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Medicine Phase 2a Respiratory > COPD > Flashcards

COPD Flashcards

1
Q

What is the major cause of COPD

A

Cigarette smoking

daily average of cigarettes smoked and years spent smoking

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2
Q

Other then Cigarettes, what else can result in COPD from chronic exposure

A

• Pollutants at work (mining, building and chemical industries)
• Outdoor air pollution
• Inhalation of smoke from biomass fuels used in heating and cooking in
poorly ventilated areas

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3
Q

What genetic deficiency can cause early COPD

A

Alpha-1 antitrypsin deficiency (due to proteolytic lung damage)

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4
Q

Pathophysiology of Alpha-1 antitrypsin deficiency

A

Mutations in the alpha-1 antitrypsin gene on chromosome 14 lead to
reduced hepatic production of alpha-1 antitrypsin which normally inhibits the proteolytic enzyme - neutrophil elastase
(Rare cause of cirrhosis due to accumulation of abnormal protein in the liver)

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5
Q

What is COPD

A

Chronic Obstructive pulmonary disease

Poorly reversible airflow limitation, usually progressive and persistent inflammatory response

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6
Q

Types of COPD

A

Blue bloaters

Pink puffers

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7
Q

Underlying pathology of Blue bloaters

A

Chronic bronchitis

Compensatory increase in Cardiac Output leads to hypoxia

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8
Q

Underlying pathology of Pink puffers

A

Emphysema

Compensatory hyperventilation prevents hypoxia

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9
Q

Pathophysiology of chronic bronchitis (blue bloaters)

A

Hypertrophy and hyperplasia of mucus secreting glands in bronchial tree, broncial wall inflammation and mucosal oedema. Ulcerations may cause metaplasia of columnar epithelium -> squamous epithelium. Capillary bed intact; body responds to increased obstruction by decreasing ventilation and increasing cardiac output. Poor ventilation to perfusion mismatch -> hypoxia (blue). Obstruction causes increasing residual lung volume (bloating).

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10
Q

Pathophysiology of pink puffers

A

Emphysematous:
Dilation and destruction of lung tissue distal to terminal bronchioles
-> loss of elastic recoil.
This usually is what allows airways to remain open following expiration, so causes air trapping.
Also causes damage to capillary bed and loss of alveoli (decreasing capacity for gas transfer)
-> Inability to oxygenate
-> Hyperventilation (puffing)

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11
Q

Are there more cases of emphysema or chronic bronchitis

A

Most people have a combination which results in severe airflow limitation

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12
Q

Different types of emphysema

A

Centri-acinar (v common)
Pan-acinar
Irregular

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13
Q

Describe Centri-acinar emphysema

A

Distension and damage of lung tissue is concentrated around the respiratory bronchioles, whilst the more distal alveolar ducts and alveoli tend to be well preserved

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14
Q

Describe Pan-acinar emphysema

A

Distension and destruction affect the whole acinus and in severe cases the lung is just a collection of bullae.
Associated with alpha-1 antitrypsin deficiency

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15
Q

Describe irregular emphysema

A

Scarring and damage that affects the lung parenchyma

patchily, independent of acinar structure

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16
Q

What causes V/Q mismatch in COPD

A

Partly due to damage and mucus plugging of smaller airways from the chronic inflammation
and partly due to rapid closure of smaller airways in expiration owing to the loss of elastic support

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17
Q

What results from V/Q mismatch in COPD

A

Fall in PaO2

Increased work or respiration

18
Q

Why is CO2 excretion sometimes less affected by V/Q mismatch and so PaCO2 is usually normal or low (Type 1 RF)

A

Due to increasing alveolar ventilation in attempt to correct their hypoxia (pink puffers)

19
Q

In shorter term for COPD patients, a rise in CO2 leads to stimulation of respiration. How does this change in longer term

A

Patients often become insensitive to CO2 and come to depend on the hypoxaemia to drive ventilation.
Such patients appear less breathless and because of renal hypoxia, they start
to retain fluid and increase erythrocyte production (leading eventually to polycythaemia) - they become bloated and cyanosed (blue).

20
Q

Example of precipitating cause of acute exacerbations in COPD

A

Respiratory infections

21
Q

Pathogenesis of cigarette smoke

A
  • Causes mucus gland hypertrophy in the larger airways and leads to an increase in neutrophils, macrophages and lymphocytes in the airways and walls of the bronchi and bronchioles
  • These cells release inflammatory mediators (elastases, proteases, IL-1,-8 & TNF-alpha) that attracts inflammatory cells (further amplify the process), induce structural changes and break down connective tissue (protease antiprotease imbalance) in the lung resulting in emphysema
  • Inactivates the major protease inhibitor alpha-1 antitrypsin
22
Q

Aetiology of COPD

A

Chronic inflammation of the airways.
Usually by smoking, also occupational irritants.
This causes the mucous gland hypertrophy, and increase in neutrophils, macrophages and lymphocytes in airways
-> Increase in inflammatory mediators (recurrent cycle)
-> Breakdown of lung tissue.

23
Q

Respiratory clinical presentation of COPD

A

Chronic cough, exertional breathlessness, regular sputum production, wheeze.

24
Q

Non-respiratory clinical presentation of COPD

A

Abnormal posture (leans forward), drowsiness/mental confusion, underweight, ankle oedema

25
Q

Signs of COPD

A 
Tachypnoea
Use of accessory muscles of respiration
Hyperinflation
Decreased expansion
Decreased cricosternal distance (<3cm)
Wheeze
Cyanosis
Cor pulmonale
Quiet breath sounds
Resonant percussion note
26
Q

Symptoms of COPD

A

Cough
Sputum
Dyspnoea
Wheeze

27
Q

Epidemiology

A

Mostly smokers

Rare under 35

28
Q

Diagnostic tests

A

CXR
FBC (increased PCV)
ABG (decreased PaO2 with or without hypercapnia)
Spirometry (obstructive and air trapping)
ECG (Right atrial and ventricular hypertrophy - cor pulmonale)

29
Q

Complications

A 
Respiratory failure
Polycythaemia
Cor pulmonale (oedema and increased JVP)
Pnuemothorax
Lung carcinoma
30
Q

Complications

A 
Respiratory failure
Polycythaemia
Cor pulmonale (oedema and increased JVP)
Pnuemothorax
Lung carcinoma
Acute exacerbations with or without infection
31
Q

Management of COPD if FEV1 <50%

A
  • Initiate Short-Acting Beta 2 agonist (SABA) or Short Acting Muscarinic antagonist (SAMA)
  • Test FEV1 (<50%)
  • Long-acting muscarinic antagonist (LAMA) or Long-acting Beta agonst (LABA) plus inhlaed corticosteroid (ICS) in combined inhaler
  • If still then LAMA plus LABA/ICS combination inhaler

COnsider LTOT if PaO2<7.3kPa

32
Q

When should Long term oxygen therapy be given for COPD

A

Clinically stable non smokers with PaO2 <7.3kPa (despite maximal Rx)
If PaO2 is between 7.3-8.0 and have pulmonary hypertension, polycythaemia, peripheral oedema or nocturnal hypoxia
Terminaly ill patients

33
Q

Management of COPD if FEV1 >50%

A

-Initiate Short-Acting Beta 2 agonist (SABA) or Short Acting Muscarinic antagonist (SAMA)
-Test FEV1 (>50%)
Two options:
1) LABA -> LABA plus Inhlaed Corticosteroid (ICS) -> LAMA plus LABA/ICS combination inhaler
2)LAMA -> LAMA plus LABA/ICS combination inhaler

34
Q

Other factors in management of COPD

A

Consider palliative care input

Air travel is risky if FEV1 <50% or PaO2 <6.7kPa on air

35
Q

Presentation of acute exacerbation of COPD

A

Increasing cough
Breathlessness
Wheeze
Decreased exercise capacity

36
Q

Hx of acute exacerbation of COPD

A

Usual/recent treatments (esp home O2)
Smoking status
Exercise capacity

37
Q

Differential diagnosis of acute exacerbation of COPD

A 
Asthma
Pulmonary oedema
Upper resp tract obstruction
Pulmonary embolus
Anaphylaxis
38
Q

Investigations of acute exacerbation of COPD

A

ABG,
CXR (to exclude pneumothorax and infection),
FBC, U and E, CRP,
Theophylline level if patient on therapy at home,
ECG,
Spend sputum for culture if purulent,
Blood cultures if pyrexial

39
Q

*Management of acute exacerbation of COPD

A

1) Nebulised bronchodilators: Salbutamol and Ipratropium
Investigate ABG, CXR
2) Controlled oxygen therapy if SaO2 <88% or PaO2 <7kPa
3) Steroids: IV hydrocortisone and oral predinsolone
4) Antibiotics (e.g. amoxicillin or doxycycline)
5) Physiotherapy to aid sputum exacerbation
6) If no response to nebulisers and steroids, consider IV aminophylline
7) If still no response consider non-invasive positive pressure ventilation (NIPPV) or respiratory stimulant drug (e.g. doxapram)

40
Q

Example of nebulised bronchodilators

A

Salbutamol and ipratropium

41
Q

What is the greatest danger in COPD

A

Hypoxia (bigger killer than hypercapnia)

Medicine Phase 2a Respiratory (22 decks)

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