THE ENDOCRINE SYSTEM AND DIABETIC EMERGENCIES

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The Endocrine System

The endocrine system is a complex system that serves many functions in the human body. Together with the nervous system, the endocrine system helps maintain homeostasis (balance of body systems), alters metabolic processes, regulates growth and development, and allows adaptation to physiologic stresses.

Hormones

The endocrine system is composed of glands and glandular tissues that secrete hormones, which are chemical messengers that affect specific target tissues in the body. These tissues have specific receptors for certain hormones in their cell membranes; this is how hormones can circulate in the entire bloodstream but only affect their specific target tissues. Chemically, there are four different classes of hormones. The following is a list of the different classes of hormones and examples of each:

·         Steroids - estrogen, testosterone, progesterone, cortisol, calcitriol, and aldosterone

·         Amines - epinephrine, norepinephrine, triiodothyronine (T3), thyroxine (T4), serotonin, and melatonin

·         Peptides and Proteins - insulin, glucagon, oxytocin, anti-diuretic hormone, parathyroid hormone, all hypothalamic releasing and inhibiting hormones, and all anterior pituitary hormones

·         Eicosanoids - prostaglandins and leukotrienes

Glands

The body contains two types of glands: exocrine and endocrine. Exocrine glands secrete their products into ducts which carry the products to body cavities, organs, or outside the body. Sweat (sudoriferous) glands, oil (sebaceous) glands, and digestive glands are all examples of exocrine glands.

Endocrine glands do not possess ducts. They secrete their products into the extracellular space around the secretory cells and then the products are diffused into the bloodstream. Endocrine tissues are thus highly vascular tissues. Following is a summary of each of the endocrine glands, the hormones each gland produces, and the effects of these hormones on the body:

ENDOCRINE GLANDS

LOCATION

HORMONES

EFFECTS

ANTERIOR PITUITARY

BASE OF BRAIN IN SMALL DEPRESSION IN THE SPHENOID BONE CALLED THE SELLA TURCICA

-PROLACTIN

-ADRENOCORTICOTROPIC HORMONE (ACTH)

-GROWTH HORMONE (GH)

-THYROID STIMULATING HORMONE (TSH)

-FOLLICLE STIMULATING HORMONE (TSH)

-LUTEINIZING HORMONE (LH)

-STIMULATES MILK PRODUCTION

-STIMULATES ADRENAL CORTEX TO PRODUCE CORTICAL HORMONES

-STIMULATES GROWTH OF ALL BODY TISSUES

-STIMULATES THYROID GLAND TO PRODUCE THYROID HORMONES

-STIMULATES GROWTH OF OVARIAN FOLLICLES AND TESTES

-CONTROLS OVULATION AND MENSTRUATION

POSTERIOR PITUITARY

SAME AS ANTERIOR PITUITARY

ANTI-DIURETIC HORMONE (ADH)

-OXYTOCIN

PROMOTES REABSORPTION OF WATER IN KIDNEYS

-CAUSES CONTRACTION OF UTERUS

PINEAL

ATTACHED TO ROOF OF 3RD VENTRICLE IN BRAIN

MELATONIN

THOUGHT TO PROMOTE SLEEPINESS

 

 

THYROID

LIES IN FRONT AND TO EACH SIDE OF THE TRACHEA IN THE LOWER NECK

TRIIODOTHYRONINE (T3)

-THYROXINE (T4)

-CALCITONIN

REGULATES METABOLIC RATE

 

-DECREASES CALCIUM LEVEL IN THE BLOOD

 

PARATHYROIDS

4 SMALL GLANDS LOCATED NEAR THE THYROID

PARATHYROID HORMONE

INCREASES CALCIUM LEVEL IN THE BLOOD

ADRENAL CORTEX

LIES ON SUPERIOR PORTION OF THE KIDNEYS

GLUCOCORTICOIDS

-MINERALCORTICOIDS

-ANDROGENS

 

 

 

METABOLISM OF CARBOHYDRATES, FATS, AND PROTEINS; ANTI-INFLAMMATORY PROPERTIES

-REGULATION OF WATER AND ELECTROLYTE BALANCE

-PROMOTE SEXUAL GROWTH

ADRENAL MEDULLA

SAME AS ADRENAL CORTEX

EPINEPHRINE

-NOREPINEPHRINE

FIGHT OR FLIGHT RESPONSE,INCREASED BLOOD PRESSURE, SPEEDS UP BODY PROCESSES

-SIMILAR TO EPINEPHRINE, NERVE CONDUCTIVITY

PANCREAS

BEHIND THE STOMACH IN THE LUQ OF THE ABDOMEN

INSULIN (BETA CELLS)

-GLUCAGON (ALPHA CELLS)

-SOMATOSTATIN (DELTA CELLS)

-PANCREATIC POLYPEPTIDE (F CELLS)

AIDS TRANSPORT OF GLUCOSE INTO BODY CELLS

-STIMULATES LIVER TO RELEASE GLUCOSE

-INHIBITS RELEASE OF INSULIN AND SLOWS ABSORPTION OF NUTRIENTS FROM THE GI TRACT

-INHIBITS RELEASE OF SOMATOSTATIN, CONTRACTION OF THE GALLBLADDER, AND SECRETION OF PANCREATIC JUICE

OVARIES

IN PELVIC CAVITY WITH FALLOPIAN TUBES AND UTERUS

ESTROGEN

-PROGESTRONE

STIMULATES GROWTH OF FEMALE SEXUAL ORGANS

-STIMULATES GROWTH OF MAMMARY GLANDS, AIDS IN MAINTAINING PREGNANCY

TESTES

IN SCROTAL SAC

TESTOSTERONE

STIMULATES GROWTH OF MALE SEXUAL ORGANS

Over- and underproduction of hormones can cause a myriad of syndromes, too many to be discussed here. In this lesson, we will discuss diabetes, the thyroid disorders hyperthyroidism and hypothyroidism, and the adrenal disorders Cushing's syndrome and Addison's disease.

DIABETES MELLITUS

Definition and Statistics

Diabetes mellitus is a condition brought on by the decreased production of insulin. Diabetes mellitus is one of the most common diseases in America. Most Type I diabetics are diagnosed before the age of nineteen. Type II diabetics are not insulin dependent. Type II diabetes usually occurs after the age of 40. Another type of diabetes is gestational diabetes. Gestational diabetes occurs during pregnancy and usually disappears following delivery. It is due to changes in glucose metabolism during pregnancy. 

Type I and Type II

Type I, also referred to as juvenile diabetes, is a form of diabetes mellitus characterized by the need for daily injections of insulin. The beta cells of the pancreas are producing little to no insulin. It is not clearly understood why this condition occurs. However, heredity seems to affect the odds on developing Type I diabetes. One theory on why the condition manifests itself is that certain people are prone to a viral attack that destroys the beta cells. Another theory holds that the body's immune system mistakes the beta cells as foreign and suppresses them or destroys them. Whatever the reason, the condition will usually present itself before nine years of age. Thus the term juvenile diabetes.

Type II diabetes occurs much more frequently than Type I. Type II is usually associated with obesity and begins much later in life than Type I. The association with obesity occurs because an increase in body weight affects inversely the number of insulin receptors. In addition, insulin receptors can become defective and less efficient in bonding to insulin.

Long Term Effects

Long term medical treatment of type II diabetes is to reduce the amount of carbohydrates in the patient's food intake. The altering of the patient's diet is designed to influence the loss of weight. Oral hypoglycemic drugs, such as Glucophage or Micronase, are prescribed to increase the insulin production in the pancreas and to increase the number of available insulin receptors. The intent of this type of therapy is to reduce the amount of glucose in the bloodstream. If unsuccessful, the use of insulin may be required.

Diabetes can have two types of long term effects. One type of damage can occur to the nervous system. Peripheral neuropathy, which can cause pain, tingling, or numbness of the extremities, is more common in diabetics. The second type of long term effect is damage to blood vessels due to increased atherosclerosis which leads to arteriosclerosis, or hardening of the arteries. This blood vessel damage can lead to gangrene of the feet due to decreased circulation in the extremities. Vessel damage can also lead to problems with the eyes and kidneys. Approximately half of all diabetics will experience eye problems within ten years of onset. Other complications of diabetes are heart disease, stroke, kidney disease, and blindness. Because of circulation problems, many diabetics have chronic ulcers in the lower extremities. Wounds in the extremities also heal very slowly in these patients.

Pathophysiology

 

The Insulin and Glucose Relationship

Diabetes is caused by a decrease or stoppage of insulin secretion. Insulin is a hormone produced by the pancreas. It is a carrier for glucose, the body's main fuel. Glucose is a simple sugar that is required by the body to produce energy. Most foods consumed by humans are in the forms of complex sugars. They are broken down by the gastrointestinal system into simple sugars - glucose, galactose, and fructose. The majority of the simple sugar distributed into the bloodstream for use by the body is glucose. The glucose molecule is too large to easily pass through the cell membranes. Glucose must be helped across the membranes by special carrier proteins in a process called facilitated diffusion. Insulin acts as a key to unlock the cell's membrane. Therefore, the rate at which glucose is transported into the cell is affected by insulin. Insulin can accelerate the process by a factor of ten. If no insulin is present, the cells cannot survive on the amount of glucose that finds its way into the cell. If the pancreas is functioning normally, glucose levels will fluctuate according to outside stimuli but remain within set limits.

Pancreas

The pancreas is the gland where insulin is produced. The pancreas plays an important role in the absorption of carbohydrates, fats, and proteins. It also is the principle regulator of blood glucose levels. It is located behind the stomach in the upper left quadrant and is approximately the length of your hand. It is a tongue-shaped organ that hangs in the folds of the duodenum. It has both exocrine and endocrine functions. The exocrine functions include the production of several key digestive enzymes and the endocrine functions include production of insulin and glucagon. Both are major players in diabetic emergencies.

Islets of Langerhans

Located inside the pancreas are special tissues called the Islets of Langerhans. This is the location of the endocrine functions. There are four types of cells that form the Islets of Langerhans - alpha, beta, delta and F cells. Each is responsible for the excretion of a particular hormone. There are 500,000 to 1 million islets in the pancreas. Beta cells comprise 70% of the islets, alpha cells - 20%, delta cells form 5%, and the remainder of the cells are F cells. Each islet is surrounded by a well-developed capillary system into which the hormones are released. The islets are activated by both divisions of the autonomic nervous system.

Alpha and Beta Cells

The alpha cells release glucagon, which increases the blood glucose levels. Whenever the glucose level falls, the alpha cells release glucagon. The glucagon stimulates the liver to release glucose stores and also to manufacture glucose from other substances. Glucagon is a protein released by the alpha cells when blood glucose levels fall. Two major effects of glucagon's release are to increase blood glucose levels by stimulating the liver to release glucose stores from glycogen, which is a polysaccharide storage molecule similar to starch in plants, and other glucose storage sites and to stimulate gluconeogenesis through the breakdown of fats and fatty acids. Both activities are designed to maintain normal glucose levels. Normally, the body should maintain a blood glucose level that varies from 60 to 120 mg/dl. However, that range will vary from one individual to another.

Beta cells produce insulin. Insulin acts as an antagonist to glucagon. The primary functions of insulin are to facilitate the transfer of glucose to the cells, increase glucose metabolism, to increase liver glycogen levels, and to decrease blood glucose concentrations to normal levels.

Other Functions of the Pancreas

The delta cells secrete somatostatin, which is identical to growth hormone inhibiting hormone. Somatostatin inhibits the release of insulin and slows the absorption of nutrients from the gastrointestinal tract. The F cells secrete pancreatic polypeptide, which inhibits the release of somatostatin, contraction of the gallbladder, and secretion of pancreatic digestive enzymes. All of the hormones produced by the pancreas work together to maintain homeostasis.

The exocrine function of the pancreas involves production of pancreatic juice by glands called acini. This juice is carried through a duct system to the small intestine where it helps in the digestive process.

Hyperglycemia

Under normal circumstances, food is broken down and transformed into glucose and proteins and absorbed into the bloodstream. Insulin is released to facilitate the transfer of glucose to the cells, thus reducing the blood glucose level. About 60% of the glucose taken in after a meal is converted by the liver into glycogen. This process occurs fairly rapidly in order to prevent excessive glucose levels.

Diabetic Ketoacidosis

About one third of the glycogen is stored in the liver. The rest is converted into fatty acids and eventually triglycerides (fats) and stored in adipose tissue. When there is a shortage of insulin, the stored fat is broken down and used as fuel. This causes an increase in triglycerides, fatty acids, and cholesterol in the bloodstream. This can lead to long term problems such as atherosclerosis and circulation problems. Short term problems caused by this abundance of fatty substances can be severe if untreated. If insulin is not present and glucose cannot be used as the primary energy source for cells, fatty acids are metabolized for food. This causes a by-product of acetate, which is then converted into acid. These substances are known as ketones which are the cause of diabetic ketoacidosis.

Pathophysiology

The pathophysiology of hyperglycemia and diabetic ketoacidosis is fairly straightforward. Insulin is required by the body to transfer glucose to the cells. If there is an inadequate supply of insulin, there will be a buildup of glucose in the bloodstream. However, the cells cannot utilize this excess because there is nothing to facilitate the transfer of the glucose across the cell membrane. The cells begin a process of finding alternative sources of energy. These alternative sources produce harmful by-products as they are consumed. Two of the by-products produced are ketones and organic acids. As the concentration of the by-products increases, the blood becomes more acidic.

Hyperglycemia can be caused by two major factors: decreased insulin intake and increased physiological stresses. Decreased insulin intake can be caused by non-compliance, improper medication adjustment, and forgetfulness. Physiologic stresses such as trauma, infection, and emotional stressors all increase the body's requirement for insulin.

Signs and Symptoms

The body will try to compensate for the increasing level of blood glucose by having the kidneys dump glucose into the urine. This causes a fluid shift and severe dehydration in the body. The patient may complain of being extremely thirsty. The skin and mucous membranes will become warm and dry.

Respirations may become fast (tachypnea) and deep (hyperpnea). This is known as Kussmaul's respirations. This is the respiratory system's mechanism to adjust the pH of the blood back to normal by breathing off excess carbon dioxide. The breath may become sweet or acetone-like because of the ketones in the blood.

If the condition continues, the patient may lose consciousness. This is often referred to as diabetic coma. The brain may suffer serious damage and death may even occur. Because of the lack of fuel and the acidic level of the blood, the patient's level of consciousness might also be affected. This might present itself as combativeness or drunken stupor. For this reason, never assume a person has been drinking. Always look for medic alert tags and other signs of diabetes.

Ketoacidosis results in 1 of 10 deaths in diabetics. Ketoacidosis is most likely to occur in the undiagnosed diabetic or those whose condition is not well controlled.

Signs and symptoms of diabetic ketoacidosis:

·         Gradual onset

·         Warm, dry skin

·         Dry mucous membranes

·         Weak, rapid pulse

·         Postural hypotension

·         Weight loss

·         Polyuria (increased urination)

·         Polydipsia (increased thirst)

·         Abdominal pain

·         Anorexia (decreased appetite)

·         Acetone breath odor

·         Kussmaul's respirations

·         Decreased level of consciousness

·         Glycosuria (sugar in the urine)

Diabetic ketoacidosis patients are rarely in a deep coma. Unresponsive patients should be assessed for other underlying causes such as head injury, stroke, or drug overdose.  When obtaining a history of the present illness, you should ask the following questions:

·         If the patient is a known diabetic:

·         Has their medication been changed lately?

·         Have they had a recent infection? trauma? emotional stress?

·         Has there been a change in eating patterns?

·         When was their last meal?

·         When did they last take their insulin?

·         If the patient is not a diabetic:

·         Has there been a recent development of increased urination, increased thirst, or weight loss? (This may indicate a new onset of diabetes)

Treatment

Assessment of the patient for ketoacidosis is similar to any medical emergency. Primary concern is always the airway. Once the airway is secure, assess respirations and circulation. Look for the signs of a possible known diabetic such as medic alert tags or evidence of insulin injection. Pay attention to breath odors and query for medical history. The best method of determining a diabetic emergency is the rapid test for blood glucose.

This test is performed by use of a glucometer. A sample of blood is taken and placed onto a special tab. The tab will change color after being exposed according to glucose levels. The tab can be measured by the assessment of color from a color chart or read more accurately by the glucometer. It is important to remember that the glucometer is a machine and the tab should always be checked with the color chart to ensure accuracy. If there is any question, always recheck your test and err on the side of caution.

Basic treatment for ketoacidosis is to maintain the ABC's, administer high-flow oxygen, and rapid transport. The patient should be monitored constantly while en route to the hospital. Vitals and the level of consciousness should be re-evaluated every three to five minutes.

Advanced treatment for ketoacidosis will be to provide BLS treatment and obtain a blood specimen in a red top tube or as your local protocols dictate. An IV of 0.9% sodium chloride or Lactated Ringer's should be started and run in at a wide open rate unless otherwise indicated. Remember, these patients may be PROFOUNDLY dehydrated and the fluid you administer might result in a dramatic improvement in their condition. Medical control may request intravenous or subcutaneous administration of insulin if available.

Non-Ketotic Hyperosmolar Coma

 

Pathophysiology

Type II diabetes does not usually lead to ketoacidosis. The fact that the body is still producing insulin does not force the body to resort to alternative forms of energy production. For this reason ketones are not produced. However, there is not enough insulin to permit glucose to be used by most of the cells or enough to prevent the liver from releasing stored glycogen. This hyperosmolar state draws fluid from the intracellular space and hence dehydration and electrolyte loss. This cell dehydration can lead to a life-threatening condition called non-ketotic hyperosmolar coma.

Non-ketotic hyperosmolar coma is a life-threatening condition that frequently occurs in older patients with Type II diabetes or undiagnosed diabetics. This condition can be predisposed in patients who have preexisting cardiac or renal disease, increased insulin requirements, medication use of diuretics. Non-ketotic hyperosmolar coma is hard to differentiate from diabetic ketoacidosis in the field. Therefore, you should treat them identically.

Signs and symptoms

·         Gradual onset

·         Weakness

·         Thirst

·         Weak, rapid pulse

·         Frequent urination

·         Weight loss

·         Extreme dehydration

·         Glycosuria

·         Altered mental status

 

HYPOGLYCEMIA

Pathophysiology

When insulin levels are extremely high, a condition known as hypoglycemia can occur. Hypoglycemia is a condition related to blood glucose levels less than 80 mg/dl. Symptoms will usually occur at levels less than 60 mg/dl. It is usually the result of excessive glucose absorption, physical exertion, decreased food intake, alcohol or drug effects, pregnancy and lactation, or too much insulin intake. Some less common causes are alcoholism, gland disorders, liver disease, tumors, hypothermia, sepsis, and administration of beta blockers or salicylates. If the patient is not treated, the insulin will cause blood glucose levels to drop very low.

Hypoglycemia, also known as insulin shock, is a true medical emergency. The brain receives almost all of its energy from glucose and if glucose is unavailable, irreversible damage can occur quickly. For this reason, if blood glucose levels cannot be measured, always err on the side of hypoglycemia and administer glucose.

Signs and symptoms

Hypoglycemia will present itself in many and different ways. Altered mental status is probably the most prevalent. In the beginning, the patient will often appear impatient or restless. Very often they will experience extreme hunger. As the condition progresses the patient may become combative and violent.

Other signs may include diaphoresis and tachycardia. The pulse will usually be strong and rapid, the skin cold and clammy, and the patient may be very weak and display a lack of coordination. If the condition persists, the patient may experience seizures and slip into a coma. Unlike hyperglycemia, hypoglycemia can occur very rapidly.  The signs and symptoms of hypoglycemia are:

·         Rapid onset

·         Nervousness, trembling

·         Irritability

·         Psychotic or combative behavior

·         Weakness and lack of coordination

·         Confusion

·         Intoxicated behavior

·         Strong, rapid pulse

·         Cold, clammy skin

·         Drowsiness

·         Seizures

·         Coma

When obtaining a history of the present illness, you should ask the following questions:

·         Is the patient a known diabetic?

·         When was their last meal?

·         When was their last insulin dose?

·         Are they an alcoholic?

·         Have they increased their activity level?

·         Has there been a change in eating patterns?

Treatment

Treatment for hypoglycemia is based on a rapid assessment. A glucose test should be performed. If glucose levels are below 60 mg/dl, you should administer glucose to the conscious patient. BLS treatment for the unconscious patient involves maintaining an adequate airway and assistance with breathing as needed. Rapid transport to hospital or ALS intercept should be initiated.

Hypoglycemia should always be suspected in any diabetic patient who displays altered mental status or unconsciousness. This condition is a true emergency that requires immediate administration of glucose to prevent permanent injury to the brain. All patients who have experienced a diabetic abnormality should be assessed by a physician.

The brain cells do not use insulin to transfer glucose into the cell membrane. The brain cells also do not use other sources of energy very well. Therefore it is a life-threatening emergency when glucose levels are low. If you are not sure as to the nature of the patient's altered mental status, administer glucose. The short term effects of too much sugar are far outweighed by the danger of not enough sugar for the brain cells.

The key to distinguishing between DKA and hypoglycemia is to remember that DKA will present with signs of dehydration: poor skin turgor, dry membranes, weak pulse. Hypoglycemia does not involve dehydration and will present with clammy skin and a strong pulse.   

Prior to administering glucose to the unconscious patient, an estimation of their social history must be made. If there is any possibility of a history of alcohol abuse, thiamine should be administered prior to the glucose. Thiamine deficiency combined with administration of IV dextrose may precipitate a condition known as Wernicke's syndrome. It is characterized by ataxia (lack of muscle coordination), eye muscle weakness, and mental derangement. Another condition that may result is Korsakoff's psychosis and is characterized by a potentially irreversible memory disorder. Both of these can be prevented by the administration of 100 mg of thiamine intravenously or intramuscularly.

Oral glucose comes in a gel form and has trade names of Glutose and Insta Glucose. Oral glucose should only be administered to patients who are conscious and can swallow. It should be placed between the cheek and gum or under the tongue. The whole tube (25 grams) should be administered. However, be careful to allow the patient to swallow or absorb the medication and not to choke. As always, the patient should be reassessed after the administration of any medication.

Contraindications for the administration of oral glucose include an unresponsive patient who cannot swallow and patients with cerebral insults. The administration of glucose could exacerbate cerebral damage in any patient over the age of 50 with a clinical history of transient ischemic attack or stroke.

During assessment you should inquire about oral intake. Alcohol can aggravate the problem. If meals and insulin are not carefully balanced, a diabetic emergency may be triggered. Foods high in simple sugars, cookies and candy, and large amounts of carbohydrates may overcome normal insulin doses. Holidays can often spawn diabetic attacks. On the other hand, excessive exercise or skipping a meal after an insulin injection is also dangerous.

You should also try to ascertain when the present condition started. Remember that a patient with an altered mental status may be uncooperative and refuse treatment. Be persistent in the pursuit of consent to treat. Advise the patient and family members of possible consequences.

Advanced treatment would include obtaining a blood specimen in a red top tube, (follow local protocols). Start an IV of normal saline ot Lactated Ringer's and administer 25 grams of 50% dextrose intravenously. If conscious, follow up with oral administration of orange juice, soda, or glucopaste for the conscious patient. Remember, if a documented glucose level cannot be obtained, treat for hypoglycemia.

If an intravenous line cannot be established, a subcutaneous or intramuscular administration of glucagon, if available, can help to raise glucose levels by stimulating the liver to break down glycogen stores. This method will not be effective in patients who are chronic alcoholics and those with liver disease.

DO NOT GIVE 50% DEXTROSE BY ANY MEANS OTHER THAN INTRAVENOUSLY OR BY THE INTRAOSSEUS ROUTE. D50 will cause tissue necrosis if given intramuscularly or subcutaneously. If given endotracheally, D50 will again cause tissue necrosis as well as lethal pulmonary edema.

The treatment of diabetic emergencies is probably one of the most rewarding in emergency medicine. You can rapidly see an improvement in your patient with the proper treatment. If treatment is prompt, recovery from diabetic emergencies is usually complete. It is important for emergency responders to recognize diabetic emergences and the forms of altered mental status they can manifest. Aggressive treatment is the key to success.

THYROID DISORDERS 

 

Hyperthyroidism

When the thyroid gland releases too much thyroid hormone into the bloodstream, a condition called hyperthyroidism results. Hyperthyroidism results in an increase in metabolism with the following signs and symptoms:

·         Anxiety, irritability

·         Warm, moist skin

·         Weight loss

·         Palpitations

·         Heat intolerance

·         Diarrhea

·         Exopthalmos (edema behind the eyes that causes an abnormal protrusion of the eyeballs)

The most common cause of hyperthyroidism is Graves' disease, which is an autoimmune disorder that causes production of antibodies that mimic the action of Thyroid Stimulating Hormone (TSH). The thyroid is contantly stimulated by these antibodies to produce the thyroid hormones.

Thyroid Storm

The most serious form of hyperthyroidism is called thyrotoxicosis, or "thyroid storm". Thyroid storm is an acute manifestation of all hyperthyroid symptoms. Signs and symptoms include:

·         Severe tachycardia and cardiac dysrhythmias

·         Heart failure

·         Hyperthermia

·         Extreme anxiety and agitation

·         Hypertension

·         Abdominal pain

·         Delirium

·         Coma

Management of hyperthyroidism and thyroid storm is primarily supportive. Monitor vital signs and cardiac rhythm, provide high-flow oxygen, establish an IV of normal saline or Lactated Ringer's, and transport to the nearest appropriate facility.

Hypothyroidism

When hypothyroidism occurs in an adult, the condition is known as myxedema. The thyroid is not producing sufficient amounts of thyroid hormones resulting in a slowed metabolic rate. Signs and symptoms of myxedema include:

·         Cold intolerance

·         Weight gain

·         Bradycardia

·         Depression, lethargy, somnolence

·         Dry, cool skin

·         Constipation

·         Hair loss

·         Edema to face and periorbital areas

·         Ataxia

As with thyrotoxicosis, management of myxedema is primarily supportive in nature.

ADRENAL DISORDERS 

 

Cushing's Syndrome

Cushing's syndrome is a hypersecretion of the glucocorticoid hormones cortisol and cortisone from the adrenal cortex. Cushing's syndrome can be caused by tumors in the pituitary gland or the adrenal cortex. It can also be caused by prolonged administration of high dose corticosteroid medications, such as prednisone for transplant patients or for inflammatory disorders including asthma.

Signs and symptoms of Cushing's syndrome include:

·         Redistribution of body fat

·         Rounded "moon face"

·         Hump on the back of the neck ("buffalo hump")

·         Pendulous (hanging) abdomen

·         Thin, spindly extremities

·         Slow wound healing

·         Easily bruises

·         Hyperglycemia

·         Hypertension

Prehospital treatment of Cushing's syndrome is supportive in nature.

Addison's Disease

Addison's disease results from an insufficiency of glucocorticoids and aldosterone. The most common cause is atrophy of the adrenal tissue but it can also be caused by infections, infarctions, and AIDS.

Signs and symptoms of Addison's disease include:

·         Weakness

·         Weight loss

·         Anorexia

·         Nausea and vomiting

·         Diarrhea

·         Hyponatremia and hyperkalemia

·         Hypotension

·         Dehydration

·         Decreased cardiac output

·         Hyperpigmentation of skin that is exposed to the sun, pressure points, and mucous membranes

Treament is based on symptoms. The patient may be quite ill and possibly in hypovolemic shock. Monitor the ABC's, monitor vital signs including cardiac rhythm, provide high-flow oxygen, establish an IV of normal saline or Lactated Ringer's and administer fluid boluses to maintain blood pressure, and rapid transport to the nearest appropriate facility.

The endocrine system can have a variety of disorders which can make assessment and management difficult. Knowledge of the endocrine glands and their hormones can help the health care provider have a greater understanding of the patient's signs and symptoms and the appropriate management of endocrine emergencies.

Try our Diabetic Emergencies Quiz on the RAEMS Blog (here)