Drug Names/Classes



|Drug Names/Classes |Used for: |

|Parasym|Indirect ACh |Reversi|Carbamates |Indicated for glaucoma. |

|pathomi|R Agonists |ble |(Physostigmine) |Antidote for atropine poisoning. |

|metics | | | | |

| | | |Quarternary Alcohol |Diagnose Myasthenia Gravis |

| | | |(edrophonium) | |

| | | |Horny Goat Weed |Indicated for erectile dysfunction |

| | |Irreversible |Insecticide |Insects… |

| | |(Organo- |(malathione) | |

| | |Phosphates) | | |

| | | |Nerve Gas |Lethal. Use atropine as antidote. |

| | | |(Sarin) | |

| |Direct ACh R |Carbachol |Indicated for glaucoma |

| |Agonists | | |

| | |Bethanechol |Indicated for urinary retention. |

| | |Pilocarpine |Indicated for Glaucoma |

|Parasym|mACh R |Atropine |Causes pupil dilation, increases HR (indicated for bradycardia), reduces |

|patholy|Blockers | |bronchosecretion (for surgery) |

|tics | | |Antidote for organophosphate poisoning. |

| | |Scopolamine |Indicated for motion sickness; antiemetic drug delivered transdermally |

| | |Pirenzipine |Indicated for peptic ulcers; selectively blocks M1 Receptors, reduces gastric acid |

| | | |secretion |

| |nACh R |Non- |Tubocuraraine |Poison; respiratory paralysis. Muscle relaxant. |

| |Blocerks |Depolar| |Competitive antagonists |

| | |izing | | |

| | | |Pancuronium |Muscle relaxants; competitive antagonists |

| | | |Atracurium | |

| | |Depolar|Succinylcholine/ |Muscle relaxants |

| | |izing |Suxamethonium |nACh R agonists, but has parasympatholytic effect |

Cholinergic System

Direct Parasympathomimetics – drugs that mimic ACh and mostly binds mAChR

Indirect Parasympathomimetics – drugs that inhibit ACh-Esterase; raises [ACh]

Muscarinic Parasympatholytics – competitive antagonists

Nicotinic Parasympatholytics – neuromuscular junction blockers; muscle relaxants

Non-Depolarizing – competitive antagonists; competes with ACh to prevent depolarization

Depolarizing – nACh R agonist; initially mimics ACh causing depolarization but it is not hydrolyzed by ACh-Esterase so the depolarization is prolonged, inhibiting other signals

Nicotine

Low Concentration – acts as a direct nAChR agonist

High Concentration – has an antagonistic effect on nAChR due to channel inactivation; similar to succinylcholine.

nAChR = nicotinic acetylcholine receptor

mAChR = muscarinic acetylcholine receptor

Adrenergic System

|Drug Name/Class |Used For: |

|Sympath|Indirec|MAO Inhibitors |Indicated for depression; inhibits metabolism of NE/E, DA, and 5HT; many side |

|omimeti|t |(Tranylcypromine, Moclobemide) |effects |

|cs |Agonist| | |

| |s | | |

| | |Ephedrine |Found in diet pills; displaces NE from storage vesicles |

| | |Amphetamines |Displaces NE from storage, inhibits reuptake, inhibits MAO |

| | |Ritalin ( ADD | |

| | |Fenfluramine ( diet pills | |

| |Direct |Non-sel|Epinephrine(Adrenaline) |Indicated for anaphylactic shock and used as an adjuvant in local anesthetics. |

| |Agonist|ective | |Dilates bronchii. |

| |s | | | |

| | | |Norepinephrine (Noradrenaline) |Limited clinical use. |

| | |Selecti|α1 Agonists |Methoxamine – treats hypotension |

| | |ve |(vasoconstrictor) |Phenylephrine – nasal decongestant |

| | | | |Naphazoline – nasal decongestant |

| | | |α2 Agonists (sympatholytic!) |Indicated for hypertension. |

| | | |Clonidine |Presynaptic α2 receptors are inhibitory, reduces sympathetic tone on cardiovascular|

| | | |Guanfacine |system. |

| | | |β1 Agonists |(+) inotropic & (+) chronotropic effect on heart |

| | | |Dobutamine |Used in Dobutamine Stress Test |

| | | |β2 Agonists |Indicated for asthma (inhaler). Dilates bronchii |

| | | |Albuterol | |

|Sympath|α-recep|Non-selective Blockers |Indicated for pheocromocytoma. |

|olytics|tor |Phentolamine |Blocking α1 causes vasodilation; reducing BP |

| |antagon| |Blocking α2 removes inhibition, increasing NE action on β receptors ( increasing HR|

| |ists | |and cardiac output |

| | |Selective α1 Blocker |Indicated for hypertension and urinary retention. |

| | |Prazosin, Terazosin, etc… |Side effects: Reflex tachycardia and postural hypotension. |

| | |Selective α2 Blocker (sympathomimetic!) |Increases sympathetic outpout. Used for male sexual dysfunction and as a weight |

| | |Yohimibine |loss drug. |

| |β-recep|Noncardioselective β blockers |-1st gen. drug, cross reaction w/ β2 causes bronchoconstriction (side effect) |

| |tor |Propranolol |-Labetalol also blocks α1 receptors (strong antihypertensive drug) |

| |antagon| |-same indications as cardioselective blockers (below) |

| |ists | | |

| | |Cardioselective β blockers |Newer drugs are more β1 selective. |

| | |Metoprolol, Atenolol… |Indicated for angina pectoris, hypertension, cardiac dysrhythmias, myocardial |

| | | |infarction, heart failure, and stage fright (anxiolytic). |

|Drug/Class |Mechanism |

|Sympathetic |α2 Receptor Agonists - Clonidine |Elicits α2 receptor’s inhibitory effect on the sympathetic nervous system. Less NE |

|Nervous | |binding to α1 and β1 receptors. |

|System | | |

|Suppressors | | |

|(sympatholyt| | |

|ics) | | |

| |α1 Receptor Antagonists |Promotes peripheral vasodilation, reducing resistance, thereby reducing BP. |

| |Prazosin, Terazosin, etc… | |

| |β-receptor antagonists |β1 receptor activation causes an increase in HR and contractility. Blocking this receptor|

| |Propranolol, Metoprolol, Atenolol, etc |will reduce the HR and contractility (reduces stroke volume) leading to a drop in blood |

| | |pressure. |

|Direct |Calcium channel blockers |Targets L-Type channels (no cardiac effects), blocking Ca2+ entry into the smooth muscle |

|Vasodilators|(Calcium antagonists) |cell ( arterial vasodilation; decreases afterload ( reducing BP |

| |Dihydropyridines |Side effects: Reflex tachycardia, postural hypotension, and peripheral edema. |

| |-Nifedipine, etc… | |

| |Potassium Channel Agonists |Increases membrane permeability to K+, K+ efflux causes membrane hyperpolarization, |

| |Minoxidil |inhibiting voltage gated Ca2+ channels ( relaxation of smooth muscles ( vasodilation ( |

| | |reduces BP |

| | |Side effect: hair growth, marketed as Rogaine |

| | |Last resort for unresponsive hypertension. |

| |Nitroprusside |Delivered thru iv only and is metabolized into NO which directly activates cGMP production|

| | |( vasodilation |

| | |Review phosphodiesterase inhibitors (Caffeine & Viagra). |

|Renin-Angiot|ACE-Inhibitors |By inhibiting the ACE enzyme, angiotensin I cannot be converted into the active peptide |

|ensin-Aldost|Captopril |(ATII) |

|erone System|Enalapril |-no aldosterone & ADH release ( no fluid retention |

|Targeting |Benazepril |-no sympathomimetic effects |

|Drugs |Lisinopril |-no vasoconstriction |

| | |Side effect – causes coughing |

| |Angiotensin II (ATII) Receptor Blocker |Inhibits the effect of AT II by blocking the receptor |

| |-Losartan |-usually used if patient cannot tolerate the cough caused by ACE inhibitors |

| |-Candesartan | |

| |-etc… | |

Antihypertensive Drugs

Other Cardiovascular Diseases

|Angina Pectoris – chest pain due to coronary heart disease; a symptom of myocardial ischemia (when heart doesn’t get enough oxygen) |

|Stable Angina |Predictable episodes; usually during/after physical exertion or stress |

| |Treatment: Nitrates & β-Blockers (Propranolol, etc.) |

|Unstable Angina |Chest pain unexpected and usually occurs at rest |

| |Treatment: Nitrates |

|Variant Angina |Chest pain almost always occurs at rest and does not follow physical exertion or stress. Due to coronary artery |

| |spasm. |

| |Treatment: Calcium channel blockers (Nifedipine, etc…) |

|Nitrates |

|Converted to nitric oxide (NO) ( guanylate cyclase ( cGMP ( smooth muscle relaxation ( vasodilation |

|Nitrate|Nitroglycerine |Drug of choice for angina pectoris. Reduces cardiac workload (and its oxygen demand) by reducing venous|

|s | |return. Causes vasodilation primarily in veins. Many different forms of administration. |

| | |Do NOT combine w/ other vasodilators (Viagra…). |

| |Isosorbide-dinitrate |Longer lasting effect when compared to nitroglycerine. |

| |(ISDN) |Tolerance may occur, give lowest dose. |

| | |Do NOT combine w/ other vasodilators. |

| |Nitroprusside |Promotes peripheral vasodilation. |

| | |IV only; rapid onset and short duration – allows for titration |

|Cardiac Arrhythmias – abnormal rhythms of the heart that cause it to pump less effectively; abnormality in pacemaker cells, conduction pathway, |

|or if other parts of the heart take over pacemaker. |

|Class I: |Slows depolarization phase of AP. |

|Sodium Channel Blockers |Procainamide – used for atrial & ventricular arrhythmias |

| |Lidocaine – used for acute ventricular arrhythmias |

| |Flecainide – used for chronic treatment of ventricular arrhythmias |

|Class II: |Propranolol |

|β-Blockers |-used for tachycardia |

|Class III: |Prolongs repolarization by blocking potassium efflux. |

|Potassium Channel Blockers |Bretylium & Amiodarone |

| |-used for intractable ventricular arrhythmias |

|Class IV: |Prolongs repolarization by blocking calcium influx |

|Calcium Channel Blockers |Verapamil – blocks both L & T Type calcium channels! |

| |Blocking T Type channels ( slows conduction |

| |(Blocking L Type channels ( coronary + arterial vasodilation) |

|Others |Adenosine – for paroxysmal supraventricular tachycardia |

| |Digoxin – atrial fibrillation |

| |Epinephrine - bradycardia |

Other Cardiovascular Diseases

|Congestive Heart Failure – inadequate contractility; ventricles unable to expel blood ( rise in venous blood pressure. Caused by blocked |

|coronary arteries, viral infections, hypertension, leaky heart vavles, myocardial infarctions… |

|-Right sided failure – lower limb edema |

|-Left sided failure – pulmonary edema & respiratory distress |

|Cardiac Glycosides |Slows heart rate and increases contractility. |

|(Digoxin) |Mechanism: Inhibits Na/K ATPase, leading to an increase intracellular Na+ |

| |Increased Na+ slows Na/Ca exchanger, leading to an increase intracellular Ca++ |

| |Low therapeutic index. |

| |Potassium competes with digoxin in binding to Na/K ATPase |

| |-antidote for cardiac glycoside poisoning |

| |-increased potassium will reduce potency of digoxin |

|ACE inhibitors & |Captopril & Losartan (review RAAS) |

|ATII antagonists |Effectively reducing cardiac workload (inhibits vasoconstriction, inhibits sodium/fluid retention, inhibits NE |

| |release…) |

|Vasodilators |Nitrates: Nitroglycerine, etc. (review Nitrates notes) |

|Diuretics |Loop Diuretics: Furosemide |

| |Thiazides: Hydrocholorothiazide |

| |K+ Sparring: Spironolactone |

Diuretics

Diuretics – increases urine output; indicated for hypertension & edema (except CA inhibitors)

|Drugs |Mechanism |

|Carbonic Anhydrase Inhibitors |Inhibits conversion of CO2 ( (H+) + (HCO3-); effectively blocking reabsorption of Na+ |

|Azetazolamide |-primarily indicated for Glaucoma! |

|Dorzolamide |Causes metabolic acidosis (lower HCO3-). |

|Loop Diuretics (high ceiling) |Inhibits Na+/K+/2Cl- symporter @ ascending limb in the Loop of Henle; effectively blocking|

|Furosemide |Na, K, Cl reabsorption |

|Torasemide |-most potent diuretic |

| |-for severe/moderate hypertension & edema |

| |Causes hypokalemia |

|Thiazide Diuretics |Inhibits Na+/Cl- symporter @ distal convoluted tube |

|Hydrochlorothiazide |-for moderate hypertension & heart failure (edema) |

|Benzthiazide |Causes hypokalemia |

|Potassium-Sparring Diuretics |Acts as distal portion of distal tube; enhances Na excretion & reduces K excretion (K |

|Spironolactone |sparring) |

|Amiloride |Spironolactone – aldosterone receptor antagonist (slow) |

| |Amiloride – directly blocks Na/K channel (fast) |

| |Used in combo w/ other diurectics |

|Osmotic Diuretics |Non-reabsorbable molecules that inhibit passive reabsorption of water (promoting water |

|Mannitol (iv only) |excretion w/ little Na excretion) |

| |-cannot cross blood-brain barrier; so water goes from brain to blood |

| |Used to reduce intracranial pressure |

Major side effects of diuretics (except K-sparing)

-Mainly Hypokalemia (loss of potassium) & hyponatremia & hypochloremia as well

(may give extra potassium orally/iv)

-Hypotension & dehydration

Interaction w/ Cardiac Glycosides (digoxin)

-cardiac glycosides are Na/K ATPase inhibitors as a competitive K antagonist

-Hypokalemia secondary to diuresis increases digoxin potency

-digoxin has a narrow therapeutic index; this may cause it to become toxic

Uricosuric Agents

Indicated for kidney stones and gouts.

@ therapeutic dose: promotes excretion and inhibits reabsorption of uric acid

@ sub-therapeutic dose: inhibits both excretion and reabsorption

-possibly increase uric acid concentration

Probenecid

-strongly inhibits penicillin excretion!!

May be beneficial when trying to elevate antibiotic plasma concentration

Gastrointestinal Pharmacology

|Antacid|Weak Bases |Neutralizes stomach acid. |

|s |Tums, PeptoBismol, etc.. |Magnesium Hydroxide – causes diarrhea |

| | |Aluminum hydroxide – causes constipation |

| | |These are often combined |

| |H2 Receptor Blockers |-competitively inhibits binding of histamine to H2 receptors on parietal cells; thus |

| |Cimetidine |reducing histamine stimulated gastric acid production (there are other signals that may |

| |Ranitidine |stimulate acid production) |

| |Proton Pump Inhibitors |-irreversible inhibition of H+/K+ ATPase in parietal cells |

| |Omeprazole |-only active at low pH (activity restricted to stomach) |

| |Lansoprazole |-inhibits acid production for 1-2days |

| | |Note: prevents acid replenishment; does not neutralize acid |

| | |already in the stomach |

| | |(GERD is primarily treated w/ PPIs) |

|Mucosal Protective Agents |Misoprostol – PGE analog; stimulates mucus and HCO3 production; used w/ NSAIDS |

|Misoprostol |Sucralfate – stabilizes mucus to inhibit H+ diffusion |

|Sucralfate |-not absorbed |

|Antieme|H1 Antagonists |Diphenhydramine, Meclizine, etc |

|tic | |Blocks H1 (histamine) receptors competitively. |

|Drugs | | |

| |Muscarinic Receptor Antagonists |Scopolamine (anticholernergic) |

| |Benzodiazepines |Lorazempam; potentiates effects of GABA in CNS |

| |D2 (dopamine) Antagonists |Competitively blocks C2 receptors in the CTZ |

| |Metoclopramide |Also increases gastric emptying |

| |Domperidone |Contraindicated in patients w/ Parkinson’s disease |

| |Cannabinoids |Synthetic cannabinoids: Nabilone & Dronabinol |

| |(marijuana) |-acts as an agonists at cannabinoid receptors in the CNS |

|Peptic Ulcers – ulcer formation in the stomach/duodenum due to insufficient mucus and/or bicarbonate and/or increased acid production |

|(autodigestion of stomach/duodenal wall) |

|Causes: |

|H. pylori (majority) – breaks down mucus and triggers inflammation |

|NSAIDS – inhibits PGE (needed for mucus/HCO3 production) |

|Smoking – stimulates gastric acid production |

|Treatment of H. pylori infection and peptic ulcer: |

|Use a combo of antibiotics and PPI (or other mucosal protectant/enhancers & antacids) |

|Antibiotics: |

|Bismuth/Amoxicillin – disrupts cell wall |

|Clarithromycin/Tetracyclin – inhibits protein synthesis |

|Metronidazole – secondary agent, used when resistance develops or other agents are intolerated |

Gastrointestinal Pharmacology

|Laxativ|Bulk Laxatives – increases bowel content volume triggering stretch receptors causing reflex peristalsis |

|es | |

| |Bulk |Carbohydrate Based |-insoluble/non-absorbable |

| | |-Vegetable Fibers |-expands with water |

| | |-Bran (husk) |May cause constipation if not enough water. |

| | |Osmotically Active |-partially soluble/non-absrobable |

| | |-Epsom salt |-potent and fast acting |

| | |-Glauber’s salt | |

| |Irritant Laxatives – irritates enteric mucosa causing an increase secretion of water softening bowel content (stool); |

| |increased volume also triggers reflex peristalsis |

| |Irritan|Ricinoleic acid (Castor Oil) |-castor oil converted to ricinoleic acid |

| |ts | |-works in the small intestine |

| | |Anthraquinones |-works in the large intestine |

| | |Diphenolmethanes | |

| | |Bisacodyl | |

| | |Sodium picosulfate | |

| |Laxative Abuse: longer interval needed to refill colon, leads to constipation |

| |Loss of water/salts in gut leads to aldosterone release; causes excretion of K+ |

| |Hypokalemia reduces peristalsis |

|Anti-di|Muscarinic receptor antagonists and opiates can cause constipation but are not useful for treating diarrhea because of its |

|arrheal|effect on other parts of the body. |

| |Loperamide |-opiod derivative that selectively acts in the GI tract (w/ no CNS activity). |

| |(Imodium) |-directly acts on the intestinal muscles reducing motility |

| | |-this increases water and electrolyte reabsorption |

| | |Dimethicone – anti-gas agent that is often combined with anti-diarrheal drugs |

Metabolic Disorders (Diabetes Mellitus)

At low blood glucose levels (hypoglycemia); the body will increase blood glucose by:

-Glucagon (secreted by α pancreatic cells) promotes glycogenolysis & gluconeogenesis…

-epinephrine also released by adrenal medulla

β-blockers will mask symptoms of hypoglycemic shock

-cortisol (anti-insulin effects) is also released by the hypothalamus

extended use of steroidal drugs may induce diabetes

At high blood glucose levels (hyperglycemia); the body will decrease blood glucose by:

-Insulin (secreted by β- pancreatic cells) promotes glucose uptake & glycolysis & glycogenesis…

Diabetes Mellitus

Type 1 Diabetes – autoimmune disease; destruction of β pancreatic cells

Treatment requires exogenous insulin replacement to control hyperglycemia

Type 2 Diabetes – hyperglycemia resulting from insulin resistance at target tissue or reduced insulin production by β pancreatic cells

Various levels of defect leading to resistance

(receptor, signaling pathway, enzymes, glucose transporter…)

Treatment with exogenous insulin replacement or oral hypoglycemic agents

|Insulin |Regular Insulin |-unmodified; short acting |

|Therapy | |-only insulin that can be administered thru iv |

| |Insulin Lispro (Humalog) |-rapid onset (fastest) & short acting |

| | |-used before a meal |

| |Insulin Lente |-insulin + zinc ( micro-precipitates (delayed absorption) |

| |(sc injection only) |-long lasting (UltraLente = longest lasting) |

| |NPH Insulin |-insulin + protamine (delayed absorption |

| | |-long lasting |

| |Insulin Glargine (Lantus) |-synthetic insulin that is soluble at low pH, but becomes insoluble and forms |

| | |precipitates at neutral pH after sc administration |

| | |-long lasting (similar to Lente) |

|Oral |Sulfonylureas |Stimulates insulin release; useful for diabetes caused by low insulin levels where β- |

|Hypoglycemi|-Tolbutamide (1st gen.) |pancreatic cells are still present |

|c Agents |-Glimepiridide | |

|(For Type |-Glipizide | |

|II only) | | |

| |Glitazones |-Increases insulin sensitivity at target cells |

| |-Rosiglitazone |-Acts as a nuclear hormone receptor (PPARγ agonist) increasing transcription of |

| |-Pioglitazone |insulin receptor signaling components and glucose transporters |

| |Biguanides |-unknown mechanism |

| |-Metformin |-increase glucose uptake & inhibits gluconeogenesis |

| | |-lowers LDL + VLDL (bad cholesterol) |

| | |-suppresses appetite |

| | |-no hypoglycemic effects |

Insulin and oral hypoglycemic agents may cause hypoglycemia (except Metformin)

Metabolic Disorders (Hyperlipidemia)

|“Statins” |-Reversible HMG-CoA Reductase inhibitors. HMG-CoA reductase is the rate-limiting enzyme in the |

|Lovastatin |production of cholesterol. Inhibition effectively reduces de novo synthesis of cholesterol precursors. |

|Atorvastatin (Lipitor) |-Lower cholesterol levels upregulates LDL receptors in liver removing LDL from the bloodstream. |

|Fibrates |PPARα agonists – stimulates β-oxidation of fatty acids |

|-Clofibrate |Promotes lipoprotein lipase activity |

|-Benzafibrate |Lowers VLDL (minor effect on LDL) |

| |Increases HDL levels |

|Resins |Bile acid binding resins prevents reabsorption of bile acids in enterohepatic circulation. |

|-Cholestyramine |-The liver responds to this loss of bile acid by increasing cholesterol synthesis to make more bile acid|

|-Colestipol |(plasma cholesterol levels remain unchanged). |

| |-The liver will also upregulate LDL receptors to increase hepatic uptake of LDL (reducing plasma LDL). |

| |Resins are not absorbed into the blood. |

Steroid Drugs

|Corticosteriods (GC) – inhibits all phases of inflammation |

|-inhibits NFκB (a transcription regulator of proinflammatory mediators |

|-upregulates lipocortin (lipocortin inhibits PLA2 ; no PT or LT synthesis) |

|-promotes fetal lung development by increasing surfactant |

|Side Effects |-immune suppression |

| |-anti-insulin effects |

| |-“steroid diabetes” |

| |-increased glucose promotes lipogenesis (fat) |

| |-increased catabolism (muscle atrophy) |

| |-salt/water retention due to cross reactivity with mineralcorticoid (aldosterone) receptors |

| |-osteoporosis |

| |Prolonged use of GC therapy causes adrenal cortex atrophy, so it is important to phase out slowly to |

| |avoid flare ups due to cortisol insufficiency. |

|Addison’s Disease |Adrenal cortex failure – low cortisol levels |

| |-hypotension |

| |-weight loss |

| |-fatigue |

| |-abnormal glucose levels |

| |-inability to cope with stress |

| |-blotchy colored skin; w/o cortisol, corticotropin is unregulated and it increases melatonin (skin |

| |pigmentation) |

|Cushing’s Syndrome |Adrenal cortex tumor – high cortisol levels |

| |(symptoms similar to GC therapy) |

| |-hypertension |

| |-weight gain (upper body obesity, “buffalo hump”) |

| |-water retention |

| |-poor wound healing |

|Hydrocortison |-equivalent to endogenous cortisol |

| |-indicated for adrenal insufficiency (Addison’s Disease) |

| |-mostly for topical application |

| |-cross-stimulation with mineralcorticoid receptors |

| |-have Na retaining effects |

|Prednisone |Pro-drug; converted to active form (prednisolone) |

|Prednisolone |Drug of choice for systemic administration |

| |-lower Na retaining effects |

|Triamcinolone |Stronger anti-inflammatory effect, 5x more potent than cortisol |

| |-no Na retaining effects |

|Halogenated GC |30x more potent than cortisol |

|(Betamethasone) |-no Na or water retaining effects |

Steroid Drugs

|Female Sex Steriods |

|Estroge|Estradiol |Primary endogenous estrogen responsible for: |

|ns | |-breast development |

| | |-improving bone density |

| | |-increase HDL |

| | |-promotes uterus growth & supports endometrium development |

| | |Rapidly metabolized by the liver and therefore not suitable as an oral drug |

| |Ethinylestradiol |Stable derivative of estradiol |

| | |Usually found as the estrogen component of birth control pills |

| |Mestranol |Oral contraceptive |

| | |Similar to ethinylestradiol with an extra methyl group; prodrug |

| | |-cleavage of the methyl group yields ethinylestradiol |

|Selecti|Raloxifene |Indicated for postmenopausal osteoporosis |

|ve | |SERM = selective estrogen receptor modifier |

|Estroge| |-anti-estrogenic effect on breast and endometrium |

|n | |-reduces stimulation in these tissues to avoid tumorgenesis |

|Recepto| |-estrogenic effect on bone and lipid metabolism |

|r | | |

|Modifie| | |

|r | | |

| |Tamoxifene |Indicated for breast cancer |

| |(antiestrogen) |-anti-estrogenic effect on breast tissue |

| | |-weak effect on bone and lipid metabolism |

| |Clomiphene |Indicated for infertility |

| |(antiestrogen) |-selectively inhibits estrogen binding in pituitary, effectively removing negative feedback |

| | |-this causes an increase in LH ( ovulation |

|Progesterone |Rapidly metabolized by the liver |

| |Stable derivatives: Hydroxy/medroxy progesterone |

| |Testosterone derivatives: norethindrone |

| |norgestrel |

| |Progesterone is important for the formation of secretory endometrium and the establishment of pregnancy.|

|Mifepristone (RU486) |Induce medical abortions ( ................
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