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PHARM 253 Exam 1 > COPD > Flashcards

COPD Flashcards

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1
Q

Define COPD

A

a respiratory disorder largely caused by smoking, and is characterized by progressive, partially reversible airway obstruction and lung hyperinflation, systemic manifestations, and increasing frequency and severity of exacerbations.”

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2
Q

Main differnce between asthma and COPD

A

Asthma is rversible, COPD is progressive

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3
Q

Define emphysema

A

abnormal enlargement of the airspace distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis

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4
Q

Define chronic bronchitis:

A

Chronic cough for at least 3 months x 2 consecutive years

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5
Q

COPD Epidemiology is primarily…. It results in how many % of deaths?

A

Cigarette smoking: principal underlying cause of COPD and responsible for about 80% of deaths

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6
Q

What is unique about COPD’s prevelance?

A

3rd leading cause of death worldwide; only chronic illness with increasing mortality

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7
Q

Risk Factors of COPD

A

Exposure to Particles
Infections
Socio-economic status

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8
Q

What is the most significant risk factor of COPD?

A
  • SMOKING/EXPOSURE TO 2ND HAND SMOKE
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9
Q

What are some host factors of COPD?

A

1) Hereditary

1-antitrypsin deficiency predisposes susceptible people to emphysema

1-antitrypsin is a serum protein produced by the liver & normally found in the lungs.

It prevents neutrophil elastase from destroying lung tissue

Accounts for <5% of cases

2) AGE
3) Lung Growth and Development
4) Airway Hyperresposiveness (Hard to seperate and define cause and effect with asthma)

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10
Q

Pathophysiology of COPD Simple

A

Stimulus (e.g smoking) –> Inflammatory process –> narrowing of perfipheral pathways –> Decreased FEV1

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11
Q

What is noted in COPD patients in regards to pathopjhysiologuy?

A

A Protease-Antiprotease Imbalance is noted in the lungs of COPD patients. (Protease Mediated destruction of elastin is an important feature of emphysema)

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12
Q

In COPD, what may amplify the inflammatory response?

A

Oxidative stress may play an important role in amplifying the inflammatory process.

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13
Q

COPD has a specific pattern of what?

A

Specific pattern of inflammation: CD8+ (cytotoxic) lymphocytes and other Inflammatory cells & mediators induce structural changes in the lung parenchyma & Pulmonary vasculature

COPD –> Increase in residual volume –> GAS TRAPPING

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14
Q

In regards to COPD pathophysiology, these things occur:

A

Expiratory Flow Limiytation

Lung Hyperinflation

Gas Exchange Abnormality

Mucous Hypersecretionm

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15
Q

What is a hallmark of COPD? Why does it occur?

A

Expiratory Flow Limitation

Hallmark of COPD
Due to increased resistance from mucosal inflammation, airway remodelling, fibrosis & secretions

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16
Q

In COPD, the lungs will ______upon inhalation. Why does it occur? What is the result?

A

Lung hyperinflation

Obstruction of the small airways results in air-trapping which causes lung hyperinflation

Develops early in disease and causes exertional dypsnea

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17
Q

In regards to gas exchange, in COPD there is ______ Result?

A

Gas exchange abnormalities
Result in hypoxemia & hypercapnia
Gas transfer for O2 & CO2 worsens as disease progresses

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18
Q

In regards to mucouis, in COPD there is ______. This results in a _____

A

Mucous hypersecretion
Results in a chronic productive cough
Not necessarily associated with airflow limitation

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19
Q

What triggers an exacerbation? What occurs during a COPD exacerbation?

A

Triggered by infection, environmental pollutants or unknown

During exacerbations there is increased hyperinflation and gas trapping, with decreased expiratory flow

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20
Q

With COPD, what other conditions may one have as a result later in life?

A

Significant Comorbid Illness
Pulmonary hypertension may develop late in course of COPD due to hypoxic vasoconstriction of small pulmonary arteries eventually leading to structural changes
Muscle wasting and cachexia, skeletal muscle dysfunction
Osteoporosis, depression and anemia, metabolic sydrome, cardiovascular, lung cancer

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21
Q

What are some comorbities associated with COPD?

A

Ischemic heart disease
Congestive heart failure
Arrhythmias
Pulmonary hypertension
Lung cancer
Osteoporosis and Fractures
Skeletal muscle dysfunction
Cachexia and Malnutrition
Glaucoma and Cataracts
Depression
Anxiety and Panic disorders
Metabolic disorders

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22
Q

Three cardinal sx of COPD?

A

Shortness of breath
Chronic cough
Phlegm

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23
Q

What other sx may be present?

A

Frequent lung infections
Reduced ability to go about daily activities
Barrel-shaped chest
Fatigue
Unexplained weight loss

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24
Q

End-stage COPD Sx?

A

Adopt positions that relieve dyspnea  relax diaphragm
Use of accessory respiratory muscles
Expiration through pursed lips
Cyanosis
Enlarged liver from right heart failure

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25
How do patients with COPD initially present?
1) Extremely sedentary lifestyle and presents with general fatigue ---> Typically have avoided exertional dyspnea ---> Shifted expectations and limited their activity 2) Patient has complaints of dyspnea and chronic cough --> Initially noted on exertion only --> Progressively triggered by less exertion or at rest --> Morning sputum production 3) Patient who presents with episodes of cough, sputum, wheezing, fatigue and dyspnea --> May be initially diagnosed as asthma --> Interval between episodes shortens
26
Asthma vs COPD: age of onset
Asthma - <40 COPD: <40
27
Asthma vs COPD: smoking History
Asthma: Not causal, but worsen control COPD: Usually >10 pack years
28
Asthma vs COPD: Sputum Production
Asthma: Infrequent COPD: Often
29
Asthma vs COPD: Allergies
Asthma: Often COPD: Infrequent
30
Asthma vs COPD: Clinical Sx Length/ How long do the sx last?
A: Intermittent and variable C: Persistet and progressive
31
Asthma vs COPD: Disease Course
A: Stable (withe xacerbations) C: Progressive (with exacerbations)
32
Asthma vs COPD: Comorbid Illness
Important for both
33
Asthma vs COPD: Spirometry
A: often normalizes C: May improve but never normalizes
34
Asthma vs COPD: Cause of Airway Inflammation
A: Eiosinophilic C: Neutrophilic
35
Asthma vs COPD: ICS response
A: Essential C: Helpful in pt's with moderate and frequent AECOPD
36
Asthma vs COPD: Bronchodilators
A: PRN only B: Regular tx
37
Asthma vs COPD: Exercise training
A: Rarely used C: Essential
38
Asthma vs COPD: End of life discussions
A: Rare C: Often essential
39
A clinical diagnosis of COPD should be considered in any pt who has:
Dyspnea Chronic Cough Sputum Production History of exposure to risk
40
What is used to diagnose COPD? What is used to stage it?
Spirometry post-bronchodilator FEV1/FVC ratio <0.7 confirms diagnosis FEV1 is used to stage
41
Who should be screened for COPD?
Evidence does not currently support population screening with spirometry -Screen patients who have risk factors: Smokers/ex-smokers ≥40 who have: - persistent cough or sputum production - frequent respiratory tract infections - progressive activity-related SOB - evening wheeze --> if yes --> Spirometry
42
MRC Scale
STUDY CHART
43
What is the CAT Test?
Validated, short (8-item) and simple patient completed questionnaire Reliable measure of the impact of COPD on a patient’s health status
44
Suspect COPD in people who are:
Age > 40 years Smokers or ex-smokers – quantify tobacco consumption Progressive dyspnea, worse with exercise
45
Spirometry is necessary for COPD ________. Values:
FEV1 / FVC < 70% after bronchodilator
46
Staging of COPD CTS
STUDY CHART
47
GOALS of TX COPD
Prevent disease progression Prevent and treat exacerbations Alleviate breathlessness and other respiratory symptoms Improve exercise tolerance and daily activity Prevent and treat complications of the disease Improve health status Reduce mortality
48
What is the most effective intervention to reduce risk of COPD? Does it stop progression? What should one ask?
Smoking Cessation --> Just slows down the rate of progression (lung function will continue decreasoing if have COPD) One should: The 5 A’s: Ask, Advise, Assess, Assist, Arrange
49
In pt education, what should be taught?
Expectations of therapy must be discussed (cannot cure, but improve QOL – progressive life long tx – most likely will add on rather than take away) Self management plans prescriptions for oral steroids and antibiotics to fill when needed advanced care directives Inhaler technique – select best device for each individual patient
50
What should be avoided in COPD? Why?
Sedatives/Narcotics: increased sensitivity to respiratory depression especially when sleeping
51
All COPD pt's should be encouraged to:
maintain an active lifestyle
52
What vaccines should people with COPD get?
Annual Influenza vaccine decreases serious illness / death by 50% Pneumococcal vaccine Recommended for all patients with COPD Covid-19 Vacinne
53
Who should get long-term oxygen tx? What is the goal?
SEVERE HYPOXEMIA Does not change pulmonary function Cornerstone of therapy improves quality/ duration of life in select patients Assess patient when stable goal PaO2 > 60 mmHg
54
Pharmacological tx is ________. The main stay of tx is.....
Empiric – individuals differ in response to treatment and side effects (start with something and go from there) Bronchodilators are the mainstay in treatment and are prescribed regularly in COPD; larger doses may be used compared to treatment of asthma.
55
Pharmacotx difference from asthma:
Compared to asthma: Muscarinic antagonists have larger role ICS have less of a role If bronchodilator fails, confirm compliance and acceptable inhaler technique.
56
SABA of Choice: Dose:
Slabutamol Terbutaline BOTH QID PRN
57
SAMA of Choice Dose
Ipratropium QID PRN
58
Can a combo be used? If so, what and dose? WHy?
Salbutamol + ipratropium --> QID PRN Synergistic --> Better than used alone
59
What is recommended in all stages of COPD?
PRN use of short acting bronchodilators is recommended in all stages of disease Higher doses = more bronchodilation May increase beyond recommended dose in severe disease
60
SAMA LAMA MOA
Airway muscle tone is partially controlled by cholinergic innervation. Inhaled anticholinergics competitively inhibit cholinergic receptors in bronchial smooth muscle. This block acetylcholine which reduces cGMP. Acetylcholine leads to bronchoconstriction.
61
SAMA vs SABA Comparison
Less effective than β2 agonists in asthma Slower onset of action than SABA
62
SAMA LAMA A/e
Dry mouth, cough, constipation, urinary retention, headache, metallic taste Avoid eye contact – can precipitate glaucoma Rinse mouth after inhalation to decrease dry mouth (less with SAMA) Cardiovascular (stroke? iffy)
63
LABA and LAMA Examples. DOSE:
Salmeterol BID Formeterol BID Indacterol OD Oldaterol OD Vilanterol (Only combo) Tiotropium OD Aclindium BID Glycopyronnium OD Umeclidium OD
64
Compare LABA and LAMA
Both improve symptoms LAMA (tiotropium) may be superior in decreasing exacerbations LAMAs may be better tolerated (decreased withdrawal in RCTs) Side effect profiles vary LAMA: dry mouth, constipation LABA: headache, dose dependent CV effects (racing heart
65
ICS COPD
In contrast to asthma, inhaled corticosteroids should not be used as first-line medication. ICS should not be used as monotherapy ICS have evidence for reducing exacerbations, but inconsistent evidence for symptom improvement Patients with a higher eosinophil count may respond better Consider ICS side effects
66
Which agent? What should one consider?
evidence, Availability, Onset, Side effects, Guidelines
67
What LABAS work fast? WHich LAMA?
Formeterol, indacterol, oldaterol LABA Glycopyrrinium -- LAMA Work within minutes
68
Prophylatic azithromycin for who?
Recommended in patients who have normal QT interval on electrocardiograms(ECGs), no significant drug interactions with concomitant medications and no evidence of either indolent or active infection with atypical mycobacteria Reduced exacerbation rates and improved QOL compared to placebo. Azithromycin group had a higher rate of colonization with macrolide-resistant bacteria, and hearing deficits. May also see dosed 3 x weekly on 250mg OD x 1 year
69
N-acetylcysteine MOA? Dosage form? Dose? USe?
A mucolytic agent with antioxidant properties Mechanism of action of NAC in COPD is not clearly understood Optimal dose of NAC has not been determined Injectable solution is administered orally High-dose NAC, 600 mg orally twice daily, may be of benefit in reducing acute exacerbations in those who had 2 or more exacerbations in the previous 2-year period chronic bronchitic phenotype at high risk of exacerbations
70
Roflimast? MOA? Dose? USe? Spirometry? Rescue?
Phosphodiesterase IV inhibitor Administered once daily (500 mcg tablet per day) could be considered for addition to existing triple therapy (LAMA + ICS/LABA) for people with COPD who have had at least 1 exacerbation in the past year. Add-on to bronchodilator treatment chronic bronchitic phenotype at high risk of exacerbations  Improves FEV1, decreases exacerbations  Not be used as a rescue medication
71
Roflimast S/e?
diarrhea, weight loss, nausea, headache, sleep disturbances Neuropsych effects – avoid in hx of depression with suicidal ideation
72
Should theophylline be used in COPD?
NO - No longe rin guidelines
73
Mild Excaerbation
worsening or new respiratory symptoms without a change in prescribed medications
74
Moderate Exacerbation
prescribed antibiotic and/or oral corticosteroids
75
Severe Exacerbation:
requiring a hospital admission or ED visit
76
Low risk Exacerbation:
if they had 1 or less moderate exacerbation in the last year and did not require an ED visit or hospitalization
77
High risk exacerbation
if they had at least 2 moderate or 1 severe exacerbation in the last year requiring a hospital admissions/ED visit.
78
COPD Guidelines
STUDY CHART
79
In the most severe cases, what is a tx of COPD?
Lung Volume Reduction Surgery Lung Transplantation --> FEV1 <25% predicted and severe sx
80
Stepping Up and Down in COPD:
Stepping up: Usually treatment is progressive and additive No absolute interval time at which evaluation should be performed after initiating change in therapy --> consider 6 months after initiating long acting bronchodilator and 12 months after initiating ICS STEPPING DOWN: QUESTIONABLE If treatment benefits not realized, or side effects exceed benefits In patients on ICS at low risk of morbidity and mortality, and exacerbation who have had a long period of stability Close supervision and monitoring necessary Taper steroids if considering stopping
81
Definition of acute exacerbation:
sustained worsening of dyspnea, cough or sputum production leading to an increase in the use of maintenance medications and / or supplementation with additional medications.
82
Consequences of AECOPD
Reduced health-related QOL Accelerated decline in Lung function Increased Mortality Increased healthr esource ultilzation and costs
83
Acute Exacerbation TX:
1) Bronchodilators SAMA and SABA (salbutamol +/-ipratropium) become scheduled Increase dose and frequency long-acting inhalers can be continued but should not replace short-acting bronchodilators 2) Steroids (systemic) Improve spirometry; decrease relapse rate. Restore lung function quicker Dose: typically 30-50 mg daily prednisone (or equivalent) x5-14 days Antibiotics – should be given to: Patients requiring mechanical ventilation OR Patients with at least 2/3 of the cardinal symptoms: sputum purulence (change in phlegm color to yellow or green) increased sputum volume increased dypsnea
84
ANTIBIOTIC CONSIDERATION:
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PHARM 253 Exam 1 (8 decks)

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