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Pulmonary > Obstructive Lung Disease > Flashcards

Obstructive Lung Disease Flashcards

1
Q

Asthma Severity:

Intermittent

A

Intermittent: Symptoms or SABA (not prevention) <2d/week, nighttime <2x/month, no interference with normal activity

  • Normal FEV1 between exacerbations, FEV1 >80%
  • 0-1 exac/year
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2
Q

Asthma Severity:

Mild

A

> 2 days/week, night sx 3-4x/mon, SABA >2d per week

  • Minor limitation
  • FEV1 >80%, FEV1/FVC normal
  • > 2 exac per year
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3
Q

Asthma Severity:

Moderate

A

daily, Night >1x/week, SABA daily

  • Some limitation
  • FEV1 >60% but <80%; FEV1/FVC reduced by 5%
  • > 2 exac per year
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4
Q

Asthma Severity:

Severe

A

throughout the day, Night often 7x/wk, SABA several times per day

  • Extremely limiting
  • FEV1 >60%, FEV1/FVC reduced by >5%
  • > 2 exac per year
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5
Q

Asthma Therapy: Step 1

A

SABA PRN

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6
Q

Asthma Therapy: Step 2

A

Low dose ICS [alt: cromolyn, LTRA, theophylline]

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7
Q

Asthma Therapy: Step 3

A

Low dose ICS+ LABA or Medium dose ICS [alt: Low dose ICS + LTRA]

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8
Q

Asthma Therapy: Step 4

A

Medium dose ICS + LABA

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9
Q

Asthma Therapy: Step 5

A

High dose ICS+ LABA AND consider omalizumab if pt has allergies

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10
Q

Asthma Therapy: Step 6

A

High dose ICS + LABA + oral steroid and consider omalizumab if allergies

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11
Q

Omalizumab: mechanism

A

anti-IgE recombinant Ab

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12
Q

Indications Omalizumab

A
  1. moderate to severe persistent asthma
  2. Inadequately controlled on ICS
  3. serum IgE 30-700
  4. Allergic sensitization (skin test or allergen-specific IgE in vitro)

*Not criteria but eos >300 predict good response

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13
Q

Mepolizumab: Mechanism

A

IgG Antibody to IL-5 Receptor (antagonist)

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14
Q

Mepolizumab: Indication

A

Severe, eosinophilic asthma, not responding to traditional therapy

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15
Q

LAMA in asthma: Indication

A

As add on to ICS/LABA has shown some efficacy on decreasing exac, improving FEV1. Did not seem to effect QOL.

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16
Q

Bronchial Thermoplasty: Criteria

A
  • Dependence on systemic steroids (intermit or continuous)
  • FEV1 >50%
  • No history of life-threatening exac
  • Understanding of risk of asthma worsening and acute exac after procedure
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17
Q

Major Cell Types

  1. Asthma-
  2. COPD-
A
  1. Epithelial cells, Th2 cells (CD4+)
    Mast cells, Eos
  2. Th1 and Tc1 cells (CD8+)
    Neutrophil, macrophage
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18
Q

Mediators

  1. Asthma’
  2. COPD
A
  1. IL4, IL5, IL13

2. LTB4, TNFa, IL8

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19
Q

Pathologic Changes

  1. Asthma
  2. COP
A
  1. Subepithelial fibrosis, smooth muscle hyperplasia, mucous metaplasia, BM thickening
  2. Peribronchial fibrosis, smooth muscle hyperplasia, mucous metaplasia, alveolar destruction
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20
Q

Alpha-1 antitrypsin Gene

  1. protein manufactured in the ?
  2. on chromosome #
A
  1. Liver

2. 14

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21
Q

Phenotypes of Alpha 1 Antitrypsin

  1. MM
  2. MZ
  3. SS
  4. SZ
  5. ZZ
  6. Null
A
  1. No increase in emphysema
  2. intermediate serum level but risk of emphysema is unclear
  3. No increase
  4. mild increase in smokers, rarely in nonsmokers
  5. High risk (80-100%), accelerated age in smokers
  6. High risk (100% by 30yo)
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22
Q

Reason to screen for AAT:

1-8

A
  1. COPD <50yo
  2. COPD without smoking history
  3. Family history of early COPD, bronchiectasis, panniculitis
  4. Predom lower lobe emphysema
  5. young asthmatic, unresponsive to therapy
  6. Necrotizing panniculitis
  7. C-ANCA vasculitis
  8. Unexplained liver disease
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23
Q

COPD interventions shown to improve mortality

A
  1. Longterm oxygen therapy (>18hr, NOTT)
  2. Smoking Cessation
  3. Long volume reduction surgery
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24
Q

COPD Indications for Lung Transplant:

A
  1. Very severe COPD 2. deterioration despite optimal medical therapy and rehab
  • History of Exac with acute hypercapnia pCO2 >50
  • pulmonary HTN/cor pulmonale despite O2 therapy

-FEV <20% with DLCO <20% or homogenous emphysema

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25
Q

Ideal candidate for LVRS

A
  • <75yo
  • upper lobe predominant emphysema
  • FEV1 between 20-45%
  • TLC >100%, RV >150%
  • PaO2 >45mmg on RA, PaCO2 <60
  • complete pulmonary rehab and low exercise tolerance (<40W in men, <25W in women)
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26
Q

Treatment for GOLD A

A

SAMA OR SABA PRN

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27
Q

Treatment for GOLD B

A

LAMA or LABA–>LAMA + LABA

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28
Q

Treatment for GOLD D

A

LAMA + LABA==> LAMA + LABA + ICS

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29
Q

Asthma: Major Cell types

A

Epithelial cells, TH2 cells (CD4+), mast cells, eosinophils

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30
Q

COPD: Major Cell types

A

TH1 and Tc1 cells (CD8), neutrophils, macrophages

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31
Q

Asthma: Mediators

A

IL-4, IL-5, IL-13

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32
Q

COPD: Mediators

A

LTB4, TNF-a, IL-8

33
Q

Asthma: Path Changes

A

Subepithelial fibrosis, smooth muscle hyperplasia +++, mucous metaplasia, BM thickening

34
Q

COPD: Path Changes

A

Peribronchial fibrosis, smooth muscle hyperplasia +, mucous metaplasia, alveolar destruction

35
Q

COPD: Mechanism of airflow limitation

A
  1. airway inflammation
  2. loss of elastin in airway wall
  3. Disappearance of small airways
  4. luminal plugs
  5. (with loss of parenchymal destruction) loss of alveolar attachment and decreased elastic recoil
36
Q

Regulatory T Cells

A

IL-10 and TGF-B to decrease transformation to Th0 to Th2 cells

37
Q

Th1 cells make:

Which:

A

INF-y
TNFa
-tissue inflammation and remodeling

38
Q

Th17 cells make:

Which:

A

IL-17

-assoc with neutrophilic inflammation in acute exac and tissue remodeling

39
Q

Th2 cells:

2 main pathways and respective mediators

A
  1. Th2–> Mast cell
    - IL-4 and IL-13 stimulated B cell to synthesize IgE
  2. Eosinophils
    - IL-3, IL-5, and GM-CSF
40
Q

Early Phase Asthma
–Drug target
Late Phase Asthma

A
  • Ag-specific IgE bound to receptors on Mast cells, released within minutes of exposure, cause mast cell to degranulate
  • -mast cell membranes stabilized by beta agonist

Influx of inflammatory cells (Eos, basophils, neutrophils, and T Cells) to site of allergen exposure

41
Q

Eos attracted to bronchial walls by

  • -secreted by
  • -clinical significant
A 
IL-3
IL-5
GM-CSF
--Th2 cells
--steroids decrease # Eos in circ, penetration into bronchial walls, and activation
42
Q

Basophils secrete

A

IL-4

IL-13

43
Q

Th1 cells secrete

–cause

A

INFy and TNF

–tissue inflammation, remodeling

44
Q

Directs B lymphocytes to synthesize IgE?

A

IL-4

45
Q

Regulates eosinophil production and maturation?

A

IL-5

46
Q

Leads to airway eosinophilia, mucous gland hyperplasia, airway fibrosis and remodeling?

A

IL-13

47
Q

Recruits neutrophils into bronchial walls

A

IL-17

48
Q

AECOPD associated with:

A
  1. Accelerated disease progression
  2. augmented decline in health status and QOL
  3. increased mortality
  4. Future exacerbation
49
Q

Pulmonary rehab within 1 mo of discharge for AECOPD:

A
  1. improves dyspnea
  2. exercise capacity
  3. QOL
  4. Reduces hospital readmission rates
50
Q

Pulmonary rehab following hospital admission for AECOPD

A
  1. significantly reduces hospital readmissions (OR 0.22)

2. mortality (OR 0.28)

51
Q

2 Types of Occupational Asthma: Presentation
Relevant exposure
Path
Associated with

A
  1. Sensitizer: latency months-yr, +immuno response
    -Complete Antigen (>10kD): animal pelt, enzyme, flour, cereal
    -Incomplete Antigen (Hapten): isocyanate, anhydride, dyes, resins, wood dust
    Path: identical to asthma
    Assoc with contact dermatitis
  2. Irritant-induced: no latency, onset min-hr, no immuno response
    -Chlorine, aldehyde, bleach, smoke
    Path: epithelial cell sloughing, hemorrhage, eventual collagen in BM
    RADS- type of irritant induced after exposure to high dose single irritant
52
Q

ABPA: Major features; if 1 present send?

A

With asthma or CF

  1. Central bronchiectasis on imaging
  2. Refractory clinical course, waxing/waning nodules
  3. Skin prick for Aspergillus
  4. Sputum cultures yield Aspergillus
  5. Periph Eos prominent

Then send:

  1. total serum IgE
  2. Aspergillus fumigatus specific IgE or IgG
53
Q

LAM markers

A

HMB-45 and CD-63

-VEGF-D- >800 in serum is sens/spec

54
Q

2 Types of Occupational Asthma:

A

Sensitizer (Latency)

Irritant-induced (No latency)

55
Q

Sensitizer induced occupational asthma:

2 types

A

Complete Antigen (MW >10kd)
-animal protein (pelt, murine labs), flour (alpha amylase), latex
Incomplete antigen (hapten, MW <8kD)
1. Isocyanate
2. Anhydride
3. Wood dust (plicatic acid with Western red cedar)

56
Q

Irritant-induced occupational asthma (no latency)

-Classic exposures

A

Chlorine gas, aldehyde, bleach, smoke from fire

57
Q

Ddx for Obstruction on Spirometry (6)

A
  1. COPD (irrev)
  2. Bronchiectasis
  3. Constrictive bronchiolitis (RA, IBD, Lung trx, inhalational injury). Progressive. Air-trapping.
  4. Central airway obstruction (flow-vol loop)
  5. Laryngeal Dysfunciton (stridor/hoarseness). Flat inspir flow-vol loop.
  6. Reactive airways viral syndrome
58
Q

Who benefits from longterm oxygen therapy in COPD?

A
  1. PaO2 < or = 55 or SaO2 < or = 88 +/- hypercapnia

2. PaO2 56-59 or SaO2 88-90% and evidence of pulm HTN (cor pulmonale) or polycythemia

59
Q

Results of LOTT trial in NEJM 2016 showed?

A

Excluded severe hypoxemia at rest
Patient with SpO2 89-93% at rest and moderate exercise hypoxemia (SpO2 80-88% >10s but > or = 5min spent >80%) showed no benefits from longterm oxygen therapy (based on hosp, QOL, dyspnea score, mortality, 6-minute walk distance)
-severe exercise induced hypoxemia (<80%) were excluded

60
Q

Key Cells involved in COPD:

A

Epithelial cells–> TGFb

Macrophage–> CCL2, CXCL, IL-8, LTB4 (attract TH1, neutrophils)

61
Q

TGFb in COPD phys

A

from epithelial cells–> small airways fibrosis

62
Q

Chemoattractants produced by macrophage in COPD

A

CXCL
IL-8, LTB-4
-Attract TH1 (CD8+ cytotoxic T cells)
-Attract Neutrophils

63
Q

Eligibility for Alpha 1 Antitrypsin Replacement:

  • critieria
  • benefot
A
  1. FEV1 25-80%
  2. No longer smoking
  3. AAT <11 (umol/L)
  4. Other therapy optimized
    - modest effect slowing lung function decline, no effect preventing exac
64
Q

mMRC 2= ?

A

I walk slower than people of the same age on the level because of breathlessness, or I have to stop for breath when walking on my own pace on the level

65
Q

Pulmonary Rehab for ?

A

GOLD group B, C, D

66
Q

Recommendation for all patients with COPD?

A

Smoking cessation
Limit Environ/Occupational exposures
Physical activity
Flu/PNA vaccines

67
Q

DDx for bronchiectasis

A 
M-Mechanical
I- Immune Defic
I-Post-infectious
C- Congenital
A- Autoimmune
M- Mucocilliary Clearance Defic
O- Other
68
Q

Treatment GOLD C

A

LAMA==> LAMA + LABA

69
Q

CF patients may benefit from inhaled abx if:

A

Colonized with PsA- improved QOL, decrease exac, improved lung function

70
Q

Chronic Azithro therapy in CF patients

A

Patient >6yo with chronic colonization of PsA have reduced exac and improved lung functions.
-must screen for NTM q6mos

71
Q

Most common organisms for acute CF exac

A

MRSA, PsA

72
Q 
GOLD Stages
I
II
III
IV
A

I. >80%

  1. > 50%, <80%
  2. > 30, <50%
  3. <30% (or <50% AND chronc resp failure)
73
Q

ATS grading obstruction

A 
Mild >70%
Moderate 60-69%
Moderately Severe 50-59%
Severe 35-49%
Very Severe <35%
74
Q

ATS grading DLCO

A

Mild >60% and

75
Q

FEV1 cut-offs

  1. LVRS
  2. Bronchial thermoplasty
  3. A1AT
  4. Bullectomy
A
  1. 25-40%
  2. > 50%
  3. 25-80%
  4. Benefits less likely in severe impairment FEV1 <40%, chronic resp failure, PH
    - DLCO <40% is contraindication to bullectomy
76
Q

Absolute Contraindication to bronchoprovocation testing:

A 
SMUK
Severe obstruction FEV1 <50%
MI or CVA within 3 months
Uncontrolled HTN (>200/100)
Known aortic aneurysm
77
Q

Exercise-induced asthma: defn

A

15% decrease in PEF or FEV1 with exertion

78
Q

Adenosine in COPD: ?

A

AVOID, as can cause bronchoconstriction

-e.g. in cardiac stress test or management of SVT

Pulmonary (14 decks)

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