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Pharm 323 Spring 22 > Anticoagulant, Thrombolytics + CHO drugs > Flashcards

Anticoagulant, Thrombolytics + CHO drugs Flashcards

1
Q

VLDLs are referring to what?

A

triglycerides

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2
Q

prototype for HMG-CoA reductase inhibitors

A

atorvastatin (Lipitor)

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3
Q

what is the 1st line tx for lipid disorders?

A

statins

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4
Q

MOA of statins

A
  1. inhibit CHO synthesis in liver
  2. stimulate liver to make more LDL receptors

more receptors = more LDL removed from blood

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5
Q

when are statins most effective? why?

A

at NIGHT - b/c CHO is made at night

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6
Q

SE of statins

A

HA, rash, memory loss, GI issues

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7
Q

what are the rare + serious SE of statins? (3)

A
  1. hepatotoxicity
  2. rhabdomyolysis
  3. increase incidence of cataracts
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8
Q

knowing SE of statins (2), what labs need to be monitored?

A
  1. LFTs - for hepatotoxicity (OK to use in fatty liver disease)
  2. CK levels - for rhabdo
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9
Q

re: the serious SE of statins (2), what s+s should we teach patients to monitor for with statin use?

A

muscle aches, tenderness, weakness (risk of rhabdomyolysis)

RUQ pain, jaundice, anorexia (risk of hepatitis)

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10
Q

what drug-food interactions are most important with statin use?

A

grapefruit

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11
Q

what are the 5 classes of lipid lowering drugs?

A
  1. HMG-CoA Reductase inhibitor
  2. bile acid sequestrants
  3. cholesterol absorption inhibitor
  4. fibric acid derivatives (fibrates)
  5. monoclonal antibodies (PCSK9 inhibitors)
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12
Q

what is the prototype for bile acid sequestrants?

A

colesevelam (Welchol)

“cole the horse is 7 and his best friend is a lamb”

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13
Q

MOA of colesevelam

A

binds to bile acids –> forms complexes that prevent them from being reabsorbed –> excreted

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14
Q

what are the 2 drugs that work ONLY in GI tract?

A
  1. colesevelam

2. ezetimibe

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15
Q

SE of colesevelam

A

GI disturbances (constipation, bloating, indigestion)

“cole the horse ate too much cole slaw”

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16
Q

administration points for colesevelam

A

with food + H2O

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17
Q

prototype for cholesterol absorption inhibitor

A

ezetimibe

“get ZET outta here!”

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18
Q

MOA for ezetimibe

A

prevents CHO from being absorbed in small intestine

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19
Q

what do we need to watch for when ezetimibe is paired with statin?

A

hepatotoxicity (DON’T use with liver disease)

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20
Q

what is vytorin?

A

ezetimibe + simvastatin

VY = BI = 2 (drugs)

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21
Q

prototype for fibric acid derivative (fibrates)

A

gemFIBrozil

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22
Q

MOA for gemfibrozil

A

accelerates clearances of VLDLs (triglycerides)

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23
Q

what drug is MOST effective to lower triglyceride levels?

A

gemfibrozil

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24
Q

SE of gemfibrozil

A
  1. GI
  2. gallstone
  3. hepatotoxicity
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25
Q

gemfibrozil + _________ = increased risk of what?

A

gemfibrozil + STATIN = increased risk of RHABDOMYOLYSIS

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26
Q

prototype for PCSK9 monoclonal antibodies

A

evolocuMAB

“you evolve to have shitty cholesterol like your family”

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27
Q

MOA for evolocumab

A

blocks PCSK9 from binding to LDL receptors –> more LDL receptors made –> LDL removed

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28
Q

what is evolocumab used to treat?

A

familial hypercholesterolemia

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29
Q

route for evolocumab

A

SQ

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30
Q

SE of evolocumab

A

injection site rxns, rash/hives

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31
Q

3 examples of other agents to reduce CHO

A
  1. red yeast rice
  2. plant sterols
  3. fish oil
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32
Q

what are the 6 lipid-lowering drugs?

A
  1. atorvastatin (HMG-CoA inhibitor)
  2. colesevelam (bile acid seq)
  3. ezetimibe (CHO absorption inhibitor)
  4. vytorin (combo CAI + statin)
  5. gemfibrozil (fibrates)
  6. evolocumab (MAb)
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33
Q

what are the 3 different drug types for clots (broad)? what is their broad MOA?

A
  1. anticoagulants: prevent clot formation (reduce fibrin)
  2. antiplatelets: inhibit clot growing (aggregation)
  3. thrombolytics: dissolves clots
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34
Q

what drug type is best for VENOUS thrombi (ex: DVT)?

A

anticoagulants

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35
Q

what drug type is best for ARTERIAL thrombi (ex: MI, stroke)?

A

antiplatelets

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36
Q

MOA of anticoagulants

A
  1. inhibit synthesis of clotting factors
    OR
  2. inhibit activity of clotting factors

prevent FUTURE clots
CO = NO!!!

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37
Q

prototype for anticoagulants

A

heparin (unfractionated)

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38
Q

MOA for heparin

A
  1. inactivates clotting factors

2. suppresses formation of fibrin

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39
Q

heparin is measured in _____

A

UNITS

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40
Q

route of admin for heparin; indicate their use based on the route

A

SQ or IV only!

SQ: prophylaxis
IV: emergency anticoagulation

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41
Q

onset for IV heparin

A

immediate

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42
Q

onset for SQ heparin

A

up to 1 hr

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43
Q

what is the DOC for rapid anticoagulation (PE, stroke, massive DVT)?

A

IV infusion heparin

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44
Q

half life of heparin

A

90 mins

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45
Q

antidote for heparin + its onset

NCLEX

A

protamine sulfate - 5 min onset

46
Q

what lab do we monitor with heparin use?

A

aPTT (INtrinsic pathway)

47
Q

what is therapeutic level of aPTT for heparin use?

A
  1. 5-2x baseline = 60-80 seconds

normal: 40

48
Q

how often should aPTT be measured with IV heparin?

A

q6h

49
Q

SE of heparin

A
  1. bleeding

2. HIT (heparin-induced thrombocytopenia)

50
Q

re: HIT, when should heparin be stopped?

A

if platelets reduce by 50% or get <100,000

51
Q

what procedure should be avoided with heparin use?

A

epidural/spinal tap (hematoma / paralysis risk)

52
Q

LMWH prototype

A

enoxaparin (Lovenox)

“it’s NOXA much as regular heparin”

“LOvenox = LOW”

53
Q

MOA for enoxaparin

A

inhibits clotting factors: inactivates Xa + thrombin

54
Q

enoxaparin dosing is based on what?

A

weight

low molecular WEIGHT heparin dosing is based on WEIGHT

55
Q

route of LMWH

A

SQ only (abdomen only)

don’t expel bubble

56
Q

SE of LMWH (enoxaparin)

A
  1. bleeding

2. HIT

57
Q

why is enoxaparin preferred over heparin?

A

safer, no blood tests + more bioavailability

58
Q

antidote for enoxaparin

A

protamine sulfate

59
Q

vitamin K antagonist prototype

A

warfarin (Coumadin)

60
Q

route of admin for warfarin (Coumadin)

A

PO
SQ
IV

61
Q

re: IV vitamin K, what is important to know?

A

can cause anaphylaxis – small dose + DILUTE!

62
Q

MOA of warfarin

A
  1. inhibits clotting factors that depend on Vit K

2. inhibits prothrombin

63
Q

antidote for warfarin

A

Vitamin K

64
Q

which drug is 99% protein bound and causes a LOT of drug-drug interactions?

A

warfarin (Coumadin)

65
Q

what are the drug-food interactions with warfarin?

A

vitamin K - green leafy veg

recommended to get a “steady state” of vitamin K and not suddenly decrease or increase the levels consumed

66
Q

SE of warfarin

A

hemorrhage

67
Q

half life of warfarin

A

1.5-2 days

68
Q

what labs are we monitoring with warfarin (Coumadin) use?

A

PT/INR (focus on this one)

waR = inR

69
Q

what is therapeutic INR for warfarin use?

A

2.0-3.0

70
Q

what things should we teach our patients on warfarin?

A
  1. same time everyday
  2. balance vit K consumption
  3. watch for s+s of bleeding
  4. avoid things that could cause bleeding (hard toothbrush, straight razors, ibuprofen or ASA, venipuncture, procedures, the “G” natural supps)
71
Q

what pain reliever is considered safe and recommended to use with warfarin? what should be avoided?

A

safe: tylenol
avoid: ASA + ibuprofen

72
Q

prototype for direct thrombin inhibitor

A

dabigatran (Pradaxa)

73
Q

route for dabigatran

A

ORAL

74
Q

MOA of dabigatran

A

direct, reversible inhibition of thrombin

75
Q

AE of dabigatran

A
  1. bleeding (less than other anticoagulants)
  2. GI issues (take with food, PPI or H2 blocker)

GI issues b/c taken orally

76
Q

why do we like dabigatran?

A 
no lab monitoring
lower risk of bleeding***
few drug-drug / drug-food interactions
no titrations (Set dose)
rapid onset
77
Q

antidote for dabigatran

A

idarucizuMAB (Praxbind)

“i DAR the DAB to CRUZ by me”

78
Q

prototype (2) for direct factor Xa inhibitors

A

apixaban (Eliquis)

rivaroxaban (Xarelto)

“Xa is BANned”

79
Q

MOA of direct factor Xa inhibitor

A

binds to Xa + inhibits thrombin

80
Q

route for apixaban + rivaroxaban

A

ORAL

81
Q

why do we like the direct factor Xa inhibitors?

A 
no lab monitoring
lower bleeding risk 
fixed dose
fewer drug-interactions
rapid onset

similar to dabigatran

82
Q

direct factor Xa inhibitors are contraindicated in which 2 scenarios?

A
  1. liver disease

2. pregnancy

83
Q

antidote for apixaban + rivaroxaban

A

andeXanet alfa

84
Q

if on IV heparin in emergency situation and need to switch to oral agent (Xa inhibitors), what’s the protocol?

A

stop heparin
immediately start oral dose
double doses for 2ish days, then move to once daily

85
Q

if on IV heparin in emergency situation and need to switch to oral agent (warfarin), what’s the protocol?

A

2-3 days administer both heparin + warfarin

  • warfarin takes a couple days for full effect*
  • increased risk of bleeding:
  • monitor pTT (heparin) + INR (warfarin)
86
Q

what are the 6 anticoagulant drugs names?

A
  1. heparin
  2. enoxaparin (LMWH)
  3. warfarin (Coumadin)
  4. dabigatran
  5. apixaban
  6. rivaroxaban
87
Q

what are the 4 antiplatelet drug names?

A
  1. ASA
  2. clopidogrel
  3. vorapaxar
  4. abciximab
88
Q

MOA of ASA

A

irreversible inhibition of COX (blocks platelet aggregation - not sticky)

89
Q

how long will you see single dose effects of ASA?

A

one week (why we have patients stop ASA 7 days before surgery)

90
Q

ASA is used to prevent clot formation in __________

A

ARTERIES (prevent MI, TIA, CVA)

91
Q

SE/risk of ASA use + how we can combat this

A

GI bleeding –> take with PPI or food/milk

92
Q

prototype for ADP antagonist

A

clopidogrel (Plavix)

93
Q

MOA of clopidogrel (Plavix)

A

blocks ADP receptors on platelet surfaces

94
Q

dual platelet therapy is often seen with which 2 drugs?

A

ASA + clopidogrel (Plavix)

95
Q

if we see s+s of bleeding with clopidogrel (Plavix) use, what’s the protocol?

A

check with provider 1st before stopping - risk of MI or CVA could increase if stopped!!!

96
Q

prototype for PAR-1 Antagonists

A

vorapaxar

97
Q

MOA of vorapaxar

A

block PAR on platelets

98
Q

route of vorapaxar

A

oral (lasts 7-10 days after last dose)

99
Q

what 3 antiplatelet drugs are often given together in some combination to prevent CV events in high risk patients (MI, CVA, PAD hx)

A

vorapaxar + clopidogrel or ASA

100
Q

prototype for glycoprotein 2B/3A receptor antagonist

A

abciximab

“easy as ABC, easy as 1, 2, 3”

101
Q

MOA of abciximab

A

reversible inhibition of ALL platelet aggregation factors!!!!!

102
Q

when would abciximab be used?

A

IV when someone is unstable (non STEMI, unstable angina, cardiac cath, stents, ACS)

103
Q

main goal of abciximab

A

SAVE CARDIAC TISSUE in procedures

“ABC = emergency!”

104
Q

how long can antiplatelet effects be seen after dose of abciximab?

A

~24 hours

105
Q

prototype for thrombolytics

A

alteplase (tPa)

106
Q

MOA of alteplase (tPa)

A

breakdown of [all] clots in the body!

107
Q

this drug is used for acute MI, PE, ischemic stroke

A

alteplase (tPa)

108
Q

when should we give alteplase?

A

best if given EARLY!

MI: 6 hours of onset (30 mins ideal)
CVA: 3 hours

all patients should be evaluated for alteplase use

109
Q

if you see any s+s of bleeding with alteplase (tPa), what should you do?

A

STOP!!!

esp. cerebral - might see mental status change

110
Q

half life of alteplase (tPa)

A

5 minutes

111
Q

contraindications for alteplase

A
  1. recent pregnancy
  2. internal bleeding
  3. other anticoagulants
  4. severe HTN
  5. PUD

Pharm 323 Spring 22 (18 decks)

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