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Pharmacology Block III > Misc. Antibiotics: Tetracyclines, Sulfonamides, Chloramphenicol and UTI Agents 9/11/15 > Flashcards

Misc. Antibiotics: Tetracyclines, Sulfonamides, Chloramphenicol and UTI Agents 9/11/15 Flashcards

1
Q

List the first and second generation tetracyclines.

A

First = Tetracycline (PO)

Second = Doxycycline (IV/PO), Minocycline (PO)

“Toast, then Drink More”

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2
Q

What is the prototypical drug of Glycylcyclines and why was it developed?

A

Tigecycline

  • Improve spectrum of activity
  • Overcome resistance mechanisms
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3
Q

What is the MOA of Tetracyclines/Glycylcyclines, and are they bacteriostatic or cidal?

A

Inhibits protein synthesis

Bacteriostatic (cidal at high concentrations)

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4
Q

What are some mechanisms of resistance against Tetracyclines/Glycylcyclines?

A

Efflux Pumps

Ribosomal protection proteins

Enzymatic inactivation

***Tigecycline resistant to these mechanisms

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5
Q

List the Spectrum of activity for the Tetracyclines.

A

Misc:

Rickettsia/Coxiella

Chlamydia

Mycoplasma

Spirochetes: Borrelia, Treponema, Leptospira

Gram Positive Aerobes:

  • MSSA
  • PSSP
  • Bacillus, Listeria, Nocardia

Gram Negative Aerobes:

  • Neisseria
  • H. flu
  • Burkholderai pseudomallei
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6
Q

What is the spectrum of activity for Tigecycline?

A

Gram Negative Aerobes:

  • E. coli
  • Klebsiella spp
  • Citrobacter spp
  • Serratia marcescens

NOT PROTEUS or P. AERUGINOSA

Gram Positive Aerobes:

  • S. aureus (MSSA, MRSA)
  • Enterococcus spp (VRE, VSE)

NOT for BACTEREMIA or UTIs

Anaerobes:

-C. perfringens, Bacteroides spp

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7
Q

What impairs absorption of Tetracyclines/Glycylcyclines, and describe their distribution?

A

Di/Trivalent Cations = Mg, Ca, Fe

Wide distribution = synovial fluid, prostate, seminal fluid, minimal CSF

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8
Q

How are the following drugs eliminated, and which of them require adjustments for disease states:

  • tetracycline
  • doxycycline
  • minocycline
  • tigecyclin
A

tetracycline = kidneys = adjust dose in RI

doxy/minocycline = metabolized

tigecycline = biliary = adjust dose with liver disease

ALL = minimally removed during HD

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9
Q

What are clinical uses for Tetracyclines/Glycylcyclines?

A

Respiratory Infections:

-Community acquired pneumonia (doxy)

STDs:

-CHLAMYDIA, Syphilis, Gonorrhea (no doxy)

Malaria prophylaxis

Others:

-RMSF, Q Fever, Lyme

Polymicrobial Infections:

-Complicated skin/soft tissue infections (tigecycline)

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10
Q

What are the major AEs of the Tetracyclines?

A

GI problems

Photosensitivity (esp doxy)

Hepatotoxicity (esp doxy)

Discolored teeth (pregnancy category D: if exposed in utero/childhood)

Fanconi Syndrome (if outdated): renal problems

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11
Q

What are the major AEs of Tigecycline?

A

GI problems = nausea, vomiting

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12
Q

What do sulfonamides inhibit, and are they bactericidal or static?

A

Inhibit dihydropteroate synthetase

Bacteriostatic

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13
Q

What does Trimethoprim inhibit and is it bacteriostatic or cidal?

A

Inhibits dihydrofolate reductase

Bacteriostatic

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14
Q

Why was Trimethoprim combined with Sulfamethoxazole (TMP-SMX = IV/PO)?

A

Static + Static = Cidal

Synergistic activity

Broader spectrum of activity (SOA)

Decreased emergence of resistance

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15
Q

List some mechanisms of resistance to Sulfonamides and Trimethoprim.

A

Sulfonamides:

PABA Overproduction

Structural change of Dihydropteroate synthetase (D.S.)

Decreased cell wall permeability

Trimethoprim:

Dihydrofolate reductase resistance

Changes in cell wall permeability

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16
Q

What is the SoA for TMP-SMX?

A

Gram Positive:

  • Staph aureus (MRSA)
  • Nocardia

Gram Negative:

  • Stenotrophomonas maltophilia
  • Haemophilus spp
  • Shigella
  • Salmonella

Anaerobes = NO ACTIVITY

Other:

-Pneumocystis carinii (esp in HIV pts)

17
Q

Describe the A and D of TMP-SMX.

A

Absorption = rapidly/completely absorbed

Distribution = Good = lungs, urine, prostate and CSF

SMX = 70% protein bound

18
Q

How is TMP-SMX eliminated?

A

Liver and kidney = adjust dose for RI

19
Q

What are some clinical uses for TMP-SMX?

A

UTI (acute, chronic, recurrent)

Bacterial prostatitis (acute, chronic)

Skin infections (CA-MRSA)

Pneumocystis carinii pneumonia

Stenotrophomonas

Nocardia

20
Q

What are some major AEs of TMP-SMX?

A

GI + Jaundice/Hepatic necrosis

Hematologic = leukopenia/thrombocytopenia/anemia

Hypersensitivity = rash, epidermal necrolysis

CNS = aseptic meningitis, seizure

Renal Toxicity = tubular necrosis/crystalluria

Drug-induced lupus

21
Q

What drug interactions occur with TMP-SMX?

A

Phenytoin = increase phen levels

Warfarin = increase anticoagulation

Methotrexate = decrease renal clearance

22
Q

Describe MOA for Chloramphenicol.

A

Prevents protein synthesis = no peptide bond formation

Bacteriostatic EXCEPT against:

H. flu, Strep pneumo, N. meningitidis

23
Q

What are the mechanisms of resistance (MoR) for Chloramphenicol?

A

Reduced permeability/uptake

Ribosomal mutation

Acetyltransferase inactivation = responsible for widespread outbreaks of typhoid fever/Shigella in developing countries

24
Q

Describe A, D and E for Chloramphenicol.

A

Absorption:

Well absorbed by GI tract

Distribution:

Lipid soluble

Not highly protein bound

Distributes to CSF

Elimination:

Metabolized by liver = decrease dose in liver failure

Excreted by kidneys: dose adjustment NOT required in RI

25
Q

What is the SoA for Chloramphenicol?

A

Gram Positive: NOT active against S. aureus and Enterococci

Gram Negative: NOT active against P. aeruginosa

IS active against:

  • Rickettsiae spp
  • Spirochetes
  • Chlamydia
  • Mycoplasma

“Rocky Mountain Spotted Cold”

26
Q

List the clinical uses for Chloramphenicol.

A

NONE in U.S.

Developing World = pneumonia, bacterial meningitis, typhoid fever, RMSF

27
Q

What are the major AEs of Chloramphenicol?

A

Gray Baby Syndrome:

  • flaccidity
  • cyanosis
  • circulatory collapse/death

Hematologic = reversible bone marrow suppression and aplastic anemia

Anaphylaxis

Porphyria

28
Q

What are the UTI agents and what are their MOAs?

A

Nitrofurantoin:

  • Inhibits translation
  • Inhibits bacterial respiration/pyruvate metabolism

Methenamine:

  • NOT an antibiotic persay
  • Converted in acidic pH to ammonia/formaldehyde
  • Formaldehyde = denaturant of proteins/nucleic acid
29
Q

Describe the absorption of the UTI Agents.

A

Nitrofurantoin:

40-50% absorbed after oral administration

Occurs in small intestine

Enhanced with food

Methenamine:

Rapid absorption after oral administration

May be partially degraded by gastric acid

30
Q

What are the differences in distribution of Nitrofurantoin and Methenamine?

A

Nitrofurantoin = Large urine concentration, Low serum concentration

Methenamine = Broad distribution in tissues

31
Q

Explain the differences in excretion of Nitrofurantoin and Methenamine.

A

Nitrofurantoin = eliminated in urine with minor biliary excretion, shorter half-life

Methenamine = renal excretion, longer half-life

32
Q

What are the indications and contraindications for Nitrofurantoin?

A

IND: Acute, uncomplicated UTIs

CONTRA: Pyelonephritis, complicated UTIs

33
Q

What are the IND and CONTRAIND for Methenamine?

A

IND: Suppression/prophylaxis against recurrent UTIs

CONTRA: Established infections, prophylaxis against catheter-associated UTI

34
Q

What is the SoA for Nitrofurantoin?

A

Active against:

  • E. coli
  • Staph saprophyticus
  • Enterococcus/VRE
  • Group B strep

NOT active against:

  • P. aeruginosa
  • Proteus
  • Providencia

“The Three P’s”

35
Q

List the major AEs of Nitrofurantoin.

A

GI intolerance

Rash

Acute pulmonary symptoms:

  • weeks to months after exposure
  • rapid onset of fever, cough, dyspnea, myalgia
  • eosinophilia/lower lobe lung infiltrates

Subacute/chronic pulmonary reaction:

  • gradual onset of non-productive cough and dyspnea
  • Interstitial infiltrate on CXR
36
Q

List the major AEs of Methenamine.

A
  • Generally well-tolerated
  • Hepatitis
  • Leukopenia
  • Hemorrhagic Cystitis (higher dose)
  • Neuropathy
  • Anemia

Pharmacology Block III (8 decks)

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