10272856
Description
Flashcards by Elizabeth Then, updated more than 1 year ago
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Created by Elizabeth Then
about 7 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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