Briefly explain what cystic fibrosis is and how dornase alfa acts to solve the problem.

Genetic metabolic disease that decreases DNase 1 that results in reduced secretions in various organs. Dornase alpha is a rhDNase inhaler that hydrolyse the proteins in the bronchial muscusto improve fluidity.

 

Briefly explain what neonatal respiratory distress syndrome is, what the general treatment strategies involve and how cortisone and exogenous surfactants solve the problem.

It is when surfactants cover the airways and therefore the lungs can fall flat causing death. Usually in premature babies. Cortisone initiates surfactant production. Exogenous surfactants are proactant alpha. Oxygen can also be used to ensure oxygenation or ventilation is used for positive pressure. 

 

What is the role of oxygen therapy in neonatal respiratory distress syndrome?  What do the dangers of oxygen toxicity involve?

Oxygen is used to ensure oxygenation but increased oxygenation over a long period leads to retinal damage and blindness.

 

Briefly explain what neonatal apnoea is and how the methylxanthines solve the problem.  Which methylxanthine is used?

It is when the respiratory centre in newborns/ premature babies' brains are not yet fully developed to stimulate continuous breathing. Methylxanthines like caffeine, theophylline IV stimulates the CNS. 

What are the general causes of rhinitis and rhinorrhoea?

Allergies, cold, chemical, or drug damage, cold air or physical damage.

 

Which drug groups can be used for the treatment of rhinorrhoea? Name examples from each group.

A-agonists: Ephedrine

Antihistamines: Loratadine

Corticosteroids: Prednisone

Mast cell stabalisers: Ketotifen

Mucolytics: Mesna

Antibodies: Neomycin

 

How do the decongestants differ with respect to the mechanism of action and duration of action?  How are they administered typically?

Vasoconstriction of mucosal blood vessels, which decreases oedema of nasal mucosa. Topical decongestants have fewer side effects than drops becuse the drops end up in the GIT. The short acting drugs have a duration of 4-6 hours, the intermediary acting 8-10 hours and the long-acting have a duration of 12 hours.  There are mainly direct acting drugs, mixed action drugs (B-phenylephrine) and mixed action (Imidazole derivatives) .

 

What is rhinitis medicamentosa?  How is it treated?

Permanent vasoconstriction with poor local blood supply that leads to damage of mucosa membranes of the nose with permanent inflammation and swelling, and deregulation of the A-adrenergic receptors on the blood vessels, making them unresponsive to A-agonists.

 

How does the first and second generations of antihistamines differ with respect to the mechanisms according to which rhinitis and rhinorrhoea are relieved?  What are the advantages of the second generation of antihistamines?  Why should they not be used to relieve cold rhinitis?

1st gen: clears up rhinorrhea, 2nd gen: treats allergic rhinitis, does not clear up cold rhinitis. 2nd generation does not cause sedation like the 1st gen. 2nd gen does not block muscarinic receptors.

 

When are corticosteroids, anti-allergic drugs, mesna and normal salt solution valid and how are they administered? 

corticosteroids are used for allergic rhinitis (topical, systemic)

anti-allergic drugs: effective for prophylactic treatment of allergic rhinitis (nasal spray- topical)

mensa: use when nasal secretion is sticky, makes mucus more liquid. (topical- nasal spray)

normal salt solution: nasal lavage 

1. Hypertension , angiotensinogen coverts renin to angiotensin 1 and that binds to angiotensin 2 which releases aldosterone and ADH or peptides through peptidases. it also causes vasoconstriction which increases the blood pressure (hypertension). 

 

2. 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.

 

3. Blocks the conversion of angiotensin 1 to angiotension 2 which decreases angiotension 2 synthesis = vasodilation, decreasing blood pressure. There is a reduction in angiotenisn 2 and ADH as well as Na+. Therefore if aldosterone is decreased the blood pressure will be decreased.

 

4. Angiotensin 2 antagonists 

no effect on type 2 receptors.

 

5. Kinins are potent vasodilators and yes, substance p, neurokinin A/B, CGRP etc.

 

6. Bradykinin 2 receptors.

 

7. They cause vasodilation which decreases blood pressure there by treating hypertension. It also increases glomerular filtration and sodium excretion, decrease renin and sodium reabsorption and the effect of angiotensin and aldosterone.

 

8. Neprylisin metabolises natriuretic peptides ANP and BNP. it is a neutral endopeptidase responsible for the degradation of natriuretic peptides in the kidney, liver and lungs. inhibiting neprilysin increases circulating levels of ANP and BNP which can cause natriuresis and diuresis It increases the protective natriuretic peptides and an example of a neprilysin inhibitor is sacubitril. 

 

9. NO and PGI2 (dilators)

ET1,2,3 and ETA,B (vasoconstrictors)

An acute migraine is due to vasodilation which can cause pain. it can be treated with vasoconstrictors like serotonin 1B/D agonists (Naratriptan, Sumatriptan and Rizatriptan). Ergovine and ergotamine also both cause vasoconstriction which reduces the pain in migraines, and cluster headaches and they fall under the ergot alkaloid. 

 

Fluvoxamine has an anti-inflammatory effect and is therefore, used to help Covid patients. Fluvoxamine binds to sigma-1 receptor in the immune cells of the body, reducing the production of inflammatory cytokines. 

https://www.covid19treatmentguidelines.nih.gov/therapies/immunomodulators/fluvoxamine/#:~:text=Anti%2DInflammatory%20Effect%20of%20Fluvoxamine,reduced%20production%20of%20inflammatory%20cytokines. 

COVID-19 could lead to serious illness as a result of an excessive immune response. Fluvoxamine could prevent clinical deterioration by stimulating the σ-1 receptor, which regulates cytokine production.