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POM Exam II > Microbiology Lecture I > Flashcards

Microbiology Lecture I Flashcards

1
Q

Antimicrobials on human life expectancy … added

a. 8-10 years
b. 20-22 years
c. 10-12 years

A

A. 8-10 years

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2
Q

Infectious disease accounts for 10%/15%/20% of deaths worldwide?

A

10%

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3
Q

25%/50% of deaths in low income countries are due to infectious disease while only 7% in high income countries.

A

50%

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4
Q

Antibacterials are classified by their mechanisms of action. What are the four main mechanisms of actions?

A
  1. Cell wall synthesis
  2. Membrane structure
  3. DNA synthesis
  4. Protein synthesis
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5
Q

minimum inhibitory concentration (MIC)

A

the lowest drug concentration required to inhibit the visual growth of a bacteria

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6
Q

minimum bactericidal concentration (MBC)

A

the concentration of drug required to kill all bacteria

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7
Q

bactericidal

A

kills bacteria; MBC will be approximately MIC

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8
Q

bacteriostatic

A

inhibits but does not kill; lowers the threshold aka bacteria stops growing; MBC&raquo_space;> than MIC (concentration that kills will be higher than concentration that inhibits)

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9
Q

methods to determine microbial susceptibility/resistance

A

disk diffusion, E-test, PCR/sequencing

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10
Q

efficacy definition

A

the ability to produce a desired or intended result

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11
Q

efficacy of antimicrobial drugs in limited by

A
  1. mechanism of action
  2. susceptibility of the target organism
  3. side effects on the host
  4. pharmacodynamics
  5. cost
  6. patient compliance
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12
Q

Cmax

A

peak concentration, maximum concentration of drug

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13
Q

AUC

A

area under the curve, total concentration of the drug that has accumulated in the patients body over a certain period of time

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14
Q

time-dependent killing (TDK)

A

antibiotic that is suppose to maximize the time above the MIC

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15
Q

concentration-dependent killing (CDK)

A

maximize Cmax and AUC

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16
Q

post antibiotic effect (PAE)

A

the time it takes for bacteria to return to log-phase growth following removal of antibiotic

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17
Q

how does TDK affect PAE

A

short PAE

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18
Q

how does CDK affect PAE

A

long PAE

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19
Q

longer PAES reduce

A
  1. required second dosages
  2. cost
  3. toxicities
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20
Q

rocephin

A

Class: B-lactam
Subclass: cephalosporin
Generic: ceftriaxone

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21
Q

gram-negative

A

stains red because pores allow flow; thinner layer of peptidoglycan, inner and outer membranes, lipopolysaccharide (LPS) on outer membrane

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22
Q

gram-positive

A

stains purple/blue; thick peptidoglycan, lipoteichoic acid (LTA)

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23
Q

peptidoglycan

A

peptides and sugars (N-acetylmuramic acid NAM and N-acetylgucosamine NAG)

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24
Q

N-acetylmuramic acid NAM

A

has the four peptides for transpeptidase

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25
Q

B-lactam antibiotics interact with peptidoglycan by…

A

affecting transpeptidation so rows of NAM-NAGS cannot form; B-lactam ex. penicillin superimposes on D-ala-D-ala (last two amino acids attached to NAM) and bind to transpeptidase and inhibit formation; transpeptidation reaction that is essential for petidoglycan synthesis

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26
Q

B-lactam works better on gram +/gram - until there were alterations on penicillin

A

gram + because pepitdoglycan is exposed

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27
Q

B-Lactam subclasses

A

penicillin, cephalosporin, monobactams, and carbapenems

28
Q

enzymatically inactivate drugs example, importance, and where they are found

A

ex. B-lactamases
antibiotic resistance mchanism
often on mobile genetic elements

29
Q

how antibiotic resistance mechanisms can alter drug target

A

mutation and can occur via horizontal exchange

30
Q

how antibiotic resistance mechanisms can alter drug exposure

A

decrease uptake or increase efflux

31
Q

two important types of B-lactamases

A
  1. extended spectrum B-lactamases (ESBL)

2. metal-dependent

32
Q

how do B-lactamases work?

A

cleave the ring on B-lactams

33
Q

clavulanic acid

A

inhibits b-lactamases

34
Q

b-lactam block

A

penicillin binding proteins

35
Q

glycoprotein works by

A

inhibiting transglycosylase by covering d-ala-d-ala amino acid chains on peptidoglycan

36
Q

glycoprotein example

A

vancomycin

37
Q

bacterial resistance to glycoproteins

A

makes enzyme to change d-ala-d-ala to d-ala-d-lac and then antibiotic cannot bind but this is energy expensive and causes the bacteria to be more susceptible to other attacks

38
Q

antibiotics that attack cell wall

A

b-lactam, glycoprotein, bacitracin, phosphomycin, and cycloserine

39
Q

mycobacterium species

A

mycolic acid waxy outer wall

ex. M. tuberculosis and M. leprae

40
Q

agents that act on mycobacterial cell walls

A

isoniazid and ethamnutol

41
Q

isoniazid mechanism of action

A

inhibits mycolic acid synthesis

42
Q

ethambutol mechanism of action

A

thought to inhibit arabinotransferases

43
Q

lipopeptides

A

disrupts the cell membrane of G+ bacteria ; cannot disrupt the G- bacteria because the molecule is too large to fit through porins

44
Q

how are lipopeptides selective for bacteria and not eukaryotic membranes?

A

bind to phosphatidylglycerol which is abundant in bacterial cell membranes but rare in eukaryotic cell membranes

45
Q

lipopeptide antibiotic example

A

daptomycin

46
Q

where in the human body is phosphatidylglycerol abundant?

A

lungs

47
Q

Why would we not use daptomycin or any lipopetides to treat pneumonia?

A

would kill normal cells and not just bacterial cells because there is high amounts of phosphotidylglycerol present in the lungs

48
Q

synergy

A

each drug works better in the presence of the other drug

49
Q

TDK two types of mechanisms

A

cell inhibitors and protein inhibitors

50
Q

TDK cell wall inhibitor examples

A

penicillins and cephalosporins

51
Q

TDK protein synthesis inhibitors

A

macrolide and clindamycin

52
Q

CDK two types of mechanisms

A

protein synthesis inhibitors and DNA inhibitors

53
Q

CDK example of DNA inhibitors

A

fluoroquinolones

54
Q

CDK example of protein inhibitors

A

aminoglycosides

55
Q

Penicillins, cephalosporins, macrolides, and clindamycin have minimal-moderate/prolonged PAE

A

minimal-moderate they are TDK antibiotics

56
Q

Fluoroquilolones and aminoglycosides have minimal-moderate/prolonged PAE

A

prolonged because they are CDK antibiotics

57
Q

sulfonamides

A

inhibit folate synthesis (folate is used in DNA synthesis), bacteriostatic on their own ex. sulfamethoxazole

58
Q

trimethoprim

A

affects DHFR (enzyme that converts folate), bactericidal, synergetic with sulfamethoxazole

59
Q

quinolones/fluoroquinolones

A

inhibit prokaryotic DNA synthesis via gyrase (prokaryotes topoisomerase II) and topoisomerase IV, bactericidal
ex. ciprofloxacin

60
Q

ciprofloxacin

A

quinolone, can cause ruptured tendons

61
Q

rifamycins

A

inhibit mRNA synthesis, bactericidal or bacteriostatic, bind to DNA-dependent- RNA- polymerase, not used often as a monotherapy because mutations occur rapidly (mutations in RNA polymerase)

62
Q

rifampin class

A

rifamycin

63
Q

nitroimidazoles

A

damage DNA, bactericidal and anaerobic

64
Q

nitroimidazole subclass

A

metronidazole

65
Q

prodrug

A

must be converted by microbial enzyme to active form

POM Exam II (11 decks)

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