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HLB > Drug Treatment for Hypertension > Flashcards

Drug Treatment for Hypertension Flashcards

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:

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:

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

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

A
  • anti-hypertensive
  • calcium channel blocker
  • dihydopyridines
  • block L type voltage-gated Ca”+
    channel
25
Q

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

A
  • anti-hypertensive
  • calcium channel blocker
  • block L type voltage-gated Ca”+
    channel
26
Q

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

A
  • anti-hypertensive
  • calcium channel blocker
  • block L type voltage-gated Ca”+
    channel
27
Q

Core Drug: Amlodipine: Clinical Use:

A

hypertension

28
Q

Core Drug: Diltiazem: Clinical Use:

A

angina
hypertension

29
Q

Core Drug: Verapamil: Clinical Use:

A

arrhythmias
hypertension

30
Q

Core Drugs: Amlodipine, Diltiazem, Verapamil: Physiological Effects:

A
  • decreases intracellular Ca2+

Arterioles:
- smooth muscle relaxation

Cardiac Muscle:
- decreased force of contraction

SA node and AV node:
- decreased heart rate

31
Q

Core Drug: Amlodipine, Diltiazem, Verapamil: Side Effects:

A
  • ankle swelling
  • palpitations
  • constipation
  • flushing
  • exacerbation of heart failure
32
Q

Balance of actions of calcium channel blockers

A
33
Q

Why do calcium channel blockers cause ankle swelling?

A
  • 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
Q

RAAS

A
35
Q

Core Drug: Ramipril: molecular mechanism and class:

A
  • anti-hypertensive
  • ACE inhibitor
  • Angiotensin Converting Enzyme
    converts Angiotensin I to
    Angiotensin II and also breaks
    down bradykinin
  • inhibits Angiotensin Converting
    Enzyme
36
Q

Core Drug: Ramipril: physiological effects:

A
  • decrease in angiotensin II, hence
    decrease in vasoconstriction
  • increase in bradykinin hence
    increase in vasodilation

overall reduces BP

37
Q

Core Drug: Ramipril: Side Effects:

A
  • Dry Cough: bradykinin
    accumulation in the lungs
  • Renal impairment: Renal Artery
    Stenoses
  • Hyperkalaemia: hence commonly
    given with a diuretic
38
Q

Core Drug: Ramipril: Clinical Uses:

A
  • hypertension
  • heart failure
39
Q

Core Drug: Ramipril: contraindications:

A

Afro-Caribbean people dont react well to ACE inhibitors

40
Q

Core Drug: Losarten: molecular mechanism and class:

A
  • anti-hypertensive
  • ARB = angiotensin II receptor
    antagonists/blockers
  • blocks action of angiotensin II on
    receptor
41
Q

Core Drug: Losarten: physiological effects:

A
  • decrease vasoconstriction
42
Q

Core Drug: Losarten: Side Effects:

A
  • less dry cough than ACE inhibitors
  • Renal impairment: Renal Artery
    Stenoses
  • Hyperkalaemia: hence commonly
    given with a diuretic
43
Q

Core Drug: Losarten: Clinical Uses:

A

hypertension

44
Q

Core Drug: Spironolactone: molecular mechanism and class:

A
  • diuretic
  • aldosterone antagonist
  • blocks upregulation of Na+
    channels in the distal convoluted
    tubule by aldosterone
45
Q

Core Drug: spironolactone: physiological effects:

A
  • reduces water reabsorption
  • reduces volume in arteries
46
Q

Core Drug: Spironolactone: Side Effects:

A
  • impaired renal function
  • hyperkalaemia
  • gynaecomastia (structurallly similar
    to oestregen) (men grow breasts)
47
Q

Core Drug: Spironolactone: Clinical Uses:

A
  • used as an add on in resistant HT
  • first line in HT due to
    hyperaldosteronism
48
Q

Specific causes of HT:

A
  • 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
Q

NICE guidance: stages of hypertension and treatment:

A
  • 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
Q

Pharmacological HT treatment

A
51
Q

NICE guidance: HT treatment targets: <80yrs:

A
  • <140/90
52
Q

NICE guidance: HT treatment targets: >80yrs:

A

<150/90

53
Q

NICE guidance: HT treatment targets: diabetes:

A

<135/85

HLB (49 decks)

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