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NURS 403 Pathophysiology Pharmacology.
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NURS 403 – Pathophysiology/Pharmacology I Quiz 4 Study Sheet – Drug ListModule 6, Lectures 1-4
Module 6: Cardiovascular System
Drugs for Hypertension (Chapter 47)
1. Diuretics: (Ch. 41)
• MOA: block Na & Cl reabsorption → ↓ passive reabsorption of H2O causing larger amount of H2O and Na to be
excreted in urine
o Urinary Output: will be equivalent to the amount of Na & Cl reabsorption blocked; diuretics acting on
earlier reabsorption sites in the nephron (PCT) will have higher diuretic effect than diuretics acting on
later reabsorption sites of the nephron (DCT & collecting duct)
• Risks: Hypovolemia and Electrolyte/acid-base imbalances
o More risk with Long-acting agents vs short-acting
o Risk is also dependent on administration timing (kidney operation b/w diuresis)
A. Thiazide Diuretics: Hydrochlorothiazide
o MOA: act on early segment DCT to decrease blood volume (initial) and induce vasodilation which
decreases arterial resistance (long-term)
o Uses: 1st line option for HTN compared to CCBs, ACE-I
▪ Renal Function: MUST be good to use thiazides – if GFR < 15-20mL/min, thiazides will be
ineffective and should be avoided
o ADEs:
▪ Electrolyte Loss: hypokalemia, hyponatremia, hypochloremia, hypomagnesemia → replace
▪ Nocturia: need to urinate during the night → Tx early in the day
▪ Dehydration: dry mouth, polydipsia, oliguria
▪ ↑ uric acid: asymptomatic initially; can increase gout attacks in gout pts
▪ ↑ glucose: be aware for diabetic pts
▪ ↑ lipids: be aware for dyslipidemia pts
▪ Pregnancy: avoid
o Interactions:
▪ Digoxin: with hypokalemia caused by thiazide → digoxin toxicity
▪ Lithium: with hyponatremia caused by thiazide → lithium toxicity
▪ NSAIDs: counteract diuresis → avoided; (Tylenol as an alternative)
B. Loop Diuretics: Furosemide
o MOA: act on the ascending loop of Henle to cause profound diuresis (>thiazides)
▪ Onset: is rapid (5min if IV, 60min if PO)
o Uses: Not routinely 1st line for HTN; used as an add-on when thiazide on its own was ineffective; DOC for
pulmonary edema due to rapid onset via IV administration
▪ Renal Function: loops can be used regardless of renal function
o ADEs: same as thiazides → risk of dehydration & electrolyte imbalance; avoid in pregnant pts
▪ Unique to Loops: hypocalcemia & ototoxicity
o Interactions: same as thiazides; be aware of other ototoxic agents (vancomycin, aminoglycosides)
C. K-Sparing Diuretics: Spironolactone (also classified as an aldosterone antagonist)
o MOA: inhibits normal action of aldosterone on distal nephron, thereby causing Na & H2O excretion & K
retention; effects are delayed, as no profound diuresis is produced for up to 48h
o Uses: due to slow onset, only used as add-ons to loop/thiazide Tx to prevent hypokalemia; not used by
itself as a diuretic agent
o ADEs:
▪ Hyperkalemia: due to “K-sparing” action
▪ Endocrine Abnormalities: can be caused by drug’s ability to bind to other steroid receptors
(reversible upon D/C)
o Interactions: avoid KCL & salt substitutes (hyperkalemia) and RAAS agents & other aldosterone
antagonists (deregulates aldosterone action)
D. Osmotic Diuretics: Mannitol (a diuretic not used for hypertension)
o MOA: not reabsorbed and remains in nephron to create an osmotic force which inhibits passive
reabsorption of H2O; has no effect on electrolytes (unique to osmotics)
o Uses: Tx of increased intracranial or intraocular pressure (i.e., cerebral edema); prophylaxis of renal
failure; Administration is IV only
o ADEs: avoid in patients presenting with CHF, HD, pulmonary edema
, 2. Drugs Acting on Adrenergic Receptors: (α & β Receptors)
A. Beta Blockers: (Ch. 18)
• MOA: blocks sympathetic nervous system action on the β-receptors (β1 or β2)
o β1 Blockade: decreases HR, heart contractility and cardiac output
o Vasodilation action: causes suppression of reflex tachycardia
o Juxtaglomerular Cell action: decreases renin, which decreases
vasoconstriction (ATII) and volume expansion (aldosterone)
o Long-term use: decreases peripheral resistance
• Efficacy: Caucasians > African Americans
i. β1-selective agents: metoprolol, atenolol (only affect the heart)
o Lipid solubility: metoprolol
o ADEs:
▪ Bradycardia: due to ↓ AV node conduction & contractility; patients with sinus bradycardia,
2nd or 3rd Degree AV Block, or HF should avoid → opt for ISA instead
▪ Masking of Hypoglycemia: by preventing tachycardia that usually accompanies
hypoglycemia; patients with diabetes should be cautious or avoid
▪ Rebound Excitation: caused by abrupt d/c of β-Blocker; presents as angina, & ventricular
dysrhythmia → temporarily resume drug therapy and then gradual titrate down over 1-2w
▪ CNS: (rare) depression, insomnia, bizarre dreams can sometimes occur – typically with lipid-
soluble agents
ii. Non-selective agents (β1 or β2): propranolol, carvedilol, labetalol (affect the heart and the lungs)
o Lipid solubility: propranolol
o Vasodilation: carvedilol, labetalol (block Alpha and Beta receptors)
o ADEs:
▪ Bronchoconstriction: due to non-selective action of drug on the lungs; patients with asthma
or COPD should avoid
▪ Hypoglycemia: due to β2 blockage of glycogen→glucose process; patients with diabetes
taking insulin should avoid → opt for selective agent for DM patients
▪ Rebound Excitation and CNS effects: same as β1-selective agents
o Interactions:
▪ Rebound Excitation and CNS effects: same as β1-selective agents
▪ Epinephrine: non-selective agents will inhibit action of epinephrine and should be avoided in
patients with history of anaphylaxis → opt for selective agent
▪ Ca Channel Blockers: avoid verapamil & diltiazem with propranolol due to potentiative
effects
▪ Insulin: non-selective agents will cause hypoglycemia in DM patients taking insulin due to
potentiative effects → opt for selective agent
iii. Intrinsic Sympathomimetic Activity: (ISA) acebutolol, pindolol; block β-receptors from action of strong
agonists (i.e., NE), but also have mild, partial β-agonism causing less resting bradycardia and less reduction in
cardiac output; Useful if symptomatic bradycardia patients
B. Alpha-1 Blockers: (Ch. 18) prazosin, doxazosin, terazosin
• MOA: blocks the sympathetic action of Alpha-1 receptors to prevent them from inducing vasoconstriction,
resulting in vasodilation
o Arterial dilation: via direct action, results in decreased arterial pressure and peripheral resistance
o Venous dilation: via indirect action, results in decreased venous return, cardiac output and arteriole
pressure
• ADEs:
o Orthostatic hypotension
o Reflex tachycardia: caused by vasodilation lowering BP which triggers baroreceptor reflex →
counteract with β-blocker
o Sexual dysfunction: due to blockage of Alpha-1 which is responsible for ejaculation → reversible
upon d/c
o Nasal congestion: due to vasodilation in nasal mucosa
o Na & H2O retention: decreased BP causes decreased renal blood flow as a compensatory
mechanism, leading to increased BV → Add-on a diuretic
2
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