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MNI (immuno pharm) > L31- Protein Synthesis Inhibitors II > Flashcards

L31- Protein Synthesis Inhibitors II Flashcards

1
Q

list the protein synthesis inhibitors

A
  • tetracyclines
  • glycylcyclines
  • aminoglycosides
  • macrolides
  • chloramphenicol
  • clindamycin
  • streptogramins
  • linezolid
  • mupirocin
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2
Q

Protein Synthesis Inhibitors:

  • bacterio-(static/cidal)
  • (2) MOA
  • (3) MOA’s effects that are basis for AEs
A

1- bacteriostatic (mostly, aminoglycoside is only bacteriocidal)

2- binds bacterial ribosome (70S = 50S + 30S) —- differs from eukaryotic ribosome (80S = 60S + 40S)

3- binds mammilian mitochondrial ribosome (due to resemblance to bacterial ribosome) => AEs

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3
Q

______ is the only bacteriocidal protein synthesis inhibitor

A

aminoglycosides

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4
Q

Chloramphenicol:

  • effective against (1) bacteria
  • usually restricted use to (2) infections, explain
A

1- aerobic and anaerobic Gram+/- bacteria

2- life-threatening infections b/c highly toxic

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5
Q

Chloramphenicol MOA:

  • (1) entry
  • binds (ir-/reversibly) to (3) in order to inhibit (4)
  • due to MOA, (5) is the main effect / toxicity in humans
A

1- active transport

2- reversibly
3- 50S ribosomal subunit
4- peptidyltransferase

5- inhibits mitochondrial ribosomal protein synthesis => BM suppression / toxicity

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6
Q

describe the mechanisms of Chloramphenicol resistance

A
  • presence of chloramphenicol acetyltransferase => enzymatic inactivation
  • change in membrane permeability (requires active transport)
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7
Q

Chloramphenicol Pharmacokinetics:

  • (1) route of administration
  • (2) describe distribution
  • major inhibitor of (3)
A

1- oral, IV, topical

2- wide distribution- including CSF

3- CYP3A4, CYP2C9

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8
Q

Chloramphenicol AEs:

  • (1) common minor AEs
  • (2) serious AE, explain
  • (3) neonate AE, explain
A

1- GI distress

2- BM suppression (reversible —> irreversible anaplastic anemia)

3- Gray Baby Syndrome / cyanosis in neonates <2wks old since they do not have metabolic enzyme yet –> crosses BBB and CNS accumulation

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9
Q

Clindamycin MOA:

  • binds to (1) in order to block (2)– similar MOA to (3) agents
  • mainly used / active against (4) bacteria and alternatively used against (5)
A

1- 50S ribosomal subunit
2- translocation
3- macrolides, chloramphenicol

4- Gram+ anaerobes
5- Gram+ aerobes, bacteroides

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10
Q

Clindamycin Resistance:

  • (1) describe mechanisms
  • (2) bacteria are intrinsically resistant
  • cross-resistant with (3) agents
A

1:

  • ribosomal receptor site mutation
  • modification of receptor
  • enzymatic inactivation

2- most Gram- aerobes, enterococci

3- macrolides

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11
Q

Clindamycin clinical applications:

  • treats (1) and (2) infections alone
  • treats (3) and (4) in combination, indicate other drug
  • alternative to (5) in certain patients
A

1- anaerobic infections
2- skin / soft tissue infections

3- PCP Tx alternative with primaquine
4- Toxoplasmosis of brain Tx alternative with pyrimethamine

5- prophylaxis in Pts allergic to penicillin (eg. dental surgeries, animal bites)

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12
Q

Clindamycin Pharmacokinetics:

  • (1) route of administration
  • (2) describe distribution
A

1- IV, oral

2- good penetration –> includes bone and abscesses

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13
Q

Clindamycin AEs:

  • (1) is the biggest and hallmark risk
  • (2) are the common milder AEs
A

1- potentiall fatal pseudomembrane colitis via C.diff. superinfection

2- GI irritation (20% diarrhea), rash (10%), neutropenia, impaired liver function

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14
Q

Streptogramins:

  • (1) agents, given in (2) fashion- explain
  • long (3) effect (hint- affects dosage)
A

1- quinupristin, dalfopristin
2- always in combination, b/c bacteriocidal —- bacteriostatic if given alone

3- long postantibiotic effect

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15
Q

Streptogramins bind (1) in order to prevent (2). (3) is the key difference in comparson to other agents with similar MOA, therefore (4) is uncommon with streptogramins.

A 
(quinupristin-dalfopristin combination)
1- 50S ribosomal subunit
2- protein synthesis
3- different site on 50S compared to other agents
4- resistance is rare
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16
Q

Streptogramins are effective against (1) and (2) bacteria, therefore are restricted clinically to be used for (3).

A

(quinupristin-dalfopristin combination)
1- gram+ cocci
2- MDR

3- MRSA + other resistance Strep. spp., VRE

17
Q

Streptogramins Pharmacokinetics:

  • (1) route of administration
  • penetrates into (2) cells
  • inhibitor of (3)
A

(quinupristin-dalfopristin combination)
1- IV
2- macrophages, PMNs
3- CYP3A4

18
Q

list Streptogramin AEs

A

(quinupristin-dalfopristin combination)
-infusion related: venous irritation, arthralgia, myalgia

  • GI effects
  • CNS effects: HA, pain
19
Q

Linezolid MOA:

-binds to unique site on (1) part of (2) in order to inhibit (3)

A

1- 23S rRNA
2- 50S ribosomal subunit
3- formation of 70S initiation complex

20
Q

describe the mechanisms of Linezolid resistance, discuss cross-resistance (explain)

A
  • dec binding to target site
  • point mutation of rRNA

-NO cross-resistance with other agents with similar MOAs b/c it binds unique site on 23S rRNA

21
Q

Linezolid is effective against (1) bacteria and is restricted to treating (2) infections

A

1- Gram+ bacteria

2- MDR infections (MRSA, VRE)

22
Q

Linezolid Pharmacokinetics:

  • (1) route of administration
  • (2) describe distribution
  • weak reversible inhibitor of (3)
A

1- oral (100% F), IV

2- wide distribution, includes CSF

3- MAOI

23
Q

Linezolid AEs:

  • (1) from short-term therapy
  • (2) from long-term therapy
  • (3) is the main contraindication
A

1- well-tolerated: GI- n/d, HA, rash

2- BM suppression (thrombocytopenia mainly), Optic/Peripheral neuropathy, lactic acidosis, Serotonin Syndrome

3- many drugs in relation to its weak reversible inhibition of MAOIs —> to avoid serotonin syndrome and hypertensive crisis

24
Q

Fidaxomicin is effective against (1) bacteria only and is the drug of choice for (2). Its MOA involves binding and inhibition of (3).

A

1- gram+ aerobes / anaerobes (no activity vs Gram-)

2- C. difficile

3- RNA polymerase (like rifampin)

25
Q

describe the pharmacokinetics and AEs of Fidaxomicin and how it relates to its functions

A

To Tx C. diff.:

  • zero or minimal oral F —> very high fecal concentration
  • good at treating GIT infections as it stays in the gut
  • all AEs are GI related
26
Q

Mupirocin MOA: it binds (1) in order to inhibit (2)

A

1- isoleucyl transfer-RNA synthetase

2- protein synthesis

27
Q

Mupirocin:

  • effective generally against (1) bacteria
  • (2)/(3): give the route of administration and the related clinical use
A

1- Gram+ cocci (MRSA, Strep. spp.)

2- Intranasal: MRSA in nasal cavity (adults, healthcare workers)

3- Topical: impetigo (Staph. aureus, Strep. pyogenes) or secondary infected traumatic skin lesions

28
Q

Mupirocin:

  • (1) discuss resistance
  • (2) list AEs
A

1- may develop with long-term use

2- local/dermatological: burning, edema, tenderness, dry skin, pruritus

MNI (immuno pharm) (15 decks)

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