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4 - Y5 a Path lectures 2021/22 > ** Histopath 7: Respiratory Pathology > Flashcards

** Histopath 7: Respiratory Pathology Flashcards

1
Q

What does this show?

A

normal lung

  • The airways are lined by ciliated respiratory epithelium (responsible for moving up mucus and pathogens)
  • Alveoli are characterised by very fine capillaries lined by type 1 pneumocytes (short diffusion distance)
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2
Q

What does this show?

A

Pulmonary Oedema

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3
Q

What is pulmonary oedema? What are its causes?

A
  • Often associated with heart failure (acute or chronic)
  • VERY COMMON cause of acute and chronic respiratory failure
  • Common finding at post-mortem
  • Defined by the accumulation of fluid in the alveolar spaces either due to leaky capillaries or backpressure from a failing left ventricle
  • This leads to poor gas exchange
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4
Q

What are the causes and pathology of pulmonary oedema?

A
  • Causes
    • Left heart failure
    • Alveolar injury (drug, inhalation, pancreatitis)
    • Neurogenic following head injury
    • High altitude
  • Pathology
    • Heavy watery lungs
    • Intra-alveolar fluid on histology
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5
Q

What does this CXR show?

A

Acute Lung Injury Pattern/Diffuse Alveolar Damage

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6
Q

What can Acute Lung Injury Pattern/Diffuse Alveolar Damage cause?

A
  • Important cause of RAPID onset respiratory failure
  • ADULTS - Acute Respiratory Distress Syndrome
  • NEONATES - Hyaline Membrane Disease of the Newborn
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7
Q

What are the causes of ARDS?

A

Causes

  • Infection
  • Aspiration
  • Trauma
  • Inhaled irritant gases
  • Shock
  • Blood transfusion
  • DIC
  • Drug overdose
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8
Q

What is NEONATES - Hyaline Membrane Disease of the Newborn?

A
  • Insufficient surfactant production
  • Premature babies
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9
Q

What is Acute Lung Injury Pattern/Diffuse Alveolar Damage?

A
  • This is acute respiratory failure NOT due to pulmonary oedema
  • It is caused by acute damage to the endothelium and/or alveolar epithelium
  • Basic pathology is the same in all cases: DIFFUSE ALVEOLAR DAMAGE
  • The lungs are expanded and firm
  • On post-mortem examination, the lungs are plum-coloured, heavy (> 1 kg) and airless
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10
Q

What is the pathophysiology of Acute Lung Injury Pattern/Diffuse Alveolar Damage?

A
  • The lungs become congested and then they become leaky (exudative phase)
  • They will then develop hyaline membranes (this is serum protein that has leaked out and ended up lining the alveolar spaces)
  • Eventually, you get organisation of the exudates to form granulation tissue sitting within the alveolar spaces (organising pneumonia)
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11
Q

What is the prognosis of Prognosis of Diffuse Alveolar Damage?

A
  • Death (40%)
  • Superimposed infection
  • Resolution (in some) - lung function returns to normal
  • Residual fibrosis - leads to chronic respiratory impairment
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12
Q

What is asthma?

A
  • DEFINITION: chronic inflammatory airway disorder with recurrent episodes of widespread narrowing of the airways that changes in severity over short periods of time.
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13
Q

What is status asthmaticus?

A
  • In a SEVERE attack, patients develop status asthmaticus
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14
Q

What are some non-atopic triggers of asthma?

A
  • Non-atopic triggers: air pollution, occupational, diet, physical exertion
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15
Q

What are the changes seen in asthma physiology-wise?

A
  • Acute Changes
    • Bronchospasm
    • Oedema
    • Hyperaemia
    • Inflammation
  • Chronic Change
    • Muscular hypertrophy
    • Airway narrowing
    • Mucus plugging

NOTE: once you’ve plugged a large airway, the distal lung will collapse

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16
Q

Describe the histological features of asthma

A
  • There are a lot of eosinophils and mast cells
  • You will also see goblet cell hyperplasia
  • Mucus plugs can be seen within the airway
  • The bronchial smooth muscle becomes thick and the blood vessels become dilated
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17
Q

What are the 2 types of COPD?

A
  • Chronic Bronchitis
  • Emphysema
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18
Q

What are the 2 types of COPD?

A
  • Chronic Bronchitis
  • Emphysema
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19
Q

What are the 2 types of COPD?

A
  • Chronic Bronchitis
  • Emphysema
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20
Q

What is COPD?

A

Very common cause of chronic respiratory failure

  • May present with acute exacerbations
  • 80% are smokers
  • Smoking causes inflammation leading to secondary damage to the airways and interstitium
  • There is a mix of airway and alveolar pathology (chronic bronchitis and emphysema), resulting in progressive airway obstruction
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21
Q

Which condition does this show?

A

chronic bronchitis

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22
Q

What is the definition of chronic bronchitis?

A
  • Defined as:
    • Chronic cough productive of sputum
    • Most days for at least 3 months over 2 consecutive years
  • Chronic injury to airways elicits reactive changes which predispose to further damage
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23
Q

Describe the pathology of chronic bronchitis

A
  • Dilated airways
  • Mucus gland hyperplasia
  • Goblet cell hyperplasia
  • Mild inflammation
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24
Q

What are the complications of chronic bronchitis?

A
  • Recurrent infections (most common cause of admission and death)
  • Chronic respiratory failure (with hypoxia and reduced exercise tolerance)
  • Chronic hypoxia results in pulmonary hypertension and right heart failure (cor pulmonale)
  • Increased risk of lung cancer (independent of smoking)
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25
Q

What does this show?

A
  • Emphysema
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26
Q

What is the definition of emphysema?

A

Defined as a permanent loss of the alveolar parenchyma distal to the terminal bronchiole

  • Damage to alveolar epithelium is secondary to inflammation, inflammation could be caused by:
    • Smoking
    • Alpha-1 antitrypsin deficiency
    • RARE: cadmium exposure, IVDU, connective tissue disorder
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27
Q

How does smoking cause emphysema?

A
  • Neutrophils and macrophages that are activated by smoking, will release proteases which degrade tissues
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28
Q

Describe the pathophysiology of emphysema?

A
  • Smoking tends to cause centrilobular damage to the alveolar tissue
  • Patients with alpha-1 antitrypsin deficiency tend to have damage throughout the lung (panacinar)
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29
Q

What are the complications of emphysema?

A
  • Bullae (large air spaces)
    • Can rupture and cause pneumothorax
  • Respiratory failure
  • Pulmonary hypertension and right heart failure
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30
Q

What does this show?

A

Bronchiectasis

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31
Q

What is the definition of bronchiectasis?

A
  • permanent abnormal dilation of the bronchi with inflammation and fibrosis extending into adjacent parenchyma
  • Varies in site depending on the cause (idiopathic often involves the lower lobe)
  • Leads to inflamed and scarred lungs with dilated airways
32
Q

What are the causes of bronchiectasis?

A
  • Infection (most common cause)
    • Post-infectious (cystic fibrosis)
    • Abnormal host defence (can be primary (e.g. hypogammaglobulinaemia) or secondary (e.g. chemotherapy))
  • Ciliary dyskinesia
  • Obstruction
  • Post-inflammatory (aspiration)
  • Secondary to bronchiolar disease and interstitial disease (e.g. sarcoidosis)
  • Systemic disease (connective tissue disorders)
  • Asthma
  • Congenital
33
Q

What are the complications of bronchiectasis?

A
  • Recurrent infections
  • Haemoptysis
  • Pulmonary hypertension and right sided heart failure
  • Amyloidosis
34
Q

How is cystic fibrosis inherited?

A
  • Autosomal recessive (approximately 1/20 are carriers)
  • Chromosome 7q3 = CFTR gene
    • Chloride ion transporter protein
    • 1400+ mutations
    • Delta F508 is the MOST COMMON mutation
  • → Abnormality leads to defective ion transport across cell membranes due to excessive resorption of water from secretions of exocrine glands
35
Q

Which organ systems does CF affect?

A
  • It is a generalised disorder of the exocrine glands resulting in abnormally thick mucus secretion - affects ALL organ systems
    • GI = meconium ileus, malabsorption
    • Pancreas = pancreatitis, malabsorption
    • Liver = cirrhosis
    • Male reproductive system = infertility
    • Lung
      • Involved in 90% of cases
      • Recurrent infections (S. pneumoniae, H. influenzae, P. aeruginosa and B. cepacia)
      • Manifestations
        • Haemoptysis
        • Pneumothorax
        • Chronic respiratory failure
        • Cor pulmonale
        • ABPA
        • Atelectasis
        • Bronchiectasis
36
Q

What is the life expectancy of CF?

A
  • Improved treatment means that most will survive 35-40 years
  • Lung transplantation will prolong survival
37
Q

What is the classification of bacterial pneumonia?

A
  • Community-Acquired
    • Streptococcus pneumoniae
    • Haemophilus influenzae
    • Mycoplasma
  • Hospital-Acquired
    • Gram-negatives (Klebsiella, Pseudomonas)
  • Aspiration
    • Mixed aerobic and anaerobic
38
Q

What are the main patterns of bacterial pneumonia?

A
  • There are a variety of PATTERNS of lung involvement depending on the organism and other co-factors:
    • Bronchopneumonia
    • Lobar pneumonia
39
Q

What is Bronchopneumonia?

A

Infection is centred around the airways

  • Compromised host defence (elderly)
  • Often LOW virulence organisms (Staphylococcus, Haemophilus, Streptococcus, Pneumococcus)
  • Patchy bronchial and peribronchial distribution often involving the lower lobes
  • There is acute inflammation surrounding airways and within alveoli
40
Q

What is Lobar pneumonia?

A
  • The infection is focused in a lobe of the lung
  • Infrequent because of antibiotics
  • 90-95% are S. pneumoniae
  • Widespread fibrinosuppurative consolidation
  • Histopathology
  1. Congestion (hyperaemia and intra-alveolar fluid)
  2. Red hepatisation (hyperaemia, intra-alveolar neutrophils)
  3. Grey hepatisation (intra-alveolar connective tissue)
  4. Resolution (restoration or normal tissue architecture)
  • Abscess formation
  • Granulomatous inflammation
41
Q

What are the complications of bacterial pneumonia?

A
  • Abscess formation
  • Pleuritis and pleural effusion
  • Infected pleural effusion (empyema)
  • Fibrous scarring
  • Septicaemia
42
Q

What is a granuloma?

A
  • A granuloma is a collection of macrophages and multi-nucleate giant cells
  • It can be necrotising or non-necrotising
  • Must think of TUBERCULOSIS + exclude
  • Other causes include fungi and parasites (travel history is important)
43
Q

What does this show?

A
  • Atypical Pneumonia
44
Q

Describe atypical pneumonia

A
  • Mycoplasma, viruses (e.g. CMV, influenza), Coxiella and Chlamydia
  • Interstitial inflammation (pneumonitis) without accumulation of intra-alveolar inflammatory cells
  • Chronic inflammatory cells within alveolar septa with oedema with or without viral inclusions
45
Q

What is Pulmonary Thromboembolism?

A
  • Occlusion of pulmonary artery by thromboembolus
  • Deep leg veins is a common site for clot formation (95%)
  • May present with a painful, swollen leg
  • Effect depends on the SIZE of the thrombus
46
Q

What is Virchow’s triad?

A
47
Q

How might a patient present with a small PTE?

A
  • Patients with small emboli may present with pleuritic chest pain or chronic progressive shortness of breath due to pulmonary hypertension
  • Repeated emboli cause increasing occlusion of the pulmonary vascular bed and pulmonary hypertension
48
Q

How might a patient present with a large PTE?

A
  • hypertension
  • Large emboli may occlude the main pulmonary trunk (saddle embolus)
  • This may present with sudden death, acute right heart failure or cardiogenic shock
  • 30% will develop a second embolus
49
Q

Name some non-thrombotic emboli

A
  • Bone marrow
  • Amniotic fluid
  • Trophoblast
  • Tumour
  • Foreign body
  • Air
  • Fat
50
Q

Which cell types do lung tumours arise from?

A
  • Tumours can arise from a variety of cell types (epithelial, mesenchymal and lymphoid)
  • Can arise in different sites
    • Airways (mainly squamous cell carcinoma)
    • Peripheral alveolar spaces (mainly adenocarcinoma)
    • Small cell carcinoma can arise either centrally or peripherally
    • Mesothelioma is a tumour of the pleura
51
Q

Describe benign lung tumours

A
  • Do NOT metastasise
  • Can cause local complications (e.g. obstruction)
  • Example: chondroma
52
Q

Describe and name the types of malignant lung tumours

A
  • Potential to metastasise
  • Most common are epithelial (90-95%)
  • Non-Small Cell Carcinoma
    • Squamous cell carcinoma (30%)
    • Adenocarcinoma (30%)
    • Large cell carcinoma (20%)
    • Small Cell Carcinoma (20%)
  • NOTE: incidence of lung cancer in men is dropping and in women is rising (because women took longer to quit smoking)
53
Q

What is the aetiology of lung tumours?

A
  • 25% of lung cancer in non-smokers is attributed to passive smoking
  • Smoke contains
    • Tumour initiators (polycyclic aromatic hydrocarbons)
    • Tumour promoters (nicotine)
    • Complete carcinogens (nickel, arsenic)
    • Strongest association with:
      • Squamous cell carcinoma
      • Small cell carcinoma
      • NOTE: adenocarcinoma is more common in non-smokers
    • Other Risk Factors
      • 25% of lung cancers are in non-smokers
      • Asbestos
      • Radiation (radon exposure)
      • Air pollution
      • Heavy metals
      • Genetics (familial lung cancers are rare)
      • Susceptibility genes
        • Chemical modification of carcinogens
        • Susceptibility to chromosomal damage
        • Nicotine addiction
54
Q

Describe the development process of a carcinoma

A
  • Multistep pathway includes:
    • Metaplasia
    • Dysplasia
    • Carcinoma in situ
    • Invasive carcinoma
    • Due to an accumulation of gene mutations
    • There are different pathways for different tumour types
55
Q

Describe SCC (lung)

A
  • Squamous epithelium is much more resilient but it does NOT have cilia
  • This leads to a build up of mucus
  • Within this mucus, you will get loads of carcinogens
  • This leads to more mutations
  • Invasive squamous carcinoma is responsible for about 35% of lung cancers
  • Closely associated with smoking
  • Traditionally centrally located arising from bronchial epithelium
  • Increasing incidence of peripheral squamous cell carcinomas (possibly because modern cigarette smoke can be inhaled more deeply)
  • Spreads locally
  • Metastasises late
56
Q

What does this show?

A

SCC (lung)

57
Q

Where does adenocarcinoma of the lung tend to arise?

A
  • Tend to arise in the periphery of the lung (often around the terminal airways)
58
Q

What is the common precursor lesion for adenocarcinoma of the lung?

A
  • Precursor lesion: atypical adenomatous hyperplasia
  • This is proliferation of atypical cells lining the alveolar walls
  • This will increase in size and eventually become invasive
59
Q

Name the Molecular Pathways in the Development of Adenocarcinoma

A
  • In smokers, the main mutations are K ras, issues with DNA methylation and p53
  • In non-smokers, EGFR mutations are very important (these are drug targets)
60
Q

Describe the epidemiology of adenocarcinoma of the lung

A
  • Incidence is INCREASING
  • More common in females, far East and non-smokers
  • Tends to occur peripherally and are often multi-centric (lots of little tumours at different stages of development)
  • Extra-thoracic metastases are COMMON and occur EARLY (80% present with metastases)
  • Histology will show evidence of glandular differentiation
61
Q

What does this show

A

cytology of adenocarcinoma of the lung

62
Q

What does this show?

A

Large Cell Carcinoma of the lung

63
Q

Describe the histopathology of large cell carcinoma of the lung

A
  • Poorly differentiated tumours composed of large cells
  • There is NO histological evidence of glandular or squamous differentiation
    • NOTE: on electron microscopy, there may be some evidence of glandular, squamous or neuroendocrine differentiation
64
Q

What is the prognosis of large cell carcinoma of the lung vs other types?

A
  • POORER prognosis
65
Q

What does this show?

A

Small cell carcinoma of the lung

66
Q

Describe small cell carcinoma of the lung

A
  • 20% of lung tumours
  • Very close association with SMOKING
  • Often CENTRAL and near the bronchi
  • 80% will present with advanced disease
  • Very chemosensitive but VERY POOR PROGNOSIS
  • May cause paraneoplastic syndromes
67
Q

Describe the histology of small cell carcinoma

A
  • Small poorly differentiated cells
  • Common mutations
    • P53
    • RB1
68
Q

What does this show?

A
69
Q

What is the survival for small cell cancer?

A
  • Survival 2-4 months if untreated
  • Survival 10-20 months on current treatment
  • Chemoradiotherapy is the mainstay (surgery is rarely performed because most cases would have spread by the time of diagnosis)
70
Q

What is the survival for non-small cell lung cancer?

A
  • Early stage 1 tumours have 60% 5-year survival
  • LESS chemosensitive
71
Q

Why are molecular changes important to know in adenocarcinoma? Which are these?

A
  • Molecular changes are important for adenocarcinoma because they can be targeted using specific therapies
  • Main molecular changes:
    • EGFR mutation (responder or resistance)
    • ALK translocation
    • Ros1 translocation
72
Q

Why is it important to know the type of lung cancer?

A
  • It is important to know the type of cancer because, for example, in some patients with squamous cell carcinoma, they can develop fatal haemorrhage with some new chemotherapeutic drugs (bevacizumab)
73
Q

What is the role of the pathologist in lung cancer?

A
74
Q

What are the Tx types for lung cancer?

A
  • Curative
    • Surgery +/- radical radiotherapy +/- immunemodulatory therapy
  • Palliative
    • Chemoradiotherapy, immunemodulatory, targeted therapy
75
Q

What does this show?

A
76
Q

Describe mesothelioma

A
  • Malignant tumour of the pleura
  • < 1% of cancer deaths but increasing incidence with a peak predicted in around 2010-2020
  • Associated with asbestos exposure
    • There is a long lag (tumour may develop decades after exposure)
    • More common in males
    • 50-70 years
  • Essentially FATAL
  • Medicolegal implications because of compensation
  • POOR prognosis
  • Several histological types

4 - Y5 a Path lectures 2021/22 (37 decks)

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