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17. Clinical Pharmacology and Therapeutics > 19. Hypertension and Heart Failure > Flashcards

19. Hypertension and Heart Failure Flashcards

1
Q

What are the mechanisms of control of blood pressure?

A

Autonomic nervous system, renin-angiotensin system, bradykinin, endothelin, nitric oxide, ANP.

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2
Q

What are the responses to increased BP?

A

Increased perfusion so increased urinary output and decreased blood volume, also decreased RAAS so less vasoconstriction. Baroreceptors detect it so more PNS and less SNS so drop in BP.

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3
Q

What are the response to falling BP?

A

Decreased renal perfusion decreases urinary output so blood volume increased, also increased RAAS so vasoconstriction so increased peripheral resistance. Baroreceptors detect it so less PNS and more SNS so BP raised.

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4
Q

What are the actions of angiotensin II?

A

Increased aldosterone, retention of salt and water (also caused by aldosterone), vasoconstriction.

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5
Q

What is the result of chronic high blood pressure?

A

Increased arterial thickening, smooth muscle hypertrophy and accumulation of arterial compliance, loss of arterial compliance, target organ damage, heart-kidneys-brain-eyes, CV morbidity and mortality.

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6
Q

What is hypertension defined as?

A

140/90mmHg or higher.

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7
Q

What are the associated risk reductions from lowering diastolic BP by 10mmHg?

A

Stroke risk reduced by 58%, CHD by 37%.

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8
Q

What are the two types of hypertension?

A

Primary (essential) hypertension with no single evident cause, secondary hypertension with discrete cause.

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9
Q

What is the treatment line of hypertension?

A

Identify and treat underlying cause if present, treat other cardiovascular risks, non-pharm therpaies, pharmacological therapy.

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10
Q

What is the lifestyle therapy for hypertension?

A

Patient education, maintain weight BMI 20-25kg/m^2, reduce salt, limit alcohol, regular aerobic physical exercise, 5 portions of fruit and veg, reduce total and saturated fat, stop smoking, relaxation therapies.

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11
Q

What are the first line pharmacological therapies for hypertension?

A

Angiotensin converting enzyme (ACE) inhibitors/ angiotensin receptor blockers (ARB), calcium channel blockers, diuretics.

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12
Q

What is the mechanism of action of ACEi?

A

Competitive inhibitors of ACE, reduce formation of angiotensin II, also means less circulating aldosterone, overall arterial vasodilators.

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13
Q

Name an ACEi.

A

Lisinopril, ramipril.

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14
Q

What is the main ADR of ACEi and the cause?

A

Dry cough due to bradykinin not being broken down.

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15
Q

What are the ADRs of ACEi?

A

Dry cough, angio-oedema, renal failure, hyperkalaemia.

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16
Q

Name an ARB.

A

Losartan, valsartan.

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17
Q

What is the mechanism of action of ARBs?

A

Inhibit vasoconstriction and aldosterone stimulation from angiotensin II.

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18
Q

What are the key ADRs of ARBs?

A

Renal failure, hyperkalaemia.

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19
Q

What is the mechanism of action of calcium channel blockers?

A

Binds to specific alpha subunits of L-type calcium channels, reducing cellular calcium entry.

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20
Q

What are the three main groups of calcium channel blockers? Give an example of each.

A

Dihydropyridines - nifedipine, amlodipine. Benzothiazepines - diltiazem. Phenylalkylamines - verapamil.

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21
Q

What is the action of calcium channel blockers?

A

Vasodilates peripheral, coronary, and pulmonary arteries.

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22
Q

What is a specific action of verapamil (a phenyalkylamine calcium channel blocker)?

A

Depresses SAN and slows AV conduction.

23
Q

What are the properties of dihydropyridine calcium channel blockers?

A

Good oral absorption, >90% protein bound, liver metabolised.

24
Q

What are the ADRs of dihydropyridine calcium channel blockers?

A

SANS activation (tachycardia and palpitations), flushing/sweating/throbbing headache, oedema , gingival hyperplasia.

25
Q

What type of anti-arrhythmic are phenylalkylamine calcium channel blockers?

A

Class IV anti-arrhythmic agent so prolongs potential/effective refractory period.

26
Q

What are the ADRs of phenylalkylamine calcium channel blockers?

A

Constipation, risk of bradycardia, reduce myocardial contractility.

27
Q

What are the ADRs of benzothiazepine calcium channel blockers?

A

Risk of bradycardia, some negative inotropic effect but not too bad.

28
Q

What is the action of thiazides/thiazide like diuretics?

A

Reduce distal tubular sodium reabsorption.

29
Q

Name a thiazide/thiazide like diuretic for hypertension.

A

Bendroflumethiazide.

30
Q

What are the ADRs of bendorflumethiazide?

A

Hypokalaemia, increased urea and uric acid, impaired glucose tolerance, cholesterol and triglyceride levels increase, RAAS activated.

31
Q

What are the four steps recommended for treatment of hypertension in patients under 55 years?

A
  1. ACE inhibitor or ARB if intolerant.
  2. Add on calcium-channel blocker or thiazide-type diuretic.
  3. Add on CCB or TTD.
  4. Add further diuretic therapy or a-blocker or B-blocker.
32
Q

What are the four steps recommended for treatment of hypertension in patients older than 55 or black patients?

A
  1. Calcium-channel blocker of thiazide-type diuretic.
  2. Add on ACEi or ARB.
  3. Add on CCB or TTD.
  4. Add further diuretic therapy or a-blocker or B-blocker.
33
Q

What is the mechanism of action of alpha blockers?

A

Selective antagonism at post-synaptic a-1 adrenoceptors, antagonises contractile effects of NA on vascular smooth muscle so reduces peripheral vascular resistance.

34
Q

What are the ADRs of alpha blockers?

A

Postural hypotension, dizziness, headache and fatigue, oedema.

35
Q

Name an alpha blocker.

A

Doxazosin.

36
Q

Name a beta blocker.

A

Atenolol, bisoprolol, nebivolol.

37
Q

What is the action of beta blockers?

A

Reduce HR and CO, inhibit renin, TPR increases initially but falls to normal.

38
Q

What are the ADRs of beta blockers?

A

Lethargy, reduced exercise tolerance, bradycardia, cold hand, impaired glucose tolerance.

39
Q

What is a contraindication for beta blocker use?

A

Asthma.

40
Q

What is the mechanism of action of aliskiren (direct renin inhibitor)?

A

Binds in renin molecule and blocks cleavage of angiotensinogen to angiotensin I.

41
Q

What is the half life of aliskiren?

A

40 hours, so can be used once-daily.

42
Q

How is aliskiren eliminated?

A

In faeces, some renally excreted.

43
Q

What is a DDI of aliskiren?

A

Furosemide.

44
Q

What is a CI of aliskiren?

A

Pregnancy.

45
Q

How can methyldopa be used to treat hypertension?

A

Converted to a-methyl-noradrenaline - a2-adrenoceptor agonists.

46
Q

How can clinidine be used to treat hypertension?

A

Direct pre-synaptic a2-adrenoceptor agonist.

47
Q

How can moxonidine be used to treat hypertension?

A

Imidazoline I1 receptor agonist and some a2 agonist effect.

48
Q

What is the general action of centrally acting agents in hypertension?

A

Reduce sympathetic outflow.

49
Q

What are the ADRs of centrally acting agents in hypertension?

A

Tiredness/lethargy, depression.

50
Q

What is the aetiology of heart failure?

A

Ischaemic heart disease, hypertension, cardiomyopathies, valve disease, others.

51
Q

What is the vicious cycle of heart failure?

A

RAAS, if output is reduced, less blood gets to kidneys so RAAS is stimulated, meaning there is vasoconstriction and more pressure to work against so output is reduced even more.

52
Q

How can prognosis of heart failure be improved?

A

RAS antagonism, beta-blockers.

53
Q

What are the physiological effects of B-blockers?

A

Reduced heart rate, reduced BP => reduced myocardial oxygen demand. Reduced mobilisation of glycogen, fewer unwanted effects of catecholamines.

54
Q

How do B-blockers reduce sudden deaths in heart failure?

A

Less ventricular tachycardia, so less ventricular fibrillation so fewer sudden cardiac deaths.

17. Clinical Pharmacology and Therapeutics (25 decks)

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