1. Pharmacokinetics (ADME) 💊

Pharmacokinetics answers the question: "What does the body do to the drug?" Remember the acronym ADME - Absorption, Distribution, Metabolism, Excretion.

Process	Definition	Key Factors	Clinical Relevance
Absorption	Drug movement from site of administration to bloodstream	Route, pH, lipophilicity, blood flow, surface area	Bioavailability, First-pass effect
Distribution	Drug movement from blood to tissues	Protein binding, lipid solubility, Vd	Drug interactions, tissue penetration
Metabolism	Chemical transformation of drug	CYP450 enzymes, Phase I/II reactions	Drug interactions, prodrugs, toxic metabolites
Excretion	Drug removal from body	Renal function, hepatic clearance	Dosing in renal/hepatic impairment

First-Pass Metabolism:

Drugs absorbed from GI tract first pass through the liver before systemic circulation. This can significantly reduce bioavailability.

High First-Pass Drugs: Morphine, Propranolol, Verapamil, Nitroglycerin

Volume of Distribution (Vd):

Hypothetical volume needed to contain all drug at plasma concentration.

Low Vd (3-5 L): Drug stays in plasma (Warfarin)
High Vd (>40 L): Drug distributes to tissues (Digoxin, Chloroquine)

💡 Board Exam Tip:

Know the half-life formula: t½ = 0.693 × Vd / Clearance. It takes approximately 4-5 half-lives to reach steady state!

2. Pharmacodynamics 💪

Pharmacodynamics answers: "What does the drug do to the body?" This involves drug-receptor interactions and mechanisms of action.

Receptor Type	Mechanism	Response Time	Examples
Ligand-Gated Ion Channels	Direct ion flow	Milliseconds	Nicotinic receptors, GABA-A
G-Protein Coupled (GPCR)	Second messengers (cAMP, IP3)	Seconds to minutes	Beta-adrenergic, Muscarinic, Opioid
Enzyme-Linked	Tyrosine kinase activity	Minutes to hours	Insulin receptor, Growth factors
Intracellular/Nuclear	Gene transcription	Hours to days	Steroids, Thyroid hormones

Agonists

Bind and activate receptors. Full agonists produce maximal response; partial agonists produce submaximal response.

Antagonists

Bind but don't activate receptors. Competitive antagonists are surmountable; non-competitive are not.

Inverse Agonists

Bind and produce opposite effect to agonist. Examples: some benzodiazepine derivatives.

Key Terms:

Efficacy (Emax): Maximum effect a drug can produce
Potency (EC50): Dose needed to produce 50% of max effect
Therapeutic Index (TI): TD50/ED50 - higher is safer!

3. Autonomic Pharmacology 🧠

Understanding the ANS is crucial - it's heavily tested in board exams! Know your sympathetic (fight or flight) vs parasympathetic (rest and digest) drugs.

Drug Class	Mechanism	Effects	Clinical Use
Sympathomimetics	Activate adrenergic receptors	↑HR, ↑BP, bronchodilation	Epinephrine, Albuterol
Sympatholytics	Block adrenergic receptors	↓HR, ↓BP	Propranolol, Prazosin
Cholinomimetics	Activate muscarinic/nicotinic	↓HR, ↑secretions, miosis	Pilocarpine, Bethanechol
Anticholinergics	Block muscarinic receptors	↑HR, dry mouth, mydriasis	Atropine, Ipratropium

🔥 High-Yield: Adrenergic Receptor Effects

α1: Vasoconstriction, mydriasis, urinary sphincter contraction
α2: ↓NE release, ↓insulin release (presynaptic)
β1: ↑Heart rate, ↑contractility (heart)
β2: Bronchodilation, vasodilation, uterine relaxation
β3: Lipolysis (adipose tissue)

4. Major Drug Classes 💉

Know the mechanism, side effects, and contraindications of major drug classes for the board exam.

Cardiovascular Drugs:

ACE Inhibitors (-pril): Dry cough, hyperkalemia, angioedema
ARBs (-sartan): Similar to ACE, no cough
Beta-blockers (-olol): Bradycardia, bronchospasm, mask hypoglycemia
CCBs (-dipine, Verapamil, Diltiazem): Edema, constipation
Diuretics: Electrolyte imbalances

Antimicrobials:

Penicillins: Hypersensitivity, cross-reactivity
Aminoglycosides: Nephro/ototoxicity
Fluoroquinolones: Tendon rupture, QT prolongation
Macrolides: GI upset, QT prolongation
Vancomycin: Red man syndrome, nephrotoxicity

CNS Drugs:

Benzodiazepines: Sedation, dependence, respiratory depression
Opioids: Constipation, respiratory depression, dependence
SSRIs: Sexual dysfunction, serotonin syndrome
Antipsychotics: EPS, metabolic syndrome, QT prolongation

Endocrine Drugs:

Insulin: Hypoglycemia, weight gain
Metformin: Lactic acidosis (rare), GI upset, B12 deficiency
Sulfonylureas: Hypoglycemia, weight gain
Corticosteroids: Cushing's, osteoporosis, hyperglycemia

5. Drug Calculations ➗

Accurate drug calculations are essential for patient safety. Master these formulas!

Essential Formulas:

Basic Dose Calculation:

Dose = (Desired / Have) × Vehicle

IV Drip Rate (drops/min):

Rate = (Volume × Drop Factor) / Time in minutes

Creatinine Clearance (Cockcroft-Gault):

CrCl = [(140 - Age) × Weight] / (72 × SCr) × 0.85 if female

Body Surface Area (BSA):

BSA = √[(Height cm × Weight kg) / 3600]

Loading Dose:

LD = (Vd × Cp) / Bioavailability

Maintenance Dose:

MD = (Clearance × Cp × τ) / Bioavailability

💡 Common Conversions:

1 grain = 65 mg (or 60 mg for quick calculations)
1 teaspoon = 5 mL
1 tablespoon = 15 mL
1 kg = 2.2 lbs
1% solution = 10 mg/mL = 10 g/L

6. Practice Questions 📝

Question 1: Pharmacokinetics

A drug has a half-life of 6 hours. How long until steady state is reached with regular dosing?

Answer: 24-30 hours (4-5 half-lives). Steady state is reached after approximately 4-5 half-lives regardless of dose. 6 hrs × 5 = 30 hours.

Question 2: Receptor Pharmacology

Which receptor subtype mediates bronchodilation when stimulated by albuterol?

Answer: Beta-2 (β2) adrenergic receptors. Albuterol is a selective β2-agonist used for asthma and COPD. β2 stimulation causes smooth muscle relaxation in bronchi.

Question 3: Drug Calculation

A patient needs 500 mg of amoxicillin. The suspension available is 250 mg/5 mL. How many mL should be given?

Answer: 10 mL. Using the formula: (Desired/Have) × Vehicle = (500/250) × 5 = 2 × 5 = 10 mL

Question 4: Autonomic Pharmacology

A patient on propranolol for hypertension develops bronchospasm. What is the mechanism?

Answer: Propranolol is a non-selective beta-blocker that blocks both β1 and β2 receptors. Blocking β2 in the lungs prevents bronchodilation, causing bronchoconstriction. This is why non-selective beta-blockers are contraindicated in asthma. A selective β1-blocker (metoprolol, atenolol) would be safer.

Pharmacology