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INDE > Bacterial Drugs > Flashcards

Bacterial Drugs Flashcards

1
Q

b-lactam cell wall inhibitors MOA

A

Looks like D-ala-D-ala; Binds PBPs (transpeptidases) and blocks peptidoglycan cross-linking; Disrupts integrity of bacterial cell wall

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2
Q

b-lactam cell wall inhibitors Adverse Effects

A

All beta lactams are associated with allergic reactions including anaphylaxis, rashes, nephritis

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3
Q

penicillin G

A

B lactam cell wall inhibitor

simple penicillins

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4
Q

amoxicillin

A

B lactam cell wall inhibitor

extended spectrum penicillins

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5
Q

nafcillin

A

B lactam cell wall inhibitor

b-lactamase-resistant penicillins

Associated with interstitial nephritis

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6
Q

piperacillin

A

B lactam cell wall inhibitor

anti-pseudomonal

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7
Q

cefazolin

A

1st gen cephalosporins (Contain FA)

Narrow spectrum; Good activity against gram pos.

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8
Q

cefuroxime

A

2nd gen cephs (contain FU)

Intermediate spectrum

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9
Q

ceftriaxone

A

3rd gen cephs (Tri)

Broad spectrum; Used for serious gram neg. infections;
Extended spectrum increases risk of secondary infections

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10
Q

cefepime

A

4th gen cephs (contain PI)

Broad spectrum; Increased activity against pseudomonas

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11
Q

ceftaroline

A

5th gen cephs (contain ROL)

Very broad spectrum; Active against MRSA; Does not cover pseudomonas

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12
Q

meropenem

A

B lactam cell wall inhibitor

carbapenems

Increased seizure risk with renal dysfunction
Broad spectrum;
Resistant to most b-lactamases;

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13
Q

aztreonam

A

B lactam cell wall inhibitor

monobactams

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14
Q

clavulanic acid

A

Binds active site of b-lactamases; Inhibits hydrolysis of b-lactam drugs

Never given alone; Always in combination with b-lactam drug

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15
Q

vancomycin

A

Binds D-ala-D-ala of cell wall precursors; Inhibits elongation of peptidoglycan chain

Nephrotoxicity, otoxocity, “Red man syndrome” flushing caused by rapid iv administration

MRSA active, oral for C.diff; Resistance can occur by altered D-ala-D-ala in peptidoglycan

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16
Q

bacitracin

A

Prevents dephosphorylation of inactive lipid carrier to active form; Hinders transport of peptidylglucan building block from inside to outside of cell

Nephrotoxicity

Toxicity limits use to topical; Treat minor skin infections

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17
Q

chloramphenicol

A

Binds 50S ribosomal subunit; Inhibits peptidyltransferase reaction (peptide transfer) in protein synthesis

Bone marrow depression; Serious and fatal blood disorders

Limited use due to toxicity

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18
Q

azithromycin

A

macrolides

Reversibly binds 50S ribosomal subunit; Blocks translocation of ribosome during protien synthesis

Cholestatic hepatitis; Arrhythmias cause by prolonged QT; GI motility issues

19
Q

clindamycin

A

licoamides

Reversibly binds 50S ribosomal subunit; Inhibits peptidyltransferase reaction (peptide transfer) in protein synthesis

MRSA active

20
Q

linezolid

A

oxazolidinones

Reversibly binds 50S ribosomal subunit; Prevents formation of initiation complex for protein synthesis

Bone marrow suppression; Serotonin syndrome (as MAO inhibitor)

MRSA active

21
Q

gentamicin

A

aminoglycosides

Irreversibly binds 30S ribosomal subunit; Inhibits initiation of protein synthesis; Causes misreading of mRNA

Nephrotoxicity; Ototoxicity

22
Q

doxycycline

A

tetracyclines

Reversibly binds 30S ribosomal subunit; Prevents entry of aminoacyl-tRNA during protein synthesis

GI stress

Some tetracyclines (e.g. doxy. and tigecycline) MRSA active; Doxycycline used to treat malaria

23
Q

tigecycline

A

glycylcyclines

Reversibly binds 30S ribosomal subunit; Prevents entry of aminoacyl-tRNA during protein synthesis

GI stress

Tetracycline derivative

24
Q

sulfamethoxazole

A

Competitive inhibitor of dihydropteroate synthase; Blocks synthesis of dihydrofolic acid

hypersensitivity reactions

Sulfa + trimeth almost always used together; Active against MRSA

25
Q

trimethoprim

A

Competitive inhibitor of bacterial DHFR (dihydrofolate reductase) in folate synthesis pathway

Bone marrow toxicity; Anemia, leukopenia

Sulfa + trimeth almost always used together; Active against MRSA

26
Q

ciprofloxacin

A

fluoroquinolones

Inhibitor of bacterial DNA gyrase (topo II) & topoisomerase IV, enzymes that unwind DNA; Disrupts bacterial DNA replication & chromosome segregation

GI stress, nausea; Tendonitis, tendon rupture in elderly

27
Q

daptomycin

A

membrane disrupter

Inserts into membranes to create channels; Causes leakage of small ions/molecules

Skeletal muscle pain and weakness

Inactivated by pulmonary surfactants (not for pneumonia); MRSA active

28
Q

rifampin

A

TB drug

RNA synthesis inhibitor

Bacterial RNA polymerase inhibitor; Binds to beta subunit of RNA polymerase

CYP450 inducer; Increases metabolism of other drugs;
Hepatotoxicity

29
Q

isoniazid

A

TB drug

cell wall inhibitor

Prodrug activated by mycobacterial KatG encoded catalase peroxidase; Inhibits synthesis of mycolic acid, important structural component unique to mycobacterial cell wall

Vitamin B6 deficiency; Hepatotoxicity

30
Q

pyrazinamide

A

TB drug

Prodrug metabolized by mycobacterial pyrazinamidase to active form pyrazinoic acid;
Exact mechanism unknown

Hyperuricemia; Hepatotoxicity

31
Q

ethambutol

A

TB drug

cell wall inhibitor

Inhibits arabinosyltransferase EmbB required for synthesis of arabinogalactan, essential component of myocobacterial cell wall

Visual disturbances

32
Q

How do bacteria become resistant to b-lactam antibiotics?

A
  1. Hydrolysis of B-lactam ring
  2. Structural changes to transpeptidase
  3. Change in porin channels found in outer membrane of Gram neg.
33
Q

How do bacteria become resistant to cycline antibiotics?

A
  1. Decreased influx or increased efflux

2. Expression of ribosome protection proteins that interfere with drug-target binding

34
Q

How do bacteria become resistant to Aminoglycoside antibiotics?

A
  1. Plasmid mediated expression of drug modification:

Acetylation of amine group; Phosphorylation or adenylation of hydroxyl group.

35
Q

How do bacteria become resistant to Chloroamphenicol antibiotics?

A
  1. Plasmid mediated expression of acetyltransferase that inactivates the drug.
36
Q

How do bacteria become resistant to Macrolides antibiotics?

A
  1. Efflux pumps

Production of methylase that adds a methyl group to rRNA which prevents drug binding site in ribosome.

37
Q

How do bacteria become resistant to Linezolid antibiotics?

A
  1. Rare
38
Q

How do bacteria become resistant to Sulfonamides antibiotics?

A
  1. Decreased intracellular accumulation.
  2. Increased PABA production
  3. Decreased sensitivity of dihydroteroate synthase
39
Q

How do bacteria become resistant to Trimethoprim antibiotics?

A
  1. Production of DHFR with reduced affinity for drug.
40
Q

How do bacteria become resistant to Floroquinolones antibiotics?

A
  1. Active efflux pumps

2. Point mutation in DNA gyrase or topo 4

41
Q

How do bacteria become resistant to Rifampin antibiotics?

A
  1. Mutation in B-subunit of RNA pol
42
Q

How do bacteria become resistant to Isoniazid antibiotics?

A
  1. Mutation on KatG and InhA
43
Q

How do bacteria become resistant to Pyrazinamide antibiotics?

A
  1. Mutation in PncA
44
Q

How do bacteria become resistant to Ethambutol antibiotics?

A
  1. Mutation in EmbB

INDE (9 decks)

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