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Diabetes Chapter 53 – Comprehensive Study Notes

Diabetes Notes – Chapter 53

  • Definition and scope

    • Diabetes (DM) is a chronic multisystem disease characterized by hyperglycemia related to absent/insufficient insulin production, impaired insulin use, or both.
    • Affects an estimated 34.2\text{ million} people in the United States.
    • Approximately 88\text{ million} have prediabetes; 17.3\text{ million} are unaware.
    • 7th leading cause of death.

  • Etiology and Pathophysiology

    • Causes can be a single factor or a combination: genetic, autoimmune, and environmental.
    • Primarily a disorder of glucose metabolism related to absent/insufficient insulin and/or ineffective use of insulin.
    • Endocrine and metabolic context: insulin promotes glucose transport into cells and storage of excess glucose; counterregulatory hormones (glucagon, epinephrine, growth hormone, cortisol) oppose insulin.
    • Insulin is synthesized from proinsulin; enzymes split proinsulin into insulin and C‑peptide in equal amounts. Serum/urine C‑peptide indicates B‑cell function and endogenous insulin levels.
    • Normal glucose and insulin dynamics:
    • Insulin is produced by beta cells in islets of Langerhans and released continuously in small increments, with larger amounts after meals.
    • Daily adult insulin secretion ≈ 40\text{ to }50\ \text{U}.
    • Glucose stabilization range: ≈ 74\text{ to }106\ \text{mg/dL}.

  • ADA classification of diabetes (4 classes)

    • Type I
    • Type II
    • Gestational diabetes
    • Other (specific types)

  • Type 1 DM (overview)

    • Accounts for 5\%\text{ to }10\% of all diabetes cases; usually affects people under 40 but can occur at any age.
    • Etiology: autoimmune destruction of pancreatic β cells; genetic predisposition (HLAs) and viral exposure contribute; idiopathic type 1 DM and latent autoimmune diabetes in adults (LADA) exist.
    • Onset: islet autoantibodies can be present for months to years before symptoms; rapid onset with ketoacidosis after insulin deficiency becomes significant.
    • Manifestations: classic symptoms—polyuria, polydipsia, polyphagia; weight loss; fatigue; risk of ketoacidosis (DKA).
    • Management: exogenous insulin required; possible temporary partial remissions after starting treatment.
    • Visual/neurological/functional considerations may arise; risk of ketoacidosis if untreated.

  • Type 2 DM (overview)

    • Most prevalent type: ~90\%\text{ to }95\% of cases.
    • Risk factors: overweight/obesity, aging, family history; higher prevalence in certain ethnic groups.
    • Pathophysiology: endogenous insulin present but not sufficient or not used effectively (insulin resistance) with impaired pancreatic insulin secretion; potential increased hepatic glucose production; adipose tissue–derived hormones (adipokines) contribute; brain/kidneys/gut also play roles.
    • Metabolic syndrome—key risk factor cluster: abdominal obesity, hypertension, high triglycerides, low HDL; presence of 3 of 5 components increases risk.
    • Onset: gradual; many years with hyperglycemia before diagnosis; about 50%–80% of β cells may be nonfunctional at diagnosis; median duration before diagnosis ≈ 6.5 years.

  • Prediabetes

    • Intermediate state with increased risk for progression to type 2 diabetes.
    • Diagnostic states:
    • Impaired glucose tolerance (IGT): OGTT 2-hour plasma glucose 140\text{ to }199\ \text{mg/dL}
    • Impaired fasting glucose (IFG): fasting plasma glucose 100\text{ to }125\ \text{mg/dL}
    • Asymptomatic but with long-term risk to heart and vessels; emphasis on screening, weight management, exercise, and risk-factor modification.

  • Gestational diabetes

    • Develops during pregnancy; in the US, prevalence ~2\%\text{ to }10\%.
    • Increases risk for cesarean delivery and perinatal complications; screen high-risk patients at first visit (obesity, advanced maternal age, family history).
    • Average-risk women screened at 24–28 weeks gestation.
    • Glycemic status usually returns to normal post partum; up to 63\% risk of developing type 2 diabetes within ~16 years.

  • Other specific types

    • Result from β-cell destruction or dysfunction due to injury or interference from medical conditions or drugs; may resolve with treatment of underlying cause or cessation of offending medication.

  • Diagnostic studies (criteria and tests)

    • A1C: A1C\geq 6.5\% defines diabetes.
    • Fasting plasma glucose (FPG): FPG>126\ \text{mg/dL}.
    • 2-hour plasma glucose during OGTT (glucose load of 75 g): \text{OGTT}_{2h}>200\ \text{mg/dL}.
    • Random plasma glucose with classic hyperglycemia symptoms: \text{random glucose}>200\ \text{mg/dL}.
    • Repeat criteria 1–3 on a separate day to confirm diagnosis.
    • Influencing factors to consider when diagnosing.

  • Islet cell autoantibody testing and other labs

    • Islet cell autoantibodies can precede symptoms in Type 1 DM.
    • C‑peptide level (from proinsulin) helps assess endogenous insulin production and β‑cell function.
    • Additional tests: lipids, BUN, creatinine, electrolytes; urine albumin; BP; eye, foot, neurologic exams; ABI;
      and comprehensive screening for organ system complications.

  • Interprofessional care goals

    • Goals (ABC framework):
    • A1C: glycemic control
    • Blood pressure
    • Cholesterol
    • Primary aims: reduce symptoms, promote well-being, prevent acute complications, prevent/delay long-term complications.
    • Diabetes management is team-based: nutrition therapy, pharmacologic therapy, exercise, and self-monitoring of glucose.

Drug therapy and insulin management

  • Insulin therapy (summary)

    • Exogenous insulin is injected or delivered via pump.
    • Required for all people with Type 1; may be required for Type 2 during stress or progression of disease.
    • Insulin preparations vary by onset, peak, and duration; categorized as rapid-acting, short-acting, intermediate-acting, and long-acting.

  • Insulin physiology and pharmacology (key points)

    • Human insulin is produced via recombinant technology; pharmacologic profiles differ by preparation.
    • Insulin regimens aim to mimic physiologic insulin production: basal (background) and bolus (mealtime).
    • Insulin also facilitates release from liver stores, uptake into muscle/adipose, and storage as glycogen; suppresses gluconeogenesis, promotes protein synthesis, and fat storage.
    • Some tissues require insulin for glucose transport (skeletal muscle and adipose tissue); liver is insulin-responsive but also has unique uptake/production dynamics.

  • Insulin preparations (examples)

    • Rapid-acting: lispro (Humalog), aspart (NovoLog), glulisine (Apidra).
    • Short-acting: Regular (Humulin R, Novolin R).
    • Intermediate-acting: NPH (Humulin N, Novolin N).
    • Long-acting: glargine (Lantus, Toujeo, Basaglar), detemir (Levemir).
    • Inhaled insulin: Afrezza (rapid-acting).
    • Insulin analogs differ in onset/peak/duration; diagrams illustrate schedules across 24 hours.

  • Insulin plans (basal-bolus regimen)

    • Intensive physiologic therapy: multiple daily injections or insulin pump with frequent glucose monitoring.
    • Bolus insulin: rapid- or short-acting before meals.
    • Basal insulin: intermediate- or long-acting, once or twice daily.
    • Goal: maintain near-normal glucose levels as much of the time as possible.
    • Planning factors include target glucose, lifestyle, meals, and activity; less intensive plans may suit some individuals.

  • Mealtime (bolus) insulin

    • Rapid-acting bolus: onset ~15 minutes; injected within 15 minutes of meals.
    • Short-acting bolus: onset ~30–60 minutes; injected 30–45 minutes before meals; higher risk of hypoglycemia.

  • Basal insulin (long-acting and intermediate-acting)

    • Long-acting: degludec, detemir, glargine; released steadily with no pronounced peak for many people; typically once or twice daily.
    • Do not mix long-acting with other insulins in the same syringe.
    • Intermediate-acting (NPH): duration ~12–18 hours; peak 4–12 hours; can mix with short-/rapid-acting; not given IV.

  • Combination insulin therapy

    • Can mix short-/rapid-acting with intermediate-acting in one syringe to provide both mealtime and basal coverage.
    • Available as premixed formulations or pens; self-mixing from two vials is possible.
    • Consider patient abilities for drawing up and managing two types in one syringe.

  • Inhaled insulin (Afrezza)

    • Rapid-acting inhaled insulin; taken at the beginning of meals or within 20 minutes after starting a meal.
    • Used in combination with long-acting insulin for Type 1 DM.
    • Adverse effects: hypoglycemia, cough, throat irritation; not recommended for DKA treatment, smokers, asthma or COPD due to bronchospasm risk.

  • Storage and administration

    • Insulin storage: extreme temperatures reduce effectiveness; avoid
    • Vials/pens can be stored at room temperature up to 4 weeks; unopened pens refrigerated.
    • Do not expose to direct sunlight; use a thermos in hot climates.
    • Prefilled syringes upright; 1 week for two insulin types, 30 days for one type.
    • Administration: subcutaneous injection; regular insulin can be given IV; not orally due to gastric inactivation.
    • Absorption fastest from the abdomen, then arm, thigh, then buttock; rotate sites within and between sites; avoid injection into exercised muscles.
    • Injection technique details: U100 insulin (1 mL contains 100 U); syringes marked in 1 U increments for 0.3/0.5 mL and 2 U increments for 1 mL syringes; needle sizes vary (6 mm, 8 mm, 12.7 mm).
    • Injection angle: typically 90°, but 45° for very lean patients.

  • Insulin devices

    • Self-injection: patient administers; proper hygiene and site cleansing.
    • Insulin pens: convenient, portable, suitable for vision-impaired patients; printed instructions.
    • Insulin pumps: continuous subcutaneous infusion of rapid-acting insulin; catheter in abdominal wall; some are tubing-free; program basal and bolus doses; requires CGM and frequent glucose checks (4–8x/day or CGM).
    • Major advantages: tighter glucose control; more flexible with meals and activity.
    • Potential concerns: infection at site, risk of DKA, cost, device burden.

  • Insulin therapy problems

    • Hypoglycemia; allergic reactions (local/systemic); lipodystrophy (atrophy or hypertrophy at injection sites) with absorption changes.
    • Somogyi effect: nocturnal hyperglycemia due to excess insulin and counterregulatory hormone response; check 2–4 AM glucose; adjust bedtime snack or insulin dose.
    • Dawn phenomenon: early morning hyperglycemia due to predawn counterregulatory hormones (growth hormone, cortisol); may require increasing insulin or adjusting timing.

  • Drug therapy: oral and noninsulin injectables (Type 2 DM)

    • Aim to improve mechanisms by which body makes/uses insulin and glucose; target 3 defects: insulin resistance, decreased insulin production, increased hepatic glucose production.
    • Drug classes and mechanisms (illustrative mappings):
    • Sulfonylureas and meglitinides: increase insulin production from pancreas.
    • DPP-4 inhibitors and GLP-1 receptor agonists: incretin-based therapy to enhance insulin secretion and suppress hepatic glucose production; affect glucagon and gastric emptying; GLP-1 agonists often reduce appetite.
    • Biguanides (metformin) and thiazolidinediones: improve insulin sensitivity and glucose uptake; influence hepatic glucose production.
    • SGLT2 inhibitors: block renal glucose reabsorption, increasing urinary glucose excretion.
    • α-Glucosidase inhibitors: delay carbohydrate absorption in the small intestine.
    • Dopamine receptor agonist (bromocriptine): may improve glucose control via unknown mechanism related to dopamine signaling.
    • Amylin analogs (pramlintide): adjunct to mealtime insulin to slow gastric emptying and suppress glucagon; cannot be mixed in the same syringe as insulin; dosing considerations around meals.
    • Examples of agents by class include:
    • Metformin (Biguanide): first-line for Type 2; reduces hepatic glucose production and improves insulin sensitivity; may cause weight loss; contraindicated with renal/liver/cardiac disease and lactic acidosis risk with renal impairment; hold around contrast imaging procedures.
    • Sulfonylureas: Glipizide, Glyburide, Glimepiride; increase insulin production; risk of hypoglycemia.
    • Meglitinides: Repaglinide, Nateglinide; rapid onset; lower hypoglycemia risk.
    • α-Glucosidase inhibitors: Acarbose, Miglitol; delay carb absorption; dosing with first bite.
    • TZDs: Pioglitazone, Rosiglitazone; improve insulin sensitivity; limited use due to adverse effects.
    • DPP-4 inhibitors: Alogliptin, Sitagliptin, Saxagliptin; enhance incretin effect.
    • SGLT2 inhibitors: Canagliflozin, Dapagliflozin, Empagliflozin; promote glycosuria.
    • GLP-1 receptor agonists: Albiglutide, Dulaglutide, Exenatide, Liraglutide, Semaglutide, etc.; subcutaneous injections; may be used as monotherapy or adjunct.
    • Amylin analogs: Pramlintide; used with mealtime insulin; requires separate administration.

  • Nutrition Therapy

    • Individualized plans with counseling, education, and ongoing monitoring; consider behavioral, cognitive, socioeconomic, cultural, religious factors.
    • ADA guidelines emphasize that people with DM can eat the same foods as those without DM; goal to achieve safe glucose, lipid, and blood pressure targets while maintaining eating pleasure.
    • Type 1 diabetes meal planning: match intake with insulin and exercise; day-to-day consistency aids glucose control; rapid-acting insulin, MDI, or pump offer flexibility based on carbohydrate content.
    • Type 2 diabetes emphasis: weight loss (5–7%), nutritionally adequate plans, reduced saturated/trans fats, and balanced carbohydrate intake; spacing meals and regular exercise; monitor via glucose, A1C, lipids, and BP.
    • Carbohydrates: primary energy source and fiber source; individualized carbohydrate amounts; include fruits, vegetables, whole grains, low-fat dairy; fiber-rich choices; 14 g of carbohydrate per 100 kcal; nutritive and nonnutritive sweeteners in moderation.
    • Fats: ADA recommends 20–35% of daily calories from fat; emphasize healthy fats from plants (olives, nuts, avocados).
    • Protein: individualized intake; aim for lean proteins; similar guidelines to non-diabetics with normal renal function.
    • Alcohol: inhibits hepatic gluconeogenesis and can cause hypoglycemia; advise carbohydrate-containing drinks and moderation (women: up to 1 drink/day; men: up to 2 drinks/day).
    • Patient teaching: carbohydrate counting basics—1 serving equals 15 g of CHO; typical meal plan 45–60 g CHO per meal; insulin dose can be adjusted per grams of CHO consumed (e.g., 1 U per 15 g CHO).
    • Involve family/caregivers in education; tailor choices to patient preferences and culture; promote self-care skills and independence.

  • Exercise

    • Regular, continuous exercise is essential; ADA recommends ≥150\text{ minutes/week} of moderate-intensity aerobic activity plus resistance training 3×/week.
    • Benefits: reduces insulin resistance, aids weight loss, may reduce medication needs (Type 2), improves triglycerides/LDL/HDL, lowers BP, enhances circulation.
    • Medical clearance recommended; start slow and progress.
    • Exercise plus glucose-lowering meds (e.g., insulin, sulfonylureas, or meglitinides) may cause hypoglycemia; sedentary activity increases hypoglycemia risk when activity increases.
    • Glucose-lowering effect may persist up to 48 hours after exercise; plan with a meal 1 hour after exercise or a 10–15 g CHO snack; test glucose before and during activity; have a snack every 30 minutes if risk of hypoglycemia.

  • Monitoring blood glucose (BGM)

    • Frequency depends on goals, DM type, drug plan, self-management capability, and access to supplies.
    • Type 1 or on intensive insulin therapy: typically 4–8 checks per day; others as needed.
    • Tools: portable glucose meters (finger-stick) and continuous glucose monitoring (CGM) systems; CGMs help identify patterns and increase time in range; insurance coverage and cost can limit access.
    • Patient/caregiver education on testing times: before meals, 2 hours after first bite, during suspected hypoglycemia, every 4 hours during illness, before and after exercise; adapt for vision/cognition/dexterity with adaptive devices.

  • Pancreas and islet transplantation

    • Pancreas transplantation considered for Type 1 DM with end-stage renal disease (ESRD) and plan for kidney transplant; criteria include frequent, severe metabolic complications and poor control with exogenous insulin.
    • Successful transplantation can improve quality of life, eliminate the need for insulin and frequent BGM, and reduce acute complications; lifelong immunosuppression required; long-term renal/neural complications may persist.
    • Islet cell transplantation is experimental in the U.S.; donor islet cells infused into portal vein to liver; less invasive but still evolving.

Nursing and clinical management

  • Nursing assessment (subjective data)

    • Past health history: infections, trauma, stress, pregnancy, chronic pancreatitis, Cushing syndrome, acromegaly; family history.
    • Medications: insulin, oral agents, corticosteroids, diuretics, phenytoin.
    • Functional health patterns: health management, nutrition/metabolic, elimination, etc.

  • Nursing assessment (objective data)

    • Eyes: soft sunken eyes, vitreal hemorrhages, cataracts.
    • Integumentary: dry, warm skin; acanthosis nigricans; ulcers.
    • Respiratory: Kussmaul respiration (DKA).
    • Cardiovascular: hypotension, tachycardia.
    • GI: dry mouth, vomiting, fruity breath.
    • Neurologic: altered mental status; restlessness; confusion; coma.
    • Musculoskeletal: muscle wasting.
    • Diagnostic findings: electrolyte abnormalities; fasting glucose ≥126 mg/dL; OGTT or random glucose criteria; leukocytosis; elevated BUN/creatinine; dyslipidemia; albuminuria; acidosis in DKA.

  • Acute care and illness management

    • Acute complications include hypoglycemia, DKA, and Hyperosmolar Hyperglycemic Syndrome (HHS).
    • Illness and surgery can elevate glucose; check glucose every 4 hours during illness; monitor for ketones when glucose >240 mg/dL; Type 2 diabetics may require temporary insulin during illness.
    • Intraoperative and ambulatory care considerations include IV fluids, insulin management, and ongoing monitoring.
    • Ambulatory care: emphasize hygiene, foot care, proper footwear, wound care, and prompt reporting of wounds.
    • Medical identification and travel planning: carry ID, plan for supplies, inform HCP, be mindful of travel-related changes and time-zone adjustments.

  • Acute complications: detailed overview

    • Hypoglycemia
    • Definition: blood glucose < 70\text{ mg/dL}; neuroendocrine response with epinephrine release; autonomic symptoms.
    • Common symptoms: shakiness, palpitations, nervousness, sweating, anxiety, hunger, pallor.
    • Neuroglycopenia: altered mental function (slurred speech, confusion, coma).
    • Hypoglycemia awareness may be reduced; higher risk in autonomic neuropathy.
    • Causes: excessive insulin/medication, insufficient food, delayed meals, or excessive exercise.
    • Management: rule of 15—consume 15 g of fast-acting carbohydrate, recheck in 15 minutes, repeat if still <70 mg/dL; if stable, provide a meal with protein; avoid high-fat foods that slow absorption.
    • Acute care treatment: 50% dextrose 20–50 mL IV push; if no IV access or cannot swallow, administer 1 mg glucagon IM or subcutaneously; monitor for nausea and aspiration.
    • DKA
    • Etiology: profound insulin deficiency; hyperglycemia; ketosis; acidosis; dehydration; most common in Type 1; may occur in Type 2 with severe illness.
    • Precipitating factors: illness, infection, insufficient insulin, undiagnosed Type 1, educational gaps, neglect.
    • Pathophysiology: insulin deficiency drives lipolysis and ketogenesis; osmotic diuresis causes dehydration; acidosis from ketone accumulation; electrolyte disturbances (Na, K, Cl, Mg, phosphate).
    • Clinical manifestations: polyuria, polydipsia, weight loss, vomiting, abdominal pain, Kussmaul respirations, fruity breath, glucose often ≥ 250\text{ mg/dL}, bicarbonate < 16\ \text{mEq/L}, pH < 7.30, ketonuria/ketonemia.
    • Interprofessional care: IV fluids (NaCl 0.45% or 0.9%), insulin drip after potassium is monitored/replaced (to avoid hypokalemia); goal gradual glucose reduction (≈ 36\text{ to }54\ \text{mg/dL per hour}).
    • Hyperosmolar Hyperglycemic Syndrome (HHS)
    • Life-threatening syndrome more common in Type 2 DM and older adults (often >60 years).
    • Features: despite some insulin, severe hyperglycemia (>600 mg/dL), osmotic diuresis, severe extracellular fluid depletion; minimal ketosis.
    • Common triggers: infections, acute illness, inadequate fluid intake, impaired thirst or cognitive impairment.
    • Management: aggressive IV fluids and insulin; monitor osmolality, electrolytes; add dextrose when glucose ~250 mg/dL; correct precipitating cause.

  • Chronic complications of diabetes

    • Angiopathy (macrovascular and microvascular complications) due to chronic hyperglycemia; leading cause of diabetes-related death.
    • Macrovascular complications: cerebrovascular disease, cardiovascular disease, peripheral vascular disease; higher risk in women and men compared with non-diabetics; management includes obesity control, smoking cessation, blood pressure control, lipid management (statins), and increased physical activity.
    • Microvascular complications: thickening of vessel membranes in capillaries and arterioles; primarily affects eyes (retinopathy), kidneys (nephropathy), and nerves (neuropathy).
    • Retinopathy: leading cause of new adult blindness; classified as nonproliferative or proliferative; annual dilated eye exams recommended; maintain glucose and BP control to prevent progression.
    • Nephropathy: damage to renal glomeruli; leading cause of ESRD in the U.S.; screening includes albuminuria and albumin-to-creatinine ratio; ACE inhibitors or ARBs delay progression; control of BP and glucose is essential.
    • Neuropathy: affects 60–70% of people with diabetes; sensory neuropathy (stocking-glove pattern) is most common; autonomic neuropathy can affect many systems, including GI and cardiovascular.
    • Sensory neuropathy: distal symmetric polyneuropathy; symptoms include loss of sensation, paresthesias, and burning pain; risk of foot ulcers due to loss of protective sensation (LOPS).
    • Autonomic neuropathy: can cause hypoglycemic unawareness, bowel incontinence/diarrhea, urinary retention, gastroparesis (delayed gastric emptying), cardiovascular autonomic changes, and sexual dysfunction.
    • Foot and lower-extremity complications: neuropathy and PAD increase risk of ulcers and infection; foot care education is essential (proper footwear, daily foot inspection, prompt wound treatment, neuropathic arthropathy/Charcot joints).
    • Skin complications: diabetic dermopathy, acanthosis nigricans, necrobiosis lipoidica diabeticorum.
    • Infections: immune defects lead to recurrent infections and poor wound healing; emphasize hand hygiene and vaccination (flu, pneumococcal).
    • Gerontologic considerations: higher prevalence and mortality in people over 65; more comorbidities and polypharmacy; hypoglycemia risk increases; adapt education and management to cognitive and functional status.

  • Practical implications and takeaways

    • Glycemic targets and management are individualized; common target range includes A1C goals around <7%, with some aiming for <6.5% depending on patient factors.
    • Early and ongoing education for patients and caregivers is critical for insulin administration, monitoring, diet, and exercise.
    • Regular screening for complications (retinopathy, nephropathy, neuropathy) is essential to prevent progression.
    • Interprofessional collaboration (nurses, dietitians, pharmacists, primary care, endocrinologists, educators) optimizes outcomes.

  • Quick reference values and guidelines (highlights)

    • Daily insulin secretion in healthy adults: 40\text{ to }50\ \mathrm{U} per day.
    • Normal fasting glucose range: 74\text{ to }106\ \mathrm{mg/dL}.
    • A1C diagnostic threshold: A1C\geq 6.5\%.
    • FPG diagnostic threshold: FPG>126\ \mathrm{mg/dL}.
    • 2-h OGTT diagnostic threshold: \text{OGTT}_{2h}>200\ \mathrm{mg/dL}.
    • Random glucose diagnostic threshold: \text{random glucose}>200\ \mathrm{mg/dL}.
    • A1C target (typical): A1C<7\% (range often discussed as 6.5\% \text{ to } 7\% depending on patient factors).
    • Alcohol and meals: limit to moderate intake; carbohydrate counting often uses 15 g CHO per serving.
    • Exercise: at least 150\text{ minutes/week} of moderate aerobic activity plus resistance training 3×/week.

  • Ethical, philosophical, and practical implications

    • Emphasis on patient autonomy and culturally sensitive care; nutrition and activity plans must respect individual preferences and beliefs while achieving health goals.
    • Access to technology (CGM, insulin pumps) and medications can be unequal; ethical considerations include equity in treatment options and education.
    • Long-term chronic disease management requires ongoing patient engagement, support systems, and health literacy enhancements.

  • Connections to foundational principles

    • Diabetes management integrates endocrine physiology (insulin, counterregulatory hormones, glucose metabolism) with nutrition, exercise science, pharmacology, and patient education.
    • The ABCs of diabetes (A1C, Blood pressure, Cholesterol) reflect a systems-based approach to reducing cardiovascular risk and long-term complications.

  • Equations and key formulas (LaTeX)

    • Diabetes diagnostic criteria:
    • A1C \ge 6.5\%
    • FPG > 126\ \text{mg/dL}
    • \text{OGTT}_{2h} > 200\ \text{mg/dL}
    • \text{random glucose} > 200\ \text{mg/dL}
    • Normal glucose range: 74 \le \text{glucose} \le 106\ \mathrm{mg/dL}
    • Daily endogenous insulin secretion: \text{Insulin}_{\text{endogenous}} \approx 40\text{ to }50\ \mathrm{U/day}
    • Mealtime CHO counting: 1 serving CHO = 15\ \mathrm{g} of carbohydrate
    • DKA treatment glucose targets: gradual reduction to avoid large shifts; insulin infusions aim for about 36\text{ to }54\ \mathrm{mg/dL}/\text{hr} decrease in serum glucose to prevent complications

  • Note

    • This study guide reflects content from the provided transcript (Chapter 53: Diabetes) and is designed to be a comprehensive, exam-focused set of notes in a structured bullet-point format.