Gutierrez Endocrine Disorders Study Guide and Note Outline PDF

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Endocrine Disorders Study Guide and Note Outline ATI Chapters: 82, 83 Textbook Chapter 51: Entire chapter Charts/Tables/Figures          

Table 51-3, Select Categories of Insulin Table 51-4, Insulin Regimens Table 51-6, Select Oral Anti-Diabetic Agents Chart 51-7, Self-Injection of Insulin Chart 51-8, Criteria for Self-Injection Figure 51-7, Patho of DKA Chart 51-9, Sick Day Rules Table 51-7, Comparison of DKA and HHS Chart 51-10, Foot Care Tips Chart 51-11, Glucose Control in Perioperative Period

Learning Objective #1: Differentiate between the types of diabetes. a. What is the patho of Type 1 diabetes? Destruction of beta cells autoimmune= no insulin production + increased glucose production by liver because it senses that cells are starving = fasting hyperglycemia --glucose from food is not stored by liver (remains in blood stream because liver thinks cells are starving) --osmotic diuresis (so many glucose particles in blood that water is pulled from cells into the vascular system) loss of electrolytes and water through urine = dehydration --kidneys cannot reabsorb all fltered glucose  glycosuria and polyuria 2/2 osmotic diuresis Usual onset: any age, but usually 30 Excretion of insulin—Y impaired insulin secretion and insulin resistance (the doorman)  pancreas works harder but can’t keep up with demand  Type 2 Does ketosis occur no, enough insulin is present to prevent the breakdown of fats by the liver

Acute complication of hyperglycemia  hyperglycemic hyperosmolar nonketotic syndrome d. What are the risk factors for Type 2 diabetes?*****

e. Describe the diet and exercise recommendations for prevention of Type 2 diabetes.

f.

Describe the symptoms of both types of diabetes.

Type 1 = fast onset; Type 2 = slower onset Fatigue and weight loss = unable to use glucose for energy

g. What are the diagnostic criteria for type 2 diabetes? FPG ≥126 mg/dL (7.0 mmol/L). Fasting is defned as no caloric intake for at least 8 h.* OR 2-h PG ≥200 mg/dL (11.1 mmol/L) during OGTT. The test should be performed as described by the WHO, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water.* OR A1C ≥6.5% (48 mmol/mol). The test should be performed in a laboratory using a method that is NGSP certifed and standardized to the DCCT assay.* OR In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose ≥200 mg/dL (11.1 mmol/L).

Learning Objective #2: Develop an education plan for diabetes. a. What are the goals and the fve key components of diabetes management? Attain and maintain recommended metabolic outcomes, Normalize insulin activity and blood glucose levels Reduce the development of vascular and neuropathic complications including glucose and A1C levels; LDL cholesterol, HDL cholesterol, and triglyceride levels; blood pressure; and body weight. b. What are the dietary teaching points? c. What are the exercise program teaching points, differentiating between Type 1 and Type 2? d. Identify the role and nursing considerations of oral antidiabetic agents in therapy for patients with Type 2 diabetes. e. What are the insulin administration considerations, including onset, peak, duration, relationship to mealtimes? f. What should be assessed and taught to patients who are prescribed insulin? g. What are the symptoms and treatments for hypo- and hyperglycemia?

h. Explain the management strategies for a person with diabetes to use during “sick days.”

i.

What are the inpatient considerations when a patient is NPO, on clear liquids, or on enteral or parenteral feedings?

j.

Explain foot care patient education.

Contributors: sensory neuropathy, autonomic neuropathy (lack of sweating to lubricate feet), peripheral vascular disease, immunocompromise Foot Care Education: What do we teach? --inspection --washing --skin care --corns, calluses, toenail care --foot protection --blood flow increase

Learning Objective #3: Differentiate between diabetic ketoacidosis or hyperglycemic hyperosmolar syndrome. a. What are the risk factors for each? DKA: Lack of sufficient insulin related to undiagnosed or untreated type 1 diabetes mellitus or nonadherence to a diabetic regimen Reduced or missed dose of insulin (insufficient dosing of insulin or error in dosage) Any condition that increases carbohydrate metabolism (physical or emotional stress, illness) Infection is the most common cause Increased hormone production (cortisol, glucagon, epinephrine) that stimulates the liver to produce glucose and decreases the effect of insulin HHS: Sustained osmotic diuresis results in a hyperglycemic hyperosmolar state, resulting from one of the following. Lack of sufficient insulin related to undiagnosed or poorly managed diabetes mellitus. There is sufficient endogenous insulin present to prevent the development of ketosis, but not enough to prevent hyperglycemia. Inadequate fluid intake or poor kidney function. Most common in adult clients age 50 to 70 years old. Mortality rates in older clients are 40% to 70%, given older clients often seek medical attention later when much sicker, and have age-related changes that affect the body’s ability to recover (decreased ability for urine concentration, decreased thirst perception). Other factors that contribute to the development of HHS include infection, stress, medical conditions (myocardial infarction, cerebral vascular injury, sepsis), and some medications (glucocorticoids, thiazide diuretics, phenytoin, beta blockers, calcium channel blockers). b. Relate the patho of DKA and HHS to the characteristics and symptoms of each. Diabetic ketoacidosis (DKA) is an acute, life-threatening condition characterized by uncontrolled hyperglycemia (greater than 300 mg/dL), metabolic acidosis, and an accumulation of ketones in the blood and urine. The onset is rapid, and the mortality rate is up to 10%. Hyperglycemic hyperosmolar state (HHS ) is an acute, life-threatening condition characterized by profound hyperglycemia (greater than 600 mg/dL), hyperosmolarity that leads to dehydration, and an absence of ketosis. Onset

generally occurs gradually over several days, and if left untreated can lead to coma and death.

DKA • • • • • • •

> T1DM Rapid onset 250 pH metabolic acidosis Ketones present BUN, creatinine elevated s/s 3 Ps; hypotension; dehydration; n/v, abdominal pain; Kussmaul’s respirations; fruity breath; neuro signs can vary

HHS • • • • • • •

> T2DM Slow onset (days) BG > 600 pH normal Ketones absent BUN, creatinine elevated s/s 3Ps, hypotension, dehydration, AMS (Altered mental status); no GI signs usually

c. Explain the treatment of DKA and HHS. Correcting dehydration with fluid resuscitation Restoring electrolytes through monitoring and replacement protocols Reversing acidosis (in DKA) with insulin infusion Treating hyperglycemia (in HHS) with insulin infusion Monitoring for complications of treatment Fluid overload Cerebral edema Management of DKA is aimed at correcting dehydration, electrolyte loss, and acidosis before correcting the hyperglycemia with insulin Rehydration to maintain tissue perfusion: NS or ½ NS; may add D5 when blood glucose levels < 300  to prevent decline in BG levels Potassium key electrolyte; initially hyperkalemia due to hyperglycemia + acidosis in DKA, but as K+ moves back into cells with insulin infusion (to reverse acidosis in DKA and hyperglycemia in both), will need to monitor for hypokalemia and replace it IV continuous infusion of regular insulin (IV doesn’t stop until SQ starts; may need to increase D5 infusion to prevent hypoglycemia  hourly BG checks When hanging the insulin drip, flush the insulin through entire IV infusion set and discard the frst 50 mL of fluid; insulin molecules adhere to the inner surface of

plastic IV infusion sets; therefore, the initial fluid may contain a decreased concentration of insulin Cerebral edema due to correction of hyperglycemia  fluid shifts Nursing assessments during fluid resuscitation?  s/s of fluid overload, VS, lung assessment, I/Os Learning Objective #4: Outline the major complications of diabetes and the self-care behaviors that are important in their prevention. a. Differentiate between the risks of complications in Type 1 and Type 2 diabetes. Kidney (microvascular) disease more common in type 1 Cardiovascular (macrovascular) complications more common in older patients with type 2 Macrovascular complications r/t medium and large vessel thickening, sclerosing, and occlusion  MI, stroke, gangrene/amputation of toes/feet/legs Microvascular complications r/t capillary membrane thickening  diabetic retinopathy and nephropathy b. What is the most effective prevention of complications? c. What are the patho and patient education for cardiovascular and cerebrovascular disease? d. What are the symptoms, and patient education for diabetic retinopathy? Damage to the small blood vessels that nourish the retina develop microaneurysms that leak fluid swelling, deposits and possibly macular edema Retinal vessels are damaged and new ones generate, but they rupture, bleeding into eye scarring from rupture can pull on retina and detach it Nursing care: education because it can be asymptomatic; blood glucose, BP control, no smoking; regular eye exams; coping with vision loss; safety as vision loss occurs

e. What are the symptoms, and patient education for peripheral and autonomic neuropathies? Peripheral Neuropathy: distal portions of the nerves, especially LEs, symmetrically, spread in a proximal direction. Clinical Manifestations: paresthesias and burning sensations (especially at night)  progressing to numbness Decreased sensations of pain and temperature  increased risk for injury and undetected foot infections. Neuropathy-related joint changes “Charcot joints” On physical examination, decrease in deep tendon reflexes and decreased vibratory sensation Management: BG control and pain management (gabapentin/Neurontin; duloxetine/Cymbalta; pregabalin/Lyrica); foot and leg care

Autonomic Neuropathies; broad dysfunctions as a result of autonomic nervous system changes Clinical Manifestations: CV: slightly tachycardia and orthostatic hypotension  lower-body elastic garments that maximize venous return and prevent pooling of blood in the extremities; GI: early satiety, bloating, n/v 2/2 delayed gastric emptying ; low-fat diet, frequent small meals, frequent blood glucose monitoring, meds that increase gastric motility (metoclopramide/Reglan, bethanechol/Myotonachol) GI: “diabetic” constipation high-fber diet, adequate hydration; laxatives and enemas may be necessary if constipation is severe; diarrhea (esp. nocturnal diarrhea)  bulk-forming laxatives or antidiarrheal agents Urinary: retention, decreased sensation of bladder fullness 2/2 neurogenic bladder; pre-disposed to UTIs b/c can’t empty bladder completely  intermittent straight cathing; Hypoglycemic unawareness: may no longer have symptoms of hypoglycemia  frequent blood glucose monitoring; teaching other symptoms such as circumoral numbness and decreased concentration Sudomotor neuropathy: decrease or absence of sweating (anhidrosis) of the extremities, with a compensatory increase in upper body sweating; dryness of the feet increases the risk for the development of foot ulcers  educate on foot care f.

What is the patho, signs/symptoms, and patient education for diabetic nephropathy?

Caused from damage to sensory nerve fbers resulting in numbness and pain Peripheral neuropathy includes focal neuropathies, caused by acute ischemic damage or diffuse neuropathies, which are more widespread and involve slow, progressive loss. This can lead to complications (foot deformities, ulcers). Autonomic neuropathy can affect nerve conduction of the heart (exercise intolerance, painless myocardial infarction, altered left ventricular function, syncope), gastrointestinal system (gastroparesis, reflux, early satiety), and urinary tract (decreased bladder sensation, urinary retention). It affects the autonomic nervous system, which minimizes manifestations of hypoglycemia (diaphoresis, tremors, palpitations), which can be dangerous for the client....