Lectures Flashcards

1
Q

What is Sarcoidosis

A

Granulomatous disease affecting mainly the lungs, but also lymph nodes in a greater frequency

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2
Q

What is Kveim test

A

subcutaneous injection of sterile homogenised sarcoid tissue induces granulomas in affected patients

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3
Q

What is asbestos

A

Inconsumable silicate

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4
Q

What is asbestosis

A

Diffuse pulmonary fibrosis

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5
Q

What can result from asbestos

A

Diffuse pleural fibrosis, persistent pleural effusion, plaque, lung cancer, mesothelioma

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6
Q

What are silicates

A

inorganic minerals abundant in stone and sand

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7
Q

What is the effect of silicates on macrophages (silicosis)

A

2μm fibres toxic to macrophages, leading to their death with release of proteolytic enzymes

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8
Q

Pathophysiology of silicosis

A

Silicates are 2μm fibres toxic to macrophages, leading to their death with release of proteolytic enzymes
Tissue destruction and fibrosis
Nodules are formed after many years of exposure -> Interstitial fibrosis
Raised incidence of TB

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9
Q

What is pneumocosis

A

Lung disease caused by inhaled dust

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10
Q

Types of pneumocosis reactions/Different ways in which lung can respond to dust exposure

A

Inert
Fibrous
Allergic
Neoplastic

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11
Q
Examples of pneumocosis:
Inert
Fibrous
Allergic
Neoplastic
A

Inert: coal worker’s pneumoconiosis
Fibrous: progressive massive fibrosis, asbestosis and silicosis
Allergic: extrinsic allergic alveolitis
Neoplastic: mesothelioma, lung cancer

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12
Q

Examples of Coal Workers pneumocosis

A

Progressive massive fibrosis (PMF)
Emphysema
Honeycomb lung and /or cor pulmonale are the terminal conditions
Caplan’s syndrome (Rh’ Arthritis association)

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13
Q

What is antracosis

A

the presence of coal dust pigment in the lung

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14
Q

Describe Macular CWP (Coal Workers pneumocosis)

A

aggregates of dust laden macrophages with no significant scarring

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15
Q

Describe Nodular CWP (Coal Workers pneumocosis)

A

nodules >10mm in a background of extensive macular CWP, with no significant scarring

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16
Q

What regions of the lung are predominantly affected by fibrosing alveolitis

A

Subpleural regions

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17
Q

Describe histology of (end-stage) fibrosing alveolitis

A

Abnormally large irregular spaces separated by thick fibrous septa (Honeycomb Lung*)

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18
Q

Complications of fibrosing alveolitis

A

Cor pulmonale

End-stage fibrosis (honeycomb lung)

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19
Q

Systemic presentation of fibrosing alveolitis

A

Finger and toe-clubbing

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20
Q

Result of cytotoxic drugs on the lung

A

e.g. Busulphan, Bleomycin

Lead to low grade alveolitis with healing interstitial fibrosis

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21
Q

What is Paraquat

A

Potent herbicide
Acts by release of hydrogen peroxide and the superoxide free radical. It remains in high concentrations in the lungs after ingestion.

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22
Q

Pathophysiology of Adult Respiratory Distress Syndrome (ARDS) and result of damage to hyaline membranes

A

Diffuse alveolar damage with hyaline membranes
Severe injury to alveolar-capillary walls leads to acute respiratory distress with tachypnoea, dyspnoea, pulmonary oedema and arterial hypoxaemia refractory to O2 therapy

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23
Q

Examples of Acute Interstitial diseases

A
Adult respiratory distress syndrome
Drug and toxin reactions
Gastric aspiration
Radiation pneumonitis
Diffuse intrapulmonary haemorrhage
24
Q

Describe pathophysiology of interstitial lung diseases and effect of FEV1 etc

A

Increased amount of lung tissue
Increased stiffness and decreased compliance
Restrictive lung defect of the pulmonary function
Reduced Tco, VC, FEV1
Relatively normal FEV1/FVC ratio and PEFR

25
Q

What is Bronchiectasis

A

The permenant dilation of bronchi and bronchioles

26
Q

Cause of bronchiectasis

A

Obstruction:
Results from bronchial obstruction with distal infection and scarring or severe infection alone -> may go on to further tissue damage and loss of lung tissue
Severe inflammation:
During acute exacerbations

27
Q

What lobes of lung are usually affected by bronchiectasis

A

Usually the lower lobes

28
Q

Symptoms of bronchiectasis

A

chronic cough with expectoration of large quantities of foul-smelling sputum, flecked with blood sometimes

29
Q

Pathophysiology of bronchioectasis

Describe types of bronchioles that can result

A

Destruction of bronchial and alveolar walls, especially interstitial elastin and fibrosis of lung parenchyma (non-reversible)
Dilatation of the airways (bronchi and bronchioles) as the surrounding scarring fibrosis contracts
Inflammation during acute exacerbations
Inflammation and fibrosis extend into adjacent lung tissue
Cylindrical, saccular or fusiform bronchioles

30
Q

Complications of Bronchiectasis

A
Pneumonia
Fungal colonisation
Emphysema
Septicaemia
Meningitis
Metastatic abscesses (e.g. brain, heart)
Amyloid formation

Further necrosis and destruction of lung tissue can lead to pulmonary fibrosis
Cor pulmonale

31
Q

What is emphysema

A

Enlargement of alveolar airspaces with destruction of elastin in walls
Frequently associated with chronic bronchitis

32
Q

Main cause of emphysema

A

Cigarette smoking

33
Q

Other causes of emphysema (not cigarette smoking)

A

alpha-1-antitrypsin deficiency,
coal dust exposure,
cadmium toxicity

34
Q

Pathophysiology of emphysema

A

Gas trapping effect from emphysema - prevents full exhalation of air, particularly if large bullae
Pathogenesis probably revolves around recruitment of neutrophils in response to free oxygen radicals with release of IL8, LTB4 and TNF.
Also released are destructive enzymes e.g. neutrophil elastase.
Tissue damage results

35
Q

True of False:

Emphysema causes an increased risk of cancer

A

False (apparently)
Emphysema does cause tho:
Pulmonary hypertension
Poor oxygen delivery to tissues

36
Q

What % of lung capacity is destroyed in emphysema before symptoms appear

A

1/3

37
Q

Clinical features of emphysema

A

Weight loss due to metabolic demands ++
Right heart failure
Overinflated chest
Poor oxygen delivery to tissues

‘pure’ emphysema appears with reduced PaCO2 and normal PaO2 at rest due to overventillation (‘pink puffers’)

38
Q

What can acute localised obstruction progress to?

A

(Chronic localised obstruction)

Bronchiectasis

39
Q

Describe asthma

A

Increased irritability of bronchi causing spasm
Overdistended lungs
Mucus plugs in bronchi
Enlarged bronchial mucous glands with excess secretions

40
Q

Clinical categories of asthma

A

Extrinsic

Intrinsic

41
Q

Subtypes of extrinsic asthma

A

Atopic
Occupational
Allergic bronchopulmonary aspergillosis

42
Q

What type of hypersensitivity is atopic asthma

A

Type 1 (IgE)

43
Q

What type of hypersensitivity is occupational asthma

A

Type 3

44
Q

Causes of intrinsic asthma

A
Aspirin
Cold
Infection
Stress
Exercise
Sulfur dioxide
Pollutants etc (induced)
45
Q

Aetiology and risk factors of extrinsic asthma

A

Environmental agents like dust, pollens, foods, animal dust etc
Family history often present

46
Q

Other atopic disorders except asthma

A

Eczema

Hay-fever

47
Q

Asthma pathogenesis

A

Bronchial obstruction with distal overinflation or atelectasis
Mucus plugging of bronchi
Bronchial inflammation (mixed)
Seromucinous gland hypertrophy
Bronchial wall smooth muscle hypertrophy
Thickening of bronchial basement membrane

48
Q

Chemicals involved in asthma pathogenesis

A

Leukotrienes C4, D4, E4
Prostaglandins D2, E2, F2a
PAF
Mast cell tryptase

49
Q

Describe intrinsic asthma

A

Associated with recurrent chest infections
Chronic bronchitis
Not immune-mediated
Possibly unusually hyper-reactive airways

50
Q

What type of asthma is associated with recurrent chest infections

A

Intrinsic asthma

51
Q

Describe aetiology/pathology of aspirin-induced asthma

A

Unknown mechanism
Possibly increased locally leukotrienes or decreased prostaglandins
Usually associated with recurrent rhinitis with nasal polyps
Skin urticaria

52
Q

Allergic bronchopulmonary aspergillosis causative organism

A

Aspergillus fumigatus

53
Q

Describe Allergic bronchopulmonary aspergillosis

A

Induces both immediate type I reaction

And delayed immune complex type III hypersensitivity reaction

54
Q

What type of hypersensitivity is occupational asthma

A

Type 1 and 3

55
Q

Describe aetiology of occupational asthma

A

Work-associated inhaled agent
This acts either as non-specific stimulus precipitating asthma in people with hypersensitive airways or capable of inducing airway hyper-reactivity