Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CRRAB II Week 6 - WLB > Chronic Obstructive Pulmonary Disease - Pathoma > Flashcards

Chronic Obstructive Pulmonary Disease - Pathoma Flashcards

1
Q

What type of obstruction occurs in Chronic Pulmonary Obstructive Disease?

A

Obstruction to getting air out of the lung?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the hallmark of Chronic Pulmonary Obstructive Disease?

A

Airway obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What changes in spirometry are seen in patients with Chronic Pulmonary Obstructive Disease?

A
  • Decreased FVC (↓)
  • Decreased FEV1 (↓↓ more)
  • Decreased FEV1:FVC ratio
  • Total Lung Capacity is increased (due to air trapping)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is Chronic Bronchitis defined?

A

Clinically:

  • Chronic productive cough lasting at least 3 months over a minimum of 2 years
  • Cough up “cups” or “buckets” of mucous
  • Highly associated with smoking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What causes the excess mucous production associated with Chronic Bronchitis?

A
  • Smoking exposes airways to pollutants
  • Hypertrophy of mucinous glands (increased thickness of mucus glands relative to overall bronchial wall thickness, Reid index >50%)
  • Increased glandular production of mucus to trap pollutants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What causes the obstruction in Chronic Bronchitis?

A

Mucus travels down airway and plugs up some smaller bronchioles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the clinical features in Chronic Bronchitis?

A
  • Productive cough
  • Cyanosis, ↑PaCO2, ↓PaO2
  • Increased risk of infection or Cor Pulmonale
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is Cor Pulmonale?

A

Diffuse pulmonary arteriole constriction causing right ventricular hyperplasia and eventually right ventricular failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What leads to the air trapping in Emphysema?

A
  1. Destruction of alveolar sacs
  2. Lose elastic recoil
  3. Collapse of small airways
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What causes the destruction of alveolar sacs in Emphysema?

A

Imbalance of proteases and antiproteases.

  • alveolar macrophages => eat pollutants in alveoli => inflammation => produces proteases
  • body produces alpha-1-antitrypsin to balance proteases
  • EMPHYSEMA: overproduction of proteases OR underproduction of antiproteases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the most common cause of Emphysema?

A

Smoking… duh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What happens in the lungs when Emphysema is due to smoking?

A
  • Overproduction of inflammation proteases that destroy lungs
  • Results in centriacinar emphysema, more severe in upper lungs (affects the central part of acinous)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the functional unit of the lung?

A

Acinous:

  • terminal bronchiole
  • alveolar sacs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is a rare cause of Emphysema?

A

Alpha-1 Antitrypsin Deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What kind of emphysema does Alpha-1 Antitrypsin Deficiency cause?

A

Panacinar emphysema => more severe in lower lobes

liver cirrhosis may also be present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the genetic considerations in Alpha-1 Antitrypsin Deficiency?

A

Disease severity is based on degree of A1AT deficiency.

  • PiM = normal allele (PiM/PiM)
  • PiZ = is most common clinically relevant mutation (misfolded protein accumulates in Endoplasmic Reticulum of hepatocytes)
17
Q

What happens if Alpha-1 Antitrypsin Deficiency is a heterozygote?

A

PiMZ Heterozygotes:

  • usually asymptomatic with decreased circulating levels of A1AT
  • significant risk for emphysema with smoking
18
Q

What happens if Alpha-1 Antitrypsin Deficiency is a homozygote?

A

PiZZ Homozygotes:
-Significant risk for panacinar emphysema and cirrhosis
(misfolded protein accumulates in Endoplasmic Reticulum of hepatocytes)

19
Q

What are the clinical features of Panacinar Emphysema?

A
  • Dyspnea and cough with minimal sputum production
  • Prolonged expiration with pursed lips (“pink-puffer”)
  • Weight loss
  • Increased AP diameter of chest (“barrel chest” due to reset FRC)
20
Q

What are late complications of emphysema?

A

-Hypoxemia (PaO2

21
Q

Why is Asthma a Chronic Pulmonary Obstructive Disease?

A

Results in airway bronchoconstriction.

but it is reversible!

22
Q

Asthma is most often due to what?

A

ALLERGIC STIMULI => Type I Hypersensitivity Reaction

23
Q

What is asthma most offten associated with?

A
  • Presents in childhood
  • Allergic rhinitis
  • Eczema
  • Family history of ATOPY
24
Q

What is the pathogenesis of Asthma?

A
  • Allergens induce Th2 phenotype in CD4+ T-cells of genetically susceptible individuals
  • Th2 cells secrete IL-4, IL-5, and IL-10
25
Q

What does IL-4 do in asthma?

A 
Allows plasma cell to class switch to IgE
(allows for production of IgE)
26
Q

What does IL-5 do in asthma?

A

Calls in Eosinophils

27
Q

What does IL-10 do in asthma?

A
  • Inhibit the production of Th1 helper T-cells
  • Induce production of Th2 helper T-cells
  • Promotes overall reaction!
28
Q

What happens when an asthma patient is reexposed to the allergen?

A
  1. IgE mediated activation of mast cells (early-phase)
  2. Mast cells dump preformed histamine granules => histamine-induced vasodilation (arterioles) + histamine-induced increased vascular permeability (post-capillary venules)
  3. Mast cell production of LTC4, LTD4, LTE4 => vasoconstriction, increased vascular permeability, bronchoconstriction
  4. Inflammation (e.g. Major Basic Protein) perpetuates bronchoconstriction (late-phase)
29
Q

What are the clinical features of Asthma?

A

Episodic Symptoms:

  • Dyspnea and wheezing
  • Productive cough
  • Curschmann spirals admixed with Charcot-Leyden crystals (aggregates of Major Basic Protein)
  • Severe, unrelenting attack can result in status asthmaticus and death
30
Q

What are the nonallergic causes of asthma?

A
  • Exercise
  • Viral infection
  • Aspirin (e.g. aspirin intolerant asthma => bronchospasm + nasal polyps)
  • Occupational exposures
31
Q

What are the important associations with nasal polyps?

A
  • Adult => Aspirin Intolerant Asthma

- Child => Cystic Fibrosis

32
Q

What is bronchiectasis?

A
  • Permanent dilation of bronchioles and bronchi

- Loss of airway tone results in air trapping

33
Q

How does the permanent dilation of bronchioles happen in Bronchiectasis?

A

Due to necrotizing inflammation with damage to airway walls.

  • **Conditions with chronic inflammation and infection:
  • Cystic fibrosis
  • Kartagener syndrome
  • Tumor or foreign body
  • Necrotizing infection
  • Allergic bronchiopulmonary aspergillosis
34
Q

What are the clinical features of Bronchiectasis?

A
  • Cough
  • Dyspnea
  • Foul-smelling sputum
35
Q

What are the complications of Bronchiectasis?

A
  • Hypoxemia with cor pulmonale

- Secondary amyloidosis

CRRAB II Week 6 - WLB (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions