Respiratory Pathology 1 Flashcards
What is bronchiectasis?
Chronic disorder characterised by permanent dilation of the bronchi, accompanied by inflammatory changes in their walls and in adjacent lung parenchyma.
Pathogenesis of bronchiectasis?
Recurrent inflammation of the bronchial walls combined with fibrosis in the surrounding parenchyma –> traction on the weakened walls causes irreversible dilatation.
Categories of bronchiectasis causes?
May be
- post inflammatory or
- post obstructive.
What are the post inflammatory causes of bronchiectasis?
- Pneumonia, measles, whooping cough
- Congenital hypogammaglobulinemia CF, immotile cilia syndrome
- ABPA
- Reactions to inhaled toxic fumes
What are the post obstructive causes of bronchiectasis?
- Neoplasm
- Foreign body
- Inspissated mucous: asthma
- External compression: hilar lymph nodes, aortic aneurysm
- Rare: bronchial webs, atresia
Pathogenesis of obstructive bronchiectasis?
Obstructive -> impairment of normal clearing mechanisms -> pooling of secretions distal to obstruction -> inflammation of the airway.
Pathogenesis of bronchiectasis in CF?
Accumulation of thick viscid secretion -> obstruct airways -> susceptibility to bacterial infections -> widespread damage to airway walls (destruction of elastin, SM) -> fibrosis -> dilation of bronchi.
What is allergic bronchopulmonary aspergillosis?
Hyeprsensitivity to fungus Aspergillosis fumigatus.
Characteristics of ABPA?
- High serum IgE
- Serum Abs to Aspergillus
- Intense airway inflammation (mostly eosinophils)
- Formation of mucous plugs
Morphology of bronchiectasis?
- Usually bilateral lower lobes
- Involves most vertical airways
- most severe in distal bronchi and bronchioles
- airways dilated (up to 4x N
How do bronchi appear on cut surface of lung in bronchiectasis?
Cysts filled with mucopurulent secretions
Histology of bronchiectasis?
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
What may isolated upper lobe bronchiectasis result from?
May be secondary to destructive tuberculous lesions
Bronchiectasis lobar involvement in CF?
Upper and middle lobes involved
Distribution of bronchiectasis in a1-antitrypsin deficiency?
Basilar distribution
What is a lung abscess?
Local suppurative process within the lung; characterised by necrosis of lung tissue.
Common causes of lung abscess?
- Aspiration
- Antecedent primary lung infection
- Septic embolism
- Neoplasia
- Direct penetration by adjacent organ / trauma
- Haematogenous seeding
Common pathogens lung abscess?
- G+ve and G-ve strep
- S. aureus
- Many G-ves!
- Anaerobic bacteria common
Most common side for lung abscess?
Most abscesses in R lung as R main bronchus more vertical
When is aspiration most likely?
-Acute alcoholism
-Coma
-Anesthesia
-Sinusitis
-Gingivodenta sepsis
When cough reflexes suppressed
Sites of septic emboli causing lung abscess?
- Thrombophlebitis (any part of systemic venous circulation)
- IE on R heart
Morphology of abscesses in the lung secondary to pneumonia / bronchiectasis?
Usually multiple, basal and diffusely scattered
what is the cardinal histologic change in abscesses?
Suppurative destruction of the lung parenchyma within the central area of cavitation. Chronic: fibroblast proliferation may develop a fibrous wall.
Clinical features of lung abscess?
- Cough
- Fever
- Copious foul smelling purulent sputum
- Fever
- CP
- May develop clubbing
What is tuberculosis?
infection by Mycobacterium tuberculosis
What are mycobacteria?
Aerobic, non-motile bacilli
What is primary TB? What characterises it?
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)
Common location of Ghon focus?
Lower portion of R upper lobe or upper portion of R lower lobe.
Healing of Ghon focus?
Fibrosis and calcification; BUT may contain viable organisms for many years.
What are the clincopathologic consequences of progressive TB?
- Cavitary fibrocaseous TB
- miliary TB
- tuberculous bronchopneumonia
What is cavitary fibrocaseous tuberculosis?
- Erosion into bronchiole -> drainage of caseous focus transforms into cavity
- infective material disseminates through airways to other lung sites
Mechanism of miliary TB?
Haematogenous dissemination:
- TB confined to lungs
- involving other organs
Favoured sites of miliary TB distal seeding?
- Bone marrow
- Liver
- Spleen
- Kidney
- LNs
- Pericardium
What is tuberculous bronchopneumonia?
TB may spread rapidly throughout large areas of lung parenchyma producing a diffuse bronchopneumonia or lobar exudative consolidation.
what is a calcified Ghon complex?
Ranke complex
What is secondary TB?
- Reactivation of dormant focus of primary infection
- Reinfection
Location of secondary TB?
Within 1-2cm of apical pleura of upper lobe of 1 or both lungs (higher oxygen tension favours growth)
Appearance of secondary TB foci?
Sharply circumscribed, firm, grey-white-yellow areas with variable central caseation and peripheral fibrosis.
Histology of TB?
- Granulomatous inflammation with epithelioid histiocytes, lymphocytes and Langhan’s giant cells.
- Caseation often present
What are Langhan’s giant cells?
Contain nuclei arranged in a horse shoe shaped pattern at cell periphery
What are the causes of granulomatous inflammation in lung?
INFECTIONS: mycobacteria, fungi, parasites
NON-INFECTIOUS: sarcoidosis, hypersensitivity pneumonitis, Wegener granulomatosis, Churg Strauss syndrome, rheumatoid nodules
What are diffuse parenchymal lung diseases?
=Interstitial lung disease.
- Interstitial inflammation, granulomatous inflammation or fibrosis.
- All compartments can be affected
Inflammation of sarcoidosis?
Non-necrotising granulomatous inflammation, distributed along lymphatic pathways (bronchovasular bundles, interlobular septa and the pleura).
What is diffuse alveolar damage?
=ARDS.
Patients develop respiratory failure and pulmonary oedema.
Radiographic appearance of diffuse alveolar damage?
Widespread consolidation
Phases of diffuse alveolar damage?
3 phases:
i) Exudative (acute)
ii) Organising
iii) Fibrotic (chronic)
Macroscopic appearance of diffuse alveolar damage?
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
Histologic appearance of diffuse alveolar damage?
ACUTE: alveolar spaces show hyaline membranes; oedema
ORGANISING phase: pneumocyte hyperplasia, interstitium inflamed with reactive fibrosis
CHRONIC phase: denser fibrosis, microscopic cysts.
Radiographic appearance of idipathic pulmonary fibrosis?
Bilateral, symmetric, irregular linear opacities causing reticular pattern; honeycombing subpleurally.
Macroscopic appearance idiopathic pulmonary fibrosis?
- decreased overall volume
- cobble stoned appearance due to scar retraction
- diffuse fibrosis with lower lobe predominance
- honeycomb cystic changes peripherally
Microscopic appearance idiopathic pulmonary fibrosis?
- patchy interstitial fibrosis in subpleural / paraseptal distribution with areas of normal lung
- dense honeycombing and fibroblastic foci
What is honeycomb lung?
Represents irreversible end stage manifestation of many interstitial inflammatory and proliferative lung diseases
Causes of honeycomb lung?
- idiopathic interstitial pneumonias
- diffuse alveolar damage
- asbestosis
- miliary TB
- sarcoidosis
- CT disease
- drugs
- radiation
Appearance honeycomb lung?
Uniformly sized cysts ranging from a few mm to >1cm in diamter; set in background of dense scarring.
What is pleuritis?
Inflammation of the pleura
Causes of pleuritis?
Infections: e.g. bacteria, TB, viral, fungal, parasitic
Non-infectious: trauma, infarction, CT disorders, uremia, tumour involvement
Normal of pleural surface?
No more than 15mL of serous, relatively acellular clear fluid.
What is a transudate?
-Low protein (
What is the pathogenesis of a transudate?
Transudate accumulates when the flow of fluid through a serous membrane exceeds normal resorptive process.
What is an exudate?
- 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
Pathogenesis of exudate?
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.
What is a large, unilateral effusion (>1L) suspicious for?
Malignancy, esp in elderly
How may pleural effusion fluid with many cancer cells appear grossly?
May form a thick, whitish layer at bottom of collection bag
What is suggested by chocolate brown pleural effusion fluid?
Fluids contains numerous pigmented melanoma cells
Characteristic of mesothelioma effusion fluid?
Often contains a high concentration of hyaluronic acid which increases the viscosity
Aetiology mesothelioma?
Strong association with asbestos
Exposure to what precipitates greatest risk of developing mesothelioma?
Crocidolite exposure
Macroscopic appearance mesothelioma? (inc progression)
- 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
What are the histological types of mesothelioma?
Epithelioid: tubulopapillary structures
Sarcomatoid: sheets and fascicles of spindle cells
Ddx mesothelioma?,
Primary lung adenocarcinoma
What is the mesothelial marker?
Calretinin
Prognosis mesothelioma?
- Avg survival from onset of symptoms 12-15m
- mortality 100%
