Flashcards
Week 4 Antibiotics, Antivirals, Antifungals, pharmacology and inflammation
Cards in this deck (37)
- 1Whats are they?pneumonia: bacteria- antibiotics
HIV: virus-antivirus
Thrush: candidosis-antifungal - 2Anti-infectives mechanism in bodyanti-infective-effector/delivery system-desired organisn-body undesired
- 3Mechanism of action: efficacyinhibit 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 - 4antibiotics 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 - 5Narrow spectrum better why?because of antibiotic resistance, doesn't kill good bacteria as well
- 6anti-infectives-immune systemantibiotics don't cure infections, immune system does.
antibiotics just kill enough bacteria and slow down their growth, especially bacteriostatic - 7Antibiotics efficacy (3)time-dependent killing: time above minimum inhibitory concentration (MIC)
concentration-dependent killing: depends on dose higher the peak - 8Antibiotics: harmful effectsGI, 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 - 9principle use of antibioticsuse narrowest specturm, use single drug, use dose high enough to achieve efficacy, and minimise dose-related toxicity
- 10antibiotic use: prophylaxisdo not exceed 7 days
single dose of antibiotics - 11Duration of therapysingle dose: prophylaxis
short course: 5 days, UTIS
longer course: 5-10 days, pnenmonia, cellulitis
prolonged course: more than 10 days, endocarditis, tuberbulosis - 12Penicillinsbactericidal= inhibit cell wall synthesis
safety: diarrhoea, nausea/vomiting - 13Pencillins narrow spectrumben 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 - 14Penicillin moderate spectrumamoxycillin/amppicillin
more effective against gram - than ben pen
oral or IV
use: pneumonia, chronic bronchitis, sinusitis - 15Penicilllins: broad spectrumamoxycillin and clavulanic acid
adverse effect: rash, hepatitis cholestatic - 16B-lactams:narrow-wdie spectrum, interferes with bacterial cell wall synthesis, bacteriacidal, can cause allergy/ hepatotoxicity
- 17Aminoglycosidesinhibits bacterial protein synthesis, bacteriacidal, gram - infections, can cause ototoxicity, nephrotoxicity
- 18Macrolidesinhibits bacterial protein synthesis, bactericidal, gram + and - infections, can cause otoxicity/ nephrotoxicity
- 19Quniolonesinhibits bacterial DNA synthesis, bactericidal, broad spcetrum, serious infections
- 20Tetracyclinesinhibits bacterial protein synthesis, bacteriostatic, broad spectrum
- 21lincosamidesinhibits bacterial protein synthesis, bacteriostatic, gram +
- 22Antibiotics, 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 - 23Antiviralsmultiple 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 - 24Antifungalsazoles
safe topical drugs for skin, nail, vaginal, oral and IV admin - 25What is inflammation?non-specific response to injury
pain, redness, swelling, white blood cells - 26Mediators involved in inflammationProstaglandins, histamine, bradykinin, cytokines, PAF,
PGS from arachidonic acid mediated by COX enzyme
two isoforms COX 1 and COX 2 - 27COX -1involved in physiological function (gastric mucosal integrtiy, platelet homeostasis, regulation of renal blood flow
- 28COX -2involved in inflammatory reactions and inflammatory pain, and fever
located in endoplasmic reticulum and nuclear membranes - 29Prostaglandins steps1. 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 - 30Prostaglandin receptorsmajor role in
inflammatory process
fever induction
pituitary function
renal function
gastric mucosal integrity - 31Steriodal agentspotent side effects
act via modulation of gene transcription
decrease production of COX
takes 24-48 hrs to have effect
mostly used in chronic inflammation - 32Non-steroidal agentsuse in relief of pain, arthirtis, headache, inflammation, rapid effects.
- 33NSAIDS 3 major effectsanti-inflammatory, analgesic, antipyretic
- 34NSAIDS adverse effectspeptic ulcer
GI bleeding
skin rash - 35Non-selective COX-1inhibitorsproduces 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 - 36Non-selective COX-2 inhibitorsblocks only COX-2, bad PGs, reduced GIT effects
produce prostaglandins, involved in inflammatory reactions and pain - 37Corticosteroidsanti-inflammatory and immunosuppressive effects
potent anti-inflammatory effects, with significant adverse effects, infection, osteoporosis, reduce in cytokines
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- Nursing Flashcards on Week 4 Antibiotics, Antivirals, Antifungals, pharmacology and inflammation, created by Elizabeth Then on 09/09/2017.
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