Drug Therapy Of Ischemic Heart Disease Flashcards

(37 cards)

1
Q

Compare ECG of classic & priznmetal anginal

A

C, ST depression

P, ST elevation with oaradixical T wave normalization

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2
Q

What is the direct cause of anginal pain?

A

By accumulation of metabolites in cardiac muscle

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3
Q

The distinguishing feature of unstable angina from MI is

A

No in serum markers in angina

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4
Q

Describe mechanism of action of nitrates

A

Nitrates bind to certain receptors on vessel wall, they release nitric oxide which bind with -SH group forming S-nitrosothiol that activates guanyl cyclase inc cGMP, dec IC Ca++, resulting SM relaxation.

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5
Q

Describe pharmacological actions of nitrates

A
  1. Relaxation of vascular SM, venodilators (dec preload) & arteriodilators (dec afterload)
  2. Brief relaxation of other smooth musces (GIT: Sphincter of Oddi & cardiac opening of oesophagus)
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6
Q

Describe mechanism of antianginal effect of nitrates

A

Dec O2 demand: venodilators & arteriodilators (in high doses) causing dec preload & afterload
Inc O2 supply: VD of large epicardial vessels & collateral & redistribution of blood to ischemic areas by dec VR, dec ventricular filling & dec coronary art compression in subendocardium (by pooling of blood in splanchnic area & extermities
Antiplatelet effect

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7
Q

Mention indications of nitrates

A

All types of angina
Congestive HF & acute pulmonary edema
Hypertensive emergencies
Acute MI (dec size)

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8
Q

Mention adverse effects of nitrates

A
  1. Throbbing headache+ flushing
  2. Withdrawal angina
  3. Postural hypotension
  4. Reflex tachycardia in high dose
  5. Methemoglobenemia
  6. Rapid tolerance
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9
Q

GR: Occurrence if throbbing headache with nitrates &ttt

A

Due to VD of meningeal arteries ttt aspirin

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10
Q

GR: Occurrence if reflex tachycardia with nitrates &ttt

A

Due to dec BP leads to worse angina ttt BB

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11
Q

GR: Occurrence if rapid tolerance with nitrates &ttt

A

Due to -SH group depletion & VC caused by activation of adrenegic system by RAAS
Nitrate free interval 8hrs/d

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12
Q

GR: Occurrence if Methemogobinemia with nitrates &ttt

A

More with nitrites due to oxidation

Methylene blue

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13
Q

Mention contraindications of nitrates

A
  1. With sildenafil
  2. HOCM
  3. RT vent innfarction
  4. In volume depletion & severe aortic stenosis (cautiously)
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14
Q

With nitrates a maximum of …. Is taken within …., if no effect ….

A

3 tablets
15 min
Refer ti hospital

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15
Q

GR: NG & ISDN are not given oral

A

Extensive 1st pass metabolism

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16
Q

Mention preparations of NG & ISDN & their indications

A
  1. Subligual/spray: 1st choice in acute attack & immediate prphylaxis
  2. Transdermal patch/oral slow release: for CHF & long term prophyalxis
  3. IV: AHF or unstable angina
17
Q

What is the difference between ISDN & ISMN

A

With ISMN

No 2st pass metabolism, high bioavailability, delayed onset & longer action.

18
Q

Mechanism of antianginal effect of BB

A

Dec O2 demand: ded HR, BP, lipolysis & fat utilization
Inc O2 supply by inc coronary filling in diatole (by dec HR), Redistribution of coronary blood flow to subendocardial ischemic areas
Antiplatelet activity

19
Q

All BB are effective except ….

A

BB with ISA may inc HR

20
Q

Role of BB in Long term prophylaxis of IHD

A

Dec frequency & severity of attacks
Control HR at rest
Blunt inc HR & BP during exercise

21
Q

Describe mechanism of action of CCBs

A

They act on alpha1 subunit of L-type Ca channel in conductive tissue, cardiac myocytes & vascular SM including coronaries.

22
Q

Mention a short & a long-acting DHP CCB

A

S, nifedipine

L, amlodipine

23
Q

Describe selectivity of DHPs & nonDHPs

A

DHP, Vessels>myocardium>SAN&AVN

NonDHP, SAN&AVN>myocardium=vessels

24
Q

Mention vascukar effects of CCBs

A

Peripheral arteriolar VD, dec PR & ABP

Mora with DHP

25
Compare cardiac effects of DHP & non DHP
DHP, No effects on nodes, reflex tachycardia (more with short-acting) & mild inhibition of contractility. Non-DHP, dec SAN & AVN conduction, bradycardia & suppress contractility
26
Verapamil is more ….. than diltiazem
Cardio-depressant
27
Mention other actions of CCBs
Relaxation of Git, bronchial, urinary, uterine SM | Inhibit platelet aggregation
28
Compare adverse effects of DHP & nonDHP
``` DHP, Reflex tachycardia…worsen angina Hypotenion….flushing & headache Ankle edema,dizziness & tinnitus Non-DHP, Bradycardia & heart block Hypotension, heart failure Constipation (verapamil) ```
29
Mention therapeutic uses of CCBs
Angina (of choice in vasospastic) diltiazem & long acting DHP Hypertension Supraventricular arrhythmia (verapamil): PSVT & AF & Af HOCM (Verapamil)
30
Describe antianginal effect of CCBs
Dec O2 demand by ive ino & chronotropic effect (more with verapamil), dec peripheral resistance (more with DHP) Inc coronary blood flow due to diltation of epicardial coronary vessels
31
Mention other uses of CCBs
Peripheral vascular disaese, prevention of premature labour, migraine prophylaxis
32
Describe mechansim & precautions of trimetazidine
It switches myocardial metabolism from fatty acid oxidation (more O2 demand to glucose oxidation, so dec demand. Given in combination with other antianginal drugs. Reduce dose by 50% in renal impairment CI parkiaonism
33
Describe mechanism, indications & precautions of ivaradine
Selectively inhibits pacemaker I-funny current leading to dec cardiac pacemaker activity & dec HR Indicated, systolic HF & IHD CI with CCBs (inhibit their metabolism) used cautiously with BB
34
Drugs dec atheroscelerosis & MI risk
Antiplatelet Hypolipedmic agents Anticoagulants
35
Management of ACS
``` Antiplatlet Anticoagulant ACEI Antianginal Statins Fibrinolytics (within 6 hr) ```
36
Revascularization and angioplasty may be needed EXCEPT in
Vasospastic angina
37
Describe mechanism, indications & side effects of ranolazine
Inhibits late phase of Na current, dec Na & Ca overload, improve diasoltic function & improve O2 supply & demand balance Used in chronic angina Side effect, prolong QT interval, drug interactions (extensively metabolised by CYP3A4)