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Medicine - Year 2 > The cardiovascular system - Pharmacology > Flashcards

The cardiovascular system - Pharmacology Flashcards

1
Q

Describe the mechanism of action of calcium channel blockers

A

Block L-type Ca2+ channels in arterial smooth muscle, cardiac muscle and cardiac pacemaking tissue

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2
Q

Describe the effect when calcium channel blockers block L-type Ca2+ channels present in:

a) Arterial smooth muscle

b) Cardiac muscle

c) Cardiac pacemaking tissue

A

a) Vasodilation

b) Reduce force of cardiac muscle contraction

c) Reduce heart rate; block AV node

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3
Q

What are the two types of Calcium channel blockers and provide 2 examples for each

A

Non-dihydropyridine/rate-limiting (negative inotropic) e.g., Verapamil, Diltiazem

Dihydroyridine (non-inotropic) e.g., Amlodopine, Nifedipine

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4
Q

Non-dihydropyridine calcium channeblockers

a) What are effects of verapamil and diltiazem

b) What are they useful for?

A

a)
Verapamil - mainly cardiac effects

Diltiazem - both cardiac and vascular

b) Useful for angina and arrhythmias (and some effect on BP)

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5
Q

Non-dihydropyridine calcium channeblockers

a) What are effects of amlodipine and nifedipine

b) What are they useful for?

A

a) Act mainly on vascular smooth muscle to reduce BP

b) Widely used for hypertension

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6
Q

What are the known effects of cardiac (negative inotropic) calcium channel blockers?

A
  • Slow heart rate
  • Reduced contraction - may worsen heart failure
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7
Q

What are the known effects of vascular (non- inotropic) calcium channel blockers?

A
  • Headache
  • flushing
  • Peripheral oedema
  • Reflex tachycardia (may be harmful to those with coronary artery disease)
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8
Q

Describe the mechanism of modern day action of beta blockers

A

Block beta-1 adrenorecpetors in the heart. This includes the cardiac muscles which prevents the heart from pumping harder and in pacemaker tissue and conduction which prevents the heart from pumping faster. This overall slows down the heart rate

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9
Q

Why must you avoid beta-blockers blocking beta-2 adrenoreceptors?

A

Beta-2 adrenoreceptors can be found in the airways (bronchial Smooth muscle). The blockage of this prevents dilation of the lungs (bronchonstriction) and so prevents an open airway. This can cause asthma to worsen

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10
Q

What are the commonly used beta-blockers

A

Non-selective: Propanolol (old generation)

Cardioselective (selective for beta-1): Atenolol, Bisoprolol and Metoprolol

Vasodilator activity: Alpha-blocking properties (carvedilol, labetolol)

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11
Q

What are the indications of beta-blocker use

A
  • ACS/MI (reduces mortality)
  • Chronic heart failure (reduces mortality)
  • Symptomatic benefit in angina
  • Resistant hypertension (4th line)
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12
Q

Describe the adverse effects of beta-blockers

A

Cardiac cause
- Bradycardia
- Initially worsens heart failure

Sympathetic blockade
- Bronchoconstriction (blockade of beta-2 adrenoreceptors)
- Tiredness, feel cold

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13
Q

Describe the mechanism of action of nitrates

A
  • Cause an increase in endothelial nitric oxide
  • This activates granulate cyclase which causes an increase in cGMP
  • increases dephosphorylation of myosin light chain
  • Decrease Ca2+ influx into the cell
  • This causes vascular smooth muscle relaxation
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14
Q

What are the effects of nitrates

A

Arterial dilation
- Improves coronary supply
- Reduce after load by lowering BP

Venous dilation that reduces blood return to heart
- Decreased preload and stretching of heart
- Decreased pressure in the ventricles (especially diastolic wall pressure)

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15
Q

What are the two most commonly used nitrates?

A

Glycerylnitrate (GTN) -

Isorbide mononitrate

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16
Q

What are the indications of nitrates

A

Symptomatic relief of angina or ACS (GTN)

Relief of heart failure in acute doses - hight doses IV are usually required

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17
Q

What are adverse effects of nitrates?

A
  • Hypotension
  • Reflex tachycardia
  • Headache
  • Flushing
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18
Q

Give 3 specialist drugs that are used as 3rd-4th line treatment of angina

A

Nicorandil (potassium channel opener)

Ranolazine (late sodium current inhibitor)

Ivabradine (Specific sinus node inhibitor - blocks cardiac conduction) (similar to beta-blocker in slowing heart rate)

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19
Q

What 2nd line anti-anginal drug would you give a patient with no haemodynamic side-effects?

A

Long-acting nitrate or nicorandil

20
Q

What 2nd-line anti-anginal would you give a patient with haemodynamic side-effects and rate control achieved?

A

Ranolazine

21
Q

What 2nd line anti-anginal drug would you give a patient with haemodynamic side-effects and no rate control achieved?

A

Ivabradine

22
Q

Describe the key targets of treating hypertension

A

Mean arterial pressure depends on cardiac output (how hard the heart is pumping) and vascular resistance (how narrow the vessels are)

Therefore a lower artery pressure is achieved when the heart pumps slowly and less vigorously and when the arteries are wide open so the volume of blood/fluid is reduced

23
Q

Describe the 4 drug classes in hypertension and provide examples for each

A
  1. Reduce intravascular volume - diuretics - thiazides
  2. Reduce sympathetic tone that is causing constriction and increased cardiac output - alpha and beta-blockers
  3. Relax the peripheral arteries - calcium channel blockers
  4. Block neuroendocrine mediators of blood pressure - ACEi, ARBs, renin inhibitors
24
Q

Describe the mechanism of action of ace inhibitor and provide 3 examples of ACEi

A

Blocks angiotensin converting enzyme. This prevents angiotensin I from converting to angiotensin II.

Angiotension II causes vasoconstriction, increased sympathetic stimulation and anti-diuretic hormone. it also causes aldosterone release which causes salt and water retention. ACEi inhibits these effects.

3 examples: Ramipril, Captopril, Enalapril

25
Q

What are the indicates of ACEi use?

A
  • 1st line for hypertension except for selected patients (> 55 or African/Caribbean descent)
  • 1st line if previous heart failure or cardiac damage
26
Q

Explain the side effects and monitoring requirements for ACEi

A

Drops blood pressure (first dose) - give small test dose and check patient not too volume depleted

Worsen renal function - check U&Es before and 1 week after

Retains potassium - stop K supplements or K+ - sparing agents

Cause cough and allergies

27
Q

Discuss the side effects and monitoring requirements for ACEi

A

Drops blood pressure (first dose) - give small test dose and check patient not too volume depleted

Worsen renal function - check U&Es before and 1 week after

Retains potassium - stop K supplements or K+ - sparing agents

Cause cough and allergies

28
Q

Angiotensin II receptor blockers (ARBs)

a) Indications

b) Mechanism of action

c) 3 examples

A

a) Use in patients who cannot tolerate ACEi

b) Block type 1 angiotensin II receptors

c) Candesartan, Losartan, Irbesartan

29
Q

What are the different types of diuretics, their indications for used an example each

A

Loop - heart failure e.g., furosemide, bumetanide

Thiazides - hypertension e.g., bendroflumethiazide

Thiazide-like diuretic - hypertension e.g., indapamide (Ineffective if GFR is less than 30 should be avoided)

Potassium-sparing - heart failure and hypertension e.g.m spironolactone (blocks aldosterone)

30
Q

Discuss the side effects and monitoring requirement of diuretics

A
  • Hypovolaemia, dehydration, and hypotension
  • Electrolyte balance: low K+ and NA+, high urea
  • Monitor BP, urine output or body weight
  • Check electrolytes regularly if on high dose
31
Q

Give possible 4th line drugs to control BP

A
  • Beta-blocker
  • Alpha-blocker e.g., doxazosin
  • Renin inhibitor e.g., doxazosin
  • Central sympathetic outflow - clonidine, methyldopa
  • Potassium Chanel openers - minoxidil
32
Q

You give ACEi/ARBs as 1st line treatment for Hyperion, except in what type of people?

A

Age over 55 years or black person of African or Caribbean family origin of age

33
Q

Describe the algorithm of antihypertensive drug treatment

A

1st line - Age under 55 years - ACE/ARB or aged over 55 years or black person of African or Caribbean family origin of age - CCB

2nd line - ACEi/ARBs + CCB

3rd line - ACEi/ARBs + CCB + Thiazide-like diuretics

4th line - ACEi/ARBs + CCB + Thiazide-like diuretics + consider further diuretic (Spiro) or alpha or beta blocker

34
Q

Name the mechanism of the 6 classes of antiarrhythmic drugs and include at least 1 example for each

A

Class Ia: sodium-channel block (intermediate dissociation) e.g., disopyramide

Class Ib: Sodium-channel block (fast dissociation) e.g.Lidocaine

34
Q

Name the mechanism of the 6 classes of Vaughan-Williams antiarrhythmic drugs and include at least 1 example for each

A

Class Ia: sodium-channel block (intermediate dissociation) e.g., disopyramide

Class Ib: Sodium-channel block (fast dissociation) e.g.Lidocaine

Class Ic: Sodium-channel block (slow dissociation) e.g., Flecainide

Class II: Beta-adrenoreceptor antagonism e.g., Propranolol, bisoprolol

Class III: Potassium-channel block e.g., Amiodarone, sotalol

Class IV: Calcium-channel block e.g., verapamil

35
Q

Class Ic: sodium-channel blocker (Flecanaide)

a) MOA

b) Abs/Distrib/Elim

c) Clinical use

d) Adverse effects

A

a) Preferential block of open sodium ion channels. Reduces the rate of phase 0 depolarisation causing an increase in the effective refractory period and slowed AV conduction

b) Oral or iv admin. half-life 20h. Mostly excited unchanged in urine

c) Prevention of AF and VT. Cardioversion of acute-onset AF

d)
- Suitable only for patients who do not have ischaemic or structural heart disease
- Increases likelihood of dysrhythmia
- May increase mortality due to VF post-infarction

36
Q

Class II: Beta-adrenoreceptor antagonist (Bisoprolol, propranolol)

a) Actions

b) MOA

c) Abs/Distrib/Elim

d) Clinical use

e) Adverse effects

A

a) Antidysrhythmic (Also antihypertensive, antiangina.) Block actions of catecholamines on beta adrenoreceptors

b) Block sympathetic drive, reducing pacemaker activity (phase 4) and increasing AV conduction time. Reduce the slow inwards Ca ion current which affects phase 2 of the action potential. Propanol has additional class I action

c) Oral and i.v. adminitstaion

c) AF, supraventrcular and ventricular tachyarrhtymias. Reduction of mortality after infarct (where dysrhythmias has a sympathetic input)

d) Bronchoconstriciton in asthma, bradycardia and heart block

37
Q

Class III: Potassium-channel blockers (amiodarone, sotalol)

a) MOA

b) Abs/Distrib/Elim

c) Clinical use

d) Adverse effects

A

a) Increases refractory period blocking potassium ion channels in the cell membrane to delay depolarisation and increase action potential duration

Amiodarone also blocks sodium channels and beta-adrenoreceptors so has class I and class II actions. Sotalol is a beta-adrenoreceptor antagonist with class II actions

d) Amiodarone - long acting; extensive tissue binding, half-life of several weeks. Sotalol half-life is 5-10h

e) Af and flutter, VT

f) Amiodarone serious toxicity: pulmonary fibrosis, liver damage, photosensitive skin rashes and thyroid malfunction. Torsades de points major problem with sotalol but less likely with amiodarone

38
Q

Class IV: Calcium-channel blockers

a) Actions

b) MOA

c) Abs/Distrib/Elim

d) Clinical use

e) Adverse effects

A

a) Anntidysrhythmic (also abtianginal and antihypertensive). Blocks Ca ion channels I. both cardiac and smooth muscle so has both negative inotropic and smooth muscle relaxant actions

b) Blocks l-type, voltage-gated Calcium ion channels, which are important in the action potential plateau, and in particular effects action potential propagation in the SA and AV nodes. Decreases automaticity and slows AV conduction

c) Oral (less commonly i.v.) admin. Half-life 6-8h

d) Supraventricular tachycardias. Control of ventricular rate in atrial fibrillation

e) Side effects due to smooth muscle relaxation: hypotension and dizziness, ankle oedema, constipation. Unwanted cardiac actions include heart block and bradycardia

39
Q

Give 7 anti-arrhythmic that are not part of the Vaughan-Williams classification and include their therapeutic use

A

Atropine - bradycardia

Adrenaline (epinephrine) - Cardiac arrest

Isoprenaline - Heart block

Digoxin - AF

Adenosine - supra ventricular tachycardia

Calcium chloride - Ventriular arrhythmia (due to hyperkalaemia)

Magensium chloride - Ventricular arrhythmia (e.g., torsades des pointes)

40
Q

Adenosine, ADP receptor agonist

a) MOA

b) Abs/Distrib/Elim

c) Clinical use

d) Adverse effects

A

a)
Activates G protein-coupled adenosine (A1 receptor). Inhibits Ca channel opening whilst increasing potassium channel opening. Negative chronotopic effect on the SA node, with slowed AV conduction

b) Given i.v. Short duration of action. Half-life 10sec

c) Termination of paroxysmal supra ventricular tachycardia. Slowing of AV conduction to enable more precise diagnosis of supraventricular tachycardias

d) Mainly flushing, chest pain, dyspnoea, bronchospasm; transient because rapid elimination of adenosine. Interacts with other drugs that exerts effects on adenosine pathways (dipyridamole, theophylline)

41
Q

Cardiac glycosides: Digoxin

a) Actions

b) MOA

c) Abs/Distrib/Elim

d) Clinical use

e) Adverse effects

f) Special points

A

a) Slows heart. Slows AV conduction. Prolongs AV node refractory period. Increases force of contraction in failing heart

b) Inhibits Na/k ATPase in plasma membrane. The increased intracellular Na reduces Ca channel extrusion thus increasing intracellular Ca ions

c) Given orally, usually with an oral or i.v. loading dose if rapid action is needed; renal excretion; plasma Half like - 36 hours

d) AF, HF (if diuretics and ACEi have not worked)

e) Dysrhythmias, due to block of AV conduction and ectopic pacemaker action; yellow vision; nausea and vomiting

f) Narrow margin between effective dose and toxic dose. Decreased plasma potassium increases toxicity due to competition between potassium and digoxin for the Na+/K+ ATPase

42
Q

Name the drugs the anti arrhythmic drugs that target the following phases of the cardiac action potential

a) Phase 4 - resting membrane potenial

b) Phase 0 - Rapid depolarisation

c) Phase 2 - Plateau

d) Phase 3 - Late repolarisation

A

a) Adenosine, metoprolol, propanolol, digoxin

b) Dispoyramide, flecainide

c) Verapamil, diltiazem, digoxin

d) Amiodarone, sotalol, digoxin

43
Q

a) What part of the kidneys does loop diuretics act on?

b) Describe it’s action

A

a) Acts on Loop of Henle

b) Blocks sodium-potassium chloride contransporter
This increases sodium, potassium and chloride excretion

44
Q

a) What part of the kidneys does thiazide diuretics act on?

b) Describe it’s action

A

a) Acts on the distal convoluted tubule

b) Blocks sodium-chloride transporter so increase sodium chloride excretion

45
Q

a) What part of the kidneys does thiazide diuretics act on?

b) Describe it’s action

A

a) Acts on the distal convoluted tubule

b) Blocks sodium-chloride transporter so increase sodium chloride excretion

46
Q

What is the difference between the action of loop and thiazide diuretics?

A

Loop diuretics increase Na, K and Cl excretion

Thiazide diuretics increase Na and Cl excretion so therefore they are potassium sparing

Medicine - Year 2 (27 decks)

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