Session 6- Chronic Obstructive Pulmonary Disease Flashcards

1
Q

What is the primary cause of COPD

A

Smoking

Alpha-1 antitrysin deficiency- imbalance in proteinase and antiprotinase - destruction in alveolar walls - emphysema

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2
Q

Pathological changes in COPD

A
  • Enlargement of mucus-secreting glands of the central airways,
  • Increased number of goblet cells (which replace ciliated respiratory epithelium)
  • Loss of cilia and ciliary dysfunction
  • Elastin breakdown leading to destruction of alveolar walls and structure, and loss of elastic recoil.
  • Formation of larger air spaces with reduction in total surface area available for gas exchange
  • Loss of capillaries with loss of the alveolar-capillary membrane secondary to destruction of elastin
  • Vascular bed changes leading to pulmonary hypertension.
  • Loss small airways
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3
Q

What is chronic bronchitis

A

Phenotype of COPD- the underlying pathology is excessive mucus secretion and impaired removal of he secretions

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4
Q

Signs of COPD

A
Cough 
SOB 
Tachypnoea 
Use of accessory muscles of respiration 
Barrel chest 
Hyper-resonance on percussion 
Reduced intensity breath sounds 
Reduced air entry 
Wheezing
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5
Q

Late features of COPD

A

Central cyanosis
Flapping tremors
Right sided heart failure signs

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6
Q

How do we investigate COPD

A

Spirometers
CXR
Pulse oximetry
Alpha-2antitrypsin level

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7
Q

What is pulmonary rehabilitation

A

Breaks the cycle of paients not wanting to exercise due to it being painful through exercise, disease education and nutritional advice

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8
Q

Wha can long term oxygen treatment lead to

A

Extended eriods of hypoxia abuse pulmonary hypertension and can lead to Cor Pulmonae `

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9
Q

What antibiotics are given in acute exacerbation if COPD

A

ones that would cover infection with

  • Streptococcus pneumoniae
  • Haemophilus influenza
  • Moraxella catarrhalis
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10
Q

What is bronchiectasis

A

Chronic, o irreversible dilatation of oneb or more bronchi due to the destruction of the elastic and muscular component of bronchial wall

The bronchi exhibit poor mucus clearance and there is predisposition to recurrent or chronic bacterial infections

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11
Q

Possible causes of brinchiectasis

A

Post infective - Whooping cough, TB measles

Immune deficiency

Genetic/ mucocillary clearance defects

Kartagener syndrome

Yellow nail syndrome

Obstruction

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12
Q

Key diagnostic features of bronchiectasis

A

Cough
Sputum production
Acrakles, high pitched insiratoty squeaks and rhonici
Dyspnoea

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13
Q

How do we differentiate between COPD and bronchiectasis

A

Diminished breath sounds in COPD

In bronchiectasis- rhonchi ma be auscultated but with inspiratory speaks and crackles

Chest CT may be normal or show emphysema in COPD as opposed to the characteristic abnormal results found i bronchiectasisp- thickened, dilated airways without ai fluid levels

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14
Q

How do we differentiate bronchiectasis fro asthma

A

Asthma younger patients and no histor of TB or pertussis

Squeaks and crackers on auscultation in B and wheezing in Asthma

Chest x-ray may show thickened small airways in asthma but will not show the enlarged or widened airways seen in bronchiectasis (thickened, dilated bronchus)

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15
Q

What is the signed ring sign

A

Seen in bronchiectasis when the dilated bronchus and accompying pulmonary Artery branch see in cross-section

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16
Q

How do we manage bronchiectasis

A

Treat underlying cause

Physiotherapist to clear mucus

Antibiotics

17
Q

What is the most common cause of bronchiectasis

A

Cystic fibrosis

18
Q

what are the goals for treatment

A

improve symptoms

reduce risk

19
Q

what is pulmonary rehabilitation

A

interdisciplinary programme of care for patients with Chronic respiratory impairement that is individually tailored and designed to optimise each patient’s physical and social performance and autonomy

20
Q

where do muscarinic receptors act

A

proximally

-inhibit bronchoconstrictor effect of acetylcholine at M3 muscarinic receptors located on airway smooth muscle

21
Q

where do b2 adrenergic receptors

A

more effective in distal airways

directly activate b2 receptors in bronchioles leading to increase in cAMP relaxation of smooth muscle, and bronchodilators