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MDRS > COPD > Flashcards

COPD Flashcards

1
Q

What is COPD? according to CDC

A 
A respiratory disorder largely caused by
smoking
characterized by:
- progressive
- partially reversible airway obstruction
- lung hyperinflation
- systemic manifestations
- increasing frequency and severity of
exacerbations
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2
Q

What is COPD according to GOLD?

A
  • A preventable and treatable disease with some significant extra pulmonary effects
  • Its pulmonary component is characterized by airflow limitation that is not fully reversible.
  • The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases.
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3
Q

What are the 2 disease included in COPD?

A

chronic bronchitis and

emphysema

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4
Q

Total pack years formula

A

Total pack years=

(# cigarettes smoked/day) / 20 x # yrs of smoking

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5
Q

What incresed risk of COPD?

A

–>10 pack yr smoking hx or ex smoker/current smoker>40yrs

  • persistent cough and sputum production
  • frequent respiratory tract infections
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6
Q

What are the risk factors of COPD

A
  • Active Exposure to Tobacco Smoke: cigarette smoking is related to 80 90% of all cases.
  • Non smoking risk factors (10 20%):
  • ->Occupational exposure to gold, coal, asbestos,
  • ->Environmental exposure to wood smoke, sulphur
  • ->Genetic factors including alpha 1 antitrypsin deficiency.
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7
Q

What is the deal with pathogenesis of COPD?

A

a combination of exposure to noxious agent and genetic factors can lead to COPD

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8
Q

How does smoke lead to COPD

A
  1. inflammatory cells
    - ->macrophages, neutrophiles, T-lymphocytes
  2. release of
    inflammatory mediators
    –>TNF, interlukins, leukotrienes
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9
Q

What is the effect of inflammatory cell after smoking

A
  • it increases the proteases (found in macrophages and neutrophiles) in the body which:
  1. breaksdown connective tissue (elastin and collagen)
    of lungs
    2.depress protease inhibitors (alpha 1 antitrypsin)
    3.loss of protective mechanism
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10
Q

What is the clinical manifestation caused by smoking ?

A
  1. emphysema
    - -> alveolar septa destruction
    - ->loss of elastic recoil of bronchial wall
  2. chronic bronchitis
    - ->hypersecretion of mucus
    - ->bronchial edema
    - ->bacterial infection
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11
Q

What are the result of the clincal manifestation?

A
  1. airway obstruction
  2. air trapping
  3. decrease gas exchange due to loss of alveolar surface area
  4. infection and bronchospasm
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12
Q

How to identify patient with POSSIBLE COPD?

A

** smoker or ex-smoker who is > 40 yrs old

Yes to ONE of these questions:

  1. do you cough regularly
  2. DO you cough up sputum regularly
  3. Do simple chores make you short of breath
  4. Do you wheeze when you exert yourself or at night
  5. DO you get frequent colds that persists longer that those ppl you know?
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13
Q

If patient answer yes to those question and is or was a smoker >40 yrs, what does it mean?

A

pt POSSIBLY have COPD

–> still need to be confirmed by SPIROMETRY

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14
Q

What is the spirometry for criteria for diagonsis COPD according to CTS?

A

Airflow obstruction is defined as post BD

FEV1/FVC <0.7 which is not fully reversible

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15
Q

Def of CB?

A

chronic productive cough for 3 months in each of 2 successive years in a patient whom
other causes of productive chronic cough have
been excluded. (TB, Bronchiectasis)

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16
Q

Def of emphysema?

A 
characterized by
1)  abnormal &amp;
permanent enlargement of airspaces distal to
the terminal bronchiole &amp;
2) destruction of
alveolar wall
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17
Q

Anatomic Alterations of the Lungs with

Chronic Bronchitis?

A
  1. Chronic inflammation and swelling of the peripheral airways
  2. Excessive mucus production and accumulation
  3. Partial or total mucus plugging of the airways
  4. bronchospasm
  5. Air trapping and hyperinflation of alveoli
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18
Q

What is the effect of anatomic alteration of CB?

A
  1. expiratory flow limitation
  2. hyperinflation of the lung
  3. decrease gas exchange
  4. V/Q mismatch , hypoventilation
  5. shunt
  6. hypoxemia
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19
Q

Why does inspiratory flow isn’t limited but expiratory flow is?

A
  1. negative pressure generated during inhalation pulls airway open, gives room for airflow to rush in
  2. positive throacic pressure compresses the bronchio, on top of existing bronchospasm , not allowing space for gas to escape
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20
Q

What is Emphysema

A

the presence of permanent enlargement of the airspaces,

  • ->distal to terminal bronchioles
  • ->with destruction of alveolar walls without fibrosis
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21
Q

What is the Anatomic Alterations of the Lungs

Associated with Emphysema

A
  1. Permanent enlargement and deterioration of
    the air spaces distal to the terminal

2.Destruction of pulmonary capillaries

3.Weakening of the distal airways, primarily the
respiratory bronchioles

4.Air trapping and hyperinflation of alveoli (air
trapping)

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22
Q

What is the deal with dynamic airway collapse?

A

caused by 2 things

  1. due to tissue destruction of distal airways, primarily the respiratory bronchioles–>tissue collapse easily
    - these tendency of collapse increase the resistance of the distal airway causing a greater pressure drop as flow is coming out of the alveolar
  2. these respiratory bronchioles are supported by cartilages thus, easily collapse when the pleural pressure is higher than the equal pressure point
    * these causes dynamic airway collapse during normal expiration in COPD or forced expiration in normal person
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23
Q

how does purse lip breathing help with dynamic airway collapse?

A
  • pursed lip breathing imposes a resistance to expiratory flow, which increases the pressure inside the airway. This pressure is transmitted to the distal airway and respiratory bronchioles helping to stent airways open, preventing dynamic airway collapse thus help with exhalation
24
Q

What are 2 types of Types of Emphysema

A

Centrilobular (centriacinar)

Panlobular (panacinar)

25
Q

characteristic of Centrilobular (centriacinar)

A

location
–> upper lung fields

  • septal destruction at the centre of the lobules
  • Abnormal
    weakening and enlargement of the respiratory
    bronchioles in the proximal portion of the acinus.
26
Q

characteristic of Panlobular (panacinar)

A

Location

  • entire acinus
  • lower and anterior lung fields
  • less common
  • bullae
  • caused by alpha 1 anti-trypsin deficiency
27
Q

What is acinus

A

the portion distal to the terminal bronchioles

including

  • respiratory broncioles
  • alveolar duct
  • alveolar sac
28
Q

What is Alpha1

Antitrypsin Deficiency

A
  • a genetic disorder Inherited genetic disorder affecting the lung, liver
29
Q

What is the fxn of Alpha1

Antitrypsin

A
  1. made in the liver

2. an enzyme that protects lung by inhibiting the protease/elastase releated by neutrophiles in response in inflammation

30
Q

What is the relationship between AATD and smoking

A

Cigarette smoking significantly increases the risk factor for early onset emphysema in patients

–> onset of dyspnea around 30 years of age.

31
Q

What are the phenotypes of AATD?

A

MM–> normal level
ZZ–>severely low AA in serum
MZ–>intermediate deficiency

32
Q

What is the symtopms of COPD

A

cough
sputum
dyspnea

33
Q

What are the goals in managing COPD

A
  • a combination of pharmcotherapy and non- pharmacological interventions in order to improve symptoms and quality of life
34
Q

what are the effects of COPD management

A
  1. Prevent progression (smoking cessation)
  2. Decrease frequency of exacerbation
  3. Alleviate respiratory symptoms
  4. Improve exercise tolerance and daily activity
  5. Treat exacerbations/complications
  6. Improve overall health
  7. Reduce mortality
35
Q

What is the purpose of the MRC dyspnea scale?

A
  • to assess severity of dyspnea
36
Q

What are the grading of the MRC dyspnea scale?

A

Grade1: breathless with strenous exercise

Grade2: short of breath when hurrying on the level/ walking up a slight hill

Grade 3: walks slower than people of the same age on the level or stops for breath while wlaking at own pace on the level

grade 4: stops for breaths after walking 100 yards

Grade 5: Too breathless to leave the house or breathless when dressing

37
Q

How to eveulate severity of COPD

A

MRC dyspnea scale

COPD assessment test (CAT)

38
Q

What is the CAT assessment

A

This is a patient completed questionnaire

assessing all aspects of the impact of COPD

39
Q

How does the scoring working on CAT test?

A

There are 8 questions on a 1 to 5 point scale.

score <10 –> mild impact

Score >10 –> mod to severe impact of COPD

40
Q

What are the 5 strategy to help patient quit smoking

A
  1. ask
  2. advise
  3. assess
  4. assist
  5. arrange
41
Q

What are 2 vaccnie to prevent AECOPD?

A

annual influenza

pnuemococcal ( every 5 - 10 yrs)

42
Q

What are the

progression of prevention of AECOPD?

A
  1. smoking cessation + vaccination
  2. self management education + written AECOPD action plan
  3. pulmonary rehabiltation
  4. optimize treatment for pharcotherapy

(short course oral systemic steriods & antibotics for purulent secretions)

5.optimize Tx for AECOPD

43
Q

What are the physical symptoms of withdrawal

A 
craving for nicotine
nervousness
irritability
anxiety
drowsiness
sleep disturbances
impaired concentration 
increase appetite/weight gain
44
Q

What are the indication of smoking cessation? drug therapy

A
  • aid to smoking cessation to relieve symptoms of withdrawal
45
Q

What is the goal of smoking cessation drug therapy?

A
  1. give inital smoking replacement, then gradual withdrawal
46
Q

What leads to nicotine addiction?

A
  • nicotine addition is bassis for tobacco dependence
  1. Nicotine binds to receptors in CNS secreting dopamine
    causing feelings of pleasure & cognitive arousal

2.Stimulates acetylcholine receptors at sympathetic and
parasympathetic autonomic ganglia

47
Q

What is the advantage of smoking cessation drug therapy?

A

prevent cause of cardiovascular and lung disease

48
Q

Definition of AECOPD

A
  1. A sustained worsening of dyspnea, cough
    or sputum production
  2. leading to an increase in the use of maintenance medications
  3. and/or supplementation with
    additional medications.

4.It is further
classified as purulent or non purulent.

49
Q

Who are COPD patient at risk of death

A
  1. FEV 1 less than 35%,
  2. MRC 4-5
  3. poor nutrition status , BM<19
  4. recurrent severe exacerbation
  5. pulmonary hypertension
  6. cor pulmonale
50
Q

what are the criteria for lung transplant

A
  1. FEV1< 25%

2. PaO2 <55 or cor. pulmonale

51
Q

What are the personal management plan for COPD

A

PRIME PLAN

  1. prevent further dmg to lung
  2. Relieve symptoms
    - ->optimize pharmacotherapy
    - ->coping mechanism
  3. improve
    - ->general health and PA level
  4. manage
    - ->excerbation
  5. establish
    - ->COPD team
52
Q

what is the treatment used in nicotine replacement therapy

A 
Nicotine polacrilex (short acting) 
nicotine transdermal (long acting)
53
Q

what is the fxn of nicotine polarcrilex

A

quick acting system that uses a specific ion channel to maximize the amount of nicotine released & absorbed by the oral mucosa

54
Q

what are the nicotine replacement devices?

A

– Inhaler
– Chewing gum
– Lozenge
– Nasal spray

55
Q

what are the drugs used in NRT

A

Bupropion (Zyban)

Varenicline (Champix)

56
Q

what is Bupropion

A

Antidepressant; also used to reduce cravings and withdrawal symptoms

57
Q

what is varencinline?

A

Low to moderate level dopamine stimulation

MDRS (23 decks)

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