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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
How does fidaxomicin and/or rifamycin work?
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.
26
What is an adverse effect of rifamycin
ORANGE - urine, saliva, tears hepatic failure - (when using other drugs) increased hepatic metabolic enzymes
27
What is fidaxomicin good for
C. Dificile. better than vancomycin, in fact, and it is well tolerated
28
What are the 4 steps in peptidoglycan synthesis
1. assembly of peptidoglycan monomers 2. transport of peptidoglycan monomers 3. polymerization of peptidoglycan 4. cross-linking of peptidoglycan polymers
29
What is an antibiotic that inhibits the laster two terminal amino acids of the 5 AA chain
cycloserine will stop the changing of an L-alanine to a D-alanine AND stop the linking of the two D-alanines
30
What is the abx that stops the formation of the sugar backbone
fosfomyin is an analogue which will block this rxn
31
What is the abx that blocks transport of the peptidoglycan monomers
bacitracin is a molecule which will bind to bactroprenol (a molecule necessary for trasnport out of the cell for peptidoglycan synthesis)
32
What is the adverse effects of cycloserine?
neurological side effects (confusion and psychosis). It is good for gram-negative enteric rods
33
What is the side effect of bacitracin ingested
nephrotoxicity. But it is good for gram +
34
What is a drug that blocks peptidoglycan polymerization
vancomycin
35
how does vancomycin block polymerization
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
What is the adverse effect of vancomycin
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
What is vanco good for?
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
What is the broad class that inhibits the cross-linking? How do they do this?
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
What determines what spectrum a beta-lactam works against?
1. ability to reach the transpeptidase 2. affinity for an essential transpeptidase 3. Whether it is cleaved by a beta-lactamase
40
What are the 4 beta-lactam classes?
penicillins, cephalosporins, monobactams, and carbapenems
41
What are the categories of penicillins
1. natural penicillins 2. staph-resistant-penicillinase resistant penicillins 3. aminopenicillins
42
What are the natural penicillins (V and G) good for
They have a narrow-spectrum of activity, but are great working against group A and B strep and T. palidum (syphilis)
43
What are the penicillinase-resistant penicillins (e.g. methicillin) good for
1 thing. Staph
44
What are the amino penicillins good for
they are charged, so they will pass through porins of Gram- bugs. also Really good for enterococci and listeria (both are gram+)
45
What are adverse affects of penicillins
IgE mediated hypersensitivity
46
What is the deal with cephalosporins and generations
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
What is used for MRSA?
Ceftaroline. Similar to other 3rd generation cephalosporin. effective for skin and soft tissue infections. Better than standard therapy for most community-acquired pneumonias
48
What are first generation cephalosporins good for
skin and soft-tissue infections
49
What are 2nd generation cephalosporins good for
respiratory infections, anaerobic infections
50
What are 3rd generation cephalosporins good for?
meningitis, gonorrhea, serious respiratory infections, infections with gram- rods
51
What are 4th generation cephalosporins good for
infections with resistant gram-negative rods
52
What are the adverse effects of cephalosporins
potential allergy to cephalosporins if allergic to penicillin, but it is far far less common. Most side effects are uncommon
53
What is unique and good about carbapenems
They have the broadest spectrum of activity against all beta-lactams.
54
How is it that carbapenems are resistant to abx-resistant bugs
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
How do protein-synthesis inhibitors work?
the will bind to the ribosomal RNA of bacteria!
56
Describe the ribosome subunit and functions
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
Are these protein-synthesis inhibitors bactericidal or bacteriostatic?
bacteriostatic... except for aminoglycosides
58
How might one remember the 5 protein synthesis inhibitors
Buy AT 30, CEL at 50. 30 S subunit are aminoglycosides tetracycline 50s subunits are chloramphenicol erythromycin (main macrolide) lincosamides
59
How do the tetracyclines work
They will block the A-site of the 30s (stopping tRNA)
60
What are the adverse effects of tetracyclines?
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
how do aminoglycosides work?
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
what are aminoglycosides synergistic with?
With beta-lactams and vancomycin. They cannot get in without the disruption of the peptidoglycan disruption
63
what are the adverse effects of aminoglycosides
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
What are some common aminoglycosides
streptomycin, gentamicin, tobramycin, amikacin
65
How does chloramphenical work?
It blocks the A-site of the 50s subunit blocking transpeptidation
66
What does chloramphenicol work against
typhoid fever and meningitis, but usually only in the developing world because it has awful side effects
67
What are some of the adverse effects of chloramphenicol
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
how do lincosamides work?
It will block the A and P site of the 50s subunit. Clindamycin
69
What are they good for
combination therapy for sever staph and strp infection. Used for anaerobic infections of the intestinal baceria.
70
What are the adverse effects of clindamycin
diarrhea is common. allergy is rare. pseudomembranous colitis is very common. It will allow c. dif. to overgrow the toxin.
71
How do the macrolides work
They will bind to the exit tunnel in the 50s subunit blocking the elongation.
72
What are the adverse effects of macrolides
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
How can the bacteria become resistant to antibiotics? 3 ways
1. inactivate the abx 2. change the target of the abx 3. keep the abx away from the target
74
What is an example of the abx inactivation
beta-lactamase secreted by the bacteria will make it resistant
75
Various beta-lactamases will have a wide range of specificity
Meth resistance is common in staph aureus. PENICILLINASE PRODUCTION
76
changes in abx targets... give an example
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
Give an example of a bug that is resistant due to inacessibility. Mechanism and stuff
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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