What are the general causes of rhinitis and rhinorrhoea?

Allergic rhinitis = allergen exposure, IgE mediated inflammation.
Non-allergic rhinitis = physiological response due to stimuli such as heat, smoke, cold.

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

Decongestants (alpha-agonists): oxymetazoline, xylometazoline, ephedrine

Antihistamines: diphenhydramine, loratadine, cetirizine 

Corticosteroids: betamethasone, prednisone, beclomethasone

Mast cell stabilizers: Sodium chromoglycate, ketotifen

Mucolytics: Mesna, acetylcysteine

Antibiotics: Mupirocin, neomycin

Diverse drugs: steam, normal saline, essential oils

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

Sympathomimetic agents, α1 agonists: vasoconstriction of mucosal blood vessels, ↓ oedema of nasal mucosa. Ephedrine, pseudoephedrine and propylhexedrine are nonselective adrenergic agonists (a and b) with additional potent indirect action. The a-adrenergic receptor stimulation (direct-acting or indirect-acting) by these drugs gives rise to decongestion of the mucous membranes of the nose. The drugs with mixed action administered topically act directly, but if they are administered orally, they reach lower concentrations in the biophase, resulting in mainly indirect action.

• short-acting drugs (4 to 6 hours), e.g. ephedrine, phenylephrine, propylhexedrine, naphazoline and tetrahydrozoline;
• intermediary acting drugs (8 to 10 hours), e.g. xylometazoline;
• long-acting drugs (12 hours), e.g. oxymetazoline.

Typically administered topically (nasal spray)

What is rhinitis medicamentosa?  How is it treated?

Also known as privinism, is a condition that may present following chronic treatment with decongestants, where the permanent vasoconstriction with poor local blood supply leads to damage of the mucous membranes of the nose with permanent inflammation and swelling, as well as deregulation of the a‑adrenergic receptors on the blood vessels, rendering them unresponsive towards the a‑agonists. Receive local corticoid therapy

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?

The first-generation antihistamines are multipotent competing antagonists and also block muscarinic receptors. Antimuscarinic drugs reduce the secretions of both the upper and lower airways and are, therefore, frequently included in preparations for colds to clear up rhinorrhoea.  They can, however, cause sedation and therefore negatively influence the ability to concentrate. The second-generation antihistamines do not block muscarinic receptors and are useful in the long-term or short-term treatment of allergic rhinitis. Because histamine plays no part in cold rhinitis (but bradykinin does) these drugs do not help to clear up cold rhinitis. They also do not cross the blood/brain barrier and thus rarely cause sedation

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

Corticosteroids: Used in allergic rhinitis, nasal polyps, inflammatory rhinitis and reversal of rhinitis, nasal spray

Anti-allergic drugs: Nasal vestibule staphylococci infection, prophylactic treatment of allergic rhinitis, nasal spray

Salt solution: dilutes mucus during sinusitis, nasal rinse/lavange