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Drug Treatment for Hypertension Flashcards

(53 cards)

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1
Q

Core Drug: Bisoprolol/Propranolol :Molecular Mechanism and class :

A
  • anti-hypertensives
  • beta blockers
  • beta blocker (non-selective)
    propranolol
  • beta 1 selective blocker
    bisoprolol
  • insert slide
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2
Q

Core Drug: Bisoprolol/Propranolol: Side effects:

A
  • heart: fatigue, bradycardia
  • lungs: breathlessness, worsens
    asthma (non-selective beta)
  • arterioles:
    - fatigue, claudication
    - cold hands/feet
    - erectile dysfunction
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3
Q

Potential targets for anti-hypertensive drugs:

A
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4
Q

Adrenoreceptors

A
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5
Q

Core Drug: Bisoprolol/Propranolol: physiological effects:

A

Heart:
- decreases force and rate of
contraction
- lowers BP

Lungs: (Beta 2)L
- bronchoconstriction

Arterioles (beta 2):
- decreases blood supply to muscle
- decreases blood supply to skin
- decreases blood supply to penis

Dangerous:
- diabetes patients prone to
episodes of hypoglycaemia
- hence body releases adrenaline
- whichc causes glucose release from
liver (gluconeogenesis)
- typical symptoms: temor, palpitations, sweats
- all blocked by beta blockers
- patients will not recognise

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6
Q

Core Drug: Bisoprolol/Propranolol: Clinical Uses:

A
  • angina, hypertension, arrhythmias
  • migraine, tremor
  • anxiety, thyrotoxicosis
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7
Q

Beta blockers are contraindicated in

A

patients that are diabetic with recurrent hypoglycaemia

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8
Q

Thiazide drugs as antihypertensive drugs target?

A

blood volume

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9
Q

Beta blockers as anti-hypertensive drugs target?

A

ionotropy
heart rate (decrease)

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10
Q

Core Drug: Bendroflumethiazide: Molecular Mechanism of action and class:

A
  • diuretic (thiazide)

Blocks Na+/Cl- symporter in distal convoluted tubule, hence less water absorbed

second mechanism of action: activate Katp in smooth muscle of blood vessels

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11
Q

Core Drug: Bendoflumethiazide: Physiological Effects:

A

Kidney (Na+/Cl symporter):
- increases Na+ loss
- increases WATER LOSS
- decreases BP

Arterioles (K-ATP):
- decreases BP

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12
Q

Core Drug: Bendoflumethiazide: Side Effects:

A

Kidney:
- hyponatraemia
- hypokalaemia
- alkalosis
- hypercalcaemia
- hypomagnesaemia
- increase in urate (gout)

Insulin Resistance: increase in glucose (diabetes)

Liver: increase in lipids (arterial disease)

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13
Q

3 other uses for thiazides apart from hypertension:

A
  • oedema
  • urinary tract stones
  • nephrogenic diabetes insipidus
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14
Q

Core Drug: Indapamide: Class and molecular mechanism of action:

A
  • diuretic
  • thiazide like drug
  • activates K+ ATP channel in smooth
    muscle of blood vessels to dilater
    arterioles
  • more K+ leaves cell

Blocks Na+/Cl- symporter in distal convoluted tubule, hence less water absorbed

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15
Q

Core Drug: Indapamide: Physiological Effects:

A

Kidney (Na+/Cl symporter):
- increases Na+ loss
- increases WATER LOSS
- decreases BP

Arterioles: lowers BP

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16
Q

Core Drug: Indapamide: Side effects:

A

Kidney:
- hyponatraemia
- hypokalaemia
- alkalosis
- hypercalcaemia
- hypomagnesaemia
- increase in urate (gout)

Insulin Resistance: increase in glucose (diabetes)

Liver: increase in lipids (arterial disease)

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17
Q

Are thiazide diuretics more aggressive than loop diuretics?

A

No
loop = aggressive (more)

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18
Q

Thiazide isnt very effective hypertensive but very effective diuretic?

A

No
Thiazide = gentle diuretic but powerful antihypertensives

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19
Q

Core Drug: Doxazosin: Molecular Mechanism and Class:

A

anti-hypertensive, alpha blocker

alpha 1 receptor acts via Gq to increase IP3 and hence Ca2+ intracellularly

Doxazosin blocks alpha 1, hence there is a decrease in intra cellular release of Ca2+ in arteriolar smooth muscle

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20
Q

Alpha blockers as anti-hypertensives are targets?

A

stroke volume

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21
Q

Core Drug: Doxazosin: Physiological Effects:

A
  • prevents contraction of arteriolar
    smooth muscle
  • relaxes bladder outflow sphincter
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22
Q

Core Drug: Doxazosin: Side Effects:

Study These Flashcards
A
  • palpitations (reflex tachycardia)
  • postural hypotension (stand up, arteries constrict, elderly patietns have a weakening of this reflex) causing dizziness
23
Q

Core Drug: Doxazoosin: Clinical Uses:

Study These Flashcards
A
  • anti-hypertensive
  • prostatic hypertrophy: relax
    bladder outflow sphincter
24
Q

Core Drug: Amlodipine: Molecular mechanism of action and class:

Study These Flashcards
A
  • anti-hypertensive
  • calcium channel blocker
  • dihydopyridines
  • block L type voltage-gated Ca”+
    channel
25
Core Drug: Diltiazem: Molecular mechanism of action and class:
- anti-hypertensive - calcium channel blocker - block L type voltage-gated Ca"+ channel
26
Core Drug: Verapamil: Molecular mechanism of action and class:
- anti-hypertensive - calcium channel blocker - block L type voltage-gated Ca"+ channel
27
Core Drug: Amlodipine: Clinical Use:
hypertension
28
Core Drug: Diltiazem: Clinical Use:
angina hypertension
29
Core Drug: Verapamil: Clinical Use:
arrhythmias hypertension
30
Core Drugs: Amlodipine, Diltiazem, Verapamil: Physiological Effects:
- decreases intracellular Ca2+ Arterioles: - smooth muscle relaxation Cardiac Muscle: - decreased force of contraction SA node and AV node: - decreased heart rate
31
Core Drug: Amlodipine, Diltiazem, Verapamil: Side Effects:
- ankle swelling - palpitations - constipation - flushing - exacerbation of heart failure
32
Balance of actions of calcium channel blockers
33
Why do calcium channel blockers cause ankle swelling?
- dilation of pre-capillary arteriole - impaired function of pre-capillary sphincter - increased hydrostatic pressure filtration - net flitration - oedema occurs when the pressure in the capillaries exceeds the suction pressure pulling fluid back into circulation
34
RAAS
35
Core Drug: Ramipril: molecular mechanism and class:
- anti-hypertensive - ACE inhibitor - Angiotensin Converting Enzyme converts Angiotensin I to Angiotensin II and also breaks down bradykinin - inhibits Angiotensin Converting Enzyme
36
Core Drug: Ramipril: physiological effects:
- decrease in angiotensin II, hence decrease in vasoconstriction - increase in bradykinin hence increase in vasodilation overall reduces BP
37
Core Drug: Ramipril: Side Effects:
- Dry Cough: bradykinin accumulation in the lungs - Renal impairment: Renal Artery Stenoses - Hyperkalaemia: hence commonly given with a diuretic
38
Core Drug: Ramipril: Clinical Uses:
- hypertension - heart failure
39
Core Drug: Ramipril: contraindications:
Afro-Caribbean people dont react well to ACE inhibitors
40
Core Drug: Losarten: molecular mechanism and class:
- anti-hypertensive - ARB = angiotensin II receptor antagonists/blockers - blocks action of angiotensin II on receptor
41
Core Drug: Losarten: physiological effects:
- decrease vasoconstriction
42
Core Drug: Losarten: Side Effects:
- less dry cough than ACE inhibitors - Renal impairment: Renal Artery Stenoses - Hyperkalaemia: hence commonly given with a diuretic
43
Core Drug: Losarten: Clinical Uses:
hypertension
44
Core Drug: Spironolactone: molecular mechanism and class:
- diuretic - aldosterone antagonist - blocks upregulation of Na+ channels in the distal convoluted tubule by aldosterone
45
Core Drug: spironolactone: physiological effects:
- reduces water reabsorption - reduces volume in arteries
46
Core Drug: Spironolactone: Side Effects:
- impaired renal function - hyperkalaemia - gynaecomastia (structurallly similar to oestregen) (men grow breasts)
47
Core Drug: Spironolactone: Clinical Uses:
- used as an add on in resistant HT - first line in HT due to hyperaldosteronism
48
Specific causes of HT:
- chronic kidney disease - structural causes: - renal artery stenosis - aortic coarctation (narrowing of aorta above kidneys) - Endocrine causes: - high aldosterone levels - high catecholamine levels - high cortisol levels - growth hormone levels - Pregnancy/ Pre-eclampsia
49
NICE guidance: stages of hypertension and treatment:
- stage 1 = BP>140/90: - treat if end-organ damage or diabetic - stage 2: BP>160/100 - treat once confirmed on 24hrBP - stage 3: systolic BP>180 - treat immediately
50
Pharmacological HT treatment
51
NICE guidance: HT treatment targets: <80yrs:
- <140/90
52
NICE guidance: HT treatment targets: >80yrs:
<150/90
53
NICE guidance: HT treatment targets: diabetes:
<135/85

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