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PT 1 > L26 Miscellaneous Antibiotics > Flashcards

L26 Miscellaneous Antibiotics Flashcards

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).

A

Bactericidal

24
Q

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

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
Q

What are the mechanisms of resistance of Sulfonamides?

A
  1. PABA overproduction
  2. Structural change of Dihydropteroate synthetase
  3. Drug resistant DHPS or decreased cell wall permeability
26
Q

What are the mechanisms of resistance of Trimethoprim?

A
  1. Production of resistant dihydrofolate reductase

2. Changes in cell permeability

27
Q

Discuss the spectrum of activity of TMP-SMX broadly.

A
  1. Gram-positive
  2. Gram-negative
  3. Other bacteria
28
Q

What are the most important Gram positive bacteria TMP-SMX have activity against?

A

S. aureus (MRSA)

Also: S. pyogenes, Nocardia, Listeria

29
Q

What are the most important Gram negative bacteria TMP-SMX have activity against?

A

S. maltophilia

Also: Acinetobacter, Enterobacter, E. coli, K. pneumoniae, Proteus, Salmonella, Shigella, Haemophilus, N. gonorrheae

30
Q

What are the most important otherbacteria TMP-SMX have activity against?

A

Pneumocystis carinii

31
Q

Discuss the absorption, distribution, and elimination of TMP-SMX.

A
  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
Q

What are the clinical uses of TMP-SMX?

A
  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
Q

What are the major adverse effects of TMP-SMX?

A

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
Q

What are the major drug interactions of TMP-SMX?

A
  1. Phenytoin (increased phenytoin levels)
  2. Warfarin (increased anti-coagulant effect)
  3. Methotrexate (decreased renal clearance)
35
Q

True or false - Chloramphenicol is not used in the U.S.

A

True

36
Q

What is the MOA of chloramphenicol?

A

Binds to 50s subunit of 70s ribosome, prevents peptide bond formation

37
Q

Chloramphenicol is ___ (cidal/static) except for…

A

Static; H. influenzae, S. pneumoniae, N. meningitidis

38
Q

What are the mechanisms of resistance of Chloramphenicol?

A
  1. Reduced permeability or uptake
  2. Ribosomal mutation
  3. Acetyltransferase inactivation
39
Q

Discuss the absorption, distribution, and elimination of Chloramphenicol.

A
  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
Q

Discuss the spectrum of activity of Chloramphenicol broadly.

A
  1. Gram positives (unreliable against S. aureus, not active against Enterococci)
  2. Gram negatives (not against P. aeruginosa)
  3. Anaerobes
41
Q

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

A

Rickettsiae sp., Spirochetes, Chlamydia, Mycoplasma

42
Q

What are the clinical uses of Chloramphenicol?

A

Third and developing world: pneumonia, bacterial meningitis, typhoid fever

RMSF

43
Q

What are the major adverse effects of Chloramphenicol?

A
  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
Q

What are the two major urinary tract agents?

A
  1. Nitrofurantoin

2. Methenamine

45
Q

What is the MOA of nitrofurantoin?

A

Binds to ribosomal proteins, inhibits translation, inhibits bacterial respiration and pyruvate metabolism

46
Q

What is the MOA of methenamine?

A

Converted in acid pH to ammonia and formaldehyde, which is a non-specific denaturant of proteins and nucleic acids

47
Q

What are the mechanisms of resistance of Nitrofurantoin?

A

Poorly understood - development of resistance is rare; E. coli shows production of nitrofuran reductase

48
Q

What are the mechanisms of resistance of Methenamine?

A

Alkaline urine; no bacterial resistance to formaldehyde itself

49
Q

Discuss the absorption, distribution, and elimination of Nitrofurantoin.

A
  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
Q

Discuss the absorption, distribution, and elimination of Methenamine.

A
  1. Rapid absorption after oral adminsitration, may be degraded by stomach acid
  2. Broad distribution
  3. Renal excretion
51
Q

What are the clinical uses of Nitrofurantoin?

A
  1. Acute uncomplicated UTIs

NOT pyelonephritis, complicated UTI

52
Q

What are the clinical uses of Methenamine?

A
  1. Suppression or prophylaxis of recurrent UTIs

NOT established infections, prophylaxis against CAUTI

53
Q

What is the spectrum of activity of Nitrofurantoin?

A

E. coli, Citrobacter, GBS, S. saprophyticus, Enterococcus (VRE)

54
Q

What is the spectrum of activity of Methenamine?

A

No antimicrobial activity; may not be effective against urease producing organisms (Proteus)

55
Q

What are the major adverse effects of Nitrofurantoin?

A

GI intolerance, rashes, acute pulmonary symptoms, subacute/chronic pulmonary reaction

56
Q

What are the major adverse effects of Methenamine?

A

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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