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Harrisons 20th A > COPd > Flashcards

COPd Flashcards

1
Q

Emphysema

A

Anatomically destruction of the lung alveoli with air space enlargement

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2
Q

Chronic bronchitis

A

Chronic cough and phlegm

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3
Q

Pathological halo mark of COPD

A

Small airways maybe narrowed by cells, mucus, and fibrosis and extensive small airway destruction

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4
Q

4 events of pathogens is of emphysema

A
  1. Chronic exposure to cigarette smoke 2. Inflammatory release proteinase 3. Structural cell death through oxidant induced damage 4. Disordered repair of elastin and other extracellular matrix components
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5
Q

genetic deficiency in α1 antitrypsin (α1AT), the inhibitor of the serine proteinase neutrophil elastase, were at increased risk of emphysema, and that instillation of elastases, including neutrophil elastase, into experimental animals, results in emphysema.

A

Elastase:Anti elastase hypothesis

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6
Q

key component of COPD pathobiology

A

Oxidative stress

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7
Q

Major regulator of oxidant-antioxidant balance

A

NRF2

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8
Q

Potent antioxidant

A

SOD3

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9
Q

Change in large airway cause

A

Cough and sputum production

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10
Q

Small airway

A

Responsible for physiologic alteration

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11
Q

Gold criteria

A

Stage I mild FEV1/FVC <0.7 and FEV1 >80% predicted II moderate FEV1 <0.7 and FEV1 >50% but 80% III severe FEV1/FVC <0.7 and FEV1 >30% but < 50% predicted IV very severe FEV1/FVC 0.7 and

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12
Q

Cellular changes

A

Goblet cell,etaplasia Mucus secreting cells replacing surfactant club cells Smooth muscle hypertrophic Luminal narrowing cause by fibrosis Reduced surfactant Mononuclear inflitration

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13
Q

Emphysema

A

Destruction of gas-exchanging air spaces, the respiratory bronchioles, alveolar ducts, and alveoli

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14
Q

Emphysema

A

Destruction of gas-exchanging air spaces, respiratory bronchioles, alveolar ducts and alveoli Dx: bronchioalveolar lavage: 5x as many macrophage as non smokers Neutrophils and T lymphocytes, particularly CD8

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15
Q

Centrilobolar emphysema

A

Type most frequently associated with cigarette smoking enlarged spaces found initially in respiratory bronchioles Most prominent in the upper lobes and superior segments of lower lobes and quite focal

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16
Q

Panlobular emphysema

A

Abnormally large air spaces evenly distributed within and across acinar units. Is commonly observed in patient with a1AT deficiency Predilection for the lower lobes

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17
Q

Partial pressure of oxygen in arterial blood pao2 usually remains near normal until

A

fFEV1 is decreased to 50% of predicted

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18
Q

Elevation of arterial carbon dioxide (PaCo2) is not expected unit

A

FEV1 is <25% of predicted

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19
Q

Pulmonary hypertension can cause

A

Cor pulmonary and right ventricular failure Occurs in individuals who have marked decrease in FEV1 (25%) and chronic hypoxemia (pao2 <55mmHg)

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20
Q

pack-years

A

average number of packs of ciga-rettes smoked per day multiplied by the total number of years of smok-ing

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21
Q

A1 antitrypsin deficiency

A

M allele- associated with normal a1AT levels S allele: associated with slightly reduced a1AT levels Z allele: associated with markedly reduced a1AT levels, also occur with frequencies of >1% in most populations.

22
Q

Most common form of severe a1AT deficiency

A

Two Z allele And one null allele

23
Q

Curve c : normal rate of decline after a reduced growth Curve B: early initiation of pulmonary function decline after normal growth Curve D: accelerate rates of lung function

A

The absolute annual loss in FEV1 tends to be highest in mild COPD and lowest in very severe COPD

24
Q

three most common symptoms in COPD

A

cough, sputum production, and exertional dyspnea

25
Q

independent poor prognostic factor in COPD

A

wasting

26
Q

advanced disease have paradoxical inward movement of the rib cage with inspiration

A

Hoover’s sign result of alteration of the vector of diaphragmatic contraction on the rib cage as a result of chronic hyperinflation

27
Q

most likely explanation for newly developed clubbing.

A

lung cancer

28
Q

hallmark of COPD

A

airflow obstruction reduction in FEV1 and FEV1/FVC lung volumes may increase, resulting in an increase in total lung capacity, functional residual capacity, and residual volume

29
Q

diffusing capacity may be reduced, reflecting the lung parenchymal destruction characteristic of this disease

A

emphysema

30
Q

Arterial blood gases provide additional information about alveolar ventilation and acid-base status by measuring arterial Pco2 and pH.

A

The change in pH with Pco2 is 0.08 units/10 mmHg acutely 0.03 units/10 mmHg in the chronic state.

31
Q

defined as Pco2 >45 mmHg

A

ventilatory failure,

32
Q

chest x-ray findings that suggests the presence of emphysema Diagnostic test

A

Obvious bullae, paucity of parenchymal markings, or hyperlucency Diagnostic test: CT scan - to rule out lung ca -to evaluate possible surgical therapy

33
Q

two main goals of therapy

A

provide symptomatic relief (reduce respiratory symptoms, improve exercise tolerance, improve health status) and reduce future risk (prevent disease progression, prevent and treat exacerbations, and reduce mortality)

34
Q

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)

35
Q

are the primary treatment for almost all patients with COPD and are used for symptomatic benefit and to reduce exacerbations

A

bronchodilators

36
Q

Anticholinergic Muscarinic Antagonists

A

Short-acting ipratropium bromide improves symptoms with acute improvement in FEV1. Long-acting muscarinic antagonists (LAMA, including aclidinium, glycopyrrolate, tiotropium, and umeclidinium) improve symptoms and reduce exacerbations

37
Q

Beta Agonists

A

ease symptoms with acute improvements in lung function. Long-acting agents (LABA) provide symptomatic benefit and reduce exacerbations, though to a lesser extent than a LAMA. long-acting inhaled β agonists are arformoterol, formoterol, indacaterol, olodaterol, salmeterol, and vilanterol. The main side effects are tremor and tachycardia.

38
Q

Inhaled Corticosteroids The main role of ICS

A

reduce exacerbations

39
Q

frequent exacerbations, defined

A

two or more per year, and in patients with features of asthma, such as eosinophilia

40
Q

chronic use of oral glucocorticoids is associated with significant side effects

A

osteoporosis, weight gain, cataracts, glucose intolerance, and increased risk of infection

41
Q

Theophylline

A

modest improvements in airflow and vital capacity Nausea is a common side effect tachycardia and tremor have also been reported

42
Q

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

A

Supplemental O2 For patients with resting hypoxemia( <88%) And with signs of pulmonary hypertension (<89%)

43
Q

Eligibility for α1AT augmentation therapy requires

A

Eligibility for α1AT augmentation therapy requires a serum α1AT level <11 μM (~50 mg/dL). Typically, PiZ individuals will qualify, although other rare types associated with severe deficiency (e.g., null-null) are also eligible

44
Q

Centrilobular emphysema

A

Severe upper lobe involvement Smoker

45
Q

Panlobular

A

Diffuse loss of lung parenchyma predominantly in the lower lobes Severe a1 deficiency

46
Q

Paraseptal emphysema

A

Marked airway inflammation

47
Q

Lung Volume Reduction Surgery important prognostic characteristics

A

anatomic distribution of emphysema and post-rehabilitation exercise capacity

48
Q

most likely to benefit from LVRS

A

upper lobe–predominant emphysema and a low post-rehabilitation exercise capacity are most likely to benefit from LVRS.

49
Q

not candidates for LVRS

A

FEV1 <20% of predicted and either diffusely distributed emphysema on CT scan or diffusing capacity of lung for carbon monoxide (DLCO) <20% of predicted have increased mortality after the procedure

50
Q

Pulmonary function curve

A
51
Q

Classification of COPD

A
52
Q

Treatment for COPD

A

Harrisons 20th A (15 decks)

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