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endocrine med surge 2

Terms in this set (111)

Causes include: noncompliance with insulin; alcohol; illness or infection; steroids or thiazide diuretic use; pancreatitis; liver failure; trauma; surgery.

Cascade: Insufficient insulin => hyperglycemia => osmotic diuresis (more water enters the kidneys and is turned into urine in attempt to get rid of glucose in the blood) => glycosuria (glucose in the urine), dehydration (increased voiding), and electrolyte imbalance (potassium, sodium, CO2, bicarb) => breakdown of glycogen in liver is activated, but synthesis into glucose is inhibited => impaired glucose uptake in adipose tissue causes impaired synthesis and release of free fatty acids into the blood => excessive free fatty acids enter liver, where they are unable to be synthesized and ketoacidosis worsens
Classic signs of DKA include: hyperglycemia (blood glucose over 300 and frequently over 500), dehydration, and acidosis (pH <7.35), increased anion gap.
Ketoacidosis is reflected in low serum bicarb (less than 15), low pH (less than 7.35), ketones in blood and urine. Sometimes a low pCO2 reflects respiratory compensation with Kussmaul respirations (fast, shallow) to blow off CO2 in an attempt to increase bicarb and pH. Electrolytes will vary according to the level of dehydration, but before insulin treatment can be started potassium and sodium must be evaluated. There may be an increase in creatinine, hematocrit, and BUN, especially if dehydration caused an acute kidney injury. Initially patients may have hyperkalemia that quickly progresses to hypokalemia. 1/3 of patients have hypocalcemia.

A common lab to confirm DKA is beta-hydroxybutyrate (referred to beta-hydroxy); this can help differentiate between nonDKA and DKA.

When a patient is in DKA, they WILL be in critical care because of fluctuating and frequent checking of electrolytes and changing of fluids based upon electrolytes and blood sugar. Patients can be on d5w, 0.9%NS, d5w0.9%NS, d5w0.45%NS, 0.45%NS, d5w0.9%NS20meqK, d5w0.45%NS20meqK, 0.9%NS20meqK, or 0.45%NS20meqK depending on their potassium, sodium, and blood glucose level.

Rehydration causes increased plasma volume, which decreases potassium concentration. Insulin causes potassium to shift from extracellular fluid into cells.
It is the treatment of choice for thyroid cancer. Occasionally radioactive iodine is used to minimize metastasis.

-Prior to surgery, focus on reducing stress and anxiety to avoid causing a thyroid storm.
-Postop care:
-monitor respirations for potential airway impairment
-monitor for potential bleeding and hematoma formation, check the posterior dressing
-assess pain and provide pain relief measures
-semi-fowler position, support head and neck
-assess voice and discourage talking
-assess for hypocalcemia related to injury or removal of parathyroid glands (refer to chart 52-6)
-Observe for Chvostek sign where a sharp tapping over the facial nerve just in front for the parotid gland and anterior to the ear causes spasm or twitching of the mouth, nose, and eye. It can be seen after a thyroidectomy and results from hypocalcemia. It manifests as numbness and tingling in the hands, soles of feet, and around the lips. It develops between 24 and 48 hours after surgery. A positive Chvostek sign is twitching of the facial muscles on the same side being tapped, which represents neuromuscular excitability from hypocalcemia.

-Provide dietary guidance to meet patient's metabolic needs
-Avoid caffeine beverages and other stimulants
-Explain tests and procedures
-Support the head and neck after surgery
-Explain that after surgery, patient's are hypothyroid and will need to take levothyroxine for the remainder of their life to prevent hypothyroidism. Levothyroxine is the synthetic version of the thyroxine (T4).
The parathyroid glands are four glands on the posterior thyroid gland.

Parathormone regulates calcium and phosphorus balance. Increased parathormone elevates blood calcium by increasing calcium absorption from the kidney, intestine, and bone. Parathormone lowers phosphorus levels.

Hyperparathyroidism occurs 2-4 times more often in women. The patient may have no symptoms or may signs and symptoms from various body system involvement, such as apathy, fatigue, muscle weakness, N/V, constipation, hypertension, and cardiac dysrhythmias. It can result in pathologic fractures due to the release of calcium and phosphate into the blood, which decreases bone density. Treatment is surgical removal of abnormal parathyroid tissue and hydration.

Hypercalcemic crisis occurs with extreme elevation of serum calcium levels causing neurologic, cardiovascular, and renal symptoms that can be life threatening. Treatment is rapid rehydration with large volumes of IV isotonic saline fluids and administration of calcitonin and corticosteroids in emergencies to reduce serum calcium levels by increasing calcium deposition in bone.

Hypoparathyroidism has several potential causes, such as:
-abnormal parathyroid development
-destruction of the parathyroid glands through surgical removal or autoimmune response
-vitamin D deficiency
It can present with tetany, numbness, tingling in extremities, stiffness of hands and feet, bronchospasm, laryngeal spasm, carpopedal spasm, anxiety, irritability, depression, delirium, and ECG changes.
A carpopedal spasm is induced by occluding the blood flow to the arm for 3 minutes with a blood pressure cuff, this is Trousseau sign.
Tetany is general muscle hypertonia, with tremor and spasmodic or uncoordinated contractions occurring with or without efforts to make voluntary movements.

Management involves:
-increasing serum calcium level to 9-10mg/dL
-administering calcium gluconate IV
-administering pentobarbital to decrease neuromuscular irritability
-administer parathormone, but watch for potential allergic reactions
-keep patients in a quiet environment ensuring no drafts, bright lights, or sudden movement
-provide a diet high in calcium and low in phosphorus
-maintain vitamin D levels

Calcium, magnesium, and vitamin D levels are decreased in hypoparathyroidism. Phosphorus levels are increased.
The adrenal glands sit on top of the kidneys.

The adrenal medulla functions as part of the autonomic nervous system. It is responsible for catecholamines, epinephrine, and norepinephrine.

The adrenal cortex is responsible for glucocorticoids, mineralocorticoids, and androgens.

Addison disease is adrenocorticortical insufficiency. The adrenal glands are suppressed by exogenous steroid use. It presents as muscle weakness, anorexia, GI symptoms, fatigue, dark pigmentation of skin and mucosa, hypotension, low blood glucose, low serum sodium, high serum potassium, apathy, emotional lability, and confusion.

Addisonian crisis

-To check for adrenal insufficiency or Addison disease, we look at adrenocortical hormone levels, ACTH (adrenocorticotropic hormone) levels, and ACTH stimulation test.
-Monitor your patient for any illness or stressors that precipitate problems.
-Monitor fluid and electrolyte status, vitals signs, and orthostatic blood pressures.
-Observe for signs and symptoms related to adrenal insufficiency, such as weight changes, muscle weakness, fatigue
-Note medications patient has been taking; administer medications as prescribed (ie appropriate steroid dose and taper)
-Monitor for signs and symptoms of Addisonian crisis; when in crisis, perform all activities for patient.

Educate your patient that stopping steroids abruptly can cause adrenal insufficiency.

Cushing syndrome is due to excessive adrenocortical activity or ACTH (growth hormone) that creates too much cortisol. Often Cushing syndrome is caused by a benign pituitary tumor releasing too much ACTH. The classic signs are central-type obesity with a "buffalo hump" and "moon face." Additional signs and symptoms include hyperglycemia, heavy trunk with thin extremities, fragile and thin skin, ecchymosis, striae, weakness, lassitude, sleep disturbances, osteoporosis, muscle wasting, hypertension, acne, infection, slow healing, virilization in women (development of male characteristics- hair growth), loss of libido, mood changes, increased serum sodium, decreased serum potassium.

To test for Cushing, a dexamethasone suppression test is done. If suppressing the activity of the adrenal glands decreases or reverses symptoms, then Cushing is likely the diagnosis.

-Encourage mild activity and ability to perform self-care
-Observe skin and changes in physical appearance in response to interventions
-Evaluate mental function and emotional status
-Administer medications as prescribed, ensure steroid tapering

Corticosteroid therapy suppresses inflammation and autoimmune response, controls allergic reactions, and reduces transplant rejection.

Make sure doses are timed appropriately and tapering is initiated prior to discontinuation. Monitor for potential side effects and implement measures to reduce side effects.
-Urine will look dark and foamy, which indicates the kidneys are filtering excess bilirubin from the blood.
-fat-soluble vitamin deficiency
-fatty stools because of inflammation in the gallbladder obstructing bile from entering the bowel and breaking down fat.
-Dietary management, ie reduced fat/cholesterol
-Medications: ursodeoxycholic acid and chenodeoxycholic acid
-Laparoscopic cholecystectomy
-nonsurgical stone removal
After surgery, maintain a low-fowler position; keep NPO until bowel sounds return, then introduce a soft, low-fat, high-carb diet
Make sure to assess respiratory status, nutritional status, potential bleeding. Observe for GI symptoms such as lack of appetite, vomiting, pain, distention, fever.
With chronic cholecystitis, make sure to tell patients to avoid foods high in fat. Ingestion of fat requires the gallbladder to release bile to break down the fat, a diet high in fat causes more episodes of biliary colic because the gallbladder is being stimulated to release more bile.

After surgery, if a patient reports pain, things you can do as a nurse to relieve pain includes giving a back rub, use incisional splinting, and changing the patient's position. Make sure to follow-up on their pain score to make sure it is improving. You can also administer prescribed pain medication, but assess if what you've given alleviates their pain to a tolerable level.

Jackson-Pratt drain. Only a surgeon can remove a JP drain, so make sure the drain is secured to the patient's gown to decrease tension and keep the weight of the bulb from pulling on the drain. Make sure to measure the output hourly after surgery and empty it when it is full.
Acute: pancreatic duct becomes obstructed and enzymes back up, causing autodigestion and inflammation of the pancreas
-Typically presents with fever, jaundice, confusion, agitation, ecchymosis in flank or umbilical area, and abdominal guarding
-Typically receive protonix or pantoprazole, a proton pump inhibitor, to decrease gastric acid production and decrease pancreatic secretions.
-Patients should be NPO to limit GI activity and stimulation of the pancreas, which decreases pain. Patients are usually on bedrest also to decrease metabolic rate and secretion of pancreatic enzymes.

-Chronic: progressive, inflammatory disorder with pancreas destruction; cells are replaced with fibrous tissue; pressure increases within the pancreas and obstructs the pancreatic and common bile ducts; refer to chart 50-3
-Typically presents with recurrent attacks of severe upper abdominal and back pain accompanied with vomiting
-prescribed pancrelipase as an enzyme replacement, but this is not recommended in acute pancreatitis. Pancrelipase is used to increase digestion of fats, carbs, and proteins. Patients will see a decrease of fat in stools.

Complications of pancreatitis include: fluid and electrolyte disturbances, necrosis of the pancreas, shock, multi-organ dysfunction syndrome (MODS), and disseminated intravascular coagulation (DIC)

Tumors of the pancreas include: pancreatic cysts and pancreatic cancer
Refer to your book for risk factors and sites for lesions for pancreatic cancer. Treatment may be palliative, but can also include chemotherapy, radiation, and surgery.
Manifestations (depends on level of hyperglycemia):
-fatigue, weakness, vision changes, tingling or numbness in hands or feet, dry skin, skin lesions or wounds that are slow to heal, recurrent infections

-Fasting blood glucose 126 mg/dL or higher
-Casual glucose exceeding 200 mg/dL
-Refer to chart 51-2 for American Diabetic Association diagnostic criteria

-Goal is to normalize insulin activity and blood glucose levels to reduce complications
-ADA recommends Hgb A1c less than 7%
-5 management components:
1. Nutritional therapy
-Part of nutritional therapy is ensuring adequate fluid intake, especially during acute illness, to prevent dehydration and build-up of ketones. Control of total caloric intake is necessary to maintain a reasonable body weight. Another goal is to normalize lipids and blood pressure to prevent heart disease. Educate clients to combine starchy foods with protein and fat to slow absorption and glycemic response. Educate about the impact of alcohol, nutritive and nonnutritive sweeteners, and misleading food labels.
-Consider food preferences, lifestyle, usual eating times, and cultural and ethnic backgrounds. Carbs should make up 50-60% of calorie distribution throughout the day; fat 30%; encourage nonanimal sources of protein with fiber. Table 51-2 has an exchange list for meal planning.

2. Exercise- lowers blood sugar, aids weight loss, eases stress, lower cardiovascular risks; Chart 51-4
-Exercise elevates blood sugar and insulin must be adjusted.
-Patients should eat a 15-g carb snack before moderate exercise when insulin dependent to prevent hypoglycemia; refer to Chart 51-5
3. Monitoring
-Patients should test their urine for ketones and report them. Ketonuria indicates the body does not have enough glucose for energy and is breaking down fats to provide glucose to cells.
4. Pharmacologic therapy
- Insulin therapy
-Oral antidiabetic agents are used for type 2 diabetics requiring more than diet and exercise
5. Education
-Nurses should educate patients and their families not to withhold insulin when a patient feels sick because acute illness causes elevated blood glucose levels. Patients should be instructed to call their provided if their blood glucose levels are greater than 250 mg/dL so treatment can be adjusted before injury occurs.