Pharmacology Of Agents For Angina

Front 1

What is angina pectoris?

Back 1

Principle symptom of heart disease

Caused by oxygen req by heart and oxygen supplied to the heart via coronary vessels

Char. by sudden, severe substernal chest pain, ceased by stopping the precipitating event - exercise, stress, eating, sex

May occur at rest or while sleep

Front 2

About how much or the artery lumen has to be blocked before there are any si/sx experienced by the pt?

Back 2

65-70% lumen..noninvasive test normal until plaque converts into obstructive atherosclerotic plaque

Front 3

Differentiate between stable and unstable angina -

Back 3

Stable - pain pattern and char relatively unchaged over past several months (Better prognosis)

Unstable - pain pattern freq increasing along with intensity and duration - poor prognosis
(MI pending)

Also, vasospastic or prinzmetal's or variant angina

Front 4

Some factors affecting myocardial O2 demand -

Back 4

Ventricular wall stress
HR
Contractility
Preload (decreased by venodilation)
Afterload (decreased by dec PVR)

Front 5

Some medication managements for angina -

Back 5

Nitrates
beta blockers
calcium channel blockers
anti-platelet agents
antihyperlipidemics

Front 6

Surgery options for angina -

Back 6

PCI
CABG

Front 7

Different types of nitrates -

Back 7

Abortive (acute)

Preventive (prevent chest pain in recurring angina episodes)

Front 8

Examples of abortive nitrates -

Back 8

Nitroglycerin (tablets, aerosol, ointment)

Front 9

Some medical uses of NTG

Back 9

Angina pectoris (ischemic HD)
HTN crisis
Uterine tone reduction
Erections in ED

IV form used for BP control in perioperative HTN, tx of CHF, ischemic pain and pulmonary edema assoc with MI

Front 10

NTG has most effect on what kind of vessels in the body

Back 10

Veins >> Arteries

Front 11

Char of NTG -

Back 11

Prototypical nitrate
Large first pass with oral form - so only topical, sublingual or aerosol
Not been shown to reduce mortality
Stored in dark amber bottle to be prevented from degrading by light/moisture

Front 12

MOA of Nitrates -

Back 12

Relaxes vascular smooth muscle by causing releasing of NO which act on GTP to be converted into cGMP -> ultimately relaxes SM

Front 13

Tolerance with nitrates -

Back 13

Longer acting nitrates causes lose of sulfhydryl groups which is necessary for efficacy of nitrates.

Typically appears with NTH patches and longer acting nitrates

Front 14

How can tolerance with nitrates be avoided?

Back 14

Omitting the evening dose in patients who do not experience angina at night.

10-12 hr nitrate free interval is reqd to prevent tolerance

Front 15

What form is NO under relaxing form?

Back 15

EDRF - responsible for resting vasodilator tone present in human resistance arterioles under basal conditions

Nitrates can cause release of NO in endothelium independent manner

Front 16

Hemodynamics effect of Nitrates -

Back 16

Selective for venous rather than arteriolar SMC

Venodilation -> reduced VF -> decrease in ventricular chamber diameter -> decrease in wall tension -> decreased Cardiac work and O2 demand

Coronary blood flow increases -> due to decreased LVEDP + NO mediated coronary art relaxation

Front 17

Some non traditional uses for Nitrates-

Back 17

Relieves the pain in esophagus spasm and biliary or renal colic be relaxing non vascular smooth muscle

Front 18

Nitrates effect on afterload -

Back 18

Don't reduce afterload when given subling/topically/patch..

Front 19

Nitrates relieve angina by -

Back 19

Arteriolar dilatation: reducing cardiac afterload and thus myocardial work and oxygen demand (only IV form)

Peripheral venodilatation: reducing venous return, cardiac preload and thus myocardial workload

Relieving coronary vasospasm

redistributing myocardial blood flow to ischaemic areas of the myocardium

Front 20

What is benefit of using Isosorbide mononitrate and isosorbide dinitrate over regular NTG?

Back 20

Long acting nitrates relatively resistant to hepatic catabolism
t1/2 = 1 hr

Front 21

Pharmacokinetics for NTG -

Back 21

t1/2 - 10mins
Extensive first pass metabolism => so given sublingual => rapid absorption and onset
Sx of angina may return after metabolization -> so given patch form for steady avail

Front 22

Main uses of long acting Nitrates

Back 22

Acute relief of angina
Prophylaxis in situations that may provoke angina
Long-term prophylaxis of angina

Front 23

Adverse effects of nitrate -

Back 23

Hypotension in pts with decreased cardiac reserve

Not to use PDE 5 inhibitor for ED in 24 hrs of Nitrate admin

Headache -> assurance that nitrate is working

Tachyphylaxis -> solved by removing patch at night to have nitrate free period

Front 24

Main uses of Beta blockers -

Back 24

prophylactic treatment of angina
Reduce risk of sudden death or reinfarction following MI

Also in HTN, arrhythmias, essential tremor and hyperthyroidism

Front 25

MOA of Beta receptors -

Back 25

β-Adrenoceptors are linked via stimulatory G-proteins to adenyl cyclase, so endogenous β-agonists (norepinephrine and epinephrine) increase cytoplasmic cAMP.

Front 26

MOA of Beta blockers -

Back 26

Decrease the HR, resulting in decreased myocardial oxygen demand and increased oxygen delivery to the heart

Decrease myocardial contractility, helping to conserve energy or decrease demand

Front 27

Clinical effectiveness of Beta blockers -

Back 27

improve the survival rate of patients with recent MI

improve the survival rate and prevent stroke and CHF in patients with hypertension

adjust the dose of -blockers to reduce heart rate at rest to 55 to 60 bpm

increase in heart rate during exercise should not exceed 75% of the heart rate response associated with onset of ischemia

Front 28

What happens in people with coronary artery vasospasm who are treated with beta blockers?

Back 28

Conversely, patients in whom coronary artery spasm is particularly important may paradoxically deteriorate if treated with β-blockers because of unopposed α-adrenoceptor-mediated coronary vasoconstriction, although this is uncommon.

DOC - nitrates

Front 29

Adverse effects of beta blockers -

Back 29

Obstructive airways
Heart block
Hyperglycemia (may mask hypoglycemia in diabetics)
Worsen perip vascular dz or raynaud's phenomenon
abrupt discontinuation -> rebound increase in freq and severity of angina

Minor effect - dizziness, fatigue, mental depression, drowsiness, impotence, wheezing, dyspnea

Front 30

Benefit of using atenolol and metoprolol over propanolol -

Back 30

Atenolol and/or metoprolol have largely replaced propranolol - "cardioselective" - need less frequent dosing, and the clinically useful range of doses is narrower than propranolol, making them easier to use.

Front 31

Pharmacokinetics of Propanolol, Metoprolol, and atenolol -

Back 31

Propanolol - variable presystemic metabolism CYP2D6
Atenolol - kidneys, largely unchnged
Metoprolol - hepatic met

Front 32

Pharmacokinetics of CCB -

Back 32

Absorbed from GI, metabolized in liver, and inactive metabolites excreted in urine

Front 33

MOA of CCB -

Back 33

 inhibits the passage of calcium ions through voltage- dependent L-type calcium channels in cell membranes in the heart and vascular smooth muscle as well as some other excitable tissues.

Ca2+ channels  open more slowly  "slow" channels (compared to Na+ channels).

In cardiac tissue Ca2+ channels
 contribute to the membrane current during the plateau phase of the cardiac action potential,
 slow initial depolarization SA and AV nodes.

Front 34

Dihydropridines -

Back 34

the ones that end in -dipine

Front 35

Pharmacologic effect of CCB -

Back 35

Relaxation of coronary VSM - in pts with coronary vasospasm

Arteriolar dilation - dec Afterload

Decreased myocardial contract

Verapamil and dilitiazem decrease cardiac conducting system - thus prevent reflex tachycardia - used in pts with unstable coronary artery dz

Front 36

Which CCB has most negative inotropic capability?

least?

Back 36

Most - verapamil
Least - nicardipine

Front 37

passport(s)

Back 37

пАспорт (А) m.

Front 38

Benefit of using CCB over beta blockers -

Back 38

In contrast to β-blockers, calcium channel blockers may be given safely to patients with asthma, chronic bronchitis, peripheral arterial disease or diabetes.

Front 39

Who is verapamil and dilitiazem CI in?

Back 39

Pts with heart block or bradycardia

Front 40

Only CCB with constipation as s/e

Back 40

Verapamil

Front 41

S/e of CCB -

Back 41

Flushing and headache - due to vasodilation..worst in dihydropyridines
Ankle swelling - only in dihydro
increased freq of urination

Front 42

Drug interactions CCB -

Back 42

Beta blockers and other negative iontropic agents

Front 43

Verapamil has severe drug interaction with -

Back 43

Digoxin - increasing its plasma conc and potentially causing toxicity -> requires dose adjustment

Front 44

Beta blocker effect on
Coronary blood supply
HR
Arterial pressure
Venous Return
Myocardial contractility

Back 44

Beta blocker effect on
Coronary blood supply - none
HR - increases
Arterial pressure - dec
Venous Return - none
Myocardial contractility - dec

Front 45

DHP CCB effect on
Coronary blood supply
HR
Arterial pressure
Venous Return
Myocardial contractility

Back 45

DHP CCB effect on
Coronary blood supply - inc
HR - increase except amlodp
Arterial pressure - dec
Venous Return - none
Myocardial contractility - dec

Front 46

nonDHP CCB effect on
Coronary blood supply
HR
Arterial pressure
Venous Return
Myocardial contractility

Back 46

nonDHP CCB effect on
Coronary blood supply - inc
HR - dec
Arterial pressure - dec
Venous Return - none
Myocardial contractility - dec

Front 47

Nitrates long acting effect on
Coronary blood supply
HR
Arterial pressure
Venous Return
Myocardial contractility

Back 47

Nitrates long acting effect on
Coronary blood supply - inc
HR - inc/none
Arterial pressure - dec
Venous Return - dec
Myocardial contractility - none