Obstructive Pulmonary Disease Flashcards

1
Q

what does air trapping result in?

A

hypoventilation and hypercapnia

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2
Q

what are present in all obstructive diseases?

A

dyspnea and wheezing

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3
Q

what is air trapping?

A

–person is not able to fully exhale
–CO2 is higher since air can’t escape
–air is trapped in alveoli –> person works harder to breathe and lungs are hyperinflated
–normal exhalation is obstructed

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4
Q

asthma

A

chronic inflammation of bronchial airways

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5
Q

risk factors for asthma

A

–usually starts in childhood
–familial link
–levels of allergen exposure
–urban residency
–exposure to indoor and outdoor air pollution
–tobacco exposure/smoke
–recurrent respiratory tract viral infections and GERD

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6
Q

early asthmatic response

A

cellular responses are activated immediately and cascade of release of inflammatory mediators occurs within minutes

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7
Q

late asthmatic response

A

4-8 hours after early response

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8
Q

two responses of asthma

A
  1. bronchoconstriction (#1 symptom)
  2. inflammation (biggest problem; causes seriousness)
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9
Q

status asthmaticus

A

–severe symptoms
–unrelenting asthma attack (silent chest, pCO2 > 70)
–life threatening

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10
Q

chronic bronchitis

A

hypersecretion of mucus and chronic productive cough for at least 3 months of the year for at least 2 consecutive years

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11
Q

simple bronchitis

A

inflammation of bronchi and bronchioles

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12
Q

etiology of simple bronchitis

A

bacterial or viral infection
NO AIRWAY OBSTRUCTION

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13
Q

etiology of chronic bronchitis

A

–cigarettes
–+ airflow obstruction = form of COPD

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14
Q

prognosis of chronic bronchitis

A

premature morbidity and mortality

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15
Q

patho of chronic bronchitis

A

–inhaled irritants result in airway inflammation
–continual bronchial inflammation
–thick, tenacious mucus produced and cannot be cleared

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16
Q

why can’t secretions be cleared in chronic bronchitis?

A

–damaged cilia bronchial walls become inflamed/thickened secondary to edema
–accumulation of inflammatory cells
–thickened smooth muscle secondary to chronic bronchospasm

17
Q

late clinical manifestations of chronic bronchitis

A

pulmonary hypertension

18
Q

patho of pulmonary HTN

A

increase in pulmonary artery pressure d/t elevated pulmonary venous pressure, increased pulmonary blood flow, pulmonary vascular obstruction, or hypoxia

19
Q

s/s of pulmonary HTN

A

syncope, DOE, and fatigue

20
Q

cor pulmonale

A

right sided heart failure

21
Q

treatment of chronic bronchitis

A

–bronchodilators
–expectorants/prophylactic antibiotic therapy
–CPT
–steroids late in disease
–home O2

22
Q

emphysema

A

abnormal, permanent enlargement of gas exchange airways, accompanied by destruction of alveolar walls

23
Q

major effect of emphysema

A

major mechanism of airflow limitation is loss of elastic recoil with collapse of the airways during expiration

24
Q

characteristics of emphysema

A

–loss of elastic recoil
–abnormal permanent enlargement of air spaces
–lung hyperinflation
–destruction = tissue changes

25
Q

causes of loss of elastic recoil in emphysema

A

–smoking
–air pollution
–childhood respiratory infections
–genetic emphysema

26
Q

symptoms of emphysema

A

–gradual increase in breathlessness
–eventually SOA at rest
–wheezing
–malnourished
–decreased muscle mass
–barrel chest
–pursed lip breathing
–decreased breath sounds

27
Q

diagnosis of emphysema

A

–PFTs (FEV1 decreased)
–CXR (hyperinflation)
–ABGs
–decrease in alpha1-antitrypsin

28
Q

treatment of emphysema

A

–smoking cessation
–bronchodilators and anti-inflammatory agents
–O2 supplementation
–breathing retraining
–relaxation techniques
–antibiotics for acute infections

29
Q

chronic bronchitis vs. emphysema

A

CB: overweight, cyanotic, elevated Hgb, peripheral edema, rhonchi, wheezing

Emphysema: older and thin, severe dyspnea, quiet chest, hyperinflation with flattened diaphragms

30
Q
A