Respiratory Flashcards
What is seretide?
Preventer product containing fluticasone (glucocorticoid) and salmeterol (long acting beta 2 agonist)
Asthma
Yourface
Pseudoephidrine mechanism of action
1) enters noradrenergic nerve and is taken up into storage vesicles in exchange for NA.
2) NA acts on post synaptic membrane and acts on alpha 1 receptors - causes vasoconstriction therefore decreased odema and fluid leakage.
Name two short acting beta agonsists
Salbutamol
Terbutaline
Name two long acting beta agonists
Salmeterol
Formoterol
Name two examples of M receptor antagonists
Ipratropium
Tiotropium
Three examples of inhaled glucocorticoids
Budesonide
Fluticasone propionate
Beclomethasone Dipropionate
Two examples of oral glucocorticoids
Prednisolone
Hydrocortisone
Mechanism of action of Beta-2 adrenoreceptor agonist
Binds to GPCR Beta-2 adrenoreceptors on lining of airways.
Activates Gs pathway -> increased adenylate cyclase activation -> PKA activation -> decrease intracellular Ca ions + dephosphorylation of MLCK -> decreased excitability of cells -> BRONCHODILATION
Mechanism of action of Glucocorticosteroids
Bind to GRalpha receptor (homodimerized complex) in cytoplasm. This complex moves into nucleus.
Transactivation:
- complex binds to positive GRE within promoter -> upregulates transcription of anti-inflammatories
Transrepression:
- complex binds to negative GRE -> displaces bound transcription factors -> reduce transcription of pro-inflammatories
What is the difference between SABA and LABA
Short acting beta agonists: - effective in minutes - 3-5 hr duration - reliever medication for attacks Long acting beta agonists - effective in 10-20 minutes - 8-12 hr duration - symptom control/preventer
Mechanism of action of M receptor antagonists
Prevent binding of ACh -> prevent activation of Galphaq pathway -> decrease PLC -> decrease IP3 -> decrease intracellular Ca ions -> dephosphorylation of MLCK -> muscle relaxation
Mechanism of action of Pseudoephedrine
- Enters cytoplasm of noradrenergic nerve terminals via Uptake 1 transporter
- Taken up into vesicles via VMAT in exchange for noradrenaline (NA) into the cytoplasm
- Some NA degraded by MAO enzyme, the rest exits nerve terminal via Uptake 1 in exchange for pseudo
- Pseudo also inhibit NA reuptake
- In the synapse, NA acts on postsynaptic receptors to cause vasoconstriction
- Pseudo is resistant to MAO breakdown
- It is used to treat non-allergic rhinitis
Mechanism of action of Antihistamines
Reversible competitive antagonism of histamine at H1 receptors
- decrease vascular permeability
- decrease pruritus
- relaxation of smooth muscle in resp and GI tract
-They are used to treat allergic rhinitis
What makes an antihistamine non-sedating?
Decreased lipophilicity -> less able to cross BBB -> less CNS side effects
Examples of non-sedating oral antihistamines
Fexofenadine
Cetirizine and Levocetirizine
Loratadine and Desloratadine
Examples of sedating oral antihistamines
Azatadine Pheniramine Chlorpheniramine Dexchlorpheniramine Cyproheptadine Promethazine
Mechanism of action of intranasal anticholinergics
.
Mechanism of action of Mast cell stabilisers
reduces hyperreactivity and reduces immediate & delayed phases of asthma
Under what cirumstances would you refer patient to doctor?
- White or yellow spots on a bright red throat
- Swollen tonsils or lymph nodes
- Pain when swallowing
- Fever (over 38.3 degrees)
- Sudden, severe sore throat
- Difficulty breathing
- Dysphagia
- Persistant sore throat
- Persistant thrush
Expectorant examples
expectorants improve the ability to expectorate mucosal secretions
- hydration with steam
- Gauiphenesin (decreases viscosity of phlegm)
- Ammonium Chloride (avaliable as “Senega & Ammonia mixture. Irritates bronchial mucoasa causing increased mucosal fluid)
Mucolytic examples
Mucolytics break down mucus
- bromhexine (break disulfide bonds between gel-forming mucins & therefore decreases viscosity)
- acetylcysteine (breaks disulfide bonds like bromhexine. Used in cystic fibrosis)
Centrally acting cough suppressants
Depress cough centre in medulla (NTS)
Narcotic
- codiene, dihydrocodeine, pholcodine
- activate opioid receptors –> results in less glutamate & NMDA activation (receptor that causes cough)
Non-Narcotic
- dextromethorphan (NMDA receptor antagonist/sigma agonist)
- diphenhydramine - antihistamine/TRPV1 antagonist
Peripherally acting cough suppressants
- Local analgesic effect or anti-inflammatory effect
- camphor, menthol
- benxydamine (difflam throat spray) - Enhance drainage of bronchial secretions by reducing viscosity (expectorants)
- relaxation of bronchial smooth muscle (bronchodilators)
- demulcent or soothing effect on irritated throat & airways (honey, syrup, thickener, expectorants)
Decongestants
- oxymetazoline (spray)
- xylometaxoline (spray)
- pseudoephedrine (oral)
- phenylephrine (oral)
Rhinitis Treatments
1) decongestants
2) antihistamine
3) leukotriene Receptor antagonist
4) Corticosteroids
5) Mast cell stabilisers
6) Intranasal anticholinergics
Drugs that can be used to treat asthma during pregnancy & breastfeeding
- bronchodilators - salbutamol, tebutaline
- glucotorticoids - budesonide
- avoid long acting beta 2 agonists during first trimester (unless already on LABA –> don’t stop)
When are leukotriene antagonists used? Give an example
3rd line use treatment in asthma
eg. montelukast
