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Pharmocolgy > P13: Pharmacological Management of Hypertension > Flashcards

P13: Pharmacological Management of Hypertension Flashcards

1
Q

What are the normal blood pressure ranges

A

90-120/60-80 mmHg

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2
Q

Equation for arterial blood pressure

A

Arterial Blood Pressure = Cardiac Output x Peripheral vascular resistance

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3
Q

Name the symptoms of Hypertension

A

There usually are none lol

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4
Q

Name risk factors for hypertension

A

Stress
Dietary salt
High saturated fat intake
High alcohol intake

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5
Q

What BP is considered hypertension

A

140/90

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6
Q

Name some of the potential consequences of hypertension

A
  • Most important cause of occlusive stroke
  • Major cause of haemorrhagic stroke
  • Kidney disease/failure
  • Angina, heart disease and cardiac infarction
  • Blindness through hypertensive retinopathy
  • Sexual dysfunction
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7
Q

How and where does hypertension cause hypertrophy in the heart

A
  • Thickening in left ventricle wall

- Hypertension causes greater pressure load on the heart to induce left ventricular hypertrophy

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8
Q

Name some drugs that can cause hypertension

A
  • Oral contraceptives (estrogen, progesterone)
  • Monoamine oxidase inhibitors
  • Indirectly acting sympathomimetic amines
  • Carbenoloxone (treatment of gastric/duodenal ulcers)
  • Steroids (glucocorticoids)
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9
Q

Name some diseases that result in hypertension

A
  • Phaeochromocytoma (adrenal chromaffin cell tumour)
  • Cushing’s syndrome (excess cortisol) - renal hypertension
  • Conn’s syndrome (excess aldosterone) - renal hypertension
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10
Q

What 2 things are pathogenesis factors for hypertension

A

Increased cardiac output

Increased peripheral resistance

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11
Q

What causes increased preload

A

Increased fluid volume
Excess sodium intake
Renal sodium retention

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12
Q

What causes increased venous constriction

A
  • excess renin/aldosterone/angiotensin stimulation
  • SNS over-activity
  • endothelial derived factors
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13
Q

What 3 major sites are pharmacological agents used to treat hypertension

A
  • Sympathetic nervous system
  • Vascular smooth muscle
  • Renal system
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14
Q

What are the aims of hypertension treatments

A
  • Suppress renin/angiotensin activity
  • Suppress heart rate and/or vasoconstriction
  • Increase vasodilation
  • Increase diuresis
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15
Q

What are the effects of Angiotensin II

A
  • Direct vasoconstrictor, acting on AT1 receptors on the vascular smooth muscle - Gq, IP3, Ca2+ mobilisation, muscle contraction
  • ADH release from anterior pituitary
  • Acts on hypothalamus to increase desire for water(dipsogen) and salt
  • Increases aldosterone release
  • Directly acts on PCT to enhance Na+ uptake
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16
Q

What are the effects/actions of aldosterone

A
  • Promotes Na+ and Na+/K+ channel expression in the DCT and CD through mineralocorticoid receptor (MR) actions
  • Enhances Na+ reuptake and K+ excretion
  • Water follows Na+
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17
Q

What are the effects of Angiotensin II from Aldosterone

A

Aldosterone is rapidly upregulated by the action of ATII in response to decreased plasma Na+

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18
Q

Name some Angiotensin Converting Enzyme (ACE) inhibitors

A

Enalapril

Captopril

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19
Q

Name an Angiotensin II (AT1 type) receptor antagonists

A

Iosartan

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20
Q

Why are there no usable renin inhibitors

A

too many side effects

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21
Q

How does Angiotensinogen form Angiotensin II

A

Angiotensinogen to ATI using renin

ATI to ATII using ACE

22
Q

Overall effects of ATII

A

Increased vasoconstriction
Increased aldosterone
Increased sympathetic function
Increased ADH

23
Q

How do diuretics reduce hypertension

A

Reduce hypertension by reducing blood volume and depleting sodium

24
Q

How do thiazide diuretics work and give an example

A
  • Inhibits reabsorption of Na+ and Cl- in the DCT
  • Increased Na+ in the CD leading to increased Na+/K+ antiporter activity - hypokalaemia
  • Hydrochlorothiazide
25
Q

How do Potassium-sparing diuretics work and give an example

A
  • Inhibits aldosterone effect on Na+ reabsorption and K+ excretion in DCT
  • MR antagonists
26
Q

Describe the mechanism of hypertension drugs that target the heart

A

Primary approach is to block Beta1 adrenoceptors in the heart, causes bradycardia

27
Q

Name some hypertension drugs that target the heart

A 
Atenolol
Oxprenolol
Pindolol
Acebutolol
Celiprolol
(these are kinds of beta blockers)
28
Q

When are hypertension drugs that target the heart used (first line etc)

A

Not first line except in patients who do not tolerate ACE inhibitors or AT1 antagonists

29
Q

What are potential side effects of hypertension drugs that target the heart

A

Anxiety
Insomnia
Bronchospam in asthamtics/COPD patients

30
Q

Describe the mechanism of Ca2+ channel blockers

A
  • Inhibits influx of extracellular Ca2+ into cardiac and smooth muscle cell
  • Block L-type Ca2+ channels - coronary and peripheral vasodilation
31
Q

Where are N-type and L-type calcium channels found

A 
N-type = in presynpatic terminals
L-type = in the T-tubules
32
Q

What type of calcium channels do Ca2+ channels block

A

No binding to N-type

Large excess of L-type Ca2+ channels in skeletal muscle - limited effect

33
Q

What are the 2 classes of Ca2+ channel blockers and give examples of each

A

Dihydropyridines - nifedipine, amlodipine

Non-dihydropyridines - diltiazem, verapmil

34
Q

Describe the actions of Dihydropyridines

A
  • Favours vasculature over the heart
  • Reflex tachycardia due to potent vasodilation
  • No effect on AV condition, (not effective in supraventricular tachyarrythmias)
35
Q

Describe the actions of Non-Dihydropyridines

A
  • Favours heart over the vasculature

- Decrease the heart rate by slowing the AV node conduction (may treat supraventricular tachyarrythmias)

36
Q

What are the adverse effects of Non-Dihydropyridines

A

Bradycardia

Atrioventricular block

37
Q

When are Ca2+ channel blockers used (first line etc)

A

First line treatment in older patients, or if ACE inhibitors cant be used

38
Q

Name some centrally acting hypertension drugs that work at the medullary CVS regulatory centres

A

Clonidine, alpha-methyldopa

Moxonidine

39
Q

Describe the mechanism and effects of clonidine

A
  • selective alpha2 agonists
  • stimulation of alpha2 receptors in medulla reduces SNS outflow
  • causes centrally mediated vasodilation and reduction in heart rate
  • sedative in ~50% of patients
40
Q

Describe the mechanism and effects of Moxonidine

A
  • Selective agonist at the imidazoline subtype 1 (I1) receptor
  • ^^receptor found in depressor areas of the medulla
  • activation = decrease in SNS activity and so BP
  • used in moderate hypertension when other approaches fail
41
Q

What are the 3 types of peripheral nerve modulator hypertension drugs and give examples

A
  1. Ganglionic transmission - trimethaphan
  2. False neurotransmitters - guanethidine
  3. Non-selective alpha-adrenoceptor antagonists - phenoxybenzamine and phentolamine
42
Q

How do peripheral nerve modulators that affect ganglionic transmission work

A
  • short-acting N1 nicotinic receptor antagonist
  • prevents SNS activity in the vasculature = vasodilation
  • net tachycardia; loss of vascular resistance governs overall effect on BP
43
Q

What are the side effects of peripheral nerve modulators that affect ganglionic transmission (trimethaphan)

A

Postural hypotension
Loss of visual accomodation
Constipation
Urinary Retention

44
Q

How do peripheral nerve modulators that are false neurotransmitters work

A
  • Taken up by NA transporters, accumulates in vesicles
  • Displaces NA, reducing effect of sympathetic stimulation
  • Used in acute hypertensive crisis, rarely long term
45
Q

What are the side effects of peripheral nerve modulators that are false neurotransmitters (guanethidine)

A

Postural hypotension
Fluid Retention
Inhibits Ejaculation

46
Q

When are peripheral nerve modulators that are non-selective alpha-adrenoceptor antagonists used (phentolamine)

A
  • not used for treatment of hypertension - postural hypotension and tachycardia
  • Used in treatment of hypertensive crisis due to MAOI or phaeochromocytoma
47
Q

What kind of hypertensive drugs are used in hypertensive crisis and give some examples

A

Direct vasodilators
Hydralazine
Sodium Nitroprusside

48
Q

Describe the mechanism of Hydralazine

A
  • Liberates NO from vascular endothelium, stimulates cGMP production in vascular smooth muscle
  • cGMP activates PKG, which phosphorylates Ca2+ channels
  • Preventing their activation and induing relaxation (arterioles>veins)
49
Q

Side effects of Hydralazine

A

Tachycardia with palpitations, often hypotension

50
Q

Describe the mechanism of Sodium Nitroprusside

A
  • Stimulates soluble guanylate cyclase
  • Increasing vascular smooth muscle cGMP
  • Causes very rapid vasodilation
51
Q

Risk of using Sodium Nitroprusside

A

Metabolism releases cyanide ions - narrow therapeutic window

Pharmocolgy (22 decks)

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