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CV II Exam 2 > Thrombosis II > Flashcards

Thrombosis II Flashcards

1
Q

endo cells release to stop platelet aggregation

A

NO, PGI2, adenosine diphosphatase

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2
Q

endo cells to inhibit 2, 9, 10, 11, 12

A

HSPG - activates antithrombin

heparan sulfate proteoglycan

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3
Q

endo inhibition of Va and VIIIa

A

thrombomodulin > thrombin

  • thrombin then activates protein C
  • with protein S - goes to inactivate Va and VIIIa
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4
Q

endo cell inhibition of VIIa/TF and Xa

A

TFPI

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5
Q

tPA activity

A

converts plasminogen to plasmin
-plasmin then causes fibrinolysis

fibrin > fibrin degradation products

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6
Q

antithrombin

A

is antithrombin III

  • neutralizes active serine proteases
  • inhibits 2a, 9a, 10a, 12a
  • mainly - IIa and Xa - no fibrin
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7
Q

heparin

A

increases antithrombin binding 1000x

no prolonged PT - but will see it with overdose

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8
Q

two main effects of antithrombin

A

1 inhibit factor Xa - decreased thrombin production

2 inhibit thrombin (IIa) from activating fibrinogen

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9
Q

tPa

A

binds fibrin

-forms plasminogen > plasmin

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10
Q

urokinase

A

from endo cells

-forms plasminogen > plasmin

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11
Q

XIIa pathway

A

converts plasminogen to plasmin

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12
Q

three things increasing plasmin

A

tPA
urokinase
XIIa pathway

all induce rapid clot dissolution

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13
Q

D dimer positive

A

indicates that clotting and fibrinolysis is occuring**

D dimer is portion of fibrin polymer once it is lysed

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14
Q

fibrin split products

A

older test - indicate plasmin breaking down fibrin

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15
Q

high thrombin, low plasmin

A

thrombosis

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16
Q

low thrombin, high plasmin

A

hemorrhage

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17
Q

low fibrin or platelets

A

hemorrhage

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18
Q

arterial thrombus

A

ischemia / infarction distal to thrombus

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19
Q

venous thrombus

A

congestion and edema proximal to occlusion

20
Q

thrombus

A

clot grown larger than required for its physiologic role

21
Q

fate of thrombus

A

propagation - grows more
embolization
dissolution - fibrinolysis
organization/recanalization - vessels

22
Q

inherited causes of hypercoagulability

A

patients under age 50 with thrombosis

-should suspect genetics

23
Q

primary causes of hypercoagulability

A

genetic causes

common

  • factor V mutation - G1691A (leiden)
  • prothrombin mutation - G20210A
  • 5,10-methylenetetrahydrofolate reductase mutation - C677T homozygous
  • increased levels of factors 8, 9, 11, fibrinogen

rare

  • antithrombin III deficiency
  • protein C deficiency
  • protein S deficiency
24
Q

factor V mutation

A

leiden
-problem with homozygote individuals

G1691A mutation

25
secondary thrombosis
high risk - bedrest/immobilization - MI - A-fib - tissue injury - cancer - heart valves - DIC - HIT - antiphospholipid antibody syndrome low risk - cardiomyopathy - nephrotic syndrome - hyperestrogen - coral contraceptive use - sickle cell anemia - smoking
26
warfarin skin necrosis
pt with protein C deficiency - pro-thrombotic state when given warfarin - hemorrhagic skin necrosis - cutaneous vessel thrombosis and skin necrosis
27
venous thrombosis
factor V mutation prothrombin G20210A mutation protein S and C deficiency antithrombin deficiency
28
venous and arterial thrombosis
hyperhomocysteinemia antiphospholipid antibody syndrome HIT
29
factor V mutation
Leiden | -protein C resistance
30
prothrombin G20210A mutation
increased prothrombin | -leads to more working thrombin
31
HIT, type II
autoantibodies for platelet factor 4 - induced by heparin - thrombocytopenia and disseminated clots
32
antiphospholipid autoantibodies
affinity for phospholipids on platelet surface that are combined with coag factors -detected clinically lupus anticoagulant when doing aPPT testing false positive VDRL syphilis test -with negative treponema test can lead to recurrent loss of babies
33
factor XII deficiency
decreased plasmin activation
34
homocysteine
elevations can be due to homozygous deficiency of beta-synthetase -results in homocystinuria increased risk of ASCVD
35
folic acid, pyridoxine, vit B12
supplements that can reduce plasma homocysteine | -DOES NOT decrease risk for ASCVD
36
number one cause of emboli
DVT | -pulmonary emboli - 60-80% clinically silent
37
diagnosis of PE
ventilation/ perfusion mismatch | -do a V/Q scan
38
periorbital edema and foamy urine
foamy urine = proteinuria likely nephrotic syndrome
39
septic shock
typically gram positive bacteria**
40
types of shock
distributive cardiogenic hypovolemic obstructive
41
distributive shock
vasodilation | -septic, neurogenic, anaphylactic
42
cardiogenic shock
pump failure
43
hypovolemic shock
hemorrhage
44
obstructive shock
obstruction of blood flow ex/ saddle embolus
45
rash and bleeding gum, malaise, joint pain, N/V
dengue fever - viral rash - thrombocytopenia
46
dengue fever
get thrombocytopenia

CV II Exam 2 (18 decks)

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