outline only pharm

[Week 3 · ACE inhibitors] Which three ACE inhibitors are on the outline?

Lisinopril, enalapril, captopril.

[Week 3 · ACE inhibitors] What suffix identifies ACE inhibitors?

-pril

[Week 3 · ACE inhibitors] How do ACE inhibitors work?

Block conversion of angiotensin I → II; vasodilation and ↓ aldosterone.

[Week 3 · ACE inhibitors] Why can ACE inhibitors cause a dry cough?

ACE inhibition increases bradykinin.

[Week 3 · ACE inhibitors] Main indications?

Hypertension, heart failure, after MI, diabetic nephropathy.

[Week 3 · ACE inhibitors] Common side effects?

Dry cough, dizziness, orthostatic hypotension.

[Week 3 · ACE inhibitors] Most urgent adverse reaction?

Angioedema: facial/tongue swelling; airway emergency.

[Week 3 · ACE inhibitors] Which electrolyte can become dangerously high?

Potassium (hyperkalemia).

[Week 3 · ACE inhibitors] What organ dysfunction is a serious risk?

Acute worsening of kidney function, especially with renal artery stenosis.

[Week 3 · ACE inhibitors] Major pregnancy precaution?

Contraindicated in pregnancy: fetal harm.

[Week 3 · ACE inhibitors] What does the nurse monitor?

BP, K⁺, BUN and creatinine; cough and facial swelling.

[Week 3 · ACE inhibitors] Key patient teaching?

Rise slowly; avoid K⁺ supplements/salt substitutes unless approved; report swelling.

[Week 3 · Angiotensin receptor blockers (ARBs)] Which two ARBs are listed?

Losartan, valsartan.

[Week 3 · Angiotensin receptor blockers (ARBs)] What suffix identifies ARBs?

-sartan

[Week 3 · Angiotensin receptor blockers (ARBs)] How do ARBs lower BP?

Block angiotensin II AT1 receptors → vasodilation and ↓ aldosterone.

[Week 3 · Angiotensin receptor blockers (ARBs)] Why do ARBs rarely cause ACE-inhibitor cough?

They do not inhibit bradykinin breakdown.

[Week 3 · Angiotensin receptor blockers (ARBs)] Main uses?

Hypertension, heart failure, ACE inhibitor intolerance.

[Week 3 · Angiotensin receptor blockers (ARBs)] Common effects?

Dizziness, fatigue; hypotension.

[Week 3 · Angiotensin receptor blockers (ARBs)] Major safety risks?

Hyperkalemia, kidney dysfunction; rare angioedema.

[Week 3 · Angiotensin receptor blockers (ARBs)] Pregnancy warning?

Avoid: ARBs can injure the fetus.

[Week 3 · Angiotensin receptor blockers (ARBs)] Monitor what?

BP, serum K⁺ and renal function.

[Week 3 · Angiotensin receptor blockers (ARBs)] What should patients avoid?

Potassium-containing salt substitutes unless approved.

[Week 3 · Aldosterone antagonists (aka potassium sparing diuretics] Which two drugs are aldosterone antagonists?

Spironolactone, eplerenone.

[Week 3 · Aldosterone antagonists] How do they affect salt and potassium?

Block aldosterone → excrete sodium/water and retain potassium.

[Week 3 · Aldosterone antagonists] Indications?

Heart failure, hypertension, hyperaldosteronism.

[Week 3 · Aldosterone antagonists] What electrolyte problem is most important?

Hyperkalemia.

[Week 3 · Aldosterone antagonists] Which agent is more likely to cause gynecomastia?

Spironolactone (less receptor-selective).

[Week 3 · Aldosterone antagonists] Why is gynecomastia less likely with eplerenone?

It is more selective for mineralocorticoid receptors.

[Week 3 · Aldosterone antagonists] Nursing priorities?

Check potassium, renal function, BP and dehydration.

[Week 3 · Aldosterone antagonists] What potassium-related advice?

Do not add K⁺ supplements or potassium salt substitutes without approval.

[Week 3 · Dihydropyridine CCBs] Which two dihydropyridine CCBs are listed?

Amlodipine, nifedipine.

[Week 3 · Dihydropyridine CCBs] What is their main site of action?

Calcium blockade mainly in vascular smooth muscle → arteriolar dilation.

[Week 3 · Dihydropyridine CCBs] Main uses?

Hypertension and angina.

[Week 3 · Dihydropyridine CCBs] Common side effects?

Peripheral edema, headache and flushing.

[Week 3 · Dihydropyridine CCBs] Important serious effect?

Excessive hypotension.

[Week 3 · Dihydropyridine CCBs] What should the nurse check?

Blood pressure and ankle/peripheral edema.

[Week 3 · Dihydropyridine CCBs] Food interaction in the outline?

Avoid grapefruit or ask pharmacist for drug-specific advice.

[Week 3 · Non-dihydropyridine CCBs] Which non-DHP CCBs are listed?

Verapamil, diltiazem.

[Week 3 · Non-dihydropyridine CCBs] How do these differ from dihydropyridines?

Slow SA/AV node conduction and heart rate, plus vasodilation.

[Week 3 · Non-dihydropyridine CCBs] Main indications?

Certain dysrhythmias, hypertension and angina.

[Week 3 · Non-dihydropyridine CCBs] What GI effect is especially linked with verapamil?

Constipation.

[Week 3 · Non-dihydropyridine CCBs] What heart-rate effect is common?

Bradycardia.

[Week 3 · Non-dihydropyridine CCBs] Serious conduction risk?

AV heart block.

[Week 3 · Non-dihydropyridine CCBs] Nursing monitoring?

Check HR/pulse, BP and ECG (especially IV use).

Which CCB group mainly dilates arteries vs slows AV conduction?

DHP: amlodipine/nifedipine → arterioles. Non-DHP: verapamil/diltiazem → heart/AV node.

[Week 3 · Hydralazine] Drug class?

Direct arteriolar vasodilator.

[Week 3 · Hydralazine] What vascular action?

Relaxation of arterioles lowers afterload/BP.

[Week 3 · Hydralazine] Outline indications?

Severe hypertension; selected heart failure treatment.

[Week 3 · Hydralazine] Typical side effects?

Headache, reflex tachycardia, orthostatic symptoms.

[Week 3 · Hydralazine] Main acute danger?

Marked hypotension.

[Week 3 · Hydralazine] What must be monitored?

BP and pulse; watch for dizziness/tachycardia.

[Week 3 · Sodium nitroprusside] How does nitroprusside lower BP?

Very rapid arterial AND venous dilation.

[Week 3 · Sodium nitroprusside] Major indication?

Hypertensive emergency (IV infusion).

[Week 3 · Sodium nitroprusside] Common immediate effects?

Severe hypotension, headache, reflex tachycardia.

[Week 3 · Sodium nitroprusside] What unique toxicity does the vasodilator lecture warn about?

Cyanide/thiocyanate accumulation during infusion.

[Week 3 · Sodium nitroprusside] Primary nursing action?

Continuous/frequent BP assessment during titrated IV infusion.

Which four classes are standard first-line BP drug options?

Thiazide diuretics, ACE inhibitors, ARBs, calcium channel blockers.

[Week 3 · Hypertension first-line treatment] What is the general thiazide mechanism?

Reduce NaCl reabsorption in distal convoluted tubule → diuresis and ↓ BP.

[Week 3 · Hypertension first-line treatment] What are major thiazide electrolyte effects?

Hypokalemia and hyponatremia.

[Week 3 · Hypertension first-line treatment] What follow-up matters beyond the BP reading?

Adherence, orthostatic symptoms and relevant labs.

[Week 3 · Hypertension first-line treatment] General BP goal in outline?

Often <130/80 mmHg; individualized to patient.

[Week 4 · Loop diuretic] What class is furosemide?

Loop diuretic.

[Week 4 · Loop diuretic] Where and how does furosemide act?

Blocks Na⁺/K⁺/2Cl⁻ transporter in thick ascending loop.

[Week 4 · Loop diuretic] Main indication in HF?

Relieve fluid overload and pulmonary/peripheral edema.

[Week 4 · Loop diuretic] Most important electrolyte loss?

Hypokalemia.

[Week 4 · Loop diuretic] Other common adverse effects?

Dehydration, hyponatremia, hypotension.

[Week 4 · Loop diuretic] What ear-related adverse effect is high yield?

Ototoxicity (higher risk with high/rapid IV doses).

[Week 4 · Loop diuretic] Best daily response to monitor?

Daily weight, intake/output, edema and breath sounds.

[Week 4 · Loop diuretic] What blood tests?

Potassium and kidney function.

[Week 4 · Loop diuretic] When should the patient take oral furosemide?

In the morning (unless instructed otherwise).

[Week 4 · Loop diuretic] What symptom may indicate low potassium?

Muscle weakness or cramps; report them.

[Week 4 · Heart failure beta blockers] Which beta blockers are named for heart failure?

Metoprolol and carvedilol.

[Week 4 · Heart failure beta blockers] Why use them in stable HF?

Block chronic sympathetic stimulation; ↓ HR/workload and adverse remodeling.

[Week 4 · Heart failure beta blockers] Other clinical uses?

Hypertension and post-MI.

[Week 4 · Heart failure beta blockers] Common adverse effects?

Fatigue, low BP and bradycardia.

[Week 4 · Heart failure beta blockers] Serious risks?

Heart block; bronchospasm (greater with nonselective drugs).

[Week 4 · Heart failure beta blockers] When can a beta blocker worsen HF?

During acute decompensation or if initiated/titrated too aggressively.

[Week 4 · Heart failure beta blockers] What do you check before administering?

HR and BP; follow prescribed hold parameters (often HR <60/min).

[Week 4 · Heart failure beta blockers] Can patients stop beta blockers suddenly?

No: rebound tachycardia/angina/ischemia risk.

[Week 4 · Cardiac glycoside] What drug is the cardiac glycoside?

Digoxin.

[Week 4 · Cardiac glycoside] Why does digoxin increase contractility?

Inhibits Na⁺/K⁺-ATPase → intracellular Ca²⁺ rises (positive inotrope).

[Week 4 · Cardiac glycoside] Why can it slow ventricular rate in AF?

Increases vagal effect → slows AV nodal conduction.

[Week 4 · Cardiac glycoside] Outline indications?

Selected heart failure patients and atrial fibrillation rate control.

[Week 4 · Cardiac glycoside] Outline therapeutic serum range?

0.5–2.0 ng/mL; many HF targets are lower (often 0.5–0.9).

[Week 4 · Cardiac glycoside] Three high-yield toxicity signs?

Nausea/vomiting, yellow-green visual changes, bradycardia.

[Week 4 · Cardiac glycoside] How does low K⁺ affect digoxin?

Hypokalemia makes digoxin toxicity more likely.

[Week 4 · Cardiac glycoside] What pulse assessment before digoxin?

Apical pulse for a full 60 seconds; use ordered hold parameters.

[Week 4 · Cardiac glycoside] Which labs are important?

Potassium, renal function, and digoxin level when indicated.

[Week 4 · Cardiac glycoside] What symptoms should patient report?

Visual halos, GI symptoms or unusual slow pulse.

[Week 4 · Class I antiarrhythmic (Na⁺ blocker)] Which Class I example is on the outline?

Lidocaine (Class IB).

[Week 4 · Class I antiarrhythmic (Na⁺ blocker)] How does lidocaine affect cardiac tissue?

Blocks fast Na⁺ channels; reduces abnormal ventricular automaticity.

[Week 4 · Class I antiarrhythmic (Na⁺ blocker)] What rhythms is IV lidocaine used for?

Selected serious ventricular dysrhythmias.

[Week 4 · Class I antiarrhythmic (Na⁺ blocker)] What neurotoxicity signs should be watched for?

Confusion, drowsiness, paresthesias; severe toxicity can cause seizures.

[Week 4 · Class I antiarrhythmic (Na⁺ blocker)] What is monitored during use?

Continuous ECG and neurologic status.

[Week 4 · Class II antiarrhythmics (beta blockers)] Which Class II examples are on the outline?

Metoprolol and propranolol.

[Week 4 · Class II antiarrhythmics (beta blockers)] How do Class II drugs affect conduction?

Beta blockade slows SA rate and AV conduction.

[Week 4 · Class II antiarrhythmics (beta blockers)] Major cardiac adverse effects?

Bradycardia, hypotension and possible heart block.

[Week 4 · Class II antiarrhythmics (beta blockers)] Which is nonselective: propranolol or metoprolol?

Propranolol blocks β1 and β2; metoprolol is relatively β1-selective.

[Week 4 · Class II antiarrhythmics (beta blockers)] What before-dose checks?

Pulse/HR, BP, and ECG if indicated.

[Week 4 · Class III antiarrhythmic (K⁺ blocker)] Class III example in outline?

Amiodarone.