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Drugs > Cardio Drugs > Flashcards

Cardio Drugs Flashcards

1
Q

Cardioselective Beta-Blockers

examples of drugs

A

Bisoprolol

atenolol

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2
Q

Cardioselective Beta-Blockers

Mechanism of action

A
  • Cardioselective beta-1-adrenoceptor antagonist.
  • Preferentially blocks beta-1 receptors in cardiac and renal tissue.
  • Inhibits sympathetic stimulation of the heart and renal vasculature.
  • Blockade of the sino-atrial node reduces heart rate (negative chronotropic effect) and blockade of receptors in the myocardium depresses cardiac contractility (negative inotropic effect).
  • Additionally, blockade of beta-1 adrenoceptors in renal tissue inhibits the release of renin, depressing the vasoconstrictive effects of the renin-angiotensin-aldosterone system.
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3
Q

Cardioslecitve Beta Blockers

Indications

A
  • Hypertension
  • Angina
  • Rate-control in atrial fibrillation
  • Carvedilol or Bisoprolol may be used as part of supportive therapy for mild / moderate heart failure.
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4
Q

Cardio selective Beta Blockers

Side Effects

A

Bradycardia
Hypotension
Bronchospasm
Fatigue (Can affect up to 10% of patients)
Cold extremities
Sleep disturbances
Loss of hypoglycaemic awareness

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5
Q

Cardio Selective Beta Blockers

Important Pharmocokinetics/ Pharmocodynamics

A
  • Avoid higher doses and use with caution in patients with Asthmatic and COPD – risk of bronchospasm.
  • Avoid in patients with history of frequent hypoglycaemia.
  • Do not combine Beta-Blockers with rate-limiting Ca2+-Channel-Blockers (Verapamil / Diltiazem) in anti-hypertensive therapy, due to risk of heart-block
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6
Q

Cardio Selective Beta Blockers

Patient Information

A
  • Compliance is important – Patients may stop beta-blockers if they do not feel any better. Remind them that hypertension is asymptomatic but nonetheless a dangerous risk factor that needs controlled.
  • Fatigue and cold extremities are common side-effects.
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7
Q

Non Cardio selctie Beat Blockers

Examples of drugs

A

Propanolol

carvedilol

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8
Q

Non Cardioselective Beta Blockers

Mechanism of Action

A
  • Propanolol: Non-cardioselective beta-1-adrenoceptor antagonist.
  • Carvedilol: Non-selective beta-1, beta-2 and alpha-1-adrenergic receptor antagonistic effects.
  • Inhibits sympathetic stimulation in the heart and vascular smooth muscle.
  • N.B Further details under Cardio-Selective Beta-Blockers.
    *
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9
Q

Non Cardio selective Beta Blockers

Indications

A
  • Hypertension
  • Angina
  • Anxiety
  • Migraine prophylaxis
  • Post-MI prophylaxis
  • Carvedilol or Bisoprolol may be used as part of supportive therapy for mild / moderate heart failure
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10
Q

Non Cardioselective Beta Blockers

Side Effects

A
  • Bradycardia
  • Hypotension
  • Bronchospasm
  • Fatigue (Can affect up to 10% of patients)
  • Cold extremities
  • Sleep disturbances
  • Loss of hypoglycaemic awareness
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11
Q

Non Cardio Slective Beta Blockers

Important pharmacokinetics / pharmacodynamics:

A
  • Caution in diabetic patients – risk of deranged carbohydrate metabolism
  • Avoid in patients with Asthma and COPD – risk of bronchospasm
  • Do not combine Beta-Blockers with rate-limiting Ca2+-Channel-Blockers (Verapamil / Diltiazem) in anti-hypertensive therapy.
  • Propanolol is lipid-soluble and is predominantly cleared by the liver. Avoid in liver impairment. Avoid abrupt withdrawal – risk of liver impairment.
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12
Q

Non Cardioselective Beta Blockers

Patient Information

A
  • Nightmares and sleep disturbances may occur.
  • Compliance is important – Patients may stop beta-blockers if they do not feel any better. Remind them that hypertension is asymptomatic but nonetheless a dangerous risk factor that needs controlled.
  • Fatigue and cold extremities are common side-effects.
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13
Q

ACE Inhibitors

Examples of Drugs

A

Ramipril
Enalapril
Lisinopril
Perindopril

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14
Q

ACE Inhibtors

Mechanism Of Action

A
  • Inhibits conversion of Angiotensin I to Angiotensin II (a more potent systemic vasoconstrictor).
  • This action subsequently inhibits Aldosterone release from the adrenal cortex, depressing renal sodium and fluid retention, thereby decreasing blood volume.
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15
Q

ACE Inhibitors

Indications

A

Hypertension
Heart Failure
Nephropathy
Prevention of Cardiovascular events in high risk patients

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16
Q

ACE Inhibtors

Side Effects

A

Dry cough (10% of Patients, causing cessation of treatment in 5%)
Hypotension
Hyperkalaemia
Renal Impairment
Angioedema

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17
Q

ACE Inhibitors

Important pharmacokinetics / pharmacodynamics:

A

Adverse drug reactions are higher in patients with:
High-dose diuretic therapy / Hypovolaemia / Hyponatraemia / Hypotension / Unstable Heart Failure / Renovascular disease

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18
Q

ACE Inhibitors

Patient Information

A

Blood test required at 1-2 weeks to check electrolyte balance.
Dry cough is a common side-effect.

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19
Q

Nitrates

Examples of Drugs

A 
Isosorbide Mononitrate
Glyceryl Trinitrate (GTN)
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20
Q

Nitrates

Mechanism Of Action

A
  • Converted to Nitric Oxide (NO), a potent vasodilator.
  • Cardioselective, acting predominantly on coronary blood vessels, enhancing flow of blood to ischaemic areas of the myocardium.
  • Additionally, reduces myocardial oxygen consumption by reducing cardiac preload and afterload.
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21
Q

Nitrates

Indications

A 
Treatment of Angina
Severe hypertension (intravenous GTN is sometimes used in this setting)
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22
Q

Nitrates

Side Effects

A
  • Headache (incidence varies greatly, between 20-82%, causing cessation of treatment in 10%)
  • Postural Hypotension / Dizziness
  • Tachycardia
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23
Q

Nitrates

Important pharmacokinetics / pharmacodynamics:

A
  • Tolerance develops with long-term use.
  • In order to avoid tolerance, patients should have a daily nitrate-free period.
  • Isosorbide Mononitrate: Oral medication, longer duration of action than GTN.
  • GTN: Rapidly inactivated by first pass (hepatic) metabolism and therefore cannot be digested – sublingual spray/tablet only. It can also be given intra-venously
24
Q

Nitrates

Patient Information

A

Headache is a common side effect initially, but incidence decreases the longer the patient is on the drug.
Take GTN before activity that you know will bring on angina.

25
Q

Rate Limiting Calcium Channel Blockers

Examples of drugs

A

Verapamil

Diltiazem

26
Q

Rate Limiting Calsium Channel Blockers

Mechanisms of action

A
  • Prevent cellular entry of Ca2+ by blocking L-type calcium channels.
  • Myocardial and Smooth muscle contractility depressed. Cardiac contractility will be reduced.
  • Dilate coronary blood vessels and reduce afterload.
  • Antidysrhythmic actions due to prolonged atrioventricular node conduction – depresses heart rate.
27
Q

Rate Limiting Calcium Channel Blockers

Indications

A
  • Supraventricular arrhythmias
  • Treatment of angina
  • Hypertension
28
Q

Rate Limting Calcium CHannel Blockers

Side Effects

A

Verapamil

  • Constipation (up to 11.7% of patients)
  • Flushing / Headache / Dizziness / Hypotension (up to 2.5% of patients)

Diltiazem

  • GI disturbances (up to 6% of patients)
  • Bradycardia (up to 3.6% of patients)
  • Peripheral oedema (up to 15% of patients)
  • Dizziness / Headache / Hypotension (up to 4.3% of patients)
29
Q

Rate Limiting Calcium Channel Blockers

Important pharmacokinetics / pharmacodynamics:

A

Contra-indicated in heart failure and left ventricular dysfunction due to potent negative inotropy.
Avoid in bradycardia and hypotension.
Do not use with beta-blockers.

30
Q

Rate Limiting calcium Channel Blockers

Patient Information

A
  • Constipation is a common side effect with Verapamil.
  • Ankle swelling is a common side effect with Diltiazem, hot weather making it worse.
  • Compliance is important – Patients may stop Calcium-channel blockers if they do not feel any better. Remind them that hypertension is asymptomatic but nonetheless a dangerous risk factor that needs controlled.
31
Q

Non rate limiting calcium channel blockers

examples of drugs

A

amlodipine

nifedipine

felodipine

32
Q

non rate limiting calcium channel blockers

mechanism of action

A
  • Prevent cellular entry of Ca2+ by blocking L-type calcium channels.
  • Myocardial and smooth muscle contractility depressed – these drugs mainly affect smooth muscle.
  • Dilate coronary blood vessels and reduce afterload
  • These drugs do not lower heart rate (heart rate may increase)
33
Q

Non rate limiting calcium channel blockers

indications

A

hypertension

treatment of angina

34
Q

non rate limiting calcium channel blockers

side effects

A

Ankle oedema (up to 15% of patients)
Abdominal pain / Nausea
Palpitations (up to 4.5% of patients)
Flushing / Headache / Dizziness

35
Q

non rate limiting calcium channel blockers

Important pharmacokinetics / pharmacodynamics:

A

Avoid in: Cardiogenic shock, Unstable Angina, Significant Aortic Stenosis

36
Q

non rate limiting calcium channel blockers

patient information

A
  • Compliance is important – Patients may stop Calcium Channel Blockers if they do not feel any better.
  • Remind them that hypertension is asymptomatic but nonetheless a dangerous risk factor that needs controlled.
  • Ankle swelling is a common side effect, hot weather making it worse.
37
Q

HMG CoA Reductase Inhibitors

Examples of Drugs

A

Simvastatin
Atorvastatin
Pravastatin

38
Q

HMG CoA Reductase Inhibitors

Mechanisms of Action

A
  • Competitively inhibits HMG CoA Reductase; the rate-determining enzyme in the mevalonate pathway synthesis of cholesterol.
  • This causes an increase in LDL-receptor expression, on the surface of hepatocytes.
  • Increases hepatic uptake of cholesterol, reducing plasma cholesterol levels.
  • Reduces development of athersclerotic plaques.
  • Statins may have additional pleotropic effects
39
Q

HMG CoA Reductase Inhibitors

Indications

A

Familial hypercholesterolaemia
Prevention of cardiovascular events in high-risk patients.

40
Q

HMG CoA Reductase Inhibitors

Side Effects

A
  • Myalgia (5-7% of patients)
  • Myopathy (with creatine kinase elevation) and rhabdomyolysis are rare.
  • GI disturbances (Varied symptoms; up to 6% of patients affected)
  • Liver abnormalities – deranged LFT’s
41
Q

HMG CoA Reductase Inhibitors

Important pharmacokinetics / pharmacodynamics:

A

Myalgia and Rhabdomyolysis are dose-related, begin with low dose, especially in patients with previous side-effects.

42
Q

HMG CoA Reductase Inhibitors

Patient Information

A

Report any unexplained muscle pains to their GP, who will check a creatine kinase blood level.
Diarrhoea and abdominal pain may be present initially.

43
Q

HMG CoA Reductase Inhibitors

Other Information

A

Hypothyroidism should be corrected before assessing need for statin use

44
Q

Cardiac Glycosides

Examples of drugs

A

Digoxin

45
Q

Cardiac Glycosides

Mechanism of action

A
  • Increases vagal parasympathetic activity and inhibits the Na+/K+ pump, causing a buildup of Na+ intracellularly.
  • In an effort to remove Na+, more Ca2+ is brought into the cell by the action of Na+/Ca2+ exchangers.
  • The buildup of Ca2+ is responsible for the increased force of contraction and reduced rate of conduction through the AV node.
46
Q

Cardiac Glycosides

Indications

A
  • Heart Failure
  • Rate control in Atrial fibrillation
47
Q

Cardiac Glycosides

Side Effects

A

Nausea
Vomiting
Diarrhoea
Confusion

48
Q

Cardiac Glycosides

Important pharmacokinetics / pharmacodynamics:

A
  • Digoxin has a narrow therapeutic index.
  • Symptoms of digoxin toxicity are similar to effects of clinical deterioration.
  • Additionally, the plasma-concentration is not a reliable indicator of toxicity.
  • Digoxin-specific antibody fragments are used for life-threatening digoxin overdose.
  • Digoxin has a long half-life and maintenance doses may only be required once-daily.
  • Renal function, age and heart disease are major determinants for safe digoxin dosage.
49
Q

Cardiac Glycosides

Patient Information

A

Risk of toxicity

50
Q

Cardiac Glycosides

Other Information

A

Digitalis Toxicity

51
Q

Anti Arrhythmic Drugs

Examples

A

Amiodarone

52
Q

Anti Arrhythmic Drugs

Mechanisms of Action

A
  • Amiodarone blocks cardiac K+ channels, prolonging repolarization of the cardiac action potential.
  • Restores regular sinus rhythm.
  • It also slows atrioventricular nodal conduction.
53
Q

Anti Arrhythmic Drugs

Indications

A

Supraventricular / ventricular arrhythmias.

54
Q

Anti Arrythmic Drugs

Side Effects

A
  • Photosensitivity skin reactions (up to 75% of patients)
  • Hypersensitivity reactions
  • Hyper / Hypothyroidism (linked to high iodine content)
  • Pulmonary fibrosis
  • Corneal deposits (69-100% of patients)
  • Neurological disturbances
  • GI disturbances / Hepatitis
55
Q

Anti Arrythmic Drugs

Important pharmacokinetics / pharmacodynamics:

A
  • Very long half-life, once daily dosing, can take weeks-months to achieve steady-state amiodarone-plasma concentrations.
  • Thyroid function tests should be performed before treatment and every six months, or where symptomatic.
  • LFTs should be taken during treatment.
56
Q

Anti Arrythmic Drugs

Patient Information

A
  • Requires good compliance and attendance for monitoring blood tests.
  • Avoid exposure to the sun, wear protective clothing and sunscreen.
  • Report presence of rash after use – hypersensitivity risk.

Drugs (8 decks)

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