Thrombopilia/Hypercoag States Flashcards

0
Q

most important part of virchow’s traid for arteries

A

vessel injury

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1
Q

Virchow’s Triad

A

blood vessel wall damage
altered blood flow( stasis)
altered blood composition (hypercoag)

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2
Q

most important part of virchow’s tria for veins

A

stasis, hypercoag

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3
Q

treatment of hyperhomocysteinemia

A

vitamins will bring down homocysteine levels but not decrease the risk of thrombosus

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4
Q

4 types of antiphospholipid antibody diseases

A

lupus anticoagulant
anti bII/Gp1
anti-prothrombin
anti-cardiolipin

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5
Q

how does lupus anticoagulant work

A

prevents binding of prothrombinase complex to phospholipid surface

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6
Q

lab studies

A

prolongs PTT and sometimes (but not commonly) PT

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7
Q

effects of lupus anticoagulant

A

in vitro- prolongs clotting time

in vivo- triggers thrombosis (by unknown mech in both arterial and venous)

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8
Q

activated protein C resistance

A

due to g–>a in factor 5 which renders factor 5a resistant to inactivation by activated protein C

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9
Q

ways to acquire APCR

A
pregnancy
cancer
thalidomide uses in multiple myeloma
oral contraceptives
lupus anticoagulants
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10
Q

Factor V Leiden

A

heterozygotes 5-8% caucasians, asymptomatic in majority, mild risk factor for venous thrombosus, homozygotes have a much higher risk

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11
Q

where does factor V affect?

A

venous circulation, little to no risk for arterial circulation

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12
Q

prothrombin G20210A

A

G–>A point mutation in 3’ untranslated region of prothrombin gene
same manifestation as factor V leiden

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13
Q

hereditary protein c deficiency genetics

A

autosomal dominant
homos lethal in utero
venous not arterial thrombosis

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14
Q

job of protein C

A

with cofactor protein S, inactivates factors V and VIII

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15
Q

lab tests for protein C deficiency

A

screen activity level–>if low screen for antigen–>if low, type 1, if normal, type 2

16
Q

how is protein S different from protein C?

A

longer half life

17
Q

protein S deficiency genetics

A

normally lethal as homozygous- autosomal dominant

18
Q

Type 1 Protein S deficiency

A

functional activity low
free antigen low
total antigen low

19
Q

type II protein S deficiency

A

functional activity low
free antigen normal
total antigen normal

20
Q

type III protein S deficiency

A

functional activity low
free antigen low
total antigen normal

21
Q

hereditary antithrombin def genetics

A

autosomal dom

homos die

22
Q

when does antithrombin deficiency present

A

usually before agre 50, typically <35

23
Q

why is antithrombin deficiency different?

A

more severe than thrombophilia

24
Q

why does factor V leiden persist in population

A

higher sperm count in males, less bleeding in childbirth–>gene persists