General Pharmacology & Key Drug Classes

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1. Principles of General Pharmacology 1.1 Drug Definition & Dosage Forms Drug: A chemical substance that affects physiological function when administered. Dosage Forms: Solid: Tablets, capsules, powders, granules. Liquid: Solutions, suspensions, emulsions, syrups, elixirs. Semi-solid: Ointments, creams, gels, pastes, suppositories. Gaseous: Inhalers, aerosols. 1.2 Routes of Drug Administration Enteral: Via GI tract Oral: Most common, convenient. Subject to first-pass metabolism. Sublingual: Under tongue, rapid absorption, avoids first-pass. E.g., Nitroglycerin. Rectal: Local or systemic effect, useful for unconscious/vomiting patients. Partial avoidance of first-pass. Parenteral: Bypasses GI tract Intravenous (IV): 100% bioavailability, rapid onset, precise dose. Higher risk of adverse effects. Intramuscular (IM): Slower absorption than IV, suitable for suspensions/oils. E.g., Vaccines. Subcutaneous (SC): Slower than IM, for small volumes. E.g., Insulin. Intradermal (ID): Into dermis, for diagnostic tests. E.g., TB test. Topical: Local effect on skin/mucous membranes. E.g., Creams, eye drops. Transdermal: Systemic effect via skin patch. Slow, sustained release. E.g., Nicotine patch. Inhalation: Rapid absorption via lungs, local (asthma) or systemic (anesthetics) effects. 1.3 Pharmacokinetics (ADME) What the BODY does to the DRUG. Absorption: Movement of drug from site of administration to systemic circulation. Factors: Lipid solubility, ionization, blood flow, surface area. Bioavailability (F): Fraction of administered dose that reaches systemic circulation unchanged. $$F = \frac{\text{AUC (oral)}}{\text{AUC (IV)}} \times 100\%$$ Distribution: Reversible transfer of drug from systemic circulation to tissues. Factors: Blood flow, plasma protein binding (e.g., albumin, $\alpha_1$-acid glycoprotein), tissue binding, volume of distribution ($V_d$). $V_d = \frac{\text{Total amount of drug in body}}{\text{Drug plasma concentration}}$. High $V_d$ means extensive tissue distribution. Metabolism (Biotransformation): Chemical alteration of drug by enzymes. Primarily in liver. Phase I reactions: Oxidation, reduction, hydrolysis. Introduce or expose polar groups. Often involves Cytochrome P450 (CYP450) enzymes. Can activate or inactivate drugs. Phase II reactions: Conjugation reactions (glucuronidation, sulfation, acetylation). Attach polar endogenous molecules to drug/metabolite to make it more water-soluble for excretion. First-Pass Metabolism: Oral drug metabolized in gut wall or liver before reaching systemic circulation, reducing bioavailability. Excretion: Removal of drug/metabolites from body. Renal: Glomerular filtration, tubular secretion, tubular reabsorption. Most common. Biliary/Fecal: Excreted into bile, then feces. Other: Lung (volatile anesthetics), sweat, milk. Half-life ($t_{1/2}$): Time for plasma drug concentration to reduce by half. $t_{1/2} = \frac{0.693 \times V_d}{\text{Clearance}}$. Clearance (CL): Volume of plasma cleared of drug per unit time. 1.4 Pharmacodynamics What the DRUG does to the BODY. Mechanism of Drug Action: How drugs interact with biological systems to produce effects. Receptors: Most drugs act by binding to specific macromolecules (receptors), usually proteins (G-protein coupled, ligand-gated ion channels, enzyme-linked, intracellular). Enzymes: Drugs can inhibit or activate enzymes. Ion Channels: Drugs can block or open channels. Transporters: Drugs can inhibit uptake or efflux transporters. Non-receptor mechanisms: Antacids (neutralize acid), osmotic diuretics (osmotic effect). Agonist: Binds to receptor and activates it, producing a biological response. (Full, partial, inverse). Antagonist: Binds to receptor but does not activate it. Blocks agonist action. (Competitive, non-competitive, irreversible, physiological, chemical). Dose-Response Relationship: Potency: Amount of drug needed to produce an effect. $EC_{50}$ (concentration for 50% max effect). Efficacy: Maximum effect a drug can produce ($E_{max}$). Therapeutic Index (TI): Ratio of toxic dose to effective dose. $TI = \frac{TD_{50}}{ED_{50}}$. A measure of drug safety. Higher TI = safer drug. 2. Drugs Acting on Central Nervous System (CNS) 2.1 Anesthetics General Anesthetics: Reversible loss of consciousness and sensation. Inhalational: Sevoflurane, Isoflurane, Desflurane, Nitrous Oxide. Mechanism: Enhance GABAergic inhibition, inhibit NMDA receptors. MAC (Minimum Alveolar Concentration): Potency measure. Lower MAC = higher potency. Intravenous: Propofol, Thiopental, Ketamine, Etomidate, Midazolam. Propofol: Rapid onset, short duration, antiemetic. Ketamine: Dissociative anesthesia, analgesia, sympathetic stimulation. Local Anesthetics: Reversible blockade of nerve conduction at site of application. Mechanism: Block voltage-gated $\text{Na}^+$ channels, preventing nerve impulse transmission. Esters (e.g., Procaine, Cocaine): Metabolized by plasma esterases. Amides (e.g., Lidocaine, Bupivacaine): Metabolized by hepatic CYP450. 2.2 Sedative-Hypnotics Drugs that depress CNS function. Sedatives reduce anxiety; hypnotics induce sleep. Benzodiazepines (BZDs): Diazepam, Lorazepam, Alprazolam, Midazolam. Mechanism: Enhance GABA action at $\text{GABA}_A$ receptors by increasing frequency of $\text{Cl}^-$ channel opening. Uses: Anxiety, insomnia, seizures, muscle spasms, alcohol withdrawal. Antidote: Flumazenil (competitive antagonist). Barbiturates: Phenobarbital, Thiopental. Mechanism: Enhance GABA action by increasing duration of $\text{Cl}^-$ channel opening. Higher abuse potential, narrower TI than BZDs. Uses: Anesthesia induction, seizures (Phenobarbital). "Z-drugs": Zolpidem, Zaleplon, Eszopiclone. Mechanism: Selective $\text{GABA}_A$ receptor agonists at BZD-1 site. Less impact on sleep architecture. Uses: Insomnia. 2.3 Antiepileptics (AEDs) Drugs that prevent or reduce seizure activity. Mechanism: Block voltage-gated $\text{Na}^+$ channels (Phenytoin, Carbamazepine, Lamotrigine, Valproate). Enhance GABAergic transmission (Phenobarbital, Benzodiazepines, Valproate, Gabapentin, Tiagabine). Block $\text{Ca}^{2+}$ channels (Ethosuximide - for absence seizures, Gabapentin). Modulate glutamate receptors (Topiramate). Key Drugs: Phenytoin: $\text{Na}^+$ channel blocker. Fosphenytoin is prodrug. ADRs: gingival hyperplasia, hirsutism, teratogenic. Carbamazepine: $\text{Na}^+$ channel blocker. Uses: partial/tonic-clonic seizures, trigeminal neuralgia. ADRs: aplastic anemia, SJS. Autoinduces metabolism. Valproic Acid (Valproate): Broad spectrum. $\text{Na}^+$ channel blocker, $\text{Ca}^{2+}$ channel blocker, GABA enhancer. ADRs: hepatotoxicity, pancreatitis, teratogenic (neural tube defects). Lamotrigine: $\text{Na}^+$ channel blocker. ADRs: SJS. Ethosuximide: Blocks T-type $\text{Ca}^{2+}$ channels. Only for absence seizures. 2.4 Antiparkinsonian Drugs Parkinson's disease: Degeneration of dopaminergic neurons in substantia nigra leading to dopamine deficiency and acetylcholine excess. Levodopa/Carbidopa: Levodopa: Dopamine precursor, crosses BBB. Carbidopa: Peripheral DOPA decarboxylase inhibitor, prevents peripheral breakdown of Levodopa, reducing side effects and increasing Levodopa reaching brain. ADRs: Dyskinesias, "on-off" phenomena, nausea, orthostatic hypotension. Dopamine Agonists: Pramipexole, Ropinirole, Bromocriptine. Directly stimulate dopamine receptors. Fewer motor fluctuations than Levodopa. ADRs: Hallucinations, impulse control disorders. MAO-B Inhibitors: Selegiline, Rasagiline. Inhibit breakdown of dopamine in brain. COMT Inhibitors: Entacapone, Tolcapone. Inhibit peripheral (Entacapone) or central/peripheral (Tolcapone) breakdown of Levodopa. Used as adjunct. Anticholinergics: Benztropine, Trihexyphenidyl. Block muscarinic receptors. Primarily for tremor and rigidity, less effective for bradykinesia. ADRs: Dry mouth, blurred vision, constipation, confusion. 2.5 Antidepressants Mechanism: Increase levels of monoamine neurotransmitters (serotonin, norepinephrine, dopamine) in synaptic cleft. Selective Serotonin Reuptake Inhibitors (SSRIs): Fluoxetine, Sertraline, Paroxetine, Escitalopram. Mechanism: Block serotonin reuptake. First-line for depression, anxiety disorders. ADRs: Sexual dysfunction, GI upset, insomnia/somnolence. Risk of Serotonin Syndrome (with other serotonergic drugs). Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs): Venlafaxine, Duloxetine. Block reuptake of both serotonin and norepinephrine. Uses: Depression, neuropathic pain (Duloxetine). Tricyclic Antidepressants (TCAs): Amitriptyline, Imipramine, Nortriptyline. Mechanism: Block reuptake of NE and 5-HT. Also block $\alpha_1$-adrenergic, muscarinic, and histamine $\text{H}_1$ receptors. ADRs: Anticholinergic effects (dry mouth, blurred vision, constipation, urinary retention), orthostatic hypotension, sedation, cardiac toxicity (widened QRS) in overdose. Monoamine Oxidase Inhibitors (MAOIs): Phenelzine, Tranylcypromine, Selegiline (patch). Mechanism: Inhibit MAO enzyme, preventing breakdown of NE, 5-HT, Dopamine. ADRs: Hypertensive crisis with tyramine-rich foods ("cheese effect"), Serotonin Syndrome. Atypical Antidepressants: Bupropion, Mirtazapine, Trazodone. Bupropion: NE and DA reuptake inhibitor. Less sexual dysfunction. Used for smoking cessation. Mirtazapine: $\alpha_2$ antagonist, increases NE and 5-HT release. Sedating, increases appetite. Trazodone: 5-HT reuptake inhibitor, 5-$\text{HT}_2$ antagonist. Highly sedating, used for insomnia. Priapism. 2.6 Antianxiety Drugs (Anxiolytics) Often overlap with sedatives. Benzodiazepines: Alprazolam, Lorazepam, Diazepam. (Refer to Sedative-Hypnotics). Rapid onset. Buspirone: Mechanism: Partial agonist at 5-$\text{HT}_{1A}$ serotonin receptors. Slow onset (weeks), no sedation, no dependence/withdrawal. Good for GAD. SSRIs/SNRIs: Many antidepressants are effective for anxiety disorders (GAD, panic disorder, social phobia). Slower onset. Beta-blockers: Propranolol. Used for performance anxiety (stage fright) to reduce somatic symptoms (tremor, palpitations). 2.7 Opioid Analgesics Drugs derived from opium poppy or synthetic analogues that act on opioid receptors. Mechanism: Agonists at $\mu$, $\kappa$, $\delta$ opioid receptors in CNS and periphery. Primarily $\mu$ receptor activation for analgesia. Effects: Analgesia, sedation, euphoria, respiratory depression, miosis (pinpoint pupils), constipation, antitussive. Key Drugs: Strong Agonists: Morphine, Fentanyl, Hydromorphone, Heroin (diacetylmorphine). Moderate Agonists: Codeine, Oxycodone, Hydrocodone. Often combined with NSAIDs/acetaminophen. Mixed Agonist-Antagonists: Buprenorphine (partial $\mu$ agonist, $\kappa$ antagonist). Less respiratory depression, used for opioid dependence. Antagonists: Naloxone, Naltrexone. Naloxone: Acute opioid overdose reversal. Short duration. Naltrexone: Long-acting, used for opioid and alcohol dependence. ADRs: Respiratory depression (dose-limiting), constipation (no tolerance), nausea, vomiting, sedation, tolerance, physical dependence. 3. Drugs Acting on Peripheral Nervous System (Somatic) 3.1 Skeletal Muscle Relaxants Used for muscle spasms (acute injury) or spasticity (CNS disorders like MS, stroke). For Acute Muscle Spasm: Cyclobenzaprine, Carisoprodol, Baclofen (oral). Mechanism: CNS depressants, reduce polysynaptic reflex activity. ADRs: Sedation, anticholinergic effects (Cyclobenzaprine). For Spasticity (Chronic): Baclofen (oral/intrathecal), Diazepam, Tizanidine, Dantrolene. Baclofen: $\text{GABA}_B$ agonist. Reduces excitatory neurotransmitter release. Tizanidine: $\alpha_2$-adrenergic agonist. Reduces spasticity by presynaptic inhibition. Dantrolene: Direct action on muscle. Blocks $\text{Ca}^{2+}$ release from sarcoplasmic reticulum. Used for malignant hyperthermia. 3.2 Local Anesthetics Refer to Section 2.1 (Anesthetics). Mechanism: Block voltage-gated $\text{Na}^+$ channels. Esters (Procaine, Cocaine), Amides (Lidocaine, Bupivacaine). Often co-administered with vasoconstrictors (e.g., Epinephrine) to prolong duration and reduce systemic absorption. 4. Autacoids and Related Drugs 4.1 Nonsteroidal Anti-inflammatory Drugs (NSAIDs) / Antipyretic & Analgesics Mechanism: Inhibit cyclooxygenase (COX) enzymes, reducing prostaglandin (PG) and thromboxane ($\text{TXA}_2$) synthesis. COX-1: Constitutively expressed, produces PGs for gastric protection, renal blood flow, platelet aggregation. COX-2: Inducible during inflammation, produces PGs that mediate pain, fever, inflammation. Effects: Analgesic, anti-inflammatory, antipyretic. Key Drugs: Non-selective COX Inhibitors: Aspirin (irreversible), Ibuprofen, Naproxen, Diclofenac, Indomethacin, Ketorolac. Aspirin: Low dose antiplatelet (irreversible COX-1 inhibition). High dose anti-inflammatory. Reye's syndrome in children with viral infections. Ibuprofen/Naproxen: Common OTC, reversible COX inhibition. Indomethacin: Potent, used for gout, patent ductus arteriosus. Selective COX-2 Inhibitors ("Coxibs"): Celecoxib. Less GI toxicity than non-selective NSAIDs. Increased risk of cardiovascular thrombotic events (due to unopposed $\text{TXA}_2$ from COX-1). ADRs (Non-selective): Gastric irritation/ulcers (due to COX-1 inhibition), renal dysfunction, increased bleeding risk. Acetaminophen (Paracetamol): Mechanism: Weak COX-1/COX-2 inhibitor in CNS (not peripheral), likely involves other pathways. Effects: Analgesic, antipyretic. NOT anti-inflammatory. ADRs: Hepatotoxicity in overdose (metabolite NAPQI depletes glutathione). Antidote: N-acetylcysteine. 5. Drugs for Respiratory Disorders 5.1 Bronchodilators Used to relieve bronchoconstriction in asthma and COPD. $\beta_2$-Adrenergic Agonists: Mechanism: Stimulate $\beta_2$ receptors in bronchial smooth muscle, leading to bronchodilation. Short-Acting ($\text{SABAs}$): Albuterol (Salbutamol), Levalbuterol. Rescue inhalers for acute symptoms. Long-Acting ($\text{LABAs}$): Salmeterol, Formoterol. Used for maintenance, always with an inhaled corticosteroid in asthma. ADRs: Tremor, tachycardia, palpitations. Anticholinergics (Muscarinic Antagonists): Mechanism: Block muscarinic receptors in airways, preventing acetylcholine-induced bronchoconstriction. Short-Acting ($\text{SAMAs}$): Ipratropium. Used for COPD, acute asthma exacerbations (synergistic with $\text{SABAs}$). Long-Acting ($\text{LAMAs}$): Tiotropium. Maintenance therapy for COPD. ADRs: Dry mouth, blurred vision. Methylxanthines: Theophylline. Mechanism: Inhibit phosphodiesterase (PDE), increasing cAMP, and adenosine receptor antagonism. Narrow therapeutic index, many drug interactions. Used less frequently. ADRs: Nausea, vomiting, arrhythmias, seizures. 5.2 Aerosols/Inhalants Delivery method for many respiratory drugs. Allows direct delivery to lungs, minimizing systemic side effects. Metered-Dose Inhalers (MDIs): Require coordination. Spacers improve delivery. Dry Powder Inhalers (DPIs): Breath-activated. Nebulizers: Converts liquid medication into a fine mist. Good for young children, elderly, or severe exacerbations. Inhaled Corticosteroids (ICS): Fluticasone, Budesonide. Mechanism: Anti-inflammatory, reduce airway hyperresponsiveness. First-line for asthma prophylaxis. ADRs: Oral candidiasis (rinse mouth after use), dysphonia. 5.3 Expectorants Drugs that increase bronchial secretion or reduce its viscosity to facilitate removal. Guaifenesin: Increases volume and reduces viscosity of respiratory tract secretions. Acetylcysteine: Mucolytic. Breaks disulfide bonds in mucus proteins, thinning secretions. Also antidote for acetaminophen overdose. 5.4 Antitussive Drugs Drugs that suppress coughing. Opioids: Codeine, Dextromethorphan. Mechanism: Act on cough center in medulla. Dextromethorphan: Opioid derivative, but no opioid analgesic or addictive properties at antitussive doses. Benxonatate: Peripheral action, anesthetizes stretch receptors in respiratory passages. 6. Cardiovascular Drugs 6.1 Antihypertensive Drugs Drugs used to lower blood pressure. Diuretics: (See section 7.1) Thiazides (Hydrochlorothiazide), Loop (Furosemide), K-sparing (Spironolactone). ACE Inhibitors (-prils): Captopril, Enalapril, Lisinopril. Mechanism: Inhibit Angiotensin Converting Enzyme, reducing Angiotensin II (vasoconstrictor, aldosterone release) and bradykinin breakdown. ADRs: Dry cough (due to bradykinin), angioedema, hyperkalemia, teratogenic. Angiotensin II Receptor Blockers (ARBs) (-sartans): Losartan, Valsartan. Mechanism: Block AT1 receptors, preventing Angiotensin II action. Similar effects to ACEIs, but no cough/angioedema (no bradykinin effect). Beta-Blockers (-olols): Metoprolol, Atenolol (cardioselective $\beta_1$), Propranolol (non-selective). Mechanism: Block $\beta$-adrenergic receptors, reducing heart rate, contractility, renin release. ADRs: Bradycardia, fatigue, bronchospasm (non-selective), sexual dysfunction. Calcium Channel Blockers (CCBs): Dihydropyridines (-dipines): Amlodipine, Nifedipine. Primarily vascular smooth muscle relaxation. Non-dihydropyridines: Verapamil, Diltiazem. Act on heart (rate, contractility) and vasculature. ADRs: Edema, headache, flushing (DHP); bradycardia, constipation (non-DHP). Alpha-1 Blockers (-zosins): Prazosin, Doxazosin. Mechanism: Block $\alpha_1$ receptors on vascular smooth muscle, causing vasodilation. ADRs: First-dose orthostatic hypotension. Central Alpha-2 Agonists: Clonidine, Methyldopa. Mechanism: Stimulate central $\alpha_2$ receptors, reducing sympathetic outflow. ADRs: Sedation, dry mouth, rebound hypertension on abrupt withdrawal. 6.2 Antianginal Drugs Used to treat angina pectoris (chest pain due to myocardial ischemia). Nitrates: Nitroglycerin, Isosorbide Dinitrate. Mechanism: Release nitric oxide (NO) in smooth muscle, causing vasodilation (venous > arterial). Reduces preload, some afterload. Uses: Acute angina (sublingual), prophylaxis (oral, patch). ADRs: Headache, flushing, orthostatic hypotension. Avoid with PDE-5 inhibitors (sildenafil). Beta-Blockers: Metoprolol, Atenolol. (See Antihypertensives) Mechanism: Reduce heart rate, contractility, and blood pressure, decreasing myocardial oxygen demand. Calcium Channel Blockers: Verapamil, Diltiazem, Amlodipine. (See Antihypertensives) Mechanism: Reduce myocardial oxygen demand (Verapamil, Diltiazem) and/or increase oxygen supply by dilating coronary arteries (all CCBs). 7. Drugs Acting on Kidney (Diuretics) 7.1 Diuretics Increase urine output by inhibiting reabsorption of $\text{Na}^+$ and $\text{Cl}^-$ in renal tubules. Loop Diuretics: Furosemide, Bumetanide. Mechanism: Inhibit $\text{Na}^+/2\text{Cl}^-/\text{K}^+$ cotransporter in thick ascending limb of loop of Henle. Most potent. Uses: Edema (heart failure, renal failure), hypertension. ADRs: Hypokalemia, hypomagnesemia, ototoxicity, dehydration. Thiazide Diuretics: Hydrochlorothiazide, Chlorthalidone. Mechanism: Inhibit $\text{Na}^+/\text{Cl}^-$ cotransporter in distal convoluted tubule. Uses: Hypertension (first-line), mild edema, $\text{Ca}^{2+}$ kidney stones (reduce $\text{Ca}^{2+}$ excretion). ADRs: Hypokalemia, hypercalcemia, hyperglycemia, hyperlipidemia, hyperuricemia. Potassium-Sparing Diuretics: Spironolactone, Amiloride, Triamterene. Mechanism: Spironolactone: Aldosterone antagonist in collecting duct. Amiloride/Triamterene: Block $\text{Na}^+$ channels in collecting duct. Uses: Heart failure (Spironolactone), hypertension (often with other diuretics to prevent K loss). ADRs: Hyperkalemia. Spironolactone: gynecomastia, menstrual irregularities. Osmotic Diuretics: Mannitol. Mechanism: Inert sugar, filtered at glomerulus but not reabsorbed, creating osmotic gradient. Uses: Cerebral edema, acute glaucoma. ADRs: Dehydration, electrolyte imbalance. 8. Drugs Affecting Blood 8.1 Haematinics Substances required for the formation of blood, especially red blood cells. Iron: Ferrous sulfate, Ferrous gluconate. Uses: Iron deficiency anemia. ADRs: GI upset, constipation, black stools. Folic Acid (Vitamin $\text{B}_9$): Uses: Megaloblastic anemia, prevention of neural tube defects in pregnancy. Vitamin $\text{B}_{12}$ (Cobalamin): Hydroxocobalamin, Cyanocobalamin. Uses: Pernicious anemia, other $\text{B}_{12}$ deficiencies. 8.2 Coagulants Drugs that promote blood clotting. Vitamin K: Phytomenadione ($\text{K}_1$). Mechanism: Essential for synthesis of clotting factors II, VII, IX, X. Uses: Warfarin overdose, vitamin K deficiency bleeding in newborns. Protamine Sulfate: Antidote for heparin overdose. Factor Concentrates: Factor VIII (for Hemophilia A), Factor IX (for Hemophilia B). 8.3 Anticoagulants Drugs that prevent blood clot formation. Heparin: Unfractionated Heparin (UFH), Low Molecular Weight Heparin (LMWH) - Enoxaparin, Dalteparin. Mechanism: Potentiate antithrombin III, inactivating thrombin and Factor Xa. UFH: Monitored by aPTT. LMWH: Longer half-life, more predictable, less HIT risk. ADRs: Bleeding, Heparin-Induced Thrombocytopenia (HIT). Warfarin: Mechanism: Vitamin K antagonist. Inhibits synthesis of clotting factors II, VII, IX, X. Oral, slow onset. Monitored by INR. Highly protein-bound, many drug/food interactions. ADRs: Bleeding. Teratogenic. Direct Oral Anticoagulants (DOACs): Direct Thrombin Inhibitors: Dabigatran. Factor Xa Inhibitors (-xabans): Rivaroxaban, Apixaban. Advantages: No routine monitoring, fewer drug interactions. ADRs: Bleeding. Antiplatelet Drugs: Aspirin: Irreversible COX-1 inhibition, preventing $\text{TXA}_2$ synthesis (platelet aggregation). $\text{P2Y}_{12}$ Inhibitors: Clopidogrel, Ticagrelor, Prasugrel. Block ADP receptor on platelets. Glycoprotein IIb/IIIa Inhibitors: Abciximab, Eptifibatide. Block final common pathway of platelet aggregation. 8.4 Hypolipidaemic Drugs Drugs used to lower blood lipid levels (cholesterol, triglycerides). Statins (HMG-CoA Reductase Inhibitors): Atorvastatin, Simvastatin, Rosuvastatin. Mechanism: Inhibit cholesterol synthesis in liver, upregulating LDL receptors, thus clearing LDL from blood. Uses: First-line for hypercholesterolemia, CVD prevention. ADRs: Myopathy, rhabdomyolysis, hepatotoxicity. Fibrates: Gemfibrozil, Fenofibrate. Mechanism: Activate PPAR-$\alpha$, increasing lipoprotein lipase activity, reducing triglycerides. Uses: Hypertriglyceridemia. Cholesterol Absorption Inhibitors: Ezetimibe. Mechanism: Inhibits cholesterol absorption from small intestine. PCSK9 Inhibitors: Alirocumab, Evolocumab. Mechanism: Monoclonal antibodies that inactivate PCSK9, increasing LDL receptor availability. Uses: Severe hypercholesterolemia, often with statins. 9. Gastrointestinal Drugs 9.1 Antacids Mechanism: Neutralize stomach acid. Systemic: Sodium Bicarbonate (rapid, but can cause alkalosis). Non-systemic: Aluminum Hydroxide (constipation), Magnesium Hydroxide (diarrhea), Calcium Carbonate (constipation, acid rebound). 9.2 Carminatives Relieve flatulence and abdominal discomfort. E.g., Peppermint oil, Dill water, Simethicone. 9.3 Digestants Enzyme preparations to aid digestion. E.g., Pancrelipase (for pancreatic insufficiency). 9.4 Antiemetics Drugs to prevent or treat nausea and vomiting. 5-$\text{HT}_3$ Receptor Antagonists (-setrons): Ondansetron. Mechanism: Block serotonin receptors in GI tract and chemoreceptor trigger zone (CTZ). Uses: Chemotherapy-induced nausea/vomiting (CINV), post-operative nausea/vomiting (PONV). Dopamine Antagonists: Metoclopramide, Prochlorperazine. Mechanism: Block $\text{D}_2$ receptors in CTZ. Metoclopramide also prokinetic. ADRs: Extrapyramidal symptoms. $\text{H}_1$ Antihistamines/Anticholinergics: Dimenhydrinate, Scopolamine. Uses: Motion sickness. 9.5 Laxatives Promote bowel evacuation. Bulk-forming: Psyllium, Methylcellulose. Increase stool bulk. Stool Softeners: Docusate. Facilitate water/fat penetration into stool. Osmotic: Polyethylene Glycol (PEG), Lactulose, Magnesium Hydroxide. Draw water into lumen. Stimulant: Bisacodyl, Senna. Directly stimulate enteric nerves. 9.6 Antidiarrhoeal Drugs Reduce frequency and liquidity of bowel movements. Opioid Agonists: Loperamide, Diphenoxylate. Mechanism: Reduce GI motility, increase water absorption. Adsorbents: Kaolin, Pectin. Absorb toxins and water. Bismuth Subsalicylate: Antisecretory, anti-inflammatory, antimicrobial. 9.7 Hepatoprotective Drugs Support liver function or protect against damage. E.g., Silymarin, Ursodeoxycholic acid (for cholestatic liver diseases). 10. Antibacterial Drugs (Antibiotics & Antitubercular) 10.1 Antibiotics (General Principles) Bactericidal: Kills bacteria. Bacteriostatic: Inhibits bacterial growth. Spectrum: Narrow vs. Broad. Resistance: Major concern. Mechanisms of Action: Cell Wall Synthesis Inhibitors: Penicillins, Cephalosporins, Carbapenems, Vancomycin. (Bactericidal) Protein Synthesis Inhibitors: 30S ribosomal subunit: Aminoglycosides (bactericidal), Tetracyclines (bacteriostatic). 50S ribosomal subunit: Macrolides, Clindamycin, Linezolid (bacteriostatic). Nucleic Acid Synthesis Inhibitors: Fluoroquinolones (DNA gyrase), Rifampin (RNA polymerase). (Bactericidal) Folate Synthesis Inhibitors: Sulfonamides, Trimethoprim. (Bacteriostatic, synergistic combination is bactericidal). Cell Membrane Disruptors: Polymyxins. 10.2 Antitubercular Drugs (RIPE) Treatment for Tuberculosis often involves multi-drug regimens due to resistance. Rifampin: Inhibits bacterial RNA polymerase. ADRs: Red-orange body fluids, hepatotoxicity. Isoniazid (INH): Inhibits mycolic acid synthesis. ADRs: Peripheral neuropathy (give $\text{B}_6$), hepatotoxicity. Pyrazinamide: Mechanism unclear, active in acidic environment. ADRs: Hyperuricemia, hepatotoxicity. Ethambutol: Inhibits arabinosyl transferase. ADRs: Optic neuritis (red-green color blindness). 11. Antifungal, Antiviral, Antimalarial and Antihelmintic Drugs 11.1 Antifungal Drugs Polyenes: Amphotericin B, Nystatin. Mechanism: Bind to ergosterol in fungal cell membrane, forming pores. Amphotericin B: Broad spectrum, severe systemic infections. ADRs: Nephrotoxicity, infusion reactions. Azoles (-azoles): Fluconazole, Ketoconazole, Voriconazole. Mechanism: Inhibit ergosterol synthesis (via CYP450 enzyme). Uses: Systemic and superficial fungal infections. ADRs: Hepatotoxicity, drug interactions (CYP450 inhibition). Echinocandins (-fungins): Caspofungin, Micafungin. Mechanism: Inhibit $\beta$-(1,3)-D-glucan synthesis (cell wall). Uses: Invasive candidiasis, aspergillosis. 11.2 Antiviral Drugs Target specific viral replication steps. Anti-herpes (HSV, VZV): Acyclovir, Valacyclovir. Mechanism: Guanosine analog, inhibits viral DNA polymerase. Requires viral thymidine kinase for activation. Anti-influenza: Oseltamivir, Zanamivir. Mechanism: Neuraminidase inhibitors, prevent viral release. Anti-HIV: Complex regimens (HAART) targeting multiple steps. Nucleoside Reverse Transcriptase Inhibitors (NRTIs), Non-nucleoside Reverse Transcriptase Inhibitors (NNRTIs), Protease Inhibitors (PIs), Integrase Strand Transfer Inhibitors (INSTIs), Entry Inhibitors. 11.3 Antimalarial Drugs Target different stages of Plasmodium life cycle. Chloroquine: Inhibits heme detoxification. Uses: Sensitive malaria. Artemisinins: Artemether-Lumefantrine. Produce free radicals. First-line for severe/resistant malaria. Mefloquine: Prophylaxis and treatment. ADRs: Neuropsychiatric. Primaquine: Active against liver stages (hypnozoites) of P. vivax and P. ovale. Requires G6PD testing. 11.4 Antihelmintic Drugs Treat parasitic worm infections. Albendazole/Mebendazole: Inhibit microtubule synthesis. Broad spectrum. Praziquantel: Increases $\text{Ca}^{2+}$ permeability, causing paralysis. For flukes and tapeworms. Ivermectin: Activates $\text{Cl}^-$ channels, causing paralysis. For strongyloidiasis, onchocerciasis. 12. Hormones and Related Drugs 12.1 Thyroid Hormones & Inhibitors Thyroid Hormone: Levothyroxine ($\text{T}_4$). Uses: Hypothyroidism. ADRs: Hyperthyroidism symptoms if dose too high. Thyroid Inhibitors (Antithyroid Drugs): Propylthiouracil (PTU), Methimazole. Mechanism: Inhibit thyroid hormone synthesis. PTU also inhibits peripheral $\text{T}_4$ to $\text{T}_3$ conversion. Uses: Hyperthyroidism (Graves' disease). ADRs: Agranulocytosis, hepatotoxicity (PTU). 12.2 Insulin & Oral Antidiabetic Drugs Insulin: Replaces endogenous insulin in Type 1 DM, or augments in Type 2 DM. Types: Rapid-acting (Lispro, Aspart), Short-acting (Regular), Intermediate-acting (NPH), Long-acting (Glargine, Detemir). ADRs: Hypoglycemia. Oral Antidiabetic Drugs (for Type 2 DM): Biguanides: Metformin. Mechanism: Decreases hepatic glucose production, increases insulin sensitivity. First-line. ADRs: Lactic acidosis (rare), GI upset. Sulfonylureas: Glyburide, Glipizide. Mechanism: Stimulate insulin release from pancreatic $\beta$-cells. ADRs: Hypoglycemia, weight gain. $\text{SGLT}_2$ Inhibitors (-flozins): Canagliflozin, Dapagliflozin. Mechanism: Block $\text{SGLT}_2$ in renal tubules, increasing glucose excretion. ADRs: Genital mycotic infections, UTIs. $\text{GLP-1}$ Receptor Agonists (-tides): Exenatide, Liraglutide. (Injectable, not oral) Mechanism: Mimic incretin effect, increasing glucose-dependent insulin secretion, suppressing glucagon. ADRs: Nausea, pancreatitis, thyroid C-cell tumors (Liraglutide). DPP-4 Inhibitors (-gliptins): Sitagliptin. Mechanism: Inhibit DPP-4 enzyme, preventing breakdown of GLP-1. 12.3 Hormonal Contraceptives Combined Oral Contraceptives (COCs): Estrogen + Progestin. Mechanism: Inhibit ovulation by suppressing FSH/LH, thicken cervical mucus, thin endometrium. ADRs: Thromboembolism, hypertension, nausea, breast tenderness. Progestin-Only Contraceptives: Mini-pills, implants, injections (Depot-Provera). Uses: When estrogen is contraindicated. Mechanism: Thicken cervical mucus, thin endometrium, sometimes suppress ovulation. Emergency Contraception: Levonorgestrel (high-dose progestin), Ulipristal acetate. 12.4 Uterine Stimulants (Oxytocics) Induce or augment labor, prevent postpartum hemorrhage. Oxytocin: Stimulates uterine contractions. Prostaglandins: Misoprostol, Dinoprostone. Ripen cervix, induce contractions. Ergot Alkaloids: Methylergonovine. Cause sustained uterine contractions. For postpartum hemorrhage. 12.5 Uterine Relaxants (Tocolytics) Inhibit uterine contractions to delay preterm labor. Beta-2 Agonists: Terbutaline. Calcium Channel Blockers: Nifedipine. NSAIDs: Indomethacin. Magnesium Sulfate: Also neuroprotective for fetus. 13. Miscellaneous Drugs 13.1 Antiseptics and Disinfectants Antiseptics: Applied to living tissue to reduce microorganisms. E.g., Povidone-iodine, Chlorhexidine, Alcohol. Disinfectants: Applied to inanimate objects to kill microorganisms. E.g., Bleach, Phenols, Aldehydes. 13.2 Vaccines Biological preparations that provide active acquired immunity to a particular disease. Live-attenuated: MMR, Varicella, Oral Polio, Rotavirus. Strong, long-lasting immunity. Risk in immunocompromised. Inactivated/Killed: Inactivated Polio, Hepatitis A, Rabies, most Flu shots. Weaker response, requires boosters. Subunit/Toxoid: Hepatitis B, Diphtheria, Tetanus. Contains specific antigen. Conjugate: Pneumococcal, Meningococcal, Hib. Polysaccharide antigen linked to protein carrier. 13.3 Vitamins Organic compounds required in small amounts for normal metabolism. Fat-soluble: A, D, E, K. Stored in body, can accumulate. Water-soluble: B complex, C. Not stored, excreted in urine. 13.4 Water Imbalance and IV Fluids Isotonic IV Fluids: Normal Saline (0.9% NaCl), Lactated Ringer's. Uses: Volume expansion (e.g., dehydration, hemorrhage). Hypotonic IV Fluids: Half-Normal Saline (0.45% NaCl), D5W (Dextrose 5% in water, becomes hypotonic after glucose metabolized). Uses: Cellular rehydration (e.g., hypernatremia). Hypertonic IV Fluids: 3% NaCl, D5 Normal Saline. Uses: Reduce cerebral edema, severe hyponatremia. Caution: Risk of osmotic demyelination syndrome.