WikiVet English - User contributions [en]

Hyoid Apparatus - Anatomy & Physiology

2009-09-28T12:35:14Z

Karag7: /* The hyoid bones */

{{toplink
|backcolour =CDE472
|linkpage =Musculoskeletal System - Anatomy & Physiology
|linktext =Musculoskeletal System
|maplink = Musculoskeletal System (Content Map) - Anatomy & Physiology
|pagetype =Anatomy
}}
 
==Introduction==

The hyoid apparatus holds the [[Larynx - Anatomy & Physiology|larynx]] in place and supports the [[Pharynx - Anatomy & Physiology|pharynx]] and [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]] from the skull.

It is made up of 5 different bones which vary in length and size depending on the species.
[[Image:Hyoid Anatomy.jpg|thumb|right|150px|Hyoid Apparatus in situ - Copyright Nottingham]]
==Structure and Function==

*Attached to the temporal region of the skull by a [[Joints - Anatomy & Physiology#Cartilaginous Joints|synchondrosis]]

*Palpable through [[Pharynx - Anatomy & Physiology|pharynx]]

*Visible when the [[Pharynx - Anatomy & Physiology|pharynx]] is viewed through the mouth

*Basihyoid is palpable within the intermandibular space

*Sternohyoid muscle pulls hyoid caudally

*Geniohyoid muscle pulls hyoid rostrally
[[Image:Hyoid Bones.jpg|thumb|right|150px|Hyoid Apparatus Drawing - Copyright nabrown]]
===The hyoid bones===

*Basihyoid
**Lingual process present in some species which protrudes into the roof of the [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]]
**Unpaired

*Stylohyoid
**Articulates with base of skull at petrus temporal
**Paired

*Epihyoid
**Paired

*Keratohyoid
**Paired

*Thyrohyoid
**Articulates with [[Larynx - Anatomy & Physiology#Thyroid Cartilage|thyroid cartilage]] of [[Larynx - Anatomy & Physiology|larynx]]
**Paired

==Species Differences==
[[Image:Canine Hyoid.jpg|thumb|right|150px|Canine hyoid apparatus - Copyright Nottingham]]
===Carnivores===
*Stylohyoid bones not palpable

===Equine===
*Epihyoid small

*Lingual process present

*Well developed stylohyoid muscle

===Ruminants===
*Lingual process present

===Porcine===
*Lingual process present

==Links==

[[Hyoid Apparatus - Musculoskeletal - Flashcards|Hyoid Apparatus Flashcards]]

Pharynx - Anatomy & Physiology

2009-09-28T12:32:05Z

Karag7: /* Muscles that shorten */

{{review}}

{{toplink
|linkpage =Cardiorespiratory System - Anatomy & Physiology
|linktext =Cardiorespiratory System
|maplink = Cardiorespiratory System (Content Map) - Anatomy & Physiology
|pagetype =Anatomy
|sublink1=Musculoskeletal System - Anatomy & Physiology
|subtext1=MUSCULOSKELETAL SYSTEM
}}
 

==Introduction==
[[Image:Developing Head.jpg|thumb|right|150px|Developing Head - Copyright RVC]]
The pharynx is part of both the [[Cardiorespiratory System - Anatomy & Physiology|respiratory]] and [[Alimentary - Anatomy & Physiology|digestive]] system. Both systems have entrances to the pharynx but they are separated from each other by the [[Soft Palate - Anatomy & Physiology|soft palate]].

During exercise or during respiratory distress, the mouth can be used as an additional opening of the respiratory system and then the [[Oral Cavity - Oropharynx - Anatomy & Physiology|oropharynx]] also becomes an air-way.

The pharynx can be split into different regions- the [[Oral Cavity - Oropharynx - Anatomy & Physiology|oropharynx]], [[Larynx - Anatomy & Physiology#Laryngeal Pharynx|laryngeal pharynx]] (sometimes referred to as the oesophageal pharynx) and the [[Nasopharynx - Anatomy & Physiology|nasopharynx]]
[[Image:Nasopharynx.jpg|thumb|right|150px|Nasopharynx Anatomy - Copyright RVC]]
==Structure and Function==

*Opening of the [[Larynx - Anatomy & Physiology|larynx]] is on the floor of the pharynx

*Caudal and dorsal to the laryngeal opening is the opening into the [[Oesophagus - Anatomy & Physiology|oesophagus]]

*In the dorsal region of the [[Nasopharynx - Anatomy & Physiology|nasopharynx]] there are paired openings into the Auditory (Eustacian) Tubes

*The lining of the middle ear cavity and auditory tube is continuous with that of the [[Nasopharynx - Anatomy & Physiology|nasopharynx]]

*Located between the base of the skull and the first two cervical vertebrae dorsally

*[[Larynx - Anatomy & Physiology|larynx]] ventrally

*[[Skull and Facial Muscles - Anatomy & Physiology#Mandible (mandibula)|Mandible]], pterygoid muscles and [[Hyoid Apparatus - Anatomy & Physiology|hyoid apparatus]] laterally

*Walls contain striated muscle
[[Image:Pharynx Anatomy.jpg|thumb|right|150px|Pharynx Labelled - Copyright C.Clarkson and T.F.Fletcher University of Minnesota]]
*During [[Deglutition|swallowing]] the [[Soft Palate - Anatomy & Physiology|soft palate]] is raised which divides the pharynx into dorsal and ventral sections
**Laterally, two pairs of palatopharyngeal arches are present from the [[Soft Palate - Anatomy & Physiology|soft palate]] to the [[Oesophagus - Anatomy & Physiology|oesophagus]]
**The dorsal compartment is the [[Nasopharynx - Anatomy & Physiology|nasopharynx]]
**The rostral compartment is the [[Oral Cavity - Oropharynx - Anatomy & Physiology|oropharynx]]

*The [[Larynx - Anatomy & Physiology#Laryngeal Pharynx|laryngeal pharynx]] is separated from the [[Oral Cavity - Oropharynx - Anatomy & Physiology|oropharynx]] by the [[Epiglottis|epiglottis]]

*[[Tonsils - Anatomy & Physiology|Tonsils]] are present on the lateral walls of the [[Oral Cavity - Oropharynx - Anatomy & Physiology|oropharynx]]
**Covered by flaps of mucosa
**Partially visible in the open mouth

*The pharynx plays an important role in [[Deglutition|deglutition]]
[[Image:Soft Palate Separating Pharyngeal Cavities.jpg|thumb|right|150x|Soft palate dividing the oropharynx and the nasopharynx - Copyright RVC]]

==Musculature==

===Muscles that constrict===

*Run dorsally to roof of pharynx

*Rostral constrictor muscles are the '''hyopharyngeous''', '''pterygopharyngeous''' and the '''palatopharyngeous muscles'''
**Originate from the [[Tonsils - Anatomy & Physiology#Pterygoid Bone (os pterygoideum)|pterygoid]] region of the skull and the aponeurosis of the [[Soft Palate - Anatomy & Physiology|soft palate]]
**Shorten the pharynx

*Middle constictor muscle is the '''thyopharyngeous muscle'''
**Origniates from the [[Hyoid Apparatus - Anatomy & Physiology|hyoid bone]]

*Caudal constictor muscles are the '''cricopharyngeous muscle'''
**Originates from the [[Larynx - Anatomy & Physiology#Thyroid Cartilage|thyroid cartilage]] of the [[Larynx - Anatomy & Physiology|larynx]]

===Muscles that dilate===

*Enclose pharynx laterally and dorsally

*Dilator muscle is the '''stylopharyngeous muscle'''

*Originates from the [[Hyoid Apparatus - Anatomy & Physiology|hyoid apparatus]]

*Widens the rostral pharynx

===Muscles that shorten===

*The '''pterygopharyngeal muscle''' and '''palatopharyngeal muscle''' shorten the pharynx

*Enclose pharynx laterally and dorsally

===Muscles that close the Pharyngeal Arch===

*The '''palatopharyngeous muscle''' also closes the pharyngeal arch

==Innervation==

*Pharyngeal muscles arise from arch 4

*Pharyngeal branch of the vagus nerve ([[Cranial Nerves - Anatomy & Physiology|CN X]]) from the cranial root of the accessory nerve ([[Cranial Nerves - Anatomy & Physiology|CN XI]])

*Stylopharyngeous muscle comes from arch 3 and is innervated by the accessory nerve ([[Cranial Nerves - Anatomy & Physiology|CN XI]])
*Glossopharyngeal nerve ([[Cranial Nerves - Anatomy & Physiology|CN IX]]) supplies taste to the pharynx
[[Image:Pharyngeal Tonsil.jpg|thumb|right|150px|Histology of Pharyngeal Tonsil - Copyright RVC]]
==Histology==

*Fibroelastic aponeurosis supports the mucosa

*[[Nasopharynx - Anatomy & Physiology|nasopharynx]] has pseudostratified columnar epithelium

*[[Oral Cavity - Oropharynx - Anatomy & Physiology|oropharynx]] and the [[Larynx - Anatomy & Physiology#Laryngeal Pharynx|laryngeal pharynx]] have stratified squamous epithelium

*[[Oral Cavity - Oropharynx - Anatomy & Physiology|oropharynx]] and the [[Larynx - Anatomy & Physiology#Laryngeal Pharynx|laryngeal pharynx]] have [[Oral Cavity - Salivary Glands - Anatomy & Physiology|salivary glands]] present
[[Image:Pharynx Anatomy.jpg|thumb|right|150px|Palatine Tonsil - Copyright C.Clarkson and T.F.Fletcher University of Minnesota]]
==Species Differences==

====Canine====
*Single duct connects [[Nasopharynx - Anatomy & Physiology|nasopharynx]] to the [[Nasal cavity - Anatomy & Physiology|nasal cavity]]

*[[Tonsils - Anatomy & Physiology|Tonsils]] are a compact mass which point away from the lumen of the pharynx

====Equine====
*Auditory tube opens into the [[Ear - Anatomy & Physiology#Equine Gutteral Pouch|gutteral pouch]]

*[[Tonsils - Anatomy & Physiology|Tonsils]] are diffuse and raised slightly

====Ruminants====
*[[Tonsils - Anatomy & Physiology|Tonsils]] are a compact mass which point towards the lumen of the pharynx

==Links==

[[Oral Cavity - Oropharynx - Anatomy & Physiology|Oropharynx - Anatomy & Physiology]]

[[Nasopharynx - Anatomy & Physiology]]

[[Larynx - Anatomy & Physiology#Laryngeal Pharynx|laryngeal pharynx]]

[[Pharynx - Musculoskeletal - Flashcards|Pharynx Flashcards]]

Equine Infectious Anemia

2009-09-18T11:09:18Z

Karag7: /* Epidemiology */

{{unfinished}}

{{toplink
|linkpage =Viruses
|linktext =VIRUSES
|sublink1=Retroviridae
|subtext1=RETROVIRIDAE
|pagetype =Bugs
}}
 

====Pathogenesis====
*Virus coats red blood cells and thrombocytes
*'''Type III Immune complex disease''' develops
*Non-neutralizing antibody and complement lyse RBC's, causing:
**Jaundice
**Vasculitis
**Hemorrhage
**Diarrhoea
**Loss of condition
**Oedema
**High mortality

====Epidemiology====
*'''Notifiable''' in UK but '''endemic''' in parts of the US
*Animals can be '''carriers''' for years despite being '''antibody-positive'''
*Transfer is '''mechanical''' via '''vectors''':
**'''Mosquitoes''' transfer infected '''macrophages
*Also transferred via infected needles, semen and milk
*Infected horses have '''lifetime latent infection of macrophages''' with recurring bouts of virus when '''immunocompromised'''

====Diagnosis====
*'''Coggins test''' required for horse movement in the US:
**Serum '''antibody''' by '''immunodiffusion''' in infected horse spleen

====Control====
*Slaughter of infected animal
*2 clear Coggins tests of all horses before movement allowed
*Vector control: stabling, etc.

Equine Influenza

2009-09-17T14:46:50Z

Karag7: /* Control */

{{unfinished}}

{{toplink
|linkpage =Viruses
|linktext =VIRUSES
|sublink1=Orthomyxoviridae
|subtext1=INFLUENZA
|pagetype =Bugs
}}
 

===Subtypes===
*Two subtypes of Equine Influenza have been described:
**H7N7 (Equine 1), which was prevalent in the UK between 1963-1977
**H3N8 (Equine 2), or the European strains, have been circulating since 1965
*Some drift has occurred, causing outbreaks of North-American-like strains of H3N8 in 1998 (EU) and 2003 (South America)
===Pathogenesis===
*Aerosol and fomite transmission infects the epithelium of the upper respiratory tract, resulting in cell necrosis
*This manifests a bronchiolitis and serous exudation
*1-3 day incubation period
*Excretion of the virus in nasal secretions peaks at 3-4 days and finishes by 10 days
*Clinical signs:
**Harsh dry cough
**Pyrexia (103-106F)
**Depression
**Loss of appetite
**Enlarged submandibular lymph nodes
*Secondary bacterial infection can follow defective muco-ciliary transport, eg ''Streptococcus zooepidemicus''
*For more, see [[Respiratory Viral Infections - Pathology#Equine influenza|here]]
===Diagnosis===
*Virus isolation: Deep nasal swabs (12 inches) deposited into 10ml of transport medium and transported at 4C
*Antigen detection via ELISA: tests for type A nucleoprotein
*Serology provides a retrospective diagnosis by '''Haemagglutination Inhibition (HI)''':
**Acute and Convalescent (2 weeks post-acute) samples are tested from the same animal
**4-fold increase of HI must be shown to confirm diagnosis
===Control===
*Isolate coughing horses to minimize spread
*Vaccination:
**All vaccines include H7 and varieties of the current circulating strains of H3
**'''Inactivated''' egg-grown vaccine is produced with alhydrogel as an adjuvant
**'''Live''' vaccines using purified haemagglutinin do not require adjuvants
**UK Jockey Club rules regarding timing:
***Horses must be certified as completing a vaccination course of 3 injections at least 8 days prior to racing
***The course consists of a primary inoculation followed by a second within 21-92 days and a third after a further 150-215 days
***Boosters are given annually to maintain immunity, and in the event a year is missed the initial course of three jabs must be repeated

Canine Breeds - WikiNormals

2009-09-11T10:33:42Z

Karag7: /* Dangerous Dogs Act 1991 */

{{toplink
|linkpage =WikiNormals
|linktext =WikiNormals
|maplink = WikiNormals Content Map
|pagetype =WikiNormals
|sublink1= Canine Section - WikiNormals
|subtext1= Canine Section
}}
 
===Overview===
The following breeds have been classified according to The Kennel Club guidelines. Any breed not part of these guidelines has been omitted, excluding the Dangerous Dogs section. The descriptions for each group are also from The Kennel Club. For further information regarding a specific breed please see http://www.thekennelclub.org.uk/.

===Gundog Group===
*Dogs that were originally trained to find live game and/or to retrieve game that had been shot and wounded. This group is divided into four categories - Retriever, Spaniels, Hunt/Point/Retrieve and Setters.^
<gallery widths="115px" perrow="6">
Image:Bracco_Italiano.jpg|'''Bracco Italiano'''WikiCommons
Image:Brittany.jpg|'''Brittany'''WikiCommons
Image:English_setter.jpg|'''English Setter'''Wikicommons
Image:German_Long-Haired_Pointer.jpg|'''German Long-Haired Pointer'''WikiCommons
Image:German-shorthaired-pointer.jpg|'''German Short-Haired Pointer'''dogfacts.org
Image:German_wirehaired_pointer.jpg|'''German Wire-Haired Pointer'''breederretriver.com
Image:Gordon_setter.jpg|'''Gordon Setter'''dyreweb.no
Image:Hungarian_Vizsla.jpg|'''Hungarian Vizsla'''WikiCommons
Image:Hungarian_Vizsla_Wirehaired.jpg|'''Hungarian Wirehaired Vizsla'''WikiCommons
Image:Irish_red_and_white_setter.jpg|'''Irish Red and White Setter'''WikiCommons
Image:Irish_Setter.jpg|'''Irish Setter'''WikiCommons
Image:Italian_Spinone.jpg|'''Italian Spinone'''WikiCommons
Image:Kooiker.jpg|'''Kooikerhondje'''WikiCommons
Image:Korthalsgriffon.jpg|'''Korthals Griffon'''WikiCommons
Image:Lagotto_Romagnolo.jpg|'''Lagotto Romagnolo'''WikiCommons
Image:Large_munsterlander.jpg|'''Large Munsterlander'''munsterlandersatlarge.com
Image:Pointer.jpg|'''Pointer'''WikiCommons
Image:Chesapeake_Bay_Retriever.jpg|'''Retriever (Chesapeake Bay)'''WikiCommons
Image:Curly_Coated_Retriever.jpg|'''Retriever (Curly Coated)'''WikiCommons
Image:Flat_Coated_Retriever.jpg|'''Retriever (Flat Coated)'''WikiCommons
Image:Golden-retriever.jpg|'''Retriever (Golden)'''WikiCommons
Image:labrador.jpg|'''Retriever (Labrador)'''WikiCommons
Image:Tollers.jpg|'''Retriever (Nova Scotia Duck Tolling)'''WikiCommons
Image:Slovakian_rough_haired_pointer.jpg|'''Slovakian Rough Haired Pointer'''WikiCommons
Image:Small_munsterlander.jpg|'''Small Munsterlander'''WikiCommons
Image:American_cocker_spaniel.jpg|'''Spaniel (American Cocker)'''dogsindepth.com
Image:American_water_spaniel.JPG‎|'''Spaniel (American Water)'''WikiCommons
Image:Clumber_spaniel.jpg‎|'''Spaniel (Clumber)'''WikiCommons
Image:Cocker_spaniel.jpg‎|'''Spaniel (English Cocker)'''WikiCommons
Image:Field_spaniel.jpg‎|'''Spaniel (Field)'''WikiCommons
Image:Irish_water_spaniel.jpg‎|'''Spaniel (Irish Water)'''WikiCommons
Image:Sussex_spaniel.jpg‎|'''Spaniel (Sussex)'''WikiCommons
Image:Welsh_Springer_Spaniel.jpg‎|'''Spaniel (Welsh Springer)'''WikiCommons
Image:SpanishWaterDog.JPG‎|'''Spanish Water Dog'''dogbreedinfo.com
Image:Weimaraner.jpg‎|'''Weimaraner'''WikiCommons

</gallery>

===Hound Group===
*Traditionally used for hunting by scent or sight. They require a significant amount of exercise and can be described as dignified, aloof but trustworthy companions.^
<gallery widths="115px" perrow="6">
Image:Afghan Hound.jpg|'''Afghan Hound'''WikiCommons
Image:Basenji.jpg|'''Basenji'''WikiCommons
Image:Basset_bleu_de_Gascogne.jpg|'''Basset Bleu De Gascogne'''WikiCommons
Image:Basset_Fauve_de_Bretagne.jpg|'''Basset Fauve De Bretagne'''WikiCommons
Image:Grand_Basset_Griffon_Vendeen.jpg|'''Basset Griffon Vendeen (Grand)'''WikiCommons
Image:Petit_BGV.jpg|'''Basset Griffon Vendeen (Petit)'''WikiCommons
Image:Bassethound.jpg|'''Bassethound'''WikiCommons
Image:Bavarian_Mountain_Hound.jpg|'''Bavarian Mountain Hound'''WikiCommons
Image:Beagle.jpg|'''Beagle'''WikiCommons
Image:Bloodhound.jpg|'''Bloodhound'''WikiCommons
Image:Borzoi.jpg|'''Borzoi'''WikiCommons
Image:Cirneco_dell_Etna.jpg|'''Cirneco Dell'Etna'''WikiCommons
Image:Minature_Dachshund.jpg|'''Dachshund (Miniature)'''WikiCommons
Image:Standard_Dachshund_(Short-haired).jpg|'''Dachshund (Standard Short-haired)'''WikiCommons
Image:Deerhound.jpg|'''Deerhound'''WikiCommons
Image:Finnish_Spitz.jpg|'''Finnish Spitz'''WikiCommons
Image:English_Foxhound.jpg|'''Foxhound'''dogfacts.org
Image:Grand_bleu_de_gascogne.jpg|'''Grand Bleu De Gascogne'''vdh.de
Image:Greyhound.jpg|'''Greyhound'''WikiCommons
Image:Hamiltonstovare.jpg|'''Hamiltonstovare'''WikiCommons
Image:Ibizan_Hound.jpg|'''Ibizan Hound'''WikiCommons
Image:Irish_Wolfhound.jpg|'''Irish Wolfhound'''WikiCommons
Image:Norwegian_Elkhound.jpg|'''Norwegian Elkhound'''WikiCommons
Image:Otterhound.jpg|'''Otterhound'''WikiCommons
Image:Pharaoh_Hound.jpg|'''Pharaoh Hound'''WikiCommons
Image:Portuguese_Podengo.jpg|'''Portuguese Podengo'''WikiCommons
Image:Rhodesian_Ridgeback.jpg|'''Rhodesian Ridgeback'''WikiCommons
Image:Saluki.jpg|'''Saluki'''WikiCommons
Image:Segugio_italiano.jpg|'''Segugio Italiano'''dogspot.de
Image:Sloughi.jpg|'''Sloughi'''WikiCommons
Image:Whippet.jpg|'''Whippet'''WikiCommons

</gallery>

===Pastoral Group===
*Herding dogs that are associated with working cattle, sheep, reindeer and other cloven footed animals. Usually this type of canine has a weatherproof double coat to protect it from the elements when working in severe conditions.^
<gallery widths="115px" perrow="6">
Image:Anatolian.jpg|'''Anatolian Shepherd Dog'''WikiCommons
Image:AustrCattleDog.jpg|'''Australian Cattle Dog'''WikiCommons
Image:Australian_Shepherd.jpg|'''Australian Shepherd Dog'''WikiCommons
Image:Bearded_Collie.jpg|'''Bearded Collie'''WikiCommons
Image:Belgian_Shepherd.jpg|'''Belgian Shepherd Dog (Groenendael)'''WikiCommons
Image:Belgian_Laekenois.jpg|'''Belgian Shepherd Dog (Laekenois)'''WikiCommons
Image:Belgian_Mali.jpg|'''Belgian Shepherd Dog (Malinois)'''WikiCommons
Image:Belgian_Tervuren.jpg|'''Belgian Shepherd Dog (Tervuren)'''WikiCommons
Image:Bergamasco.jpg|'''Bergamasco'''WikiCommons
Image:Border_Collie.jpg|'''Border Collie'''WikiCommons
Image:Briard.JPG|'''Briard'''WikiCommons
Image:Catalan_Sheepdog.jpg|'''Catalan Sheepdog'''WikiCommons
Image:Rough_Collie.jpg|'''Collie (Rough)'''WikiCommons
Image:Smooth_Collie.jpg|'''Collie (Smooth)'''WikiCommons
Image:ESTRELA_MOUNTAIN_DOG.jpg|'''Estrella Mountain Dog'''WikiCommons
Image:Finnish_Lapphund.jpg|'''Finnish Lapphund'''WikiCommons
Image:GermanShep.jpg|'''German Shepherd (Alsatian)'''WikiCommons
Image:Hungarian_Kuvasz.jpg|'''Hungarian Kuvasz'''WikiCommons
Image:Puli.jpg|'''Hungarian Puli'''WikiCommons
Image:Komondor.jpg|'''Komondor'''WikiCommons
Image:Lancashire_Heeler.jpg|'''Lancashire Heeler'''WikiCommons
Image:Maremma.JPG|'''Maremma Sheepdog'''WikiCommons
Image:Norwegian_Buhund.jpg|'''Norwegian Buhund'''WikiCommons
Image:Old_English_Sheepdog.jpg|'''Old English Sheepdog'''WikiCommons
Image:Polish_Lowland_Sheepdog.jpg|'''Polish Lowland Sheepdog'''WikiCommons
Image:Pyrenean_Mountain_Dog.jpg|'''Pyrenean Mountain Dog'''WikiCommons
Image:Pyrenean-Sheepdog.jpg|'''Pyrenean Sheepdog'''breedersonline.co.uk
Image:Samoyed.jpg|'''Samoyed'''WikiCommons
Image:Shetland.jpg|'''Shetland Sheepdog'''WikiCommons
Image:Swedish_lapphund.JPG|'''Swedish Lapphund'''WikiCommons
Image:swedish_vallhund.jpg|'''Swedish Vallhund'''WikiCommons
Image:Cardigan_Welsh_Corgi.jpg|'''Welsh Corgi (Cardigian)'''WikiCommons
Image:Pembroke_Welsh_Corgi.jpg|'''Welsh Corgi (Pembroke)'''WikiCommons

</gallery>

===Terrier Group===
*Dogs originally bred and used for hunting vermin. This hardy collection of dogs were selectively bred to be extremely brave and tough, and to pursue fox, badger, rat and otter (to name but a few) above and below ground.^
<gallery widths="115px" perrow="6">
Image:Airedale_Terrier.jpg|'''Airedale Terrier'''WikiCommons
Image:Aus_Terrier.jpg|'''Australian Terrier'''WikiCommons
Image:Bedlington.jpg|'''Bedlington Terrier'''WikiCommons
Image:Border_terrier.jpg|'''Border Terrier'''WikiCommons
Image:Bull_Terrier.jpg|'''Bull Terrier'''WikiCommons
Image:Miniature_bull_terrier.jpg|'''Bull Terrier (Miniature)'''breedersonline.co.uk
Image:Cairn_terrier.JPG|'''Cairn Terrier'''WikiCommons
Image:Cesky_terrier.jpg|'''Cesky Terrier'''ridleyceskyterriers.co.uk
Image:Dandie_Dinmont_Terrier.jpg|'''Dandie Dinmont Terrier'''WikiCommons
Image:Fox_terrier_smooth.jpg|'''Fox Terrier (Smooth)'''WikiCommons
Image:Fox_terrier_wire.jpg|'''Fox Terrier (Wire)'''WikiCommons
Image:Glen_of_imaal_terrier.jpg|'''Glen Of Imaal Terrier'''WikiCommons
Image:Irish_terrier.jpg|'''Irish Terrier'''WikiCommons
Image:Kerry_blue_terrier.jpg|'''Kerry Blue Terrier'''WikiCommons
Image:Lakeland_terrier.jpg|'''Lakeland Terrier'''WikiCommons
Image:Manchester_terrier.jpg|'''Manchester Terrier'''WikiCommons
Image:Norfolk_terrier.jpg|'''Norfolk Terrier'''WikiCommons
Image:Norwich_terrier.jpg|'''Norwich Terrier'''WikiCommons
Image:Parson_russell_terrier.jpg|'''Parson Russell Terrier'''WikiCommons
Image:Scottish_terrier.jpg|'''Scottish Terrier'''WikiCommons
Image:Sealyham_terrier.jpg|'''Sealyham Terrier'''WikiCommons
Image:Skye_terrier.jpg|'''Skye Terrier'''WikiCommons
Image:Soft_coated_wheaten_terrier.jpg|'''Soft Coated Wheaten Terrier'''WikiCommons
Image:Staffordshire_bull_terrier.jpg|'''Staffordshire Bull Terrier'''WikiCommons
Image:Welsh_Terrier.png|'''Welsh Terrier'''WikiCommons
Image:West_highland_white_terrier.jpg|'''West Highland White Terrier'''WikiCommons

</gallery>

===Toy Group===
*Small companion or lap dogs. Many of the Toy breeds were bred for this capacity although some have been placed into this category due to their size. They should have friendly personalities and love attention. They do not need a large amount of exercise and some can be finicky eaters.^
<gallery widths="115px" perrow="6">
Image:Affenpinscher.jpg|'''Affenpinscher'''WikiCommons
Image:Australian_Silky_Terrier.JPG|'''Australian Silky Terrier'''Kennel Club
Image:Bichon_Frise.jpg|'''Bichon Frise'''WikiCommons
Image:Bolognese.jpg|'''Bolognese'''WikiCommons
Image:Cavalier_king_charles_spaniel.jpg|'''Cavalier King Charles Spaniel'''WikiCommons
Image:Chihuahualongcoat.jpg|'''Chihuahua (Long Coat)'''WikiCommons
Image:Chihuahuasmoothcoat.jpg|'''Chihuahua (Smooth Coat)'''WikiCommons
Image:Chinese_Crested.jpg|'''Chinese Crested'''WikiCommons
Image:Coton_de_Tular.jpg|'''Coton de Tular'''WikiCommons
Image:English_Toy_Terrier.jpg|'''English Toy Terrier'''WikiCommons
Image:Griffon_Bruxellois.jpg|'''Griffon Bruxellois'''Kennels.co.uk
Image:Havanese.jpg|'''Havanese'''WikiCommons
Image:Italian_Greyhound.jpg|'''Italian Greyhound'''WikiCommons
Image:Japanese_Chin.jpg|'''Japanese Chin'''WikiCommons
Image:King_Charles_Spaniel.jpg|'''King Charles Spaniel'''WikiCommons
Image:Lowchen.jpg|'''Lowchen'''WikiCommons
Image:Maltese.jpg|'''Maltese'''WikiCommons
Image:miniature_pinscher.jpg|'''Miniature Pinscher'''WikiCommons
Image:Papillon.jpg|'''Papillon'''petplanet.co.uk
Image:Pekingese.jpg|'''Pekingese'''WikiCommons
Image:Pomeranian.jpg|'''Pomeranian'''WikiCommons
Image:Pug.jpg|'''Pug'''WikiCommons
Image:Yorkshire_Terrier.jpg|'''Yorkshire Terrier'''WikiCommons

</gallery>

===Working Group===
*Over the centuries these dogs were selectively bred to become guards and search and rescue dogs. Arguably, the working group consists of some of the most heroic canines in the world, aiding humans in many walks of like, including the Boxer, Great Dane and St. Bernard.^
<gallery widths="115px" perrow="6">
Image:Alaskan_Malamute.jpg|'''Alaskan Malamute'''WikiCommons
Image:Beauceron.jpg|'''Beauceron'''WikiCommons
Image:Bernese_mountain_dog.jpg|'''Bernese Mountain Dog'''WikiCommons
Image:Bouvier_des_Flandres.jpg|'''Bouvier Des Flandres'''WikiCommons
Image:Boxer.jpg|'''Boxer'''dogsindepth.com
Image:Bull_mastiff.jpg|'''Bull Mastiff'''aboutpedigreedogs.com
Image:Canadian_Eskimo_Dog.jpg|'''Canadian Eskimo Dog'''WikiCommons
Image:Dobermann.jpg|'''Dobermann'''WikiCommons
Image:Dogue_de_Bordeaux.jpg|'''Dogue De Bordeaux'''WikiCommons
Image:Entlebucher_Mountain_Dog.jpg|'''Entlebucher Mountain Dog'''WikiCommons
Image:Pinscher.jpg|'''German Pinscher'''WikiCommons
Image:GiantSchnauzer.jpg|'''Giant Schnauzer'''WikiCommons
Image:greatdane.jpg|'''Great Dane'''WikiCommons
Image:Swiss_mdog.jpg|'''Greater Swiss Mountain Dog'''WikiCommons
Image:Greenland_dog.jpg|'''Greenland Dog'''WikiCommons
Image:Hovawart.jpg|'''Hovawart'''WikiCommons
Image:Leonberger.jpg|'''Leonberger'''WikiCommons
Image:Mastiff.JPG|'''English Mastiff'''WikiCommons
Image:Neapolitan-mastiff.jpg|'''Neapolitan Mastiff'''gotpetsonline.com
Image:Newfoundland.jpg|'''Newfoundland'''WikiCommons
Image:pwaterdog.jpg|'''Portuguese Water Dog'''WikiCommons
Image:Pmdog.jpg|'''Pyrenean Mastiff'''WikiCommons
Image:Rottweiler.jpg|'''Rottweiler'''WikiCommons
Image:Russianblack.jpg|'''Russian Black Terrier'''WikiCommons
Image:Stbernard.jpg|'''St. Bernard'''WikiCommons
Image:Siberian-husky.jpg|'''Siberian Husky'''WikiCommons
Image:Tmastiff.jpg|'''Tibetan Mastiff'''WikiCommons

</gallery>

===Utility Group===
*The name "Utility" basically means fitness for a purpose and this group consists of an extremely mixed and varied bunch, most breeds having been selectively bred to perform a specific function not included in the sporting and working categories.^
<gallery widths="115px" perrow="6">
Image:Akita.jpg|'''Akita'''WikiCommons
Image:Boston_terrier.jpg|'''Boston Terrier'''WikiCommons
Image:Bulldog.jpg|'''Bulldog'''WikiCommons
Image:Canaandog.jpg|'''Canaan Dog'''WikiCommons
Image:Chow_chow.jpg|'''Chow Chow'''WikiCommons
Image:Dalmatian.jpg|'''Dalmatian'''WikiCommons
Image:Eurasier.jpg|'''Eurasier'''WikiCommons
Image:French_bulldog.jpg|'''French Bulldog'''WikiCommons
Image:German_spitz.jpg|'''German Spitz (Klien)'''WikiCommons
Image:German_spitz_mittal.jpg|'''German Spitz (Mittal)'''WikiCommons
Image:Japanese_akita.jpg|'''Japanese Akita'''WikiCommons
Image:Japanese_shiba.jpg|'''Japanese Shiba'''WikiCommons
Image:Japanese_spitz.jpg|'''Japanese Spitz'''WikiCommons
Image:Keeshond.jpg|'''Keeshond'''WikiCommons
Image:Korean_Jindo.jpg|'''Korean Jindo'''WikiCommons
Image:Lhasa_apso.jpg|'''Lhasa Apso'''WikiCommons
Image:Mexican_hairless.jpg|'''Mexican Hairless (Standard/Miniature)'''WikiCommons
Image:Miniature_schnauzer.jpg|'''Miniature Schnauzer'''WikiCommons
Image:Miniature_Poodle.jpg|'''Miniature Poodle'''WikiCommons
Image:Standard_poodle.jpg|'''Standard Poodle'''WikiCommons
Image:Toy_poodle1.jpg|'''Toy Poodle'''WikiCommons
Image:Schipperke.jpg|'''Schipperke'''WikiCommons
Image:Schnauzer.jpg|'''Schnauzer (Standard)'''WikiCommons
Image:Shar_pei.jpg|'''Shar Pei'''WikiCommons
Image:Shih_tzu.jpg|'''Shih Tzu'''WikiCommons
Image:Tibetan_spaniel.jpg|'''Tibetan Spaniel'''WikiCommons
Image:Tibetan_terrier.jpg|'''Tibetan Terrier'''WikiCommons

</gallery>

===Dangerous Dogs Act 1991===
*It is an offence to own or keep any of the types of dog listed below, unless it is on the Index of Exempted Dogs and is in compliance with the requirements. In any event it is an offence to breed from, sell or exchange (even as a gift) such a dog, irrespective of whether it has been placed on the Index of Exempted Dogs.^^ See http://www.defra.gov.uk/animalh/welfare/domestic/dogs.htm

<gallery widths="115px" perrow="6">
Image:pit_bull.jpg|'''American Pit Bull Terrier'''WikiCommons
Image:tosa.JPG|'''Japanese Tosa'''dogbreedinfo.com
Image:dogo.JPG|'''Dogo Argentino'''WikiCommons
Image:fila.jpg|'''Fila Brasileiro'''pedigreedatabase.com

</gallery>

{|width="700px" align="center"
{{citation
|initiallast = ^
|initialfirst =
|2last =
|2first =
|3last =
|3first =
|year = 2006
|title = Breed Group Listings
|ed =
|city = London
|pub = The Kennel Club
|range =
}}

{|width="700px" align="center"
{{citation
|initiallast = ^^
|initialfirst =
|2last =
|2first =
|3last =
|3first =
|year = 1991
|title = Dangerous Dogs Act
|ed = Department for Environmental, Food and Rural Affairs
|city = London
|pub = Government Legislation
|range =
}}
|}

Respiratory Gas Analysis

2009-09-03T13:00:35Z

Karag7: /* End-Tidal Carbon Dioxide */

{{unfinished}}
{{toplink
|linkpage =Anaesthesia
|linktext =Anaesthesia
|maplink= Anaesthesia Content Map - WikiClinical
|sublink1=Monitoring Anaesthesia
|subtext1=Monitoring Anaesthesia
|pagetype=Clinical
}}
 
==Introduction==
Most patients undergoing a general anaesthetic are maintained on inhalation agents and therefore in a situation where they will be connected to an anaesthetic machine. This means that with the inhalation agent, oxygen or medical air will also be delivered as well as nitrous oxide in some cases. It is important, as in any anaesthetic, to monitor the respiratory function of the patient, including respiratory rate, rhythm, and effort, as well end-tidal carbon dioxide and anaesthetic agent levels if the equipment is available to do so.

==End-Tidal Carbon Dioxide==
End-tidal carbon dioxide is often measured via capnometry and capnography.
*''Capnometry'' is the numerical display of carbon dioxide levels in the respiratory gas throughout the cycle.
*''Capnography'' is the graphical display of carbon dioxide levels in the respiratory gas throughout the cycle.
Capnometers are either ''sidestream'' or ''mainstream''. In sidestream capnometers, a sample line is attached to a small connector which is placed between the endotracheal tube and breathing system. Mainstream capnometer sampling chambers are small enough that they can be fitted directly to the endotracheal tube between that and the breathing system. Readings are based on absorption of infrared light by carbon dioxide.

===Capnograph===
[[Image:Capnograph.JPG|left]]

<center>
{| border="0.5" cellpadding="6"
|-style="background:#B0E0E6; color:black"
!'''Stage'''
!'''Represents'''
|-
| '''A''' 
|Exhalation of Carbon Dioxide from dead space.
End tidal carbon dioxide should be zero at this point
|- style="background:#F0F8FF; color:black"
|'''B''' 
|Start of phase 1.

The beginning of the respiratory upstroke.
|-
|'''C''' 
|End of phase 1.

The beginning of the expiratory plateau.
|- style="background:#F0F8FF; colour:black"
|'''D''' 
|End of the expiratory plateau.
This is the maximum end tidal carbon dioxide level.

It is the beginning of the inspiration and phase 4.
|-
|'''E''' 
|End of inspiration.
End tidal carbon dioxide should reach zero at this point.
|-
|}
</center>

* Phase 1 is the inspiratory baseline and indicates inspired carbon dioxide, therefore should be zero.
* Phase 2 is the expiratory upstroke and indicates the alveoli and conducting airway carbon dioxide levels.
* Phase 3 is the expiratory plateau which indicates pure alveoli carbon dioxide levels.
* Phase 4 is the inspiratory downstroke indicating the start of inspiration.

===Increases in End Tidal Carbon Dioxide===
*Impaired alveolar ventilation.
*Increased metabolism.
*Increased cardiac output.
*Rebreathing.

===Decreases in End Tidal Carbon Dioxide===
*Hyperventilation.
*Low cardiac output.
*Pronounced hypothermia.
*Failing circulation and cardiac arrest.

==Inhaled and Exhaled Anaesthetic Agents==
With some of the monitors now available it is also possible to monitor the inhaled and exhaled anaesthetic agent concentration. This allows monitoring of dosing of inhalant anaesthetics (inhaled value) and the exhaled value indicates the concentration in the circulation and brain.

Local Anaesthetics

2009-09-03T10:01:59Z

Karag7: /* Procaine */

{{toplink
|linkpage =Anaesthesia
|linktext =Anaesthesia
|maplink= Anaesthesia Content Map - WikiClinical
|sublink1=Anaesthetic Drugs
|subtext1=Anaesthetic Drugs
|pagetype=Clinical
}}
 
==Mechanism of Action==

* Local anaethetic drugs reversibly interfere with action potential generation and conduction in the neurons around which they are administered. To reach the neuronal plasma membrane where they act, local anaethetic drugs must first enter the nerve sheath. Only molecules lacking ionic charge may do this, and so local anaesthetic agents work more effectively in an alkaline pH when charge is neutral. Once inside the sheath, the drug gains charge and can then bind to voltage-gated Na+ channels, preventing depolarisation of the cell. Local anaesthetics also infiltrate and change the composition of the cell membrane to take effect. However, they do NOT alter resting membrane potential.

* Small diameter nerve fibres are blocked before large fibres by local anaesthetics, and fibres which are myelinated are blocked before those which are unmyelinated. Therefore, A-delta fibres are blocked before C fibres, and so the sensation of pain is eliminated before that of gentle touch.

* The blocking effects of local anaethetics is more effective in neurons which are firing. This is because action potentials cause channels in the nerve sheath to cycle between open, resting inactive conformations. The drugspenetrate the sheath through open channels, and bind most readily to inactivated channels.

* Local anaesthetic drugs also cause vasodilation. To prevent this effect leading to increased systemic absorption of drug, vasoconstrictors (e.g. adrenaline) are commonly added to preparations.

==Pharmacokinetic Considerations==

Local anaesthetic agents consist of a lipid-soluble (hydrophobic) aromatic ring joined to a basic (hydrophilic) amide group. The two groups may be either:
* '''Ester linked'''
** For example, [[#Procaine|procaine]] and cocaine.
** Local anaesthetics linked in this way are less stable in solution.
** Metabolism by tissue esterases, hepatic esterases and hydrolysis occurs. Products are subsequently excreted by the kidney. However, one product of metabolism is para-amino benzoic acid (PABA), which may cause allergic reactions.
* '''Amide linked'''
** For example, [[#Lidocaine|lidocaine]] and [[#Bupivicaine|bupivicaine]].
** Amide linked local anaesthetics can be stored longer than ester-linked drugs and are heat stable.
** Metabolism is by hepatic amidases, and excretion occurs via the kidney.

===Protein Binding===

The degree of plasma protein binding of individual drugs affects their distribution within the body and the duration of their action. Drugs which have a higher degree of binding have effects for a longer period of time, and in hypoproteinaemic animals, local anaesthetics have a shorter duration of action. For example, [[#Bupivicaine|bupivicaine]] is 95% protein bound, compared to 65% for [[#Lidocaine|lidocaine]], and so its effects will persist longer.

===Ionisation===

Local anaesthetics are weak bases and so the degree of ionisation will be greatest at low pHs. Since only unionised drug can cross the nerve sheath to enter the nerve and take effect, local anaesthetics work best in alkaline surroundings where the unionised form predominates. Infected tissue has a lower pH, increasing the proportion of ionised molecules and causing poor uptake of drug. For more about the effect of pH on drugs, see the [[Pharmacokinetics#Physiological Variables|pharmacokinetics]] page.

==Side Effects and Contraindications==

Local anaesthetics may have undesirable effects on the CNS. These include termors, convulsions and respiratory depression. The cardiovasular system may also be adversely affected, with drug administration leasing to reduced cardiac contractility, vasodilation and hypotension. [[#Bupivicaine|bupivicaine]] is particularly cardiotoxic, but stereoisomerism exists. The cardio- and neuro-toxic effects of dextrobupivicaine are greatly increased compared to that of levobupivicaine. Commercially available preparations of [[#Bupivicaine|bupivicaine]] are a 50:50 mixture of the two forms of the drug.

Local anaesthetic drugs are known to reduce epithelial repair, and so it it wise to administer them away from the site of surgical incision so that healing is not impaired. Inadvertent intravenous administration of these drugs can result in tissue irritation and allergic reactions.

==Drugs in this Group==

===Lidocaine===

Lidocaine is an amide-linked local anaesthetic, which aslo has anti-arrhythmic properties. The time to onset of action is 3-10mins, after which the drug's effects last 60-90mins. The duration of action may be prolonged by the addition of adrenaline to the preparation. Lidocaine is a very cheap drug, and is a component of EMLA cream.

===Bupivicaine===

Bupivicaine is also an amide-linked local anaesthetic, but with a duration of action of around 8 hours, it is longer acting than lidocaine. It also has a longer time to onset (20-30mins). It is very cardiotoxic, casuing asystole by decreasing the force of contraction, and therefore must NOT be given intravenously.

===Mepivicaine===

Another amide-linked drug, mepivicaine has the same potency as lidocaine but is less irritant and vasodilatory. The time to onset is only 5-10 mins, and the effects last 90-180 mins. However, the drug is expensive, and is not formulated with a preservative and so the vial must be discarded once the seal is broken.

===Procaine===

Procaine is ester-linked, and so may cause allergic reactions to the PABA metabolite. It has an onset of action of 15-20 minutes and a duration of action of 45-60 minutes and may be added to penicillin to reduce pain on injection.

===Proxymetacaine===

Proxymetacaine is amide-linked. It has a 10 second onset, with 10-20 min duration. It may be used on the conjunctival sac, but is toxic to corneal epithelium with long-term use.

===EMLA===

"EMLA" stands for Eutectic Mix of Local Anaesthetic, and is formulated as a cream containing [[#Lidocain|lidocaine]] and prilocaine. It is used for topical anaesthesia of the skin, for example before venupuncture. It must be applied 30-60mins before the anticipated insult to allow absorption and effect to take place.

Barbiturates

2009-09-02T11:36:36Z

Karag7: /* Drugs in this Group */

{{unfinished}}
{{toplink
|linkpage =Anaesthesia
|linktext =Anaesthesia
|maplink= Anaesthesia Content Map - WikiClinical
|sublink1=Anaesthetic Drugs
|subtext1=Anaesthetic Drugs
|sublink2=Injectable Agents
|subtext2=Injectable Agents
|pagetype=Clinical
}}
 
The drugs within this group are '''short acting''' and have been classically used agents for anaesthesia. They produce a state of hypnosis and higher doses are required to produce an anaesthetised state but they are '''poor analgesics'''.

==Mechanism of Action==
Barbituates act by depressing the central nervous system (CNS) by acting at the ''Gamma Aminobutyric Acid A'' receptors (GABAa). They mimic and enhance GABA, which is the principle inhibitory neurotransmitter in the CNS. Once bound to the GABAa receptor they reduce the rate of GABA dissocation and thereby ''increase chloride conductance'' is maintained resulting in hyperpolarisation of the membrane and reduced neuronal excitability. However, as the concentration of barbituate increases, it starts to have a direct effect on the chloride conductance and it is this that is thought to bring about the anaesthetic effects, while the GABA related increases causes a sedative effect. They act to depress the motor centres allowing there use as an ''anticonvulsant'' agent, as well as depressing the sensory centres and inducing an anesthetised state.

==Pharmacological Considerations==
Barbituates are usually powders of the salt that require reconsititution using sterile water or saline. Onset of action and doses depends upon the amount of unbound and unionised form of the barbituate in the circulation. This is due to the ability of the drug to cross the blood-brain barrier. Barbituates are ''cumulative'' making them unsuitable to maintain anaesthesia.

==Side Effects and Contraindications==
*Patients with an acidaemia and hypoproteinaemia often require lower doses to produce an anaesthetised state due to the increase in unbound and unionised forms.
*Causes respiratory depression, particularly in the cat.
*Dose and rate depended cardiovascular depression.
*Hypotension due to peripheral vasodilation and reduction in cardiac output from myocardial depression and tachyarrhythmias.

==Drugs in this Group==
===Thiopental===
Thiopental (also ''Thiopentone'') causes a rapid loss of conciousness with time of onset being influenced by premedication agents. It is considered a '''ultra short acting''' barbituate, with effects seen within 15-30s following injection, and has a rapid recovery period, commonly 10-15 minutes. The duration and depth of anaesthetic, however, depends upon the ''amount'' of drug injected, ''speed'' of injection, and ''rate of distribution'' in non-fatty and fatty tissues. Recovery is dependent on redistribution of thiopental from plasma to adipose tissue so animals with minimal fat will take longer to recover.

Thiopental is available as a yellowish powder, which once reconsituted and stored correctly, can be used for up to 3-4 days. It comes as 2.5%, 5% and 10% solutions.

As thiopental causes a reduction in intracranial pressure (ICP), it can be used in patients with head traumas, brain tumours or other reasons for a raised ICP.

The commercial preparation is a sodium salt which requires dilution in water or saline. The resulting solution has a strong alkaline pH which is extremely irritant and if injected extravascularly it causes tissue necrosis and skin sloughing. It is best to inject via an intravenous catheter but if it is injected subcutaneously, then bathe immediately with saline and lidocaine solution which will cause a local vasodilation and help dissipate the subcutaneous thiopental.

Thiopental is highly protein-bound and so the dose should be reduced, or thiopental avoided in animals with hypoproteinaemia.

Care should also be taken in sighthounds as they take longer to recover this may be because they have minimal fat or because they metabolise it differently.

===Pentobarbital===
Pentobarbital is an oxybarbiturate which is no longer available at anaesthetic doses, but used as an euthansia agent. It causes a rapid onset of anaesthesia (40-120s) but has a longer duration of action compared with thiopental (1-2 hours). Recovery is dependent on hepatic metabolism. Its main indication of use is for the treatment of intractable seizures, long term sedation in ICU and euthansia.

Bovine Forelimb - Anatomy & Physiology

2009-09-02T09:44:42Z

Karag7: /* Carpal bones */

{{no pics}}

{{toplink
|backcolour =CDE472
|linkpage =Musculoskeletal System - Anatomy & Physiology
|linktext =Musculoskeletal System
|maplink = Musculoskeletal System (Content Map) - Anatomy & Physiology
|pagetype =Anatomy
|sublink1=Forelimb - Anatomy & Physiology
|subtext1=FORELIMB
}}
 
==Structures of the Proximal Forelimb and Shoulder==

===Scapula===
*The ox possesses a small '''tuber scapular'''
*It has '''acromion''' present
*It has extensive scapular cartilage

===Humerus===
*The humerus is essentially the same conformation as that of the dog.

===Radius and Ulna===
*These are complete bones in the ox but are entirely fused
*There is a proximal and distal interosseous space which are the only two places where the shafts are seperated
*The ulna's proximal end is caudal to the radius and it's distal end forms the lateral styloid process, distal to the radius and articulating with the ulnar carpal bone.

==Joints of the Proximal Forelimb==
===Shoulder Joint===

*The joint capsule attaches a very short distance from the periphery of the articular surfaces.
*The '''intertubercular (bicipital) bursa''' lies between the humeral tubercles cushioning the bicipital tendon.
*The bursa and tendon are held in place by the '''transverse humeral retinaculum''' running between the greater and lesser tubercles of the humerus.

===Elbow Joint===

*The joint capsule attaches to the articular surface of the condyle, the periphery of the olecranon fossa and the articular cartilage of the trochlear notch of the ulna. It fuses with the collateral ligaments.
*Paired collateral ligaments attach the epicondyles to the tuberosities of the radius and ulna.

==Structures of the Distal Forelimb==

===Carpal bones===

Carpal bones comprise two rows:
*Proximally, (mediolaterally), radial, intermediate, ulnar and accessory bones
*Distally, 1st is missing, 2 and 3 are fused and there is also a 4th carpal bone

===Metacarpal bones===

These are covered in detail in the [[Bovine Phalanges - Anatomy & Physiology|bovine phalanges]] section.

==Joints of the Distal Forelimb==
===Carpal Joint===

The carpal joint is a compound joint composed of:
*The '''antebrachiocarpal joint''' between the radius/ulna and the proximal carpal bones
*The '''middle carpal joint''' between the two rows of carpal bones
*The '''carpometacarpal joint''' between the distal carpal bones and the proximal metacarpals

The joint is a synovial joint, comprised of a common outer fibrous capsule and three inner synovial pouches, one for each joint.
*'''Collateral ligaments''' extend from the radius to the metacarpal bones on the medial and lateral aspect of the carpus.
*The carpal canal houses both the deep digital flexor tendon and the deep branch of the superficial digital flexor.

==Muscles of the Forelimb==
===Extrinsic Musculature===

These muscle are responsible for joining the forelimb to the trunk, forming a synsarcosis rather than a conventional joint. Collectively, they act to transfer the weight of the body to the forelimbs as well as stabilize the scapula.

'''''Trapezius''''': Accessory n.
*Origin: mid-dorsal raphe and supraspinous ligament
*Insertion: spine of the scapula
*Body: two parts, cervical and thoracic separated by aponeurosis
*Action: raises scapula against the trunk and swings cranially to advance the limb

'''''Brachiocephalic m.''''': Accessory n.
*Two parts separated by the clavicle where it exists
*Origin: occipital bone, nuchal ligament, mastoid process
*Insertion: deltoid tuberosity and fascia of limb
*Actions:
**advances the limb and extends the shoulder joint when limb is in motion
**draws head and neck ventrally when limb is fixed

'''''Omotransversarius''''': Accessory n.
*Origin: transverse processes of the atlas
*Insertion: acromion and spine of scapula
*Action: advancing the limb
*Innervation

'''''Latissimus dorsi''''': local branch of brachial plexus
*The '''broadest muscle of the back'''
*Origin: thoracolumbar fascia
*Insertion: teres tuberosity of the humerus
*Actions: antagonist to the brachiocephalic m.
**cranial fibers strap scapula to the chest
**retracts free limb and flexes shoulder joint
**draws trunk forward over the fixed limb

'''''Pectoral mm.''''': brachial plexus
*Two superficial parts, cranial and caudal, these aren't very distinct in the ox
**Origin: cranial sternum
**Insertion:
***cranial ('''descending'''): crest of the humerus distal to the deltoid tuberosity
***caudal ('''transverse'''): covers elbow joint to insert on the medial fascia of the forearm
**Action: adduct the forelimb, assist in protraction and retraction
*One deep part ('''pectoralis profundus'''), with cranial and caudal parts
**Origin: ventral sternum and adjacent cartilage
**Insertions:
***cranial (subclavius): supraspinatus m.
***caudal (pectoralis ascendens): lesser tubercle of the humerus
**Actions:
***slinging trunk between forelimbs
***may also retract free limbs
***draw trunk forward when limb is fixed

'''''Serratis ventralis''''': branch of brachial plexus
*Origin: C4 to 10th rib
*Insertion: medial scapula and scapular cartilage
*Action: supporting the weight of the trunk
**reinforced by strong fascia
**cervical portion can retract the limb
**caudal portion can advance the limb

'''''Rhomboids''''': brachial plexus,
*Origin: nuchal ligament
*Insertion: dorsal border and adjacent scapula
*Action: retracting the limb, may also raise limb

===Intrinsic Musculature===
====Muscles of the Shoulder====
These muscles are grouped:
*Lateral:'''Supraspinatus ''' and '''Infraspinatus''', Suprascapular n. of the brachial plexus
**Origin: the fossae of the scapula
**Insertion: both tubercles of the humerus
**Action: brace the shoulder
**Clinical significance: bursa between the tendon of the infraspinatus and lateral tubercle of the humerus can be the site of inflammation
*Medial:
**'''Supscapularis''': Subscapular n. from the brachial plexus
***Origin: Deep surface of the scapula
***Insertion: medial tubercle of the humerus
***Action: braces medial shoulder joint, potential adductor
**'''Coracobrachialis''': Musculocutaneous n. of the brachial plexus
***Origin: medial supraglenoid tubercle
***Insertion: proximal shaft of the humerus
***Action: fixator
*Caudal (Flexors): Axillary n. of the brachial plexus
**'''Deltoids'''
***Origin: caudal border and spine of the scapula, acromion
****Two heads of origin
***Insertion: deltoid tuberosity on the humerus
**'''Teres Major'''
***Origin: dorsal part of the caudal scapula
***Insertion: teres tuberosity midway down humerus
**'''Teres Minor'''
*There are no defined extensors of the shoulder. Those involved (brachiocephalic m., biceps brachii, supraspinatus, and ascending pectorals) have other, more primary roles.

====Muscles of the Elbow====
''Extensors'': Radial n. from the brachial plexus
*'''Triceps brachii''': Three heads,the medial branch is the most developed
**Long head: caudal margin of the scapula
**Lateral, medial, and accessory heads: shaft of the humerus
**Insertion: olecranon, proteced by tricipital bursa against the bone and subcutaneous bursa against the skin
*'''Tensor fasciae antebrachii'''
**Overlies triceps extending from scapula to olecranon

''Flexors'': Musculocutaneous n. from the brachial plexus
*'''Biceps brachii'''
**Origin: supraglenoid tubercle of the scapula
**Insertion: medial tuberosity of proximal radius and adjacent ulna
**Runs through the intertubercular groove of the humerus
*'''Brachialis'''
**Origin: proximocaudal humerus
**Insertion: spirals to insert next to biceps

====Muscles of the Carpal and Digital Joints====
''Extensors'': Radial n. from the brachial plexus
*Craniolateral position on the forearm
*Almost all originate from the lateral epicondyle of the humerus
*'''Extensor carpi radialis''': most medial, inserts on 2nd/3rd metacarpal bone
*'''Ulnaris lateralis''': most lateral, inserts on accessory carpal bone
*'''Extensor carpi obliquus''': aka '''abductor pollicis longus'''
**Origin: cranial radius
**Insertion: most medial metacarpal bone
*Last two may also serve in medial deviation of the foot
*'''Common Digital Extensor'''
**Insertion: extensor process of the distal phalanx of each digit
*'''Lateral Digital Extensor'''
**Insertion: dorsal proximal phalanges
*'''Medial Digital Extensor'''
**Insertion: middle and distal phalanges

''Flexors'': Median or Ulnar n. of the brachial plexus
*Caudal position on the forearm
*Originate from the caudal medial epicondyle of the humerus
*'''Flexor carpi radialis''': most medial, inserts on upper 2nd/3rd metacarpal bone
*'''Flexor carpi ulnaris''': most lateral, inserts on the accessory carpal bone
*'''Superficial Digital Flexor'''
**Insertion: palmar surface of middle phalanges
*'''Deep Digital Flexor'''
**Passes through carpal canal before branching and continues to palmar distal phalanges

''Interosseus muscles''
*This is covered in more detail in the [[Bovine Phalanges - Anatomy & Physiology|bovine phalanges]] section.

==Vasculature of the Forelimb==
*'''[[Arteries of the Forelimb - Anatomy & Physiology|Arteries of the Forelimb]]'''
*'''[[Veins of the Forelimb - Anatomy & Physiology|Veins of the Forelimb]]'''
*'''[[Lymphatics of the Forelimb - Anatomy & Physiology|Lymphatics of the Forelimb]]'''

Sevoflurane

2009-09-01T16:44:42Z

Karag7: /* Pharmacokinetics */

Halothane

2009-09-01T16:40:05Z

Karag7: /* Pharmacokinetics */

{{Unfinished}}
{{toplink
|linkpage =Anaesthesia
|linktext =Anaesthesia
|maplink= Anaesthesia Content Map - WikiClinical
|sublink1=Anaesthetic Drugs
|subtext1=Anaesthetic Drugs
|sublink2=Inhalation Agents
|subtext2=Inhalation Agents
|pagetype=Clinical
}}
 

'''Halothane''' was one of the most widely used inhalation agents in veterinary patients. However, it has now been overtaken by other agents such as [[Isoflurane|isoflurane]]. It is most commonly used to maintain anaesthesia after induction with an [[Injectable Agents|injectable agent]], although it has also been used to induce anaesthesia when injection is not possible e.g. poor intravenous access.

==Pharmacokinetics==
At room temperature, halothane is a liquid and so requires a [[Vaporisers|vaporiser]] before it reaches the patient. It needs to be stored in a darkened bottle due to ultraviolet degradation. It contains a preservative, Thymol, which can accumulate within the vaporiser The '''blood:gas partition coefficient''' is moderately low meaning that it is relatively insoluble in blood. This results in relatively rapid induction, recovery and depth change. The [[Inhalation Agents#General Pharmacokinetics#Minimum Alveolar Concentration|'''MAC''']] for halothane is approximately ''0.9%'' in dogs and ''1.1%'' in cats, meaning it is highly potent. Halothane undergoes a degree of hepatic metabolism by the cytochrome P450 system found in hepatocytes.

==Adverse Effects==
===Central Nervous System===
*Causes dose dependent depression but poor analgesic effect.
*Cause cerebral vasodilation but increases intracranial pressure (ICP) therefore should not be used in patients with an increased ICP.

===Cardiovascular System===
*Decreased cardiac output due to myocardial contraction depression.
*Decreased arterial blood pressure.
*Sensitizes the myocardium to catecholamines so may cause cardiac arrhythmias.

===Respiratory System===
*Beneficial in patients with increased airway resistance due to bronchodilatory effect.

===Other Systems===
*Blood flow through the hepatic artery and portal vein are both reduced, which may result in hepatic damage, although unlikely to see clinical signs.
*Reduced renal blood flow and therefore a reduction in glomerular filtration rate.
*Of all the inhalation agents, halothane is the most likely to cause malignant hyperthermia.

==Contraindications==
Halothane should be avoided in patients with increased ICP, cardiac dysfunction, hepatic disease and susceptibility to malignant hyperthermia.

Isoflurane

2009-09-01T16:30:37Z

Karag7: /* Pharmacokinetics */

Halothane

2009-09-01T16:19:06Z

Karag7: /* Cardiovascular System */

{{Unfinished}}
{{toplink
|linkpage =Anaesthesia
|linktext =Anaesthesia
|maplink= Anaesthesia Content Map - WikiClinical
|sublink1=Anaesthetic Drugs
|subtext1=Anaesthetic Drugs
|sublink2=Inhalation Agents
|subtext2=Inhalation Agents
|pagetype=Clinical
}}
 

'''Halothane''' was one of the most widely used inhalation agents in veterinary patients. However, it has now been overtaken by other agents such as [[Isoflurane|isoflurane]]. It is most commonly used to maintain anaesthesia after induction with an [[Injectable Agents|injectable agent]], although it has also been used to induce anaesthesia when injection is not possible e.g. poor intravenous access.

==Pharmacokinetics==
At room temperature, halothane is a liquid and so requires a [[Vaporisers|vaporiser]] before it reaches the patient. It needs to be stored in a darkened bottle due to ultraviolet degradation. It contains a preservative, Thymol, which can accumulate within the vaporiser The '''blood:gas partition coefficient''' is moderately low meaning that it is relatively insoluble in blood. This results in relatively rapid induction, recovery and depth change. The [[Inhalation Agents#General Pharmacokinetics#Minimum Alveolar Concentration|'''MAC''']] for halothane is approximately ''0.9%'', meaning it is highly potent. Halothane undergoes a degree of hepatic metabolism by the cytochrome P450 system found in hepatocytes.

==Adverse Effects==
===Central Nervous System===
*Causes dose dependent depression but poor analgesic effect.
*Cause cerebral vasodilation but increases intracranial pressure (ICP) therefore should not be used in patients with an increased ICP.

===Cardiovascular System===
*Decreased cardiac output due to myocardial contraction depression.
*Decreased arterial blood pressure.
*Sensitizes the myocardium to catecholamines so may cause cardiac arrhythmias.

===Respiratory System===
*Beneficial in patients with increased airway resistance due to bronchodilatory effect.

===Other Systems===
*Blood flow through the hepatic artery and portal vein are both reduced, which may result in hepatic damage, although unlikely to see clinical signs.
*Reduced renal blood flow and therefore a reduction in glomerular filtration rate.
*Of all the inhalation agents, halothane is the most likely to cause malignant hyperthermia.

==Contraindications==
Halothane should be avoided in patients with increased ICP, cardiac dysfunction, hepatic disease and susceptibility to malignant hyperthermia.

Halothane

2009-09-01T16:16:07Z

Karag7: /* Cardiovascular System */

{{Unfinished}}
{{toplink
|linkpage =Anaesthesia
|linktext =Anaesthesia
|maplink= Anaesthesia Content Map - WikiClinical
|sublink1=Anaesthetic Drugs
|subtext1=Anaesthetic Drugs
|sublink2=Inhalation Agents
|subtext2=Inhalation Agents
|pagetype=Clinical
}}
 

'''Halothane''' was one of the most widely used inhalation agents in veterinary patients. However, it has now been overtaken by other agents such as [[Isoflurane|isoflurane]]. It is most commonly used to maintain anaesthesia after induction with an [[Injectable Agents|injectable agent]], although it has also been used to induce anaesthesia when injection is not possible e.g. poor intravenous access.

==Pharmacokinetics==
At room temperature, halothane is a liquid and so requires a [[Vaporisers|vaporiser]] before it reaches the patient. It needs to be stored in a darkened bottle due to ultraviolet degradation. It contains a preservative, Thymol, which can accumulate within the vaporiser The '''blood:gas partition coefficient''' is moderately low meaning that it is relatively insoluble in blood. This results in relatively rapid induction, recovery and depth change. The [[Inhalation Agents#General Pharmacokinetics#Minimum Alveolar Concentration|'''MAC''']] for halothane is approximately ''0.9%'', meaning it is highly potent. Halothane undergoes a degree of hepatic metabolism by the cytochrome P450 system found in hepatocytes.

==Adverse Effects==
===Central Nervous System===
*Causes dose dependent depression but poor analgesic effect.
*Cause cerebral vasodilation but increases intracranial pressure (ICP) therefore should not be used in patients with an increased ICP.

===Cardiovascular System===
*Decreased cardiac output due to myocardial contraction depression.
*Decreased arterial blood pressure.
*Sensitises the myocardium to catecholamines so may cause cardiac arrhythmias.

===Respiratory System===
*Beneficial in patients with increased airway resistance due to bronchodilatory effect.

===Other Systems===
*Blood flow through the hepatic artery and portal vein are both reduced, which may result in hepatic damage, although unlikely to see clinical signs.
*Reduced renal blood flow and therefore a reduction in glomerular filtration rate.
*Of all the inhalation agents, halothane is the most likely to cause malignant hyperthermia.

==Contraindications==
Halothane should be avoided in patients with increased ICP, cardiac dysfunction, hepatic disease and susceptibility to malignant hyperthermia.

Barbiturates

2009-09-01T15:22:35Z

Karag7: /* Thiopental */

{{unfinished}}
{{toplink
|linkpage =Anaesthesia
|linktext =Anaesthesia
|maplink= Anaesthesia Content Map - WikiClinical
|sublink1=Anaesthetic Drugs
|subtext1=Anaesthetic Drugs
|sublink2=Injectable Agents
|subtext2=Injectable Agents
|pagetype=Clinical
}}
 
The drugs within this group are '''short acting''' and have been classically used agents for anaesthesia. They produce a state of hypnosis and higher doses are required to produce an anaesthetised state but they are '''poor analgesics'''.

==Mechanism of Action==
Barbituates act by depressing the central nervous system (CNS) by acting at the ''Gamma Aminobutyric Acid A'' receptors (GABAa). They mimic and enhance GABA, which is the principle inhibitory neurotransmitter in the CNS. Once bound to the GABAa receptor they reduce the rate of GABA dissocation and thereby ''increase chloride conductance'' is maintained resulting in hyperpolarisation of the membrane and reduced neuronal excitability. However, as the concentration of barbituate increases, it starts to have a direct effect on the chloride conductance and it is this that is thought to bring about the anaesthetic effects, while the GABA related increases causes a sedative effect. They act to depress the motor centres allowing there use as an ''anticonvulsant'' agent, as well as depressing the sensory centres and inducing an anesthetised state.

==Pharmacological Considerations==
Barbituates are usually powders of the salt that require reconsititution using sterile water or saline. Onset of action and doses depends upon the amount of unbound and unionised form of the barbituate in the circulation. This is due to the ability of the drug to cross the blood-brain barrier. Barbituates are ''cumulative'' making them unsuitable to maintain anaesthesia.

==Side Effects and Contraindications==
*Patients with an acidaemia and hypoproteinaemia often require lower doses to produce an anaesthetised state due to the increase in unbound and unionised forms.
*Causes respiratory depression, particularly in the cat.
*Dose and rate depended cardiovascular depression.
*Hypotension due to peripheral vasodilation and reduction in cardiac output from myocardial depression and tachyarrhythmias.

==Drugs in this Group==
===Thiopental===
Thiopental (also ''Thiopentone'') causes a rapid loss of conciousness with time of onset being influenced by premedication agents. It is considered a '''ultra short acting''' barbituate, with effects seen within 15-30s following injection, and has a rapid recovery period, commonly 10-15 minutes. The duration and depth of anaesthetic, however, depends upon the ''amount'' of drug injected, ''speed'' of injection, and ''rate of distribution'' in non-fatty and fatty tissues.

Thiopental is available as a yellowish powder, which once reconsituted and stored correctly, can be used for up to 3-4 days. It comes as 2.5%, 5% and 10% solutions.

As thiopental causes a reduction in intracranial pressure (ICP), it can be used in patients with head traumas, brain tumours or other reasons for a raised ICP.

The commercial preparation is a sodium salt which requires dilution in water or saline. The resulting solution has a strong alkaline pH which is extremely irritant and if injected extravascularly it causes tissue necrosis and skin sloughing. It is best to inject via an intravenous catheter but if it is injected subcutaneously, then bathe immediately with saline and lidocaine solution which will cause a local vasodilation and help dissipate the subcutaneous thiopental.

Thiopental is highly protein-bound and so the dose should be reduced, or thiopental avoided in animals with hypoproteinaemia.

Care should also be taken in sighthounds as they do not possess the enzyme to cleave the sulphur molecule from the thiopental, which is the first stage of metabolism of the drug, and so recovery may be prolonged in these patients.

===Pentobarbital===
Pentobarbital is an oxybarbiturate which is no longer available at anaesthetic doses, but used as an euthansia agent. It causes a rapid onset of anaesthesia (40-120s) but has a longer duration of action compared with thiopental (1-2 hours). Recovery is dependent on hepatic metabolism. Its main indication of use is for the treatment of intractable seizures, long term sedation in ICU and euthansia.

Barbiturates

2009-09-01T15:10:44Z

Karag7: /* Thiopental */

{{unfinished}}
{{toplink
|linkpage =Anaesthesia
|linktext =Anaesthesia
|maplink= Anaesthesia Content Map - WikiClinical
|sublink1=Anaesthetic Drugs
|subtext1=Anaesthetic Drugs
|sublink2=Injectable Agents
|subtext2=Injectable Agents
|pagetype=Clinical
}}
 
The drugs within this group are '''short acting''' and have been classically used agents for anaesthesia. They produce a state of hypnosis and higher doses are required to produce an anaesthetised state but they are '''poor analgesics'''.

==Mechanism of Action==
Barbituates act by depressing the central nervous system (CNS) by acting at the ''Gamma Aminobutyric Acid A'' receptors (GABAa). They mimic and enhance GABA, which is the principle inhibitory neurotransmitter in the CNS. Once bound to the GABAa receptor they reduce the rate of GABA dissocation and thereby ''increase chloride conductance'' is maintained resulting in hyperpolarisation of the membrane and reduced neuronal excitability. However, as the concentration of barbituate increases, it starts to have a direct effect on the chloride conductance and it is this that is thought to bring about the anaesthetic effects, while the GABA related increases causes a sedative effect. They act to depress the motor centres allowing there use as an ''anticonvulsant'' agent, as well as depressing the sensory centres and inducing an anesthetised state.

==Pharmacological Considerations==
Barbituates are usually powders of the salt that require reconsititution using sterile water or saline. Onset of action and doses depends upon the amount of unbound and unionised form of the barbituate in the circulation. This is due to the ability of the drug to cross the blood-brain barrier. Barbituates are ''cumulative'' making them unsuitable to maintain anaesthesia.

==Side Effects and Contraindications==
*Patients with an acidaemia and hypoproteinaemia often require lower doses to produce an anaesthetised state due to the increase in unbound and unionised forms.
*Causes respiratory depression, particularly in the cat.
*Dose and rate depended cardiovascular depression.
*Hypotension due to peripheral vasodilation and reduction in cardiac output from myocardial depression and tachyarrhythmias.

==Drugs in this Group==
===Thiopental===
Thiopental (also ''Thiopentone'') causes a rapid loss of conciousness with time of onset being influenced by premedication agents. It is considered a '''ultra short acting''' barbituate, with effects seen within 15-30s following injection, and has a rapid recovery period, commonly 10-15 minutes. The duration and depth of anaesthetic, however, depends upon the ''amount'' of drug injected, ''speed'' of injection, and ''rate of distribution'' in non-fatty and fatty tissues.

Thiopental is available as a yellowish powder, which once reconsituted and stored correctly, can be used for up to 3-4 days. It comes as 2.5%, 5% and 10% solutions.

As thiopental causes a reduction in intracranial pressure (ICP), it can be used in patients with head traumas, brain tumours or other reasons for a raised ICP.

The commercial preparation is a sodium salt which requires dilution in water or saline. The resulting solution has a strong alkaline pH which is extremely irritant and if injected extravascularly it causes tissue necrosis and skin sloughing. It is best to inject via an intravenous catheter but if it is injected subcutaneously, then bathe immediately with saline and lidocaine solution which will cause a local vasodilation and help dissipate the subcutaneous thiopental.

Care should also be taken in sighthounds as they do not possess the enzyme to cleave the sulphur molecule from the thiopental, which is the first stage of metabolism of the drug, and so recovery may be prolonged in these patients.

===Pentobarbital===
Pentobarbital is an oxybarbiturate which is no longer available at anaesthetic doses, but used as an euthansia agent. It causes a rapid onset of anaesthesia (40-120s) but has a longer duration of action compared with thiopental (1-2 hours). Recovery is dependent on hepatic metabolism. Its main indication of use is for the treatment of intractable seizures, long term sedation in ICU and euthansia.

Opioids

2009-09-01T11:17:23Z

Karag7: /* Buprenorphine */

The opioid drugs include [[#Morphine|morphine]] and its synthetic derivatives. They are powerful '''analgesics''', and have dose-dependent '''sedative''' properties.

Opioids have additional recognised effects. They:
* Decrease the sensitivity of the respiratory centres of the brain to carbon dioxide.
* Give potent cough suppression.
* Cause emesis.
* Constrict the pupils (miosis).
* Reduce gastro-intestinal motility.
* Lead to histamine release.

==Mechanism of Action==

Opiods act on opioid (OP) receptors. OP receptors are G-protein coupled: activation of the receptors causes inhibition of adenylate cyclase, decreasing cAMP levels within the cell. Thus, receptor-ligand interaction promotes the opening of K+ channels within the plasma membrane, and also inhibits that of voltage-gated calcium channels. There are three types of opioid receptors:
* '''OP1''': These are located spinally and supraspinally. The primary effect of receptor engagement is sedation.
* '''OP2''': Located spinally, the main effect of OP2 activation is sedation.
* '''OP3''': OP3 receptor interaction gives rise to analgesia, on a spinal and supraspinal level.

Following interaction with the receptor and the subsequent cascade of events, opiods exert their effects by a variety of mechanisms. Neuronal excitability is decreased, along with reductions in the release of the neurotransmitters glutamate and substance P. In this manner, transmission of nociceptive impulses is inhibited and the actions detailed above are elicited.

==Pharmacokinetic Considerations==

Opioids can be administered intramuscularly, intravenously, subcutanously, intrathecally or orally. Absorption following oral administration is variable with the drug used, but first-pass metabolism decreases the efficacy of the drug when given this way.

The half-life of opioids is around 3-6 hours.

==Side Effects and Contraindications==

Side effects of opioid drugs include:
* Emesis. This is worst in animals that are not in pain at the time of administration, e.g. when morphine is administered as a pre-operative pre-medication.
* Negative chronotropic effects
* Respiratory depression
* Reduced gastro-intestinal motility. This is of most clinical significance in the horse, which is prone to post-operative ileus.

==Drugs in this Group==

===Morphine===

Morphine is indicated for severe pain, but is an unlicensed, Schedule 2 controlled drug. It may be administered by the i/m, i/v, s/c and i/t routes, and may also be given as a constant rate infusion.

Morphine is a full OP3 agonist, with a 10-15 min onset and a duration of 2-4 hours. Its side effects are as detailed above.

Glucuronidation in the liver produces an active metabolite of the drug, morphine-6-glucuronide (morphine-3-glucuronide is also formed). Metabolites are then excreted in the urine. Enterohepatic circulation of morphine does occur, but this is not clinically important.

===Buprenorphine===

Buprenorphine is a Schedule 3 controlled drug used for the relief of moderate pain. It is licensed for veterinary used and may be given i/v, i/m, s/c or p/o. There is an onset time of 45 mins and its actions last 6-8 hours.

Buprenorphine is a partial OP3 agonist. This gives it a bell-shaped dose response curve, with large experimental doses actually causing opioid receptor antagonism. Buprenophine may therefore cause partial reversal of administration of full OP3 agonists such as [[#Morphine|morphine]], [[#Methadone|methadone]], [[#Pethidine|pethidine]] or [[#Fentanyl|fentanyl]].

===Butorphanol===

Butorphanol may be used to combat mild pain. It is a poor analgesic but has excellent sedative properties, and also acts as a cough suppressant. Butorphanol is licensed for veterinary use, and is a mixed partial agonist; it is an antagonist at the OP3 receptor and an agonist at the OP2 receptor.

There is an onset time of 15 mins following i/v, i/m or s/c administration, and effects then last for 2-4 hours.

===Pethidine===

A full OP3 agonist, pethidine is used for moderate to severe pain. It may be given i/m or s/c, but NOT intravenously as it will cause massive histamine release. The onset time is 10-15 mins, and the drug has as duration of 30-60 mins. Pethidine is chronotropic and also spasmolytic. It is therefore a good drug choice to provide analgesia and facilitate rectal examination of colic-ing horses. Pethidine is a licensed, Schedule 2 controlled drug.

===Methadone===

Methadone is an unlicensed, Schedule 2 controlled, full OP3 agonist. It is used i/v, i/m, s/c or by constant rate infusion for the relief of moderate to severe pain. Advantageously, it does not cause emesis. There is an onset time of 15-30 mins following i/v, i/m or s/c administration, and effects then last for around 4 hours.

===Fentanyl===

Fentanyl may be used i/v or via slow release patches for severe pain. It is a full OP3 agonist with a rapid onset of action and a duration of 15-20 mins. It is therefore useful as "rescue analgesia" to top-up levels of analgesia during particularly painful stages of surgery. It is a Schedule 2 controlled drug which is licensed as a formulation containing fluanisone as a neuroleptanalgesic for use in mice, rats, rabbits and guinea pigs.

===Etorphine===

Etorphine is a hugely potent opioid that is a component of large animal and small animal immobilon. (Large animal immobilon consists of etorphine plus [[Phenothiazines#Acepromazine|acepromazine]]; small animal immobilon comprises etorphine and [[Phenothiazines#Methotrimeprazine|methotrimeprazine]] ). It may be fatal to man following self administration, when opioid antagonism with [[#Opioid Antagonists|naloxone]] is required.

==Opioid Antagonists==

Naloxone is an antagonist to endogenous opioids. It is frequently used in human medicine to antagonise opioid narcotics in the incidence of overdose. Naloxone may be administered intravenously, intramuscularly, intrathecally or subcutaneously. It has a short duration of action (1-2 hours) and so repeated administrations may be necessary.

Opioids

2009-09-01T11:13:52Z

Karag7: /* Methadone */

The opioid drugs include [[#Morphine|morphine]] and its synthetic derivatives. They are powerful '''analgesics''', and have dose-dependent '''sedative''' properties.

Opioids have additional recognised effects. They:
* Decrease the sensitivity of the respiratory centres of the brain to carbon dioxide.
* Give potent cough suppression.
* Cause emesis.
* Constrict the pupils (miosis).
* Reduce gastro-intestinal motility.
* Lead to histamine release.

==Mechanism of Action==

Opiods act on opioid (OP) receptors. OP receptors are G-protein coupled: activation of the receptors causes inhibition of adenylate cyclase, decreasing cAMP levels within the cell. Thus, receptor-ligand interaction promotes the opening of K+ channels within the plasma membrane, and also inhibits that of voltage-gated calcium channels. There are three types of opioid receptors:
* '''OP1''': These are located spinally and supraspinally. The primary effect of receptor engagement is sedation.
* '''OP2''': Located spinally, the main effect of OP2 activation is sedation.
* '''OP3''': OP3 receptor interaction gives rise to analgesia, on a spinal and supraspinal level.

Following interaction with the receptor and the subsequent cascade of events, opiods exert their effects by a variety of mechanisms. Neuronal excitability is decreased, along with reductions in the release of the neurotransmitters glutamate and substance P. In this manner, transmission of nociceptive impulses is inhibited and the actions detailed above are elicited.

==Pharmacokinetic Considerations==

Opioids can be administered intramuscularly, intravenously, subcutanously, intrathecally or orally. Absorption following oral administration is variable with the drug used, but first-pass metabolism decreases the efficacy of the drug when given this way.

The half-life of opioids is around 3-6 hours.

==Side Effects and Contraindications==

Side effects of opioid drugs include:
* Emesis. This is worst in animals that are not in pain at the time of administration, e.g. when morphine is administered as a pre-operative pre-medication.
* Negative chronotropic effects
* Respiratory depression
* Reduced gastro-intestinal motility. This is of most clinical significance in the horse, which is prone to post-operative ileus.

==Drugs in this Group==

===Morphine===

Morphine is indicated for severe pain, but is an unlicensed, Schedule 2 controlled drug. It may be administered by the i/m, i/v, s/c and i/t routes, and may also be given as a constant rate infusion.

Morphine is a full OP3 agonist, with a 10-15 min onset and a duration of 2-4 hours. Its side effects are as detailed above.

Glucuronidation in the liver produces an active metabolite of the drug, morphine-6-glucuronide (morphine-3-glucuronide is also formed). Metabolites are then excreted in the urine. Enterohepatic circulation of morphine does occur, but this is not clinically important.

===Buprenorphine===

Buprenorphine is a Schedule 3 controlled drug used for the relief of moderate pain. It is licensed for veterinary used and may be given i/v, i/m, s/c or p/o. Its actions last 6-8 hours.

Buprenorphine is a partial OP3 agonist. This gives it a bell-shaped dose response curve, with large experimental doses actually causing opioid receptor antagonism. Buprenophine may therefore cause partial reversal of administration of full OP3 agonists such as [[#Morphine|morphine]], [[#Methadone|methadone]], [[#Pethidine|pethidine]] or [[#Fentanyl|fentanyl]].

===Butorphanol===

Butorphanol may be used to combat mild pain. It is a poor analgesic but has excellent sedative properties, and also acts as a cough suppressant. Butorphanol is licensed for veterinary use, and is a mixed partial agonist; it is an antagonist at the OP3 receptor and an agonist at the OP2 receptor.

There is an onset time of 15 mins following i/v, i/m or s/c administration, and effects then last for 2-4 hours.

===Pethidine===

A full OP3 agonist, pethidine is used for moderate to severe pain. It may be given i/m or s/c, but NOT intravenously as it will cause massive histamine release. The onset time is 10-15 mins, and the drug has as duration of 30-60 mins. Pethidine is chronotropic and also spasmolytic. It is therefore a good drug choice to provide analgesia and facilitate rectal examination of colic-ing horses. Pethidine is a licensed, Schedule 2 controlled drug.

===Methadone===

Methadone is an unlicensed, Schedule 2 controlled, full OP3 agonist. It is used i/v, i/m, s/c or by constant rate infusion for the relief of moderate to severe pain. Advantageously, it does not cause emesis. There is an onset time of 15-30 mins following i/v, i/m or s/c administration, and effects then last for around 4 hours.

===Fentanyl===

Fentanyl may be used i/v or via slow release patches for severe pain. It is a full OP3 agonist with a rapid onset of action and a duration of 15-20 mins. It is therefore useful as "rescue analgesia" to top-up levels of analgesia during particularly painful stages of surgery. It is a Schedule 2 controlled drug which is licensed as a formulation containing fluanisone as a neuroleptanalgesic for use in mice, rats, rabbits and guinea pigs.

===Etorphine===

Etorphine is a hugely potent opioid that is a component of large animal and small animal immobilon. (Large animal immobilon consists of etorphine plus [[Phenothiazines#Acepromazine|acepromazine]]; small animal immobilon comprises etorphine and [[Phenothiazines#Methotrimeprazine|methotrimeprazine]] ). It may be fatal to man following self administration, when opioid antagonism with [[#Opioid Antagonists|naloxone]] is required.

==Opioid Antagonists==

Naloxone is an antagonist to endogenous opioids. It is frequently used in human medicine to antagonise opioid narcotics in the incidence of overdose. Naloxone may be administered intravenously, intramuscularly, intrathecally or subcutaneously. It has a short duration of action (1-2 hours) and so repeated administrations may be necessary.

Opioids

2009-09-01T10:44:22Z

Karag7: /* Etorphine */

The opioid drugs include [[#Morphine|morphine]] and its synthetic derivatives. They are powerful '''analgesics''', and have dose-dependent '''sedative''' properties.

Opioids have additional recognised effects. They:
* Decrease the sensitivity of the respiratory centres of the brain to carbon dioxide.
* Give potent cough suppression.
* Cause emesis.
* Constrict the pupils (miosis).
* Reduce gastro-intestinal motility.
* Lead to histamine release.

==Mechanism of Action==

Opiods act on opioid (OP) receptors. OP receptors are G-protein coupled: activation of the receptors causes inhibition of adenylate cyclase, decreasing cAMP levels within the cell. Thus, receptor-ligand interaction promotes the opening of K+ channels within the plasma membrane, and also inhibits that of voltage-gated calcium channels. There are three types of opioid receptors:
* '''OP1''': These are located spinally and supraspinally. The primary effect of receptor engagement is sedation.
* '''OP2''': Located spinally, the main effect of OP2 activation is sedation.
* '''OP3''': OP3 receptor interaction gives rise to analgesia, on a spinal and supraspinal level.

Following interaction with the receptor and the subsequent cascade of events, opiods exert their effects by a variety of mechanisms. Neuronal excitability is decreased, along with reductions in the release of the neurotransmitters glutamate and substance P. In this manner, transmission of nociceptive impulses is inhibited and the actions detailed above are elicited.

==Pharmacokinetic Considerations==

Opioids can be administered intramuscularly, intravenously, subcutanously, intrathecally or orally. Absorption following oral administration is variable with the drug used, but first-pass metabolism decreases the efficacy of the drug when given this way.

The half-life of opioids is around 3-6 hours.

==Side Effects and Contraindications==

Side effects of opioid drugs include:
* Emesis. This is worst in animals that are not in pain at the time of administration, e.g. when morphine is administered as a pre-operative pre-medication.
* Negative chronotropic effects
* Respiratory depression
* Reduced gastro-intestinal motility. This is of most clinical significance in the horse, which is prone to post-operative ileus.

==Drugs in this Group==

===Morphine===

Morphine is indicated for severe pain, but is an unlicensed, Schedule 2 controlled drug. It may be administered by the i/m, i/v, s/c and i/t routes, and may also be given as a constant rate infusion.

Morphine is a full OP3 agonist, with a 10-15 min onset and a duration of 2-4 hours. Its side effects are as detailed above.

Glucuronidation in the liver produces an active metabolite of the drug, morphine-6-glucuronide (morphine-3-glucuronide is also formed). Metabolites are then excreted in the urine. Enterohepatic circulation of morphine does occur, but this is not clinically important.

===Buprenorphine===

Buprenorphine is a Schedule 3 controlled drug used for the relief of moderate pain. It is licensed for veterinary used and may be given i/v, i/m, s/c or p/o. Its actions last 6-8 hours.

Buprenorphine is a partial OP3 agonist. This gives it a bell-shaped dose response curve, with large experimental doses actually causing opioid receptor antagonism. Buprenophine may therefore cause partial reversal of administration of full OP3 agonists such as [[#Morphine|morphine]], [[#Methadone|methadone]], [[#Pethidine|pethidine]] or [[#Fentanyl|fentanyl]].

===Butorphanol===

Butorphanol may be used to combat mild pain. It is a poor analgesic but has excellent sedative properties, and also acts as a cough suppressant. Butorphanol is licensed for veterinary use, and is a mixed partial agonist; it is an antagonist at the OP3 receptor and an agonist at the OP2 receptor.

There is an onset time of 15 mins following i/v, i/m or s/c administration, and effects then last for 2-4 hours.

===Pethidine===

A full OP3 agonist, pethidine is used for moderate to severe pain. It may be given i/m or s/c, but NOT intravenously as it will cause massive histamine release. The onset time is 10-15 mins, and the drug has as duration of 30-60 mins. Pethidine is chronotropic and also spasmolytic. It is therefore a good drug choice to provide analgesia and facilitate rectal examination of colic-ing horses. Pethidine is a licensed, Schedule 2 controlled drug.

===Methadone===

Methadone is an unlicensed, Schedule 2 controlled, full OP3 agonist. It is used i/v, i/m, s/c or by constant rate infusion for the relief of moderate to severe pain. Advantageously, it does not cause emesis.

===Fentanyl===

Fentanyl may be used i/v or via slow release patches for severe pain. It is a full OP3 agonist with a rapid onset of action and a duration of 15-20 mins. It is therefore useful as "rescue analgesia" to top-up levels of analgesia during particularly painful stages of surgery. It is a Schedule 2 controlled drug which is licensed as a formulation containing fluanisone as a neuroleptanalgesic for use in mice, rats, rabbits and guinea pigs.

===Etorphine===

Etorphine is a hugely potent opioid that is a component of large animal and small animal immobilon. (Large animal immobilon consists of etorphine plus [[Phenothiazines#Acepromazine|acepromazine]]; small animal immobilon comprises etorphine and [[Phenothiazines#Methotrimeprazine|methotrimeprazine]] ). It may be fatal to man following self administration, when opioid antagonism with [[#Opioid Antagonists|naloxone]] is required.

==Opioid Antagonists==

Naloxone is an antagonist to endogenous opioids. It is frequently used in human medicine to antagonise opioid narcotics in the incidence of overdose. Naloxone may be administered intravenously, intramuscularly, intrathecally or subcutaneously. It has a short duration of action (1-2 hours) and so repeated administrations may be necessary.

Opioids

2009-09-01T10:21:50Z

Karag7: /* Buprenorphine */

The opioid drugs include [[#Morphine|morphine]] and its synthetic derivatives. They are powerful '''analgesics''', and have dose-dependent '''sedative''' properties.

Opioids have additional recognised effects. They:
* Decrease the sensitivity of the respiratory centres of the brain to carbon dioxide.
* Give potent cough suppression.
* Cause emesis.
* Constrict the pupils (miosis).
* Reduce gastro-intestinal motility.
* Lead to histamine release.

==Mechanism of Action==

Opiods act on opioid (OP) receptors. OP receptors are G-protein coupled: activation of the receptors causes inhibition of adenylate cyclase, decreasing cAMP levels within the cell. Thus, receptor-ligand interaction promotes the opening of K+ channels within the plasma membrane, and also inhibits that of voltage-gated calcium channels. There are three types of opioid receptors:
* '''OP1''': These are located spinally and supraspinally. The primary effect of receptor engagement is sedation.
* '''OP2''': Located spinally, the main effect of OP2 activation is sedation.
* '''OP3''': OP3 receptor interaction gives rise to analgesia, on a spinal and supraspinal level.

Following interaction with the receptor and the subsequent cascade of events, opiods exert their effects by a variety of mechanisms. Neuronal excitability is decreased, along with reductions in the release of the neurotransmitters glutamate and substance P. In this manner, transmission of nociceptive impulses is inhibited and the actions detailed above are elicited.

==Pharmacokinetic Considerations==

Opioids can be administered intramuscularly, intravenously, subcutanously, intrathecally or orally. Absorption following oral administration is variable with the drug used, but first-pass metabolism decreases the efficacy of the drug when given this way.

The half-life of opioids is around 3-6 hours.

==Side Effects and Contraindications==

Side effects of opioid drugs include:
* Emesis. This is worst in animals that are not in pain at the time of administration, e.g. when morphine is administered as a pre-operative pre-medication.
* Negative chronotropic effects
* Respiratory depression
* Reduced gastro-intestinal motility. This is of most clinical significance in the horse, which is prone to post-operative ileus.

==Drugs in this Group==

===Morphine===

Morphine is indicated for severe pain, but is an unlicensed, Schedule 2 controlled drug. It may be administered by the i/m, i/v, s/c and i/t routes, and may also be given as a constant rate infusion.

Morphine is a full OP3 agonist, with a 10-15 min onset and a duration of 2-4 hours. Its side effects are as detailed above.

Glucuronidation in the liver produces an active metabolite of the drug, morphine-6-glucuronide (morphine-3-glucuronide is also formed). Metabolites are then excreted in the urine. Enterohepatic circulation of morphine does occur, but this is not clinically important.

===Buprenorphine===

Buprenorphine is a Schedule 3 controlled drug used for the relief of moderate pain. It is licensed for veterinary used and may be given i/v, i/m, s/c or p/o. Its actions last 6-8 hours.

Buprenorphine is a partial OP3 agonist. This gives it a bell-shaped dose response curve, with large experimental doses actually causing opioid receptor antagonism. Buprenophine may therefore cause partial reversal of administration of full OP3 agonists such as [[#Morphine|morphine]], [[#Methadone|methadone]], [[#Pethidine|pethidine]] or [[#Fentanyl|fentanyl]].

===Butorphanol===

Butorphanol may be used to combat mild pain. It is a poor analgesic but has excellent sedative properties, and also acts as a cough suppressant. Butorphanol is licensed for veterinary use, and is a mixed partial agonist; it is an antagonist at the OP3 receptor and an agonist at the OP2 receptor.

There is an onset time of 15 mins following i/v, i/m or s/c administration, and effects then last for 2-4 hours.

===Pethidine===

A full OP3 agonist, pethidine is used for moderate to severe pain. It may be given i/m or s/c, but NOT intravenously as it will cause massive histamine release. The onset time is 10-15 mins, and the drug has as duration of 30-60 mins. Pethidine is chronotropic and also spasmolytic. It is therefore a good drug choice to provide analgesia and facilitate rectal examination of colic-ing horses. Pethidine is a licensed, Schedule 2 controlled drug.

===Methadone===

Methadone is an unlicensed, Schedule 2 controlled, full OP3 agonist. It is used i/v, i/m, s/c or by constant rate infusion for the relief of moderate to severe pain. Advantageously, it does not cause emesis.

===Fentanyl===

Fentanyl may be used i/v or via slow release patches for severe pain. It is a full OP3 agonist with a rapid onset of action and a duration of 15-20 mins. It is therefore useful as "rescue analgesia" to top-up levels of analgesia during particularly painful stages of surgery. It is a Schedule 2 controlled drug which is licensed as a formulation containing fluanisone as a neuroleptanalgesic for use in mice, rats, rabbits and guinea pigs.

===Etorphine===

Etorphine is a hugely potent opioid that is a component of large animal and small animal immobilon. (Large animal immobilon consists of etorphine plus [[Phenothiazines#Acepromazine|acepromazine]]; small animal immobilon comprises etorphine and [[Phenothiazines#Methotrimeprazine|methotrimeprazine]] ). It may be fatal to man follwing self administration, wehn opioid antagonism with [[#Opioid Antagonists|naloxone]] is required.

==Opioid Antagonists==

Naloxone is an antagonist to endogenous opioids. It is frequently used in human medicine to antagonise opioid narcotics in the incidence of overdose. Naloxone may be administered intravenously, intramuscularly, intrathecally or subcutaneously. It has a short duration of action (1-2 hours) and so repeated administrations may be necessary.

Opioids

2009-09-01T10:07:48Z

Karag7: /* Butorphanol */

The opioid drugs include [[#Morphine|morphine]] and its synthetic derivatives. They are powerful '''analgesics''', and have dose-dependent '''sedative''' properties.

Opioids have additional recognised effects. They:
* Decrease the sensitivity of the respiratory centres of the brain to carbon dioxide.
* Give potent cough suppression.
* Cause emesis.
* Constrict the pupils (miosis).
* Reduce gastro-intestinal motility.
* Lead to histamine release.

==Mechanism of Action==

Opiods act on opioid (OP) receptors. OP receptors are G-protein coupled: activation of the receptors causes inhibition of adenylate cyclase, decreasing cAMP levels within the cell. Thus, receptor-ligand interaction promotes the opening of K+ channels within the plasma membrane, and also inhibits that of voltage-gated calcium channels. There are three types of opioid receptors:
* '''OP1''': These are located spinally and supraspinally. The primary effect of receptor engagement is sedation.
* '''OP2''': Located spinally, the main effect of OP2 activation is sedation.
* '''OP3''': OP3 receptor interaction gives rise to analgesia, on a spinal and supraspinal level.

Following interaction with the receptor and the subsequent cascade of events, opiods exert their effects by a variety of mechanisms. Neuronal excitability is decreased, along with reductions in the release of the neurotransmitters glutamate and substance P. In this manner, transmission of nociceptive impulses is inhibited and the actions detailed above are elicited.

==Pharmacokinetic Considerations==

Opioids can be administered intramuscularly, intravenously, subcutanously, intrathecally or orally. Absorption following oral administration is variable with the drug used, but first-pass metabolism decreases the efficacy of the drug when given this way.

The half-life of opioids is around 3-6 hours.

==Side Effects and Contraindications==

Side effects of opioid drugs include:
* Emesis. This is worst in animals that are not in pain at the time of administration, e.g. when morphine is administered as a pre-operative pre-medication.
* Negative chronotropic effects
* Respiratory depression
* Reduced gastro-intestinal motility. This is of most clinical significance in the horse, which is prone to post-operative ileus.

==Drugs in this Group==

===Morphine===

Morphine is indicated for severe pain, but is an unlicensed, Schedule 2 controlled drug. It may be administered by the i/m, i/v, s/c and i/t routes, and may also be given as a constant rate infusion.

Morphine is a full OP3 agonist, with a 10-15 min onset and a duration of 2-4 hours. Its side effects are as detailed above.

Glucuronidation in the liver produces an active metabolite of the drug, morphine-6-glucuronide (morphine-3-glucuronide is also formed). Metabolites are then excreted in the urine. Enterohepatic circulation of morphine does occur, but this is not clinically important.

===Buprenorphine===

Buprenorphine is a Schedule 3 controlled drug used for the relief of moderate pain. It is licensed for veterinary used and may be given i/v, i/m, s/c or p/o. Its actions last 6-8 hours.

Buprenorphine is a partial OP3 agonist/antagonist. This gives it a bell-shaped dose response curve, with large experimental doses actually causing opioid receptor antagonism. Buprenophine may therefore cause partial reversal of administration of full OP3 agonists such as [[#Morphine|morphine]], [[#Methadone|methadone]], [[#Pethidine|pethidine]] or [[#Fentanyl|fentanyl]].

===Butorphanol===

Butorphanol may be used to combat mild pain. It is a poor analgesic but has excellent sedative properties, and also acts as a cough suppressant. Butorphanol is licensed for veterinary use, and is a mixed partial agonist; it is an antagonist at the OP3 receptor and an agonist at the OP2 receptor.

There is an onset time of 15 mins following i/v, i/m or s/c administration, and effects then last for 2-4 hours.

===Pethidine===

A full OP3 agonist, pethidine is used for moderate to severe pain. It may be given i/m or s/c, but NOT intravenously as it will cause massive histamine release. The onset time is 10-15 mins, and the drug has as duration of 30-60 mins. Pethidine is chronotropic and also spasmolytic. It is therefore a good drug choice to provide analgesia and facilitate rectal examination of colic-ing horses. Pethidine is a licensed, Schedule 2 controlled drug.

===Methadone===

Methadone is an unlicensed, Schedule 2 controlled, full OP3 agonist. It is used i/v, i/m, s/c or by constant rate infusion for the relief of moderate to severe pain. Advantageously, it does not cause emesis.

===Fentanyl===

Fentanyl may be used i/v or via slow release patches for severe pain. It is a full OP3 agonist with a rapid onset of action and a duration of 15-20 mins. It is therefore useful as "rescue analgesia" to top-up levels of analgesia during particularly painful stages of surgery. It is a Schedule 2 controlled drug which is licensed as a formulation containing fluanisone as a neuroleptanalgesic for use in mice, rats, rabbits and guinea pigs.

===Etorphine===

Etorphine is a hugely potent opioid that is a component of large animal and small animal immobilon. (Large animal immobilon consists of etorphine plus [[Phenothiazines#Acepromazine|acepromazine]]; small animal immobilon comprises etorphine and [[Phenothiazines#Methotrimeprazine|methotrimeprazine]] ). It may be fatal to man follwing self administration, wehn opioid antagonism with [[#Opioid Antagonists|naloxone]] is required.

==Opioid Antagonists==

Naloxone is an antagonist to endogenous opioids. It is frequently used in human medicine to antagonise opioid narcotics in the incidence of overdose. Naloxone may be administered intravenously, intramuscularly, intrathecally or subcutaneously. It has a short duration of action (1-2 hours) and so repeated administrations may be necessary.

Opioids

2009-09-01T10:06:04Z

Karag7: /* Fentanyl */

The opioid drugs include [[#Morphine|morphine]] and its synthetic derivatives. They are powerful '''analgesics''', and have dose-dependent '''sedative''' properties.

Opioids have additional recognised effects. They:
* Decrease the sensitivity of the respiratory centres of the brain to carbon dioxide.
* Give potent cough suppression.
* Cause emesis.
* Constrict the pupils (miosis).
* Reduce gastro-intestinal motility.
* Lead to histamine release.

==Mechanism of Action==

Opiods act on opioid (OP) receptors. OP receptors are G-protein coupled: activation of the receptors causes inhibition of adenylate cyclase, decreasing cAMP levels within the cell. Thus, receptor-ligand interaction promotes the opening of K+ channels within the plasma membrane, and also inhibits that of voltage-gated calcium channels. There are three types of opioid receptors:
* '''OP1''': These are located spinally and supraspinally. The primary effect of receptor engagement is sedation.
* '''OP2''': Located spinally, the main effect of OP2 activation is sedation.
* '''OP3''': OP3 receptor interaction gives rise to analgesia, on a spinal and supraspinal level.

Following interaction with the receptor and the subsequent cascade of events, opiods exert their effects by a variety of mechanisms. Neuronal excitability is decreased, along with reductions in the release of the neurotransmitters glutamate and substance P. In this manner, transmission of nociceptive impulses is inhibited and the actions detailed above are elicited.

==Pharmacokinetic Considerations==

Opioids can be administered intramuscularly, intravenously, subcutanously, intrathecally or orally. Absorption following oral administration is variable with the drug used, but first-pass metabolism decreases the efficacy of the drug when given this way.

The half-life of opioids is around 3-6 hours.

==Side Effects and Contraindications==

Side effects of opioid drugs include:
* Emesis. This is worst in animals that are not in pain at the time of administration, e.g. when morphine is administered as a pre-operative pre-medication.
* Negative chronotropic effects
* Respiratory depression
* Reduced gastro-intestinal motility. This is of most clinical significance in the horse, which is prone to post-operative ileus.

==Drugs in this Group==

===Morphine===

Morphine is indicated for severe pain, but is an unlicensed, Schedule 2 controlled drug. It may be administered by the i/m, i/v, s/c and i/t routes, and may also be given as a constant rate infusion.

Morphine is a full OP3 agonist, with a 10-15 min onset and a duration of 2-4 hours. Its side effects are as detailed above.

Glucuronidation in the liver produces an active metabolite of the drug, morphine-6-glucuronide (morphine-3-glucuronide is also formed). Metabolites are then excreted in the urine. Enterohepatic circulation of morphine does occur, but this is not clinically important.

===Buprenorphine===

Buprenorphine is a Schedule 3 controlled drug used for the relief of moderate pain. It is licensed for veterinary used and may be given i/v, i/m, s/c or p/o. Its actions last 6-8 hours.

Buprenorphine is a partial OP3 agonist/antagonist. This gives it a bell-shaped dose response curve, with large experimental doses actually causing opioid receptor antagonism. Buprenophine may therefore cause partial reversal of administration of full OP3 agonists such as [[#Morphine|morphine]], [[#Methadone|methadone]], [[#Pethidine|pethidine]] or [[#Fentanyl|fentanyl]].

===Butorphanol===

Butorphanol may be used to combat mild pain. It is a poor analgesic but has excellent sedative properties, and also acts as a cough suppressant. Butorphanol is licensed for veterinary use, and is a mixed partial agonist; it is an antagnoist at the OP3 receptor and an agonist at the OP2 receptor.

There is an onset time of 15 mins following i/v, i/m or s/c administration, and effects then last for 2-4 hours.

===Pethidine===

A full OP3 agonist, pethidine is used for moderate to severe pain. It may be given i/m or s/c, but NOT intravenously as it will cause massive histamine release. The onset time is 10-15 mins, and the drug has as duration of 30-60 mins. Pethidine is chronotropic and also spasmolytic. It is therefore a good drug choice to provide analgesia and facilitate rectal examination of colic-ing horses. Pethidine is a licensed, Schedule 2 controlled drug.

===Methadone===

Methadone is an unlicensed, Schedule 2 controlled, full OP3 agonist. It is used i/v, i/m, s/c or by constant rate infusion for the relief of moderate to severe pain. Advantageously, it does not cause emesis.

===Fentanyl===

Fentanyl may be used i/v or via slow release patches for severe pain. It is a full OP3 agonist with a rapid onset of action and a duration of 15-20 mins. It is therefore useful as "rescue analgesia" to top-up levels of analgesia during particularly painful stages of surgery. It is a Schedule 2 controlled drug which is licensed as a formulation containing fluanisone as a neuroleptanalgesic for use in mice, rats, rabbits and guinea pigs.

===Etorphine===

Etorphine is a hugely potent opioid that is a component of large animal and small animal immobilon. (Large animal immobilon consists of etorphine plus [[Phenothiazines#Acepromazine|acepromazine]]; small animal immobilon comprises etorphine and [[Phenothiazines#Methotrimeprazine|methotrimeprazine]] ). It may be fatal to man follwing self administration, wehn opioid antagonism with [[#Opioid Antagonists|naloxone]] is required.

==Opioid Antagonists==

Naloxone is an antagonist to endogenous opioids. It is frequently used in human medicine to antagonise opioid narcotics in the incidence of overdose. Naloxone may be administered intravenously, intramuscularly, intrathecally or subcutaneously. It has a short duration of action (1-2 hours) and so repeated administrations may be necessary.

Opioids

2009-09-01T10:05:22Z

Karag7: /* Fentanyl */

The opioid drugs include [[#Morphine|morphine]] and its synthetic derivatives. They are powerful '''analgesics''', and have dose-dependent '''sedative''' properties.

Opioids have additional recognised effects. They:
* Decrease the sensitivity of the respiratory centres of the brain to carbon dioxide.
* Give potent cough suppression.
* Cause emesis.
* Constrict the pupils (miosis).
* Reduce gastro-intestinal motility.
* Lead to histamine release.

==Mechanism of Action==

Opiods act on opioid (OP) receptors. OP receptors are G-protein coupled: activation of the receptors causes inhibition of adenylate cyclase, decreasing cAMP levels within the cell. Thus, receptor-ligand interaction promotes the opening of K+ channels within the plasma membrane, and also inhibits that of voltage-gated calcium channels. There are three types of opioid receptors:
* '''OP1''': These are located spinally and supraspinally. The primary effect of receptor engagement is sedation.
* '''OP2''': Located spinally, the main effect of OP2 activation is sedation.
* '''OP3''': OP3 receptor interaction gives rise to analgesia, on a spinal and supraspinal level.

Following interaction with the receptor and the subsequent cascade of events, opiods exert their effects by a variety of mechanisms. Neuronal excitability is decreased, along with reductions in the release of the neurotransmitters glutamate and substance P. In this manner, transmission of nociceptive impulses is inhibited and the actions detailed above are elicited.

==Pharmacokinetic Considerations==

Opioids can be administered intramuscularly, intravenously, subcutanously, intrathecally or orally. Absorption following oral administration is variable with the drug used, but first-pass metabolism decreases the efficacy of the drug when given this way.

The half-life of opioids is around 3-6 hours.

==Side Effects and Contraindications==

Side effects of opioid drugs include:
* Emesis. This is worst in animals that are not in pain at the time of administration, e.g. when morphine is administered as a pre-operative pre-medication.
* Negative chronotropic effects
* Respiratory depression
* Reduced gastro-intestinal motility. This is of most clinical significance in the horse, which is prone to post-operative ileus.

==Drugs in this Group==

===Morphine===

Morphine is indicated for severe pain, but is an unlicensed, Schedule 2 controlled drug. It may be administered by the i/m, i/v, s/c and i/t routes, and may also be given as a constant rate infusion.

Morphine is a full OP3 agonist, with a 10-15 min onset and a duration of 2-4 hours. Its side effects are as detailed above.

Glucuronidation in the liver produces an active metabolite of the drug, morphine-6-glucuronide (morphine-3-glucuronide is also formed). Metabolites are then excreted in the urine. Enterohepatic circulation of morphine does occur, but this is not clinically important.

===Buprenorphine===

Buprenorphine is a Schedule 3 controlled drug used for the relief of moderate pain. It is licensed for veterinary used and may be given i/v, i/m, s/c or p/o. Its actions last 6-8 hours.

Buprenorphine is a partial OP3 agonist/antagonist. This gives it a bell-shaped dose response curve, with large experimental doses actually causing opioid receptor antagonism. Buprenophine may therefore cause partial reversal of administration of full OP3 agonists such as [[#Morphine|morphine]], [[#Methadone|methadone]], [[#Pethidine|pethidine]] or [[#Fentanyl|fentanyl]].

===Butorphanol===

Butorphanol may be used to combat mild pain. It is a poor analgesic but has excellent sedative properties, and also acts as a cough suppressant. Butorphanol is licensed for veterinary use, and is a mixed partial agonist; it is an antagnoist at the OP3 receptor and an agonist at the OP2 receptor.

There is an onset time of 15 mins following i/v, i/m or s/c administration, and effects then last for 2-4 hours.

===Pethidine===

A full OP3 agonist, pethidine is used for moderate to severe pain. It may be given i/m or s/c, but NOT intravenously as it will cause massive histamine release. The onset time is 10-15 mins, and the drug has as duration of 30-60 mins. Pethidine is chronotropic and also spasmolytic. It is therefore a good drug choice to provide analgesia and facilitate rectal examination of colic-ing horses. Pethidine is a licensed, Schedule 2 controlled drug.

===Methadone===

Methadone is an unlicensed, Schedule 2 controlled, full OP3 agonist. It is used i/v, i/m, s/c or by constant rate infusion for the relief of moderate to severe pain. Advantageously, it does not cause emesis.

===Fentanyl===

Fentanyl may be used i/v or via slow release patches for severe pain. It is a full OP3 agonist with a rapid onset of action and a duration of 15-20 mins. It is therefore useful as "rescue analgesia" to top-up levels of analgesia during particularly painful stages of surgery. It is a Schedule 2 controlled drug which is licensed in combination with fluanisone as a neuroleptanalgesic for use in mice, rats, rabbits and guinea pigs.

===Etorphine===

Etorphine is a hugely potent opioid that is a component of large animal and small animal immobilon. (Large animal immobilon consists of etorphine plus [[Phenothiazines#Acepromazine|acepromazine]]; small animal immobilon comprises etorphine and [[Phenothiazines#Methotrimeprazine|methotrimeprazine]] ). It may be fatal to man follwing self administration, wehn opioid antagonism with [[#Opioid Antagonists|naloxone]] is required.

==Opioid Antagonists==

Naloxone is an antagonist to endogenous opioids. It is frequently used in human medicine to antagonise opioid narcotics in the incidence of overdose. Naloxone may be administered intravenously, intramuscularly, intrathecally or subcutaneously. It has a short duration of action (1-2 hours) and so repeated administrations may be necessary.

Opioids

2009-09-01T10:03:52Z

Karag7: /* Pethidine */

The opioid drugs include [[#Morphine|morphine]] and its synthetic derivatives. They are powerful '''analgesics''', and have dose-dependent '''sedative''' properties.

Opioids have additional recognised effects. They:
* Decrease the sensitivity of the respiratory centres of the brain to carbon dioxide.
* Give potent cough suppression.
* Cause emesis.
* Constrict the pupils (miosis).
* Reduce gastro-intestinal motility.
* Lead to histamine release.

==Mechanism of Action==

Opiods act on opioid (OP) receptors. OP receptors are G-protein coupled: activation of the receptors causes inhibition of adenylate cyclase, decreasing cAMP levels within the cell. Thus, receptor-ligand interaction promotes the opening of K+ channels within the plasma membrane, and also inhibits that of voltage-gated calcium channels. There are three types of opioid receptors:
* '''OP1''': These are located spinally and supraspinally. The primary effect of receptor engagement is sedation.
* '''OP2''': Located spinally, the main effect of OP2 activation is sedation.
* '''OP3''': OP3 receptor interaction gives rise to analgesia, on a spinal and supraspinal level.

Following interaction with the receptor and the subsequent cascade of events, opiods exert their effects by a variety of mechanisms. Neuronal excitability is decreased, along with reductions in the release of the neurotransmitters glutamate and substance P. In this manner, transmission of nociceptive impulses is inhibited and the actions detailed above are elicited.

==Pharmacokinetic Considerations==

Opioids can be administered intramuscularly, intravenously, subcutanously, intrathecally or orally. Absorption following oral administration is variable with the drug used, but first-pass metabolism decreases the efficacy of the drug when given this way.

The half-life of opioids is around 3-6 hours.

==Side Effects and Contraindications==

Side effects of opioid drugs include:
* Emesis. This is worst in animals that are not in pain at the time of administration, e.g. when morphine is administered as a pre-operative pre-medication.
* Negative chronotropic effects
* Respiratory depression
* Reduced gastro-intestinal motility. This is of most clinical significance in the horse, which is prone to post-operative ileus.

==Drugs in this Group==

===Morphine===

Morphine is indicated for severe pain, but is an unlicensed, Schedule 2 controlled drug. It may be administered by the i/m, i/v, s/c and i/t routes, and may also be given as a constant rate infusion.

Morphine is a full OP3 agonist, with a 10-15 min onset and a duration of 2-4 hours. Its side effects are as detailed above.

Glucuronidation in the liver produces an active metabolite of the drug, morphine-6-glucuronide (morphine-3-glucuronide is also formed). Metabolites are then excreted in the urine. Enterohepatic circulation of morphine does occur, but this is not clinically important.

===Buprenorphine===

Buprenorphine is a Schedule 3 controlled drug used for the relief of moderate pain. It is licensed for veterinary used and may be given i/v, i/m, s/c or p/o. Its actions last 6-8 hours.

Buprenorphine is a partial OP3 agonist/antagonist. This gives it a bell-shaped dose response curve, with large experimental doses actually causing opioid receptor antagonism. Buprenophine may therefore cause partial reversal of administration of full OP3 agonists such as [[#Morphine|morphine]], [[#Methadone|methadone]], [[#Pethidine|pethidine]] or [[#Fentanyl|fentanyl]].

===Butorphanol===

Butorphanol may be used to combat mild pain. It is a poor analgesic but has excellent sedative properties, and also acts as a cough suppressant. Butorphanol is licensed for veterinary use, and is a mixed partial agonist; it is an antagnoist at the OP3 receptor and an agonist at the OP2 receptor.

There is an onset time of 15 mins following i/v, i/m or s/c administration, and effects then last for 2-4 hours.

===Pethidine===

A full OP3 agonist, pethidine is used for moderate to severe pain. It may be given i/m or s/c, but NOT intravenously as it will cause massive histamine release. The onset time is 10-15 mins, and the drug has as duration of 30-60 mins. Pethidine is chronotropic and also spasmolytic. It is therefore a good drug choice to provide analgesia and facilitate rectal examination of colic-ing horses. Pethidine is a licensed, Schedule 2 controlled drug.

===Methadone===

Methadone is an unlicensed, Schedule 2 controlled, full OP3 agonist. It is used i/v, i/m, s/c or by constant rate infusion for the relief of moderate to severe pain. Advantageously, it does not cause emesis.

===Fentanyl===

Fentanyl may be used i/v or via slow release patches for severe pain. It is a full OP3 agonist with a rapid onset of action and a duration of 15-20 mins. It is therefore useful as "rescue analgesia" to top-up levels of analgesia during particularly painful stages of surgery. It is an unlicensed, Schedule 2 controlled drug.

===Etorphine===

Etorphine is a hugely potent opioid that is a component of large animal and small animal immobilon. (Large animal immobilon consists of etorphine plus [[Phenothiazines#Acepromazine|acepromazine]]; small animal immobilon comprises etorphine and [[Phenothiazines#Methotrimeprazine|methotrimeprazine]] ). It may be fatal to man follwing self administration, wehn opioid antagonism with [[#Opioid Antagonists|naloxone]] is required.

==Opioid Antagonists==

Naloxone is an antagonist to endogenous opioids. It is frequently used in human medicine to antagonise opioid narcotics in the incidence of overdose. Naloxone may be administered intravenously, intramuscularly, intrathecally or subcutaneously. It has a short duration of action (1-2 hours) and so repeated administrations may be necessary.

Opioids

2009-09-01T10:02:12Z

Karag7: /* Buprenorphine */

The opioid drugs include [[#Morphine|morphine]] and its synthetic derivatives. They are powerful '''analgesics''', and have dose-dependent '''sedative''' properties.

Opioids have additional recognised effects. They:
* Decrease the sensitivity of the respiratory centres of the brain to carbon dioxide.
* Give potent cough suppression.
* Cause emesis.
* Constrict the pupils (miosis).
* Reduce gastro-intestinal motility.
* Lead to histamine release.

==Mechanism of Action==

Opiods act on opioid (OP) receptors. OP receptors are G-protein coupled: activation of the receptors causes inhibition of adenylate cyclase, decreasing cAMP levels within the cell. Thus, receptor-ligand interaction promotes the opening of K+ channels within the plasma membrane, and also inhibits that of voltage-gated calcium channels. There are three types of opioid receptors:
* '''OP1''': These are located spinally and supraspinally. The primary effect of receptor engagement is sedation.
* '''OP2''': Located spinally, the main effect of OP2 activation is sedation.
* '''OP3''': OP3 receptor interaction gives rise to analgesia, on a spinal and supraspinal level.

Following interaction with the receptor and the subsequent cascade of events, opiods exert their effects by a variety of mechanisms. Neuronal excitability is decreased, along with reductions in the release of the neurotransmitters glutamate and substance P. In this manner, transmission of nociceptive impulses is inhibited and the actions detailed above are elicited.

==Pharmacokinetic Considerations==

Opioids can be administered intramuscularly, intravenously, subcutanously, intrathecally or orally. Absorption following oral administration is variable with the drug used, but first-pass metabolism decreases the efficacy of the drug when given this way.

The half-life of opioids is around 3-6 hours.

==Side Effects and Contraindications==

Side effects of opioid drugs include:
* Emesis. This is worst in animals that are not in pain at the time of administration, e.g. when morphine is administered as a pre-operative pre-medication.
* Negative chronotropic effects
* Respiratory depression
* Reduced gastro-intestinal motility. This is of most clinical significance in the horse, which is prone to post-operative ileus.

==Drugs in this Group==

===Morphine===

Morphine is indicated for severe pain, but is an unlicensed, Schedule 2 controlled drug. It may be administered by the i/m, i/v, s/c and i/t routes, and may also be given as a constant rate infusion.

Morphine is a full OP3 agonist, with a 10-15 min onset and a duration of 2-4 hours. Its side effects are as detailed above.

Glucuronidation in the liver produces an active metabolite of the drug, morphine-6-glucuronide (morphine-3-glucuronide is also formed). Metabolites are then excreted in the urine. Enterohepatic circulation of morphine does occur, but this is not clinically important.

===Buprenorphine===

Buprenorphine is a Schedule 3 controlled drug used for the relief of moderate pain. It is licensed for veterinary used and may be given i/v, i/m, s/c or p/o. Its actions last 6-8 hours.

Buprenorphine is a partial OP3 agonist/antagonist. This gives it a bell-shaped dose response curve, with large experimental doses actually causing opioid receptor antagonism. Buprenophine may therefore cause partial reversal of administration of full OP3 agonists such as [[#Morphine|morphine]], [[#Methadone|methadone]], [[#Pethidine|pethidine]] or [[#Fentanyl|fentanyl]].

===Butorphanol===

Butorphanol may be used to combat mild pain. It is a poor analgesic but has excellent sedative properties, and also acts as a cough suppressant. Butorphanol is licensed for veterinary use, and is a mixed partial agonist; it is an antagnoist at the OP3 receptor and an agonist at the OP2 receptor.

There is an onset time of 15 mins following i/v, i/m or s/c administration, and effects then last for 2-4 hours.

===Pethidine===

A full OP3 agonist, pethidine is used for moderate to severe pain. It may be given i/m or s/c, but NOT intravenously as it will cause massive histamine release. The onset time is 10-15 mins, and the drug has as duration of 30-60 mins. Pethidine is chronotropic and also spasmolytic. It is therefore a good drug choice to provide analgesia and facilitate rectal examination of colic-ing horses. Pethidine is a Schedule 2 controlled drug.

===Methadone===

Methadone is an unlicensed, Schedule 2 controlled, full OP3 agonist. It is used i/v, i/m, s/c or by constant rate infusion for the relief of moderate to severe pain. Advantageously, it does not cause emesis.

===Fentanyl===

Fentanyl may be used i/v or via slow release patches for severe pain. It is a full OP3 agonist with a rapid onset of action and a duration of 15-20 mins. It is therefore useful as "rescue analgesia" to top-up levels of analgesia during particularly painful stages of surgery. It is an unlicensed, Schedule 2 controlled drug.

===Etorphine===

Etorphine is a hugely potent opioid that is a component of large animal and small animal immobilon. (Large animal immobilon consists of etorphine plus [[Phenothiazines#Acepromazine|acepromazine]]; small animal immobilon comprises etorphine and [[Phenothiazines#Methotrimeprazine|methotrimeprazine]] ). It may be fatal to man follwing self administration, wehn opioid antagonism with [[#Opioid Antagonists|naloxone]] is required.

==Opioid Antagonists==

Naloxone is an antagonist to endogenous opioids. It is frequently used in human medicine to antagonise opioid narcotics in the incidence of overdose. Naloxone may be administered intravenously, intramuscularly, intrathecally or subcutaneously. It has a short duration of action (1-2 hours) and so repeated administrations may be necessary.

Opioids

2009-09-01T10:01:32Z

Karag7: /* Butorphanol */

The opioid drugs include [[#Morphine|morphine]] and its synthetic derivatives. They are powerful '''analgesics''', and have dose-dependent '''sedative''' properties.

Opioids have additional recognised effects. They:
* Decrease the sensitivity of the respiratory centres of the brain to carbon dioxide.
* Give potent cough suppression.
* Cause emesis.
* Constrict the pupils (miosis).
* Reduce gastro-intestinal motility.
* Lead to histamine release.

==Mechanism of Action==

Opiods act on opioid (OP) receptors. OP receptors are G-protein coupled: activation of the receptors causes inhibition of adenylate cyclase, decreasing cAMP levels within the cell. Thus, receptor-ligand interaction promotes the opening of K+ channels within the plasma membrane, and also inhibits that of voltage-gated calcium channels. There are three types of opioid receptors:
* '''OP1''': These are located spinally and supraspinally. The primary effect of receptor engagement is sedation.
* '''OP2''': Located spinally, the main effect of OP2 activation is sedation.
* '''OP3''': OP3 receptor interaction gives rise to analgesia, on a spinal and supraspinal level.

Following interaction with the receptor and the subsequent cascade of events, opiods exert their effects by a variety of mechanisms. Neuronal excitability is decreased, along with reductions in the release of the neurotransmitters glutamate and substance P. In this manner, transmission of nociceptive impulses is inhibited and the actions detailed above are elicited.

==Pharmacokinetic Considerations==

Opioids can be administered intramuscularly, intravenously, subcutanously, intrathecally or orally. Absorption following oral administration is variable with the drug used, but first-pass metabolism decreases the efficacy of the drug when given this way.

The half-life of opioids is around 3-6 hours.

==Side Effects and Contraindications==

Side effects of opioid drugs include:
* Emesis. This is worst in animals that are not in pain at the time of administration, e.g. when morphine is administered as a pre-operative pre-medication.
* Negative chronotropic effects
* Respiratory depression
* Reduced gastro-intestinal motility. This is of most clinical significance in the horse, which is prone to post-operative ileus.

==Drugs in this Group==

===Morphine===

Morphine is indicated for severe pain, but is an unlicensed, Schedule 2 controlled drug. It may be administered by the i/m, i/v, s/c and i/t routes, and may also be given as a constant rate infusion.

Morphine is a full OP3 agonist, with a 10-15 min onset and a duration of 2-4 hours. Its side effects are as detailed above.

Glucuronidation in the liver produces an active metabolite of the drug, morphine-6-glucuronide (morphine-3-glucuronide is also formed). Metabolites are then excreted in the urine. Enterohepatic circulation of morphine does occur, but this is not clinically important.

===Buprenorphine===

Buprenorphine is a Schedule 3 controlled drug used for the relief of moderate pain. It is licensed for veterinary used and may be given i/v, i/m, s/c or p/o. Its actions last 6-8 hours.

Buprenorphine is a partial OP3 agonisy/antagonist. This gives it a bell-shaped dose response curve, with large experimental doses actually causing opioid receptor antagonism. Buprenophine may therefore cause partial reversal of administration of full OP3 agonists such as [[#Morphine|morphine]], [[#Methadone|methadone]], [[#Pethidine|pethidine]] or [[#Fentanyl|fentanyl]].

===Butorphanol===

Butorphanol may be used to combat mild pain. It is a poor analgesic but has excellent sedative properties, and also acts as a cough suppressant. Butorphanol is licensed for veterinary use, and is a mixed partial agonist; it is an antagnoist at the OP3 receptor and an agonist at the OP2 receptor.

There is an onset time of 15 mins following i/v, i/m or s/c administration, and effects then last for 2-4 hours.

===Pethidine===

A full OP3 agonist, pethidine is used for moderate to severe pain. It may be given i/m or s/c, but NOT intravenously as it will cause massive histamine release. The onset time is 10-15 mins, and the drug has as duration of 30-60 mins. Pethidine is chronotropic and also spasmolytic. It is therefore a good drug choice to provide analgesia and facilitate rectal examination of colic-ing horses. Pethidine is a Schedule 2 controlled drug.

===Methadone===

Methadone is an unlicensed, Schedule 2 controlled, full OP3 agonist. It is used i/v, i/m, s/c or by constant rate infusion for the relief of moderate to severe pain. Advantageously, it does not cause emesis.

===Fentanyl===

Fentanyl may be used i/v or via slow release patches for severe pain. It is a full OP3 agonist with a rapid onset of action and a duration of 15-20 mins. It is therefore useful as "rescue analgesia" to top-up levels of analgesia during particularly painful stages of surgery. It is an unlicensed, Schedule 2 controlled drug.

===Etorphine===

Etorphine is a hugely potent opioid that is a component of large animal and small animal immobilon. (Large animal immobilon consists of etorphine plus [[Phenothiazines#Acepromazine|acepromazine]]; small animal immobilon comprises etorphine and [[Phenothiazines#Methotrimeprazine|methotrimeprazine]] ). It may be fatal to man follwing self administration, wehn opioid antagonism with [[#Opioid Antagonists|naloxone]] is required.

==Opioid Antagonists==

Naloxone is an antagonist to endogenous opioids. It is frequently used in human medicine to antagonise opioid narcotics in the incidence of overdose. Naloxone may be administered intravenously, intramuscularly, intrathecally or subcutaneously. It has a short duration of action (1-2 hours) and so repeated administrations may be necessary.

Alpha-2 Agonists

2009-09-01T09:05:51Z

Karag7: /* Actions */

Alpha-2 agonists have sedative, anxiolytic and analgesic effects.

==Mechanism of Action==

Alpha-2 agonists act on alpha-2 adrenoreceptors, and mimic the effects of the actual ligand binding. The sedative and anxiolytic effects arise from this process leading to pre-synaptic inhibition of noradrenaline release.

==Pharmacokinetic Considerations==

There is great variation between species sensitivity to alpha-2 agonists. Cattle are ten times as sensitive to the drugs as horses.

==Actions==

Alpha-2 agonists have a wide range of actions, due to the presence of alpha-2 receptors throughout the body. The actions most useful pharmacologically are '''sedation''', '''anxiolysis''' and '''analgesia'''. The drugs also have a huge '''anaesthetic sparing effect''', reducing MAC by 50-95%. They also give '''muscle relaxation'''.

Other systems affected by alpha-2 agonists include:
* Cardiovascular System
** Post synaptic alpha-2 effects and non-selective action on alpha-1 receptors cause vasoconstriction, hypertension and reflex bradycardia.
** Pre-synaptic inhibition of noradrenaline release gives a reduced sympathetic outflow. This decreases heart rate and offsets vasoconstriction.
* Respiratory System
** The drugs cause mild depression of the respiratory systsem.
** The response to hypercapnoea is reduced.
* Gastrointestinal Tract
** Alpha-2 agonists cause extreme vomiting in dogs and cats. [[#Xylazine|Xylazine]] is the worst culprit for this.
** Huge reductions in gut motility occur following drug administration, as well as decreased salivation and secretion.
* Endocrine System
** Alpha-2 agonists inhibit ADH, leading to diuresis.
** Insulin is also inhibited, causing hyperglycaemia which leads to osmotic diuresis. This, along with the above, causes excessive urination.
** Growth hormone release is triggered by alpha-2 agonists.
* Urogenital Tract
** Uterine contraction occurs with alpha-2 agonist administration.

==Side Effects and Contraindications==

Side effects relate to the wide range of action of the drugs. These particularly include vomitting, hypertension and uterine contraction.

==Drugs in this Group==

===Xylazine===

Xylazine is available as a 2% solution for use in cattle, horses, cats and dogs. A 10% solution for horses may be used for pre-medication prior to [[NMDA Antagonists|ketamine]] anaesthesia or analgesia in, for example, colic cases. A powdered form is also licensed in horses. Intramuscular and intravenous administration both have a short onset time of 5 minutes. The peak effect occurs 10 minutes after intramuscular injection, and the duration of the drug's actions is 20 mins following intravenous administration. Intravenous use is only licensed in dogs and cats.

Xylazine must not be used in the last month of pregnancy, since it causes uterine contractions. The drug is also arrhythmogenic.

===Detomidine===

Detomidine is available as a 10mg/ml solution in multidose vials. It is licenced for use in cattle and horses. It can be administered via an intravenous or intramuscular route. Although oral dosing is ineffective, it is readily absorbed across mucous membranes so may be adminstered sublingually. Its main indication for use is sedation in the horse for examinations, such as rectal or endoscopic, minor surgical procedures, as part of a premedication regime or before treatment, such as shoeing.

===Medetomidine===

Medetomidine is available as a 1mg/ml solution for use in dogs and cats.It is non irritant so therefore can be administered via an intravenous, intramuscular or subcutaneous route. Intravenous administration produces the most rapid effects, and the least amount of vomiting compared to other routes of administration. When given via an intramuscular route, maximal effects are not seen until 20 minutes after administration, although some sedation may be seen as early as 5 minutes. It is a very effective premedicant reducing the MAC of inhalation agents, and can be used in combination with [[NMDA Antagonists|ketamine]] in cats to induce anaethesia.

===Romifidine===

Romifidine is available as a 10mg/ml solution for use in horses. Its main indication for use is as a sedation agent and may be used in a premedication regime. It produces less ataxia and the head does not lower as much when compared to [[#xylazine|xylazine]] but the duration of action is longer.

Phenothiazines

2009-08-31T16:04:05Z

Karag7: /* Acepromazine */

==Actions==

Phenothiazines have tranquilising, sedative and anxiolytic properties, but do NOT provide analgesia. As well as these effects on the CNS, phenothiazines also affect the cardiovascular system and the gastrointestinal tract (see [[#Side Effects and Contraindications|Side Effects and Contraindications]]).

==Drugs in this Group==

Phenothiazines include:
* [[#Acepromazine|Acepromazine]]
* Proprionylpromazine
* Chlorpromazine
* Promazine
* [[#Methotrimeprazine|Methotrimeprazine]]
* Promethazine

===Acepromazine===

Acepromazine (ACP) is commonly used in veterinary practice as a sedative and as a premedicant. It is available in liquid, gel and tablet form and so may be administered orally (with 20-55% bioavailability), i/m, i/v or s/c. The intramuscular route is preferred as fewer side effects are apparent. Administration in this way leads to a 20 minute onset of drug action. The time to onset is only 5 minutes if acepromazine is given intravenously, but the drug must be given slowly to avoid causing vasodilation and hypotension. The duration of effects is 4-6 hours.

Lower doses of acepromazine affect animal behaviour, whereas higher doses give sedation. However, the level of sedation is not increased by increasing the drug dose further; this merely increases the duration of sedation. Acepromazine's sedative effect is greatest in young, anxious animals.

Acepromazine potentiates the actions of several other drugs. These include [[Local Anaesthetics|local anaesthetic agents]], general anaesthetics and opioids (forming the principal of neurolept analgesia). Administration of the drug may also lower the threshold for seizures but, interestingly, acepromazine may be used as an anticonvulsant. ACP is also anti-emetic.

Use of acepromazine is contra-indicated in breeding stallions, as it may cause penis protrusion and priapism. In Boxers spontaneous fainting and syncope can occur due to sinoatrial block caused by excessive vagal tone, so acepromazine should be given in low doses or avoided in this breed. Giant breeds of dog require lower doses of the drug.

===Methotrimeprazine===

Methotrimeprazine has potent analsgesis as well as tranquilising, sedatice and anxiolytic actions. It si a component of small animal immobilon, along with [[Opioids#Etorphine|etorphine]].

==Side Effects and Contraindications==

In addition to the CNS, phenothiazines also act on:
* The '''cardiovascular system''', where they bind to alpha-1 adrenoreceptors leading to vasodilation, hypotension and hypothermia.
* The '''gastrointestinal tract''', where they have an antispasmodic effect.
* Other '''receptors'''. Blockade of muscarinic receptors, histamine receptors and 5-HT occurs.
* '''Hypovolaemia''' - due to the vasodilator effects of ACP it's use is contraindicated in animals with, or suspected of having hypovolaemia

Acepromazine can cause penis protrusion and priapism in stallions, and may lower the seizure threshold.

Phenothiazines

2009-08-31T16:03:44Z

Karag7: /* Acepromazine */

==Actions==

Phenothiazines have tranquilising, sedative and anxiolytic properties, but do NOT provide analgesia. As well as these effects on the CNS, phenothiazines also affect the cardiovascular system and the gastrointestinal tract (see [[#Side Effects and Contraindications|Side Effects and Contraindications]]).

==Drugs in this Group==

Phenothiazines include:
* [[#Acepromazine|Acepromazine]]
* Proprionylpromazine
* Chlorpromazine
* Promazine
* [[#Methotrimeprazine|Methotrimeprazine]]
* Promethazine

===Acepromazine===

Acepromazine (ACP) is commonly used in veterinary practice as a sedative and as a premedicant. It is available in liquid, gel and tablet form and so may be administered orally (with 20-55% bioavailability), i/m, i/v or s/c. The intramuscular route is preferred as fewer side effects are apparent. Administration in this way leads to a 20 minute onset of drug action. The time to onset is only 5 minutes if acepromazine is given intravenously, but the drug must be given slowly to avoid causing vasodilation and hypotension. The duration of effects is 4-6 hours.

Lower doses of acepromazine affect animal behaviour, whereas higher doses give sedation. However, the level of sedation is not increased by increasing the drug dose further; this merely increases the duration of sedation. Acepromazine's sedative effect is greatest in young, anxious animals.

Acepromazine potentiates the actions of several other drugs. These include [[Local Anaesthetics|local anaesthetic agents]], general anaesthetics and opioids (forming the principal of neurolept analgesia). Administration of the drug may also lower the threshold for seizures but, interestingly, acepromazine may be used as an anticonvulsant. ACP is also anti-emetic.

Use of acepromazine is contra-indicated in breeding stallions, as it may cause penis protrusion and priapism. In Boxers spontaneous fainting and syncope can occur due to sinoatrial block caused by excessive vagal tone, so acepromazien should be given in low doses or avoided in this breed. Giant breeds of dog require lower doses of the drug.

===Methotrimeprazine===

Methotrimeprazine has potent analsgesis as well as tranquilising, sedatice and anxiolytic actions. It si a component of small animal immobilon, along with [[Opioids#Etorphine|etorphine]].

==Side Effects and Contraindications==

In addition to the CNS, phenothiazines also act on:
* The '''cardiovascular system''', where they bind to alpha-1 adrenoreceptors leading to vasodilation, hypotension and hypothermia.
* The '''gastrointestinal tract''', where they have an antispasmodic effect.
* Other '''receptors'''. Blockade of muscarinic receptors, histamine receptors and 5-HT occurs.
* '''Hypovolaemia''' - due to the vasodilator effects of ACP it's use is contraindicated in animals with, or suspected of having hypovolaemia

Acepromazine can cause penis protrusion and priapism in stallions, and may lower the seizure threshold.

Phenothiazines

2009-08-31T15:04:46Z

Karag7: /* Acepromazine */

==Actions==

Phenothiazines have tranquilising, sedative and anxiolytic properties, but do NOT provide analgesia. As well as these effects on the CNS, phenothiazines also affect the cardiovascular system and the gastrointestinal tract (see [[#Side Effects and Contraindications|Side Effects and Contraindications]]).

==Drugs in this Group==

Phenothiazines include:
* [[#Acepromazine|Acepromazine]]
* Proprionylpromazine
* Chlorpromazine
* Promazine
* [[#Methotrimeprazine|Methotrimeprazine]]
* Promethazine

===Acepromazine===

Acepromazine (ACP) is commonly used in veterinary practice as a sedative and as a premedicant. It is available in liquid, gel and tablet form and so may be administered orally (with 20-55% bioavailability), i/m, i/v or s/c. The intramuscular route is preferred as fewer side effects are apparent. Administration in this way leads to a 20 minute onset of drug action. The time to onset is only 5 minutes if acepromazine is given intravenously, but the drug must be given slowly to avoid causing vasodilation and hypotension. The duration of effects is 4-6 hours.

Lower doses of acepromazine affect animal behaviour, whereas higher doses give sedation. However, the level of sedation is not increased by increasing the drug dose further; this merely increases the duration of sedation. Acepromazine's sedative effect is greatest in young, anxious animals.

Acepromazine potentiates the actions of several other drugs. These include [[Local Anaesthetics|local anaesthetic agents]], general anaesthetics and opioids (forming the principal of neurolept analgesia). Administration of the drug may also lower the threshold for seizures but, interestingly, acepromazine may be used as an anticonvulsant. ACP is also anti-emetic.

Use of acepromazine is contra-indicated in breeding stallions, as it may cause penis protrusion and priapism. Boxers and giant breeds of dog require lower doses of the drug.

===Methotrimeprazine===

Methotrimeprazine has potent analsgesis as well as tranquilising, sedatice and anxiolytic actions. It si a component of small animal immobilon, along with [[Opioids#Etorphine|etorphine]].

==Side Effects and Contraindications==

In addition to the CNS, phenothiazines also act on:
* The '''cardiovascular system''', where they bind to alpha-1 adrenoreceptors leading to vasodilation, hypotension and hypothermia.
* The '''gastrointestinal tract''', where they have an antispasmodic effect.
* Other '''receptors'''. Blockade of muscarinic receptors, histamine receptors and 5-HT occurs.
* '''Hypovolaemia''' - due to the vasodilator effects of ACP it's use is contraindicated in animals with, or suspected of having hypovolaemia

Acepromazine can cause penis protrusion and priapism in stallions, and may lower the seizure threshold.

Breathing Systems

2009-08-31T14:52:21Z

Karag7: /* Circle */

{{unfinished}}
==Introduction==
Breathing systems are the connecting component between the anaesthetic machine and patient. Their role is to deliver oxygen and anaesthetic agent to the patient from the machine, remove exhaled carbon dioxide and provided a means of ventilation via pressure on the reservoir bag.

Basic components of a breathing system are -
*''Breathing tubes'' - Deliver gases to patient and allow for flexibility.
*''Reservoir bag'' - Allows for gas accumulation during exhalation and can be used to assist breathing.
*''Carbon dioxide absorbent'' - To absorb carbon dioxide from the circuit to allow complete rebreathing.
*''One way valve'' - Ensures gases flowing towards the patient do not mix with those exhaled i.e. make a one way system within circuit.
*''Pressure relief valve'' - Limit pressure build up and allows for removal of waste gases.
*''Fresh gas inlet'' - Connects the circuit to the gas outlet on the anaesthetic machine.

==Classification==
Breathing systems have been classified in a number of different ways, including open and closed, but current classification is -

*'''''Non-rebreathing''''' - The patient breathes from the anaesthetic machine and then exhaled into the atmosphere.
*'''''Rebreathing''''' - The patient rebreathes exhaled gases, but a carbon dioxide absorbant is present to remove any waste gases.

===Non Rebreathing Systems===
====''T-piece''====
*Used on patients less than 10kg.
*Circuit factor - 2.5 - 3 x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Low resistance so suitable for small patients.
**Can use Intermitent Positive Pressure Ventilation (IPPV).
*'''Disadvantages'''
**Cold dry gases delivered to patients.
**Uneconomical on larger patients.

====''Bain''====
*Either parallel or co-axial circuits.
*Used on patients between 10-20kg.
*Circuit factor - 2.5 - 3 x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Can use IPPV.
**In a co-axial circuit the fresh gases are warmed by the exhaled gases surround the tubing.
*'''Disadvantages'''
**Uneconomical as high fresh gas flows required.

====''Magill''====
*Used on patients between 10-35kg
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Ecomonical on gas compared to T-piece and Bain.
**Low resistance
*'''Disadvantages'''
**Cannot use for IPPV.
**Reservoir bag near patient making positioning difficult.

====''Lack''====
*Also parallel and mini circuits available.
*Used on patients between 10-35kg (Mini lack used on patients less than 10kg)
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Economical due to lower flow rates
**Rebreathe some warm and moist gas from anatomical dead space.
*'''Disadvantages'''
**Cannot use for IPPV.

===Rebreathing Systems===
====''Circle''====
*Also mini circle circuit available.
*Used on patients over 10kg.
*Minimum gas flow = 10ml/kg. It does not have a circuit factor!
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
**Very economical on gas.
**Can use IPPV
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.

====''To-and-Fro''====
*Not commonly used due to disadvantages.
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.
**Increased dead space as carbon dioxide absorbant used.

==Checking Breathing System for Use==
#Check that system has been assembled correctly and that all components are present.
#Check for any obvious holes, obstructions etc within the tubing - If any found the replace affected part.
#Securely attached the system to the common gas outlet on the anaesthetic machine.
#Close the pressure relief valve.
#Turn on the oxygen and fill the circuit by occluding the end which would usually attach to the patient using thumb, and use oxygen flush to fill if necessary.
#Listen for leaks and gently squeeze reservoir bag to check that pressure is maintained indicating no leaks.
#Open the pressure relief valve to ensure pressure relieved.
#Ensure inspiratory and expiratory valves move freely on a circle circuit by squeezing reservoir bag and releasing thumb off the end of the circuit.

==Calculating Fresh Gas Flow==
*The formula for working out the fresh gas flow rate is:

<center>
{| border="1" cellpadding="1"
|-style="background:#B0E0E6; color:black"
!'''Fresh gas flow''' = ''Tidal volume (weight x 10 - 15mls)'' x ''Respiratory rate'' x ''System factor''
|-
|}
</center>

*For patients under 10kg, the tidal volume is weight times 15mls, for patients over 10kg the tidal volume is weight times 10mls.

Breathing Systems

2009-08-31T12:49:31Z

Karag7: /* Calculating Fresh Gas Flow */

{{unfinished}}
==Introduction==
Breathing systems are the connecting component between the anaesthetic machine and patient. Their role is to deliver oxygen and anaesthetic agent to the patient from the machine, remove exhaled carbon dioxide and provided a means of ventilation via pressure on the reservoir bag.

Basic components of a breathing system are -
*''Breathing tubes'' - Deliver gases to patient and allow for flexibility.
*''Reservoir bag'' - Allows for gas accumulation during exhalation and can be used to assist breathing.
*''Carbon dioxide absorbent'' - To absorb carbon dioxide from the circuit to allow complete rebreathing.
*''One way valve'' - Ensures gases flowing towards the patient do not mix with those exhaled i.e. make a one way system within circuit.
*''Pressure relief valve'' - Limit pressure build up and allows for removal of waste gases.
*''Fresh gas inlet'' - Connects the circuit to the gas outlet on the anaesthetic machine.

==Classification==
Breathing systems have been classified in a number of different ways, including open and closed, but current classification is -

*'''''Non-rebreathing''''' - The patient breathes from the anaesthetic machine and then exhaled into the atmosphere.
*'''''Rebreathing''''' - The patient rebreathes exhaled gases, but a carbon dioxide absorbant is present to remove any waste gases.

===Non Rebreathing Systems===
====''T-piece''====
*Used on patients less than 10kg.
*Circuit factor - 2.5 - 3 x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Low resistance so suitable for small patients.
**Can use Intermitent Positive Pressure Ventilation (IPPV).
*'''Disadvantages'''
**Cold dry gases delivered to patients.
**Uneconomical on larger patients.

====''Bain''====
*Either parallel or co-axial circuits.
*Used on patients between 10-20kg.
*Circuit factor - 2.5 - 3 x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Can use IPPV.
**In a co-axial circuit the fresh gases are warmed by the exhaled gases surround the tubing.
*'''Disadvantages'''
**Uneconomical as high fresh gas flows required.

====''Magill''====
*Used on patients between 10-35kg
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Ecomonical on gas compared to T-piece and Bain.
**Low resistance
*'''Disadvantages'''
**Cannot use for IPPV.
**Reservoir bag near patient making positioning difficult.

====''Lack''====
*Also parallel and mini circuits available.
*Used on patients between 10-35kg (Mini lack used on patients less than 10kg)
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Economical due to lower flow rates
**Rebreathe some warm and moist gas from anatomical dead space.
*'''Disadvantages'''
**Cannot use for IPPV.

===Rebreathing Systems===
====''Circle''====
*Also mini circle circuit available.
*Used on patients over 10kg.
*Minimum gas flow = 10ml/kg.
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
**Very economical on gas.
**Can use IPPV
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.

====''To-and-Fro''====
*Not commonly used due to disadvantages.
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.
**Increased dead space as carbon dioxide absorbant used.

==Checking Breathing System for Use==
#Check that system has been assembled correctly and that all components are present.
#Check for any obvious holes, obstructions etc within the tubing - If any found the replace affected part.
#Securely attached the system to the common gas outlet on the anaesthetic machine.
#Close the pressure relief valve.
#Turn on the oxygen and fill the circuit by occluding the end which would usually attach to the patient using thumb, and use oxygen flush to fill if necessary.
#Listen for leaks and gently squeeze reservoir bag to check that pressure is maintained indicating no leaks.
#Open the pressure relief valve to ensure pressure relieved.
#Ensure inspiratory and expiratory valves move freely on a circle circuit by squeezing reservoir bag and releasing thumb off the end of the circuit.

==Calculating Fresh Gas Flow==
*The formula for working out the fresh gas flow rate is:

<center>
{| border="1" cellpadding="1"
|-style="background:#B0E0E6; color:black"
!'''Fresh gas flow''' = ''Tidal volume (weight x 10 - 15mls)'' x ''Respiratory rate'' x ''System factor''
|-
|}
</center>

*For patients under 10kg, the tidal volume is weight times 15mls, for patients over 10kg the tidal volume is weight times 10mls.

Breathing Systems

2009-08-31T12:49:19Z

Karag7: /* Calculating Fresh Gas Flow */

{{unfinished}}
==Introduction==
Breathing systems are the connecting component between the anaesthetic machine and patient. Their role is to deliver oxygen and anaesthetic agent to the patient from the machine, remove exhaled carbon dioxide and provided a means of ventilation via pressure on the reservoir bag.

Basic components of a breathing system are -
*''Breathing tubes'' - Deliver gases to patient and allow for flexibility.
*''Reservoir bag'' - Allows for gas accumulation during exhalation and can be used to assist breathing.
*''Carbon dioxide absorbent'' - To absorb carbon dioxide from the circuit to allow complete rebreathing.
*''One way valve'' - Ensures gases flowing towards the patient do not mix with those exhaled i.e. make a one way system within circuit.
*''Pressure relief valve'' - Limit pressure build up and allows for removal of waste gases.
*''Fresh gas inlet'' - Connects the circuit to the gas outlet on the anaesthetic machine.

==Classification==
Breathing systems have been classified in a number of different ways, including open and closed, but current classification is -

*'''''Non-rebreathing''''' - The patient breathes from the anaesthetic machine and then exhaled into the atmosphere.
*'''''Rebreathing''''' - The patient rebreathes exhaled gases, but a carbon dioxide absorbant is present to remove any waste gases.

===Non Rebreathing Systems===
====''T-piece''====
*Used on patients less than 10kg.
*Circuit factor - 2.5 - 3 x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Low resistance so suitable for small patients.
**Can use Intermitent Positive Pressure Ventilation (IPPV).
*'''Disadvantages'''
**Cold dry gases delivered to patients.
**Uneconomical on larger patients.

====''Bain''====
*Either parallel or co-axial circuits.
*Used on patients between 10-20kg.
*Circuit factor - 2.5 - 3 x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Can use IPPV.
**In a co-axial circuit the fresh gases are warmed by the exhaled gases surround the tubing.
*'''Disadvantages'''
**Uneconomical as high fresh gas flows required.

====''Magill''====
*Used on patients between 10-35kg
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Ecomonical on gas compared to T-piece and Bain.
**Low resistance
*'''Disadvantages'''
**Cannot use for IPPV.
**Reservoir bag near patient making positioning difficult.

====''Lack''====
*Also parallel and mini circuits available.
*Used on patients between 10-35kg (Mini lack used on patients less than 10kg)
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Economical due to lower flow rates
**Rebreathe some warm and moist gas from anatomical dead space.
*'''Disadvantages'''
**Cannot use for IPPV.

===Rebreathing Systems===
====''Circle''====
*Also mini circle circuit available.
*Used on patients over 10kg.
*Minimum gas flow = 10ml/kg.
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
**Very economical on gas.
**Can use IPPV
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.

====''To-and-Fro''====
*Not commonly used due to disadvantages.
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.
**Increased dead space as carbon dioxide absorbant used.

==Checking Breathing System for Use==
#Check that system has been assembled correctly and that all components are present.
#Check for any obvious holes, obstructions etc within the tubing - If any found the replace affected part.
#Securely attached the system to the common gas outlet on the anaesthetic machine.
#Close the pressure relief valve.
#Turn on the oxygen and fill the circuit by occluding the end which would usually attach to the patient using thumb, and use oxygen flush to fill if necessary.
#Listen for leaks and gently squeeze reservoir bag to check that pressure is maintained indicating no leaks.
#Open the pressure relief valve to ensure pressure relieved.
#Ensure inspiratory and expiratory valves move freely on a circle circuit by squeezing reservoir bag and releasing thumb off the end of the circuit.

==Calculating Fresh Gas Flow==
*The formula for working out the fresh gas flow rate is:

<center>
{| border="1" cellpadding="1"
|-style="background:#B0E0E6; color:black"
!'''Fresh gas flow''' = ''Tidal volume (weight x 10 - 15mls)'' x ''Respiratory rate'' x ''System factor''
|-
|}
</center>

*For patients under 10kg, the tidal volume is weight times 15mls, for patients over 10kg the tidal volume is weight times 10mls.

Breathing Systems

2009-08-31T12:47:58Z

Karag7:

{{unfinished}}
==Introduction==
Breathing systems are the connecting component between the anaesthetic machine and patient. Their role is to deliver oxygen and anaesthetic agent to the patient from the machine, remove exhaled carbon dioxide and provided a means of ventilation via pressure on the reservoir bag.

Basic components of a breathing system are -
*''Breathing tubes'' - Deliver gases to patient and allow for flexibility.
*''Reservoir bag'' - Allows for gas accumulation during exhalation and can be used to assist breathing.
*''Carbon dioxide absorbent'' - To absorb carbon dioxide from the circuit to allow complete rebreathing.
*''One way valve'' - Ensures gases flowing towards the patient do not mix with those exhaled i.e. make a one way system within circuit.
*''Pressure relief valve'' - Limit pressure build up and allows for removal of waste gases.
*''Fresh gas inlet'' - Connects the circuit to the gas outlet on the anaesthetic machine.

==Classification==
Breathing systems have been classified in a number of different ways, including open and closed, but current classification is -

*'''''Non-rebreathing''''' - The patient breathes from the anaesthetic machine and then exhaled into the atmosphere.
*'''''Rebreathing''''' - The patient rebreathes exhaled gases, but a carbon dioxide absorbant is present to remove any waste gases.

===Non Rebreathing Systems===
====''T-piece''====
*Used on patients less than 10kg.
*Circuit factor - 2.5 - 3 x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Low resistance so suitable for small patients.
**Can use Intermitent Positive Pressure Ventilation (IPPV).
*'''Disadvantages'''
**Cold dry gases delivered to patients.
**Uneconomical on larger patients.

====''Bain''====
*Either parallel or co-axial circuits.
*Used on patients between 10-20kg.
*Circuit factor - 2.5 - 3 x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Can use IPPV.
**In a co-axial circuit the fresh gases are warmed by the exhaled gases surround the tubing.
*'''Disadvantages'''
**Uneconomical as high fresh gas flows required.

====''Magill''====
*Used on patients between 10-35kg
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Ecomonical on gas compared to T-piece and Bain.
**Low resistance
*'''Disadvantages'''
**Cannot use for IPPV.
**Reservoir bag near patient making positioning difficult.

====''Lack''====
*Also parallel and mini circuits available.
*Used on patients between 10-35kg (Mini lack used on patients less than 10kg)
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Economical due to lower flow rates
**Rebreathe some warm and moist gas from anatomical dead space.
*'''Disadvantages'''
**Cannot use for IPPV.

===Rebreathing Systems===
====''Circle''====
*Also mini circle circuit available.
*Used on patients over 10kg.
*Minimum gas flow = 10ml/kg.
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
**Very economical on gas.
**Can use IPPV
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.

====''To-and-Fro''====
*Not commonly used due to disadvantages.
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.
**Increased dead space as carbon dioxide absorbant used.

==Checking Breathing System for Use==
#Check that system has been assembled correctly and that all components are present.
#Check for any obvious holes, obstructions etc within the tubing - If any found the replace affected part.
#Securely attached the system to the common gas outlet on the anaesthetic machine.
#Close the pressure relief valve.
#Turn on the oxygen and fill the circuit by occluding the end which would usually attach to the patient using thumb, and use oxygen flush to fill if necessary.
#Listen for leaks and gently squeeze reservoir bag to check that pressure is maintained indicating no leaks.
#Open the pressure relief valve to ensure pressure relieved.
#Ensure inspiratory and expiratory valves move freely on a circle circuit by squeezing reservoir bag and releasing thumb off the end of the circuit.

==Calculating Fresh Gas Flow==
*The formula for working out the fresh gas flow rate is:

<center>
{| border="1" cellpadding="1"
|-style="background:#B0E0E6; color:black"
!'''Fresh gas flow''' = ''Tidal volume (weight x 10 - 15mls)'' x ''Respiratory rate'' x ''System factor''
|-
|}
</center>

Breathing Systems

2009-08-31T12:47:31Z

Karag7:

{{unfinished}}
==Introduction==
Breathing systems are the connecting component between the anaesthetic machine and patient. Their role is to deliver oxygen and anaesthetic agent to the patient from the machine, remove exhaled carbon dioxide and provided a means of ventilation via pressure on the reservoir bag.

Basic components of a breathing system are -
*''Breathing tubes'' - Deliver gases to patient and allow for flexibility.
*''Reservoir bag'' - Allows for gas accumulation during exhalation and can be used to assist breathing.
*''Carbon dioxide absorbent'' - To absorb carbon dioxide from the circuit to allow complete rebreathing.
*''One way valve'' - Ensures gases flowing towards the patient do not mix with those exhaled i.e. make a one way system within circuit.
*''Pressure relief valve'' - Limit pressure build up and allows for removal of waste gases.
*''Fresh gas inlet'' - Connects the circuit to the gas outlet on the anaesthetic machine.

==Classification==
Breathing systems have been classified in a number of different ways, including open and closed, but current classification is -

*'''''Non-rebreathing''''' - The patient breathes from the anaesthetic machine and then exhaled into the atmosphere.
*'''''Rebreathing''''' - The patient rebreathes exhaled gases, but a carbon dioxide absorbant is present to remove any waste gases.

===Non Rebreathing Systems===
====''T-piece''====
*Used on patients less than 10kg.
*Circuit factor - 2.5 - 3 x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Low resistance so suitable for small patients.
**Can use Intermitent Positive Pressure Ventilation (IPPV).
*'''Disadvantages'''
**Cold dry gases delivered to patients.
**Uneconomical on larger patients.

====''Bain''====
*Either parallel or co-axial circuits.
*Used on patients between 10-20kg.
*Circuit factor - 2.5 - 3 x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Can use IPPV.
**In a co-axial circuit the fresh gases are warmed by the exhaled gases surround the tubing.
*'''Disadvantages'''
**Uneconomical as high fresh gas flows required.

====''Magill''====
*Used on patients between 10-35kg
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Ecomonical on gas compared to T-piece and Bain.
**Low resistance
*'''Disadvantages'''
**Cannot use for IPPV.
**Reservoir bag near patient making positioning difficult.

====''Lack''====
*Also parallel and mini circuits available.
*Used on patients between 10-35kg (Mini lack used on patients less than 10kg)
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Economical due to lower flow rates
**Rebreathe some warm and moist gas from anatomical dead space.
*'''Disadvantages'''
**Cannot use for IPPV.

===Rebreathing Systems===
====''Circle''====
*Also mini circle circuit available.
*Used on patients over 10kg.
*Minimum gas flow = 10ml/kg.
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
**Very economical on gas.
**Can use IPPV
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.

====''To-and-Fro''====
*Not commonly used due to disadvantages.
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.
**Increased dead space as carbon dioxide absorbant used.

==Checking Breathing System for Use==
#Check that system has been assembled correctly and that all components are present.
#Check for any obvious holes, obstructions etc within the tubing - If any found the replace affected part.
#Securely attached the system to the common gas outlet on the anaesthetic machine.
#Close the pressure relief valve.
#Turn on the oxygen and fill the circuit by occluding the end which would usually attach to the patient using thumb, and use oxygen flush to fill if necessary.
#Listen for leaks and gently squeeze reservoir bag to check that pressure is maintained indicating no leaks.
#Open the pressure relief valve to ensure pressure relieved.
#Ensure inspiratory and expiratory valves move freely on a circle circuit by squeezing reservoir bag and releasing thumb off the end of the circuit.

==Calculating Fresh Gas Flow==
*The formula for working out the fresh gas flow rate is:

<center>
{| border="1" cellpadding="1"
|-style="background:#B0E0E6; color:black"
!'''Fresh gas flow''' = ''Tidal volume (weight x 10 - 15mls)'' x ''Respiratory rate'' x ''System factor''
|-
|}
</center>

Breathing Systems

2009-08-31T12:45:11Z

Karag7:

{{unfinished}}
==Introduction==
Breathing systems are the connecting component between the anaesthetic machine and patient. Their role is to deliver oxygen and anaesthetic agent to the patient from the machine, remove exhaled carbon dioxide and provided a means of ventilation via pressure on the reservoir bag.

Basic components of a breathing system are -
*''Breathing tubes'' - Deliver gases to patient and allow for flexibility.
*''Reservoir bag'' - Allows for gas accumulation during exhalation and can be used to assist breathing.
*''Carbon dioxide absorbent'' - To absorb carbon dioxide from the circuit to allow complete rebreathing.
*''One way valve'' - Ensures gases flowing towards the patient do not mix with those exhaled i.e. make a one way system within circuit.
*''Pressure relief valve'' - Limit pressure build up and allows for removal of waste gases.
*''Fresh gas inlet'' - Connects the circuit to the gas outlet on the anaesthetic machine.

==Classification==
Breathing systems have been classified in a number of different ways, including open and closed, but current classification is -

*'''''Non-rebreathing''''' - The patient breathes from the anaesthetic machine and then exhaled into the atmosphere.
*'''''Rebreathing''''' - The patient rebreathes exhaled gases, but a carbon dioxide absorbant is present to remove any waste gases.

===Non Rebreathing Systems===
====''T-piece''====
*Used on patients less than 10kg.
*Circuit factor - 2.5 - 3 x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Low resistance so suitable for small patients.
**Can use Intermitent Positive Pressure Ventilation (IPPV).
*'''Disadvantages'''
**Cold dry gases delivered to patients.
**Uneconomical on larger patients.

====''Bain''====
*Either parallel or co-axial circuits.
*Used on patients between 10-20kg.
*Circuit factor - 2.5 - 3 x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Can use IPPV.
**In a co-axial circuit the fresh gases are warmed by the exhaled gases surround the tubing.
*'''Disadvantages'''
**Uneconomical as high fresh gas flows required.

====''Magill''====
*Used on patients between 10-35kg
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Ecomonical on gas compared to T-piece and Bain.
**Low resistance
*'''Disadvantages'''
**Cannot use for IPPV.
**Reservoir bag near patient making positioning difficult.

====''Lack''====
*Also parallel and mini circuits available.
*Used on patients between 10-35kg (Mini lack used on patients less than 10kg)
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Economical due to lower flow rates
**Rebreathe some warm and moist gas from anatomical dead space.
*'''Disadvantages'''
**Cannot use for IPPV.

===Rebreathing Systems===
====''Circle''====
*Also mini circle circuit available.
*Used on patients over 10kg.
*Minimum gas flow = 10ml/kg.
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
**Very economical on gas.
**Can use IPPV
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.

====''To-and-Fro''====
*Not commonly used due to disadvantages.
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.
**Increased dead space as carbon dioxide absorbant used.

==Checking Breathing System for Use==
#Check that system has been assembled correctly and that all components are present.
#Check for any obvious holes, obstructions etc within the tubing - If any found the replace affected part.
#Securely attached the system to the common gas outlet on the anaesthetic machine.
#Close the pressure relief valve.
#Turn on the oxygen and fill the circuit by occluding the end which would usually attach to the patient using thumb, and use oxygen flush to fill if necessary.
#Listen for leaks and gently squeeze reservoir bag to check that pressure is maintained indicating no leaks.
#Open the pressure relief valve to ensure pressure relieved.
#Ensure inspiratory and expiratory valves move freely on a circle circuit by squeezing reservoir bag and releasing thumb off the end of the circuit.

==Calculating Fresh Gas Flow==
*The formula for working out the fresh gas flow rate is:

Breathing Systems

2009-08-31T12:43:47Z

Karag7:

{{unfinished}}
==Introduction==
Breathing systems are the connecting component between the anaesthetic machine and patient. Their role is to deliver oxygen and anaesthetic agent to the patient from the machine, remove exhaled carbon dioxide and provided a means of ventilation via pressure on the reservoir bag.

Basic components of a breathing system are -
*''Breathing tubes'' - Deliver gases to patient and allow for flexibility.
*''Reservoir bag'' - Allows for gas accumulation during exhalation and can be used to assist breathing.
*''Carbon dioxide absorbent'' - To absorb carbon dioxide from the circuit to allow complete rebreathing.
*''One way valve'' - Ensures gases flowing towards the patient do not mix with those exhaled i.e. make a one way system within circuit.
*''Pressure relief valve'' - Limit pressure build up and allows for removal of waste gases.
*''Fresh gas inlet'' - Connects the circuit to the gas outlet on the anaesthetic machine.

==Classification==
Breathing systems have been classified in a number of different ways, including open and closed, but current classification is -

*'''''Non-rebreathing''''' - The patient breathes from the anaesthetic machine and then exhaled into the atmosphere.
*'''''Rebreathing''''' - The patient rebreathes exhaled gases, but a carbon dioxide absorbant is present to remove any waste gases.

===Non Rebreathing Systems===
====''T-piece''====
*Used on patients less than 10kg.
*Circuit factor - 2.5 - 3 x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Low resistance so suitable for small patients.
**Can use Intermitent Positive Pressure Ventilation (IPPV).
*'''Disadvantages'''
**Cold dry gases delivered to patients.
**Uneconomical on larger patients.

====''Bain''====
*Either parallel or co-axial circuits.
*Used on patients between 10-20kg.
*Circuit factor - 2.5 - 3 x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Can use IPPV.
**In a co-axial circuit the fresh gases are warmed by the exhaled gases surround the tubing.
*'''Disadvantages'''
**Uneconomical as high fresh gas flows required.

====''Magill''====
*Used on patients between 10-35kg
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Ecomonical on gas compared to T-piece and Bain.
**Low resistance
*'''Disadvantages'''
**Cannot use for IPPV.
**Reservoir bag near patient making positioning difficult.

====''Lack''====
*Also parallel and mini circuits available.
*Used on patients between 10-35kg (Mini lack used on patients less than 10kg)
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Economical due to lower flow rates
**Rebreathe some warm and moist gas from anatomical dead space.
*'''Disadvantages'''
**Cannot use for IPPV.

===Rebreathing Systems===
====''Circle''====
*Also mini circle circuit available.
*Used on patients over 10kg.
*Minimum gas flow = 10ml/kg.
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
**Very economical on gas.
**Can use IPPV
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.

====''To-and-Fro''====
*Not commonly used due to disadvantages.
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.
**Increased dead space as carbon dioxide absorbant used.

==Checking Breathing System for Use==
#Check that system has been assembled correctly and that all components are present.
#Check for any obvious holes, obstructions etc within the tubing - If any found the replace affected part.
#Securely attached the system to the common gas outlet on the anaesthetic machine.
#Close the pressure relief valve.
#Turn on the oxygen and fill the circuit by occluding the end which would usually attach to the patient using thumb, and use oxygen flush to fill if necessary.
#Listen for leaks and gently squeeze reservoir bag to check that pressure is maintained indicating no leaks.
#Open the pressure relief valve to ensure pressure relieved.
#Ensure inspiratory and expiratory valves move freely on a circle circuit by squeezing reservoir bag and releasing thumb off the end of the circuit.

==Calculating Fresh Gas Flow==

Breathing Systems

2009-08-31T12:41:20Z

Karag7: /* Bain */

{{unfinished}}
==Introduction==
Breathing systems are the connecting component between the anaesthetic machine and patient. Their role is to deliver oxygen and anaesthetic agent to the patient from the machine, remove exhaled carbon dioxide and provided a means of ventilation via pressure on the reservoir bag.

Basic components of a breathing system are -
*''Breathing tubes'' - Deliver gases to patient and allow for flexibility.
*''Reservoir bag'' - Allows for gas accumulation during exhalation and can be used to assist breathing.
*''Carbon dioxide absorbent'' - To absorb carbon dioxide from the circuit to allow complete rebreathing.
*''One way valve'' - Ensures gases flowing towards the patient do not mix with those exhaled i.e. make a one way system within circuit.
*''Pressure relief valve'' - Limit pressure build up and allows for removal of waste gases.
*''Fresh gas inlet'' - Connects the circuit to the gas outlet on the anaesthetic machine.

==Classification==
Breathing systems have been classified in a number of different ways, including open and closed, but current classification is -

*'''''Non-rebreathing''''' - The patient breathes from the anaesthetic machine and then exhaled into the atmosphere.
*'''''Rebreathing''''' - The patient rebreathes exhaled gases, but a carbon dioxide absorbant is present to remove any waste gases.

===Non Rebreathing Systems===
====''T-piece''====
*Used on patients less than 10kg.
*Circuit factor - 2.5 - 3 x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Low resistance so suitable for small patients.
**Can use Intermitent Positive Pressure Ventilation (IPPV).
*'''Disadvantages'''
**Cold dry gases delivered to patients.
**Uneconomical on larger patients.

====''Bain''====
*Either parallel or co-axial circuits.
*Used on patients between 10-20kg.
*Circuit factor - 2.5 - 3 x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Can use IPPV.
**In a co-axial circuit the fresh gases are warmed by the exhaled gases surround the tubing.
*'''Disadvantages'''
**Uneconomical as high fresh gas flows required.

====''Magill''====
*Used on patients between 10-35kg
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Ecomonical on gas compared to T-piece and Bain.
**Low resistance
*'''Disadvantages'''
**Cannot use for IPPV.
**Reservoir bag near patient making positioning difficult.

====''Lack''====
*Also parallel and mini circuits available.
*Used on patients between 10-35kg (Mini lack used on patients less than 10kg)
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Economical due to lower flow rates
**Rebreathe some warm and moist gas from anatomical dead space.
*'''Disadvantages'''
**Cannot use for IPPV.

===Rebreathing Systems===
====''Circle''====
*Also mini circle circuit available.
*Used on patients over 10kg.
*Minimum gas flow = 10ml/kg.
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
**Very economical on gas.
**Can use IPPV
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.

====''To-and-Fro''====
*Not commonly used due to disadvantages.
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.
**Increased dead space as carbon dioxide absorbant used.

==Checking Breathing System for Use==
#Check that system has been assembled correctly and that all components are present.
#Check for any obvious holes, obstructions etc within the tubing - If any found the replace affected part.
#Securely attached the system to the common gas outlet on the anaesthetic machine.
#Close the pressure relief valve.
#Turn on the oxygen and fill the circuit by occluding the end which would usually attach to the patient using thumb, and use oxygen flush to fill if necessary.
#Listen for leaks and gently squeeze reservoir bag to check that pressure is maintained indicating no leaks.
#Open the pressure relief valve to ensure pressure relieved.
#Ensure inspiratory and expiratory valves move freely on a circle circuit by squeezing reservoir bag and releasing thumb off the end of the circuit.

Breathing Systems

2009-08-31T12:41:06Z

Karag7: /* T-piece */

{{unfinished}}
==Introduction==
Breathing systems are the connecting component between the anaesthetic machine and patient. Their role is to deliver oxygen and anaesthetic agent to the patient from the machine, remove exhaled carbon dioxide and provided a means of ventilation via pressure on the reservoir bag.

Basic components of a breathing system are -
*''Breathing tubes'' - Deliver gases to patient and allow for flexibility.
*''Reservoir bag'' - Allows for gas accumulation during exhalation and can be used to assist breathing.
*''Carbon dioxide absorbent'' - To absorb carbon dioxide from the circuit to allow complete rebreathing.
*''One way valve'' - Ensures gases flowing towards the patient do not mix with those exhaled i.e. make a one way system within circuit.
*''Pressure relief valve'' - Limit pressure build up and allows for removal of waste gases.
*''Fresh gas inlet'' - Connects the circuit to the gas outlet on the anaesthetic machine.

==Classification==
Breathing systems have been classified in a number of different ways, including open and closed, but current classification is -

*'''''Non-rebreathing''''' - The patient breathes from the anaesthetic machine and then exhaled into the atmosphere.
*'''''Rebreathing''''' - The patient rebreathes exhaled gases, but a carbon dioxide absorbant is present to remove any waste gases.

===Non Rebreathing Systems===
====''T-piece''====
*Used on patients less than 10kg.
*Circuit factor - 2.5 - 3 x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Low resistance so suitable for small patients.
**Can use Intermitent Positive Pressure Ventilation (IPPV).
*'''Disadvantages'''
**Cold dry gases delivered to patients.
**Uneconomical on larger patients.

====''Bain''====
*Either parallel or co-axial circuits.
*Used on patients between 10-20kg.
*Circuit factor - 2-3 x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Can use IPPV.
**In a co-axial circuit the fresh gases are warmed by the exhaled gases surround the tubing.
*'''Disadvantages'''
**Uneconomical as high fresh gas flows required.

====''Magill''====
*Used on patients between 10-35kg
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Ecomonical on gas compared to T-piece and Bain.
**Low resistance
*'''Disadvantages'''
**Cannot use for IPPV.
**Reservoir bag near patient making positioning difficult.

====''Lack''====
*Also parallel and mini circuits available.
*Used on patients between 10-35kg (Mini lack used on patients less than 10kg)
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Economical due to lower flow rates
**Rebreathe some warm and moist gas from anatomical dead space.
*'''Disadvantages'''
**Cannot use for IPPV.

===Rebreathing Systems===
====''Circle''====
*Also mini circle circuit available.
*Used on patients over 10kg.
*Minimum gas flow = 10ml/kg.
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
**Very economical on gas.
**Can use IPPV
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.

====''To-and-Fro''====
*Not commonly used due to disadvantages.
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.
**Increased dead space as carbon dioxide absorbant used.

==Checking Breathing System for Use==
#Check that system has been assembled correctly and that all components are present.
#Check for any obvious holes, obstructions etc within the tubing - If any found the replace affected part.
#Securely attached the system to the common gas outlet on the anaesthetic machine.
#Close the pressure relief valve.
#Turn on the oxygen and fill the circuit by occluding the end which would usually attach to the patient using thumb, and use oxygen flush to fill if necessary.
#Listen for leaks and gently squeeze reservoir bag to check that pressure is maintained indicating no leaks.
#Open the pressure relief valve to ensure pressure relieved.
#Ensure inspiratory and expiratory valves move freely on a circle circuit by squeezing reservoir bag and releasing thumb off the end of the circuit.

Peripheral Nervous System Pathology Overview

2009-08-28T12:32:13Z

Karag7: /* Peripheral Nerve Disease in Large Animals */

{{review}}

{{toplink
|backcolour = E0EEEE
|linkpage = Nervous System - Pathology
|linktext =Nervous System
|maplink = Nervous System (Content Map) - Pathology
|pagetype =Pathology
}}
 
==Nerve Injury==
===Classification of Peripheral Nerve Disease===
{| cellpadding="4" cellspacing="0" border="2"
|-
|style="background:#B0E0E6; color:black" width="200"|'''By Nerve Type
|style="background:#B0E0E6; color:black" width="200"|'''By Anatomy'''
|style="background:#B0E0E6; color:black" width="250"|'''By Pathology'''
|-
|
*Mixed
|
*NMJ
|'''Neuronopathy :''' ''The Whole nerve cell''
|-
|
*Motor
|
*Distal / Proximal
|'''Axonopathy :''' ''The axon''
|-
|
*Sensory
|
*Root / Spinal Cord
|'''Demyelination:''' ''Schwann cell''
|-
|}
 

===Types of Injury===
{| cellpadding="4" cellspacing="0" border="2"
|-
|style="background:#B0E0E6; color:black"|'''Neuropraxia:'''||
*Temporary interruption of conduction - no histological change.
|-
|style="background:#B0E0E6; color:black"|'''Axonotmesis:'''||
*Axon interupted but basal lamina intact (e.g. crush injury)
*Regeneration occurs along original path - prospect for functional recovery good.
|-
|style="background:#B0E0E6; color:black"|'''Neurotmesis:'''||
*Axon '''and''' basal lamina interupted (e.g. transection injury)
*Success of regeneration depends on finding the correct distal stump
|}
 

===Clinical Signs with Peripheral Nerve Disease===
{| align="center" cellpadding="4" cellspacing="0" border="0"
|width="350"|
:'''Motor Neuropathy Signs (LMN signs)'''
|width="350"|
:'''Sensory Neuropathy'''
|width="350"|
:'''Autonomic Neuropathy'''
|-
|
*Flaccid paresis/paralysis of innervated structures
|
*Decreased or abherrant 'pain' response or sensation
|
*Anisocoria (dilated / constricted pupils)
|-
|
*Neurogenic muscle atrophy (very rapid)
|
*Proprioceptive defects
|
*Decreased tear production
|-
|
*Reduced / absent reflexes and muscle tone
|
*Abnormal sensation (paraesthesia)/sensitivity (dysthesia)
|
*Decreased salivation
|-
|
|
*Reduced / absent reflexes without muscle atrophy
|
*Bradycardia
|}
 

==Peripheral Nerve Disease in Small Animals==
{| cellpadding="4" cellspacing="0" border="2"
|- style="background:#B0E0E6; color:black"
|width="150"|<center><big>'''Disease'''</big></center>
|width="200"|<center><big>'''Pathology'''</big></center>
|width="250"|<center><big>'''Clinical Signs'''</big></center>
|width="250"|<center><big>'''Diagnosis'''</big></center>
|width="250"|<center><big>'''Prognosis + Treatment'''</big></center>
|-
|<center><big>'''Distal Denervating Disease'''</big></center>
|
*Distal axonopathy, possibly of toxic origin
|
*Tetraparesis
*Dysphonia / Aphonia
*Neck Weakness
*Tetraparesis developing to tetraplegia in severe cases ''floppy dog''
*Sensory function preserved: Pain but '''no''' withdrawal
|
*Biopsy / EMG unhelpful
|
*Very good prognosis
*Recovery in 3-6 weeks by '''axon regeneration'''
*Good nursing to prevent pressure sores in the recumbant animal
|- style="background:#F0F8FF; color:black"
|<center><big>'''Idiopathic Polyradiculoneuritis'''</big></center>
|
*Immune mediated demyelination often involving roots, directed against unknown epitopes in peripheral myelin.
*May be post infection
*May get axonal injury if severe
|
*As for distal denervating (although more rapid onset)
*May have sensory involvement.
|
*By clinical signs
*CSF changes if roots involved
*Slower nerve conduction
*H reflexes and F-waves may be lost
|
*Very good prognosis
*Recovery in 3-6 weeks by '''remyelination'''
*Immunosuppresive levels of corticosteroids (although may delay remyelination)
|-
|<center><big>'''Cauda Equina Traction'''</big></center>
|
*Tail pull injury
*Esp. cats after RTA
*Lesion via longitudinal traction
*Sacrocaudal dislocation/fracture
|
*Limp tail
*Incontinence
*Hindlimb Paresis
|
*Diagnosis on Clinical signs and history
*+/- Radiographs to show dislocation/fracture
|
*Prognosis difficult to predict
*Poor prognosis if tail limp & no anal tone
*Supportive treatment
*'''Persist for >3 months if possible'''
|- style="background:#F0F8FF; color:black"
|<center><big>'''Peripheral Nerve Tumours'''</big></center>
|
*Nerve sheath tumours
*Generally tumours of Schwann cells
*Common in dog Brachial plexus
|
*Chronic single forelimb lameness
*Weakness
*Muscle Atrophy
*Pain in Axilla
*LMN signs (may get UMN if grows into spinal cord
|
*Clinical signs
*Imaging
|
*Prognosis dependant on location
*Poor prognosis if in spinal cord
*Amputation of limb?
|-
|<center><big>'''Feline Dysautonomia'''</big></center>
|
*Common in 1980's - Sporadic now
*Degeneration (toxic?) of autonomic ganglia
|
*Mainly Parasympathetic
*Vomiting
*3rd Eyelid protrusion
*Dilated pupils + poor PLR
*Reduced Lacrimation
*Megaoesophagus
*Bradycardia
|
*Clinical signs
|
*Poor Prognosis
*Supportive therapy only
*Similar sporadic disease seen in dogs
|-
|}

==Peripheral Nerve Disease in Large Animals==
{| cellpadding="4" cellspacing="0" border="2"
|-- style="background:#B0E0E6; color:black"
|width="150"|<center><big>'''Disease'''</big></center>
|width="200"|<center><big>'''Pathology'''</big></center>
|width="250"|<center><big>'''Clinical Signs'''</big></center>
|width="250"|<center><big>'''Diagnosis'''</big></center>
|width="250"|<center><big>'''Prognosis + Treatment'''</big></center>
|-
|<center><big>'''Idiopathic Laryngeal Hemiplagia (ILH)'''</big></center>
|
*Progressive loss of fibres (esp. large diameter) within left recurrent laryngeal nerve compared to right
*[[PNS Repsonses to Injury - Pathology#The 'Dying Back' Phenomenon|Dying back]] axonopathy with myelin sheath involvement:
**Degenerating fibres
**Regenerating clusters
**De/Re-myelination
*Flattening of nerve between aorta & trachea
|
*Inspiratory 'roaring' noise - flapping of vocal fold
|
*'Slap test' - adduction of contralateral arytenoid during expiration
*Endoscopic examination - assymetric arytenoids, poor abduction of left vocal fold.
*Palpable atrophy of laryngeal musculature
|
*Laryngeal Ventriculectomy (Hobday procedure)
*'Tie Back'
*Laryngeal muscle prosthesis
*Prognosis usually good
|-style="background:#F0F8FF; color:black"
|<center><big>'''Cauda Equina Neuritis'''</big></center>
|
*Equine version of [[#IPRN|Idiopathic polyradiculoneuritis]]
*Extradural nerve roots of cauda equina thickened and discoloured
*Inflammatory infiltrate (lymphocytes, plasma cells, macrophages)
*Extensive axonal damage and demyelination
*Cranial nerve involvement often occurs
*Aetiology unknown:
**Antecedent infection?
**Antibodies to PNS myelin?
|
*Paralysis & anaesthesia of tail
*Urinary incontinence
*Loss of anal reflex
*Failure to defaecate
*Pain/hypersensitivity in gluteal/tail-head area
|
*Clinical signs
|
*Recovery unlikely - most animals are destroyed.
|-
|<center><big>'''Stringhalt'''</big></center>
|
*Causes poorly understood - similar signs caused by sweat pea plant ingestion (lathyrism)
*Distal axonopathy (esp. large diameter fibres)
|
*Abrupt onset continuous / intermittent hyperflexion of one or both hind limbs
*May also have ataxia, urinary incontinence, perineal flaccidity
|
*Differential diagnosis : Upward fixation of patella
|
*May get spontaneous recovery
*Move pasture
*Tenectomy of lateral digital extensor may help
|-
|-style="background:#F0F8FF; color:black"
|<center><big>'''Equine Motor Neuron Disease'''</big></center>
|
*Generalised LMN disorder
*Degeneration of Ventral horn motor neuron
*[[PNS Repsonses to Injury - Pathology#Chromatolysis|Chromatolysis]]
*Neurofilament accumulation
*Gliosis
*[[PNS Repsonses to Injury - Pathology#Wallerian Degeneration|Wallerian degeneration]]
*Denervation changes in muscle
|
*Weight Loss
*Muscle atrophy
*Generalised Weakness
*Short strided gait + narrow based stance
*Trembling
*Sweating and fasiculations
*Increased recumbency
|
*Elevated CK
*CSF protein
*Denervation of EMG
|
*May progress to constant recumbency (destroy), stabilise or improve
|-
|<center><big>'''Suprascapular Nerve Injury'''</big></center>
|
*'''"Sweeney"'''
*Commonly damaged by horse colliding into objects
*Fibrous entrapment as nerve reflected around wing of scapula
*Atrophy of supra- and infra- spinatous muscles
|
*Lateral luxation of shoulder when weight bearing
*Muscle wasting around shoulder
|
*Clinical signs
*History
|
*No more than 30cm regrowth in 12 months expected due to irreversible muscle fibrosis.

|-
|}

==Other Polyneuropathies==
*Tick Paralysis
*Vincristine Toxicity
*Endocrine polyneuropathy
**Dogs - hypothyroidism, insulinoma, diabetes mellitus
**Cats - diabetes mellitus
*Genetic polyneuropathies
*Protozoan polyradiculoneuritis
*Idiopathic facial paralysis (e.g. Bell's Palsy)
*Botulism

==Learning Tools==

Peripheral Nervous System Pathology Overview

2009-08-28T11:41:04Z

Karag7: /* Clinical Signs with Peripheral Nerve Disease */

{{review}}

{{toplink
|backcolour = E0EEEE
|linkpage = Nervous System - Pathology
|linktext =Nervous System
|maplink = Nervous System (Content Map) - Pathology
|pagetype =Pathology
}}
 
==Nerve Injury==
===Classification of Peripheral Nerve Disease===
{| cellpadding="4" cellspacing="0" border="2"
|-
|style="background:#B0E0E6; color:black" width="200"|'''By Nerve Type
|style="background:#B0E0E6; color:black" width="200"|'''By Anatomy'''
|style="background:#B0E0E6; color:black" width="250"|'''By Pathology'''
|-
|
*Mixed
|
*NMJ
|'''Neuronopathy :''' ''The Whole nerve cell''
|-
|
*Motor
|
*Distal / Proximal
|'''Axonopathy :''' ''The axon''
|-
|
*Sensory
|
*Root / Spinal Cord
|'''Demyelination:''' ''Schwann cell''
|-
|}
 

===Types of Injury===
{| cellpadding="4" cellspacing="0" border="2"
|-
|style="background:#B0E0E6; color:black"|'''Neuropraxia:'''||
*Temporary interruption of conduction - no histological change.
|-
|style="background:#B0E0E6; color:black"|'''Axonotmesis:'''||
*Axon interupted but basal lamina intact (e.g. crush injury)
*Regeneration occurs along original path - prospect for functional recovery good.
|-
|style="background:#B0E0E6; color:black"|'''Neurotmesis:'''||
*Axon '''and''' basal lamina interupted (e.g. transection injury)
*Success of regeneration depends on finding the correct distal stump
|}
 

===Clinical Signs with Peripheral Nerve Disease===
{| align="center" cellpadding="4" cellspacing="0" border="0"
|width="350"|
:'''Motor Neuropathy Signs (LMN signs)'''
|width="350"|
:'''Sensory Neuropathy'''
|width="350"|
:'''Autonomic Neuropathy'''
|-
|
*Flaccid paresis/paralysis of innervated structures
|
*Decreased or abherrant 'pain' response or sensation
|
*Anisocoria (dilated / constricted pupils)
|-
|
*Neurogenic muscle atrophy (very rapid)
|
*Proprioceptive defects
|
*Decreased tear production
|-
|
*Reduced / absent reflexes and muscle tone
|
*Abnormal sensation (paraesthesia)/sensitivity (dysthesia)
|
*Decreased salivation
|-
|
|
*Reduced / absent reflexes without muscle atrophy
|
*Bradycardia
|}
 

==Peripheral Nerve Disease in Small Animals==
{| cellpadding="4" cellspacing="0" border="2"
|- style="background:#B0E0E6; color:black"
|width="150"|<center><big>'''Disease'''</big></center>
|width="200"|<center><big>'''Pathology'''</big></center>
|width="250"|<center><big>'''Clinical Signs'''</big></center>
|width="250"|<center><big>'''Diagnosis'''</big></center>
|width="250"|<center><big>'''Prognosis + Treatment'''</big></center>
|-
|<center><big>'''Distal Denervating Disease'''</big></center>
|
*Distal axonopathy, possibly of toxic origin
|
*Tetraparesis
*Dysphonia / Aphonia
*Neck Weakness
*Tetraparesis developing to tetraplegia in severe cases ''floppy dog''
*Sensory function preserved: Pain but '''no''' withdrawal
|
*Biopsy / EMG unhelpful
|
*Very good prognosis
*Recovery in 3-6 weeks by '''axon regeneration'''
*Good nursing to prevent pressure sores in the recumbant animal
|- style="background:#F0F8FF; color:black"
|<center><big>'''Idiopathic Polyradiculoneuritis'''</big></center>
|
*Immune mediated demyelination often involving roots, directed against unknown epitopes in peripheral myelin.
*May be post infection
*May get axonal injury if severe
|
*As for distal denervating (although more rapid onset)
*May have sensory involvement.
|
*By clinical signs
*CSF changes if roots involved
*Slower nerve conduction
*H reflexes and F-waves may be lost
|
*Very good prognosis
*Recovery in 3-6 weeks by '''remyelination'''
*Immunosuppresive levels of corticosteroids (although may delay remyelination)
|-
|<center><big>'''Cauda Equina Traction'''</big></center>
|
*Tail pull injury
*Esp. cats after RTA
*Lesion via longitudinal traction
*Sacrocaudal dislocation/fracture
|
*Limp tail
*Incontinence
*Hindlimb Paresis
|
*Diagnosis on Clinical signs and history
*+/- Radiographs to show dislocation/fracture
|
*Prognosis difficult to predict
*Poor prognosis if tail limp & no anal tone
*Supportive treatment
*'''Persist for >3 months if possible'''
|- style="background:#F0F8FF; color:black"
|<center><big>'''Peripheral Nerve Tumours'''</big></center>
|
*Nerve sheath tumours
*Generally tumours of Schwann cells
*Common in dog Brachial plexus
|
*Chronic single forelimb lameness
*Weakness
*Muscle Atrophy
*Pain in Axilla
*LMN signs (may get UMN if grows into spinal cord
|
*Clinical signs
*Imaging
|
*Prognosis dependant on location
*Poor prognosis if in spinal cord
*Amputation of limb?
|-
|<center><big>'''Feline Dysautonomia'''</big></center>
|
*Common in 1980's - Sporadic now
*Degeneration (toxic?) of autonomic ganglia
|
*Mainly Parasympathetic
*Vomiting
*3rd Eyelid protrusion
*Dilated pupils + poor PLR
*Reduced Lacrimation
*Megaoesophagus
*Bradycardia
|
*Clinical signs
|
*Poor Prognosis
*Supportive therapy only
*Similar sporadic disease seen in dogs
|-
|}

==Peripheral Nerve Disease in Large Animals==
{| cellpadding="4" cellspacing="0" border="2"
|-- style="background:#B0E0E6; color:black"
|width="150"|<center><big>'''Disease'''</big></center>
|width="200"|<center><big>'''Pathology'''</big></center>
|width="250"|<center><big>'''Clinical Signs'''</big></center>
|width="250"|<center><big>'''Diagnosis'''</big></center>
|width="250"|<center><big>'''Prognosis + Treatment'''</big></center>
|-
|<center><big>'''Idiopathic Laryngeal Hemiplagia (ILH)'''</big></center>
|
*Progressive loss of fibres (esp. large diameter) within left recurrent laryngeal nerve compared to right
*[[PNS Repsonses to Injury - Pathology#The 'Dying Back' Phenomenon|Dying back]] axonopathy with myelin sheath involvement:
**Degenerating fibres
**Regenerating clusters
**De/Re-myelination
*Flattening of nerve between aorta & trachea
|
*Inspiratory 'roaring' noise - flapping of vocal fold
|
*'Slap test' - adduction of contralateral arytenoid during expiration
*Endoscopic examination - assymetric arytenoids, poor abduction of left vocal fold.
*Palpable atrophy of laryngeal musculature
|
*Laryngeal Ventriculectomy (Hobday procedure)
*'Tie Back'
*Laryngeal muscle prosthesis
*Prognosis usually good
|-style="background:#F0F8FF; color:black"
|<center><big>'''Cauda Equina Neuritis'''</big></center>
|
*Equine version of [[#IPRN|Idiopathic polyradiculoneuritis]]
*Extradural nerve roots of cauda equina thickened and discoloured
*Inflammatory infiltrate (lymphocytes, plasma cells, macrophages)
*Extensive axonal damage and demyelination
*Cranial nerve involvement often occurs
*Aetiology unknown:
**Antecedent infection?
**Antibodies to PNS myelin?
|
*Paralysis & anaesthesia of tail
*Urinary incontinence
*Loss of anal reflex
*Failure to defaecate
*Pain/hypersensitivity in gluteal/tail-head area
|
*Clinical signs
|
*Recovery unlikely - most animals are destroyed.
|-
|<center><big>'''Stringhalt'''</big></center>
|
*Causes poorly understood - similar signs caused by sweat pea plant ingestion (lathyrism)
*Distal axonopathy (esp. large diameter fibres)
|
*Abrupt onset continuous / intermittent hyperflexion of one or both hind limbs
*May also have ataxia, urinary incontinence, perineal flaccidity
|
*Differential diagnosis : Upward fixation of patella
|
*May get spontaneous recovery
*Move pasture
*Tenectomy of lateral digital extensor may help
|-
|-style="background:#F0F8FF; color:black"
|<center><big>'''Equine Motor Neuron Disease'''</big></center>
|
*Generalised LMN disorder
*Degeneration of Ventral horn motor neuron
*[[PNS Repsonses to Injury - Pathology#Chromatolysis|Chromatolysis]]
*Neurofilament accumulation
*Gliosis
*[[PNS Repsonses to Injury - Pathology#Wallerian Degeneration|Wallerian degeneration]]
*Denervation changes in muscle
|
*Weight Loss
*Muscle atrophy
*Generalised Weakness
*Short strided gait + narrow based stance
*Trembling
*Sweating and fasiculations
*Increased recumbency
|
*Elevated CK
*CSF protein
*Denervation of EMG
|
*May progress to constant recumbency (destroy), stabilise or improve
|-
|<center><big>'''Suprascapular Nerve Injury'''</big></center>
|
*'''"Sweeny"'''
*Commonly damaged by horse coliding into objects
*Fibrous entrapment as nerve reflected around wing of scapula
*Atrophy of supra- & infra- spinatous muscles
|
*Lateral luxation of shoulder when weight bearing
*Muscle wasting around shoulder
|
*Clinical signs
*History
|
*No more than 30cm regrowth in 12 months expected due to irreversible muscle fibrosis.

|-
|}

==Other Polyneuropathies==
*Tick Paralysis
*Vincristine Toxicity
*Endocrine polyneuropathy
**Dogs - hypothyroidism, insulinoma, diabetes mellitus
**Cats - diabetes mellitus
*Genetic polyneuropathies
*Protozoan polyradiculoneuritis
*Idiopathic facial paralysis (e.g. Bell's Palsy)
*Botulism

==Learning Tools==

Peripheral Nervous System Pathology Overview

2009-08-28T10:59:38Z

Karag7: /* Types of Injury */

{{review}}

{{toplink
|backcolour = E0EEEE
|linkpage = Nervous System - Pathology
|linktext =Nervous System
|maplink = Nervous System (Content Map) - Pathology
|pagetype =Pathology
}}
 
==Nerve Injury==
===Classification of Peripheral Nerve Disease===
{| cellpadding="4" cellspacing="0" border="2"
|-
|style="background:#B0E0E6; color:black" width="200"|'''By Nerve Type
|style="background:#B0E0E6; color:black" width="200"|'''By Anatomy'''
|style="background:#B0E0E6; color:black" width="250"|'''By Pathology'''
|-
|
*Mixed
|
*NMJ
|'''Neuronopathy :''' ''The Whole nerve cell''
|-
|
*Motor
|
*Distal / Proximal
|'''Axonopathy :''' ''The axon''
|-
|
*Sensory
|
*Root / Spinal Cord
|'''Demyelination:''' ''Schwann cell''
|-
|}
 

===Types of Injury===
{| cellpadding="4" cellspacing="0" border="2"
|-
|style="background:#B0E0E6; color:black"|'''Neuropraxia:'''||
*Temporary interruption of conduction - no histological change.
|-
|style="background:#B0E0E6; color:black"|'''Axonotmesis:'''||
*Axon interupted but basal lamina intact (e.g. crush injury)
*Regeneration occurs along original path - prospect for functional recovery good.
|-
|style="background:#B0E0E6; color:black"|'''Neurotmesis:'''||
*Axon '''and''' basal lamina interupted (e.g. transection injury)
*Success of regeneration depends on finding the correct distal stump
|}
 

===Clinical Signs with Peripheral Nerve Disease===
{| align="center" cellpadding="4" cellspacing="0" border="0"
|width="350"|
:'''Motor Neuropathy Signs (LMN signs)'''
|width="350"|
:'''Sensory Neuropathy'''
|width="350"|
:'''Autonomic Neuropathy'''
|-
|
*Flaccid paresis/paralysis of innervated structures
|
*Decreased or abherrant 'pain' response or sensation
|
*Aniscoria (dilated / constricted pupils)
|-
|
*Neurogenic muscle atrophy (very rapid)
|
*Proprioceptive defects
|
*Decreased tear production
|-
|
*Reduced / absent reflexes and muscle tone
|
*Abnormal sensation (paraesthesia)/sensitivity (dysthesia)
|
*Decreased salivation
|-
|
|
*Reduced / absent reflexes without muscle atrophy
|
*Bradycardia
|}
 

==Peripheral Nerve Disease in Small Animals==
{| cellpadding="4" cellspacing="0" border="2"
|- style="background:#B0E0E6; color:black"
|width="150"|<center><big>'''Disease'''</big></center>
|width="200"|<center><big>'''Pathology'''</big></center>
|width="250"|<center><big>'''Clinical Signs'''</big></center>
|width="250"|<center><big>'''Diagnosis'''</big></center>
|width="250"|<center><big>'''Prognosis + Treatment'''</big></center>
|-
|<center><big>'''Distal Denervating Disease'''</big></center>
|
*Distal axonopathy, possibly of toxic origin
|
*Tetraparesis
*Dysphonia / Aphonia
*Neck Weakness
*Tetraparesis developing to tetraplegia in severe cases ''floppy dog''
*Sensory function preserved: Pain but '''no''' withdrawal
|
*Biopsy / EMG unhelpful
|
*Very good prognosis
*Recovery in 3-6 weeks by '''axon regeneration'''
*Good nursing to prevent pressure sores in the recumbant animal
|- style="background:#F0F8FF; color:black"
|<center><big>'''Idiopathic Polyradiculoneuritis'''</big></center>
|
*Immune mediated demyelination often involving roots, directed against unknown epitopes in peripheral myelin.
*May be post infection
*May get axonal injury if severe
|
*As for distal denervating (although more rapid onset)
*May have sensory involvement.
|
*By clinical signs
*CSF changes if roots involved
*Slower nerve conduction
*H reflexes and F-waves may be lost
|
*Very good prognosis
*Recovery in 3-6 weeks by '''remyelination'''
*Immunosuppresive levels of corticosteroids (although may delay remyelination)
|-
|<center><big>'''Cauda Equina Traction'''</big></center>
|
*Tail pull injury
*Esp. cats after RTA
*Lesion via longitudinal traction
*Sacrocaudal dislocation/fracture
|
*Limp tail
*Incontinence
*Hindlimb Paresis
|
*Diagnosis on Clinical signs and history
*+/- Radiographs to show dislocation/fracture
|
*Prognosis difficult to predict
*Poor prognosis if tail limp & no anal tone
*Supportive treatment
*'''Persist for >3 months if possible'''
|- style="background:#F0F8FF; color:black"
|<center><big>'''Peripheral Nerve Tumours'''</big></center>
|
*Nerve sheath tumours
*Generally tumours of Schwann cells
*Common in dog Brachial plexus
|
*Chronic single forelimb lameness
*Weakness
*Muscle Atrophy
*Pain in Axilla
*LMN signs (may get UMN if grows into spinal cord
|
*Clinical signs
*Imaging
|
*Prognosis dependant on location
*Poor prognosis if in spinal cord
*Amputation of limb?
|-
|<center><big>'''Feline Dysautonomia'''</big></center>
|
*Common in 1980's - Sporadic now
*Degeneration (toxic?) of autonomic ganglia
|
*Mainly Parasympathetic
*Vomiting
*3rd Eyelid protrusion
*Dilated pupils + poor PLR
*Reduced Lacrimation
*Megaoesophagus
*Bradycardia
|
*Clinical signs
|
*Poor Prognosis
*Supportive therapy only
*Similar sporadic disease seen in dogs
|-
|}

==Peripheral Nerve Disease in Large Animals==
{| cellpadding="4" cellspacing="0" border="2"
|-- style="background:#B0E0E6; color:black"
|width="150"|<center><big>'''Disease'''</big></center>
|width="200"|<center><big>'''Pathology'''</big></center>
|width="250"|<center><big>'''Clinical Signs'''</big></center>
|width="250"|<center><big>'''Diagnosis'''</big></center>
|width="250"|<center><big>'''Prognosis + Treatment'''</big></center>
|-
|<center><big>'''Idiopathic Laryngeal Hemiplagia (ILH)'''</big></center>
|
*Progressive loss of fibres (esp. large diameter) within left recurrent laryngeal nerve compared to right
*[[PNS Repsonses to Injury - Pathology#The 'Dying Back' Phenomenon|Dying back]] axonopathy with myelin sheath involvement:
**Degenerating fibres
**Regenerating clusters
**De/Re-myelination
*Flattening of nerve between aorta & trachea
|
*Inspiratory 'roaring' noise - flapping of vocal fold
|
*'Slap test' - adduction of contralateral arytenoid during expiration
*Endoscopic examination - assymetric arytenoids, poor abduction of left vocal fold.
*Palpable atrophy of laryngeal musculature
|
*Laryngeal Ventriculectomy (Hobday procedure)
*'Tie Back'
*Laryngeal muscle prosthesis
*Prognosis usually good
|-style="background:#F0F8FF; color:black"
|<center><big>'''Cauda Equina Neuritis'''</big></center>
|
*Equine version of [[#IPRN|Idiopathic polyradiculoneuritis]]
*Extradural nerve roots of cauda equina thickened and discoloured
*Inflammatory infiltrate (lymphocytes, plasma cells, macrophages)
*Extensive axonal damage and demyelination
*Cranial nerve involvement often occurs
*Aetiology unknown:
**Antecedent infection?
**Antibodies to PNS myelin?
|
*Paralysis & anaesthesia of tail
*Urinary incontinence
*Loss of anal reflex
*Failure to defaecate
*Pain/hypersensitivity in gluteal/tail-head area
|
*Clinical signs
|
*Recovery unlikely - most animals are destroyed.
|-
|<center><big>'''Stringhalt'''</big></center>
|
*Causes poorly understood - similar signs caused by sweat pea plant ingestion (lathyrism)
*Distal axonopathy (esp. large diameter fibres)
|
*Abrupt onset continuous / intermittent hyperflexion of one or both hind limbs
*May also have ataxia, urinary incontinence, perineal flaccidity
|
*Differential diagnosis : Upward fixation of patella
|
*May get spontaneous recovery
*Move pasture
*Tenectomy of lateral digital extensor may help
|-
|-style="background:#F0F8FF; color:black"
|<center><big>'''Equine Motor Neuron Disease'''</big></center>
|
*Generalised LMN disorder
*Degeneration of Ventral horn motor neuron
*[[PNS Repsonses to Injury - Pathology#Chromatolysis|Chromatolysis]]
*Neurofilament accumulation
*Gliosis
*[[PNS Repsonses to Injury - Pathology#Wallerian Degeneration|Wallerian degeneration]]
*Denervation changes in muscle
|
*Weight Loss
*Muscle atrophy
*Generalised Weakness
*Short strided gait + narrow based stance
*Trembling
*Sweating and fasiculations
*Increased recumbency
|
*Elevated CK
*CSF protein
*Denervation of EMG
|
*May progress to constant recumbency (destroy), stabilise or improve
|-
|<center><big>'''Suprascapular Nerve Injury'''</big></center>
|
*'''"Sweeny"'''
*Commonly damaged by horse coliding into objects
*Fibrous entrapment as nerve reflected around wing of scapula
*Atrophy of supra- & infra- spinatous muscles
|
*Lateral luxation of shoulder when weight bearing
*Muscle wasting around shoulder
|
*Clinical signs
*History
|
*No more than 30cm regrowth in 12 months expected due to irreversible muscle fibrosis.

|-
|}

==Other Polyneuropathies==
*Tick Paralysis
*Vincristine Toxicity
*Endocrine polyneuropathy
**Dogs - hypothyroidism, insulinoma, diabetes mellitus
**Cats - diabetes mellitus
*Genetic polyneuropathies
*Protozoan polyradiculoneuritis
*Idiopathic facial paralysis (e.g. Bell's Palsy)
*Botulism

==Learning Tools==

Peripheral Nervous System Pathology Overview

2009-08-28T10:59:22Z

Karag7: /* Types of Injury */

{{review}}

{{toplink
|backcolour = E0EEEE
|linkpage = Nervous System - Pathology
|linktext =Nervous System
|maplink = Nervous System (Content Map) - Pathology
|pagetype =Pathology
}}
 
==Nerve Injury==
===Classification of Peripheral Nerve Disease===
{| cellpadding="4" cellspacing="0" border="2"
|-
|style="background:#B0E0E6; color:black" width="200"|'''By Nerve Type
|style="background:#B0E0E6; color:black" width="200"|'''By Anatomy'''
|style="background:#B0E0E6; color:black" width="250"|'''By Pathology'''
|-
|
*Mixed
|
*NMJ
|'''Neuronopathy :''' ''The Whole nerve cell''
|-
|
*Motor
|
*Distal / Proximal
|'''Axonopathy :''' ''The axon''
|-
|
*Sensory
|
*Root / Spinal Cord
|'''Demyelination:''' ''Schwann cell''
|-
|}
 

===Types of Injury===
{| cellpadding="4" cellspacing="0" border="2"
|-
|style="background:#B0E0E6; color:black"|'''Neuropraxia:'''||
*Temporary interruption of conduction - no histological change.
|-
|style="background:#B0E0E6; color:black"|'''Axonotmesis:'''||
*Axon interupted but basal lamina intact (e.g. crush injury)
*Regeneration occurs along original path - prospect for functional recovery good.
|-
|style="background:#B0E0E6; color:black"|'''Neurotemesis:'''||
*Axon '''and''' basal lamina interupted (e.g. transection injury)
*Success of regeneration depends on finding the correct distal stump
|}
 

===Clinical Signs with Peripheral Nerve Disease===
{| align="center" cellpadding="4" cellspacing="0" border="0"
|width="350"|
:'''Motor Neuropathy Signs (LMN signs)'''
|width="350"|
:'''Sensory Neuropathy'''
|width="350"|
:'''Autonomic Neuropathy'''
|-
|
*Flaccid paresis/paralysis of innervated structures
|
*Decreased or abherrant 'pain' response or sensation
|
*Aniscoria (dilated / constricted pupils)
|-
|
*Neurogenic muscle atrophy (very rapid)
|
*Proprioceptive defects
|
*Decreased tear production
|-
|
*Reduced / absent reflexes and muscle tone
|
*Abnormal sensation (paraesthesia)/sensitivity (dysthesia)
|
*Decreased salivation
|-
|
|
*Reduced / absent reflexes without muscle atrophy
|
*Bradycardia
|}
 

==Peripheral Nerve Disease in Small Animals==
{| cellpadding="4" cellspacing="0" border="2"
|- style="background:#B0E0E6; color:black"
|width="150"|<center><big>'''Disease'''</big></center>
|width="200"|<center><big>'''Pathology'''</big></center>
|width="250"|<center><big>'''Clinical Signs'''</big></center>
|width="250"|<center><big>'''Diagnosis'''</big></center>
|width="250"|<center><big>'''Prognosis + Treatment'''</big></center>
|-
|<center><big>'''Distal Denervating Disease'''</big></center>
|
*Distal axonopathy, possibly of toxic origin
|
*Tetraparesis
*Dysphonia / Aphonia
*Neck Weakness
*Tetraparesis developing to tetraplegia in severe cases ''floppy dog''
*Sensory function preserved: Pain but '''no''' withdrawal
|
*Biopsy / EMG unhelpful
|
*Very good prognosis
*Recovery in 3-6 weeks by '''axon regeneration'''
*Good nursing to prevent pressure sores in the recumbant animal
|- style="background:#F0F8FF; color:black"
|<center><big>'''Idiopathic Polyradiculoneuritis'''</big></center>
|
*Immune mediated demyelination often involving roots, directed against unknown epitopes in peripheral myelin.
*May be post infection
*May get axonal injury if severe
|
*As for distal denervating (although more rapid onset)
*May have sensory involvement.
|
*By clinical signs
*CSF changes if roots involved
*Slower nerve conduction
*H reflexes and F-waves may be lost
|
*Very good prognosis
*Recovery in 3-6 weeks by '''remyelination'''
*Immunosuppresive levels of corticosteroids (although may delay remyelination)
|-
|<center><big>'''Cauda Equina Traction'''</big></center>
|
*Tail pull injury
*Esp. cats after RTA
*Lesion via longitudinal traction
*Sacrocaudal dislocation/fracture
|
*Limp tail
*Incontinence
*Hindlimb Paresis
|
*Diagnosis on Clinical signs and history
*+/- Radiographs to show dislocation/fracture
|
*Prognosis difficult to predict
*Poor prognosis if tail limp & no anal tone
*Supportive treatment
*'''Persist for >3 months if possible'''
|- style="background:#F0F8FF; color:black"
|<center><big>'''Peripheral Nerve Tumours'''</big></center>
|
*Nerve sheath tumours
*Generally tumours of Schwann cells
*Common in dog Brachial plexus
|
*Chronic single forelimb lameness
*Weakness
*Muscle Atrophy
*Pain in Axilla
*LMN signs (may get UMN if grows into spinal cord
|
*Clinical signs
*Imaging
|
*Prognosis dependant on location
*Poor prognosis if in spinal cord
*Amputation of limb?
|-
|<center><big>'''Feline Dysautonomia'''</big></center>
|
*Common in 1980's - Sporadic now
*Degeneration (toxic?) of autonomic ganglia
|
*Mainly Parasympathetic
*Vomiting
*3rd Eyelid protrusion
*Dilated pupils + poor PLR
*Reduced Lacrimation
*Megaoesophagus
*Bradycardia
|
*Clinical signs
|
*Poor Prognosis
*Supportive therapy only
*Similar sporadic disease seen in dogs
|-
|}

==Peripheral Nerve Disease in Large Animals==
{| cellpadding="4" cellspacing="0" border="2"
|-- style="background:#B0E0E6; color:black"
|width="150"|<center><big>'''Disease'''</big></center>
|width="200"|<center><big>'''Pathology'''</big></center>
|width="250"|<center><big>'''Clinical Signs'''</big></center>
|width="250"|<center><big>'''Diagnosis'''</big></center>
|width="250"|<center><big>'''Prognosis + Treatment'''</big></center>
|-
|<center><big>'''Idiopathic Laryngeal Hemiplagia (ILH)'''</big></center>
|
*Progressive loss of fibres (esp. large diameter) within left recurrent laryngeal nerve compared to right
*[[PNS Repsonses to Injury - Pathology#The 'Dying Back' Phenomenon|Dying back]] axonopathy with myelin sheath involvement:
**Degenerating fibres
**Regenerating clusters
**De/Re-myelination
*Flattening of nerve between aorta & trachea
|
*Inspiratory 'roaring' noise - flapping of vocal fold
|
*'Slap test' - adduction of contralateral arytenoid during expiration
*Endoscopic examination - assymetric arytenoids, poor abduction of left vocal fold.
*Palpable atrophy of laryngeal musculature
|
*Laryngeal Ventriculectomy (Hobday procedure)
*'Tie Back'
*Laryngeal muscle prosthesis
*Prognosis usually good
|-style="background:#F0F8FF; color:black"
|<center><big>'''Cauda Equina Neuritis'''</big></center>
|
*Equine version of [[#IPRN|Idiopathic polyradiculoneuritis]]
*Extradural nerve roots of cauda equina thickened and discoloured
*Inflammatory infiltrate (lymphocytes, plasma cells, macrophages)
*Extensive axonal damage and demyelination
*Cranial nerve involvement often occurs
*Aetiology unknown:
**Antecedent infection?
**Antibodies to PNS myelin?
|
*Paralysis & anaesthesia of tail
*Urinary incontinence
*Loss of anal reflex
*Failure to defaecate
*Pain/hypersensitivity in gluteal/tail-head area
|
*Clinical signs
|
*Recovery unlikely - most animals are destroyed.
|-
|<center><big>'''Stringhalt'''</big></center>
|
*Causes poorly understood - similar signs caused by sweat pea plant ingestion (lathyrism)
*Distal axonopathy (esp. large diameter fibres)
|
*Abrupt onset continuous / intermittent hyperflexion of one or both hind limbs
*May also have ataxia, urinary incontinence, perineal flaccidity
|
*Differential diagnosis : Upward fixation of patella
|
*May get spontaneous recovery
*Move pasture
*Tenectomy of lateral digital extensor may help
|-
|-style="background:#F0F8FF; color:black"
|<center><big>'''Equine Motor Neuron Disease'''</big></center>
|
*Generalised LMN disorder
*Degeneration of Ventral horn motor neuron
*[[PNS Repsonses to Injury - Pathology#Chromatolysis|Chromatolysis]]
*Neurofilament accumulation
*Gliosis
*[[PNS Repsonses to Injury - Pathology#Wallerian Degeneration|Wallerian degeneration]]
*Denervation changes in muscle
|
*Weight Loss
*Muscle atrophy
*Generalised Weakness
*Short strided gait + narrow based stance
*Trembling
*Sweating and fasiculations
*Increased recumbency
|
*Elevated CK
*CSF protein
*Denervation of EMG
|
*May progress to constant recumbency (destroy), stabilise or improve
|-
|<center><big>'''Suprascapular Nerve Injury'''</big></center>
|
*'''"Sweeny"'''
*Commonly damaged by horse coliding into objects
*Fibrous entrapment as nerve reflected around wing of scapula
*Atrophy of supra- & infra- spinatous muscles
|
*Lateral luxation of shoulder when weight bearing
*Muscle wasting around shoulder
|
*Clinical signs
*History
|
*No more than 30cm regrowth in 12 months expected due to irreversible muscle fibrosis.

|-
|}

==Other Polyneuropathies==
*Tick Paralysis
*Vincristine Toxicity
*Endocrine polyneuropathy
**Dogs - hypothyroidism, insulinoma, diabetes mellitus
**Cats - diabetes mellitus
*Genetic polyneuropathies
*Protozoan polyradiculoneuritis
*Idiopathic facial paralysis (e.g. Bell's Palsy)
*Botulism

==Learning Tools==

CNS Congenital Abnormalities - Pathology

2009-08-28T09:41:03Z

Karag7: /* Meningoencephalocoele */

{{review}}

{{toplink
|backcolour = E0EEEE
|linkpage = Nervous System - Pathology
|linktext =Nervous System
|maplink = Nervous System (Content Map) - Pathology
|pagetype =Pathology
}}
 
==Introduction==

* Congenital malformations may involve the spinal cord, brain, meninges, calvaria or vertebral column.
* Abnormalities typically result from defects in neural tube development.
* Congenital malformations are present at or before birth, and manifest as either:
** Morphological problems
** Functional problems
*** Tend to arise as biochemical abnormalities, such as the lysosomal diseases or leukodystrophies.
* Causes of congenital abnormalities include:
** Environmental causes
*** For example, these may be toxic, infectious, nutritional, or physical (e.g. radiation)
*** This is by far the most common cause.
** Inherited traits.

==Meningoencephalocoele==

* A defect in the cranium allows protrustion of the brain and meninges.
** There is always crania bifida (a split skull).
* Meningoencephalocoele may be inherited in pigs and cats.

==Hydrocephalus==
[[Image:hydrocephalus.jpg|thumb|right|150px|Hydrocephalus in situ]] [[Image:hydrocephalussection.jpg|thumb|right|150px|Hydrocephalus. Image courtesy of BioMed Archive.]] [[Image:aqueductstenosis.jpg|thumb|right|150px|Aqueduct stenosis. Image courtesy of BioMed Archive.]]
* Hydrocephalus is an increased accumulation of fluid in the cranial cavity.
* There are several different types of hydrocephalus relating to where the fluid is located within the cavity.
** '''Internal''' hydrocephalus - fluid is within the ventricles
*** The most common type.
*** There is unilateral or bilateral dilation of the ventricles.
** '''External''' hydrocephalus - fluid is within the arachnoid space
** '''Communicating''' hydrocephalus - fluid is within the ventricles and arachnoid space
** '''Hydrocephalus ex vacuo''' - the ventricle is dilated secondary to loss of cerebral tissue
*** Also known as compensatory hydrocephalus.

[http://w3.vet.cornell.edu/nst/nst.asp?Fun=F_KSsrch&kw=HYDROCEPHALUS View images courtesy of Cornell Veterinary Medicine]

===Causes===

* Hydrocephalus may be '''congenital'''.
** Congenital hydrocephalus is common in brachycephalic and small breed dogs.
*** It occurs sporadically in cattle.
** Obstructive lesions are often not found.
** Amalformed mesencephalic aqueduct may be involved.
** The cranium may be abnormal, for example, doming.
* '''Acquired''' hydrocephalus is the result of obstruction, usually due to inflammation or compression.
** Space-occupying lesions include :
*** Neoplasms
*** Abscesses
*** Cholesteatomas
** Inflammation of meninges and/or ependymal cells can lead to hydrocephalus.
*** For example, FIP causes ependymitis which can obstruct flow if it affects the mesencephalic aqueduct.
* Hydrocephalus may also arise with:
** Increased ventricle size due to loss of brain parenchyma.
** Overproduction of CSF
*** Rare
*** Associated with choroid plexus tumours.

===Breed predisposition===

* Some breeds are predisposed to hydrocephalus.
** Chihuahua, pomeranian, yorkshire terrier, english bulldog, lhasa apso, toy poodle, cairn terrier, boston terrier, pug, pekingese, maltese terrier.
** Hydrocephalus has also been described in
*** Bullmastiffs, in association with cerebellar ataxia.
*** Siamese cats, as an autosomal recessive trait.

===Clinical Signs===

* Clinical signs are the result of:
** Loss of neurons or neuronal function
** Alterations in intercranial pressure
** Pathophysiological effects of intracranial disease
* Signs reflect the anatomical level of disease involvement.
** Rostrotentorial, vestibular and cerebellar signs are most common.
* Signs are not related to the degree of ventricular dilation. They are more associated with other damage caused by the disease proces:
** Intracranial pressure changes
** Intraventricular haemorrhage
** Speed of ventricular obstruction
* Hydrocephalus may contribute to abnormalities of skull development, where it is a congenital disease.
** Thinning of the bone structure
** Dome-shape head
** Persistent fontanelles
* Ventral or lateral strabismus may occur, although the reason for this is unknown.
** May be related to distortion of the orbits, due to skill deformity.
** May be realted with pressue on the mesencephalic tegementum.

===Diagnosis===

* Diagnosis is by a variety of imaging and electrophysiologic methods.
** MRI allows examination of the ventricular system, and give better resolution of the brain parenchyma than CT.

===Treatment===

* Prognosis is generally poor.
* Medical treatment:
** General supportive care
** Medications to limit CSF production and reduce intracranial pressure.
* Surgical treatment:
** Aims to allow drainage of CSF from the brain to another site for absorption.

==Cerebellar Defects==

* Cerebellar defects include:
** [[Cerebellar Pathology - Pathology#Cerebellar Hypoplasia|Cerebellar hypoplasia]]
** [[Cerebellar Pathology - Pathology#Cerebellar Abiotrophy|Cerebellar abiotrophy]]

CNS Inflammation - Pathology

2009-08-28T09:15:27Z

Karag7: /* Prion Diseases */

{{review}}

{{toplink
|backcolour = E0EEEE
|linkpage = Nervous System - Pathology
|linktext =Nervous System
|maplink = Nervous System (Content Map) - Pathology
|pagetype =Pathology
}}
 
==Introduction==

* Although the CNS is well protected, its defences against organisms that have already invaded are less well developed. This is due to:
*# Minimal antibody production
*# Cerebrospinal fluid providing a good culture medium for invading organisms.
*# Inflammatory cell, antibody and drug entry to the CNS being impeded by the blood-brain barrier.

===Classification of Inflammation===

* CNS inflammation may manifest as encephalitis or meningitis.
** These often co-exist.
* The aetiology CNS inflammation may be:
** Infectious
*** Bacteria
*** Fungi
*** Protozoa
*** Viruses or non-infectious.
*** Infectious agents vary geographically.
** Non-infectious
*** No infectious cause can be found in 60% of meningitis cases.
* Inflammation may also be broadly classified based on the nature of the exudate present.
** '''Fibrinous'''
*** Caused by bacteria infection (including ''Mycoplasma'').
** '''Suppurative'''
*** Caused by bacteria and fungi.
** '''Granulomatous'''
*** Caused by bacteria or fungi.
** '''Lymphoplasmacytic'''
*** Caused by viruses.
** '''Haemorrhagic'''
*** This is rare.
*** Usually associated with septicemia or infarcts.

==Routes of Entry==

* CNS inflammation is usually the result of infection.
** This may be caused by:
*** Bacteria
*** Fungi
*** Protozoa
*** Viruses
* Organisms must first enter the CNS in order to establish infection.
** There are several routes of entry that allow this:
**# '''Haematogenous entry'''
**#* This is the most common route.
**# '''Entry via the peripheral nerves'''
**#* Organisms track within the axoplasm of axons.
**#* For example, ''Listeria monocytogenes''.
**# '''Penetrating trauma'''
**#* For example, dehorning wounds, skull fracture or tail docking.
**# '''Direct spread of infection'''
**#* From the nasal cavity, middle ear or paranasal sinuses.

==Localisation of Infectious Organisms==

* After entry, organisms may establish in one or more of four main areas:
*# '''Epidural space'''
*#* Infection tends to manifest as abscess formation.
*# '''Subdural space'''
*#* Manifests as abscess formation.
*#* Fairly uncommon.
*# '''Leptomeninges'''
*#* Causes leptomeningitis, which may be:
*#*# Suppurative
*#*#* The most common form.
*#*#* Neutrophils are the predominant cell type.
*#*#* Caused by bacteria
*#*#** E.g. ''E. coli'' and ''Streptococcus''
*#*#* There are often no gross lesions, but the brain may appear swollen and the meninges opaque.
*#*#* Usually results in death.
*#*# Eosinophilic meningoencephalitis
*#*#* The classic example of this is porcine salt poisoning, when water has been restricted and the suddenly replenished.
*#*#* Perivascular eosinophilic cuffing is seen in the cerebrum and meninges.
*#*# Lymphocytic
*#*#* Usually of viral origin.
*#*# Granulomatous
*#*#* Caused by fungal diseases and Mycobacteriosis.
*# '''CNS parenchyma'''

==Bacterial Infections==
[[Image:pneumococcalmeningitis.jpg|thumb|right|150px|Pneumococcal meningitis. Image courtesy of BioMed Archive]]
* Bacterial infections typically result in abscesses.
** These may be single or multiple depending on the route of entry, and vary in size.
** They contain a central, liquefied cavity.
* There are differences between cerebral abscesses and those occuring elsewhere.
** Encapsulation is slow.
*** This is due to a lack of fibroblasts.
*** There is therefore less collagen in the capsule.
** Astrocytic glial fibers are not as strong as collagen
* Other organisms may cause similar infections:
** Rickettsial organisms
*** E.g. ''Ehrlichia''
** Spirochates
*** E.g. Leptospirosis

==Viral Infections==

* Viral infections tend to reach the CNS by haematogenous spread and via peripheral nerves.
* There are three hallmark lesions of CNS viral infections:
*# Neuronal necrosis
*# Gliosis
*# Vascular changes
* Several types of virus may cause inflammation in the CNS. [[Image:negribodies.jpg|thumb|right|150px|Negri bodies, as seen in rabies. Image courtesy of BioMed Archive]]
** '''Neurotropic''', e.g.
*** Rabies (rhabdovirus)
*** Aujesky’s disease (herpesvirus)
*** Visna (ovine lentivirus)
** '''Endotheliotropic''', e.g.
*** Infectious canine hepatitis (canine adenovirus)
*** Classical swine fever (pestivirus)
*** Equine herpesvirus type 1 (herpes)
** '''Pantropic'''
*** Infectious canine distemper (morbillivirus)
*** Infectious bovine rhinotracheitis (bovine herpesvirus type 1)
* Other examples of viruses affecting the CNS:
** Distemper
** Parvovirus
** Parainfluenza
** Herpes
** FIP
** FIV
** FeLV
** Pseudorabies
** Rabies

==Prion Diseases==

* Prion diseases are also knowns as transmissible spongiform encephalopathies (TSEs).
* They are a group of fatal neurodegenerative diseases which occur in a number of species, including man.
** For example:
*** Bovine spongiform encephalopathy (BSE) in cattle
*** Scrapie in sheep
*** Chronic wasting disease in elk
*** Creutzfeldt-Jakob disease (CJD), Gerstmann-Sträussler-Scheinker disease (GSS), fatal familial insomnia (FFI) and kuru in man
* TSEs have a long incubation period, making them difficult to diagnose.

===Aetiology===

* The aetiology of prion diseases is still highly controversial.
** However, an abnormal isoform of the host-encoded prion protein (PrP) is seen in the brains of affected animals.
*** The normal host PrP changes its structure into the disease-associated form PrPSc.
** The abnormal proteint (PrPSc) accumulates as amyloid fibrils in nervous tissue.
* The agent appears to be highly resistant.

===Pathology===

====Gross====

* Prion diseases cause NO GROSS LESIONS.

====Hisological====

* TSEs typically cause what is known as the "microscopic triad":
*# Spongiform change.
*#* Vacuolation of neurons.
*#* Particularly in nuclei.
*# Astrogliosis
*# Amyloid plaques
*#* These are not always seen.

==Non-Infectious Inflammatory Diseases==

===Granulomatous Meningoencephalitis (GME)===

* An [[CNS Idiopathic Conditions - Pathology|idiopathic CNS conditon]]
* May occur as:
** A disseminated disease
** A focal mass lesion
** A primary occular disease
* Brainstem signs are common, although the forebrain is primarily affected.
* May be incorrectly diagnosed as lymphoma.
* Changes are apparent in the CSF.
** There is usually a mononucloear pleocytosis.
** Sometimes only protein is elveated.
* Diffuse inflammatory changes or a mass lesion will be seen by advanced imaging.
** However, biopsy is required for a definative diagnosis.
* Life span is between 6 months and 1 year from diagnosis.

====Treatment====

* Immunosuppression:
** Corticosteroids
** Azathioprine
** Cycophosphamide
* Surgery
** This is only appropriate if there is a focal mass.
* Radiation therapy.

===Pug Encephalitis===

* A [[CNS Idiopathic Conditions - Pathology|CNS idiopathic condition]]
* Affects pugs.
** Similar conditions are seen in yorkshire and maltese terriers.
* Officially known as necrotising meningoencephalitis of small dogs.
* Characterised by histological forebrain inflammation and necrosis.
* The disease is uniformly fatal.
** Corticosterid treatment has no effect.

==Clinical Signs of CNS Inflammation==

* Signs often reflect multiple levels of neurological involvement.
* Generalised [[Forebrain Disease - Pathology#Clinical Signs|forebrain signs]] are seen.
* Neck pain may be seen alone, or with other signs.

==Diagnosis==

* History, physical and neurological examination.
* Fundic examination may give clues as to whether a systemic infection is present.
* CSF examination may help define the problem.

==Treatment==

* Treatment is directed at a specific cause, if one can be found.
** If a cause cannot be found, trimethoprim, clindamycin or doxycycline plus or minus corticosteroids may be used.

CNS Response to Injury - Pathology

2009-08-28T09:01:22Z

Karag7: /* Chromatolysis */

{{review}}

{{toplink
|backcolour = E0EEEE
|linkpage = Nervous System - Pathology
|linktext =Nervous System
|maplink = Nervous System (Content Map) - Pathology
|pagetype =Pathology
}}
 
==Introduction==

* The CNS is composed of two major cell types:
*# Neurons
*# Glial cells, which include:
*#* Astrocytes
*#* Oligodendrocytes
*#* Microglial cells
*#* Ependymal cells
*#* Choroid plexus epithelial cells
* The response to injury varies with the cell type injured.

==Response of Neurons to Injury==

* Neurons are particularly vulnerable to injury, due to their:
** High metabolic rate
** Small capacity to store energy
** Lack of regenerative ability
** Axons being very dependent on the cell body.
*** Axons cannot make their own protein as they have no Nissl substance.
*** The cell body produces the axon's protein and disposes of its waste.
*** Death or damage of the cell body causes axon degeneration.

* There are four ways in which neurons may react to insult:
*# Acute Necrosis
*# Chromatolysis
*# Wallerian Degeneration
*# Vacuolation

===Acute Necrosis===

* Acute necrosis is the most common neuronal response to injury.
* Causes of actue necrosis include:
** Ischaemia
*** Diminution of the blood supply causes a lack of nutrients and oxygen, inhibiting energy production. A decrease in the levels of ATP leads to:
***# Failure of the Na+/K+pumps, causing cell swelling and an increase in extracellular potassium.
***# Failure to generate NAD required for DNA repair.
** Hypoxia
** Hypoglycaemia
** Toxins, such as lead and mercury

====Laminar Cortical Necrosis====

* Laminar cortical necrosis refers to the selective destruction of neurons in the deeper layers of the cerebral cortex.
** These neurons are the most sensitive to hypoxia.
* The laminar cortical pattern of acute necrosis occurs in several instances:
*# Ischaemia
*#* For example, seizure-related ischaemia in dogs.
*# Polioencephalomalacia in ruminants
*#* Also called cerebrocortical necrosis or CCN.
*# Salt poisoning in swine
*# Lead poisoning in cattle
* It is most likely that gross changes will not be seen. When they are visible, changes may be apparent as:
** Oedema
*** Causes brain swelling, flattened gyri and herniation
** A thin, white, glistening line along the middle of the cortex.
*** In ruminants, this fluoresces with UV-light.
* Ultimately the cortex becomes necrotic and collapses.

[http://w3.vet.cornell.edu/nst/nst.asp?Fun=F_KSsrch&kw=POLIOENCEPHALOMALACIA View images courtesy of Cornell Veterinary Medicine]

===Chromatolysis===

* Chromatolysis is the cell body’s reaction to axonal insult.
* The cell body swells and the Nissl substance (granular cytoplasmic reticulum and ribosomes found in nerve cell bodies) disperses.
** Dispersal of the Nissl substance allows the cell body to produce proteins for rebuilding the axon.
* IT IS NOT A FORM OF NECROSIS.
** It is an adaptive response to deal with the injury.
** It can, however lead to necrosis.
* Seen, for example, in grass sickness in [[Hindgut Fermenters - Horse - Anatomy & Physiology|horses]] (equine dysautonomia).

[http://w3.vet.cornell.edu/nst/nst.asp?Fun=Display&imgID=13353 View images courtesy of Cornell Veterinary Medicine]

===Wallerian Degeneration===

* Wallerian degeneration is the axon’s reaction to insult.
* The axon and its myelin sheath degenerates distal to the point of injury.
* There are several causes of wallerian degeneration:
** Axonal transection
*** This is the "classic" cause
** Vascular causes
** Inflamatory reactions
** Toxic insult
** As a sequel to neuronal cell death.

[http://w3.vet.cornell.edu/nst/nst.asp?Fun=F_KSsrch&kw=WALLERIAN View images courtesy of Cornell Veterinary Medicine]

====The Process of Wallerian Degeneration====

# '''Axonal Degeneration'''
#* Axonal injuries initially lead to acute axonal degeneration.
#** The proximal and distal ends separate within 30 minutes of injury.
#* Degeneration and swelling of the axolemma eventually leads to formation of bead-like particles.
#* After the membrane is degraded, the organelles and cytoskeleton disintegrate.
#** Larger axons require longer time for cytoskeleton degradation and thus take a longer time to degenerate.
# '''Myelin Clearance'''
#* Following axonal degeneration, myelin debris is cleared by phagocytosis.
#* Myelin clearance in the PNS is much faster and efficient that in the CNS. This is due to:
#** The actions of schwann cells in the PNS.
#** Differences in changes in the blood-brain barrier in each system.
#*** In the PNS, the permeability increases throughout the distal stump.
#*** Barrier disruption in CNS is limited to the site of injury.
# '''Regeneration''' [[Image:neuronalvacuolation1.jpg|thumb|right|150px|Neuronal vacuolation. Image courtesy of BioMed Archive]]
#* Regeneration is rapid in the PNS.
#** Schwann cells release growth factors to support regeneration.
#* CNS regeneration is much slower, and is almost absent in most species.
#** This is due to:
#*** Slow or absent phagocytosis
#*** Little or no axonal regeneration, because:
#**** Oligodendrocytes have little capacity for remyelination compared to Schwann cells.
#**** There is no basal lamina scaffold to support a new axonal sprout.
#**** The debris from central myelin inhibits axonal sprouting.

===Vacuolation===
[[Image:neuronalvacuolation2.jpg|thumb|right|150px|Neuronal vacuolation. Image courtesy of BioMed Archive]]
* Vacuolation is the hallmark of transmissible spongiform encephalopathies.
** For example, BSE and Scrapie.
* Vacuolation can also occur under other circumstances:
** Artefact of fixation
** Toxicoses
** It may sometimes be a normal feature.

==Glial Cell Response to Injury==

* The order of susceptibility of CNS cells to injury runs, from most to least susceptible:
*# Neurons
*# Oligodendroglia
*# Astrocytes
*# Microglia
*# Endothelial cells

===Astrocytes===

* The response of astrocytes to insult include:
** '''Necrosis'''
** '''Astrocytosis'''
*** An increase in the number of astrocytes (i.e. astrocyte hyperplasia).
** '''Astrogliosis'''
*** An increase in the size of astrocytes (i.e. astrocyte hypertrophy).
** '''Gliosis'''
*** Formation of glial fibres.
*** This is a form of scarring in the CNS.

===Oligodendrocytes===

* Oligodendrocytes are prone to hypoxia and degeneration
* Oligodendrocytes proliferate around damaged neurons.
** This is known as '''satellitosis'''.
* Death of oligodendrocytes causes demyelination.

===Microglial Cells===

* Microglial cells can respond in two ways to CNS injury.
*# They may phagocytose cell debris to transform to gitter cells.
*#* Gitter cells are large macrophages with foamy cytoplasm. [http://w3.vet.cornell.edu/nst/nst.asp?Fun=F_KSsrch&kw=GITTER View images courtesy of Cornell Veterinary Medicine]
*# They may form glial nodules.
*#* These are small nodules that occur notably in viral diseases.

==General Responses to Injury==

===Ischaemic Damage===

* The CNS is particularly sensitive to ischaemia, because it has few energy reserves.
* The CNS is protected by its bony covering.
** Despite offering protection, the covering also makes the CNS vulnerable to certain types of damage, for example:
*** Damage due to fractures and dislocation.
*** Damage due to raised intracranial pressure.
**** Raised intracranial stimulates a compensatory increase in blood flow, further raising intracranial pressure. This stimulates a further increase in blood flow, and the cycle continues until intracranial pressure is so high that blood flow is impeded.
***** The result of this is '''ischaemia'''.
* Survival of any cell is dependent on having sufficient energy.
** Ischaemia causes cell death by impeding energy supply to cells.
*** Cells directly affected by ischamia die rapidly.
**** For example, those suffering a failure of pefusion due to an infarct.
*** Neurons surrounding this area of complete and rapid cell death exist under sub-optimal conditions and die over a more prolonged period.
**** This area of gradual death is known as the '''lesion penumbra'''.
**** There are several mechanisms implicated in cell death in the penumbra:
****# Increase in intracellular calcium
****# Failure to control free radicals
****# Generation of nitrogen species (e.g NO and ONOO) are the main damaging events.

===Oedema===

* There are three types of cerebral oedema:
*# '''Vasogenic oedema'''
*#* Vasogenic oedema follows vascular injury.
*#* Oedema fluid gathers outside of the cell.
*#* This is the most common variation of cerebral oedema.
*# '''Cytotoxic oedema'''
*#* Cytotoxic oedema is due to an energy deficit.
*#** The neuron can’t pump out sodium and water leading to swelling within the cell.
*# '''Interstitial oedema'''
*#* Associated with hydrocephalus.
*#* This type of cerebral oedema is of lesser importance.
* One serious consequence of oedema is that the increase in size leads to the brain trying to escape the skull.
** This causes herniation of the brain tissue.
** The most common site of herniation is at the foramen magnum.
*** The medulla is compressed at the site of the respiratory centres, leading to death.

===Demyelination===

* Demyelination is the loss of initially normal myelin from the axon.
* Demyelination may be primary or secondary.

====Primary Demyelination====

* Normally formed myelin is selectively destroyed; however, the axon remains intact.
* Causes of primary demyelination:
** Toxins, such as hexachlorophene or triethyl tin.
** Oedema
** Immune-mediated demyelination
** Infectious diseases, for example canine distemper or caprine arthritis/encephalitis.

====Secondary Demyelination====

* Myelin is lost following damage to the axon.
** I.e. in [[CNS Response to Injury - Pathology#Wallerian Degeneration|wallerian degeneration]]

===Vascular Diseases===

* Vascular diseases can lead to complete or partial blockage of blood flow which leads to ischaemia.
** Consequences of ischaemia depend on:
**# Duration and degree of ischaemia
**# Size and type of vessel involved
**# Susceptibility of the tissue to hypoxia
* Potential outcomes of vascular blockage include:
** Infarct, and
** Necrosis of tissue following obstruction of its blood supply.
* Causes include:
** Thrombosis
*** Uncommon in animals but may be seen with DIC or sepsis.
** Embolism. e.g.
*** Bone marrow emboli following trauma or fractures in dogs
*** Fibrocartilaginous embolic myelopathy
** Vasculitis, e.g.
*** Hog cholera (pestivirus)
*** Malignant catarrhal fever (herpesvirus)
*** Oedema disease (angiopathy caused by E.coli toxin)

===Malacia===

* Malacia may be used:
** As a gross term, meaning "softening"
** As a microscopic term, meaning "necrosis"
* Malacia occurs in:
** Infarcted tissue
** Vascular injury, for example vasculitis.
** Reduced blood flow or hypoxia, e.g.
*** Carbon monoxide poisoning, which alters hemoglobin function
*** Cyanide poisoning, which inhibits tissue respiration

==Excitotoxicity==

* The term "excitotoxicity" is used to describe the process by which neurons are damaged by glutamate and other similar substances.
* Excitotoxicity results from the overactivation of excitatory receptor activation.

===The Mechanism of Excitotoxicity===

* '''Glutamate''' is the major excitatory transmitter in the brain and spinal cord.
** There are four classes of postsynaptic glutamate receptors for glutamate.
*** The receptors are either:
**** Directly or indirectly associated with gated ion channels, '''OR'''
**** Activators of second messenger systems that result in release of calcium from intracellular stores.
*** The receptors are named according to their phamacological agonists:
**** '''NMDA receptor'''
***** The NMDA receptor is directly linked to a gated ion channel.
***** The ion channel is permeable to Ca++, as well as Na+ and K+.
***** The channel is also voltage dependent.
****** It is blocked in the resting state by extracellular Mg++, which is removed when membrane is depolarised.
***** I.e. both glutamate and depolarisation are needed to open the channel.
**** '''AMPA receptor'''
***** The AMPA receptor is directly linked to a gated ion channel.
***** The channel is permeable to Na+ and K+ but NOT to divalent cations.
***** The receptor binds the glutamate agonist, AMPA, but is not affected by NMDA.
***** The receptor probably underlies fast excitatory transmission at glutamatergic synapses.
**** '''Kainate receptor'''
***** Kainate receptors work in the same way as AMPA receptors, and also contribute to fast excitatory transmission.
**** '''mGluR''', the '''metabotropic receptor'''
***** Metabotropic receptors are indirectly linked to a channel permeable to Na+ and K+.
***** They also activate a phoshoinositide-linked second messenger system, leading to mobilisation of intra-cellular Ca++ stores.
***** The physiological role ot mGluR is not understood.

* Under normal circumstances, a series of glutamate transporters rapidly clear glutamate from the extracellular space.
** Some of these transporters are neuronal; others are found on astrocytes.
* This normal homeostatic mechanism fails under a variety of conditions, such as ischaemia and glucose deprivation.
** This results in a rise in extracellular glutamate, causing activation of the neuronal glutamate receptors.
* Two distinct events of excitiotoxicity arise from glutamate receptor activation:
*# The depolarisation caused mediates an influx of Na+, Cl- and water. This give '''acute neuronal swelling''', which is reversible.
*# There is a '''rise in intracellular Ca++'''.
*#* This is due to:
*#** Excessive direct Ca++ influx via the NMDA receptor-linked channels
*#** Ca++ influx through voltage gated calcium channels following depolarisation of the neuron via non-NDMA receptors
*#** Release of Ca++ from intracellular stores.
*#* The rise in neuronal intracellular Ca2+ serves to:
*#** Uncouple mitochondrial electron transport and activate nitric oxide synthase and phospholipase A, leading to generation of reactive oxygen and nitrogen species which damage the neurone.
*#** Activats a number of enzymes, including phospholipases, endonucleases, and proteases.
*#*** These enzymes go on to damage cell structures such as components of the cytoskeleton, membrane, and DNA.
* Excitotoxicity is, therefore, a cause of acute neuron death.

Bones Developmental - Pathology

2009-08-28T08:19:38Z

Karag7: /* Localised */

{{review}}

{{toplink
|backcolour =CDE472
|linkpage =Musculoskeletal System - Pathology
|linktext =Musculoskeletal System
|maplink = Musculoskeletal System (Content Map) - Pathology
|pagetype =Pathology
|sublink1=Bones - Pathology
|subtext1=BONES
}}
 
==Generalised==
===Proportionate dwarfism===
*Miniature breeds
*Due to growth factor deficit
===Chondrodysplasia===

*Literally means “abnormal cartilage development”
*Defective cartilage growth at the physis
*Usually genetic cause
*Occurs in cattle, dogs, sheep, pigs and cats
*Leads to '''disproportionate dwarfism''' (contrast with miniature breeds)
**Generally, growth is disproportionate because only the growth of bones which form from cartilage models is retarded – growth of other bones is normal (i.e. long bones shorter than normal)

In Dogs:
*'''Localised''' forms occur in dogs (e.g. affecting skulls of Pekingese and Bulldogs or the limbs of Dachshunds and Bassett hounds)
*Occasionally seen in immature Beagles, Poodles, Alaskan Malamutes, Scottish Deerounds and Norwegian Elkhounds

In Cattle:
*'''Dexter cattle'''
**Are heterozygous for incompletely dominant gene
**When homozygous - lethal, producing 'buldog calf'
**Usually aborted prior to seven month of pregnancy
**Also occurs in Holstein, Jerseys and Charolais
**Grossly:
***Limbs and vertebral column are short
***Domed cranium
***Protruding [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]]
***Absent hard palate
***Large umbilical hernia with eventrated abdominal organs
**Histologically:
***Proliferative and hypertrophic zones in the physes are irregularly separated by fibrovascular tissue
***Chondrocytes are not properly arranged
***Irregular ossification and mineralisation

*'''Telemark type'''
**Cattle of Norwegian origin
**Also seen in Jersey cows
**Calves born alive, unable to stand and die soon after birth
**Grossly:
***Domed cranium
***Brachygnatic face
***Protruding [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]]
***Cleft palate
***Short neck and limbs

*'''Brachycephalic 'Snorter' type'''
**Hereford and Aberdeen Angus
**Show nasal dyspnoea and chronic rumenal tympany
**Grossly:
***Short, broad head
***Prominent, laterally displaced eyes
***Short and compressed vertebral column
***Distal long bones shorter than proximal
**Histologically:
**Physes appear normal
**Pallisading chondrocytes fewer in number
**Less hypertrophy

In Sheep:
*'''Ancon type'''
**Short limbs due to premature closure of growth plates
**Now rare
*'''Spider lamb'''
**Hereditary (autosomal recessive) in Suffolk and Hampshire breeds in North America
**Long, thin, angular limbs
**May be born alive or dead, aborted or develop symptoms within a month of birth
**Grossly:
***Fine bones, poor musculature, small heads, scoliosis
**Histologically:
***Abnormal centres of [[Bones - normal#Bone development|endochondral ossification]]
***Nodular cartilage hypertrophy

In Pigs:
*Occurs in Danish Landrace
*Autosomal recesive inheritance
*Dwarfs with short legs, forelegs shorter than hind legs
*Abnormal movement is noticable at weaning
*Sequel is [[Joints Degenerative - Pathology#Degenerative joint disease (DJD)|arthrosis]]

===Osteopetrosis (Marble bone disease)===

*Occurs in sheep, dogs, cattle, horses
*Failure of resorption by osteoclasts -> failure of remodelling of [[Bones - normal#Bone organisation|cancellous bone]]
*Bones become thickened and dense but brittle
*Marrow cavites are full of unresorbed primary spongiosa
*Thickened intramembranous bones of skull -> altered shape of brain
*Associated with severe viral infections, e.g. '''FeLV''', [[Cavity & Gingiva - Pathology#Bovine Viral Diarrhoea / Mucosal disease|BVD]]
*Hereditary in Angus cattle

===Lysosomal storage disease===

*Excess accumulation of metabolites in lysosomes
*Affects mainly nervous system
*Also affects growth of cartilage

===Osteogenesis Imperfecta===

*Cause of fragile bones in humans, very rarely in animals
*Reported in Holstein and Charolais calves
*Poor mineralisation of bones and teeth
*Fractures are often present at birth

===Congenital hyperostosis of pigs===
[[Image:Hyperostosis.jpg|right|thumb|100px|<center>Hyperostosis (Image sourced from Bristol Biomed Image Archive with permission)</center>]]

*Rare, genetic
*Diaphysial dysplasia
*Excessive periosteal intramembranous bone, particularly in long bones
*Grossly:
**Greatly thickened long bones
**Tense, shiny skin, closely adherent to tissues below
*Born dead or die soon after birth

===Retention of elongated primary trabeculae===

*Happens due to impaired osteoclastic activity
*Primary trabeculae do not transform into secondary and tertiary
*Continue to elongate
*Form a dense band beneath growth plate - growth retardation lattice
*Dense spikules apparent on radiographs
*Can be caused by [[Paramyxoviridae#Canine Distemper Virus (CDV)|distemper virus]], [[Flaviviridae|bovine viral diarrhoea virus]]

==Localised==

*'''Hemimelia''' - abscence of one of limb bones
*'''Syndactylia''' - fusion of toes
*'''Polydactylia''' - increased number of digits
*'''Ectrodactylia''' - cleft in paw extending to metacarpus of dogs and cats

===Cervical Vertebral Stenotic Myelopathy (Wobblers)===

*Equine disease
*Narrowing of the vertebral canal due to malalignment or maldevelopment of the vertebrae
*Fast growing male TBs ranging from 8 months to 4 years
*Hind limb ataxia due to cord compression

===Angular limb deformity===

*Lateral deviation of distal portion of limb (valgus)
*Medial deviation of distal portion of limb (varus) - more rare
*Most common in foals
**Carpal joint
**Tarsal joint
**Fetlock joint
*Congenital or acquired
*Due to:
**Malpositioning in utero
**Excessive joint laxity
**[[Thyroid Gland - Pathology#Hypothyroidism|Hypothyroidism]]
**Trauma
**Overnutrition
**Defective endochondral ossification
**Poor conformation
**Disruption of blood supply to one side of bone
**Secondary to [[Bones Developmental - Pathology#Physitis|physitis in horses]]
*Usually resolves spontaneously in one to two weeks of life
*More severe cases exceding compensatory capabilities will persisist
*[[Bones - normal#Bone development|Cartilage development]] is affected

===Fibrous dysplasia===

*See [[Bones Hyperplastic and Neoplastic - Pathology#Fibrous dysplasia|Bones and Cartilage - hyperplastic and neoplastic]]

===Physitis===

*In horses
*Often associated with [[Bones Developmental - Pathology#Angular limb deformity|angular limb deformity]]
*Also called '''epiphysitis''' and '''physeal dysplasia'''
*Problem of [[Bones - normal#Bone development|endochondral ossification]]
*Two age groups
**Weanlings
**Yearlings in early training and two-year-olds
*May cause contracted tendons and flexural deformities
*Factors probably involved in its development:
**Genetically fast growth rate
**Large quantities of imbalanced, high energy feed
**Imbalanced weight-bearing on joints
**Excessive activity
**Growth spurts
*Histologically: (appearance similar to [[Bones Developmental - Pathology#Angular limb deformity|angular limb deformity]])
**Lateral aspect of radius
***Thickened metaphyseal part of physeal cartilage
***-> Delay or disturbance of endochondral ossification
***Compression
**Central part
***No obvious deformity
**Medial aspect
***Tension
***-> Transverse [[Bones Fractures - Pathology|fractures]] and repair
**Laxity of periarticular attachements in young foals allows [[Bones Developmental - Pathology#Angular limb deformity|angular limb deformity]]; not occuring in older foals and young horses
**(Sustained trauma produces similar lesions)

[http://www.omafra.gov.on.ca/english/livestock/horses/facts/info_congenital.htm#musculoskeletal Developmental abnormalities]

Breathing Systems

2009-08-27T15:46:01Z

Karag7: /* Magill */

{{unfinished}}
==Introduction==
Breathing systems are the connecting component between the anaesthetic machine and patient. Their role is to deliver oxygen and anaesthetic agent to the patient from the machine, remove exhaled carbon dioxide and provided a means of ventilation via pressure on the reservoir bag.

Basic components of a breathing system are -
*''Breathing tubes'' - Deliver gases to patient and allow for flexibility.
*''Reservoir bag'' - Allows for gas accumulation during exhalation and can be used to assist breathing.
*''Carbon dioxide absorbent'' - To absorb carbon dioxide from the circuit to allow complete rebreathing.
*''One way valve'' - Ensures gases flowing towards the patient do not mix with those exhaled i.e. make a one way system within circuit.
*''Pressure relief valve'' - Limit pressure build up and allows for removal of waste gases.
*''Fresh gas inlet'' - Connects the circuit to the gas outlet on the anaesthetic machine.

==Classification==
Breathing systems have been classified in a number of different ways, including open and closed, but current classification is -

*'''''Non-rebreathing''''' - The patient breathes from the anaesthetic machine and then exhaled into the atmosphere.
*'''''Rebreathing''''' - The patient rebreathes exhaled gases, but a carbon dioxide absorbant is present to remove any waste gases.

===Non Rebreathing Systems===
====''T-piece''====
*Used on patients less than 10kg.
*Circuit factor - 2-3x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Low resistance so suitable for small patients.
**Can use Intermitent Positive Pressure Ventilation (IPPV).
*'''Disadvantages'''
**Cold dry gases delivered to patients.
**Uneconomical on larger patients.

====''Bain''====
*Either parallel or co-axial circuits.
*Used on patients between 10-20kg.
*Circuit factor - 2-3 x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Can use IPPV.
**In a co-axial circuit the fresh gases are warmed by the exhaled gases surround the tubing.
*'''Disadvantages'''
**Uneconomical as high fresh gas flows required.

====''Magill''====
*Used on patients between 10-35kg
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Ecomonical on gas compared to T-piece and Bain.
**Low resistance
*'''Disadvantages'''
**Cannot use for IPPV.
**Reservoir bag near patient making positioning difficult.

====''Lack''====
*Also parallel and mini circuits available.
*Used on patients between 10-35kg (Mini lack used on patients less than 10kg)
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Economical due to lower flow rates
**Rebreathe some warm and moist gas from anatomical dead space.
*'''Disadvantages'''
**Cannot use for IPPV.

===Rebreathing Systems===
====''Circle''====
*Also mini circle circuit available.
*Used on patients over 10kg.
*Minimum gas flow = 10ml/kg.
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
**Very economical on gas.
**Can use IPPV
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.

====''To-and-Fro''====
*Not commonly used due to disadvantages.
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.
**Increased dead space as carbon dioxide absorbant used.

==Checking Breathing System for Use==
#Check that system has been assembled correctly and that all components are present.
#Check for any obvious holes, obstructions etc within the tubing - If any found the replace affected part.
#Securely attached the system to the common gas outlet on the anaesthetic machine.
#Close the pressure relief valve.
#Turn on the oxygen and fill the circuit by occluding the end which would usually attach to the patient using thumb, and use oxygen flush to fill if necessary.
#Listen for leaks and gently squeeze reservoir bag to check that pressure is maintained indicating no leaks.
#Open the pressure relief valve to ensure pressure relieved.
#Ensure inspiratory and expiratory valves move freely on a circle circuit by squeezing reservoir bag and releasing thumb off the end of the circuit.

Breathing Systems

2009-08-27T15:16:05Z

Karag7: /* Bain */

{{unfinished}}
==Introduction==
Breathing systems are the connecting component between the anaesthetic machine and patient. Their role is to deliver oxygen and anaesthetic agent to the patient from the machine, remove exhaled carbon dioxide and provided a means of ventilation via pressure on the reservoir bag.

Basic components of a breathing system are -
*''Breathing tubes'' - Deliver gases to patient and allow for flexibility.
*''Reservoir bag'' - Allows for gas accumulation during exhalation and can be used to assist breathing.
*''Carbon dioxide absorbent'' - To absorb carbon dioxide from the circuit to allow complete rebreathing.
*''One way valve'' - Ensures gases flowing towards the patient do not mix with those exhaled i.e. make a one way system within circuit.
*''Pressure relief valve'' - Limit pressure build up and allows for removal of waste gases.
*''Fresh gas inlet'' - Connects the circuit to the gas outlet on the anaesthetic machine.

==Classification==
Breathing systems have been classified in a number of different ways, including open and closed, but current classification is -

*'''''Non-rebreathing''''' - The patient breathes from the anaesthetic machine and then exhaled into the atmosphere.
*'''''Rebreathing''''' - The patient rebreathes exhaled gases, but a carbon dioxide absorbant is present to remove any waste gases.

===Non Rebreathing Systems===
====''T-piece''====
*Used on patients less than 10kg.
*Circuit factor - 2-3x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Low resistance so suitable for small patients.
**Can use Intermitent Positive Pressure Ventilation (IPPV).
*'''Disadvantages'''
**Cold dry gases delivered to patients.
**Uneconomical on larger patients.

====''Bain''====
*Either parallel or co-axial circuits.
*Used on patients between 10-20kg.
*Circuit factor - 2-3 x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Can use IPPV.
**In a co-axial circuit the fresh gases are warmed by the exhaled gases surround the tubing.
*'''Disadvantages'''
**Uneconomical as high fresh gas flows required.

====''Magill''====
*Used on patients between 10-25kg
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Ecomonical on gas compared to T-piece and Bain.
**Low resistance
*'''Disadvantages'''
**Cannot use for IPPV.
**Reservoir bag near patient making positioning difficult.

====''Lack''====
*Also parallel and mini circuits available.
*Used on patients between 10-35kg (Mini lack used on patients less than 10kg)
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Economical due to lower flow rates
**Rebreathe some warm and moist gas from anatomical dead space.
*'''Disadvantages'''
**Cannot use for IPPV.

===Rebreathing Systems===
====''Circle''====
*Also mini circle circuit available.
*Used on patients over 10kg.
*Minimum gas flow = 10ml/kg.
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
**Very economical on gas.
**Can use IPPV
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.

====''To-and-Fro''====
*Not commonly used due to disadvantages.
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.
**Increased dead space as carbon dioxide absorbant used.

==Checking Breathing System for Use==
#Check that system has been assembled correctly and that all components are present.
#Check for any obvious holes, obstructions etc within the tubing - If any found the replace affected part.
#Securely attached the system to the common gas outlet on the anaesthetic machine.
#Close the pressure relief valve.
#Turn on the oxygen and fill the circuit by occluding the end which would usually attach to the patient using thumb, and use oxygen flush to fill if necessary.
#Listen for leaks and gently squeeze reservoir bag to check that pressure is maintained indicating no leaks.
#Open the pressure relief valve to ensure pressure relieved.
#Ensure inspiratory and expiratory valves move freely on a circle circuit by squeezing reservoir bag and releasing thumb off the end of the circuit.

Breathing Systems

2009-08-27T10:58:02Z

Karag7: /* Introduction */

{{unfinished}}
==Introduction==
Breathing systems are the connecting component between the anaesthetic machine and patient. Their role is to deliver oxygen and anaesthetic agent to the patient from the machine, remove exhaled carbon dioxide and provided a means of ventilation via pressure on the reservoir bag.

Basic components of a breathing system are -
*''Breathing tubes'' - Deliver gases to patient and allow for flexibility.
*''Reservoir bag'' - Allows for gas accumulation during exhalation and can be used to assist breathing.
*''Carbon dioxide absorbent'' - To absorb carbon dioxide from the circuit to allow complete rebreathing.
*''One way valve'' - Ensures gases flowing towards the patient do not mix with those exhaled i.e. make a one way system within circuit.
*''Pressure relief valve'' - Limit pressure build up and allows for removal of waste gases.
*''Fresh gas inlet'' - Connects the circuit to the gas outlet on the anaesthetic machine.

==Classification==
Breathing systems have been classified in a number of different ways, including open and closed, but current classification is -

*'''''Non-rebreathing''''' - The patient breathes from the anaesthetic machine and then exhaled into the atmosphere.
*'''''Rebreathing''''' - The patient rebreathes exhaled gases, but a carbon dioxide absorbant is present to remove any waste gases.

===Non Rebreathing Systems===
====''T-piece''====
*Used on patients less than 10kg.
*Circuit factor - 2-3x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Low resistance so suitable for small patients.
**Can use Intermitent Positive Pressure Ventilation (IPPV).
*'''Disadvantages'''
**Cold dry gases delivered to patients.
**Uneconomical on larger patients.

====''Bain''====
*Either parallel or co-axial circuits.
*Used on patients between 10-20kg.
*Circuit factor - 1-2x Minute Volume.
*Reservoir bag on expiratory limb.
*'''Advantages'''
**Can use IPPV.
**In a co-axial circuit the fresh gases are warmed by the exhaled gases surround the tubing.
*'''Disadvantages'''
**Uneconomical as high fresh gas flows required.

====''Magill''====
*Used on patients between 10-25kg
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Ecomonical on gas compared to T-piece and Bain.
**Low resistance
*'''Disadvantages'''
**Cannot use for IPPV.
**Reservoir bag near patient making positioning difficult.

====''Lack''====
*Also parallel and mini circuits available.
*Used on patients between 10-35kg (Mini lack used on patients less than 10kg)
*Circuit factor - 1-1.5x Minute Volume.
*Reservoir bag on inspiratory limb.
*'''Advantages'''
**Economical due to lower flow rates
**Rebreathe some warm and moist gas from anatomical dead space.
*'''Disadvantages'''
**Cannot use for IPPV.

===Rebreathing Systems===
====''Circle''====
*Also mini circle circuit available.
*Used on patients over 10kg.
*Minimum gas flow = 10ml/kg.
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
**Very economical on gas.
**Can use IPPV
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.

====''To-and-Fro''====
*Not commonly used due to disadvantages.
*'''Advantages'''
**Patient breathes warm humidified air due to rebreathing.
*'''Disadvantages'''
**Amount of inhalant gas the patient is receiving is not known.
**Risk of anoxia if system closed.
**Increased dead space as carbon dioxide absorbant used.

==Checking Breathing System for Use==
#Check that system has been assembled correctly and that all components are present.
#Check for any obvious holes, obstructions etc within the tubing - If any found the replace affected part.
#Securely attached the system to the common gas outlet on the anaesthetic machine.
#Close the pressure relief valve.
#Turn on the oxygen and fill the circuit by occluding the end which would usually attach to the patient using thumb, and use oxygen flush to fill if necessary.
#Listen for leaks and gently squeeze reservoir bag to check that pressure is maintained indicating no leaks.
#Open the pressure relief valve to ensure pressure relieved.
#Ensure inspiratory and expiratory valves move freely on a circle circuit by squeezing reservoir bag and releasing thumb off the end of the circuit.