Pharmacology Final

MOA: Resistant to AChE. Highly selective for Muscarinic (M) receptors. Zero nicotinic activity.

Toxicity: Cholinergic crisis (sweating, salivation, diarrhea, bronchospasm, hypotension).

Key Features: Treats postoperative/postpartum non-obstructive urinary retention and GI atony. Antidote: Atropine.

MOA: Tertiary amine partial agonist. Topically causes rapid miosis and ciliary muscle contraction

Toxicity: Crosses BBB (CNS effects), extreme sweating/salivation

Key Features: Drug of choice for emergency lowering of IOP in acute angle-closure glaucoma. Also treats xerostomia in Sjögren's.

MOA: Highly selective M3 receptor agonist.

Toxicity: Excessive sweating, nausea, rhinitis.

Key Features: Used to enhance salivation/tearing in Sjögren’s syndrome with fewer off-target cardiac side effects.

MOA: Reversible alcohol blocker of AChE. Short-acting, peripheral only.

Toxicity: Cholinergic crisis, depolarizing neuromuscular blockade.

Key Features: Historically used to diagnose Myasthenia Gravis (Tensilon test). Rapid onset, ultra-brief duration (10-20 min).

MOA: Reversible carbamate inhibitor of AChE. Uncharged tertiary amine (crosses BBB).

Toxicity: Convulsions, skeletal muscle fasciculations, bradycardia.

Key Features: Definitive antidote for life-threatening atropine/anticholinergic overdose. Duration: 2 - 4 hours

MOA: Reversible carbamate inhibitor of AChE. Charged quaternary nitrogen (cannot cross BBB).

Toxicity: Peripheral muscarinic overstimulation, flaccid paralysis.

Key Features: Used to reverse non-depolarizing neuromuscular blockers post-surgery and manage Myasthenia Gravis symptoms.

MOA: Organophosphates. Covalently and permanently bind AChE serine site.

Toxicity: DUMBBELSS profile (miosis, cramps, bronchoconstriction, neuromuscular paralysis, seizures).

Key Features: Subject to "aging" (permanent chemical bond change). Echothiophate: Glaucoma drug with cataract risk.

MOA: Competitive antagonist/inverse agonist at M1, M2, M3 receptors.

Toxicity: Mydriasis, delirium, flush, hyperthermia, anhidrosis.

Features: Low dose bradycardia, high dose tachycardia. Organophosphate antidote. Avoid in narrow angle glaucoma and benign prostatic hyperplasia.

MOA: Competitive muscarinic antagonist. Exhibits deep central CNS and vestibular penetration.

Toxicity: Heavy sedation, somnolence, amnesia, high abuse potential.

Key Features: Most effective prophylactic anti-motion sickness drug. Must be taken before motion starts.

MOA: Charged quaternary atropine derivatives. Locally block muscarinic bronchoconstriction via inhalation.

Toxicity: Local dry mouth, bitter taste. No muscle tremors or tachycardia (unlike beta 2 - agonists).

Key Features: Maintenance therapy for COPD and asthma. Tiotropium is long-acting (once-daily).

MOA: Nucleophilic oxime chemical antagonist. Cleaves organophosphate from AChE to restore enzyme function.

Toxicity: Neuromuscular block, transient hypertension.

Key Features: Must be given early before "aging" occurs. Reverses both nicotinic (muscle paralysis) and muscarinic signs. Cannot cross BBB.

MOA: Direct agonist at alpha1, alpha2, beta1, beta2. Dose-dependent: low doses = beta2 vasodilation; high doses = alpha1 vasoconstriction.

Toxicity: Severe anxiety, headache, cerebral hemorrhage, cardiac arrhythmias.

Key Features: Drug of choice for Type I anaphylactic shock (beta2 bronchodilates, alpha1 reverses vascular collapse). Added to local anesthetics to prolong action.

MOA: Agonist at alpha 1, 2 and beta 1, 2. Low dose dilates vessels, high dose constricts.

Toxicity: Anxiety, headache, brain bleed, arrhythmias.

Features: First choice for anaphylactic shock. Prolongs local anesthetics.

MOA: Pure beta 1 and 2 agonist. Increases heart rate and dilates muscle vessels, lowering diastolic pressure.

Toxicity: Extreme tachycardia, palpitations, ischemia risk.

Features: Rarely used. Treats refractory AV block or severe bradycardia.

MOA: Low dose: D1/D2 (renal vasodilation). Medium dose: beta 1 (cardiac output increase). High dose: alpha 1 (vasoconstriction).

Toxicity: Nausea, hypertension, arrhythmias.

Features: Treats cardiogenic/septic shock. Retains renal perfusion at low/medium doses.

MOA: Stimulates presynaptic alpha-2 autoreceptors in brainstem vasomotor centers. Shuts down peripheral sympathetic outflow.

Toxicity: Heavy sedation, xerostomia, severe constipation. Abrupt withdrawal triggers life-threatening rebound hypertension.

Key Features: Treats essential hypertension and counters autonomic symptoms during opiate/nicotineenzodiazepine withdrawal.

MOA: Direct beta 2 agonists. Increase cAMP for rapid bronchodilation.

Toxicity: Muscle tremor, restlessness. High dose causes beta 1 tachycardia.

Features: First line rescue for acute asthma. Terbutaline stops premature labor.

MOA: Highly lipophilic, long-acting beta-2 selective agonists (12 hours duration).

Toxicity: Tachycardia, tremors, hypokalemia. Black Box Warning: Monotherapy use in asthma is contraindicated (increases mortality).

Key Features: Prophylaxis of asthma and COPD. Must always be combined with an Inhaled Corticosteroid (ICS). Too slow for acute rescue.

MOA: Irreversible alpha 1 and 2 blocker. Lowers vascular resistance, causes reflex tachycardia.

Toxicity: Orthostatic hypotension, fainting, stuffy nose, impaired ejaculation.

Features: Given before pheochromocytoma surgery. Causes epinephrine reversal where epinephrine lowers blood pressure instead of raising it.

MOA: Reversible alpha 1 and 2 blocker. Causes extreme reflex tachycardia and epinephrine reversal.

Toxicity: Severe tachycardia, arrhythmias, angina.

Features: Used for pheochromocytoma and reversing tissue damage from norepinephrine leaks.

MOA: Alpha 1 blockers. Tamsulosin is selective for prostate alpha 1A.

Toxicity: First dose fainting so take at bedtime. Tamsulosin causes floppy iris syndrome.

Features: Prazosin treats hypertension. Tamsulosin treats benign prostatic hyperplasia.

MOA: Nonselective beta 1 and 2 blocker. Lowers cardiac output and renin. Causes bronchoconstriction and blocks glycogen breakdown.

Toxicity: Bronchospasm in asthma and COPD. Masks low blood sugar signs in diabetics. Nightmares, depression. Never stop abruptly due to rebound heart attacks.

Features: Treats hypertension, angina, post heart attack, thyroid storm, and prevents migraines.

MOA: Selective beta 1 blockers. Selectivity is lost at high doses.

Toxicity: Bradycardia, AV block, acute heart failure.

Features: Safe for patients with asthma, COPD, or diabetes. Metoprolol improves lipids. Esmolol is ultra short acting for acute IV use.

MOA: Partial beta agonists. Weakly stimulate receptors but block stronger catecholamines.

Toxicity: Minimal bradycardia. Avoid in arrhythmias.

Features: Used for hypertension with baseline bradycardia. Preserves HDL levels.

MOA: Alpha 1, beta 1, and beta 2 blockers. Alpha 1 block causes vasodilation.

Toxicity: Orthostatic hypotension, dizziness.

Features: IV Labetalol treats hypertensive emergencies. Carvedilol lowers mortality in chronic heart failure.

MOA: Synthetic PGE 1 analog. Lowers gastric acid secretion and increases bicarbonate/mucus production. Stimulates uterine smooth muscle.

Toxicity: Abdominal pain, cramping, diarrhea. Pregnancy Category X: Triggers complete uterine contraction and abortion.

Key Features: Prevents NSAID-induced gastric ulcers in chronic arthritis populations.

MOA: Prostaglandin PGF2 alpha analog. Increases uveoscleral outflow of aqueous humor to lower intraocular pressure.

Toxicity: Local conjunctival hyperemia, permanent brown pigmentation of the iris, increased thicknessrowth of eyelashes.

Key Features: First-line topical choice for chronic open-angle glaucoma. Lacks systemic or pupillary side effects.

MOA: Blocks central and peripheral H1 and muscarinic receptors. Crosses blood brain barrier.

Toxicity: Severe sedation. Dry mouth, blurred vision, urinary retention, constipation.

Features: Treats acute allergies, hives, motion sickness, and vomiting.

MOA: Selective competitive blockers of peripheral H1 receptors. Low lipid-solubility, polar structures prevent BBB crossover.

Toxicity: Very low/no sedation. Can cause mild headache, cough, or back pain.

Key Features: First-line baseline therapy for seasonal allergic rhinitis and hives. Safe for long-term use in children. Fexofenadine is excreted unchanged in feces.

MOA: Serotonin 1B and 1D agonist. Constricts meningeal blood vessels and stops inflammatory peptide release.

Toxicity: Chest, neck, and jaw pressure. Risk of coronary vasospasm and heart attacks.

Features: First line to stop acute migraines and cluster headaches. Do not use in coronary artery disease.

MOA: Selective competitive antagonist of 5HT3 receptors centrally (chemoreceptor trigger zone) and peripherally (vagal enteric gut nerves). Blocks emetic reflex arc.

Toxicity: Headache, diarrhea. Associated class agent dolasetron can cause QRS and QT interval prolongation.

Key Features: Premier anti-emetic for controlling severe nausea and vomiting from cancer chemotherapy, radiation, or surgery.

MOA: Partial agonists at serotonin, alpha, and dopamine receptors. Ergotamine acts via 5HT1D. Ergonovine contracts the uterus.

Toxicity: Nausea, vomiting. Severe vasoconstriction causes gangrene. Chronic use damages heart valves.

Features: Ergotamine stops acute migraines. Ergonovine stops postpartum bleeding. Never give before placenta delivers.

MOA: Inhibits phosphodiesterase to increase cAMP and bronchodilate. Blocks adenosine receptors.

Toxicity: Narrow safety window. Mild toxicity causes vomiting and tremors. Severe causes seizures and arrhythmias.

Features: Oral drug for asthma and COPD. Aminophylline is the shorter acting salt form.

MOA: Inhibits the degranulation of mast cells, preventing the release of preformed histamine and leukotrienes in response to IgE cross-linking.

Toxicity: Local throat irritation, dry cough. Zero systemic side effects (highly insoluble).

Key Features: Purely prophylactic agent for seasonal rhinitis, exercise-induced asthma, or food allergies. Completely useless for acute asthma attacks (zero bronchodilator activity).

MOA: Inhibits phospholipase A2 and COX 2 to suppress airway inflammation.

Toxicity: Oral thrush and hoarseness. Rinse and spit after use.

Features: First line maintenance for persistent asthma. Prevents airway remodeling.

MOA: Blocks CysLT1 leukotriene receptors to prevent bronchoconstriction.

Toxicity: Very low toxicity. Rare risk of Churg Strauss syndrome.

Features: Oral prophylaxis for exercise, antigen, and aspirin induced asthma. Safe for kids.

MOA: Inhibits 5 lipoxygenase to block all leukotriene synthesis.

Toxicity: Liver toxicity and elevated enzymes. Requires liver monitoring.

Features: Oral prevention for asthma. Highly effective for exercise and aspirin induced asthma.

MOA: Weak opioid agonist. Depresses brainstem cough center.

Toxicity: Severe constipation, thickens sputum. Addiction and respiratory depression risk.

Features: Short term cough syrup. Avoid in asthma and COPD because retained sputum worsens breathing.

MOA: Synthetic morphine derivative. Acts as an uncompetitive NMDA receptor antagonist centrally in the medulla to elevate the cough threshold.

Toxicity: Mild nausea, dizziness. Safest antitussive profile: virtually zero risk of addiction, respiratory depression, or constipation.

Key Features: Displays equal clinical cough-suppression efficacy to codeine but with a vastly superior safety profile.

MOA: Inhibits HMG CoA reductase. Lowers liver cholesterol and increases LDL receptors to clear blood LDL.

Toxicity: Elevated liver enzymes, muscle damage, rhabdomyolysis. Grapefruit juice increases toxicity risk.

Features: Only lipid drug proven to lower overall mortality and strokes. Rosuvastatin and atorvastatin are high intensity. Simvastatin and lovastatin are prodrugs.

MOA: Binds bile acids in the intestine to prevent recycling. Liver uses cholesterol to make new bile acids, increasing LDL receptors.

Toxicity: Bloating, flatulence, severe constipation. Impairs absorption of fat soluble vitamins and other oral drugs.

Features: Lowers LDL but can cause a dangerous spike in triglycerides.

MOA: Selectively inhibits the NPC1L1 transporter protein on the enterocyte brush border, blocking dietary and biliary cholesterol absorption. Leads to a compensatory up-regulation of high-affinity LDL receptors.

Toxicity: Well-tolerated. Minor additive transaminase risk or mild myopathy when paired with statins.

Key Features: Lowers LDL-C by 20% alone. highly effective when combined with a statin (e.g., ezetimibe + simvastatin).

MOA: Inhibits hormone sensitive lipase in adipose tissue, lowering VLDL and LDL.

Toxicity: Severe flushing prevented by aspirin. Causes gout flares, high blood sugar, and liver toxicity.

Features: Raises HDL but adding it to statins does not improve cardiovascular outcomes.

MOA: Activates PPAR-alpha, increasing lipoprotein lipase (LPL) expression to rapidly clear triglycerides.

Toxicity: Nausea, cholesterol gallstones. High risk of rhabdomyolysis if combined with statins (especially gemfibrozil).

Features: Primary treatment for severe hypertriglyceridemia to prevent acute pancreatitis.

MOA: Antibodies (Alirocumab, Evolocumab) bind PCSK9 to prevent LDL receptor destruction, continuously clearing blood LDL. Inclisiran (siRNA) blocks PCSK9 synthesis intracellularly.

Toxicity: Injection site reactions, flu-like symptoms.

Features: Lowers LDL up to 70%. Used for familial hypercholesterolemia or high-risk coronary disease. Subcutaneous injection.

MOA: Class IA antiarrhythmics. Block open sodium channels to slow Phase 0 depolarization and block potassium channels to prolong Phase 3 and the effective refractory period.

Toxicity: Quinidine causes cinchonism (tinnitus, headache) and vasodilation. Procainamide causes a reversible lupus-like syndrome. Both risk QT prolongation and Torsades de Pointes.

Features: Treats atrial fibrillation, atrial flutter, and ventricular tachycardias.

MOA: Class IB antiarrhythmic. Binds inactivated sodium channels with fast dissociation. Selectively targets ischemic tissue and shortens the action potential duration.

Toxicity: Neurological symptoms like dizziness, slurred speech, numbness, and seizures. No risk of QT prolongation or Torsades de Pointes.

Features: Treats only ventricular arrhythmias, especially acute post heart attack or digoxin induced. Ineffective for atrial arrhythmias. Given IV only due to high first pass metabolism.

MOA: Profoundly powerful blocker of voltage-gated Na+ channels with slow binding/dissociation kinetics. Markedly flattens Phase 0 depolarization, massively slowing conduction velocity. Zero effect on APD or QT interval (widens QRS instead).

Toxicity: Prominently pro-arrhythmic. Can cause sudden lethal ventricular tachycardias in patients with structural or ischemic heart disease (verified by CAST trial).

Key Features: Indicated for refractory SVT and atrial fibrillation only in patients with structurally normal hearts.

MOA: Class III antiarrhythmic. Blocks potassium channels to prolong Phase 3. Also possesses Class I, II, and IV properties.

Toxicity: Pulmonary fibrosis, thyroid dysfunction, corneal deposits, blue-gray skin discoloration.

Features: Treats ventricular and supraventricular arrhythmias. Low risk of Torsades de Pointes despite QT prolongation. Extremely long half-life.

MOA: Binds A1 receptors on the AV node. Increases potassium conductance to hyperpolarize the membrane and blocks calcium influx, temporarily halting AV conduction.

Toxicity: Transient chest pressure, flushing, shortness of breath, and a feeling of impending doom. Effects are intensified by dipyridamole and blocked by caffeine or theophylline.

Features: First choice for the immediate conversion of paroxysmal supraventricular tachycardia (PSVT). Given as a rapid IV bolus. Half-life is less than 10 seconds.

MOA: Synthetic Prostaglandin E1. Relaxes vascular smooth muscle.

Toxicity: Hypotension, flushing, local pain.

Key Features: Keeps the ductus arteriosus open in neonates awaiting heart surgery. Also used for erectile dysfunction.

MOA: Powerful endogenous vasodilator and potent inhibitor of platelet aggregation.

Toxicity: Flushing, headache, hypotension, jaw pain.

Key Features: Used via continuous IV infusion for Pulmonary Arterial Hypertension (PAH).

MOA: Non-selective Cyclooxygenase (COX-1 and COX-2) inhibitors. Stop prostaglandin synthesis.

Toxicity: Gastric ulcers, renal impairment, bleeding risk.

Key Features: Indomethacin is used to close a patent ductus arteriosus (PDA) in premature infants. Aspirin irreversibly inhibits platelet TXA2 to prevent MI.

MOA: Competitive blockers of H2 histamine receptors on gastric parietal cells. Turn down cAMP to reduce gastric acid secretion.

Toxicity: Cimetidine causes anti-androgenic effects (gynecomastia, impotence) and is a potent CYP450 inhibitor. Famotidine lacks these side effects.

Key Features: First-line baseline therapy for GERD and peptic ulcer disease.

MOA: Competitively blocks 5HT2 serotonin receptors and H1 histamine receptors.

Toxicity: Marked sedation, dry mouth, increased appetite/weight gain.

Key Features: The definitive antidote for Serotonin Syndrome caused by SSRI/MAOI overdoses.

MOA: Releases nitric oxide to increase cGMP, causing vascular smooth muscle relaxation. Primarily dilates veins to lower cardiac preload.

Toxicity: Throbbing headache, orthostatic hypotension, reflex tachycardia.

Features: Treats acute angina (sublingual) and used for prophylaxis (patch). Requires a 10–12 hour daily nitrate-free interval to prevent tolerance. Strictly contraindicated with sildenafil due to risk of fatal hypotension.

MOA: Blocks L-type calcium channels in the heart to lower heart rate, AV conduction, and contractility.

Toxicity: Bradycardia, AV block, worsening heart failure, and severe constipation (especially Verapamil).

Features: First line prophylaxis for stable and vasospastic angina. Never combine with beta blockers due to the risk of severe bradycardia and AV block.

MOA: Block L-type voltage-gated calcium channels. Highly selective for vascular smooth muscle (systemic arteriodilation and coronary vasodilation) with minimal direct cardiac effects.

Toxicity: Peripheral ankle edema, flushing, dizziness, and reflex tachycardia (greatest with short-acting nifedipine).

Key Features: Used for chronic stable angina and vasospastic angina. Paired with beta-blockers to neutralize reflex tachycardia.

MOA: Blocks late inward sodium currents to reduce intracellular calcium overload. Improves myocardial relaxation and lowers wall tension without altering heart rate or blood pressure.

Toxicity: Prolongs QT interval, dizziness, constipation.

Features: Reserved for chronic refractory angina uncontrolled by standard therapies.

MOA: Selectively inhibits the cardiac pacemaker current in the SA node. Slows sinus heart rate without altering contractility, conduction, or blood pressure.

Toxicity: Luminous visual phenomena , bradycardia.

Key Features: Used for chronic stable angina or chronic heart failure in patients who cannot tolerate or are insufficiently managed by maximal beta-blocker therapy.

MOA: Inhibits carbonic anhydrase in the proximal convoluted tubule to block bicarbonate reabsorption.

Toxicity: Hyperchloremic metabolic acidosis, hypokalemia, sulfa allergy, and paresthesias.

Features: Weak diuretic. Used to treat glaucoma and prevent altitude sickness.

MOA: Inhibits the Na/K/2Cl cotransporter in the thick ascending limb of the loop of Henle. Destroys the medullary concentration gradient to eliminate water reabsorption.

Toxicity: Hearing impairment, hypokalemic metabolic alkalosis, hypocalcemia, gout, and sulfa allergy.

Features: Most potent diuretics. First line for acute pulmonary edema and peripheral fluid overload in heart failure.

MOA: Inhibits the Na+/Cl- cotransporter (NCCT) in the distal convoluted tubule.

Toxicity: Hypokalemic metabolic alkalosis, hypercalcemia, hyperglycemia, hyperuricemia (gout), and sulfa allergy risk.

Features: The most common diuretic for primary hypertension. Chlorthalidone is preferred due to its longer half-life. It lowers urinary calcium, making it useful to prevent recurrent calcium kidney stones.

MOA: Competitively antagonizes intracellular aldosterone receptors in the cortical collecting tubule. This prevents the synthesis of ENaC channels and sodium/potassium pumps, reducing sodium reabsorption and potassium excretion.

Toxicity: Hyperkalemia, metabolic acidosis. Spironolactone causes endocrine side effects (gynecomastia, erectile dysfunction) due to cross-reactivity with androgen/progesterone receptors. Eplerenone is more selective and avoids these.

Features: Weak diuretics used primarily to block aldosterone-mediated cardiac remodeling, significantly reducing mortality in chronic heart failure.

MOA: Directly block the luminal Epithelial Sodium Channels (ENaC) in the Cortical Collecting Tubule (CCT), independent of aldosterone.

Toxicity: Hyperkalemia, muscle cramps. Triamterene can precipitate as kidney stones.

Key Features: Co-administered with loop diuretics or thiazides to actively prevent/offset hypokalemia.

MOA: Hydrophilic, non-reabsorbable sugar that acts freely inside the tubule lumen (primarily PCT and descending loop) to create an osmotic gradient that opposes water reabsorption. Also draws water out of cells into the bloodstream.

Toxicity: Acute extracellular volume expansion (can precipitate acute pulmonary edema/heart failure if given too fast), dehydration, hypernatremia.

Key Features: Administered strictly IV to rapidly reduce intracranial pressure in cerebral edema or to lower intraocular pressure before eye surgery.

MOA: Inhibit Angiotensin-Converting Enzyme (ACE). Blocks conversion of Angiotensin I to Angiotensin II (vasoconstriction decrease, aldosterone decrease). Prevents breakdown of bradykinin (a potent vasodilator).

Toxicity: Dry, hacking cough and life-threatening Angioedema (both due to bradykinin accumulation). Hyperkalemia, acute kidney injury in patients with bilateral renal artery stenosis. Teratogenic (fetal kidney damage).

Key Features: First-line for hypertension, especially in Diabetics (provides diabetic nephroprotection) and Heart Failure (reduces cardiac remodeling and overall mortality).

MOA: Competitively block AT1 receptors to inhibit the effects of Angiotensin II.

Toxicity: Hyperkalemia, acute kidney injury. Teratogenic. No effect on bradykinin metabolism, so no dry cough or angioedema risk.

Key Features: First-line alternative to ACE inhibitors for hypertension and heart failure if the patient cannot tolerate the ACE-inhibitor cough.

MOA: Directly binds and inhibits Renin, blocking the initial, rate-limiting conversion of angiotensinogen to Angiotensin I.

Toxicity: Hyperkalemia, diarrhea, acute kidney injury. Teratogenic.

Key Features: Used orally as an alternative therapy for essential hypertension. Never combine with ACE inhibitors or ARBs.

MOA: Directly relaxes arteriolar smooth muscle (minimal effect on veins) by stimulating the release of Nitric Oxide (NO) from vascular endothelium.

Toxicity: Profound compensatory reflex tachycardia and fluid retention/edema. Promotes a classic reversible Drug-Induced Lupus Erythematosus (SLE)-like syndrome in slow acetylators.

Key Features: Used for severe, refractory hypertension. Safe in pregnancy (often used for preeclampsia). Always paired with a beta-blocker (to stop reflex tachycardia) and a loop diuretic (to handle fluid retention).

MOA: Active sulfate metabolite opens ATP-sensitive K+ channels in vascular smooth muscle, causing membrane hyperpolarization and arteriolar relaxation.

Toxicity: Extreme reflex tachycardia, severe fluid retention, and hypertrichosis.

Key Features: Reserved for severe, refractory hypertension. Topical form is used for male pattern baldness.

MOA: Spontaneously releases nitric oxide in the bloodstream, activating cGMP to cause balanced dilation of arterioles and venules.

Toxicity: Releases cyanide, which can lead to thiocyanate toxicity during prolonged infusions or in patients with renal failure, resulting in metabolic acidosis and seizures. Antidote: Sodium thiosulfate or hydroxocobalamin.

Key Features: First-line IV drug for hypertensive emergencies. Immediate onset and ultra-short duration; requires continuous blood pressure monitoring.

MOA: Postsynaptic D1 receptor agonist; induces arteriolar vasodilation, maintains renal perfusion, and promotes diuresis.

Toxicity: Reflex tachycardia, headache, flushing, increased intraocular pressure.

Key Features: IV treatment for hypertensive emergencies, particularly useful in patients with renal insufficiency.

MOA: Sacubitril inhibits neprilysin to increase natriuretic peptides. Valsartan blocks AT1 receptors to stop angiotensin II.

Toxicity: Hypotension, hyperkalemia, renal impairment, angioedema.

Key Features: First-line therapy for HFrEF. Must never be used within 36 hours of an ACE inhibitor due to the risk of severe angioedema.

MOA: Inhibits the Na+/K+ ATPase pump to increase intracellular calcium, providing a positive inotropic effect. Also stimulates the vagus nerve to slow heart rate.

Toxicity: Narrow therapeutic window. Aggravated by hypokalemia. Symptoms include nausea, vomiting, confusion, yellow-green vision, and scooped ST segments on ECG. Can cause any cardiac arrhythmia. Antidote: Digoxin immune Fab and potassium replacement.

Key Features: Used for symptom relief in chronic heart failure and ventricular rate control in atrial fibrillation.

MOA: Binds to GH receptors, activating the JAK/STAT signaling pathway to stimulate production of IGF-1 in the liver.

Toxicity: Idiopathic intracranial hypertension (pseudotumor cerebri), slipped capital femoral epiphysis, hyperglycemia/insulin resistance, peripheral edema.

Key Features: Promotes growth in children with GH deficiency, Turner syndrome, chronic renal failure, or AIDS-associated wasting syndrome. Contraindicated if epiphyses are fused.

MOA: Long-acting synthetic somatostatin analog. Potently inhibits the secretion of Growth Hormone (GH), TSH, insulin, glucagon, and gastrin.

Toxicity: Biliary sludge and gallstones (due to cholecystokinin inhibition), steatorrhea, abdominal cramps, bradycardia.

Key Features: First-line medical therapy for Acromegaly. Also used for symptomatic control of carcinoid syndrome diarrhea and acute esophageal variceal bleeding.

MOA: Genetically modified GH analog that binds to and blocks the GH receptor, preventing functional receptor dimerization and downstream IGF-1 production.

Toxicity: Injection site reactions, significant transaminase elevations (requires liver function monitoring).

Key Features: Reserved for Acromegaly refractory to surgery, radiation, or octreotide therapy. Does not shrink pituitary tumors; may cause them to expand.

MOA: Continuous administration down-regulates pituitary GnRH receptors, halting LH and FSH secretion. Pulsatile administration stimulates them.

Toxicity: Hot flashes, bone loss, erectile dysfunction, and initial tumor flare in prostate cancer.

Key Features: Treats precocious puberty, advanced prostate cancer, and endometriosis. Used to suppress endogenous cycles during ovulation induction.

MOA: Competitive antagonist at pituitary GnRH receptors. Immediately suppresses LH and FSH secretion without causing an initial flare or surge.

Toxicity: Ovarian hyperstimulation syndrome, headache, injection site hypersensitivity.

Key Features: Used in controlled ovarian hyperstimulation protocols to prevent premature LH surges during assisted reproduction techniques.

MOA: Direct FSH receptor agonists. Purified from postmenopausal urine (urofollitropin) or recombinant human form (follitropin). Direct stimulus for ovarian follicle maturation and spermatogenesis.

Toxicity: Ovarian hyperstimulation syndrome (OHSS), multiple pregnancies, gynecomastia in men.

Key Features: Indicated for ovulation induction in infertile women and to promote spermatogenesis in infertile men with hypogonadotropic hypogonadism.

MOA: Activates oxytocin receptors on uterine smooth muscle to trigger rhythmic contractions. Also stimulates mammary myoepithelial cells to promote milk ejection.

Toxicity: Risk of uterine rupture and fetal distress. High doses may cause water intoxication and dilutional hyponatremia due to weak V2 receptor cross-reactivity.

Key Features: Drug of choice for labor induction and preventing postpartum uterine hemorrhage.

MOA: Selective renal V2 receptor agonist that inserts aquaporin-2 channels into the collecting tubule to increase water reabsorption. Also stimulates release of Factor VIII and von Willebrand factor from endothelial cells.

Toxicity: Water retention and severe dilutional hyponatremia.

Key Features: Drug of choice for central diabetes insipidus. Also used for mild hemophilia A and von Willebrand disease.

MOA: Blocks vasopressin receptors. Conivaptan blocks V1 and V2. Tolvaptan is selective for V2. Induces aquaresis by increasing free water clearance.

Toxicity: Polyuria, intense thirst, dry mouth. Risk of hepatotoxicity with Tolvaptan (treatment limited to 30 days).

Key Features: Used to treat euvolemic or hypervolemic hyponatremia in patients with SIADH, liver cirrhosis, or congestive heart failure.

MOA: Bind intracellular receptors to alter gene transcription. They inhibit Phospholipase A2 to prevent leukotriene and prostaglandin synthesis, block COX-2 expression, reduce inflammatory cytokines, and inhibit white blood cell proliferation.

Toxicity: Chronic use causes osteoporosis, muscle wasting, hyperglycemia, fat redistribution, impaired wound healing, cataracts, and growth suppression in children.

Key Features: Hydrocortisone has balanced glucocorticoid and mineralocorticoid activity. Dexamethasone provides high anti-inflammatory potency without salt retention. Abrupt withdrawal after chronic use triggers acute adrenal insufficiency

MOA: Potent aldosterone receptor agonist with high salt-retaining activity. Promotes sodium reabsorption and potassium/hydrogen excretion in the collecting tubule.

Toxicity: Hypertension, edema, severe hypokalemia, hypokalemic metabolic alkalosis.

Key Features: Long duration of action. Favored replacement therapy for primary adrenal insufficiency (Addison's disease) and post-adrenalectomy, paired with a glucocorticoid.

MOA: Inhibits CYP450 enzymes, specifically 17-alpha-hydroxylase and 11-beta-hydroxylase, to block cortisol synthesis.

Toxicity: Severe hepatotoxicity and inhibition of androgen production, resulting in gynecomastia, impotence, and decreased libido in men.

Key Features: Used to reduce clinical symptoms in Cushing syndrome caused by adrenal tumors or ectopic ACTH secretion.

MOA: Competitive pharmacologic antagonist at both Glucocorticoid (GR) and Progesterone receptors. Blocks endogenous cortisol and progesterone activity.

Toxicity: Vaginal bleeding, abdominal pain, nausea, headache, hypokalemia.

Key Features: Used to treat hypercortisolism in patients with endogenous Cushing syndrome who have type 2 diabetes and have failed surgery. Also utilized as an abortifacient via progesterone blockade.

MOA: Binds nuclear thyroid receptors to increase basal metabolic rate, oxygen consumption, and cardiac beta1 receptor expression. T4 is converted to T3 in the periphery.

Toxicity: Hyperthyroidism signs: tachycardia, arrhythmias, tremors, heat intolerance, weight loss.

Key Features: Levothyroxine (T4) is the standard drug of choice for hypothyroidism due to its stable, long 7-day half-life. Elderly patients require careful starting doses to avoid triggering cardiac collapse or arrhythmias.

MOA: Inhibit thyroid peroxidase to block iodide organification and the coupling of tyrosine residues on thyroglobulin. PTU also inhibits the peripheral conversion of T4 to T3.

Toxicity: Agranulocytosis, which is a lethal drop in white blood cells. PTU carries a black-box warning for severe hepatotoxicity. Methimazole is teratogenic and can cause aplasia cutis, which is why PTU is preferred in the first trimester of pregnancy.

Key Features: Mainstay treatment for hyperthyroidism and Graves disease. Methimazole is generally preferred due to a longer half-life and lower risk of liver toxicity, except during the first trimester of pregnancy and in cases of thyroid storm.

MOA: Inhibit thyroid peroxidase to block iodide organification and the coupling of tyrosine residues on thyroglobulin. PTU also inhibits the peripheral conversion of T4 to T3.

Toxicity: Agranulocytosis, which is a lethal drop in white blood cells. PTU carries a black-box warning for severe hepatotoxicity. Methimazole is teratogenic and can cause aplasia cutis, which is why PTU is preferred in the first trimester of pregnancy.

Key Features: Mainstay treatment for hyperthyroidism and Graves disease. Methimazole is generally preferred due to a longer half-life and lower risk of liver toxicity, except during the first trimester of pregnancy and in cases of thyroid storm.

MOA: Actively taken up by thyroid follicular cells and incorporated into storage. Emits beta particles that selectively destroy local thyroid parenchymal tissue without injuring surrounding organs.

Toxicity: High incidence of delayed, permanent hypothyroidism, requiring lifelong thyroid replacement. Completely contraindicated in pregnancy as it destroys fetal thyroid tissue.

Key Features: The only medical therapy that produces a permanent reduction of thyroid activity in severe hyperthyroidism or thyroid carcinoma.

MOA: Recombinant fragment of human PTH. Given intermittently (once-daily SC injection), it preferentially stimulates osteoblasts over osteoclasts to increase bone formation. (Continuous high levels stimulate osteoclasts via RANKL, causing bone resorption).

Toxicity: Hypercalcemia, hyperuricemia, osteosarcoma risk (black-box warning; avoid in Paget's disease or unexplained elevated alkaline phosphatase).

Key Features: Used for severe osteoporosis in patients at high risk for fractures. Stimulates true bone architecture restoration.

MOA: Pyrophosphate analogs that bind to bone hydroxyapatite. They are ingested by osteoclasts and disrupt the cholesterol synthesis pathway, leading to osteoclast apoptosis and inhibition of bone resorption.

Toxicity: Severe chemical esophagitis and gastric erosion with oral forms. Associated with osteonecrosis of the jaw and atypical subtrochanteric femur fractures.

Features: First-line therapy for osteoporosis. Oral doses must be taken with a full glass of water, and patients must remain upright for 30 minutes before eating to prevent esophageal perforation. Zoledronate is administered via yearly IV infusion.

MOA: Human monoclonal antibody that binds and neutralizes RANKL. Mimics natural osteoprotegerin (OPG), preventing RANKL from binding to the RANK receptor on osteoclast precursors. This completely blocks osteoclast maturation and survival.

Toxicity: Hypocalcemia, increased risk of infections (RANKL plays a role in immune function), osteonecrosis of the jaw.

Key Features: Given via subcutaneous injection every 6 months for postmenopausal osteoporosis.

MOA: Peptide hormone (usually salmon sequence) that binds directly to receptors on osteoclasts, inhibiting bone resorption and increasing renal calcium excretion.

Toxicity: Rhinitis and nasal irritation (nasal spray formulation), flushing, nausea.

Key Features: Used to treat hypercalcemia and Paget's disease. Less effective than bisphosphonates for osteoporosis, but unique for providing analgesic relief for acute painful osteoporotic vertebral compression fractures.

MOA: Activates the calcium-sensing receptor (CaSR) on parathyroid gland principal cells. Increases the receptor's sensitivity to extracellular ionized calcium, turning down and suppressing PTH synthesis and release.

Toxicity: Severe hypocalcemia, nausea, vomiting.

Key Features: Indicated for the treatment of secondary hyperparathyroidism in chronic kidney disease patients on dialysis, and for hypercalcemia in parathyroid carcinoma.

MOA: Active 1,25-dihydroxyvitamin D3 binds nuclear vitamin D receptors to increase calcium and phosphate absorption from the GI tract and kidney tubules, while suppressing PTH synthesis.

Toxicity: Hypercalcemia, hyperphosphatemia, soft tissue calcification, renal stones.

Key Features: Does not require renal activation. It is the preferred agent for secondary hyperparathyroidism and hypocalcemia in chronic kidney disease and dialysis patients.

MOA: Activates tyrosine kinase insulin receptors to promote glucose uptake into muscle and fat via GLUT4 translocation and inhibit hepatic gluconeogenesis and glycogenolysis.

Toxicity: Hypoglycemia, lipodystrophy at injection sites, and hypokalemia.

Key Features: Regular insulin is used IV for Diabetic Ketoacidosis (DKA). Insulin Lispro is ultra-rapid acting and injected at mealtimes to mimic normal postprandial insulin surges.

MOA: Activate insulin tyrosine kinase receptors. Modified chemical structures cause slow, sustained release from subcutaneous injection sites.

Toxicity: Hypoglycemia, weight gain.

Key Features: Provide a peakless, flat basal insulin profile over 24+ hours. Used as baseline background therapy for Type 1 and advanced Type 2 diabetes. Cannot be mixed in the same syringe with other insulins due to pH precipitation risks.

MOA: Block ATP-sensitive potassium channels on pancreatic beta-cells to cause membrane depolarization, calcium influx, and insulin release.

Toxicity: High risk of hypoglycemia and weight gain. Glyburide is contraindicated in renal impairment and the elderly due to prolonged action.

Key Features: Require functional beta-cells, so they are useless in Type 1 Diabetes. Not first-line therapy because they cause weight gain and hypoglycemia compared to metformin.

MOA: Activates AMP-activated protein kinase (AMPK), inhibiting hepatic gluconeogenesis and glucose output. Increases peripheral insulin sensitivity and glucose uptake in skeletal muscle. Does not stimulate insulin release.

Toxicity: Gastrointestinal distress and decreased Vitamin B12 absorption. Risk of lethal lactic acidosis. Contraindicated in renal insufficiency (GFR < 30)

Key Features: First-line, gold-standard therapy for Type 2 Diabetes. Weight-neutral and carries zero risk of hypoglycemia when used as monotherapy.

MOA: High-affinity ligands that bind and activate the nuclear PPAR-gamma receptor to regulate gene transcription, increasing the expression of GLUT4 and adiponectin to improve peripheral insulin sensitivity in fat and muscle tissue.

Toxicity: Severe fluid retention, weight gain, and peripheral edema. Can precipitate or worsen congestive heart failure. Increased risk of bone fractures.

Key Features: Euglycemics that do not cause hypoglycemia when used alone. They have a slow onset of action because they require time to alter gene expression. Contraindicated in patients with NYHA Class III or IV heart failure.

MOA: Reversibly inhibits membrane-bound alpha-glucosidase enzymes in the intestinal brush border. Delays carbohydrate digestion and breakdown into absorbable monosaccharides.

Toxicity: Profound GI distress including severe flatulence, abdominal bloating, and diarrhea due to osmotic fermentation of undigested carbohydrates by colonic bacteria.

Key Features: Lowers postprandial blood glucose spikes. Euglycemic. If a patient experiences hypoglycemia while taking this in combination with a sulfonylurea, they must be treated with pure glucose (dextrose), not sucrose, because acarbose blocks the breakdown of sucrose.

MOA: Injectable synthetic analogs of incretin GLP-1. They activate GLP-1 receptors to stimulate glucose-dependent insulin secretion, suppress glucagon release, delay gastric emptying, and signal central satiety to reduce appetite.

Toxicity: Nausea, vomiting, and diarrhea are common. Associated with a risk of acute pancreatitis and thyroid C-cell tumors. Contraindicated in patients with a history of Multiple Endocrine Neoplasia Type 2 (MEN2).

Key Features: Provide significant cardiovascular risk reduction and notable weight loss. Recommended for patients with a high risk of hypoglycemia because insulin release is strictly glucose-dependent.

MOA: Orally active inhibitors of dipeptidyl peptidase-4 (DPP-4) that prevent the breakdown of endogenous GLP-1, increasing the half-life of incretins and promoting glucose-dependent insulin release.

Toxicity: Nasopharyngitis, upper respiratory tract infections, headache, rare joint pain, and risk of acute pancreatitis.

Key Features: Oral alternative to injectable GLP-1 agonists. They are weight-neutral and have a low risk of hypoglycemia.

MOA: Inhibit the Sodium-Glucose Co-transporter 2 in the Proximal Convoluted Tubule of the kidney. Blocks the reabsorption of filtered glucose, forcing therapeutic glucosuria and osmotic diuresis.

Toxicity: Genital mycotic infections (candidal vulvovaginitisalanitis) and Urinary Tract Infections due to high urine glucose. Dehydration, hypotension, and euglycemic diabetic ketoacidosis.

Key Features: Reduce cardiovascular mortality and provide renoprotection or decrease heart failure hospitalizations. Cause mild weight loss and drop blood pressure. Empagliflozin is highly favored for heart failure protection.

MOA: Binds G-protein coupled glucagon receptors on the liver, activating adenylyl cyclase to spike cAMP. Accelerates hepatic glycogenolysis and gluconeogenesis, elevating blood glucose. Bypasses cardiac beta receptors to directly increase heart rate and force via cAMP.

Toxicity: Nausea, vomiting, transient tachycardia/hypertension.

Key Features: Used for emergency treatment of severe hypoglycemia in unconscious diabetic patients when IV access cannot be established. Also the definitive antidote for Beta-Blocker overdoses due to its direct cardiac-stimulating properties that bypass blocked betareceptors.

MOA: Lipophilic weak bases that act as prodrugs. They accumulate in the acidic canaliculi of parietal cells and form a covalent disulfide bond that irreversibly inhibits the H+/K+ ATPase pump.

Toxicity: Diarrhea, headache, and decreased absorption of Vitamin B12 and calcium. Chronic use increases the risk of bone fractures and is associated with a high risk of Clostridioides difficile infection.

Key Features: The most effective inhibitors of gastric acid secretion. They must be administered 30 to 60 minutes before breakfast to ensure the pump is active and the drug is effectively incorporated.

MOA: Competitively block histamine H2 receptors on parietal cells, reducing intracellular cAMP and blunting acid secretion stimulated by histamine, gastrin, or acetylcholine.

Toxicity: Cimetidine is a potent CYP450 inhibitor and has anti-androgenic effects including gynecomastia and erectile dysfunction. Famotidine lacks these toxicities.

Key Features: Highly effective for controlling nocturnal acid secretion but subject to tachyphylaxis (tolerance) within a few days of continuous use.

MOA: Synthetic analog of Prostaglandin E1. Binds to EP receptors on parietal cells to decrease acid production while stimulating mucus and bicarbonate secretion.

Toxicity: Profound abdominal cramping and watery diarrhea. Pregnancy Category X as it induces uterine contractions and can cause abortion.

Key Features: Indicated specifically for the prevention of NSAID-induced gastric ulcers.

MOA: Sulfated sucrose complexed with aluminum hydroxide. Polymerizes in an acidic environment into a thick, sticky paste that selectively binds to the positively charged proteins in the ulcer bed, creating a physical barrier.

Toxicity: Constipation (due to aluminum). May trap and bind other concurrent oral medications.

Key Features: Requires an acidic environment to activate; do not co-administer with antacids, H2 blockers, or PPIs.

MOA: Highly selective competitive antagonists of 5HT3 receptors in the central chemoreceptor trigger zone (CTZ) and on peripheral vagal afferents in the intestinal tract.

Toxicity: Headache, dizziness, constipation. Can cause QT interval prolongation on ECG.

Key Features: First-line, premier choice for preventing chemotherapy-induced nausea and vomiting (CINV), post-radiation emesis, and post-operative emesis.

MOA: Blocks dopamine D2 receptors centrally in the chemoreceptor trigger zone (CTZ). It also acts as a prokinetic agent by enhancing acetylcholine sensitivity in the upper gastrointestinal tract.

Toxicity: Extrapyramidal symptoms (EPS) including dystonia, akathisia, and Parkinson-like tremors. Can also cause hyperprolactinemia, leading to galactorrhea and gynecomastia.

Key Features: Metoclopramide is the drug of choice for diabetic gastroparesis and severe bloating due to its dual antiemetic and prokinetic properties.

MOA: Crosses the blood-brain barrier to competitively block central Neurokinin-1 NK1 receptors, preventing the binding of substance P in the emetic center.

Toxicity: Fatigue, diarrhea, and hiccups. It is a potent inhibitor of CYP3A4.

Key Features: Used in combination with a 5-HT3 antagonist and dexamethasone for the prevention of delayed nausea and vomiting caused by highly emetogenic chemotherapy.

MOA: Actively stimulate central CB1 cannabinoid receptors in and around the vomiting center.

Toxicity: THC-like central effects: euphoria, sedation, hallucinations, paranoid reactions, and prominent tachycardia.

Key Features: Reserved for refractory chemotherapy-induced emesis when standard cocktails fail. Also acts as an appetite stimulant in AIDS-wasting syndrome.

MOA: Stimulate opioid receptors in the enteric nervous system; inhibit circular and longitudinal muscle activity to prolong transit time.

Toxicity: Constipation, abdominal cramps, CNS depression.

Key Features: Loperamide does not cross the BBB (low abuse potential). Diphenoxylate crosses the BBB and is combined with atropine to discourage abuse via unpleasant anticholinergic effects.

MOA: Potent selective 5HT3 receptor antagonist; slows colonic transit time and reduces visceral pain signaling in the gut.

Toxicity: Black Box Warning for severe, life-threatening ischemic colitis and catastrophic constipation that may require surgery.

Key Features: Highly restricted use; strictly indicated for women with severe, chronic diarrhea-predominant IBS (IBS-D) who have failed all other standard therapies.

MOA: Non-absorbable solutes draw water into the intestinal lumen via an osmotic gradient; the resulting increase in luminal volume stretches the colon, stimulating peristalsis.

Toxicity: Electrolyte imbalances, dehydration, and abdominal cramps. Magnesium can accumulate to toxic levels in patients with renal insufficiency.

Key Features: Magnesium hydroxide is fast-acting. Polyethylene glycol (PEG) is the standard for bowel cleansing before colonoscopy.

MOA: Selectively activates type-2 chloride channels (ClC-2) on the small intestine's luminal epithelial surface. This stimulates chloride-rich fluid secretion into the lumen, softening stool and accelerating transit.

Toxicity: Nausea (due to delayed gastric emptying), diarrhea, abdominal pain.

Key Features: Indicated for chronic idiopathic constipation and constipation-predominant IBS (IBS-C) in women.

MOA: Binds to and activates guanylyl cyclase-C (GC-C) on the luminal surface of enterocytes. This increases intracellular cGMP, activating the CFTR channel to pump out chloride and bicarbonate, driving fluid secretion and speeding transit.

Toxicity: Diarrhea, flatulence, abdominal distension.

Key Features: Orally active drug used to treat chronic idiopathic constipation and IBS-C.

MOA: Unabsorbed prodrug formulations (e.g., sulfasalazine is 5-ASA linked to sulfapyridine). Cleaved locally by bacterial azoreductases in the colon to release free 5-ASA (mesalamine), which acts locally to inhibit cyclooxygenase (COX) and lipoxygenase (LOX), suppressing the localized inflammatory cascade.

Toxicity: Sulfasalazine causes significant sulfonamide toxicities (nausea, hemolytic anemia, oligospermia, rash). Mesalamine formulations lack the sulfa component and are much better tolerated.

Key Features: Mainstay of therapy for inducing and maintaining remission in mild-to-moderate Ulcerative Colitis.

MOA: Activates G-coupled oxytocin receptors on uterine smooth muscle triggers IP3 calcium pathways to cause rhythmic, coordinated contractions.

Toxicity: Dose-related hypotension, reflex tachycardia, uterine rupture, fetal distress. High doses cross-activate V2 receptors causing water intoxication/dilutional hyponatremia.

Key Features: Drug of choice for induction of labor and prevention/treatment of postpartum hemorrhage.

MOA: Partial agonist at 5HT1, alpha-adrenergic, and dopamine receptors. Induces powerful, sustained tetanic uterine contractions that compress leaking vessels.

Toxicity: Vasoconstriction, hypertension, nausea/vomiting.

Key Features: Strictly indicated for postpartum hemorrhage control. Safety Rule: Never administer before full delivery of the placenta.

MOA: Inhibit phosphodiesterase-5 (PDE-5), preventing the breakdown of cGMP in the corpora cavernosa smooth muscle relaxation and increased blood flow.

Toxicity: Headache, facial flushing, nasal congestion, blue-green visual tint (sildenafil).

Key Features: Treats erectile dysfunction and pulmonary hypertension. Tadalafil has a longer half-life.

Strict Contraindication: Never combine with organic nitrates (e.g., nitroglycerin) causes synergistic cGMP accumulation leading to severe, fatal hypotension.

MOA: Synergistic feedback mechanism: Estrogen suppresses FSH (preventing follicle maturation); Progestin suppresses LH (blocking the midcycle LH surge and ovulation). Progestin also thickens cervical mucus and inhibits implantation.

Toxicity: Breakthrough bleeding, weight gain, nausea. Increased risk of deep vein thrombosis (DVT), thromboembolism, and stroke.

Key Features: Highly effective. Contraindicated in smokers over 35, or patients with a history of thromboembolic disease, stroke, or estrogen-dependent tumors.

MOA: Selective Progesterone Receptor Modulator (SPRM) with partial agonist and antagonist properties. Delays or inhibits ovulation and alters the endometrium.

Toxicity: Headache, nausea, abdominal pain, dysmenorrhea.

Key Features: Single oral dose (30 mg) for emergency contraception. Maintains high efficacy up to 120 hours (5 days) after unprotected intercourse.

MOA: Bind to intracellular estrogen receptors (ER\alpha, EReta) to modulate gene transcription. Regulate female reproductive development and protect bone mineral density.

Toxicity: Endometrial hyperplasia/cancer (if given without a progestin), thromboembolism, gallbladder disease.

Key Features: Ethinyl estradiol is synthetic and resistant to first-pass metabolism. Diethylstilbestrol (DES) is a nonsteroidal agonist historically associated with clear cell vaginal adenocarcinoma in female offspring exposed in utero.

MOA: Selective Estrogen Receptor Modulators (SERMs) with tissue-specific actions:
Tamoxifen: Antagonist in breast tissue; Agonist in bone and endometrium.
Raloxifene: Antagonist in breast and endometrium; Agonist in bone.

Toxicity: Hot flashes, increased risk of DVT/thromboembolism. Tamoxifen increases endometrial cancer risk; Raloxifene does not.

Key Features: Tamoxifen is first-line for ER-positive breast cancer. Raloxifene is used to prevent/treat postmenopausal osteoporosis, especially in patients with a high risk of breast cancer.

MOA: Competitively inhibit Aromatase, the enzyme responsible for the peripheral conversion of androgens to estrogens.

Toxicity: Hot flashes, severe arthralgias, accelerated bone loss (osteoporosis/fractures).

Key Features: First-line baseline therapy for ER-positive breast cancer in postmenopausal women (where peripheral fat tissue is the primary source of estrogen).

MOA: Activate intracellular androgen receptors to promote male secondary sex characteristics (androgenic) and muscle wasting recovery (anabolic).

Toxicity: Cholestatic jaundice, elevated liver transaminases (AST/ALT), virilization in females, gynecomastia (via peripheral aromatization to estrogen), and testicular atrophy/azoospermia (via negative feedback on LH/FSH).

Key Features: Large doses used by athletes increase cardiovascular risks and cause aggressive behavior.

MOA: Competitive antagonists at the intracellular androgen receptor. Block endogenous testosterone and DHT binding.

Toxicity: Hot flashes, gynecomastia, hepatotoxicity (requires liver enzyme monitoring).

Key Features: Used to treat metastatic prostate carcinoma. Co-administered with GnRH agonists (like leuprolide) during the first week of therapy to prevent the dangerous "tumor flare" caused by the initial testosterone surge.

MOA: Inhibit 5$\alpha$-reductase, blocking the conversion of testosterone to its more potent cellular metabolite, Dihydrotestosterone (DHT).

Toxicity: Erectile dysfunction, decreased libido, gynecomastia. Teratogenic (pregnant women must not handle crushed tablets).

Key Features: Treats Benign Prostatic Hyperplasia (BPH) by actively shrinking prostate volume, and male pattern baldness (alopecia) by reducing hair follicle DHT exposure.

MOA: Bind to GABA_A receptors to increase the frequency of chloride channel opening, causing neuronal hyperpolarization.

Toxicity: CNS depression, anterograde amnesia, respiratory depression (severe with alcohol). Antidote: Flumazenil (can trigger seizures in chronic users).

Key Features: Lorazepam and Oxazepam are safe in liver failure due to extrahepatic metabolism. Alprazolam is highly addictive due to its short duration. Contraindicated in sleep apnea.

MOA: Bind to GABA_A receptors to increase the duration of chloride Cl- channel opening. At high doses, they act directly as GABA mimetics.

Toxicity: Profound respiratory and cardiovascular depression. No pharmacological antidote exists. They are potent CYP450 enzyme inducers, reducing the efficacy of concurrent medications like warfarin.

Key Features: Thiopental is ultra-short acting and used for anesthesia induction. Phenobarbital is used for chronic tonic-clonic seizures. Strictly contraindicated in porphyria.

MOA: Selectively bind the BZ1 alpha1-containing subunit of the GABA A receptor complex to induce sedation.

Toxicity: Daytime somnolence, ataxia, and complex sleep behaviors (e.g., sleepwalking). Effects are reversed by flumazenil.

Key Features: Pure hypnotics that lack the anxiolytic, muscle relaxant, or anticonvulsant properties of standard benzodiazepines. They cause minimal disruption to sleep architecture.

MOA: Partial agonist at presynaptic 5HT1A serotonin receptors.

Toxicity: Dizziness, headache, nausea.

Key Features: Treats Generalized Anxiety Disorder (GAD). Lacks sedative, hypnotic, or muscle relaxant properties. Zero abuse potential, zero synergy with alcohol. Catch: Takes 2–4 weeks to manifest clinical efficacy.

MOA: Selectively inhibit the presynaptic serotonin transporter (SERT), prolonging serotonin neurotransmission.

Toxicity: GI distress, sexual dysfunction (anorgasmia), insomnia. Combined with MAOIs triggers lethal Serotonin Syndrome (hyperthermia, rigidity, clonus; treat with cyproheptadine).

Key Features: First-line baseline therapy for depression and anxiety. Fluoxetine inhibits CYP2D6 (blocks tamoxifen activation). Safe in elderly over TCAs.

MOA: Inhibit both serotonin (SERT) and norepinephrine (NET) presynaptic reuptake transporters.

Toxicity: SSRI side effects plus noradrenergic spikes: increased blood pressure, tachycardia, insomnia, and agitation.

Key Features: Duloxetine is highly effective for treating depression accompanied by chronic pain states (neuropathic pain, fibromyalgia).

MOA: Inhibit presynaptic reuptake of NE and 5-HT. Also block H1 histamine, alpha1 adrenergic, and muscarinic receptors.

Toxicity: The 3 C's of Overdose: Cardiotoxicity (blocks Na+ channels causing fatal QRS widening/arrhythmias; treat with sodium bicarbonate), Convulsions, and Coma. Massive anticholinergic profile.

Key Features: Clomipramine is highly specific for OCD. Amitriptyline handles neuropathic pain. High toxicity profile limits first-line utility.

MOA: Phenelzine is a non-selective inhibitor of MAO-A and MAO-B. Selegiline is a selective MAO-B inhibitor at low doses (preserves dopamine).

Toxicity: Ingesting tyramine-rich foods (aged cheese, red wine) causes a catastrophic Hypertensive Crisis (Cheese Reaction) due to uncontrolled NE release.

Key Features: Requires a 2-week washout period before switching to or from SSRIs to prevent fatal Serotonin Syndrome.

MOA: Inhibits norepinephrine and dopamine reuptake (NDRI).

Toxicity: High risk of inducing seizures at high doses or in susceptible populations.

Key Features: Zero sexual side effects and weight-neutral. Highly favored for smoking cessation. Strictly contraindicated in patients with Bulimia or Anorexia due to lowered seizure thresholds.

MOA: Suppresses inositol signaling pathways (IP3/DAG) and inhibits glycogen synthase kinase-3 (GSK-3).

Toxicity: Ultra-narrow therapeutic window. Fine hand tremor, polyuria/polydipsia (causes Nephrogenic Diabetes Insipidus), hypothyroidism, Ebstein's anomaly (teratogenic cardiac defect)

Key Features: First-line for bipolar disorder mania prophylaxis. Thiazide diuretics increase lithium reabsorption, rapidly precipitating lethal lithium toxicity.

MOA: Potent, high-affinity competitive Dopamine D2 receptor antagonists in the mesolimbic pathway.

Toxicity: Extrapyramidal Symptoms (EPS): acute dystonia (treat with diphenhydramine or benztropine), akathisia, and tardive dyskinesia. Hyperprolactinemia. Triggers Neuroleptic Malignant Syndrome (NMS) (lethal hyperthermia, "lead-pipe" rigidity; treat with dantrolene).

Key Features: High-potency agents (Haloperidol) cause high EPS but low autonomic effects. Low-potency agents (Chlorpromazine) cause high anticholinergic and alpha1 blockade orthostatic hypotension.

MOA: Combined 5-HT2A serotonin and lower-affinity D2 dopamine receptor antagonists.

Toxicity: Severe metabolic syndrome (profound weight gain, hyperglycemia, hyperlipidemia). Clozapine causes life-threatening agranulocytosis (requires strict, mandatory regular WBC monitoring) and seizures. Ziprasidone carries a high risk of QT prolongation.

Key Features: First-line for schizophrenia due to vastly lower EPS risk and superior management of negative symptoms. Quetiapine is safe in bipolar depression.

MOA: Binds to and prolongs the inactivated state of voltage-gated Na+ channels, blocking high-frequency repetitive firing.

Toxicity: Nystagmus, ataxia, diplopia. Chronic signs: Gingival hyperplasia, hirsutism, megaloblastic anemia (folate depletion), and fetal hydantoin syndrome.

Key Features: Follows zero-order elimination kinetics at therapeutic or high ranges, meaning small dose changes cause massive blood level spikes. It is also a potent CYP450 inducer.

MOA: Blocks voltage-gated Na+ channels (similar to phenytoin).

Toxicity: Diplopia, ataxia, severe Hyponatremia (SIADH), agranulocytosis/aplastic anemia, and Stevens-Johnson syndrome (especially in HLAB1502 patients). Teratogenic.

Key Features: First-line agent for Trigeminal Neuralgia and focal seizures. Characterized by autoinduction (induces its own hepatic metabolism over the first few weeks of therapy).

MOA: Multi-action profile: Blocks voltage-gated Na+ channels, inhibits T-type Ca2+ channels, and increases GABA synthesis/inhibits GABA degradation.

Toxicity: Severe Hepatotoxicity (requires liver function monitoring), weight gain, tremor, pancreatitis. Highest teratogenic risk across the class (neural tube defects/spina bifida).

Key Features: Highly versatile broad-spectrum agent for generalized tonic-clonic, focal, and myoclonic seizures. Acts as a CYP450 inhibitor (contrasts with phenytoin/carbamazepine).

MOA: Selectively inhibits T-type voltage-gated calcium channels in thalamic pacemaker neurons.

Toxicity: GI distress (nausea, pain), headache, drowsiness, urticaria.

Key Features: The definitive drug of choice for pure Absence Seizures. Completely ineffective against focal or generalized tonic-clonic seizures.

MOA: Reversibly bind to the intracellular domain of voltage-gated Na+ channels, blocking influx and halting nerve action potential propagation. Target small, myelinated fibers (pain/autonomic) before large unmyelinated fibers (motor).

Toxicity: CNS stimulation (tremors, seizures) followed by CNS depression. Bupivacaine is highly cardiotoxic (precipitates refractory ventricular arrhythmias). Prilocaine creates an accumulation of o-toluidine, causing Methemoglobinemia (chocolate-colored blood).

Key Features: Paired with Epinephrine to cause local vasoconstriction, which extends block duration, limits systemic toxic bleeding, and counters baseline vasodilation (except Cocaine, which has intrinsic vasoconstriction). Systemic toxicity is exacerbated by acidosis or hyperkalemia.

MOA: Direct potentiation of GABA A receptor-mediated chloride currents.

Toxicity: Marked hypotension (profound vasodilation) and respiratory depression.

Key Features: Premier agent for day-case/outpatient surgery due to its rapid clearance and ultra-fast, clean recovery. Features intrinsic antiemetic properties and does not cause cumulative effects.

MOA: Uncompetitive NMDA glutamate receptor antagonist.

Toxicity: Post-operative emergence delirium, vivid hallucinations, and unpleasant dreams (prevented by co-administering midazolam).

Key Features: Induces "Dissociative Anesthesia" . Acts as a cardiovascular stimulant (spikes HR and BP via central sympathetic stimulation), making it ideal for patients in hypovolemic or septic shock. Minimally depresses respiration.

MOA: Alter activity of multiple ion channels (GABA, potassium) in the CNS to disrupt synaptic transmission.

Toxicity: Halothane causes severe fulminant hepatotoxicity ("Halothane Hepatitis"). Volatile liquids trigger Malignant Hyperthermia when paired with succinylcholine (treat with dantrolene). Nitrous oxide can cause megaloblastic anemia via vitamin B12 inactivation.

Key Features: Nitrous oxide has a low blood:gas partition coefficient (ultra-fast inductionecovery) but low potency (high MAC). Halothane has high solubility (slow induction) but high potency (low MAC).

MOA: Levodopa is a prodrug that crosses the BBB and is decarboxylated into functional Dopamine centrally. Carbidopa is a peripheral dopamine decarboxylase inhibitor that cannot cross the BBB; it stops peripheral breakdown of Levodopa.

Toxicity: Nausea/vomiting, orthostatic hypotension, visual hallucinations, and tardive-like dyskinesias.

Key Features: Carbidopa markedly lowers peripheral dopamine generation, neutralizing severe systemic vomiting and arrhythmias while boosting central brain delivery. Chronic use is plagued by the "on-off" phenomenon (unpredictable motor fluctuations).

MOA: Reversible central acetylcholinesterase (AChE) inhibitors. Increase the concentration of ACh in the cerebral cortex.

Toxicity: Generalized cholinergic side effects: nausea, vomiting, diarrhea, abdominal cramps, anorexia, and bradycardia.

Key Features: Produce modest, temporary cognitive stabilization in mild-to-moderate Alzheimer's disease; exert zero effect on altering actual neurodegenerative disease progression. Rivastigmine is available as a daily skin patch.

MOA: Uncompetitive, low-affinity NMDA glutamate receptor antagonist. Blocks pathological tonic levels of glutamate that cause excitotoxic neuronal death.

Toxicity: Dizziness, headache, confusion, and mild constipation.

Key Features: Indicated for moderate-to-severe Alzheimer's disease. Can be safely combined with AChE inhibitors like donepezil.

MOA: Reversible inhibitor of Vesicular Monoamine Transporter 2 (VMAT2). Depletes presynaptic stores of dopamine, norepinephrine, and serotonin.

Toxicity: Severe sedation, akathisia, depression, and increased suicidal ideation.

Key Features: Used specifically to alleviate the hyperkinetic motor symptoms and chorea characteristic of Huntington's disease. Less toxic than reserpine.

MOA: Copper chelating agent (dimethylcysteine) that forms a stable soluble complex with copper, facilitating its urinary excretion.

Toxicity: GI distress, bone marrow suppression (blood dyscrasias), optic neuropathy, and drug-induced myasthenia.

Key Features: Standard therapy to halt and reverse lethal hepatic and neurological copper deposition in Wilson's disease.

MOA: Competitive antagonists at nicotinic receptors NM on the skeletal muscle motor end plate. Prevent ACh binding.

Toxicity: Tubocurarine triggers prominent histamine release, causing profound bronchospasm, flushing, and hypotension.

Key Features: Blockade is completely reversed by AChE inhibitor paired with an antimuscarinic (atropine) to block off-target parasympathetic surges. Rocuronium is intermediate-acting and fast, making it ideal for rapid sequence intubation without histamine release.

MOA: Nicotinic receptor NM agonist that resists AChE breakdown. Causes persistent depolarization of the motor end plate, manifesting as transient muscle fasciculations followed by flaccid paralysis (Phase 1 block).

Toxicity: Hyperkalemia (can trigger cardiac arrest, especially in burn, crush, or denervation injuries). Postoperative muscle pain. Triggers Malignant Hyperthermia.

Key Features: Phase 1 block is worsened/intensified by AChE inhibitors (neostigmine). Ultra-short acting due to rapid hydrolysis by plasma pseudocholinesterase. Fasciculations can be blunted by a tiny pre-dose of a nondepolarizing blocker

MOA: GABA B receptor agonist in the spinal cord. Activates G protein mechanisms to open K+ channels, hyperpolarizing neurons and reducing the release of excitatory neurotransmitters.

Toxicity: Marked sedation, drowsiness, muscle weakness, and a risk of seizures if stopped abruptly.

Key Features: Used to reduce severe spasticity resulting from spinal cord transections, multiple sclerosis, or trauma.

MOA: Directly binds and inhibits Ryanodine Receptors (RyR1) on the skeletal muscle sarcoplasmic reticulum. Blocks the intracellular release of calcium needed for excitation-contraction coupling.

Toxicity: Significant muscle weakness, drowsiness, and dose-dependent hepatotoxicity.

Key Features: The life-saving drug of choice for Malignant Hyperthermia (triggered by volatile anesthetics/succinylcholine) and Neuroleptic Malignant Syndrome (NMS).

MOA: Enhances GABA-mediated current at GABA A receptors and competitively inhibits glutamate-induced opening of NMDA receptor channels.

Toxicity: Acute: medullary respiratory depression, coma. Chronic: cirrhosis, Wernicke-Korsakoff syndrome (thiamine deficiency deficiency). Leading cause of mental retardation in offspring when consumed during pregnancy (Fetal Alcohol Syndrome).

Key Features: Exhibits zero-order elimination kinetics because metabolic enzymes (alcohol dehydrogenase) are saturated at low concentrations. Chronic use induces CYP2E1, which shifts acetaminophen metabolism into a cytotoxic hepatotoxic pathway. Acute withdrawal is treated with diazepam; dependence craving is reduced by Naltrexone or Acamprosate.

MOA: Irreversibly inhibits Aldehyde Dehydrogenase, halting the conversion of toxic acetaldehyde into acetate.

Toxicity: If ethanol is consumed concurrently, it triggers a violent Acetaldehyde Syndrome: throbbing headache, severe nausea/vomiting, flushing, sweating, hypotension, and chest pain.

Key Features: Used purely as a behavioral modifier/deterrent for recovering alcoholics.

MOA: Highly potent competitive inhibitor of Alcohol Dehydrogenase (ADH).

Toxicity: Well tolerated. May cause transient headache or nausea.

Key Features: The definitive antidote for acute Methanol or Ethylene Glycol poisoning.

MOA: Bind to G-protein-coupled opioid receptors MOP centrally and peripherally. Close voltage-gated Ca2+ channels presynaptically (stopping neurotransmitter release) and open K+ channels postsynaptically (hyperpolarizing pain pathways).

Toxicity: The Overdose Triad: Pinpoint Pupils (Miosis), Coma, and Severe Respiratory Depression.

Key Features: Methadone has high oral bioavailability and a long half-life >24, making it the gold standard for controlled heroin detoxification and maintenance programs. Fentanyl is ultra-short acting (60-90 min) given IV or transdermally.

MOA: Bind to opioid receptors with lower affinity than morphine.

Toxicity: Standard opioid profile: constipation, sedation, respiratory depression in overdose.

Key Features: Codeine is heavily utilized at sub-analgesic doses as an oral syrup antitussive (cough suppressant) .

MOA: Pure, high-affinity competitive antagonists at mu, kappa, and delta opioid receptors. Completely displace bound opioid agonists.

Toxicity: Will immediately precipitate acute, severe withdrawal symptoms (rhinorrhea, lacrimation, severe diarrhea, yawning, hyperthermia, piloerection) in opioid-dependent individuals.

Key Features: Naloxone is short-acting given IV or intranasally for emergency reversal of acute lethal opioid overdose respiratory depression. Naltrexone has a long half-life (up to 2 days) given orally to prevent relapse compliance in opioid dependence and to reduce alcohol craving.

MOA: Cocaine blocks the reuptake transporters of dopamine, NE, and 5-HT (intrinsic vasoconstrictor). Amphetamines enter nerve terminals to actively displace and force the non-vesicular release of stored catecholamines into the synapse.

Toxicity: Severe agitation, paranoid psychosis, tachyarrhythmias, malignant hypertension, and coronary artery vasospasm/myocardial infarction.

Key Features: Highly addictive. Withdrawal produces deep dysphoria, depression , and intense hyperphagia

MOA: Antagonist at the NMDA glutamate receptor channel.

Toxicity: Psychomotor agitation, extreme unpredictable aggressiveness, delirium, and analgesic insensitivity to pain.

Key Features: Pathognomonic indicator: The presence of both horizontal AND vertical nystagmus combined with violent, detached behavior. Overdose management involves benzodiazepines for seizures and nasogastric suction/activated charcoal

MOA: Exerts its central effects by binding and activating G-protein-coupled CB 1 cannabinoid receptors in the brain.

Toxicity: Impaired psychomotor performance, short-term memory lapses, and transient panic reactions.

Key Features: Pathognomonic indicators: Notable increase in resting pulse rate combined with deep injectioneddening of the conjunctiva (bloodshot eyes). Pupils remain completely unchanged in size (distinguishes it from opioids or stimulants).

MOA: Selective Serotonin Reuptake Inhibitor (SSRI).

Treats: Depression, anxiety disorders, and bulimia.

Tox: Sexual dysfunction and insomnia.

Key: Longest half-life; inhibits CYP2D6, which can interfere with Tamoxifen activation.

MOA: Selective inhibition of SERT.

Toxicities: GI distress, jitters, and sexual dysfunction. Citalopram overdose can cause QT prolongation.

High Yield Info: Often the best choice for elderly patients due to lower autonomic side effects compared to TCAs.

MOA: Blocks NE and 5-HT reuptake; also blocks muscarinic, H_1, and alpha_1 receptors.

Treats: Major depression and chronic neuropathic pain.

Tox: Atropine-like effects and dangerous cardiac arrhythmias in overdose.
Coma, Convulsions, and Cardiotoxicity

Key: Overdose management focuses on lidocaine for arrhythmias and bicarbonate for acidosis.

MOA: Irreversible inhibition of both MAO-A and MAO-B, increasing vesicular stores of NE, 5-HT, and Dopamine.

Toxicities: CNS stimulation (agitation/convulsions), and orthostatic hypotension in the absence of tyramine.

High Yield Info: "Cheese Reaction": Hypertensive crisis when combined with tyramine-rich foods (aged cheese, wine). Can cause life-threatening Serotonin Syndrome if combined with SSRIs.

MOA: Selective inhibitors of MAO-B (monoamine oxidase type B), the enzyme that metabolizes dopamine in the brain.
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Toxicities: Insomnia, mood changes, dyskinesias, GI distress, and hypotension.

​High Yield Info: Lacks the "cheese effect" (hypertension) of non-selective MAOIs used in depression.

MOA: Weak reuptake inhibitor of NE and Dopamine (NDRI).

Treats: Major depression and nicotine withdrawal.

Tox: Seizures at high doses.

Key: Least likely to cause sexual dysfunction.

MOA: Antagonist at presynaptic alpha2 adrenoceptors (increasing amine release) and 5-HT2 receptors.

High Yield Info: Useful for depressed patients with insomnia or severe weight loss.

Toxicities: Marked sedation and significant weight gain

MOA: Postsynaptic 5-HT_2A receptor antagonist.

Toxicities: Highly sedating.

High Yield Info: Widely used as a sleeping aid in depressed patients with insomnia.