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HistoPath > Respiratory > Flashcards

Respiratory Flashcards

1
Q
  1. Define asthma.
A

Chronic inflammatory airway disorder with recurrent reversible episodes of widespread narrowing of the airways

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2
Q
  1. List some non-atopic triggers of asthma.
A

Air pollution
Occupational
Exercise

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3
Q
  1. Describe the pathogenesis of asthma?
A

Immediate phase – mast cells degranulate when they come into contact with antigen. Inflammatory mediators are released which causes increased vascular permeability= recruitment of eosinophils and mast cells and bronchospasm
Late phase – tissue damage = increase mucus production and muscle hypertrophy

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4
Q
  1. List some acute changes seen in asthma.
A

Bronchospasm
Oedema
Hyperaemia
Inflammation

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5
Q
  1. List some chronic changes seen in asthma.
A

Muscular hypertrophy
Airway narrowing
Mucus plugging

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6
Q
  1. Describe the main histological features of asthma.
A

Lots of eosinophils and mast cells
Goblet cell hyperplasia
Mucus plugs within airways
Thickening of bronchial smooth muscle and dilatation of blood vessels

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7
Q
  1. Define chronic bronchitis.
A

Chronic cough productive of sputum presents for most days for at least 3 months over 2 consecutive years

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8
Q
  1. List some histological features of chronic bronchitis.
A

Dilated airways
Mucus gland hyperplasia
Goblet cell hyperplasia
Mild inflammation

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9
Q
  1. List some complications of chronic bronchitis.
A

Recurrent infections
Chronic respiratory failure
Pulmonary hypertension and right heart failure (cor pulmonale)
Increased risk of lung cancer (independent of smoking)

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10
Q
  1. Define bronchiectasis.
A

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

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11
Q
  1. Which part of the lungs tends to be affected most frequently in idiopathic bronchiectasis?
A

Lower lobe

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12
Q
  1. List some causes of bronchiectasis.
A 
Infection (MOST COMMON)
•	Post-infectious (e.g. CF)
•	Abnormal host defence (e.g. chemotherapy, immunodeficiency)
•	Ciliary dyskinesia
Obstruction 
Post-inflammatory (aspiration)
Interstitial disease (e.g. sarcoidosis)
Asthma
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13
Q
  1. List some complications of bronchiectasis.
A

Recurrent infections
Haemoptysis
Pulmonary hypertension and right heart failure
Amyloidosis

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14
Q
  1. Where is the CFTR gene found?
A

7q3

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15
Q
  1. What is the most common mutation associated with CF?
A

Delta F508

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16
Q
  1. List some clinical manifestations of CF.
A 
GI – meconium ileus, malabsorption 
Pancreas – pancreatitis 
Liver – cirrhosis 
Male reproductive system – infertility 
Recurrent chest infections
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17
Q
  1. What is pulmonary oedema?
A

Accumulation of fluid in the alveolar spaces either due to leaky capillaries or back pressure from a failing left ventricle
This leads to poor gas exchange

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18
Q
  1. List some causes of pulmonary oedema.
A

Left heart failure
Alveolar injury (e.g. drugs)
Neurogenic following head trauma
High altitude

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19
Q
  1. What is diffuse alveolar disease?
A

Acute damage to alveolar epithelium/endothelium leading to exudative inflammatory rection

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20
Q
  1. Describe the appearance of the lungs on post-mortem examination in a patient who died from ARDS.
A

Plum-coloured
Heavy
Airless

21
Q
  1. Outline the pathophysiology of ARDS.
A

Capillary congestion
Exudative phase – the lungs become congested and leaky
Hyaline membranes – form when serum protein that is leaked out of vessels end up lining the alveoli
Organising phase – organisation of the exudates to form granulation tissue sitting within the alveolar spaces

22
Q
  1. List some causes of hospital-acquired bacterial pneumonia.
A

Gram-negatives (Klebsiella, Pseudomonas)

23
Q
  1. Which types of bacteria tend to be implicated in aspiration pneumonia?
A

Mixture of aerobic and anaerobic

24
Q
  1. What is bronchopneumonia?
A

Infection is centred around the airways
Tends to be associated with compromised host defence (mainly the elderly) and is caused by low virulence organisms (e.g. Staphylococcus, Haemophilus, Pneumococcus)
It will show patchy bronchial and peribronchial distribution often involving the lower lobes

25
Q
  1. What is lobar pneumonia?
A

Infection is focused in a lobe of the lung
90-95% caused by S. pneumoniae
Widespread fibrinosuppurative consolidation

26
Q
  1. What are the histopathological stages of lobar pneumonia?
A

Stage 1: congestion (hyperaemia and intra-alveolar fluid)
Stage 2: red hepatisation (hyperaemia, intra-alveolar neutrophils)
Stage 3: grey hepatisation (intra-alveolar connective tissue)
Stage 4: resolution (restoration of normal tissue architecture)

27
Q
  1. List some complications of pneumonia.
A 
Abscess formation 
Pleural effusion 
Empyema
Fibrous scarring 
Septicaemia
28
Q
  1. What is a granuloma?
A

Collection of macrophages and multi-nucleate giant cells

29
Q
  1. Define emphysema.
A

Permanent loss of alveolar parenchyma distal to the terminal bronchiole due to protease activation

30
Q
  1. List some causes of alveolar damage that can lead to emphysema.
A

Smoking
Alpha-1 antitrypsin deficiency
Rare: cadmium exposure, IVDU, connective tissue disorder

31
Q
  1. Describe how the pattern of alveolar damage is different with smoking compared to alpha-1 antitrypsin deficiency.
A

Smoking – centrilobular damage – loss centred around bronchioles
Alpha-1 antitrypsin deficiency – panacinar (throughout the lungs)

32
Q
  1. List some complications of emphysema.
A

Bullae (can rupture to cause pneumothorax)
Respiratory failure
Pulmonary hypertension and right heart failure

33
Q
  1. What is a long term consequence of repeated small pulmonary emboli?
A

Increase occlusion of pulmonary vascular bed = Pulmonary hypertension

34
Q
  1. List some types of non-thrombotic emboli.
A 
Bone marrow 
Amniotic fluid 
Trophoblast 
Tumour 
Foreign body 
Air 
Fat
35
Q
  1. What are some causes of pulmonary hypertension?
A 
Pre-capillary
	Vasoconstrictive - chronic hypoxia
	Embolic – thromboelmbolism 
Capillary
	Widespread pulmonary fibrosis
Post capillary
	Veno-occlusive disease
Left sided heart failure
36
Q
  1. What are the main types of lung cancer?
A 
Non-small cell carcinoma
•	Squamous cell carcinoma (30%)
•	Adenocarcinoma (30%)
•	Large cell carcinoma (20%)
Small cell carcinoma (20%)
37
Q
  1. Which types of lung cancer are most strongly associated with smoking?
A

Squamous cell carcinoma

Small cell carcinoma

38
Q
  1. Which type of lung cancer tends to occur in non-smokers?
A

Adenocarcinoma

39
Q
  1. Describe the sequence of histological changes that results in lung cancer.
A

Metaplasia  dysplasia  carcinoma in situ  invasive carcinoma

40
Q
  1. What feature of squamous epithelium makes it vulnerable to undergoing malignant changes?
A

It does not have cilia leading to a build-up of mucus

Within the mucus carcinogens accumulate

41
Q
  1. Where do squamous cell carcinomas and adenocarcinomas tend to arise?
A

Squamous cell
Centrally – arising from the bronchial epithelium
Adeno - Peripherally – around the terminal airways

42
Q
  1. Which mutations are associated with adenocarcinoma in smokers AND non smokers?
A

SMOKERS
Kras
Issues with DNA methylation
P53

NON SMOKERS
EGFR

43
Q
  1. Where does small cell lung cancer tend to arise?
A

Central – around the bronchi

44
Q
  1. What is large cell carcinoma of the lung?
A

Poorly differentiated tumour composed of large cells
There is no evidence of squamous or glandular differentiation
It has a poor prognosis

45
Q
  1. List some common mutations seen in small cell lung cancer.
A

P53

RB1

46
Q
  1. What is the difference in the chemosensitivity of small cell lung cancer and non-small cell lung cancer?
A

Small cell – sensitive

Non-small cell – not very chemosensitive

47
Q
  1. Which molecular changes are important to test for in adenocarcinoma?
A

EGFR (responder or resistance)
ALK translocation
Ros1 translocation

48
Q
  1. What is cancer of the pleura?
A

Mesothelioma

HistoPath (7 decks)

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