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Cardiac drugs Flashcards

1
Q

Loop diuretic

A

Furosemide

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2
Q

Indications of furosemide (3)

A

Relief of breathlessness in pulmonary oedema
Symptomatic treatment of fluid overload in CHF (1st line)
Symptomatic treatment of fluid over load in other oedematous stated (e.g. renal/kidney failure)

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3
Q

Main side effects of furosemide (4)

A

Ototoxicity - tinnitus and hearing loss at high doses due to blockage of transporter in the ear
Hyperuricaemia
Hyperglycaemia
Hypokalaemia

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4
Q

What part of the nephron does furosemide act on?

A

Loop of Henle

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5
Q

What transporter channel does Furosemide inhibit?

A

Na+/K+/2Cl- co-transporter
Ca
Inhibits ion transport from the lumen into epithelial cells, thus reducing the gradient for osmosis, having a diuretic effect

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6
Q

Other effects of furosemide (1)

A

Dilation of capitance veins, reducing preload and improving contractile function

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7
Q

Metabolism and excretion of furosemide

A

Hepatic metabolism
Renal glucuronidation
Renal and biliary excretion

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8
Q

Interactions of furosemide

A

Aspirin and salicylates - may potentiate effects
Synergistic effects with other antihypertensives and diuretics
Affects drugs excreted by the kidneys (e.g. lithium and digoxin, aminoglycosides), risking toxicity

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9
Q

Thiazide diuretic

A

Bendroflumethiazide

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10
Q

This drug is used when CCBs, ACEIs and ARBs are insufficient in the control of hypertension

A

Bendroflumethiazide

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11
Q

Side effects of bendroflumethiazide (2)

A

Hyponatraemia

Hypokalaemia -> arrhythmias

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12
Q

Bendroflumethiazide acts on what part of the nephron?

A

Distal convoluted tubule

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13
Q

Bendroflumethiazide takes its action through inhibition of which channel?

A

Na+/Cl- transporter

Increases sodium and chloride ion secretion, with water following

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14
Q

Contraindications of bendroflumethiazide

A

Hypoklaemia
Hyponatraeima
Gout (reduces uric acid secretion)

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15
Q

Interactions of bendroflumethiazide (3)

A

Alcohol - causes sudden drop in BP
NSAIDs - reduces effectiveness
Other thiazides that lower potassium (e.g. furosemide)

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16
Q

Potassium-sparing diuretic

A

Spironolatone

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17
Q

Indications of spironolactone (2)

A

Combination therapy for treatment of hypokalaemia

Hypertension

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18
Q

Side effects of spironolactone

A

Dizziness, hypotension and urinary symptoms

May lead to hyperkalaemia - potentially fatal

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19
Q

MoA of spironolactone

A

Antagonist of mineralocorticoid receptor
Competitive antagonist of aldosterone
Increases sodium excretion and reduces potassium loss

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20
Q

Site of action of spironolactone

A

DCT

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21
Q

Metabolism and excretion of spironolactone

A

Hepatic metabolism to active metabolites

Urinary and biliary excretion

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22
Q

Interactions of spironolactone (4)

A

Avoid using with potassium supplements (hyperkalaemia)
Increased likelihood of hyperkalaemia with trimethoprim/sulphamethoxazole
Induces CYP3A4
Increases serum digoxin concentration

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23
Q

Beta blocker

24
Q

Indications of atenolol (5)

A

Management of hypertension when other hypertensives are insufficient
1st line IHD to improve Sx and prognosis
CHF - first line
AF - reduced ventricular rate and maintains sinus rhythm
SVT - first line in patients with circulatory compromise to restore sinus rhythm

25
Serious side effect of beta-blockers
Bronchospasm in patients with asthma - mediated by blockade of beta-2 adrenoceptors in the airways
26
MoA of atenolol
Beta-1 adrenoceptor blocker (mainly in the heart) Reduce speed of conduction and force of contraction, relieving myocardial ischaemia by reducing cardiac work and oxygen demand, increasing myocardial perfusion Protect the heart from the effects of chronic sympathetic stimulation Prolong refractory period of AVN (treatment of SVT) Reduce renin secretion from the kidney (metabolised by beta-1 adrenoceptors) - Rx of hypertension
27
Excretion and metabolism of atenolol
Excretion is renal and lactic in lactiferous females | Metabolism is hepatic
28
Interactions of atenolol (1)
Non-dihydropyridine CCBs - verapamil, diltiazem | Can cause HF, bradycardia and asystole
29
Thrombolytic
Tissue Plasminogen Activator (tPA)
30
Indications of tPA (3)
Management of MI, acute ischaemic stroke, and lysis for acute pulmonary emboli
31
Side effect of tPA
Haemorrhage, IC bleeding (high dose)
32
Contraindication
Haemorrhagic stroke
33
MoA of tPA
Bind fibrin in thrombi and convert pladminogen to plasmin which degrades the fibrin matrix of the thrombus Also produces conversion of plasminogen in the absence of fibrin
34
Metabolism of tPA
Hepatic
35
Interactions of tPA
Coumarin derivatives, oral anti-coagulants, platelet aggregation inhibitors, unfractioned heparin, LMWH or active substances interfering with coagulation - risk of haemorrhage Use of GPiib/iiia antagonists - increased risk of bleeding
36
Statin
Simvastatin
37
Indications of simvastatin (3)
1. Primary prevention of CVD 2. Secondary prevention of CVD 3. Primary hyperlipidaemia (1st line in hypercholesterolaemia)
38
Side effects of statins
Muscle ache, myopathy and rarely, rhabdomyolysis
39
Contraindications of statins
Renal impairment and pregnancy and breastfeeding (cholesterol is essential for foetal growth)
40
MoA of simvastatin
Inhibition of HMG coenzyme A reductase - decrease cholesterol production by the liver and increased clearance of LDL from the blood Directly reduce triglycerides and increase HDL level Slow and reverse the atherosclerotic process
41
Metabolism and excretion of simvastatin
Hepatic metabolism by CYP3A4 | Renal and faecal excretion
42
Interactions of simvastatin
Metabolism reduced by CYP450 inhibitors - amiodarone, diltiazem, itraconazole, macrolides, protease inhibitors - reduces risk of adverse effects due to accumulation
43
Novel anticoagulant
Rivaroxaban
44
Indications of rivaroxaban (4)
1. Prevention of VTE in pts undergoing joint replacement 2. Prevention of stroke and ischaemic embolism in pts with non-valvular AF 3. Treatment of DVT and PE 4. Reduce risk of recurrent DVT and PE
45
Side effects of rivaroxaban
Bleeding (but lower rate than warfarin) Renal toxicity Liver impairment
46
MoA of rivaroxaban
Inhibition of free and clot-bound factor Xa, which activates prothrombin (ii) to thrombin (iia) One molecule of factor Xa can generate > 1000 molecules of thrombin Action is irreversible
47
Metabolism and excretion of rivaroxaban
Metabolism: CYP3A4 and CYP2J2 Excretion: renal
48
Interactions of rivaroxaban
CYP3A4 and P-gp inhibitors e.g. ketoconazole and ritonavir - increased risk of bleeding Othe anticoagulants - increased risk of bleeding NSAIDs/platelet aggregation inhibitors e.g. clopidogrel - increased risk of bleeding CYP3A4 inducers - reduced plasma concentrations - thrombosis
49
Nitrate
Isosorbide mononitrate
50
Indications of isosorbide mononitrate (2)
1) Prophylaxis of angina | 2) Treatment of pulmonary oedema, usually with furosemide and oxygen
51
Side effects of isosorbide mononitrate
Headache, hypotension | Can lead to tolerance - minimise dose to avoid unnecessary administration
52
MoA of isosorbide mononitrate
Converted to nitric acid which increases CMP synthesis and reduces IC calcium in vascular SMCs, causing relaxation and vasodilation
53
Effects on isosorbide mononitrate
Relaxation of venous capacitance vessels, reducing cardiac preload and LV filling - these effects reduce cardiac work and oxygen demand, relieving angina and cardiac failure
54
Metabolism and excretion of isosorbide mononitrate
Hepatic metabolism | Renal excretion
55
Interactions of isosorbide mononitrate (4)
Phosphodiesterase inhibitors (viagra, slidenafil) - enhance and prolong hypotensive effects Antihypertensives - hypotension Propranolol - causes fall in portal pressure, reduction in hepatic flow and CO, and mean arterial BP Calcium antagonists - orthostatic hypotension when used in combination
56
Anti-dysrrhythmic
Amiodarone
57
Indications of amiodarone
Management of tacchycardias - AF, atrial flutter, SVT, VT, refractory VF

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