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

** Histopath 7: Respiratory Pathology Flashcards

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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
What does this show?
* **Emphysema**
26
What is the definition of emphysema?
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
27
How does smoking cause emphysema?
* Neutrophils and macrophages that are activated by smoking, will release proteases which degrade tissues
28
Describe the pathophysiology of emphysema?
* Smoking tends to cause **centrilobular** damage to the alveolar tissue * Patients with alpha-1 antitrypsin deficiency tend to have damage _throughout_ the lung (**panacinar**)
29
What are the complications of emphysema?
* Bullae (large air spaces) * Can rupture and cause pneumothorax * Respiratory failure * Pulmonary hypertension and right heart failure
30
What does this show?
**Bronchiectasis**
31
What is the definition of bronchiectasis?
* 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
What are the causes of bronchiectasis?
* **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
What are the complications of bronchiectasis?
* Recurrent infections * Haemoptysis * Pulmonary hypertension and right sided heart failure * Amyloidosis
34
How is cystic fibrosis inherited?
* 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
Which organ systems does CF affect?
* 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
What is the life expectancy of CF?
* Improved treatment means that most will survive 35-40 years * **Lung transplantation** will prolong survival
37
What is the classification of bacterial pneumonia?
* **Community-Acquired** * *Streptococcus pneumoniae* * *Haemophilus influenzae* * *Mycoplasma* * **Hospital-Acquired** * Gram-negatives (*Klebsiella*, *Pseudomonas*) * **Aspiration** * Mixed aerobic and anaerobic
38
What are the main patterns of bacterial pneumonia?
* There are a variety of _PATTERNS of lung involvement_ depending on the organism and other co-factors: * **Bronchopneumonia** * **Lobar pneumonia**
39
What is **Bronchopneumonia?**
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
What is **Lobar pneumonia?**
* 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
What are the complications of bacterial pneumonia?
* Abscess formation * Pleuritis and pleural effusion * Infected pleural effusion (empyema) * Fibrous scarring * Septicaemia
42
What is a granuloma?
* 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
What does this show?
* **Atypical Pneumonia**
44
Describe atypical pneumonia
* 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
What is **Pulmonary Thromboembolism?**
* 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
What is Virchow's triad?
47
How might a patient present with a small PTE?
* 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
How might a patient present with a large PTE?
* 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
Name some non-thrombotic emboli
* Bone marrow * Amniotic fluid * Trophoblast * Tumour * Foreign body * Air * Fat
50
Which cell types do lung tumours arise from?
* 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
Describe benign lung tumours
* Do _NOT_ metastasise * Can cause local complications (e.g. obstruction) * Example: chondroma
52
Describe and name the types of malignant lung tumours
* 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
What is the aetiology of lung tumours?
* 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
Describe the development process of a carcinoma
* 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
Describe SCC (lung)
* 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
What does this show?
SCC (lung)
57
Where does adenocarcinoma of the lung tend to arise?
* Tend to arise in the **periphery** of the lung (often around the _terminal airways_)
58
What is the common precursor lesion for adenocarcinoma of the lung?
* 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
Name the **Molecular Pathways in the Development of Adenocarcinoma**
* 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
Describe the epidemiology of adenocarcinoma of the lung
* 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
What does this show
cytology of adenocarcinoma of the lung
62
What does this show?
**Large Cell Carcinoma** of the lung
63
Describe the histopathology of large cell carcinoma of the lung
* _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
What is the prognosis of large cell carcinoma of the lung vs other types?
* **POORER** prognosis
65
What does this show?
Small cell carcinoma of the lung
66
Describe small cell carcinoma of the lung
* 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
Describe the histology of small cell carcinoma
* Small poorly differentiated cells * Common mutations * P53 * RB1
68
What does this show?
69
What is the survival for small cell cancer?
* 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
What is the survival for non-small cell lung cancer?
* Early stage 1 tumours have 60% 5-year survival * _LESS_ chemosensitive
71
Why are molecular changes important to know in adenocarcinoma? Which are these?
* 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
Why is it important to know the type of lung cancer?
* 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
What is the role of the pathologist in lung cancer?
74
What are the Tx types for lung cancer?
* **Curative** * Surgery +/- radical radiotherapy +/- immunemodulatory therapy * **Palliative** * Chemoradiotherapy, immunemodulatory, targeted therapy
75
What does this show?
76
Describe mesothelioma
* 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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