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Lung Pathology Flashcards

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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
Signs, symptoms, pathology of desquamative interstitial pneumonia
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
26
Signs and symptoms of non-specific interstitial pneumonia
Dyspnoea Cough Middle aged adults Underlying connective tissue disease in some patients Steroid responsive in most patients Microscopy --> uniform interstitial inflammatory and fibrosing process
27
Antigens implicated in extrinsic allergic alveolitis
Wide range Including drugs In a significant number NO antigen can be found
28
What is extrinsic allergic alveolitis otherwise known as
Hypersensitivity pneumonitis
29
Clinical presentation of hypersensitivity pneumonitis
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
Hypersensitivity pneumonitis radiological features
Lower love ground glass and fine nodular densities characteristic
31
Hypersensitivity pneumonitis histological features
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
Occupational disease in the lung
``` Occupational asthma Pneumonitis with ARDS appearance - acute respiratory distress syndrome Hypersensitivity pneumonitis Emphysema Pulmonary or pleural fibrosis Malignancy - lung, pleura ```
33
Types of fibrogenic dusts
Silicosis Asbestos Hard metal disease - tungsten, cobalt
34
What is the most prevalent chronic occupational disease worldwide
Silicosis
35
Occurrence of crystalline silica
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
What does silicosis do to the lungs
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
Microscopy of silicosis
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
Immune dysfunction in silicosis
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
Coal workers pneumoconiosis
``` 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
Progressive massive fibrosis
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
Pulmonary massive fibrosis pathology
``` 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
Asbestos types
Amphibioles | Serpentine
43
Amphiboles
Crocidolite and amosite (blue and brown asbestos) Stiff, straight and brittle Fibres less prevalent More pathogenic as impacted in airways and lungs
44
Serpentines
Chrysotile white asbestos Cleared reasonably effectively from airway Less pathogenic than amphiboles
45
Asbestos chest disease
Can affect pleura and lungs and can benign and malignant
46
Asbestos benign disease
Pleural plaques Benign pleural thickening Pleural effusion Interstitial fibrosis (asbestosis)
47
Pleural plaques
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
Asbestos malignant disease
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
Risk of cancer
Non smoker RR =1 Asbestos and no smoker = rr 5 Asbestos and smoker RR = 55
50
How is asbestos inhalation assessed
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
What is pulmonary hypertension
When the means pulmonary arterial pressure is greater than 25mmHg at rest or 30mmHg during exercise
52
Primary pulmonary hypertension
Rare Females > males Often affects young adults Very poor prognosis - transplant may be necessary
53
Secondary pulmonary hypertension
``` Left to right cardiac shunts Venous back pressure - mitral stenosis Hypoxaemic lung disease - chronic bronchitis - emphysema Drugs Vascular obstruction - repeated Pulmonary thromboembolism ```
54
Cause of pulmonary hypertension
``` 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
Pulmonary hypertension morphology
``` Muscularisation of the arterioles Medical thickening of muscular arteries Intimal thickening Plexiform lesions Fibrinoid necrosis ```
56
Pathophydiology of acute asthma
``` 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
Lung mechanics in asthma
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
What are the abnormalities in measurements
Dec FEV1, FEV1/FVC Dec FVC as airways close prematurely Inc RV obstruction Inc FRR and TLC
59
Asthma presentation
Cough Tight chest Wheeze Dyspnoea
60
Asthma history
``` 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
Asthma examination
``` Inc resp rate Accessory muscles -sternocleidomastoid Tachycardia Talking in full sentence - difficult due to dyspnoea Wheeze polyphonic ```
62
How to recognise asthma severity
``` 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
Pathophydiology of acute asthma
``` 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
Lung mechanics in asthma
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
What are the abnormalities in measurements
Dec FEV1, FEV1/FVC Dec FVC as airways close prematurely Inc RV obstruction Inc FRR and TLC
66
Asthma presentation
Cough Tight chest Wheeze Dyspnoea
67
Asthma history
``` 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
Asthma examination
``` Inc resp rate Accessory muscles -sternocleidomastoid Tachycardia Talking in full sentence - difficult due to dyspnoea Wheeze polyphonic ```
69
How to recognise asthma severity
``` 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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