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Pulmonary > COPD > Flashcards

COPD Flashcards

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?

A

Exacerbation

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?

A

Symptoms

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
Q

Triple therapy for COPD

A

ICS + LABA/LAMA
-ICS effect on muscarinic receptors is emerging
-has been shown to improve QOL (more evidence needed)

26
Q

When are Phosphodiester-4 inhibitors appropriate to use?

A

-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
Q

What are the signs of chronic bronchitis?

A

wet cough

28
Q

MOA of PDE-4 inhibitors

A

-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
Q

Side effects of PDE-4 inhibitors

A

-GI disturbance
-Weight loss (not for older patients)
-Sleep disturbances
-Headache
-Worsening of depression
-Suicidal ideation

30
Q

When is Roflumilast (oral) added to the regimen?

A

-Exacerbation, FEV1 < 50%
-chronic bronchitis

31
Q

When is Azithromycin added to the regimen instead of Roflumilast?

A

preferred in smokers

BUT associated with bacterial resistance and hearing test impairment

32
Q

What are the cardinal symptoms of an exacerbation?

A

-Increased dyspnea
-Increased sputum
-increased sputum purulence

33
Q

Therapy options after Exacerbation

A

-Short-acting Bronchodilator
ß2 agonists with or w/o anticholinergics
-Corticosteroids
-Antibiotics
-Supplemental oxygen/mechanical support
-Adjunct therapies

34
Q

What is the baseline recommendation duration for antibiotics and steroids in COPD patients?

A

5 days

35
Q

Bronchodilator - COPD Exacerbation

A

-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
Q

What is the dose to treat COPD Exacerbation with oral Corticosteroids?

A

-40 mg/day oral prednisone equivalent for 5 days

37
Q

Benefits of Corticosteroids in COPD Exacerbation

A

-limit recovery time
-improve lung function
-reduce relapse and treatment failure
-shorten length of stay (LOS) in the hospital

38
Q

The patient population to be treated with antibiotics

A

-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
Q

What are the antibiotics used in COPD exacerbation?

A

-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

Pulmonary (13 decks)

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