192489
| Question | Answer |
| what is a stress leukogram? what do you see? | changes in cellular profiles in response to cortisol (endogenous or exogenous) neutrophilia, eosinopaenia, monocytosis, lymphocytopaenia |
| what are the physiological and pathological causes behind lymphocytosis? | physiological: mobilisation of lymphocytes due to immune response (i.e. infection, vaccination), epinenephrine release pathological: lymphoid neoplasias |
| reasons behind lymphocytopaenia? (6) | 1. steroids / HerAC - stress leukogram 2. acute and drastic inflammation - calls all the lymphocytes out of the blood 3. cytotoxic drugs 4. early viral disease e.g. distemper, FeLV, parvovirus (FPV and dog), FIV 5. immunodefiency syndrome 6. loss of lymph - chylothorax |
| what is leukaemia? what is the difference between acute and chronic leukaemia? what are the different types of leukaemia (4) | progressive disease of bone marrow that results in abnormal proliferation and differentiation of cells from myeloid lineage acute: neoplastic transformation during differentiation = lots of immature cells = cytopaenia (as lack of normal cells) chronic: neoplastic transformation after differentiation = lots of mature cells = rarely cytopaenia granlocytic: acute myeloid leukaemia (AML), chronic myeloid granulocytic leukaemia (CML/GML) monocytic: acute monocytic leukaemia (AMoL) mixed: acute myelomonocytic leukaemia (AMML) |
| what is lymphoid leukaemia? how is lymphoid leukaemia different to lymphoma? | neoplastic transformation and proliferation of lymphocytes in the bone marrow - therefore effects CLP / pre t cells / pre b cells lymphoma = neoplasm arising in the lymph node - still get abnormal lymphocyte proliferation but is in LN NOT BM |
| Are lymphoid proliferative or myeloid proliferative disorders more common in dogs or cats? what are the main mechanisms behind bone marrow change? | dogs: more likely to get lymphoid proliferative (lymphoid leukaemia, lymphoma) cats: myeloproliferative - AML, CML/GML, AMoL, AMML DNA damage virus (cats only) - FeLV |
| macrocytic + hypochromic? macrocytic + normochromic normocytic + normochromic microcytic + hypochromic microcytic + normoblastosis +/- basophillic stippling | regenerative anaemia (haemolysis, haemorrhage, oxidative damage) non-regnerative anaemia - myeloprolifertive diseases (leukamias, FeLV), vit B12/ folic acid deficiency, some chemo non-regen: acute haemorrhage, anaemia of chronic disease, bone marrow suppression/destruction iron deficiency Pb toxicity |
| 3 broad causes of regenerative anaemia? main principle behind regenerative anaemia? what does it look like? | haemorrhage/blood loss, haemolysis, oxidative damage bone marrow can spew out RBC - something is happening to them in circulation reticulocytes, anisocytosis, poikilocytosis, normoblastosis, howell jolly bodies, basophilic stipling, +/- heinz bodies |
| potential causes of haemorrhage/blood loss? | ext and/or int bleed e.g.trauma, haemangiosarcoma, ruptured spleen, GI bleed etc Parasites - endo and ecto coagulopathies |
| what is the mechanism behind anaemia associated w/ chronic blood loss? what does Fe deficiency anaemia look like? causes of chronic blood loss? | iron depeletion over time leads to iron deficiency anaemia hypochromic, microcytosis, increased platelets parasites - endo and ecto coagulopathies |
| what is the most important thing in acute blood loss? what is the first thing you do? then what? in acute haemorrhage when will reticulocyte response be seen int he blood? | replacing circulating volume start giving IVFT prevent further haemorrhage, consider blood transfusion (>30% loss - whole blood is generally what is given in haemorrhage), Tx underlying cause after ~4days |
| what is oxidative damage a cause of? what does it look like? causes of oxidative RBC damage (3)? Tx | regenerative anaemia eccentrocytes, heinz bodies, schistocytes (plus other signs of regeneration) heavy metals - Zn, Cu food - onions, garlic, brassiacs drugs- paracetamol propofol (cats) phenothiazines (pony) Tx: remove oxidative agent give anti-oxidants suppotive care - O2 tent, transfusion? |
| what does haemolysis cause? what CSx are a big clue? what are the main 4 causes? | regenerative anaemia icterus, haemoglobinaemia, haemoglobinurea 1. immune mediated e.g. neonatal isoerythrolysis, idiopathic, transfusion reaction, drug reaction 2. parasites - babesia, FIA 3. toxicity - Cu 4. rare genetic disorders |
| what spp is chronic Cu toxicity seen in? pathophysiology? Cause? CSx? Tx? | sheep accumulate excess Cu in liver over mo-yrs w/o CSx. Sudden release of Cu = haemolytic anaemia and oxidative damage cause: high Cu intake or low Mo,S, Co, Zn CSx pale gums, >CRT, tachycardia, weak/lethargic, icterus, haemoglobinaemia/urea Tx daily trench containing S and Mo |
| what is non regenerative anaemia characterised by? what is are the primary and secondary underlying mechanisms? | lack of reticulocytes + low PCV - everything else normal primary: intramarrow suppression - myeloplasia, myelodysplasia, myeloproliferative disorders (leukaemias), myelofibrosis secondary: extramarrow suppression - anaemia of chronic disease endocrine - HoT, HoAC, oestrogen suppression renal failure - no EPO infectious - erlichiosis |
| primary haemostasis tests (4) | buccal mucosal bleeding time (BMBT) dog: 1.7-4 cat: 1-2.5 platelet count - automated or manual NB cats and CKCS clot retraction - allow blood to clot in real time - should start clotting w/i min and retract w/i 2hrs wWF test (lab) - tests conc and function of vWF |
| secondary haemostasis: intrinsic + common pathway tests (3) | 1. activated clotting time (ACT) - time it takes for fresh blood to clot once you've added a substance to start the cascade dog: 1-2min cat: ~1min 2. whole blood clotting time - time it takes for whole blood to clot ~7min 3. activated partial thromboplastin time (APTT) time it takes for fresh blood to clot once you've added a phospholipid and activator (e.g. Ca or silica) - lab test |
| extrinsic pathway test (1) | one stage prothrombin time (OSPT) time it takes for fresh blood to clot once you've added thromboplastin and Ca |
| why should you not use an EDTA tube to collect blood for an APTT or OSPT? | has EDTA has Ca in which will fuck with the chelation - use sodium citrate tube |
| 6 causes of primary haemostatic disorder? | decrease in production fault in production destruction consumption loss sequestrianism |
| classic CSx for primary haemostasis disorder? | petechiae, ecchymosis mucosal bleeding oozing from small cuts/wounds abnormal intra-op bleeding occular haemorrhage |
| what might cause thrombocytopaenia (lack of production) | anything that suppresses/destroys bone marrow - intra or extrasuppression e.g. neoplasia, chemotx, drugs, hyperoestrogenaemia, liver failure (no TPO) |
| fault in production - what is thrombocytopathy diagnosis? causes? (acquired and hereditary) | normal platelet numbers but they are shit at their job normal platelet count, prolonged BMBT, normal secondary haemostasis tests, platelet function assays acquired: reaction to many drugs and disease hereditary: chedak higashi syndrome (persian cats) basset hound thrombopathia scotts syndrome (GSD) |
| 3 types of vWF disease and severity? CSx? diagnosis? Tx? common in which breed? what does desmopressin do? limitations? | 1 = low # of normal vWF - mild 2 = normal # of abnormal vWF - severe 3 = no vWF - severe classic signs of primary haemostatic disorder BMBT 5-12min = mild >12min = severe vWF ELISA Tx - replace what is missing fresh whole blood, fresh frozen plasma and cryoprecipitate have vWF in +/- packed RBC dobermann (type I) desmopressin will cause release of vWF factor from cells. Get rapid tachyphylaxis |
| what is immune mediated thrombocytopaenia? how common is it? primary cause? secondary cause? | immune destruction of thrombocytes in circulation (not in spleen) most common acquired primary haemostatic disorder in dogs (middle age female) primary: idiopathic autoimmune destruction secondary: drugs, infection |
| how does consumption of platelets cause primary haemostatic disorder? | use of platelets (e.g. DIC, mending a haemorrhage) causes a drop in circulation |
| what is sequestrianism (platelets)? | spleen eats the thrombocytes - seen in hypermegaly |
| normal platelet count for dog? at what point does spontaneous haemorrhage occur? | 150-400 x(10^9) /L <30 x (10^9)/L |
| what test(s) for... a) intrinsic + common pathways b) extrinsic + common pathways c) common pathway | a) activated clotting time (1-2min), whole blood clotting time (~7min), APTT b) OSPT c) thrombin clot time, TCT (8-10s in dog) |
| classic CSx of secondary haemostatic disorders | bleeding from big places / wear and tear places! joint bleed epistaxis (nose bleed) melena (GIT) bleeding from big vessels - internal haemorrhage |
| inherited secondary haemostatic disease: what is it? examples (intrinsic, extrinsic, common) | born lacking one or more clotting factors intrinsic pathway = haemophilia a = x VIII b = x IX c = x XI extrinsic = x VII - mild-moderate CSx common = no X or V - die as neonate |
| diagnosis of inherited secondary disease: typical age? determine whether or not extrinsic, intrinsic or common? what to do about it? | tend to be young animals. Haemophilia more often in males (a and b) intrinsic - APTT - if increased, then add in one by one an exogenous clotting factor to determine which one is missing from the sample extrinsic - OSPT - if increased = missing VII common: TCT - tells you whether or not have enough fibrinogen/if something if is inhibiting the thrombin replace what is missing! |
| Tx for... a joint bleed? more severe haemophilic bleed? severe haemophiliac w/ repeat incidences? | movement restriction, pain relief (essential), antifibrinolytics to prevent tertiary haemostasis from happening to quickly whole blood or fresh frozen plasma - replace volume as well as products. Wary of just IVFT - do not want to dilute blood further euthanasia viable |
| what are the 2 main acquired secondary haemostatic disorders? | secondary to liver disease - may also see issues with primary haemostasis due to lack of TPO = thrombocytopaenia coumarin poisoning |
| how does coumarin toxicity work? which clotting factors does it affect? how long does it take for CSx to appear and why? CSx? diagnosis Tx a) if just ingested poison b) if have clinical signs | coumarin drugs inhibit vit K activation in the body; several clotting factors are vit K dependent - II, VII, IX, X 2-3d are delayed as existing clotting factors need to deplete first, will run out of VII first typical secondary haemostatic CSx = epistaxis, joint bleeds, melena, haematoma, internal haemorrhage + signs of anaemia (regenerative) = tachycardic, dyspnoic, weakness, collapse, pale mm, >CRT CSx and history of exposure prolonged APTT and OSPT a) apomorphine followed by activated charcoal then watch for CSx b) synthetic vit K administration, consider whole blood transfusion in severe cases |
| what would a) too much, b)too little tertiary haemostasis result in? | a) too much break down b) too little breakdown (DIC and thrombosis) |
| causes of thrombosis - virchows triad? diagnosis clinical example | turbulent flow, hypercoagubility, endothelial damage decrease in antithrombin increase in FDPs feline thromboembolic disease |
| what is DIC, why does it occur? why do you get secondary haemostatic disorder CSx? CSx? diagnosis? Tx? | disseminated intravascular coagulopathy - formation of microthrombi can be a result of many diseases e.g. FIP, trauma, pancreaitis, some neoplasias, endothelial damage.. very long list! acute form: presents as secondary haemostatic disorder due to secondary secondary HD - used up all clotting factors making tiny clots CSx: regenerative anaemia signs secondary haemostatic CSx diagnosis: increase APTT, OSPT + FDP + decreased antithrombin - need to look for underlying cause also - bloods, biochem, urinalysis etc heparin - only work if have enough antithrombin whole blood - for volume and clotting factors etc treat underlying cause supportive |
| what % of normal antithrombin are you at risk of thrombosis? | <50% |
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