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Respiratory Pathology > Obstructive & Restrictive Lung Diseases > Flashcards

Obstructive & Restrictive Lung Diseases Flashcards

1
Q

Define emphysema

A

Abnormal irreversible dilatation of air spaces distal to terminal bronchioles accompaied by destruction of their walls without fibrosis.

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2
Q

Compare centriacinar & panacinar emphysema

A

C: central (proximal) part of acinus with spared distal part, common in upper lobes, associated with smoking/chronic bronchitis.
PA: the whole acinus is uniformly involved, common in lower lobes, associated with alpha-1-antitrypsin deficiency.

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3
Q

Compare paraseptal & irregular emphysema

A

PS: the distal part of acinus while proximal part is normal, more common in upper lobes, adjacent to the pleura, along the lobular connective tissue septa & margins of lobules. Unknown cause, leads to spontaneous pneumothorax.
I: the acinus is irregularly involved, associated with scarring.

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4
Q

Mention the main steps of pathogenesis of emphysema

A

Lung damage and inflammation by inflammatory cells & mediators
Protease-Anti-Protease Imbalance
Oxidative stress
Insufficient wound repair
Loss of elastic tissue causing the respiratory bronchioles to collapse during expiration, leading to functional (not mechanical) obstruction.

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5
Q

Describe the gross & microscopic features of emphysema

A

G: panacinar it is pale & voluminous in lower lobes, centriacinar less pale and less voluminous thant PA, present in upper 2/3.
M: destruction alveolar wall without fibrosis, enlarged air spaces & decreased number of alveoli.

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6
Q

Mention clinical features of predominant emphysema

A
  1. Dyspnea, in chronic bronchitis or chronic asthmatic bronchitis, wheezing can occur.
  2. Weight loss
  3. Hyperventilation or better hyper respiration
  4. Barrel shaped chest
  5. Prolonged expiration: sitting in hunched position
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7
Q

Mention the reason of secondary pulmonary hypertension in COPD with
1, Predominant emphysema
2, Predominant chronic bronchitis

A

1, due to loss of pulmonary capillary surface area from alveolar destruction
2, due to hypoxia induced vascular spasm

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8
Q

Write a note on conditions confused with emphysema

A
  1. Compensatory emphysema: dilatation following surgical removal of diseased lung lobe.
  2. Obstructive Over-inflation: due to subtotal obstruction of an airway
  3. Bullous emphysema
  4. Mediastinal emphysema: air in mediasium , interstitium m subcutaneously. Due to whooping cough, excess vomitting or accidents and fractured ribs.
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9
Q

Define 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.

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10
Q

Pathogenesis of chronic bronchitis

A
  1. Mucus hypersection, smoke interfere with ciliary action, prevent clearance of mucus & predisposes to infection
  2. Inflammation: neutrophils, lymphocytes, mabrophages, end with fibrosis & obstructive airway disease.
  3. Infection
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11
Q

Mention the most important diagnostic criterion of chronic bronchitis

A

Increased Reid Index

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12
Q

Mention microscopic features of chronic bronchilitis

A

Goblet cell metaplasia, mucus plugging, inflammation & fibrosis (bronchiolitis oblterans)

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13
Q

Clinical features and complications of chronic bronchitis

A
  1. Persistent productive cough
  2. Dyspnea with effort
  3. Hypercapnia, hypoxemia and mild cyanosis
  4. Repeated infection
  5. Cor pulmonale
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14
Q

Define bronchiectasis

A

Its is permenant dilatation of bronchi & bronchioles caused by destruction of the muscle and the supporting elastic tissue resulting from or associated with chronic necrotizing infection.

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15
Q

Mention predisposing factors of bronchietasis

A
  1. Bronchial obstruction
  2. Necrotizing/suppurative inflammation. Post-tuberculous bronchiectasis, Staph aureus, Klebsiella.
  3. Immunodeficiency states
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16
Q

Describe the pathogenesis of bronchiectasis

A

Obstruction AND chronic persistent infection
Either normal secretions are hindered by obstruction so secondary infection will follow
Or infection causes accumulation of sectretion and obstruction
Weakening of bronchial walls, traction & irreversible dilatation

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17
Q

Describe bronchiectasis grossly

A

Lower lobes of lung, most distal bronchi & bronchioles can be followed to pleural surface.
Segmental affection

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18
Q

Describe bronchiectasis microscopically

A
  1. Extensive desquamtion and ulceration of the surface epithelium
  2. Dense inflammatory cellular infiltrate
  3. Fibrosis
  4. Dilatation
  5. Lung abscess formation
  6. Mixed flora can be cultures
19
Q

Mention clinical features & complications of bronchiectasis

A
  1. Severe persistent cough, sputum with changing position
  2. Dyspnea
  3. Hemoptysis
  4. Lung abscess
  5. Hypoxemia, hypercapnia, pulmonary hypertension , cor pulmonale
  6. Spread
  7. Amyloidosis
20
Q

Define bronchial asthma

A

Chronic inflammatory disorder of airways that causes recurrent episodes of wheezing, breathlessness, chest tightness & cough.

21
Q

What are the hallmarks of bronchial asthma?

A

Intermittent and reversible airway obstruction, bronchial muscles hypertrophy, hyper-activity, increased mucus secretion & chronic bronchial inflmmation with eosinophils.

22
Q

Describe clinical picture of bronchial asthma

A

Sym:
Coughing more at nigh & excercise, dyspnea, tight chest, short breath & wheezing.
Signs:
Chest: high pitch wheezes with expiration
Skin/nose allergy

23
Q

Underlying aetiology of bronchial asthma, most important cellular & humoral agents.

A

Type 1 hypersensitvity
TH2, mast cells, basophils
IL4,5,13

24
Q

Late phase reaction of bronchial asthma occurs with ….. of contact with antigen

A

2-4 hrs

25
Q

Compare type 2 & non-type 2 asthma

A

Type 2: severe, airway/systemic eosinophilia, responsive to corticosteroids & inhibitors of type 2 inflammation, may be atopic with early onset, IgE mediated, positive skin test.
Non-type 2: older age of onset, viral infection may play a role, neutrophilic, smooth-muscle mediated, less severe, no eosinophilia, no response to corticosteroids. No evidence of allergy or positive skin test.

26
Q

Mention types of type 2 asthma

A

Allergic (atopic, extrinsic)
Exercise-induces asthma
Late onset eosinophilic asthma

27
Q

Comapre early & late phases of asthma

A

Early: within 30-60 min, immediate bronchospasm, mucus production, inc vascular permeability & chemotaxis.
Late: 2-4 hrs, exaggerated initial response, epithelial damage, inflammation & wall edema , inc chemostaxis.

28
Q

Describe gross & microscopic picture of bronchial asthma

A

G: overdistended with areas of atelactasis
M: Curschman spirals & charcot crystal, thickened BM, hyperplasia of mucus glands and smooth muscles, eosinophils & increased vascularity in submucosa.

29
Q

Hallmark features of restrictive lung disease

A

Reduced compliance with increased effort of breathing

Hypoxia with abnormalities in V/Q ratio,

30
Q

Mention genetic defects associated IPF

A

Telomerase gene defect, MUC5B, surfactant gene defects

31
Q

Mention proposed causes of injury in IPF

A

GERD, smoking, occupational irritants, toxins & viral infection

32
Q

TGF beta downregulates …. Which

A

Fibroblast caveolin

Inhibits pulmonary fibrosis

33
Q

Mention gross features of IPF

A

Pleural surface shows cobblestone appearance due to retraction of scars along ther interlobar septa.
Honeycomb appearance, fibrosis, firm rubbery greyish white areas.

34
Q

Describe microscopic features of IPF

A
  • Early, exuberant fibroblastic foci, late, it is more collagenous less cellular.
  • Cystic spaces lines by type II pneumocytes or bronchiolar epithelium (honeycomb fibrosis)
35
Q

Clinical features of IPF

A
  1. Dyspnea & dry cough
  2. Dry crackles during inspiration
  3. Hypoxemia, cyanosis & clubbing
  4. Gradual deterioration
  5. Acute execration
36
Q

Non-specific interstitial pneumonia is associated with

A

Collagen vascular disorders as rheumatoid arthritis

37
Q

Describe morphology of NSIP

A

Cellular (inflmmatory cells) pattern: mild to moderate interstitial inflammation.
Fibrotic pattern: diffuse or patchy fibrosis, no temporal heterogeneity or honeycombing.

38
Q

The lung reaction in pneumoconiosis depends on

A

Size of particles

Reactivity

39
Q

Manifestions of complicated coal worker pneumocniosis

A 
Pulmonary massive fibrosis
Caplan syndrome (rheumatoid arthritis & pneumoconiosis)
40
Q

Mention disaeses caused by silica in the lung

A

Acute silicosis
Chronic silicosis with concentrically arranged hyaline collagen fibers
PMF

41
Q

Mention effects of asbestos on pleura

A

Pleural effusions, fibrous plaques, diffuse pleural fibrosis, mesothelioma.

42
Q

Mention malignancies associated with asbestosis

A

Mesothelioma, bronchogenic carcinoma & laryngeal carcinoma.

43
Q

Mention features of asbestosis

A

Interstital fibrosis in lower lobes & subpleural, enlarged air spaces enclosed by areas of fibrosis (honeycomb appearance)

44
Q

GR: Silicosis causes increased frequency of TB

A

As it affects the capability of macrophages to kill the bacilli

Respiratory Pathology (3 decks)

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