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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
Q

secondary thrombosis

A

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
Q

warfarin skin necrosis

A

pt with protein C deficiency

  • pro-thrombotic state when given warfarin
  • hemorrhagic skin necrosis
  • cutaneous vessel thrombosis and skin necrosis
27
Q

venous thrombosis

A

factor V mutation
prothrombin G20210A mutation
protein S and C deficiency
antithrombin deficiency

28
Q

venous and arterial thrombosis

A

hyperhomocysteinemia
antiphospholipid antibody syndrome
HIT

29
Q

factor V mutation

A

Leiden

-protein C resistance

30
Q

prothrombin G20210A mutation

A

increased prothrombin

-leads to more working thrombin

31
Q

HIT, type II

A

autoantibodies for platelet factor 4

  • induced by heparin
  • thrombocytopenia and disseminated clots
32
Q

antiphospholipid autoantibodies

A

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
Q

factor XII deficiency

A

decreased plasmin activation

34
Q

homocysteine

A

elevations can be due to homozygous deficiency of beta-synthetase
-results in homocystinuria

increased risk of ASCVD

35
Q

folic acid, pyridoxine, vit B12

A

supplements that can reduce plasma homocysteine

-DOES NOT decrease risk for ASCVD

36
Q

number one cause of emboli

A

DVT

-pulmonary emboli - 60-80% clinically silent

37
Q

diagnosis of PE

A

ventilation/ perfusion mismatch

-do a V/Q scan

38
Q

periorbital edema and foamy urine

A

foamy urine = proteinuria

likely nephrotic syndrome

39
Q

septic shock

A

typically gram positive bacteria**

40
Q

types of shock

A

distributive
cardiogenic
hypovolemic
obstructive

41
Q

distributive shock

A

vasodilation

-septic, neurogenic, anaphylactic

42
Q

cardiogenic shock

A

pump failure

43
Q

hypovolemic shock

A

hemorrhage

44
Q

obstructive shock

A

obstruction of blood flow

ex/ saddle embolus

45
Q

rash and bleeding gum, malaise, joint pain, N/V

A

dengue fever

  • viral rash
  • thrombocytopenia
46
Q

dengue fever

A

get thrombocytopenia

CV II Exam 2 (18 decks)

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