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Clinical Pathology > Respiratory Disease > Flashcards

Respiratory Disease Flashcards

1
Q

What is the principle epithelium comprising the respiratory system?

A

Pseudo stratified columnar epithelium with mucus secreting goblet cells

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2
Q

What comprises the conductive airways

A
  • Nasal/oral cavities
  • Trachea
  • Left and right bronchi
  • Segmental & smaller bronchi
  • Bronchioles and terminal bronchioles

Warm and humidify air

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3
Q

What comprises the respiratory airway?

A
  • Respiratory bronchioles
  • Alveolar ducts
  • Alveolar sacs
  • Alveoli
  • gas exchange takes place here
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4
Q

What are the main epithelium cells of the alveoli

A

Type I pneumocytes (respiratory)

Type II pneumocytes - secrete surfactant

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5
Q 
What are the following..
Residual volume (RV)
Tidal volume (TV) 
Inspiratory reserve volume (IRV)
Expiratory reserve volume (ERV)
A

RV - amount of air remaining in lungs after max expiration
TV - amount of air breathed in/out during normal breathing
IRV - max amount of air breathed in after normal expiration
ERV - max amount of air breathed out after normal inspiration

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6
Q

What are the following?
Total lung capacities
Vital capacity
functional residual capacity

A

TLC = TV + RV =IRV + ERV
VC - TV + ERV + IRV
FRC - RV + ERV

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7
Q

Respiratory failure can result from the following 3 things…

A
  • Impaired ventilation (mechanical/neural)
  • impaired perfusion
  • impaired gas exchange
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8
Q

What is defined as respiratory failure (kPaO2)

A

PaO2

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9
Q

What defines and what are the clinical features of type I and type II respiratory failure?

A

Type I (paCO2 less than 6.3kPa) - hypocapnic

Type II (paCO2 more than 6.3kPa) - hypercapnic

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10
Q

What does a wheeze indicate?

A

DISTAL airway obstruction

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11
Q

What does a stridor indicate?

A

PROXIMAL airway obstruction

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12
Q

What is pleuritic pain a result of?

A

Irritation of pleura due to inflammation, infarction or tumour

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13
Q

What is dyspnoea?

A

Reduced oxygen in the blood due to impaired alveolar gas exchange

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14
Q

What is cyanosis?

A

Reduced oxygenation of Hb

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15
Q

What can clubbing of the fingers indicate?

A
  • Carcinoma of the lung
  • Bronchiectasis
  • Pulmonary fibrosis
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16
Q

What could weight loss be associated with?

A

Protein catabolic state due to chronic inflammatory disease or tumours

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17
Q

What do crackles with lung auscultation indicate?

A

Resisted opening of the small airways due to fibrosis/fluid)

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18
Q

What does a wheeze indicate

A

Generalised/localised narrowing of the small airways

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19
Q

What does a pleural rub indicate?

A

Pleura roughened by exudate (rubs against inflamed viscera)

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20
Q

What does a dull and hyper resonate percussion indicate?

A

Dull - lung consolidation/lung effusion

Hyper resonate - pneumothorax or emphysema

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21
Q

Are the majority of lung neoplasms carcinogenic?

A

YES - 90% are malignant. Benign lung tumours are RARE

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22
Q

What are the causes of lung neoplasms?

A
  • Cigarette smoking (80%)
  • Asbestos exposure
  • Lung fibrosis - including asbestosis and silicosis
  • Radon
  • Chromates, nickel, tar, arsenic, mustard gas
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23
Q

What does asbestos causes?

A

Pulmonary interstitial fibrosis

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24
Q

Highe incidence of asbestosis is associated with…

A

Higher exposure (in regards to dose and time) to asbestos

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25
Q

What are the main diagnostic features of asbestosis

A

Evidence of structural pathology consistent with asbestosis (histology/shortness of breath)

Evidence of causation by asbestos (occupational and environmental history, markers of exposure, recovery of asbestos bodies, or other means

Exclusion of alternative plausible causes for the findings

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26
Q

What are the main classifications of carcinomas in the lung?

A
  • non-small cell carcinoma (85%)

- Small cell carcinomas (15%)

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27
Q

What do non small cell carcinomas include

A
  • Squamous cell carcinoma (20-30%) - smoking, mostly central, possibly keratinised, intracellular desmosomes
  • Adenocarcinoma (30-40%) - most common, central=peripheral, evidence of glandular/mucoid differentiation (80% due to smoking)
  • Large cell undifferentiated - no evidence of squamous/glandular differentiation,
  • Large cell neuroendocrine carcinoma - neuroendocrine differentiation - associated with smoking
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28
Q

What are all small cell carcinomas?

A

Poorly differentiated neuroendocrine carcinomas
All due to smoking
Rapidly progressive malignant tumours (NOT IN-SITU)

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29
Q

What are bronchial carcanoid tumours and how do they present?

A
  • Low grade malignant tumours
    Highly vascular - haemoptysis and potential airway obstruction
  • NOT associated with smoking
  • rarely metastasise
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30
Q

What are most common; primary or secondary lung tumours?

A

Secondary

  • most commonly from breast, kidney and gastrointestinal tract.
  • Difficult to distinguish if origin = primary or secondary
  • Usually multiple bilateral nodules but can be solitary
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31
Q

What is squamous cell metaplasia in the context of normal epithelium in respiratory?

A

Normal psuedostratified columnar epithelium undergoes reversible metastatic change to squamous type (possible keratinised) in response to irritants e.g. smoking - more able to resist chemicals

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32
Q

What does dysplasia comprise?

A

Irreversible genetic change of metastatic cell - first neoplastic cell. Neoplastic cell undergoes clonal expansion/proliferation, replacing metastatic cell. Produces dysplasia intraepithelial neoplasia/ CARCINOMA-IN-SITU. Squamous cell carcinoma - neoplastic cells breach through basement membrane, access lymph/vasculature - produces metastases/distant sites

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33
Q

How is lung cancer graded/staged?

A

TMN system

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34
Q

How is lung cancer treated

A

Non-small cell carcinoma - complete surgical resection if not metastasised - if spread = contraindicated
Small cell carcinoma - usually metastasised at time of diagnosis
Chemotherapy/radiotherapy - used radically or palliatively - prevents ‘worsening’ of symptoms

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35
Q

Complications of primary lung cancer..

A
  • pleural effusion
  • obstructive pneumonia
  • bronchiectasis
  • Clubbing
  • Cachexia - weight loss
  • lymph metastasis…
    - Epilepsy - cerebral metastasis
    - Bone metastasis - increased Ca+ - fractures
    - Endocrine effects - increased ACTH, ADH, and PTH
    hypokalaemia, hyponatraemia, hypercalcaemia
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36
Q

Name the types of pleura

A
  • visceral pleura - associated with lungs themselves

- Parietal pleura - covers thoracic cavity, heart, mediastinum, and diaphragm

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37
Q

Name the disorders due to collection of fluid (effusions) and air (pneumothorax) in the pleural cavities

A 
Haemothorax - blood 
Pneumothorax - air
Hydrothorax - exudate and transudate - pleural effusion
Chylothorax - lymph 
Pyrothorax - pus
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38
Q

What are the causes of pleural effusion?

A
  • Inflammatory - inflammation/infection in adjacent lung e.g. TB, pneumonia, lupus, rheumatic fever, rheumatoid disease, pleural embolism
  • Non-inflammatory - e.g congestive heart failure
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39
Q

What is inflammation of pleura called?

A

Pleuritis/pleurisy

40
Q

Malignancies of pleura. Are beingn tumours rare/common and what are the most common cause of plural malignancies?

A
  • Benign tumours = rare
  • Malignant tumours = usually SECONDARY to adenocarcinomas of lung/breast
  • Primary mesothelioma = rare
41
Q

What is the main cause of mesothelioma? (i.e. primary tumour of pleura)

A

Asbestos exposure - latent development (can develop 30 years later after asbestos exposure)

42
Q

How do mesotheliomas develop?

A
  • initial nodule and effusion -> obliteration of pleural cavity around lung -> chest wall invasion (pain) and lung -> possible metastasis
  • no treatment and fatal in usually under a year
43
Q

Abnormalities predisposing individuals to lung infection

A 
MUSCULOCILIARY ELEVATOR DYSFUNCTION
Obstruction - foreign object/tumour
Loss of Cough reflex
Mucous viscosity - CF
Ciliary motility - Kartagener's syndrome

IMMUNITY
Hypogammaglobulinaemia , lymphomas, immunosuppressive drugs, AIDS
Macrophage function – smoking, hypoxia

PULMONARY OEDEMA

44
Q

What is the other name for acute bronchitis?

A

Croup - most severe in children - excessive coughing/sputum

45
Q

What are the major causes of acute bronchitis?

A

RSV (respiratory syncitical virus), H influenzae, Strepp pneumoniae, chemical agents we.g. smoke, sulphur dioxide

46
Q

What structures does acute bronchitis involve?

A

Bronchi, larynx, trachea

47
Q

What is the definition for chronic bronchitis?

A

Excessive sputum/coughing for 3 months over 2 consecutive years (common in people with chronic obstructive airway disease)

48
Q

What is broncholitis caused by?

A

usually primary RSV infection in INFANTS

49
Q

What are the main symptoms of broncholitis

A

Tachypnoea and dyspnoea

50
Q

If bronchiolitis does not resolve, what can it develop into?

A

Bronchopneumonia

51
Q

What is bronchopneumonia characterised by?

A

Patchy distribution - inflamed bronchioles and bronchi which spread to neighbouring alveoli. Often several lobes or bilateral.

52
Q

What people are usually effected by bronchopneumonia?

A

Elderly, young children, or secondary to disease

53
Q

What is lobar pneumonia?

A

Pneumonia that effects anatomically delineated segments OR entirety of lobes/lung

54
Q

Who is effect by lobar pneumonia most/least

A
  • Mostly young, healthy individuals

- Uncommon in infancy/elderly

55
Q

What is the main cause of lobar pneumonia?

A

90% causes by Streptococcus pneumoniae

56
Q

What are the main symptoms of lobar pneumonia?

A

Fever, cough and ‘rusty’ purulent sputum

57
Q

What is the main cause of TB

A

Mycobacterium tuberculosis

58
Q

What are the main associations of TB infection?

A

Socioeconomic deprivation

Immunosuppression (i.e. AIDS)

59
Q

What is the vaccine for TB?

A

BCG vaccine

60
Q

What are the main symptoms of TB

A

VARIABLE - Fever, night sweats, dyspnoea, bronchopneumonia, respiratory distress

61
Q

Name the stages of TB

A

Primary TB - lung initially, usually asymptomatic, Granulomas with multinucleated Langhans’ giant cells & caseous necrosis, usually resolves but TB can still persist (dampened down by macrophages).

Secondary TB - reanimation of TB usually with immunosuppression/elderly - occurs in lung apices

Military TB - spread to other organs. Granulomas in multiple organs. AntiTB chemo required to prevent death (EMERGENCY)

62
Q

How does primary TB appear?

A

fibrous calcified scar

63
Q

What is bronchiectasis?

A

Permanent dilation of bronchi/bronchioles due to destruction of muscle and elastic tissue and contraction of fibrous tissue

64
Q

What are the predisposing conditions of bronchiectasis?

A

Infections and disease…

  • Cystic fibrosis
  • Kartagener syndrome
  • Tumour, foreign body
  • Lupus, rheumatoid arthritis, inflammatory bowel disease, TB, whooping cough
65
Q

What is the main symptom/sign of bronchiectasis?

A

Copious production of foul smelling sputum

clubbing of fingers

66
Q

What are the two types of obstructive airway disease?

A

Diffuse

Localised

67
Q

How are localised obstructive airway diseases caused?

A

Localised obstruction e.g. foreign body/tumour

68
Q

How do localised obstructive airway diseases appear in pulmonary function tests?

A

Normal

69
Q

How to diffuse obstructive airway diseases appear on pulmonary function tests?

A

‘Obstructive’ pulmonary test

70
Q

What are diffuse obstructive airway diseases caused by?

A

Reversible/irreversible abnormalities of the bronchi/bronchioles - main ‘resistance vessel’ in the lungs

71
Q

How will diffuse obstructive diseases appear in pulmonary function tests?

A

Obstructive
Reduced FEV1 and VC and reduced FEV1:VC ratio
Reduced PEFR

72
Q

What are the principle conditions of diffuse obstructive airway disease?

A 
Chronic bronchitis 
COPD
Asthma
Emphysema 
Obliterate brochilitis
73
Q

What is the definition of chronic bronchitis and what is the main cause?

A
  • Sputum production and coughing for 3 months on 2 consecutive years
  • Smoking = major cause
74
Q

What are the clinical features of chronic bronchitis?

A

Mucus hyper secretion and hypertrophy of mucus glands

75
Q

What is emphysema?

A

Abnormal dilation of the of alveolar spaces DISTAL to terminal bronchioles

76
Q

Name the 3 classifications of emphysema and their aetiology

A

Centrilobular/centriacinar - respiratory bronchioles - smoking and coal dust

Panlobular/panacinar - dilation of airspaces distal to terminal alveolar spaces - due to Alpha 1 antitrypsin deficiency

Paraseptal/distalacinar - alveoli - fibrosis and scarring (mainly due to smoking)

77
Q

What is COPD?

A

Condition where both chronic bronchitis and emphysema coexist (associated with smoking)

78
Q

Where are the clinical features of COPD?

A

Dyspnea
Sputum production
Chronic cough
Cor Pulmonale (chronic bronchitis)

79
Q

What are the two types of patients with COPD?

A

Blue bloaters - predominately chronic bronchitis

Pink puffers - predominately emphysema

80
Q

Why blue bloaters? (cyanosis, bloated, cor pulmonale)

A

COUGHING Musculociliary dysfunction and increased goblet cell numbers/secretion (increased mucus production/coughing) - infections common

BLUE Obstruction leads to alveolar hypoxia (cyanosis). Increased pulmonary constriction and increased pulmonary hypertension. Increased back flow of blood to right side of heart (cor pulmonale).

Decreased circulating volume - increased RAAS activation - increased fluid retention

81
Q

Why pink puffers? (Barrel chested, breathless, thin)

A
  • Inflammatory response - proteases and elastase - destruction of capillary beds (reduced perfusion) and alveolar integrity (reduced elastic recoil - reduced ventilation)
  • Reduced ventilation - ‘air trapping’ - barrel chested
  • Reduced ventilation - increased work to breath - dyspnea and cachexia
82
Q

What is asthma?

A
  • Reversible small airway obstruction
83
Q

What is acute asthma characterised by?

A
  • Bronchial obstruction (wheeze, dyspnoea, tachypnoea) - leads to distal overinflation or collapse
  • Bronchospasm
  • Bronchial inflammation - eosinophils, plasma cells, lymphocytes
  • Oedema
  • MUCUS PLUGGING
84
Q

What is chronic asthma (repeated attacks) characterised by?

A
  • Mucus gland hypertrophy
  • Bronchial wall smooth muscle hypertrophy and fibrosis
  • Thickening of bronchial basement membrane
85
Q

What are the clinicopathological classifications of asthma?

A

Atopic- environmental
Non-atopic - bronchospasm with respiratory infections
Aspirin-induced
Occupational
Allergic bronchpulmonary aspergillosis (ABPA) - inhalation of Aspergillus fumigatus

86
Q

What are interstitial diseases of the lung and what do they usually present?

A 
Heterogenous group of conditions 
Increasing breathlessness
Hypoxia
RESTRICTIVE LUNG FUNCTION  
Bilateral shadowing of lungs on X-ray
87
Q

What part of lung do interstitial lung diseases mostly affect?

A

Alveoli (mainly walls)

88
Q

What is the major cause of interstitial lung diseases?

A

Inflammatory infiltrates and/or increased fibrous tissue
in the lung
- increases stiffness, decreases compliance and increased gas exchange distance

89
Q

What happens with acute interstitial disease? aka acute interstitial pneumonia

A

Type I pneumocyte death
Alveolar exudate
Formation of hyaline membranes
Type II pneumocyte hyperplasia

90
Q

What is the main causes of adult respiratory distress syndrome?

A

Massive insult to alveolar capillary walls,

leading to alveolar damage e.g. trauma, injury, radiation etc

91
Q

What are the major symptoms of chronic interstitial lung disease?

A
  • Increasing dyspnoea over months - years
  • Fibrotic/inflammatory in nature
  • clubbing, crackles, dry cough
92
Q

What are the main chronic interstitial lung diseases?

A 
idiopathic pulmonary fibrosis,  
pneumoconioses  
sarcoidosis,  
collagen vascular diseases
associated lung diseases
93
Q

What are the lung pneumoconiosis?

A

Dust diseases

94
Q

What types of dust diseases are there?

A

inert
fibrogenic
allergenic
oncogenic

95
Q

What is silicosis?

A

Diseases involving silica - sand & stone dust

Clinical Pathology (50 decks)

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