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CVS Pharmacology > Drug Therapy Of Ischemic Heart Disease > Flashcards

Drug Therapy Of Ischemic Heart Disease Flashcards

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
Q

Compare cardiac effects of DHP & non DHP

A

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
Q

Verapamil is more ….. than diltiazem

A

Cardio-depressant

27
Q

Mention other actions of CCBs

A

Relaxation of Git, bronchial, urinary, uterine SM

Inhibit platelet aggregation

28
Q

Compare adverse effects of DHP & nonDHP

A 
DHP, 
Reflex tachycardia…worsen angina
Hypotenion….flushing & headache
Ankle edema,dizziness & tinnitus 
Non-DHP,
Bradycardia & heart block
Hypotension, heart failure
Constipation (verapamil)
29
Q

Mention therapeutic uses of CCBs

A

Angina (of choice in vasospastic) diltiazem & long acting DHP
Hypertension
Supraventricular arrhythmia (verapamil): PSVT & AF & Af
HOCM (Verapamil)

30
Q

Describe antianginal effect of CCBs

A

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
Q

Mention other uses of CCBs

A

Peripheral vascular disaese, prevention of premature labour, migraine prophylaxis

32
Q

Describe mechansim & precautions of trimetazidine

A

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
Q

Describe mechanism, indications & precautions of ivaradine

A

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
Q

Drugs dec atheroscelerosis & MI risk

A

Antiplatelet
Hypolipedmic agents
Anticoagulants

35
Q

Management of ACS

A 
Antiplatlet
Anticoagulant
ACEI
Antianginal
Statins
Fibrinolytics (within 6 hr)
36
Q

Revascularization and angioplasty may be needed EXCEPT in

A

Vasospastic angina

37
Q

Describe mechanism, indications & side effects of ranolazine

A

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)

CVS Pharmacology (6 decks)

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