Cardio Pharmacology Flashcards

1
Q

Fill table.

A
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2
Q

Beta-blockers used in patient who have had a previous MI.

A

Metoprolol (standard release), propranolol, timolol or atenolol.

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3
Q

Beta-blocker agents used in patients with angina and/or heart failure.

A

Bisoprolol, carvedilol, or nebivolol

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4
Q

Which one is non-selective beta-blocker.
a. Atenolol
b. Metoprolol
c. Propranolol
d. Carvedilol
e. Labetalol
f. Bisoprolol

A

(d) Carvedilol and (e) Labetalol

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5
Q

Mechanism of beta blocker

A

A. Beta 1 antagonist
1. Reduces renin secretion (renin secretion meditated by beta-1 receptors) and plasma levels of angiotensin II, leads to diuresis
2. block sympathetic stimulation of heart, reduce cardiac output. Reduces cardiac contractility and conduction.

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6
Q

Adverse effects of beta-blocker

A

Cold extremities
Fatigue
Bronchospasm

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7
Q

Carvidolol mechanism of action

A

Alpha-1-receptor and Beta-1-receptor antagonist.

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8
Q

Aim of resting pulse rate for beta-blockers

A

55-60 bpm

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9
Q

Counselling beta blocker

A

For men advice that it can cause impotence let us know.

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10
Q

Contraindication beta-blockers

A

Heart block
COPD
Acute asthma
Liver failure

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11
Q

Drug interactions to AVOID with beta blocker

A

Non-dihydropyrimidine calcium channel blocker: verapamil and diltiazam

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12
Q

Mechanism of ACE-inhibitor

A

ACE-I
Mechanism: Blocks the production of angiotensin 2 and inhibits bradykinin breakdown through inhibition of angiotensin-converting-enzyme.

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13
Q

Indication for ACE-inhibitor

A

Hypertension patient age <55 years and not of African/Caribbean descent.
Diabetic nephropathy with proteinuria
Chronic heart failure
Ischemic heart disease.

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14
Q

Adverse effects of ACE-inhibitors

A

Chronic dry cough
Hypotension
Renal injury
Hyperkalemia

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15
Q

Why does ACE-inhibitors cause hyperkalemia.

A

Blockade of angiotensin II prevents the downstream secretion aldosterone preventing the reabsorption of sodium and water and excretion of potassium.

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16
Q

Important contraindication with ACE-inhibitors

A

Pregnancy (teratogenic)
Renal failure
Bilateral renal stenosis
Angioedema due to bradykinin

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17
Q

Why is ACE inhibitor contraindicated in renal artery stenosis.

A

In renal artery stenosis the stenosis at the renal afferent arterioles leads to a compensatory mechanism taking place causing the constriction of efferent arterioles, via Ang II. Therefore by blocking ACE there is no vasoconstriction but rather vasodilation of the efferent arterioles causing acute renal injury.

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18
Q

Patient X has been on Ramipril 5 mg OD and is experiencing dry cough. How will you manage the patient.

A

Patient should be switched to ARB.

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19
Q

Monitoring required for ACE-I

A

Renal function 1-2 weeks.
Urea and electrolyte function (especially potassium)
Cough.

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20
Q

ARB example

A

Losartan

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21
Q

Side effects of ARBs

A

Upper respiratory infection
Dizziness
Back pain.

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22
Q

ACE-inhibitors cause decrease in X which result in Y without any increase in heart rate.
a. Preload
b. Afterload
c. Systolic wall stress
d. Cardiac output
e. Stroke volume

A

X: preload, after load and systolic wall stress
Y: cardiac output.

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23
Q

Aldosterone Antagonist (AA)

Give examples of AA

A

Spironolactone, eplerenone

24
Q

Give the indications for AA

A
  1. Ascites and oedema due to liver cirrhosis: First-line treatment Spironolactone alone increasing from 100 mg/day to a dose of 400 mg/day.
  2. Chronic heart failure (with reduced ejection fraction): Add-on therapy for Moderate-severe heart failure.
  3. Primary hyperaldosteronism awaiting surgery
25
Q

Mechanism of aldosterone.

A

Aldosterone is mineralocorticoid produced by cholesterol. Binds to cytoplasmic receptors and influence mRNA transcription —> protein synthesis. Aldosterone increases expression of Na+ channels on luminal side of the principal cells of the distal tubules—> increasing sodium reabsorption. Meanwhile, potassium excreted. Water follows Na+ provide ADH makes the tubules permeable to water.

26
Q

When is aldosterone secreted.

A

In hypovolemia, dehydration, hypokalaemia to increase blood volume & water retention.

27
Q

What is mechanism and effect of AA.

A

Inhibition of aldosterone binding to miner corticoid receptor. Na+ and water is excreted and K+ retained.

28
Q

Aldosterone antagonist cause decrease in …X… and reduce left ventricular …Y.
a. Preload
b. Afterload
c. Workload
d. Conduction

A

X= Preload
Y=Workload.

29
Q

Patient R has LF reduced ejection heart failure and come into the ward with hypokalaemia and is very dehydrated. Med History
Praidel 40 mg tablets
Spironolactone 25 mg OD
Fluoxetine 40 mg OD
Cyanocobalamin 50 microgram OD
Atorvastatin 80 mg OD
Aspirin 75 mg OD
Clopidogrel 75 mg OD
Ramipril 10 mg OD
Bisoprolol 5 mg OD
(a) Which one of these medicines caused the hypokalaemia presentation.
(b) Which medicine will continue to potentiate the hypokalaemia and dehydration.

A

(a) Praidel 40 mg tablets
(b) Spironolactone due to its aldosterone antagonist effects.

30
Q

AA are contraindicated in patients with…

A

Hyperkalemia
Renal impairment
Addisons disease

31
Q

Monitoring for AA

A

Monitor potassium and creatinine 1 week after initiation and after dose increase, monthly for the first 3 months, then every 3 months for 1 year and then every 6 months.

32
Q

Adverse side effects of AA

A

Hyperkalemia: due to potassium retention
Liver impairment and jaundice
Gynaecomastia: due to it binding to androgen receptor decreasing tester ones levels
Steven-johnson syndrome
Hypovolemia

33
Q

Administration of AA in terms of food.

A

With food allows for it be solubilised in foods containing lipids.

34
Q

Counselling for AA

A

Impotence and growth and tenderness of tissues under nipples. Reassure patient that it is benign and reversible. Ask patients to return if they may be uncomfortable/experiencing troublesome side effects, as they may respond to dose reduction. Reinforce importance of attending blood test for monitoring [K+] levels.

35
Q

Indication for CCB: selective and non-selective.

A

Hypertension: amlodipine.
Rate control in supra ventricular arrhythmias
Stable angina.

36
Q

Which CCB is rate limiting.
a. Amlodipine
b. Diltiazem
c. Felodipine
d. Verapamil
e. Nicardipine

A

(b) and (d)

37
Q

Which CCB is selective.
a. Amlodipine
b. Diltiazem
c. Felodipine
d. Verapamil
e. Nicardipine

A

(b) and (d)

38
Q

What effects does CCB have on the afterload/ preload/ cardiac work- increase decrease or no effects.

A

CCB decreases after load because is decrease total peripheral resistance.
CCB reduces left ventricular preload due to its diuretic effect+ vasodilation.
CCB (selective) reduces cardiac work by reducing the conduction rate at AV node.

39
Q

Selective CCB are negative or positive inotrope or chronotrope.

A

Selective CCB are negative inotrope.

40
Q

In order of the CCB: which one produces the most vasodilation: DHP, Verapamil, diltiazem.

A

DHP>Diltiazem>Verapamil.

41
Q

In order of the CCB: which one produces the most negative inotropy: DHP, Verapamil, diltiazem.

A

Verapamil> Diltiazem> DHPs

42
Q

Mechanism of CCB.

A

Inhibits constriction of arteriole by agonist (e.g. NA, Ang II) by blocking voltage-gated Ca2+ channels

43
Q

Pharmacodynamic effect of non-selective CCB

A

Decrease in total peripheral resistance due to relaxation of smooth muscle (through hyper polarisation and removal Ca2+). And as result venous and arterial vasodilation leading to reduce after load/preload—> reducing cardiac demand.

44
Q

Pharmacodynamic effect of selective CCB

A

Suppress cardiac conduction at AV node slowing ventricular rate. Reducing cardiac rate, contractility may reduce cardiac demand for oxygen and increase coronary flow.

45
Q

Adverse effects of CCB

A

Ankle swelling (oedema): Vasodilatory effects
Headaches + lightheadness + hypotension : due to vasodilatory effect.
Palpitation: due to reflexive tachycardia —> drop in blood pressure activating baroreceptor in heart to increase HR to increase blood pressure.

46
Q

Additional adverse effects associated with verapamil

A

Verapamil: constipation

47
Q

CCB contraindicated

A

Pregnancy.
Heart failure.

48
Q

Select the best option
a. Bisoprolol
b. Spironolactone
c. Amlodipine
d. Diltiazam
e. Ramipril
f. Clopidogrel

  1. A 54 year old south Asian male has been admitted to hospital with chest pain. After several tests are performed he is diagnosed with stable angina. He is a smoker and has PMH of hypercholestremia. He has no known allergies.
  2. A 64 year old male who has not tolerated beta blockers in the past as stable angina and requires anti-anginal medicine.
  3. A 67 year old male who has recovered from unstable angina is currently on aspirin. What other agent should be added.
A
  1. (a) Bisoprolol is first line in stable angina to increase cardiac perfusion and reduce HR.
  2. (c) offer NDHP agents.
  3. (f)
49
Q

Organic nitrates have major effect on arterioles leading to decrease in after load.
(A) True
(B) False

A

(B) False

50
Q

Organic nitrates (GTN) have major effect on venules and veins leading to drop in preload.
(A) True
(B) False

A

(B) True

51
Q

Organic nitrates (GTN) mechanism of action.
a. Vasodilation of arterial blood vessels
b. Vasodilation of coronary venules.
c. Vasodilation of peripheral venules.

A

(b) Vasodilation of coronary venules.

52
Q

MAO of Sacubatril/Valsartan

A

Neprolysin inhibitor and Valsartan is ARB.

53
Q

Indication for Sacubatril/Valsartan
a. Chronic heart failure with reduced ejection fraction, 35% or less
b. Chronic heart failure with reduced ejection fraction, 45% or less.
c. Acute heart failure, with reduced ejection fraction 40%

A

(a)

54
Q

MAO Ivabradine
a. Blocks funny sodium channel on nodal cell.
b. Blocks potassium channels.
c. Blocks chloride channels

A

a. Blocks funny sodium channels on nodal cells.

55
Q

Hydralazine effect on preload/afterload/stroke volume/HR- increased of decreased.

A

Hydralazine has negligible effect on preload.
Hydralazine decreases after load
Hydralazine increases stroke volume and heart rate in turn will increase cardiac output. CO= HR x SV.