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AAPathology (Robbins) > The lungs > Flashcards

The lungs Flashcards

1
Q

Type of epithelium lining the respiratory tree (except vocal cords)

A

Pseudostratified tall columnar ciliated epithelial cells.

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2
Q

Features of bronchi that bronchioles do not share

A

Cartilage and submucosal glands.

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3
Q

Epithelium covering vocal cords

A

Stratified squamous epithelium.

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4
Q

Other cells in the bronchi and trachea

A

Goblet cells
Submucosal glands
Neuroendocrine cells (bronchial only).

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5
Q

Structure of alveolar walls.

A

Type I and type II pneumocytes (synthesises surfactant).
Basement membrane and interstitial tissue.
Endothelial cells lining capillaries.

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6
Q

Congenital abnormalities of the lung

A

Pulmonary hypoplasia (due to lung compression in utero)
Foregut cysts.
Pulmonary sequestration.

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7
Q

What is pulmonary sequestration?

A

An area of lung without connection to airway system and abnormal blood supply arising from the aorta.

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8
Q

Types of atelectasis

A

Resorption
Compression
Contraction

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9
Q

Cause of resorption atelectasis

A

Obstruction (mucus plug, exudate, foreign body) of an airway leads to air resorption.
Mediastinum shift toward atelectic lung.

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10
Q

Which way does the mediastinum shift in compression atelectasis?

A

Away from the affected lung.

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11
Q

What causes contraction atelectasis?

A

Pulmonary or pleural fibrosis preventing full expansion.

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12
Q

Types causes of pulmonary edema

A

Haemodynamic (haemodynamic or cardiogenic) or increases in capillary permeability

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13
Q

Gross histology of haemodynamic pulmonary edema.

A

Basal regions of lower lobes affected first (dependent edema) due to higher hydrostatic pressure.

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14
Q

Microscopic histology of pulmonary edema.

A

Engorged alveolar capillaries.
Pale pink granular intra-alveolar transudate.
Haemosiderin laden macrophages may be present.

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15
Q

Pathology of microvascular alveolar injury

A

Inflammatory exudate leaks into interstitial space and sometimes the alveoli. When diffuse can lead to acute respiratory distress syndrome.

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16
Q

Production of inflammatory exudate in acute lung injury/ARDS.

A

Endothelial activation due to cytokines (local or systemic)
Adhesion and extravasation of neutrophils - release of proteases, ROS, cytokines.
Accumulation of intraalveolar fluid and formation of hyaline membranes. (damage to type II pneumocytes leads to surfactant abnormalities as well)
Epithelial necrosis impedes resolution of injury, but resolution can be achieved by macrophages.

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17
Q

Key histological features of ARDS

A

Heavy, firm, red, boggy lungs with diffuse alveolar damage. Alveolar walls lined with hyaline membranes.

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18
Q

Clinical features of acute lung injury

A

Profound dyspnea and tachypnea.
Increasing cyanosis and hypoxemia, resp filure and diffuse bilateral infiltrates.
V/Q perfusion mismatch.

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19
Q

What FEV1/FVC ratio suggests lung obstruction?

A

Less than 0.7

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20
Q

What FEV1/FVC ratio suggests restrictive disease?

A

Both are lowered, so ratio is normal.

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21
Q

What are the types of restrictive lung deficit?

A

Chest wall disorders

Chronic interstitial and infiltrative diseases

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22
Q

List some common obstructive lung diseases

A

Emphysema, chronic bronchitis, asthma and bronchiectasis.

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23
Q

What percentage of heavy smokers develop COPD?

A

35-50%

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24
Q

What is emphysema?

A

Irreversible enlargement of the airspaces distal to the terminal bronchiole, accompanied by destruction of their walls without obvious fibrosis. Small airway fibrosis is also involved.

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25
Q

Classifications of emphysema

A

Centriacinar, panacinar, paraseptal and irregular, but only the first two cause clinical obstruction.

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26
Q

Describe the pathogenesis of emphysema

A

Smoking or air pollution and genetic predisposition leads to oxidative stress (apoptosis and senescence), inflammatory cells and mediators and a disruption of the protease-antiprotease balance. These lead to alveolar wall destruction.

27
Q

What inflammatory mediators are associated with emphysema?

A

leukotriene B4, IL-8 and TNF.

28
Q

What antiprotease deficiency leads to emphysema?

A

Antiprotease a1-antitrypsin deficiency leads to panacinar emphysema (About 1% of all emphysema patients)

29
Q

Causes of small airway inflammation in emphysema leading to increased obstruction.

A

Goblet cell hyperplasia and mucus plugging.
Inflammatory infiltrates in bronchial walls.
Muscle hypertrophy and peribronchial fibrosis leading to thickening of the wall.

30
Q

How much emphysema do you need to have symptoms?

A

Damage to 1/3 of the functioning parenchyma.

31
Q

Clinical course of emphysema

A

Dyspnoea is usually first, with cough or wheezing being other possible main complaints.
Weight loss is common.
Pink puffers.
Cor pulmonale and heart failure.

32
Q

Death in patients with emphysema is usually due to one of 4 things which are…

A

Coronary artery disease, respiratory failure, right sided heart failure and massive collapse of the lungs due to pneumothorax.

33
Q

Treatments of emphysema

A

Smoking cessation, oxygen therapy, long acting bronchodilators with inhaled corticosteroids, physical therapy and surgery.

34
Q

Other forms of emphysema

A

Compensatory hyperinflation due to loss of tissue elsewhere.
Obstructive overinflation (air trapping by tumour or foreign object); life threatening.
Bullous emphysema
Interstitial emphysema

35
Q

Clinical definition of chronic bronchitis

A

Persistent cough with sputum production for at least 3 months in at least 2 consecutive years in the absence of any other identifiable cause.

36
Q

Pathogenesis of chronic bronchitis

A

Initiating factor - exposure to irritating substance such as tobacco smoke or dust. This leads to mucus hypersecretion and inflammation and is maintained by infection.

37
Q

How tobacco smoke leads to mucus hypersecretion in chronic bronchitis

A

Involves histamine and IL-13 inflammatory mediators, and, over time, increase in size of mucous glands and in goblet cells (a protective reaction, which causes damage here).

38
Q

Morphology of chronic bronchitis

A

Hyperaemia, swelling and edema.

Increase in size of mucous glands.

39
Q

What is the Reid index?

A

A ratio of the thickness of the mucous gland layer to the thickness of the wall; normally it is 0.4, but is increased in chronic bronchitis.

40
Q

What is the cardinal symptoms of chronic bronchitis?

A

Persistent cough productive of sparse sputum.

Over many years, SOBOE develops.

41
Q

Define asthma

A

A chronic disease of reversible bronchoconstriction usually caused by an immunological reaction resulting in increased airway sensitivity, inflammation of the bronchial walls and increased mucous secretion.

42
Q

Categorization of asthma

A

Atopic or non-atopic.
Drug induced. Occupational.
Can be classified by clinical features such as triggers

43
Q

Triggers to asthma

A

Resp infections
Exposure to irritants
Cold air
Stress

44
Q

Atopic asthma is an example of what type of hypersensitivity reaction?

A

IgE mediated (Type I) hypersensitivity.

45
Q

How is childhood atopic asthma often triggered?

A

Exposure to environmental allergens on a background of a respiratory infection.

46
Q

What are key features of non-atopic asthma?

A

No evidence of allergen sensitization.

Less common family history of asthma

47
Q

Common triggers for non-atopic asthma

A

Respiratory infections, inhaled air pollutants.

48
Q

Discuss aspirin induced asthma

A

Uncommon, but sufferers exquisitely sensitive, and also get urticaria.
Aspirin inhibits COX, leading to decrease in prostaglandine E which normally inhibits proinflammatory mediators.

49
Q

Occupational asthma triggers

A

Usually fumes, dusts, gases or other chemicals.

50
Q

Atopic asthma is an example of what type of hypersensitivity reaction?

A

IgE mediated (Type I) hypersensitivity.

51
Q

Th2 responses in asthma

A

Exaggerated to normally harmless environmental antigens.
Secrete cytokines which stimulate the production of IgE (IL-4), actively recruit eosinophils (IL-5) and stimulate mucus secretion (IL-13).
IgE binds Fc receptors on mast cells leading to degranulation; the early-phase and late-phase reactions.

52
Q

Early phase reaction following mast cell degranulation in asthma

A

Bronchoconstriction (vagal), mucus production, vasodilation and increased vascular permeability.

53
Q

Common triggers for non-atopic asthma

A

Respiratory infections, inhaled air pollutants.

54
Q

Discuss aspirin induced asthma

A

Uncommon, but sufferers exquisitely sensitive, and also get urticaria.
Aspirin inhibits COX, leading to decrease in prostaglandine E which normally inhibits proinflammatory mediators.

55
Q

Occupational asthma triggers

A

Usually fumes, dusts, gases or other chemicals.

56
Q

Asthma pathogenesis

A

Th2 and IgE response to environmental allergens in genetically predisposed individuals.

57
Q

Th2 responses in asthma

A

Exaggerated to normally harmless environmental antigens

58
Q

Late phase reaction following mast cell degranulation in asthma

A

Recruitment of leukocytes including eosinophils, neutrophils and more T cells (Th2 and Th17)

59
Q

Pharmacological targets in asthma (confirmed, scene of crime, suspects)

A

Intervention clearly effective; leukotrienes and acetylcholine.
On the scene of the crime, but pharmacological intervention not effective; histamine, prostaglandin D2, platelet-activating factor.
Suspects; IL-13/IL4 pathways. IL-1, TNF, IL-6, chemokines.

60
Q

Genetic susceptibility in asthma

A

Multigenic. Many patients also have other allergic disorders.

61
Q

Susceptibility loci for asthma

A 
Chromosome 5q, near cytokine genes.
HLA class II
Metalloprotease ADAM33
B2-adrenergic receptors
IL-4
62
Q

Enviromental factors in asthma

A

High exposure to airborne allergens with low exposure to microbial allergens

63
Q

Histological findings in asthma

A 
Mucus plugs (BAL findings; Curschmann spirals)
Eosinophils and Charcot-Leyden crystals; airway remodelling
64
Q

Features of airway remodelling in asthma

A

Thickened wall, Subbasement membrane fibrosis.
Increased vascularity.
Hypertrophy of muscle.

AAPathology (Robbins) (2 decks)

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