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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
How do Potassium-sparing diuretics work and give an example
- Inhibits aldosterone effect on Na+ reabsorption and K+ excretion in DCT - MR antagonists
26
Describe the mechanism of hypertension drugs that target the heart
Primary approach is to block Beta1 adrenoceptors in the heart, causes bradycardia
27
Name some hypertension drugs that target the heart
``` Atenolol Oxprenolol Pindolol Acebutolol Celiprolol (these are kinds of beta blockers) ```
28
When are hypertension drugs that target the heart used (first line etc)
Not first line except in patients who do not tolerate ACE inhibitors or AT1 antagonists
29
What are potential side effects of hypertension drugs that target the heart
Anxiety Insomnia Bronchospam in asthamtics/COPD patients
30
Describe the mechanism of Ca2+ channel blockers
- Inhibits influx of extracellular Ca2+ into cardiac and smooth muscle cell - Block L-type Ca2+ channels - coronary and peripheral vasodilation
31
Where are N-type and L-type calcium channels found
``` N-type = in presynpatic terminals L-type = in the T-tubules ```
32
What type of calcium channels do Ca2+ channels block
No binding to N-type | Large excess of L-type Ca2+ channels in skeletal muscle - limited effect
33
What are the 2 classes of Ca2+ channel blockers and give examples of each
Dihydropyridines - nifedipine, amlodipine | Non-dihydropyridines - diltiazem, verapmil
34
Describe the actions of Dihydropyridines
- Favours vasculature over the heart - Reflex tachycardia due to potent vasodilation - No effect on AV condition, (not effective in supraventricular tachyarrythmias)
35
Describe the actions of Non-Dihydropyridines
- Favours heart over the vasculature | - Decrease the heart rate by slowing the AV node conduction (may treat supraventricular tachyarrythmias)
36
What are the adverse effects of Non-Dihydropyridines
Bradycardia | Atrioventricular block
37
When are Ca2+ channel blockers used (first line etc)
First line treatment in older patients, or if ACE inhibitors cant be used
38
Name some centrally acting hypertension drugs that work at the medullary CVS regulatory centres
Clonidine, alpha-methyldopa Moxonidine
39
Describe the mechanism and effects of clonidine
- 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
Describe the mechanism and effects of Moxonidine
- 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
What are the 3 types of peripheral nerve modulator hypertension drugs and give examples
1. Ganglionic transmission - trimethaphan 2. False neurotransmitters - guanethidine 3. Non-selective alpha-adrenoceptor antagonists - phenoxybenzamine and phentolamine
42
How do peripheral nerve modulators that affect ganglionic transmission work
- 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
What are the side effects of peripheral nerve modulators that affect ganglionic transmission (trimethaphan)
Postural hypotension Loss of visual accomodation Constipation Urinary Retention
44
How do peripheral nerve modulators that are false neurotransmitters work
- Taken up by NA transporters, accumulates in vesicles - Displaces NA, reducing effect of sympathetic stimulation - Used in acute hypertensive crisis, rarely long term
45
What are the side effects of peripheral nerve modulators that are false neurotransmitters (guanethidine)
Postural hypotension Fluid Retention Inhibits Ejaculation
46
When are peripheral nerve modulators that are non-selective alpha-adrenoceptor antagonists used (phentolamine)
- not used for treatment of hypertension - postural hypotension and tachycardia - Used in treatment of hypertensive crisis due to MAOI or phaeochromocytoma
47
What kind of hypertensive drugs are used in hypertensive crisis and give some examples
Direct vasodilators Hydralazine Sodium Nitroprusside
48
Describe the mechanism of Hydralazine
- 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
Side effects of Hydralazine
Tachycardia with palpitations, often hypotension
50
Describe the mechanism of Sodium Nitroprusside
- Stimulates soluble guanylate cyclase - Increasing vascular smooth muscle cGMP - Causes very rapid vasodilation
51
Risk of using Sodium Nitroprusside
Metabolism releases cyanide ions - narrow therapeutic window

Pharmocolgy (22 decks)

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