Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHARMACOLOGY - Antibiotics and Immunosuppressives > Antibiotics MOA and Resistance Mechs. > Flashcards

Antibiotics MOA and Resistance Mechs. Flashcards

1
Q

T or F: drugs that mess with the structure of bacteria are typically bacteriostatic

A

False

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the most common drugs to form allergies?

A

-Penicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the preferred oral treatment for non-penicillinase producing streptococci?

A

-Penicillin V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Differentiate between

  • Penicillin
  • Monobactam
  • Carbapenem
  • Cephalosporins
  • Vancomycin
A

Penicillin – Thiazole Ring
Monobactam –sulfonic acid
- gets it inside the cell wall
Carbapenem
- Replaces thiazole sulfur with carbon giving it MORE RESITANCE to ß-lactamases, better penetration and affinity for more PBP
Cephalosporins
- 6 membered ring to make it more stable
Vanco – inhibits d-ala d-ala binding by transpeptidases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What drugs bind the 30S RSU? Which bind 50S?

A

Buy AT 30, CELL at 50
A = Aminoglycosides
T = Tetracyclines
30S

C = Chloramphenicol
E = Erthromycin (macrolides) 
L = Linezolid 
L = cLindomycin
50S
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why use muti-drug therapy?

A
  1. Treat polymicrobial infections
  2. Decrease emergence of resistance
  3. Descrease Dose-related toxicity
  4. Enhanced cell-kill
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why might tetracyclines and chloramphenicol antagonize bactericidal cell wall agents?

A

Cell wall agents require that the cell be dividing to be effective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Why might giving a ß-lactam antagonize an infection?

A

Some gram (-) bacilli possess inducible lactamases that will be induced by the presence of ß-lactams

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Bactericidal Antibiotics

A
  1. Aminoglycosides*
  2. Fluroquinolones
  3. Nitrofurantion
  4. Sulfonamides with DHFR inhibitors
  5. Metronidazole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Bacteriostatic antibiotics

A

Protein synthesis inhibitors

Sulfonamides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What bacteria are often treated by combining Penicillins with aminoglycosides?

A
  1. Staphylococci
  2. Enterococci
  3. Streptococci
  4. P aeruginosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

4 methods by which antibiotic work

A
  1. Inhibition of Cell Wall Synthesis
  2. Inhibition of Protein Synthesis
  3. Inhibition of Folic acid biosynthetic paths
  4. Inhibition of DNA/RNA synth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

MOA of ß-lactams

A

Bind Penicillin binding proteins (transpeptidase) which causes destruction of the bacterial cell wall gram (+) bacteria are really the only type of microbe affected by this

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the protype penicillins?

A

Penicillin G and Penicillin V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the narrow spectrum penicillins?

A

Oxacillin and Nafcillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the aminopenicillins?

A

Ampicllin and Amoxicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the broad spectrum penicillins?

A

Pipercillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are 2 examples of ß-lactamase inhibtors being combined with penicillins?

A
  • Clavulanic acid with Amoxicillin

- Tazobactam with Piperacillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is a common structural characteristic of Broad Spectrum Penicillin?

  • why are they called broad spectrum ?
  • What are they usually administered with?
A

Broad spectrum because AMINO group added increases ability to cross lipid layer in gram (-) bacteria
Usually administered with ß-lactamase inhibitors (clavulanic acid, or Tazobactam)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are narrow spectrum penicillins?

A

Have larger molecules on their side chain that confers steric hinderance and ß-lactamase can’t twist molecule into different stereoisomers
- these are narrow spectrum because bulky side groups limit the amount of different bacterias that can be targeted

21
Q

What are the 3 major categories of ß-lactams?

A
  • Penicillins
  • Carbaenems
  • Cephalosporins
22
Q

General problem with aminoglycoside administration:

- affected organs?

A

Poorly absorbed in GI Tract so oral administration is not possible. In general intracellular concentrations are low except in proximal tubule of the kidney where they can accumulate and cause NEPHROTOXICITY

23
Q

Drugs ending in –mycin or –micin typically have what general function?

A
  • mycin = macrolides
  • micin = aminoglycosides
  • both inhibit protein synthesis
24
Q

T or F: most protein synthesis inhibitors are bactericidal

A

False, they are bacteriostatic with the exception of aminoglycosides, and Synpristin/dalfopristin (streptogramins) that are bactericidal

25
Q

What is the general trend of cephalosporins across generations?

A

They get increasingly better at attacking gram (-) bacteria and worse at gram (+) bacteria

26
Q

Fluroquinolones to know

A

CIPROFLOXACIN

Levofloxacin

27
Q

Rifamycins to know

A

RIFAMPIN

Rifaximin

28
Q

DHFR drugs to know

A

COTRIMOXAZOLE

Trimethroprim

29
Q

Sulfonamides to know

A

COTRIMOXAZOLE

Sulfamethoxazole

30
Q

MOA for Aminoglycosides

A

Initial site of Action:
Outer bacterial membrane creating holes

Low conc.
Irreversibly bind the 30S ribosomal subunit at low concentrations causing misreading of mRNA.

High conc.
Halt protein synthesis by trapping AUG codon

31
Q

Are aminoglycosides more effective against gram (+) or gram (-) bacteria?

  • aerobic bacteria or anaerobic bacteria?
  • Bacteriostatic or Bactricidal
  • Why?
A

Gram (-) because they deteriorate the outer membrane which is more protected in gram positive
Aerobic because energy is needed for aminoglycoside uptake
Typically bactericidal against aerobic gram (-) bacteria

32
Q

MOA for Lincosamides

A

(protein synth targeting)
Bind 50S ribosomal subunit (23S rRNA part) and inhibit Peptidyl Transferase, are phagocytosed by macrophages carrying them to the site of infection (ideally)

**also slows toxin production by inhibiting bacterial growth

33
Q

Lincosamides to know

A

CLINDAMYCIN

34
Q

MOA of Tetracyclines

A

Bind 30S RSU (16S part) and inhibit protein synthesis by weaking ribosome-tRNA interaction

35
Q

Tetracyclines to know:

A

DOXYCYCLINE
TIGECYCLINE
Minocycline
Tetracycline

36
Q

MOA for Macrolides

A

(protein synth targeting)
Bind 50S ribosomal subunit (23S rRNA part) and inhibit Peptidyl Transferase, are phagocytosed by macrophages carrying them to the site of infection (ideally)

37
Q

Macrolides: Bacteriostatic or Bactericidal

A

Bacteriostatic at most concentrations but become bactericidal at high enough concentrations

38
Q

Why would you give penicillin with an aminoglycoside?

A

Penicillin can break the cell wall and the aminoglycoside can then be absorbed

39
Q

Aminoglycosides to know

A 
GENTIMICIN
Amikacin
Neomycin
Stretomycin
Tobramycin
40
Q

Macrolides to know

A

AZITHROMYCIN
CLARITHROMYCIN
ETYHTROMYCIN

41
Q

MOA for Streptogramins

A

Binds 50S ribosomal subunit (at the same site as macrolides)

42
Q

Bacterial response to Aminoglycosides

  • Gram (+)
  • Gram (-)
  • Anaerobes
  • MRSA
  • VRE
  • Pseudomonas
A
  • Gram (+) – Poor
  • Gram (-) – Great
  • Anaerobes – Resistant
  • MRSA – Resitant
  • VRE – Resistant
  • Pseudomonas - Good
43
Q

Bacterial response to macrolides

  • Gram (+)
  • Gram (-)
  • Anaerobes
  • MRSA
  • VRE
  • Pseudomonas
A
  • Gram (+) – Good
  • Gram (-) – Good
  • Anaerobes – Resistant
  • MRSA – Resistant
  • VRE – Resistant
  • Pseudomonas - Resistant
44
Q

Bacterial response to Lincosamides

  • Gram (+)
  • Gram (-)
  • Anaerobes
  • MRSA
  • VRE
  • Pseudomonas
A
  • Gram (+) – Good
  • Gram (-) – Resitant
  • Anaerobes – Very Good
  • MRSA – Pretty good
  • VRE – Resistant
  • Pseudomonas – Resistant
45
Q

Bacterial response to Tetracyclines

  • Gram (+)
  • Gram (-)
  • Anaerobes
  • MRSA
  • VRE
  • Pseudomonas
A
  • Gram (+)- Good
  • Gram (-) – Good
  • Anaerobes – Pretty good
  • MRSA – Resistant
  • VRE – Resistant
  • Pseudomonas – Resistant
46
Q

What is Cilastin?

- how does it work?

A
  • Cilastin is a reversible, competitive inhibitor of Renal Dehydropeptidase (DHP-1), an enzyme that breaks down Imipenem to inactive BUT NEPHROTOXIC metabolites
47
Q

What group of bacteria is thought to be intrinsically resistant to aminoglycosides because of permability barriers?

A

Enterococci

48
Q

Why are gram (-) bacteria less prone to lysis via ß-lactams?

A

They have a thinner peptidoglycan layer and LPS layer

49
Q

When is a bacteria determined to be resistant to a drug?

A

When the MIC exceeds the breakpoint

PHARMACOLOGY - Antibiotics and Immunosuppressives (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions