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► Med - Pathology > Pulmonary Pathology III > Flashcards

Pulmonary Pathology III Flashcards

1
Q

What is the general feature of restrictive lung disease?

A

Decreased total lung capacity

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2
Q

What are the two categories of restrictive lung disease?

A
  • Interstitial lung disease

- Chest wall disease

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3
Q

What are the characteristics of interstitial lung disease?

A 
Group of disorders which result in inflammation and fibrosis of alveolar walls (septa) with similar features:
-Dyspnea
-Tachypnea
-Decreased lung volume
and compliance
-Diffuse infiltration by small nodules
-"Honeycomb lung" at the end stage
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4
Q

What are the categories of interstitial lung disease?

A

-􏰀 Fibrosing
􏰀- Granulomatous
􏰀- Eosinophilic
􏰀- Smoking related

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5
Q

What is Idiopathic Pulmonary Fibrosis AKA?

A

Usual interstitial pneumonia

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6
Q

What is the pathogenesis of IPF?

A

Repeated cycles of epithelial activation/injury by some unidentified agent lead to abnormal epithelial repair and fibroblastic proliferation resulting in fibrosis with increased collagen from wound healing

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7
Q

What are the gross findings in IPF?

A

 Scarring of pleural surfaces - cobble stoned
 Fibrosis of lung parenchyma which appear as firm, rubbery, white areas
 Findings most prominent subpleural and along interlobular septa

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8
Q

What is the histology of IPF?

A

Honeycomb fibrosis represents the destruction of alveolar architecture and formation of cystic spaces lined by pneumocytes type II and bronchial epithelium

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9
Q

What will stain areas of fibrosis in IPF blue?

A

Trichrome Stain

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10
Q

What is the typical patient of IPF?

A

Male between 40-70 years

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11
Q

What is the prognosis of IPF and definitive treatment for it?

A

 Definitive treatment is lung transplant

 Mean survival is 3 years after diagnosis

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12
Q

Pneumoconiosis

A

The accumulation of dust in the lungs and the tissue reaction to its presence

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13
Q

Agent in Siderosis

A

Iron - welding

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14
Q

Agent in Anthracosis

A

Coal - mining

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15
Q

Agent in Silicosis

A

Silica - sand blasting

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16
Q

Agent in Asbestosis

A

Asbestos - ship building

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17
Q

What size particles are the most dangerous when inhaled and why?

A

1-5 􏰃m particles most dangerous - they can reach terminal small airways, air sacs, settle in linings

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18
Q

Pathogenesis of Pneumoconiosis

A

Macrophages endocytose and trap particles. Reactive particles trigger release of inflammatory mediators from macrophages which initiate fibroblast proliferation and activation. End result – collagen deposition and fibrosis.

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19
Q

What are the 3 states of Coal Worker’s Pneumoconiosis?

A

􏰀Anthracosis
Simple coal worker’s pneumoconiosis 􏰀
Progressive massive fibrosis

20
Q

What is the pathogenesis of anthracosis?

A

Inhaled carbon pigment is engulfed by alveolar/interstitial macrophages. Accumulates in connective tissue, pleural lymphatics, lymph nodes - no sequelae

21
Q

What is the patient population of anthracosis?

A

Seen in urban dwellers, tobacco smokers and coal miners

22
Q

What is seen with simple coal worker’s pneumoconiosis?

A

􏰀Coal macules, nodules with accumulations of dust-laden macrophages and fibrosis - not many other symptoms though

23
Q

Pathogenesis of Progressive Massive Fibrosis

A

Results from coalescence of coal nodules leading to haphazard fibrosis, large scars (2-10cm) with dense collagen and pigment leading to: progressive dyspnea, pulmonary dysfunction, pulmonary hypertension, cor pulmonale

24
Q

What is the finding in progressive massive fibrosis - anthracosis?

A

“Black Lung”

25
Q

What is Caplan Syndrome and what is it AKA?

A

AKA rheumatoid pneumoconiosis

Form of Coal Worker Pneumoconiosis associated with rheumatoid arthritis

26
Q

What is the most prevalent occupational disease?

A

Silicosis

27
Q

Silicosis

A

Inhalation of crystalline silica causes macrophage activation and the release of cytokines that are ultimately fibrogenic

28
Q

Simple Nodular Silicosis

A

 Upper zones of lungs with concentric hyalinized collagen with a whorled appearance
 Fibrotic lesions may be present in hilar lymph nodes

29
Q

Progressive Massive Fibrosis - Silicosis

A

Coalescence of nodules that can lead to: progressive dyspnea, pulmonary dysfunction, pulmonary hypertension, cor pulmonale

30
Q

What disease is silicosis associated with?

A

Silicosis is associated with increased susceptibility to tuberculosis. It is postulated that silicosis depresses cell mediated immunity and silica may inhibit ability of pulmonary macrophages to kill phagocytosed myocbacteria

31
Q

What are the effects of asbestos?

A
  • Acts as tumor initiator and promoter (mediated by reactive free radicals)
  • Adsorbs toxic chemicals (tobacco smoke)
  • Fibrinogenic effect
32
Q

What are the plethora of asbestos effects?

A 
􏰀 Interstitial fibrosis (asbestosis)
􏰀 Localized fibrous plaques - pleural plaques
􏰁 Diffuse fibrosis of pleura
􏰀 Pleural effusions
􏰀 Bronchogenic carcinoma
􏰀 Malignant mesothelioma
􏰀 Largyngeal carcinoma
33
Q

What is the interaction of asbestos with smoking?

A

Synergistically increased risk of bronchogenic cancer with smoking - 55x more likely chance of cancer

34
Q

What is the most common manifestation of asbestos exposure?

A

Localized fibrous pleural plaques - well circumscribed plaques of dense collagen usually on parietal pleura and
domes of diaphragm.

35
Q

What cancer is highly related to asbestos but NOT smoking?

A

Mesothelioma

36
Q

What is the pathogenesis of malignant mesothelioma?

A

 Asbestos fibers settle near mesothelium

 Reactive oxygen free radicals induce DNA damage

37
Q

What stain will mesothelioma be positive for?

A

Positive staining for calretinin

38
Q

Sarcoidosis

A

 Multisystem disease of unknown etiology

 Characterized by non-caseating granulomas

39
Q

How is sarcoidosis diagnosed?

A

Diagnosis of exclusion because other diseases may present as non-caseating granulomas: TB, fungal infection, berylliosis

40
Q

Pathogenesis of Sarcoidosis

A

Unknown, however evidence suggests disordered immune regulation in genetically predisposed individuals exposed to certain environmental agents - hypothesized to be CD4 T-cell driven

41
Q

What are some findings with sarcoidosis?

A
  • Uveitis
  • Bell’s Palsy - CN VII
  • Pulmonary interstitial fibrosis
  • Restrictive cardiomyopathy
  • Hypercalcemia
  • Asteroid and Schaumann bodies
42
Q

What are Asteroid and Schaumann bodies?

A
  • Schauman bodies – laminated concretions composed of calcium and proteins
  • Asteroid bodies – stellate inclusions
43
Q

What is the typical patient of sarcoidosis?

A

Young adult - under the age of 40

African Americans, Danish and Swedish

44
Q

Why is there hypercalcemia in sarcoidosis?

A

Granulomas autonomously convert 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D which increases calcium absorption

45
Q

A 66-year-old man has had increasing dyspnea for the past year. He is a smoker. He is retired from the construction business. There are some rales auscultated in both lungs on physical examination. A chest radiograph reveals bilateral diaphragmatic pleural plaques with focal calcification as well as diffuse interstitial lung disease. A sputum cytology shows no atypical cells. Pulmonary function studies reveal a low FVC and a normal
FEV1/FVC ratio. These findings are most likely to suggest prior exposure to which of the following environmental agents?

A Cotton fibers
B Silica dust
C Fumes with iron particles 
D Asbestos crystals
E Beryllium
A

D Asbestos crystals

46
Q

Hypersensitivity Pneumonitis

A

Abnormal hypersensitivity response from spores of thermophilic bacteria, fungi, animal proteins, bacterial products - Immunologically mediated response to an extrinsic antigen that involves both immune complex and delayed type hypersensitivity reactions (Type III and IV)

► Med - Pathology (203 decks)

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