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Clinical Pathology > Lecture 7: Benign lung pathology > Flashcards

Lecture 7: Benign lung pathology Flashcards

1
Q

Name 3 factors involved in how tubes conduct air in and out?

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

What is the most important factor in tubes conducting air?

A

Size of lumen

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3
Q

What 2 features of an alveolar wall affect gas exchange?

A
  1. Quantity
  2. Thickness
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4
Q

What 2 features of an alveolar wall affect gas exchange?

A
  1. Quantity
  2. Thickness
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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

Aside from swelling what other key features of inflammation could result in the wall of a tube narrowing the lumen?

A

redness, heat, pain, loss of function (Rubor, Calor, Dolor, Fucntio Laesae)

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7
Q

What does inflammation casue?

A

Swelling

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8
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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9
Q

What 4 things does inflammation cause?

A

Swelling
Tissue damage
Tissue loss
Fibrosis

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10
Q

Name 4 ways tissue may respond locally after an episode of acute inflammation?

A

1 - complete resolution,
2 - chronic inflammation,
3 - loss of tissue or
4 - scarring.

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11
Q

What 2 responses of inflammation impacts on the function of the lung tissue the most?

A

LOSS OF TISSUE and SCARRING will / can often reduce the function of the tissue

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12
Q

What does resolution mean?

A

RESOLUTION mean the tissue returns to how it was before

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13
Q

What disease is loss of tissue seen in?

A

Emphysema

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14
Q

What are 2 factors seen in scarring in chronic interstitial lung disease?

A
  1. Fibrosis of interstitium
  2. More normal alveolar tissue
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15
Q

What does fibrosis of interstitium involve?

A
  1. Thicker walls
  2. Less capillary exchange
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16
Q

What is asthma?

A

Reversible intermittent narrowing of conducting airways

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17
Q

Who can get asthma?

A

Children and young adults (atopic), non-atopic (intrinsic) more common in adults but is less common

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18
Q

What causes asthma?

A

Allergens, drugs (NSAIDs), cold, exercise, infections, emotion

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19
Q

How does the trigger cause pathology /dysfunction in asthma?

A

Sensitisation to trigger followed by re-exposure to trigger causing airway narrowing - See upcoming explanation

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20
Q

What are morphological abnormalities are present?

A

Wall – thick (inflammation, tissue hyperplasia)
contracted (smooth muscle),
lumen - mucus

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21
Q

How do the morphological abnormalities commonly present clinically?

A

SOB, Wheeze, cough, hyperinflation

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22
Q

What causes SOB and wheezing?

A

TUBES THICKENED and NARROWED.
This is caused by 3 main things –
smooth muscle contraction, (see hyperplastic/hypertrophied smooth muscle in bronchioles and bronchi)
inflammation, (wall of conducting airways is swollen with vasodilatation, fluid and inflammatory cells)
Mucus (goblet cells and mucus glands are increased in number/size and increase in mucus filling lumen)

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23
Q

What are 4 features of Bronchitis?

A
  1. The wall of the bronchus is thickened by inflammation
    2.Increased goblet cells and overlying luminal mucus
  2. Mucus gland hyperplasia
  3. Increased mucus production
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24
Q

What is COPD?

A

A combination of chronic bronchitis and emphysema, 2 commonly co-existent obstructive lung diseases associated mainly with cigarette smoking

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25
Q

Who gets COPD?

A

Mainly long standing cigarette smokers

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26
Q

What triggers COPD?

A

Tobacco smoke mainly

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27
Q

How does the trigger cause pathology /dysfunction in 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)

28
Q

What are morphological abnormalities are present in COPD?

A

Bronchitis – Chronic inflammation, mucus gland hyperplasia

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

29
Q

What are 2 features of Bronchiectasis?

A
  1. Dilated Bronchus
  2. Muco-Purulent Debris in airway Lumen
30
Q

What is Bronchiectasis?

A

Permanent dilation of bronchi and bronchioles due to wall damage secondary to chronic necrotising infection

31
Q

What triggers/causes bronchiectasis?

A

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

32
Q

How does the trigger cause pathology /dysfunction in Bronchiectasis?

A

Obstruction causes infection (or infection arises de novo), inflammation damages wall tissues, walls dilate but also contain inflammatory debris and mucus

33
Q

What morphological abnormalities are present in Brocheictasis?

A

Dilated inflamed airway walls

34
Q

How do the morphological abnormalities commonly present clinically in Brochiectasis?

A

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

35
Q

What is Chronic ILD?

A

scarring +/- inflammation in multiple areas of both lungs that reduces lung compliance (ie stiff lungs) = restrictive.
Most common are Idiopathic Pulmonary Fibrosis (IPF) , Pneumoconiosis, Sarcoid, Hypersensitivity Pneumonitis (HP)

36
Q

What are 2 features of Idiopathic Pulmonary Fibrosis (IPF)?

A
  1. Fibrosis of the interstitium
  2. More normal alveolar tissue
37
Q

What is IPF?

A

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

38
Q

What gets IPF?

A

Mainly Males over females
and over 60yrs

39
Q

What triggers IPF?

A

Idiopathic

40
Q

How does the trigger cause pathology /dysfunction in IPF?

A

Speculated is repeated epithelial injury leads to inflammation and fibrosis

41
Q

What morphological abnormalities are present in IPF?

A

Patchy interstitial fibrosis, especially lung bases at periphery

42
Q

How do the morphological abnormalities commonly present clinically in IPF?

A

Insidious dry cough and progressive SOB

43
Q

What is Pneumoconiosis?

A

Lung damage secondary to particle inhalation -mixed group.

44
Q

What is the commonest type of particle inhalation in Pneumoconiosis?

A

Commonest coal dust/ silica from mining, asbestos or other fibrogenic dust inhalation from occupational exposure (eg stone or metal workers)

45
Q

Who gets Pneumoconiosis?

A

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

46
Q

What triggers pneumoconiosis?

A

Chronic particle inhalation

47
Q

How does the trigger cause pathology /dysfunction in Pneumoconiosis?

A

Particles ingested by macrophages – trigger fibrosis – smoking makes it worse

48
Q

What morphological abnormalities are present in Pneumoconiosis?

A

Dust accumulation and fibrosis, often centred on smaller conducting airways (main route in)

49
Q

How do the morphological abnormalities commonly present clinically in Pneumoconiosis?

A

Slowly increasing SOB, often picked up on CXR

50
Q

What is sarcoid in the lung?

A

Multisystem granulomatous disease that most commonly involves lymph nodes and lungs

51
Q

What can get 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

52
Q

what triggers sarcoid?

A

Idiopathic

53
Q

How does the trigger cause pathology /dysfunction in sarcoid?

A

Granulomatous inflammation leads to fibrosis

54
Q

What morphological abnormalities are present in Sarcoid of the lung?

A

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

55
Q

How do the morphological abnormalities commonly present clinically in Sarcoid of the lung?

A

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

56
Q

What is HP?

A

Inflammatory and fibrotic bronchiolar response to inhaled antigens

57
Q

What triggers/causes Hypersensitivity Pneumonitis (HP)?

A

Inhaled organic antigens such as mold (eg in hay - farmer’s lung), animal faeces (eg bird fanciers lung), paint fumes, etc

58
Q

How does the trigger cause pathology /dysfunction in HP?

A

Hypersensitivity response to antigen in wall of bronchioles, inflammation triggering fibrosis if antigen not removed

59
Q

What morphological abnormalities are present in HP?

A

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

60
Q

How do the morphological abnormalities commonly present clinically in HP?

A

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

61
Q

What is cystic fibrosis?

A

Disease from abnormally thickened mucus

62
Q

Who gets CF?

A

1 in 2500 births in UK (1 in 25 people carries defective gene in UK) - common

63
Q

What triggers/causes CF?

A

Chloride channel recessive gene abnormality

64
Q

How does the trigger cause pathology /dysfunction in 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

65
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

66
Q

How do the morphological abnormalities commonly present clinically in CF?

A

Depends on predominant organ involvement. Respiratory and exocrine pancreas often most prominent. Chronic cough, persistent lung infections and eventually right heart failure. Malabsorption from pancreatic insufficiency

Clinical Pathology (6 decks)

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