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STEP 2 Pulmonary > Pulmo. COPD > Flashcards

Pulmo. COPD Flashcards

1
Q

Emphysema. ,,pink puffer”

A

.

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2
Q

Emphysema. CO2, O2, cyanosis?

A

CO2 retention
No change in oxygen –> No cyanosis

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3
Q

Emphysema. AP diameter?

A

increased

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4
Q

Emphysema. exhalation?

A

prolonged

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5
Q

Emphysema. what characteristic breathing?

A

through pursed lips

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6
Q

Emphysema. what type in smoking?

A

Centriacinar

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7
Q

Emphysema. what type in A1AT deficiency?

A

Panacinar (lower lobes)

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8
Q

Emphysema. A1AT. liver disease associated.

A

.

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9
Q

Emphysema. A1AT. 4 characteristic?

A

● COPD at a young age (</=45 years).
● COPD with minimal or no smoking history.
● Basilar-predominant COPD.
● History of unexplained liver disease.

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10
Q

Emphysema. xray?

A

narrow heart shadow, flat diaphragm, decreased vascular markings and hyperinflated lungs.
inc. AP diameter

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11
Q

Chronic bronchitis. ,,blue bloaters”

A

.

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12
Q

Chronic bronchitis. definition?

A

Productive cough for 3 or more months over 2 consecutive years.

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13
Q

Chronic bronchitis. O2?

A

Decreased oxygen –> cyanosis.

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14
Q

Chronic bronchitis. heart dysfunction?

A

Pulmonary HTN
CHF
edema

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15
Q

Chronic bronchitis. xray?

A

CXR: prominent bronchovascular markings and a mildly flattened diaphragm.

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16
Q

COPD and chronic bronchitis most of the time is in combination.

A

.

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17
Q

hyperinflation. static mechanism.

A

Static mechanisms: equilibrium between negative pressure of chest wall and positive pressure by the lungs at the FRC. Decreased elasticity of the lungs decreases the positive pressure created by the lungs to expel air. Thus, decreasing the negative pressure created by the chest wall. FRC is reached at a higher lung volume (higher FRC).

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18
Q

hyperinflation. dynamic mechanism.

A

Dynamic mechanisms: “air stacking”. Increased airway resistance leading to
prolonged expiratory phase. When exertional demands trigger an increase in minute ventilation, the patient is forced to begin inhalation prior to completion of exhalation –> further air trapping and hyperinflation.

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19
Q

Hyperinflation.
diaphragmatic flattening in COPD.

A

In COPD, the diaphragmatic flattening and muscular shortening caused by
hyperinflation result in more difficulty in decreasing intrathoracic pressure
during expiration and therefore increases work of breathing.

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20
Q

COPD. pulmonary tests.
4?

A

PFT, DLCO, A1AT, ABG

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21
Q

COPD. PFT? 2

A

Decreased FEV1/FVC ration
Not reversibel

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22
Q

COPD. DLCO?

A

DLCO decreased in emphysema, normal in chronic bronchitis

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23
Q

COPD. A1AT?

A

Tiesiog measue serum AAT levels

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24
Q

COPD. ABG?

A

chronic respiratory acidosis and secondary metabolic alkalosis.

▪ Vs CHF exacerbation: respiratory alkalosis.

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25
Q

COPD. treatment. medication groups?

A

Treatment: add more medications if condition is getting worse.
o SABA.
o Add LAMA.
o Add LABA.
o Add ICS.
o Add PDE4 inhibitors.
o Add oral corticosteroids.

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26
Q

COPD. treatment mneumonic - COPDER

A

Corticosteroids, oxygen, prevention, dilators, experimental, rehabilitation

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27
Q

COPD. treatment mneumonic - C? what effect?

A

Corticosteroids: decreases COPD exacerbations and improves quality of life.

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28
Q

COPD. Mild - what corticosteroids?

A

ICS

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29
Q

COPD. severe - what corticosteroids?

A

Oral CS

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30
Q

COPD. exacerbation - what corticosteroids?

A

IV CS

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31
Q

COPD. mneumonic - O. What Spo2, what pO2?

A

SpO2 is less than 88%.
o Keep it between 88 and 92 since they’re dependent on hypoxic drive to ventilate.

● Or PaO2 is less than 55.

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32
Q

COPD. mneumonic - O. Long term supplemental oxygen has mortality benefit with significant hypoxemia.
What SpO2 or pO2?

A

SpO2</= 88% or PaO2 <55 mmHg.

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33
Q

COPD. mneumonic - O. Long term supplemental oxygen has mortality benefit with significant hypoxemia.
What SpO2 or pO2 with cor pulmonale or RHF or erythrocitosis (>55 proc.)?

A

SpO2</=89% or PaO2 <59 mmHg with cor pulmonale or RHF or erythrocytosis (>55%)).

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34
Q

COPD. mneumonic - O. Long term supplemental oxygen has mortality benefit with significant hypoxemia. SpO2 maintai above 90proc. when?

A

SaO2 should be maintained above 90% during sleep, walk, and at rest.

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35
Q

COPD. mneumonic - O. Long term supplemental oxygen has mortality benefit with significant hypoxemia. how long to use to get benefit?

A

Survival benefits are significant when used for 15 hours or more.

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36
Q

COPD. mneumonic - O. why not above 92 proc?

A

Why not above 92? ((The hypercapnia would lead to cerebral vasodilation –> may induce seizures.))

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37
Q

oxygen induced CO2 retention in COPD schema atspausdinti

A

.

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38
Q

oxygen induced CO2 retention in COPD.
Baseline: decr. ventilation,
decr. gas exchange (hypoxic vasoconstriction) –> what after O2 –> what effect?

A

post O2: vasodilation –> effect: ventilation/perfusion mismatch

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39
Q

oxygen induced CO2 retention in COPD.
Baseline: decr. PaO –> incr. CO2 affinity (Haldane effect) –> what after O2 –> what effect?

A

after O2: Incr. PaO2 –> decr. CO2 affinity –> Effect: Decr. CO2 uptake from tissues

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40
Q

oxygen induced CO2 retention in COPD.
Baseline: rapid, shallow breathing (incr. RR) –> what after O2 –> what effect?

A

after O2: decr. RR –> effect: decr. minute ventilation

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41
Q

COPD. mneumonic - P. 2 aspects?

A
  1. smoking cessation - decrease the rate of decline of FEV1 and decrease mortality
  2. vaccines: flu and pneumococcal
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42
Q

COPD. mneumonic - D. 3 drugs in general?

A

Short acting, long acting, and orals.

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43
Q

COPD. mneumonic - ER
E - experimental
R- rehabilitation

nieko nebuvo prirasyta prie situ.

A

.

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44
Q

COPD. Rofumilast - ?

A

Rofumilast: PDE inhibitor that decreases mucociliary malfunction and pulmonary remodeling; reduces future exacerbation.

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45
Q

COPD in A1AT. what specific treatment?

A

A1AT: IV supplementation with pooled human AAT + bronchodilators + steroids.

▪ Lung & liver transplant if needed.

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46
Q

COPD. to improve survival? 3

A

o Smoking cessation.
o LTOT.
o Lung reduction surgery.

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47
Q

COPD - progressive condition of limited airflow during expiration that is not entirely reversible.

Encompasses chronic bronchitis and emphysema

A

.

48
Q

COPD most important risk factor?

A

smoking

49
Q

COPD compliance and elasticity?

A

loss of elasticity, increase compliance

50
Q

COPD. features? symptoms

A

a. Progressive dyspnea
b. Cough with sputum production
c. decr. breath sounds
d. Prolonged expiratory phase
e. Barrel-shaped chest (due to air trapping and hyperinflation of lungs)
f. Elongated and narrow heart shadow on X-ray
g. Chronic hypoxemia may be seen in advanced disease, which leads to secondary polycythemia.

51
Q

COPD. Hyperinflation in COPD - It occurs through both static and dynamic mechanisms.

A

.

52
Q

COPD. air stacking phenomenon?

A

a. It is the dynamic mechanism for hyperinflation in COPD
b. It is more responsible for hyperinflation than static mechanism

53
Q

COPD. air stacking phenomenon. pathophysiology?

A

The expiratory phase is prolonged in COPD

When exertional demands trigger an increase in minute ventilation, the patient is forced to begin inhalation prior to completion of exhalation

This results in additional air trapping and hyperinflation

54
Q

most important factor for prolonged survival in COPD?

A

Abstinence from smoking (most important)

(NOT long term O2 or lung reduction surgery)

55
Q

COPD treatment. what inhaled bronchodilators?

A

Inhaled bronchodilators (especially anti-cholinergics medications like ipratropium and
tiotropium)

56
Q

COPD treatment. what combination of drugs?

A

Anti-cholinergics may be combined with short-acting beta agonists (eg, albuterol)

57
Q

COPD treatment. for severe COPD drug?

A

Inhaled steroids and long-acting beta agonists

58
Q

chronic vs acute-on-chronic COPD.
what metabolic change in chronic? apie hypercarbia

A

In chronic COPD, there is hypercarbia with normal pH and high serum bicarbonate

59
Q

chronic vs acute-on-chronic COPD.
what metabolic change in acute-on-chronic COPD? apie hypercarbia

A

In acute-on-chronic COPD, there is hypercarbia with associated acidosis and low bicarbonate level

This is because of mixed-acid base disorder

60
Q

selection of bronchod. for stable COPD. Lentele buvo, bbz ten vapsie.

Lower symptom severity + lower disease risk?

A

SABA or SAMA as needed

61
Q

selection of bronchod. for stable COPD.

Higher symptom severity + lower disease risk?

A

LAMA

62
Q

selection of bronchod. for stable COPD.

Lower symptom severity + higher disease risk?

A

LAMA +/- LABA

63
Q

selection of bronchod. for stable COPD.

Higher symptom severity + higher disease risk.

A

LAMA +/- LABA +/- ICS

64
Q

selection of bronchod. for stable COPD.
Kas skaitosi disease risk?

A

In general: Based on frequency of exacerbations

65
Q

selection of bronchod. for stable COPD.
Kas skaitosi [higher symptom severity]?

A

Dyspnea with neutral exertion (light housework) or at rest. Assessed using validated instruments, such COPD assessment test (CAT)

nu mazdaug impact of respiratory symptoms in daily life

66
Q

selection of bronchod. for stable COPD.
Kas skaitosi lower disease risk?

A

No hospitalization
AND
<2 outpatient exacerbations requiring systemic corticoisteroids

67
Q

selection of bronchod. for stable COPD.
Kas skaitosi higher disease risk?

A

> = 1 hospitalization
OR
=2 outpatient exacerbations requiring systemic corticoisteroids

68
Q

LAMA’s are always superior to LABA’s in COPD

A

.

69
Q

COPD exacerbation.
most common trigger?

A

upper respiratory infection

70
Q

COPD exacerbation.
characterized by symptoms?

A
  1. It is characterized by change in >=1 of the following cardinal symptoms:

a. COUGHT severity or frequency (increased frequency or severity)
b. Volume or character of SPUTUM production (change in color or volume)
c. Level of DYSPNEA (increased)

71
Q

COPD exacerbation.
physical examination?

A

a. Wheezing
b. Tachypnea
c. Prolonged expiration
d. Use of accessory respiratory muscles
e. Jugular venous distension is observed, especially during expiration, due to increased intrathoracic pressure
f. Distal heart sounds may be heard due to hyperinflation of lungs

72
Q

COPD exacerbation.
Diagnosis - xray ->?

A

hyperinflation

73
Q

COPD exacerbation.
treatment. initial? 3

A

a. Initial intervention:
i. SABA
ii. Systemic glucocorticoids (inhaled glucocorticoid have no role in management of COPD exacerbation)
iii. Antibiotics

74
Q

COPD exacerbation. ABG?

A

hypoxia, CO2 retention (chronic and/or acute)

75
Q

COPD exacerbation. persistent symptoms even after initial intervention? what to do

A

Noninvasive positive pressure ventilation (NPPV)

76
Q

COPD exacerbation. when need intubation?

A

i. Failure of 2-hour trial of NPPV
ii. pH <7.1
iii. Hemodynamic instability
iv. Poor mental status (eg, somnolence, lack of cooperation, inability to clear secretions)

77
Q

COPD exacerbation. prevention. what drug?

A

Roflumilast

78
Q

COPD exacerbation. prevention. Roflumilast. mechanism?

A

It is a phosphodiesterase inhibitor with anti-inflammatory properties

79
Q

COPD exacerbation. prevention. Roflumilast. action 2?

A

decr. mucociliary malfunction
decr. pulmonary remodeling

80
Q

COPD exacerbation. prevention. Roflumilast. use? 2

A
  1. It is useful as maintenance therapy to reduce future exacerbations in patients with severe COPD and history of exacerbations
  2. It is not indicated during an acute exacerbation
81
Q

COPD exacerbation. management is lenteles?

A

oxygen
inhaled bronchodilators
systemic glucocorticoids
antibiotics if >=2 cardinal symptoms
Oseltamivir if evidence influenza
NPPV if ventilatory failure
intubation if NPPV failed or contraindicated

82
Q

COPD exacerbation. MCC?

A

upper respiratory infection

83
Q

COPD exacerbation. moderate exacerbation, how defined?

A

Moderate exacerbation: 2 or more cardinal symptoms.

84
Q

COPD exacerbation. JVP?

A

Jugular venous distention noted during expiration.

85
Q

COPD exacerbation. Abs?

A

Antibiotics (3-7 days): azithromycin, respiratory fluoroquinolones, or penicillin/beta-lactamase inhibitors (amoxiclav).

86
Q

COPD exacerbation. bronchodilators 2?

A

Bronchodilators: albuterol and ipratropium.

87
Q

COPD exacerbation. steroids 2?

A

Steroids: PO prednisone or IV methylprednisolone.
▪ Given for 5 days.
▪ Improve lung function and hypoxemia, decreased risk of relapse, treatment failure, and length of hospital stay.

88
Q

COPD exacerbation. altered mental status indicates what?

A

hypercapnia

89
Q

COPD exacerbation. mild treatment combination?

A

Mild: MDI albuterol and ipratropium and PO prednisone.

90
Q

COPD exacerbation. severe treatment combination?

A

Severe: Nebulizer albuterol and ipratropium IV methylprednisolone.

91
Q

COPD exacerbation. severe treatment –> gets better?

A

▪ Gets better –> home. PO CS and MDI.

92
Q

COPD exacerbation. severe treatment –> gets worse?

A

Gets worse (rising CO2, absent lung sounds) –> ICU.

IV CS, and nebulizer.

Preferred method of respiratory support is NPPV. If fails –> invasive mechanical ventilation.
o Required in hypercapnic patients with poor mental
status, hemodynamic instability, or profound acidemia
(pH <7.1).

93
Q

COPD exacerbation. severe treatment –> needs more time to evaluate?

A

Needs more time –> ward.
PO CS and nebulizer.

94
Q

PFT. table. normal FEV1?

A

> 80 proc. (of predicted)

95
Q

PFT. table. normal FVC?

A

> 80 proc. (of predicted)

96
Q

PFT. table. normal FEV1/FVC?

A

> 70 proc

97
Q

PFT. table. OLD FEV1?

A

decreased

98
Q

PFT. table. OLD FVC?

A

normal to decreased

99
Q

PFT. table. OLD FEV1/FVC?

A

decreased

100
Q

PFT. table. restrictive (including obesity) FVC?

A

decreased

101
Q

PFT. table. restrictive (including obesity) FEV1?

A

decreased

102
Q

PFT. table. restrictive (including obesity) FEV1/FVC?

A

normal to increased

103
Q

Therapeutically relevant to differentiate between COPD and asthma since inhaled steroids are the primary long-term intervention for asthma and a long-acting anticholinergic inhaler is preferred for COPD.

A

.

104
Q

COPD exacerbation. ABs duration?

A

3-7 days

105
Q

COPD exacerbation. 3 abs groups?

A

Macrolides (eg azithromycin)
Resp fluoroquinolones (levoflox, moxiflox)
Penicillin/beta-lactamase inhibitors (amoxiclav)

106
Q

COPD exacerbation. symptomatic hypercapnia. what symptom cause initial suspicion? what to do?

A

Altered mental status in the setting of COPD exacerbation should raise suspicion for symptomatic hypercapnia

DO ABG

107
Q

COPD exacerbation. symptomatic hypercapnia. pathophysiology?

A

a. Some patients with COPD retain CO2 during an exacerbation due to shallow breathing and high levels of ventilation-perfusion mismatch
b. Hence, despite tachypnea, patient may be hypercapnic

108
Q

COPD exacerbation. symptomatic hypercapnia.
Symptomatic hypercapnia may present without significant hypoxemia.

A

.

109
Q

COPD exacerbation. symptomatic hypercapnia. mild to moderate hypercapnia symptoms?

A

headache
hypersomnolence

110
Q

COPD exacerbation. symptomatic hypercapnia. severe hypercapnia symptoms? (eg > 75-80 mmHg)

A

i. Delirium
ii. Confusion
iii. Lethargy
iv. Coma (CO2 narcosis)
v. Seizures

111
Q

OXYGEN-INDUCED CO2 RETENTION IN COPD. schema jau buvo anksciau. what changes in brain hormones when acidosis?

A
  1. Acidosis caused by an acute increase in CO2 leads to altered level of consciousness due to following changes in the brain:
    a. incr. GABA and glutamine
    b. decr. Glutamate and aspartate
112
Q

OXYGEN-INDUCED CO2 RETENTION IN COPD. what hormones in brain incr in case of acidosis?

A

GABA and glutamine

113
Q

OXYGEN-INDUCED CO2 RETENTION IN COPD. what hormones in brain decr in case of acidosis?

A

glutamate and aspartate

114
Q

OXYGEN-INDUCED CO2 RETENTION IN COPD.

Hypercapnia -> Cerebral vasodilation
-> Seizures

A

.

115
Q

OXYGEN-INDUCED CO2 RETENTION IN COPD.
prevention of CO2 retention?

A

a. Oxygen should be cautiously used with following goals:
i. SaO2 of 90%-93% OR
ii. PaO2 60-70 mm Hg

b. Patients who develop significant acidosis or have severely reduced level of consciousness require mechanical ventilation

STEP 2 Pulmonary (19 decks)

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