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Y3 > Lung Pathology > Flashcards

Lung Pathology Flashcards

1
Q

Define asthma

A

Paroxysmal contraction of airways resulting in decreased airflow due to reversible airway obstruction over a period of time
Restricted airway causes - increased production of mucus, enlarged smooth muscle, narrowed bronchiole

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2
Q

Types of asthma

A

Extrinsic -
- children predominate
- exposure to external agent e.g. Pollen, chemicals, (occupational), drugs Aspergillus
Intrinsic
- adults predominate
- causes include exercise, infection, stress

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3
Q

Causes of asthma

A

Genetic - atopic individual those who have hay fever and eczema
Environmental- pollution, smoke, particular allergens
Viral bacterial infection
Medication beta blockers and NSAIDS
Emotional factors and stress

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4
Q

What happens at the mast cells

A 
Allergen binds to IgE 
Mast cells degranulate 
Histamine and leukotrienes released 
Inflammation of the lung tissue 
Introduces other inflammatory cells to the area cause epithelia also shredding, goblet cell discharge, plasma leak and oedema
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5
Q

Signs of asthma at the lung tissue

A

Shedding of bronchial epithelial cells - due to specific failure on intercellular adhesion mechanisms
Thickening of epithelial basement membrane
Eosinophils and by products of their degranulation
(Charcot Leyden crystals)
Increased bronchial gland mass with increased mucus- curschmanns spirals
Increased smooth muscle
Inflammation of bronchial mucosa: t lymphocytes, eosinophils, +/- neutrophils

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6
Q

What is status asthmaticus

A

Hyperinflation - not due to emphysema
Petechial haemorrhages
Mucoid plugging of large and small airways
Atelectasis (resorption collapse distal to mucoid impaction in segmental bronchi)

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7
Q

What are the components of COPD

A

Chronic obstructive pulmonary disease
Chronic bronchitis
Emphysema

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8
Q

Chronic bronchitis facts

A

Essentially a clinical diagnosis
May be prone to recurrent infections
‘Blue bloater’
Increased mass of bronchial mucus glands

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9
Q

Emphysema

A

Essentially a pathological/morphological diagnosis
Pink puffer clinically
Loss of alveolar walls and dilatation of air spaces clinically

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10
Q

Chronic bronchitis definition

A

A persistent cough with sputum production for at least 3 months over the past 2 consecutive years

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11
Q

Causes of chronic bronchitis

A

Tobacco smoking

Atmospheric pollution

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12
Q

The pathological changes in the large airways in chronic bronchitis

A

Increase in submucosal gland mass
Increase no of goblet cells
Increase in smooth muscle
Chronic inflammatory cell infiltrate of lamina propria

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13
Q

Define emphysema

A

Abnormal permanent enlargement of air spaces distal to the terminal bronchiole, accompanied by destruction of their walls without obvious fibrosis

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14
Q

Morphological types of emphysema

A

Centrilobular - 75% cases generally caused by cigarette smoking
Panacinar (panlobular) - associated with alpha 1 antitrypsin deficiency
Paraseptal (distal acinar) - cause unclear may be a cause of spontaneous pneumothorax
Irregular emphysema - associated with scarring clinically not significant

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15
Q

Other Types of emphysema

A

Compensatory emphysema - response to loss of lung elsewhere e.g. Through surgery
Senile emphysema - age related
Obstructive emphysema - tumour, overinflation e.g. Congenital abnormality
Bullous emphysema - associated with bullae often with a background of centrilobular emphysema
Interstitial emphysema - air in connective tissue of lung, pleura or mediastinum

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16
Q

Centrilobular emphysema facts

A

Common
Linked with tobacco smoking and atmospheric pollution
Involves preferentially the centre of the acinus around the terminal bronchiole

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17
Q

Complications of COPD

A

Cor pulmonale
Respiratory failure
Polycythaemia
Lung cancer - double the incidence in male bronchitis
Pneumothorax - ruptured Bullae can occur if there is coexistant emphysema

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18
Q

What is Interstitial pulmonary fibrosis

A

A condition characterised by progressive interstitial scarring leading to respiratory incapacity, and effacement of the lung architecture, which in extreme cases may result in a honeycomb pattern

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19
Q

What is honeycomb lung

A

‘Cysts’ several mm to >1cm diameter, in background of dense fibrous scarring
Most prominent in subpleural parenchyma at the lung bases

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20
Q

Honeycomb lung causes

A

Antecedent lung diseases:
Idiopathic interstitial pneumonia (UIP, DIP)
DAD
Inorganic dust exposure
Interstitial granulomatous disease e.g. Infections, hypersensitivity pneumonia (EAA), sarcoidosis, berylliosis
Histiocytosis X

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21
Q

Types of interstitial fibrosing alveolitis

A 
Idiopathic (cryptogenic [CFA] ) 
- diagnosis is by exclusion
- incidence 3-5/1000000
Secondary including 
- connective tissue diseases
- dust and smoke inhalation 
- asbestos
- EEA, sarcoidosis
- shock lung, radiation 
- drugs
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22
Q

Morphological patterns of interstitial pulmonary fibrosis

Mortality rates

A

AIP - acute interstitial pneumonia -60%
UIP - usual interstitial pneumonia - nearly 80%
DIP - desquamate interstitial pneumonia - nearly 40%
NSIP - non specific interstitial pneumonia -10%
GIP, LIP probably not as important

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23
Q

What is acute interstitial pneumonia

A

Individuals are well
Signs of URTI
they have progressive rapid respiratory failure
High mortality
Essentially signs of diffuse alveolar damage
Necrosis of alveolar lining cells with exudate
Hyaline membranes are frequently seen
Later organisation by fibrosis occurs
Hugh mortality

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24
Q

Signs, symptoms and pathology of usual interstitial pneumonia

A

Insidious onset of dyspnoea, in adults 40-70 years
Progressive down hill course, median survival 4-5 years
Seen with CFA but may also be associated with collagen vascular diseases, especially rheumatoid arthritis and scleroderma
Pathology - heterogenous, non-uniform inflammatory and fibrosing process, fibroblastic foci, honeycomb damage

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25
Q

Signs, symptoms, pathology of desquamative interstitial pneumonia

A

Uncommon
Occurs in Middle Aged smokers
Dyspnoea and cough
Usually responds to steroid treatment
Relatively good prognosis
Now believed to be related to respiratory bronchiolitis
Pathology- increased numbers of macrophages in alveolar spaces, uniform interstitial fibrosis

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26
Q

Signs and symptoms of non-specific interstitial pneumonia

A

Dyspnoea
Cough
Middle aged adults
Underlying connective tissue disease in some patients
Steroid responsive in most patients
Microscopy –> uniform interstitial inflammatory and fibrosing process

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27
Q

Antigens implicated in extrinsic allergic alveolitis

A

Wide range
Including drugs
In a significant number NO antigen can be found

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28
Q

What is extrinsic allergic alveolitis otherwise known as

A

Hypersensitivity pneumonitis

29
Q

Clinical presentation of hypersensitivity pneumonitis

A

Acute: follows exposure to large amounts of antigen. Sudden onset of dyspnoea, fever, chills. Symptoms subside following cessation of exposure, reappear on rexposure
Chronic: results from prolonged exposure to small amounts of antigen. Insidious onset of dyspnoea, dry cough, fatigue, reticulonodukar infiltrates on CXR, can progress to irreversible lung damage if exposure persists.

30
Q

Hypersensitivity pneumonitis radiological features

A

Lower love ground glass and fine nodular densities characteristic

31
Q

Hypersensitivity pneumonitis histological features

A

Variable lymphoplasmocellular infiltrate centred on small airways and alveolar ducts
Small non-necrotising loose granulomas
Foamy macrophages
BOOP like pattern in 50% of cases
BOOP - bronchiolitis-obliterates-organising-pneumonia

32
Q

Occupational disease in the lung

A 
Occupational asthma
Pneumonitis with ARDS appearance - acute respiratory distress syndrome 
Hypersensitivity pneumonitis 
Emphysema
Pulmonary or pleural fibrosis 
Malignancy - lung, pleura
33
Q

Types of fibrogenic dusts

A

Silicosis
Asbestos
Hard metal disease - tungsten, cobalt

34
Q

What is the most prevalent chronic occupational disease worldwide

A

Silicosis

35
Q

Occurrence of crystalline silica

A

Silicone dioxide basic component of sand, quartz, granite
Second most common mineral in the earths crust
Airborne silica produced by
Sandblasting
Rock drilling
Foundry work
Quarrying

36
Q

What does silicosis do to the lungs

A

Collagenous nodules form within the lungs and in the mediastinal lymph nodes
It is irreversible
Low mortality but of severe tends to cause respiratory incapacity
Many cases asymptomatic
Often long latency between exposure and development of silicosis
Pathology -well defined nodular opacities in the upper and posterior lung zones
Lung nodules may coalesce to form confluence complicated nodules

37
Q

Microscopy of silicosis

A

Whorled laminated well circumscribed nodules of collagen (onion skin)
Anthracotic pigment may also be present
May be found anywhere in the lung
Hilar lymph node involvement invariably involved and may be the sole representation of the disease
Alveolar lipoproteinosis may be seen in acute silicotic workers

38
Q

Immune dysfunction in silicosis

A

Promotes development of mycobacterial infection - TB and atypical forms
Up to 5% cases complicated by TB
Increased risk of connective tissue disorders particularly scleroderma
Patients with silicosis have increased levels of autoantibodies in the blood
Likely due to depressed cell immunity and macrophage function

39
Q

Coal workers pneumoconiosis

A 
May be asymptomatic 
Variable quartz and carbon 
Pathological findings 
Coal dust macule 
Upper lobe predominance 
Histologically 
- accumulation of coal dust around respiratory bronchioles
- nodular lesions with silicotic morphology maybe found 
- emphysema invariably present
40
Q

Progressive massive fibrosis

A

Progressive from dust macules
By definition - nodules >10mm
Probably related to quartz/silica content of inspired particles
Not related to cigarette smoking
May progress in the absence of any coal mining exposure

41
Q

Pulmonary massive fibrosis pathology

A 
Upper zone predominant - related to poor lymphatic drainage 
Locally destructive rubbery 
Cavitation may occur but exclude TB 
Microscopy - 
Black lipid debris 
Deposition of cholesterol clefts 
Necrosis 
Giant cells
42
Q

Asbestos types

A

Amphibioles

Serpentine

43
Q

Amphiboles

A

Crocidolite and amosite (blue and brown asbestos)
Stiff, straight and brittle
Fibres less prevalent
More pathogenic as impacted in airways and lungs

44
Q

Serpentines

A

Chrysotile white asbestos
Cleared reasonably effectively from airway
Less pathogenic than amphiboles

45
Q

Asbestos chest disease

A

Can affect pleura and lungs and can benign and malignant

46
Q

Asbestos benign disease

A

Pleural plaques
Benign pleural thickening
Pleural effusion
Interstitial fibrosis (asbestosis)

47
Q

Pleural plaques

A

Fairly common
Non neoplastic and invariably asymptomatic
Irreversible and composed of hyalinised collagen possibly also showing calcification
Implies asbestos exposure
BUT
Does not indicate asbestosis

48
Q

Asbestos malignant disease

A

Mesothelioma - 90% associated with asbestos exposure often decades previously
Bronchiogenic carcinoma
- invariably associated with accompanying asbestosis
- all forms of lung cancer may occur but particularly adenocarcinomas
Other cancers
-laryngeal carcinoma
Colon cancer ?

49
Q

Risk of cancer

A

Non smoker RR =1
Asbestos and no smoker = rr 5
Asbestos and smoker RR = 55

50
Q

How is asbestos inhalation assessed

A

Inspection for the pressence of asbestos bodies
- characteristics beaded rod shaped structures coated with iron salts
Only a few asbestos fibres become coated in the way to become visible and their presence indicates significant asbestos inhalation
Digestion of tissue and manually counting asbestos fibres by microscopy

51
Q

What is pulmonary hypertension

A

When the means pulmonary arterial pressure is greater than 25mmHg at rest or 30mmHg during exercise

52
Q

Primary pulmonary hypertension

A

Rare
Females > males
Often affects young adults
Very poor prognosis - transplant may be necessary

53
Q

Secondary pulmonary hypertension

A 
Left to right cardiac shunts 
Venous back pressure - mitral stenosis 
Hypoxaemic lung disease 
- chronic bronchitis 
- emphysema 
Drugs 
Vascular obstruction 
- repeated Pulmonary thromboembolism
54
Q

Cause of pulmonary hypertension

A 
Prepulmonary 
Increased pressure and flow 
- congenital heart disease 
Pulmonary 
- disruption +\- loss of lung parenchyma 
- emphysema
- vascular obstruction 
-- chronic thromboembolism
- hyooxaemia 
-- COPD 
-- living at high altitudes 
Post pulmonary 
-- mitral stenosis
55
Q

Pulmonary hypertension morphology

A 
Muscularisation of the arterioles 
Medical thickening of muscular arteries 
Intimal thickening
Plexiform lesions 
Fibrinoid necrosis
56
Q

Pathophydiology of acute asthma

A 
Trigger which causes inflammation in the bronchioles 
-> airway hyper responsiveness
And smooth muscle contraction 
And increased mucous secretion
->
Airway obstruction and then clinical symptoms 
Inc mast cell 
Inc eosinophil 
Inc NKT
Inc T helper 2
57
Q

Lung mechanics in asthma

A

Incomplete expiation as the airways close prematurely leads to hyperinflation can’t breath out so inspiration is difficult
Tachypnoea
Positive end expiratory pressure (PEEP)
-gas trapping
- dynamic hyperinflation breath in and can’t completely breath out
- auto PEEP
Inc work of breathing and patient can tire
Inc residual volume due to unable to breath out, inc elastic load on respiratory muscle
Respiratory muscle must Uber come this for breathing so may tire
AutoPEEP / intrinsic positive end reps pressure

58
Q

What are the abnormalities in measurements

A

Dec FEV1, FEV1/FVC
Dec FVC as airways close prematurely
Inc RV obstruction
Inc FRR and TLC

59
Q

Asthma presentation

A

Cough
Tight chest
Wheeze
Dyspnoea

60
Q

Asthma history

A 
Pro drone of a cough, rhinorrhea, wheeze, fever, GI 
Speed of onset 
Associated illness
Precipitating exposure 
Number of admission 
No of ITU admission and intubation 
Best peak flow
Dec in activity
61
Q

Asthma examination

A 
Inc resp rate 
Accessory muscles 
-sternocleidomastoid 
Tachycardia
Talking in full sentence - difficult due to dyspnoea 
Wheeze polyphonic
62
Q

How to recognise asthma severity

A 
Moderate PEFR 50-75% of best or predicted 
Acute severe
PEF 33-50% best/predicted 
Resp rate more than 25 breaths min 
HR 110 above 
Inability to com
63
Q

Pathophydiology of acute asthma

A 
Trigger which causes inflammation in the bronchioles 
-> airway hyper responsiveness
And smooth muscle contraction 
And increased mucous secretion
->
Airway obstruction and then clinical symptoms 
Inc mast cell 
Inc eosinophil 
Inc NKT
Inc T helper 2
64
Q

Lung mechanics in asthma

A

Incomplete expiation as the airways close prematurely leads to hyperinflation can’t breath out so inspiration is difficult
Tachypnoea
Positive end expiratory pressure (PEEP)
-gas trapping
- dynamic hyperinflation breath in and can’t completely breath out
- auto PEEP
Inc work of breathing and patient can tire
Inc residual volume due to unable to breath out, inc elastic load on respiratory muscle
Respiratory muscle must Uber come this for breathing so may tire
AutoPEEP / intrinsic positive end reps pressure

65
Q

What are the abnormalities in measurements

A

Dec FEV1, FEV1/FVC
Dec FVC as airways close prematurely
Inc RV obstruction
Inc FRR and TLC

66
Q

Asthma presentation

A

Cough
Tight chest
Wheeze
Dyspnoea

67
Q

Asthma history

A 
Pro drone of a cough, rhinorrhea, wheeze, fever, GI 
Speed of onset 
Associated illness
Precipitating exposure 
Number of admission 
No of ITU admission and intubation 
Best peak flow
Dec in activity
68
Q

Asthma examination

A 
Inc resp rate 
Accessory muscles 
-sternocleidomastoid 
Tachycardia
Talking in full sentence - difficult due to dyspnoea 
Wheeze polyphonic
69
Q

How to recognise asthma severity

A 
Moderate PEFR 50-75% of best or predicted 
Acute severe
PEF 33-50% best/predicted 
Resp rate more than 25 breaths min 
HR 110 above 
Inability to com

Y3 (22 decks)

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