Respiratory Flashcards

1
Q

3 basic types of atelectasis

A
  1. Resoprtion - after complete obstruction eg excessive bronchial secretions
  2. Compressive - pleural space expanded by fluid eg effusion
  3. Patchy - loss of surfactant eg IRDS
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2
Q

Histology of pulmonary oedema

A

Engorged capillaries
Filling of airspace’s with granular pink pink precipitate

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3
Q

3 classifications of pulmonary oedema

A

Harmodynamic oedema
Oedema due to microvascular injury
Oedema of undetermined origin

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4
Q

Causes of increased hydrostatic pressure causing haemodynamic oedema

A

Left sided heart failure
Mitral stenosis
Volume overload
Pulmonary vein is obstruction
(Increase pulmonary venous pressure)

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5
Q

Causes of decreased oncotic pressure causing haemodynamic oedema in the lungs

A

Hypoalbunaemia
Nephrotic syndrome
Liver disease
Protein losing enteropathies

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6
Q

3 causes of haemodynamic oedema causing pulmonary oedema

A

Increased hydrostatic pressure
Decreased oncotic pressure
Lymphatic obstruction

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7
Q

Causes of pulmonary oedema due to microcsacular injury

A

Infections
Inhaled gas
Liquid aspiration
Drugs and chemicals eg chemo
Shock/trauma
Radiation
DIC
Transfusion related

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8
Q

2 causes of pulmonary oedema of undetermined origin

A

High altitude
Neurogenic

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9
Q

Define acute respiratory distress syndrome

A

Diffuse alveolar capillary damage that leads to severe pulmonary oedema, respiratory failure and arterial hypoxia

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10
Q

Top 4 conditions associated with ARDS

A

Sepsis
Diffuse pulmonary infections
Gastric aspiration
Mechanical trauma

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11
Q

Mechanism of injury in Acute Respiratory Distress

A

Activation of lung macrophages which release oxidants, proteases, pro inflammatory cytokines
Causes aggregation of activated neutrophils secreted onjurious factors
Damage to endothelium and epithelium
Loss of surfactant = atelectasis
Increased alveolar permeability = pulmonary oedema

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12
Q

Morphology of acute respiratory distress syndrome

A

Diffuse alveolar damage - oedema, hyaline membranes, acute inflammation
Patchy interstitial fibrosis and type II epithelial proliferation

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13
Q

In ARDS what forms hyaline membranes

A

Composed of necrotic epithelial cell debris and exuded protein

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14
Q

Definition and example of obstructive pulmonary disease

A

Increased resistance to air flow
Emphysema
Chronic bronchitis
Bronchiectasis
Asthma

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15
Q

Definition and example of restrictive disease

A

Decreased expansion of lung parenchyma
Chest wall disorders
Acute or chronic interstitial or infiltration diseases

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16
Q

Define emphysema

A

Abnormal enlargement of airspace’s distal to the terminal bronchioles, with destruction of their walls

17
Q

4 classifications and causes of emphysema according to anatomical distribution

A
  1. Centriacinar emphysema - seen on tobacco smoking
  2. Panacinar - uniform distraction and enlargement, predominance in the lower zones, associated with alpha 1 antitrypsin deficiency
  3. Paraseptal - involves distal acinus, often underlying lesion of spontaneous pneumothorax
  4. Irregular - bullous emphysema
18
Q

Explain the protease-antiprotrease hypothesis causing emphysema

A

Imbalance between proteases and their inhibitors in the lung
Emphysema invariably results in hereditary deficiency of the major protease inhibitor alpha 1 antitrypsin

19
Q

How does smoking contribute to emphysema

A

Activating alveolar macrophages
Secrete chemotactic factors
Recruit neutrophils
Stimulate release of elastase from neutrophils
Enhance macrophage elastase activity
Inactivating alpha 1 antitrypsin by oxidants in tobacco smoke and free radicals in neutrophils

20
Q

Define chronic bronchitis

A

Persistent cough with sputum production for at least 3 months in at least 2 consecutive years

21
Q

Morphology of chronic bronchitis

A

Hyperaemia and oedema of mucus membranes of the lung
Mucinous secretions
Increased size in mucus glands
Mucus plugging inflammation fibrosis
Squamous metaplasia/dysplasia of bronchial epithelium

22
Q

Pathogenisis of chronic bronchitis

A

Chronic irritation of the airways
Hyper secretion of mucus
Hypertophy of mucus glands
Goblet cell metaplasia bronchiolitis

23
Q

What are the 2 major types of asthma

A

Extrinsic atopic allergin mediated
Intrinsic nonreaginic (idiopathic)

24
Q

What type of hypersensitivity is asthma

A

Type 1 IgE mediated

25
Q

What happens in the acute phase in asthma

A

Binding of antigen IgE coated mast cells
Release primary mediators (leukotrienes)
Then release secondary mediators (cytokines)
Cause bronchospasm, oedema, mucus secretion, recruitment of leukocytes

26
Q

What happens in the late phase reaction of asthma

A

Mediated by recruited leukocytes
Persistent bronchospasm and oedema
Leokocytic infiltration
Loss of damaged epithelial cells

27
Q

What is the morphology in asthma

A

Lungs are overinflated, show patchy atelectasis with occlusion of airways by mucus plugs

28
Q

In asthma what are curschmann spirals

A

Whorled mucus plugs

29
Q

In asthma what are Charcot Leyden crystals

A

Crystalloid debris of eosinophil membranes within airways

30
Q

What is seen microscopically in asthma

A

Oedema
Inflammatory infiltrate with numerous eosinophils
Hypertrophy of bronchial wall musculature and mucous glands
Whorled mucous plugs
Crystalloid debris of eosinophil membranes within airways