Chapter 15: Lung Flashcards

1
Q

Types of foregut cysts

A
  • bronchogenic
  • esophageal
  • enteric
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2
Q

Types of atelectasis

A
  • resorption (obstruction): complete obstruction with resorption of oxygen and mediastinal shift toward atelectasis
  • compression: pleural filling, etc; with mediastinal shift away from atelectasis
  • contraction: fibrotic chnages prevent full expansion
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3
Q

Causes of pulmonary edema

A
  • hemodynamic (increased hydrostatic pressure, decreased oncotic pressure)
  • microvascular/alveolar injury (inhalations, shock, burns, etc)
  • other (high altitude, neurogenic)
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4
Q

Pathologic features of organizing phase of ARDS

A
  • type II pneumocyte hyperplasia

- granulation tissue response in alveolar walls, sometimes resolving with fibrosis

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5
Q

Pathogenesis of ARDS

A
  • imbalance of pro and anti-inflammatory mediators
  • interleukins and other cytokines cause neutrophil activation and sequestration in the lung
  • neutrophils release proteases that damage the lung and loss of surfactant preventing the alveoli from expanding
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6
Q

What is the most prevalent alveolar lining cell?

A

-type I pneumocyte (95% of cells)

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7
Q

Types of chronic lung disease

A
  • obstructive

- restrictive: divided into chronic fibrosing diseases and chest wall disorders

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8
Q

What part of the lung is affected in centriacinar emphysema

A
  • the respiratory bronchioles, with alveolar sparing

- more pronounced in upper lobes

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9
Q

What is the pattern of injury in panacinar emphysema?

A
  • entire acinus from respiratory bronchioles to distal alveoli is distended
  • more common in lower lung zones and is associated with alpha 1 antitrypsin deficiency
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10
Q

What is the best hypothesis for the pathogenesis of damage in COPD?

A

Protease-antiprotease hypothesis

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11
Q

How does lung damage occur in smoking?

A
  • neutrophils and macrophages accumulate in the lungs possibly due to chemoattractant effects or production of ROS
  • these cells release granules including elastases, causing lung damage
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12
Q

Microscopic features of COPD

A
  • early changes: goblet cell metaplasia, inflammation and smooth muscle hyperplasia
  • established: large blebs with large pores of Kohn such that septa appear to be floating; mild centriacinar fibrosis
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13
Q

Causes of death in emphysema

A

1) Respiratory acidosis and coma
2) Right heart failure
3) Massive lung collapse due to ptx

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14
Q

Define chronic bronchitis

A

-persistent cough with sputum production lasting at least 3 months in at least 2 consecutive years

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15
Q

Main features of asthma

A
  • increased airway responsiveness resulting in bronchoconstriction
  • mucus hypersecretion
  • inflammation
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16
Q

Potential mediators in asthma

A
  • leukotrienes: bronchoconstriction, increased vascular permeability
  • histamine: bronchoconstriction
  • prostaglandins
  • platelet activating factor
  • cytokines: IL1, IL6, TNF
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17
Q

Findings in status asthmaticus

A
  • hyperinflation
  • mucus plugs grossly visible
  • eosinophils and Charcot-Leyden crystals
  • airway remodelling: thickened bronchial wall with sub-basement membrane fibrosis, muscular hypertrophy and increased goblet cells
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18
Q

Define bronchiectasis

A
  • permanent dilatation of bronchi and bronchioles due to destruction of muscle and elastic tissue by chronic/recurrent infection
  • probably requires both obstruction and infection
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19
Q

Causes of bronchiectasis

A
  • inherited (CF, Kartagener syndrome)
  • infectious (viral, bacterial (tb) and fungal)
  • obstruction (by tumor, etc)
  • chronic conditions including lupus, IBD, RA and post-transplant and chronic GVHD
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20
Q

Possible complications of bronchiectasis

A
  • cor pulmonale
  • amyloidosis
  • brain abscess
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21
Q

Major categories of chronic interstitial lung disease

A
  • fibrosing
  • granulomatous
  • eosinophilic
  • smoking related
  • other (e.g. PAP)
22
Q

Features of NSIP

A
  • better prognosis than UIP; best prognosis is in cellular pattern
  • cellular and fibrosing forms
  • temporal and spatial homogeneity
  • no fibroblastic foci or honeycombing
23
Q

Features of COP

A
  • subpleural accentuation
  • intraalveolar plugs of organizing connective tissue (Masson bodies)
  • no interstitial fibrosis or architectural distorsion
24
Q

Types of lung involvement in RA

A
  • chronic pleuritis
  • interstitial fibrosing
  • pulmonary rheumatoid nodules
  • pulmonary hypertension
25
Factors determining the development of a pneumoconiosis
- amount inhaled - size of the particles (worst size: 1-5 microns b/c these reach terminal airways) - particle solubility - additional effects of other irritants (e.g. smoking)
26
Features of silicosis
- early, nodules in upper lobes - later, collagenized scars, sometimes with central necrosis - concentric layers of hyalinized collagen surrounded by a dense capsule of more condensed collagen with polarizable birefrigent particles
27
Oncogenic effects of asbestos
- ROS generation | - toxic chemicals attached to the fibres
28
Features of asbestos
-fibrosis that begins around respiratory bronchioles and becomes diffuse and leads to honeycombing; identical to UIP except has asbestos bodies
29
Immunologic pathogenesis in sarcoidosis?
- T cell mediated response to an unidentified antigen driving by CD4 cells - CD4:CD8 ratios> 5:1 - increased levels of Th1 cytokines IL2 and TNFgamma -> T cell expansion and macrophage activation
30
Histologic features of hypersensitivity pneumonitis
- bronchiolocentric interstitial pneumonitis with lymphocytes, plasma cells and macrophages - non caseating granulomas - interstitial fibrosis - intraalveolar infiltrate in 50%
31
Categories of pulmonary eosinophilia
- acute eosinophilia with respiratory failure - simple eosinophilia (Loeffler syndrome) - tropical eosinophilia (filiaria) - secondary eosinophilia (fungi, parasites, hypersensitivity, allergy, aspergillosis, vasculitis) - idiopathic chronic eosinophilic pneumonia
32
Histologic features of DIP
- intraalveolar macrophages with iron pigment | - sparse septal inflammation (lymphocytes, plasma cells, sometimes eos)
33
What are causes of secondary PAP?
- hematologic and other malignancies - immunodeficiency - silicosis and other inhalational disorders
34
Treatments for acquired PAP
- whole lung lavage | - GM-CSF administration
35
Main consequences of pulmonary embolism
- respiratory compromise: nonperfused, ventilated segment | - hemodynamic compromise: increased resistance to pulmonary blood flow
36
Causes of death in pulmonary embolism
- sudden death if a large saddle embolism due to obstructed blood flow - acute cor pulmonale -multiple small emboli over time lead to pulmonary htn
37
Classification of pulmonary hypertension
1) Pulmonary arterial hypertension 2) Associated with left heart disease 3) Associated with chronic interstitial lung disease 4) Associated with recurrent emboli 5) Other
38
Effects of BMPR2 in vascular smooth muscle?
-inhibits proliferation and favours apoptosis
39
Mechanism of development of secondary pulmonary hypertension?
-Endothelial dysfunction resulting from initial damage, e.g. shear stress, fibrin
40
Histologic features of pulmonary hypertension
- medial hypertrophy of muscular and elastic arteries - pulmonary artery atheromas - right ventricular hypertrophy - intimal fibrosis - plexiform lesion (most common in familial and idiopathic forms): tuft of capillary formations that spans the lumen of thin walled small arteries - dilated vessels and arteritis may also be present
41
Complications of pneumonia
- empyema - abscess - septic embolism to other organs causing metastatic abscesses
42
Histologic features of atypical pneumonia
- interstitial mononuclear inflammation and edema (rarely with neutrophilis) - may have superimposed bacterial infection and intraalveolar exudates
43
Describe the influenza virus
- eight helices of ssRNA | - lipid bilayer with viral hemaglutinin and neuraminidase which determine subtype
44
Cause of influenza epidemics
-antigenic drift: mutations in H and N that allow avoidance of host T cell response
45
Causes of lung abscesses
- septic embolism - pneumonia - malignancy - aspiration pneumonia - direct infection from trauma, adjacent organs, etc
46
Histologic features of blastomycosis
- suppurative granulomas | - 5-15 micron yeasts that exhibit broad based budding
47
What is the San Joachin Valley fever complex
- pulmonary coccidiodomycosis - erythema multiforme - erythema nodosum - fever
48
Histologic features of coccidio
- resembles histoplasmosis granulomas - intracellular 20-60 micron yeasts filled with endospores - if endospores are released: pyogenic inflammation
49
Morphologic features of chronic lung transplant rejection
- bronchiolitis obliterans, sometimes completely occluding the airways - active inflammation may or may not be present - findings often patchy therefore may not be sampled on biopsy
50
Common cytogenetic abnormalities in mesothelioma
del 1p, 3p, 6q, 9p, 22q p16 mutations not usually p53 mutations SV40 sequences in > half
51
Histochemical and immunohistochemical features of mesothelioma
- contain acid mucopolysaccharide - CEA negative - CK positive, particularly perinuclear - calretinin, WT1, CK5/6, D2-40 positive - long microvilli by EM