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NSG 323 > LL agents, Anticoags, antiplatelets and thrombolytics > Flashcards

LL agents, Anticoags, antiplatelets and thrombolytics Flashcards

1
Q

HMG-CoA reductase inhibitors are also called

A

statins

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2
Q

1st line therapy for lipid disorders

A

statins

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3
Q

MOA for statins

A

inhibit CL synthesis in the liver
stimulate hepatocytes to produce more LDL receptors
LDL receptors remove the LDL from the blood

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4
Q

prototype for statins

A

Atorvostatin AKA Lipitor

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5
Q

common SE of statins

A

headache, rash, memory loss, GI disturbance

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6
Q

serious SE of statins

A

hepatotoxicity, myopathy/rhabdomyolysis, cataracts

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7
Q

special considerations for statins

A

monitor for increased SE when statins combined with other lipid lowering agents.
no grapefruit
no pregnancy!
d-d interactions!

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8
Q

Bile-acid sequestrants MOA

A

bind to bile acids to form complexes that excreted.

bile acids are made from CL –> liver makes more bile acids using LDL –> increases LDL receptors to uptake more LDL

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9
Q

bile acid sequestrants prototype

A

colesevelam (welchol)

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10
Q

where do bile acid sequestrants work?

A

only in GI tract! so they have GI side effects, like constipation, bloating and indigestion.
admin with food and h2o

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11
Q

Cholesterol absorption inhibitor prototype

A

ezetimibe (zetia)

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12
Q

CL absorption inhibitor MOA

A

blocks CL absorption in the small intestine

also blocks CL secreted in bile

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13
Q

Ezetimibe se

A

equal placebo

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14
Q

what should you watch for with ezetimibe?

A

increased liver toxicity with statin.

no liver disease!

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15
Q

what is vytorin?

A

ezetimibe + simvistatin

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16
Q

Fibric acid derivatives (fibrates) moa

A

accelerates the clearance of VLDLs
little to no effect on LDLs
increases HDLs too

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17
Q

Fibrates prototype

A

gemfibrozil (lopid)

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18
Q

SE of gemfibrozil

A

rash and GI upset
increased risk of gallstones
myopathy
liver toxicity

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19
Q

d-d interactions of gemfibrozil

A

warfarin: increased risk of bleeding
statins: increased risk of rhabdo

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20
Q

MAB PCSK9 inhibitors MOA

A

binds to PCSK9 which blocks PCSK9 binding to LDL receptors. this increases LDL receptors, allowing LDL to bind to the receptors and be removed from the blood.

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21
Q

MAB PCSK9 prototype

A

evolocumab (repatha)

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22
Q

who is evolocumab approved for?

A

those who have familial high CL OR atherosclerotic heart problems who maxed out on statins.

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23
Q

how is evolocumab administered?

A

subq or IV. NO ORAL

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24
Q

SE of MAB PCSK9 inhibitors

A

injection site reactions, vasculitis, rask, urticaria.

antibody production can occur.

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25
Q

Other lipid lowering agents

A

fish oil
plant sterols and sterol esters
cholestin: made from rice fermented with red yeast

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26
Q

anticoagulants

A

prevents the formation of clots

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27
Q

antiplatelets

A

inhibits platelet aggregation

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28
Q

thrombolytic

A

dissolves life threatening clots

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29
Q

general MOA for anticoagulants

A

inhibit syn clotting factors (factor X and thrombin)
or
inhibit the activity of clotting factors (factor Xa, thrombin)

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30
Q

general uses of anticoags.

A

PREVENTION of VENOUS thrombosis

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31
Q

Heparin MOA

A

inactives several clotting factors (factor Xa) as well as inhibits thrombin activity and suppresses formation of fibrin

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32
Q

admin of heparin

A

must be IV or subq

33
Q

half life of heparin

A

90 mins.

takes 6 hours to become therapeutic!

34
Q

heparin/LMWH antidote

A

protamine sulfate

35
Q

what sort of monitoring do you need to do with heparin

A

aPTT

platelets

36
Q

normal aPTT levels

A

40 secs. with heparin we want to get it to 1.5-2x baseline, 60-80 seconds.
with IV heparin, test aPTT every 6 hours

37
Q

se of heparin

A

bleeding, heparin induced thrombocytopenia (HIT)

38
Q

HIT management

A

monitor platelets. if <100K, reduce by 50% then stop heparin

39
Q

LWMH characteristics

A

same MOA but safer!
no frequent blood tests
can be admined at home
dosage based on weight

40
Q

what is the drug of choice for DVT?

41
Q

LWMH prototype

A

enoxaparin (lovenox)

42
Q

Vitamin K antagonist prototype

A

warfarin (coumadin)

43
Q

MOA of warfarin

A

acts by inhibiting hepatic syn of vitamin K dependent clotting factors and prothrombin

44
Q

antidote for warfarin

A

vitamin K, effects in 6 hours

45
Q

uses of warfarin

A

prevent DVT, PE, clots in patients with afib, prosthetic heart valves, or who had TIA or recurrent MI

46
Q

considerations for warfarin

A

no pregnancy!
highly protein bound
lots of d-d interactions
narrow therapeutic index
genetic testing is recommended (VKORC1 and CYP2C9) variants (increased risk of bleeding )
foods high in vitamin K– eat consistently

47
Q

monitoring for warfarin

A

PT or INR, normally look at INR

half-life is 1.5-2 days.

48
Q

direct thrombin inhibitors MOA

A

direct, reversible inhibitor of thrombin

49
Q

admin of direct thrombin inhibitors?

A

can be IV, subQ or oral

50
Q

when do you use dabigatran?

A

afib, hip/knee replacement

51
Q

prototype for direct thrombin inhibitors

A

dabigatran (pradaxa)

52
Q

AE of dabigatran

A

bleeding and GI issues

53
Q

considerations for dabigatran

A 
no lab monitoring
lower risk of bleeding
few d-d interactions/d-f interactions
rapid onset
set dose
stop before surgery!
54
Q

antidote for dabigatran

A

idarucizumab (praxbind)

55
Q

direct factor Xa inhibitors MOA

A

bind with factor Xa and inhibits thrombin

56
Q

considerations for factor Xa inhibitors

A 
NO monitoring
Oral formulation
rapid onset
fixed dose
lower bleeding risk
few drug interactions
57
Q

prototype for factor Xa inhibitors (2)

A

rivaroxaban (xarelto)

apixaban (eliquis)

58
Q

antidote for factor xa inhibitors

A

andexanet alfa

59
Q

indications for factor xa inhibitors

A

post hip/knee replacement
Afib
tx of DVT/PE

60
Q

se of factor xa inhibitors

A

bleeding; spinal/epidural hematoma

contra in: liver disease and pregnancy

61
Q

Aspirin moa

A

interfere with platelet aggregation

used to prevent clot formation in ARTERIES

62
Q

what does ASA prevent

A

MI, TIA and stroke

63
Q

what does COX have to do with ASA

A

asa irreversibly inhibits COX and COX interferes with TXA 2, which is platelet aggregation

64
Q

dosing for ASA

A

81 mg 1x/week

give with proton pump inhibitor to protect GI system

65
Q

ADP antagonists prototype

A

clopidogrel (Plavix)

66
Q

ADP antagonists MOA

A

irreversible blockade of ADP receptors on platelet surfaces

67
Q

SE of ADP antag

A

same as ASA

68
Q

ACS pts and ADP

A

give ASA too!

69
Q

What should you do if there are s/s of bleeding pts taking clopidogrel?

A

call provider! they’ll clot up super quickly, may keep them on.

70
Q

PAR-1 antagonists prototype

A

vorapaxar (Zontivity)

71
Q

Vorapaxar MOa

A

reversibly blocks the PAR-1 expressed on platelets

72
Q

admin of PAR-1 antagonists

A

oral, lasts 7-10 days. given with clopidogrel and/or ASA to prevent CV events.
given to high risk patients!

73
Q

glycoprotein IIb/IIIa receptor antagonists prototype

A

abciximab (ReoPro)

74
Q

admin of abciximab

A

IV for short term use (like surgery or procedures)
given with ASA and heparin
stops working in 24-48 hours

75
Q

MOA for abciximab

A

reversible inhibition of all factors in platelet aggregation

76
Q

Thrombolytics MOA

A

bust up a clot baby

77
Q

thrombolytics prototype

A

alteplase (tPa)

78
Q

considerations for tPa

A

most effective if given early: within 6 hrs of MI or 3 of CVA
have to see if they are eligible for tPa, screen for risk of hemorrhage
narrow margin of safety, stop if ANY sign/sym of bleeding

79
Q

contraindications for tPa

A

pregnancy, severe HTN, peptic ulcer, history of MI/CVA.

NSG 323 (12 decks)

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