NURSE-UN 240 NURSE-UN 240 A&E I– FINAL EXAM STUDY GUIDE WEEK 8 –DIABETES MELLITUS
- Glucose – efficient fuel – when metabolized in presence of
... [Show More] O2, breaks down to form carbon dioxide and water – brain & nervous system rely almost exclusively on glucose as fuel
o Brain cannot synthesize nor store more than a few min’s supply of glucose needs continuous supply
from circulation to maintain normal cerebral fxn
o Body tissues obtain glucose from the blood – glucose that is not needed for energy is removed from the blood and stored in the liver as glycogen or converted to fat.
- Pancreas – endocrine fxn for blood glucose regulation, controlled by 2 types of islet cells
o Alpha cells – secrete glucagon
▪ Glucagon prevents hypoglycemia by triggering release of glucose from cell storage sites
o Beta cells – produce insulin
▪ Insulin prevents hyperglycemia by allowing body cells to take up, use and store carbs, fat, protein
o Need specific carrier proteins and insulin to move glucose into cells
▪ Insulin binds to insulin receptors in order to change membrane permeability to glucose
▪ Insulin stimulates glucose uptake in skeletal muscle and heart muscle; suppresses gluconeogenesis (liver production of glucose)
o Insulin levels increase as blood glucose levels increase; insulin decreases when blood glucose levels decline – insulin secreted at low levels during fasting and at increased levels after eating
Diabetes Mellitus (DM)
- DM – a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both.
o In the absence of insulin, cells are prevented from using glucose for energy, so they begin breaking down fat and protein. Glucose builds up in the blood, causing high blood glucose levels (hyperglycemia).
Because glucose, like sodium, has a high pull for water, hyperglycemia causes fluid and electrolyte imbalances, leading to the classic manifestations of diabetes:
▪ Polyuria is frequent and excessive urination and results from an osmotic diuresis caused by excess glucose in the blood and urine. With diuresis, electrolytes are excreted in the urine and water loss is severe. Dehydration results, and polydipsia (excessive thirst) occurs. Because the cells receive no glucose, cell starvation triggers polyphagia (excessive eating).
▪ Dehydration with diabetes leads to hemoconcentration, hypovolemia, poor tissue perfusion, and hypoxia. Hypoxic cells do not metabolize glucose efficiently, the Krebs’ cycle is blocked, and lactic acid increases, causing more acidosis.
▪ Excess acids cause by absence of insulin increase hydrogen ion and carbon dioxide levels in the blood. These products trigger the brain to increase the rate and depth of respiration in an attempt to “blow off” carbon dioxide and acid; this type of breathing is known as Kussmaul respiration.
▪ Insulin facilitates the transport of potassium into cells, so insulin lack initially causes potassium depletion, as it is excreted in the urine. High serum potassium levels may occur in acidosis because of the shift of potassium from the inside of cells into the blood.
- Involves improper metabolism of carbohydrates, fats and proteins
- The chronic hyperglycemia of diabetes is associated with long-term damage, dysfunction, and failure of various organs, especially the eyes, kidneys, nerves, heart, and blood vessels.
DM Facts:
- Increasingly affects all age groups
- Shortens average life expectancy by 15 years
- Especially prevalent in American Indian, African and Hispanic Americans
- 34.2 million people in the US (10.5% population)
- 34.1 million diagnosed, 7.3 million undiagnosed adults
The disease is classified by the underlying problem causing a lack of insulin or its action and the severity of the insulin deficiency:
Type 1 Type 2
A.K.A. Juvenile-Onset DM Adult-Onset DM
Prevalence 10% of diabetes cases 90% of diabetes cases
Age Usually younger than 40, occurs at any age Peaks in 50s, may occur earlier
Etiology Associated with a cell-mediated autoimmune reaction (Type IV hypersensitivity): we develop autoantibodies that
destroy beta cells in the pancreas, which are responsible for the production of insulin. We don’t know what causes this. Not well understood; we become less sensitive to the action of insulin or decrease production of insulin.
Hallmark Lack of insulin and presence of islet cell antibodies (ICA) Decreased insulin production and insulin resistance
Onset Abrupt Insidious, gradual
Symptoms Weight loss (loss of calories and water in urine)
Polyuria (increased urination due to the increased glucose in the blood, creating a hypertonic solution)
Polydipsia (increased thirst due to the body’s need to dilute the hypertonic blood by pulling water out of cells, as well as to replenish what’s lost in excessive urination) Polyphagia (increased hunger due to the fact that cells are
starved for glucose) Frequently none and non-specific: Fatigue b/c brain doesn’t store glc
Recurrent infections (predosed to infection) Prolonged wound healing
Visual changes
Treatment Insulin injections Increase insulin production or increase sensitivity
of cells to insulin
- Type 1 DM:
o Autoantibodies are present for months to years before sx occur
o Manifestations develop when pancreas can no longer produce insulin, then rapid onset w/ ketoacidosis
o Necessitates insulin (exogenous insulin for life)
o Pt may have temporary remission after initial treatment
- Type 2 DM:
o Metabolic syndrome increases risk for type 2 DM (elevated glucose level, abdominal obesity, elevated BP, high levels of triglycerides, decreased levels of HDLs)
o Hyperglycemia may go many years w/o being detected
o Many times discovered with routine labs
- Risk factors
o Abdominal obesity (greatest risk factor)
o A high triglyceride level
o A low HDL cholesterol level
o High blood pressure
o High fasting blood sugar
- Checking insulin levels can distinguish between Type 1 (very low or non-existent) and Type 2 diabetes (likely high).
- 4 test to dx DM (note: 1 abnormal reading not enough to dx DM unless pt presents w/ s/s of hyperglycemia and has random plasma glucose >200 mg/dL)
o Hemoglobin A1C: measures glucose that is permanently attached to hemoglobin, which is an accurate indicator of glucose level for the past 3 months (the life of a RBC), > 6.5% could be diagnostic (pre- diabetes 5.7−6.4%); this test is the gold standard of diagnosing diabetes, and is also used to measure the success of treatment
o Fasting plasma glucose (FPG): NPO from midnight and tested the following day, > 126 mg/dL could be diagnostic
o 2-hr plasma glucose: NPO night before, come into clinic, drink a solution of 75g of glucose and take blood test two hours later to see a trend of the glucose, ≥ 200 mg/dl could be diagnostic during OGTT (oral glucose tolerance test)
• 4 options
• FPG ≥126 mg/dL (7.0 mmol/L)*
Fasting is defined as no caloric intake for ≥8 hours
• A1C ≥6.5% (48 mmol/mol)*
Performed in a lab using NGSP-certified method and standardized to DCCT assay
Diagnostic Tests
- If you have prediabetes:
o Known as impaired glucose tolerance (IGT) or impaired fasting glucose (IFG)
▪ IFG: fasting glucose lvls higher than normal (100 mg/dL < x < 126 mg/dL)
▪ IGT: 2 hour plasma glucose higher than normal (140 mg/dL < x <199 mg/dL)
o If no preventative measures taken, diabetes could develop within 10 years
- Hemoglobin A1C:
o Normal is less than 6.5% (pre-diabetes: 5.7-6.4%)
o Normal A1C reduces risk of retinopathy, nephropathy, and neuropathy
o Useful in determining glycemic levels over time
o Diagnostic and monitors success of treatment *golden standard*
- Urine tests for patients with DM:
o Ketone bodies are a product of fat metabolism, and the presence of moderate to high urine ketones (hyperketonuria) indicates a severe lack of insulin.
o Tests for kidney function are important in detecting kidney disease in diabetes. A urine microalbumin test detects very small levels of a blood protein (albumin) in the urine. Persistent albuminuria is an indicator of early-stage diabetic nephropathy.
o Urine glucose testing is an indirect measurement of blood glucose and is not accurate – this test is not used for monitoring DM management!
Acute Complications
- Hypoglycemia (Blood Glucose less than 70 mg/dl)
o Primary Causes: Receiving too much insulin, decreased food intake, alcohol intake, exercise
o Common Manifestations: NEURO – Confusion/irritability, Diaphoresis, Tremors, Hunger, Weakness and visual disturbances
▪ Can mimic alcohol intoxication
▪ Untreated can progress to loss of consciousness, seizures, coma, and death
o Treatment of Mild Hypoglycemia
▪ If alert enough to swallow, give 15 to 20 grams of simple carbohydrate, ½ cup fruit juice or, ½ cup regular soft drink; then repeat until blood sugar is > 70 mg/dL
▪ Patient should eat regularly scheduled meal/snack to prevent rebound hypoglycemia
o Treatment Severe Hypoglycemia (Blood Sugar less than 20 mg/dL)
▪ Administer 1 mg of glucagon IM or subcutaneously.
• Side effect: Rebound hypoglycemia
▪ In acute care settings
• 20 to 50 ml of 50% Dextrose intravenous (IV) push
▪ Have patient ingest a complex carbohydrate after recovery
- Hyperglycemia (Blood Glucose more than 200 mg/dL)
o Type 1: Diabetic Ketoacidosis (DKA): no insulin production in the body
▪ Blood Glucose Level >250 mg/dL
▪ CLINICAL MANIFESTATIONS: Positive ketones in the blood and urine (d/t fat breakdown), Kussmaul’s Respiration, “Fruity” breath (from presence of ketones), Nausea and abdominal pain (d/t vomiting, delayed gastric emptying and hyperosmolarity),
Clinical manifestations of Dehydration/hypovolemia d/t electrolyte depletion
• Tx: fluid replacement therapy, slow insulin administration, also watch for hypokalemia (insulin facilitates transfer of K+ into cells)
o Type 2: Hyperglycemic Hyperosmolar State (HHS): minimal amount of insulin to prevent fatty acid breakdown
▪ Blood Glucose Level > 600 mg/dL
▪ CLINICAL MANIFESTATIONS: No ketones in the blood and urine, hemoconcentrated = aggregated, thick blood = blood clots, Neurologic symptoms,
Clinical manifestations of Dehydration!
• Tx: fluid replacement therapy
Chronic Complications: decreased in ATP, decreased insulin, decreased AA affects peripheral tissues (lacking O2 and nutrients tissue death
- The chronic hyperglycemia of diabetes is associated with long-term damage, dysfunction, and failure of various organs, especially the eyes, kidneys, nerves, heart, and blood vessels. Chronic hyperglycemia thickens basement membranes, which causes organ damage, and changes in large blood vessels and small blood vessels in tissues and organs result in poor tissue perfusion and cell death.
o Macrovascular complications include coronary heart disease, cerebrovascular disease (stroke), and peripheral vascular disease.
o Microvascular complication of blood vessel structure and function lead to nephropathy (kidney dysfunction), neuropathy (nerve dysfunction), and retinopathy (vision problems).
- Glaucoma
- Cataract
- Diabetic Retinopathy
o Microvascular changes in retina
o Exam: funduscopic (dilated eye exam), fundus photography – annually
- Nephropathy
o Exam: urine for albuminuria, serum creatinine – annually
- Neuropathy
o Exam: visual examination of foot (daily), comprehensive foot exam (annually), sensory examination w/ monofilament and tuning fork (annually), palpation for pulses, temperature, callus formation (annually), avoid OTC cream, dry toes, and toe nail clipping should be done at podiatrist
o Foot injury/ulcers (due to loss of sensation in the feet) is the most common complication of diabetes leading to hospitalization. Once a failure of tissue integrity has occurred and an ulcer has developed, there is an increased risk for wound progression that will eventually lead to amputation. Therefore, patients with DM need intensive teaching about proper foot care behaviors:
▪ Inspect the feet daily
▪ Wash feet daily with lukewarm water and soap – do not soak the feet!
▪ Wear properly fitting shoes made with breathable material
▪ Wear socks to keep the feet warm
▪ Avoid walking in bare feet
▪ Trim toenails properly – straight across with the nail clipper
▪ Report non-healing breaks in the skin of the feet to the health care provider immediately – do not treat blisters, sores, or infection with home remedies
- CV Disease
o Risk factor assessment: HTN, high cholesterol, smoking, FHx of CAD and presences of albuminuria
o Exam: stress EKG test, stress echo, nuclear stress (as needed)
- Nervous System Disease
- Amputations (due to reduced feeling in the feet)
- Delayed Wound Healing
- Dental Disease
- Complications of Pregnancy
- Urinal distention
- Sexual Dysfunction
DIABETES – THE NURSING PROCESS
Assessment – subjective data (PMHx, medications, recent surgeries), ROS, objective data
Subjective PMHx, meds, SHx Subjective ROS Objective data Objective lab values
PMHx: viral infections, infection, trauma, stress, pregnancy, chronic pancreatitis, Cushing syndrome, acromegaly, FHx of DM
Meds: insulin, OA, corticosteroids, diuretics (hyperglycemia when, phenytoin (predisposes for increase glc)
Recent surgeries - Malaise
- Obesity, wt gain or loss
- Thirst, hunger, n/v
- Poor healing
- Dietary compliance
- Constipation, diarrhea
- Frequent urination, bladder infections
- Nocturia, urinary incontinence
- Muscle weakness, fatigue
- Abdomen pain, HA, blurred vision
- Numbness/tingling, pruritus
- Impotence, frequent vaginal infection
- Decreased libido
- Depression, irritability, apathy
- Commitment to lifestyle changes - Sunken eyeballs, vitreal hemorrhages, cataracts
- Dry, warm, inelastic skin (poor skin turgor)
- Pigmented skin lesions, ulcers, loss of hair on toes, acanthosis nigricans (velvety discoloration of darker tone, in the flexors of arm and neck, more in DM 2)
- Kussmaul respiration, fruity breath (DKA)
- Hypotension (d/t fluid loss)
- Weak, rapid pulse
- Dry mouth
- Vomiting
- Altered reflexes, restlessness
- Confusion, stupor, coma
- Muscle wasting (atrophy) - Serum electrolyte imbalance
- FGB > 126+
- OGTT > 200+
- Leukocytosis
- Increased BUN/creatinine
- Increased TGC and LDL, VLDL chol
- Decreased HDL
- A1C > 6.0%
- Glycosuria, ketonuria, albuminuria
- Metabolic and DK acidosis
Possible Diagnoses
- Ineffective tissue perfusion r/t interrupted blood flow secondary to development and progression of macroangiopathy and microangiopathy
- Risk for infection r/t dz process
- Risk for impaired skin integrity
- Knowledge deficit
- Ineffective therapeutic regimen management
- Imbalanced nutrition
- Risk for peripheral neurovascular dysfunction
- Risk for unstable blood glucose levels
Planning
- Overall goals and collaborative care: active pt participation, few or no episodes of acute hyperglycemic emergencies or hypoglycemic, maintain normal blood glc lvls, prevent or minimize chronic complication, adjust lifestyle to accommodate diabetes regimen, promote well-being
Nursing implementation
- Health promotion: identify, monitor and teach pt at risk, obesity: primary risk factor, routine screening for all overweight adults and those older than 45
- Acute intervention for:
o Hypoglycemia – rule of 15 (blood sugar <70 mg/dL)
▪ If alert enough to swallow give 15-20 g of simple carbohydrate, ½ cup OJ, 5-8 lifesavers, ½ cup soda
▪ Recheck blood sugar 15 mins after treatment
▪ Repeat until blood sugar above 70 mg/dL
▪ Pt should eat regularly scheduled meal/snack to prevent rebound hypoglycemia
▪ Check blood sugar again 45-60 mins after treatment
▪ SEVERE HYPOGLYCEMIA -- <20 mg/dL OR if no improvement after 2-3 doses of carbs OR pt not alert enough to swallow administer 1 mg of glucagon IM or subQ (s/e: rebound hypoglycemia)
• Acute care settings – 20-50 mL of 50% Dextrose IV push
• Have pt ingest complex carb after recovery
o DKA / HHS
- Acute illness, injury, surgery
o Blood glucose level may be elevated secondary to counter-regulatory hormones
o Frequent blood glc monitoring (ketone testing if glc > 240 mg/dL, report glc lvl > 300mg/dL for two tests or moderate to high ketone levels)
o Increase insulin for DM type 1
o DM type 2 may need insulin
- Acute illness – sick day
o Continue taking meds and insulin as usual, check and keep track of your blood glc
o Check temp every morning and evening (fever may indicate infection), weigh yourself every day (wt loss is a sign of high blood glc)
o Drink extra liquids and try to eat as you normally would
o If regular diet is not possible, supplement with carbohydrate containing fluid while continuing meds
- Intraoperative period
o IV fluids and insulin
o Frequent monitoring of blood glucose
- Ambulatory and homecare
o Overall goal to enable pt or caregiver to reach an optimal level of independence
o Use services of certified diabetes educator (CDE) or registered dietician
o Establish individualized goals for teaching
o Include family and caregivers
o Mental health check
o Assess pt’s ability to perform SMBG and insulin injection
o Assess pt/caregiver knowledge and ability to manage diet, medication, and exercise therapy
o Teach s/s and how to treat hypoglycemia and hyperglycemia
o Frequent oral care
o Foot care: inspect daily, avoid going barefoot, proper footwear, and how to treat cuts
o Travel needs: meds, supplies, food, and activity
Goals of DM management
- Reduce symptoms
- Promote well-being
- Prevent acute complications
- Delay onset and progression of long-term complications
Continuing Care Visits
- Minimum standards of American Diabetic Association
- Lab Evaluation
o HbA1c (quarterly for those not meeting goals, semiannually for stable pts)
o Lipids annually
- Annually need:
o Ophthalmology Exam
o Foot Exam (more often in those at high risk)
Pharmacologic Treatment
- Type I - Insulin
- Type II - Oral Agents (Many different classes and may progress to insulin at some point)
- Different types of insulin from immediate release to long release and individualized
Two conditions of fasting (overnight) hyperglycemia can occur. They are distinguished by whether or not they’re triggered by hypoglycemia, so to diagnose the patient would have to test their blood sugar around 2-4am:
- Dawn phenomenon results from a nighttime release of growth hormone that causes release of liver glucose resulting in blood glucose elevations at about 5-6am. It’s managed by providing more insulin for the overnight period and limiting evening snacks.
- Somogyi phenomenon is morning hyperglycemia from the counter-regulatory response to nighttime hypoglycemia resulting in release of liver glucose. It’s managed by ensuring adequate dietary intake at bedtime.
We have special concerns for older adults with diabetes, including increased risk for falls, a slower metabolism, and decreased ability to self-manage (they’re more likely to live alone).
Nonsurgical management of DM involves nutrition interventions, blood glucose monitoring, and a planned exercise program. Patients with type 1 DM require insulin therapy for blood glucose control. Drug therapy is indicated when a patient with type 2 DM does not achieve blood glucose control with diet changes, regular exercise, and stress management. Several categories of drugs are available to lower blood glucose levels. Drugs are started at the lowest effected dose and increased every 1-2 weeks until the patient reaches desired blood glucose control or the maximum dosage.
- Shorter-acting agents are preferable in older patients, those with irregular eating schedules, or those with liver, kidney, or cardiac dysfunction.
- Longer-acting agents with one-a-day dosing are better for adherence.
Continuous subcutaneous infusion of a basal dose of insulin (CSII) with increases in insulin at mealtimes is more effective in controlling blood glucose levels than other schedules. It allows flexibility in meal timing, because if a meal is skipped, the additional mealtime does of insulin is not given. CSII is given by an externally worn pump containing a syringe and reservoir with rapid-acting insulin and is connected to the patient by an infusion set. However, injection devices including a needleless system and a pen-type injector in addition to traditional insulin syringes are still commonly used.
Minimum standards for continuing care visits have been set by the American Diabetes Association and include a lab evaluation (HbA1c) quarterly for those not meeting goals or semiannually for stable patients, as well as ophthalmology exam and foot evaluation annually. [Show Less]