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Clinical Pathology Year 2 > Respiratory Pathology > Flashcards

Respiratory Pathology Flashcards

1
Q

Describe the pathology of asthma?

A

Type I hypersensitivity reaction (allergens/ cold/ exercise).
-Degranulation of IgE bearing mast cells: histamine initiated bronchoconstriction & mucus production, obstructing air flow. Also eosinophil chemotaxis.

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2
Q

What are the persistent/ irreversible changes of asthma?

A
  • Bronchiolar smooth wall hypertrophy
  • Mucus gland hyperplasia
  • Respiratory bronchiolitis leading to centrilobar emphysema
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3
Q

What is bronchiectasis?

A

Permanent dilation of bronchi & bronchioles caused by destruction of the muscle and elastic tissue.
Results from chronic necrotizing infection (like from CF, primary ciliary dyskinesia, bronchial obstruction)

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4
Q

What is COPD?

A

A combination of emphysema & chronic bronchitis (basically chronic inflammation and infections).

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5
Q

What are the 3 classifications of emphysema?

A

1) Centrilobar (centiacinar) - coal dust, smoking
2) Panlobar (panacinar) - >80% are antitrypsin deficient, severest in lower lobe bases.
3) Paraseptal (distal acinar) - upper lobe subpleural bullae adjacent to fibrosis.

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6
Q

How can you tell if the COPD is predominantly bronchitis or emphysema?

A

Bronchitis: 40-45, cough with copious sputum, common infections, prominant vessels & larger heart on xray, blue bloater.
Emphysema: 50-75, late cough, infections rare, small heart & hyperinflated lungs on xray, pink puffer.

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7
Q

Characteristics of interstitial lung disease?

A 
Restrictive lung disease.
Increased tissue in alveolar-capillary wall.
Inflammation and fibrosis
Decreased lung compliance
Increased gas diffusion distance
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8
Q

What is acute interstitial lung disease?

A

Diffuse alveolar damage- exudate & death of type I pneumocytes –> form hyaline membranes lining alveoli, followed by type II pneumocytes.

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9
Q

What is chronic interstitial lung disease?

A

Dyspnoea increasing for months to years.
Interstitial fibrosis & chronic inflammation with varying radiological & histological patterns.
Common end-stage fibrosed ‘honey-comb lung’

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10
Q

Describe the histological appearance of Idiopathic Pulmonary Fibrosis?

A

(sub-pleural, lower lobes affected most)

  • Interstitial chronic inflammation & variably mature fibrous tissue
  • Similar pattern in asbestos
  • Bosselated ‘cobblestone’ pleural surface
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11
Q

What is sarcoidosis?

A

(typically young adult females)

  • Non-caseating perilymphatic pulmonary granulomas, then fibrosis. Hilar nodes involved.
  • Hypercalcaemia & elevated serum ACE
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12
Q

What are the types of coal worker’s pneumoconiosis?

A

1) Anthracosis (asymptomatic, milder type- caused by accumulation of carbon)
2) Simple (macular) CWP (nodular aggregations in lungs)
3) Progressive massive fibrosis (if prolonged exposure. Large masses of dense fibrosis in the lungs).

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13
Q

What is silicosis, and what might it lead to?

A

(silica= sand and stone dust). Kills phagocytosing macrophages. Fibrosis & fibrous silicotic nodules.

  • Possible reactivation of TB
  • Increased risk of lung carcinoma (prescribed occupational disease in UK)
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14
Q

What is Hypersensitivity Pneumonitis? (aka extrinsic allergic alveolitis)

A

Type III hypersensitivity reaction, repeated episodes lead to interstitial fibrosis.

  • FARMER’S LUNG= actinomycetes in hay
  • PIGEON FANCIER’S LUNG= pigeon antigens
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15
Q

What aspects of the GI system are affected by Cystic Fibrosis?

A

Small Bowel: mucus plugging- meconium ileus
Liver: plugging of bile cannaliculi- cirrhosis
Salivary glands & pancreas: atrophy & fibrosis

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16
Q

What are the 4 major types of primary malignant lung tumours (mostly carcinomas)?

A
  1. Squamous cell carcinoma (20-30%)
  2. Small cell carcinoma (15-20%)
  3. Adenocarcinoma (30-40%)
  4. Large cell undifferentiated carcinoma (10-15%)
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17
Q

Aetiology of Lung tumours?

A 
Tobacco smoking
Occupational/ Industrial hazards (eg asbestos, arsenic)
Radiation (mines- radon)
Lung fibrosis
Genetic Mutations (EGFR, KRAS, ALK)
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18
Q

What are the electrolytic disturbances of small cell carcinoma?

A

Hyponatraemia
Hypokalaemia
Hypercalcaemia

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19
Q

What happens in a normal pleural mesothelium?

A

Single layer of mesothelial cells lines the pleural cavity

Secrete hyaluronic acid rich mucinous pleural fluid (lubricates movement of visceral & parietal pleura)

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20
Q

What are the 2 types of asbestos associated pleural fibrosis?

A
  • Parietal pleural fibrous plaques

- Diffuse pleural fibrous

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21
Q

Characteristics of Parietal pleural fibrous plaques?

A
  • Associated with low level asbestos dust exposure
  • Asymptomatic, may be visible of chest radiographs
  • Dense poorly cellular collagen
  • Not eligible for Industrial Injuries Disablement Benefit
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22
Q

Characteristics of Diffuse pleural fibrosis?

A
  • Associated with high level asbestos dust exposure
  • Usually bilateral, prevents normal expansion of lung causing breathlessness.
  • Dense cellular collagen (not extending into interlobar fissures)
  • Eligible for Industral Injuries Disablement Benefit
23
Q

What are features of Transudate Pleural Effusion?

A

1- Low capillary oncotic pressure (due to hypoalbumenaemia) & high capillary hydrostatic pressure
2- Low protein and low lactate dehydrogenase
3- Intact capillaries retain semipermeability

24
Q

What is an Exudate Pleural Effusion caused by?

A

Inflammation (with or without infection)

Neoplasms either primary or secondary

25
Q

What are features of Exudate Pleural Effusion?

A

1- Normal capillary oncotic pressure & normal vascular hydrostatic pressure
2- High protein & high lactate dehydrogenase
3- Capillaries lose semipermeability

26
Q

What is an open pneumothorax?

A

Chest wall perforation (usually traumatic- ‘sucking chest wound’)
External air is drawn into the pleural cavity during inspiration, reducing potential lung expansion.

27
Q

What is a closed pneumothorax?

A 
Lung perforation (usually not traumatic), connects the lung air spaces to the pleural cavity.
Lung air is drawn into the pleural cavity during inspiration, reducing potential lung expansion.
28
Q

What is a tension pneumothorax?

A

The perforation into the pleural cavity can be valvular (allowing air into cavity during inspiration, but not out during expiration)
Pressure in pneumothorax can rise above atmospheric pressure.
Can compress mediastinal structures

29
Q

What is a malignant mesothelioma?

A

A neoplasm of the mesothelial cells that line serious cavities (pleura, peritoneum, peridcardium) 92% are pleural (and more common in men), 8% are peritoneal.

30
Q

Causes of malignant mesothelioma?

A
  • Asbestos (80-90% of cases)
  • Thoracic irradiation
  • BAP1 (BRCA1-associated protein)
31
Q

What are 3 types of asbestos? (fibrous metal silicates)

A
  • Amphibole: blue aspestos (crocidolite)
  • Brown aspestos (amosite)
  • Serpentine: white aspestos (chrysotile)
32
Q

What is the oncogenicity of amphiboles and chrysotile?

A

Amphiboles: most oncogenic and persists in the lungs.
Chrysotile: less oncogenic and is more readily cleared from the lungs.

33
Q

What is asbestosis?

A

Interstitial pneumonia-like progressive pulmonary fibrosis caused by exposure to aspestos dust.
Fibrosis of the alveolar walls impairs both gas exchange and lung expansion.

34
Q

What are asbestos corns?

A

Benign hyperkeratotic wart-like skin lesions

35
Q

What is the Centor criteria?

A

(indication of the likelihood of a sore throat being due to bacterial infection)

  • Tonsillar exudate
  • Tendor anterior cervical lymphadenopathy
  • Fever over 38C
  • Absence of cough
36
Q

What are the triad of symptoms in Infectious mononucleosis/ glandular fever/ kissing disease (EPV)?

A

Fever, tonsillar pharyngitis and cervical lymphadenopathy.

avoid ampicillin due to mac-pap rash

37
Q

What is the commonest cause of epiglottitis?

A

Haemophillusinfluenzae type b (Hib) - in 90% paediatric cases.

38
Q

What are the 2 causes of acute otitis externa? (Acute OE)

A
  • 90% bacterial (Pseudonomas aeruginosa & Staphylococcus aureus)
  • 10% fungal
39
Q

What is malignant (necrotising) Otitis Externa?

A

Occurs when external otitis spreads to the skull base (soft tissue, cartilage and bone of the temporal region & skull)
Commonly develops in elderly diabetic or immunocompromised patients.
Severe pain, otorrhoea, granulation tissue in canal floor, cranial nerve palsy.

40
Q

What is chronic Otitis Externa?

A

Pruritus, mild discomfort, erythematous external canal devoid of wax
White keratin debris may fill ear canal
Common cause is allergic contact dermatitis

41
Q

What organisms cause Otitis Media?

A

Viruses! = Streptococcus pneumoniae, Haemophilusinfluenzae and Moraxella catarrhalis

42
Q

What is mastoiditis?

A

Complication of Otitis Media.
Infection of the mastoid bone and air cells. Rare in adults.
CT scan always required.

43
Q

What are the 2 anatomical patterns of pneumonia?

A

1) Bronchopneumonia- characteristic patchy distribution centred on inflamed bronchioles/bronchi, then subsequent spread to surrounding alveoli.
2) Lobar pneumonia- affects a large part, or the entire lobe (90% due to S. pneumoniae)

44
Q

What are some causative organisms in Community-Acquire Pneumonia?

A

Bacterial causes often divided into ‘typical’ and ‘atypical’…
Typical (have cell wall): Strep. pneumoniae, Haemophillus influenzae, Staph. aureus
Atypical (no cell wall): Mycoplasma pneumoniae, Legionella pneumophilia

45
Q

What is used as an assessment of disease severity in CAP?

A

CURB-65 score

sputum culture, blood culture, pneumococcal/ legionella urinary antigen

46
Q

What are 3 complications of pneumonia?

A

1) 3-5% pleural effusion
2) 1% Empyema (pus in pleural space)
3) Lung abscess (suppuration & destruction of lung parenchyma)

47
Q

Viral LRTI, what are the causative agents for pneumonia in the normal host?

A

Adults: Influenza A & B, Adenovirus, Varicella zoster virus (VZV)
Children: RSV, Parainfluenza

48
Q

What is Rhinovirus?

A

Agent responsible for most ‘common colds’, can cause LRTI and trigger exacerbations of asthma.

49
Q

What is a method of prevention of LRTIs?

A 
Pneumococcal vaccination (S. pneumoniae)
-for patients with chronic heart/ lung/ kidney disease and splenectomy.
50
Q

What is PCP (Pneumocystis jiroveci Pneumonia)?

A

A fungus, but lacks ergosterol in its cell wall & is not susceptible to a number of antifungals.

51
Q

What sort of % of tobacco smokers develop lung cancer, and what are some other risks associated?

A

11%

  • P450 polymorphisms
  • Industrial hazards
  • Air pollution
52
Q

What is the most common tumour found in lung?

A

Metastatic

if primary= squamous cell

53
Q

Why may young females (<50yrs) who have never smoked but develop lung cancer (adenocarcinoma)?

A

Associated with EGFR mutation.

54
Q

What is paraneoplastic syndrome of inappropriate antidiuretic hormone secretion (SIADH) associated with?

A

Small cell lung carcinoma
(Paraneoplastic syndromes: caused by ectopic hormone production or immune-mediated tissue destruction caused by antigens expressed on cancer cells- caused by a number of malignancies but most commonly lung, breast, ovary )

Clinical Pathology Year 2 (11 decks)

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