Care of Clients WITH ENDOCRINE DISORDERS (Part II) ANTERIOR PITUITARY DISORDERS Overview

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short pitched voice slow maturing skeletal system hyperlipidemia hypercholesterolemia

Hyperfunction of the anterior pituitary (hyperpituitarism)

results in excess production and secretion of one or more hormones; GH, PRL, or ACTH; leading to the manifestation such as tissue overgrowth seen in hyperpituitarism Cause: Benign adenoma (most common) Hypofunction of the anterior pituitary (hypopituitarism) results in deficiency of one or more of the pituitray hormones: GH, FHS, TSH, LH and ACTH Cause: Surgical removal of pituitary gland, pituitary tumors, pituitary infection, pituitary trauma, congenital defects, and radiation GIGANTISM the result of GH hypersecreation that begins before the

Nursing Assessment 1. Assessment for gigantism includes growth chart for height and weight by age and visual exam 2. Assessment for acromegaly includes VS, visual disturbances, signs and symptoms of CHF or DM, growth and development, symptoms analysis of any pain 3. Assessment of dwarfism includes growth chart for height and weight by age, development of sex organs

Diagnostic Tests:

closure of epiphyseal plate

This hypersecretion leads the person to become abnormally tall, often reaching 7 8 ft in height Body proportions are generally normal Cause: tumor of the pituitary gland Signs and Symptoms: excessive height and acromegaly in adult ACROMEGALY the result of GH hypersecretion beginning during adulthood; bone and connective tissue to continue to grow, leading to disproportionate enlargement of tissues

Cause: pituitary adenoma (most common) Signs and Symptoms o Soft tissue swelling of the hands and feet o Facial features Prognathism enlargement of the jaw Skull is thickened Supra orbital ridges protrusion o Enlarging hands o Enlarging feet o Signs of osteoporosis o Arthritis and carpal tunnel syndrome (the median nerve is compressed at the wrist causing symptoms like tingling, numbness, night time wakening, pain, coldness, and sometimes weakness in parts of the hand) o Teeth spacing increase o Heart failure o Compression of the optic chiasm leading to loss of vision in the outer visual fields o Diabetes mellitus o Hypertension o Increased palmar sweating and sebum production over the face (seborrhea) are clinical indicators of active growth hormone (GH) producing pituitary tumors. These symptoms can also be used to monitor the activity of the tumor after surgery although biochemical is confirmatory o Amenorrhea o Organomegaly (enlarged adrenal, thyroid and parathyroid gland) DWARFISM results from deficient secretion of anterior pituitary hormones inadequate secretion of these hormones leads to growth retardation and accompanying metabolic disorders Signs and Symptoms: o short stature o obesity

1. bone scan 2. cholesterol, lipid panel, hormone levels Nursing Management 1. Pharmacologic Therapy o Cortisol and thyroid replacement drugs o Growth hormone for dwarfism o Bromocriptine mesylate (Parlodel) for acromegaly o Somatrem for dwarfism (given at bedtime) o Assist client in obtaining proper counseling to facilitate psychosocial adjustment to altered body image 2. Monitor for diabetes insipidus since posterior pituitary gland may be affected simultaneously 3. Surgery: Transsphenoidal Hypophysectomy o A general anaesthetic is used o Incision: through the mouth by making an incision at the junction of the upper lip and upper gum. o The surgeon will be using key-hole surgery to remove the adenoma or part/whole of the pituitary gland o At the end of the operation the neurosurgeon will make a decision about the need to insert a fat graft to stop fluid leakage (one of the potential complications of trans-sphenoidal surgery). Fat grafts are obtained from the outer side of the right thigh. o Postoperative Management: Monitor for CSF leak (frequent swallowing, patch/incision is disrupted) Monitor for signs of infection Avoid toothbrushingEncourage deep breathing exercises Position clients to semi-fowlers Advice client to avoid coughing (this increases ICP and can cause CSF leak)

POSTERIOR PITUITARY DISORDERS SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE Overview an excessive amount of serum ADH resulting in water intoxication and hyponatremia further water retention Causes: o Malignant tumors secrete ADH independent of a normally functioning hypothalamus and feedback mechanisms o Hypersecretion of ADH by the hypothalamus o Positive pressure ventilation and other conditions causing increased pressure may stimulate the aortic baroreceptors and cardiopulmonary receptors that trigger the hypothalamus to secrete ADH o Trauma, pain, stress, and acute pyschosis may activate the limbic system that, in turn, stimulates the hypothalamus to secrete ADH o Increase vasopressin therapy 1

Handouts/CARE OF CLIENTS WITH ENDOCRINE DISORDERS II/RAY ANDREW S. DEL ROSARIO, RN, MAN

Pathophysiology o The usual feedback mechanism does not function to decrease posterior pituitary secretion of ADH with decreased serum osmolality o High levels of ADH leads to renal absorption of water and suppression of the renin angiotensin mechanism, causing renal excretion of sodium o This leads to water intoxication, cellular edema, and dilutional hyponatremia Nursing Assessment General manifestations of fluid volume excess, possibly including increased blood pressure, crackles auscultated in lung fields, distended jugular neck veins, taut skin and intake greater than output Diagnostic Tests: 1. high urine osmolality (>1200 mOsm/kg H20) 2. specific gravity > 1.032 3. low serum osmolality (<275 mOsm.kg) 4. decreased Hct 5. hyponatremia Normal Serum Osmolality Normal solute and solvent Normal Value Na 135 145 mEq/L Hyponatremia Na water Hypernatremia Na water Normal Urine Specific Gravity Value 1.010 1.025

DIABETES INSIPIDUS Overview water excretion Causes: 1. Hyposecretion of ADH or the kidneys inability to respond to ADH 2. Subsequent polyuria (excessive urine output ranging from 4 30 L in 24 hours) that leads to severe dehydration 3. Trauma 4. Transsphenoidal Hypophysectomy (removal of pituitary gland) Pathophysiology 1. Normally fluid balance is maintained by actions of the hypothalamus, kidneys and pituitary gland a. The hypothalamus detects dehydration, sends a message to the pituitary, which in turn releases ADH and sends it to the kidney b. In the kidney it acts on the collecting and dital tubules to reabsorb water; promoting retention to restor fluid balance c. When excess fluid volume occurs, the hypothalamus sends s message to the pituitary to inhibit secretion of ADH, promoting excretion to restore fluid balance 2. Neurogenic DI: renal tubules excrete excessive amounts of water in the urine caused by insufficient ADH secretion by the posterior pituitary gland 3. Nephrogenic DI: the inability of the kidney to respond to ADH 4. Lithium carbonate and demeclocycline ca cause the kidneys to alter response to ADH 5. Primary DI results from an inherited malfunction of the posterior pituitary gland 6. Secondary DI is caused by brain tumors, head trauma, infection, surgery, metastatic tumors, cerebrovascular hemorrhage, and granulomatous diseases Nursing Assessment 1. Assess for a history of head injury, brain surgery, infection or tumor 2. Obtain a list of current and past medications 3. Assess LOC, VS, skin turgor, I/O, weight, skin intergrity, polydypsia, sagging skin, bowel sounds, constipation 4. Diagnostic Test: o Hypernatremia o Urine specific gravity: low o Serum osmolality: high o Urine osmolality: decreased o Serum ADH levels: decreased o Vasopressin test and water deprivation test: increased (hyperosmolality) Signs and Symptoms o Polyuria o Polydipsia o Weight loss o Dehydration o Hypovolemic shock increased RR and PR, decreased BP o Hypernatremia o Hyperosmolality o Diluted urine (<1.005) Nursing Management 1. Pharmacologic Therapy o Vasopressin (Pitressin, Pressyn) for treatment of neurogenic diabetes insipidus o Hypotonic intravenous fluids o Desmopressin as supplemtal ADH o Chlorpropamide (Diabenese)/Carbamazepine (Tegretol) to potentiate the renal effect of ADH 2. Increase oral fluid intake 3. Treatment is lifelong for chronic diabetes insipidus 2

Signs and Symptoms o decreased urinary output o weight gain o increased BP o confusion due to water intoxication o dilutional hyponatremia o hypoosmolality decreased solute (Na) o concentrated urine ( 1.025) Decreased solvent (water) excretion but increase solute (Na) excretion Nursing Management: 1. Pharmacologic Therapy o IV hypertonic saline (3%) o Demeclocycline (Declomycin) o Diuretics 2. Restrict oral fluids including ice chips to 80 ml/day to prevent further hemodilution 3. Flush all enteral and gastric tubes with NS instead of water to replace sodium and prevent further hemodilution 4. Monitor intake and output accurately 5. Monitor serum sodium, and urine osmolality and specific gravity 6. Weigh daily; a weight loss of 2 pounds indicates a loss of 1L of fluid 7. Assess for changes in LOC, mentationm cognition, nutrition, muscle twitching and comfort 8. Client education: a. Instruct client about SIADH and symptoms to report b. Medication may be for life depending on the cause c. Identify hidden sources of water and fluids, such as ice and ice cream, to prevent accidental excessive intake d. Plan meal pattern and maintain fluid limitation and sodium prescription e. Weigh daily on same scale and report gain of 2 pounds in1 day

Handouts/CARE OF CLIENTS WITH ENDOCRINE DISORDERS II/RAY ANDREW S. DEL ROSARIO, RN, MAN

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Monitor intake and output Monitor daily weight Dietary instructions for low sodium diet and to avoid caffeine Client Education: o Teach client about DI; self-administration of medication, and about possible need for lifelong treatment o Instruct client to wear a Medic-Alert bracelet listing DI and treatments o Instruct client to weigh self daily, on same scale at same time of day, and to report weight loss o Instruct client to consult practitioner before taking over-the-counter medications

Type 2 Diabetes Mellitus o results from a decrease in the beta cell weight and number or from insulin resistance o there is inadequate secretion of insulin or an insensitivity (resistance) to insulin, which leads to hyperglycemia o the symptoms are generally the same as type 1 diabetes, but, type 2 has a gradual onset and may be undetected for years (later adulthood); additionally, ketones are not usually present and excess weight rather than weight loss is noted

DISORDERS OF THE ENDOCRINE PANCREAS DIABETES MELLITUS a lack if or inadequate secretion of insulin, or insulin resistance resulting in hyperglycemia the pancreas (beta cells of the islets of Langerhans) fails to secrete an adequate amount of insulin, the hormone responsible for glucose metabolism the lack of adequate insulin secretion results in inappropriate hyperglycemia obesity, especially when centralized in the abdomen, may lead to insulin resistance Types: o Type 1 diabetes (insulin dependent diabetes o

TABLE 1. TYPE 1 VS TYPE 2 DM TYPE 1 NORMAL Beta cells destroyed Pancreas; Decreased or no insulin Functional receptors Rapid Before 36 years old (children/adolescents) Thin More common in male

beta cells insulin Insulin output Receptors Onset Age Physique Gender

TYPE 2 Beta cells intact Normal; above normal; below normal Receptors defective (insulin resistance) Slow Occurs after 35 years old (older adults) Obese Indefinite

Pathophysiology Type 1 Diabetes Mellitus o damage to the pancreatic beta cells lead to uncontrolled glucose production by the liver and subsequently results in hyperglycemia (elevated serum glucose) o the renal threshold for glucose is approximately 180 200 mg/dl, therefore glucose spills into the urine once it has surpassed the renal threshold because glucose is highly osmotic, fluids follow the glucose and are excreted out of the body in large amounts of urine (osmotic diuresis), causing an excessive loss of fluids and electrolytes; polyuria the loss of fluids leads to polydypsia (excessive thirst) o because of the lack of insulin, the body is unable to utilize CHO, its primary source of energy; therefore it must use CHON and fats for energy, leading to unexplained weight loss the use of fats results in ketones, the acid end products of fat metabolism as ketones build in the body, acidosis occurs the breakdown of nutritional stores leads to excessive hunger, known as o classis signs of diabetes and are known as the 3 Ps failure to receive adequate amounts of insulin results in continued fat metabolism, which produces ketone bodies leading to acidosis diabetic ketoacidosis (DKA) results in severe metabolic, fluid and electrolyte disturbances, and is life threatening condition of hyperglycemia and metabolic acidosis requiring immediate action

mellitus) Type 2 diabetes (non-insulin dependent diabetes mellitus)

polyphagia Polyuria, polydipsia and polyphagia are

Nursing Assessment: o General assessment include: health history, cognitive and mentation function, pattern of weight loss organ, nutrition pattern, elimination pattern, VS, skin, wound healing, eyes.vision, sensory perception, energy level and activity tolerance. Diagnostic Tests: o Fasting Blood Sugar (FBS) NPO (6 8 hours), check the blood sugar Normal Value: 70 110 mg/dl 111 125 mg/dL is at risk for DM (+) DM > 126 mg/dL: to be checked twice o 2 hour Post Prandial Blood Sugar patient is given 75 100 g of glucose after meals Normal Value: 70 140 mg/dL 141 199 mg/dL is at risk for DM (+) DM > 200 mg.DL] o Oral Glucose Tolerance Test (OGTT) test to tolerate the glucose by mouth/oral cavity fast overnight patient is given 75 100 g of glucose collect blood glucose specimen at 1, 2 and 3 hours after drinking glucose 4 specimens for 2 hours (most accurate) and checked blood sugar every 30 minutes o Capillary glucose monitoring o Glycosylated hemoglobin test to check how well the individual manages glucose in the past 3 4 months glucose normally bind to Hgb (permanent) RBC life span is 120 days (4 months) 3

Handouts/CARE OF CLIENTS WITH ENDOCRINE DISORDERS II/RAY ANDREW S. DEL ROSARIO, RN, MAN

Normal Value: below 7.5 % - good; 7.6 8.9 % - fair; above 9 % - poor o Urine for protein: positive o Urine for glucose and ketones: positive (Type 1 (+) ketones) o Cholesterol and triglyceride levels: elevated o Serum K: decreased (hypokalemia) Signs and Symptoms Type 1 DM o 3 Ps, glucosuria, fatigue, weight loss, nausea and vomiting, abdominal pain Type 2 DM o 3 or 2Ps (except polyphagia), blurred vision, weight gain General Multisystem Findings o Sensory/neurological: diabetic neuropathy, cataracts, glaucoma, paresthesias, loss of sensation, peripheral neuropathy o Cardiovascular: coronary artery disease, peripheral vascular disease, hypertension o Gastrointestinal: constipation/diarrhea o Integumentary: atrophy, foot ulcers, poor wound healing, chronic skin infections o Renal: edema, chronic renal failure, albuminuria, UTI o Reproductive: sexual dysfunction, vaginitis o Metabolic: hyperglycemia, hypokalemia, metabolic acidosis Nursing Management 1. Diet o Follow the diet recommended in the Food Pyramid Guide or the exchange system diet (Meat, Milk, Fruits within fruits, Fats, Bread/Starch and Vegetables within vegetables) o Follow caloric intake distribution: CHO 50-60%; Fats 20-30%; and Proteins 10-20%; caloric intake is based on individual needs o Needs to be tailored to individual and cultural preferences whenever possible to increase adherence 2. Oral Antidiabetic Agents TABLE 2: ORAL ANTIDIABETIC AGENTS Sulfonylureas Acetohexamide (Dymelor) Chlorpropramide (Diabenese) Glimeperide (Amaryl) Glipizide (Glucotrol) Glyburide (DiaBeta, Micronase) Tolazamide (Tolinase) Tolbutamide (Orinase) Nonsulfonylureas Alpha Glucosidase Inhibitor Acarbose (Precose) Miglitol (Glyset) Biguanide Metformin (Glucophage) Meglitinide Nateglinide (Starlix) Replaglinide (Prandin) Thiozolidinediones Pioglitazone (Actos) Rosiglitazone (Avandia) Sulfonylureas stimulate the beta cells to produce more insulin Nonsulfonylureas affect the hepatic and gastrointestinal production of glucose; it may be used alone or in combination with sulfonylureas

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Used in Type 2 DM only, and are indicated when diet and exercise alone fail to control blood glucose o Consist of oral sulfonylureas (Chlorpropamide [Diabenese], alpha-glucosidase inhibitor, biguanide and a miscellaneous agent o Instruct client taking oral sulfonylureas that concurrent use of alcohol can cause a disulfiramtype reaction (hypoglycemia, flushing, headache and abdominal cramps) o Instruct client about risk of metabolic acidosis and to discuss with primary care provider about need to discontinue medicine if severe diarrhea, infection or dehydration occur Insulin Therapy o Is used in Type 1 DM or when exercise and oral agents are insufficient to control Type 2 DM o Combinations of insulin preparations are usually administered to mimic pancreatic activity of the pancreas in response to variations in blood glucose levels o Only regular insulin may be given IV; insulin preparations are usually given via the subcutaneous route; continuous SC insulin infusion, also called insulin pump is also available to deliver a basal rate of insulin and allow for additional bolus doses of insulin based on requirements; insulin patch, nasal spray, and inhaled aerosolized preparations have been developed but are not yet widely used o DURATION (WEARS OFF) 6 8 hours

TABLE 3. COMMON TYPES OF INSULIN TYPES ONSET PEAK (MOST POTENT) Rapid Acting (clear) Insulin lispro 30 1 2 4 hours Humalog hour Regular Humulin R Intermediate Acting (cloudy) 12 6 12 hours NPH/Lente hours Humulin N Long acting 46 18 24 hours (cloudy) hours Ultralente/Lantus

18 24 hours 36 72 hours

Instructions: Storage: Opened/used vial: room temperature; Closed/extra: refrigerator; away from direct sunlight Preparation: if regular insulin appears cloudy: discard; do not shake to avoid inactivation; roll non regular insulin gently between hands; draw regular insulin first when mixing it with other types of insulin.

Inject air in the vial of non regular insulin and also to regular insulin; then withdraw regular insulin first then non regular insulin next (N R ; R N) 1. Injection: rotate injection sites to prevent lipoatrophy/lipodystrophy; do not inject in an area that will be involved in exercise as it will increases the rate of absorption, onset and peak action Site: Abdomen, anywhere except within 2 inches of the navel (absorbs insulin faster); upper arms, outside part (absorbs insulin

2.

Handouts/CARE OF CLIENTS WITH ENDOCRINE DISORDERS II/RAY ANDREW S. DEL ROSARIO, RN, MAN

TABLE 4. TYPES OF MORNING HYPERGLYCEMIA Type: Description/Causes Dawn Relatively normal blood glucose Phenomenon until about 3 am, when the glucose level begins to RISE Results from the nightly surges of GROWTH HORMONE secretion Somogyi Normal or elevated blood glucose Effect at bedtime, decrease blood glucose at 2-3 am due to hypoglycemic levels and a subsequent increase in blood glucose (rebound hypergycemia) Due to the production of counter regulatory hormones: glucagon, cortisol and epinephrine Insulin Progressive rise in blood glucose Waning from bedtime to morning Seen when the NPH evening dose is administered before dinner

9. Management Bedtime injection of NPH Decrease evening dose of NPH or increase bedtime snack

Develop with a plan of for wellness, including EXERCISE: o Daily cardiovascular exercises decrease the risk for insulin resistance, reduce risk for complications and improve glucose management. o Check blood glucose before exercise: check for urine ketones if fasting glucose is 250 mg/dL; notify physician if ketones present and avoid exercise

ACUTE COMPLICATIONS OF DIABETES MELLITUS Hypoglycemia Occurs when blood glucose falls below 60 mg/dL Caused by too much insulin or oral hypoglycemic agents, too little food, drinking too much alcohol or excessive activity Assessment Mild hypoglycemia: less than 60 mg/dL (hunger, nervousness, palpitations, sweating, tachycardia, tremor) Moderate hypoglycemia: less than 40 mg/dL (confusion, double vision, drowsiness, emotional changes, headache, impaired coordination, inability to concentrate, irrational or combative behavior, light-headedness, memory lapses, numbness of the lips and tongue, slurred speech) Severe hypoglycemia: less than 20 mg/dL (the client is unable to swallow, in unconscious or is experiencing seizures) (difficulty of arousing from sleep, disoriented behavior, loss of consciousness, seizures) Interventions: Mild hypoglycemia: Give 10 15 g of a fast-acting simple CHO Retest the blood glucose in 15 minutes and repeat treatment if not resolve Once resolve, a snack containing CHO and CHON, such as milk or chess and crackers are recommended unless the client plans to eat a regular meal within 60 minutes. Moderate hypoglycemia: Administer 15 30 g of a fast-acting CHO Administer additional food such as low-fat milk or chess after 10 15 minutes Severe hypoglycemia: If unconscious or unable to swallow: glucagon SQ or IM is administered Administer a second dose in 10 minutes if still unconscious A small meal is given to client when the client awakens as long as the client is not nauseated The physician is notifies if a severe hypoglycemic reaction occurs In the hospital or ER, the client may be treated with an IV injection of 25 50 ml of 50% dextrose in water Diabetic Ketoacidosis (DKA) a life threatening metabolic acidosis resulting from persistent hyperglycemia and breakdown of fats into glucose, leading to presence of ketones in blood; can be triggered by emotional stress, uncompensated exercise, infection, trauma, or insufficient or delayed insulin administration hyperglycemia causes uncompensated polyuria, hemoconcentration, dehydration, hyperosmolarity, and electrolyte imbalance; a significant accumulation of serum ketones leads to acidosis Assessment o anorexia, nausea and vomiting and abdominal pain o blurred vision 5

Move the insulin injection at bedtime

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slowly), buttocks, anywhere & thigh, front and outside parts, not inner thigh, not just above the knee (absorbs insulin even more slowly) Monitor for signs of hypoglycemia: have candy or foods with simple carbohydrates available (crackers, candy or orange juice) Avoid alcohol while taking insulin because it lowers blood glucose levels and can cause hypoglycemia Client Education o Instruct client about type of DM, symptoms to report, self administration of medication, fingerstick glucose monitoring, plan for regular exam, need for lifelong medication and lifestyle adjustments o Instruct client about foot care: keep clean and dry inspect feet daily using mirror to see soles of feet avoid walking bare footed; protect feet by wearing slippers/shoes avoid snug fitting socks or stockings use cotton socks in cutting nails, cut across not on sides/edge of nails Develop with client a plan for sick day management of DM o maintain food and fluid intake o continue to take insulin o increase frequency of blood glucose monitoring o monitor urine for ketones Instruct client on symptoms of hypoglycemia (restlessness, irritability, hunger, nausea, pale diaphoretic skin, shakiness or trembling, headache, confusion, inability to concentrate, deteriorating LOC to coma, seizures) o Check blood glucose as scheduled o Treat hypoglycemia with 15 g of CHO snack such as: 8 oz skim/low fat milk 6 10 lifesaver candies or hard candy 3 large marshmallows 6 oz juice/ cup fruit juice or regular (nondiet) soft drink 4 tsp sugar/4 sugar cubes/ 1 Tbs of honey or syrup 6 saltine crackers/3 graham crackers o Recheck blood glucose Discuss with prevention and management of the acute complications of DM: hyperglycemia, hypoglycemia, diabetic ketoacidosis, hyperglycemic hyperosmolar non ketotic coma; and the chronic complications: diabetic retinopathy, nephropathy and neuropathy.

Handouts/CARE OF CLIENTS WITH ENDOCRINE DISORDERS II/RAY ANDREW S. DEL ROSARIO, RN, MAN

headache hypotension weak, rapid pulse malaise and lethargy polyuria, polydipsia warm dry skin flushed face acetone (fruity) breath Kussmauls respiration (deep, nonlabored, rapid respirations) o Blood glucose levels: 300 800 mg/dL o Low serum bicarbonate and low pH Nursing Management 1. Insulin a. IV bolus of regular insulin (5 10 units) followed by a continuous IV drip b. Mix the prescribed IV dose of RI for continuous infusion in 0.9% or 0.45% saline c. IM administration of insulin hourly as an alternative for IV infusion 2. Fluid therapy to diminished hyperglycemia and to treat large fluid deficit a. Normal Saline Solution or 0.45 % saline b. 5 % glucose/dextrose solution to prevent hypoglycemia and cerebral edema (given when the blood glucose level reaches 250 300 mg/dL) 3. Potassium replacement (serum K may be elevated as a result of dehydration and acidosis but when client receives treatment, the serum K will decrease) 4. Promote safety 5. Maintain skin integrity o o o o o o o o o

TABLE 5. LONG-TERM COMPLICATIONS OF DIABETES MELLITUS Tissue or What Happens Complications Organ Affected Blood vessels Fatty material (atherosclerotic Poor circulation causes plaque) builds up and blocks wounds to heal poorly and large or medium-sized arteries can lead to heart disorders, in the heart, brain, legs, and strokes, gangrene of the feet penis. and hands, erectile dysfunction (impotence), and infections. The walls of small blood vessels are damaged so that the vessels do not transfer oxygen to tissues normally, and the vessels may leak. Eyes The small blood vessels of the Decreased vision and, retina are damaged. ultimately, blindness occur (diabetic retinopathy) Kidney Blood vessels in the kidney The kidneys malfunction, and thicken. ultimately, kidney failure occurs (diabetic nepropathy) Protein leaks into urine. Blood is not filtered normally. Nerves are damaged because Legs suddenly or gradually glucose is not metabolized weaken. normally and because the blood supply is inadequate. People have reduced sensation, tingling, and pain in their hands and feet. The nerves that control blood (Diabetic neuropathy) pressure and digestive processes are damaged. Swings in blood pressure occur. Swallowing becomes difficult. Digestive function is altered, and sometimes bouts of diarrhea occur. Erectile dysfunction develops. Sores and deep infections (diabetic ulcers) develop. Healing is poor. People become more susceptible to infections, especially of the urinary tract and skin. Carpal tunnel syndrome and Dupuytren's contracture develop.

Nerves

Hyperglycemic Hyperosmolar Non Ketotic Syndrome (HHNS) a life threatening metabolic disorder of hyperglycemia usually occurring with DM type 2 and triggered by a variety of situations: medications, infection, acute illness, invasive procedure or a chronic illness increased insulin resistance along with increased CHO intake lead to hyperglycemia, followed by polyuria, decreased plasma volume, decreased glomerular filtration rate (GFR) leading to glucose retention and sodium and water excretion; hyperosmolarity causes dehydration and reduced intracellular water (cellular shrinkage) Signs and Symptoms o decreased LOC o polydipsia; dry mucous membranes o hyperthermia o impaired sensory and motor function o positive Babinski sign (the hallux (large toe) extends upward, and the other toes fan out) o seizure Nursing Management 1. Determine and treat the triggering situation 2. Treat co existing health deviations 3. Provide fluid and electrolyte replacement a. IV infusion of NS to replace of fluids and sodium b. regular insulin IV to manage hyperglycemia c. Potassium to replace losses and shifts d. Maintain intact skin by turning every 2 hours, use of pressure relief aids, nutritional support, use of skin moisturizers and barriers and management of incontinence. e. Prevent aspiration by using appropriate feeding precautions, elevated head of bed to 15 30 degrees during and after feeding for 1 HOUR

Autonomic nervous system

Skin

Blood flow to the skin is reduced, and sensation is decreased, resulting in repeated injury. White blood cell function is impaired.

Blood

Connective tissue

Glucose is not metabolized normally, causing tissues to thicken or contract.

Handouts/CARE OF CLIENTS WITH ENDOCRINE DISORDERS II/RAY ANDREW S. DEL ROSARIO, RN, MAN