COPD Flashcards

1
Q

Etiopathogenesis of COPD

A
  • Characterized by expiratory airflow limitation not fully reversible
  • Unusual in the absence of smoking or prior history of smoking,e xcept for patients with alpha-1 antitrypsin deficiency
  • Elastase-antielastase hypothesis: remains a prevailing mechanism for iths pathophysiology
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2
Q

Hallmark of COPD

A

Airflow Obstruction

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3
Q

Main risk exposure for COPD

A

Smoking tobacco

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4
Q

Pathologic Changes in COPD

A
  • Chronic inflammation and structural changes resulting from repeated injury and repair
  • Increased number sof specific inflammatory cell types in different parts of the lung
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5
Q

Anatomically defined conditioned characterized by enlargement and destruction of alveoli

A

Emphysema

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6
Q

Clinical condition characterized by chronic cough and spurum production

A

Chronic Bronchitis

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7
Q

Condition where the bronchioles and smaller airways are narrowed

A

Small airway disease

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8
Q

Cardinal symptoms of COPD

A
  • cough
  • sputum production, exertional dyspnea
  • punctauated by exacerbations (acute worsening of symptoms)
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9
Q

Most common symptoms for COPD

A

cough and sputum

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10
Q

Signs of COPD

A
  • May be normal in early stages
  • Pink puffers (predominantly emphysema): thin, non-cyanotic, prominent use of accessory muscles
  • Blue bloaters (predominantly chronic bronchitis): heavy and cyanotic
  • “tripod” position”: to faciliate use of accessory muscles
  • Signs of hyper inflation: barrel chest, hyperresonance on percussion
  • Others: pursed-lip breathing, expiratory wheezing, systemic wasting, weigh loss
  • Signs of cor pulmonale (bipedal edema, ascites) in severe cases
  • Clubbing is not a sign of COPD
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11
Q

Pink puffers

A
  • predominantly emphysema
  • thin, non-cyanotic prominent use of accessory muscle
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12
Q

Blue bloaters

A
  • predominantly chronic bronchitis: heavy and cyanotic
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13
Q

Signs of hyerinflation

A
  • barrel chest
  • hyperresonance on percussion
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14
Q

Diagnosis of COPD

A
  • A clinical diagnois of COPD should be considered in any patient who has:
    • dyspnea
    • chronic cough or sputum production
    • history to risk factors for the disease
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15
Q

Risk factors for for COPD

A
  • Tobacco smoke
  • smoke from home cooking ang heating fuels
  • occupational dusts and chemicals
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16
Q

Spirometry in COPD

A
  • Required to make the diagnosis of COPD
  • post-bronchodilator FEV1/FVC <0.70: confirms presence of persistent airflow limitation
  • FEV1, FEV1/FVC and all other measures of expiratory airflow are reduced
  • TLC, FRC, RV may be increased indicating air trapping
  • DLCO may be reduced
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17
Q

Chest Radiograph for COPD

A
  • Useful for excluding other differential diagnoses
  • low flattened diaphragms
  • Increase in the volume of retrosternal airspace (hyperinflation)
  • Hyperlucent lung zones with possible bullae formation and diminished vascular markings
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18
Q

CT Scan for COPD

A
  • Not routinely requested
  • Maybe helpful when the diagnosis is in doubt to rule out concomitant diseases
  • useful if surgical procedure such as lung volume reduction and diminished vascular markings
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19
Q

Pulse oximetry for COPD

A
  • To evaluate a patient’s O2 saturation and need for supplemental oxygen therapy
  • Should be used to assess all stable patients with FEV1 <35% predicte owith clinical signs suggestive of respiratory failure or right heart failure
  • If peripheral stauration is <92% arterial blood gases should be assessed
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20
Q

Arterial blood gases

A
  • Resting or exertional hypoxemia
  • Increased alveolar-arterial oxygen tension gradient
  • In-long standing disease, may have chronically increased arterial PaCO2 but metabolic compensation (increased HCO3) maintains pH to near Normal
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21
Q

Approach to Classification of COPD

A
  • Step 1 : Confirm diagnosis of COPD
  • Step 2: Assess Airflow limitation (also by spirometry)
  • Step 3: Assess for symproms and risk of exacerbations
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22
Q

Assessing Airflow Limitation (by spirometry)

A
  • The classification is based on severity of airflow limitation in COPD using spirometry (post-bronchodilator FEV1)
  • Spirometry should be performed after the administration of an adequate dose of a short-acting inhaled bronchodilator (to minimize variability)
23
Q

Assessing Symptoms and Risk of Exarcerbations

A
24
Q

deined as an acute event chacracterized by worsening of the patient’s respiratory symptoms that is beyond normal day to day variations and leads to a change in medication

A

Exaerbation

25
Q

Fequent exacerbation

A

>= 2 per year

26
Q

simple measure of breathlessness

Relates well to ther measures of health status and predicts future mortality risks

A

Modified Medical Reaserch council (mMRC) Questionnaire for Assessng Severity of Breathlessness

27
Q

Modified Medical Research council (mMRC)

A
28
Q

COPD assessment test (CAT)

A
  • Comprehensive assessment of symptoms
  • Consist of 8 questions which pertain to symptoms of COPD - patient will give a score (0-5 point rating scale) and the points will be added
29
Q

Beta 2 Aonists for COPD

A
  • Alters airway smooth muscle tone improvng emptying of the lungs
  • Effects usualy wears off 4-6 hours (short acting)
  • and >12 hours (long acting)
  • Regular treatment with LABA is more effective and convenient than SABA
  • appears to provide subjective benefit in acute episodes but is not necessarily helpful in satble disease
  • Adverse effectL tachycardia, arrythmia, tremors, hypokalemia

SHORT ACTING

  • Salbutamol
  • terbutaline

LONG ACTING

  • Formoterol
  • Salmeterol
  • Vilanterol
  • Olodaterol
  • Indacetrol
30
Q

Anticholinergics for COPD

(Anti-muscarinic)

A
  • Blocks acetycholine’s effect on muscarinic receptors
  • Bronchodilating effect of short acting inhaled antichholinergics last longer than that of short acting B2 agonists
  • Improves symptoms and health status and effectiveness of pulmonary rehabilitation and reduces exacerbations
  • Adverse effects:
    • Dry mouth,bitter metallic taste, arrhythmias
  • SHORT ACTING
    • Ipratropium bromdie
    • Oxitropium bromide
  • LONG ACTING
    • Triotropium
    • Umeclidinium
    • Glycopyrronium
31
Q

Methylxantines for COPD

A
  • Acts as nonselective phosphodiesterase inhibitor
  • Improves FEV1 and breathlessness when added to salmeterol
  • Advserse effects:
    • tachycardia, arrhythmias, headache, insomnia
  • Example:
    • Theophylline
    • Aminophylline
    • Doxofylline
32
Q

Inhaled Corticosteroids for COPD

A
  • Adition of ICS to nronchodilator treatment is appropriate for:
    • Symptomatic patients with FEV1 <50% predicted (stage III and Stage IV)
    • Repeared exacerbations
  • Chronic treatment with systemic glucocorticoids should be avoided
  • ICS combined with LABA in moderate to very severe COPD is more ffecteive than either component alone
  • Adverse effects:
    • hoarseness, candidiasis
  • EXAMPLES:
    • Beclomethasone
    • Budesonide
    • Mometasone
    • Fluticasone
33
Q

PDE-4 Inhibitors for COPD

A
  • Improves lung function and reduces moderate and severe exacerbations in patients with chronic bronchitis or those whoa re in fixed-dose LABA/ICS combiantions
  • Adverse effects:
    • Anorexia, weight loss, diarrhea, headache
34
Q

Antibiotics for COPD

A
  • Long term azithromycin and erythromycin use reduces exacerbations over 1 year
  • Azithromycin 250 mg/day or 500 mg 3x/week or erythromycin 500 mg 2x/day for 1 year
35
Q

Mucolytics/Antioxidants for COPD

A
  • Antioxidants (N-acetylcysteine and carbocysteine) reduce the risk of exacerbations in select populations
36
Q

Vaccination for COPD

A
  • Influenza vaccine: decrease incidence of lower respiratory tract infections
  • PCV13 andPPSV23 are recommended for all >65 years of age
    • 23 valent pneumococcal polysaccharide vaccine (PPSV23): reduces incidence of CAP in COPD patients <65 years and FEV1 <40% predicted and in those with commorbidities
    • 13 valent conjugate pneumococcal vaccine: efficient in reducing bacteremia and serious invasive pneumococcal disease in the general population >65 years
37
Q

3 interventions that have been demonstrated to influence the natural history of COPD

A
  • Smoking Cessation
  • Oxygen Therapy
  • Lung volume Reduction surgery
38
Q

Biggest impact in the natural history of COPD

A

Smoking cessation

39
Q

Only pharmacologic therapy demonstrated to unequivocally decrease mortality rates in COPD

A

Oxygen

  • >15 hours/day (long term oxygen therapy)
40
Q

Management of Stable COPD

A
  • Main goals:
    • Reduction of symptoms
    • Reductionof future exacerbations
41
Q

Non pharmacologic management of COPD

A
42
Q

Pharmacologic Management of Stable COPD

A
  • Most are inhaled (proper inhaler technique is important)
  • LABAs and LAMAs: preferred over short-acting agents, except for those with only occasional dyspnea
  • Patients may be started on a single long-acting bronchodilator therapy
  • Long term monotherapy with ICS is NOT recommended
43
Q

Supplemental Oxygen to COPD patients

A
  • Prescribe oxygen and titrate SaO2 >90% in patients with arterial hypoxemia, defined as:
    • PaO2 <55 mmHg or SaO2 <88% or
    • PaO2 55-59 mmHg with right heart failure or erythrocytosis
  • Recheck and reassess in 60-90 days
44
Q

Etiopathogenesis in Exacerbations in COPD

A
  • Associated with increased airway inflammation, increased mucus production, and arked gas trapping
  • Mainly triggered by respiratory viral infections (others: bacterial infetons, environmental factors)
45
Q

Key symptom during exacerbations in COPD

A
46
Q

Manifestations of Exacerbations in COPD

A
  • Increased dyspnea
  • Increased sputum purulence and volume
  • Increased cough
  • wheezing
  • Symptoms usually last between 7-10 days during exacerbations; but 20% of patients do not recover at 8 weeks
47
Q

Classification of exacerbated COPD among hospitalized patients

A
48
Q

most important sign of a severe exacerbation in patients with very severe COPD

A

Change in metal status

49
Q

Management of Acute Exacerbations

A
50
Q

Management of Severe but NOT life threatening Exacerbations of COPD at the ER

A
  • Assess severity of symptoms, blood gases and chest radiographs
  • Administer controlled oxygen therapy and repeat ABG after 30-60 minutes
  • Increase doses and/or frequency of use of bronchodilators
  • Add oral or IV glucocorticoids
  • Consider ntibiotics (oral or occasionally IV) when there are signs of bacterial infection
  • Consider non-nvasive mechanical ventilation
51
Q

Therapy for Acute Exacerbations in COPD

A
52
Q

Indications for NON INVASIVE VENTILATION

A
  • Selection Criteria
    • Severe yspnea with use of accessory muscles and paradoxical abdominal motion
    • Respiratory acidosis (pH <7.35) and/or hypercapnia (PaO2 >45 mmHg)
    • Progressive hypoxemia despite supplemental O2 therapy
  • Exclusion Criteria (presence of any of the following)
    • Respiratory arrest
    • Cardiovascular instability
    • Change in mental status, uncooperative patient
    • High aspiration risk
    • Viscous or copious secretions
    • Recent facial or gastroesophageal surgery
    • Craniofacial trauma
    • Fixed nasopharyngeal abnormalities
    • Burns
    • Extreme Obesity
53
Q

Indications for INVASIVE MECHANICAL VENTILATION

A
  • Unable to tolerateNIV or NIV failure
  • Respiratoty or cardiac arrest
  • Somnolence, impaired mental status
  • Massive aspiration or persistent vomiting
  • Persistent inability to remove respiratory secretions
  • Severe hemodynamic instability without response to fluids and vasoactive drugs
  • Severe venticular or supraventricular arrhythmias
  • Life-threatening hypoxemia in those unable to tolerate NIV
54
Q

Discharge Criteria for COPD

A
  • Inhaled beta-agonist use no more fequent than q4 hours
  • Patient is able to walk across room
  • PAtient able to eat and sleep without frequent awakening by dyspnea
  • Aptient has been clinically stable for 12-24 hours
  • Patient (or home caregiver) fully understands the use of medications
  • Follow-up plans and home care arrangements have been completed, follow up <30 days following discharge