Cardiology Drugs Flashcards

1
Q

List the 7 main types of cardiology drugs.

A
Beta blockers
ACE inhibitors
Nitrates
Calcium channel blockers 
HMG CoA reductase inhibitors
Cardiac glycosides
Anti-arrhythmic drugs
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2
Q

List the 2 types of beta blockers.

Give 2 examples of each.

A

CARDIOSELECTIVE:

  • Bisoprolol
  • Atenolol

NON-SELECTIVE:

  • Propranolol
  • Carvedilol
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3
Q

Describe the mechanism of action of beta blockers. (5)

What is the difference between selective and non-selective beta blockers?

A

MECHANISM OF ACTION:
1. Blocks beta 1 adrenoreceptors in cardiac and renal tissue

  1. Inhibits sympathetic stimulation of heart and renal vasculature
  2. Negative chronotropic effect:
    a. Caused by blockage of SAN
  3. Negative inotropic effect:
    a. Caused by blocked receptors in the myocardium
  4. Effects on renal tissue:
    a. Inhibits release of renin
    b. Inhibits RAS, causing vasodilation

NON-SELECTIVE BETA BLOCKERS:
-Block beta 1 and 2 adrenoreceptors

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4
Q

List 4 indications of cardioselective beta blockers.

List 6 indications of non-selective beta blockers.

A
CARDIOSELECTIVE:
Hypertension
Angina
AF
Mild-moderate heart failure
NON-SELECTIVE:
Hypertension
Angina
Anxiety
Migraine prophylaxis
Secondary MI prophylaxis
Mild-moderate heart failure
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5
Q

List 7 side effects of beta blockers.

A
Bradycardia
Hypotension
Bronchospasm
Fatigue
Cold extremities
Sleep disturbances
Loss of hypoglycaemic awareness
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6
Q

List 5 contraindications for beta blockers.

Give 1 condition in which beta blocker use requires caution.

A
AVOID IN:
Peripheral vascular disease
Asthma
COPD
Liver impairment
Rate-limiting CCB use

CAUTION IN:
Diabetes

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7
Q

What would you tell the patient when prescribing beta blockers? (3)

A

Nightmares and sleep disturbances may occur
Compliance is important
Fatigue and cold extremities are common

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8
Q

Give 4 examples of ACE inhibitors.

A

Ramipril
Enalapril
Lisinopril
Perindopril

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9
Q

Describe the mechanism of action of ACE inhibitors. (2)

List 4 indications for ACE inhibitors.

A

MECHANISM OF ACTION:
1. Inhibits conversion of angiotensin I into angiotensin II

  1. This inhibits aldosterone release from the adrenal cortex
    a. This causes decreased sodium/fluid retention
    b. This decreases blood volume
INDICATIONS:
Hypertension
Heart failure
Nephropathy
Prophylaxis of cardiovascular events
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10
Q

List 5 side effects of ACE inhibitors.

A
Dry cough
Hypotension
Hyperkalaemia
Renal impairment
Angioedema
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11
Q

Describe important pharmacokinetics/dynamics of ACE inhibitors. (6)

What would you tell the patient when prescribing ACE inhibitors?

A
IMPORTANT PHARMA INFO:
Adverse drug reactions are higher in patients with:
-High dose diuretics
-Hypovolaemia
-Hyponatraemia
-Hypotension
-Unstable heart failure
-Renovascular disease

PATIENT INFO:
Dry cough is very common
Blood tests required at 1-2 weeks to check electrolyte balance

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12
Q

Give 3 examples of nitrates.

A

Isosorbide mononitrate
Glyceryl trinitrate (GTN)
Sodium nitroprusside

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13
Q

Describe the mechanism of action of nitrates. (3)

List 2 indications for nitrates.

A

MECHANISM OF ACTION:
1. Converted to nitric oxide (NO), a potent vasodilator

  1. Cardioselective, acting predominantly on coronary blood vessels
    a. This enhances blood flow to ischaemic areas of myocardium
  2. Reduces cardiac preload and afterload
    a. This decreases myocardial oxygen demand

INDICATIONS:
Angina
Severe hypertension

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14
Q

List 4 side effects of nitrates.

What would you tell the patient when prescribing nitrates? (2)

A
SIDE EFFECTS:
Headache
Postural hypotension
Dizziness
Tachycardia

PATIENT INFO:
Headaches are common initially, but decrease the longer the patient takes nitrates
Take GTN before activity you know will bring on angina

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15
Q

Describe important pharmacokinetics/dynamics of nitrates. (4)

A

Tolerance develops with long term use
To avoid tolerance, patients should have a daily nitrate-free period

Isosorbide mononitrate: oral
GTN: sublingual spray/tablet or IV

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16
Q

What are the 2 types of calcium channel blockers?

Give examples of each.

A

RATE-LIMITING CCBS:

  • Verapamil
  • Diltiazem

NON-RATE-LIMITING CCBS:

  • Amlodipine
  • Nifedipine
  • Felodipine
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17
Q

Describe the mechanism of action of rate-limiting calcium channel blockers. (3)

How do non-rate-limiting calcium channel blockers differ? (2)

A

RATE-LIMITING CCBS:

  1. Prevent cellular entry of Ca2+ by blocking L-type calcium channels
    a. This reduces myocardial and smooth muscle contractility
    b. Therefore has a negative inotropic effect
  2. Causes dilation of coronary blood vessels and reduced cardiac afterload
  3. Anti-dysrhythmic actions caused by prolonged AVN conduction rate
    a. This decreases HR

NON-RATE LIMITING CCBS:

  • Act mainly on smooth muscle; therefore no negative inotropic effect
  • Do not decrease HR
18
Q

List 3 indications for rate-limiting CCBs.

List 2 indications for non-rate-limiting CCBs.

A

RATE LIMITING CCBS:
Supraventricular arrhythmias
Angina
Hypertension

NON-RATE-LIMITING CCBS:
Hypertension
Angina

19
Q

List 5 side effects of verapamil.

List 7 side effects of diltiazem.

A
VERAPAMIL:
Constipation
Flushing
Headache
Dizziness
Hypotension
DILTIAZEM:
GI disturbance
Ankle swelling
Bradycardia
Peripheral oedema
Dizziness
Headache
Hypotension
20
Q

List 4 contraindications for rate-limiting CCBs.

Which drug can you NOT combine them with?

A

Heart failure
Left ventricular dysfunction
Bradycardia
Hypotension

Beta blockers

21
Q

What would you tell the patient when prescribing rate-limiting CCBs? (3)

A

Compliance is important
Constipation is common with verapamil
Ankle swelling is common with diltiazem

22
Q

List 7 side effects for non-rate-limiting CCBs.

A
Ankle oedema
Abdominal pain
Nausea
Palpitations
Flushing
Headache
Dizziness
23
Q

In which conditions would you avoid using non-rate-limiting CCBs? (3)

A

Cardiogenic shock
Unstable angina
Significant aortic stenosis

24
Q

What would you tell the patient when prescribing non-rate-limiting CCBs? (2)

A

Compliance is important

Ankle swelling is common

25
Q

Give 1 example of a cardiac glycoside.

A

Digoxin

26
Q

Describe the mechanism of action of digoxin. (4)

A
  1. Inhibits Na+/K+ pump, therefore causes increased levels of intracellular Na+
  2. This increases Na+/Ca2+ exchanger activity
    a. Therefore increased intracellular Ca2+
  3. This has a positive inotropic effect
  4. Also decreases rate of conduction through AVN
27
Q

List 2 indications of digoxin.

What would you tell the patient when prescribing digoxin? (1)

A

INDICATIONS:
Heart failure
Atrial fibrillation

PATIENT INFO:
Risk of toxicity

28
Q

List 4 side effects of digoxin.

A

Nausea
Vomiting
Diarrhoea
Confusion

29
Q

Describe important pharmacokinetics/dynamics of digoxin. (5)

A

Narrow therapeutic index
Plasma concentration NOT reliable indicator of toxicity

Symptoms of toxicity similar to clinical deterioration

Treatment of toxicity:
-Digoxin specific antibody fragments

Long half-life

30
Q

Give 1 example of an anti-arrhythmic drug.

A

Amiodarone

31
Q

Describe the mechanism of action of amiodarone. (2)

List 2 indications of amiodarone.

A

MECHANISM OF ACTION:

  1. Blocks cardiac K+ channels, causing prolonged repolarisation of cardiac AP
    a. This restores regular sinus rhythm
  2. Decreases rate of AVN conduction, which decreases HR

INDICATIONS:
Supraventricular/ventricular tachycardia
Atrial fibrillation

32
Q

List 8 side effects of amiodarone.

A
Photosensitivity skin reaction
Hypersensitivity
Hyper/hypothyroidism
Pulmonary fibrosis
Corneal deposits
Neurological disturbances
GI disturbances
Hepatitis
33
Q

Describe the important pharmacokinetics/dynamics of amiodarone. (4)

A

Very long half-life:

  • Once daily dosing
  • Weeks-months needed for steady state

Monitoring needed:

  • Thyroid function tests
  • LFTs
34
Q

What would you tell the patient when prescribing amiodarone? (3)

A

Good compliance is necessary
Avoid sun exposure
Report any rash

35
Q

List 4 examples of statins.

A

Simvastatin
Atorvastatin
Pravastatin
Rosuvastatin

36
Q

Describe the mechanism of action of statins. (3)

A
  1. Competitively inhibits HMG CoA reductase, the rate-determining enzyme in the mevalonate pathway synthesis of cholesterol
  2. This causes an increase in LDL receptor expression on hepatocytes
    a. This increases hepatic uptake of cholesterol, reducing plasma cholesterol levels
    b. This reduces the development of atherosclerotic plaques
  3. Some statins may have additional pleiotropic effects (i.e. additional benefits unrelated to lowering cholesterol levels)
37
Q

List 2 indications for statins.

A

Familial hypercholesterolaemia

Prevention of CVD in high risk patients

38
Q

List 3 common side effects of statins.

List 2 uncommon side effects of statins.

A

COMMON SIDE EFFECTS:
Myalgia
GI disturbance
Deranged LFTs

RARE SIDE EFFECTS:
Myopathy
Rhabdomyolysis

39
Q

Describe important pharmacokinetics/dynamics of statins. (2)

A

Hypothyroidism should be corrected before assessing need for statins
Myalgia and rhabdomyolysis are dose related, so start low

40
Q

What would you tell the patient when prescribing statins? (2)

A

Report any unexplained muscle pain to GP (to check serum creatinine kinase)
Diarrhoea and abdominal pain may occur initially