Drugs to Treat PAD and DVT Flashcards

1
Q

Why can fondaparinux and low molecular weight heparins be administered at home?

A

Because of their predictable pharmacokinetics

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2
Q

What is an example of drugs that can contain vasoconstrictors that can exacerbate PAD?

A

Cold remedies

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3
Q

What is the function of CYP2C9?

A

Metabolizes the more potent S warfarin; numerous polymorphisms in this gene and those decreasing its activity against warfarin are more common in Caucasians, increasing Warfarin potency 3-5x

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4
Q

Contraceptive use is associated with increased risk of what?

A

DVT in younger women due to increased clotting factor synthesis

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5
Q

Name risk factors for PAD

A

obesity, smoking, diabetes, increased cholesterol levels

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6
Q

What are white clots?

A

Abundance of platelets in arteries; reason platelet targeting drugs are chosen for problems there

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7
Q

What is the first line tx for decreasing risk of PAD?

A

Statins

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8
Q

What is a common cause of PAD?

A

atherosclerosis

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9
Q

Kidney disease can hasten the elimination of what?

A

clotting factors

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10
Q

What are red clots?

A

Blood clots in the venous circulation; consequence of large fibrin mesh that forms

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11
Q

What is a potential sx of DVT?

A

pain

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12
Q

What is a surgical tx option for PAD?

A

angioplasty

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13
Q

What is a sign of PAD?

A

bruits

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14
Q

Petechiae are a common sign of what?

A

platelet defects, uncommon with clotting factor defects

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15
Q

What is often recommended to reduce risk of DVT?

A

exercise; cardiomyositis is an instance where it is not recommended

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16
Q

What assay can be used to measure anticoagulation for drugs such as rivaroxaban?

A

Anti-Xa

17
Q

What was the first use for warfarin?

A

rat poison

18
Q

what is a stent?

A

Wire mesh placed in stenotic blood vessels to keep the lumen open; often drug-eluting

19
Q

What is cilostazol?

A

Type 3 phosphodiesterase inhibitor that prolongs the life of cAMP in platelets; used to surpress platelet aggregation and cause peripheral vasodilation; indicated for intermittent claudication associated with PAD

20
Q

How do deficiencies of clotting factors manifest?

A

as deep tissue bleeding forming large subcutaneous and soft tissue hematomas or hemarthroses; may be delayed/oozing after procedures

21
Q

what is a frequent consequence of PAD?

A

erectile dysfunction

22
Q

Which drug can cause necrosis?

A

Warfarin; occurs when there is a rapid fall in protein C leading to a hyper coagulable state; reason why pts must be transitioned to warfarin therapy rather than abruptly started on it

23
Q

How are the legs characterized in PAD?

A

have shiny skin

24
Q

What can also contribute to DVT risk?

A

genetic variability; also seen in VKORC1 (reason why AA can be resistant to warfarin and Asians more sensitive to it)

25
Q

Liver disease can impair the synthesis of what?

A

clotting factors

26
Q

What leads to platelet activation/thrombosis and platelet removal by splenic macrophages?

A

Platelet Fc receptors bind an IgG bound to heparin and PF4 in heparin induced thrombocytopenia

27
Q

What is released by thrombin?

A

fibrin; polymerized form is a substrate for plasmin

28
Q

What is a black box contraindication for cilostazol?

A

hepatic failure

29
Q

Pedal pulses tend to be weak or absent with what?

A

PAD

30
Q

What is generated as a consequence of factor X activation?

A

thrombin; inhibited by unfractionated heparin but not LMW heparin or fonaparinux

31
Q

What is an element of treatment strategy when switching from a DOAC to warfarin, but not when switching from one DOAC to another?

A

overlap

32
Q

Carbamazepine, phenytoin, and phenobarbital all decrease the effects of what?

A

Warfarin because they induce the synthesis of its metabolic enzymes

33
Q

What is a challenge associated with both heparin and warfarin?

A

dosing; which is a reason for frequent coagulation tests are required

34
Q

What is the generic name reference to the drug class that inhibits factor Xa?

A

Xaban