10-9 DSA - COPD by Kinder Flashcards

1
Q

What is COPD?

A

Disease characterized by progressive, mostly irreversible airflow obstruction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

When is the onset of COPD?

A

middle age or elderly 20-30 years after exposure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the burden of COPD?

A

4th leading cause of mortality in the United States with mortality in women now exceeding mortality in men.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What role does cigarette smoking play in COPD?

A

Cigarette smoking is by far the leading cause of COPD. Lung function decline is related to both the duration and intensity of cigarette smoking.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What decreases in lung function can smokers expect?

A

Non-smokers after the age of 30 have approximately a 25ml per year reduction of their FEV1.

Smokers have a 40ml per year reduction of FEV1.

A small percentage of smokers develop FEV1 reduction of a 100ml per year and may develop COPD in their 4th or 5th decades of life.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does exposure to smoke or second hand smoke do to children?

A

Lung growth can be impaired from maternal smoking in pregnancy, 2nd hand exposure during childhood, and smoking during adolescence.

This reduced lung growth increases risk of COPD later in life.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What other exposures can cause COPD?

A

workplace dusts from mining, cotton mills, and grain-handling facilities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is alpha-1 antitrypsin deficiency?

A

Genetic risk factor for COPD. 1-2 % of COPD.

A serine protease inhibitor secreted by the liver that protects the lung tissue against the action of neutrophil elastase and serine proteases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are people with alpha 1 antitrypsin deficiency at risk for?

A

These patients are very susceptible to damage caused by cigarette smoking. Consider this in patients that are young at onset.

Also leads to LFT abnormalities and cirrhosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is emphysema?

A

enlargement of the air spaces distal to the terminal bronchiole with destruction of the alveolar walls

Emphysema is caused by an imbalance of elastase-antielastase in the lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is centriacinar emphysema?

A

affects respiratory bronchioles distal to the terminal bronchiole, remainder of acinus spared.

Occurs with smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is panacinar emphysema?

A

alveolar ducts, adjacent alveoli, coalescence and bullae formation.
Common in alpha 1 antitrypsin deficiency.

Occurs with smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What type of emphysema is common with people with COPD?

A

Most severe COPD patients have a combination of centriacinar and panacinar emphysema.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is chronic bronchitis and bronchiolitis?

A

enlargement of bronchial mucous glands and increased epithelial goblet cell production leads to cough and increased mucous production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is pulmonary HTN (PHTN)?

A

hypoxemia leads to vasoconstriction and increased pulmonary vascular resistance in small pulmonary arteries. This leads to vascular remodeling including medial smooth muscle enlargement and intimal fibrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the lung mechanics in COPD?

A

Elastic recoil is the lungs innate ability to deflate following inflation.

Elastic fibers in the lung parenchyma, along with surface tension at the alveolar air-liquid interface are responsible for this elastic recoil.

Elastic recoil maintains the patency of small airways.

1) This elastic recoil is markedly decreased in COPD.
2) Airway resistance is increased in COPD. The sites of airflow obstruction in COPD are the distal airways of less than 2mm diameter.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is hypoxemia in COPD? When does it present?

A

mild hypoxemia can be detected in early COPD.

Hypercapnea presents only in severe COPD.

Ventilation perfusion mismatching is common secondary to uneven ventilation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are some questions regarding HPI to ask patients with suspected COPD?

A

History: current or past cigarette use, dyspnea with slow progression, history of acute bronchitis, chronic cough, sputum production, and wheezing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What physical findings do you expect to find with COPD?

A

barrel chest,

prolonged expiratory phase,

accessory muscle use,

low diaphragm,

distant heart sounds,

diminished breath sounds,

rhonchi,

wheezing,

cyanosis,

pedal edema,

distended jugular veins,

hepatic congestion, and

cachexia.

“blue bloaters” “pink puffers”

20
Q

What are the PFTs consistent with mild COPD?

A

Mild FEV1/FVC < 70%, FEV1 ≥ 80% of predicted

21
Q

What are the PFTs consistent with moderate COPD?

A

Moderate FEV1/FVC < 70%, 50% ≤ FEV1 < 80% of predicted

22
Q

What are the PFTs consistent with severe COPD?

A

Severe FEV1/FVC < 70%, 30% ≤ FEV1 < 50% of predicted

23
Q

What are the PFTs consistent with very severe COPD?

A

Very Severe FEV1/FVC <70% < 30% of predicted

or FEV1 < 50% of predicted plus chronic respiratory failure

24
Q

What would you see on CXR with someone with COPD?

A

hyperinflation,

flattened diaphragms,

increased retrosternal space,

bullae,

can be normal in mild to moderate COPD

25
Q

What are some diff Dx’s for someone with COPD?

A

asthma, bronchiectasis, bronchiolitis obliterans

26
Q

What are the treatments for COPD?

A

Smoking cessation

Bronchodilators

Oxygen

Immunizations

Pulm rehab

Surgery

27
Q

What types of medications are helpful in treating COPD?

A

beta 2 adrenergic agonists

anticholinergics

methyxanthines

PDE-4 inhibitor

corticosteroids

28
Q

Which beta 2 adrenergic agonists are helpful in treating COPD?

A

B2-adrenergic agonists - inhaled

Short Acting: albuterol, levalbuterol

Long Acting: salmeterol, formoterol

29
Q

Which anticholinergics are helpful in treating COPD?

A

Anticholinergics - inhaled

Short Acting: ipatroprium bromide

Long Acting: tiotropium

30
Q

Why are methylxanthines useful in treating COPD?

A

Theophylline oral

antagonizes adenosine receptors, increases cAMP, weak bronchodilator,

requires close monitoring,

narrow therapeutic window,

numerous side effects,

numerous drug interactions

31
Q

What is a PDE-4 inhibitor? What can it help with in COPD?

A

Phosphodiesterase-4 Inhibitor

Roflumilast: can increase FEV1 by 50 ml

reduce exacerbations in moderate to severe exacerbations of COPD,

  • even in patients already treated with tiotropium
32
Q

What are the corticosteroids that are helpful in treating COPD?

A

Inhaled: Reduces COPD exacerbations by 15-20%. Added benefit when combined with long acting beta agonist

Systemic: Prednisone – no proven benefits of chronic, low dose prednisone, many adverse effects

33
Q

In long vs. short acting bronchodilators, which are more effective in treating COPD?

A

Generally, long acting

Long acting bronchodilators provide improvement in 10-15% of patients.

Tiotropium once daily superior to salmeterol twice daily.

Long acting bronchodilators reduce exacerbations by 15-20%.

34
Q

Why is oxygen helpful in treating COPD?

A

chronic hypoxemia can lead to pulmonary hypertension and cor pulmonale. Long term oxygen extends life in patients with chronic hypoxemia

35
Q

Which immunizations should people with COPD get?

A

influenza and pneumococcus

36
Q

What is pulmonary rehab?

A

exercise endurance training, will improve walking distance

37
Q

What are the surgical options for treating COPD?

A

Lung volume reduction surgery: used in severe emphysema involving the upper lobes

Lung transplantation: used for severe incapacitation, no other major comorbities, median survival of about 5 years.

38
Q

What is COPD exacerbation?

A

combination of dyspnea, cough, and productive sputum that is worse than usual stable state

39
Q

What causes most COPD exacerbations?

A

respiratory infections

40
Q

What are the common bacterial infections that cause COPD exacerbation?

A

Bacterial:

Haemophilus influenzae,

Streptococcus pneumoniae,

Moraxella catarrhalis

41
Q

What are the less common bacteria that cause COPD exacerbations?

A

Pseudomonas aeruginosa and enteric bacilli are less common, but are present in more severe disease and recently hospitalized or intubated patients

42
Q

What viruses and other factors can cause COPD exacerbation?

A

Viral:

rhinoviruses,

influenza,

parainfluenza, and

respiratory syncytial virus

Airborne pollution

43
Q

What should be assessed to see if a COPD patient with exacerbation needs to be hospitalized?

A

Dyspnea, accessory muscle use, ABG, hemodynamic stability, and mental alertness

44
Q

What drugs should a COPD patient with exacerbation be given while hospitalized?

A

Antibiotics when cough and purulent sputum present

Systemic corticosteroids

Increase short acting bronchodilator frequency

Oxygen to maintain saturation greater than 90%

45
Q

What interventions should be done with the patient hospitalized with COPD exacerbation?

A

Noninvasive positive-pressure ventilation

Intubation, mechanical ventilation

46
Q

What is the prognosis of a COPD patient?

A

Only ½ of patients with FEV1 that is 40% will survive 5 years

Smoking cessation reduces mortality in patients with mild to moderate COPD

Oxygen reduces mortality in subset with chronic hypoxemia