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PT 1 > L26 Miscellaneous Antibiotics > Flashcards

L26 Miscellaneous Antibiotics Flashcards

(56 cards)

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1
Q

What are the three Tetracyclines? What is the one Glycylcyline?

A
  1. Tetracycline
  2. Doxycycline
  3. Minocycline
  4. Tygecycline
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2
Q

What is the MOA of tetra/glycylcyclines?

A

Protein synthesis inhibition via REVERSIBLE binding to the 30S ribsomal subunit; this inhibits binding of aminoacyl tRNA, preventing addition of amino acids

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3
Q

Tetra/glycylcyclines are ___ (cidal/static).

A

Static, but can be cidal at higher concentrations against susceptible organisms

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4
Q

What are the mechanisms of resistance for tetra/glycylcyclines?

A
  1. Efflux pumps
  2. Ribosomal protection proteins
  3. Enzymatic inactivation

Tigecycline is resistant to this resistance

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5
Q

Discuss the spectrum of activity of Tetracyclines broadly.

A
  1. Gram positive aerobes
  2. Gram negative aerobes
  3. Anaerobes
  4. Other bacteria
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6
Q

What are the most important Gram positive bacteria Tetracyclines have activity against?

A

MSSA

Also: PSSP, Bacillus, Listeria, Nocardia

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7
Q

What are the most important Gram negative bacteria Tetracyclines have activity against?

A

B. pseudomallei

Also: N. gonorrhea, H. influenzae, H. ducreyi, Campylobacter jejuni, H. pylori, V. cholera, V. vulnificus

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8
Q

What are the most important anaerobic bacteria Tetracyclines have activity against?

A

Actinomyces and Propionibacterium

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9
Q

What are the most important other bacteria Tetracyclines have activity against?

A

Legionella, Chlamydophila, Chlamydia, Mcyoplasma, Ureaplasma, Rickettsia

Also: Bordetella, Brucella, Pasteurella, Borrelia, Trepenoma, Leptospira, Coxiella, M. fortuitum, Bartonella

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10
Q

Discuss the absorption, distribution, and elimination of Tetra/glycylcyclines.

A

Absorption: impaired by di- and trivalent cations
Distribution: wide, synovial fluid, prostate, seminal fluid, minimal CSF
Elimination: renal (tetra), metabolic (doxy, mino), biliary (tige)

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11
Q

What are the clinical uses of Tetra/glycylcylines?

A

RMSF, respiratory infections, CA pneumonia (doxy), pertussis, STDs, malaria, Q fever, Lyme disease, Burcellosis, Bartonellosis, plague, Tularenmia, chanchroid, anthrax, H. pylori, acne, SIADH

Also: Polymicrobial infections (tige)

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12
Q

What are the major adverse effects of tetra/glycylcylcines?

A

GI (nausea, vomiting), photosensitivity, Fanconi-like syndrome (outdated tetra), contraindicated in pregnancy

Also: diarrhea, pseudomembranous colitis, hypersensitivity, reversible diabetes insipidus, hepatic enzyme elevation

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13
Q

Discuss the spectrum of activity of Glycylcyclines broadly.

A
  1. Gram positive aerobes
  2. Gram negative aerobes
  3. Anaerobes
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14
Q

What are the most important Gram positive bacteria Tigecycline has activity against?

A

MSSA, MRSA, VRE, VSE (NOT for bacteremias or UTIs)

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15
Q

What are the most important Gram negative bacteria Tigecycline has activity against?

A

NOT Proteus or P. aeruginosa

A. baumannii, A. hydrohpila, Citrobacter, E. coli, Klebsiella S. marcescens, S. maltophila

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16
Q

What are the most important anaerobes Tigecycline has activity against?

A

Bacteroides

Also: C. perfringens

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17
Q

What is the MOA of sulfonamides?

A

Inhibition of dihydropteroate synthetase (inhibits incorporation of PABA into tetrahydropteroic acid)

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18
Q

Sulfonamides are ___ (static/cidal).

A

Bacteriostatic

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19
Q

What are the 4 short/medium-acting sulfonamides?

A
  1. Sulfisoxazole
  2. Sulfamethoxazole
  3. Sulfadiazine
  4. Sulfamethizole
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20
Q

What is the 1 long-acting sulfonamide?

A

Sulfadoxine

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21
Q

What is the MOA of trimethoprim?

A

Inhibition of dihydrofolate reductase (interferes with conversion of dihydrofolate to tetrahydrofolate)

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22
Q

Trimethoprim is ___ (static/cidal).

A

Bacteriostatic

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23
Q

TMP-SMX is ___ (static/cidal).

24
Q

Describe the steps of the pathway at which Sulfamethoxazole and Trimpethoprim act to inhibit metabolism.

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A

PABA is converted to Dihydrofolic acid via Dihydropterate Synthetase (Sulfamethoxazole acts here). Dihydrofolic acid is converted to tetrahydrofolic acid via Dihydrofolate reductase (trimpethoprim acts here).

25
What are the mechanisms of resistance of Sulfonamides?
1. PABA overproduction 2. Structural change of Dihydropteroate synthetase 3. Drug resistant DHPS or decreased cell wall permeability
26
What are the mechanisms of resistance of Trimethoprim?
1. Production of resistant dihydrofolate reductase | 2. Changes in cell permeability
27
Discuss the spectrum of activity of TMP-SMX broadly.
1. Gram-positive 2. Gram-negative 3. Other bacteria
28
What are the most important Gram positive bacteria TMP-SMX have activity against?
S. aureus (MRSA) Also: S. pyogenes, Nocardia, Listeria
29
What are the most important Gram negative bacteria TMP-SMX have activity against?
S. maltophilia Also: Acinetobacter, Enterobacter, E. coli, K. pneumoniae, Proteus, Salmonella, Shigella, Haemophilus, N. gonorrheae
30
What are the most important otherbacteria TMP-SMX have activity against?
Pneumocystis carinii
31
Discuss the absorption, distribution, and elimination of TMP-SMX.
1. Rapidly and completely absorbed; IV, PO 2. Good distribution (lungs, urine, prostate, CSF) 3. SMX is 70% protein bound 4. Liver and kidney elimination
32
What are the clinical uses of TMP-SMX?
1. UTI (acute, chronic, recurrent) 2. Bacterial prostatitis (acute/chronic) 3. Skin infections due to CA-MRSA Also: bacterial sinusitis, Stenotrophomonas, Toxo, Listeria, Nocardia
33
What are the major adverse effects of TMP-SMX?
GI (nausea, vomiting, diarrhea, glossitis, jaundice, hepatic necrosis), Hematologic (leukopenia*, thrombocytopenia*, eosinophilia, acute hemolytic anemia, aplastic anemia, agranulocytosis, megaloblastic anemia), Hypersensitivity (rash*, urticaria, epidermal necrolysis, Steven-Johnson, drug fever), CNS (headache, aspecti meningitis, seizures), renal toxicity (tubular necrosis,, interstitial nephritis), drug-induced lupus, serum sickness-like syndrome, cyrstalluria*
34
What are the major drug interactions of TMP-SMX?
1. Phenytoin (increased phenytoin levels) 2. Warfarin (increased anti-coagulant effect) 3. Methotrexate (decreased renal clearance)
35
True or false - Chloramphenicol is not used in the U.S.
True
36
What is the MOA of chloramphenicol?
Binds to 50s subunit of 70s ribosome, prevents peptide bond formation
37
Chloramphenicol is ___ (cidal/static) except for...
Static; H. influenzae, S. pneumoniae, N. meningitidis
38
What are the mechanisms of resistance of Chloramphenicol?
1. Reduced permeability or uptake 2. Ribosomal mutation 3. Acetyltransferase inactivation
39
Discuss the absorption, distribution, and elimination of Chloramphenicol.
1. Well-absorbed by the GI tract 2. Lipid soluble, not highly protein bound, CSF levels 3. Metabolized by the liver, excreted by the kidneys; decrease dose in liver failure, no adjustment in renal failure
40
Discuss the spectrum of activity of Chloramphenicol broadly.
1. Gram positives (unreliable against S. aureus, not active against Enterococci) 2. Gram negatives (not against P. aeruginosa) 3. Anaerobes
41
What are the most important other bacteria Chloramphenicol have activity against?
Rickettsiae sp., Spirochetes, Chlamydia, Mycoplasma
42
What are the clinical uses of Chloramphenicol?
Third and developing world: pneumonia, bacterial meningitis, typhoid fever RMSF
43
What are the major adverse effects of Chloramphenicol?
1. Gray baby syndrome (abdominal distention, vomiting, flaccidity, cyanosis, circulatory collapse/death) Also: hematologic (reversible bone marrow suppression, aplastic anemia), optic neuritis, hypersensitivity reaction, anaphylaxi, GI intolerance, stomatitis, porphyria
44
What are the two major urinary tract agents?
1. Nitrofurantoin | 2. Methenamine
45
What is the MOA of nitrofurantoin?
Binds to ribosomal proteins, inhibits translation, inhibits bacterial respiration and pyruvate metabolism
46
What is the MOA of methenamine?
Converted in acid pH to ammonia and formaldehyde, which is a non-specific denaturant of proteins and nucleic acids
47
What are the mechanisms of resistance of Nitrofurantoin?
Poorly understood - development of resistance is rare; E. coli shows production of nitrofuran reductase
48
What are the mechanisms of resistance of Methenamine?
Alkaline urine; no bacterial resistance to formaldehyde itself
49
Discuss the absorption, distribution, and elimination of Nitrofurantoin.
1. 40-50% absorption following oral administration, occurs in small intestine, enhanced with food 2. Large urine concentrations, low serum concentration, no prostate distribution 3. Urine elimination, some biliary
50
Discuss the absorption, distribution, and elimination of Methenamine.
1. Rapid absorption after oral adminsitration, may be degraded by stomach acid 2. Broad distribution 3. Renal excretion
51
What are the clinical uses of Nitrofurantoin?
1. Acute uncomplicated UTIs NOT pyelonephritis, complicated UTI
52
What are the clinical uses of Methenamine?
1. Suppression or prophylaxis of recurrent UTIs NOT established infections, prophylaxis against CAUTI
53
What is the spectrum of activity of Nitrofurantoin?
E. coli, Citrobacter, GBS, S. saprophyticus, Enterococcus (VRE)
54
What is the spectrum of activity of Methenamine?
No antimicrobial activity; may not be effective against urease producing organisms (Proteus)
55
What are the major adverse effects of Nitrofurantoin?
GI intolerance, rashes, acute pulmonary symptoms, subacute/chronic pulmonary reaction
56
What are the major adverse effects of Methenamine?
Generally well-tolerated, GI, rash, pruritis, bladder irritaiton, hemorrhagic cystitis, peripheral sensory neuropathy, hepatitis, hemolytic anemia, leukopenia, aplastic anemia, megaloblastic anemia, eosinophilia

PT 1 (34 decks)

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