Cystic fibrosis occurs when the mucus secreted in the body is very thick and sticky. There is also a build-up of mucus in the body due to the body’s inability to clear the mucus in the body. This will lead to mucus blocking the alveoli in the lungs. This can cause recurrent bacterial infections. Dornase alpha assist in the treatment of Cystic fibrosis due to its mucolytic effects (it hydrolyze the extra-cellular DNA of the neutrophils in the bronchial mucus)  on the mucus thereby, improving the fluidity of the mucus making it easier to be excreted from the body.

Neonatal respiratory distress syndrome is also called hyaline membrane disease and it only occurs in in premature babies. It is when the lung falls flat because the surfactants that cover the airways which are essential for gas exchange are not formed yet because it is only formed shortly before birth. Treatment includes oxygen therapy. Ventilation is used to keep a positive pressure in the lungs. Intensive monitoring of respiratory status is used in order to prevent too high oxygen levels which can lead to retinal damage and blindness. Before labour corticosteroids are given to the mother. This will initiate the baby’s surfactant production. Exogenous surfactants are administered to the baby through a catheter into the lungs. This augment lung surfactant.

Oxygen therapy is induced in order to assure that the baby oxygen levels is in its requires index. Oxygen is also used to maintain a positive ventilation pressure, thereby ensuring that the alveoli in the lungs do not colapse. Too high oxygen levels can lead to retinal damage and blindness.

Neonatal apnoea occurs when continuous breathing by a baby is not stimulated because the respiratory centre in the Medulla is not yet fully developed. Methylxanthines are lipophilic and can therefore cross the blood brain barrier and stimulate the CNS. Methylxanthines used for this treatment includes caffeine and theophylline.

Rhinitis is mostly associated with the inflammation of the nasal mucosa due to colds and flu. Allergic rhinitis refers to the inflammation of the nasal mucosa due exposure of allergens. Mucosal rhinitis is associated with sinitus. Rhinorrhea can occur because of: allergies, a cold, exposure to chemicals and physical damage.

drug groups that can be used for the treatment of rhinorrhoea:

A1-agonists: ephedrine

Antihistamines: Bromopheniramine

Corticosteroids: Prednisone

Anti-allergic drugs: Ketotifen

Mucolytics: Mesna

Antibiotics: Neomycin

The mechanism of action of the decongestants is that the A1-receptors in the nasal cavity is stimulated and then leads to vasoconstriction of the mucosal blood vessels. Thereby, reducing the volume of nasal mucosa. Their duration of action differs between long and short acting. However, the short-acting decongestants are administered topically through nasal sprays and they are usually preferred because long acting decongestants tends to cause cardiac and CNs side effects thereby, leading to a decrease in local concentrations.

Rhinitis medicamentosa can also be conferred to as rebound congestion. This happens when a patient tends to develop a tolerance for the current treatment that they are using. Treatment includes to progressively decrease the using of the medication (note that abruptly stopping can lead to even greater swelling and congestion). A nasal steroid (corticosteroids) such as Prednisone can help to limit the symptoms.

Frist generation antihistamines act as muscarinic blockers (thereby, decreasing the mucus secretion in the upper and lower airways.) Second generation does not have any muscarinic blocking effects and is therefore only used as short/long term treatment for allergic rhinitis. The 1^st generation antihistamines are lipophilic and can therefore easily cross the blood brain barrier. This can then lead to sedation and a decrease in the concentration of the patient. 2^nd generation antihistamines however, are not lipophilic and will therefore not lead to these side effects. 2^nd generation antihistamines are not effective in the use of cold rhinitis because histamine plays no part in cold rhinitis (unlike Bradykinins).

Corticosteroids are used in allergic rhinitis, nasal polyps, inflammatory rhinitis and to reverse rhinitis medicamentosa. They are administered through nasal sprays.

 Anti-allergic drugs: are used in allerdic rhinitis to stabalise mast cells. They are administered through nasal sprays.

 Mesna: Is a mucolytic and is used to liquefy sticky mucus. It can be administered through steam inhalation.

 Normal salt solution: It is administered through nasal drops in order to hydrate (humidify) dry and inflamed mucus membranes in the nasal cavity.

ACE inhibitors such as omeprazole and leflumide can cause a cough

A COPD is a chronic condition where the pulmonary airways are obstructed by either a buildup of mucus or uncontrollable contraction of the airways known as bronchoconstriction.

Chronic bronchitis is a progressive inflammatory condition. This condition arises because of long term exposure to irritants in the airways, resulting in the inflammation of these airways. It is also characterized by the increase in mucus secretion and the decrease of the clearance of this mucus. This can also lead to an increase in infections in the airways.

Emphysema occurs due to structural damages found in the alveoli and bronchioles caused by smoking and irritants in the airways. This leads to a difficulty to breathe because old air is trapped within the alveoli.

In the case of bacterial infections antibiotics are given. Bronchodilators are given if the airways are obstructed. Steam therapy is usually used to dilute excessive mucus secretions, rehydration therapy is also used here. Oxygen inhalation therapy can be given to a patient that suffers from hypoxia. Regular light to moderate exercise is recommended to patients that have poor lung capacity.
Usually the first step in COPD treatment will be to provide a patient with anticholinergic drugs that will inhibit bronchoconstriction. A B2 stimulant is also given with this treatment.

Ipratropium is a short acting anticholinergic drug. Therefore, it stimulates the relaxation of bronchial smooth muscles leading to bronchodilation. In Chronic Bronchitis there is an increase in the secretion of mucus, Ipratropium is an anticholinergic drug and will therefore decrease the secretion thereof. As well with the bronchodilation effect this drug has proven to be effective in the use for chronic bronchitis. The effects of short acting anticholinergic drugs in asthma cases have been proven to be almost as effective as sympathomimetic drugs, thus meaning still less effective. Therefore, in cases of bronchial asthma anticholinergic drugs are only used as alternative therapy for patients that has developed a tolerance for B-adrenoceptor agonists.

Theophylline increases the skeletal muscle strength of the diaphragm. This is very useful in patients with COPD that requires a higher O2 intake, because it improves ventilation response.

Because of the obstruction of the airways a patient might find it difficult to breathe in enough oxygen. Oxygen therapy is then induced to ensure that the oxygen levels in the body stays at the required level.

Fluvoxamine is a selective serotonin reuptake inhibitor (SSRI). It has been found that fluvoxamine reduces inflammatory cytokine production by binding to sigma-1 receptors in immune cells. This is FDA approved for the treatment of obsessive-compulsive disorder. It is still currently undergoing studies to determine the effectiveness thereof in Covid-19. (Covid-19 Treatment guidelines).

https://www.covid19treatmentguidelines.nih.gov/therapies/immunomodulators/fluvoxamine/

Endothelium dependent vasodilation refers to the production of nitric oxide by the endothelial cell. Nitric oxide is a strong vasodilator.

Constitutive means that something is synthesized at a constant level (this includes nNOS and eNos enzymes). Inducible enzymes is only present during pathological states such as inflammation (this will include INOS enzymes.

NO contributes to the fatal pathology of septic shock by causing hypotension due to excessive No mediated vasodilation.

Nitric oxide

NO binds to superoxide species, this can be cytotoxic This toxicity can be prevented by glutathione which protects cells.

NO stimulates the release of inflammatory prostaglandins by activating COX-2. This causes NO to be pro-inflammatory. Advantages thereof is: there is a increase in permeability, causing White blood cells to move through the endothelium to the site of action easily. Disadvantages is that an excess of NO production can cause acute inflammatory oedema which will lead to cell injury.

Parkinson’s disease, stroke.

Diseases that increase the levels of angiotensinogen and the implications thereof:

Diseases that cause an increase in the release or production of corticosteroids, estrogens, thyroid hormones as well as ANG II will lead to an increase in angiotensinogen levels. These types of diseases include hyponatremia, hyperthyroidism as well as heart failure. The increase of angiotensinogen concentration will lead to an increase in the production in ANG II which in turn will lead to hypertension.

Drugs that inhibit the angiotensinogen system by acting on angiotensin receptors have fewer side effects than those that inhibit ACE because of:

ACE plays a role in the degradation of bradykinin. Therefore, if ACE is inhibited there will be an increase in the concentration of bradykinin. Bradykinin have adverse side effects namely cough as well as angioedema. Drugs that inhibits the angiotensinogen system avoids these side effects.

ACE inhibitors have a two-fold mechanism of action in the treatment of hypertension

• A decrease in the degradation of bradykinin leads to an increase in the concentration of bradykinin in the blood. This contributes to the antihypertensive effect.
• Blood pressure as well as vascular resistance is decreased by the blockage of the conversion of ANG I to ANG II by ACE inhibitors.

AT₁ receptors are inhibited by losartan as well as similar drugs. This indirectly stimulate AT₂ receptors through the increase in the concentration of ANG II (caused by the disinhibition of renin release).

Kinins causes a vasodilatory effect in the arteries. This is caused by either a direct inhibition of vascular smooth muscles or by indirectly stimulating the release of Nitric Oxide or vasodilator prostaglandins. However, the effect of kinins on veins is the complete opposite. Kinins in veins causes an inhibition of vascular smooth muscles, or indirectly causes a release of vasoconstrictor prostaglandins. This leads to vasoconstriction in veins.

Receptors that are probably the most involved in the important clinical effects of kinins will be B₂-receptors.

Natriuretic peptides cause an increase in sodium excretion as well as the flow of urine. This leads to a decrease in blood volume. Natriuretic peptides also cause vasodilation and a decrease in arterial blood pressure. All of this will be effective in the treatment of hypertension as well is congestive heart failure.

Neprilysin is a neutral endopeptidase (enzyme) that metabolize natriuretic peptides. The inhibition of this enzyme will lead to an increase in Natriuretic peptides concentration. This will lead to an increase in natriuresis as well as diuresis. This will be effective in the treatment of heart failure. A drug that can be used for this outcome is Sacubitril.

• Endothelium-derived vasodilators: Nitric Oxide
• Endothelium-derived vasoconstrictors:  ET-_B1 receptors

Peptide neurotransmitters (calcitonin gene-related peptides especially) are very powerful vasodilators. They are released through the stimulation of the trigeminal nerve that is distributed into the intracranial arteries. Perivascular edema occurs (this is caused by the increase in the concentration of plasma as plasma proteins in the perivascular space). This in turn leads to mechanical stretching which then leads to activation of the pain nerve endings found in the dura. This is then called a migraine.

Drugs that is used in the treatment of migraines include: ergot alkaloids, NSAID’s, β-adrenoceptor blockers, Calcium channel blockers, tricyclic antidepressants and SSRI’s as well as antiseizure agents.

The mechanism of action of these drugs helps in the treatment of migraines in two ways. Firstly, by preventing vasodilation through the activation of direct 5-HT agonists that causes vasoconstriction. This leads to the inhibition of the stretching of the pain endings in the dura.
Secondly by inhibiting the release of vasodilation peptides. This is done by the activation of 5-HT_1D/1B receptors found on the nerve endings on presynaptic trigeminal. This causes a decrease in excessive firing of these nerve endings.