Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Inflammatory Drugs
Kaplan
| Question | Answer |
|---|---|
| What are the stimulants of the H/K+ channel on Parietal cells? (3) And which is INHIBITORY? (1) | 1. Histamine (H2 receptor) 2. Ach (muscarinic receptor) 3. Gastrin ( G receptor) INHIBITORY: Prostaglandin (PG receptor) |
| Which drugs are the H2 (histamine) antagonists ? (3) | “-tidine” 1. Famotidine (preferred, less s/e) 2. Cimetidine (p450 inhibitor) 3. Ranitidine (discontinued) |
| What is a major side effect of Cimetidine? | P450 inhibitor which DECREASE production of androgens and cortisol ( —> gynecomastia and libido) *p450 enzymes form androgen + cortisol |
| What are the PPIs? And MOA | “-prazole” Omeprazole MOA: directly and irreversibly bind to H/K pump |
| MOA of Misoprostole | PGE1 analog. Increase mucus and bicarbonate secretion and decrease HCl (gastro protective) |
| Sucralfate (peptic ulcer drug) MOA | Polymerizes on GI luminal surface to form gel like prortective coating of ulcer beds. REQUIRES ACIDIC pH so it can work |
| Bismuth subsalicylate MOA and side effect | MOA (same as Sucralfate) forms gel like protective coating on ulcer beds Side effect:BLACK tongue and stool AVOID IN KIDS, same effect as Aspirin |
| What are the Antacids (3) and their MOA | 1. Al Hydroxide (OH) 2. Mg Hydroxide (OH) 3. Ca CO3- Calcium carbonate MOA: neutralize protons in gut lumen (they are bases) Se: Al - constipation Mg- diarrhea (mg= must go) |
| What are the receptors that an antiemetic medication blocks ? ( 4) | 1. 5HT3 ("-setron") 2. D2 3. M1 4. NK1 (neurokinin, receptor to substance P) |
| What are the receptors that an antiemetic medication stimulate? | CB1 (cannabinoid receptor) |
| What is a cannabinoid agonist? | Dronabinol |
| What are the serotonin receptor(5HT3,)ANTAGONIST? (2) | “-setron” 1. Odansetron 2. Granisetron |
| Which drug is NK1 receptor antagonist? | “-pitant” APREPITANT NK 1 receptor to substance P found on spinal cord) |
| Antiemetic DA2 antagonist?(2) | 1. Prochlorperazine 2. Metoclopramide |
| Antiemetic H1 antagonists? (3) | 1. Diphenhydramine 2. Meclizine 3. Promethazine can also have can have muscarinic block efects and sedation |
| Antiemetic muscarinic antagonist? (1) | Scopolamine |
| What are the 2 drugs used in Chron’s disease and Ulcerative colitis? | 1. Mesalamine (aka 5ASA) 2 Sulfasalazine ( composed of 5 ASA) If these do not work go for immunosuppressants |
| Where is serotonin synthesized and stored? (3) | 1. GI cells (neurochromaffin cells) 2. Neurons ( Raphe nuclei) 3. Platelets 5 hydroxyindoleacetic acid (5HIAA) is its metabolite, broken down by MAO-A |
| All 7 serotonin receptor subtype all are G coupled EXCEPT for… | 5HT3 is coupled to ion channel (in area postrema) |
| Sumatriptan and other triptan's work at which serotonin receptor and MOA? | 5HT 1b and 1d. MOA: 1. decrease substance P and CGRP (calcitonin gene related peptide)release in the PRESYNAPTIC 2. Vasoconstrictions Used in ACUTE MIGRAINES (they are agonists) |
| Olanzapine and other atypical antipsychotic drugs work on which serotonin receptor subtype. Receptor? | 5HT2 (a-c) |
| What is the difference in COX 1 and 2 in the sense of their activity? | COX 1 = constitutive (Always on) - found in most tissues COX 2= Inducuble (needs to be activated) - found in brain, kidney, site of inflammation COX 2 is the main COX to block in inflammatory states |
| What are PGE1 analog? (2) | 1. Misoprostol (protects gastric mucosa) 2. Alprostadil (maintains PDA and used in male impotence LOCALLY) so it can be used with nitrates |
| What are the PGE2 analog? (1) | Dinoprostone (uterine smooth muscle contraction) |
| What are the PGF2a? (2) | 1. Carboprost 2. Latanoprost (treatment for glaucoma) |
| What is a PGI2 analog? | Epoprostenol Platelet stabilizer and vasodilator USED in PULMONARY HTN |
| What are the two subtypes of prostaglandins that are INCREASED in dysmenorrhea (Painful periods) ? | PGE2 and PGF2 |
| What is the mechanism of TXA2? | Platelet aggregator |
| What is the relationship of “free” calcium and platelet? | HIGH free calcium: platelet AGGREGATION LOW free calcium: platelet STABILIZATION |
| Where does NSAIDs work? | Nonselective inhibitors of cyclooxygenases, work on COX1 and 2. they are: Analgesic, Antipyretic and Antiinflammatory |
| MOA of Acetylsalicyclic Acid (Aspirin)? and what makes it irreversible? | IRREVERSIBLY inhibits of COX (irreversible d/t covalent bond via acetylation of serine hydroxyl group at active site) Actions are dose dependent Low:inhibit platelet aggregation Moderate: analgesic + antipyresis High: anti inflammatory |
| What is an “early” and “late” sign of Aspirin overdose? | Early: Respiratory alkalosis (compensated) Late: Metabolic acidosis |
| What are some unique side effects of Aspirin (compared to other NSAIDs)? | GI ulcers Salicylism: tinnitus, vertigo, decrease hearing Retention syndrome Increased bleeding time (low platelet) |
| How is Aspirin overdose treated? (Time dependent) | < 1 hour: Gastric lavage Few hours: INCREASE excretion |
| What are some other NSAIDs (reversible inhibitors)? | Naproxen Ibuprofen Indomethacin Ketorolac / Tromethamine(best analgesic of all) Sulindac |
| What are the selective COX 2 inhibitors? (2) | 1. Celecoxib 2. Meloxicam They have fewer GI side effects compared to conventional NSAIDs |
| MOA of Acetaminophen | NO inhibition of COX but has similar analgesic and antipyretic activity of NSAIDs |
| Acetaminophen gets metabolized by what? (2 pathway) | 1. Phase 2 metabolism mostly (GLUCURONIDATION and SULFATION) 2. Phase 1 a little (by P450) Metabolism by P450 results in NAPQI |
| How does NAPQI gets metabolized to an inactive metabolite? | Via GSH (glutathione, which is limited supply) |
| NAPQI is toxic which part of the liver | CENTRILOBULAR (causes necrosis there) That is known as the Zone 3 and where P450 is found thus drug gets metabolized there |
| How is Gout treated (Acute vs Chronic) ? | Acute: treat pain and inflammation Chronic: treat uric acid by DECREASE production, INCREASE excretion or INCREASE metabolism |
| What is the drug of choice for acute gout? (2) | Colchicine and steroids |
| What is the MOA of Colchicine | MOA: DECREASE microtubular polymerization |
| What is the drug of choice to treat chronic gout? (5) | 1. Allopurinol 2. Febuxostat 3. Pegloticase 4. Probenecid 5. Rasburicase |
| MOA of Allopurinol and FEbuxostat? (Chronic gout) | inhibits Xanthine Oxidase —> decrease purine metabolism and uric acid |
| What are the 2 mechanism that we treat Asthma? | 1. Bronchodilators 2. Anti-inflammatory drugs Early asthmatic response are associated w/ bronchospasm (dt histamine and leukotrines) Late asthmatic response involve eosinophils and lymphocytes into airway (inflammatory) |
| What are the 3 substances that cause bronchoconstriction? | 1. Acetylcholine 2. Adenosine 3. Leukotrines |
| What are the (3/4) drugs that inhibit bronchoconstrction and by what mechanism? | 1. Ipratropium (inhibits acetylcholine) 2. Theophylline (inhibits adenosine) 3+4. "-lukasts" and Zileuton (inhibits leukotrienes) |
| What type (SABA or LABA) B2 agonists are used for ACUTE asthma attacks and which for PROPHYLAXIS? | SHORT ACTING (SABA) for Acute asthma attacks LONG ACTING (LABA) for PROPHYLAXIS (but glucocorticoids are preferred for prophylaxis) |
| What are the Short acting B2 agonists? (3) | 1. Albuterol 2. Metaproterenol 3. Terbutaline |
| Formoterol MOA | Rapid onset and long lasting (mix between SABA and LABA) |
| What are the choice of drug group in bronchospasm caused by B-blockers (in asthmatic pt)? | MUSCARINIC RECEPTOR BLOCKERS 1. Ipratropium (short acting) 2. Tiotropium (long acting) causes bronchodilation |
| Theophylline MOA (2) | 1. antagonism of adenosine (a bronchoconstrictor) 2. INHIBITS phosphodiesterase --> Increase cAMP (which causes bronchodilation) most dangerous asthma drugs bc of LOW TI |
| Cromolyn and Nedocromil MOA (athma drug) | PREVENT DEGRANULATION OF pulmonary MAST CELLS Omalizumab has similar MOA but used in severe asthma |
| Glucocorticoids MOA (in asthma) | Block mediator release AND decrease brochial hyperreactivity (via decrease prostaglandins, leukotrines and inflammatory interleukins) |
| S/E of glucocorticoids (used for asthma)? | Oropharyngeal candidiasis (oral thrush) dt drug deposits in the mouth. |
| Zileuton MOA | selective inhibitor of LIPOXYGENASES (LOX) decrease all Leukotrines. |
| Zafirlukast and Montelukast (Antileukotrines) MOA | Antagonists at LTD4 receptors |
| Roflumilast MOA | PDE4 inhibitor that increase cAMP in proinflammatory cells and decrease inflammation. |
| What are the 2 Glucocorticoids that HAS aldosterone effects? | 1. Hydrocortisone 2. Prednisone |
| Which 3 Glucocorticoids does NOT have aldosterone effects? | 1. Betamethasone 2. Dexamethasone 3.Triamcinolone |
Created by:
DVD27