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pharmacotherapy 2 > copd > Flashcards

copd Flashcards

1
Q

systemic consequences of copd progression

A

cardiac and skeletal muscle dysfunction, osteoporosis, depression, and anemia.
COPD is a major cause of morbidity and mortality and a significant cause of disability worldwide

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2
Q

copd classifies to:

A

Chronic bronchitis
characterized by chronic cough for at least 3 months for 2 consecutive years with inflammation and fibrosis of the small airways
Emphysema
characterized by alveolar wall destruction and airspace enlargement resulting in loss of gas-exchange surface area.

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3
Q

genetic factor in development of emphysema

A

The best documented genetic factor is a rare hereditary deficiency of α1-antitrypsin (Antiproteinase)
Severe deficiency of this enzyme results in premature and accelerated development of emphysema.

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4
Q

Difference in inflammatory reaction
asthma and copd cells and mediators

A

Asthma
* Eosinophils and mast cells
* IL-1, IL-8, and TNF-α.
COPD
* Neutrophils, macrophages, and CD8+ T lymphocytes
* proteinases such as elastase and proteinase-3.

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5
Q

protinease and antiprotinease imbalance

A

Increase: proteinase: lung prenchyma –> loss elasticity and remodling –>narrow

Decrease: antiprotinease( inhibit trypsin, elastase enzymes which cause destruction to lungs)

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6
Q

pathalogical changes due to obstruction aiflow

A
  • pulmonary hyperinflation
  • pulmonary HTN
  • mucus hypersecretion
  • ciliary dysfunction
  • airflow limitation
  • gas exchange abnormal
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7
Q

Emphysema

A

Permanent enlargement of the airway distal to the terminal bronchiole with destruction of alveolar walls.
Both airway and blood vessels destroyed
PaO2 is low and paCO2 is normal
Pink color, muscle wasting and weight loss, better prognosis

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7
Q

sign and symtpoms of copd

A
  1. chronic cough for 3 mnths
  2. Chronic Sputum Production
    3: dyspnea on rest and exertion and othopenea
    4: of heaviness in the chest.
    5: use of accessory muscles for respiration
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8
Q

Clinical Presentation and Diagnosis

A

1: pursed lips
2: barrel chest
3: lung auscultation
4: hypoxemia cynosis and tachycardia
5: corpulmonale : second heart sound, jugular venous distention (JVD), lower extremity edema, and hepatomegaly.

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9
Q

d

chronic bronchitis

A

Productive cough on most days for 3 months, for 2 consecutive years
Mucus hyper-secretion,
Loss of ventilation due to obstruction by mucus
paCO2 is high
Bluish face and lips, obese, poor prognosis

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10
Q

GOLD guidelines for diagnosis of copd

A
  1. perform spirometry
  2. cough
  3. dyspnea, worsning, persistant
  4. cough with suptum
  5. History of exposure to risk factors, especially tobacco smoke.
    * Spirometry revealing an FEV1/FVC less than 70% of predicted is the hallmark of COPD.
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11
Q

GOLD grade
Classification
Spirometry Results fev1

A
  • I mild ≥ 80
  • II moderate 50-79%
  • III severe 30% -49%
  • IV very severe <30% predicted or FEV1 <50% predicted plus chronic respiratory failure
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12
Q

difference between asthma and copd

A

age:Asthma < 40 copd >40
smoking: asthma not cause copd,(>10 pack-years).
sputum: infrequent copd often
allergies: asthma often copd infreqent.
course: asthma stable, copd progressive
spirometery: ashtma normla copd not normalixe
hyperactivity: ashtma
corticosteroid response: asthma
brnchodialtor response: asthma

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13
Q

Smoking Cessation
critical part of any COPD treatment plan because

A
  • it slows the rate of decline in pulmonary function
  • It reduces cough & sputum production
  • It decreases airways reactivity

Smoking cessation is the only intervention that has been shown to reduce mortality in COPD

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14
Q

5A and 5R

A
  1. ask
  2. advice
  3. assess
  4. assist
  5. arrange
  6. Relevance
  7. Risks
  8. Rewards
  9. Roadblocks
  10. Repetition
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15
Q

pulmonary rehabilitation program

A
  • exercise training, smoking cessation, nutrition counseling & education.
  • for symptomatic patients with FEV1 <50% predicted.
  • The minimum length of an effective program is 6 weeks
  • Pulmonary rehabilitation results in significant and clinical improvements in dyspnea, exercise capacity, health status, and health care utilization.
16
Q

Long-Term Oxygen Therapy

(LTOT)

A

indication: for resting hypoxemia (PaO2 ≤ 55 mm Hg or oxygen saturation ≤ 88%). pulmonary hypertention, peripheral edma suggesting chf, polycythemia
delivery of Oxygen: dual-prong nasal cannul for more thn 15 hr day
Goals of LTOT: O2 saturation to ≥ 90% and/or PaO2 to ≥ 60 mm Hg, allowing adequate oxygenation of vital organs.

Continue lifetime after using
air travel increase to 3l/min
smoking with o2 may cause explosion

17
Q

surgurical option for cods

A
  • Bullectomy
  • volume reduction surgery
  • lung transplantation

result in improved spirometry, lung volumes, exercise capacity, dyspnea, health-related quality of life, and possibly survival.

18
Q

lama vs laba

A

poet trail: lama> laba in reducing excerbation
cochrane review: lama> laba in hopitilization and excerbation prevention
while symptoms and qol same
flame trail: laba/lama> ics/ ;aba

19
Q

α1-Antitrypsin Augmentation Therapy
indicated for?

A
  • Augmentation therapy consists of weekly transfusions of human AAT
  • for individuals with AAT deficiency and moderate airflow obstruction (FEV1 35%–60% predicted).
  • it reduce overall mortality and slow decline in FEV1
20
Q

Triple Therapy

A
  • Ellipta® is a combination of ICS/LAMA/LABA (Fluticasone furoate/umeclidinium/vilanterol) “Available in Bahrain
  • improve lung function and HQOL while reducing the number of exacerbations.
    The ETHOS trial:
    ICS/LAMA/LABA had lower mortality in symptomatic COPD patients compared to LABA/LAMA and no differences were found when compared with LABA/ICS.
21
Q

Antibiotics – Chronic Therapy
Azithromycin / Erythromycin

A

Actions are anti-inflammatory and antibacterial.
Daily azithromycin at 250 mg orally for 1 year has been shown to:
1. Lengthen time to first exacerbation.
2. . Decrease overall exacerbation rate.
3. . Improve quality of life

  • Azithromycin 500 mg orally 3 times per week and erythromycin500 mg orally twice daily have reduced exacerbations
  • Recommended as add-on to treatment intensification with
     LABA + LAMA +/- ICS if eosinophils < 100 cells/mcL and former smoker.
22
Q

Antibiotics – Active Infections

A

Antibiotics are beneficial if 2 of the following 3 symptoms are present during an acute exacerbation:
* increased dyspnea
* sputum volume
* sputum purulence

23
Q

Antibiotics for hospitlize and outpatient

A

hospitilize patient:Pseudomonas aeruginosa.
outpatients: amoxicillin
risk factors for poor outcomes should receive a broader-spectrum antibiotic
* beta-lactam + beta-lactamase inhibitor
* quinolones
* 2nd or 3rd generation cephalosporin

24
Q

patient group A
symp, excerbation
treatment

A

symptoms and excerbations
1. CAT <10
2. no hospitilization
3. ≥1 excerbation

treatment
bronchodilator ( short or long)

25
Q

patient group B
symp, excerbation
treatment

A

symptoms and excerbations
1. CAT ≥10
2. no hospitilization
3. ≥1 excerbation

treatment
LAMA or LABA

26
Q

patient group C
symp, excerbation
treatment

A

symptoms and excerbations
1. CAT <10
2. ≥1 hospitilzation
3. ≥2 excerbation

treatment
LAMA

27
Q

patient group D
symp, excerbation
treatment

A

symptoms and excerbations
1. CAT ≥10
2. ≥1 hospitilzation
3. ≥2 excerbation

treatment
LAMA,
LAMA + LABA (if cat>20)
LABA+ ICS( if esnophil >300)

28
Q

An exacerbation is defined as

A

an acute event characterized by a worsening of the patient’s respiratory symptoms that is beyond normal day-to-day variations and leads to a change in medication

COPD Patients have on average 1 - 2 exacerbations / yr with the frequency increasing with disease progression.

29
Q

Severity of an exacerbation is assessed by

A

clinical presentation, not through spirometry due to the difficulty of doing the test and interpretation of the results.

30
Q

clinical signs of excerbation

A

severe COPD exacerbation (e.g. use of accessory muscles to breathe, cyanosis, peripheral edema) should be admitted to the hospital.

** life threatening exacerbation** (e.g. mental status changes, worsening respiratory status despite ventilator support, hemodynamic instability) should be admitted to ICU

31
Q

Pharmacological Management of excerbation

A
  • SABA ± ipratropium is standard bronchodilator therapy during COPD exacerbation.
  • I.V. aminophylline is a 2nd-line for critical p
  • On discharge, maintenance therapy should include long-acting anticholinergic or inhaled corticosteroid plus LABA.

Previous medications should be continued during an exacerbation. However, long-acting anticholinergics should be discontinued if ipratropium is used.

pharmacotherapy 2 (15 decks)

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