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Pharm 3 Shea > COPD - MJ > Flashcards

COPD - MJ Flashcards

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
Q

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

A

Long-acting

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26
Q

What is the MOA of antimuscarinic bronchodilators?

A

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
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27
Q

The following describes the short acting or long acting antimuscarinic bronchodilators?

  • Slower onset of action (10-20 min) and a more prolonged bronchodilator effect vs. albuterol
  • Does not affect the progressive decline in lung function
A

Short acting

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28
Q

The following describes the short acting or long acting antimuscarinic bronchodilators?

  • 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
A

Long acting

29
Q

What are the 3 ADEs of antimuscarinic (anticholinergic) bronchodilators?

A
  1. Dry mouth
  2. Nausea
  3. Occasional metallic taste
30
Q

The following are examples of what type of therapies?

  • Stiolto Respimat - tiotropium bromide/olodaterol
  • Anoro Ellipta - umeclidinium bromide/vilanterol
  • Bevespi Aerosphere - glycopyrrolate and formoterol
  • Utibron Neohaler - glycopyrrolate/indacaterol)
A

Combination therapies of LAMA + LABA

31
Q

What is the antiinflammatory mechanisms of corticosteroids?

A
  • reduction in capillary permeability to decrease mucus
  • inhibition of release of proteolytic enzymes from leukocytes
  • inhibition of prostaglandins
32
Q

What are the 5 ADEs of systemic corticosteroid therapy? Why might this be used in COPD?

A
  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
Q

T/F: There is a role of ICS therapy for patients with severe or very severe COPD and at high risk of exacerbation

A

TRUE

34
Q

LABA & ICS have greater improvements in clinical outcomes such as what 3 things?

A
  1. FEV1
  2. Health status
  3. Frequency of exacerbations
35
Q

The following are examples of what type of meds?

  • salmeterol plus fluticasone
  • budesonide plus formoterol
  • mometasone plus formoterol
A

LABA & ICS

(-sone or -sonide= corticosteroids)

36
Q
A
37
Q

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?

A

Better

38
Q

What type of medication is Trelegy Ellipta

A
  • A combination of an ICS, a LAMA, and a LABA
  • Delivered once daily in Ellipta dry powder inhaler
39
Q

Which phosphodiesterase is:

•found in airway smooth muscle cells and inflammatory cells

•responsible for degrading cAMP

A

Phosphodiesterase 4 (PDE4)

40
Q

What is indication for Romflumilast, a phosphodiesterase 4 inhibitor?

A

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
Q

The following is the mechanism of which med?

  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
A

Phosphodiesterase 4 (PDE4) inhibitors

42
Q

What are the ADEs of PDE4 inhibitors? (8)

A
  • HA, dizziness, insomnia
  • Diarrhea, weight loss, nausea, decreased appetite
  • Back pain
43
Q

When are PDE 4 inhibitors contraindicated?

A

in moderate to severe hepatic impairment

44
Q

What interaction do PDE 4 inhibitors have with Cimetidine?

A

May increase serum concentrations of the active metabolite(s) of Roflumilast.

45
Q

What interaction do PDE4 inhibitors have with Ciprofloxacin (systemic)?

A

May increase the serum concentration of Roflumilast

46
Q

What interaction do PDE 4 inhibitors have with immunosuppressants? What are the 2 exceptions?

A

Roflumilast may enhance the immunosuppressive effect of Immunosuppressants. Exceptions: Beclomethasone; Budesonide

47
Q

Why is it not recommended to use theophylline and roflumilast (a PDE 4 inhibitor) together for the management of COPD?

A

Both theophylline and roflumilast have similar mechanisms of action through inhibition of phosphodiesterases

48
Q

What is the indication for α1-Antitrypsin Replacement Therapy?

A

inherited AAT deficiency-associated emphysema

49
Q

What is the treatment for patients with inherited AAT deficiency-associated emphysema?

A
  • 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
Q

What are the 5 A’s in th 5 step strategy for smoking cessation program

A

Ask

Advise

Assess

Assist

Arrange

51
Q

What are the 6 first line pharmacotherapies for smoking cessation and what is the common complaints for each?

A
  1. Buproprion SR- insomnia, dry mouth
  2. Nicotine gum- sore mouth, dyspepsia
  3. Nicotine inhaler- 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
Q

What are 3 prevention/maintenance therapies for patients w/ COPD?

A
  1. Inhaler technique assessed regularly.
  2. Influenza/pneumococcal vaccination decreases the incidence of lower respiratory tract infections.
  3. Pulmonary rehabilitation improves symptoms, quality of life, and physical and emotional participation in everyday activities.
53
Q

In COPD patients with severe resting chronic hypoxemia, what has been shown to improve survival?

A

long-term oxygen

54
Q

In patients with stable COPD and resting or exercise-induced moderate desaturation, What treatment should be prescribed routinely?

A

long-term oxygen treatment

However, individual patient factors must be considered when evaluating the patient’s need for supplemental oxygen.

55
Q

What are considered “cardinal symptoms”, which are used in the staging of acute COPD exacerbations?

A
  1. Worsening of dyspnea
  2. Increase in sputum volume
  3. Increase in sputum purulence.
56
Q

Staging of acute exacerbations of COPD:

What constitutes an exacerbation as Mild?

A

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
Q

Staging of acute exacerbations of COPD:

What constitutes an exacerbation as moderate (type 2) vs severe (type 3)?

A
  • 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
Q

Therapeutic options for acute exacerbations of COPD:

When are abx recommended?

A

If 2+ of the following are present:

  • Increased dyspnea
  • Increased sputum production
  • Increased sputum purulence
59
Q

Therapeutic options for acute exacerbations of COPD:

Bronchodilators: β-Agonists also may ______ mucociliary clearance.

A

increase

60
Q

Therapeutic options for acute exacerbations of COPD:

When should noninvasive mechanical ventilation be considered? When is it not appropriate?

A
  • Consider for patients with acute respiratory failure.
  • Not appropriate for patients with altered mental status, severe acidosis, respiratory arrest, or cardiovascular instability.
61
Q

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
A

Macrolide (azithromycin, clarithromycin)

(not recommended: TMP/SMX, amox, first gen ceph and erythromycin)

62
Q

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
A

Amoxicillin/clavulanate

63
Q

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
A

Fluoroquinolone with enhanced pneumococcal and P. aeruginosa activity (levofloxacin)

64
Q
A
65
Q

What is the best Fluoroquinolone against pseudomonas?

A

Ciprofloxacin

66
Q

Pneumococcal vaccine:

Who is PCV13 recommended for?

A
  • 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
Q

Pneumococcal vaccine:

Who is PPSV23 recommended for?

A
  • 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
Q

Pneumococcal Vaccine:

How long must you wait between giving PCV13 and PPSV23?

A

At least 1 year apart (must give both)

Pharm 3 Shea (17 decks)

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