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Exam 2 adv pharm study guide 2024/2025
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Exam 2 adv pharmFactors that regulate BP - Baroreceptors - Carotid arteries and arch of aorta
Stimulation of Baroreceptors by ↑ B/P- Sends inhibitory impulse to Sympathetic Vasomotor Center
in Brain- decrease in HR and force of contraction- vasodilation of arteries Short term effect, in long
standing HTN baroreceptors adjust to elevated B/P Endothelial Factors- Endothelin- a potent
vasoconstrictor
- Prostacyclin- local vasodilator
Kidneys- Renin Angiotensin Aldosterone System
- Renin converts Angiotensinogen → Angiotensin I → Angiotensin II (by ACE enzyme)
-Angiotensin II - Vasoconstrictor
- Angiotensin II- Stimulates adrenal gland →Aldosterone →promotes sodium and water retention
Genetic Factors- Strong familial tendency
Diuretic Thiazide - Thiazide and thiazide-like diuretics have been a mainstay of the therapy of primary
hypertension.
Hydrochlorothiazide- HCTZ- most popular
Chlorthalidone and Indapamide- Thiazide like diuretics
MOA: The mechanisms responsible for BP decline are incompletely understood.
Acts on the distal tubule and inhibits sodium reabsorption--à decreased plasma volume
Vasodilatory action of Chlorthalidone and Indapamide
Fall in BP is blunted by hypovolemia-induced activation of the renin-angiotensin system in non-
responders
Contraindication/adverse effects in Diuretics-Thiazide - ◦ Anuria (CrCl<30 ml/minute), renal
decompensation
◦ Hypersensitivity to thiazides or sulfonamides (HCTZ is a sulfonamide
,Adverse events
◦ Potential for negative impact on dyslipidemia, glucose control ◦ Monitor for Na+, K+, Mg+ depletion
◦ Elevated calcium, uric acid, glucose, cholesterol
◦ Sexual dysfunction and sleep disturbance (cause unknown)
◦ HCTZ enhances DNA damage induced by ultraviolet radiation and therefore may increase the risk of
skin cancer
Electrolyte adverse effects with Diuretics - Hypokalemia due to urinary potassium loss.
Hyperuricemia due to interference with renal clearance of uric acid. (Risk of acute gout)
Hyperglycemia possibly related to hypokalemia. (Risk of new onset diabetes)
Hypercalcemia due to reduced renal clearance of calcium Erectile dysfunction by an unknown
mechanism.
Thrombocytopenia and skin rashes. Rare
(Fall in serum potassium > 0.3 mmol/l with low-dose thiazide or thiazide-like diuretics raises suspicion of
primary hyperaldosteronism if serum sodium is in high-normal range: refer for investigation).
Potassium sparing diuretics MOA - -Amiloride & Triamterene- Non- aldosterone antagonist - directly
block sodium channels but do not affect the mineralocorticoid receptor
-Spironolactone & Eplerenone- Aldosterone antagonist - competitively inhibit the mineralocorticoid
receptor MOA- decrease sodium absorption in the principal cells in the connecting and collecting
tubules.
Adverse reactions in diuretics - Adverse Reactions:
Central nervous system: Dizziness, fatigue, headache
Endocrine & metabolic: Hyperkalemia, dehydration, gynecomastia, hyperchloremic metabolic acidosis,
hyponatremia
Gastrointestinal: Abdominal pain, change in appetite, constipation, diarrhea, gas pain, nausea, vomiting
Genitourinary: Impotence
,Hepatic - Hepatotoxictiy
Neuromuscular & skeletal: Muscle cramps, weakness
Respiratory: Cough, dyspnea
Renal: Acute renal failure, acute interstitial nephritis
Hematologic & oncologic: Agranulocytosis, leukopenia, thrombocytopenia
Contraindications in diuretics - Hypersensitivity , serum potassium levels (>5.5 mEq/L)
Use with other potassium-conserving agents or with potassium supplementation is contraindicated
except in severe and/or refractory cases of hypokalemia
Anuria, acute or chronic renal insufficiency; evidence of diabetic nephropathy.
Beta-adrenergic antagonist - (-olol or -lol suffix): atenolol, metoprolol, propranolol, etc. Widely used
drugs
MOA
oThe physiologic effects of catecholamines (norepinephrine and epinephrine) are mediated by
activation of specific alpha and beta adrenergic receptors. Beta blockers act by competitively inhibiting
catecholamines from binding to these receptors.
o β-1 receptors (heart)
β-2receptors(lungs,liver,pancreas,arteriolarsmoothmuscle)
◦Cardioselectivebindspecificallytoβ-1receptors
◦ Non cardioselectivebindtoβ-1andβ-2receptors
-Inhibit sympathetic stimulation;which lowers HR & decs CO to lower BP
• Reduced HR
• Reduced force of contraction
• Reduced velocity of impulse conduction through the AV node
• Suppresses secretion of renin
, Nonselective beta blockers - Nonselective- Nadolol, Propanolol, Pindolol, Timolol
Cardioselective beta blockers - Cardio selective- Atenolol, Metoprolol, Esmolol, Bisoprolol
Beta blockers with alpha blocking activity - With alpha-blocking activity- Labetalol, Carvedilol
Adverse affects with beta adrenergic antagonist - Adverse events
◦ Use with caution in untreated heart block
◦ May cause bronchospasm
◦ May worsen insulin resistance
◦ May mask hypoglycemia
◦ Risk vs benefit?
◦ With discontinuation: taper over 10-14 days
Alpha-beta adrenergic antagonist - (-lol) suffix: Carvedilol, labetalol
MOA: Block adrenergic β-1, β-2, alpha-1 receptor sites, blunt catecholamine response
Adverse events
◦ Same as non-cardioselective beta-blocker for airway disease & DM
◦ Less insulin resistance compared to BB
◦ Taper over 10-14 days
ACE inhibitor - (-pril siffix) Mechanism of Action
◦ Inhibit Angiotensin Converting Enzyme; decrease conversion of angiotensin I to angiotensin II (potent
vasoconstrictor).
Contraindications
◦ Renal artery stenosis (bilateral/unilateral) ◦ History of angioedema
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