CH 54 Endocrine System Saunders Flashcards

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1
Q

Addisons diseases

A

hyposecretion of the adrenal cortex hormones (glucocorticoid and mineralocorticoids) can be fatal if left untreated. Assessment includes: lethargy, fatigue, muscle weakness, GI disturbance, weight loss, menstrual changes, impotence, hypoglycemia, hyponatremia, HYPERkalemia, HYPERcalcemia, hypotension, hyper pigmentation with primary disease.

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2
Q

Addisons crisis is a

A

life threatening disorders caused by acute adrenal insufficiency
precipitated by stress, infection, trauma, surgery or abrupt withdrawal of exogenous corticosteroid use
can cause HYPOnatremia, HYPERkalemia, HYPOglycemia and shock. *prepare to administer glucocorticoid iv as prescribed; iv hydrocortisone sodium succinate is usually prescribed initially.

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3
Q

Cushings disease V. Cushings syndrome (hypercortisolism)

A

hyper secretion of cortisol from the adrenal cortex.

Cushings disease is a metabolic disorder characterized by increased secretion (endogenous) of cortisol, caused by increased amount of ACTH secreted by the pituitary gland.
Cushings syndrome is a metabolic disease resulting from the chronic and extensive production of cortisol by the adrenal cortex or by the administration of glucocorticoids in large doses for sever weeks or longer.

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4
Q

Primary hyperaldosteronism (Conn’s syndrome)

A

hypersecretion of mineralocorticoids (aldosterone) from the adrenal cortex of the adrenal glands, most commonly caused by an adenoma. Assessment, symptoms r/t hypokalemia, hypernatremia, and hypertension. polydipsia, polyuria paresthesias, visual changes, low urine specific gravity.
Monitor vital signs. Spironolactone (aldactone) may be prescribed to promote fluid balance and control hypertension.

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5
Q

Pheochromocytoma

A

a catecholamine-producing tumor usually found in the medulla, but extra-adrenal locations include the chest, bladder, abdomen, and brain, typically benign but can become malignant.
excessive amount of epi and norepi are secreted
diagnostic test include a 24 hour urine collection for vanillymandelic acid (VMA) a product of catecholamines. normal levels are 14mcg/mL with higher levels occurring in pheochromocytoma. Surgical removal of adrenal gland is primary treatment.
Assessment; paroxysmal or sustained hypertension, severe headaches, palpitations, flushing and profuse diaphoresis, pain in the chest or abdomen with n/v, heat intolerance, weightless, tremors, hyperglycemia.
* for a client with pheochromocytoma, avoid stimuli that can precipitate a hypertensive crisis, such as increased abdominal pressure and vigorous abdominal palpitation.

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6
Q

hypothyroidism

A

results from hypo-secretion of thyroid hormones T3 and T4 and is characterized by a decrease rate of the body metabolism.
Assessment: lethargy, fatigue weakness, muscle aches, paresthesias, intolerance to cold, weight gain, dry skin and hair and loss of body hair, bradycardia constipation, generalized puffiness and edema around the eyes and face (myxedema) forgetfulness and loss of memory, menstrual disturbance, cardiac enlargement, tendency to develop hf, goiter may or may not be present.
interventions: administer thyroid replacement, levothyroxine sodium (synthroid) is most commonly prescribed.

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7
Q

myxedema coma

A

rare but serious disorder result from persistently low thyroid production.
Coma can be precipitated by acute illness, rapid withdrawal of thyroid medication, anesthesia and surgery, hypothermia, or the use of sedatives and opioid analgesics.
*Monitor for hypoglycemia, hypotension, brady, hypothermia, hyponatremia, edema, respiratory failure and coma.

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8
Q

Hyperthyroidism

A

results from hyper secretion of thyroid hormone T3 and T4. characterized by an increased rate of body metabolism. A common cause of graves disease, also known as toxic diffuse goiter. Clinical manifestation are referred to as thyrotoxicosis.
Assessment: personality changes such as irritability, agitation and mood swings, nervousness, and fine tremors of the hand, heat intolerance, weight loss, smooth soft skin and hair, palpitation, cardiac dysrhythmias, such as tachy and afib, diarrhea, protruding eyeballs, diaphoresis, hypertension, enlarged thyroid gland (goiter)
Intervention: administer antithyroid medications (propylthiouracil, PTU) that block thyroid synthesis as prescribed. administer iodine preparations that inhibit the release of thyroid hormone as prescribed.
administer propranolol foor tachy as prescribed.
prepare the client for radioactive iodine treatments or thyroidectomy if prescribed.

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9
Q

Thyroid storm

A

is an acute life threatening condition that occurs in client with uncontrollable hyperthyroidism. It can be caused by manipulations of the thyroid gland during surgery and the release of thyroid hormone into the blood stream; it can occur from severe infection and stress.
antithyroid medication, beta-blockers, glucocorticoids and iodides may be administered to the client before thyroid surgery to prevent its occurrence.
Use cooling blanket to decrease temperature as prescribed. Removal of thyroid gland maybe necessary.
* after removal of thyroid gland (thyroidectomy) maintain the client in the semi-Fowlers position. Monitory the surgical site for edema and for signs of bleeding and check the dressing anteriorly at the back of the neck.

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10
Q

hypoparathyroidism

A

a condition caused by hypo-secretion of parathyroid hormone by the parathyroid gland. can occur following thyroidectomy.
Assessment. hypocalcemia and hyperphospatemia, numbness and tingling of the face, muscle cramps and cramps of the abdomen or in the extremeties. Positive trousseau’s sign or chvostek’s sign. Signs of overt tetany, such as bronchospasm, laryngospasm, carpopedal spasm, dysphagia, photophobia, cardiac dysrhythmias, seizures, hypotension, anxiety, irritability, depression.
Interventions monitor v/s. monitor for signs of hypocalcemia and tetany, initiate seizure precaution, teachetomy set, sx on bedside. High calcium low phosphorus diet

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11
Q

Trousseau’s sign

A

A sign of latent TETANY. A SPHYGMOMANOMETER cuff is applied to the upper arm and inflated. Within 4 minutes the forearm muscles go into spasm.

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12
Q

Chvostek’s sign

A

Chvostek’s sign is the twitching of the facial muscles in response to tapping over the area of the facial nerve.

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13
Q

hyperparathyroidism

A

assessment: hypercalcemia and hypophosphatemia, fatigue, muscle weakness, skeletal pain and tenderness, bone deformities that result in pathological fractures, anorexia, n/v, epigastric pain, weight loss, constipation, hypertension, cardiac dysrhythmias, renal stones
interventions: monitor v/s, i/o, administer furosemide as prescribed to lower calcium levels, administer calcitonin as prescribed to decrease skeletal calcium release and increase renal exertion of calcium, monitor calcium and phosphorus levels, prepare the client for parathyroidectomy as prescribed.

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14
Q

postoperative interventions for parathyroidectomy

A

monitory for respiratory distress. Have a trachemotomy set, oxygen, and suction at the bedside. Limit client talking and assess for level of hoarseness. monitory of laryngeal nerve damage as evidenced by respiratory obstruction, dysphonia, high-pitched voice, stridor, dysphagia and restlessness. Monitory for signs of hypocalcemia, tetany, which can be caused by trauma to the parathyroid gland. Prepare to administer calcium gluconate as prescribed for tetany. Monitory for thyroid storm. * After removal of thyroid gland (thyroidectomy) maintain the client in the semi-Fowlers position.

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15
Q

Signs of tetany

A

cardiac dysrhythmias, corpopedal spasm, dysphagia, muscle and abdominal cramps, numbness of tingling of the face and extremities, positive chvostek’s sign, trousseaus sign, photophobia, wheezing and dyspnea (bronchospasm, laryngospams) seizures.

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16
Q

Diabetes mellitius

A

chronic disorder of impaired carb, proteins and lipid metabolism caused by deficiency of insulin
an absolute or relative deficiency of insulin results in hyperglycemia.

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17
Q

Type 1 DM is nearly absolute deficiency of

A

insulins (primary beta cell destruction); if insulin is not given, fats or metabolized for energy resulting in ketonemia (acidosis.)

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18
Q

Type 2 DM is relative lack of

A

insulin or resistance to the action of insulin; usually, insulin is sufficient to stabilize fat and protein metabolism but not carbohydrate metabolism.

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19
Q

metabolism syndrome is also known as

A

syndrome X and the individual has coexisting risk factors for developing type 2 DM; these risk factors include abdominal obesity, hyperglycemia, hypertension, high triglyceride levels, and lowered HDL cholesterol levels.

20
Q

Exercise and DM

A

Exercise lowers blood glucose levels, encourages weight loss, reduces cv risk, improves circulation and muscle tone, decreases total cholesterol and triglyceride levels and decreases insulin resistance and glucose intolerance.
Instruct the client that dietary adjustments during exercise is very individualized. If the client requires extra food during exercise to prevent hypoglycemia, it need not be deducted form the regular meal plan. If the blood glucose level is higher than 250mg/dL and urinary ketones are present (type 1 DM), the client is instructed not to exercise until the blood glucose levels is closer to normal and urinary ketones are absent.
*Instruct a person with DM to monitor blood glucose levels before, during and after exercising.

21
Q

Oral hypoglycemic medication: oral medications are prescribed for clients with DM type 2

A

when diet and weight control therapy have failed to maintain satisfactory blood glucose levels.
*Pts taking sulfonylurea should not consume alcohol

22
Q

Insulin

A

is used to treat type 1&2 DM when diet and weight control and oral hypoglycemic agents have failed. Illness, infection and stress increase the blood glucose levels and the need for insulin. Insulin should not be withheld during illness, infection or stress because hyperglycemia and DKA can result. The peak action time of insulin is important to explain to the pt because of the possibility of hypoglycemic reactions occurring during this time.
* Only short-duration (lispro, aspart, glulsine, ,and regular insulin) can be administered IV

23
Q

Lipohypertrophy

A

is the development of fibrous fatty masses at the injection site and is caused by repeated us of an injection site. P 651

24
Q

dawn phenomenon

A

is the result from reduced tissue sensitivity to insulin ad usually develops between 5-8am; it may be caused by the nocturnal release of growth hormone. Treatment includes administering an evening dose of intermediate acting insulin at about 10pm

25
Q

Somogyi phenomenon

A

normal or elevated blood glucose levels are present at bedtime; hyperglycemia occurs at around 2-3am which causes an increase in the production of counterregulatory hormones. By 7am the blood glucose rebound significantly to the hyperglycemia range. Treatments includes decreasing the evening (predinner or bedtime) dose of intermediated-acting insulin or increasing the bedtime snack

26
Q

lipoatrophy

A

is the loss of subcut fat and appears as slight dimpling or more serious pitting of subcut fat; the use of human insulin helps prevent this complication. P 651

27
Q

Insulin pumps

A

is a subcut insulin infusion administered by an externally worn device containing a syringe attached to along thin narrow lumen tube with a needle or teflon catheter attached to the end. Pt. inserts the cath into the subcut tissue and secures it with tape and should be change q2-3 days. A continuous basal rate of insulin is infused and the client can deliver bolus before each meal. BOTH rapid-acting insulin and regular short acting insulin are appropriate for use in the pumps.

28
Q

Insulin pump and skin sensor devices

A

monitor the clients blood glucose continuously, the information is transmitted to the pump, determines the need for insulin and then the insulin is injected.

29
Q

Urine testing and diabetes

A

Urine testing is not reliable indicator of the blood glucose level and is not used for monitoring purposes.
Instruct the client in the procedure for testing for urine ketones
The ketones may indicated impending ketoacidosis.
Urine ketone testing should be performed during illness and whenever the client with type 1 DM has persistently elevated blood glucose levels (higher than 24-mg/dL or as prescribed for two consecutive test periods.)

30
Q

Priority nursing actions for hypoglycemia

A
  1. check the clients blood glucose level
  2. give the client a 10-15g carbohydrate item such as 1/2 cup of sugar.
  3. take the clients vital signs
  4. retest blood glucose levels
  5. give the client a small snack of carbohydrate and protein.
  6. document the clients complains, actions taken, and outcome.
31
Q

What is hypoglycemia

A

occurs when the blood glucose levels falls below 70mg/dL or when the blood gluocse levels drops to rapidly from an elevated level.
hypoglycemia is caused by too much insulin or oral hypoglycemic agents, too little food, or excessive activity.
the client should be instructed to always carry fast acting simple carbs
if the clients does not have simple carbs, and available food should be eaten.

32
Q

mild hypoglycemia

A

the client remains fully awake but displays adrenergic symptoms; (hunger, tremors, tachy, nervous) the blood glucose levels is usually lower than 60 mg/dL.
intervention: administer 15g of fast acting simple carbohydrates (4-6 hard candys, 4 tsp of sugar etc.) P 653. Repeat test in 15 minutes and repeat if neseccary.

33
Q

moderate hypoglycemia

A

the client displays symptoms of worsening hypoglycemia; (confusion double visions, headache, impaired coordination) the blood glucose level is usually lower than 40mg/dL
intervention: Administer 15-30 g of fast acting simple carbs. Administer additional food such as low fat milk after 10-15 minutes.

34
Q

sever hypoglycemia

A

the client displays sever neuropglycopenic symptoms; the blood glucose level is usually lower than 10mg/dL.
intervention: If pt is unconscious and cannot swallow an injection of glucagon is administered IM or subcut. Administer a second dose in 10 minutes if pt remains unconscious. When pt wakes give pt small meal as long as the pt is not nauseated. The NCP is notified if a sever hypoglycemic reaction occurs. Family members should be instructed about he administration of glucagon.

35
Q

DKA definition and mainifestation

A

is a life threatening complication of type 1 DM that develops with a sever insulin deficiency occurs. Main clinical manifestation include hyperglycemia, dehydration, ketosis, and acidosis.

36
Q

Kussmaul breathing

A

is a deep and labored breathing pattern often associated with severe metabolic acidosis, particularly diabetic ketoacidosis (DKA) but also kidney failure.

37
Q

DKA interventions

A

Restore the circulating blood and protect from cerebral, coronary and renal hypo-perfusion.
Treat dehydration with rapid IV infusion of .9 or .45 NS as prescribed; dextrose is added to IV fluids when the blood glucose levels reaches 250-300 mg/dL/
Treat hyperglycemia with insulin administered IV as prescribed. Correct electrolyte imbalance. (K may be elevated as a result of dehydration and acidosis)

38
Q

Insulin IV administration during DKA

A

use short-duration insulin only. An IV bolus dose of insulin (usually 5-10 unites) may be prescribed for continuous infusion is begun. Mix the prescribed IV dose of insulin for continuous infusion of .9 or .45 NS as prescribed. Flush the insulin solution through the enitre IV inufusion set and discard the first 50-100mL of slution before connecting and administering it the pt (the insulin molecules adhere to the plastic IV infusion set.) Always place the insulin infusion on an IV infusion controller. Insulin is infused continuously until subcut administration resumes to prevent rebound blood glucose levels.

Monitor v/s. monitor i/o. monitor K. K will fall rapidly within first hour of treatment as the dehydration and acidosis are treated. K is administer IV in a diluted solution when K reaches normal levels to prevent hypokalemia; * ensure adequate renal function before administering K.

39
Q

Why do we monitor clients with DKA closely for signs for increased ICP.

A

if blood glucose falls too far or too fast before the brains has to to equilibrate, water is pulled from the blood to the CSF and the brain, causing cerebral edema and increased ICP

40
Q

What is hyperglycemic hyperosmolar nonketotic syndrome (HHNS)

A

extreme hyperglycemia occurs without ketosis or acidosis. Most often occurs with type 2 DM. The major difference between HHNS and DKA is that ketosis and acidosis do not occur with HHNS; enough insulin is present with HHNS to prevent the break down of fats for energy, thus preventing ketosis.

41
Q

Treatment for HHNS

A

is very similar to DKA. Fluid and electrolyte correction is important along with insulin administration. However, rehydration alone may decrease glucose levels enough.

42
Q

Assessment and interventions for diabetic nephropathy

A

Assessment: microalbuminuria, thirst, fatigue, anemia, weight loss, signs of malnutrition, frequent UTI, sings of neurogenic bladder
Intervention: early prevention measures include control of hypertension and blood glucose levels. Monitor v/s, monitor blood urea nitrogen, creatinine and urine albumin levels. Restrict dietary protein, sodium and K.

43
Q

Preoperative care for diabetic client undergoing surgery

A

Check with HCP about withholding oral hypoglycemic medication or insulin. Some long acting oral anti diabetic meds are discontinued 24-48 presurgery.
Metformin (glucophage) may be discontinued 48 before surgery and may not be restarted until renal function is normal postop. Insulin dose may be adjusted or withheld if the Iv insulin administration during surgery is planned. Monitor blood glucose and administer IV fluids as prescribed.

44
Q

Intraoperative care for diabetic client undergoing surgery

A

monitor blood glucose frequently. Administer IV short- or rapid-acting insulin as prescribed to maintain blood glucose levels lower than 200 mg/dL.

45
Q

Postoperative care for diabetic client undergoing surgery

A

Administer IV glucose and insulin infusion as prescribed based on blood glucose results. Administer supplement short-acting insulin as prescribed. Moniotr blood glucose levels frequently if the client is recieving parenteral nutrition. PT is at higher risk for cardiovascular, impaired wound healing and renal complications post op.