Module 6 Diabetes & Glucose Regulation

NUR1460C; Diabetes

Pancreatic exocrine function

Produces digestive enzymes:

• Amylase

• Lipase

• Protease

Pancreatic exocrine cells

Acini cells 

-Secrete pancreatic juice 

Pancreatic endocrine function

Islet of Langerhans:

-Alpha cells

-Beta cells

-Delta cells

Alpha cells

Release Glucagon

• Raises blood glucose

• Prevents hypoglycemia

Beta cells

Release Insulin

• Lowers blood glucose

• Moves glucose into cells

Delta cells

release somatostatin

Insulin function

• Decreases blood glucose

• Stimulates glucose uptake

• Promotes glycogen storage

• Inhibits ketone formation

-prevents hyperglycemia

Insulin production in the body

The body produces insulin in the beta cells of the pancreas.

This production is triggered by rising glucose levels in the bloodstream after eating

Glycogenesis

the metabolic process by which the body converts excess glucose molecules into glycogen for storage

-activated by insulin

Glycogenolysis

the biochemical process of breaking down stored glycogen into glucose

-immediate energy source

Gluconeogenesis

the metabolic process where the liver and kidneys synthesize new glucose from non-carbohydrate sources

Type 1 Diabetes

autoimmune destruction of beta cells

• Absolute insulin deficiency

• Requires lifelong insulin

• More common in younger patients

Glucagon

a peptide hormone produced by the pancreas (alpha cells) that raises blood glucose levels

• Raises blood glucose

• Stimulates glycogen breakdown

Type 2 Diabetes

a progressive disorder in which the person initially has insulin resistance that progresses to pancreatic beta-cell dysfunction

-insulin resistance- the body's cells do not respond properly to insulin causing pancreas to make more insulin (hyperinsulinemia)

-beta-cell failure- the pancreas cannot produce enough insulin to overcome this resistance

Latent Autoimmune Diabetes of Adult Onset (LADA)

often called "Type 1.5 diabetes"—is a form of autoimmune diabetes that begins in adulthood

-immune system attacks insulin-producing cells, but the damage happens much more slowly, so insulin isn't required right away

• Initially may not require insulin

-”LATEnt” to remember

Normal fasting glucose

70–100 mg/dL

Prediabetic glucose levels

100–125 mg/dL

Diabetic glucose levels

Diabetes

≥126 mg/dL (two occasions)

Random Glucose

≥200 mg/dL + symptoms

Hemoglobin A1C

Normal: 4–6%

Diabetes: ≥6.5%

*Remember: A1C reflects approximately 3 months of glucose control

Metabolic syndrome

the simultaneous presence of metabolic factors known to increase risk for developing Type 2 DM

• Obesity

• Coronary heart disease

• Dyslipidemia (high LDL & low HDL)

• Hypertension

• Microalbuminuria (protein in the urine)

• Increased risk for thrombotic (blood clotting) events

Primary diabetes prevention

balanced diet

exercise

weight control

Secondary diabetes prevention

Lab tests:

-hemoglobin A1C

-cholesterol

-microalbuminuria

Screening to detect complication: BP, dental care, foot care, eye exams

Hyperglycemia (“High & Dry”)

High blood glucose (125-180+ mg/dL)

-result of insufficient insulin production or secretion, excessive counter-regulatory hormones secretion and deficient hormone signaling

-body burning fat instead of using glucose for energy

-leads to metabolic acidosis or DKA

-hemoconcentration, hypovolemia, hyperviscosity, hypoperfusion, hypoxia

Hyperglycemia S/S

polyuria

polydipsia

polyphagia

• Weight loss

• Fatigue

• Blurred vision

• Recurrent infections

• Numbness

Hyperglycemia pathophysiology

-insulin absent > fat breakdown > ketones > metabolic acidosis

signs: Kussmaul respirations, fruity breath, dehydration

Hyperglycemia complications

• Hot dry flushed skin, the 3 P’s, fruity breath – Kussmaul’s Respiration

  • Restless, drowsy- unconsciousness

  • Treatment: check BG

  • IV fluids, Insulin infusion

  • Continue to monitor BG

  • Basic Metabolic Panel (BMP) for Electrolytes: K+ (may be below 3.5) Supplementation of K+ may be needed

Hyperglycemia treatment/interventions

-Insulin therapy

-Isotonic fluids

-Blood glucose tracking

-Assess for complications - altered mental status, fruity breath, Kussmaul respirations, and severe dehydration

Hypoglycemia

low blood glucose levels (70 mg/dL)

-typically occurs as a result of insufficient nutritional intake

-adverse reaction to medications

-excessive exercise, and/or a consequence of disease states

Levels of hypoglycemia

-Level 1 hypoglycemia is a glucose less than 70 mg/dL but greater than or equal to 54 mg/dL

-Level 2 hypoglycemia is less than 54 mg/dL.

-Level 3 hypoglycemia is any event requiring external assistance because of mental or physical alterations.

Hypoglycemia S/S

“Low is Slow”

• Irritability

• Confusion

• Tremors

• Fatigue

• Seizures

• LOC changes

• Gastroparesis -delay in gastric emptying

Hypoglycemia treatment/interventions

15g carbohydrates (juice, crackers, glucose tablets)

reassess in 15 minutes

• severe patients (< 30 mg/dL):

-glucagon IM/SQ- repeating the dose in 10 minutes if the patient remains unconscious; notify the PCP immediately

-25 to 50 mL of D50W via IV push at a rate of 10 mL/min

Hypoglycemia complications

• Confusion, irritability, tremor, sweating

  • Hypothermia, seizures

  • Coma and death will occur if not treated

• Treatment – check BG

• IF ALERT AND ABLE TO SWALLOW

  • Oral forms of concentrated glucose

  • Orange juice – may repeat if BG still low

• If NOT ALERT

  • 5% dextrose in water (D50W)

  • Glucagon IV or IM

Blood-free glucose monitoring

FreeStyle Libre (continuous glucose monitoring system)

-detects highs & lows

-have to reapply a new sensor to your arm every 14 days

Continuous Subcutaneous Infusion of Insulin (CSII)

Continuous Subcutaneous Infusion of Insulin (CSII)

-An insulin pump administers insulin on a continual basis. Rapid Acting Insulin Used

Patient Education:

-Hand washing Use aseptic technique when cleaning site

-The cannula should be changed every 1-2 days.

-Ketoacidosis may occur because of infection, obstruction, or mechanical pump problems.

-If BG levels ↑than 300 mg/dL – Need for Ketone testing

Rapid-acting Insulin

-Blocks hepatic production of glucose

-Tx: Type I & Type 2 Diabetes

Aspart (Novolog)- peak 1 hour

Lispro (Humalog)- peal 40-50 minutes

-onset: 15 minutes

-durations: 3-5 hours

Short-acting Insulin

Regular insulin (Humulin R, Novolin R)

Tx: Type I & Type II Diabetes, Acute Hyperglycemia, DKA, Severe Hyperkalemia, Insulin in D5W

-The only type of insulin that should be given intravenously is regular human insulin (can be SQ too)

-onset: 0.5-1 hour

-peak: 2-3 hours

-duration: 4-6 hours

Intermediate-acting Insulin

Isophane insulin (NPH)

Tx: Type I & Type II Diabetes

-onset: 2-4 hours

-peak: 6-8 hours

-duration: 12-16 hours

Long-acting Insulin

Glargine (Lantus) & Detemir (Levemir)

-Tx: Type I & Type II Diabetes

-onset: 2 hours

-peak: no peak

-duration: 24 hours

-should be drawn up in a separate syringe*

Single dosing

Intermediate or long acting Insulin

-Some Type II DM patients once-daily for basal coverage

-Oral antidiabetic to stimulate Insulin secretion

Multiple Insulins

a combination of short/intermediate based on blood glucose levels pre and postprandial (before and after meals)

Intensified (insulin) Regimes

Rapid/short/intermediate/long acting – the aim is to attain the target range

-Blood glucose levels will determine Insulin dosage-Sliding-Scale

Insulin injection sites

Subcutaneous injection

-45° ANGLE FOR OLDER FRAIL PATIENTS

-90° ANGLE FOR YOUNGER AND THOSE THAT ARE OVERWEIGHT

-Rotation of injection sites to prevent a decrease in absorption and lipodystrophy of the SQ Tissue

Importance of Insulin Peak times

-Peak time is the period when a medication has its strongest effect

-It’s essential to know the peak time of the insulin so that one can predict how much and when a person should eat to keep the blood sugar constant.

-Snacks should be ingested around peak times to avoid hypoglycemia

Insulin Sliding Scale

a reactive dosing method where short-acting or rapid-acting insulin is administered in increasing amounts based on pre-meal or bedtime blood sugar levels

-Basically, add ordered insulin and units to administer based on pts blood glucose levels (scheduled insulin + correction insulin)

Metformin (Glucophage)

-Biguanides Oral - Antidiabetic

-Tx: Type II Diabetes

-Blocks glucose production from the liver and prevents glucose reabsorption in the intestines, & increases insulin sensitivity

-It DOES NOT cause HYPOglycemia

-GI upset, and bloating can occur, take with food to lessen symptoms

-Avoid alcohol (EtOH), may induce Latic Acidosis (do not take with kidney disease*)

Contrast & Metformin

-Hold metformin for 48 hours before procedures that require iodine-containing contrast agents because these agents cause renal failure in patients treated with metformin.

-Resume medication no earlier than 48 hours following the procedures, after renal function is confirmed to have returned to baseline.

Micronase (Glyburide)

Sulfonylurea

-Tx: Type II Diabetes

-Stimulates the pancreas to produce more insulin

-Longer duration (up to 24 hours), not recommended for adults 65+

-Take before a meal can decrease the potential for hypoglycemia

-Severe effects for those with liver/renal disease

-Interacts with many medications

Glipizide (Glucotrol)

Sulfonylurea

-Tx: Type II Diabetes

-stimulates insulin release

-shorter duration (12-24 hours), lower risk, generally safe for 65+ adults

-risk: hypoglycemia

Injectables:

-Exenatide (Bydureon/ Byetta)

-Dulaglutide (Trulicity)

-Liraglutide (Victoza)

-Semaglutide (Ozempic)

Incretin Mimetics (GLP-1 Agonists) Antidiabetic Injectables

-Tx: Type II Diabetes

-stimulate glucose-dependent insulin secretion, inhibit glucagon release, slow gastric emptying, and promote satiety

-Once a week subq. injectables

-Not a replacement for insulin

-Risk: hypoglycemia, weight loss, delay gastric emptying

Antidiabetic Drugs Patient Education

-Antidiabetic drugs are not a substitute for dietary modification and exercise.

-Nutritional considerations

-Exercise

-All patients with DM should monitor blood glucose levels regularly

Diabetic Ketoacidosis (DKA)

-The combination of insulin deficiency and an increase in hormone release that leads to increased liver and kidney glucose production and decreased glucose use in peripheral tissues.

-uncontrolled hyperglycemia, metabolic acidosis, and increased production of ketones

-DKA occurs in Type I DM, but it can occur in Type II DM under severe stress.

-The most common precipitating factor for DKA is INFECTION

S/S of Diabetic Ketoacidosis (DKA)

Polyuria, Polydipsia, Polyphagia

-Fruity breath

-Kussmaul respirations

-Weakness

-Confusion

-Abdominal pain

-Hypokalemia (after treatment starts)

DKA treatment

-IV fluids FIRST

-Regular insulin IV in D5W

-Frequent monitoring of BG

-Monitor anion gap (normal 7-9 mEq/L), if high indicates metabolic acidosis

-Common cause of death is Hypokalemia**

-Monitor ECG

Hyperglycemia-Hyperosmolar State (HHS)

a life-threatening complication of diabetes (mostly type 2; older adults) characterized by extremely high blood sugar, severe dehydration, and concentrated blood (high osmolality)

-ketone levels are absent or low compared to DKA

-BG level may exceed 600mg/dL

-blood osmolarity may exceed 320 mOsm/kg

-”High high sugar” (HHS) to remember

HHS in Older Adults

-Most common cause is DEHYDRATION

-Kidney impairment in HHS allows for extremely high blood glucose levels.

-Many are unaware they have the disease.

-Mortality rates in older patients are high.

-The onset of HHS is slow and may not be recognized.

HHS Treatment

• IV fluids

• Insulin

• Electrolyte correction (K+)

-Important to continually monitor the patient being managed for HHS state to recognize status changes

-Assess the patient hourly for signs of cerebral edema with abrupt changes in mental status, abnormal neurologic signs, and coma

-Notice changes in LOC, as well as pupil size, shape, or reaction, and seizures. If any of these signs are present notify the care provider immediately

DKA & HHS Comparison

DKA occurs in < 40 yr. old Type 1 Diabetic

HHS occurs in older adults Type 2 Diabetic

DKA is caused by infection & stress

HHS is caused by dehydration

HHS blood glucose are higher compared to DKA (600mg/dL)

DKA has high ketones while HHS has high serum osmolality

Dawn Phenomenon

Early AM hyperglycemia

-caused by natural early-morning hormone release, not hypoglycemia like Somogyi

Tx: Increase evening insulin

Somogyi Effect

a controversial diabetes concept suggesting that an episode of low blood sugar overnight triggers the body to overcompensate, causing high blood sugar in the morning

-”rebound hyperglycemia”- rebound from nighttime hypoglycemia

-Tx: bedtime snack, adjust insulin, exercise program

Macrovascular Diabetic Complications (macroangiopathy)

• CAD

• Stroke

• PVD

• Blood vessel walls thicken, sclerosis, and become occluded by plaque that adheres to the vessel walls

• Leads to coronary artery disease, cerebrovascular disease, and peripheral vascular disease

• Focus of management is aggressive modification and reduction of risk factors

-Think Brain, Heart, Extremities

Microvascular Diabetic Complications

• Retinopathy - vision loss

• Nephropathy - kidney disease

• Neuropathy - Peripheral neuropathy (Gabapentin med)

Think Eyes, Kidneys, Nerves

Cardiovascular Autonomic Neuropathy

affects sympathetic and parasympathetic nerves of the heart and blood vessels.

-This leads to orthostatic (postural) hypotension, resting tachycardia, exercise intolerance, silent ischemia

Autonomic Neuropathy

can also affect the GI system (gastroesophageal reflux, delayed gastric emptying and gastric retention, early satiety, heartburn) nausea, vomiting, constipation and diarrhea, and anorexia

Peripheral Neuropathy

chronically high blood glucose levels- numbness, loss of sensation, pain in feet and legs or hands

-Medication - *Gabapentin (Neurontin)*

Gabapentin (Neurontin)

anticonvulsant and nerve pain medication for diabetic peripheral neuropathy

Tx: Seizures, Neuropathic Pain, Migraines, Post-herpetic neuralgia- following Shingles, Fibromyalgia

-not recommended for pts with COPD or other respiratory issues

Foot Care for Diabetics

• Shoes on at all times.

• Properly fitted shoes.

• Shop late in the day

• Inspect feet daily.

• Keep feet and skin moist to prevent cracks.

• Apply lotion to feet except between toes.

• Seamless hose and stockings

• Toenails clipped by a podiatrist (recommended).

-Neuropathy main cause of diabetic ulcer

Charcot foot

a type of diabetic foot deformity with any abnormalities, often including a hallux valgus (turning inward of the great toe).

Walking collapses the arch, shortens the foot, and gives the foot a “rocker bottom” shape.

Claw toe

-Thinning or shifting of the fat pad under the metatarsal heads decreases cushioning and increases areas of pressure.

-In claw toe deformity, toes are hyperextended and increase pressure on the metatarsal heads (ball of the foot).

-These changes predispose the patient to callus formation, ulceration, and infection

Diabetes Surgery

Risks:

• Hyperglycemia

• Infection

• Delayed healing

Monitor:

• BG

• Skin

• Hydration

• Stress response

Diabetic Teaching

-Patient must be willing to focus on reducing modifiable risk factors such as smoking cessation, diet, exercise, blood pressure control, maintaining prescribed aspirin use – maintain prescribed lipid-lowering drug therapy.

-The patient must be able to plan for periodic evaluation of blood glucose control by the PCP, as well as periodic dental and eye examinations.

-The patient must be able to integrate the demands of diabetes into daily and recreational schedules while keeping blood glucose stable.

-Encourage all patients to participate regularly in exercise or physical activity appropriate to their health status for better blood glucose regulation

Diabetes Insipidus

Caused by a deficiency of—or resistance to—antidiuretic hormone (ADH), also called vasopressin

-severe polyuria (very diluted urine)

-polydipsia

-dehydration

-increased electrolyte levels (hypernatremia)

-normal blood sugar

-Tx: Vasopressin

Vasopressin (synthetic ADH)

Tx for Diabetes Insipidus

-Close monitor of vital signs, ECG, I&O

Interventions for Diabetes Insipidus

• Drug therapy with Desmopressin

• Urine output can be lowered with a low-salt, low-to-normal protein diet and diuretics.

• Restricting sodium intake to less than 2.3 g/day and reducing protein intake to less 1.0mg/kg daily diminishes urine output.

• Thiazide diuretic induces mild volume depletion; even a weight loss of 1 to 1.5 kg can reduce urine output significantly.

• Measure fluid intake and output

• Check urine specific gravity

• Record the patient’s daily weight.

• Urge the patient to drink fluid in an amount equal to urine output

• Ensure the patency of the access catheter and accurately monitor the amount infused intravenously hourly

DI vs. SIADH

SIADH is the excessive retention of water, while DI is the excessive loss of water

SIADH think LOW- oliguria, hyponatremia, low blood osmolality (diluted)

DI think HIGH- polyuria, hypernatremia, high blood osmolality (concentrated)

Desmopressin (DDAVP)

synthetic hormone that mimics vasopressin; signals kidneys to reabsorb water, thus reducing urine production (water regulation)

-Tx for Diabetes Insipidus

-monitor sodium levels (hyponatremia), I&O, & neuro changes

-daily weights

-restrict fluid intake to prevent water intoxication