Treatment for common cold, flu, allergic rhinitis and sinusitis (2.2) Flashcards
A) What does common cold, flu, allergic rhinitis and sinusitis have in common?
B) How does this mechanism work and how does it contribute to the symptoms associated with this conditions
A) Inflammation
B)
- Injurious agent infection
- Activation of mast cells
- Release of mediators of inflammation eg HISTAMINE
- Vasodilation and increased vascular permeability –> Nasal congestion, headache, runny nose, phlegm
- Increase sensitivity to pain –> sore throat, aching body
What are some pharmaloogical interventions to the below physiological changes and associated symptoms;
A) Injurious agents – bacterial infection + Flu – viral infection
B) Activation of mast cells
C) Release of histamine
D) Vasodilation and increase vascular permeability with associaed symptoms: nasal congestion, mucossal swelling, runny nose
E) Inflammatory responses to cellular injury –> allergic reactions
F) Increase sensitivity to pain
A) Antibiotics
B) Mast cell stabiliser (prevent further release of mediators)
C) Inhiibit action of histamine - Antihistamine
D)
- Vasconstrictor to reduce congestion
- Sympathomimetics - oral and intranasal decongestants
E) Intransal corticosteroids
F) Analgesics –> paracetamol, ibuprofen, aspirin
A) What are mast cells
B) What happens when they are activated?
A)
- Typically present in tissues that surround neurovascular tissue (skin, mucosa of lungs + digestive tract, mouth, nosew)
- Play a key role in modulating the intial inflammatory responses
- Respond to cellular injury - infection - by rapidy degranulating and releasing histamine and other chemical mediators
B)
Imp activator of inflammatory response
- Release mediators ( Histamine, arachidonic acid, prostaglandins & leukotrienes, cytokines)
- Temporary rapid SM contraction in vessles –> vasconstriction
- Then VASODILATION –> Increased vascular permeability –> decreased in blood pressure (BP)
- CONTRACTION of smooth muscle cells in lung causing constriction of airways
Give some examples of mast cell stabilisers and their mechanism of action
Intranasal mast cell stabiliser: Cromoglycate and prophylactic treatment for allergic rhinitis
Mechanism of action
- Prevent release of histamine and other chemical mediators from mast cells
- Inhibit mast cell degranulation and stabilise mast cell by blocking calcium channel regulated by IgE in response to immune challenge
- Block entry of calcium –> prevent histamine vesicles fusing to cell membrane –> inhibit histamine release
For antihistamines;
A) Provide an example of a sedating antihistamine, oral antihistamine (less sedating) and a intranasal antihistamine
B) Provide thier mechanisms of action
A)
- Sedating antihistamine: Chlorpheriamine, promethazine
- Oral antihistamine: Cetrizine, fexofenadine
- Intransal antihistmaines: Azelastine, levocabastine
B)
- Histamine 1 antagonists –> Block action of histamine on H1-receptors
- Reduce vasodilation and vascular permeability –> reduce congestion and dry up mucous
- Seading antihistamines can cause BBB –> sedating effects
What happpens when antishistamines are used with cytochrome inhibitors?
They will stay in the body for longer if they are taken with cytochrome inhibitors such as CYP3A4/5 inhibitors;
- Antifungals – ketoconazole
- HIV protease inhibitors – ritonavir, darunavir
- Grapefruit juice
What are some adverse effects of antihistamines due to their mechanisms of action?
- H1 - receptor - blockade
> decreased neurotransmission in CNS, cognitive & psychomotor function
> increased seation, appetite
- Muscarinic receptor - blockade
> increased dry mouth, urinary retention, sinus tachycardia
- a-Adrenergic receptor-blockade
> Hypotension, dizziness, reflex tachycardia
- Serotonin receptor-blockade
> increase appetite and weight gain
- Cardiotoxicity –> Cardiac ion channels-blockade – less with 3rd gen drugs
> Prolonged QT interval –> possible ventricular arrhythmias
For Sympathominimetics;
A) Give an example of an oral decongestant, ocular vasoconstrictor and intransal decongestant
B) What is the mechanism of action
A)
- Oral decongestant: pseudoephedrine, phenyelphrine
- Ocular vasoconstrictor: phenylephrine
- Intranasal decongestants: ephedrine, phenylephrine, xylometazoline
B)
- Stimulates the alpha-1 receptors in the wall of blood vessels –> contraction of smooth muscle –> vasoconstriction
- Narrows blood vessels, decrease nasal blood flow –> reduces congestion
- Decreases vascular permeability –> reduce mucus secretion
- Ocular administration –> contraction of iris –> dilation of pupil (mydriasis)
What are some adverse efffects that drugs that target adrenergic receptors eg Sympathomimetics
- Hypertension and tachycardia
- Beta 1 –> tachycardia
- Alpha 1 –> increased BP
- Prolonged use –> rebound congestion
Give some examples of anticholinergic agents and their mechanism of action
Intranasal Anticholinergic agent: Ipratropium (use of allergic rhinitis –> hayfever)
Mechanism of action
- Block muscarinic M3 receptor in the bronchi and bronchioles –> relaxation of smooth muscle –> bronchodilation –> reduce chest tightness
- Potent inhibitor of mucus secretion in the upper and lower respiratory tract –> reduce congestion and nasal discharge
Give some examples of corticosteroids and their mechanism of action
Intranasal contricosteroids: Beclomethasone, budesonide, fluticasone, mometasone, triamiconolone –> first line treatment for allergic rhinitis
Mechanism of action:
- Act by binding to glucocorticosteroid receptor
- Inhibit pro-inflammatory molecules and cells including mast cells, basophils, eosinophils and lymphocytes (inflammatory blood cells) –> reduce release of chemical mediators such as histamine
- Increased activity of anti-inflammatory molecules –> reduce inflammation –> reduce mucosal swelling, congestion and secretion
