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Pathophysiology > 22 Obstructive Pulmonary Disorders > Flashcards

22 Obstructive Pulmonary Disorders Flashcards

1
Q

Spirometry

A

pulmonary function testing [PFT]

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2
Q

common ventilatory parameters

A

1 tidal vol
2 residual vol
3 vital capacity/forced capacity
4 functional residual capacity

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3
Q

when chest vol INCREASES…

A

alveolar pressure decreases

air flows INTO respiratory synth

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4
Q

when chest vol DECREASES

A

alveolar pressure increases

air flows out to atmosphere which has lower pressure

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5
Q

tidal volume [Vt]

A

amt that moves during a single inspiration or expiration

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6
Q

residual vol [RV]

A

vol of air still in lungs after MAX expiration

-keeps alveoli fr collapsing since no smooth muscles to contract

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7
Q

forced vital capacity [FVC]

A

*total vol of air exhaled
*time required for air xchange is also measured
VT + IRV + ERV

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8
Q

Inspiratory + expiratory reserve [IRV and ERV]

A

addition vol you inspire or expire maximally

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9
Q

FEV1

A

forced expiratory volume in 1 second

*reliable + index of OBSTRUCTIVE AIRWAY DISEASE

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10
Q

Arterial Blood Gas [ABG]

A

-assesses oxygenation + acid-base status

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11
Q

air flows towards ____

A

low pressure or low resistance

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12
Q

normal PaO2

A

80-100 mmHg

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13
Q

normal PaCO2

A

45-35 mmHg

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14
Q

normal HCO3-

A

22-26 mEq/L

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15
Q

normal O2 Saturation

A

96-100%

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16
Q

normal pH

A

7.35-7.45

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17
Q

lethal pH range

A

below 6.9

above 7.6

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18
Q

PaCO2: respiratory function

A

respiratory acidosis/alkalosis

-opposite change to CO2 to pH

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19
Q

hco3: renal (metab) function

A

metab acidosis or alkalosis

-same changes of HCO3 as pH

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20
Q

retaining CO2 leads to

A

acidosis

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21
Q

Obstructive Pulmonary Disorder

A

-manifested by increased resistance to airfloww

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22
Q

Obstructive Pulmonary Disorder

diagnosis

A

INCR: residual vol, functional residual capacity,
DECR: FEV1, FEV1/FVC ratio (less than 70%)

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23
Q

Bronchodilator for Obstructive Pulmonary Disorder

A
  • diagnosis test should be repeated in 15-20 mins
  • improvement in FEV1 after use of bronchodilator helps diagnose Asthma
  • no significant improvement = COPD
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24
Q

Postive Bronchodilaroe Response

A

FEV1 improves >15%

-partially reversible bronchospasms of smooth muscles (asthma, asthmatic bronchitis)

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25
Q

Restrictive Pulmonary Disorders

A

manifested by decreased lung expansion

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26
Q

Restrictive Pulmonary Disorders

diagnosis

A

DECR: VC, TLC, FRC, RV

-normal FEV1/FVC ratio since both of them are reduced

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27
Q

the greater the DECR in lung vol, the ____ the severity of the disease

A

GREATER

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28
Q

Restrictive Pulmonary Disorders

ABG

A

1 DECR PaO2
2 NORM/DECR Pa CO2
3 INCR Ph (alkalosis)

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29
Q

functional residual capacity [FRC]

A

ERV + RV

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30
Q

why is restrictive pulmonary disorder more prone to alkalosis?

A
  • decreased PaO2 means HYPOXEMIA
  • low O2 in tissue
  • baroreceptors are triggered by low O2
  • baroreceptors tells lungs to hyperventilate
  • hyperventilation decreases CO2
  • decrease in CO2 leads to alkalosis
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31
Q

Normal Range for FEV1/FVC

A

FEV1/FVC: 75%
FEV1: 3.0L
FVC: 4.0L

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32
Q

Restrictive Range for FEV1/FVC

A

FEV1/FVC: 83%
FEV1: 2.5L
FVC: 3.0L

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33
Q

Obstructive Range for FEV1/FVC

A

FEV1/FVC: 25%
FEV1: 1.0L
FVC: 4.0L

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34
Q

Obstructive Pulmonary Disorder

Classifications

A

1 obstruction in wall of lumen (asthma/bronchitis)
2 obstruction fr incr pressure around outside of airway lumen
3 obstruction of airway of lumen

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35
Q

Asthma

A

airway obstruction in the wall of lumen

  • reversible
  • airway inflammation
  • incr airway responsiveness to a variety of stimuli
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36
Q

Asthma

etiology

A
  • occurs in 5-12% of US pop

- most common chronic disease of children

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37
Q

2 types of Asthma

A

1 Intrinsic

2 Extrinsic

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38
Q

Intrinsic Asthma

A
  • non-allergic, adult onset
  • dvlps in midl age w less favorable prognosis
  • no hx of allergies
  • resp infections or psych factors appear to be contributory
  • allergen-specific immunotherapy + environmental control NOT helpful
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39
Q

Extrinsic Asthma

A
  • allergic, pediatric onset
  • .3-.5 of asthma cases
  • IgE response - mast cells activation (histamine)
  • inflammatory cell infiltration (neutro, eosino, + lymphocytes)
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40
Q

histamine

A

vasodilator

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41
Q

leukotriene

A

bronchoconstrictor

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42
Q

Asthma

clinical manifestations

A 
1 wheezing (expiratory)
2 tightness of chest
3 dyspnea
4 dry cough 
5 productive cough (incr sputum)
6 hyperinflated chest (barrel chest, xray)
7 decr breath sounds (phys exam)
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43
Q

Severe Attck of Asthma

clinical manifestations

A 
1 orthopnea
2 agitation
3 tachypnea: >30 breaths/min
4 tachycardia: >120 bts/min
5 pulsus paradoxus
6 PEFR: <80L/min
7 intercostal retractions
8 distant breathes w inspiratory wheezing
9 use of accessory muscles (chest + neck)
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44
Q

pulsus paradoxus

A
  • normally, when inhaling, BP falls, but not by much

- in pulsus paradoxus, BP falls by >10mmHg

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45
Q

Asthma

diagnosis

A 
1 radiographic finding
2 physical finding
3 sputum examination
4 PFT
5 skin testing
6 ABG
7 CBC
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46
Q

radiographic finding as a diagnosis for Asthma

A

hyperinflation w flattening of diaphragm

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47
Q

sputum examination as a diagnosis for Asthma

A
  • Charcot-Leyden Crystals
  • eosinophils
  • Cruschmann Spirals
48
Q

Charcot-Leyden Crystals

A

formed fr crystallized enzymes fr eosinophilic membranes

-a form of sputum exam for asthma

49
Q

Cruschmann Spirals

A

mucous casts of bronchioles

-form of sputum exam for asthma

50
Q

Asthma

PFT

A
  • DECR in forced expiratory vol

- PEFR

51
Q

PEFR

A

peak expiratory volumes decrease

  • ratio of FEV1/FVC before + after administration of short-acting bronchodilator
  • —- >15% change
52
Q

skin testing as a diagnosis for Asthma

A

for young patients w extrinsic asthma

53
Q

Asthma

ABG

A

MILD ATK: normal
BRONCHOSPASM INTENSIFIES: RESP. ALKA + hypoxemia
LATE STG: PaCO2 elevation, sign that patient is getting worse

54
Q

Asthma

CBC

A

elevated WBC + eosinophil

55
Q

Asthma

Treatments

A

1 avoid triggers
2 environ control (dust, allergens, air purifiers)
3 preventative therapy (stop smoking, aerosols, odors)
4 desensitization
5 anti type I hypersensitivity

56
Q

desentization

A

allergen specific immunotherapy

57
Q

anti type I hypersensitivity medications

A 
1 O2 therapy
2 small-vol nebulizers
3 B2 agonist
4 corticosteroids
5 leukotriene modifiers
6 mast cell inhibitors
58
Q

nebulizers

A

machine to help inhale med

59
Q

B2 agonist

A

beta 2 agonist like ibutrol

-dilate bronchi

60
Q

corticosteroids

A

counters histamine/inflammatory rxn

61
Q

leukotrine modifier

A

med to counter bronchoconstriction

62
Q

Chronic Bronchitis

A

aka type B COPD, “blue bloater”

  • obstruction in the wall of lumen
  • chronic recurrent productive cough that lasts more than 3 months for 2 cosuccessive years
  • hypersecretion of bronchial mucus
63
Q

Chronic Bronchitis

etiology

A
  • persistent, IRREVERSIBLE, when paired w emphysema
  • 1:2 male to female ratio
  • > 30-40 rys
64
Q

Chronic Bronchitis

pathogenesis

A

1 Chronic Inflammation + swelling of bronchial mucosa results w Scarring
2 Hyperplasia of bronchial mucous gland/goblet cells
3 Incr bronchial wall thickness
4 Pulmonary Hypertension [cor pulmonle]

65
Q

inflammation + swelling in chronic bronchitis

A
  • results w scarring
  • –INCR IL8 (recruit neutrophil actvtn), CD8 T-lymph
  • –extends to surrounding alveoli prevents proper oxygentn + potentiates airway obstrctn
66
Q

hyperplasia of bronchial mucous in chronic bronchitis

A

–incr mucus prodctn w formtn of mucus plugs

67
Q

incr brochial wall thickness in chronic bronchitis

A
  • resistance increases work for breathing + o2 demands

- ventilation-perfusion mismatch w hypoxemia + hypercarbia; incr pulmonary artery resistance

68
Q

pulmonary hypertension in chronic bronchitis

A
  • inflammation in bronchial walls w vasoconstriction of pulmonary vessels + arteries
  • SNS activation
  • autoregulatn
  • RSHF may occur w/t high pulmonary resistance
69
Q

last stage of chronic bronchitis pathogenesis

A

destruction of bronchial walls - dead space/emphysema

  • -results in dilation of airway sacs:bronchiectasis
  • dilated sacs contain pools of infected secretion that DO NOT clear themselves
  • —can cause further infection that can spread to adjacent lung fields by the lymphatics or venous drainage to other areas of the body (commonly the brain)
70
Q

chronic bronchitis

clinical manifestations

A

1 typically patient is overweight
2 commonly assoc w Emphysema (late stage)
3 SOB on expiration
4 excessive sputum
5 chronic cough
6 evidence of excess body fluids (edema, hypervolemia)
7 cyanosis (late sign)

71
Q

why are chronic bronchitis patients generally overweight?

72
Q

Chronic Bronchitis

diagnosis

A 
1 Chest XRay
2 PFT
3 ABG
4 ECG
5 Secondary polycythemia****
73
Q

chest xray for chronic bronchitis

A

looks for signs of pulmonary hypertension or cor pulmonale

1 incr bronchial vascular markings
2 enlarged horizontal cardiac silhouette
3 congested lung fields
4 evidence of previous pulmonary infection

74
Q

Chronic Bronchitis

PFT

A

1 normal TLC
2 INCR RV
3 DECR FEV1
4 DECR FEV1/FVC

75
Q

chronic bronchitis

ABG

A

INCR PaCO2

DECR PO2

76
Q

chronic bronchitis

ECG

A
  • atrial arrythmias

- evidence of right ventricular hypertrophy (cor pulmonale)

77
Q

secondary polycythemia

A

incr in RBC

-due to LOW O2 (nocturnal hypoxemia)

78
Q

chronic bronchitis

mgmt

A

a form of treatment for chronic bronchitis

  • smoking cessation
  • bronchodilator therapy
  • reduction to exposure of irritants

other:

  • adequate rest
  • proper hydration
  • physical conditioning (treadmill/walk/bike)
  • influenza + pneumococcal vaccines
79
Q

chronic bronchitis

treatments

A

1 mgmt
2 low dose O2 therapy
3 medication

80
Q

chronic bronchitis

medication

A

1 inhaled short-acting B2 agonist
2 inhaled anticholinergic bronchodilators
3 cough suppressants
4 antimicrobial agents (bacterial infections)
5 inhaled/oral corticosteroids
6 theophylline products

81
Q

low-dose o2 for chronic bronchitis

A

normally, low O2 sends a signal to baroreceptors to prevent CO2 fr accumulating

high dose will prevent that pathway and will try to increase CO2 retention.

low dose wont interfere w the pathway

82
Q

2 types of COPD

A

chronic obstructive pulmonary diseases
Type A: Emphysema aka pink puffer
Type B: Chronic Bronchitis aka blue bloater

83
Q

Emphysema

A

aka Type a COPD aka pink puffer (not cyanotic, puffy bc hyperventilation)

  • obstruction related to loss of lung parenchyma
  • destructive changes of alveolar walls w/o fibrosis
  • abnormal enlargement of distal air sacs
  • IRREVERSIBLE damage
  • assoc w Chronic Bronchitis
84
Q

the bigger the alveoli, the ___

A

the less recoil force/tension we have

-thats why abnormal enlargement is bad

85
Q

Emphysema

causes

A
  • smoking >70 packs/year
  • air pollution
  • certain occupations (mining, welding, asbestos)
  • a1-antitrypsin deficiency (could be genetic or acquired due to inflammation)
86
Q

smoking causes alveolar damage

A
  • inflammation leads to release of proteolytic enzymes

- inactivates a1-antitrypsin

87
Q

a1-antitrypsin

A

protects surfactant which protects lung parenchyma

88
Q

lung parenchyma

A

substance of the lung outside of the circulatory system that is involved with gas exchange and includes the pulmonary alveoli

89
Q

neutrophils + macrophage cause alveolar damage

A

by release of proteolytic enzymes

90
Q

loss of elastic tissue in lung

A

results in loss of radial traction (normally holds airway open)

91
Q

Emphysema pathogenesis

A

1 loss of elastic tissue in lungs
2 air becomes trapped in distal alveoli
3 loss of alveolar wall + air trapping leads to Bullae formation
4 reduction in pulmonary capillary bed

92
Q

Bullae

A

large thin walled cysts in the lung

93
Q

reduction in pulmonary capillary bed

A

exchange of O2 + CO2 bw alveolar + capillary blood impaired

94
Q

Emphysema

clinical manifestations

A 
1 progressive, exertional dyspnea
2 THIN
3 barrel chest
4 use of accesory muscles
5 pursed-lip breathing
6 cough (minimal or absent)
7 digital clubbing
95
Q

Thin emphysema

A

R/t incr respiratory effect, incr caloric expenditure, decr ability to consume adequate calories

96
Q

barrel chest emphysema

A

incr total lung vol to compensate the lost lung capacity due to dead space

97
Q

Emphysema

Diagnosis

A 
1 PFT
2 chest xray
3 ECG
4 ABG
5 patient Hx
6 physical findings
98
Q

Emphysema

PFT

A

INCR: RV, TLCl, functional residual capacity,
DECR: FEV1, FVC

99
Q

Emphysema

chest x ray

A
  • hyperventilation
  • low, flat diaphragm
  • presence of blebs or bullae
  • narrow mediastinum
  • normal or small vertical heart
  • barrel chest
100
Q

Emphysema

ABG

A
  • mild DECR in PaO2

- normal PaCO2 (elevated in late stages)

101
Q

Emphysema

phys findings

A

thin, wasted individual hunched forward

  • using accessory muscles
  • *decr breath sounds, lack of crackles + rhonchi
  • *decr heart sounds
  • prolonged expiration
  • hyperresonance
  • decr diaphragmatic excursion
  • chronic morning cough
102
Q

Emphysema

treatment

A

similar to chronic bronchitis

1 o2 therapy
2 smoking cessation
3 medication

103
Q

Emphysema

medication

A

similar to chronic bronchitis

1 inhaled short acting B2 agonist
2 inhaled anticholinergic bronchodilators
3 inhaled/oral corticosteroids
4 theophylline products
5 cough suppressants
6 antimicrobial agents
104
Q

air gets trapped in distal alveoli

105
Q

pursed lips

106
Q

presence of bullae

107
Q

abnormal enlargement of distal sac

108
Q

obstruction due to loss of lung parenchyma

109
Q

_____ may result with pulmonary hypertension in chronic bronchitis

110
Q

cor pulmonale is more associated with

A

chronic bronchitis

111
Q

secondary polycythemia is a diagnosis for

A

chronic bronchitis

112
Q

theophylline is to treat

A

emphysema + chronic bronchitis

113
Q

antimicrobial is to treat

A

emphysema + chronic bronchitis

114
Q

leukotriene modifiers is to treat

A

asthma

-leukotriene is a bronchoconstrictor

115
Q

sputum testing is for

A

diagnosis of asthma

116
Q

loss of elastic tissue is a characteristic of

117
Q

which OLD starts with resp alkalosis and then leads to acidosis?

Pathophysiology (32 decks)

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