Module 7 Diabetes

Diabetes Mellitus

A chronic disorder of impaired carbohydrate, protein, and lipid metabolism caused by an absolute or relative deficiency of insulin, resulting in hyperglycemia

Type 1 Diabetes Mellitus

Nearly absolute deficiency of insulin due to primary beta cell destruction; without insulin, fat is metabolized for energy, resulting in ketonemia (acidosis)

Type 2 Diabetes Mellitus

Relative lack of insulin or resistance to insulin action; insulin is sufficient to stabilize fat and protein metabolism but not carbohydrate metabolism

Metabolic Syndrome

Coexisting risk factors for developing Type 2 DM, including abdominal obesity, hyperglycemia, hypertension, high triglycerides, and low HDL

Polyuria, Polydipsia, Polyphagia

The classic triad of diabetes symptoms (excessive urination, thirst, and hunger); more common in Type 1 DM

HbA1c

A lab test measuring average blood glucose over ~3 months; used alongside fasting glucose and OGTT to diagnose and monitor diabetes

Dawn Phenomenon

Morning hyperglycemia upon awakening caused by excessive release of growth hormone and cortisol in the early morning hours; more common in Type 1 DM; treated by increasing insulin dose or changing timing

Somogyi Effect

Normal/elevated glucose at bedtime → hypoglycemia around 2am → rebound hyperglycemia by 7am due to counterregulatory hormones; more common in Type 1 DM; treated by decreasing insulin dose and/or having a larger bedtime snack

Lipodystrophy

A fibrous mass that develops at an insulin injection site caused by repeated use of the same site

Insulin Pump

A device that delivers continuous subcutaneous insulin (basal rate) with the ability to self-administer bolus doses; needle/catheter changed every 2–3 days; can hold up to a 3-day supply

Sulfonylureas

Oral hypoglycemics (e.g., Glipizide) that lower blood glucose by increasing insulin secretion from the pancreas

Meglitinides

Oral hypoglycemics (e.g., Repaglinide) that lower blood glucose by stimulating insulin secretion; similar mechanism to sulfonylureas

Thiazolidinediones

Oral hypoglycemics (e.g., Pioglitazone, Rosiglitazone) that lower blood glucose by improving insulin sensitivity

Biguanides (Metformin)

Oral hypoglycemic that lowers blood glucose by decreasing liver glucose output; must be held 48 hours before surgery and restarted only when renal function is normal

Alpha-Glucosidase Inhibitors

Oral hypoglycemics (e.g., Acarbose, Miglitol) that lower blood glucose by delaying intestinal glucose absorption

GLP-1 Receptor Agonists

Oral/injectable hypoglycemics (e.g., Semaglutide, Liraglutide) that lower blood glucose by enhancing incretin activity

DPP-4 Inhibitors

Oral hypoglycemics (e.g., Sitagliptin) that lower blood glucose by enhancing incretin activity

SGLT-2 Inhibitors

Oral hypoglycemics (e.g., Canagliflozin, Dapagliflozin) that lower blood glucose by promoting renal glucose excretion independent of insulin; the only oral hypoglycemic NOT contraindicated in Type 1 DM

Hypoglycemia

Blood glucose

Hypoglycemia – Mild (54–70 mg/dL)

Symptoms include shakiness, sweating, hunger, irritability, and mild confusion

Hypoglycemia – Moderate (

Symptoms include increased heart rate, headache, pronounced confusion, difficulty concentrating, and blurred vision

Hypoglycemia – Severe (

Symptoms include severe confusion, inability to perform routine tasks, seizures, loss of consciousness, and potentially coma

Hypoglycemia Unawareness

Condition where warning signs of hypoglycemia are not evident until blood glucose is dangerously low; seen in frequent hypoglycemia episodes, older patients, or those on beta-adrenergic blockers

The 15/15 Rule

If blood glucose is

Glucagon

Hormone secreted by pancreatic alpha cells that raises blood glucose; used to treat insulin-induced hypoglycemia; given SC, IM, or IV; takes effect within 5–20 minutes

Altered LOC Hypoglycemia Treatment

First-line therapy is injectable glucagon or 50% dextrose IV (not oral carbohydrates, as the patient cannot swallow safely)

Diabetic Ketoacidosis (DKA)

A life-threatening complication of Type 1 DM caused by severe insulin deficiency; characterized by glucose >300 mg/dL, positive urine ketones, elevated K+ with acidosis, and ABG showing acidosis

DKA – Key Labs

Glucose >300 mg/dL, creatinine >1.5 mg/dL, positive urine ketones, elevated potassium, ABG shows acidosis

DKA Treatment

Restore blood volume with rapid IV NS or ½NS (with dextrose added); IV short-acting insulin; monitor and correct potassium imbalances; cardiac monitoring if indicated

IV Insulin for DKA

Short-acting insulin only; a bolus dose may precede continuous infusion; infused continuously until SC administration resumes to prevent rebound hyperglycemia; watch for potassium drop within first hour

Hyperosmolar Hyperglycemic Syndrome (HHS)

Extreme hyperglycemia (glucose >800 mg/dL) without ketosis or acidosis; occurs more often in Type 2 DM; gradual onset; enough insulin present to prevent fat breakdown = no ketosis

HHS vs DKA Key Difference

HHS has no ketosis or acidosis (ABG normal, urine ketones negative); DKA has ketosis and acidosis; HHS glucose is typically much higher (>800 mg/dL vs >300 mg/dL in DKA)

HHS Treatment

Fluid and electrolyte repletion (similar to DKA); insulin is less critical since there is no ketosis or acidosis

Diabetic Retinopathy

Chronic, progressive impairment of retinal circulation leading to rupture of microaneurysms in retinal blood vessels; can cause permanent vision changes, retinal detachment, and cataracts

Diabetic Retinopathy Interventions

HTN management and tight glucose control for prevention; laser therapy for hemorrhagic tissue; vitrectomy for vitreous hemorrhages; cataract removal with lens implant

Diabetic Nephropathy

Progressive decline in kidney function from diabetes; signs include microalbuminuria, fatigue, anemia, frequent UTIs, and neurogenic bladder

Diabetic Nephropathy Interventions

HTN and glucose management; monitor BUN, creatinine, urine albumin; restrict dietary protein, sodium, and potassium; avoid nephrotoxic medications; prepare for dialysis or transplant as indicated

Diabetic Neuropathy

A generalized deterioration of the nervous system; classified as focal, sensory/peripheral, or autonomic (cardiovascular, pupillary, gastric, urinary, skin, adrenal, reproductive)

Autonomic Neuropathy – Cardiovascular

Cardiac denervation syndrome and orthostatic hypotension (OH) due to loss of autonomic regulation

Autonomic Neuropathy – Adrenal

Results in hypoglycemic unawareness due to impaired adrenal response to low blood glucose

Diabetic Neuropathy Pain Management

Anti-seizure drugs (pregabalin, gabapentin) and antidepressants (duloxetine); topical capsaicin or lidocaine patches; non-pharmacological: TENS, acupuncture, CBT

Diabetic Foot Care

Daily inspection for sores, cuts, or infections; proper well-fitting footwear; regular podiatry visits; essential due to decreased sensation and impaired wound healing

Exercise Contraindication in Diabetes

Do NOT exercise if blood glucose is >250 mg/dL AND urinary ketones are present (Type 1 DM) — risk of worsening ketoacidosis

Insulin Injection Site and Exercise

Do not inject insulin into an area that will be exercised, as exercise increases the rate of insulin absorption

Diabetes and Preoperative Care

Hold oral hypoglycemics 24–48 hours before surgery; hold Metformin 48 hours prior; hold other diabetes management on day of surgery; monitor blood glucose

Diabetes and Postoperative Care

Administer short-acting insulin based on blood glucose levels; monitor glucose frequently (especially with parenteral nutrition); risk for impaired wound healing

Carbohydrate Counting

A simple dietary strategy for diabetes management that helps control blood glucose by tracking carbohydrate intake; easy to comply with