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HistoPath - Respiratory disease Flashcards

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1
Q

Give examples of congenital lung disease

A

Lung agenesis or hypoplasia – LBW, impaired foetal respiratory movements
Tracheal and bronchial stenosis – associated with other malformations
Congenital cysts

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2
Q

Define asthma

A

widespread reversible narrowing of the airways (bronchi) that changes in severity over short periods of time

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3
Q

What are the causes/triggers of asthma

A

Recent RTI
Allergens/atopy
Pollution
Drugs (NSAIDs)
Occupational (gases)
Diet
Physical exertion
Intrinsic
Genetics

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4
Q

What is the pathogenesis of asthma

A

Immediate phase = mast cell degranulation → mediator release → increased vascular permeability → eosinophil + mast cell recruitment → bronchospasm

Late phase = tissue damage, increased mucous production, muscle hypertrophy

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5
Q

What are the histological features of asthma

A

Smooth muscle cell hyperplasia
Excess mucous → goblet cell hypertrophy
Inflammation
Whorls of shed epithelium (Cusrchmann spirals)
eosinophils
Charcot-Leyden crystals

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6
Q

Define Chronic bronchitis and what are the causes

A

Chronic bronchitis = type of COPD (other type = emphysema)
Dilatation of the airways (bronchi) and excess mucus production → Chronic cough productive of sputum; most days for ≥3 months over ≥2 consecutive years

Causes = smoking, air pollution, occupational exposures

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7
Q

What are the histological features of Chronic bronchitis

A

Dilatation of the airways
Goblet cell hyperplasia
Hypertrophy of mucous glands

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8
Q

What are the complications of COPD

A

Repeat infections
Chronic hypoxia
Reduced exercise tolerance, pulmonary HTN → RHF
Lung cancer risk

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9
Q

Define bronchiectasis and what are the histological features

A

Permanent abnormal dilatation of the terminal bronchi

Permanent fibrotic dilatation of the bronchi

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10
Q

What are the causes of bronchiectasis

A

Inflammatory
- Post-infectious
- Abnormal host defence (1º (hypogammaglobulinaemia) and 2º (chemotherapy, NG))
- Obstruction
- Post-inflammatory e.g. aspiration
- Secondary to bronchiolar disease and interstitial fibrosis (CFA, sarcoidosis)
- Systemic disease (connective tissue disorders)
- Asthma

Congenital
- Cystic fibrosis
- Primary ciliary dyskinesia (kartagener’s)
- Hypogammaglobulinaemia
- Young’s syndrome (rhinosinusitis, azoospermia and bronchiectasis)

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11
Q

What are the complications of bronchiectasis

A

Recurrent infections
Haemoptysis
Cor pulmonale
Amyloidosis

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12
Q

What is the cause of cystic fibrosis

A

Autosomal recessive
mutation in CFTR gene on Chr 7 (F508del) → defective Cl ion transfer → less water transfers to secretions → abnormally thick secretions
Allows growth of bacteria + frequent lung infections → bronchiectasis

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13
Q

What are the clinical features of cystic fibrosis

A

Lung → obstruction, recurrent infection → bronchiectasis → infection (pseudomonas, S. aureus, H. influenza, B. epacia)
Gi tract → meconium ileus, malabsorption
Pancreas → pancreatitis
Liver → cirrhosis
Male infertility

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14
Q

What is pulmonary oedema, its causes and its pathology

A

Parenchymal lung disease where fluid accumulation in alveolar spaces → poor gas exchange
Causes – LHF, alveolar injury, neurogenic, high altitude

  • Intra-alveolar fluid on histology
  • “Heart failure cells” = iron-laden macrophages
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15
Q

What is ARDS

A

Parenchymal disease of diffuse alveolar damage
Acute damage to endothelium ± alveolar epithelium leading to an exudative inflammatory reaction

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16
Q

What are the causes of ARDS in adults and neonates

A

Adults → acute respiratory distress syndrome / ARDS
- Infection
- Aspiration
- Trauma
- Inhaled irritant
- Shock
- Blood transfusion
- DIC
- Drug overdose
- Pancreatitis

Neonates = respiratory distress syndrome/ hyaline membrane disease of the newborn
- Insufficient surfactant in premature babies

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17
Q

What is the pathology of respiratory distress syndrome

A

Gross: fluffy white infiltrates in all lung fields, lungs expanded/firm, plum-coloured lungs, airless lungs, >1kg
Micro: capillary congestion, exudative phase, hyaline membranes, organising phase

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18
Q

What are the patterns of lung involvement in bacterial pneumonia

A

Bronchopneumonia
Lobar pneumonia
Abscess formation
Granulomatous inflammation

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19
Q

Describe the epidemiology, cause, and pathology of bronchopneumonia

A

Elderly
Low virulence organisms (staph, H. influenzae, strep, pneumococcus)
Pathology = patchy bronchial and peribronchial distribution, lower lobes, inflammation surrounding the airways themselves and is within the alveoli

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20
Q

What are the stages of lobar pneumonia

A

(1) Congestion: Hyperaemia, Intra-alveolar fluid
(2) Red hepatization: Hyperaemia, Intra-alveolar neutrophils (non-atypical)
(3) Grey hepatization: Intra-alveolar connective tissue
(4) Resolution: Restoration normal architecture

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21
Q

What are the causes and complications of lobar pneumonia

A

90-95% pneumococcus
Complications: abscess, pleuritis, effusion, empyema (infected effusion), fibrosis, sepsis

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22
Q

What are the features of atypical pneumonia

A

Mycoplasma, viruses (CMV, influenza), Coxiella, chlamydia, etc.
I.E. CMV pneumonia in those immunosuppressed
Interstitial inflammation without the accumulation of intra-alveolar inflammatory cells
Chronic inflammatory cells within alveolar septa with oedema ± viral infections

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23
Q

Define emphysema and what is the histology/pathology

A

Parenchymal type of COPD
permanent loss of alveolar parenchyma distal to terminal bronchiole

Pathology = Airspace enlargement, wall destruction

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24
Q

What are the causes of emphysema

Study These Flashcards
A

Damage to alveolar epithelium:
Smoking (centrilobular loss)
A1AT deficiency (panacinar loss)
Rare (IVDU, connective tissue disease)

25
What are the complications of emphysema
Bullae formation → pneumonthorax Respiratory failure Cor pulmonale
26
What is interstitial lung disease
Group of >200 diseases characterized by inflammation and fibrosis of the pulmonary connective tissue, accounting for 15% of respiratory disease burden
27
What are the features of interstitial lung disease on presentation and investigation
Chronic SOB Fine end-inspiratory crackles Cyanosis, pulmonary HTN and cor pulmonale rRduced FEV1 and FVR but normal FEV1/FVC ratio i.e. >70%) - RESTRICTIVE picture Decreased CO diffusion capacity Decreased lung volume Decreased compliance Advanced → ground glass/honeycomb appearance on CT CAP
28
What are the categories of interstitial lung disease
1. Fibrosing - Cryptogenic Fibrosing Alveolitis/ Idiopathic pulmonary fibrosis - Pneumoconiosis - Cryptogenic organizing pneumonia - Associated with connective tissue disease - Drug-induced - Radiation pneumonitis 2. Granulomatous - Sarcoid - Extrinsic allergic alveolitis - Associated with vasculitides e.g. Wegener’s, Churg-Strauss, microscopic polyangiitis 3. Eosinophilic 4. Smoking related
29
What are the features of Cryptogenic Fibrosing Alveolitis/ Idiopathic pulmonary fibrosis
Idiopathic pulmonary fibrosis >50yo, male >50% die in 2-3 years progressive SOB/cough Diagnosed on HR-CT
30
What are the histological features of Cryptogenic Fibrosing Alveolitis/ Idiopathic pulmonary fibrosis
Usual Interstitial Pneumonia Progressive patchy interstitial fibrosis with loss of normal lung architecture and honeycomb change, beginning at periphery of the lobule, usually sub-pleural Hyperplasia of type II pneumocytes causing cyst formation – honeycomb fibrosis.
31
Give examples of pneumoconiasis causes
Occupational lung disease - inhalation of mineral dusts/inorganic particles Industrial lung diseases: asbestosis, silicosis, coal-miner’s lung - Asbestosis → fine sub-pleural fibrosis with asbestos bodies in tissues (typically lower lobe)→ increased risk of adenocarcinoma/mesothelioma
32
What are granulomas
collection of histiocytes, macrophages ± giant multinucleate cells
33
What are the causes of granulomatous disease of the lung
TB Fungal (histoplasma, Cryptococcus, coccidioides, aspergillus, mucor) Others (pneumocystis, parasites) Sarcoidosis Foreign body (aspiration, IVDU) Drugs Occupational lung disease
34
What is the pathophysiology of Extrinsic allergic alveolitis and its presentation
Immune-mediated lung disorders caused by intense/prolonged exposure to inhaled ORGANIC antigens → widespread alveolar inflammation (pts. get better over weekend away from work) Presents with productive cough/SOB/clubbing/severe weight loss
35
What are the histological features of Extrinsic allergic alveolitis
Polypoid plugs of loose connective tissue within the alveoli/bronchioles Granuloma formation organising pneumonia
36
Give examples of occupation causes of granulomatous lung disease
Farmer's lung: mouldy hay/grain/silage – Saccharopolyspora rectivirgula) Pigeon fancier's lung: proteins in excreta/feathers Humidifier's lung: heated water reservoirs – thermactinomyces spp. Malt-worker's: germinating barley – Aspergillus clavatus/fumigatus Cheese washer's lung: mouldy cheese – Aspergillus clavatus/penicillium casei
37
What is the pathogenesis of sarcoidosis
abnormal host immunological response to variety of commonly encountered antigens, probably environmental in origin Affects lungs, skins, lymph nodes and eyes Lungs: discrete epithelioid and giant cell granulomas (usually upper zones → peri-lymphatic and peri-bronchial) → advanced disease becomes fibrocystic
38
How is sarcoidosis diagnosed
Non-caseating granulomas Elevated serum ACE Hypercalcaemia (1a-hydroxylase)
39
What are the risk factors for pulmonary embolism
Female Immobility Cardiac disease Cancer Primary and secondary hypercoagulable states (Virchow’s triad = stasis + vessel wall injury + hypercoagulability).
40
What is the pathophysiology of pulmonary embolism
95% originate from DVTs Large emboli impact in the main pulmonary arteries → acute cor pulmonale, cardiogenic shock and death if >60% of pulmonary bed occluded (N.B. occluding pulmonary trunk = saddle embolus) Small emboli may can be silent or cause peripheral wedge infarctions Repeated infarctions → pulmonary HTN
41
Give examples of non-thrombotic emboli
Bone marrow Amniotic fluid Trophoblast tumour Foreign body Air Fat
42
What is the definition of pulmonary hypertension
Mean pulmonary arterial pressure of >25mmHg at rest N.B. normal response of lungs to hypoxia is to reduce blood supply to hypoxic areas of lungs and divert it to aerated zones → chronic hypoxia results in chronic vasoconstriction to pulmonary arterioles (COPD, fibrosing lung disease)
43
What is the pathophysiology of pulmonary hypertension
Pre-capillary (chronic hypoxia/embolus) Capillary (Pulmonary Fibrosis) Post-capillary (left heart disease/ veno-occlusive disease) Pulmonary vasoconstriction of arterioles – intimal fibrosis, thickened walls
44
What are the complications of pulmonary hypertension
Right heart failure → venous congestion of organs (nutmeg liver), peripheral oedema
45
Describe pulmonary vasculitis
Uncommon Present as life threatening haemorrhage, chronic haemoptysis, mass lesion, interstitial lung disease Variety of patterns from granulomatous vasculitis involving small-medium sized vessels (GPA) through to a leukocytoclastic vasculitis involving capillaries (e.g with Rheumatoid arthritis)
46
Describe squamous cell carcinomas of the lung (representation, RFs, site, response to chemo, subtypes)
30-50% RF: Men, smoking, p53/c-myc mutations Proximal bronchi →local spread → late mets Less responsive to chemo There are a variety of subtypes e.g. papillary, basaloid Associated with cavitation and hypercalcaemia due to paraneoplastic syndrome (PTHrp secretion).
47
Describe the histology and cytology of squamous cell carcinomas of the lung + progression
Histology: Keratinisation, intercellular prickles (desmosomes). Cytology: Squamous cells
48
Describe the progression of squamous cell carcinomas
Progression: Epithelium → hyperplasia →squamous metaplasia→angiosquamous dysplasia→carcinoma in situ→invasive carcinoma
49
What are the features of adenocarcinoma of the lung (representation, definition, RF, site)
20-25% Malignant epithelial tumour with glandular differentiation or mucin production RF: women, non-smokers In peripheral alveolar spaces → early mets
50
Describe the histology and cytology of adenocarcinomas of the lung
Histology: Glandular differentiation (gland formation and mucin production). Cytology – cells containing mucin vacuoles. Molecular – EGFR mutations (non-smokers), K-rase (smokers)
51
Describe the progression of adenocarcinomas of the lung
Atypical adenomatous hyperplasia→non-mucinous BAC→mixed pattern adenocarcinoma
52
What are the features of small cell carcinomas (representation, RFs, site, prognosis, association)
10-15% RF: smoking, p53, RB1 Occurs centrally, proximal bronchi Highly malignant, metastasize early, usually by diagnosis commonly to bone, adrenal, liver and brain Poor prognosis Arises for neuroendocrine cells → ectopic ACTH secretion → Lamber-Eaton → SIADH
53
Describe the cytology and histology of small carcinomas
Cytology: small cells, ciliated normal resp. cell Histology: Small, poorly differentiated “oat cells”
54
Describe large cell carcinomas and its histology
Poorly differentiated malignant epithelial tumour – large cells, large nuclei, prominent nucleoli. Poor prognosis Histology: No evidence of glandular or squamous differentiation
55
Give examples of paraneoplastic syndromes
ADH → SIADH (Small cell) ACTH → Cushing’s syndrome (Small cell) PTH/ PTHrP → primary hyperparathyroidism, hypercalcaemia and bone pain (Squamous cell) Calcitonin → hypocalcaemia Serotonin → carcinoid syndrome (flushing + diarrhoea + bronchoconstriction) Bradykinin → cough
56
What are the molecular associations with lung cancers
ERCC1 – NSCLC = poorer response to cisplatinEGFR – adeno (usually) = target for Anti-EGFR (usually tyrosine kinase inhibitor (TKI)) therapy Kras – adeno/squamous = poor prognosis, non-response to TKI EML4-ALK – adeno (usually) = no benefit from TKI
57
How are lung cancers staged
TNM staging Tumour (T1-4) – based on size and invasion of pleura, pericardium Node metastasis (N0-2) - - N0: lymph node not involved by tumour - N1 or N2: lymph nodes involved (1 vs 2 depends on extent of involvement) Distant metastasis (M0 or 1) - M1 – tumour has spread to distant sites.
58
Describe mesotheliomas
Malignant tumour of the pleura (parietal or visceral), associated with asbestos exposure Extensive pleural effusion, chest pain and dyspnoea Long latent (lag) period of 25-45 years for development Poor prognosis

Y5 Pathology (71 decks)

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