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Pathology - Y5 > Pathology of Respiratory Disease > Flashcards

Pathology of Respiratory Disease Flashcards

1
Q

Define asthma.

A

A condition in which breathing is periodically rendered difficult by widespread narrowing of the airways that changes in severity over short periods of time.

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2
Q

What are the signs and symptoms of asthma?

A

Presents with wheezing, acute SOB.

In a severe attack patients develop status asthmaticus.

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3
Q

Explain the aetiology/risk factors for asthma.

A

Allergens and atopy (house dust mites)

Pollution

Drugs - NSAIDs

Occupational – inhaled gases/fumes

Diet

Physical exertion – “cold”

Intrinsic underlying genetic factors

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4
Q

What is involved in the immediate phsae of asthma?

A

Mast cells degranulate on contact with antigen

Mediators released cause vascular permeability, eosinophil and mast cell recruitment, and bronchospasm.

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5
Q

What is involved in the late phase of asthma?

A

Tissue damage

Increased mucus production

Muscle hypertrophy

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6
Q

Define COPD.

A

Chronic cough productive of sputum – Most days for at least 3 months over at least 2 consecutive years.

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7
Q

Explain the aetiology/risk factors for COPD.

A

Chronic injury to airways elicits local inflammation and reactive changes which predispose to further damage.

Common causes:

  • Smoking
  • Air pollution
  • Occupational exposures
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8
Q

What are complications associated with COPD?

A

Repeated infections (most common cause of hospital admission and death)

Chronic hypoxia and reduced exercise tolerance

Chronic hypoxia results in pulmonary hypertension and right sided heart failure (cor pulmonale)

Increased risk of lung cancer independent of smoking

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9
Q

Define bronchiectasis.

A

Permanent abnormal dilatation of bronchi.

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10
Q

What are common causes of bronchiectasis?

A

Congenital

Inflammatory:

  • Post-infectious(especially children or cystic fibrosis patients)
  • Ciliary dyskinesia 1º [Kartagener’s] and 2º
  • Obstruction (extrinsic/intrinsic/middle lobe syn.)
  • Post-inflammatory (aspiration)
  • Secondary to bronchiolar disease (OB) and interstitial fibrosis (CFA, sarcoidosis)
  • Systemic disease (connective tissue disorders)
  • Asthma
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11
Q

What are some complications associated with bronchiectasis?

A

Recurrent infections

Haemoptysis

Pulmonary Hypertension and right sided heart failure

Amyloidosis

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12
Q

Explain the aetiology/risk factors of cystic fibrosis.

A

Affects 1 in 2,500 live births

  • Autosomal recessive (approx 1/20 of population are heterozygous carriers)
  • Chr 7q3 = CFTR gene (Cystic Fibrosis Transmembrane Conductance Regulator) = ion transporter protein.
  • Abnormality leads to defective ion transport and therefore excessive resorption of water from secretions of exocrine glands.
  • Results in abnormally thick mucus secretion - affects all organ systems.
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13
Q

Which organs are affected in cystic fibrosis?

A

Lung: Airway obstruction, respiratory failure, recurrent infection

GI tract: Meconium ileus, malabsorption

Pancreas: Pancreatitis, secondary malabsorption

Liver: Cirrhosis

Male reproductive system: Infertility

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14
Q

What are treatment options for cystic fibrosis?

A

Improved treatment (physio, antibiotics, enzyme supplements, parenteral nutrition) has led to survival often into fourth decade.

Lung transplantation offers longer survival.

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15
Q

Define pulmonary oedema.

A

Accumulation of fluid in alveolar spaces as consequence of “leaky capillaries” or “backpressure” from failing left ventricle.

Common cause hospital admission and of respiratory failure.

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16
Q

What are causes of pulmonary oedema?

A
  • Left heart failure
  • Alveolar injury
  • Neurogenic
  • High altitude
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17
Q

What is the pathology of pulmonary oedema?

A

Acute: Heavy watery lungs, intra- alveolar fluid on histology

Chronic: Iron laden macrophages, fibrosis

Poor gas exchange therefore hypoxia and respiratory failure.

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18
Q

What is diffuse alveolar damage?

A

Pattern of acute diffuse lung injury in which patients present with rapid onset of respiratory failure, requiring ventilation on ITU. CXR shows “white out” all lung fields.

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19
Q

What is the pathogenesis of diffuse alveolar damage?

A

Acute damage to endothelium and/or alveolar epithelium leading to exudative inflammatory reaction.

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20
Q

What is diffuse alveolar damage also known as in adults?

A

Acute respiratory distress syndrome “shock lung”.

Numerous causes in adults:

Infection (local or generalised sepsis), aspiration, trauma, inhaled irritant gases, shock, blood transfusion, DIC, drug overdose, pancreatitis, idiopathic.

Common on ITU.

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21
Q

What is diffuse alveolar damage also known as in neonates?

A

Hyaline membrane disease of newborn.

Insufficient surfactant production leading to stiff lungs and secondary alveolar epithelial damage.

Premature babies.

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22
Q

What is the clinical outcome of diffuse alveolar damage?

A

Death ~ 40% of cases

Superimposed infection

Resolution: Lung returns to normal

Residual fibrous scarring of lung leading to chronic respiratory impairment

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23
Q

What is the general clinical presentation of bacterial pneumonia?

A

Variety of patterns of lung involvement depending upon organism and other cofactors.

  • Bronchopneumonia
  • Lobar pneumonia
  • Abscess formation
  • Granulomatous inflammation
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24
Q

What are features of bronchopneumonia?

A

Compromised host defense - Elderly

Often low virulence organisms - Staphylococcus, Haemophilius, Streptococcus, Pneumococcus.

Pathology - Patchy bronchial and peribronchial distribution, often lower lobes

25
Q

What can be seen on a histology slide of a patient with bronchopneumonia?

A

Peribronchial distribution

Acute inflammation surrounding airways and within alveoli

26
Q

What are features of lobar pneumonia?

A

Acute bacterial infection of a large portion of a lobe or entire lobe.

Infrequent with advent of antibiotics.

High virulence organism: 90-95% pneumococci (S. pneumoniae).

Widespread fibrinosuppurative consolidation.

27
Q

What can be seen on a histology slide of lobar pnuemonia?

A
  1. Congestion – Hyperaemia – Intra-alveolar fluid
  2. Red hepatization – Hyperaemia – Intra-alveolar neutrophils
  3. Grey hepatization – Intra-alveolar connective tissue
  4. Resolution – Restoration normal architecture
28
Q

What are complications associated with infectious respiratory disease?

A

Abscess formation

Pleuritis and pleural effusion

Infected pleural effusion (EMPYEMA)

Fibrous scarring

Septicaemia

29
Q

Define emphysema.

A

Emphysema is a permanent loss of the alveolar parenchyma distal to the terminal bronchiole.

Damage to alveolar epithelium:

  • SMOKING
  • Alpha 1 antitrypsin deficiency
  • Rare: IVDU, connective tissue disease
30
Q

What are complications associated with emphysema?

A
  • Large air spaces (bullae) – Rupture - pneumothorax
  • Respiratory failure – Loss of area for gas exchange – Compression of adjacent normal lung.
  • Pulmonary hypertension and cor pulmonale
31
Q

What is a granuolma?

A

Collection of histiocytes/macrophages +/- multinucleate giant cells.

Necrotising or non necrotising.

32
Q

What are some causes of granulomatous disease?

A
  • Infection
  • Sarcoidosis
  • Foreign body
  • Aspiration or IVDU
  • Drugs
  • Occupational lung disease
33
Q

Define fibrosing lung disease.

A

Chronic and progressive fibrosing diseases of lung

34
Q

What are some important types of fibrosing lung disease?

A

Idiopathic pulmonary fibrosis: Cryptogenic fibrosing alveolitis

Extrinsic allergic alveolitis: Farmers lung

Industrial lung diseases: Pneumoconiosis

35
Q

What is idiopathic pulmonary fibrosis?

A

Also known as cryptogenic fibrosing alveolitis

Chronic: SOB and cough

Over 50 years, male predominance

Diagnosis by HRCT +/- biopsy

  • Macro: Basal and peripheral fibrosis and cyst formation
  • Micro: Interstitial fibrosis at varying stages

Progressive disease

Over 50% die in 2-3 years

36
Q

What is pulmonary thromboembolism?

A

Embolisation of peripheral thrombus to lung.

Common cause of admission to A&E/Medical Admission Unit.

37
Q

What are common site formations of thromboembolism?

A

Common site formation in deep veins of leg (95%):

  • Present with swelling of leg (Deep Vein Thrombosis)
  • Present with symptoms of spread to lung (Pulmonary Embolism)
38
Q

What are small emboli?

A

Small peripheral pulmonary arterial occlusion

Haemorrhagic infarct

Repeated emboli cause increasing occlusion of pulmonary vascular bed and pulmonary hypertension. Patients present with pleuritic chest pain, acute SOB and/or chronic progressive shortness of breath.

39
Q

What are large emboli?

A

Large emboli can occlude the main pulmonary trunk (saddle embolus).

Sudden death, acute right heart failure, or cardiovascular shock occurs in 5% of cases when >60% of pulmonary bed is occluded. If patient survives, the embolus usually resolves. 30% develop second or more emboli.

40
Q

What are some non-thrombotic emboli?

A

Bone marrow

Amniotic fluid

Trophoblast

Tumour

Foreign body

Air

41
Q

What is pulmonary hypertension?

A

Mean pulmonary arterial pressure > 25mmHg at rest

42
Q

What are some precapillary causes of pulmonary hypertension?

A

Vasoconstrictive:

  • Chronic hypoxia
  • Hyperkinetic congenital heart disease
  • Unknown (Primary pulmonary hypertension)
  • Chronic liver disease, HIV infection, Connective tissue disease

Embolic:

  • Thromboembolic
  • Parasitic (schistosomal)
  • Tumour emboli
43
Q

What are some capillary causes of pulmonary hyptertension?

A

Widespread pulmonary fibrosis - mechanical vascular distortion and chronic hypoxia

44
Q

What are some post-capillary causes of pulmonary hypertension?

A

Veno-occlusive disease

Left-sided heart disease

45
Q

Define lung tumours.

A

Variety of benign and malignant tumours arise in the lungs.

Arise from a variety of cell types: epithelial, mesenchymal (soft tissue), lymphoid.

Arise at a variety of sites: airways, seromucinous glands, alveolar parenchyma, vessels, pleura.

46
Q

What are benign lung tumours?

A

Do not metastasise

Can cause local complications e.g. Airway obstruction

e.g. Chondroma

47
Q

What are metastatic lung tumours?

A

Potential to metastasise, but variable clinical behaviour from indolent to aggressive. Commonest are epithelialtumours, and of these main types (90-95%).

NON-small cell carcinoma

  • Squamous cell carcinoma (30%)
  • Adenocarcinoma (30%)
  • Large cell carcinoma (20%)

SMALL cell carcinoma

  • Small cell carcinoma (20%)
48
Q

Which lung cancers does smoking have the strongest association with?

A

Strongest association with squamous cell carcinoma and small cell carcinoma.

49
Q

What are other risk factors for lung cancer?

A

10-20% of lung cancers worldwide in non-smokers.

Asbestos exposure (Asbestos + smoking = 50 fold increase risk)

Radiation (Radon exposure, theraputic radiation, uranium miners)

Air pollution

Other: Heavy metals (Chromates, arsenic, nickel)

Genetics: Familial lung cancers rare. Epidemiological evidence of increased risk for first degree relatives. Typically young age, non-smoking cases.

50
Q

What are features of invasive squamous cell carcinoma?

A

Frequency: 35% pulmonary carcinoma.

Risk factor: Closely associated with smoking

Site: Traditionally centrally located arising from bronchial epithelium, however increasing number of peripheral squamous cell carcinomas.

Behaviour: Local spread, metastasise late.

51
Q

What is the pathway of development of adenocarcinoma?

A

Precursor lesion: Atypical adenomatous hyperplasia. Proliferation of atypical cells lining the alveolar walls. Increases in size and eventually can become invasive.

AAH > Non-mucinous adenocarcinoma in situ > Mixed pattern invasive adenocarcinoma

52
Q

What are features of invasive adenocarcinoma?

A

Frequency: Increasing incidence: 27% pulmonary carcinomas.

Risk factor: Smoking + other – Commoner in far east, females and non-smokers.

Site: Peripheral and more often multicentri.

Behaviour: Extrathoracic metastases common and early.

Histology: Histology shows evidence of glandular differentiation. Variety patterns relate underlying molecular abnormalities and prognosis.

53
Q

What are large cell carcinomas?

A

Peripheral or central 10% of tumours.

Poorly differentiated tumours composed of large cells.

No histological evidence of glandular or squamous differentiation – BUT on electron microscopy many show some evidence of glandular, squamous or neuroendocrine differentiation – i.e are probably very poorly differentiated adeno/squamous cell carcinomas.

Poorer prognosis.

54
Q

What are small cell carcinomas?

A

Frequency: 20% tumours.

Risk factor: Very close association with smoking.

Site: Often central near bronchi.

Behaviour: 80% present with advanced disease. Although very chemosensitive, have an abysmal prognosis. Paraneoplastic syndromes.

Histology: Small poorly differentiated cells; p53 and RB1 mutations common.

55
Q

What is the prognosis and treatment of small cell carcinomas?

A

Survival 2-4 months untreated

10-20 months with current therapy

Chemoradiotherapy (surgery very rarely undertaken as most have spread at time of diagnosis)

56
Q

What is the prognosis and treatment of non-small cell carcinomas?

A

Early Stage 1: 60% 5 yr survival

Late Stage 4: 5% 5 yr survival – 20-30% have early stage tumours suitable for surgical resection.

Less chemosensitive.

57
Q

What are common clinical presentations for lung cancer?

A

Asymptomatic:

  • Incidental finding of mass on chest X-ray

Symptomatic:

  • Cough
  • Haemoptysis
  • Recurrent infections
  • Other: Weight loss, metastasis
58
Q

What is cytology and how can pathologists study this?

A

Looking at cells.

  • Sputum
  • Bronchial washings and brushings
  • Pleural fluid
  • Endoscopic fine needle aspiration of tumour/enlarged lymph nodes
59
Q

What is histology and how can pathologists study this?

A

Looking at tissue.

  • Biopsy at bronchoscopy: Central tumours
  • Percutaneous CT guided biopsy: -Peripheral tumours
  • Mediastinoscopy and lymph node biopsy: For staging
  • Open biopsy at time of surgery if lesion not accessible otherwise: Frozen section
  • Resection specimen: Confirm excision and staging

Pathology - Y5 (59 decks)

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