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antibiotics Flashcards

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1
Q

what is an antibiotic

A

anti-bacterial

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2
Q

how do antibiotics basically work

A

molecules that work by binding a target site on a bacteria

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3
Q

how will the binding site vary

A

vary due to the antibiotic class

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4
Q

how do antibiotic classes differ

A

due to the location of binding

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5
Q

three classes of antibiotics

A

cell wall synthesis
nucleic acid synthesis
protein synthesis

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6
Q

main group with cell wall synthesis

A

beta lactans

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7
Q

examples of beta lactans

A

penicillins
cephalosporins
carbapenems

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8
Q

examples of some penicillins

A

peniccilin v
penicillin g
flucoxallinin

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9
Q

examples of glycopeptides

A

vancomycin
teicoplan

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10
Q

beta lactam antibiotics mechanism?

A

-disrupt peptidoglycan production
-binding covalently and irreversibly to the Penicillin Binding Proteins
-cell wall is disrupted and lysis occurs
-results in a hypo-osmotic or iso-osmotic environment

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11
Q

why is gram negative bacteria hard to use with beta lactams

A

it has an additional lipopolysaccharide layer which makes penetration difficult

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12
Q

most used examples of nucleid acid synthesis medicines

A

metronidazole
ciprofloxacin

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13
Q

nucleic acid synthesis antibiotic mechanism?

A

prevent production of folic acid so you cant make pyrine bases ro make dna

affect enzymes that are involved in dna replcate such as dna gryase, rna polymerase

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14
Q

PROTEUN SYN

A

aminoglycosides- gentamincin
tetracylince

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15
Q

Folate synthesis mechanism ?

A

NO FOLATE- NO REPLCIATION OF CELLS

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16
Q

examples of folate synthesis antibiotics

A

trimethoprim
co- trimoxazole

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17
Q

consequences of bacteria

A
  • destroy phagocytes or cells in which bacteria replicate
  • inflammation - necrotic cells
    -diarrhoea
  • exotoxin- protein production
18
Q

two main ways antibiotics work

A
  • kill the bacteria
  • prevent growth of bacteria
19
Q

how would an antibiotic work effectively

A

should remain at binding site, for a sufficient period of time in order for the metabolic processes to be sufficiently inhibited.

20
Q

two major determinants of bacterial efficacy?

A

concentration
time

21
Q

pharmcokinetics relation to antibiotics ?

A

its release from dosage
its absorption
its distribution
rate of elimination

22
Q

how do bacteria resist antibiotics

A

change antibiotic target- by changing binding site
destroy antibiotic -
prevent antibiotic access- modify the bacterial membrane porin channel, size and selectivity
remove antibiotic from bacteria-proteins in bacterial membranes act as an export or efflux pump

23
Q

what two ways do bacteria become resistant

A

intrinsic
acquired

24
Q

what happens in intrinsic resistance

A

naturally resistant

25
Q

example of intrinsic resistance

A

Aerobic bacteria are unable to reduce metronidazole to its active form

Vancomycin cannot penetrate outer membrane of gram negative bacteria

26
Q

what happens in acquired resistance

A

spontaneous gene mutation
horizontal gene transfer

27
Q

what can mrsa become resistant to

A

flucloxacillin

28
Q

why would you never give trimethoprim to a pregnant woman

A

it prevents folate production which is key to prevent spina bifida

29
Q

how can horizontal gene transfer cause antibiotic ressitance

A

conjugation
transformation
transduction

30
Q

WHAT can streptococcus be treated with

A

penicillin’s

31
Q

What factors to consider when deciding if an antibiotic is safe to prescribe?

A

Intolerance, allergy and anaphylaxis
Side effects
Age
Renal and Liver function
Pregnancy and breast feeding
Drug interactions
Risk of Clostridium difficile

32
Q

what is amoxicillin- clavulanate

A

amoxicillin and clavulonic acid

33
Q

what can cause cellulitis of the foot

A

s.aureus
group a c g strep

34
Q

what woudl you give to someone w s,aureus and beta haemolysis

A

flucloxacillin

35
Q

who would you give penicillin to

A

pharyngitis
penicillin

36
Q

what does MRSA stand for

A

Methicillin*-resistant Staphylococcus aureus

37
Q

examples of macrolides and use

A

clarithromycin and erythromycin
for s.aureus

38
Q

what does clindamycin do

A

turns off nasty toxins made by gram positive bugs

39
Q

main difference between gram neg and pos

A

neg has a thin cell wall
pos has a thick lipolysaccaride layer

40
Q

main difference between gram neg and pos

A

neg has a thin cell wall
pos has a thick liposaccharide layer

41
Q

what will gram neg cause

A

intra abdo infections
diarrohoea
appendicitis

42
Q

what is gentamicin used for

A

UTI’s

microbiology (9 decks)

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