Pharmacology

ANTI-FUNGALS (Anti-mycotics)

 “mycosis”: an infection caused by fungus

 FUNGUS has a rigid cell wall that is made up of chitin and various polysaccharides andmembrane
that contains ergosterol (makes them resistant to antibiotics)
 Treatment for systematic (candidiasis histoplasmosis) and superficial (tinea pedis/ athletes foot)

I. Polyenes
a. Amphotericin B (Fungizone)
i. MOA: binding to the fungal cell membrane; forming open channels >> increase
cell permeability and leakage of intracellular components.
ii. Very potent but with many unpleasant side effects (renal failure)
iii. DOC: severe systematic infection; IV
iv. SE/AD: fever. N/V, decreased BP, paresthesia, thrombophlebitis, neohrotoxicity,
hypersensitivity, electrolyte imbalance (hypokalemia & hypomagnesemia)
b. Nystatin (Mycostatin)
i. MOA: increases permeability of fungal cell membrane
ii. Oral preparation – intestinal candidiasis, poorly absorb in GIT
iii. Suspension – mouth or throat fungal infection**** swish>>gargle>>swallow
iv. Oitment, suppository, cream-vaginal
v. SE: fever, N/V, rash, diarrhea (large dose)
II. Azole Group
i. MOA: Interference with the formation of ergosterol (major sterol in fungal cell
membrane)
1. Ketoconazole (Nizoral)
a. First effective antifungal – orally absorbed
b. Used to treat some mycoses with amphotericin B (give with
food; no antacid)
c. Shampoo = dandruff
d. SE: dizziness, blurred vision
e. AE: hepatomegaly;photosensitivity
2. Itraconazole (Sporanox) PO
a. Systemic fungal infection
3. Miconazole (monistat)
a. Ointment – vaginitis; IV- fungal bladder infection
4. Fluconazole (diflucan) PO
a. Orpharyngeal and systemic; hepatotoxic
 5. Voriconazole
6. Posaconazole
a. *****NOTE: vaginal tablet, cream, ointment and solution
(topical preparation to treat candidiasis and tinea infections)
III. Antimetabolite
a. MOA: disrupts fungal DNA and RNA synthesis
i. Fluctosine (ancoban)
1. Combination therapy with other antifungal drugs (amphotericin B)
2. Well absorbed in GIT
IV. Antiprotozoal
a. Atozaquone (Mepron)
i. Used to tx mild to moderate pneumosytis carinii pneumonia

CONSIDERATIONS:

 GSCS
 Monitor IV Sites
 Check liver enzymes creatinine, BUN, I/O
 Take with meals – oral forms (NAVDA)
 Check for hypersensitivity reaction (rash)
 For topical: wash hands before & after application
 For athletes foot: wear cotton socks, change 2-3 times daily
 Jock itch worm or wing worm: wear well fitting, non-constrictive, ventilated clothing
 Intravaginal
o Read instructions carefully
o Insert high into the vagina
o Continue use through menstruation
o Wear a minipad to avoid staining clothing, do not use tampon
o Wash applicator with mild soap and rinse thoroughly after each use
o Avoid sexual intercourse while using the drug

ZOLE

 Z ole – many drug interactions can occur

 O bserve hygiene measures to control infections
 L iver Function tests – monitor
 E ducate to take with food
Meet “ZOLE” the toad who destroys fungal infections, such as ringworm. “ZOLE” will help you remember
some key points with these drugs. It will also help you remember the medication used for these
infections, since they have the letters zole in them.

AMPHOTERRIBLE

 Amphoterrible is a monster. He treats monster infections such as histoplasmosis and other life
threatening fungal infections. He has a terrible habit of creating irregularities in the heart
(arrhythmias). The X marks the spot of the kidney since 80% of clients receiving this drugs may
develop some nephrotoxicity.

AMINOGLYCOSIDES

BACTERIOSTATIC

Examples:

 Chloramphenicol
 Erythromycin
 Clindamycin
 Sulfonamides
 Trimehtroprim
 Tetracyclines

BACTERICIDAL

Examples:

 Aminoglycosides
 Beta-lactams
 Vancomycin
 Quiolones
 Ritampin
 Metronidazole

MOA: bacteria cannot synthesize the CHONs necessary for their function and replication
INDICATION:

 Reserved for infections that did not respond to less toxic drugs
 Gram (-) bacteria ( E. Coli. Proteus pseudomonas)
 Some gram (+) are resitstant

DOC: tularemia & bubonic forms of plaques

1. Streptomycin Sulfate
a. First aminoglycoside
b. Used in treatment of TB
c. Derived from bacterium Streptomyces griseus in 1944
d. Ototoxicity and bacterial resistant can develop
i. Medicines
1. Amikacin
a. Has a broader spectrum; it resists degredation by most enzymes
that inactivate gentamycin and tobramycin
2. Gentamycin
a. (-) esp pseudomonas
3. Netilmicin
a. Less toxic
4. Tobramycin sulfate
a. Burn wounds/ ocular infection; cystic fibrosis
5. Streptomycin sulfate
6. Kanamycin
a. For hepatic coma
7. Cannot be absorbed from GIT; cannot cross CSF (BBB of adults)
8. Prep: IM & IV except neomycin & paromomycin
9. Oral preparation
a. Given to decrease bacteria in the bowel
ii. Side Effects:
1. Anorexia, nausea, vomiting, photosensitivity
iii. Adverse effects:
1. Nephrototoxicity
a. (cast, albumin, RBC, WBC in urine, decrease creatinine
clearance, increased serum creatinine and BUN)
2. Ototoxicity
a. (due to damage of 8th cranial nerve: deafness or decreased
hearing, tinnitus, dizziness, ataxia)
3. Neurotoxicity
a. Visual disturbances, respiratory paralysis, apnea
 4. Hypersensitivity
iv. Interactions
1. Increase action of anticoagulants
2. Loop diuretics may increase ototoxicity & nephrotoxicity
3. Penicillins, vancomycin, & amphotericin B may increase nephrotoxicity
4. Decrease if with penicillin
a. Administer 1 hour before/ after aminoglycosides
v. Considerations:
1. Monitor audiograms, BUN, creatinine, & vestibular studies over 10 days
therapy
2. Adjust for renal insufficiency ****
3. Monitor VS, peak serum levels
4. For IV administration: dilute & administer slowly to prevent toxicity
5. Monitor I&O, hydrate well before & during therapy
6. Manage S/E (anorexia, N/V, photosensitivity)
7. Establish plan safety if vestibular nerve effects occurs

“THE AMINO MICE” (toxic mice!!!)

 “ONE CAN’T HEAR” – Ototoxicity

 “ONE CAN’T PEE..” - Nephrotoxicity
 “ONE CAN’T FEEL” - Neurotoxicity