WEEK 3 - chronic breathlessness Flashcards
sympathetic innervation of bronchiolar smooth muscle is mediated by ______ acting on ________ to cause ________.
parasympathetic innervation of bronchiolar smooth muscle is mediated by _______ acting on ______ to cause ________.
- noradrenaline
- beta receptors
- bronchodilation
- acetylcholine
- muscarinic receptors
- bronchoconstriction
type I vs type II alveolar cells
type I
- gas exchange between the alveoli and capillaries
- larger squamous (flattened) cells
- no secretory organelles present
- less numerous than type II
type II
- secrete surfactant to lower surface tension
- smaller cuboid-shaped cells
- secretory organelles present
- more numerous than type I
the lungs have dual arterial supply and venous drainage, comprised of the ________ arteries and veins, and the __________ arteries and veins.
the pulmonary arteries supply _________ from the ______ to the _____ capillary network. the pulmonary veins drain _______ blood to the _________.
the bronchial artiereis supply ________ blood from the ________ to the lung tissues. the bronchial veins drain ________ blood to the pulmonary and systemic venom systems
- pulmonary
- bronchial
- deoxygenated
- right ventricle
- alveolar
- oxygenated
- left atrium
- oxygenated
- thoracic aorta
- deoxygenated
what is the MRC (medical research council) dyspnoea scale?
a scale to make an objective assessment of the symptom of breathlessness when taking a history
breathlessness when lying flat is a key symptom of what?
congestive cardiac failure (CCF) (orthopnoea)
bilateral vs unilateral ankle swelling
bilateral — sign of cardiac pathology, esp CCF
unilateral — may indicate DVT/PE
what classically can cause breathlessness with lightheaded mess?
aortic stenosis
why ask about exposure to birds?
hypersensitivity pneumonitis
a type of hypersensitivity pneumpnitis due secondary to repeated inhalation of avian antigens is seen in bird keeps
sometimes known as ‘Pigeon Fancier’s Lung’
what are the hallmark symptoms of COPD?
- SOB
- chronic cough
- sputum production
other features:
- winter exacerbations
- wheeze
what are the physical signs of COPD?
- accessory muscle use
- auscultation
- chest hyperexpansion
- chest wall movement
- tar-staining
- peripheral oedema
- palpable liver
- pursed lip breathing
explain pursed lip breathing
this enables a patient to reduce their resp rate by increasing their period of expiration; it creates resistance to expiratory airflow and development of a positive expiratory pressure in the airways, reducing airway collapse and aiding ventilation
in COPD, what impede the effective chest expansion by the diaphragm and intercostal muscles? what does the patient do instead?
air trapping and hyperinflation
instead the patient used accessory muscles (inc SCM, scalene, trapezius and abdominal muscles) to aid ventilation
what does peripheral oedema in COPD indicate?
right-sided heart failure due to cor pulmonale
what is cor pulmonale?
abnormal enlargement of the right side of the heart as a result of disease of the lungs or the pulmonary blood vessels
why might you get a palpable liver in COPD?
may be due to hyperinflation of the lungs or congestive heart failure
what would you hear in auscultation of COPD?
- reduced breath sounds
- reduced heart sounds
- tachypnoea
- wheeze
during an exacerbation there may also be crepitations
describe chest wall movement in COPD
- reduced lateral (bucket handle) chest expansion
- increased vertical (pump handle) chest expansion
what rare genetic condition can cause COPD at a young age, esp in smokers?
alpha-1 anti trypsin deficiency
what is the gold standard investigation for diagnosing COPD and grading COPD severity?
spirometry
what are 3 histological features of COPD? what symptoms do they cause?
- goblet cell hyperplasia — cough and sputum
- airway narrowing — breathlessness and wheeze
- alveolar destruction — breathlessness
inflammation mediated by the toxic substances of tobacco smoke cause these things
how does NICE define airflow obstruction?
post-bronchodilator FEV1/FVC ratio such that FEV1/FVC is less than 0.7
(above 70% is normal)
FEV1/FVC obstructive vs restrictive disease
O = <75%
R = > 75% (FEV1 and FVX are reduced in roughly the same proportion so the ratio remains within the normal range)
premature airway ______ is a key feature of COPD
collapse
list some restrictive vs obstructive disorders
restrictive — pulmonary fibrosis, sarcoidosis., chest wall deformity, and neuromuscular disorders
obstructive — COPD, asthma, bronchiectasis, cystic fibrosis
describe COPD natural history
- progressive decline in lung function
- progressive dyspnoea and disability
- right ventricular failure (cor pulmonale)
- exacerbations become more frequent and contribute to morbidity and disability
describe hypoxia to RV failure
hypoxia —> pulmonary artery vasoconstriction —> increased pulmonary artery pressure —> right ventricular hypertrophy —> right ventricular failure
what are the fundamentals of COPD care?
- treatment and support to stop smoking
- vaccinations — influenza and pneumococcal
- physiotherapy/pulmonary rehabilitation if indicated
- co-develop a personalised self-management plan
- optimise treatment for co-morbidities
what is the best combination to achieve smoking cessation?
champix combined with NRT and behavioural support
what is champix?
varenicline
nicotine receptor partial agonist
for COPD, inhaled therapies should only be offered if what?
- needed to relieve SOB and exercise limitation
- patient has been trained to use inhalers and has satisfactory technique
what is the most common short-acting muscarinic antagonist?
ipratropium
what is step 1 of COPD treatment?
offer SABA or SAMA
what is step 2 of COPD treatment if no asthmatic features (previous secure diagnosis of asthma or autopsy, raised blood eosinophil counts substantial variation in FEV1 over time pr diurnal variation in PEF) ?
offer DUAL therapy : LABA + LAMA
LABA eg. formoterol, salmeterol
LAMA eg. tiotropium, glucopyrronium
what is step 2 of COPD treatment if asthmatic features present?
DUAL therapy with LABA + inhaled corticosteroids (ICS)
ICS eg. beclomethasone — brown inhaler
salmeterol with fluticasone — purple inhaler
what is step 3 of COPD treatment? (continue to have day-to-day symptoms that adversely impact QoL, OR have 1 severe or 2 moderate exacerbations within a year, even on dual therapy)
triple therapy : LABA + LAMA + ICS
who is home oxygen therapy for in COPD?
patients with a paO2 < 7.3 on air
or paO2 7.3-8.0 on air and either:
- secondary polycythaemia
- peripheral oedema
- pulmonary hypertension
only available to NON-SMOKING HOUSEHOLDS
magnesium in asthma/COPD?
bronchodilator typically used for treating acute exacerbations of asthma, and rarely used in acute COPD exacerbations
long-acting muscarinic antagonists are used in management of ____ but not ____
COPD but not asthma
brand names for inhalers?!
surely not
what are the side effects of inhaled corticosteroid therapy?
inhaled corticosteroids generally have less systemic absorption and therefore less systemic side effects than oral corticosteroids, and the main side effects are candidiasis and hoarseness.
however, with prolonged use at higher doses you may see side effects of adrenal suppression, osteoporosis and growth restriction in children
COPD exacerbation treatment
- oxygen
- high dose SABAs, usually nebulised
- high dose corticosteroids (usually prednisone 40mg/day — 7 days)
- antibiotic only if purulent sputum or very severe illness
- reassess after 1 hr
if after 1 hour still respiratory acidosis, consider all of:
- iv bronchodilator (salbutamol or theophylline)
- urgent intensive care opinion
- non-invasive ventilation
- intubation and assisted ventilation
What is the pathological process that leads to Type II respiratory failure in COPD? What physiological compensatory mechanisms occur in the body to reduce the level of acidaemia?
In COPD the elastic recoil of the lungs is lost. This causes gas trapping and reduced excretion of carbon dioxide. Sputum retention also means there is less surface area for gas exchange. In the blood, the carbon dioxide combines with water to form carbonic acid.
In an acute setting, the increased acid levels in the blood would lower the pH levels and the patient would become unwell very quickly. However, when carbon dioxide retention is slowly progressive, as is often the case in chronic COPD, the body can compensate for this by utilising the bicarbonate buffer system of the blood. The kidneys are stimulated to reabsorb more bicarbonate, which acts as a base and neutralises the carbonic acid, thus restoring the pH back to the normal range.
what can been seen in this x ray that might suggest COPD?
- flattened diaphragms
- nipple shadows
- smaller heart size
- hyper inflated lung
- horizontal ribs
fibrotic vs inflammatory causes of ILD?
inflammatory eventually turn into fibrotic if left unchecked
salmeterol inhaler and tiotropium inhaler
uncompensated type II respiratory failure
hyper-resonant percussion note, polyphonic wheeze
PaO2 7.2kPa
bronchoscopy with biopsy EBUS
bronchiectasis
honeycombing
nitrofurantoin
