Pcol II Exam 4

Gram POSITIVE vs Gram NEGATIVE bacteria

1. POS → CM + thick cell wall → purple/blue → mostly cocci

2. NEG → CM + thin cell wall + outer memb w porins + lipopolysach → red/pink → mostly bacilli

GRAM-POSITIVE SPECIES + identification

1. Staphylococcus → cluster → catalase + → aureus coag +, epi coag -

2. Streptococcus → chains → catalase - → a, b, y hemolytic

3. enterococcus → catalase -

Common infections of STAPHYLOCOCCUS (gram +)

1. Staphylococcus aureus → 6

2. Staphylococcus epidermidis

3. Staphylococcus saprophyticus

1. abscesses, osteomyelitis, food poisoning, TSS, nosocomial, endocarditis

2. endocarditis, line infxns

3. UTI

STREPTOCOCCUS SPECIES (gram +)

1. a hemolytic (partial lysis)

2. b hemolytic + Lancefield classification (full lysis)

3. y hemolytic (no lysis)

1. pneumoniae, viridans

2. group A pyogenes, B agalactiae, D bovis

3. enterococcus

Common infections of STREPTOCOCCUS (gram +)

1. Streptococcus pneumoniae

2. Viridans Streptococcus

3. Streptococcus pyogenes

4. Streptococcus agalactiae

1. community adult meningitis, acute sinusitis

2. endocarditis

3. soft tissue infxns, pharyngitis, rheumatic fever

4. neonatal meningitis

Enterococcus ___________ is typically vancomycin RESISTANT (VRE)

faecium

Gram-POSITIVE

1. shape =

1. _________ species + diseases (2)

2. _________ species + disease

1. +bacilli

2. listeria → meningitis, food poisoning

3. bacillus → anthrax

Gram-NEGATIVE

1. Shape =

2. ____________ gonorrhea, meningitis

1. -cocci

2. Neisseria

Gram-NEGATIVE coccobacillus

1. found in respiratory tract → ________ species

2. ______ species

1. haemophilus

2. moraxella

GRAM NEGATIVE DRUGS → SPACE

1. serratia

2. pseudomonas aeruginosa

3. acinetobacter

4. citrobacter

5. enterobacter

GRAM-NEGATIVE BACCILI

Enterobacterales (from the GUT) → YES PECKSS

1. Yersinia

2. Escherichia

3. serratia

4. proteus

5. enterobacter

6. citrobacter

7. Klebsiella

8. salmonella

9. shigella

1. Salmonella can cause (3)

2. Shigella can cause

3. Yersina can cause

4. Which can cause UTIs? (5)

1. typhoid fever, enterocolitis, sepsis

2. entercolitis

3. plague

4. E. coli, proteus, Klebsiella p, serratia, enterobacter

GRAM-NEGATIVE BACCILI:

Pseudomonas aeruginosa

1. “___________”

2. Highly ________ to antibiotics

3. Diseases → 7

1. non-fermenters

2. resistant

3. CF/lower resp, nosocomial, endocarditis, ear infxn, UTI, hot tub folliculitis, burn wound sepsis

GRAM-NEGATIVE BACCILI:

Burkholderia cepacia diseases

CF/lower resp, catheter + IV line infxns

ATYPICAL ORGANISMS

1. 3 major species

2. all 3 can cause _______

1. mycoplasma, chlamydia, legionella

2. pneumonia

ANAEROBIC organisms

1. _______ species (C diff)

2. -

1. clostridium

2. bacteroides

RESISTANT PATHOGENS → No ESKAPE

1. Enterococcus faecium (VRE, gram +)

2. Staph aureus (MRSA, gram +)

3. Klebsiella pneumoniae (ESBL, gram -)

4. Acinetobacter (gram -)

5. Pseudomonas aeruginosa (gram -)

6. Enterobacter (gram -) → C diff, E. coli

Important Resistance Genes:

1. MRSA

2. VRE

3. fluoroquinolone

4. plasmid mediated resistance in clindamycin + macrolides

5. E.coli to tetracyclines

6. P.aeruginosa to carbapenems

1. MecA

2. Van A/B/C

3. GyrA/B, parC

4. Erm

5. Tet A/B/C

6. OprD

AMINOGLYCOSIDES

1. The 3 most commonly used aminoglycosides

2. IRREVERSIBLE Inhibitors of __________ → _____ subunit

3. Mostly used against _________ bacteria

4. Including __________

5. Significant toxicities → 2

6. Other ADEs → 2

7. Polycationic → amine group is ______ at phys pH

8. _________ prevents oral absorption / penetration into CSF

9. Excretion →

10. How are AGs taken up by bacteria?

1. gentamicin, tobramycin, amikacin

2. protein synth → 30S

3. Aerobic gram -

4. pseudomonas

5. nephrotox, ototox

6. neuromusc blockade (myasthenia gravis susceptible), apnea

7. protonated

8. polarity

9. renal

10. passive porins → then active O2 depend process

Spectrum of Activity - AMINOGLYCOSIDES

1. Gram + bacteria → combination w cell wall active agent to produce ________ bactericidal effect

2. Gram - bacteria → active against … (3)

3. ______________ (3) are active against mycobacteria

4. _________ active against Entamoeba histolytica and other intestinal protozoa

1. synergistic

2. enterobacteriaceae, pseudomonas, gram - cocci (neisseria, moraxella, haemophilus)

3. streptomycin, tobramycin, amikacin

4. paromomycin

which aminoglycoside is the most active against M. tuberculosis?

streptomycin

Mechanisms of RESISTANCE against Aminoglycosides

1. Production of _______________ (most common) → 3 reactions

2. -permeability and -intracellular accumulation of drug → ______ systems seen w P. aeruginosa

3. Target ________

1. *inactivating enzymes → acetylation, adenylation, phos

2. efflux

3. alteration

AMINOGLYCOSIDES PK/PD

1. ________-dependent killing and __________

2. Goal of therapy:

3. Efficacy goal:

4. Dosing: Traditional vs extended, TYPICALLY GIVEN _____

1. conc, PAE

2. maximized concentrations

3. peak/MIC >10-12

4. IV

Other Aminoglycosides Dosage Forms

1. Ophthalmic →

2. Topical →

3. Inhalation + use →

1. gentamicin, tobramycin, neomycin-bacitracin-polymyxin B

2. neomycin-bacitracin-polymyxin B

3. tobramycin, amikacin → CF

AMINOGLYCOSIDES ADEs → Ototoxicity differences btwn AGs

1. strepto, genta → vestibular (balance)

2. amikacin, kanamycin, neomycin → auditory

3. tobra → both (equally)

Aminoglycosides Monitoring

1. Therapeutic effect → 5

2. Toxicity → 3

1. vitals signs (BP, HR, T, O2), WBC, procalcitonin, ESR, CRP

2. renal fx, urine output, hearing fx

AMINOGLYCOSIDES NEW AGENT:

1. Agent =

2. Resistant to enzyme _________ (acetyl, adenyl, phos)

3. Approved for ________

   Similar spectrum

   Similar ADEs

1. plazomicin (Zemdri)

2. modification

3. complicated UTIs

POLYMYXINS

1. Used against _______ organisms (last line of defense)

2. MOA: act as __________ → disrupt the structure of the ________ of GNB → leakage of intracell contents → rapidly bactericidal

3. Significant toxicity →

4. Other ADE

5. ACTIVE AGAINST →

6. Abs?

7. Excretion

8. Resistance?

1. MDR gram - bacilli

2. cationic detergents → outer memb

3. nephrotox

4. neurotox

5. gram - ONLY

6. poor PO abs

7. colistin → urine (unchanged), polymyxin B → non renal

8. RARE

POLYMYXIN PK/PD

1. _____-dependent and _______

2. Goals of therapy

3. Efficacy goal

1. conc, MODERATE PAE

2. maximize amt of drug received

3. AUC/MIC >12

Concomitant NEPHROTOXINS → 7

(DDI AGs & polymyxins)

1. vancomycin

2. ampho B

3. cisplatin

4. ACEi

5. NSAIDs

6. diuretics

7. radiocontrast

Which AG has good oral absorption?

A. gentamicin

B. tobramycin

C. amikacin

D. none

D

Which AG was recently approved for cUTI?

A. amikacin

B. plazomicin

C. gentamicin

D. tobramycin

B

Which is Colistin’s MOA?

A. causes rapid loss of K+ and membrane depolarization

B. inhibits transpeptidase

C. cationic detergents that disrupts bacterial cell membranes

D. bind 30S subunit and inhibit protein synthesis

C

Colistin is also known as polymyxin ____

E

Which is given IV as a prodrug?

A. polymyxin B

B. polymyxin E

B (colistin)

GLYCOPEPTIDES

vancomycin, teicoplanin, telavancin, dalbavancin, oritavancin

1. MOA: inhib ____________ by inhibiting ________ and is __________

2. ACTIVE AGAINST →

3. Mostly used against …

1. cell wall synth, D-ala-D-ala, bactericidal

2. gram + → kills staphylococci rel slowly

3. MRSA

Spectrum of Activity - GLYCOPEPTIDES (5)

1. MRSA

2. MRSE

3. strep

4. strep pneumoniae (PCN resistant)

5. enterococcus faecalis

GLYCOPEPTIDE RESISTANCE

1. _____ is a major concern

2. Occurs as a result of alteration of the last ________ terminus to either ________ or _____

3. Some concern about _____ and ______ (rare)

1. VRE

2. ala → lac or ser

3. VRSA/VISA

GLYCOPEPTIDES PK/PD

1. all have ______ PO abs

2. Vd → ________ has best CNS penetration

3. Excretion → RENAL (renal adjust)

4. Excretion → nonrenal

5. t1/2

6. Killing characteristics: ________ and ________ dependent

7. Goal of therapy:

8. Efficacy goal: _________ for MRSA

1. poor

2. vancomycin

3. vancomycin, telavancin, dalbavancin (Dalvance)

4. oritavancin (Orbactiv)

5. dalba 346 hr, orita 245 hr

6. conc, time

7. maximize amt of drug received

8. AUC/MIC 400-600

Which glycopeptides are given as a SINGLE dose?

oritavancin, dalbavancin

ADEs - VANCOMYCIN

1. “____________” syndrome → erythematous, urticaria, flushing, tachycardia, hypotension

2. _________ release from mast cells

3. *DO NOT EXCEED AN INF RATE OF ________

4. Reaction NOT observed w _____

5. Other ADE → ________ → risk factors (4)

1. red man syndrome

2. histamine

3. 1 g/hr

4. teicoplanin

5. nephrotox → total daily dose >4g, coadmin w piperacillin-tazobactam (Zosyn)/AGs, TR>15, AUC>800

ADES - TELEVANCIN (3)

1. nephrotox

2. teratogenic

3. +QT

GLYCOPEPTIDES: Therapeutic uses

1. vancomycin

2. telavancin

3. dalbavancin

4. oritavancin

1. MRSA/MRSE, PO for C diff, sev + non sev infxns

2. hosp acquired pneumonia, skin + soft tissue infxn

3. skin + soft tissue infxn

4. skin + soft tissue infxn

CYCLIC LIPOPEPTIDE

1. Agent →

2. MOA: ________ agent that is rapidly ________ for ____________ bacteria

3. ^ causes rapid _________ possibly by pore formation + membrane depolarization

4. kills _____ than vancomycin

5. *NOT USED FOR _________

6. May cause __________

1. daptomycin

2. cell memb, bactericidal, resistant gram +

3. loss of K+

4. FASTER

5. NO pneumonia

6. muscle injury

DAPTOMYCIN PK/PD

1. Abs

2. Vd

3. Excretion

4. Killing characteristics

5. goal of therapy

6. efficacy goal

7. Dose _______ for more severe infxns (blood stream, joint, etc) & VRE (monitor muscle injury)

1. poor PO, muscle toxicity → NO IM

2. very small → ECF

3. renal

4. conc, PAE

5. maximize conc

6. peak/MIC

7. inc

Why is daptomycin inappropriate for pneumonia even though it penetrates adequately into the lung?

inactivated by pulmonary surfactants

ADES - DAPTOMYCIN

Usually well tolerated

1. Monitor _____________ during therapy → rapidly resolves after DC

2. Daptomycin-induced acute __________________ is very rare, unpredictable, potentially serious AE → fever, hypoxia, pulm infiltrates

3. DRUG INTERACTIONS →

1. CPK weekly

2. eosinophilic pneumonia

3. statins (+CPK)

Which is vancomycin’s MOA?

A. inhib protein synthesis by binding 30S subunit

B. complex formation in cytoplasmic memb, rapid loss of K+

C. inhib cell wall synth by inhibiting transpeptidase

D. inhib cell wall synth by binding to D-ala-D-ala

D

Which may increase risk of nephrotoxicity with vancomycin?

A. rate >1 gram/hr

B. AUC <400

C. trough of 10-15

D. concurrent piperacillin-tazobactam

D

(A is for red man syndrome

TR >15 and AUC >800 would be risk nephro)

Daptomycin is active vs:

A. E.coli

B. VRE

C. Bacteroides sp

D. Mycoplasma

B (active vs resistant gram+)

Which is a common ADE of daptomycin?

A. nephrotoxicity

B. elevated CPK

C. hepatotox

D. QTc prolongation

B

BETA-LACTAMS

1. Includes … (4)

2. All share B-lactam ring and same MOA →

3. ^ these are involved in the final stages of the synthesis of _________

4. bacterial resistance continues to increase at a dramatic rate, unfortunately there are ________ of resistance

1. penicillin, cephalosporins, carbapenems, monobactams

2. inhib PBPs (cell wall synth)

3. peptidoglycan

4. multiple forms

BETA-LACTAMS: PENICILLINS

1. Narrow spectrum → 5

2. Broad spectrum → 2

3. BROADEST spectrum (pen + B-lactamase INHIBITOR) → 3

1. pen G, pen V, nafcillin, oxacillin, dicloxacillin

2. ampicillin, amoxicillin

3. ampicillin/sulbactam, amoxicillin/clavulanate, piperacillin/tazobactam

NATURAL PENICILLINS

1. Agents → 2

2. Used for _________ infxns →

3. Significant ADEs →

1. pen G, pen V

2. streptococcal → strep throat

3. allergic rxn, AB assoc diarrhea

Crucial enzymatic activities of PBPs:

1. ___________ → crosslinking of peptidoglycan

2. ___________ → links subunits of glycopeptide polymer

1. transpeptidase

2. glucosyltransferase

BETA-LACTAMS MOA OF RESISTANCE:

1. Decreased __________ to target site → must pass through porin channels

2. ________ of the target site (MRSA, MRSE, PRSP)

3. ________ pump

4. *MAJOR MOA: ___________ by a bacterial enzyme (AmpC, ESBL, CRE. plasmid-mediated)

1. penetration

2. alteration

3. efflux

4. inactivation

PENICILLINS PK/PD

1. Good PO abs = 4

2. ______ distribution

3. Excretion → Most eliminated _______ 60-90%

4. EXCEPT …

5. ______ half-lives

6. Killing characteristic: ____-dependent

7. Goal of therapy

8. Efficacy goal

1. PCN, amp, amox, dicloxa

2. wide

3. renally

4. antistaph → naf, ox, diclox (no renal adj)

5. short (1-2h)

6. time

7. maximize duration of exposure

8. T>MIC = 50%

ANTI-STAPH PENICILLINS

aka penicillinase-resistant penicillin

1. Agents → 3

2. ONLY active against (2)

3. Resist ________ of penicillinase

4. Significant ADEs

5. Dosing:

1. nafcillin, oxacillin, dicloxacillin

2. staph, strep (gram +)

3. hydrolysis

4. allergic rxn

5. NO renal adj

EXTENDED-SPECTRUM PENICILLINS

1. Aminopenicillins + activity →

2. Ureidopenicillins → almost always used in comb w tazobactam

3. Significant ADEs →

1. ampicillin, amoxicillin → strep, enterococci, listeria

2. piperacillin

3. allergic rxn, AB assoc diarrhea

B-LACTAMASE INHIBITORS

1. Have very _______ AB activity on their own

2. Prevent ______________ of beta-lactam ABs and thus extend the spectrum of activity

3. Aminopenicillins + BLI activity →

4. Piperacillin/tazobactam activity →

5. All extended-spectrum penicillins w or w/o BLI require __________

1. little

2. bacterial degradation

3. +MSSA, MORE GNB and ANAEROBES

4. MSSA, PSEUDOMONAS, anaerobes, enterobacter

5. renal adjust

ANTI-PSEUDOMONAL DOSING for piperacillin/tazobactam

4.5 g IV q 6h

1st line agents for diabetic foot infxns / animal bites

amox/clavulanate, amp/sulbactam

Meningitis → AB combination

aminopenicillin (amp/amox) + vanco + 3rd gen ceph

Piperacillin/tazobactam (ZOSYN) reserved for SERIOUS infxns caused by __________ organisms, often ______, often in combination

gram -, nosocomial

PCN ADEs

1. _______ rash 10%

2. Antibiotic-associated diarrhea type 1 → higher with ____________ PCNs

3. Antibiotic-associated diarrhea type 2 → _____ infxn as a concern

4. ______________ contains 1.7 mEQ of K+ → caution cardiac arrest w rapid infusion and hyperkalemia in renal failure

5. ________ at very high blood levels

1. amp

2. broader spectrum

3. C diff

4. IV Pen G

5. seizures

SUMMARY - PCNS SPECTRUM OF ACTIVITY

1. Natural PCNs

2. Anti-Staph PCNs

3. Amino PCNs

4. Amino + BLI (additional)

5. Piperacillin/tazobactam

1. enterococcus, strep, minimal GNB + anaerobes

2. MSSA, strep

3. enterococcus, strep, listeria, some H influenza + enterobacter

4. +MSSA, anaerobes, acinetobacter w sulbactam

5. enterococcus, strep, MSSA, anaerobes, pseudomonas, GNB

CEPHALOSPORINS:

1. MOA:

2. Resistance: particular concern w AmpC beta-lactamase producing _______/________

1. Bind PBPs

2. SPACE/SPICE -> I = indole + proteus

CEPHALOSPORINS PK/PD:

1. Killing characteristic: _____-dependent

2. Efficacy goal

3. _____ distribution 

4. ______ half lives 

5. Elimination

1. Time

2. T>MIC 50-70%

3. Wide

4. Short

5. Renal

Which cephalosporins have excellent CNS penetration?

cefotaxime, ceftriaxone, ceftazidime

Which cephalosporin has the longest half-life (5-9h vs 1-3h)?

ceftriaxone

Which cephalosporin is NOT renally eliminated (no dose adj)?

ceftriaxone

1ST GEN CEPHALOSPORINS

1. Agents =

2. Often used for …

3. Spectrum of activity

1. Cephalexin, cefadroxil, cefazolin 

2. Skin + soft tissue infxn, surg prophylaxis

3. MSSA, strep, some GNB/anaerobe

2ND GEN CEPHALOSPORINS

1. Agents = 4

2. MAY be used for …

3. Cephamycins may be used for _____ and _____ procedures

4. Spectrum of activity

1. Cefuroxime, cefprozil, cephamycins → cefoxitin & cefotetan

2. Upper resp infxn 

3. Intra-abdominal, gyn

4. Strep, Less MSSA than 1st gen, better GNB/anaerobe

___________ (2nd gen) or ___ gen cephalosporins used for otitis media in PCN allergic patients

cefuroxime + 3rd

3RD GEN CEPHALOSPORINS

1. Agents IV = 3

   Agents PO = cefpodoxime, cefixime, cefdinir, cefditoren, ceftibuten 

2. WIDELY used for … (4)

3. Spectrum of activity

1. Cefotaxime, ceftriaxome, ceftazidime 

2. Pneumonia, meningitis, bacteremia, sinusitis

3. Strep, Less MSSA than 1st gen, GNB

__________ is therapy of choice for all forms of gonorrhea

ceftriaxone

ANTI-PSEUDOMONAL CEPHS

1. Agents → ______ and ______ for pseudomonas infection

2. ___________ for RESISTANT pseudomonas infection

3. ___________ and __________ for ESBL + CRE organisms

1. Ceftazidime (3rd gen), cefepime (4th gen)

2. ceftolozane/tazobactam (Zerbaxa)

3. ceftazidime/avibactam (Avycaz), cefiderocol (gen 5)

4th and 5th generation cephalosporins

1. 4th = cefepime

2. 5th = ceftaroline, ceftolozane, cefiderocol

CEFTAZIDIME & CEFTOLOZANE

Spectrum of activity

NO STAPH, strep <ceftriaxone, pseudomonas, HIGHLY GNB

1. 4th Generation ceph = 

2. Spectrum of activity =

1. cefepime

2. MSSA, strep, HIGHLY GNB, pseudomonas, anaerobes

1. 5th generation ceph = 

2. Spectrum of activity =

1. Ceftaroline

2. MSSA, MRSA, VISA, Strep + PRSP (PCN resist strep pneumoniae), GNB

BLI + CEPH COMBINATIONS

1. Comb 1

2. Comb 2

3. Differences

4. FDA indication: complicated _________________ infections with ________

1. Avycaz → ceftazidime/avibactam

2. Zerbaxa → ceftolozane/tazobactam 

3. Zerbaxa ESBL < Avycaz, Zerbax NO CRE (Avycaz does)

4. Intra-abdominal, metronidazole

ADES OF CEPHALOSPORINS:

1. _________

2. _________ problematic in NEONATES → interacts with ________________, also biliary sludging that has produced ________

3. _________ w _______ at high doses/renal dysfx

4. _________

1. Allergic rxns

2. Ceftriaxone → calcium to form crystal deposits in lungs + kidneys → hyperbilirubinemia 

3. Encephalopathy → cefepime

4. AB assoc diarrhea

NEW CEPHALOSPORIN AGENT → Gen V

Cefiderocol (Fetroja) 

1. MOA: binds ______

2. Chelates _____ ions and uses bacterial iron transport systems (Trojan horse strategy)

3. Spectrum

1. PBP3

2. Ferric

3. MDR GNB

Which class has the BROADEST coverage of all beta-lactams?

Carbapenems

CARBAPENEMS

1. MOA:

2. Used in polymicrobial infxns to cover _____

3. GENERALLY RESISTANT to cleavage by most plasmid/chromosomal beta-lactamases, but _____ is a growing concern 

4. Spectrum of activity

1. Bind PBP

2. Resistant GNB

3. CRE

4. MSSA, strep, enterococ/pseudomonas/acinetobacter EXCEPT ertapenem, listeria, GNB, anaerobes

CARBAPENEMS PK/PD

1. Killing characteristics: _____ dependent

2. Goal efficacy

1. Time

2. T>MIC >40%

___________ and __________ are highly active against many CRE (carbapenem-resistant Enterobacteriaceae) + difference?

1. Vabomere - meropenem/vaborbactam 

2. Recarbrio - imipenem/cilastatin-relebactam

3. Vabomere 3h infusion vs Recarbrio 30 min

Which carbapenem can only be given once a day?

Ertapenem

CARBAPENEMS ADEs (3)

1. Allergic rxn

2. CNS tox

3. AB associated diarrhea

MONOBACTAMS

1. Agent = 

2. Structural similarities to _______

3. Active vs

4. Used for serious infxn in place of an _____ in patients with a history of ________

5. Spectrum of activity 

6. Elimination

1. Aztreonam

2. Ceftazidime 

3. pseudomonas aeruginosa

4. ESBL → PCN anaphylaxis 

5. GNB

6. renal

1. AZTREONAM is resistant to many of the β-lactamases produced by most GNB, including the metallo-β-lactamases but NOT THE ______ B-lactamases

2. _________ being developed -> activity against class A, class C, and select class D beta-lactamase enzymes

1. KPC

2. aztreonam/avibactam

CLINDAMYCIN

1. Class =

2. Active against ____ and _____

3. MOA: binds ______ subunit and suppress protein synth

4. ADEs → 3

5. Spectrum of activity

6. RESISTANCE → 2

7. GNB are intrinsically resistant due to ________ and ______

8. Therapeutic uses → 4

1. lincosamide

2. GPC, anaerobes

3. 50S

4. C diff, diarrhea/GI, allergic rxn

5. staph, strep, CA-MRSA, anaerobes

6. target modification, inactivation

7. poor perm, efflux pumps

8. skin/soft tissue infxn, polymicrobial, TSS, PID

Which agent is active vs CA-MRSA (community acquired)?

clindamycin

CLINDAMYCIN PK/PD

1. Abs

2. Vd

3. Metabolism

4. Excretion

5. Killing characteristic: _____ dependent

1. good PO

2. poor CSF

3. CYP3A4 substrate → N-demethyl clindamycin more active

4. not much renal

5. time

CLINDAMYCIN should be used with CAUTION in patients receiving _________

neuromusc blockers (clindamycin has some NM blockade)

1. DIAPHRAGM UP / oral anaerobes → use _______

2. Diaphragm down → use ______

1. clindamycin

2. metronidazole

NITROIMIDAZOLES

1. Primary tx of ________ and _______ infxns

2. Therapeutic uses: _________ infections w aerobic + anaerobic

3. MOA: production of ________ that are toxic to microbe → _________

4. Drug _______ activation by intracellular transport proteins ONLY IN ANAEROBIC CELLS

5. ADEs → 2

1. anaerobic, protozoal

2. polymicrobial

3. free radicals → disrupt DNA structure

4. reduction

5. GI/altered taste, CNS/disulfiram like

Which drug class used for anaerobic and protozoal infxns?

nitroimidazoles

NITROIMIDAZOLE PK/PD

Metronidazole

1. Abs

2. Vd

3. Metabolism

4. Excretion

Tinidazole

5. Abs

6. Vd

7. Metabolism

8. Excretion

1. good PO

2. tissues+CSF

3. hydroxymethyl = active; glucuronide/ox = inactive

4. renal

5. good PO

6. tissues

7. CYP3A4 substrate, ox/hydrox/conjug

8. little