• Cystic fibrosis is a genetic metabolic disease (decrease DNase 1) that results in reduced secretions in various organs. Dornase alpha (rhDNase) inhalations improve fluidity by hydrolyzing proteins in bronchial mucus.
• Surfactants that cover airways and are essential for gas exchange are not formed completely because baby is born premature and lungs can fall flat. Treatment involves oxygen, ventilation for positive pressure and drugs like beractant and poractant alfa. Betamethasone a corticosteroid is given prophylactically to the mother before labour to initiate the baby's surfactant production.
• It is to ensure oxygenation where there may be a lack in that. Over a long term increased oxygen can lead to retinal damage and blindness.
• The respiratory center of the brain of premature or newborns is not fully developed to stimulate continuous breathing and this results in apnoea with bradycardia. Methylxanthines stimulate the CNS and caffeine is used. 

• Sinusitis, allergen exposure, stimuli such as heat, smoke and cold, cold air, chemical or drug damage and physical damage.
• Alfha 1-agonists- ephedrine, antihistamines- diphenhydramine, corticosteroids-prednisone, mast cell stabilisers- ketotifen, mucolytics- acetylcysteine, antibiotics- neomycin, diverse drugs- normal saline.
• Decongestants can have systemic side effects if administered by another route other then topical because they are agonists for alpha 1 receptors and there duration of treatment is also longer with topical administration. They are administered topically with nasal sprays and gels.
• Rhinitis medicamentosa is a condition that develops due to long term use of decongestant nasal spray that causes it to not have an effect anymore. It can be treated with cortisone nasal sprays, like beclomethasone.
• The first generation is effective, but it gives sedation and lowers concentration. Second generation doesn't and can be used for long term. They should not be used to relieve cold Rhinitis, because the fast action and long term duration of the first generation is preferred. 
• They decrease mucus production and decrease bronchodilation in nasal Rhinitis. They are administered through nasal sprays. 

• COPD's are a combination of different diseases that can have one common characteristic and that is that they a affect the lungs and leads to the degeneration of the airways in the lungs.COPD's all affect breathing and make it more difficult.
• Chronic bronchitis develops due to bacterial respiratory infections and the aiway becomes swollen and filled with mucus that results in structural changes in the bronchial walls and a chronic cough. Emphysema develops due to smoking and irritants and it leads tothe aveoli being dilated and damaged and air is trapped in the lungs and can not be exhaled. This causes the capillary blood vessels to stop gas exchange.
• Smoking cessation, bacterial infection treatreatment like immunization against influenza and antibiotic treatment like erythromycin, airway obstruction treatment like bronchodilators, secretions by diluting mucus (rehydration and steam), hypoxia treatment by oxygen inhalation and to increase poor lung capacity- regular light to moderate exercise.
• With asthma a anti-inflammatory drug is most suitable to relieve asthma and ipratropium effects are more directed to bronchodilation and decreased mucus production which are specific side-effects of bronchitis.
• Theophylline causes the contraction of the diaphragm skeletal muscles and this improves in COPD patients the ventilation response, and it reduces hypoxia and dyspnea.
• The role is to increase the oxygen levels at tissues where there may by a shortage of oxygen and treats hypoxia. 

The SSRI fluvoxamine can not be used for treatment in covid patients, because SSRI are usually used in the treatment in patients with depression and anxiety by increasing the amount of serotonin in the brain by blocking the reabsorption of serotonin into neurons. This causes more serotonin to be available to transmit messages between the neurons in the brain. Fluvoxamine can not be used in the treatment of covid patients, because it leads to some side effects that can worsen a patients condition if they have covid. These side effects include headache, drowsiness, dizziness, nausea and diarrhea, nervousness and loss of appetite. Thus by using this medication while diagnosed with covid can lead to a worsened state. According to https://www.mayoclinic.org > ssris

• Endothelial cells respond to vasorelaxants by releasing EDRF that act on vascular muscle to cause relaxation and consequently vasodilitation. Thus for vasodilation to occur it is dependent on the endothelium.
• A "constitutive" enzyme is an enzyme that is formed at a constant rate and amout in a cell. A "inducible" enzyme is an enzyme that is only produced in the presence of their substrate thus the production is not constant. The iNOS (inducible) is not normally readily detectable until inflammatory mediators induce iNOS gene transcription that results in synthesis of to much NO, because of the  accumulation of iNOS. The constitutive NOS enzyme forms at a constant rate and is not trigered or regulated by calsium.
• Cytokines induce synthesis of iNOS during an infection. It causes a widespread generation of NO which results in exaggerated hypotension, shock and death. This leads to septic shock and can be treated by the inhibition of NOS or compounds that prevent the action of NO. There is no improvement in survival in patients with gram-negative sepsis that is treated with NOS inhibitors, despite the ability of NOS inhibitors to ameliorate hypotension in sepsis treatment.
• Guanylyl Cyclase is converted to Activated Guanylyl Cyclase by adding NO and Activated Guanylyl Cyclase changes GTP to cGMP.
• NO reacts with the iron in hemoglobin in the blood and can therefore be inhibited by hemoglobin who is always present in the body.
• When infection and injury occurs it leads to an increase in leukocytes, and inflammatory mediators and causes an increase in iNOS which results in higher levels of NO. This causes inflammation. The advantages is that NO, with interaction with superoxide, is a microbicide. NO also protects the body via immune cell function. It also stimulates the synthesis of inflammatory prostaglandins. The disadvantages are exacerbation of tissue injury, psoriasis lesions, airway epithelium in asthma and inflammatory bowl lesions.
• Stroke, amyotrophic lateral sclerosis and Parkinson's disease. 

• Hypertension increases angiotesinogen levels. Angiotensinogen is converted to Angiotensin I by Renin. Angiotensin I is converted to Angiotensin II which binds to the receptors and causes the release of aldosterone and ADH. Aldosterone stimulates the increased reabsorption of Na+ and H2O and increased excretion of K+. ADH stimulates the increased reabsorption of H2O. Both leads to an increase in blood pressure. 
• ACE inhibitors in addition to converting ANGI to ANG II, also inhibit the degradation of bradykinin, substance P, and interleukins. The inhibition of bradykinin metabolism leads to increased bradykinin levels which causes side effects, like cough and angioedema. With the inhibition of angiotensin receptors these side effects are not present.
• ACE inhibitors block the conversion of ANG I to ANG II. ACE inhibitors also inhibit the metabolism of bradykinin to inactive peptides. This contributes to the decrease in blood pressure and treats hypertension.
• Losartan and similar drugs act on the angiotensin AT1 receptors. They have an indirect effect on the ANG II receptors. When these drugs are given for a long period of time they disinhibit renin release and increase the ANG II levels that circulate in the body. That increases the stimulation of AT2 receptors.
• Kinins causes vasodilation in arteries and vasoconstriction in veins. Autacoids play a role, because during vasodilation the release of nitric oxide or vasodilator prostaglandins for example PGE2 and PGI2 is mediated. During vasoconstriction there is a release of vasoconstrictor prostaglandins such as PGF2α.
• The B2 receptor.
• ANP causes urine flow and sodium excretion. The natriuresis induced by the ANP is because of an increase in glomerular filtration rate and decreased proximal sodium reabsorption. ANP inhibits the release of renin, aldosterone and AVP, which causes increased sodium and water excretion. ANP also causes vasodilation and all these effects contribute to the treatment of hypertension and congestive heart failure.
• Neprilysin is responsible for the degeneration of natriuretic peptides in the lungs, kidneys and liver. It is also a neutral endopeptidase. Neprilysin inhibition causes ANP and BNP levels to increase in the circulation, causing diuresis and natriuresis. It increases protective natriuretic peptides. The inhibitor's name is Sacubitril.
• Bosentan, macitentan, ambrisentan and sitaxsentan. 

Pathology of migraine: During a migraine trigeminal nerve distribution to intracranial arteries are involved and the nerves release powerful vasodilators, like calcitonin gene-related peptide, and other peptide neurotransmitters. Migraine involves an ion channel in the aminergic brain stem nuclei. It consist of neural events resulting in the dilation of blood vessels that cause pain and result in further nerve activation. Substance P and neurokinin A may be involved and extravasation of plasma and plasma proteins into the perivascular space is a common, because of the action of the neuropeptides on the vessels. Mechanical stretching because of the perivascular edema may cause pain in the nerve endings of the dura.

Treatments: Sumatriptan, Naratriptan and Rizatriptan (triptans) are used in the treatment of acute migraine. Ergot alkaloids, non-steroidal anti-inflammatory analgesic agents, β-adrenoceptor blockers, calcium channel blockers, tricyclic antidepressants and SSRIs, and several anti-seizure agents are also used (some drugs for prophylaxis are also used). The 5-HT 1D/1B receptors on are activated by triptans, ergot alkaloids and antidepressants to inhibit the release of vasodilating peptides. Excessive firming of these nerve ends are suppressed by anti-seizure agents. Or the vasodilation and stretching of pain ends may be prevented by the vasoconstrictive effect of 5-HT agonists, like triptans and ergot alkaloids.