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SBM > Bleeding Disorders > Flashcards

Bleeding Disorders Flashcards

0
Q

genetics of vWF

A

autosomal dominant

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1
Q

vWF function

A

tethers platlets to subendo in vascular injury–>localizes and holds factor 8 to site of injury

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2
Q

vWF type 1

A

most common

low levels of vWF activity

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3
Q

vWF type 2

A

normal levels of vWF protein, but reduced activity due to abnormal molecule or decreased high molecular weight multimers

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4
Q

vWF type 3

A

absent vWF activity

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5
Q

aspirin and bleeding disorder

A

makes it worse!

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6
Q

lab testing in vWF

A

prolonged aPTT but normal PT
decreased or normal factor VIII fx
prolonged PFA-100
abnormal ristocetin test

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7
Q

DDAVP

A

desmopression;synthetic vasopression
stimulates release of vWF and favtor VIII from endothelial cells
good for type I, but not really type II because if no functional protein doesnt matter if you pump out more

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8
Q

other treatments for vw def

A

vw factor replacement- humate P, alphanate, cryoprecipitate
antifibronlytic therapy
contraceptives
medic alert bracelets

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9
Q

x linked recessive hemophilia

A

hemo A

hemo B

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10
Q

autosomal recessive hemophilia

A

hemo C

parahemophilia

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11
Q

heterozygotes of hemo

A

will have low levels but will generally not bleed (except maybe C)

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12
Q

hemo A

A

factor VIII def

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13
Q

hemo B

A

factor IX def (christmas disease)

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14
Q

hemo C

A

factor XI def

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15
Q

parahemophilia

A

factor V def

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16
Q

factor levels for different severities

A

mild: 5-40%
moderate 2-5%
severe: less than or equal to 1%

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17
Q

joint disease in hemophilia

A

bleeding into joing–>Fe causes synovial proliferation–> chronic synovitis–>arthritis–>joint destruction

18
Q

labs in hemo

A

aptt prolonged

19
Q

treatment of hemo

A

coagulation factor concentrations on demand

prophylaxis to reduce bleeding episodes

20
Q

complications with hemophilia

A

chronic arthropathy
infectious diseases- hiv, hep c
inhibitors to missing coag factors (can complicate treatment)

21
Q

Coagulation Factor Inhibitor disease

A

acquired hemophilia- spontaneous autoantibody to factor VIII

22
Q

lab studies in aquired hemophilia

A

aPTT will be prolonged, but will NOT correct with mixing study
bethesda assay is used to measure antibody titer: if less than or equal to 5 BUs, may correct temporarily

23
Q

treatment methodology of bleeding disorders

A

treat bleeding and do something about antibody

24
Q

if low BU titer,

A

treat with high doses of factor VIII concentrate

25
Q

if titer high

A

treat with bypass agent

–recombinant factor VII, FEIBA, porcine factor VIII

26
Q

you can also do this for acquired hemophilia

A

immunosuppresion

27
Q

hereditary fibrinolytic defects

A

deficient inhibitors

overexpression of plasminogen activator

28
Q

deficinet inhibitor diseases

A

alpha 2 antiplasmin

plasminogen activator inhibitor deficiency

29
Q

overexpression of plasminogen activator

A

quebec platelet disorder

30
Q

acquired fibrinolytic defects

A

cancer
liver disease
DIC
local relase plasminogen activators from prostate surgery

31
Q

lab results of fibrinolytic diseases

A

prolonged PTT and PT

increased d-dimers

32
Q

treatment of fibrinolytic disorders

A 
supportive with plasma infusions
antifibrinolytic drugs (if NO DIC)
33
Q

antifibrinolytic drugs

A

epsilon aminocaproic acid

tranexamic acid

34
Q

DIC labs

A

prolonged PT, aPTT
elevated d-dimers
decreased fibrinogen, platlet count, rbcs, antithrombin, protein c, protein S
presence of schistocytes

35
Q

treatment DIC

A

plasma to replace coagulation factors and anticoagulants
cryoprecipitate (to replace fibrinogen)
platelets, RBC

**heparin will stop DIC, but may lead to bleeding

36
Q

liver disease parameters

A

bleeding due to decreased synthesis of coagulation factors, fibronlytic factor inhibitors

clotting due to decreased clearance of activated coagulation factors

37
Q

liver disease labs

A

prolonged PTT and PT, but this doesnt correspond with bleeding
low factor levels except VIII

38
Q

treatment of liver disease

A

transplant; everything else is only temporary

39
Q

vitamin K is required for

A

gamma-carboxylation of coagulation factors which improves coagulation factor binding to phospholipid surface of platelet

40
Q

ways to get vitamin K def

A

dietary-poor intake, malabsorption due to pancreatic or small-bowel disease, alcoholism
medications
warfarin!

41
Q

lab studies vitamin k def

A 
prolonged PT, PTT
factor 2, 7, 9, 10 decreased
normal 5 (so we know it's not liver disease)
42
Q

treatment vitamin k def

A

give vitamin K

fresh frozen plasma can get you out of a quick bind, but not long lasting

43
Q

must give vitamin K concurrently because

A

short half life of factor VII in plasma

SBM (18 decks)

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