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P2 Spring: PHRM 845 > Exam 1: Sowinksi > Flashcards

Exam 1: Sowinksi Flashcards

1
Q

What are the different types of angina? (hint= 3 types)

A
  1. Printzmetal’s Variant (vasospasm)
  2. Stable Angina (fixed stenosis)
  3. unstable angina (thrombus)
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2
Q

What are the two types of supply ischemia? What is considered demand ischemia?

A
  1. Supply: variant and unstable angina
  2. Demand: stable angina
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3
Q

When does ischemia happen?

A

when there is an imbalance in oxygen supply and demand

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4
Q

what factors impact oxygen supply and demand?

A
  1. contractility
  2. HR
  3. Preload-LVEDV
  4. Afterload
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5
Q

What does decreasing contractility do?

A

decreases o2 consumption

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6
Q

what does decreasing HR do?

A
  • decreases O2 consumption
  • increases coronary perfusion
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7
Q

what does decreasing Preload-LVEDV do?

A
  • decreased by venodilation
  • decrease in o2 consumption
  • increases in myocardial perfusion
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8
Q

what does decreasing afterload do?

A
  • by dilation of arteries
  • decreases O2 consumption
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9
Q

There is 2 pathways that leads to ischemia that then leads to Angina, what are they and what causes them?

A
  1. Fixed stenosis, vasospasm, thrombus —-> dec. coronary blood flow
  2. increased HR, contractility, afterload, and preload –> inc. oxygen consumption
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10
Q

what is the main cause of angina and ischemia?

A

a build up of atherosclerotic plaque

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11
Q

what is the definition of stable angina?

A

discomfort in the chest caused from myocardial ischemia and disturbs heart function without necrosis and goes away quickly

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12
Q

What are some precipitating factors of angina?

A
  1. exertion
  2. large meals
  3. very cold or very hot weather
  4. walking against wind
  5. smoking
  6. shoveling/ gardening
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13
Q

what are quality feeling/ quantity feelings of pain with angina?

A
  1. squeezing
  2. heavy
  3. tight
  4. SOB
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14
Q

what areas do most people get angina?

A

substernal (down left arm into left jaw)

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15
Q

how long should the stable angina last and how severe in pain?

A
  1. severe >5/10
  2. lasts <20 min, norm 5-10 min
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16
Q

what are the clinical characteristics for typical angina on a ECG?

A

ST depression during event (ischemia)
or elevation in variant angina

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17
Q

what is a exercise tolerance test for CHD?

A
  1. tread or bike
  2. looking at duration, ECG, BP, ect.
  3. MVO2 and BO readings and levels
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18
Q

what cardiac imagine can be done for CHD?

A
  1. stress test
  2. CT
  3. PET/SPECT
  4. coronary angiography
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19
Q

what are some other risk factor modifications we should consider also?

A
  1. RSV vaccine
  2. min. alcohol consumption
  3. min. environ exposure
  4. manage psych factors
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20
Q

Aspirin is both a cox-1 and cox-2 at higher levels. What is the difference?

A
  1. COX-1 (thromboxane)
    –> increase platelet aggregation and vasoconstriction (aspirin prevents aggregation)
  2. COX-2 (prostacyclin)
    –> inhibits platelet aggregation and vasodilation (higher thrombotic risk)
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21
Q

what is the loading dose for asprin?

A

162-325mg

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22
Q

what is the maintenance dose of aspirin?

A

75-162mg

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23
Q

what is the loading dose of plavix?

A

300-600mg

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24
Q

what is the generic name for plavix?

A

clopidogrel

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25
Q

what is the generic name for effient?

A

prasugrel

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26
Q

what is the generic name for brilinta?

A

ticagrelor

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27
Q

what is the brand name for kengreal?

A

cangrelor

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28
Q

what is the maintenance dose of plavix?

A

75mg qd

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29
Q

what is the loading dose of effient?

A

60mg

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30
Q

what is the maintenance dose of effient?

A

10mg qd

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31
Q

what is the loading dose of ticagrelor?

A

180mg

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32
Q

what is the maintenance dose of ticagrelor?

A

90mg bid

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33
Q

what is the mechanism for P2Y12 inhibitors?

A

Selectively inhibit adenosine diphosphate
induced platelet aggregation with no direct effect on TXA2

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34
Q

what are the SEs of aspirin?

A

GI: bleed, ulcer, gastiritis
Brain bleeds
Hypersensitivity

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35
Q

what P2y12 inhibitors have to be converted to their active form?

A

plavix and effient

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36
Q

which P2Y12 is more CYP dependent?

A

plavix and effient is less

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37
Q

which P2Y12 is direct acting?

A

ticagrelor

38
Q

what are the side effects of plavix and effient?

A

bleeds, rash, diarrhea

39
Q

what are the side effects for ticagrelor?

A

bleeding, bradycardia, heart block, dyspnea

40
Q

what do we do when a patient has CCD but does not have a stent?

A

SAPT: ASA 81mg or plavix 75mg if ASA CI
DAPT: certain people, tho not more helpful in reducing MACE

41
Q

what do we do when a patient has CCD and has an elective PCI and DES? (more so in terms of before and after procedure based off of low or high bleeding risk)

A
  1. B4 procedure
    –> ASA and P2Y12 loading dose
  2. After procedure
    –> LOW
    - DAPT: min 6 m
    - SAPT: LT
    –> HIGH
    - DAPT: 1-3m
    -SAPT: P2Y12 12m & LT
42
Q

what do we do when a patient has CCD with SIDH: CABG?

A
  1. emergent
    - restart after CCABG
  2. CABG
    - DAPT: both (ASA 81 and plavix 75)
    -SAPT: ASA LT
    - plavix may be good for 12 m
43
Q

What are the types of generation and drugs for DES?

A

1st gen
–> sirolimus, paclitaxel
2nd gen
–> everolimus, zotarolimus
3rd gen
–> biolimus, sirolimus, everolimus

44
Q

if using ticagrelor and ASA what is the limit of ASA?

A

< or equal to 100mg

45
Q

when is Prasugrel CI?

A

stroke, ICH, TIA

46
Q

is someone has a high ischemic risk and low-mod risk of bleeding what can you give them in addition to dec. MACE?

A

rivaroxiban 2.5mg bid and ASA 81mg

47
Q

what are RAS inhibitors? What are some important notes about them?

A
  1. do not improve symptomatic ischemia
  2. dec. cv events
48
Q

What is colchicine? What is important to know about it?

A
  • reduces inflammation via reduction of IL-1b and IL-18
  • reduces MACE
  • CI in severe renal and hepatic disease
  • caution with CYP3A and PGP
49
Q

What meds are used to relieve acute ischemia and angina?

A

nitrates

50
Q

What is the MOA and activity of nitrates?

A

nitric oxide donors/releasers and leads to activation of guanylate cyclase
1. marked venodilation (dec.preload)
2. less arteriole dilation and inhibition of platelet aggregation

51
Q

what are the clinical effects of nitrates?

A
  1. increased myocardial o2 supply
  2. decreased myocardial o2 demand
52
Q

what are the acute agents for nitrates?

A

tabs,spray, powder, buccal, ISDN chew and SL

53
Q

what are the dosing ranges for all nitrates (tabs,spray, powder, buccal, ISDN chew and SL)?

A

Tab: .3-.6mg
Spray: 0.4mg
Powder: 0.4mg
Buccal: 1-3mg
ISDN Chews: 5-10mg
ISDN SL: 2.5-10mg

54
Q

what are the instructions to nitroglycerin?

A

take one wait, 5 minutes, call 911

55
Q

what are the patient eduction points for nitro tabs?

A
  1. keep in orginal container
  2. no safety cap
  3. place under tongue, do not swallow
  4. dont store in bathroom or in humid locations
  5. keep
  6. need for refills -6m
56
Q

what are the pt education points for nitro spray?

A
  1. spray under tongue, do not inhale
  2. dont shake
  3. 2 yr and renew
57
Q

what are the AEs and monitoring parameters for nitrates?

A

headache, hypotension, dizziness, light headed, facial flushing, reflex tachycardia

58
Q

what are the drug interactions/ CIs for nitrates?

A
  1. PDEs
59
Q

what pharmacotherapy is used to prevent recurrent ischemia and angina symptoms?

A

bbs
ccbs
nitrates

60
Q

what is the mechanism for beta blockers?

A

competitive, reversible inhibitors of beta-
adrenergic stimulation by catecholamines

61
Q

what are the primary effects for bbs?

A
  1. Desired effects on myocardial oxygen demand
    - Reduce HR (mainly during sympathetic stimulation)
    - Reduce myocardial contractility
    - Reduce arterial BP (afterload)
  2. Undesired effect on myocardial oxygen demand
    - Reduce HR → Increase diastolic filling time → Increase LVEDV →
    Increase Preload
62
Q

what are the AEs for BBs?

A

sinus bradycardia, sinus arrest, AV bloack, bronchoconstriction, fatique, depression, masked hypoglycemia

63
Q

what is the parameters for BBs?

A
  1. initiate lowest dose and titrate to symptoms reduction
  2. goal HR
    –> rest 5-60
    –> exercise <100BPM
64
Q

what is the MOA for Ca2+ blockers?

A
  • Decrease influx of
    trigger Ca2+ in
    myocytes
  • Decreased
    chronotropy in nodal
    cells; Inotropy in
    myocytes
65
Q

what are the AEs of DHP CCBs?

A

hypotension, flushing, headache, dizziness, peripheral edema

66
Q

what are the AEs of non-DHP CCBs?

A

reduced myocardial contractility, hypotension, constipation, headache, dizziness, flushing

67
Q

what is the monitoring for CCBs?

A
  1. initiate at lowest dose and titrate
68
Q

what is nitrate intolerance?

A

dec. response in the presence of continuously or frequently administered nitrates
– LT use, continuous infusions

69
Q

how can you prevent nitrate intolerance?

A
  1. nitrate free period of at least 1-012 hrs
  2. biopharmaceutics and PK contribute to the amount of time required to be dosage-free
70
Q

what is the pharmacology of nitrate tolerance?

A
  1. Reversible (hours) in
    absence of drug
  2. ALDH2 inactivation in
    mitochondria3. ISMN and ISDN also elicit
    tolerance but via a slower, less understood process
71
Q

what is the pt counseling for nitrate patches?

A
  1. Apply the patch between elbows and knees
  2. Apply the patch to clean, dry, hairless (or nearly free)
    skin that is not irritated, scarred, burned, broken, or calloused.
  3. Choose a different area each day.
  4. You may shower while you are wearing a NTG skin patch.
  5. Do not cut the patch
  6. Wash hands before and after
72
Q

what is the pt counseling for nitrate ointment?

A
  1. do not rub or massage ointment
  2. do not cover area
73
Q

what is the MOA of Ranolazine?

A

Inhibition of late inward Na+ current in
ischemic myocytes, ↓ intracellular Na+ → ↓ Ca2+ influx

74
Q

what does Ranolazine not affect?

A

DOES NOT affect HR, BP,
inotropy, or perfusion like traditional anti-ischemic agents

75
Q

when should you use ranolazine and how do you use it and when?

A
  1. tx for chronic angina
  2. add-on therapy for the symptomatic treatment of patients with stable angina pectoris who are inadequately controlled or intolerant to first-line antianginal therapies
  3. can add on to anything when not responding to monotherapy
76
Q

what is the dosing for ranolazine and titration regimen?

A

500 bid titrated to 1000 bid over 1-2 wks

77
Q

what are some important drug interactions of ranolazine?

A
  1. 3A4 inhibitors or inducers
  2. limit to 500 bid when with dilt, ver, ery, and flz
78
Q

what are the AEs of ranolazine?

A

constipation, nausea, dizziness, and headache

79
Q

what are the beta-blockers place in therapy?

A
  • can be selected as initial therapy in pts w/o CIs
80
Q

what are beta-blockers contraindications?

A

bradycardia (HR <50), high degree Av block or sick sinus syndrome
AVOID IN: vasospastic/Prinzmetal’s angina

81
Q

what is CCBs role in therapy?

A

use non-DHP if Ci to bbs, unacceptable SEs

82
Q

what are the CIs for DHP/Non-DHP CCBs?

A

NON-DHP: HFrEF, bradycardia, high degree AV block or sick sinus syndrome
DHP: HFrEF (except amlodipine)

83
Q

what are the CIs for nitrates?

A

HOCM, severe aortic stenosis, PDI use

84
Q

what conditions are BBs favored in?

A

prior ACS/MI, HF/LVD

85
Q

what are the combination of medications that should be given to people if symptomatic?

A
  1. nitrate&BBs
  2. nitrates&non-DHP
  3. DHPs&BBs
  4. BBs&non-DHP (generally avoided)
  5. triple therapy (BB, Nitrate, CCBs)
86
Q

what therapies/ medications are not beneficial or harmful to CCD?

A
  1. PM HRT
  2. antioxidants (vit c, E, b-carotene)
  3. Folic acid, Vit B6-B12
  4. Garlic, CoQ10, selenium
  5. NSAIDS
87
Q

what is the stance on NSAIDS in CV disease?

A
  1. look at risk vs. benefit (cv, renal, GI, other risks)
  2. review meds
  3. look at non-pharm approaches first
88
Q

what should you do if a systemic NSAID is chosen?

A
  • temporary adjunct
  • lowest dose for shortest time
  • ibuprofen/naproxen first
  • celebrex at 200mg qd max
  • avoid diclofenac
  • take ASA at least 2 hrs prior to NSAID
  • adj. may min NSAID needs
89
Q

what is a vasospasm?

A

—- BF is constricted during an artery spasm ——-
1. Ischemia/angina usually occurs at rest,
not precipitated by physical exertion or
emotional stress
2. Associated with ECG ST-segment
elevation
3. Ischemic episodes occur most
frequently in the early morning hours
4. Not necessarily associated with
atherosclerosis

90
Q

what is the management for vasospastic angina?

A

acute tx: SL NTG
chrinic tx: CCBs, nitrates, combo therapy
NO BBs

P2 Spring: PHRM 845 (2 decks)

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