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119 Cards in this Set

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Penicllin
forms
MOA
Penicillin G (IV), penicillin V (oral)

MOA--
1) Binds penicillin binding proteins
2) blocks transpeptidase cross linking of cell wall
3) Activates autolytic enzymes
Penicillin
Clinical use
bacteriacidal for gram negative cocci, gram + rods, gram+ cocci, and spirochetes

Not penicillinase rresistant
Penicillin
SE
hypersensitivity rxts
hemolytic anemia
Methicilin, nafcillin, dicloxacillin
Mechanism
same as penicillin---review

penicillinase resistant dt bulkier R group
Methicilin, nafcillin, dicloxacillin

clinical use
S. aureus
Methicilin, nafcillin, dicloxacillin:
SE
Hypersensitivity rxts

methicillin--interstitial nephritis
Ampicillin, amoxicillin
MOA
same as penicillin--review

Wider spectrum--can combine with clavulanic acid to enhance spectrum

AmOxicillin has greater Oral bioavailability vs ampicillin

Penicillinase sensitive
Ampicillin, amoxicillin:
clinical use
extended coverage penicillin: HELPS kills enterococci (gram + bacteria and gram - rods)

Haemophilus influenza
E coli
Listeria monocytogenes
Proteus mirabilis
Salmonella
enterococci
Ampicillin, amoxicillin: Tox
Hypersensitivity rxts
ampicillin rash
pseudomembranous colitis
carbenicillin, piperacillin, ticarcillin
MOA
same as penicillin, extended spectrum
carbenicillin, piperacillin, ticarcillin:
Clinical use
Pseudomonas spp
gram -rods
susceptible to penicillinase

use with clavulanic acid
carbenicillin, piperacillin, ticarcillin: SE
Hypersensitivity rxts
Cephalosporins:
MOA
B lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases

bacteriacidal
Cephalosporins:Clinical use
Generation 1
PEcK:
proteus mirabilis
E coli
Klebsiella pneu
gram + cocci
Cephalosporins: clinical use
Generation 2
HEN PEcKS
gram + cocci
H. influenza
Enterobacter aerogenes
Neisseria spp
Proteus mirabilis
E coli
Klebsiella pneu
Serratia marcescens
Cephalosporins: clinical use
3 generation
serious gram - infectiosn resistant to other B lactams
meningitis

ie) ceftazidime for Pseudomonas

ceftriaxone for gonorrhea
Cephalosporins: clinical use
4 generation
increased activity against pseudomonas and gram + organisms
Cephalosporins: tox
Hypersensitivity rxts--cross hypersensitivity with penicillin occurs in 5-10% of patients

increased nephrotoxicity of aminoglycosides

disulfiram like reaction with ETOH (in cephalosporins with a methylthiotetrazole group ie cefamandole)
Aztreonam
MOA
monobactam resistant to B lactamases
Bind PBP and inhibit cell wall synthesis

Synergistic with aminoglycosides

No cross allergicity with penicillins
Aztreonam: Clinical use
Gram - rods: klebsiella spp, Pseudomonas spp, Serratia spp,

no activity against gram + or anaerobes

Use with pts who are penicillin allergic or who have renal insufficiency and cannot handle aminoglycosides
Aztreonam: SE
Usually non-toxic
occasional GI upset
Imipenem/Cilastatin:
MOA
broad spectrum, B lactamase resistant carbapenem

Always administered with cilastatin (inhibitor of renal dihydropeptidases) to increase inactivation of renal tubules
Imipenem/Cilastatin: Clinical use
Gram + cocci
gram - rods
anaerobes

drug of choice for Enterobacter
Imipenem/Cilastatin: SE
GI distress
skin rash
CNS toxicity--seizures

at high plasma levels
vancomyocin:
MOA
resistance
binds D-Ala D-ala and prevents cell wall mucopeptide formation

bacteriacidal

resistance occurs with changes of D-ala to D lac
vancomyocin:
Clinical use
serious, gram positive MDR organisms including S Aureus, C. difficile (pseudomembranous colitis)
vancomyocin: tox
Well tolerated, NOT many problems


Nephrotoxicity
Ototoxicity
Thrombophlebitis
diffuse flushing--Red Man syndrome (prevent with antihystamines or slow infusion)
Protein Synthesis inhibitors
name them
buy AT 30, CELL at 5o

30:
Aminoglycosides--streptomycin,tobramycin, amikacin
tetracyline--

50:
Chloramphenical
Erythromycin
Lincomycin
cLindamycin
Protein Synthesis Inhibitors:
bacteriacidal

bacteriostatic
cidal--Aminoglycosides

static--tetracycline, Chloramphenical, Erythromycin, Lincomycin, cLindamycin
Aminoglycosides--
streptomycin
tobramycin
amikacin
Aminoglycosides..name them
Gentamycin, neomycin, amikacin,tobramycin,streptomycin
Aminoglycosides:
MOA
Bacteriacidal
inhibit formation of initiating complex and cause misreading of mRNA

Require O2 for uptake so are ineffective against anaerobes
Aminoglycosides;
clinical use
severe gram negative rod infection
synergistic with b lactam Ab

Neomycin for bowel surgery
Aminoglycosides:
SE/Tox
Nephrotoxicity (esp when used with a cephalosporin)

Ototoxicity--esp with a loop diuretic
tetracyclines name
Tetracycline, doxycycline, democlocycline, minocycline
Tetracyclines MOA
bacteriostatic
binds 30S and prevents attachment of aminoacyl-tRNA

limited CNS penetration

Doxycycline is fecally eliminated and cannot be used with pts who are renal failure

Inhibited by divalent ions inhibit absoprtion in gut (milk, antacids, iron-containing preps)
Tetracyclines Clinical use
VACUUM your Bed Room Tonight
V. cholera
Acne
Chlamydia
Ureaplasma
Urealyticum
M. Pneumonia
Borrelia (lyme)
Rickettsia
Tularemia
Tetracyclines..SE/Tox
Gi distres

discoloration of teeth and inhibition of growth in children

photosensitivity
Macrolides--name
Erythromycin
Azithromycin
Clarithromycin
Macrolides MOA
prevent protein synthesis by blocking translocation
bind 23S RNA of 50S

Bacteriostatic
Macrolides--Clinical use
URI
pneumonia
STD gram + cocci (strptoccocal inf in pts allergic to penicillin)
Mycoplasma
Legionella
Chlamydia
Neisseria
Macrolides--Tox, SE
GI discomfort
Acute cholestatic hepatitis
eosinophilia
skin rashes
Chloramphenicol MOA
Bacteriostatic

Inhibits 50S peptidyltransferase
Chloramphenicol Clinical use
Meningitis -- H. INfl, N. meningitidis, Strep Pneumo

Use conservatively dt toxicities
Chloramphenicol--SE/ Tox
Anemia--dose dependent
Aplastic anemia--dose dependent
gray baby syndrome (preemies without UDP glucuronyl transferase
Clindamycin--MOA
block peptide bond formation at 50S

bacteriostatic
Clindamycin--Clinical use
Anaerobic infections (bacteriodes fragilis, clostridium perfringens)

Anaerobes above the diaphragm
Clindamycin--Tox
Psuedomambranous Colitis

fever diarrhea
Sulfonamides name
Sulfamethoxazole (SMX), sulfisoxazole, triple sulfas, sulfadiazine
Sulfonamides MOA
PABA antimetabolites inhibit dihydropteroate synthase

Bacteriostatic
Sulfonamides--Clinical use
Gram +
Gram -
Nocardia
Chlamydia
Triple sulfas or SMX for simple UTIs
Sulfonamides--SE/Tox
Hypsty rxts
hemolysis if G6PD deficient
nephrotoxicity
kernicterus in infants
displaces other drug from albumin (warfarin)
Trimethoprim MOA
Inhibits bacterial dihydrofolate reductase

bacteriostatic
Trimethoprim Clinical use
Used in combo with sulfonamides (TMP-SMX) causing sequential block of folate synthesis

Combo used for recurrent UTIs shigella, Salmonella, P. carini
Trimethoprim SE/Tox
Megaloblastic anemia

Leukopenia

granulocytopenia

May alleviate with supplemental folic acid
Fluroquinolones name
Cipro-
Norflox-
oflox-
sparflox-
moxiflox-
gatiflo-
enoxacin

nalidixic acid (quinolone)
Fluoroquninolones MOA
Inhibit DNA gyrase (Topoisomerase II)
bacteriacidal
Fluoroquninolones Clinical use
gram negative rods of urinary and GI tracts including pseudomonas, Neisseria, some gram +
Fluoroquninolones--SE, Tox
Gi upset
superinfections
skin rashes
HA
dizzy

Contraindicated --pregnant, children dt damage to cartilage (Tendonitis, tendon rupture)
Metronidazole--MOA
Forms toxic metabolites in bacterial cell wall

bacteriacidal
Metronidazole--Clinical use
Antiprotozoal GET on METRO

Giardia
Entamoeba
Trichomonas
Gardnerella vaginalis

anaerobes
bacteriodes
Clostridium

Used with bismuth adn amoxicillin (or tetracycline) for "triple therapy" against H. pylori
Metronidazole SE/Tox
Disulfram like reaction with alcohol
Polymixins--MOA
Bind to cell membranes of bacteria and disrupt their osmotic properties

Cationic, basic proteins that act like detergents
Polymixins--Clinical use
resistant gram - infections
Polymixins--SE, TOX
Neurotoxicity, acute tubular necrosis
Anti-Tb drugs
Rifampin
Ethambutol
Streptomycin
Pyrazinamide
Isoniazid

All hepatotoxic
Isoniazid--MOA
decrease synthesis of mycolic acid
Isoniazid--clinical use
M. Tb---the only agent used as solo prophylaxis against TB
Isoniazid--TOX
INH Injures Neurons and Hepatocytes

Hemolysis if G6PD deficient
neurotoxic
hepatotoxic
SLE like syndrome
Pyridoxine (vit B6) can prevent neurotoxicity
Rifampin--MOA
Inhibits DNA dependent RNA pol
Rifampin--Clinical use
M. TB--delays resistance to dapsone when used for leprosy

Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children with H inf Type B
Rifampin--Tox
minor hepatotoxicity and drug interactions (P450)

What are the 4 Rs of Rifampin?? (p290)
resistances mechanism for:
1) penicillin/cephalosporins

2) Aminoglycosides

3) vancomycin

4) Chloramphenicol
1) B lactamase cleavage of B lactam ring

2) Modification via acetylation, adenylation, phosphorolation

3)Terminal D-Ala of cell wall replaced with D-lac which reduces afinity

4)Acetylation
resistances mechanism for:

1)Macrolides

2) Tetracycline

3)Sulfonamides
1) Methylation of rRNA near erythromycins ribosome binding site

2)decreased uptake or increased transport out of cell

3)Altered enzyme (bacterial dihydropteroate synthetase), decreased uptake, increased PABA synthesis
nonsurgical antimicrobial prophylaxis

1) meningococcal

2)Gonorrhea

3) Syphilis

4)recurrent UTIs

5) P. carinii pneumonia
1) rifampin (drug of choice)

2) Ceftriaxone

3)benzathine penicillin G

4) TMP-SMX

5) TMP-SMX (drug of choice) aerosolized pentamidine

^
Amphotericin B
MOA
Binds ergosterol and forms membrane pores that allow leakage of electrolytes

Ergosterol is unique to fungi
Amphotericin B Clinical use
Side spectrum use for mycoses

Cryptococcus
Blastomyces
Coccidioides
Aspergillus
Histoplasmosis
Candida
Mucor (systemic mycoses)

Intrathecally for fungal menigitis

doe snot cross BBB
Amphotericin B Tox
fever and chills (shake and bake)

Hypotension

nephrotoxicity
arrythmias (amphoterrible)
Nystatin...
MOA

Cinical use
Binds to ergosterol nad disrupts fungal membranes

Swish and swallow for oral candidiasis
Azoles...
MOA
inhibit ergosterol (fungal steroid) synthesis
Azoles..Clinical use
Systemic mycoses
Fluconazole for cryptoccocal meningitis in AIDS pts and candidal infections in all types

Ketoconazole for blastomyces, Coccidiodes, Histoplasma, C. Albicans,

hypercortilism
Azoles..Tox
Hormone sysnthesis inhibition (gynecomastia)

liver dysfunction (inhibits P450)

fever chills
Flucytosine
MOA
Inhibits DNA synthesis by converting to fluorouracil which competes with uracil
Flucytosine...Clinical Use
Systemic funal infections (Candida, Cryptococus)
Flucytosine SE/Tox
Nausea
vomiting
BM suppression
caspofungin MOA
Inhibits cell wall synthesis
caspofungin Clinical use
invasive aspergillosis
caspofungin SE/Tox
GI upset, flushing
Terbinafine MOA

Clinical use
Inhbits fungal enzyme squalene epoxidase

dermatophytes especially onychomycosis
Griseofulvin MOA
Interferes with microtubule fxn
disrupts mitosis
deposits in keratin containing tissue
Griseofulvin Clinical use
oral treatment of superficial infections

inhibits growth of dermatophytes (tinea and ringworm)
Griseofulvin..Tox
teratogenic
carcinogenic
confusion
HA
inc warfarin metabolism
Amantadine MOA
Blocks viral penetration and uncoating

may buffer pH of endosome

causes the release of dopamine from intact nerves
Amantadine Clinical use
prophylaxis for inf A

Parkinsons dz
Amantadine SE, Tox
Amantadine blocks influenz A and rubellA and causes problems with the cerebellA

ataxia, dizziness, slurred speech

rimantidine is derivative with fewer side effects
Zanamivir, Oseltamivir

MOA

Clinical use
Inhibits influenza neuraminidase


Both A and B
Ribavarin
MOA
inhibits synthesis of guanine by competitively inhibiting IMP dehydrogenase
Amantadine Clinical use
RSV, chronic Hep C
Amantadine Tox
Hemolytic anemia

severe teratogen
Acyclovir MOA
preferentially inhibits viral DNA pol when phophorylated by viral thymidine kinase
Amantadine Clinical use
HSV
VZV
EBV
mucocutaneous and genital herpes lesions

prophylaxis in immunocompromised pts
Amantadine SE, Tox
Delirium
tremor
nephrotoxicity
Ganciclovir MOA
Phosphorylation by viral kinase

preferentially inhibits CMV DNA pol
Ganciclovir Clinical use
CMV
Ganciclovir Tox
Leukopenia
neutropenia
thrombocytopenia
renal tox
More toxic to hosts than acyclovir
Foscarnet MOA
Viral DNA pol inhibitor that binds to the pyrophosphate binding site of the enzyme

Does not require activation by viral kinase
Foscarnet Clinical use
CMV retinitis in immunocompromised pts when ganciclovir fails
Foscarnet Tox, SE
Nephrotoxicity
Interferons MOA
glycoproteins from human leukocytes that block various stages of viral DNA and RNA synthesis
Interferons Clinical use
Chronic Hep B and C
Kaposi's sarcoma
Interferons Tox
Neutropenia
HIV
Protease inhibitors: name
Saquinavir
Ritonavir
Nelfinavir
Amprenavir
HIV
Protease inhibitors: MOA
Block protease enzyme and prevents new virus from being made
HIV
Protease inhibitors: Tox
GI intolerance (D, N)
hyperglycemia
lipid abnormalities
thrombocytopenia (indinavir)
HIV
RT Inhibitors: MOA
Inhibit RT and prevent incorporation of viral genome into host DNA
HIV
RT Inhibitors: TOX
BM suppression (neutropenia, anemia)

peripheral neuropathy

lactic acidosis (nucleosides)

rash (non nucleosides)

megaloblastic anemia ( AZT)
HIV
RT Inhibitors:
Nucleoside-
AZT (zidovudine)
didanosine (ddI)
zalcitabine (ddC)
stavudine (d4T)
lamivudine (3TC)
abacavir
HIV
RT Inhibitors: non-nucleosides
Nevirapine
delaviridine
efavirenz
HIV treatment Clinical use
HAART includes combo therapy of Protease inhibitirs and RT inhibitors

started with low CD4 (<500) or high viral load

AZT used during pregnancy