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Medicine Phase 2a Respiratory > Lectures > Flashcards

Lectures Flashcards

(55 cards)

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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

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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

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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
What is Bronchiectasis
The permenant dilation of bronchi and bronchioles
26
Cause of bronchiectasis
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
What lobes of lung are usually affected by bronchiectasis
Usually the lower lobes
28
Symptoms of bronchiectasis
chronic cough with expectoration of large quantities of foul-smelling sputum, flecked with blood sometimes
29
Pathophysiology of bronchioectasis | Describe types of bronchioles that can result
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
Complications of Bronchiectasis
``` 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
What is emphysema
Enlargement of alveolar airspaces with destruction of elastin in walls Frequently associated with chronic bronchitis
32
Main cause of emphysema
Cigarette smoking
33
Other causes of emphysema (not cigarette smoking)
alpha-1-antitrypsin deficiency, coal dust exposure, cadmium toxicity
34
Pathophysiology of emphysema
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
True of False: | Emphysema causes an increased risk of cancer
False (apparently) Emphysema does cause tho: Pulmonary hypertension Poor oxygen delivery to tissues
36
What % of lung capacity is destroyed in emphysema before symptoms appear
1/3
37
Clinical features of emphysema
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
What can acute localised obstruction progress to?
(Chronic localised obstruction) | Bronchiectasis
39
Describe asthma
Increased irritability of bronchi causing spasm Overdistended lungs Mucus plugs in bronchi Enlarged bronchial mucous glands with excess secretions
40
Clinical categories of asthma
Extrinsic | Intrinsic
41
Subtypes of extrinsic asthma
Atopic Occupational Allergic bronchopulmonary aspergillosis
42
What type of hypersensitivity is atopic asthma
Type 1 (IgE)
43
What type of hypersensitivity is occupational asthma
Type 3
44
Causes of intrinsic asthma
``` Aspirin Cold Infection Stress Exercise Sulfur dioxide Pollutants etc (induced) ```
45
Aetiology and risk factors of extrinsic asthma
Environmental agents like dust, pollens, foods, animal dust etc Family history often present
46
Other atopic disorders except asthma
Eczema | Hay-fever
47
Asthma pathogenesis
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
Chemicals involved in asthma pathogenesis
Leukotrienes C4, D4, E4 Prostaglandins D2, E2, F2a PAF Mast cell tryptase
49
Describe intrinsic asthma
Associated with recurrent chest infections Chronic bronchitis Not immune-mediated Possibly unusually hyper-reactive airways
50
What type of asthma is associated with recurrent chest infections
Intrinsic asthma
51
Describe aetiology/pathology of aspirin-induced asthma
Unknown mechanism Possibly increased locally leukotrienes or decreased prostaglandins Usually associated with recurrent rhinitis with nasal polyps Skin urticaria
52
Allergic bronchopulmonary aspergillosis causative organism
Aspergillus fumigatus
53
Describe Allergic bronchopulmonary aspergillosis
Induces both immediate type I reaction | And delayed immune complex type III hypersensitivity reaction
54
What type of hypersensitivity is occupational asthma
Type 1 and 3
55
Describe aetiology of occupational asthma
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

Medicine Phase 2a Respiratory (22 decks)

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