COPD - MJ Flashcards

(68 cards)

1
Q

Are the following reversible or irreversible etiologies of airflow limitation in COPD?

  • Presence of mucus and inflammatory cells and mediators in bronchial secretions
  • Bronchial smooth muscle contraction in peripheral and central airways
  • Dynamic hyperinflation during exercise
A

reversible

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2
Q

Are the following reversible or irreversible etiologies of airflow limitation in COPD?

  • Fibrosis and narrowing of airways
  • Reduced elastic recoil with loss of alveolar surface area
  • Destruction of alveolar support with reduced patency of small airways
A

Irreversible

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3
Q

The following are sxs of what dz?

  • Chronic and progressive dyspnea
  • Cough
  • Sputum production
  • Wheezing and chest tightness
  • Others – fatigue, weight loss, anorexia, syncope, rib fractures, ankle swelling, depression, anxiety
A

COPD

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4
Q

What are the 7 goals of treatment for COPD? (According to GOLD guidelines)

A
  1. Prevent disease progression
  2. Relieve symptoms
  3. Improve exercise tolerance
  4. Improve overall health status
  5. Prevent and tx exacerbations
  6. Prevent and txcomplications
  7. Reduce morbidity and mortality
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5
Q

What are the 3 steps (in general) to determine drug therapy for COPD?

A

Step 1: Spirometrically confirmed dx: Post-bronchodilator FEV1 (determine if pt is mild- very severe)

Step 2: Assessment of airflow limitation (questionnaires- CAT, mMRC, )

Step 3: Assessment of sxs/risk of exacerbations (ABCD assessment tool)

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6
Q

Process used to determine drug therapy for COPD:

  • Step 1: post-bronchodilator FEV1- what values of FEV1 correspond to mild, moderate, severe and very severe ?
A
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7
Q

Process used to determine drug therapy for COPD:

Which questionnaires are used in step 2 (choice of thresholds)

A

►COPD Assessment Test (CAT)

►Chronic Respiratory Questionnaire (CCQ® )

►St George’s Respiratory Questionnaire (SGRQ)

►Chronic Respiratory Questionnaire (CRQ)

Modified Medical Research Council (mMRC) questionnaire

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8
Q

What are COPD exacerbations defined as?

A

an acute worsening of respiratory symptoms that result in additional therapy

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9
Q

How are mild COPD exacerbations treated?

A

w/ SABDs only

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10
Q

How are moderate COPD exacerbations treated?

A

SABDs + antibiotics/oral corticosteroids

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11
Q

How are severe COPD exacerbations treated?

A
  • patient requires hospitalization or visits the ER
  • Severe exacerbations may also be associated with acute respiratory failure.
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12
Q

Step 3: Assessment of exacerbation risk-

Blood _______ count may also predict exacerbation rates (in patients treated with LABA without ICS).

A

eosinophil

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13
Q

ABCD assessment tool

A
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14
Q

What is initial pharmacotherapy for a COPD pt in group A? (less sxs, low risk)

A

SABA

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15
Q

What is initial pharmacologic tx for a COPD pt in group B? (more sxs, low risk)

A

LABA or LAMA

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16
Q

What is initial pharmacologic tx for a COPD pt in group C? (Low sxs, high risk)

A

LAMA

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17
Q

What is initial pharmacologic tx for a COPD pt in group D? (more sxs, high risk)

A

LAMA

or

LAMA + LABA

or

ICS + LABA (consider if eos>200)

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18
Q

Tx for COPD exacerbations

A
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19
Q

What is the onset and duration of bronchodilators- beta agonist (ex: albuterol)

A

Onset- 5 min

Duration- 2-6hrs

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20
Q

T/F: the response to bonchodilators-beta agonists (ex: albuterol) is generally less than that seen in asthma

A

True

  • only a sm improvement in FEV1
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21
Q

Bronchodilators- beta agonists (ex: albuterol) may improve what 2 things?

A
  1. Respiratory sxs
  2. Exercise tolerance
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22
Q

Long acting bronchodilators: both beta agonists and antimuscarinics:

  • _____ outcomes in lung function as measured by spirometry
  • symptoms including ______
  • reductions in exacerbation frequency
  • improved quality of life
A
  • Superior
  • dyspnea
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23
Q

What are the ADEs of bronchodilators- beta agonists?

A
  • sinus tachycardia, rhythm disturbances in predisposed patients
  • skeletal muscle tremors can occur initially but subside as tolerance develops
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24
Q

Is Ipatropium a short acting or long acting anti-muscarinic bronchodilator?

A

shor-acting

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25
Is tiotropium a short acting or long acting anti-muscarinic bronchodilator?
Long-acting
26
What is the MOA of antimuscarinic bronchodilators?
Bronchodilation by competitively inhibiting cholinergic receptors in bronchial smooth muscle * Activation of M1 and M3 receptors by acetylcholine results in bronchoconstriction * Activation of M2 receptors inhibits further acetylcholine release
27
The following describes the short acting or long acting antimuscarinic bronchodilators? ## Footnote * **Slower onset** of action (10-20 min) and a **more prolonged bronchodilator effect** vs. albuterol * **Does not affect the progressive decline in lung function**
Short acting
28
The following describes the short acting or long acting antimuscarinic bronchodilators? ## Footnote * Significantly **greater improvements in lung function**, **quality of life** and **reduces the frequency of exacerbation** and need for hospitalization * Equal or superior efficacy compared with LABAs in various studies * Lower overall risk of mortality, including deaths from respiratory and cardiac causes
Long acting
29
What are the 3 ADEs of antimuscarinic (anticholinergic) bronchodilators?
1. Dry mouth 2. Nausea 3. Occasional metallic taste
30
The following are examples of what type of therapies? ## Footnote * Stiolto Respimat - tiotropium bromide/olodaterol * Anoro Ellipta - umeclidinium bromide/vilanterol * Bevespi Aerosphere - glycopyrrolate and formoterol * Utibron Neohaler - glycopyrrolate/indacaterol)
Combination therapies of LAMA + LABA
31
What is the antiinflammatory mechanisms of corticosteroids?
* reduction in capillary permeability to decrease mucus * inhibition of release of proteolytic enzymes from leukocytes * inhibition of prostaglandins
32
What are the 5 ADEs of _systemic_ corticosteroid therapy? Why might this be used in COPD?
1. Osteoporosis 2. Muscular atrophy 3. Thinning of the skin 4. Development of cataracts 5. Adrenal suppression/insufficiency ? clinical benefit including slowing of disease progression
33
T/F: There is a role of ICS therapy for patients with **severe or very severe COPD and at high risk of exacerbation**
TRUE
34
LABA & ICS have greater improvements in clinical outcomes such as what 3 things?
1. FEV1 2. Health status 3. Frequency of exacerbations
35
The following are examples of what type of meds? * salmeterol plus fluticasone * budesonide plus formoterol * mometasone plus formoterol
LABA & ICS | (-sone or -sonide= corticosteroids)
36
37
**Once-Daily Single Inhaler Triple Therapy for COPD: LABA + LAMA + ICS--\>** This inhaler provides better or worse control than 2 or more individual drug inhalers?
Better
38
What type of medication is Trelegy Ellipta
* A combination of an ICS, a LAMA, and a LABA * Delivered once daily in Ellipta dry powder inhaler
39
Which phosphodiesterase is: ## Footnote •found in airway smooth muscle cells and inflammatory cells _•responsible for degrading cAMP_
Phosphodiesterase 4 (PDE4)
40
What is indication for Romflumilast, a phosphodiesterase 4 inhibitor?
Indication: with bronchodilator therapy in the maintenance treatment of **severe or very severe COPD patients at high risk of exacerbation** (Groups C and D) and are **not controlled by inhaled bronchodilators**
41
The following is the mechanism of which med? ## Footnote 1. _Selectively inhibit \_\_\_\_\__- leads to accumulation of cAMP w/in inflammatory/structural cells important in the pathogenesis of COPD 2. _Anti-inflammatory effects-_ _suppression of cytokine release_ and inhibition of lung infiltration by neutrophils and other leukocytes 3. _Pulmonary remodeling_ and _mucociliary malfunction_ are also attenuated
Phosphodiesterase 4 (PDE4) inhibitors
42
What are the ADEs of PDE4 inhibitors? (8)
* HA, dizziness, insomnia * Diarrhea, **weight loss**, nausea, **decreased appetite** * Back pain
43
When are PDE 4 inhibitors contraindicated?
in moderate to severe hepatic impairment
44
What interaction do PDE 4 inhibitors have with Cimetidine?
May increase serum concentrations of the active metabolite(s) of Roflumilast.
45
What interaction do PDE4 inhibitors have with Ciprofloxacin (systemic)?
May increase the serum concentration of Roflumilast
46
What interaction do PDE 4 inhibitors have with immunosuppressants? What are the 2 exceptions?
Roflumilast may enhance the immunosuppressive effect of Immunosuppressants. Exceptions: Beclomethasone; Budesonide
47
Why is it not recommended to use theophylline and roflumilast (a PDE 4 inhibitor) together for the management of COPD?
Both theophylline and roflumilast have similar mechanisms of action through inhibition of phosphodiesterases
48
What is the indication for α1-Antitrypsin Replacement Therapy?
inherited AAT deficiency-associated emphysema
49
What is the treatment for patients with inherited AAT deficiency-associated emphysema?
* focus on reduction of risk factors such as smoking, symptomatic treatment with bronchodilators * augmentation therapy with replacement AAT * weekly infusions of pooled human AAT * ? significant reduction in lung tissue loss and destruction
50
What are the 5 A's in th 5 step strategy for smoking cessation program
Ask Advise Assess Assist Arrange
51
What are the 6 first line pharmacotherapies for smoking cessation and what is the common complaints for each?
1. **Buproprion SR**- insomnia, dry mouth 2. **Nicotine gum**- sore mouth, dyspepsia 3. **Nicotine inhale**r- Sore mouth and throat 4. **Nicotine nasal spray**- nasal irritation 5. **Nicotine patches**- skin reaction, insomnia 6. **Varenicline (Chantix)**- Nausea, sleep disturbances (vivid dreams)
52
What are 3 prevention/maintenance therapies for patients w/ COPD?
1. **Inhaler technique** assessed regularly. 2. **Influenza/pneumococcal vaccination** decreases the incidence of lower respiratory tract infections. 3. **Pulmonary rehabilitation i**mproves symptoms, quality of life, and physical and emotional participation in everyday activities.
53
In COPD patients with severe resting chronic hypoxemia, what has been shown to improve survival?
long-term oxygen
54
In patients with stable COPD and _resting or exercise-induced moderate desaturation,_ What treatment should be prescribed routinely?
**long-term oxygen treatment** However, individual patient factors must be considered when evaluating the patient’s need for supplemental oxygen.
55
What are considered "cardinal symptoms", which are used in the staging of acute COPD exacerbations?
1. _Worsening of dyspnea_ 2. _Increase in sputum volume_ 3. _Increase in sputum purulence._
56
Staging of acute exacerbations of COPD: What constitutes an exacerbation as Mild?
Mild (type 1)= 1 cardinal symptom plus at least 1 of the following: * URTI w/in 5 days * unexplained fever * increased wheezing * increased cough * increase in respiratory or heart rate \>20% above baseline (cardinal sx= worsening of dyspnea, increase in sputum volume and increase in sputum purulence)
57
Staging of acute exacerbations of COPD: What constitutes an exacerbation as moderate (type 2) vs severe (type 3)?
* Moderate (type 2)= 2 cardinal sxs * Severe (type 3)= 3 cardinal sxs (cardinal sxs= worsening of dyspnea, increase in sputum volume and increase in sputum purulence)
58
Therapeutic options for acute exacerbations of COPD: When are abx recommended?
If 2+ of the following are present: * Increased dyspnea * Increased sputum production * Increased sputum purulence
59
Therapeutic options for acute exacerbations of COPD: Bronchodilators: β-Agonists also may ______ mucociliary clearance.
increase
60
Therapeutic options for acute exacerbations of COPD: When should noninvasive mechanical ventilation be considered? When is it not appropriate?
* **Consider** for patients with **acute respiratory failure.** * **Not appropriate** for patients with **altered mental status**, **severe acidosis, respiratory arrest, or cardiovascular instability.**
61
What is the recommended antimicrobial therapy in an aute COPD exacerbation in a patient w/: * Uncomplicated exacerbations * \<4 exacerbations per year * No comorbid illness * FEV1 \>50% of predicted
**Macrolide** (azithromycin, clarithromycin) (not recommended: TMP/SMX, amox, first gen ceph and erythromycin)
62
What is the recommended antimicrobial therapy in an aute COPD exacerbation in a patient w/: * Complicated exacerbations: *  Age ≥65 and \>4 exacerbations per year *  FEV1 \<50% but \>35% of predicted
Amoxicillin/clavulanate
63
What is the recommended antimicrobial therapy in an aute COPD exacerbation in a patient w/: * Complicated exacerbations with risk of P. aeruginosa *  Chronic bronchial sepsis *  Need for chronic corticosteroid therapy *  Resident of nursing home with \<4 exacerbations per year * FEV1 \<35% of predicted
Fluoroquinolone with enhanced pneumococcal and P. aeruginosa activity (levofloxacin)
64
65
What is the best Fluoroquinolone against pseudomonas?
Ciprofloxacin
66
Pneumococcal vaccine: Who is PCV13 recommended for?
* All adults \>65 * Adults \>19y/o with certain health conditions (ones that weaken the immune system- HIV, organ transplant, leukemia, lymphoma, and severe kidney disease)
67
Pneumococcal vaccine: Who is PPSV23 recommended for?
* **All adults \>65** * **19- 64 years old w/ certain health conditions** (chronic illnesses like asthma, DM or alcoholism; HIV, etc) or who smoke cigarettes **•(in group child care, have chronic conditions)**
68
Pneumococcal Vaccine: How long must you wait between giving PCV13 and PPSV23?
At least **1 year apart** (must give both)