Brainscape's Knowledge GenomeTM

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


See full index

From Flashcardlet > Pharmacology: Antimicrobial Drugs II > Flashcards

Pharmacology: Antimicrobial Drugs II Flashcards

1
Q

Protein Synthesis Inhibitors

A
  • Aminoglycosides (gentamicin, neomycin, streptomycin, toramycin, and amikacin)
  • Tetracyclines (Tetracycline, doxycycline, minocycline)
  • Macrolides (azithromycin, clarithormycin, erythromycin)
  • Clindamycin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Types of aminoglycosides

A
  • Gentamicin
  • Neomycin
  • Streptomycin
  • Tobramycin
  • Amikacin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Drugs that affect 30S ribosomal subuint

A
  • Aminoglycosides

- Tetracyclines

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

Drugs that affect 50S ribosomal subunit

A
  • Macrolides
  • Chloramphenicol
  • Clindamycin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Aminoglycoside amino groups are

A

Basic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Aminoglycosides are administered ___ for systemic infecitons

A

Parenterally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Aminoglycosides are administered ___ to treat hepatic coma and GI infections

A

Orally

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

Aminoglycosides are administered ___ for infections of skin, mucous membrane, and ocular tissues

A

Topically

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

Aminoglycosides do not penetrate

A
  • Body cells

* CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Aminoglycoside excretion

A

as unmetabolized drugs by renal glmerulcar filtration

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

Aminoglycosides- mechanism

A
  • Bind to 30S ribosomal subuit
  • Interfere with initiation of protein synthesis
  • Cause misreading of genetic code = post-antibiotic effect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Resistance among aminoglycosides is primarily due to

A
  • Inactivation of drugs*

- Decreased uptake and binding of drugs to 30S ribosomal subunit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Aminoglycosides are most commmon cause of

A

Drug-induced renal failure = acute tubular necrosis

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

Aminoglycoside risk factors

A
  • Old age
  • Other nephrotoxic drugs
  • Diabetes
  • Liver cirrhosis
  • Aminoglycoside therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Adverse effects of aminoglycosides

A
  • Renal toxicity

- Ototoxicity (cochlear toxicity and vestibular toxicity)

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

To minimize toxicity of aminoglycosides

A
  • Once daily dosing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cohlear toxicity vs. Vestibular toxicity

A 
Cochlear = irreversible
Vestibular = reversible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Clincial use of Aminoglycosides

A

Active against Gram-negative bacilli

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

Gentamicin- clinical use

A
  • Treatment of endocarditis

- Enterococcal, staphylcoccal, or viridans strep infections

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

Sttreptomycin- clinical use

A
  • Treat multi-resistant TB
  • Yersinia pestis
  • Fracisella tularensis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Tobramycin- clinical use

A

P. aeruginosa

22
Q

Amikacin- clinicla use

A
  • Most resistant to inactivation by bacterial enzymes than gentamicin and tobramycin
  • Treats organisms resistant to gentamicin and tobramycin
23
Q

Synergistic interaction with penicillins and vancomycin

A
  • Ampicllin or vancomysin makes pores in bacterial cell wall –> entry of aminoglycosides (gentamicin) –> block protein synthesis
24
Q

Tetracyclines- ex.

A
  • Tetracycline
  • Doxycycline
  • Minocycline
25
Q

Oral bioavailability of tetracyclines is reduced if they are taken with

A
  • Dairy products
  • Antacids
  • Iron supplements
26
Q

Doxycycline is predominately excreted in

A
  • Bile

- Does not require dose adjustment in renal failure

27
Q

Tetracycline- Mechanism

A
  • Competitivelly block binding of tRNA to 30S subunit

- Prevent addition of new amino acids

28
Q

Tetracycline resistance

A

Accomplished by Mg 2+ efflux of drug mediated by resistance protein TetA

29
Q

Adverse effects of tetracyclines

A
  • Epigastic distress
  • Calcified tissues
  • Nephrotoxicity
  • Phototoxicity
30
Q

Tetracyclines are contraindicated in

A

Children below 8

31
Q

Tetracyclines- spectrum

A

Broad spectrum, bacteriostatic drugs

32
Q

Clincial uses of tetracyclines

A
  • Rickettsiae
  • Spriochetes
  • Mycoplasmas
  • Chlamydiae
  • Management of acne vulgaris
  • Shortens course of cholera
33
Q

Ex. of macrolides

A
  • Azithromycin
  • Clarithromycin
  • Erythromycin
34
Q

Macrolides- pharmacokinetics

A
  • Do not readily enter CSF

* Diffuse into tissues and prostatic fluid

35
Q

Macrolides that are metabolized by cytochrome P450

A
  • Erythromycin

- Clarithromycin

36
Q

Excretion of Erythromycin, azithromycin, and clarithromycin

A

Erythro and Zithro are excreted by bile

Clarithro is eliminated by kidney and liver

37
Q

Macrolides- mechanism

A
  • Bind to 50S subunit
  • prevents translocation of nascent peptide
  • prevents binding of next tRNA to ribosome
  • Blocks peptidyl transferase
38
Q

Macrolides- resistance

A
  • Acquire resistance due to active transport of drugs out of bacteria via specialized transport systmes
  • Decreased binding of macrolides to ribosomes
  • Plasmid-associated erythromycin esterase
39
Q

Adverse effects of macrolides

A
  • Epigastic distress
  • Cholestatic jaundice
  • Ototoxicity
40
Q

Macrolides- contraindications

A
  • Drug accumulates in live

* Erythromycin is not administered to patients with hepatic dysfunction

41
Q

Drug interactions- Erythromycin and clarithromycin

A
  • Inhibit cytochrome P450

- Increase plasma concentration and toxicity of other drugs metabolized by this enzyme

42
Q

Clinical uses of macrolides

A
  • More for G+ than G-
43
Q

Clinical use- Erythromycin

A
  • Used for patients who are allergic to penicillin
  • Treatment of stretococcal and pneumococcal infections
  • Treatment, prophylaxis, or reduction of risk of pathogens
  • Mycoplasma pneumonia
  • Legionella pneumophila
  • Chlamydia trachomatis
  • Chlamydia pelvic infection during pregnancy
  • Carrier state of Corynebacterium diphtheria
44
Q

Azithromycin- clinilcal use

A

More active against:

  • H. influenza
  • M. catarrhalis
  • M. pneumoniae
  • Chlamydia trichomatis than erythromycin
45
Q

Clarithromycin- clinical use

A

Used in combination with amoxicillin and a gastric acid inhibitor for treatment of peptic ulcer caused by H. pylori

46
Q

Clindamycin- mechanism

A
  • Binds to 50S ribosomal subunit

- Inhibits translocation of nascent peptide

47
Q

Clindamycin- adequate levels are not achieved in

A

CSF

48
Q

Clindamycin- drug is excreted

A

In bile or urine by golmerular filtration

49
Q

Clindamycin- adverse effects

A
  • Pseudomembranous colitis caused by C. difficile
50
Q

Pseudomembranous colitis caused by clindamycin is treated with

A
  • Vancomycin

- Metronidazole

51
Q

Clindamycin- clinical uses

A
  • Active against gram-positive cocci and anaerobes (Bacteroides fragilis)
  • Treats infectious caused by penicillin-resistant streptococci
  • Treats wound infections in patients allergic to penicillin
52
Q

___ are resistant to clindamycin

A

Gram negative aerobes

From Flashcardlet (110 decks)

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