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MHD VI: Pulm > 11.20: Pulm III > Flashcards

11.20: Pulm III Flashcards

1
Q

What is decreased TLC consistent with?

A

Restrictive lung disease

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2
Q

2 categories of restrictive lung disease?

A
  1. Chest wall disorder

2. Chronic interstitial and infiltrative disease

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3
Q

Characteristics of interstitial lung diseases?

A
  • Dyspnea
  • End inspiratory crackles
  • Hypoxia
  • Nodules and irregular lines on cxr
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4
Q

2 Main categories and 3 main types of chronic interstitial lung disease?

A
  1. Fibrosing
    a. Usual interstitial pneumonia: 15%
    b. Pneumoconiosis: 25%
  2. Granulomatous
    a. Sarcoidosis: 20%
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5
Q

What is interstitial lung disease?

A
  • Inflammatory and fibrotic disease of alveolar walls and septa leading to reduced pulmonary compliance
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6
Q

What will interstitial lung disease lead to?

A
  • Pulmonary htn.
  • Cor pulmonale
    “Honey comb lung” is end stage pathology
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7
Q

What is honeycomb lung characteristic of?

A

End stage restrictive interstitial lung disease

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8
Q

Difference between interstitial lung disease and emphysema?

A

There is fibrosis seen in interstitial disease but not in emphysema

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9
Q

What is idiopathic pulmonary fibrosis?

A

“IPF”

- Clinical term for “usual interstitial pneumonia”

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10
Q

Pathogenesis of IPF?

A
  • Repeated epithelial injury leading to TGFbeta
  • TGFB leads to fibroblasts
  • Fibroblasts deposit collagen and ECM
  • Pulmonary fibrosis ensues
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11
Q

Another name for idiopathic pulmonary fibrosis?

A

“IPF”

- Usual interstitial Pneumonia “UIP”

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12
Q

Another name for Usual interstitial Pneumonia “UIP”?

A

“IPF”

- Idiopathic pulmonary fibrosis

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13
Q

Characteristics of fibrosis in IPF?

A
  • Non uniform pattern
  • Varies in intensity and age
  • Early “exuberant” fibroblastic proliferation
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14
Q

What is patchy interstitial fibrosis indicative of?

A

IPF

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15
Q

What is the impact of fibrosis in IFP?

A
  • Patchy fibrosis destroys interstitial architecture
  • Contraction of scarring pulls to destroy alveolar spaces
  • Cystic spaces are created with Type II pneumocytes
    “Honeycomb fibrosis”
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16
Q

What is cobblestone lung indicative of?

A
  • IPF
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17
Q

Characteristics of IPF?

A
  • Variable fibrosis more common in lower lobes
  • “Cobblestone lung”
  • Fibrosis more common in subpleural layers than in paraseptal
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18
Q

Clinical appearance of IPF?

A
  • 40 - 70
  • M > W
  • Dyspnea on exertion
  • Dry cough
  • Velcro crackles
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19
Q

Prognosis of IPF/UIP? Treatment?

A
  • Rapid deterioration with mean survival
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20
Q

What is pneumoconioses?

A

Accumulation of particulate, chemical fume, or vapor in lung and the reaction to its presence

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21
Q

3 main types of pneumoconioses?

A
  1. Anthracosis: coal dust
  2. Silicosis: silica from sand blasting
  3. Asbestosis: ships, roofing, plumbing
22
Q

What causes largest risk for development of pneumoconioses?

A
  • Small 1 to 5 micrometer particles have greats danger of settle in linings of small airways and sacs and fester
  • Too small to be caught by cilia and mucus
  • Too big to be engulfed by macs
23
Q

How is most inhaled particulate removed?

A
  • Trapped in mucus and removed by ciliary elevator if > 1 microns
24
Q

Pathogenesis of pneumoconiosis?

A
  • Macs endocytose particles releasing inflammatory mediators

- Fibrogenesis and collagen deposition ensues

25
Q

Presentation of anthracosis?

A
  • Seen in coal, urban, and smokers
  • Inhaled carbon pigment engulfed by interstitial macs
  • Accumulates in tissues them moves to lymph
  • Will see some black on autopsy but not other problems
    • NO SYMPTOMS NOTES
26
Q

Pathogenesis of simple coal workers pneumoconiosis?

A
  • Same carbon irritant forms macules / nodules

- Patchy fibrosis noted but not extensive

27
Q

Pathogenesis of progressive massive fibrosis?

A

“Black lung”

  • Coalescence of coal nodules into large scars
  • Fibrotic, bulky, heavily pigmented black tissue masses
28
Q

Clinical course of coal workers pneumoconiosis?

A

Bening with progression to pulmonary dysfunction, pulm htn, or cor pulmonale

29
Q

What is Caplan syndrome?

A

“Rheumatoid pneumoconiosis”

  • Ptn. w/ rheumatoid arthritis exposed to coal
  • Get fibrotic lesions with cavitating nodules on radiology
  • Hints that RA alters bodies response to coal
30
Q

Who is likely to get silicosis?

A
  • Most prevalent occupational disease in world
  • Workers in foundries, sandblasting, mines
  • Caused by inhalation of crystalline silica engulfed by mac releasing fibrotic mediators
31
Q

Appearance of silicosis?

A
  • Nodules of “Whorled” hyalinized collagen
  • Nodules can coalesce leading to massive fibrosis extending to hilar lymph nodes and pleura
    “Eggshell calcification” of lymph nodes
32
Q

When is egg shell calcification of lymph nodes seen?

A
  • Silicosis
33
Q

What does silicosis lead to increased susceptibility to?

A
  • Tuberculosis

- Silicosis suppresses cell mediated immunity and impairs macrophage phagocytosis

34
Q

What can silicosis lead to?

A
  1. Dyspnea
  2. Pulm htn
  3. Cor pulmonale
35
Q

Disease often associated with silicosis?

A

TB

36
Q

Disease often associated with coal workers?

A

Rheumatoid arthritis

37
Q

Which form of Pneumoconioses is carcinogenic?

A

Asbestosis

38
Q

Why is asbestos often used?

A
  1. Cheap
  2. Durable
  3. Head resistant for insulation
39
Q

Which type of asbestos is most dangerous?

A
  • Rigid, rod like molecule that can poke hole through macrophage
40
Q

What does asbestos lead to?

A
  1. Interstitial Fibrosis
  2. Localized fibrotic pleural plaques
  3. Malignant mesothelioma
  4. Bronchogenic carcinoma
  5. Laryngeal Carcinoma
  6. Pleural effusion
41
Q

What cause malignant mesothelioma?

A

Asbestos

42
Q

Hallmark of asbestos?

A
  • Fibrinous “Asbestos bodies”
  • Looks like beaded structure with nobby head
  • Fe will sit on and coat the asbestos body
43
Q

How much does asbestos increase cancer risk?

A
  • 55x if a smoker
  • 5 x if not a smoker
  • 1000x increased risk in mesothelioma
  • **Family members are at risk through indirect exposure
  • **Can occur 20 - 40 years after exposure
44
Q

Characteristics of Sarcoidosis?

A
  • Multisystem disease of unknown etiology
  • Characterized by non caseating granulomas
  • Diagnosis of exclusion in which TB or fungus must be ruled out when granulomas are seen
45
Q

What is a granuloma?

A
  • Lymphocytes, macrophages that have fused to form giant cells
46
Q

Clincial presentation of sarcoidosis?

A
  • 90% with bilateral hilar lymphadenopathy or parenchymal abnormality on chest xray
47
Q

What leads to sarcoidosis?

A
  • Genetic abnormality with environmental trigger
48
Q

When are asteroid and schaumann bodies seen?

A

Sarcoidosis

49
Q

Manifestations of sarcoidosis?

A
  • SOB with dry cough
  • Fever fatigue sweats
  • Eye in inflammation: Uveitis
  • Erythema nodosum
  • Restrictive cardiomyopathy
50
Q

What is erythema nodosum?

A

Inflammatory lesions of subcutaneous fat see in skin in sarcoidosis

51
Q

Why is vitamin D hypercalcemia see in sarcoidosis?

A
  • Granulomas produce enzyme increase conversion of Vitamin D to active form to increase Ca absorption

MHD VI: Pulm (20 decks)

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