Graves’ Thyrotoxicosis Leading to Adrenal Decompensation and Hyperandrogenemia in a Pediatric Patient with Salt-Wasting Congenital Adrenal Hyperplasia

Introduction. Thyroid hormone is known to accelerate glucocorticoid turnover. In a thyrotoxic state, individuals with adrenal insufficiency are unable to increase endogenous cortisol production to compensate for increased turnover, placing them at risk for symptoms of glucocorticoid deficiency and adrenal crisis. In patients with salt-wasting congenital adrenal hyperplasia (SW-CAH), hyperandrogenemia is a measurable reflection of relative glucocorticoid insufficiency. Case Presentation. A 12-year-old girl with SW-CAH reported 3 recent episodes of vomiting without diarrhea, and accompanying tachycardia, responsive to stress dose steroids. In the previous 9 months, she unintentionally lost 2.6 kg. She had tachycardia and new thyromegaly. Labs showed suppressed TSH, elevated free T4 and total T3, and elevated thyroid stimulating immunoglobulin (TSI) consistent with Graves’ disease. Adrenal androgens were markedly elevated. Maintenance hydrocortisone dose was 25 mg/m²/day and was not changed. Methimazole was initiated. Four weeks later, free T4 and adrenal androgens normalized. She had no further vomiting episodes. Conclusions. Thyrotoxicosis must be included in the differential diagnosis of individuals with SW-CAH who present with episodes concerning for adrenal crises, escalating hydrocortisone requirements, and/or inadequate suppression of adrenal hormones.

1. Introduction

Salt-wasting congenital adrenal hyperplasia (SW-CAH) is the most common cause of primary adrenal insufficiency in pediatric patients, and in over 95% of cases it is caused by a mutation in the CYP21A2 gene, which causes a deficiency of the enzyme 21-hydroxylase [1]. Deficiency in 21-hydroxylase causes both gluco- and mineralocorticoid deficiency as well as hyperandrogenism due to the diversion of adrenal steroid precursors to adrenal androgens. Treatment consists of mineralocorticoid supplementation, as well as supraphysiologic glucocorticoid doses to suppress ACTH and minimize formation of adrenal androgens.

Management of glucocorticoid dosing in the growing child with SW-CAH is challenging. Typical dosing of hydrocortisone ranges from 10 to 15 mg/m² daily in 3 divided doses [1]. Cortisol clearance increases in puberty, and glucocorticoid dose requirements often increase [2]. Glucocorticoid overtreatment can compromise height and result in symptoms of glucocorticoid excess. Undertreatment can also compromise height due to accelerated epiphyseal maturation and can result in bothersome virilization and prompt adrenal crises. Close monitoring of growth and biochemical measurement of androgens are essential for the care of the pediatric patient with SW-CAH.

In this case report, we describe a 12-year-old female with previously well-controlled SW-CAH, who presented to a pediatric emergency department with multiple episodes concerning for adrenal crises, responsive to stress dose steroids. She was found to have poorly suppressed androgens on supraphysiologic glucocorticoid doses. Ultimately, she was diagnosed with Graves’ disease.

2. Case Presentation

A 12-year-old female with SW-CAH presented to the pediatric endocrinology clinic for routine follow-up. She was diagnosed with SW-CAH in the newborn period after presenting with ambiguous genitalia and was treated with supraphysiologic hydrocortisone divided three times daily throughout her life (prepubertal dosing range 10-15 mg/m²/day, pubertal dosing range 15-25 mg/m²/day), as well as fludrocortisone (0.1 mg daily). She was monitored every 3-4 months with clinical examinations, growth parameters, and serum measurements of 17-hydroxyprogesterone (17-OHP), androstenedione, and testosterone (Esoterix Laboratory, Calabasas Hills, CA), which together guided her medication dosing. She had no evidence of glucocorticoid excess and her growth velocity was normal, without evidence of acceleration or suppression. She and her parents reported continued excellent compliance with her medication regimen.

At age 12 3/12 years, she reported 3 recent emergency department visits for persistent vomiting without diarrhea, abdominal pain, inability to tolerate oral steroids, and tachycardia. One of the episodes was accompanied by fever >39°C. There was no hypotension during any of these episodes, but heart rates were elevated ranging from 124 to 154 beats per minute. Sodium and potassium were normal: Na 137-140 meq/L (reference range, 133-143 meq/L) and K 3.6-4.1 meq/L (reference range 3.4-4.7 meq/L). Each episode was treated with normal saline boluses and intravenous stress dose steroids, and treatment led to immediate improvement in symptoms. She was discharged from the emergency department with recommendations for stress dose steroids by mouth. Over the prior 9 months, she had also unintentionally lost 2.6 kg and had an accelerated annualized growth velocity of 10.6 centimeters per year. BMI was 15.4 kg/m² (Z-score -1.38). She denied any heat intolerance, jitteriness, palpitations, sweating, diarrhea, or vision complaints. While in clinic, her resting pulse was elevated at 136 beats per minute and blood pressure was normal. She was noted to have new symmetric thyromegaly without nodules. She had no lid lag or stare. She was in mid-puberty, with tanner 3 breasts. There was no family history of autoimmune disease or thyroid disease. Labs (Table 1) showed a suppressed TSH, and an elevated free T4 and Total T3. Thyroid antibodies were consistent with Graves’ disease, with a thyroid stimulating immunoglobulin (TSI) of 652% (reference range <140%). She had no prior thyroid studies for comparison. Adrenal androgens were markedly elevated with 17-OHP 11,600 ng/dl (reference range 11-155 ng/dl, target <1000 ng/dl in SW-CAH). At a clinic visit 15 weeks prior to this evaluation, her 17-OHP on the same dose of hydrocortisone (25 mg/m²/day) was improved at 639 ng/dl. She was initiated on methimazole 0.5 mg/kg/day. Her hydrocortisone dose was not changed and remained at 25 mg/m²/day. Four weeks later, repeat labs demonstrated normal free T4 with mildly suppressed TSH and normal total T3. 17-OHP was stable at 717 ng/dl (Figure 1). She had no further vomiting episodes after initiation of methimazole, and her tachycardia resolved.

Three months after treatment began for Graves’ disease, her TSH and free T4 were in the reference range, and methimazole was decreased to 0. 3 mg/kg/day. Repeat 17-OHP was low at 33 ng/dl, indicating suppression on the unchanged hydrocortisone dose of 25 mg/m²/day. Her hydrocortisone dose was decreased to 21 mg/m²/day.

3. Discussion

Thyroid hormone is well-known to accelerate the metabolism of cortisol. In the adrenally sufficient individual, the thyrotoxic state both increases the production of cortisol, and shortens the half-life of cortisol due to an increased turnover rate, with a net effect of normal circulating cortisol levels [3]. Cortisol requirements are increased due to the stress and increased metabolic demands of thyrotoxicosis. The mechanism of increased cortisol clearance appears to be due to thyroid hormone effects on the activity of 11βHSD and 5-α reductase enzymes [4].

Patients with adrenal insufficiency are unable to mount an adrenal response by increasing cortisol levels in the setting of excess thyroid hormone, placing them at risk for adrenal crises. Recurrent adrenal crises have been reported in individuals with autoimmune primary adrenal insufficiency upon development of autoimmune thyrotoxicosis [5]. Similarly, it is well documented that hypothyroid patients initiated on thyroid hormone repletion with undiagnosed primary or secondary adrenal insufficiency can present with adrenal crisis [6, 7]. In the hypothyroid state, cortisol clearance is slowed, protecting the hypothyroid, adrenally insufficient patient from symptoms of adrenal insufficiency. With thyroid hormone initiation, cortisol clearance increases, and adrenal crisis may occur, similar to the thyrotoxic patient with adrenal insufficiency.

The literature includes only 2 cases of adult patients with congenital adrenal hyperplasia who experienced symptomatic adrenal insufficiency and/or adrenal crisis associated with thyrotoxicosis. Takasu et al. described a 75-year-old female who was admitted for treatment of Graves’ thyrotoxicosis and was found unconscious due to adrenal crisis during her hospitalization [8]. She was ultimately diagnosed with nonclassical 21-hydroxylase deficiency. Kim et al. reported the case of a 23-year-old male with Graves’ thyrotoxicosis who was diagnosed with nonclassic 11-beta hydroxylase deficiency after he presented with hypokalemia and hypertension and was found to have adrenal hyperplasia on imaging [9]. Our report is the first case describing a pediatric patient with CAH, who experienced repeated episodes concerning for adrenal crises and hyperandrogenemia secondary to the onset of Graves’ thyrotoxicosis, demonstrating the impact of thyroid hormone excess on the metabolism of glucocorticoids in vivo.

4. Conclusions

This unusual case demonstrates the unique findings of thyrotoxicosis in a pediatric patient with SW-CAH on glucocorticoid supplementation. She presented with classic signs and symptoms of Graves’ disease including thyromegaly, weight loss, and tachycardia, as well as SW-CAH specific symptoms reflecting cortisol deficiency including biochemical hyperandrogenemia and repeated episodes concerning for adrenal crises. Increased clearance of cortisol in the setting of thyrotoxicosis resulted in recurrent adrenal decompensations due to insufficient cortisol, though 1 episode was accompanied by fever and thus may have been triggered by illness. Hyperandrogenemia and episodes concerning for adrenal crises resolved with normalization of thyroid levels, without any change in glucocorticoid dose. Thyrotoxicosis must be included in the differential diagnosis of individuals with any form of adrenal insufficiency, including CAH, who present with escalating glucocorticoid requirements, or recurrent adrenal crises despite appropriate glucocorticoid adherence and dosing.

Disclosure

This case was presented as a poster at the 99th Annual Meeting of the Endocrine Society.

Conflicts of Interest

The authors declare that they have no conflicts of interest.

Copyright

Copyright © 2018 Meghan E. Fredette and Lisa Swartz Topor. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Overactive thyroid (hyperthyroidism) – NHS

An overactive thyroid, also known as hyperthyroidism or thyrotoxicosis, is where the thyroid gland produces too much of the thyroid hormones.

The thyroid is a small butterfly-shaped gland in the neck, just in front of the windpipe (trachea). It produces hormones that affect things such as your heart rate and body temperature.

Having too much of these hormones can cause unpleasant and potentially serious problems that may need treatment.

An overactive thyroid can affect anyone, but it’s about 10 times more common in women than men, and typically happens between 20 and 40 years of age.

Symptoms of an overactive thyroid

An overactive thyroid can cause a wide range of symptoms, including:

Find out more about the symptoms of an overactive thyroid.

When to see a GP

See a GP if you have symptoms of an overactive thyroid.

They’ll ask about your symptoms and if they think you might have a thyroid problem, they can arrange for a blood test to check how well your thyroid is working.

If the blood test shows that you have an overactive thyroid, you may be referred for further tests to identify the cause.

Find out more about how an overactive thyroid is diagnosed.

Treatments for an overactive thyroid

An overactive thyroid is usually treatable.

The main treatments are:

• medicine that stops your thyroid producing too much of the thyroid hormones
• radioiodine treatment – where a type of radiotherapy is used to destroy cells in the thyroid, reducing its ability to produce thyroid hormones
• surgery to remove some or all of your thyroid, so that it no longer produces thyroid hormones

Each of these treatments has benefits and drawbacks. You’ll usually see a specialist in hormonal conditions (endocrinologist) to discuss which treatment is best for you.

Find out more about how an overactive thyroid is treated.

Causes of an overactive thyroid

There are several reasons why your thyroid can become overactive.

These include:

• Graves’ disease – a condition where your immune system mistakenly attacks and damages the thyroid (about 3 in every 4 people with an overactive thyroid have Graves’ disease)
• lumps (nodules) on the thyroid – this extra thyroid tissue can produce thyroid hormones, causing your levels to be too high
• some medicines such as amiodarone, which can be used to treat an irregular heartbeat (arrhythmia)

Find out more about the causes of an overactive thyroid.

Further problems

An overactive thyroid can sometimes lead to further problems, particularly if it’s not treated or well controlled.

These include:

Find out more about the complications of an overactive thyroid.

Page last reviewed: 24 September 2019
Next review due: 24 September 2022

Feeling Tired? Stress Hormones & Thyroid Lab Tests

The information presented in Supplement Guide is for informational purposes only and should not be considered medical advice. Nutritional recommendations are based on established guidelines for people of average health and on associations between vitamins, minerals, and herbs with health conditions from published scientific studies (human, animal, or in vitro), clinical experience, or traditional usage. These associations may not be true for all individuals and are not based on specific product brands or formulations. Nutritional and herbal products may vary widely in ingredient purity, concentration, and combinations, which may affect people differently. Consult your doctor, pharmacist, or other professional for any health problem and before adding supplements to your self-care practices or discontinuing any prescribed medications. It is important not to make any changes in your self-care, including taking supplements, before or after a surgery without your doctor’s express recommendation. In addition, please consult with your healthcare practitioner to make sure that your cumulative daily intake of copper, selenium, zinc, vitamin B6, folic acid, or any other nutrient, does not exceed established, tolerable upper intake levels.

Information and statements regarding dietary supplements have not been evaluated by the Food and Drug Administration and are not intended to diagnose, treat, cure, or prevent any disease.

By using Supplement Guide you understand that recommendations are in no way intended as a substitute for medical counseling and neither the publisher nor the authors have liability or responsibility to any person or entity receiving or using this information.

Copyright© 2021 Life Extension. All rights reserved.

Thyroid and Parathyroid Disorders – Diabetes and Endocrinology

Assessing Thyroid and Parathyroid Function

An accurate evaluation of the way your thyroid or parathyroid glands are functioning is essential to determine the most appropriate therapy. We use a number of noninvasive procedures to accomplish this, including lab tests, ultrasound, thyroid scans, function stimulation tests, bone x-rays, and biopsy. You can receive any procedures you need in our hospital.

Graves’ Disease and Overactive Thyroid Care

In people with hyperthyroidism, the thyroid gland produces high levels of thyroid hormones, increasing metabolism and causing symptoms such as rapid heartbeat, nervousness, high blood pressure, and weight loss. Graves’ disease is a type of hyperthyroidism that can also cause a goiter (bulge in the neck from an enlarged thyroid gland), bulging eyes, and thickened skin. Our team tests thyroid hormone levels in the blood and performs a thyroid scan to diagnose Graves’ disease and other types of hyperthyroidism. Treatments may include one or more of these approaches:

• Medication to block or change how the thyroid gland uses iodine. These drugs may be used as long-term treatment, or to control an overactive thyroid gland before surgery or radioiodine therapy.
• Radioiodine therapy, in which radioactive iodine is given by mouth. It concentrates in overactive thyroid tissue and destroys it. Thyroid hormone replacement therapy is prescribed for the rest of your life after this treatment to provide the hormones that your thyroid used to make.
• Surgery to remove the thyroid. We perform thyroidectomy using small incisions. Thyroid hormone replacement therapy is also prescribed after thyroid surgery.

Hypothyroidism Treatment

Hypothyroidism (under-active thyroid) is the most common thyroid disorder. It most often results from an autoimmune disorder or the treatment of hyperthyroidism. You may have hoarseness, weight gain, a puffy face, coarse skin and hair, and a reduced heart rate. Our doctors will treat you with thyroid hormone replacement therapy.

Care for Thyroiditis

Thyroiditis is inflammation of the thyroid gland. Hashimoto’s thyroiditis is the most common form of thyroiditis and can cause goiter, fatigue, muscle weakness, and weight gain. It is often associated with other endocrine disorders, such as diabetes, under-active parathyroid or adrenal glands, or autoimmune disorders. Hashimoto’s thyroiditis can cause under-active thyroid activity and is typically treated with thyroid hormone replacement therapy.

Thyroid Cancer

Benign thyroid tumors (adenomas) may over-produce thyroid hormone and require treatment, or become very large and cause symptoms. For patients with “indeterminate” thyroid nodules—growths for which it is hard to tell if they are benign or malignant, using standard pathology techniques—we can perform molecular testing. Thyroid cancers are frequently curable through surgery and/or hormone and radioactive iodine therapy. The endocrine cancer specialists at NewYork-Presbyterian Brooklyn Methodist Hospital treat thyroid cancer using a multidisciplinary approach. Learn more.

Genetic Endocrine Disorders

Some people have a hereditary predisposition to endocrine disorders, such as multiple endocrine neoplasia (MEN). People with MEN I have a defect in a gene that carries the code for a protein called menin. The condition causes tumors of the pancreas, parathyroid, or pituitary glands to appear in the same person, but not necessarily at the same time. People with MEN II have a defect in the RET gene and may develop overactivity or tumors in the thyroid gland as well as the adrenal or parathyroid glands. Treatment for MEN may include medication or surgery. At NewYork-Presbyterian Brooklyn Methodist, we provide genetic counseling and screening for families with MEN and other hereditary endocrine syndromes to detect problems and complications early, when they may be treated most effectively.

Parathyroid Disorders

Our doctors are experienced treating disorders of the parathyroid glands.

• Parathyroid tumors may cause high levels of calcium in the blood, increasing the risk of osteoporosis and possibly damage to organs such as the kidneys, bones, heart, and blood vessels. They rarely affect more than one of the four glands. Typically only the affected gland needs to be surgically removed—resulting in a cure in more than 95 percent of patients
• Hyperparathyroidism (overactive parathyroid) may result from another problem in the body, such a kidney failure, which leads to low blood levels of calcium and triggers an increase in parathyroid activity to compensate. We treat hyperparathyroidism using medication, and surgery to remove some or all four of the parathyroid glands if medication is not sufficient. Our surgeons perform minimally invasive parathyroidectomy as well as conventional surgery to remove all four glands. Your doctor will discuss the most appropriate treatment for you.
• Hypoparathyroidism (under-active thyroid) can lead to blood low calcium levels, which can result in seizures or uncontrollable spasms of the face, hands, arms, and feet. Your doctor may prescribe calcium and vitamin D supplements to correct blood calcium levels and treat your symptoms.

Adrenal Tumors

Adrenal tumors may produce excess hormones that can adversely affect your quality of life. They are best treated through surgical removal of the affected adrenal gland, which we typically do in a minimally invasive manner (“laparoscopic adrenalectomy”).

Warning Signs of High Cortisol and Low Thyroid

When a person feels stressed, they may reach for comfort foods that contain carbohydrates and sugars and proclaim that they’re “eating their feelings. ”

Many patients have a sense that stress, metabolism, and sugar are related to one another. They often can make the connection between eating poorly and feeling sluggish. What they may not know is that changes in diet and other lifestyle behaviors that lead to alterations in coping skills can impact cortisol, insulin, and thyroid levels, which can result in fatigue and slowed metabolism.

Receptors for all three hormones are located in nearly every cell of the body, so the relationship between them and the adrenal gland, thyroid, and pancreas is critical for energy production and balanced physiology.

When this relationship is functioning normally, people tend to feel vital and well. When they aren’t functioning properly, or when their function is impacted by poor rest, diet, and exercise, patients feel unwell, gain weight, and appear in your office with issues related to adrenal fatigue and thyroid problems.

Identifying Hormone Issues

Some of the initial questions you’ll ask when identifying issues with cortisol, insulin, and thyroid hormones include:

• Do you have enough energy to complete daily tasks?
• Do you sleep deeply at night?
• Have you gained weight?

Within our interconnected metabolic pathways, each of these individual regulatory hormones influences the other two, making their triangular relationship a complex web of physiological function. We’ll focus on problems associated with high cortisol and low thyroid, how insulin production is affected by each scenario, and how changes in the stress response impact these bodily systems.

Physical Symptoms of High Cortisol

Cortisol is produced by the adrenal glands, which sit atop each kidney. The glands are about the size of a nutmeg. The inside of the adrenal, called the adrenal medulla, produces epinephrine and norepinephrine, while the gland’s outer rind, called the cortex, produces cortisol.

Cortisol influences the brain, and high cortisol can decrease neurogenesis and inhibit immune function. Cortisol is a catabolic hormone that limits anabolic drive. Problems with cortisol production can also result in lower growth hormone production, changes in reproductive status, blood pressure abnormalities, blood sugar control issues, and excess abdominal visceral adiposity.

We know that abnormal states of stress lead to increased production of cortisol, and the effects on the body can be vast. The physical symptoms of high cortisol can include thinning of the bones, sarcopenia (or muscle wasting), fat deposition, the presence of metabolic syndrome or syndrome X, problems with blood sugar, obesity, lipid abnormalities, cognitive decline due to alteration in the hippocampus and prefrontal cortex, compromised immune system, poor cardiovascular health, memory loss, and other complications.

Stress has even greater implications. It can result in permanent abnormalities in blood sugar, protein wasting, immune dysfunction, mineral loss, and changes in kidney function and blood pressure. The stress response should activate and go back to normal. If it doesn’t, there can be dire consequences. 

High Cortisol Levels at Night

Cortisol is important for sleep. Its release is controlled in slow wave sleep and cortisol levels follow circadian rhythms; levels should be higher in the morning and lower at the end of the day.

Nocturnal hypercortisolism, or high cortisol levels at night, can lead to sleep fragmentation, which increases cortisol even more. In this hyper vigilant state, the body struggles to enter rest and repair mode, and the immune system remains hyperactive and in a neuro-excited mode. The brain can’t settle down and the body can’t enter slow wave or REM sleep.

The Body’s Response to High Cortisol

When the body has produced too much cortisol, known as hypercortisolism, it enters self-defense mode. The brain and the body say, “Enough is enough.”

There is too much stress, too much cortisol, and there are possibly alterations or injuries to key centers of physiology. To further protect itself, the body’s next step is to turn down the stress response by entering the flattened cortisol curve.

In nearly every scenario when there’s flattening of the cortisol curve and alterations in the HPA axis, there tend to be worse outcomes overall.

When your patient presents with any of the issues related to high cortisol levels, you’ll want to determine the state of their cortisol, and whether excess stress, an immune threat, or other metabolic pressures have played a role.

Symptoms of Low Thyroid

When we eat, insulin levels and glucose levels go up. Cortisol goes up, too, because it wants to create a blunting mechanism for glycemic control. Stress can influence the body’s insulin response and blunt thyroid function. Cortisol plays an important role in thyroid balance.

Increased cortisol due to high stress can shift the thyroid into a more inactive state, elevating reverse T3 levels rather than converting Free T4 to Free T3, which is important for glucose control as it affects the number of insulin receptors available and how receptive they are to insulin.

When the body’s sympathetic nervous system has been activated, such as when an athlete trains, you’ll see increased cardiac output, peripheral blood flow, and oxygenation of peripheral tissues. When that’s already occurring, the body’s in a hypervigilant state and doesn’t really need excess Free T3. If the body isn’t shifting into rest and repair mode, such as when an athlete is overtraining without proper down time, the response is metabolic stress. This can lead to neuro, endocrine, and immune balances, resulting in an increased baseline of inflammatory cytokines.

Just like over-trained athletes, people who have a lot of stress will have similar physical symptoms. You’ll see the same inflammatory drive, insulin resistance, low thyroid levels, loss of anabolic hormones, low libido, and low sex hormones.

The metabolic effects of suboptimal thyroid function are linked to glucose tolerance. The thyroid hormone influences the rate at which glucose is absorbed from the GI tract and taken up by cells. Insulin signaling and receptor problems also arise from low thyroid, which reduces target insulin binding and number of insulin receptors expressed.

If your patient exhibits cardiovascular issues you’ll want to check their thyroid levels. Decreased metabolism of fats, increased serum lipids, and decreased availability of fatty acids are all associated with low thyroid levels. Additionally, inadequate T3 lowers oxygen consumption, contributes to lipids peroxidation, and adds to free-radical damage.

Controlling Blood Sugar to Control Stress

Stress, metabolism, and sugar have a triangular relationship. Normal physiology confers good conversion of glucose to glycogen, proper insulin regulation and glucose uptake, and good cortisol regulation of carbohydrates, lipids, and nucleic acids.

Blood sugar swings, such as with episodes of hypoglycemia, will activate the stress response and lead to that bidirectional relationship between cortisol and insulin. Controlling blood sugar through diet is key, but it’s not enough to simply eliminate carbs. Managing and modifying stress levels is also necessary.

RELATED CONTENT: How Cortisol Impacts Weight Gain

Key Supplements for Regulating Cortisol*

Cortisol, especially when it’s related to occasional anxiety and mind racing at night, may be helped by L-theanine.* If the patient has GI tract issues, holy basil may be substituted to clam the gut and phenyl-gaba or gaba may be used to help calm the brain and induce sleep.*

Stress management for cortisol control is promoted with magnolia/phellodendron, while iodine can help with thyroid.*

For insulin resistance cravings and stress, we recommend tryptophan to boost serotonin levels.* It can have a sedative effect, but if the patient is already activated, tryptophan has a calming effect on the brain and elevates mood. *

Managing the complex relationship between adrenal, thyroid, and pancreas can involve many potential choices for patient care. It’s important to choose the options that relate to the situation of the individual patient and what you identify as the primary driver in the problems they present. This may involve managing stress response, breaking insulin resistance, or enhancing thyroid function. But it’s important to remember that even when you’re treating the primary driver, you’re not just addressing one thing because these functions are deeply interconnected. Though your primary focus may be linked to one corner of the triangle, clinical strategy should give attention to all three.

*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.

Thyroxine and adrenaline – Higher – Hormonal coordination and control in humans – Eduqas – GCSE Biology (Single Science) Revision – Eduqas

2dw6m3i8e84.0.0.0.1:0.1.0.$0.$1.$0″>Thyroxine is produced by the thyroid gland, which stimulates the basal metabolic rate. It controls the speed at which oxygen and food products react to release energy for the body to use. Thyroxine plays an important role in growth and development. Thyroxine levels are controlled by negative feedback.

The hypothalamus and pituitary gland have important roles in detecting and controlling thyroxine levels.

1. Low thyroxine levels in the bloodstream stimulate the hypothalamus to release TRH (Thyrotropin releasing hormone) and this causes the pituitary to release TSH (Thyroid stimulating hormone) so the thyroid releases more thyroxine. So blood levels return to normal.
2. Normal thyroxine levels in the bloodstream inhibit TRH release from the hypothalamus and this inhibits the release of TSH from the pituitary, so less thyroxine is released from the thyroid gland and normal blood levels are maintained.

This is an example of negative feedback.

Adrenaline is produced by the adrenal glands in times of fear or stress. It targets vital organs, increases the heart rate and boosts the delivery of oxygen and glucose to the brain and muscles, preparing the body for ‘flight or fight’.

Adrenaline is controlled by 2dw6m3i8e84.0.0.0.1:0.1.0.$0.$1.$6.$1″>positive feedback.

When adrenaline is released into the bloodstream, it creates multiple effects:

• an increase in pulse rate and volume of blood pumped by the heart with each beat
• increase in the depth of breathing
• dilation of the blood vessels supplying muscles

The effects of adrenalin allow the body to prepare for action in situations where a quick response may be essential.

Adrenaline is then converted into a less active compound by the liver.

Endocrinology | Dartmouth-Hitchcock

The Endocrinology Department cares for patients with hormone conditions. The endocrine system produces the hormones your body needs to work correctly. Glands in the endocrine system include the thyroid, parathyroid, pituitary, and adrenal glands, among others.

Conditions we treat

We diagnose, evaluate, and treat a number of hormone-related conditions. Many of these conditions are caused by the endocrine system producing too few, or too many, hormones. Some of the conditions we treat include:

• Addison’s disease occurs when the adrenal glands do not produce enough of the hormones your body needs to work properly. This affects the balance of water, sodium, and potassium in the body, and harms its ability to control blood pressure and react to stress.
• Adrenal tumors are abnormal growths on the adrenal glands. Most are benign (non-cancerous), and are called adenomas. Malignant adrenal growths (cancers) are rare.
• Cholesterol disorders include hyperlipidemia, and hypolipidemia. Cholesterol is essential for life, and is found in the body cells of all animals, including humans. Your body needs cholesterol to work properly. Hyperlipidemia means you have an unusually high level of fat (lipids) in your blood. This puts you at risk for many health problems, including heart attack and stroke. It is sometimes called high blood cholesterol. Hypolipidemia means you have an unusually low level of fat in your blood. It is sometimes called low blood cholesterol.
• Congenital adrenal hyperplasia (CAH) is an inherited disorder that is present at birth. It affects the adrenal glands, causing them to produce low levels of the hormones cortisol and aldosterone, and high levels of male sex hormones (androgens). There are two forms of CAH: non-classical (the most common and least severe), and classical. Non-classical CAH is one of the most common genetic disorders.
• Conn’s disease is a condition in which the adrenal glands produce too much aldosterone. It is frequently caused by a benign (non-cancerous) tumor of an adrenal gland.
• Cushing’s syndrome is a condition in which the adrenal glands produce too much cortisol. It is frequently caused by a benign (non-cancerous) tumor of the pituitary gland.
• Diabetes is a condition marked by high levels of glucose (sugar) in the blood. Over the last few decades, the condition has become relatively common in the United States with more than 18 million Americans living with diabetes—most often type 2. People can acquire diabetes at any age. Our Diabetes Program supports the full range of diabetes care, including dietary counseling, insulin pumps and a wide range of diabetes educational activities.
• Graves’ disease is the most common cause of hyperthyroidism, which means that the thyroid gland produces more hormones than the body needs. It is caused by an autoimmune disorder, where the body’s immune system destroys its own tissues.
• Growth hormone disorder (acromegaly) is a condition in which the pituitary gland secretes growth hormone after the normal growth of the skeleton and other organs is complete. In almost all cases, it is caused by a benign (non-cancerous) tumor of the pituitary gland.
• Hyperparathyroidism (excess parathyroid hormones) in a condition in which one or more of the parathyroid glands makes too many hormones. This can lead to osteoporosis, or loss of bone density.
• Hypopituitarism is a condition in which the pituitary gland is not producing one or more of its hormones, or is producing them at lower than normal levels. These hormones stimulate other endocrine glands to produce their hormones. For example, if the pituitary gland doesn’t make thyroid stimulating hormone (TSH), the thyroid gland doesn’t work correctly. Hypopituitarism is a rare disorder.
• Hyperthyroidism (excess thyroid hormones) is a condition in which the thyroid gland produces more hormones than the body needs.
• Hypothyroidism (low thyroid hormones) is a condition in which the thyroid gland produces fewer hormones than the body needs.
• Male hypogonadism (low testosterone) is caused by a man’s testes failing to produce normal levels of the male sex hormone, testosterone. Some men are born with hypogonadism, while others may develop the condition later in life. There are two kinds of male hypogonadism: primary hypogonadism, in which the testes do not work properly, and secondary hypogonadism, in which the testes are not being stimulated to produce hormones. This happens because of a problem with the pituitary or hypothalamus glands, such as a tumor.
• Male infertility is a condition in which a problem with a man’s reproductive systems is the reason why a couple is unable to become pregnant after having regular, unprotected sexual intercourse for a year. Infertility affects men and women equally. About half of infertility problems are caused by male infertility.
• Metabolic syndrome is a condition that includes several disorders of the body’s metabolism. Metabolism refers to how your body creates energy from the food you eat. Metabolic syndrome includes high blood pressure, insulin resistance, obesity, and high levels of “bad” cholesterol in your blood. All of these conditions increase your risk of getting heart disease, kidney disease, diabetes, or having a stroke.
• Multiple endocrine neoplasia (MEN) is the name of three rare, inherited disorders that cause extra tissue (hyperplasia) or adenomas (tumors) to grow on the endocrine glands. This can cause several endocrine glands to become overactive (produce too many hormones) at the same time. The three kinds of MEN are Type 1 (the most common), Type 2A, and Type 2B. The glands most often affected are the parathyroid, the pancreas, and the pituitary.
• Osteoporosis is a condition in which more calcium from the bones is being lost than is being replaced. Healthy bone is a living tissue, made up mainly of calcium and protein. As such, bone is always gaining and losing cells. When bones lose too much calcium, they becomes less dense and can weaken. Weak bones tend to break more easily.
• Pituitary tumors are abnormal growths on the pituitary gland. Most are benign (non-cancerous), and are called adenomas. Even though they are benign, such adenomas can cause significant symptoms if they produce excess pituitary hormones, or grow large enough to press on the brain or nearby nerves.
• Prediabetes (hyperglycemia) is a condition in which a person’s blood sugar (glucose) levels are higher than normal, but not high enough to be classified as diabetes. A person with pre-diabetes is at risk of developing type 2 diabetes. However, by making some lifestyle changes, a person with pre-diabetes can reduce his or her risk of developing type 2 diabetes.
• Thyroid nodules are lumps or growths on the thyroid gland. They are fairly common, especially among people over 50. In most cases, these growths are benign (non-cancerous), but about five percent of thyroid nodules may be malignant, or cancerous.

Glands that produce hormones

Many of the conditions listed above mention the following glands that produce hormones:

• The pituitary gland is about the size of a pea, and is located at the base of the brain. It controls the production of hormones in all endocrine glands. The pituitary gland secretes hormones that regulate growth, sexual function, and the body’s balance of fluids.
• The adrenal glands are located on the top of your kidneys. They produce adrenaline, cortisol, aldosterone, and other steroid hormones that enable the body to respond to stress.
• The thyroid gland is a butterfly-shaped organ found in the center of the neck, below the Adam’s apple. It creates and stores hormones that control the body’s heart rate, blood pressure, and metabolism (how the body makes energy from food).
• The parathyroid glands control the level of calcium in your blood. These four small glands are located in the neck, at the corners of the thyroid gland.

90,000 Influence of adrenaline and corticosterone on the uptake and distribution of atherogenic and antiatherogenic lipoproteins in the myocardium | Panin

The role of lipoproteins (LP) in the development of cardiovascular pathology is discussed in the literature in various aspects: due to the influence of stress hormones and activation of the lysosomal apparatus of cells [6], with the development of autoimmune processes [1], impaired metabolism of saturated and unsaturated fatty acids [10] and others. However, the effect of catecholamines, glucocorticoids and blood LP (atherogenic and antiatherogenic) directly on the myocardium is practically not disclosed in the literature.This is especially true in relation to LP, which are the most important supplier of fatty acids as an energy material in many tissues, including the heart. Under stress conditions, the regulatory effect of catecholamines and glucocorticoids on myocardial energetics is complemented by the regulatory properties of individual apolipoproteins (apo-LP). For example, apoSP increases the activity of lipoprotein lipase [14], anoAI – the activity of LCAT [15]. We can talk about other regulatory properties of apo-LP. We have shown for the first time that anoAI is also present in the nuclei of many cells, including the heart [7].It turned out that in combination with the reduced forms of ste

‘This work was supported by the Regional Public Fund for the Promotion of Domestic Medicine. roid hormones (tetrahydro compounds), they are involved in the regulation of gene expression [7, 8].

In this work, we tried to assess the effect of adrenaline, corticosterone, high density lipoprotein (HDL) and low (LDL) density on the myocardium in a model of a perfused rat heart, and to show the role of hormones in the uptake and intercellular distribution of atherogenic and antiatherogenic drugs.

Materials and methods

In experiments with Langendorff heart perfusion, Wistar rats weighing about 300 g were used. Krebs-Henseleit buffer solution served as perfusate [3]. Colloidal gold-labeled serum LDL (1.006-1.063 g / ml, 15-20 mg%) or HDL (1.063-1.21 g / ml, 200-250 mg%) (6 experiments) were added to the perfusion solution. In other series, LP was added to the perfusate together with adrenaline at a concentration of 1 mg / L (6 experiments) or corticosterone 2 mg / L (8 experiments). Five experiments with cardiac perfusion with Krebs-Henseleit solution and 7 experiments with the addition of hormones without LP were used as controls.

The rate of glycogenolysis in the heart was determined in Wistar rats weighing 180-200 g. The animals were sacrificed under light ether anesthesia, the heart was removed and washed from the blood in chilled Tris-HC1 buffer, pH 7.4. After homogenization and centrifugation at 50,000 g for 30 min, a supernatant was obtained, in which glycogenolysis was studied in a reconstructed system containing all the necessary cofactors and substrates. The composition of the incubation medium: 20 mM Tris-HC1 buffer pH 7.4, 7 mM phosphate buffer pH 7.4, 5 mM MgCl ₂ , 0.2 mM NAD, 1 mM ATP, 5 mM nicotinamide, 2 mM cysteine ​​and 0.1% glycogen solution.The lactate content was determined by NADP at a wavelength of 340 nm and expressed in nanomoles per minute per 1 mg of protein.

For electron microscopic examination, the left ventricular myocardium after 30 min of perfusion was fixed in a 2.5% glutaraldehyde solution and a 2% paraformaldehyde solution, supplemented in a 1.5% solution of OsO ₄ , and poured into a mixture of epona with araldite. Ultrathin sections were contrasted with uranyl acetate and lead citrate, viewed in a JEM 100SX electron microscope at magnification from 5 to 20 thousand. once. The distribution of the label (as a percentage of the total) was assessed by counting the gold granules in endotheliocytes, macrophages and interstitial space on a cut area of ​​0.01 μm ² . The distribution of the label in invaginations, endosomes, lysosomes and freely in the cytoplasm of endothelial cells (as a percentage of the number of granules in the endothelium) was determined. A qualitative analysis of the structures of cardiomyocytes and interstitial macrophages was carried out.

Statistical data processing was performed using the Statgraphics 4 software package.0. Differences were assessed using the nonparametric Mann-Whitney test at a 5% significance level.

Results and discussion

In the experiments carried out in the recirculation mode with Krebs-Henseleit solution, the heart could work quite stably, maintaining the frequency and amplitude of contractions, as well as the value of the coronary flow constant for at least 2 hours.

Effect of adrenaline and corticosterone on the biochemical and structural characteristics of the myocardium

Adrenaline added to the perfusion medium caused an increase in coronary flow, amplitude and frequency of contractions by an average of 1. 5 times.Morphologically, the microcirculatory bed was widened, and myofibrils overcontraction, expansion of the sarcoplasmic reticulum channels and dense sediments in mitochondria were revealed in cardiomyocytes, which corresponds to ultrastructural signs of mild calcium overload according to VG Sharov [11]. In the cytoplasm of some cardiomyocytes, dust-like granularity was located in place of glycogen.

It is known that an increase in the contractile activity of the myocardium under the influence of adrenaline is associated not only with an increase in coronary blood flow and the supply of oxygen to the heart, but also with the activation of glycogenolysis.Perhaps the last mechanism is decisive. It is associated with an increase in the concentration of cAMP in the tissue and the activity of phosphorylase under the influence of adrenaline [19]. It turned out that cAMP at a concentration of 10 “ ⁴ – 10″ ³ M significantly increased the rate of glycogenolysis both in the heart and in the muscles (Table 1). This process was expressed to an even greater extent under the influence of AMP, a specific activator of phosphorylase B. The obtained biochemical results are in good agreement with the patterns of glycogen breakdown in cardiomyocytes under the influence of adrenaline, revealed using electron microscopy.

The addition of corticosterone to the perfusate did not have a significant effect on cardiac activity, did not reduce perfusion changes in the myocardium, revealed in control experiments with Krebs-Henseleit solution [2], which confirms the absence of a direct effect of corticosteroids on the heart [4]. However, at the same time, the content of glycogen in the muscle cells of the heart decreased, its sequestration in the sarcoplasm and the release of residues in the interstitium were observed. The mechanism of increased breakdown of glycogen under the influence of corticosterone is similar to that described above.It is associated with the possibility of hormone action through [3-adrenergic receptors as in the case of adrenaline [6], ie, with an increase in phosphorylase activity under the influence of cAMP.

Effect of HDL and LDL on myocardial ultrastructure

The addition of native LDL to the perfusate did not affect myocardial contractility, while HDL increased the frequency and amplitude of contractions under the same conditions. We associate an increase in the efficiency of the heart under the influence of HDL with the activation of glycolysis.Previously, we have shown that under the influence of HDL, the rate of glycolysis in the liver increases [5], but the mechanism of this phenomenon remained unrevealed. Electron microscopic studies showed that in 30 min labeled drugs of both classes interacted with endotheliocytes (Table 2). More actively receptor-mediated pathway captured HDL and located in pubescent vesicles, without leaving the walls of the capillaries. LDL penetrated into the interstitium faster and accumulated in the lysosomes of activated macrophages

Table 1

Effect of cAMP at various concentrations and AMP on glycogenolysis in cardiac and skeletal muscles of rats

Heart 61 ± 8. 6 74 ± 10.0 * 73 ± 9.7 * 94 ± 8.0 *

Muscle 93 ± 10.4 113 ± 15.0 * 121 ± 13.7 * 163 ± 18.0 *

Note.The rate of glycogenolysis is given in nanomoles of lactate per minute per mg of protein (M ± m). Each group consisted of 7 animals. * – statistically significant differences with control at p <0.05.

Table 2

Number (M, min – max ) and distribution of the label within endothelial cells (in%) during perfusion of an isolated rat heart with labeled LP and hormones

Note. Hell is adrenaline, X is corticosterone.

Effect of adrenaline and corticosterone on the binding and distribution of LP in the myocardium

The combined addition of epinephrine and labeled HDL to the perfusate did not affect the penetration and distribution of the latter in the myocardium. There were a lot of marks on the sections, but, as in experiments without adrenaline, they were not detected outside the vascular bed (see Fig. 1). At the same time, almost 3/4 of the mark was located on the luminar surface of endotheliocytes and in pubescent invaginations, the rest was in pubescent vesicles (see Fig.tab. 2). In these experiments, endotheliocytes and macrophages acquired ultrastructural signs of active functioning. Cardiomyocytes contained activated nuclei with a minimal amount of heterochromatin, numerous pores in the membrane, and very large nucleoli of a nucleonemic structure. In the sarcoplasm, there were moderate reversible injuries characteristic of functional overstrain of organelles. It is known that HDL is an active participant in lipolytic processes that provide tissues with free fatty acids [10].

With the combined addition of adrenaline and LDL, the amount of the label associated with the endothelium increased 3 times, and its distribution indicated a slower penetration into tissues compared to LDL without adrenaline (see Fig. 1, Table 2). The absolute majority of the label (see Table 2) was in contact with the luminar surface of endothelial cells (adhesion and invagination). For 30 min of perfusion with adrenaline, only 11% of the label penetrated into macrophages, while it was concentrated exclusively in endosomes (Fig.2, see inset), while without adrenaline, four times more tags were recorded in macrophages (see Fig. 1), and almost half of them were already located in lysosomes. These experiments revealed some features of the penetration of labeled LDL into the myocardium, which were not completely absorbed, but underwent partial destruction (lysis) on the surface of endotheliocytes. This is in good agreement with the data that lipoprotein lipase is able to bind to endothelial cell membranes via glucosaminoglycans and simultaneously interact with LP [1].In this case, the amount of the enzyme determines the number of LP particles that it retains on the cell surface [13]. Thus, the flow of the main energy material – fatty acids into the myocardium is regulated. There is evidence that the cardiotoxic effect of catecholamines is due to an increase in the formation of free radicals [17]. The ability of drugs to bind free radicals may underlie their cardioprotective effect [12, 16].

With the joint perfusion of the heart with corticosterone and LP of both classes, a decrease in the content of glycogen in cells, its sequestration inside cardiomyocytes, separation of cytoplasm areas with glycogen residues (clasmatosis) into the interstitium and the capillary bed were noted.This effect is probably associated with the relative excess of the hormone in relation to the LP.

The addition of corticosterone caused an increase in the number of endothelium-associated label almost 5-fold compared with all other experiments with HDL (see Fig. 1). A sharp increase in receptor-mediated endocytosis (Fig. 3, see inset) in the endothelium was manifested in the fact that the label was accumulated mainly in pubescent vesicles (see Table 2). By the end of the experiment, many markers were located near the basal surface of the endothelium, where numerous patterns of endosome opening were recorded.Sometimes accumulations of granules were located near the expanded intercellular contacts, which did not exclude their exit, bypassing endotheliocytes. The fundamental difference between the experiments with corticosterone and HDL was that the label was found in the interstitium and macrophages, albeit in small amounts (see Fig. 1). An unexpected find was the discovery of me-

Hell – adrenaline, Ks – corticosterone.

On the ordinate axis – the number of marks in 0. 01 mm ² .

a – LDL; b – Ad + LDL; to – Ks + LDL; g – HDL; d – Ad + HDL; 90,029 e – 90,030 Ks + HDL.complexes not only in the endothelium and interstitium, but also in the lumens of the lymphatic vessels, which were located in close intertwining with the blood capillaries (this mark was not taken into account in the calculations).

HDL is known to bind and transfer a wide range of glucocorticoids [9]. In this case, a complex complex of LP with corticosterone is visualized with colloidal gold. It can be assumed that this complex is absorbed much more actively than HDL alone. Possibly, in the heart, as in the liver, the cooperative effect of HDL and glucocorticoids is triggered, aimed at activating the genome and enhancing protein biosynthesis in cells [2, 18].This indicates that blood LP can not only take part in the transport of various ligands (hormones), but together with them have a regulatory effect on the cell genome.

With the joint administration of LDL and corticosterone, their stimulating effect on the functional parameters of the heart has been convincingly shown. Most of the cardiomyocytes were in a state of mild overcontraction, only some of them showed signs of moderate myocytolysis. The lumens of most of the capillaries were enlarged, sometimes very strongly.The mark associated with the endothelium (see Fig. 1) was very small (13 by 0.01 mm ² ), it was mainly associated with LA on the luminar surface and in invaginations, and only a few granules were located in the pubescent bubbles (see Table 2). This can be explained by the actively proceeding process of lipolysis on the surface of the endothelium, which provides the myocardium with free fatty acids.

Conclusions

1. Epinephrine enhances the dissolution of colloidal gold-labeled LDL on the endothelial surface, the total number of bound label increases, and its distribution indicates a slower penetration into the myocardium compared to the perfusion of the heart with LDL without epinephrine. When adrenaline was added to the perfusate together with HDL, no changes were noted in the penetration and distribution of the label, which does not leave the capillary walls.
2. Joint perfusion of the heart with LDL with adrenaline protects the structure of cardiomyocytes from the damaging effect of adrenaline, completely removing the signs of calcium overload.
3. Corticosterone in all experiments caused a decrease in the content of glycogen in the muscle cells of the heart, the sequestration of its residues in the sarcoplasm and their release into the interstitium.
4. The addition of HDL to the perfusate together with corticosterone increased their receptor-mediated absorption by the endothelium of capillaries by 5 times and ensured their penetration into interstitial macrophages. Corticosterone hindered the penetration of labeled LDL into the myocardium when added together to the perfusate compared to similar experiments without the hormone.

Epinephrine and corticosterone have different effects on the penetration and distribution of LDL and HDL in the myocardium. Under stress conditions, this ensures the mobilization of various metabolic pathways for the energy supply of the myocardium.

1. Klimov A. N., Nikulcheva I. G. Metabolism of lipids and lipoproteins and its disorders: A guide for physicians. – SPb., 1999.

2. Maksimov, V.F. and Korostyievskaya, I.M., Byull. SB RAMS. – 1998. – T. 89, No. 3. – S. 47-51.

3.Maksimov V.F., Kolpakov A.R., Korostyshevskaya I.M. et al. // Tsitologiya. – 2002. – T. 44, No. 1. – S. 40-47.

4. Opi L. X. And Physiology and pathophysiology of the heart / Ed. N. Sperelakis: Per. from English – M., 1990 .– T. 2. – S. 7-63.

5. Panin LE Biochemical mechanisms of stress. – Novosibirsk, 1983.

6.Panin L.E., Mayanskaya N.N. Lysosomes: role in adaptation and recovery. – Novosibirsk, 1987.

7. Panin LE, Russkikh GS, Polyakov LM // Biochemistry. —2000- T. 65, No. 12. — S. 1684-1689.

8. Panin LE, Kleimenova E. Yu. // Immunology. – 2002. No 4. – S. 206-208.

9.Polyakov L.M., Panin L.E. // Uspekhi sovrem, biol. – 2000. – T. 120, No. 3. – S. 275-282.

10. Titov VN Atherosclerosis as a pathology of polyene fatty acids. Biological foundations of the theory of atherogenesis. – M., 2002.

11. Sharov VG, Igrashev Sh. B., Mavrodi DI, Mogilevsky GM // Heart ultrastructure. – Tashkent, 1988.- S. 53-65.

12. Ahotupa M., Ruutu M., Mantyla E. // Clin. Biochem. – 1996. Vol. 29, No. 2. – P. 139-144.

13. Amies D., Greten H. // Esterases, Lipases, and Phospholipases: From Structure to Clinical Significance. – 1994. – P. 121-128.

14.Baggio G., Manzato E., Gabelli C. et al. // J. Clin. Invest. – 1986. – Vol. 77. – P. 520-527.

15. Jones A. I I J. Lipid Res. – 1986. – Vol. 27. – P. 689-698.

16. Matsumoto F, Mitchell A., Kurata H. et al. // J. Biol. Chem. – 1997. – Vol. 272, No. 27. -P. 16778-16789.

17.Noronha-Dutra F. E, Steen-Dutra E. M., Woolf N. // Br. Heart J. – 1991. – Vol. 65, No. 6. – P. 322-325.

18. Panin L. E., Usynin I. F, Kharkovski A. V. et al. // Cells of the Hepatic Sinusoid. – 1997. – Vol. 6. – P. 156-157.

19. Sutherland E. W., Rail T. W. // Pharmacol. Rev. – 1960. – Vol. 42. – P. 265.

90,000 epinephrine, norepinephrine, dopamine.Laboratory tests at the WTC medical center.

Interpretation of results / Information for specialists

An increase in the excretion of adrenaline in the urine is observed in diseases associated with pain, poor sleep, anxiety; during the period of hypertensive crises, in the acute period of myocardial infarction, with attacks of angina pectoris; with hepatitis and cirrhosis of the liver; exacerbation of gastric ulcer and duodenal ulcer; during attacks of bronchial asthma; after the introduction of insulin, ACTH and cortisone. With pheochromocytoma, the adrenaline content in urine increases tenfold. The sensitivity of the determination of adrenaline in urine for the diagnosis of pheochromocytoma is 82%, the specificity is 95%.

A decrease in the concentration of adrenaline in the urine is noted with a decrease in the filtration capacity of the kidneys; collagenoses; acute leukemia, especially in children, due to degeneration of chromaffin tissue; symptomatic crises caused by damage to the diencephalic region.

Norepinephrine differs from adrenaline in a stronger vasoconstrictor and pressor effect, a lesser stimulating effect on the contraction of the heart, a weak bronchodilator effect, a weak effect on metabolism (no pronounced hyperglycemic effect).With pheochromocytoma, the content of norepinephrine in the urine increases tenfold. The sensitivity of the determination of norepinephrine in urine for the diagnosis of pheochromocytoma is 89-100%, the specificity is 98%.

Separate determination of adrenaline and norepinephrine in urine makes it possible to obtain approximate data on the possible localization of the tumor: if the tumor originates from the adrenal medulla, then more than 20% of catecholamines excreted in the urine will be adrenaline. With the predominant excretion of norepinephrine, extraadrenal localization of the tumor is possible, most often it is a neuroblastoma.

A decrease in the concentration of norepinephrine in the urine is noted with a decrease in the filtration capacity of the kidneys; collagenoses; acute leukemia, especially in children, due to degeneration of chromaffin tissue; sympathetic crises caused by damage to the diencephalic region.

An increase in the excretion of catecholamines in the urine is observed in diseases associated with pain syndrome, poor sleep, anxiety; during the period of hypertensive crises, in the acute period of myocardial infarction, with attacks of angina pectoris; with hepatitis and cirrhosis of the liver; exacerbation of gastric ulcer and duodenal ulcer; during attacks of bronchial asthma; after the introduction of insulin, ACTH and cortisone; during flights with pilots and passengers; with hyperthyroidism and manic-depressive psychosis.With pheochromocytoma, the content of dopamine in the urine increases tenfold; an increase in its content is characteristic of neuroblastoma.

A decrease in the concentration of dopamine in the urine is noted with a decrease in the filtration capacity of the kidneys, collagenoses, acute leukemias, especially in children, due to degeneration of chromaffin tissue, sympathetic crises caused by damage to the diencephalic region, neuropathy (including diabetes mellitus), parkinsonism.

Endocrinologist Yuri Poteshkin – on the influence of hormones on our life

On whether hormones change our behavior

– Let’s first define: what are hormones?

– In general, a hormone is a substance that is produced inside the body, affects certain cells and at the same time changes their metabolism.Hormones are released when the body needs to adapt to a new situation. Cells have receptors for hormones (but for vitamins, for example, there are no receptors). But these receptors are not found on all cells, but only on some that perform a certain function in the body. For example, thyroid hormones affect the metabolic rate, the amount of heat produced. Cortisol, a hormone of the adrenal glands, is produced during prolonged stress and helps to cope with this stress. And there are substances that act over short distances and are not released for long.For example, adrenaline also modulates the body’s response to stress and activates the nervous system. But, unlike cortisol, adrenaline will not be produced for several days in a row.

Hormones are the “old” regulation, primitive organisms have only it, but no nervous system. Higher organisms have a nervous system, and it is it that normally controls hormones, and not vice versa. With organ pathologies, the situation may change and hormones will begin to affect the nervous system. For example, a tumor has developed in the adrenal gland, and it releases cortisol uncontrollably.Of course, its lion’s dose will affect human behavior. There is such a condition – “steroid psychosis”: this behavior disorder is just manifested with an unhealthy excess of cortisol.

There is a higher nervous activity, the cerebral cortex is responsible for it. It can affect the hypothalamus, which is part of the nervous system. The hypothalamus produces neurotransmitters that activate the pituitary gland. But the pituitary gland already acts on most of the endocrine glands, giving them signals to secrete or not secrete hormones.In addition, feedback from these glands comes to the pituitary gland, it also gives information about which hormones and how much needs to be produced.

– Nowadays they often say: “the chemistry of love”, “the hormone of attachment” (about oxytocin) or “the hormone of happiness” (about serotonin) and so on. Can you even say that?

– It all depends on what people understand by this. In science, there is cause and effect, and there are correlations. People don’t always distinguish between them. Correlation means that two things happen simultaneously with each other.Moreover, they may not depend on each other at all. If we add serotonin to the human body, will a person be happy from this? No. He is more likely to have the prerequisites for becoming happy. Again, it is the central nervous system that signals the release of hormones to adapt to the situation. If there is love, it means that certain hormones will be released. No need – no hormones will be released.

– That is, in a normal situation, it is not hormones that cause some kind of condition, but this condition causes the release of hormones?

– Yes.Hormones are designed to adapt us to what’s going on. It will not be possible to cure some disorders of mood and psyche with the help of hormones, the reasons for these disorders are different.

– One example of situations where certain hormones are needed is prolonged stress.

– The main hormone released during prolonged stress is cortisol. By the way, this is an example of how a hormone can produce different effects in different parts of the body due to different intracellular signal pathways.Cortisol breaks down adipose tissue, but when it is in excess, it occurs mainly on the arms and legs, and in the abdomen, cortisol rather promotes the accumulation of fat. Therefore, people with an excess of cortisol (hypercortisolism) look very characteristic: they have thin limbs, but a large belly.

– Could there be obesity from stress in this case?

– You cannot call it obesity. Cortisol does not contribute to the formation of new adipose tissue; under its action, it rather changes its place of dislocation in the body.In prehistoric times, this hormone was released in response to physical danger and mobilized the body’s strength to survive this danger. On the limbs, fat is destroyed, but on the trunk, on the contrary, it accumulates, the limbs are not so sorry to lose. In addition, cortisol itself stimulates appetite: earlier, in difficult times, a person had to look for food in order not to die of hunger. At the same time, cortisol has a destructive effect on the bones, although it would seem that bone density in any situation should be kept at a high level.The fact is that bones in a stressful situation serve as a source of calcium.

In fact, cortisol is not intended for long-term release, it, like adrenaline, is needed at short distances: now everything is bad, cortisol is released, the person went and got food. After that, cortisol should already stop being produced. But the fact is that now a person is threatened much more often by psychological than physical danger, and it does not pass so quickly. Therefore, for example, with constant stress at work, cortisol will continue to be produced, although there is no need to look for any food.The release of cortisol is also controlled by the pituitary gland, in particular the pituitary hormone ACTH (adrenocorticotropic). Its level often rises with stress and depression.

– Hence the question: is it possible theoretically with hormones to correct a person’s condition with depression?

– Depression comes from the central nervous system, that is, the problem is not with hormones, but with the head. Here you need to work with the psychological reactions of a person to what worries him, and this is the work of psychotherapists. If a person is doing well, hormones will not drive him into depression.On the other hand, if he has depression, with which he does nothing – does not go to a specialist, does not take antidepressants – the hormones of such a person will not relieve depression.

– Yet hormones can influence behavior.

– Of course, hormones can change a person’s behavior a little. For example, with thyrotoxicosis, when there is a lot of thyroid hormone, thyroxine, irritability and irascibility may appear. It is unpleasant to communicate with such a person, but at the same time he likes himself and is completely confident in himself.And there are patients with thyrotoxicosis who are very easy to bring to tears. For example, you advise one person to be treated, and he replies in an explosive way: “No, I will not!” Say the same to another patient, and he goes into tears. The reaction depends on what character the person had before the disease. That is, how hormones work depends on the underlying data. The same thyroxine aggravates the behavioral characteristics of a person, therefore it is almost impossible to correct the behavior with hormones. It is necessary to change the connections between neurons in the head, but this is not done by hormones.

– It turns out that you need to see a psychotherapist.

– Yes, the endocrinologist will not help here. But in our country there is such a tendency that if a person comes to a doctor of any specialization and this person is strange, that is, it is not clear what is wrong with him, he is referred to an endocrinologist. First of all, doctors think positively about patients and believe that if people cannot control behavior, this is the result of the pathological release of any hormones from the endocrine glands – for example, the same thyrotoxicosis.To exclude this pathology, they ask for help from endocrinologists. Most often, endocrinologists do not find any pathology. This only proves that a person needs to go to a psychotherapist or psychiatrist and solve their mental problems. But, unfortunately, we do not have a culture of referring to psychiatrists and such a recommendation can cause a negative reaction. This is a legacy from the days of punitive psychiatry: there is a prejudice that if you go to a psychiatrist, your active social life may end there. But today we do not have punitive psychiatry, but there are doctors who treat.Provided that the patient came to them, of course.

Ten masks of the hormone

nina bashkirova

Society

10 January 2017

It is customary to think that if a person is overly excited and does not know how to control himself, it means that his nerves are out of control and it is time to visit a psychotherapist. And when the pressure jumps, go to a neurologist. And only a cardiologist will help with pain in the heart.But all this is only partly true. You can be treated by these specialists for years and continue to suffer from pressure, heart and neuroses. Because the real cause of these symptoms often lies in the disruption of the endocrine system. The head of the Department of Endocrinology of the North-Western State Medical University named after N.I. Mechnikova Zulfiya SHAFIGULLINA.

Art by Marcos Mesa Sam Wordley / shutterstock.com

– Zulfiya Rifgatovna, can a person himself understand that his thyroid gland is out of order? And what signs indicate that you need to visit an endocrinologist?

– Let’s start with the fact that thyroid diseases are quite common all over the world.When the activity of this organ is disrupted, it produces either too little or too much hormones.

For example, a tendency to neurotic and depressive states is a hallmark of hyperthyroidism, which is characterized by an excess of hormones. A person loses weight, there is a rapid heartbeat, increased sweating, weakness, fatigue … You may also have complaints about the feeling of sand in the eyes, watery eyes.

With hypothyroidism (insufficient production of hormones by the thyroid gland), on the contrary, all processes in the body are inhibited, the pulse becomes less frequent and even the body temperature decreases.A person feels tired, weak, dizzy, sometimes chilly and drowsy. Without changing the usual diet, he suddenly begins to gain weight, fluid is retained in the tissues and puffiness appears on the face, especially noticeable in the morning. Women notice that the skin becomes drier. By the way, the diagnosis of “hypothyroidism” can be made as soon as the patient enters the office. It is given by the pasty face, pallor and lack of shine in the eyes.

– And the patient is immediately put on hormones?

– The first study, which is prescribed for suspicious symptoms, is to determine the level of thyroid-stimulating hormone (TSH).If it is higher or lower than normal, the patient is first observed and only with the final confirmation of the diagnosis, the appropriate dosage of hormones is prescribed.

With hypothyroidism, hormone replacement drugs will have to be taken for life. Only in the case when autoimmune thyroiditis proceeds in waves, that is, at first there is a decrease in the functions of the thyroid gland, and then an increase, medication can be canceled. Wave-like transient hypothyroidism occurs in women after pregnancy and childbirth.

– And if the disease is not diagnosed for a long time or the person refuses to take hormones?

– Lack or excess of thyroid-stimulating hormones affects the work of all internal organs. With hyperthyroidism, the cardiovascular system is primarily affected, atrial fibrillation and myocardial dystrophy may develop. Sometimes people with such symptoms walk in circles for a long time, referring to a neurologist, cardiologist, therapist, and drink a lot of pills… And they get an appointment with an endocrinologist when serious pathologies already appear in the body. And if the doctor is able to restore the function of the thyroid gland, then it is already impossible to get rid of complications. Uncompensated hyperthyroidism is especially dangerous in old age. Therefore, the earlier treatment is started, the better.

– At what age does the thyroid gland begin to malfunction and why?

– We often diagnose hyperthyroidism in young people, and hypothyroidism mainly develops with age, when body functions slow down physiologically.Stress and micronutrient deficiencies have a very strong effect on morbidity. Women, who are more emotionally susceptible, suffer from thyroid diseases much more often than men.

– In what cases is it necessary to run to the endocrinologist immediately?

– If the thyroid gland has increased and pain appears, while the temperature has risen and chills have begun, these are obvious symptoms of subacute thyroiditis, an inflammatory disease of the thyroid gland.This is a fairly rare disease, but it can be cured without a trace if measures are taken in time.

Signs of diabetes are known to many – severe thirst, dry mouth, weight loss, frequent urination. You also need to urgently see a doctor. And, finally, one more endocrine pathology that cannot be pulled – adrenal tumors. This disease has recently become almost an epidemic. It can also hide behind the masks of arterial hypertension, neurological and other diseases.It is important to know: when the pressure “jumps” up to 200 and even 300 mm Hg, while it cannot be brought back to normal, it is necessary to exclude the pathology of the adrenal glands.

In addition to hypertension that cannot be corrected, the disease gives out muscle weakness, unexplained weight gain, “stretch marks” that appear on the body in the form of red stripes. Very characteristic symptoms in pheochromocytoma (one of the types of adrenal pathology) – blood pressure rises suddenly, accompanied by sweating, palpitations and headache.People often attribute these symptoms to fatigue, depression, stress, do not attach importance to them and do not go to the doctor. And the disease is revealed quite by accident, for example, by radiologists who find neoplasms in the adrenal glands in the images.

Today we receive a whole stream of patients with this pathology. According to the latest data, adrenal tumors affect up to 7 percent of the population.

– And you can’t do without surgery?

– A benign tumor can be hormonally active and inactive.Most often it turns out to be inactive, then the patient is recommended to be monitored by an endocrinologist. Once every six months or a year, he undergoes hormonal research and CT diagnostics. If the tumor does not exceed 4 cm, does not increase in size, then surgical treatment is usually not carried out.

The task of doctors is to determine the risk of a tumor turning into a malignant form. And this happens when the tumor becomes hormonally active, that is, it overproduces cortisol, aldosterone, adrenaline, norepinephrine.Then the operation is necessary. Any tumor larger than 4 cm that is at risk of becoming cancerous must also be removed. But there is no need to be afraid – operations on the adrenal glands are well developed today, they are carried out by the laparoscopic method and practically do not give complications.

You can discuss and comment on this and other articles in our VKontakte group

Material published in the newspaper “St. Petersburg Vedomosti” No. 002 (5864) from 10.01.2017.

90,000 57. Thyroid gland.

Characteristic
feature of thyroid cells
is their ability to absorb iodine,
which is then part of the hormones,
produced by the follicles of this gland.
The main hormones of the thyroid gland
are thyroxine and triiodithyronine.
Entering the bloodstream, they bind to
plasma proteins, which are
their carriers, and in tissues these complexes
break down, releasing hormones.

Characteristic
by the action of thyroid hormones
is to enhance energy
exchange by stimulating oxidative
processes. At the same time, significantly
basal metabolism increases, increases
consumption of proteins, fats and carbohydrates, which
accompanied by weight loss. Hormones
the thyroid gland accelerate the development
organism.

Hypofunction
thyroid gland, in childhood,
leads to the development of cretinism, and during
as an adult – to the development of myxedema
(“mucous edema”), i.e.because as a result
disorders of protein metabolism in the intercellular
the amount of fluid increases
mucin and albumin, which leads to
increased osmotic pressure
tissue fluid and water retention in
tissues, especially in the subcutaneous tissue.
With a lack of iodine in food and water
its hypofunction with growth is observed
gland tissue and education so
called a goiter. Although the iron itself
hypertrophied, but hormone production
it is reduced.

Hyperfunction
thyroid gland (hyperthyroidism).It manifests itself in an increase in the thyroid
glands, bulging eyes, tachycardia, high
irritability, a sharp increase
basal metabolic rate and body temperature,
increased food intake and, together
with weight loss. This disease
called Graves’ disease. Because
this disease is the result
hyperthyroidism, i.e. surplus production
thyroid hormone and enlargement
their content in the blood to concentration,
causing toxic phenomena, its
called thyrotoxicosis.

V
thyroid gland, except for iodine-containing
hormones, thyrocalcitonin is formed.The place of its formation is
parafollicular cells located
outside the glandular follicles of the thyroid
glands. Under the influence of calcitonin
there is a decrease in calcium content
in blood. This is due to the fact that he
inhibits the function of osteoclasts,
promoting the formation of bone
tissue and absorption of calcium ions from
blood. Therefore, thyrocalcitonin
contributes to the conservation of calcium in
the body.

Regulation
internal secretion of the thyroid gland.
The thyroid gland is richly supplied
afferent and efferent nerves.Impulses coming to the gland by
sympathetic fibers, stimulate
its activity. Hormone formation
the thyroid gland is under the influence
hypothalamic-pituitary system. At
decrease in the secretion of iodine-containing
hormones in the blood plasma rises
content of triotropic hormone (TSH),
the level of which, in turn,
depends on the stimulation of thyrotropin-releasing hormone
(TRG). Thyrotropin causes an increase
synthesis of hormones and their secretion by
stimulation of adenylate cyclase in epithelial
cells of the gland.TSH stimulates everything
phases of iodine metabolism, iodization of tyrosine
and synthesis of thyroxine, as well as proteolytic
cleavage of thyroglobulin and recoil
thyroid hormones. Isolation of thyroid
hormones leads to a decrease in TSH. V
the regulation system is also included
hypophysotropic zone of the hypothalamus, where
produced by TRH, stimulating
the production of TSH by the pituitary gland. Thyroxine
inhibits the secretion of TRH and TSH.

57.
Parathyroid glands.

Have
human has four parathyroid
glands that produce parathyroid hormone.It is due to the activation of the function of osteoclasts
causes destruction of bone tissue,
the release of calcium ions from it and increase
their concentration in the blood. Parathyroid hormone
activates other processes that cause
an increase in the level of calcium in the blood.
For example, it enhances absorption
calcium in the intestine and reabsorption in
tubules of the kidney. All this leads to
significant increase in calcium levels
and a simultaneous decrease in concentration
inorganic phosphates in the blood.

At
insufficient parathyroid function
glands in childhood are disturbed
growth of bones, teeth, hair, arise
prolonged spastic contractions
muscle groups.An adult in
these conditions significantly increases
CNS excitability, seizures occur
convulsions.

Hyperfunction
parathyroid glands accompanied
increased calcium in the blood
and a decrease in the amount of inorganic
phosphate. In these cases, it develops
osteoporosis, i.e. the destruction of bone
tissue, muscle weakness, back pain,
limbs.

Regulation
the formation of hormones that regulate
calcium exchange. Normal concentration
plasma calcium ions are maintained
at a constant level.Maintaining
a certain concentration of calcium ions
in the blood due to the interaction
two hormones – parathyroid hormone and
thyrocalcitonin. Decrease in level
calcium in the blood washing the gland,
leads to an increase in income
calcium into the blood from his bone depots.
An increase in the content of calcium in the blood,
washing the parathyroid glands,
inhibits the secretion of parathyroid hormone and
enhances the formation of thyrocalcitonin,
resulting in the amount of calcium
in the blood decreases. Hence, between
the content of calcium in the blood and internal
secretion of the parathyroid glands and
parafollicular cells of the thyroid
the gland has a two-way connection:
changes in the concentration of calcium in the blood
causes changes in the secretion of parathyroid hormone
and thyrocalcitonin, and they regulate
the content of calcium in the blood.These
relationships are not mediated nor
nervous or humoral mechanisms.

59.
Adrenal glands.

Adrenal glands
consist of cerebral and cortical
substances whose hormones differ
in its action.

Brain
adrenal gland substance.
Adrenal medulla hormone
adrenaline, formed from its predecessor
– norepinephrine. Adrenaline and norepinephrine
are combined under the name catecholamines,
or sympathomimetic amines, since their
the effect on organs and tissues is similar to
by the action of sympathetic nerves.

Adrenalin
affects many functions
organism:

*v
muscle glycogenolysis increases;

*
it causes an increase in heart rate
activities, improves performance
excitement in the heart;

*
narrows the arterioles of the skin, abdominal organs
and non-working muscles;

*
weakens contractions of the stomach and thin
intestines;

*
relaxes the bronchial muscles,
resulting in the lumen of the bronchi and
the bronchiole increases;

*
causes contraction of the radial muscle
iris, resulting in
destruction of the pupils;

*
increases the sensitivity of receptors,
in particular, the retina, auditory
and the vestibular apparatus.

Hence,
adrenaline causes emergency restructuring
functions aimed at improving
interaction of the body with the environment
environment.

Action
norepinephrine is similar to the action
adrenaline, but not in everything. Norepinephrine,
for example, causes a contraction of a smooth
rat uterus muscles, adrenaline relaxes
her. In humans, norepinephrine increases
peripheral vascular resistance,
as well as systolic and diastolic
pressure, and adrenaline leads to an increase
only systolic pressure.Adrenalin
stimulates the secretion of hormones in the anterior
lobes of the pituitary gland, norepinephrine-like
has no effect.

At
irritation of secretory nerves
adrenal secretion increases
them adrenaline and norepinephrine. With all
conditions that are accompanied
excessive body activity and
increased metabolism (emotional
arousal, muscle load, cooling
organism, etc.) secretion of adrenaline
increases. Increased secretion
adrenaline provides those physiological
changes that accompany
emotional states.

Bark
adrenal glands.
Hypofunction of the adrenal cortex
observed in humans with illness
Addison’s (bronze disease). Signs
hers are the bronze coloration of the skin,
weakening of the work of the heart muscle,
asthenia, cachexia. With hyperfunction
there is a change in sexual development,
because they begin to stand out vigorously
Sex hormones Adrenal cortex hormones
are divided into three groups:

*
mineralocorticoids;

*
glucocorticoids;

*
sex hormones.

1.
Mineralocorticoids .
Of the mineralocorticoids, the most active
aldosterone and deoxycorticosterone.
They are involved in the regulation of mineral
metabolism of the body, primarily sodium
and potassium.

Aldosterone .
In the cells of the tubular epithelium of the kidneys
it activates the synthesis of enzymes that increase
sodium pump activity that
leads to increased reabsorption
sodium and chlorine in the kidney tubules and,
hence, increasing the content
sodium in blood, lymph and interstitial fluid.At the same time, there is a decrease
reabsorption of potassium ions in the renal
tubules and a decrease in its content
in organism. Increased concentration
sodium in blood and interstitial fluid.
At the same time, there is a decrease
reabsorption of potassium ions in the renal
tubules and a decrease in its content
in organism. Increased concentration
sodium in blood and interstitial fluid
increases their osmotic pressure, which
accompanied by water retention in the body
and an increase in the level of arterial
pressure.

At
lack of mineralocorticoids, in
as a result of reduced sodium reabsorption
in the tubules, the body loses a lot
the number of these ions, which is often
incompatible with life.

Regulation
the level of mineralocorticoids in the blood .
The secretion of mineralocorticoids is
in direct proportion to the content
sodium and potassium in the body. Hanged man
the sodium content in the blood inhibits
secretion of aldosterone, and the lack
sodium in the blood causes increased secretion
aldosterone. Potassium ions also act
directly on the cells of the ravine
zones of the adrenal glands and provide
opposite effect on secretion
aldosterone. ACTH increases secretion
aldosterone.Decreased volume of circulating
blood stimulates its secretion, and
the increase in volume inhibits, which leads
to urinary excretion of sodium, and together with
him and water. This leads to normalization
circulating blood volume and quantity
body fluids.

2.
Glucocorticoids
– cortisone, hydrocortisone, corticosterone
have an effect on protein, fat
and carbohydrate metabolism. They are able to increase
blood sugar levels (hence their
name) by stimulating education
glucose in the liver as a result of acceleration
amino acid deamination processes
and converting their protein-free residues
into carbohydrates.They accelerate the breakdown of proteins,
which leads to a negative
nitrogen balance. Protein change
exchange influenced in different tissues
different. So, in muscles the synthesis of proteins
inhibited, occurs in the lymphoid tissue
their increased decay, and in the liver synthesis
protein is accelerated.

Glucocorticoids
enhance the mobilization of fat from fat
depot and its use in processes
energy metabolism. They excite
Central nervous system, contribute to the development of muscle
weakness and atrophy of skeletal muscles,
which is associated with increased decay
contractile proteins of muscle fibers.

At
insufficient secretion of glucocorticoids
the body’s resistance decreases
to various harmful effects.

Gain
the release of glucocorticoids occurs
in case of emergency conditions of the body
(pain, injury, blood loss, overheating,
hypothermia, poisoning, infectious
diseases, etc.), when reflexively
increased production of adrenaline. He
enters the bloodstream and affects
hypothalamus, stimulating ‘- formation
in its cells of a factor that promotes
formation of ACTH.ACTH stimulates
secretion of glucocorticoids.

3.
Sex
hormones
adrenal cortex. Sex hormones
adrenal cortex (androgens and estrogens)
play an important role in the development of genital
organs in childhood, which is especially
important, since during this period the intrasecretory
the function of the gonads is still poorly expressed.
After puberty, the role of
sex hormones of the adrenal glands are small.
However, in old age, after termination
intrasecretory function of genital
glands, the adrenal cortex again becomes
the only source of secretion
estrogens and androgens.

60.
Sex glands.

Sexual
glands secrete sex hormones,
which are divided into two groups: androgens
–
male sex hormones and estrogens
–
female sex hormones. Those and others
are formed in both male and female
gonads, but in different quantities.
The physiological role of sex hormones
consists in ensuring sexual functions.
These hormones support development
secondary sexual characteristics, and in the female
the body play an important role in
the occurrence of sexual cycles, in
ensuring the normal flow
pregnancy and in preparation for feeding
newborn.

At
dysfunction of the sex glands (ovaries
or testes), the ratio
the production of these hormones and, therefore,
related functions. Such a state
received the name of intersexuality.
It in men can be manifested by the presence
some physical and mental
characteristics peculiar to women,
and for women – for men.

Regulation
activity of the gonads. Activity
the gonads are regulated by the nervous
system, as well as pituitary hormones and
pineal gland.Nervous regulation of the genital
glands is carried out by reflex
changes in the internal secretion of the pituitary gland,
especially the secretion of gonadotropic hormones
or gonadotropins of the anterior lobe
pituitary gland, which dramatically increase
endocrine function of the gonads.
After removal of the pituitary gland in immature
animals development of gonads
slows down and remains unfinished
– no formation occurs in the testes
sperm, and in the ovaries follicles
do not reach maturity. When deleting
pituitary gland in sexually mature animals
atrophy of the gonads is observed.

Hormone
pineal gland – melatonin – inhibits development
sex glands and their activity.

Placenta .
The placenta secretes estrogen, progesterone
and choreonic gonadotropin. At
removal of the pituitary gland or ovary in animals,
when the placenta is already well developed,
miscarriage does not occur, because hormones
placenta are able to replace the corresponding
hormones of the pituitary gland and ovaries and provide
normal course of pregnancy.

Epiphysis.

V
the pineal gland forms a substance – melatonin,
which has an impact on
melanophores (pigment cells of the skin).Its action is opposite to action
intermedin and causes lightening
skin. With damage to the pineal gland in children
there is premature sexual
maturation. Influenced by lighting
the formation of melatonin in the pineal gland
decreases. The pineal gland contains a large
the amount of serotonin, which is
a precursor to melatonin. Education
serotonin in the pineal gland increases in
period of greatest illumination.

Internal
the secretion of the pineal gland is regulated by the sympathetic
department of the autonomic nervous system,
since the cycle of biochemical processes
in the pineal gland reflects the change of periods of the day
and nights, it is believed that this cyclical
activity is a kind
the biological clock of the body.

Testing on the topic “Endocrine system”, grade 8.

Test on the topic: “Endocrine system”

Option-1

1. Endocrine glands secrete:

A) vitamins B) hormones

C) digestive juices D) sweat and sebum 9000

2 . The endocrine system includes:

A) sweat glands B) salivary glands

C) sebaceous glands D) adrenal glands

3. Dysfunction of the thyroid gland may be associated with a lack of food

A) iodine B) chlorine B) vitamin A D) carbohydrates

4. Increased body temperature, thinness, “bulging” eyes and increased excitability can serve as signs of impairment
A) liver B) thyroid

C) pancreas D) sweat glands

5. The pancreas is considered a gland of mixed secretion, because

A) secretes digestive juice and the hormone insulin

B) produces digestive enzymes

C) contains various tissues

D) its work is regulated by the nervous and humoral paths

6. A person suffering from diabetes should regularly
A) take vitamins B) inject insulin

C) walk in the fresh air

D) exercise

7. The main adrenal hormone is

A) vitamin D B ) insulin B) growth hormone D) adrenaline.

8. In a person who is late for an important event, the secretion of

A) digestive juices B) insulin

C) adrenaline D) growth hormone

9. Growth hormone is released liters is

A) pancreas B) thyroid

C) liver D) pituitary

10. The hypothalamus is a section

A) medulla oblongata C) thyroid 2) B) cerebellum 9000) gland D) cerebral cortex

Test on the topic: “Endocrine system”

Option-2

1. Endocrine glands, in contrast to the external, secrete their secret:

A) to the surface body B) into the ducts

C) into the cavity of the internal organs D) into the blood

2. The secretion of hormones is carried out by iron:

A) sweat B) sebaceous

C) salivary D) thyroid

3. Diabetes mellitus develops with a lack of hormone
A) pituitary gland B) thyroid gland

C) pancreas D) pancreas adrenal glands
4. Lagging in mental and physical development, violation of body proportions m / b is associated with impaired activity
A) liver B) thyroid gland

C) circulatory system D) vestibular apparatus

5. With insufficient secretion of the thyroid gland, an adult develops:

A) Basedow’s disease C) Myxedema

B) Cretinism D) Diabetes mellitus

6. Mixed secretion glands do not include:

A) pituitary gland B) liver

B) pancreas D) thyroid

7. With strenuous physical work, the amount of

A) vitamin D B) bile C) growth hormone D) adrenaline increases in the blood.

8. With an excess of thyroid hormone,
develops A) rickets B) scurvy

C) Graves’ disease D) gigantism

9. Dwarfism m / b result of insufficient function

A) pituitary gland B) thyroid gland

C) circulatory system D) vestibular apparatus

10. The hypothalamus affects the work of the endocrine glands using as an “intermediary”

A) pituitary gland C) somatic NS

B) digestive system D) adrenal glands

Test on the topic: “Endocrine system”

Option-3

1. Glands consist of tissue

A) epithelial B) connective

C) smooth muscle D) nervous

2. Adrenaline is produced in
A) pituitary gland B) sebaceous gland

C) adrenal glands D) thyroid

3. As a result of hyperfunction of the thyroid gland
A) Graves’ disease B) rickets

C) diabetes mellitus D) gigantism
4. Iodine is necessary for the synthesis of
A) pancreatic hormone

B) thyroid hormone

C) pancreatic juice D) bile

5. With a lack of insulin, not

A) starch is digested B) glucose is absorbed by cells

B) glucose is absorbed D) enzymes are produced

6. The pancreas produces a hormone:

A) adrenaline B) thyroxin 9000) D) growth hormone

7. Adrenaline has an effect on the body similar to the effect of

A) somatic NS B) sympathetic NS

C) parasympathetic NS D) insulin hormone

8. In case of danger, a person increases the secretion of hormone
A) pancreas B) liver

C) adrenal glands D) sebaceous glands

9.

A) pituitary gland B) thyroid gland

C) liver D) pancreas

10. Neurohormones secreted by the hypothalamus through blood vessels are delivered to

A) muscles C) liver

B) heart D) pituitary gland

Option-4

1. Biologically active substances secreted by endocrine glands are called

A) enzymes B) vitamins

C) hormones D) nucleic acids

2. Mixed secretion glands include

A) sweat and sebaceous glands B) sex glands glands and pancreas

C) thyroid and pituitary gland D) adrenal glands

3 . Gigantism develops with an excess of:

A) noradrenaline B) insulin

C) growth hormone D) adrenaline.

4. Insufficient function of the thyroid gland leads to the development of
A) diabetes mellitus B) gastritis

C) myxedema D) gigantism

5. The constancy of glucose concentration in the blood is disturbed with insufficient function

A) sweat glands C) the pituitary gland

B) the adrenal glands D) the pancreas

6. The insulin secreted by the pancreas stimulates:

A) the conversion of glucose into glycogen

B) the breakdown of glycogen to glucose)

Digestion

7. As a result of adrenaline entering the bloodstream,

A) an increase in blood pressure B) a weakening of the heart

C) a decrease in blood sugar D) narrowing of the bronchi

8. A release of adrenaline into the blood occurs
A) after a hearty meal B) during sleep

C) during a quarrel D) during rest

9. Pituitary hyperfunction can cause the development of

A) gigantism B) diabetes

C) rickets D) Graves’ disease

10. The main center of humoral regulation is the system

A) spinal cord-brain B) liver-pancreas

B) pituitary-hypothalamus

D) sympathetic NS-parasympathetic NS

Functional state of the sympathetic-adrenal system | Laboratory and Diagnostic Center in Togliatti

The central and peripheral parts of the sympathetic system, as well as the adrenal medulla and accumulations of chromaffin cells, constitute the sympathoadrenal system.Chromaffin cells secrete two hormones, but a large amount of adrenaline and a small amount of norepinephrine. At that time, postganglinar cells secrete mainly norepinephrine.

Adrenaline actively secretes the adrenal medulla. Entering the bloodstream, it has an active effect on organs far from the adrenal glands.

The level of adrenaline in the body depends on the tone of the sympathetic system. Adrenaline in hepatocides promotes the breakdown of glycogen and an increase in blood glucose levels.At high concentration, intensified and accelerated contractions of the heart appear, and blood pressure rises.

Epinephrine plays an important role in stressful situations, increases the sensitivity of the thyroid gland to the action of thyrotropic hormone (TSH).

Epinephrine and norepinephrine are chemically different. The first has no methyl group.

The origin of norepinephrine is provided by nerve endings. Most of the hormone is absorbed by neurons, and only 10% of it is in the blood.

The nucleation of chromaffin cells and sympathetic ganglia occurs in neural crest cells at the stage of embryonic development.

Cells of the neural crest and newly formed cells can provoke the development of neoplastic neoplasms:

• sympathoblasts form tumors called sympathoblastomas;
• pheochromoblasts form pheochromoblastoma tumors;
• cells of the sympathetic ganglion form ganglioneuromas.

In modern medicine, the above types of tumors are diagnosed in most cases in children and newborns.Young people rarely suffer from such pathologies.

Pheochromocytoma, a tumor formed by chromaffin cells, is often diagnosed in adult patients. Moreover, in most cases, the tumor is located in the adrenal medulla. In some cases, it is localized elsewhere.

In the presence of chromaffin tumors in the body, an increase in the concentration of adrenaline and norepinephrine is observed.

As a result of which:

• hypertensive crises, while blood pressure remains normal;
• constantly increased blood pressure indicators with periodic cases of its increase to critical values;
• permanent persistent hypertension without hypertensive crises;
• some patients are diagnosed with an unusual form of pathology with a predominance of symptoms of cardiovascular failure against the background of cardiomyopathy in the absence of hypertension.

Laboratory blood tests to assess the state of the sympathetic-adrenal system

To assess the system, patients are assigned laboratory blood tests:

• Tests to determine the level of norepinephrine and adrenaline. The norm of the first is in the range of 104-548 mcg / l, of the second – less than 88 mcg / l.
• Blood test for the concentration of intermediate metabolism products;
• Urine test for vanilla-mandelic acid content,
• Pharmacological test studies are also being carried out.

As practice shows, pheochromocytoma is diagnosed in 1 out of 200 patients with hypertension.

The diagnostic center in Togliatti, which employs the best specialists, invites you to undergo laboratory tests to assess the functional state of the sympathetic-adrenal system. Call us!

.