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69 Cards in this Set
- Front
- Back
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Alpha 2 adrenergic antagonist for Emisis
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Chlorpromazine
A2 ant Dopa ant Histamine ant Cholinergic ant Block Emetic Center and CTZ Slight sedative and used in cats and dogs NOT IN HORSES |
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Antihistamines for motion sickness and antiemesis
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Dimenhydrinate
= Blockade of H1 in CRTZ Sedation is common Not effective in preventing motion sickness in cats (NOT WITH CRTZ) - Ear goes straight to emetic center in cat MEclizine has less sedation |
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Anticholinergic by blocking muscarinic receptor in emetic center
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Scopolamine - topane alkaloid with antimuscarinic activity
Propantheline and Isopropantehline |
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Neurokinin 1 Antagonists
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Maropitant and Aprepitant - Blocks NK1 activation
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Cannabinoids for antiemesis
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THC, more than 60 cannabinoids in canabis, THC is psychoactive ingredient
Binds to CB1&2 GPCRS in many areas of CNS CB1 is very high density |
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Drugs that Make you Emetic - Direct
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Apomorphine and Xylazine
- Apo is nonselective dopa agonist, stims CRTZ, can cause paradoxical excitement in cats = contraindic Xylazine = alpha 2 agonist in cats then mild sedation = dose for emesis is lower than sedation in cats! |
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Peripherally acting emeitcs
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Sodium Chloride
Hydrogen Peroxide Syrup of Ipecac - alkaloid, induces vomiting in 15-30 mins for dogs = DO NOT USE IN CATS! |
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D2 Dopamine Antagonist Antiemesis
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Metoclopramide - Blocks D2 Dopamine to CRTZ - higher doses also blocks 5HT3 (prokinetic within GI)
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5Ht3 Antagonist Antiemesis
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Ondansteron, Granisteron - Block 5ht3 receptors in CRTZ and GI - used for oral control of Nausea due to radiation and chemotherapy
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Opiod Antagonist antiemesis
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Butorphanol - synthetic opiod antagonist - blocks emetic and higher CNS cetners
Sedation is common |
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Short Acting Synthetic Steroids
Med-Acting Long Acting |
Prednisone, Prednisolone, Methylprednisolone - short
Triamcinolone - med Dexamethasone - long |
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Prednisolone
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4-5 x anti-inflammatory activey
70% less mineralcorticoid activity Water Soluable Oral, Topical, Injectable |
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Methylprednisolone
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Methylated C6 of prednisolone
Short acting 4-5 anti-inflammatory activity Low minarlcorticoid activity (very little) oral, topical, injectable |
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Dexamethasone and Betamethasone
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Long Acting - Lower dose, slow onset (6h)
30x Anti-inflammatory activity little mineralcorticoid activity oral, topical, injectable |
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Triamcinolone
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Similar to dexamethasone
Intermediate acting Oral (5x antiinflammatory activity) Topical (5000x anti-inflammatory activity) - acetonid increases surface activity Very little mineralcorticoid activity |
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2 types of therapy for Glucocorticoids
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Short term
- Fast acting to reduce inflammation associated damage - Taper Withdrawl to allow adrenal gland to recover Long Term - Alternate Day Therapy (short half-life drug), ensures less suppression of adrenal gland endogenous cortisol and ACTH - Repositol therapy for CATS, long lasting methylprednisolone acetate and triamcinolone acetonide (weeks to months) |
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NSAIDs
Specifically Aspirin and Salicylates |
Aspirin = 3.5 pKa
Na-Salicylate = 3.0 pka Absorbed in stomacha nd upper small intestine - keeps them in non-ionized form Salicylate binds albumin Esterases in tissue and blood cleave aspirin |
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Aspirin and salicylates
Only NSAID TO DO THIS |
Irreversible Cyclooxygenase inhibitor
Acetylates COX, better for inhibiting Cox-1 than Cox-2 Scavanges Oxygen Free Radicals Platelet effects - inhibit COX-1 and therefore blocks thromboxane development - inhibit agregation and is irreversible till new platelets are formed Glucocorticoids can't do this cause there is no nucleus in RBC or platelets |
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Inactivation of Aspirin
Mechanism, Activity level by species and clearance |
Glucuronic acid conjugation
1h in horses 37h in cats 4 h in dogs Conjugates are cleared via kidney - glutathione if glucuronic acid is absent |
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Adverse Effects of Salicylate
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COX-1 inhibition gastric cytoprotection
- prostaglandins synthesis stimulate bicarb and mucous secretion -Gastric irritation can be decreased by increasing pH or a prostaglandin analogue High Doses - Salicylism, Fever, Dehydration, Renal damage, gen hemorrhage, convulsions or coma |
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Para-Aminophenols
Types What does it inhibit, where, type of inhibition |
Acetaminiphen/Phenacetin
- Reversible COX Compete with arachidonic acid Not really used in antiinflammatory 80% rapidly conjugates to glucuronic acid - Byproduct is toxic |
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Phenylproprionic acids
What are they What do they inhibit |
Ibuprofen
- Selective for Cox-2 (some cox-1) - Toxic to Dogs Naproxen - Equipotent on both COX-1/COX-2 - 74h in dog for T1/2 Carprofen/Etodolac/Deracoxib/Firocoxib - Side effect = PGI decrease which means more thromboxane relative = clotting All copete with aspirin for plasma binding protein, Competitive reversible inhibitors of COX |
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Carprofen
- Official Species Type Inhibitor Solubility Excretability Contraindiciations |
Only in Dogs
Proprionic Acid More Selective for Cox-2 Insoluable in Water and excreted in feces Renal Side effects from COX-1 inhibition (Excess water consumption) Loss of balance and hyperactivity/depression/;aggression Contraindiciations - preexisting liver, kidney, GI disease - other NSAID or corticosteroid drug - Pregnant or nursing females |
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Other NSAIDs
Animal, T1/2, Sideffects, Metabolized |
Etodolac
- Approved for Dogs - T1/2 1-14 hours - Metabolized in Liver/Excreted in feces - Side Effects: gastrointestinal ulceration Deracoxib - Approved in dogs for postoperative pain and inflammation COX 1/2 Ratio Aspirin = 0.28 Etodolac = 3.4 Carprofen = 65 Deracoxib = 1275 Higher the number the more COX-2 specific |
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Flunixin meglumine
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Irreversible Non-covalent COX inhibit
Weak 5-lipox (Leukotrienes) Powerful analgesic Long duration (24-36h) 2h onset action (IV/IM) Horses and Cattle = NOT CATS!! Advantages - more potent than other PG hinibitors - Rapid Action with long action (2 hours of admin) - Useful for relieving pain associated w/ muscoskeletal disorders, surgery, GI spasm (colc) and endotoxic shock Adverse effects - ulceration of mucosa - CNS depression, Acute renal failure? |
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Phenyl butazone
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Irreversibly binds COX
- Oxyphenbutazone is active form (can become hydroxyphenylbutazone as well) - >99% of drub binds plasma proteins - approved for dogs and horses Long Duration (24-72h) - New Cox to synthesize PGs - Excreted via kidneys Orally or IV in dogs and horses Phlebitis if perivascular Adverse Effecs - oral and GI erosions, diarrhea, depression - death if enteropathy -> hypovolumic shock |
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Tepoxalin
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Dual LOX/COX inhibit
Approved for dogs Lipophilic and coverted into an active carboxylated metabolite Hepatic Clearance (12-14h T1/2) Preven Leukotrienes |
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DMSO
Mechanism of Action Route Adverse Effect Random Drug = Orgotein |
Non-Cyclooxygenase inhibitor
Anti-Inflam/analgesi/microb/fungal/diuretic/cholinesterase Scavanges Oxygenated Free Radicals Appears to slow conductance of non-myelinated nerve fibers T/12 Horses = 9hour Halitosis and DMS as a metabolite Topically ONLY!!! Hemolysis when injected IV Adverse - Transports toxins into body - Degranulation of mast cells - Cataracts of dogs - Teratogenic Orgotein - Bovine superoxide dismutase - Scavanges cytotoxic free radicals - Dampens inflammatory response - Not Analgesic Approved for horses and dogs |
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Oxygen Therapy Concepts
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Mixed Venous PO2 is adequacy of tissue oxygenation
- Combination of Oxygen COnsumption, blood flow, and arterial O2 content PAlveolarO2 = PInspiredO2 - 1.2 x PAlveolarCO2 |
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Causes of Tissue Hypoxia
- Pulmonary |
DIffusion Block (Overcome by O2 admin)
Ventilation/Perfusion Inequalities - Lung disease Shunts - blood bypasses lung = no ventilation, small increase in O2 from passive ventilation |
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Causes of Tissu Hypoxia
- Post-pulmonary |
Low Cardiac output
Impaired carrying capacity (Anemia/CO) Impaired O2 release (Low DPG, Low CO2) Cellular and Enzyme Abnormalities Aterial PO2 = Normal/Content may be normal Oxygen therapy more limited since not enough aspects Whole Blood may be of benefit |
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List of Chemical Buffers
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Bismuth Subsalicylate
Montmorillonite Sucralfate |
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Bismuth Subsalicylate
Mechanism of Action |
Chemical diffusion barriers
Bismuth = coats ulcerated mucosal surfaces/absorbs toxins/mild antibacterial action Salicylate = anti inflammatory |
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Montmorillonite
Mechanism of Action |
Smectite Clay
Combines with mucus to form a protective layer on intestinal mucosa High Capacity to absorb and adsorb tocins, bacteria, viruses, enzymes, and free radicals |
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Sucralfate
Mechanism of Action |
Chemical diffusion barrier
Sucros octasulfate polymerized and formas a paster that binds to damaged gastric epithelial cells Formas a physical barrier against stomach acid Binds and inactivated bile salts and pepsin Increase Prostaglandin synth Increase Mucosal blood flow and Increase NO production |
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Acetylcholine Receptor Antagonists
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Used prior to H2-selective antagonists
Atropine would work, but large side effects Pirenzepine |
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Pirenzepine
mechanism of action |
Acetylcholine recepter antagonist
Protective of Stomach Barrier M1-selective antagonist (decreases antimuscarinic-mediated side effects) Location of M1 receptors unknown M3 receptor on parietal cell |
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Histamine Receptor Antagonist
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h1, H2, H3, H4 (GPCR)
H1 = Smooth muscle and endothelium/Vasodilation/Bronchoconstriction/SM activation H2 = Parietal cells and regulates histamine mediated gastric acid secrtion H3 = Inhibitory autoreceptor regulating histamine release H4 = ??? Drugs Cimetidine = h2 antagonist - CP450 Inhibition Ranitidine = 2nd Gen H2 antagonist - CP450 Inhibition (less) Famotidine = 3rd Gen h2 antagonist - no CP450 inhibition Nizatidine = last gen H2 antagonist - no CP450 inhibition |
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Cimetidine
Method of Action Limitations |
H2 selective antagonist
Imidazole on Left of structure, Guanl on right Suppression of gastric acid secetion without H1 side effects Adverse - Inhibits many CP450 enzymes which results in numerous drug interaction (oral contraceptives theophylline, coumadine,benzodiazepens) - Decrease hepatic blood flow = less clearance of drugs such as propranolol and lidocaine |
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Rantidine
Method of Action Limitations |
2nd generation of H2-selective antagonist
less CP450 inhibition Longer lasting than cimetidine 10x more activity than cimetidine |
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Famotidine
Method of action |
Poor bioavailability
30 x more potent than cimetidine and more potent than ranitidine No CP450 inhibition with Famotidine Promotility effects on stomach |
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Pepcid Complete
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Combines Famotidine, CaCO3 and MgOHCO3
The latter two help neutralize acid and also counteract the Ca constipating and Mg diarrhea |
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Nizatidine
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Last gen H2-Selective Antagonist
No CP450 inhibition Primarily excreted unchanged promotility effects on the stomach Thiazole instead of a furan (ranitidine) |
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Gastrin Receptor Antagonists
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Experimental compounds (decreased ethanol-induced damage to gastric mucosa), Gastrin receptor antagonists may have utility as an adjunct therapy to ulcer disease by countering release of gastrin
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H/K/ATPase antagonist (proton Pump)
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Omeprazole
Lansoprazole Esomeprazole Rabeprazole |
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Oemprazole
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Prolonged decrease in gastric acid production = increased stomach pH
- Can lead to bacterial growth and penumonia Sustaine HCl reduction can lead to increased gastrin levels (hypergastrinemia) Can cause parietal cell hyperplasia in animal models the S-Enatiomeris more effective |
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Prostaglandin
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Inhibit gastric acid secretion
Stimulate HCO3 Stimulate mucous Increase mucosal blood flow Decrease local resposne to inflamatory response Misoprostol |
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Misoprostol
Indications/OffLabel uses |
Primary indications
- increase mucous productions for fastric ulcers - Co-admin with nsaids to prevent ulceration Off-Label Uses - Labor induction due to SM contractiion - Abortion - Erectile dysfunction |
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Laxatives and Cathartics
Stimulants Surfactant Laxitive Lubricants Bulk Forming Laxatives Osmotic Agents |
Bisacodyl - Stimulant, effects colon and slow onset
Docusate - surfactant laxative, anionic surfactants that ahve a detergent-like action Mineral Oil - nonabsorb, literally lubricate Dietary Fiber - increasing bulk and stimulates bowl peristalsis Osmotic Agents - Hypertonic and Isotonic - Hypertonic = Mg, Tartate Na, Lactulose, glycerin, sorbitol, mannitol = more water in lumen = dehydrate body by movement into colon - Isotonic = PEG = copious watery stools but no dehydration since no water movement from body MgOH = Diarrhea |
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Antidiarrheal Agents
Rehydration Opioid agonists Bismuth salicylates Kaolin-pectin |
Rehydration helps balance water loss
Opiod - Lperamide/Diphenoxylate = mu and delta opiod receptors to decrease myenteric activation Bismuth Subsalicylate = unknown but don't use in cats Kaolin-pectin = Clay mineral which absorbs water from intestines |
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Anti-emesis
The 4 Brain Center Their Receptors |
CRTZ = D2, 5-HT3, H1, M1, NK1
Vestibular to 2 different paths = pathway to CRTZ or to Emetic Center Emetic Center = Alph2, 5HT1, Opiod Stomach = Ach, 5HT3 |
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Alpha 2 Adrenergic Antagonists
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Chlorpromazine, Prochlorperazine
- Blocks at emetic and CRTZ - Mild sedation due to weak histamine receptor antagonism - No Horses due to ataxia - D2, H1, M1, and Strong Alpha 2 |
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D2 Antagonists
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Metoclopramide
- Blocks D2 at CRTZ - Higher doses = 5HT3 blockage - Still have vomitting due to direct feed from vestibular - prokinetic = muscarinic, D2 antagonism, and 5HT4 agonism Side Effects: Hyperactivity, Tremors, Constipation |
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5HT3 Serotonin Antagonists
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Ondansteron, Granisteron
Anti-emetic from CRTZ and Gastrointestinal cat |
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Opioid antagonists
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Butorphanol
Blocks opiod receptor in emetic receptor and higher CNS |
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Antihistamines
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Dimenhydrinate
Blockade of H1 histamine at emetic Sedation (CNS H1) Not effective in cats - Vestibular center to emetic center directly Meclizine (less drowsy) |
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Anticholinergics
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Scoplolamine - blocks receptors at stomach and in brain
Propantheline, Isoporpamiede - dogs and cats anticholinergic combine with pheno |
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NK1
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Maropitant and Aprepitant
CRTZ! |
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Centrally Acting Emetics
Agonists |
Apomorphine = dopamine AGONIST
Xylazine = alpha 2 agonist |
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Peripherally acting
mechanism |
Salt = High salt content = vomit
H2O2 = vomiting Ipecac = induce vomitting 15-30, do not use in cats All are irritants |
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Types of Diuretics
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Osmotic
Carbonic Anhydrase Inhibit Loop Thiazide Natriuretic K-Sparing Others (Aquaretic/Glomelular) |
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Osmotic
Site Mechanism Response Example |
PCT and Loop of Henle
Osmotic Mechansim (gradients) 20-30% excretion Mannitol/Urea/Glucose |
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Carbonic Anhydrase Inhibitors
Site Mechanism Response Example |
PCT
Inhibits Carbonic Anhydrase 2-3% response Acetazolamide |
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Loop
Site Mechanism Response Example |
Thick Ascending Loop
Inhibit NA/K/2CL cotransport System 25-30% Furosemide, Bumetanide, Ethacrynic acid, Piretanide, Muzolimine |
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Thiazides
Site Mechanism Response Example |
PCT and Early DCT
Inhibit distal Na/Cl transport 5-8% Hydrochlorothiazied, Chlorthalidone, Metolazone |
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Natriuretic K-Sparing
Site Mechanism Response Example |
Late DCT and CT
Inhibit luminal Na permeability and aldosterone action 2-3% Amiloride, triamterene, spironolactone |
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Aquaretic
Site Mechanism Response Example |
CT
Antagonize ADH and inhibit Na transport 1-2% Lithium, demechlortetracycline, ADH antagonists, ANP? |
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Glomerular
Site Mechanism Response Example |
Glomerulus
Vasodilation 0-1% Theophyline, ANP |
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PDGF
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Macrophage, endothelial Cells, Fibroblasts, platelets
Fibroblast chemotaxis and proliferation |
