Brainscape's Knowledge GenomeTM

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


See full index

CPR Exam 2 > Pulmonary Pathology Part 2 > Flashcards

Pulmonary Pathology Part 2 Flashcards

1
Q

What are some components of restrictive lung disease?

A
  • Volume restriction
  • FEV1/FVC normal
  • FVC reduced
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are some components of obstructive lung disease?

A
  • Decreased flow

- Low FEV1/FVC ratio

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

What is the key fact of restrictive lung disease?

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

What is the key fact of obstructive lung disease?

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

Where does the loop shift in flow volume loops with obstructive lung disease?

A
  • To the left

- Lung volume is greater than normal but FEV1 is greatly reduced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where does the loop shift in flow volume loops with restrictive lung disease?

A
  • To the right

- Lung volume is less than normal and both FEV1 and FVC are reduced

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

What is the most common cause of obstructive pulmonary disease?

A
  • COPD/Chronic bronchitis due to smoking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens in chronic bronchitis?

A
  • Mucous gland hyperplasia causing damage to airway epithelium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does chronic bronchitis present as?

A
  • Persistent cough with sputum production for 3 months out of 2 consecutive years (Diagnostic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are some complications of chronic bronchitis?

A
  • Bronchiectasis
  • Death from respiratory infection
  • Squamous metaplasia/dysplasia/carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is emphysema?

A
  • Alveolar ducts are narrowed causing alveolar sacs to collapse and develop holes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does emphysema look like on clinical presentation?

A
  • Enlarged lungs on CXR
  • Flattened diaphragm
  • Barrel chest with increased AP diameter (same diameter all around chest)
  • Diminished breath sounds with prolonged expiratory wheezes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What do PFTs show in patients with emphysema?

A
  • Obstructive pattern
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is good description of someone with chronic bronchitis?

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

What is a good description of someone with emphysema?

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

Is emphysema reversible or irreversible?

A
  • Irreversible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does a1-antitrypsin do in the lungs?

A
  • Coats lungs, protecting them from neutrophil elastase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What happens physiologically in a1-antitrypsin deficiency?

A
  • A1-antitrypsin stays in the liver rather than going to lungs causing liver damage
  • Due to the lack of a1-antitrypsin, the lung is susceptible to damage from neutrophil elastase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does the lung look like in a1-antitrypsin?

A
  • Panacinar or pan lobar emphysema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are some other types of emphysema?

A
  • Spontaneous PTX
  • COPD
  • Localized
  • A1-AT deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What gene encodes for a1-AT?

A
  • Pi gene on chromosome 14
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the Z allele associated with in a1-AT deficiency?

A
  • Decreased circulating a1-AT
23
Q

What is seen in individuals that are homozygous for PiZZ?

A
  • Markedly decreased a1-AT with a majority developing panacinar emphysema
24
Q

How do you diagnose a1-AT deficiency?

A
  • Serum testing for a1-AT
25
Q

What are some complications of emphysema?

A
  • Respiratory failure
  • Pneumothorax with lung collapse
  • Coronary artery disease
  • Right heart failure
26
Q

What kind of emphysema does a spontaneous PTX present with?

A
  • Distal acinar or paraseptal
27
Q

What kind of emphysema does COPD present with?

A
  • Centrilobular, centriacinar, or proximal acinar
28
Q

What kind of emphysema does localized present with?

A
  • Irregular
29
Q

What are the three components of asthma?

A
  • Recurrent airway obstruction with a reversible component
  • Airway hyper-responsiveness
  • Airway inflammation
30
Q

What is atopic asthma classified as?

A
  • 2/3 of all patients
  • May be at any age, typically childhood
  • Family history of asthma
  • Elevated IgE levels (eosinophils, mast cells, lymphocytes)
  • Triggers may include a variety of allergens
31
Q

What is non-atopic asthma classified as?

A
  • 1/3 of all patients
  • Often older patients
  • Typically normal IgE levels (T-lymphocytes, neutrophils)
  • Triggers may include cold, exercise, infection
32
Q

What kind of hypersensitivity reaction is atopic asthma?

A
  • Type 1
33
Q

What cells are increased in atopic asthma?

A
  • Eosinophils
  • Mast cells
  • Lymphocytes
34
Q

What cells are increased in non-atopic asthma?

A
  • T-lymphocytes

- Neutrophils

35
Q

What is the pathogenesis of asthma?

A
  • Allergen is presented to dendritic cell
  • Th2 cell releases IL4 and IL5
  • IL4 recruits IgE B cells which help get mast cells
  • IL5 recruits eosinophils which release granules and mediators
36
Q

What mediators cause the bronchoconstriction in asthma?

A
  • Leukotrienes C4, D4, E4
  • Histamine
  • Prostaglandin D2
  • Acetylcholine
37
Q

What mediators cause the mucus secretion in asthma?

A
  • Leukotrienes C4, D4, E4
38
Q

What mediators cause the increased vascular permeability?

A
  • Leukotrienes C4, D4, E4
39
Q

What mediators cause the recruitment of inflammatory cells?

A
  • Interleukins
40
Q

What happens in airway remodeling?

A
  • Progressive structural changes to airways with characteristic histologic findings
41
Q

What is seen histologically in airway remodeling?

A
  • Fibrosis
  • Smooth muscle hyperplasia
  • Increased goblet cells and submucosal glands
42
Q

What is status asthmaticus?

A
  • An unremitting, potentially fatal asthma attack

- Causes a bronchial occlusion by thick mucus

43
Q

What is a “Curschmann’s spiral”?

A
  • A coiled thick mucus plug
44
Q

What are some genetic associations with atopic asthma?

A
  • Associated with seasonal allergies and eczema

- May be linked to various alleles controlling factors like IgE, cytokines, adrenergic receptors

45
Q

What are some environmental associations with atopic asthma?

A
  • Disease of industrialized societies (pollution and lack of allergen exposure at early age)
  • Early infection
46
Q

What is aspirin sensitive asthma?

A
  • Due to the COX blocking effect of aspirin, all of the arachidonic acid is pushed to make leukotrienes C4, D4, E4 which cause bronchoconstriction
47
Q

What is aspirin associated asthma associated with?

A
  • Nasal polyps and recurrent rhinitis (Samter’s triad)
48
Q

What is bronchiectasis?

A
  • Necrotizing inflammatory response

- Usually the end stage process of multiple processes (Infection or Obstruction)

49
Q

What can bronchiectasis be seen in?

A
  • Allergic bronchopulmonary aspergillosis (ABPA)
  • Cystic fibrosis
  • Chronic infection (TB)
  • Primary ciliary dyskinesia
50
Q

What is kartagener’s syndrome?

A
  • Dysfunction of dynein arm of microtubules
51
Q

What is the triad seen in kartagener’s syndrome?

A
  • Sinusitis
  • Bronchiectasis
  • Situs inversus
    (will often see male infertility too)
52
Q

What is primary ciliary dyskinesia?

A
  • Microtubules are vital to motility of various cell populations (cilia and flagella)
53
Q

What is allergic bronchopulmonary aspergillosis (ABPA)?

A
  • Exaggerated hypersensitivity response to aspergillus infection overlying chronic lung disease
54
Q

What is seen in ABPA?

A
  • Background of asthma or cystic fibrosis
  • Increased IgE on serum testing
  • Positive skin test
  • Thick dark mucus in bronchi
  • Associated with bronchiectasis in advanced disease

CPR Exam 2 (12 decks)

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