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ENDOCRINE SYSTEM DISEASES

PARATHYROID GLANDS

HYPERPARATHYROID ISM

H Y P E R PA R A T H Y R O I I M D S

Caused by an overproduction of parathormone hormone (PTH) by the parathyroid glands. Characterized by bone decalcification and the development of renal calculi (containing calcium).

ASSESSMENT

Fatigue Muscle weakness Nausea and vomiting Constipation Hypertension Skeletal pain Cardiac dysrhythmia (may occur) Psychological manifestations (e.g irritability, apathy) COMPLICATION: Kidney Stones

DIAGNOSTIC PROCEDURE
B l o d Te sts: S e ru m C a l u m o ci Le ve l B o n e M i e ra lD e n si te st n ty U ri a l s n ysi M R I C T sca n / S e sta m i isca n b

MEDICAL MANAGEMENT

D RUG S

Calcimimetics (Sensipar) Biphosphonates Calcitonin Loop diuretics (furosemide) Parathyroidectomy

NURSING INTERVENTION
Increase fluid intake (2L) Limit activity Low Calcium Diet Monitor serum calcium levels Dont Smoke Avoid Calcium-raising drugs (e.g Lithium, Thiazides, Potassium-sparring diuretics)

HYPOPARATHYROID ISM

HYPOPARATHYROIDISM
a rare condition in which your body secretes abnormally low levels of parathyroid hormone (parathormone). This hormone plays a key role in regulating and maintaining a balance of your body's levels of two minerals calcium and phosphorus.

ASSESSMENT

Chief Symptom: TETANY Tingling or burning sensation Muscle aches or cramps Twitching or spasms of your muscles Trousseau and Chvosteks sign Brittle nails Anxiety or nervousness Depression, mood swings

For Diagnostic findings: A low blood-calcium level A low parathyroid hormone level A high blood-phosphorus level A low blood-magnesium level prolonged ST wave on ECG

DIAGNOSTIC PROCEDURE

Serum Calcium Level ECG Urine tests X-ray and bone-mineral density test

MEDICAL MANAGEMENT

DRUGS
Oral Calcium Carbonate Vitamin D supplements (e.g Calcitriol) Thiazide Diuretics

NURSING INTERVENTION
High Calcium and Vitamin D, Low Phosphorus Diet Provide an environment free of noise or bright lights Monitor serum calcium levels Monitor cardiac activity Keep Calcium Glocunate at bedside

ADRENAL GLANDS

CUSHINGS SYNDROME

C U S H I G S S Y N D R O M E N
Results from excessive adrenocortical activity. It may result from excessive administration of corticosteroids or ACTH or from hyperplasia of the adrenal cortex. Characterized by oversecretion of glucocorticoids, androgens and mineralocorticoids.

ASSESSMENT

Weight gain Truncal obesity Moon face Buffalo hump Purple striae Thin, fragile skin (easily bruised) Fatigue and Muscle weakness Increased Blood Pressure Hyperglycemia

Hypernatremia Hirsutism (women), Gynecomastia (men) Men: Erectile Dysfunction Women: Irregular or Absent menstrual periods

DIAGNOSTIC PROCEDURE
Overnight Dexamethasone suppression test (measures plasma cortisol level) CT scan, MRI CBG

MEDICAL MANAGEMENT

DRUGS Radiation therapy Potassium-sparring diuretics Insulin Adrenal enzyme inhibitors Post operative meds: adrenal cortex hormone SURGERY: Transphenoidal hypophysectomy Adrenalectomy

NURSING INTERVENTION
Monitor weight daily Monitor Sodium and Glucose intake Encourage moderate activity High protein, calcium and vit. D; Low Sodium diet Provide skin care regularly and plan rest periods Monitor serum Na and Glucose levels

ADDISONS DISEASE

A D D I O N S D I E A S E S S
a disorder that occurs when your body produces insufficient amounts of certain hormones produced by your adrenal glands. In Addison's disease, your adrenal glands produce too little cortisol and often insufficient levels of aldosterone as well.

ASSESSMENT

Muscle weakness and fatigue Weight loss and decreased appetite Hyperpigmentation (bronze skin) Hypotension Hypoglycemia Nausea, diarrhea or vomiting Muscle or joint pains Irritability

ADDISONIAN CRISIS
Cyanosis Fever Classic signs of circulatory shock: pallor rapid and weak pulse rapid respirations hypotension

DIAGNOSTIC PROCEDURE
ACTH stimulation test Blood tests: Serum Na Serum Potassium Serum Cortisol levels CBC CBG MRI, CT scan

MEDICAL MANAGEMENT

DRUGS
Oral Corticosteroids Fludrocortisone Hydrocortisone Prednisone Hormone replacement therapy Dextrose and Saline Solution

NURSING INTERVENTION
Monitor weight daily Increase fluid intake High Sodium, Glucose, Low Potassium diet Provide food choices or patients preferred food Provide rest Instruct patient to report increased thirst Assess for signs and symptoms of Addisonian Crisis, report to physician immediately

PANCREAS

PANCREATITIS

PA N C R E A T I I T S
inflammation of the pancreas commonly described as an autodigestion of this organ by the exocrine enzymes it produces. common cause of acute episodes are biliary tract disease and long term alcohol use

ASSESSMENT

mid-epigastric pain nausea and vomiting Turners sign (ecchymosis in the flank) Cullens sign (ecchymosis around the umbilicus) rigid or boardlike abdomen abdominal muscle guarding decreased or absent bowel sounds hyperglycemia Tachypnea

CULLENS SIGN

TURNERS SIGN

DIAGNOSTIC PROCEDURE
CBC WBC (increased) Bilirubin (conjugated bilirubin) Lipase Amylase

CGB Abdominal ultrasound CT scan

MEDICAL MANAGEMENT

DRUGS
Demerol Antacids H receptor antagonists (cimetidine, ranitidine) Parenteral Nutrition is administered instead of food Insulin (if neccessary) TREATMENT Biliary drainage

NURSING INTERVENTION
monitor bowel sounds Assess nutritional status NPO during acute pancreatitis attack low fat diet is encouraged, after and acute episode avoid heavy meals and alcoholic beverages, excessive intake of coffee and spicy foods. monitor laboratory values monitor serum glucose levels Position patient in semi-fowlers, change position frequently Nasogastric suctioning as ordered (to relieve nausea and vomiting)

DIABETES MELLITUS

DIABETES MELLITUS
group of metabolic disorders characterized by elevated levels of blood glucose resulting from defects in insulin production and secretion, decreased cellular response to insulin, or both.

TYPES:

TYPE I/ Insulin-Dependent Diabetes Mellitus TYPE II/ Non-Insulin-Dependent Diabetes Mellitus

COMPLICATIONS:
Diabetic Ketoacidosis Hyperglycemic Hyperosmolar Nonketotic Syndrome Neuropathy Nephropathy Retinopathy Cerebrovascular Accident Myocardial Infarction

ASSESSMENT

TYPE I

TYPE II

Hereditary Juvenile onset < 40 years old Insulin dependent

Slow progressive onset Obesity > 40 years old Oral hypoglycaemic agent

Polyphagia Polydipsia Polyuria hyperglycemia fatigue and weakness sudden visual changes tingling or numbness wounds that heal slowly Increased BP hypertensive Acetone breath (DKA)

DIAGNOSTIC PROCEDURE
Fasting Blood Glucose level (126 mg/dL) Random Blood Glucose level (200 mg/dL) CBG

MEDICAL MANAGEMENT

DRUGS
TYPE I

TYPE II

Primary treatment: Insulin

Primary treatment: weight loss Oral Hypoglycemic agents

NURSING INTERVENTION
TYPE I TYPE II Encourage to eat foods low in Encourage patient to eat foods low glucose, carbohydrates in glucose, carbohydrates Encourage patient to avoid vigorous Encourage patient to do regular activity exercises Educate patient on proper wound Monitor blood glucose levels Monitor weight frequently care Monitor blood glucose levels Educate patient on proper wound Administer Insulin as ordered care Educate patient self administration Administer OHA as ordered Educate patient to report signs of of insulin for home medication Educate patient how to monitor hypotension or seizures blood glucose level using a CBG immediately. monitor

hank you for listenin

Prepared by : Chinee Marie Talosig , RN

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