Antimicrobial agents 110821 Flashcards Preview

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Flashcards in Antimicrobial agents 110821 Deck (34)
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1
Q

name some beta lactam antibiotics

A

penicillins
cephalosporins
carbapenems

2
Q

How do beta lactams work

A

bactericidal. Inhibit cell wall synthesis by being a substrate to penicillin binding protein

3
Q

Why might beta lactams not be effective

A

if the cell wall has already been formed or if the bacteria does not have a peptidoglycan cell wall e.g. mycoplasma, clamydia

4
Q

Describe how penicillin works

A

works against Gram +ve streptococci, clostridia

broken down by beta lactamases which are produced by staph aureus etc

5
Q

Describe amoxicillin

A

Broad spectrum to enterococci and gram -ve

6
Q

Flucloxacillin

A

effective against STAPH AUREUS as it is NOT broken down by beta lactamase produced by SA

7
Q

Piperacillin

A

broad spectrum (pseudomonas, non-enteric gram -ve, broken down by beta lactamase

8
Q

Clavulanic acid and tazobactam

A

beta lactamase inhibitors,

9
Q

Name some examples of Cephalosporins

A

Ceforoxime, ceftriaxone, ceftazidime

10
Q

What is the significance of the generations of cephalosporins

A

Increasing activity against gram negative bacilli

11
Q

ceftazidime vs. ceftriaxone vs. cefotaxime

A

ceftriaxone (associated with c. diff, treat meningitis, no cover against pseudomonas); ceftazidime (activity against pseudomonas), cefotaxime (paediatric ceftriaxone)

12
Q

Do cephalosporins work against ESBL producing organisms

A

No they don’t - use carbapenems

13
Q

what are Carbapenems used for

A

Stable against ESBL producing organisms

14
Q

Examples of CARBAPENEMS

A

Meropenem, imipenem, ertapenum

15
Q

What are examples of beta lactams

A

penicillins, cephalosporins, carbapenems, monobactams

16
Q

Key features of beta lactams

A

o Relatively non-toxic
o Renally excreted so decrease dose if renal impairment
o Short T1/2 (many are type 2 drugs so aim to maximise the time > MIC)
o Will not cross BBB
o Cross allergenic – penicillin has 10% cross reactivity with cephalosporins and carbapenems

17
Q

Glycopeptides

A

Active against gram +ve, large molecules so unable to penetrate gram -ve.
Slowly bactericidal
nephrotoxic

18
Q

Important uses of glycopeptides

A

MRSA, c dif

19
Q

Why must you monitor glycopeptides

A

nephrotoxic

20
Q

Examples of glycopeptides

A

Vancomycin
Teicoplanin
Telavancin

21
Q

Give examples of antibiotics that inhibit protein synthesis

A

aminoglycosides, tetracyclines, macrolides, cloramphenicol, oxazolidinones

22
Q

Aminoglycosides, examples, MOA

A

• Aminoglycosides – gentamicin, amikacin, tobramycin
o Bind to amino-acyl site of 30s ribosome subunit
o Rapid, concentration-dependent bactericidal
o Require specific transport mechanisms to enter
 Accounts for some intrinsic resistance
o Ototoxic and nephrotoxic – monitor levels
o Gentamicin and tobramycin are particularly active against pseudomonas aeruginosa
o Synergistic combination with beta lactams
 Endocarditis treatment, pneumonia
o No activity against anaerobes

23
Q

Tetracyclines

A

o Broad spectrum, activity against intracellular pathogens – chlamydia, rickettsia, mycoplasma
o Bacteriostatic (stops bacteria from reproducing)
o Widespread resistance now
o Deposited in growing bone
 Don’t give to children, pregnant women
o SE: photosensitivity rash (summer effect)
 Particularly doxycycline

24
Q

Which protein synthesis inhibitor should you NOT give to children and pregnant women

A

Tetracyclines as it deposits in growing bone

25
Q

Macrolides

A

o Bacteriostatic
o Useful agent for treating mild staphylococcal or streptococcal infections in pen-allergic patients
o Active against campylobacter species, legionella, pneumophilia
o Newer agents include clarithromycin and azithromycin due to a better half-life
o Little activity against gram -ve bacteria (membrane)
o Useful to inhibit toxins produced by bacteria

26
Q

Cloramphenicol

A

o Bacteriostatic
o Broad antibacterial activity
o Rarely used apart from eye preparations
 Risk of aplastic anaemia
 Risk of grey-baby syndrome in neonates because of inability to metabolise the drug

27
Q

Oxazolidinoes

A

o Highly active against gram +ve (MRSA & VRE)
o Not active against most gram -ve

o Expensive, may cause thrombocytopenia & optic neuritis; should only be used with micro/ID approval
o Binds to 23S component of 50s subunit  prevents formation of a functional 70s initiation complex

28
Q

Which antibiotics inhibit DNA synthesis

A

Quinolones and nitromidazoles

29
Q

Nitromidazoles

A

o Under anaerobic conditions, an active intermediate is produced which causes DNA strand breakage
o Rapidly bactericidal
o Active against anaerobic bacteria and protozoa (Giardia)
o Nitrofurans are related compounds (nitrofurantoin is good for cystitis and lower UTIs)

30
Q

Quinolones

A

o Act on alpha unit of DNA gyrase, bactericidal
o Broad antibacterial activity versus gram -ve (pseudomonas aeruginosa)
o Newer agents (levofloxacin, moxifloxin) better against gram +ve and intracellular bacteria (Chlamydia spp.)
o Well absorbed after PO administration (good bioavailability)
o Use for UTI, pneumonia, atypical pneumonia, bacterial gastroenteritis
o Lower your seizure threshold, also causes achilles tendonitis

31
Q

Rifamycin

A

• Rifamycins – rifampicin and rifabutin
o Inhibits protein synthesis by binding to DNA-dependent RNA polymerase, inhibiting initiation
o Bactericidal
o Active against mycobacteria and chlamydia
o Interactions with other drugs metabolised in the liver (OCP) and so need to monitor LFTs
o Turns secretions orange (urine and contacts) – can check compliance

o Rifampicin resistance (never used as a single):
 Resistance due to chromosomal mutation
 Causes single amino acid change in beta subunit of RNA polymerase which fails to bind rifampicin

32
Q

Inhibitors of folate metabolism include

A

• Sulphonamides
o Resistance is common
o Combination of sulphamethoxazole + trimethoprim (co-trimoxazole) is important in treating pneumocystis jiroveci pneumonia (PCP – HIV-defining disease)

• Diaminopyrimidines – trimethoprim
o Used as treatment for community acquired UTIs

33
Q

How does MRSA and strep pneumoniae have resistance to flucloxacillin

A

target modification

34
Q

How do ESBLs have resistance

A

enzyme modification/iniactivation