Drug Treatment for Hypertension Flashcards
Core Drug: Bisoprolol/Propranolol :Molecular Mechanism and class :
- anti-hypertensives
- beta blockers
- beta blocker (non-selective)
propranolol - beta 1 selective blocker
bisoprolol - insert slide
Core Drug: Bisoprolol/Propranolol: Side effects:
- heart: fatigue, bradycardia
- lungs: breathlessness, worsens
asthma (non-selective beta) - arterioles:
- fatigue, claudication
- cold hands/feet
- erectile dysfunction
Potential targets for anti-hypertensive drugs:
Adrenoreceptors
Core Drug: Bisoprolol/Propranolol: physiological effects:
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
Core Drug: Bisoprolol/Propranolol: Clinical Uses:
- angina, hypertension, arrhythmias
- migraine, tremor
- anxiety, thyrotoxicosis
Beta blockers are contraindicated in
patients that are diabetic with recurrent hypoglycaemia
Thiazide drugs as antihypertensive drugs target?
blood volume
Beta blockers as anti-hypertensive drugs target?
ionotropy
heart rate (decrease)
Core Drug: Bendroflumethiazide: Molecular Mechanism of action and class:
- 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
Core Drug: Bendoflumethiazide: Physiological Effects:
Kidney (Na+/Cl symporter):
- increases Na+ loss
- increases WATER LOSS
- decreases BP
Arterioles (K-ATP):
- decreases BP
Core Drug: Bendoflumethiazide: Side Effects:
Kidney:
- hyponatraemia
- hypokalaemia
- alkalosis
- hypercalcaemia
- hypomagnesaemia
- increase in urate (gout)
Insulin Resistance: increase in glucose (diabetes)
Liver: increase in lipids (arterial disease)
3 other uses for thiazides apart from hypertension:
- oedema
- urinary tract stones
- nephrogenic diabetes insipidus
Core Drug: Indapamide: Class and molecular mechanism of action:
- 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
Core Drug: Indapamide: Physiological Effects:
Kidney (Na+/Cl symporter):
- increases Na+ loss
- increases WATER LOSS
- decreases BP
Arterioles: lowers BP
Core Drug: Indapamide: Side effects:
Kidney:
- hyponatraemia
- hypokalaemia
- alkalosis
- hypercalcaemia
- hypomagnesaemia
- increase in urate (gout)
Insulin Resistance: increase in glucose (diabetes)
Liver: increase in lipids (arterial disease)
Are thiazide diuretics more aggressive than loop diuretics?
No
loop = aggressive (more)
Thiazide isnt very effective hypertensive but very effective diuretic?
No
Thiazide = gentle diuretic but powerful antihypertensives
Core Drug: Doxazosin: Molecular Mechanism and Class:
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
Alpha blockers as anti-hypertensives are targets?
stroke volume
Core Drug: Doxazosin: Physiological Effects:
- prevents contraction of arteriolar
smooth muscle - relaxes bladder outflow sphincter
Core Drug: Doxazosin: Side Effects:
- palpitations (reflex tachycardia)
- postural hypotension (stand up, arteries constrict, elderly patietns have a weakening of this reflex) causing dizziness
Core Drug: Doxazoosin: Clinical Uses:
- anti-hypertensive
- prostatic hypertrophy: relax
bladder outflow sphincter
Core Drug: Amlodipine: Molecular mechanism of action and class:
- anti-hypertensive
- calcium channel blocker
- dihydopyridines
- block L type voltage-gated Ca”+
channel
Core Drug: Diltiazem: Molecular mechanism of action and class:
- anti-hypertensive
- calcium channel blocker
- block L type voltage-gated Ca”+
channel
Core Drug: Verapamil: Molecular mechanism of action and class:
- anti-hypertensive
- calcium channel blocker
- block L type voltage-gated Ca”+
channel
Core Drug: Amlodipine: Clinical Use:
hypertension
Core Drug: Diltiazem: Clinical Use:
angina
hypertension
Core Drug: Verapamil: Clinical Use:
arrhythmias
hypertension
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
Core Drug: Amlodipine, Diltiazem, Verapamil: Side Effects:
- ankle swelling
- palpitations
- constipation
- flushing
- exacerbation of heart failure
Balance of actions of calcium channel blockers
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
RAAS
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
Core Drug: Ramipril: physiological effects:
- decrease in angiotensin II, hence
decrease in vasoconstriction - increase in bradykinin hence
increase in vasodilation
overall reduces BP
Core Drug: Ramipril: Side Effects:
- Dry Cough: bradykinin
accumulation in the lungs - Renal impairment: Renal Artery
Stenoses - Hyperkalaemia: hence commonly
given with a diuretic
Core Drug: Ramipril: Clinical Uses:
- hypertension
- heart failure
Core Drug: Ramipril: contraindications:
Afro-Caribbean people dont react well to ACE inhibitors
Core Drug: Losarten: molecular mechanism and class:
- anti-hypertensive
- ARB = angiotensin II receptor
antagonists/blockers - blocks action of angiotensin II on
receptor
Core Drug: Losarten: physiological effects:
- decrease vasoconstriction
Core Drug: Losarten: Side Effects:
- less dry cough than ACE inhibitors
- Renal impairment: Renal Artery
Stenoses - Hyperkalaemia: hence commonly
given with a diuretic
Core Drug: Losarten: Clinical Uses:
hypertension
Core Drug: Spironolactone: molecular mechanism and class:
- diuretic
- aldosterone antagonist
- blocks upregulation of Na+
channels in the distal convoluted
tubule by aldosterone
Core Drug: spironolactone: physiological effects:
- reduces water reabsorption
- reduces volume in arteries
Core Drug: Spironolactone: Side Effects:
- impaired renal function
- hyperkalaemia
- gynaecomastia (structurallly similar
to oestregen) (men grow breasts)
Core Drug: Spironolactone: Clinical Uses:
- used as an add on in resistant HT
- first line in HT due to
hyperaldosteronism
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
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
Pharmacological HT treatment
NICE guidance: HT treatment targets: <80yrs:
- <140/90
NICE guidance: HT treatment targets: >80yrs:
<150/90
NICE guidance: HT treatment targets: diabetes:
<135/85
