174 terms

First Aid - Antmicrobials

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Methicillin
Penicillinase-resistant penicillins
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MOA: same as PCN. Narrow spectrum: penicillinase resistance because of bulkier R group
Use: S. aureus (except MRSA; resistant because of altered PCN-binding protein target site)
Toxicity: HSN Rxns, methicillin - interstitial nephritis
Nafcillin
Penicillinase-resistant penicillins, only one (along with oxacillin) not eliminated by the kidney
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MOA: same as PCN. Narrow spectrum: penicillinase resistance because of bulkier R group
Use: S. aureus (except MRSA; resistant because of altered PCN-binding protein target site)
Toxicity: HSN Rxns, methicillin - interstitial nephritis
Dicloxacillin
Penicillinase-resistant penicillins
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MOA: same as PCN. Narrow spectrum: penicillinase resistance because of bulkier R group
Use: S. aureus (except MRSA; resistant because of altered PCN-binding protein target site)
Toxicity: HSN Rxns, methicillin - interstitial nephritis
Penicillinase-resistant penicillins
methicillin, nafcilin, dicloxacillin
"use naf for staph"

MOA: same as PCN. Narrow spectrum: penicillinase resistance because of bulkier R group
Use: S. aureus (except MRSA; resistant because of altered PCN-binding protein target site)
Toxicity: HSN Rxns, methicillin - interstitial nephritis
Aminopenicillins
ampicillin, amoxicillin
"(AMPed up penicillin)"

MOA: same as PCN. Wider spectrum: penicillinase SENSITIVE. Also combine w/ clavulanic acid to protect against B-lactamase. AmOxicillin has greater Oral bioavailability than ampicillin
Use: extended spectrum penicillin - H flu, E. coli, Listeria, Proteus, Salmonella, Shigella "(HELPSS kill enterococci)"
Toxicity: HSN rxns, ampicillin rash, pseudomembranous colitis
REsistance: B-lactamases cleave B-lactam ring
penicillins
pen G, pen V. DOC for prophylaxis of endocarditis with surgical or dental procedures

MOA: 1) bind penicillin binding proteins 2) block transpeptidase cross-linking of peptidoglycan 3) activate autolytic enzymes
Use: GRAM + ORGANISMS (S. pneumo, S. pyo, actinomcyes) + SYPHILIS. Bactericidal for Gram + cocci, gram + rods, gram - cocci, spirochetes. NOT PENICILLINASE RESISTANT
Toxicity hypersensitivity rxns, hemolytic anemia
Resistance: B-lactamases cleave B-lactam ring
penicillin G
IV penicillin
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pen G, pen V
MOA: 1) bind penicillin binding proteins 2) block transpeptidase cross-linking of peptidoglycan 3) activate autolytic enzymes
Use: GRAM + ORGANISMS (S. pneumo, S. pyo, actinomcyes) + SYPHILIS. Bactericidal for Gram + cocci, gram + rods, gram - cocci, spirochetes. NOT PENICILLINASE RESISTANT
Toxicity hypersensitivity rxns, hemolytic anemia
Resistance: B-lactamases cleave B-lactam ring
Penivillin V
Oral penicillin
---------
pen G, pen V
MOA: 1) bind penicillin binding proteins 2) block transpeptidase cross-linking of peptidoglycan 3) activate autolytic enzymes
Use: GRAM + ORGANISMS (S. pneumo, S. pyo, actinomcyes) + SYPHILIS. Bactericidal for Gram + cocci, gram + rods, gram - cocci, spirochetes. NOT PENICILLINASE RESISTANT
Toxicity hypersensitivity rxns, hemolytic anemia
Resistance: B-lactamases cleave B-lactam ring
antipseudomonals
ticarcillin, carbenicillin, piperacillin

MOA: same as PCN, extended spectrum
Use: PSeudomonas and Gram neg rods; susceptible to penicillinase so use with clavulanic acid
Toxicity: HSN rxns

"TCP: Takes Care of Pseudomonas"
ticarcillin
antipseudomonal (carboxypenicillin), high Na load - caution in CHF/RF
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MOA: same as PCN, extended spectrum
Use: Empiric therapy for hospital aquired infection - Pseudomonas and Gram neg rods; susceptible to penicillinase so use with clavulanic acid
Toxicity: HSN rxns

"TCP: Takes Care of Pseudomonas"
carbenicillin
antipseudomonal (carboxypenicillin), poor F so use for UTI (high concentration in urine)
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MOA: same as PCN, extended spectrum
Use: Pseudomonas and Gram neg rods; susceptible to penicillinase so use with clavulanic acid
Toxicity: HSN rxns

"TCP: Takes Care of Pseudomonas"
piperacillin
antipseudomonal (ureidopenicillin), also has activity against anaerobes
------
MOA: same as PCN, extended spectrum
Use: Empiric therapy for hospital aquired infection - Pseudomonas and Gram neg rods; susceptible to penicillinase so use with clavulanic acid
Toxicity: HSN rxns

"TCP: Takes Care of Pseudomonas"
B-lactamase inhibitors
clavulanic acid, sulbactam, tazobactam
"CAST"
Augmentin: amoxicillin-cclavunate, only one that is PO, use for OM/sinusitis, URI/LRI and BITE WOUNDS.
Unasyn (ampicillin + sulbactam), zosyn (piperacillin + tazobactam) + timentin (ticarcillin + clavulanate) - all IV, use for polymicrobial infections (aspiration pneumo, abd, gyne and DM foot inf). Zosyn for empiric therapy of hisopital acquired infection

MOA: protects antibiotic from destruction by B-lactamase (penicillinase)
Use: often added to penicillin abx
clavulanic acid
B-lactamase inhibitor (+ amoxicilin = augmentin, + ticarcillin = timentin)
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MOA: protects antibiotic from destruction by B-lactamase (penicillinase)
Use: often added to penicillin abx
sulbactam
B-lactamase inhibitor (+ ampicillin = unasyn)
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MOA: protects antibiotic from destruction by B-lactamase (penicillinase)
Use: often added to penicillin abx
tazobactam
B-lactamase inhibitor (+ piperacillin = zosyn)
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MOA: protects antibiotic from destruction by B-lactamase (penicillinase)
Use: often added to penicillin abx
cephalosporins
1st gen: cefazolin, cephalexin
2nd gen: cefoxitin, cefaclor, cefuroxime
3rd gen: ceftriaxone, cefotaxime, ceftazidime
4th gen: cefepime
(Only cefuroxime, 3rd gen, and 4th gen cross BBB)

"Organisms not covered by cephalosporins are LAME: Listeria, Atypicals (chalmidya, mycoplasma), MRSA, Enterococci"

MOA: B-lactam drugs that inhibit CW synthesis, but LESS susceptible to penicilinases. BACTERICIDAL
Use: varies by generation
Toxicity: HSN rxns,
vit K deficiency.
Cross-HSN with penicilins occurs in 5-10% of pts.
Inc Nephrotoxicity of AGs
Disulfuram-like reaction with ethanol (in those with a methylthiotetrazole group like cefamandole)
cefazolin
first generation cephalosporins,
Used for prophylaxis of infectino during surgery


MOA: B-lactam drugs that inhibit CW synthesis, but LESS susceptible to penicilinases. BACTERICIDAL
Use: FIRST GEN = GRAM + COCCI: PEcK - Proteus, E. Coli, Klebsiella
Toxicity: HSN rxns,
vit K deficiency.
Cross-HSN with penicilins occurs in 5-10% of pts.
Inc Nephrotoxicity of AGs
Disulfuram-like reaction with ethanol (in those with a methylthiotetrazole group like cefamandole)
cephalexin
first generation cephalosporins
Used for SSTIs due to staph (does NOT cover MRSA)


MOA: B-lactam drugs that inhibit CW synthesis, but LESS susceptible to penicilinases. BACTERICIDAL
Use: FIRST GEN = GRAM + COCCI: PEcK - Proteus, E. Coli, Klebsiella
Toxicity: HSN rxns,
vit K deficiency.
Cross-HSN with penicilins occurs in 5-10% of pts.
Inc Nephrotoxicity of AGs
Disulfuram-like reaction with ethanol (in those with a methylthiotetrazole group like cefamandole)
cefoxitin
2nd generation cephalosporins, has activity against anaerobes and can be used in polymicrobial inf/infection prophylaxis for abdominal surgery

MOA: B-lactam drugs that inhibit CW synthesis, but LESS susceptible to penicilinases. BACTERICIDAL
Use: SECOND GEN: GRAM + COCCI (HEN PEcKS): H. flu, Enterobacter, Neiserria, Proteus, E. coli, Klebsiella, Serratia marcescens
Toxicity: HSN rxns,
vit K deficiency.
Cross-HSN with penicilins occurs in 5-10% of pts.
Inc Nephrotoxicity of AGs
Disulfuram-like reaction with ethanol (in those with a methylthiotetrazole group like cefamandole)
cefaclor
2nd generation cephalosporins

MOA: B-lactam drugs that inhibit CW synthesis, but LESS susceptible to penicilinases. BACTERICIDAL
Use: SECOND GEN: GRAM + COCCI (HEN PEcKS): H. flu, Enterobacter, Neiserria, Proteus, E. coli, Klebsiella, Serratia marcescens
Toxicity: HSN rxns,
vit K deficiency.
Cross-HSN with penicilins occurs in 5-10% of pts.
Inc Nephrotoxicity of AGs
Disulfuram-like reaction with ethanol (in those with a methylthiotetrazole group like cefamandole)
cefuroxime
2nd generation cephalosporins

MOA: B-lactam drugs that inhibit CW synthesis, but LESS susceptible to penicilinases. BACTERICIDAL
Use: SECOND GEN: GRAM + COCCI (HEN PEcKS): H. flu, Enterobacter, Neiserria, Proteus, E. coli, Klebsiella, Serratia marcescens
Toxicity: HSN rxns,
vit K deficiency.
Cross-HSN with penicilins occurs in 5-10% of pts.
Inc Nephrotoxicity of AGs
Disulfuram-like reaction with ethanol (in those with a methylthiotetrazole group like cefamandole)
ceftriaxone
third generation cephalosporins
CEFTRIAXONE USED ALSO FOR MENINGITIS AND GONORRHEA, best gram + activity (including PRSP) NO pseudomonas activity (same as cefotaxime in this regard)

MOA: B-lactam drugs that inhibit CW synthesis, but LESS susceptible to penicilinases. BACTERICIDAL
Use: THIRD GEN: serious gram neg inf resistant to other B-lactams
Toxicity: HSN rxns,
vit K deficiency.
Cross-HSN with penicilins occurs in 5-10% of pts.
Inc Nephrotoxicity of AGs
Disulfuram-like reaction with ethanol (in those with a methylthiotetrazole group like cefamandole)
cefotaxime
third generation cephalosporins best gram + activity (including PRSP) NO pseudomonas activity (same as ceftriaxone in this regard)

MOA: B-lactam drugs that inhibit CW synthesis, but LESS susceptible to penicilinases. BACTERICIDAL
Use: THIRD GEN: serious gram neg inf resistant to other B-lactams
Toxicity: HSN rxns,
vit K deficiency.
Cross-HSN with penicilins occurs in 5-10% of pts.
Inc Nephrotoxicity of AGs
Disulfuram-like reaction with ethanol (in those with a methylthiotetrazole group like cefamandole)
ceftazidime
third generation cephalosporins
CEFTAZIDIME ALSO USED FOR PSEUDOMONAS

MOA: B-lactam drugs that inhibit CW synthesis, but LESS susceptible to penicilinases. BACTERICIDAL
Use: THIRD GEN: serious gram neg inf resistant to other B-lactams
Toxicity: HSN rxns,
vit K deficiency.
Cross-HSN with penicilins occurs in 5-10% of pts.
Inc Nephrotoxicity of AGs
Disulfuram-like reaction with ethanol (in those with a methylthiotetrazole group like cefamandole)
cefepime
4th gen cephalosporins

MOA: B-lactam drugs that inhibit CW synthesis, but LESS susceptible to penicilinases. BACTERICIDAL
Use: FOURTH GEN: inc activity against PSEUDOMONAS and gram + organisms (good for febrile neutropenia)
Toxicity: HSN rxns,
vit K deficiency.
Cross-HSN with penicilins occurs in 5-10% of pts.
Inc Nephrotoxicity of AGs
Disulfuram-like reaction with ethanol (in those with a methylthiotetrazole group like cefamandole)
azotreonam
MOA: monobactam resistant to B-lactamases. Inhibits CW synthesis (binds to PBP3). Synergistic witha minoglycosides. No cross-allergenicity with penicillins
Use: Gram NEG RODS ONLY - no activity against Gram +! For *PCN-allergic pts* and those with renal insuff who cannot tolerate aminoglycosides
Toxicity: usually nontoxic; occasional GI upset
NO CROSS SENSITIVITY WITH PCNS OR CEPHALOSPORINS!
Carbipenems
Imipenem (+cilasatin), meropenem
"With impienem, killin is LASTIN with ciLASTATIN"
MOST BROAD SPECTRUM AGENTS

MOA: broad-spectrum, B-lactamase-resistant carbapenem. Always admin with cilastatin (inhibitor of renal dehydropeptidase I) to dec inactivation of drug in renal tubules
Use: Gram + cocci, GNR, anaerobes. Wide spectrum, but significant side effects limit use to life-threatening infections or after other drugs have failed. Meropene, has reduced risk of seizures and is stable to dihydropeptidase I.
Toxicity: GI distress, skin rash, CNS TOXICITY (SEIZURES) at high plasma levels
Imipenem/cilastatin
Carbipenem
"With impienem, killin is LASTIN with ciLASTATIN",
(Imipenem is nephrotoxic, so NEED to give with cilastin which inhibits its hydrolysis by DHP in the renal brush border)
Worst carbipenem in terms of SEIZURE risk

MOA: broad-spectrum, B-lactamase-resistant carbapenem. Always admin with cilastatin (inhibitor of renal dehydropeptidase I) to dec inactivation of drug in renal tubules
Use: Gram + cocci, GNR, anaerobes. Wide spectrum, but significant side effects limit use to life-threatening infections or after other drugs have failed.
Toxicity: GI distress, skin rash, CNS TOXICITY (SEIZURES) at high plasma levels
meropenem
carbipenem
Meropenem has reduced risk of seizures and is stable to dihydropeptidase I.
also the carbipenem that is best for MENINGITIS

MOA: broad-spectrum, B-lactamase-resistant carbapenem.
Use: Gram + cocci, GNR, anaerobes. Wide spectrum, but significant side effects limit use to life-threatening infections or after other drugs have failed
Toxicity: GI distress, skin rash, CNS TOXICITY (SEIZURES) at high plasma levels
vancomycin
MOA: Inhibits CW mucopeptide formation by binding D-ala D-ala portion of CW precursors. BACTERICIDAL.
USE: GRAM POSITIVE ONLY (NO GRAM NEGATIVE ACTIVITY, so does NOT cover pseudomonas) - serious, multi-drug resistant oranisms, icluding S. auerus, enterococci and C. diff (oral dose for pseuodmembranous colitis). ALSO COVERS COAG NEG STAPH!
Toxicity: "Well tolerated in general - does NOT have many problems":
Nephrotixicity,
Ototoxicity,
Thrombophlebitis (NOT),
diffuse flushing (Red man syndrome - prevent w/ pretreatment with anthistamines and slow infusion rate)

Resistance: W/ amino acid change of D-ala D-ala to D-ala D-lac "Pay back 2 D-alas (dollars) for vandalizing."
protein synthesis inhibitors
30s: aminoglycosides (bactericidal), tetracyclines (bacteriostatic)
50s: chloramphenicol, clindamycin (bacteriostatic), erythromycin (macrolides, bacteriostatic), linezolid (Variable)

"Buy AT 30, CEL at 50"
aminoglycosides
gentamicin, neomycin, amikacin, tobramycin, streptomycin
"Mean GNATS canNOT kill anaerobes"

MOA: BACTERICIDAL; inhibits formation of initiation complex and causes misreading of mRNA. Require O2 for uptake; therefore ineffective against anaerobes.
Use: severe ENTERIC GRAM NEGATIVE ROD infections. Amikacin best for pseudomonas. Synergistic with B-lactam antiobiotics (Staph, Strep viridans, enterococcus and gram negs). Neomycin for bowel surgery.
Toxicity: Nephrotoxicity (esp when used with cephalosporins)
Ototoxicity (esp when used with loop diuretics)
Teratrogen, neuromuscular blockade (do not give to a pt with myasthenia gravis)
Resistance: Transferase enzymes that inactivate the drug by acetylation, phosphorylation or adenylation
tetracyclines
tetracycline, doxycycline, demeclocycline, minocycline
"*D*emeclocycline - ADH antagonist, acts as a DD*emeclocycline - ADH antagonist, acts as a *D*iuretic in SIADH"

MOA: BActeriostatic,
bind to 30S and prevent attachment of aminoacyl-tRNA; limited CNS penetration.
Doxycycline is fecally elimianted and can be used in pts with renal failure.
Must NOT take with milk, antacids or iron-containing preps b/c divalent cations inhibit absorption in the gut
Use: Borellia burgdorferi, M. pneumoniae.
Drugs ability to accumulate intracellularly makes it very effective against Rickettsia and Chlamidya
Toxicity: GI distress, discoloration of teeth and inhibition of bone growth in repgnancy, photosensitivity, contraindicated in pregnancy
Resistance: Dec uptake into cells or inc efflux out of cell by plasmid-encoded transport pumps
gentamicin
aminoglycoside
most nephrotoxic

MOA: BACTERICIDAL; inhibits formation of initiation complex and causes misreading of mRNA. Require O2 for uptake; therefore ineffective against anaerobes.
Use: severe GRAM NEGATIVE ROD infecitons. Synergistic with B-lactam antiobiotics. Neomycin for bowel surgery.
Toxicity: Nephrotoxicity (esp when used with cephalosporins)
Ototoxicity (esp when used with loop diuretics)
Teratrogen
Resistance: Transferase enzymes that inactivate the drug by acetylation, phosphorylation or adenylation
neomycin
aminoglycoside
BOWEL SURGERY

MOA: BACTERICIDAL; inhibits formation of initiation complex and causes misreading of mRNA. Require O2 for uptake; therefore ineffective against anaerobes.
Use: severe GRAM NEGATIVE ROD infecitons. Synergistic with B-lactam antiobiotics. Neomycin for bowel surgery.
Toxicity: Nephrotoxicity (esp when used with cephalosporins)
Ototoxicity (esp when used with loop diuretics)
Teratrogen
Resistance: Transferase enzymes that inactivate the drug by acetylation, phosphorylation or adenylation
amikacin
aminoglycoside
best one against pseudomonas

MOA: BACTERICIDAL; inhibits formation of initiation complex and causes misreading of mRNA. Require O2 for uptake; therefore ineffective against anaerobes.
Use: severe GRAM NEGATIVE ROD infecitons. Synergistic with B-lactam antiobiotics. Neomycin for bowel surgery.
Toxicity: Nephrotoxicity (esp when used with cephalosporins)
Ototoxicity (esp when used with loop diuretics)
Teratrogen
Resistance: Transferase enzymes that inactivate the drug by acetylation, phosphorylation or adenylation
tobramycin
aminoglycoside


MOA: BACTERICIDAL; inhibits formation of initiation complex and causes misreading of mRNA. Require O2 for uptake; therefore ineffective against anaerobes.
Use: severe GRAM NEGATIVE ROD infecitons. Synergistic with B-lactam antiobiotics. Neomycin for bowel surgery.
Toxicity: Nephrotoxicity (esp when used with cephalosporins)
Ototoxicity (esp when used with loop diuretics)
Teratrogen
Resistance: Transferase enzymes that inactivate the drug by acetylation, phosphorylation or adenylation
streptomycin
aminoglycoside
Also used against Tb


MOA: BACTERICIDAL; inhibits formation of initiation complex and causes misreading of mRNA. Require O2 for uptake; therefore ineffective against anaerobes.
Use: severe GRAM NEGATIVE ROD infecitons. Synergistic with B-lactam antiobiotics. Neomycin for bowel surgery.
Toxicity: Nephrotoxicity (esp when used with cephalosporins)
Ototoxicity (esp when used with loop diuretics)
Teratrogen
Resistance: Transferase enzymes that inactivate the drug by acetylation, phosphorylation or adenylation
tetracycline
tetracycline

MOA: BActeriostatic,
bind to 30S and prevent attachment of aminoacyl-tRNA; limited CNS penetration.
Doxycycline is fecally elimianted and can be used in pts with renal failure.
Must NOT take with milk, antacids or iron-containing preps b/c divalent cations inhibit absorption in the gut
Use: Borellia burgdorferi, M. pneumoniae.
Drugs ability to accumulate intracellularly makes it very effective against Rickettsia and Chlamidya
Toxicity: GI distress, discoloration of teeth and inhibition of bone growth in repgnancy, photosensitivity, contraindicated in pregnancy
Resistance: Dec uptake into cells or inc efflux out of cell by plasmid-encoded transport pumps
doxycycline
tetracycline
Doxycycline is fecally elimianted and can be used in pts with renal failure.
Good drug against chlamidya (but azithro often preferred b/c it is only 1 dose)

MOA: BActeriostatic,
bind to 30S and prevent attachment of aminoacyl-tRNA; limited CNS penetration.
Doxycycline is fecally elimianted and can be used in pts with renal failure.
Must NOT take with milk, antacids or iron-containing preps b/c divalent cations inhibit absorption in the gut
Use: Borellia burgdorferi, M. pneumoniae.
Drugs ability to accumulate intracellularly makes it very effective against Rickettsia and Chlamidya
Toxicity: GI distress, discoloration of teeth and inhibition of bone growth in repgnancy, photosensitivity, contraindicated in pregnancy
Resistance: Dec uptake into cells or inc efflux out of cell by plasmid-encoded transport pumps
demeclocycline
tetracycline
ADH antagonist, acts as a diuretic in SIADH (AE: Can cause reversible nephrogenic diabetes insipidus)
----
MOA: BActeriostatic,
bind to 30S and prevent attachment of aminoacyl-tRNA; limited CNS penetration.
Doxycycline is fecally elimianted and can be used in pts with renal failure.
Must NOT take with milk, antacids or iron-containing preps b/c divalent cations inhibit absorption in the gut
Use: Borellia burgdorferi, M. pneumoniae.
Drugs ability to accumulate intracellularly makes it very effective against Rickettsia and Chlamidya
Toxicity: GI distress, discoloration of teeth and inhibition of bone growth in repgnancy, photosensitivity, contraindicated in pregnancy
Resistance: Dec uptake into cells or inc efflux out of cell by plasmid-encoded transport pumps
minocycline
tetracycline, can use for prophylaxis of meningococcal inf

MOA: BActeriostatic,
bind to 30S and prevent attachment of aminoacyl-tRNA; limited CNS penetration.
Doxycycline is fecally elimianted and can be used in pts with renal failure.
Must NOT take with milk, antacids or iron-containing preps b/c divalent cations inhibit absorption in the gut
Use: Borellia burgdorferi, M. pneumoniae.
Drugs ability to accumulate intracellularly makes it very effective against Rickettsia and Chlamidya
Toxicity: GI distress, discoloration of teeth and inhibition of bone growth in repgnancy, photosensitivity, contraindicated in pregnancy
Resistance: Dec uptake into cells or inc efflux out of cell by plasmid-encoded transport pumps
macrolides
erythromycin, azithromycin, clarithryomycin

MOA: Inhibits synthesis by blocking translocaiton ("macroSlides"); bind to the 23S rRNA of the 50s ribosomal subunit. BacterioSTATIC
Use: atypical pneumonias (MYCOPLASMA, CHLAMIDYA, LEGIONELLA), URIs (azithro for H. flu), STDs (Azithro for chlamidya), gram + cocci (STreptococcal infections in pts allergic to penicillin) and Neisseria
Toxicity: Prolonged QT interval (esp erythromycin), GI discomfort (most common cause of noncompliance), acute choelstatic hepatitis, eosinophilia, skin rashes. Otototoxic. P450 inhibitors: Increases serum concentration of theophyllines, oral anticoagulants.
Resistance: Methylation of 23S rRNA binding site
erythromycin
Macrolide

MOA: Inhibits synthesis by blocking translocaiton ("macroSlides"); bind to the 23S rRNA of the 50s ribosomal subunit. BacterioSTATIC
Use: atypical pneumonias (MYCOPLASMA, CHLAMIDYA, LEGIONELLA), URIs, STDs, gram + cocci (STreptococcal infections in pts allergic to penicillin) and Neisseria
Toxicity: Prolonged QT interval (esp erythromycin), GI discomfort (most common cause of noncompliance), acute choelstatic hepatitis, eosinophilia, skin rashes. Increases serum concentration of theophyllines, oral anticoagulants.
Resistance: Methylation of 23S rRNA binding site
azithromycin
Macrolide (used for H. Flu, STDs/Chlamidya and MAC prophylaxis)

MOA: Inhibits synthesis by blocking translocaiton ("macroSlides"); bind to the 23S rRNA of the 50s ribosomal subunit. BacterioSTATIC
Use: atypical pneumonias (MYCOPLASMA, CHLAMIDYA, LEGIONELLA), URIs, STDs, gram + cocci (STreptococcal infections in pts allergic to penicillin) and Neisseria
Toxicity: Prolonged QT interval (esp erythromycin), GI discomfort (most common cause of noncompliance), acute choelstatic hepatitis, eosinophilia, skin rashes. Increases serum concentration of theophyllines, oral anticoagulants.
Resistance: Methylation of 23S rRNA binding site
clarithromycin
Macrolide

MOA: Inhibits synthesis by blocking translocaiton ("macroSlides"); bind to the 23S rRNA of the 50s ribosomal subunit. BacterioSTATIC
Use: atypical pneumonias (MYCOPLASMA, CHLAMIDYA, LEGIONELLA), URIs, STDs, gram + cocci (STreptococcal infections in pts allergic to penicillin) and Neisseria
Toxicity: Prolonged QT interval (esp erythromycin), GI discomfort (most common cause of noncompliance), acute choelstatic hepatitis, eosinophilia, skin rashes. Increases serum concentration of theophyllines, oral anticoagulants.
Resistance: Methylation of 23S rRNA binding site
chloramphenicol
Mainly used in 3rd world for Meningitis, Typhoid fever, Rocky Mt Spotted Fever
MOA: blocks peptidyl transferase, and thus peptide bond formation at teh 50S ribosomal subunit. BacterioSTATIC.
Use: MENINGITIS (H. influ, N. meningiditis, S. pneumo). Conservative use owing to toxicities but often still use in developing countries due to low cost.
Toxicity: Anemia (dose-dependent), aplastic anemia (dose-independent), gray baby syndrome (in premature infants bc they lack liver UDP-guluronyl transferase, see abd distention, vomitting, cyanosis, death)
Resistance: plasmid-encoded acetyltransferase that inactivates drug
clindamycin
BEST DRUG FOR anaerobes outside of CNS: pulmonary, diabetic foot, intraabd, pelvic, decubitus ulcers
MOA: blocks peptide bond formation at 50s ribosomal subunit. BacterioSTATIc (inhibits translocation during elongation)
USE: Gram + only (aerobes and anaerobes). Anaerobic infections (e.g. Bacteroides, fragilis, Clostridium perfringens) in aspiration pneumonia or lung abscesses
Treats anaerobes above the diaphragm vs. metronidazole (anaerobes below the diaphragm)
Toxicity: PSeudomembraous colitis (C. Diff overgrowth), fever, diarrhea
sulfonamides
sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine
Great activity against gram negative and positive aerobes, but none against pseudomonas or anaerobes

MOA: PABA antimetabolites inhibit dihydropteroate synthetase. Bacteriostatic.
Use: Gram +, gram -, Nocardia, Chlamidya. Triple sulfas or SMX for simple UTI.
Toxicity: Hypersensitivity reactions, hemolysis if G6PD deficient, npehrotixicity (tubulointerstitial nephritis), phoeotsensitivity, kernicterus in infants, displace other drugs fromalbumin (e.g. warfarin)
Resistance: Altered enzyme (abcterial dihydropteroate synthetase), dec uptake, or inc PABA
sulfamethoxazole (SMX)
sulfanamide

MOA: PABA antimetabolites inhibit dihydropteroate synthetase. Bacteriostatic.
Use: Gram +, gram -, Nocardia, Chlamidya. Triple sulfas or SMX for simple UTI.
Toxicity: Hypersensitivity reactions, hemolysis if G6PD deficient, npehrotixicity (tubulointerstitial nephritis), phoeotsensitivity, kernicterus in infants, displace other drugs fromalbumin (e.g. warfarin)
Resistance: Altered enzyme (abcterial dihydropteroate synthetase), dec uptake, or inc PABA
sulfisoxazole
sulfanamide

MOA: PABA antimetabolites inhibit dihydropteroate synthetase. Bacteriostatic.
Use: Gram +, gram -, Nocardia, Chlamidya. Triple sulfas or SMX for simple UTI.
Toxicity: Hypersensitivity reactions, hemolysis if G6PD deficient, npehrotixicity (tubulointerstitial nephritis), phoeotsensitivity, kernicterus in infants, displace other drugs fromalbumin (e.g. warfarin)
Resistance: Altered enzyme (abcterial dihydropteroate synthetase), dec uptake, or inc PABA
sulfadiazine
sulfanamide

MOA: PABA antimetabolites inhibit dihydropteroate synthetase. Bacteriostatic.
Use: Gram +, gram -, Nocardia, Chlamidya. Triple sulfas or SMX for simple UTI.
Toxicity: Hypersensitivity reactions, hemolysis if G6PD deficient, npehrotixicity (tubulointerstitial nephritis), phoeotsensitivity, kernicterus in infants, displace other drugs fromalbumin (e.g. warfarin)
Resistance: Altered enzyme (abcterial dihydropteroate synthetase), dec uptake, or inc PABA
trimethropim
"TMP: Treats Marrow Poorly"

MOA: inhibits bacterial dihydrofolate reductase. BacterioSTATIC
Use: USed in combo with sulfonamides (TMP-SMX) causing sequential block of folate synthesis. Combination used for UTIs, shigella, salmonella, PCP pneumonia
Toxicity: Megaloblastic anemia, leukopenia, granulocytopenia (may aleviate with supplemental folinic acid - leucovorin rescue)
fluoroquinolones
ciprofloxacin, norfloxacin, levofloxacin, ofloxacin, sparfloxacin, moxifloxacin, gatifloxacin, enoxacin
quinolon: nalidixic acid
"FluoroquinoLONES hurt attachments to your BONES"

MOA: inhibits DNA gyrase (topoisomerase II). Bactericidal. Must NOT be taken with antacids.
Use: gram neg rods of urinary and GI tracts - including pseuodmonas, Neisseria, some gram + organisms
Toxicity: GI upset, superinfections, skin rashes, headache, dizziness. Contraindicates in pregnant women and in children because animal studies show damage to cartilage. Tendonitis and tendon rupture in adults leg cramps and myalgias in kids.
Resistance: chromosome-encoded mutation in DNA gyrase
ciprofloxacin
Fluoroquinolones, best for pseudomonas, not for PSRP, caution in transplant pts on cyclosporine. DOC FOR PROPHPYLAXIS OF MENINGOCOCCAL INFECTION

MOA: inhibits DNA gyrase (topoisomerase II). Bactericidal. Must NOT be taken with antacids.
Use: gram neg rods of urinary and GI tracts - including pseuodmonas, Neisseria, some gram + organisms
Toxicity: GI upset, superinfections, skin rashes, headache, dizziness. Contraindicates in pregnant women and in children because animal studies show damage to cartilage. Tendonitis and tendon rupture in adults leg cramps and myalgias in kids.
Resistance: chromosome-encoded mutation in DNA gyrase
norfloxacin
Fluoroquinolones

MOA: inhibits DNA gyrase (topoisomerase II). Bactericidal. Must NOT be taken with antacids.
Use: gram neg rods of urinary and GI tracts - including pseuodmonas, Neisseria, some gram + organisms
Toxicity: GI upset, superinfections, skin rashes, headache, dizziness. Contraindicates in pregnant women and in children because animal studies show damage to cartilage. Tendonitis and tendon rupture in adults leg cramps and myalgias in kids.
Resistance: chromosome-encoded mutation in DNA gyrase
levofloxacin
Fluoroquinolones, active against BOTH pseudomonas and PRSP

MOA: inhibits DNA gyrase (topoisomerase II). Bactericidal. Must NOT be taken with antacids.
Use: gram neg rods of urinary and GI tracts - including pseuodmonas, Neisseria, some gram + organisms
Toxicity: GI upset, superinfections, skin rashes, headache, dizziness. Contraindicates in pregnant women and in children because animal studies show damage to cartilage. Tendonitis and tendon rupture in adults leg cramps and myalgias in kids.
Resistance: chromosome-encoded mutation in DNA gyrase
moxifloxacin
Fluoroquinolones,
only one that doesn't cover pseudomonas, can't use in UTI, covers anaerobes

MOA: inhibits DNA gyrase (topoisomerase II). Bactericidal. Must NOT be taken with antacids.
Use: gram neg rods of urinary and GI tracts - including pseuodmonas, Neisseria, some gram + organisms
Toxicity: GI upset, superinfections, skin rashes, headache, dizziness. Contraindicates in pregnant women and in children because animal studies show damage to cartilage. Tendonitis and tendon rupture in adults leg cramps and myalgias in kids.
Resistance: chromosome-encoded mutation in DNA gyrase
sparfloxacin
Fluoroquinolones

MOA: inhibits DNA gyrase (topoisomerase II). Bactericidal. Must NOT be taken with antacids.
Use: gram neg rods of urinary and GI tracts - including pseuodmonas, Neisseria, some gram + organisms
Toxicity: GI upset, superinfections, skin rashes, headache, dizziness. Contraindicates in pregnant women and in children because animal studies show damage to cartilage. Tendonitis and tendon rupture in adults leg cramps and myalgias in kids.
Resistance: chromosome-encoded mutation in DNA gyrase
moxifloxacin
Fluoroquinolones

MOA: inhibits DNA gyrase (topoisomerase II). Bactericidal. Must NOT be taken with antacids.
Use: gram neg rods of urinary and GI tracts - including pseuodmonas, Neisseria, some gram + organisms
Toxicity: GI upset, superinfections, skin rashes, headache, dizziness. Contraindicates in pregnant women and in children because animal studies show damage to cartilage. Tendonitis and tendon rupture in adults leg cramps and myalgias in kids.
Resistance: chromosome-encoded mutation in DNA gyrase
gatifloxacin
Fluoroquinolones

MOA: inhibits DNA gyrase (topoisomerase II). Bactericidal. Must NOT be taken with antacids.
Use: gram neg rods of urinary and GI tracts - including pseuodmonas, Neisseria, some gram + organisms
Toxicity: GI upset, superinfections, skin rashes, headache, dizziness. Contraindicates in pregnant women and in children because animal studies show damage to cartilage. Tendonitis and tendon rupture in adults leg cramps and myalgias in kids.
Resistance: chromosome-encoded mutation in DNA gyrase
enoxacin
Fluoroquinolones

MOA: inhibits DNA gyrase (topoisomerase II). Bactericidal. Must NOT be taken with antacids.
Use: gram neg rods of urinary and GI tracts - including pseuodmonas, Neisseria, some gram + organisms
Toxicity: GI upset, superinfections, skin rashes, headache, dizziness. Contraindicates in pregnant women and in children because animal studies show damage to cartilage. Tendonitis and tendon rupture in adults leg cramps and myalgias in kids.
Resistance: chromosome-encoded mutation in DNA gyrase
nalidixic acid
Just a QUINOLONE (not a fluoroquinolone)

MOA: inhibits DNA gyrase (topoisomerase II). Bactericidal. Must NOT be taken with antacids.
Use: gram neg rods of urinary and GI tracts - including pseuodmonas, Neisseria, some gram + organisms
Toxicity: GI upset, superinfections, skin rashes, headache, dizziness. Contraindicates in pregnant women and in children because animal studies show damage to cartilage. Tendonitis and tendon rupture in adults leg cramps and myalgias in kids.
Resistance: chromosome-encoded mutation in DNA gyrase
metronidazole
One of the only drugs that can penetrate abscesses. NOT active in O2 environment (opposite of aminoglycosides) b/c activated by a reductive process.
MOA: Forms free radical toxic metabaolites in bacterial cell that damage DNA. Bactericidal, antiprotozoal
Use: Anaerobic inf below the diaphragm.
Treats GIARDIA,
ENTAMOEBA
TRICHOMONAS,
GARDNERLLA VAGINALIS,
ANAEROES (bacteroids, C. difF).
Used with BISMUTH and AMOXICILIN (or tetracycline) for Triple therapy against H. pylori
"GET GAP on the METRO!"
Toxicity: Disulfiram-like reaction with alcohol; headache, metallic taste. Peripheral neuropathy and seizures. DO NOT GIVE IN PREGNANCY (Teratrogen).
antimycobacterial drugs
-M tb
-MAC
-M. leprae

prophylaxis and treatment?
M. Tb: isoniazid to prevent, RIPE to treat (rifampin, isoniazid, pyrazinamide, ethambutol)
MAC: azithromycin to prevent, azithromycin, rifampin, ethambutol and streptomycin to treat
M. Leprae: nothing for prophylaxis, to treaT: dapsone, rifampin, clofazimine
isoniazid
"INH: Injuries Neurons and Hepatocytes"

MOA: Dec synthesis of mycolic acids. Bacteria catalase negative peroxidase (KatG) needed to convert INH-> active metabolite
USE: M. Tuberculosis. The ONLY agent used as solo prophylaxis against TB
Toxicity: neurotox, hepatotox (esp in elderly, alcoholics, previous liver damage, pregnancy, active hep B), lupus
Pyroxidine (B6) can prevent neurotoxicity and lupus

Metabolized in the liver via ACETYLATION. (rapid acetylator: inc risk of hepatitis), slow acetylator (inc risk of peripheral neuropathy)
rifampin
"4 R's: RNA pol inhibitor, Revs up mitochondrial p450, Red/Orange body fluids, Rapid resistance if used alone" In pts on HIV meds, use RIFABUTIN INSTEAD!

MOA: inhibits DNA dependent RNA polymerase
USE: M TUBRCULOSIS;
Delays resistance to dapsone when used for leprosy.
Used for meningococcal prophylaxisand chemoprophylaxis inc ontacts of kids with H. influ type B

Toxicity: Minor hepatotoxicity and drug interactions (induces P-450)
Red/Orange body fluids (nonhazardous AE). IMPAIRS OCPs AND HIV DRUGS! (major inducer of P450s)
pyrazinamide
MOA: Inhibits mycolic acid production by blocking mycobacterial Fatty acid synthase I; effective in acidic pH of phagolysosomes where Tb engulfed by macs is found (ACTIVE AGAINST INTRACELLULAR ORGANISMS)
*USE: M. Tb
Toxicity: Hyperuricemia/arthralgia, hepatotoxicity, avoid in renal failure
ethambutol
MOA: dec carbohydrate polymerization of Mb cell wall by blocking arabinosyltransferase.
USE: mycobacterial Tb
Toxicity: OPTIC NEUROPATHY (green-red color blindness) - DO NOT USE IN KIDS TOO YOUNG TO ASSESS ISUAL ACUITY!
prophylaxis of meningococcal inf
ciprofloxcin (DOC), rifampin, minocycline
prophylaxis of gonorrhea
ceftriaxone
prophylaxis of syphilis
benzathine penicillin G
history of recurrent UTIs, prophylaxis of UTIS?
TMP-SMX
prophylaxis of endocarditis with surgical or dental procedures
penicillins
CD4< 200 prophylaxis
TMP-SMX: PCP
CD4< 100 prophylaxis
TMP-SMX: PCP and toxoplasmosis
CD4<50 prophylaxis
azithromycin: MAC
treatment of MRSA
vancomycin
Treatment of VRE
linezolid and streptogramins (quinupristin, dalfopristin)
streptogramins
quinupristin, dalfopristin
treatment of VRE
quinupristin
streptogramin
tx of VRE
dalfopristin
streptogramin
tx of VRE
empiric tx of outpt pneumonia
macrolides
empiric tx of inpt pneumoni
FQs
empiric tx of pneumonia in ICU
B-lactam + (FQ or azithromycin)
Antifungals that inhibit membrane function
polyenes: amphotericin B, nystatin
antifungals that inhibit cell wall synthesis
echinocandins: capsfungin
Antifungals that inhibit nucleic acid synthesis
5-fluorocytosine
antifungals that inhibit lanosterol synthesis
naftifine, terbinafine
antifungals that inhibit ergosterol synthesis
fluconazole, itraconazole, voriconazole
amphociterin B
Polyene
amphociterin "TEARS" holes in the fungal memb by forming pores
ONLY ANTIFUNGAL SAFE IN PREGNANCY.


MOA: binds ergosterol (unique to fungi); forms membrane pores that allow leakage of electrolytes (binds only weakly to cholesterol -> fungal lysis)
Use: serious, systemic mycoses. Cryptococcus, blastomyces, coccidioides, aspergillus, histoplasma, candida, DOC FOR MUCOR (systemic mycoses)
Intrathecal for fungal meningitis (does NOT cross BBB)
Supplement K and Mg due to altered renal tube permeability
Toxicity:
fever/chills ("shake and bake")
hypotension
nephrotoxicity (hypoK, hypoMg)
arrythmias
anemia (dec EPO)
IV phlebitis ("amphoterrible")
Hydration reduces nephrotoxicity
Liposomal amphotericin reduces toxicity

Can premedicate with anti-pyretics and anti-histamines to diminish acute infusion related rxns
nystatin
Polyene
"Swish and swallow"

MOA: same as amphoB, but TOPICAL b/c too toxic fo rsystemic use
Use: Swish and swallow for oral candidiasis (thrush - ex. in pt on inhaled corticosteroids who develops thrush), topical for diaper rash or vaginal candidiasis - NOT active against dermatophytes
Azoles
fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, vorconizole

MOA: inhibit fungal sterol (Ergosterol) synthesis, by inhibiting the P-450 enzyme that converts lanosterol to ergosterol
Use: systemic mycoses.
Fluconazole: cryptococcal meningitis in AIDS pts (can cross BBB) and candidal inf of all types
Ketoconazole: blastomyces, coccidioes, histoplasma, Candida, hypercortisolism
Clotrimazole and miconazole: topical fungal infections
Variconazole: invasive aspergillus (also crosses BBB)
Toxicity: hormone synthesis inhibition (gynecomastia), liver dysfn (inhibit cytochrome P450), fever, chills, GI sx, fetal abnormalities (NOT for pregnancy)
fluconazole
Azole
3 C's: Cryptococcal meningitis in AIDS pts (can cross BBB), Candidal inf of all types, coccidiodes (narrowest spectrum)
Can cause alopecia (but well tolerated and has fewest drug interactions)
Along w. voriconazole - only one that can enter CSF

MOA: inhibit fungal sterol (Ergosterol) synthesis, by inhibiting the P-450 enzyme that converts lanosterol to ergosterol
Use: systemic mycoses.
Toxicity: hormone synthesis inhibition (gynecomastia), liver dysfn (inhibit cytochrome P450), fever, chills, GI sx, fetal abnormalities (NOT for pregnancy)
ketoconazole
Azole
blastomyces, coccidioes, histoplasma, Candida, hypercortisolism
Decreases adrenal/gonadal hormone synth b/c it inhiits the CYP450 enzymes that synthesize them (dec cortisol/testosterone/estrogen -> can lead go gynceomastia, libido, impotence, menstrual irregularities, hypotension, fatigue)

MOA: inhibit fungal sterol (Ergosterol) synthesis, by inhibiting the P-450 enzyme that converts lanosterol to ergosterol
Use: systemic mycoses.
Toxicity: hormone synthesis inhibition (gynecomastia), liver dysfn (inhibit cytochrome P450), fever, chills, GI sx, fetal abnormalities (NOT for pregnancy)
clotrimazole
azole, topical fungal infections

MOA: inhibit fungal sterol (Ergosterol) synthesis, by inhibiting the P-450 enzyme that converts lanosterol to ergosterol
miconazole
azole
topical fungal infections

MOA: inhibit fungal sterol (Ergosterol) synthesis, by inhibiting the P-450 enzyme that converts lanosterol to ergosterol
itraconazole
DOC for dermatophytes, onchomycosis, non-meningeal inf of blasto/histo/sporothrix/occidiomyoces, also active against Candida, aspergillus
AE: hypertension, hypokalemia, peripheral edema (can cause CHF in pts with ventricular dysfn!)

MOA: inhibit fungal sterol (Ergosterol) synthesis, by inhibiting the P-450 enzyme that converts lanosterol to ergosterol
Use: systemic mycoses.
Toxicity: hormone synthesis inhibition (gynecomastia), liver dysfn (inhibit cytochrome P450), fever, chills, GI sx, fetal abnormalities (NOT for pregnancy)
voriconazole
Variconazole: DOC for invasive aspergillus (also crosses BBB)
AE: vision changes, periostitis, photosensitivity, hallucinations/seizures

MOA: inhibit fungal sterol (Ergosterol) synthesis, by inhibiting the P-450 enzyme that converts lanosterol to ergosterol
Use: systemic mycoses.
Toxicity: hormone synthesis inhibition (gynecomastia), liver dysfn (inhibit cytochrome P450), fever, chills, GI sx, fetal abnormalities (NOT for pregnancy)
flucytosine
MOA: inhibits DNA synthesis by conversion to 5-flucouracil by cytosine deaminase
Use: systemic fungal infections (e.g. cryptococcus) in combo with ampho B (mainly used for synergy in ampho B to lower resistance)
Toxicity: nausea, vomiting, darrihea, bone marrow suppression, teratrogenic
capsofungin
echinocandin - first to TARGET CELL WALL DIRECTLY
MOA: inhibist cell wall synthesis, inhibits synthesis of B-glucan
Use: invasive aspergillosis, Candida
Toxicity: GI upset, flushing (histamine-like effect with itching associated with rapid infusion)
terbinafine
Allylamine

MOA: inhibits fungal enzyme SQUALENE EPOXIDASE (impairs fungal memb fn by inhibition synthesis of ergosterol)
Use: dermatophytes (esp ONCHOMYCOSIS: fungal inf of finger or toe nails)
Toxicity: Abnormal LFTs, visual disturbances

USed topically or orally, accumulates in skin and nails
griseofulvin
For MUCOCUTANEOUS INF

MOA: interferes with MT function; disrupts mitosis. Deposits in keratin-containing tissues (nails)
REquires long term tx
Use: ONLY active against DERMATOPHYTES (tineal ringworm)- oral tx of superficial infections
Toxicity: teratrogenic, carcinogenic, confusion, headaches, inc P-450 and warfarin metabolism and OCPs (LOTS of drug interactions)
antiprotoazoan therapy for
1) Toxoplasmosis?
2) T. crusi?
3). Leishmaniasis?
4) Giardia?
5) E. histolytica?
6) Trichomonas?
Toxoplasmosis: Pyrimethamine + sulfadiazine
Trypanosoma brucei: suramin and melarsoprol
T. crusi: nifurtimox
Leishmaniasis: sodium stiboclugonate
Giardia: metronidazole
E. histolytica: metronidazole
Trichomonas: metronidazole
chloroquine
MOA: blocks plasmodium heme polymerase
Use: Plasmodium species
Toxicity: retinopathy, G6PD hemolysis
pyrimethamine
toxoplasmosis (+sulfadiazine) or plasmodium falciparum
suramin + melarsoprol
trypanosoma brucei
nifurtimox
T. cruzi
Sodium stibogluconate
leishmaniasis (lots of AE: joint pain, QT prolongation, others)
Antihelmnthic therapy
mebendazole, pyrantel pamoate, ivermectin diethylcarbamazine, praziquantel (imobilize helminths)
mebendazole
anti-helminth, DOC for trichinosis (can also use for hookworm, ascariasis, pinworm, taeniasis, strongyloides),
pyrantel pamoate
anti-helminth, DOC for ascaris, pinworm (not trichuris or strongyloides). Can also use for hookworm.
ivermectin
anti-helminth, DOC for river blindness (onchocerciasis) and strogyloidiasis (AE: MAZOTTI REACTION - fever, HA, dizziness (hypersensitivity from worm death)
diethylcarbamazine (DEC)
anti-helminth
Use: DOC for lymphatic filariasis (W. bancrofit), loiasis, tropical eosinophilia, toxocare canis/catis.

AE: hypersensitivity rxn to onchocerciasis (to dying parasite) -use ivermectin instead (same rxn but not as bad)
praziquantel
anti-helminth, DOC for all trematodes (flukes): schistosomiasis, chinese liver fluke (chlonorchis sinensis/viverrini), lung fluke (paragonimus westermani) AND for some cestodes: T. solium (bendazoles + steroids better for neurocysticercosis), D. Latum
amantidine
"A Man 2 dine" takes off his COAT
"Amantadine blocks influ A and causes problems with cerebellA"
(Rimantidine = derivative w/ fewer CNS side effects, does not cross BBB)

MOA: blocks viral penetration/uncoating (M2 protein)
Also causes release of DA from intact nerve terminals
Use: prophylaxis and tx of influenza A ONLY, Parkinson's disease
Toxicity: ataxia, dizziness, slurred speech
REsistance: Mutated M2, 90% of all influenza A strains are resistant so it's not used.
zanamivir
MOA: inhibit influenza neuraminidase, decreasing release of progeny virus
Use: influenza A AND B
osteltamivir
MOA: inhibit influenza neuraminidase, decreasing release of progeny virus
Use: influenza A AND B
ribavirin
MOA: inhibist synthesis of guanine nucleotides by competitive inhibiting IMP dehydrogenase.
Use: RSV, chronic hep C
Toxicity: hemolytic anemia. Severe teratrogen
acylcovir
MOA: monophosphorylated by HSV/VZV thymidine kinase. Guanosine analog. Triphosphate formed by cellular enzymes. Preferentially inhibits viral DNA pol by chain termination.
Use: HSV, VZV, EBV. Used for HSV-induced mucocutaneous and genital lesions as well as for encephalitis. Prophylaxis in immunocompromised pts. No effect on latent forms of HSV and vZV. Valacyclovir (prodrug) has better oral bioavailability.
For herpes zoster, use drelated agent, famciclovir
Toxicity: few serious AE
Resistance: Lack of viral thymidine kinase
gancicylovir
MOA: 5-monophosphate formed by CMV viral kinase. Guanosine analog. Triphosphate formed by cellular kinases. Preferentially inhibits viral DNA polymerase.
Use: CMV, esp in immunocomp pts. Valganciclovir, prodrug of gancicloir, has better oral bioavailability
Toxicity: leukopenia, neutropenia, thrombocytopenia, renal toxicivity. More toxic to host enzymes than acyclovir. Caution when giving with zidovudine (bad neutropenia/BM suppression)!!
MOR: mutated CMV DNA polymerase or lack of viral kinase
foscarnet
"FOScarnet = pyroFOSphate analog"

MOA: viral DNa pol inhibitor that binds to the pyrophosphate-binding site of the enzyme. Does NOT require activatio by viral kinase
Use: CMV retinitis in immunocompromised pts when gangicovir fails, acyclovir-resistant HSV
Toxicity: nephrotoxicity (renal Mg wasting and loss of Ca due to chelation and dec PTH -> hypocalcemia, hypomagnesemia -> seizures)
*AE: Mutated DNA pol
cidofovir
MOA: preferentially inhibits DNA pol. does NOT require phosphorylation by viral kinase.
USE: CMV retinitis in immunocompromised pts; acyclovir-resistant HSV. Long half-life. Nephrotoxicivity (coadminister with probenecid).
protease inhibitors:
lopinavir, atazanavir, darunavir, fosamprenavir, saquinavir, ritonavir
All end in NAVIR
"NAVIR TEASE a proTEASE"

MOA: prevent maturation of new viruses (assembly of virions depends on HIV-1 protease - pol gene, which cleaves polypeptide products of HIV mRNA into their functional parts). Ritonavir BOOSTS other drugs by inhibiting P450
USE: HAART (HIV)
Toxicity: hyperglycemia, GI intolerance (nausea, diarrhea, lipodystrophy, metabolic syndrome (only use pravastatin or fluvastatin - non Cyp substrates, for HL)
lopinavir
HIV, Protease inhibitor

MOA: prevent maturation of new viruses (assembly of virions depends on HIV-1 protease - pol gene, which cleaves polypeptide products of HIV mRNA into their functional parts). Ritonavir BOOSTS other drugs by inhibiting P450
USE: HAART (HIV)
Toxicity: hyperglycemia, GI intolerance (nausea, diarrhea, lipodystrophy, metabolic syndrome (only use pravastatin or fluvastatin - non Cyp substrates, for HL)
atazanavir
HIV, Protease inhibitor

MOA: prevent maturation of new viruses (assembly of virions depends on HIV-1 protease - pol gene, which cleaves polypeptide products of HIV mRNA into their functional parts). Ritonavir BOOSTS other drugs by inhibiting P450
USE: HAART (HIV)
Toxicity: hyperglycemia, GI intolerance (nausea, diarrhea, lipodystrophy, metabolic syndrome (only use pravastatin or fluvastatin - non Cyp substrates, for HL)
darunavir
HIV, Protease inhibitor

MOA: prevent maturation of new viruses (assembly of virions depends on HIV-1 protease - pol gene, which cleaves polypeptide products of HIV mRNA into their functional parts). Ritonavir BOOSTS other drugs by inhibiting P450
USE: HAART (HIV)
Toxicity: hyperglycemia, GI intolerance (nausea, diarrhea, lipodystrophy, metabolic syndrome (only use pravastatin or fluvastatin - non Cyp substrates, for HL)
fosamprenavir
HIV, Protease inhibitor

MOA: prevent maturation of new viruses (assembly of virions depends on HIV-1 protease - pol gene, which cleaves polypeptide products of HIV mRNA into their functional parts). Ritonavir BOOSTS other drugs by inhibiting P450
USE: HAART (HIV)
Toxicity: hyperglycemia, GI intolerance (nausea, diarrhea, lipodystrophy, metabolic syndrome (only use pravastatin or fluvastatin - non Cyp substrates, for HL)
saquinavir
HIV, Protease inhibitor

MOA: prevent maturation of new viruses (assembly of virions depends on HIV-1 protease - pol gene, which cleaves polypeptide products of HIV mRNA into their functional parts). Ritonavir BOOSTS other drugs by inhibiting P450
USE: HAART (HIV)
Toxicity: hyperglycemia, GI intolerance (nausea, diarrhea, lipodystrophy, metabolic syndrome (only use pravastatin or fluvastatin - non Cyp substrates, for HL)
ritonavir
HIV, Protease inhibitor
Ritonavir BOOSTS other drugs by inhibiting P450

------
MOA: prevent maturation of new viruses (assembly of virions depends on HIV-1 protease - pol gene, which cleaves polypeptide products of HIV mRNA into their functional parts).
USE: HAART (HIV)
Toxicity: hyperglycemia, GI intolerance (nausea, diarrhea, lipodystrophy, metabolic syndrome (only use pravastatin or fluvastatin - non Cyp substrates, for HL)
NRTIs
tenofovir
emtricitabine
abacavir
lamivudine
zidovudine
didanosine
stavudine
"Have YOU DINED (vudine) with my NUCLEAR (nucleosides) family?
-Slow resistance

MOA: competitive inhibit nucleotide binding to RT and termiante the DNA chain (lack a 3-OH group). Must be phosphorylated by thymidine kinase to be active.
Use: ZDV for general prophylaxis and during pregnancy to reduce fetal transmission
Toxicity: Bone marrow suppression (can be reversed with G-CSF and erythropoetin), peripherla neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (ZDV)
NNRTIs
neVIRapine
EfaVIRenz
DelaVIRdine

MOA: bind to RT at site diff from NRTIs. Do NOT require phosphorylation to be active or compete with nucleotides
Use: HIV HAART
Toxicity: same as NRTIs:
Toxicity: Bone marrow suppression (can be reversed with G-CSF and erythropoetin), peripherla neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (ZDV)

Disaadvantage: rapid resistance
tenofivir
HIV - NRTI
-Slow resistance

MOA: competitive inhibit nucleotide binding to RT and termiante the DNA chain (lack a 3-OH group). Must be phosphorylated by thymidine kinase to be active.
active.
Use: HAART
Toxicity: Bone marrow suppression (can be reversed with G-CSF and erythropoetin), peripherla neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (ZDV)
emtricitabine
HIV - NRTI
-Slow resistance

MOA: competitive inhibit nucleotide binding to RT and termiante the DNA chain (lack a 3-OH group). Must be phosphorylated by thymidine kinase to be active.
active.
Use: HAART
Toxicity: Bone marrow suppression (can be reversed with G-CSF and erythropoetin), peripherla neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (ZDV)
abacavir
HIV - NRTI
-Slow resistance

MOA: competitive inhibit nucleotide binding to RT and termiante the DNA chain (lack a 3-OH group). Must be phosphorylated by thymidine kinase to be active.
active.
Use: HAART
Toxicity: Bone marrow suppression (can be reversed with G-CSF and erythropoetin), peripherla neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (ZDV)
lamivudine
HIV - NRTI
-Slow resistance

MOA: competitive inhibit nucleotide binding to RT and termiante the DNA chain (lack a 3-OH group). Must be phosphorylated by thymidine kinase to be active.
active.
Use: HAART
Toxicity: Bone marrow suppression (can be reversed with G-CSF and erythropoetin), peripherla neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (ZDV)
zidovudine
HIV - NRTI
-Slow resistance
ZDV for general prophylaxis and during pregnancy to reduce fetal transmission

MOA: competitive inhibit nucleotide binding to RT and termiante the DNA chain (lack a 3-OH group). Must be phosphorylated by thymidine kinase to be active.
Use: HAART
Toxicity: Bone marrow suppression (can be reversed with G-CSF and erythropoetin), peripherla neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (ZDV)
didanosine
HIV - NRTI
-Slow resistance

MOA: competitive inhibit nucleotide binding to RT and termiante the DNA chain (lack a 3-OH group). Must be phosphorylated by thymidine kinase to be active.
Use: ZDV for general prophylaxis and during pregnancy to reduce fetal transmission
Toxicity: Bone marrow suppression (can be reversed with G-CSF and erythropoetin), peripherla neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (ZDV)
stavudine
HIV - NRTI
-Slow resistance

MOA: competitive inhibit nucleotide binding to RT and termiante the DNA chain (lack a 3-OH group). Must be phosphorylated by thymidine kinase to be active.
Use: ZDV for general prophylaxis and during pregnancy to reduce fetal transmission
Toxicity: Bone marrow suppression (can be reversed with G-CSF and erythropoetin), peripherla neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (ZDV)
nevirapine
HIV-NNRTIS

MOA: bind to RT at site diff from NRTIs. Do NOT require phosphorylation to be active or compete with nucleotides
Use: HIV HAART
Toxicity: same as NRTIs:
Bone marrow suppression (can be reversed with G-CSF and erythropoetin), peripherla neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (ZDV)

Disaadvantage: rapid resistance
efavirenz
HIV-NNRTIS

MOA: bind to RT at site diff from NRTIs. Do NOT require phosphorylation to be active or compete with nucleotides
Use: HIV HAART
Toxicity: same as NRTIs:
Bone marrow suppression (can be reversed with G-CSF and erythropoetin), peripherla neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (ZDV)

Disaadvantage: rapid resistance
delavirdine
HIV-NNRTIS

MOA: bind to RT at site diff from NRTIs. Do NOT require phosphorylation to be active or compete with nucleotides
Use: HIV HAART
Toxicity: same as NRTIs:
Bone marrow suppression (can be reversed with G-CSF and erythropoetin), peripherla neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (ZDV)

Disaadvantage: rapid resistance
raltegravir
HIV, Integrase inhibitors

MOA: inhibits HIV genome integration into host ell chormosome by inhibiting HIV integrase REVERSIBLY

AE: Hypercholesterolemia
interferons
MOA: glycoproteins synthesized by virus-inf cells block replication of both RNA and DNA viruses.
USE: IFN-a chronic hep B and C, Kaposi's sarcoma.
IFN-B - MS,
IFN-Y: NADPH oxidase deficiency
AE: Neutropenia
antimicrobials to avoid in pregnancy
clarithromycin - embryotoxic
sulfonamides - kernicterus
aminoglycosides - ototoxicity
fluroquinolones - cartilage damage
metronidazole - mutagenesis
tetracyclines - discolored teeth, inhibition of bone growth
ribavirin (antiviral) -teratrogenic
griseofulvin (Antifungal) -teratrogenic
chloramphenicol - gray baby
"Countless SAFe Moms Take Really Good Care"
block cell wall synthesis by inhibition of peptidoglycan cross linking
penicillin, methicillin, ampicilin, piperacillin, cephalosporins, aztreonam, imipenem
block peptidoglycan snthesis
bacitracin, vancomycin
block nucleotide synthesis
sulfonamides, trimethoprim
blcok DNA topoisomerases
fluoroquinolones
block mRNA synthesis
rifampin
Damage DNA
metronidazole
block protein synthesis at 50s ribosomal subnit
chloramphenicol, macrolides, clindamycin, streptogrammins (quinupristin, dalfopristin, linezolid)
block protein synthesis at 30 s ribosomal subunit
aminoglycosides, tetracyclines
amipcillin
aminopenicillin
"(AMPed up penicillin)"

MOA: same as PCN. Wider spectrum: penicillinase SENSITIVE. Also combine w/ clavulanic acid to protect against B-lactamase. AmOxicillin has greater Oral bioavailability than ampicillin
Use: extended spectrum penicillin - H flu, E. coli, Listeria, Proteus, Salmonella, Shigella "(HELPSS kill enterococci)"
Toxicity: HSN rxns, ampicillin rash, pseudomembranous colitis
REsistance: B-lactamases cleave B-lactam ring
amoxicillin
ampicillin, amoxicillin
"(AMPed up penicillin)"
-------------
MOA: same as PCN. Wider spectrum: penicillinase SENSITIVE. Also combine w/ clavulanic acid to protect against B-lactamase. AmOxicillin has greater Oral bioavailability than ampicillin
Use: extended spectrum penicillin - H flu, E. coli, Listeria, Proteus, Salmonella, Shigella "(HELPSS kill enterococci)"
Toxicity: HSN rxns, ampicillin rash, pseudomembranous colitis
REsistance: B-lactamases cleave B-lactam ring
Mefloquine
Treatment or prophylaxis of plasmodium species
Quinine
Treatment of resistant plasmodium species in combo with pyrimethamine/sulfonamide
Rimantidine
Rimantidine = derivative of amantidine w/ fewer CNS side effects, does not cross BBB

MOA: blocks viral penetration/uncoating (M2 protein)
Use: Influenza A
Valacyclovir
prodrug of acyclovir, better oral bioavailability
--------
acyclovir:
MOA: monophosphorylated by HSV/VZV thymidine kinase. Guanosine analog. Triphosphate formed by cellular enzymes. Preferentially inhibits viral DNA pol by chain termination.
Use: HSV, VZV, EBV. Used for HSV-induced mucocutaneous and genital lesions as well as for encephalitis. Prophylaxis in immunocompromised pts. No effect on latent forms of HSV and vZV. Valacyclovir (prodrug) has better oral bioavailability.
For herpes zoster, use drelated agent, famciclovir
Toxicity: few serious AE
Resistance: Lack of viral thymidine kinase
Famciclovir
related to acyclovir, use for herpes
---------
acyclvori:
MOA: monophosphorylated by HSV/VZV thymidine kinase. Guanosine analog. Triphosphate formed by cellular enzymes. Preferentially inhibits viral DNA pol by chain termination.
Use: HSV, VZV, EBV. Used for HSV-induced mucocutaneous and genital lesions as well as for encephalitis. Prophylaxis in immunocompromised pts. No effect on latent forms of HSV and vZV. Valacyclovir (prodrug) has better oral bioavailability.
For herpes zoster, use drelated agent, famciclovir
Toxicity: few serious AE
Resistance: Lack of viral thymidine kinase
valganciclovir
prodrug of gangiclovir with better oral bioavailability
------
gangiclyovir:
MOA: 5-monophosphate formed by CMV viral kinase. Guanosine analog. Triphosphate formed by cellular kinases. Preferentially inhibits viral DNA polymerase.
Use: CMV, esp in immunocomp pts. Valganciclovir, prodrug of gancicloir, has better oral bioavailability
Toxicity: leukopenia, neutropenia, thrombocytopenia, renal toxicivity. More toxic to host enzymes than acyclovir. Caution when giving with zidovudine (bad neutropenia/BM suppression)
MOR: mtuated CMV DNA polymerase or lack of viral kinase
HAART
highly active antiretroviral therapy
-initiated when pts present with
1) AIDs-defining illness
2) LOW CD4 (<350)
3) High viral load

Regiment = 3 drugs to prevent resistance:
2 NRTIs + 1 NNRTI OR 1 Protease inhibitor OR 1 integrase inhibitor
IFN-A
MOA: glycoproteins synthesized by virus-inf cells block replication of both RNA and DNA viruses.
USE: IFN-a chronic hep B and C, Kaposi's sarcoma.
AE: Neutropenia
IFN-B
MOA: glycoproteins synthesized by virus-inf cells block replication of both RNA and DNA viruses.
USE: IFN-B - MS,
AE: Neutropenia
IFN-Y
MOA: glycoproteins synthesized by virus-inf cells block replication of both RNA and DNA viruses.
USE: IFN-Y: NADPH oxidase deficiency
AE: Neutropenia
Linezolid
Use: Gram + aerobes and anaerobes, esp those that are multi-drug resistant.
MRSA, VRE, MSSA
AE: lactic acidosis, perpiheral neuropathy, thrombocytopenia/annemia. EXPENSIVE.
can cause serotonin syndrome with MOA-i.
Dapsone
Use: leprosy, 2nd lien for Tb, PCP pneumonia and prophylaxis
AE: Hemolytic anemia (G6PD deficiency)
Clofazimine
Use: Leprosy, MDR Tb
AE: SKIN PIGMENTATION
Posaconazole
only azole active against zygomycoses (broadest spectrum)
Albendazole
DOC for T. solium - neurocysticercosis (no effect on calcified brain cysts). Can also use in pinworm, ascariasis, hookworm trichuriasis, strongyloides, echinococcus. Can give with steroids to dec inflammation
DOC for STIs
1) Syphillis
2) Gonorrhea
3) Chalmidya
1) Pen G for syphillus
2) Ceftriaxone for ghonorrhea
3) Azithromycin (1 dose) or Doxycycline Chalmidya
4) Gonorrhea and chlamidya commonly appaeartogether so usually need to cover for both.
Options for treating CMV retinitis
1) Ganciclovir (only one of the 3 that requires phosphorylation to be active)
2) Foscarnet
3) Cidofovir
Which antivirals require phosphorylation by thymidine kinase to be active? which don't?
Require phosphorylation: NRTIs, acyclovir, valacyclovir, famciclovir, ganciclovir
Don't require phosphorylation: Protease inhibitors, NNRTIs, integrase inhibitors, foscarnet, cidofovir