2 Flashcards

(27 cards)

1
Q

What two main groups of antibiotics inhibit cell wall synthesis

A

Beta lactams

Glycopeptide

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2
Q

Name the three subgroups of beta lactams

A

Penicillins
Cephalosporins
carbapenems

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3
Q

Between pen v and pen g which is better orally absorbed

A

Penicillin v

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4
Q

Which beta lactam is good against staphylococci

A

Flucloxacillin

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5
Q

Give two examples of cephalosporins

A

Cefalexin

Ceftazidime

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6
Q

Name two examples of carbapenems and what they do

A

Ertapenem- orally absorbed

Meropenem - very broad spectrum

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7
Q

Mode of action of beta lactams

A

Block active site of penicillin binding protein and stops cross linking between cell wall components therefore is susceptible to osmotic lysis

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8
Q

What are beta lactams often given in combination with and why

A

Beta lactamase inhibitors because many bacteria produce beta lactamases that hydrolyse the beta lactam ring and inactivate it

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9
Q

Give an example of a beta lactamase inhibitor and an example of a well known combination

A

Clavulanic acid

Co-amoxiclav (amoxicillin and clavulanic acid)

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10
Q

What is the mode of action of glycopeptide antibiotics

A

Block the binding site of the penicillin binding protein and stop cell wall cross-linking

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11
Q

Give two examples of glycopeptide antibiotics

A

Vancomycin

Teicoplanin

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12
Q

Name some bacteria that glycopeptides are useful for due to beta lactam resistance

A

MRSA
Coagulase negative staphylococci
Penicillin resistance entercocci and streptococci
Clostridium difficile

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13
Q

Name the three groups of protein synthesis inhibitors

A
Macrolides 
Tetracyclines 
Aminoglycosides 
Rifamycins
Lincosamides
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14
Q

Give two examples of macrolides

A

Erythromycin

Clarithromycin- community acquired pneumonia (legionella and mycoplasma)

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15
Q

Give examples of tetracyclines

When you use them and when you don’t

A

doxycycline and tigecycline
Broad spectrum.
Not in pregnancy children or in neutropenia ( bacteriostatic)

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16
Q

Give examples of aminoglycosides

Why do you have to be careful with them

A

Gentamicin- sepsis
Amikacin
Tobramycin - anti-pseudomonal in CF

Narrow therapeutic window

17
Q

How do protein synthesis inhibitors work?

A

Inhibit either the 30s subunit ( aminoglycosides, tetracyclines)
50s (macrolides, chloramphenicol)
Or mRNA ( rifamycins)

18
Q

Name two modes of DNA synthesis/replication inhibitors

A

Nucleotide synthesis- folate inhibition

DNA gyrase inhibition- stop unwinding for replication

19
Q

Name three groups of DNAsyn/rep inhibitors

A

Sulphonamides- folate synthesis inhibitors
Diaminopyrimidines- folate synthesis inhibitors
Quinolones- additions of fluorine atom - fluoroquinolones

20
Q

What are the groups of fungi

A

Yeasts, molds and diamorphic

21
Q

Give examples of mycosis

A

Tinea ( ringworm)
Candidiasis
Mucormycosis
Aspergillosis

22
Q

What are the three main groups of antifungal drugs

A

Azoles
Polyenes
Echinocandins

23
Q

How do triazoles act

Give examples of them

A

Inhibit ergosterol synthesis (fungal alternative to cholesterol of cell membrane)
Fluconazole

24
Q

How do Polyenes act

Give examples

A

Bind ergosterol

Amphotericin B
Nystatin

25
How do Echinocandins act | give examples
Inhibit glucan ( cell wall) Caspofungin Micafungin
26
Name all the modes of antibiotic action
Inhibits cell wall synthesis Inhibits protein synthesis Interferes with DNA synthesis and replication Disrupts cell membrane
27
How is acyclovir selective
Only activated in infected cells Becomes concentrated in infected cells due to gradient Higher affinity for viral DNA polymerase then cellular enzymes