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YR5 Histopathology > 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 5 signs and symptoms of asthma?

A

Wheezing
Acute SOB
Chest tightness
Night-time cough
Severe attack: status asthmaticus.

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3
Q

Give 8 aetiology/ risk factors for asthma.

A

Atopy (house dust mites)
Pollution
Drugs: NSAIDs
Occupational: inhaled gases/ fumes
Diet
Physical exertion: “cold”
Intrinsic
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 + mast cell recruitment, + bronchospasm.

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5
Q

What acute changes are seen in asthma?

A

Bronchospasm: constricted
Oedema + Hyperaemia: swollen

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6
Q

What is involved in the late phase of asthma?

A

Tissue damage

Increased mucus production

Muscle hypertrophy (GFs triggered)

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7
Q

What are 3 chronic changes seen in asthma?

A

Muscle hypertrophy

Airway narrowing

Mucus plugging

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8
Q

What is this? What disease is this associated with?

A

Mucus plug
Asthma

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9
Q

What is this? What disease is this associated with?

A

Hyperaemia: v dilated blood vessel
Asthma

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10
Q

What is this? What disease is this associated with?

A

Eosinophilic inflammation + goblet cell hyperplasia
Asthma

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11
Q

What is this? What disease is this associated with?

A

Hypertrophic constricted muscle
Asthma

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12
Q

What is this? What disease is this associated with?

A

Mucus plugging + inflammation
Asthma

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13
Q

Define COPD.

A

Chronic cough productive of sputum – Most days for at least 3/12 over at least 2 consecutive years.
Mix of airway + alveolar pathology
(chronic bronchitis + emphysema)

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14
Q

Explain the aetiology/ risk factors for COPD.

A

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

Common causes:
* Smoking
* Air pollution
* Occupational exposures

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15
Q

Give 4 pathological features of COPD

A

Dilated airways- lose structure
Mucus gland hyperplasia
Goblet cell hyperplasia
Inflammation

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16
Q

What are 4 complications associated with COPD?

A

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

Chronic hypoxia + reduced exercise tolerance

Chronic hypoxia results in pulmonary HTN + right HF (cor pulmonale)

Increased risk of lung cancer independent of smoking

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17
Q

Define bronchiectasis.

A

Permanent abnormal dilatation of bronchi with inflammation + fibrosis extending into adjacent parenchyma

Inflamed scarred lungs with dilated airways

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18
Q

What are 9 causes of bronchiectasis?

A

Congenital

Inflammatory:
Infection
* Post-infectious (esp. kids/ CF patients)
* Ciliary dyskinesia 1º [Kartagener’s] + 2º
*Abnormal host defence1º [hypogammagl] + 2º [chemo, NG]
* Obstruction (extrinsic/ intrinsic/ middle lobe syn.)
* Post-inflammatory (aspiration)
* Secondary to bronchiolar disease (OB) + interstitial fibrosis (Idiopathic PF, sarcoidosis)
* Systemic disease (connective tissue disorders)
* Asthma

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19
Q

What are 4 complications associated with bronchiectasis?

A

Recurrent infections (massively dilated + full of mucus)

Haemoptysis (severe infection causes erosion into vessels)

Pulmonary HTN + right HF

Amyloidosis

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20
Q

Explain the aetiology of cystic fibrosis.

A

Affects 1 in 2,500 live births

  • Autosomal recessive (~ 1/20 of pop. heterozygous carriers)
  • Chr7q3 = CFTR gene (Cystic Fibrosis Transmembrane Conductance Regulator) = ion transporter protein.
  • Abnormality leads to defective ion transport across cell membranes leading to excessive resorption of water from secretions of exocrine glands.
  • Abnormally thick mucus secretion - affects all organ systems.
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21
Q

What is the most common mutation causing cystic fibrosis?

A

Delta F508

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22
Q

Which organs are affected in cystic fibrosis?

A

GIT: Meconium ileus, malabsorption

Pancreas: Pancreatitis, secondary malabsorption

Liver: Cirrhosis

Male reproductive system: Infertility

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23
Q

How is the lung affected in cystic fibrosis?

A

Airway obstruction
Recurrent infections
Resp. failure + cor pulmonale
Haemoptysis
Pneumothorax

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24
Q

What are treatment options for cystic fibrosis?

A

Physio
Abx
Enzyme supplements
Parenteral nutrition
Lung transplantation

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25
Q

Define pulmonary oedema.

A

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

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26
Q

What is pulmonary oedema commonly associated with?

A

Heart failure (acute or chronic)
Common cause hospital admission + resp. failure.

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27
Q

List 4 causes of pulmonary oedema

A
  • Left HF
  • Alveolar injury: drugs, inhalation, infection, pancreatitis
  • Neurogenic following head injury
  • High altitude: altitude sickness
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28
Q

What is shown here? What condition is this?

A

Iron laden macrophages
(Haemosideren)
Pulmonary oedema: “Heart failure cells”

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29
Q

What is shown here? What condition is this?

A

Alveolar spaces full of plasma
Pulmonary oedema

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30
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 + resp failure.

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31
Q

What is diffuse alveolar damage?

A

Pattern of acute diffuse lung injury in which patients present with rapid onset resp. failure, requiring ventilation on ITU.

CXR shows “white out” all lung fields.

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32
Q

What is the pathogenesis of diffuse alveolar damage?

A

Acute damage to endothelium +/- alveolar epithelium leading to exudative inflammatory reaction.

Diffuse alveolar damage

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33
Q

What is diffuse alveolar damage also known as in adults?

A

Acute respiratory distress syndrome “shock lung”.

Common on ITU.

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34
Q

List 10 causes of diffuse alveolar damage in adults

A

Infection (local or generalised sepsis)
Aspiration
Trauma
Inhaled irritant gases
Shock
Blood transfusion
DIC
Drug OD
Pancreatitis
Idiopathic

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35
Q

What is diffuse alveolar damage also known as in neonates? Describe the aetiology

A

Hyaline membrane disease of newborn.

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

Premature babies.

36
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

37
Q

What is seen here? What condition is this?

A

Fluffy white infiltrates in all lung fields, filled with liquid + exudate
“white out”
Diffuse alveolar damage

38
Q

Describe the lung in diffuse alveolar damage as seen here

A

Lungs expanded + firm
Plum coloured
Airless
Often weigh >1kg

39
Q

What is the general clinical presentation of bacterial pneumonia?

A

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

  • Bronchopneumonia (most common)
  • Lobar pneumonia
  • Abscess formation
  • Granulomatous inflammation
40
Q

What are features of bronchopneumonia?

A

Compromised host defense - Elderly

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

Pathology - Patchy bronchial + peribronchial distribution, often lower lobes

41
Q

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

A

Peribronchial distribution

Acute inflammation surrounding airways and within alveoli

42
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.

43
Q

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

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
44
Q

What are 5 complications associated with infectious respiratory disease?

A

Abscess formation

Pleuritis and pleural effusion

Infected pleural effusion (EMPYEMA)

Fibrous scarring

Septicaemia

45
Q

In which patients are abscesses a more common complication of infectious respiratory disease? Give an example

A

Immune compromised
Alcoholics a/w Klebsiella abscess

46
Q

Define emphysema.

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

47
Q

How does the pattern of damage differ in different causes of emphysema?

A

Smoking: Loss centred on bronchiole- CENTRILOLOBULAR

Alpha-1-antitrypsin deficiency: Diffuse loss of alveolae- PANACINAR

48
Q

What are 3 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 HTN + cor pulmonale
49
Q

What is a granuolma?

A

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

Necrotising or non necrotising.

50
Q

What are 5 causes of granulomatous disease?

A
  • Infection: ?TB, fungi, parasites
  • Sarcoidosis
  • Foreign body: aspiration or IVDU
  • Drugs
  • Occupational lung disease
51
Q

Define fibrosing lung disease.

A

Chronic + progressive fibrosing diseases of lung

52
Q

What are 3 important types of fibrosing lung disease?

A

Idiopathic pulmonary fibrosis aka. Cryptogenic fibrosing alveolitis

Extrinsic allergic alveolitis aka Farmers lung

Industrial lung diseases aka Pneumoconiosis

53
Q

What is idiopathic pulmonary fibrosis? What symptoms does it cause? Describe the epidemiology

A

Aka. cryptogenic fibrosing alveolitis

Chronic SOB + cough

> 50y
M > F

54
Q

How is idiopathic pulmonary fibrosis diagnosed? What is seen?

A

Dx: HRCT +/- biopsy

  • Macro: Basal + peripheral fibrosis + cyst formation
  • Micro: Interstitial fibrosis at varying stages
55
Q

What is the prognosis in idiopathic pulmonary fibrosis?

A

Progressive disease

> 50% die in 2-3y

56
Q

What is pulmonary thromboembolism?

A

Occlusion of pulmonary artery by embolisation of peripheral thrombus to lung.

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

57
Q

What are common site formations of thromboembolism?

A

Deep veins of leg (95%):
* Present with swelling of leg (DVT)
* Present with Sx of spread to lung (PE)

58
Q

What promotes thrombus formation?

A

Virchows triad
1. Factors promoting blood STASIS: obesity, immobility, cardiac failure, pregnancy, abdo masses

  1. DAMAGE to ENDOTHELIUM: local trauma, cannulation
  2. Increased COAGULATION: malignancy, haemoconcentration, polycythaemia, DIC, OCP, cannulation, anti-phospholipid syndrome
59
Q

What are small emboli? What do they cause?

A

Small peripheral pulmonary arterial occlusion

Cause local haemorrhagic infarct

Repeated emboli cause increasing occlusion of pulmonary vascular bed + pulmonary HTN.

Present with pleuritic chest pain, acute SOB +/- chronic progressive SOB

60
Q

What are large emboli? What do they cause?

A

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

Sudden death, acute right HF, or cardiovascular shock occurs in 5% of cases when >60% of pulmonary bed is occluded.

If patient survives, the embolus usually resolves.

30% develop 2nd or more emboli.

61
Q

What are 6 non-thrombotic emboli?

A

Bone marrow

Amniotic fluid

Trophoblast

Tumour

Foreign body

Air

62
Q

What is pulmonary hypertension?

A

Mean pulmonary arterial pressure > 25mmHg at rest

(Normal pulmonary circulation is low pressure ~12mmHg)

63
Q

What are 9 precapillary causes of pulmonary hypertension?

A

Vasoconstrictive:
* Chronic hypoxia
* Hyperkinetic congenital heart disease
* Unknown (Primary pulmonary HTN)
* Chronic liver disease
* HIV infection
* Connective tissue disease

Embolic:
* Thromboembolic
* Parasitic (schistosomal)
* Tumour emboli

64
Q

What are capillary causes of pulmonary hyptertension?

A

Widespread pulmonary fibrosis: mechanical vascular distortion + chronic hypoxia

65
Q

What are 2 post-capillary causes of pulmonary hypertension?

A

Veno-occlusive disease

Left-sided heart disease

66
Q

What are 2 features of benign lung tumours? Give an example

A

Do not metastasise

Can cause local complications e.g. Airway obstruction

e.g. Chondroma

67
Q

What are 2 features of malignant lung tumours?

A

Potential to metastasise, but variable clinical behaviour from indolent to aggressive.

Commonest are epithelial tumours

68
Q

Which are the main types of malignant lung tumour?

A

NON-small cell carcinoma:
* Squamous cell carcinoma (30%)
* Adenocarcinoma (30%)
* Large cell carcinoma (20%)

SMALL cell carcinoma:
* Small cell carcinoma (20%)

69
Q

Which lung cancers does smoking have the strongest association with?

A

Squamous cell carcinoma
+
Small cell carcinoma.

70
Q

What are 5 other risk factors for lung cancer?

A

25% of lung cancers worldwide is in non-smokers.

Asbestos exposure

Radiation (Radon, theraputic radiation, miners)

Air pollution

Other: Heavy metals (Chromates, arsenic, nickel)

Genetics: Familial lung cancers rare.

71
Q

Describe the pathway of development of squamous cell carcinoma

A

Normal epithelium
Hyperplasia
Squamous metaplasia
Dysplasia
Carcinoma in situ
Invasive carcinoma

72
Q

What are features of invasive squamous cell carcinoma?
Frequency
Risk factors
Site
Behaviour

A

Freq: 35% of pulmonary carcinoma.

Risk factor: Closely a/w smoking

Site: Traditionally CENTRAL arising from bronchial epithelium (but increasing number of peripheral SCCs)

Behaviour: Local spread, metastasise late.

73
Q

What is the pathway of development of adenocarcinoma?

A

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

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

74
Q

What are features of invasive adenocarcinoma?
Frequency
Risk factors
Site
Behaviour

A

Freq: Increasing incidence- 27% pulmonary carcinomas.

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

Site: Peripheral + more often multicentric

Behaviour: Extrathoracic metastases common + early.

75
Q

Describe the histology of invasive adenocarcinoma

A

Evidence of glandular differentiation.
Variety of patterns relate to underlying molecular abnormalities + prognosis.

76
Q

What are large cell carcinomas?

A

Poorly differentiated tumours composed of large cells.

Peripheral or central

10% of tumours.

No histological evidence of glandular or squamous differentiation- on EM may show glandular, squamous or NE differentiation= probs v poorly differentiated adeno/ squamous cell carcinomas.

Poorer prognosis.

77
Q

What are small cell carcinomas?
Frequency
Risk factors
Site
Behaviour

A

Freq: 20% tumours.

Risk factor: Very close a/w smoking.

Site: Often central near bronchi.

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

78
Q

Describe the histology and common mutations seen in small cell carcinoma

A

Small poorly differentiated cells

p53 + RB1 mutations common.

79
Q

Which lung cancer has the worst prognosis?

A

Small cell carcinoma

80
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 rarely undertaken as most have spread at time of dx)

81
Q

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

A

Early Stage 1: 60% 5y survival

Late Stage 4: 5% 5y survival 20-30% have early stage tumours suitable for surgical resection.
Less chemosensitive.

82
Q

How is non-small cell carcinoma sub-typed? Why is this important?

A

Adenocarcinoma: target mutations- EFGR, ALK translocation, Ros1 translocation

SCC: may develop fatal haemorrhage with new chemotherapeutic drugs e.g. Bevacizumab

83
Q

What are common clinical presentations for lung cancer?

A

Asymptomatic:
* Incidental finding of mass on CXR

Symptomatic:
* Cough
* Haemoptysis
* Recurrent infections
* Other: Weight loss, metastasis

84
Q

What is cytology and how can pathologists study this?

A

Looking at cells.

  • Sputum
  • Bronchial washings + brushings
  • Pleural fluid
  • Endoscopic fine needle aspiration of tumour/ enlarged LNs
85
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 + LN biopsy: For staging
  • Open biopsy at time of surgery if lesion not accessible otherwise: Frozen section
  • Resection specimen: Confirm excision + staging
86
Q

List 10 causes of diffuse alveolar damage in adults

A

Infection (local or generalised sepsis)
Aspiration
Trauma
Inhaled irritant gases
Shock
Blood transfusion
DIC
Drug OD
Pancreatitis
Idiopathic

87
Q

I’ve been smoking for 30y, stopping now is not going to reduce my risk of lung cancer. True or false.

A

FALSE
Even at older age, stopping smoking significantly reduces risk of lung cancer

YR5 Histopathology (27 decks)

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