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Endocrine System JUSTINE WILLMAN MED, MSN, RN 2015-2016 Glands & Conditions of Focus 2 PANCREAS- DIABETES (I & II) & DKA ADRENAL- CUSHING'S, ADDISON'S & PHEOCRYOCYTOMA PITUITARY- SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE SECRETION (SIADH) & DIABETES INSIPIDUS (DI) 3 Type I DM is the failure of the beta cells to Pancreas Review Located posterior to the liver- LUQ Contains the islets of Langerhans (glands) The islets contain alpha and beta cells which produces insulin and glucagon Influences fat, protein and carbohydrate metabolism secrete any or enough insulin Most type II DM is the result of abnormalities of the insulin receptors Pancreas- Diabetes Review 4 Type 1 Diabetes Type II Diabetes Body’s immune system destroys 90-95% of all diagnosed cases of pancreatic beta cells. This can happen early in life of up into adulthood 5-10% of all documented cases of DM Depends on insulin to sustain life Risk factors include autoimmune, genetic, and environmental factors DM Usually begins as insulin resistance, cells do not use insulin properly Associated with older age, obesity, family history of diabetes, prior history of gestational diabetes, impaired glucose tolerance, physical inactivity, and race/ethnicity. Most important risk factor is family history and obesity 5 Often the presentation is nonspecific, the client Diabetes Clinical Manifestations Review Polyuria Polydipsia Polyphagia As times, ketones are present (ketosis) Hyperglycemia, weight loss, weakness and fatigue may go to physician with “other” problems such as fatigue, visual problems, recurrent infection, prolonged wound healing, etc. Clinical manifestations can occur so gradually that before the person knows it, he or she may have complications. Presentation ranges from asymptomatic to profound ketosis and coma. 6 Blood glucose Monitoring of Pancreas Review Common medications such as corticosteroids, oral contraceptives and albuterol often elevate glucose levels and may require the client to have regular glucose checks and at times, receive SQ insulin What is total parenteral nutrition (TPN) and how can it impact glucose levels? Normal 70-110mg/dL (fasting). This is the basic monitoring test for diabetics Glucose Tolerance Test (GTT) GTT can take up to 3-5 hours, requires IV or oral administration of glucose and multiple blood draws Glycosylated Hemoglobin (HbA1c) Monitors a diabetic’s glucose management over the past 3 months Test result >7 is considered poor management of DM and/or an indicator of newly diagnosed DM How long should your patient fast before having a HbA1c test? 7 Daily Routines for Diabetics Review Glucose monitoring and recording Insulin injections and oral agent administration Know the signs and symptoms of hypo and hyperglycemia Meal planning, exercise/ daily activities Skin care & foot care Carry fast acting glucose at all times What lifestyles or circumstances can impact or alter the way in which a client incorporates the daily routines listed above? What are the nurse’s roles in assisting the client as a result? 8 If you live alone, have someone call and check on you Sick Day Schedule Review Flu shots are recommended every year for people with diabetes Also, pneumonia vaccines and tetanus shots should be kept up to date Try to stay away from people who are sick, especially young children If you are around people who are sick, wash your hands often two or three times a day. NEVER omit insulin or diabetic meds, even if you can't eat. Test your blood sugar every 2-4 hours. Rest. Do not exercise during an illness Drink plenty of fluids to prevent dehydration Eat carbs of BS <150 Call Your Doctor or Diabetes Educator if: You have an obvious infection Your illness lasts longer than 2 days You have vomiting or diarrhea more than 8 hours Your blood sugar is over 400 mg in two consecutive tests All urine tests are positive for large amounts of sugar You have moderate to large urine ketones for more than 8 hours You have extreme fatigue, shortness of breath, or dizziness 9 What situation concerns you more? The client Endocrine Conditions of Focus- Pancreas Hyperglycemia Hypoglycemia Ketoacidosis (DKA) Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS) with a 42mg/dL glucose or the client with a 420 mg/dL glucose; or are you equally concerned? Think- is one client more likely to have a rapid decline in status? Would one need your attention first if you were caring for both clients? Once you’ve prioritized, what interventions are needed for these clients? Are you able to delegate any of the interventions to the LPN or CNA? List your interventions based on priority, figuring in your delegations… 10 Hypoglycemia is very dangerous as low sugar in the blood leads to low sugar in the brainconfusion, stupor, coma and death Although dangerous, hyperglycemia still supplies the brain with sugar and is more of a chronic concern in comparison to the immediate concerns of hypoglycemia Rapid, shallow respirations Nauseated Diaphoresis (cold sweats) Weakness and trembling Palpitations, tachycardia, jitters Technically a BGL below 70 mg/dl 11 Treatments for Hypoglycemia Review Carbs, Peanut butter, cheese and crackers Recheck glucose 15 min after initial treatment, and treatment should be repeated until achieving a glucose of 70. Once over 70, regular diet or snack to prevent hypoglycemia should be given Recheck glucose in 30-45 minutes Emergency treatment: D50 IV or glucagon (IV, SC, IM) At what rate is an amp of Dextrose 50% given? 12 Hyperglycemia Review Polyuria Polydipsia Blurred vision Weight loss Polyphagia Increased and/or unexplained sense of fatigue Skin infections, wounds don't heal easily Warm, dry skin SCENARIO- A client arrives in the ER via family member. The client is week and febrile (101.2). Labs reveal the following: Serum glucose of 511 mg/dL, WBC 18.3 thousand, sodium 129 mEq, potassium 6.8 mEq, anion gap 17, positive serum ketones & arterial blood pH 7.29. Analyze the labs and client presentation and make the connections to a “hyperglycemia” diagnosis. Once completed continue the scenario on next slide. 13 What is likely happening to this client as a result of Hyperglycemia View the next slide for a visual on how low insulin (leading to high blood glucose) impacts the body hyperglycemia, as evidenced in presentation and lab data? Why do you think the client is febrile? Regardless if the client knew he was diabetic on his ER admission or not, what type of DM do you think he has and why? Based on the client's blood pH (7.29) and glucose of 511 mg/dL, what compensatory measures are likely to be observed on this client and why? What are your priority actions? Can you delegate any interventions to the ER Tech? What was your correlation of the sodium and potassium levels to this state of hyperglycemia? Based on your interventions and the client’s condition, what specific assessments will you do on this client and how frequently will you assess? 14 15 DKA An acute life-threatening complication of uncontrolled IDDM (type I) Urinary loss of water, potassium, ammonium and sodium results in hypovolemia, electrolyte imbalance, extremely high glucose and breakdown of free fatty acids, causing acidosis, often leading to coma Most commonly brought on by infection DKA vs. HHNS 16 HHNS- Type II DM DKA- Type I DM Basics of DKA http://www.bing.com/videos/search?q=what+is+dka&FORM= HDRSC3#view=detail&mid=FD2E83EF5AD293D93915FD2E83EF 5AD293D93915 Kussmaul Breathing http://www.youtube.com/watch?v=gy7VEVPnOn4 &list=PLKBbwyYL5BYHR9u-prSR3IZ9Z04iISRJo Fruity breath (from acetone), dry mucous membranes from polyuria Deep respirations possibly kussmaul respirations Drowsiness, stupor or coma Low BP from polyuria Glucosuria and ketonuria Polyuria and polydipsia n/v, no hunger Glucose: 300-800mg/dl Basics of HHSN http://on.aol.com/video/what-is-hyperosmolarnonketotic-hyperglycemic-coma-234756250 Elevated glucose NO elevation of serum or urine ketones NO fruity scent NO acidosis NO Kussmauls Treat with fluids and decrease glucose levels 17 Treatment involves IV Insulin, fluid administration & Ketoacidosis Treatment Since DKA is an emergency, often we treat these clients in the ER or ICU settings Due to impaired insulin action and hyper osmolality, use of potassium by skeletal muscle is greatly diminished leading to K+ shifting out of the cell (extracellular) leading to intracellular potassium depletion. Also, potassium is lost via osmotic diuresis causing profound total body potassium deficiency. Goal is to return to normal intracellular K+ levels, increase fluid volume and lower glucose possibly IV potassium Why is IV K+ sometimes given when the potassium levels in the blood (extracellular) are already so high in DKA? How quickly can IV K+ be given and how is it administered? (find this in your drug reference) Are there ways in which potassium should not be given? Awesome potassium movement VIDEO http://www.dnatube.com/video/5282/Maintaining-potassium-level-in-cells 18 What type of insulin will be used to treat DKA and Ketoacidosis Treatment how can it be given as an IV infusion? (find this in your drug reference) If you were to mix & prepare this insulin for IV infusion, how would you make a 1:1 dilution from this bottle? ORDER: Infuse 0.1 U/kg of Regular insulin STAT Client weight is 170 lbs Now that you have prepared your med, prime your line and infuse the proper dose of insulin based on the order to the left. What rate will your pump be set at? How to add a medication to an IV solution VIDEO http://www.bing.com/videos/search?q=adding+medication+to+iv+solution&FORM=H DRSC3#view=detail&mid=728DD66FCE3F15482859728DD66FCE3F15482859 19 Importance of Insulin for DKA Look at the next slide for an example of IV insulin protocol Would you consider the structured decrease in glucose for DKA to be a fast or slow? Critically ill patients with DKA should be given a loading dose of regular insulin at 0.1 units/kg body weight to a maximum of 10 units followed by an infusion of regular insulin at 0.1 units/kg body weight/hour, to a maximum of 10 units/hour. Other doses and routes of insulin administration have been studied, but these have not been evaluated outside of the research setting or in critically ill patients. Less seriously ill patients with DKA should be given an infusion of regular insulin at 0.1 units/kg body weight/hour without a loading dose to minimize the risk of hypoglycemia. Insulin should not be started until hypovolemia has been addressed and serum potassium has been confirmed to be > 3.5 mEq/L. Giving insulin to patients with a serum potassium level < 3.5 mEq/L may precipitate life-threatening arrhythmias. Expert opinion regarding the use of insulin for patients with HHNS is mixed because some patients with HHNS achieve euglycemia (normal glucose levels) with fluid resuscitation alone. However, if the patient’s serum glucose does not decrease by 50–70 mg/dl per hour despite appropriate fluid management, a bolus of IV regular insulin at 0.1 units/kg body weight to a maximum of 10 units may be given. doi: 10.2337/diaclin.29.2.51 Clinical Diabetes April 2011 vol. 29 no. 2 51-59 20 IV Insulin Protocol Example Consider the likelihood of hypoglycemia and need for constant nursing assessment This is an example of titration in action, the nurse should stay at the bedside for close monitoring Nursing Management of Insulin Infusion If K+ < 3.3 at the time of insulin administration, promptly notify physician Initiate insulin drip at 0.1 units/kg/hour (or other dose written by physician) Monitor glucose q1 hour. Titrate insulin drip using the below table TABLE: Insulin Drip Titration (for use after insulin drip initiation) Glucose (mg/dL) Insulin Drip (units/hr) Glucose >500 Increase drip by 4 units/hr (or 25 %, which ever increase is less) Glucose 251-500 Do not adjust rate if blood glucose is decreasing by 50-75 mg/dL/hr If blood glucose is NOT decreasing by 50-75 mg/dL/hr, then increase the drip rate by 2 units/hr Glucose 151-250 When the plasma glucose reaches 250 mg/dl in DKA, decrease the insulin infusion rate to 0.05 - 0.1 unit/kg/h IV fluids should contain D5W if glucose is <250mg/dL. Call physician, if needed. Glucose 101-150 Decrease insulin drip by 50% Glucose 71-100 Hold insulin drip for 1 hour. (if still 71-100 at next hour, continue to hold and call MD Glucose <70 Hold insulin drip (if not already held) , Give dextrose 50%, 12.5 grams IV, Contact physician. Recheck blood, glucose in 15 minutes , Follow titration as above, Physician may change IV fluids to D10W 21 Fluid Replacement Ketoacidosis Treatment Fluid Replacement As the nurse, also think about IV access, urine output, electrolyte imbalance, should the client have a Foley? etc. Critically ill patients with severe hyperglycemia resulting from DKA or HHNS should be treated immediately with a bolus of normal saline. The average fluid deficit for patients with DKA is 3–5 liters; fluid resuscitation in young, otherwise healthy patients should begin with a rapid bolus of 1 liter of normal saline followed by an infusion of normal saline at 500 ml/hour for several hours. Patients with HHNS are often severely dehydrated, with cumulative fluid deficits of 10 liters or more. However, because they tend to be older and sicker, they require careful resuscitation. Expert opinion advocates for a rapid bolus of 250 ml of normal saline repeated as needed until the patient is well perfused. Fluid therapy is then continued at a rate of 150–250 ml/hour based on cardiopulmonary status and serum osmolality. The choice and rate of IV fluid for patients with DKA who are not critically ill should be based on their corrected serum sodium and overall fluid status. While awaiting laboratory study results, most of these patients may be given a bolus of 500 ml of normal saline. Patients with mild to moderate DKA should be given normal saline at 250 ml/hour; those with an elevated corrected serum sodium should be given half-normal saline at 250 ml/hour. doi: 10.2337/diaclin.29.2.51 Clinical Diabetes April 2011 vol. 29 no. 2 51-59 22 Adrenal Glands Adrenal Cortex is the outer shell that secretes corticoids (aldosterone, glucocorticoids and hydrocortisone) and sex hormones Adrenal Medulla is the Inner core produces epi/norepi via the sympathetic nervous system Conditions of focus for the adrenal glands are Cushing’s Syndrome, Addison's Disease & Pheochromocytoma Addison’s Disease 23 Addison’s is the result of the HYPO secretion of the adrenal cortex hormones Condition is fatal if left untreated Presentation Hypotension and weakness Bronze pigment of skin and mucous membranes changes Emotional disturbances Electrolyte imbalances Hypoglycemia 24 Interventions Addison’s It is believed that President Kennedy had Addison’s Consider the effects on his body as a result of the stress associated with holding the Presidency Monitor VS, I&O, fluid and electrolyte balance Inform the client on the need for life long steroid therapy, avoid stress and observe for Addisonian crisis (acute adrenal insufficiency) Clients with Addison’s are unable to tolerate physical or emotional stress without additional supplemental cortisone Keeping the patient stress and infection free is very important. Why do you think infection prevention is such an important factor? Cushing’s Syndrome 25 The HYPERsecretion of glucocorticosteriods from the adrenal cortex Most commonly the result of prolonged administration of corticosteroids Less likely from an adrenal gland tumor or benign tumor of the pituitary gland Interventions: Monitor glucose, I&O, weight Administer insulin when ordered Teach about the risk for infection and skin tears Surgical removal of tumor on adrenal gland or taper off steroid therapy if possible Client’s body image concerns Do the side effects of Cushing's remain after the cause is removed? 26 Pheochromocytoma Benign tumor on the adrenal gland leading to HYPERsecretion of epinephrine and norepinephrine, causing persistent or intermittent hypertension BP as high as 300/175 Many times not very responsive to medications Extreme HTN leads to: CVA, kidney damage and retinopathy Presentation Severe HTN Complaints of anxiety and heart palpitations Classic symptoms Severe pounding headache Tachycardia Profuse sweating Interventions Surgical excision is usual treatment Non-surgical candidates can be treated with adrenergic blocking agents http://www.bing.com/videos/search?q=pheochromocytoma&qs=PA&sk= &FORM=QBVR&pq=pheocry&sc=87&sp=1&qs=PA&sk=#view=detail&mid=919EA9B021DC73F5F5BE919EA9B 021DC73F5F5BE 27 Endocrine Conditions of Focus- Pituitary Diabetes Insipidus (DI) Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) What does the word diabetes mean? Knowing this can help explain what is happening in Diabetes Insipidus and you will see that overall DM and DI have little in common What does anti diuretic hormone (ADH) do in our bodies? http://www.bing.com/videos/search?q=diabetes+insipidus&qs=n&form=QBVR&pq=di abetes+insipidus&sc=8-18&sp=1&sk=#view=detail&mid=942A92486701F91E0CDA942A92486701F91E0CDA 28 Diabetes Insipidus The HYPOsecretion of ADH from the pituitary gland (and/or a deficiency of vasopressin) resulting in the failure of reabsorption of water in the kidneys, thus, a largely increased output Can occur after trauma to the pituitary gland Presentation and Assessment Polyuria of 4-24 liters a day Polydipsia Dehydration Tachycardia & postural hypotension, why? Urine specific gravity (measurement of urine concentration) of < 1.006 Why should we monitor VS, I & O, neuro, electrolyte and cardiac status? 29 30 Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) Pituitary gland HYPER secretes ADH and leads to water intoxication May happen to those under great stress or trauma Severity depends on how rapid it progresses Most S/S appear when blood NA+ levels < 125mEq/L Presentation- what are the reasons for each? Change in LOC and mental status Tachycardia and hypertension Weight gain Na+ less than 135mEq/L Interventions- what are the reason for each? Monitor VS, I & O, daily weight, labs, fluid restrictions, fluid retention Monitor neurological and cardiac status Push foods high in Na+ 31