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HARRISSONS > Copd > Flashcards

Copd Flashcards

1
Q

The most characteristic symptom of COPD

A

Chronic and progressive DYSNEA

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2
Q

The FIRST SYMPTOM OF COPD

A

Chronic Cough

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3
Q

Test required to establish diagnosis of COPD

A

Spirometry

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4
Q

Consider COPD In px with dyspnea that is

A

PROGRESSIVE OVER TIME
Characteristically worse with exercise
Persistent

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5
Q

COPD chest X-ray findings:

A

Diaphragmatic flattening
Increase in retrosternal air space
Attenuation of vascular markings (hyperinflation)

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6
Q

Genetic factors that have

also been related to a decline in lung function or risk of COPD

A
  1. alpha-1 antitrypsin (AATD) 15 ;
  2. metalloproteinase 12 (MMP-12)
  3. glutathione S-transferase
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7
Q

How to diagnose COPD?

A

Spirometry is required to make the diagnosis; the presence of a post-bronchodilator FEV1/FVC < 0.70 confirms the presence of persistent airflow limitation.

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8
Q

The World Health Organization recommends that all patients with a diagnosis of COPD should be screened once especially in areas with high AATD diagnostic test because of its weak specificity.

A

Alpha-1 antitrypsin deficiency (AATD) screening

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9
Q

Classification of airflow limitation severity post bronchodilator:
What is the classification if FEV1> or = 80%

A

MILD

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10
Q

Classification of airflow limitation severity post bronchodilator:
What is the classification if FEV1 is 50-80%

A

Moderate

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11
Q

Classification of airflow limitation severity post bronchodilator:
What is the classification if FEV1 is 30-50%

A

Severe

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12
Q

Classification of airflow limitation severity post bronchodilator:
What is the classification if FEV1 is <30%

A

Very severe

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13
Q

What is the MMRC scale:

I only get breathless with strenuous activity

A

MMRC 0

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14
Q

What is the MMRC scale:

I get short of breath when “hurrying” on the level
Or
Walking up a slight hill

A

MMRC 1

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15
Q

What is the MMRC scale:

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

A

MMRC 2

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16
Q

What is the MMRC scale:

I stop for breath after walking 100 meters or after a few minutes on the level

A

MMRC 3

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17
Q

What is the MMRC scale:

I am too breathless to leave the house or I am breathless when dressing or undressing

A

MMRC 4

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18
Q

is a once daily LABA that improves breathlessness, health status and exacerbation rate

A

Indacaterol

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19
Q

are additional once daily LABAs that improve lung function and symptoms

A

Oladaterol and vilanterol

OV

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20
Q

have prolonged binding to M3 muscarinic receptors, with faster dissociation from M2 muscarinic receptors, thus prolonging the duration of bronchodilator effect.

A

Long-acting antimuscarinic antagonists (LAMAs), such as tiotropium
aclidinium
glycopyrronium bromide
umeclidinium

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21
Q

also block the inhibitory neuronal receptor M2, which potentially can cause vagally induced bronchoconstriction

A

Short-acting antimuscarinics (SAMAs),

namely ipratropium and oxitropium

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22
Q

systematic review of randomized controlled trials concluded that this SAMA/ short acting muscarinic antagonist, used alone provided small benefits over short-acting beta2-agonist in terms of lung function, health status and requirement for oral steroids

A

ipratropium

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23
Q

improve symptoms and health status. They also improve the effectiveness of pulmonary rehabilitation and reduce exacerbations and related hospitalizations

A

LAMA treatments (tiotropium)

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24
Q

Main side effect of anticholinergic drugs

A

Dry mouth

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25
Q

The most commonly used methylxanthine, is metabolized by cytochrome P450 mixed function oxidases. Clearance of the drug declines with age.

A

Theophylline

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26
Q

an anatomically defined condition characterizedby destruction of the lung alveoli with air space enlargement

A

emphysema

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27
Q

a clinically defined condition with chronic cough andphlegm;

A

Chronic bronchitis

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28
Q

a condition in which small bronchiolesare narrowed and reduced in number.

A

small airway disease

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29
Q

has been demonstratedto be a hallmark of advanced COPD.

A

extensive small airway destruction

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30
Q

The major site of increased resistance in most individuals with COPDis in airways ≤2 mm diameter.

A

The small airways

31
Q

undergo squamous metaplasia, predisposing to carcinogenesis and disrupting mucociliary clearance.

A

Large airways

32
Q

the type most frequently associated with cigarette smoking,is characterized by enlarged air spaces found (initially) in association with respiratory bronchioles.

A

Centrilobular emphysema

33
Q

Centrilobular emphysema is usually most prominent in what part and-is often quite focal

A

upper lobes and superior segments of lower lobes

34
Q

refers to abnormally large airspaces evenly distributed within and across acinar units.

A

Panlobular emphysema

35
Q

Panlobular emphysema is commonly observed in patients with α1AT deficiency,which has a predilection for the

A

lower lobes

36
Q

occurs in 10–15% of cases and is distributed along the pleural margins with relative sparing of the lung core or central regions

A

Paraseptal emphysema

37
Q

is the most typical finding in COPD.

A

Persistent reduction in forced expiratory flow rates FEV1

38
Q

the total volume of air exhaled during the entire spirometric maneuver

A

forced vital capacity [FVC]

39
Q

In contrast to asthma, the reduced FEV1 in COPD seldom shows largeresponses to inhaled bronchodilators, although improvements up to% are common.

A

15%

40
Q

The partial pressure of oxygen in arterialblood Pao2 usually remains near normal until the FEV1 is decreased to~% of predicted, and even much lower FEV1 values can be associatedwith a normal Pao2, at least at rest.

A

50%

41
Q

An elevation of arterial level of carbon dioxide (Paco2) is not expected until the FEV1 is _% of predicted and even then may not occur

A

<25%

42
Q

Pulmonary hypertension severe enough to cause cor pulmonale and right ventricular failure due to COPD typically occurs in individuals who have marked decreases in FEV1 __% of predicted) and chronic hypoxemia (Pao2 __ mmHg);

A

FEV1 (<25% of predicted) and chronic hypoxemia (Pao2 <55 mmHg);

43
Q

accounts for essentially all of the reduction in Pao2 that occurs in COPD; shunting is minimal.

A

Ventilation-perfusion mismatching

44
Q

often described as increased effort to breathe, heaviness, air hunger, or gasping, can be insidious.

A

The development of exertional dyspnea

45
Q

are thin and noncyanotic at rest and have prominent use of accessory muscles, pursed lip breathing, decreased breath sounds thru out the lungs

A

pink puffers

Predominantly emphysema

46
Q

are more likely to be heavy and cyanotic , fluid retention

A

patients with chronic bronchitis

blue bloaters

47
Q

Some patients with advanced disease have paradoxical inward movement of the rib cage with inspiration, the result of alteration of the vector of diaphragmatic contraction on the rib cage as a result of chronic hyperinflation.

A

Hoover’s sign

48
Q

Increased hematocrit and signs of RVH on ECG

A

Chronic hypoxemia

49
Q

Obvious bullae, paucity of parenchymal markings, or hyperlucency on chest x-ray suggests the presence of

A

emphysema

50
Q

Increased lung volumes and flattening of the diaphragm suggest

A

hyperinflation

51
Q

is the current definitive test for establishing the presence or absence of emphysema, the pattern of emphysema, and the presence of significant disease involving medium and Large airways

A

Chest computed tomography (CT) scan

52
Q

subjects with low α1AT levels, the definitive diagnosis of α1AT deficiency requires

A

PI type determination

53
Q

Only three interventions——have been demonstrated to improve survival of patients with COPD

A

smoking cessation, oxygen therapy in chronically hypoxemic patients, and lung volume reduction-surgery (LVRS) in selected patients with emphysema

54
Q

There are principal pharmacologic approaches to quitting smoking:

A
  1. nicotine replacement therapy
  2. bupropion
  3. varenicline -a nicotinic-acid receptor agonist/antagonist.
55
Q

Short-acting anticholinergic that improves symptoms with acute improvement in FEV1.

A

ipratropium bromide

56
Q

Long acting anticholinergic there was a trend toward reduced mortality rate in-treated patients that approached statistical significance

A

tiotropium

57
Q

Main role of ICS in COPD

A

Reduce exacerbation

58
Q

selective phosphodiesterase 4 (PDE4) inhibitor that has been demonstrated to reduce exacerbation frequency in patients with severe COPD, chronic bronchitis, and a prior history of exacerbations; its effects on airflow obstruction and symptoms are modest.

A

roflumilast

59
Q

administered daily to subjects with a history of exacerbation in the past 6 months demonstrated a reduced exacerbation frequency and longer time to first exacerbation

A

Azithromycin

60
Q

is the only pharmacologic therapy Demonstrated to unequivocally decrease mortality rates in patients with COPD.

A

Supplemental O2

61
Q

Indication for O2 supplementation

A

For patients with “RESTING” hypoxemia
(resting O2 saturation ≤88% in any patient
or
≤89% with signs of pulmonary hypertension or right heart failure)

62
Q

Vaccines for COPD

A

ANNUAL INFLUENZA VACCINATION
Pneumococcal vaccination
Bordetella pertussis vaccination

63
Q

Patients that are not candidates for LVRS due to increased post procedure mortality

A
  1. FEV1 <20% of predicted
  2. diffusely distributed emphysema on CT scan
  3. diffusing capacity of lung for Carbon monoxide (DLCO) <20% of predicted
64
Q

are episodic acute worsening of respiratory symptoms, including increased dyspnea, cough, wheezing, and/or change in the amount and character of sputum.

A

Exacerbations

65
Q

Strongest predictor of Exacerbations

A

Previous Exacerbations

66
Q

Bacteria frequently implicated in COPD exacerbations include

A

Streptococcus pneumoniae,
Haemophilus influenzae
Moraxella catarrhalis

Mycoplasma pneumoniae
Chlamydia pneumoniae are found in 5–10% of exacerbations.

67
Q

In patients admitted to the hospital, the use of systemic glucocorticoids reduces the length of stay, hastens recovery, and reduces the chances of subsequent exacerbation or relapse.

A

2 weeks of OCS glucocorticoid therapy produced benefit indistinguishable from 8 weeks of therapy.

68
Q

Gold recommendation for OCS

A

Current recommendations suggest 30–40 mg of oral PREDNISOLONE or its equivalent typically for a period of 5–10 days in outpatients

69
Q

Supplemental O2 should be supplied to maintain oxygen saturation of.

A

≥90%

70
Q

The initiation of noninvasivepositive-pressure ventilation (NIPPV) in patients with respiratory failure, defined as, results in a significantreduction in mortality rate, need for intubation, complications oftherapy, and hospital length of stay.

A

Paco2 >45 mmHg

71
Q

The mortality rate of patients requiring mechanical ventilatory support is ___ for that particular hospitalization

A

17–30%

72
Q

For patients aged >65 admitted to the intensive care unitfor treatment, the mortality rate doubles over the next year to __%,regardless of whether mechanical ventilation was required.

A

60%

73
Q

Following a hospitalization for COPD, about of __ % patients are re-hospitalized in the subsequent 30 days and __% are hospitalized in the next year.

A

20%

45%

74
Q

Mortality following hospital discharge is about ___ %in the following year

A

20%

HARRISSONS (62 decks)

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