Pathology Flashcards

Question

What are the cellular events of necrosis that can be observed microscopically?

Answer 1

1/ **Pyknosis** 2/ **Karyorrhexis** 3/ **Karyolysis** 4/ **Cytoplasm sometimes stains brighter pink** (more eosinophilic due to lower pH)

Answer 2

It's a cellular event in necrosis that can be seen histologically: chromatin condenses & becomes small, dark & shrunken

Answer 3

It's a cellular event in necrosis that is more advanced than pyknosis. Histologically, the nucleus can be seen to have broken up into several dense pieces.

Answer 4

It's a cellular event in necrosis that is more advanced than pyknosis and karyorrhexis. It's dissolution of the cell's nucleus. Staining of nucleus with haematoxylin becomes faint & only ghost outline remains.

Answer 5

It stains brighter pink ie., more eosinophilic due to lower pH. (Eosinophilic is more acidic = pink Basophilic is more basic/alkaline = blue)

Answer 6

1. Coagulative 2. Liquefactive - Malacia (CNS) 3. Liquefactive - Abscesses 4. Caseous 5. Fat

Answer 7

**CAUSES**: Bacteria that produce toxins esp. *Clostridium* spp; Infarction; some foci of viral replication eg. *Canine herpesvirus-1* **GROSS**: Remains firm; drier on cut surface but still resembles in outline the adjacent viable tissue **MICRO**: General architecture preserved. Cells may appear slightly larger & outline lost. Cytoplasm appears structureless & homogenous. Important nuclear changes (pyknosis, karyorrhexism karyolysis); might see inclusion bodies

Answer 8

They affect different tissues and look different grossly & microscopically. ## Footnote **1. Liquefactive necrosis involving malacia of CNS tissue**: **GROSS**: Gaps apparent in white matter of brain and spinal cord **MICRO**: Vacuoles appear where grey matter of brain is becoming necrotic **CAUSES**: Thiamine (Vit. B) deficiency in cereborcortical necrosis in ruminants Lead toxicity in ruminants Salt poisoning in pigs **2. Liquefactive necrosis involving abscesses: ** **GROSS**: Whitish, yellowish watery or clumpy pus **MICRO**: Necrotic area composed of: varying stages of degeneration & death of neutrophils; homogenous structureless mixture of remnants staining faintly bluish _Pyogenic membrane - _reddish membrane on inner surface of capsule composed of blood vessels responsible for transporting the vast # of neutrophils to lesion _Fibrous tissue capsule- _part of host inflammatory response walls off the irritant **CAUSES**: Pyogenic (pus-producing) organisms. Pus = dead & dying neutrophils, dead tissue & organisms causing necrosis Bacteria cause necrosis & attract vast #s of neutrophils ➔ neutrophils kill ➔ dying neutrophils release proteolytic enzymes ➔ digest necrotic tissue ➔ kill further tissue cells ➔ kill other incoming neutrophils

Answer 9

**CAUSE**: Mixture of coagulation & liquefactive necrosis Specific organisms eg. *Mycobacterium tuberculosis* can cause granulomas; fungi, parasites & foreign bodies also cause granulomas **GROSS**: - “Cottage-cheese”-like; white/grey/yellowish; consistency varies according to fluid content; some dry & crumbling **MICRO**: Complete loss of cell architecture. Purplish necrotic material due to: - _random intermixing of nuclear & cytoplasmic components_ that stain with H&E - _lots of MACROPHAGES in granulomas_: large proportion of necrotic tissue is composed of macrophages recruited into tissue to engulf organism - _can see multinucleate giant cells_: merger of macrophages in histo sample of M. tuberculosis-infected tissue; *Mycobacteria* have fatty cell wall that resists digestion & other factors, allowing replication within macrophage & evasion of phagolysis ➔ organisms burst macrophage ➔ engulfed by other macrophages

Answer 10

Adipocytes die ➔ fat broken down into fatty acids ➔ these combine with Ca++, Na+ & K+ to form **soaps** (saponification) ➔ soaps provoke inflammatory response ➔ do not dissolve but remain indefinitely & often calcify ## Footnote **GROSS**: Areas of focal opacity, very hard consistency **MICRO**: Vacuoles surround inflammation **CAUSES:** _Enzymatic_ - release of pancreatic enzymes esp lipase from damaged pancreas into adjacent mesenteric fat eg., pancreatitis _Traumatic_ - in subcutaneous tissue following trauma to area; quite common in brisket of recumbent animals due to prolonged pressure _Diet-related_ - rarely in cats with antioxidant-deficient diets eg., Vit. E, eating only fish.

Answer 11

Post-necrotic change - degradation of dead tissue AFTER necrosis - it is NOT necrosis

Answer 12

**Wet**: Life-threatening; Eg., common in bovine mastitis due to *S. aureus* (primary) _Primary_ - agent that initially kills tissue also putrefies it Live skin rotting, malodourous _Secondary_ - dead tissue invaded by organisms that putrefy ittissue already dead/necrotic, black, pus-y, rotten, starting to putrefy **Dry**: Like mummification Eg., Post-septicaemic *salmonellosis;* appears leathery, dessicated then sloughs off; occurs on extremities; air passing over extremities removes fluid content of dead tissue; appears leathery

Answer 13

Programmed death of scattered single cells in living tissues NOT NECROSIS Eg., mammary gland after lactation, endometrial cells during menstruation, death of lymphocytes in tolerance, low levels of injurious substances, some viruses & tumours, extra cells produced in embryogenesis **GROSS**: No reaction, no inflammation **MICRO**: Cell membrane intact

Answer 14

**Hyperaemia**: *Engorgement of the vascular bed due to ↑ INFLOW of blood*. There is more blood in circulation/in blood vessels because there is more physiological demand for blood flow. Eg., from muscles during exercise, loss of heat from skin or digestion of food. Hyperaemia can also be the earliest response in inflammation (eg., swelling). **Congestion**: *Engorgement of vascular bed due to ↓ OUTFLOW of blood*. There is more blood clogging up the veins because it can’t flow out from one end to the other. It can lead to hypoxia or cyanosis, since oxygenated blood doesn’t make it through the circulation, the stagnant blood loses its oxygen. Eg., local obstruction or congestive heart failure.

Answer 15

**Venous Congestion** - ↓ flow of blood to tissues caused by functional or structural blockage to blood flow. ## Footnote **Chronic** - congestive heart failure - buildup of blockage **Acute** - acute heart failure - sudden blockage (lung & abdominal viscera don’t get enough blood); spleen after barbiturate euthanasia; accidental compression of tissues eg., abdominal twist Can be localised to an organ or generalised, affecting the whole body.

Answer 16

Compression of the vessels occludes the thin-walled veins, stopping blood from leaving the tissue ↓ For a time blood can still enter tissue, passing through the muscular arteries ↓ Dark red venous blood collects in capillaries and veins ↓ Organ may become red/black and if the condition persists anoxic necrosis will occur

Answer 17

Obstruction of blood flow through the heart ↓ Blood is held back or “pools” behind the point of obstruction in the circulation ↓ Left-sided heart failure - due to congestion of pulmonary (lung) circulation or Right-sided heart failure - due to congestion of hepatic (liver) circulation

Answer 18

**Damage to heart valves** - eg., endocardiosis (congenital in King Charles Cavaliers), endocarditis (bacterial) **Changes to heart muscle** - cardiomyopathy **Compression of heart from outside** - eg. wire, hydropericardium **Neoplasia affecting heart**

Answer 19

Hypostatic congestion occurs *after death:* Before blood clots, it pools due to gravity to lowest parts of organ/body; important to distinguish from pathological congestion, which occurs during life to cause or as a symptom of disease.

Answer 20

Abnormal accumulation of fluid in INTERSTITIAL TISSUES or BODY CAVITIES. It occurs when there is an imbalance in the forces that retain blood/fluid in the blood vessels and those that retain fluid in the interstitial spaces & body cavities.

Answer 21

1/ **Exudate** - protein-rich, containing many inflammatory cells, produced during _inflammatory oedema_ 2/ **Transudate** - low in protein & cells, clear-running, produced during non-inflammatory aka _haemodynamic oedema_

Answer 22

1. ↑ Capillary Blood Pressure aka Hydrostatic Pressure 2. Plasma Osmotic Pressure - loss or lack of blood protein (mainly albumin) 3. ↑ Capillary Permeability - usually inflammatory in origin 4. Blockage of Lymphatic Flow - cells, including tumour cells

Answer 23

Increase in blood pressure prevents adequate resorption of fluid at venous end of the capillary bed. Blood can’t flow out of the veins, so pressure increases in the capillary bed, forcing fluid out into the interstitial space between cells. Examples: _Localised - occlusion of veins_: Venous congestion: Intestinal torsion, heart-valve disease, cardiomyopathy, left-sided or right-sided heart failure _Generalised - cardiac failure_: - Ventral subcutaneous oedema - seen in heart failure in horses & cattle - Anasarca - generalised tissue oedema most noticeable in subcutaneous tissues

Answer 24

Osmotic (oncotic) pressure is the force responsible for pulling tissue fluid BACK INTO BLOOD VESSELS at venous end; it’s the protein gradient where water goes from low-protein concentration to area of high-protein concentration. ## Footnote Reduction in albumin due to malnutrition, loss or reduction in formation by liver or protein-losing pathologies means proteins can’t be absorbed across tissues into blood vessels, so fluid flows OUT of blood, where protein is low, into tissue or body cavities where there is higher protein levels. **Examples**: _Protein-losing enteropathy_ - loss of protein due to chronic inflammation of GIT; animal can’t absorb protein via GIT or it passes in faeces. Water leaves blood vessels (area of low protein) into GIT tissue. *Haemonchus contortus* - blood-sucking nematode in sheep abomasum leading to “bottle jaw” _Protein-losing nephropathy aka Nephrotic Syndrome_ - subcutaneous oedema as fluid accumulates in body cavities because proteins are lost via urine in cases of glomerulonephritis & amyloidosis * Ascites* - excessive fluid in abdominal cavity, common in dogs * Hydrothorax* - excessive fluid in thorax, common in cats. ``` _Chronic liver disease_ - may interfere with albumin synthesis Liver fluke (*Fasciola hepatica*) - in sheep *Fibrosis* of liver - in dogs ```

Answer 25

Increased capillary permeability allows escape of plasma protein into interstitial fluid & thereby ↑ osmotic pressure Fluid then is drawn INTO the interstitial fluid FROM the plasma. **Systemic causes:** Bacterial toxins Various chemicals Some immune-mediated conditions - *Feline Infectious Peritonitis* (FIP) **Local causes:** Inflammation - vasoactive substances eg., histamine, substance P, ↑vascular permeability so fluid & inflammatory cells move out of vessels into extracellular tissue, forming cell-rich exudate

Answer 26

Blockage of lymphatic flow refers to an obstruction from inside or outside the blood vessels, or removal of lymphatics. Lymphatics help maintain interstitial fluid at normal homeostatic volume by draining waste out of blood, produces localised oedema ## Footnote Can be caused by trauma, surgery, inflammation or neoplasia. **Examples**: Cells of malignant epithelial tumours (metastases) travel through lymphatic system to seed other tissues & may cause obstruction Breast cancer

Answer 27

Haemorrhage is the escape of blood from vessels. Distinguished from congestion because the blood is OUTSIDE of vessels as opposed to inside.

Answer 28

Rhexis is a type of haemhorrhage due to physical rupture of a blood-vessel wall. **CAUSES**: - Trauma - Haemorrhagic enteritis - Erosion of blood vessels by tumours or absesses - Idiopathic rupture of arteries

Answer 29

Intrapericardial rupture of aorta in horse Arterial rupture in pigs associated with Cu deficiency Adult turkeys often have rupture of various arteries

Answer 30

They are all types of haemhorrage into body cavities caused by rhexis (physical rupture of blood-vessel wall).

Answer 31

Both are haemhorrages within tissue due to rhexis. **Haematoma**: release of blood into tissue forming clot; can be associated with angiogenic tumours **Bruise**: red for 48 hrs, then turns yellow due to macrophages converting haemoglobin to haemosiderin (not as serious)

Answer 32

They are all forms of loss of blood (haemhorrage) from the body, due to rhexis (rupture of blood vessel).

Answer 33

Nosebleed; originates anywhere in respiratory system; can occur in lungs after heavy exercise or in problem with gutteral pouch in horses. Example of haemhorrage out of the body.

Answer 34

Gastric secretion turns blood dark brown, “coffee-ground” appearance; called ***haematomesis*** when vomited up & ***melena*** when passed in faeces (blood originated in stomach/upper SI, often due to ulceration) Example of haemorrhage OUT of the body due to rhexis.

Answer 35

Blood in faeces when bleeding is low down in the GIT & when blood is passed in faeces relatively unchanged. Example of haemhorrage OUT of the body due to rhexis.

Answer 36

Blood in urine; loss of whole blood. Distinguish from ***haemoglobinuria*** (loss of haemoglobin into bladder following intravascular haemolysis). Example of haemhorrage OUT of the body due to rhexis.

Answer 37

Loss of haemoglobin into bladder following intravascular haemolysis. Distinguish from haematuria - loss of whole blood. Example of haemhorrage OUT of the body due to rhexis.

Answer 38

Both diapedesis & rhexis are forms of haemorhorrage. **Diapedesis** are small losses of blood, usually from tiny ruptures in microvasculature. **Rhexis** is bigger, physical rupture that lead to bigger haemorrhages.

Answer 39

Usually seen on skin, mucous membranes & serosal surfaces: ## Footnote **Petechiae** - minute, pinpoint **Ecchymoses** - 1-3 cm diameter & blotchy **Purpura** - mix

Answer 40

***Purpura haemorrhagica*** - in horses after an infection, esp. strangles. Endothelial damage caused by accumulation of immune complexes. ## Footnote ***Haemophilia*** - rare but reported in dogs & pigs; failure of normal blood clotting of blood due to absence of clotting factors ***Dicoumeral poisoning*** - warfarin, an antagonist to Vit. K, or prolonged feeding of sweet clover ***Astrongylus vasorum*** - worm that parasitises pulmonary artery, right ventricle & lungs of dogs & foxes; secretes anticoagulant causing sporadic haemorrhage

Answer 41

Shock comes about when the entire body suffers a severe lack of blood flow, or hypoperfusion. This is due either to decreased effective circulating blood volume, in the case of haemorrhage, thromboembolism or heart failure, and/or increased peripheral vascular resistance (ie., higher blood pressure), which reduces blood flow to tissues. Shock can also occur with hypotension, or very reduced blood pressure, which can result in impaired blood flow, hypoxia and a shift to anaerobic metabolism of cells, cellular degeneration and apoptosis. It is a common final outcome for severe haemorrhage, dehydration, severe trauma, burns, major myocardial infarction, massive pulmonary embolism & sepsis.

Answer 42

Hypovolaemic Cardiogenic Maldistribution of blood

Answer 43

Reduced circulating blood volume; loss of 10% blood volume can occur without causing a fall in blood pressure. When loss of more than 35% blood volume occurs, BP falls dramatically & tissue perfusion cannot be maintained - 80-90% young, healthy animals survive **CAUSES**: Haemhorrhage Vomiting Diarrhoea Burns

Answer 44

Heart fails to pump enough blood or fails to do so forcefully enough to perfuse the systemic circulation. Unsuccessful compensation by sympathetic stimulation results in stagnation of blood & progressive tissue hypoperfusion **CAUSES**: Myocardial infarction Cardiac arrythmias Obstruction of blood flow from the heart (pulmonary embolism) Cardiac dysfunctions

Answer 45

Decrease in vascular resistance (ie., increase in systemic vasodilation) resulting in relatively reduced perfusion to vital organs. Peripheral blood-pooling & stagnation. **CAUSES**: _Septic_ - most common & important; infectious organisms (eg. bacterial endotoxin) induce excess release of vascular & inflammatory mediators (eg. DIC) → multi-organ failure _Anaphylactic_ - generalised hypersensitivity reaction, eg., plant allergens, drugs, vaccines (IgE on mast cells →histamine → vasodilation →vascular permeability) _Neurogenic_ - induced by trauma, electrocution, fear, emotional stress (profound autonomic stimulation → widespread vasodilation)

Answer 46

Blood-clotting, or haemostasis, begins with **vasoconstriction** of the ruptured blood vessel. This is caused by myogenic spasm (contraction of the vascular muscle cells initiated by themselves), production of vasoconstrictor **thromboxane** by platelet enzymes and nervous stimulation by pain sensation. This is followed by **primary & secondary clotting**, then **fibrolysis**. **Primary clotting** involves the *adhesion, activation and aggregation* of platelets to the site of rupture. When the blood is exposed to collagen in the ruptured vessel, platelets change shape and begin secreting factors that cause them to **adhere** to the ruptured vessel’s endothelial cells, which normally prevent such sticking of platelets. Platelets especially adhere to **Von Willebrand Factor**, which leaks into the tissues from the plasma. **Activation** occurs when the irregularly shaped, contracting platelets secrete factors such as **ADP** and **5-HT** (**seratonin**, a vasoconstrictor), while the phospholipid in the platelets’ cell membrane generate **arachidonic acid**, which acts as a substrate for the enzyme **cyclooxygenase** (**COX**). COX, reacting with the platelets’ arachidonic acid, catalyses synthesis of **TxA2, aka thromboxane**, another vasoconstrictor. Together, ADP and thromboxane **activate** nearby platelets. The **aggregating** platelets express **GP IIb/IIIa** surface receptors, which bind **soluble fibrinogen** in a cross-link pattern, forming a **temporary platelet plug**. **Secondary clotting** occurs via the **coagulation cascade**. This can be triggered **extrinsically** when the vessel wall is ruptured, and **intrinsically**, when there’s trauma to the blood or exposure to collagen. The first step in the extrinsic pathway is the release of **tissue factors (TF)** from the nearby tissue. These factors are made of lipoproteins and phospholipids especially that act like proteolytic enzymes and activate many of the clotting factors. A key factor is the **conversion of Factor X to Factor Xa**, which sets in motion the interaction of **prothrombin activator in the presence of Ca++ to convert prothrombin, which is already in the blood, to thrombin.** Thrombin then converts soluble fibrinogen into insoluble **fibrin fibres**, forming a **haemostatic clot**. This is a **rapid process** that protects the body. The **intrinsic pathway** starts by the activation of **Factor XII (Hageman) to Factor XIIa**, and there is no interaction with the TF of the extrinsic pathway. The common final pathway they share begins with the conversion of Factor X to Factor Xa, after which prothrombin + Ca++ converts prothrombin to thrombin, etc. This is a **slow process** that occurs outside of the body, eg., in a test tube. Finally, the clot undergoes **fibrinolysis**. The tissue around the clot and the underlying endothelial cells release **tPA, aka tissue plasminogen activator, which converts plasminogen already in the blood to plasmin, which digests the fibrin until it disappears.** Plasmin also digests key clotting factors, including prothrombin.

Answer 47

A failure to clot, or dyscrasia, can mean the body lacks or has defective clotting factors, as in the case of haemophilia. It can also be due to liver disease, which cuts down on the production of prothrombin, fibrinogen and other clotting factors. A deficiency of Vitamin K can also lead to dyscrasia, and it can occur with the ingestion of warfarin, which blocks Vit. K, or sweet clover, which has a similar effect. *Angiostrongylus vasorum* secretes an anticoagulant into the blood. Thrombocytopaenia is a condition in which there is a decrease in platelets due to infection, drugs, bone-marrow tumours or poisons. Septicaemia can lead to widespread damage to the vascular endothelium.

Answer 48

Pathological clotting means clotting that occurs when it’s not supposed to. This is called **THROMBOSIS**. It is typically due to three primary influences (Virchow’s Triad): i/ _Endothelial injury_ - this also triggers the normal clotting cascade, due to all the same things that can cause normal clotting, as well as depletion of plasminogen activator inhibitors. Remember that tissue plasminogen activator tPA sets in motion fibrinolysis so a tPAI, or PAI, would inhibit fibrinolysis, resulting in a clot not dissolving. ii/ _Alteration of blood flow_ - stasis (usually venous) or turbulence (usually arterial) caused by intestinal torsion, external compression of vessel or cardiac disease causing a blockage. iii/ _Hyper-coagulability of blood_ - could be due to ↑ number of platelets (diabetes mellitus, cancer, heartworm, uraemia, nephrotic syndrome) , ↑ in clotting fibres and fibrin (nephrotic syndrome, DIC, neoplasia), ↓ in fibrinolytic system, metabolic abnormalities (eg. hyperadrenocorticism).

Answer 49

**Arterial/Cardiac Thrombi**: Usually non-occlusive (result of rapid & high vol flow; turbulence) Smaller arterial thrombi may be occlusive All begin at sites of endothelial injury or turbulence Grey-red, laminated *layers* (platelets + fibrin and RBCs) Major sites: left ventricle, faulty heart valves, sometimes in peripheral circulation **Venous Thrombi:** Occlusive Occur in sites of stasis Long red-blue cast of lumen Enmeshed RBCs + fibrin - red-blue MESH instead of thrombus Major sites: veins of distal limbs (DVT - deep vein thrombosis)

Answer 50

A **thrombosis** is an inappropriate clot. A **thromboembolism** is a fragment of a thrombus (clot) that breaks away and flows through the blood stream and ends up blocking a blood vessel. The vascular occlusion can be complete or partial, and can lead to ischaemia & necrosis.

Answer 51

* *Venous emboli** (ie., found in veins) tend to lodge in the pulmonary circulation (ie., pulmonary veins coming back from the lungs). These are called **pulmonary infarcts**, or right-sided heart failure because the emboli tend to lodge in the vessels leaving the heart to the lungs, ie., pulmonary artery. * *Arterial emboli** tend to lodge in smaller downstream arteries, often near a bifurcation site, such as at the iliac arteries that branch off the aorta. * *Left-sided cardiac emboli** are basically arterial emboli, and are often saddle emboli like the emboli of the iliac arteries.

Answer 52

Infarction occurs when blood supply to tissues is so impaired (ischaemia) that it leads to necrosis of the tissue. The ischaemia can be caused by a thrombosis, emboli, compression from outside the vessel like a tumour, vasoconstriction or vasculitis (inflammatory destruction of blood vessels). The effects in tissue might be reversible, depending on the duration of the ischaemic period or the metabolic demands of the tissue.

Answer 53

Infarction affects, most importantly, the following **end-arteries aka terminal arteries**: renal artery & its branches splenic artery & its branches coronary arteries (heart) some cerebral & spinal-cord arteries anterior mesenteric artery & its branches The **organs** most sensitive to infarction are those that have an “end-artery” structure & are thus very sensitive to hypoxia (ie. organs whose tissue only receives oxygenated blood from one artery, therefore a blockage would cut off all oxygen to that organ): Brain, Kidney, Heart cells Lung, liver, muscle and intestines are less sensitive because they have alternative blood supplies.

Answer 54

An area of ischaemic necrosis. It is usually arterial & not venous.

Answer 55

Large or more proximal artery blockage that causes more severe or extensive infarction, eg. to the whole kidney or the whole lung. **Example**: _DIC - Disseminated Intravascular Coagulation_ - widespread intravascular coagulation/clot, especially microthrombi in the capillaries, caused by widespread generation of thrombin (complication of diffuse thrombin activation, diffuse activation of extrinsic coagulation).

Answer 56

**Disseminated Intravascular Coagulation** Widespread intravascular coagulation/clot, especially microthrombi in the capillaries, caused by widespread generation of thrombin (complication of diffuse thrombin activation, diffuse activation of extrinsic coagulation). Generation of TF by endothelial cells in response to bacteraemia, toxaemia, other stimuli or systemic infections that activate widespread release of inflammatory mediators. Concurrently, high levels of thrombin stimulate various anti-coagulant functions, so fibrinolysis goes into overdrive, while platelets and clotting factors get used up, so paradoxically the body bleeds in widespread haemorrhagic diathesis. Clinically this presents as shock, acute respiratory distres, heart failure and renal failure.

Answer 57

Hyaline degeneration is a segmental (affects a portion but not all) necrosis of the muscle fibres. **CAUSES**: Vitamin E and/or Selenium deficiency: both these substances protect cellular membranes from the effects of radicals produced during normal cellular metabolism

Answer 58

Subclinical ill-thrift. Vitamin E and Selenium protect all cells, so the immune system cells are also reduced in their ability to counteract infections.

Answer 59

**Protein-losing nephropathy aka Nephrotic Syndrome** - subcutaneous oedema as fluid accumulates in body cavities because proteins are lost via urine in cases of glomerulonephritis & amyloidosis Caused by chronic, sometimes purulent (pus producing), inflammatory process elsewhere in the body. Following continuous stimulation from the chronic inflammatory process (due to chronic liver disease or a liver-fluke infestation), the **liver** produces a substance (serum associated amyloid –SAA) that deposits and polymerises into fibrils in the **glomeruli**. This allows protein to leak into the urine (**proteinuria**), thereby lowering the plasma protein level (**hypoproteinaemia**) and resulting in transudation of low-protein fluid into the body cavities and tissue spaces.

Answer 60

See picture. Note: a. The circular nature of the lesions due to sporing heads of Aspergillus fungus b. The nuclear changes in the necrotic area (pyknosis, karyorrhexis, karyolysis) Remember, Aspergillus spp is a filamentous fungus (mycelium), that causes Aspergillosis: Some strains of Aspergillosis, which spreads by the fragmentation of its septate mycelium into sporing heads that release spores that we see as blue- green mould, are other examples of mycotoxosis as the spores are easily ingested. - *A. fumigatus, A. nidulans, A. flavus, A. niger* - fungus abundant in hay, straw & grain heated during storage - produce large numbers of dry light spores that become airborne

Answer 61

Immunosuppression caused by primary FIV or FeLV infection.

Answer 62

The pigment that makes the mass dark is melanin. Melanophage: round and contains lots of pigment Melanocyte: also contains melanin but of lesser intensity. Produces the melanin and IS the tumour cell. Varies in size and shape.

Answer 63

There could be spread (metastasis) of the melanoma tumour to the lungs. Melanomas on the extremities i.e. digits of dogs tend to be malignant and readily metastasise to the lungs. The oral cavity is another predilection site for malignant melanomas in dogs

Answer 64

Bilirubin (hyperbilirubinaemia), which is major component of bile from erythrocyte breakdown.

Answer 65

Hyperaemia. It is part of the acute inflammatory reaction. The vessels actively dilate to bring fluid and inflammatory cells to the damaged tissue. Bacterial bronchopneumonia results in hyperaemia (parasite enters via the airways). Cattle and pigs have a well developed interstitium between lung lobules and for the infection to spread from one to the other, it must go back up the airway of the affected lobule and down into the unaffected lobule. This does not apply to lesions produced by bacteria secreting necrotising toxins.

Answer 66

As pieces of the thrombus break off, they go through the systemic circulation and a usual site for them coming to rest is the renal vessels and blocking them. The kidney has an ‘end artery’ supply and so the tissue whose supplying vessel has been blocked undergoes an ischaemic necrosis (termed infarction).

Pathology Flashcards

(90 cards)