A brief explanation of what cystic fibrosis is and how Dornase alfa works to solve the problem. Cystic fibrosis is a hereditary metabolic disorder (decrease in DNase 1) that reduces secretions in the body. Dornase Alpha hydrolyzes enzymes in bronchial mucus to improve fluidity What is neonatal respiratory distress syndrome, what are common treatment strategies, cortisone and extrinsic I will briefly explain how it is contained. Surfactants solve the problem. Infant respiratory distress syndrome is also known as vitreous membrane disease. It occurs in premature babies whose lungs sink and die when the surfactant required for gas exchange develops shortly before birth. Extrinsic Surfactant and Poraktanto Alpha Increase Pulmonary Surfactant What role does oxygen therapy play in neonatal respiratory distress syndrome? What is the risk of oxygen toxicity? To ensure oxygen supply Toxicity is retinal damage and blindness A brief explanation of what neonatal apnea is and how methylxanthine solves the problem. Which methylxanthine is used? Neonatal apnea occurs in premature and newborn babies, and continuous breathing is not guaranteed because the respiratory center of the brain is not yet fully developed. Bradycardia and apnea last 15 seconds longer and recur. Methylxanthines such as theophylline, which lead to nerve damage and hypoxia, are given intravenously to stimulate the CNS.

What are the common causes of rhinitis and rhinorrhea? Response to stimuli such as colds, colds, influenza, sinusitis, allergen exposure, heat, smoke, cold Rhinorrhea Can be used to treat allergies, colds, chemical or drug damage, cold or physical damage rhinorrhea Which is the drug group? Give an example for each group. How do first-generation antihistamines (eg, B. diphenhydramine decongestants differ in terms of mechanism of action and duration of action? ) How are they normally managed? Short effect (4-6 hours)-Example: B. Ephedrine Long effect (12 hours)-Example: B. Oxymetazoline Decongestant causes vasoconstriction of mucosal blood vessels and reduces nasal mucosal edema Can be administered topically or orally. This is the best way to distribute the drug and is usually given topically because it easily falls into the stomach and administers the spray. The safest. Oral decongestants cause more side effects and slower onset of action. What is Rhinitis Pharmaceuticalosa? How is it treated? Rhinitis excipientosa is caused by excessive use of decongestants, permanent contraction of blood vessels with inadequate blood circulation, permanent inflammation and swelling of the nasal mucosa, and alpha receptors in the blood vessels. It leads to the adjustment release. It no longer responds to alpha agonists. Can be treated with corticosteroids How do 1st and 2nd generation antihistamines differ in the mechanism by which rhinitis and rhinorrhea are alleviated? What are the benefits of second-generation antihistamines? Why shouldn't it be used to relieve a cold? First-generation antihistamines are pluripotent competing agonists that block muscarinic receptors. It is often included in cold remedies to reduce upper and lower respiratory tract secretions and eliminate rhinorrhea. However, they cause sedation and thus impair the ability to concentrate. Second generation antihistamines do not block muscarinic receptors and are suitable for long-term or short-term treatment of allergic rhinitis. Second-generation antihistamines have no sedative side effects Histamine is not involved in colds, but bradykinin does not help cure colds. When are corticosteroids, antiallergic drugs, mesna, and saline effective and how are they administered? Topically administered corticosteroid (nasal drops) effective in reversing allergic rhinitis, inflammatory rhinitis, nasal polyps, and rhinitis pharmaceuticals Anti-allergic drug preventive treatment for allergic rhinitis administered as nasal drops Mesna is used for local administration of nasal discharge

Provides a unique definition of COPD. A group of diseases that cause airway obstruction and respiratory distress, including emphysema, chronic bronchitis, and bronchial asthma. A brief description of the proposed etiology and pathophysiology of chronic bronchitis and emphysema. Chronic bronchitis is a non-specific obstructive airway disease that causes increased and decreased mucous secretions, with frequent bacterial respiratory infections, structural changes in the bronchi, and smoking and irritants. Damage causes irreversible dilation of the bronchi and arteries of the airways, trapping air in the lungs, making it difficult to exhale, reducing the size of capillaries, and inadequate gas exchange Which treatment Is it part of the treatment of COPD patients? Quit smoking if smoking is the cause Wide spectrum with bacterial infection, influenza vaccination, and infection AB-ampicillin, amoxicillin, erythromycin Airway obstruction bronchodilator Secretions thin the mucus Oxygen inhalation in hypoxia Decreased vital capacity Regular mild to moderate exercise Why is ipratropium more effective in treating chronic bronchitis than in treating bronchial asthma? Ipratropium has anticholinergic properties that block the release of Ach and reduce mucus production. Bronchial asthma is not good because chronic bronchitis is characterized by increased mucus secretion. How does theophylline's effect on skeletal muscle help treat COPD? Theophylline improves diaphragmatic contractile function, increases ventricular volume, thereby reducing hypoxia and dyspnea, and COPD What role does oxygen therapy play in COPD? Prevents hypoxia and improves airflow and gas exchange

Which blood vessel changes can be observed before and during a migraine? When chemicals are released, they travel to the outer layers of the brain, called the meninges, causing inflammation and swelling of blood vessels and increasing blood flow to the brain. This can be the result of the throbbing, throbbing pain that most people experience during a migraine. What role does serotonin play in migraine? Serotonin is a chemical substance required for communication between nerve cells. Blood vessels throughout the body may narrow. Changes in serotonin or estrogen levels can result in migraine headaches. Serotonin levels can affect both sexes, but fluctuating estrogen levels affect only women. How is ergotamine used in migraine attacks? Take ergotamine as soon as the symptoms of migraine begin. Place the tablet under your tongue and let it melt. Take 1 tablet every 30 minutes as needed. Do not use more than 3 tablets within 24 hours. What are the side effects of taking ergotamine? What are the contraindications to the use of ergotamine? The side effects are: Overdose can cause vomiting, confusion, drowsiness, weakness in the wrists of the legs and arms, numbness and tingling and pain in the hands and feet, scratches on the fingers and toes, fainting, and seizures. Contraindications: High blood pressure, coronary artery disease, cerebral ischemia, lack of blood supply to the brain, Reynaud phenomenon, diseases in which blood vessels contract too much during cold or tension, peripheral vascular disease, thrombotic venitis, veins due to inflammatory clots What other medications can be used for acute ischemic attacks? What are the effects of all these drugs? Currently, nonsteroidal anti-inflammatory drugs (NSAIDs) and triptans (serotonin 5HT1B / 1D receptor agonists) are recommended for the acute treatment of migraine attacks. Metoclopramide or domperidone can help with NSAIDs and triptans. Subcutaneous sumatriptan is the first choice for very severe attacks Migraine is a common neuropathy with severe socio-economic burden. Nonsteroidal anti-inflammatory drugs (NSAIDs) reduce the synthesis of prostaglandins involved in the pathophysiology of migraine by blocking cyclooxygenase. Triptans are selective 5HT1 receptor agonists shown in severe migraine attacks. These drugs work primarily by constricting the cranial blood vessels. However, vasoconstriction outside the central nervous system is also possible. Divalproex (Depakote), sodium valproate, and topiramate (Topamax)

What is the mechanism of action of colchicine in the treatment of gouty arthritis? colchicine regulates various pro-inflammatory and anti-inflammatory signaling pathways associated with Jigartritis. Colchicine prevents the accumulation of microtubules, thereby interfering with inflammatory activation, microtubule-based inflammatory cell chemotaxis, leukotriene and cytokine production, and phagocytosis. What are the indications for the use of colchicine, its side effects and dosages? Colchicine indications: acute and recurrent pericarditis, prevention of postpericardial syndrome, primary biliary cirrhosis, cirrhosis, dermatitis herpetitis, Paget's disease, chronic immune thrombocytopenia and idiopathic thrombocytopenia Purpura, pseudogout. Side effects of colchicine: Diarrhea, nausea, cramps, abdominal pain and vomiting may occur. If any of these side effects persist or worsen, tell your doctor or pharmacist immediately. The doses of colchicine are: Oral dosage form (capsule, solution): To prevent gout attacks: Adults 0.6 mg (mg) (5 ml [ml]) once or twice daily. However, the dose is usually 1.2 mg or less per day. Oral use (tablets): Prevention of seizures: Adults 0.6 mg (mg) once or twice daily. However, the dose is usually 1.2 mg or less per day. To treat a ziga attack: 1.2 mg (mg) for adults at the first sign of a ziga attack, 0.6 mg 1 hour later. The dose is usually 1.8 mg per hour. What are the other medications that can be used to treat acute gout attacks? Colchicine is an effective anti-inflammatory drug to relieve the pain of gout. Non-steroidal anti-inflammatory drug (NSAID). Which drug group does probenecid belong to? How do the drugs in this group work? Probenecid belongs to a class of drugs called uricosuric drugs. It lowers your body's levels of uric acid by helping the kidneys excrete uric acid. If the uric acid level becomes too high, crystals can form in the joints and cause gout. How does allopurinol work? What are its indications, precautions, and key interactions? Allopurinol works by reducing the amount of uric acid produced by the cells of the body. In gout, it helps prevent uric acid crystals from accumulating in the joints. Prevents joint swelling and pain. Allopurinol is indicated for reduced uric acid / uric acid formation in diseases in which uric acid / uric acid deposition has already occurred or is at foreseeable clinical risk. Take as directed by your doctor. Do not take more often or longer than your doctor recommends. This can increase the likelihood of side effects. You can take this medicine after meals to prevent stomach problems

What is the mechanism of action of paracetamol? Not a weak peripheral COX1 and COX2 inhibitor, anti-inflammatory agent. It blocks COX3 in the CNS and activates the reduction of serotonergic analgesic pathways. Antipyretic: Direct effect on the thermoregulatory center of the hypothalamus. How is it different from aspirin? Aspirin is an irreversible non-selective blocker of cyclooxygenase (COX) that blocks COX1 and 2. This reduces the production of prostaglandins (PG), thromboxane (TXA), and prostacyclin (PGI). Name the indication for paracetamol. Under what circumstances is the drug of choice for the treatment of mild pain and fever? • Relief of mild to moderate pain of somatic origin • Suitable for patients with contraindications for NSAIDs Asthma, gastric ulcer, hemophilia • Treatment choices for children • Rash and urticaria • No effect on platelet adhesion • No effect Therefore, for uricosuric, it can be used with uricosuric drugs. Name the side effects that you may experience when using paracetamol. • Antipyretic • False safety delusion: 1015g (ie 2030 tablets) can be fatal • Chronic consumption of 2g / day can also lead to acetaminophen poisoning. • Painkiller combinations can increase toxicity. • Alcohol addicts: Even therapeutic doses can be hepatotoxic • Overdose: Hepatotoxicity Discusses acute acetaminophen toxicity and produces reports highlighting doses, signs and symptoms, and treatment increase. Signs and symptoms: Within 12 days: • Abdominal pain • Nausea and vomiting • Loss of appetite • Tired and weak 12 days later: • Lower right rib • Jaundice • Tar liver • Development of renal failure • Liver necrosis and death Dosage: 1015 g (Ie 2030 tablets) can be fatal. Chronic intake of 2 g / day can also lead to acetaminophen poisoning. Treatment: • Immediate supplementation of the SH group to supplement liver glutathione and prevent hepatocellular necrosis. • N-Acetylcysteine ​​(Parvolex®) IV administration within 812 hours. • Starting dose: 200 ml in 15 minutes 150 mg / kg with 5% glucose, • 500 ml in 4 hours 50 mg / kg with 5% glucose, • 1,000 ml 100 mg / kg with 5% glucose 16 hours • Oral treatment: Acetylcysteine ​​(Solmucol®, ACC®), 140 mg / kg or Carboscistein (Mucosirop®, Flemex®) 150 mg / kg • Within 1 hour after poisoning: • Inducing vomiting • Gastric lavage • Administer activated charcoal when using IV treatment • Note: Treatment is only effective within 10 hours of poisoning

Provides a concise and critical explanation of why fluvoxamine, a selective serotonin reuptake inhibitor (SSRI), is used to treat Covid patients (NIH, 2021). Fluvoxamine is a selective serotonin reuptake inhibitor (SSRI). Yes, it is approved by the Food and Drug Administration (FDA) for the treatment of obsessive-compulsive disorders and is also used for depression and other illnesses. Studies conducted have shown that fluvoxamine has been found to bind to the sigma 1 receptor in immune cells and reduce the production of inflammatory cytokines. In vitro studies of human endothelial cells and macrophages also reduced the expression of inflammatory genes. The Medical Letter (Medical Letter, 2021: 63) states that Sigma1 agonism has been shown to inhibit SARSCoV2 replication and regulate the inflammatory response to sepsis. Theoretically, COVID 19 can prevent the development of life-threatening cytokine storms and acute respiratory distress syndrome. According to the source by K. Hashimoto (NIH, 2021) The sigma 1 receptor in the endoplasmic reticulum plays an important role in intracellular SARSCoV2 replication. Knockouts and knockdowns of SIGMAR1 (Sigma1 receptor encoded by SIGMAR1) cause a significant reduction in SARSCoV2 replication, suggesting that the Sigma1 receptor is an important therapeutic target for SARSCoV2 replication.

Why do you think aspirin is contraindicated for people with allergic asthma? Because it blocks both COX 1 and 2, more arachidonic acid is available for the production of leukotrienes, thus producing more leukotrienes. This leads to bronchoconstriction, which is not good for asthma patients. Arachidonic acid is the most important precursor of eicosanoids, but how is this fatty acid released from the cell membrane and through what stimulus? For eicosanoid synthesis, arachidonic acid (AA) must first be released from membrane phospholipids. There are at least three classes of phospholipases that contribute to the release of AA from membrane phospholipids. Cytosol PLA2 (phospholipase A2) Secretory PLA2 (calcium dependence) Calcium-independent PLA2 (Chemical and physical stimulation activates Ca2 + translocation of PLA2 to the plasma membrane, where it releases arachidonic acid for the synthesis of eicosanoids.) In addition to prostanoids and leukotrienes, which other nonnicosanoid products of cell membrane hydrolysis are deeply involved in asthma? Why do you say that COX-II inhibitors, not COX-I inhibitors, have a selective effect on the inflammatory response? COX 1: Always present in the body and has housekeeping functions such as cell protection of the gastric epithelium. COX 2: Easy to induce and its level depends on the stimulus. It is often found in kidney and vascular tissue. Release occurs via inflammatory stimuli, shear stresses, and growth factors. Drugs that inhibit any of the following enzymes, such as tumor promoters: Phospholipase A; Cyclooxygenase; Lipoxygenase, Phospholipase A: Hydrocortisone Cyclooxygenase: Aspirin Lipoxygenase: Giroton Prostaglandin and antileukotriene receptors A drug that can act as a target. How does that happen? Cox1 & Cox2 irreversibly block What are the benefits of alprostadil in the treatment of congenital heart disease? This is given to the patient as an infusion to keep the heart valve open during surgery. What is the value of misoprostil in the treatment and prevention of gastric ulcer? It protects the lining of the stomach by increasing mucus production and reducing acid secretion. Prostaglandins may help with asthma. Which PGE2 or PGF2A analog is effective in such cases? Epoprostenol What is the value of latanoprost in the treatment of glaucoma? Increased outflow of aqueous humor.

1. In which diseases are angiotensinogen levels increased? What are the implications of this?
Estrogens, corticosteroids, thyroid hormones, and ANG II all raise angiotensinogen levels. It is increased among women who take estrogen-containing oral contraceptives and in pregnant women. As a result, an increase in plasma angiotensinogen concentration could lead to hypertension.

2.Why do drugs which inhibit the angiotensinogen system by acting on angiotensin receptors have fewer side effects than those that inhibit ACE

ACE inhibitors can cause angioedema and dry cough by increasing the level of bradykinin in the body.

3. In which way do ACE inhibitors have a two-fold mechanism of action in the treatment of Hypertension?

ACE inhibitors prevent the conversion of ANG I to ANG II and the degradation of other compounds such as enkephalins, bradykinin, and substance P. As a result, the activity of ACE inhibitors in inhibiting substances like bradykinin helps to reduce blood pressure.

4. At which type of angiotensinogen receptor do losartan and similar drugs act? Do they have any effect, direct or indirect, at other angiotensinogen II receptors?

The medications bind to AT1 receptors and, as ANG II levels rise, they bind to AT2 receptors.

5. What are the physiological effects of kinins on arteries and veins?  Do other autacoids play a role in this action?  Explain.

Kinins promote artery vasodilation due to their direct inhibitory impact on arteriolar smooth muscle; however, it can also be mediated through the release of vasodilator prostaglandins or nitric oxide, such as PGE2 and PGI2. Because of the release of venoconstriction prostaglandin PGF 2 alpha or direct activation of venous smooth muscle, kinins causes veins to constrict. Autacoids, such as bradykinin, which is a powerful vasodilator, have a function.

6. Which receptor is probably the most involved in the important clinical effects of kinins? Type B2 receptor.

7. In which way are natriuretic peptides possibly effective in the treatment of hypertension, as well as congestive heart failure?

For the treatment of congestive heart failure, natriuretic peptides such as ularitide, carperitide, nesiritide, and urodilatin cause natriuresis and vasodilation.

8.What is neprilysin and what is the rationale for inhibiting its action in the treatment of heart failure?

The enzyme neprilysin is involved in the breakdown of natriuretic peptides. The major goal of neprilysin inhibitor therapy in cardiovascular disease was to raise endogenous natriuretic peptide levels, which would result in the vasodilation and natriuresis that these peptides cause.

9. Give examples of endothelium-derived vasodilators and vasoconstrictors. Vasodilators: Nitric oxide and PGI2 Vasoconstrictors: ET 1 and receptor subtypes ETA and ETB

Migraines are caused by the distribution of the trigeminal nerve to the intracranial arteries. The trigeminal nerves secrete peptide neurotransmitters, including calcitonin gene-related peptide (CGRP), a powerful vasodilator. Extravasation of plasma and plasma proteins into the perivascular space results in mechanical stretching, which activates the dura's pain receptors.

Treatment:

Triptans, such as Sumatriptan, are selective 5-HT1D and 5-HT1B agonists, causing vasoconstriction and preventing the migraine's vasodilatory effects as well as the discomfort associated with it. They also control neurotransmitter release, lowering the quantity of CGRP.

Ergot alkaloids, such as Ergotamine, act as a partial agonist at 5-HT and alpha adrenoreceptors, reducing the vasodilation that is associated with migraines.

Anti-inflammatory analgesics, such as aspirin, can help with migraine pain.

Calcium channel blockers, such as Verapamil, are effective in migraine prevention.

Beta blockers, such as Propranolol, are useful in migraine prevention.