Endocrine Problems

Question 1

Endocrine Glands: Function and risk factors for problems

Answer 1

Endocrine Glands:
- Adrenal, Hypothalamus, Ovaries, Pancreas, Parathyroid, Pituitary, Testes, Thyroid.
Function:
- maintenance and regulation of vital functions, response to stress and injury, growth and development, energy metabolism, reproduction, fluid, electrolyte, and acid-base balance.
Risk Factors:
- age, heredity, congenital factors, trauma, environmental factors, consequence of other health problems or surgery.

Question 2

Hypothalamus

Answer 2

• portion of the diencephalon of the brain, forming the floor and part of the lateral wall of the third ventricle.
• activates, controls, and integrates the peripheral autonomic nervous system, endocrine processes, and many somatic functions, such as body temp, sleep, and appetite.
• hormones: corticotropin-releasing hormone (CRH); gonadotropin-releasing hormone (GnRH); growth hormone-inhibiting hormone (GHIH); growth hormone-releasing hormone (GHRH); melanocyte-inhibiting hormone (MIH); prolactin-inhibiting hormone (PIH); thyrotropin-releasing hormone (TRH).

Question 3

Pituitary Gland

Answer 3

• the master gland; located at the base of the brain.
• influenced by the hypothalamus; directly affects the function of the other endocrine glands.
• promotes growth of body tissue, influences water absorption by the kidney, and controls sexual development and function.
• anterior lobe production: adrenocorticotropic hormone (ACTH), follicle-stimulating hormone (FSH), growth hormone (GH), luteinizing hormone (LH), melanocyte-stimulating hormone (MSH), prolactin (PRL), somatotropic growth-stimulating hormone, thyroid-stimulating hormone (TSH).
• posterior lobe: oxytocin, vasopressin (antidiuretic hormone ADH). These hormones are produced by the hypothalamus, stored in the posterior lobe, and secreted into the blood when needed.

Question 4

Adrenal Gland

Answer 4

• one on top of each kidney; regulates sodium and electrolyte balance; affects carbohydrate, fat, and protein metabolism; influences the development of sexual characteristics; and sustains the fight-or-flight response.
• adrenal cortex: is the outer shell of the adrenal gland; synthesizes glucocorticoids and mineralocorticoids and secretes small amounts of sex hormones (androgens, estrogens).
• adrenal medula: is the inner core of the adrenal gland; works as part of the sympathetic nervous system and produces epinephrine and norepinephrine.

Question 5

Glucocorticoids and Mineralocorticoids

Answer 5

Glucocorticoids:
- cortisol, cortisone, corticosterone
- responsible for glucose and protein metabolism
- responsible for fluid and electrolyte balance
- suppression of the inflammatory response to injury
- protective immune response to invasion by infectious agents
- resistance to stress
Mineralocorticoids:
- aldosterone
- regulation of electrolyte balance by promoting sodium retention and potassium excretion.

Question 6

Thyroid and Parathyroid glands

Answer 6

Thyroid gland:
- located in the anterior part of the neck; controls the rate of body metabolism and growth and produces thyroxine (T4), triiodothyronine (T3), and thyrocalcitonin
Parathyroid glands:
- located on the thyroid gland; controls calcium and phosphorus metabolism; produces parathyroid hormone.

Question 7

Pancreas

Answer 7

• located posteriorly to the stomach;
• influences carbohydrate metabolism, indirectly influences fat and protein metabolism, and produces insulin and glucagon.

Question 8

Ovaries and Testes

Answer 8

• the ovaries are located in the pelvic cavity and produces estrogen and progesterone.
• the testes are located in the scrotum, control the development of the secondary sex characteristics, and produce testosterone.

Question 9

Negative-feedback loop

Answer 9

• regulates hormone secretion by the hypothalamus and pituitary gland.
• increased amounts of target gland hormones in the bloodstream decrease secretion of the same hormone and other hormones that stimulate its release.

Question 10

Diagnostic Tests: Stimulation tests

Answer 10

• in a client with suspected under-activity of an endocrine gland, a stimulus, measured amounts of selected hormones or substances, may be provided to stimulate the target gland to produce its hormone, therefore determining whether it is capable of normal hormone production.
• hormone levels produced by the target gland are measured.
• failure to of the hormone level to increase indicates hypofunction.

Question 11

Diagnostic Tests: Suppression tests

Answer 11

• used when hormone levels are high or in the upper range of normal.
• agents that normally induce a suppressed response are adm to determine whether normal negative feedback is intact.
• failure of hormone production to be suppressed indicates hyperfunction.

Question 12

Diagnostic Tests: Overnight dexamethasone suppression test

Answer 12

• used to distinguish between Cushing’s syndrome and Cushing’s disease.
• in Cushing’s disease the source of excess cortisol is the pituitary gland rather than the adrenal cortex or exogenous corticosteroid adm.
• dexamethasone, a potent long-acting corticosteroid given at bedtime, should suppress the morning cortisol in clients without the disease by suppressing adrenocorticotropic hormone (ACTH) production; in the client with disease, this suppression will not occur.

Question 13

Diagnostic Tests: Radioactive iodine uptake

Answer 13

• measures the absorption of an iodine isotope to determine how the thyroid gland is functioning.
• a small dose of radioactive iodine is given by mouth or IV; the amount of radioactivity is measured in 2-4h and again at 24h.
• normal values are approx 3-10% ate 2-4h and 5-30% in 24h.
• elevated values indicate hyperthyroidism, decreased iodine intake, or increased iodine excretion.
• decreased values indicate a low T4 level, the use of antithyroid meds, thyroiditis, myxedema, or hypothyroidism.
• contraindicated in pregnancy.

Question 14

Diagnostic Tests: T3 and T4 resin uptake test

Answer 14

• used to diagnose thyroid disorders.
• T3 and T4 regulate thyroid-stimulating hormone.
  Normal values (lab variations):
  = total T3: 110.4 to 337.7 ng/dL (1.7 to 5.2 pmol/L)
  = total T4: 5 to 12 mcg/dL (64 to 154 nmol/L)
  = Thyroxine, free (FT4): 0.8 to 2.8 ng/dL (10 to 36
  pmol/L).
• the T4 level is elevated in hyperthyroidism and decreased in hypothyroidism.

Question 15

Diagnostic Tests: Thyroid-stimulating hormone

Answer 15

• blood test used to differentiate the diagnosis of primary hypothyroidism.
• normal value is 2-10 mclU/mL (mlU/L).
• elevated values indicate primary hypothyroidism.
• decreased values indicate hyperthyroidism or secondary hypothyroidism.

Question 16

Diagnostic Tests: Thyroid scan

Answer 16

• performed to identify nodules or growths in the thyroid gland.
• a radioisotope of iodine or technetium is adm before scanning.
• determine whether the client has received radiographic contrast agents within the past 3 months, because they may invalidate the scan.
• meds containing iodine may be discontinued 14 days before and thyroid meds before the test.
• NPO status is needed before the test and an additional 45 min after ingestion of the oral isotope.
• If technetium is used, it is adm by the IV route 30 min before the scan.
• contraindicated in pregnancy.

Question 17

Diagnostic Tests: Needle aspiration of thyroid tissue

Answer 17

• done for cytological examination.
• client preparation is necessary and NPO status may be prescribed.
• light pressure is applied to the aspiration site after the procedure.

Question 18

Diagnostic Tests: Glycosylated hemoglobin

Answer 18

• HgbA1c is blood glucose bound to hemoglobin.
• hemoglobin A1c is a reflection of how well blood glucose levels have been controlled for the past 3-4 months.
• hyperglycemia in clients with DM is usually a cause of an increase in HbA1c.
• Fasting is not required before the test.
• normal reference: <6% (adult without DM).

Question 19

Diagnostic Tests: 24h urine collection for vanillylmandelic acid (VMA)

Answer 19

• diagnostic tests for pheochromocytoma include a 24h urine collection for VMA, a product of catecholamine metabolism, metanephrine, and catecholamines, all of which are elevated in the presence of pheochromocytoma.
• the normal range of urinary catecholamines:
  = epinephrine: < 20 mcg/day (<109nmol/day)
  = norepinephrine: < 100 mcg/day (<590nmol/day)

Question 20

Pituitary Gland Problems: Hypopituitarism

Answer 20

• hyposecretion of 1 or more of the pituitary hormones caused by tumors, trauma, encephalitis, autoimmunity, or stroke.
• hormones most often affected are GH, gonadotropic hormones (luteinizing and follicle-stimulating hormones), but TSH, ACTH, or ADH may be involved.
• assessment: mild to moderate obesity (GH, TSH); reduced cardiac output (GH, ADH); infertility and sexual dysfunction (gonadotropins, ACTH); fatigue and low BP (TSH, ADH, ACTH, GH); tumors of the pituitary also may cause headaches and visual defects (because of its location close to the optic nerve).
• interventions: client may need hormone replacement.

Question 21

Pituitary Gland Problems: Hyperpituitarism (acromegaly)

Answer 21

• hypersecretion of growth hormone by the anterior pituitary gland in an adult; caused primarily by tumors.
• assessment: large hands and feet; thickening and protrusion of the jaw; arthritic changes and joint pain, impingement syndromes; visual disturbances; diaphoresis; oily, rough skin; organomegaly; hypertension, artherosclerosis, cardiomegaly, heart failure; dysphagia; deepening of the voice; thickening of the tongue, narrowing of the airway, sleep apnea; hyperglycemia; colon polyps, increased colon cancer risk.
• interventions: pharmacological interventions to suppress GH or to block the action of GH; prepare client for radiation or stereotactic radiosurgery or hypophysectomy if planned.

Question 22

Hypophysectomy

Answer 22

• pituitary adenectomy, sublabial transsphenoidal pituitary surgery.
• removal of a pituitary tumor via craniotomy or a sublabial transsphenoidal (edoscopic transnasal and less complications associated) approach.
• complications for craniotomy include increased ICP, bleeding, meningitis, and hypopituitarism.
• complications for the sublabial transsphenoidal surgery include cerebrospinal fluid leak, infection, diabetes insipidus, and hypopituitarism.
• if the sublabial approach is used, an incision is made along the gum line of the inner upper lip. Following this type of procedure, monitor for postnasal drip or clear nasal drainage, which might indicate a cerebralspinal fluid leak and should be checked for glucose.
• postop: elevated head of bed, monitor for complications, report excessive urinary output; if the pituitary gland was removed, clients will require lifelong replacement of ADH, cortisol, and thyroid hormone.

Question 23

Pituitary Gland Problems: Diabetes Insipidus

Answer 23

• hyposecretion of ADH by the posterior pituitary gland caused by stroke, trauma, or surgery, or it may be idiopathic.
• kidney tubules fail to reabsorb water.
• in central diabetes insipidus there is decreased ADH production.
• in nephrogenic diabetes insipidus, ADH production is adequate, but the kidneys do not respond appropriately to the ADH.
• assessment: excretion of large amounts of dilute urine; polydipsia; dehydration; inability to concentrate urine; low urinary specific gravity; fatigue, muscle pain, and weakness; headache; postural hypotension that may progress to vascular collapse without rehydration; tachycardia.
• vasopressin or desmopressin acetate (SC, IV, IN, OR) may be prescribed; these are used when the ADH deficiency is severe or chronic. Monitor for signs of water intoxication (overtreatment).

Question 24

Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

Answer 24

• condition of hyperfunctioning of the posterior pituitary gland in which excess ADH is released, but not in response to the body’s need.
• causes include trauma, stroke, malignancies (often lungs or pancreas), meds, and stress.
• results in increased intravascular volume, water intoxication, and dilutional hyponatremia; may cause cerebral edema and seizures.
• assessment: sings of fluid volume overload; changes in level of consciousness and metal status; weight gain without edema; hypertension, tachycardia; anorexia, nausea, vomiting; hyponatremia; low urinary output.
• interventions: elevate head of bed a max of 10 degrees; loop diuretics may be prescribed (if sodium is at least 125), potassium replacement may be necessary; vasopressin antagonists may be prescribed to decrease the renal response to ADH.

Question 25

Adrenal Gland Problems: Adrenal cortex insufficiency (Addison’s disease)

Answer 25

• refers to hyposecretion of adrenal cortex hormones (glucocorticoids, mineralocorticoids, and androgen); autoimmune destruction is a common cause.
• requires lifelong replacement of glucocorticoids and possibly mineralocorticoids if significant hyposecretion occurs; the condition is fatal if left untreated.
• secondary adrenal insufficiency is caused by hyposecretion of ACTH from the anterior pituitary gland; mineralocorticoid release is spared.
• loss of glucocorticoids in Addison’s disease leads to decreased vascular tone, decreased vascular response to the catecholamines epinephrine and norepinephrine, and decreased gluconeogenesis.
• loss of the mineralocorticoid aldosterone leads to dehydration, hypotension, hyponatremia, and hyperkalemia.
• assessment: lethargy, fatigue, muscle weakness; GI disturbances and weight loss; menstrual changes in women and impotence in men; hypoglycemia, hyponatremia, hyperkalemia, hypercalcemia; hypotension; hyperpigmentation of skin with primary disease.
• observe for addison’s crisis caused by stress, infection, trauma, or surgery (avoid risk situations) and corticosteroid replacement will need to be increased during times of stress.
• diet should be high on protein and carbohydrates; clients taking glucocorticoids should be prescribed calcium and vit D supplements to maintain normal levels and to protect against corticosteroid-induced osteoporosis.

Question 26

Adrenal Gland Problems: Addisonian Crisis

Answer 26

• a life-threatening disorder 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.
• assessment: severe headache, abdominal, leg, and lower back pain; generalized weakness; irritability and confusion; severe hypotension and shock.
• interventions: adm IV fluids and glucocorticoids, after resolution adm glucocorticoids and mineralocorticoids orally.

Question 27

Adrenal Gland Problems: Cushing’s Syndrome

Answer 27

• a metabolic disorder resulting from the chronic and excessive production of cortisol by the adrenal cortex or from the adm of glucocorticoids in large doses for several weeks or longer.
• ACTH secreting tumors (most often of the lung, pancreas, or GI tract) can cause Cushing’s syndrome.

Question 28

Adrenal Gland Problems: Cushing’s Disease

Answer 28

• a metabolic disorder characterized by abnormally increased secretion (endogenous) of cortisol, caused by increased amounts of ACTH secreted by the pituitary gland.

Question 29

Cushing’s syndrome and disease: assessment and interventions

Answer 29

• generalized muscle wasting and weakness; moon face, buffalo hump; truncal obesity with thin extremities, supraclavicular fat pads, weight gain; hirsutism (masculine characteristics in females); hyperglycemia, hypernatremia, hypokalemia, hypocalcemia; hypertension; fragile skin that bruises easily; reddish-purple striae on the abdomen and upper thighs.
• prepare for radiation therapy or chemotherapy (for inoperable tumors). Prepare for removal of the pituitary tumor if the condition results from increased pituitary secretion of ACTH.
• prepare for adrenalectomy if the condition results from an adrenal adenoma.
• assess for postop protection against thrombus formation (cushing’s syndrome predisposes to thromboemboli).

Question 30

Adrenal Gland Problems: Primary Hyperaldosteronism (Conn’s Syndrome)

Answer 30

• hypersecretion of mineralocorticoids (aldosterone) from the adrenal cortex of the adrenal gland; most commonly caused by an adenoma.
• excess secretion of aldosterone causes sodium and water retention and potassium excretion, leading to hypertension and hypokalemic alkalosis.
• assessment: symptoms related to hypokalemia, hypernatremia, and hypertension; headache, fatigue, muscle weakness; cardiac dysrhythmias; paresthesias, tetany; visual changes; glucose intolerance; elevated aldosterone levels.
• interventions: potassium supplement, adrenalectomy, sodium restriction, glucocorticoids preop and postop therapy.

Question 31

Adrenal Gland Problems: Pheochromocytoma

Answer 31

• catecholamine-producing tumor usually found in the adrenal medulla, but extraadrenal locations include the chest, bladder, abd, and brain; typically is a benign tumor but can be malignant.
• excessive amounts of epinephrine and norepinephrine are secreted.
• diagnostic test include a 24h urine collection for VMA.
• surgical removal of the adrenal gland is the primary treatment; symptomatic treatment is initiated if surgical removal is not possible.
• the complications associated include hypertensive crisis, hypertensive retinopathy and nephropathy, cardiac enlargement, and dysrhythmias; heart failure, myocardial infarction, increased platelet aggregation, and stroke.
• death can occur from shock, stroke, renal failure, dyshrythmias, or dissecting aortic aneurysm.
• assessment: paroxysmal or sustained hypertension, severe headche, palpitations, flushing and profuse diaphoresis, chest and abd pain with nausea and vomiting, heat intolerance, weight loss, tremors, hyperglycemia.
• interventions: avoid smoke, caffeine drinks or changing position suddenly; adm a-adrenergic blocking agents and b-adrenergic blocking agents to control hypertension; diet high in calories, vitamins, and minerals.; adrenalectomy.

Question 32

Adrenalectomy

Answer 32

• surgical removal of an adrenal gland.
• lifelong glucocorticoid and mineralocorticoid replacement is necessary with bilateral adrenalectomy.
• temporary glucocorticoid replacement, usually up to 2 years, is necessary after a unilateral adrenalectomy.
• catecholamine levels drop as a result of surgery, which can result in cardiovascular collapse, hypotension, and shock, and the client needs to be monitored closely.
• hemorrhage also can occur because of the high vascularity of the adrenal glands.

Question 33

Thyroid Gland Problems: Hypothyroidism

Answer 33

• hyposecretion of thyroid hormones and characterized by a decreased rate of body metabolism; T4 is low and the TSH is elevated.
• in primary hypothyroidism, the source of dysfunction is the thyroid gland, which cannot produce the necessary amount of hormones; in secondary hypothyroidism, the thyroid is not being stimulated by the pituitary to produce hormones.
• assessment: lethargy and 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; mestrual disturbances; goiter may be present; cardiac enlargement and tendency to develop heart failure.
• interventions: thyroid replacement (levothyroxine sodium most common); low calorie, cholesterol, and saturated fat diet; avoid sedatives and opioids because of increased sensitivity to these meds (may precipitate myxedema coma).

Question 34

Thyroid Gland Problems: Myxedema Coma

Answer 34

• rare but serious disorder, results from persistently low thyroid production.
• coma can be precipitated by acute illness, rapid withdrawal of thyroid med, anesthesia and surgery, hypothermia, or the use of sedatives and opioid analgesics.
• assessment: bradycardia, hypothermia, hyponatremia, hypoglycemia, generalized edema, respiratory failure, coma.
• interventions: adm IV fluids ( normal or hypertonic saline), levothyroxine sodium IV, glucose IV, and corticoteroids as prescribed.

Question 35

Thyroid Gland Problems: Hyperthyroidism

Answer 35

• hypersecretion of thyroid hormones (T3 and T4); characterized by an increased rate of body metabolism; the T3 and T4 are usually elevated and TSH low.
• common cause is Graves’ disease, also known as toxic diffuse goiter; clinical manifestations are referred to as thyrotoxicosis.
• assessment: personality changes such as irritability, agitation, and mood swings; nervousness and fine tremors of the hands; weakness, muscle aches, paresthesias; heat intolerance; weight loss; smooth, soft skin and hair; palpitations, cardiac dysrhythmias (tachycardia or atrial fibrillation); diarrhea; protuding eyeballs (exophthalmos); diaphoresis; hypertension; enlarged thyroid gland (goiter).
• interventions: high-calorie diet; adm antithyroid meds (methimazole or propylthiouracil); adm iodine preparations that inhibit the release of thyroid hormone; proponolol for tachycardia; radioactive iodine therapy; subtotal thyroidectomy; elevate head of bed, use artificial tears and tape eyelids closed at night if necessary.

Question 36

Thyroid Gland Problems: Thyroid Storm

Answer 36

• this acute and life-threatening condition occurs in a client with uncontrollable hyperthyroidism.
• it can be caused by manipulation of the thyroid glans during surgery and the release of thyroid hormone into the bloodstream; it also can occur from severe infection and stress.
• antithyroid meds, beta-blockers, glucocorticoids, and iodides may be adm to the client before thyroid surgery to prevent its occurence.
• assessment: fever, tachycardia, systolic hypertension, nausea, vomiting, diarrhea, agitation, tremors, anxiety, irritability, restlessness, confusion, and seizures; delirium and coma with progression.
• interventions: antithyroid meds, iodides, propranolol, and glucocorticoids as prescribed; nonsalicylate antipyretics (salicylates increase free thyroid hormone levels); cooling blankets.

Question 37

Thyroidectomy

Answer 37

• removal of the thyroid gland; performed when persistent hyperthyroidism exists.
• subtotal (removal of portion) is the preferred surgical intervention.
• preop: adm antithyroid meds, iodides, propranolol, and glucocorticoids as prescribed to prevent the occurrence of thyroid storm.
• postop: limit client talking, avoid neck flexion and stress on the suture line; monitor for laryngeal nerve damage; adm calcium gluconate for tetany; monitor for thyroid storm.

Question 38

Parathyroid Gland Problems: Hypoparathyroidism

Answer 38

• caused by hyposecretion of parathyroid hormone; can occur folowing thyroidectomy because of removal of parathyroid tissue.
• assessment: hypocalcemia and hyperphosphatemia; numbness and tingling in the face; muscle cramps and cramps in the abd or extremities; positive Trousseau’s sign or Chvostek’s sign; signs of overt tetany (such as bronchospasm, laryngospasm, carpopedal spasm, dysphagia, photophobia, cardiac dysrhythmias, seizures).
• interventions: adm calcium gluconate IV (if hypoCa); high-calcium diet, low-phosphorus; vit D sup as it enhances the absorption of calcium from the GI tract; thiazide diuretics (protect kidney if vit D is also taken); phosphate binders to promote the excretion of phosphate through the GI tract.

Question 39

Parathyroid Gland Problems: Hyperparathyroidism

Answer 39

• caused by hypersecretion of parathyroid hormone (PTH) by the parathyroid gland.
• assessment: hypercalcemia and hypophosphatemia; fatigue and muscle weakness; skeletal pain and tenderness; bone deformities that result in pathological fractures; anorexia, nausea, vomiting, epigastric pain, weight loss, constipation; hypertension, cardiac dysrhythmias; renal stones.
• interventions: furosemide to lower calcium levels; phosphates which interfere with calcium reabsorption; calcitonin to decrease skeletal calcium release and increase renal excretion; IV or oral bisphosphonates to inhibit bone resorption; high fiber diet and moderate calcium diet.

Question 40

Parathyroidectomy

Answer 40

• removal of 1 or more of the parathyroid glands.
• auto transplantation is a common procedure; parathyroid tissue is transplanted in the forearm or near the sternocleidomastoid muscle, alowing PTH secretion to continue.
• preop: ensure that calcium levels are decreased to near-normal values.
• postop: semi-fowler’s position; monitor for hypocalcemic crisis and assess for tetany signs; calcium + vit D sup.

Question 41

Problems of the Pancreas: Diabetes Mellitus

Answer 41

• chronic disorder of impaired carbohydrate, protein, and lipid metabolism caused by a deficiency of insulin; resulting in hyperglycemia.
• type 1 DM is a nearly absolute deficiency of insulin (primary beta cell destruction); if insulin is not given, fats are metabolized for energy, resulting in ketonemia (acidosis).
• type 2 DM is a relative lack of insulin or resistance to the action of insulin; usually insulin is sufficient to stabilize fat and protein metabolism but not carbohydrate metabolism.
• metabolic syndrome is also known as syndrome X, and the individual has coexisting risk factors for developing type 2 DM (abd obesity, hyperglycemia, hypertension, high triglyceride level, and a lowered HDL cholesterol level.
• DM can lead to chronic health problems and early death as a result of complications.
• macrovascular complications: coronary artery disease, cardiomyopathy, hypertension, cerebrovascular disease, and peripheral vascular disease.
• microvascular complications: retinopathy, nephropathy, and neuropathy.
• infection is also a concern because of reduced healing ability.
• male erectile dysfunction can also occur.

Question 42

DM: assessment

Answer 42

• polyuria, polydipsia, polyphagia (more common in type 1 DM).
• hyperglycemia
• weight loss (common in type 1, rare in type 2)
• blurred vision
• slow wound healing
• vaginal infections
• weakness and paresthesias
• signs of inadequate circulation to the feet
• signs of accelerated atherosclerosis (renal, cerebral, cardiac, peripheral).

Question 43

DM: diet, exercise, and oral hypoglycemic med

Answer 43

• diet should take into account weight, med, activity level, and other health problems.
• carbohydrate counting may be a simpler approach for some clients.
• if the client requires extra food during exercise to prevent hypoglycemia, it need not to be deducted from the regular meal plan.
• if the blood glucose level is higher than 250mg/dL and urinary ketones (DM1) are present, the client is instructed not to exercise until the blood glucose level is closer to normal and urinary ketones are absent.
• client should try to exercise at the same time each day and should exercise when glucose from the meal is peaking, not when insulin or glucose lowering meds are peaking.
• insulin should not be injected into an area of the body that will be exercised following injection, as exercise speeds absorption.
• oral hypoglycemic med: prescribed for clients with DM2 when diet and weight control therapy have failed to maintain satisfactory blood glucose levels.

Question 44

DM: Insulin

Answer 44

• used to treat DM1 and may be used to treat DM2 when diet, weight control therapy, and oral hypoglycemic agents have failed to maintain satisfactory blood glucose levels.
• illness, infection, and stress increase the blood glucose level and the need for insulin; therefor should not be withheld during these times (to prevent ketoacidosis).
• regular insulin and the short-duration insulins (lispro, aspart, and glulisine) can be adm via IV infusion; regular insulin can also be done by IV push.

Question 45

DM: complications of insulin therapy

Answer 45

• local allergic reactions: redness, swelling, tenderness, and induration or a wheal at the site of injection may occur 1-2h after adm; reactions usually occur during the early stages; instruct to cleanse the skin with alcohol before injection.
• insulin lipodystrophy: development of fibrous fatty masses at the injection site caused by repeated use of an injection site; instruct the client about the importance of rotating injection sites; avoid using the same site more than once in a 2-3 week period; injections should be 1.5in (3.8cm) apart.
• dawn phenomenon: characterized by hyperglycemia upon morning awakening that results from excessive early morning release of GH and cortisol; treatment requires an increase of insulin dose or a change in the time of adm.
• somogyi phenomenon: normal or elevated blood glucose are present at bedtime; hypoglycemia occurs at about 2-3 am, which causes an increase in the production of counter-regulatory hormones; by about 7am, in response to the hormones, blood glucose rebounds to the hyperglycemic range; treatment includes a decrease of insulin dose or increase in the bedtime snack, or both; clients usually complain of early morning headache, night sweats, or nightmares caused by the early morning hypoglycemia.

Question 46

DM: insulin administration

Answer 46

• insulin pumps: continuous SC insulin infusion is adm by an externally worn device that contains a syringe and pump; client inserts needle or teflon catheter into the SC tissue (usually abd or upper arm) and secures it with tape or transparent dressing (should be changed every 2-3 days); a continuous basal rate of insulin infuses, in addition, client can deliver a bolus before meals and when needed; both rapid-acting and regular short-acting insulin are appropriate for use.
• insulin pump and skin sensor: skin sensor device can be used for monitoring continuously; information is transmitted to the pump, which determines the need for insulin, and injects; pump upholds up to a 3 day supply and can be disconnected easily if necessary for certain activities such as bathing.

Question 47

DM: pancreas transplants

Answer 47

• goal is to halt or reverse the complications of DM.
• are performed on a limited number of clients (in general, these are clients who are undergoing kidney transplantation simultaneously).
• immunosuppressive therapy is prescribed to prevent and treat rejection.

Question 48

DM: self-monitoring of blood glucose level

Answer 48

• provides the client with the current blood glucose level and information to maintain good glycemic control.
• requires a finger prick to obtain a drop of blood for testing.
• alternative site testing (forearm, upper arm, abd, thigh, or calf) is available, using specific measurement devices.
• tests must be used with caution in clients with diabetic neuropathy.

Question 49

DM: urine testing

Answer 49

• not a reliable indicator of the blood glucose level and is not used for monitoring purposes.
• presence of ketones may indicate impending ketoacidosis.
• urine ketone testing should be performed during illness and whenever the client with type 1 DM has persistently elevated blood glucose levels (> 250 mg/dL or as prescribed for 2 consecutive testing periods).

Question 50

Acute Complications of DM: Hypoglycemia

Answer 50

• occurs when blood level is < 70mg/dL or when drops rapidly from an elevated level.
• caused by too much insulin or too large an amount of an oral hypoglycemic agent, too little food, or excessive activity.
• instruct client to always carry a form of fast-acting simple carbohydrate.
• high-fat foods slow the absorption of glucose, and the hypoglycemic symptoms may not resolve quickly.
• clients who experience frequent episodes of hypoglycemia, older clients, and clients taking b-adrenergic agents may not experience the warning signs of hypoglycemia until level is critically low; this phenomenon is termed hypoglycemia unawareness.
• mild hypoglycemia: fully awake but displays adrenergic symptoms(hunger, nervousness, palpitations, sweting, tachycardia, tremor); <70mg/dL.
• moderate hypoglycemia: symptoms are worsening (confusion, double vision, drowsiness, emotional changes, headache, impaired coordination, inability to concentrate, irrational or combative behavior, lightheadedness, numbness of lips and tongue, slurred speech); <40mg/dL.
• severe hypoglycemia: severe neuroglycopenic symptoms (difficulty arousing, disoriented behavior, loss of consciousness, seizures); <20mg/dL.
• interventions: 15/15 rule.

Question 51

Hypoglycemia: the 15/15 rule

Answer 51

1. <70 mg/dL or symptoms (diaphoresis, hunger, pallor, and shakiness) with no monitor available, assume hypo and treat.
2. 15g of a simple carbohydrate (1/2 cup of fruit juice or 15g of glucose gel).
3. recheck in 15 min
4. if <70 adm another 15g of a simple carbohydrate.
5. recheck in 15 min
6. if <70 adm another 15g of a simple carbohydrate.
7. recheck in 15 min
8. if still <70, treat with 25-50ml of 50% dextrose IV, or 1mg of glucagon SC or IM (if IV not available).
9. after blood glucose level is recovered, have the client ingest a snack that includes a complex carbohydrate and a protein.
10. document and explore causes
11. if the client is experiencing altered level of consciousness, bypass oral treatment and start with injectable glucagon or 50% dextrose.

Question 52

Acute Complications of DM: diabetic ketoacidosis (DKA)

Answer 52

• a life-threatening complication of type 1 DM that develops when a severe insulin deficiency occurs.
• main clinical manifestations include hyperglycemia, dehydration or electrolyte loss (polyuria, polydipsia, weight loss, dry skin, sunken eyes, soft eyeballs, lethargy, coma), ketosis (kussmaul’s resp, fruity breath, nausea, abd pain), and acidosis.
• onset is sudden and precipitating factors include infection, inadequate insulin dose, and other stressors.
• lab: glucose >300mg/dL; ketones +; pH<7.35; HCO3 <15mEq/L; K elevated with acidosis (decreases following hydration; BUN >20mg/dL; creatinine >1.5mg/dL; urine ketones +
• monitor potassium, glucose levels and for signs of increased intracranial pressure; potassium level will fall rapidly within the first hour of treatment as the dehydration and the acidosis are treated; potassium is adm IV in a diluted solution as prescribed and ensure adequate renal function before adm.

Question 53

Acute Complications of DM: hyperosmolar hyperglycemic syndrome (HHS)

Answer 53

• extreme hyperglycemia occurs without ketosis or acidosis; most often in type 2 DM.
• major difference between HHS and DKA is that ketosis and acidosis do not occur with HHS; enough insulin is present with HHS to prevent the breakdown of fats for energy, thus preventing ketosis.
• precipitating factors: infection, poor fluid intake, and other stressors.
• assessment: gradual onset, altered CNS function with neurological symptoms; dehydration or electrolyte loss (polyuria, polydipsia, weight loss, dry skin, sunken eyes, soft eyeballs, lethargy, coma).
• treatment is similar to DKA, includes fluid replacement, correction of electrolyte imbalances, and insulin adm.
• insulin plays a less critical role in the treatment of HHS because ketosis and acidosis is not present; rehydration alone may decrease glucose levels.

Question 54

Chronic Complications of DM: diabetic retinopathy

Answer 54

• chronic and progressive impairment of the retinal circulation that eventually causes hemorrhage; permanent vision changes and blindness can occur.
• a change in vision is caused by the rupture of small microaneurysms in retinal blood vessels; blurred vision results from macular edema; sudden loss of vision results from retinal detachment; cataracts result from lens opacity.
• interventions: early prevention; photocoagulation (laser therapy) may be done to remove hemorrhagic tissue; vitrectomy may be done to remove vitreous hemorrhages and thus decrease tension on the retina, preventing detachment; cataract removal with lens implantation improves vision.

Question 55

Chronic Complications of DM: diabetic nephropathy

Answer 55

• progressive decrease in kidney function.
• assessment: microalbuminuria, thirst, fatigue, anemia, weight loss, signs of malnutrition, frequent urinary tract infections, signs of a neurogenic bladder.
• interventions: early prevention; monitor urea, creatinine, and urine albumin levels; restrict dietary protein, sodium, and potassium intake; avoid nephrotoxic meds; prepare for possible dialysis, kidney transplant, or pancreas transplant.

Question 56

Chronic Complications of DM: diabetic neuropathy

Answer 56

• general deterioration of the nervous system; complications include the development of nonhealing ulcers of the feet, gastric paresis, and erectile dysfunction.
• assessment (finding depend on the classification): paresthesias; decreased or absent reflexes; decreased sensation to vibration or light touch; pain, aching and burning in the lower extremities; poor peripheral pulses; skin breakdown and signs of infection; weakness or loss of sensation in cranial nerves III, IV, V, and VI; dizziness and postural hypotension; nausea and vomiting; diarrhea or constipation; incontinence, dyspareunia; impotence; hypoglycemic unawareness.
• interventions: early prevention, foot care, pain relief, bladder training, instruct treatment for dyspareunia (estrogen-containing lubricants) and impotence (penile injections), prepare for surgical decompression related to cranial nerves.

Question 57

Diabetic Neuropathy: classifications

Answer 57

• focal or mononeuropathy: involves a single nerve or group of nerves, most frequently cranial nerves III and VI, resulting in diplopia.
• sensory or peripheral: affects distal portion of nerves, most frequently in the lower extremities.
• autonomic: symptoms vary according to the organ system involved.
• cardiovascular: cardiac denervation syndrome (HR does not respond to changes in oxygenation needs) and orthostatic hypotension occur.
• pupillary: pupil does not dilate in response to decreased light.
• gastric: decreased gastric emptying (gastroparesis).
• urinary: neurogenic bladder.
• skin: decreased sweating.
• adrenal: hypoglycemic unawareness.
• reproductive: impotence (male), painful intercourse (female).

Question 58

Care of the Diabetic Client Undergoing Surgery

Answer 58

• check with PHCP regarding withholding oral hypoglycemic meds or insulin.
• some long-acting oral antidiabetic meds are discontinued 24-48h before surgery.
• metformin may need to be discontinued 48h before surgery and may not be restarted until renal function is normal postop.
• all other oral antidiabetic meds are usually withheld on the day of the surgery.
• postop adm IV glucose and insulin infusions as prescribed until the client can tolerate oral feedings.
• client is at higher risk for cardiovascular and renal complications postop, also impaired wound healing.