Hemostasis 1 Flashcards

1
Q

define hemostasis - response to, what components are involved, what is outcome

A

response to vascular injury, interactive process between BVs, platelets, coat proteins, and fibrinolytic system; leads to formation and resolution of hemostatic plug to stop bleeding

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2
Q

describe 5 basic steps of hemostasis

A

vascular injury, vasospasm/vasoconstriction, platelet plug formation (primary hemostasis), coagulation (secondary hemostasis), clot retraction and fibrinolysis

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3
Q

what are platelets and what is lifespan

A

nucleate cytoplasmic fragments from megakaryocytic in bone marrow, 4-6 days in circulation

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4
Q

production of platelets can be dramatically produced in presence of

A

thrombopoeitin

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5
Q

what causes platelet activation and what happens to a platelet when activated

A

exposure to sub endothelial collaged and adhesive protein vWF leads to platelet adhesion and activation. shape change from disc to sphere and develops projections.

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6
Q

describe steps of primary hemostasis after an injured blood vessel occurs

A
  1. Endothelin release causes vascular constriction within minutes of injury.
  2. vWF (von Willebrand factor) is present on the subendothelium of injured vessels and acts as a tether for platelets.
    • NOTE: vWF is esp important for vessels with high blood flow.
  3. Exposure to subendothelial collagen and vWF leads to platelets ADHERING to wall and becoming ACTIVATED.
    • Once activated, they change shape from disk to sphere and develop projections.
  4. Activate platelets release GRANULES, RECRUIT others to site of injury, and AGGREGATE to form a HEMOSTATIC PLUG.
    Surface for firbirn formation and leukocytes are binding also.
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7
Q

clinical signs of hemostasis

A

petechia 1-2 mm, purpura 3mm-2cm, ecchymosis 2-3 cm; persistent oozing from incisions or skin, epistaxis, melon, hematochezia, hematuria

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8
Q

2 types of platelet disorders (primary hemostasis disorders)

A

thrombocytopenia = decreased platelet numbers (acquired or congenital); thrombopathia = platelet dysfunction disorder (again, acquired or congenital)

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9
Q

if you see less than 2-3 platelets/hpf what do you do

A

consistent with thrombocytopenia, investigate for clinical hemorrhage

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10
Q

name 3 mechanisms of acquired thrombocytopathia

A

increased platelet destruction, increased platelet consumptions, or decreased platelet production

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11
Q

name a congenital thrombocytopenia, what is it in dogs

A

inherited macrothrombocytopenia; Cavalier King Charles Spaniel

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12
Q

what are 2 causes of increased platelet destruction in acquired thrombocytopenia

A

primary (idiopathic) or secondary immune mediated thombocytopenia, IMT

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13
Q

what are 2 causes of increased platelet consumption in acquired thrombocytopenia

A

DIC, thrombosis

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14
Q

what are 3 causes of decreased platelet production in acquired thrombocytopenia

A

infiltrative bone marrow disease (myelophthisis) or myelofibrosis, drug induced, viral induced

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15
Q

describe clin path change seen with primary (idiopathic) IMT, why is this happening, how is it diagnosed

A

severe platelet number drop, due to Abs being generated in response to target self antigen on platelets and potentially megakaryocytic as well, this is a diagnosis of exclusion

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16
Q

describe clin path change seen with secondary IMT, why is this happening

A

as with primary IMT, see a severe platelet number drop; occurs with formation of immune complexes on platelet surfaces and can be associated with vaccines, drugs, rickettsial disease, viral disease, or neoplasia

17
Q

what effect does intravascular coagulation (localized or DIC) have on platelets

A

the increased clotting depleted platelets (and clotting factors). vasculitis can also damage endothelial cells, exposing sub endothelium so platelets will adhere and activate

18
Q

3 most common causes of severe thrombocytopenia are

A

primary or secondary IMT, drug induced, and decreased platelet production (neoplasia, fibrosis) ***

19
Q

define myelophthisis. what is clin path finding seen?

A

replacement normal hematopoietic tissue with normal tissue (eg. neoplasia); leads to severe drop in platelet numbers, like IMT

20
Q

define myelofibrosis

A

replacement of normal hematopoietic tissue with fibrous tissue

21
Q

name at least 2 and at least 2 viruses that decrease platelet production; what is mechanism

A

estrogen, griseofulvin, cyclophosphamide, chloramphenicol suppress bone marrow. FeLV, FIV, Parvo, distemper, EIA, BVD destroy directly or indirectly platelets and potentially MKs

22
Q

characteristic findings and C/S inherited macrothrombocytopenia

A

large platelets and decreased platelet numbers; thrombocytopenia persistent and no C/S; not associated with hemorrhage

23
Q

breeds affected by inherited macrothrombocytopenia (a congenital thrombocytopenia)

A

CKCS! Chihuahuas, lab retrievers, poodles, shih tzus, maltese, jack russels

24
Q

name the most common hereditary bleeding disorder in dogs, pigs, and people. is it extrinsic or intrinsic?

A

von Willebrands disease vWD. [this is an extrinsic disorder of platelet dysfunction, and an inherited thrombopathia (platelet disorder)]

25
Q

what is cause of vWD.

A

extrinsic disorder of platelet dysfunction that is caused by a deficiency in vWF. (vWF is a tether for platelets to sxbendothelial collagen at site of vessel injury and is important in vessels with high shear stress, ie. the small vessels)

26
Q

species vWD is common in? rare in?

A

dog pig people. rare in cat horse cattle

27
Q

there are 3 types of vWD reported in dogs. describe type 1: how common? how severe? breeds?

A

type 1, most common over 95% cases, variable severity. LOW vWF protein but NORMAL strx and fxn, many breeds eg. Doberman pinschers.

28
Q

there are 3 types of vWD reported in dogs. describe type 2: how common? how severe? breeds?

A

LOW numbers vWF proteins and ABNORMAL strx and fin, severe but rare. German shorthaired and wire-haired pointers

29
Q

there are 3 types of vWD reported in dogs. describe type 3: how common? how severe? breeds?

A

markedly reduced to absent vWF protein. severe but rare. Chesapeake bay retrievers, Scottish terriers, shetland sheepdogs and others.

30
Q

what should you look at in your blood tests for primary hemostasis? include CBC and morphology and tube type.

A

blood smear look for giant placements and platelet clumps (which are normal in monolayer). EDTA purple top is best. thrombocytopenia will be under 50 x 10^9 platelets/L on our CBC with platelet count

31
Q

what clinical test should you perform for primary hemostasis (except in cases of thrombocytopenia)? what does it evaluate, what is normal range, what should you consider if prolonged

A

buccal mucosal bleeding time, usually <4 min, if prolonged consider thrombopathia likely vWD. evaluates platelet function WHEN NORMAL PLATELET NUMBERS. if you have thrombocytopenia–>don’t perform, test will likely be prolonged.

32
Q

what test might you perform to differentiate between IMT and myeloproliferative disease, for primary hemostasis

A

bone marrow aspirate

33
Q

you suspect vWF disease because of a mild to severe bleeding tendency, prolonged BMBT (a fairly insensitive test) and normal platelet numbers. what test can you perform for vWF deficiency or vWD? what range would you expect? what sample should you use?

A

vWF antigen assay, vWF:Ag. vWF:Ag <50% considered decreased and a carrier of vWF trait, and you would expect <25% in bleeding dogs, often <15%. use EDTA or citrated plasma sample.

34
Q

an 8 y/o Staffy has been mildly lethargic, has petechial hemorrhages in his mucus membrane, and biochemistry results are WNL. his bloodwork shows slight polychromatic, occasional nRBCs, mild leukocytosis monocytosis, neutrophilia, and thrombocytopenia. what is going on?

A

leukogram–could be inflammation of stress component.