Endocrine Hormones & Functions

 Endocrine Hormones & Functions:    Type       Type  1 Diabetes: Age of onset- common in younger people Type of onset: usually abrupt Islet Cell Antibodies: absent/ minimal insulin production Symptoms: Polydipsia, polyuria, polyphagia, fatigue, weight loss Ketosis: Present at onset or during insulin deficiency Inulin Therapy: REQUIRED FOR ALL 2 Diabetes Age of onset: common in adults        Type of onset: gradual Islet Cell Antibodies: initially increased in response to insulin resistance-secretion decreases overt time Symptoms: Often none- fatigue, recurrent infections Ketosis: not present except during infection/ stress Insulin Therapy: not required for all Diagnosis of Diabetes:  A1C- 6.5% or higher: amount of glycosylated hemoglobinprovides measurement of previous 2-3 months- if A1C is kept at a normal level risk for developing complications is lowered.  Fasting plasma glucose of 126 or higher  2-hr plasma glucose test of 200 or higher Insulin: Exogenous insulin I s needed when a pt has inadequate insulin to meet metabolic need. Basal Bolus plan- mocks natural exogenous insulin production. Insulin Onset, Peak, and Duration Times Rapid-Acting Insulin: Novolog (aspart), Humalog ( lispro), Apidra (glulisine) Onset: 15 minutes Peak: 1 hour Duration: 3 hours “15 minutes feels like an hour during 3 rapid responses.” Short-Acting Insulin: Humulin R, Novolin R (regular)- remember these as "R"    Onset: 30 minutes Peak: 2 hours Duration: 8 hours “Short-staffed nurses went from 30 patient to (2) 8 patients.” Intermediate-Acting Insulin: NPH- Humulin N & Novolin N( remember these as "N")    Onset: 2 hours Peak: 8 hours Duration: 16 hours “Nurses Play Hero to (2) eight 16 year olds.” Long-Acting Insulin: Basaglar, Lantus, Toujeo( glargine), Levemir (detemir), Tresiba (degludec)    Onset: 2 hours Peak: NONE Duration: 24 hours “The two long nursing shifts never peaked but lasted 24 hours.”      Storage of insulin: vials & pens last at room temp for up to 4 weeks. Avoid direct sunlight. Store unopened in fridge. Prefilled syringes w/ 2 types of insulins are stable for up to 1 week when in the fridge, syringes w/ 1 type for 30 days in fridge. Store vertical. Preparing Insulin Injection: o Wash hands o Inspect bottle for proper type and expiration date o For IMMEDIATE acting- ROLL between palms to mix- never shake o Choose site o Clean & dry site o Push needle @ 90 degree angle, if skin is thin you make pinch and/or use 45 degree angle o Push plunger fully down and leave in place for 5 seconds o Destroy needle properly o Insulin drawing up- air to draw up insulin = cloudy clear --> clear cloudy Fastest absorption area is ABDOMEN, followed by arm, thigh, & buttocks Caution injecting site where client will be exercising- this can increase rate of absorption Rotate injection site        100U syringe- 6mm (1/2 in), 8in ( 5/16in), 12.7mm (1/2in). Insulin Pump: delivers continuous subQ infusion, small device worn on the belt, in a pocket, or under clothing. o Rapid acting insulin 24 hours a day- basal rate o At meal time users programs the pump to deliver a bolus o Infusion site changed every 2-3 days o Check glucose levels at least 4 times per day OR a continuous monitoring system that checks 8 or more times a day. Lipodystrophy- may occur if the same injection site are use frequently Somogyi Effect: Hyperglycemia in the morning-high dose of insulin causes a decline in blood glucose levels during the night. This stimulates lipolysis, gluconeogenesis, & glycogenolysis. The danger of this is when the glucose reading is hyperglycemic and the pt increases the insulin dose. o If morning hyperglycemia occurs- check glucose b/w 2-4am for hypoglycemia o May report headaches on awakening & recall night sweats Dawn Phenomenon: Hyperglycemia in the A.M o Two hormones- GH & Cortisol which are excreted in increased amounts in the early A.M- may be the cause o Tends to more severe when GH is at peak in adolescence & young adulthood Medications: o Biguanides: Metformin- only drug in class. Most effective first-line treatment.  Primary Action: reduce glucose production by liver. Enhances insulin sensitivity at tissue level & improves glucose transport into cells. May cause moderate wt loss  IV CONTRAST: D/C medication for 2 days b/f procedure, resume 48 hours after procedure. IV contrast poses a risk for contrast induced kidney injury. Monitor serum creatine levels. Do not use in people who drink excess alcohol. Do not use w/ kidney disease, liver disease, HF. Lactic acidosis is a rare complication of metformin accumulation. o Sulfonylureas: Glyburide- primary action is to increase insulin production by pancreas- hypoglycemia is a side effect Diabetic Meal Planning: goal is to achieve glucose, lipid, & BP levels. Modest wt loss will also help. o Appropriate serving sizes, reduce trans & saturated fats, low carbs. Regular exercise. o Alcohol inhibits gluconeogenesis by liver= hypoglycemia    o Carbohydrate counting-keep track of amount of carbs eaten w/ each meal. o Diet exchange list: instead of carb counting- exchanges are carbs, fruits, milk, meats, veg, fats, free foods.  Half plate= nonstarchy veg, 1/4 starch, 1/4 protein, 8 oz glass of milk & small piece of fruit. Exercise: o Does not have to be vigorous o Proper footwear o Start program gradual then increase intensity o Monitor BS before, during, and after o If BS <100 east 15mg carb snack, after 15-30 min recheck- delay if <100 o Before exercise if BS >250 with TYPE ONE & ketones are present- delay exercise until ketones are gone- drink WATER Diabetic Teaching: Asses ability of pt & caregiver in performing activities-SMBG & insulin injection o Proper administration of insulin, assessment of insulin response, teach about storage, & side effects o Teach proper foot & dental care o Medical identification bracelet o Herbs effecting blood glucose: aloe, ginger, cinnamon, St Johns Wort, garlic, ginseng Diabetic Ketoacidosis: profound deficiency of insulin- characterized by hypoglycemia, ketosis, acidosis, & dehydration o TYPE 1 Diabetics o Precipitating factor- illness, infection, inadequate insulin, undiagnosed diabetes, neglect o S/SS- dehydration, dry mucous membrane, tachycardia, orthostatic hypotension, lethargy, weakness, fruity breath, kussmaul respirations  Treatment: O2, fluid resuscitation, regular insulin drip, VS, ECG, sodium bicarb for acidosis, dextrose to IV fluids for BS <250. Give K+ for hypokalemia o Hyperosmolar Hyperglycemia Syndrome: life threatening- occur in pt with diabetes who is able to make enough insulin to prevent DKA, but not enough to prevent SEVERE hyperglycemia.  Causes: infections, illness, pneumonia, sepsis  HHS if often related to impaired thirst sensation &/or functional inability to replace fluids DIFFERENCE B/W DKA & HHS= pt w/ HHS usually has enough circulation insulin so that ketoacidosis doesn’t occur  TYPE 2 DIABTEIC  Can cause severe neurologic manifestations- seizures, coma, hemiparesis, aphasia.  Labs- over 600 BS. Ketones are ABSENT  Immediate IV admin of insulin & either 0.9% or 0.45% NaCl. Large volume fluid replacement. Hypokalemia not usually present o Hyperglycemia vs Hypoglycemia    Retinal Neuropathy: microvascular damage to the retina d/t hyperglycemia, neuropathy, and HTN o Proliferative- retina & vitreous- damage forming new blood vessels--> extremely fragile & hemorrhage easily o Nonproliferative: most common: partial occlusion of small blood vessels in retina causes micraneurysms  Prevention of retinal neuropathy is managing HTN & regular eye exams Cardiovascular Complications: Optimizing BP control prevents CVD & renal disease. Pt should be screening BP.  Peripheral Neuropathy: nerve damage d/t metabolic imbalances- lead to loss of protective sensation in lower extremities o Sensory: most common- hands/feet  s/ss: loss of sensation, pain, paresthesia, burning, cramping, crushing worse at night, increased sensitivity to touch.  Managing BS is the only tx  Medications: Gabapentin Endocrine Disorders- Ch. 49   Acromegaly: overproduction of GH o Benign GH secreting pituitary adenoma o Results in overgrowth of soft tissues, bones in the hands, feet and face. Develops after epiphyseal closure-arms & legs do NOT grow o Manifestations: thickening/enlargement of bony & soft tissues of face, feet, dead, proximal muscle weakness, joint pain o Voice depends d/t hypertrophy of vocal cords. o Prone to diabetes d/t antagonizes action of insulin, glucose intolerance and diabetes may occur o Treatment: Surgery. Octreotide medication: reduces GH levels Hypophysectomy: removal of pituitary gland o Permanent loss of pituitary hormones o Life long hormone replacement therapy of: thyroid & sex hormones & glucocorticoids o Monitor for formation of hematoma compressing optic nerveperipheral vision changes, visual acuity, extraocular movements, pupillary response. o CSF leaks & epistaxis are common complication o Monitor "moustache" dressing- check clear drainage for glucose o Monitor for severe supraorbital headache may indicate CSF leak into sinuses o Strict I&O and monitor for fluid imbalances- DI or SIADH o HOB elevated o Avoid coughing, sneezing, blowing nose, bending over the waist, use of toothbrushes  SIADH: overproduction of ADH or release of ADH despite normal or low plasma osmolarity. o s/ss: low urine output, increased body wt, fatigue, hyponatremia,  Tx: fluid restriction, loop diuretics, seizure precautions, HOB flat or no more than 10 Degrees.  Diabetes Insipidus: deficiency of production or secretion of ADH o s/ss: increased urine output, polydipsia. Large quantities of urineup to 20L/day. Serum Osmolarity increased, hypernatremia o Tx: DDAVP- vasopressin given, IV fluid replacement, monitor glucose levels, limit Na+  Nontoxic Goiter: diffuse enlargement if thyroid gland that does not result from cancer or An inflammatory process. Normal thyroid levels Goitrogen foods: broccoli, Brussel sprouts, cabbage, cauliflower, kale, mustard, peanuts, Strawberries, turnips Tx: thyroid hormone replacement & surgery  Hyperthyroidism vs. Hypothyroidism  Hyperthyroidism: Low TSH levels, increased T4. o Tx: antithyroid drugs- methimazole. Iodine- tx of thyrotoxicosis. Radioactive Iodine Therapy- common tx. Teach about radiation exposure @ home- separate bathrooms, laundry, do not prepare food for others o Graves Disease: autoimmune. o Acute Thyrotoxicosis: acute, severe- excess thyroid hormones released. Life threatening. Result from stressors or thyroidectomy. S/ss are = to hyperthyroidism- severe tachycardia, HF, shock, hyperthermia, agitation, delirium, seizures, abd pain, v/d, coma.  Tx: meds that block thyroid hormone production       o Total Thyroidectomy: d/t- large goiter causing tracheal compression, lack of response to med therapy, thyroid cancer  Subtotal Thyroidectomy: tx of choice  Nursing care: VS q 15min first 24 hrs, monitor airway, monitor for s/ss hemorrhage or tracheal compression, assist w/ cough & deep breathing, O2, suction equipment, assess ability to speak, monitor Ca levels, keep Ca salts available, semi fowlers, avoid neck flexion Hypothyroidism: high TSH levels. Iodine deficiency is most common cause. Associated w/ Hashimotos. o Myxedma: accumulation of hydrophilic mucopolysaccharides in dermis. Alter appearance of skin- pufÏness, facial & periorbital edmea, masklike effect.  Myxedema coma: Medical emergency- precipitated by infection, drugs, exposure to cold, trauma.  s/ss- subnormal temp, hypotension, hypoventilation o IV Thyroid hormone replacement for client to survive  Tx: wt loss lifelong Synthroid( monitor HR, report chest pain, wt loss, nervousness, tremors, insomnia) Hyperparathyroidism: high PTH--> leads to hypercalcemia o s/ss- asymptomatic. Loss of appetite, constipation, fatigue, muscle weakness o Tx: surgery- if fails= calcium supps for life. IV NaCl and loop diuretics, or IV bisphosphates to lower serum calcium  Monitor for tetany w/ immediate decrease in Ca or after surgery Hypoparathyroidism: Low PTH and low Ca+. o Caused typically from parathyroid removal- IV calcium for tx  Parathyroid Scan: used to find parathyroid glands- check for iodine allergy  Cushing's vs. Addison's  Cushing's: chronic exposure to corticosteroids.  s/ss: moon face, wt gain, buffalo hump, hyperglycemia, muscle wasting, osteoporosis, thin skin, purple striae.  Diagnostics: midnight salivary cortisol, low dose dexamethasone suppression test, 24hr urine. Urine cortisol higher than 100mcg/24 hr indicated Cushing's.  Tx: find the cause- surgical tx for adrenal tumor or pituitary tumor. If cause is prolong use of steroids= decrease slowing and d/c steroid.  Addison's: Adrenocortical insufÏciency.  Diagnostics: ACTH stimulation test- baseline labs checked, IV injection of synthetic ACTH give, labs rechecked 30-60 min later. Positive Addison's is little to no increase in cortisol levels  Adrenal Crisis: triggered by- stress, sudden w/d of steroids, adrenal surgery, sudden pituitary gland destruction  Tx is high dose hydrocortisone replacement, large volume fluid replacement saline & dextrose.  Prescribed Corticosteroid's:  Do not abruptly stop, monitor for s/ss infection, monitor BS w/ diabetics, take early in the AM, monitor for induced osteoporosis for long term therapy