ACE inhibitors (ACEi) and angiotensin II receptor blockers (ARB) Drugs ACEi include enalapril, ramipril, and lisinopril. ARBs include losartan and candesartan. Mechanism Reduce levels (ACEi) or effects (ARB) of angiotensin II. Angiotensin II increases BP via systemic vasoconstriction, sodium retention, and aldosterone and ADH release. Lower efficacy in black patients, so not 1st line in this group. The medicos PDF app was used to collect this information. I stumbled discovered this amazing app when searching for various slides and books and decided to share it with you all. The Google Play Store has a free version of the app.

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2. Drugs
 ACEi include enalapril, ramipril, and lisinopril.
 ARBs include losartan and candesartan.
Mechanism
 Reduce levels (ACEi) or effects (ARB) of angiotensin II.
 Angiotensin II increases BP via systemic vasoconstriction, sodium
retention, and aldosterone and ADH release.
 Lower efficacy in black patients, so not 1st line in this group.

3. ACEi-specific:
 Dry cough (10%). Switch to ARB if occurs.
 Angio-oedema: rare (0.1%) but 3x commoner in black patients.
ACEi and ARB:
 ↑K+ due to ↓aldosterone.
 ↓↓BP when starting, so start low and titrate.
Renal effects:
 Can impair renal function: ↓GFR via efferent dilation, especially dangerous in
bilateral renal artery stenosis.
 However, it is often kidney protective via increased renal blood flow, so is used in
chronic kidney disease and diabetes.
 ↓GFR only occurs when efferent dilation outweighs the increased blood flow.

4. Absolute:
 K+ >5.5.
 Bilateral renal artery stenosis. However, used in unilateral disease.
 Pregnancy: causes cleft palate.
Cautions:
 K+ >5.
 Use ↓dose in kidney failure.

5. Check K+ and creatinine at the following times:
 Baseline: 1 wk pre + post starting.
 After each dose increase.
 During severe illness, especially if dehydration risk.
 Routinely: annually, or more if ↓GFR.
Actions:
 If creatinine ↑20% from baseline or GFR ↓ 15%, recheck within 2 wks
and if no better discuss with nephrologist.
 If K+ >5.5, reduce dose, if K+ >6, stop.

6. Mechanism
 Cardiac β1 receptors increase HR at the sinus node and contractility in the
myocytes; blockade therefore provides negative chronotropy and negative
inotropy.
 Selective for β1 receptors, B1
MAN: BIsoprolol, Metoprolol, Atenolol, Nebivolol.
 Non-selective: carvedilol, labetalol, propranolol, timolol.
 Metoprolol is the most short-acting, so often used IV acutely.

7.  Fatigue. Consider dose reduction if occurs.
 Cardiac: ↓HR, heart block.
 Symptomatic hypotension. Consider stopping other agents (e.g. nitrates)
first if β-blocker given for prognostic improvement e.g. in heart failure.
 Wheeze
 Erectile dysfunction.
 May worsen diabetes control if combined with thiazide.
 Cold peripheries from vasoconstriction, mainly with non-selective drugs.
Switch to nebivolol if this occurs.
 Sleep disturbance.

8.  Asthma
 Non-selective agents should be avoided in COPD, but selective agents
should be given when indicated.
 Heart block.
 ↓HR or ↓BP.
 Pregnancy: restricts fetal growth.
Cautions
 May not be appropriate for those who are physically active. st

9. Mechanism
Block L-type Ca2+ channels, reducing calcium inflow to cells:
 Rate-limiting CCBs — verapamil and diltiazem — mainly affect
myocardiocytes and nodal tissue, causing negative inotropy and chronotropy.
 Non rate-limiting CCBs: amlodipine, nifedipine, lercanidipine. Known as
dihydropyridines, the molecule from which they’re derived. Mainly affect
arterial smooth muscle, causing vasodilation and hence ↓BP.

10.  Head and face: flushes, headache (especially non rate-limiting), gum
hyperplasia.
 Peripheral oedema. Less common with lercanidipine.
 Constipation, especially verapamil.
 Rate-limiting CCBs: heart failure.

11.  Heart block.
 HF, especially rate-limiting CCBs.
 β-blockers interact with rate-limiting CCBs.

12. Mechanisms
 Loop diuretics (furosemide, bumetanide) block Na+-K+-2Cl- cotransporter in
loop of Henle.
 Thiazide (bendroflumethiazide) and thiazide-like diuretics (chlorthalidone,
indapamide, metolazone) block Na+-Cl- cotransporter in distal convoluted
tubule (DCT).
 Potassium-sparing diuretics block ENaC in DCT (amiloride) or block
aldosterone (spironolactone) which works via Na+-K+ ATPase and ENaC.

13. All:
 Urinary frequency.
 Altered electrolytes.
 Renal impairment, mainly due to volume depletion.
Furosemide:
 ↓K+
 Muscle cramps.
 Kidney stones, due to ↑Ca2+ excretion.
 Gout

14. Thiazides:
 Electrolytes: ↓Na+, ↓K+ (↑Na+ is left in DCT then Na+-K+ ATPase
removes some in exchange for K+), ↓Mg2+, ↑Ca2+.
 Photosensitive rash.
 ↑Glucose
 Gout
Spironolactone:
 ↑K+
 Tender gynecomastia.

15.  Gout
 Renal failure
 Pregnancy: thiazides, which cause oligohydramnios.

16. Drugs
 Tamsulosin, doxazosin, and prazosin.
Mechanism
 Systemic vasodilation by blocking α1 receptors.
 Good for HTN in patients with prostatism, as they also help relieve urinary
obstruction by relaxing smooth muscle in the prostate and bladder neck.

17.  Peripheral oedema.
 Worsen heart failure.
 Postural ↓BP.
Contraindications
 Urinary incontinence.

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