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Internal medicine: pulmonary > COPD > Flashcards

COPD Flashcards

1
Q

acute bronchitis

A

Acute bronchitis or tracheobronchitis is a
poorly defined but common clinical condition
caused by acute inflammation of the
trachea and bronchi.

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2
Q

acute bronchitis: etiology

A
  • infectious agents -> influenza A and B viruses, parainfluenza viruses, respiratory syncytial virus, adenovirus, rhinovirus and other.
  • non specific irritants (dust or smoke)
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3
Q

acute bronchitis; symptoms

A
  • cough (initially nonproductive but later productive of muccopurulent sputum)
  • substernal discomfort worsened by coughing
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4
Q

acute bronchitis: physical findings

A

minimal or absent

  • ronchi (may disappear after productive cough and wheezing)
  • fever (usually minimal or absent except in influenza)
  • chest xray: in whom influenza is suspected, with underlying copd and those with physical findings suggestive of pneumonia.
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5
Q

acute bronchitis: TTT

A
  • is symptomatic, aimed at controlling cough, chest discomfort and fever
  • inhaled bronchodilator: metaproterenol or albuterol (2 puff every 4h) if chest tightening or wheezing.
  • persistent dry cough -> diagnosis cough variant asthma
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6
Q

COPD: essential for diagnosis: 2 components

A
  • > chronic bronchitis
  • > pulmonary emphysema
  • history of cigarette smocking
  • chronic cough and sputum production (in chronic bronchitis)
  • dyspnea (in emphysema)
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7
Q

COPD: defintion

A

disease characterized by the presence of airflow obstruction due to chronic bronchitis or emphysema

  • airflow is generally progressive may be accompanied by airway hyperactivity and may be partially reversible
  • 3rd death cause
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8
Q

COPD: clinical characteristics

A
  • excessive secretion of bronchial mucus
  • productive cough for 3 months or more in at least 2 consecutive years
  • emphysema
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9
Q

COPD: causes

A
  • smoking, air pollution
  • airway infection
  • familial factors
  • allergy
  • hereditary factors (deficiency of alfa 1-antiprotease)
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10
Q

symptoms and signs of copd:

A
  • excessive cough, productive cough often occurs in the morning
  • sputum production
  • dyspnea initially only on extreme exertion, in severe dis it occurs at rest
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11
Q

symptoms and signs of copd : inflammation and exacerbation

A

-> rpz a further amplification of the inflammatory response in the airways of patients, may triggered by infection with bacteria or viruses or environmental pollutants

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12
Q

symptoms and signs of copd : late stage

A

pulmonary hypertension, cor pulmonale and chronic respiratory failure
death usually occurs during an exacerbation of illness in association with acute respiratory failure
hemoptysis -> occasionally

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13
Q

symptoms and signs of copd :

A
  • barrel chest: this deformity most commonly in individuals with emphysema
  • use of accessory respiratory muscles due to diaphragmatic dysfunction
  • hyper resonant lungs, reduced diaphragmatic excursion
  • decreased breath sounds on auscultation: prolonged expiratory phase, end-expiratory wheezing, coarse rhonchi on auscultation
  • congested neck veins, peripheral edema, hepatomegaly, signs of right heart failure and cor pulmonale.
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14
Q

symptoms and signs of copd :

A

cyanosis
confusion (due tp hypoxemia and hypercapnia)
nail clubbing is non specific

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15
Q

2 categories of patients ?

A
  • PINK PUFFER: -> emphysema
  • noncyanotic, cachectic, pursed lip breathing, mild
  • PaO2: sightly reduced
  • PaCO2: normal
  • bBLUE BLOATER -> chronic bronchitis
  • productive, overweight, peripheral
  • PaO2: markedly reduced
  • PaCO2: increased
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16
Q

laboratory findings: putum exam, ecg…

A
  • secondary policytemia (as a result of hypoxemia)
  • examination of sputum -> streptococcus pneumonia, hemophilus influenzas or mortadella catarrhales
  • ECG: sinus tachycardia, electrocardiographic abnormalities typical of cor pulmonale
    supraventricular arrhythmias and ventricular irritability
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17
Q

Investigations: Pulsoximetry, arterial blood gas (abg)…

A
  • pulsocimetry measures SO2
  • ABG: show no abnormalities in early COPD
  • hypoxemia, hypercapnia occurs in advanced dis
    compensated respiratory acidosis occurs in patients with chronic respiratory failure -> chronic bronchitis
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18
Q

investigations: spirometry, pulmonary function test, lung volume measurements…

A
  • spirometry: provides objective info about pulmonary function and assesses the results of therapy
  • pulmonary function test: in the early course of the dis reveals only evidence of dysfunction in small airways
    reduction in FEV1 and in the ratio of forced expiratory volume to forced vital capacity (FEV1 : FVC) occur later. in severe dis, the forced vital capacity is reduced
  • lung volume measurements: increased in total lung capacity (TLC), a marked increase in the residual volume (RV) and elevation of the RV/TLC ration, indicative of air trapping
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19
Q

bronchodilator test

A

assesses the reversibility of pulmonary obstructive dysfunction

  • inhalation Salbutamol and repeat spirometry after 10-15 min
  • Delta FEV1 < 12%, means irreversible obstruction COPD is more likely than asthma
  • Delta FEV1> 12% means reversible obstruction, asthma is more likely than COPD
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20
Q

imaging: what is apparent when emphysema is the main clinical feature ?

A

Hyperinflation is apparent

- parencymal bull are pathognomic of emphysema

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21
Q

imaging: what does radiographs with chronic bronchitis show?

A

only nonspecific peribronchial and perivascular markings

22
Q

imaging: what becomes evident in advanced dis?

A

pulmonary hypertension becomes evident as enlargement of central pulmonary arteries in advanced dis

23
Q

chest X ray hyper inflated lungs:

A
  • hyper lucency of lung tissue
  • increased A-P diameter
  • diaphragm pushed down and flattened
  • horizontal ribs
  • long now heart shadow
  • parenchimal bullae or sub pleural bleds
  • increased retrosternal space in lateral view
24
Q

differential diagnosis: what are the others obstructive pulmonary dis?

A 
bronchial asthma 
bronchiectasis 
cystic fibrosis 
bronchopulmonary aspergillosis 
central airway obstruction
25
Q

differential diagnosis: how is bronchiectasis distinguished from copd?

A

by features such as recurrent pneumonia and hemoptysis, digital clubbing and radiographic abnormalities

26
Q

differential diagnosis: how are patients with alfa-1 antiprotease deficiency recognized ?

A

->by the appearance of panacinar emphysema early in life (usually in the 3rd of 4th decade); and hectic cirrhosis and hepatocelullar carcinoma may occur

27
Q

differential diagnosis: cystic fibrosis

A
  • occurs in children and younger adults.
  • rarely mechanical obstruction of central airway simulates copd
  • flow-volume loops may helps separate patients with central airway obstruction from those with diffuse intrathoracic airway obstruction which is characteristic of copd
28
Q

complications of copd

A 
-acute bronchitis 
asthma 
pulmonary embolization 
concomitant left ventricular failure 
- pulmonary hypertension 
cor pulmonale 
chronic respiratory failure 
are common in advanced copd
29
Q

ttt: ambulatory patients: goals in the ttt of copd includes:

A
  • control of symptoms
  • improvement in ability to carry out daily activities
  • reduction in the need for hospitalization
  • réhabilitation
30
Q

ttt: Bronchodilator drugs

A

-> inhaled IPRATROPIUM BROMIDE or SYMPATHOMIMETIC DRUGS = mainstay of this therapy
the response to bronchodilator is assessed with spirometry

31
Q

ttt: ipratropium bromide?

A
  • > > to sympathomimetic aerosol
  • > has a slower onset but a longer duration of action
  • > can be combined to enhances and prolonge bronchodilator
  • > side effect = min
  • > confers only a small improvement in FEV 1 in mid aged smokers with mild airway obstruction.
  • > 2 to 4 inhalation every 6 hours
32
Q

ttt: Anticholinergics

A
  • short acting muscarinic antagonists
    ipratropium bromide - onset 10-15 min, duration 4-6h
  • long acting muscarinic antagonists
  • tiotropium bromide - duration 12h
33
Q

ttt: beta agonists

A
  • > short acting = salbutamol, fenoterol

- > long acting = salmeterol, formoterol

34
Q

ttt: maintenance therapy

A
  • > théophylline in ambulatory patients with copd is controversial
  • its principal value in copd may relate to improving respiratory muscle performance
  • improvement in dyspnea, exercice performance and pulmonary function
  • oral sustained release theophylline improves oxyhemoglobin saturation during sleep
  • 1ce daily
35
Q

ttt: patients with moderate to severe copd are treated with a combination of ?

A
  • Ipratropium + beta 2 agonist + theophylline
36
Q

ttt: oral corticosteroids: how and for who?

A
  • > prescribed in the same way as in asthma
  • > for :
  • patients with asthmatic bronchitis
  • patients with frequent exarcebations or disabling symptoms who fail to respond to conventional therapy with ipratropium bromide, simpathmimetics and theophylline
  • > corticosteroids should be discontiuated after 2)4 weeks I there is no objective improvements.
37
Q

ttt: inhaled corticosteroids

A
  • responsive patients with chronic bronchitis, particularly those requiring less than 20 mg prednisone daily
  • inhaled corticosteroids (budesonide, fluticasone, beclomethsone) may permit discontinuance of systemic therapy
  • cromolyn has not role in treatment of chronic bronchitis or emphysema
38
Q

ttt: other measures: if airway infection is suspected?

A

-> amoxicillin or amoxicillin clavulanate (500 mg every 8h)
-> ampicilline or tetracycline (250-500 mg four times daily)
-> trimethoprim-sulphametaxole (160/800 mg every 12h)
may be given PO for 7-10 days

39
Q

ttt: In patients with chronic bronchitis,
increased mobilization of secretions
may be accomplished through:

A

-the use of adequate systemic hydration
- effective cough training methods
- and postural drainage
- sometimes with chest percussion or
vibration.

40
Q

ttt: coughing up retained secretion

A
  • Postural drainage and chest percussion should be
    used only in selected patients with excessive
    amounts of retained secretions that cannot be
    cleared by coughing and other methods. These
    measures are of no benefit in pure emphysema.
  • Expectorant- Mucolytics (e.g., N-acetylcysteine)
  • Cough supressants and sedatives should be avoided
    as routine measures.
41
Q

ttt: home oxygen therapy

A
  • is prescribed for selected patients with COPD or other severe lung
    diseases who have significant hypoxemia. Oxygen may be prescribed for continuous use, only at
    night, or with exercise.
  • Hypoxemic patients with pulmonary hypertension,
    chronic cor pulmonale, erythrocytosis, impaired
    cognitive function, exercise intolerance, nocturnal
    restlessness or morning headache are particularly
    likely to benefit from home oxygen therapy.
  • Survival in hypoxemic patients with COPD
    treated with supplemental oxygen therapy is
    directly proportionate to the number of hours per
    day oxygen is administered.
42
Q

ttt: long term oxygen therapy

A

indicated in the case of:
A. PaO2 ≤ 55 mm Hg or SaO2 ≤ 88% at rest
- Increases the chance of survival in patients with
COPD
- Supplemental O2 can worsen hypercapnia
- The target oxygen saturations is 90–93%.
B. PaO2 between 55 and 60 mm Hg or SaO2 of 88%,
if there is evidence of pulmonary hypertension,
congestive cardiac failure, or polycythemia

43
Q

COPD rehabilitation

A
  • Human α1- proteinase inhibitor is available for
    replacement therapy of emphysema due to
    congenital deficiency of α-1 antiproteinase.
  • Patients over 18 years of age with obstructive lung
    dysfunction and alfa-1 antiproteinase levels less
    than 11 μmol/L are potential candidates for
    replacement therapy.
  • Human alfa-1 proteinase inhibitor is administered
    intravenously in a dose of 60 mg/kg body weight
    once weekly
44
Q

surgery for Copd: requirements

A

Experience with both single and bilateral sequential
lung transplantation for severe COPD is growing
rapidly.
-> Requirements for lung transplantation are severe lung disease, limited activities of daily living, exhaustion of medical therapy, ambulatory status, potential for pulmonary rehabilitation, limited life expectancy without
transplantation, adequate function of other organ
systems and a good social support system.

45
Q

surgery for copd: 2 years survival rate and complications

A
  • The two- year survival rate after lung transplantation for COPD is 75%.
  • Complications include rejection, opportunistic infection and obliterative bronchiolitis
46
Q

surgery for copd: volume reduction surgery (reduction pneumoplasty)

A

surgical approach to relief of dyspnea and improvement in exercise tolerance in patients with advanced diffuse emphysema and lung hyperinflation.

47
Q

surgery for copd: bullectomy

A

older surgical procedure for
palliation of severe dyspnea in patients with severe
bullous emphysema. In this procedure, the surgeon
removes a very large emphysematous bulla that
demonstrates no ventilation or perfusion on lung scanning and compresses adjacent lung that has
preserved function. Bullectomy can now be performed with a CO2 laser, via thoracoscopy.

48
Q

need for hospitalization: indicted for?

A

acute worsening of COPD that fails to respond to
measures for ambulatory patients. Patient with acute
respiratory failure or complications such as cor
pulmonale and pneumothorax should also be hospitalized.

49
Q

management of hospitalizated patients with an acute exarcebation of copd includes:

A
  • supplemental oxygen
  • ipatropium bromide
  • inhaled sympathomimetics
  • broad spectrum antibiotics
  • corticosteroids
  • in selected cases, chest physiotherapy.
50
Q

prognosis of copd

A
  • The outlook for patients with clinically significant
    COPD is poor.
  • The median survival time of patients with severe COPD ( FEV 1≤1 L) is about 4 years.
  • The degree of pulmonary dysfunction (as measured
    by FEV 1) at the time the patient is first seen is
    probably the most important predictor of survival.
  • The prognostic is better in the chronic asthmatic form of COPD than in the emphysematous form.

Internal medicine: pulmonary (8 decks)

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