thrombosis Flashcards

1
Q

what is virchow’s triad

A

endothelial injury, blood stasis or turbulence of blood flow, blood hypercoagulaboilty

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2
Q

what dirction do thrombi grow

A

toward the heart

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3
Q

what are some antiplatelete effects

A

no binding to endothelium and PGI2 and NO prevent platelet adhesion

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4
Q

what are some anticoagulant properties

A

herparin like molecule activate anti thrombin 3, thrombomodulin activates protein c

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5
Q

what are some fibronlytis properties

A

endothelium made tPA

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6
Q

what inhibits platelests

A

ASA?

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7
Q

what is the diffence between a hemostatic plug and a clot

A

plug is still reversible whereas a clot is not

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8
Q

how does turbulence and stasis of effect thrombosis

A

turbulance will enhance endothelial injury and stasis leads to venous thrombosis,

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9
Q

what happens to von willebrand factor with increased blood flow

A

it will unfold and become more sticky.

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10
Q

what makes the fibrin clot

A

when the plug made of fibrin gets cross likes it will make the fibrin clot.

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11
Q

how does the degradation process start

A

plasminogen is converted to plasmin and then it degrades the clot.

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12
Q

tell me about pulmonary thrombolism

A

small will be silent, medium will have an acute respiratory and cardiac symptoms and fear, large right heart failure and collapse, massive sudden death with saddle embolus.

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13
Q

what are some causes of hypercoagulability primary

A

Factor 5 leiden mutation, antithrombin 3 deficeincy, protein c or s defeciency, prothrombin G20210A gene mutation

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14
Q

what are some causes of hypercoagulability secondary

A

anti phospholipid syndrome, lups anticoagulant, cancer, nephrotic syndrom, contraceptive pills, smoking, prolonged immobilazation.

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15
Q

what are some other hypercoagulability states

A

heparin induced thrombocytopenia, and antiphospholipid syndrom [lupus] antibodies to phospholipids, invitro inhibits coagulation in vivo indueds it,

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16
Q

where do you get DVT from

A

popliteal femoral iliac veins

17
Q

what leads to DIC

A

disseminated intravascular coagulation can be caused by shock infection pregnancy with malignancy.

18
Q

what is the second most common medical complication

A

VTE venous thrombi embolism

19
Q

what is the most common cause of preventable hospital death

A

pulmonary embolism

20
Q

what is a parodoxical embolus

A

when it will pass from right side to left of the heart by a septal defect

21
Q

what is the vulnerability to hypoxia of neurons heart and fibrous tissue

A

3-4 min neuron, 20-30- heart, and hours for fibrous tissue

22
Q

what the inherirted hypercoagulabilities with highes relative risk

A

antithrombin deficiency 10x but only 5% of pop, prothrombin mutation 7%, defeciecy in protein c and protein s 5% and 10 rr

23
Q

what should you look for before oral contraceptives prescription

A

possible factor 5 leiden because it will increaase rr by 34.7

24
Q

what are some threpuetic options for thrombosis

A

heparin LMW heparis, throbolysis, warfarin, ASA PGP 2B/3a inhibititors.

25
Q

what is purple skin syndrom

A

3% of people who go on warfarin will get this common on toes and skin reversible with heparin.

26
Q

what percent of thrombosis is accounted by factor 5 leiden

A

About 50%

27
Q

how do you test for factor 5 and prothrombin

A

DNA genetic tests.

28
Q

what is the overall risk of thrombosis

A

1:1000 adults children less need several factors to really be at risk.