Path Flashcards
What should samples be fixed in?
at least 10x their volume of bufferred formalin.
What stain is used for fat?
Oil Red O
What stain is used for fibrous tissue?
massons trichome - stains ct green
What stain is used for haemosiderin?
Perls Prussian blue
What is pyknosis?
Small shrunken densely staining nuclei
What is karyorrhexis?
The nuceus has fragmented into small pieces
What is karyolysis?
Nucleus has lysed
What is lipidosis?
Accumulation of intracytoplasmic lipid. the central role of the liver means that it is especially susceptible. the major mechanisms are excessive FFas into the liver or toxic damage affecting metabolism of fatty acids and triglycerides.
What is pseudomelanosis?
green/black discolouration due to conversion of iron to iron sulphide by GI bacteria.
What is biliary imbibition?
Pigment imbibed - onto liver and any organs in contact e.g GI tract.
How does Rigor mortis occur?
Beings approx 2-4 hours after death. Burst of metabolic activity as substrates depleted on cessation of circulation progressive decrease in muscle Ph, Oxygen and ATP. Ca2+ efflux from sarcoplasmic reticulum of muscle cell > contraction of muscle fibres. Generally the head and neck musculature is affected first then the changes spread to the extremities. disappears as putrefaction begins (approx 1-2 days) Completely disappeared by 72 hours.
what PM signs are seen when an animal is euthanased with barbiturates?
Spleen is congested & crystal deposition on the endocardium of the heart.
What is splenic siderofibrosis?
yellow, dry encrustations on the capsule of the spleen thought to represent sites of previous local haemorrhage with usbsequent deposits of Fe, Ca and fibrosis.
What does steroid use do to the liver?
long term steroid use can lead to steroid induced hepatopathy. pathogenesis : glucocorticoids induce the enzyme glycogen synthetase leading to increased storage of glycogen within hepatocytes. The hepatocytes in midzonal areas are often preferentially affected and can be up to 10x normal size.
What is the role of the renin-angiotensin and aldosterone system?
Main role is in maintaining effective circulating volume. Renin is produced by specialised juxtaglomerular cells in the glomerular afferent arertiole. renin is released in response to decreased renal perfusion due to decreased blood pressure and decreased blood volume. Renin converts angiotensin to angiotensin I which then converts to angiotensin II. Angiotensin II increases aldosterone production by adrenal cortex > aldosterone enhances renal sodium absorption.
What is the function of ADH?
ADH is made in the hypothalamus and released when hypothalamic osmoreceptors are stimulated. ADH controls permeability of distal tubules and collecting ducts. if ADH is present, urine volume is low. if ADH is absent, urine volume is high. Another stimulus for ADH secretion is decreased blood volume and pressure. Baroreceptors in the left atrium are stimulated by increased blood volume. Impulses pass in neurons to the hypothalamus where they inhibit ADH producing cells > urine volume is high which reduces blood volume and pressure. Decreased BP leads to decreased firing of baroreceptors and increased ADH secretion > urine volume is low > increased blood volume and pressure.
What are Atrial natriuretic peptides?
A group of diverse peptide hormones produced by the heart in response to stretching of the heart, they reduce cardiac output and blood pressure through loss of NA and water from the kidneys as well as through vasodilation.
What are the possible reasons for hypokalaemia?
Increased insulin activity, anorexia in herbivores, low K diet, GI disease especially horses, profuse sweating in horses, increased renal loss.
What are the possible reasons for Hyperkalaemia?
Diabetes mellitus, high K fluid therapy, post renal obstruction, anuric renal failure, addisons disease.
What are the possible reasons for Hypomagnesaemia?
Hypoporteinaemia, decreased absorption (grass tetany), anorexia, excess urinary excretion eg e.g ketonuria, blister beetle poisoning in horses, lactation tetany in shetland pony mares.
What are the possible reasons for hypermagnesaemia?
Decreased renal excretion (renal failure, Decreased GFR), increased PTH (milk fever), increased intestinal absorption. Excess Iv administration.
What are the possible reasons for hypocalcaemia?
Milk fever and eclapmsia in bitches, hypoproteinaemia, chronic renal failure, acute pancreatitis.
What are the possible reasons for hypercalcaemia?
Malignant neoplasia
Renal failure in hrose
Thiazide diuretics, increased vit D activity.
What is the protein content of transudate and exudate comparitively?
Tranusdate is 0.05-0.5% mainly albumin. Exudate is usually 2-4%, but can be higher. Transudate does not coagulate as no fibrinogen but exudate contains fibrinogen so will coagulate.
What is the cell content like in transudate compared to exudate?
Very low in transudate - mesothelial cells, some macrophages & lymphocytes. High cell count in exudates, any cel type potentially but more commonly macrophages, lymphocytes and neutrophils.
What is the difference in hyperaemia and congestion?
Hyperaemia occurs when arteriolar dilation increase blood flow to the tissue, which leads to tissue erythema e.g reddening at sites of inflammation. Congestion is due to reduced outflow of blood from a tissue ( a passive process e.g heart failure or vennous obstruction)
What does heart failure cause to happen to macrophages in the lung?
In chronic congestive heart failure - haemosidering laden macrophages within the lung alveoli due to capillary rupture in congested areas which leads to microscopic haemorrhages.
Classify the haemorrhages Petechiae, purpura, ecchymoses or rhetic?
Petechiae are very small 1-2mm and may be associated with locally increased vascular pressure, thrombocytopenia or decreased platelet function. Purpura is slightly larger >3mm and may be associated with the same conditions that cause petechiae or due to trauma, vasculitis or increased vascular fragility. Ecchymoses are larger (1-3cm) and rhetic affects large contiguous areas of tissue.
Give a summary of the process of haemostasis.
Injury > increased blood viscosity and RBC packing occur due to plasma loss > sludging effect > activated platelets change from small rounded discs to flat plates > release secretory granules which recruit more platelets > form a haemostatic plug > tissue factor III or thromboplastin is exposed at the point of vascular injury > this initiates coagulation cascade which results in formation of thrombin. Thrombin converts circulating fibrinogen into fibrin which is insoluble. Fibrin accumulates and forms a meshwork that recruits and activates more platelets to consolidate a primary haemostatic plug. Polymerization of this material forms a plug which stops further haemorrhage.
What is the fibrinolytic cascade?
prevents over production or persistence of fibrin. plasminogen in plasma is converted to plasmin by a factor XII dependent pathway or via plasminogen activators. Plasmin breaks down fibrin into fibrin degradation products.
What is the kinin system?
Predominantly associated with inflammation eg bradykinin acts as a vasodilator, increases vascular permeability which allows increased leucocyte migration, causes contraction of smooth muscle & pain.
What is the complement system
another cascade system with classic and alternative pathways. Inactive precursors in plasma are triggered by bacterial enzymes, antigen antibody complexes and thrombin. Complement system contributes to inflammation, phagocytosis of microbes and cell lysis.
What is thrombocytopenia and what are the possible causes?
Decreased platelet numbers in the blood. May be due to decreased production or increased destruction/utilisation of platelets. Decreased production due to bone marrow disease may be secondary to damage to megakaryoblasts in the bone marrow e.g myeloprofilerative disease, some viral infections, radiation injury, neoplasia and some drugs. Increased destruction of platelets may occur due to primary immune mediated disease, feline leukaemia virus, neoplasia or secondary to some drugs or diffuse endothelial damage such as disseminated intravascular coagulation, septicaemia or vasculitis.
What is von willebrands disease?
Due to a deficiency of the plasma glycoprotein von willebrands factor which is produced by endothelial cells. it acts as an adhesion molecule and is essential for primary haemostasis. it is common in dogs such as scottish terriers, dobermans and shelties. there are three types which vary in severity (type 3 is most severe form and is an absolute deficiency). Acquired coagulopathies include vitamin K antagonism, vitamin K deficiency and liver disease.
What is a thrombus?
A layered mass containing red blood cells, granular leucocytes and platelets held together by fibrin. An antemortem thrombus will be granular, dry, dull, and atatched to vessel wall or chordae tendinae in heart.
What are the three factors of virchows triad?
Damage to endothelium
Stasis or irregular /turbulent flow
Hypercoagulability of blood.
What is a common cause of arterial thrombosis in horses?
Secondary to strongylus vulgaris infection, seen in the root of the cranial mesenteric artery, renal artery and aorta
What is a common cause of arterial thrombosis in cats?
Iliac thrombosis secondary to cardiomyopathy and atrial thrombosis
What is an embolus?
A solid or gaseous mass carried by the bloodstream form its point of origin to a distant site within the circulation. Blockage of a major vessel such as the pulmonary arterial trunk tends to cause sudden death, blockage of a small end arteriolar vessels lead to ischaemia and infarction of the area supplied by the vessel.
What is an infarction?
A segmental or localised area of ischaemic necrosis due to occlusion of blood supply usually due to thromboembolic occlusion of an artery.
What is DIC?
DIC is characterised by the activation of coagulation within the vascular system resulting in deposition o fibrin in the small blood vessels and consumption of coagulation factors and platelets. The fibrin deposition within blood vessels leads to vascular obstruction and microinfarction. The fibrinolytic system is activated which removes some fibrin but also uses up clotting factors and forms fibrin degradation products which have anticoagulant properties. Causes include septicaemia, bacterial endotoxaemia, viral e.g feline infectious peritonitis
What are the three different types of shock?
Cardiogenic - failure of heart to pump blood adequately eg DCM or arrhythmias.
Hypovolaemic - reduced circulating volume resulting from blood loss or fluid loss.
Blood maldistribution - decreased peripheral vascular resistance and pooling of blood in peripheral tissues. It is usually caused by neural or cytokine induced vasodilation eg hypersensitivity, endotoxaemia. (Neurogenic, anaphylactic and septic shock)
what is neurogenic shock?
Usually induced by trauma, generally to the nervous system, electrocution, fear or emotional stress. Autonomic discharges > vasodilation > venous pooling.
What is anaphylactic shock?
Generalised type I hypersensitivity commonly caused by allergens, drugs or vaccines. the inciting substance interacts with IgE bound to mast cells > widespread mast cell degranulation > release of histamine > systemic vasodilation and increased vascular permeability > hypotension and hypoperfusion.
What is septic shock?
This is the most common form of shock due to maldistribution. it is mediated by vascular and inflammatory mediators released in response to bacteria or funal elements. the most common cause is endotoxin, a lipopolysaccharide in the cell wall of gram negative bacteria. LPS is a pattern associated molecular pattern. it binds CD14 and toll like receptor 4.
What are the clinical features of shock?
Hypotension, weak pulse, tachycardia, hyperventilation, urine production, hypothermia.
What is granulomatous inflammation?
Inflammation in which macrophages predominate, there is also giant cells and lymphocytes.
What is granuloamtous meningoencephalomyelitis?
An idiopathic disease which causes granulomatous disease in the central nervous system of young to middle aged small breed dogs. It causes a variety of neurological signs. Grossly there are few lesions. there may be some grey discolouration of affected areas in the brain and spinal cord.
What is salmon poisoning in dogs?
The etiologic agent of the disease is the rickettsia, Neorickettsia helminthoeca, which is vectored by the intestinal fluke, Nanophyetus salmincola. Dogs get the disease by eating salmonid fish infected with the cercaria of the fluke, which harbor the rickettsia. Clinical signs along with finding fluke eggs in the feces of the dog is usually enough to make the diagnosis. Paragonimus kellicotti is a lung fluke of the dog.
What is an adenoma ?
benign neoplasia of glandular epithelium
What is a papilloma?
benign neoplasia of surface epithelium
Which dogs are predisposed to developing mast cell tumours?
Boxers, boston terriers, bull terriers, bull mastiffs, cocker spaniels, labs, golden retrievers.
Which mutation is very common in mast cell tumours?
c-kit gene. which encodes for the KIT protein, which signals cells to proliferate.
Which granules do mast cells contain?
Histamine & heparine. Histamine causes vasodilation. It also binds to H2 receptor on parietal cells in the stomach and encourages them to produce gastric acid.
What is the neoplastic cell in Ovine pulmonary adenocarcinoma?
The clara cell found in the terminal bronchioles of the lung or the type II pneumocyte which lines the alveoli of the lung. Both of these cell types are surfactant producing cells and overproduction of surfactant is one of the more obvious clinical signs of this disease.
Histologically, how are squamous cell carcinoma made up?
Made up of cords or whorls of pleomorphic epithelial cells. Sometimes they have keratin pearls at the centre of the whorls.
What are the three main categories of cells?
Epithelial, mesenchymal and round cells.
List the general criteria of malignancy
Pleomorphism (variable size, shape and nucleus:cytoplasm ratio), macrocytosis, hypercellularity (increased cell exfoliation). Anisokaryosis, macrokaryosis, increased nucleus: cytoplasm ratio, multinucleation, increased mitotic figures, abnormal mitosis, atypical chromatin pattern, nuclear moulting (deformation of nuclei by other nuclei within the same celll or adjacent cells.
What is concentric hypertrophy?
There is an increase in the mass of the ventricle, the wall of which becomes thicker. there is either no change or a decrease in the end diastolic volume.
What is eccentric hypertrophy?
There is an increase in the mass of the ventricle, the wall becomes longer and chamber dilates resulting in an increase in end diastolic volume. In eccentric hypertrophy the ventricular wall may appear thin because it is dilated, but its mass is still greater than normal because the cells have increased in size by elongating.
Describe the pathophysiology of an atrial septal defect?
blood goes from LA > RA > RV = RA dilation and increased RV preload = eccentric RV hyertrophy.
increased pulmonary return = LA dilation.
Describe the pathophysiology of a ventricular septal defect?
LV > RV = inreased RV preload and afterload = RV hypertrophy
Pulmonary overperfusion = increased pulmonary return = LA dilation and Increased LV preload = eccentric hypertrophy.
Which defects will be present in a tetralogy of fallot?
Ventricular septal defect, pulmonic stenosis, RV hypertrophy, dextro rotated aorta.
What is the pathophysiology of a PDA?
Patent ductus arteriosus (From aorta to Pulmonary artery). Increased RV aterload = concentric hyertrophy. Pulmonary overperfusion, increased pulmonary return, LA dilation and LV preload = eccentric hyertrophy.
What is a persistent aortic/branchial arch/vascular ring anomaly?
Of the six pairs of branchial arches present in the early embryo, normally only the left fourth arch persists as the aortic arch. persistent branchial arches are most commonly recognised in dogs and cats. the basic anomaly is constriction of the oesophagus as a result of anomalous vascular rings or associated structures. This results in megaoesophagus with regurgitation of undigested food i.e food never reaches stomach compared to vomiting. persistent right aortic arch is the most common manifestation.
Which of the following is the causative agent of Feline Infectious Anemia?
Mycoplasma haemofelis
What is ectopia cordis?
The heart is normal but is situated abnormally in the body. Cattle and pigs show the highest incidence of the condition. usually situated pre sternally in the lower cervical region or more rarely in the abdomen.
Which disease is hyaline degeneration of the myocardium typical of?
Most commonly a microscopic manifestation o the vitamin E/selenium deficiency white muscle disease, together with cardiomyocyte ncerosis, inflammation and dystrophic calcification. this disease presents as acute left heart failure or acute ataxia/collapse. muscles affected in white muscle disease include skeletal, intercostal, diaphragmatic and cardiac muscle.
What is visceral gout and why does this occur?
It occurs in reptiles and birds as in these species uric acid is the nitrogen metabolisms end product vs urea in mammals. Uric acid will precipitate in tissues as urate tophi (crystals) under certain circumstances (high protein diet, dehydration).
What is mulberry heart disease?
Seen in 3-4 month old thriving pigs. Considered to be the result from lack of selenium/vitamin E. This may be the result of low dietary vit/e selenium or genetic derangements of vit E /se metabolism. The cardiac presentation is similar to white muscle disease, with necrosis, although in this case there are also myocardial haemorrhages resulting from arteriolar fibrinoid necrosis.
What is malignant hyperthermia in pigs?
A rare genetic disease, due to a point mutation in the skeltal muscle ryanodine receptor. It is triggered by stress e.g handling, transportation and by halothane anaesthesia. This results in necrosis of cardiac and skeletal muscles which are then pale, soft and exudative interfering with the maturation of these into meat.
What is dilated cardiomyopathy?
Typically affects giant breed dogs such as boxers, dobermans, great danes, st bernards. Cases of DCM have been strongly associated with taurine deficiency in cats & correction of comercially available diets has reduced the incidence. Monensin toxicity has been associated with DCM in the horse and long term administration of drugs such as doxorubicin and adriamycin in dogs. Affected hearts are enlarged with uni or bilateral ventricular dilation, pale & flabby.
what is hypertrophic cardiomyopathy?
More common in cats, rare in dos. maine coons & ragdolls have mutations identified. The myocardial fibres are hypertrophied, and are accompanied by interstitial fibrosis and arteriosclerosis. There is marked cardiomegaly, Left ventricular concentric hypertrophy with concurrent thickening of the interventricular septum and normal or reduced internal left ventricular chamber size. Thrombus formation in the left atrium is common and when this thrombus breaks these animals develop aorti iliac thromboembolism with sudden onset posterior paresis.
What is restrictive cardiomyopathy?
Occurs less commonly in cats. these animals have marked myocardial fibrosis or endomyocardial fibrosis of the left ventricular endocardium. Marked left atrial dilation with a left ventricle of normal dimensions.
What is arrhythmogenic right ventricular cardiomyopathy?
This is primarily a familial disease of boxer dogs and is rare in cats. the right ventricular myocardium is replaced by fat and fibrous tissue. May present with arrhythmia, syncope, heart failure or sudden death.
What is the most common bacterial cause of endocarditis in cattle?
Arcanobacterium pyogenes
What is the most common cause of endocarditis in pigs?
Erysipelothrix rhusopathiae, strep suis
When a vegetative endocarditis lesion ruptures where do these cause lesions in cattle and in other species?
Right sided lesions in cattle causing pulmonary embolism and abscessation. Left sided lesions in pig dog and horse - myocardial and peripheral infarction and infection especially in the kidneys.
What are jet lesions?
Fibrous thickenings of the endocardium adjacent to an incompetent valve caused by back flow during systole. lesions may also occur in the aorta/pulmonary artery as a result of high pressure abnormal jets of blood passing through a narrowed stenotic semilunar valve and striking the vessel endothelium.
