Diabetes Management: Diet, Exercise & Monitoring

Diabetes Mellitus Overview

• Diabetes Mellitus (DM) is a syndrome of disordered metabolism resulting in inappropriate hyperglycemia.
• DM may be due to deficiency of insulin secretion or a combination of insulin resistance and inadequate insulin secretion.
• In the US, over 37 million people have DM, representing 10.5% of the population.
• Type 1 diabetes accounts for 5-10% of DM cases, with the remainder being Type 2.
• DM can be primary or secondary, potentially temporary depending on the cause.

Primary DM Etiologies

• Type 2 Diabetes is the most common primary etiology.
• Other primary etiologies include Type 1 Diabetes, gestational diabetes, and malnutrition-related diabetes (rare and involves beta cell dysfunction and blood sugar imbalances).

Secondary DM Etiologies

• Pancreatic diseases like pancreatitis and malignancy can lead to DM.
• Other endocrine disorders like Cushing's, acromegaly, pheochromocytoma, and glucagonoma can cause DM.
• Medications like corticosteroids, diuretics, beta-blockers, and niacin, particularly with chronic use, can be secondary etiologies.
• Genetic disorders like cystic fibrosis, can cause DM due to sludging within the pancreas.

Glucose Metabolism and Insulin Regulation

• Serum glucose is a major energy source for all tissues, especially the brain, muscles, and RBCs.
• Glucose metabolism occurs through glycogenolysis (breakdown of glycogen) and gluconeogenesis (synthesis of new CHO from non-CHO sources).
• Insulin is the key regulator of serum glucose concentration.
• Insulin is synthesized in the beta-cells of islets in the pancreas as a precursor, then cleaved into its active form with a C-peptide residual.
• A basal amount of insulin is normally produced and secreted steadily.
• There is also release of a bolus of insulin in response to a glucose load, spurring with meals.

Role of Other Hormones

• Glucagon acts in the liver to promote gluconeogenesis and glycogenolysis.
  • Incretins (GLP-1 Proteins) are hormones that inhibit glucagon secretion and stimulate insulin secretion during meals.
• Epinephrine works on receptors in the liver to produce the same changes as glucagon.
  • Epinephrine also works on alpha-2 receptors of beta cells to inhibit insulin release and it induces symptoms of hypoglycemia (tremor, sweating, anxiety).
• Cortisol and growth hormone inhibit glucose utilization by promoting gluconeogenesis and inhibiting glucose uptake in tissues, which raises serum glucose when needed, like in stressful situations.

DM Diagnostic Criteria

• Hemoglobin A1C of 6.5% or higher is a diagnostic criterion.
• Fasting plasma glucose of 126 mg/dL or higher after an 8-hour fast is another criterion.
• A casual plasma glucose level > 200 mg/dL with classic symptoms such as polydipsia, polyuria, polyphagia, unexplained weight loss, fatigue is also a diagnostic criterion.
• A 2-hour plasma glucose level of 200 mg/dL or greater after a glucose load during an oral glucose tolerance test (OGTT) is diagnostic.
• Tests should be repeated to confirm diagnosis.

DM Signs and Symptoms

• Classic "3-P's": Polyuria, polydipsia, and polyphagia are common.
• Weight loss is another sign, and more common in Type 1 DM.
• Dehydration and altered mental status (DKA) can be signs.
• Blurred vision.
• Fungal and/or bacterial infections.
• Polyneuropathy.
• Most patients have NO symptoms and are found on screening tests.

Type 1 Diabetes Mellitus Characteristics

• Caused by autoimmune destruction of pancreatic islet beta cells.
• Rate of destruction is variable, involves progression from Stage 1 (autoantibodies, normal glucose tolerance) and Stage 2 (autoantibodies, glucose intolerance) to Stage 3 (symptomatic disease).
• Commonly occurs in children/young adults, but can appear at any age.
• Insulin is absent.
• Plasma glucagon is elevated, but beta cells cannot respond to stimuli to produce insulin.
• Exogenous insulin is required to prevent ketosis and reduce blood glucose.
• Latent Autoimmune Diabetes of Adults (LADA) is a latent form of Type 1 DM that slowly leads to insulin deficiency.
• Latent Autoimmune Diabetes of Adults (LADA) is often confused in adults with Type 2 DM

Type 1 DM Autoantibodies

• Evaluation is helpful to differentiate Type 1 vs Type 2 if diagnosis unclear.
• Can screen family members of patients with Type 1 DM.
• Autoantibodies presence can precede onset of disease by 5 years or more -New medication aims to slow these.
• Anti-islet cell antibodies, insulin autoantibodies, glutamate decarboxylase (GAD) antibodies, and insulinoma-related antigen-2 have high sensitivity (~80%) and specificity (~99%) for Type 1 DM.
• Risks associated with Type 1 DM are Diabetic Ketoacidosis (DKA), chronic complications like in Type 2 DM and higher rate of other autoimmune disorders. Since Type 1 is due to severe insulin deficiency, therapy must include insulin replacement. Medications to stimulate insulin production or activity are not effective.

Diabetic Ketoacidosis (DKA)

• DKA is an emergency with greater risk in Type 1 DM due to severe insulin deficiency.
• Lack of insulin leads to:
  • Accumulation of ketones in the serum -> lowering of pH.
  • Insulin deficiency which leads to glycogenolysis, gluconeogenesis, lipolysis.
  • Ketones are a product of fat breakdown to form glucose.
• High serum glucose causes osmotic diuresis -> dehydration, electrolyte loss, and a worsening of acidosis.
• Causes inadequate insulin, infection (UTI, pneumonia), or vascular issue (MI, CVA).

DKA Diagnostic Criteria

• Serum glucose > 250mg/dL (usually 400s or 500s).
• Arterial pH ≤ 7.30.
• HCO3 ≤ 18mmol/L.
• Anion gap > 10.
• Urine/serum ketones positive.

DKA Signs/Symptoms

• Vomiting induced by acidosis.
• Thirst and Polyuria.
• Weight loss is caused by dehydration
• Abdominal pain.
• Tachycardia and dry skin/mucous membranes, hypotension.
• Kussmaul breathing (hyperventilation).
• Acetone smell to breath and in urine.
• Confusion and coma

DKA Work-Up

• Serum electrolytes, ketones.
• CBC and blood cultures (signs of infection).
• Blood gas.
• Urinalysis and urine ketones.
• EKG (peaked T waves if hyperkalemia).
• CRX (evaluate infection or CHF)
• CT/MRI if altered mental status (cerebral edema).
• Abdominal US/imaging if needed

DKA Treatment

• Restore hydration with normal saline (closely monitor electrolytes).
• Replace insulin with IV insulin (closely monitor glucose).
• Replace electrolytes (especially potassium).
• Restore acid-base balance (IV fluids and insulin will remove ketones).
• Determine cause of DKA .
• Treat precipitating factor: treatment non-compliance, infection, MI

DKA Complications

• Altered mental status (monitor for cerebral edema).
• Hypotension (pre-renal from dehydration).
• Hypothermia (rapid IV fluid replacement).
• DVT caused by acidosis.
• Hypoglycemia and hypokalemia.
• Congestive Heart Failure (CHF).
• ICU is needed if altered mental status, severe acidosis (pH < 6.9), severe electrolyte abnormalities, or risk of cerebral edema.

Type 1 DM Management and Monitoring

• Prone to hypoglycemia, especially in kids
• Long-term complications are same ones as with Type 2 DM
• Retinopathy Screening (annual eye exam) should start if there are symptoms, but if not then it should start at age 10 or after 3-5 years from diagnosis duration, or by age 12 if no Fhx
• Check urine for microalbumin annually to look for occult kidney disease which should start at age 10 or after 5 years after diagnosis.
• HTN Screening which should be routinely checked on routine visits, including an annual eye exam Screen lipid profile at diagnosis if +Fhx, or by age 12 if no Fhx If abnormal, monitor annually Treat with low fat diet
• Initiate lipid lowering med if LDL > 160 if/no RFs for CV disease (>130 if + RFs) in children
• Screening annually for Thyroid disease and Celiac disease

Type 1 DM Second Most Frequent Childhood Illness #2

• Also critical to educate parents and child about disease state, diet, insulin and end-organ damage screenings
• Can be a time that is very difficult during adolescence

DM - Other: MODY (maturity-onset diabetes of the young)

• Genetic defects with beta cell dysfunction (genetic disorder).
• MODY is neither Type 1 nor Type 2.
• Autosomal dominant inheritance.
• Often characterized as the "young and skinny" type 2 DM.
• No insulin resistance.
• Islet function typically preserved for at least 3-5 years after onset.

Pathophysiology of Type 2 Diabetes Mellitus

• The incidence increases as people age with onset typically happens after age 40.
• Associated with obesity and increased caloric intake with decreased caloric expenditure.
• Has strong genetic links
• Ask about FHx! Concordance can reach as high as 90% in identical twins; While 15-25% for non-identical siblings
• Endogenous insulin is present (normal or increased) with insulin resistance nearly always present Impairs insulin secretion from pancreas, which can cause a loss of beta cells over time High levels commonly seen in most people with diabetes, especially early as High insulin levels are commonly asscoiated with other complications, such as dyslipidemia, hypercoagulability, Atherosclerosis , and further weight gain/obesity (insulin acts as a growth hormone)

Diagnosing Impaired Fasting Glucose

• Prediabetes
• Impaired fasting glucose registers between 100-125mg/dL
• Impaired glucose tolerance Measurements for this diagnostic feature includes: Glucose level is measured 2hrs after 75mg glucose oral load 140-199mg/dL
• Hgb A1C - registers as 5.7-6.4%
• Without significant hange/weight loss, high rate of conversion into the Diabetes Mellitus (Frank DM) type 2
• Educate patient on lifestyle modifications (l/s) such as weightloss and diet to prevent Type 2 DM
• Risk of having Impaired glucose tolerance (IGT) which means it is the biggest predictor of cardiovascular risk.

Risk Factors for Type 2 DM

• Family history.
• Low birth weight and low weight as a 1-year-old.
• Male gender.
• Age greater than 45 years.
• Ethnicity: Hispanic, Native-American, African-American, Asian-American, and Pacific Islanders.
• History of gestational diabetes (gestational diabetes).
• Hypertension (HTN).
• Dyslipidemia.
• PCOS and acanthosis nigricans (a/w insulin resistance).
• Obesity (abdominal circumference).
• Sedentary lifestyle.
• Western diet.
• Stress.

Metabolic Sydrome is 3 or more of the following:

• Cluster of conditions that happen together, increasing overall risk for diabetes and cardiovascular disease. Involves 3 or more of the following:
  • Central (abdominal) obesity as measured by waist circumference (Men > 40 inches, women > 35 inches) -Fasting triglycerides : ≥ 150mg/dL = (or under tx for this)
• HDL cholesterol: Low (Men < 40, women < 50)
• BP: ≥ 130/85 = (or under tx for this)
• Fasting glucose : ≥ 100mg/dL

Diagnosing Obesity

• Can be primary or secondary etiologies (Cushing's, hypothyroid) and the measurements include:
• BMI = kg/m2
• Waist circumference (measured midway between lowest rib and iliac crest while standing)
• Both Ghrelin and leptin are known as the 2 feedback mediators that help manage patients’ appetite
• However it is also Current area of interest for rsearch and development on the role of all those feedback meds in weight loss

What is a BMI?

• 18.5-24.9 = healthy weight
• 25-29.9 = overweight
• 30-34.9 = obese (Class 1)
• 35-39.9 = severe obesity (Class 2)
• 40+ = profound obesity (Class 3) Diet
• Consuming a Healthy, balanced diet means:
• To eat more F/Vg, fiber w/ protein, and
• To limit foods that are high is Sugar such as Soda, white breads, baked goods.
• Eat More Low - Fat foods (Saturated fats) - Aerobic Excersie
• Doing at least 150 min of moderate exercise per week will help keep you in shape
• Weight loss/maintaining a healthy weight can also help fight against obesity
• 5% Weight loss will also help in the associated with 74% reduction in risk of developing diabetes!

Prevention against Type 2 DM and early monitoring is important

• In all patients every 3 years starting at age 45 are already considered for type 2 prevention
• Current guidelines recommend annual checkups for all adults
• Screening patients (30yo) are and more frequently if they have:
• BMI 25+ and acanthosis nigricans Sedentary
• 1st degree of someone with relevant family members w DM
• High-risk ethnicity
• H/o gestation DM or delivery of > 9lb infant H/o impaired fasting glucose
• Having HTN
• Low HDL< 36mg/dL or triglycerides > 249
• Have PCOS
• Having h/o Vascular disease

Diagnosing Symptoms with (HONK)Hyperosmolar Nonketotic Hyperglycemia State 

• It is a state that typically found in Type 2 DM, Though can also occur in Type 1's
  • Severe hyperglycemia - Diuresis due to high osmotic load through nephrons

Treatment

  Presence of insulin prevents Ketosis
  But most often has insulin present at insufficient levels

HONK diagnostic criteria Plasma glucose > 600mg/dL Arterial pH > 7.30 Serum HCO3 > 15 Anion gap can be variable Urine/serum ketones absent (or minimal) Serum osmolality > 320mOsm/kg

Presentation

Altered mental status/coma Severe dehydration Stroke/MI/Acute lower extremity arterial insufficiency Arterial thrombosis due to pro-inflammatory effect of extreme hyperglycemia

(Hyperviscosity and glycosylated proteins)

• Treatment Fluid replacement with normal saline Cautious, slow infusion of insulin Frequent monitoring of serum osmolality, glucose, & electrolytes

Monitoring

Monitor for signs of cerebral edema and thrombotic complications

Managing and treating HONK entails lifestyle changes such as: Lifestyle (lifestyle/S) modifications to prevent and/or change DM - such Diet, exercise, weight loss, self monitoring/screening, reduction of other RFs (HTN, lipids) Meds can be used as (oral, injectables, insulin)

• Typical Treatment progression is : lifestyle modifications alone -> lifestyle mods + oral medications -> lifestyle mods + oral meds + insulin , In some cases, may progress right to insulin management depending on severity

Consider the Types of DM: Diet

• Patients should avoid refined sugars and eat less than 30% of calories from fat
• atleast 15%+ should come from protein and remeainder should be "healthy" carbohydrates such as whole grains, fruits, vegetables, legumes, low-fat dairy _ The average amount of calories should be dependent on patients' BMI. If ideal weight is present, 1800cal/day is the total amount calories they should ingest If overweight - caloric restriction based on weight loss of 1kg/wk Lastly, remember Referall to RD/diabetic Educator! - is something you to help your paitent better understand

Glycemic index = measure how foods affect blood sugar levels

• It measures the Area under the curve of blood glucose for the values that elicits a carbohydrate in the blood The working principle behind using the Glycemic Index (GI) with foods is very prevalent with the Atkins's and South Beach diet, which involves the following Utilizing a low glycemic index diet to elicit the normal glucose levels will naturally cause lower GI on foods with its own properties to inhibit patients appetite. That is the goal!

DM Treatment

• Carbohydrate counting should be done often, it's a important role to prevent Dm (type 1 or type 2)
• Educate patients on how to estimate the grams of carbohydrate (or the GI) of food items, It's Especially useful for insulin-dependent patients (Type 1 or Type 2)
• The average Carbohydrate count should typically be taught as a first education process to a registered dietician/diabetic educator to help provide a simple understanding for the patient and to help guide them better towards their goal.
• When prescribing a good diet a patient must know that they are doing it for Lifelong and change is the goal, not what people expect as crash diets or even those trending diets
• In turn, they are supposed to have or expect Slow weight loss and limit the amount of alcohol they ingest

Remember Exercise:

• At least 150 minutes per week of moderate exercise (50-70% max HR) There should be a mix with Resisrance excersies for all muscle groups And this process will have to carefully be slowly built up if the paitents tend to be more on or less of the ssedentary spectrum

What should be taking when excersing

• Caution with potential should be excersices if hypoglycemia (low blood sugar) Especially if your that patient is with Type 1 DM
• In this case CHO (20-40g) prior to and during exercise
• Lastly, they may need to reduce the actual insulin dose if intense exercise is planned!

DM important patient processes

• Self-monitoring/screening - this includes how to perform foot excercises on the daily, perform annual eye exams, look at their body Weight, check blood pressure, and monitor lipid levels and the glucose of their body
• Make sure the patients take Weight - BP, lipid screening/monitoring Stay Uptodate and perform Glucometer/CGM
• It is also important to note that the goal for those who go trhough this all is to Stay UTD with vaccinations (flu, pneumonia, hep B series)

Optimal management of DM Glucose:

• Fasting is around are 80-139 mg/dL
• And to not have any post-prandial (after easting) spike and stay within 130-180 mg/dL Pregnancy guidelines can be even stricter however!
• Such the goal is to keep Fadtinf under: 60-99 mg/dL (also before meals) Peak is between 1-2hr post-prandial = 100-129 mg/dL -> Very tight control - can be at risk for hypoglycemia

How do Glucose monitories:

• Can have performed their reading and their value with the actual finger stick On the other hand, newer monitoring such Continuous Glucose Monitors
• 10 day (Dexcom) to 14 day (Libre) where Subcutaneous interstitial glucose sensor Worn can show where the sensor which can communicate a patient's glucose level through a smartphone app or reader device, has alarms to alert patients of when theyre low or high, and for the most part insurances do cover this is and only if you are a daily insulin

In the setting of DM treatment

• Multi Medication can be very common given the patient's status but it's extremely important to practice shared decision making!
• Some things patient have to take in consideration are : Patient preference, what they find for their own comfort of use (PO vs injectable) What their schedule is? (How many times/day must take it), Cost of all the medication
• Remember it's also important to understand that patient cases are Not a Static conditions. - which means this rquiers continual monitoring in treatment
• Patients can not assume that by Initiating on a medication = thatlifestyle/S modifications are no longer needed!

Diabetes Medication

• Lastly Side effect and organ damage monitoring should be a routine step! Most Common Oral medications are : Metformin, Sulfonylureas, Meglitinides, Alpha-glucosidase inhibitors, Thiazolidinediones, DPP-4 inhibitors, Incretin memetics, & SGLT-2 inhibitors

Assess knowledge of diabetes management, including dietary approaches, exercise recommendations, carbohydrate counting, self-monitoring, and treatment plan modifications for both Type 1 and Type 2 Diabetes Mellitus. Includes gestational diabetes management and target glucose ranges.