Endocrine Overview.docx

**Endocrine System Overview** The endocrine system is diverse and has complex interrelationships with the nervous, immune, and other systems. Its major functions include controlling metabolic functions of the body, controlling the rate of cellular chemical reactions, cellular membrane transport, fl...

**Endocrine System Overview** The endocrine system is diverse and has complex interrelationships with the nervous, immune, and other systems. Its major functions include controlling metabolic functions of the body, controlling the rate of cellular chemical reactions, cellular membrane transport, fluid and electrolyte balance and regulating growth and development. Two principle endocrine glands are the **hypothalamus** and **pituitary gland.**  The hypothalamus is found beneath the cerebral hemispheres on each side of the third ventricle in the brain. The posterior portion of the pituitary gland is connected to the hypothalamus with nerve fibers in the hypophyseal stalk. The endocrine function of the hypothalamus is to produce regulatory hormones. Some of these hormones are released into the bloodstream and travel to the anterior pituitary where they either stimulate or inhibit the release of anterior pituitary hormones. The hypothalamus also synthesizes vasopressin (antidiuretic hormone \[ADH\]), which is stored in the posterior pituitary and released into adjacent blood vessels when needed. \[remember, when you have the \"d\" you do NOT pee\] **The Adrenal Glands** The adrenal glands are also a major part of the endocrine system. These vascular glands, which are tent shaped, sit on top of each kidney and are only about 1 1/2 inches long. The outer portion of the gland, which is the cortex, and the inner part of the gland, which is the medulla, have independent functions. **The Renin-Angiotensin System** [Renin] is produced in the kidneys and its **release occurs** when there is a decrease in extracellular fluid volume **\[blood loss, sodium loss\]**. When renin is released then angiotensinogen \[plasma protein from the liver\] is converted to angiotensin I. Angiotensin I is converted to angiotensin II, which is the active form of angiotensin. It is the angiotensin II which stimulates the secretion of aldosterone. Serum potassium also helps regulate aldosterone secretion. The adrenal cortex secretes aldosterone when the ratio of serum potassium to serum sodium increases. The increased serum potassium concentration then directly stimulates the adrenals to release mineralocorticoids. **The Adrenal Cortex** The adrenal cortex is also responsible for secreting glucocorticoid steroids, specifically [cortisol]. The main responsibilities of cortisol are that it **affects carbohydrate, protein,** and fat **metabolism; plays a role in the body\'s response to stress; supports emotional stability;** and **affects immune functions**. The release of glucocorticoids is directly regulated by the anterior pituitary hormone ACTH \[adrenocorticotropic hormone\] and indirectly by the hypothalamic corticotropin-releasing hormone (CRF). The release of CRH and ACTH is affected by the serum concentration of free cortisol, the diurnal sleep-wake cycle, and stress. When serum levels of cortisol are low, the hypothalamus secretes CRH, which stimulates the pituitary to release ACTH. ACTH then stimulates the adrenal cortex to secrete cortisol. When cortisol levels are normal or increased, then CRH and ACTH release are inhibited. Glucocorticoid release peaks in the morning and reaches its lowest level 12 hours before and after each peak. This means that cortisol levels are highest around 6 to 8 am and gradually fall during the day to their lowest point around midnight. The loss of this diurnal variation is sometimes the earliest sign of adrenal hyper-function \[ If a free cortisol level is ordered by the doctor, then two specimens should be drawn. The first will be around 8 am and then repeated at 4 pm. If the patient is following a normal diurnal variation, then the 4 pm specimen will be 1/3 to 2/3 of the 8 am level. Normal findings 8 am 6-28 ug/dl, 4pm 2-12ug/dl\]. **The Adrenal Medulla** The [adrenal medulla], in response to sympathetic nervous stimulation, is responsible for **secreting** two catecholamines which are **norepinephrine** and **epinephrine**. During times of physical or psychological stress these catecholamines result in \"**fight-or-flight**\" response and a state of heightened physical and emotional awareness. **The Pancreas** The [pancreas] lies retroperitoneally behind the stomach and is comprised of 1 million islet cells. The [islets of Langerhans] is made up of: *alpha cells* which **secrete glucagon** *beta cells* which **secrete insulin** *delta cells* which **secrete somatostatin** The primary endocrine function is to [regulate blood glucose]. This regulation is done by stimulating the release of **glucagon when blood glucose levels are low**. The [liver] is the **primary target** of **glucagon**. Remember that glucagon promotes glycogenolysis, which is the conversion of glycogen to glucose. [Glucagon] also **raises blood sugar** by enhancing amino acid transport from muscle and promotes \[conversion of amino acids and fatty acids to glucose\]. [Insulin] is responsible for **lowering blood sugar**. This is done by promoting glucose diffusion across cell membranes in most tissues. Carbohydrates is the major stimulus for insulin secretion. Insulin will be further discussed with Diabetes. [Somatostatin], the substance produced by the *delta cells*, is also responsible for regulating blood glucose levels. This neurotransmitter does this because it **inhibits the production of both glucagon and insulin.** **Hormones** The structures of the endocrine system include exocrine glands whose secretions are emptied to the outside of the body \[such as the sweat glands\] or into the lumen of an organ with same epithelium as the gland \[such as when the pancreas secretes its enzymes into the pancreatic duct, and it is transported to the intestine\]. The [endocrine glands] are **ductless** and make **hormones** that are **secreted directly into the blood** and **affect specific target organs**. These hormones are a chemical substance that are secreted in minute amounts. In a healthy state the concentration of most hormones is maintained at a relatively constant level. When the **hormone concentration rises,** further **production of that hormone** **is inhibited**. When the **hormone concentration falls**, the rate of the **production of that hormone increases**. This mechanism for hormone regulation is called [negative feedback]. **GLAND HORMONES** ================== **Anterior Pituitary:** Thyroid-stimulating hormone (TSH)\ Adrenocorticotropic hormone (ACTH, corticotropin)\ Luteinizing hormone (LH)\ Follicle-stimulating hormone (FSH)\ Prolactin (PRL)\ Growth hormone (GH)\ Melanocyte-stimulating hormone (MSH) **Posterior Pituitary:** Vasopressin (antidiuretic hormone \[ADH\]) Pancreas\ Oxytocin Insulin\ Adrenal Cortex Glucagon\ Glucocorticoids (cortisol) Somatostatin\ Mineralocorticoids (aldosterone) **Nursing Assessment: Endocrine System** A thorough understanding of normal endocrine function is essential for assessment and management of endocrine problems. The subjective data within the functional health pattern is of interest and the effects of aging on the endocrine system and non- specific manifestations of hormone dysfunction are important to understand the functioning of the system. Laboratory and radiologic studies used to measure hormone levels, to estimate the production, transport, and catabolism of hormones, and to evaluate the effect of hormone activity are also important and the nursing responsibilities associated with the studies. **Disorders of the Endocrine System** Disorders of the endocrine system include: **anterior pituitary gland** (hyperpituitarism: gigantism, acromegaly; hypopituitarism: adrenocortical insufficiency secondary to decreased ACTH) **posterior pituitary gland** (hyper-secretion: SIADH; hypo-secretion: DI) **adrenal cortex** (hyper-secretion: cushing\'s syndrome, hyperaldosteronism; hypo-secretion: adrenocortical insufficiency) **adrenal medulla** (hyper-secretion: pheochromocytoma).  **Anterior Pituitary Gland: Hyperpituitarism** Hyper-secretion of the anterior pituitary gland causes increased amounts of the hormone [galactorrhea] [(]*growth hormone*) to result in **gigantism in children** and **acromegaly in adults**..\ **Hyper-secretion of the anterior pituitary gland** is usually **caused by an** [adenoma]; these adenomas can cause neurologic problems, including: **vision changes** **headache** **changes in mental status** (compressing normal neural tissue) GH-secreting tumors are resected. Surgical removal of the pituitary tumor does not usually disrupt normal pituitary action. Anterior Pituitary Gland: Hypopituitarism **Hypo-secretion of ACTH** results in **adrenocortical insufficiency**. **Posterior Pituitary Gland: Hyper-function** [Syndrome of inappropriate antidiuretic hormone] (SIADH) results from **hyper-secretion of the posterior pituitary gland**. SIADH causes abnormal **water reabsorption,** as well as **hyponatremia** and **hypoosmolality**, which cause fluid movement from the extracellular to the intracellular compartment and change electrical activity of nerves, potentially resulting in **seizures.** Nursing care in SIADH is focused on increasing osmolality and sodium by **water restriction**, **monitoring for** and **reporting critical changes (low sodium levels, neuro changes),** maintaining a **safe environment,** and **patient education**. **\ Posterior Pituitary Gland:** **Hypo-function** [Diabetes insipidus], is a **deficiency of ADH**, results from **posterior pituitary gland insufficiency.** Although diabetes insipidus can cause volume deficit and hypernatermia, it usually does not because the thirst precipitated will cause increased fluid intake. [Vasopressin] in a **nasal spray** is **used to treat permanent diabetes insipidus**. Diagnostics may include: radiographic image of pituitary, normal, gross radiographic image of pituitary adenoma, gross and microscopic **Adrenal Cortex Gland: Hyper-function (cortisol excess)** The adrenal cortex secretes glucocorticoids and mineralocorticoids that are essential for life and adrenal androgens. Glucocorticoids excess (**Cushing\'s syndrome**) can result from excessive production of ACTH by the pituitary gland, excessive production of ectopic tumors, excessive production of glucocorticoids by the adrenal glands, or intake of large doses of exogenous steroids. Glucocorticoid excess (Cushing's syndrome) results in: **increased protein breakdown** **muscle wasting** **abnormal metabolism of fats** **changes in fat stores** **increased serum lipid levels** **increased glucose production** **Abnormal retention of sodium and water** **increased excretion of potassium and hydrogen ions** **bone demineralization** **Suppression of** the **immune system** and **inflammatory response** Patients with [glucocorticoid excess] have: **fluid volume excess** **hypernatremia** **hypocalcemia** **alkalosis, infections** **muscle wasting** **osteoporosis** **hyperglycemia** **peptic ulcers** **mental changes** **body changes** (thin extremities, truncal obesity, **moon face**, [kyphosis] (aka. **Hunchback**) **poor wound healing** **bruising** Nursing care for patients with Cushing\'s syndrome focuses on the nursing diagnoses of activity intolerance, disturbances in body image, ineffective coping, fluid volume excess, high risk for infection and injury, nutrient excess, pain, and knowledge deficit. The most frequent cause of Cushing\'s syndrome is iatrogenic, and the treatment focuses on dealing with the signs and symptoms of glucocorticoid excess.\ When patients have been taking long-term steroids, drug therapy must be tapered as it is discontinued. **Adrenal Cortex Gland: Hyper-function (aldosterone excess)** [Aldosterone excess] results in: **sodium** and **water** **[excess], volume expansion, hypokalemia,** and **hypertension**. [Treatment of aldosterone excess] is designed to lower blood pressure using **sodium restriction** and **spironolactone diuretics** or **surgery**. **Adrenal Cortex Gland: Hypo-function** Adrenocortical insufficiency is a medical emergency because the person is not able to mount a compensatory response to a major stressor. When glucocorticoids are deficient and a stressor is present, the person is unable to retain needed water and sodium, maintain blood pressure, and produce energy substrates (glucose, fatty acids). Untreated glucocorticoid deficiency results in **shock**. Patients with deficient in glucocorticoids require [lifetime] replacement therapy. They must know what to monitor to identify signs of a deficit or an excess, must know when to ask additional hormones, and must wear or carry proper identification. [Hyperpigmentation] occurs in patients with Cushing\'s syndrome resulting from increased ACTH and primary adrenocortical insufficiency, which is associated with increased ACTH. **Adrenal Medulla: Hyper-secretion** Tumors of the adrenal medulla cause **excessive production of catecholamines** are called [pheochromocytomas]. **Hypertension**, constant or paroxysmal, is [the major sign of pheochromocytoma]. Activities such as increased abdominal pressure, Valsalva maneuver, straining, and bending over can increase release of catecholamines and worsen hypertension in pheochromocytoma. Before surgery for pheochromocytoma, blood pressure is lowered using alpha-adrenergic blockers. **Surgery is the treatment of choice** for [patients with pheochromocytoma]. If bilateral tumors are present, after surgery the patient will be deficient in glucocorticoids and will need lifelong replacement therapy. **Diabetes Mellitus/Hypoglycemia** [Diabetes mellitus] is complex metabolic disorder that may be classified into two major classifications: **non-insulin-dependent diabetes mellitus** (NIDDM) or **insulin-dependent diabetes mellitus** (IDDM). Genetic, heredity, autoimmunity, and environmental factors have a role in the causes of both IDDM and NIDDM. Diabetes occurs more often in: **Native Americans** **Hispanics** **African Americans** **Elderly** [Insulin deficit] is a central feature of the disease; insulin deficit may be absolute, when B-cells do not secrete insulin, or relative, when B-cell defect and peripheral resistance to insulin is present.\ Insulin deficit and hyperglycemia lead to many immediate alterations in metabolism, including hyperosmolarity and osmotic diuresis, glycosuria, cellular starvation, calorie loss, and increased fat metabolism and catabolism. The classic signs and symptoms of insulin-dependent diabetes mellitus (IDDM) are **polyuria, polydipsia, polyphagia, weight loss, weakness**, and **fatigue**. Patients with IDDM may have these symptoms or signs and symptoms of diabetic ketoacidosis (DKA). Patients with non-insulin-dependent diabetes mellitus (NIDDM) may have the same symptoms, except that they usually have **weight gain instead of weight loss**, or they may have signs and symptoms of **hyperglycemic, hyperosmolar, nonketotic coma** or **vascular changes** and **neuropathy**. **Prevention** Taking measures to prevent and treat obesity is the focus of primary prevention of NIDDM; screening to detect undiagnosed cases (50%) is the focus of secondary prevention; detecting and preventing progression of complications is the focus of tertiary prevention. The five primary modalities of treatment for diabetes mellitus are **diet, exercise, hypoglycemic agents, monitoring,** and **education**. Dietary recommendations include calorie distribution of **carbohydrates (CHO) \[55% to 60%\]**; **fat** **(20% to 30%)** with restriction in saturated fat to 10%; **protein (20%)**; limitation of cholesterol, sodium, and refined simple CHO; and increased use of complex, unrefined CHO. Exercise has a hypoglycemic action in most instances; it can increase hyperglycemia if blood glucose levels are above 300 mg/dl or if exercise is intense. Exercise does aid in cardiovascular fitness and weight reduction and maintenance, and it decreases peripheral resistance to insulin. **Nursing Management Diabetes Mellitus** Assessment of the patient includes collecting objective data about metabolic status and assessing cardiovascular-renal status, vision, and nerve function. The lower extremities should be examined carefully. Diabetes education must be individualized and planed over time. Initial instruction should be restricted to \"survival skills\" with plans for continued education. The treatment of hypoglycemia must be prompt; **10 to 15 g of simple CHO** is given as soon as symptoms are detected. The [first signs] present are those of **epinephrine excess**; [later signs] are those of **cerebral dysfunction**. The signs and symptoms may be prolonged if the patient is taking oral hypoglycemic agents. Insulin or oral hypoglycemic agents should not be omitted when short illness occurs; about 50% of normal daily CHO intake be distributed over 24 hours. Monitoring should dictate the need for more or less medication. Foot care includes daily inspection, measures to maintain integrity of skin, and prevention of injury. Referral to podiatric services is highly recommended. Patient should verbalize knowledge of feet at risk. **Complications of Diabetes Mellitus** Diabetic ketoacidosis (DKA) and hyperglycemic, hyperosmolar, nonketotic coma (HHNC) are two life-threatening situations that occur in uncontrolled diabetes mellitus; they are usually precipitated by infection, stressors, or failure to follow regimen. Medical management of DKA and HHNC include **intensive fluid replacement, low-dose insulin infusion,** and **potassium replacement**. The patient may also need \*phosphate and magnesium replacement. Hyperglycemia, from poorly controlled diabetes mellitus, seems to be a major predictor of the development of **microvascular lesions** (nephropathy, retinopathy), **macrovascular lesions** (atherosclerotic disease), and **neuropathy** (autonomic and peripheral). Amputation of a limb may be necessary because of alterations in blood vessels and nerve trauma, tissue trauma, or infections occurring persons with inadequate skin integrity and insensitivity to pain and pressure. Proper foot care, which helps to prevent an infection, can reduce the chance of amputation. The major nursing focuses on patients with DKA or HHNC are: **monitoring intake and output, weight, vital signs, mental status, ECG, blood glucose, urine ketones, serum electrolytes,** and **osmolality**. The medical plan must be implemented and unexpected changes reported immediately.