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RHS > L8- Pulmonary Pathology IV > Flashcards

L8- Pulmonary Pathology IV Flashcards

1
Q

NSIP:

(1) etiology
(2) prognosis in comparison to IPF/UIP
(3) age group affected
(4) Tx

A 
(nonspecific insterstitial pneumonia)
1- unknown
2- better prognosis
3- younger people
4- steroids or immunomodulatory therapy
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2
Q

Describe the histology of NSIP

A

(nonspecific insterstitial pneumonia)
-uniform fibrosing process (chicken-wire): i) cellular variant (lymphocyte infiltration), ii) fibrosing variant, iii) both

-lacks honeycomb change, fibroblast foci (in comparison to IPF/UIP)

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3
Q

Cryptogenic Organizing Pneumonia:

(1) alternate names
(2) etiology
(3) Sxs
(4) Radiographic findings
(5) Tx

A

1- BOOP (bronchiolitis obliterans organizing pneumonia)
2- unknown
3- cough, dyspnea
4- patchy peribronchial or subpleural consolidation
5- spontaneous recovery or with 6 mos steroids

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4
Q

Describe the histology Cryptogenic Organizing Pneumonia

A

-Masson Bodies: polyploid plugs of loose fibroblastic tissue filling alveolar spaces

  • normal underlying parenchyma / alveolar architecture not destroyed
  • no interstitial fibrosis or honey combing
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5
Q

(1) cause of Organizing Pneumonia

(2) cause of Cyptogenic Organizing Pneumonia

A

1- viral/bacterial pneumonia, inhaled chemicals/toxins, transplantation (lung, bone marrow), collagen vascular disease

2- unknown (or obscure)

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6
Q

Describe the histology of Organizing Pneumonia

A

(not cryptogenic)

  • interstitial fibrosis
  • honeycombing
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7
Q

AIP = (1)

  • (2) affected age group
  • (aggressive/benign) disease
  • follows (4) event or is apart of (5) event
  • (6) prognosis
A

(acute interstitial pneumonia)
1- Hamman-Rich Syndrome
2- older Pts, ~59 y/o
3- very aggressive
4- 2 wks post-URI
5- acute phase of IPF (interstitial pulmonary fibrosis)
6- significant mortality rate - survivors with recurrences and chronic conditions

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8
Q

AIP presents with (1) and (2) histologically, very similar to people who have (3)

A

(acute interstitial pneumonia)
1- diffuse alveolar damage
2- hyaline membranes
3- ARDS / DAD

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9
Q

LIP = (1)

  • (2) interstitial changes
  • (3) associated conditions
  • (4) etiology / pathogenesis
  • (5) possible complication
A

1- lymphoid interstial pneumonia
2- interstitial expansion by groups/sheets of lymphoid cells
3- CT disease, autoimmune disease, HIV infection
4- idiopathic (possibly)
5- progression to lymphoma in small number of cases

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10
Q

Majority of interstitial lung diseases are related to (1), three examples include: (2)

A

1- smoking
2:
-DIP, desquamative interstitial pneumonia
-respiratory bronchiolitis associated interstitial lung disease
-Pulmonary Langerhans cell histiocytosis

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11
Q

DIP = (1)

  • (2) affected group, age/sex
  • characterized by the presence of (3) in airspaces, seen in (4) patients
  • may also present with (5)
A 
1- desquamative interstitial pneumonia
2- 50-60s, M=F
3- macrophages (filled alveolar space)
4- current/former smokers
5- emphysema
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12
Q

DIP = (1)

  • (2) clinical presentation
  • (3) pulmonary function test
  • (4) Tx
A

1- desquamative interstitial pneumonia
2- insidious onset of dry cough, dyspnea, clubbing of fingers
3- mild restrictive pattern (reduced volumes, inc/normal FEV1:FVC), moderately dec diffusion capacity
4- steroids, smoking cessaion

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13
Q

DIP = (1)

  • (2) histological results, hint- 3
  • (3) possible progression
A

1- desquamative interstitial pneumonia
2- alveolar macrophages (filled alveolar spaces), septal thickening, mild interstitial fibrosis
3- interstitial fibrosis (severe)

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14
Q

Respiratory bronchiolitis associated interstitial lung disease:

  • (1) are the 2 hallmark features
  • may also be present with (2)
  • (3) affected age group / smoker status
A

1- chronic inflammation, peribronchiolar fibrosis
2- centrilobar emphysema
3- 50-60 y/o /// >30 pack years

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15
Q

Respiratory bronchiolitis associated insterstitial lung disease:

  • (1) hallmark histological feature
  • (2) clinical presentation
  • (3) Tx
A

1- intraluminal pigmented macrophage (intracellular carbon) accumulation in 1st/2nd order respiratory bronchioles
2- mild disease, gradual onset of dyspnea, cough
3- steroids, smoking cessation

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16
Q

PAP = (1)
-(2) is the defect => (3) dysfunction and issue

Causes: (4), (5), (6)

A

1- pulmonary alveolar proteinosis (rare disease)
2- GM-CSF defect
3- pulmonary macrophage dysfunction => surfactant accumulation in alveolar/bronchiolar spaces

4- Autoimmune (90% cases): adults
5- Secondary: many disorders impairing macrophage maturation / activity
6- Congenital/hereditary: rare, GM-CSF related mutations

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17
Q

PAP = (1)

  • (2) clinical presentation
  • (3) Tx (hint- 2)
A

1- pulmonary alveolar proteinosis (rare disease)

2- very productive (gelatinous) cough, progressive dyspnea / cyanosis / respiratory failure [or a benign course with resolution]

3- pulmonary lavage (therapeutic) + GM-CSF replacement therapy

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18
Q

Sarcoidosis:

  • (1) affected organs
  • (2) is the hallmark feature seen in affected organs
  • (3) etiology / pathogenesis
  • highest prevalence in (4) patients
A

1- multiple organs / tissues
2- non-caseating / non-necrotizing granulomatous inflammation
3- unknown- evidence it involves Immune Response via Th cells to specific Ag (possible genetic pre-disposition)
4- young adults (<40 y/o) and smokers

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19
Q

Sarcoidosis results from a (1) hypersensitivity reaction to (2), driven by (3) cells

A

1- type IV hypersensitivity reaction
2- unknown Ag
3- Th cells (CD4+)

20
Q

Sarcoidosis clinical presentation:

  • (1) is an important feature related to its presentation
  • (2) lung Sxs
  • (3) constitutional Sxs
  • (4) other organs involved –> (5) organs may have severe impairment
A

1- variable presentation, asymptomatic to serious presentation
2- (90% cases involve lungs) gradual respiratory Sx development: dry cough, SOB/dyspnea, vague discomfort)
3- fever, weight loss, fatigue, night sweats
4- skin (erythema nodosum), eyes (lacrimal glands - sicca syndrome), parotid glands (bilateral parotitis), spleen, liver, bone marrow
5- CNS, cardiac system, ocular system, skin

21
Q

Sarcoidosis:

1) lab results
(2) CXR results (note hallmark feature

A

1- hypercalcemia + its resulting Sxs; elevated ACE (60% cases)

2- bilateral hilar lymadenopathy, +/- parenchymal infiltrates or fibrosis

22
Q

Sarcoidosis Histology:

  • (1) hallmark feature
  • (2) progressive feature
  • (3) rare feature
  • (4)/(5) are the special histological and other hallmark features
A

1- non-necrotizing epithelioid granuloma w/ lymphangitic distribution
2- hyalinized scar (via collagen replacing granuloma)
3- (5-15%) progression to interstitial fibrosis and honeycombing

4- Schaumann bodies (Ca-protein concretions)
5- Astroid bodies (giant cell stellate inclusions)

23
Q

define:

(1) Schaumann bodies

(2) Asteroid bodies

A

(for Sarcoidosis Histo)
1- laminated concretions of Ca and protein

2- stellate inclusions in giant cells

24
Q

Sarcoidosis Tx

  • 65-70% result in (1)
  • 20% result in (2)
  • 5-15% result in (3)

-(4) can occur post-lung transplantation

A

(Note- remission is spontaneous or with therapy)
1- recovery
2- permanent lung dysfunction
3- progressive fibrosis and cor pulmonale
4- sarcoidosis can reocur in 35% of Pts

25
Q

HP / EAA = (1)

  • (2) is the general pathogenesis
  • (3), (4), (5) are possible causes
A

1- hypersensitivity pneumonia / extrinsic allergic alveolitis
2- inhaled Ag (organic Ag) => granulomatous interstitial pneumonitis (= EAA) –> restrictive lung disease

(occupational exposures)
3- Farmer’s lung: moldy hay from thermophilic bacteria
4- Silo filler’s disease: plant material gas inhalation (oxides of nitrogen)
5- Byssinosis: cotten, linen, hemp, textile factory worker

26
Q

HP / EAA = (1)

  • general pathogenesis (2)
  • (3) first exposure
  • (4) second exposure
  • (5) chronic exposure
A

1- hypersensitivity pneumonia / extrinsic allergic alveolitis
2- Type III hypersensitivity reaction; immunologic mediated response to extrinsic Ag

3- => IgG in serum
4- Ig-Ag complex –> interstitial inflammatory response
5- granuloma formation via Type IV hypersensitivity response

27
Q

HP / EAA = (1)

-histopathology = (2)

A

1- hypersensitivity pneumonia / extrinsic allergic alveolitis

2- airway centered process with chronic inflammatory infiltrate, organizing pneumonia, poorly formed non-necrotizing granulomas with giant cells

28
Q

define Pneumonconiosis + list 3 most common conditions

A
  • non-neoplastic lung diseases secondary to inhalation of mineral dusts (occupational)
  • asbestosis, silicosis, CWP (coal workers pneumoconiosis)
29
Q

define and list the causes of the 2 types of Pneumonconiosis

A

Fibrogenic: asbestos, silica

Inert of Weakly Fibrogenic: C, Fe oxides

30
Q

Pneumonconiosis pathogenesis includes the participation of (1) cells that will release and secrete (2) and (3) in order to get (4) overall in the lung

A

1- macrophages
2- lysosomal enzymes / free radicals –> tissue injury + reparative response
3- IL-1 + GFs –> fibroblast proliferation
4- 2/3 —> fibrosis

31
Q

Asbestosis:

  • (1) define asbestos
  • (2) high risk occupations
  • (3) associated lung developments
A

1- family of hydrated silicates, fibrous geometry / fibrous silicates, proinflammatory

2- mining, milling, insulation, construction, demolition

3- parenchymal interstitial fibrosis (asbestosis), localized/dissue fibrous plaques, pleural effusions, lung Ca, malignant pleural / peritoneal mesothelioma and laryngeal CA

32
Q

Asbestosis: exposure of asebestos fibers to (1) leads to its ‘uptake’ by (2) cells. (2) activation will initiate a (3) reaction and long-term exposure will eventually lead to (4) because of chronic (3) reaction.

A

1- deep lung tissue
2- phagcytosis via alveolar macrophages
3- inflammatory (inflammasome –> CK release)
4- diffuse interstitial fibrosis

33
Q

Asbestosis in the lung histologically is exhibited by….

A

Asbestos Bodies: golden-brown, beaded rods, translucent center
-consists of asbestos fiber w/ Fe containing proteinaceous material

34
Q

list the associated lung lesions from asbestos

A
  • asbestos body deposition
  • peribronchilar fibrosis
  • diffuse interstitial fibrosis
  • lung Ca
35
Q

list the pleural associated lung lesions from asbestos

A
  • Plaques

- Mesothelioma***

36
Q

pleural plaques from asbestos is usually made up of (1), but (2) are absent and it is usually found in (3) area

A

1- dense collagen, calcification
2- asbestos bodies
3- over domes of diaphragm

37
Q

list the clinical presentation of Asbestosis

A

(similar to most other diffuse interstitial lung diseases)

  • cough, dyspnea
  • possible progression to respiratory failure and cor pulmonale
38
Q

Silicosis:

(1) definition
(2) risks
(3) associated materials

A

1- inhalation of proinflammatory crystalline silicon dioxide (silica)
2- mining, demolition, stonecutting, sandblasting, grinding, foundry work, ceramics
3- silica (amorphous / crystalline forms), Quartz, cristobalite / tridymite (crystalline form is most fibrogenic/toxic)

39
Q

In silicosis, the inhaled material interacts with (1) and (2) leading to activation of (3) and release of (4). There is an increased risk for (5) because of (6).

A

1- epithelial cells
2- alveolar macrophages
3- inflammasome
4- IL-1, IL-8 + TNF, fibronectin, lipid mediators, free radicals, IL-18

5- pulmonary Tb
6- crystalline silica inhibits pulmonary macrophages ability to phagocytose bacteria

40
Q

Silicosis:

  • (1) and (2) are the main gross morphological changes
  • (3) is the main histological change, with (4) seen under polarized light
A

1- collagenous scar/nodule: hilar lymph nodes and upper lung fields
2- Eggshell calcification: calcified sheet in lymph nodes (radiographically seen)

3- central area with whorled collagen fibers + dust-laiden macrophages
4- weakly birefringent (polarized microscopy)

41
Q

Silicosis:

  • (slow/fast) progression
  • (2) in early stages, only (3) is noticeable
  • (4) Sx in later stages
  • (5) complications in later stages (hint- 4)
  • (6) important correlation possibly related to (5)
A

1- slow progression
2- asymptomatic
3- on CXR: fine nodularity in upper zones of lung field
4- SOB
5- progressive massive fibrosis, pulmonary HTN, cor pulmonale, inc susceptibility to Tb
6- inc risk of Lung CA

42
Q

CWP = (1)

  • (2) definition
  • (3) particle description
  • (4) typical presentation (early stages)
A

1- coal workers pneumoconiosis
2- inhalation of coal particles and other admixed forms of dust
3- mostly carbon with other silica/minerals and organic/metallic compounds
4- asymptomatic

43
Q

list the 3 possible morphological changes seen in CWP

A

(coal workers’ pneumoconiosis)

  • Anthracosis
  • Simple CWP
  • Complicated CWP
44
Q

describe anthracosis (histologically + clinical presentation

A

(seen in CWP)
-accumulation of carbon pigment from alveolar/interstitial macrophage phagocytosis along CT in lymphatic regions (lymph nodes)

-asymptomatic (no appreciable pathologic changes)

45
Q

describe simple CWP (histologically + clinical presentation)

A
  • macule 1-2 mm + nodules
  • aggregation of dust-laden macrophages
  • minimal or absent fibrosis
  • associated with centrilobar emphysema (smokers)

-little to no pulmonary dysfunction

46
Q

describe complicated CWP (histologically + clinical presentation)

A

(progressive massive fibrosis)
-coalescence of nodules –> fibrinous scars; appear blackened and >1cm

  • impaired pulmonary function (restrictive)
  • <10% of simple CWP progress to this stage

RHS (35 decks)

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