Drug List Block 2 Reversed Flashcards by Oladipo Fagbemi

Synthetic analog of PGE2

Therapeutic uses:

Cervical ripening
Terminating early pregnancy/abortion

Mechanism:
1. Activation of collagenase also relaxing cervical smooth muscle EP4 receptor subtype (for cervical ripening)

Uterine contractions via EP1/3 receptors

SE:
GI related (nausea, vomiting, diarrhea)
Fever
Uterine rupture: contraindicated in women having history fo cesarean section or other uterine surgery

Dinoprostone

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Analog of PGF2alpha

Therapeutic use:

Termination of pregnancy in 2nd trimester
Control postpartum hemorrhage that is not responding to conventional treatment methods

Mechanism:

Stimulates uterine contractility by action at FP receptors
Postpartum, the drug cause myometrial contractions via FP receptors. This provides hemostasis at the stie of placenta formation

SE: 
GI related (nausea, vomiting, diarrhea)
Fever
Uterine rupture (contraindicated in women having history of cesarean section or other uterine surgery)
Rare case of bronchoconstrictino

Carboprost

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PGE1 analog

Therapeutic use:
Replacement therapy for prevention of ulcers caused by long term NSAIDS

Mechanism:
Suppresses gastric acid secretion by stimulating EP3 receptors on parietal cells; causes decrease in cAMP
Increase mucin and bicarbonate secretion
Increase mucosal blood flow

SE: Diarrhea-common and contraindicated in pregnancy

*(Misoprostol used with methotrexate or mifepristone for termination of early pregnancy)

Misoprostol

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PGE1

Use:

Impotence/ED
Maintenance of patent ductus arteriosus

Mechanism of action

Increase in cAMP which relaxes smooth muscle fo corpus cavernosum
cAMP mediated relaxation of ductus arteriosus smooth muscle

SE:
1. Pain at site of injection (reason for intra-urethral formulation)
Priapism: prolonged erection
2. Apnea in 10% of neonates,

Alprostadil

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PGI2 agonist

Therapeutic use: Primary pulmonary hypertension.

Mechanism: cAMP mediated dilation of pulmonary artery vascular smooth muscle

SE: Nausea, vomiting, headache, flushing

Epoprostenol

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Prostaglandin PGF2alpha analog

Uses: glaucoma and eyelash hypotrichosis

Mechanism: Increases outflow of aqueous humor and Increases the percent and duration of hairs in the growth phase.

Pharmacology: administered as opthalmic drops

SE: Eye redness, itching, permanent changes in eye color (increased brown pigment), eyelid skin; may increase length and number of eyelashes

Bimatoprost

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Mechanism: Blocks 11 beta hydroxylation so synthesis is stopped at 11-desoxycortisol. Does not inhibit ACTH release, so plasma ACTH increases stimulating synthesis and excretion of 17-hydroxycorticoids as 11-desoxycortisol.

Used as a diagnostic test

Metyrapone

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Competitive antagonist at progesterone and glucocorticoid receptors

Progesterone antagonist- Termination of pregnancy
Glucocorticoid antagonist- Treat cushing syndrome etc.

Mifepristone

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Competitive antagonists at mineralcorticoid receptor

Uses: diuretics, cardiac fibrosis/hypertrophy, HTN

Spironolactone

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Competitive antagonists at mineralcorticoid receptor

Uses: diuretics, cardiac fibrosis/hypertrophy, HTN

Eplerenone

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Progesterone and Mineralocorticoid and Androgen receptor antagonist

Mineralcorticoid antagonist-diuretic, antagonizes the salt retaining effects of estrogen
Progesterone Agonist- Used with estrogen to suppress ovulation and as hormone replacement therapy in post menopausal women
Androgen receptor antagonist

Drospirenone

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Responses: 1. Lymphocytopenia and monocytopenia, Prevent neutrophil adherence to endothelium, Inhibit action of chemotactic factors
2. Interferes with macrophage antigen processing, blocks the actions of lymphokines, inhibits binding to Fc receptors

Toxicity: 1. Suppression of adrenal-pituitary axis (acute adrenal insufficiency on abrupt withdrawal
2. Cushing’s syndrome

Contraindication: in presence of existing infection

Uses: in combination with other drugs in autoimmune diseases and to prevent graft rejection

Prednisolone

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Mechanism: Metabolized to 6-mercaptopurine, a purine antimetabolite that inhibits purine biosynthesis thereby inhibitng DNA synthesis, inhibits De novo AND salvage pathways.

Pharmacology: Orally active

Used to inhibit rejection of transplanted organs and some autoimmune diseases such as rheumatoid arthritis

SE: Bone marrow depression, GI and hepatic toxicity

Azathioprine

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Mechanism: alkylating agent that cross links DNA to kill replicating and nonreplicating cells.

Pharmacology: Toxic effect more pronounced on B cells so more effective in suppressing humoral immunity.
Orally active.

Use: treatment of autoimmune diseases in combination with other drugs.
NOT EFFECTIVE IN PREVENTING GRAFT REJECTION

SE: Bone marrow depression

Cyclophosphamide

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Mechanism: inhibitor of dihydrofolate reductase, inhibits folate dependent steps in purine synthesis, inhibiting DNA synthesis

Use: treat autoimmune diseases

SE: Hepatic toxicity

Methotrexate

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Mechanism: Lymphocyte selective immunosuppressant by inhibiting IMP dehydrogenase (necessary for de novo purine synthesis w no effect on salvage pathway). Lymphocytes cannot make GMP via salvage. More selective than AZA or methotrexate but equally effective

Pharmacology: Orally active
Used with cyclosporine and corticosteroids to prevent renal allograft rejection (allowing lower dose of cyclosporine)

Use: treat autoimmune diseases– rheumatoid arthritis and refractory psoriasis

Contraindications: Active GI disease, reduced renal function and infections. Also pregnancy (loss and congenital malformations)

SE: infection, leukopenia, anemia

Mycophenolate Mofetil

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Mechanism: binds to cellular receptor Cyclophilin and inhibits calcineurin (a calcium dependent phosphatase), blocking activation of transcription factor NFAT necessary for IL 2 production. Blocks T cell helper function.

Pharmacology: Orally active

Use: Prevent rejection of transplanted organs. some autoimmune diseases. more effective than other agents used with fewer side effects

SE: nephrotoxicity. Hepatotoxicity

Cyclosporine

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Mechanism: binds FK binding protein a cyclophilin related protein, same mechanism as cyclosporine. Spectrum is same but 50-100 more potent

SE: less nephro and hepatotoxicity

Tacrolimus

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Mechanism: Inhibits T cell activaiton and proliferation downstream of IL-2. Binds FKBP-12, binds and inhibits mTOR (not calcineurin), this mTOR is a kinase involved in cell cycle progression blocking G1->S transition

Use: Same as cyclosporine. Coating of cardiac stents.

Sirolimus

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Mechanism: Irreversible inhibitor of cyclooxygenase 1 and 2.

Uses:
Cancer?
CV disease (low dose)
Fever, pain, (intermediate dose)
Chronic inflammatory disease/rheumatoid arthritis (high dose)

SE: Typical NSAIDs side effects + Salicylism + Reye’s Syndrome

Pharmacology:
Non COX inhibition effects (1. Uric acid excretion 2. CNS 3. Respiration)

At low dose decrease uric acid secretion. at high dose increase uric acid excretion.
CNS (b/c crosses BBB) delirium psychoses, nausea, vomiting.
Respiration (Direct stim of respiratory center to increase RR, leading to respiratory alkalosis, compensated by a renal excretion of bicarbonate.
Salicylism
Reye’s syndrome (liver failure and death related to viral epidemics

Acetylsalicylic Acid/Aspirin

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Mechanism: Reversible inhibitor of COX 1 and COX 2. Naproxen has a much longer plasma half life (14 hr vs. 2) than ibuprofen

Uses:
Both: Rheumatoid disorders (including juvenile rheumatoid arthritis), osteoarthritis, mild-to-moderate pain, dysmenorrhea, fever,
Ibuprofen: Inflammatory diseases, IV preparation to induce closure of PDA in premature infants less than 32 wk gestational age when usual treatments ineffective.
Naproxen: manage ankylosing spondylitis, acute gout/bursitis/tendonitis,

SE: Less GI effects than Aspirin

Ibuprofen and Naproxen

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Mechanism: Reversible inhibitor of COX 1 and COX 2

Uses:
gout
preterm labor (investigational)
IV form used for closure of patent ductus arteriosus in neonates,
not routinely used to treat pain or fever.

SE: Frequent adverse rxns, CNS severe frontal headache, better tolerated if given at night

Indomethacin

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Mechanism: Reversible inhibitor of COX 1 and COX 2

Uses:
Alternative for opioid analgesics in treatment of post-operative pain (short term, and much more effective for pain than inflammation)

SE: Serious adverse effects

Ketorolac

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Mechanism: Active metabolite (6methoxy2naphthylacetic acid) is reversible inhibitor of COX2 moreso than COX-1.

Uses:
Osteoarthritis
Rheumatoid arthritis

SE: Well tolerated with less GI effects

Nabumetone

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Mechanism: Reversible inhibitor of COX 1 and COX 2. SUPER LONG HALF LIFE plasma T1/2 50 hours Uses: Symptomatic treatment of acute and chronic rheumatoid arthritis and osteoarthritis, advantage in osteoarthritis treatment because of LONG HALF LIFE. SE: GI toxicity

Piroxicam

Mechanism: 5-aminosalicylic acid (mesalamine) active component linked to sulfapyridine (a sulfa antibiotic) by azo bond (which prevents absorption in upper GI tract). NOT CYCLOOXYGENASE INHIBITION. Possibly inhibition of IL-1, TNFalpha, lipoxygenase pathway, scavenging of free radicals oxidants, inhibition of NF-kappaB. Uses: Mild or moderately active ulcerative colitis (b/c of mesalamine) Rheumatoid arthritis and ankylosing spondylitis (b/c of sulfapyridine) SE: High % for b/c sulfa moiety Allergic rxns (rash, fever, hepatitis, pneumonitis, hemolytic anemia, bone marrow suppression) Decreases number and motility of sperm Therapeutic application: mild or moderately active ulcerative colitis, rheumatoid arthritis, and ankylosing spondylitis

Sulfasalazine

Mechanism: COX-2 selective inhibition. Metabolized by CYP450 2C9 ``` Uses: Rheumatoid arthritis and osteoarthritis Primary dysmenorrheal Management of acute pain reduce # of intestinal polyps in familial adenomatous polyposis (COX2 contributory to certain cancers) ``` SE: Hypersensitivity Increase risk in GI irritation, ulceration, bleeding Increased risk of adverse CV thrombotic events Anemia (rare) ``` Contraindications: Sulfonamide toxicity Prior NSAID hypersensitivity CV risk factors/disease GI disease Coronary artery bypass graft surgery CYP2C9 deficiency ```

Celecoxib

Mechanism: No aff for COX1 or COX2 active site. inhibits reduction of COX to peroxidase form, brain selective? COX3? Metabolized partially by liver microsomal system (CYP2E1, CYP1A2, CYP3A4), but mostly by glucoronidation and sulfation (95%) Uses: Treatment of mild-to-moderate pain and fever; does not have antirheumatic or anti-inflammatory effects SE: Well tolerated with little to no GI issues at normal doses. But with excessive use results in hepatic toxicity... evidenced by elevated liver enzymes like aminotransferase. NAPQI (N-acetyl-p-benzoquinoneimine toxicity if glutathione reduced), covalently binds amino acids in proteins and enzymes. N-acetylcysteine used to replenish glutathione stores to manage toxicity. Contraindication: Ethanol use, as alcohol induces CYP450 (producing NAPQI) and depletes glutathione.

Acetaminophen

1st generation with most sedative effect | Uses: Allergies, Motion sickness, Sleeping, Early stage Parkinson's disease

Diphenhydramine

1st generation | Uses: Allergies, Motion sickness, Vestibular disturbances

Dimenhydrinate

1st generation

Chlorpheniramine

1st generation | Uses: Allergies, Motion sickness, Chemotherapy induced nausea and vomiting

Promethazine

2nd generation | NOT metabolized by P450

Fexofenadine

2nd generation | Metabolized by CYP450 to desloratadine

Loratadine

2nd generation with most sedative effect | Active metabolite of hydroxyzine

Cetirizine

H2 receptor antagonist | Has the most potential for adverse effect due to inhibiting P450 metabolism

Cimetidine

H2 receptor antagonist

Famotidine

H2 receptor antagonist | Also inhibits P450 metabolism but to less of an extent than Cimetidine

Ranitidine

Mechanism: Stabilizes mast cell membrane to prevent release of histamine. Uses: Chronic control of asthma and prophylaxis of bronchospasm (allergen or exercise induced). NOT A RESCUE MEDICINE Nasal formulation for allergies Opthalmic formulation for conjunctivitis Oral formulation for systemic mastocytosis (significant increases in mast cell numbers in the skin and internal organs) Off label uses for food allergy and irritable bowel syndrome SE: Safe drug/few side effects

Cromolyn sodium

Mechanism: IgG monoclonal antibody for which the antigen is the Fc region of the IgE antibody. Forms omalizumab-IgE complexes ergo no affinity for FcRI Uses: Decreases amount of antigen specific IgE that normally binds to and sensitizes mast cells, SE: Injection site reaction, anaphylaxis after the first dose and in some cases >1 year after initiation of regular treatment.

Omalizumab

5-HT2 receptor agonist. Hallucinogen

lysergic acid diethylamide

5-HT1A receptor partial agonist- antianxiety

buspirone

Agonist for 5-HT1D receptor on cerebral blood vessels. Promote vasoconstriction. Treatment of migraine headaches, stops existing ones. SE: nausea, vomiting, angina, dizziness, flushing

sumatriptan

Serotonin specific reuptake inhibitors (SSRIs), block active reuptake of serotonin. Increases amount of transmitter in synapse. Uses: Treatment of affective disorders,, OCD, panic attacks. SE:Sexual dysfunction nausea etc.

fluoxetine

Monoamine oxidase inhibitor, block metabolism of serotonin, NE, and DA. Increased synaptic serotonin. Uses: Treatment of affective disorders and narcolepsy SE: hypertensive crisis

phenelzine

5-HT2 antagonist, also histamine H1 antagonist. Uses: Treatment of allergies, pruritis, urticaria. Carcinoid.

cyproheptadine

5-HT3 antagonist, CNS and GI action Uses: Treatment of chemotherapy induced nausea and vomiting, post op and x ray therapy induced nausea and vomiting

ondansetron

Selective 5-HT3 antagonist Uses: treat diarrhea predominant IBS in women. SE: Can produce severe GI adverse effects. A restricted prescribing program must be followed

alosetron

Syntheized from serotonin in pineal. Own receptors M1, M2- Gi associated Uses: Entrains circadian clock, target for insomnia treatment.

Melatonin

Vasodilator drugs

Nitroglycerin, Nitroprusside, Hydralazine, Minoxidil, Diazoxide, Ca2+ channel blockers, Verapamil, Diltiazem, Milrinone, Inamrinone, Cilostazol, Sildenafil, Tadalafil, ACE inhibitors, Fenoldopam, Prazosin

Bronchodilator drugs:

Albuterol, Pirbuterol, Terbutaline, Salmeterol, Formoterol, Ipratropium, Tiotropium, Theophylline, Aminophylline

Mechanism: Generation of nitric oxide, activating guanylate cyclase, increasing cGMP, resulting in relaxation. Venous dominant, Uses: Heart failure Effects: hypotension

Nitroglycerin/Isosorbide Dinitrate/Isosorbide-5-mononitrate

Mechanism: NO releasing, guanylate cyclase action, increase cGMP, relaxation. Arterial/venous both affected Use: hypertensive emergencies SE: hypotension

Nitroprusside

Mechanism: Unknown. Direct vasodilator Uses: Heart failure patients, pill with Isosorbide dinitrate (works on venous circulation), working on arterial circulation. Severe/emergencies hypertension.

Hydralazine

Mechanism: K+ATP channel opening. Works on arterial circulation. Direct vasodilator Uses: Severe hypertension and hair growth for males. SE: Fluid retention (so use with diuretics)

Minoxidil

Mechanism: K+ channel opener, efflux of K+ leads to hyperpolarization, closing Ca2+ channel, preventing contraction Uses: in hypertensive emergencies (and hypoglycemia) and in hypoglycemia

Diazoxide

Ca2+ Channel blockers

Examples: Nifedipine, Verapamil, Diltazem Mechanism: Block the L-type Ca2+ channels. Non selective, and affect arterial circulation, block Ca2+ influx. Heart vs. Vascular Smooth Muscle: PKA phosphorylates Ca2+ channel causing influx and contraction. Versus. PKA phosphorylates and inactivates MLCK, normally activating by phosphorylation Myosin light chain.

PDE3 inhibitors

Milrinone, inamrinone, cilostazol Intracellular signaling Used for heart failure (and dilate vacular smooth muscle)

PDE5 inhibitors

Sildenafil, tadalafil Intracellular signaling Erectile dysfunction

Mechanism: Vasodilator on endothelial through action on B2 receptor through release prostaglandins, nitric oxide, and epoxygenase metabolites. Increased by ACE inhibitor. (because ACE breaks down bradykinin). *SO A LITTLE DIFF THAN AT1 RECEPTOR BLOCKER*. Works on both arterial and venous circulation

Bradykinin

Mechanism: Dopamine 1 receptor agonist. Arterial and venous circulation Use: Good for hypertensive crisis. Renal blood flow and Na excretion increased

Fenoldopam

Mechanism: Vasodilator that blocks NE acting on Alpha-adrenergic receptors. Arterial and venous circulation

Prazosin

B2 adrenergic agonists

Bronchodilators Examples: Albuterol (most widely used), Pirbuterol, terbutaline, Simeterol, Formoterol Mechanism: Beta 2 agonist causes rise in cAMP/PKA resulting in relaxation. Also acts on Calcium activated potassium channels to cause Potassium efflux and hyperpolarization and relaxation. SE: Cardiotoxicity-tachycardia (Beta 2 on the cardiac smooth muscle)

Anti cholinergic bronchodilator

Bronchodilators Examples: Ipratropium, tiotropium Mechanism: Block muscarinic receptors, blocking a contraction pathway. (Acetylcholine acting on M3 receptor typically causes contraction) Use: Can also be used for inhibiting mucous secretion

Methylxanthine

Bronchodilator Examples:Theophylline, aminophylline Mechanism: Adenosine receptor antagonism and phosphodiesterase inhibition. Increasing cAMP leading to bronchodilation. Also inhibits Adenosine from causing bronchoconstriction. Use: Good for mucous clearance, antiinflammatory actions, prevent edema by decreasing permeability.

ACE inhibitors

Examples: captopril, enalapril, lisinopril Improves CHF survival, regardless of BP Increases Bradykinin levels, resulting in increase in Nitric oxide and Prostaglandins Decreases MAP when Angiotensin I given Does not change MAP when Angiotensin II given Does not change MAP when NE given Increases decrease in MAP when Brady kinin given (enhances bradykinin response) Does not change loss in MAP when other vasodilators given SE: Cough and rash (due to elevation in bradykinin), Taste disturbance, rarely an allergic reaction resulting in angioedema (life threatening, and thus CANNOT USE ACE INHIBITOR. CONTRAINDICATION) Pharmacology: Racial differences in antihypertensive response (Blacks less response to ACE inhibition or angiotensin renin system. Thus the first antihypertensive you would prescribe is diuretic. Cauc/asian have same response to either)

Renal Vasodilators

Examples: Dopamine, Fenoldopam, Caffiene, Atriopeptins Mechanism: Selectively dilates renal vasculature that modifies proximal tubular function. Increases RBF with no change to GFR, decreasing filtration fraction, resulting in decreased proximal tubular sodium reabsorption which is compensated by more distal nephron segments limiting diuretic effect Therapeutic uses: Limited, hypertensive crisis and shock

Osmotic Diuretics

Examples: Mannitol Mechanism: (1. Freely filtered. 2. Not reabsorbed. 3. Metabolically inert) Given IV, act in tubular lumen as nonreabsorbable solute, Urine volume and Na+ excretion are proportional to osmotic load. Thus increased urinary excretion of sodium, potassium, chloride, water, and mannitol. Therapeutic uses: Edema, glaucoma, acute renal failure SE: Related to volume overload and expansion of intravascular fluid volume. Also a rare hypersensitivity

Inhibitors of carbonic anhydrase

Examples: Acetazolamide Mechanism: Weak diuretic Inhibited by acidosis-limits clinical use Filtered and secreted by Organic Acid Transporter, acts from tubular lumen Inhibits Carbonic anhydrase in the proximal distal tubule (which normally provides H+ ions for bicarbonate reabsorption) Increases excretion of Na+, K+, bicarbonate, H2O Alkalinize the urine ``` Therapeutic uses: Glaucoma Alkalize the urine for decreasing drug toxicity Altitude sickness Anticonvulsant ``` SE: Metabolic acidosis and Hypokalemia

Loop diuretics

Examples: Furosemide, Bumetanide, Etharynic acid Mechanism: High efficacy (20-30%) Rapid in onset and short duration of action (20 min) Na+ K+ 2Cl- Symport inhibitors Filtered and secreted by the OAT Acts on the cortical and medullary segments of the ascending limb of the loop of Henle Increase the excretion of sodium, potassium, chloride, and water Increases the renal blood flow and GFR Enhances calcium excretion Large urine volume Therapeutic uses: Edema of cardiac, hepatic, or renal origin, Acute pulmonary edema Hypertension ``` SE: Hypokalemia Alkalosis Hypovolemia Hyperuricemia Hyperglycemia (furosemide only) Ototoxicity ```

Thiazide diuretics

Examples: Chlorothiazide, Hydrochlorothiazide, Metolazone ``` Mechanism: Intermediate efficacy Moderate onset (60 min) Long duration Filtered and secreted by the OAT Inhibits Na-Cl symporter Acts on cortical segment of distal tubule Increases excretion of Na+ K+ Cl- H2O Urine is hypertonic-unable to dilute Increases K= secretion Enhances urate reabsorption (PT) ``` Therapeutic uses: Edema due to CHF Hypertension Hypercalcinuria/Ca salt-renal caliculi ``` SE: Hypokalemia Alkalosis Hyperuricemia Hyperglycemia Decrease in GFR ```

Potassium sparing diuretics

Examples: Spironolactone, Eplerenone (Aldosterone antagonists): Block aldosterone action on collecting duct Triamterene, Amiloride (Na+ channel inhibitors): Block Na+ entry into principal cells of the collecting duct ``` Mechanism: Low efficacy Weak diuretic Increases Na+ excretion without K+ loss Increase Na+ excretion Decrease K+ excretion Increase urinary excretion of sodium, chloride, and H2O ``` Therapeutic uses: Edema Hypertension Seldom used alone but with thiazide or loop diuretics to enhance naturesis without potassium loss Aldosterone antagonism improves survival in heart failure SE: Low efficacy Hyperkalemia if used alone, thus usually used with thiazide Gynecomastia (spironolactone>>eplerenone) Triamterene decreases RBF and GFR Na+ channel inhibitors-mild azotemia