3- Respiratory Diseases and treatment Flashcards
Name 2 obstructive respiratory disease
- asthma
2. COPD
What functions can respiratory diseases impact?
- Gas exchange
2. Lung Inflation
Name 7 diseases that affect gas exchange?
- Pulmonary oedema
- Acute respiratory distress syndrome
- Obstructive lung disease
- Congenital diseases
- Pulmonary infections
- Carcinomas
- Pulmonary embolism
What is pulmonary oedema and what causes it?
Pulmonary oedema is when fluid fills alveolar spaces from the interstitial spaces. one key cause is congestive heart failure (backflow of blood leads to an increase in hydrostatic pressure forcing fluid into alveoli)
What is acute respiratory distress syndrome?
endothelial cells get damaged. e.g drowning/infection/pneumonia/chemical injury (Drugs)
What is obstructive lung disease? give examples?
partial/complete blockage of the airway obstructing airflow. leads tp build-up of co2 lack of o2 shortness of breath.
e.g. asthma, emphysema, chronic bronchitis, bronchiectasis
What would the FEV1:FVC be in obstructive lung disease?
FEV1:FVC is less than 0.7
Give an example of congenital disease and how it would impact gas exchange
cystic fibrosis -> build up of mucus in airways
Who are pulmonary infections more common in?
immunocompromised patients e.g. HIV
What is a pulmonary embolism?
blood clot blocking pulmonary arteries, leads to large parts of lungs not receiving blood supply.
What 2 types of disease affect lung inflation?
- restrictive lung disease
2. surfactant deficiencies
What 2 types of restrictive lung diseases are there?
- chest wall disorders
2. infiltrative diseases
give 3 examples of chest wall disorders
- pneumothorax - obstruction to visceral/pleural membrane
- neuromuscular disease
- pleural disease e.g. severe obesity
How do infiltrative diseases affect lung inflation?
causes fibrosis (scarring) of the lungs
What is a surfactant?
made up of phospholipids disrupts surface tension created by water surrounding epithelium increasing compliance.
How does surfactant deficiency affect lung inflation?
They will have more surface tension around the alveoli making it harder to inflate the airways.
Who is likely to have surfactant deficiency?
premature babies
people with mutations
which obstructive lung disease is reversible?
asthma
2 types of asthma?
bronchial hyper-responsiveness
bronchoconstriction
2 types of bronchial hyper-responsiveness?
- atopic - allergen causing sensitisation
2. non-atopic - not caused by an allergen
give some examples of what can trigger an asthma attack?
- cold air
- exercise
- environmental stimulus (smoke,dust,pollen)
- occupational triggers (chemicals,fumes, gas)
- stress/emotion
- respiratory infections
- drug induced e.g. NSAIDs
2 stages of an asthma attack?
- immediate phase
2. late phase
briefly describe the immediate phase
allergen/stimulus detected -> results in recruitment of mast calls -> mast cells degranulate to release histamine which constricts bronchioles. {mast cells also produce chemokines used in the late phase}
what do chemokines do?
attract inflammatory cells
briefly describe the late phase
chemokines cause t-helper2 cells to be recruited -> leads to exaggerated response and production of cytokines. this leads to :
- damage to airway
- airway inflammation
- hypertrophy of smooth muscle cells
what happens to the cells when the airway is inflamed?
- blood vessels become dilated
- basement membrane thickens
- epithelial cells damaged (desquamated) leading to more mucus production which blocks the airway
- oedema
- hypertrophied smooth muscle (leads to more constriction)
- infiltration of inflammatory cells which damage the epithelial cells
in what 2 ways can we control airway diameter?
- dilation (Sympathetic NS)
2. constriction (Parasympathetic NS)
what chemical causes dilation of the airway?
adrenaline {beta 2 adrenoreceptor}
which chemical causes constriction of the airway?
Acetylcholine (Ach) {m3 cholinergic receptor}
what type of receptor does adrenaline bind to?
a beta 2 adrenoreceptor
what type of receptor does acetylcholine bind to?
an m3 cholinergic receptor
what can we use to dilate the airway?
- beta 2 agonist
- muscarinic antagonist
- xanthine
- steroid
how does a muscarinic antagonist dilate the airway?
it prevents Ach binding (which constricts the airway) allowing relaxation of the airway
what can we use to constrict the airway?
- histamine
- cigarette smoke
how is histamine released?
from the degranulation of mast cells
What treatments can we use to relieve asthma attacks? (bronchodilators)
- beta 2 agonist
- antimuscarinic drugs
- xanthines
what treatments can we use to prevent asthma attacks (prophylactic)
- sodium cromoglicate and nedocromil
- leukotriene receptor antagonist
- glucocorticoids
- monoclonal antibodies
how do sodium cromoglicate and nedocromil prevent asthma attacks?
they prevent the degranulation of mast cells, therefore, no histamines are released (so no constriction)
how do leukotriene receptor antagonists prevent asthma attacks?
inhibits leukotrienes (which constrict airways)
how do monoclonal antibodies prevent asthma attacks?
inhibit the involvement of IGE antibodies
what do beta 2 agonists act on?
beta 2 adrenoreceptors (which relaxes smooth muscles in the airway)
2 types of beta agonists?
- short acting e.g. salbutamol [lasts 3-5 hrs]
2. long acting e.g. salmetorol [lasts 8-12 hrs]
Side effects of beta agonists?
- muscle tremor/cramp
- heart: tachycardia, palpitations, arrhythmias
- nervous tension
- headaches
- hypokalemia
3 ways of administering salbutamol?
- metered dose inhaler
- spacer device
- nebuliser
what is hypokalemia and what causes it?
drop in plasma potassium due to lack of k+ in the blood. this is caused by b2 agonist stimulating the na+/k+ pump causing more k+to be taken up in the cells
how can we minimise the side effects of beta 2 agonists?
by taking the drug via an inhaler rather than orally
what do glucocorticoids do?
dampen down the inflammatory response
what is the special feature of glucocorticoids?
they are lipid soluble (lipophilic)
briefly explain how glucocorticoids work
change mRNA levels
- steroid diffuses across lipid bilayer
- binds to receptor forming a dimer
- dimer moves into nucleus and binds to dna
- affects mRNA levels
what effect does increasing mRNA have on protein production?
increasing mRNA increases protein production
what effect does decreasing mRNA have on protein production?
decreasing mRNA decreases protein production
side effect of glucocorticoids
- oral candida (reduces number of t-helper cells)
- adrenal suppression
- decrease in bone mineral density
- bruising, weight loss, osteoporosis
- increased glucose production leading to hyperglycemia (possibly diabetes)
- reduction in protein synthesis and increase protein breakdown leads to muscle wasting
what can steroid drugs lead to?
Adrenal atrophy
what does COPD encompass
emphysema and chronic bronchitis
what is emphysema?
loss of elastin fibre, less able for lungs to inflate
what is chronic bronchitis?
inflamed bronchial tubes produce a lot of mucus
what does alpha 1 antitrypsin do?
protects trypsin from attacking the airway
signs and symptoms of emphysema?
- dyspnoea
- severe weight loss
- pulmonary hypertension
- right sided heart failure
signs and symptoms of chronic bronchitis?
- persistent cough with sputum
- dyspnea
- hypercapnia
- hypoxaemia
- mild cyanosis
- cardiac failure
what is hypercapnia?
elevated co2 levels in the blood
what is hypoxaemia?
abnormally low levels of o2 in the blood
treatments of COPD?
- smoking cessation
- immunisation against flu etc (due to increased likelihood of infections)
- trial of inhaled or oral glucocorticoids
- short/long-acting bronchodilators
- oxygen therapy (at 24%)
why should you avoid rubber dam in pts with COPD?
more obstruction to airways
why should you avoid general anaesthesia in pts with COPD?
risk of respiratory depression
