Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology > Protein Synthesis Inhibitors I > Flashcards

Protein Synthesis Inhibitors I Flashcards

1
Q

Protein synthesis inhibitors types?

A

Buy AT 30, CCELL(sell) at 50

30S Inhibitors

  1. Aminoglycosides
  2. Tetracyclines

50S Inhibitors

  1. Chloramphenicol
  2. Clindamycin
  3. Erythromycin /Macrolides

MOLD FKS

Mupirocin
Oxazolidinones
Lipopeptides
Disruption of bacterial plasma membrane

Fusidic acid
Ketolides
Streptogramins

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

Aminoglycosides

  1. MOA
  2. Bacteria MOA
A
  1. Inhibit 30S Ribosomal subunit
  2. Bactericidal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Aminoglycosides drugs?

A

TANGS

Tobramycin
Amikacin
Neomycin
Gentamicin
Streptomycin

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

Aminoglycosides resistance mechanims-3?

A
  1. Inhibit of transport into cell
  2. Inactivation by enzymes
    -Acetyl transferases
    -Adenyl transferases
    -Nucleotidyl Transferases
  3. Mutation of binding site on 30S ribosomal subunit (Streptomycin Only)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Streptomycin resistance mechanims?

A

Mutation of binding site on 30S ribosomal subunit (Streptomycin Only)

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

Aminoglycosides antibiotic effect?

A

Prolonged post-antibiotic effect

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

Aminoglycosides admin & not?

A

IM/IV (Not oral)

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

Aminoglycosides admin for eye infections?

A

Topical for sight-threatening eye infections

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

Aminoglycosides S/E and ir/reversible-7?

A
  1. Nephrotoxicity-reversible
    -All of them
  2. Ototoxicty-Irréversible
  3. Neuromuscular Blockage
  4. Liver damage
  5. Headache
  6. Skin Rashs
  7. Fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Aminoglycosides nephrotoxicity levels in all drugs?

A

GeNeTo

Increased nephrotoxicty

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

Which aminoglycosides causes deafness in children?

A

Streptomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Ototoxicty amnioglycosides intensities?

A

NeoKanAmi

Neomycin
Kanamycin
Amikacin

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

Vestibulotoxic amnioglycosides intensities?

A

StreGen

Streptomycin
Gentamycin

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

Aminoglycosides CI?

A
  1. Pregnancy(Streptomycin)
  2. Myasthenia Gravis (Due to neuromuscular blockage)
  3. Renal insufficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Aminoglycosides DI-4?

Mention two drugs that cause Nephrotoxic agents

A
  1. General Anaesthetics-prolonged paralysis
  2. NMB-Prolonged paralysis, Resp depression, prolonged apnea
  3. Oto-or-Nephrotoxic agents
    -Vancomycin
    -Amphotericin
    -Above is the increased
    risk of oto-and
    nephrotoxicity
  4. Loop diuretics-Increased risk of ototoxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which aminoglycosides have increased risk of oto-and-nephrotoxicty?

A

Vancomycin

   &

Amphotericin

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

Tetracyclines

  1. MOA
  2. Bacteria MOA
A
  1. Inhibit 30S ribosomal subunit-prevent the formation of initiation complex
  2. Bacteriostatic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Tetracyclines drugs?

A

Tetracycline
Doxycycline
Minocycline

19
Q

Tetracyclines and glycyclines and name?

A

A new class derived from minocycline(Inf resistant to tetracyclines)

Tigecyline

20
Q

Tetracyclines drugs of choice against?

A
  1. Rickettsia
  2. Chlamydia
  3. Brucellosis
21
Q

Tetracyclines resistance mechanisms?

A

-Decreased intracellular accumulation-Decrease influx or Increase Efflux

-Enzymatic Inactivation

-Production of a protein that interferes with the binding of tetracyclines on the ribosomes

22
Q

Tetracyclines S/E-7?

Mention one specific for minocycline too

A
  1. Discolouration of nails & teeth
  2. Bone growth retardation
  3. Pseudomembranous colitis (clostridium difficle)
  4. Photosensitivity
  5. Nephrotoxcity & Heptoxicty
  6. Destruction of normal gut flora
  7. Minocycline-Specific S/E
    -Blue-grey pigmentation of
    the skin & acne
    scars=vestibulotoxic
23
Q

Tetracyclines DI & why?

A

-Vit A and other retinoids
-Risk of increased
intracranial pressure BECAUSE tetracycline and a form on Vit A cross the BBB

-Decreased Efficacy of combined oral contraceptives-ALL antibiotics do this

24
Q

Tetracyclines CI-6 & why?

A

-Pregnancy & Children < 8-12 years ‘coz it causes bone retardation

-Myasthenia gravis-tetracyclines have a weak NMB effect

-Systemic lupus erythematosus(Minocycline)

-Hepatic Impairement -causes hepatoxicty as a S/E

-Porphyria

-Elderly-Crosses BBB thus DUH!

25
Q

Chloramphenicol

  1. MOA
  2. CYP450
  3. Admin/Bioavailability
A
  1. Inhibits 50S ribosomal unit-inhibit peptidyltransferase
  2. CYP450 Inhibitor
  3. Oral-80% bioavailability
26
Q

Chloramphenicol treatment?

A

-Rickettsidal Infections
-Bacterial Meningitis (Crosses BB)
-Typhoid Fever
-Bacterial eye Infections

27
Q

Chloramphenicol resistance mechanisms?

A

-Production of Chloramphenicol acetyltransferase
-inactivation of the drug

28
Q

Chloramphenicol S/E-3?

A

BAG

-Bone marrow suppression
-Aplastic anemia(fatal)
-Grey-baby syndrome

29
Q

Chloramphenicol CI?

A

-Neonates( Grey-baby syndrome)
-Pregnancy (3rd trimester) & Lactation

30
Q

Clindamycin

  1. MOA
  2. Bacteria MOA and differing concentrations
A
  1. Inhibits 50S ribosomal subunit
  2. Bacteriostatic at low concentrations & Bactericidal at increased concentrations
31
Q

Clindamycin resistance of mechanisms?

A

-Mutations of ribosomal binding site

-Enzymatic inactivation -usually for protein synthesis

32
Q

Clindamycin S/E-3?

A

1.Pseudomembranous colitis

  1. Transient increased liver enzymes and bilirubin
  2. Transient leucopenia eosinophilia, thrombocytopenia and agranulocytosis’
33
Q

Clindamycin S/E?

A
  1. Pseudomembranous colitis
  2. Transient increased liver enzymes and bilirubin
  3. Transient leucopenia, eosinophillia, thrombocytopenia
34
Q

Clindamycin cautions?

A

Pregnancy/Lactation

35
Q

Clindamycin and malaria?

A

Sometimes treated for malaria

36
Q

Macrolides drugs?

A
  1. Erythromycin
  2. Azythromycin
  3. Clarithromycin
37
Q

Macrolides CYP450 and p-glycoproteins?

A

Inhibit CYP450 & P-glycoprotein

38
Q

Macrolides

  1. MOA
  2. Bacteria MOA @ different concentrations?
  3. Placenta/BBB
  4. Best absorption
A
  1. Inhibits 50s ribosomal subunit
  2. Bacteriocidal at increased concentrations and bacteriostatic at decreased concentration
  3. Crosses the placenta but not BBB
  4. Best absorbed as estolate form
39
Q

Macrolides I?

A

Respiratory bacterial infections

40
Q

Macrolides treatment?

A
  1. Rickettsial infections (Azythromycin & Clarithromycin)
  2. Helicobacter pylori(Peptic ulcer)
41
Q

Which macrolides drugs treat ricketsial infection?

A

Azythromycin & Clarithromycin

42
Q

Macrolides resistance mechanisms?

A

-Decreased cell membrane permeability or active efflux

-Modification of binding site

-Production of esterases that hydrolize macrolides

43
Q

Macrolides S/E?

A
  1. Hepatotoxicity
  2. Cholestatic jaudice

Pharmacology (44 decks)

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