Pharmacology (Antiplatelets/Anticoagulation) Flashcards

1
Q

what is the advantage that dabigatran has over rivaroxaban in terms of ADRs

A

Dabigatran (pradaxa) is not a CYP450 substrate

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2
Q

what is a disadvantage of rivaroxaban that Heparin and Warfarin and Enoxaparin have

A

no antidote

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3
Q

what are some ADRs for rivaroxaban

A

GI upset, bleeding, HS, don’t stop abruptly, elevated LFTs

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4
Q

what is rivaroxabans MOA

A

is a direct Xa irreversible antagonist; indicated to prevent & tx VTE, MI, and ACS

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5
Q

what is Dabigatrans Indications for use and MOA

A

prevents/tx VTE, MI, ACS by directly inhibiting thrombin

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6
Q

what is the onset of action for both dabigatran and rivaroxaban

A

2-4 hours

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7
Q

what are some ADRs of ferrous sulfate (feosol)

A

GI upset, toxicity in children, black stools, HS, *compliance an issue

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8
Q

what are some ADRs of cyanacobalamin B12

A

diarrhea, PE, CHF, anaphylaxis, polycythemia vera

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9
Q

what are some DI’s of cyanocobalamin B12

A

folic acid (masks B12 def.) drugs that reduce absorption or stomach acidity

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10
Q

what are some ADRs of folic acid

A

GI disturbance, CNS symptoms, HS, can mask Vit B12 def.

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11
Q

DI with Folic Acid

A

anticonvulsants

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12
Q

what is 5-fluorouracil Indications & MOA

A

tx cancer, skin conditions; acts as a purine/pyrimidine preventing DNA replication

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13
Q

what are some ADRs of 5-fluorouracil

A

cardiotoxicity, alopecia, pancytopenia, nystagmus, PE photosensitivity

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14
Q

what is methotrexates MOA

A

inhibits folic acid reductase, antirheumatic MOA unknown

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15
Q

ADRs of methotrexate

A

mucositis, diarrhea, stomatitis, N&V, myelosuppresion, hepatotoxicity

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16
Q

what is the MOA of both Heparin and Enoxaparin

A

potentiates antithrombin to inactivate factor Xa, preventing prothrombin-thrombin and fibrinogen-fibrin.

17
Q

what are the ADRs of Heparin and Enoxaparin

A

**Bleeding (reversible with protamine), alopecia, osteoporosis, HIT, thrombocytopenia

18
Q

what is Heparins Onset, time to FE, and time to wear off

A

45 minutes, FE-few hours, 4 hrs to wear off

19
Q

Enoxaparin’s onset, time to FE, and to wear off

A

onset-4-5 hrs, FE-1 day and 24 hrs to wear off

20
Q

what is the advantages of Enoxaparin over heparin

A

more selective, predictable, improved bioavailability, more consisten molecular size, longer half-life

21
Q

what are the DI’s of both heparin and enoxaparin

A

anticoagulants and antiplatelets

22
Q

what are some ADRs of warfarin

A

blue toe syndrome, skin necrosis, rash, bleeding (reversible with Vit. K) *contraindicated with pregnant

23
Q

what causes skin necrosis from warfarins effect

A

blocking Protein C which normally has a function to be cytoprotectant by inhibiting apoptosis in healthy endothelium

24
Q

what are some ADRs with aspirin

A

bleeding GI ulcers, asthma exacerbation, tinnitus, occult bleeding, thrombocytopenia, AKI, hepatits, Reye syndrome (brain/liver) HS , don’t give children <20

25
what are some DI's of aspirin
ADR x2, Live Vaccines,
26
what is clopidrogel's MOA
irreversibly inhibits P2Y12 on surface of plts
27
what are some DI's of clopidrogel
it is a prodrug that requires liver metabolism hence CYP450 substrate
28
what are some ADRs of clopidrogel
bleeding, GI ulcers, HS, bone marrow toxicity
29
what is warfarins Onset, time to FE, and to wear off
Onset-8-12 hours, FE at 5-7 days, and 4 days to wear off
30
this is a pentasacchide similar to heparin and enoxaparin which increases antithrombin 300 fold, however is not reversible with protamine, and takes longer to wear off (4-5 days)
fondaparinux
31
describe the mechanism of how B12 is absorbed...
first they bind to R protein in saliva; R protein protects it from stomach acid & then destroyed in duodenum. Next, B12 binds to intrinsic factor made from parietal cells in stomach and can be absorbed in terminal ileum.
32
this is an autoimmune dz where antibodies against parietal cells reduces intrinsic factor which can cause B12 def.
pernicious anemia