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244 Cards in this Set

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Left Ventricle Hypertrophy


Individual cadiomyocytes hypertrophied

Osteoporosis - Atrophy

Atrophic liver - hepatocytes smaller/narrower & sinusoids correspondingly wider

Cerebellar hypoplasia

MetaplasiaAirway epithelium in response to chronic inflammation




Normal Columnar cells replaced with abnormal stratefied squamous epithelium

Metaplasia




Vitamin A necessary for maintenance of normal epithelium. Deficiency → epithelium and goblet cells in glands replaced by keratinised stratified squamous epithelium

Canine Mammary Gland




Dysplastic duct with crowded and disorganised epithelial cells projecting into lumen.

Anaplastic cells - failure to differentiate - cant tell what type of cells they are

Hydropic ('watery') degeneration of hepatocytes

Hydropic degeneration - squamous epitheliumBlack arrow identifies swollen but still viable cellNucleus displaced, ‘clearing’ of cytoplasm, cell borders remain intact

Fatty Degeneration of Liver

Liver Necrosis




Cells around central vein showing signs of necrosis




Cytoplasmic palor - loss of RNA and protein


Nucleus shrinkage (karyopyknosis), fragmentation (karyorrhexis), lysis (karyolysis)



Karyorrhexis in splenic lymphocytes - dog with parvovirus infection. Lymphocyte nuclei fragmented as a result of viral attack (arrow).

Coagulation necrosis of renal tubular epithelial cells




Necrotic cells have ‘ghostly’ appearance - homogeneous pale eosinophilic cytoplasm but retained cell outlines (structured necrosis) and nuclear changes such as karyopyknosis and karyolysis.

Liquefactive necrosis, lung abscesses, cow




Liquified material consists of cell debris & large numbers of mostly neutrophils (bacteria not visible with H&E stain)

Liquefactive necrosis, brain, dog




The clear/pale zone in the cerebral cortex represents areas of near total loss of cells and tissue. The cells in the spaces are macrophages attempting to clear up the damage. Grossly, this would have a fluid consistency.

Caseous Necrosis




Tuberculosis, lymph node, cow




Necrosis is structureless - cell walls disrupted, tissue architecture lost, a mixture of nuclear and cytoplasmic amorphous granular debris

Fat necrosis, dog.




Necrosis with inflammation, basophilic foci of saponification & cholesterol clefts

Apoptosis, Pancreas, rat




Individual acinar cells shrunken with chromatin condensed and fragmented (arrows). Inflammation absent.

Pathological mineralisation/calcification




If present in large amounts it appears as gritty white granular deposits grosslyMicroscopically as amorphous basophilic granules of varying size – intra or extra cellular




Dystrophic Where deposited in areas of necrosis

Amyloidosis, kidney, cross section, dog




Black foci (dots) are glomeruli-containing amyloid stained by Lugol’s iodine




Renal glomerulus contains large amounts of pale homogeneous eosinophilic material (amyloid) using H&E stain

Amyloidosis, liver, dog




Spaces of Disse expanded by eosinophilic proteinaceous material (amyloid) that has caused atrophy of hepatic cords (H&E stain)

JaundiceBile casts in bile canaliculi - result of a high rate of bilirubin excretion by liver secondary to widespread haemolysis

Acute Hyperaemia of the brain in acute encephalitis



Fibrin exudate of acute inflammation



Granuloma formation




Lymphocytes and area walled off with fibronous material - Tuberculosis in the lung



Neutrophils




First line of defense in acute inflammation




Death of large numbers can lead to liquefaction of tissues - formation and accumulation of pus



Eosinophils




Present in allergic or parasitic disease




Can also phagocytose







Macrophages (Monocytes in circulation)




Acute and Chronic Inflammation




Large oval with kidney bean nuclei and foamy cytoplasm




Develop into multinucleated giant cells with horse shoe nuclei



Lymphocytes




B or T lymphocytes (cant be distinguished by histological appearance)




Small round sounds mostly nucleus




Enter areas of acute inflammation after 24-48hrs



Plasma Cells




Activated B lymphocytes - producing antibodies




Pink/red cytoplasm possibly with halo of white above the nucleus



Fibroblasts




Proliferate in chronic inflammatory lesions




Play a role in healing and repair




Produce collagen and extracellular matrix proteins



Diffuse acute fibronous pericarditis



Serous inflammation in the coelmic cavity of a bird (clear fluid - very little protein)



Serous Inflammation microscopic view



Catarrhal inflammation microscopic view




Thick mucus with abundant goblet cells




Occurs in parasitic disease and chronic inflammation




Exudate if opaque thick fluid



Fibronous peritonitis




Gelatinous exudate due to coagulation by the amount of fibrin




Can adhere to tissues and create casts of areas



Purulent (suppurative) inflammation




Pus exudate due to death of neutrophils




Thoracic empyema or pyothorax



Cellulitis




Non-encapsulated suppurative inflammation in the subcutaneous tissue



Eosinophilic myositis




Exudate contains large numbers of eosinophils




Associated with parasites, hypersensitivity and unknown mechanics




Exudate is green discoloured







Haemorrhagic Inflammation




Haemorrhagic Enteritis




Large number of erythrocytes associated with sever damage to endothelial cells



Pyogranuloma




Neutrophils at center of granuloma - could be bacterial cause

Myocardial fibrosis




Pale areas of fibroblasts - regeneration could not occur so switched to repair



Granulation tissue




Fibroblasts forming in perpendicular to blood vessels with lymphocytes throughout



Fibrous connective tissue (Fibrosis)




Decrease in blood vessels and cells - scar formation



Scar; Renal Infarct



Proud Flesh




Excess/exuberant proliferation of granulation tissue



Anaphylaxis




Pulmonary oedema (alveolar spaces filled with proteinous fluid)




Vascular congestions (alveolar wall filled with blood)



Hypersensitivity type 1




Oedema and mast cells present



Flea Bite Nibble




A break of the epidermis - replaced with degranulated eosinophils and neutrophils



Heave line on horse




Muscles used to struggle for breath



Brincho thickening




Inflammatory cells within the lumen




Even slight thickening of airways cause massive increases in resistance



Tuberculosis lesion




Bright eosinophilic material is fibrin




Clear spaces are oedema




Lymphocytes and macrophages present

Local Congestion due to small intestine volvulus (twisted bowel)




Blue color due to deoxygenated haemoglobin, wet, swollen




Can lead to necrosis




Passive process due to decreased venous outflow from affected area




(General caused by congestive heart failure)



Local Congestion due to gastric volvulus (twisted stomach)




Vein drainage from the stomach is blocked




Blue color due to deoxygenated haemoglobin, wet, swollen




Passive process due to decreased venous outflow from affected area




(General caused by congestive heart failure)



Hyperaemia of the small and large intestine and cecum




Increased arterial blood flow to the area




Red due to oxygenated haemoglobin, heat, swollen




Pathological - secondary to inflammatory mediators due to tear in colon




(Physiological due to normal increased workload and flow)



Hyperaemia due to ruminal tear leading to peritonitis




Red due to increased blood flow to the area due to inflammatory mediators and oxygenated haemoglobin



Hyperaemia of the trachea - bright red luminal appearance




Commonly seen in animals that have major respiratory distress prior to death



Diagram of haemorrhage due to rupture of blood vessel




Escape secondary to vascular damage (trauma/ inflammation)



Diagram of haemorrhage due to diapedesis




Red blood cells pass through intact blood vessel walls secondary to congestion (increased pressure)



Petechiae of gums




Small 1-2mm spots of haemorrhage



Petechiaetion on kidney




1-2mm spots of haemorrhage



Petechiae in cortex of crossection of kidney




Damage due to toxin



Haemorrhage within cortex of kidney




Red blood cells accumulating between tubules




Coagulative necrosis of tubular epithelial cells due to toxin



Areas of petechiae and ecchymoses




Petechiae 1-2mm spots of haemorrhage (purpura slightly larger vasculitis)




Ecchymoses 2-3cm spots of haemorrhage



Haematoma formation in a kidney




Substantial solid clot




Blood clotting in a localized area



Large area of extravasation at medial aspect of left hind leg due to tearing of abducters of the leg




Large region of haem within tissue




Hyperaemia and oedema also present



Extravasation near the rostral aspect of the nose (on the right side of image)




Dura is expanded by large amounts of blood




Subdural haemorrhage secondary to traffic accident



Contrecoup




Haemotoma just caudal to the cerebellum




Caused by blunt trauma to the front of the head




Brain moves forward in impact resulting in tearing of blood vessels in the back of the brain



Cerebellar coning




Pressure in the brain case increases pushing the cerebellum through the opening of the foramen magnum




Cerebellum becomes flattened and cone shaped



Microscopic view of subdural haemorrhage



Microscopic view of haemorrhage of tissue due to leaky and faulty blood vessel





Bulging haemotoma in the lateral ventricle of the brain




Site of loss can determine how critical the haemorrhage is - brain very critical



Pericardial sack - blue due to deoxygenated blood



Resolving haemorrhage




Macrophages phagocytose red blood cells resulting in haemosiderin

Macroscopic view of oedema filling the abdominal cavity



Pitting Oedema




When you push your finger into an area of oedema if takes a moment to return to previous shape



Diagram of 3 main reasons for oedema formation



Diagram of Oedema formed due to increased intravascular hydrostatic pressure




Increased pressure within the vessels pushes fluid out of the vessels




Factors that increase venous pressure more important than those that increase arteriole pressure




Local Oedema - vain or lymphatic occlusion




Generalized oedema - congestive heart failure




Transudate - Fluid passed through intact capillary walls due to imbalanced hydrostatic +/- oncotic pressures- Little or no protein or cells, low sg



Diagram of oedema formed due to decreased oncotic pressure




Fewer proteins within the vessels leading to the movement of fluid out of them




Caused by nephro/enteropathies causing loss or decreased synthesis by liver disease




Leads to generalized oedema




Transudate - Fluid passed through intact capillary walls due to imbalanced hydrostatic +/- oncotic pressures- Little or no protein or cells, low sg



Diagram of oedema formed due to increased capillary permeability




Caused by inflammatory or allergic responses




Usually local




Exudate - Fluid passed through injured/inflamed capillary wallsContains protein (straw coloured) & leucocytes (also known as inflammatory oedema)



Oedema within trachea




Fluid tends to be frothy due to air passing back and forth over it and it mixing with surfactant



Macroscopic transsection of arteries showing thrombosis formation




Can distinguish between post mortem clots by their attachment to the artery wall (PM clots dont attach)



Arteriole thrombosis transsection




Contains dense eosinophilic material containing fibrin and red and white blood cells




Attached to the endothelial lining



Pulmonary thrombosis (macro)




Coagulation of blood in blood vessels during life




Abnormal triggering of clotting mechanism



Macroscopic image of Parasitic thrombus




Strongylus vulgaris presence leads to damage to the endothelium resulting in thrombus formation




Both intrinsic and extrinsic pathways are triggered




Lead to hypoxic damage and thromboembolic colic



Microscopic image of Parasitic thrombus




Angiostrongylus vasorum presence leads to damage to the endothelium resulting in thrombus formation




Both intrinsic and extrinsic pathways are triggered - clot filled entire vasculature



Thrombus forming on the valve of the heart




White head visible with black portion being the red tail




White head is made up of the white constituents of the blood




Red tail is the stagnation of red cells distal to the site of attachment of the white head - formed in the direction the blood is flowing

Diagram of the fate of thrombi




Removal by Fibrinolysis: Plasminogen to plasmin allows fibrin to turn into FDPs breaking down the clot




Propogation - Increase in size (in arteries form a white head and red tail) (in veins form a dark red cast of vein lumen)




Organization - decrease in size and formation of fibrous scar within vessel wall




Embolism - Before organization occurs, fragments break off and lodge in distant smaller vessels



Thrombosis of the caudal (posterior) vena cava



Organisation of blood vessel after thrombus




Endothelial cells proliferate to seal off surface of thrombus




New capillaries form through it - recanalisation



Emboli lodged at the aortic bifurcation



Fat embolism



Fibrocartilaginous embolism



Infarction Diagram of Stages




Obstructed arterial supply Initially swollen and poorly delineated




After 48 hrs coagulation necrosis occurs - pale with hyperaemic border




After 10 days organization occurs - indented




Infarction red in loosely structured organisms




Infarction pale in solid organs

Renal Infarction (Macro)




After 48 hrs coagulation necrosis occurs - pale with hyperaemic border



Renal Infarction (Micro)


After 48 hrs coagulation necrosis occurs - pale with hyperaemic border





Renal Infarction Macro




Organization have occurred (greater than 10 days) - indented



Cardiac infarction Macro




Solid organ so infarction appears white in color



Splenic Infarction macro




Loosely structured organism so red in color



Intestinal Infarction do to small intestine volvulus




Venous infarcts full of deoxygenated blood leading to very dark blue/black coloration

2

2

Bracken Fern




Toxin causing suppression of bone marrow




Trilineage depression - suppression of red blood cells, white blood cells, and platelets



Petechiae of mucus membranes (eye) of calves




Bovine neonatal pancytopaenia - bleeding calf syndrome, haemorrhagic diathesis of neonatal calves, blood 'sweating' disease




Thrombocytopaenic (increased consumption of clotting factors) and leucopaenic



Liver failure




Green hue to liver with rough bumpy surface, jaundice, and blood within the cavity (incapable of clotting)




Acquired haemostatic disorder




No ability to produce coagulation factors - inadequate synthesis




Retention of bile may also interfere with vit K absorption





Lung of animal suffering DIC (Disseminated Intravascular Coagulation)




Microthrombi within the venule of the lung (with alveoli surrounding) with platelets stuck between the meshwork



Kidney of animals suffering DIC (Disseminated Intravascular Coagulation)




Thombus in glomerular tuft and microthrombi throughout the capillary loops - impair glomerular filtration



Dark orange fibrin filling up glomerular tuft in animal suffering from DIC

Lymph node




During immune response to antigen a primary follicle, composed of re-circulating B cells and Follicular Dendritic Cells, forms a Germinal Center and becomes a secondary follicle




Follicular Dendritic Cells take up antigen and can hold this on their surface for periods of >1 yr (antigen ‘depots’)


Lymph Node




Intravascular lymphocytes migrate into paracortex via high endothelial venules




Specialised cuboidal endothelium have receptors that bind passing lymphocytes facilitating their transmigration into node


Medullary cords and sinuses of lymph node




If very activated, medullary cords will contain large numbers of lymphocytes and plasma cells (many of the sinuses cells would be plasma cells)


Reactive hyperplasia of lymph nodes (microscopic whole node section)




Response to infection/immune-mediated disease (Draining/filtering antigens/immune complexes)




Characterised by Nodal enlargement (hyperaemia/oedema)




Enlarged & increased # of secondary follicles




Possibly expanded paracortex (depends on antigen involved)




Medullary cords distended with plasma cells




Prominent sinus cell ‘traffic’ – sinus histiocytosis


Reactive hyperplasia, Outer cortex of lymph node




When follicles are antigenically stimulated (e.g. bacterial antigen) B lymphocytes in developing GCs undergo massive clonal expansion (hyperplasia) and hypermutation of their Ig-producing genes




B lymphocytes with augmented affinity for the antigen selected and move to mantle zone (edges) of follicle.




They then migrate to medullary cords as plasmacytes or memory cells




Non-selected lymphocytes (>90%) undergo apoptosis


Reactive hyperplasia, medulla - sinus histiocytosis of lymph node




Medullary sinusoids filled with macrophages & a few neutrophils (small dark nuclei)




Most macrophages derived from perisinusoidal macrophages - some arrive via afferent lymphatics




Medullary cords filled with lymphocytes and plasma cells




Plasma cell precursors formed in GCs in follicles in cortex, mature into plasma cells, and migrate to cords. Their presence in large numbers in cords indicate ongoing Ig production following an antigenic stimulus


Caseous lymphadenitis - Clinical Presentation




Caused by Corynebacterium pseudotuberculosis




Enters skin by contaminated wound with soil, faeces, or discharge




Bacteria drains to regional LNs




Neutrophils and eosinophil rich inflammatory response (eosinophil = greenish tint)




Has onion ring appearance due to sequential episodes of necrosis and repair




Collagenous layer to wall off abscess and then another around it and around that


Caseous lymphadenitis - Lymph node cross section




Caused by Corynebacterium pseudotuberculosis




Enters skin by contaminated wound with soil, faeces, or discharge




Bacteria drains to regional LNs




Neutrophils and eosinophil rich inflammatory response (eosinophil = greenish tint)




Has onion ring appearance due to sequential episodes of necrosis and repair




Collagenous layer to wall off abscess and then another around it and around that


Lymphadenitis




Dorsal view of opened larynx showing left and right retropharyngeal LNs grossly distended and effaced by pus




Streptococcus equi causing inflammation of upper respiratory tract LNs which drain to regional retropharyngeal LNs




Causes purulent lymphadenitis leading significant enlargement of periairway LNs and compression of trachea --> Strangles




Lymphadenitis (Micro)




Streptococcus equi causing inflammation of upper respiratory tract LNs which drain to regional retropharyngeal LNs




Causes purulent lymphadenitis leading significant enlargement of periairway LNs and compression of trachea --> Strangles




Greater hyperaemia/oedema




Influx of leucocytes +/- necrosis


Granulomatous lymphadenitis with caseous/structureless necrosis and dystrophic mineralisation




Caused by Mycobacterium bovis infection growing within macrophages




Infected macrophages carry mycobacteria to draining LNs (bronchial/mediastinal)




Multifocal to coalescing gritty pale abscesses


Lymph node atrophy (Micro big picture)




# and size of follicles decreased (arrowhead)




Paracortical lymphocytes depleted (arrow).




Node reduced in size




Hypocellular ‘ghost’ follicles and paracortical areas




Potential Causes:




Cachexia (starvation/malabsorption) cause decrease in T lymphocytes




Ageing causes decrease in both T & B lymphocytes




LN ‘exhaustion’ with some persistent infections


Lymph node atrophy - Cloe up of ghost follicle




Paracortical lymphocytes depleted




Node reduced in size




Hypocellular ‘ghost’ follicles and paracortical areas




Potential Causes:




Cachexia (starvation/malabsorption) cause decrease in T lymphocytes




Ageing causes decrease in both T & B lymphocytes




LN ‘exhaustion’ with some persistent infections


Primary Neoplasia of Lymph Node (lymphosarcoma) - Macro cross section




Bulging soft white homogeneous ‘fish-flesh’ Cortex/medulla obliterated




Note infarct as neoplastic lymphocytes cause vascular obstruction




No difference between cortex and medulla


Primary Neoplasia of Lymph Node (lymphosarcoma) - Micro




Monotonous sheets of often atypical neoplastic lymphoid cells




Clones of cancerous lymphocytes that have taken over and are expanding the lymph nodes




Lymph node architecture gone


Secondary neoplasia of Lymph Node (metastatic carcinoma)




Embolisation, lodgement, invasion, and growth of neoplastic emboli in subcapsular sinus (arrows)




Lymph node filters emboli of metastatic neoplastic cells draining from neoplastic epithelium




Cell type not normally found within the lymph node




Secodary Neoplasia of lymph node




Left are normal node lymphocytes while right side of section are large epitheliod cells which have metastasized from epithelial surface


Close up of secondary neoplasia of lymphocyte




Central cells neoplastic surrounded by normal lymphoid tissue




Variation in nuclear size, cell shape, strange appearance to cell chromatin


Normal Spleen with Activated Lymph Follicles




C - splenic capsule




WP - white pulp - Composed of B (follicles) and T (sheaths along arterioles) lymphocytes




RP - red pulp - collection of erythrocytes within sinusoids being filtered for recycling and bacterial killing




Ln - lymphoid nodule




GC - germinal center




CA - central arteriole




TR - trabecula


Terminal Capillaries within spleen




Connect directly into venous sinuses ‘closed system’ (97%)




Terminate in splenic cords ‘open system’ (3%)




Other capillaries release blood into marginal zone at periphery of white pulp




Blood eventually reaches sinuses of red pulp which are continuous with venules which connectto veins returning to the surface of the spleen via vessels in trabeculae


Normal Splenic Sinuses




Four splenic sinuses (1-4) joining to form a larger sinus (arrowhead) ultimately empties into venous system




Lined by discontinuous endothelial cells and surrounding framework of cellular splenic cords


Splenomegaly (Macro)




Can be caused by:




Splenitis




Haemolytic anaemia




Torsion




Chronic venous congestion




Barbituates




Splenic tumours


Peracute splenitis caused by anthrax - Macro slice into spleen




Bacterial toxins inhibit platelet aggregation




Necropsy shows splenomegaly with 'black berry jam' consistency


Peracute splenitis caused by anthrax - micro




Extensive lymphoid necrosis and depletion within the white pulp




Expansion of red pulp with increased clear space indicating oedema




Chains of basophilic rods with very few neutrophils or macrophages in the area


Splenomegaly, pig with haemolytic anaemia (macro)




Extremely enlarged and diffusely congested




Immune mediated haemolytic anaemia




Causes: Babesiosis, Haemobartonellosis (mycoplasma haemofelis infection)


Immune mediated haemolytic anaemia (micro)




Common in dog - idiopathic




Immune-mediated attack on rbcs




Macrophages proliferate in spleen, remove portions of rbc membranes where Ig attached marked haemosiderin accumulation


Haemosiderosis, spleen, dog (Not stained)




Haemosiderin - golden brown granules in splenic macrophages - product of phagocytosis of large numbers of red blood cells




Stain blue by Prussian blue reaction specific for Fe


Haemosiderosis, spleen, dog (Prussian blue stain)




Haemosiderin - golden brown granules in splenic macrophages results of phagocytosis of large numbers of red blood cells




Stain blue by Prussian blue reaction specific for Fe


Neonatal isoerythrolysis, foal




Immune-mediated haemolytic anaemia




Enlarged spleen (S) and liver (L) & very slight jaundice




Newborn foal ingested colostrum containing maternal abs which reacted against its own erythrocytes




Macrophages in splenic red pulp proliferate & remove erythrocytes whose membranes have bound ab


Splenic congestion following barbiturate euthanasia, horse (Macro)




Spleen enlarged & congested from storage of blood




Red pulp vascular spaces markedly distended by blood




One focus of white pulp to lower right of microscopic image


Splenic congestion following barbiturate euthanasia, horse (Micro)




Spleen enlarged & congested from storage of blood




Red pulp vascular spaces markedly distended by blood




One focus of white pulp to lower right of microscopic image


Hyperplastic nodules (aka nodular hyperplasia) of spleen




Incidental - old dogs




One or more bulging smooth hemispherical nodules 2-4 cm diameter




Composed of both red & white pulp




May occasionally rupture – haemoabdomen




Cross-section of bulging mass shows intermixed red & white pulp areas composed of rbcs & proliferating lymphocytes


Haemangioma of spleen




Benign tumour of endothelial cells




May grow to considerable size




May haemorrhage → haematoma


Haemangiosarcoma of spleen




Highly malignant tumour of endothelial cells




Solid & blood-filled regions




Metastasise & can rupture→ haemoabdomen


Haemangiosarcoma of spleen (micro)




Histopathology reveals haphazardly arranged vascular channels lined by anaplastic endothelial cells. Mitotic figure (arrow).


Haemic (haemopoietic) neoplasms in spleen (macro)




Tumours of blood cell-forming cells arising in bone marrow & resulting in significant No.s of neoplastic cells in bloodstream - leukaemias




Diffuse infiltration of sinuses of spleen → diffuse enlargement


Lymphosarcoma in spleen cross section (macro)




Spleen can get involved in lymphosarcoma




Neoplastic lymphocytes can cause a multifocal distribution (expanding the white pulp) or more discrete nodules - often detected on ultrasound scan


Secondary metastatic neoplasia




Metastatic carcinoma, spleen, cow




Lobulated white soft mass bulges from the cut surface


Siderofibrosis of spleen (macro)




Yellow colour grossly due to haemosiderin (blue microscopically) & bilirubin (orange microscopically)




White colour due to presence of calcium & fibrosis




Siderotic plaques - opaque pale yellow with roughened texture




Typically over capsule and along tip




Incidental, often seen on dog spleen




Ongoing trauma to capsule – local haemorrhage – fibrous repair & breakdown of heme - haemosiderin & bilirubin


Siderofibrosis of spleen (micro)




Yellow colour grossly due to haemosiderin (blue microscopically) & bilirubin (orange microscopically)




White colour due to presence of calcium & fibrosis




Siderotic plaques - Incidental, often seen on dog spleen




he plaque lies within the fibrous connective tissue of the capsule and consists of haemosiderin (purple) and bilirubin (orange) within fibrous scarring.




Ongoing trauma to capsule – local haemorrhage – fibrous repair & breakdown of heme - haemosiderin & bilirubin


Splenic rupture/ Haemotoma (macro)




Subcapsular haematoma, spleen, dog




Elevation of capsule from underlying parenchyma by a mass of blood




Caused by trauma




Sometimes observe fissures as incidental findings are necropsy




Splenic amyloidosis




When amyloidosis generalised (horses, dogs, cats and cattle)




Splenomegaly and high fragility - risk of spontaneous rupture






Normal Thymus




Lobulated




Clear corticomedullary differentiation




Prothymocytes from bm ‘home’ to & colonize outer cortex




Cortex - selection (proliferation/ apoptosis) and ‘training’ of T-lymphocytes - undergo rearrangement of T-cell receptor genes – ‘randomly shuffling gene segments’ – creates TCR diversity




Medulla – removal of auto-reactive T-lymphocytes (thymic epithelial cells express proteins from elsewhere in body)




Mature T-lymphocytes migrate to paracortical region of LNs, periarteriolar splenic white pulp & Peyer’s patches


Lymphocytolysis of splenic lymphocytes in a dog with parvo




Can see bits of broken nuclei


Lymph node, dog (whole picture Micro)




Nodal architecture replaced by monotonous sheets of neoplastic lymphoid cells




Monomorphic population of atypical lymphocytes that disrupt normal tissue architecture


Osteosarcoma (malignant osteoblasts) in the humerus of a retriever




Mesenchymal tumors




Bone, osteoblast, malignant



Osteosarcoma (outlined) in the distal femur of a St. Bernard. This tumor does not cross the joint space. The proximal tibia (arrow) is unaffected.




Mesenchymal tumors




Bone, osteoblast, malignant



Fibroma (fibroblasts) in the hind leg of a beagle




Mesenchymal tumors




Connective tissue, fibroblast, benign



Fibroma (fibroblasts) in the subcutaneous tissues of the muzzle in a dog. This tumor is growing by expansion, compressing surrounding tissues, It is not invasive




Mesenchymal




Connective tissue, fibroblast, benign



Mammary carcinoma in an Old English Sheepdog




Epithelial tumors




Malignant, does not form from glands



Dermal papillomas (keratinocytes) in a cow




Epithelial tumors




Benign, does not form from glands



Multiple well-demarcated non-infiltrative papillomas of the lips of a dog




Epithelial tumors




benign, dos not form from glands



Histology from well demarcated non-infiltrative pailloma of the lips of a dog




Shows a pedunculated, exophytic well-differentiated population of cells not arranged in glands



A well-demarcated non-infiltrative mass developing on the eyelid of a dog is most likely either a sebaceous gland adenoma or a benign dermal melanoma




Adenoma = benign, form from glands







Histology from a well-demarcated non-infiltrative mass developing on the eyelid of a dog




Shows a sebaceous gland adenoma with well-differentiated sebaceous cells arranged within well-formed glands



A well-demarcated non-infiltrative mass in the ventricles of a dog




Mmost likely a choroid plexus papilloma



An expansile non-infiltrative mass in the cerebrum of a dog




A possible astrocytoma



A canine oral melanoma is infiltrating into overlaying maxillary bone




Most neoplasms initially spread this way




Direct invasion



Canine lung with multifocal metastases from an osteosarcoma originally located in a femur




Sarcomas typically spread this way




Spread via the vascular system



Malignant cells (arrow) from an osteosarcoma in the blood vessel of a dog (outlined)




Spread via the vascular system



A prostatic carcinoma has spread to the subinguinal lymph nodes in this dog.




Arrow highlights necrotic lymph node




Epithelial tumors often metastasize via the lymph to regional lymph nodes




Spread via the lymph system



Enlargement of lymph nodes in this Weimaraner (arrows)




In this case the enlargement is due to lymphosarcoma, but they can also be enlarged due to the spread of epithelial tumors




Epithelial tumors often involve regional lymph nodes




Spread via the vascular system



Transcoelomic spread




Examples:




Hemangiosarcomas




Ovarian carcinomas




Mesotheliomas



Abdominal mesothelioma in an adult cow




Transcoelomic spread



Abdominal mesothelioma in an adult ewe




Note multifocal variably sized nodules and plaques covering most serosal surfaces (arrows)



Transcoelomic spread of an ovine small intestinal adenocarcinoma




Note numerous white metastases overlying the peritoneum of the mesentery and overlying the intestinal serosa



Histology of transcoelomic spread of an ovine small intestinal adenocarcinoma




Shows numerous poorly formed glands adhered to, and infiltrating through, the peritoneum



An invasive thyroid carcinoma (star) in-situ a dog



An invasive thyroid carcinoma (star) of a dog after excision



An invasive hemangiosarcoma in the leg muscle of a dog




Note that it would be impossible to locally excise the neoplasm



Ovine small intestine adenocarcinoma showing anaplasia, poor differentiation and the presence of a cluster of neoplastic cells within a lymphatic vessel (arrow)




Microscopic




Degree of differentiation



A leiomyosarcoma of the pulmonary artery found invading the heart




Note nuclear atypia, bizarre mitoses, high mitotic rate etc.




Smooth muscle, myocyte, malignant



Osteoma in the nasal cavity of a horse




Note that not all benign tumors are clinically silent



Hemangioma in the skin of a dog




Note the reddened areas which are due to the presence of neoplastic blood vessels

Bovine papilloma virus




BPV-1: Papillomas of the skin


BPV-2: Papillomas of the urinary bladder


BPV-3: Papillomas of the upper GIT




Viral oncogenes can initiate tumor formation




Factors involved in tumor transformation: intrinsic



Vaccine induced sarcoma in a cat due to chronic inflammation




Macro view and cut-surface of tumor




Factors involved in tumor transformation: intrinsic



Trauma (and chronic inflammation) induced ocular sarcomas are seen in cats




Chronic inflammation




Factors involved in tumor transformation: intrinsic



Squamous cell carcinoma on the nose of a cat




UV Light - Radiation




Factors involved in tumor transformation: extrinsic



Squamous cell carcinoma removed from the ear pinna of a cat




UV Light - Radiation




Factors involved in tumor transformation: extrinsic



Squamous cell carcinomas in the eyes of cattle




UV light - radiation




Factors involved in tumor transformation: extrinsic



Cutaneous and genital lesions in water buffalo due to infection with BPV-1




Viruses




Factors involved in tumor transformation: extrinsic



Dermal and genital papillomas and carcinomas in badicoot due to a papilloma virus




Viruses




Factors involved in tumor transformation: extrinsic



Cutaneous and corneal fibro-papillomas in a green sea turtle due to CFPHerpes V




Viruses




Factors involved in tumor transformation: extrinsic



Dermal papillomas in a green lizard due to an as yet unnamed herpes virus




Viruses




Factors involved in tumor transformation: extrinsic



Severe fibropapillomas in a cottontail rabbit due to Shope papilloma virus




Viruses




Factors involved in tumor transformation: extrinsic

Despite all these tumors being benign, the bulk and weight of these mammary gland fibroadenomas severely affected this rat




Effects of neoplasia




Disruption of normal tissue



Even benign neoplasms of the CNS can have severe clinical effects due to compression of the brain or spinal cord




Effects of neoplasia




Disruption of normal tissue



Intestinal lipomas in horses can result in intestinal obstruction and death if the pedunculated lipoma becomes wrapped around a segment of intestine




The necrotic intestine is dark red




Disruption of normal tissue



Metastases from a colonic adenocarcinoma in the liver of a dog




Disruption of normal tissue



Bovine cardiac lymphosarcomas can infiltrate the myocardium (pale areas) resulting in congestive heart failure or dysrhythmias and death




Macro and Micro




Disruption of normal tissue



Lymphosarcoma (pale areas) in a dog's heart




Disruption of normal tissue




Macro only



Dog skin




Although cutaneous lymphosarcoma rarely spreads from the skin to other organs, the ulcerative lesions become repeated infected, severely decreasing quality of life for the patient




Ulceration, haemorrhage, infection




Disruption of normal tissue



Ulcerated mammary tumor in a bitch.




Note also the non-ulcerated mammary masses (circled)




Mammary carcinomas can have rapid growth, necrosis, and ulceration




Disruption of normal tissue



Sheep skin.




Squamous cell carcinomas often result in ulceration, haemorrhage and secondary infection




Ulceration, haemorrhage, infection




Disruption of normal tissue



Transitional cell carcinomas of the canine bladder (left) often bleed resulting in hematuria




Ulceration, haemorrhage




Disruption of normal tissue



Rectal adenocarcinomas can lead to hematochezia




Anemia can occur if bleeding is chronic




Ulceration, Haemorrhage




Disruption of normal tissue



An adenoma of pancreatic beta-cells (insulinoma) can result in greatly increased insulin levels and sometimes fatal hypoglycemia even when barely visible




Increased function




Altered hormone production




Disruption of normal tissue



Thyroid adenomas in cats are common tumors and often result in increased levels of thyroid hormone with resultant clinical effects




Increased function




Altered hormone production




Disruption of normal tissue



Adenocarcinoma (circled) in a dog's thyroid gland is unlikely to produce thyroid hormone




Instead it's more likely ti result in hypothyroidism due to infiltration and destruction of surrounding thyroid gland




notice the numerous white metastases (arrows) in the lungs




Reduced function




Altered hormone production




Disruption of normal tissue



Hypertrophic pulmonary osteopathy in the distal radius of a dog

Circle indicates region of extra osseous growth

Paraneoplastic syndromes


Radiograph of Hypertrophic pulmonary osteopathy in the distal radius of a dog




Circle indicates region of extra osseous growth




Paraneoplastic syndromes



Hypertrophic pulmonary osteopathy in P1 of a horse




Arrow indicates extra osseous growth




Paraneoplastic syndromes



Section through a dog's kidney which has a lone of calcification at the cortico-medullary function (circled)




Hypercalcemia of malignancy




Mediated through an osteoclast activity factor or PTH-rP




Paraneoplastic syndromes




Muscle weakness, anorexia, vomiting




Neuropathy (decreased ADH sensitivity)



Cancer cachexia




Likely due to cytokines such as TNF-alpha




Not due to increased metabolic demands of the tumor




Disproportionately greater loss of muscle mass than loss of body fat




Animal anorexic and depressed




In veterinary medicine cachexia onset often indicates the appropriate time for eithanasia

Cytological preparation of an FNA from a Boxer skin lump




Note the strongly staining purple granules in the cytoplasm of mast cells (green arrows)




Also note that cytoplasmic granules in less well-differentiated mast cells (solid circle) may not stain well




Abundant eosinophils are also present (dashed circles)




Gross exam: breed




Boxers have a strong predisposition in developing mast cell tumors. These can be diagnosed cytologically



German shepherds are more likely to develop hemangiosarcomas than other breeds




Gross exam: breed



A histiocytoma should always be suspected if a lump develops on a young dog, especially around the head and feet.




Cytology should allow for diagnosis




An aspirate from a skin lump on a dog shows numerous histiocytes some with mitotic figures (circled)




Gross exam: age



Skin leukosis with generalized lymphadenopathy




A lymph node form of sporadic bovine leukosis in cattle usually affects animals <6 months old while the cutaneous form of sporadic bovine leukosis presents mostly in animals 1-3 years old




Gross exam: age



Pituitary pars intermedia dysfunction (PPID) a pituitary tumor which affects horses mainly in their late teens




Gross exam: age



Squamous cell carcinomas commonly develop on the nose and ears of cats (left)




The presence of an anaplastic population of keratinizing cells can be confirmed by impression smear (right)




Gross exam: location



Squamous cell carcinomas are the most common tumor in the feline oral cavity



Melanoma of dog oral cavity




Melanomas in the oral cavity of dogs are frequently malignant compared to those in the skin which are more likely to be benign




Gross exam: location



This benign follicular tumor has been traumatized and ruptured resulting in inflammation




The inflammatory response may be interpreted as 'rapid growth'




Gross exam: Growth rate



Nasal squamous cell carcinoma which grew faster than the blood supply could sustain resulting in necrosis and ulceration of the tumor




Necrosis often due to rapid growth and outstripping of blood supply by malignant tumors. Benign tumors are less likely to have necrosis




Gross exam: necrosis



Canine right atrial hemangiosarcoma with extensive metastases to the lungs




If there is a single mass in one organ and lots of masses in another organ then they are likely to be due to malignant/ metastatic tumors




Gross exam: number of masses



Multiple metastatic malignant melanomas in the thoracic cavity of a horse




If there is a single mass in one organ and lots of masses in another organ then they are likely to be due to malignant/ metastatic tumors




Gross exam: number of masses



White sun-bathing dogs often develop squamous cell carcinomas on the ventrum (left)




Anaplastic keratinocytes are visible cytologically (right)




Gross exam: Other factors: Amount of Pigment



Periocular sqaumous cell carcinomas are much more common in white faced cattle




Gross exam: Other factors: Amount of Pigment



Pancreatic adenocarcinoma




The cells are arranged in poorly-formed glands that have little resemblance to normal pancreatic architecture.




Microscopic features: differentiation




How similar to a normal cell is the neoplastic cell? (better differentiation = less mutation = more likely to be benign)



Anaplastic sarcoma showing marked variation in cell appearance and size




Microscopic features: anaplasia




How much variation is there between individual tumor cells? (More variation (anaplasia) = more genetic diversity = more likely to be malignant)



Anaplastic rhabdomyosarcoma (muscle tumor). Cells dont resemble normal muscle cells at all




Microscopic features: anaplasia




How much variation is there between individual tumor cells? (More variation (anaplasia) = more genetic diversity = more likely to be malignant)

Physiological causes of pre-analytical variation




Stress produces neuroendocrine changes

Hemoconcentration (horse, dog)




Physiological lymphocytosis (high) (young cats, horses)




Mild mature neutrophilia (high), slight monocytosis (high), eosinopenia (low), and lymphopenia (low)

Physiological causes of pre-analytical variation




Exertion

Increases CK, LDH, ALT, and AST

Biochemistry Profiles: Relations




Protein

Total protein (TP)




Albumin (A)




Calculated globulins (G = TP - A)




Calculated A/G ratio (1/G)

Biochemistry Profiles: Relations




Renal parameters

Urea




Creatinine

Biochemistry Profiles: Relations




Metabolites

Glucose




Cholesterol




Triglycerides

Biochemistry Profiles: Relations




Muscle

Creatine Kinase (CK)




Aspartate aminotransferase (AST) (Not specific)




Alanine aminotransferase (ALT) (Not specific)

Biochemistry Profiles: Relations




Liver disease

Alanine aminotransferase - ALT




Aspartate aminotransferase - AST




Alkaline phosphate - ALP




Glutamate dehydrogenase - GLD




Bile acids




Bilirubin

Biochemistry Profiles: Relations




Pancreas

Amylase




Lipase




Pancreatic lipase




TLI = trypsin-like immunireactivity

Biochemistry Profile




High Values: ALP, ALT, Bilirubin, Bile acids, Ammonia




Low Values: Urea, Cr, Total Protein, Albumin, A/G ratio, Glucose, Ca, Cholesterol

Severe liver disease - aquired porto-systemic shunt




Hypoproteinemia due to hypoalbuminemia, hypoglycemia, hypocholesterolemia, andlow urea indicate marked reduction in biosynthetic function (likely marked decrease in liver mass)




Low Cr likely reflects low muscle mass.




Low Ca due to low albumin, a major carrier of Ca (free Ca probably ok)




Slight to mild hepatocellular injury with cholestasis (ALT, ALP, TB)




Markedly impaired detoxification / excretion ammonium




Markedly impaired metabolism / excretion of bile acids

History: Lethargy, depression, ataxia,vomiting,oliguria




Biochemistry Profile




High Values: hematocrit, hemoglobin, erythrocytes, leukocytes, neutrophils, phosphate, potassium, glucose, urea, creatinine, total protein, albumin, anion gap




Low Values: lymphocytes, calcium, sodium, chloride, A/G ratio, Total CO2




Presence of: Calcium oxalate monohydrate crystals in urinalysis

Ethylene glycol poisoning (antifreeze) - producing oxalate nephrosis with marked azotemia, hemoconcentration and mild metabolic acidosis




Mild hypocalcemia due to hyperphosphatemia and possibly some chelation (by oxalate)




Market azotemia (elevated blood urea nitrogen), marked hyperphosphatemia, moderate hyperkalemia due to decreased GFR. With urine unconcentrated this indicates the azotemia is renal




Mild hyperglycemia due to stress with mild glucosuria due to exceeding renal threshold




Mild hyperproteinemia due to mild hyperglobinemia and slight hyperalbuminemia




Mild hyponatremia and moderate hypochloremia likely due in part to renal losses and for Cl, vomiting as well




Very high AG due to metabolic acidosis, uremic acids, and possible oxalate crystals or some other related metabolite




Mild proteinuria likely due to renal tubular injury as there is no inflammation nor haemorrhage and no evidence for glomerular loss




Oxalate crystalluria with renal injury and failure, and high AG, suggest ethylene glycol




Mild metabolic acidosis with partial respiratory compensation

History: lymph nodes seem enlarged




Biochemistry Profile




High Values: leukocytes, neutrophils, monocytes, calcium, urea, creatinine, albumin




Low Values: Hematocrit, hemoglobin, erythrocytes




Presence of: 1-2 granular cats/ high power field (sediment - urinalysis)

Lymphoma causing psuedohyperparathyroidism with secondary anaemia of chronic disease and renal tubular nephrosis and mild dehydration




Mild anaemia




Mild leukocytosis due to mild mature neutrophilia with mild monocytosis




Marked hypercalcemia




Marked azotemia due to decreased GFR. With urine unconcentrated this indicates the azotaemia is renal in origin, likely due to impaired renal tubular concentration by hypercalcemia




Mild hyperalbuminemia which can only occur due to dehydration




Mild hyperglycemia likely due to renal tubular injury and impairment of glucose absorption




Mild hyperglycemia likely due to renal tubular injury and impairment of glucose absorption

History: diarrhea, anorexia, weakness, pyrexia, dehydration, hypernea




Biochemistry Profile




High Values: Hematocrit, hemoglobin, erythrocytes, neutrophil bands, calcium, urea, creatinine, total protein, fibrinogen




Low Values: Leukocytes, neutrophil segs, lymphocytes, sodium, Total CO2, Anion Gap, pH, HCO3-, pCO2

Salmonellosis causing mild dehydration, moderate to marked inflammation, moderate metabolic acidosis




Mild polycythemia & hyperalbuminemia due to dehydration




Mild leukopenia due to marked neutropenia with degenerative left shift.




Neutrophilia and marked lymphopenia due to stress& azotemia and enteritis




Markedhypercalcemia




Marked hyponatremia and hypobicarbonatemia due to intestinal fluid loss




Moderate to markedazotemia due to decreased GFR




Marked hyperfibringoenemia and mild hyperglobulinemia




Moderatemetabolic acidosis with partial respiratorycompensation

History: anorexia,weakness, pyrexia, clinical dehydration of 7%, circling, ataxia, yawning, pushesagainst objects, muscle quivers, icterus




Biochemistry Profile




High Values: Leukocytes, neutrophil bands and segments, GGT, AST, SDH, GLDH, LDH, Bilirubin, Bile acids, Ammonia




Low Values: None

Hepatic encephalopathy due to liver failure with moderate inflammation.




Mild leukocytosis due to mild neutrophilia with mild left shift, likely associated with hepatocellular injury.




Marked cholestasis




Marked to moderate hepatocellular injury




Marked to moderate hepatocellular and hepatobiliary dysfunction (bilirubin and bile acid uptake and excretion and ammonia detoxification by urea production

History: hematuria, clinical dehydration of 8%




Biochemistry Profile




High Values: Neutrophil segs, total protein, urea, creatinine, firbinogen, sodium, glucose, total CO2, Anion Gap, AST, CK, pH, HCO3-




Low Values: lymphocytes, A/G ratio, potassium, chloride




Presence of: red, cloudy, protein, glucose, RBC, 1-2 granular casts in urinalysis

Tubular nephrosis with mixed metabolic alkalosis due to abomasal stasis and metabolic acidosis due to uremia, and hematuria, mild to moderate neutrophilic inflammation, and general systemic stress




Mild mature neutrophilia




Mild lymphopenia due to stress & azotemia




Marked hyperfibringoenemia and mild hyperglobulinemia likely due to renal disease




Marked azotemia due to decreased GFR. With urine unconcentrated this indicates the azotemia is renal




Moderate to marked hyponatremia and profound hypochloremia likely due in part to renal losses and for Cl, gastric sequestration as well




Mild hypochloremic metabolic alkalosis with hypokalemia




Mild muscle injury




Moderate to marked hematuria.




Moderate hyperglycemia and glucosuria due to stress and exceeding renal threshold




Moderate renal tubular injury

History: anorexia, depression, vomiting, unable to urinate, tense,enlarged abdomen




Biochemistry Profile




High Values: Neutrphil (segs), phosphate, potassium, glucose, urea, creatinine, ALP, Anion Gap, pH, urine protein




Low Values: Sodium, chloride, total CO2




Presence of: reddish brown, cloudy, protein, occult bloodm RBC, 15-20 WBC, triple phosphate crystals, 3+ bacterial rods

Feline urologic syndrome with hemorrhagic cystitis, mild neutrophilic inflammation, general systemic stress, and mild metabolic acidosis




Mild mature neutrophilia




Moderate hyperglycemia due to stress




Marked azotemia, marked hyprphosphatemia, moderate hyperkalemia due to decreased GFR




Mild hyponatremia and moderate hypochloremia likely due in part to sequestration in abdomem and for Cl, vomiting as well.




Mild metabolic acidosis causing increased anion gap along with accumulation of uremic acids




Moderate to marked hematuria




Mild paradoxic alkaluria




Moderate septic neutrophilic inflammation