COPD Flashcards

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1
Q

What does COPD stand for, and the epidemiology of it in ireland?

A

chronic obstructive pulmonary disease

Studies in Europe estimate the prevalence of COPD to be approximately 10%, however it varies considerably between European countries.

—-Ireland has the highest rate of admissions for exacerbations of COPD in the Organisation for Economic Co-operation and Development (OECD) countries.

——COPD is more common in older people; European studies in people aged >70 years showed a prevalence of COPD of 20% in men and 15% in women.

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2
Q

What does COPD stand for, and the epidemiology of it in ireland?

A

chronic obstructive pulmonary disease

Studies in Europe estimate the prevalence of COPD to be approximately 10%, however it varies considerably between European countries.

—-Ireland has the highest rate of admissions for exacerbations of COPD in the Organisation for Economic Co-operation and Development (OECD) countries.

——COPD is more common in older people; European studies in people aged >70 years showed a prevalence of COPD of 20% in men and 15% in women.

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3
Q

what are the causes of COPD

A

Causes
• Cigarette smoking
• Genetic—bronchial hyperresponsiveness; α1-antitrypsin deficiency • Race—Chinese and Afro-Caribbeans have d susceptibility
• Diet—poor diet and low birthweight

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4
Q

what are the presenting symptoms of COPD

A

A diagnosis of COPD should be considered in patients over the age of 35 who have a risk factor (generally smoking) and who present with one or more of the following symptoms:

  • -Exertional breathlessness
  • -Chronic cough
  • -Regular sputum production

Frequent winter ‘bronchitis’
Wheeze

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5
Q

what is the diagnosis for COPD

A

A diagnosis of COPD should be considered in patients over the age of 35 who have a risk factor (generally smoking, occupational exposure) and who present with one or more of the following symptoms:

  • -Exertional breathlessness (dyspnoea)- dyspnea that is progressively getting worse, and persistent
  • -Chronic cough-may be intermittend and may be unproductive
  • -Regular sputum production- any pattern

The diagnosis of COPD is based on a combination
of history and physical examination with confirmation of the diagnosis using spirometry.

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6
Q

Diagnosis of COPD…

what fev/fev1 ratio for clinical diagnosis?
what FEV1 ?
% response to bronchodilator reversibility test?

A

less than 0.7
less than 70% predicted
less than 15% response

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7
Q

what are the causes of COPD

A

Causes
• Cigarette smoking
• Genetic—bronchial hyperresponsiveness; α1-antitrypsin deficiency • Race—Chinese and Afro-Caribbeans have d susceptibility
• Diet—poor diet and low birthweight

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8
Q

what are the presenting symptoms of COPD

A

A diagnosis of COPD should be considered in patients over the age of 35 who have a risk factor (generally smoking) and who present with one or more of the following symptoms:

  • -Exertional breathlessness
  • -Chronic cough
  • -Regular sputum production

Frequent winter ‘bronchitis’
Wheeze

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9
Q

what is the diagnosis for COPD

A

A diagnosis of COPD should be considered in patients over the age of 35 who have a risk factor (generally smoking) and who present with one or more of the following symptoms:

  • -Exertional breathlessness (dyspnoea)
  • -Chronic cough
  • -Regular sputum production

The diagnosis of COPD is based on a combination
of history and physical examination with confirmation of the diagnosis using spirometry.

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10
Q

what is spirometry? what does it measure.

A

Spirometry measures

—the volume of air forcibly exhaled from the point of maximal inspiration (FVC - forced vital capacity)

—-the volume of air exhaled during the 1st second of this manoeuvre (FEV1 forced expiratory volume in one second);

—-the ratio of these two measurements (FEV1/FVC) is calculated

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11
Q

what fev/fev1 ratio confirms COPD post bronchodilator?

A

less than

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12
Q

What investigations should be carried out to rule out other conditions that may be attributing to the COPD?

A

—–a chest x-ray to exclude other conditions such as lung cancer and tuberculosis.

—-serial peak flow measurements (to exclude asthma, which is frequently indistinguishable from COPD),

—–ECG and echocardiography (to assess cardiac status if there are clinical features of cor pulmonale)

—-and alpha-1 antitrypsin deficiency (if early onset, minimal smoking history or positive family history)

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13
Q

describe the MRC dyspnea scale? (used to provide an objective measure of breathlessness)

A

MRC dyspnoea scale

Grade Degree of breathlessness related to physical
activity

1 Not troubled by breathlessness, except on strenuous
exercise


2 Short of breath when hurrying or walking up a slight hill


3 Walks slower than contemporaries on level ground
because of breathlessness or has to stop for breath
when walking at own pace


4 Stops for breath after walking 100m or after a few
minutes on level ground


5 Too breathless to leave the house or breathless on
dressing/undressing

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14
Q

describe the classification system (GOLD) for COPD? (based on FEV1 values)

A

GOLD 1 Mild FEV1 ≥80% predicted

GOLD 2 Moderate 50%- 80% FEV1 predicted

GOLD 3 severe 30%-49% FEV1 predicted

GOLD 4 VERY severe less than 30% predicted

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15
Q

what are the 4 main goals of COPD management?

A

The main goals in the management of COPD are to improve the patient’s health by:

(1) reducing symptoms,
(2) reducing the rate of lung function decline,
(3) preventing exacerbations and
(4) reducing mortality

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16
Q

what are the signs of COPD?

A

Signs May be none. Possible signs:

• Hyperinflated chest ± poor chest expansion on inspiration
• dec cricosternal distance
• Hyperresonant chest with d
cardiac dullness on percussion
• Wheeze or quiet breath sounds
• Paradoxical movement of
lower ribs
• Use of accessory muscles
• Tachypnoea
• Pursing of lips on expiration
(purse lip breathing) 
• Peripheral oedema 
• Cyanosis
• inc JVP
• Cachexia
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17
Q

what is the DDX for COPD?

A

asthma, bronchiectesis, lung cancer, heart failure

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18
Q

compare COPD with asthma under these headings:

onset, smoking hx, breathlessness, chronic prod cough, waking at night with wheeze/cough

A

COPD ——>

onset opposite to all of above

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19
Q

Assessment of a patient with COPD is based on three things, what are they?

A

severity of airflow
severity of symptoms
risk of future exacerbations

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20
Q

how is the risk of exacerbation assessed?

A

by spirometry- this helps us classify according to the GOLD classification

by assessing the no of exacerbations in the past 12 months

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21
Q

non-pharm treatment of COPD?

A

Smoking cessation & nicotine replacement therapy
Patient education
exercise
pulmonary rehabilitation programmes
ambulatory oxygen therapy (AOT)
LTOT- long term administration of oxygen therapy
Non-invasive positive pressure ventilation (NIV)

other—
pollution- indoor and outdoor
occupational exposure
physical activity

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22
Q

what Pharmacotherapeutic agents should be offered to aid smoking cessation?

A

need to do this

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23
Q

what is LTOT?
what are the indications?
how beneficial is it?

A

Long-term administration of oxygen therapy (LTOT) (> 15 hours per day) in patients with chronic respiratory failure has been
shown to increase survival in patients with severe resting hypoxaemia.1,8 LTOT is indicated for patients who have a PaO2
≤7.3
kPa or a PaO2 of 7.3-8.0 kPa with evidence of pulmonary hypertension, peripheral oedema with congestive cardiac failure or
polycythaemia, when assessed on two separate occasions

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24
Q

what is NIV?

A

Non-invasive positive pressure ventilation (NIV) is increasingly being
used in patients with stable very severe COPD, who may have required assisted ventilation during an exacerbation

refers to positive pressure ventilation delivered through a noninvasive interface (nasal mask, facemask, or nasal plugs), rather than an invasive interface (endotracheal tube, tracheostomy).

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25
Q

list the main classes of pharmacological treatment of COPD?

inhaled ones….

A
SABA
LABA
SAMA
LAMA
combination of LABA and LAMA
ICS
Combination of LABA and ICS
26
Q

list the main classes of pharmacological treatment of COPD?

oral ones….

A

methylxanthines
phosphodiesterase 4 inhibitors
systemic corticosteroids

27
Q

name nicotine replacement therapy

A

varenicline or bupropion

28
Q

drug treatment of COPD, flow pathway, fig 11.4 Oxford Handbook GP

A

fig 11.4 Oxford Handbook GP

29
Q

DDX of COPD?

give the clinical signs associated with each of them that differentiate it from COPD

A

Asthma- onset early in life, symptoms very widely from day to day, symptoms worse at night/early morning, allergy/rhinitis/ezcema present, family hx also present

CHF- chest xray would show dilated heart, PFT’s indicate volume restriction not airflow limitation

bronchiectasis- large volumes of purulent sputum, commonly associated with abcterial infection, chest xray would show bronchial dilation, bronchial wall thickkening

TB- chest xray shows lung infiltrate, micro confirmation,

30
Q

what is normal FVC? normal FEV1? (in litres)

A

5L…….4L

31
Q

in obstructive lung diseases (COPD) which is affected more, the FVC or the FEV1?

A

FEV1- the lower the FEV1 the worse the prognosis

expiration is longer than normal

FVC is less than normal (not to the same extent as FEV1) but just takes longer to breath out

32
Q

when performing spirometry are patients seated/standing?

how long are they advised to breathe out for? (secondds)

A

exhalation must conatinue until no more air can be exhaled, it must be at least 6 seconds and no longer than 15 seconds

33
Q

what happens to the FVC/FEV1 ratio in restrictive lung diseases?

A

greater or equal to 80%…not really changed. this is in stark contrast to obstructive lung diseases!

34
Q

what happens to TLC, FRC, RV in obstructive and restrictive lung diseases?

A

Obstructive lung volumes > normal (􏰄TLC,􏰄FRC,􏰄RV)

restrictive lung volumes

35
Q

describe/defiine COPD?

A

COPD is a disease state characterised by airflow limitation that is not fully reversible.

The airflow limitation is in most cases both progressive and associated with an abnormal inflammatory response of the
lungs to noxious particles or gases.

36
Q

describe the pathology of COPD?

and the changes that occur in the lungs?

A

COPD is the result of a chronic inflammatory response in the

  • ——-large airways (chronic bronchitis),
  • ——-the small airways (bronchiolitis which may progress to fibrosis)
  • ——and the lung parenchyma (emphysema).

Airflow obstruction arises as a result of progressive thickening, fibrosis and smooth muscle hypertrophy of the
small airways, along with the loss of elastic recoil pressure due to pulmonary emphysema.

Pathological changes that occur include mucus hypersecretion, ciliary dysfunction, airflow limitation, pulmonary hyperinflation and gas exchange abnormalities

37
Q

what happens in advanced COPD disease to the heart?

other systemic associations?

A

In advanced disease, pulmonary hypertension, right ventricular
hypertrophy and right ventricular failure may occur.

Systemic changes that may occur in advanced disease
include osteoporosis, low body-mass index, and abnormal skeletal muscles with reduced muscle strength.

38
Q

what is the average decline in FEV1 per year?

normal adults?
COPD patients?
smokers?

A

Normal ageing results in an
average decrease in FEV1 of 20 ml/year, which is increased in smokers to 45 ml/year. Those who are
susceptible to COPD have an accelerated decline of 50-70 ml/year.1

39
Q

main DDx of COPD?

A

The main differential diagnoses
are chronic bronchitis, chronic asthma or congestive cardiac failure. These may be difficult to differentiate
and frequently co-exist.

Rarer differential diagnoses include: bronchiectasis, lung cancer, bronchopulmonary obliterans and chronic sarcoidosis

40
Q

name 3 B2 agonists (bronchodilators)?

A

albuterol, salmeterol, terbutaline

Albuterol for acute asthma; salmeterol for long- term asthma or COPD control;

terbutaline to reduce premature uterine contractions

41
Q

name 2 muscarinic antagonists? (aka anticholinergic)

A

ipatropium, tiotropium

42
Q

what do anticholinergics do? MOA?

A

Anticholinergics prevent the increase in intracellular concentration of Ca++ which is caused by interaction of acetylcholine with the muscarinic receptor on bronchial smooth muscle. Ca++ release is mediated by the second messenger system consisting of IP3 (inositol triphosphate) and DAG (diacylglycerol)

increased calcium leads to smooth muscle contraction……

43
Q

what drugs may cause exacerbations of asthma?

A
beta blockers (antiarrhythmiacs, class II)
ending in -olol

Nonselective antagonists (β1 = β2)—nadolol, pindolol (partial agonist), propranolol, timolol

Nonselective antagonists mostly go from N to Z (β2 with 2nd half of alphabet)

ASPIRIN/ NASAIDS (ibuprofen)

ACE InHIBITORS-

44
Q

describe the pathology of chronic bronchitis?

A

A form of COPD along with emphysema. Hyperplasia of mucus-secreting glands in the bronchi􏱪Reid index (thickness of gland layer/total thickness of bronchial wall) > 50%.

Productive cough for > 3 months per year (not necessarily consecutive) for > 2 years. Disease of small airways.
Findings: wheezing, crackles, cyanosis (early- onset hypoxemia due to shunting), late-onset dyspnea, CO2 retention.

45
Q

describe the pathology of emphysema?

A

Enlargement of air spaces, dec 􏰃recoil, 􏰄inc compliance,􏰃 dec DLCO resulting from destruction of alveolar walls

Two types:
􏱰 Centriacinar—associated with smoking B . 􏱰 Panacinar—associated with α1-antitrypsin
deficiency.

inc 􏰄elastase activity——􏱪loss of elastic fibers increased 􏱪􏰄lung compliance.
Exhalation through pursed lips to 􏰄 increases airway pressure and prevent airway collapse during respiration.

46
Q

name the 3 types of bronchodilators?

A

The available agents are divided into three categories:
ß2 agonists (short- and long-acting),
anticholinergics (short- and long-acting)
methylxanthines.

47
Q

describe the MOA of methylxanthines?

and their contraindications?

A

Methylxanthines (theophylline, aminophylline) have been used both orally and intravenously for many
years. While effective, their usefulness is limited by the need for plasma level monitoring, their adverse
reactions and the potential for interactions with other medications

Theophylline—likely causes bronchodilation by inhibiting phosphodiesterase􏱪􏰄cAMP levels due to􏰃cAMP hydrolysis. Usage is limited because of narrow therapeutic index (cardiotoxicity, neurotoxicity); metabolized by cytochrome P-450. Blocks actions of adenosine.

48
Q

what is the metacholine challenge test?

A

Muscarinic receptor agonist. Used in bronchial provocation challenge to help diagnose asthma.

49
Q

describe the MOA of Corticosteroids?

and give 2 exaplmes of asthmatic corticosteroid drugs?

A

Beclomethasone, fluticasone—

inhibit the synthesis of virtually all cytokines. Inactivate NF-κB, the transcription factor that induces the production of TNF-α and other inflammatory agents. 1st-line therapy for chronic asthma.

50
Q

describe the MOA of some antileukotrienes in the treatment of asthma?

see page 614 of USMLE…NB!!!

A

Montelukast, zafirlukast—block leukotriene receptors. Especially good for aspirin-induced asthma

Zileuton—a 5-lipoxygenase pathway inhibitor. Blocks conversion of arachidonic acid to leukotrienes.

51
Q

what is normal pulmonary artery pressure?

and what does chronic COPD do to this?

A

Normal pulmonary artery pressure = 10–14 mmHg

pulmonary hypertension ≥ 25 mmHg at rest. Results in arteriosclerosis, medial hypertrophy, and intimal fibrosis of pulmonary arteries.

COPD can cause this

52
Q

what is omalizumab useful for?

describe its MOA?

A

Monoclonal anti-IgE antibody.

Binds mostly unbound serum IgE and blocks binding to FcεRI.

Used in allergic asthma resistant to inhaled steroids and long-acting β2-agonists.

53
Q

describe when (FEV1 values) to start using ICS in COPD?

and disadvantages of their use?

A
Inhaled corticosteroids (beclomethasone, budesonide, fluticasone) reduce the number of
exacerbations and the decline in health status in patients with severe disease (FEV1
54
Q

what practical advice would you give to someone taking ICS for COPD?

A

Practical Advice:

Patients taking inhaled steroids should be advised on appropriate oral hygiene, e.g.
brush teeth or rinse well after each inhalation. Patients should be monitored for potential complications of steroid use, which include proximal myopathy, osteoporosis, hypertension and abnormal glucose
tolerance

remember CORTISOL and BIG FIB

55
Q

how to manage an acute exacerbation of COPD?

A

management includes

  • —-prompt maximisation of bronchodilator therapy,
  • —–short courses of broad-spectrum antibiotics (if there is a change in the volume and purulence of the sputum)
  • ——addition of oral corticosteroids.
56
Q

Give the causative agents involved in acute exacerbations of COPD?

DDX of an acute exacerbation?

A

Causes:

Acute bacterial infections account for 30-50% of episodes (common pathogens: Haemophilus
influenza (amoxicillin), Moraxella catarrhalis and Strep pneumonie (penicillin)),

30% are viral (common pathogens: rhino-,
influenza, parainfluenza, corona-, adeno- and respiratory syncytial virus).

In up to 30% of cases the cause
may be unidentifiable.

Differential diagnoses include pneumonia, pneumothorax and pulmonary
embolism

57
Q

what is corpulmonale?

what are the 2 main causes of cor pulmonale?

A

Pulmonary heart disease also known as Cor pulmonale is the enlargement and failure of the right ventricle of the heart as a response to increased vascular resistance or high blood pressure in the lungs (pulmonary hypertension).

To be classified as pulmonary heart disease, the cause must originate in the pulmonary circulation system.

Two major causes are vascular changes as a result of tissue damage (e.g. disease, hypoxic injury, chemical agents, etc.), and chronic hypoxic pulmonary vasoconstriction. If left untreated, then death may result. RVH due to a systemic defect is not classified as pulmonary heart disease.

58
Q

what is the BODE index?

A

The BODE index (= BMI, airflow Obstruction, Dyspnoea and Exercise capacity index)[6] should be used to assess the prognosis when the component information is available: measurement of the BODE index includes measurement of BMI, FEV1 as a percentage of predicted, dyspnoea (modified MRC score) and exercise tolerance (six-minute walking distance).

59
Q

describe the GOLD classification?

A

The GOLD (= Global Initiative on Obstructive Lung Disease) classification of severity is also still used:[1]

Stage 0: at risk; chronic cough and sputum production. Spirometry is normal.
Stage I: mild COPD; mild airflow limitation (FEV1/FVC) less than 70% but FEV1 80% or more than predicted; usually, but not always, chronic cough and sputum production.
Stage II: moderate COPD; worsening airflow limitation (FEV1 50-79% predicted) and usually progression of symptoms, with shortness of breath, especially on exertion.
Stage III: severe COPD; further worsening of airflow limitation (FEV1 30-50% predicted), increased shortness of breath, and repeated exacerbations.
Stage IV: very severe COPD; severe airflow limitation (FEV1 less than 30% predicted) or the presence of chronic respiratory failure.

60
Q

complications of COPD?

A

Complications
Chronic hypoxaemia causes slowly progressive pulmonary hypertension with the development of right ventricular hypertrophy and possible cor pulmonale.
Pneumothorax.
Respiratory failure.
Arrhythmias, including atrial fibrillation.
Infection.
Secondary polycythaemia.

61
Q

SIGNS of COPD?

under the following categories:

respiratory
posture
Neuro
Overall
pallor?
Palpation of abdomen?
Auscultation?
A

Signs
Respiratory distress: tachypnoea, breathlessness on exertion, increased use of accessory muscles of respiration, pursed lip breathing.
Abnormal posture: patients may lean forward and rest their arms on the table to ease breathing.
Drowsiness, flapping tremor and mental confusion (these are features of elevated carbon dioxide levels).
Other signs include being underweight, ankle oedema, cyanosis, hyperinflation of the chest, downward displacement of the liver, relatively quiet vesicular breath sounds, wheezing, prolonged forced expiratory time.

62
Q

why would you never add a LABA to an asthmatic?

Look up treatment protocaols for astheman

A

cxvsdfg