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91 Cards in this Set

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  • Back
Define somatic death
The disappearance of life from the individual.
List the four predictable changes associated with somatic death
1) Cooling (aka algor mortis)
2) Rigor mortis
3) Blood changes
4) Post mortem degeneration
Describe the factors that control the rate of post mortem body cooling.
1) initial temp of the body
2) insulation (fat, fibre or housing)
3) external temp
4) glycogen reserve in muscle
5) muscle pH
6) antemortem muscle activity
Describe rigor mortis
General stiffening of muscles that sets in approx 1-9 hrs after death.
Due to the contraction of muscle fibres as their ATP source is depleted (a state of muscle relaxation requires a source of energy). Occurs in the defined order - head, heart, diaphragm then limbs. Degree of onset dependent on environment and state of the individual.
Describe the blood changes associated with post mortem changes
Blood accumulates in gravity dependent parts of the body.
'Currant jelly' clots are formed post mortem and are distinguished by being able to peel away from the intima of the blood vessel.
'Chicken fat clots' are formed due to the sedimentation of RBC's - indicates that the animal took some time to die. Esp in horses due to rouleaux formation.
Distinguish between ante and post mortem clots
Ante-mortem clots are pink, dull and adhere to the wall of the blood vessel.
Post mortem clots are deep red, shiny and peel away.
Describe post mortem degeneration
Decay of the the body/organs
1) autolysis. Affects the whole organ due to to release of enzymes from lysozymes.

2) Putrefaction. Breakdown of body protein by saprophytic microorganisms. Produces gas, odour, discolouration of tissue through various pigments.
Describe reversible cell injury (cell degeneration)
Results form dysfunction of the membrane bound sodium/potassium pump. Intracellular Na increases, drawing in water - leads to swelling. Can continue to a point at which ribosomes detach which then compromises cell function. If the damaging stimulus is severe or repeated this can progress to cell death.
Describe irreversible cell injury (cell death)
Results from sever mitochondrial vacuolisation, extensive membrane damage, lysosymal swelling and calcification of mitochondria. Results in the leakage of lysosomal enzymes into the cell and its external environment. Ca rushes in, leading to further mitochondrial dysfunction.
Severe mitochondrial dysfunction and membrane damage are definitive to irreversible cell death. Describe the mechanisms of membrane damage.
1) increased intracellular Ca activates endogenous phospholipase which depletes membrane phospholipids
2) cytoskeletal defects caused by cell swelling, inc detachment of the cell membrane from the cytoskeleton
3) production of free radicals esp in reperfusion injusry
4) lipid breakdown products produced through phospholipase activity have a detergent effect on membrane components.
What are the causes of cell damage?
1) hypoxia
2) free radical damage
3) physical agents
4) chemicals
5) immunological reactions
6) genetic defects
7) nutrition
8) aging
9) microbiological agents
Describe the appearance of cellular degeneration
1) cell swelling
2) increased cytoplasmic eosinophilia
3) fatty change
Define necrosis
The local death of cells within a living individual. The siginificance of the necrosis depends on site, size speed of progression and sequelae
Describe the morphological changes associated with necrosis.
Nuclear changes;-
1) pyknosis = a shrunken dark staining nucleus (with H&E) due to condensation of chromatin
2) karyorrhexis = fragmentation of the nucleus. Fragments may appear pyknotic.
3) karyolysis = nuclear loss of affinity for basic dye. Fades away essentially.
Describe in detail the four types of necrosis
1) coagulative necrosis = necrosis in which the original tissue architecture remains, though cellular detail is lost. Caused when autolysis is delayed by slow endogenous enzyme action or absence of extracellular lytic enzymes
2) caseous = necrosis in which both cellular and tissue architecture is lost. Caused by specific bacterial infiltration inc. Mycobacteria tuberculosis
3) liquefactive = disintegration of necrotic tissue into a liquid mass. Complete obliteration of any cell or tissue detail. Often seen in the CNS or from the action of pyogenic bacteria. Aided by the presence of neutrophils producing hydolytic enzymes.
4) fat necrosis = involves the breakdown of fat into glycerol and FAs. FAs combine with Ca, K or Na to form soaps.
Describe the desposal of necrotic tissue.
1) liquefaction. Commonly occurs when the necrotic area is small, the tissue enzyme rich and moist and neutrophils are in the vicinity.
2) liquefaction with pus formation or suppuration. Pyogenic bacteria. Formation of pus within a tissue leads to an abscess, which has a tendency to expand towards the point of weakness in the tissue and burst.
3) encapsulation w/o liquefaction is known as sequestration. Produced in situations where there are very little lytic enzymes or the tissue is dry. Necrotic region stimulates an immune response and a fibrous capsule is laid around the area. The necrotic area may become more inspissated and eventually replaced by fibrous tissue
4) Erosion/ulceration. Detachment of dead cells form the underlying living tissue of the body surface into the surrounding space of lumen. Erosion means loss of epithelial cells, while ulceration involves the basement mmb as well.
5) organisation/repair. Invasion of the necrotic tissue by leucocytes, capillaries and fibroblasts to repair the damage and form living tissue.
6) regeneration. Dead cells are replaced by division of the remaining cells that escaped damage. Not possible in post mitotic tissues.
Define gangrene and its classification
Ischaemic necrosis of extremeties.
1) dry. Uncomplicated ischaemic necrosis.
2) moist. Complicated by presence of bacteria. Normal body defence mechanisms are not present in dead tissue.
3) gas. Gangrene produced by the bacterial genus Clostridia. Anaerobic spore-forming saprophytes produce necrotising exotoxins (and thus produce a viscious infiltration cycle)
Describe the appearance of gangrenous tissue
Cool to the touch, unresponsive to stimuli and will not bleed upon incision.
Dark colour due to the presence of anoxic blood, haemosiderin and iron sulphie (breakdown of SH containing aa's produce hydrogen sulphide which reacts with RBCs to produce iron sulphide - responsible for the foul smell). Often has a marked line of demarcation. Absorption of toxic breakdown products can produce systemic toxaemia and death.
Define apoptosis
Programmed cell death that, unlike necrosis, occurs without inflammation and release cell contents.
Define atrophy
Organ, tissue or cell that is smaller than normal. Due to the individual cells shrinking. The organ, tissue or cell MUST have reached it's potential normal size and shrunken to be determined as atrophic, thus the distinction between atrophy and hypoplasia.
Define hypertrophy
Organ, tissue or cell that is larger than normal. Due to the individual cells enlarging. Can be both physiological or pathological. Hypertrophy is the only option for enlargement of post mitotic cells
Define hypoplasia
Incomplete growth of and organ or tissue. Marked degrees of variability in the condition form complete lack of an organ/tissue (aplasia or agenesis) to only a small decrease in size. Atresia refers to a congenital (not acquired) lack of a lumen.
Define hyperplasia
An increase in the number of cells in an organ/tissue. Can increase the gross size of the tissue. Limited to cells that have the ability to divide.
Define dysplasia
Describes the lack of normal histological architecture. Can either be congenital or acquired. Such as hip dysplasia as congenital and tissue healing as acquired.
Define metaplasia
The acquisition of one fully differentiated cell type fromt the original. It is NOT a neoplastic change and the cells are completely normal. Often stimulated in response to chronic irritation.
Define hamartoma
An improper mix of NORMAL tissues within an organ.
Define purulent exudate.
A highly cellular inflammatory exudate composed mainly of neutrophils and necrotic debris.
Define fibrinous exudate.
An exudate composed largely of fibrin due to the activation of coagulation. An increase in vascular permeability stimulates the change from serous to fibrinous exudate.
Define serous exudate.
A high protein exudate lacking normal cellular components. Resembles plasma
Differentiate between granulation tissue and granulomatous inflammation.
Granulation tissue is the new tissue formed in repair and wounds of soft tissue. Consists of the connective tissue forming fibroblasts and angiogenesis forming new blood vessels.

Granulomatous inflammation is a sub type of chronic inflammation where the body fails to rid itself of the causative agent. It is characterised by often focal collections of macrophages, epithelioid cells and multinucleated giant cells.
What is the distinction between a transudate and an exudate?
An exudate is an inflammatory extravascular fluid with a high protein concentration, cellular debris, and specific gravity above 1.020.

A transudate is an extracellular fluid of low protein content and specific gravity of less than 1.012.

A transudate occurs with an intact endothelium, and results from a net increase in capillary hydrostatic pressure.

In contrast, an exudate results from a significant increase in permeability of the endothelium of blood vessels leading to an outpouring of protein rich fluid.
What are the 5 cardinal signs of inflammation and what are they a direct result of?
Redness from tissue hyperemia
Warmth from tissue hyperemia
Swelling from tissue oedema
Pain from vasoactive amine stimulation of nociceptors
Loss of function from a combination of all of the above
What are the major categories of mediators of the inflammatory response and important mediators in each category?
a) Vasoactive amines, including histamines and serotonin;

b) Plasma proteases consisting of three interrelated systems: the kinin system, the complement system, and the clotting system;

c) Arachidonic acid metabolites, namely prostaglandins and leukotrines;

d) Products of neutrophils including cationic proteins, acid proteases and neutral proteases;

e) Products of monocytes and macrophage including enzymes, lymphokines, monokines, and cytokines;

f) Oxygen derived free radicals;

g) Platelet activating factor.
What are the hallmarks that differentiate between acute and chronic inflammation?
Acute inflammation involves the accumulation of fluid in the tissue space(interstitial edema), altered microvasculature, platelet stimulation and the presence of PMNs particularly neutrophils.

Chronic inflammation involves
interstitial fibrosis, the presence of lymphocytes, plasma cells (clock face nucleus) and macrophages/monocytes
Define inflammation.
Inflammation is the stereotypic, complicated, vascular and cellular response of an individual to a non lethal irritant.
Define dystrophic calcification
The local deposition of calcium salt in dead or dying tissues and is a common occurance. It is NOT accompanied by hypercalcaemia. The pathogenesis of the mechanism is complex, but most likely involves a local increase in Ca and phosphate ions, breakdown of substances able to bind calcium and phosphate in their non ionic form and the release of inorganic phosphate from organic phosphate (through the action of lysomal phosphatase)
Define metastatic calcification
Occurs through elevated levels of calcium and phosphate in the blood. It is a systemic manifestation of a disturbance in the calcium and/or phosphate level. Deposits are characteristically in the blood vessel wall, gastric mucosa, bronchi and alveoli, renal tubules and thoracic pleura.
Describe four causes of metastatic calcification
a) Primary hyperparathyroidism (results from a functional PTH secreting tumour, or overdose of PTH. Increased PTH leads to excessive osteoclastic breakdown of bone mineral, producing an increase in blood calcium and phosphate. This is rare in animals.
b) Secondary hyperparathyroidism is most commonly caused by renal failure.
c) Pseudohyperparathyroidism can be produced when certain neoplasms can produce a PTH analogue.
d) Excessive vitamin D. Promotes retention and resorption of calcium and phosphate from the bone, gut and kidneys. Essentially overloads the system. Commonly caused by ingestion of Vit D based rodenticides or certain plant species.
Outline the mechanism by which renal failure can produce metastatic calcification.
Phosphate is actively secreted by the kidneys, and levels can be maintained partly by the reabsorption in the tubular epithelium. The control over this is via PTH - inc PTH inc the phosphate in the urine. In renal failure, the excretion of phosphate is impaired due to the loss of renal tissue. Results in the accumulation of phosphate in the blood. Should the ionic constant for the two ions be exceeded, calcium and phosphate will combine and precipitate into tissue, and some of the complex is lost through the GIT. This leads to an overall decrease in blood calcium, which then stimulates PTH secretion. This increases the osteoclastic activity releasing calcium, but also phosphate. PTH also attempts to promote decreased reabsorption of phosphate, but since renal function is compromised, this isn't possible.
List the clotting factors involved in the following pathways:

a) intrinsic
b) extrinsic
c) common
Intrinsic = XII, XI, IX and VIII
Extrinsic = VII
Common = X, V and II
Which part of the coagulation cascade to the following diagnostic tests assess?

a) ACT
c) PT
d) TT
Activated clotting time asses the intrinsic and common

Activated partial thromboplastin time assess the intrinsic and common

Prothrombin time assess the extrinsic and common

Thrombin time assess the converstion of fibrinogen to fibrin
Define thrombus
A solid structure formed within the flowing blood stream from the normal constituents of blood
Define thrombosis
The process by which a thrombus forms
Define embolus
An abnormal mass circulating in the blood stream
Define embolism
The process by which an embolus becomes lodged and occludes a blood vessel.
What are the three components of Virchow's triad for the pathogenesis of a thrombus? Give an example for each. Which of the three is the most important initiator?
Endothelial injury (through direct trauma, inflammation, or infectious agents and such)

Abnormal blood flow (through dilated veins, disturbance to laminar flow)

Changes to coagulability (dehydration and some drugs)

Endothelial injury is the single most important initiating factor, while the other two are important since they influence the progression and severity of the thrombus
List the possible fates of a thrombus that remains attached to the vessel wall.
a) A small thrombus may undergo lysis by the plasminogen/plasmin system

b) If the occluding thrombus is fibrin rich, it may shrink, permiting blood to pass. This new channel will become lined by endothelium and is thus termed recanalized

c) A thrombus remaining after partial lysis and recanalization may become organised. The thrombus will be invaded by fibroblasts and new capillaries - forming granulation tissue. This new tissue eventually forms dense fibrious tissue. Organised thrombi may eventually become calcified.

d) The thrombus may at some point detach to form and embolus

Define anaplasia and state its microscopic features.
Lack of differentiation. Characterized by pleomorphism, anisocytosis, anisokaryosis, hyperchromasia, high nuclues:cytoplasm ration, chromatin clumping, large numbers of mitotic figures and heterokaryons
Outline the steps in primary haemostasis.
Damaged blood vessels constrict (local axonal reflex). Damaged endothelium has exposed collagen, platelets attach to the collagen via vWF (stored in endothelial cells and released upon damage). Once adhered to collagen, platelets change shape and are now activated. This results in exposure of binding sites (on the platelets) which allow platelet-platelet binding, and sites for clotting factors. They release factors which increase platelet adhesion and aggregation (ADP and thromboxane). These mediators also activate fibrinolysis, inflammation and secondary haemostasis.
What is the main component of secondary haemostasis?
How is fibrin produced?
Thrombin produced by the intrinsic and extrinsic cascade activates fibrinogen, which then produces fibrin.
How is the clotting cascade triggered?
The intrinsic pathway is triggered by the contact of blood with negatively charged surfaces eg. collagen. This pathway is known as intrinsic because all of the components needed are found in the blood.

The extrinsic pathway is activated by tissue factor produced by damaged endothelium.

All components of the cascade must be present and functional for secondary haemostasis to work.
What are the two other essential factors for the clotting cascade?
Calcium ions are essential cofactors for many of the clotting factors. This fact is exploited by the use of EDTA in blood sample tubes (chelating agents removes calcium so the blood won't clot)

Platelet factor 3 (phospholipid found on platelets) helps to confine the deposition of fibrin to the primary platelet plug
What is the role of thrombin?
Activates platelets, activates fibrinolysis, has an autocatalytic effect and converts fibrinogen to soluble fibrin.
What are the constituents of Hb?
4 subunits of globin each of which contains a molecule of heme (tetrapyrollic ring with a central atom of Fe)
Distinguish between extravascular and intravascular haemolysis.
Extravascular haemolysis involves diseases in which large numbers of RBCs are damaged, resulting in greatly inc. removal and haemolysis by splenic macrophages. egs inc Mycoplasma haemofelis.

Intravascular haemolysis involves the breakdown of RBCs directly in the blood vessels, so that Hb is released into the plasma (haemoglobinaemia). Should the level in the blood increase it may spill through the glomerular tuft to produce haemoglobinuria.
What is haemosiderin?
An insoluble yellow pigment consisting of iron (from heme) complexed loosely with protein.
What is ferritin?
A soluble storage form of iron complexed with another protein
What is the fate of the iron freed from the breakdown of RBCs
Haemosiderin or ferritin.
What is haemosiderosis and when would it be produced?
Large accumulation of haemosiderin. Can be produced in systemic overload of iron such as in haemolytic disease, diseases involving impaired iron utilisation, blood transfusions or increased dietary absorption of iron.
What is bilirubin?
The remnant of heme once the iron has been removed to form haemosiderin or ferritin. Its a linear tetrapyrrolic orange pigment, and becomes 'loosely' bound to albumin.
What happens to the bilirubin in circulation?
A small amount of it is normal. Because it is relatively insoluble, it is taken up by the liver and conjugated with glucuronic acid. It is then excreted in the bile
What are urobilinogens?
Formed from bilirubin in the intestine. Some of it is reabsorbed, then oxidised and excreted in the urine (which makes it yellow)

The rest that's left behind is oxidised to stercobilin, which makes faecal matter brown.
Define icterus.
Abnormal accumulation of bilirubin in the tissues, producing the characteristic yellow colour of mucous membranes and sclera.
What are the three causes of icterus?
Haemolytic or pre-hepatic
Toxic or hepatic
Obstructive or post hepatic
Outline the mechanism of pre-hepatic icterus.
Results from the increased breakdown of RBCs, which can either be intra or extravascular. NB that free Hb is only seen in the plasma in intravascular haemolysis.

egs inc. certain Leptospira spp, Mycoplasma haemofelis, blood transfusions, neonatal icterus.
Outline the mechanism of hepatic icterus.
Occurs when there is significant damage to the liver to such an extent that the conjugation of bilirubin and excretion is compromised. Can be produced by any condition that results in significant liver damage.

egs include certain Leptospira causing hepatocellular necrosis, infections such as canine infectious hepatitis and copper poisoning.
What is the main mechanism by which copper poisoning leads to hepatic icterus?
Excessive copper is mainly stored in the liver, and may reach toxic levels leading to hepatocellular necrosis. This releases copper into the liver, potentiating further liver damage. Damage disrupts the livers ability to conjugate and excrete bilirubin.
What is the secondary mechanism by which this occurs?
Released copper from necrotic hepatocytes spills over into the circulation, and once it exceeds the carrying capacity of plasma proteins it can damage the membranes of RBCs. This vacilitates intravascular haemolysis.
Outline the mechanism of post-hepatic icterus.
Occurs when there is obstruction to the excretion of conjugated bile from blockage of the duct system aka cholestasis. Can either be extra or intra-hepatic. Extra hepatic occurs when there is blockage of the large bile ducts that drain the liver, while intra hepatic occurs when there is blockage of the bile canaliculi
What is haematoidin?
A yellow/brown pigment derived from blood found in sites of local haemorrhage in tissues with low oxygen tension. Does not contain active iron
What are porphyrins?
A group of pigmented compounds, some of which are precursors of Hb synthesis. Inherited defects in porphyrin metabolism results in the accumulation of the substance in teeth and bone, makeing them pinky/brown and fluroesent. May cause photosensitivty in tissues containing it.
What is amyloid?
An amorphous eosinophilic extracellular material that is sometimes deposited in tissues. Contains glycoproteins arranged in a beta pleated sheet.
How is amyloid formed?
The glycoproteins come from incompletely degraded proteins, notably immunoglobulin light chains and an acute phase protein known as serum amyloid A. Associated with chronic inflammatory processes
Describe glycogen infiltration.
Has an osmotic effect on cells, making them swell aka hydropic degeneration. Often occurs in damaged hepatocytes, myocardial cells and renal tubular epithelium.
What is ceroid and how is it formed?
Ceroid is a lipopigment formed during the degeneration of lipids. Free radical oxidation of unsaturated FAs is important. Necrotic fat is taken up by macrophages and combined with proteins to produce ceroid.
What two things can cause increased blood in the terminal vascular bed?
Hyperaemia and congestion. Hyperaemia is an active acute process involving more blood being pumped through the TVB. It can either be pathological or physiological.

Congestion is produced because of obstructed venous outflow from the TVB. Can be produced by physical obstruction, failure of flow (such as in CHF)

Both tissues are red, but congested tissue is darker because of the deoxygenated Hb.
What are the subtypes of congestion?
Localised, systemic and hypostatic.

Localised is due to a restriction of venous flow from a small area. Can be due to an embolism/thrombus, tight tourniquet, tumour etc

Systemic congestion is commonly seen in heart failure as deficient forward flow results in the blood backing up in the great veins and affecting a number of organs.

Hypostatic congestion occurs due to the force of gravity. Occurs because of peripheral circulatory failure and relaxed blood vessels.
What may limit the effects of congestion?
Gradual onset allows the development of collateral circulation
What are the effects of congestion?
Oedema, ischaemia, diapedesis or haemorrhage.
Define ischaemia
Inadequate blood supply to an organ relative to its needs.
What are the consequences of ischaemia?
Anoxia or hypoxia, nutrient deprivation, and accumulation of metabolic byproducts. Oxygen deprivation is the most important factor because what the small amoung of nutrient that gets through wouldn't be metabolised anyway because oxygen is so limiting. The accumulation of byproducts causes pain in muscle ischaemia.
What are the factors that determine the effects of ischaemia?
Sensitivity of the tissue to hypoxia, duration of onset, degree of oxygenation ie anaemia is not a good thing and temperature of the tissue (since cooling reduces metabolic rate)
Define reperfusion injury.
Phenomenon by which ischaemic injury worsens when blood supply is restored. Postulated that the resupply of oxygen increases the production of oxygen free radicals.
Define infarction.
An infarct is a localised area of necrotic tissue that occurs as a result of ischaemia. The process by which this occurs is known as infarction. Commonly occurs in organs with a terminal vascular bed.
Describe the development of an infarct.
An artery becomes obstructed, and this reduces the hydrostatic pressure in the capillary bed, dragging the blood back. The endothelium will become hypoxic and the blood vessels become leaky, fluid leaches out into the interstitium. The hypoxic tissue degenerates and begins to swell. This swelling pushes fluid out of the region, and this combined with the lysis of leached RBCs means the area lightens. Necrotic tissue stimulates an inflammatory response, line of demarcation produced. Assuming the infarct isn't lethal, eventually macrophages invade, and fibroblast lay down a ECM to result in fibrosis.
Describe the compensatory mechanisms for haemorrhage.
Redistribution of blood by splanchnic and cutaneous vasoconstriction. Contraction of the spleen. Restoration of plasma volume (intravascular capillary pressure in deflated capillary beds draws in extravascular fluid). Replacement of RBCs via erythropoiesis, seen as reticulocytes in the blood.
Haemorrhagic diatheses
Predisposition of haemorrhage associated iwht disorders of the clotting cascade, disorders of the vascular system (inc vasculitisfrom endotheliotropic viruses, bacterial toxins, parasites or weakness of the endothelial connective tissues inc. inherited and congenital defects in collagen formation.
Outline the pathogeneis of DIC.
DIC is widespread, generalized activation of clotting. Whenever clotting is activated, so is fibrinolysis. Fibrinolysis products (FDPs) also have an anticoagulant effect. But the stimulus that triggered clotting in the first place is still there, so clotting is still occuring else where. This depletes platelets and clotting factors, known as a consumptive coagulopathy. Thus paradoxically presents as multifocal haemorrhage.
Describe the appearance of DIC.
Clinically manifests as petechiae and ecchymoses in the skin, mucous membranes and serosal surfaces. May also see lesions associated with congestion and infarction leading to organ failure.
What are the causes of DIC?
Any agent that causes widespread endothelial damage, abnormal blood flow or abnormal coagulability.