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Robbins systemic pathology > Chapter 15: Lung > Flashcards

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
Q

Factors determining the development of a pneumoconiosis

A
  • 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
Q

Features of silicosis

A
  • 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
Q

Oncogenic effects of asbestos

A
  • ROS generation

- toxic chemicals attached to the fibres

28
Q

Features of asbestos

A

-fibrosis that begins around respiratory bronchioles and becomes diffuse and leads to honeycombing; identical to UIP except has asbestos bodies

29
Q

Immunologic pathogenesis in sarcoidosis?

A
  • 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
Q

Histologic features of hypersensitivity pneumonitis

A
  • bronchiolocentric interstitial pneumonitis with lymphocytes, plasma cells and macrophages
  • non caseating granulomas
  • interstitial fibrosis
  • intraalveolar infiltrate in 50%
31
Q

Categories of pulmonary eosinophilia

A
  • 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
Q

Histologic features of DIP

A
  • intraalveolar macrophages with iron pigment

- sparse septal inflammation (lymphocytes, plasma cells, sometimes eos)

33
Q

What are causes of secondary PAP?

A
  • hematologic and other malignancies
  • immunodeficiency
  • silicosis and other inhalational disorders
34
Q

Treatments for acquired PAP

A
  • whole lung lavage

- GM-CSF administration

35
Q

Main consequences of pulmonary embolism

A
  • respiratory compromise: nonperfused, ventilated segment

- hemodynamic compromise: increased resistance to pulmonary blood flow

36
Q

Causes of death in pulmonary embolism

A
  • 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
Q

Classification of pulmonary hypertension

A

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
Q

Effects of BMPR2 in vascular smooth muscle?

A

-inhibits proliferation and favours apoptosis

39
Q

Mechanism of development of secondary pulmonary hypertension?

A

-Endothelial dysfunction resulting from initial damage, e.g. shear stress, fibrin

40
Q

Histologic features of pulmonary hypertension

A
  • 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
Q

Complications of pneumonia

A
  • empyema
  • abscess
  • septic embolism to other organs causing metastatic abscesses
42
Q

Histologic features of atypical pneumonia

A
  • interstitial mononuclear inflammation and edema (rarely with neutrophilis)
  • may have superimposed bacterial infection and intraalveolar exudates
43
Q

Describe the influenza virus

A
  • eight helices of ssRNA

- lipid bilayer with viral hemaglutinin and neuraminidase which determine subtype

44
Q

Cause of influenza epidemics

A

-antigenic drift: mutations in H and N that allow avoidance of host T cell response

45
Q

Causes of lung abscesses

A
  • septic embolism
  • pneumonia
  • malignancy
  • aspiration pneumonia
  • direct infection from trauma, adjacent organs, etc
46
Q

Histologic features of blastomycosis

A
  • suppurative granulomas

- 5-15 micron yeasts that exhibit broad based budding

47
Q

What is the San Joachin Valley fever complex

A
  • pulmonary coccidiodomycosis
  • erythema multiforme
  • erythema nodosum
  • fever
48
Q

Histologic features of coccidio

A
  • resembles histoplasmosis granulomas
  • intracellular 20-60 micron yeasts filled with endospores
  • if endospores are released: pyogenic inflammation
49
Q

Morphologic features of chronic lung transplant rejection

A
  • 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
Q

Common cytogenetic abnormalities in mesothelioma

A

del 1p, 3p, 6q, 9p, 22q
p16 mutations
not usually p53 mutations
SV40 sequences in > half

51
Q

Histochemical and immunohistochemical features of mesothelioma

A
  • contain acid mucopolysaccharide
  • CEA negative
  • CK positive, particularly perinuclear
  • calretinin, WT1, CK5/6, D2-40 positive
  • long microvilli by EM

Robbins systemic pathology (17 decks)

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