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PREPARED BY: MARJORIE C. CABUAL, RN, MN
ANTERIOR PITITUARY GLAND
² TSH, ACTH, LH, FSH, MSH ² GROWTH HORMONE, PROLACTIN
POSTERIOR PITUITARY GLAND
² ADH OR VASOPRESSIN ² OXYTOCIN
THYROID GLAND ² THYROXINE (T4) ² TRIIODOTHYRONINE (T3) ² THYROCALCITONIN .
PARATHROID GLAND PARATHYROID HORMONE (PTH) OR PARATHORMONE ² Regulates calcium and phosphorus blood levels ² Increases intestinal absorption of calcium .
PANCREAS ALPHA CELLS ² GLUCAGON BETA CELLS ² INSULIN DELTA CELLS ² SOMATOSTATIN F CELLS ² PANCREATIC POLYPEPTIDE .
g. Aldosterone ² SEX HORMONES or ANDROGENS e.ADRENAL GLANDS ADRENAL CORTEX ² GLUCOCORTICOIDS e. Testosterone and Estrogen ADRENAL MEDULLA ² EPINEPRINE (Adrenaline) ² NOREPINEPHRINE .g.g. Cortisol ² MINERALOCORTICOIDS e.
Gonads OVARIES ² Estrogen ² Progesterone TESTES ² Testosterone .
Assessment of the Endocrine System .
Health history Subjective data ² Past health history ² Diet history ² Medications ² Surgery or treatments ² Functional health patterns (Gordon·s) .
Objective data ² V/S ² Height and weight ² Mental-emotional status Mental² Head-to-toe physical examination Head-to- .
Lab/Diagnostic studies Serum studies Radiologic studies Urine studies .
DIABETES MELLITUS A chronic disease of absolute or relative insulin deficiency characterized by alteration in metabolism of CHO. .
stress Lifestyle and diet .g.Etiology Genetic Autoimmune Race/ethnicity Obesity/hypertension Environmental factor e.
Incidence Higher among African-American and Hispanics Africanthan whites. .
2 TYPES TYPE I (IDDM/JUVENILE TYPE II (NIDDM/MATURE-ONSET DM (NIDDM/MATURE- .
Feedback mechanism between blood glucose and insulin Normal insulin production .
TYPE I ABRUPT ONSET OCCURS BEFORE 35 Y. ABSOLUTE INSULIN DEFICIENCY .O.
Risk factors Genetic predisposition for increased susceptibility Environmental triggers stimulate an autoimmune response e. chemical toxins .g. viral infections.
malaise Visual changes Abnormal discomfort and pain .Manifestations Polyuria Polydipsia Polyphagia Glycosuria Weight loss Fatigue.
Pathophysiology Autoimmune reaction.beta cells are destroyed reaction² Beta cell destruction occurs slowly ² Hyperglycemia occurs when 80-90% are destroyed 80- Alpha cells produce excess glucagons causing hyperglycemia .
Diagnostic tests Blood glucose greater than 250mg/dl Ketones in blood and urine Glucose present in urine Electrolyte abnormalities (Na. K. Cl) Opthalmologic exam may show diabetic retinopathy .
9% saline at 500 ² 1000 mL/hr Correct electrolyte imbalance.Treatment Blood glucose monitoring Insulin subcutaneous/IV Restore fluid balance: initially 0.potassium is imbalancemonitored frequently Assess risk for dysrrhythmias Treat underlying condition precipitating DKA .
O. & ABOVE USUALLY AFFECTS OBESE PERSON LACK OF INSULIN RECEPTORS .TYPE II INSIDOUS ONSET OCCURS 40 Y.
Pathophysiology insulin insufficiency insulin resistance. poor utilization of tissues. inappropriate glucose production by the liver .
Clients with hypertension . Physical inactivity 4. Women: history of gestational diabetes 6. Race/ethnicity: African American. Hispanic.RISK FACTORS: 1. or American Indian origin 5. History of diabetes 2. Obesity (especially of upper body) 3.
Complications of DM Hyperglycemia ² DKA ² HHNS Hypoglycemia .
Dawn phenomenon: rise in blood sugar between 4 am and 8 am. not associated with hypoglycemia (associated with Diabetes Type 1 and 2) Somogyi effect: combination of hypoglycemia during night with a rebound morning hyperglycemia that may lead to insulin resistance for 12 to 48 hours .
Hypertension C. Complications Affecting System/Organ Function A. Coronary Artery Disease B. Peripheral (Somatic) Neuropathies H. Peripheral Vascular Disease E. Visceral (Autonomic) Neuropathies . Diabetic Nephropathy G. Stroke: Type 2 diabetics are 2 ² 6 times more likely to have stroke D. Diabetic Retinopathy F.
ASSESSMENT Clinical manifestations Classic symptoms associated with Type 1 Weight loss Malaise/Fatigue Recurrent infections Prolonged wound healing Visual changes Glycosuria .
90² Goal: 7% or less .Diagnostic studies Fasting plasma glucose level 126 mg/dl RBS 200mg/dl 2-hour OGTT 200mg/dl Glycosylated hgb or hemoglobin A1c (HgbA1C) (HgbA1C) ² Indicates overall glucose control for the previous 90-120 days.
PLANNING/NURSING DX Deficient knowledge Ineffective renal tissue perfusion Imbalanced nutrition Pain Impaired oral mucous membrane Impaired urinary elimination .
Constipation/diarrhea Overflow incontinence Risk for impaired skin integrity Risk for infection Risk for deficient fluid volume Risk for injury .
Risk for ineffective sexuality patterns Sexual dysfunction Situational low self-esteem selfAnxiety Fear Powerlessness Social isolation Noncompliance Ineffective health maintenance .
NURSING INTERVENTIONS Collaborative Care Goals: Reduce symptoms Promote well-being well Prevent acute complications Delay the onset and progression of long term complications .
Diabetes Management Drug therapy Nutritional therapy SMBG or urine ketone testing Exercise .
acting Rapid² Short-acting Short² Intermediate ² Long-acting Long² Mixed type ORAL AGENTS ² Sulfonylureas ² Meglitinides ² Biguanides ² a-Glucosidase inhibitors ² Thiazolidinediones .DRUG THERAPY INSULIN injections ² Rapid.
1. Biguanide ² reduces hepatic glucose production and enhances tissue response to insulin (metformin(metformin-Glucophage) . Sulfonylureas ² stimulate insulin release from the pancreas (Glipizide) 2. Meglitinide ² acts like sulfonylureas at a faster rate 3.
Thiazolidinediones ² increase insulin sensitivity at receptor sites on cells (rosiglitazone(rosiglitazone-Avandia) 6. D-phenylalanine (Amino Acid) Derivative : stimulates very rapid and short insulin secretion to decrease spikes in glucose following meals.4. reduces overall glucose level . Alpha-glucosidase Inhibitors ² limits the Alphaabsorption of carbohydrates from the small intestine (Acarbose) 5.
Maintain blood glucose levels as near normal. Achieve lipid profiles and BP levels that reduce the risk for disease. 3. Address individual nutritional needs while taking into account personal and cultural preferences and respecting the individual·s willingness to change. .Nutritional Therapy OverOver-all Goal To assist in making changes in nutrition and exercise habits Specific Goals 1. Improve health through healthy food choices & physical activity 5. Modify lifestyle 4. 2.
Nutritional therapy Reduction in caloric intake LowLow-fat diet Consistency of CHO for weight reduction Uniform timing of meals desirable but not essential Intermeal and bedtime snacks not usually recommended Nutritional supplement for exercise programs may be necessary if patient controlled on sulfonylyurea or insulin .
Food composition: Protein 15-20% 15 Fat less than 10% CHO 60-70% 60- Alcohol.high in calories Alcohol Diet teaching. Food Guide teachingPyramid as teaching tool or (food exhange list) Exercise.regular and consistent (Guidelines on Exercise(Guidelines exercise for patients with DM) .nurse works with dietician.
promotes intestinal motility and gives feeling of fullness Sodium: recommended intake 1000 mg per 1000 kcal Sweeteners approved by FDA Limited use of alcohol: potentiates hypoglycemic effect of insulin and oral hypoglycemics . Fiber: 20 to 35 grams/day.
SelfSelf-monitoring of Blood Glucose (SMBG) Provides current blood glucose readings Enables the patient to make self-management selfdecisions Detects episodic hyperglycemia and hypoglycemia Portable glucose meters G2 Biographer from GlucoWatch .
Exercise Increases uptake of glucose by muscle cells Decreases cholesterol and triglyceride levels Clients should consult with health care provider before beginning or changing exercise program .
² Ask exercise preference ² Ascertain action of oral hypoglycemic agents ² Meal 1-3 hours before exercise 1² Monitor blood sugar level before exercise. sugar level and results in weight loss ² Keep a diary of food intake and exercise. a graph of body measurements & blood sugar level. Knowledge deficit ² Teach patient that exercise will decrease bld. .
Surgical Management Pancreas Transplantation (Type 1 DM) .
New Developments in Diabetic Therapy Inhaled insulin Skin patch Oral spray Insulin pills .
minimize or delay occurrence of chronic complications . be active participant in the management 2. experience few or no episodes of acute hyper/hypoglycemic emergencies 3. prevent. maintain blood glucose levels at normal or near normal 4.Nursing management Asssessment Planning Goals : The patient to: 1.
personal hygiene. oral agents. Nursing implementation ² Health promotion and maintenance ADA recommends routine screening for all overweight adults over age 45. medical identification and travel. patient and family teaching (empowerment approach) . ² Acute interventions Hypoglycemia DKA (Diabetic Ketoacidosis) HHNS (Hyperosmolar Hyperglycemic Nonketotic Syndrome) Syndrome) ² Stress of acute illness and surgery ² Ambulatory and Home Care Insulin therapy.
g.Organizations American Diabetes Associations ² Affiliates located in all states (1-800-DIABETES) (1-800² Publishes materials ² Sponsors conferences for healthcare professionals ² Research and management of patients. American Associations of Diabetes Educators ² Pamphlets ² Booklets ² Bimonthly magazine e. Diabetes Forecast Drug Companies .
Organizations/resources American Diabetes Associations (ADA) Affiliates located in all states (1-800-DIABETES) (1-800Publishes materials Sponsors conferences for healthcare professionals Research and management of patients.g. American Associations of Diabetes Educators Pamphlets Booklets Bimonthly magazine e. Diabetes Forecast Drug Companies .
COMPLICATIONS & NURSING MANAGEMENT HYPOGLYCEMIA DIABETIC ACIDOSIS OR COMA DIABETIC FOOT .
Cool. Faintness.Hypoglycemia Also referred to as insulin reaction or low blood glucose <45-60mg/dl <45 S/S: a. Nervousness. dizziness f. Vision changes h. Rapid heartbeat c. coma . Unsteady gait. slurred and/or incoherent speech g. clammy skin b. tremor e. Hunger d. Seizures.
juice. INTERVENTIONS Worsening symptoms/unconscious: Subcutaneous or IM glucagon IV 50ml 50% glucose Determine cause of hypoglycemia (after correction of condition) . soda. crackers ² Immediate notification of provider/emergency service.HYPOGLYCEMIA Conscious Patient: ² administer 15-20g of 15quick ²acting CHO e. slice of bread.g.g. ² Administration of longlongacting CHO e. low-fat milk low² Repetition of treatment in 15min.
Occurs in people with type1 but may be seen in type 2 DM. and dehydration. ketosis. acidosis.Diabetic ketoacidoses (DKA) (mainly associated with DM type 1) Profound deficiency of insulin characterized by hyperglycemia. ETIOLOGY ² Undiagnosed DM ² Inadequate treatment ² Insulin not taken as prescribed ² Infection ² Change in diet. insulin or exercise regimen .
DKA S/S: ² Manifestations of dehydration ² Lethargy and weakness ² Abdominal pain ² Anorexia and vomiting ² Kussmaul respirations ² Acetone breath Lab findings: Glucose level 250 mg/dl Arterial blood pH 7.35 Serum bicarbonate 15mEq/L Ketones in blood & urine .
O2 sat. LOC. Assess breath sounds monitor serum glucose and K Administer K to correct hypokalemia Administer Na Bicarbonate if severe acidosis (pH <7. . u. time & amount of insulin injection Ongoing monitoring: Monitor V/S.9 NaCL sol. time of last food. ² Identify hx of diabetes.1 u/kg/hr. ² Continous regular insulin drip 0.0).. cardiac rhythm.o.DKA Interventions Initial: ² Patent airway ² O2 ² IV access ² Fluid resucitation of 0.
Occurs in type 2 ETIOLOGY: ² Fluid vol.HHNS (mainly associated with DM type 2) A life-threatening lifesyndrome that can occur in patient with DM who is unable to produce enough insulin to prevent DKA but not enough to prevent severe hyperglycemia. & extracellular fluid depletion. deficit ² Mental depression . osmotic diuresis.
HHNS S/S: ² Somnolence ² Coma ² Seizures ² Hemiparesis ² aphasia Lab findings: ² Blood sugar 400mg/dl ² Marked increased in serum osmolality ² Ketone bodies absent or minimal in both blood and urine .
DKA & HHNS COLLABORATIVE CARE
IV IV INSULIN ELECTROLYTE REPLACEMENT ASSESSMENT OF MENTAL STATUS RECORDING OF I & O CVP if indiccated ASSESSMENT OF GLUCOSE LEVELS AND KETONES ECG MONITORING ASSESSMENT OF C/P STATUS
Definition: excessive delivery of thyroid hormone to peripheral tissues Also known as thyrotoxicosis Pathophysiology a. Autoimmune reactions (Grave·s disease) b. Excess secretion of TSH from pituitary gland c. Neoplasms (toxic multinodular goiter) d. Thyroiditis e. Excessive intake of thyroid medications
lithium.Etiology Genetic factors Excessive dietary iodine intake Medications e.g. amniodarone Toxic nodules or tumors .
S/S Enlarged goiter Nervousness Heat intolerance and sweating Weight loss. hypertension Exophthalmos . appetite Frequent bowel movements Tremor and palpitations.
Difficulty concentrating Fine tremor. shaky handwriting. clumsiness Pretibial myxedema Ackopachy. clubbing of the fingers and toes .
jaundice. tachycardia. ² Confusion. Thyroid storm ² Hypertension. stupor. and hyperglycemia . vomiting. coma. tremors. nausea and vomiting. high fever ² Pulmonary edema. psychosis. delirium. apathy. shock. emotional lability. diarrhea. abdominal pain.
and paralysis Vision loss or diplopia Heart failure. arrhythmias Hypoparathyroidism after thyroidectomy Hypothyroidism after radioactive iodine treatment . atrophy.Complications Muscle wasting.
Diagnostic test findings Radioimmunoassay: serum T4 and T3 Blood testing: TSH level Thyroid scan: uptake of 131I in Graves· dse. Electrocardiography: shows tachycardia .
and cool environment . sponge baths.Management V/S q4 Rest Quiet environment Frequent bed linen changes.
Drug therapy: ² Antithyroid drugs Propylthioucil (PTU) Methimazole (Tapazole) ² Iodine preparations decrease blood flow to the thyroid gland. Propanolol Beta² Radioactive Iodine therapy . Carbonate² Beta-adrenegic blocking drugs e.g. ² Lithium Carbonate-inhibits thyroid hormone release.
Surgical ² Total thyroidectomy Client must take lifelong thyroid replacement ² Subtotal thyroidectomy .
Pre-op care: Pre² Drug therapy to achieve euthyroid state before surgery with iodine preparations ² Control of cardiac problems ² High protein. high CHO diet ² Deep breathing and coughing exercises .
Post-op care: Post² V/S ² Sandbags or pillows to support the neck ² Semi-fowlers position when awake Semi² Avoid neck extension ² Pain meds ² Humidification of air ² Exercises and suction when needed ² Watch for complications .
Post-op complications Post² Hemorrhage ² Respiratory distress ² Hypocalcemia and tetany ² Larengyl nerve damage ² Thyroid storm .
Hypothyroidism The result of decreased metabolism from low levels of thyroid hormones .
Pathophysiology Thyroid cells may fail to produce sufficient levels of thyroid hormones The cells themselves are damaged and no longer function normally Other times thyroid cells are functional but the person does not ingest enough substances needed to make thyroid hormones .
forming a goiter. . the blood levels of TH are very low and the client decreased BMR The hypothalamus and Anterior Pit. TH is too low or absent. G make stimulatory hormones (TSH) as compensation TSH binds to thyroid cells and causes the Thyroid gland to enlarged.
Cellular energy production is decreased & metabolites build up Myxedema. Decreased perfusion results in tissue and organ failure . tongue thickened and edema to form in the larynx. course hair Myxedema Coma (decreased in metabolism in cardiac tissue causes the heart muscle to become flabby and chamber size to increase. making the voice more husky. Mxedema facefacedull puffy skin.
Etiology Most causes occur as a result of thyroid surgery and radioactive iodine treatment of hyperthyroidism Common in areas where soil and water have little natural iodide (endemic goiter) .
Incidence/prevalence Women 30-60 years old 30 Women are affected 7-10x more often than 7men. .
changes in menses For men. constipation Cold intolerance Decrease in libido Infertility. muscle aches.Assessment Increase in time spent sleeping (14-16hrs/day) (14 Generalized weakness. and paresthesias. anorexia. impotence and fertility .
Nursing Diagnosis Hypothermia Imbalanced nutrition Constipation Activity intolerance Disturbed thought process .
Provision of extra clothing, warm environment Low-calorie, high protein diet Low Assess bowel pattern, provide 2-3L of 2fluids/day Foods high in bulk and roughage Encourage activity Laxatives
Thyroid replacement Rest periods Assess thingking process, repeat information to patient Provide clock and calendar to maintain orientation to time and day Provide handouts with all instructions
(Adrenal gland hypofunction)
adrenocortical steriods as a result of production of ACTH Dysfunction of hypothalamic-pituitary control hypothalamicmechanism Complete or partial destruction of the adrenal glands
anorexia. Effects of aldosterone. resistance to stress . ECF aldosteronevolume depletion.water excretion. gluconeogenesisweakness. emotional disturbances.Pathophysiology Insufficiency of adrenocortical steroids through the loss of mineralocorticoid (aldosterone) and glucocorticoid (cortisol) action. hypotension. cardiac output Impaired secretion of cortisol results in decreased gluconeogenesis.hypoglycemia.
Assessment Health history/PA Lethargy. muscle weakness Salt craving Gastrointestinal symptoms Weight loss Menstrual changes. male clients may report impotence Meds-steriods. anticoagulants. fatigue. cytotoxic drugs Meds- .
Hyperkalemia (elevated blood levels of K) Hyperpigmentation of hand r/t adrenocortical deficiency Decreased energy level Mood swings Client is forgetful .
the most definitive test for testadrenal insufficiency .Diagnostic assessment Low serum cortisol Low FBS Low Na Elevated K Plasma cortisol levels fail to rise during stimulation tests glucocorticoid metabolites in urine Radiologic exams.may show atrophy of the gland examsACTH stimulation test.
primary insufficiency cortisol- .25-1mg given IM or IV 0. ² Result: absent or markedly decreased cortisol.25² Plasma cortisol levels are obtained at 30-min and 1 30hr interval after the baseline value is established. ACTH stimulation test can be done on outpatient basis ² Cosyntropin 0.
Management V/S Promote fluid balance Weight daily I and O Monitor lab values Replacement therapy: ² Hydrocortisone ² Fludrocortisone (Florinef) Salt additives for excess heat or humidity Teach patient symptoms of steroid overdose .
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