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Year 3 Drug Formulary > Cardiovascular drugs > Flashcards

Cardiovascular drugs Flashcards

1
Q

What type of diuretic is furosemide?

A

Loop diuretic (inhibits salt and water reabsorption from ascending limb of loop of Henle)

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2
Q

When should furosemide be used?

A

Pulmonary oedema due to LVF, chronic heart failure, oedema, resistant HTN

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3
Q

Important furosemide interactions?

A

NSAIDs may reduce effect of drug
K+ loss leads to digoxin toxicity
Increased risk of ototoxicity with aminoglycosides, colistin and vancoymcin
Increased risk of nephrotoxicity with aminoglycosides
Increased risk of toxicity with lithium

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4
Q

What type of diuretic is bendroflumethiazide?

A

Thiazide diuretic - inhibits Na+ and water reabsorption in distal convoluted tubule

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5
Q

3 states/conditions thiazide diuretics should be avoided?

A 
Refactory hypokalaemia, hyponatraemia and hypercalcaemia
Symptomatic hyperuricaemia
Addison's disease
Sever liver disease
Gestational HTN
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6
Q

Bendroflumethiazide administration alongside what can lead to arrhythmias?

A

Terfenadine, as diuretics can cause electrolyte disturbances –> more at risk of arrhythmias

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7
Q

What type of drug can increase K+ loss with thiazide diuretics?

A

Corticosteroids

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8
Q

How do thiazide diuretics work to reduce HTN?

A

Initial decrease in cardiac output due to reduced fluid volume but long term effect is due to reduced total peripheral resistance

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9
Q

What type of diuretic is spironolactone?

A

K+ sparing diuretic and aldosterone antagonist

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10
Q

How does spironolactone produce its effects?

A

Competitive inhibitor of aldosterone and acts on distal portion of renal tubule thereby increasing NA+ and H2O excretion and reducing K+ excretion

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11
Q

Indictations for spironolactone?

A

Oedema and ascites in liver cirrhosis, malignant ascites, nephrotic syndrome, oedema in congestive heart failure, resistant HTN, primary hyperaldosteronism

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12
Q

Contra-indications for spironolactone?

A

Addison’s disease, hyperkalaemia, anuria

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13
Q

What drugs can increase K+ levels and potentiate spironolactone?

A

ACE-i, NSAIDs, ARBs, cyclosporine, tacrolimus, potassium salts

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14
Q

Which diuretics are more effective: loop or thiazide?

A

Loop diuretics are more effective

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15
Q

Examples of cardioselective (B1) B-adrenoreceptor blockers?

A

Atenolol, propanolol, carvedilol

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16
Q

Effects of beta-blockers?

A

Decrease HR and force, reduce renin production by kidneys, decrease conduction in heart (anti-arrhythmic effect)

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17
Q

Which drugs may reduce the antihypertensive effects of beta blockers?

A

Decongestants and NSAIDs

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18
Q

What drug when given with beta blockers may mask symptoms of hypoglycaemia?

A

Insulin

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19
Q

What class of drugs are diltiazem and amlodipine?

A

Ca2+ channel blockers

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20
Q

How do calcium channel blockers work?

A

Selectively reduce calcium entry into vascular smooth muscle and myocardial cells thus lowering intracellular calcium so less activation of contractile proteins resulting in coronary artery dilation and therefore increased oxygen supply

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21
Q

Indications for diltiazem?

A

Angina, HTN, dysrrhythmias

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22
Q

Which drug is known to undergo extensive 1st pass metabolism and which drug undergoes no 1st pass metabolism?

A

Diltiazem
and
Isosorbide Mononitrate

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23
Q

Why is it important not to suddenly withdraw diltiazem?

A

May exacerbate angina

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24
Q

Examples of ACE inhibitors?

A

Ramipril, lisinopril

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25
Q

What do ACE inhibitors prevent?

A

Conversion of Angiotensin I to Angiontensin II and the downstream effects of this

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26
Q

Why is persistent dry cough sometimes a side effect of ramipril use?

A

Bradykinin can accumulate

27
Q

When should the first dose of ramipril be taken?

A

Before bed to avoid 1st dose hypotension

28
Q

Example of Angiontensin Receptor Blocker?

A

Losartan - behave similarly to ACE-i but don’t cause cough as they don’t inhibit bradkinin breakdown

29
Q

In which group of patients are ARBs less effective?

A

Black people

30
Q

How does Isosorbide Mononitrate (belonging to nitrate drug class) produce its effect?

A

Acts as a donor of NO to relax vascular smooth muscle, decreasing preload and therefore increases oxygen to myocordium

31
Q

Indications for nitrates use?

A

Angina prophylaxism, adjunct in congestive heart failure

32
Q

What cardiac conditions are contra-indicators for Nitrates use?

A

Hypertrophic cardiomyopathy, Aortic stenosis, cardiac tamponade, constrictive pericarditis, mitral stenosis. Also don’t use in toxic pulmonary oedema and raised ICP due to cerebral haemorrhage/trauma

33
Q

A maximum of how many tablets of isosorbide mononitrate should be taken per day?

A

1 as tolerance can be built

34
Q

What drug class is digoxin in?

A

Cardiac glycoside

35
Q

How does digoxin work?

A

Digitalis inhibits NA+/K+ pump, raising intracellular Na+ conc. inhibiting Na+/Ca++ pump so less Ca++ pumped out of cell so greater force of contraction. Vagal activity is increased so decreased HR and AV node conduction

36
Q

Indications for digoxin?

A

Heart failure, supraventricular tachycardias

37
Q

What drugs increase risk of digoxin toxicity?

A

Antiarrhythmics, Ca channel blockers, and non-K+ sparing diuretics

38
Q

Does digoxin have a narrow therapeutic index?

A

Yes

39
Q

What class of drug is Amiodarone?

A

Anti-dysrhythmic (when other drugs can’t be used)

40
Q

How does amiodarone work?

A

Slows impulses in heart, prolongs refractory period in all parts of the conduction system

41
Q

Why is amiodarone often a last drug of choice?

A

Serious side effects including, N+V, metallic taste, jaundice, reversible corneal microdeposits causing night glare, photosensitivity, pulm. toxicity, tremor, sleep disturbances, altered thyroid function, grey skin discolouration, cough, SOB. Can also worsen arrhythmias!

42
Q

Amiodarone interaction with phenytoin and warfarin?

A

Inhibits their metabolism

43
Q

How does aspirin work to produce its effects?

A

Aspirin is a weak acid, pronated in stomach, crosses the mucosa, absorbed in ileum, hydrolysed to form esterase, enters active site of COX1 and 2 and acetylates serine 530 irreversibly inactivating them so reduces PGE2 and TXA2 production

44
Q

Which group of patients must not be given aspirin?

A

Children (under 16s) due to risk of Reye’s syndrome (hepatic encephalopathy after acute viral illness).
Also avoid in: peptic ulceration, haemophilia, gout, severe liver and kidney disease.

45
Q

What symptoms are seen in Salicylism (a potential side effect of aspirin use)?

A

Tinnitus, vertigo, reduced hearing, N+V

46
Q

How does clopidogrel work?

A

Inhibits platelet aggregation and thrombus formation in arterial circulation

47
Q

What class of drug is streptokinase?

A

Thrombolytics

48
Q

Why can streptokinase be used twice in the same year?

A

The body develops antibodies to it

49
Q

How do heparins/LMWH (such as enoxaparin) work?

A

Activate Antithrombin III thus inhibiting, in particular Factor Xa.

50
Q

What are LMWHs used for?

A

Venous thromboses (DVT/PE) and VTE prophylaxis

51
Q

What drugs increase the risk of hyperkalaemia in heparin use?

A

ACE-i and potassium supplements

52
Q

Considering heparin use, what can be the result of antithrombin III deficiency?

A

Heparin resistance and thrombophilia

53
Q

What can be used to reverse the effects of heparins?

A

IV protamine sulfate

54
Q

How does the oral anticoagulant warfarin work?

A

Inhibits synthesis of vitamin K dependent clotting factors (2,7,9,10) by inhibiting vitamin K epoxide reductase

55
Q

Indications for warfarin?

A

Prophylaxis of embolisation in rheuamtic heart disease, AF, VTE and PEs. Prophylaxis after prosthetic heart valve insertion. TIAs.

56
Q

After how long does warfarin begin to have its effect?

A

2-3 days

57
Q

What is the target INR for warfarin use?

A

2-3 (lower the number, more likely to clot)

58
Q

Examples of novel oral anticoagulants?

A

Rivororaxaban, Dabigatran, Apixaban

59
Q

How does rivoroxaban work?

A

Highly selective direct factor Xa inhibitor, preventing thrombus formation. (No effect on platelets)

60
Q

Examples of statins?

A

Simvastatin, atorvastatin, fluvastatin

61
Q

How do statins work?

A

Competitive, reversible inhibiton of HMG CoA reductase, preventing cholesterol synethesis. Response is increased LDL receptor expression, LDL cellular intake, reduced plasma tricglyceride conc.

62
Q

Side effects of statins?

A

MYALGIA, myopathy, myositis, rhabdomyolysis, altered LFTs, sleep and GI disturbances, abdominal pain

63
Q

When should statins be taken?

A

At night, full effect within 6 weeks

Year 3 Drug Formulary (10 decks)

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