Clin Path - Midterm Fast Review 2

drraythe's version from 2015-12-05 14:01

thrombo review

Question Answer
what are some 1* hemostatic disorders? what are some 2* hemostatic disorders?1*= petechiae, ecchymosis, has to do with endothelial/platelet probs. 2*= hematomas (rapid onset and large), multi organ involvement
which tests for clotting would you use a sodium citrate?PTT and PT (plain tube has all Cs in it, these dont have Cs in them, so, sodium citrate) (THE MAJOR TWO TESTS USE SODIUM CITRATE! why he emphasized sodium citrate as the clot test tube)
which tests for clotting would you use a EDTA?platelet counts (preserve morphology)
which tests for clotting would you use a plain tube?CT, ACT, CRT ((you want to have a Clot, use a plain tube, for tests that have a "C" IN THEM)
what would a high MPV indicate?mean platelet volume--> high means immature (like RBCs)--> IMT (immune mediated thrombocytopenia)
what might cause pseudothrombocytopenia? who is susceptible to it?platelet clumping or bad sample collection(would trigger tissue thromboplastin) or bad sample handling (refrigeration). cats and pigs susceptible this, and horse blood when in EDTA
immune mediated thrombocytopenia would be in what range of # of thrombocytes?<30-50x10^3
DIC would be strongly indicated with the platelet count of what?50-90x10^3 thrombocytes
IMP?aka IMT (immune mediated thrombocytopenia)
thrombocytopathy can be hereditary or acquired. examples?herid= vWD, bovine thrombopathy, Thrombastheniain Otterhounds. ACQUIRED= nsaids, or secondary to dz like Multiple myeloma, renal failure, MPDs
most common canine hereditary bleeding disorder? whats happening? signs?vWD, from dec vWF. inherited. vWF is for platelet to endothelium or p-to-p adhesion. Bleeding in gums, epistaxis, hematuria, melena
what is SUPER IMPORTANT TO KNOW ABOUT CLINICAL SHIT IN vWD? which tests are useful?THE COAGULATION TESTS WILL BE WRI (bc they check intrinsic, extrinsic and common paths, and this has nothing to do with that). platelet count will also be WRI. BMBT, CRT, CL will be abnormal (these are platelet tests) and obv low vWF
what is bleeding time (BMBT) testing for?Vascular or platelet, or vWF test (long time= abnormal)
CRT tests for what? explain itcrude test for thrombocytopathy (platelet shit) (small clot= abnormal)
CL tests for what? explain itCrude test for stability of the clot (platelet shit) if clot lysis appears before 24 hr= abnormal. Excess of Fibrin Degradation Products (FDPs) »induced by excess plasmin(dissolves clots)
Platelet Aggregation Test tests for what? explain itMeasures the ability of platelets to clot. measures speed of clot formation and aggregating ability. if there is INC TURBIDITY--> vWF is low
DIC is what kinda coagulopathy? what does it look like clinically?consumptive coagulopathy. thrombopenia (50-90), Prolonged PT, PTT, ACT, BMBT (intrinsic, extrinsic, common path AND platelet tests), and Increased FDPs and D-dimers
what are FDP/FSPs? what are you looking at them for? caution?fibrin degradation products/fibrin split products. Plasminogen converts to plasmin and plasmin digests the fibrin in clots.. increased fibrinolysis (lysis of clots). Strong sign of DIC (lots of clots being formed, lots of clots being broken up). caution: Absence of FSPs doesn’t rule out DIC (MPS can be clearing them)
if you are checking D-dimers, what are you prolly looking for?DIC (D-DIC)
do you wanna look for fibrin or fibrinogen? and which of these does FDPs/FSPs/D-DIMERS come from?look for fibrin (fibrinogen is less concise) and then FDPs come from that, and then D-dimers come from the FDPs so D-dimers are most accurate
Purpura hemorrhagica is what? caused by? what are the clin path signs?acute injury to small blood vessels in horses. Streptococcus equi respiratory infections and vx cause complexes which damage the vessels. abnormalities are: BLEEDING HORSE! low PCV, other coag tests WRI
secondary hemostasis has to do with what? (is it platelets or is it pathways? )pathways
what is the point of the pathways?make fibrin to stabalize the platelet plug
what keeps a clot from continuing to clot out of control?antithrombin III
if you put a bunch of needles in the skin, which pathway are you activating?extrinsic
whats some basic stuff you need to know about extrinsic path?tissue based, rapid, more important in vivo (both paths activate common path)
what some basic stuff you need to know about the intrinsic path?less important in vivo, plasma-based, slow, (both paths activate common path)
if there was an intrinsic and common path defect (which diseases would this deal with?) what would the clin path abnormalities be?HEMOPHILIAS! prolonged PTT, CT, ACT, mildly prolonged PT or WRI
what does PTT (aptt) (activated partial thromboplastin time) test? what should you perform it with?intrinsic and common paths. result is time it takes to clot. should be performed with OSPT (PT)
what does ACT test?(Activated coag time) intrinsic and common paths. value is time when clotting is first observed.
what are the best tests for the intrinsic and extrinsic and common paths?(a)PTT (intrinsic) and (os)PT (extrinsic) (diatemaceous earth and warm bath)
what does CT test?intrinsic and common factors, not very sensitive. (break the capillary tube one)
which number is NOT A clotting factor?VI (6)
which defects are more common, intrinsic+common or extrinsic+common?EXTRINSIC
what is the main cause of an extrinsic clotting issue?vitamin K deficiency/warfarin poisoning
what are the clinpath abnormalities like for vit K deficiency/warfarin poisoning?prolonged (os)PT, mildly prolonged PTT, regenerative hemmorhagic anemia, hypoproteinemia
(OS)PT tests for what path?extrinsic+common *should be performed with a (a)PTT
what is PIVKA for?tests for Absence of or presence of VitK antagonists. abnormal is a prolonged PIVKA, which strongly suggests warfarin (has to do with the external path)
what is TCT/TT?thrombin clottin time, if it's prolonged it indicates Hypofibrinogenemia-->Dysfunction of fibrinogen
what is tertiary hemostasis?lysis of fibrin clot after repair to the vessel
hypercoagulation leads to what? possible causes?thrombosis--> DIC. possibly caused by inflammation or infection
hypocoagulation = _________coagulopathy

BM abnormalities

Question Answer
reversible BM abnormalities initially present as? then as?neutropenia--> non-regen anemias/thrombocytopenia or all together as aplastic pancytopenia
main causes of reversible BM abnormalities?viruses, toxins, estrogens
explain endogenous vs exogenous estrogen toxestrogen tox suppresses BM. endogeous sources of estrogen are genetic susep. in errets, sertoli cell tumor in testes, cystic ovaries. exogenous reasons are tx for mismating, pseudopreg, and incontinence.
irreversible BM abnormalities can present as what two things? mechanisms?cytopenia or unregulated prolif. If it was cytopenia-->Lack of differentiation/ maturation of stem cells. if it was neoplasm--->Unregulated proliferation
main causes for irreversible BM abnormalities?Viruses, toxins, radiation, idiopathic--> and TX WONT HELP
what conditions are required for a label of aplastic pancytopenia?Leukopenia+ Anemia +Thrombocytopenia
which is more common, hypoplasia or atrophy?atrophy way more common
is atrophy of BM reversible or irreversible?irreversible (cant fix itself if it's gone)
what is going on in hyperplasia of BM?its a BM response, often to inflammation, or hemolysis or acute hemm. (we need to make more blood!) yellow BM-->red
what does hypertrophy of the spleen/liver possibly indicate?extramed. hematopoeisis
what is MDS? what are the results of it? causes?myelodysplastic syndrome.Maturation of precursor cell stops at a certain point! can be selective or non-selective (just red cell, or is it aplastic pancytopenia?) either way, MDS ALWAYS LEADS TO A PENIA (bc immature cells and not enough to spill out). usually cased by Viruses, toxins, radiation, idiopathic
describe what's going on in the BM with MDShave too many blast cells (over the healthy 20%) but not too many to be considered a MPD/leukemia (which would be 30 or above). MDS will always cause penia then, because they are babies staying in the bone marrow. It can be considered a pre-MPD or a pre-leukema because it is above normal but not yet to 30%blast in BM
who is very suseptible to MDS?CATS! i guess theyre bitches because theyre so full of immature
what is Myelophthsis/panmyelophthsis? what happens because of this?BM failure due to replacement of “normal” hematopoietic tissue with “abnormal” tissue--> fibrous or neoplastic. causes penias or aplastic pancytopenia
what is MPD? charateristics?MyeloproliferativeDisease (MPD)--> Neoplastic clonal proliferation of one or more myeloid cells. chara incld hypercellular BM, Distorted or disorderly maturation sequence, may or may not spill into blood. causes might be Retroviruses, radiation, toxins
acute vs chronic MPD?acute= >30%blast cells in the BM, PENIA, cells dont last long/get destroyed---> poor prog. chronic= lots of mature cells in BLOOD (cytosis) AND in the BM. longer survival time, slightly better prognosis. this excess of cells can lead to splenomegaly and hepatomegaly
explain Erythrocytic Sarcoma in DOGS. whats happening, charateristics, aka?aka polycythemia vera. Neoplastic clonal proliferation of RBCs Rare, occurs latein production line»mature RBC (so erythrocytosis). charateristics incld a lack of heart/lung/lkidney/EPO problems, plasma proteins and albumin normal (not dehydration) and leads to high vscosity,cyanosis, depression, etc
explain erythrocytic sarcoma in CATSNeoplastic clonal proliferation of RBCs. in cats, happens EARLY in production line-->RBCsare unstable and disintegrate »non-reganemia. clinpath abnormalities incld: severe anemia, nRBCs in blood, atypical cells on blood smear, hepatomegaly and splenomegaly are possible
what is Myelomonocytic Sarcoma? what are the types?Neoplasticclonalproliferation of granulcytes/monocytes/both. if non-circulatory, its staying in the BM, EARLY PRECURSORS AFFECTED, so WBC is WRI-low. If circulatory, has spilled into the blood. and there are a lot of atypical(blast cells) in the BLOOD. Acute» high numbers of blast cells. Chronic» bands, metamyelocytes, myelocytes
Megakaryocytic Sarcoma? what are the diff situations for this?Neoplasticclonalproliferation of megakaryocytes. if early in production line, leads to thrombocytoPENIA(Neoplasticmegakaryocytes), and can leads to myelophthisis and aplastic pancytopenia. LATE occurance can lead to thrombosis and megaplatelets (bc old enough to hold up so are too many in blood)
what is LymphoproliferativeDisease (LPD)? aka? causes? sp diffs? how does it present?neoplastic prolif of lymphocytes. Aka: Lymphosarcomaor malignant lymphoma. can be caused by Retroviruses: cats (FeLV), cattle (BoLV), birds (avian leukosis), toxins, and radiation. very common in cats/dogs/cows but NOT IN HORSES. presents as leukemia (blast/atyical cells in blood), masses of unknown origin, lyphadenopathy
diff between dog with LPD and a cat/cow/horse with LPD?in dogs, you wont see the lymphocytes in the blood (lymphocytic leukemia) until the TERMNIAL STAGES where the BM is involved. but, in cats/cows/horses, you will see lymphocytic leukemia in the earlier stages when the LNs are involved, before the BM does.
what are two possible causes of lymphadenopathy?Chronic lymphocytic leukemia (CLL), or, Rarely: Acute lymphoblastic leukemia (ALL)
how could you possibly diagnose LPD?you could look for blood abnormalities (atypical lymphocytes, blast cells) but CBC might be WRI (if not circulatory). so you can also do a FNA of LNs (look for malignancy) or do a biopsy/histopathy
describe the unique features of LPD in a DOGusually multicentric! usually B cell lymphoma, usually non-functional with generalized lymphadenopathy (multicentric). If it were a T-cell lymphoma, could Lead to increased globilinsand calcium---> renal failure. (other forms are cuteaneous, mediasteinal, alimentary)
Pyrexia of unknown/ recurring infection might be due to what? extreme leukopenia
is aspiration or biopsy the clin path one?aspiration(faster, easier, less expensive, looks at cell morphology) is clin path, biopsy(Establish cellularityof BM & metastatic neoplasia) is path
where are sites for BM aspiration?prox humerus, illiac crest(lg animal), trochanteric fossa(sm animal)
how do you prepare for the BM aspirate?STERLIZE, and cut path (stab skin) to make path for needle bc needle is blunt and dont want other tissue in needle.
TUBE for BM aspirate?EDTA
whats a good way to know you have a BM sample on your slide from your aspirate?Yellow floccules and blood»BM. if only blood, gotta try again.
BM aspirate--> what are you looking for at 10x?cellularity (is it hypercellular/hyperplasia? is it Hypocellular/ hypoplasia? are there megakaryocytes? large vacuoles-->fat)
BM aspirate--> what are you looking for at 40x?proportions of precursors (in general)
BM aspirate--> what are you looking for at 100x?RBC and WBC precurosor lines, cell morph, CALC G/E ratio
what do you gotta do to determine the G/E ratio?count 500-1000 precursors. then put the Granulycyte precursors/Erythroid precursors.
**what are the possible reasons for a HIGH G/E ratio?HIGH G and normal E (leukocytosis, inflammation), or NORMAL G and small E.(non-regen anemia). BOTH OF THESE CAN OCCUR AT THE SAME TIME= anemia of inflammatory dz
**what are the possible reasons for a LOW G/E ratio?SMALL G and normal E(Leukopenia, might be an infection against WBC precursors). or it could be a normal G/HIGH E(anemia with regeneration)

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