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Flashcards in Thrombosis II Deck (46):
1

endo cells release to stop platelet aggregation

NO, PGI2, adenosine diphosphatase

2

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

HSPG - activates antithrombin

heparan sulfate proteoglycan

3

endo inhibition of Va and VIIIa

thrombomodulin > thrombin
-thrombin then activates protein C
-with protein S - goes to inactivate Va and VIIIa

4

endo cell inhibition of VIIa/TF and Xa

TFPI

5

tPA activity

converts plasminogen to plasmin
-plasmin then causes fibrinolysis

fibrin > fibrin degradation products

6

antithrombin

is antithrombin III
-neutralizes active serine proteases
-inhibits 2a, 9a, 10a, 12a
-mainly - IIa and Xa - no fibrin

7

heparin

increases antithrombin binding 1000x

no prolonged PT - but will see it with overdose

8

two main effects of antithrombin

1 inhibit factor Xa - decreased thrombin production

2 inhibit thrombin (IIa) from activating fibrinogen

9

tPa

binds fibrin
-forms plasminogen > plasmin

10

urokinase

from endo cells
-forms plasminogen > plasmin

11

XIIa pathway

converts plasminogen to plasmin

12

three things increasing plasmin

tPA
urokinase
XIIa pathway

all induce rapid clot dissolution

13

D dimer positive

indicates that clotting and fibrinolysis is occuring**

D dimer is portion of fibrin polymer once it is lysed

14

fibrin split products

older test - indicate plasmin breaking down fibrin

15

high thrombin, low plasmin

thrombosis

16

low thrombin, high plasmin

hemorrhage

17

low fibrin or platelets

hemorrhage

18

arterial thrombus

ischemia / infarction distal to thrombus

19

venous thrombus

congestion and edema proximal to occlusion

20

thrombus

clot grown larger than required for its physiologic role

21

fate of thrombus

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

22

inherited causes of hypercoagulability

patients under age 50 with thrombosis
-should suspect genetics

23

primary causes of hypercoagulability

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

factor V mutation

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