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Pathology (Guide) > Histopathology - Lung Pathology > Flashcards

Histopathology - Lung Pathology Flashcards

1
Q

What are some obstructive lung diseases?

A
  • Chronic bronchitis
  • Bronchiectasis
  • Asthma
  • Emphysema
  • Small airway disease/bronchiolitis
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2
Q

What is the pathology, aetiology + histological features of bronchitis?

A
  • P = Dilation of the airways + excess mucus production
  • A = tobacco smoke, air pollution
  • H = Dilation of airways, goblet cell hyperplasia, hypertrophy of mucous glands
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3
Q

What is the pathology, aetiology + histological features of bronchiectasis?

A
  • P = Airway dilatation + scarring
  • A = Recurrent infections (e.g. CF, primary ciliary dyskinesia)
  • H = Permanent fibrotic dilatation of the bronchi with mucous plugging
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4
Q

What is the pathology, aetiology + histological features of asthma?

A
  • P = Widespread airway constriction due to mast cell degranulation
  • A = Immunologic, allergens, drugs, cold air, exercise
  • H = SM cell hypertrophy, goblet cell hyperplasia, eosinophilia, Curschmann spirals, Charcot-Leyden crystals
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5
Q

What is the pathology, aetiology + histological features of emphysema?

A
  • P = airspace enlargement, wall destruction
  • A = tobacco smoke, α1-AT deficiency
  • H = Loss of alveolar parenchyma distal to terminal bronchiole
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6
Q

What is the pathology, aetiology + clinical features of bronchiolitis?

A
  • P = inflammatory scarring/obliteration
  • A = tobacco smoke, air pollutants
  • C = dyspnoea, cough
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7
Q

What is the pathophysiology of cystic fibrosis?

A
  • AR mutation in CTFR gene affects Cl ion transport, leading to abnormally thick secretions
  • Secretions allow growth of bacteria, causing frequent lung infections, resulting in bronchiectasis
  • Multisystem disease as secretions affect other organs (e.g. pancreatic insufficency = malabsorption)
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8
Q

What pathogen is commonly seen in patients with lung infections in cystic fibrosis?

A

Pseudomonas Aeruginosa

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9
Q

What is interstitial lung disease?

A

Group of >200 disease characterised by inflammation + fibrosis of pulmonary connective tissue, accounting for 15% of resp disease burden

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10
Q

What typical features are seen in interstitial lung disease

A
  • Restrictive picture (spirometry)
  • Chronic SOB
  • Fine-end inspiratory crackles
  • cyanosis
  • pulmonary HTN
  • Cor pulmonale
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11
Q

In advanced interstitial lung idease, what is seen on a CT CAP?

A

Ground glass/honeycomb appearance

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12
Q

What are the different types + categories of interstitial lung disease?

A

Fibrosing:
- Idiopathic pulmonary fibrosis
- Pneumoconiosis
- A/w connective tissue disease
- Drug-induced
- Radiation pneumonitis

Granulomatous:
- Sarcoid
- Extrinsic allergic alveolitis
- A/w vasculitides

Eoisinophilic

Smoking-related

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13
Q

What is the clinical picture of patient with idiopathic pulmonary fibrosis?

A
  • Male
  • 40-70y
  • Exertional dyspnoea
  • Non-productive cough
  • Clubbing
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14
Q

How is idiopathic pulmonary fibrosis diagnosed and managed?

A
  • D: high resolution CT +/- niopsy
  • T: Steroids, cyclophosphamide, azathioprine, pirfenidone
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15
Q

What is pneumoconiosis + its typical presentation?

A
  • Occupational lung disease causes by inhalation of minerla dusts or inorganic particles
  • Coal miners
  • Predilection for upper lobes
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16
Q

What is asbestosis + its typical presentation?

A
  • Fibrosis resulting from asbestos exposure
  • Affects lower lobes
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17
Q

What is a granuloma?

A

A collection of histiocytes, macrophages +/- multinucleate giant cells

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18
Q

What is extrinsic allergic alveolitis/pneumonitis etc. examples of?

A

Group of immune-mediated lung disorders caused by intense/prolonged exposure to inhaled organic antigens causing widespread alveolar inflammation

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19
Q

What is seen on histology for extrinsic allergic alveolitis?

A
  • Presence of polypoid plugs of loose connective tissue within alveoli/bronchioles
  • Granuloma formation + organising pneumonia
20
Q

What are some typical features of bronchopneumonia?

A
  • Patchy bronchial/peri-bronchial distribution
  • Low virulence organisms
  • Elderly + frail people
21
Q

What are some typical features of lobar pneumonia?

A
  • Fibrosuppurative consolidations
  • High virulence organisms (e.g. Strep. pneumoniae = rust-coloured sputum)
22
Q

What stages are seen in lobar pneumonia?

A
  1. Consolidation
  2. Red hepatisation (neutrophilia)
  3. Grey hepatisation (fibrosis)
  4. Reolution
23
Q

What are some typical features of atypical pneumonia?

A
  • Interstital pneumonitis
  • No intra-alveolar inflammation
  • Chronic + progressing fibrosing disease of lung
24
Q

What are some tumours of the lung + their prevalence?

A
  • Squamous cell carcinoma (30-50%)
  • Adenocarcinoma (20-30%)
  • Small cell carcinoma (20-25%)
  • Large cell carcinoma (10-15%)
25
Q

What are the risk factors, mutations, location and histological findings of Squamous Cell Carcinoma?

A
  • RFs: Male, SMOKING
  • M: p53/c-myc
  • L: Proximal bronchi, local spread with late metastases
  • H: sQaumous = hyperQualcaemia (of malignancy), Qeratin pearls (keratinisation), cell Qonnections (intercellular prickles)
26
Q

What is adenocarcinoma of the lung, its risk factors, location and histological findings?

A

Malignant epithelial tumour with glandular differentiation of mucin-production

  • RFs: Women + non-smokers
  • L: Peripherally (type 2 pneumocytes in alveoli) + metastasizes early
  • H: glandular differentiation (gland formation + mucin production)
27
Q

What are the risk factors, mutations, location and histological findings of Small Cell Carcinoma + its associations?

A
  • RFs: Smoking
  • M: p53 + RB1
  • L: Centrally, proximal bronchi + rapid metastases
  • H: Small, poorly differentiated “oat cells” (kulchitsky cell)
  • A: SIADH, Cushing’s Lambert-Eaton
28
Q

What is large cell carcinoma and it’s histological findings?

A
  • Poorly differentiated malignant epithelial tumour
  • H: No evidence of glandular or squamous differentiation
29
Q

What are some paraneoplastic syndromes?

A
  • ADH –> SIADH (small cell)
  • ACTH –> Cushing’s syndrome (Small cell)
  • PTH/PTHrP –> primary hyperparathyroidism, hypercalcaemia + bone pain (squamous cell)
  • Calcitonin –> hypocalcaemia
  • Serotonin –> Carcinoid syndrome (flushing, diarrhoea, bronchoconstriction)
  • Bradykinin –> cough
30
Q

How is lung cancer staged?

A
  • Tumour (T1-4): based on size, invasion of pleura, pericardium
  • LN metastasis (N0-2): N0 = no involvement, N1/2 = involvement, dependant on extent
  • Distant Mets (M0/1): Tumour spread to distant sites
31
Q

Where does mesothelioma originate, where does it spread and what is its typical presentation?

A
  • Arises from parietal/visceral pleura
  • Spreads in pleural space
  • Presentation: extensive pleural effusion, chest pain, dyspnoea
32
Q

What is a pulmonary embolus?

A

The embolisation of a peripheral thrombus to the lung

33
Q

What are some RFs for developing a PE?

A
  • Female
  • Immobility
  • Cardiac disease
  • Cancer
  • Primary + Secondary hypercoagulable states
34
Q

What are the different types of emboli and how do they differ?

A
  • Large Emboli: Impact in main pulmonary arteries leads to acute cor pulmonale, cardiogenic shock + death if >60% pulmonary bed occluded
  • Small Emboli: Silent or cause peripheral wedge infarctions. Repeated infarctions = pulmonary HTN
  • Non-thrombotic emboli: Bone marrow, amniotic fluid, tumour, air, foreign body
35
Q

What is the term used to describe a large emboli occluding the pulmonary trunk?

A

Saddle embolus

36
Q

What is pulmonary hypertension?

A

Mean pulmonary arterial pressure >25mmHg at rest

37
Q

What are the different classes of pulmonary hypertension and how do they differ?

A
  • Class 1: Pulmonary arterial hypertension - most common in women 20-40yrs (Causes: idiopathic, hereditary, congenital HD)
  • Class 2: Due to left heart disease (e.g. valve disease)
  • Class 3: Due to lung disease (e.g. ILD)
  • Class 4: Chronic thromboembolic pulmonary hypertension (e.g. due to many clots over time which causes fibrosis)
  • Class 5: With unclear multifactorial mechanisms (e.g. metabolic/systemic/haematological disorders)
38
Q

What is the pathophysiology of pulmonary hypertension?

A
  • Pre-capillary: chronic hypoxia/embolus
  • Capillary: Pulmonary fibrosis
  • Post-capillary: Left heart disease/veno-occlusive disease
  • Pulmonary vasoconstriction of arterioles: intimal fibrosis, thickened walls
39
Q

What are some complications of pulmonary hypertension?

A

RHF - venous congestion of organs (nutmeg liver), peripheral oedema

40
Q

What is pulmonary oedema, its aetiology + histology?

A

Intra-alveolar fluid accumulation leads to poor gas exchange

Aetiology:
- LHF

Histology:
- Intra-alveolar fluid
- Iron laden macrophages

41
Q

What is diffuse alveolar damage, its complications + histology?

A

Acute damage to alveoli (alveolar epithelium) leading to exudative inflammatory reaction, rapid onoset of respiratory failure + requiring ventilation in ITU

Cx:
- ARDS
- Hyaline Membrane Disease (HMD) in neonates

Histology:
- Lung expanded, firm, plum-coloured, airless

42
Q

What is seen on the CXR of diffuse alveolar damage?

A

White out of all lung fields

43
Q

What is COPD, it’s symptoms, causes + histological findings?

A

Chronic bronchitis + emphysema

Sx:
- Frequent coughing
- Wheezing
- Excessive sputum
- SOB

Causes:
- Smoking
- α-1 antitrypsin deficiency (SOB + liver Sx)

Histo:
- Neutrophilic infiltration into airways
- Loss of alveoli, elastic fibres + lung parenchyma

44
Q

What is cystic fibrosis, its inheritance, complications + histological findings?

A

AR mutation in CFTR gene on Chr 7

Cx:
- Recurrent lung infections
- Pancreatic insufficiency
- Malabsorption

Histo:
- Mucous clogged airways
- Inflammatory cell infiltration

45
Q

What is the mechanism of action of cystic fibrosis?

A
  • Mutation on CFTR gene (Chr 7) leads to defective ion transport
  • Excessive resorption of water from secretions of exocrine glands
  • Abnormally thick mucous secretions
  • Affects all organ systems

Pathology (Guide) (84 decks)

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