Pulmonary conditions - Pathology 1 Flashcards

(69 cards)

1
Q

what is an acinus (terminal respiratory unit)

A
  • this is a functional unit, the part of the respiratory tract distal to terminal bronchioles
  • where the gas exchange occurs
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2
Q

for normal gas exchange what should only be allowed to be there structurally

A
  • flat epithelial cell that forms the lining of the alveoli sac
  • basement membrane of that
  • blood
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3
Q

describe the structure of the trachea

A
  • c shaped cartilage rings

- mucous glands

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4
Q

Describe the structure of the bronchi

A
  • discontinuous cartilage plates

- mucous glands

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5
Q

describe the structure of bronchioles

A
  • No cartilage or mucous glands
  • terminal bronchioles are less than 2mm in diameter
  • respiratory bronchioles is where the gas exchange begins
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6
Q

describe the structure of alveolar ducts

A
  • flat epithelium

- no glands or cilia

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7
Q

Describe the structure of the alveolar sacs

A
  • no glands

- no cilia

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8
Q

What is the definition of pulmonary oedema

A
  • accumulation of fluid in the paraenchyma and interstitial of the lung
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9
Q

What is the usual cause of pulmonary oedema

A
  • haemodynamic - usually cardiogenic due to a problem in the heart
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10
Q

What does pulmonary oedema look like on autopsy

A
  • heavy wet lungs
  • alveolar pink granular fluid in the alveoli - may contain haemosiderin-laden macrophages
  • resolution or brown induration if long standing
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11
Q

What is diffuse alveolar damage (ARDS; Shock lung)

A
  • oedema caused by injury to alveolar capillary endothelium

- rapidly developing life-threatening respiratory insufficiency

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12
Q

What can cause diffuse alveolar damage (ARDS; Shock lung)

A
  • shock
  • trauma
  • sepsis
  • viral infection
  • noxious gases
  • radiation
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13
Q

What does diffuse alveolar damage (ARDS; Shock lung) look like on microscopy

A
  • oedema fluid and fibrinous membranes lining the alveoli

- does not resolve but proceeds to severe scarring and lung parenchyma is often lost

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14
Q

Name two types of pulmonary emboli

A
  • large saddle emboli

- smaller emboli

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15
Q

What are large saddle emboli

A
  • immediately fatal

- lodge at the bifurcation of pulmonary trunk

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16
Q

What are smaller emboli

A
  • these lodge peripherally and result in characteristic wedge shaped infarcts
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17
Q

How do the pulmonary arteries become occluded

A
  • pulmonary arteries occlusion by circulating clots usually from the lower limb veins in bed-ridden
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18
Q

What can cause pulmonary hypertension

A
  • COPD
  • left heart valvular disease
  • recurrent thromboembolism
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19
Q

What can pulmonary hypertension cause to happen to the heart

A
  • this can cause right ventricular hypertrophy and failure = chronic cor pulmonale
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20
Q

describe what happens to the airway in obstructive pulmonary disease

A
  • increased resistance to airflow at any level

- this is due to airway narrowing or loss of recoil

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21
Q

Describe what happens to total lung capacity and FEV1 in obstructive airway

A
  • there is no decrease in lung capacity

- reduced FEV1

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22
Q

What happens to cause a restrictive lung disease

A
  • reduced expansion of lung parenchyma

- caused by chest wall disorders or interstitial/infiltrative diseases

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23
Q

What happens to total lung capacity and FEV1 in restrictive pulmonary diseases

A
  • Decreased total lung capacity

- reduced TLC with proportionate reduction in FEV1

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24
Q

define chronic obstructive airway disease

A
  • a group of disease characterised by obstruction to airflow - this obstruction can be intermittent, reversible or irreversible and at any level of the respiratory tract
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25
Name examples of COPDs
- chronic bronchitis - emphysema - bronchial asthma - bronchiectasis
26
what two COPDs are always co existent
- chronic bronchitis and emphysema
27
What causes chronic bronchitis and emphysema
- almost always entirely due to smoking
28
what is the Clinical definition of chronic bronchitis
- productive cough for longer than 3 months in 2 consecutive years
29
describe what happens to the structure of the lung in chronic bronchitis
Effects of smoking: - mucous gland hypertrophy due to smoking - mucus hyper secretion due to the hypertrophy - this leads to obstruction of the airway - this can then become infected which causes more mucus secretion and can become worse - therefore it is a progressive disease
30
Describe the characteristics of chronic bronchitis
- hypoxia - hypercapnia (excess carbon dioxide) - cyanosis prone
31
What is the pathological definition of emphysema
- permanent dilatation of airway distal to terminal bronchiole
32
Describe what happens to the structure of the lungs in emphysema
- centriacinar/panacinar/irregular - elastin destruction that leads to the loss of elastic recoil therefore have problems exhaling - tends to hyperventilate and blood gases are normal
33
What do the blood gases in emphysema
Blood gases are normal
34
What are the types of emphysema
- centriacinar - panacinar - paraseptal - irregular
35
define centriacinar emphysema
- central/proximal parts of respiratory bronchioles are affected - distal spared - seen in smokers
36
Define panacinar emphysema
- uniform dilatation of acini from respiratory bronchiole to alveoli, seen in alpha-1-anti trypsin deficiency
37
Define paraseptal emphysema
- peripheral along lung margins - occurs adjacent to scarring, collapse or fibrosis - predisposes to spontaneous pneumothorax in young adults
38
define irregular emphysema
- irregular involvement of acini seen with scarring
39
Describe the pathogenesis of emphysema in smoking and hereditary
- all of the normal elastin is kept in check by elastase and anti elastase - there are enzymes that synthesis and get rid of the elastin - if you mess up that balance this results in a net elastic damage - there is a congenial absence of an anti elastase, such as in alpha 1 anti trypsin, therefore shifting to more elastase activity therefore causing more damage of elastin - in smoking there is a shift to elastase due to macrophages and pro inflammatory response due to inflammation
40
what emphysema leads to a pneumothorax
- peripheral emphysema with sub pleural bullae
41
What is bronchial asthma
- increased irritability of the bronchial treat | - paroxysms of reversible bronchospasm
42
What is the cause of bronchial asthma
- atopic caused by type 1 hypersensitivity to common allergens such as pollen and house dust - others: aspirin-induced, occupational, infection (allergic bronchopulmonary aspergillosis)
43
What causes bronchiectasis
- permanent dilatation of bronchi and bronchioles with necrosis of their walls
44
What causes bronchiectasis
- usually obstruction or childhood viral pneumonia | - airways become saclike, filled with foul-smelling pus
45
What are the symptoms of bronchiectasis
- chronic paroxysmal cough only brought on by a change in posture as the cough moves into a viable position in the bronchial tree
46
What are the complications of bronchiectasis
- abscess - fibrosis - amyloid - clubbing - cor pulmonale
47
what are restrictive lung diseases characterised by
- diffuse and chronic damage to delicate pulmonary interstitium, basement membrane, collagen fibres, elastic tissue fibroblasts and few leucocytes
48
What are the physiological restrictive lung diseases characterised by
- reduced oxygen diffusing capacity | - lung volume and lung compliance
49
What does the chest x ray of restrictive lung diseases look like
- Diffuse infiltration by small nodules, irregular lines or ground glass shadows
50
What are the causes of restrictive lung diseases
- environmental diseases, including occupational (25%) - sarcoidosis (20%) - collagen vascular disease (10%) - idiopathic pulmonary fibrosis (15%)
51
What is the definition of occupational lung disease
- Diseases caused by the inflation of dust particles, mineral or organic substances over many years due to occupational exposure
52
What are the two broad mechanisms of injury to lung in occupational lung disease
- Scarring from chronic irritation; inert substances such as coal workers pneumoconiosis - hypersensitivity; organic dusts
53
Name examples of occupational lung diseases
- Coal workers pneumoconiosis: antracosis, macule, progressive massive fibrosis - silicon - silicosis, Caplan's syndrome - asbestos = asbestosis, pleural plaques, Caplan syndrome, mesothelioma, cancer of lung, stomach and colon - farmers lung: baggassosis, byssinosis, bid breeders' lung due to organic dusts
54
What causes sarcoidosis
- Systemic disease of unknown cause
55
What is the characteristics of sarcoidosis
- caused by non caveating granulomatous reaction in many tissues; lungs involved in 90%
56
what is the treatment for sarcoidosis
- steroid therapy is unpredictable
57
What can cause lung cancer
- cigarette smoking - asbestos - mineral dusts - radiation - pollution - scarring
58
What cancers can be caused by smoking
- lip - tongue - floor of mouth - larynx - oesophagus - urinary bladder - pancreas - kidney
59
How does cancer develop as a result of smoking
- respiratory epithelium is irritated by ciagrette smoke - the epithelium undergoes a process of metaplasia and the ciliated, mucus-secreting pseudo stratified columnar tissue changes to stratified squamous - this leads to squamous dysplasia - this leads to carcinoma
60
What are the types of lung cancer
- Squamous cell carcinoma (25-40%) - adenocarcinoma (25-40%) - small cell (oat cell) carcinoma (20-25%) - large cell carcinoma (10-15%)
61
what is the difference between small cell carcinoma or non small cell carcinoma
Small cell carcinoma - more aggressive - not treatable surgically, usually widely disseminated at time of diagnosis - treatment is chemotherapy Non small cell carcinoma - surgically treatable
62
What is the treatment therapy of non small cell carcinoma of the lung
- targeted therapy for non small cell lung cancers 1. tumour cells express growth factor receptors; blocking these signals stop cancer cells from dividing; to block these we can do one of the following - block the receptor using an antibody - block the cell pathway by using a small molecule that goes into the cell 2. stop erratic growth of blood vessels by the tumour 3 encourage immune response to fight against tumour cells
63
What receptors do we have for the treatment of non small cell carcinoma of the lung
- EGFR - VEGF - ALK-EMLF - ROS - MET - BRAF - PDE1 Blockage
64
What are the clinical features of lung cancer
Local - cough - haemoptysis - pain General - weight loss - clubbing - hypertrophic pulmonary osteoarthropathy Paraneoplastic syndromes - due to ectopic hormone production by tumour cells such as hypercalcaemia, SIADH
65
What is a paraneoplastic syndromes
- signs and symptoms that are not related to the physical presence of the tumour or its metastases but due to the hormonal production of the tumour
66
what is the prognosis of lung cancer
- staging is most important determinant - non small cell versus small cell tumour - overall 5 year survival is less than 10%
67
What is the cause of bronchiectasis
- Post infective – TB, measles, pneumonia - Bronchial obstruction e.g. lung cancer/foreign body - Immune deficiency: selective IgA - Allergic bronchopulmonary aspergillosis - Yellow nail syndrome - Kartageners syndrome
68
What is the management of bronchiectasis
hysical training – e.g. inspiratory muscle training - Postural drainage - Antibiotics for exacerbations and long term rotating antibiotics - Bronchodilators in selected cases - Immunisations
69
What are the causes of clubbing
- Lung cancer - bronchiectasis - interstitial lung disease - pulmonary fibrosis - tuberculosis - lung abscess - cystic fibrosis - empyema - sarcoidosis