antibiotics Flashcards

1
Q

5 classes of antibiotics

A
Antibiotics against bacteria 
Anti-virals 
Anti-fungals 
Anti-protosoals  
Anti-nematodes
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2
Q

what are most antibiotics made from

A

natural products of bacteria and fungi, chemically modified to increase their pharmacological properties and amplify the antimicrobial effect.

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3
Q

principle of selective toxicity of antibiotics

A

occurs due to the differences in structure and metabolic pathways between host and pathogen .’. host unaffected pathogen destroyed

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4
Q

principle of therapeutic margin of antibiotics

A

minimum effective dosage that will inhibit or kill the bacteria.
cannot be too high bc will then affect the host cells

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5
Q

what is the theraoeutic margin

A

difference between therpeutic dosage and toxic dosage

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6
Q

what is microbial antagonism

A

normal flora of the body antagonising the survival of pathogenic bacteria by competing for nutrients and space

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7
Q

effect of antibiotics on microbial antagonism

A

antibiotics cannot distinguish between bacteria .’. kill off normal flora and the pathogen. .’. allows overgrowth of pathogenic bacteria .’. opportunistic infection

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8
Q

symptoms of overgrowth of pathogenic bacteria

A

ulceration

severe diarrhoea

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9
Q

classes of bacteria based on their type of action

A

bactericidal

bacteriostatic

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10
Q

what do bacteriostatic antibiotics do

A

imit the growth of bacteria by interfering with bacterial protein production, DNA replication, or other aspects of bacterial cellular metabolism.
work w/ immune system to remove the microorganisms from the body.

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11
Q

what are bactericidal antibiotics

A

kill bacteria by slowing growth/reproduction of pathogen. inhibit cell wall synthesis: the Beta-lactam antibiotics (penicillin derivatives (penams), cephalosporins (cephems), monobactams, and carbapenems) and vancomycin.

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12
Q

what are broad spectrum antibiotics

A

effective against many different types of bacteria e.g. cefotaxime

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13
Q

what are narrow spectrum antibiotics

A

effective only against a very few types of bacteria e.g. Penicillin G

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14
Q

when do we use broad spectrum antibiotics

A

emergency situations

when we don’t know exact pathogen we may use broad-spectrum antibiotics until we know the pathogen

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15
Q

role of flagella on bacteria

A

enable mobility

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16
Q

role of pillion bacteria

A

allow adhesion

17
Q

targets of bacteriostatic bacteria

A

inhibit: cell wall synthesis, protein synthesis, DNA gyrate, mRNA formation, antifolates

18
Q

what do dan gyrate inhibitors do

A

DNA gyrase unwinds the bacterial DNA to allow its replication, if it is inhibited the bacteria cannot replicate its DNA and divide)

19
Q

what do poymixins do

A

Act at the bacterial cell membrane, makes it more toxic towards human cells as our membranes are very similar to bacteria

20
Q

what do antifolates do

A

inhibit the ability of the bacteria to form THFA (tetrahydrofolic acid) required to make DNA precursors.

21
Q

characteristics of gram +ve bacteria

A

cell membrane encloses cytoplasm. outside the cell membrane we have large peptidoglycan cell wall.

22
Q

characteristics of cell wall in gram

A

synthesised by enzymes released grin the cell membrane.

cell wall is porous so can give b-lactam antibiotics will ps through cell wall and affect the cell membrane

23
Q

characteristics of gram -ve bacteria

A

cell membrane encloses cytoplasm. outside the cell membrane we have thin peptidoglycan cell wall, and surrounding this is an impermeable lipopolysaccharide layer. can only enter cell through porins

24
Q

why are gram -ve bacteria more resistant to antibiotics

A

have impermeable lipopolysaccharide layer .’. things can only get through via porins .’. difficult to get to periplasmic space (to inhibit peptidoglycan synthesis) or into cytoplasm (to inhibit protein synthesis

25
Q

how is peptidoglycan synthesised

A

in cytoplasm - precursor dimer made (NAG & NAM joint by UDP). D-ala added onto terminal ends. precursors then transported to space between cell membrane and wall where chain is built up. vancomycin bind to D-ala (imp to allow peptide cross linkage between carbohydrate chains) transpeptidase and carboxypeptidase then cleave one D-ala and make cross links chains.

26
Q

mechanism of penicillins and b-lactams

A

inhibit transpeptidase and carboxypeptidase .’. stop bacteria from forming cross links between the chains .’. bacteria cannot make cell wall and lyses

27
Q

how do b-lactams get into gram +ve bacteria

A

diffuse through porous cell wall

28
Q

how do b-lactams get into gram -ve bacteria

A

impermeable lipopolysaccharide membrane .’. cannot diffuse in. b-lactam has to go through the porins in impermeable layer into periplasmic layer and then moves through to bind to PBP in cell membrane

29
Q

what are PBP

A

penicillin binding proteins e.g. transpeptidase and carboxypeptidase

30
Q

mechanism of b-lactam in game -ve

A

b-lactam has to go through the porins in impermeable layer into periplasmic layer and then moves through to bind to PBP in cell membrane .’. cell wall cannot ve cross linked properly eptidoglycan subunits build up.’. autolytic enzymes induced

31
Q

how do we treat bacterial infection

A

1 - antibiotic
2 - surgery (e.g. draining abscess)
3 - immunological (e.g. antitoxin)

32
Q

why do we use antibiotics before surgery

A

used to prevent the person getting infected with organisms at the wound site

33
Q

what do we need to consider when deciding the antiobiotic we prescribe

A

Type of bacteria, Sensitivity of that bacteria, Route of administration, The clinical condition, The spectrum of activity, Level of toxicity, Can they excrete the drug

34
Q

why may antibiotic therapy not work

drug issues

A

Inappropriate drug used, Improper route of administration, Poor tissue penetration e.g. endocarditis, Inadequate dose (not reaching MIC)

35
Q

why may antibiotic therapy not work

host issues

A

Immuocompromised host, Poor circulation or damaged tissue, Unusual site for a pathogen

36
Q

why may antibiotic therapy not work

bacteria issues

A
  • > Natural or acquired resistance
  • > Dual infections
  • > biofilms (e.g. in endocarditis)