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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
Does Desquamative Interstitial PNA have a good or bad prognosis?
Good, >95% survival at 5yrs
26
What is the treatment for Desquamative Interstitial PNA?
- smoking cessation | - corticosteroids
27
What other separated disease is on a spectrum with Desquamative Interstitial PNA (DSIP)?
Respiratory Bronchiolitis - Interstitial Lung Disease --also caused by smoking
28
Which is generally less symptomatic: Desquamative Interstitial PNA (DSIP) or Respiratory Bronchiolitis-Interstitial Lung Disease?
Respiratory Bronchiolitis - Interstitial Lung Disease
29
When does Respiratory Bronchiolitis - Interstitial Lung Disease typically present?
3rd-4th decades
30
What is a feature seen on histology slides of Respiratory Bronchiolitis - Interstitial Lung Disease?
peribronchiolar metaplasia (abnormally-located ciliated cells lining the alveoli)
31
What demographic is most commonly affected by Langerhans Cell Histiocytosis?
-young smokers
32
What do you see on histology of a patient with Langerhans Cell Histiocytosis?
- stellate lung lesions - eosinophils - Langerhans cells (immature dendritic cells) - fibrosis - cysts
33
What is the typical clinical presentation of Langerhans Cell Histiocytosis?
-young smoker presents w/ a pneumothorax (d/t rupture of peripheral cysts)
34
What staining is positive in Langerhans Cell Histiocytosis?
CD1a | and S-100
35
What is defective in Pulmonary Alveolar Proteinosis?
GM-CSF (granulocyte-macrophage colony stimulating factor)
36
What type of Pulmonary Alveolar Proteinosis is the most common?
autoimmune
37
What happens in Pulmonary Alveolar Proteinosis as a result of the GM-CSF deficiency?
-surfactant metabolism is impaired and surfactant proteins accumulate throughout the alveoli air spaces
38
Why is it important to identify the cause of pneumoconiosis due to occupational exposure?
- it's often insidious | - there's more than just one patient affected
39
What factors make pneumoconiosis worse?
- high, repetitive exposure (ex: workplace) - small particle size - impaired ciliary clearance (ex: smoking)
40
What are the three main points on the spectrum of Coal Workers' Pneumoconiosis?
1) anthracosis (carbon pigment coating lungs) 2) coal macules/nodules 3) progressive massive fibrosis -the first two are not debilitating
41
True or False: Coal Workers' Pneumoconiosis increases the risk of cancer and TB
False
42
What are risk factors of developing Silicosis?
- mining/quarry work - concrete repair/demolition - inhaled silicon dioxide
43
Is Silicosis an acute or insidious onset, and can it progress to massive pulmonary fibrosis?
Insidious Yes
44
True or False: Silicosis increases the risk of cancer
True, a two-fold risk
45
What do you see on histology and radiology of a patient with Silicosis?
Histology: dense collagenous nodules Radiology: eggshell calcification (calcified hilar LN's)
46
What is asbestosis?
-interstitial and pleural disease resulting from inhalation of asbestos fibers
47
Who is at risk for Asbestosis?
- insulation workers - Navy shipyard workers - paper mill workers - oil/chemical refinery workers
48
What are conditions of the pleura and the lungs due to asbestosis?
Pleura: fibrous plaques, effusions, mesothelioma Lung: interstitial fibrosis, carcinoma
49
Which type of asbestos fibers (serpentine vs. amphibole) are more dangerous and why?
the amphibole ones, because they're small, sharp, and straight ... so they are able to be inhaled deeper into the lungs
50
What are asbestos bodies?
- asbestos fibers that macrophages tried to "eat" | - called ferruginous bodies d/t iron deposition
51
What does pleural plaque look like?
- "candlewax drippings" | - histology shows hyalinized collagen
52
What does a Pulmonary Infarct look like on a CXR?
wedge-shaped lesion
53
What is the progression of a Pulmonary Infarct?
begins as hemorrhagic, then fibrosis sets in
54
What are Lines of Zahn?
-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
In what situation would you see a marrow embolism?
- trauma where bones are broken | - CPR when ribs are broken
56
In what situation would you see a talc embolism?
-IV drug users (some oral meds contain substances that were never meant to be in blood vessels)
57
In what situation would you see septic emboli?
- IV drug users, thrombi come from heart valve vegetations (do an echocardiogram) - appear as abscesses on a CT scan
58
What heart valve is linked to infective endocarditis that can send septic emboli to the lungs?
tricuspid valve
59
What are symptoms of endocarditis?
- Janeway Lesions (skin microemboli) - Roth Spots (retinal microemboli) - Splinter Hemorrhages (vascular damage in nail bed)
60
What is the definition of Pulmonary HTN?
-pulmonary artery pressure > 25 mmHg
61
What is a characteristic visualization of Pulmonary HTN on histology?
-plexiform lesions --tortuous knots creating multiple tiny lumen instead of one big lumen in the vessel
62
What is Goodpasture Syndrome?
- an antibody response against the glomerular basement membrane (against a noncollagenous subunit of collagen IV) - a Type II Hypersensitivity
63
What is the typical presentation of someone with Goodpasture Syndrome?
-young adult male (2nd and 3rd decades of life) w/ pulmonary hemorrhage
64
How is Goodpasture Syndrome seen on immunofluorescence?
--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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