HYPERTHYROIDISM

 Definition
- Increased synthesis of thyroid hormone from overactivity (Graves’ disease) or change in thyroid gland (toxic nodular goiter)

 Causes
- Autoimmune disease - Thyroid adenomas
- Genetic - Pituitary tumors
- Psychological or physiologic stress - Infection

 Pathophysiology
- Thyroid-stimulating antibodies have a slow, sustained, stimulating effect thyroid metabolism
- Accelerated metabolism causes increased synthesis of thyroid hormone andd signs and symptoms of sympathetic nervous
system stimulation

 Assessment findings
- Anxiety - Increased hunger
- Flushed, smooth skin - Increased systolic blood pressure
- Heat intolerance - Tachypnea
- Mood swings - Fine hand tremors
- Diaphoresis - Exophthalmos
- Tachycardia - Weight loss
- Palpitations - Diarrhea
- Dyspnea - Hyperhidrosis
- Weakness - Bruit or thrill over thyroid

 Diagnostic test findings

- Thyroid scan: nodules
- Blood chemistry: increased T3, T4, protein-bound iodine, radioactive iodine (131]); decreased TSH, cholesterol
- ECG: atrial fibrillation
- RAIU: increased

 Medical management
- Diet: high-protein, high-carbohydrate, high-calorie; restrict stimulants, such as coffee and caffeine
- IV therapy: saline lock
- Activity: bed rest
- Monitoring: vital signs and I/O
- Laboratory studies: T3, T4
- Sedative: lorazepam (Ativan)
- Radiation therapy
- Antihyperthyroids: methimazole (Tapazole), propylthiouracil (Propyl-Thyracil)
- Iodine preparations: potassium iodide, radioactive iodine
- Beta-adrenergic blocking agents: propranolol (Inderal)
- Vitamins: thiamine (vitamin B,), ascorbic acid (vitamin ©)
- Cardiac glycoside: digoxin (Lanoxin)
- Glucocorticoids: prednisone (Deltasone); IV hydrocortisone (Solu-Cortef) for thyroid storm
- IV glucose

 Nursing interventions
- Maintain the patient's diet
- Avoid stimulants, such as drugs and foods that contain caffeine
- Administer IV fluids
- Assess fluid balance
- Assess cardiovascular status
- Monitor and record vital signs, I/O, and laboratory studies

pg. 1
 - Administer medications, as prescribed
- Weigh the patient daily
- Provide rest periods
- Provide a quiet, cool environment
- Provide eye care
- Allay the patient’s anxiety
- Encourage the patient to express his feelings about changes in his body image
- Provide postradiation nursing care
o Provide prophylactic skin, mouth, and perineal care
o Monitor dietary intake
o Provide rest periods
- Individualize home care instructions (for teaching tips, see Patients with endocrine disorders)
o Stop smoking
o Recognize the signs and symptoms of thyroid storm
o Adhere to activity limitations
o Avoid exposure to people with infections
o Monitor self for infection

 Complications
- Thyroid storm (thyroid crisis): tachycardia, delirium, agitation, coma, death, hyperpyrexia, dehydration, arrhythmias, diarrhea
(see understanding thyroid storm)
- Arrhythmias
- Diabetes mellitus

 Surgical intervention
- Subtotal thyroidectomy when euthyroid state is established

Patients with Endocrine disorders

Be sure to include the following topics in your teaching plan when caring for patients with endocrine disorders.
 Follow-up appointments
 Optimal body weight maintenance
 Medication therapy including the action, adverse effects, and scheduling of medications
 Dietary recommendations and re strictions
 Fluid intake recommendations and restrictions
 Rest and activity patterns, including any limitations or restrictions
 Community agencies and resources for supportive services
 Ways to reduce stress
 Medical identification jewelry
 Safe, quiet environment

Understanding thyroid storm

Thyrotoxic crisis — also known as thyroid storm — usually occurs in patients with preexisting, though often unrecognized,
thyrotoxicosis. Left untreated, it's usually fatal.

PATHOPHYSIOLOGY
The thyroid gland secretes the thyroid hormones triiodothyronine (T3) and thyroxine (T4). When T3, and T4, are overproduced,
systemic adrenergic activity increases. The result is epinephrine overproduction and severe hypermetabolism, leading rapidly to
cardiac, GI, and sympathetic nervous system decompensation.

ASSESSMENT FINDINGS
Initially, the patient may have marked tachycardia, vomiting, and stupor. If left untreated, he may experience vascular collapse,
hypotension, coma, and death. Other findings may include a combination of irritability and restlessness; visual disturbances such as

pg. 2
diplopia; tremor and weakness, angina; shortness of breath; cough: and swollen extremities. Palpation may disclose warm, moist,
flushed skin,
and a high fever that begins insidiously and rises rapidly to a lethal level.

PRECIPITATING FACTORS
Onset is usually abrupt and evoked by a stressful event, such as trauma, surgery, or infection, Other less common precipitating factors
include:
 insulin-induced ketoacidosis
 hypoglycemia or diabetic ketoacidosis
 stroke
 myocardial infarction
 pulmonary embolism
 sudden discontinuation of antithyroid drug therapy
 initiation of radioactive iodine therapy
 preeclampsia =
 subtotal thyroidectomy with accompanying excessive intake of synthetic thyroid hormone.

HYPOTHYROIDISM

 Definition
- Underactive state of thyroid gland, resulting in absence or decreased secretion of thyroid hormone

 Causes
- Autoimmune disease: Hashimoto's thyroiditis
- Thyroidectomy
- Overuse of antithyroid drugs
- Malfunction of pituitary gland
- Use of radioactive iodine

 Pathophysiology
- Thyroid gland fails to secrete a satisfactory quantity of thyroid hormone
- Hyposecretion of thyroid hormone results in overall decrease in metabolism
 Assessment findings
- Fatigue
- Weight gain
- Dry, flaky, “doughy” skin
- Edema
- Cold intolerance
- Coarse hair
- Alopecia
- Thick tongue, swollen lips
- Mental sluggishness
- Menstrual disorders
- Constipation
- Hypersensitivity to narcotics, barbiturates, and anesthetics
- Anorexia
- Decreased diaphoresis
- Hypothermia

 Diagnostic test findings

- Blood chemistry: decreased T3, T4, protein-bound iodine, sodium; increased TSH, cholesterol
- RAIU: decreased
- ECG: sinus bradycardia

pg. 3
 Medical management
- Diet: high-fiber, high-protein, low-calorie with increased fluid intake
- Activity: as tolerated
- Monitoring: vital signs and I/O
- Laboratory studies: T3, T4, and sodium
- Stool softener: docusate (Colace)
- Thyroid hormone replacements: levothyroxine (Synthroid), liothyronine (Cytomel), thyroglobulin (Proloid), liotrix
(Thyrolar)

 Nursing interventions
- Maintain the patient's diet
- Encourage fluids
- Monitor and record vital signs, 1/O, and laboratory studies
- Administer medications, as prescribed
- Encourage the patient to express his feelings of depression
- Encourage physical activity and mental stimulation
- Provide a warm environment
- Avoid sedation: administer one-third to one-half the normal dose of sedatives or narcotics
- Check for constipation and edema
- Prevent skin breakdown
- Provide frequent rest periods
- Individualize home care instructions
o Exercise regularly
o Recognize the signs and symptoms of myxedema coma (see understanding myxedema coma)
o Monitor self for constipation
o Use additional protection in cold weather
o Limit activity in cold weather
o Avoid using sedatives
o Complete skin care daily

 Complications Medic
- Coronary artery disease (CAD)
- Heart failure
- Acute organic psychosis
- Angina
- Myocardial infarction (MI)
- Myxedema coma: hypoventilation, hypothermia, respiratory acidosis, syncope, bradycardia, hypotension, seizures, and
cerebral hypoxia

 Surgical interventions
- None

Understanding myxedema
Myxedema coma is a medical emergency that commonly has a fatal outcome. Progression is usually gradual but when strass — such
as infection, exposure to cold, or trauma — aggravates severe or prolonged hypothyroidism, coma may develop abruptly. Other
precipitating factors are thyroid medication withdrawal and the use of sedatives, narcotics, or anesthetics.

WHAT HAPPENS
Patients in myxedema coma have significantly depressed respirations, so their partial pressure of carbon dioxide in arterial blood may
rise. Decreased cardiac output and worsening cerebral hypoxia may also occur. The patient becomes stuporous and hypothermic. Vital
signs reflect bradycardia and hypotension. Lifesaving interventions are necessary.

HYPERPARATHYROIDISM

pg. 4
 Definition
- Overactivity of one or more parathyroid glands, resulting in increased PTH secretion

 Causes
- Chronic renal failure - Malignant tumors of parathyroid gland
- Bone disease - Vitamin D deficiency
- Benign adenomas - Malabsorption
- Hypertrophy of parathyroid gland

 Pathophysiology
- Excessive secretion of PTH leads to bone demineralization and hypocalcemia
- Hypercalcemia increases the risk of renal calculi

 Assessment findings
- Renal colic - Fatigue
- Renal calculi - Osteoporosis
- Arrhythmias - Muscle weakness
- Constipation - Mood swings
- Bowel obstruction - Deep bone pain
- Anorexia - Hematuria
- Weight loss - Paresthesia
- Nausea and vomiting - Thick nails
- Depression - Pathologic fractures
- Mental dullness

 Diagnostic test findings

- ECG: shortened QT interval
- Urine chemistry: decreased phosphorus; increased calcium
- Blood chemistry: increased calcium, BUN, creatinine, chloride, alkaline phosphatase; decreased phosphorus
- X-ray: osteoporosis

 Medical management
- Diet: low-calcium, high-fiber, high-phosphorus in small frequent feedings; increase fluid intake to 3,000 ml/day
- IV therapy: saline lock
- Activity: as tolerated
- Monitoring: vital signs and I/O
- Laboratory studies: calcium, phosphorus, BUN, creatinine, potassium, and sodium
- Radiation therapy
- Treatments: strain urine, bed cradle
- Analgesic: oxycodone (Vicodin)
- Diuretics: furosemide (Lasix), ethacrynic acid (Edecrin)
- Antacid: aluminum hydroxide gel (AlternaGEL)
- Estrogen: estrogen (Premarin)
- Antineoplastic: plicamycin (Mithracin)
- Phosphate salts: K-Phos, Neutra-Phos
- Dialysis using calcium-free dialysate
- IV saline

 Nursing interventions
- Maintain the patient's diet
- Encourage fluids with acidifying solutions: cranberry juice
- Administer IV fluids
- Assess urinary status
- Monitor and record vital signs, 1/O, and laboratory studies
- Administer medications, as prescribed

pg. 5
 - Encourage the patient to express his feelings about chronic illness
- Encourage the patient to walk
- Prevent falls
- Strain urine
- Assess bone and flank pain
- Move the patient carefully to prevent pathologic fractures
- Limit strenuous activity
- Assess the patient for constipation
- Provide postradiation nursing care
o Provide skin and mouth care
o Monitor dietary intake
o Provide rest periods
- Individualize home care instructions
o Recognize the signs and symptoms of renal calculi
o Strain urine
o Prevent falls
o Prevent constipation

 Complications
- Peptic ulcer

 Surgical intervention
- Parathyroidectomy

HYPOPARATHYROIDISM
 Definition
- Decrease in PTH secretion

 Causes
- Thyroidectomy - Radiation
- Autoimmune disease - Use of radioactive iodine
- Parathyroidectomy - Parathyroid tumor

 Pathophysiology
- Decreased PTH decreases stimulation to osteoclasts, resulting in decreased release of calcium and phosphorus from bone (see
What happens in acute hypoparathyroidism)
- Decreased circulating PTH reduces GI absorption of calcium and increases absorption of phosphorus
- Decreased blood calcium causes a rise in serum phosphates and decreased phosphate excretion by the kidney

 Assessment findings
- Lethargy - Personality changes
- Calcification of ocular lens - Brittle nails
- Muscle and abdominal spasms - Alopecia
- Trousseau’s sign: positive - Deep tendon reflexes: increased
- Chvostek’s sign: positive  Diagnostic test findings
- Tingling in fingers - Blood chemistry: decreased PTH, calcium; increased
- Arrythmias phosphorus
- Seizures - Urine chemistry: decreased calcium
- Vision disturbances: diplopia, photophobia, blurring - X-ray: calcification of basal ganglia; increased bone
- Dyspnea density
- Laryngeal stridor - ECG: prolonged QT interval

 Medical management
- Diet: high-calcium, low-phosphorus, low-sodium with spinach restriction
- Activity: as tolerated
- IV therapy: saline lock

pg. 6
 - Monitoring: vital signs and I/O
- Laboratory studies: PTH, calcium, and phosphorus
- Precautions: seizure
- Antacid: aluminum hydroxide gel (AlternaGGEL)
- Sedative: zolpidem (Ambien)
- Anticonvulsants: phenytoin (Dilantin), magnesium sulfate (Epsom salt)
- Vitamins: ergocalciferol (vitamin D), dihydrotachysterol (Hytakerol)
- Oral calcium salts: calcium gluconate (Kalcinate), calcium Carbonate (Os-Cal)
- Diuretic: furosemide (Lasix)
- Hormone replacement: parathyroid extract (PTH)
- IV calcium salts: calcium chloride or calcium gluconate

 Nursing interventions
- Maintain the patient's diet
- Assess neurologic status
- Maintain seizure precautions
- Monitor and record vital signs, I/O, and laboratory studies
- Administer medications, as prescribed
- Allay the patient's anxiety
- Keep tracheostomy tray and LV. calcium gluconate available
- Maintain a calm environment
- Individualize home care instruction
o Recognize the signs and symptoms of seizure activity
o Follow dietary recommendations

 Complications
- Heart failure - Blindness
- Mental retardation

 Surgical interventions
- None

What happens in acute hypoparathyroidism

Causes of acute hypoparathyroidism include injury to the glands, accidental removal of the parathyroid glands during thyroidectomy
or other neck surgery, autoimmune disease, tumor, tuberculosis, sarcoidosis, hemochromatosis, and severe magnesium deficiency
associated with alcoholism and intestinal malabsorption. These disorders and conditions cause a cascade of effects that result in severe
hypocalcemia and hyperphosphatemia, which can lead to seizures, tetany, laryngospasm, and central nervous system (CNS)
abnormalities, as shown in the flow chart below.

Causative factor
[gland injury. accidental gland removal, autoimmune disease, tumor, or conditions)

Diminished or absent parathyroid hormone levels

Excessive Decreased release of Decreased renal Decreased intestinal

reabsorption of
phosphate by renal
tubules
Hyperphosphatemia
calcium from bone calcium reabsorption calcium absorption
Hypocalcemia
pg. 7
 Seizures
Tetany
Laryngospasm
CNS abnormalities

CUSHING’S SYNDROME (HYPERCORTISOLISM)

 Definition
- Hyperactivity of the adrenal cortex that results in excessive secretion of glucocorticoids, particularly cortisol
- Possible increase in mineralocorticoids and sex hormones

 Causes
- Hyperplasia of the adrenal glands
- Hypothalamic stimulation of the pituitary gland
- Adenoma or carcinoma of the pituitary gland
- Exogenous secretion of corticotropin by malignant neoplasms in the lungs or gallbladder
- Excessive or prolonged administration of glucocorticoids or corticotropin
- Adenoma or carcinoma of the adrenal cortex

 Pathophysiology on
- Hypothalamic stimulation of the pituitary gland causes excessive secretion of corticotropin
- Excessive secretion of corticotropin causes increased plasma cortisol
- Elevated blood cortisol levels don’t diminish secretion of hypothalamic corticotropin-releasing hormone se

 Assessment findings
- Weight gain (see Symptoms of cushingoid syndrome) - Poor wound healing
- Hirsutism - Truncal obesity
- Amenorrhea - Buffalo hump
- Weakness and fatigue - Moon face
- Pain in joints - Gynecomastia
- Ecchymosis - Enlarged clitoris
- Edema - Decreased libido
- Hypertension - Muscle wasting
- Mood swings - Recurrent infections
- Fragile skin Girdle - Acne
- Purple striae on abdomen

 Diagnostic test findings

- Dexamethasone suppression test: no decrease in 17-OHCS
- X-ray: pituitary or adrenal tumor; osteoporosis
- Angiography: pituitary or adrenal tumors
- CT scan: pituitary or adrenal tumors
- Urine chemistry: increased 17-OHCS and 17-K5; decreased specific gravity; glycosuria
- Blood chemistry: increased cortisol, aldosterone, sodium, corticotropin, glucose; decreased potassium
- Ultrasonography: pituitary or adrenal tumors
- Hematology: increased WECs, RBCs; decreased eosinophils
- GTT: hyperglycemia

pg. 8
 Medical management
- Diet: low-sodium, low-carbohydrate, low-calorie, high-potassium, and high-protein
- Activity: as tolerated
- Monitoring: vital signs, I/O, urine glucose and ketones, and specific gravity
- Laboratory studies: sodium, potassium, cortisol, BUN, glucose, WBCs, and RBCs
- Radiation therapy
- Diuretics: furosemide (Lasix), ethacrynic acid (Edecrin)
- Potassium supplements: potassium chloride (K-Lor), potassium gluconate (Kaon)
- Adrenal suppressants: metyrapone (Metopirone), aminoglutethimide (Cytadren)
- Hypoglycemics: rapid-acting (Lispro); short-acting (regular); intermediate-acting (NPH); long-acting (Lente, Lantus-insulin
glargine); glyburide (DiaBeta, Micronase, Amaryl); glipizide (Glucotrol, Glucotrol XL)

 Nursing interventions
- Maintain the patient's diet
- Assess fluid balance
- Monitor and record vital signs, [/O, specific gravity, blood glucose levels, urine glucose and ketones, and laboratory studies
- Assess edema
- Check for infections of skin, respiratory, and urinary tracts
- Protect the patient from falls and bruising
- Protect from infection
- Provide meticulous skin care
- Limit water intake
- Weigh the patient daily
- Administer medications, as prescribed
- Encourage the patient to express his feelings about changes in his body
- image and sexual function
- Provide rest periods
- Minimize environmental stress
- Provide postradiation nursing care
o Provide prophylactic skin care
o Monitor dietary intake
o Provide rest periods
o Assess for hypoglycemia
- Individualize home care instructions
o Recognize the signs and symptoms of infection and fluid retention
o Avoid exposure to people with infections
o Monitor self for infection

 Complications
— Adrenal insufficiency — Heart failure
— Infection — Psychosis
— Peptic ulcers — Arrhythmias
— Hypertension — Diabetes mellitus
— Fractures — Arteriosclerosis

 Surgical interventions
— Adrenalectomy
— Hypophysectomy

Symptoms of cushingoid syndrome

Long-term treatment with corticosteroids may produce an adverse effect called cushingoid syndrome —a condition marked by
widespread systemic abnormalities and obvious fat deposits between the shoulders and around the waist.

pg. 9
In addition to the symptoms shown in the illustration, observe for signs of hypertension, renal disorders, hyperglycemia, tissue
wasting, muscle weakness, and
labile emotional state. The patient may also have amenorrhea and glycosuria.

Fluid retention around eyes and face Thinning of extremities

Acne, moon face, hirsutism Girdle obesity
Cervicodorsal fat (buffalo hump) Purplish striae
Protruding abdomen Edema

ADDISON'S DISEASE
 Definition
- Chronic hypoactivity of the adrenal cortex, resulting in insufficient secretion of glucocorticoids (cortisol) and
mineralocorticoids (aldosterone)

 Causes
- Idiopathic atrophy of adrenal glands - Metastatic lesions from lung cancer
- Surgical removal of adrenal glands - Pituitary hypofunction
- Autoimmune disease - Histoplasmosis
- Tuberculosis - Trauma

 Pathophysiology
- Autoimmune theory: body produces adrenocortical antibodies, resulting in adrenal hypofunction
- Decreased aldosterone causes disturbances in sodium, water, and potassium metabolism
- Decreased cortisol causes abnormal metabolism of fal, protein, and carbohydrate

 Assessment findings
- Hypoglycemia - Decreased pubic and axillary hair
- Weakness and lethargy - Orthostatic hypotension
- Bronzed skin pigmentation of nipples, scars, and - Diarrhea
buccal mucosa - Nausea
- Dehydration - Weight loss
- Anorexia - Depression
- Thirst

 Diagnostic test findings

- Blood chemistry: decreased HCT, Hb, cortisol, glucose, sodium, chloride, aldosterone; increased BUN, potassium
- Urine chemistry: decreased 17-KS and 17-OHCS
- Basal metabolic rate (EMR): decreased
- Fasting serum glucose: hypoglycemia
- ECC: prolonged PR and OT intervals

 Medical management
- Diet: high-carbohydrate, high-protein, high-sodium, low-potassium in small, frequent feedings before steroid therapy; high-
potassium and low sodium when on steroid therapy
- IV therapy: hydration, electrolyte replacement: saline lock
- Activity: bed rest
- Monitoring: vital signs, I/O, and specific gravity
- Laboratory studies: sodium, potassium, osmolality, cortisol, chloride, glucose, BUN, creatinine, Hb, and HCT
- IV saline
- Vasopressors: phenylephrine (Neo-Synephrine), norepinephrine (Levophed), dopamine (Intropin)
- Antacids: magnesium and aluminum hydroxide (Maalox), aluminum hydroxide gel (Gelusil)
- Mineralocorticoid (aldosterone): fludrocortisone (Florinef)
- Glucocorticoids: cortisone (Cortone), hydrocortisone (Solu-Cortef)

pg. 10
 Nursing interventions
- Maintain the patient's diet
- Administer IV fluids
- Monitor and record vital signs, I/O, specific gravity, and laboratory studies
- Weigh the patient daily
- Administer medications, as prescribed
- Allay the patient's anxiety
- Protect the patient from falls
- Encourage fluid intake
- Assist with activities of daily living
- Maintain a quiet environment
- Individualize home care instructions
o Avoid strenuous exercise, particularly in hot weather
o Recognize the signs and symptoms of adrenal crisis
o Increase fluid intake in hot weather
o Carry injectable dexamethasone (Decadron)
o Avoid using OTC drugs

 Complications
- Addisonian crisis (adrenal crisis); marked hypotension, cyanosis, abdominal cramps, diarrhea, costovertebral tenderness,
fever, confusion, coma
- Arrhythmias
- Hypovolemic shock
- Renal failure

 Surgical interventions
- None

PHEOCHROMOCYTOMA

 Definition
- Catecholamine-secreting neoplasm associated with hyperfunctioning adrenal medulla

 Causes
- Genetics
- Pregnancy
- Trauma

 Pathophysiology
- Tumor in the adrenal medulla secretes large amounts of catecholamines (epinephrine and norepinephrine)
- Increased catecholamines cause hypertension, increased BMR, and hyperglycemia

 Assessment findings
- Labile malignant hypertension - Weight loss
- Throbbing headaches - Dyspnea
- Diaphoresis - Vertigo
- Palpitations - Angina
- Tachycardia - Nausea
- Excessive anxiety - Vomiting
- Hyperactivity - Anorexia
- Dilated pupils - Visual disturbances
- Cold extremities - Polyuria
- Weakness - Diarrhea

pg. 11
 - Tinnitus - Tremors

 Diagnostic test findings

- CT scan: adrenal tumor
- Angiography: adrenal tumor
- Magnetic resonance imaging: adrenal tumor
- VMA: increased
- BOG: tachycardia
- Blood chemistries: increased BUN, creatinine, glucose, and catecholamines
- Urine chemistries: increased glucose and catecholamines

 Medical management
- Diet: high-calorie, high-vitamin, and high-mineral with restricted use of stimulants such as caffeine beverage
- Activity: as tolerated
- Monitoring: vital signs, I/O, and urine glucose and ketones
- Position: semi-Fowlers
- Laboratory studies: BUN, creatinine, and glucose
- Sedative: lorazepam (Ativan)
- Alpha-adrenergic blockers: prazosin (Minipress), doxazosin (Cardura), terazosin (Hytrin)
- Beta-adrenergic blocker: propranolol (Inderal)
- Vasodilator: clonidine (Catapres), IV nitroglycerine
- Catecholamine inhibitor: metyrosine (Demser)

 Nursing interventions
- Maintain the patient's diet
- Assess cardiovascular status
- Keep the patient in semi-Fowler’s position
- Monitor and record vital signs, I/O, orthostatic blood pressure, specific gravity, urine glucose and ketones, neurovital signs,
and laboratory studies
- Weigh the patient daily
- Administer medications, as prescribed
- Encourage the patient to express his feelings about fear of dying
- Protect the patient from falls
- Minimize environmental stress
- Provide rest periods
- Keep phentolamine (Regitine) available
- Provide postradiation nursing care
o Provide skin and mouth care
o Monitor dietary intake
o Provide rest periods
- Individualize home care instructions
o Stop smoking
o Recognize the signs and symptoms of renal failure
o Monitor blood pressure, urine glucose, and ketones daily

 Complications
- Cardiac arrest - Renal failure
- Cerebral hemorrhage - MI
- Blindness - Heart failure

 Surgical interve ntions

- Adrenal medulla resection after administration of phentolamine (Regitine)
- Adrenalectomy

pg. 12
 HYPERALDOSTERONENISM (PRIMARY ALDOSTERONISM, CONN’S SYNDROME)

 Definition ‘
- Hypersecretion of aldosterone (mineralocorticoids) from adrenal cortex

 Causes
- Adenoma of adrenal cortex
- Adrenal hyperplasia
- Adrenal carcinoma

 Pathophysiology
- Aldosterone’s primary effect on the renal tubules causes the kidneys to retain sodium and water and excrete potassium and
hydrogen

 Assessment findings
- Muscle weakness - Headache
- Polyuria - Paresthesia
- Polydipsia - Pyelonephritis
- Metabolic alkalosis - Nocturia
- Hypertension - Chvostek's sign: positive
- Postural hypotension - Trousseau's sign: positive

 Diagnostic test findings

- Blood chemistry: decreased potassium; increased sodium, carbon dioxide
- Arterial blood gas (ABG) analysis: metabolic alkalosis
- Urine chemistry: increased aldosterone, protein, pH; decreased specific gravity

 Medical management
- Diet: high-potassium, low-sodium
- Activity: as tolerated
- Monitoring: vital signs and I/O
- Laboratory studies: potassium, sodium, calcium, and ABG analysis
- Potassium salts: potassium chloride (KCI), potassium gluconate (Kaon)
- Diuretics: spironolactone (Aldactone), acetazolamide (Diamox)
- Calcium salts: calcium gluconate (Kalcinate), calcium carbonate (Os-Cal)

 Nursing interventions
- Maintain the patient's diet, as tolerated
- Monitor and record vital signs, I/O, orthostatic blood pressure, specific gravity, and laboratory studies
- Monitor laboratory results: ABG analysis, sodium, potassium, and calcium
- Administer medications, as prescribed
- Allay the patient's anxiety
- Weigh the patient daily
- Provide a quiet environment
- Individualize home care instructions cells
o Recognize the signs and symptoms of fluid overload and muscle irritability
o Comply with medical follow-up

 Complications
- Neuropathy
- Arrhythmias
 Surgical intervention
- Adrenalectomy

pg. 13
 DIABETES MELLITUS

 Definition
- Chronic disorder of carbohydrate metabolism with subsequent alteration of protein and fat metabolism
- Results from a disturbance in the production, action, and rate of insulin use
- Five types of diabetes mellitus
o Type 1 (insulin-dependent diabetes mellitus or ketosis-prone): usually develops in childhood
o Type 2 (non-insulin-dependent diabetes mellitus or ketosis-resistant): usually develops after age 30
o Gestational diabetes mellitus: occurs with pregnancy
o Secondary diabetes: induced by trauma, surgery, pancreatic disease or medications; can be treated as type 1 or type 2
o Maturity-onset diabetes: type 2 that develops in teens and young adults under age 30

 Causes
- Failure of body to produce insulin - Hyperthyroidism
- Blockage of insulin supply - Infection
- Autoimmune disease - Surgery
- Receptor defect in normally insulin-responsive cells - Stress
- Genetics - Medications
- Exposure to chemicals - Pregnancy
- Hyperpituitarism - Trauma
- Cushing’s syndrome

 Pathophysiology
- Type 1 results from an inability to produce endogenous insulin by the beta cells in the islets of Langerhans in the pancreas
- Type 2 is a deficit in insulin release or an insulin-receptor defect in peripheral tissues
- Insulin deprivation of insulin-dependent cells leads to a marked decrease in the cellular rate of glucose uptake
- Glucogenesis increases because of decreased stimulation of glucose metabolism with resulting hyperglycemia and glycosuria
- Decreased insulin triggers release of free fatty acids that can’t be metabolized and are released as ketone bodies in blood and
urine
- Decreased insulin depresses protein synthesis, causing a release of amino acids that the liver converts into glucose and
ketones
- The formation of urea results in overall nitrogen loss

 Assessment findings
- Weight loss - Kussmaul's respirations
- Anorexia - Multiple infections and boils
- Polyphagia - Flushed, warm, smooth, shiny skin
- Acetone breath - Atrophic muscles
- Weakness - Poor wound healing
- Fatigue - Mottled extremities
- Dehydration - Peripheral and visceral neuropathies
- Pain - Retinopathy
- Paresthesia - Sexual dysfunction
- Polyuria - Blurred vision
- Polydipsia

 Diagnostic test findings

- Blood chemistry: increased glucose, potassium, chloride, ketones, cholesterol, and triglycerides; decreased carbon dioxide;
pH less than 7.4
- Urine chemistry: increased glucose, ketones
- Fasting serum glucose: increased
- GIT: hyperglycemia
- Postprandial blood glucose: hyperglycemia
- Glycosylated Hb assay: increased

 Medical management

pg. 14
 - Diet: individually prescribed diet based on ideal weight, metabolic activity, and personal activity levels
- Use the American Diabetes Association's exchange list for meal planning to design a diet that will distribute an individual’s
caloric needs, carbohydrate, fat, and protein intake over 24 hours
- Avoid refined and simple sugars and saturated fats
- Limit cholesterol
- Include high fiber and high complex carbohydrates
- Activity: as tolerated
- Monitoring: vital signs and I/O
- Laboratory studies: glucose, potassium, glycosylated Hb, and pH, and liver and renal function tests
- Hypoglycemics: rapid-acting (Lispro), short-acting (regular), intermediate- acting (NPH), long-acting (Ultralente, Lantus-
insulin glargine); glyburide (DiaBeta, Micronase, Amaryl); glipizide (Glucotrol, Glucotrol XL); metformin (Glucophage);
pioglitazone (Actos); rosiglitazone (Avandia); repaglinide (Prandin)
- Vitamin and mineral supplements

 Nursing interventions
- Maintain the patient's diet
- Encourage fluids
- Assess acid-base balance
- Monitor and record vital signs, I/O, blood glucose levels, and laboratory studies
- Administer medications, as prescribed
- Encourage the patient to express his feelings about diet, medication regimen, and body image changes
- Encourage activity, as tolerated
- Weigh the patient weekly
- Provide meticulous skin and foot care
- Monitor the patient for infection
- Maintain a warm and quiet environment
- Monitor wound healing
- Observe for Somogyi phenomena and Sjögren’s syndrome
- Provide information about the American Diabetes Association
- Foster independence
- Determine the patient's compliance to diet, exercise, and medication regimens
- Individualize home care instructions
o Exercise regularly
o Stop smoking
o Recognize the signs and symptoms of hyperglycemia and hypoglycemia
o Monitor self for infection, skin breakdown, changes in peripheral circulation, poor wound healing, and numbness in
extremities
o Know and use proper dietary substitutions if unable to take prescribed diet because of illness
o Adjust diet and insulin for changes in work, exercise, trauma, infection, fever, and stress
o Demonstrate administration of hypoglycemics
o Demonstrate home blood glucose monitoring technique
o Complete daily skin and foot care
o Carry an emergency supply of glucose
o Seek counseling for sexual dysfunction and feelings about body image changes
o Avoid use of OTC medication
o Avoid alcohol
o Demonstrate use of the subcutaneous insulin infusion therapy (insulin pump)
o Adhere to the treatment regimen to prevent complications

 Complications
- Ketoacidosis (diabetic coma): abdominal pain; acetone breath; altered consciousness; hot, flushed skin; Kussmaul's
respirations; nausea; vomiting; hypotension; oliguria; tachycardia (see Understanding DKA and HHNS)
- Insulin reaction (hypoglycemia): hunger, weakness, hand tremors, pallor, tachycardia, diaphoresis, irritability, confusion,
diplopia, slurred speech, headaches
- Infections

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 - Peripheral neuropathies
- Glaucoma
- Impotence
- CAD
- Gangrene
- Stroke
- Chronic renal failure
- Hyperosmolar hyperglycemic nonketotic syndrome: severe dehydration, severe hypotension, fever, stupor, and seizures
- Hypovolemia
- Diabetic retinopathy
- Peripheral vascular disease

 Surgical interventions
- None

DIABETES INSIPIDUS
 Definition
- Deficiency of ADH (vasopressin) that's secreted by the posterior lobe of the pituitary gland (neurohypophysis)

 Causes
- Trauma to posterior lobe of pituitary gland - Head injury
- Tumor of posterior lobe of pituitary gland - Idiopathic
- Brain surgery - Meningitis

 Pathophysiology
- Decreased ADH reduces the ability of distal and collecting renal tubules to concentrate urine
- Copious, dilute urine, and intense thirst result

 Assessment findings
- Polyuria (greater than 5 L/day) - Weight loss
- Polydipsia (4 to 40 L/day) - Muscle weakness and pain
- Fatigue - Headache
- Dehydration - Tachycardia

 Diagnostic test findings

- Urine chemistry: specific gravity less than 1.004, osmolality 50 to 200 mOsm/kg
- Blood chemistry: decreased ADH by radioimmunoassay
- Water deprivation test: inability to concentrate urine

 Medical management
- Diet: regular with restriction of foods that exert a diuretic effect
- IV therapy: hydration, electrolyte replacement; saline lock
- Activity: bed rest
- Monitoring: vital signs, CVP, and I/O
- Laboratory studies: potassium, sodium, BUN, creatinine, specific gravity; and osmolality
- Treatments: indwelling urinary catheter
- ADH stimulant: carbamazepine (Tegretol)
- ADH replacement: lypressin (Diapid nasal spray)

 Nursing interventions
- Maintain the patient's diet - Administer medications, as prescribed
- Encourage fluids - Allay the patient's anxiety
- Administer LV. fluids - Weigh the patient daily
- Maintain patency of indwelling urinary catheter - Individualize home care instructions
- Monitor and record vital signs, CVF [/O, specific o Recognize the signs and symptoms of
gravity, and laboratory studies dehydration

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 o Increase fluid intake in hot weather o Carry medications on person at all times

 Complications
- Dehydration
- Arrhythmias
- Hypovolemic shock

 Surgical intervention
- Hypophysectomy, when etiology is tumor

Understanding DKA and HHNS

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic nonketotic syndrome (HHNS) are acute complications of
hyperglycemic crisis that may occur with diabetes. If not treated property, either may result in coma or death.
DKA occurs most often in patients with type 1 diabetes and may be the first evidence of the disease. HNNS occurs most
often in patients with type 2 diabetes, but it also occurs in anyone whose insulin tolerance is stressed and in patients who have
undergone certain therapeutic procedures, such as peritoneal dialysis, hemodialysis, tuba feedings, or total parenteral nutrition.
Acute insulin deficiency (absolute in DKA; relative in HHNS) precipitates both conditions. Causes include illness, stress,
infection and, in patients with DKA, failure to take insulin.

BUILDUP OF GLUCOSE
Inadequate insulin hinders glucose uptake by fat and muscle cells, Because the to convert to energy, glucose accumulates in the blood.
At the same time, the liver responds to the demands of the energy-starved cells by converting glycogen to glucose and releasing
glucose into the blood, further increasing the blood glucose level. When this level exceeds the renal threshold, excess glucose is
excreted in the urine. Still, the insulin-deprived cells can't utilize glucose. Their response is rapid metabolism of protein, which results
in loss of intracellular potassium and phosphorus and excessive liberation of amino acids. The liver converts these amino acids into
urea and glucose.
As a result of these processes, blood glucose levels are grossly elevated. The aftermath is increased to serum osmolarity and
glycosuria (high amounts of glucose in the urine), leading to osmotic diuresis. Glucosuria is higher in HHNS than in DKA” because
blood glucose levels are higher in HHNS.

A DEADLY CYCLE
The massive fluid loss from osmotic diuresis causes fluid and electrolyte imbalances and dehydration. Water loss exceeds glucose and
electrolyte loss, contributing to hyperosmolarity. This, in turn, perpetuates dehydration, decreasing the glomerular filtration rate and
reducing the amount of glucose excreted in the urine. This leads to a deadly cycle: Diminished glucose excretion further raises blood
glucose levels, producing hyperosmolarity and dehydration and finally causing shock, coma, and death.

DKA complication
All of these steps hold true for DKA and HHNS, but DKA involves an additional, simultaneous process that leads to metabolic
acidosis. The absolute insulin deficiency causes cells to convert fats into glycerol and fatty acids for energy. The fatty acids can't be
metabolized as quickly as they're released, so they accumulate in the liver, where they're converted into ketones (ketoacids). These
ketones accumulate in the blood and urine and cause acidosis. Acidosis leads to more tissue breakdown, more ketosis, more acidosis,
and eventually shock, coma, and death.

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