Endocrine Study Guide (Diabetes Mellitus / Cushings / Addisons) Addison’s & Cushing Syndrome Understand the underlying pathophysiology and which hormones are involved. Cortisol/steroids Which prescribed medications mimic adrenal production of cortisol and cause concern for Cushing Syndrome? Steroids Too much steroids/cortisol = Cushings Syndrome What are precautions with corticosteroids that need to be taken to prevent Addison’s / Addisonian Crisis? Too little adrenal cortisol or abrupt withdraw of glucocorticoids= Addison Diabetes Mellitus Know the common insulins, as well as the onset and peak. [Lantus (Glargine), NPH (Humulin N), Regular (Humulin R), Detemir (Levemir)] o Lantus(Glargine) Long acting- Duration 24 hours Onset: 1-2 hr No Peak o NPH (Humulin N) Intermediate-acting, usually mixed with regular, is cloudy Onset 2-4 hrs Peaks 4-12 hours Remain in 10-20 hours o Regular (Humulin R) Short acting, clear, inject 30-45 min before meal Onset ½ to 1 hour Peaks 2-3 hours Remains in body 2-6 hours Only one allowed to drip with an IV o Detemir (Levemir) Long-acting insulin Onset: 1-2 hr No Peak Duration: 24+ hr What is insulin sliding scale? Which insulin would you use to “cover” a blood sugar based on a sliding scale order? What is the onset and peak of the insulin associated with sliding scale coverage? o Insulin Sliding cale o Regular, short acting used for sliding cover o Insulin drip- People with DKA What is Hgb A1C? What is the goal for a patient with diabetes mellitus related to Hgb A1C? o Lifespan of rbc is 120 day- 3 mo o Hemocrit and hemoglobin make up RBC o If Hgb A1C is high, we know patient has had uncontrollable BS in the last three months. o For diabetic patients the Hgb A1C goal is 6.5% What is the effect of corticosteroids, such as prednisone, on blood glucose? What is the effect on WBC’s? o Steroids increase white count. Ex)If someone with an infection has high WBC o Corticoidsteriods increase blood sugar o Blood sugar will fuel an infection o If the steroid is driving up the BS then you give insulin to off set the BS Which lab values are most important to monitor in a patient with diabetes mellitus? Which labs are most important with IV insulin therapy? o DM-Potassium levels Monitor DM patients on IV Inulin drip for hypokalemia. o IV Insulin to lower postassium levels to a non-diabetic IV Insulin moves glucose from blood to the cells along with potassium. What are Kussmaul respirations? Why does this type of breathing occur? How would Kussmaul breathing present on assessment of the patient? o Patients that are DKA have kussmal respirations to blow off extra CO2 acid to get back to an alkaline state, because they are at a Its done naturally o Breath faster indication they are acidic o Kussmaul resp., teach patient pursed lip breathing to blow off CO2, to blow off ketones. o Get rid of acids through CO2 o Blowing off CO2, which is not the problem, ketones are which cause the acid. Compentesory mechanism. o Blow more air than normal What would cause a “fruity” or “acetone-like” odor to the breath? o The ketones (acidic waste products of fat metabolism) from DKA. Ketone=acid Due to the breakdown of fat and protein as an energy source because the body doent have enough insulin to use all the sugar Define polyuria, polydipsia, and polyphagia. o Polyuria- increase urination, due to kidney wanting to flush the sugar out until given water o Polydipsia- Increase thirst cause kidneys register that you need to filter the sugar out and your hyperglycemic, so you need water to filter stuff out. So thirst because blood sugar is crazy high o Polyphagia- increased hunger, if blood sugar is low. What are common signs & symptoms of HYPOglycemia? o Clammy, cold confusion, irritable, o Blood Sugar- <70 Treat with glucose source ( 15g of carbs) You will not use glucagon Give patient glucose- amp of d50 straight into IV or 15g of Oral Glucose. Given based on level on of consciousness. Wait 15 mins after administration and reassess BS before any new interventions. o Diaphoresis o Hunger o Generalized weakness or seizures o Alert to coma state o Can be in result to too much insulin What are common signs & symptoms of HYPERglycemia? o Blood sugar 250 or higher o Alert to Como state- from the ketotic acidoic state o Hot and dry skin o Nausea and vomiting with DKA o Kussmals respiration- blowing off ketones through CO2 o Acetone (fruit breath) o Treat with oral hypoglycemics or insulin What are common microvascular complications of poorly controlled diabetes mellitus? What are macrovascular complications? o Macrovascular Complications Moderate to large arteries and veins Cardiovascular Disease (MI, CAD, HF) Cerebrovascular disease (CVA)- stroke Peripheral Vascular (foot ulcers) o Microvascular Complications Damage to small arteries and veins o o Retinopathy (vision)- microcapillaries, no perfusion to the capillaries Diabetic neuropathy-tingling/ pins and needles sensation in feet causing ulcers. DM have poor blow flow to lower extremities Diabetic nephropathy- inadequate perfusion in kidney due to blood being very viscous blood so it wont make its way to the capillaries leading to damage. Sexual dysfunction Cognitive dysfunction What is the underlying patho of diabetic ketoacidosis? What are common signs & symptoms of diabetic ketoacidosis (DKA)? o DKA more common in type 1 diabetic o Glucose > 300 mg/dL o Ketones, acidic waste products of fat metabolism o Body can’t use glucose for energy o Severe dehydration, electrolyte imbalance and acidosis can lead to coma and death o Develops rapidly when cold, flu or infection o Kussmaul’s respirations (low pH) What interventions would the nurse expect for a patient with diabetic ketoacidosis? o Hydrate first with Hypotonic 0.9 Normal Saline IV Bolus to shift the amount of insulin they need then Short acting insulin drip o Check potassium hypokalemic due to insulin driving potassium out of the cell Regarding hypoglycemia and administration of 50% dextrose (D50) vs. 15 grams of oral glucose, when would it be appropriate to administer one medication over the other? o Level of consciousness, aspiration risk, alert & orientated, slow to respond, gargle speaking. Regarding management of diabetes mellitus and exercise, what would the nurse include in a teaching plan? Consider presence of ketones in the urine, foot care, blood glucose monitoring, when to avoid exercise, timing of food intake around exercise. o Exercise burns glucose so check blood sugar before working out and making sure eat something so BS doesn’t crash espically if on a antihyperglycemic or an insulin o If patient is at a ketotic state, should not exercise due to not having access to carbs or glucose to burn off Regarding diabetes mellitus and “sick day” management, what would the nurse include in a teaching plan? Consider frequency of blood glucose monitoring, exercise while sick, expected effect illness will have on blood glucose, when to hold insulin, what to do if vomiting / not tolerating oral intake, importance of adequate hydration. o You would teach the patient to increase blood sugar check o Making sure staying hydrated to dilute the glucose o Give long acting insulin and hold short acting before surgery due to NPO and cortisol levels increasing BS o When stressed, relase cortisol, increasing BS What is metabolic syndrome? What are the signs & symptoms that identify metabolic syndrome? Why is it important to consider metabolic syndrome in a patient with diabetes? o Simultaneous Metabolic factors that increase risk of type 2 diabetes and cardiovascular disease Risks: Abdominal Obesity (40 inches (100 cm) or more for men and 35 inches (88 cm) or more for women), hyperlipidemia, hyperglycemia, stress, hypertension What is Metformin? What is the safety concern with Metformin that results in patients being taken off of this medication while hospitalized? o Metformin helps to control the amount of glucose (sugar) in your blood. It decreases the amount of glucose you absorb from your food and the amount of glucose made by your liver. o Contraindicated with contrast. Cannot be combined with contrast for diagnostics so must be off it in the hospital. Any contrast for diagnostics combined with metformin will cause irreversible kidney failure. What is diabetic neuropathy? How can the patient with diabetes reduce the chance of developing neuropathy? If the patient has diabetic peripheral neuropathy, what should the nurse include in the teaching plan to prevent complications? o Neuropathy- damage to nerve ending and blood flow problem leaving tingles in the feet o Reduce by managing blood sugar o How to prevent: Blood sugar checks Protect the feet from injury, check for integrity of feet, cuts, tissue damage, ulcers o Type 1 Diabetes o Always need insulin o Not ability to produce insulin. Absolute absence of insulin o Insulin made in pancreas made in beta cells o Cannot receive oral antihyperglycemics, must have insulin o Use protein and fat to burn energy because type 1 cant use gluecose or carbs o Biproduct of protiene and fat used for energy is ketones, and ketones are highly acidic o DKA is producing ketones cause not using crabs and acidic bec of all the ketones that is in their blood stream o DKA more common in TYPE 1 o Type 2 Diabetic o Produce insulin, they just don’t produce enough. Or cells aren’t receptive enough o Working out and dietary makes insulin work better by decreasing BS o Because they are able to have carbs for energy, they do not have ketones In addition to the ATI practice assessment, consider practice NCLEX questions from the Lewis textbook online resources (Evolve website), the Lewis Study Guide, Saunders Comprehensive OR Saunders Q&A book or online questions in Evolve or the Saunders app. Success truly comes from exposure to as many NCLEX practice questions as possible.