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Antibiotics Flashcards

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1
Q

What is the therapeutic index

A

the ratio between the dose which has a certain toxic effect in half of people divided by the dose with is effective in half of people.

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2
Q

minimum inhibitory concentration… describe

A

concentration of abx at which this is no longer inhibition of visible growht of the bacteria.

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3
Q

minimum bactericidal concentration

A

concentration at which 99.9% of the bacteria are dead

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4
Q

Give a list of the bactericidal abx (there are 5 classes)

A

What kind of car is bactericidal? Ford Rimjob AWD WDFRA

F - fluoroquinolones
R - rifamycin
A - aminoglycosides
W - cell Wall synthesis inhibitors
D - Daptomycin
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5
Q

What are the bacteriostatic abx (there are 3)

A

to be static is the PITS

PI - other Protein-synthesis inhibitors
T - trimethoprim
S - sulfonadmides

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6
Q

ABX indifference

A

combi is as effective as the more effective of the two abx

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7
Q

abx antagonism

A

less effective than the more effective of the 2

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8
Q

abx synergism

A

more effective than the more effective of the two abx

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9
Q

What are the 4 forms of synergy

A

Synergy is achieved by bottle CAPS

C - Concentration. One abx allows the 2nd one to achieve higher concentration
A - Affinity. One abx enhances binding of a 2nd abx
P - Pathway. Both abx block separate steps in a synthetic pathway. Trimethoprim and sulfa-abx are an example.
S - Survival. One abx blocks the destruction of another abx.

,, Survival, Pathway

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10
Q

What’s the deal with the CNS, abx, and inflammation

A

There are some abx which only reach the CNS in high enough concentrations in the presence of inflammation

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11
Q

What are these abx that work in the CNS with inflammation

A

P, A, 3, 4 (tell me that you love me more)

Penicillin
Ampicillin
3rd and 4th generation cephalosporins

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12
Q

What are the 5 major abx classes

A

what do immature people do? Draw things using pee. P-DRAW

P - protein-synthesis inhibitors
D - DNA-stability inhibitors
R -  RNA-synthesis inhibitors
A - antimetabolites
W - peptidoglycan (wall)-synthesis inhibitors
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13
Q

What are the antimetabolites

A

Trimethoprim and sulfonamides

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14
Q

What are the 5 protein-synthesis inhibitors

A

What is the public transport underseas? T-CLAM

T - tetracycline
C - chloramphenicol
L - Lincosamides
A - Aminoglycosides
M - Macrolides
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15
Q

What are the Wall (peptidoglycan)-synthesis inhibitors

A

Baby, Come For Valium! BB-CFV

B - beta-lactams
B - bacitracin
C - cycloserine
F - Fosfomycin
V - vancomycin
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16
Q

What are the DNA-stability inhibitors

A

Fluorquinolones

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17
Q

What are the RNA-synthesis inhibitors

A

FR-ance

Fidaxomicin
Rifamycin

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18
Q

Talk about how the antimetabolites work and the blockade that they work

A

tetahydrofolate is an important enzyme used to transfer single carbons in the synthetic pathway for amino acids and nucleotides. The two enzymes (sequentially) that make tetrahydrafolate. The first crucial enzyme is dihydropteroate synthase which is inhibited by synthase, and the 2nd crucial enzyme is dihydrofolate reductase which is inhibited by trimethoprim.

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19
Q

What are the adverse effects of sulfonamides?

A

hypersensitivity leading to rash and itch. Stevens-johnson syndrome sometimes occurs leading to desquamation of the skin and mucosa

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20
Q

What is special about these antimetabolites

A

using sulfonamides and trimethoprim together is syngergistic and has a broad spectrum of effect against bacteria

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21
Q

What are the adverse effects of trimethoprim (a bacterial DHFR inhibitor)

A

rarely - a suppressive effect on bone marrow cells leading to reduction of RBCs, WBCs, and platelets

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22
Q

Describe how a fluoroquinolone works?

A

All bacteria have specific topoisomerases that will help to repair DNA with breaks. The quinolones will block the important type II topoisomerase.

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23
Q

what makes fluoroquinolones interesting?

A

There is one for every malady and every bug!

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24
Q

What are the adverse effects of quinolones

A

rarely will cause tendinitis and tendon rupture in adults.

might predispose people to cardiac arrythmias

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25
Q

How does fidaxomicin and/or rifamycin work?

A

fidaxomycin: blocks separation of DNA strands. It FIGHTS the DNA separating and letting it’s genetic code go.
rifamycin: blocks bond formation of the nascent RNA. Creates a rift between the polymerase and the RNA bits floating around.

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26
Q

What is an adverse effect of rifamycin

A

ORANGE - urine, saliva, tears
hepatic failure - (when using other drugs)
increased hepatic metabolic enzymes

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27
Q

What is fidaxomicin good for

A

C. Dificile. better than vancomycin, in fact, and it is well tolerated

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28
Q

What are the 4 steps in peptidoglycan synthesis

A
  1. assembly of peptidoglycan monomers
  2. transport of peptidoglycan monomers
  3. polymerization of peptidoglycan
  4. cross-linking of peptidoglycan polymers
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29
Q

What is an antibiotic that inhibits the laster two terminal amino acids of the 5 AA chain

A

cycloserine will stop the changing of an L-alanine to a D-alanine AND stop the linking of the two D-alanines

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30
Q

What is the abx that stops the formation of the sugar backbone

A

fosfomyin is an analogue which will block this rxn

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31
Q

What is the abx that blocks transport of the peptidoglycan monomers

A

bacitracin is a molecule which will bind to bactroprenol (a molecule necessary for trasnport out of the cell for peptidoglycan synthesis)

32
Q

What is the adverse effects of cycloserine?

A

neurological side effects (confusion and psychosis). It is good for gram-negative enteric rods

33
Q

What is the side effect of bacitracin ingested

A

nephrotoxicity. But it is good for gram +

34
Q

What is a drug that blocks peptidoglycan polymerization

A

vancomycin

35
Q

how does vancomycin block polymerization

A

vancomycin will bind to the last 2 AA’s of the peptidoglyca polymer (d-ala d-ala) and block the transglycolase from binding together the polysaccharide backbone of the peptidoglycan

36
Q

What is the adverse effect of vancomycin

A

it can cause histamine release and lead to red man syndrome. Not an allergic rxn, but a generalized histamine release. Also, uncommonly causes neutropenia and nephrotoxicity

37
Q

What is vanco good for?

A

good for all gram-positive bacteria. does not work against gram-negative bacteria because it cannot get into the outer membranes of the gram-negative bacteria to get into the periplasmic space.

38
Q

What is the broad class that inhibits the cross-linking? How do they do this?

A

BETA-LACTAMS!!!!!!! They work by disrupting the transpeptidase (AKA penicillin-binding proteins) that will link the 4th AA in one chain to the 3rd AA of another chain. This makes the peptidoglycan unable to resist the osmotic forces which will eventually lyse the cell. Beta-lactams bind irreversibly to the transpeptidases and thus inhibit it from creating cross-linking

39
Q

What determines what spectrum a beta-lactam works against?

A
  1. ability to reach the transpeptidase
  2. affinity for an essential transpeptidase
  3. Whether it is cleaved by a beta-lactamase
40
Q

What are the 4 beta-lactam classes?

A

penicillins, cephalosporins, monobactams, and carbapenems

41
Q

What are the categories of penicillins

A
  1. natural penicillins
  2. staph-resistant-penicillinase resistant penicillins
  3. aminopenicillins
42
Q

What are the natural penicillins (V and G) good for

A

They have a narrow-spectrum of activity, but are great working against group A and B strep and T. palidum (syphilis)

43
Q

What are the penicillinase-resistant penicillins (e.g. methicillin) good for

A

1 thing. Staph

44
Q

What are the amino penicillins good for

A

they are charged, so they will pass through porins of Gram- bugs. also Really good for enterococci and listeria (both are gram+)

45
Q

What are adverse affects of penicillins

A

IgE mediated hypersensitivity

46
Q

What is the deal with cephalosporins and generations

A

There are 4 generations of cephalosporins which are ranked in order of their spectrum of activity with 1st generation being really good against staph and increasingly becoming better for gram- (why? because they become increasingly able to cross porins and achieve stability within the Gram -‘s)

47
Q

What is used for MRSA?

A

Ceftaroline. Similar to other 3rd generation cephalosporin. effective for skin and soft tissue infections. Better than standard therapy for most community-acquired pneumonias

48
Q

What are first generation cephalosporins good for

A

skin and soft-tissue infections

49
Q

What are 2nd generation cephalosporins good for

A

respiratory infections, anaerobic infections

50
Q

What are 3rd generation cephalosporins good for?

A

meningitis, gonorrhea, serious respiratory infections, infections with gram- rods

51
Q

What are 4th generation cephalosporins good for

A

infections with resistant gram-negative rods

52
Q

What are the adverse effects of cephalosporins

A

potential allergy to cephalosporins if allergic to penicillin, but it is far far less common. Most side effects are uncommon

53
Q

What is unique and good about carbapenems

A

They have the broadest spectrum of activity against all beta-lactams.

54
Q

How is it that carbapenems are resistant to abx-resistant bugs

A

they are resistant to almost all beta-lactamases. They use a different porin than other drugs to get into the periplasmic space of the gram- bacteria (although they do just fine for gram+’s too)

55
Q

How do protein-synthesis inhibitors work?

A

the will bind to the ribosomal RNA of bacteria!

56
Q

Describe the ribosome subunit and functions

A

There are two sbunits: 30s and 50s.

30s = A&P sites, decodes the mRNA
50s = A&P sites, pepidyl transferase (to link the AA's), exit tunnel
57
Q

Are these protein-synthesis inhibitors bactericidal or bacteriostatic?

A

bacteriostatic… except for aminoglycosides

58
Q

How might one remember the 5 protein synthesis inhibitors

A

Buy AT 30, CEL at 50.

30 S subunit are
aminoglycosides
tetracycline

50s subunits are
chloramphenicol
erythromycin (main macrolide)
lincosamides

59
Q

How do the tetracyclines work

A

They will block the A-site of the 30s (stopping tRNA)

60
Q

What are the adverse effects of tetracyclines?

A

mess up ca+ binding and thus will damage and discolor growing teeth enamel. NOT to be given to children <8 years or during pregnancy. Must be taken on an empty stomach and can cause GI upset

61
Q

how do aminoglycosides work?

A

They will interfere with the decoding of the 30s subunit which will lead to incorporation of many incorrect amino acids in the protein and thus it will die.

62
Q

what are aminoglycosides synergistic with?

A

With beta-lactams and vancomycin. They cannot get in without the disruption of the peptidoglycan disruption

63
Q

what are the adverse effects of aminoglycosides

A

so many. nephrotoxicity although it is reversible. IRREVERSIBLE oto-toxicity and hearing loss. mild to complete hearing loss and/or nausea or vertigo
RARELY: neuromuscular blockade. very rare, reversible flaccid paralysis (including the respiratory musculature)

64
Q

What are some common aminoglycosides

A

streptomycin, gentamicin, tobramycin, amikacin

65
Q

How does chloramphenical work?

A

It blocks the A-site of the 50s subunit blocking transpeptidation

66
Q

What does chloramphenicol work against

A

typhoid fever and meningitis, but usually only in the developing world because it has awful side effects

67
Q

What are some of the adverse effects of chloramphenicol

A

commonly will suppress (transiently) RBC’s, WBC’s, and platelet production
uncommonly: SEVERE suppression of RBC (aplastic anemia), WBC’s, or platelet production

Toxic for babies: gray baby syndrome since they can’t excrete the drug. Leads to abdominal distention, vomiting, flaccidity, cyanosis, and hypotension AND death

68
Q

how do lincosamides work?

A

It will block the A and P site of the 50s subunit. Clindamycin

69
Q

What are they good for

A

combination therapy for sever staph and strp infection. Used for anaerobic infections of the intestinal baceria.

70
Q

What are the adverse effects of clindamycin

A

diarrhea is common. allergy is rare. pseudomembranous colitis is very common. It will allow c. dif. to overgrow the toxin.

71
Q

How do the macrolides work

A

They will bind to the exit tunnel in the 50s subunit blocking the elongation.

72
Q

What are the adverse effects of macrolides

A

it is really safe and well-tolerated. The GI upset is common with erythromycin. cholestatic hepatitis can occur rarely with prolonged therapy (reversible with ending treatment)

73
Q

How can the bacteria become resistant to antibiotics? 3 ways

A
  1. inactivate the abx
  2. change the target of the abx
  3. keep the abx away from the target
74
Q

What is an example of the abx inactivation

A

beta-lactamase secreted by the bacteria will make it resistant

75
Q

Various beta-lactamases will have a wide range of specificity

A

Meth resistance is common in staph aureus. PENICILLINASE PRODUCTION

76
Q

changes in abx targets… give an example

A

MRSA. The MRSA bugs have developed a new PBP2a which not only will not bind penicillin, but it won’t even bind methicillin which should bind normally at rates that are 10000 stronger than penicillin. ALTERNATIVE PBP.

77
Q

Give an example of a bug that is resistant due to inacessibility. Mechanism and stuff

A

erythromycin given for a staph infection can quickly gain resistance if the bug has a msrA channel which will just pump it right out of the cell. PUMP FOR MACROLIDES

Microbiology (10 decks)

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