COPD Flashcards

(39 cards)

1
Q

ETIOLOGY
What are the main causes of COPD?

A

-Smoking and pollutants
-Host factors

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2
Q

Pathophysiology

A

-Starts with chronic inflammation
-inflammation leads to peripheral airway obstruction -> smaller bronchioles -> trapped air in the lungs
-the body upregulates goblet cells to clear the inflammation (get inflammatory particles out of the lungs with mucus)
-Hyperinflation causes goblet cells to get bigger and to proliferate -> more mucus secretion
-Hyperinflation causes Mucus hypersecretion
-Exacerbations
-Alpha-1 antitrypsin deficiency

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3
Q

What are the factors that cause Exacerbation in COPD?

A

-illness (viral, bacterial)
-environmental exposure
-med nonadherence
-can’t afford meds

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4
Q

Alpha-1 antitrypsin deficiency

A

-protease, which helps the lung tissues to stretch and recoil as we exhale and inhale

-people under the age of 40 with COPD get tested for it

-deficiency results in fibrotic lungs and their breakdown, early in life and aggressively

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5
Q

Symptoms of COPD

A

-Shortness of breath (dyspnea)
-chronic cough
-sputum

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6
Q

Risk factors of COPD

A

-smoking
-air pollution
-host factors
-Occupation (job)

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7
Q

What are the GOLD ABE assessment tools?

A

-modified MRC Dyspnea Assessment tool: how COPD affects daily life
-CAT assessment (COPD effect on daily life)
-Assessing airflow obstruction: GOLD 1 to GOLD 4 (comparing FEV1 to standard)
-Exacerbation history (per year)

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8
Q

How are patients treated based on the Assessment tools?

A

Group A and B: treat symtoms

Group E: prevent further exacerbation

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9
Q

When would a patient be categorized into Group E?

A

more than 2 moderate exacerbations per year or more than 1 exacerbation with hospitalization

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10
Q

What is an Exacerbation of COPD?

A

Any acute event causing the worsening of the respiratory symptoms that results in additional therapy

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11
Q

Nonpharmacologic Treatment in COPD

A

-Smoking cessation
-Reduce indoor air pollution
-Reduce environmental triggers
-Pulmonary rehabilitation

-Nutrition counseling (high carbohydrate diet can worsen the condition bc it increases the level of CO2, which is high already due to trapped air)

-Pursed-lip breathing (helps regulate and slow their breathing down)

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12
Q

What are recommended vaccinations for COPD patients?

A

-Influenza
-COVID
-Pneumococcal: PVC20 or PVC15 followed by PVC23
-Tdap

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13
Q

Pharmacologic therapy

A

-Bronchodilator - BACKBONE in COPD therapy
ß2-agonists
Anticholinergic drugs
Methylxanthines (Theophylline)

-Inhaled steroids
-Phosphodiester-4 inhibitors (Roflumilast, Daliresp)

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14
Q

What are the cholinergic effects on the lungs?

A

-Acetylcholine causes bronchial smooth muscles to constrict - binding to M1 and M3
-once a certain amount of Acetylcholine binds to M2 a negative feedback signal is triggered

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15
Q

Why is LAMA and SAMA not appropriate for dyspnea (shortness of breath) treatment?

A

-If a patient is on LAMA (tiotropium (LAMA) binds specifically to M3 (newer LAMA’s)
-SAMA (ipratropium) binds to all M1, M2 and M3

-since the M3 receptors are predominantly occupied by tiotropium, so if the patient uses ipratropium (SAMA) it will bind to M2 and prevent negative feedback of Acetylcholine release

-Patients on LABA (Salmeterol) can still be treated with SABA (Albuterol) in shortness of breath

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16
Q

Side effects of Anticholinergics

A

-Dry mouth
-Urinary retention (more with BPH and oral and systemic rather than inhaler)
-Metallic taste
-Cardiovascular events?
-Face mask nebs can precipitate acute glaucoma

17
Q

LABA is superior to LAMA in reducing exacerbation risk in COPD patients?

A

False - LAMA (tiotropium) is superior
(improves the number of exacerbations and the time it takes for the next exacerbation)

LAMA (tiotropium) also superior to SAMA (Ipratropium) for monotherapy in COPD

18
Q

What do COPD patients in Group E struggle with the most?

19
Q

What is the recommended first-line therapy for COPD patients in Group E?

A

LAMA/LABA Combo

also #1 for Group A and Group B patients providing relief in their symptoms as compared to each of them alone

20
Q

What do COPD patients in Group A and Group B struggle with the most?

21
Q

When is ICS not appropriate/appropriate to use in COPD Exacerbation?

A

appropriate: if the eosinophile blood count (causing inflammation) is high
(appropriate for asthma)

not appropriate: ICS alone in COPD

22
Q

Side effects of Inhaled Corticosteroids

A

-Oral Candidiasis (rinse mouth after every use)
-skin-bruising, hoarse voice
-Pneumonia
-decrease in bone-mineral density?

23
Q

Strongly favors the use of ICS

A

-History of hospitalization for COPD
-2 exacerbations per year
-Blood eosinophile over 300
-history or concomitant asthma

24
Q

Against the use of ICS

A

-Repeated Pneumonia
-Eosinophile under 100
-History of mycobacterial infection

25
Triple therapy for COPD
ICS + LABA/LAMA -ICS effect on muscarinic receptors is emerging -has been shown to improve QOL (more evidence needed)
26
When are Phosphodiester-4 inhibitors appropriate to use?
-in patients with chronic bronchitis (wet cough with a lot of mucus) -history of exacerbation -Roflumilast (Daliresp) - one daily tab (added to LAMA/LABA)
27
What are the signs of chronic bronchitis?
wet cough
28
MOA of PDE-4 inhibitors
-PDE-4 degrades cAMP -cAMP activates PKA -> PKA inactivates inflammatory pathways -PDE-4 inhibitor will block PDE-4 -> increasing cAMP and inflammatory deactivation -stopping inflammatory mediators and the migration of immune cells
29
Side effects of PDE-4 inhibitors
-GI disturbance -Weight loss (not for older patients) -Sleep disturbances -Headache -Worsening of depression -Suicidal ideation
30
When is Roflumilast (oral) added to the regimen?
-Exacerbation, FEV1 < 50% -chronic bronchitis
31
When is Azithromycin added to the regimen instead of Roflumilast?
preferred in smokers BUT associated with bacterial resistance and hearing test impairment
32
What are the cardinal symptoms of an exacerbation?
-Increased dyspnea -Increased sputum -increased sputum purulence
33
Therapy options after Exacerbation
-Short-acting Bronchodilator ß2 agonists with or w/o anticholinergics -Corticosteroids -Antibiotics -Supplemental oxygen/mechanical support -Adjunct therapies
34
What is the baseline recommendation duration for antibiotics and steroids in COPD patients?
5 days
35
Bronchodilator - COPD Exacerbation
-Short-acting ß-agonists -> short-acting anticholinergic (SAMA) often used as adjunct to SABA -nebulizer in very ill patients nebulizer may be used, but for other patients, inhalers are appropriate
36
What is the dose to treat COPD Exacerbation with oral Corticosteroids?
-40 mg/day oral prednisone equivalent for 5 days
37
Benefits of Corticosteroids in COPD Exacerbation
-limit recovery time -improve lung function -reduce relapse and treatment failure -shorten length of stay (LOS) in the hospital
38
The patient population to be treated with antibiotics
-when hospitalized they are likely to be qualified -all with the 3 cardinal symptoms increased sputum increased sputum purulence increase in dyspnea -2 cardinal symptoms if sputum purulence is involved -anyone medical ventilated length of therapy: 5-7 days
39
What are the antibiotics used in COPD exacerbation?
-Augmentin or Pip/Tazo (Zosyn) Atypicals: -Azithromycin 500 mg IV/PO x 3-5 days -Doxy 100 mg IV/PO Q12H -Quinolones (reserve these) -H. flu -M. cat -S. pneumo -C. pneumo -Pseudomonas or enterobacteriaceae