ALEXIA DUARTE
1. Cold, allergies, physical damage, drug or chemical damage.
2. Alpha- antagonist- phenylephrine, corticosteroids- betamethasone, antihistamines- Loratadine, antibiotics- mupirocin, mucolytics- mensa, mast cell stabilizers- ketoifen.
3. Decongestants cause vasoconstricion of mucosal blood vessels that reduces oedema of nasal mucosa. Local Decongestants have fewer SE eg oxymetazoline (drops). Short acting drugs have a duration of 4 to 6 hours, intermediate acting drugs have a 8 to 10 hour duration and long acting drugs have a 12 hour duration.
4. Rhinitis medicamentosa is the permanent vasoconstriction that has a poor local blood supply leading to the damage of mucosa membranes in the nose and gives permanent swelling and inflammation. Xylomethazoline may only be used for a few days cause rhinitis medicamentosa may develop.
5. 1st gen, used for rhinorrhea, 2nd gen used for allergic rhinitis. 2nd gen doesn't block muscarinic receptors and doesn't cause sedation like the first gen.
6. Corticosteroids- used for allergic rhinitis, administration is topical, anti-allergic drugs- prophylactic treatment of allergic rhinitis given as a nasal spray. Mensa- makes mucus a liquid given as a nasal spray. Normal salt solution- nasal lavage.
Blog 2.2
14 Oct 2021, 13:22
In which diseases are angiotensinogen levels increased? What are the implications of this?
This disease is Hypertension ,an increase in the angiotensinogen through renin causes it to convert to angiotensin II. This causes vasoconstriction and increases the secretion of aldosterone.
Why do drugs which inhibit the angiotensinogen system by acting on angiotensin receptors have fewer side effects than those that inhibit ACE?
Drugs which block ACE will also reduce the amount of bradykinin 2.However, drugs which act on angiotensin receptors may not inhibit the breakdown of bradykinin.
In which way do ACE inhibitors have a two-fold mechanism of action in the treatment of hypertension?
ACE inhibitors block the conversion of angiotensin 1 to angiotension 2. This prevents the breakdown of natriuretic peptides which decreases angiotension 2 synthesis leading to vasodilation, decreasing blood pressure. Aldosterone secretion is also decreased which would normally reabsorb NaCl if the BP is low in order to increase it . Since aldosterone is decreased the blood pressure will be decreased leading to the treatment of hypertension.
At which type of angiotensin receptor do losartan and similar drugs act? Do they have any effect, direct or indirect, at other angiotensin II receptors?
Angiotensin 2 type 1 receptors which have no effect on type 2 receptors.
What are the physiological effects of kinins on arteries and veins? Do other autacoids play a role in this action? Explain.
Kinins are potent vasodilators causing dilation of arteries and veins, and many autacoids play a role such as Natriuretic peptides, vasoactive peptides, substance P, neurokinin A and B and CGRP.
Which receptor is probably the most involved in the important clinical effects of kinins? Bradykinin 2 receptors.
In which way are natriuretic peptides possibly effective in the treatment of hypertension, as well as congestive heart failure?
Natriuretic peptides cause vasodilation which can cause a decrease in blood pressure, effective in the treatment of hyperstion. It increases GF and Na secretion, decrease renin and aldosterone secretion, which relieves fluid build up helping with congestive heart failure.
What is neprylisine and what is the rationale for inhibiting its action in the treatment of heart failure? Can you name the drug being used as such? Refer to Study unit 1 where you have also come across this drug.
Neprylisin metabolises natriuretic peptides ANP and BNP. In a reduction of ANP and BNP their effect on CHF patients will be reduced, leading to vasoconstriction with an increase in GF and Na excretion as well as renin secretion being increased causing an increase in blood pressure. Sacubitril which is a Neprilysin inhibitor.
Give examples of endothelium-derived vasodilators and vasoconstrictors.
Endothelium-derived vasodilators: NO and PGI2, Endothelium-derived vasoconstrictors: ET1,2,3 and ETA,B