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Week 120 > Antibiotics - don't do these.. use "fever" below, which has ABx in > Flashcards

Antibiotics - don't do these.. use "fever" below, which has ABx in Flashcards

1
Q

MOA of macrolide? (2)

A

> Bind to 50s ribosome sub-unit and inhibit protein synthesis (block translocation)
BACTERIOSTATIC

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2
Q

Which bacteria are macrolides active against? (7)

A

Gram +ve e.g. staph, strep

Some gram -ve including:
> H flu (not erythro)
> N meningitidis
> Legionella
> Mycoplasma
> N gonorrhoea
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3
Q

What clinical uses do macrolides have? (4)

A

> Skin infections
Respiratory infections including pneumonia, legionella, mycoplasma, H flu, chlamydia
STDs (chlamydia, gonorrhoea)
Any strep / staph infections

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4
Q

Common side effects of macrolides? (5)

A

> N&V
Diarrhoea (erythro ++)
Prolonged QT interval -> arrythmias
Liver dysfunction -> cholestatic jaundice
Increased risk of statin-induced myopathy

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5
Q

Cautions with macrolides? (2)

A

> Patients with risk of QT prolongation e.g. electrolyte disturbances, other medications that prolong QT
Patients with MG (may aggravate)
Patients taking warfarin, theophylline, statins (CYP metabolised drugs)

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6
Q

Which macrolide causes diarrhoea most commonly and why?

A

> Erythromycin

> Due to pro-motility effect

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7
Q

When would a macrolide be used in a non-infection setting, why, and which one?

A

> Erythromycin
Pro-motility
Gastroparesis

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8
Q

Which antibiotics must caution be taken with warfarin and why? What other drugs should be monitored?

A

> Macrolides
Quinolones
INHIBITION of hepatic CYP450 enzymes
Theophylline, statins

> Also Rifampicin but thats the other way, it INDUCES hepatic CYP450 enzymes

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9
Q

What is the dosing regime and routes available for azithromycin?

A

> OD

> PO only

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10
Q

What is the dosing regime and routes available for erythromycin?

A

> QDS or BD

> PO or IV

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11
Q

What is the dosing regime and routes available for clarithromycin?

A

> BD (modified release = OD)

> PO or IV

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12
Q

What are the names of the macrolides, and their routes?

A

> Erythromycin PO/IV
Clarithromycin PO/IV
Azithromycin IV

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13
Q

What are the names of the aminoglycosides? (5)

A 
> Gentamicin 
> Tobramycin
> Amikacin
> Streptomycin
> Neomycin
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14
Q

What is the MOA of aminoglycosides?

A

> Enter bacterial cells via oxygen-dependent transport system
Bind to 30s sub-unit of ribosome to inhibit protein synthesis

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15
Q

Spectrum of aminoglycosides? (1+5+3)

A

> Aerobes only as they require oxygen-dependent transport system

> Gram -ve aerobic rods
e.g. E coli, pseudomonas, klebsiella, proteus, enterobacter

> Gram +ve aerobes e.g. staph, strep, mycobacteria

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16
Q

Routes of administration of aminoglycosides? (3 main points)

A

> Poor oral absorption (highly polar), low lipid diffusion and poor penetration across body membranes so PO not available

> IV or IM injection

> Tobramycin = inhaler/neb

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17
Q

Clinical uses of aminoglycosides?

A

Gentamicin is the aminoglycoside of choice in the UK usually. It’s used in serious infections.

Usually given in combination therapy.

> Endocarditis (gent)
> Bacteraemia / sepsis
> TB (streptomycin)
> S aureus food poisoning
> CF (tobra)
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18
Q

What other antibiotics are aminoglycosides usually administered with and why?

A

Penicillin or a macrolide because they increase the activity of the aminoglycoside and reduce its toxicity

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19
Q

How are aminoglycosides excreted?

A

Renal (urine)

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20
Q

Adverse effects of aminoglycosides?

A

There are many:

> Nephrotoxicity can lead to renal failure
Ototoxicity due to damage of VIIIth cranial nerve causing irreversible deafness and vestibular damage
NMJ breakdown
Headache, fever, dizziness

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21
Q

Why are the aminoglycosides considered more dangerous than many other ABx?

A

Narrow therapeutic window and serious side effects

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22
Q

Contraindications for aminoglycoside use?

A

> Myasthenia gravis

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23
Q

Cautions for aminoglycosides?

A

> Elderly: vulnerable to nephrotoxicity and ototoxicity

> Regular monitoring of serum levels (high peak = lower dose, high trough = longer interval)

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24
Q

Oral absorption, lipid diffusion and membrane penetration of aminoglycosides?

A

> Poor oral absorption
Low lipid diffusion
Poor penetration

Therefore no PO formulations available

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25
Q

Tetracyclines drug names? (4)

A

> Doxycycline
Tetracycline
Oxytetracycline
Minocycline

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26
Q

Tetracyclines MOA?

A

> Protein sythesis inhibitor

> Binds to 30s ribosome subunit - prevents amino acids being added during protein synthesis

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27
Q

Tetracyclines spectrum of activity?

A

> Broad spectrum

> Gram +ve aerobes (staphs & streps)

> Gram -ve rods

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28
Q

Tetracyclines clinical application? (2 main ones in caps, and several others)

A

First line for:

> CAP (LOCALLY)
> Chlamydia infections
> Rickettsia infections
> Brucella
> Borrelia

Also used in:

> ACNE
Respiratory mycoplasma

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29
Q

Cautions associated with tetracyclines administration?

A

> May increase muscle weakness associated MG
May worsen SLE
Forms chelates with Mg/Ca/Al - so not taken with antacids or dairy, and not suitable for children, breastfeeding or pregnant females

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30
Q

Contraindications associated with tetracycline administration?

A

> Not for 1. children under 12 2. pregnancy 3. breast-feeding women, as concentrates within tissues undergoing calcification causing STAINING and occasional DENTAL HYPOPLASIA, and can cause GROWTH STUNTING

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31
Q

Adverse effects associated with tetracyclines?

A

> Phototoxicity reactions

> Irritation of gastric mucosa so take with food (but not dairy)

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32
Q

Why are tetracyclines less commonly used clinically than they were several years ago?

A

> Development of resistance to tetracyclines among many bacteria

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33
Q

Excretion of tetracyclines is via which route?

A

> Excreted unchanged in bile (so via liver)

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34
Q

Are tetracyclines safe for patients with renal impairment?

A

> Doxycycline & minocycline are safe for patients with renal impairment

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35
Q

Are tetracyclines safe for patients with hepatic impairment?

A

> Tetracyclines shouldn’t be used, or should be used with caution in patients with hepatic impairment

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36
Q

Metronidazole MOA?

A

> Direct DNA damage via reactive oxygen species formation

> Bactericidal

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37
Q

Metronidazole spectrum of activity?

A

> Anaerobes e.g. clostridium, h. pylori, bacteroides fragilis

> Protozoa e.g. giardia, amoebae

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38
Q

Clinical application of metronidazole?

A

> Activity against anaerobes e.g. abdominal infections / abscesses, brain/liver abscesses, oral infections, aspiration pneumonia, C diff, bacterial vaginosis

> Protozoal infections e.g. giardiasis, amoebiasis

> GI surgery prophylaxis

> Also polymicrobial infections (as one is possibly going to be anaerobic!)

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39
Q

Does metronidazole have good oral bioavailability?

A

Yes, metronidazole has 100% oral bioavailability

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40
Q

How is metronidazole metabolised?

A

Metronidazole is metabolised by the liver, which means it is excreted in faeces, and needs to be used in caution in those with hepatic impairment

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41
Q

What is “oral bioavailability”?

A

It is the concentration of drug available after oral administration, when compared to intravenous infusion.

E.g. if 100mg of drug X is administered orally and 10mg is within the blood, but 100mg of drug X is administered IV and 100mg is available in the blood, the oral bioavailability is 10/100 = 10%.

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42
Q

Adverse effects of metronidaole? (4)

A

> Metallic taste
Rashes
“Disulfiram effect” (reaction when taken with alcohol)
GI effects e.g. N&V

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43
Q

Safety of metronidazole in pregnancy?

A

Mutagenic especially in 1st trimester, but manufacturer suggests only avoiding high dose regimens

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44
Q

Metronidazole routes available?

A

IV, PO and rectal

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45
Q

Which antibiotic classes shouldn’t be taken with dairy or antacids?

A

> Tetracyclines

> Quinolones

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46
Q

Examples of quinolones? (4)

A

> Ciprofloxacin
Ofloxacin
Levofloxacin
Gatifloxacin

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47
Q

MOA of quinolones?

A

> DNA/RNA synthesis inhibitor by inhbiition of DNA gyrase (topoisomerase II), preventing supercoiling
Bactericidal (eventually degrades DNA after preventing supercoiling if concentration high enough)

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48
Q

Spectrum of quinolones?

A

> Gram +ve and gram-ve

> Particularly active against gram -ve e.g. salmonella, neiserria, pseudomonas, shigella, campylobacter

> Some efficacy against anaerobes (not first line)

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49
Q

Clinical uses of quinolones?

A

> Wide usage

> Respiratory tract infections
> Bone & joint infections
> UTIs (not first line though)
> GI infections
> Gonorrhoea
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50
Q

Oral bioavailability of quinolones?

A

> Good oral bioavailability so can treat severe infections orally (70-90% for cipro)

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51
Q

Excretion route of quinolones?

A

Kidneys primarily

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52
Q

What instructions would you give in regards to taking quinolones?

A

> Not with dairy or antacids as chelates with Ca/Al/Mg/Zn/Fe which can interfere with absorption

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53
Q

What drugs would you monitor the effects of in a patient newly started on ciprofloxacin?

A

Theophylline, warfarin etc

CYP450 inhibition = higher concentrations in blood = possible toxicity

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54
Q

Adverse effects of quinolones? (

A

> Reduces seizure threshold so careful with epilepsy (even worse with NSAIDs)
Tendon damage (may occur within 48h of treatment)
Can prolong QT interval
Confusion/drowsiness/dizziness (driving)
N&V/diarrhoea/headache

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55
Q

Which drug class has synergistic effects on reducing seizure threshold when used concurrently with ciprofloxacin?

A

> NSAIDs

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56
Q

Cautions of quinolones?

A

> Epilepsy history (seizure threshold lowers)
Concurrent NSAIDS (makes seizure A/E worse)
Myasthenia gravis (risk of exacerbation)
Patients with risk of QT prolongation e.g. bradycardia, long QT syndrome
History of tendon disorders related to quinolone use

> Children / adolescents (arthropathy in weight-bearing joints in young animals)

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57
Q

Trimethoprim MOA?

A

> Antimetabolite

> Inhibits bacterial conversion of folate to active folate by inhibition of dihydrofolate reductase

> Bacteriocidal

58
Q

Trimethoprim spectrum of activity?

A

> Enterococci (a gram +ve diplococci species, 90% are E. faecalis)

> Some gram -ves

59
Q

Trimethoprim clinical use?

A

> First line treatment of UTIs

> UTI prophylaxis (low dose at night)

> Pneumocystis pneumonitis?

60
Q

Trimethoprim is first line treatment for what, and why is it so effective?

A

> UTIs

> Because it is in high concentrations in the urinary tract as it is excreted from there unchanged (therefore still active!)

61
Q

What would you give and how, for prophylaxis of UTIs?

A

> Trimethoprim, low dose at night

62
Q

Cautions/contra-indications to trimethoprim use?

A

> Contraindicated in first trimester of pregnancy

(though patient likely to refuse at any stage in pregnancy!)

> Contra-indicated in blood dyscrasias

> Caution in those with pre-disposition to folate deficiency

63
Q

Alternative for UTI treatment if trimethoprim allergic?

A

> Cefalexin or nitrofurantoin

64
Q

Which drug would you want to be sure the patient wasn’t taking if you were going to prescribe trimethoprim, and why?

A

> Methotrexate (anti-cancer)

> Also lowers folate so can cause serious depression of haematopoiesis

65
Q

What is co-trimoxazole?

A

Trimethoprim and sulfamethoxazole

66
Q

MOA of co-trimoxazole?

A

Inhibits folate processing at 2 sequential steps:

> Inhibits dihydrofolate synthetase

> Inhibits dihydrofolate reductase

67
Q

Cautions/adverse effect of co-trimoxazole?

A

Associated with rare but serious side effects such as Stevens-Johnson syndrome & bone marrow depression

68
Q

Clinical use of co-trimoxazole?

A

Pneumocystis jiroveci pneumonia, toxoplasmosis

e.g. in patients with AIDS / immunocompression

69
Q

Absorption of trimethoprim?

A

Rapid and complete oral absoprtion from GIT

70
Q

Glycopeptide drug examples and their dosing regimen?

A

> Vancomycin (BD)

> Teicoplanin (OD)

71
Q

MOA of glycopeptides

A

> Cell wall synthesis inhibitors: bind to cell wall causing blockage of polymerisation of glycopeptide

> Causes secondary damage to cytoplasmic membrane (as well as cell wall synthesis inhibition)

> BACTERICIDAL (because of the cell membrane damage)

72
Q

Spectrum of glycopeptides?

A

> Gram +ve organisms (including B lactamase producing gram +ves)

> Multi-resistant organisms e.g. MRSA

Note that some MRSA now resistant to vancomycin!

73
Q

Clinical use of glycopeptides?

A

> MRSA

> Oral used for C diff if metronidazole doesn’t work or is contraindicated

> Endocarditis (also for prophylaxis before prosthesis insertion)

> Serious gram +ve infections

74
Q

How is the oral absorption for vancomycin?

A

> Poor

> This means that IV is the usual route, except in C diff when oral is suitable (as C diff exists in gut, not within the cells)

75
Q

Excretion of vancomycin?

A

> Renal excretion - dose needs to be adjusted in renal impairment

76
Q

Are the glycopeptides concentration-dependent or time-dependent?

A

Time dependent

77
Q

Adverse effects of glycopeptides?

A

> “red man syndrome” if infused too rapidly (vanc)

> phlebitis if not diluted sufficiently (vanc)

> Nephrotoxicity (particularly in renal impairment and elderly)

> Ototoxicity (particularly in renal impairment and elderly)

> Neutropenia (1w+)

78
Q

Which antibiotics require monitoring of serum concentrations and why? How often would you monitor them?

A

> Glycopeptides (vancomycin particularly)

> Can cause nephrotoxicity and ototoxicity

> Monitor after 3rd or 4th dose in everybody, but even sooner in renal impairment (as renally excreted)

> Also monitor in pregnancy as toxic concentrations can cause fetal harm

79
Q

Are the glycopeptides safe in pregnancy?

A

> If benefits outweigh risk, but serum concentrations must be regularly monitored to prevent toxic doses reaching the foetus

80
Q

What is Rifampicin’s mechanism of action?

A

> Inhibits DNA-dependent RNA polymerase activity in bacterial cells

81
Q

Spectrum of activity of Rifampicin?

A

> Active in mycobacteria (TB)

> Staphylococci including MRSA

> N. meningiditis (nasal carriage)

82
Q

Clinical uses of rifampicin?

A

> TB

> Always used in combination with a second antibiotic to avoid conferring resistance

> Eliminating nasal carriage of N. meningitidis*

> Serious staph infections including MRSA, endocarditis

> Leprosy

  • (so meningitis prophylaxis basically)
83
Q

Which drug causes your bodily fluids to go orange? (Bile, urine, tears, contact lenses)

A

> Rifampicin

84
Q

What cautions are taken with rifampicin?

A

> Hepatic monitoring during treatment

> Those on contraceptive pill (alternative should be taken)

> Warn patient that contact lenses / bodily fluids likely to turn orange

> CYP450 enzyme inducer - may need to alter levels of warfarin, theophylline etc

85
Q

Which antibiotic would require family planning advice to be given in certain situations and why?

A

> Rifampicin

> Effectiveness of hormonal contraceptives are reduced and so alternative family planning advice should be given

86
Q

What significant drug interaction(s) are caused by Rifampicin?

A

> CYP450 induction

> Therefore affects concentrations (lowers them) of warfarin, theophylline, statins etc

87
Q

What are the 1st generation cephalosporins?

A

> Cefadrine
Cefadroxil
Cefalexin

88
Q

What are the 2nd generation cephalosporins?

A

> Cefaclor

> Cefuroxime

89
Q

What are the 3rd generation cephalosporins?

A

> Cefotaxime
Ceftazidime
Ceftriaxone

90
Q

What is the MOA of the cephalosporins?

A

> Interferes with cross-linking of the bacterial cell wall

> Only active in rapidly dividing cells (e.g. not effective in abscesses)

91
Q

Spectrum of cephalosporins

A

Primary coverage (not absolute limitations but a good general rule of thumb):

> 1st gen: Gram +ves (not MRSA)

> 2nd gen: Anaerobes and some gram -ves

> 3rd gen: Gram -ves

> 4th gen: Pseudomonas

> 5th gen: ?MRSA

92
Q

Name 3 first generation cephalosporins and their clinical use

A

> Cefadrine
Cefadroxil
Cefalexin

> Skin and soft tissue infections

93
Q

Name 2 second generation cephalosporins and their clinical use

A

> Cefaclor
Cefuroxime

> Infections that should be self limiting that don’t clear up e.g. otitis media, sinusitis, upper respiratory tract, skin and soft tissue

94
Q

Name 3 third generation cephalosporins and their clinical use

A

> Cefotaxime
Ceftazidime
Ceftriaxone

> Greatest gram -ve activity; meningitis, pseudomonas

95
Q

Which cephalosporin can be used in meningitis due to good CSF penetration? What class is it?

A

> Ceftriaxone

> Third-generation

96
Q

Which cephalosporin is active against pseudomonas? What class is it?

A

> Ceftazidime

> Third-generation

97
Q

Adverse effects of cephalosporins?

A

> 10% of patients allergic to penicillins will be allergic to cephalosporins due to same beta-lactam ring

> Diarrhoea / GI upset

98
Q

Excretion of cephalosporins?

A

> Renal, except ceftriaxone

99
Q

Which cephalosporin is excreted differently to the others?

A

> Ceftriaxone, hepatically

100
Q

Do cephalosporins have good oral absorption?

A

No

101
Q

What is the treatment for TB?

A

RIPE

Rifampicin
Isoniazid
Pyrazinamide
Ethambutol

6 months??

102
Q

Why is benzylpenicillin a treatment for meningitis even though penetration through the healthy blood brain barrier is poor?

A

> When the meninges are inflamed, the BBB is more permeable to penicillins and the drug can reach the CSF

103
Q

MOA of penicillins?

A

> Cell wall synthesis inhibitor - interfering with cross-linking of the cell wall

> Not useful in abscesses as only active during production of cell wall e.g. in rapidly dividing cells

> Bactericidal

104
Q

Excretion of penicillins?

A

> Urine

105
Q

What percentage of patients is hypersensitivity to penicillin prevalent in? (according to the BNF)

A

10%

106
Q

What percentage of patients is anaphylaxis due to penicillins estimated to be prevalent in?

A

0.2%

107
Q

Which individuals are at higher risk of anaphylaxis to penicillins?

A

> Atopic individuals (asthma, eczema, hay fever)

> History of anaphylaxis, rash, urticaria due to penicillins

> Those who had a history of minor rash, or a rash occurring more than 72 hours after penicillins should not have penicillins withheld for serious infectons!

108
Q

Adverse effects of penicillins?

A

> Hypersensitivities are most common e.g. rash, anaphylaxis

> Diarrhoea due to disturbance of bowel flora

> Cholestatic jaundice (Fluclox over 2/52)

> Convulsions/encephalopathy due to cerebral irritation in poor renal function

109
Q

Which drug has a possible risk of causing cholestatic jaundice?

A

> Flucloxacillin (particularly if used for > 2/52)

110
Q

What demographic of patients is at risk of convulsions, and due to which drug class, and why?

A

> Those with impaired renal function

> Due to penicillins

> Impaired renal function means high concentrations can accumulate and cause cerebral irritation which can cause convulsions

111
Q

Which is the adverse effect most commonly caused by penicillins?

A

> Diarrhoea, due to disruption of bowel flora. Can also cause ABx associated colitis.

112
Q

Which commonly used penicillin is best by a non-oral route, what is the route, and why?

A

> Benzylpenicillin (Pen G)

> IV

> Pen G is inactivated by gastric acid and so absorption from the gut is low

113
Q

Spectrum of action of benzylpenicillin?

A

> Gram -ve cocci & bacilli
Gram +ve cocci
Spirochetes eg. syphilis

BUT NOT BETA LACTAMASE PRODUCERS e.g. most staph aureus, and many of the common gram -ve rods!

114
Q

Spectrum of action of phenoxymethylpenicillin (Pen V)?

A

> Gram -ve cocci & bacilli
Gram +ve cocci
Spirochetes eg. syphilis

BUT NOT BETA LACTAMASE PRODUCERS e.g. most staph aureus and many of the common gram -ve rods e.g. E coli, Klebsiella, Proteus

** Note that Pen V and Pen G have basically the same spectrum, Pen V is just PO and Pen G is IV **

115
Q

Clinical use of Pen G?

A 
> Throat infections
> Otitis media
> Endocarditis
> MENINGOCOCCAL DISEASE
> Anthrax

I reckon the main things to remember are that penicillins are given for throaty stuff, endocarditis (as its common caused by gram positives), and a dose of Pen G is given as soon as meningitis is suspected, even before the patient gets to hospital if possible

116
Q

Clinical use of Pen V?

A

> Otitis media
Throat infections e.g. tonsils etc
Some skin infections such as cellulitis
Group A strep infections

I think its important to remember perhaps that Pen G is active against Strep B and Pen V against Strep A. Also that all throaty stuff is generally penicillins.

117
Q

Are penicillins safe in pregnancy / breast feeding etc?

A

Yes

118
Q

What bacteria are particularly known to be beta lactamase producers, and therefore are not treated with Pen V or Pen G? What drug is used instead?

A

> Staphylococci spp.

> Flucloxacillin

119
Q

Clinical use of flucloxacillin?

A

> Only used in staph infections as they are penicillin-resistant

> Otitis externa 
> Impetigo
> Cellulitis
> Pneumonia (in combo therapy)
> Staph endocarditis
> Osteomyelitis

So basically if its on the skin, or endocarditis, its likely to be flucloxacillin as the infective organism is probably a staph.

120
Q

Cautions with flucloxacillin?

A

> Risk of kernicterus in jaundiced neonates

> Risk of cholestatic jaundice in long term use (> 2/52)

121
Q

Adverse effects of flucloxacillin?

A

> Gi upsets

> Cholestatic jaundice

122
Q

Clinical use of amoxicillin?

A

> Broad-spectrum penicillin

> Gram +ve and gram -ves but inactivated by beta lactamases so not useful against Staph, E Coli or H flu

> Acute exacerbations of chronic bronchitis

> Otitis media

123
Q

What is the combination formulation involving amoxicillin, and why?

A

> Co-amoxiclav

> Amoxicillin + clavulanic acid

> Clavulanic acid is a beta lactamase inhibitor so extends spectrum of action

> Used in infections where beta lactamase producers may be likely e.g. S aureus, H flu, E coli, Klebsiella, Bacteroides

124
Q

Clinical use of co-amoxiclav?

A

> Used in infections where beta lactamase producers may be likely e.g. S aureus, H flu, E coli, Klebsiella, Bacteroides

> Respiratory tract infections (particularly nosocomial) - this is the main one to know I think

> Abdominal infections

> Hospital acquired infections

125
Q

What is tazocin?

A

> Piperacillin (beta lactam antibiotic) and tazobactam (beta lactamase inhibitor)

> Extends spectrum

126
Q

What is the use of tazocin?

A

> Hospital acquired pneumonia

> Complicated abdominal infections

> Infections in neutropenic patients

> “Anti-pseudomonal”

** This is a good drug to know - it’s commonly given in the hospital. Imagine an old lady who has been in for a week or so, and she develops a fever and crackly chest. It sounds like pneumonia but because its hospital acquired, the likely cause is aspiration, meaning a gram negative, or a penicillin resistant bacteria, and so tazocin or co-amoxiclav are commonly given **

127
Q

Which class of bacteria do not have a cell wall, and how does that directly impact their susceptibility to certain antibiotics?

A

> Mycoplasma

> Not susceptible to penicillins as they act on the cell wall

128
Q

Which penicillin is “anti-pseudomonal”? (and therefore heavily utilised in nosocomial respiratory tract infections)?

A

> Tazocin

129
Q

How should oral penicillins be taken and why?

A

> 60 minutes before food on an empty stomach

> Absorption is delayed by food

130
Q

Why is delayed absorption particularly harmful in penicillins, and how could this occur? (2 reasons)

A

>

  1. Delayed can mean incomplete absorption if they reach the lower GIT beyond the absorptive region, and so low levels of penicillins = incomplete therapeutic benefit

>

  1. Active drug reaching the lower GIT (colon) can affect bowel flora -> ABx associated colitis

> Delayed absorption can be due to food, hence penicillins should be taken on an empty stomach

131
Q

What drug class are penicillins often prescribed with and why?

A

> Aminoglycosides e.g. gentamicin

> The penicillins boost the efficacy of the aminoglycosides, and lowers their toxic effects (e.g. gentamicin is often given with a penicillin to lower chance of nephrotoxicity and ototoxicity)

132
Q

How are penicillins excreted? >

A

> Renal (urine)

133
Q

What new class of drug is active against multi-resistant microbes and so is reserved only for these purposes?

A

> Oxazolidinones

134
Q

What drugs are within the oxazolidinones class?

A

> Linezolid

135
Q

MOA of linezolid?

A

> Binds to bacterial ribosome 50s subunit preventing formation of functional 70s initiation complex, preventing protein synthesis

> Protein synthesis inhibitor (prevents translation)

136
Q

Spectrum of action of linezolid?

A

> Gram positive bacteria, including MRSA and VRE

137
Q

Clinical uses of linezolid?

A

> Serious infections only, where other antibiotics have failed e.g. refractory MRSA, VRE

(usually skin/soft tissue infections, and respiratory infections)

138
Q

Cautions with linezolid?

A

> Not licensed for Monitor full blood count at least weekly to monitor for signs of haematopoietic suppression

> Monitor optic function as can cause optic neuropathy

> Higher chance of neuropathy and bone marrow suppression in elderly

> Those taking SSRIs, TCAs, MAOIs (serotonin syndrome)

139
Q

Adverse effects of linezolid?

A

> Haematopoietic disorders e.g. thrombocytopaenia, anaemia, leucopenia, pancytopenia - MONITOR FBC WEEKLY … elderly are more vulnerable

> Acts as MAOI so avoid tyramine-rich foods and serotonin sparing drugs (serotonin syndrome)

> Optic neuropathy (28 days+ = increased chance)

140
Q

What are the three main adverse effects associated with linezolid?

A

> Bone marrow suppression leading to haematopoietic disorders

> Optic neuropathy

> Serotonin syndrome

141
Q

Which bacteria commonly cause UTIs?

A

> Coliforms
Proteus spp.

(Coliforms are gram negative rods: Citrobacter, Enterobacter, Hafnia, Klebsiella, Escherichia)

Week 120 (3 decks)

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