J Letchford Lec 5 Inhibs of protein synthesis Flashcards
Inhibitors of protein synthesis include Am_______
e.g g_____, ami____, tobra_____, str______
Gentamicin, amikacin, tobramycin, streptomycin
Amino glycosides are used _._for serious infections from a____ bacteria
e.g se____, co____ ___, nosocomial ___
These antibiotics are active against many G_ve incl P_____
Active against some G_ve incl St_____
Streptomycin used for _ _, mycoplasma
Aerobic
Septicaemia, complicated UTI, nosocomial RTI
G-ves incl Pseudomonas
G+ves incl Staphylococci
TB, mycoplasma
Inhibitors of protein synthesis include A________s
MOA and PK:
- Bind the __S subunit
- ____ assembly of initiation ____ and binding of ____ in A site
- . or . and _______ for wounds
- 1/2 life of - hours
- Crosses placenta but poor penetration inside cells and ___
- _____ excretion
Aminoglycosides
Bind the 30S subunit (not in mammals)
Decrease assembly of initiation complex and binding of tRNA in A site
I.V or I.M and topically for wounds
t1/2 of 2-3 hours
CSF
Renal
Side effects of Gentamicin, A_____, Tobramycin, Streptomycin (A________s):
N_______
O_______
_____ daily doses least toxic
MONITOR
Amikacin
Aminoglycosides
Nephrotoxic
Ototoxic (damages 8th cranial nerve)
Single daily doses
Inhibitors of protein synthesis include T_______.
e.g D____, M_____, Tig______.
These can sometimes be used as an alternative to macrolide and B-lactams
Used in A____, R__, C_____, SSTIs, mycoplasma and periodontal disease
MANY S________ and S________ are now resistant
Tetracyclines
Doxycycline, minocycline, Tigecycline
Acne, RTIs, Chlamydia, Skin and soft tissue infections
Staphylococci and streptococci
Inhibitors of protein synthesis include T_______.
MOA and PK
Bind __s ribosomal subunit and _____ ____ binding to _ site.
- ____ administration
- Abs ____ by _____ and neutral/high pH
- Well distributed incl foetal circulation but NOT ___.
- Accumulation in bile
- Excreted in bile and kidney
Tetracyclines
30S ribosomal subunit and decreases tRNA binding to A site
Oral admin
Decreased by cations (milk, food, antacids)
CSF
SE’s of tetracyclines:
- GIT effects - why is this?
(Candida albicans, Proteus, Pseudomonas)
- Deposition in forming _____/_____ so not used in preg or under __ years
- Kidney and liver damage
- Headache/vertigo
- _____toxicity
- Due to alteration of the usual bacterial flora in the gut
- Bone/teeth (stain teeth)
- 12 years
- Phototoxicity (skin red)
Inhibitors of protein synthesis include M_____/K_____
These can be used as an alternative to penicillin for treating step infections
e.g E_____, A______, C______
Used orally or I.V for R__, S__, G_, S___
K____ include: T_____
This is a more potent macrolide and is designed to overcome _____.
Macrolides/Ketolides
Erythromycin, Azithromycin, Clarithromycin
RTI, STI, GI, SSTIs
Ketolides (kept group) include Telithromycin
Resistance
Erythromycin is a M______.
MOA: binds __S subunit to ____ _____ and release of _____.
PK:
- Oral or I.V
- Acid labile: so given as _____ _____ capsule or tabs
- Rapidly abs and distributed but not in the ____
- Metab in ____ and t 1/2 _hrs
- Excreted in bile
Macrolide
50S subunit to decrease translocation and release of tRNA.
Enteric coated
CSF
Liver
t1/2 = 2hours
Side effects of Tetracyclines include:
GIT effects: direct and \_\_\_\_\_\_\_ Cholestatic jaundice Reversible O\_\_\_\_\_ Allergic reactions Cardiac effects
Superinfection
Ototoxicity
Inhibitors of protein synthesis include L_____:
e.g Cl_____ (Cleocin)
Used IV, IM or orally for St_____ bone and joint infections, RTIs, peritonitis and sep_____
SE’s:
AB associated d_____
Associated with pseudomembranous colitis caused by _.___
More active against gram _ve bacteria
Lincosamides
Clindamycin
Staphylococcal bone and joint infections
Septicaemia
AB associated diarrhoea
C.diff
Positive (cocci)
Inhibitors of protein synthesis included O______.
e.g L______
This is an orally active, synthetic antimicrobial possessing a bacteriostatic action against g_ve organisms with no activity against g_ves.
Active against e.g: M___, Vancomycin Resistant E_______(VRE).
Oxazolidinone’s
Linezolid
G+ve
G-ves
MRSA
Vancomycin resistant enterococci (VRE)
Linzolid is an O_______.
It works by binding __S ____ in 50S subunit
This decreases assembly of the _____ _______.
- It is given i.v or orally
- Rapid and extensive abs
- Wide distribution
- peak levels - hours after oral dose
- ____ excretion
Oxazolidinone antibiotic.
23S rRNA in 50s Subunit
Initiation complex
1-2 hours after oral dose
Renal excretion
SE’s of Linezolid:
- Mild: GIT, hypersensitivity, headache
- Severe: Ps\_\_\_\_\_\_ \_\_\_\_\_\_ Severe allergic reaction Thro\_\_\_\_\_\_\_ Pan\_\_\_\_\_\_ Neuropathy
Pseudomembranous colitis
Thrombocytopenia (decrease in platelets)
Pancytopenia (reduction red and white blood cells)
Fusidic acid is a _____ spectrum antibiotic for S______ infections.
Gram-negative ____ are completely resistant
BUT active against ____.
It affects EF-G which supplies ____ for _____.
Binds EF-G:GDP complex to ribosome ______ translocation of ____.
Used topically for skin and eye infections
Used orally or IV infusion for os_____ and en______.
Narrow spectrum antibiotic
For Staphylococcal infections
Gram negative bacilli = resistant
MRSA
Energy translocation
Decreasing translocation of tRNA
Osteomyelitis and endocarditis
