Exam 1: Sowinksi Flashcards

(90 cards)

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
what is the generic name for effient?
prasugrel
26
what is the generic name for brilinta?
ticagrelor
27
what is the brand name for kengreal?
cangrelor
28
what is the maintenance dose of plavix?
75mg qd
29
what is the loading dose of effient?
60mg
30
what is the maintenance dose of effient?
10mg qd
31
what is the loading dose of ticagrelor?
180mg
32
what is the maintenance dose of ticagrelor?
90mg bid
33
what is the mechanism for P2Y12 inhibitors?
Selectively inhibit adenosine diphosphate induced platelet aggregation with no direct effect on TXA2
34
what are the SEs of aspirin?
GI: bleed, ulcer, gastiritis Brain bleeds Hypersensitivity
35
what P2y12 inhibitors have to be converted to their active form?
plavix and effient
36
which P2Y12 is more CYP dependent?
plavix and effient is less
37
which P2Y12 is direct acting?
ticagrelor
38
what are the side effects of plavix and effient?
bleeds, rash, diarrhea
39
what are the side effects for ticagrelor?
bleeding, bradycardia, heart block, dyspnea
40
what do we do when a patient has CCD but does not have a stent?
SAPT: ASA 81mg or plavix 75mg if ASA CI DAPT: certain people, tho not more helpful in reducing MACE
41
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)
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
what do we do when a patient has CCD with SIDH: CABG?
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
What are the types of generation and drugs for DES?
1st gen --> sirolimus, paclitaxel 2nd gen --> everolimus, zotarolimus 3rd gen --> biolimus, sirolimus, everolimus
44
if using ticagrelor and ASA what is the limit of ASA?
< or equal to 100mg
45
when is Prasugrel CI?
stroke, ICH, TIA
46
is someone has a high ischemic risk and low-mod risk of bleeding what can you give them in addition to dec. MACE?
rivaroxiban 2.5mg bid and ASA 81mg
47
what are RAS inhibitors? What are some important notes about them?
1. do not improve symptomatic ischemia 2. dec. cv events
48
What is colchicine? What is important to know about it?
- 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
What meds are used to relieve acute ischemia and angina?
nitrates
50
What is the MOA and activity of nitrates?
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
what are the clinical effects of nitrates?
1. increased myocardial o2 supply 2. decreased myocardial o2 demand
52
what are the acute agents for nitrates?
tabs,spray, powder, buccal, ISDN chew and SL
53
what are the dosing ranges for all nitrates (tabs,spray, powder, buccal, ISDN chew and SL)?
Tab: .3-.6mg Spray: 0.4mg Powder: 0.4mg Buccal: 1-3mg ISDN Chews: 5-10mg ISDN SL: 2.5-10mg
54
what are the instructions to nitroglycerin?
take one wait, 5 minutes, call 911
55
what are the patient eduction points for nitro tabs?
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
what are the pt education points for nitro spray?
1. spray under tongue, do not inhale 2. dont shake 3. 2 yr and renew
57
what are the AEs and monitoring parameters for nitrates?
headache, hypotension, dizziness, light headed, facial flushing, reflex tachycardia
58
what are the drug interactions/ CIs for nitrates?
1. PDEs
59
what pharmacotherapy is used to prevent recurrent ischemia and angina symptoms?
bbs ccbs nitrates
60
what is the mechanism for beta blockers?
competitive, reversible inhibitors of beta- adrenergic stimulation by catecholamines
61
what are the primary effects for bbs?
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
what are the AEs for BBs?
sinus bradycardia, sinus arrest, AV bloack, bronchoconstriction, fatique, depression, masked hypoglycemia
63
what is the parameters for BBs?
1. initiate lowest dose and titrate to symptoms reduction 2. goal HR --> rest 5-60 --> exercise <100BPM
64
what is the MOA for Ca2+ blockers?
- Decrease influx of trigger Ca2+ in myocytes - Decreased chronotropy in nodal cells; Inotropy in myocytes
65
what are the AEs of DHP CCBs?
hypotension, flushing, headache, dizziness, peripheral edema
66
what are the AEs of non-DHP CCBs?
reduced myocardial contractility, hypotension, constipation, headache, dizziness, flushing
67
what is the monitoring for CCBs?
1. initiate at lowest dose and titrate
68
what is nitrate intolerance?
dec. response in the presence of continuously or frequently administered nitrates -- LT use, continuous infusions
69
how can you prevent nitrate intolerance?
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
what is the pharmacology of nitrate tolerance?
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
what is the pt counseling for nitrate patches?
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
what is the pt counseling for nitrate ointment?
1. do not rub or massage ointment 2. do not cover area
73
what is the MOA of Ranolazine?
Inhibition of late inward Na+ current in ischemic myocytes, ↓ intracellular Na+ → ↓ Ca2+ influx
74
what does Ranolazine not affect?
DOES NOT affect HR, BP, inotropy, or perfusion like traditional anti-ischemic agents
75
when should you use ranolazine and how do you use it and when?
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
what is the dosing for ranolazine and titration regimen?
500 bid titrated to 1000 bid over 1-2 wks
77
what are some important drug interactions of ranolazine?
1. 3A4 inhibitors or inducers 2. limit to 500 bid when with dilt, ver, ery, and flz
78
what are the AEs of ranolazine?
constipation, nausea, dizziness, and headache
79
what are the beta-blockers place in therapy?
- can be selected as initial therapy in pts w/o CIs
80
what are beta-blockers contraindications?
bradycardia (HR <50), high degree Av block or sick sinus syndrome AVOID IN: vasospastic/Prinzmetal's angina
81
what is CCBs role in therapy?
use non-DHP if Ci to bbs, unacceptable SEs
82
what are the CIs for DHP/Non-DHP CCBs?
NON-DHP: HFrEF, bradycardia, high degree AV block or sick sinus syndrome DHP: HFrEF (except amlodipine)
83
what are the CIs for nitrates?
HOCM, severe aortic stenosis, PDI use
84
what conditions are BBs favored in?
prior ACS/MI, HF/LVD
85
what are the combination of medications that should be given to people if symptomatic?
1. nitrate&BBs 2. nitrates&non-DHP 3. DHPs&BBs 4. BBs&non-DHP (generally avoided) 5. triple therapy (BB, Nitrate, CCBs)
86
what therapies/ medications are not beneficial or harmful to CCD?
1. PM HRT 2. antioxidants (vit c, E, b-carotene) 3. Folic acid, Vit B6-B12 4. Garlic, CoQ10, selenium 5. NSAIDS
87
what is the stance on NSAIDS in CV disease?
1. look at risk vs. benefit (cv, renal, GI, other risks) 2. review meds 3. look at non-pharm approaches first
88
what should you do if a systemic NSAID is chosen?
- 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
what is a vasospasm?
---- 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
what is the management for vasospastic angina?
acute tx: SL NTG chrinic tx: CCBs, nitrates, combo therapy NO BBs