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?

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?

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
how is HIT treated?
stop all heparin products and give alternative anticoag no platelet infusions, no warfarin until platelet over 150,000
25
what are some alternative anticoags used to treat HIT?
lepirudin argatroban bivalirudin fondaparinux
26
what type of heparin has reduced incidence of HIT?
LMWH
27
what type of heparin is SQ dosing?
LMWH
28
what type of heparin has renal dysfunction dosing?
enoxaparin (lovenox)
29
what drugs are LMWH?
enoxaparin (lovenox) dalteparin (fragmin)
30
when should patients be monitored during LMWH therapy?
consider for children, severe kidney failure, obesity, long courses, and pregnancy usually not recommended
31
what is trough monitoring?
used in once daily dosing in LMWH measured immediately before the dose is given on day 2
32
what is peak monitoring?
used in twice daily dosing in LMWH measured 4 hours post dose