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167 Cards in this Set

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What antifungal drug is NOT used to treat systemic fungal infections?
Griseofluvin
Also absorbed well with a high fat diet
Itraconazole [Sporanox]Administration
Capsule= wide range fungal infections [take with food] Oral solution= Candidiasis [take without food]
Injection= Empiric Tx for febrile neutropenia & blastomycosis [DOC]
3 forms
Itraconazole [Sporanox]cautions
WARNING for CHF patients!!!
AEs- GI [Nausea], rash, HTN, HA
Mepiridine is used in Amphtericin B administration to treat:
IV infusion related rxns [rigors, fever, chills; post op]
Used to treat onchomycosis of the great toe
Terbinafine [Lotramin]
Cicloprox [Loprox] [Penlac]
Griseofulvin [Fulvicin UF]
*New- Itraconaole [Sporonox]
4 antifungals
Ketoconazole [Nizoral] MOA
Inhibits fungal CYP450 enzyme [critical in ergosythesis pathway], interupting synthsis of ergosterol---> increased permeability of azoles into cell---> inhibits fungal growth
Ketoconazole Cautions
WARNING- Hepatotoxicity
AEs-
CNS [Dizzy, HA, somnolence]
GI [NV 10%, D, ab pain, hepatotoxicity]
Psychiatric- SUICIDAL, SEVERE DEPRESSION [although rare]
Miscellaneous- pruritis, fever/chills, IMPOTENCE, GYNECOMASTIA, thrombocytopenia, leukopenia, hemolytic anemia, bulging fontanells, hypersens, oligospermia
Ketoconazole Administration
BROAD SPECTRUM Antifunal
Systemic- Candidiasis, Oral thrush, histoplasmosis [target lesion],Coccidiomycosis
Topical- Tineas & cutaneous candidiasis
2 Forms
What antifungals cross CSF?
Terbinafin [Lotramin]
Flucytosine [Ancobon]
Fluconazole [Diflucan]
3
Which antifungals require dose adjustment for renal PTs?
Flucytosine [Ancobon]
Fluconazole [Diflucan]
2 Fs
Ketoconazole Drug Drug Interactions
Amphotericin B
Rifampin
Other CYP450 metabolized drugs
3
Itraconazole Drug Interactions
CYP 450 metabolized drugs [could lead to seroius cardiac events--> QT elongation, V-Tach, cardiac arrest, sudden death]
Lamasil Indication
Dermatophytosis [Tineas]
What antifungal is FUNGICIDAL?
Lamisil [Terbinafine]
What 2 Antifungals are listed as FUNGISTATIC in our notes?
Flucytosine & Griseofulvin
Griseofulvin is FUNGISTATIC against what 3 infections?
Trihopyton
Microsporum
Epidermophyton
Griseofulvin MOA
Inhibits fungal mitosis by disrupting formation of mitotic spidles & inhibiting fungal mitosis
Griseofulvin- length/description of therapy?
Requires LONG TERM therapy [weeks-months-up to 6 months]
Must wait for infected keratinized tissue to grow out & be replaced by normal tissue
Griseofulvin Gooooooooooooo Grow Out
Griseofulvin Administration
Oral [good absorption with high fat diet] but NOT Topical!!!
Griseofulvin Drug Interactions
Phenobarbital [Dec. Gris.]
Oral Anticoagulants [Gris. INCREASES the rate of their metabolism]
ETOH [Gris. potentiates the effects]
3 major
What antifungals are CYP450 INHIBITORS?
All Azole Antifungals
What antifungal (s) are CYP450 INDUCERS?
Griseofulvin Fulvicin UF]
Why can't you treat Candida with Ketoconazole if a PT is also on Cyclosporin for immunosuppression?
Ketoconazole inhibits the CYP450 enzymes that inactivate cyclosporin
What drug is now used to treat Onchomycosis, but originally was only used for blastomycosis & histoplasmosis in immunocompromised PTs?
Intraconazole [Sporanox]
Itraconazole distribution/penetration
Does NOT penetrate CNS, however DOES penetrate most all other body tissue well
Vehicle/Antifungal for topical application in the treatment of onchomycosis?
Laquer- Cicloprox [PenLac]
Cream- Cicloprox [Loprox], Terbinafine [Lotramin]
* Griseofulvin is INEFFECTIVE topically
CHF "Black Box" Warning
Itraconazole [Sporanox]
Cicloprox MOA
Inhibits transport of essential elementsin fungal cell---> problems in synthesis of DNA, RNA, proteins
Caspofungin in 2001 was approved for treatment of
*Invasive aspergillosis IV Infusion for PTs who can't tolerate standard Tx [AmB, Lipid AmB, Itraconazole]
[Also used to treat candidemia, oropharyndeal/esophageal candidiasis]
Caspofungin belongs to this class of anti-fungals
Glucan Sythesis Inhibitors
Echinocandin
Nucelotide Reverse Transcriptase Inhibitors MOA & Target
Target- HIV
MOA- Phosphorylated by cellular enzymes to nucleotide triphosphate--> Inhibits reverse transcriptase b/c doesn't have 3'OH groups to continue Viral DNA elongation
Binding site of the nuclotide molecule
Nucleotides are added to the OH group of the 3' end--> OH of one forms an ester bond with phosphate of another--> eliminates a molecule of H2o
Major toxicities of the reverse transcriptase inhibitors
Lactic acidosis [esp. Stavudine], hepatotoxicity [mainly Zidovudine], All NRTIS- Renal Toxicities [except ABC], Pancreatitis, Peripheral Neuropathy, Fat redistribution syndrome [suggested]
The 4 main Antiviral inducers of the SEs Pancreatitis & Peripheral Neuropathy
Zalcitibine, Stavudine, Didanosine, Lamivudine [but notes say ALL RTIs cause these 2 SEs
Abacavir [Ziagen] [ABC] Toxicity
Some FATAL HYPERSENSITIVITY RXN [Watch PT for signs of respiratory distres- discontinue immediately]; rash, fever, fatigue
Numbness & pain in lower extremities [peripheral neuropathy] is a SE that is REVERSIBLE in what NRTI?
Didanosine [ddL, Videx]
Peripheral Neuropathy is a SE that is NOT ALWAYS REVERSIBLE in what NRTI?
Zalcitabine [Hivid]
Which antiviral has been discontinued/taken off the market?
Zalcitabine [Hivid]
Didanosine Administration
Tablet [ddL]- chew or crush up
Enteric coated capsule [Videx]- DON'T chew, crush
Lamivudine Drug Interactions
Zalcitabine [Lamivudine inhibits phosphorylization of it so it never gets activated]
Which antiviral must undergo glucuronidation in the liver b/f it can be excreted renally?
Zidovudine [AZT, Retrovir]
NRTIs special MOA slight differences
Zidovudine- Non listed
Didanosine-metab to dideoxadenosine triphosphate
Zalcitabine- ddC, dideoxycytidine
Lamivudine- 3TC
Stavudine- dTTT
Abacavir-dGTP
Tenofovir- diPO4/ doxyadenosine 5'triPO4
Abacavir
NRTI, competes with dGTP, take orally, FATAL HYPERSENSITIVITY
Non-Nucleoside RTIs [NNRTIs] MOA & drugs in class
Bind DIRECTLY to HIV reverse transcriptase to inhibit formation of viral DNA; Efavirenz, Delaviridine, Nevirapine, Atripia
HIV Protease MOA
Jam the catolytic site of precursor proteins encoded by viral mRNA--> inhibit the enzyme responsible for cleavage of viral polyprotein into essential enzymes [reverse transcriptase, protease, integrase, capsid, & matrix proteins]
What drug is used in combo with Lopinavir to inhibit the CYP-450 metabolism?
Ritonavir
Major SEs of Protease Inhibitors
Lipodystrophy, fat redistribution syndrome, elevated TG & cholesterol, glucose intolerance, CYP-450 Inhibition, HEPATIC IMPAIRMENT, parasthesias, NVD
DDI of PIs
Rifampin [decreases effectiveness b/c inhibits CYP-450]
Chronic fat redistribution in abdomen & base of neck caused by PIs is aka:
"Buffalo hump"
Which PI is available as a soft gel?
Saquinavir [Invirase, Fortovase]
Which Antiviral has MORE DRUG INTERACTIONS than any other HIV drug?
Ritonavir [Norvir]
Which PI was specifically stated in our notes to have good oral bioavilability when given WITH FOOD?
Saquinavir [Fortovase]
Which PI causes kidney stones in 3-4% of PTs?
Indinavir [Crixivan]
Ritonavir is a major problem b/c it:
Induces metabolic enzymes--> induces own metabolism potent inhibitor of cyp3A--> increases levels of many other drugs
Which PI seems to be well tolerated in PTs?
Nelfinavir [Viracept]
Which PI has serious/life-threatening Drug interactions with amiodarone, lidocaine, tricyclic antidepressants, quinidine?
Amprenovir [Agenerase]
Which PI has a drug interaction with ST. JOHN'S WORT?
Amprenavir [Agenerase]- ST.JOHN'S decreases the concentration of Ampernavir
What's a good PI combo drug, & why?
Lopinavir + Ritonavir [Lopinavir is completely metabolized by cyp3A; Ritonavir enhances b/c it inhibits cyp3A, so levels of Lopinavir are INCREASED]
What are the life-threatening/serious Drug Interactions of Amprenovir [Agenerase]?
Amiodarone, lidocaine, tricyclic antidepressants, quinidine; St. John's Wort
Discuss Hepatic Failure & some specific PIs.
1- Increased risk for transaminase elevations [esp. in PTs w/Hep B/C]
2- Ritonavir is assoc. w/ abnormal LFTs in PTs with Viral Hep.
3- Tipranavir increases risk for severe hepatotoxicity in combo with Ritonavir.
4- Amprenavir concentration is increased when a PT has cirrhosis [inc risk of AEs].
Tipranavir Drug Interaction [Reaction description]
Ritonavir [Norvir]- Tipranavir increases risk for severe hepatotoxicity when given in combo with Ritonavir.
Which PIs are listed as cyp3A inhibitors in our notes?
Ritonavir & Amprenavir
What drug can Ritonavir be given with to enhance it's effects?
Liponavir [This combo is called Kaletra]
Effects of AntiHTN meds on PIs:
AntiHTN meds are metabolized by cyp450 so may increase or decrease the metabolism of a PI [CCBs & Verapamil are most likely to do this]
Of the PIs, Ritonavir [RTV?] most interactions with antihypertensives?
CCB & BB
When to/to not adjust therapy for an HIV Pt
do NOT change therapy based on 1 viral load result [esp. after vaccination]
Acycolvir indications
HSV, VZV
Acyclovir MOA
Competes with dGTP & causes DNA chain termination
Acyclovir is the DOC for
herpes Simplex Encephalitis
Acyclovir inhibits [active/latent] viruses.
ACTIVE ONLY!
Ganciclovir [Cytovene] Indications
CMV retinitis in ImmC PTs,
CMV DZ & preventative Tx in transplant PTs, CMV congenital in newborns
Foscavir [Foscarnet] Indications
CNV retinitis, CMV colitis, CMV esophagitis, Acyclovir-resistant HSV/VZV infections
Foscavir [Foscarnet] Toxicities
Nephrotoxicity, HA, Fever, NV, Anemia
Foscavir [Foscarnet] Toxicities are increased when...
Administered rapid/bolus IV or Injection; Use an infusion pump!
Oral therapy for CMV retinitis is
Gancyclovir for AIDS PTs
This anti-CMV drug is most likely to cause additive myelosuppression when administered with Zidovudine
Gancyclovir
Ribavirin treats the following in children...
RSV in hospitalized children [It's also used to Tx Hep C, Lassa fever, & Hanta virus]
Black Box warnings for Ribavirn
Birth defects &/or fetal death, genotoxic & mutagenic, potential carcinogen, causes hemolytic anemia
Name the Anti-Influenza drugs
Amantadine & Rimantadine
Zanavamir & Oseltavimir
Amantidine & Rimantidine MOA
Interfere with viral coating & nucleic acid release of influenza A, but B inhibits the ion channel formed by the viral M2 protein, which promotes dissociation of the ribonucleoprotein complex & uncoating of the viron
Zanavimir & Oseltavimir MOA
Neuraminidase inhibitors- inhibit viral neuraminidase; Analogs of salicilic acid & act to block the active site of neuraminidase for influenza A & B with < 2 days symptoms
Anti-Influenza Drugs Indications
Amantidine & Rimantidine- Influenza A ONLY
Zanamivir & Oseltavimir- Influenza A & B
Used SOLEY in the treatment of influenza A infections
Amantidine
The test used to definitavely diagnose HIV infection:
ELISA
The nucleoside reverse transcriptase inhibitors MOA
Phosphorylated by cellular enzymes to nucleotide triphosphate; inhibits reverse transcriptase; causes viral DNA chain to be terminated if it is incorporated into one b/c it lacks the 3'OH group
Protease Inhibitors suffix
"NAVIR"
Drug therapy for HIV should be a combination of 3 drugs:
2 NRTIs & 1 potent PI
Name the 2 neuraminidase inhibitors we've discussed
Zinamivir & Oseltavimir
MOA of Neuroaminidase inhibitors
Zinamivir & Oseltavimir inhibit viral neuraminidase, an enzyme that cleaves sialic acid residues resulting in release of viral progeny
Zanamivir is for ages ____
Oseltamivir is for ages ____
With less than ___ days symptoms
zanimiavir- > 7 YO
Oseltamivir- > 1 YO
< 2 days symptoms
Discuss Enfuviritide [Fuzeon] Use
1st in a new class of anti-HIV drugs known as Fusion Inhibitors; granted accelerated approval on March 13, 2003; used in combo with other antiretroviral agents; No studies of enfuzeon in antiretroviral naive PTs; no results on clinical progression
Fuzeon [Enfuviritide] MOA
Blocks HIV's ability to infect healthy immune [CD4] cells; Slows HIV progression in PTs who have developed resistance; blocks gp41 protein; disrupts the structural arrangement necessary for the virus to fuse
High concentration of Hep B virus can be found in the _____ of an infected carrier.
High- blood/serum/wound exuda
Mod- Semen/vaginal fl/saliva
Low- urine/ feces/ sweat/ tears/ breastmilk
Oral or esophageal thrush [candida] is considered an AIDS defining Illness along with _____ at what CD4 count?
oral hairy leukoplakia & TB @ CD4 counts of 200-300
@ CD4 Counts of 200-100, what are the AIDS definfing illnesses?
PCP, Histoplasmosis, Cocci, Crypto, toxoplasmosis
@ CD4 counts <100, what are the AIDS defining illnesses?
HSV, crypto, CMV, MAI
In reference to "AIDS defining illnesses", check for associated pathogens such as":
T.pallidium & Hep B
Clinical latency symptoms with viral tendency?
Clinical Latency is NOT SYNONYMOUS with viral or immunologic latency!!!!!
Combivir is a combination ...
Pill with 150 Lamivudine & 300 mg Zidovudine
Rifampin should be avoided in combination with:
Protease inhibitors, Ketoconazole, etc.
Ribaviren's Black Box warning
Birth defects/death of fetus, genotoxic & mutagenic, pathogenic carcinogen, hemolytic anemia [may result in worsening cardiac disease]
Drugs & their metabolites can be excreted via:
Urine/renal, bile, saliva, sputum, milk
INH excretion
Saliva, sputum, milk, renal
Amphotericin B & Rifampin excretion
urine & bile
Anti-tubercular agent associated with ototoxicity
Streptomycin
INH is metabolized by
a liver N-acetyltransferase
TB history/epidemilolgy
Leading killer of IDZ worldwide [1/3 infected die; 3 million/year] Men 2x Women; Rate of increase is 0.4% but a lot faster in Africa
The short couse chemotherapy for TB
INH & RIF [others are weaker & take longer]
Rifampin is an [inducer/inhibitor] of the CYP-450 system
INDUCER
The 2 CYP-450 inducers in this section that we've talked about
Griseofulvin & Rifampin
Drug regimen for the treatment of leprosy
Dapsone, Clofazimine, Rifampin x 6-24 months
INH is usually administered
PO
High risk post exposure to TB should be treated with
Isoniazid [INH] 300 mg/day for 12 months
Antibiotics associated with the development of Hepatitis
Isonazid [INH] is most closely associated
INH & ____ should be used together whenever possibl
Rifampin
Mycobacterium infections include
TB, M.bovis, Atypical Mycobacterial Infxn, & M. leprosae
TB therapy began with these 3 drugs:
Streptomycin
Isoniazid
P-aminosalicylic acid
Extrapulmonary TB can be found in:
CNS, peritoneum, genitourinary tract, lymph system, skeletal system, pericardium, adrenal glands, liver
TB Etiology:
1- Mycobacterium tuberculosis
2- 60 species [aerobic, non-spore-forming rods]
3- Ghon Complex [calcification in hilar lymph nodes]
4- Acid-fast bacilli [AFB]- stain with carbol-fuchsin
5- Cavitary & laryngeal TB- high transimission rate
Ghon Complex- From the host’s point of view, the residue of a successful encounter with the tubercle bacillus is
a peripheral, rounded scar, less than 1 cm in diameter, in the lower half of the lung. Together with a similar scar in a hilar lymph node, it is known as the Ghon complex.
Chemotherapy of TB first line therapy
1- Isoniazid [INH]
2- Rifampin [RIF]
3- Pyrazinamide
4- Ethambutol
5- Rifabutin [Mycobutin]
6- Rifapentine
Second line TB therapy
1- Amikacin [Amikin]
2- Ethionamide
3- Aminosalicylic Acid
4- Levofloxacin
5- Capreomycin
6- Moxifloxacin
7- Streptomycin
8- Gatifloxacin
9- Cycloserine
Desired outcome of TB treatment
1- Identification of new TB case
2- Isolation of active case PT
3- Sample collection
4- TB treatment [Multi drug therapy- @ least 2 active agents]
5- Signs & symptoms resolution
6- Achieving non-infectious state
7- Medication compliance/ cure
The MOST ACTIVE agent for treatment of TB is
Isoniazid [INH]
INH AB spectrum
1- Bacteriostatic against stationary phase
2- Bactericidal against dividing organisms
3- NEVER USED ALONE Given alone, INH administration selects out resistant mutants which
necessitates additional agents.
Resistance mechanisms agaisnt INH
1- Inability of organism to accumulate drug
2- Altered target enzyme [no binding with INH]
3- Excessive enzyme to overwhelm drug
*about 10% of TB isolates are INH resistant
INH MOA
INH inhibits mycolic acid synthesis, an essential part of mycobacterial cell walls.
INH Metabolism/ Excretion
Hepatic by acetylation [influenced by genetic predisposition for fast or slow acetylation
*May need to DOSE ADJUST for Liver PTs
Renal excretion
INH Dose
Dose 300 mg QD
—> 6 months [65- 69%] to 12 months [75-93%]
INH administration instructions
EMPTY stomach, AVOID ANTACIDS w/in 2 hrs of INH
INH is absorbed _____
orally [avoid food & aluminum]
INH t 1/2
Greater in infected tissues
INH Drug interactions
Phenytoin [metabolism inhibited]
Rifampin [RIF] MOA
Inhibits RNA synthesis in prokaryotes; NEVER USE ALONE!!!
RIF indications
1- Treat carriers of N.meningitidis
A- Prophylaxis for household against meningitis [meningococci or H.influenzae]
B- Effective against many gram (+) & gram (-) species
2- MOST ACTIVE ANTI-LEPROSY DRUG
The most active anti-leprosy drug is
RIF
RIF is administered in what form?
Oral
RIF & CNS penetration?
Good CNS penetration
RIF & CYP-450
INDUCER
RIF & Discoloration
Red-orange discoloration in urine, tears, feces, contact lenses
Pyrazinamide is orally effective in combo with
INF & RIF
Pyrazinamide Spectrum
Bactericidal or Bacterialstatic
[Bactericidal to DIVIDING organisms]
Pyrazinamide Metabolism
MUST be metabolized to active drug form
[pyrazinoic acid; Resistance to hydrolysis by certain
strands of TB]
Pyrazinamide distribution
Good throughout body, PENETRATES CNS
Pyrazinamide AEs
1- Hepatotoxicity/ Liver dysfunction [1-5% of PTs on INF/RIF/Pyrazinamide combo]
2- Gout Attack [ Due to Urate retention]
3- Thrombocytopenia
4- Interstitial Nephritis
5- N& V
6- Anorexia
7- Siderblastic Anemia
8- Rash, urticaria, pruritis
Pyrazinamide Dose
1- 15-30 mg/kg/day
2- Max- 2 gms/day if on daily regimen; may be administered in twice-weekly doses of 50-70 mg/kg
Pyrazinamide CIs
1- Severe hepatic damage
2- Acute Gout
3- Pregnancy category C [risk to fetus can’t be ruled out; use only if benefit outweighs risk]
When PTs are on Pyrazinamide, you should monitor levels of ...
Monitor levels of LFTs, Uric Acid, follow up of TB symptoms, CXR, & sputum
Ethambutol Spectrum/ resistance/ combination indications
1- Bacteriostatic
2- Specific for strains of M.tuberculosis & M.kansasi
3- Resistance- not a big problem if given with other anti-TB agents
4- MUST BE USED IN COMBO [Pyrazinamide, Isoniazid, Rifampin]
Ethambutol Kinetics
1- Good oral absorption
2- Distributed well throughout body
3- CNS penetration adequate in TB meningitis
4- Excretion- Glomerular Filtration & Tubular Secretion
Ethambutol AEs
1- Optic Neuritis [results in diminished visual acuity & loss of ability to discriminate b/t red & green]
2- Gout attack [decreased Urate excretion]
3- Toxic effects on discontinuation ARE REVERSED
Ethambutol Dose
1- Myambutol 100 mg, 400 mg tablets available
2- 15 mg/kg/day PO
3- Max- 1500 mg/day
For PTs on Ethambutol, Monitor ...
Visual acuity, uric acid, LFTs
Streptomycin MOA
MOA- inhibits protein synthesis [aminoglycoside] binds to 30S ribosomal sub unit
Streptomycin duration of treatment
Duration- 12 months of MULTI-DRUG therapy [INH, RIF, PYR] MINIMUM
—> Usual treatment of TB is 2 months of [INH, RIF & PYR] followed by 4 months [INH & RIF]
—> Streptomycin is added in
Streptomycin Dosing
Dose- based on body weight
1- Serum concentration: 20-30 mcg/mL
2- Toxic serum levels: > 50 mcg/mL [peak]
Streptomycin is usually administered ___ & toxic serum levels are ____
IM, > 50mcg/ml
Streptomycin AEs & CIs
1- Severe N& V & dizziness, rash, & fever
2- Loss of hearing w/long term use reported
CIs- PTs with renal impairment
Para- aminosalicylate Na [PAS] Spectrum, MOA, Kinetics
a- Spectrum- Bacteriostatic only against M.tuberculosis
b- MOA- inhibits folic acid synthesis—> inhibited bacterial synthesis
c- Kinetics
1- Oral administration [take with/after meals or with antacid]
2- Readily absorbed from GI tract
Para- aminosalicylate Na [PAS] SEs, dosing, & CIs
d- SEs
1- NVD
2- peptic ulcer [rare]
3- hemorrhage [rare]
e- Dose
1- PAS sodium must not be used alone for treatment of TB
2- Adults: 10-12 g orally per day in 2-4 divided doses
f- CIs- Dose adjustment in renal PTs
3 DRUG regimen for Leprosy "Hansen's DZ"
3 Drug Regimen:
a- Dapsone
b- Clofazimine
c- Rifampin
Dapsone Related to ____, indications, MOA
—> Related to sulfonamides
a- Indications- Bacteriostatic for M.leprae & PCP
b- MOA- PABA antagonist [inhibits folate synthesis]
Dapsone Kinetics
1- Good oral bioavailability
2- Metabolism- Hepatic
3- Excretion-Urine
4- Distribution- good throughout whole body
Dapsone AEs
1- Hemolytic Anemia [G6P deficiency]
2- Methemoglobinemia
3- Peripheral Neuropathy
4- Possible dev of Erythema Nodosum leprosum [treat with corticosteroids or thalidomide]
Clofazimine [Lamprene] Indications, MOA, Spectrum
a- Indications- Therpay for Hansen’s Disease [Dapsone resistant- 20% cases] b- MOA- inhibits DNA replication & forms toxic O2 radicals
c- Bacteriacidal against M.leprae
Clofazimine AEs
1- Skin [including retina] & urine colored RED
2- Lesions colored blue-black
3- NOT Erythema Nodosum like Dapsone [b/c it’s anti-inflammatory]
Clofazimine CIs
1- Hypersensitivity to clofazimine
2- Liver or Kidney Damage
3- Pregnancy/Lactation safety not yet established