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Medicine: Pharmacology > Cardio > Flashcards

Cardio Flashcards

0
Q

Mode of action of furosemide

A

Short acting, within an hour, diuresis takes 6 hrs

  • acts on the ascending loop of henle to inhibit Na/K/2Cl pump causing inhibition of Na K and water reabsorption, leading to an increased loss of salt, water K
  • blood becomes hypovolaemic, reducing BP
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1
Q

Drug class of furosemide

A

Loop diuretic

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2
Q

Indications for furosemide

A
  • pulmonary oedema (secondary to left ventricular failure)
  • chronic HF - oedema
  • oliguria secondary to renal failure
  • resistant hypertension
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3
Q

Contraindications of furosemide

A

Hypovolaemia
Dehydration
Hyponatraemia (severe)
Comatose States (associated with liver cirrhosis)

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4
Q

Side effects of furosemide

A

Mild GI disturbances
Hypotension
Hyperglycaemia
Electrolyte disturbance

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5
Q

Which type of diuretic, loop or thiazide, is more likely to cause hyperglycaemia as a side effect ?

A

Thiazide

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6
Q

When May a particularly high dose of furosemide be required ?

A

In renal impairment - may cause deafness as a side effect

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7
Q

What are the possible interactions of furosemide ?

A

Antibacterials: increased risk of ototoxicity with amino glycosides, colistin, vancomycin
Digoxin: furosemide-induced hypokalaemia with digoxin causes arrhythmias

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8
Q

What class of drug is bendoflumethiazide

A

Thiazide diuretic

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9
Q

How do thiazide diuretics work ?

A

Inhibit sodium reabsorption at the beginning of the distal convoluted tubule

  • act within 1to 2 hrs
  • diuresis usually takes 12 to 24 hrs, usually given early in day so doesn’t interfere with sleep
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10
Q

Indications for bendoflumethiazide

A

Oedema
Hypertension (alone in mild or combo in severe)
Mild to moderate HF

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11
Q

Contraindications of bendoflumethiazide

A
  • (Refractory) hypokalaemia, hyponatraemia, hypercalcaemia
  • (symptomatic) hyperuricaemia
  • Addison’s disease (primary adrenal insufficiency)
  • caution with: gout, diabetes, SLE
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12
Q

Side effects of bendroflumethiazide

A 
GI disturbances 
Postural hypotension
Altered plasma/lipid concentrations 
Metabolic/electrolyte disturbances 
Gout
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13
Q

Possible interactions of bendroflumethiazide

A

Digoxin: hypokalaemia caused by diuretic with digoxin can cause dysthymia
Lithium: increases excretion further causing inc plasma conc and inc risk of toxicity

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14
Q

What drug class is spironalactone

A

Potassium sparing diuretic

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15
Q

How does spironalactone work ?

A

Acts on receptors in distal Tubule: competitive inhibition if aldosterone
Inhibits Na retention; increased Na excretion

(Often given in combo with another diuretic instead of potassium supplements)

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16
Q

Indications for spironalactone

A 
Oedema
Ascites (cirrhosis of liver, malignant)
Nephrotic syndrome
Congestive heart failure
Primary hyperaldosteronism (conn syndrome)
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17
Q

Contraindications of spironalactone

A

Hyperkalaemia
Hyponatraemia
Anuria
Addison’s disease (primary adrenal insufficiency)

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18
Q

Side effects of Spironolactone ?

A 
GI disturbances
Impotence
Gynaecomastia 
Menstrual irregularities
Lethargy/headache/confusion
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19
Q

Possible. Interactions of Spironolactone

A

Can increase blood levels of other drugs due to hypovolaemia, therefore increasing their potency

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20
Q

Why a class of drug is atenolol?

A

Beta blocker

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21
Q

How do beta blockers work ?

For hypertension, anti-arrhythmic, angina

A

Acts on beta 1 receptors in the heart (peripheral vasculature, bronchi, pancreas and liver)

  • Decreases HR and force of contraction therefore decreasing workload of the heart
  • reduced renin production from kidneys = anti-hypertensive
  • reduced conduction/AP initiation of heart = anti-arrhythmic
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22
Q

Indications for atenolol

A 
Hypertension 
Angina
Supra ventricular dysrhymias
MI prophylaxis
Migraine prophylaxis
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23
Q

Contraindications for atenolol

A 
Asthma
HF
2nd/3rd degree heart block
Bradycardia
COPD
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24
Q

Side effects of atenolol?

A 
Lethargy
Bradycardia
Cold extremities
AV block 
Sleep disturbance/nightmares
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25
Q

Which beta blockers are less likely to cause nightmares as a side effect ?

A

Those that are water soluble e.g. Atenolol, celiprolol, nadolol, sotalol

  • less likely to to enter brain
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26
Q

Possible interactions of atenolol

A

Verapamil: increased risk of HF/bradycardia/AV block
Insulin: masks symptoms of hypoglycaemia
Diltiazem: (ca channel blocker) increased risk of bradycardia/AV block

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27
Q

What drug class is diltiazem ?

A

Calcium channel blocker

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28
Q

How do calcium channel blockers work ?

A

Inhibit Ca influx into vascular smooth muscle and myocardium by inhibiting L-type Ca channel
Causing relaxation of vascular smooth muscle which results in:
- decreased myocardial contractility
- decreased conduction at AV node (inc refractory period)
- decreased after load and HR meaning decreased oxygen consumption

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29
Q

Which calcium channel blockers should usually be avoided in heart failure and why ?

A

They may further depress cardiac function and cause significant clinical deterioration

Can use dihydropyridine ca channel blockers instead e.g. Amlodipine etc which have more effect on the vessels and less on the myocardium

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30
Q

Indications for diltiazem

A

Angina (prophylaxis and treatment)
Hypertension (longer acting formulation used)
* may be used in patients who are contraindicated to beta blockers or ineffective*

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31
Q

Contraindications of diltiazem

A

Severe bradycardia
Heart failure
2nd/3rd degree heart block
Pregnancy/breastfeeding

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32
Q

Side effects of diltiazem

A

Headache, nausea, dizziness, hypotension, bradycardia, ankle swelling

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33
Q

Possible interactions of diltiazem

A

Antiarrythmics: cause increased myocardial depression
Beta blockers: increased risk of AV block/bradycardia
Causes increased plasma conc of cyclosporins and digoxin

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34
Q

What class of drug is ramipril ?

A

Ace inhibitor

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35
Q

How do ace inhibitors work ?

A

Inhibits angiotensin converting enzyme, causing:

  • decreased angiotensin 2 synthesis = decreased peripheral resistance/fluid overload
  • increased bradykinin = peripheral vasodilation
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36
Q

Indications for ramipril ?

A

Hypertension
Heart failure
Post-MI
Diabetic neuropathy

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37
Q

Which medications should be stopped before starting an ACE inhibitor for treatment of HF in order to avoid hyperkalaemia?

A

Potassium supplements and potassium sparing diuretics

*note: low dose Spironolactone in severe HF may be beneficial if serum potassium levels monitored carefully *

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38
Q

An ACE Inhibitor may be most appropriate initial drug for hypertension in which patients ?

A

Younger Caucasian

Respond less well:
Afro Caribbean
Aged over 55
Primary aldosteronism

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39
Q

Why are ACE inhibitors particularly indicated for hypertension in patients with type 1 diabetes with nephropathy ?

A

ACE inhibitors potentate the hypoglycaemic effect of insulin and oral antidiabetic drugs

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40
Q

Contraindications of ramipril

A 
Renovascular disease
Aortic stenosis
Pregnancy
Acute porphyria
Angioedema
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41
Q

Common side effects of ramipril ?

A

Postural hypertension
Dry cough
Renal impairment
GI & other upper resp

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42
Q

Possible interactions of ramipril ?

A

Diuretics = pronounced hypotension
K- sparing diuretic = inc risk hyperkalaemia
Lithium & NSAIDs = inc plasma conc
NSAID also risk of renal damage

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43
Q

What class of drug is losartan ?

A

Angiotensin 2 receptor antagonist

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44
Q

In what way are AT2 blockers different to ACE inhibitors ?

A

Do not inhibit the breakdown of bradykinin- therefore unlike,y to cause persistent dry cough

45
Q

Indications for losartan ?

A 
Hypertension 
Chronic HF (when ACEi unsuitable)
Diabetic nephropathy in type 2 diabetes
46
Q

Contraindications of losartan

A 
Pregnancy/breastfeeding
Caution with:
Renal artery stenosis
Aortic or mitral valve stenosis 
Hepatic or renal impairment
47
Q

Possible interactions of losartan

A

Antibacterials: plasma conc of losartan its active metabolite reduced by rifampicin

48
Q

Side effects of losartan

A

Hypotension/ dizziness
Hyperkalaemia occasionally

usually very MILD

49
Q

How do cardiac glycoside drugs work ?

A

Reduce conductivity within AV Node
- increased AV refractory period -> decreased HR
Increase force of contraction of myocardium
- inhibits Na/K pump causing increased intracellular conc of Na which in inhibits Na/Ca pump -> less Ca pumped out, increased intracellular Ca -> increased force of contraction

50
Q

What is the most commonly used cardiac glycoside ?

A

Digoxin

51
Q

Why is digoxin rarely used for rapid control of heart rate ?

A

Even with IV admin response may take hours

52
Q

For what are cardiac glycosides most useful for ?

A

Controlling ventricular response in atrial fibrillation and flutter

53
Q

What electrolyte disturbance predisposes to digitalis toxicity in patient taking digoxin ?

A

Hypokalaemia

54
Q

Indications for digoxin

A

Supraventricular arrhythmias - Atrial fibrillation and flutter
HF (sinus rhythm, unresponsive to ACE inhibitors, b blocker and diuretic)

55
Q

What is the effect of digoxin on heart failure ?

- how affects symptoms, exacerbation, mortality

A

Improves symptoms and exercise tolerance
Reduces hospitalisation due to acute exacerbations
Does not reduce mortality

56
Q

Contraindications of digoxin

A

Complete heart block
Wolff-Parkinson-white syndrome
Ventricular tachycardia or fibrillation
Hypertrophic cardiomyopathy

57
Q

Possible interactions of digoxin

A

Increased risk of digoxin toxicity with:

Antiarrythmics: Amiodarone, propafenone, quinidine
Ca channel blockers
Diuretics

58
Q

Side effects of digoxin

A

Nausea, vomiting, anorexia, diarrhoea

Visual disturbances

59
Q

What class of drug is isosorbide mononitrate ?

A

Nitrate

60
Q

How do nitrates work?

A

Metabolised to NO in smooth muscle cells causing activation of guanylyl cyclise, which causes vascular smooth muscle relaxation resulting in vasodilation of coronary arteries and systemic veins = decreased preload and increased oxygen supply to myocardium
+ reduction in venous return reducing left ventricular work

61
Q

Indications for isosorbide mononitrate

A

Angina prophylaxis

Congestive heart failure

62
Q

Contraindications of isosorbide mononitrate

A

Hypotension/hypovolaemia
Hypertrophic cardiomyopathy
Aortic/mitral stenosis

63
Q

Side effects of isosorbide mononitrate ?

A

Headache, dizziness, postural hypertension, flushing, tachycardia

64
Q

Interactions of isosorbide mononitrate

A

Sildenafil (Viagra): increased hypotensive effects

65
Q

How can nitrate tolerance be avoided when taking isosorbide mononitrate ?

A

Drug free periods of 8 hours

66
Q

How do beta blockers act as anti arrhythmics?

A

By attenuating the effects of sympathetic nervous system on automaticity and conductivity within the heart

67
Q

What class of drug is amiodarone ?

A

(Class III) anti arrhythmic

68
Q

What is the mechanism of action of amiodarone ?

A

Block K+ channels, slowing cell depolarisation and increasing refractory period; also blocks Na, Ca channels and beta receptors

69
Q

Indications for amiodarone

A

Ventricular fibrillation
Haemodynamically unstable ventricular tachycardia
Wolff-Parkinson-White tachyarrhythmias

70
Q

Contraindications of amiodarone ?

A

Severe sinus node dysfunction causing bradycardia
2nd/3rd degree heart block
Hepatitis
Thyroid dysfunction

71
Q

What function tests should be monitored before treatment with amiodarone and then every 6 months ?

A

Liver and thyroid function

72
Q

Side effects of amiodarone

A 
Arrhythmia
Nausea/vomiting
Skin discolouration
Vision disturbances
Photo sensitivity 
Thyroid disorders 
Hepatotoxicity
73
Q

Possible Interactions of amiodarone

A

B blockers and diltiazem /verapamil: increased risk of bradycardia, AV block and myocardial depression
Digoxin and phenytoin: increased risk of toxicity
Warfarin: inhibits warfarin metabolism, increased risk of bleeding

74
Q

What drug class is aspirin ?

A

Anti platelet/salicylate

75
Q

Mechanism of action of aspirin ?

A 
Inhibits cyclooxygenase (COX) enzymes;
Anti platelet actions due to irreversible acetylation of COX1 in platelet preventing their activation
76
Q

Indications of aspirin

A

Acute MI & primary/secondary prophylaxis
Secondary prophylaxis of cerebrovascular events
Analgesic, antipyretic, anti inflammatory

77
Q

Contraindications of aspirin

A

Active peptic ulcer
Bleeding disorders
NSAID/aspirin hypersensitivity
Breast feeding (Reyes syndrome)
Caution with:asthma, third trimester of pregnancy
not to be given <16yrs unless for anti-platelet

78
Q

Elimination of aspirin hepatic or renal ?

A

Renal

79
Q

Side effects of aspirin ?

A

Dyspepsia
Urticaria
Bronchospasm
GI bleeding/ulceration

80
Q

What drug class is clopidogrel ?

A

Anti platelet: adenosine diphosphate (ADP) receptor blocker

81
Q

Mechanism of action of clopidogrel ?

A

Inhibits platelet activation by blocking the actions of ADP on P2Y12 (subtype of ADP receptor) which inhibits eventual cross linking by fibrin (aggregation)

82
Q

Indications for clopidogrel

A

Prevention of atherosclerotic events in PAD + STEMI

Post MI/Ischaemic stroke

83
Q

Contraindications of clopidogrel

A

Active bleeding
Severe hepatic impairment (bleeding risk)
Pregnancy and breastfeeding

84
Q

Side effects of clopidogrel ?

A

Diarrhoea, dyspepsia, abdo pain
Rash
Haemorrhage

85
Q

Possible interactions of clopidogrel ?

A

NSAIDS and aspirin increase risk of bleeding

86
Q

What class of drug is streptokinase ?

A

Thrombolytic

87
Q

How do Thrombolytic drugs work ?

A

Promote conversion of plasminogen to plasmin. Plasmin is a proteolytic enzyme which dissolves the clots

88
Q

Indications for streptokinase ?

A
  • Acute MI (within 12hrs, preferably within 1) - biggest benefit in this with STEMI (anterior infarct) and bundle branch block
  • DVT
  • PE
  • acute arterial thromboembolism
  • central retinal venous or arterial thrombosis
89
Q

Contraindications of streptokinase

A

Recent haemorrhage, trauma, surgery
Coagulation defects, bleeding conditions, aortic dissection, aneurysm

anything that will increase risk of bleeding

90
Q

Side effects of streptokinase

A 
Nausea/vomiting
Bleeding
Reperfusion arrhythmias, recurrent Ischaemia, angina (MI), cerebral oedema 
Hypotension
Fever
91
Q

Interactions of streptokinase

A

Activated by liver enzyme cytochrome p450:

Decreased warfarin metabolism, more in blood, increased risk of bleeding

92
Q

What drug class is enoxaparin

A

Heparin (LMWH)

93
Q

Why are low molecular weight heparins usual,y preferred over unfractionated heparin in the prevention of venous thromboembolism ?

A

As LMWHs are equally as effective with less risk if heparin induced thrombocytopenia
Also don’t require monitoring and have longer duration if action so can use once daily for convenience

94
Q

Indications for enoxaparin

A 
PE
DVT
Prophylaxis of thromboembolic disorders 
Unstable angina
STEMI and non-Q-wave MI
95
Q

Contraindications of enoxaparin

A 
Active bleeding 
Neonates
Severe liver disease
Peptic ulcer
Bacterial endocarditis
96
Q

Side effects of enoxaparin ?

A

Haemorrhage
Thrombocytopenia
Elevated liver aminotransferases

97
Q

Possible interactions of enoxaparin

A

Aspirin increased risk of bleeding

98
Q

What is the main route of elimination of enoxaparin ?

A

Renal

99
Q

What drug class is warfarin ?

A

Vitamin k antagonist (anticoagulant)

100
Q

Mechanism of action of warfarin ?

A

Prevents activation of vitamin k, a key cofactors in the coagulation cascade, therefore inhibiting coagulation

Clotting factors 2,7,9&10 dependent on vit k

101
Q

Indications of warfarin ?

A

Prophylaxis of embolisation in rheumatic heart disease and AF
Prophylaxis after prosthetic heart valves
Prophylaxis after treatment of PE and venous thrombosis
TIA

102
Q

Contraindications of warfarin

A

Peptic ulcer
Severe hypotension
Pregnancy (1st and 3rd trimester) & avoid breastfeeding
Severe Renal or kidney disease

103
Q

Main route of elimination for warfarin ?

A

Liver

104
Q

Side effects of warfarin

A

Haemorrhage
Headache
Nausea/vomiting/diarrhoea
Purple toe syndrome

105
Q

Possible interactions of warfarin

A

Amiodarone : increases effect of warfarin by inhibiting metabolism (cyt P450)
Cranberry juice: increased anticoagulant effect

106
Q

How do statins work ?

A

Competitively inhibit HMG CoA-Reductase, the key enzyme in cholesterol synthesis, therefore reducing cholesterol production

107
Q

Indications for simvastatin

A

Hypercholesterolaemia/hyperlipidaemia

Prophylaxis of CV events in those with atherosclerotic disease/diabetes

108
Q

Contraindications of simvastatin

A

Active liver disease

Pregnancy/breast feeding

109
Q

Side effects of simvastatin

A

Myositis -> rhabdomyolysis (rare but significant)
GI disturbances
Rarely pancreatitis, anaemia

110
Q

Possible interactions of warfarin

A

Cyclosporins and fibrates: increased risk of myositis

Warfarin: increased effects of warfarin

111
Q

Elimination of warfarin

A

Liver

Medicine: Pharmacology (10 decks)

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