weber pre-lecture pt 1 Flashcards

pages 1-21

1
Q

how are venous thrombi formed?

A

stasis blood leads to decreased clotting factor clearance

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2
Q

what is the composition of venous thrombi?

A

RBCs
fibrin
platelets

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3
Q

when do symptoms result?

A

flow is obstructed
vascular tissue wall is inflamed (after surgery/trauma)
thrombus ocurs and affects venous blood flow or emboli occur and enter pulmonary circulation

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4
Q

what is virchow’s triad?

A

hypercoagulable state
endothelial injury
circulatory stasis

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5
Q

what is a hypercoagulable state?

A

abnormalities of clotting components
example – pregnancy, cancer

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6
Q

what is endothelial injury?

A

abnormality of surfaces in contact with blood flow
example - surgery/trauma

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7
Q

what is circulatory stasis?

A

abnormalities in blood flow
example - long periods of immobility

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8
Q
A
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9
Q

what happens in the initiation stage?

A

injury exposes tissue factor bearing cell
X is converted to Xa/Va
Prothrombin is converted to Thrombin (in trace amounts) via Xa/Va

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10
Q

What happens in the amplification stage?

A

in the collagen-activated platelet, thrombin converts V, VIII/vWF, and XI to Va, VIIa + vWF, XI

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11
Q

what happens in the propagation stage?

A

in the collagen/thrombin-activated platelet,
prothrombin is converted into thrombin (in large amounts) via Xa/Va
fibrinogen is converted into fibrin via thrombin

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12
Q

what is postthrombotic syndrome?

A

long term complication of DVT caused by damage to venous valves
results in chronic venous obstruction, chronic pain/swelling, stasis ulcers, and development of infection
caused by venous hypertension

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13
Q

what are some risk factors of DVT?

A

> 40 yo
fam h/o of DVT
HF
immobilization greater than 10 days
pregnancy
malignancy
MI
obesity
orthopedic injury
oral contraceptives/estrogen
paralysis
postop state (within 3 months)
prior DVT
varicose veins

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14
Q

what are some non-pharmacologic txs of DVT?

A

bed rest with proper anticoag meds
elevation of feet
pain management
compression stocking

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15
Q

what are some non-pharm tx of PE?

A

oxygen
mechanical ventilation

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15
Q

what is UFH?

A

unfractionated heparin

16
Q

what dosage form is UFH?

A

rapid, parenteral anticoagulation
IV

17
Q

what is the monitoring parameters for UFH?

A

activated Partial Thromboplastic Time (aPTT)
goal –> 1.5 to 2.5 time control

18
Q

how is UFH dosed?

A

by weight

19
Q

what are AE of UFH?

A

bleeding
thrombocytopenia

20
Q

what are the platelet count associated with HAT/HIT?

A

HAT –> mild decrease
HIT –> major decrease from baseline (over 50%) or under 100,000 mm3

21
Q

in what type of thrombocytopenia, does all heparin need to be stopped?

A

in HIT

22
Q

what are the associated characteristics of HAT?

A

non-immune mediated
occurs around 48-72 hours after admin
transient
do not d/c

23
Q

what are the associated characteristics of HIT?

A

immune mediated
occurs between 1-2 weeks
can occur up to 9 days after stopping therapy

24
Q

how is HIT treated?

A

stop all heparin products and give alternative anticoag
no platelet infusions, no warfarin until platelet over 150,000

25
Q

what are some alternative anticoags used to treat HIT?

A

lepirudin
argatroban
bivalirudin
fondaparinux

26
Q

what type of heparin has reduced incidence of HIT?

A

LMWH

27
Q

what type of heparin is SQ dosing?

A

LMWH

28
Q

what type of heparin has renal dysfunction dosing?

A

enoxaparin (lovenox)

29
Q

what drugs are LMWH?

A

enoxaparin (lovenox)
dalteparin (fragmin)

30
Q

when should patients be monitored during LMWH therapy?

A

consider for children, severe kidney failure, obesity, long courses, and pregnancy
usually not recommended

31
Q

what is trough monitoring?

A

used in once daily dosing in LMWH
measured immediately before the dose is given on day 2

32
Q

what is peak monitoring?

A

used in twice daily dosing in LMWH
measured 4 hours post dose