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==An Introduction to General Pathology==
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#REDIRECT[[:Category:General Pathology]]
 
 
* The term '''pathology''' is derived from:
 
** '''Pathos''', or suffering
 
** '''Logos''', or reasoning/logic.
 
* Pathology is defined as the study of disease including:
 
** '''Aetiology''' - causal factor(s)
 
** '''Pathogenesis''' - the development of the disease within the body.
 
** '''Lesions''' - the observable structural changes in the tissues and fluids of the body.
 
** '''Pathophysiology''' - the functional changes in diseased tissues.
 
** '''Sequel''' - the consequences of the disease in the body.
 
** '''Remote effects''' - the effect of disease in one tissue on other tissues in the body.
 
 
 
===Lesions===
 
 
 
* Lesions are the abnormalities or changes seen in living tissues due to disease.
 
* Observed in
 
** The live animal
 
** Tissues surgically removed from the live animal
 
*** Biopsy/ excision
 
** Animals soon after death
 
*** Necropsy, post-mortem examination.
 
 
 
====Decription of Lesions====
 
 
 
* Descriptions of lesions is very important
 
* Whole organs, tissues or individual lesions are described under headings such as
 
*# Size
 
*# Shape
 
*# Colour
 
*# Weight
 
*#* Generally in relation to body weight
 
*# Texture and Consistency
 
*# Appearance of the cut surface
 
*# Contents of hollow organs
 
*# Position, relationships and effects on adjacent tissues
 
 
 
===Disease===
 
 
 
====Definition and Type====
 
 
 
* '''Disease''' is  a definite morbid (illness producing) process, having a characteristic train of symptoms or signs.
 
** May affect the whole body or any of its parts.
 
** The disease's aetiology, pathology and prognosis may be known or unknown.
 
* There are two main categories of disease.
 
*# '''Acute'''
 
*#* Characterised by sudden onset and short duration.
 
*#* The outcome of acute disease may be:
 
*#** Death
 
*#** Resolution due to host defence response or clinical therapy
 
*#** Progression to chronic disease
 
*# '''Chronic'''
 
*#* Characterised by insidious onset and protracted course.
 
*#* The outcome of chronic disease may be:
 
*#** Progressive destruction of tissue
 
*#*** Compromises funtion and  endangers life,
 
*#** The halting of the course of disease, with tissue repair by scarring.
 
 
 
====Factors Involved in the Development of Disease====
 
 
 
* There are three factors which conspire with each other to produce disease.
 
*# '''The individual animal'''.
 
*#* In particular, the animal's nutritional and immune status
 
*#** This is modified by:
 
*#*** Recent or concurrent disease
 
*#*** Previous exposure to the agent(s) responsible
 
*# '''The disease-causing agent(s)'''.
 
*#* Most do not cause a uniform pattern of disease
 
*#** Host defences are important in determining the presentation of the disease.
 
*#* An agent's capacity to produce disease depends upon:
 
*#** The dose
 
*#** The virulence of the agent
 
*#* Several agents may be involved.
 
*#** Usually one agent debilitates, allowing others to exert a greater effect within the body
 
*#* The presence of an agent does not necessarily mean it is the cause of the disease!
 
*#* A pathogenic agent may be absent from the tissues, due to:
 
*#** Clinical therapy
 
*#** Host defence systems
 
*# '''Environment''', for example:
 
*#* Overcrowding of animals
 
*#* Mixing animals from differing origins
 
*#** Carriers are allowed to infect susceptible animals.
 
*#*** Carriers are animals which harbour the pathogenic agent but do not show signs of disease.
 
*#* Changes in management routine
 
 
 
====Types of Agents Causing Disease====
 
 
 
# '''Infectious organisms'''
 
#* [[Viruses|Viruses]]
 
#* [[Bacteria|Bacteria]]
 
#* [[Fungi|Fungi]]
 
#* [[Parasites|Parasites]]
 
# '''Physical'''
 
#* Trauma
 
#* Pressure
 
#* Heat
 
#* Cold
 
#* Radiation
 
# '''Chemical'''
 
#* Toxic organic and inorganic substances
 
#* Toxins produced by infectious organisms
 
# '''Nutritional'''
 
#* Deficiencies of vitamins and trace elements
 
#* Excess vitamins and trace elements
 
# '''Genetic defects'''
 
#* There is a very wide range of potential defects.
 
#** Some are incompatible with life
 
#** Others affect specific systems within the body
 
 
 
====Aspects of Disease====
 
 
 
* There are many aspects of a disease that must be considered in order to understand it in full.
 
*# '''Incidence'''
 
*#* How much of the disease is present?
 
*#* Where is the disease found?
 
*#* In what species is the disease seen?
 
*# '''Aetiology'''
 
*#* Causal agent(s)
 
*#* Predisposing factors
 
*# '''Transmission'''
 
*#* How is the disease spread between individuals?
 
*#* Is the disease zoonotic?
 
*# '''Pathogenesis'''
 
*#* How the causal agent(s) exert their effect within the body.
 
*# '''Diagnosis'''
 
*#* History
 
*#* Clinical findings
 
*#** Clinical examination
 
*#** Clinical pathology
 
*#* Biopsy or post-mortem examination
 
*# '''Prognosis and Treatment'''
 
*# '''Control and Prevention'''
 
*#* The ideal situation
 
 
 
====Post-Mortem Examination====
 
 
 
* Post-mortem examination (PME) investigates the observable structural changes in the animal.
 
* Information relating to the disease withing the body or specific tissue is gained from PME.
 
** This includes information on the disease's
 
*** Aetiology (cause).
 
*** Pathogenesis (development).
 
* Several types of changes are encountered at post-mortem examination.
 
*# Those due to the '''disease'''
 
*#* Lesions
 
*# Those occuring '''immediately prior to death'''
 
*#* Agonal
 
*# Those occuring '''after death'''
 
*#* Post-mortem
 
 
 
====Techniques Involved in Pathological Examination====
 
 
 
* '''Fluid examination'''
 
** E.g. blood, urine, discharges from orifices and so on.
 
* '''Cytology'''
 
** Examination of cells in smears, aspirates and fluids.
 
* '''Necropsy'''
 
** Visual examination of the gross changes in the dead body.
 
* '''Histopathology'''
 
** Microscopic examination of:
 
*** Tissues selected from the dead body after necropsy.
 
*** Biopsy/excision materials from lesions in the living animal.
 
* '''Histochemistry'''
 
** Microscopic visualisation of enzymatic activity in tissues.
 
* '''Immunological methods'''
 
** Specific antibody activity can be detected in tissues and fluids.
 
*** Examination of serum can show prior exposure to a particular infectious agent (i.e. specifice antibodies).
 
** Specific antigens can be detected in tissues.
 
*** When linked to a marking agent (e.g. a fluorescent dye), an antibody can localise its antigen in the tissue.
 
* '''Electronmicroscopy'''
 
** Electronmicrosopcy shows fine detail of the surfaces or internal structures of cells.
 
* '''Bacteriology/ Virology/ Parasitology'''
 
** These techniques allow the isolation and identification of pathogenic bacteria, viruses and parasites.
 
* '''Toxicology'''
 
** Analysis of tissues for particular poisons and toxins.
 
 
 
==General Pathology - Contents==
 
 
 
==Degenerations and Infiltrations==
 
 
 
*  Degenerations and infiltrations are the morphological manifestation of an altered metabolism within the cell.
 
** A particular kind of change within a cell or tissue may suggest that a specific type of alteration has occurred.
 
* Degenerations and infiltrations are types of structural changes.
 
** These are best considered at a cellular level.
 
** These structural changes are deviations from the cell's normal structure and function.
 
*** Parameters are outside the normal physiological range for the cell.
 
* '''Degeneration'''
 
** The tissue cell shows some change in itself.
 
* '''Infiltration'''
 
** Something accumulates in the cell or tissue.
 
 
 
===Cellular Swelling===
 
 
 
* Cellular swelling is
 
** The earliest detectable degenerative change.
 
** The mildest from of cellular degeneration.
 
** The first stage in injury to a cell.
 
** Caused by a variety of insults, e.g.
 
*** Lack of oxygen (anoxia) to a tissue.
 
*** Toxic influences.
 
* Is due to the impairment of the integrity of the cell membrane.
 
* Cellular swelling is characterised by a moderate swelling of the individual cells.
 
** Due to an influx of water into the cell.
 
 
 
====Gross Appearance====
 
 
 
* Organs diffusely affected with cloudy swelling grossly appear pale.
 
** This may be partly due to the swollen cells impeding the tissue's blood supply.
 
* Without cutting into an organ, it may be difficult to appreciate a gross enlargement of it.
 
** Each individual cell is increased in size, meaning the entire volume of the organ is also increased.
 
** E.g. on cutting the liver or kidney capsule, the underlying swollen parenchyma bulges outwards, making the cut ends of the capsule retract.
 
* The degree of gross swelling is not great.
 
** Could be easily confused with early post-mortem changes in the organ.
 
 
 
====Histological Appearance====
 
 
 
* Individual cells appear somewhat swollen.
 
* The cytoplasm appears more red in colour in hematoxylin and eosin (H&E) stained sections.
 
* The nucleus of the cell remains normal.
 
* Cellular swelling is best histologically appreciated in the liver and kidney in damage caused by circulating toxins that are not powerful enough to actually kill the cells.
 
 
 
====Significance of Cellular Swelling====
 
 
 
* Cellular swelling is an important stage in degeneration.
 
** Not commonly observed on its own without more serious changes
 
*** Not easy to identify at post-mortem unless the examination os perfomred very soon after the animal's death.
 
**** Early post-mortem (autolytic) change in dead tissue looks rather similar.
 
*** Cellular swelling is also reversible.
 
**** When the toxin is no longer exerting its effect, the tissue returns to normal.
 
*** Cellular swelling may be a transient stage in the more serious forms of degenerations which follow.
 
 
 
===Hydropic Degeneration===
 
 
 
* Hydropic degeneration often indicates severe cellular damage due to viruses.
 
** Is a more severe or advanced form of cellular swelling.
 
* There are two types of hydropic degeneration, in which:
 
*# The cells may swell up like a balloon prior to their destruction.
 
*#* '''Balloning Degeneration'''
 
*# There is a discrete bleb (vacuole) of fluid within the cytoplasm.
 
*#* '''Vacuolar Degeneration'''
 
 
 
====Ballooning Degeneration====
 
 
 
* May occur in a variety of conditions.
 
** Is particularly seen in viral conditions of epithelial tissue.
 
* [[Oral Cavity - Cavity & Gingiva#Foot and Mouth disease|Foot and Mouth Disease]] is the best example.
 
** Foot and Mouth virus attacks the stratum spinosum of the epithelium of the tongue and feet.
 
** Affected cells balloon up with water containing the replicating virus, swelling until they burst.
 
*** The fluid contained in the cells then forms microvesicles (blisters) in the stratum spinosum.
 
**** Blisters may later burst, shedding vast quantities of the virus.
 
** On bursting, the edges of the erosions look ragged.
 
*** Within weeks, the germinal epithelium at the base of the erosion regenerates the epithelium, leaving no trace of a scar.
 
 
 
====Vacuolar Degeneration====
 
 
 
* In vacuolar degeneration, excess water is transferred to the endoplasmic reticulum (ER).
 
* The ER  swells and eventually fragments.
 
** A fluid vacuole remains in the cytoplasm.
 
* Commonly occurs in cells that are very metabolically active and have well developed pumping mechanisms.
 
** E.g. as the hepatocyte, renal tubular epithelium and pancreatic acinar cell.
 
 
 
===Cellular Fatty Change===
 
 
 
* DOES NOT REFER TO THE THE FAT STORES OF THE BODY!
 
** Fatty substances accumulate or increase within the cytoplams of specific cells.
 
** In some instances, the fat stores may be involved in the transfer of fat to these specific cells.
 
* Cellular fatty change is an important intracellular abnormality.
 
** Principally concerns the intracellular fat in hepatocytes.
 
* Fatty change is commonly seen in three organs of the body.
 
** Prinicpally in the '''liver'''.
 
** Also in the '''kidney''' and the '''heart'''.
 
** This is  because these organs are either:
 
*** Involved in the metabolism of fat, or
 
*** Dependant upon lipids as an energy source.
 
* Fatty change can be readily recognised at post-mortem.
 
 
 
==== Gross Appearance of Fatty Change====
 
 
 
* '''Liver'''
 
** This is the main organ involved in fatty change.
 
** May be greatly increased in size.
 
** Is tan to yellowish in colour.
 
*** Is normally reddish brown.
 
** Very prone to rupture with slight pressure (friable).
 
** Parenchyma bulges outwards on being freed from the constraint of the capsule when cut.
 
** Parenchyma is dull, yellowish and greasy.
 
* '''Kidney'''
 
** The cortex appears paler.
 
***N.B. This is normal in e.g. the cat!
 
*** Diffuse paleness is not the prominent feature, unlike in the liver.
 
* '''Heart'''
 
** Anoxia, as a result of anaemia, causes fatty change.
 
** The heart is flabby.
 
** Fatty change may occur as streaks in the papillary muscles.
 
*** I.e. those muscles furthest away from the blood supply.
 
** Contractile ability is reduced, and blood is therefore not umped efficiently.
 
 
 
====Histological Appearance of Fatty Change====
 
 
 
* The fat either appears as globules or is contained in varying sizes of vacuoles in the cytoplasm.
 
** In the heart, fat appears as groups of tiny vacuoles dispersed along the myofibrils.
 
** In the liver and kidney, vacuoles tend to coalesce to form larger ones.
 
*** One or more large globules may fill the cytoplasm.
 
**** The nucleus is displaced to the periphery of the cell.
 
* The nucleus remains normal.
 
** Nuclear changes are only seen if the degree of fatty change becomes incompatible with the continued existence of the cell.
 
* In hepatocytes, it is necessary to stain for fat in order to ellucidate if a vacuole in the cytoplasm is fat-containing.
 
** Two further conditions may produce vacuoles in hepatocytes.
 
*** [[General Pathology#Vacuolar Degeneration|Vacuolar hydropic degeneration]]
 
*** Glycogen accumulation
 
** Stains commonly used include Sudan 111, Sudan 1V, and Oil Red O.
 
*** Stain fat varying shades of orange to red.
 
** Sections must be prepared differently to the routine paraffin embedding (used e.g. in H&E staining).
 
*** The strong solvents used in paraffin embedding dissolve the fat out of the cell.
 
*** When staining for fat,  the tissue to be examined is frozen and sectioned in a cryostat before being stained.
 
**** These sections are more than twice as thick as those attained by sectioning paraffin blocks
 
***** There may be some overlap of cells on the section.
 
***** Individual cells are less clear.
 
 
 
====Causes of Fatty Change====
 
 
 
=====Dietary and Metabolic=====
 
 
 
# '''Starvation'''
 
#*  A reduction in dietary intake neccessitates the increased mobilisation of fat from body fat stores to meet energy needs.
 
#* Fat from stores is transported in the blood as fatty acids.
 
#** The liver cannot cope with them all properly.
 
#*** The fatty acids are stored in the liver as neutral fats.
 
# '''Overeating'''
 
#* When the dietary intake is greater than the energy expenditure, the fat is temporarily stored prior to movement to the body fat stores.
 
#** Also occurs in fat-rich diets.
 
# '''Lipotrope Derangement'''
 
#* Lipotropes are substances which hasten the removal of fat from the liver cells.
 
#* Lipotropes include the amino acids that allow conjugation of fat with proteins to form the lipoprotein that is excreted from cells.
 
#** E.g. choline, methionine.
 
#** Dietary deficiency of these leads to fatty change within the cells.
 
#* Some poisons also prevent stages of lipoprotein formation.
 
#** E.g. CCl4, phosphorus and alcohol
 
 
 
=====Metabolic diseases=====
 
 
 
* Certain metabolic diseases may result in deranged carbohydrate metabolism.
 
* Glucose is not made available for uptake into the tissues.
 
** The celles still require energy, and so alternative pathways are resorted to.
 
*** This leads to fatty change.
 
* Examples:
 
** Diabetes mellitus in dogs
 
*** Deficiency of the hormone insulin required for cellular glucose utilisation.
 
** Ketosis in ruminants
 
*** The body is exhorted to find another source of energy following drainage of the glucose reserves.
 
**** Fat reserves are mobilised and transported to the liver.
 
*** E.g.
 
**** Twin lambs in sheep
 
***** The condition is known as Pregnancy Toxaemia
 
**** Milk producion in high-yielding dairy cattle shortly afer parturiton.
 
***** Acetonemia
 
 
 
=====Anoxia=====
 
 
 
* Any condition that reduces the oxygen supply to the tissues will cause fatty change in the
 
liver.
 
* Examples:
 
** Anaemia
 
*** Reduced numbers of red blood cells circulating in the blood
 
*** Caused by sustained loss of erythrocytes from the vessels by
 
**** Chronic haemorrhage
 
**** Excessive destruction of erythrocytes (haemolysis).
 
** Circulatory disorders
 
*** Ischaemia
 
**** Reduced blood supply to a tissue
 
*** Chronic venous congestion
 
**** Slowing of blood flow through the vasculature e.g. due to a failing heart.
 
 
 
=====Toxins=====
 
 
 
* Many toxins will cause fatty change in the liver.
 
** In these cases fatty change may be considered to be a more severe form of [[General Pathology#Cellular Swelling|cellular swelling]].
 
* Examples:
 
** Bacterial and fungal toxins
 
*** May be:
 
**** Produced in the bloodstream by circulating bacteria (septicaemia/bacteraemia)
 
**** Produced elsewhere and absorbed into the bloodstream.
 
** Chemical toxins
 
*** For example, CCl4, phosphorus, arsenic and lead.
 
** Plant toxins
 
*** Some plant toxins will cause fatty change in the very early stages of poisoning.
 
 
 
====Distribution of Fatty Change in the Liver====
 
 
 
* Fatty change in the liver tends to be throughout the whole lobule.
 
* Occasionally there is a preferential localiasation -  this may give some clue as to the inciting cause.
 
** E.g. in chronic venous congestion
 
*** Due to a failing heart (a cause of anoxia).
 
*** Blood pools in the centrilobular area (due to ineffective blood flow back to the heart), as well as fatty change being induced.
 
**** Gives a striking gross appearance - areas of yellow interspersed with red.
 
***** Described as a 'nutmeg liver'.
 
*** When found post-mortem examination, indicated the heart should be examined for the cause.
 
 
 
====Significance of fatty change====
 
 
 
* Fatty change is '''reversible''', provided that the underlying cause is brought under control.
 
* '''Necrosis'''
 
** From the distribution of fat in a cell, it may be difficult to decide whether the fatty change is due to a toxic or metabolic defect.
 
*** In toxic effects, the fatty change can be considered as a more serious form of cellular swelling.
 
**** There may be evidence of necrosis.
 
*** If a metabolic defect is prolonged, cellular function may be impaired by the substantial amount of fat.
 
**** Necrosis may also result in this instance.
 
* '''Wallerian Degeneration'''
 
** A special form of fatty change in the nervous system.
 
** Damage to myelinated nerves results in the degeneration of the myelin that ensheaths them.
 
* '''Extracellular accumulation of lipids'''
 
** Necrosis of cells containing lipid may release lipid into the extracellular space. 
 
*** Haemorrhage or tissue damage may result in cholesterol being released from cells or pooled from lipoproteins in crystalline form (cholesterol clefts).
 
 
 
===Mucoid Degeneration===
 
 
 
* Mucoid degeneration is also known as mucinous or myomatous degeneration.
 
* Mucoid degeneration involves chanages in epithelial tissue or the extracellular matrix/ ground substance.
 
* An extracellular phenomenon of some specific cells.
 
** Tend to show a bluish tinge in H&E stained sections.
 
 
 
====Epithelium====
 
 
 
* The specific cells involved in mucoid degeneration in the eptihelium are:
 
** The goblet cells of wet mucous membranes.
 
** The mucous glands themselves.
 
* This is not really a degeneration, but an increased production of mucin.
 
** It is a beneficial reaction; the product
 
*** Is important as a lubricant.
 
*** Soothes inflamed surfaces.
 
*** Traps and dilutes harmful agents.
 
*** Carried specific antibodues against infectious agents.
 
*** Provides a means for removal of infectious agents.
 
 
 
====Connective tissue====
 
 
 
* Here, the mucin forms part of the ground substance between the fibroblasts that produce it.
 
* A disturbance in the metabolism of the fibroblasts under some circumstances,means the ground substance takes on a bluish hue in H&E sections.
 
* Mucoid degenration in the heart valves of middle-aged and older dogs is a common example.
 
** Causes '''endocardiosis'''.
 
*** A condition specific to the dog.
 
 
 
====Endocardiosis====
 
 
 
* Tends to affects middle-aged and older dogs.
 
* Primarily occurs in the mitral valve.
 
* Results in slowly developing heart failure
 
* The valves become swollen and misshapen
 
** The heart cannot pump blood effectively to the circulation from the left ventricle.
 
*** Blood passes back into the left atrium, compromising the filling from the pulmonary vein.
 
**** Leads to back pressure on the pulmonary capillaries.
 
***** Oedema forms in the lungs, and can be heard as moist sounds on ausculatation.
 
***** Reduces the oxygenation of blood leading to exercise intolerance.
 
*** Failure of the left side eventually compromises the function of the right side.
 
**** There is pooling of blood in the venous system i.e. in the liver.
 
 
 
===Hyaline Degeneration===
 
 
 
* The term "hyaline degeneration" is applied to several types of degeneration or infiltration.
 
** "Hyaline" is a descriptive term meaning "glassy".
 
*** Used in pathology when structureless material appears in section, and stains red with eosin
 
**** Describes a variety of conditions in which structureless materials are present.
 
* Is applied to both extra-  and intra-cellular degenrations/ infiltrations.
 
** '''Extracellular'''
 
*** Protein hyaline casts in the renal tubules.
 
**** From excessive protein passing through glomerulus.
 
**** When fresh urine is examined under the microscope, casts may be seen as elongated glassy tubes.
 
***  Hyaline membranes
 
**** Proteinaceous effusions into pulmonary alveoli
 
**** Prevent gaseous exchange.
 
** '''Intracellular'''
 
*** Hyaline degeneration of skeletal muscle.
 
**** In vitamin E/ selenium deficiency.
 
* There are two forms of hyaline degeneration that deserve their own mention.
 
** Fibrinoid degeneration.
 
** Amyloid infiltration.
 
 
 
====Fibrinoid Degeneration====
 
 
 
* Fibrinoid degeneration features a material which is fibrin-like.
 
* Is essentially a focal death of cells in the walls of small blood vessels (usually arterioles).
 
** Parts of the vessel wall become replaced by a granular material.
 
*** Pinkish-red (i.e. eosin-staining).
 
*** Has some of the appearance and staining properties of fibrin.
 
*** Consists partly of degenerated muscle and elastic fibres, and partly of an increased amount of protein ground substance around the degenerated fibres.
 
*** Looks like a red smudge in the vessel wall when viewed histologically.
 
* The presence of the fibrin-like material may suggest
 
** A local hypersensitivity reaction
 
** Hypertension
 
 
 
====Amyloidosis====
 
 
 
* Also known as amyloid infiltration
 
* Deposition of a proteinaceous hyaline substance in extracellular sites.
 
** Sites of deposition vary with species.
 
* The kidney is a common site of deposition.
 
** Amyloid is deposited under the capillary endothelium and progressively increases in volume.
 
* There are various categories of amyloid.
 
** Is essentially an abnormal protein produced in the body
 
** In most cases, it is produced in response to sustained antigenic stimulation caused by a chronic suppurative process.
 
*** E.g. a foot abscess, mastitis.
 
* Amyloid is a relatively inert substance.
 
** When it accumulates, it is not easily removed.
 
 
 
===Glycogen Infiltration===
 
 
 
* Glycogen is normally present in substantial amounts in the liver and muscle.
 
** Is a readily utilisable source of energy.
 
* Moderate glycogen infiltration in the liver:
 
** '''Grossly'''  - doesn't have much effect.
 
** '''Histologically''' - shows up as foamy cytoplasmic vacuoles, similar to that of fat.
 
* Some conditions may result in an increase in glycogen deposits.
 
** '''Diabetes mellitus'''
 
*** Gives an increase in hepatic glycogen stores.
 
*** May be overshadowed by the increased fat in the hepatocytes, and therefore difficult to see.
 
**** Renal tubular deposits are more easily observed.
 
** '''Excessive glucocorticoids'''
 
*** Could be due to:
 
**** Hyperadrenocortism
 
**** Animals being maintained on glucocorticoid therapy over a long period of time.
 
***** Has more dramatic effect.
 
*** Huge amounts of glycogen infiltration.
 
**** Liver appears larger and paler.
 
**** Vacuoles may be so extensive that the rest of the cytoplasm appear as pink strands passing from the nucleus to the plasma membrane.
 
***** A "feathery appearance" or "web-like effect".
 
** '''Glycogen storage diseases'''
 
*** Due to an inherited deficiency of an enzyme required for the breakdown of glycogen to glucose.
 
**** Cells continuously accumulate glycogen.
 
*** Seen in all tissues of the body but exerts its major effect in the CNS.
 
* Selective staining must be employed to distinguish glycogen vacuoles from fatty vacuoles in the liver.
 
** Alcohol fixation is preferred. T
 
** Best's Carmine is the commonly used stain.
 
*** Stains the intracellular glycogen red.
 
 
 
===Cellular Inclusions===
 
 
 
==Necrosis==
 
===Causes of Necrosis===
 
===Gross and Histological Features of Necrotic Lesions===
 
====Coagulation Necrosis====
 
====Liquefactive Necrosis====
 
====Caseation Necrosis====
 
===Sequel to Necrosis===
 
====Fat Necrosis====
 
====Gangrene====
 
 
 
==Post Mortem Change==
 
===Types of Post Mortem Change===
 
====Rigor Mortis====
 
 
 
====Post Mortem Clotting of Blood====
 
====Hypostatic Congestion====
 
====Post Mortem Imbibition of Blood====
 
====Inbibition of Bile Pigment====
 
====Gaseous Distenstion of the Alimentary Tract====
 
====Autolysis====
 
====Putrefaction====
 
 
 
==Pigmentation and Calcification==
 
 
 
===Exogenous Pigmentation===
 
====Carbon (Anthracosis)====
 
====Pneumoconiosis====
 
====Carotenoids====
 
 
 
===Endogenous Pigmentation===
 
====Melanin====
 
====Blood Pigments====
 
=====Haemoglobin=====
 
=====Haemosiderin=====
 
=====Haematin=====
 
=====Jaundice=====
 
=====Haematoidin=====
 
=====Porphyria=====
 
====Lipofuscin====
 
 
 
 
 
===Mineralisation===
 
 
 
====Calcification====
 
=====Dystrophic=====
 
=====Metastatic (Hypercalcaemia)=====
 
 
 
==Circulatory Disorders==
 
 
 
===Introduction====
 
 
 
====Venous Congestion and Hyperaemia====
 
 
 
====Oedema====
 
 
 
 
 
====Dehydration====
 
 
 
====Shock====
 
 
 
====Haemorrhage====
 
=====Rhexis=====
 
=====Diapedesis=====
 
 
 
====Haemostasis====
 
 
 
====Thrombus====
 
=====Causes=====
 
=====Evolution=====
 
=====Embolism=====
 
=====Post Mortem Clots=====
 
 
 
====Disseminated Intravascular Coagulation====
 
 
 
==Inflammation==
 
 
 
===Cardinal Signs===
 
 
 
===Causes===
 
 
 
===Acute===
 
====Introduction====
 
====Sequence of Events====
 
====Fluids====
 
=====Serous=====
 
=====Catarrhal=====
 
=====Fibrinous=====
 
=====Diptheritic=====
 
=====Haemorrhagic=====
 
=====Purulent=====
 
=====Functions of Exudate=====
 
=====Sequel to Exudation=====
 
====Cells====
 
=====Neutrophils=====
 
=====Eosinophils=====
 
=====Mast Cells=====
 
=====Basophils=====
 
 
 
===Chronic===
 
====Introduction====
 
====Cells====
 
=====Macrophages=====
 
=====Lymphocytes=====
 
====Types====
 
=====Granulomatous Inflammation=====
 
=====Granulation Tissue=====
 
=====Lymphocytic Inflammation=====
 
 
 
===Changes in Inflammatory Cells Circulating in Blood===
 
====Neutrophilia====
 
====Neutopenia====
 
====Eosinophilia====
 
====Eosinopenia====
 
====Lymphocytosis====
 
====Lymphopenia====
 
====Plasma Cells====
 
====Monocytosis====
 
 
 
===Role of The Lymph Node in Inflammation===
 
 
 
===Healing and Repair===
 
====Introduction====
 
====Repair====
 
=====Regeneration=====
 
=====Replacement=====
 
====In Particular Tissues====
 
=====Skin=====
 
======First Intention======
 
======Second Intention======
 
=====Bones=====
 
=====Respiratory Tract=====
 
=====Alimentary Tract=====
 
=====Urinary Tract=====
 
=====Genital Tract=====
 
=====Central Nervous System=====
 
 
 
==Growth Disorders==
 
 
 
===Congenital===
 
====Causes====
 
====Malformations====
 
=====Cyclops=====
 
=====Bulldog Calf=====
 
=====Cleft Palate=====
 
=====Cystic Kidney=====
 
=====Spina Bifida=====
 
=====Hydrocephalus=====
 
=====Cerebellar Hypoplasia=====
 
=====Skeletal Malformations=====
 
=====Skin Defects=====
 
=====Muscular Defects=====
 
=====Cardiac Defects=====
 
=====Sexual Organ Malformation=====
 
=====Metabolic Diseases=====
 
 
 
===Growth Disorders During Life===
 
====Atrophy====
 
====Hypertrophy====
 
====Hypoplasia====
 
====Hyperplasia====
 
====Metaplasia====
 
====Dysplasia====
 
====Anaplasia====
 
====Neoplasia====
 
=====Benign Tumours=====
 
=====Malignant Tumours=====
 
=====Aetiology of Tumours=====
 
=====Phases of Tumour Growth=====
 
=====Tumour Classification and Nomenclature=====
 

Latest revision as of 12:42, 15 February 2011