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Block 9 Week 3 > Obstructive Lung Disease - Parks and Baker > Flashcards

Obstructive Lung Disease - Parks and Baker Flashcards

1
Q

what values do full PFTs give you that spirometry doesn’t?

A

total lung capacity

residual volume

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2
Q

how do you measure residual volume?

A

TCL-FVC

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3
Q

Emphysema results in an (inc/dec) DLCO

A

decreased

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4
Q

what is DLCO?

A

measures the ability of the lungs to transfer gas from inhaled air to the red blood cells in pulmonary capillaries

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5
Q 
Describe the changes in lab values for obstructive pulmonary dz:
FEV1
FEV1/FVC
FEF25-75
TLC
RV
A 
dec. FEV1
dec FEV1/FVC ratio
dec FEF25-75
normal to inc. TLC
inc. RV
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6
Q

why do you get an increased rv in OPD?

A

air trapping

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7
Q

what is the characteristic pattern of emphysema on flow-volume loops?

A

scooped-out

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8
Q

t/f: most patients are somewhere between emphysema and chronic bronchitis

A

true

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9
Q

what is the biggest risk factor for COPD?

A

smoking

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10
Q

only what percent of smokers develop COPD?

A

10-15%

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11
Q

do more men or women die of COPD?

A

women

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12
Q

What are the three leading causes of death?

A
  1. heart disease
  2. Cancer
  3. Chronnic lower resp. tract disorder
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13
Q

is emphysema defined clinically or anatomically?

A

anatomically

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14
Q

what are the two criteria for emphysema Dx?

A
  1. irreversible enlargemnt DISTAL to terminal bronchioles

2. airspace destruction WITHOUT fibrosis

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15
Q

What are the four types of emphysema?

A

Centriacinar
Panacinar
Paraseptal
Irregular

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16
Q

t/f: you tend to see a combo of types of emphysema

A

true

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17
Q

what is the most common type of emphysema?

A

centriacinar

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18
Q

centriacinar emph. has initial sparing of what structure?

A

distal acinus

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19
Q

which lobes of the lung are affected in centriacinar emph?

A

upper lobes and apical segments

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20
Q

centriacinar emph is assc’d wit….

A

heavy smoking; walls black with pigment

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21
Q

centriacinar emph is assc’d with what other diz?

A

chronic bronchitis

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22
Q

describe the histo of a slide for centriacinar emph

A

huge alveoli with dilated airspaces. Alveolar walls and capillaries have been destroyed

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23
Q

what are the anatomical boundaries of panacinar emph?

A

airspace enlargement from respiratory bronchiole to alveoli (NO SPARING)

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24
Q

which lobes of the lung are affected in panacinar emph?

A

lower lobes and anterior margins

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25
Q

which type of emph is assc’d with a1-antitrypsin def?

A

panacinar emph

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26
Q

t/f: nicotine indirectly causes inflammation via TLR on mac’s

A

false; DIRECTLY causes inflammation

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27
Q

Which three chemokines are released in response to ROS from tobacco smoke?

A

IL9
leukotriene B4
TNF-a

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28
Q

The release of IL9, LTB4, and TNF-a recruit neutrophils to the lung which then break down..

A

elastin

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29
Q

The tissue damage in the alveoli from smoke is due to a (blank-blank) imbalance

A

protease-antiprotease

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30
Q

A1-AT helps to reduce (blank) activity

A

elastase

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31
Q

t/f: A1-AT def can be congenital or acquired as a result of oxidative damage

A

true

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32
Q

A1-AT def is coded by the Pi gene on which csome?

A

14

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33
Q

what are the two alleles of Pi gene?

A

M and Z

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34
Q

What is the normal A1AT alleles?

A

2 copies of PiMM

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35
Q

What is the genotype for panacinar emph?

A

2 copies of PiZZ

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36
Q

What is the result of the PiMZ allelle combo?

A

reduced levels of A1AT in the lungs; but asymptomatic. adding smoke increases risk sig.

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37
Q

popping a bleb can lead to a….

A

pneumothorax

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38
Q

What are the two ways that airspace enlargement leads to pathophys?

A
  1. loss of elastic recoil

2. small airway inflammation

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39
Q

in small airway inflamm, goblet cell metaplasia leads to…

A

mucus plugging

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40
Q

in small airway inflamm, there is a (blank) infiltrate

A

inflamm cell

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41
Q

in small airway inflamm, there is smooth muscle hypertrophy and (blank) fibrosis

A

peribronchial

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42
Q

Is chronic bronchitis defined anatomically or clinically?

A

clinically

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43
Q

What are the criteria for chronic bronchitis Dx?

A

Persistent cough with sputum production for at least three months in at least two consecutive years.

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44
Q

What are the four ways that the body tries to protect itself in response to tobacco smoke?

A
  1. deploy inflamm cells (neutrophils, mac’s, lymphs)
  2. hypertrophy of submucosal glands in trachea/bronchi
  3. hypersecretion of mucus in large airways
  4. small airway obstruction
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45
Q

T/F: the causes of small airway obstruction are the same in emphysema and chronic bronchitis

A

true;

  1. increased goblet cellls
  2. increased mucus production
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46
Q

What is the Reid index?

A

thickness of bronchial glands:total bronchial wall thickness

abnl: submucosal glands are greater than 50% of the thickness

47
Q

Who are the pink puffers?

A

emphysema

48
Q

Describe the clinical presentation of emphysema?

A 
dyspnea; slow decline in function
cough not necessary
wt. loss
BARREL-CHESTED
prolonged expiratory phase
hunched over
PURSED LIP BREATHING
49
Q

who are the blue bloaters?

A

chronic bronchitis

50
Q

After the chronic cough, what are the symptoms of chronic bronch?

A

Dyspnea on exertion
Hypercapnea
Hypoxemia
Mild cyanosis

51
Q

how will exacerbations of COPD affect dz course?

A

they will ultimately increase the speed of disease progression

52
Q

what are common exacerbations of COPD?

A

URI or smoke in the air. seen more in CB than in E

53
Q

What are the GOLD criteria for COPD?

A
  1. preventable and treatable
  2. persistent airflow limitation
  3. enhanced chronic inflamm response to noxious particles/gas
  4. exacerbations and comorbidities contribute
54
Q

t/f: spirometry is necessary for the Dx of COPD

A

true

55
Q

What are the spirometer criteria for a dx of COPD?

A

Post-bronchodilator FEV1/FVC <0.70

56
Q

is the FEV1/FVC ratio or FEV1 %predcited value determinant of the severity of COPD?

A

%predicted value FEV1

57
Q

What % predicted is mild COPD?

A

> 80

58
Q

What % predicted is moderat COPD?

A

50-80

59
Q

What % predicted is severe COPD?

A

30-50

60
Q

What % predicted is very severe COPD?

A

<30

61
Q

After smoking cessation, lung function decline is (worse than/equal to) non-smokers

A

equal to

62
Q

what distinguishes asthma from other COPD?

A

reversible

63
Q

are there more male or female kids with asthma?

A

2x more males

64
Q

are there more men or women with asthma?

A

equal

65
Q

when is the peak of asthma presentation?

A

3 years

66
Q

t/f: some kids grow out of asthma

A

true

67
Q

t/f; asthma is progressive

A

false
mild will be mild
severe will be severe

68
Q

what are the Sx of acute asthma exacerbation

A

chest tightness
wheezing
dyspnea
cough w/wo sputum

69
Q

What is status asthmaticus?

A

persistent Sx lasting days to weeks

can result in cyanosis and death

70
Q

what changes do you see to peripheral blood in asthma?

A

eosinophilia

71
Q

What do you see in asthma sputum?

A
  1. Curschmann spirals
    (Whorls of shed epithelium forming spiral shaped mucous plugs)
  2. Charcot-Leyden Crystals
72
Q

What is the most common type of asthma?

A

atopic

73
Q

what is the MOA of atopic asthma?

A

immediate type I hypesensitivty rxn

74
Q

what will RAST show in atopic asthma?

A

positive skin tests for specific allergens

75
Q

which type of asthma has a family history?

A

atopc

76
Q

Non-atopic asthma is assciated with hyper-irritability of the…

A

bronchial tree

77
Q

Which type asthma tends to be more severe?

A

non-atopic

78
Q

which three chemokines are released 5-30 mins after beginning of asthma attack?

A

IL4
IL5
IL13

79
Q

which cell mediates the type I rxn and release the chemokines in atopic asthma?

A

TH2 cells

80
Q

What is the result of release of chemokines from Th2 cells?

A
  1. tissue inflammation
  2. IgE production
  3. Mast cell degranulation
81
Q

What three things do mast cells release when stimulated by Th2 cells?

A

LT C4, D4, E4

82
Q

What are the four changes to the respiratory structure during an asthma attack?

A
  1. bronchoconstriction
  2. increased mucus
  3. vasodilation
  4. increased vascular permeability
83
Q

Mast cell degranulation leads to a loss of..

A

integrity of the mucus membranes (inc. vascular permeability)

84
Q

T/F: asthma attacks can last for days without additional exposure

A

true

85
Q

What are the changes that wee see in an asthma attack 2-24 hours after it begins?

A
  1. increased inflamm cells
  2. major basic protein
  3. continued airway constriction
  4. epithelial destruction
86
Q

Which four inflammatory cells invade the airways 2-24 hours after the beginning of an asthma attack?

A

Eos
Basophils
neutrophils
lymphs

87
Q

What is the best way to interrupt the continued asthma cascade?

A

inhaled corticosteroids

b2 agonists for SMC

88
Q

If a pt is unresponsive to bronchiodilators or corticosteroids, what type of med should you give them?

A

mAb to IL4/5/13

89
Q

Describe the bronchiole remodeling in chronic asthma

A
  1. goblet cell hyperplasia
  2. smooth muscle hypertrophy
  3. inflammation
  4. fibrosis
90
Q

T/F: inflammation and fibrosis are the main causes of chronic asthma

A

false.

while present, they are secondary to smooth muscle hypertrophy and goblet cell hyperplasia in causing symptoms

91
Q

what is another name for non-atopic asthma?

A

intrinsic asthma

92
Q

When does intrinsic asthma begin?

A

adulthood

93
Q

What is Samter’s triad?

A

Nasal polyps
asthma
Aspirin sensitivty

94
Q

in which type of asthma do we see Samter’s triad?

A

intrinsic

95
Q

Describe the spirometry values that confirm asthma
FEV1
FEV1/FVC
PEF

A

Decreased FEV1
dec. FEV1/FVC
Dec. PEF

96
Q

The reversible nature of asthma is measured how?

A

> 12% AND 200mL improvement in FEV1 15 minutes post-inhaled beta-2 agonist

97
Q

What med do you give people to trigger an asthma attack?

A

Methacholine;
PC20 = conc’n of methacholine reduceds FEV1 by 20%
can also have them exercise

98
Q

what symptom is especially important in determining asthma severity?

A

night time symptoms

99
Q

what is bronchiectasis?

A

Permanent dilation of the bronchi and bronchioles

Caused by destruction of the muscle and elastic tissue

100
Q

bronchiectasis is assc’d with what type of infx?

A

necrotizing infx

101
Q

What are the three things that can form an obstruction in the bronchiole?

A

mucus plug
tumor
foreign body

102
Q

explain how blockage of a bronchiole leads to bronchiectasis

A
  1. secretions and bacteria are not cleared.

2. infection and infalmm leads to destruction of smooth muscle and elastic fibers

103
Q

in what lobes of the lungs do you tend to see bronchiectasis?

A

lower lobes

104
Q

in what genetic dz do you see bronchiectasis?

A

CF

105
Q

what other dz will cause LOCALIZED bronchiectais

A

if there’s a tumor there!

106
Q

Using pathology words, describe what you see in bronchiectasis destruction

A

cystic appearing with mucopurulent secretions

107
Q

What is Kartagener syndrome and what is it assc’d with?

A

Primary ciliary dyskinesia

assc’d with bronchiectasis

108
Q

What are the bacterial causes of necrotizing pneumonia asscciated with bronchiectasis?

A

TB
S. aurues
H. flu.
pseudomonas

109
Q

What are the vira lcauses of necrotizing pneumonia asscciated with bronchiectasis?

A

adenovirus
influenza
HIV

110
Q

What are the fungal causes of necrotizing pneumonia asscciated with bronchiectasis?

A

aspergillus

111
Q

What are other dz states associated with bronchiectasis?

A

RA
SLE
IBD
post-transplant

112
Q

What are the Sx of bronchiectasis?

A
  1. LOTSA COUGHING
  2. foul-smelling, bloody sputum
  3. worse in morning
  4. dyspnea and cyanosis
  5. severe hemoptysis
113
Q

Describe the morphologic changes to the airways in bronchiectasis

A
  1. acute and chronic inflamm of the bronchiole walls
  2. desquamation of epithelium
  3. ulcerations
  4. fibrosis
  5. MULTIPLE POS. CULTURES
114
Q

Which abx do you give prophylactically or chronically for bronchiectasis?

A

doxycycline

Block 9 Week 3 (8 decks)

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