P10 - Pulmonary pathology Flashcards

1
Q

What are clinical presentations of lung disease?

A
  • Cough, wheeze
  • Breathlessness (dyspnoea)
  • Chest pain (often due to pleural disease)
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2
Q

Are the lungs themselves sensitive to pain?

A

No- but the chest wall is

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3
Q

What are the 2 functional classifications of lung disease?

A
  • Obstructive

- Restrictive

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4
Q

Describe obstructive lung disease.

A

Normal volume but difficulty getting air out (asthma)

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5
Q

Describe restrictive lung disease.

A

Decreased lung volumes (scarring /fibrosis in lungs)

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6
Q

Name 5 ways of investigation of a patient with lung disease.

A
  • Chest x-ray +/- CT scan
  • Hb, white cell count etc
  • Arterial blood gases (pO2, pCO2, pH)
  • Physiology (spirometry, pulmonary function tests)
  • Bronchoscopy +/- biopsy and lavage
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7
Q

what is the lungs function?

A

to facilitate transfer of O2 to blood and CO2 in the other direction

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8
Q

What is type 1 respiratory failure?

A

decreased arterial pO2

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9
Q

What is type II respiratory failure?

A

decreased arterial pO2 plus increased arterial pCO2

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10
Q

which is worse of the two respiratory failures?

A

Type II - pulmonary function is terminal

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11
Q

What does decreased Pa O2 lead to?

A

• Dyspnoea and increased respiratory rate
• Pulmonary vasoconstriction (and pulmonary
hypertension)
• Eventually right sided heart failure

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12
Q

What can cause airway narrowing /obstruction?

A
  • Muscle spasm
  • Mucosal oedema (inflammatory or otherwise
  • Airway collapse due to loss of support
  • (Localised obstruction due to tumour or foreign body)
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13
Q

What are the main categories of obstructive disease?

A
  • Asthma

* Chronic obstructive pulmonary disease (COPD/COAD/COLD)

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14
Q

What is bronchial asthma?

A

A chronic inflammatory disorder characterised by hyperreactive airways leading to episodic reversible bronchoconstriction

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15
Q

What is extrinsic asthma?

A

response to inhaled antigen

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16
Q

What is intrinsic asthma?

A

non-immune mechanisms (cold, exercise, aspirin)

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17
Q

What is type I hypersensitivity ?

A

Allergen binds to IgE on surface of mast cells

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18
Q

what effects does type 1 hypersensitivity have?

A

• Degranulation (histamine)
– muscle spasm
– inflammatory cell influx (eosinophils)
– mucosal inflammation/oedema
• Inflammatory infiltrate tends to chronicity

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19
Q

Name the types of pathology.

A
  • Narrowed oedematous airways
  • Mucus plugs
  • Inflammatory cells (lymphocytes, plasma cells, eosinophils)
  • Epithelial cell damage
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20
Q

What is mucosal oedema?

A

airways narrowed and blocked by mucous

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21
Q

Name 2 types of chronic obstructive disease.

A
  • Chronic bronchitis

* Emphysema

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22
Q

what do symptomatic patients have?

A

Often have both chronic bronchitis and emphysema

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23
Q

What is the epidemiology of COPD?

A
  • Smoking
  • Atmospheric pollution
  • Genetic factors
24
Q

what is the epidemiology definition of chronic bronchitis?

A

Cough productive of sputum on most days for 3 months of at least 2 successive years

25
Q

what does chronic bronchitis not imply?

A

airway inflammation

26
Q

What is emphysema?

A

• Increase beyond the normal in the size of the airspaces distal to the terminal bronchiole
• Without fibrosis
-The gas-exchanging compartment of the lung

27
Q

What is emphysema due to?

A

“Dilatation” is due to loss of alveolar walls (tissue destruction)
• Appears as “holes” in the lung tissue

28
Q

Discuss the diagnosis and treatment of emphysema.

A

• Difficult to diagnose in life (apart from in
extremis)
• Radiology (CT) can show changes in lung
density
• Correlation with function known from autopsy studies

29
Q

what is panacinar emphysema?

A

Tissue destructtion-extreme -big dilated airspaces, loss of tissue between gives illusion of dilation

30
Q

what do emphysema impair?

A

respiratory function

31
Q

How does emphysema impairs respiratory function?

A
  • Diminished alveolar surface area for gas exchange

* Loss of elastic recoil and support of small airways leading to tendency to collapse with obstruction

32
Q

What causes restrictive lung disease?

A
  • Decreased lung volumes due to scarring +/- inflammation in the alveolar walls
  • Many causes (idiopathic pulmonary fibrosis, sarcoidosis, farmer’s lung, asbestosis)
33
Q

Name 3 pulmonary infections.

A
  • Pneumonia
  • Chronic infection – abscess/bronchiectasis
  • Tuberculosis
34
Q

what is pneumonia?

A

Infection involving the distal airspaces usually with inflammatory exudation (“localised oedema”)
-fluid filled spaces lead to consolidation

35
Q

what is bronchopneumonia?

A

Common in older people -after flu - common terminal cause of death

36
Q

what is the clinical context of bronchopneumonia?

A
  • COPD
  • Cardiac failure (elderly)
  • Complication of viral infection (influenza)
  • Aspiration of gastric contents
37
Q

Name 4 complications of pneumonia.

A
  • Scarring
  • Abscess
  • Bronchiectasis
  • Empyema (pus in the pleural cavity)
38
Q

Describe lung abscess.

A
  • Localised collection of pus •Tumour-like

* Chronic malaise and fever •Context - aspiration

39
Q

what is tuberculosis?

A
  • Mycobacterial infection

* Chronic infection described in many body sites – lung, gut, kidneys, lymph nodes, skin

40
Q

what is tuberculosis pathology characterised by?

A

delayed (type IV) hypersensitivity (granulomas with necrosis)

41
Q

what are the 2 types of lung neoplasm?

A
  • Primary

- Metastatic

42
Q

What are the 2 types of primary lung neoplasms.

A

– benign (rare)

– malignant (very common)

43
Q

What is metastatic?

A

coming from somewhere else in the body

44
Q

what is the commonest cause of cancer death in men?

A

33% in men

45
Q

what is the mortality rate 1 year after diagnosis?

46
Q

What does tobacco smoke contain?

A
  • polycyclic hydrocarbons
  • aromatic amines
  • phenols
  • nickel
  • cyanates
47
Q

What percentage of smokers die of lung cancer and what do they also suffer from?

A
  • 20% of smokers die of lung cancer

- (also suffer laryngeal, cervical, bladder, mouth, oesophageal, colon cancer)

48
Q

What is the clinical presentation of a primary neoplasm?

A

Local effects:

  • obstruction of airway (pneumonia)
  • invasion of chest wall (pain)
  • ulceration (haemoptysis
49
Q

What is the clinical presentation of metastases?

A

– nodes
– bones
– liver
– brain

50
Q

How many common smoking -associated lung tumours are there (heterogenous)?

A
4:
– adenocarcinoma (35%)
– squamous carcinoma (30%)
– small cell carcinoma (25%)
– large cell carcinoma (10%)
51
Q

what other classification of lung tumours are there?

A
  • Neuroendocrine tumours

* Bronchial gland tumours

52
Q

what is different about different type of tumours?

53
Q

what is the most simple classification of lung cancer?

A
  • Small cell lung cancer (SCLC)

- Non-small cell lung cancer (NSCLC)

54
Q

What is the treatment of small cell lung cancer?

A
  • Small cell known to be chemosensitive but with rapidly emerging resistance
  • Surgery the treatment of choice in other types. “Non-small cell” regimens have also been developed in chemotherapy/radiotherapy
55
Q

What are new development in chemotherapy?

A
  • Differing NSCLC regimens for squamous cell and adenocarcinoma (e.g. pemetrexed contraindicated in squamous carcinoma)
  • Molecular abnormalities, particularly in adenocarcinoma, can define susceptibility to new targeted drug treatments
56
Q

Describe the molecular pathology and targeted treatment (epithelial growth signalling in lung epithelium.

A
  • Specific point mutations render the EGFR gene active in the absence of ligand (epidermal growth factor) binding
  • These mutations can be identified in DNA extracted from biopsy or cytology samples
  • Mutation seen almost exclusively in adenocarcinoma (esp. non-smokers and in Asian populations)
  • These tumours respond to tyrosine kinase inhibitors (erlotinib)
  • EML4-ALK fusion oncogene also identifies a target for specific drug treatment (crizotinib)