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Y5 Pathology > HistoPath - Respiratory disease > Flashcards

HistoPath - Respiratory disease Flashcards

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

A

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

25
Q

What are the complications of emphysema

A

Bullae formation → pneumonthorax
Respiratory failure
Cor pulmonale

26
Q

What is interstitial lung disease

A

Group of >200 diseases characterized by inflammation and fibrosis of the pulmonary connective tissue, accounting for 15% of respiratory disease burden

27
Q

What are the features of interstitial lung disease on presentation and investigation

A

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
Q

What are the categories of interstitial lung disease

A
  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
Q

What are the features of Cryptogenic Fibrosing Alveolitis/ Idiopathic pulmonary fibrosis

A

Idiopathic pulmonary fibrosis
>50yo, male
>50% die in 2-3 years
progressive SOB/cough
Diagnosed on HR-CT

30
Q

What are the histological features of Cryptogenic Fibrosing Alveolitis/ Idiopathic pulmonary fibrosis

A

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
Q

Give examples of pneumoconiasis causes

A

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
Q

What are granulomas

A

collection of histiocytes, macrophages ± giant multinucleate cells

33
Q

What are the causes of granulomatous disease of the lung

A

TB
Fungal (histoplasma, Cryptococcus, coccidioides, aspergillus, mucor)
Others (pneumocystis, parasites)
Sarcoidosis
Foreign body (aspiration, IVDU)
Drugs
Occupational lung disease

34
Q

What is the pathophysiology of Extrinsic allergic alveolitis and its presentation

A

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
Q

What are the histological features of Extrinsic allergic alveolitis

A

Polypoid plugs of loose connective tissue within the alveoli/bronchioles
Granuloma formation
organising pneumonia

36
Q

Give examples of occupation causes of granulomatous lung disease

A

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
Q

What is the pathogenesis of sarcoidosis

A

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
Q

How is sarcoidosis diagnosed

A

Non-caseating granulomas
Elevated serum ACE
Hypercalcaemia (1a-hydroxylase)

39
Q

What are the risk factors for pulmonary embolism

A

Female
Immobility
Cardiac disease
Cancer
Primary and secondary hypercoagulable states (Virchow’s triad = stasis + vessel wall injury + hypercoagulability).

40
Q

What is the pathophysiology of pulmonary embolism

A

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
Q

Give examples of non-thrombotic emboli

A

Bone marrow
Amniotic fluid
Trophoblast
tumour
Foreign body
Air
Fat

42
Q

What is the definition of pulmonary hypertension

A

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
Q

What is the pathophysiology of pulmonary hypertension

A

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
Q

What are the complications of pulmonary hypertension

A

Right heart failure → venous congestion of organs (nutmeg liver), peripheral oedema

45
Q

Describe pulmonary vasculitis

A

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
Q

Describe squamous cell carcinomas of the lung (representation, RFs, site, response to chemo, subtypes)

A

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
Q

Describe the histology and cytology of squamous cell carcinomas of the lung + progression

A

Histology: Keratinisation, intercellular prickles (desmosomes).
Cytology: Squamous cells

48
Q

Describe the progression of squamous cell carcinomas

A

Progression: Epithelium → hyperplasia →squamous metaplasia→angiosquamous dysplasia→carcinoma in situ→invasive carcinoma

49
Q

What are the features of adenocarcinoma of the lung (representation, definition, RF, site)

A

20-25%
Malignant epithelial tumour with glandular differentiation or mucin production
RF: women, non-smokers
In peripheral alveolar spaces → early mets

50
Q

Describe the histology and cytology of adenocarcinomas of the lung

A

Histology: Glandular differentiation (gland formation and mucin production).
Cytology – cells containing mucin vacuoles. Molecular – EGFR mutations (non-smokers), K-rase (smokers)

51
Q

Describe the progression of adenocarcinomas of the lung

A

Atypical adenomatous hyperplasia→non-mucinous BAC→mixed pattern adenocarcinoma

52
Q

What are the features of small cell carcinomas (representation, RFs, site, prognosis, association)

A

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
Q

Describe the cytology and histology of small carcinomas

A

Cytology: small cells, ciliated normal resp. cell
Histology: Small, poorly differentiated “oat cells”

54
Q

Describe large cell carcinomas and its histology

A

Poorly differentiated malignant epithelial tumour – large cells, large nuclei, prominent nucleoli.
Poor prognosis
Histology: No evidence of glandular or squamous differentiation

55
Q

Give examples of paraneoplastic syndromes

A

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
Q

What are the molecular associations with lung cancers

A

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
Q

How are lung cancers staged

A

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
Q

Describe mesotheliomas

A

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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