253 - Study Guide for Endocrine System
Terms in this set (32)
Describe diabetic ketoacidosis.
Caused by a profound deficiency of insulin and is characterized by hypergylcemia, ketosis, acidosis, and dehydration. When the circulation supply of insulin is insufficient, glucose cannot be properly used for energy so that the body breaks down fat stores as a secondary source of fuel. Ketones are acidic by-products of fat metabolism that can cause serious problems when they become excessive in the blood. Ketosis alters the pH balance, causing metabolic acidosis to develop. Ketonuria is a process that begins when ketone bodies are excreted in the urine. During this process, electrolytes become depleted as cations are eliminated along with the anionic ketones in an attempt to maintain electrical neutrality. Insulin deficiency impairs protein synthesis and causes excessive protein degradation. This result in nitrogen losses from the tissues. Insulin deficiency also stimulates the production of glucose from amino acids (from proteins) in the liver and leads to further hyper-glucosemia. Because there is a deficiency of insulin, the additional glucose cannot be used and the blood glucos level rises further, adding to the osmotic diuresis.
Who is at risk for DKA?
It is most likely to occur in people with type 1 diabetes but may be seen in type 2 conditions of severe illness or stress when the pancreas cannot meet the extra demand for insulin.
Describe the presentation of a patient with DKA.
Dry mouth, thirst, abdominal pain, nausea and vomiting, gradually increasing restlessness, confusion, lethargy, flushed, dry skin, eyes appear sunken, fruity breath odor of ketones, rapid, weak pulse, labored breathing (Kussmaul's), fever, urinary frequency, serum glucose over 300, glucosuria and ketoneuria.
Describe the assessment findings of a patient with DKA.
Dehydration such as poor skin turgor, dry mucous membranes, tachycardia, and orthostatic hypotension. Early symptoms include lethargy and weakness. As the patient becomes severly dehydrated the skin becomes dry and loose and the eyeballs become soft and sunken. Abdominal pain is another symtom of DKA that may be accompanied by anorexia and vomiting. Finally, Kussmaul respiration (rapid, deep breathing associated with dyspnea) are the body's attempt to reverse metabolic acidosis through the exhalations of excess carbon dioxide. Acetone is noted on the breath as a sweet, fruity odor. Laboratory finding include a blood glucose level above 300, serum bicarb level less than 15 and ketones in the blood and urine.
Describe the interventions you would expect for a patient with DKA.
- Ensure patent airway, administer oxygen via NC or non-rebreather mask.
- Establish IV access with large-bore catheter, begin fluid resuscitation with 0.9% NS 1L/hr until BP stabilized and urine output 30-60 ml/hr, begin continuous regular insulin drip 0.1 U/kg/hr.
- Identify history of diabetes, time of last food and time/amount of last insulin injection.
Describe the ongoing monitoring you would expect for a patient with DKA.
- Monitor V/S, LOC, cardiac rhythm, oxygen saturation, and urine output.
- Assess breath sound for fluid overload.
- Monitor serum glucose and serum potassium.
- Administer potassium to correct hypokalemia.
- Administer sodium bicarbonate if sever acidosis; pH < 7.0
What is HHNS (HHS/HHNK) and how is it managed?
Hyperosmolar hyperglycemic syndrome is a life-threatening syndrome that can occur in the patient with diabetes who is able to produce enough insulin to prevent DKA but not enough to prevent severe hyperglycemia, osmotic diuresis, and extracelluar fluid depletion. If often occurs in patient over 60 years of age with type 2 diabetes.
What is the relationship between hypocalcemia and thyroidectomy?
Hypocalcemia is a complication of throidectomy. Postoperative complications include hypothyroidism, damage to or inadvertent removal of parathyroid glands causing hypoparathroidism and hypocalcemia, hemorrhage, injury to the recurrent or superior laryngeal nerve, thyrotoxic crisis, and infection.
What are the manifestations of thyroid storm, and what interventions should the nurse be prepared to implement?
Thyroid storm is also called thyrotoxic crisis. This is an acute, rare condition in which all hyperthyroid manifestations are heightened. Although it is considered a life-threatening emergency, death is rare when treatment is vigorous and initiated early. The cause is thought to be stressors (trauma, infection, surgery) in a patient with preexisting hyperthyroidism, either diagnosed or undiagnosed. Manifestations include severe tachycardia, heart failure, shock, hyperthermia (up to 105.3), restlessness, agitation, seizures, abdominal pain, nausea, vomiting, diarrhea, delirium, and coma. Treatment is aimed at reducing circulating manifestations of this disorder by appropriate drug therapy. Supportive therapy is directed at managing respiratory distress, fever reduction, fluid replacement, and elimination or management of the initiating stressors.
What are the clinical manifestations of myxedema?
Patients with severe long-standing hypothyroidism may display myxedema, the accumulation of hydrophillic mucopolysaccharides in the dermis and other tissues. This mucinous edema causes the characteristic faces of hypothyroidism (i.e. puffiness, periobital edema, and masklike affect).
What happens in myxedema coma?
The mental sluggishness, drowsiness, and lethargy of hypothyroidism may progress gradually or suddenly to a notable impairement of consciousness or coma. This situation, termed myxedema coma, constitutes a medical emergency. Myxedema coma can be precipitated by infection, drugs (especially opiods, tranquilizers, and barbiturates), exposure to cold, and trauma. it is characterized by subnormal temperature, hypotension, and hypoventilation. For the patient to survive, vital functions must be supported and IV thyroid hormone replacement must be administered.
What causes diabetes insipidus?
DI is associated with a deficiency of production or secretion of ADH or a decreased renal response to ADH. The decrease in ADH results in fluid and electrolyte imbalances cause by increased urinary output and increased plasma osmolality. Depending on the cause, DI may be transient or a chronic lifelong condition.
Decreased antidiuretic hormones ---> Decreased water reabsorption in renal tubes ---> Decreased intravascular fluid volume ---> Increased serum osmolality (hypernatremia) and excessive urine output.
What is the characteristic feature of DI? What happens as a result?
The primary characteristic of DI is the excretion of large quantities of urine with a very low specific gravity and urine osmolality. Serum osmolality is elevated as a result of hypernatremia due to pure water loss in the kidney. Most patients compensate for fluid loss by drinking great amounts of water so that serum osmolality is normal or only moderately elevated. The patient may be fatigued from nocturia and may experience generalized weakness.
What are some causes of DI? What patients are at risk for developing DI?
CENTRAL DI (neurogenic):
- Problem results from an interference with ADH synthesis or release. Multiple cause include brain tumor, head injury, brain surgery, CNS infections.
- Problem results from inadequate renal response to ADH despite presence of adequate ADH. Caused by drug therapy (especially lithium), renal damage, or hereditary renal disease.
Problem results from excessive water intake. Caused by structural lesion in thirst center of psychologic disorder.
What signs and symptoms are associated with DI?
Central DI usually occurs suddenly with excessive fluid loss. After intracranial surgery, DI usually has a triphasic pattern: the acute phase, with abrupt onset of polyuria; and interphase, in which urine volume apparently normalizes; and a third phase, in which central DI is permanent.
What is the vasopressin test?
Because DI maybe central, nephrogenic, or psychogenic in origin, identification of the cause is the initial step. A complete history and physical is done. Psychogenic DI is associated with overhydration and hypervolemia rather than with dehydration and hypovolemia seen in other forms of DI. A water deprivation test is usually done to confirm the diagnosis of central DI. Before a water deprivation test is done, the patient's baseline weight, pulse, urine and plasma osmolalities, urine specific gravity, and blood pressure are obtained. All fluids are withheld for 8-16 hours. The patient may be anxious and should be reassured that the test will be stopped if fluid volume deficit becomes severe. The patient should be observed throughout the test because of the craving to drink. During the test, the patient's BP, weight, and urine osmolality are assessed hourly. The test continues until urine osmlality stabilizes or body weight declines by 3%, or orthostatic hypotension develops. ADH is then given, and urine osmolality is measured 1 hr later. In central DI, the rise in urinary osmolality after vasopressin exceeds 9%. Individuals with nephorgenic DI will have no response.
What type of IV fluids would you expect to use for a patient with DI?
Hypotonic saline or dextrose 5% in water is administered intravenously and titrated to replace urinary output.
What are the nursing considerations for the patient with DI?
Early detection, maintenance of adequate hydration, and patient teaching for long-term management, serum glucose should be monitored, accurate records of intake and output, urine specific gravity, daily weights, administration of DDAVP, assess for weight gain, headache, restlessness and signs of hyponatremia and water intoxication. The health care provider should be notified immediately if the individual with DI develops increased urine volume with low specific gravity because this indicates need for increase dosing of DDAVP, instruction in self-management, nasal irritation, nausea. The patient should be instructed to report any of these symptoms.
What are the 3 causes of excessive levels of ADH?
SIADH caused by malignant tumors, central nervous system disorders, and drug therapy.
What is the effect on serum sodium and osmolality with SIADH?
Plasma osmolality declines, sodium levels decline.
What the clinical signs and symptoms associated with SIADH?
Muscle cramps, weakness, initially; thirst, dyspnea on exertion, fatigue, and dulled sensorium, low urinary output and increased body weight. As the serum sodium level falls manifestations become more severe and include vomiting, abdominal cramps, muscle twitching, and seizures. As plasma osmolaltiy and serum sodium levels continue to decline, cerebral edema may occur, leading to lethargy, anorexia, confusion, headache, seizures, and coma.
What treatments are used for SIADH?
Treatment is directed at the underlying cause. Medications that stimulate the release of ADH should be avoided or discontinued. The immediate treatment goal is to restore normal fluid volume and osmolality. IF symptoms are mild and serum sodium is greater that 125, the only treatment may be restriction of fluid to 800-100 ml per day. In cases of severe hyponatremia, less that 120, especially in the presence of neurologic symptoms such as seizures, intravenous hypertonic saline may be administered. A diuretic such as furosemide (Lasix) may be used to promote diuresis. A fluid restriction 500 ml per day is also indicated for those with sever hyponatremia.
Addisonian crisis is a deficiency of both mineralocorticoids and glucocorticoids. What fluid and electrolyte imbalances result?
Hyperkalemia, hypochloremia, hypoglycemia, anemia, and increased blood urea nitrogen levels.
What might addsonian crisis develop?
Patients with adrenocortical insufficiency are at risk for an acute adrenal insufficiency (addisonian crisis), a life-threatening emergency caused by insufficient adrenocotical hormones or a sudden sharp decrease in these hormones. Addisonian crisis is triggered by stress (i.e. from infection, surgery, trauma, hemorrhage, or psychologic distress); the sudden withdrawal of corticosteroid hormone replacement therapy (which is often done by a patient who lacks knowledge of the importance of replacement therapy); after adrenal surgery; or following sudden pituitary gland destruction.
What interventions would you expect in the care of the patient in addisonian crisis?
Vital signs and signs of fluid volume deficit and electrolyte imbalance should be assessed every 30 minutes to 4 hours for the first 24 hours. Daily weights, diligent corticosteroid administration, protection against exposure to infection, complete assistance with daily hygiene should be practiced. The patient should be protected from noise, light and environmental temperature extremes. The patient cannot cope with these stressors because of the inability to produce corticosteroids.
Describe Cushing's syndrome.
This is a spectrum of clinical abnormalities caused by an excess of corticosteroids, particularly glucocorticoids. The most common cause is iatrogenic administration of exogenous corticosteroids. Other causes of Cushing's syndrome include adreanal tumors and ectopic ACTH production by tumors. It is more common in women 20-40 years old.
What are the characteristic physical changes in the patient with Cushing's syndrome?
Thinning hair, acne, red cheeks, buffalo hump on upper back, moon face, supraclavicular fat pod (fat around neck), increased body and facial hair, weight gain in middle section of body, purple striae, pendulous abdomen, ecchymosis resulting from easy bruising, slow wound healing, thin skin and subcutaneous tissue, thin extremities with muscle atrophy.
What information do you need to give a patient regarding daily use of cortisol?
Don't DC abruptly, monitor for signs and symptoms of infection, if diabetic, closely monitor glucose, get up slowly, avoid sick people, take early in the morning with food.
Phenochromocytoma - what is released by this tumor?
This is a tumor of the adrenal medulla that produces excessive catecholamines (epinephrine, norepinephrine).
List signs and symptoms of pheochromocytoma.
Severe, episodic hypertension accompanied by the classic manifestations of severe, pounding headache, tachycardia with palpitations, profuse sweating, and unexplained abdominal or chest pain.
Surgery is the treatment of choice. What type of postop care is required?
High doses of corticosteroids are administered IV during surgery and for several days afterward. Fluid intake and output are monitored carefully. Morning urine levels of cortisol (obtained at the same time each morning) are measured to evaluate the effectiveness of the surgery. The nurse must constantly be alert for signs of corticosteroid imbalance. After surgery the patient is usually maintained on bed rest until the BP stabilizes. The nurse must be alert for subtle signs of postoperative infections because the usual inflammatory responses are suppressed. BP fluctuations from catecholamine excesses tend to be severe and must be carefully monitored. Because hypertension may persist even when the tumor is removed, the nurse should stress the importance of follow-up care and routine BP monitoring.
What treatment is given for the patient who is not a candidate for surgery?
Metyrosine is used to diminish catecholamine production by the tumor and simplify chronic management.