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Year 3 - CR > Pulmonary conditions - Pathology 1 > Flashcards

Pulmonary conditions - Pathology 1 Flashcards

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
Q

Name examples of COPDs

A
  • chronic bronchitis
  • emphysema
  • bronchial asthma
  • bronchiectasis
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26
Q

what two COPDs are always co existent

A
  • chronic bronchitis and emphysema
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27
Q

What causes chronic bronchitis and emphysema

A
  • almost always entirely due to smoking
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28
Q

what is the Clinical definition of chronic bronchitis

A
  • productive cough for longer than 3 months in 2 consecutive years
29
Q

describe what happens to the structure of the lung in chronic bronchitis

A

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
Q

Describe the characteristics of chronic bronchitis

A
  • hypoxia
  • hypercapnia (excess carbon dioxide)
  • cyanosis prone
31
Q

What is the pathological definition of emphysema

A
  • permanent dilatation of airway distal to terminal bronchiole
32
Q

Describe what happens to the structure of the lungs in emphysema

A
  • 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
Q

What do the blood gases in emphysema

A

Blood gases are normal

34
Q

What are the types of emphysema

A
  • centriacinar
  • panacinar
  • paraseptal
  • irregular
35
Q

define centriacinar emphysema

A
  • central/proximal parts of respiratory bronchioles are affected
  • distal spared
  • seen in smokers
36
Q

Define panacinar emphysema

A
  • uniform dilatation of acini from respiratory bronchiole to alveoli, seen in alpha-1-anti trypsin deficiency
37
Q

Define paraseptal emphysema

A
  • peripheral along lung margins
  • occurs adjacent to scarring, collapse or fibrosis
  • predisposes to spontaneous pneumothorax in young adults
38
Q

define irregular emphysema

A
  • irregular involvement of acini seen with scarring
39
Q

Describe the pathogenesis of emphysema in smoking and hereditary

A
  • 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
Q

what emphysema leads to a pneumothorax

A
  • peripheral emphysema with sub pleural bullae
41
Q

What is bronchial asthma

A
  • increased irritability of the bronchial treat

- paroxysms of reversible bronchospasm

42
Q

What is the cause of bronchial asthma

A
  • atopic caused by type 1 hypersensitivity to common allergens such as pollen and house dust
  • others: aspirin-induced, occupational, infection (allergic bronchopulmonary aspergillosis)
43
Q

What causes bronchiectasis

A
  • permanent dilatation of bronchi and bronchioles with necrosis of their walls
44
Q

What causes bronchiectasis

A
  • usually obstruction or childhood viral pneumonia

- airways become saclike, filled with foul-smelling pus

45
Q

What are the symptoms of bronchiectasis

A
  • chronic paroxysmal cough only brought on by a change in posture as the cough moves into a viable position in the bronchial tree
46
Q

What are the complications of bronchiectasis

A
  • abscess
  • fibrosis
  • amyloid
  • clubbing
  • cor pulmonale
47
Q

what are restrictive lung diseases characterised by

A
  • diffuse and chronic damage to delicate pulmonary interstitium, basement membrane, collagen fibres, elastic tissue fibroblasts and few leucocytes
48
Q

What are the physiological restrictive lung diseases characterised by

A
  • reduced oxygen diffusing capacity

- lung volume and lung compliance

49
Q

What does the chest x ray of restrictive lung diseases look like

A
  • Diffuse infiltration by small nodules, irregular lines or ground glass shadows
50
Q

What are the causes of restrictive lung diseases

A
  • environmental diseases, including occupational (25%)
  • sarcoidosis (20%)
  • collagen vascular disease (10%)
  • idiopathic pulmonary fibrosis (15%)
51
Q

What is the definition of occupational lung disease

A
  • Diseases caused by the inflation of dust particles, mineral or organic substances over many years due to occupational exposure
52
Q

What are the two broad mechanisms of injury to lung in occupational lung disease

A
  • Scarring from chronic irritation; inert substances such as coal workers pneumoconiosis
  • hypersensitivity; organic dusts
53
Q

Name examples of occupational lung diseases

A
  • 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
Q

What causes sarcoidosis

A
  • Systemic disease of unknown cause
55
Q

What is the characteristics of sarcoidosis

A
  • caused by non caveating granulomatous reaction in many tissues; lungs involved in 90%
56
Q

what is the treatment for sarcoidosis

A
  • steroid therapy is unpredictable
57
Q

What can cause lung cancer

A
  • cigarette smoking
  • asbestos
  • mineral dusts
  • radiation
  • pollution
  • scarring
58
Q

What cancers can be caused by smoking

A
  • lip
  • tongue
  • floor of mouth
  • larynx
  • oesophagus
  • urinary bladder
  • pancreas
  • kidney
59
Q

How does cancer develop as a result of smoking

A
  • 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
Q

What are the types of lung cancer

A
  • Squamous cell carcinoma (25-40%)
  • adenocarcinoma (25-40%)
  • small cell (oat cell) carcinoma (20-25%)
  • large cell carcinoma (10-15%)
61
Q

what is the difference between small cell carcinoma or non small cell carcinoma

A

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
Q

What is the treatment therapy of non small cell carcinoma of the lung

A
  • 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
Q

What receptors do we have for the treatment of non small cell carcinoma of the lung

A
  • EGFR
  • VEGF
  • ALK-EMLF
  • ROS
  • MET
  • BRAF
  • PDE1 Blockage
64
Q

What are the clinical features of lung cancer

A

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
Q

What is a paraneoplastic syndromes

A
  • 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
Q

what is the prognosis of lung cancer

A
  • staging is most important determinant
  • non small cell versus small cell tumour
  • overall 5 year survival is less than 10%
67
Q

What is the cause of bronchiectasis

A
  • 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
Q

What is the management of bronchiectasis

A

hysical training – e.g. inspiratory muscle training

  • Postural drainage
  • Antibiotics for exacerbations and long term rotating antibiotics
  • Bronchodilators in selected cases
  • Immunisations
69
Q

What are the causes of clubbing

A
  • Lung cancer
  • bronchiectasis
  • interstitial lung disease - pulmonary fibrosis
  • tuberculosis
  • lung abscess
  • cystic fibrosis
  • empyema
  • sarcoidosis

Year 3 - CR (44 decks)

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