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anti bacterial drugs > Antifungal drugs > Flashcards

Antifungal drugs Flashcards

1
Q

why are fungal infections hard to treat

A
  1. They are slow growing
  2. occur in tissues that are poorly penetration by anti microbial agents

3require prolonged treatment

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2
Q

List the types of anti fungal infections

A

1.Superficial infections
eg they affect your nails ,skin

  1. Systemic infections eg deep tissues
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3
Q

List the types of superficial infections

A
  1. Dermatomycoses
    * infections of skin ,hair and nails eg ring warm
  • Tinea pedis ;foot
  • tinea cruris -groin
  • tinea corporis -body
  • tinea capitis -scalp
  • tinea unguium -nails

2.Candidiasis
yeast like infections that affect mucous membranes of eg mouth , skin , vagina

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4
Q

Discuss the types of systemic infections

A
  1. Systemic candidiasis
    * can disseminate vital organs
  2. Cryptococcosis
    * Enter through lungs and travel to the brain and can cause meningitis (crytpotomeningitis)
  3. Systemic aspergillosis
    * seen in immunocompromised patients eg aids, patients
  4. Blastomycosis
    * Affect the lungs
  5. histoplasmosis : affects the lungs
  6. Emergomycosis: affect the lungs in immune incompetent patients
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5
Q

What are the uses of amphotericin B

A

*Used intravenously for systemic fungal infections
*Oral preparations are used to treat thrush
*

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6
Q

What can amphotericin treat (systemic infections )

A
  • candida albicans and Cryptococcus neoformans ,mycoses eg histoplasma and blastomycoses
  • molds like aspergillus
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7
Q

What are the MOA of amphotericin

A
  • binds with ergosterol(component of fungal cell membrane )
  • Forming a pore that leads to monovalent ion eg K+,Ca+,H+ and Cl- leakage

*leading to fungal death

Amphotericin B are insoluable in water and are poorly absorbed from the GIT

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8
Q

What are the side effects of amphotericin

A

*infusion reactions toxicity eg high fever ,shaking ,chills ,hypotension
INFUSE OVER 4 HOURS OR REDUCE DAILY DOSE IN ORDER TO REDUCE INFUSION REACTION

NB; NEPHROTOXIC

cUMULATIVE TOXICITY
*renal damage

  • intrathecal( admin into spinal cord) admin may cause seizures
  • anamia
  • hypokalaemia
  • ABNORMALITIES IN LIVER FUNCTION

PATIENT MUST BE

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9
Q

Must knows

A

Liposomal amphotericin b is newer and has less side effects but is more costly

Nystatin has similar structure to amphotericin but too toxic thus not given through IV but through orally

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10
Q

What are the pharmacokinetics of amphotericin

A

*admin IV
*not absorbed orally thus it is not useful for systemic infections but it can be used for local infections in the lumen of GIT
*Used as induction therapy then replaced by newer Azole drug of choice once the fungal burden is reduced
*t1/2 of 24 hrs
*widely distributed but poor BBB crossing
*Eliminated via urine
*

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11
Q

Drug interaction of amphotericin B with others drugs

A

Drugs like aminoglycosides ,tenofovir ,ciclosporin ,diuretics and digoxin also inhibit renal function thus they must not be combined

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12
Q

T/F ; Some Triazoles can be used for systemic and topical functions

A

true

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13
Q

Discuss the characteristics of azoles

A
  • They are a class of drugs

* They have a broad spectrum against dermatophytes and invasive yeast infections eg candida ,Cryptococcus

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14
Q

Discuss the MOA of Azoles

A

*Inhibit fungal Cytp450(enzymes-demethylase) ,leading to a reduction in ergosterol synthesis

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15
Q

What are the adverse effects of azole

A

*nausea
*vomiting
*diarrhea
*skin rash
hepatotoxity(incraese hepatic enzymes)

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16
Q

what are the contraindications of azole

A

*Pregnancy ,it is excreted in breast milk and it is thus not recommended

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17
Q

What are the adverse effects of voriconazole

A
  • visual disturbance which resolves in 30 min
  • photosensitivity dermatitis
  • toxicity : rash and raised hepatic enzymes

NB should not be given to pregnant woman

18
Q

what are the pharmacokinetics of voriconazole

A
  • well absorbed orally ,with more than 90% bioavailability
  • Absorption is reduced by food
  • it is hepatically metabolized
  • It is excreted as an inactivated metabolite
  • It is an cytp450 inhibitor
  • can be administered as oral or IV
19
Q

What can voriconazole be used to treat

A
  • TREATMENT CHOICE FOR INVASIVE ASPERGILLOSIS ( mold type of infection ,usually inhaled and cause respiratory infections )
  • candida spp and infections resistant to fluconazole
  • oropharyngeal and esophageal candidiasis
  • less toxic than amp

*Treats invasive fungal infections
*These are generally seen in immune incompetent’s
patients

It is not useful for urinary tract infections

20
Q

What is fluconazole used to treat

A

Used for treatment and prevention of superficial and systemic infections and mostly commonly used in treatment of mucocutaneous candida eg
*Viginal and oropharyngeal candidiasis not responding to topical tx

  • Oesophageal and systemic candidiasis
  • cryptococcal meningitis and to prevent relapse of of cryptococcal diseases in aids patients

has not activity against aspergillus

21
Q

MOA of fluconazole

A

inhibits the fungal cytochrome p45 enzyme .This inhibition interferes with ergosterol synthesis

22
Q

fluconazole pharmacokinetics

A
  • good oral absorption
  • distribution is wide in the body including CSF
  • T1/2 is 20-50 hours
  • excreted in the urine *Penetrates the CSF best
  • has widest therapeutic index thus allows aggressive dosing
23
Q

Side effects of fluconazole

A

rash ,headache , vomiting ,nausea, abdominal pain and elevated hepatic enzymes ( has least increase in hepatic enzymes’ among azole drugs)

rare: anorexia ,fatigue ;constipation

24
Q

What can itraconazole treat

A
  • Dermatophytosis
  • onychomycosis( infection of the nail and it only respnds to systemic treatments )
  • candidiasis if not responding to topcal treatment
  • DRUG OF CHOICE for
  • dimorphic fungi infections
  • alternative therapy for aspergillosis

oral solutions are preferred in oropharyngeal and oesophageal candidiasis

25
Q

mechanism of itraconazole

A

similar to fluconazole

26
Q

pharmacokinetics of itraconazole

A
  • food and gastric acid increases absorption
  • widely distributed except for CSF
  • t1/2 is 21 hrs
  • metabolized in the liver
  • excreted in urine and feces
  • admin orally or IV
  • Has broader spectrum than fluconazole but not as broad as voriconazole
  • low bioavailability when taken orally and liquid solution must be taken on an empty stomach
27
Q

Side effects of itraconazole

A

rash ,headache, nausea ,diarrhea

abdominal pain ,elevated hepatic enzymes

28
Q

what are posaconazole treat

A
  • Most species of candida , alternate in oropharyngeal or oesophageal candidiasis
  • Has activity against aspergillosis ,used when voriconazole doesnt work

murcomyscosis

29
Q

The pharmacokinetics of posaconazole

A
  • available as oral suspension in SA
  • metabolized by liver
  • fatty meal increase absorption
30
Q

Echinocandins -capsofungin MOA

A

Specifically inhibit D-glucan synthesis essential to cell wall integrity of fungi thus compromising integrity of cell wall to become permeable causing cell lysis

31
Q

What can echinocandins -capsofungin treat

A

Candidasis ( invasive oropharyngeal and oesopharyngeal )

  • Aspergillus ( last resort)
  • Emperic therapy for febrile neutropenia
  • No activity against cryptococcus
32
Q

Echinocandins -capsofungin pharmacokinetics

A
  • Only through IV
  • t1/2 is 9 - 11 hrs
  • poor CSP
  • well tolerated with minor GIT and flushing
33
Q

What are the examples of echinocandins

A

capsofungin and micafungin and anidulfungin

34
Q

How are anidulfungin and micafungin admin and what do they treat

A

Treat :
*ANI ; Invasive candidiasis

Availiable as IV

MIC ; Invasive candisiasis and availiable as IV

35
Q

MOA and pharmacokinetics of griseofulvin

A

inhibit fungal mitosis

  • Used to treat dermatophytosis via oral treatment
  • 2-6 weeks for skin and hair infection
  • months of treatment for nail infection and it allows regrowth of the new protected nail
  • Largely been replaced by itraconazole and terbinafine

*fatty food increase absorption

*

36
Q

griseofulvin side effects

A

headache , skin rash,dry mouth and altered taste sensation

37
Q

What can terbinafine treat

A
  • Dermatophytsosis of skin ,hair and nails
  • Candida albicans

*oncmycosis

38
Q

Pharmacokinetics of terbinafine

A
  • distributed preferentially to skin ,skin ,nail bed
  • Metabolized in liver
  • Available in oral and topical formulation
  • highly lipophilic
39
Q

What is the adverse effects of terbinafine

A

GIt upset ,headache ,skin reactions , arthralhia ,hepatotoxicity and taste disturbance

40
Q

What is the terbinafine MOA

A

inhibits squalene epoxidase which inhibits ergosterol synthesis( Squalene is not converted to lanosterol and ultimately ergosterol)

41
Q

What is nystatin used to treat

*topical antifungals

A
  • Used in candida yeast infections
  • Not effective against dermatophyte skin infection
  • oropharyngeal thrush
  • vaginal candidiasis
  • intertriginous candidal infections
42
Q

How is nystatin ( topical)

A
  • Too toxic for parental admin thsu it is used for suppression of local candidial infection
  • treatment for 14 days is usually adequate but prolonged therapy needed in some cases
  • Poorly absorbed through skin ,mucous membrane or GIT low toxicity
  • unpleasent taste
  • safe for use in infants

anti bacterial drugs (7 decks)

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