Polisegmental osteochondrosis

Autoimmune thyroiditis, most commonly known as Hashimoto's thyroiditis, is a chronic inflammatory disease of the thyroid gland. In this condition, the body's protective system—the immune system—mistakenly perceives the hormone-producing cells of its own thyroid gland as "foreign" and attacks them. This continuous attack by the immune system leads to the gradual destruction of thyroid tissue over the years. As a result, the gland's ability to produce hormones is limited, and over time, thyroid underactivity—hypothyroidism—develops. Hashimoto's thyroiditis is considered one of the most common causes of hypothyroidism. Causes The main factors for the onset of the disease are diverse and often interconnected: 1. Family predisposition – if there are cases of thyroid or other autoimmune diseases in the family, the risk increases significantly. 2. Iodine-rich diet – especially in cases where a genetic predisposition exists. 3. Certain viral and bacterial infections – which can activate the autoimmune process. Initial Symptoms In the early stages of the disease, symptoms resembling increased thyroid function are often observed, which can be temporarily misleading: 1. Increased sweating 2. Weight loss 3. Nervousness and irritability 4. Palpitations This phase can be transient and gradually change into thyroid underactivity. Symptoms of Hypothyroidism As the disease develops, signs characteristic of hypothyroidism manifest, which can significantly affect the quality of life: 1. Fatigue, general weakness 2. Dry skin 3. Hair loss 4. Weight gain 5. Constipation 6. Difficulty concentrating 7. Memory impairment 8. Edema (swelling) in the upper and lower extremities Diagnosis A combination of several research methods is used for accurate diagnosis: 1. Palpation of the thyroid gland 2. Checking thyroid hormones and specific antibodies in the blood 3. Ultrasound examination of the thyroid gland 4. Scintigraphy (if necessary) Treatment The main approach to treating Hashimoto's thyroiditis is hormone replacement therapy: 1. Thyroid hormone replacement medications are prescribed. 2. It is necessary to periodically monitor thyroid hormone levels to determine and adjust the correct dosage of the pill. Thyroid function usually deteriorates gradually over the course of life; therefore, the dosage of the hormonal medication may change over time. Treatment, as a rule, continues throughout life because the damaged tissue of the thyroid gland does not recover, and the underactivity remains permanent.

Polyneuropathy is a disease of the peripheral nervous system in which multiple nerves are affected simultaneously. These nerves connect the brain and spinal cord to the muscles, skin, and internal organs. Damage is usually symmetrical and often begins in the extremities—hands or feet—but in some cases, internal organs are also affected. Causes of the Disease By origin, polyneuropathies are divided into primary (hereditary) and secondary. Hereditary forms are associated with genetic disorders and include, for example, hereditary motor-sensory neuropathies, amyloidosis, Fabry and Refsum diseases, and other rare syndromes. Secondary polyneuropathies, which occur as a complication of other diseases or under the influence of external factors, are significantly more common. These include toxic, infectious, metabolic, vascular, and autoimmune forms. The development of polyneuropathy can be promoted by: • Infections (HIV, diphtheria, Epstein–Barr virus, botulism, etc.); • Autoimmune and allergic diseases, including Guillain–Barré syndrome; • Intoxication with drugs, alcohol, heavy metals, and other toxic substances; • Diabetes mellitus, liver and kidney diseases, deficiency of B vitamins; • Exposure to cold, vibration, radiation; • Tumors and their metastases compressing the nerves. The risk of the disease increases with age. In some cases, a precise cause cannot be established—such a form is called idiopathic. Classification Depending on the type of fibers affected, the following forms are distinguished: • Sensory form — with impaired sensitivity; • Motor form — with muscle weakness and reduced movement; • Autonomic form — with disorders of internal organ function; • Mixed form — a combination of several types. According to the mechanism of damage, a distinction is made between axonal forms (damage to the axon) and demyelinating forms (damage to the myelin sheath). By localization, polyneuropathy can affect the upper or lower limbs, cranial nerves, or autonomic nerves of internal organs. According to its course, the disease can be acute, subacute, or chronic. Symptoms Most often, the first manifestations occur in the feet and hands. Numbness, tingling, and burning appear, followed by pain and muscle weakness. Over time, symptoms spread upward along the limbs. Other observations may include: • Reduction or loss of sensitivity; • Muscle atrophy; • Tremors, muscle twitching; • Swelling, changes in skin and nails; • Delayed wound healing. When autonomic or cranial nerves are affected, disturbances in sweating, heart rhythm, breathing, digestion, vision, hearing, speech, and swallowing are possible. Pathogenesis In axonal forms, nerve fibers are primarily damaged, leading to muscle weakness and atrophy, especially in the distal parts of the limbs. These forms are characteristic of toxic and some hereditary polyneuropathies. During demyelination, the conduction of nerve impulses is disrupted, manifesting as reduced reflexes and muscle weakness without pronounced atrophy. These changes are typical for autoimmune and hereditary diseases. Diagnosis Diagnosis begins with an interview and a neurological examination. The doctor assesses sensitivity, reflexes, muscle strength, and coordination. To clarify the diagnosis, the following are used: • Blood and urine tests; • Immunological and genetic studies; • Cerebrospinal fluid examination; • Electroneuromyography (the main method); • Ultrasound of the nerves, biopsy — as indicated. Treatment Treatment tactics depend on the cause of the disease. Hereditary forms are treated symptomatically. For autoimmune polyneuropathies, immunoglobulins, glucocorticoids, and plasmapheresis are used. In diabetic, alcoholic, and toxic forms, main attention is paid to treating the underlying disease and eliminating the damaging factor. To reduce pain, anticonvulsants, antidepressants, B vitamins, and thioctic acid are used. Non-drug therapy includes physical therapy and rehabilitation, and in severe cases, support of vital functions. Complications and Prognosis Without treatment, polyneuropathy can lead to persistent muscle atrophy, injuries, impaired function of internal organs, and, in rare cases, life-threatening conditions. The prognosis depends on the form of the disease. In toxic and infectious polyneuropathies, complete recovery is possible after eliminating the cause. Chronic forms usually progress slowly, but with proper therapy, quality of life can be maintained. Prevention To reduce risk, it is important to control blood sugar levels, avoid alcohol, avoid contact with toxic substances, follow safety regulations at work, and ensure adequate intake of vitamins, especially group B. Medications should only be taken as prescribed by a doctor.

Kidney stone disease, also known as renal calculi or nephrolithiasis, is a condition in which hard mineral deposits form inside the kidneys. These stones develop when urine becomes too concentrated, allowing minerals and salts to crystallize and stick together. Kidney stones can affect anyone at any age, but they occur more often in men, with the highest incidence between the ages of 30 and 40. While some kidney stones remain small and pass without causing problems, others can grow, recur, or move into the urinary tract, leading to severe pain and complications. If left untreated, kidney stones may result in kidney infections, damage to the ureters, sepsis, or long-term loss of kidney function, including chronic kidney disease. Recognizing the condition early is key to preventing serious outcomes.Kidney stones vary in size—from tiny, sand-like grains to much larger stones—and they may form anywhere along the urinary tract, from the kidneys to the bladder. Even after successful treatment, stones can return, making prevention and follow-up especially important. Why do kidney stones form? Several factors increase the likelihood of developing kidney stones. These factors often affect how much calcium, oxalate, uric acid, or water is present in the urine: • Diet and hydration habits: Not drinking enough water, eating excessive salt, sugar, animal protein, or oxalate-rich foods (such as spinach, nuts, and chocolate) can promote stone formation. • Medical conditions and body chemistry: Obesity, gout, overactive parathyroid glands, digestive disorders (like inflammatory bowel disease or chronic diarrhea), and high calcium or uric acid levels in the blood raise the risk. • Medications and supplements: High-dose vitamin C, calcium supplements, and certain medications may contribute to stone development. Warning signs and symptoms Kidney stones may not cause symptoms until they move within the kidney or become lodged in the ureter, blocking urine flow. When symptoms do appear, they can be sudden and intense: • Severe, sharp pain in the side, back, or lower abdomen that may come in waves • Pain during urination, frequent urination, or difficulty passing urine • Cloudy, pink, red, or brown urine, sometimes with sand-like particles • Nausea, vomiting, fever, or chills if an infection is present Some people, however, may have kidney stones without any noticeable symptoms. Diagnosis and treatment If kidney stones are suspected, healthcare providers use urine and blood tests along with imaging studies—such as ultrasound, X-rays, or CT scans—to confirm the diagnosis and determine stone size and location. Treatment depends on the type and size of the stone and the severity of symptoms. Small stones often pass on their own with increased fluid intake and, in some cases, medications to relax the ureter and ease pain. Larger or problematic stones may require specialized procedures, such as shock wave therapy to break them apart, endoscopic removal with a ureteroscope, or surgical techniques for very large stones. Prevention and outlook Most people with kidney stones recover fully, but recurrence is common. Preventive strategies focus on long-term lifestyle and dietary adjustments, including staying well hydrated, maintaining a balanced diet, limiting salt and animal protein, and following medical advice tailored to the type of stone formed. With early diagnosis, appropriate treatment, and preventive care, kidney stone disease can be effectively managed, helping protect kidney health and quality of life.

A C-peptide test measures the level of C-peptide in your blood or urine to evaluate how much insulin your pancreas is producing. Because C-peptide and insulin are released into the bloodstream at the same time and in equal amounts, this test provides a reliable picture of your body’s natural insulin production. Unlike insulin levels, C-peptide is not affected by injected or inhaled insulin used for diabetes treatment. For this reason, healthcare providers often rely on a C-peptide test to distinguish between insulin made by the body and insulin taken as medication. Understanding C-Peptide and Insulin C-peptide is a short chain of amino acids created when the pancreas produces insulin. Insulin is the hormone responsible for helping glucose enter the body’s cells, where it is used for energy. Proper insulin function is essential for maintaining healthy blood sugar levels. In people with Type 1 diabetes, the pancreas produces little or no insulin. In Type 2 diabetes, insulin is produced, but the body may not use it effectively, or insulin production may decline over time. Measuring C-peptide helps clarify which situation is present. Why Is a C-Peptide Test Performed? Healthcare providers may order a C-peptide test to better understand blood sugar disorders and guide treatment decisions. Common reasons include: • Determining whether diabetes is Type 1 or Type 2 when the diagnosis is unclear • Evaluating how well current diabetes treatment is working • Deciding whether insulin therapy is necessary • Investigating unexplained low blood sugar (hypoglycemia) • Differentiating between insulin produced by the body and insulin taken as medication • Monitoring or diagnosing rare insulin-producing pancreatic tumors (insulinomas) How Is the Test Done? A C-peptide test is usually performed using a blood sample taken from a vein in the arm. In some cases, especially when more detailed information is needed, the test may be done using urine collected over a 24-hour period. Blood testing is more common and quicker. Depending on the clinical situation, your provider may ask you to fast for 8–12 hours or may measure C-peptide after eating to see how your pancreas responds to food. The test is often performed alongside a blood glucose measurement. Understanding the Results C-peptide results must always be interpreted together with blood sugar levels and clinical findings. In general: • Low C-peptide levels suggest reduced insulin production, which may occur in Type 1 diabetes, advanced Type 2 diabetes, after insulin injections, or with certain conditions such as Addison disease or severe liver disease. • High C-peptide levels indicate excessive insulin production, which may be associated with insulin resistance, Type 2 diabetes, Cushing syndrome, kidney disease, low potassium levels, or insulin-producing tumors. • If no C-peptide is detected, insulin replacement therapy is usually required. Important Notes A C-peptide test does not diagnose diabetes on its own. Blood glucose tests and hemoglobin A1c (HbA1c) remain the primary tools for diagnosing diabetes. Instead, the C-peptide test plays a supportive role by showing how well the pancreas is functioning and helping tailor long-term treatment strategies.