Week 4 Antibiotics, Antivirals, Antifungals, pharmacology and inflammation


Nursing Flashcards on Week 4 Antibiotics, Antivirals, Antifungals, pharmacology and inflammation, created by Elizabeth Then on 09/09/2017.
Elizabeth Then
Flashcards by Elizabeth Then, updated more than 1 year ago
Elizabeth Then
Created by Elizabeth Then over 6 years ago

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Question Answer
Whats are they? pneumonia: bacteria- antibiotics HIV: virus-antivirus Thrush: candidosis-antifungal
Anti-infectives mechanism in body anti-infective-effector/delivery system-desired organisn-body undesired
Mechanism of action: efficacy inhibit cell wall synthesis= bactericidal e.g. penicillin, cephalsporins disrupt cell membrane= bactericidal or bacteriostatic e.g antifungals inihibit metabolism = folic acid bacteriostatic=trimethoprim sulphamethoxazole inhibit protein synthesis, bacteriostatic=tetracyclines, macrolides bactericidal= gentamicin
antibiotics spectrum of activity: efficacy (2) narrow spectrum: active against a few species, ben pen, gram + moderate spectrum: active against several species, amoxycillin Broad spectrum: effective against many species, tetracyclines
Narrow spectrum better why? because of antibiotic resistance, doesn't kill good bacteria as well
anti-infectives-immune system antibiotics don't cure infections, immune system does. antibiotics just kill enough bacteria and slow down their growth, especially bacteriostatic
Antibiotics efficacy (3) time-dependent killing: time above minimum inhibitory concentration (MIC) concentration-dependent killing: depends on dose higher the peak
Antibiotics: harmful effects GI, nausea, vomiting, diarrhoea, CNS superinfection, candidosis, thrush hypersensitivity: interaction with antigens-rash, anaphylaxis antibiotic associated colitis, penicillins, tetracyclines WHY? prevent access to microbe microbe produces destructive enzyme microbe changes drug binding site etc
principle use of antibiotics use narrowest specturm, use single drug, use dose high enough to achieve efficacy, and minimise dose-related toxicity
antibiotic use: prophylaxis do not exceed 7 days single dose of antibiotics
Duration of therapy single dose: prophylaxis short course: 5 days, UTIS longer course: 5-10 days, pnenmonia, cellulitis prolonged course: more than 10 days, endocarditis, tuberbulosis
Penicillins bactericidal= inhibit cell wall synthesis safety: diarrhoea, nausea/vomiting
Pencillins narrow spectrum ben pen: IM, IV, not acid stable, endocarditis, meningitis, pneumonia Phenoxymethyl pencillin: tonsillitis, skin infections, acid stable benzathine penicillin: IM, long-acting, rheumatic fever prevention procaine penicillin: resp tract infections, IM
Penicillin moderate spectrum amoxycillin/amppicillin more effective against gram - than ben pen oral or IV use: pneumonia, chronic bronchitis, sinusitis
Penicilllins: broad spectrum amoxycillin and clavulanic acid adverse effect: rash, hepatitis cholestatic
B-lactams: narrow-wdie spectrum, interferes with bacterial cell wall synthesis, bacteriacidal, can cause allergy/ hepatotoxicity
Aminoglycosides inhibits bacterial protein synthesis, bacteriacidal, gram - infections, can cause ototoxicity, nephrotoxicity
Macrolides inhibits bacterial protein synthesis, bactericidal, gram + and - infections, can cause otoxicity/ nephrotoxicity
Quniolones inhibits bacterial DNA synthesis, bactericidal, broad spcetrum, serious infections
Tetracyclines inhibits bacterial protein synthesis, bacteriostatic, broad spectrum
lincosamides inhibits bacterial protein synthesis, bacteriostatic, gram +
Antibiotics, which one? use narrow specturm use safest and short duration use dose hgih enough to reach MIC but avoid resistance routes oral dont use in combination and prophylaxis
Antivirals multiple daily dosing influenza A and B: block viral uncoating or neuramidinases of virus HIV protease inhibitors cause drug-drug interactions due to inhibition of metabolism (CYP3A enzyme) adverse effects, nausea, diarrhoea, CNS disturbances
Antifungals azoles safe topical drugs for skin, nail, vaginal, oral and IV admin
What is inflammation? non-specific response to injury pain, redness, swelling, white blood cells
Mediators involved in inflammation Prostaglandins, histamine, bradykinin, cytokines, PAF, PGS from arachidonic acid mediated by COX enzyme two isoforms COX 1 and COX 2
COX -1 involved in physiological function (gastric mucosal integrtiy, platelet homeostasis, regulation of renal blood flow
COX -2 involved in inflammatory reactions and inflammatory pain, and fever located in endoplasmic reticulum and nuclear membranes
Prostaglandins steps 1. cell damage, hormone stimulation causes release of arachidonic acid 2. prostaglandins synthesised form arachidonic acid 3. initial steps catalysed by COX enzyme 4. prostaglandins are released during inflammation: acute inflammation chronic inflammation
Prostaglandin receptors major role in inflammatory process fever induction pituitary function renal function gastric mucosal integrity
Steriodal agents potent side effects act via modulation of gene transcription decrease production of COX takes 24-48 hrs to have effect mostly used in chronic inflammation
Non-steroidal agents use in relief of pain, arthirtis, headache, inflammation, rapid effects.
NSAIDS 3 major effects anti-inflammatory, analgesic, antipyretic
NSAIDS adverse effects peptic ulcer GI bleeding skin rash
Non-selective COX-1inhibitors produces prostaglandins involved in physiological functions: platelet homeostasis, gastric mucosal integrity, renal blood flow e.g. aspirin, blocks both COX-1 and COX-2, good and bad PGs side effects: GIT erosion, bleeding, skin rash, prolonged bleeding
Non-selective COX-2 inhibitors blocks only COX-2, bad PGs, reduced GIT effects produce prostaglandins, involved in inflammatory reactions and pain
Corticosteroids anti-inflammatory and immunosuppressive effects potent anti-inflammatory effects, with significant adverse effects, infection, osteoporosis, reduce in cytokines
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