General drug info for IPT2

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Last updated 3:13 PM on 5/31/26
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30 Terms

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Ace Inhibitors MOA

Inhibit angiotensin II formation by inhibiting the ACE enzyme. Therefore, vasodilation occurs. Reduces aldosterone causing a decrease in BV, sodium and water extcretion and potassium retention. Causes arterial and to a lesser extent venous dilation. Mainly reduces afterload, but also preload.

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ACEi AEs

Hyperkaleamia

Fetopathic potential - preg C/I

Dry cough → build up of bradykinin in lungs due to ACE being inhibited.

facial flushing

headache

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ACEi C/I or precautions

Renal impairment → avoid use (hyperkalaemia risk)

T1DM

C/I in pregnancy

Angioedema history

ARNI → increased angioedema isk → wait 36 hrs before acei start

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ACEi drug interaction

Loop diuretics → hyperkalaemia

NSAIDs → reverse ACEi antihyperintensive effect + increased risk of hyperkalemia and renal impairment

ARB → similiar MOA

Thiazide and loop diuretics → can cause hypotension (1st dose), less with thiazide

K+ supplements → hyperkalemia → renal impairment

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Ramiprill dose

2.5mg d

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ARB MOA

competitively binds to Ang II receptor sub-type 1, inhibiting the hypertensive effects of Ang II. This causes mainly arterial vasodilation but also venous dilation and decreases mainly afterload but less of a in preload. Decreased aldosterone causes a decrease in BV, sodium and water excretion and causes potassium retention.

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AEs of ARBs

No dry cough

Facial flushing

hyperkaleamia

headache

Hypotension

Dizziness

Fetopathic potential - preg C/I

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Drug interaction - ARBs

Potassium-sparing dieuretics → hyperkaleamia → renal impairment

NSAID - reverse antihypertensive effect of ARA + renal impairment + hyperkaleamia

Lithium→ reduced Li excretion → toxicity

Thiazide and loop diuretucs → hypotension

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Candesartan dose

16mg d

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Hypertension BP target

Uncomplicated: 140/90mmHg

High CVD risk (>15%): <120mmHg

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Monitoring - Acei

SeCr 1-2 weeks after starting (usually increases a bit)

Hyperkaleamia??

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CCB MOA - dihydropyridines

Block the L-type calcium channels of smooth muscle cells. This reduces Ca2+ influx into arteriolar smooth muscle cells, which causes vasodilation of the arteries. Also reduces peripheral smooth muscle vascular resistance. Hence reduces afterload → reduces BP.

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Amlodipine dose

5mg

elderly, hepatic impairment = 2.5mg

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CCB precautions + C/I

Simvastatin – toxicity due to enzyme being inhibited/used by CCB

Ritonavir – CCB toxicity → ritonavir inhibits CCB’s enzyme

C/I → HF (amlodipine and felodipine are good). Verapamil → further depression of cardiac function.

Angina → dihydrohydropyridine can excacberate via tachycardia → ?usually given w B-blocker?

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CCB AEs

Peripheral oedema

Reflex tachycardia - dihydropyridines

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Reflex tachycardia

Caused by the baroreceptors detecting drop in BP → reflex tachycardia (increased HR)

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CCB drug interactions

Simvastatin → statin toxicity

Ritonavir → CCB toxicity

diltiazem and verapamil + digoxin → digoxin toxicity = cardiac effects

Verapamil + antiarrhythmics → HF risk

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MOA of verapamil

Blocks the L-type calcium channels in the vascular smooth muscle and cardiac cells. This reduces the influx of calcium, causing slowed AV conduction. Also reduces HR and contractility. Mild vasodilation effects.

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MOA diltiazem

Blocks L-tyoe calcium channels in vascular smooth muscle and cardiac muscle. Slows AV node conduction + HR + contractility. Causes moderate peripheral vasodilation.

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Thiazide drug examples

Indapamide, Hydrochlorothiazide, Chlorthalidone

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Thiazide diuretics

Inhibit electroneutral Na+/Cl⁻ co-transport in the distal convoluted tubule, leading to fluid retention in tubule and more sodium and water excretion. This reduces BV → reduces BP.

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AEs and precautions of Thiazides

Hypercalceamia

Hypokaleamia

C/I in history of GOUT → causes hyperuricaemia → can precipitate GOUT

Hyperglyceamia

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Triple Whammy

Diuretics decrease BV. Causes hypoperfusion

ACEi and ARBs cause vasodilation of the efferent arteriole

NSAIDs cause the vasoconstriction of the afferent arteriole. Also, reduce the effect of diuretics

Decrease in transglomerular pressure → decreased eGFR.

NEVER combine these drugs

High dose aspirin (not low dose as an antiplatelet)

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Hydrochlorothiazide dose

Low dose for hypertension

Up to 25mg d

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Best combo for hypertension

ACEi + CCB

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2nd best combo for hypertension

Thiazide (HCTZ 25mg) + ACEi/ARB

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Hypertension comlications if not managed

can develop into stroke, MI, HF, and other cardiovascular events

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Hypertension lifestyle modification

regular excersise, more wholef oods, vegetales, fruits, less salt intake and saturated foods and sugary foods.

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Verapamil dose

120mg - 240mg CR!!!

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High dose statin

If patient has micro/macroalbuminuria + Diabetes

Rosuvastatin 40mg OR

Artorvastatin 80mg