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Laz's Path Questions > Histo: Respiratory Disease > Flashcards

Histo: Respiratory Disease Flashcards

1
Q

List some examples of airway diseases.

A
  • Asthma
  • COPD-chronic bronchitis
  • Bronchiectasis
  • Infections
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2
Q

List some examples of Parenchymal disease.

A
  • Pulmonary oedema and diffuse alveolar damage (includes Acute respiratory distress syndrome and HMD)
  • Infections
  • COPD-Emphysema
  • Granulomatous diseases
  • Fibrosing interstitial lung disease and occupational lung disease
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3
Q

What is lung agenesis or hypoplasia?

A
  • Low weight underdeveloped lungs
  • Impaired fetal respiratory movements (movement is important in lung development)
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4
Q

List some examples of congenital lung disease.

A
  • Lung agenesis or hypoplasia
  • Tracheal & bronchial stenosis
  • Congenital cysts
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5
Q

Define asthma.

A

A condition in which breathing is periodically rendered difficult by widespread narrowing of the airways that changes in severity over short periods of time.

NOTE: Prevalence increased in recent decades

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6
Q

What is the typical presentation of asthma?

A
  • Presents with wheezing, acute SOB
  • In a severe attack patients develop status asthmaticus
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7
Q

List some causes and associations of Asthma.

A
  • Allergens and atopy (house dust mites)
  • Pollution
  • Drugs - NSAIDs
  • Occupational - inhaled gases/fumes
  • Diet
  • Physical exertion - “cold”
  • Intrinsic
  • Underlying genetic factors
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8
Q

Describe the pathogenesis of asthma.

A
  1. Sensitisation to allergen
  2. Immediate phase:
    • Mast cells degranulate on contact with antigen
    • Mediators released cause vascular permeability, eosinophil and mast cell recruitment and bronchospasm
  3. Late phase:
    • Tissue damage
    • Increased mucus production
    • Mucus hypertrophy
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9
Q

What are the macroscopic features of asthma?

A
  • Mucus plug
  • Overinflated lung
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10
Q

List the histological feeatures of asthma.

A
  • Hyperaemia
  • Eosinophilic inflammation and goblet cell hyperplasia - mucus
  • Hypertrophic constricted muscle
  • Mucus plugging and inflammation
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11
Q

Define COPD.

A
  • Chronic cough productive of sputum
  • Most days for at least 3 months over at least 2 consecutive years
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12
Q

Describe the pathophysiology of COPD.

A

Chronic injury to airways elicits local inflammation and reactive changes which predispose to further damage.

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13
Q

What are some common causes of COPD?

A
  • Smoking
  • Air pollution
  • Occupational exposures
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14
Q

List some histological features of COPD.

A
  • Dilatation of airways
  • Hypertrophy mucous glands - Reid Index
  • Goblet cell hyperplasia
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15
Q

What are some complications of chronic bronchitis?

A
  • Repeated infections (most common cause of hospital admission and death)
  • Chronic hypoxia and reduced exercise tolerance
  • Chronic hypoxia results in pulmonary hypertension and right sided heart failure (cor pulmonale)
  • Increased risk of lung cancer independent of smoking
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16
Q

Define Bronchiectasis.

A

Permanent abnormal dilatation of bronchi

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17
Q

What are common causes of bronchiectasis?

A
  • Congenital
  • Inflammatory
    • Post-infectious (especially children or cystic fibrosis)
    • Ciliary dyskinease 1° (Kartagener’s) and 2°
    • Obstruction (extrinsic/intrinsic/middle lob syn.)
    • Post-inflammatory (aspiration)
    • Secondary to bronchiolar disease (OB) and interstitial fibrosis (CFA, sarcoidosis)
    • Systemic disease (connective tissue disorders)
    • Asthma
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18
Q

List some complications of bronchiectasis.

A
  • Recurrent infections
  • Haemoptysis
  • Pulmonary hypertension and right sided HF
  • Amyloidosis
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19
Q

Describe the inheritance pattern of Cystic Fibrosis.

A
  • Autosomal recessive (approx 1/20 of population are heterozygous carriers)
  • Affects 1 in 2,500 live births
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20
Q

Mutation in which gene causes Cystic Fibrosis?

A
  • Chr 7q3 = CFTR gene (Cystic Fibrosis Transmembrane Conductance Regulator) = ion transporter protein
  • Abnormality leads to defective ion transport and therefore excessive resorption of water from secretions of exocrine glands
  • Results in abnormally thick mucus secretion - affects all organ systems
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21
Q

How does CF affect various organs?

A
  • Lung: airway obstruction, respiratory failure, recurrent infection
  • GI tract: meconium ileus, malabsorption
  • Pancreas: pancreatitis, secondary malabsorption
  • Liver: cirrhosis
  • Male reproductive system: infertility
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22
Q

What is the management of cystic fibrosis?

A
  • Improved treatment (physio, antibiotics, enzyme supplements, parenteral nutrition) has led to survival often into fourth decade
  • Lung transplantation offers longer survival
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23
Q

What are the main consequences of CF?

A
  • Over 90% of patients have lung involvement: patter of bronchiectasis
  • Recurrent infections (S. aureus, H. influenzae, P. aeruginosa, B. cepacia)
  • Other complications:
    • Haemoptysis
    • Pneumothorax
    • Chronic respiratory failure and cor pulmonale
    • Allergic bronchopulmonary aspergillosis (ABPA)
    • Lung collapse
    • Small airway disease
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24
Q

Define pulmonay oedema.

A

Accumulation of fluid in alveolar spaces as consequence of ‘leaky capillaries’ or ‘backpressure’ from failing left ventricle.

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25
Q

What are the main causes of pulmonary oedema?

A
  • Left heart failure
  • Alveolar injury
  • Neurogenic
  • High altitude
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26
Q

Describe the pathology of pulmonary oedema.

A
  • Heavy watery lungs, intra-alveolar fluid on histology
  • Poor gas exchange therefore hypoxia and respiratory failure
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27
Q

List some causes of acute respiratory distress syndrome in adults.

A
  • Infection
  • Aspiration
  • Trauma
  • Inhaled irritant gases
  • Shock
  • DIC
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28
Q

What causes hyaline membrane disease in newborns?

A

Lack of surfactant (mainly in premature babies)

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29
Q

On a cellular level, what insult results in ARDS?

A
  • Acute damage to the endothelium and/or alveolar epithelium
  • The basic pathology is the same regardless of cause: diffuse alveolar damage
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30
Q

Describe the appearance of the lungs on post-mortem examination in a patient who died from ARDS.

A
  • Plum-coloured
  • Heavy
  • Airless
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31
Q

Outline the pathophysiology of ARDS.

A
  1. Exudative phase - the lungs become congested and leaky
  2. Hyaline membranes - form when serum protein that is leaked out of vessels end up lining the alveoli
  3. Organising phase - organisation of the exudates to form granulation tissue sitting within the alveolar spaces
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32
Q

What are the outcomes of ARDS?

A
  • Death
  • Superimposed infection
  • Resolution (restoration of normal lung function)
  • Residual fibrosis (leads to chronic respiratory impairment)
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33
Q

What are the various patterns of bacterial pneumonia?

A
  • Bronchopneumonia
  • Lobar pneumonia
  • Abscess formation
  • Granulomatous inflammation
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34
Q

List some causes of community-acquired bacterial pneumonia.

A
  • Streptococcus pneumoniae
  • Haemophilus influenzae
  • Mycoplasma
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35
Q

List some causes of hospital-acquired bacterial pneumonia.

A

Gram-negatives (Klebsiella, Pseudomonas)

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36
Q

Which types of bacteria tend to eb implicated in aspiration pneumonia?

A

Mixture of aerobic and anaerobic

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37
Q

What is bronchopneumonia?

A
  • Infection is centred around the airways
  • Tends to be associated with compromised host defence (mainly the elderly) and is caused by low virulence organisms (e.g. Staphylococcus, Haemophilus, Pneumococcus)
  • It will show patcy bronchial and peribronchial distribution often involving the lower lobes
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38
Q

What is lobar pneumonia?

A
  • Infection is focused in a lobe of the lung
  • 90-95% caused by S. pneumoniae
  • Widespread fibrinosuppurative consolidation
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39
Q

What are the histopathological stages of lobar pneumonia?

A
  • Stage 1: congestion (hyperaemia and intra-alveolar fluid)
  • Stage 2: red hepatisation (hyperaemia, intra-alveolar neutrophils)
  • Stage 3: grey hepatisation (intra-alveolar connective tissue)
  • Stage 4: resolution (restoration of normal tissue architecture)
40
Q

List some complications of pneumonia.

A
  • Abscess formation
  • Pleural effusion
  • Empyema
  • Fibrous scarring
  • Septicaemia
41
Q

What is a granuloma?

A

Collection of macrophages and multi-nucleate giant cells

42
Q

Describe the histological appearance of atypical pneumonia.

A
  • Interstitial inflammation (pneumonitis) without accumlation of intra-alveolar inflammatory cells

NOTE: causes include Mycoplasma, viruses, Coxiella and Chlamydia

43
Q

What is a long term consequence of repeated small pulmonary emboli?

A

Pulmonary hypertension

44
Q

List some types of non-thrombotic emboli.

A
  • Bone marrow
  • Amniotic fluid
  • Trophoblast
  • Tumour
  • Foreign body
  • Air
  • Fat
45
Q

Define COPD.

A

Emphysema is a permanent loss of alveolar parenchyma distal to the terminal bronchiole

46
Q

What are the main causes of COPD?

A

Damage to alveolar epithelium

  • Smoking
  • Alpha-1 antitrypsin deficiency
  • Rare - IVDU, connective tissue disease
47
Q

Describe the pathogenesis of emphysema.

A
48
Q

How does pathogenesis of COPD differ depending on cause?

A
  • Smoking: Loss centred on bronchiole → CENTRILOBULAR
  • Alpha 1 antitrypsin deficiency: Diffuse loss of alveolae → PANACINAR
49
Q

What are the complications of COPD?

A
  • Bullae - large air spaces
    • Rupture → pneumothorax
  • Respiratory failure
    • Loss of area for gas exchange
    • Compression of adjacent normal lung
  • Pulmonary hypertension and cor pulmonale
50
Q

What is a granuloma?

A
  • Collection of histiocytes/macrophages +/- multinucleate giant cells
  • Necrotising or non-necrotising
51
Q

List some causes of Granulomatous disease.

A
  • Infection
  • Sarcoidosis
  • Foregin body - aspiration or IVDU
  • Drugs
  • Occupational lung disease
52
Q

What must be excluded when considering causes of granulomatous infection?

A
  • TB must be excluded before considering other causes of granulomatous inflammation
  • TB is fairly common in urban community and immunosuppressed
53
Q

List some causes of granulomatous infections.

A
  • Fungal (IS or foreign travel)
    • Histoplasma
    • Cryptococcus
    • Coccidioides
    • Aspergillus
    • Mucor
  • Other
    • Pneumocystis
    • Parasites
54
Q

What is sarcoidosis?

A

Idiopathic granulomatous disease that most commonly affects lungs, skin, lympho nodes and eyes (may affect any organ)

55
Q

What is the presumed pathogenesis of sarcoidosis?

A

An abnormal host immunological response to a variety of commonly encountered antigens, probably of environmental origin

56
Q

Describe the lung involvement by sarcoid.

A
  • Discrete epitheloid and giant cell granulomas, preferential distribution in upper zones with tendency to be perilymphatic, peribronchial
  • Advanced disease may be fibrotic and peribronchial
57
Q

How is diagnosis of sarcoidosis in the lung made?

A
  • Biopsy (Bronchial/OLB) - Non-necrotising granulomas, either singly or coalescent. May undergo fibrosis.
  • Elevated serum ACE
58
Q

What are other causes of non-infectious granulomas?

A
  • Intravascular talc granulomas in IV drug users
  • Aspirated food
59
Q

What are the different types of fibrosing lung disease?

A
  • Idiopathic pulmonary fibrosis (Cryptogenic fibrosing alveolitis)
  • Extrinsic allergic alveolitis - “farmers lung”
  • Industrial lung disease - “pneumoconiosis”
60
Q

What is idiopathic pulmonary fibrosis also known as?

A

Cryptogenic fibrosing alveolitis

61
Q

What are the macro and microscopic features of idiopathic pulmonary fibrosis?

A
  • Macro = basal and peripheral fibrosis and cyst formation
  • Micro = interstitial fibrosis at varying stages

NOTE: It is a progressive disease with over 50% mortality in 2-3 years

62
Q

What are the features of asbestosis?

A
  • Fine subpleural basal fibrosis with asbestos bodies in tissue
  • May also see pleural disease - fibrosis, pleural plaques
  • Increased risk of lung cancer in the presence of asbestosis
63
Q

What are some common pulmonary vascular diseases?

A
  • Pulmonary hypertension
  • Pulmonary thromboembolism
  • Pulmonary vasculitis
64
Q

What is the requirement for pulmonary hypertension diagnosis?

A

PHBP = mean pulmonary arterial pressure > 25 mmHg at rest

65
Q

What are the main causes of pulmonary hypertension?

A

Precapillary:

  • Vasoconstrictive
    • Chronic hypoxia
    • Hyperkinetic congenital heart disease
    • Unknown (Primary pulmonary hypertension)
    • Chronic liver disease, HIV infection, connective tissue disease
  • Embolic
    • Thromboembolic
    • Parasitic (schistosomal)
    • Tumour emboli

Capillary

  • Widespread pulmonary fibrosis - mechanical distortion and chronic hypoxia

Postcapillary

  • Veno-occlusive disease
  • Lef-stided heart disease
66
Q

What does chronic hypoxia result in?

A
  • Normal response of lung is to reduce blood supply to hypoxic areas of lung and divert it to aerated zones
  • Chronic hypoxia results in chronic vasoconstriction pulmonary arterioles
    • COPD
    • Fibrosing lung disease
67
Q

What morphological changes in the lung does chronic hypoxia cause?

A
  • Morphological changes in vessels
    • Eccentric intimal fibrosis
    • Thickening muscle wall
68
Q

Where is the most common site of embolisism formation in pulmonary thromboembolism?

A
  • Deep veins of leg (95%)
    • Present with swelling leg (DVT)
    • Present with symptoms of spread to lung (pulmonary embolism)
69
Q

What determines risk of thrombus formation?

A

Virchow’s Triad:

  1. Factors promoting blood stasis
  2. Damage to endothelium
  3. Increased coagulation
70
Q

List some risk factors of pulmonary thromboembolism.

A
  • Advanced age
  • Femal sex
  • Obesity
  • Immobility
  • Cardiac failure
  • Malignancy
  • Trauma
  • Surgery
  • Childbirth
  • Haemoconcentration
  • Polycythaemia
  • DIC
  • Contraceptive pill
  • Cannulation
  • Anti-phospholipid syndrome
71
Q

How might patients with small pulmonary emboli present?

A
  • Patients present with pleuritic chest pain or chronic progressive shortness of breath
72
Q

How does repeated emboli cause pulmonary hypertension?

A
  • Small peripheral pulmonary arterial occlusion
  • Haemorrhagic infarct
  • Repeated emboli cause increasing occlusion of pulmonary vascular bed and pulmonary hypertension
73
Q

What are the consequences of large pulmonary embolism?

A
  • Large emboli can occlude the main pulmonary trunk (saddle embolus)
  • Can cause:
    • Sudden death
    • Acute right heart failure
    • Cardiovascular shock occurs in 5% of cases when >60% of pulmonary bed is occluded
  • If patient survives, the embolus usually resolves
  • 30% develop second or more emboli
74
Q

List some causes of non-thrombotic emboli.

A
  • Bone marrow
  • Amniotic fluid
  • Trophoblast
  • Tumour
  • Foreign body
  • Air
75
Q

What is pulmonary veno-occlusive disease? List some causes.

A

Fibrotic occlusion of pulmonary veins

Causes:

  • IDIOPATHIC
  • Some “herbal” teas and diet pills
  • Chemotherapy
  • Radiotherapy
  • Bone marrow transplantation
  • Renal transplantation
  • HIV infection
  • Systemic sclerosis
76
Q

What are the complications of pulmonary hypertension?

A

Right sided heart failure

  • Venous cngestion of visceral organs - “nutmeg liver”
  • Peripheral oedema
  • Pleural effusions and ascites
  • Poorl lung perfusion and hypoxia
77
Q

How may pulmonary vasculitis present?

A

Present as life threatening haemorrhage, chronic haemoptysis, mass lesion, interstitial lung disease

NOTE: it is uncommon

78
Q

What are the different patterns of pulmonary vasculitis?

A

Variety of patterns from granulomatous vasculitis involving small-medium sized vessels (GPA) through to a leukocytoplastic vasculitis involving capillaries (e.g. with Rheumatoid arthritis)

79
Q

What are the main types of lung cancer?

A

Non-small cell carcinoma

  • Squamous cell carcinoma (30%)
  • Adenocarcinoma (20%)
  • Large cell carcinoma (20%)

Small cell carcinoma

80
Q

What components of cigarette smoke are responsible for its carcinogenicity?

A
  • Tumour initiators (polycyclic aromatic hydrocarbons)
  • Tumour promoters (nicotine)
  • Complete carcinogens (nickel, arsenic)
81
Q

Which types of lung cancer are most strongly associated with smoking?

A
  • Squamous cell carcinoma
  • Small cell carcinoma
82
Q

Which type of lung cancer tends to occur in non-smokers?

A

Adenocarcinoma

83
Q

List some risk factors for lung cancer.

A
  • Smoking
  • Asbestos
  • Radiation
  • Air pollution
  • Heavy metals
  • Susceptibility genes (e.g. nicotine addiction)
84
Q

Describe the sequence of histological changes that results in lung cancer.

A

Metaplasia → dysplasia → carcinoma in situ → invasive carcinoma

85
Q

What feature of squamous epithelium makes it vulnerable to undergoing malignant changes?

A

It does not have cilia leading to a build-up of mucus

Within the mucus carcinogens accumulate

86
Q

Where do squamous cell carcinomas tend to arise?

A

Centrally - arising from the bronchial epithelium

NOTE: there is an increasing incidence of peripheral squamous cell carcinomas (possibly due to deeper inhalation of modern cigarette smoke)

87
Q

Where does adenocarcinoma of the lung tend to arise?

A

Peripherally - around the terminal airways

NOTE: it tends to be multi-centric and extra-thoracic metastases are common and occur early

88
Q

What is the precursor lesion for adenocarcinoma of the lung?

A

Atypical adenomatous hyperplasia (proliferation of atypical cells lining the alveolar walls)

89
Q

Which mutations are associated with adenocarcinoma in smokers?

A

Kras

Issues with DNA methylation

P53

90
Q

Which mutation is associated with adenocarcinoma in non-smokers?

A

EGFR

91
Q

What is large cell carcinoma of the lung?

A
  • Poorly differentiated tumour composed of large cells
  • There is no evidence of squamous or glandular differentiation
  • It has a poor prognosis
92
Q

Where does small cell lung cancer tend to arise?

A

Central - around the bronchi

NOTE: 80% present with advanced disease and it carries a poor prognosis

93
Q

List some common mutations seen in small cell lung cancer.

A

P53

RB1

94
Q

What is the difference in the chemosensitivity of small cell lung cancer and non-small cell lung cancer?

A
  • Small cell - sensitive
  • Non-small cell - not very chemosensitive
95
Q

Which molecular changes are important to test for in adenocarcinoma?

A
  • EGFR (responder or resistance)
  • ALK translocation
  • Ros1 translocation
96
Q

Why is it important to know the tumour type precisely?

A

Some treatments can be fatal if the cancer is misdiagnosed

E.g. bevacizumab can cause fatal haemorrhage if used for squamous cell carcinoma

97
Q

What is cancer of the pleura?

A

Mesothelioma

Laz's Path Questions (9 decks)

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