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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
 
 
 
*'''See [[General Pathology - Recognition and Description of Lesions|Recognition and Description of Lesions]]'''
 
 
 
===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==
 
 
 
===[[General Pathology - Recognition and Description of Lesions|Recognition and Description of Lesions]]===
 
 
 
===[[General Pathology - Degenerations and Infiltrations|Degenerations and Infiltrations]]===
 
 
 
===[[General Pathology - Necrosis|Necrosis]]===
 
 
 
==Necrosis==
 
Necrosis
 
The term necrosis means death of cells within the living body.
 
Two things happen when necrosis occurs:
 
a. further changes can take place in the tissue itself; and
 
b. the surrounding unaffected living tissue can react against this necrotic tissue.
 
Causes of Necrosis.
 
There are three main causes of necrosis:
 
1. loss of blood supply - tissues depend upon their blood supply to remain alive,
 
2. non-living agents such as chemicals or physical injuries,
 
3. living agents such as bacteria, viruses, fungi or parasites.
 
1. Loss of blood supply
 
.A diminished blood supply to a tissue is called ischaemia. This type of necrosis is called
 
ischaemic necrosis, also called infarction - defined as necrosis of a portion of tissue due to
 
an interruption (usually sudden) in the blood supply to that portion. The effects of
 
ischaemia on a tissue will vary according to:
 
a. the type of tissue affected - some tissues are more susceptible than others.
 
b. the type of cell in the tissue - the general rule is that parenchymatous cells, the
 
essential functioning cells, are more susceptible than the stromal supporting cells.
 
c. the metabolic activity of the tissue - very active organs i.e. those that work continuously
 
are more susceptible.
 
d. whether or not there is a good or potential collateral blood supply
 
25
 
There are three ways in which tissue ischaemia can be brought about
 
a. compression of the blood vessel
 
from without e.g. too tight a bandage
 
will cause tissue ischaemia. A
 
common cause of tissue ischaemia is
 
strangulation of the intestine by a
 
twist upon itself, or a mass such a
 
lipoma ( a relatively common growth
 
of mature fat tissue ) forms in the
 
mesentery, becomes pedunculated (
 
attached by a fine band of the
 
mesentery) and can encompass a
 
portion of intestine. Initially, the
 
compression of the mesenteric veins
 
will prevent outflow of blood leading
 
to congestion and swelling of the
 
affected portion. When the arterial
 
supply becomes occluded or cannot
 
supply sufficient blood to the tissue
 
because of pressure in the swollen
 
intestine and its vessels, the affected area undergoes an ischaemic necrosis with disastrous
 
sequelae of rupture and peritonitis or gangrene and toxaemia due to absorption of toxic
 
products of the necrosis and intestinal bacteria.
 
b. a narrowing of the lumen e.g. thickening of the wall in arteriosclerosis.
 
c. blocking of the lumen of the vessel, important causes are thrombi and emboli. Renal
 
vessels are commonly affected. See the effects of emboli in Circulatory Disorders.
 
2. The action of physical or chemical agents.
 
The physical agents include burns, cold, frostbite, X-rays, pressure, and actual pinching or
 
crushing of the tissue. The necrosis is direct in the case of burns and indirect in the case of
 
crushing or pinching which causes occlusion of the vessels supplying the tissue which will
 
undergo necrosis. Chemical agents may be directly caustic or corrosive in action or exert
 
their effects when absorbed and metabolised to a more toxic substance.
 
3. Living agents - their effect is either through their toxic effects on cells or their
 
colonisation of the cells.
 
Appearance of necrotic lesions
 
In a typical necrotic lesion there are three zones.
 
1. Where the effect of the causal agent is maximal, there is a sphere of necrosis.
 
2. A little further away, the tissue will be damaged but not yet dead, and so there is a
 
zone of degeneration short of death.
 
3. Still farther away, where the effect of the agent is insufficient to cause death or
 
degeneration of cells, we have a zone where the body is reacting to the dead tissue
 
26
 
Gross and histological features of necrotic tissue.
 
1. Colour change in the tissue. In contrast to living tissue, dead tissue tends to be paler,
 
partly because there is no circulation in dead tissue
 
2. Consistency (texture) of the tissue. The appearance of the centre of the necrotic lesion
 
will vary according to the
 
1. type of agent responsible and
 
2. the tissue in which it is acting.
 
This appearance may give a clue to the agent responsible, and the types of necrosis
 
encountered are based on their gross description
 
a. Coagulation necrosis
 
Gross: The necrotic lesion will be
 
firmer and dryer on the cut surface. The
 
gross appearance still resembles
 
somewhat the nearby living tissue. It is
 
a feature of bacteria which produce
 
toxins, infarction, and some foci of
 
viral replication.
 
Micro: the general architecture of the
 
tissue is preserved. Certain changes
 
present can be recognised in an ordinary
 
H&E section, and are related to loss of
 
cellular detail.
 
a. the cells may appear somewhat
 
larger and their outline may be lost
 
b. the cytoplasm appears structureless
 
and homogenous.
 
c. there are nuclear changes - the most important
 
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There are three types of nuclear change.
 
i. Pyknosis - Greek for dense - is a
 
condition in which the normal nuclear
 
structure is replaced by a very dense,
 
heavily staining, somewhat smaller angular
 
mass of chromatin.
 
ii. Karyorrhexis - Greek karyon =
 
nucleus; rhexis = breaking up. This
 
appearance is rather the reverse of the
 
above. It appears as though the nucleus has
 
exploded rather than condensed in the
 
cytoplasm, and irregular-sized bits of dense
 
nuclear material are found scattered
 
throughout the centre of the cytoplasm.
 
iii. Karyolysis - this means dissolution of the nucleus. The nuclear staining with
 
haematoxylin becomes fainter and only the ghost outline of the nucleus remains.
 
Apoptosis - is a term used to denote the programmed death of scattered single cells in living
 
tissues. Unlike necrosis, there is no reaction to the death of the cell. It is thought that some
 
cells are programmed to die - a form of cell regulation in a tissue - unless there is a change in
 
circumstances in a tissue that require them to continue living. One such circumstance is the
 
development of tumours in which cellular regulation is absent. Cellular apoptosis is thought
 
to be important in deleting extra cells produced in embryogenesis, in cyclical physiological
 
changes in the genital tract of females, in the death of lymphocytes, in graft rejection, and in
 
cellular death by the same injurious substances that cause necrosis in higher doses.
 
The cells undergoing
 
apoptosis lose their
 
connections with their
 
neighbours and shrink; the
 
nucleus becomes pyknotic;
 
and the cytoplasm becomes
 
eosinophilic. The cell
 
breaks up into fragments
 
that are engulfed by
 
neighbouring cells or local
 
macrophages. Their
 
remnants can be seen in the
 
neighbouring cells’ cytoplasm.
 
28
 
b. Liquefactive (Colliquative)
 
Necrosis.
 
Gross: In the brain where there is a lot of
 
lipid, the intracellular enzymatic changes
 
make it softer and more fluid in nature. This
 
is known as 'malacia'. Initially it becomes
 
swollen with a gelatinous, sometimes bloodtinged
 
appearance due to disruption of the
 
blood vessels but later becomes fluid.
 
Micro: the microscopic appearance will
 
not resemble the nearby living tissue as it
 
may have already lost any semblance of the
 
nearby living tissue because it is becoming
 
a fluid.
 
Another type of liquefactive necrosis,
 
quite important is pus formation which
 
occurs when the organism causing the initial
 
necrosis in the tissue, is capable of attracting
 
to the necrotic area large numbers of
 
neutrophils and also capable of killing them.
 
These are the so-called pyogenic bacteria.
 
When the neutrophils die they release
 
proteolytic enzymes which digest the dead
 
tissue and also more incoming neutrophils.
 
The liquid formed is called pus, and it is
 
composed mainly of the dead and dying
 
neutrophils together with the remnants of
 
the necrotic tissue cells.
 
29
 
In favourable cases, the neutrophils may
 
eventually kill the organisms, but in most cases
 
the organisms persist, all the time producing
 
more pus. This produces an expanding
 
sphere of pus that is called an abscess. The
 
pressure will build up and if near to the skin
 
will cause pressure on the overlying skin, and
 
when the pressure is sufficient or the surgeon
 
lances it, the abscess will burst discharging the
 
pus, and hopefully with it the organisms responsible. This is nature’s way of ridding the body
 
of an injurious agent.
 
Micro: In the case of an
 
abscess, the necrotic area will
 
show varying stages of
 
degeneration of the
 
neutrophils, ranging from
 
nearly normal neutrophils, to
 
pyknosis, karyorrhexis and
 
karyolysis, and finally to a
 
homogenous structureless
 
admixture of remnants staining
 
faintly bluish.
 
As this sphere of pus is
 
forming, there is a host
 
inflammatory response directed against it. This is composed of a capsule of fibrous tissue in
 
which there are many blood vessels on its inner surface, which transport the vast number of
 
neutrophils into the necrotic centre. This is called the 'pyogenic membrane'. In superficial
 
abscesses, when the abscess has discharged to the surface, this membrane can be viewed as a
 
crater that has a reddish somewhat ragged lining. Where the abscess is deep within an organ
 
such as the liver, there is nowhere to discharge to, and the fibrous capsule around the pus is
 
markedly thickened. .
 
c. Caseation necrosis.
 
The necrotic tissue appears grossly like
 
cheese. The colour varies from white to
 
grey to yellowish. In sheep it appears
 
whitish while in cattle there may be a
 
yellowish tinge. The fluid content also
 
varies giving a dry crumbling consistency
 
in some cases to being more like cottage
 
cheese in others. It is really a mixture of
 
coagulation and liquefactive necrosis,
 
and is a feature of necrosis caused by
 
some specific organisms.
 
30
 
Micro: On histological section, there is a
 
complete loss of the architecture, the
 
necrotic material being purplish in colour
 
due to random intermixing of the
 
components that stain with haematoxylin
 
and eosin i.e. bits of nuclear material
 
interspersed with cytoplasmic fragments.
 
This type of necrosis is a feature of
 
granulomatous (tumour-like
 
proliferation of chronic inflammatory
 
cells) processes such as tuberculosis in
 
some species, as in the ox, pig and sheep.
 
The necrotic tissue is not derived
 
principally from the organ in which it
 
occurs, but from a special type of host
 
inflammatory cell - the macrophage -
 
which is sent into the tissue in large
 
numbers to engulf the organism. The
 
organism has defences against the enzymes of the macrophages and is quite willing to
 
continue to grow and multiply within these macrophages eventually causing their death. In
 
some granulomas, the macrophages will combine together and form giant cells.
 
Fungi and parasites also cause granulomas.
 
Calcification. In the condition of calcification, calcium salts are deposited within the
 
necrotic tissue in an effort to make it more inert. It is seen quite commonly in necrosis in
 
cattle and sheep, and is a common feature in lesions which show caseation necrosis, and
 
usually indicates a lesion of long standing. Such calcified necrotic tissue can be appreciated
 
grossly. The deposits of calcium salts can be palpated and on cutting into the necrotic
 
portion, the calcified material may be both felt as a gritty substance and heard by a grating
 
sound against the knife.
 
The colour is usually chalk-white but may have a yellowish green tinge if the inciting cause
 
is a parasite. Parasites attract a large number of eosinophils that are responsible for this
 
colour. This type of calcium deposition in necrotic tissue is called dystrophic calcification.
 
It is an attempt to make the tissue more inert. It does not result from elevated levels of
 
calcium in the blood.
 
Micro: In sections stained by H&E, calcium has a
 
distinctive dark blue colour. You may also see some
 
shattering of the calcium and adjacent tissue due to the
 
effect of the microtome knife
 
passing through it. It blunts the knife and there may be
 
score marks throughout the rest of the section. Difficulty
 
sometimes arises in distinguishing calcium from
 
bacterial colonies that stain a similar colour. A
 
definitive special stain for calcium is to stain the
 
section with silver nitrate (the von Kossa method).
 
The calcium stains black.
 
31
 
Sequel to necrosis
 
These will vary in relation to the causes of necrosis, but by and large it is important to
 
distinguish between dead tissue on the surface of the body and dead tissue in the depths of
 
the body; a piece of dead skin as compared with a portion of dead liver.
 
Dead tissue on the surface can be shed and is said to slough, whereas dead tissue in the centre
 
of the liver cannot naturally be shed from the surface. Something else happens to it. It can
 
either be absorbed or replaced by fibrous tissue, or it can be enclosed by fibrous tissue. This
 
is part of the process of inflammation - the response of the body to local injury. It is a
 
general rule that small areas of necrosis become absorbed and replaced by fibrous tissue
 
(scars) while larger areas become encapsulated by fibrous tissue, the necrotic portion
 
remaining in the centre. This effectively cuts off any contact with living tissue, and allows
 
perhaps further changes to occur within the necrotic portion to make it more inert. The
 
encapsulated portion is called a sequestrum. It can be, as mentioned before, be calcified to
 
make it more inert.
 
When necrosis occurs on an epithelial surface, two things may happen depending upon the
 
depth of the necrosis. In a case like 'Foot and Mouth' where the necrosis is confined to the
 
middle and outer layers of the epithelium, the remaining underlying germinal layer divides
 
and replaces the shed portion. This type of necrosis confined to the epithelium is called an
 
erosion. It leaves no scar.
 
When the necrosis extends below the basement membrane of the epithelium as might be
 
caused by an applied corrosive substance or a burn, the body reacts to this interruption in the
 
integrity of the epithelium with an underlying inflammatory reaction attempting to repair the
 
deficit by fibrous tissue. This type of necrosis is called ulceration, and the resultant
 
contraction of the fibrous tissue leaves a scar.
 
Fat necrosis
 
This is confined to the fat depots of the body.
 
It has a very distinctive appearance grossly: instead
 
of the fat being semi- translucent and malleable, it
 
shows areas of focal opacity and is very hard in
 
consistency. This appearance is due to the
 
intracellular fat after the fat cells have died, being
 
broken down into fatty acids which combine with
 
Ca++, Na+ and K+ ions to forms soaps. These soaps
 
are substances foreign to the body and they provoke a
 
host inflammatory response. Unlike fat, they do not
 
dissolve out in routine preparation of sections,
 
These areas of fat necrosis remain indefinitely, may
 
show great scarring, and quite often calcify. It occurs
 
principally in two ways in the body.
 
32
 
a. Enzymatic necrosis of fat. This happens when there is a release of pancreatic enzymes
 
into the neighbouring mesenteric fat, the release being caused by a damaged pancreas e.g.
 
due to an adjacent tumour.
 
b. Traumatic necrosis of fat. This is seen in the
 
subcutaneous tissue following trauma to the area.
 
It is quite common in the brisket of recumbent
 
animals due to the prolonged pressure on the area.
 
It is worth mentioning here another condition of fat that can also undergo necrosis and
 
calcify. This is the so-called lipomatosis that occurs for some unknown reason in Channel
 
Island breeds of cattle. In this condition, there are focal areas of increased fat in the
 
mesentery. They often surround several loops of the gut, and if they become necrotic, they
 
may strangle the enclosed gut with disastrous consequences for the animal.'
 
Gangrene
 
Gangrene is a post-necrotic change, and in some cases is the ultimate degradation of necrotic
 
tissue. The tissue is already dead. There are two main types
 
a. Wet gangrene - life threatening
 
b. Dry gangrene - non life threatening
 
a. Wet gangrene can either be due to:
 
a. the agent which initially kills the tissue, further putrefying it, or
 
b. the gangrene may be due to dead tissue killed by some other means being invaded by
 
organisms which putrefy it.
 
In other words the former may be viewed as a primary gangrene, while the latter is
 
secondary.
 
An example of the former is gangrenous mastitis of the udder of the cow caused by
 
Staphylococcus aureus, the organism killing the tissue and then putrefying it.
 
An example of secondary gangrene is that which occurs when a portion of gut twists on its
 
mesentery or when a lipomatous mass attached to a strand of mesentery, loops around a piece
 
of intestine as depicted earlier with regard to tissue ischaemia. The blood supply to the gut is
 
cut off, and the affected portion becomes necrotic. Wet gangrene supervenes when the
 
putrefactive organisms that are normally present in the gut invade the dead tissue.
 
33
 
A further cause of wet gangrene is when a ligature around an extremity causes ischaemic
 
necrosis of tissue distal to it and the necrotic tissue becomes invaded with putrefactive
 
bacteria.
 
The gross appearance is of a swollen puffy tissue cold to the touch and with a horrible smell
 
owing to the hydrogen sulphide (the smell of rotting flesh) produced in the putrefying tissue.
 
In comparison to other dead tissue the zone of inflammation between the dead putrefying
 
tissue and living tissue is indistinct. This type of gangrene is overwhelming disastrous for the
 
animal unless treated quickly and effectively, as the organisms produce potent toxins either
 
themselves or in their breakdown of the dead tissue and the animal rapidly succumbs to
 
toxaemia.
 
A variation of wet gangrene is that produced by Clostridia organisms such as Clostridium
 
chauvei and C. septicum whereby they also form gas. This is called gas gangrene. The
 
conditions of Blackleg and Clostridia contamination of wounds produce this type of
 
gangrene.
 
Dry gangrene, on the other hand, is not life threatening. This is really mummification
 
(like an Egyptian mummy) of an extremity, such as the tail, foot or ears of animals. There is
 
an occlusion of the blood supply to the extremity. The tissue becomes necrotic.
 
Because of air circulating around the extremity, water is drawn out of the tissue, drying and
 
preserving it. There is little if any bacterial growth in the tissue and it eventually sloughs off.
 
In small animals crushing of the tail may cause this by cutting off the blood supply.
 
34
 
In large animals, it is seen commonly following a septicaemic condition in which bacteria
 
are growing and passing around in the circulation. An embolus blocks the blood supply.
 
When seen in calves, the possibility of Salmonellosis must be kept in mind. Other causes
 
are frostbite and ergot poisoning.
 
Finally, necrosis is irreversible.
 
===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