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Respiration > COPD > Flashcards

COPD Flashcards

1
Q

Define COPD?

A

Chronic obstruction of lung airflow that interferes with normal breathing and is not fully reversible.
Its common, preventable and treatable

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2
Q

What is the prevalence and incidence of COPD?

A

Prevalence = increasing
- greater in males than females (due to different jobs and smoking habits)
Incidence = decreasing
- possibly due to increased cessation of smoking

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3
Q

How can COPD be caused (aetiology)?

A

Smoking
- may affect foetal lung growth and priming of the immune system
- <50% will develop COPD
Occupation
- exposure to dust and fumes
Genetic
- Alpha-1-antitrypsin deficiency = early onset of COPD <45 years
Childhood disadvantage
- shunted lung development increases risk
Lower socioeconomic group
Asthma/airway hyperreactivity
Chronic bronchitis
Childhood infection

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4
Q

What is the patho-biology of COPD?

A

Impaired lung growth
Accelerated decline
Lung injury
Lung and systematic inflammation

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5
Q

What is the pathology of COPD?

A

Small airway disorders
Abnormalities
Emphysema
Systemic effects

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6
Q

What are the symptoms of COPD?

A

Cough
SOB
Sputum
Frequent chest infections
Wheezing
Other:
- Weight loss - due to inc metabolic activity
- Fatigue
- Swollen ankles
- Depression, anxiety

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7
Q

Upon examination what could a COPD patient present with?

A

Cyanosis (blue)
Raised JVP
Cachexia
Wheeze
Pursed lip breathing
Hyperinflated chest
Use of accessory muscles
Peripheral oedema

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8
Q

When do you diagnose COPD?

A

Typical symptoms
>35 years old
Presence of a risk factor (e.g. smoking)
Absence of clinical features of asthma
AND
Airflow obstruction confirmed by lung function tests

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9
Q

What does a chest x-ray show

A

Vascular hila (more prominent)
Hyperinflation (>6 anterior ribs showing)
Bulla (reduced lung markings)
Small heart (squashed by lungs)
Flat diaphragm

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10
Q

What does spirometry results show?

A

80% predicted = mild
50-70% = moderate
30-49% = severe
<30% = very severe

*useful but not always diagnosis

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11
Q

What are the differences between COPD and asthma?

A

COPD
- Smoker = nearly all
- Rarity to have symptoms under 35
- Common chronic productive cough
- Uncommon night time waking with SOB and wheeze
- Persistent SOB
- Uncommon variability

Asthma
- Possible smoker
- Often symptoms under 35
- Uncommon chronic productive cough
- Variable SOB
- Common nocturnal variability

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12
Q

How to manage acute exacerbations in primary care?

A

Change inhalers (technique, device, add bronchodilator, increase or add inhaled steroid)
Oral steroids
Antibiotics
Self management for select patients

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13
Q

When do acute exacerbations need hospital treatment?

A

Confusion
Cyanosis
Severe SOB
Flapping tremor
Drowsy
Pyrexial
Wheeze
Tripod possition
Tachypnoea
Low O2 sats (<90-92%)
Hypotension

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14
Q

How to manage acute exacerbations in secondary care?

A

Oxygen
Nebulised bronchodilator
(B2 & anti-muscarinic)
Oral/IV corticosteroid
Oral/IV antibiotics
Ventilation

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15
Q

What investigations are done in secondary care?

A

CXR
Blood gases
FBC
U&E
Sputum culture
VTS

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16
Q

How do you measure severity?

A

Nature and magnitude
- MRC SOB scale and COPD assessment tool
History of moderate/severe exacerbations and future risk
- Number of attacks & admissions per year
Presence of co-morbidity
- Heart disease, atrial fibrillation, obesity

17
Q

Describe severe COPD

A

End point = respiratory failure
- Caused by matched reduced ventilation/perfusion

Increased PCO2 = ventilatory failure

18
Q

What happens in hypoxic drive?

A

Rely on chemoreceptors in cartic body/aortic arch to detect drops in O2
(don’t give high O2 as will make it worse - 88-92%)

19
Q

What is cor pulmonale?

A

Right side of the heart failure due to lung disease, caused by smoking and hypoxia.

Results in thickening of muscle on the right side of the heart. Increasing pressure on the left side, increasing JVP.
This reduces circulatory volume and leads to fluid retention.

20
Q

Describe secondary polycythaemia

A

Body produces more erythropoietin in response to low O2
Increased haemoglobin and haematocrit
Leading to increased viscosity
Resulting in strokes

21
Q

What happens during end stage COPD?

A

Terminal illness
Unpredictable decline
Acute decline possible
Palliation of symptoms
- SOB anxiety in particular
Social aspects
- Care, housebound, O2 at home

22
Q

What is the main COPD management?

A

Improve exercise tolerance
Prevent exacerbations

23
Q

What is secondary COPD management?

A

Nutrition/weight loss management
Complications (cor-pulmonale, resp failure)

24
Q

What is tertiary COPD management?

A

Co-morbidities
Dysfunctional breathing
Palliative care

25
Q

Non pharmacological managements?

A

Smoking cessation
Vaccines (flu/pneumococcal)
Pulmonary rehab
Nutritional assessment
Psycological support

26
Q

What are some pharmacological benefits?

A

Relieve symptoms
Prevent exacerbations
Improve quality of life

27
Q

What types of inhaled therapies are there?

A

Short acting bronchodilators
- SABA (e.g. salbutamol)
- SAMA (e.g. Ipratropium)
Long acting bronchodilators
- LAMA (long acting anti-muscarinic agents)
- LABA (long acting B2 agonists)
High dose inhaled corticosteroids (ICSL and LABA
- Relvar
- Fostair MDI

28
Q

What investigations are required for patients admitted to hospital?

A

Full blood count
Biochemistry and glucose
Theophylline concentration
Arterial blood gas
Electrocardiograph
Chest X-ray
Blood cultures in febrile patients
Sputum microscopy, culture and sensitivity

29
Q

What does ward based management look like?

A

Oxygen - target saturation 88-92% (too much O2 can supress respiratory drive)
Nebulised bronchodilators
Corticosteroids
Antibiotics (oral/IV)
Assess for evidence of respiratory failure
- clinical
- Arterial blood gas

30
Q

What does palliative care look like?

A

Management of SOB and dysfunctional breathing
- Pharmacological (morphine)
- Psychological support
- Palliative care referral
Anticipatory care plan (death plan)
- Hospital admission
- Ceiling of treatment - ward based, HDU, ventilation
- DNACPR

Respiration (27 decks)

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