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Respiratory System > COPD > Flashcards

COPD Flashcards

1
Q

Pathology of COPD

A

Obstruction due to narrowing of airways - combination of bronchitis and emphysema

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2
Q

Pathology of chronic bronchitis

A

Causes excess mucous production and inflammation of respiratory tract

Inflammation leads to scarring and fibrosis which thickens the walls of the airways, reducing size of lumen and increases diffusion distance

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3
Q

Pathology of emphysema

A

Causes increased in airspaces due to dilation or from destruction of the walls without obvious fibrosis

Loss of alveolar tissue means loss of elasticity and thus recoil of the lungs

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4
Q

Chronic bronchitis aetiology

A
  • SMOKING
  • Air pollution
  • Occupation (dust)
  • a-1-antitrypsin deficiency (cant inhibit protease which destroys tissue)
  • Effect of age & susceptibility (metabolism of irritants in tobacco smoke)

Smoke paralyses cilia that sweeps debris and mucous out of the airways and smoke irritation increased mucous production - without functional cilia, mucous & debris pool in airways

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5
Q

Morphological changes in chronic bronchitis

A

Small airways:

  • Goblets appear
  • Fibrosis and inflammation I along standing disease

Large airways:

  • Mucous and goblet cell hyperplasia
  • Inflammation and fibrosis
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6
Q

Emphysema aetiology

A
  • SMOKING: protease-antiprotease imbalance

- a-1-antitrypsin deficiency

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7
Q

Describe centri-acinar emphysema

A

Begins with bronchiolar dilation, then alveolar tissue loss

Enlargement of airways in the proximal part of bronchial tree due to LACK OF ELASTIN

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8
Q

Describe panacinar

A

a-1-antitrypsin deficiency allows elastase to inhibit elastin, so all acinar structures destroyed

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9
Q

What is a bulla?

A

Emphysematous space > 1cm

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10
Q

What is a bleb?

A

A space (bulla) underneath the pleura which can cause a pneumothorax

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11
Q

Effect of hypoxaemia

A

Low O2 concentration in blood due to airway obstruction which decreased inhaled air in alveoli - alveolar hypoventilation

Most alveoli are hypoxic, so arterioles constrict due to shunt (V/Q mismatch) which increased BP and cause pulmonary HPT

Pul. HPT increases work of RV to pump blood in pul. circulation, causing it to hypertrophy and dilate -> Cor pulmonale

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12
Q

Symptoms of COPD

A 
SOB (decreased gas exchange and abnormal diaphragm mechanism)
Cough (cilia impaired)
Recurrent chest infection - specific 
Sputum purulence 
Wheeze 
Dyspnoea
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13
Q

Signs

A

May be normal in early stages
Reduced chest expansion
Wheeze
Hyperinflated chest (gas trapping)

Respiratory failure:
Cyanosis 
Tachypnoea 
Accessory muscles 
Pursed lip breathing 
Peripheral oedema

Cor Pulmonale
Weight loss

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14
Q

Clinical history

A

PH:
Asthma as child
Ischaemic heart disease

Drugs:
List of current inhalers and doses
Previous meds and effect on breathing (steroids)

Social:
Occupation (exposure to dust, vapours, fumes)
Smoking - pack years

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15
Q

Exacerbating factors

A

Viral/bacterial infections, sedative drugs, trauma and pneumothorax

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16
Q

Useful Investigations

A

CXR (flattened diaphragm, hyperinflation: > 6 anterior and > 10 posterior ribs, bullae)
ABG (type I or II res failure)
FBC (high WBC - anaemia, high Hb or eosinophil)
ECG (cor pulmonale)
Sputum culture (Strep. pneumonia, H influenza, M catarrahlis)

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17
Q

Effect of loss of elastic recoil in emphysema

A

Can cause collapse of the lungs - this makes expiration hard and air is ‘trapped’ -> hyperinflation of lungs

18
Q

Main pathological changes in the small airways

A

Goblet cells appear

Inflammation and fibrosis

19
Q

Main pathological changes in the large airways

A

Mucous gland hyperplasia
Goblet cell hyperplasia
Inflammation and fibrosis

20
Q

How does smoking cause COPD?

A

Tobacco in cigarettes releases a reactive oxygen species - free radicals. This causes the inactivation of antiproteases leading to an increase in neutrophil elastase which cause tissue damage -> emphysema

Paralyses the cilia that sweep debris and mucus out of the airways -> mucous and debris pool in the airways

21
Q

Why does hypoxaemia occur?

A

Airway obstruction
Reduced respiratory drive
Loss of alveolar surface area (less gas exchange)
V/Q mismatch - responds well to small increases in FiO2

22
Q

What other molecules can increase neutrophil elastase?

A

Nicotine in tobacco
IL-8, LTB4 and TNF from free radicals

Both cause the release of neutrophils causing an increase in neutrophil elastase

23
Q

What can COPD lead to?

A

Loss of muscle mass (SOB)
Weight loss
Cardiac disease - R HF then L HF which will decrease CO
Depression, anxiety

24
Q

How is COPD diagnosed?

A

Clinical history: cough, SOB, recurrent chest infections, winter bronchitis

Examination: normal or tachypnoea, wheeze, hyper inflated chest

Spirometry: confirms and assesses severity

25
Q

Interpretation of spirometry

A

Based on the patient’s FEV1 and its percentage of predicated FEV1

> 80% : mild AFO
50-79% : moderate AFO - cough, SOBOE
30-49% : severe AFO - SOBOE, cough/sputum
<30% : v severe AFO - SOBOE+, wheeze, cough, cor pulmonale

26
Q

Essential investigations

A

Spirometry
Full pulmonary function testing
Response to drug therapy

27
Q

Explain use of PFT

A

Looking for emphysema

Gas trapping present: increase residual volume and total lung capacity
RV/TLC > 30%

Carbon monoxide gas transfer:
Decreased diffusion of CO sign of emphysema (loss of surface area)

28
Q

Explain response to drug therapy in COPD

A

Should show:
Minimal bronchodilator reversibility (salbutamol)
Minimal response to oral corticosteroids
- 30mg prednisone daily for 2 weeks
- Measure baseline and final FEV1

29
Q

What are 4 exacerbating factors?

A

Viral/bacterial infection
Sedative drugs
Pneumothorax
Trauma

30
Q

What are 5 signs of AECOPD?

A 
Confusion 
Cyanosis 
SOB
Flapping tremor 
Pyrexia
31
Q

Aims and interventions of COPD

A

Prevent progression -> smoking cessation
Relieve SOB -> inhalers
Prevent exacerbation -> inhalers, vaccines, pulmonary rehabilitation
Manage complications -> long term O2 therapy

32
Q

Non-pharmacological management

A 
Smoking cessation 
Vaccinations (flu, pneumococcal)
Pul. rehab 
Nutritional assessment 
Psychological support
33
Q

Benefits of pharmacological management

A

Relieves symptoms
Prevent exacerbations
Improves quality of life

34
Q

Stages to treatment

A
  1. SABA
  2. LABA or LAMA
  3. Further LABA or LAMA
  4. Triple therapy: ICS, LABA, LAMA
35
Q

Name short acting bronchodilators

A

SABA - salbutamol

SAMA - ipratropium

36
Q

Name long acting bronchodilators

A

LABA (long acting B2 agonist) - salmeterol

LAMA (long acting anti-muscarinic agents) - umeclidium

37
Q

Name inhaled corticosteroids

A

Revlar

38
Q

Criteria for long term oxygen (LTOT)

A 
PaO2 < 7.3kPa 
or 
PaO2 = 7.3-8 kPa if:
polycythaemia
nocturnal hypoxia 
peripheral oedema 
pul. HPT
39
Q

Management of AECOPD

A 
SABA (salbutamol)
Steroids (prednisone)
Antibiotics - if evidence of infection (fever, increase in sputum volume/purulence)
Consider hospital:
-Tachypneoa
-Low O2 sat <92%
-Hypotension
40
Q

Investigations for AECOPD

A 
FBC
Biochem and glucose 
Theophylline concentration 
ABG
Electrocardiograph
CXR
Blood culture 
Sputum microscopy, culture and sensitivity
41
Q

Why do you get a hyper inflated chest in COPD?

A

Obstruction is usually with air being expired so air trapped in lungs

Respiratory System (29 decks)

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