Session 6- Chronic Obstructive Pulmonary Disease Flashcards
What is the primary cause of COPD
Smoking
Alpha-1 antitrysin deficiency- imbalance in proteinase and antiprotinase - destruction in alveolar walls - emphysema
Pathological changes in COPD
- 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
What is chronic bronchitis
Phenotype of COPD- the underlying pathology is excessive mucus secretion and impaired removal of he secretions
Signs of COPD
Cough SOB Tachypnoea Use of accessory muscles of respiration Barrel chest Hyper-resonance on percussion Reduced intensity breath sounds Reduced air entry Wheezing
Late features of COPD
Central cyanosis
Flapping tremors
Right sided heart failure signs
How do we investigate COPD
Spirometers
CXR
Pulse oximetry
Alpha-2antitrypsin level
What is pulmonary rehabilitation
Breaks the cycle of paients not wanting to exercise due to it being painful through exercise, disease education and nutritional advice
Wha can long term oxygen treatment lead to
Extended eriods of hypoxia abuse pulmonary hypertension and can lead to Cor Pulmonae `
What antibiotics are given in acute exacerbation if COPD
ones that would cover infection with
- Streptococcus pneumoniae
- Haemophilus influenza
- Moraxella catarrhalis
What is bronchiectasis
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
Possible causes of brinchiectasis
Post infective - Whooping cough, TB measles
Immune deficiency
Genetic/ mucocillary clearance defects
Kartagener syndrome
Yellow nail syndrome
Obstruction
Key diagnostic features of bronchiectasis
Cough
Sputum production
Acrakles, high pitched insiratoty squeaks and rhonici
Dyspnoea
How do we differentiate between COPD and bronchiectasis
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
How do we differentiate bronchiectasis fro asthma
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)
What is the signed ring sign
Seen in bronchiectasis when the dilated bronchus and accompying pulmonary Artery branch see in cross-section
How do we manage bronchiectasis
Treat underlying cause
Physiotherapist to clear mucus
Antibiotics
What is the most common cause of bronchiectasis
Cystic fibrosis
what are the goals for treatment
improve symptoms
reduce risk
what is pulmonary rehabilitation
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
where do muscarinic receptors act
proximally
-inhibit bronchoconstrictor effect of acetylcholine at M3 muscarinic receptors located on airway smooth muscle
where do b2 adrenergic receptors
more effective in distal airways
directly activate b2 receptors in bronchioles leading to increase in cAMP relaxation of smooth muscle, and bronchodilators
