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Stage 3 Block 2 > CVS > Flashcards

CVS Flashcards

1
Q

How does the sympathetic nervous system regulate cardiac function?

A

At the SA node, NA binds B1 to increase pacemaker current

At the AV node, NA binds B1 to increase calcium current and hence conduction velocity

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2
Q

How does the parasympathetic nervous system regulate cardiac function?

A

At the SA node, ACh binds M receptors to slow depolarisation by opening potassium channels and inhibiting sodium channels form opening
At the AV node, ACh binds M receptors to decrease conduction velocity

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3
Q

Summarise the effect the SNS and PNS has on cardiac function.

A

SNS - increase pacemaker current and conduction velocity

PNS - slows depolarisation and decreases conduction velocity

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4
Q

What changes occur with increased BP?

A

Baroreceptors activate PNS to inhibit SA firing rate, inhibiting SNS from inducing vasoconstriction

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5
Q

What changes occur with decreased BP?

A

Baroreceptors activate SNS to increase SA firing rate, increase vasoconstriction, increase venous return and increase cardiac output (hence increasing BP)

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6
Q

What are the 3 types of heart failure?

A

Acute left ventricular failure
Cardiogenic shock
Chronic heart failure

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7
Q

Describe acute left ventricular failure

A

Where there is inadequate output leading to pulmonary oedema, reflex contraction (which increases venous return hence exacerbating the issue)

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8
Q

What is the treatment goal for acute left ventricular failure and what treatments are used to achieve this goal?

A

To reduce venous return using loop diuretics, GTN, and opioids

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9
Q

Describe cardiogenic shock

A

Where there is sudden impairment to left ventricular systole, impairing organ perfusion

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10
Q

What is the treatment goal for cardiogenic shock and what treatments are used to achieve this goal?

A

Resuscitation, dobutamine to increase tissue perfusion

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11
Q

Describe chronic heart failure

A

Where there is myocardium disease due to excess load because of e.g. IHD, valve dysfunction, HTN

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12
Q

What is the treatment goal for chronic heart failure and what treatments are used to achieve this goal?

A

Reduce compensatory mechanisms and increase CO using ACEI, diuretics, beta-blockers and digoxin

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13
Q

Outline the mechanism of cardiac contraction

A

Action potential arrives at sodium channel, opening the channel and allowing sodium influx. This causes further membrane depolarisation, opening calcium channels and causing calcium influx. The increased calcium concentration inside the cytoplasm causes calcium-induced calcium release from the SR, causing myofibre contraction.

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14
Q

Describe the mechanism of action of digoxin

A

Inhibits Na+/K+ ATPase, causing less sodium to leave the cell, ultimately slowing down the Na+/Ca2+ exchanger, causing the concentration of calcium inside the cell to remain high, allowing more calcium to enter the SR causing a stronger contraction next time (increasing contractility)

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15
Q

Describe the mechanism of action of dobutamine

A

Beta-1 agonist, activates ACy, increasing the concentration of cAMP, activating PKA causing calcium channels to open, increasing contractility, and stimulating the calcium pump to allow more calcium to enter the SR. Also inhibits Na+/K+ ATPase, increasing concentration of calcium in the cell, increasing contractility.

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16
Q

Describe the mechanism of action of enoximone

A

PDE inhibitor, increases concentration of cAMP, activating PKA, causing calcium channels to open and increasing contractility, allowing more calcium to enter the SR, and inhibiting the Na+/K+ ATPase, increasing the concentration of calcium inside the cell, increasing contractility

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17
Q

What class of drug is digoxin?

A

Cardiac glycoside

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18
Q

How does digoxin cause arrhythmia?

A

More calcium in the cell, more calcium-induced calcium release, more spontaneous contraction

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19
Q

What are the indications for digoxin?

A

Symptomatic relief in heart failure

Supraventricular arrhythmia

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20
Q

Describe the PK of digoxin

A

Fp.o. ~75%
T1/2 ~40h
Vd ~640L/70kg (binds Na+/K+ ATPase in skeletal muscle)
Eliminated through p-GP

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21
Q

Describe the ADRs of digoxin

A

Arrhythmia, nausea, vomiting, fatigue, confusion, impaired coloured vision

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22
Q

What are the cautions for digoxin?

A

Hypokalaemia (digoxin binds with more affinity in the absence of potassium)
Hypothyroidism (reduced GFR -> increased toxicity)
Elderly (reduced GFR)

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23
Q

What are the contraindications to the use of digoxin?

A

Heart block, as digoxin inhibits AV node conduction

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24
Q

What interactions are associated with digoxin?

A

Diuretics (hypokalaemia)
Verapamil, quinidine, amiodarone (displace digoxin from tissue binding sites -> reduced Vd)
Antibiotics (increase Fp.o)
Beta-blockers (inhibit AV conduction and decrease contractility)
CCBs (decrease contractility)
p-GP inhibitors (reduce elimination)

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25
Q

Describe the two forms of IHD and give example of each

A

Chronic arterial disease e.g. stable angina

Acute coronary syndromes e.g. unstable angina, NSTEMI and STEMI

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26
Q

Describe how stable angina occurs

A

Where there is partial vessel block.
Exertion causes the oxygen demand to exceed the supply due to the reduced blood flow, resulting in chest pain radiating to arm and jaw, however this pain resolves on rest

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27
Q

Describe how unstable angina occurs

A

Where the plaque ruptures, causing platelet aggregation and thrombus formation hence blocking the vessel further. This results with pain at rest

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28
Q

Describe how an NSTEMI occurs

A

Coronary artery still not fully blocked so some tissue perfusion remains. This results in a small area of tissue death
(NSTEMI = non-ST elevated myocardial infarction)

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29
Q

Describe how a STEMI occurs

A

Where there is complete occlusion leading to a large area of tissue death
(STEMI = ST-elevated myocardial infarction)

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30
Q

Describe the mechanism of action of organic nitrates

A

NO activates guanylate cyclase, increasing the concentration of cGMP, activating PKG, resulting in vasodilation

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31
Q

What are the indications of organic nitrates?

A

Angina

Left ventricular failure

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32
Q

Describe the PK of organic nitrates

A

Glyceryl trinitrate - t1/2 ~5mins, sublingual, buccal, transdermal, i.v.
Isosorbide mononitrate - slower onset, low first pass metabolism, t1/2 ~ 5h
Isosorbide dinitrate - extensive first pass metabolism to mononitrate (active)

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33
Q

What are the ADRs of nitrates?

A

Dizziness, headache, flushing, tolerance

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34
Q

What interactions are associated with nitrates?

A 
Diuretics
Hypotensive drugs
Drugs affecting CO
Drugs causing vasodilation
PDE inhibitors 
Heparin
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35
Q

What cautions are associated with nitrates?

A

Pregnancy (affects placental blood flow)

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36
Q

What are the contraindications of nitrates?

A

Hypotension
Hypovolaemia
Hypersensitivity

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37
Q

What is the mechanism of action of beta-blockers?

A

Block beta2-receptor, increasing the concentration of cAMP, block the phosphorylation of MLCK, causing vasodilation

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38
Q

What are the indications for beta-blockers?

A

Prophylactic treatment of stable angina, HTN, MI, arrhythmia, HF, anxiety

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39
Q

Describe the ADRs of beta-blockers

A

Bronchoconstriction, bradycardia, reduced cardiac contractility, erectile dysfunction, sleep disturbances

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40
Q

Describe the cautions associated with beta-blockers

A

Pregnancy, avoid suddenly stopping therapy, can mask signs of hypoglycaemia, diabetes

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41
Q

What are the contraindications associated with beta-blockers?

A

Asthma, heart block, uncontrolled HF, bradycardia, hypotension, prolong QT(sotalol)

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42
Q

What interactions are associated with beta-blockers?

A

Verapamil (asystole)

Reduced renal/hepatic perfusion

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43
Q

Describe the mechanism of action of the dihydropyridines

A

Have only vascular effects:
Arteriolar dilation - lower resistance, lower workload, lower oxygen demand
Coronary artery dilation - reduced vasospasm, improved oxygen supply

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44
Q

Describe the mechanism of action of verapamil and diltiazem

A

Vascular and cardiac effects:
Arteriolar dilation - lower resistance, workloads and oxygen demand
Coronary artery dilation - reduced vasospasm and improved oxygen supply
Reduced rate and cardiac contractility: lower workload and lower oxygen demand

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45
Q

What are the indications for dihydropyridines?

A

HTN

Stable angina prophylaxis

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46
Q

What ADRs are associated with the dihydropyridines?

A

Flushing, headache, oedema, reflex tachycardia, increased contractility

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47
Q

What cautions are associated with the dihydropyridines?

A

HF (amlodipine and felodipine preferred)

Pregnancy

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48
Q

What contraindications are associated with the use of dihydropyridines?

A

Breast feeding, unstable angina, 1 month after MI

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49
Q

What interactions are associated with the use of dihydropyridines?

A

Drugs that cause hypotension
Grapefruit juice
Ciclosporin and digoxin (inhibit renal secretion by p-GP)

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50
Q

What are the indications for use of diltiazem?

A

HTN

Stable angina prophylaxis

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51
Q

What ADRs are associated with diltiazem?

A

Bradycardia (inhibits AV node conduction)

Teratogenic

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52
Q

What cautions surround the use of diltiazem?

A

Hepatic and renal failure

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53
Q

What are the contraindications for the use of diltiazem?

A

Breast feeding
Pregnancy
HF
AV block

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54
Q

What interactions are associated with diltiazem?

A 
Hypotensive drugs
Beta-blockers (asystole)
Propranolol
Ciclosporin (inhibits CYP3A4 metabolism)
Digoxin (inhibits renal secretion by p-GP)
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55
Q

What are the indications for use of verapamil?

A

Supraventricular tachycardia

HTN, stable angina prophylaxis

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56
Q

What ADRs are associated with verapamil?

A

Bradycardia
Hypotension
Constipation

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57
Q

What cautions surround the use of verapamil?

A

Hepatic impairment

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58
Q

What are the contraindications for the use of verapamil?

A

Breastfeeding
Pregnancy
HF
AV block

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59
Q

What interactions are associated with the use of verapamil?

A

Hypotensive drugs
Beta-blockers
Ciclosporin and digoxin
Grapefruit juice

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60
Q

What class of drug is nicorandil?

A

Potassium channel opener

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61
Q

What are the indications for nicorandil?

A 
Stable angina
Nitrate tolerance (its an NO donor)
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62
Q

What ADRs are associated with nicorandil?

A

Headache, flushing, reflex tachycardia

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63
Q

What caution are associated with the use of nicorandil?

A

Hypovolaemia

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64
Q

What are the contraindications for the use of nicorandil?

A

Cardiogenic shock, hypotension

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65
Q

What interactions are associated with the use of nicorandil?

A

Sildenafil (slower turnover of cGMP -> hypotension)

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66
Q

What is the mechanism of action of nicorandil?

A

Open potassium channels causing hyperpolarisation of calcium channels thus closing them, decreasing concentration of calcium in the cell, leading to vasodilation

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67
Q

Describe the mechanism of action of loop diuretics

A

Inhibit NKCC2, inhibiting sodium and water reabsorption

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68
Q

What are the indications for loop diuretics?

A

Oedema, HTN, hypercalcaemia, hyperkalaemia, hyponatraemia

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69
Q

Describe the PK of loop diuretics

A 
Furosemide t1/2~1h
Bumetanide t1/2~1.5h
Torasemide t1/2~3h
Highly protein bound
Secreted into proximal tubule
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70
Q

What ADRs are associated with loop diuretics?

A

Hypokalaemia, sulpha allergy, hypotension, hypocalcaemia, hypomagnesaemia, hyperuricaemia and gout, ototoxicity

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71
Q

What cautions are associated with the use of loop diuretics?

A

Gout

Diabetes

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72
Q

What are the contraindications for use of loop diuretics?

A

Hypokalaemia, hypovolaemia, pregnancy

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73
Q

What interactions are associated with loop diuretics?

A

Aminoglycoside antibiotics (ototoxicity)
Cardiac glycosides (arrhythmia)
NSAIDs
Lithium

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74
Q

Describe the mechanism of action of thiazides and thiazide-like diuretics

A

Inhibit NCC1, inhibiting Sodium and water reabsorption

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75
Q

What are the indications for use of thiazides?

A

Mild oedema, HTN, diabetes insipidus

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76
Q

Describe the PK of thiazides

A

Bendroflumethazide t1/2~6h
Indapamide t1/2~16h
Metolazone t1/2~4h
Plasma protein bound

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77
Q

Which thiazide/thiazide-like diuretic is preferred in advanced renal failure?

A

Metolazone

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78
Q

What ADRs are associated with the use of thiazides?

A

Hypokalaemia, nocturia, hypotension, hyponatraemia, hypomagnesaemia, decreased calcium excretion, impotence

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79
Q

What can hypokalaemia lead to?

A

Arrhythmia, encephalopathy, diabetes mellitus, fatigue and lethargy

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80
Q

How is hypokalaemia treated?

A

Potassium sparing diuretics
Potassium supplement
Diet - bananas

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81
Q

What cautions are associated with he use of thiazides?

A

Gout

Diabetes

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82
Q

What interactions are associated with thiazides?

A

Sulfonylureas
Antiarrhythmic agents that prolong QT
Cardiac glycosides
NSAIDs

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83
Q

Describe the mechanism of action of potassium sparing diuretics

A

Amiloride - inhibit ENaC, inhibiting sodium and water reabsorption

Spironolactone and eplerenone - block aldosterone receptor, inhibiting the expression of ENaC

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84
Q

What are the indications for the use of potassium sparing diuretics?

A

Conserving potassium
Concomitant digoxin therapy
Secondary hyperaldosteronism
Elderly

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85
Q

What ADRs are associated with potassium sparing diuretics?

A

Hyperkalaemia
Metabolic acidosis
Spironolactone - impotence, gynaecomastia, menstrual cycle irregularities

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86
Q

What interactions are associated with potassium sparing diuretics?

A

NSAIDs (impair renal function and cause hyperkalaemia)

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87
Q

Describe the mechanism of action of alpha-blockers

A

Block alpha-1 receptor, inhibiting activation of Gq, inhibiting vasoconstriction
Relax arteriolar resistance vessels and dilate venous capacitance

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88
Q

What class of drug is doxazosin?

A

Alpha-blocker

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89
Q

What are the indications for the use of alpha-blockers?

A

HTN

BPH

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90
Q

What ADRs are associated with alpha-blockers?

A 
Postural hypotension
Reflex tachycardia (palpitations)
Lethargy 
Dizziness
Headache
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91
Q

What cautions are associated with the use of alpha-blockers?

A

Pregnancy

HF

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92
Q

What are the contraindications for the use of alpha-blockers?

A

Incontinence

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93
Q

What interactions are associated with alpha-blockers?

A

Diuretics and beta-blockers (potentiate hypotensive effect)

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94
Q

Describe the mechanism of action of alpha-agonists

A

Activate alpha-2 receptor, inhibiting sympathetic output from CNA by inhibiting NA release, inhibiting vasoconstriction

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95
Q

What is the mechanism of action of ACE inhibitors?

A

Prevent conversion of angiotensin I to angiotensin II by inhibiting Angiotensin Converting Enzyme (ACE)
Inhibits vasoconstriction and aldosterone release caused by angiotensin II and reduces metabolism of bradykinin

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96
Q

What are the indications for the use of ACEIs?

A

HTN, HF, MI, diabetic nephropathy

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97
Q

What ADRs are associated with the use of ACEIs?

A

Hypotension, hyperkalaemia, persistent dry cough, rash

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98
Q

What cautions are associated with the use of ACEIs?

A

Hepatic insufficiency

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99
Q

What contraindications are associated with the use of ACEIs?

A

Reduced renal perfusion

Pregnancy

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100
Q

What interactions are associated with ACEIs?

A

Hypotensive drugs
Potassium sparing diuretics (hyperkalaemia)
NSAIDs (reduced GFR)

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101
Q

What is the mechanism of action of ARBs?

A

Block Angiotensin 1 receptor (AT1), blocking angiotensin 2 from causing vasoconstriction

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102
Q

What are the indications for use of ARBs?

A

HTN

Prevention of diabetic nephropathy

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103
Q

What ADRs are associated with ARBs?

A

Headache, dizziness, fatigue

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104
Q

What cautions are associated with the use of ARBs?

A

Renal insufficiency

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105
Q

What are the contraindications for the use of ARBs?

A

Pregnancy

106
Q

What interactions are associated with ARBs?

A

Hypotensive drugs
Potassium sparing diuretics (hyperkalaemia)
NSAIDs

107
Q

What are the 3 classes of arrhythmia?

A

Supraventricular
Ventricular
Heart block

108
Q

Describe supraventricular arrhythmias

A

Where the origin is in the SA, AV nodes or atria
Can result in sinus tachycardia/bradycardia (due to altered SA firing), AT (due to an alternative SA pacemaker), atrial flutter, AF (due to re-entry impulses in the atrium)

109
Q

Describe ventricular arrhythmias

A

Origin in ventricles

VT, VF (due to re-entry impulses)

110
Q

What are the treatment goals for arrhythmias?

A

Restore normal cardiac rhythm
Prevent recurrence of arrhythmia
Prevent more severe arrhythmia
Deal with haemodynamic consequences

111
Q

What are the general actions of anti-arrhythmic drugs?

A

Alter the baseline/threshold potential in SA cells
Alter the rate of phase 4 repolarisation
Alter the baseline/threshold potential in contractile cells
Alter the duration of action potential (by altering the refractory period)

112
Q

Give an example of a class Ia anti-arrhythmic

A

Disopyramide

113
Q

Describe the mechanism of action of class Ia anti-arrhythmics

A

Block sodium channels thus slowing phase 0 and decreasing conduction velocity
Block potassium channels thus prolonging repolarisation and increasing the refractory period
Block parasympathetic inhibition of AV node

114
Q

What are the indications of Class Ia anti-arrhythmics?

A

VT following MI

115
Q

What ADRs are associated with class Ia anti-arrhythmics?

A

Negative inotrope

Dry mouth, urinary retention, blurred vision, constipation

116
Q

What cautions surround the class Ia anti-arrhythmics?

A

Pregnancy

117
Q

What are the contraindications for the use of disopyramide?

A

HF

118
Q

What interactions are associated with disopyramide?

A 
Prolong QT (sotalol etc.)
Negative inotrope (beta-blockers etc.)
119
Q

Give an example of a class Ib anti-arrhythmic

A

Lidocaine

120
Q

What are the indications for the use of lidocaine?

A

VT, local anaesthesia

121
Q

What ADRs are associated with lidocaine?

A

Nausea, vomiting, drowsiness, convulsions

122
Q

What is the mechanism of action of lidocaine?

A

Block open and refractory sodium channels, shortening the action potential

123
Q

What cautions are associated with the use of lidocaine?

A

Hepatic impairment, HF

124
Q

What are the contraindications for the use of lidocaine?

A

AV block

125
Q

What interactions are associated with the use of lidocaine?

A

Diuretics (hypokalaemia predisposes to arrhythmia)

126
Q

Give an example of a class Ic anti-arrhythmic

A

Flecainide

127
Q

What is the mechanism of action of felcaininde?

A

Sodium channel blocker, slows conduction in all cardiac tissue, suppresses premature ventricular contraction and increases PR and QRS intervals

128
Q

What are the indications for the use of flecainide?

A

AF and AT

129
Q

What ADRs are associated with the use of flecainide?

A

Negative inotrope, lightheadedness, arrhythmia

130
Q

What cautions are associated with the use of flecainide?

A

Heart block
Pregnancy
Hepatic insufficiency

131
Q

What are the contraindications for the use of flecainide?

A

HF, previous MI

132
Q

What interactions are associated with flecainide?

A

Diuretics (risk of arrhythmia due to hypokalaemia)
Amiodarone
Fluoxetine
Negative inotropes

133
Q

Give an example of a class II anti-arrhythmic

A

Atenolol

134
Q

What is the mechanism of action of class II anti-arrhythmics?

A

Block beta-receptors, inhibit pacemaker and slows pacemaker current, prolong repolarisation

135
Q

What are the indications for the use of class II anti-arrhythmics?

A

Supraventricular arrhythmia e.g. AF

136
Q

Give an example of a class III anti-arrhythmic

A

Amiodarone

137
Q

Describe the mechanism of action of amiodarone

A

Blocks potassium channels to prolong repolarisation, increases refractory period (reduced re-entry)

138
Q

What are the indications for the use of amiodarone?

A

Arrhythmia

139
Q

What cautions surround the use of amiodarone?

A

Bolus i.v. In HF

140
Q

What are the contraindications for the use of amiodarone?

A 
Bradycardia 
Heart block
Iodine sensitivity 
Pregnancy
Breastfeeding
141
Q

What ADRs are associated with the use of amiodarone?

A

Pulmonary fibrosis, visual halo (deposits of lipofuscin of cornea), sensitivity to sunlight, grey skin discolouration, hyperthyroidism

142
Q

What interactions are associated with amiodarone?

A

CYP3A4 substrate, inhibits metabolism of warfarin
Inhibits renal excretion of digoxin by p-GP
Prolong QT

143
Q

Give an example of a class IV anti-arrhythmic

A

Verapamil/diltiazem

144
Q

Describe the mechanism of action of class IV anti-arrhythmics

A

CCBs, slows SA rate, slows phase 0 in AV node

145
Q

What type of arrhythmia are CCBs used to treat?

A

Re-entrant, e.g. supraventricular tachycardia, that involve the AV node

146
Q

Describe the structure of lipoproteins

A

Hydrophobic core consisting of cholesterol and TAG
Surface monolayer of phospholipid
Apolipoprotein on surface

147
Q

Outline the transport of lipids

A

Lipids get broken down into triglycerides and cholesterol and combine with bile to make a micelle, which then gets packaged into chylomicrons containing ApoB48 protein on the surface. They also obtain an ApoCII protein from HDL which is a ligand for lipoprotein lipase, which breaks down 50% into free fatty acids that go to the muscle. The other 50% is present as a remnant that exchanges its ApoCII for ApoE from HDL, allowing VLDL to be taken up into the liver by LDL-R. LDL containing ApoB100 becomes oxidised LDL in blood vessels leading to atherosclerosis.

148
Q

What are the three different types of hyperlipidaemia?

A

Hypercholesterolaemia
Hypertriglyceridaemia
Mixed hyperlipidaemia

149
Q

Describe the mechanism of action of statins

A

Inhibit HMG CoA Reductase, prevent synthesis of cholesterol so concentration of cholesterol decreases, switching on SREBP, which up-regulates the LDL-R, increasing LDL uptake thus decreasing plasma cholesterol concentration

150
Q

What are the indications for use of statins?

A

Occlusive arterial disorders
Coronary heart disease
Patients at risk of atherosclerosis even if asymptomatic (diabetics >40, FH)

151
Q

Describe the metabolism of statins

A

CYP3A4 - simvastatin and atorvastatin
CYP2C9 - fluvastatin
Renal - pravastatin and rosuvastatin

152
Q

What ADRs are associated with statins?

A

Myopathy progressing to rhabdomyolysis

153
Q

What cautions surround the use of statins?

A

Risk of myopathy (risk increased by renal insufficiency, co-treatment with fibrates or ciclosporin)

154
Q

What are the contraindications for the use of statins?

A

Liver disease
Pregnancy
Breastfeeding

155
Q

What interactions are associated with the use of statins?

A

Warfarin
CYPs
Fibrates

156
Q

Describe the mechanism of action of bile acid binding resins

A

Decrease reabsorption of bile, increased bile synthesis, reduced liver cholesterol, switched on SREBP, increased expression of LDL-R, reduced plasma cholesterol

157
Q

Give an example of a bile acid binding resin

A

Cholestyramine and colestipol

158
Q

What are the indications for the use of bile acid binding resins?

A

Patients in which statins are insufficient on own or contraindicated

159
Q

What ADRs are associated with bile acid binding resins?

A

Constipation, bloating, flatulence

160
Q

What cautions surround the use of bile acid binding resins?

A

May also bind vitamin A, D, and K thus supplements Amy be necessary
May also bind drugs e.g. warfarin, digoxin, statins, thiazides, aspirin, so give other drug 1h before or 4h after the resin

161
Q

What is the mechanism of action of ezetimibe?

A

Inhibit NPC1L1 to inhibit transport of cholesterol across the intestinal brush border, decreasing the concentration of cholesterol in chylomicrons, the liver, VLDL and LDL, thus switching on SREBP, up regulating the LDL-R and reducing plasma cholesterol

162
Q

What are the indications of ezetimibe?

A

Hypercholesterolaemia

Used with statin or on own if statin now appropriate

163
Q

What cautions surround the use of ezetimibe?

A

Hepatic impairment

164
Q

What are the contraindications for the use of ezetimibe?

A

Breastfeeding

165
Q

What ADRs are associated with ezetimibe?

A

Diarrhoea, abdominal pain

166
Q

What interactions are associated with ezetimibe?

A

Fibrates

167
Q

Describe the mechanism of action of fibrates

A

Activate PPAR-alpha, decrease plasma triglyceride by increasing lipoprotein lipase, fatty acid uptake and oxidation, and increase HDL, increasing LDL clearance

168
Q

Give an example of a fibrate

A

Bezafibrate

169
Q

What are the indications for the use of fibrates?

A

Hypercholesterolaemia where statin unsuccessful or inappropriate
Hypertriglyceridaemia

170
Q

What cautions surround the use of fibrates?

A

Myotoxicity especially in patients with renal disease

Displaces warfarin from plasma proteins

171
Q

What are the contraindications for the use of fibrates?

A

Hepatic and renal impairment
Pregnancy
Breastfeeding

172
Q

What ADRs are associated with fibrates?

A

Nausea, abdominal discomfort, anorexia, myopathy

173
Q

What interactions are associated with fibrates?

A

Statins
Warfarin
Ezetimibe

174
Q

Give an example of a PCSK9 inhibitor

A

Alirocumab and evolucumab

175
Q

What is the mechanism of action of PCSK9 inhibitors?

A

Inhibit PCSK9 which increases the number of LDL-Rs thus promoting LDL clearance

176
Q

Describe the mechanism of action of nicotinic acid

A

Precursor of NADP
Increases HDL
Decreases lipolysis in adipose tissue, decreased flux of FFA to liver, reduced production of VLDL thus decreases LDL and triglycerides

177
Q

What is the indication for use of nicotinic acid?

A

Hyperlipidaemia with statin or if statin not tolerated

Hypertriglyceridaemia

178
Q

What ADRs are associated with nicotinic acid?

A

Flushing and pruritus (PG release and vasodilation - treat with aspirin)
Diarrhoea, nausea, vomiting
Hyperuricaemia (inhibits uric acid secretion -> may cause gout))
Reduced insulin sensitivity (may cause diabetes)

179
Q

What cautions are associated with the use of nicotinic acid?

A

Unstable angina
MI
Diabetes
Gout

180
Q

What are the contraindications for the use of nicotinic acid?

A

Arterial bleeding
Peptic ulcer disease
Breast feeding

181
Q

What are the three causes of thrombosis?

A

Endothelial injury
Abnormal blood flow
Hypercoagulability

182
Q

Describe an arterial thrombosis

A

More platelet rich
Can result in a stroke or MI
Risk factors include smoking, diabetes, BP, weight and cholesterol
Treatment involves reducing risk factors and the use of antiplatelet drugs

183
Q

Describe a venous thrombosis

A

More fibrin rich
Can result in a DVT or PE
Risk factors include genetic predisposition and slow blood flow
Treatment involves anticoagulants

184
Q

Describe the mechanism of action of aspirin

A

Inhibits COX1 by acetylation, inhibiting PG synthesis in platelets which inhibits TxA2 synthesis, inhibiting aggregation

185
Q

What are the indications for the use of aspirin?

A

Primary and secondary prevention of thromboembolism in atherosclerotic disease: angina, MI, stroke, peripheral vascular disease
Analgesia, anti-inflammatory for rheumatoid arthritis

186
Q

What ADRs are associated with aspirin?

A

Haemorrhage

Hypersensitivity

187
Q

What are the cautions and contraindications for aspirin?

A

Risk of bleeding
Asthma
Renal insufficiency

188
Q

What interactions are associated with aspirin?

A

Anticoagulants
Antiplatelets
NSAIDs
Diuretics (antagonise effect)

189
Q

Give an example of a PDE inhibitor

A

Dipyridamole

190
Q

What is the mechanism of action of dipyridamole?

A

PDE inhibitor, promotes activation of PKA which inhibit platelet activation
Inhibits reuptake of adenosine into platelets

191
Q

What are the indications for use of dipyridamole?

A

Prevention of embolism from prosthetic heart valve with warfarin
Prevention of vessel block in patients with ischaemic stroke with aspirin

192
Q

What ADRs are associated with dipyridamole?

A

Bleeding, headache, diarrhoea, facial flushing

193
Q

What cautions surround the use of dipyridamole?

A

Risk of bleeding

194
Q

What interactions are associated with dipyridamole?

A

Anticoagulants

195
Q

Give an example of an ADP receptor antagonist

A

Clopidogrel

196
Q

What is the mechanism of action of clopidogrel?

A

Inhibits P2Y which inhibits the inhibition of ACy, increasing the concentration of cAMP, activating PKA which inhibits GP-IIbIIIa, inhibiting platelet activation

197
Q

What ADRs are associated with clopidogrel?

A

Haemorrhage
Abdominal pain
Nausea

198
Q

What cautions surround the use of clopidogrel?

A

Risk of bleeding

199
Q

What are the contraindications for the use of clopidogrel?

A

Active bleeding

Breastfeeding

200
Q

What interactions are associated with clopidogrel?

A

Aspirin
Antiplatelets
Warfarin

201
Q

Give an example of a GP-IIbIIIa antagonist

A

Eptifibatide, abciximab, tirofiban

202
Q

What is the mechanism of action of GP-IIbIIIa antagonists?

A

Inhibit end-point of platelet aggregation

203
Q

What ADRs are associated with GP-IIbIIIa antagonists?

A

Haemorrhage

204
Q

What cautions surround the use of GP-IIbIIIa antagonists?

A

Risk of bleeding or active bleeding

205
Q

What are the contraindications for the use of GP-IIbIIIa antagonists?

A

Recent abnormal bleeding or stroke

206
Q

What is the mechanism of action of heparin?

A

Inhibit clotting factors IX, Xa, XIa, XIIa and thrombin by catalysing irreversible binding of anti-thrombin III

207
Q

What ADRs are associated with heparin?

A

Haemorrhage

Thrombocytopenia

208
Q

What are the contraindications for the use of heparin?

A

Haemophilia
Thrombocytopenia
Severe hepatic disease

209
Q

What interactions are associated with heparin?

A

Increase risk of bleeding

NSAIDs

210
Q

What is the mechanism of action of warfarin?

A

Inhibit vitamin K reductase, preventing reduction of vitamin K which prevents the carboxylation of clotting factors, preventing clot formation

211
Q

What ADRs are associated with warfarin?

A

Haemorrhage

212
Q

What are the contraindications for the use of warfarin?

A

Pregnancy

Peptic ulcer

213
Q

What interactions are associated with warfarin?

A

NSAIDs (displace from plasma proteins)
Antibiotics
CYP2C9 (inhibitors - amiodarone, cimetidine, clopidogrel, fluconazole, fluoxetine, inducers-barbiturates, carbamazepine, phenytoin, alcohol)

214
Q

Give an example of a thrombin inhibitor

A

Dabigatran

215
Q

What is the mechanism of action of dabigatran?

A

Thrombin inhibitor

216
Q

What ADRs are associated with the use of dabigatran?

A

Bleeding

217
Q

What cautions surround the use of dabigatran?

A

Assess renal function before use and annually

218
Q

What are the contraindications for the use of dabigatran?

A

Active bleeding/risk of bleeding

219
Q

What interactions are associated with dabigatran?

A

Anticoagulants

220
Q

Give and example of a factor Xa inhibitor

A

Rivaroxaban

221
Q

What ADRs are associated with rivaroxaban?

A

Bleeding

222
Q

What cautions surround the use of rivaroxaban?

A

Renal impairment

Risk of bleeding

223
Q

What are the contraindications for the use of rivaroxaban?

A

Active bleeding

224
Q

What interactions are associated with rivaroxaban?

A

Anticoagulants

225
Q

Name the 4 different fibrinolytic agents

A

Late please
Relteplase
Tenecteplase
Streptokinase

226
Q

What ADRs are associated with fibrinolytic agents?

A

Haemorrhage
Streptokinase generates bradykinin => hypotension
Allergy to streptokinase

227
Q

What are the contraindications for the use of fibrinolytic agents?

A

Previously received streptokinase

228
Q

Define normal BP

A

90-120/60-80mmHg

229
Q

Define the two classifications of HTN

A

Primary (essential) - no know identifiable cause

Secondary - underlying cause known

230
Q

What is essential HTN associated with?

A

Stress response, race, age, heredity, socioeconomic background

231
Q

What can secondary HTN be caused by?

A

Renal disease, endocrine disease, vascular disease, pregnancy, drugs

232
Q

Outline the pathophysiology of HTN

A

Arterial BP -CO+TPR
Increased HR/stroke volume = increased CO (also increased by SNS)
Vasoconstriction (arteriosclerosis, atherosclerosis, increased blood viscosity) = increased TPR (decreased by PNS)

233
Q

A patient has a clinic BP of >140/90 and an ABPM of over 135/85, what stage of HTN do they have?

A

Stage 1

234
Q

A patient has a clinic BP >160/100 and an ABPM of over 150/95, what stage of HTN do they have?

A

Stage 2

235
Q

A patient’s SBP is >180 and DBP is>110, what stage of HTN do they have?

A

Severe (stage 3)

236
Q

What are the long-term consequences of HTN?

A

ESKD, CVD, arteriosclerosis, retinopathy, stroke

237
Q

What is first line treatment for a patient over 40 years old with stage 1 HTN and no other risk factors?

A

Lifestyle interventions including weight loss, healthy diet, increasing exercise, reducing salt, smoking cessation, decreasing alcohol, decreasing caffeine

238
Q

What is first line treatment for someone who is under 80, with stage 1 HTN and renal disease?

A

Antihypertensives

239
Q

What are the risk factors that mean someone gets offered antihypertensives first-line?

A 
Target organ damage
Established CVD
Renal disease
Diabetes
10y CVD risk of ≥20%
Stage 2 HTN
240
Q

What is the BP target for someone under 80?

A

140/90

241
Q

What is the BP target for someone over 80?

A

150/90

242
Q

What is the BP target for someone with diabetes?

A

140/80

243
Q

What is the BP target for someone with diabetes and retinopathy/nephropathy/neuropathy?

A

130/80

244
Q

Define gestational HTN

A

New HTN occurring after 20 weeks gestational age without significant proteinuria

245
Q

Define pre-eclampsia

A

Gestational HTN with significant proteinuria

246
Q

What are the symptoms of pre-eclampsia?

A

Severe headaches, visual disturbances, new epigastric pain (persistent), nausea, vomiting, sudden swelling of face and extremities

247
Q

What is HTN in pregnancy defined as being?

A

Single DBP reading of ≥90mmHg on two or more occasions more than 4h apart AND/OR a single DBP reading of >110mmHg

248
Q

What is first line treatment for someone with type 1 diabetes and a BP reading of ≥135/85mmHg?

A

Antihypertensives

249
Q

What is the threshold BP for starting antihypertensives in someone with type 1 diabetes and albuminuria and 2 or more features of metabolic syndrome (obesity, insulin resistance, tiredness)?

A

≥130/80mmHg

250
Q

What are the BP reading for someone with postural hypotension?

A 
Lying/sitting = 120/76mmHg
Standing = 97/60mmHg
251
Q

Define heart failure

A

A failure to meet normal perfusion demands of the body or where perfusion needs can only be met by an elevated filling pressure

252
Q

Describe the compensatory mechanisms that kick in when the heart fails as a pump

A

RAAS - sodium and water retention and vasoconstriction -> increased TPR
SNS - muscle stretches -> remodelling

253
Q

What are natriuretic peptides?

A

Hormones released by the blood stream in response to the body’s increased ventricular wall stress, myocardial damage and volume overload

254
Q

Define the normal, suspect HF and high levels of BNP and NT-proBNP

A

Normal: BNP<100pg/mL NT-proBNP<400pg/mL
Suspect HF: BNP 100-400pg/mL NT-proBNP 400-2000pg/mL
High - refer: BNP >400pg/mL NT-proBNP >2000pg/mL

255
Q

What are the main underlying causes of HF?

A 
Myocardial dysfunction
Volume overload
Pressure overload
Impaired filling
Arrhythmias
High output
256
Q

Describe the changes in ejection fraction

A

Normal >50%
LVSD <45%
Symptoms <35%
Thrombosis <10%

257
Q

Outline the signs and symptoms of HF

A

SOB, swelling of feet and legs, chronic lack of energy, orthopnoea, hepatomegaly=>ascites, cough with frothy sputum, increased urination at night, confusion and/or impaired memory, arrhythmias, raised JVP, presence of a third heart sound, reduced exercise tolerance

258
Q

Outline the NYHA classification of heart failure

A

Class I - no limitations
Class II - ordinary activity=symptoms
Class III - less than ordinary activity = symtpoms
Class IV - symptoms at rest

259
Q

What lifestyle interventions can be recommended to someone with HF?

A 
Avoid excessive alcohol intake (=> dilated cardiomyopathy)
Smoking cessation
Low intensity exercise
Decrease salt to <6g per day
Daily weight monitoring
260
Q

What invasive procedures are available for someone with HF?

A

Cardiac resynchronisation therapy with pacing (CRT-P)
Implantable cardioverter defibrillators (ICDs)
Coronary revascularisation
Cardiac transplantation
Assisted ventilation

261
Q

What are the desirable lipid ranges?

A

TC <5mmol/L
LDL <3mmol/L
HLD >1.2mmol/L (F), >1mmol/L (M)
Triglycerides <1.7mmol/L

Stage 3 Block 2 (8 decks)

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