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Pathology > Respiratory Pathology 1 > Flashcards

Respiratory Pathology 1 Flashcards

1
Q

What is bronchiectasis?

A

Chronic disorder characterised by permanent dilation of the bronchi, accompanied by inflammatory changes in their walls and in adjacent lung parenchyma.

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2
Q

Pathogenesis of bronchiectasis?

A

Recurrent inflammation of the bronchial walls combined with fibrosis in the surrounding parenchyma –> traction on the weakened walls causes irreversible dilatation.

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3
Q

Categories of bronchiectasis causes?

A

May be

  • post inflammatory or
  • post obstructive.
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4
Q

What are the post inflammatory causes of bronchiectasis?

A
  • Pneumonia, measles, whooping cough
  • Congenital hypogammaglobulinemia CF, immotile cilia syndrome
  • ABPA
  • Reactions to inhaled toxic fumes
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5
Q

What are the post obstructive causes of bronchiectasis?

A
  • Neoplasm
  • Foreign body
  • Inspissated mucous: asthma
  • External compression: hilar lymph nodes, aortic aneurysm
  • Rare: bronchial webs, atresia
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6
Q

Pathogenesis of obstructive bronchiectasis?

A

Obstructive -> impairment of normal clearing mechanisms -> pooling of secretions distal to obstruction -> inflammation of the airway.

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7
Q

Pathogenesis of bronchiectasis in CF?

A

Accumulation of thick viscid secretion -> obstruct airways -> susceptibility to bacterial infections -> widespread damage to airway walls (destruction of elastin, SM) -> fibrosis -> dilation of bronchi.

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8
Q

What is allergic bronchopulmonary aspergillosis?

A

Hyeprsensitivity to fungus Aspergillosis fumigatus.

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9
Q

Characteristics of ABPA?

A
  • High serum IgE
  • Serum Abs to Aspergillus
  • Intense airway inflammation (mostly eosinophils)
  • Formation of mucous plugs
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10
Q

Morphology of bronchiectasis?

A
  • Usually bilateral lower lobes
  • Involves most vertical airways
  • most severe in distal bronchi and bronchioles
  • airways dilated (up to 4x N
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11
Q

How do bronchi appear on cut surface of lung in bronchiectasis?

A

Cysts filled with mucopurulent secretions

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12
Q

Histology of bronchiectasis?

A

Varies with stage/chronicity
Active:
-intense inflammatory exudate in bronchial walls;
-desquamation of lining epithelium
-extensive necrotising ulceration
Chronic complication: fibrosis bronchi-al/-olar walls with gradual lumen obliteration

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13
Q

What may isolated upper lobe bronchiectasis result from?

A

May be secondary to destructive tuberculous lesions

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14
Q

Bronchiectasis lobar involvement in CF?

A

Upper and middle lobes involved

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15
Q

Distribution of bronchiectasis in a1-antitrypsin deficiency?

A

Basilar distribution

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16
Q

What is a lung abscess?

A

Local suppurative process within the lung; characterised by necrosis of lung tissue.

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17
Q

Common causes of lung abscess?

A
  • Aspiration
  • Antecedent primary lung infection
  • Septic embolism
  • Neoplasia
  • Direct penetration by adjacent organ / trauma
  • Haematogenous seeding
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18
Q

Common pathogens lung abscess?

A
  • G+ve and G-ve strep
  • S. aureus
  • Many G-ves!
  • Anaerobic bacteria common
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19
Q

Most common side for lung abscess?

A

Most abscesses in R lung as R main bronchus more vertical

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20
Q

When is aspiration most likely?

A

-Acute alcoholism
-Coma
-Anesthesia
-Sinusitis
-Gingivodenta sepsis
When cough reflexes suppressed

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21
Q

Sites of septic emboli causing lung abscess?

A
  • Thrombophlebitis (any part of systemic venous circulation)

- IE on R heart

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22
Q

Morphology of abscesses in the lung secondary to pneumonia / bronchiectasis?

A

Usually multiple, basal and diffusely scattered

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23
Q

what is the cardinal histologic change in abscesses?

A

Suppurative destruction of the lung parenchyma within the central area of cavitation. Chronic: fibroblast proliferation may develop a fibrous wall.

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24
Q

Clinical features of lung abscess?

A
  • Cough
  • Fever
  • Copious foul smelling purulent sputum
  • Fever
  • CP
  • May develop clubbing
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25
Q

What is tuberculosis?

A

infection by Mycobacterium tuberculosis

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26
Q

What are mycobacteria?

A

Aerobic, non-motile bacilli

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27
Q

What is primary TB? What characterises it?

A

Occurs following first exposure to the organisms. Usually self limited and characterised by area of necrotising granulomatous inflammation in the lung and draining LNs (Ghon’s complex)

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28
Q

Common location of Ghon focus?

A

Lower portion of R upper lobe or upper portion of R lower lobe.

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29
Q

Healing of Ghon focus?

A

Fibrosis and calcification; BUT may contain viable organisms for many years.

30
Q

What are the clincopathologic consequences of progressive TB?

A
  • Cavitary fibrocaseous TB
  • miliary TB
  • tuberculous bronchopneumonia
31
Q

What is cavitary fibrocaseous tuberculosis?

A
  • Erosion into bronchiole -> drainage of caseous focus transforms into cavity
  • infective material disseminates through airways to other lung sites
32
Q

Mechanism of miliary TB?

A

Haematogenous dissemination:

  • TB confined to lungs
  • involving other organs
33
Q

Favoured sites of miliary TB distal seeding?

A
  • Bone marrow
  • Liver
  • Spleen
  • Kidney
  • LNs
  • Pericardium
34
Q

What is tuberculous bronchopneumonia?

A

TB may spread rapidly throughout large areas of lung parenchyma producing a diffuse bronchopneumonia or lobar exudative consolidation.

35
Q

what is a calcified Ghon complex?

A

Ranke complex

36
Q

What is secondary TB?

A
  • Reactivation of dormant focus of primary infection

- Reinfection

37
Q

Location of secondary TB?

A

Within 1-2cm of apical pleura of upper lobe of 1 or both lungs (higher oxygen tension favours growth)

38
Q

Appearance of secondary TB foci?

A

Sharply circumscribed, firm, grey-white-yellow areas with variable central caseation and peripheral fibrosis.

39
Q

Histology of TB?

A
  • Granulomatous inflammation with epithelioid histiocytes, lymphocytes and Langhan’s giant cells.
  • Caseation often present
40
Q

What are Langhan’s giant cells?

A

Contain nuclei arranged in a horse shoe shaped pattern at cell periphery

41
Q

What are the causes of granulomatous inflammation in lung?

A

INFECTIONS: mycobacteria, fungi, parasites
NON-INFECTIOUS: sarcoidosis, hypersensitivity pneumonitis, Wegener granulomatosis, Churg Strauss syndrome, rheumatoid nodules

42
Q

What are diffuse parenchymal lung diseases?

A

=Interstitial lung disease.

  • Interstitial inflammation, granulomatous inflammation or fibrosis.
  • All compartments can be affected
43
Q

Inflammation of sarcoidosis?

A

Non-necrotising granulomatous inflammation, distributed along lymphatic pathways (bronchovasular bundles, interlobular septa and the pleura).

44
Q

What is diffuse alveolar damage?

A

=ARDS.

Patients develop respiratory failure and pulmonary oedema.

45
Q

Radiographic appearance of diffuse alveolar damage?

A

Widespread consolidation

46
Q

Phases of diffuse alveolar damage?

A

3 phases:

i) Exudative (acute)
ii) Organising
iii) Fibrotic (chronic)

47
Q

Macroscopic appearance of diffuse alveolar damage?

A

Acute: 3-4x heavier than N; congested, oedematous w/ dark red cut surface
Chronic: rubbery firm with yellow grey appearance; fine cysts may be present

48
Q

Histologic appearance of diffuse alveolar damage?

A

ACUTE: alveolar spaces show hyaline membranes; oedema
ORGANISING phase: pneumocyte hyperplasia, interstitium inflamed with reactive fibrosis
CHRONIC phase: denser fibrosis, microscopic cysts.

49
Q

Radiographic appearance of idipathic pulmonary fibrosis?

A

Bilateral, symmetric, irregular linear opacities causing reticular pattern; honeycombing subpleurally.

50
Q

Macroscopic appearance idiopathic pulmonary fibrosis?

A
  • decreased overall volume
  • cobble stoned appearance due to scar retraction
  • diffuse fibrosis with lower lobe predominance
  • honeycomb cystic changes peripherally
51
Q

Microscopic appearance idiopathic pulmonary fibrosis?

A
  • patchy interstitial fibrosis in subpleural / paraseptal distribution with areas of normal lung
  • dense honeycombing and fibroblastic foci
52
Q

What is honeycomb lung?

A

Represents irreversible end stage manifestation of many interstitial inflammatory and proliferative lung diseases

53
Q

Causes of honeycomb lung?

A
  • idiopathic interstitial pneumonias
  • diffuse alveolar damage
  • asbestosis
  • miliary TB
  • sarcoidosis
  • CT disease
  • drugs
  • radiation
54
Q

Appearance honeycomb lung?

A

Uniformly sized cysts ranging from a few mm to >1cm in diamter; set in background of dense scarring.

55
Q

What is pleuritis?

A

Inflammation of the pleura

56
Q

Causes of pleuritis?

A

Infections: e.g. bacteria, TB, viral, fungal, parasitic

Non-infectious: trauma, infarction, CT disorders, uremia, tumour involvement

57
Q

Normal of pleural surface?

A

No more than 15mL of serous, relatively acellular clear fluid.

58
Q

What is a transudate?

A

-Low protein (

59
Q

What is the pathogenesis of a transudate?

A

Transudate accumulates when the flow of fluid through a serous membrane exceeds normal resorptive process.

60
Q

What is an exudate?

A
  • Higher protein (>3g/dL)
  • Higher specific gravity >1.015
  • High LDH
  • High cellular content
  • Contains many inflammatory cells or neoplastic cells
  • Implies local problems: infection, inflammatory condition, neoplasm
61
Q

Pathogenesis of exudate?

A

Exudate results from altered permeability of or damage to the capillaries that are in the serosal CT. Allows escape of cells and protein into the serous cavity.

62
Q

What is a large, unilateral effusion (>1L) suspicious for?

A

Malignancy, esp in elderly

63
Q

How may pleural effusion fluid with many cancer cells appear grossly?

A

May form a thick, whitish layer at bottom of collection bag

64
Q

What is suggested by chocolate brown pleural effusion fluid?

A

Fluids contains numerous pigmented melanoma cells

65
Q

Characteristic of mesothelioma effusion fluid?

A

Often contains a high concentration of hyaluronic acid which increases the viscosity

66
Q

Aetiology mesothelioma?

A

Strong association with asbestos

67
Q

Exposure to what precipitates greatest risk of developing mesothelioma?

A

Crocidolite exposure

68
Q

Macroscopic appearance mesothelioma? (inc progression)

A
  • Initially numerous small nodules or plaques covering series
  • nodules fuse, form diffuse thickening
  • Final: massive encasement of viscera, causes complete obliteration of pleural / peritoneal cavity
  • Can invade into lungs or through chest / abdo wall
  • tumour is firm, rubbery, grey-white or soft and gelatinous
69
Q

What are the histological types of mesothelioma?

A

Epithelioid: tubulopapillary structures
Sarcomatoid: sheets and fascicles of spindle cells

70
Q

Ddx mesothelioma?,

A

Primary lung adenocarcinoma

71
Q

What is the mesothelial marker?

A

Calretinin

72
Q

Prognosis mesothelioma?

A
  • Avg survival from onset of symptoms 12-15m

- mortality 100%

Pathology (11 decks)

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