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Pathology > Chronic Diffuse (Interstitial) Lung Disease > Flashcards

Chronic Diffuse (Interstitial) Lung Disease Flashcards

1
Q

clinical presentation of restrictive lung dz?

A
  • dyspnea
  • tachypnea
  • end-repsiratory crackles
  • NO WHEEZING - b/c there is no airway obstruction
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2
Q

draw volume-pressure curves of obstructive vs restrictive disease. how does each dz effect the lung capacities (RV, FRV, VC, TLC)

A
  • both decrease VC
  • obstuctive: can’t get air out –> inc RV–> inc FRV –> inc TLC
  • restrictive: can’t get air in –> dec RV –> dec FRV –> dec

obstructive: total air lung volume = being normal. RV makes up a higher portion of that TLC than in normal.

restrictive (interstitial) : total lung volume is significantly less than normal.

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3
Q

discuss the general findings seen on images of restrictive (interstitial) lung dz

A
  • bilateral
    • nodules
    • irregular lines
    • ground glass shadows
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4
Q

what are the major potential sequale of restricive (interstitial) lung dz?

A
  • pulmonary HTN –> right HF (cor pulmonale)
  • severe lung scaring
    • “honeycomb” lung
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5
Q

usual interstitial pneumonia (UIP)

  • restrictive or obstructive?
  • demographics?
  • clinical presentation?
A
  • interstitial = restrictive
  • demographics = 50-70, M > F
  • clinical:
    • subacute onset
    • non-productive cough (vs typical pneumo)
    • LOW/NO fever (vs typical pneumo)
    • later in dz –> inspiratory crackles
    • +/- finger clubbing
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6
Q

usual interstitial pneumonia - gross appearance

A

*gross appearance not very telling)

  • outside (pleural surface): cobblestone
  • inside (cut surface): rubbert/white/firm fibrosis in LOWER LOBES
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7
Q

usual interstitial pneumonia (UIP) - microscopic appearance

A
  • alveolar wall lesions that
    • fibrotic
    • contain lymphocytes + some plasma cells
    • are patchy - adjacent to mormal lung tissue
    • are temporarily heterogenous: become less cellular over tme
      • early on: fibroblastic cells > collagen - bluer
      • later on: collagen >>>> cells - pinker

again, mostly in the lower lung.

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8
Q

what can morphology can develop in late stage UIP?

A
  • “honeycombing” of lung:
    • the fibrosis can lead to massive, multicystic changes:
      • dilated air spaces at lung periphery
  • squamous metaplasia
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9
Q

how to dx UIP?

A
  • first, microscopic & radiographc findings: patchy interstitial fibrosis + lymphocytes / ground glass, honeycombing in lower lungs
  • if not diagnostic, must do:
    • multiple open lung biopsies from multiple lobes
      • ​transbronchial biopdsies not useful
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10
Q

non-specific interstitial pneumonia (NSIP_

  • restrictive vs obstructive
  • demographic
  • clinical presentation
A
  • interstitial = restrictive
  • demographics: 25-60, F > M
  • clinical presentation
    • similar to UIP (dyspnea, cough, +/- clubbing)
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11
Q

NSIP gross appearance

A

not telling

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12
Q

clinical differences between UIP (IPF) vs NSIP

A
  • Unspecific Interstitial Pneumonia / Idiopathic Pulmonary Fibrosis
    • no known etiology
    • demographics: 50-70 (older), M > F
    • prognosis: poor
    • NO response to corticosteroids
  • Non-Specific Interstitial Pneumonia
    • linked to collagen-vascular dz
    • demographics: 25-60 (younger), F > M
    • prognosis: better than UIP
    • DRAMATIC response toto corticostreroids
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13
Q

NSIP microscopic apperance

A
  • wall lesions that
    • are fibrotic
    • contain lymphocytic infiltates
    • uniform throughout age - NO temporal heterogeneity
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14
Q

compare/contrast morphology of UIP and NSIP

A

both: dz in lower lung, ground class on radiograph, interstitial fibrosis

UIP:

  • temporal heterogeneity: fibroblastics –> collagenous
  • can form cysts (honeycomb fibrosis)

NSIP:

  • < fibrosis than UIP, architecture more retained
  • no temporal heterogeneity
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15
Q

cryptogenic organizing pneumonia (COP)

  • demographics
  • clinical presentation
A
  • no demographic predilection
  • clinical
    • cough/dyspnea + flu like symptoms
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16
Q

cryptogenic organizing pneumonia (COP) - morphology

A

no gross

  • microscopic - can effect ANY PART of the lung!.
    • loose granulation tissue in terminal airways + alveoli
    • INTRALUMINAL fibroblast plugs - i.e. within - bronchioles/alveoli/alveolar ducts
      • NO interstitial fibrosis
        • so, NO honeycomb lung
      • no temporal changes
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17
Q

tx for COP (cryptogenic organization pneumonia)

A

corticosteroids

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18
Q

contrast COP to UID & NSIP

A
  • found in ANY part of the lung - unlike UID/NSIP (ower lobes only)
    • NO interstitial fibrosis - unlike UID/NSIP
    • INTRAluminal fibrosis (unlike UID/NSIP)
    • no temporal heterogeneity (unlike UID, like NSIP)
  • presents with flu-like symptoms (unlike UID & NSIP)
  • improves w/ corticosteroids (unlike UID, like NSIP)
19
Q

what is coal workers pneumoconiosis (CWP)?

describe its pathogenesis:

A
  • chronic lung disease caused by inhalation of coal particles + dust
  • pathogenesis:
    • inhaled irritatants induce macrophages to –> produce ROS & fibrogenic cytokines
    • development of disease depends ondepends on:
      • [] of particles
      • duration of exposure
      • efficacy of lung clearance mechanisms
        • cigarrette smoking lowers
      • size/shape of particles
      • particle solubility
  • variations of coal workers pneumoconiosis:
    • anthracocis
    • simle CWP
    • complicated CWP
20
Q

anthracosis

  • defintion
  • morphology
  • sequelae
A
  • type of CWP
  • characterized by accumulation of carbon pigment-filled macrophages in the connective tissue of the lymphatics/lymph nodes/lung him amongst otherwise intact parynchyma
  • sequelae: innocuous
21
Q

simple CWP

  • pathogenesis
  • morphology
  • sequelae
A
  • pathogenesis: like all CWP
  • mophology: characterized by
    • coal macules + coal nodules scattered throughout the lungs but especially in the ubber lobes (adj to resp. bronchioles)
      • coal macules: 1-2mm carbon laden macrophages
      • coal nodes: larger carbon filled macrophages + c_ollagen fibers_
  • seqelae –> poss emphysema
22
Q

complicated CWP

  • pathogenesis
  • morphology
  • sequelae
A
  • pathognesis: due to progressive massive fibrosis (PMF) that typically follows years of simpe CWP that destroys lung parynchma
  • mophology: intensely blackened scars (1-10 cm) that consist of haphazardly distributed dense collagen bunds + carbon pigment
    • +/- necrotic cefnter
23
Q

who is at higher risk of CWP?

A

pt who inhale a lot of silica

24
Q

silicosis

  • demographics
  • pathogenesis
  • clinical presentaiton
A
  • demographics:
    • AA> caucasion
    • workers exposed to silicon
  • pathogenesis:
    • crystalline silica inhaled –> phagocytzed by macrophages –> _activates inflammasom_e – IL-1 release –> fibrosis
      • amorphous crysals less severe, still = fiboriss
    • progression depends on exposure:
      * mos/yrs (acute)–> lipoprotein accumulation
      * decades (chronic) –> fibrosis
25
Q

silicosis - gross morphology

A
  • early: discrete nodules in hilar lymph nodes + upper lung zones
  • then, hard, colllagenous scars (formed by discrete nodules)
  • then, eggshell calcification
    • ​shees of calficiation around non-calcified zone
  • late: progressive massive fibrosis (PMF)
26
Q

silicosis - microscopic morphology

A

l_ight microscope_: coalescent collagenous nodules

polarized light microscopy: bright white needle like crystals (“befringmenet” silica)

27
Q

what is the most chronic occupational disease in the world?

A

silicosis

28
Q

silicosis sequelae

A
  • slow to kill but can cause serious diability
    • increases risk of contracting tuberuosis
    • doubles the risk for lung cancer
29
Q

what is asbestos and asbestos related diseases?

A
  • asbestos: a family of pro-inflammatory crystalline hydrated silicates (silica + iron + magnesium)
  • asbestos related diseases: come from inhalation of asbestos
    • fibrous plaques, interstitial fibrosis
    • pleural effusions
    • tumors:
      • lung carcinoma
      • mesothelioma
      • neopasma of larnx/ovary/colon
30
Q

what are the two main geometric forms of asbestos?

A
  1. serptentine (chrystotile)
  2. amphibole (amosite and crocidolite)
31
Q

serptentine asbestos

  • also called?
  • shape
  • pathological effects
  • prevalence?
A
  • chrysotile
  • flexible, curved
    • due to shape, it easily gets lodged lodged in upper respiratory passages then removed by mucociliary action
      • thus, less pathogenic than amphibole
  • more prevalent than amphibole
32
Q

amphibole asbestos

  • is also called?
  • shape
  • pathogenic effects
  • prevalence
A
  • amosite and crocidolite
  • straight, stiff
    • ​less likely to get “caught” in airstream, and may carried deeper in to the lungs to penetrate epithelial cells
      • thus, more pathogenic than serpentine
  • prevalence: less prevalent then serpentine
33
Q
A

serptentin (crysotile) asbestos - flexible, curved

less pathogenic asbestos

34
Q
A

amphibole asbestos (amosite and crocidolite)

more pathogenic asbestos

35
Q

asbestos morphology (gross, histologic)

A

gross - unimportant

  • histologic:
    • characterized by diffuse interstitial fibrosis that begins in the lower lobes subpleurally and spreads to middle, superior lobes, as well as:
      • asbestos & ferruginous bodies:
        • abestos bodies = brown, fusiform beaded rods
      • pleural plaque: well circumscribed plaqutes of DENSE CT that dont contain asbestos bodies
36
Q
A

abestos bodies

37
Q
A

dense CT comprising pleural plaques seen in asbestos

38
Q

sarcoidosis

  • demographics
  • clinical presentation
A
  • AA, 20-40, F > M
  • clinical presentation
    • triad:
      • erythema nodosum
      • bilateral hilar lymphadenopahty
      • polyarthralgia
39
Q

sarcoidosis morphology

A
  • characterized by small, non-necrotizing, epitheliod interstitial granulomas made of
    • histiocytes
    • mutinucleated giant cells, which can contain
      • asteroid bodies
      • schumann bodies
40
Q

hypersensitivity pneumonitis

  • pathognesis
  • morphology
  • treatment
A
  • pathogenesis: immune mediated reaction to various antigens
    • animal protein from bird feathers/feces
    • thermophillic actinomycetes in moldy hay
    • thermophilic bacteria in heated water reserroirs
  • morphology
    • small, ill defined non-caseating granulomas
  • tx
    • stop exposure to allergn
41
Q

desquamative interstitial pneumonia

  • pathogenesis
  • demographics
  • clinical presentation
  • morphology
A
  • pathogenesis: directly related to cigaratte smoking
  • demographics: middle aged smokers
  • clinical: cough, dyspnea
  • morphology
    • microscopic
      • intra-alveolar collections of macrophages
      • NO fibroblast foci
        • minimal fibrosis / wall thickening
          • (in contrast to other interitial dz - UIP, NSIP)
42
Q

pulmonary langerhans cell histiocytosis

  • pathogenesis
  • clinical presentation
  • morphology
A
  • pathogenesis - highly linked to cigarette smoking
  • clinical presentation - cough/dyspnea
  • morphology: collections of langerhans cells
    • ​langerhans cells:
      • have round/oval nuclei w/ frequent nuclear grooves
      • can contain Birbeck granules (zipper like structures)
      • are associated with eisonophils
      • form innto –> stellate nodules
        • ​(around bronchioles)
43
Q

pulmonary alveolar proteinosis

  • pathogenesis
  • clinical presentation
  • morphology
A
  • pathogenesis: defects in GM-CSF –> alveoli filled with surfactant proteinaceous material
  • clinical presentation: cough w/ abundant gelatinous sputum
  • morphology:
    • gross:
      • marked increase in lung size/weight
      • congested lung parenchyma
    • microscopic:
      • alveoli filled with granular, proteinatious material that stains PAS positive

Pathology (8 decks)

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