UNRS 212 Diabetes:Hyper:Hypothryoidism PDF

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Diabetes-chronic for lifetime, characterized by sustained hyperglycemia due to abnormal insulin production or insulin receptor on cell 10/2/19 Normal physiology & Biochemistry  Glucose is the primary source of energy for the cells of the body Thru diet, useless unless it can get into cells. Insulin opens the door to let glucose into muscle cells Will store excess glucose in liver as glycogen ! Pancreas-endocrine Insulin is made by Beta cells ! Glucagon made by Alpha cells Work together to regulate glucose in blood Pancreas:  Two main hormones are produced by the pancreas:  Insulin  Glucagon  These two hormones play an important role in the regulation of glucose homeostasis  Insulin  Promotes cellular uptake of glucose (use it)  Converts glucose into glycogen (store it)  Glucagon “glucose be gone”  A hormone formed in the pancreas that promotes the breakdown of glycogen to glucose in the liver. Causes the liver to release glucose into the bloodstream.

Reference range: 70-110! Homeostasis  There is a continuous homeostatic balance in the body between the actions of insulin and those of glucagon.  This natural balance serves to maintain physiologically optimal blood glucose levels between 70-110 mg/dL (fasting).

Pathophysiology Diabetes  Definition:  Chronic disease characterized by hyperglycemia related to abnormal insulin production, impaired insulin utilization, or both.  Incidence:  Major public health problem around the world  29.1 million people (9.3% of population) in U.S.  86 million have prediabetes.  7th leading cause of death in U.S.  Etiology:  Genetics  Autoimmune  Environmental (obesity)  Pathophysiology:  Diabetes is primarily a disorder of glucose metabolism related to absent or insufficient insulin supply and/or poor utilization of insulin that is available.  Type I DM  5-10% of cases  Generally affects those under 40 years of age  Autoimmune disorder in which the body develops autoantibodies against insulin and/or pancreatic beta cells that produce insulin.  Destruction of beta cells means the patient always requires insulin.  Must have insulin!  Type II  90 to 95% of cases  Risk factors include being overweight/obese and having a family history of type II (first degree relative).  It is more prevalent in some populations (African American, Asian Americans, Hispanics, Native Hawaiians and other Pacific Islanders).

 Characterized by insulin resistance.  Can have insulin if not managed by diet/exercise Hyperinsulinemia Type 2  When insulin is not properly used, the entry of glucose into the cell is impeded, resulting in hyperglycemia.  In the early stages of insulin resistance, the pancreas responds to high blood glucose by producing greater amounts of insulin (if β-cell function is normal).  This creates a temporary state of hyperinsulinemia that coexists with hyperglycemia. High glucose tries to compensate but makes way too much insulin -Body first tries to compensate for hypoglycemia, but too much insulin being produced is not used efficiently Beta Cell Fatigue Type 2  A second factor in the development of type 2 diabetes is a marked decrease in the ability of the pancreas to produce insulin, as the β-cells become fatigued from the compensatory overproduction of insulin or when β-cell mass is lost. -Due to overproduction of insulin Inappropriate release of glucose from the liver  This leads to a third factor, which is inappropriate glucose production by the liver. Instead of properly regulating the release of glucose in response to blood levels, the liver does so in a haphazard way that does not correspond to the body's needs at the time. Metabolic Syndrome-high risk for getting Diabetes

A cluster of conditions that together significantly increase the risk for Type II DM. (Big waist circumference) Gestational Diabetes  Diabetes that develops during pregnancy.  Those who are at high risk are screened at the first prenatal visit:  Obese, advanced maternal age, family history of DM  Women at average risk are screened by at 24-28 weeks of gestation. (OGTT oral glucose tolerance test to rule out gestational diabetes)  Usually resolves within 6 weeks of delivery.!  63% chance of developing Type II within 16 years. Clinical manifestations  Signs and symptoms  Sustained hyperglycemia (≥126 mg/dL while fasting)  Glycosuria

 Polyuria-large amounts of urine  Polydipsia-always thirsty  Polyphagia-always hungry  Unexplained weight loss-body breaks up fat to get energy  Fatigue-cells do not have energy they need Diagnosing Diabetes  HgA1C (%):  7% is ideal, this is the goal for EVERY diabetic!  ≥ 6.5 not pregnant, healthy diabetic  5.7-6.4 prediabetic, insulin resistance  /=600mg/dL) that leads to osmotic diuresis and vascular depletion. Patient presents with seizures, somnolence, coma, seizure IV fluid replacement, give insulin, watch K (potassium levels) If >60years with impaired, decreased thirst sensation, dependent Macrosomia in Gestational Diabetes  Hyperglycemia that develops during pregnancy  Usually subsides after delivery  Insulin must be given to prevent birth defects  30% of patients may develop type 2 DM within 10 to 15 years Treatment for both  Drug therapy  Insulin (first treatment for type 1)  Oral and noninsulin injectables (first treatment for type 2)  Nutrition therapy  Exercise  Self-monitoring of blood glucose (SMBG) Type 2-Oral (first treatment for type 2), noninsulin injectable, nutrition, exercise, self-monitoring Insulins  Mechanism of action:  Functions as a substitute for the endogenous hormone. Promotes cellular uptake of glucose and converts extra glucose to glycogen for storage.  Onset, peak, duration different from real insulin

 Drug effects:  Effects are the same as normal endogenous insulin. Glycemic control of diabetes mellitus. Types of Insulin  Various insulins are available to manage diabetes. These insulins differ in their onset, peak, and duration. (See study sheet & study!)  Four major classes of insulin:  Rapid acting  Short acting  Intermediate acting  Long-acting Clnical Pearl  When the nurse administers insulin, he/she (you!) must monitor for the adverse reaction of hypoglycemia.  In order to do this, he/she (you!) must know when your patient is at risk for hypoglycemia based on the type of insulin you are giving.  In other words, you must know the onset, peak, and duration of any insulin that you administer. Types of Insulin  Rapid-acting insulin “shoot & eat”  Onset 10-15 minutes  Peak 30-90 minutes  Duration 3-5 hours  Examples: lispro (Humalog), aspart (Novolog)  Short-acting insulin  Onset 30-60 minutes  Peak 2-4 hours  Duration 4-8 hours  Examples: regular insulin (Humulin R, Novolin R) Examples of Sliding Scale order  The following is an example of a sliding scale order:  No insulin for a blood glucose less than 150 mg/dL  2 units for a blood glucose 150-199 mg/dL  4 units for a blood glucose 200-249 mg/dL  6 units for a blood glucose 250-299 mg/dL  Call MD for glucose >300 mg/dL Insulin Pen  An insulin pen is used to inject insulin for the treatment of diabetes. It is composed of an insulin cartridge and a dial to measure the dose, and is used with disposable pen needles to deliver the dose. Insulin Pump Count their carbs, pt HAS to eat, esp if they’re receiving a bolus Types of Insulin

 Intermediate-acting insulin  Onset: 2-4 hours  Peak: 4-10 hours  Duration: 10-18 hours  Examples: NPH (Humulin N, Novolin N)  Long-acting insulin  Onset: 2-4 hours  Peak: Peakless  Duration: Up to 24 hours  Examples: detemir (Levemir), glargine (Lantus) Side effect  Too much insulin can result in hypoglycemia (blood glucose below 60 mg/dL)  Severe hypoglycemia can result in convulsions, coma, and death Hypoglycemic Signs and Symptoms

Mealtime insulin (bolus)

Basal insulin

Hypoglycemic Signs and Symptoms  Tachycardia  Palpitations  Tremor or shakiness  Diaphoresis (sweating)  Headache  Weakness  Sudden moodiness or behavior changes  Confusion or difficulty paying attention Hypoglycemia  Treatment: rule of 15  Consume 15 g of a simple carbohydrate  Fruit juice or regular soft drink, 4 to 6 oz  Recheck glucose level in 15 minutes  Repeat if still < 70 gm/dL  Avoid foods with fat  Decrease absorption of sugar  Avoid overtreatment  Give complex carbohydrate (CHO) after recovery ex. turkey & milk Nursing Implications Are they eating? Any N/V?  Before giving drugs that lower glucose levels:  Hypoglycemia may be a problem if antidiabetic drugs are given and the patient does not eat  Assess the patient’s ability to consume food  Assess for nausea or vomiting  If a patient is NPO for a test or procedure, consult physician to clarify orders for antidiabetic drug therapy  Ensure adequate glucose is available at the time of onset and during all peak times High-Alert Medication-2 certified RN double check  When insulin is ordered, ensure:  Right patient  Right med  Right dose  Right route  Right time

 All insulin dosages are double checked by a second licensed nurse prior to administration Side effect: Somogyi effect  Hyperglycemia in the morning may be due to the Somogyi effect.  Too much insulin at bedtime, become hypoglycemic at 2-4am, hormones try to compensate but overshoots, patient is hyperglycemic when they wake up  Must decrease the amount of insulin they take at night  Problem: Too much insulin at bedtime  A high dose of insulin produces a decline in blood glucose levels during the night. As a result, counterregulatory hormones (e.g., glucagon, epinephrine, growth hormone, cortisol) are released, stimulating lipolysis, gluconeogenesis, and glycogenolysis, which in turn produce rebound hyperglycemia. Side effect: Dawn phenomenon  The dawn phenomenon is also characterized by hyperglycemia that is present on awakening.  Hyperglycemic at 2-4 am, need MORE insulin before they go to bed  Two counterregulatory hormones (growth hormone and cortisol), which are excreted in increased amounts in the early morning hours, may be the cause of this phenomenon.  Adolescence and young adulthood. (both hyperglycemic when they wake up) Oral Antidiabetics  Used in Diabetes type II along with life style modifications:  Diet  Exercise  Smoking cessation  Medication may not work without lifestyle modification  Therapy may require one or more drugs  Classes  Biguanide  Sulfonylureas  Glinides  Thiazolidinediones (glitazones)  Alpha-glucosidase inhibitors  Gliptins (DPP-4 Inhibitors)  SGLT-2 Inhibitors  Incretin Mimitics (GLP-1 Receptor Agonists) Biguanide  Mechanism of action:  Decreases the production of glucose by the liver. Also, improves insulin receptor sensitivity to insulin.  Example:  metformin HCl (Glucophage)  Indication:  First-line drug choice for most people with type 2 diabetes mellitus

 Adverse effects  Does not cause hypoglycemia  Gastrointestinal effects including loss of appetite, nausea, and diarrhea  May alter vitamin B12 absorption resulting in folic acid deficiency  Lactic acidosis is rare but lethal if it occurs Black Box Warning  Nursing alert:  Use of metformin with iodine containing radiologic contrast can lead to acute renal failure.  Client should be off drug for at least 24 hours before the test and for 48 hours after undergoing any radiologic study that requires contrast materials. Sulfonylureas  Mechanism of action:  Stimulates beta cells to release insulin (requires functioning beta cells to be effective).  Adverse effects:  Hypoglycemia  Nursing implications:  Hold if NPO; teach patient to avoid ETOH  Examples:  glyburide (Glynase, DiaBeta, Micronase), glipizide (Glucotrol), glimepiride (Amaryl) Glinides  Mechanism of action:  Similar to sulfonylureas, stimulates beta cells to insulin secretion  Adverse Effect:  Hypoglycemia  Nursing Implications:  Must eat within 30 minutes of taking dose  Examples:  repaglinide (Prandin), nateglinide (Starlix) Thiazolidinediones (glitazones)  Mechanism of action:  Improves insulin receptor sensitivity to insulin. Decreases the production of glucose by the liver.  Nursing implications:  Contraindicated in heart failure (BLACK BOX WARNING), bladder cancer, and active hepatic disease  Examples:  pioglitazone (Actos), rosiglitazone (Avandia)

Alpha-Glucosidase Inhibitors  Mechanism of action:  Inhibits the enzyme alpha-glucosidase which is found in small intestine. When blocked, carbohydrate absorption is decreased.  Adverse effects:  GI: Abdominal distention, cramping, diarrhea, flatulence  Nursing implication:  Must be taken with first bite of food.  Examples:  acarbose (Precose), miglitol (Glyset) Gliptins (DPP-4)  Mechanism of action:  Enhance the actions of incretin hormones, endogenous compounds that (1) stimulate glucose-dependent release of insulin and (2) suppress postprandial release of glucagon.  Adverse effects:  Generally, well tolerated; pancreatitis (rare)  Examples:  sitagliptin (Januvia) Sodium-Glucose Co-Transport (SGLT-2) Inhibitors  Mechanism of action:  Blocks the reabsorption of glucose. Glucose ends up staying in the nephron and being excreted by the kidneys (causing glycosuria).  Adverse affects:  Genital yeast infection  Orthostatic hypotension  Examples:  empagliflozin (Jardiance), dapaglifozin (Farxiga) Incretin Mimetics (GLP-1 Receptor Agonists)  Mechanism of action:  Works the same way as the endogenous hormone. Delays gastric emptying. Stimulates release of insulin. Suppresses post-prandial glucagon release.  Adverse effects:  N/V, diarrhea, pancreatitis  Examples:  exenatida (Byetta) In conclusion…  Monitor for adverse response  Hypogylcemia

 Monitor for therapeutic response  Decrease in blood glucose levels to the level prescribed by physician  Monitor for hypoglycemia and hyperglycemia  Self-monitoring of blood glucose (SMBG)  Measure hemoglobin A1c (HgbA1C) to monitor long-term compliance with diet and drug therapy (goal 7.0) Patient education: Carb counting  Diet teaching  Dietitian initially provides instruction, tells how much insulin they should get  Carbohydrate counting  Serving size is 15 g of CHO  Typically 45 to 60 g per meal  Insulin dose based on number of CHOs consumed  Patient teaching essential Patient education: Exercise  Type/amount  Minimum 150 minutes/week aerobic activity  3 days moderate activity, brisk walk  Resistance training three times/week  Do not exercise if hypoglycemic, or hyperglycemic (above 300)  Benefits  ↓ Insulin resistance and blood glucose  Weight loss  ↓ Triglycerides and LDL , ↑ HDL  Improve BP and circulation  Start slowly after medical clearance  Monitor blood glucose  Glucose-lowering effect up to 48 hours after exercise  Exercise 1 hour after a meal  Snack to prevent hypoglycemia  Do not exercise if blood glucose level > 300 mg/dL and if ketones are present in urine Patient education: SMBG  Enables decisions regarding diet, exercise, and medication  Accurate record of glucose fluctuations  Helps identify hyperglycemia and hypoglycemia  Helps maintain glycemic goals  A must for insulin users  Frequency of testing varies  Patient teaching  How to use, calibrate  When to test  Before meals  Two hours after meals

 When hypoglycemia is suspected  During illness  Before, during, and after exercise Patient education: Storage of insulin:  Storage of insulin  Do not heat/freeze  In-use vials may be left at room temperature up to 4 weeks  Extra insulin should be refrigerated  Avoid exposure to direct sunlight, extreme heat or cold  Store prefilled syringes upright for 1 week if 2 insulin types; 30 days for one Patient should wear medical alert jewelry

Patient education: Foot care  Inspect daily  Avoid going barefoot  Proper footwear  How to treat cuts

Hyperthyroidism & Hypothyroidism  Thyroid gland is responsible for the secretion of thyroid hormone which is essential for proper regulation of metabolism.  Thyroxine (T4)  Triiodothyronine (T3) Hypothalamus-Pituitary-Thyroid Axis  Hypothalamus  Thyrotropin-releasing hormone (TRH)  Anterior pituitary  Thyroid stimulating hormone (TSH)  Thyroid gland  Thyroxine (T4)  Triiodothyronine (T3) Parathyroid Glands on the Thyroid Gland  Two pairs of parathyroid glands lie behind each thyroid lobe.  Parathyroid glands secrete parathyroid hormone (PTH).  Increased parathyroid hormone regulates (increases) calcium in body T3/t4  Both are produced in the thyroid gland through the iodination and coupling of the amino acid tyrosine.  Body needs about 1 mg of iodine per week from the diet. Iodine & tyrosine are coupled (married) in thyroid gland, out come the babies t3 & t4

Iodine deficiency - not common in US, bc– table salt in America, overstimulation of TSH, compressing trachea T3=active form T4=becomes T3

Hyperthyroidism – everything’s speed  Definition:

 Hyperactivity of the thyroid gland with sustained increase in synthesis and release of thyroid hormone.  Incidence:  More common in women than men  Highest frequency in those 20 to 40 years old Spotlight on Grave’s disease  Autoimmune disorder of unknown etiology (idiopathic) characterized by diffuse enlargement of the gland and excess thyroid hormone secretion, chronic with exacerbations & remissions, hyperthyroid issue  Development of autoantibodies that stimulate the gland to release thyroid hormone (T3 & T4).  Patient will experience remissions and exacerbations.  May ultimately result in destruction of thyroid tissue and hypothyroidism.  Causes goiter Thyrotoxicosis The term thyrotoxicosis refers to the clinical syndrome of hypermetabolism resulting from excess circulating levels of thyroid hormone. Clinical manifestations  Nervousness  Palpitations, tachycardia  Tremors  Insomnia  Increased appetite  Weight loss  Diaphoresis-sweating  Diarrhea  Heat intolerance-cannot get cool  Elevated basal temperature ExophthalmosProtrusion of the eyeballs from the orbits that is usually bilateral.  Results from increased fat deposits and edema in the orbital tissues and ocular muscles  White sclera visible above and below eyes, not normal Edema in eyes, HOB bed should be elevated Diplopia Double vision may occur due to weakening of ocular muscles. Acropachy Acropachy (clubbing of the digits) may occur with advanced disease. Complications  Thyrotoxicosis (also called thyrotoxic crisis or thyroid storm) is an acute, severe, and rare condition.  Medical emergency that requires aggressive treatment to prevent death, (admitted to ICU)

 Symptoms: Severe tachycardia, heart failure, shock, hyperthermia (up to 106 F), agitation, delirium, abdominal pain, vomiting, diarrhea, coma. Diagnosis  Laboratory values: Hyperthyroidism  Decreased TSH level (< 0.4 mU/L)  Elevated T3 and T4 levels (thyroid hormone)  Radioactive iodine uptake test (RAUI)  Used to differentiate Grave’s disease from other forms of hyperthyroidism Treatment  Antithyroid drugs  propylthiouracil (PTU), most common  methimazole (Tapazole) “parents” tells t3&4 they cannot be coupled  B-adrenergic blockers  propanolol (*nonselective, blocks beta 1 & 2)  atenolol (*cardioselective blocks beta1) inhibits sympathetic NS  Radioactive iodine (RAI) therapy, swallowed, and kills bacteria  Surgery  Thyroidectomy Subtotal Thyroidectomy  A subtotal thyroidectomy is the preferred surgical procedure for removal of thyroid. Antithyroid drugs  Mechanism of action/ drug effects:  Inhibits the incorporation of iodine molecules into the amino acid tyrosine. This prevents the formation of the thyroid hormone (T3 and T4). Neither drug can inactivate already existing thyroid hormone.  Usual regime:  Begin to improve within 1 to 2 weeks with peak results taking up to 4 to 8 weeks  Continue medication for 6 to 15 months in hopes patient will go into spontaneous remission (20-40% of patients) Complication: hypothyroidism  Following removal of all or part of the thyroid gland patient may develop hypothyroidism which would necessitate life long treatment with thyroid hormone replacement. Nursing Care reminders  Acu...