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Myocardial infarction (MI) is ischemic necrosis of the heart muscle caused by an acute disruption of its blood supply. It is one of the most dangerous cardiovascular diseases and remains one of the leading causes of death worldwide. According to statistics, most cases occur in individuals aged 45–65. Men tend to develop the disease at a younger age than women. In recent years, due to preventive measures in developed countries, the incidence of infarction has somewhat decreased, but it remains a major global health problem. Etiology and Risk Factors The main cause of myocardial infarction is atherosclerotic damage to the coronary arteries. After rupture of an atherosclerotic plaque, a thrombus forms, blocking the artery and leading to myocardial ischemia.The main risk factors are: • High blood pressure. • High cholesterol or lipid disorders. • Diabetes mellitus. • Smoking. • Overweight and physical inactivity. • Age, especially over 50. • Stress and unhealthy lifestyle. Clinical Picture 1. The main symptom of MI is a compressive, burning, or pressing chest pain lasting more than 20 minutes. 2. The pain may radiate to the left arm, neck, lower jaw, or back. 3. It is often accompanied by cold sweats, weakness, shortness of breath, and nausea. 4. In elderly patients and those with diabetes, pain may be mild or absent. Classification Myocardial infarction is classified according to several principles. 1. Based on ECG findings: • ST-segment elevation MI (STEMI). • Non-ST-segment elevation MI (NSTEMI). 2. Based on localization: • Anterior wall infarction. • Posterior wall infarction. • Lateral, inferior, or extensive infarction. 3. Based on stages: • Early stage — first 24 hours. • Acute stage — up to 7 days. • Subacute stage — up to 4 weeks. • Chronic stage — formation of myocardial scar. Diagnosis 1. Diagnosis is based on three main criteria: • Typical clinical symptoms. • ECG changes — ST-segment elevation or depression, Q-wave formation. • Elevated biochemical markers of myocardial injury (Troponin I/T, CK-MB). 2. Echocardiography helps detect areas of segmental hypokinesia or akinesia. Complications The complications of acute myocardial infarction are divided into early and late stages. Early Complications (from the first hours to the first days) 1. Arrhythmias: • Ventricular tachycardia or fibrillation. • Atrioventricular block. • Sinus bradycardia or tachycardia. 2. Heart failure: • Acute left ventricular failure. • Pulmonary edema. 3. Cardiogenic shock. 4. Myocardial rupture (often on the 3rd–5th day): • Free wall rupture leading to cardiac tamponade. • Ventricular septal rupture. • Papillary muscle rupture leading to acute mitral insufficiency. 5. Early fibrinous pericarditis. Late Complications (weeks to months) 1. Myocardial aneurysm, acute or chronic. 2. Impaired ejection of blood from the heart. 3. Thrombosis in the aneurysmal cavity. 4. Thromboembolic complications — cerebral stroke or pulmonary embolism. 5. Late pericarditis (Dressler’s syndrome) of autoimmune origin. 6. Chronic heart failure. 7. Recurrent infarction or ischemic attacks. Treatment The main goal of treatment is to restore coronary blood flow as quickly as possible to prevent myocardial damage. Coronary angiography is considered the “gold standard” because it identifies the occlusion site and allows restoration of circulation. Thrombolysis is most effective during the first hours after onset, while percutaneous coronary intervention (PCI, stenting) is the preferred method. If PCI is not possible, coronary artery bypass grafting (CABG) is performed. Additional medications are used, including morphine for pain relief, antiplatelet therapy with aspirin and P2Y12 inhibitors, heparin for anticoagulation, as well as beta-blockers and ACE inhibitors to reduce cardiac workload. This comprehensive approach lowers the risk of complications and improves recovery outcomes. Prevention Secondary prevention is essential after myocardial infarction to reduce the risk of recurrence and complications. Patients should remain under regular cardiologist supervision, with strict control of blood pressure, glucose, and lipid levels. Cardiac rehabilitation exercises play an important role in restoring cardiac function. Prescribed medications must be taken consistently and according to medical recommendations. Myocardial infarction is a severe but controllable disease if diagnosed and treated in time. Early detection and appropriate therapy can save lives and prevent complications. Prevention begins with every individual — through a healthy lifestyle and regular medical check-ups.

Adrenal insufficiency, also known as Addison’s disease, is an endocrine disorder in which the adrenal cortex fails to produce adequate amounts of vital hormones. The adrenal cortex secretes several steroid hormones — cortisol, aldosterone, and androgens. Cortisol production is regulated by the adrenocorticotropic hormone (ACTH), produced by the pituitary gland. Cortisol is a vital “stress hormone” that affects fat and carbohydrate metabolism, supports immune regulation, and helps the body respond to physical and emotional stress. Aldosterone maintains water and electrolyte balance, regulating blood pressure and sodium–potassium levels. There are three types of adrenal insufficiency: primary, secondary, and tertiary. Primary Adrenal Insufficiency In this form, the adrenal glands themselves are damaged. Main causes: 1. Autoimmune destruction, where antibodies attack the steroid-producing cells of the adrenal cortex. 2. Amyloidosis 3. Metastatic lesions 4. Hemorrhagic infarction of the adrenal glands 5. Infectious diseases such as tuberculosis, meningococcal infection, or cytomegalovirus. Secondary Adrenal Insufficiency This type results from pituitary gland dysfunction, which leads to reduced secretion of ACTH and, consequently, decreased adrenal activity and cortisol production. Main causes: 1. Tumors 2. Head injuries 3. Circulatory disturbances 4. Inflammatory conditions Main Symptoms of Adrenal Insufficiency 1. Muscle weakness 2. Brownish skin pigmentation 3. Low blood pressure 4. Bradycardia 5. Low sodium levels 6. Elevated potassium levels 7. Hypoglycemia 8. Eosinophilia 9. Fatigue 10. Nausea, vomiting, diarrhea 11. Abdominal pain 12. Dizziness 13. Drowsiness Diagnosis A detailed medical history is essential, including any past or current use of glucocorticoid medications (pills, injections, or creams). These drugs have anti-inflammatory properties and are often prescribed for chronic conditions, but they must be used according to a strict medical schedule. Abrupt dose reduction or sudden discontinuation may suppress ACTH production in the pituitary gland, leading to adrenal insufficiency. Laboratory and imaging tests: • Hormonal assays (cortisol and ACTH levels) • MRI of the brain and CT scan of the adrenal glands Treatment The cornerstone of treatment is hormone replacement therapy to compensate for the lack of adrenal hormones. During stress (surgery, infections, fever, trauma, or intense emotional or physical exertion), the body’s need for cortisol increases, so the medication dose must be temporarily raised. After recovery, the dose should return to the previous level. Conclusion Adrenal insufficiency is a serious endocrine disorder that requires timely diagnosis and carefully monitored hormone therapy. If the above symptoms occur, it is essential to consult an endocrinologist for proper evaluation and treatment.

Dry eye syndrome is one of the most common eye conditions, in which the surface of the eye loses its normal moisture. This happens when the tear film becomes unstable or when tear production is insufficient. As a result, the eyes “dry out,” causing irritation, fatigue, and a feeling of grittiness. According to ophthalmologists, almost one in five people experiences this condition, most often women over 40. Modern habits — long computer use, air conditioning, and contact lenses — make the problem even more widespread. Causes and development The tear film protects the cornea from drying and irritation. It consists of three layers — oily, watery, and mucous. When any of these layers are disrupted, moisture evaporates quickly and the eye surface becomes unprotected. Causes can be internal or external. Internal factors include hormonal changes (such as during menopause or pregnancy), chronic illnesses, and deficiency of vitamins A and E. External ones include dry air, wind, air conditioners, and infrequent blinking while using screens. Improperly fitted lenses or long-term use of some medications can worsen the problem. Symptoms The main symptoms are dryness, burning, redness, and a feeling of sand or a foreign body in the eyes. Sometimes excessive tearing occurs as a reaction to irritation. Vision may become blurry or fluctuate during the day. Symptoms often worsen by evening, after prolonged reading or computer work, or in dry environments. In severe cases, corneal inflammation and visual impairment may develop. Diagnosis An ophthalmologist can diagnose dry eye syndrome during an eye exam. The doctor evaluates the eyelids, cornea, and tear film. Common diagnostic tests include: • Schirmer’s test – measures tear production; • Norn’s test – checks how quickly the tear film evaporates; • Fluorescein test – identifies dry spots on the cornea. These tests are painless and take just a few minutes. Treatment and care The main goal of treatment is to restore normal eye moisture and relieve irritation. Most patients benefit from “artificial tears” — drops or gels that imitate natural tears and protect the cornea. Inflammation may require anti-inflammatory or regenerative medications. It’s also important to remove triggering factors: avoid dry or dusty environments, choose lenses carefully, and take breaks from screens. In rare severe cases, minor surgery can help retain natural moisture. Prevention To prevent dry eye syndrome: • blink more often when using a computer, • maintain indoor humidity, • drink enough water and eat foods rich in vitamin A and omega-3, • avoid using eye drops without a doctor’s advice. Even mild dry eye requires attention. Early treatment helps preserve eye health and visual clarity.

Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system, in which the immune system mistakenly attacks the myelin sheath of nerve fibers in the brain, spinal cord, and optic nerves. Damage to myelin disrupts the transmission of nerve impulses and leads to numerous neurological symptoms. Etiology The exact causes of multiple sclerosis are unknown. It is believed that the development of the disease is promoted by a combination of factors such as: • genetic predisposition, • environmental factors (infections, vitamin D deficiency, stress, smoking). Pathogenesis Immune cells (lymphocytes) penetrate the blood–brain barrier and damage myelin. As a result, inflammation develops, and over time, destruction of the nerve fibers (axons) themselves may occur. Forms of Multiple Sclerosis • Relapsing-remitting (RRMS) — the most common form, characterized by alternating periods of relapses and remissions. • Secondary-progressive (SPMS) — initially presents as RRMS, then gradually transitions into a progressive form. • Primary-progressive (PPMS) — gradual worsening of symptoms without distinct remissions. • Progressive-relapsing (PRMS) — a rare form in which disease progression is accompanied by periodic relapses. Symptoms The clinical picture is diverse and depends on which parts of the nervous system are affected. Possible manifestations include: • weakness in the limbs, muscle spasticity, • numbness, tingling, sensation of “electric shocks” in the body, • urinary and bowel dysfunction, • visual disturbances (diplopia, blurred vision, blindness in one eye), • problems with coordination, balance, and gait, • chronic fatigue, dizziness, • cognitive impairments (memory, attention), • depression and emotional instability. Diagnosis The diagnosis is made based on a combination of findings: • MRI of the brain and spinal cord — detection of demyelinating lesions, • Evoked potentials — assessment of nerve impulse conduction speed, • Cerebrospinal fluid analysis — detection of oligoclonal antibodies, • Clinical presentation and history of relapses. Treatment The main goals of therapy are to reduce disease activity, slow progression, and alleviate symptoms. Disease-modifying therapy (DMT): • interferon-beta, • glatiramer acetate, • monoclonal antibodies (natalizumab, ocrelizumab, alemtuzumab), • oral medications (fingolimod, dimethyl fumarate, etc.). Management of relapses: high doses of corticosteroids (e.g., methylprednisolone). Symptomatic therapy: medications to relieve spasticity, pain, fatigue, and urinary problems. Rehabilitation: physiotherapy, therapeutic exercise, psychological support. Prognosis Multiple sclerosis is a chronic and currently incurable disease. However, modern medications can significantly slow disease progression and maintain quality of life for many years. Most patients, especially those who start treatment early, retain mobility for decades.