Cardiovascular Drugs Flashcards

1
Q

What are some examples of cardioselective beta-blockers?

A

Bisoprolol

Atenolol

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2
Q

What is the mechanism of action for cardioselective beta-blockers?

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 SAN reduces HR(negative chronotropic effect) and blockade of receptors in the myocardium depresses cardiac contractility (negative inotropic effect).
  • blockade of beta-1 adrenoceptors in renal tissue inhibits release of renin, depressing vasoconstrictive effects of the RAAS.
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3
Q

What are the indications of cardioselective beta-blockers

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

List the side effects of cardioselective beta-blockers

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

What is important clinically regarding Pharmacokinetics/dynamics for cardioselective beta-blockers?

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

What information should you tell the patient before starting on a cardioselective beta blocker

A
  • Compliance is important – 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

What are some examples of non-cardioselective beta-blockers?

A

Propranolol

Carvedilol

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8
Q

What is the mechanism of action for non-cardioselective beta-blockers?

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.
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9
Q

What are the indications of non-cardioselective beta-blockers?

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

List the side effects of non-cardioselective beta-blockers

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

What is important clinically regarding Pharmacokinetics/dynamics for non-cardioselective beta-blockers?

A

Caution in diabetic patients – risk of deranged CHO metabolism
Avoid in patients with Asthma & 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 mostly cleared by the liver. Avoid in liver impairment. Avoid abrupt withdrawal – risk of liver impairment.

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12
Q

What information should you tell the patient before starting on a non-cardioselective beta blocker

A
  • Nightmares and sleep disturbances may occur.
  • Compliance is important – 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

What are some examples of ACE Inhibitors?

A

Ramipril
Enalapril
Lisinopril
Perindopril

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14
Q

What is the MoA for ACE Inhibitors?

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

What are the indications for ACE Inhibitors?

A
  • Hypertension
  • Heart Failure
  • Nephropathy
  • Prevention of Cardiovascular events in high risk patients
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16
Q

List some side effects of ACE Inhibitors:

A
  • Dry cough (10% of Patients, causing cessation of treatment in 5%)
  • Hypotension
  • Hyperkalaemia
  • Renal Impairment
  • Angioedema
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17
Q

What is important clinically regarding Pharmacokinetics/dynamics for ACE Inhibitors?

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

What information should you tell the patient before starting on an ACE Inhibitor

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

What are some examples of Nitrates?

A
Isosorbide Mononitrate
Glyceryl Trinitrate (GTN)
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20
Q

What is the MoA for Nitrates?

A

• Converted to Nitric Oxide, a potent vasodilator.
Cardioselective, acting predominantly on coronary blood vessels, enhancing flow of blood to ischaemic areas of the myocardium.
• reduces myocardial oxygen consumption by reducing cardiac preload and afterload.

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21
Q

What are the indications for Nitrates?

A
  • Treatment of Angina

* Severe hypertension (intravenous GTN is sometimes used in this setting)

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22
Q

List some side effects of Nitrates

A
  • Headache
  • Postural Hypotension/dizziness
  • Tachycardia
23
Q

What is important clinically regarding Pharmacokinetics/dynamics for Nitrates?

A
  • Tolerance develops with long-term use.
  • 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 IV.
24
Q

What information should you tell the patient before starting on a Nitrate?

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

What are some examples of rate limiting calcium channel blockers?

A

Verapamil

Diltiazem

26
Q

What is the MoA for rate limiting calcium channel blockers?

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

What are some side effects of rate limiting calcium channel blockers?

A

Verapamil:
• Constipation
• Flushing / Headache / Dizziness / Hypotension

Diltiazem:
• GI disturbances 
• Bradycardia
• Peripheral oedema 
• Dizziness / Headache / Hypotension
28
Q

What is important clinically regarding Pharmacokinetics/dynamics for rate limiting calcium channel blockers?

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.
29
Q

What information should you tell the patient before starting on a rate limiting calcium channel blockers?

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 – hypertension is asymptomatic but nonetheless a dangerous risk factor that needs controlled.
30
Q

what are some examples of non-rate limiting calcium channel blockers?

A

amlodipine
nifedipine
felodipine

31
Q

What is the MoA for non-rate limiting calcium channel blockers?

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)
32
Q

What are some indications for non-rate limiting CCBs?

A

Hypertension

Treatment of Angina

33
Q

What are some side effects of non-rate limiting calcium channel blockers?

A

Ankle oedema
Abdominal pain / Nausea
Palpitations
Flushing / Headache / Dizziness

34
Q

What is important clinically regarding Pharmacokinetics/dynamics for non-rate limiting calcium channel blockers?

A

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

35
Q

What information should you tell the patient before starting on a non-rate limiting calcium channel blockers?

A
  • Compliance is important – Patients may stop CCB f they do not feel any better.
  • HPT is asymptomatic but a dangerous risk factor that needs controlled.
  • Ankle swelling is a common side effect, hot weather making it worse.
36
Q

What are some indications for rate limiting CCBs?

A

Supraventricular arrhythmias
Treatment of angina
Hypertension

37
Q

What are some examples of HMG CoA Reductase Inhibitors?

A

Simvastatin
Atorvastatin
Pravastatin

38
Q

What is the MoA of HMG CoA Reductase Inhibitors?

A
  • Competitively inhibits HMG CoA Reductase; the rate-determining enzyme in the mevalonate pathway synthesis of cholesterol.
  • causes increase in LDL-receptor expression, on hepatocyte surface
  • Increases hepatic uptake of cholesterol, reducing plasma cholesterol levels.
  • Reduces development of athersclerotic plaques.

(Statins may have additional pleotropic effects)

39
Q

what are the indications for HMG CoA reductase inhibitors?

A

familial hypercholesterolaemia

prevention of CV events in high risk patients

40
Q

What are the side effects of HMG CoA reductase inhibitors?

A

Myalgia
Myopathy (with creatine kinase elevation) and rhabdomyolysis are rare.
GI disturbances
Liver abnormalities – deranged LFT’s

41
Q

What is important clinically regarding Pharmacokinetics/dynamics for HMG CoA reductase inhibitors?

A

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

Hypothyroidism should be corrected before assessing need for statin use.

42
Q

What information should you tell the patient before starting on a HMG CoA reductase inhibitors?

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

What is an example of a Cardiac Glycoside?

A

Digoxin

44
Q

What is the MoA for Cardiac glycosides?

A

Increases vagal parasympathetic activity and inhibits the Na+/K+ pump, causing a buildup of Na+ intracellularly.
T try remove Na+, more Ca2+ enters cell by Na+/Ca2+ exchangers.
The buildup of Ca2+ causes increased force of contraction and reduced rate of conduction through AV node.

45
Q

What are the indications for digoxin?

A

heart failure

rate control in atrial fibrillation

46
Q

What are some side effects of Cardiac glycosides?

A

nausea
vomiting
diarrhoea
constipation

47
Q

What is important clinically regarding Pharmacokinetics/dynamics for digoxin?

A
  • narrow therapeutic index.
  • Symptoms of digoxin toxicity are similar to effects of clinical deterioration.
  • plasma-concentration is not a reliable indicator of toxicity.
  • Digoxin-specific antibody fragments are used for life-threatening digoxin overdose.
  • 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.
48
Q

What information should you tell the patient before starting on a Cardiac glycoside?

A

risk of toxicity

49
Q

what is an example of an anti-arrhythmic drugs?

A

amiodarone

50
Q

what is the mechanism of action for anti-arrhythmic drugs?

A

Amiodarone blocks cardiac K+ channels, prolonging repolarization of the cardiac action potential.
Restores regular sinus rhythm.
It slows AV nodal conduction.

51
Q

what is the indication for amiodarone?

A

supraventricular / ventricular arrhythmias

52
Q

What are the side effects of anti-arrhythmic drugs?

A
Photosensitivity skin reactions 
Hypersensitivity reactions
Hyper / Hypothyroidism
Pulmonary fibrosis
Corneal deposits 
Neurological disturbances
GI disturbances / Hepatitis
53
Q

What is important clinically regarding Pharmacokinetics/dynamics for anti-arrhythmic drugs?

A
  • long half-life, once daily dosing, can take weeks-months to achieve steady-state amiodarone-plasma concentrations.
  • Thyroid function tests before Tx and every six months, or where symptomatic.
  • LFTs should be taken during treatment.
54
Q

What information should you tell the patient before starting on a anti-arrhythmic drug?

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.