COPD Flashcards

1
Q

COPD definition

A

Disease state characterized by airflow
limitation that is not fully reversible but
progressive with an abnormal inflammatory
response of the lung to noxious particles or
gases

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2
Q

COPD is comprised of

A

Chronic bronchitis + emphysema

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3
Q

difference between bronchitis and emphysema

A

Bronchitis is inflammation of large airways
emphysema is inflammation of alveoli

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4
Q

Difference between COPD and asthma

A

COPD- Onset in mid-life
Symptoms slowly
progressive
Long smoking history
Largely irreversible
airflow limitations

Asthma- Onset early in life,
family history of
asthma
Symptoms vary from
day to day
Symptoms at
night/early morning
Allergy, rhinitis,
eczema also present
Largely reversible
airflow limitation

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5
Q

Risk factors of COPD main two categories

A

Host factors
Environmental factors

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6
Q

Host factors that affects COPD

A

Genes- alpha 1 antitrypsin deficiency
Gender- female smokers at higher risk
Lung growth- childhood infections, maternal infections

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7
Q

Environmental factors that affect COPD

A

o Tobacco smoke
o Occupational dust- wood dust
o Pollution
o Infections
o Socioeconomic status

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8
Q

Pathophysiology of COPD - central airways

A

mucus hypersecretion,
ciliary dysfunction → chronic cough, sputum
production

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9
Q

Pathophysiology of COPD - peripheral airways

A

Airway remodelling, scar
tissue formation → fixed airway limitation,dynamic hyperinflation → low FEV1, high TLC,
rhonchi, barrel chest

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10
Q

Pathophysiology of COPD - parenchyma

A

emphysema → loss of elastic
recoil, impaired gas exchange → low DLCO,
hypoxaemia

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11
Q

Pathophysiology of COPD - vasculature

A

hypoxia →pulmonary
vasoconstriction → pulmonary hypertension
→ right ventricular hypertrophy (RAD< R in
V1, RBBB) → Right ventricular failure
(oedema, raised JVP, hepatomegaly)

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12
Q

Hx in COPD

A


* chronic cough (intermittent or daily-cough
and sputum production for >3months,>2
years),
* chronic sputum production,
* breathlessness (progressive and
exertional),
* wheeze
* minimal day to day variation,
* worsening of symptoms with infections
* exposure to risk factors (smoking,
occupational dusts, smoke from home
cooking)

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13
Q

Physical signs of COPD

A
  • usually late,
  • thin wasted person,
  • hyperinflation of chest, barrel shaped
    chest, reduced cardiac dullness, liver
    pushed down
  • Prolong expiration, B/L rhonchi on
    auscultation,
  • cyanosis and polycythaemia,
  • oedema
  • cor-pulmonale
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14
Q

Two clinical presentations of COPD

A

Blue bloaters
Pink puffers

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15
Q

Blue bloaters Sx

A

Chronic, productive cough
Purulent sputum
Hemoptysis
Mild dyspnea (initially)
Cyanosis
Peripheral edema
Crackles, Wheezes
Prolonged expiration
Obese

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16
Q

Pink puffers Sx

A

Dyspnea
Minimal cough
Increased minute ventilation
Pink skin, Pursed lip breathing
Accessory muscle use
cachexia
Hyperinflationm Barrel chest
Decreased breath sounds
Tachypnea

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17
Q

Complications of blue bloaters

A

Secondary polycythemia vera due to hypoxemia
Pulmonary HTN due to reactive vasoconstriction from hypoxemia
Cor pulmonale from chronic pulmonary HTN

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18
Q

Complications of Pink puffers

A

Pneumothorax due to bullae
Weight loss due to work of breathing

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19
Q

FEV1/FVC ratio of COPD

A

<70% ( Obstructive disease)

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20
Q

FEV1 level in COPD

A

<80% predicted

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21
Q

TLC, FRC, RV

22
Q

DLCO levels in COPD

23
Q

DDs of COPD

A
  • Long standing breathlessness –
    1. chronic persistent asthma, chronic
    heart failure
  • Chronic cough – bronchiectasis,
    tuberculosi
24
Q

Management of COPD

A
  • Diagnose, assess, monitor
  • Reduce risk factors
  • Manage stable COPD
  • Management of exacerbation
    o Controlled oxygen through mask
    o Nebulized bronchodilators (salbutamol,
    ipratropium
    o Antibiotics
    o Oral prednisolone – 40 mg/day
25
Pulmonary rehabilitation
Education and training program to help patient to live an active life within the limitation of symptoms
26
Pulmonary rehabilitation
* Stopping smoking * Controlling breathlessness o Breathing control o Pursed lip breathing o Correct posture * Stopping smoking * Controlling breathlessness o Breathing control o Pursed lip breathing o Correct posture
27
Complications of COPD
* recurrent exacerbations by URTI, * cor-pulmonale, * type II respiratory failure, * pneumothorax, * polycythaemia * systemic effects (muscle wasting, muscle fatigue
28
MMRC dyspnea scale
0 - vigourous exertion 1- rapid walking / climbing uphill 2- normal speed wailking 3- 100m / few minutes of level ground walk 4- Stationary activity – dressing, undressing etc. Can’t leave home
29
CAT ( COPD assessment tool)
score each from 0-5 (good - 0 to worst -5) 1. Cough 2. Sputum 3. Chest tightness 4. Dyspnoea 5. ADL 6. Sleep 7. Confidence in walking out 8. Energy
30
Dx steps in COPD
1. Spirometrically confirmed Dx - Post bronchodilator FEV1/FVC <70% 2. Assessment of airflow limitation - Predicted FEV1 GOLD 1 >= 80 GOLD 2 50-79 GOLD 3 30-49 GOLD 4 <30 3. Assessment of Sx/risk of exacerbations - table
31
Assessment of Sx/ risk of exacerbations. Y axis and X axis
Y axis - exacerbation Hx X axis - Sx
32
Y axis
0 or 1 (not leading to hospital admission) >=2 or >=1 leading to hospital admission
33
X axis
mMRC 0-1 and CAT <10 mMRC >=2 and CAT >=10
34
Group A in COPD Mx
mMRC 0-1 CAT <10 0-1 exacerbations and no hospital admissions
35
Group B in COPD Mx
mMRC >=2 CAT >=10 0-1 exacerbations and no hospital admissions
36
Group C in COPD Mx
mMRC 0-1 CAT<10 >=2 or >=1 w hospital admission
37
Group D COPD Mx
mMRC >=2 CAT >=10
38
Group B Drugs COPD
LAMA or LABA persistent Sx LAMA+LABA
38
Group A Drugs in COPD
LAMA or LABA evaluate the effect Continue, stop or try alternative class or bronchodilator
39
Group C drugs COPD
LAMA further exacerbations LAMA+LABA or LABA+ICS
40
Group D drugs COPD
Start w LAMA further exacerbations LAMA+LABA or LABA+ICS further worsening LAMA+LABA+ICS further exacerbations Consider Roflumilast (if FEV1 <50% predicted and pt has chronic bronchitis) OR Consider Macrolides (in former smokers)
41
When to consider LTOT for COPD
if PaO2 <55mmHg Should be given at least 15h/d
42
Mortality benefit in COPD
Cessation of smoking Long term O2 therapy Lung vol reduction therapy
43
Indications of NIV for COPD exacerbations
PaCO2 >45mmHg Persistent hypoxia despite other exacerbation measures Clinical severe dyspnea w progression to exhaustion
44
Pack years calculation
(No of Cig smoked per day/ 20) x No of years smoked
45
Barrel chest
AP diameter > transverse
46
How does COPD cause the right heart to fail
In alveoli that are not adequately oxygenated, blood supply for perfusion will not happen. BV will undergo vasoconstriction. (Coz there's no point sending blood to these alveoli) This causes pulm HTN ( causes RVH coz of extra pressure in RV) RVH causes RAD ( tall wave in V1) At some point, R heart will fail ( Ascites, Edema, increases JVP, Hepatomegaly)
47
meaning behind Pink puffers
usually in people increasing CO2 levels stimulate the respi centre in the medulla. But in pink puffers, hypoxia stimulates the respi centre, so they are always gasping for breaths. Therefore, they are not cyanosed.
48
meaning behind blue bloaters
they are not sensitive to hypoxia. ( Respi centre is not stimulated by hypoxia) so they are not cyanotic. Kidneys will also undergo hypoxia. Renal hypoxia will trigger RAAS. causing Sodium- water retention giving edema
49
% of controlled oxygen given in COPD and the target SpO2
25-28% target SpO2 - 88-92%
50