• What are the general causes of rhinitis and rhinorrhoea?

General causes of rhinitis and rhinorrhoea are allergens, cold chemical or drug damage, cold air and physical damage

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

Mucolytics – acetylcysteine, mensa

Alpha1 agonists – ephedrine

Corticosteroids – prednisone, betamethasone

Antihistamine – rupatadine

Diverse drugs – steam, normal saline

Antibiotics – neomycin

Mast cell stabilizers - ketotifen

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

We have:

short-acting drugs (4-6 hours) ephedrine, phenylephrine

intermediate acting drugs (8-10 hours), xylometazoline

long acting drugs (12 hours) oxymetazoline

• What is rhinitis medicamentosa?  How is it treated?

A condition that is caused by overusing nasal decongestants and it is firstly treated by the cessation of nasal decongestants or using a saline nasal spray or corticosteroids nasal spray in topical form

• 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?

1^st generation drugs block muscarinic and histaminic receptors leading to increased vasoconstriction leading to mucus thickening however, it will have anti-inflammatory effects  but also have sedation effects. While 2^nd generation drugs block only histaminic receptors having anti-inflammatory effects and anti-allergic effects and the can be used long term without side effects. Histamine has no effects on cold rhinitis

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

normal saline solution is highly recommended in the treatment of children, corticosteroids are administered in the treatment of rhinitis medicamentosa and the are recommended in allergic rhinitis and all these are administered through topical nasal spray

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

It is a genetic metabolic disease that results in reduced secretion in various organs, the mucus is thick and sticky and this leads to recurrent bacterial infections. Dornase alpha helps to hydrolyse proteins in bronchial mucus to improve fluidity, antibiotics helps with the recurrent bacterial infections and sometimes the use of corticosteroids as well as bronchodilators.

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

Neonatal respiratory distress syndrome is when the surfactant that covers the airways for gaseous exchange only develops shortly before birth. Exogeneous surfactants such as beractant and poractant alpha as well as administering the corticosteroid before labour to a mother will help in the production of the surfactant.

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

Oxygen therapy helps so that there babies does not experience hypoxia as well as the level of oxygen needed in the body is met. Oxygen toxicity can cause retinal damage and blindness

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

neonatal apnoea is a condition in which the respiratory centre in the brain has not yet fully developed to stimulate continuous breathing. The methylxanthine used are caffeine and theophylline which causes bronchodilation so that more oxygen can reach the lungs

• Give your own definition of COPD.

Chronic obstructive pulmonary disease is a combination of bronchial asthma which is a an inflammatory disease where the respiratory system becomes hypersensitive to stimuli like allergens, exercise, smoking and cold air - chronic bronchitis which is inflammation of the bronchi which transport oxygen to and from the alveoli - as well as emphysema which is the irreversible structural damage of the alveoli which prevents air from entering or leaving the air sac.

• Briefly describe the proposed aetiology and pathophysiology of chronic bronchitis and emphysema.

chronic bronchitis which is inflammation of the bronchi which transport oxygen to and from the alveoli

emphysema which is the irreversible structural damage of the alveoli which prevents air from entering or leaving the air sac. Causing physical damage to the alveoli

• Which types of therapy are included in the treatment of a COPD patient?

The cessation of smoking, diluting the mucus by rehydration and steam, increased inhalation of oxygen, use of bronchodilators such as your B2 agonist, M-antagonist as well as xanthine derivatives, the use of antibiotics such as ampicillin

• Why is ipratropium more effective in the treatment of chronic bronchitis than in the treatment of bronchial asthma?

Ipratropium is an anticholinergic antagonist which blocks the activity of M3 receptors found in the airway to stimulate the vagus nerve which will stimulate the release of Ach leading to vasoconstriction. Chronic bronchitis is characterised by inflammation and bronchial asthma is not and ipratropium does not have any anti-inflammatory effects.

• In which way do the skeletal muscle effects of theophylline have advantages in the treatment of COPD?

Theophylline causes that skeletal muscles to contracts much harder and reduce hypoxia and dyspnoea in COPD patients by increasing ventilation

• What is the role of oxygen therapy in COPD?

COPD leads to hypoxia which is decreased level of oxygen intake so oxygen therapy will help so that a person has the required oxygen levels in the body

1.Ach and bradykinin are Endothelium-dependent vasodilators and they act by increasing intracellular calcium levels in endothelial cells, leading to the synthesis of NO. NO diffuses to vascular smooth muscle leading to vasodilation.

2. constitutive enzyme = any enzyme formed at a constant rate and amount in given cell regardless of the metabolic state of the cell. They have a great physiological effect because they are always present.

Inducible enzyme = an enzyme whose rate of synthesis can be controlled by an addition of a substance implying that the body must first get rid of a substance before the enzyme can have an effect having a smaller pathological effect.

3. Sepsis is a systemic inflammatory response caused by infection. Endotoxin components from the bacteria and endogenously generated tumor necrosis factor-α and other cytokines induce synthesis of iNOS in macrophages, neutrophils, and T cells, as well as hepatocytes, smooth muscle cells, endothelial cells, and fibroblasts. This widespread generation of NO results in exaggerated hypotension, shock, and, in some cases, death.

4. Nitric Oxide

5. The body secrete NO inhibitors like sGC inhibitor methylene blue which prevents the action NO and NO reacts with oxygen to form nitrogen dioxide which inactivates NO

6.When there is foreign antigens in the body, TH1 cells synthesise NO which stimulates inflammatory prostaglandin by activating COX-2. COX-2 has direct vasodilatory effects with NO. NO generated during inflammation contributes to the erythema, vascular permeability, and subsequent edema associated with acute inflammation.  

7. when there is an excess of NO synthesis it can lead to excitotoxic neuronal death, a  stroke and Parkinson’s disease.

1.Angiotensin levels are increased in Hypertension. It is increased by intake of corticosteroids (they upregulate angiotensin II synthesis), estrogen, thyroid hormones and angiotensin which stimulate the renin-angiotensin which increases the blood pressure by causing vasoconstriction which leads to hypertension.

2.ACE inhibitors not only block the conversion of ANG I to ANG II but also inhibit the degradation of bradykinin which causes vasodilation implying that there will be a decrease in blood pressure leading to hypotension. Inhibition of the metabolism of Bradykinin increases vascular permeability causing angioedema and a cough. Whereas the drugs that block the angiotensin receptors are specific competitive antagonists and have a lower incidence of a cough.

3.ACE inhibitors inhibit the d=metabolism of bradykinin which has vasodilatory effects, therefore it decreases the blood pressure. They also decrease peripheral ventricular resistance which decreases the blood pressure.

4. Losartan blocks angiotensin AT1 receptor only. Prolonged treatment with the use of Losartan causes may cause stimulation of angiotensin AT2 receptors

5. Kinins causes vasodilation on the arteries and vasoconstriction on the veins. The vasodilation may result from a direct inhibitory effect of kinins on arteriolar smooth muscle or may be mediated by the release of nitric oxide or vasodilator prostaglandins such as PGE2 and PGI2. Vasoconstriction may result from direct stimulation of venous smooth muscle or from the release of venoconstrictor prostaglandins such as PGF2α. Prostaglandin is a potent vasodilator.

6. The receptors involved in the clinical effects of kinins are the beta receptors.

7. Natriuretic peptides produce vasodilation which will decrease your blood pressure therefore brin helpful in the treatment of hypertension and congestive heart failure. increase in ANP and BNP causes natriuresis and vasodilation, as well as a compensatory increase in renin secretion and plasma ANG II levels. The development of drugs that combine neprilysine inhibition with an ACE inhibitor in order to prevent the increase in plasma ANG II, or with an ARB to block the actions of ANG II.

8. Neprilysin is a neutral endopeptidase and it is inhibited to prevent an increase in plasma ANG II  which increases hypertensive effects and heart failure and an example is Sacubitril (valsartan).

9. vasodilators: PGI2 and Nitric Oxide

vasoconstrictors: Endothelin ET1, ET2, ET3

A migraine is an intensified type of headache which attributes nausea, vomiting visual scotomas or even hemianopsia, and speech abnormalities. It is caused by these characteristics, however, are not part of “Common migraine”

Pathology:

A migraine involves the Trigeminal nerve which is responsible for sending pain, touch, and temperature sensations from the head to the brain. These nerves release the calcitonin gene-related peptides which are extreme vasodilators. Mechanical stretching caused by the perivascular oedema activates the pain nerve and the onset of a headache my also sometimes be increased by the increase in the magnitude of the temporal artery pulsations.

Treatment:

Triptans, ergot alkaloids and antidepressants activate 5HT1D/1B receptors on the presynaptic trigeminal nerve endings to inhibit vasodilating peptides excessive firing of nerve endings. He Triptans and ergot alkaloids also prevent stretching of the pain endings. The use of anti-inflammatory analgesic and beta-blockers, and anti-depressants also play a role in the treatment of Migraines however the Triptans (mainly Sumatriptan) are first in line to trat migraines.