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Nursing-Sem 1 > Pharm Section 3 > Flashcards

Pharm Section 3 Flashcards

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1
Q

more than ____% of americans have 1 or more types of CVD (cardiovascular disease)

A

20% of males and females (more than 60 million)

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2
Q

heart disease, tx, and prevention accounts for ____% of healthcare expenditures in the US

A

17%

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3
Q

_______ from heart disease has gone down, but the number of ________ has remained virtually the same

A

death; coronary events

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4
Q

stent

A

sleeve inserted into an obstructed artery that has been ballooned open by angioplasty (PCTA).

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5
Q

rapamycin

A

an imunosuppresant that prevents rejection (coats stents)

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6
Q

traditional risk factors for CVD

A

increasing age (45+ male, 55+ female)
fam hx of premature cardiac heart disease
smoking, second-hand smoke
HDL <40mg/dL
hypertension (double risk for every 20/10mmHg increase)
lack of physical activity, being overweight
diabetes/insulin resistance

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7
Q

newer markers for CVD

A 
Lipoprotein a (Lp(a))
Apolipoproetin B (APOB)
homocysteine
hematological factors
troponin
Myeloperoxidase (MPO)
Brain natriuretic peptide (BNP)
high sensitivity C-reactive protein (hs-CRP)
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8
Q

BNP is used to rule out….

A

heart failure

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9
Q

C-reactive protein levels are indicative of…

A

inflammation. hs-CRP levels >3mg/L = high risk; 1-3 mg/L normal, <1mg/L = low risk

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10
Q

c-reactive protein can be lowered by

A

diet, exercise, statins, aspirin, alcohol

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11
Q

CAD spectrum of acute coronary syndromes & ST elevation

A

stable angina > unstable angina > NSTEMI > STEMI. ST elevation @ STEMI only.

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12
Q

ACS (acute coronary syndrome) treatments strategies

A

reperfusion or revscularization therapy including thrombolysis, PCI +/- stunting, CABG, and medical therapy. antithrombic cotherapy (ASA, UFH, LMWH, Penta., DTI, GP IIb, IIIa), ADP agonist) and acute and long-term medical therapy (Nitrates, beta blockers, ACEIs, ARBs, CCBs, Statins, APT)

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13
Q

antithrombic drugs include what types of drugs?

A

anticoagulants, antiplatelets, and thrombolytic agents

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14
Q

drug of choice for prevention and tx of arterial thrombosis?

A

anti platelet drugs. Used primarily for ACS (acute coronary syndrome) and STEMI (ST-elevation myocardial infarction)

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15
Q

ACS is an all-encompassing term that refers to…

A

Unstable angina (UA), Non-Q wave myocardial infarction, and Q-wave myocardial infarction

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16
Q

drug of choice for prevention and treatment of venous thromboembolism (VTE), DVT, PE in patients undergoing PCI or PTCA or for prevention of cardioembolic events in pts with a fib

A

anticoagulants

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17
Q

arterial thrombi are composed of…

A

mainly of platelet aggregates held together by small amounts of fibrin. Anti platelet drugs are #1 for pv/tx of arterial thrombosis, but anticoagulants also effective/can add to effect of antiplatelets

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18
Q

venous thrombi are composed of…

A

mainly of fibrin and trapped RBCs (relatively few platelets). anticoagulants are #1 for pv/tx

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19
Q

what are fibrinolytic agents used for?

A

rapid dissolution of thromboemboli, usually during MIs

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20
Q

clotting cascade

A

intrinsic and extrinsic pathways, common pathway.

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21
Q

vitamin K antagonists

A

aka warfarin. disrupt extrinsic pathway of clotting cascade during transition from Factor VII to VIIa. also disrupt @ intrinsic pathway during transition from Factor IX to IXa, @ common pathway between Factor X and Xa and prothrombin to thrombin.

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22
Q

oral Xa inhibitors

A

inhibit Factor Xa directly in common pathway

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23
Q

direct thrombin inhibitors

A

act to directly inhibit thrombin in common pathway

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24
Q

parenteral anticoagulant agents include

A

Unfractionated heparni (UFH), low-molecular-weight heparins (LMWHs), Pentasaccharide (selective Factor Xa inhibitors), Thrombin-Specific anticoagulants or direct thrombin inhibitors (DTIs), oral anticoagulants, newer oral anticoagulants (NOACs), new antithrombis for A fib, anti platelet drugs, glycoprotein IIb/IIIa inhibitors

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25
Q

heparin is only administered via what route?

A

parenteral with small gauge needle to avoid hematoma formation at injection site

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26
Q

heparin is derived from…?

A

hog mucosa or bovine lung

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27
Q

heparin MOA (mechanism of action)

A

decreases thrombin by binding to antithrombin II. forms complex, inactivates factor Xa, prevents conversion of prothrombin to thrombin (inhibits fibrinogen to fibrin).

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28
Q

heparin does NOT have ________ activity

A

fibrinolytic

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29
Q

effects of heparin

A

anticoagulation, inhibits platelet function, increases vascular permeability (all contribute to hemorrhagic effects of heparin)

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30
Q

antidote for bleeding related to heparin overdose

A

protamine sulfate

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31
Q

how do you test for heparin?

A

activated partial thromboplastin time (aPTT) or anti-Xa heparin assay (HA)
aPTT levels should remain between 1.5 and 2.5 times the normal control level

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32
Q

herpain-induced thrombocytopenia (HIT)

A

prothrombic adverse drug effect. platelet activating antibodies react against complexes of platelet factor IV and heparin. Rare, but significant mortality. Less common with LMWH. Associated with thrombosis, not bleeding.

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33
Q

is suspect HIT, what do you do?

A

immediately stop heparin tx. initiate alternative anticoagulant (i.e. argatroban, bivalirudin, fondaparinux)

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34
Q

heparin is available in two strengths…?

A

10 units/mL and 10,000 units/mL

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35
Q

LMWH derivatives are formed by…

A

cleaving standard heparin into shorter chains

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36
Q

benefits of LMWHs

A
  • more effect on factor Xa
  • more bioavailable with with dose-dependent plasma levels
  • produce more predictable plasma heparin concentrations (can use fixed doses w.o monitoring)
  • have longer half life (need fewer doses)
  • decreased risk of bleeding/HIT (less effect on platelet function)
  • less bone loss
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37
Q

protamine and LMWHs

A

doesn’t neutralize b/c absorbed faster than UFH, but reverses 60% of its effects

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38
Q

LMWH does is dependent on…?

A

actual body weight

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39
Q

1st line prevention and treatment for venous thromboembolism (VTE)?

A

LMWHs

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40
Q

LMWH agents

A

enoxaparin (Lovenox–inpt and outpt approved), dalteparin (Fragmin), Ardeparin (Normiflo), and Tinzaparin (Innohep)

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41
Q

Fondaparinux (Arixta)

A

antithrombotic action. inhibits single, targeted step in coagulation cascade (factor Xa). does NOT directly inhibit thrombin. Evidence suggests works as well as LMWH Lovenox and may cause fewer bleeds.

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42
Q

protamine and fondaparinux

A

protamine will not reverse its effects. must monitor factor Xa levels.

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43
Q

fondaparinux black box warning

A

warning for risk of bleeding with spinal or epidural hematoma, which could lead to long term or permanent paralysis.

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44
Q

fondaparinux contraindications

A

don’t give to patients with severe renal impairment (levels can accumulate).

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45
Q

thrombin specific anticoagulant/ direct thrombin inhibitors (DTIs)

A

cause the inhibition of thrombin independent of antithrombin. greater specificity. reduced tendency for bleeding b/c don’t directly affect platelet function.

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46
Q

injectable DTIs

A

Bivalirudin (Angiomax)
Desirudin (Iprivask)–recombinant of leech anticoagulant protein. Expensive.
Argatroban (no brand name)

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47
Q

oral anticoagulants (antithrombotics)

A

warfarin (Coumadin), newer oral anticoagulants (NOACs)

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48
Q

warfarin MOA

A

used orally. primary MOA is to interfere with the production of vitamin-K dependent clotting factors II, VII, IX, and X.

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49
Q

vitamin K

A

fat soluble vitamin. “K” derived from german word “koagulation”

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50
Q

clotting factor activity reduced by _____% when therapeutic doses of warfarin are given

A

30-50%

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51
Q

warfarin action @ liver

A

interferes with hepatic recycling of vitamin K by inhibiting reductase enzyme system that converts Vit K epoxide to Vit K. Accumulation of Vitamin K epoxide reduces effective concentration of Vit K and reduces the synthesis of coagulation factors.

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52
Q

vitmin K supplementation in pts taking warfarin?

A

usually pts educated to avoid vitamin K, but recent research shows supplementation with low dose k vitamins might reduce serious bleeding complications associated with warfarin therapy.

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53
Q

antidote for warfarin

A 
vitamin K (injection or oral)
can also administer: fresh frozen plasma, recombinant factor VIIa, prothrombin complex concentrates,
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54
Q

current vitamin K recommendations

A

take orally. use less.

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55
Q

warfarin INR (international normalized ratio)

A

2-3. anything =+4 shows no added benefit and increases risk of bleeding.

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56
Q

complications of long term anticoagulant therapy

A

major bleeding events like intracranial hemorrhaging. black box warning for potential fatal bleeding

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57
Q

warfarin original use

A

rat poison

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58
Q

warfarin and pregnancy

A

contraindicated for use in pregnancy

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59
Q

why is warfarin involved in so many drug interactions?

A

metabolized at the liver by P450 system. highly plasma protein bound ,but easily displaced so easy to interact with other drugs (tylenol, celebrex)

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60
Q

genetic testing and warfarin

A

CYP2C9 and VKORC1 genetic carriers face higher risk of bleeding on warfarin

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61
Q

NOACs

A

new oral anticoagulants. all have boxed warning for discontinuation and increased risk of stroke. shorter acting w. 12 hour half lives (40 hours for warfarin). includes dabigatran (Pradaxa), rivaroxaban (Zarelto), apixaban (Eliquis), and Edoxaban (Savaysa)

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62
Q

Dabigatran (Pradaxa)

A

NOAC. has an antidote: idarucizumab (Praxbind). IV injection. Expensive.

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63
Q

the only once-daily factor Xa inhibitor?

A

endoxaban (Savaysa)

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64
Q

black box warning for endoxaban (Savaysa)

A

don’t use in A fib patients with creatinine clearance < 95 mL/min. avoid using in patients with STRONG renal function.

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65
Q

NOACs vs warfarin

A

NOACs at least as effective as warfarin

NOACs have faster onset, fewer interactions, cause less bleeding

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66
Q

Afib pts 4x more likely to die from ______ than ______.

A

stroke than GI bleed.

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67
Q

NOACs and adherence

A

strict adherence is critical with NOACs because most don’t have antidotes and missing just a couple of doses increases risk for stroke (NOACs have much shorter durations than warfarin).

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68
Q

In what patient populations would warfarin be recommended over NOACs?

A

end-stage kidney disease pts, hemodialysis pts, and pts with mechanical heart valves.

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69
Q

Compared to warfarin, NOACs were associated with a _____% reduction in stroke or systemic embolic events and ____% inc. in GI bleeding.

A

19% reduction in stroke and 25% inc. in GI bleed.

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70
Q

NOACs and MIs/ ischemia strokes?

A

meta-analyses show a small, statistically insignificant reduction in stroke and MIs with NOACs

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71
Q

anticoagulation in afib patients after a GI bleed?

A

15% of pts on anticoagulant will have GI bleed, 25% of those won’t restart. Much more likely to die of stroke than GI bleed, so it’s recommended they do start back if @ high risk for stroke. Take warfarin or Eliquis over others, less chance of GI bleed. NOT PRADAXA–riskiest. Also recommended PPI in pts with upper GI bleed (benefits outweigh risks).

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72
Q

Some afib patients will need warfarin plus…?

A

an anti-platelet drug. CAUTION against triple anti-thrombotic therapy b/c inc. bleeding risk.

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73
Q

who is at high risk for stroke?

A

those with prior stroke or TIA, 75 years or older, diabetes, hypertension, etc.

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74
Q

what anti-thrombotic for VTE tx?

A

direct oral anticoagulants (DOACs) like Eliquis (apixaban) or Xarelto (rivaroxaban)

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75
Q

Why are Eliquix (apixaban) and Xarelto (rivaroxaban) preferred for tx of VTEs?

A

they don’t require pretreatment with LMWHs like dabigatran (Pradaxa) and edoxaban (Savaysa), work as well as warfarin, and have lower risk of bleeding.

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76
Q

what anticoagulant is recommended for pts with severe renal impairment, esp those over 75 or who are underweight?

A

warfarin

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77
Q

what anticoagulant is recommended when adherence is problematic?

A

warfarin. longer duration so more forgiving when doses are missed.

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78
Q

what anticoagulant is recommended for pts with mechanical heart valves? what kind are not recommended?

A

warfarin is recommended, DOACs are not (less effective with mechanical valves)

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79
Q

When might you see anticoagulants and LMWHs?

A

special cases like pregnancy, severe liver diseases, or in pts that develop clots while on oral anticoagulants

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80
Q

What is recommended tx for pts with clots above the knee or clots that result in PE?

A

tx with anticoagulant for at least three months

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81
Q

BOTTOM LINE for anticoagulants for afib pts?

A

Pts well controlled on warfarin should remain on warfarin; for all others, one of the DOACs might be a better choice.

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82
Q

DOACs are _______ as effective as warfarin in preventing stroke or systemic embolism in fib pts, and they appear to be _______.

A

at least as effective and appear to be safer.

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83
Q

PAIs…?

A

platelet aggregation inhibitors aka anti-platelet drugs.

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84
Q

mechanisms of action for PAIs?

A 
COX inhibition
ADP or P2Y12 inhibition
GP IIb-IIIa inhibition
PDE inhibition
PAR-1 inhibition
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85
Q

COX inhibitors include…?

A

aspirin and NSAIDs

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86
Q

antiinflammatory agents inhibit what?

A

COX-1 (prostaglandins and thromboxane > GI protection and platelet function) and COX-2 (prostaglandins > mediate inflammation, pain, fever. All starts with arachidonic acid (beginning of pathway).

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87
Q

drug used for secondary prevention (second heart attack)?

A

aspirin (since 1974!)

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88
Q

how does aspirin work to inhibit platelet activation/aggregation?

A

acetylates COX-1, blocking thromboxane synthesis and inhibiting platelet activation/aggregation IRREVERSIBLY for the life of the platelet (usually 5-7 days, up to 10 days.

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89
Q

Platelets have daily turnover of about _____%?

A

10-15%

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90
Q

Durlaza

A

RX extended release aspirin, most feel it’s no more effective than OTC aspirin.

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91
Q

aspirin effect on thromboxane synthesis?

A

one dose of oral aspirin almost completely suppresses the biosynthesis of thromboxane within one hour (non-aspirin, non-acetylated salicylates do not have this effect)

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92
Q

Aspirin vs traditional NSAIDS?

A

both alter aggregation of platelets, but NSAIDs have limited effects that disappear after 1-3 days. (similar effect, but NSAIDs not as much and reversible)

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93
Q

ibuprofen and aspirin together?

A

ibuprofen impairs the effect of aspirin by blocking its access to the TXA2 receptor. Reduces aspirins cardioprotective effect and may worsen cardiovascular risk if taken together.

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94
Q

COX-2 inhibitors and platelets?

A

COX-2 inhibitors (like Celebrex) don’t affect platelets.

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95
Q

reasons why people take aspirin?

A

mostly to prevent heart attack and stroke, but 20% also list cancer prevention as reason

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96
Q

____% of surveyed adults report using aspirin regularly?

A

50%

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97
Q

Low dose aspiring as secondary prevention reduces all-cause mortality by ____% and subsequent MIs by ____% in people with CVD.

A

18% and 30%

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98
Q

aspirin as primary prevention for MIs?

A

controversial.

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99
Q

effective dose of aspirin

A

10-325mg daily. Usually 1mg/kg/day, so ~81mg (“low dose” aspirin) closest dose.

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100
Q

twice daily dosing and aspirin?

A

no advantage to twice daily dosing

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101
Q

risks associated with increased doses of aspirin?

A

GI bleed

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102
Q

taking aspirin @ what time of day might reduce acute cardiac events?

A

bedtime

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103
Q

why should you use caution when giving aspirin to babies, children, adolescents?

A

it’s been linked to Reye’s syndrome (swelling @ liver, brain)

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104
Q

what’s recommended for secondary prevention of stroke?

A

mono therapy of aspirin (50-325mg/daily)

combination therapy of aspirin (25mg) and XR dipyridamole/Aggrenox (200mg 2x/daily

mono therapy of clopidrogrel/Plavix (75mg/daily)

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105
Q

when deciding whether or not to use aspirin for primary prevention of heart attack or stroke, what parameter should you use?

A

age.

generally low dose aspirin for men 45-79 and women 55-79. Only for those 80 if have no risk for GI bleed.

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106
Q

what should you give in combination with aspirin to a pt with GI risks who requires aspirin therapy?

A

PPI

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107
Q

recommendations for avoiding local effects during aspirin administration?

A

give regular aspirin with food or use enteric coated to avoid/reduce stomach irritation

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108
Q

aspirin and cancer?

A

aspirin can help prevent colorectal cancer

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109
Q

what happens when you rapidly stop taking aspirin?

A

cessation of aspirin can cause platelet rebound phenomenon and pro-thrombotic state leading to major adverse cardiovascular events

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110
Q

aspirin before surgery

A

traditionally has been discontinued 7-10 days before surgery, but meta-analysis suggests this increases thrombo-embolitic risks and the practice should be discontinued

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111
Q

NSAIDs and platelet function

A

all NSAIDs work in varying degrees to inhibit platelet function and prolong bleeding time. All (except aspirin) reversible when drug cleared (1-3 days).

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112
Q

ibuprofen an aspirin together?

A

ibuprofen interferes with the cardio-protective and anti-platelet effects of aspirin. if take together, take aspirin 2 hours before ibuprofen. Acetaminophen, diclofenac, COX-2 inhibitors better than ibuprofen with aspirin.

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113
Q

P2Y12 receptor

A

receptor for ADP

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114
Q

Theinopyridine anti-platelet drugs are used for?

A

prevention of coronary stent thrombosis in pts undergoing percutaneous coronary intervention with stent placement

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115
Q

P2Y12 inhibitors include…(drugs)?

A

Ticlopidine (Ticlid), clopidrogel (Plavix), prasurgrel (Effient), and ticagrelor (Brilinta), cangrelor (Kengreal)

116
Q

dual anti-platelet therapy to decrease cardiac events in ACS pts undergoing percutaneous coronary interventions consists of..?

A

combination of aspirin and ADP/P2Y12 inhibitors

should be continued minimum of 12 months in those with drug-eluting stents and up to 12 months in those with bare metal stents

PPIs recommended in addition for those with hx or risk of GI bleeding

117
Q

Ticlopidine (Ticlid)

A

largely replaced by clopidogrel (Plavix) bc of its toxicities and hematological adverse reactions

118
Q

Clopidogrel (Plavix)

A

pro drug converted to CYP2C19
onset of action delayed
more effective than aspirin @ reducing atherosclerotic events
similar tolerability to aspirin, but lower risk of bleeding
more expensive than aspirin

119
Q

clopidogrel (plavix) dosing

A

300 mg tablets for loading dose

75 mg tablets for chronic use

120
Q

clopidogrel and timing

A

early initiation is important. if wait to fill RX after drug-eluting stent is placed, inc risk of poor outcomes

121
Q

clopidogrel (plavix) and PPIs?

A

reports of loss of efficacy of clopidogrel when taken concurrently with PPIs b/c PPIs inhibit the enzyme that converts clopidogrel to its active form CYP2C19

122
Q

clopidogrel boxed warning

A

for people who carry a variant of the CYP2C19 gene, may be poor metabolizers (lack of drug effect). 2-14% of patients. genetic test can be used to tell ($500).

123
Q

if poor metabolizer, what can pts do?

A

take double dose of plavix or use Effient, which is not affected by the CYP2C19 gene

124
Q

which specific PPI is not recommended for use in pts taking clopidogrel? Which one is recommended if PPI is required?

A

omeprazole (Prilosec) is not recommended; if must take one, take prantoprazole (Protonix)

125
Q

prasugrel (Effient) compared to clopidogrel (Plavix)

A

prasugrel (Effient) is ten times more potent and has quicker onset of action (not a prodrug so doesn’t require bio-activation)
also less prone to drug-drug interactions and pt nonresponsiveness

126
Q

prasugrel (Effient) boxed warning

A

potential for significant, sometimes fatal bleeding.

DONT USE in pts with bleeding, hx of stroke, or urgent need for surgery

127
Q

Ticagrelor (Brilinta)

A

binds to same P2Y12 receptors as thienopyridines

recommended to give with aspirin, but only @ doses < 100 mg/day

128
Q

Ticagrelor (Brilinta) boxed warning

A

warns against giving with aspirin doses < 100 mg/day b/c of inc risk for bleeding

129
Q

ticagrelor (Brilinta) compared to clopidogrel (Plavix) Plavix and prasugrel (Effient)?

A
  • -faster onset than other two (not a prodrug) but binds REVERSIBLY instead of permanently
  • -more effective than clopidogrel (Plavix)
  • -must be taken twice a day (possible disadvantage)
130
Q

cangrelor (Kengreal)

A

I.V. P2Y12 inhibitor
used in pts undergoing percutaneous coronary intervention (PCI), but have not been treated with P2Y12 platelet inhibitor or GP IIb/IIIa inhibitor

131
Q

cangrelor (Kengreal) compared to clopidogrel (Plavix)

A

cangrelor has rapid, reversible anti-pletelet effect

conflicting results on which is better, but overall cangrelor appears more effective.

132
Q

PAR-1 antagonist/inhibitor does what?

A

blocks PAR-1 (major thrombin receptor on platelets), inhibiting thrombin-induced platelet aggregation

133
Q

vorapaxar (Zontivity)

A
  • -PAR-1 antagonist/inhibitor
  • -used to reduce risk of MI, stroke, cardiovascular death, need for re-vascularization procedures
  • -approved for use with aspirin or clopidogrel
  • -high risk of bleeding
  • -long 1/2 life (8 days) and no antidote to reverse effects
  • -unsure if it’s better than standard therapy (aspirin + clopidogrel)
134
Q

PDE inhibitors do what?

A

block phosphodiesterase, resulting in an inc in cAMP levels, inhibition of platelets, and vasodilation

135
Q

dypyridamole (Persantine)

A

PDE inhibitor
alternative to aspirin
available in combination with low-dose aspirin as Aggrenox

136
Q

pentoxyfylline (Trental)

A
  • -PDE inhibitor, rarely used
  • -increases erythrocyte flexibility, decreases fibrinogen concentration, prevents aggregation of RBCs and platelets
  • -decreases viscosity of blood, improves flow
137
Q

cilostazole (Pletal)

A
  • -PDE inhibitor
  • -contraindicated with any CHF
  • -most effective drug available for tx of PVD, PAD, intermittent claudication
  • -improves maximal walking distance, absolute claudication distance, and pain-free walking distance
138
Q

PVD/IC

A
  • -result from poor blood flow to muscles
  • -exertional aching pain, cramping, fatigue
  • -@muscle groups, not joints
  • -consistent/reproducible from 1 day to next
  • -resolves completely in 2-3 min
139
Q

GPIs

A
  • -glycoprotein IIb/IIIa inhibitors
  • -most potent platelet aggregation inhibitors available
  • -directly block GPIIb/IIIa receptor preventing platelet aggregation induced by ALL agonsits
  • -indicated for PCI adjunct and tx of ACS (including unstable angina, nonQwave MI)
140
Q

populations where GPIs indicated?

A

use in addition to aspirin and heparin in pts with continuing ischemia, elevated CK-MB, elevated myoglobin, elevated cardiac troponin, and in pts with planned PCI

141
Q

Interesting chemical similarity of GPI drugs?

A

they are chemically similar to proteins derived from snake venom

142
Q

most common side effect of GPIs?

A

bleeding

143
Q

essential monitoring with GPIs?

A

monitor for bleeds and thrombocytopenia (too few platelets in blood)

–baseline platelet count before admin and 6 hours after infusion; thrombocytopenia usually seen 1-24 hours after infusion

144
Q

contraindications for GPIs?

A

thrombocytopenia
<100K/mm3

use with caution in folks with platelet count <150K/mm3

145
Q

abcixamab (ReoPro)

A
  • -very effective GPI
  • -fast tracked by FDA because showed 70% reduction in MIs in 30 days, not fair to continue control group
  • -longer acting than other GPIs
146
Q

eptifibatide (Integrilin)

A

GPI

147
Q

Tirofiban (Aggrastat)

A

GPI

148
Q

standard of care for pts undergoing PCI for acute MI?

A

dual-agent anti platelet therapy with aspirin and a P2Y12 inhibitor

149
Q

standard of care for pts undergoing PCI for acute MI that also have fib or prosthetic valves?

A

dual therapy with oral anticoagulants replacing anti platelet agents (plus P2Y12 inhibitor)

150
Q

MI patients treated with triple therapy show…?

A

significant bleeding risks after PCI

151
Q

dual therapy vs triple therapy?

A 
dual = anti-platelet + P2Y12 inhibitor
triple = oral anticoagulant + P2Y12 inhibitor, + aspirin
152
Q

epidurals and anti coagulated patients?

A

epidurals, spinal anesthesia, spinal punctures (esp indwelling epidural catheters) in patients taking anticoagulants run increased risk of resulting in epidural or spinal hematoma, which can result in long-term or permanent paralysis

153
Q

largest malpractice case in TN history

A
  • -22.2 million
  • -auto accident
  • -nurse put in epidural catheter for pain control
  • -should have considered inc risk for bleeding @ spinal cord when cath removed
  • -no consent form on record
154
Q

thrombolytic therapy

A

“clot busters”

  • -commonplace in 1990s for acute MI
  • -now use angioplasty, so use of thrombolytics unnecessary for MIs
  • -now, used mostly for tx of ischemic stroke
155
Q

gold standard for tx of ischemic stroke or “brain attack”

A

tx with thrombolytic agents within 3-4.5 hours of acute ischemic strokes (in certain eligible patients) significantly improves outcomes

heparin often give in conjunction to reduce risk of another clot formation

156
Q

streptokinase [SK] (Kabikinase, Streptase)

A

thrombolytic drug, protein produced by group C streptococci

binds with plasminogen to form activator complex, converts plasminogen (in circulation and bound to fibrin) to plasmin

157
Q

adverse effects of SK?

A
  • -antigenicity (induce formation of antibodies–subsequent doses may be ineffective from 6mo-life)
  • -hypotension
  • -bleeding complications
158
Q

alteplase [tPA] (Activase)

A

tPA is a naturally occurring enzyme
produced by recombinant DNA technology
not antigenic or allergic

159
Q

adverse effects of tPA?

A

bleeding

rapid drop in BP

160
Q

anistreplase (Eminase)

A

anisolayted plasminogen-sk activator complext (APSAC)
active portion is SK
longer lasting than SK, more bleeding risk

161
Q

Reteplase (Retavase)

A

tPA derivative

162
Q

Tenecteplase (TNKase)

A

modification of alteplase (tPA)
longer 1/2 life, so 1st thrombolytic than can be administered over 5 sec in single dose
Fastest admin of any thrombolytic agent

163
Q

hemostatic agents for surgical bleeding include

A

Absorbable gelatin songes (USP) and thrombin for oozing

thrombin drugs include (Thrombin JMI, Thrombogen, and Evithrom)

164
Q

antifibrinolytics (hemorrhage-sparing medications)

A

aminocaproic acid (Amicar) and Tranexamic acid (Cyklokapron, Lysteda)

Tranexamic acid;;anti hemophilic agent for SAH, also used for heavy menstrual bleeding (Lysteda)

165
Q

anticoagulants/antiplatelets and dental surgery?

A

almost never since risk of thrombosis if stopped higher than risk of bleeding if stay on it

can usually manage dental bleeding with gelatin sponges, sutures, compression, aminocaproic mouth rinse

166
Q

aspirin and surgery?

A

can be continued before and after surgery if high risk for thrombosis or for procedures with low bleed risk

if held, stop 7-10 days out to minimize anti platelet effects

167
Q

clopidogrel (Plavix) and surgery?

A

stop 7-10 days out unless a stent patient (prevent clots)

168
Q

Pradaxa or Xarelto and surgery?

A

stop one day before if low bleed risk and at least 2 days before if higher bleed risk. restart 24 hours after.

169
Q

NSAIDs and surgery?

A

stop 5 1/5 lives before surgery. 1 day for ibuprofen, 10 days for nabumetone (Relafen)

170
Q

warfarin and surgery?

A
  • -continued for minor dental/derm procedures
  • -stop 5 days before invasive procedures
  • -restart 12-24 hours after surgery
  • -can bridge therapy with heparin to use during gap (start 2 days after warfarin, hold —-for surgery, resume 24-72 h after surgery until warfarin resumed)
171
Q

Vitamin E, A, & beta carotene as tx for CVD/CAD?

A

meta-analysis shows mortality actually increases as follows:
E: 4%
A: 16%
beta-carotene: 7%

172
Q

vitamin C as tx for CVD/CAD?

A

no long-term studies published; small/short trials show no benefit on mortality

173
Q

Vit B6, B12, and folic acid for CVD/CAD

A

gen used to lower plasma homocysteine levels
–may lower levels, but no evidence of corresponding benefit on incidence of major vascular events, cancer, or all-cause mortality

174
Q

multivitamins and CVD/CAD

A

no cardiovascular effect
most in developed countries eating normal diet get necessary nutrients
may be “waste of money”
not harmful @ correct doses, not sure if helpful

175
Q

alcohol and CVD/CAD

A

thought to reduce platelet aggregation and thrombotic markers, plus have anti-inflammatory effects

scientific world divided on its cardio-protective effects; studies problematic b/c of confounders

“goldilocks amount” - 1 or 2 drinks daily, but this also may be associated with inc risk for hypertension

176
Q

reservatrol and CVD/CAD?

A

polyphenol compound found in red wine, dark chocolate

studies show it doesn’t inc longevity or reduce CVD risks; has anti-inflammatory, antioxidant effects in vitro and in animals

177
Q

omega 3 fatty acids (fish oil, flaxseed, krill oil) and CVD/CAD?

A

refers to DHA and EPA (acids), not plant-based alpha-linolenic acid
older studies show it lowers triglycerides, increases HDL
more recently, no benefit shown, esp in those already well treated
three FDA approved “fish oil” drugs: Lovaza, Viscera, and Epanova

178
Q

side effect of omega3s?

A

“fish burp”

179
Q

fish oil vs flax seed and krill oil

A

stick to fish oil

DHA, EPA better than plant based acid or kill oil

180
Q

high blood pressure is mathematically defined as…?

A 
B.P = C.O. * SVR
CO = cardiac output
SVR = systemic vascular resistance
181
Q

antihypertensives are the ____ largest selling class of meds worldwide

A

3rd largest

51.6 billion in 2012

182
Q

hypertension in the US population

A

1/3 of pop are hypertensive

  • > 1/3 of those are medicated
    • > 1/3 of those are actually controlled

so, 1/9th well controlled

183
Q

risk of death from heart disease and stroke _______ for each 20/10 mmHg inc beginning at 115/75 mmHg

A

risk of death doubles

184
Q

____% of middle-aged americans will at some point develop high BP

A

90%

!!!

185
Q

why are so few people with HTN adequately controlled

A

silent disease (“i feel fine”)
med compliance b/c side effects
lack of knowledge about harmful effects
cost of medications

186
Q

hypertension definition

A

elevation of systolic BP, diastolic BP, or both

187
Q

non-pharmacologic tx of HTN

A

lifestyle measures: smoking cessation, lose weight, restrict sodium, restrict sat fat, stop drugs that inc BP, supplement K+/Ca2+/Mg2+, more exercise

188
Q

four classes of meds equally recommended as antihypertensive agents for non-black HTN population?

A

ACEIs (ACE inhibitors)
ARBs (angiotensin receptor blockers)
CCBs (calcium channel blockers)
thiazide-type diuretics

189
Q

which two classes of antihypertensive agents should not be used together?

A

ACEIs and ARBs should not be used together

190
Q

recommended initial therapy for black HTN population?

A

BBC or thiazide-type diuretic

191
Q

diuretics (mechanism of action)

A

aka NaCl inhibitors b/c prevent reabsorption of sodium (water follows sodium, so excrete more water)

thiazides also have direct smooth muscle relaxant effect

loop diuretics work @ loop of Henle to inhibit Na-K-Cl

192
Q

DCT or thiazide-type diuretics include…?

A

hydrochlorothiazide (HCTZ), chlorothalidone (Hygroton), inapamide (Lozol), and metolazone (Zaroxolyn)

193
Q

diuretics are usually taken when?

A

once daily preferably in the AM

some with shorter 1/2 life are twice daily

194
Q

initial drug of choice for hypertension?

A

thiazide diuretics, particularly chlorothalidone 12.5-25 mg

195
Q

HCTZ vs chlorothalidone

A

chlorothalidone most evidence of improved outcomes, but causes more K+ loss
HCTZ shorter acting

196
Q

thiazides and osteoporosis

A

may reduce the risk of fractures from osteoporosis b/c decrease calcium secretion and bone loss

197
Q

thiazides and diabetes

A

may increase blood glucose, but still recommended as 1st line therapy

198
Q

side effects of thiazides?

A 
hypokalemia (low K+)
hyperurecemia (excess uric acid @ blood)
hyperglycemia (excess glucose @ blood)
hyperlipidemia (excess lipids)
hypercholesterolemia (excess cholesterol)
199
Q

loop diuretics va thiazide type diuretics?

A
  • -loops less effective in pts with normal renal function (no vasodilatory action), but more effective in pts with renal insufficiency
  • -loops more effective at diuresis, but less effective at controlling BP
200
Q

loop diuretics and hypersensitivity?

A

loops contain sulfonamide moiety and may illicit allergic reaction in those allergic to sulfas

201
Q

side effects of loop diuretics?

A

same as thiazides, plus ototoxicity with furosemide (Lasix)

202
Q

loop diuretic agents include…?

A

bumetanide (Bumex)
furosemide (Lasix) primary. also ototoxic
torsemide (Demadex)
ethacrynic acid (Edecrin) only sulfa free loop diuretic

203
Q

replacement of _____ is essential in pts taking diuretics that cannot obtain enough from diet

A

potassium, b/c hypokalemia is a side effect of diuretics

204
Q

potassium supplementation with diuretics is especially important in patients taking what other drug? why?

A

digoxin (Lanoxin) b/c hypokalemia increases risk for digoxin toxicity

205
Q

potassium supplements are notoriously irritating to what area of the body?

A

GI tract

206
Q

potassium supplementation agents include…?

A

potassium chloride, postassium gluconate

207
Q

potassium-sparing diuretics or CCT diuretics

A

used with thiazide and loop diuretics to correct hypokalemia

if used alone can cause hyperkalemia (too much K+) esp in pts with renal probe or taking drugs that reduce aldosterone secretion (NSAIDs, ACEI, ARBs)

208
Q

K+ sparing or CCT diuretics include..?

A

spironolactone (Aldactone), triamterene (Dyrenium), amilorider (Midamor), and eplerenone (Inspra)

209
Q

spironolactone (Aldactone)

A

aldosterone receptor agonist with anti androgen (estrogen) effects

Used with heart failures, b/c blocks aldosterone which causes water and salt retention

also used in acne for androgen blocking effects

210
Q

side effects of spironolactone

A

hyperkalemia, mastodynia (breast pain), gynecomastia (breast swelling), and menstrual abnormalities

211
Q

patiromer (Veltassa)

A

oral powder option for reversing hyperkalemia (side effect of heart failure meds, antialdosterone agents, ACEIs, and ARBs)

212
Q

eplerenone (Inspra)

A

1st SARA (selective aldosterone receptor antagonist) agent for HTN tx

213
Q

RAAS

A

in response to low BV or BP: liver secretes angiotensinogen, which is cleaved to angiotensin I by renin (secreted @ kidney). Angiotensin I is converted to angiotensin II by angiotensin converting enzyme (ACE) @ the lungs. Angiotensin II is a potent vasoconstrictor and stimulates adrenal gland to make/secrete aldosterone. Aldosterone increases Na+ and H2O reabsorption @ kidneys, as well as inc. secretion of K+ and H+ into urine. Retain more sodium, water, which increases blood volume and returns BP to normal.

214
Q

what effect to beta blockers have on renin?

A

beta blockers decrease renin production

215
Q

RAAS agonists include…?

A

ACEIs, ARBs

216
Q

renal effects of RAAS antagonists

A

may have renal protective effects or cause renal failure, depending on how used and in whom. slows progression of kidney diseases in pts with macroalbuminuria. can cause renal failure in pts taking multiple agents (ACEIs, ARBs, diuretics, NSAIDs)

217
Q

patients with (micro/macro)albuminuria should take and ACEI or an ARB. (choose)

A

macroalbuminuria indicates ACEI or ARB use.

218
Q

RAAS agents and creatinine

A

RAAS agents might slightly bump creatinine levels up, but okay. protects kidneys in the long run.

as BP imporves, SCr should move back toward baseline. continue using as long as SCr inc less than 30% above baseline

219
Q

“beta blockers of the kidneys”

A

ACEIs and ARBs

220
Q

when using ARB, ACEIs in pts with chronic kidney disease, what are some important points for patient education?

A

force fluids to avoid dehydration
avoid NSAIDs, especially chronically
both dehydration and NSAIDs compromise kidney fucntion.

221
Q

RAAS agents in pts with diabetes

A

recommended for diabetes patients with HTN and/or macroalbuminuria, not micro. for both populations, suggest lowering glucose to lower renal risk and lowering lipids/BP to lower CV risk. IF DIABETES + HTN, recommend ACEI/ARB to improve CV risk.

222
Q

current diabetes guidelines do/do not recommend starting ACEI or ARB for microalbuminuria? (choose one)

A

current guidelines do recommend it, but recent research shows diabetes pts don’t benefit from ACEI/ARB to prevent kidney disease

223
Q

ACEIs

A

prevent ACE from converting angiotensin I to angiotensin II (powerful vasoconstrictor)

224
Q

effects of angiotensin II

A
  • -powerful vasoconstrictor

- -increase in glomerular hypertension, inflammation, and fibrosis

225
Q

ACEIs used for?

A
  • -standard therapy for HTN
  • -also for diabetic nephropathy in pts with macroalbuminuria
  • -CHF
  • -post MI secondary prevention
226
Q

ACEIs in black patients

A

less effective, unless combines d with thiazide diuretic or CCB.

associated with higher incidence of angioedema and worse cardiovascular outcomes in black patients

227
Q

ACEIs and plasma lipids + glucose

A

no effect on plasma lipids or glucose tolerance

228
Q

major side effects of ACEIs?

A

dry, non-productive cough (rule out post nasal drip, GERD/reflux)

hyperkalemia, angioedema

229
Q

how to ACEIs cause cough?

A 
catalyzes the hydrolysis of bradykinin and substance P and also induce prostaglandins (accumulation of these causes cough).
prostaglandin inhibitors (aspirin, NSAIDs) may help prevent/relieve cough.
230
Q

ARB or ACEI more likely to cause angioedema?

A

ACEI

most common in black populations

231
Q

ACEI boxed warning

A

discontinue use as soon as possible after detecting pregnancy. Don’t use during 2nd or 3rd trimester b/c of fetal injury or death.

232
Q

drugs ending in -pril belong to what class?

A

ACEIs

233
Q

drugs ending in -sartan belong to what class?

A

ARBs

234
Q

ARBs are also called…?

A

A-II blockers because they interfere with the binding of A-II to the AT-1 receptor site.

235
Q

ARBs and heart failure

A

not all ARBs are effective for heart failure, just some are

236
Q

ARB and cough?

A

No effect on prostaglandins, bradykinin, so no cough side effect. Still can have angioedema, but less likely than with ACEIs

237
Q

if get angioedema on ACEI, can you give ARB?

A

2% of patients who have angioedema with ACEI will also have it with ARB

238
Q

ARBs and pregnancy?

A

contraindicated (relatively)

239
Q

ARBs in black and low renin hypertension populations?

A

less effective than in white populations

240
Q

direct renin inhibitor (DRI)

A

aliskiren (Tekturna)

no longer promoted because increases incidence of nonfatal stroke, renal complications, hyperkalemia, and hypotension.

241
Q

drugs ending in -pine belong to what class?

A

dihydropyridine calcium channel blockers

242
Q

CCBs

A
  • -calcium channel blockers
  • -divided into two groups (dyhydropyridines and non-dihydropyridines)
  • -block voltage-dependent Ca2+ channels on cell membranes (keep Ca2+ from entering cell), resulting in lower systolic calcium, relaxation/vasodilation of vascular smooth muscle, and decrease in cardiac contractility and AV conduction.
243
Q

dihydropyridine vs nondihydropyridine CCBs

A

both decrease peripheral resistance
both mostly increase cardiac output
dihydros (mostly) increase HR, nondihydros decrease HR (mostly)

244
Q

caution with short acting dihydropyridine CCBs!

A

don’t use with tachyarrythmias or tachycardia, can cause reflex tachycardia due to vasodilation, which in turn may cause MI or arrhythmia.

245
Q

primary side effect of CCB class of drugs?

A

peripheral edema

diuretics won’t help & doesn’t change over time.

246
Q

side effects of verapamil (nondihyrdo)

A

muscle relaxant
constipation (most common complaint)
GERD
bronchial relaxation worsening of COPD

247
Q

caution with nondihydro CCBs and beta blockers

A

nondihydro CCBs can affect AV conduction, use with caution in clients taking beta blockers or with heart failure.

248
Q

CCBs and lipids?

A

they are lipid neutral

249
Q

drug of choice for isolated systolic hypertension (ISH) in older clients?

A

long-acting CCBs

250
Q

nifedipine (Procardia) caution

A

DONT ADMINISTER SUBLINGUALLY. pseudo-emergency to real emergency if BP precipitously (too quickly) lowered

251
Q

CCB food interaction

A

grapefruit

serious adverse reactions

252
Q

class of drugs ending in -olol

A

beta blockers

253
Q

beta blockers are notorious for adverse side effects including…?

A

mask hypoglycemia
bradycardia
fatigue/mental dullness
prevents bronchodilation, can cause spasms
decrease in HDL cholesterol
cautions: don’t use in asthma/COPD pts, use with caution in diabetics, don’t stop abruptly, don’t use with PVD

254
Q

beta blockers and uncomplicated HTN

A

beta blockers are no longer recommended for initial tx of uncomplicated HTN. recommended for pts with CAD b/c improve outcomes in pts with angina, systolic heart failure, and after heart attack.

255
Q

how to beta blockers affect BP?

A

reduce BP by lowering adrenergic stimulation to beta receptors and by decreasing renin release from the kidneys.

256
Q

beta blockers and cardioselectivity?

A

beta-1- blockers are more cadioselective (less selective as dosage increases, even low doses may cause broncho-spasms in pts with asthma).

257
Q

benefits of beta blockers with ISA

A

those with ISA (intrinsic symptathomimetic activity) may have fewer side effects (esp bradycardia)

258
Q

beta blockers with ISA should NOT be used for what?

A

angina, cardiac protection during surgery, or after MI

259
Q

contraindications for beta blockers

A

asthma, COPD
diabetes
don’t stop therapy abruptly (super sensitive myocardium if you do)

260
Q

cardiac sympatholytics include..?

A

central alpha adrenergic agonists
peripheral adrenergic neuron antagonists
alpha adrenergic blockers

261
Q

central alpha adrenergic agonists do what?

A

agonists, but result in drop in peripheral drop in BP

agonist effect with antagonist outcomes by blocking an increased effect to decrease BP

act centrally*

262
Q

central alpha adrenergic agonists include…?

A

clonidine (most used), methyldopa, and guanfacine

263
Q

central alpha adrenergic agonists side effects

A

sedation, dry mouth impotence, depression

264
Q

clonidine

A

most used central alpha adrenergic agonist
short half life, must be taken 2-3x/day
often used for HTN emergencies
sometimes used in opioid detox programs to reduce withdrawal
sometime abused for sedative effects or to “boost” effects of opiods
recently approved for ADHA as Kapvay

265
Q

Kapvay

A

clonidine form approved for ADHD

266
Q

peripheral adrenergic neuron antagonists do what?

A

taken up by adrenergic nerve endings and then decrease the release of catecholamines

267
Q

peripheral adrenergic neuron antagonists include…?

A

guanadrel (Hylorel) and rauqolfia alkaloids (primarily reserpine)

268
Q

side effect of peripheral adrenergic neuron antagonists?

A 
severe depression (reserpine)
snake dreams (reserpine &amp; serpent roots)
postural/exertional hypotension (guanadrel)
269
Q

alpha adrenergic blockers do what?

A

block post synaptic alpha1 adrenoreceptors

cause less tachycardia than direct vasodilators

270
Q

alpha adrenergic blockers used to treat what?

A

hypertension

benign prostatic hyperplasia (BPH)

271
Q

side effects of alpha adrenergic blockers

A

1st dose syncope! take @ bedtime
postural hypotension
floppy iris syndrome which complicates cataract surgery

272
Q

drugs that end in -zosin belong to what class?

A

alpha adrenergic blockers

273
Q

alpha adrenergic blockers include…?

A

prazosin (Minipress), terazosin (Hytrin), and doxazosin (Cardura)

274
Q

direct vasodilators

A

directly dilate blood vessels via vascular smooth muscle relaxant effect

2nd or 3rd line agents for hypertension b/c side effects

275
Q

side effect of direct vasodilators

A

reflex tachycardia

276
Q

give direct vasodilators with what else?

A

beta blocker or centrally-acting drug to minimize reflex tachycardia and inc c.o.

also with loop diuretic to avoid Na2+ and H2O retention.

277
Q

can patients quit taking BP meds?

A

no

possibly if very mild and make necessary lifestyle changes to control it.

278
Q

self-BP readings

A

home blood pressure monitoring good as long as pts are educated to look for patterns, take at same time each day.
may reduce need to antihypertensives.
recommended that all patients receiving HTN tx monitor BP at home.

279
Q

tx HTN during pregnancy

A 
not usually treated unless SBP>160 or DBP>100
use labetalol (oral or IV)
280
Q

labetalol

A

1st line therapy for htn in pregnancy

alpha and beta blocker so doesn’t compromise fetal blood flow or cause growth restriction or still births

281
Q

another option for HTN tx in pregnancy?

A 
ER nifedipine (Procardia XL) or methyldopa (Aldomet), but methyldopa is weak antihypertensive with more side effects. only use if can't use the other two.
hydralazine falling out of favor b/c fetal and maternal side effects
282
Q

what HTN drugs should you definitely avoid during pregnancy?

A

ACEIs and ARBs

283
Q

HTN tx in athletes/active people?

A

Use ACEIs or ARBs

diuretics and beta blockers (precision) banned in many sports

284
Q

chronotherapeutics with CV meds

A

BP dips at night, increases in early AM
Blockers lower BP more @ daytime
ACEIs better at lowering BP @ night
recommend taking BP meds at bedtime

285
Q

agents used only for hypertensive crisis include…?

A

nitroprusside (Nipride) *cyanide toxicity
fenoldopam (Corlopam) *reflex tachycardia
Clevidipine (Cleviprex) most used today; is latest-gen IV dihydro CCB

286
Q

anti-hypotensive agents are used to treat what?

A

orthostatic hypotension (dec SBP by 20 or DBP by 10)

287
Q

what drugs are considered antihypotensives?

A

midodrine (ProAmatine) most often used, also for syncope
Pyridostigmine (Mestinon) * for myasthenia gravis primarily*
Fludrocortisone (Florinef) pressor effect, volume expander
Droxidopa (Northera) prodrug of norepi

Nursing-Sem 1 (13 decks)

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