Hypertension Flashcards
Typically uses what approach?
ABCD
What do angiotensin converting enzyme inhibitors end in?
-pril
e.g. of ace inhibitors
captopril, enalapril, perindopril, ramipril
How do ACE inhibitors work
by blocking conversion of angiotensin I to angiotensin II by inhibiting ACE, thus relaxing blood vessels and decreasing the force of cardiac contraction and also o decrease the release of aldosterone from the adrenal cortex leading to sodium loss and potassium retention and block breakdown of bradykinin
Common AEs of ACE inhibitors
dry persistent cough (10-20%), metallic taste (captopril), hyperkalaemia, confusion, restlessness, irregular HR, numbness and tingling of lips and limbs, muscle weakness and hypotension (common with first dose). Administer at night to avoid dizziness and syncope
Clinical considerations of ACE inhibitors
avoid use with potassium supplements and spironolactone. When commencing treatment, start with the lowest dose.
What to check before administering ace inhibitors
Renal function and electrolyte levels should be checked prior to administration and reviewed after 1-2 weeks
Angiotensin II receptor blockers end in what
-artan
E.g. of Angiotensin II receptor blockers
losartan, candesartan, irbesartan
How do angiotensin II receptor blockers work?
By blocking binding of angiotensin II to angiotensin (AT1) receptors reducing vasoconstriction, blocking the release of aldosterone from adrenal cortex increasing sodium loss and potassium retention
Common AEs of angiotensin II receptor blockers
hypotension, dizziness headache, hyperkalaemia, GI disturbances. The incidence of cough is less when compared to ACR inhibitors, however the clinical considerations are the same
Alpha blockers end in
-osin
Types of alpha blockers
There are alpha-adrenoceptors alpha1 and alpha2 medications
Selective alpha1 blockers are
antagonists and include prazosin and terazosin
Non-selective blockers are
both antagonist and agonist and include phentolamine (pheochromocytoma)
mechanism of action of alpha1 blocker
block alpha1 receptors on arterioles and venules, reducing systemic vascular resistance, thus decreasing BP
AEs of alpha1 blockers
o postural hypotension, nasal congestion, pupil constriction, fatigue, diarrhoea
Hypotension is common on the first dose
In older people there may be fluid depletion and diuretics
The patient should slowly rise from a laying/sitting position to minimise postural hypotension
Medications should start at a low dose at bedtime to avoid this complication
Beta blockers end in
-lol
beta1 blockers block
beta1 receptors causing decrease in the heart rate and force of contraction and decreases renin release
beta2 blockers block
beta2 receptors causing bronchoconstriction, peripheral vasoconstriction and impaired insulin release (chronic use increases the risk of diabetes mellitus)
E.g. of beta1 blockers that are cardio-selective
atenolol, bisoprolol and metoprolol
E.g. of beta1 blockers that are non-cardio-selective (block beta1 and 2)
include carvedilol, pindolol and propranolol
AEs of beta blockers
o bradycardia, hypotension, impaired peripheral circulation (cold extremities), vivid dreams, erectile dysfunction in males
Treatment may mask hypoglycaemic symptoms (palpitations, tremor, hunger) in diabetic patients
Abrupt withdrawal can also cause rebound HT
Contraindications for beta blockers
asthma, COPD, bradycardia, cardiogenic shock, severe hypotension and diabetes
If there is a need to reduce the dose…
always do it slowly to prevent rebound HT
When is it best to administer beta blockers
in the morning to avoid vivid dreams (consider atenolol as it is less likely to enter the brain)
calcium channel blockers end in
-pine
e.g. of calcium channel blockers
amlodipine, felodipine, nifedipine, diltiazem, verapamil
what do calcium channel blockers do
Act by blocking movement of calcium into cells (block L-type calcium channels) which relax muscle, cardiac contractility, cardiac conduction and vascular tone
Which calcium channel blockers work on vascular smooth muscle
nifedipine
Which calcium channel blockers work on cardiac and vascular muscle
diltiazem and verapamil. Verapamil has a greater effect in AV node function when compared to diltiazem
AEs of calcium channel blockers
headache, hypotension, dizziness, palpitations, facial flushing and skin rashes
Contraindications of calcium channel blockers
cardiogenic shock
E.g. of potassium-sparing diuretics
spironolactone and amiloride
What does spironolactone do
Inhibits sodium absorption in the distal tubule by blocking sodium channels and aldosterone.
It interferes with the sodium/potassium exchange causing sodium excretion and a decrease in urinary potassium excretion
What does amiloride do
acts independently of aldosterone and inhibits sodium reabsorption in the distal convoluted tubule which decreases water retention
AEs of potassium-sparing diuretics
hyperkalaemia, gynaecomastia in men, postmenopausal bleeding in women.
What to avoid when taking potassium-sparing diuretics
Avoid potassium supplements and ACE inhibitors
Clinical considerations for potassium-sparing diuretics
monitoring potassium levels
Contraindications of potassium-sparing diuretics
patients with hyperkalaemia
A once-daily dose of a potassium-sparing diuretic may
prevent nocturia
Approaches to hypertensive management depends on
the presence of other coexisting factors
treatment of mild to moderate HT usually starts with
One drug e.g. a diuretic or a beta-blocker
If the BP remains above the target, consider
other factors such as nonadherence
when one drug is only partially successful in lowering the BP, it is preferable to try
a combo of drugs rather than a higher dose of the one drug
the combos that are effective and pharmacologically complementary are:
A diuretic with either a beta-blocker or an ACE inhibitor
A calcium channel blocker with either a beta-blocker or an ACE inhibitor
