NUR130 Metabolism -Diabetes, DKA, HHS $xam 3

diabetes mellitus

a metabolic disorder resulting from either an inadequate production of insulin (type 1) or an inability of the body’s cells to respond to insulin that is present (type 2)

hyperglycemia (high glucose levels)

Type I diabetes

is characterized by the autoimmune destruction of insulin-producing beta cells in the pancreas, leading to little or no insulin production.

Glucose unable to be stored into liver due to lack of insulin

Genetic

Treatment for Type I diabetes

insulin ONLY and blood glucose monitoring.

what can poor maintenance of Type I Diabetes lead to?

DKA

Type II diabetes

is characterized by insulin resistance and relative insulin deficiency, often associated with obesity and a sedentary lifestyle

body storing more energy than client is using —→storage space is too full—> decreased tissue sensitivity to insulin

treatment for Type II diabetes

antidiabetics, supplemental insulin, diet modification

metabolic syndrome

combination of conditions that include abdominal obesity, hyperglycemia, hyperlipidemia, and hypertension

often precedes type II diabetes

How is blood sugar regulated?

blood sugar is regulated primarily by insulin and glucagon

Insulin lowers blood sugar by facilitating cellular uptake of glucose, while glucagon raises blood sugar by promoting glucose release from liver stores

• Transports glucose to tissues, muscles, organs 

• Then stimulates the storage of glucose (which has now become glycogen)

• Once adequate amounts of glucose and glycogen are disbursed- insulin regulates the release of more by inhibiting further release of glucose. 

• Pancreas simultaneously, and continuously releases tiny amounts of insulin (basal insulin) and glucagon to maintain and prevent glucose spikes

risk factors for diabetes

metabolic syndrome

insulin resistance

pancreatitis and Cushing’s Syndrome

Age (older adult clients can have impaired liver and kidney function)

obesity

physical inactivity

family history

poor diet

diabetes expected findings

• polyuria

• excessive thirst (polydipsia)

• dehydration (dry mucus membranes, loss of skin turgor/ skin warm and dry, weakness and malaise, rapid weak pulse and hypotension)

• polyphagia (excessive hunger) due to the inability of cells to receive glucose and the body using fat and protein for energy(ketosis)

• kussmaul respirations

• recurrent infections

• blurred vision

• fruity breath

• Lethargy

kussmaul respirations

deep, labored breathing pattern often seen in metabolic acidosis, particularly diabetic ketoacidosis.

expected screenings - DM

• HgA1C greater than 5.7%, impaired fasting glucose, or impaired glucose tolerance

• HDL level less than 35 mg/dL or triglyceride level greater than 250 mg/dL

client education: DM

• Consume a diet low in saturated fats to decrease low-density lipoprotein (LDL), assist with weight loss for secondary prevention of diabetes, and reduce risk of heart disease.

• Modify the diet to include sources of omega-3 fatty acids and fiber to lower cholesterol, improve blood glucose for clients who have diabetes, for secondary prevention of diabetes, and to reduce the risk of heart disease.

• Perform physical activity at least three times per week (150 min/week).

diagnostic criteria for DM

two findings (on separate days) of at least one of the following.

• Manifestations of diabetes plus casual blood glucose concentration greater than 200 mg/dL (without regard to time since last meal)

• Fasting blood glucose greater than 126 mg/dL (no caloric intake within 8 hr of testing)

• 2-hr glucose greater than 200 mg/dL with oral glucose tolerance test

• Glycosylated hemoglobin (A1C) greater than 6.5%

glycosylated hemoglobin (HbA1c)

A measure of average blood glucose levels over the past two to three months, used to diagnose and monitor diabetes.

• The expected reference range is 4% to 6%, but an acceptable reference range for clients who have diabetes can be 6.5% to 8%, with a target goal of less than 7%.

ketones

Chemicals produced in the blood during the breakdown of fat for energy when glucose (and insulin) is in short supply, often present in diabetic ketoacidosis (DKA).

tested by urine dipstick

rapid-acting insulin

A type of insulin that begins to work within 15 minutes, peaks in about 1 hour, and lasts for 2 to 4 hours, commonly used to control blood sugar spikes after meals.

aspartate and lispro

short-acting insulin

A type of insulin that takes effect within 30 minutes, peaks in 2 to 3 hours, and lasts for 3 to 6 hours, often used to manage blood sugar levels during meals.

intermediate acting insulin

A type of insulin that takes effect within 2 to 4 hours, peaks in 4 to 12 hours, and lasts for 12 to 18 hours, commonly used for long-term blood sugar management.

long-acting insulin

A type of insulin that takes effect within 1 to 2 hours, has no pronounced peak, and lasts for 24 hours or more, used for basal insulin coverage.

glargine

Which insulin is drawn up first, regular or cloudy (NPH)?

regular insulin

manifestations of hypoglycemia

cold/clammy skin, mild shakiness, mental confusion, sweating, palpitations, headache, lack of coordination, blurred vision, seizures, and coma (CNS affects and activation of sympathetic nervous system)

manifestations of hyperglycemia

increased thirst, frequent urination, fatigue, hot/dry skin, fruity breath

hypoglycemia blood glucose levels

less than 70 mg/dL

hyperglycemia blood glucose levels

greater than 130 mg/dL after fasting or greater than 180 mg/dL after meals

normal blood glucose levels

typically between 70 and 99 mg/dL when fasting.

diabetic ketoacidosis

a metabolic derangement, most commonly occurring in type 1 diabetes, that results from a deficiency of insulin; highly acidic ketone bodies are formed, resulting in acidosis

pathophysiology of DKA and compensatory mechanisms

• without insulin, glucose cannot enter cells —> excess glucose in blood (hyperglycemia)

• the body breaks down fat for energy

  • free fatty acids —> converted into ketones by liver

  • excess ketones cause ketosis and metabolic acidos

• In an attempt to rid the body of the excess glucose, the kidneys excrete the glucose along with water and electrolytes (e.g., sodium, potassium). This osmotic diuresis, which is characterized by polyuria, leads to dehydration and marked electrolyte loss

• Body compensates with Kussmaul Respirations (deep/rapid breathing) to blow off CO2

• Acetone production due to elevated ketones —> fruity breath odor

• perfusion interrupted due to excess glucose / O2 not getting to where it needs to go

causes of DKA

primarily due to insufficient insulin, often triggered by infections, stress,missed insulin doses, or untreated/undiagnosed diabetes.

manifestations of DKA

include polyuria (body trying to rid excess glucose)

polydipsia (due to fluid loss)

polyphagia (3Ps)

fluid loss leads to—> dehydration, confusion, agitation, nausea, weakness

fruity breath odor

volume depletion —> orthostatic hypotension, hypotension, weak/rapid pulse

Kussmaul respirations (body trying to blow off excess CO2;) —> increased RR

Electrolyte imbalance

Kidneys working hard**

blood glucose > 250

what kind of ABGs would you see in DKA?

low PH (<7.35), low Bicarbonate (<22), CO2 depends (can be low due to compensatory mechanisms), low levels of electrolytes, increased levels of BUN/creatinine/ hematocrit due to dehydration

nursing interventions DKA

rehydration (fluid and electrolyte replacement/ BEFORE insulin), monitoring vital signs, listening to lungs, monitoring intake and output, administering insulin, assessing blood glucose levels, monitoring EKG, calorie count, BUN/creatinine (kidney function), and educating the patient on diabetes management.

monitor feet

Why do we give NS first then Dextrose?

Normal Saline (NS) is administered first to correct volume depletion and restore hydration, while Dextrose is given later to prevent hypoglycemia after insulin administration.

Why is hyperkalemia often seen in diabetic patients?

Hyperkalemia occurs in diabetes due to insulin deficiency, which impairs the ability of cells to uptake potassium, leading to elevated potassium levels in the bloodstream.

However, Insulin treatment can help drive potassium back into cells, potentially lowering serum potassium levels (hypokalemia)

How does insulin reverse acidosis?

inhibits fat breakdown, thereby ending ketone production and acid buildup.

Hyperglycemia Hyperosmolar Syndrome

• metabolic disorder most often of type 2 diabetes resulting from a relative insulin deficiency initiated by an illness that raises the demand for insulin

• serious condition in which hyperosmolality and hyperglycemia predominate, with alterations of the sensorium (sense of awareness). At the same time, ketosis is usually minimal or absent.

• Insulin too low to control glucose- but too high to cause fat breakdown (ketosis)

causes of HHS

• 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.

expected findings in HHS

polydipsia

polyuria (Osmotic diuresis causing excess loss of fluids resulting in dehydration and increased thirst)

polyphagia (Cell starvation due to inability to receive glucose resulting in increased appetite)

weight loss (fluid volume depletion)

blurred vision, headache, weakness (due to fluid volume depletion caused by osmotic diuresis)

orthostatic hypotension

mental status changes

seizures

reversible paralysis

nursing interventions for HHS

• Intake and output- very important

• IV fluidsand electrolyte replacement.

• Capillary blood glucose

• Kidney function- BUN/ Creat

• Monitor mentation

• Calorie count

blood glucose levels for DKA

typically greater than 250 mg/dL

blood glucose levels for HHS

typically greater than 600 mg/dL

nursing interventions and care for complications of DM

• Check vital signs every 15 min until stable, then every 4 hr.

• Check for indications of dehydration (weight loss, decreased skin turgor, oliguria, rapid, weak pulse).

• Always treat the underlying cause (infectious process).

• Provide isotonic fluid replacement to maintain perfusion to vital organs. The client can require 6 to 10 L of IV fluid in 24 hrs.

• Start with a rapid infusion of 0.9% sodium chloride for the first 1 to 3 hr. (Clients who have elevated blood sodium levels might require 0.45% sodium chloride.)

• Follow with a hypotonic fluid (0.45% sodium chloride) to continue replacing losses to total body fluid.

• When blood glucose levels decrease to 250 mg/dL, change the IV solution to one containing 5% dextrose to minimize the risk of cerebral edema associated with drastic changes in blood osmolarity and prevent hypoglycemia.

• Administer IV regular insulin

• Monitor blood glucose hourly

• Monitor blood potassium levels (insulin therapy can cause hypokalemia due to it being pulled into cells)

• client education

• monitor changes in mental status

client education - DM

• Wear a medical alert bracelet.

• Take measures to decrease the risk of dehydration.

  • Unless contraindicated by other health problems, consume 2 to 3 L/day of fluid from food and beverages with artificial sweetener, and drink an adequate amount of water.

  • If blood glucose levels are low, consume liquids with sugar.

• Monitor glucose every 4 hr when ill and continue to take insulin.

• Check urine for ketones if blood glucose is greater than 240 mg/dL

• Consume liquids with carbohydrates and electrolytes (sports drinks) when unable to eat solid food.

• Notify the provider for the following.

  • Illness that lasts longer than 24 hr

  • Blood glucose greater than 250 mg/dL

  • Inability to tolerate food or fluids

  • Ketones in urine for more than 24 hr

  • Temperature of 38.6° C (101.5° F) for 24 hr