Disorders of the Parathyroid Glands

Click to edit Master subtitle style Hypoparathyroidism -Hyperparathyroidism

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Hyperparathyroidism

Primary hyperparathyroidism is an edenoma of one of the parathyroid gland Excessive secretion of parathyroid hormone{parathormone} results in increased urinary excretion of phosphorous and loss of calcium from the bones Renal stones develop as calcium becomes concentrated in the urine

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Secondary hyperparathyroidism, the parathyroid glands secrete excessive parathormone in response to hypocalcemia {low serum calcium level} Which may result from vit D deficiency , chronic renal failure, large doses of thiazide diuretics and excessive use of laxatives and calcium supplements.

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Signs and Symptoms

Fatigue Muscle weakness Cardiac dysrhythmias Skeletal tenderness and pain on bearing weight Bones may become demineralized that they break with little or no trauma Nausea, vomiting and constipation

Formation of stones in the urinary 11/28/12 tract,pyelonephritis and uremia

Diagnostic findings

Elevated serum calcium and decreased serum phosphorus levels without other causes of hypercalcemia 24 hr urine test: increased urine calcium levels Skeletal radiographs: calcium loss from bones MRI or CT scan: parathyroid adenoma Parathormone levels are elevated in hyperparathyroidsm

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Medical and surgical management

Primary hyperthyroidism: only treatment is surgical removal of hypertrophied gland tissue or of an individual tumor of one of the parathyroid glands. One or more of the parathyroid is left in place because they are necessary for calcium and phosphorous metabolism

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parathyroidectomy

*Removal of 1 or more

parathyroid gland
*PRE-OPERATIVE

CARE:

-monitor calcium, phosphate & magnesium 11/28/12 level

Secondary hyperparathyroidism is managed by correcting the cause {example, for a vitD deficiency , vitD therapy, correction of renal failure, calcium restricted diet Sodium and phosphorous replacements are often ordered. Hormone replacement with synthetic calcitonin {calcimar} is avoided allergic reaction and drug resistance

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Nursing management

Closely monitoring of I/o Observes signs of urinary calculi from hypercalcemia, flank pain and decreasing urine output Encourage to increase fluid intake Assess clients ability to perform self care Provide safe environment Encourages frequent rest periods Monitors fatigue level for s/sx of hypoparathyroidism

Observe 11/28/12

Hypoparathyroidism

Deficiency of parathormone that results in hypocalcemia Most common cause are trauma to the glands and inadvertent removal of all or nearly all these structures during thyroidectomy or parathyroidectomy.

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Signs and Symptoms

Main symptom is TETANY Numbness and tingling in the fingers or toes or around the lips A voluntary movement may be followed by an involuntary, jerking spasm Muscle cramping Tonic flexion of an arm or a finger Positive Chvosteks sign Trousseaus sign

Positive 11/28/12

Laryngeal spasm occur in the larynxdyspnea Cyanosis Danger of asphyxia and cardiac dysrythmias Nausea, vomiting, abdominal pain and seizure can develop In chronic hypoparathyroidism: neuromuscular irritability, constipation or diarrhea, numbness and tingling of the arms and legs, loss of tooth enamel and muscle pain. chvosteks and trousseaus signs

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Diagnostic findings

Serum calcium level is decreased Serum phosphorous level is increased Urine levels of both are decreased In chronic hypoparathyroidism, radiographs show increased bone density

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Medical management

Administration of IV calcium salt, such as calcium gluconate for immediate treatment of tetany and severe hypoparathyroidism Endotracheal intubation and mechanical ventilation Brochodilators Parathyroid replacement therapy is not the usual treatment

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Long term treatment after trauma or inadvertent removal of the parathyroids includes: Administration of oral calcium, vit D or vit D2{calcifor} increases the serum calcium level Diet high in calcium and low in phosphorous usually is recommended

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Nursing management

Be alert for signs of tetany Assess for chvosteks and trousseaus sign Administration of IV calcium salt and observes for adverse effect such as flushing, cardiac dysrhythmia{bradycardia}, tingling of arms and legs and metalllic taste Monitor serum calcium levels is important esp.heart rate and rhythm

Vs monitoring 11/28/12

Emergency tracheostomy tray, mech vent equipment, artificial airway and endotracheal intubation equipment at bedside if hypocalcemia is severe Inserts Iv line for emergency administration of calcium Observe for respiratory distress and notify physician Assist in pts ADL Consultation to a dietitian is necessary

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Diabetes Mellitus

Metabolic disorder of the pancreas, affects carbohydrate, fat and protein metabolism No age group is exempt from diabetes Diabetes is the sixth cause of death in the US

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2 major forms

Type 1: insulin dependent diabetes mellitus IDDM, also referred to as juvenile diabetes because it affects children and adolescents, is characterized by no insulin production by the beta cells in the islets of langerhans of the pancreas Type 2: non insulin dependent diabetes mellitus NIDDM is characterized by insulin resistance or insufficient insulin production. More common in aging adults and being detected in obese children.

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Pre- diabetes mellius

The national health institute of diabetes and digestive and kidney diseases has developed criteria which can lead to type2 diabetes, heart disease and stroke. People with pre diabetes may have either impaired fasting glucose IFG or impaired glucose tolerance IGT or both. Person with IFG has a fasting blood glucose level of 100-125mg/dl after an overnight fast. , a person has a blood glucose

In 11/28/12 IGT

Signs and symptoms

3 classic symptoms of both types of DM are: polyuria, polydipsia and polyphagia Also include weight loss, weakness, thirst, fatigue and dehydration Some develop skin, urinary tract and vaginal infections possibly because the elevated level of blood glucose supports bacterial growth. Blurred vision

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Diagnostic findings Diagnostic tests for detecting glucose intolerance

Random blood glucose: blood specimen is drawn without preplanning : 200mg/dl in the presence of symptoms is suggestive of DM

Fasting blood glucose: blood specimen is obtained after 8hrs of fasting: in the nondiabetic client the glucose level will be between 70 and 110 mg/dl. In diabetic client glucose is 110mg/dl but 11/28/12

Postprandial glucose: blood sample is taken 2hrs after a high carbohydrate meal: in the nondiabetic client, the glucose level wil be between 70 and 110mg/dl. In client with DM, the result is 140mg/dl but < 200mg/dl Oral glucos tolerance test: diet high in carbohydrates is eaten fo 3days.client then fasts for 8hrs. A baseline blood sample is drawn and a urine specimen is collected. An oral glucose solution is given and time of ingestion recorded. Blood is drawn at 30mins and 1,2 and 3hrs after the ingestion of glucose

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Drinking water is encouraged to promote urine excretion: in nondiabetic client, the glucose returns to normal in 2-3hrs and urine is negative for glucose. In diabetic client, blood glucose level returns to normal slowly , urine is positive for glucose Glycosylated hemoglobin or hemoglobin A1c: single sample of venous blood is withdrawn: the amount of glucose stored by the hemoglobin is elevated above 7.0% in the newly diagnosed client with DM in one who is noncompliant or in one who is inadequately treated

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Glucometer: measures a capillary blood glucose from blood sampled from a finger stick or through the skin on the arm

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Medical management

Diet and weight loss

Exercise

Insulin Oral antidiabetic agents

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Oral Hypoglycemic Agents

Sulfonylureas

Chlorpropamide (Diabinase) Tolbutamide (Orinase) Glimepinide (Solosa) Acetohexamide (Dymelor) Repaglinide (Novonorm) Rosiglitazone (Avandia)

Prandial Glucose Regulator

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Insulin

Insulin increases glucose transport into cells & promotes con- version of glucose to glycogen, decreasing serum glucose levels *Primarily acts in the liver, muscle, adipose tissue by attaching to receptors on cellular membranes & facilitating transport of glucose, potassium & magnesium

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Glucagon

Hormone secreted by the alpha cells of the islets of Langerhans in the pancreas *Increase blood glucose by stimulating glycogenolysis in the liver *given SC, IM or IV routes to treat insulin-induced

*Used 11/28/12

Common Types of Insulin TYPE

ONSET

PEAK

DURATION

RAPID-ACTING INSULIN 10-15 mins

Lispro (Humalog) 1 hour 3 hours

SHORT-ACTING INSULIN 4-6 hours 0.5-1

Humulin Regular hour 2-3 hours 11/28/12

Major Complications of Diabetes Mellitus

HYPOGLYCEMIA *DIABETIC KETOACIDOSIS (DKA) *HYPERGLYCEMIC HYPEROSMOLAR

NONKETOTIC SYNDROME (HHNS)

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Signs of Hypoglycemia

sweating tremor tachycardia palpitations

11/28/12 nervousness

Simple Carbohydrate to Treat Hypoglycemia

3 or 4 commercially prepared glucose tablets CHILD: 2-3 GLUCOSE TABS *4-6 ounces of fruit juice or regular soda

CHILD: CUP OR 120 ML OF ORANGE JUICE OR SUGAR-SWEETENED JUICE

*6-10 Life Savers or hard candy CHILD: 3-4 HARD CANDIES OR 1 CANDY BAR *2-3 teaspoons of sugar or honey 1 SMALL BOX OF RAISINS

CHILD: 11/28/12

Assessment:

Diabetic Ketoacidosis

3 Ps Blurred Vision Weakness Headache Hypotension Weak, rapid pulse nausea, vomiting & abdominal

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DKA
Progressive insulin deficiency Glucogenolysis Gluconeogenesis Contribute to further hyperglycemia Breakdown of fats
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Hyperglycemic Hyperosmolar Nonketotik Coma

Similar to DKA but without Kussmaul Respirations and acetone breath.

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Chronic Complications of Diabetes Mellitus

DIABETIC RETINOPATHY

DIABETIC NEUROPATHY

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IF OTHERS MADE IT, WHY CANT I!

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Preventive Foot Care Instructions

Meticulous skin care & proper foot care Inspect feet daily & monitor feet for redness, swelling or break in skin integrity

Avoid thermal injuries from hot water, heating pads & baths

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Client Education During Illness

Take insulin or oral hypoglycemic agents as prescribed. Test blood glucose & test the urine for ketones every 3-4 hours If meal plan cannot be followed, substitute with soft food 6-8 x

per day
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