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Cardio Drugs Flashcards

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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:

Study These Flashcards
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

Study These Flashcards
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
Rate Limiting Calcium Channel Blockers Examples of drugs
Verapamil Diltiazem
26
Rate Limiting Calsium Channel Blockers Mechanisms of action
* 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
Rate Limiting Calcium Channel Blockers Indications
* Supraventricular arrhythmias * Treatment of angina * Hypertension
28
Rate Limting Calcium CHannel Blockers Side Effects
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
Rate Limiting Calcium Channel Blockers ## Footnote Important pharmacokinetics / pharmacodynamics:
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
Rate Limiting calcium Channel Blockers Patient Information
* 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
Non rate limiting calcium channel blockers examples of drugs
amlodipine nifedipine felodipine
32
non rate limiting calcium channel blockers mechanism of action
* 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
Non rate limiting calcium channel blockers indications
hypertension treatment of angina
34
non rate limiting calcium channel blockers side effects
Ankle oedema (up to 15% of patients) Abdominal pain / Nausea Palpitations (up to 4.5% of patients) Flushing / Headache / Dizziness
35
non rate limiting calcium channel blockers Important pharmacokinetics / pharmacodynamics:
Avoid in: Cardiogenic shock, Unstable Angina, Significant Aortic Stenosis
36
non rate limiting calcium channel blockers patient information
* 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
HMG CoA Reductase Inhibitors Examples of Drugs
Simvastatin Atorvastatin Pravastatin
38
HMG CoA Reductase Inhibitors Mechanisms of Action
* 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
HMG CoA Reductase Inhibitors Indications
Familial hypercholesterolaemia Prevention of cardiovascular events in high-risk patients.
40
HMG CoA Reductase Inhibitors Side Effects
* 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
HMG CoA Reductase Inhibitors ## Footnote Important pharmacokinetics / pharmacodynamics:
Myalgia and Rhabdomyolysis are dose-related, begin with low dose, especially in patients with previous side-effects.
42
HMG CoA Reductase Inhibitors Patient Information
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
HMG CoA Reductase Inhibitors Other Information
Hypothyroidism should be corrected before assessing need for statin use
44
Cardiac Glycosides Examples of drugs
Digoxin
45
Cardiac Glycosides Mechanism of action
* 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
Cardiac Glycosides Indications
* Heart Failure * Rate control in Atrial fibrillation
47
Cardiac Glycosides Side Effects
Nausea Vomiting Diarrhoea Confusion
48
Cardiac Glycosides ## Footnote Important pharmacokinetics / pharmacodynamics:
* 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
Cardiac Glycosides Patient Information
Risk of toxicity
50
Cardiac Glycosides Other Information
Digitalis Toxicity
51
Anti Arrhythmic Drugs Examples
Amiodarone
52
Anti Arrhythmic Drugs Mechanisms of Action
* Amiodarone blocks cardiac K+ channels, prolonging repolarization of the cardiac action potential. * Restores regular sinus rhythm. * It also slows atrioventricular nodal conduction.
53
Anti Arrhythmic Drugs Indications
Supraventricular / ventricular arrhythmias.
54
Anti Arrythmic Drugs Side Effects
* 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
Anti Arrythmic Drugs ## Footnote Important pharmacokinetics / pharmacodynamics:
* 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
Anti Arrythmic Drugs Patient Information
* 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.

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