Benign Lung Pathology

Question 1

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

Answer 1

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

Question 2

What are the 3 most important characteristics of airways?

Answer 2

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

Question 3

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?

Answer 3

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.

Question 4

What does the quality and thickness of alveolar walls affect?

Answer 4

Gas exchange

Question 5

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

Answer 5

Swelling (Tumour)

Question 6

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?

Answer 6

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

Question 7

Histological view of tissue damage in airway

Answer 7

Question 8

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

Answer 8

1 - complete resolution,

2 - chronic inflammation,

3 - loss of tissue

4 - scarring

Question 9

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

Answer 9

lymphocytes or macrophages forming granulomas

Question 10

How can fibrosis affect the lungs?

Answer 10

fibrosis restricts expansion of the lung parenchyma

Question 11

What can inflammation result in?

Answer 11

• swelling
• tissue damage
• tissue loss
• fibrosis

Question 12

What is asthma?

Answer 12

Reversible intermittent narrowing of conducting airways

Question 13

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

Answer 13

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.

Question 14

What are the 2 types of asthma?

Answer 14

Atopic (extrinsic) and non-atopic (intrinsic)

Question 15

What can trigger asthma?

Answer 15

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

Question 16

Pathogenesis behind the trigger causing asthma?

Answer 16

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

Question 17

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

Answer 17

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

Lumen - mucus

Question 18

Clinical presentation of asthma?

Answer 18

SOB, Wheeze, cough, hyperinflation

Question 19

Airway during asthma exacerbation

Answer 19

Question 20

What causes SOB and wheeze in asthma?

Answer 20

Tubes thickened and narrowed

Question 21

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

Answer 21

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)

Question 22

Asthma pathogenesis when exposed to allergen:

Answer 22

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

Question 23

How does sensitisation occur during asthma?

Answer 23

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

Question 24

Which 3 main changes occur during asthma?

Answer 24

1. inflammation
2. smooth muscle contraction
3. mucus production

Question 25

What is **c****hronic****obstructive pulmonary disease** a combination of?

Answer 25

Chronic bronchitis & emphysema

Question 26

How is chronic bronchitis defined?

Answer 26

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

Question 27

Site of bronchitis?

Answer 27

Bronchus

Question 28

Describe the; a) wall of the bronchus b) mucus gland c) mucus production in bronchitis? What will this do to airflow?

Answer 28

a) thickened by inflammation b) mucus gland hyperplasia c) by increased mucus production This will obstruct airflow

Question 29

What will this persistent mucus in bronchitis predispose to?

Answer 29

Infection if mucus isn't cleared quickly

Question 30

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

Answer 30

Airways may get scarred, become weakened and bronchiectatic

Question 31

What is emphysema?

Answer 31

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

Question 32

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

Answer 32

Cigarette smoking

Question 33

How does tobacco smoke lead to COPD?

Answer 33

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).

Question 34

What morphological abnormalities are present in bronchitis?

Answer 34

Chronic inflammation, mucus gland hyperplasia

Question 35

What morphological abnormalities are present in emphysema?

Answer 35

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

Question 36

Define centriacinar emphysema

Answer 36

Centrilobular emphysema primarily affects the **upper** **lobes** of the lungs

Question 37

What is bronchiectasis?

Answer 37

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

Question 38

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

Answer 38

Collapse

Question 39

What is bronchiectasis due to?

Answer 39

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)

Question 40

Bronchi vs bronchiole?

Answer 40

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.

Question 41

What triggers/causes bronchiectasis?

Answer 41

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

Question 42

How does obstruction lead to bronchiectasis?

Answer 42

Obstruction causes infection (or infection can arise de novo)

Question 43

Pathogenesis behind bronchiectasis?

Answer 43

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

Question 44

What morphological abnormalities are present in bronchiectasis?

Answer 44

Dilated inflamed airway walls

Question 45

How do the morphological abnormalities of bronchiectasis commonly present clinically?

Answer 45

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

Question 46

What is chronic ILD?

Answer 46

Chronic interstitial lung disease; mixed group. Most common are: * Idiopathic Pulmonary Fibrosis (IPF) * Pneumoconiosis * Sarcoid * Hypersensitivity Pneumonitis (HP)

Question 47

What does chronic ILD involve?

Answer 47

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

Question 48

What happens in idiopathic pulmonary fibrosis?

Answer 48

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

Question 49

What is idiopathic pulmonary fibrosis?

Answer 49

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

Question 50

Where does IPF tend to occur?

Answer 50

Lower zones of both lungs

Question 51

Age of IPF?

Answer 51

Typically over 60

Question 52

Speculated pathogenesis of IPF?

Answer 52

Speculated is repeated epithelial injury leads to inflammation and fibrosis

Question 53

What morphological abnormalities are present in IPF?

Answer 53

Patchy interstitial fibrosis, especially lung bases at periphery

Question 54

What is the cough like in IPF?

Answer 54

Insidious dry cough

Question 55

What is Pneumoconiosis? What is it caused by?

Answer 55

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)

Question 56

What triggers Pneumoconiosis

Answer 56

Chronic particle inhalation

Question 57

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

Answer 57

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

Question 58

How does chronic particle inflammation lead to Pneumoconiosis?

Answer 58

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

Question 59

What morphological abnormalities are present in Pneumoconiosis?

Answer 59

Dust accumulation and fibrosis, often centred on smaller conducting airways

Question 60

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

Answer 60

coal dust/ silica from mining

Question 61

Who is Pneumoconiosis more common in?

Answer 61

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

Question 62

How does Pneumoconiosis present?

Answer 62

Slowly increasing SOB, often picked up on CXR

Question 63

What is sarcoid/sarcoidosis?

Answer 63

A condition where inflamed cells clump together to make small lumps called **granulomas**. Multisystem granulomatous disease that most commonly involves **lymph** **nodes** and **lungs**

Question 64

What do granulomas cause in sarcoid?

Answer 64

Scarring; affects lung compliance and gas exchange

Question 65

Epidemiology of sarcoid?

Answer 65

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

Question 66

Trigger of sarcoid?

Answer 66

Granulomatous inflammation leads to fibrosis (idiopathic)

Question 67

Is sarcoid more common in smokers or non-smokers?

Answer 67

Non-smokers

Question 68

What morphological abnormalities are present in sarcoid?

Answer 68

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

Question 69

How does sarcoid typically present?

Answer 69

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

Question 70

What is Hypersensitivity Pneumonitis (HP)?

Answer 70

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.

Question 71

Effect on interstitium in HP?

Answer 71

Interstitium **widened** by inflammatory infiltrate

Question 72

What are examples of inhaled antigens in HP?

Answer 72

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

Question 73

What morphological abnormalities are present in HP?

Answer 73

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

Question 74

Clinical presentation of HP?

Answer 74

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

Question 75

What is cystic fibrosis?

Answer 75

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

Question 76

How many people carry defective genes in UK for CF?

Answer 76

1 in 25 (common)

Question 77

Pathogenesis behind CF?

Answer 77

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**.

Question 78

What morphological abnormalities are present in CF?

Answer 78

* 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

Question 79

What do the clinical features of CF depend on?

Answer 79

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

Question 80

What can pancreatic insufficiency in CF lead to?

Answer 80

Malabsorption

Question 81

In this slice of lung, what do you see?

Answer 81

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

Question 82

Answer 82

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

Question 83

What is number 1, 2, 3 and 4?

Answer 83

1 - bronchiectasis 2 - cigarette smoke leading to emphysema 3 - asthma 4 - CF

Question 84

Answer 84

2 - CF

Question 85

What is 1, 2, 3 and 4?

Answer 85

1 - cigarette smoking leading to bronchitis 2 - CF 3 - sarcoidosis 4 - asthma or HP

Question 86

Answer 86

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

Question 87

What is 1, 2, 3 and 4?

Answer 87

1 - bronchiectasis 2 - sarcoid 3 - bronchitis 4 - asthma

Question 88

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

Answer 88

Chronic bronchitis

Question 89

morphological change of heart in chronic bronchitis vs emphysema?

Answer 89

Chronic bronchitis; prominent vessels and large heart Emphysema; small heart (and hyperinflated lungs)

Question 90

Describe cough in emphysema vs chronic bronchitis

Answer 90

Emphysema; late, scanty sputum Chronic bronchitis; early in disease, copious sputum

Question 91

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

Answer 91

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.