DISORDERS OF THE ENDOCRINE SYSTEM

ENDOCRINE SYSTEM ENDOCRINE GLANDS ENDOCRINE SYSTEM*ENDOCRINE GLANDS*Secrete their products directly into the bloodstream *Different from exocrine glands *Exocrine glands: secrete through ducts onto epithelial surfaces or into the gastrointestinal tract

HORMONES*Are chemical substances that are secreted by the endocrine glands. *Can travel moderate to long distances or very short distances. *Acts only on cells or tissues that have receptors for the specific hormone. *Target organ: the cell or tissue that responds to a particular hormone.

HYPOTHALAMUS AND PITUITARY GLAND REGULATION OF HORMONES: NEGATIVE FEEDBACK MECHANISM*If the client is healthy, the concentration or hormones is maintained at a constant level. *When the hormone concentration rises, further production of that hormone is inhibited. *When the hormone concentration falls, the rate of production of that hormone increases.

Diseases of the Endocrine System*Primary disease problem in target gland; autonomous *Secondary disease problem outside the target gland; most often due to a problem in the pituitary gland

Disorders of the Anterior Pituitary GlandHYPOPITUITARISM HYPERPITUITARISM

HYPOPITUITARISM*Caused by low levels of one or more anterior pituitary hormones. *Lack of the hormone leads to loss of function in the gland or organ that it controls.

Causes of Primary Hypopituitarism*Pituitary tumors *Inadequate blood supply to pituitary gland*Sheehan syndrome

*Infections and/or inflammatory diseases*Sarcoidosis *Amyloidosis

*Radiation therapy *Surgical removal of pituitary tissue *Autoimmune diseases *Congenital absence

Causes of secondary hypopituitarism (affecting the hypothalamus):

*Tumors of the hypothalamus *Inflammatory disease *Head injuries *Surgical damage to the pituitary and/or blood vessels or nerves leading to it

Signs and Symptoms Signs and Symptoms*Gonadotropin deficiency*Congenital onset *Delayed or absent secondary sexual characteristics *May have micropenis, cryptorchidism *Acquired *Loss of body hair *Infertility, decreased libido, impotence in males, amenorrhea in females *Osteopenia, muscle atrophy

*Prolactin deficiency*Failure to lactate

Signs and Symptoms*Thyroid-stimulating (TSH) deficiency*Causes hypothyroidism with manifestations such as fatigue, weakness, weight change, and hyperlipidemia

*Adrenocorticotropic hormone (ACTH) deficiency*Results in diminished cortisol secretion *Symptoms include weakness, fatigue, weight loss, and hypotension

Signs and Symptoms Diagnostics Treatment*Surgery for tumors: transsphenoidal hypophysectomy *Radiation therapy for tumors *Hormonal substitution: maybe for life*Corticosteroids *Levothyroxine *Androgen for males *Estrogen for females *Growth hormone

HYPERPITUITARISM*Hyperfunction of the anterior pituitary gland oversecretion of one or more of the anterior pituitary hormones *Usually caused by a benign pituitary adenoma *Most common hormones affected:*Prolactin

*Growth hormone

PITUITARY TUMOR: PROLACTINOMAGrowth Hormone Hypersecretion0 Early onset Late onset Acromegaly epiphyseal closure occur at normal times Gigantism acromegalic gigantism 25 50 years

Gigantism vs. Acromegaly Gigantism vs. AcromegalyGrowth Hormone Hypersecretion: Signs and Symptoms*Enlarged hand and feet; carpal tunnel syndrome common *Coarsening of features esp. in acromegaly; prominent mandible, tooth spacing widens *Macroglossia *Hypertension, cardiomegaly, heart failure *Insulin resistance DM *Visual fields defect: bitemporal hemianopsia complete blindness *Headaches *Arthritis *Hypogonadism

Treatment*Medication*Bromocriptine and cabergoline (dopamine agonist) for prolactinoma and GH hypersecretion *Octreotide (somatostatin) for GH hypersecretion

*Surgery*Transsphenoidal hypophysectomy

*Radiation therapy for large tumors *Diet

NURSING INTERVENTIONS*Provide emotional support striking body change can cause psychological stress *Perform or assist with range of motion exercises to promote maximum joint mobility and prevent injury *Evaluate muscle weakness

NURSING INTERVENTIONS*Keep the skin dry

*Be aware that pituitary tumor may cause visual problems. *Warn relatives that hyperpituitarism can cause inexplicable mood changes

NURSING INTERVENTIONS*If the patient is a child, explain to the parents that surgery prevents permanent soft-tissue deformities but wont correct bone changes that have already occurred. *Emphasize the importance of continuing hormonal replacement therapy.

Question*What is the medication of choice in the treatment of GH hypersecretion and prolactinoma?*Bromocriptine *Cabergoline *Octreotide *Vasopressin

Question*As a nurse which of the following is the most important nursing consideration?*Ensuring a safe environment *Giving the medications as prescribed *Providing emotional support and counseling *Assisting in ROM exercises to prevent contractures

Question*The hypothalamus has direct control over which of the following organs? *Adrenal gland *Thyroid gland *Kidneys

*Ovaries *Prostate

Disorders of the Posterior Pituitary GlandDiabetes Insipidus SIADH

Vasopressin or Antidiuretic Hormone

Diabetes Insipidus Diabetes Insipidus*Central diabetes insipidus: Deficiency of vasopressin*Primary diabetes insipidus*Maybe familial, occurring as a dominant trait, or sporadic (idiopathic)

*Secondary diabetes insipidus*Due to damage to the hypothalamus or pituitary stalk by tumor, surgical or accidental trauma, infection

Diabetes Insipidus Diabetes InsipidusSIGNS AND SYMPTOMS *Polyuria *Intense thirst *Dehydration *Inadequate water replacement*hyperosmolality *hypovolemia

Diabetes InsipidusDIAGNOSTICS *Fluid deprivation test *Administration of desmopressin *24 hour urine collection for volume, glucose, and creatinine *Serum for glucose, urea nitrogen, calcium, uric acid, potassium, sodium

Diabetes Insipidus

MEDICATIONS *For Central DI*Desmopressin; intranasal *Lypressin; intranasal *Vasopressin tannate in oil; IM

*For Nephrogenic DI*Indomethacin-hydrochlorothiazide *Indomethacin-desmopressin *Indomethacin-amiloride

*Clofibrate, chlorpropamide *Psychotherapy

Diabetes Insipidus: Nursing Management*Maintain fluid and sodium balance*Record I and O. Weigh patient daily. *Maintain fluid intake to prevent severe dehydration *WOF: dehydration and shock *Keep the side rails up and assist with walking if the patient is dizzy or has muscle weakness *Monitor urine specific gravity between doses. Watch for decreased specific gravity with increased urine output. *Add more bulk food and fruit juices to diet

Diabetes Insipidus: Nursing Management*Provide meticulous skin and mouth care, an apply a lubricant to cracked or sore lips *Diet: low in sodium

*Carry out drug therapy*Caution with vasopressin if coronary disease is present vasoconstriction

*Assist in searching for the underlying pathology

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)*Disorder due to excessive ADH release *Signs and symptoms: *Persistent excretion of concentrated urine *Signs of fluid overload *Change in level of consciousness *Hyponatremia *No edema

Syndrome of Inappropriate Antidiuretic Hormone (SIADH): Causes of SIADH*Tumors*Bronchogenic CA

*Lymphoma *Pancreatic cancer *Mesothelioma

*Pulmonary*TB *Pneumonia *Lung abscess *COPD *Pneumothorax *P. carinii pneumonia

Syndrome of Inappropriate Antidiuretic Hormone (SIADH): Causes of SIADH *CNS*Meningitis *Subdural hematoma *Subarachnoid hemorrhage

*Drugs*Vincristine *Phenothiazines *Tricyclic antidepressants

Syndrome of Inappropriate Antidiuretic Hormone (SIADH): Diagnostic Tests*Low serum sodium < 135 meq/LO *Low serum osmolality *High urine osmolality ( >100 mosmol/kg) *High urine sodium excretion ( >20 mmol/L) *Normal renal function (low BUN 100, withhold the drug. Assess for tachyarrhytmias and chest pain.

Nursing Management of replacement therapy*Thyroid hormones alter thyroid function test results*For I uptake studies *D/C levothyroxine 4 wks before the test *D/C liothyronine 7 to 10 days before the test

*Monitor prothrombin time*WOF: unusual bleeding and bruising

Hypothyroidism: Nursing Interventions*Diet: high-bulk, low calorie diet *Encourage activity *Maintain warm environment *Administer cathartics and stool softeners *To prevent myxedema coma, tell the patient to continue course of thyroid medication event if symptoms subside *Maintain patent airway *Administer medications synthroid, glucose, corticosteroids *IV fluid replacement *Wrap patient in blanket *Treat infection or any underlying illness

Disorders of the PancreasDiabetes Mellitus

Hormones of the Pancreas*Insulin*Decreases blood sugar by: *Stimulating active transport of glucose into muscle and adipose tissue *Promoting the conversion of glucose to glycogen for storage *Promoting conversion of fatty acids into fat *Stimulating protein synthesis *Secreted in response to high blood sugar *Found in cells of the Islets of Langerhans

Hormones of the Pancreas*Glucagon*Increases blood glucose by*Causing gluconeogenesis and glycogenolysis in the liver

*Secreted in response to low blood sugar *Found in the -cells of the Islets of Langerhans

Diabetes Mellitus*Chronic disease characterized by hyperglycemia *It is due to total or partial insulin deficiency or insensitivity of the cells to insulin *Characterized by disorders in the metabolism of CHO, FATS, CHON as well as changes in the structure and function of blood vessels

Types of Diabetes Mellitus*Type 1 or IDDM*Usually occurs in children or in non-obese adults

*Type 2 or NIDDM*Usually occurs in obese adults or over age 40

*Gestational DM *Secondary DM*Induced by trauma, surgery, pancreatic disease or medications *Can be treated as either type 1 or type 2

Pathophysiology*Lack of insulin causes hyperglycemia (insulin is necessary for the transport of glucose across the membrane) *Body excretes excess glucose through kidneys osmotic diuresis polyuria

dehydration polydipsia *Cellular starvation polyphagia *The body turns to fats and proteins for energy; but in the absence of glucose in the cell, the fats cannot be completely metabolized and ketones are produced

Chronic Complications*Microangiopathy: retinopathy, nephropathy *Macroangiopathy: peripheral vascular diseae, atherosclerosis, CAD *Neuropathy

Instruction in the Care of the Feet*Hygiene of the feet*Wash feet daily with mild soap and lukewarm water. Dry thoroughly between the toes by pressure. Do not rub vigorously, as this is apt to break the delicate skin. *Rub well with vegetable oil to keep them soft, prevent excess friction, remove scales, and prevent dryness. *If the feet become too soft and tender, rub them with alcohol abut once week.

Instruction in the Care of the Feet*Hygiene of the feet*When rubbing the feet, always rub upward from the tips of the toes. If varicose veins are present, massage the feet very gently; never massage the legs. *Of the toenails are brittle and dry, soften them by soaking for 1 hour each night in lukewarm water containing 1 tbsp of powdered sodium borate (borax) per quart. Clean around the nails with an orangewood stick. If the nails become too long, file them with an Amery board. File them straight across and no shorter than the underlying soft tissue of the toes. Never cut the corner of the nails.

Instruction in the Care of the Feet*Wear low heeled shoes of soft leather that fit the shape of the feet correctly. The shoes should have wide toes that will cause no pressure, fit close in the arch, and grip the heels snugly. Wear new shoes one-half hour only on the first day and increase by 1 our each day following. Wear thick, warm, loose stockings.

Instruction in the Care of the Feet*Treatment of corns and calluses*Corns and calluses are due to friction and pressure, most often from improperly fitted shoes and stockings. Wear shoes that fit properly and cause no friction or pressure. *To remove excess calluses or corns, soak the feet in lukewarm water, using a mild soap, for about 10 minutes and then rub off the excess tissue with a towel or file. Do not tear it off. Under no circumstances must the skin be irritated.

Instruction in the Care of the Feet*Treatment of corns and calluses*Do not cut corns or calluses. If they need attention it is safer to see a

podiatrist. *Prevent callus formation under the ball of the foot (a) by exercise, such as curling and stretching the toes several times a day; (b) by finishing each step on the toes and not on the ball of the foot; and (c) by wearing shoes that are not too short and that do not have high heels.

Diagnostics: FBS and OGTTDiagnostics: Glycosylated hemoglobin*NV = 7.5% or less, good control *7.6% to 8.9% fair control *9% or greater, poor control

Therapeutic Interventions:*Life-style changes*Weight control and exercises *Planned diet*50 60% of calories are complex carbohydrates, high fiber *12 20% daily calories is CHON *Fat intake not to exceed 30% of daily calories, more of polyunsaturated fats *Basic tools: food exchange groups

*Self-monitoring of blood glucose

Therapeutic Interventions:*Insulin administration*Type 1 IDDM and type 2 DM when diet and weight control therapy failed *Aspirin, alcohol, oral anticoagulants, oral hypoglycemics, beta blockers, tricyclic antidepressants, tetracycline, MAOIs increase the hypoglycemic effects of insulin *Glucocorticoids, thiazide diuretics, thyroid agents, oral contraceptives increase blood glucose levels *Illness, infection, and stress increase the need for insulin

Insulin AdministrationComplications of Insulin Therapy*Local allergic reaction, lipodystrophy, insulin resistance *Dawn phenomenon*Increase in blood sugar because of release of growth hormone at around 3AM *TX: give at 10PM, intermediate-acting insulin

*Somogy effect*Rebound hyperglycemia at 7 AM after a bout of hypoglycemia at around 2-3AM *Tx: decrease the evening dose of intermediate acting insulin

Complications of Insulin Therapy*Hypoglycemia*If awake, give 10-15 g of fast-acting simple juice carbohydrate (glucose

tablets, fruit juice, and soda) *If unconscious, glucagon SQ or IM *If in the hospital, 25-50 cc of D50%

Oral Hypoglycemic Agents*For DM type 2 *May have to be shifted to insulin when sick, under stress, during surgery *Necessary to shift to insulin when pregnant

Oral Hypoglycemic Agents*Sulfonylureas*Promotes increase insulin secretion from pancreatic beta cells through direct stimulation *First Generation Agents:*Tolbutamine, Acetohexamide, Tolzamide, Chlorpropamide

*Second Generation Agents*Glypizide, Glyburide

Oral Hypoglycemics*Biguanides*Reduces hepatic production of glucose by inhibiting glycogenolysis *Decrease the intestinal absorption of glucose and improving lipid profile *Agents:*Phenformin, Metformin, Buformin

Oral Hypoglycemics*Alpha-glucosidase inhibitors*Inhibits alpha-glucosidase enzymes in the small intestine and alpha amylase in the pancreas *Decreases rate of complex carbohydrate metabolism resulting to a reduced rate postprandially *Agents:*Acarbose (precose), Miglitol (glyset)

Oral Hypoglycemics*Thiazolidinediones*Enhances insulin action at the cell and post-receptor site and decreasing insulin resistance *Agents:*Pioglitazone (Actos), Rosiglitazone (Avandia)

Acute Complication: DKA*Characterized by hyperglycemia and accumulation of ketones in the body causing metabolic acidosis

*Occurs in Insulin-Dependent Diabetic Client *Precipitating Factors: undiagnosed diabetes, neglect of treatment, infection, other physical or emotional stress *Onset slow, maybe hours to days

DKA: Signs and Symptoms*Polydipsia, polyphagia and polyuria *Nausea and vomiting, abdominal pain *Skin warm, dry and flushed *Dry mucous membrane *Kussmauls respirations or hyperventilation; acetone breath *Alterations in LOC *Hypotension, tachycardia

Hyperglycemic Hyperosmolar Nonketotic Coma (HHNK)*Characterized by hyperglycemia and a hyperosmolar state without ketosis *Occurs in NIDDM or non-diabetic persons (typically elderly persons) *Precipitating factors: undiagnosed diabetes, infection, or other stress; certain medications, dialysis, hyperalimentation, major burns

Emergency Management:*For both DKA and HHNK, treat dehydration first with 0.9% or ).45% saline solution*Shift to D5W when glucose level is down to 250-300mg/dl *WOF to rapid correction, it can cause rapid fluid shifts (brain edema and increased ICP, ARDS)

*IV regular insulin 0.1 unit/kg bolus then 0.1 unit/kg/h drip *Correcting electrolyte imbalance: watch out for hypokalemia as a result of treatment.

Disorders of the Adrenal GlandsCushings Syndrome Hyperaldosteronism Adrenal Insufficiency Pheochromocytoma

Adrenal Glands Adrenal Medulla Adrenal Cortex Hormones*Glucocorticoids*Cortisol, corticosterone *Increase blood glucose levels by increasing rate of gluconeogenesis

*Increase protein catabolism *Increase mobilization of fatty acids *Promote sodium and water retention *Anti-inflammatory effect *Aid the body in coping with stress

Adrenal Cortex Hormones*Mineralocorticoids*Aldosterone, Corticosterone, Deoxycorticosterone *Regulate fluid and electrolyte balance *Stimulate reabsorption of sodium, chloride and water *Stimulate potassium excretion

*Under the control of Renin-Angiotensin-Aldosterone system

Adrenal Cortex Hormones*Sex hormones*Androgens, Estrogens *Influences the development of sexual characteristics

Hypercortisolism (Cushings Syndrome)*Cluster of physical abnormalities due to excessive cortisol release *Cortisol excess is due either to:*Autonomous steroid release from adrenals *Increased ACTH release from pituitary *Complication from exogenous steroid tx

Hypercortisolism (Cushings Syndrome) Hypercortisolism (Cushings Syndrome)

Complications*Osteoporosis *Peptic ulcer *Immune and inflammatory response is also compromised *Other complications include HPN, and sexual and psychological complications

Cushings Syndrome: Diagnostics*ACTH levels determines whether the syndrome is ACTH dependent *24 hr urine collection for cortisol, midnight serum cortisol *Dexamethsone suppression test 1 mg dexamethasone is given at 11 pm and serum cortisol taken at 8 AM the next day

*Radiologic evaluation

Cushings Syndrome: Management*Transsphenoidal resection of pituitary tumor *Medications:*Aminogluthetimide: adrenal enzyme inhibitor *Metyrapone and ketokonazole: suppress hypercrtisolism in unresectable adrenal tumor

*Antihypertensives *Adrenalectomy as needed

Cushings Syndrome: Nursing Considerations*Monitor VS, WOF for HPN *Safety precaution: *Maintain muscle tone *Prevent accidents or falls and provide adequate rest *Protect client from exposure to infection, monitor WBC *Maintain skin integrity *Minimize stress *Provide diet low in calories, sodium, and high in protein, potassium, calcium and Vitamin D *Monitor for urine glucose and acetone, administer insulin if necessary *Prepare client for adrenalectomy if needed

Hyperaldosteronism*Hypersecretion of aldosterone from the adrenal cortex *Two types:*Primary disease of the adrenal cortex *Secondary condition due to increased plasma renin activity

*Causes:*Excessive reabsorption of sodium and water *Excessive renal excretion of potassium

Hyperaldosteronism: Causes*Primary aldosteronism: autonomous secretion of aldosterone from adrenals*Benign adrenal adenoma (Conns syndrome) *Bilateral adrenocortical hyperplasia

Hyperaldosteronism: Causes*Secondary hyperaldosteronism: high renin state stimulating aldosterone release*Renal artery stenosis *Wilms tumor *Pregnancy *Oral contraceptive use *Nephritic syndrome *Cirrhosis with ascites *Idiopathic edema

*Heart failure *Extrarenal sodium loss

Hyperaldosteronism: Signs and Symptoms*Hypertension*Headache and visual disturbance

*Hypokalemia*Muscle weakness and fatigue *Paresthesia and arrhythmias *Polyuria and polydipsia *Tetany from alkalosis

*Hypernatremia

Hyperaldosteronism: Diagnostics*Hypokalemia (145 meq/L) *Elevated serum bicarbonate and pH *Hypomagnesemia *Elevated plasma and urinary aldosterone * Renin in primary hyperaldosteronism * Renin in secondary hyperaldosteronism *Low specific gravity urine (diluted urine)

Hyperaldosteronism: Treatment*Primary aldosteronism:*Unilateral adrenalectomy

*Potassium-sparing diuretic *Antihypertensives *Aminogluthemide *Diet: sodium restriction, increase potassium *Treatment of secondary hyperaldosteronism

Adrenal Insufficiency*Addisons disease- the most common form of adrenal hypofunction *Autoimmune process, circulating antibodies react specifically against the adrenal tissue *Acute adrenal insufficiency, or adrenal crisis (Addisonian crisis) is a medical emergency requiring immediate, vigorous treatment

Adrenal Insufficiency: Causes*Autoimmune destruction of the adrenal gland, tuberculosis, bilateral adrenalectomy, hemorrhage into the adrenal gland, neoplasm, fungal infection *Secondary adrenal hypofunction

*Hypopituitarism *Abrupt withdrawal of long-term corticosteroid therapy

Adrenal Insufficiency: Signs and Symptoms*Weakness, fatigue *Weight loss, nausea and vomiting, anorexia *Chronic constipation or diarrhea *Cardiovascular abnormalities*Postural hypotension, decreased heart size and cardiac output *Weak, irregular pulse *Decreased tolerance for minor stress

Adrenal Insufficiency: Signs and Symptoms*Conspicuous bronze skin coloration *Poor coordination *Fasting hypoglycemia: and craving for salty food *Amenorrhea *Adrenal crisis

Adrenal Insufficiency: Diagnostic tests*Decreased plasma cortisol and serum sodium levels *Increased ACTH (in Addisons), serum potassium, and blood urea nitrogen level

Adrenal Insufficiency : Treatment*Corticosteroid replacement *Fludrocortisone acetate acts as mineralocorticoid to prevent dehydration and hypotension *Adrenal crisis: prompt IV bolus of corticosteroids, 3 to 5 L of IV fluids, dextrose

Adrenal Insufficiency: Nursing Management*WOF: adrenal crisis*Hypotension and signs of shock *Decreased level of consciousness and urine output *Watch for hyperkalemia before treatment and for hypokalemia after treatment (from excessive mineralocorticoid effect)

*If patient has diabetes, check blood glucose levels periodically because replacement may necessitate changing the insulin dosage

Adrenal Insufficiency: Nursing Management*Diet: maintain sodium and potassium balance, high protein, and carbohydrates

*If the patient is anorexic, suggest six small meals per day to increase calorie intake *Observe the patient receiving steroids for cushingoid signs, such as fluid retention around the eyes and face

Adrenal insufficiency: Nursing management*Instruct on lifelong cortisone replacement therapy. Do not omit medications. Give 2/3 of dose in AM and 1/3 in PM *Instruct the patient that hell need to increase the dosage during times of stress *Warn that infection, injury, profuse sweating may precipitate crisis

Pheochromocytoma*Rare disorder, a chromaffin-cell tumor of the sympathetic nervous system, usually in the adrenal medulla, secrets an excess of the catecholamine epinephrine and norepinephrine *Causes episodes of hypertension and symptoms of catecholaine excess *Usually benign but may be malignant

Pheochromocytoma Pheochromocytoma: Signs and Symptoms*Think sympathetic!*Persistent or paroxysmal hypertension *Palpitations, tachycardia, headache, visual disturbance, diaphoresis, pallor, warmth or flushing, paresthesia, tremor, excitation *Anxiety, fright, nervousness, feelings of impending doom, abdominal or chest pain, tachypnea, nausea and vomiting, fatigue, weight loss, constipation

Pheochromocytoma:*Diagnostic tests:*Increased plasma levels of catecholamines, elevated blood sugar, glucosuria *Elevated urinary catecholamines and urinary vanilymandelic acid levels*Avoid coffee, nuts, chocolates, banana

*Tumor on CT scan

Pheochromocytoma: Treatment*Surgical removal of the tumor with sparing of normal adrenals*WOF: hypo or hypertension post-op

*Antihypertensives

*Alpha-adrenergic blocker *Beta-adrenergic blocker *Calcium channel blockers

*Metyrosine may be used to block catecholamine synthesis

Adrenalectomy*Resection or removal of one or both adrenal glands *The treatment of choice:*For adrenal hyperfunction and hyperaldosteronism *Adrenal tumors, such as adenomas and pheochromocytomas

Adrenalectomy: Pre-op*Correct electrolyte imbalance*Potassium *Sodium *Calcium

*Manage hypertension

Adrenalectomy: Post-op*Monitor vital signs *WOF: shock from hemorrhage *Keep in mind that post-op hypertension is common because of handling of the adrenal glands stimulate catecholamine release *WOF: adrenal crisis hypotension, hyponatremia, hyperkalemia

Adrenalectomy: Nursing Interventions*Instruct the patient to take prescribed medication as directed *If patient had unilateral adrenalectomy, explain that he may be able to taper his medication in a few months *Inform patient that sudden withdrawal of steroids can precipitate adrenal crisis

Disorders of the Parathyroid GlandsHyperthyroidism Hypothyroidism

Parathyroid glands Hyperparathyroidism Hyperparathyroidism: Causes*Primary hyperparathyroidism:

*Single adenoma, genetic disorders, or multiple endocrine neoplasias

*Secondary hyperparathyroidism:*Rickets, vitamin D deficiency, chronic renal failure, or phenytoin or laxative abuse

Hyperparathyroidism*Effect of PTH secretion: calcium*Through increased bone resorption, increased GI and renal absorption of calcium

*Complications*Renal calculi renal failure *Osteoporosis *Pancreatitis *Peptic ulcer

Hyperparathyroidism: Signs and Symptoms*Think of Hypercalcemia:*CNS; psychomotor and personality disturbances, loss of memory for recent event, depression, overt psychosis, stupor and, possibly coma *GI: anorexia, nausea, vomiting, dyspepsia, and constipation *Neuromuscular: fatigue, marked muscle weakness and atrophy, particularly in the legs

Hyperparathyroidism: Signs and Symptoms*Renal: symptoms of recurring nephrolithiasis renal insufficiency *Skeletal and articular: chronic lower back pain and easy fracturing from bone degeneration, bone tenderness, joint pain *Others: skin pruritus, vision impairment from cataracts, subcutaneous calcification

Hyperparathyroidism:Diagnostics* serum PTH levels * serum calcium and phosphorus levels *X-rays may show diffuse demineralization of bones *Elevated alkaline phosphatase

Hyperparathyroidism: Treatment*Surgery to remove adenoma *Force fluids: limiting dietary calcium intake *For life threatening hypercalcemia: promote sodium and calcium excretion, using normal saline solution, furosemide; and administering oral sodium or potassium phosphate, calcitonin *Postmenopausal women: estrogen supplements

Hypoparathyroidism*A deficiency of parathyroid hormone (PTH) *PTH primarily regulates calcium balance; hypoparathyroidism leads to hypocalcemia and produces neuromuscular symptoms ranging from paresthesia to tetany

Hypoparathyroidism: Causes*Congenital absence or malfunction of the parathyroid glands *Autoimmune destruction *Removal or injury to one or more parathyroid glands during neck surgery *Massive thyroid radiation therapy *Ischemic infarction of the parathyroids during surgery

Hypoparathyroidism: Signs and Symptoms*Neuromuscular irritability *Increased deep tendon reflexes *Dysphagia *Paresthesia *Tetany seizures *Psychosis

Hypoparathyroidism: Signs and Symptoms*Arrhythmias *Abdominal pain *Dry, lusterless hair *Brittle fingernails *Dry and scaly skin *Weakened tooth enamel

Hypoparathyroidism: Diagnostic tests* PTH and serum calcium levels * serum phosphorus levels *X-rays reveal increased bone density

*ECG: prolonged QTi, QRS-complex and ST-elevation changes

Hypoparathyroidism: Treatment*Vitamin D with supplemental calcium *Lifelong therapy, except for patient with the reversible form of the disease *Acute life-threatening tetany calls for immediate IV administration of calcium *Sedatives and anticonvulsants are given to control spasms until calcium levels rise *Seizure precautions