migraine pathology: Migraines are thought to be caused by the release of peptide neurotransmitters (primarily the calcitonin gene-related peptide, viz. CGRP) from the trigeminal nerve distribution into the intracranial arteries. These neurotransmitters are known to be powerful vasodilators resulting in cranial vasodilation. This may further lead to extravasation of blood plasma and plasma proteins resulting in perivascular oedema. Perivascular oedema can cause mechanical stretching, leading to activation of pain nerve endings in the dura which may be the cause of the painful headache associated with migraines.
migraine treatment:
Allergies, colds and flue, cold air, physical damage, chemical or drug damage.
First generation antihistamines: diphenhydramine, promethazine, chlorpheniramine, brompheniramine
Alpha 1 agonist/decongestants: phenylephrine, ephedrine, phenylpropanolamine, naphazoline, xylometazoline, oxymetazoline
Ephedrine, pseudoephedrine and propylhexidrine are non-selective for adrenoceptors and thus stimulate alpha and beta adrenoceptors with a potent indirect action and mixed action.
Phenylephrine is direct acting.
Naphazoline, xylometazoline and oxymetazoline are imidazole derivatives with mixed action.
They are administered as nasal sprays, gels/jellies, drops and inhalations.
Short acting (4-6 hours): ephedrine, phenylephrine, naphazoline
Intermediate acting (8-10 hours): xylometazoline
Long acting (more than 12 hours): oxymetazoline
It happens when decongestants/alpha 1 agonist are used chronically.
The permanent vasoconstriction of nasal capillaries and reduced blood supply to the nasal mucosa/nasal walls, damages the nasal mucosa which cause permanent swelling and inflammation of the nasal walls. Alpha 1 receptor deregulation also happens which leads to the receptors not acting on alpha 1 stimuli. Tachyphylaxis (depletion of l-NA) also occur.
Treatment: Corticosteroid/cortisone nasal sprays such as beclomethasone.
First generation antihistamines only relieve rhinorrhoea caused by colds. They are multipotent antagonists which also antagonizes muscarinic receptors and thus reduce mucus secretions/mucus production in the upper and lower airways.
Second generation antihistamines only relieve allergic rhinitis. They only antagonize histamine 1 receptors which has an anti-inflammatory effect. The second generation drugs to not cause sedation or reduced concentration and can be used in prophylactic/chronic treatment of allergic rhinitis.
They should not be used to relieve cold rhinitis because they do not have an effect on bradykinin receptors (bradykinin and not histamine are released during colds and thus bradykinin receptors and not histamine receptors should be blocked).
Corticosteroids (nasal drops/topical): allergic rhinitis, inflammatory rhinitis, nasal polyps, reversal of rhinitis medicamentosa/privinism
Anti-allergic drugs/mast cell stabilizers (topical): prophylaxis of allergic rhinitis
Mesna (topical/nasal sprays): diluting sticky nasal mucus
Normal salt saline solution (topical/nasal sprays): nasal lavage to dilute mucus caused by sinusitis.
Question 1: Giver your own definition of COPD
It is a combination of lung diseases that prevent airflow resulting in difficulty in breathing. Some of the most common conditions that make up COPD are: Emphysema (condition where the walls of the air sacs of the lungs are damaged), bronchial asthma (condition where a persons airway become swollen and produces extra mucus which makes breathing difficult) and chronic bronchitis (inflammation of lining of bronchial tubules). Damage to the lungs from COPD can not be reversed.
Question 2: Briefly describe the proposed aetiology and pathophysiology of chronic bronchitis and emphysema
The cause of emphysema is generally continuous exposure to irritants that damage your lungs and their airways. The damage done to the alveoli eventually leads to reduced elasticity and over-inflation. This therefore causes swelling of the bullae where the CO2 becomes trapped. Due to this reason the lungs are being deprived of continuous flow of oxygen therefore causing deeper breathing. Emphysema is therefore known as a lung condition that causes shortness of breath.
It is a non-specific obstructive airway disease which is characterized by: reduced mucus secretion and mucosal clearance, recurring bacterial respiratory infections, changes in bronchial walls and chronic cough due to sticky mucus. The bronchial lining becomes inflamed and continuous exposure to smoke, excessive dust or chemicals will eventually cause damage to the bronchioles. Chronic bronchitis is due to hypersecretion of mucus by the goblet cells. The epithelial cells lining the airway responds to infectious stimuli by freeing inflammatory mediators.
Question 3: Which types of therapy are included in the treatment of a COPD patient?
Question 4: Why is ipratropium more effective in the treatment of chronic bronchitis than in the treatment of bronchial asthma?
Ipratropium is a muscarinic Ach receptor antagonist which prevents the function of parasympathetic nervous system. The function includes: the production of bronchial secretions as well as constriction. If this is prevented it will result in bronchodilation and less secretions. Ipratropium is therefore more effective in the treatment of chronic bronchitis since it is characterized by increased mucus secretion. With bronchial asthma, the increased mucus secretion does not have the same effect.
Question 5: In which way do the skeletal muscle effects of theophylline have advantages in the treatment of COPD
Theophylline improves ventilation response, decreases hypoxia and dyspnea in COPD patients. It causes the smooth muscle relaxation which further causes bronchodilation. This allows for easier flow of air to the bronchial air passage therefore, significantly improves breathing.
Question 6: What is the role of oxygen therapy in COPD?
Increases the amount of oxygen that flows into your lungs and bloodstream and as a result this improves breathing.