Minor resp 1 Flashcards
(14 cards)
What changes occur during congestion?
Inflammatory response causes inflammation of goblet cells and excessive release of mucus. Mast cell releases histamine which binds to histamine receptor and causes vasodilation and inflammation causing increased release of mucus from goblet cells.
What mechanisms can you use to reduce congestion?
Activate alpha 1 receptor to induce vasoconstriction, block histamine receptor, prevent histamine release (mast cell stabiliser), antibodies which inactivate inflammatory mediators (too expensive). Target the DNA and prevent expression of proteins (inflammatory mediators) that cause inflammation (corticosteroids).
What are the alpha 1 receptor agonists and what are the 2 kinds and how do they work?
Ephedrine & Pseudoephedrine: Noradrenaline equivalent- non selective. Lead to vasoconstriction, reducing congestion. Phenylephrine, Oxymetazoline & Xylometazoline: Direct alpha-1 adrenergic receptor agonists. Cause vasoconstriction, reducing nasal swelling. (Gq PIP 2 to IP3 and DAG so increases Ca2+ release resulting in contraction).
Give examples of antihistamines, explain their mechanism and side effects.
Examples: Cetirizine, Loratadine, Levocetirizine, Chlorphenamine, Diphenhydramine, Azelastine. Mechanism: Allergen-activated IgE binds to mast cells, mast cells degranulate releasing histamine. Histamine binds to H1 receptors riggers allergic reactions, leading to mucus secretion. Antihistamines block H1 receptors, preventing histamine effects (allergic reaction and mucous secretion). Administered orally, intravenously, or via inhalation. Side effects: Drowsiness (especially first-generation antihistamines) (this is because first gens can cross the brain blood barrier).
Give examples of glucocorticoids, explain their mechanism and list their side effects.
Examples: Fluticasone, Budesonide, Prednisolone. Mechanism: Bind to nuclear receptors to induce inhibitory proteins. Inhibit the release of arachidonic acid, preventing leukotriene and prostaglandin synthesis. Suppress inflammatory immune cells and cytokine release. Administered nasally, orally, parenterally, or via inhalation. Side effects: Dysphonia, oral candidiasis.
What causes coughing?
Viral infection, allergies, airway irritants, chronic conditions like asthma. Overproduction of mucus which is kept in balanced production. If you have too little or too much mucus it will trigger inflammation and cause coughing.
What is the cough reflex pathway?
Inflammation in resp system induces vagus nerve which sends signal to medulla which induces a signal to the effectors (vagus to larynx, phrenic to diaphragm) which induces cough - inspiratory, compression, expiratory
What are the three phases of coughing?
Inspiratory phase - air is taken into the lungs. Compressive phase - epiglottis closes and intrathoracic pressure builds due to expiratory muscle contraction. Expiratory phase - Sudden release of air in high velocity.
What are the different types of drugs for treating a cough?
Mucolytic - clear mucus from resp tract
expectorant promote production of mucus and phlegm
antitussive - cough suppressant ,
decongestant - relieve nasal congestion
How do mucolytic agents work?
They clear mucus from the respiratory tract-e.g. Bromhexine depolymerises muco-polysaccharides in mucus making it less viscous.
How do expectorants work and give an example of one?
Expectorants like guaifenesin - induces parasympathetic nervous system, reduces mucous production and increases clearance of mucus by triggering more coughing (not preferred for patients).
How do cough suppressants work?
Cough suppressants like codeine bind to the mu receptor, activate Gi subunit on neurons in the brainstem (neuron to diaphragm which is normally stimulated by vagus nerve), means less stimulation and action potential as it decreases calcium conductance and increases potassium conductance. Inhibits action potential and NT release.
What are the dangers of cough suppressants (Codeine and codeine metabolites)?
Codeine is a prodrug so is inactive unless metabolised by enzyme in liver CYP2D6 which will result in morphine being produced which causes the cough suppressing effect. However if someone is a rapid metaboliser (or a child which have an immature version of the enzyme) they produce too much morphine which causes morphine to bind to receptors all over the body which can cause respiratory depression and death.
What is an alternative to codeine that can be used but why can’t it be used with children?
Dextromethorphan which is a derivative of codeine but not an opiate but activates the parasympathetic nervous system and activates serotonin pathway which inhibits cough reflex pathway. Still not recommended for peds as it can cause palpitations and cardiac complications based on serotonin effect.
