Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pulmonary Week 2 > COPD/Emphysema > Flashcards

COPD/Emphysema Flashcards

1
Q

What are some things that characterize COPD?

A
  • Fibrosis of airways walls
  • Inflammation with lymphocytes, neutrophils, and macrophages
  • Smooth muscle hyperplasma
  • hyper-secretion of mucus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which disease of airway limitation is fully reversible?

A

Asthma

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

Which parts of the breathing cycle are hindered in COPD?

A

expiration

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

T or F. COPD is progressive

A

T.

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

What is the most common cause of COPD in the WORLD?

A

Wood smoke exposure

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

Risk factors for COPD?

A
  • Smoking
  • Occupational dust and chemicals
  • Air pollution
  • Aging
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What protein is usually deficient in COPD?

A

alpha-1 antitrypsin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does alpha-1 antitrypsin do?

A

protect the lungs from neutrophil elastase, an enzyme that can disrupt connective tissue

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

What cells promote Asthma inflammation?

A

mast cells, eosinophils, CD4, macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What cells promote COPD inflammation?

A

neutrophils, CD8, macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What mediators promote Asthma inflammation?

A

LTD, histamine, IL-4/5, ROS

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

What mediators promote COPD inflammation?

A

LTB, IL-8, TNF-a, ROS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Steroids in COPD mainly target what cell and what mediator?

A

macrophages and ROS

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

How does COPD limit airway flow?

A
  • small airway disease via inflammation, fibrosis, and increased resistance
  • parenchymal destruction via loss of alveolar attachments and decrease in elastic recoil
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is emphysema?

A

loss of alveolar attachments

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

T or F. The amount of residual air in COPD patients is higher

A

T. Leading to a barrel chest appearance (so the tendency for the airways to collapse is higher)

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

What are the two parts of COPD?

A

chronic bronchitis and emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is chronic bronchitis?

A

chronic or recurrent cough present on most days for a minimum of 3 months in a year and for not less than 2 straight years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the Reid index?

A

bronchial gland depth /total bronchial wall thickness (normally higher than 0.4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does the Reid Index change in chronic bronchitis?

A

increases, bronchial gland hypertrophy and goblet cell metaplasia lead to excessive mucous production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What kinds of airway changes accompany chronic bronchitis?

A

squamous metaplasia of airway epithelium, loss of cilia, and ciliary function, and increased smooth muscle and connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What cells make up the inflammation in chronic bronchitis?

A

CD8 and neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What do you see in small airways (less than 2mm) in CB?

A
  • formation of goblet cells and mucus secretion
  • fibrosis and collagen deposition
  • this is the MAJOR site of airflow resistance
24
Q

What is emphysema?

A

an abnormal enlargement of air spaces distal to the terminal bronchioles

25
What is centrolobular emphysema?
dilation and destruction of the respiratory bronchioles
26
What mainly causes centrolobular emphysema?
mostly an upper lobe process associated with smoking
27
What causes panlobular emphysema?
destruction of the entire acinus, predominantly a lower lobe process associated with A1AT deficiency
28
What are bull?
emphysematous spaces greater than 1cm in diameter
29
Common complication of emphysema?
small airway collapse during exhalation (dynamic airway collapse)
30
What things lead to IRREVERSIBLE airflow limitation in COPD?
- fibrosis - loss of elastic recoil - destruction of alveolar attachments
31
What things lead to REVERSIBLE airflow limitation in COPD?
- accumulation of inflammatory cells and mucus in bronchi | - smooth muscle contraction
32
What are 'pink puffers' (Type A COPD)?
- good spiratory drive - intense dyspnea; purse-lip breathing - thin and often elderly - small sputum volume
33
What are 'blue bloaters' (Type A COPD)?
- poor respiratory drive - mild dyspnea - obese - large sputum volume often associated with CHF
34
When should COPD be suspected?
considered in any patients with those complaining of dyspnea, chronic cough or sputum production, or risk factors
35
How is COPD diagnosed?
spirometry with FEV1/FVC less than 0.70 after bronchodilation with drugs
36
T or F. FEV1 AND FVC decrease in COPD
T. But FEV1 decreases more (both in chronic bronchitis and emphysema)
37
T or F. Lung volumes, compliance, elastic recoil, and diffusing capacity for CO (DLCO) are normal in pure chronic bronchitis
T. Note that DLCO is low in pure emphysema due to destruction of alveoli
38
In Emphysema, are lung volumes and compliance increases or decreased
Increased because elastic recoil decreases
39
How does COPD present?
- prolonged expiration - wheezing during auscultation on slow breathing - barrel chest - pursed lip breathing
40
Cor pulmonale is seen in COPD. What is this?
split of S2, JVD, peripheral edema
41
How are the symptoms of suspected COPD rated?
mMRC ratio or FEV1:FVC ratios
42
mMRC criteria
Grade 0- only SOB with strenuous exercise Grade 1- SOB when hurrying Grade 2- walks slower than normal and gets SOB Grade 3- Stops to breath after 100 m when level Grade 4- too SOB to leave house
43
FEV1:FVC criteria in COPD severity
GOLD 1: 80+% GOLD 2: 50-80% GOLD 3: 30-50% GOLD 4: less than 30%
44
Exacerbations in COPD rating (most important)
Two or more within 1 yr or an FEV1 less than 50% are HIGH risk One or more hospitalizations= HIGH risk
45
Co-morbidites of COPD?
- CV disease - Osteoporosis - Respiratory infection - Anxiety and Depression
46
What vaccines should be considered with COPD?
Influenza and Pneumococcal
47
Treatment for Group A COPD Patients?
SAMA or SABA
48
Treatment for Group B COPD Patients?
LABA or LAMA
49
Treatment for Group C COPD Patients?
ICS+ LABA or LAMA
50
Treatment for Group D COPD Patients?
ICS+LABA and/or LAMA
51
What do B2-agonists do to bronchodilate?
-act through PKA (increased cAMP)
52
Side effects of B2 agnosts?
- muscle tremor - tachycardia - hypokalemia - restlessness
53
How do muscarinic antagonists combat broncho-constriction?
decreased cGMP
54
Side effects of muscarinic antagonists?
- bitter taste - glaucoma - dryness of mouth - urinary retention
55
How do corticosteroids work in asthma?
Inflammatory genes are activated by inflammatory stimuli (IL-1β, TNF-α, etc.), resulting in activation of IKKβ (inhibitor of I-κB kinase-β), which activates the transcription factor nuclear factor κB (NF-κB). A dimer of p50 and p65 NF-κB proteins translocates to the nucleus and binds to specific κB recognition sites and also to coactivators, such as CREB-binding protein (CBP), which have intrinsic histone acetyltransferase (HAT) activity. This results in acetylation of core histones and consequent increased expression of genes encoding multiple inflammatory proteins. Cytosolic glucocorticoid receptors (GR) bind corticosteroids; the receptor-ligand complexes translocate to the nucleus and bind to coactivators to inhibit HAT activity in two ways: directly and, more importantly, by recruiting histone deacetylase-2 (HDAC2), which reverses histone acetylation, leading to the suppression of activated inflammatory genes.
56
What is there rescuer bronchodilator of choice in COPD?
Ipratropium
57
T or F. All other drugs must be discontinued for a methacholine test
T. This has a HIGH negative predictive value

Pulmonary Week 2 (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions