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
Q

what are some DI’s of aspirin

A

ADR x2, Live Vaccines,

26
Q

what is clopidrogel’s MOA

A

irreversibly inhibits P2Y12 on surface of plts

27
Q

what are some DI’s of clopidrogel

A

it is a prodrug that requires liver metabolism hence CYP450 substrate

28
Q

what are some ADRs of clopidrogel

A

bleeding, GI ulcers, HS, bone marrow toxicity

29
Q

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

A

Onset-8-12 hours, FE at 5-7 days, and 4 days to wear off

30
Q

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)

A

fondaparinux

31
Q

describe the mechanism of how B12 is absorbed…

A

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
Q

this is an autoimmune dz where antibodies against parietal cells reduces intrinsic factor which can cause B12 def.

A

pernicious anemia