UNIT 9: Introduction to pathology
1. Pathology: pathology is a subject dealing with abnormal biology in a living
organism, its causes, development, structural and functional alterations and
termination.
Pathology starts as soon as disease starts but does not end with the death of the
organism. Pathological studies continue even after death requiring post mortem to
correlate the lesions with the symptoms observed during life, to assess the line of
treatment, to explain the cause of the death and even to record the changes as legal
evidence.
Pathology is broadly divided into general pathology, special pathology and clinical
pathology.
General pathology deals with general causes and effects as expressed by as expressed
by cells and tissues in response t o abnormal stimuli.
Special pathology deals with specific response of specific tissues or organs to specific
stimuli or disease.
Clinical pathology deals with specific alterations in the tissue fluids, cells, excretions
and secretions which pinpoint harmful stimuli or diseases.
There are highly specialized branches of pathology such as diagnostic pathology,
surgical pathology, histopathology and physiopathology.
2. Pathogenesis: Pathogenesis refers to sequence of events in anatomy or histology,
physiology, chemistry and in general, progress of disease from onset to the end.
3. Disease: any deviation in normal structure and function of any part of the body which
may lead to a symptom or symptoms.
4. Syndrome: means a set of symptoms which occur together. In other words it is a
collection of symptoms related to a disease.
5. Etiology: it denotes theoretical study of factors which result into a particular disease.
6. Lesion: any pathological change or discontinuity of organs or tissue including loss of
function.
7. Necropsy: examination of a body after death which includes external examination as
well as internal examination by dissection.
8. Biopsy: removal and examination of tissues from living body for microscopic or
other types of examinations.
9. Signs: objective evidences or characteristics of any disease, such as excitement,
lameness, deformities, breathlessness, etc.
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10. Symptom: symptom means any subjective evidences which characterize a particular
disease. A symptom being subjective can be felt by human beings. For example
headache is felt and can be described by a man. Nausea, pain, burning sensation, etc
are subjective evidences which cannot be seen.
11. Pathognomonic: any alteration which is characteristic or distinctive for the diagnosis
of a particular disease.
12. Morbid: unhealthy or deviated from normal
13. Morbidity: it means rate of sickness. It is the ratio of sick animals to healthy animals
living in a farm.
14. Mortality: it means death rate. It is generally expressed as death per 100 of a
particular population of animals.
15. Incineration: burning a body or a material to ashes.
16. Prognosis: predicting the possible course or progress of a disease (favorable, grave,
guarded, etc)
17. Sequalae: consequences or end results of a disease.
Inflammation
Inflammation is a series of changes that occur in the tissues following infliction of injury
or infection
Causes: inflammation can be induced by any injurious agent, which includes:
1. physical causes such as mechanical injury, radiation, x-rays, burns, etc
2. bacterial infections or bacterial toxins
3. viral infections
4. fungal infections or fungal toxins
5. parasitic infections
6. chemical; toxins or plant toxins
7. immune mediated reactions- hypersensitivity reactions
Inflammation is the basic reaction of all living multicellular organisms which is primarily
defence-oriented. In fact it is the single most powerful weapon of a living animal to fight
against and in most cases kill or remove the cause of the disease.
However, sometimes inflammation may prove to be harmful to the organism or to an
organ if there is severe inflammation especially in any vital organs such as eyes,
kidneys, brains, etc which can result in irreparable or even fatal damage to the organ.
Usefulness of inflammation
Mild infections or injuries such as enteritis, abscesses, cuts, wounds, etc are often
overcome through defensive inflammatory reactions. Infection may be removed by
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formation of abscess and discharge of pus or by dilution and removal of toxins of stings.
After infection is overcome our second line of defence- healing of wounds or
regeneration- comes into play.
Cardinal signs of inflammation
Celsus, a Roman described in the first century the four cardinal signs of inflammation.
Rudolf Virchow, a German pathologist added loss of function, as the fifth cardinal sign in
1858. The cardinal signs of inflammation are the basic reactions of acute inflammation.
The five cardinal signs of inflammation are;
1. Rubor or redness
2. Tumor or swelling
3. Calor or heat
4. Dolor or pain, and
5. Functiolesia or loss of function
1. Rubor- rubor or redness is caused by dilatation of microcirculation in the area of
injury.
2. Heat- heat is due to increased blood flow in the inflamed area. More blood flow in
inflamed skin makes it hotter than the normal skin.
3. Swelling: swelling in the inflamed tissue is mainly due to infiltration of exudates
and inflammatory cells. Exudates and cells infiltrate due to increased vascular
permeability.
4. Pain: pain in inflamed tissue is due to several factors:
a. Increased pressure or tension
b. Chemical mediators as prostaglandins, histamines and bradykinin
c. Potassium release from intracellular locations and
d. Formation of lactic acid
5. Loss of function- loss of function may be due to pain induced by the inflamed part
subjected to movement. This is mediated by reflexes of sensory nerves. But the
normal cells in an inflamed area continue to function normally unless their
oxygen and nutrient requirement is compromised.
Vascular changes in inflammation
The inflammation has been shown to pass through a sequence of vascular and cellular
alterations as described:
1. Momentary vasoconstriction- momentary vasoconstriction affects arterioles,
which is of a few seconds duration. In cases where injury is very severe the
duration of vasoconstriction may be prolonged to several minutes.
2. Vasodilatation- vasodilatation initially occurs in arterioles but soon the
capillaries open up and get dilated. E.g., PGE1 and leukotrienes are
substances which cause vasodilatation. Vasodilatation may last for a variable
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3.
4.
5.
6.
7.
8.
period up to days or weeks depending on severity and persistence of injurious
stimulus.
Slowing of blood flow- slowing of blood flow occurs mainly due to exudation
of fluid causing increased viscosity of blood or haemoconcentration. It is also
partly due to swelling of endothelial cells and formation of roleaux. The small
blood vessels become virtually packed with erythrocytes, which is called
stasis. The blood flow returns to normal as inflammation subsides.
Margination and pavementing of leukocytes- the leukocytes, particularly
neutrophils, in the blood vessels with stasis tend to move towards the
endothelium which is called margination. After sometime the leukocytes
adhere to the endothelium, forming almost a layer of adherent leukocytes
which is called pavementing.
Emigration of leukocytes and diapedesis- the adherent leukocytes,
particularly the neutrophile move out through the junctions of endothelial;
cells and the basement membrane. The neutrophils dissolve the basement
membrane by proteolytic enzymes and come out into the extra vascular tissue.
This process is called emigration. Along with leukocytes some erythrocytes
may also pass out of the vessels passively which is called diapedesis.
Changes in vascular permeability- as the leukocytes emigrate the protein
rich fluid also comes out of the blood vessel to form exudate or the
inflammatory oedema
Adhesion of leukocytes to endothelium- adhesion of leukocytes to
endothelium at the site of inflammation is to some extent dependent on
availability of calcium which acts as cationic bridge between the two cells.
Emigration and chemotaxis- the endothelial cells form a single layer of
vascular channels but they are tightly joined to each other in arterioles, less
tightly in capillaries and least in venules, in which maximum exudation and
cellular emigration occurs. The leukocytes are attracted to extravascular
locations by some chemical stimuli which is termed chemotaxis.
Chemical mediators of inflammation
Several chemical factors are known to mediate in the inflammatory process particularly
in increasing permeability of blood vessels
1. Kinins system- e.g., Bradykinin
2. Complement system- complements are extra cellular proteins present in inactive
form in plasma as complement cascade numbered C1 to C9. They help in
liberation of histamine by mast cell degranulation.
3. Prostaglandins- prostaglandins (PG) are a group of chemicals related to fatty
acids. They are produced from intracellular phospholipids, through arachidonic
acid. PGE1, PGE2 and prostacyclin (PGI2) are most important in causing
increased permeability, vasodilatation and potentiation of other chemotactic
factors. Prostaglandin synthesis is inhibited by aspirin and indomethacin. The
most important source of prostaglandins is macrophage.
4. Lymphokines- lymphokines are proteins secreted by T lymphocytes on
stimulation by an antigen.
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5. Histamines- histamine is richly found in granules of mast cells (present around
blood vessels), basophils of blood and blood platelets. Histamine acts in early
stages of inflammation.
6. Seratonin or 5-hydroxytryptamine- mostly found and released from blood
platelets and mast cells.
7. Leukotrienes- product of metabolism of arachidonic acid by lipoxigenase
pathway. Prostaglandins are formed by cytoxigenase pathway.
8. Lysosomal constituents- lysozyme, proteases, cationic proteins, hydrolases
9. Free radicals- oxygen derived free radicals such as H2O2 and OH which are
formed by neutrophils and macrophages during phagocytosis cause endothelial
damage particularly in the lungs, causing increased vascular permeability.
PhagocytosisNeutrophils or polymorphonuclear cells or heterophils (in poultry and rodents) are the
most important cells which not only phagocytose bacteria and kill many but not all of
them. They constitute the first line of defence because they are mostly the first cells to
emigrate at the site of inflammation. They destroy bacteria by their phagocytic activity
and by antibacterial and lytic enzymes contained in their granules. The optimum pH for
exocytosis and phagocytosis is 6.75 which is slightly acidic. They can also kill virus
infected cells if they become coated with antibodies and probably complement. They also
act as scavengers by their ability to dissolve infected or damaged tissue such as in an
abscess the tissue is converted into liquid pus. They also dissolve basement membrane of
endothelium, collagen, elastic fibers and fibrin with proteolytic enzymes such as elastase,
collagenase, proteases, etc.
Steps of phagocytosis
Phagocytosis can be divided into three steps although it is one continuous process. These
steps are identification of phagocytic particle or organisms, engulfment, and degradation
of phagocytosed material.
1. Recognition- material or organism to be phagocytosed by the cells cannot be
phahgocytosed unless it is covered by some proteins called opsonins. The particles or
organism with opsonic covering attract neutrophils or macrophages which have
receptors for opsonins.
2. Engulfment- the organism or particle to be engulfed is enclosed in phagocytic cups.
Phagocytic cups are formed from tentacles or cytoplasmic projections. The tentacles
fuse to form phagocytic vacuole. The lysosomes begin to fuse with phagocytic
vacuole to form phogolysosome. In phagolysosome large number of enzymes is
poured in, such as proteases, lipases, phospholipases, which work optimally in acidic
pH. The macrophages summon the neutrophils, the profesessional killers to the site of
infection.
3. Digestion phase –the granules empty their contents into phagosomes and this is called
degranulation because granules lose their identity. Digestion of phagocytosed nucleic
acids, proteins, lipids, glycans and glycoproteins is brought about by specific
enzymes.
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4. Disposal phase- the materials digested to basic things like amino acids, lipids,
carbohydrates and nuleosides are discharged by exocytosis for utilization by the body,
but indigestible materials continue to accumulate during life time till the macrophage
dies.
Sequelae of acute inflammation
1. Death: inflammation itself may be fatal if it is very severe and involves vital organs
such as brains, liver, kidneys etc.
2. Resolution: when the cause of inflammation such as infection, pollens, parasites,
toxins etc is removed, the process of resolution starts.
3. Regeneration: if inflammation occurs in parenchymatous organs skin or lungs then
the functional, specialized cell such as hepatocytes in liver, kidney tubular epithelium
or the alveolar epithelium or epidermis may be regenerated to replace the necrosed
cells or if the damage is extensive then replacement occurs by fibrous scar tissue.
Inflammatory cells
1. Neutrophils- neutrophils proliferate and get matured in bone marrow. When they
enter into blood they are divided into two pools namely marginal pool and circulating
pool. In the marginal pool, neutrophils are located along the walls of small blood
vessels, from where they leave blood and enter the tissue pool. Circulating pool
consists of neutrophils in blood circulation. Increased level of neutrophils in
circulating pool is called neutrophilia. Neutrophilia with less than 3% immature or
band neutrophils is called regenerative left shift. Low to slightly elevated neutrophilia
in which immature neutrophils outnumber the mature ones is called degenerative left
shift. If the mature or old cells increase in percentage then it is called right shift.
Thus, the right and left shifts indicate number of immature neutrophils, designated as
Schilling index.
The principal function of neutrophils is phagocytosis of small particles and
organisms. They infiltrate in large numbers in inflammation produced by pyogenic
organisms such as Staphylococci, Streptococci, Corynebacteria, Pseudomonas and in
variable numbers in other bacterial infections.
2. Lymphocytes- lymphocytes are small round cells usually not larger than 5 to 6 µm.
Nucleus constitute about 50% of the volume of the cell.
3. NK cells- NK cells were earlier called ‘null’ or ‘N cells’. Now it is known that NK
cells are made of heterogenous cell population of derived from several subsets of
lymphocytes. Morphologically they all look alike. They are larger than lymphocytes
and contain large granules.
4. T-lymphocytes- functionally T-lymphocytes can be divided into two subsets. Helper
T (Th) cells are those which on activation secrete hormone like proteins called
lymphokines. The other type of T cells are cytotoxic T (Tc) cells which on activation
by exposure to cells carrying specific surface antigens get activated to lyse the cells
on further exposure to such cells. These cells are mainly responsible for cell mediated
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immunity (CMI) which gives protection against cancer, viruses, fungi and some
bacteria causing chronic infections. The third category of suppressor T cells (Ts)
secrete on stimulation substances which inhibit response of other cells.
5. Macrophages- macrophages are large mononuclear cells which perform the important
function of phagocytosis due to which they are also called as scavenger cells.
6. Other phagocytic cells are basophils, mast cells and eosinophils.
Classification of inflammation
Classification of inflammation can be based on:
I. Adequacy of the reaction
II. Duration of occurrence of inflammation
III. Nature of the exudates
IV. Predominance of degenerative changes
V. Sequelae (result) of inflammation
I. Adequacy of the reaction
 Adequate reaction- through inflammation, body attempts to kill, remove the irritant,
repair the damaged tissues of the body and bring to normal or as normal as possible.
When the injured part has been brought back to normal state, after a brief period of
inflammation, such a reaction is called adequate reaction.
 Inadequate reaction-when the defence forces of the body are not capable of killing or
removing the irritant fully, it is considered as inadequate reaction. Inadequate reaction
is usually observed in chronic diseases. However, in such diseases, the gross lesions
reveal large sized abnormalities in the organs due to overgrowth.
 Excessive reaction- when the body over reacts to an irritant it is called excessive
reaction. The body reacts excessively to those substances to which it is allergic. In
most of the substances, the individual may die as a result of reaction to allergies even
before any inflammatory response is produced. Such type of reaction is described as
allergic reaction or anaphylactic shocks.
II. Duration of occurrence of inflammation-inflammation can also be classified
according to length of time for which it persists. Vascular, exudative and
proliferative changes are three important events of inflammation. Vascular changes are
the first alterations in inflammation followed by exudative and then proliferative changes.
The inflammation can be classified as:
a. Per acute: in this type the causative agents is very severe. The vascular changes
are predominant and duration of inflammation is very short, may be a few hours
so the end results are either recovery without permanent damage to the tissues
or death. Examples- septicaemia, anthrax, black quarter, etc. in cattle.
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b. Acute: in this type the duration is of a few days may be up to a week or so. The
causative agent is very severer but less so when compared to per acute
inflammation.
c. Subacute: this type of inflammation usually lasts longer, usually several weeks.
The causative agent is less severe but usually persists. Vascular changes are less
prominent.
d. Chronic: The causative agent in this type is mild, but persistent in nature. The
irritant, thought mild will continue to act. The body reacts slowly but
continuously pouring in the mononuclear cells. Thus after several weeks or at
times after several months, large sized inflammatory tissues is the result. A
typical of such inflammation is tuberculous nodule.
III. Nature of exudate- this type of classification is based on the prominent constituent of
the exudates. When two constituents are almost equal, it is usually mentioned by a
combined name. The types of inflammation based on the principal constituents are:
a. Serous inflammation- principal constituent is plasma or lymph.
b. Fibrinous inflammation- exudate constituent is fibrin.
c. Diphtheria inflammationd. Serofibrinous inflammation
e. Catarrhal or mucous inflammation
f. Suppurative inflammation
Different types of suppurative lesions, viz.
 Pustule: small focal suppurative area in the epidermis.
 Boil or furuncle: small focal suppurative area in the hair follicle or sebaceous
gland.
 Erosion: small area in which superficial layers of epidermis are lost and stratum
germinatum is intact. Erosion may form by rupture of pustule or in viral infection
viz. foot-and- mouth disease.
 Ulcer: small area in which epidermis of skin or epithelium of mucous membrane
is lost. The dermis or submucosa is usually exposed.
 Empyema: pus in the pleural or peritoneal body cavities or bone sinuses.
 Pyaemia: literally means pus in the blood but it means the presences of pyogenic
bacteria in the blood.
 Pyorrhea: (literally means discharge of pus).this pertains to suppurative
inflammation of gums.
IV. Predominance of degenerative changes
Classification according to predominance of degenerative changes or necrosis: the irritant
bring about degenerative changes to which the body reacts resulting in inflammation. The
most typical examples for such nomenclature are caseous lymphadenitis, atrophic rhinitis,
necrotic enteritis, etc.
V. Sequelae of inflammation
This type of classification is based on the outcome of inflammation. Some of the
examples are:
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a. Atrophic inflammation: the typical example is atrophic rhinitis in the pigs in
which the ultimate result is the atrophy of turbinates and nose.
b. Hypertrophic inflammation: this type is seen in pox in various animals, typical
hypertrophy being in fowl pox.
c. Adhesive inflammation: when two structures adhere together either by fibrinous
exudates or by fibrous tissue. The fibrous tissue adhesions develop as a result of
organization of inflammatory exudates.
d. Obliterate inflammation: when certain structures are completely replaced or
when any tubular structure is obstructed primarily by fibrous tissue. Example of
such inflammation is bronchiolitis obliterans.
e. Fibrous inflammation: when there is excessive proliferation of fibrous tissue
and after fibrous tissue matures scar tissue is produced.
Terminologies for inflammation of different organs
Organ
condition
Organ
Condition
Brain
Meninges
Ear
Conjunctiva
Iris
Buccal cavity
Lips
Gums
Palates
Tongue
Pharynx
Oesophagus
Crop
Stomach
Intestine
Cecum
Colon
Rectum
Liver
Gall bladder
Pancreas
Larynx
Encephalitis
Meningitis
Otitis
Conjunctivitis
Iritis
Stomatitis
Chelitis
Gingivitis
Palatitis
Glossitis
Pharyngitis
Oesophagitis
Ingluvitis
Gastritis
Enteritis
Typhlitis
Colitis
Proctitis
Hepatitis
Cholecystitis
Pancreatitis
Laryngitis
Bronchus
Lung
Pericardium
Myocardium
Endocardium
Arteries
Veins
Lymph nodes
Lymphanges
Skin
Muscle
Joints
Vertebrae
Kidney
Ureter
Urinary bladder
Urethra
Testis
Penis
Vagina
Uterus
Cervix
Bronchitis
Pneumonitis
Pericarditis
Myocarditis
Endocarditis
Arteritis
Phlebitis
Lymph adenitis
Lymphangitis
Dermatitis
Myositis
Arthritis
Spondylitis
Nephritis
Ureteritis
Cystitis
Urethritis
Orchitis
Balanitis
Vaginitis
Metritis
Cervicitis
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CIRCULATORY DISTURBANCES
i.
ii.
iii.
iv.
v.
vi.
vii.
Circulatory disturbances include the pathological conditions in which circulation of
arterial, venous blood, lymph and intercellular fluid is disturbed.
The circulatory disturbances may occur mainly due to:
Inflammation
Obstruction in the flow of blood in the vessels or lymphatic
Failure of function of heart
Disturbances in the structure of blood or lymphatic vessel
Disturbances in the factors controlling vascular permeability
Variation in the hormonal, enzymatic or nervous control of circulation
Disturbances in the volume of blood, chemical composition of blood or circular
alterations in blood.
HYPERAEMIA OR CONGESTION
This term denotes increased flow of blood to an organ or tissue due to increased arterial
blood flow associated with dilatation of blood vessels and capillaries.
Etiology:
Hyperaemia may be physiological or pathological. In physiological hyperaemia there is
increased blood supply due to increased physiological function such as hyperaemia of
stomach or intestine during digestion, hyperaemia of uterus during pregnancy, or
hyperaemia of muscles during exercise.
Pathological conditions which cause inflammation also lead to hyperaemia of the
inflamed tissue or organ. Healing or regeneration of wounds is also accompanied by
hyperaemia. Exposure to irritants, heat or massage also results in localized hyperaemia.
Gross changes:
The hyperaemic tissue appears red due to increased blood flow. The arteries and their
tributaries appear prominent. The hyperaemic tissue may become hot and swollen.
PASSIVE CONGESTION
Passive congestion means more than normal retention of blood in an organ or tissue due
to obstruction or retardation of venous return. The venules and capillaries therefore
become dilated.
OEDEMA
Oedema can be defined as increased accumulation of fluid of non-inflammatory origins
in the interstitial tissue or in the cavities of the body.
Oedema may be generalized or localized. In generalized oedema the fluid accumulates
under the skin as well as in the serous cavities. Localized oedema may involve an organ
or part of limbs or a body cavity such as hydropericardium.
EMBOLISM
Embolism means circulation of abnormal material (solid, liquid or gas) in the blood.
Emboli can be made of even blood constituents such as a piece of thrombus when
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circulating in the blood becomes an embolus. The emboli get lodged or impacted in an
artery or an arteriole or capillary depending on their size. If the embolus is a piece of
thrombus it is called thrombo-embolism. Examples of emboli are fat emboli, gas emboli,
bacterial or septic emboli, parasitic emboli, etc.
HAEMORRHAGE
Haemorrhage means escape of blood outside the normal blood channels. Haemorrhage is
generally due to rupture of blood vessels by trauma or due to injury to the vessel walls by
viruses such as hog cholera, equine viral arteritis, infectious canine hepatitis, etc.
Haemorrhages are also seen in internal organs in severe, usually septicaemic bacterial
diseases such a pastuerellosis, anthrax and salmonellosis.
Types of haemorrhages:
Depending on the size of haemorrhagic spots, different terms are used for haemorrhagic
foci as follows:
Petechiae: indicates minute or pinpoint haemorrhage
Purpura: haemorrhage smaller than 1 cm but larger than petechiae.
Ecchymosis: haemorrhages between 1 to 2 cm diameters.
Extravasation: term used for larger and more diffuse haemorrhagic patches. When there
are wide spread, diffuse haemorrhages in organs or tissues they are called extravasation.
Suffusions: irregular areas of haemorrhage.
Haematoma: means a mass of blood in a tissue space caused by bleeding
Bleeding or accumulation of blood in natural body cavities is named according to
location such as:
Hydrothorax: accumulation of blood in pleural cavity.
Haemopericardium: accumulation of blood in pericardial sac.
Haemoperitoneum: accumulation of blood in the peritoneal cavity
Haematemesis: vomiting of blood.
Epistaxis: bleeding from nose.
Haemoptysis: blood in sputum
Haematuria: blood in urine
Melena: blood in feces
Metrorrhegia: bleeding from uterus.
Significance of haemorrhages:
Loss of blood by about 15 to 20% may not cause any clinical signs. Minute haemorrhage
in vital organs like brain may produce severe nervous signs, in contrast to a haematoma
or bleeding in body cavities in which it may not cause clinical effects. Bleeding into
pericardium or bronchi or bronchioles will interfere with cardiac or respiratory functions
respectively. Massive haemorrhage results in shock.
Blood loss stimulates haematopioesis which may replenish the erythrocytes and
leukocytes in a few weeks to one and half months. Persons who donate blood can do so
after about three months.
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THROMBOSIS
Intravascular coagulation of blood, in other words formation of clot in the blood vessels
of a living animal is called thrombosis. The intravascular clot is called thrombus.
Thrombus and postmortem clot:
Blood also clots after death of animal which is called postmortem clot. Postmortem clot
has to be differentiated from thrombus or antemortem clot.
Thrombus
1. Thrombus has irregular shape.
2. Its surface is generally rough and is
almost invariably attached to the
endothelium of heart or blood vessel.
3. Attached to blood vessel wall.
4. Colour and consistency variable due
to deposition of different blood
components at different periods.
5. Thrombus generally crumbles on
pressure (friable consistency).
6. Thrombus forms in living animal
Postmortem clot
1. Postmortem clot takes the shape
of the blood vessels in which it is
formed.
2. Its surface is smooth and not
attached to vascular endothelium
3. Not attached to blood vessel
wall.
4. The colour and texture is uniform
red or reddish brown. It contains
mostly fibrin and erythrocytes.
5. It is rubbery in consistency and
does not crumble easily on
pressure.
6. Postmortem clot forms after
death.
Significance of thrombus
1. Obstruction of veins and arteries.
2. Cardiac thrombi which develops in case of vegetative endocarditis cause
incompetence of valves or stenosis resulting in passive venous congestion
3. When fragments of thrombi detach from the thrombus they enter in to arterial or
venous side of circulation. They may be arrested in brain or in minute pulmonary
vessels with chances of fatal outcome.
INFARCTION
An infarct is defined as an area of the ischemic necrosis in tissues or organs due to
sudden and almost complete stoppage of blood flow in an end artery or venous drainage
of the affected area.
Ischemic necrosis is quicker if an artery is blocked and slow if a vein is blocked.
Infarction usually results from obstruction of blood in an ‘end artery’.
The most important causes of infarction are thrombosis and thrombo-embolism.
Endothelial damage by viruses are the common causes of infarction in animals. Other
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causes of infarction are pressure due to tumours or space occupying lesions, cysts,
narrowing of arterial lumen, etc.
SHOCK
Shock means collapse of blood circulation due to reduction in volume of blood or
ineffective cardiac output or due to acute generalized vasodilatation of capillary bed. The
result of collapse of blood circulation is hypoperfusion of cells and tissues leading to
death of vital cells, mainly due to hypoxia. The most vital are the heart and nervous
system.
Etiology:
The causes of shock are listed below:
1. Cardiac: cardiac output can be insufficient due to cardiac diseases such as cardiac
infarction, myocarditis, cardiac temponade, etc.
2. Hypovolaemia: reduction in blood volume due to haemorrhage or loss of fluid
(dehydration) by vomiting, diarrhea or severe burns. Reduction in 15-20% blood
volume may be compensated by increased heart rate or vasoconstriction.
3. Septic: severe bacterial infections usually of septicemic or toxaemic type can cause
shock.
4. Neurogegic or traumatic or surgical: peripheral vasodilatation may occur due to
uncontrolled anaesthesia, or injury to spinal cord, large wounds or trauma or crushing
injury of muscles.
DISTURBANCES OF GROWTH
The disturbances of growth occur at any stage of life starting from embryo to old
individuals. The science dealing with developmental defects in embryo is known as
teratology.
Aplasia: Aplasia (‘A’ denotes without; plasia means formation) is defined as complete
failure of an organ or its parts to form whereas agenesis (a= without; genesis=
development) is applied synonymously to indicate complete failure to develop during
embryogenesis.
Etiology:
1. Inherited genetic defects such as aplasia of left cecum and right kidney in chicks,
adactylia (absence of digits) and atresia ani (absence of anal opening) in calves.
2. Physical causes such as mechanical injuries and radiations initiate this disorder.
3. Chemical poisons result in aplasia. For example, thalidomide causes Amelia (absence
of limbs).
4. Prenatal bacterial and viral infections of the dam.
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There is complete absence of the tissue or organ. Aplasia involving vital organs such as
brain, heart, pituitary gland is always fatal and death is the outcome.
Hypoplasia: when the cell, tissue or organ fails to develop to its normal size, the
condition is called hypoplasia (hypo=less; plasia= formation)
Atrophy: atrophy apparently indicates shrinking. The tissue or organs are decreased in
size and shape after they get fully developed.
Hypertrophy: an enlargement in the size of the organ or tissue due to increase in size of
its constituent cells is termed as hypertrophy.
Hyperplasia: hyperplasia means an increase in the size of tissue or organ due to absolute
increase in the number of its constituent cells, in response to stimuli or functional needs.
Anaplasia: reversion of cells to primitive and undifferentiated cells.
Metaplasia: it’s the substitution of one type of matured cell or tissue into another adult
variety of cell or tissue, in response to an irritant as a protective mechanism. For example,
columnar or cuboidal epithelium can be changed to stratified squamous epithelium.
Dysplasia: (dys= abnormal; plasia= development) refers to abnormal development of
cells or tissues because of their variation in size, shape and oriental make up.
NECROSIS
Necrosis means death of cells in a living body usually due to disease.
Causes:
1. Obstruction of blood: continuous supply of oxygenated blood is essential for life of
each cell. Impaired blood supply can cause cellular death as in case of infarction
resulting from obstruction of an end artery.
2. Toxins of bacteria: many of the bacteria produce potent toxins which can directly kill
the cells. Example, alpha, beta, gamma, toxins of Staphylococci.
3. Viral infections: viruses are intracellular parasites. They do not produce any toxins
but injure the cells by various mechanisms.
4. Chemical, plant and animal poisons by way of interfering with oxidation and
metabolism.
5. Physical injury: physical injury may be caused by heat, freezing, radiation, trauma or
by parasites migrating in tissues. For example, larva of Ascaris suum in liver.
6. Immunological injury: the hypersensitivity reactions or autoimmune diseases may be
accompanied by necrosis of target cells.
7. Fungal toxins: aflatoxins cause necrosis of liver cells; Ochratoxins bring about
necrosis of kidney tubular epithelium.
Notes/Fundamentals of Veterinary Medicine
14
8. Nutritional: vitamin and selenium deficiency causes necrosis of cardiac or skeletal
muscles in new born animals. Thiamine deficiency can cause necrosis of brain tissue.
Somatic death
Somatic death means death of an organism or an individual. Earlier cessation of
respiration and heart beat continuously for at least five minutes was considered as
somatic death for medically legal declaration of death. Because by that time the neurons
are not likely to survive hence it was thought that revival of life was not possible.
However, it is now possible to revive respiration and cardiac functions for long time after
somatic death. But such revival is of value only to salvage organs for transplant but not
life of an individual.
Gangrene:
Invasion of the necrotic area by saprophytic organisms leading to putrefaction is called
gangrene. Gangrene is one of the outcomes of necrosis.
POSTMORTEM EXAMINATION
Postmortem (PM) examination is the systematic and scientific examination of tissues and
organs of a cadaver to determine the cause of death, the extent of the lesion or the nature
of illness. Terms such as “necropsy” and “autopsy” are used to designate a PM
examination.
PM examination is performed to ascertain the cause of death or for diagnosis of a disease.
Usually, it is conducted in a special room called the Postmortem Room.
Objectives of Postmortem examination
1. To arrive at a rational diagnosis.
2. To correlate clinical symptoms with postmortem lesions.
3. To assess the efficacy of the line of treatment followed.
4. For issuing an insurance certificate.
5. In medico-legal/vetero-legal cases.
Describing the post mortem lesions/organs
While describing the lesions or organs, the following points must be considered.
1. Position: whether the organ is in normal position, relation to its neighbouring
organs/structure, adhesions, if any.
2. Size: normal size, smaller, hypertrophied, etc
3. Colour: accurate description of the colour must be given- blue, light-green, dark red,
etc
4. Consistency: this must be judged by palpation. For example, soft, hard, firm, etc.
Fluids and exudates must be described as watery, serous, viscid, turbid, etc.
5. Odour: Any abnormal odour must be recorded. For example, the odour of Black
Quarter muscle is like that of rancid butter.
6. Shape: alteration of the shape if any, of organs must be described.
Notes/Fundamentals of Veterinary Medicine
15
7. Contents: the contents of pleural cavities, urinary bladder, gall bladder, intestinal
tract, etc must be described as to quantity and nature.
8. Lumen of tubular organs: the presence of strictures or dilatations must be noted.
Patent, obstructed, diverticula present, etc.
9. surface: hairy, ulcerated, covered with exudates, smooth, irregular, eroded, rough,
pitted, elevated, depressed, glistening, dull, scaly, etc
Details of postmortem examination
1. External examination- Brand marks, scars, gun shot wounds, etc must be clearly
described noting the anatomical part involved. If the animal has met with an accident,
feel the body for fractures.
a. Examinations of natural orifices- mouth, nostrils, anus, vulva, penis- look
for discharges. Note the colour of visible mucous membranes-eye, nose,
mouth, vulva. It may be congested, pale, icteric or cyanosed.
b. Note the nutritive condition of the animal- emaciated, hide-bound or in
good condition. Examine eye for corneal opacity or ulcer.
c. Presence or absence of rigor mortis must be noted.
d. Make an incision on the skin, linearly from the chin, right up to the anus
or vulva, in the center along the plane of linea alba. The hind limbs are
abducted by cutting through the medial thigh muscles opening the hip
joint.
e. As the skin is incised, the condition of the skin and subcutaneous tissues is
noticed for normal amount of fat, exudates, haemorrhage, congestion,
icterus, etc.
f. The abdomen is then opened (after removal of udder in female and
backward drawing of penis and prepuce in male) by incision along the line
of linea alba.
g. Now inspect the abdominal cavity contents. Look for fluids, observe the
position of organs, etc.
h. Remove the GIT and liver.
i. Remove the urogenital organs, adrenals and rectum.
j. The diaphragm is cut beginning at the xiphoid cartilage.
k. Inspect the pleura.
l. The structures of oral cavity and neck are then removed.
m. The thoracic aorta is removed along with other thoracic organs.
n. The head with the salivary glands attached, is removed by cutting through
the atlanto-occipital joint.
Postmortem changes
Factors influencing the occurrence of PM changes:
1. Environmental temperature: higher is the temperature faster is the onset of PM
changes. At higher temperatures, bacterial and enzymatic activity is increased, thus
degrading the tissues.
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16
2. Size of the animal: heat dissipation in larger animals is slow which increases bacterial
and enzymatic activity.
3. External insulations: External insulations such as hair coat, wool, etc help retain heat
which enhances bacterial and enzymatic activity.
4. Adiposity of the animal: it refers to the fat content of the animal. Fat layer provides
insulation thereby retaining heat in the body.
5. Species of the animal: e.g., Swine have soft muscles so faster PM changes as
compared to horse.
Important postmortem changes
1. Algor mortis: cooling of the body after death. It usually starts at stoppage of
circulation or before stoppage of circulation. When an animal dies suddenly, cooling
of body occurs at stoppage of circulation. In chronic disease conditions, it occurs
before stoppage of circulation.
2. Rigor mortis: It’s the stiffening of the body with contraction of muscles leading to the
rigidity of the body. Presence or absence of rigor mortis can be understood by;
o Trying to flex the limbs.
o Trying to open the mouth
o Trying to depress the neck
The different stages of rigor mortis are:
o Rigor mortis setting in: stiffness in cranial portion (usually 2-6 hours after
death).
o Rigor mortis set in: whole body is stiff. It occurs usually between 6-12 hours
after death.
o Rigor mortis passing off: the cranial portion is relaxed while the caudal
portion is stiff.
o Rigor mortis passed off: the whole body is in a relaxed state. This stage of
rigor mortis can be differentiated from rigor mortis not set in by PM
discolouration, decomposition, and distension which are seen while rigor
mortis has passed off.
3. Livor mortis: it’s the bluish or bluish-purple discolouration of the tissues due to
gravitational settling of blood. Livor mortis is also known as PM staining or
hypostatic congestion. Livor mortis usually occurs by 4 hours after death and reach
maximum at 6- 12 hours after death. Livor mortis is highly appreciable in lungs,
kidneys and skin.
4. PM decomposition: PM decomposition refers to degradation of soft tissues in the
body. It is usually brought about by two factors:
o Bacteria- putrefaction
o Enzyme- autolysis
5. P.M. discolouration: it refers to any deviation from normal colouration which occurs
after death.
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o Red colouration- due to imbibation of hemoglobin
o Yellow discolouration: due to imbibation of bile
o Greenish-yellow to greenish black- due to deposition of melanin in abnormal
locations (pseudomelanosis)
6. P.M. clots: blood clots within the vessel after death.
7. PM emphysema/distension/bloat: it results from accumulation of gases that are due
to PM decomposition. It can occur anywhere in the body.
8. PM displacement of organs: PM displacement occurs due to excessive accumulation
of air and handling of carcass.
9. PM rupture of organs and tissues: Excessive accumulation of gases may result in
PM rupture. Antemortem rupture shows blood clot, haemorrhages and congestion at
the affected site.
Neoplasms
The terms tumour and neoplasm are used synonymously to mean any new growth of cells
or tissues.
Although the very name tumour means swelling, but all swellings are not tumours such
as haematomas, cysts, nodules or granulomas in chronic inflammations, abscesses, etc.
these pathological processes are developed by known etiological agents and they cease
when the causative agents are removed. However, in a tumour, the proliferative growth is
purposeless, persisting and progressive.
In hyperplasia, we also observe proliferation of cells in response to functional needs of
the body, hormonal stimulation, infection or other stimuli, although the condition may be
adaptive compensatory as in the case of cardiac hypertrophy in race horses and
greyhound dogs. This proliferation of cells is limited in amount and purposeful. It is
terminated and regressed when the stimulus is withdrawn.
By definition, a tumour or neoplasm is a growth of cells that proliferate without control,
retain considerable resemblance to the parent cells from which they arise, and serve no
beneficial function to the body. The growth persists in the same fashion even after the
cessation/removal of the stimuli and the growth lacks orderly structural arrangement.
Oncology: a branch of pathology that deals with the study of all neoplastic growth
irrespective of their behaviour pattern- benign or malignant.
Cancer: (Cancrum, latin means crab): refers to all types of malignant neoplasms
irrespective of their origin.
Carcinoma: all malignant neoplasms of epithelial cells of either glandular or nonglandular type.
Sarcoma: term used for all malignant neoplasms of connective tissue including muscular,
lymphoid and haemopoietic tissues.
Carcinogenesis: the conversion of a normal cell in to a cancer cell.
Carcinogens:the agents involved in the process of carcinogenesis.
Metastasis: transport of neoplastic cells and their remnants from the primary site to other
location, where they set a new growth which behaves as the primary growth. Such growth
Notes/Fundamentals of Veterinary Medicine
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is a metastatic or secondary neoplasm. Carcinomas normally metastasize by lymphatics
and sarcomas by blood or through tissues by infiltration.
Classification:
1. Based on the shape: the shape of neoplastic growths vary and may be round or oval,
elliptical, polypoid, wart-like, spherical, multilobulated, etc.
2. Based on the cell or tissue of origin: on this basis, all neoplasms are classified as
epithelial, connective tissue (including muscles), lymphoid, haematopoietic, neural
and other tissue neoplasms according to the cells/tissues of origin.
The suffix –oma is used for benign growth of epithelial and mesenchymal tissues. In
malignant neoplasm, the suffix carcinoma, if the growth arises from the epithelium or
sarcoma when it is of mesenchymal origin.
Histogenic classification of neoplasms:
Cell/tissue of origin
Epithelium
Non-glandular
Glandular
Benign
Malignant
Papilloma
Adenoma
Squamous cell carcinoma
Adenocarcinoma
Connective tissue
Mature
Immature
Fat cells
Mast cell
Bone
Cartilage
fibroma
Myxoma
lipoma
mast cell tumour
osteoma
chondroma
Fibrosarcoma
Myxosarcoma
Liposarcoma
Malignant mast cell tumour
osteosarcoma
chondrosarcoma
Muscular tissue
Smooth muscle
Striated muscle
leiomyoma
rhabdomyoma
leiomyosarcoma
rhabdomyosarcoma
Haemopoietic tissues
Myeloblasats
Erythroblasts
-
Myeloid leukaemia
Erythroid leukaemia
Lymphatic tissues
Lymphoid cell
Blood vessels
Lymph vessels
Melanocytes
lymphoma
haemangioma
lymphangioma
melanoma
Lymphosarcoma
Haemangiosarcoma
lymphangiosarcoma
melanosarcoma
Neural tissues
Neurons
Glial cells
Nerve sheath
glioma
neurofibroma
neuroblastoma
glioblastoma
neurofibrosarcoma
Notes/Fundamentals of Veterinary Medicine
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Mesenchyme: the cells within the embryo that develop into connective tissue, bone,
cartilage, blood, and the lymphatic system.
3. Based on behaviour pattern: Benign and malignant
Comparative features of benign and malignant neoplasms
Features
Benign
Malignant
a. Growth rate
Slow without prominent
mitosis
Expansion
Normally capsulated
Circumscribed
Rapid with mitosis
b. Nature of growth
c. Capsule
d. Limit
e. Metastasis
f. Recurrence after
removal
g. Prognosis
h. Haemorrhagic
degeneration and
necrosis
Never occurs
Rare
Invasion and infiltration
Mostly noncapsulated
Unlimited/poorly
defined
Always occurs
Frequent
Favourable
Seldom seem
Always poor
Frequently seen
Etiology of neoplasms:
I. Chemical carcinogens- Some chemical and other biological carcinogens are listed
below:
Name of the chemical/biological
component
Target organ
Coaltar and soot
Nickel compounds
Chromium compounds
Arsenic compounds
Benzene
Asbestos
Aflatoxin B1
Phenacetin
Azodyes and aromatic amines
Skin, lungs
Lungs, nasal passage
Lungs
Skin, lungs
Blood cells (leukaemia)
Lungs
Liver (fish, ducks)
Pelvis of kidney
Bladder, liver
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II. Oncogenic viruses
a. DNA viruses
i. Papilloma viruses .e.g., bovine papilloma virus, human papilloma
virus
ii. Hepatitis B virus causes hepatocellular carcinoma.
iii. SV40 or Polyoma virus.
iv. Adenoviruses
b. RNA viruses- all RNA tumour viruses belong to the retrovirus group.
III. Parasites: fibrosarcoma due to Spirocerca lupi in dogs
IV. Physical causes: x-rays, UV rays and ionizing rays are known to produce cancer in
human beings and animals
V. Chromosomal abnormalities:- chromosomal abnormalities either in their number or
structure can lead to oncogene activation. Example: Wilms tumour, disseminated
neuroblastoma, etc show chromosome defects.
VI. Hormones: hormones in general have a strong control on the metabolism and
growth of their target tissues. Sex hormones play a major role in hormone dependent
tumours. For example, cancer of prostrate gland apparently induced by testosterone.
The cancer can be controlled by orchiectomy or by injections of estrogen. In bitches
the incidence of mammary tumours gets drastically reduced by overiectomy which
removes the effect of estrogen and progesterone on the gland. Crytorchidism in dogs
favour development of sertoli cell tumours of testes.estrogen may act as a
cocarcinogen since its administration over long periods can lead to cancer of uterus,
mammary gland, testes, etc.
In general, the hormones are associated with the cancer of target organs.
VII. Food: food may be contaminated with carcinogenic substances like aflatoxin B
produced by the fungus Aspergillus flavus. Chronic aflatoxicosis may be associated
with hepatocellular carcinomas in some animals.
VIII. Heredity: heredity plays a role as a promoting factor for carcinogenesis. For
example, the cancer of eye in cattle is more in Hereford cattle. Boxers and terrier
breeds of dogs have high incidence of tumour.
IX. Sex: The incidences of tumours in the two sexes differ from breed to breed.
Tumours are more common in female dogs than in the males while in cats it’s more
in males.
X. Age: tumour incidence in general increases in direct proportion to age. But some
cancers, for example, embryonal nephroma in pigs, canine histocytomas in calves
occur in younger age. The higher incidence of cancer with age possible occurs due
to more mutogenic effect in the older animals or due to declining immune
competence or both.
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Pigmentations
Abnormal deposition of coloured substances of diverse origin in the cells or tissues is
called pathological pigmentation. The pigments may be formed within the body and
they are called endogenous pigmentation. If the pigments come from outside the body
such as medicines, plants, etc are called exogenous.
Exogenous pigments: carbon or coal, lead compounds, tattoo pigments, etc
Endogenous pigments: melanin, iron, bile pigments, haemoglobin pigments, etc.
Fatty changes
Fatty change means abnormal accumulation of fat in the cells which normally do not
show fat I microscopically visible form. Fatty change may occur after cellular
swelling or even independently. Fatty change is seen mostly in liver cells, tubular
epithelium of kidneys and heart muscles.
Etiology and pathogenesis: appearance of fat in parenchmatous cells in which it is not
normally found is called fatty metamorphosis which is supposed to be due to
accumulation of fat which should normally be mobilized after formation of
phospholipids with the help of lipotrophic factors. The causes of fatty change are:
1. Overfeeding of carbohydrates, fats or B vitamins: in poultry a condition called
fatty liver is due to feeding of high energy ration.
2. Deficiency of lipotrophic factors: deficiency of choline, methionine, inositol
and other lipotrophic factors can help in inducing fatty changes especially in
liver, kidney and heart.
3. Vitamin E and selenium deficiency: vitamin E and selenium help in preventing
degeneration and necrosis of liver cells particularly in low protein diet.
4. Toxins such as aflatoxins produced by fungus Aspergillus flavus and other
fungal species, chemical poisons like carbontetrachloride, phosphorus, lead,
arsenichelp in fatty changes in liver.
5. Alcohol intake and cirrhosis: in alcoholics, in nutritional cirrhosis and
pancreatic disease the fatty changes can be attributed to lack of availability of
protein, or poor quality of food or due to inadequate digestion of protein in
pancreatic diseases.
6. Advanced and chronic anaemia or anoxia: in cases of iron deficiency anaemia
of piglets, fatty changes in liver, kidneys and heart are remarkable. Lack of
oxygen to vital cells result in lack of glucose metabolism.
Calcification:
Calcificatrion means grossly or microscopically visible deposition of calcium salts in
soft tissues i.e., other than bone and teeth. The calcium salts which are usually
deposited are calcium phosphjate and calcium carbonate.
The term ossification is used for deposition of calcium salts in bones while the term
chondrofication is used for deposition of calcium salts in cartilage.
In the normal body calcium salts are precipitated only in bones, cartilage and teeth.
Therefore, calcification of soft tissues is pathological.
Pathological calcification may be classified into two main types:
1. local or dystrophic calcification
2. general or metastatic calcification
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Local or dystrophic calcification is the deposition of calcium salts in a local area of
tissue which is degenerated, dying or dead. This type of calcification is more
commonly encountered than the general calcification.
Hypercalcaemia is not necessary for this type of calcification and it occurs when the
amount of calcium in the blood is normal (about 10mg/dl). It may occur in any organ
or tissue. The most common disease is tuberculosis where calcium salts are deposited
in the central area of necrosis. It also occurs in old infarcts, in the areas of fat necrosis,
in atherosclerosis of arteries, degenerating tumours, chronic parasitic lesions, etc.
General or metastatic calcification is the deposition of calcium salts in many tissues
in several organs at a time throughout the body. This type if calcification occurs in
previously normal tissues. It can occur in all the tissues and organs but the most
common sites are tunica media of arteries, kidneys, lungs and gastric mucosa.
General or metastatic calcification occurs when there is persistently high
concentration of calcium in the blood (more than 12mg %). Any factor which causes
hypercalcaemia will also result in this type of calcification. The causes of
hypercalcaemia are the following:
 hyperparathyroidism
 excess vitamin D in the diet
 decreased secretion of calcitonin hormone
 chronic hypomagnesaemia
 variety of chronic debilitating diseases such as Johne’s disease
Macroscopic appearance of calcification
Small amounts of calcium deposits are within tissues are usually not observed. Large
deposits appears as white or grey, chalky masses within the tissue. Calcified tissue has
a firm consistency. If the calcified area is incised with a knife, a definite gritty sound
and feeling can be detected against the edge of the knife.
Microscopic appearance
In haematoxylin and eosin stained sections, calcium salts appear as purplish to deep
blue granules or masses. They take colour from the basic haematoxilin stain. Calcium
salts can be confirmed by special stains such as von Kossa and alizarine Red-S stains.
With von Kossa stain, calcium salts appear as black spheres or masses within the
tissue. With alizarine Red-S stain, calcium salts appear as red granules or masses.
Significance of calcification depends on the organ affected. If it occurs in the aorta
and arteries their elasticity is lost. If it occurs in the interalveolar septa of lungs, the
normal gaseous exchange will be interfered. When it occurs in kidneys renal failure
results. Calcification of flexor tendons of limbs will lead to difficulty in movements as
it occurs in Manchester wasting disease.
Concretions or calculi
Concretions or calculi are abnormal, solid usually stony hard or soft masses of
minerals in varying proportion with organic matter.
Calculi are usually formed in hollow organs such as pelvis, ureter, urinary bladder,
gall bladder, and intestine, ducts of pancreas or salivary glands but sometimes they
may develop in kidney parenchyma. Various names are given to concretions
depending on locations. The most common site is urinary organs in which they are
Notes/Fundamentals of Veterinary Medicine
23
called uroliths and the pathological condition is called urolithiasis. The names of
calculi are listed below:
Location
Name of calculi
Common/clinical name
Urinary system
Gall bladder
Intestine
Pancreatic ducts
Salivary glands
Tooth
Uroliths
choleliths
enteroliths
pancreatic calculi
sialoliths
dental calculus
Urinary calculi
gall stones
intestinal calculi
pancreatic calculi
salivary calculi
dental tartar
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