DIABETES MELLITUS

PNR 221

WHAT IS DIABETES MELLITUS?

Diabetes Mellitus (DM) is a chronic multisystem disease related to either:

• Abnormal insulin production (pancreas doesn’t produce insulin) • Impaired insulin utilization (body can not use insulin properly) • Or both • Results in hyperglycemia

• Canada needs a nation-wide diabetes strategy now - Diabetes Canada • http://www.who.int/mediacentre/factsheets/fs312/en/

3 INCIDENCE OF DM

• Diabetes Mellitus (DM) is the leading cause of end-stage renal disease, adult blindness and non-traumatic lower limb amputations • DM is a major contributing factor in the development of heart disease and stroke • DM is a financial burden to the client and the Canadian health care system • 6.2 % incidence in Canada – 6.7% in Windsor • Medical costs are 2-3 times higher than non-DM patient • People with DM pay $1000 - $15,000/yr in direct costs for meds and supplies.

4 INSULIN IS KEY

What is insulin? • Insulin is a hormone produced by the pancreas to control the amount of glucose (sugar) in the blood. Normal insulin metabolism: • Produced in pancreas by the  cells in the Islets of Langerhans • Released continuously (basal) into bloodstream in small increments and in larger amounts after food ingestion Like your housekey, it is unique to your • Stable glucose: 4 to 6 mmol/L or home, it only opens a specific “door” 4 to 7 mmol/L (Varies between or receptor site on the cell. sources) 5 FIG. 52-1: NORMAL INSULIN SECRETION NORMAL INSULIN SECRETION CONT’

• Insulin moves glucose from bloodstream into the cell • Thus: It ____________’s glucose level in the bloodstream

• Insulin specific receptors are found on skeletal muscles, adipose tissue and liver cells: • Skeletal muscle, adipose and some liver tissues are insulin- dependent tissues

• Other tissues (brain, liver, blood cells) do not directly depend on insulin for glucose transport FUNCTIONS OF INSULIN

• Insulin facilitates glucose transport from the bloodstream to the cell to provide nutrition/energy for cell function • Required for survival • It continuously provides the body with energy and the need for insulin increases after ingestion of food • Stimulates storage of glucose in the form of glycogen in the liver and muscle • Inhibits (prevents) gluconeogenesis • Enhances (increases) fat deposition • Increases protein synthesis • Counter regulatory hormones oppose (go against) the effects of insulin. In DM, these hormones may have abnormal production. Normally: • Provides regulated release of glucose for energy i.e. following food intake, during fasting • Help maintain normal blood glucose levels COUNTER- R E G U L ATO RY In Diabetes: HORMONES • Stimulates glucose production, increases blood glucose levels • Glucose production increased from the liver • Decreases movement of glucose into cells (remain in bloodstream)= ___________ • Examples: Glucagon, epinephrine, growth hormone, cortisol (all increased 9 in diabetes mellitus) NORMAL BLOOD GLUCOSE LEVELS

• A normal fasting blood glucose level is 4 - 6 mmol/L • BS rise after eating • Within 2-3 hours of eating, the glucose should be return to normal levels (less than 6.1mmol/L)

10 TYPES OF DIABETES MELLITUS

Two most Other types common types • Type 1 • Gestational • Type 2 • Prediabetes

11 TYPE 1 DIABETES ETIOLOGY AND PATHOPHYSIOLOGY

• An autoimmune disease – the immune system (T cells) attack and destroys the cells in the pancreas (islet  cells) that make insulin. The body is left without insulin. • Long, progressive onset • Symptoms occur when the autoantibodies destroy 80% to 90% of the  cells leading to hyperglycemia

https://www.diabetes.ca/en-CA/about-diabetes/causes-of-diabetes 12 TYPE 1 DIABETES MELLITUS

Less than 10% of adults with DM have type 1 DM

Formerly known as “juvenile onset” or “insulin dependent” diabetes • Most often occurs in people under 30 years of age • Peak onset is between ages 11 and 13. Why?________ TYPE 1 DM RELATED FACTORS

Causes/theories: • Auto-immune – thought to occur in individuals with genetic predisposition • Environmental – sedentary lifestyle, obesity, stress • Viral exposure • Nonimmune factors unknown (idiopathic) causes (rare) COMMON SYMPTOMS TYPE 1 DIABETES

Onset of symptoms occur rapidly once critical level of beta cell destruction is reached (80-90%) The pancreas can no longer produce insulin. • POLYDIPSIA - unusual thirst • POLYURIA - frequent urination • POLYPHAGIA – hunger • weight change (gain or loss) • extreme fatigue or lack of energy • blurred vision • frequent or recurring infections • cuts and bruises that are slow to heal • tingling or numbness in the hands or feet • trouble getting or maintaining an erection • Present to ER with diabetes ketoacidosis (DKA) - Complication of type I DM (3rd sem) 15 PREDIABETES/ IMPAIRED GLUCOSE TOLERANCE • Prediabetes is a condition where blood sugar levels are higher than normal, but are not yet high enough to be diagnosed as type 2 DM. • Estimated 6 million Canadians are prediabetic = left unmanaged leads to an increased risk of cardiovascular disease and the development of DM 2 • Often asymptomatic or may have same symptoms as diabetics • Not everyone with prediabetes will develop type 2 diabetes, but many will • Taking steps to manage blood sugar can prevent or delay type 2 diabetes. The key is a healthy lifestyle. • https://www.diabetes.ca/about-diabetes/prediabetes-1 PREDIABETES – REDUCING RISK • Long-term damage already occurring to heart and blood vessels (macrovascular changes) • Health teach symptoms of diabetes • Lifestyle changes - maintenance of a healthy diet, moderate exercise, cessation of smoking and reduction of stress • Goal: Normal BS levels and maintain BP • Research large study: • 58% at risk people reduced risk of DM2 by losing weight and moderate exercise for 30 minutes daily. Risk reduced by 71% in people over 60 years of age. TYPE 2 DIABETES MELLITUS ETIOLOGY AND PATHOPHYSIOLOGY

• Accounts for over 90% of people with diabetes • Usually occurs in people over the age of 40 with a parent or sibling with diabetes • Increased incidence of DM2 and obesity seen in children and adolescents • Genetics – increased risk for those with a parent or sibling with DM. Similar lifestyle and diets. • Risk increased in: Indigenous , African, Arab, Asian, Hispanic, or South Asian descent • Obesity – 80 - 90% of DM 2 clients are overweight at time of diagnosis. Increased abdominal and visceral fat increased risk of _____________ TYPE 2 DM RELATED FACTORS

• Hypertension (high blood pressure) • High levels of cholesterol or other fats in the blood • Elevated BMI or are overweight -especially if that weight is in abdomen • Prediabetes (impaired glucose tolerance) • Polycystic Ovary Syndrome (PCOS) • Psychiatric disorders (schizophrenia, depression, bipolar disorder) • Obstructive sleep apnea • Darkened patches of skin called acanthosis nigricans • Glucocorticoid medication (long term, increases BS)

19 TYPE 2 DIABETES MELLITUS ETIOLOGY AND PATHOPHYSIOLOGY

• The pancreas cannot make enough insulin (islet beta cells) or does not properly use the insulin it makes (at cell level). • Pancreas continues to produce some endogenous (self-made) insulin • Insulin produced is either insufficient or poorly utilized by cells/tissues Leads to: • Insulin resistance – body tissues do not respond to the action of insulin • Insulin receptors are unresponsive to the action of insulin (i.e. skeletal, muscle, fat and liver-insulin dependent tissues) • Hyperglycemia Insulin resistance • Body tissues and receptors for insulin are not responsive Pancreas ↓ ability to produce insulin • β cells fatigued from compensating or β-cell mass lost Inappropriate glucose production from liver TYPE 2 DM • Liver’s release of glucose is not regulated i.e. MAJOR with food intake M E TA B O L I C Alteration in production of hormones and ABNORMALITIES adipocytokines (for glucose and fat metabolism) • Contribute to pathophysiology of type 2 diabetes

21 Fig. 52-2: Altered mechanisms in type 1 and type 2 diabetes TYPE 2 DIABETES MELLITUS ONSET OF DISEASE

• Gradual onset

• Person may go many years with undetected hyperglycemia causing underlying damage to organs • Diagnosis often accidental - routine blood work, eye exam, wound not healing, recurrent yeast infections, frequent UTIs…. • Osmotic fluid/electrolyte loss from hyperglycemia may become severe resulting in significant dehydration ➢ May lead to Hyperosmolar Hyperglycemic Coma (HHS a complication of DM2 will discuss in 3rd sem) • Symptoms appear gradually and tend to be non-specific: • Fatigue • Recurrent infections • Recurrent vaginal yeast CLINICAL infections M A N I F E S TAT I O N S TYPE 2 DIABETES • Prolonged wound healing MELLITUS • Visual acuity changes • Painful peripheral neuropathy of the feet • May also have a few classic symptoms of type 1 GESTATIONAL DIABETES

• Develops during third trimester of pregnancy • High blood sugar levels during pregnancy could lead to: • Preeclampsia (high blood pressure that occurs during pregnancy) • Abnormal glucose level in baby • Large birth weight, increasing the need of a caesarean section • Possible birth injury due to the baby's size and difficulties during delivery • Higher risk of DM and CVD later in life (5-10 years, approx. 10%) Treatment: • manage weight, healthy diet, exercise before and during pregnancy • If lifestyle changes ineffective – exogenous insulin • BS levels return to normal approx. 6 weeks postpartum SECONDARY DIABETES

• Results from another medical condition or treatment of a medical condition • i.e. Schizophrenia, Hyperthyroidism, Cystic fibrosis, Prednisone, TPN, phenytoin,etc • Abnormal blood glucose levels • Usually resolves once underlying condition treated Four methods of diagnosis of diabetes:

1. Hemoglobin A1C (A1C) 2. Fasting plasma glucose (FPG) DI AG NOSI S 3. Casual (random) plasma glucose level OF DM 4. Oral glucose tolerance test • Same test should be repeated for confirmation of DM diagnosis • Exception: if FPG >7 AND client presents with 3 polys, no additional testing required

s2 7 DIABETES MONITORING IN C ANADA

LDL Kidney Test A1C Blood pressure cholesterol (urine ACR) How many were tested at the recommended 17% 69% 32% 17% frequency? How many tests are 2 (if at target); recommended in a 2- 4-8 3+ (if above 2 2 year period? target) Blindness, Cardiovascular amputation, Cardiovascular What can it help disease, Kidney kidney disease, disease, prevent? amputation, failure cardiovascular amputation kidney disease disease

28 HEMOGLOBIN A1C (A1C) G LY C O S Y L AT E D H E M O G L O B I N

• Assesses blood glucose average (percentage) over 2-3 months • Glucose remains attached to hemoglobin (Hgb) for the life span of the RBC (~ 120 days) • Example: A1C of 7% means that 7% of the total hemoglobin has glucose attached to it

• Should be assessed in all diabetic clients every 3-6 months

29 HEMOGLOBIN A1C (A1C) GLYCOSYLATED HEMOGLOBIN

Results: • Prediabetes – 6.0-6.4% • Diagnosis of diabetes – >6.5% Target for DM: ≤ 6.5 (dr. may set individual A1C goals) or good Goal: good glycemic control (4-6.5%)

Advantages: Can be taken at any time, doesn’t require fasting, fewer day-to-day variations • Elevated glucose = damages blood vessels and leads to chronic complications • Near normal A1C levels greatly reduces risks of developing retinopathy, nephropathy, and neuropathy 30 FASTING BLOOD GLUCOSE (FBS)

Simple blood test, requires a minimum of 8 hours of fasting Results: • ≥ 7.0 mmol/L = Diabetes Mellitus • 6.1 – 6.9 mmol/L = prediabetes, Impaired Fasting Glucose (IFG), • < 6.1 mmol/L = Normal value

• Hold insulin and oral diabetic meds until after blood is obtained • Most accurate from venipuncture sample, in hospital at bedside or client at home uses capillary sample

3 1 C ASUAL OR RANDOM PLASMA GLUCOSE .

• If doctor suspects a client has diabetes, they may test the blood at any time of day without regard to the meals

• Results indicate diabetes mellitus if: • Casual Plasma Glucose ≥ 11.1 mmol/L and symptoms of DM, such as polyuria, polydipsia, unexplained weight change 3 2 ORAL GLUCOSE TOLERANCE TEST (OGTT)

This test measures the body’s ability to use glucose, requires fasting of 8 hours Procedure: • Fasting blood sugar taken (FPG) = baseline • Client is given a flavored beverage containing 75g of glucose, must drink all of beverage within 5 minutes. • After 2 hours, plasma glucose reassessed Results: • ≥ 11.1 mmol/L = diabetes • 7.8 to 11.0 mmol/L = prediabetes, Impaired Glucose Tolerance (IGT) • Disadvantage: expensive, time-consuming • Used to diagnose gestational diabetes at wks 24-28 gestation 3 3 SELF-MONITORING OF BLOOD GLUCOSE

• Cornerstone of diabetic management • Provides “real-time” blood glucose levels, allowing the client to make decisions regarding diet, exercise, and medications. • Allows client to respond quickly to high and low BG levels • Method: client washes hands with soap and water, pricks side of finger tip, applies blood drop to strip, waits for results • Frequency and timing of SBGM ordered by doctor; it will depend on stability of BG readings, type of meds used, healthy vs illness, activity level

3 4 ADDITIONAL TESTS FOR MONITORING

• Urine Test for Ketones – Part of urinalysis or urine strips. • Normal: NO ketones are present in the urine. • +ve ketones indicates control of DM type 1 is deteriorating and impending ketoacidosis (DKA) is high. • Assessed in type 1 DM when blood glucose is high, positive glucose in urine, illness, wt loss program. • May also be indicated for DM type 2 if on insulin

• Tests for Renal Function • Identification of chronic kidney disease in diabetes requires screening for proteinuria (urine albumin) as well as an assessment of renal function (BUN, Creatinine). • First morning void or 24-hr urine collection preferred 3 5 C ASE STUDY APPLIC ATION OF KNOWLEDGE

Mrs. HR is a 48 year old being screened for diabetes since she is over 40, and has a family history of diabetes. The doctor orders an A1C test. Her first A1C comes back 6.5%. Should you tell her she has Type 2 diabetes? Yes or No Resource: https://www.diabetes.ca/managing-my-diabetes/tools---resources/how- do-i-make-the-diagnosis-of-diabetes- 36 TYPE I OR 2?

Determine whether the conditions below relate to DM type I or 2?

a) Insulin resistance b) Beta-cell secretory exhaustion c) Genetic (inherited) defect in insulin receptors d) Production of islet cell antibodies e) Inappropriate glucose production by the liver f) Beta-cell destruction g) Impaired glucose tolerance occurs gradually h) Compensatory increased insulin production

37