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Sven's Flashcards > 228 - Fungal Disease > Flashcards

228 - Fungal Disease Flashcards

1
Q

what is allergic bronchopulmonary aspergillosis?

A

a hypersensitivity pneumonitis caused by aspergillus antigen in bronchi/aveoli

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2
Q

Hypersensitivity pneumonitis causes a immune mediated response, name the 2 pathways?

A
  • Ty3 hypersensitivity reaction with cross linking of Th2 and B-cell mediated antibodies and antigens to form large immune complexes. These deposit in tissues causing an inflammatory response and vascular permeabilty
  • Ty4 hypersensitvity reaction - delayed hypersensitivity reaction/cell mediated immune memory response with Th1 memory cells (previous aspergillus exposure) and macrophages - granulomas and inflammatory damage due to complement activation
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3
Q

what are the symptoms/signs of hypersensitivity pneumonitis?

A
  • bronchospasm, mucous plugging, bronchocentric inflammation (bronchiectasis, smooth muscle hypertrophy and pulm. fibrosis)
  • fever, dyspnoea, cough, wheeze, fine expiratory crackles
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4
Q

who is at risk from hypersensitivity pneumonitis?

A

px with underlying lung disease (asthma, COPD) as cant clear spores, pigeon fanciers, farmers, brewers, cheese workers, textiles

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5
Q

what investigations should be carried out in suspected hypersensitivity pneumonitis?

A
  • peak flow/ spirometry for restrictive defects
  • CXR - pulm infiltrates/consolidation (ring and glove signs )
  • allergy testing - prick test
  • sputum - evidence of hyphae
  • bronchoalveolar lavage (↑WCC, ↑eosinophils, aspergillus present
  • bloods for ↑IgE and aspergillus antibodies
  • CT thorax - bilateral areas of consolidation and air trapping (ground glass infiltrates)
  • VATS biopsy
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6
Q

what treatment should be given for hypersensitivity pneumonitis?

A
  • oral corticosteroids (prednisolone) +/- oral antifungals

* immunosuppressants if necessary (cytophosphamide)

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7
Q

What is aspergilloma?

A

a pre-existing cavity in the lung parynchyma from previous cavitating disease (TB, abcess, bronciectasis, sarcoidosis) that has been colonised by aspergillus to form a mycetoma (fungal ball - pink necrotic centre of dead cells and debris surrounded by rim of active hyphae). Toxin released and cause erosion with haemoptysis

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8
Q

how does aspergilloma present?

A
  • often asymptomatic
  • haemoptysis in 50%
  • solitary mass on CXR
  • fever, cough, weight loss
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9
Q

how would you investigate suspected aspergilloma?

A
  • CXR - solitary pulm mass with crescent if air around mass that can move if px moves
  • biopsy/fine needle aspiration to exclude TB or neoplasia
  • bloods - aspergillus antibodies raised
  • sputum culture
  • skin sensitivity
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10
Q

how should aspergilloma be treated?

A
  • conservatively / monitoring
  • oral antifungals eg itraconazole not very efficient
  • surgical resection or bronchial artery embolisation for severe haemoptysis
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11
Q

What is Chronic Necrotising Pulmonary Aspergillosis?

A

Aspergillus colonises bronchi/alveoli any invades locally in those with mild/mod immunosuppression (alcoholism, steroid treatment, pre-existing lung disease). Bronchocentric granulomas formed by Th1.macrophage immune response - necrosis and cavitation

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12
Q

how does Chronic Necrotising Pulmonary Aspergillosis present?

A
  • hx of exposure

* fever, productive cough +/- haemopytisis, night sweats, weight loss, consolidation

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13
Q

how should suspected Chronic Necrotising Pulmonary Aspergillosis be invesitgated?

A
  • CXR - pum infiltrates/consolidation
  • sputum culture
  • broncho alveolar lavage / needle biopsy
  • Galactomnnan Assay
  • bloods - antibodies
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14
Q

how should Chronic Necrotising Pulmonary Aspergillosis be treated?

A

*antifungals - voriconazole, itraconazole, amphotericin

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15
Q

what is invasive apergillosis?

A

aspergillus colonisation of bronchi/alveoli and invasion of lung intersitium in immunosuppressed (neutropaenic - HIV, organ transplant, steroids, chemo). Angioinvasion occurs causing multiple lung infarcts

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16
Q

how does invasive apergillosis present?

A
  • Hx of immunosuppression (neutropaenia) & exposure
  • gravely ill, fever, cough, dyspnoea, pleuritic pain
  • organ involvement
17
Q

how would you investigate suspected invasive apergillosis?

A
  • CXR - pulm infiltrates - multi-focal opacities “halo sign” due to film of blood
  • sputum, bronchoalveolar lavage, biopsy
  • galactomannan assay
18
Q

how would you treat invasive apergillosis?

A

IV voriconazole or amphotericin plus flucytosine

*reduce immunosuppresants

19
Q

what does the plasma membrane of a fungus consist of?

A
  • phospholipid bilayer
  • sterols - ergosterol
  • embedded proteins
  • synthases
20
Q

what does the external cell walls of fungi consist of?

A

carbohydrate polymers - B glucans, chitinss, mannose sugars

*mannoproteins

21
Q

how are fungal infections classified?

A

by region affected

  • superficial and cutaneous (dermatophytosis, pityriasis versicolour, candidiasis)
  • subcutaneous - rare and mainly travel associated
  • systemic infections (invasive candidiasis, asperigillosis, cryptococcosis, pneumocytosis) also true pathogens (histoplasmosis, coccidiomycosis, blastomycosis, paracoccidiomycosis)
22
Q

what is affected by dermatophytosis (tinea)?

A

localised infection of keratinised tissue (skin, hair, nails) spread by direct contact or indirect contact

23
Q

what is pityriasis versicolor?

A

superficial infection of strateum corneum producing hyperpigmented or depigmented macules on trunk/proximal limbs caused by malassezia furfur - use ketoconazole shampoo topically or itraconazole/fluconazole orally

24
Q

whar is superficial candidiasis?

A

superficial infection of mucous membranes (mouth vagian) with white patches and tinea like lesions caused by candida albicans
*invasive candidiasis in immunocompromised

25
Q

what is cryptococcosis?

A

CNS infection or pulm infection in immunosuppressed caused by crptococcus neoformans via inhalation of fungal aerosols from soil

26
Q

what is pneumocystosis?

A

infection of lungs by pneumocystis jiroveci (protozoan like fungus) in immunosuppressed - use co-trimoxazole

27
Q

where do travel associated true pathogens come from?

A
  • hystoplasmosis -east USA, Latin America, west africa
  • coccidiomycosis - latin america
  • blastomyscosis - E USA and canada
28
Q

what investigations can be carried out to determine what fungus species?

A
  • macroscopic exam - IV light for lesions, pus, bloody, necrosis - wood lamp to make fungi fluoresce
  • microscopic exam
  • culture - sugar agar plates - 1-3 weeks
  • serology - rapid identification in systemic infection
29
Q

what antifungals inhibit membrane synthesis?

A

azoles, echinocandins, allylamines

30
Q

what antifungals inhibit membrane function?

A

polyenes

31
Q

what antifungals inhibit nucleic acid synthesis and mitosis?

A

flucytosine (narrow spectrum so used with amphotericin IV- systemic candidiasis and cryptococcus) and griseofulvin

32
Q

how do azoles work?

A

inhibit fungal cytochrome P450 enzyme which produces ergosterol necessary form cell membrane formation (also inhibits human p450 enzyme - toxicity) - inhibits growth, makes membrane permeable and builds up toxic sterol intermediates

33
Q

name some imidazoles and what are they used for?

A
  • ketoconazole, mionazole, clotrimazole

* candida and tinea

34
Q

name some triazoles and what are they used for?

A
  • fluconazole - candida, cryptococcus, dermatophytes - topical and oral but GI disturbances and liver damage
  • voriconazole - life threatening candida, aspergillus -oral and IV (danger in renal impirment) - GI and visual impairment
  • itraconazole - candida, aspergillus, cryptococcus - oral but mostly IV - negative ionotrope (less muscle contractions in heart) and liver damage
35
Q

how do echinocandins like caspofungin work?

A

inhibit 1.3 beta glucan synthase and weakens cell wall. IV only and start with loading dose (caution in hepatic impairment) - few side effects

36
Q

how do polyenes work?

A

increase membrane permeability by binding to ergosterol and increasing pore formation and ion leakage

  • amphotericin - systemic aspergillis, candida, cryptococcus - IV or intrathecally (high protein bound) - high toxicity esp renal (hypokalaemia)
  • nystatin - only topical against superficial candidiasis
37
Q

how do allylamines work?

A

inhibit ergosterol synthesis by inhibiting squalene epoxidase enzyme
*Terbafine used for superficial dermatophyte infections top and oral - allergic skin reactions, GI disturbance and liver toxic

Sven's Flashcards (32 decks)

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