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invasive fungal infections Flashcards

1
Q

where is fungi freely present?

A

the environment ( soil)
some parts of the normal flora in humans/ animals

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2
Q

what are 3 endemic fungi (not part of the normal human flora)

A

histoplasmosis
blastomycosis
coccidiomycosis

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3
Q

what are the 4 opportunistic fungi (part of the normal human flora ( microbiota))

A

candidiasis
aspergillosis
mucormycosis
cryptococcosis

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4
Q

what is the primary defense mechanism against endemic and opportunistic fungi ?

A

innate immunity

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5
Q

why are fungi increasingly recognized as a major pathogen

A

intentional immunosuppression
-cancer treatments, immunosuppressive agents

use of broad spectrum antibiotics
-imbalances normal flora
-increast risk of opportunistic fungi

general advances in medical care
-surgery, aggressive treatment, organ treatment, HIV/AIDS

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6
Q

invasive infections

A

high mortality
disseminated, deep organ

effects blood, heart, brain, lungs, eyes, bones

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7
Q

esgrosterol inhibitors/binders class includes

A

polyenes
azoles
allylamines (terbinafin)

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8
Q

cell wall active agents include

A

echinocandins

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9
Q

intracellular active agents include

A

flucytosine

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10
Q

MOA of Polyenes

A

intercalate the cell membrane by directly binding to ergosterol –.> leakage of intracellular contents

concentration- dependent

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11
Q

spectrum of activity for polyenes : AMB

A

all candida
aspergillus terreus
some mucorales
some fusarium
all endemic

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12
Q

what is the formulation of amphoterin B

A

IV

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13
Q

conventional amphotericin B

A

amphotericin B deoxylate (AmB-d, fungizone)

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14
Q

lipid amphotericin B

A

amphotericin B lipid complex ( ABLC, abelcet)

liposomal amphotericin B (L-AmB, AMbisome)
- more favorable
- more expensive for dose escalations

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15
Q

amphotericin B ADME

A

A; poor, all formulations are IV products
D: tissue, blood, liver, body fluid,urin, CSF (poor, best L-AmB)
M; none
E: feces/ urine (AmB-d)

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16
Q

amphotericin B side effects

A

infusion-related reactions
-preventable: pre-medication, slow infusion, pre-hydration

nephrotoxicity
-tubular damage, vasoconstriction

electrolyte abnormalities
-hypokalemia
-hypomagnesemia

thrombophlebitis

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17
Q

monitoring parameters for amphotericin B

A

signs and symptoms of nephrotoxicity , potassium (4) , magnesium (2)

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18
Q

MOA of -azoles

A

Bind to 14 alpha-demethylase, a fungal CYP450, which subsequently depletes ergosterol in the cell membrane, leading to:

(1) impaired membrane fluidity
(2) accumulation of toxic 14 alpha-methylated sterols intracellularly
(3) collateral inhibition of human CYP enzymes leading to DDIs

AUC:MIC ratio dependent killing

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19
Q

what azole drugs have >90% bioavailability

A

fluconazole
voriconazole
isavuconium

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20
Q

what azole drugs have 50% bioavailability

A

itraconazole

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21
Q

what azole drugs unpredictable bioavailability

A

posaconazole

-especially unpredicatble if pt has poor appetite due to N/D, mucositis, GvHD invoking gut/colon

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22
Q

formulation and specific instructions for fluconazole

A

IV and PO
take with or without food

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23
Q

formulation and specific instructions for voriconazole

A

IV and PO
take on empty stomach

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24
Q

formulation and specific instructions for isavunconazonium

A

IV and PO
take with or without food

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25
Q

formulation and specific instructions for itraconazole

A

PO only
- caps: take with high fat meal or acidic beverages
-OS take on empty stomach

26
Q

formulation and specific instructions for posaconazole

A

PO only
-OS: the with high fat meal
- devide dosed to improve absorption

-

27
Q

metabolism and drug interactions of azoles

A

inhibit CYP2C19, 2C9, and 3A4 to varying degree

28
Q

azoles that are strong inhibitors of CYP3A4

A

itraconazole
posaconazole

29
Q

azoles that are strong inhibitors of CYP2C19

A

Voriconazole

30
Q

fluconazole SE

A

QT prolongation
GI, rash, hepatotoxicity

31
Q

ItraconazoleSE

A

QT prolongation;
Contraindication in CHF
GI, rash, hepatotoxicity

32
Q

Voriconazole SE

A

QT prolongation photosensitivity, visual changes
GI, rash, hepatotoxicity

33
Q

Posaconazole SE

A

, QT prolongation
GI, rash, hepatotoxicity

34
Q

Isavuconazonium SE

A

elevated LFTs,
hypokalemia,
peripheral edema,
infusion related reactions,
shortening of QT
GI, headache

35
Q

MOA of each echinocanins

A

Competitive inhibition of ß-1,3-D-glucan polymers (the crosslinking structural components of fungal cell walls)

AUC:MIC ratio dependent killing

36
Q

echinocanins ADME

A

A: poor; IV only

D: Blood,liver, kidneys, large intestines, spleen, and lungs
- Minimal or undetectable in urine, CSF, eye
-Highly protein bound

M: hepatic (C, M)

E: Caspofungin (Urine); Micafungin and Anidulafungin (feces)

37
Q

SE of echinocandins

A

GI, headache, flushing, infusion-related pruritus, increased LFTs

38
Q

monitoring of echinocandins

A

LFTs, Hypersensitivity

39
Q

echinocandins drug interactions

A

minimal

40
Q

what is the most common invasive fungal infection

A

invasive candidiasis

41
Q

clinical presentation of invasive candidiasis

A

-Single or multi-organ involvement

-Kidney, brain, myocardium, skin, eye, bone / joints
–Liver and spleen (common in patients undergoing chemotherapy for acute leukemia, lymphoma)

-Symptoms: acute onset fever, tachycardia, tachypnea, chills, hypotension

-Diagnosis:
–Cultures: blood culture sensitivity ~ 50 %
—-Lung, urine, GU/GI: Sometimes can be difficult to discern whether colonization or pathogen if there are co-infections w bacteria, etc.

42
Q

what is the 1st line treatment for Candidemia/Disseminated Candidiasis

A

1st line: echinocandins

43
Q

what is the alternative empiric treatment for noncritical ill pts & without azole exposure for Candidemia/Disseminated Candidiasis

A

azole

used once culture / susceptibility data known & patients are clinically sta

44
Q

what is the alternative agent if intolerance or antifungal resistance develops for Candidemia/Disseminated Candidiasis

A

Amphotericin B

Lipid formulation preferred to minimize side effects, toxicities

45
Q

what is the duration for treatment of candidemia and Disseminated candidiasis

A

Candidemia:14 days from negative blood cultures, symptom resolution (repeatblood cultures q24-48h)​

Disseminated candidiasis:weeks to months until lesions have resolved on imaging​

46
Q

clinical presentation of invasive aspergillosis

A

Single or multiorgan involvement

Sites:
-Common: lung ,sinuses
-Other: CNS, skin, liver, spleen, heart, pericardium (uncommon)

Symptoms:
-pleuritic chest pain, fever, wheezing, hemoptysis; stuffiness, runny nose, headache

Diagnosis –>Challenging
-Cultures & histopathology
Imaging: CT

47
Q

what is first line for invasive aspergillosis

A

Voriconazole

48
Q

what are second line options for invasive aspergillosis

A

-AmB deoxycholate / lipid derivatives

-Isavuconazole: newer agent, indicated for Invasive Aspergillosis; less data compared with voriconazole, AmB

-Echinocandins: effective in salvage therapy; not recommended routinely as monotherapy for primary treatment

-Posaconazole: only suspension studied in treatment/prophylaxis studies

-Itraconazole: rarely recommended, reserved for less severe disease

49
Q

what is the treatment duration for invasive aspergillosis

A

a minimum of 6–12 weeks, and suppression therapymay follow if immunosuppression state persists

50
Q

what class covers dimorphic/ endemic fungi ?

A

Polyene: AMB

trizoles

51
Q

epidemiology of blastomycosis

A

MS and OH river valleys; great lakes region

Found in moist soils, decomposing matter (wood, leaves)

Higher risk in persons participating in outdoor activities in wooded areas (forestry work, hunting, camping)

52
Q

etiology of blastomycosis

A

Inhalation of conidia from air

53
Q

risk factors of blastomycosis

A

Travel to/residence in an endemic area

Occupational soil exposure

Immunocompromised host

54
Q

Presentation and diagnosis of blastomycosis

A

Clinical presentation
–Asymptomatic infection, acute/chronic pneumonia, disseminated disease
—Fever, cough, night sweats, myalgias, arthalgias, chest pain

–Disseminated blastomycosis
—Skin, bone / joint, or genitourinary tract
—Cutaneous blastomycosis reported in 40-80 % of cases, marker for multi-organ involvement

Diagnosis
-HISTORY, including travel
-Direct visualization in cytology/histologic specimens
-Culture (respiratory)
-Urine antigen; may cross-react w/ H. capsulatum

55
Q

epidemiology of histoplasmosis

A

MS and OH river valleys; Central/South America; Asia; Africa

Organism grows best in soil containing bird/bat droppings (accelerate sporulation)

56
Q

etiology of histoplasmosis

A

Inhalation of microscopic fungal spores

57
Q

risk factors of histoplasmosis

A

Travel to/residence in an endemic area

Occupational soil exposure, chicken coops, areas with bird droppings, cave exposure, demolition of old buildings

Immunocompromised host

58
Q

presentation and diagnosis of histoplasmosis

A

Clinical presentation depends on comorbidities, immune status, previous exposure
–Environment: duration, enclosed area, inoculum size

Sites:
–Disseminated disease: pulmonary, liver, spleen, GI, bone marrow, CNS, ocular, pericarditis (rare)

Symptoms:
–fever, malaise, headache, weakness, myalgias; cough, chest pain

Diagnosis:
Medical/travel history
Cultures/histopathology, direct
Antigen detection (serum, urine); antibody assays
Imaging (pulmonary)

59
Q

epidemiology of Coccidioidomycosis (valley fever)

A

San Joaquin Valley, CA
SW US, N. Mexico, Central / S. America
Organism grows best in soil

60
Q

etiology of of Coccidioidomycosis (valley fever)

A

Inhalation of conidia

61
Q

risk factors of Coccidioidomycosis (valley fever)

A

Travel to/residence in an endemic area

Race: African-American, Filipino; Asian, Hispanic, Native Americans

Pregnancy (especially 3rd trimester)

Immunocompromised host

62
Q

presentation & diagnosis of Coccidioidomycosis (valley fever)

A

Clinical presentation
–Variable; majority of patients are asymptomatic
—Fever, cough, chest pain –> may mimic CAP
–Sites: primarily pulmonary
—Disseminated (skin, bone/joints, CNS)

Diagnosis
HISTORY, including travel!
Imaging (CXR, CT scans)
Cultures/histopathology/direct microscopy
Serologic (EIAs), PCR, and/or antigen testing

ID (27 decks)

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