Selective-Serotonin reuptake inhibitors increase serotonin levels in the brain improving depression and stabilizing emotions. Serotonin also has anti-inflammatory action by preventing the release of IL-6 and TNF-alpha, which are pro-inflammatory cytokines. This anti-inflammatory action  can be useful in the treatment of COVID-19, as this condition occurs as an overstimulation of the body’s pro-inflammatory action. Fluvoxamine is a SSRI and may have this anti-inflammatory activity and other possible antivirus abilities. Inhibition of the acid sphingomyelinase or ceramide system by fluvoxamine also plays a role in the infection. The use of fluvoxamine in COVID-19 has shown to decrease mortality. 
References: 
1. Oskotsky T, Marić I, Tang A, et al. Mortality risk among patients with COVID-19 prescribed selective serotonin reuptake inhibitor antidepressants. JAMA Net. 2021;4(11):e2133090-e2133090. doi: 10.1001/jamanetworkopen.2021.33090.
2. Carpinteiro  A, Edwards  MJ, Hoffmann  M,  et al.  Pharmacological inhibition of acid sphingomyelinase prevents uptake of SARS-CoV-2 by epithelial cells.   Cell Rep Med. 2020;1(8):100142. doi:10.1016/j.xcrm.2020.100142
 

1.    Endothelium-dependent vasodilation is vasodilation initiated by endothelial cells.
2.    Constitutive form of NOS is found in endothelial cells while the inducible form is found in macrophages. Constitutive NOS enzyme is always produced regardless of the metabolic state of the body while an inducible NOS enzyme is produced situationally. 
3.    Indirect release of NO by stimulation of PG via COX2 in inflammatory response leads to vasodilation and a further decrease in blood pressure occurs, increasing the severity of septic shock.
4.    Substance P, neurokinin A and B and endothelins.
5.     NO can be inhibited by hemoglobin and excreted in the kidneys.
6.    Tissue damage releases NO and indirect release is also stimulated by PG release leading to vasodilation and allowing migration of neutrophils to affected areas. This can be a disadvantage in inflammatory conditions such as arthritis. 
7.    Alzheimer’s disease, anxiety, and depression. 

1.    Hypertension: Increased angiotensinogen levels increases angiotensin leading to increased blood pressure.
Oedema: increased angiotensinogen levels increases water retention leading to increased blood pressure.
2.    ACE is also involved in bradykinin metabolism which will decrease prostaglandin synthesis and increases vasoconstriction. Angiotensin receptor blockers are selective causing less side effects.
3.    Angiotensin 1 is not converted to angiotensin 2 by ACE, preventing the cascade leading to increased blood pressure. ACE inhibitors prevent inactivation of bradykinin leading to increased prostaglandin synthesis, vasodilation and decreased blood pressure. 
4.    Losartan and other similar drugs are selective AT1 receptor blockers and will have a direct effect on AT1 receptors by decreasing angiotensin 2.
5.    Kinins are vasodilatory peptides and they increase capillary permeability. Other autocoids which are vasodilatory include natriuretic peptides, CGRP, vasoactive intestinal peptides, substance P, neurokinin A and B.
6.    G-protein coupled receptors.
7.    They are vasodilatory, therefore they are used to decrease blood pressure by vasodilation and renin excretion. Atrial natriuretic peptide plays a role in congestive heart failure and intravenous netritide (Brain natriuretic peptide) is used in severe heart failure.  
8.    Sacubitril inhibits neprilysin, which is a neutral endopeptidase responsible natriuretic peptide metabolism in the liver and kidneys. Natriuretic peptides are useful in heart failure. Sacubitril is also used in bleeding disorders and post-myocardial infarction by controlling blood volume.
9.    Bosentan is an ETA antagonist leading to vasodilation.
Nitric oxide and PG12 also cause vasodilation but their action is followed by prolonged vasoconstriction.   

Migraine can be considered as a severe headache but is characterised by vasodilation of intracranial arteries via vasodilators such as CGRP, causing oedema and stimulating pain nerve endings. Treatment of migraine will therefore need to include analgesia (for pain treatment, eg paracetamol and aspirin), anti-inflammatory drugs (NSAIDs) and vasoconstrictors (ergotamine). NSAIDs block the production of mediators which stimulate pain receptors while ergotamine relieves vasodilatory effects in the intracranial arteries via vasoconstriction. 

1.    Cystic fibrosis is a genetic mutation where the CFTR (Cystic Fibrosis Transmembrane Conductance Regulator) protein is not produced or is ineffective, leading to reduced secretions in various organs. Dornase alfa inhalation hydrolyses extracellular DNA from neutrophils (which increases the stickiness of the mucus, making a suitable environment for bacterial infections) ,thereby increasing the viscosity of mucus.
2.    Neonatal respiratory distress syndrome is the absence of the surface active material, which covers the respiratory system airways, causing disrupted gas exchange the possibility of atelectasis. Monitoring of the respiratory system, oxygen therapy and continuous positive airway pressure is required. Exogenous surfactants are administered and corticosteroids boost the surfactant production.
3.    Oxygen therapy is necessary to ensure oxygenation, but toxicity can lead to blindness.
4.    Neonatal aponea is a condition in premature babies where the medulla has not been fully developed, leading to insufficient breathing stimulation. Methylxanthines (theophylline) help by stimulating the central nervous system.
 

1.    Allergies, cold air, physical and chemical damage.
2.    Alpha-1 agonists .eg Ephedrine. Antihistamines and antimuscasrinic drugs.eg Diphenhydramine. Corticosteroids(budesonide), Mast cell stabilizers(ketotifen), Mucolytics(mesna), volatile oils.
3.    Decongestants may be selective or direct-acting and non-selective adrenergic agonists. They range from short-acting drugs (4-6 hours), intermediary-acting (8-10hours) and long-acting (12 hours). They are normally administered topically as nasal sprays, drops or gels. 
4.    Rhinitis medicamentosa or privinism is a condition caused by long term use of decongestants, where nasal blood vessels are irreversibly constricted and the adrenergic receptors are unresponsive. It is treated by stopping the use of alpha-1 agonists and temporarily using corticoid therapy.
5.    First generation antihistamines are competing antagonists on the H1 receptor and also have antimuscarinic effects. Second generation anihistamines are not however not multipotent ant are only useful in allergic rhinitis, for long term and short term.
6.    Corticosteroids are valid in non-infection conditions and administered topically. Anti-allergy drugs are only useful in allergic rhinitis and are administered . Mesna is a mucolytic and is administered topically. Normal saline solution is first choice for children and pregnant women and is administered topically.       
 

1.    Chronic Obstructive Pulmonary Disease is an umbrella term for the combination of varying degrees of conditions affecting the respiratory system, namely bronchial asthma, chronic bronchitis and emphysema.
2.    Chronic bronchitis is associated with changes to the structure of bronchial walls due to long term exposure to stimulants such as smoking, which leads to inflammation and increased mucus production.
3.    Cessation of smoking, antibiotic therapy, beta-2 agonists for bronchodilation, oxygen inhalation therapy, rehydration and steaming to dilute mucus, antibiotic therapy and regular light exercise to improve lung capacity. 
4.    They have influence on the vagus nerve and are long-acting which is beneficial in chronic bronchitis, where as in bronchial asthma beta agonists are preferred for quick action.
5.    Theophylline improves the contraction of diaphragm skeletal muscles improving ventilation.
6.    To improve hypoxia.