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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
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2
Q

Which disease of airway limitation is fully reversible?

A

Asthma

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3
Q

Which parts of the breathing cycle are hindered in COPD?

A

expiration

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4
Q

T or F. COPD is progressive

A

T.

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5
Q

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

A

Wood smoke exposure

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6
Q

Risk factors for COPD?

A
  • Smoking
  • Occupational dust and chemicals
  • Air pollution
  • Aging
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7
Q

What protein is usually deficient in COPD?

A

alpha-1 antitrypsin

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8
Q

What does alpha-1 antitrypsin do?

A

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

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9
Q

What cells promote Asthma inflammation?

A

mast cells, eosinophils, CD4, macrophages

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10
Q

What cells promote COPD inflammation?

A

neutrophils, CD8, macrophages

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11
Q

What mediators promote Asthma inflammation?

A

LTD, histamine, IL-4/5, ROS

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12
Q

What mediators promote COPD inflammation?

A

LTB, IL-8, TNF-a, ROS

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13
Q

Steroids in COPD mainly target what cell and what mediator?

A

macrophages and ROS

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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
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15
Q

What is emphysema?

A

loss of alveolar attachments

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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)

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17
Q

What are the two parts of COPD?

A

chronic bronchitis and emphysema

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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

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19
Q

What is the Reid index?

A

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

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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

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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

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22
Q

What cells make up the inflammation in chronic bronchitis?

A

CD8 and neutrophils

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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
Q

What is centrolobular emphysema?

A

dilation and destruction of the respiratory bronchioles

26
Q

What mainly causes centrolobular emphysema?

A

mostly an upper lobe process associated with smoking

27
Q

What causes panlobular emphysema?

A

destruction of the entire acinus, predominantly a lower lobe process associated with A1AT deficiency

28
Q

What are bull?

A

emphysematous spaces greater than 1cm in diameter

29
Q

Common complication of emphysema?

A

small airway collapse during exhalation (dynamic airway collapse)

30
Q

What things lead to IRREVERSIBLE airflow limitation in COPD?

A
  • fibrosis
  • loss of elastic recoil
  • destruction of alveolar attachments
31
Q

What things lead to REVERSIBLE airflow limitation in COPD?

A
  • accumulation of inflammatory cells and mucus in bronchi

- smooth muscle contraction

32
Q

What are ‘pink puffers’ (Type A COPD)?

A
  • good spiratory drive
  • intense dyspnea; purse-lip breathing
  • thin and often elderly
  • small sputum volume
33
Q

What are ‘blue bloaters’ (Type A COPD)?

A
  • poor respiratory drive
  • mild dyspnea
  • obese
  • large sputum volume

often associated with CHF

34
Q

When should COPD be suspected?

A

considered in any patients with those complaining of dyspnea, chronic cough or sputum production, or risk factors

35
Q

How is COPD diagnosed?

A

spirometry with FEV1/FVC less than 0.70 after bronchodilation with drugs

36
Q

T or F. FEV1 AND FVC decrease in COPD

A

T. But FEV1 decreases more (both in chronic bronchitis and emphysema)

37
Q

T or F. Lung volumes, compliance, elastic recoil, and diffusing capacity for CO (DLCO) are normal in pure chronic bronchitis

A

T. Note that DLCO is low in pure emphysema due to destruction of alveoli

38
Q

In Emphysema, are lung volumes and compliance increases or decreased

A

Increased because elastic recoil decreases

39
Q

How does COPD present?

A
  • prolonged expiration
  • wheezing during auscultation on slow breathing
  • barrel chest
  • pursed lip breathing
40
Q

Cor pulmonale is seen in COPD. What is this?

A

split of S2, JVD, peripheral edema

41
Q

How are the symptoms of suspected COPD rated?

A

mMRC ratio or FEV1:FVC ratios

42
Q

mMRC criteria

A

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
Q

FEV1:FVC criteria in COPD severity

A

GOLD 1: 80+%
GOLD 2: 50-80%
GOLD 3: 30-50%
GOLD 4: less than 30%

44
Q

Exacerbations in COPD rating (most important)

A

Two or more within 1 yr or an FEV1 less than 50% are HIGH risk

One or more hospitalizations= HIGH risk

45
Q

Co-morbidites of COPD?

A
  • CV disease
  • Osteoporosis
  • Respiratory infection
  • Anxiety and Depression
46
Q

What vaccines should be considered with COPD?

A

Influenza and Pneumococcal

47
Q

Treatment for Group A COPD Patients?

A

SAMA or SABA

48
Q

Treatment for Group B COPD Patients?

A

LABA or LAMA

49
Q

Treatment for Group C COPD Patients?

A

ICS+ LABA or LAMA

50
Q

Treatment for Group D COPD Patients?

A

ICS+LABA and/or LAMA

51
Q

What do B2-agonists do to bronchodilate?

A

-act through PKA (increased cAMP)

52
Q

Side effects of B2 agnosts?

A
  • muscle tremor
  • tachycardia
  • hypokalemia
  • restlessness
53
Q

How do muscarinic antagonists combat broncho-constriction?

A

decreased cGMP

54
Q

Side effects of muscarinic antagonists?

A
  • bitter taste
  • glaucoma
  • dryness of mouth
  • urinary retention
55
Q

How do corticosteroids work in asthma?

A

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
Q

What is there rescuer bronchodilator of choice in COPD?

A

Ipratropium

57
Q

T or F. All other drugs must be discontinued for a methacholine test

A

T. This has a HIGH negative predictive value

Pulmonary Week 2 (25 decks)

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