Pharmacology for Nurses

Pharmacology is the study of drugs — their properties, mechanisms of action, pharmacokinetics, pharmacodynamics, therapeutic uses, and adverse effects. For nurses, pharmacology is a critical clinical science because nurses are the healthcare professionals who most frequently administer medications, monitor for therapeutic and adverse effects, and are often the first to detect drug-related problems. The HAAD examination tests pharmacological knowledge heavily, particularly in areas relevant to common conditions seen in the UAE: cardiovascular disease (hypertension, coronary artery disease), diabetes mellitus, infectious diseases, and pain management. This chapter covers the essential pharmacology knowledge required for the HAAD nursing examination.

Pharmacokinetics: What the Body Does to the Drug

Pharmacokinetics describes the absorption, distribution, metabolism, and excretion (ADME) of drugs.

Absorption

Absorption is the process by which a drug enters the bloodstream from its site of administration.

Factors affecting absorption:

• Route of administration: IV (fastest — 100% bioavailability, bypasses absorption); IM (fast, good bioavailability); SC (slower than IM due to less vascularity); PO (most common, but subject to first-pass metabolism)
• First-pass effect: Drugs absorbed from the GI tract are transported via the portal vein to the liver before entering systemic circulation. Many drugs are significantly metabolized in the liver on first pass (e.g., propranolol, morphine, lidocaine), reducing their bioavailability. Drugs with significant first-pass effect may require higher oral doses or IV administration.
• pH and ionization: Drugs that are weak acids (e.g., aspirin, warfarin) are better absorbed in the acidic stomach environment; weak bases (e.g., morphine, catecholamines) are better absorbed in the alkaline small intestine
• Surface area: Larger surface area → faster absorption (small intestine has largest surface area due to villi)
• Blood flow: Areas with high blood flow (IM, sublingual) have faster absorption

Distribution

Distribution is the movement of drugs from the bloodstream to tissues and organs.

Factors affecting distribution:

• Blood flow: Highly perfused organs (brain, heart, liver, kidneys) receive drugs faster
• Protein binding: Many drugs bind to plasma proteins (mainly albumin) — only unbound (free) drug is pharmacologically active and can cross membranes. Protein-bound drug acts as a reservoir. In hypoalbuminemia (liver disease, nephrotic syndrome), more free drug is available → increased effect and toxicity risk.
• Blood-brain barrier: Only lipophilic (fat-soluble) drugs can cross into the CNS; polar/ionized drugs cannot — this protects the brain from many substances but also limits drug entry (e.g., many antibiotics cannot treat meningitis)
• Volume of distribution (Vd): A theoretical volume that a drug would need to distribute in to achieve the observed plasma concentration. Large Vd → drug distributes extensively into tissues.

Metabolism (Biotransformation)

Drug metabolism occurs primarily in the liver (by cytochrome P450 enzymes), but also in the GI tract, kidneys, lungs, and plasma.

Phase I reactions (Functionalization): Oxidation, reduction, hydrolysis — convert drugs to more polar, water-soluble metabolites. The cytochrome P450 system (CYP450) is the most important enzyme system. Key isoforms include CYP3A4 (metabolizes ~50% of drugs), CYP2D6, CYP2C9, CYP2C19.

Phase II reactions (Conjugation): Glucuronidation, sulfation, acetylation, methylation — attach endogenous molecules to the drug or its Phase I metabolite to make it water-soluble for renal excretion.

First-order kinetics: Rate of elimination is proportional to drug concentration (most drugs at therapeutic doses). Half-life (t½) is constant.

Zero-order kinetics: Rate of elimination is constant regardless of concentration (e.g., alcohol, phenytoin at high doses). Half-life increases as concentration rises → risk of accumulation.

Factors affecting metabolism: Age (neonates have immature liver enzymes; elderly have reduced hepatic function), genetics (some populations have genetically determined fast/slow metabolizer status), liver disease (cirrhosis reduces metabolic capacity), drug interactions (inducers: carbamazepine, rifampin, phenytoin; inhibitors: erythromycin, ketoconazole, grapefruit juice).

Excretion

Renal excretion is the most important route for most drugs. Glomerular filtration, tubular secretion, and tubular reabsorption all play roles. In renal impairment, drugs excreted by the kidneys require dose adjustment.

Other routes: Biliary/fecal (drugs secreted in bile → feces), pulmonary (volatile anesthetics, alcohol), sweat, saliva (some drugs appear in breast milk).

Drug half-life (t½): The time required for the plasma concentration to fall by 50%. After 4–5 half-lives, a drug reaches steady state (steady-state concentration = Css). The steady-state concentration is directly proportional to the dose and dosing frequency, and inversely proportional to clearance.

Pharmacodynamics: What the Drug Does to the Body

Mechanisms of Drug Action

Agonists: Drugs that bind to a receptor and produce a biological response (mimic the endogenous ligand). Full agonists produce a maximal response; partial agonists produce less than maximal response.

Antagonists: Drugs that bind to a receptor without producing a response, blocking the action of an agonist. Competitive antagonists bind reversibly to the same site as the agonist; non-competitive antagonists bind to a different (allosteric) site.

Other mechanisms: Enzyme inhibition (e.g., ACE inhibitors block angiotensin-converting enzyme), direct receptor interaction (insulin binding to insulin receptor), cytotoxic agents (chemotherapy — acting on rapidly dividing cells).

Dose-Response Relationship

Therapeutic window: The range of drug concentrations between the minimum effective concentration (MEC) and the toxic concentration (TC). Drugs with a narrow therapeutic window (e.g., digoxin, lithium, aminoglycosides, warfarin) require careful monitoring (therapeutic drug monitoring — TDM).

Potency: The dose required to produce a given effect — a more potent drug requires a lower dose to achieve the same effect (not the same as efficacy).

Efficacy (intrinsic activity): The maximum effect a drug can produce (Emax) — determines whether it can produce the desired clinical effect.

Efficacy vs. Potency: A drug can be highly potent (low dose effective) but have low efficacy (cannot produce a maximal response). A drug can have high efficacy but low potency (requires high dose).

Adverse Drug Reactions (ADRs)

Type A (Predictable, dose-dependent): Excessive pharmacological effect — e.g., bleeding from warfarin, hypoglycemia from insulin, constipation from opioids. Account for ~75% of ADRs. Preventable by dose adjustment.

Type B (Unpredictable, dose-independent): Idiosyncratic or allergic — e.g., anaphylaxis from penicillin, Stevens-Johnson syndrome from sulfonamides. Not predictable from the known pharmacology. Not preventable by dose reduction.

Drug allergy vs. intolerance: Allergy involves immune-mediated IgE or cell-mediated mechanisms; intolerance is a non-immune adverse reaction (e.g., nausea from opioids — not an allergy).

Drug Categories Important for HAAD

Cardiovascular Drugs

Antihypertensives:

• ACE inhibitors (–pril): Enalapril, lisinopril. Block conversion of angiotensin I → angiotensin II. Side effects: dry cough (bradykinin accumulation), angioedema, hyperkalemia, hypotension (first-dose effect). Contraindicated in pregnancy, bilateral renal artery stenosis.
• ARBs (–sartan): Losartan, valsartan. Block AT1 receptors. Less cough than ACEIs.
• Beta-blockers (–olol): Metoprolol, atenolol. Block β1-adrenergic receptors → reduce HR, contractility, BP. Side effects: bradycardia, bronchospasm (non-selective), sexual dysfunction, depression, masking of hypoglycemia symptoms. Contraindicated in asthma, severe bradycardia, AV block.
• Calcium channel blockers: Amlodipine (dihydropyridine — mainly vasodilation), Verapamil/Diltiazem (non-dihydropyridine — also reduce HR and contractility).

Diuretics:

• Thiazides (hydrochlorothiazide): First-line for hypertension; cause hypokalemia, hyperuricemia, hyperglycemia, hypercalcemia
• Loop diuretics (furosemide/bumetanide): More potent; cause hypokalemia, hypocalcemia, ototoxicity (furosemide)
• Potassium-sparing (spironolactone, amiloride): Block aldosterone or ENaC; cause hyperkalemia

Anticoagulants:

• Heparin (unfractionated): IV/SC; potentiates antithrombin III; monitored by aPTT; reversal with protamine
• LMWH (enoxaparin): SC; predictable pharmacokinetics; monitored by anti-Xa levels if needed; reversal with protamine partially
• Warfarin: Oral; vitamin K antagonist (inhibits factors II, VII, IX, X, proteins C and S); narrow therapeutic window; monitored by INR (target 2–3 for most indications, 2.5–3.5 for mechanical heart valves); many drug and food (vitamin K) interactions
• DOACs (apixaban, rivaroxaban, dabigatran): Direct oral anticoagulants; do not require routine monitoring; dabigatran (direct thrombin inhibitor) requires reversal with idarucizumab

Antiplatelet agents:

• Aspirin: Irreversibly inhibits COX-1 → reduced thromboxane A2 → reduced platelet aggregation. Low dose (75–100 mg) for cardiovascular prevention.
• Clopidogrel: P2Y12 ADP receptor antagonist; requires CYP2C19 activation; drug interactions with omeprazole (reduces activation)

Antimicrobials

• Penicillins (amoxicillin, ampicillin, piperacillin): Bactericidal; inhibit cell wall synthesis; allergy (Type I — anaphylaxis) is the most important concern; broad-spectrum with beta-lactamase inhibitors (augmentin = amoxicillin-clavulanate)
• Cephalosporins: Similar to penicillins; cross-reactivity ~1–2% with penicillin allergy; divided into generations (1st = mainly Gram-positive; 3rd/4th = broader Gram-negative coverage)
• Aminoglycosides (gentamicin, amikacin): Bactericidal; inhibit protein synthesis (30S ribosome); nephrotoxic and ototoxic; requires TDM
• Fluoroquinolones (ciprofloxacin, levofloxacin): Bactericidal; inhibit DNA gyrase and topoisomerase IV; side effects: tendon rupture, QT prolongation, neuropathy; contraindicated in children (<18) — cartilage damage
• Vancomycin: Bactericidal; inhibits cell wall synthesis; used for MRSA; nephrotoxic and ototoxic; requires TDM (trough levels 15–20 µg/mL for serious infections)

Hypoglycemic Agents

• Metformin: First-line for T2DM; reduces hepatic gluconeogenesis, improves insulin sensitivity; contraindicated in renal impairment (creatinine >130 µmol/L), liver failure, conditions causing hypoxia (MI, sepsis); causes vitamin B12 deficiency
• Sulfonylureas (glibenclamide, gliclazide): Stimulate insulin secretion from pancreatic beta cells; risk of hypoglycemia and weight gain
• Insulin: Essential for T1DM; used in T2DM when oral agents fail; types: rapid-acting (aspart, lispro — given with meals), intermediate-acting (NPH), long-acting (glargine, detemir — basal coverage). Side effect: hypoglycemia (treat with oral glucose or IV dextrose/glucagon IM/SC)

⚡ Exam tip: Drug half-life determines time to steady state (~4–5 half-lives). Narrow therapeutic index drugs require TDM (digoxin, aminoglycosides, vancomycin, warfarin, lithium, phenytoin). For anaphylaxis (Type I allergic reaction):肾上腺素 (epinephrine) IM is first-line — NOT antihistamine. For hypoglycemia: if patient unconscious → IV dextrose 50% (D50); if conscious → oral glucose.

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