Session 7 Flashcards

1
Q

Define COPD.

A

Disease characterised by airflow obstruction which is usually progressive, not fully reversible and does not change markedly over several months. it encompasses emphysema and/or chronic bronchitis.

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2
Q

What is the most common cause of COPD?

A

Smoking.

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3
Q

What is emphysema?

A

pathological process where there is destruction of the terminal bronchioles and distal airspaces causing loss of alveolar surface area and impairment of gas exchange.

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4
Q

Why do the lungs hyperinflate in emphysema?

A

The loss of elastic tissue means that the lungs cant resist the natural tendency of the rib cage to expand outwards so hyperinflation occurs.

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5
Q

What is chronic bronchitis?

A

Chronic inflammation with excess mucus secretion in the large airways of the lungs.

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6
Q

What can cause COPD?

A

Smoking, alpha-1 antitrypsin deficiency, occupational exposure, pollution.

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7
Q

How does COPD usually present?

A

Cough and sputum production are usually the first signs, most patients wont present until they become breathless.

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8
Q

What is exacerbation of COPD?

A

Increased breathlessness, increased cough and increased sputum production compared to the baseline.

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9
Q

What is the MRC dyspnoea score?

A

A way of quantifying the level of breathlessness in a patient typically used in COPD.

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10
Q

What are typical signs on examination of COPD?

A

Pursed lip breathing, tachypnoea, using accessory muscles to breathe, barrel chest, wheeze, quiet breath sounds, cyanosis, oedema.

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11
Q

How is airflow obstruction measured in COPD?

A

Using spirometry.

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12
Q

What does spirometry show in COPD sufferers?

A

Reduced total expiratory volume as obstructive condition, FEV1.0 us usually low, FEV1.0/FVC is usually low.

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13
Q

How is COPD diagnosed?

A

Using a combination of the suggestive symptoms and presence of airflow obstruction on spirometry. CXR used to exclude other diagnoses

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14
Q

How is COPD managed?

A

Stop smoking, bronchodilators, antimuscarinics, steroids, mucolytics, diet supplements, may need oxygen therapy and lung volume reduction.

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15
Q

How do beta-2 agonists work?

A

Binds to beta-2 receptor activating adenyl cyclase; [cAMP] increases and PKA activated; MLCK is phosphorylated and activated; smooth muscle relaxes and causes bronchodilation in the lungs.

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16
Q

What are the adverse effects of beta-2 agonists used in COPD therapy?

A

Tachycardia and tremor due to activation of other beta-2 receptors; anxiety; palpatations; hypokalaemia due to increased skeletal muscle potassium uptake.

17
Q

How do methylxanthines work?

A

Inhibit phosphodiesterases so less cAMP is broken down, causing bronchodilation.

18
Q

What are the potential side effects of long term steroid use?

A

Think skin, bruising, cataracts, adrenal insufficiency, osteoporosis, DM, fluid retention, mental disturbance, GI symptoms, proximal myopathy.

19
Q

Why is pulmonary rehabilitation performed in COPD?

A

To prevent deconditioning from social anxiety and inactivity.

20
Q

When is long-term oxygen therapy offered to COPD patients?

A

If pO2 is consistently below 7.3kPa (8kPa with cor pulmonale) if patients are non-smokers and don’t retain high CO2 levels.

21
Q

What is the aim of COPD treatment?

A

To improve sufferers’ quality of life as the condition can’t be reversed or cured.

22
Q

How are acute exacerbations of COPD treated?

A

Controlled oxygen therapy, nebs, steroids, antibiotics if infective, repeat ABG, consider IV bronchodilators.

23
Q

What are the contraindications to non-invasive ventilation?

A

Untreated pneumothorax, impaired consciousness, increased upper airway secretions, facial injury, vomiting, agitation, life threatening hypoxia.

24
Q

Briefly describe the epidemiology of lung cancer.

A

Most common cancerous cause of death in UK, very low 5 year survival rate, lowest one year survival rate, more common in less affluent socio-economic groups, large link to smoking, link to occupational carcinogens.

25
Q

What are the advantages of lung cancer screening?

A

Detects disease before critical point, causes little morbidity, affordable, available, allows earlier treatment so better prognosis.

26
Q

What are the disadvantages of lung cancer screening?

A

Detects some pseudo-disease so can lead to overdiagnosis.

27
Q

How is lung cancer staged?

A

Using TNM staging based on primary tumour, lymph nodes and metastases.

28
Q

Which stages of lung cancer are operable?

A

IA-IIB.

29
Q

Which stages of lung cancer are non-operable?

A

IIIA.

30
Q

Which stages of lung cancer are palliative?

A

IIIB and IV.

31
Q

Where does lung cancer typically spread to?

A

Brain, draining lymph nodes, pericardium, lungs, pleura, liver, adrenal glands, bone.

32
Q

How is lung cancer staged?

A

Using imaging (usually CXR) and tissue sampling.

33
Q

What are the typical presenting symptoms of lung cancer?

A

Cough, dyspnoea, wheezing, haemoptysis, lung infection, chest/shoulder pain, weight loss, lethargy/malaise, metastatic symptoms (bone pain, bloated face, hoarseness, etc.), metabolic symotoms (hypercalcaemia, hyponatraemia).

34
Q

What is paraneoplastic syndrome?

A

Consequence of cancer in the body where the syndrome isn’t due to the presence of local cancer cells.

35
Q

What paraneoplastic symotoms can occur in lung cancer?

A

Hypercalaemia, Cushing’s syndrome, SIADH, anaemia, thrombocytosis, peripheral neuropathy, dermatomyositis, finger clubbing.

36
Q

Describe the pathology of lung cancer.

A

Carcinoma (invasive malignant epithelial tumour). Usually non-small cell lung cancer but may also be small-cell or other rare tumours. Molecular markers are EGFR, ALK, KRAS and PD1 mutations.

37
Q

How is lung cancer treated?

A

Surgery if operable; radical/palliative radiotherapy; combination chemotherapy if appropriate; combination chemo-radiotherapy; biological therapies; palliative care.