Pharmacology Exam 4 Study Guide

Introduction

This Study Guide integrates essential pharmacology content from Module 11 (Drugs Affecting Blood Coagulation, Diuretics, and Renal Function) and Module 12 (Cardiac/Blood Vessel Drugs: Antihypertensives, Antiarrhythmics, Antianginals, and Lipid-Lowering Agents). It is organized by major drug categories and learning outcomes, highlighting mechanisms of action, therapeutic uses, adverse effects, and key nursing implications. Superscript numbers throughout refer to the “References” section at the end¹.

Use this guide to prepare for Exam 4, ensuring you understand each class of drugs, their clinical applications, and relevant nursing interventions. Whenever you see a visual aid placeholder, imagine or insert a table/diagram to reinforce the concepts.

1. Drugs Affecting Blood Coagulation

Blood coagulation modifiers include anticoagulants, antiplatelet agents, and thrombolytics. All can increase bleeding risk^1,3,5.

1.1 Anticoagulants

Heparin (unfractionated) and Enoxaparin (LMWH)
- Mechanism: Enhance antithrombin, inhibiting factors IIa (thrombin) and Xa^1,3.
- Therapeutic Uses: Prophylaxis and treatment of venous thromboembolism (VTE), such as DVT and PE; also used in acute coronary syndromes¹.
- Monitoring: Heparin: IV infusion or SubQ; monitor aPTT (goal ~60–80 sec). Antidote = Protamine sulfate¹. Watch for heparin-induced thrombocytopenia (HIT). Enoxaparin (LMWH): SubQ; more predictable; typically no lab monitoring. Reversed by protamine if needed¹.
Warfarin
- Mechanism: Inhibits Vitamin K–dependent clotting factors (II, VII, IX, X)^1,3.
- Therapeutic Uses: Long-term prevention of thromboembolism (AFib, mechanical valves). Slow onset¹.
- Monitoring: PT/INR (goal usually 2–3). Antidote = Vitamin K¹.
- Patient Education: Maintain consistent Vitamin K intake; check INR regularly; multiple drug/food interactions¹.
DOACs (e.g., Dabigatran, Rivaroxaban, Apixaban)
- Benefits: Fixed dosing, minimal lab monitoring^1,3.
- Reversal Agents: Idarucizumab (for dabigatran), Andexxa (for Xa inhibitors)¹.

Nursing Considerations (Anticoagulants): Double-check doses, monitor for bleeding, implement precautions (soft toothbrush, etc.)¹.

1.2 Antiplatelet Agents

Aspirin (ASA) Mechanism: Irreversible COX-1 inhibition → reduced thromboxane A₂ → decreased platelet aggregation^1,3. Use: Secondary prevention post-MI, stroke, TIA. Watch for GI bleeding¹.
Clopidogrel (Plavix) Mechanism: Blocks ADP receptor on platelets → prevents aggregation³. Use: Often combined with or used instead of ASA in stent placement, post-MI/stroke¹.

1.3 Thrombolytics

Alteplase (tPA) Mechanism: Converts plasminogen to plasmin → dissolves existing clots^1,3. Use: Acute MI, ischemic stroke, massive PE (strict time window)³. Major Risk: Severe bleeding (intracranial hemorrhage). Reversal: Aminocaproic acid¹.

Visual Aid Placeholder: Table – Comparison of Anticoagulants vs. Antiplatelets vs. Thrombolytics

2. Diuretics & Renal Function

Diuretics increase urine output by blocking sodium (and water) reabsorption in different nephron sites^2,3. They treat hypertension, edema, and can help prevent renal failure².

2.1 Loop Diuretics

Furosemide (Lasix), Bumetanide, Torsemide
Mechanism: Block Na⁺/Cl⁻ reabsorption in ascending loop of Henle².
Uses: Rapid fluid removal (acute pulmonary edema, HF).
Adverse: Hypokalemia, hypotension, ototoxicity (if pushed IV too fast)^2,3.

2.2 Thiazide Diuretics

Hydrochlorothiazide (HCTZ)
Mechanism: Block Na⁺ reabsorption in distal convoluted tubule².
Uses: First-line for HTN, mild edema².
Adverse: Hypokalemia, hyperglycemia, dehydration².

2.3 Potassium-Sparing Diuretics

Spironolactone (aldosterone antagonist)
Mechanism: Retains K⁺, excretes Na⁺ in distal nephron².
Adverse: Hyperkalemia, endocrine effects (e.g., gynecomastia)².

2.4 Osmotic Diuretics

Mannitol
Mechanism: Increases osmotic pressure → major fluid shift².
Uses: Reduce intracranial/intraocular pressure².
Adverse: Edema initially due to fluid shifts².

Visual Aid Placeholder: Table – Diuretics Comparison

3. Antihypertensive Agents & RAAS

Hypertension can be managed by reducing cardiac output, peripheral resistance, and/or blood volume. RAAS inhibitors (ACEIs, ARBs) are cornerstone therapies³.

3.1 RAAS Pathway & Inhibitors

ACE Inhibitors (e.g., Lisinopril) Mechanism: Block Ang I → Ang II → vasodilation, lower aldosterone³.
Adverse: Dry cough, hyperkalemia, angioedema, first-dose hypotension, teratogenic³.
ARBs (e.g., Losartan) Mechanism: Block angiotensin II receptors → no cough³.
Adverse: Hyperkalemia, rare angioedema, avoid in pregnancy³.
Renin Inhibitors (e.g., Aliskiren) Mechanism: Directly inhibit renin; not first-line³.

3.2 Beta Blockers

e.g., Metoprolol, Propranolol
Mechanism: Decrease HR, contractility, renin release³.
Adverse: Bradycardia, hypotension, fatigue, bronchospasm (if non-selective)³.

3.3 Calcium Channel Blockers

Dihydropyridines (Amlodipine) → vasodilation
Non-dihydropyridines (Verapamil, Diltiazem) → also slow AV conduction³.
Adverse: Hypotension, edema, bradycardia, constipation (verapamil). Avoid grapefruit juice³.

3.4 Other Antihypertensives

Alpha-1 Blockers (Prazosin): vasodilation; first-dose orthostatic hypotension³.
Central Alpha-2 Agonists (Clonidine, Methyldopa): sedation, dry mouth, rebound HTN if abrupt stop³.
Direct Vasodilators (Hydralazine, Minoxidil): reflex tachycardia; often need BB + diuretic³.

4. Heart Failure Management: Cardiac Glycosides

4.1 Digoxin

Mechanism: Positive inotrope (↑ contractility); negative chronotrope (↓ HR). Inhibits Na⁺/K⁺-ATPase⁴.
Uses: HF symptom control, rate control in AF⁴.
Therapeutic Range: ~0.5–2.0 ng/mL (narrow).
Signs of Toxicity: GI upset (nausea, anorexia), visual halos, arrhythmias, confusion⁴.
Predisposing Factors: Hypokalemia, renal dysfunction.
Antidote: Digoxin immune Fab (Digibind)⁴.

Nursing Considerations: Check apical pulse for 1 min; hold if <60. Monitor K⁺, renal function, and digoxin levels⁴.

5. Antiarrhythmic Drugs

Classified by Vaughan Williams Classes I–IV; can be proarrhythmic⁵. Continuous cardiac monitoring is essential when initiating or changing doses.

Class I (Na⁺ Channel Blockers)

IA: Procainamide, Quinidine – moderate Na⁺ block + K⁺ block, prolong repolarization⁵.
IB: Lidocaine IV – mild block, shortens repolarization; used for ventricular arrhythmias⁵.
IC: Flecainide – strong block; avoid in structural heart disease⁵.

Class II (Beta Blockers)

Decrease SA/AV nodal conduction, used in rate control (AF, flutter), post-MI prophylaxis⁵.

Class III (K⁺ Channel Blockers)

Amiodarone – used for atrial & ventricular arrhythmias; can cause pulmonary fibrosis, hepatotoxicity, thyroid issues, corneal deposits⁵.

Class IV (Calcium Channel Blockers, Non-DHP)

Verapamil, Diltiazem – slow AV node conduction; used for rate control in AF/flutter⁵.

Other Antiarrhythmics

Adenosine: For PSVT; causes brief asystole to reset rhythm⁵.
Atropine: Anticholinergic; used in symptomatic bradycardia⁵.
Digoxin: Slows AV conduction; add-on for rate control^4,5.

6. Antianginal Medications

Angina is chest pain from myocardial ischemia. Treatment reduces myocardial O₂ demand or increases O₂ supply⁶.

6.1 Nitrates

Nitroglycerin (NTG), Isosorbide dinitrate/mononitrate
Mechanism: Venous dilation → decreased preload; also arterial/coronary dilation⁶.
Uses: Acute relief (sublingual) or prophylaxis (transdermal, oral).
Adverse: Headache, hypotension, reflex tachycardia⁶.
Contraindication: PDE-5 inhibitors (e.g., sildenafil) within 24–48 hours⁶.

6.2 Beta-Blockers (for Angina)

Decrease HR & contractility → lower O₂ demand. Good for chronic stable angina prophylaxis, post-MI⁶.

6.3 Calcium Channel Blockers (for Angina)

Dihydropyridines: reduce afterload; Non-DHP: also slow HR⁶. First-line for variant (Prinzmetal) angina.

7. Lipid-Lowering Agents (Antilipemics)

Hyperlipidemia → atherosclerosis. Antilipemics target elevated LDL, TG, and raise HDL⁷.

7.1 HMG-CoA Reductase Inhibitors (Statins)

Atorvastatin, Simvastatin
Mechanism: Inhibit hepatic cholesterol synthesis⁷.
Effects: Lower LDL 20–60%, reduce CV events⁷.
Adverse: Hepatotoxicity, myopathy/rhabdomyolysis (rare). Avoid grapefruit juice⁷.

7.2 Bile Acid Sequestrants

Cholestyramine, Colestipol
Bind bile acids in intestine → lower LDL. GI side effects (constipation, bloating)⁷.

7.3 Niacin (High-Dose Vitamin B₃)

Lowers LDL/TG, significantly raises HDL. Common flushing (mitigate with aspirin)⁷.

7.4 Fibric Acid Derivatives (Fibrates)

Gemfibrozil, Fenofibrate
Mainly lower triglycerides; risk of gallstones, myopathy with statins⁷.

7.5 Ezetimibe

Blocks dietary cholesterol absorption. Often used with a statin⁷.

References

Open RN Nursing Pharmacology (2020) – Section 6.12: Blood Coagulation Modifiers. Open Resources for Nursing (Chippewa Valley Technical College). Used for information on anticoagulant, antiplatelet, and thrombolytic drug classes, including mechanisms and nursing considerations.
Open RN Nursing Pharmacology (2020) – Section 6.9: Diuretics. Open Resources for Nursing. Source for diuretic classes, their effects on renal function, electrolyte implications, and patient teaching.
Open RN Nursing Pharmacology (2020) – Section 6.10: Antihypertensives. Open Resources for Nursing. Referenced for RAAS system, ACE inhibitors, ARBs, beta-blockers, CCBs, and other blood pressure agents’ mechanisms and side effects.
Open RN Nursing Pharmacology (2020) – Section 6.7: Cardiac Glycosides. Open Resources for Nursing. Provided details on digoxin’s mechanism, therapeutic range, toxicity signs, and management.
Open RN Nursing Pharmacology (2020) – Section 6.6: Antiarrhythmics. Open Resources for Nursing. Used for classification of antiarrhythmic drugs (Classes I–IV) and their effects on cardiac conduction.
Open RN Nursing Pharmacology (2020) – Section 6.8: Antianginal – Nitrates. Open Resources for Nursing. Information on nitroglycerin’s action, contraindications (e.g., sildenafil), and patient education for angina management.
Open RN Nursing Pharmacology (2020) – Section 6.11: Antilipemics. Open Resources for Nursing. Source for lipid-lowering agents including statins (mechanism, rhabdomyolysis risk), bile sequestrants, niacin, fibrates, and key patient teaching points.