NC AHEC test presentation

Caring for the Patient with Diabetes

Courtesy of Pixabay.com

Learning Activity Goals - At the conclusion of this educational activity the learner will be able to:

1. Contrast between different types of diabetes diagnosis and the associated pathophysiology.

2. Differentiate between the classifications of medications used to treat diabetes.

3. Identify symptoms associated with the complications of diabetes

Pre-Quiz Time

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Part I Pathophysiology of Diabetes

Pathophysiology of Type I Diabetes

• Destruction of the islet cells in the pancreas (most often believe to occur from a faulty immune system response) causing insufficient insulin and excess glucagon
• Serum glucose increases causing hyperglycemia
• Elevated blood glucose filters into the kidneys causing osmotic diuresis and glycosuria (sugar in urine)
• Polydipsia and polyuria result due to osmotic diuresis and excessive loss of water
• Ketosis (breakdown of fat stores) combined with weight loss occurs due to the body’s inability to use carbohydrate for fuel then resulting in the breakdown of fat and protein
• Fatigue and polyphagia as a result of limited absorption of nutrients
• In the setting of inadequate insulin supply the patient will begin to develop hyperglycemia, ketosis, abnormal lipid and protein metabolism, and hyperglucagonemia. The person with T1DM must receive exogenous insulin for life in order to survive. T1DM most often presents itself from infancy up through the third decade of life.

https://youtu.be/3B73j1tKkpI

Type 1 Diabetes

Stomach breaks down food Courtesy of Pixabay.com

Glucose travels to bloodstream Courtesy of Pixabay.com

• Absolute insulin deficiency

• Results in hyperglycemia

• Lifelong insulin requirement

Requires exogenous insulin for life Courtesy of Pixabay.com

Pancreas secretes NO insulin Courtesy of Dreamstime.com

Pathophysiology of Type 2 Diabetes

• Insulin-related abnormalities: insulin resistance and beta-cell dysfunction
• Insulin resistance is induced by the breakdown of many cellular pathways, which results in a reduced response or sensitivity of cells in peripheral tissues, notably muscle, liver, and adipose tissue, to insulin.
• In the early stages of the condition, decreased insulin sensitivity leads to hyperfunction of beta-cells requiring a compensatory increase in insulin secretion to maintain normal blood glucose response. Higher levels of circulating insulin attempt to aid in the prevention of a hyperglycemic state.
• Beta-cell activity decreases, leading to insulin insufficiency.

https://youtu.be/RlLrvnnTDDU?si=2mWBFwcWFHUW84Rk

Type 2 Diabetes

• Progressive loss of insulin secretion from beta-cells
• Insulin resistant
• Hyperglycemia
• Treatments may include insulin, oral/injectable medication, diet/exercise

Glucose travels to bloodstream Courtesy of Pixabay.com

Stomach breaks down food Courtesy of Pixabay.com

Depending on glucose control the patient may be taking insulin, pills, diet/ exercise or a combination Courtesy of Pixabay.com

Insulin secretion has decreased Courtesy of Dreamstime.com

Pathophysiology of Gestational Diabetes

• Glucose intolerance presentation during pregnancy causing elevated blood glucose
• No history of diabetes prior to pregnancy
• Hormones during pregnancy (cortisol, human placental lactogen and estrogen) cause cells to become more resistance to using insulin effectively. This resistance is usually seen by the 20-24 week of gestation and continues on through until around the 36 week of gestation prior to decreasing.
• Abnormal shift in circulating adipokines during pregnancy. Adipokines are molecules made within adipose (fat) tissue that work to maintain systemic homeostasis of energy.
• Decreased risk of congenital anomalies in fetus as compared with pregnancy in patient with preexisting T1DM or T2DM.
• Blood glucose levels return to normal once delivery has taken place.

Atypical Diabetes Diagnoses

• Rare forms affecting children and adolescents
• Require different approaches to treatment
• Monogenic diabetes - caused by mutation in single gene
• Neonatal diabetes mellitus (NDM)
• Maturity-onset diabetes of the young (MODY)
• Monogenic diabetes can by often misdiagnosed as Type 1 diabetes and treated incorrectily
• Mitochondrial disease
• Lipodystrophy

Pathophysiology of Mature Onset Diabetes in the Young (MODY)

• Single gene mutation (monogenic) causing defective beta cell secretion of the hormone insulin causing glucose intolerance
• Non-ketotic and no pancreatic autoantibodies present
• 14 known MODY gene mutations; 6 subtypes
• The different genes vary with respect to the age of onset, response to treatment, and the presence of extra-pancreatic manifestations
• Autosomal dominant inheritance (remember….autosomal dominant means a trait passed from one parent onto their child. In the case of autosomal recessive it would mean both parents passed on the trait to their child)
• Commonly mistaken for T1DM or T2DM; usually presents by 25 year of age; accounts for <5% of all diabetic cases
• Most often treated with oral antihyperglycemics, diet and exercise and then insulin

Pathophysiology of Latent Autoimmune Diabetes Adults (LADA)

• Slow autoimmune damage causing decreased amounts of insulin secretion from the beta cell of the pancreas
• A faulty autoimmune response similar to the damage causing T1DM but at an older age. Individuals with LADA suffer slower complete insulin-secreting beta cell destruction due to lymphocytic infiltration

• Presence of autoantibodies (Glutamic acid decarboxylase-GAD) indicating the likelihood of an attack on the immune system

• Pathogenesis thought to be related to intestinal microbiota influencing immunity and progression of disease

• Commonly referred to as Diabetes 1.5

Part II Pharmacological Therapy

Medication for Diabetes Type I

Basal Insulin

• Basal insulin works by mimicking the action of the pancreas
• Slow and steady action over 24 hours
• Maintains homeostasis of blood glucose levels within the bloodstream
• Prescribed once to twice daily

Action Generic Name Brand Name Onset/hrs Peak/hr Duration/hrs Intermediate NPH 2-4 4-10 10-16 Long Acting detemir Levemir 3-8 None 6-24 glargine Lantus 2-4 None 20-24 Basaglar Semglee degludec Tresiba ~1 None <42

Note: Patients with Type 2, Mody and LADA may require insulin if oral medications fail to control glucose

Medication for Diabetes Type I - continued

Bolus Insulin

• Bolus insulin works to maintain homeostasis of blood glucose following meal intake
• Bolus insulin starts to work in 10-15 minutes and lasts approximately 3 hours in the body
• Can be used as a fixed dose to manage carbohydrate at meal time or as a correction dose to bring

down an already elevated blood glucose

• Administered via insulin syringe, insulin pen or insulin pump

Action Generic Name Brand Name Onset/min Peak/min Duration/hrs Very Rapid Acting aspart Fiasp 2-5 ~60 3-5 lispro-aabc Lyumjev 1 ~60 4-5 Rapid Acting aspart Novolog 5-15 30-60 <5 lispro Humalog Admelog glulisine Apidra Short Acting Regular 30-60 120-180 5-8

Medication for Diabetes Type I - continued

Basal/Bolus Insulin (referred to as “mixed” insulin)

• Basal/Bolus insulin contains a pre-mixed combination of rapid acting or short acting

insulin with intermediate acting insulin

• Prescribed twice daily but some patients may take it differently
• Maintains homeostasis of blood glucose levels within the bloodstream
• AM injection covers both breakfast and lunch meal intake
• PM injection (generally administered 12 hours later from AM dose) covers dinner intake

and glucose surges typically seen in early morning hours before waking

Action Combo of NPH + Regular Onset/min Peak/hrs Duration/hrs Intermediate+Short 70/30 = 70% NPH + 30% Regular 30-60 Dual 10-16 50/50 = 50% NPH + 50% Regular Intermediate+Rapid Novolog Mix 70/30 5-15 Dual 24 Humalog Mix 75/25 or 50/50

Medication for Diabetes Type I - continued

Concentrated & Inhaled Insulin

• Used often in patients requiring higher unit dosing
• Increased risks of side effects if taken inappropriately
• Concentrated insulins deliver doses in less volume of fluid
• Use of U-500 insulin syringe is needed with U-500 insulin to avoid incorrect dosing
• Insulin U-200/U-300 strength are available in pen option only (vial not an option)
• Maintains homeostasis of blood glucose levels within the bloodstream
• Regimen will vary based on type of insulin prescribed

Action Generic Name Brand Name Onset/hrs Peak/hr Duration/hrs Basal/Bolus Regular U-500 Humulin U-500 30-60 120-180 5-8 Bolus Lispro U-200* Humalog U-200 5-15 30-60 <5 Basal glargine U-300* Lantus-Toujeo 2-4 None 20-24 Ultra Basal degludec U-300* Tresiba ~1 None <42 Bolus-Rapid Acting Inhaled regular Afrezza ~12 35-45 1.5-3

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https://youtu.be/CrmU3tKzhmU?si=nOp-SybZpBHXOgE5

Medication for Diabetes Type 2

Glucagon like peptide receptor agonist referred to as GLP-1 Receptor Agonist

• Injectable medication with exception of Rybelus*
• GLP-1 Agonists work to mimic incretin
• Incretin is a hormone produced by the small intestine during PO intake to trigger secretion of insulin into the bloodstream.
• Slows gastric emptying
• Promotes satiety
• Suppresses glucagon (glucagon secretion from the pancreas causes stored glucose to be released from the liver

Biguanides

• Stops liver from making too much glucose from stored glycogen
• Enhances absorption of glucose in the cells
• Lowers the absorption of glucose into the small intestine

Dipeptidase 4 inhibitor referred to as DPP-4

• DPP-4 is an enzyme that destroys the hormone incretin so insulin secretion decreases
• DPP-4 inhibitor therefore allows incretin to continue so the pancreas will secrete additional insulin

*Rybelus is the only GLP-1 Agonist that is available in a daily pill form

Medication for Diabetes Type 2 - continued

Sulfonylureas*

• Increase secretion of pancreatic insulin into the bloodstream

SGLT-2 Inhibitors

• Inhibit sodium glucose transport proteins found in the small intestine and proximal tube of nephrons from reabsorbing glucose into kidneys thus allowing glucose to pass through kidneys and out of the body

Thiazolidinediones (TZD)

• Referred to as glitazones
• Decreases insulin resistance and makes fat cells more sensitive to insulin

Meglitinides

• Increases rapid insulin burst from the pancreas following PO intake

Alpha glucosidase Inhibitors

• Delays the absorption of carbohydrate from the small intestine
• Lower postprandial (after eating) blood glucose

*Sulfonylureas are often first line treatment for MODY Note: There are also combinations of oral medications used to treat Type 2 diabetes

Part III Complications of Diabetes

Retinopathy

• Diabetic retinopathy is a condition that causes loss of vision and possible blindness in those individuals diagnosed diabetes.
• The retina (light sensitive portion of the eye that sends information to the brain allowing the formation of images) is damage due to chronic elevated blood glucose
• Early symptoms may include trouble reading or seeing objects at a distance
• Later on in the disease blood vessels will bleed into the vitreous causing what appears as spider webs or dark spots and streaks
• Untreated symptoms will form scars and cause further damage

Signs and Symptoms (vary from patient to patient)

• Blurry or reduced vision, difficulty reading, floaters and/or “rings” around lighted objects, flashing lights, and rapid onset of vision change

Nursing Intervention

• Promote importance on healthy lifestyle (blood glucose control, diet, exercise, annual dilated eye exam, no smoking, limit alcohol intake, lowering cholesterol, and maintain healthy weight)

https://youtu.be/JxMOsMDM1UM?si=mBpkq369txUHf5ro

Neuropathy

• Nerve damage caused by changes and stress at the cellular level
• Degree of nerve damage varies patient to patient depending on type of diabetes, length of the disease and other factors including but not limited to age, weight, and blood pressure
• Negative symptoms of neuropathy are referred to as nerve dysfunction and loss of nerve fiber and sensation
• Positive symptoms of neuropathy are referred to as abnormal or reduced function in nerve fibers and cause pain and tingling sensation

Possible Side Effects

• Decreased muscle tone, numbness, muscle twitching, balance issues due to loss of feeling in extremities, cramps, changes in peripheral sensation, dizziness, lightheaded, diarrhea/constipation, trouble swallowing, issues w/ bladder/bowel control

Nursing Interventions

• Educate patient on importance of self checks for blood glucose/blood pressure, adherence to recommended sodium/consistent carbohydrate intake, and daily skin checks to assess for cuts and wounds that are not healing.

https://youtu.be/bnd5scg7Fik?si=sZQfh9NZTijQbEYg

Nephropathy

• Abnormal kidney function causing improper filtration and removal of excess waste products and water from the blood.
• Kidney filtration system leaks albumin (protein) into urine causing fluids to move from bloodstream into surrounding tissues (swelling-edema)
• Nephropathy (loss of normal kidney function) causes inflammation, fibrosis and progressive decline in glomerular filtration (GFR)
• Risk factors include high blood pressure, elevated cholesterol, overweight, and smoking.
• Associated diagnosis of peripheral vascular disease, retinopathy and cardiovascular disease

Signs and Symptoms

• Passing of foamy urine
• Puffy eyes and swelling of feet and ankles
• Fatigue and swelling of feet, ankles
• Albumin to creatinine ratio >300 mg/g

Nursing Interventions

• Promote importance on healthy lifestyle (blood glucose control, diet, exercise, no smoking, limit alcohol intake, lowering cholesterol, and maintain healthy weight)

https://youtu.be/F4Lt0AjMxEY?si=C9IfI2t-66DZeUL5

Hypoglycemia When you you have diabetes you are at an increased risk of low blood glucose <70 mg/dL

• Contributing factors:

Excessive insulin and/or oral hyperglycemic medication, vomiting/diarrhea, decreased intake of food, and renal failure (the kidney are responsible for the metabolism of insulin). Untreated hypoglycemia can result in seizures, coma and even death. Diabetic Ketoacidosis (DKA) When you have diabetes you are at an increased risk of DKA. This is especially true for T1DM but can also occur with T2DM.

• Contributing factors:

Absence of insulin causing dysfunction in the metabolism of nutrients including carbohydrates, fats, and proteins. Breakdown of fat stores causes ketones in blood and urine. Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS) Patients with T2DM are at risk of HHNS without appropriate management of blood glucose levels

• Contributing factors:

Stressors including but not limited to cardiac events, severe dehydration, inappropriate management of glucose

Cardiovascular Disease When you have diabetes you have an increased risk for both cardiovascular disease and stroke

• Contributing factors:

Hypercholesterolemia, obesity, hypertension, elevated blood glucose levels secondary lifestyles contributing to INSULIN RESISTANCE (the body’s inability to use both endogenous and exogenous insulin These associated risk factors increase large and small vessel disease (heart and brain blood vessels) Sexual and Bladder Health

• Contributing factors:

Changes in blood vessels, nerves and hormones can cause urinary incontinence and bowel issues in both the male and female and erectile dysfunction in males. Men with diabetes who are overweight are more likely to have decreased testosterone levels Both genders may suffer from diabetes associated depression which may cause sexual dysfunction Gum Disease

• Contributing factors:

Diabetes causes less saliva in the mouth, increased sugar and bacterial leading to buildup of plaque and gum disease

Putting the Pieces Together….Let’s Play

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Click on link, select No Teams on the dropdown box and click on start. https://jeopardylabs.com/play/everything-diabetes

Case Study - “Ellie” 31 year old female History of T1DM diagnosed 12 months ago Weight 115 Height 5’8” BMI 17.5 BP 102/54 Pulse 110-125 R 32 Sats 93% BG 348 Ellie, 31 year old female, with a history of T1DM presents to the emergency room with complaints of abdominal pain with nausea and multiple episodes of vomiting. Denies illness with any other members of her family or coworkers. She reports checking her blood glucose before each meal, bedtime and prn (for low blood glucose). She reports her fasting and pre meal glucose normally averages in the 180-210 range. Reports for the past few days her blood glucose results are reading “high”. Pulse is rapid. Respirations are labored, skin is pale and dry. She reports leaving her last long acting insulin pen in the car with extreme weather conditions of 94 degrees daily and 70’s at night and decided not take her long acting insulin times two nights believing it had gone bad. She reports trying to keep up with elevated sugars by giving extra rapid acting insulin. She denies the use of ketone strips. Reports unwanted weight loss of 10# over the past 2 months. Question: What treatments and education will Ellie need prior to being discharged from the hospital? Click to next slide for answers……

Treatments (Provider suspects DKA and orders the following labs)

1. Venous Blood Gas (VBG) or Arterial Blood Gas (ABG), Comprehensive Metabolic Panel and Basal Metabolic Panel
2. IV fluids-0.9% NaCl or Ringer’s Lactate is commonly used. 15-20 mL/Kg of body weight over 1 hour then maintenance IV fluids dependent on electrolyte status
3. Potassium (K+) levels monitored
4. IV insulin typically started once K+ levels are >/=3.3 mmol/L
5. Point of Care testing POCT BG every hour
6. Serum glucose adjunct to POCT BG every 2 hours until patient stable
7. Monitor for hypoglycemia. When glucose decreases to <250 IV dextrose will help to decrease risk of low glucose in the setting of IV insulin administration

Education

1. Sick Day Management including testing glucose every hour, checking for urine ketones when BG >250 mg/dL. Increase water intake. Call provider if unable to control elevation in ketone levels. Trace to small continue drinking water to flush system. Moderate to large call provider/ED
2. Maintain insulin in a safe environment. Unopened insulin should remain in refrigerator. Once opened may keep insulin at room temperature between 46-86 degrees F. Never freeze insulin. Monitor for refill needs in order not to completely run out of insulin
3. Maintain blood glucose supplies in a proper controlled temperature/environment
4. Review guidelines for decreasing complications associated with diabetes including healthy nutrition, following medication regimen, exercise, sleep, and follow up as recommended with physicians.
5. Blood glucose goals: A1c
6. Educate on the connection between elevated and weight loss in diabetes. Chronic hyperglycemia especially in T1DM causes glucose to be excreted through renal system and end outcome = unintentional weight loss + starving cells

Post Quiz Time

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References Diabetes Care. (n.d.). American Diabetes Association. https://diabetesjournals.org/care/issue/47/Supplement_1 Hoffman L.S., Fox T.J., Anastasopoulou C., & Ishwarlal, J. (2023, August 14). Maturity onset diabetes in the young. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK532900/ Intermediate Acting Insulin Mnemonic for Nursing Pharmacology (NCLEX). (n.d.). www.youtube.com. Retrieved April 22, 2024, from https://www.youtube.com/watch?si=C2S-ZzGq7cz8iL2I&v=CqWbINKy_90&feature=youtu.be Long Acting Insulin Mnemonic for NCLEX | Nursing Pharmacology. (n.d.). www.youtube.com. Retrieved April 22, 2024, from https://youtu.be/CrmU3tKzhmU?si=nOp-SybZpBHXOgE5 Mallardo, M., Ferraro, S., Daniele, A., & Nigro, E. (2021). GDM-complicated pregnancies: Focus on adipokines. Molecular Biology Reports, 48(12), 8171–8180. https://doi.org/10.1007/s11033-021-06785-0 Mayo Clinic. (2020). Peripheral neuropathy: Mayo Clinic Radio. In YouTube. https://www.youtube.com/watch?v=bnd5scg7Fik Pathophysiology - Type I diabetes | Endocrine system diseases | NCLEX-RN | Khan Academy. (n.d.). www.youtube.com. https://youtu.be/3B73j1tKkpI Qualtrics. (n.d). The leading research & experience software. https://qualtricsxmfs38djz7w.qualtrics.com/jfe/form/SV_bpzLI2ZpGSpM2Fw Rajkumar V, Levine S.N. Latent Autoimmune Diabetes. (2022 June, 21). StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK557897/ Rapid Acting Insulin Mnemonic Nursing Pharmacology (NCLEX). (n.d.). www.youtube.com. Retrieved April 22, 2024, from https://youtu.be/0Pux_usFxDk?si=KAO7WVnLMk74Ptxy Short Acting Insulin Mnemonic for NCLEX | Nursing Pharmacology. (n.d.). www.youtube.com. Retrieved April 22, 2024, from https://www.youtube.com/watch?si=VLZ_-Iw-TlJxdXOq&v=aECo__PnVV4&feature=youtu.be