90% of hypertension is ‘primary’ which means of ❌ cause. 'Secondary’ is due to kidney disease, Cushing syndrome, thyroid disease, and drug-induced. Drug treatments include drugs to: ❌ blood vessels, reduce ❌ of vessels, reduce blood ❌, and reduce cardiac load.
If we give a Beta1 blocker then we anticipate a decrease in heart rate.
If we give an alpha blocker then we anticipate vasoconstriction.
Non-selective β−blockers (e.g. Propanolol) should be avoided in asthmatics as they may constrict the airways.
The RAAS system maintains fluids and electrolyte balances. Renin is released from the arterioles near the ❌, in response to reduced ❌ or reduced renal blood ❌. Renin: - Converts ❌ to ❌ - Angiotensin is converted to ❌ by the ❌ ATII causes ❌ and aldosterone release from the adrenals. Aldosterone promotes ❌ excretion in exchange for ❌ reabsorption to maintain plasma volume and cardiac output (ie to retain volume and raise BP.)
If we give an ACE inhibitor or an angiotensin II receptor blocker (ARB) we anticipate vasodilation.
Side effects of ACE inhibitors and ARBs: - dizziness/postural ❌ - ❌kalaemia (increase K+) - ACEI can cause ❌ due to build up of bradykinin (broken down by ACE)
❌ are also side effects of thiazide diuretics.
Which of these is not a side effect of calcium channel blockers?
Peripheral oedema
Constipation
Dizziness/postural hypotension
Flushing
Headache
Nausea
Non-dihydropyridine calcium channel blockers can cause bradycardia (Caution if patient also on a β-blocker).
