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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
How does smoking lead to emphysema?
Pollutants in smoke lead to excessive inflammation and protease-mediated damage.
26
What type of emphysema does smoking cause? Where does it occur in the lungs?
``` Centriacinar emphysema (at terminal bronchiole) Most severe in upper lobes (smoke moves upward) ```
27
What is a rare cause of emphysema?
A1AT deficiency
28
How does A1AT deficiency lead to emphysema?
Lack of antiprotease leaves air sacs vulnerable to protease mediated damage.
29
What type of emphysema does A1AT deficiency cause? Where does it occur in the lungs?
It causes panacinar emphysema (entire acinus which includes terminal bronchiole and alveolar air sacs). Most severe in lower lobes.
30
What may also be present with A1AT deficiency?
Liver cirrhosis!
31
What causes A1AT deficiency?
Misfolding of the mutated protein.
32
How does A1AT deficiency cause liver cirrhosis?
Mutant A1AT accumulates in the endoplasmic reticulum of hepatocytes, resulting in liver damage.
33
What is seen on biopsy of A1AT deficiency induced liver cirrhosis?
Pink, PAS-positive globules in hepatocytes
34
In A1AT deficiency, what is disease severity based upon?
Degree of A1AT deficiency!
35
What is the normal allele for A1AT?
PiM. | Two copies are usually expressed (PiMM)
36
What is the most common clinically relevant mutation in A1AT deficiency? What does it result in?
PiZ. | Significantly low levels of circulating A1AT.
37
What happens in PiMZ heterozygotes?
They are usually asymptomatic with decreased circulating A1AT levels. However, significant risk for emphysema with smoking exists.
38
What are PiZZ homozygotes at significant risk for?
Panacinar emphysema and Cirrhosis.
39
What are four clinical features of emphysema?
1. Dyspnea 2. Cough (with minimal sputum) 3. Prolonged expiration with pursed lips 4. Weight loss
40
Why are emphysema patients known as "pink puffers"?
Prolonged expiration with pursed lips.
41
Why do emphysema patients purse their lips?
They want to create back pressure and prolong expiration (to counter airway collapse).
42
What will you see on X-ray with emphysema?
Increased anterior-posterior diameter of chest ('barrel-chest'). FRC (functional residual capacity) is increased!
43
What determines FRC (functional residual capacity)?
It is a set point determined by the balance between the lung and chest wall.
44
What are late complications of emphysema?
- Hypoxemia | - Cor pulmonale
45
What causes Hypoxemia in late emphysema?
Destruction of capillaries in the alveolar sac. [destruction of air sacs]
46
What causes Cor Pulmonale in late emphysema?
It's preceded by hypertrophy.
47
Wha is Asthma?
Reversible airway bronchoconstriction.
48
Asthma is most often due to. . .
Allergic stimuli (atopic asthma)
49
When does asthma present?
In childhood
50
What is asthma often associated with?
- Allergic rhinitis - Eczema - Family history of atopy
51
What type of hypersensitivity is asthma?
Type I
52
What do allergens do in asthma?
Allergens induce TH2 phenotype in CD4+ T cells of genetically susceptible individuals.
53
What do TH2 cells do in asthma?
TH2 cells secrete IL-4, IL-4 and IL-10.
54
What is IL-4 responsible for?
Mediating class switch to IgE
55
What is IL-5 responsible for?
Attracting eosinophils
56
What is IL-10 responsible for?
Stimulating TH2 cells and inhibiting TH1 cells.
57
What does re-exposure to an antigen lead to in asthma?
IgE-mediated (IgE cross linking) activation of mast cells.
58
What happens when mast cells are activated?
They release histamine --> Histamine induced vasodilation (arterioles) and increased vascular permeability (post-capillary venules)
59
What is generated in asthma after the release of preformed histamine granules?
Leukotrienes C4, D4 and E4
60
What do LTC4, LTD4 and LTE4 lead to?
Early phase reaction: Bronchoconstriction (smooth muscle of bronchus is constricted), inflammation (blood vessel constriction), and edema (pericytes constrict and increase vascular permeability)
61
What is the late phase reaction in asthma?
Inflammation, especially major basic protein derived from eosinophils, damages cells and perpetuates bronchoconstriction.
62
What are two characteristics of the symptoms of asthma?
1. Episodic | 2. Related to allergic exposure
63
What are the clinical features of asthma (three)?
1. Dyspnea 2. Wheezing 3. Productive cough
64
What does the mucus show in asthma (two things)?
1. Classically spiral-shaped mucus plugs (Curschmann spirals) 2. Eosinophil-derived crystals (Charcot-Leyden crystals)
65
What can a severe unrelenting asthma attack result in?
Status asthmatics and DEATH
66
What may asthma also arise from?
Nonallergic causes (non-atopic asthma)
67
What are examples of nonallergic causes of asthma?
- Exercise - Viral Infection - Aspirin (esp. aspirin intolerant asthma) - Occupational exposure
68
What should you think of when you see a child with nasal polyps?
Cystic fibrosis
69
What is the classic triad of Aspirin induced asthma?
- Nasal polyps - Bronchospasms - Asthma
70
What is Bronchiectasis?
Permanent dilatation of bronchioles and bronchi
71
What causes Air Trapping in Bronchiectasis?
Loss of airway tone (as air is exhaled, it cannot be accelerated - like someone blowing into a wide diameter pipe)
72
What pathology causes Bronchiectasis?
Necrotizing inflammation and damage to airway walls.
73
What are the four main causes of Bronchiectasis?
1. Cystic fibrosis 2. Kartagener syndrome 3. Tumor or foreign body 4. Necrotizing infection 5. Allergic bronchopulmonary aspergillosis
74
What is Kartagener syndrome?
Inherited defect of the dynein arm, which is necessary for ciliary movement.
75
What other symptoms is Kartagener syndrome associated with?
- 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
What is Allergic Bronchopulmonary Aspergillosis?
Hypersensitivity reaction to Aspergillus leads to chronic inflammatory damage
77
What is Allergic Bronchopulmonary Aspergillosis seen in?
Individuals with asthma or cystic fibrosis.
78
What are three clinical features of Bronchiectasis?
1. Cough 2. Dyspnea 3. Foul-smelling sputum (sitting in lungs rotting for a long time)
79
What complications are associated with Bronchiectasis?
- Hypoxemia (from CO2 trapping) - Cor Pulmonale - Secondary (AA) Amyloidosis
80
What is Amyloidosis?
Deposition of a misfolded protein.
81
What is local and systemic amyloidosis?
``` Local = one organ Systemic = multiple organs ```
82
What is Primary Systemic Amyloidosis?
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
What is Secondary Systemic Amyloidosis?
Chronic inflammation --> over production of SAA --> over production of AA --> DEPOSITS

Pathoma - Respiratory Tract Pathology (9 decks)

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