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Yr 2 - Clinical Pathology > Benign Lung Pathology > Flashcards

Benign Lung Pathology Flashcards

1
Q

Which of these 3 cross-sections would most likely work best at transmitting the fluid?

A

1 = size of lumen – 1 and 2 will allow greater volume of flow in short space of time

2 =wall strength - 1 may collapse as very thin, 2 and 3 probably strong enough

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2
Q

What are the 3 most important characteristics of airways?

A
  1. Size of lumen
  2. Wall strength
  3. Wall support
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3
Q

In this diagram, each length of the vertical blue line represents a set area of a gas exchange surface, and increased thickness, as in No 3, represents increased width and density of that gas exchange surface. The red arrow represents the gas being transferred across the surface. In this example, if we say a wide arrow represents 1 litre per second of gas transfer and a narrow arrow represents ½ litre per second, then which one enables the greatest gas transfer?

A

No 1 has 2 quantities of thin surface area = 2 litres per second.

No 2 has 1 quantity of thin surface area = 1 litre per second.

No 3 has 2 quantities of thick surface area = 1 litre per second.

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4
Q

What does the quality and thickness of alveolar walls affect?

A

Gas exchange

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5
Q

What is one of the key features of inflammation that could result in the wall of a tube narrowing the lumen?

A

Swelling (Tumour)

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6
Q

Acute inflammatory cells like neutrophils release chemicals such as proteases and active oxygen species to kill micro-organisms. What is the downside of these on the local tissues?

A

The downside is damage to the normal healthy cells / tissues and thereby potentially triggering further inflammation and damage

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7
Q

Histological view of tissue damage in airway

A
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8
Q

What are the 4 ways the tissues may respond locally after an episode of acute inflammation?

A

1 - complete resolution,

2 - chronic inflammation,

3 - loss of tissue

4 - scarring

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9
Q

What are acute inflammatory cells like neutrophils and macrophages replaced by as inflammation becomes chronic?

A

lymphocytes or macrophages forming granulomas

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10
Q

How can fibrosis affect the lungs?

A

fibrosis restricts expansion of the lung parenchyma

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11
Q

What can inflammation result in?

A
  • swelling
  • tissue damage
  • tissue loss
  • fibrosis
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12
Q

What is asthma?

A

Reversible intermittent narrowing of conducting airways

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13
Q

What is non-atopic asthma? When does it tend to develop?

A

Non-allergic asthma, or non-atopic asthma, is a type of asthma that isn’t related to an allergy trigger like pollen or dust, and is less common than allergic asthma. The causes are not well understood, but it often develops later in life, and can be more severe.

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14
Q

What are the 2 types of asthma?

A

Atopic (extrinsic) and non-atopic (intrinsic)

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15
Q

What can trigger asthma?

A

Allergens (pollen, house dust mite, animals), drugs (NSAIDs), cold, exercise, infections, emotion

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16
Q

Pathogenesis behind the trigger causing asthma?

A

Sensitisation to trigger followed by re-exposure to trigger causing airway narrowing

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17
Q

What morphological abnormalities are present in asthma? (wall, lumen)

A

Wall; thick (inflammation, tissue hyperplasia) and contracted (smooth muscle)

Lumen - mucus

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18
Q

Clinical presentation of asthma?

A

SOB, Wheeze, cough, hyperinflation

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19
Q

Airway during asthma exacerbation

A
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20
Q

What causes SOB and wheeze in asthma?

A

Tubes thickened and narrowed

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21
Q

What 3 main things cause the tubes to thicken and narrow in asthma?

A
  1. Smooth muscle contraction, (see hyperplastic/hypertrophied smooth muscle in bronchioles and bronchi)
  2. Inflammation, (wall of conducting airways is swollen with vasodilatation, fluid and inflammatory cells)
  3. Mucus (goblet cells and mucus glands are increased in number/size and increase in mucus filling lumen)
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22
Q

Asthma pathogenesis when exposed to allergen:

A
  1. Allergen/cold air etc triggers basophils/eosinophils
  2. These release histamine, prostaglandins and leukotrienes
  3. These cause;
    1. contraction of smooth muscle
    2. inflammation; vascular dilation and oedema
    3. increase mucus production
  • Airway surrounded by thickened smooth muscle which contracts and narrows the lumen
  • Inflammatory cells; cause vasodilation of vessels and oedema
    • This thickens the bronchial wall and narrows the lumen
  • Mucus in lumen narrows it even further
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23
Q

How does sensitisation occur during asthma?

A
  1. APC (with MHC II) presents antigen to Th2 cells
  2. Th2 cells release certain cytokines (IL-4);
    1. Cause B cells to switch from producing IgM to IgE
    2. Recruite and stimulate various inflammatory cells
  3. Antigen is then encountered again (cells are already there)
  4. Antigen reacts with IgE to cause widespread release of histamine/PGs/leukotrienes for eosinophils/basophils
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24
Q

Which 3 main changes occur during asthma?

A
  1. inflammation
  2. smooth muscle contraction
  3. mucus production
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25
Q

What is chronicobstructive pulmonary disease a combination of?

A

Chronic bronchitis & emphysema

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26
Q

How is chronic bronchitis defined?

A

Cough and sputum for 3 months in each of 2 consecutive years

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27
Q

Site of bronchitis?

A

Bronchus

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28
Q

Describe the;

a) wall of the bronchus
b) mucus gland
c) mucus production

in bronchitis? What will this do to airflow?

A

a) thickened by inflammation
b) mucus gland hyperplasia
c) by increased mucus production

This will obstruct airflow

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29
Q

What will this persistent mucus in bronchitis predispose to?

A

Infection if mucus isn’t cleared quickly

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30
Q

What might happen to the wall of the airway with persistent inflammation and/or recurrent bouts of infection in bronchitis?

A

Airways may get scarred, become weakened and bronchiectatic

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31
Q

What is emphysema?

A

Reduction in the number alveolar walls around the bronchiole. Normal thickness walls but less of them –> less SA so reduced gas exchange

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32
Q

What are co-existent obstructive lung diseases associated mainly with?

A

Cigarette smoking

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33
Q

How does tobacco smoke lead to COPD?

A

Chemicals and heat trigger inflammation in bronchi and lung parenchyma. In the bronchi this leads to persistent inflammation, scarring, mucus hyperplasia. In the parenchyma inflammation leads to alveolar wall loss (emphysema).

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34
Q

What morphological abnormalities are present in bronchitis?

A

Chronic inflammation, mucus gland hyperplasia

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35
Q

What morphological abnormalities are present in emphysema?

A

Emphysema - alveolar wall loss, especially around the bronchioles (centriacinar)

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36
Q

Define centriacinar emphysema

A

Centrilobular emphysema primarily affects the upper lobes of the lungs

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37
Q

What is bronchiectasis?

A

Permanent dilation of bronchi and bronchioles caused by destruction of the muscle and elastic tissue

38
Q

If the alveolar wall is damaged and weakened by chronic inflammatory damage, what might happen to the wall on expiration?

A

Collapse

39
Q

What is bronchiectasis due to?

A

secondary to chronic necrotising infection (often with pre-disposing conditions)

  • Cystic fibrosis
  • Primary ciliary dyskinesia, Kartagener syndrome
  • Bronchial obstruction: tumour, foreign body
  • Lupus, rheumatoid arthritis, inflammatory bowel disease, GVHD (graft-versus-host-disease)
40
Q

Bronchi vs bronchiole?

A

Bronchi are the main passageway into the lungs. The bronchi become smaller the closer they get to the lung tissue and are then considered bronchioles.

41
Q

What triggers/causes bronchiectasis?

A

Mainly obstruction (eg by tumour, thick mucus in CF) and / or infection

42
Q

How does obstruction lead to bronchiectasis?

A

Obstruction causes infection (or infection can arise de novo)

43
Q

Pathogenesis behind bronchiectasis?

A
  1. Obstruction/infection leads to inflammation
  2. inflammation damages wall tissues
  3. walls dilate but also contain inflammatory debris and mucus
44
Q

What morphological abnormalities are present in bronchiectasis?

A

Dilated inflamed airway walls

45
Q

How do the morphological abnormalities of bronchiectasis commonly present clinically?

A

Productive cough, may be blood, obstructive ventilatory defects, repeated infections

46
Q

What is chronic ILD?

A

Chronic interstitial lung disease; mixed group.

Most common are:

  • Idiopathic Pulmonary Fibrosis (IPF)
  • Pneumoconiosis
  • Sarcoid
  • Hypersensitivity Pneumonitis (HP)
47
Q

What does chronic ILD involve?

A

Often = scarring +/- inflammation in multiple areas of both lungs that reduces lung compliance (ie stiff lungs) = restrictive

48
Q

What happens in idiopathic pulmonary fibrosis?

A
  • Fibrosis of interstitium causes reduced gas exchange
  • If fibrosis slowly replaces normal lung;
    • Shortness of breath etc
    • Increased severity of symptoms
49
Q

What is idiopathic pulmonary fibrosis?

A

Progressive patchy scarring especially lower zones of both lungs that is fatal (mean survival 3 yrs).

50
Q

Where does IPF tend to occur?

A

Lower zones of both lungs

51
Q

Age of IPF?

A

Typically over 60

52
Q

Speculated pathogenesis of IPF?

A

Speculated is repeated epithelial injury leads to inflammation and fibrosis

53
Q

What morphological abnormalities are present in IPF?

A

Patchy interstitial fibrosis, especially lung bases at periphery

54
Q

What is the cough like in IPF?

A

Insidious dry cough

55
Q

What is Pneumoconiosis? What is it caused by?

A

Lung damage secondary to particle inhalation. Commonest coal dust/ silica from mining, asbestos or other fibrogenic dust inhalation from occupational exposure (eg stone or metal workers)

56
Q

What triggers Pneumoconiosis

A

Chronic particle inhalation

57
Q

What is the effect of damaged alveolar walls on the heart? What can this lead to?

A

Increased resistance for right ventricle –> can lead to 2ary RHF

58
Q

How does chronic particle inflammation lead to Pneumoconiosis?

A

Particles ingested by macrophages –> trigger fibrosis (inflammation) N.B. smoking makes it worse

59
Q

What morphological abnormalities are present in Pneumoconiosis?

A

Dust accumulation and fibrosis, often centred on smaller conducting airways

60
Q

Which type of particle is the most common cause of Pneumoconiosis?

A

coal dust/ silica from mining

61
Q

Who is Pneumoconiosis more common in?

A

Male due to occupational exposure, as dose dependent, often older

62
Q

How does Pneumoconiosis present?

A

Slowly increasing SOB, often picked up on CXR

63
Q

What is sarcoid/sarcoidosis?

A

A condition where inflamed cells clump together to make small lumps called granulomas.

Multisystem granulomatous disease that most commonly involves lymph nodes and lungs

64
Q

What do granulomas cause in sarcoid?

A

Scarring; affects lung compliance and gas exchange

65
Q

Epidemiology of sarcoid?

A

All ages (20-60 most common), both genders, all round world, more in non-smokers, more in those of African or Northern European descent

66
Q

Trigger of sarcoid?

A

Granulomatous inflammation leads to fibrosis (idiopathic)

67
Q

Is sarcoid more common in smokers or non-smokers?

A

Non-smokers

68
Q

What morphological abnormalities are present in sarcoid?

A

Non-caseating granulomas in multiple sites, often accompanied by scarring

69
Q

How does sarcoid typically present?

A

Nodal enlargement (esp mediastinal) , respiratory symptoms (cough, SOB), constitutional symptoms (fever, fatigue, weight loss, sweats)

70
Q

What is Hypersensitivity Pneumonitis (HP)?

A

Inflammatory and fibrotic bronchiolar response to inhaled antigens leads to hypersensitivity response to antigen in wall of bronchioles. This inflammation triggering fibrosis if antigen not removed.

71
Q

Effect on interstitium in HP?

A

Interstitium widened by inflammatory infiltrate

72
Q

What are examples of inhaled antigens in HP?

A

mold (eg in hay - farmer’s lung), animal faeces (eg bird fanciers lung), paint fumes, etc

73
Q

What morphological abnormalities are present in HP?

A

Chronic inflammation around bronchioles spilling out into interstitium, sometimes accompanied by interstitial fibrosis

74
Q

Clinical presentation of HP?

A

Respiratory symptoms (cough, SOB), constitutional symptoms (fever, fatigue, weight loss, sweats)

75
Q

What is cystic fibrosis?

A

Disease from abnormally thickened mucus caused by chloride channel recessive gene abnormality

76
Q

How many people carry defective genes in UK for CF?

A

1 in 25 (common)

77
Q

Pathogenesis behind CF?

A

Reduced sodium and chloride in lumen of: respiratory tract, GI tract (inc ducts in pancreas and liver) and seminiferous tubules. This causes dehydrated mucus which is thicker and blocks the lumina, also predisposing to infections, inflammation and scarring.

78
Q

What morphological abnormalities are present in CF?

A
  • Lungs (often the most life threatening complication) – infections, bronchitis and bronchiectasis
  • Pancreas – exocrine atrophy and fibrosis, small intestine in infants – blockage (meconium ileus)
  • Liver – bile canalicular blockage can lead to cirrhosis
  • Seminiferous tubules – 95% males infertile
79
Q

What do the clinical features of CF depend on?

A

Depends on predominant organ involvement - Respiratory and exocrine pancreas often most prominent

80
Q

What can pancreatic insufficiency in CF lead to?

A

Malabsorption

81
Q

In this slice of lung, what do you see?

A

Emphysema (lost lots of alveolar walls), fibrosis, scarring

82
Q
A

3 - smooth muscle contraction, airway swelling and luminal mucus production triggered by histamine release

83
Q

What is number 1, 2, 3 and 4?

A

1 - bronchiectasis

2 - cigarette smoke leading to emphysema

3 - asthma

4 - CF

84
Q
A

2 - CF

85
Q

What is 1, 2, 3 and 4?

A

1 - cigarette smoking leading to bronchitis

2 - CF

3 - sarcoidosis

4 - asthma or HP

86
Q
A

Loss of alveolar walls leading to enlarged airspaces; emphysema

This is one part of COPD, so bronchitis is most likely to accompany.

3 - inflammation, mucus hypersecretion in the bronchi and bronchioles

87
Q

What is 1, 2, 3 and 4?

A

1 - bronchiectasis

2 - sarcoid

3 - bronchitis

4 - asthma

88
Q

Are you more prone to cor pulmonale if your COPD is predominated by emphysema or chronic bronchitis?

A

Chronic bronchitis

89
Q

morphological change of heart in chronic bronchitis vs emphysema?

A

Chronic bronchitis; prominent vessels and large heart

Emphysema; small heart (and hyperinflated lungs)

90
Q

Describe cough in emphysema vs chronic bronchitis

A

Emphysema; late, scanty sputum

Chronic bronchitis; early in disease, copious sputum

91
Q

What is the main difference in symptoms between chronic bronchitis and emphysema?

A

The main difference between these conditions is that chronic bronchitis produces a frequent cough with mucus. The main symptom of emphysema is shortness of breath.

Yr 2 - Clinical Pathology (80 decks)

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