Respiratory Flashcards
What is COPD?
Describes progressive and irreversible obstructive airway disease. It is a combination of emphysema and chronic bronchitis
Describe the epidemiology of COPD
1.2 million people in the UK
4th leading cause of death globally
What are the risk factors for developing COPD?
Tobacco smoking (biggest risk factor)
Air pollution
A1AD
Occupational exposure such as dust, coal, cotton, cement and grain
What are the two things that make up COPD?
Emphysema and bronchitis
What is emphysema?
Alveolar air sacs become damaged or destroyed:
- They become enlarged and lose their elasticity.
- Individuals have difficulty exhaling which depends heavily on lung recoil
Describe the pathophysiology of emphysema
When lung tissue is exposed to irritants it triggers an immune response
This attracts various immune cells such as elastases and collagenases which causes a loss in elastin in the alveoli
The elastin loss causes collapse meaning:
- air is trapped distal to the point of collapse
-lungs become more compliant when air is inhaled, the lungs expand easily and hold onto air
- Breakdown if the thin alveolar walls, which reduces the surface area for gas exchange
What are some signs of emphysema?
Barrel shaped chest due to air trapping and hyperinflation
Downward displacement of liver due to hyperexpansion of the lungs
What is bronchitis
Inflammation of the bronchial tubes of the lungs. It is said to be chronic when it causes a productive cough for at least 3 months every year for 2 or more years
Describe the pathophysiology of chronic bronchitis?
-Due to chemicals and irritants the squamous epithelium may become ulcerated and when it heals it is replaced with columnar cells (metaplasia). Irritants also stimulate hypertrophy and hyperplasia of mucinous glands so there is an increase in mucus production in bronchioles with narrow lumen this can cause obstruction
This inflammation is also followed by scarring and thickening of the walls which narrows the small airways and makes cilia shorter making it harder to move mucus meaning coughing is the only way to remove it
Overall, there is airway narrowing due to hyperplasia, inflammation and oedema.
Why is there V/Q mismatch in COPD?
Due to damage and mucus plugging of smaller airways. This leads to a fall in PaO2 and increased respiration. CO2 will remain unaffected until patient can no longer maintain respiratory effort
What is the usual drive for respiration and how does this change in how does this change in COPD?
The usual drive for respiration is CO2 however body becomes desensitised to high CO2.
- Hypoxaemia (low arterial blood oxygen) becomes the new drive for respiration.
What are the signs of COPD?
Tachypnoea
Barrel chest
Cyanosis
Quiet breath sounds and wheeze
What are the symptoms of COPD
Dyspnoea
Productive cough
Wheeze
Chest tightness
Weight loss
What are signs of CO2 retention?
Drowsy
Asterixis (flapping tremor of hands)
Confusion
What are the differentials for COPD?
Lung cancer, lung fibrosis or heart failure
COPD does not cause clubbing or haemoptysis/chest pain
What is the MRC dyspnoea scale?
5 point scale for assessing impact of breathlessness.
Grade 1 – Breathless on strenuous exercise
Grade 2 – Breathless on walking up hill
Grade 3 – Breathless that slows walking on the flat
Grade 4 – Stop to catch their breath after walking 100 meters on the flat
Grade 5 – Unable to leave the house due to breathlessness
What is FEV1 and FVC?
FEV1 = forced expiratory volume in one second
FVC = forced vital capacity
What would happen to FVC (max air exhaled in one breath) in COPD?
It would be lowered
What would happen to FEV1 (first second of air breathed out in a single breath) in COPD?
Lowered more than FVC
What would happen to TLC in COPD?
Increased due to air trapping
How would you make a diagnosis of COPD?
Clinical presentation plus spirometry
What would spirometry show for COPD?
FEV1/FVC ratio less than 0.7
Important to note that it does not show a dramatic response to reversibility testing with salbutamol (beta-2 agonist). If it does then consider asthma as a differential
What is used to classify the severity of airway obstruction?
GOLD classification
Stage 1: FEV1 >80% of predicted
Stage 2: FEV1 50-79% of predicted
Stage 3: FEV1 30-49% of predicted
Stage 4: FEV1 <30% of predicted
What other investigations might you perform for COPD?
Chest x-ray to rule out other pathology
BMI for a baseline to asses weight loss/weight gain form steroids
ECG
CT thorax to rule out fibrosis, cancer or bronchiectasis
Serum alpha-1 antitrypsin
What is the initial management for COPD?
STOP SMOKING
Annual flu vaccine and the pneumococcal vaccine (this is a one off vaccine)
What are the GOLD groups in COPD?
GOLD A = 1 or less exacerbations per year not requiring admission with mild symptoms, >80% FEV1
GOLD B = 1 or less exacerbations per year not requiring admission severe symptoms, 50-79%
GOLD C = 2 exacerbations per year or 1 per year requiring admission with mild symptoms, 30-49%
GOLD D = 2 exacerbations per year or 1 per year requiring admission with severe symptoms, <30%
What are the different bronchodilators used to treat COPD?
SABA:short-acting beta-agonist (e.g. salbutamol)
SAMA: short-acting muscarinic antagonist (ipratropium)
LABA: long-acting beta-agonist (e.g. salmeterol)
LAMA: long-acting muscarinic antagonist (e.g. tiotropium)
What is the treatment for GOLD group A?
Any short or long acting bronchodilator
(saba/laba)
What is the treatment for GOLD group B?
LAMA/LABA
What is the treatment for GOLD group C?
LAMA
What is the treatment for GOLD group D?
LAMA or LABA+LAMA or LABA+ICS
(ICS: inhaled corticosteroid e.g. beclomethasone)
When is long term oxygen therapy used to treat COPD?
Long term oxygen therapy
- is used for severe COPD that is causing problems such as chronic hypoxia, polycythaemia, cyanosis or heart failure secondary to pulmonary hypertension (cor pulmonale).
- It can’t be used if they smoke as oxygen plus cigarettes is a significant fire hazard.
What other treatments can be given alongside inhalers?
Mucolytics (carbocisteine)
Systemic corticosteroids (prednisolone)
Phosphodiesterase- 4 inhibitors (roflumilast)
Azithromycin
Long term antibiotics
What are the pros and cons of adding ICS to an bronchodilator?
Pro:
- history of hospitalisation for exacerbations of COPD
- >2 moderate exacerbations of COPD per year
- bloody eosinophils >300 cells
Cons:
- repeated pneumonia events
- blood eosinophils < 100 cells
- history of mycobacterial infection
What is an exacerbation of COPD?
COPD presents as an acute worsening of symptoms such as cough, shortness of breath, sputum production and wheeze
What causes an exacerbation of COPD?
Usually triggered by viral or bacterial infection
Can be heart failure, pulmonary embolism or medications
What would an exacerbation look like on an ABG?
CO2 will make blood more acidotic. This will show as a type 2 respiratory acidosis high CO2 and low oxygen with low pH
If this chronic there will be some metabolic compensation by kidneys releasing more bicarbonate to try and neutralise pH
What is the treatment for an exacerbation of COPD where the patient is well enough to stay at home?
Prednisolone for 7-14 days
Regular inhalers or home nebulisers
Antibiotics if there is presence of infection
What is the treatment for an exacerbation of COPD where the patient is in hospital?
Nebulised bronchodilators (e.g. salbutamol 5mg/4h and ipratropium 500mcg/6h)
Steroids (e.g. 200mg hydrocortisone or 30-40mg oral prednisolone)
Antibiotics if evidence of infection
Physiotherapy can help clear sputum
What are the treatment options for an exacerbation of COPD not responding to treatment?
IV aminophylline
Non-invasive ventilation
Intubation and ventilation
-Doxapram can be used as a respiratory stimulant if ventilation not appropriate
Why should you not give beta blockers to someone with asthma?
Beta blockers = bronchoconstriction
e.g. atenolol
Why do you have to be careful giving oxygen to someone with COPD and how would you manage this?
Too much oxygen in someone that is prone to retaining CO2 can depress their respiratory drive.
Venturi masks are designed to deliver specific percentage concentrations of oxygen
If retaining CO2 aim for oxygen saturations of 88-92% titrated by Venturi mask
If not retaining CO2 and their bicarbonate is normal (meaning they do not normally retain CO2) then give oxygen to aim for oxygen saturations > 94%
What is the difference between COPD and asthma?
Spirometry:
COPD = always abnormal
Asthma = may be normal
Serial Peak Flow
COPD = minimal variation
Asthma = day to day + diurnal variation
Reversibility
COPD = usually <15%
Asthma = usually > 15%
What is asthma
A chronic inflammatory airway disease characterised by intermittent airway obstruction and hyperreactivity
What are the two types of asthma?
Allergic/eosinophilic
Non-allergic e.g. exercise, cold air and stress
What are some risk factors for developing asthma?
History of atopy (allergies)
Viral URTI
Occupational exposur
What causes asthma?
There is often an excessive reaction for the Th2 cells against specific antigens. Allergens from environmental triggers are picked up by dendritic cells and presented to Th2 cells leading to the release of cytokines.
This leads to the production of IgE antibodies which lead to histamine release
What are some genetic causes of asthma ?
Genes controlling cytokines IL-3 -4 -5 -9 -13
ADAM33 is associated with airway hyper-responsiveness and tissue remodelling
Generally asthma before 12 is more genetic after this it is more environmental
What is the hygiene hypothesis?
Reduced early immune-system exposure to bacteria and viruses might increase the risk of later developing asthma, possibly by altering the overall proportion of immune cell subtypes.
What are the signs and symptoms of asthma?
Episodic
Diurnal variability- worse at night and in the morning
Dry cough with wheeze and shortness of breath
Bilateral widespread “polyphonic” wheeze heard by a healthcare professional
Family history of other ectopic disease such as eczema and hayfever
What are the primary investigations for asthma?
Fractional exhaled nitric oxide a value of >40 ppb is positive
Spirometry = will show a FVC/FEV1 ratio of less than 70% but will improve by 12% and increase by >200ml when using a bronchodilator
FBC = look for eosinophils
Skin prick tests
Bronchial hyperesponsivness to e.g. histamine
Sputum eosinophil count
What tests would you perform if you were unsure of a diagnosis of asthma?
PEFR: measured multiple times a day over a 2-4 week period. Variability of >20% throughout the day is diagnostic
Airway hyperreactivity testing: a histamine or methacholine direct bronchial challenge
What are Short acting beta 2 adrenergic receptor agonists?
They work quickly but the effect only lasts for an hour or 2. Nor Adrenalin acts on smooth muscle of airways to cause relaxation.
Reliver or rescue medication salbutamol
What are Long-acting beta 2 agonists (LABA)?
Same as short acting but last for longer salmeterol
What are Long-acting muscarinic antagonists (LAMA)?
block acetylcholine receptors
- stimulated by the parasympathetic nervous system which cause bronchoconstriction.
E.g. tiotropium
What are Inhaled corticosteroids (ICS)?
They reduce inflammation and reactivity of the airways. They are used for maintenance and prevention.
Beclomethasone
What are Leukotriene receptor antagonists?
Leukotrienes are produced by the immune system and cause inflammation, bronchoconstriction and mucus secretion.
Montelukast
What is MART?
Maintenance and Reliever Therapy (MART).
- a combination inhaler = containing a low dose inhaled corticosteroid and a fast acting LABA.
- This replaces all other inhalers and the patient uses this single inhaler both regularly as a “preventer” and also as a “reliever” when they have symptoms.
What is the BTS/SIGN stepwise ladder for treatment of asthma?
- SABA as required for wheezy episodes
- Regular low dose ICS inhaler
- Add LABA e.g. salmeterol
- Consider LTRA e.g. Montelukast or oral beta 2 agonist, oral theophylline or an inhaled LAMA (i.e. tiotropium).
- Titrate up ICS
- Add oral steroids at lowest possible dose
What is the NICE Guidelines (adapted from 2017 guidelines) for asthma
- SABA as required or wheezy episodes
- Regular lose dose ICS inhaler
- Add LTRA e.g. Montelukast
- Add LABA
- Consider MART
- Increase steroid dose
What are the triggers for an asthma attack?
Allergy exposure
Viral infection
Smoking exposure
Pollution
Exercise
What is the presentation of an asthma attack?
Fast respiratory rate
Symmetrical wheeze
Tight sounding chest with reduced air entry
What is investigated in an asthma attack?
PEFR
ABG: patients will initially have respiratory alkalosis. Abnormal or high PCO2 is concerning as it implies the patient is tiring
What would be considered an moderate asthma attack?
PEFR 50-75% of predicted
What would be considered a severe asthma attack?
PEFR 33-50%
Resp rate >25
Heart rate above 110
unable to complete sentences
What would be considered a life threatening asthma attack?
PEFR <33%
Sats <92%
Becoming tired
No wheeze. This occurs when the airways are so tight that there is no air entry at all. This is ominously described as a “silent chest”.
Haemodynamic instability (i.e. shock)
What is the treatment for a moderate asthma attack?
Nebulised salbutamol
Nebulised ipratropium bromide
Steroids oral continue for 5 days after
What is the treatment for a severe asthma attack?
Oxygen is required to maintain stats
Aminophylline infusion
Consider IV salbutamol
What is the treatment for a life threatening asthma attack?
IV magnesium sulphate
Admission to ICU
Intubation in worst cases
What is dyspnoea?
Shortness of breath
What is the MRC dyspnoea scale?
Grade 1
Not troubled by breathlessness except on strenuous exercise
Grade 2
Short of breath when hurrying or walking up a slight hill
Grade 3
Walks slower than contemporaries on level ground because of breathlessness, or has to stop for breath when walking at own pace
Grade 4
Stops for breath after walking about 100 metres or after a few minutes on level ground
Grade 5
Too breathless to leave the house, or breathless when dressing or undressing
What are the causes of dyspnoea?
Cardiac:
Acute pulmonary oedema
Cardiac arrhythmia
Cardiac tamponade
Chronic heart failure
MI
Pulmonary:
Asthma
Bronchiectasis
COPD
Interstitial Lung disease
Pleural effusion
lung collapse
Pneumonia
pulmonary embolism
other:
Anaemia
anaphylaxis
anxiety
diaphragmatic splinting (ascites, obesity, pregnancy)
What is type 1 respiratory failure?
Hypoxemia
- failure of lungs to provide adequate O2 to meet metabolic needs
What are the causes of type 1 respiratory failure?
R-L shunt
V/Q mismatch
Alveolar hypoventilation
Diffusion defect
Inadequate FIO2
e.g. Asthma, ILD, cardiac septal defect, COPD, PE
What is the criteria for type 1 respiratory failure?
PaO2 < 60mmHg on FiO2 or pO2 <8kpa
Low PaO2 with normal or low PaCO2
What is type 2 respiratory failure?
the failure of the lungs to eliminate adequate CO2
What are the causes of type 2 respiratory failure?
Pump failure
Increased Co2 production
R-L shunt
Increased deadspace
e.g. COPD, drug OD, obesity, chest wall deformity, neuromuscular weakness
What is the criteria for a type 2 respiratory failure?
Acute increase in PaCO2 > 50mmHg
Low PaO2 with raised PaCO2
What are the signs of hypercapnia in type 2 respiratory failure?
Bounding pulse
Flapping tremor
Confusion
Drowsiness
Reduced consciousness
What is DLCO a measure of?
Transfer Coefficient of oxygen/CO
Measure of ability of oxygen to diffuse across the alveolar membrane
How is DLCO measured?
Can calculate by inspiring a small amount of carbon monoxide (not too much since can kill)
hold breath for 10 seconds at total lung capacity (TLC) then the gas transferred is measured
What causes a high DLCO?
Pulmonary haemorrhage
- can absorb O2 very efficiently due to bleeding resulting in more red blood cells being available
What causes a low DLCO?
Severe emphysema
Fibrosing alveolitis
Anaemia
Pulmonary hypertension
Idiopathic pulmonary fibrosis
COPD
What is the pleura? and the layers?
Lining of the lung
1. Visceral pleura – forms the
outer covering of the lung
2. Parietal pleura – forms the inner lining of the chest wall
Between the 2 linings is the pleural space
In health this space is almost non-existent, contains 5- 10mls of fluid
What is the purpose of the pleura?
Allows for optimal expansion and contraction of the lungs
Pleural fluid allows for visceral and pareital pleurae to glide over without friction during respiration
What is pneumothorax?
‘collapse of the lung’
Presence of air in the pleural
space
what occurs during a pneumothorax?
Air enters due to
- Hole in the lung/pleura
- Chest wall injury
intrapluerla pressure is negative, leads to air beinf sucked into cavity
What are the causes of a pneumothorax?
- primary spontaneous pneumothorax
- secondary spontaneous pneumothorax
- traumatic pneumothorax
- iatrogenic pneumothorax
What is primary spontaneous pneumothorax? and risk factors?
- No underlying lung disease
- Rupture of apical pleural bleb
Risk Factors
Male
Smoker
Tall (lung stretched)
Age 20-40 y/o
Annual incidence 9 per 100,000
Risk of recurrence high
What are the causes of secondary spontaneous pneumothorax?
- known lung disease = COPD, Asthma. lung cancer, cystic lung disease (cyst pops)
- infection = PCP/TB, lung abscess
- genetic predisposition = Marfan’s, Birt- Hogg Dube, lymphangioleiomyomatosis LAM
- Catamenial pneumothorax = occur with menstruation + PCOS (only in females)
What are the difference in traumatic and iatrogenic causes of pneumothorax?
Traumatic
Penetrating chest wall injury
Puncture from rib
Rupture bronchus/ oesophagus
Iatrogenic:
‘Doctor induced’
Risk
Pacemakers,
CT lung biopsies,
Central line insertion
Mechanic ventilation
Pleural aspiration
What is the presentation for a pneumothorax?
Asymptomatic
Acute/ sudden
Breathlessness
Pleuritic chest pain
Cough
Life threatening resp failure/ cardiac arrest
sweating
What are the signs of a pneumothorax?
Tachyopnoea
Hypoxia
Unilateral chest wall expansion
Reduced breath sounds
Hyper-resonant percussion note
Tension penumothorax:
Deviated trachea (away)
Surgical emphysema
Distended neck veins
Cardiovascular compromise
What is a tension pneumothorax?
- air pushing against the healthy lung, squashing it
- displaces mediastinum and cardiac compromise
- medical emergency
- requires urgent decompression
What is the first line investigation for a pneumothorax?
If tension pneumothorax is suspected then don’t wait
Chest x-ray would be first line and would show:
- no pleural edge with no lung markings
- Look for mediastinal shift in tension
What is the gold standard investigation for a pneumothorax?
CT chest:
will show an accurate size of the pneumothorax will be rarely used though
What is the management for a pneumothorax?
- No intervention
Reabsorb spontaneously 2% volume a day
Consider high flow oxygen (10L) - Pleural Aspiration
Up to 1.5Litre of air can be aspirated - Ambulatory devices
stick one way valve on chest and send home - Chest Drain
Needed for most secondary pneumothoraxes - Surgery
For persistent and recurrent pneumothorax
What is the management for a tension pneumothorax?
Initially inset a large bore cannula into the second intercostal space in the midclavicular line do not wait to do this
Once the pressure is relieved then use a chest drain
Where are chest drains usually inserted?
- The 5th intercostal space (or the inferior nipple line)
- The mid axillary line (or the lateral edge of the latissimus dorsi)
- The anterior axillary line (or the lateral edge of the pectoris major)
Why is a tension pneumothorax dangerous?
Air is drawn in to the pleural space with each breath and cannot escape.
This is dangerous as it creates pressure in the thorax and will push the mediastinum across kinking the big vessels causing cardiorespiratory arrest
What is general advice to prevent future pneumohtoraxes?
(very high re-occurence rate)
stop smoking
no air flight until 6 week after resolution
no scuba diving ever
What is a pleural effusion?
collection of fluid in the pleural space
- fluid presses against lung, compressing it and making it smaller
What are the 2 types of pleural effusions?
(light’s criteria)
Transudates
- pleural fluid protein < 30g/L or 1/2 serum protein
- low protein count fluid moving across into the pleural space (fluid shifting)
(increased hydrostatic pressure or reduced osmotic pressure in microvascular circulation)
Exudates
- pleural fluid protein > 30g/L or 1/2 serum protein
- high protein count caused by inflammation proteins leak out of tissue
(increase capillary permeability and impaired reasborption)
What are the causes of transudative pleural effusion?
Congestive heart failure
Hypoalbuminemia
Hypothyroidism
Meig’s syndrome (right sided pleural effusion with ovarian malignancy)
(cirrhotic liver disease)
What are the causes of exudative causes of pleural effusion?
Lung cancer
Pneumonia
Rheumatoid arthritis
TB
(inflammation increase protein levels)
What are the symptoms for a pleural effusion?
Asymptomatic
Breathlessness
Cough
Pain
Fever
What are the signs for pleural effusion)
Reduced chest wall
expansion
Quiet breath sounds
“Stony” Dull Percussion
Reduced tactile/ vocal fremitus
Mediastinal shift away from affected side
What investigations are done for a pleural effusion?
X-ray = blunting of diaphragm + costcophrenic angle, fluid, larger effusions, tracheal + medialstinal deviation
Thoracic USS = before doing needle aspiration, to exclude other causes
pleural aspiration = take sample of fluid
What do the appearances of the pleural fluids signify?
- straw coloured = transudate/exudate
- turbid/foul smelling= empyema/parapneumonic effusion
- milky = chylothorax
- blood stained = trauma, cancer, PE
- food particles = oesophageal rupture
What tests are done on the lung fluid?
Biochemistry
pH
Protein
LDH
Glucose
(Amylase)
Microscopy and culture
- AAFB
Cytology
What is a medical thoracoscopy?
- local anaesthetic
- put tube in and draw out all the fluid
- and take some biopsies
What is the management for a pleural effusion?
Depends on size, symptoms and underlying cause
Small effusions often treated conservatively
Pleural infection/empyema
- Antibiotics
- Chest drain if pus/ complex infection
Malignant effusion
- Consider chest drain if symptomatic (+/- talc)
- If re-current consider long term chest drain
Treat underlying cause e.g.
Diuretics for heart failure
Dialysis for renal failure
NSAIDS/ steroids for SLE effusion
What is the criteria for a pleural infection?
Criteria that would support a diagnosis of
pleural infection
pH < 7.2
Glucose < 3.4mmol/L
PF LDH > 1000 IU/L
Bacterial growth on culture
Macroscopic appearance of pus (can do a chest drain straight away)
What is the progression of a pleural infection?
- Simple parapneumoni effusion
- complex parapneumonic effusion
- Empyema (pus)
What is a complication of pleural effusion?
Empyema
What is empyema?
pus in the pleural space
What are the causes of empyema?
community/acquired
- S. milleri/ S. pneumo/ S. Aureus/
Anaerobes
Hospital Acquired
MRSA/ S. Aureus/ Enterococcus
What are the symptoms for empyema?
Symptoms
Patient unwell/ not improving
Swinging fevers/ rigor
Cough/ Chest Pain
What is the treatment for empyema?
Antibiotics (prolonged course)
Chest Drain
Surgery
What is the treatment for malignant effusions?
Drain and ‘pleurodesis’
- chest drain (talc via drain)
- thoracoscopy (spray talc - cause inflammatory response making lung expand and stick to pleura to stop from refilling with fluid)
if recurrent = indwelling pleural catheter (IPC)
What is a haemothorax?
Blood in pleural cavity
(haemocrit ratio >50%)
What are the causes of a haemothorax?
Trauma
Post-operative
Bleeding disorders
Lung cancer
PE
Aortic rupture
Thoracic endometriosis
What is the management for haemothorax?
- Large bore chest drain
- Possible vascular intervention = embolise vessel to stop bleed
- Surgical opinion
What is a hydropneumothorax? A
air and fluid in pleural space
What are the causes for a hydropneumothorax?
Iatrogenic
Gas forming organisms
Thoracic trauma
What is the cause of thickening of pleura?
- Related to asbestos exposure
- Following infection/ empyema/ chest trauma/ haemothorax
- Cancer (Consider if nodular/ >1cm depth)
What is a pneumomediastinum?
Air in mediastinum
- Air from lungs/ trachea/ oesophagus/ peritoneal cavity
What are the features and causes of a pneumomediastinum?
Can track to neck/ face and abdomen
Often seen with surgical emphysema/ pneumothorax
Oesophageal rupture (Boerhaave’s syndrome - also get mediastinitis)
What is a normal alveolar-arterial gradient?
normally less than 2kPa
What are the causes of a raised A-a gradient?
- V/Q mismatch (ventilation perfusion)
- Diffusion limitation
- Shunt (right-to-left)
What are the features and treatment of a high altitude pulmonary oedema?
1%at4000m
* 2-3 days after ascent
* Exaggerated hypoxic pulmonary vasoconstriction
* Treatment: Descent, oxygen, pulmonary vasodilators
What are the classfications for obstructive and restrictive lung conditions?
Obstructive vs. Restrictive
* Low FEV1 (< 80% predicted)
* FEV1/FVC ratio (< 0.7 aka 70%) = obstructive
* FEV1/FVC ratio normal = restrictive
What is transfer factor?
Diffusing capacity
- the extent to which oxygen passed from the air sac of the lungs into the blood
What does a low or high Transfer factor of the lungs for Carbon Monoxide (TLCO) indicate?
Low TLCO
* Thickening of the alveolar-capillary membrane
* Reduced lung volumes
Raised TLCO
* Increased capillary blood volume
* Pulmonary haemorrhage
What conditions have low TLCO?
Pulmonary fibrosis
What conditions have a high TLCO?
- Alveolar haemorrhage (blood is sitting there so has more time to diffuse)
- left to right intracardial shunt (blood goes past twice)
What is the difference between pneumonia, pulmonary fibrosis, pulmonary TB, emphysema, asthma and bronchitis?
Pneumonia = alveoli fill with thick fluid, making gas exchange harder
Pulmonary fibrosis = fibrous connective tissue build up in lung, reduce elasticity
Pulmonary TB = TB encapsulate bacteria + elasticity reduced
Emphysema = alveoli burst and fuse into enlarged air spaces reducing surface area
Asthma = airways are inflamed due to irritation and bronchioles constrict due to muscle spasms
Bronchitis = airways are inflamed due to infection or irritants
What are the advantages of inhaled medicines?
- lungs are robust
- large surface ares
- rapid absorption
- fewer systemic side effects (as drug is ending up just in lungs where you want it)
- non-invasive
- act directly on the lung or enter the systemic circulation
What are the different delivery systems for inhaled devices?
- pressurised metered dose inhalers
- spacer devices = slow down particles so more of drug can be inhaled
- dry powder inhalers = person needed sufficient inspiratory effort to breathe in powder
- Nebuliziers = less coordination needed
What occurs during bronchoconstriction?
Constriction of the airways due to:
- tightening of airway smooth muscle (ASM)
- lumenal occlusion by mucus and plasma
- airway wall thickening
Leads to airflow obstruction.
Most commonly seen in asthma & COPD
Reversible vs non-reversible
How do airway smooth muscle cells react in asthma?
ASM is both primed to contract and is resistant to relaxation
What are the two categories of bronchodilators?
Adrenergic (sympathetic)
bronchodilation
Anti-cholinergic (parasympathetic)
Block bronchoconstriction