Hypertension and HF Flashcards

1
Q

What are the ranges for the different grades of hypertension?

A

Grade I: 140-159/90-99

Grade II: 160-179/100-109

Grade III: >180/>110

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2
Q

What are some drugs that can cause hypertension?

A

OCP
Corticosteroids
NSAIDs

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3
Q

Problems and complications of hypertension?

A
Increased arterial thickening
Smooth muscle cell hypertrophy
Accumulation of vascular matrix
Loss of arterial compliance
Target organ damage such as heart, kidneys, brain, eyes
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4
Q

Endocrine causes of secondary hypertension?

A
Conn's syndrome
Congenital adrenal hyperplasia
Cushing's
Phaeochromocytoma
Thyroid disease
Acromegaly
Hyperparathyroidism
Carcinoid
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5
Q

Renal causes of hypertension?

A
Renovascular hypertension
Chronic pyelonephritis
Diabetic renal disease
Renal parenchymal disease
Liddle's syndrome
Gordon's syndrome
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6
Q

What is phaeochromocytoma?

A

Adrenal catecholamine-secreting tumour - produces large amounts of adrenaline and NA

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7
Q

How is phaeochromocytoma treated?

A

Non-selective alpha-adrenoreceptor antagonists

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8
Q

What is Conn’s syndrome?

A

An aldosterone-secreting adenoma causing fluid reabsorption

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9
Q

How is Conn’s syndrome treated?

A

Aldosterone antagonists eg spironolactone

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10
Q

How is mild (grade I) hypertension treated?

A

Normally a non-pharmacological therapy (lifestyle changes)

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11
Q

What is isolated systolic hypertension and what is it due to?

A

A low diastolic BP and a high systolic BP (>140mmHg)

Common with increasing age due to loss of compliance of arteries

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12
Q

What are some non-pharmacological interventions?

A

Maintain normal body weight
Reduce salt intake
Consume 5+ portions of fruit and veg a day
Limit alcohol
Regular exercise
Reduce total and saturated fat
Stop smoking (just reduces CV risk, not BP)

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13
Q

When is blood pressure treated pharmacologically?

A

When it is above 160/100mmHg

Above 140/90mmHg in diabetics

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14
Q

What is someone under 55 initially treated for hypertension with?

A

ACE inhibitors

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15
Q

What is someone over 55 or black of any age initially treated with?

A

Calcium channel blockers

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16
Q

If there is no response in someone with hypertension with initial treatment, what is done?

A

Combine ACE inhibitors and Ca channel blockers

Then add diuretics

Then add alpha-blockers, beta-blockers, centrally acting drugs or vasodilators

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17
Q

Name some ACE-i

A

Lisinopril

Ramipril

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18
Q

What is the mechanism of action of ACE-i?

A

Competitively inhibits ACE activity

  • reducing formation of angiotensin II
  • preventing degradation of bradykinin
  • minimising production of aldosterone
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19
Q

What are the overall effects of ACE-i?

A

Reduce effect of RAAS

  • reduce Na and water reabsorption
  • reduce peripheral vasoconstriction
  • some venodilation action
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20
Q

ADRs of ACE-i?

A
HARD
Hyperkalaemia
Angioedema
Renal problems/failure
Dry cough
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21
Q

Name some angiotensin-II receptor blockers (ARBs)

A

Losartan

Valsartan

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22
Q

ADRs of ARBs?

A

Renal failure

Hyperkalaemia

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23
Q

Indications for ARBs?

A

For individuals who cannot tolerate adverse effects of ACE-i

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24
Q

Mechanism of action of calcium-channel blockers?

A

Bind to the alpha-subunit of L-type calcium channels, reducing calcium entry
Causes vasodilation of peripheral, coronary and pulmonary arteries by smooth muscle relaxation

25
Q

What are the main groups of calcium channel blockers? Name a drug in each group

A

Dihydropyridines - nifedipine, amlodipine

Phenylalkylamines - verapamil

Benzothiazepines - dilitiazem

26
Q

Absorption, distribution and metabolism of dihydropyridines?

A

Good oral absorption
90% protein bound
Metabolised by liver

27
Q

ADRs of dihydropyridines?

A
Baroreflex-mediated tachycardia 
SNS activation - tachycardia and papitations
Flushing and sweating
Ankle oedema
Throbbing headache

However normally well-tolerated

28
Q

Mechanism of action of phenylalkylamines eg verapamil and overall effects?

A

Act on myocardial and smooth muscle cell membrane calcium transport - leads to vasodilation, reducing cardiac preload and myocardial contractility

Class IV anti-arrhythmic - prolongs action potential/effective refractory period

29
Q

ADRs of phenylalkylamines?

A

Constipation
Bradycardia
Negative inotropy

30
Q

DDIs of phenylalkylamines?

A

Cannot be given with beta-blockers as they cause bradycardia

31
Q

Effects of benzothiazepines?

A

Peripheral vasodilation and reduced myocardial contractility

Prolongs action potential/effective refractory period

32
Q

ADRs of benzothiazepines?

A

Bradycardia

Negative inotropy

33
Q

What are benzothizaepines mostly used for?

A

Angina rather than hypertension

34
Q

Overall effects of thiazide diuretics?

A

Act on Na-Cl symport in DCT
Reduced sodium and water absorption, reduced blood volume
Long-term, reduces TPR

35
Q

ADRs of thiazides?

A

Hypokalaemia
Increased urea and uric acid
Impaired glucose tolerance
Raised cholesterol and triglyceride levels

36
Q

Name an alpha blocker

A

Doxazosin

37
Q

Mechanism of action of alpha blockers?

A

Antagonise alpha-1 adrenoreceptors and antagonises contractile effects of NA, reducing TPR

38
Q

ADRs of alpha-blockers?

A

Postural hypotension
Dizziness
Headache and fatigue
Oedema

39
Q

Mechanism of action of beta blockers?

A

Antagonise beta-1 adrenoceptors on ventricular myocardium, reducing HR and CO
Inhibit renin release
Rarely used as anti-hypertensive as have little significant effect

40
Q

Why are beta-blockers good for angina?

A

Slow heart rate, increasing diastolic filling of coronary arteries

41
Q

ADRs of beta-blockers?

A
Lethargy
Impaired concentration
Reduced exercise tolerance
Bradycardia
Raynaud's
Impaired glucose tolerance
42
Q

Contra-indications of beta-blockers?

A

Asthma

43
Q

How do direct renin inhibitors work?

A

Bind to the renin molecule, preventing cleavage of angiotensinogen to angiotensin I

44
Q

Name a renin inhibitor

A

Aliskiren

45
Q

Bioavailability and excretion of aliskiren?

A

Low bioavailability
Eliminated unchanged in faeces
1% renally excreted

46
Q

In which patients must care be taken in prescribing renin inhibitors?

A

Patients at risk of hyperkalaemia, sodium and volume-depleted patients, patients with HF, severe renal impairment, renal stenosis

47
Q

Examples of centrally acting agents?

A

Methyldopa - alpha-2 adrenoceptor agonist
Clonidine - pre-synaptic alpha-2 agonist
Monoxidine - alpha-2 agonist

48
Q

Effects of centrally acting agents?

A

Reduce sympathetic outflow which reduces blood pressure

49
Q

Benefits of centrally acting agents?

A

Good response

Safe in pregnancy

50
Q

ADRs of centrally acting agents?

A

Tiredness and lethargy

Depression

51
Q

What can happen in withdrawal of clonidine?

A

Rebound hypertension - due to NA release leading to desensitisation of alpha 2 receptors and super-sensitivity of post-synaptic alpha-1 receptors

52
Q

What is a hypertensive emergency?

A

Very high BP of >220/120

53
Q

What can happen in a hypertensive emergency if BP is not reduced by around 20% within 1-2 hours?

A

Pulmonary oedema
Renal failure
Aortic dissection

54
Q

Treatment of hypertensive emergencies?

A

Sodium nitroprusside - acts as an endogenous nitrous oxude causing vasodilation and rapid onset of reduction of BP

55
Q

What are the goals in HF treatment?

A

Symptomatic improvement
Delay progression
Reduce mortality
Treat complications/associated conditions/CVS risk factors

56
Q

What are the drugs used in HF?

A

ACE inhibitors and ARBs
Aldosterone antagonists
Diuretics (loop and thiazide)

57
Q

What can aldosterone do/cause in HF?

A

Can return to normal even with ACE-i/ARB therapy

Endothelial dysfunction leading to myocardiac fibrosis and acute coronary events
Potassium and magnesium leading to arrhytmias
Myocardiac fibrosis leading to arrhythmias

All of these increase risk of sudden cardiac death

58
Q

Why are beta-blockers good in HF?

A

Reduce myocardial oxygen demand

  • reduce heart rate via beta receptors
  • reduce BP, reducing CO

Reduce metabolism of glycogen
Negate unwanted effects of catecholamines

59
Q

Why do beta-blockers need to be prescribed with care in HF?

A

A failing myocardium is dependent on HR