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CPR 2 Pulm Section > Respiratory Pathology Pt. 3 > Flashcards

Respiratory Pathology Pt. 3 Flashcards

1
Q

What do you see on the histology of Idiopathic Pulmonary Fibrosis?

A
  • normal areas
  • inflammation
  • fibroblast foci
  • peripheral honeycombing
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2
Q

What are contributing factors to Idiopathic Pulmonary Fibrosis?

A

Environmental: industrialization, smoking
Genetics: telomerase or surfactant mutations,
Age > 50yrs

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3
Q

What are the clinical findings of Idiopathic Pulmonary Fibrosis?

A
  • dyspnea (most prominent symptom)
  • crackles
  • restrictive PFT pattern
  • basilar infiltrates (progress to “honeycomb lung”)
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4
Q

Is Idiopathic Pulmonary Fibrosis a progressive disease?

A

Yes, most patients die within 4yrs of diagnosis

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5
Q

What are the potential therapies for Idiopathic Pulmonary Fibrosis?

A
  • -lung transplant
  • -tyrosine kinase inhibitors
  • -TGF-B inhibitors
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6
Q

True or False: Non-specific Interstitial PNA (NSIP) has a uniform pattern of inflammation and fibrosis.

A

TRUE

  • uniform infiltrates
  • no heterogeneity, no fibroblast foci, no granulomata
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7
Q

True or False: Usual Interstitial PNA has a better prognosis than Non-specific Interstitial PNA (NSIP).

A

False, NSIP has a better prognosis.

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8
Q

What will you see on histology of Cryptogenic Organizing PNA?

A
  • fibroblast foci (Masson Bodies … looks like cotton candy)
  • organizing plugs of connective tissue
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9
Q

What “sets the stage” for Cryptogenic Organizing PNA?

A

-Cryptogenic Organizing PNA occurs superimposed on a prior infection or inflammatory process (ex: URI)

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10
Q

What is the clinical presentation of Cryptogenic Organizing PNA?

A
  • -PNA-like consolidation

- -5th-6th decades of life

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11
Q

How is Cryptogenic Organizing PNA diagnosed?

A
  • a diagnosis of exclusion
  • -not an active infection
  • -not drug- or toxin-induced
  • -not related to a connective tissue disorder
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12
Q

Does Cryptogenic Organizing PNA have a good or bad prognosis?

A

Good, full recovery w/ oral steroids.

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13
Q

When autoimmune or connective tissue diseases manifest as Interstitial Lung Disease, what determines the prognosis?

A
  • the prognosis is linked to the Tx of the underlying condition
  • this accounts for 20% of Interstitial Lung Disease!
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14
Q

How does Sarcoidosis manifest clinically, as it relates to lung pathology?

A

–non-caseating granulomata in various organs (90% of cases of Sarcoidosis involve the lungs or hilar LN’s)

–dyspnea … or just an incidental abnormal radiograph!

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15
Q

What cell types stand out in granulomatous inflammation?

A
  • multinucleated giant cells

- histiocytes (epithelioid cells)

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16
Q

What are the stages of Sarcoidosis?

A

0) no abnormalities
1) hilar lymphadenopathy only
2) hilar lymphadenopathy and pulmonary infiltrates
3) pulmonary infiltrates only
4) fibrosis

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17
Q

How do patients move from one stage of Sarcoidosis to another?

A
  • patients can move around between stages
  • not entirely progressive
  • hard to get out of Stage 4 (kinda stuck there)
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18
Q

What population is more commonly afflicted with Sarcoidosis?

A

< 40 yrs

10x greater predominance in blacks

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19
Q

What enzyme level is abnormal in Sarcoidosis?

A

Angiotension Converting Enzyme (ACE) is elevated

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20
Q

What do you see on histology of Hypersensitivity Pneumonitis?

A
  • -no fibrosis
  • -multinucleated giant cells
  • -airway-centered granulomata
  • -lymphocytes!
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21
Q

What is the etiology of Hypersensitivity Pneumonitis?

A

immune rxn to inhaled antigen

  • Pigeon Breeder Lung: protein in bird feces
  • Farmer Lung: actinomycetic spores in hay
  • Hot Tub Lung: rxn to Mycobacterium Avium Complex
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22
Q

What is the most important component of the exam to make the diagnosis of Hypersensitivity Pneumonitis?

A

history

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23
Q

What population is most at-risk for Desquamative Interstitial PNA (DSIP)?

A

smokers

4th-5th decade

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24
Q

What does Desquamative Interstitial PNA look like on histology?

A

-alveolar spaces stuffed with macrophages

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25
Q

Does Desquamative Interstitial PNA have a good or bad prognosis?

A

Good, >95% survival at 5yrs

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26
Q

What is the treatment for Desquamative Interstitial PNA?

A
  • smoking cessation

- corticosteroids

27
Q

What other separated disease is on a spectrum with Desquamative Interstitial PNA (DSIP)?

A

Respiratory Bronchiolitis - Interstitial Lung Disease

–also caused by smoking

28
Q

Which is generally less symptomatic: Desquamative Interstitial PNA (DSIP) or Respiratory Bronchiolitis-Interstitial Lung Disease?

A

Respiratory Bronchiolitis - Interstitial Lung Disease

29
Q

When does Respiratory Bronchiolitis - Interstitial Lung Disease typically present?

A

3rd-4th decades

30
Q

What is a feature seen on histology slides of Respiratory Bronchiolitis - Interstitial Lung Disease?

A

peribronchiolar metaplasia (abnormally-located ciliated cells lining the alveoli)

31
Q

What demographic is most commonly affected by Langerhans Cell Histiocytosis?

A

-young smokers

32
Q

What do you see on histology of a patient with Langerhans Cell Histiocytosis?

A
  • stellate lung lesions
  • eosinophils
  • Langerhans cells (immature dendritic cells)
  • fibrosis
  • cysts
33
Q

What is the typical clinical presentation of Langerhans Cell Histiocytosis?

A

-young smoker presents w/ a pneumothorax (d/t rupture of peripheral cysts)

34
Q

What staining is positive in Langerhans Cell Histiocytosis?

A

CD1a

and S-100

35
Q

What is defective in Pulmonary Alveolar Proteinosis?

A

GM-CSF (granulocyte-macrophage colony stimulating factor)

36
Q

What type of Pulmonary Alveolar Proteinosis is the most common?

A

autoimmune

37
Q

What happens in Pulmonary Alveolar Proteinosis as a result of the GM-CSF deficiency?

A

-surfactant metabolism is impaired and surfactant proteins accumulate throughout the alveoli air spaces

38
Q

Why is it important to identify the cause of pneumoconiosis due to occupational exposure?

A
  • it’s often insidious

- there’s more than just one patient affected

39
Q

What factors make pneumoconiosis worse?

A
  • high, repetitive exposure (ex: workplace)
  • small particle size
  • impaired ciliary clearance (ex: smoking)
40
Q

What are the three main points on the spectrum of Coal Workers’ Pneumoconiosis?

A

1) anthracosis (carbon pigment coating lungs)
2) coal macules/nodules
3) progressive massive fibrosis

-the first two are not debilitating

41
Q

True or False: Coal Workers’ Pneumoconiosis increases the risk of cancer and TB

A

False

42
Q

What are risk factors of developing Silicosis?

A
  • mining/quarry work
  • concrete repair/demolition
  • inhaled silicon dioxide
43
Q

Is Silicosis an acute or insidious onset, and can it progress to massive pulmonary fibrosis?

A

Insidious

Yes

44
Q

True or False: Silicosis increases the risk of cancer

A

True, a two-fold risk

45
Q

What do you see on histology and radiology of a patient with Silicosis?

A

Histology: dense collagenous nodules

Radiology: eggshell calcification (calcified hilar LN’s)

46
Q

What is asbestosis?

A

-interstitial and pleural disease resulting from inhalation of asbestos fibers

47
Q

Who is at risk for Asbestosis?

A
  • insulation workers
  • Navy shipyard workers
  • paper mill workers
  • oil/chemical refinery workers
48
Q

What are conditions of the pleura and the lungs due to asbestosis?

A

Pleura: fibrous plaques, effusions, mesothelioma
Lung: interstitial fibrosis, carcinoma

49
Q

Which type of asbestos fibers (serpentine vs. amphibole) are more dangerous and why?

A

the amphibole ones, because they’re small, sharp, and straight … so they are able to be inhaled deeper into the lungs

50
Q

What are asbestos bodies?

A
  • asbestos fibers that macrophages tried to “eat”

- called ferruginous bodies d/t iron deposition

51
Q

What does pleural plaque look like?

A
  • “candlewax drippings”

- histology shows hyalinized collagen

52
Q

What does a Pulmonary Infarct look like on a CXR?

A

wedge-shaped lesion

53
Q

What is the progression of a Pulmonary Infarct?

A

begins as hemorrhagic, then fibrosis sets in

54
Q

What are Lines of Zahn?

A

-alternating fibrin and RBC’s that mean the clot was formed during active blood flow, and it’s not a result of postmortem coagulation

55
Q

In what situation would you see a marrow embolism?

A
  • trauma where bones are broken

- CPR when ribs are broken

56
Q

In what situation would you see a talc embolism?

A

-IV drug users (some oral meds contain substances that were never meant to be in blood vessels)

57
Q

In what situation would you see septic emboli?

A
  • IV drug users, thrombi come from heart valve vegetations (do an echocardiogram)
  • appear as abscesses on a CT scan
58
Q

What heart valve is linked to infective endocarditis that can send septic emboli to the lungs?

A

tricuspid valve

59
Q

What are symptoms of endocarditis?

A
  • Janeway Lesions (skin microemboli)
  • Roth Spots (retinal microemboli)
  • Splinter Hemorrhages (vascular damage in nail bed)
60
Q

What is the definition of Pulmonary HTN?

A

-pulmonary artery pressure > 25 mmHg

61
Q

What is a characteristic visualization of Pulmonary HTN on histology?

A

-plexiform lesions

–tortuous knots creating multiple tiny lumen instead of one big lumen in the vessel

62
Q

What is Goodpasture Syndrome?

A
  • an antibody response against the glomerular basement membrane (against a noncollagenous subunit of collagen IV)
  • a Type II Hypersensitivity
63
Q

What is the typical presentation of someone with Goodpasture Syndrome?

A

-young adult male (2nd and 3rd decades of life) w/ pulmonary hemorrhage

64
Q

How is Goodpasture Syndrome seen on immunofluorescence?

A

–an anti-Ig antibody tagged w/ dye is added to a sample and binds to any anti-basement membrane antibodies

  • a linear pattern of deposition around alveoli
  • blood cells inside alveolar spaces

CPR 2 Pulm Section (9 decks)

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