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92 Cards in this Set
- Front
- Back
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MI & Angina treatments: |
Decrease workload/ O2 demand |
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Three families of anti-anginal agents |
Organic nitrates Beta-blockers Calcium channel blockers |
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Three types of Angina Pectoris |
Chronic Stable Angina (exertional) Variant angina (Prinzmetal's) Unstable angina |
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Fast acting Nitro |
Fast: Nitrostat Slow: Isordil Bind vascular SM receptor > |
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Six adverse effects of nitrates |
1. Hypotension (worse with alcohol) 2. Orthostatic hypotension 3. Headache/flushing 4. Dizzy 5. Dilates bronchial/uterine/urethral/GI SM 6. Reflex tachycardia |
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Six routes of admin. for Nitrates |
1. IV 2. Oral sustained-release (isosorbide dinitrate) 3. Sublingual 4. Topical 5. Transdermal delivery system 6. Translingual spray |
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3 important teachings for Nitrates |
1. don't expose it to air, heat, or moisture 2. check expiry, it becomes inactive over time 3. don't give with other hypotensive drugs |
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5 adverse effects of Beta Blockers for Angina |
1. Asthmatic effects 2. Bradycardia 3. Caution with diabetes 4. Decreased AV conduction 5. Reduced contractility |
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Three Calcium channel blockers used for Angina |
1. Diltiazem 2. Verapamil 3. Nifedipine |
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3 adverse effects of Calcium Channel Blockers for Angina |
1. Hypotension 2. Reflex Tachycardia 3. Bradycardia |
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4 phases of a clot |
1. Platelet aggregation 2. Platelet-fibrin plug 3. Clot retraction 4. Fibrinolysis |
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Clot life cycle: 7 Steps of platelet aggregation |
1. platelet adhesion to site of injury 2. platelet activates and releases serotonin 3. serotonin causes vasospasm 4. cyclooxygenase changes to thromboxane A2 5. TXA2 binds other platelets + ADP 6. platelets change shape, bind glycoprotein IIa/IIIb receptors 7. glycoprotein IIa/IIIb bind with fibrinogen and platelets aggregate |
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Clot life cycle: 4 Steps of Platelet-fibrin plug formation |
1. Activated platelets & damaged tissue stimulate coagulation cascade 2. Fibrin is incorporated into the plug 3. traps platelets/RBCs to plug damage 4. lays mesh for new epithelial cells |
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Clot life cycle: Steps of Clot Retraction & Fibrinolysis |
1. Platelet proteins contract pulling clot tight 2. ruptured edges together, endothelial cells multiply and damage is repaired 3. fibrinolysis pathway activated during plug formation by plasminogen activators in endothelial cells 4. plasminogen activator turns plasminogen into plasmin 5. plasmin degrades fibrin |
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MOA of IV Heparin - High Doses |
Activates antithrombin III Suppresses fibrin formation and limits extension of thrombi |
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Why is Heparin normally given as IV or s/c? |
It's not absorbed well from the GI |
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When dosing Heparin you should measure aPTT every _________ hours until therapeutic and stable, then daily. |
4-6 1.5-2 |
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3 adverse effects of IV heparin: high doses |
1. Hemorrhage (10%) 2. Heparin-induced thrombocytopenia Protamine sulfate |
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MOA of s/c Heparin: Low Doses |
Binds to endothelium, causing local anti-thrombin III activity (no change in aPTT) Binds to platelets and decreases activation |
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What are the two low-molecular weight heparins |
Lovenox/ Enoxaparin 1. no aPTT monitoring, can use fixed dose schedule, so good for home therapy 2. less incidence of thrombocytopenia 3. costs more but less lab tests and hospital stay |
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MOA of Warfarin (Coumadin) Therapeutic uses? |
Competes with Vitamin K at the same sites in the liver to inhibit production of clotting factors. Interferes with synthesis of factors VII, IX, X, prothrombin that require Vit K. MI, Atrial Fib., Heart valve disease/replacement, pulmonary embolism, venous thrombosis, systemic embolism |
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Warfarin (Coumadin): Antidote: |
1-3 days 5-7 days 2-3 IM vitamin K |
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3 Antiplatelet drugs: 1. Cyclooxygenase inhibitor 2. ADP receptor antagonist 3. ADP receptor antagonist |
1. Aspirin (ASA) 2. Ticlopidine (Ticlid) 3. Clopidogrel (Plavix) |
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MOA of ASA - antiplatelet drug Keep below ______ mg/day |
irreversibly blocks COX 1 (&2) so TXA2 can't be synthesized. 325 mg/day |
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MOA of Clopidrogel (Plavix) - antiplatelet drug ________ mg/day; route ____ effects in _____ hours Platelet function & bleeding time return to baseline in _________ days after last dose |
irreversibly inhibits ADP-mediated platelet aggregation 75, PO, 2, 7-10 |
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Prototypical Statin used for LDL lowering: MOA |
Lovastatin (Mevacor) inhibits HMG CoA reductase, which is needed to make LDL. increases LDL receptors in the liver, so less LDL in circulation. |
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Cholesterol synthesis occurs primarily in the _________ so you should give statins in the _________. Route ________. |
Night eventing PO |
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When starting a patient on Lovastatin (Mevacor), they are at slight risk for hepatotoxicity. Therefore you must check their liver function every _________ weeks for ______ months, then check every ___________ weeks. |
4-6 3 6-8 |
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Chemicals against invading organisms: Produced by one mincroorganism that harms other microbes: Any agent, natural or synthetic, that has ability to kill or suppress microorganisms: |
Chemotherapy Antibiotic Antimicrobial Agent |
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__________ agents kill microbes __________ agents slow down their growth enough that WBCs and immune system can overcome the invaders |
Bactericidal Bacteriostatis |
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4 Ways microbial resistance occurs: |
1. increase production of metabolizing enzymes 2. cease active uptake of certain drugs 3. change drug receptors decreasing binding 4. synthesize compounds that antagonize drug action |
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Explain how selection pressure favours growth of newly resistant microbes. |
Microbes compete for nutrients to survive. Killing off the non-resistant microbes frees up the nutrients for the resistant microbes. |
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Preferred drug for Staph. Aureus: resists methicillin (MRSA) |
Vancomycin |
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Preferred drug for Streptococcus Pneumoniae - Resists Pen G |
Cefotaxime |
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What three factors may rule out a drug of first choice? |
1. allergy
2. inability of drug to penetrate site of infection 3. unusual susceptibility to toxicity - pregnancy/ age/ site of infection/ host defences |
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What are the three appropriate indications for prophylactic antibiotic use? |
1. surgery 2. bacterial endocarditis 3. neutropenia (recurrent UTIs in young women) |
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An infection that appears during the course of treatment for a primary infection. |
suprainfection |
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These broad spectrum drugs are the first drugs available for systemic tx. of bacterial infections. Primary use is UTIs. |
Sulfonamides |
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MOA of sulfonamides for bacterial infection |
Bacteriostatics. Inhibits synthesis of folic acid - needed for DNA/RNA/Protein synthesis. Microbes only synthesize Folic Acid using PABA. Thus f's with PABA so you don't get Folic Acid. |
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4 adverse effects of sulfonamides |
1. hypersensitivity rxns 2. kernicterus-bilirubin toxic to brain 3. renal damage - crystallization 4. hematologic effects |
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Sulfonamides can cause inhibition of hepatic metabolism of what three drugs? |
Warfarin Dilantin Oral hypoglycemics |
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Two classes of sulfonamides: Routes for each. Which one is safer? Water solubility? |
Short acting: PO, IM, IV, or s/c, high Intermediate acting: PO only, low |
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This broad-spectrum anti-microbial agent is used to treat respiratory, urinary, GI tract, bone, joint, and soft tissue infections. It has mild side effects, and resistance is slow to develop. |
Fluoroquinolones |
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Prototypical Fluoroquinolone and its MOA |
Ciprofloxacin inhibits bacterial DNA gyrase, needed to supercoil circular DNA. Without that, it can't replicate and the bacteria fkin dies babay. |
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Cipro route, dose, and half life |
oral or IV 250 - 500 mg BID 4 hours |
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Cipro adverse effects for GI: 3 CNS: 4 Elderly: 3 Candida infections of: 2 |
Nausea, vomiting, diarrhea dizzy, confused, headache, restless confusion, psychosis, visual disturbances vagina and pharynx |
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Cipro increases the plasma levels of what 2 drugs? |
theophylline and warfarin cationic |
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MOA of Metronidazole (Flagyl) |
taken up, converted into active form in anaerobes. Causes DNA strang breaks, loss of helical structure = can't make nucleic acids = death |
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Two side effects of Flagyl |
metallic taste in mouth dizzy |
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Used for protozoal infections and those caused by anaerobic bacteria mostly in GI or deep tissue. Route is IV initially. |
Flagyl |
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When given with tetracyclin, this bactericidal drug eradicates h.pylori for people with PUD |
flagyl |
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3 categories of anti-virals |
1. Purine nucleoside analogs 2. Hep B and C 3. Influenza |
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This anti-viral is used for the herpes virus family! (Herpes, varcilla-zooster, cytomegalovirus) In immunocompromised pts its given: |
Acyclovir topical, PO, IV IV |
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MOA of Acyclovir for virus' |
suppresses synthesis of viral DNA decreases symptoms |
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Adverse effects of acyclovir: GI: 3 CNS: 3 Topical: 2 IV: 1 How to reduce nephrotoxicity |
Nausea, vomiting, diarrhea dizzy, headache, vertigo burning, stinging phlebitis infuse IV slowly over 1 hour, hydrate well during and for 2 hrs after |
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Flu vaccine begins to protect ________ weeks after admin and lasts for _______ months. Only ____ in elderly. Targets ____ strains. |
1-2 6 4 3 |
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Who should get vaccinated for the flu? |
Age 6-23 mo. 6mo. and older - LT health problems or weakened immune system >50 yo Nursing home residents, HCPs, living in dormitories |
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Amantadines MOA against the flu What's used for Influenza B? MOA? |
Fights Influenza A by preventing its penetration of host cells, and inhibits viral uncoating. Tamiflu targets both. Inhibits neuraminidase, viral enzyme needed for rep. |
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MOA of Pen G |
inhibits transpeptidases > no cross-linkage occurs of peptigoglycan chains> Bacterial autolysins also activated> together they disrupt cell wall synthesis. promotes cell wall destruction> Cell lysis = bactericidal |
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Is penicillin more effective against Gram neg or positive bacteria? |
Gram positive. Penicillin can't penetrate the cell envalope of Gram negative bacteria. |
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What is the main part of penicillins that is destroyed in resistant bacteria? |
The beta-lactam ring by beta-lactamase/penicillinases |
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1. Narrow spectrum: penicillinase sensitive 2. Narrow spectrum: penicillinase resistant 3. Broad spectrum (3) 4. Extended spectrum (2) |
1. Pen G 2. Cloxacillin 3. Ampicillin, Amoxicillin, Bacampicillin 4. Ticarcillin, Pipercillan |
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1. How is Pen G given? Why? 2. half life? 3. Adverse effects? What % of pts. |
1. IM, IV only; destroyed by stomach acid 2. 30 minutes 3. Allergy in 1-10% |
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Three types of Pen allergy and their time? What other drug type should you avoid? |
1. Immediate 2-30 min 2. Accelerated 1-72 hours 3. Late days to weeks Cyclosporins |
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What makes Pen V different from Pen G? |
Can be taken with food. Stable in stomach acid, can be given PO. Food reduces chemical irritation to the gut. |
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1. What is the primary target for extended-spectrum penicillins? 2. Prototype? 3. Route? |
1. pseudomonas aeruginosa (antipseudomonal) 2. Piperacillin 3. IV or IM 4. Gentamicin |
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MOA of cephalosporins? |
Binds to penicillin-binding proteins> Disrupts cell wall synthesis/activates autolysins> Cell wall destroyed & cell dies from lysis |
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What is the difference in antimicrobial use of Cephalosporins from 1st gen to 4th gen? |
Increased:
1. activity against Gram - germs 2. resistance to destruction by beta-lactamases 3. ability to reach |
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Cephalosporins: Interactions? Adverse effects? Route? |
1. if taken with alcohol = vomiting and GI distress 2. Allergy, bleeding, throbophlebitis at IV site 3. IM, IV, soooome PO |
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Indication and MOA of Vancomycin |
Indication = antibiotic-related pseudomembranous colitis (C.diff), MRSA, srs infections if pts are alergic to penicillins binds to precursor molecules for cell wall > inhibits cell wall synthesis > Weakened cell wall = lysis = bacteriocidal ***Doesn't interact with PBPs |
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Vancomycin route: Rate and dilution: Adverse effects: (3) |
IV 1 hr, in 250 mL Ototoxicity, thrombophlebitis at IV site, allergy (allergy is rare) |
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MOA of Aminoglycosides: |
binds to 30S ribosomal subunit of bacteria > blocks init. of protein synth/term. protein synth> causes misreading of genetic code> synthesis of faulty proteins (bactericidal) |
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3 Aminoglycosides |
1. Gentamicin 2. Amikacin 3. Tobramycin |
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Indications for Aminoglycosides. Narrow or broad spectrum? What can't it be used on? |
Serious infections due to aerobic Gram Neg. Narrow spectrum Can't be used on anaerobes because it uses O2 to cross the cell wall. |
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Aminoglycosides: Route: |
Parenterally or topically - not absorbed in GI tract |
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Aminoglycosides: Loading dose: Maintenance dose: Why use either |
1. 15 mg q24h - quicker therapeutic effect, quicker to reach plateau levels. 2. 5 mg q8h - to keep blood levels in therapeutic range |
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Aminoglycosides: Gentamicin When should serum blood levels be taken? IV: |
- 30 minutes after IM injection OR - right after a 30 minute IV infusion |
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______________: the highest blood level achieved from a dose - should be in the therapeutic range |
Peak levels |
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____________: lowest blood level achieved before giving the next dose. Important to achieve washout of ______ and _________ to avoid ___________ and _______________. |
Trough Kidneys Hair of the cochlea Nephrotoxicity Ototoxicity |
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Aminoglycosides: Gentamicin Checking for proper trough levels, what time do you draw blood? q8h maintenance dose: |
prior to next dose once at 2 hr, once at 12 hr post infusion |
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Aminoglycosides: Gentamicin Isn't metabolized, putting pt at risk of nephrotoxicity and ototoxicity, SO why give over tobramycin or amikacin? |
Cheaper. Moulah babay. |
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MOA of Beta-2 Adrenergic Agonists for Asthma |
selectively activates Beta-2 receptors > Acts on smooth muscle of lungs> Bronchodilation/ H1 release suppression> Increased ciliary action/motility **Opposite effect on vascular smooth muscle |
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Beta-2 Adrenergic Agonists for Asthma Short acting prototype: Onset: Peak: Duration: Route & Dose: |
Ventolin O: 5-15 min P: 30-60 min D: 3-5 hr R&D: 2 puffs q4-6hr PRN |
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Beta-2 Adrenergic Agonists for Asthma Inhaled Long acting prototype: Dose: |
Salmeterol (serevent) 2 puffs q12hr |
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Beta-2 Adrenergic Agonists for Asthma Oral Long acting prototype: Dose: |
Terbutaline (Brethine) 5 mg PO TID |
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Five common side effects of beta-2 agonists |
1. Tachycardia 2. High FOC 3. Vasoconstriction 4. Angina 5. Tremors/Diaphoresis/Agitation |
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Methylxanthines for asthma: Prototype: Indication: Route: Effects (3) |
Theophylline (Theodur) chronic asthma Orally 1. CNS excitation (vasoconstriction) 2. Bronchodilation 3. Diuresis |
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What makes Theophylline so dangerous compared to other asthma drugs? |
1. narrow TP range 2. Many interactions (caffeine, cigarettes) (drugs like antibiotics & anticonvulsants, it increases their effectiveness) |
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Theophylline normal blood levels: mild effect blood levels: adverse effects blood levels: |
<20 mcg
20-25 mcg >30 mcg |
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Theophylline mild effects: adverse effects: |
N&V Diarrhea Insomnia Restlessness severe dysrhythmias (Vent. Fib) convulsions death |
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MOA of glucocorticoids |
bind & stabilize mast cells > block phospholipase A activity> decrease synthesis & release of H1, Lt's> decreased infiltration & activity of eosinophils> decreased infiltration & activity of leukocytes> decreased edema in airway mucosa> suppressed inflammation |
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Two examples of glucocorticoids Routes: Ling term adverse effects: |
Flovent, Pulmicort PO, IV Infection (less defensive response), fluid & electrolytes (Na H2O retention, K+ loss), Hyperglycemia (phuks wit glucose production) slows children's growth ****only give to children when all else fails |
