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Pathoma - Respiratory Tract Pathology > Chronic Obstructive Pulmonary Disease > Flashcards

Chronic Obstructive Pulmonary Disease Flashcards

1
Q

What characterizes the group of diseases making up Chronic Obstructive Pulmonary Disease?

A
  • Airway obstruction
  • Lung does not empty
  • Air is trapped (air trapping)
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2
Q

What is seen on Spirometry with COPD?

A
  • Dec. FVC (volume of air that can be forcefully expired)
  • Dec. (ALOT) FEV1 (first second of expiration)
  • Dec. FEV1:FVC ratio
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3
Q

What happens to total lung capacity in COPD?

A

TLC is increased due to AIR TRAPPING

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4
Q

What is the normal FEV1:FVC ratio?

A

80%

4L/5L

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5
Q

What is Chronic Bronchitis?

A

Chronic productive cough lasting at least 3 months over a minimum of 2 years

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6
Q

What is Chronic Bronchitis highly associated with?

A

Smoking!

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7
Q

What characterizes Chronic Bronchitis histologically?

A

Hypertrophy of bronchial mucinous glands.

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8
Q

How much of the wall do mucinous glands usually take up?

A

Less than 40% of the wall

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9
Q

What does hypertrophy of bronchial mutinous glands lead to?

A

Increased thickness of mucus glands relative to bronchial wall thickness

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10
Q

What is the Reid index and how does it change in Chronic Bronchitis?

A

Reid index measures thickness of mucinous glands in relation to the wall.
It increases to greater than 50% when normal is less than 40%

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11
Q

What two things does the increased thickness of mucinous glands in relation to the wall cause?

A

Production of mucus —> Goes to lumen —> (1) Mucus coughed up and (2) Some goes back and plugs airways or causes obstruction

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12
Q

What are the clinical features of Chronic Bronchitis?

A
  • Productive cough
  • Excessive mucus production
  • Cyanosis
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13
Q

What are Chronic Bronchitis patients referred to as?

A

‘Blue bloaters’

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14
Q

What causes Cyanosis in Chronic Bronchitis?

A

Mucus plugs trap carbon dioxide. This leads to increased PaCO2 and decreased PaO2.

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15
Q

What is there an increased risk for with Chronic Bronchitis?

A

Infection (due to mucus plugging) and Cor Pulmonale

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16
Q

What causes Cor Pulmonale in Chronic Bronchitis?

A

The entire lung is clamping down on blood vessels (trying to send blood to other areas of the lung)

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17
Q

What is Emphysema?

A

Destruction of alveolar air sacs

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18
Q

How does Emphysema result in Air Trapping?

A

Loss of elastic recoil (alveoli become shopping bags) and collapse of airways during exhalation results in obstruction and air trapping.

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19
Q

What causes Emphysema?

A

An imbalance of proteases and antiproteases

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20
Q

What are the normal roles of proteases and antiproteases?

A

Inflammation in lung normally leads to to release of proteases by neutrophils and macrophages (alveolar).
Alpha1-antitrypsin (A1AT) neutralizes proteases.

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21
Q

What is the most important antiprotease?

A

Alpha1-antitrypsin

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22
Q

What leads to the destruction of air sacs in emphysema (what protease/antiprotease imbalance)?

A

Excessive inflammation or lack of A1AT leads to destruction of the alveolar air sacs.

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23
Q

What two things cause Emphysema?

A
  1. Smoking

2. A1AT deficiency

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24
Q

What is the most common cause of emphysema?

A

Smoking

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25
Q

How does smoking lead to emphysema?

A

Pollutants in smoke lead to excessive inflammation and protease-mediated damage.

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26
Q

What type of emphysema does smoking cause? Where does it occur in the lungs?

A 
Centriacinar emphysema (at terminal bronchiole)
Most severe in upper lobes (smoke moves upward)
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27
Q

What is a rare cause of emphysema?

A

A1AT deficiency

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28
Q

How does A1AT deficiency lead to emphysema?

A

Lack of antiprotease leaves air sacs vulnerable to protease mediated damage.

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29
Q

What type of emphysema does A1AT deficiency cause? Where does it occur in the lungs?

A

It causes panacinar emphysema (entire acinus which includes terminal bronchiole and alveolar air sacs).
Most severe in lower lobes.

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30
Q

What may also be present with A1AT deficiency?

A

Liver cirrhosis!

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31
Q

What causes A1AT deficiency?

A

Misfolding of the mutated protein.

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32
Q

How does A1AT deficiency cause liver cirrhosis?

A

Mutant A1AT accumulates in the endoplasmic reticulum of hepatocytes, resulting in liver damage.

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33
Q

What is seen on biopsy of A1AT deficiency induced liver cirrhosis?

A

Pink, PAS-positive globules in hepatocytes

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34
Q

In A1AT deficiency, what is disease severity based upon?

A

Degree of A1AT deficiency!

35
Q

What is the normal allele for A1AT?

A

PiM.

Two copies are usually expressed (PiMM)

36
Q

What is the most common clinically relevant mutation in A1AT deficiency? What does it result in?

A

PiZ.

Significantly low levels of circulating A1AT.

37
Q

What happens in PiMZ heterozygotes?

A

They are usually asymptomatic with decreased circulating A1AT levels.
However, significant risk for emphysema with smoking exists.

38
Q

What are PiZZ homozygotes at significant risk for?

A

Panacinar emphysema and Cirrhosis.

39
Q

What are four clinical features of emphysema?

A
  1. Dyspnea
  2. Cough (with minimal sputum)
  3. Prolonged expiration with pursed lips
  4. Weight loss
40
Q

Why are emphysema patients known as “pink puffers”?

A

Prolonged expiration with pursed lips.

41
Q

Why do emphysema patients purse their lips?

A

They want to create back pressure and prolong expiration (to counter airway collapse).

42
Q

What will you see on X-ray with emphysema?

A

Increased anterior-posterior diameter of chest (‘barrel-chest’).
FRC (functional residual capacity) is increased!

43
Q

What determines FRC (functional residual capacity)?

A

It is a set point determined by the balance between the lung and chest wall.

44
Q

What are late complications of emphysema?

A
  • Hypoxemia

- Cor pulmonale

45
Q

What causes Hypoxemia in late emphysema?

A

Destruction of capillaries in the alveolar sac. [destruction of air sacs]

46
Q

What causes Cor Pulmonale in late emphysema?

A

It’s preceded by hypertrophy.

47
Q

Wha is Asthma?

A

Reversible airway bronchoconstriction.

48
Q

Asthma is most often due to. . .

A

Allergic stimuli (atopic asthma)

49
Q

When does asthma present?

A

In childhood

50
Q

What is asthma often associated with?

A
  • Allergic rhinitis
  • Eczema
  • Family history of atopy
51
Q

What type of hypersensitivity is asthma?

A

Type I

52
Q

What do allergens do in asthma?

A

Allergens induce TH2 phenotype in CD4+ T cells of genetically susceptible individuals.

53
Q

What do TH2 cells do in asthma?

A

TH2 cells secrete IL-4, IL-4 and IL-10.

54
Q

What is IL-4 responsible for?

A

Mediating class switch to IgE

55
Q

What is IL-5 responsible for?

A

Attracting eosinophils

56
Q

What is IL-10 responsible for?

A

Stimulating TH2 cells and inhibiting TH1 cells.

57
Q

What does re-exposure to an antigen lead to in asthma?

A

IgE-mediated (IgE cross linking) activation of mast cells.

58
Q

What happens when mast cells are activated?

A

They release histamine –> Histamine induced vasodilation (arterioles) and increased vascular permeability (post-capillary venules)

59
Q

What is generated in asthma after the release of preformed histamine granules?

A

Leukotrienes C4, D4 and E4

60
Q

What do LTC4, LTD4 and LTE4 lead to?

A

Early phase reaction:
Bronchoconstriction (smooth muscle of bronchus is constricted), inflammation (blood vessel constriction), and edema (pericytes constrict and increase vascular permeability)

61
Q

What is the late phase reaction in asthma?

A

Inflammation, especially major basic protein derived from eosinophils, damages cells and perpetuates bronchoconstriction.

62
Q

What are two characteristics of the symptoms of asthma?

A
  1. Episodic

2. Related to allergic exposure

63
Q

What are the clinical features of asthma (three)?

A
  1. Dyspnea
  2. Wheezing
  3. Productive cough
64
Q

What does the mucus show in asthma (two things)?

A
  1. Classically spiral-shaped mucus plugs (Curschmann spirals)
  2. Eosinophil-derived crystals (Charcot-Leyden crystals)
65
Q

What can a severe unrelenting asthma attack result in?

A

Status asthmatics and DEATH

66
Q

What may asthma also arise from?

A

Nonallergic causes (non-atopic asthma)

67
Q

What are examples of nonallergic causes of asthma?

A
  • Exercise
  • Viral Infection
  • Aspirin (esp. aspirin intolerant asthma)
  • Occupational exposure
68
Q

What should you think of when you see a child with nasal polyps?

A

Cystic fibrosis

69
Q

What is the classic triad of Aspirin induced asthma?

A
  • Nasal polyps
  • Bronchospasms
  • Asthma
70
Q

What is Bronchiectasis?

A

Permanent dilatation of bronchioles and bronchi

71
Q

What causes Air Trapping in Bronchiectasis?

A

Loss of airway tone (as air is exhaled, it cannot be accelerated - like someone blowing into a wide diameter pipe)

72
Q

What pathology causes Bronchiectasis?

A

Necrotizing inflammation and damage to airway walls.

73
Q

What are the four main causes of Bronchiectasis?

A
  1. Cystic fibrosis
  2. Kartagener syndrome
  3. Tumor or foreign body
  4. Necrotizing infection
  5. Allergic bronchopulmonary aspergillosis
74
Q

What is Kartagener syndrome?

A

Inherited defect of the dynein arm, which is necessary for ciliary movement.

75
Q

What other symptoms is Kartagener syndrome associated with?

A
  • Sinusitis
  • Infertility (poor motility of sperm)
  • Situs inversus (position of major organs is reversed e.g. heart is on right side of thorax)
  • Inflammation and infection of the lung due to impaired mucociliary elevator
76
Q

What is Allergic Bronchopulmonary Aspergillosis?

A

Hypersensitivity reaction to Aspergillus leads to chronic inflammatory damage

77
Q

What is Allergic Bronchopulmonary Aspergillosis seen in?

A

Individuals with asthma or cystic fibrosis.

78
Q

What are three clinical features of Bronchiectasis?

A
  1. Cough
  2. Dyspnea
  3. Foul-smelling sputum (sitting in lungs rotting for a long time)
79
Q

What complications are associated with Bronchiectasis?

A
  • Hypoxemia (from CO2 trapping)
  • Cor Pulmonale
  • Secondary (AA) Amyloidosis
80
Q

What is Amyloidosis?

A

Deposition of a misfolded protein.

81
Q

What is local and systemic amyloidosis?

A 
Local = one organ
Systemic = multiple organs
82
Q

What is Primary Systemic Amyloidosis?

A

Deposition of amyloid light chain due to plasma cell problem –> cells over produce light chain amyloid and it goes into blood and deposits in tissues

83
Q

What is Secondary Systemic Amyloidosis?

A

Chronic inflammation –> over production of SAA –> over production of AA –> DEPOSITS

Pathoma - Respiratory Tract Pathology (9 decks)

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