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Year 1 Systems (JBR) > Cardio Drugs > Flashcards

Cardio Drugs Flashcards

1
Q

What is Ivabradine?

A

Selective blocker of HCN channels

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2
Q

What is the effect of ivabradine?

A

Reduces slope of pacemaker potentialSlow HR reduces oxygen consumption

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3
Q

What are the side effects of ivabradine?

A

Arrythmias

Hypotnesion

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4
Q

What are examples of beta-adrenoceptor agonists?

A

Dobutamine (beta-1 selective)
Adrenaline
Noradrenaline

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5
Q

What is the mechanism of a beta-adrenoceptor agonist?

A

Results in stimulation of adenylyl cyclase and production of cAMP which generates protein kinase A

Phosphorylation increases Ca-influx & CICR

Increased contractility, force and rate

Decrease cardiac efficiency

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6
Q

What are side effects of beta-adrenoceptor agonists?

A

Arrhythmias

Acute MI

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7
Q

What is an example of a non-selective beta-blocker?

A

Propranolol

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8
Q

What is an example of a selective for beta-1 beta blocker?

A

Metprolol

Atenolol

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9
Q

What is the effect of a beta blocker?

A

Decrease HR, contractility and MAP

Decrease O2 consumption

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10
Q

What are the side effects of beta-blockers?

A 
Asthma
Fatigue
Cold peripheries
Heart failure 
Bradycardia (heart block)
Hypoglycaemia
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11
Q

What is an example of a non-selective muscarinic antagonist?

A

Atropine

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12
Q

What is the effect of atropine?

A

Increase heart rate

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13
Q

What are the side effects of atropine?

A

Arrythmias
Hallucinations
Confusion

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14
Q

What type of drug is digoxin?

A

Cardiac glycoside

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15
Q

What is the mechanism of of digoxin`

A

Competes with K+ at the alpha subunit and blocks the Na/K/ATPase pump
Increase contractility by backing the sarcolemma ATPase

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16
Q

What are the indirect effects of digoxin?

A

Increased vagal activity, slows SA node discharge

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17
Q

What re the direct effects of digoxin?

A

Shortens action potential and refractory period

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18
Q

What are the overall effects of digoxin?

A

Increase force, contraction and CO

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19
Q

The effects of digoxin are dangerously enhanced with?

A

Hypokalaemia

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20
Q

What are the side effects of digoxin?

A

Heart block
Dysrhythmias
Myocarditis

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21
Q

What is Levosimendan?

A

Calcium sensitizer

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22
Q

What is the mechanism of Levosimendan?

A

Binds to troponin C in myocytes sensitising them to Ca

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23
Q

What are calcium sensitisers used for?

A

Acutely decompensated congestive heart failure

Increased contractility

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24
Q

What are the side effects of calcium sensitisers?

A

Headaches
Arrhythmias
Hypokalaemia

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25
Q

Class I AADs act on?

A

Voltage activated Na+ channels

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26
Q

Example of Class I AAD?

A

Flecainide

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27
Q

What is the effect of Flecainide?

A

Reduce Na channel current

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28
Q

What are the side effects of flecainide?

A

Negative inotropic effects

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29
Q

What is Flecainide used for?

A

Rhythm control

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30
Q

What is an example of a Class II AAD?

A

Propanolol (beta-adrenoceptor)

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31
Q

What is propranolol used for?

A

Rate control

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32
Q

What is an example of a Class III AAD?

A

Amiodarone

Sotalol

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33
Q

What do Class III AADs act on?

A

Activated K channels

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34
Q

What is the effect of Class III AADs?

A

Action potential prolongation

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35
Q

What are Class III AADs used for?

A

Rhythm control

36
Q

What is an example of a Class IV AAD?

A

Verapamil

37
Q

Verapamil is an example of a?

A

Ca channel antagonist

38
Q

Class IV AADs are used to control`

A

rate

39
Q

What are examples of nitrates?

A

Isosobride mononitrate

GTN spray

40
Q

What is the mechanism of nitrates?

A

Mimic effect of endothelium
Produce nitric oxide which is formedthorugh influx of calcium, activation of eNOS and L-arginine
NO caused efflux of calcium producing hyper polarisation and relaxation
cGMP is also produced which regulates protein kinase G activity causing relaxation
Endothelin is also produced

41
Q

What is the effect of nitrates?

A

Venorelaxation (decreased preload and after load, CO maintained as HR increase)
Arteriolar dilation, increased coronary blood flow

42
Q

What are side effects of nitrates?

A

Headache
Hypotension
Tolerance is common

43
Q

What are examples of ACEI?

A

Lisinopril

44
Q

What is the mechanism of ACEI?

A

Block conversion of angiotensin I - II

Aldosterone and ADH not stimulation

45
Q

What is the effect of an ACEI?

A

Vasodilation and arterial dilation

46
Q

What are side effects of ACEI?

A

Dry cough
Renal dysfunction (bas with renal artery stenosis / god for diabetic nephropathy)
Angioneurotic oedema
Fetal abnormalities

47
Q

What is an example of an ARB?

A

Losartan

48
Q

What are side effects of ARBs`

A

Renal dysfunction
Oedema
Contraindicated in pregnancy

49
Q

What are examples of calcium antagonists?

A

Amlodipine
Verapamil
Diltiazem

50
Q

What is the mechanism of calcium antagonsits?

A

Decrease conduction at SA and AV node

Decrease heart rate

51
Q

What are side effects of calcium antagonists?

A

Ankle oedema

Bradycardia

52
Q

What are examples of alpha Blockers?

A

Doxazosin

53
Q

What is the mechanism of alpha blockers`

A

Block alpha-adrenoceptors to cause vasodilation

54
Q

What are side effects of alpha blockers?

A

Postural hypotension

55
Q

What are examples of potassium channel openers?

A

Minoxidil

Nicorandil

56
Q

What is the mechanism of K-channel openers?

A

Causes hyperpolarisation whcih striches of calcium channels
Mediated by ATP
Relaxation of vascular smooth muscle

57
Q

What are side effects of K-channel blockers?

A

Tachycardia

Salt and water retention

58
Q

What is the mechanism of a thiazide diuretic?

A

Inhibit NaCl reabsorption in distal tubules by blocking NaCl co-transporter
Increase excretion of Na, Cl, water – decrease blood volume

59
Q

What is the mechanism of a loop diuretic?

A

inhibit NaCl reabsorption in the thick ascending limb of the loop of Henle
Increase excretion of Na, Cl, water – decrease blood volume

60
Q

What are side effects of diuretics?

A 
Hypokalaemia
Arrythmias
Fatigue
Hyperglycaemia 
Increase uric acid = gout (arthritis due to uric acid deposits)
61
Q

What are examples of statins?

A

Sim/Atorvastatin

62
Q

What is the mechanism of statins?

A

Block HMG CoA reductase which inhibits the formation of cholesterol
Decrease LDL and total cholesterol
Stabilise atherosclerotic plaque and decrease thrombosis

63
Q

What are side effects of statins?

A

Myalgia, myopathy, myositis (rarely rhabdomyolosis)

64
Q

What are examples of fibres?

A

Bezafibrate

Gemfibrozil

65
Q

What is the mechanism of fibres?

A

Agonsit of nuclear receptors which enhances transcription of lipoprotein lipase (LPL) which hydrolyses triglycerides to fatty acids and glycerol

66
Q

What are side effects of fibres?

A

Myositis

67
Q

What are examples of bile acid binding resins?

A

Colestyramine, colestipol, colsevelam

68
Q

What is the effect of bile acid binding resins?

A

Inhibit cholesterol absorption

69
Q

What is the mechanism of bile acid resins?

A

Causes the excretion of bile salts resulting in more cholesterol to be converted to bile salts
Bile resins bind bile in th intestine so it is not absorbed in the duodenum
Liver uses metabolised cholesterol to compensate for loss

70
Q

What are the side effects of bile acid resins?

A

GI tract irritation

71
Q

What is the mechanism of ezetimibe?

A

Decrease in LDL

72
Q

What are side effects of Ezetimibe?

A

Diarrhoea
Abdominal pain
Headache
Contraindicated in breast feeding

73
Q

What is the mechanism of warfarin?

A

Blocks clotting factors 2, 7, 9, and 10 (serine proteases - glycoprotein precursors of active thrombin factors)

G-carboxylase enzyme is stimulated by vitamin K and modifies the serine proteases
Anticoagulants act as vitamin K antagonists which prevents production of mature coagulation factors

74
Q

What are side effects of warfarin?

A

Haemorrhage anywhere

Reversed by vitamin K

75
Q

What is the mechanism of heparin?

A

Binds to antithrombin II, increasing its affinity for serine proteases to greatly increase their rate of activation

76
Q

What is the mechanism of LMWH (enoxaparin and date-aron)?

A

Inhibit factor Xa (activates thrombin IIa - fibrin - blood clot)

77
Q

Dabigatran and etexilate directly inhibit?

A

Thrombin

78
Q

Ravaroxaban directly inhibits?

A

Factor Xa

79
Q

What are side effects of anticoagulants (heparin, LMWH, Dbigatran, rivaroxaban)?

A

haemorrhage
Osteoporosis
hypoaldosteronism
Hypersensitivity reactions

80
Q

What is the mechanism of aspirin?

A

Blocks COX inhibiting formation of TXA2 which causes cross linking of platelets

81
Q

What is the mechanism of clopidgrel?

A

Blocks ADP from binding to P2Y12 receptor and formation of fibrin

82
Q

What are the side effects of anti platelets (aspirin/clopidogrel)?

A

Haemorrhage anywhere
Peptic ulcer
Aspirin sensitivity –> asthma

83
Q

What are examples of fibrinolytic drugs?

A

Streptokinase
Tissue plasminogen activator
Alteplase, duteplase

84
Q

The fibrinolytic cascade opposes the?

A

Coagulation cascade

85
Q

Fibrinolytic drugs activate formation of plasmid from plasminogen which …

A

lyses fibrin into fibrin fragments causing lysis of the clot

86
Q

What are side effects of fibrinolytic drugs?

A

Haemorrhage risk (controlled by tranexamic acid which inhibits plasminogen activation)

Year 1 Systems (JBR) (21 decks)

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