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pulmonary > immunologic lung diseases > Flashcards

immunologic lung diseases Flashcards

1
Q

th2 cytokines

A

il-4,5,10,13

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2
Q

th1 cytokines

A

il-2, ifn-y

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3
Q

th1 role

A

killing microbes, autoimmunity, activate macrophages

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4
Q

th2 role

A

antibodies, extracellular parasites, allergy

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5
Q

th17 role

A

induction of inflammatory response, autoimmunity

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6
Q

treg role

A

dampening immune activation, tolerance

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7
Q

innate immunity immunologic lung diseases

A

pneumonia, ards

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8
Q

granulomatous immunologic lung disease

A

tb
sarcoid
egpa (esosinophilic granulomatosis with polyangitis)

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9
Q

autoimmune and vasculitis lung disease

A

gpa (granulomatosis with polyangitis)
sle
rheumatoid lung
anti-gbm disease

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10
Q

th-1 related lung diseases

A

hypersensitivity pneumonitis, copd

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11
Q

th-2 related lung diseases

A

allergic asthma, abpa (allergic bronchopulmonary aspergillosis)

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12
Q

extrinsic allergic alevolitis= ?

A

hypersensitivity pneumonitis

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13
Q

signs of hypersensitive pneumonitis?

A

cough, dyspnea, fever

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14
Q

most common causes of HP?

A

thermophilic actinomycetes, fungi, bird proteins

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15
Q

how do you diagnose hp?

A

ouchterlony test for igG directed against allergen

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16
Q

pathology of hp?

A

in a genetically susceptible host, antigen exposure activates the immune system, causing alveolitis, granulomatous inflammation, and fibrosis

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17
Q

cells involved in hp?

A

b cell (igG antibodies) and t cell mediated (th1, IFN-gamma)

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18
Q

clinical features of acute HP?

A

4-48 hrs: fever, chills, cough, hypoxemia, aches, tachypnea, fine rales

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19
Q

clinical features of subacute HP?

A

weeks-4 mo: dyspnea, cough, episodic flares, tachypnea, diffuse rales

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20
Q

clinical features of chronic HP?

A

4 mo-years: dyspnea, cough, fatigue, weight loss, +/- clubbing

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21
Q

hrct on acute hp?

A

ground glass infilatrates

22
Q

hrct in subacute hp?

A

micronodules, air-trapping

23
Q

hrct in chronic hp?

A

fibrosis, honeycombing, emphysema

24
Q

prognosis in HP?

A

good for acute and subacute, chronic is poor

25
Q

immunopathology of acute hp?

A

macrophage, lymphocyte response (th1) to antigen, immune complexes

26
Q

immunopathology of subacute hp?

A

formation of GRANULOMAS and lymphoid follicles containing plasma cells, activated b cells

27
Q

immunopathology of chronic hp?

A

lymphocytic infiltration, collagen formation, FIBROSIS, neutrophil-mediated air space destruction

28
Q

bronchoalveolar lavage in HP?

A

inc. total cell count, increased T lymphocytes (more CD8/CD4)

29
Q

diagnostic criteria for hypersensitivity penumonitis

A
  1. exposure to known antigen
  2. precipitating antibodies to antigen
  3. recurrent episodes
  4. inspiratory crackles on PE
  5. symptoms occur 4-8 hours after exposure
  6. weight loss
30
Q

spirometry of HP?

A

restrictive patterns and reduced diffusion

31
Q

management of hp?

A

trial of corticosteroids in acute phase; longer course at higher doses often necessary for subacute phase–efficacy not established

32
Q

immunology of abpa?

A

th2 and eosinophils

33
Q

what is allergic bronchopulmonary aspergillosis?

A

allergic inflammatory response to colonization by aspergillus and other fungi; characterized by asthma, pulmonary infiltrates, mucus plugging, proximal bronchiectasis

34
Q

what is aspergillus?

A

ubiquitous fungus that grows in organic debris; hyphae branch at 45 degree angles, macrophages ingest and kill spores

35
Q

normal response to aspergillus

A

macrophages ingest and kill spores, neutrophils bind to hyphae and damage cell walls with an oxidative burst

36
Q

what happens in abpa?

A

virulence factors/mycotoxins cause th2 mediated inflammation
generation of eosinophil-rich mucoid impaction
activation of cd20 b cells which generate igE antibodies

37
Q

criteria for diagnosis of abpa?

A
  1. asthma
  2. central bronchiectasis (inner 2/3 of chest CT)
  3. immediate cutaneous reactivity to aspergillus species
  4. total igE > 417
  5. elevated igE and or igG to A. fumigatus
    non essential but supportive: infiltrtes on Cxr/ct; serum precipitating antibodies to Af, eosinophilia
38
Q

lobe predominance in abpa?

A

upper lobe

39
Q

spirometry in abpa?

A

obstructive; bd response in fewer than 1/2, air trapping, deification is reduced in minority (bronchiectasis)

40
Q

drugs for abpa?

A

itraconazole (anti-fungal)

omalizumba (anti-igE–> use in CF patients where you can’t use steroids)

41
Q

GPA stands for?

A

granulomatosis with polyangitis

42
Q

what is vasculitis?

A

leukocytes in vessel wall with reactive damage to rural structures; loss of wall integrity leads to bleeding; compromise of lumen leads to ischemia and necrosis

43
Q

gpa is an example of what kind of vasculitis?

A

small vessel that most commonly affects the upper airways, lower airways, and kidneys

44
Q

upper airway disease in GPA:

A

sinus disease, epistaxis, septal perforation, subglottic stenosis

45
Q

how do you diagnose gpa?

A

at least 2 of the following:
1) nasal or oral inflammation (painful or painless oral ulcers or purulent or bloody nasal discharge)
2) abnormal chest CT showing nodules, fixed infiltrates, or cavities
3) abnormal urinary sediment (microscopic hematuria with or without rbc casts)
4) granulomatous inflammation on biopsy of an artery or perivascular area
AND positive c-anca

46
Q

what else is anca associated vasculitis?

A

gpa, mpa (microscopic polyangiitis), egpa (eosinophilic…), renal limited vasculatis

47
Q

egpa is ____=anca?

A

perinuclear (p-anca)–> antibodies to strong cations (myeloperoxidase)

48
Q

what is c-anca?

A

antibodies to neutral proteins or weak cations (proteinase 3)

49
Q

immunopathogenesis of gpa?

A

activated Cd4 T cells; B cells, neutrophils

50
Q

spirometry in gpa?

A

restrictive with reduced diffusion

pulmonary (4 decks)

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