LYMPHORETICULAR AND HAEMATOPOEITIC

what is obstructive nephropathy?

"big kidney, little kidney" stones: calcium oxalate ureteroliths - cat ureter is small and gets blocked easily. - obstruction of first kidney is typically asymptomatic (little), and second kidney grows in response - obstructs second kidney, then clinical signs leads to CKD

what are the inhibitors of coagulation?

- ATIII - inhibits thrombin, activated X - increased by heparin from endothelium - protein C inactivates V, VIII - fibrinolysis: enzymatic breakdown of fibrin by plasmin - derived from plasminogen in platelet membrane

how do you test for fibrinolysis?

- FDP's (fibrin degredation products) - latex agglutination test - special test and kit: requires special tubes - done on serum - increased if DIC, not specific (haemorrhage, jugular vein thrombosis, liver disease)

what are possible rxns to transfusions? what are clinical signs of a reaction?

- FNHTR - allergic - TACO - disease transmission - acute haemolytic - septic - anaphylactic clinical signs often non-specific: - pyrexia - tachycardia/tachypnoea/dyspnoea - erythema/urticaria - haemoglobinurea/haemolysed serum mgmt: - stop transfusion, check ECG/BP, symptomatic (adrenaline/CPR, anti-histamines, anti-pyretics)

what might be some ddx for the clinical picture of renal lymphoma?

- PCKD - FIP - acute renal failure - hydronephrosis - perinephric psuedocysts - other renal tumours (bilateral carcinoma)

for a dog, when should your cross-match a transfusion? why? how?

- a transfusion > 4 days ago - history of transfusion rxn - recipients history unknown why: there are blood types we don't check for or know about. major: donor cells, recipient plasma. spin them down in a centrifuge and look on a microscope. minor: recipient cells and donor plasma can be confusing if there is auto-agglutination or rouleax formation due to an autoimmune disease

how can you ensure adequate intake of an end-stage renal animals?

- appetite stimulants: don't really work that well. can try omega-3 fatty acids. often also sedatives (like mirtazipine) which can just cause them to sleep - can consider feeding tubes: short term solution for end-stage. discuss quality of life.

what is the diagnostic approach to the bleeding patient? what will the different tests tell you about most likely ddx?

- are the haemorrhages ecchymotic or petechial? if so - platelet defect most likely - if not: coagulation defect. consider age of animal (if very young, could be hereditary) - history: exposure to toxins - check CBC - evaluate HCT + plt numbers if thrombocytopenia: check for clots, check smear, recheck #s, assess degree - if 100 e9 - consider haemorrhage. if <25e9, may be thrombocytopenia causing haemorrhage if plt normal: consider vWD or function defects as cause - if possible check BMBD - assess vWF: AG - check PTT (factor VIII) and PT. if both prolonged: consider vit K deficiency or DIC if PTT alone: consider defects of intrinsic pathways (haemophilia A and B) if PT alone: early vit K, liver disease, early DIC

what organs produce leukocytes? which organs differentiate them?

- bone marrow - all cell lines - spleen/liver maintain protential for all - thymus, spleen, lymph nodes, bursa of Fabricius (birds): differentiation

what leads you to want to transfuse a patient?

- can the owners afford it - can you get a hold of it - are there any procedures plannes - is the anaemia regenerating/nonregenerating, and what is the expected disease progression? - is the animal coping (CVS status)

what can affect leukocyte numbers?

- dynamic equilibrium: balance b/w peripheral demand and BM ability to supply adequate replacements - other factors include position of leukocyte within blood vessel (marginated or circulating), availability for sampling

what parasitic infections might be a ddx for a highly thrombocytopaenic dog? how are they tested?

- erlichia canis, anaplasma platys, a. phagocytophilum, neorickettsiea risticii, bartonella visonii, rickettsia rickettsii = immunofluorescent antibody or PCR tests - leishmania infatum: amastigotes in macrophages, immunofluorescent antibody, ELISA, or PCR tests - e. canis, a. phagocytophilum, d. immitis, b. burgdorferi = SNAP tests also, haemotrophic mycoplasma spp (m. haemocanis in dogs, haemofelis in cats)

what are some hereditary defects of coagulation? how are they treated?

- factor VII deficiency - haemophilia A - factor VIII - Haemophilia B - factor IX - factor XI - factor XII Treatment: - transfusions of whole blood or plasma to replace factor deficiency, red cells - use of fresh or frozen plasma not enough - need cryoprecipitate (10x more factor VIII)

what are the indications for lymph node sampling? how do you know which one to sample?

- lymphadenomegaly (single/multiple nodes) evaluation of metastatic disease (based on drainage) - head: submandibular - caudal head/thoracic limb/thoracic wall: prescapular - thoracic wall, deep structures of thoracic limb/neck, thoracic/cranial abdominal mammary glands: axillary - caudal abdominal and inguinal mammary glands, ventral half of abdominal wall, penis, prepuce, scrotal skin, ventral pelvis, medial part of thigh/stifle: superficial inguinal - distal to stifle: popliteal classification of lymphoma (histo) if there are multiple large ones: avoid submandibular. often more complex things (inflammation, etc)

how is FIV transmitted? what is the common signalment?

- male, aggressive, free-roaming cats (not-neutered) - transmission: direct inoculation of blood/saliva during fighting - not transmissible via uterus/feeding of kittens. - don't put them in isolation (but don't let them bite other cats) avg age: 5-6 years very uncommon in indoor cats.

what is the role of basophils? what is their lifespan?

- maturation, release from bone marrow over 2.5 days - persist for 6 hours - role in type 1 hypersensitivities (anaphylaxis, rhinitis, asthma, GI, parasites) - ? role in delayed hypersensitivities? - poorly understood

what is DIC? what is aetiology? how is it treated

- mixed haemostatic defect when excessive coagulation leads to widespread thrombosis and then haemorrhage (all coagulation factors consumed) aetiology: secondary to other underlying diseases (neoplasia, liver, immune, infectious) diagnostics: - haemostatic anormalities: thrombocytopenia, prolonged PT/PTT, elevated FDPs, decreased fibrinogen, decreased ATIII tx: - stop coagulation process: heparin (different regimens) - transfusion of whole blood, plasma, or cryoprecipitate as a source of ATIII - aspirin to stop platelet activation prognosis: poor

how do monocytes develop and how are they distributed?

- monoblasts to monocytes in 6 days in bone marrow - no storage pool, do have marginated circulating pools - persistence in circulation varies, shortens w/inflammation - leaves circulation into tissues where they differentiate into macrophages with inflammatory cytokines

how should you collect a blood sample if you are evaluating coagulation time?

- most tests require citrated plasma (citrate tube) - ratio of anticoagulant: blood should be 1:9. fill to line - do not sample thru heparinised catheters - minimise trauma to prevent coagulation activation - centrifuge to separate within 1 hr - analyse with in 4 hrs or freeze - always include species specific control CHECK for clots in tube

what is polycystic kidney disease? aetiology/pathology

- persians + related breeds, autosomal dominant (DNA test available) clinical picture: - kidneys are palpably enlarged in azotemic cats - azotaemia doesn't develop until middle age - detected ultrasonographically before azotemia occurs (from 8m) - leads to CKS there is now a screening program.

what does metastatic neoplasia look like on a LN cytology?

- presence of "foreign" cells, even if no ample features of malignancy. - need to examine all slides!! - can't rule it out! - if you see mast cells: ask an expert. hard to tell, there can be mast cells in a LN.

IMHA in cats: how to diagnose, how it's different, how to treat

- primary (idiopathic) less common or more difficult to diagnose - giving blood products tends to be more challenging NO azathioprine - only give pred or cyclosporine/chlorambucil

what is the role of colostrum in cows? what are the most important diseases does it prevent? how does it work?

- primary prevention against neonatal septicaemia, joint/naval ill - enteropathogens - enzootic pneumonia (BRDC) nutrition: - first feed, with additional vitamins, trace elements 8.8% of cows die, mostly because of diarrhoea, pneumonia, and FPT physiology: starts 4-6 weeks before calving (dry period), IgG tranfered into udder - IgG, IgM systemically - re-secretion of IgG into gut lumen, passage of IgA in colostrum (+ milk) thru gut lumen need to get it at first milking, and with a high concentration (only 29% of holsteins have 100g in 2 L) - pre-calving milking or leaking, a short dry period, and premature calving can all affect this - mastitis too - heifers have fewer/different pathogen exposure - vaccinate

what is the treatment for FIP? how is it prevented at home, in a cattery? is there a vaccine?

- prognosis is grave - this is fatal - current options: palliative care, immunomodulators (interferon?), maybe glucocorticoids +/- chlorambucil most likely no survivors recorded prevention: very difficult - requires no contact with FCoV - test new cats before entering household if known to be negative - more likely not to re-infect if toilet outside. houses can spontaneously become FCoV free - hard to manage in shelters breeding catteries/shelters: - very difficult to be FCoV free - reduce number of young cats, strict hygiene - segregate antibody negative cats - test RT-PCR to identify shedding cats and remove persistent shedders (>6 wks) - wean kittens early vaccination: many failed attempts at producing vaccines due to antibody-dependent enhancement - if vaccinated and contract FCoV - more likely to develop FIP - ideally need vaccine that induces CMI but not humoral response - intranasal vaccine (IgA) has questionable efficacy but appears safe. not available in UK, not useful if cat already has FCoV

what are the requirements for RBC production?

- space in the cell - space in the marrow - growth factors (IL-3, GM-CSF, EPO) - iron - cholesterol/lipids for membrane - enzyme pathways for construction and maintenance

how is FCoV spread and what CS does it cause? how common is it? what is the outcome of infection?

- spread by faecal-oral - replicates in enterocytes Clinical Signs: usually none - kittens more likely affected (D+, V+/-), stunted growth outcomes: approx 80% of cats have FCoV - 60-70% transient (no immunity) - 10-15% PI - 5-10% FIP - 2-5% resistant

how is vWD treated?

- transfusion - cryoprecipitate best at 6-12 ml/kg - whole blood if anaemic - desmopressin as a pre-operative prophylaxis for dogs with type I - human intranasal preparation: give 1ul/kg SQ 30 min prior to surgery

what is the signalment and 3 clinical presentations of canine lymphoma?

- very common signalment: - median age 6-9 yrs, but can be any age - breeds deisposition (mastiff, boxers for T cell) presentation: 1) multicentric lymphoma most common: - generalised lymphadenomegaly (80-85%), often marked - often asymptomatic (can be malaise, lethargy, anorexia, pyrexia, PU/PD) - +/- hepatosplenomegaly 2) GI lymphoma (approx 7% of cases) - wt loss, anorexia - diarrhoea/vomiting - ddx IBD, other GI tumours, FB, intussuscepton 3) mediastinal lymphoma (appx 3% of cases) - dyspnoea/tachypnoea + cough - wt loss - regurgitation - heart sounds displaced, lung sounds reduced ventrally - loss of compressibility if small - horner's syndrome: sympathetic trunk runs thru cranial medastinum - hypercalcaemia (dog) - PU/PD, dehydration, vomiting - usually T-cell - caval syndrome (swelling of face from compression of cranial VC) 4) cutaneous lymphoma other ones less common (CNS, renal, hepatic, ocular, etc)

when would you do diagnostic imaging for an animal with CKD?

- young animals - dogs > cats - asymmetric kidneys - severe proteinuria - uncertain chronicity - "do everything" owners

what is the aetiology of feline lymphoma? what are the risk factors?

1) FeLV/Retroviruses. - ssRNA -- DNA via reverse transcriptase. integrates into host genome, can integrate next to a proto-oncogene - p27 antigenaemia cats increased risk - vaccination has reduced lymphoma cases and age of onset - could also be FIC? 2) genetic (siamese/oriental) 3) passive smoking 4) sites of chronic inflammation (IBD?) 5) post-transplant

what are the 7 clinical presentations of feline lymphoma? list in order of most to least common

1) GI lymphoma most common site. (50% of cases) - wt loss, anorexia - d+/v+ 2) mediastinal lymphoma: 10-20% of cases - dyspnoea/tachypnoea - cough, regurgitation - heart sounds displaced/lung sounds reduced ventrally - loss of chest compressibility - caval syndrome/horner's 3) renal lymphoma: 5-10% - median age 9 y - +/- alimentary involvement - 40-50% develop CNS involvement - PU/PD, anorexia, wt loss - renomegaly, usually bilateral (image) 4) hepatic/splenic: 5-10% of feline cases - general malaise, organomegaly, jaundice 5) nasal/nasopharyngeal lymphoma: 5-10% - nasal discharge - epistaxis - facial pain/distortion - loss of airflow 6) nodal lymphoma: rare (4-10%) - single nodes > multiple - >25% have lymphadenopathy as a component - there is a hodgkin's-like lymphoma variant (head + neck LNs) - ddx infections, benign hyperplasia (cats only) 7) CNS/ocular lymphoma - ocular infiltrates, uveitis, glaucoma - one of the most common CNS tumours in cats, often multifocal neuro deficits,

what are disorders of platelet function?

1) Glanzmann's thrombasthenia: defect in GPIIbIIIA - otterhounds, great pyrenees - quarter horse - defective plt aggregation, clot rxn 2) canine thrombopathia - abnormal GPIIBIIIa exposure, impaired degranulations - basset hounds 3) bovine thrombopathia - not known - simmentals - mild/severe bleeding

what are the four functions of the spleen?

1) RBC maintenance, iron metabolism (also repairing RBC, removing RBC) 2) blood reservoir (contracts during exercise) 3) haematopoiesis 4) immune functions

what are ways 3 to evaluate clotting time? how do you evaluate?

1) activated clotting time: evaluates intrinsic and common pathways of coagulation - collect 2 ml of whole blood into ACT tube w/ diatomeceaous earth - incubate, check every 5-10 second - interpret like PTT but less sensitive - affected by thrombocytopenia 2) PTT (partial thromboplastin time) - screening for intrinsic and common pathways - incubate with excess phospholipid, contact activator, and calcium - measure time to form clot - interfered by lipemia, haemolysis, oxygloben tx, and icterus -activity must be <30% of normal to prolong, such as haemophilia, DIC, vit K, liver disease - not affected by thrombocytopenia 3) PT (Prothrombin time) - screening test for defects in extrinsic and common pathways of coagulation - incubated citrated plasma with tissue thromboplatin (TF) and calcium. - measure time to clot formation - must be <30% - expect prolonged if factor VII deficiency, DIC, vit K, liver failure - not affected by thrombocytopenia, might be normal in early vit. K

causes of non-regenerative anaemia in small animals?

1) anaemia of CHRONIC DISEASE/ chronic inflammation. very common cause of mild/moderate anaemia (25-36% PCV, cats 18-26%) due to poor iron storage/utilisation, shortened red cell survival, impaired erythrocyte production 2) renal disease. normocytic, normochromic. inadequate EPO prod/decreased erythrocyte lifespan, decreased marrow response to EPO 3) FeLV - test for in anaemic cats. macrocytic normochromic or normocytic normochromic. can induce IMHA/bone marrow 4) miscellaneous: - nutrient deficiency (iron, copper, folate, cobalamin) - endocrine (hypothyroid, hypoadrenocorticism, hyperestrogen). usually only mild to moderate. can get severe pancytopenia with hyperestrogenism. - liver: mild to moderate. PSS due to iron deficiency. 5) Bone Marrow Disease: pure red cell aplasia, aplastic anaemia, neoplasia (myelophthsis from overcrowding), myelodysplasia, myelofibrosis

infectious causes of haemolytic anaemia? miscellaneous causes?

1) babesiosis (b. anis) in europe - travel scheme. B gibsoni in other areas. often have intravasculary haymolysis, thrombocytopaenia, often sicker (pancreatitis, AKI) 2) mycoplasma spp in cats (common) - often give doxy while waiting for results. dogs can b clinical after splenectomy also: leptospirosis, borrelia (Lyme), anaplasma, erlichia, dirofilaria, angiostrongylus any infection theoretically MISCELLANEOUS - oxidative damage: paracetamol (cats), onions, garlic, zn, cu - hypophosphataemia - shear injury - damaged endothelium

what are the steps of primary haemostasis?

1) damage to endothelium, exposure of subendothelial collagen - vWF released from damaged endothelium - platelet adhesion occurs - platelets bind to collagen via receptor GPIb, vWF from endothelium and become spherical with filipodia - additional receptors for vWF and Fibrinogen are exposed 2) platelet aggregation: platelets bind fibrinogen via receptor GPIIbIIIa between adjacent platelets, forming a clump/aggregate. 3) platelet secretion: platelets rapidly degranulate, releasing ADP, fibrinogen vWF, thromboxane A2, Factors V and VIII

how can we try to minimise electrolyte imbalances in the kidney?

1) dietary phosphate reduction (renal diet) slows the progression of renal disease. can live 2-3x as long. has higher calories though. if not, feed a senior diet. 2) IRIS phosphorus targets. phosphate binders if diet not enough. - palatability issues, constipation - aluminium, hydroxide (limited), lanthanum carbonate (expensive) ipakitin/epakitin or calcium carbonate (can cause hypercalcaemia)

what are common Ddx for generalised lymphadenomegaly? where are the lymph nodes?

1) disseminated infection: bacterial, viral, riccketsial, protozoal, parasitic, fungal 2) immune-mediated diseases 3) metastatic neoplasia (lymphoma) or leukemia, myeloma 4) skin disease 5) sterile granulomatous lymphadenitis

what are the 4 components of haemostasis?

1) endothelium - flattened cells that line blood vessels. have pro and anticoagulant properties - normally are anticoagulant and via inhibiting platelet aggregation and acting as a barrier to supendothelial collagen which is procoagulant 2) platelets - small, discoid, anuclear cells - 3-5um, bale basophilic - derived from cytoplasm of megakaryocytes in BM (thrombopoiesis) - mediated by thrombopoetin - circulate for 5-9 days in most species 3) coagulation factors - Von willebrands: produced by endothelium and platelets, stored in weibel palade bodies - released in early coagulation process - responsible for platelet adhesion to collagen 4) fibrinolytic factors

how should you evaluate a LN aspirate, generally, from slide to microscope?

1) evaluate quality of preparation - # of intact cells. neoplastic/imm cell can be very fragile. - adequate spread - want to be able to see - adequate staining (purple) - thick areas tend to under stain. understained slides look like lymphoma 2) access cellular arrengement - look like foreign cells. 3) try to decide if uniform (small matures, etc) or variable 4) LN are "easy" - only 5 big categories in which you have to fit it into

what nutritional aspects are changed with renal diets?

1) food intake/calories - anorexia is a big problem with CRF. need to eat it - don't do it while in the hospital - often reject prescribed diets, can try home-made or senior diet - end-stage: just need calories. doesn't matter what the diet is. 2) protein restriction (<5g/100cal for dogs, <8g/100 for cats, need more because they can't conserve protein or stop breaking down protein) - minimise generation of nitrogenous wastes, "relieving" kidney of extra urea filtering - controlling azotaemia might mitigate clinical signs - severe protein restriction might break-down muscle and worsen cachexia - might be useful with protein-losing nephropathies 3) phosphorus/phosphate : - best evidence involves reducing phosphorus and reducing renal secondary hyperparathyroidism and MBD. - preserves renal morphology - as soon as hyperphosphataemic (early disease) - might need phosphate binders 4) potassium: this varies from patient to patient. supplementation of potassium might be added in for hypokalaemic late stage cats. 5) sodium - low sodium. (in humans, it is important. in animals, it's not) 6) fibre - fermentable fibre addition lowers BUN via enhancement of colonic degradation of urea, increase of faecal nitrogen conten - "nitrogen trap" but not proven in cats'dogs 7) fatty acids - fish oils may dampen inflammation, modulate progression - omega-6 worsen renal injury in certain models. need omega-3 acids - also lowers SAP and glomerular pressure, may improve appetite

what are some ddx for acute bloodloss (regenerative, haemorrhagic anaemia) in horses?

1) haemoabdomen: - trauma (ruptured spleen/liver) - ruptured mesenteric vessel - uterine artery rupture - neoplasia 2) haemothorax - trauma (fractured rib, foals, or lacerated heart/vessel) - pulmonary haemorrhage - necrotising pneumonia 3) epistaxis - trauma - ethmoid haematoma - EIPH - neopasia - GP mycosis - pulm. haemorrhage - coagulopathy/DIC 4) haematuria - trauma - pyelonephritis - cystitis/urolithiasis - idiopathic renal haematuria - urethral rent (male) - neoplasia

what are the 4 basic mechanisms of neutrophilia and ddx for each?

1) increased demand - infections - immune-mediated diseases (IMHA, polyarthritis) - neoplasia - haemolysis, haemorrhage, necrosis, thrombosis 2) increased production independent of demand - well-differentiated neutrophils transformed: chronic granulocytic leukemia - poorly-differentiated: acute myeloid leukemia. prognosis poor 3) increased persistence in circulation - stress/steroid response - may be hypersegmented (rigth shift) - often seen w/ monocytosis, lymphopenia 4) redistribution - stress/excitement increased BP leading to marginated neutrophils swept off vessel walls - may increase WBC numbers by up to 200% - lymphocytes prevented from leaving circulation

what are 3 causes of monocytosis and some ddx for each?

1) increased demand - infectious (bacterial, fungal, protozoal) - immune-mediated disease (IMHA, meningitis, polyarthritis) - necrosis, trauma, burns - neoplasia 2) independent of demand - 2ary to immune neutropenia (common precursors) - myelomonocytic leukemia - acute and chronic forms - acute monocytic leukemia - with or without maturations 3) redistribution - steroids may move them

what are are 3 causes of Lymphocytosis and some ddx?

1) increased demand - persistent antigenic stimulation (fungal, protozoal, FeLV, leishmania, brucellosis) - post-vaccination - Young animals 2) increased #s independent of demand - chronic lymphocytic leukemia - well differentiated - acute lymphoblastic leukemia - poorly differentiated - stage V lymphoma: BM involvement, release of neoplastic lymphocytes into circulation 3) Redistribution: - physiological leukocytosis - hypoadrenocorticism

what are the 3 mechanisms of eosinophilia and their ddx?

1) increased demand - sensitised T cells/mast cells (IL-5 release) - parasite antigen - allergic disease (atopy, drug allergy, asthma, pulmonary infiltrate) - inflammation of mast cell rich tissue (gut, skin, lungs, uterus) 2) independent of demand - paraneoplastic (lymphoma, mast cell tumours, others with IL-5) - hypereosinophilic syndrome: numbers increase in circulation, tissue without obvious cause - eosinophilic leukemia

what are 4 mechanisms of lymphopenia and ddx of each?

1) increased demand - some protein-losing enteropathies (lose lymphocyte-rich chyle) - chylothorax - recruitment and emigration into tissue with antigens 2) redistribution - steroids (exogenous or endogenous): redistribution to bone marrow, tissues, trapping in lymph noodes - trapp in lymph rich fluid (chylothorax) 3) decreased production - infectious causes: viruses (canine distemper virus, parvovirus, panleukopenia virus, FeLV, FIV) - lympholytic drugs - chemotherapeutics (cyclophosphamide, azathioprine, long term corticosteroids) - congenital immunodeficiences (Bassett Hounds)

what are three mechanisms of neutropenia? what are ddx for each? how should this be treated, generally?

1) increased demand (endotoxaemia) - peracute bacterial infections (peritonitis, pyothorax) - immune-mediated (decreased neutrophil survival time) 2) redistribution (vasodilatory shock) - endotoxaemia, anaphylaxis - neutrophils marginate to vessel walls 3) decreased production (BM disorders) - infectious causes: parvo, FIV, FeLV, Ehrlichia - toxicities: commonly iatrogenic (azathioprine, cyclophosphamide, drug rxns) - ineffective prod: myelodysplasia (FeLV) - changes in marrow environment - myelofibrosis, myelophthisis (neoplasia) - stage V lymphoma - congenital abnormalities: cyclic neutropenia, higashi syndrome intervention: most give broad spectrum antibiotics if neutrophils <2e9

what can cause basophilia?

1) increased demand: immediate or delayed hypersensitivies or paratasism (dirofilaria, also GI parasites, fleas, and ticks) 2) paraneoplastic (MCT), rare basophilic leukemia

what are the mechanisms of thrombocytopenia and some ddx?

1) increased platelet destruction/consumption - immune-mediated: most common, often very low numbers (<10 x10 ^9). evan's syndrome. - haemorrhage - DIC: low numbers, other signs of a coagulation deficit - sequestration: rare, can occur with splenomegaly or large cavitate mass 2) decreased production - BM disease - neoplasia - drugs 3) infectious - numerous causes - FeLV, BVD, Ehrlichia, Lieshmania, borrelia (Lyme, not specifically thrombocytopaenia), anaplasma, angiostrongylus (mixed clotting), leptospirosis

how is CKD managed?

1) investigate cause 2) renoprotective tx 3) symptomatic at the end

what 3 specific tests can you do for VW disease? how can you interpret the results?

1) measure levels of vWF: Ag - blood into EDTA or citrate. will be decreased by clots in the sample and haemolysis - separate plasma immediately, 2) ELISA, immunoelectrophoresis (required for Type II) - <50% = carrier, likely to transmit, at risk for disease - 50-69%: borderline, can transmit - 70-180%: free from trait 3) genetic testing

how can you monitor for adverse effects of canine lymphoma tx? what should you do about them?

1) myelosuppression via haematology. ideally weekly initially/prior to tx. neutrophil count: - if < 1.5 e9, delay 3-7 d tx - if <1, reduce dose of drug bu 10-25% - if <.75e9, consider prophylaxtic Abx platelet: if <50e9, delay tx 5-7 days or change tx 2) biochem for abnormal parameters, toxicity (ALT for lomustine) 3) urinalysis (renal function, sterile haemorrhagic cystitis from cyclo, UTIs) 4) GI: prophylactics - anti-emetics (maropitant, odansetron) - GI protectants (omeprazole) - appetite stimulants

what are three causes of thrombocytosis?

1) physiological (Transient) - epinephrine induced splenic contraction 2) reactive (Secondary) - increased thrombopoietin, IL-6) - inflammation, haemorrhage, iron deficiency 3) essential thrombocythemia - myeloproliferative disorder - marked persistent increase in platelets - BM megakaryocytes increased, may have abnormal morphology

what lab tests can evaluate platelets and coagulation (primary haemostasis)? how should they be interpreted? when are they accurate?

1) platelet concentration (CBC): good accuracy except cat, sheep, goat because of overlap b/w RBC and size, and clumping - blood smear (do in cats, CKCs which can get giant platelets counted as RBCs) <100 x 10^ 9 = thrombocytopenia > 1000 x 10^ 8 = thrombocytosis, increased risk of thrombosis 2) buccal mucosal bleeding time: measures length of time for a platelet plug to form, evaluates primary haemostasis and platelet function - use a spring loaded cassette to make small incision in buccal mucosa - low sensitivity, increased in thrombocytopenic animals, von willebrand's disease, and disorders of platelet funcitoin - not increased with coagulation deficiencies

how can you monitor a positive response to canine lymphoma chemotherapy?

1) regular physical exams - measure LNS - complete response = not enlarged - partial reduction = >30% reduced - progressive disease > 20% increase - stable disease = between PR/PD 2) resolution of clinical signs like BW 3) Xrays for internal lesions 4) repeat FNAS of liver/spleen if done originally

what are the FIV diagnostic tests? how should you interpret the results? what causes false +ve/-ve?

1) serology to detect FIV antibody by ELISA: first line, usually in house, often combined with FeLV. detects with core + envelope protein positive could mean: - FIV + - circulating MDA - retest > 6 months - vaccination (not UK) - false +ve. retest with another kit negative could mean - FIV -ve - infected but not yet seroconverted. retest in 60 days - false negatives are uncommon 2) confirmatory tests: - western blot or IFA - PCR: only used to differentiate between vaccinated and naturally infected cats

how is canine lymphoma clinically staged (WHO staging)? what is the scheme?

1. single LN II. multiple LNs regional area III. generalised LN involvement IV: liver +/- splenic involvemenet V. BM involvement +/- other organs a - without systemic signs b- with systemic signs

how should you administer IV plasma to foals with FPT? what should you do if a foal has a reaction?

1.0L of plasma (15-17g/L IgG): Increases IgG concentrations by 2-3g/L 1.0L of plasma >25g/L of IgG: Increases IgG concentrations by 4-8g/L Several liters may be required, particularly in sick foals. use plasma giving set and monitor carefully for signs of plasma rxn. - 1 drop/second (3mL/min). - check heart, resp rate, temp every 5 minutes. - if no rxn after 15 minutes: administer quickly if plasma reaction: stop transfusion, give 1 mg/kg flunixin +/- IV fluids - wait 1-2 hrs, restart infusion slowly - if rxn persists, use different plasma batch/donor

how does FCov become FIP? what is the pathogenesis of the fatal infection?

5% of FCoV cats - sporadic mutation, poss @ S (spike) gene. allows the virus to enter and replicate in macrophages!! ultimately fatal immune-mediated reaction. - if humoral response: WET - (no cellular response) - complexes leading to vasculitis, formation of protein-rich effusions - if moderate CMI response: DRY - cytokine overproduction by macrophages - activates neutrophils which then extravasate and cause granulomas

what is the incidence of haemangiosarcoma and what are the effects? diagnostics? tx?

50% of all splenic masses are haemangiosarcoma. very likely if also anaemic/haemoabdomen (rupture) highly metastatic (liver, omentum, mesentery, brain, sq) diagnostics: - difficult to diagnose, FNA not rec, not on imaging, even histopath hard treatment: splenectomy if no mets, but palliative - median survival with surgery alone 3-12 wks (+ chemo = 6 month) - if haemoabdomen, worse prognosis <10% alive >1 year even with adjuvant therapy

what does lymphoma look like on cytology? how can you use these cells to do further tests?

> 50% immature, medium to large lymphocytes - monotony - the #s count (monoclonal) - possibly increased numbers of mitotic figures - only low numbers of small, mature lymphocytes - +/- plasma cells can send them from a slide to do a few tests: - PCR for T or B cell receptor arrangement, and look for clonality (PARR - same receptor arrangement if neoplasia) - flowcytometry for immunophenotyping (look at CD3, etc markers) - immunocytochemistry

what is the tx of acute vs chronic leukaemia? lymphoblastic vs myeloid?

ACUTE: difficult to tx. poor prognosis. lymphoblastic ( ALL) - L-aspararinase/prednisone + cytarabine first - then lymphoma type protocol. ~30% response rate myeloid (AML) - cytarabine - 6-thioranine + doxorubicin - ?TKIs? - worse prognosis than ALL CHRONIC: more treatable lymphocytic: - chlorambucil, prednisolone. - MST 1 yr myeloid (rare) - hydroxycarbamide

what are the clinical signs of FeLV and how do they develop? what is the main cause of morbidity and mortality? when should you test it?

BEGINNING: - many cats asymptomatic and can be healthy for years - early infection can have pyrexia, lethargy, lymphadenomegaly (but might be ignored) LATER: progressively infected cats: go on to have varied, non-specific and depends on organ involved - immunosuppression (most common noticed) leads to secondary infection - neoplasia (lymphoma, thymic or multicentric) - BM disorders (non-regen anaemia, or mycoplasma, cytopaenias) - miscellaneous (repro, fading kittens, neuro, etc) - most common signs: wt loss, fever, dehydration, rhinitis. vague. morbidity and mortality: due to secondary infections. depletion of interference with function of lymphocytes and neutrophils. opportunistic pathogens. test if: - struggling to treat an infection or it keeps recurring

what BM disorders are common with FeLV+ cats? why? what about neoplasias?

BM suppression due to viral infection of haematopoeitic stem cells and stromal cells. - anaemia: usually non-regenerative, pure red cell aplasia. if regen: check for mycoplasma or IMHA - cytopaenias: plateles or neutrophils. can wax/wane. some get myelodysplasia NEOPLASIAS: lymphomas. - 60x more likely, 25% of +ve cats get in 2 years

what are the causes of IMTP? what are clinical findings? diagnostics?

CAUSES: primary: antibodies produced against platelet antigens secondary: many causes - SLE or other immune diseases - drugs or vaccines - neoplasia - infectious (parasitic, lepto) clinical findings: - often very low numbers (<10 x10 ^9). evan's syndrome. recheck, look at smear for clots - evidence of petechial or ecchymotic haemorrhages - history of bleeding from gums, mucosal surfaces, wounds, etc diagnostics: diagnosis of exclusion - may see megakaryocyte hyperplasia ni BM - BM exam can be done, they rarely bleed - anti-platelet antibodies (need large volume of blood) - response to tx

what are the diagnostics for FIA? how is it treated?

CBC: regenerative anaemia - PCV drops suddenly - can have "latent" infection that lapses with stress/illness - RBCs destroyed by extravascular haemolysis by macrophages (spleen, liver, lungs, BM) - might rise once parasite burden drops - if peracute, may be pre-regenerative - +/- agglutination - +/- monocytosis blood smear: often not found, but have a look - FRESH smear, no EDTA - check that they aren't howell-jolly bodies (those are inside the cell) - no stained precipitate, no basophilic stippling, etc. coomb's test may b +ve PCR: sensitive. amplifies from in vitro, can distinguish b/w spp. - may be negative if you have already started tx - take sample first - evaluate for FIV/FeLV (which can also cause IMHA) radiograph: enlarged abdomen, enlarged organs - image: splenomegaly, hepatomegaly treatment: doxycycline - give with food/water (really important), can cause oesophagitis/stricture - flea control - may need blood transfusion (cross-match) - may try steroids for the IMHA before you make sure it has mycoplasma (can stop once diagnosis is confirmed) prognosis: excellent with tx - chronically infected is possible

what is haemoabdomen (equine)? what are CS, causes, diagnosis, outcome?

CS: often colic as presenting complaint - hypovolaemia - increased HR, slow capillary and jugular refill time, increased plasma lactate diagnosis: US - avoid abdominocentesis, introduces bacteria causes: - trauma - neoplasia - uterine artery rupture (periparturient haemorrhage) - mesenteric injury - idiopathic outcome: depends on cause. survival ~ 50%

what is the clinical presentation/diagnosis of leukaemia?

Clinical Presentation: non-specific - lethargy, weakness, anorexia, GI - pyrexia, pallor, petechiae - mild generalised lymphadenopathy - hepatosplenomegaly haematology: cytopaenias, often >1 cell line - abnormal circulating cells - perform flow cytometry to assess what markers they are expressing other diagnostics: BM aspirate/core

Nutritional MGMT of renal disease

Dan Chan

how is FIP diagnosed? what are all the tests you can do? (think about all the organ systems)

FCoV antibodoes are nonspecific (80% of cats are positive) but a very high titre + CS is suggestive - can have -ve titres with advanced FIP - FCoV PCR only tells you if a cat has FCoV extremely challenging to diagnose BIOCHEM: can be normal - hyperglobulinaemia: polyclonal increase on serum protein electrophoresis. albumin: globulin ration low, alb: glob < .5 highly suspicious - hyperbilirubinaemia: liver enzymes usually normal. if an animal has hyperbilirubin and no elevated liver enzymes, think FIP or sepsis - usually non-azotaemic, can be normal CBC: can also be normal - lymphpaenia (50% cases) - rest within reference interval - mild neutrophilia +/- mild left shift - mild non-regenerative anaemia FLUID ANALYSIS: - if peritoneal or pleural fluid then always sample - typically clear yellow and sticky - high protein content >35 g/l (exudate) but low cell count - predominantly macrophages and neutrophils - ddx lymphoma, HF, cholangiohepatitis, bacterial peritonitis, pleuritis - consider rivalta's test CSF analysis: increased proteins but non-specific profiles offered by lab: a-1 acid glycoproein (acute inflammatory but non-specific). >1500 increases suspicion. immunocyto/histochemistry: - stains FCoV in macrophages (only mutated FCoV should be in macrophages) - cannot differentiate strains - 100% positive predictive value - needs a biopsy, takes some time (often euthanise before results come back) IMAGING: xrays, etc. - fluid in the abdomen/chest/lungs, - US for fluid in abdomen (FAST) can do post-mortem ex-laps

a cat has non-specific malaise. hyperglobulinaemia (low albumin: globulin ratio) and hyperbilirubinaemia on biochem. CBC only has lymphopenia. liver enzymes are normal, everything else is normal. what might you suspect? what might you do next?

FIP (or sepsis) - do fluid analysis.

what are the ddx for regenerative anaemia caused by haemorrhage?

HAEMORRHAGE: external: - Melena - can have occult blood. need to test after 5 days of a meat free diet (check addison's) - severe parasitic infection (angiostrongylus) - Urinary tract - Epistaxis - Post trauma/surgery internal: - bleeding tumours (spleen) - amyloidosis (hepatic in cats) - trauma - into tissue (bleeding diathesis) - surgery

what are 5 main ddx for (regenerative) anaemia caused by haemolysis? what are signs? how can you tell b/w intra and extravascular?

IMHA: anti-red cell antibodies. can agglutinate, Coomb's test, can be severe/rapid and are usually strongly regenerative - neutrophilia, monocytosis - platelets affected (evan's syndrome) INTRAVASCULAR: - Ghost cells (lost haemoglobin, membrane only) assoc w/ deposition of complement. EXTRAVASCULAR: - spherocytes: red cells which survive macrophage attack. diameter looks small, volume is normal (MCV doesn't decrease) - increased bilirubin (yellow plasma) PARASITES - mycoplasma haemofelis, M. haemominutum - bloodborne, epicellular. increases cell fragility. - erhlichiosis/anaplasma - leptospirosis - dirofilariasis - cyclical - diagnosis: PCR - Babesia: dogs, tick-born. pyriform bodies. tx imidocarb. HYPOPHOSPHATAEMIA: diabetic ketoacidosis OXIDATIVE DAMAGE: HEINZ BODIES - heinz body = denatured haemoglobin caused by oxidative damage - cats more vulnerable than dogs, low numbers could be unremarkable - causes: onions, paracetamol, vit. k, propylene glycol, garlic, zinc - eccentrocytes (image) - Hb has uneven distribution within the cell. often dogs, horses with red maple toxicosis MICROANGIOPATHIC DAMAGE: SHEAR INJURY - tumours with narrow vessels (haemangiosarcoma) - organ inflammatory beds (severe hepatitis, DIC) with fibrin stranding - acanthocytes: projections. splenic - keratocytes: helmet shaped. intravascular trauma (vasculitis, DIC) - shistocytes: red cell fragments. fibrin deposition, DIC

how do you differentiate between stage V lymphoma and acute lymphoblastic leukemia (ALL)?

LYMPHOMA: - usually relatively well - LNs grossly enlarged - mild cytopenia - CD34 -ve ALL: - often sick - LN mildly enlarged - marked cytopenia - CD34 +ve

what is the appropriate stocking density for camels? what is the approximation vaccination strategy for alpacas?

MAXIMUM 5-7 adult alpacas per acre. vaccination: - clostridial diseases once annually, also bluetongue - worming - ivermectin not enough - nematodirus is not sensitive. can also use pyrantel, fenbendazole - liver flukes can be a significant problem.

what does MCV tell you about the type of anaemia you have? when would you see it change?

MCV = size of a single cell. normocytic: often mild, non-regen anaema, acute haemorrhage microcytic (image): iron deficiency anaemia, because the MCHC determines when division stops. Fe deficiency = one more division. - PSS, Fe deficiency, hepatick failure - akitas macrocytic: regenerative anaemia - polychromatophils larger than mature cells. - some poodles. - FeLV cats - myelodysplasia - stored/posted blood artefact

what is the prognosis for canine lymphoma with diff treatments? what about b vs t cell? what are negative prognostic indicators?

NO TX: 4-6 weeks PRED alone: 2-3 months b-cell multicentric: - median remission 6-9 months - median survival 12-13 months t-cell: - CHOP: 6 months - LOPP: 11-16 months negative prognostic indicators: - T-cells (high grade) with CHOP - substage b - hypercalcaemia - prolonged pre-tx with corticosteroids > stage III, stage V - failure to achieve CR - primary GI, hepatic, hepato-splenic, renal

what does a normal vs. reactive lymph node look like?

NORMAL - dominated by small mature lymphocytes (90%). 1-1.5x RBC, clumped - low #s of medium to large, immature lymphocytes - occasional macrophages, rare neutrophils, eiosinophils, etc REACTIVE (image) - enlarged, similar populations as normal = hyperplastic - 10-50% medium to large lymphocytes, but <50% - possibly increased % plasma cells - possibly increased # of mitotic figures - always look for reason

what is the treatment for FeLV for well vs. sick cats? what is the prognosis?

NOT a good reason for euthanasia. if well: - good preventative healthcare - neuter if entire and confine indoors - tx infections promptly - could be healthy for years if sick: - supportive care and tx as if would do otherwise - tx secondary infections - confine indoors no evidence for antivirals or immunomodulators median survival time: 2-3 years

what is the PCR test for antigen receptor rearrangement (PARR)?

PCR the antigen receptor region and assess presence of band. if single bland: malignant population (clonal) if multiple bands of diff. sizes: reactive population watch slide about this

a cocker spaniel is previously healthy and then quiet. vomited, anorexic, reluctant to stand. on PE: HR 150, pulses tall and narrow. MM pale, crt .5 seconds. HCT is 15% PCV is 18, lymphopaenia, thrombocytopenia. should you transfuse this dog? why or why not? what factors should you consider? what would you give bertie?

PCV is halved, acutely. is it regenerating or able to replace red cells? what is the progression? are there any procedures planned? (surgery/GA needs a lot of blood). in this dog: if the owners can afford it, then yes. you can give whole blood or backed red blood cells - the dog is hypovolaemic (melaena) and anaemic.

how can you differentiate between a primary and secondary clotting disorder and what are the common ddx?

PRIMARY platelet disorders (usually thrombocytopaenia) - IMTP (primary or secondary)/Evan's syndrome - increased consumption (haemorrhage, DIC is both) - sequestration (rare, splenomegaly, large mass) - decreased production (BM disease, neoplasia, drug therapy) - infectious disease (parasites: FeLV, BVD, Ehrlichia, Leishmania) - inherited (vW disease - dobermans, thrombathia,) diagnostics: - platelet concentration (CBC) - severe thrombocytopaenia - buccal mucosal bleeding time (not increased with coagulation deficiencies) SECONDARY coagulation cascade - congenital (haemophilia A/B, factor VII/XI/XII deficiency) - Vit K inhibitor (warfarin, sweet clover in cattle) - SLE (inhibition of coagulation factors by antibodies) - hepatic failure (impaired production) - drugs: heparin administration, phenylbutazone - DIC (both) diagnostics: - very high activating clotting (less sensitive) /prothrombin/PTT time (much higher than a primary). no changes in platelets - can test for fibrinolysis - latex agglutination (DIC)

what are the different pools of neutrophils and what is their relative volume?

ProNP: proliferation neutrophil pool - myeloblasts, progranulocytes, and myelocytes. mitotic pool, stimulated by a bunch of IL-s. timeframe ~ 3 days. MatNP: maturation neutrophil pool. Metamyelocytes, bands, and semgented nutrophils. 2-3 days of replenishing in dogs. - SNP: storage neutrophil pool. subpool of MatNP, ready to be released to marrow sinusoids CNP: circulating neutrophil pool. what's sampled during blood collection MNP: marginated pool ready to exit circulation and migrate into the tissues (TNP - tissue neutrophil pool)

what are some inherited deficiencies that can cause haemolysis?

Pyruvate kinase: basenjis, beagles - chronic, severe haemolysis, initially very regenerative but may go on to develop myelofibrosis PFK deficiency: english springers. - red cells sensitive to alkaline pH causing low-grade haemolysis, with severe episodes feline porphyria

what are some ddx for regenerative vs non regenerative, chronic blood loss in the horse?

REGENERATIVE 1) GI: paratasism, neoplasi 2) Haemolysis (immune-mediated, toxic red maple) - or infectious (EIA, piroplasmosis) NON-REGEN: 1) iron deficiency (chronic disease) 2) BM failure (myelophthisis, myeloproliferative disease, toxins - PBZ) 3) miscellaneous (rhEPO)

what is a stress leukogram? what is it a response to? what is the reverse? what is the difference between a stress leukogram, an acute inflammatory leukogram, and a chronic inflammatory leukogram?

STRESS LEUKOGRAM: a response to corticosteroids, whether endogenous (cortisol) or exogenous (pred). consists of: - mild-moderate neutrophilia - monocytosis - lymphopenia - eosinopenia ADDISON'S: REVERSE STRESS leukogram - lymphocytosis, eosinophlia - neutrophils/monocytes usually within normal limits - changes usually mild ACUTE INFLAMMATORY: - neutrophilia may or may not have left shift - everything else the same CHRONIC INFLAMMATORY: - may or may not have left shift - lymphocytosis instead of lymphopenia

treatment of primary IMHA in dogs? what is the prognosis?

TX: 1) IV fluid/blood transfusion 2) IMMUNOSUPPRESSANTS - prednisolone: suppression of macrophage activity, impair Ab binding, suppress Ig-G production - high dose and then taper down - Azathioprine (never use in cats) - cyclosporine, chlorambucil (cats) 3) aspirin/clopidrogrel: antithrombotic. 4) gastroprotectants - high dose steroids prognosis: guarded. icterus, haemoglobinuria/aemia, all poor prognostic indicators. common cause of death is pulmonary thromboembolism. may relapse in future. need regular MONITORING - regular PCV, TP, haematology , prior to each dose reduction. regular biochem - toxicity.

what are the three types of VW disease?

Type 1: most common (90%) - all multimers present, decreased concentrations - variable severity of bleeding but not until concentraion < 20% - dobermans, autosomal Type II: disp. decrease in large multimers - abnormalities in structure/function - severe, uncommon - german shorthaired/wirehaired pointers - autosomal recessive type III: absence of all multimers - scottish terriers, chesapeake bay retrievers, shetland sheepdogs, dutch kooiker

how can you diagnose GI lymphoma in cats? how can you grade/stage it?

US plays pivotal role high grade: 1) US: mass lesions in gut - loss of layering - LN enlargement - effusion 2) FNA of mass lesions/ mesenteric LNS/liver/spleen? - monomorphic large lymphoid cells 3) analysis effusions low grade: 1) US: diffuse thickening of gut (esp. muscularis) - masses uncommon - LN enlargement (mild) 2) difficult to FNA. LN may be too small, only small lymphocytes like reactive hyperplasia 3) endoscopy: visualisation of stomach, duodenum/colon - operator dependent, can only see mucosa - superficial biopsy - lymphoma vs. IBD? 4) Laparotomy: complete visualisation, can do full thickness biopsy, look for obstruction (can resect) grade is important, particularly in cats - immunophenotyping (b vs T cell, low grade GI usually T cell) - morphological subtypes affect prognosis staging: - CBC - Biochem - UA - B12

is it safe to take an FIP+ cat home if you have other cats? why or why not?

Yes - actually stop shedding once they mutate. Don't pass from cat to cat. however, littermates are more likely to get FIP if one does, because there is some genetic predisposition. but if the cat dies, clean the home thoroughly and wait 60 days.

what is multiple myeloma? signalment, CS, diagnostics, tx?

a plasma cell tumour, starting in BM/spleen. - older animal CS: - pyrexia, lethargy, pallor, lymphadenopathy, hepatosplenomegaly - signs of hyperviscosity (due to Ab production): neurological, bleeding - signs of bone pain diagnostics: - haematology: cytopenias - Biochem: increased globulins, +/- hypercalcaemia, azotemia - urine: bence-jones proteins (Ig light chains. special test). - serum protein electrophoresis - BM: excess plasma cells. >20% indogs tx: - melphalan, prednisolone (dogs0 - MST 12-18 mo

what is CKD-MBD?

a result of renal secondary hyperparathyroidism (metabolic bone disease). abnormalities of calcium, phosphorus, or vit. D metabolisms leading to problems in bone turnover, mineralisation, volume, linear growth, strength. can cause vascular or other soft tissue in calcification. this can lead to bone pain or pathological fractures.

what parasite can cause hyphaema? where is it normally found? what is the normal clinical picture?

a. vasorum - rare, but happens. normally in the right ventricle of the heart and pulmonary arteries of dogs, red foxes, and other carnivores. french heartworm - from foxes, then mollusks. 1) cardio-respiratory signs (coughing, exericse intolerance, dyspnoea, tachypnoea) 2) coagulopathies -

what are disorders of coagulation?

acquired factor deficiencies - main one: vitamin K deficiency - typically seen with rodenticide toxicity or sweet clover ingestion - vitamin K: factors II, VII, IX, X. produced in the liver, activated by a vit. k dependent carboxylase. inhibited by rodenticides (coumarin) - usually affects factor VII first because it's shortest half life

contrast acute vs chronic leukemia.

acute: rapid progression, severe signs - immature, poorly differentiated cells (blasts) with a high capacity to divide - prognosis poor (days/weeks - months) chronic: slow progression, mild signs - well-differentiated late precursor cells, less capacity to divide - prognosis reasonable (several months-years)

what is the leukocyte adrenaline response? how is it different from a stress leukogram?

adrenaline response: neutrophilia, lymphocytosis stress leukogram: lymphopenia, also monocytosis/eosinopenia

What is neonatal isoerythrolysis? what is the cause/prerequisites/=?

an immune-mediated haemolytic anaemia of newborn foals. cause: incompatibility between mare's and foals' blood group. 1) First foal inherits RBC antigens (Aa/Qa) from Sire but mare is negative - mare exposed to foals' RBC (transplacental haemorrhage, parturition) and produces antibodies 2) second foal inherits same antibodies - mare has built antibodies against Aa/Qa and foal ingests them 3) antibodies coat RBC, intra, extravascular haemolysis. clinical signs develop at 1-12 days of age, usually <3 days - onset of signs depend on amt of antibodies ingested and affinity - Aa > Qa

what is a blood type? how do we type cats/dogs? do we need to blood type animals before transfusions?

antigen on erythrocyte surface. proteins, glycoproteins, glycolipids, carbohydrates. feline: A/B scheme. more likely to react. ALWAYS blood type cats, DONOR AND RECIPIENt, they MUST match. - if type B receives type A or AB: peracute fatal reaction - if B receives A/AB: fever, icterus, destruction of cells - AB: A is acceptable, B is worse, AB is rare DOGS: dogs: DEA scheme (1-7can be + or -. should match DA1 even tho no antibodies. if you give a DEA + blood to a DEA 1 - RECIPIENT, i t will FORM ANTIBODIES AND DESTROY THOSE CELLS WITHIN 4 DAYS. (acute haemolytic transfusion reaction) - can be delayed the first time, the second time will be within 12 hours - other blood types less severe

what is combined immunodeficiency? (equine)

autosomal recessive genetic disease of Arabian Foals - enzymatic defect: non-functional DNA-dependent protein kinase - no mature functional T or B cells CS: - recurrent infections after passive immunity decreases - associated with infection with uncommon pathogens (adenovirus), pneumonia, diarrhoea - fatal at approx. 5 months of age (when foal IgG supposed to take over) - dam and sire both carriers of gene - genetic testing

what is normochromic/hypochromic anaemia? how is it determined?

based on MCHC/MCH on panel. hypochromic - iron deficiency/poor iron incorporatoin (with microcytosis) hyperchromic not possible

Equine Neonatal diseases and Equine Anaemia

bettina dunkel

how should colostrum be stored?

can be room temp for a day, refrigerated for 7 days, or frozen for 6+ months thaw at <55c - DONT microwave collect from first milking only. fermented colostrum not suitable for first feed but can use IgA for rotavirus

ideal blood donor?

can only buy dog blood in the UK. - want bigger dogs/cats, >4kg, ideally 5. they use human blood bags even though they are half the size. dogs > 25kg. - not stressed/sedated. good dogs, good temperament. - healthy, age 1-8 years old, negative on FeLV, FIV, Mycoplasma, etc. UTD on vaccinations/worms - no travel abroad - no transfusions themselves the animal is given fluid afterwards.

how is immune-mediated haemolytic anaemia caused, diagnosed, and treated in horses?

causes: 1) .primary uncommon 2) secondary: antibody formation via - primary disease process - drug admin (penicillin, PBZ) - neoplasia - immune-mediated disease - EIA diagnosis: - can attempt coomb's test (anti-RBC antibodies on surface or parent) but false +ve, -ve possible - flow cytometry to demonstrate antibodies on RBC tx: - treat primary disease if possible, stop all medications if possible - transfusion only if signs of inadequate oxygen - immunosuppression: corticosteroids, azathioprine, cyclophosphamide (rarely in horses)

describe the causes (2 main) and clinical picture of anaemia due to inadequate erythropoesis in horses.

chronic disease - chronic inflammation/infection - neoplasia - sequestration of iron - shortened RBC lifespan - defective epo response clinical picture: - mild to moderate - normocytic, normochromic - non-regen - no clinical signs tx: treat primary disease. iron deficiency - chronic blood loss - treat with oral iron supplementation others: - chronic renal failure - admin of human recombinant EPO

what are the 5 LN cytology classifications? what are the cell types?

classifications: 1) normal 2) hyperplastic/reactive 3) lymphadenitis 4) lymphoid neoplasia 5) non-lymphoid neoplasia cell types: can only judge size if adequate spread 1) small lymphocytes: 1-1.5x RBC (should b 80%) 2) medium lymphocyte: 2-2.5x RBC. chromatin pattern much finer. 3) large lymphocyte (>3x RBC. if there's a lot of them -- neoplastic. if there's a few of them -- reactive) 4) plasma cell (vary in #) 5) macrophage: eccentric nucleus, busy cytoplasm may have few inflammatory cells, mast cells, foreign cells

what are the clinical and lab findings of neonatal isoerythrolysis? what are the diagnostics?

clinical findings: - signs may occur >12 days pp - weakness, depression, not nursing - tachycardia/tachypnoea - +/- fever - icterus +/- neurological signs - foals may be septic laboratory findings: - anaemia - haemoglobinuria/haemoglobinaemia - increased unconjugated bilirubin - metabolic acidosis - pre-renal/renal azotaemia - toxic hepatopathy/hypoxic hepatocellular necrosis diagnosis: - history + clinical signs (often can dx with just this) - haemolytic cross match: requires external (rabbit) complement, but negative doesn't rule out

what are the most common clinical findings with FIV? which cats should you test?

clinical signs: - gingivostomatitis - neoplasia (5x risk of lypmhoma, usually high grade) - ocular signs: uveitis, chorioretinitis - anaemia, leucopaenia - opportunistic infections - chronic kidney test: - sick cats with those clinical signs or anaemia, TCP, mycoplasma haemofelis, or polyclonal gammopathy - cats to be rehomed - kittens from FIV +ve queens - cats at risk of infection (bite wounds), living with FIV+ cat - cats to be vaccinated (not uk) - blood donors

what are perioperative + intraoperative considerations of a splenectomy? complications?

considerations: perioperative: 1) increased risk of DIC: perform PT/APTT tests, blood type, PCV/TP - be ready to provide extra stablisation/postop care - unsure why, could be blood pooling 2) increased risk of cardiac arrhythmias: treat hypovolaemic shock, antidysthythmic drugs intra-op: - fluid loss. need suction: so much fluid in the way - time: LDS, vascular clips, vessel sealant devices can all speed up surgery complications: - haemorrhage (technical failure, DIC) - cardiac arrhythmias - use an ECG of you have one. often self-limiting, perfusion relation. just monitor it and monitor the BP. can last for several days. - gastritis/pancreatitis - infection risk?

how to decide aspirate vs biopsy of LN?

cytology is great for cell details histo is great for architecture. classic lymphoma = easty to recognize on cytology if more unique lymphomas - histo is better

which farm animals need supplemented colostrum? what factors affect how much is colostrum is absorbed (by baby, mother, and colostrum)

dairy calves - selective breeding of dairy cows leads to dilute colostrum, shape of udders makes it difficult for calves to nurse properly. - can do assisted suckling, bottle + teat (need patience) or oesophageal feeder (not a stomach tube) needs: - need 2L at first feed. 3-4 for a 45k calf more effective. dairy and sheep probably ok. - 5g/L plasma = protection, 10g/L plasma = no disease baby factors: - weakness - acidosis - dystocia - mouth issues (belgian blues have large tongues) - timing - most efficient immediately after calving. by 12 hrs < 50% udder: - sore teats - teat shape - teat alignment - dropped udder mother: - poor mothering - heifers - disturbance/stress - overcrowding of calving area - c-section (some lose interest in calf) - milk fever/downer cow - slippery floors

what should your diagnostic approach be to non-regenerative anaemia?

depends on severity. similar investigation path to regenerative anaemia but different ddx - look for the disease. if severe and no cause found - issue may be in bone marrow, esp if bi/pancytopenia how to sample BM: sedation and local if aspirate, anaesthesia if biopsy - iliac crest or proximal humerus - clip, prepare aseptically - aspirate, smear quickly (clots within seconds/minutes) - core biopsy - roll prep into formalin - thrombocytopenia not a contraindication to BM sampling

what are 3 FeLV diagnostic test options? when would you use them?

detect antigen (p27) by ELISA/serology/SNAP (in house): capsid protein on virus - SNAP test, for FeLV/FIV - first line for all cats. - serum better than whole blood. - if negative, highly reliable (unless recent exposure - retest in 30 days) - can get false positives. use a diff. manufacturers kit - kittens can be tested at any time (no vaccination interference) confirmatory tests: 1) PCR (most common) for FeLV provirus or RNA to confirm progressive or regressive infection (latent cats) 3) testing for neutralising antibody: not diagnostic. but might identify immunity (regressor cats with complete virus slim)

diagnostic appch to pale MM?

determine anaemia vs. poor perfusion 1) manual PCV/TP - TP will decrease with haemorrhage, but normal/increase with haemolysis/NRA 2) regen or non/regen? think about timescale (3-5 days before signs of regen) - reticulocyte count (smear) - blood smear eval: in house? signs of regen, evidence of cause? 3) in saline agglutination test

when anaemia is determined, what is the first question to ask? what should you do?

determine between regenerative and non-regenerative anaemia - timescale - measure reticulocyte count/polychromatophils - blood smear eval (in house?): signs of regen (anisocytosis, polychromasia, nRBC), evidence of underlying cause (IMHA, mechanical, infectius agent) - take CORRECTD RETICULOCYTE PERCENTAGE.

how is angiostrongylus vasorum diagnosed and treated?

diagnosis: - angiosnap - bearmann - faecal smear treatment: - imidacloprid/moxidectin spot on - milbemycin - fenbendazole

what are the signalment and clinical signs of FIA?

disease more common in young males (more out + about), more common if FIV/FeLV +ve CS: acute: normal anaemia signs - lethargy, anorexia - fever - pale MMs - splenomegaly, icterus Chronic - wt loss, weakness, depression - can have "latent" infection that lapses with stress/illness

how does CKD progress? how does one control the factors important in the progression of CKD?

dogs progress more rapidly than cats. most dogs will die >1 yr of diagnosis but cats can live 2-3 years, at least half will die of something else. the way progression goes is periods of worse and getting better until a certain threshold of no return and the renal disease is fatal. probably due to secondary renal hyperparathyroidism, glomerular hypertension, and direct proteinuria induced renal injury. treatments: 1) dietary therapy to reduce secondary renal hyperparathyroidism 2) ACE-inhibitors to reduce proteinuria

what are the clinical signs of FIP? what are the two types?

early signs - non-specific: - pyrexia of unknown origin (waxes and wanes), often referred WET: 60-75% of cases - inappetance, anorexia, wt loss, listlessness - dehydration - icterus - abdominal masses and distension - tachypnoeas with pleural effusion DRY (non-effusive): 25-40% of cases - granulomas in the eye, brain/CNS, kidney, liver, intestines - always perform ocular and fundic exam if suspicious of dry FIP - iritis, keratic precipitates on the cornea/AC, cuffing in the vitreous/fundus

what are the most common neonatal diseases of calves?

early weeks - pre-weaning: navel ill, diearrhoea later weeks: BRDC diarrhoea least of ur worries

what is the epidemiology and pathogenesis of FeLV? how is it transmitted and what are the three different pathogenesis after exposure?

epi: - 1-2% of healthy cats are +ve - 20% of sick cats? - similar rates worldwide but decreasing since vaccines/testing pathogenesis -once exposed, it can cause transient viraemia (in lymph tissues) or no clinical signs be eliminated (abortive, rare). this leads to lifelong immunity - populates salivary glands and mucosal glandular epithelium - 3 wks later: BM cells involved - neutrophils and platelets: viraemia. can still go to a latent infection and become a regressor cat - after 3-14 weeks: becomes lifelong host and gets progressive infection (vast majority) transmission: - saliva, nasal secretions of PI cats, and faeces, urine, milk - prolonged intimate contact: sharing food/water, intimate grooming. multi-cat households - kittens in utero or feeding - blood transfusions

describe the transmission, clinical syndromes, and diagnosis of EIA. what type of pathogen is it?

epi: lentivirus (like FIV, caprine arthritis encephalitis virus, maedi-visna) - transmitted via insects, blood contaminated equipment - not present in UK but risk from imports - persistent - lifelong carrier syndromes: acute, chronic, inapparent - anaemia caused by intra + extravascular haemolysis - BM suppression - thrombocytopaenia common diagnosis: coggins' test (AGID) or ELISA - euthanasia or lifelong quarantine if horse is positive as danger to other horses

what are the two types of canine cutaneous lymphoma?

epitheliotropic: affects the most superficial layer of the dermis non-epitheliotropic: affects the deeper layers

when is a partial splenectomy indicated? how is it performed?

focal and benign disease (like trauma) - ligate hilar vessels along a line of demarcation close: - with forceps, form two rows of continuous overlapping mattress suture, then close cut end with continuous suture - or linear stapler if there is any doubt, do a total splenectomy.

where are RBC's produced in the neonate vs growing animals?

foetus: liver/spleen neonate: bone marrow growing animal: BM of all bones. red marrow = making RBC, yellow marrow = not - liver/spleen maintain erythropoietic capacity, especially if increased demand

review the splenic vasculature and how it informs splenectomies. how should you perform a splenectomy?

gastrosplenic ligament + short gastric vessels are very short, so the spleen is attached there. (bottom image). often rupture in a GDV, can cause necrosis in the spleen and require removal. it's easier to start at the mobile end. main splenic artery. make sure you don't remove the branch to the pancreas from the splenic artery. try to ligate the gastroepiploic closer to the spleen. best help is to use abdominal retractors (better than a person) so that you can see what you are doing. pack everything else off so you can see what you are doing. start at the mobile end. big area of fat: you will see the splenic artery (white) and the dark one is the vein. ligate near the spleen. (splenic artery + vein, left gastroepiploic, and 2 from stomach)

how should transfusions be administered?

give with hartmann's and through a filter. slow initial rate (.5-1 ml/kg/hr for first half hour). give over 4-6 hrs. don't want it at room temp for too long.

how is anaemia due to haemorrhage treated in the horse? what indicators do you use to guide treatment?

guided by clinical and lab indicators (HR, RR, lactate, PvO2, not PCV) - PCV not good indicator in first 24 hrs - if source of bloodloss can be ID'd, attempt to control blood loss (ligate etc) - severe acute blood loss - IV fluid resuscitation anaemia may not need to be treated if animal can be stabilised

what should you assess after a diagnosis of canine lymphoma is achieved? (what tests need to be done to properly stage it?) what are you looking for?

haematology: essential - neutrophils/platelets - anaemia - BM involvement (neutropenia, thrombocytopenia, anaemia, abnormal circulating cells) biochem: essential - organ involvement (disease extent, drug metablolism) - liver enzymes, urea, creatinine - concurrent morbidities - hypercalcaemia urinalysis: general health screen - urine SG to assess renal functin - check for blood before starting cyclophosphamide thorax Xray/CT: nice, not essential - 60-70% of dogs with multicentric lymphoma will have abnormalities - mediastinal LN enlargement, pleural effusion, various lung patterns US: not essential - liver and spleen, abdominal LNS, other organs - need FNA to confirm infiltration - mass lesions, thickening of gut, loss of GI layering (image)

what is periparturient haemorrhage? clinical signs, tx?

haemorrhage from uterine (reproductive tract) vessels after parturition important cause of post-partum colic and death CS: - delivery often uneventful - bleeding may be confined by broad ligament or may bleed into abdomen (haemoabdomen - often rapidly fatal) - mares may repeat bleed during subsequent pregnancies tx: - aimed at cardiovascular stabilisation

what is FIA? what is the pathogenesis of FIA? how is it transmitted?

haemotropic mycoplasmas (m. haemofelis, candidatus mycoplasma haemominutum, candidatus mycoplasma turicensis) - parasites with no cell wall, then attach to RBCs - cause immune-mediated destruction. more severe with concurrent diseases or immunosuppression - more sever if concurrent disease, immunosuppressed - more common with chronic infections transmission: - fleas - blood transfusion - neonates - not sure if fighting/oral, urine/salive not thought to be infective

what are the steps of secondary haemostasis? what are the coagulation factors and cascade? what is the intrinsic vs. extrinsic factory?

happens simultaneously with formation of platelet plug because damage to endothelium releases tissue factor which activates the extrinsic coagulation pathway coagulation cascade: - soluble enzymes in circulation, activated from proenzyme - each step amplifies the system - end result is insoluble fibrin, which stabilises the primary platelet plug extrinsic system: initiation - TF from vascular injury released from damaged tissue binds to, activates FVII in presence of calcium intrinsic system: amplification - FXII activated by contact with negatively charged surface and platelets - slower than extrinsic - a bunch of shit with calcium - IX activates X of common pathway common pathway: - X binds with V and calcium eventually prothrombin turns into thrombin, which turns into fibrinogen, and finally insoluble fibrin

what are oxidative injuries to the horse? what are the most common signs? what are blood smear signs?

heinz body formation - leads to haemolytic anaemia - oxidatively denatured Hb precipitates on RBC membrane - makes RBC less deformable, rapidly cleared from circulation causes: 1) drugs (phenothiazine, methylene blue) 2) plants (onions, brassica, red maple) - red maple (not UK) - wilted leaves toxic (gallic acid + ???) - methaemoglobin results from oxidative damage of haemoglobin iron from ferrous (2+) to ferric (3+) state - not usable for oxygen transport - heinz body formation also present - causes chocolate brown MMs

clinical picture of high grade vs low grade feline GI lymphoma?

high grade: - older cats (10y) - short history - GI signs, wt loss - thickened intestinal loops - mass lesions (gut, mesenteric LNS) - may be obstructed - +/- peritoneal effusion low grade: - older cats - more chronic history (months) - +/- thickened intestinal loops - mildly enlarged LNs

how does the haemogram of young animals differ?

higher numbers of WBC lower haematocrit changes usually mild, normalised by 3 months

what is the diagnostic approach to a suspect canine lymphoma case?

history/physical - palate all peripheral LNs - MMS (pallor, petichiae) - chest auscultation/percussion/compression - abdominal palpation - rectal examination FNA of LN/mass lesion (might need US if mediastinal): - shows a monomorphic population of intermediate/large lymphoid cells (image) Biopsy/Histo may be needed (remove whole node preferrable) - if GI, can do endoscopic biopsy of cut cytology of effusions when diagnosis is tricky, IHT may help, look for B/T cells PCR for antigen receptor rearrangement (PARR))

what are the paraneoplastic syndromes of lymphoma? what are the CS? when are they most common?

hypercalcaemia in 10-40% of dogs, rare in cats. more common with t-cell (PTHrP) CS: - PU/PD, dehydration - depression, weakness - anorexia, vomiting - constipation - bradyarrhythmias - muscle tremors

how does FeLV transmit to fetuses from pregnant queens? how are they affected? what should you do?

if < 2 months pregnant when contracted, they will always be progressively infected often don't survive the pregnancy consider spaying or euthanising the kittens.

what is "rescue therapy" for canine lymphoma?

if it relapses when not receiving therapy/ in maintenance phase restart original protocol if relapse during induction (resistant), try different drugs or dif. combo doxorubicin, L-asparaginase + lomustine, or DMAC (dexamethasone, melphalan, actinomycin D cytosine arabinonside)

how can you prevent FeLV at home and in practice? what about the vaccine?

in practice: - good routine hygiene: virus susceptible to regular disinfectants/detergents - no sharing food/water bowls - care with multidose vials - confirm blood donors are -ve at home: - only introduce negative cats into household - consider keeping indoors or confining when outdoors or vaccination Vaccine: - vaccine available (5 types) - whole inactive virions or inactivated gp70 + envelope. - not core: consider exposure risk (indoor cats don't need) - associated with injection site sarcomas - left pelvic limb - consider testing before (if immune, don't need to vacine)

what can cause erythrocytosis/polycythemia?

increase in HCT/RBC/Haemoglobin. relative: - dehydration (volume contraction) - RBC redistribution (splenic contraction) absolute: - primary = polycythemia vera. disorder of erythoid stem cells, EPO lowered or decreased. - secondary: chronic hypoxia, EPO secreting tumours, EPO levels elevated

what does lymphadenitis look like on cytology?

increased % of inflammatory cells. - neutrophils = neutrophilic, eosinophils = eosinophilic - macrophages: histiocytic/macrophagic - can have combination, can also have mast cell % increase

what is FIV? what is the pathogenesis of FIV?

infects CD4+ T cells, B cells, activated macrophages. contains two identical RNA strands and enzymes surrounded by a host cell envelope. similar to HIV. primary stage: weeks. surge in viral replication. - transient - nonspecific illness asymptomatic stage: years. - no clinical signs - CBC normal - CD4+ : CD8+ ratio inverted - most cats just die of something else in this stage secondary stage (AIDS): - months. rare to reach this. - immune dysfunction - lymphoma - wasting - neuro signs

internal vs. external haemorrhage: causes in SA. what should you check when an animal has regenerative anaemia due to haemorrhage? how should you treat blood loss anaemia?

internal: spleen (dogs), thorax, trauma, amyloidosis (hepatic in cats) external: epistaxis, gut, severe parasitic infection (young animals), angiostrongylus vasorum urinary tract CHECK: - total protein - coagulation profile - platelet count (in haematology profile) - faecal lungworm (angiostrongylus - cough, scleral bleeding) - ACTH stim test (addisons can lead to GI ulcerations and melaena) - search body cavities tx: treat underlying cause (remove spleen, piece of gut) - gastro-protectants if ulceration

what is rivalta's test? how is it interpreted?

it's an FIP test of peritoneal fluid. plastic tube filled with water. add acetic acid/vinegar. then mixed and effusion is layered if positive: - drop stays attached, retains shape and keeps connection, or slowly floats down to bottom - if it doesn't stay but turns into upside-down jellyfish - if it disperses into little cloudy pieces if negative: - drop disappears - clear or cloudy cords seen falling which dissolve before reaching bottom, but no drop or "upside-down jellyfish" 90% positive predictive value if cat < 2 years.

how is GFR regulated normally? how is this affected by kidney disease? how can we maintain this in the kidney under disease conditions?

kidney glomerulus has autoregulation over a wide range of blood pressures to maintain constant GFR. ANG II constricts the efferent arteriole. in CKD, autoregulation less well developed. systemic hypertension and renal injury lead to glomerular capillary hypertension and proteinuria. the hyperfiltrating nephrons cannot maintain the barrier. proteinuria is a sensitive prognostic indicator. possibly cause inflammation of renal injury like a self-fulfilling cycle. ANG II blockers (ACE-I) or ARBs relax efferent arteriole Calcium channel blockers (amlodipine) affect afferent arteriole

what is a feline coronavirus? what can it lead to?

large, single stranded RNA molecules which cause rep. and enteric infections in mammals. enveloped but can survive up to 7 weeks in faeces. mutates into FIP. very common. replicate in cytoplasm, get envelopes from membranes or ER/golgi. released by lysis or fusion with membrane. relatively unstable outside host but if protected, can survive.

what diseases can animals get from rats?

leptospirosis - dogs. Leptospires are in the urine of infected animals,and are transmitted through direct contact with urine or tissuesvia skin abrasions or contact with mucous membranes. Transmission can also occur through inhalation of infectious droplet aerosols and by ingestion. multisystemic - vomiting, diarrhoea, anaemia, jaundice, haemorrhage campylobacter

what is the fast total splenectomy method?

ligate the large vessels and not the short gastric vessels or the tiny blood supplies to the spleen. it's quicker but you need to be confident that you have the right vessels. easier if there's no tumour in practice, she does about a mixture of both - ligate the big vessels and some of the other ones.

what are ddx of local vs diffuse splenomegaly?

local: - haematoma - abscess - nodular hyperplasia (older dogs, can look alarming) - infarction - neoplasia (haemangio (sarcoma), leiomyoma, fibroma, lipoma, etc) diffuse: - infection (bacterial, viral, fungal parasitic) - congestion (drugs, torsion, DGV, RHS failure) - neoplasia (acute/chronic leukaemia, systemic MCT, lymphoma, multiple myeloma, malignant histiocytosis) - IMTP

how is feline grade lymphoma treated? how does it vary depending on presentation? grade? what's the prognosis?

low grade: - chlorambucil, prednisone - supplement B12 if needed - rescue with cyclophsophamide or lomustine med/high grade: - COP protocol: 8 weekly vincrisctine, pulse cyclophosphamide renal/CNS: incorporate cytarabine (crosses BBB) - COAP

what is the suggested testing protocol for low risk vs. high risk FeLV cats?

low risk: whole blood or serum for FeLV p27 antigen (ELISA) 1) if positive: retest with another immunochromatographic in 2 months. to rule out false +ve. - if negative the second time: could also be regressive infection, could be false +ve (could PCR) 2) if negative: uninfected or regressive high risk (blood donors, breeders, highly suggestive clinical signs): - first ELISA - then PCR to either confirm positive infection or test for regressive infection

what is the leukocyte differential count? what is percentage vs. absolute concentration?

machine can do it but it's not always accurate. have a quick look at the blood smear to confirm. - neutrophils - lymphocytes - monocytes - eosinophils - basophils percentage often gives ref. interval concentration is more accurate

what is the most common method of measuring leukocytes? what are other methods?

machine: impedance + optical. machine lyses of cells so the nuclei are left and then counts the nuclei (might include nuclear RBC). fairly robust (total #s) but take blood smear to check for nuclear RBC smaller machines: scans a spun down large PCV tube and relates fractions. not as accurate. manual methods: used for birds blood smear estimates from monolayer. count in a x100 field and divide by 4. difficult to accurately do of all the cells. should avg 10 fields. rough estimate better.

what is leukemia? what is lympoid vs myeloid?

malignant neoplasm originating from haematopoeitic precursor cells in bone marrow (or spleen) - neoplastic cells be present in the circulation in large numbers lymphoid/myeloid depending on which cell line is involved - lymphoid = lymphocytes and NK cells - myeloid = monocytes, mast cells, erythrocytes, megakaryocytes

how does failure of passive transfer occur? what does it depend on? how is it diagnosed? how is it treated?

maternal factors: - lack of colostrum (premature lactation) - poor quality colostrum: amt of IgG dependent on environment, farm mgmt, etc. foal: - lack of intake: can't nurse (sepsis, perinatal asphyxia, orthopaedic problems) or rejection - lack of absorption: too late, GI disease (hypoxic damage) greatly increases chance of infection (sepsis, septic arthritis, diarrhoea, pneumonia, meningitis) diagnosis: - problems standing/never stood - not nursing until 8-12 hrs - rejected - colostrum exam: specific gravity <1.060 - IgG concentration SNAP test (ELISA) treatment: - colostrum via nasogastric tube if < 12hr old, no signs of systemic compromise. 1-2L of equine colostrum, 200-400 ml at a time. no syringe/bottle (aspiration) - if foal >8-12 hrs: IV plasma (or if showing signs of systemic disease, no high quality colostrum available). however no antibodies against local diseases. might need several liters.

how do eosinophils mature/distribute? w

mature in 2-6 days (species dependent) - variable persistence in circulation (<1 hr in dog) - random entry into tissues. skin, resp, GIT in particular under normal circumstances, directional with chemokines/inflammatory mediators

what is the mechanism of vit K deficiency, and what are the main clinical signs, diagnostics, tx ?

mechanism: - dog eats courmarin- type rodenticide - vitamin K reductase is inhibited (produces vitamin K) - Vit K dependent carboxylase: produces factors II, VII, IX, X in the liver - factor VII decreased first (shortest half life) main CS: haemorrhage (chest/abdomen full of blood) diagnostics: - elevated PT (prolonged first), PTT - PLT numbers, buccal mucosal bleeding time should be normal but mild thrombocytopenia is possible due to consumption associated w/haemorrhage - same results as hepatic disease tx: 1) emetics, cathartics, activated charcoal if recent 2) transfusions of whole fresh blood or fresh frozen plasma to replace factors. may also need packed RBC if anaemia 3) vitamin K1 oral or parenterally. NOT IV or IM. do not OVERDOSE - haemolytic anaemia. can also give with a fatty meal - may take 12 hrs before shortens PT, decrease bleeding - course: 1 week if warfarin/1st gen, >3 weeks if 2nd or 3rd gen. check PT 24-48 hrs after last dose.

what can cause eosinopenia?

mechanisms unclear. - corticosteroids (endogenous or exogenous) via apoptosis, possible neutralisation of histamine/mast cell degranulation and other mechanisms - catecholamines

what is the prognosis for feline lymphoma? general vs. GI, stage, grade, etc? what are the prognostic indicators?

medium/high grade (general) - response rate < dogs (50-80%) - less predictable: medium remission 3-8 mo, survival variable 3-10 mo - 30% have long remission > 1 year GI lymphoma: - low grade/small cell: 70-96 CR rate - MST > 2 yr with chlormabucil/prednisolone - high/intermediate: 30-40% CR, MST 3-10 mo positive factors: - achieving CR - low grade - hodgkin's like subtype - nasal with RT negative: - FeLV +Ve - high grade - LGL subtype

what might be some ddx for a CNS lymphoma clinical picture?

meningioma, trauma, disc herniation, FIP, aortic thromboembolism, discospondylitis, FeLV myelopathy

what are CS of mild vs moderate vs severe anaemia?

mild: from normal PCV to appx 10 below - may not affect animal until exercised - common in animals with longstanding disease, endocrine disorders, etc moderate: varies b/w species - may show weakness or may adapt over time - MM pallor, fast bounding pulse severe: PCV < low teens - pale, weak, unable to exercise - may need O2/stabilisation before diagnostic procedures. - don't fight w/ very anaemic cats!

what are causes of CKD in the dog?

more mixed than cat. not as common (1/3 cases) - tubulointerstitial nephritis - familial (breed-related) disease syndromes - primary glomerular disease

how should FIV be treated? what is the prognosis?

most cats: doesn't affect lifespan manage healthy cats: - 6 month vet checks + regular flea/worming - consider killed vaccines - prevent transmission (indoors or enclosed) - no new cats and test in contact cats sick cats: as any other cat but be careful with glucocorticoids - gingivostomatitis: test for calicivirus - can try lots of stuff but often extraction of pre-molars and molars secondary stage - cytopaenias: try to treat other causes first. if this stage, prognosis poor - rare - little data on immunomodulators. could try interferon - no anti-retrovirals licensed, could try but lots of side effects.

what are signs of non-regenerative anaemia? what are ddx?

most common: inflammatory/chronic disease - normocytic, normochromic - mild, slowly progressing - Fe sequestraion, inflammatory mediators, shortened erythrocyte survival renal: kidneys produce EPO - EPO injections available, can develop antibodies - aim to increase PCV, not necessarily to normal endocrine: hypothyroid/hypoadrenocorticism - thyroid hormone/cortisol have facultative effect on RBC production FeLV: - up to 70% of anaemic cats - selective depression of erythropoiesis - dyplastic production - usually non-specific erythroid hypoplasia - can be normal or macrocytic - subgroup C Marrow: - Aplastic anaemia (all precursors wiped out): needs core biopsy. can be FeLV, estrogen, phenylbutazone, chemo, unknown - myelodysplasia: abnormal maturation/production, but adequate cellularity - myelopthisis: neoplasia crowding out BM - myelofibrosis: response to dry taps, maybe after prolonged regenerative attempts exceptions: - iron deficiency can become non-regen in the long run - immune medatied attack against precursors may give non-regen

how are RBC's removed?

most of them: senescent cells taken up by phagocytic macrophages, components recycled some of them: intravascular haemolysis

how do RBC's vary in shape and nucleation depending on species?

most species: biconcave disc, area of central pallor. high surface are: volume ratio, allows for deformability camelids: elliptical RBCs birds/reptiles nucleated

what is the difference between chronic kidney disease and renal failure?

need to lose >75% of nephrons before a patient becomes azotemic. before then, the remaining nephrons hyperfiltrate (increase in single-nephron GFR) and actually grow to preserve overall renal function. replaces the term "renal insufficiency" - vague term. better to stage it.

what are causes of CKD in the cat?

non-renal: - lymphoma - FIP - toxins renal: - PCKS - amyloidosis - primary glomerular disease - pyelonephritis - recovery from ARF/AKI - obstructive uropathy - chronic tubulointerstitial nephritis (garbage, most common cause)

what is tubulointerstitial nephritis?

not a condition, a description. most common "diagnosis" with CKD, end stage renal disease with fibrosis.

what is anaemia? CS? how do the clinical signs vary? how is the singalment relevant?

not a diagnosis alone. decreased PCV, HCT, Hb, RBS. may be obvious on clinical exam CS: - none/vague if mild/chronic - non-specific: lethargy, anorexia, collapse - specific: pale MMs, increased HR, RR, heart murmur, hyperdynamic pulses. heart has to try harder to pump the remaining RBC to the tissues. - severity of signs reflects cause, chronicity, and severity of anaemia signalment likely to be relevant. younger = parasites, older = neoplastic/CKD, cocker spaniels = IMHA

how can you treat splenic trauma?

not common. they either die or self-resolve. can suture the capsule and omentalise or do a partial splenectomy.

when is the appropriate time to begin nutritional intervention of renal disease?

not fully known, but there are guidelines. must evaluate each patient individually. - stage 2-3 prevent nutritional imbalance: BUN > 27 g/L or when azotaemia is "pathological" - earlier stage can start on ACE inhibitor - nutritional status of animal (growing or older?) - body condition score - concurrent diseases: thyroid issues - practical considerations

how can you reduce patient morbidity with chronic renal disease?

not improving survival, but reducing other diseases. - UTIs are common, often subclinical. pyelonephritis can also incite CKD (in the dog) - cats: Hypokalaemia due to decreased appetite, increased urinary loss, hperaldoseronism. we know, it's weird. - dehydration. may result in azotemia, will benefit from subcut fluids but be careful administering fluids to an animal with CKD, esp if it's more advanced - feeding tubes? some owners aren't ready to give up on their animal. - constipation (cats) - can treat with lactulose or miralax - appetite spimulants: maropitant (no evidence) or mitazipine (unlicensed, but works, but is also a sedative) - anaemia (lack of epo): can give recombinant human erythropoeitin for moderate/severe anaemia. - acidosis: corrected with fluid

what are other ddx for symptoms of a mediastinal tumour?

other mediastinal masses: thymomas, other, cyst pulmonary mass: primary lung tumour, metatatic chest wall mass other causes of pleural effusion: transudate mod. transudate, exudate (pyothorax, haemothorax)

what are the tx options for canine lymphoma? B cell vs T cell? what is maintenance?

palliative. combination chemo has a high response rate (80-90%) MULTICENTRIC: - B cell: COP (cyclophosphamide, vincristine, prednisolone) , 8 weeks - CHOP (^^ + doxorubicin) can be more expensive in beginning, more adverse effects, but longer remissions. 19 weeks. - T cell: LOPP: a cycle. vincristine, lomustine, procarbazine, prednisolone 6 months maintenance: chlorambucil, methotrexate, prednisolone other forms: - surgery if solitary lesion/obstructive GI lesion - radiation? maybe for nasal/oral lymphoma, solitary lesions to prolong remissions

reticulocytes vs. polychromatophils: what are they? how is reticulcyte count measured?

polychromatophils: Diff-Quik/Giemsa stained smear. larger, bluer. reticulocytes: New Methylene Blue. RNA precipitates, forming aggregates (reticulum.) - in cats: released as aggregate retics and then mature to punctate retics over time. counts: counts should record either aggregate or both in cats - should use corrected reticulocyte % because the PCV will be decreased. - regenerative = > 1% corrected (dog), .4% (cat)

describe the three steps of haemostasis, generally

primary: formation of primary platelet plug secondary: activation of coagulation cascade, generation of insoluble fibrin which stabilises the platelet plug fibrinolysis: breakdown of fibrin and platelet plug

how would a progressively infected cat, regressive cat, and immune cat test differently for the various FeLV diagnostics? (p27 ELISA, PCR, neutralising antibody)

progressive: - positive on p27 ELISA (may take 30 days and be negative on the first one) - confirm not false positive via PCR regressive/latent: - positive on PCR (not routinely done in gen. practice, but done in RVC) abortive infection/immunity: - positive on virus neutralising antibody - unlikely in clinical practice

how can you assess colostrum quality of a cow? what about uptake? what can affect colostrum quality?

quality affected by: - exposure of dam to pathogens - vaccination - can ferment after vaccination to produce IgA but don't use for first feed assessment of quality: - IgG cut-off point of 50 g/L - gives 10g/L plasma in calf - specific gravity (>1.048) - brix refractomter - "thicker the better" assessment of uptake: - serum of calf (IgG) - Total protein (can use refractomter) - >55g/L - GammaGT, ZST, sodium sulphite)

what is the definition of anaemia? how is it measured?

reduction in red blood cell mass, evidence in decreased: - haemoglobin concentration [HGB] = total oxygen carrying capacity - PCV = % or RBC in a volume of blood. manual, also allows buffy coat assmt (larger if inflammatoin/leukaemi) - HCT (calculated PCV, less accurate) - RBC concentration [RBC] = total RBC #

what does regenerative anaemia usually indicate? how do RBC's regenerate?

regeneration: kidneys respond to low blood oxygen by releasing EPO -- BM makes more cells. takes 2-3 days, polychromatophils increase. interpretation: RBC lost or destroyed. implies animal is responding.

define regenerative vs. degenerative left shift, and right shift

regenerative: - neutrophilia - segmented > bands degenerative: - neutropenia - bands > segmented right shift: hypersegmentation

review the RAAS. what drugs can we use to treat CKD along its pathway and what considerations should be made once we understand their mechanism?

renin is produced by the kidney when the nephrons is hypoperfused. ACE converts ANG I into ANG II (and also breaks down bradykinin) AT I receptor binding from ANG II is what leads to all the effects: - vasoconcstriction - aldosterone secretion - tubular sodium reabsorption - thirst - vasopressin secretion - cellular hypertrophy - calcium transport ATII receptor: - opposite to ANG II receptor. DRUGS: ACE-inhibitors prevent ANG II formation. - some say long-term ANG II will be produced by other means. - ARBs might prevent then and also allow the AT2 receptors to be bound. - considered to be equivalent. spironalactone is an aldosterone antagonist. CONSIDERATIONS: - the CK will go up initially because the GFR goes DOWN, but will self- regulate - therefore, ONLY use in MILD disease. an animal with end-stage disease will not be able to accommodate the reduction in GFR and will end up dying. CATS: - long-term, benazepril and telmistartin will preserve renal function but neither has been shown to improve survival. - benazepril is licensed DOGS: - proven to work in managing pimary glomerular disease, but not licensed

how does anaemia in horses differ from that of small animals? what are the clinical signs? diagnosis?

respond slower and take longer to recover: - large splenic reserve - circulating lifespan is 140-150 days (long) no release of reticulocytes into circulation - regenerative vs. non-regenerative can't be diagnosed in horses unless BM aspirate howel-jolly bodies normal (don't indicate responsive anaemia) CS: similar to SA. - pale MM, tachycardia/tachypnoea, weakness/exercise intolerance - plasma lactate concentration increased - decreased PO2 in blood diagnosis: clinical signs more important than PCV, Hb, RBC.

what kind of viruses are FeLV and FIV?

retroviruses. FeLV = gammaretrovirus, FIV = lentivirus - single stranded RNA - poor survival outside host - neither is zoonotic differences: route of transmission, outcome of infection, testing methods

what is a rouleax formation vs. agglutination? what causes it?

rouleaux = artefact. agglutination = stacks/aggregations of RBC because they are discoid shape. large surface area. occur when plasma protein conc is high. non-specific indicator of disease.

how should you take a history for an anaemic dog? signalment? PE?

signalment likely to be relevant. younger = parasites, older = neoplastic/CKD, cocker spaniels = IMHA- lifestyle - signs stable/deteriorating - site of bleeding? - access to drugs/toxins? - TRAVEL HISTORY physical exam: - is the patient stable? - RR/HR/ demeanour - icterus? (prehepatic haemolysis, bleeding liver tumours) - concurrent disease? - bleeding into pleural/peritoneal spaces? (rodenticide) - masses/pain? - rectal (melaena)

what are causes of IMHA? what are signs?

signs: - regen anaemia, no signs of blood loss - signs of haemolysis: jaundice, autoagglutination, spherocytes, ghost cells - rule out infectious diseases - cats less common, challenging to give blood products 1) primary - spaniels, maltese 2) secondary: - infection (erlichiosis, babesiosis, anaplasma, lepto, dirofilarias, histoplasmaosis) - neoplasia: lymphosarcoma, haemangiosarcoma, lymphocytic leukemia, gastric/lung carcinoma, diffuse carcinoma - drugs: trrimethoprim-sulfonamide, penicillins, cephalosporins, levimasole, PBZ, dipyrone, chlorpromazine - oxidative damage: onion, garlic, zinc, bee-stings, vaccines - intrinsic: PFK deficiency, PK, osmotic fragility

how does the kidney regulate phosphate? (where is it reabsorbed and which molecules regulate this?) how is this affected by renal disease? how can we combat this?

some is reabsorped in the proximal tubules by special transporters. regulated by PTH and FGF23. the increase of FGF-23 raises PTH which prevents absorption. in advanced disease, when the GFR is very low, the body can't get rid of all the phosphate, and it accumulates in the body. this drops ionised calcium which raises PTH directly. dietary phosphate reduction (renal diet) slows the progression of renal disease. can live 2-3x as long. has higher calories though. if not, feed a senior diet.

how is canine lymphoma graded/further subtyped?

specific subtypes exist with varying diagnosis most lymphomas in dogs are intermediate or high grade. low grade lymphomas are uncommon - tx/prognosis difference low grade: small lymphocytes intermediate: medium-sized high: large cells (blasts) 1) immunophenotyping to determine B vs T cell (cell surface markers, flow cytometry) - also tells you subtype, CD4 vs CD8, etc

what is a splenic torsion? CS, causes, diagnostics, tx?

spleen twists on its vascular pedicle occluding hilar vessels. - leads to splenic congestion +/- splenic vessel thrombosis. cause: unknown. breed? conformation? organo-instability? presentation: acute, progressive abdominal pain, distension, hypovolaemic shock - chronic also possible (nonspecific, lethargy, anorexia, +/- pancreatitis) diagnostics: US most useful. unique pattern of linear echoes separating large anechoic areas. (shaken snowglobe) - may visualise twisted pedicle - doppler assmt of splenic artery/vein, may see thrombosis tx: splenectomy. excellent prognosis - do not untwist pedicle prior to removing spleen. gradually divide and ligate pedicle. - may help to ligate first

how is FeLV integrated?

ssRNA -- dsDNA (retrovirus, uses reverse transcriptase) -- to nucleus in nucleus - integrates into host dna -- destroys virus-infected cells, transformation into tumour cells, or may do nothing

Farm animal neonatal anaemias

steven van winden

describe the structure and function of platelets. what molecules to they contain?

structure: - outer membrane creates receptors important for adhesion and aggregation - has cytoskeleton with actin and myosin that allows for shape change - contains membrane bound granules: alpha (vWF, fibrinogen, factors V, VIII) - dense granules: ADP, calcium surface receptors: - glycoproeins associated with the platelet membrane - CP Ib binds VWF, BP IIbIIIA binds fibrinogen - defects in receptors lead to abnormal platelet function, clot formation

what is SDMA? what is the IRIS staging scheme for renal disease?

symmetrical dimethyl arginine, marker of GFR developed commercially by Idexx. - Suggested to be more sensitive in detecting renal dysfunction (but this is likely to be at the expense of specificity) - Not as affected by changes in lean body mass as creatinine. staging: - Dogs/Cats varies, but >440 is severely azotaemic. cut off point around stage 2. - Patients must be diagnosed with CKD first (elevation > 3 months, look at patient clinically) azotaemia must be stable. - staging also includes urea: protein creatinine ratio, systolic blood pressure, creatinine stage 1: no clinical signs stage 2: clinical signs other than PU/PD are very mild or absent stage 3: PU/PD, extrarenal clinical signs may be present stage 4: vomiting, dehydration, wt loss likely

how do RBC's mature and what is the lifespan of one?

they start out nucleated and large and blue, then shrink and become basophilic and then eventually lose their nucleus. lifespan: - dog = 100 days - cat = 70 days - horse/cattle = 150 days

What is erlichiosis?

tick-borne, rickettsial bacterial infection (erlichio canis, anaplasma phagocytophilum) from the brown dog tick. causes fever, petechiae, bleeding, vasculitis, lymphadenopathy, and throbocytopaenia. similar to rocky mountain spotted fever, but no rash

what's a toxic vs. degenerate neutrophil?

toxic: in peripheral blood - accelerated production - no need for toxins - vacuoles degenerate/lytic in tissues/fluids - fighting with bacteria - bacterial toxins

how is neonatal isoerytholysis prevented and treated? if you are going to do a transfusion, what type should you give?

treatment: - prevent further colostrum intake: muzzle foal or separate from mare, provide with alternate source of nutrition/passive immunity - supportive care: may need IV fluids if sever haemoglobinuria - blood transfusion: washed RBC's from mare (NOT PLASMA) or blood donor -ve for Aa/Qa or can do x-match prevention: - mare with history of NI: determine blood group of sire - test serum for alloantibodies

how can you differentiate the two main ddx of pale mm? what are they?

two main ddx = anaemia or hypovolaemia? CRT: <2 sec = anaemia (euvolemic), prolonged = hypovolaemic/poor peripheral perfusions PULSE: strong/bounding = anaemia, weak = hypovolaemia

what is vWF? von willebrand's disease? what are the clinical signs/diagnostics?

vWF = plasma glycoprotein needed for platelet adherence to collagen and formation of primary plug, - synthesized by endothelial cells, platelets, and megakaryocytes - may see concurrent decrease in factor VII - common in dogs clinical signs/diagnostics - may have mucosal bleeding (GI, epistaxis, haematuria) - prolonged buccal mucosal time but no thrombocytopenia, no petichiae - clotting times usually normal, may increaese PTT due to factor VIII decrease - specific testing: measure vWF: AG, ELISA, immunoelectrophoresis, or genetic test [ three types: type 1 (most common) - all multimers present type 2 - disp. decrese in large multimers type 3 - absence of all]

how does the foal's immune system develop? where does it get antibodies? how is the body primed for this at birth?

very susceptible to disease. CELLS: - functional T (100 days) and B (200 days) in gestation - capable of mounting a complete immune response - no MDA across placenta (epitheliochorial) - born agammaglobulinaemic, but produce them upon exposure COLOSTRUM: produces all antibodies - secretion of Ig from serum in last 2 weeks of pregnancy - soluble: IgG, some IgM/IgA, growth factors, cytokines, lactoferrin, CD14, enzymes/lysozymes - cellular: lymphocytes, macrophages, neutrophils, epithelial cells - foals need 1-2L colostrum in first 3L of life Foal has specialised enterocytes to absorb IG via pinocytosis for 12-24 hr, maximal efficacy immediately after birth. half-life 20-30 days. - at 1-2 months, foals particularly susceptible to infection (foal Ig prod reaches max at 5-10 months)

splenic disorders

vicky lipscomb

what might protein electrophoresis from a lymph node sample inform you of?

what might be causing a hyperglobulinaemia. polyclonal: broad-based, wide gamma peak - infectious (leishmanaia, erlichia), immune-mediated - inflammatory monoclonal: narrow gamma peak/spike - neoplasia (myeloma, B- cell lymphoma)

what can you transfuse with besides whole blood? when would you use it?

whole blood: only used really for convenience. packed RBC: centrifuged whole blood, additive solutions, refrigerated. - indications: anaemia w/out hypovolaemia or other deficits, or anaemia with risk of volume overload fresh plasma: separated w/in 24 hrs, frozen < 1 year. - high in all clotting factors - indications: coagulopathies, haemophilia, etc could also be used as a source of immunoglobulin or albumin (pancreatitis?) liquid/frozen plasma: refrigerated 24 hours - 6 wks post collection, frozen <5 years. - inadequate factors V, VIII, wWF >1 yr - indications: rodenticide, haemophilia B cryoprecipitate: enriched in VIII, vWF fibrinogen. - partial thawing, centrifugation of FFP, re-frozen >1 yr. - indications: can use for dogs with von willebrands disease. cryosupernatant: everything minus cryoprecipitate. cheaper. contains vit k. dependant factors, albumin, anti-thrombin, etc - indications: rodenticide, vit k, haemophilia

when is whole blood used vs component therapy (blood products, platelets, etc)?

whole blood: when blood required immediately and not able to produce competent products. product of convenience. - substantial, acute haemorrhage - haemorrhage due to haemostatic disorders COMPONENTS: multiple products from one donation, decreases # of donations required. also decreases risk of side effects from volume overload/transfusion rxns. - it's spun down or squeezed into a different bag.

What is caval syndrome?

worms in caudal vena cava (but also mediastinal tumours) can cause swelling of face, etc leads to: collapse and death almost complete blockage of all blood flow he superior vena cava (SVC) and nerves can become trapped, resulting in vein distention, edema of the face or upper extremities, and nervous system symptoms (1)