PANCE Blueprint Endocrinology (7%)

Diabetes Mellitus (PEARLS)


NCCPA™ PANCE Endocrine System Blueprint diabetes mellitus type I and type II (PEARLS)

Diabetes mellitus type 1 Etiology: Autoimmune- HLA-DR3/4/O antibodies. Islet cell antibodies

Presentation of Type I DM:

  • Children
  • Polyuria, polydipsia, polyphagia, fatigue, and weight loss
  • Often first recognized as diabetic ketoacidosis:
    • Symptoms: Fruity breath, nausea, vomiting, dehydration
    • Treatment: IV regular insulin

Treatment of Type I DM: Insulin

Dawn Phenomenon: Normal glucose until 2-8 am when it rises. Results from decreased insulin sensitivity and a nightly surge of counter-regulatory hormones during nighttime fasting

  • Treat with bedtime injection of NPH to blunt morning hyperglycemia, avoiding carbohydrate snack late at night

Somogyi effect: Nocturnal hypoglycemia followed by rebound hyperglycemia due to a surge in growth hormone

  • Treat with decreased nighttime NPH dose or give bedtime snack

Insulin waning: a progressive rise in glucose from bedtime to morning

  • Treat with a change of insulin dose to bedtime

DKA: Fruity breath, weight loss, rapid respirations, hypotension

  • Diabetic ketoacidosis (DKA) should always be handled in a hospitalized setting, usually an intensive care unit, and often with an endocrinologist’s consultation, if appropriate.
  • TREAT WITH FLUIDS! Patients with DKA are always dehydrated and need large-volume IV fluid resuscitation, usually isotonic fluids such as normal saline. If corrected serum sodium level is high, this can be reduced to half-normal saline. Insulin should always be administered by an IV pump to guard against accidental overdose.

Diagnosis of DM is made by one of the following:

  • Random blood glucose level of > 200 mg/dL + diabetic symptoms
  • 2 separate fasting (8 hours) glucose levels of > 126 mg/dL
  • 2-hour plasma glucose of > 200 on an oral glucose tolerance test (3-hour GTT is the gold standard in GDM)
  • Hemoglobin A1c of > 6.5%

Insulin and C-peptide levels –  low or inappropriately normal fasting C-peptide and insulin levels with concomitant hyperglycemia

  • High fasting insulin and C-peptide levels suggest T2DM

Insulin, GAD65, and IA-2 antibodies -  If one or more of the antibodies is present, and especially if two or more are positive, the patient should be presumed to have type 1 diabetes and should be treated with insulin replacement therapy

Monitoring/evaluation of glycemic control

  • Hemoglobin A1c
    • represents mean glucose level from previous 8-12 weeks (approx lifespan of an RBC)
    • useful to gauge the 'big-picture' overall efficacy of glucose control in patients (either Type 1 or Type 2) to assess the need for changes in medication/insulin levels
    • Treatment goal of A1c < 7.0%
  • "finger-stick" blood glucose monitoring
    • useful for insulin-dependent (either type 1 or 2) diabetics to monitor their glucose control and adjust insulin doses according to variations in diet or activity
    • Treatment goals: < 130 mg/dL fasting and < 180 mg/dL peak postprandial 
Diabetes Mellitus Type 2 Diagnosis: random glucose > 200 x 2 or fasting glucose > 126 x 2

Diabetes Medications:

Metformin - decreases hepatic glucose production and peripheral glucose utilization, decreases intestinal glucose absorption (these are reasons it leads to weight loss)

  • Side effects: Lactic acidosis, GI side effects, initiation is contraindicated with eGFR <30 mL/min and not recommended with eGFR 30 to 45 mL/min, discontinue 24 hours before contrast and resume 48 hours after with monitoring for creatinine, stop if creatinine is > 1.5
  • Benefits: Weight loss, inexpensive

Sulfonylureas - stimulates pancreatic beta cell insulin release (insulin secretagogue)

  • Glyburide (Diabeta), glipizide (Glucotrol), glimepiride (Amaryl)
  • Side effects: Hypoglycemia
  • Benefits: cheap, rapidly effective

Thiazolidinediones - increases insulin sensitivity in peripheral receptor site adipose and muscle has no effect on pancreatic beta cells

  • Pioglitazone (Actos), Rosiglitazone (Avandia)
  • Contraindications: CHF, liver disease, fluid retention, weight gain, bladder cancer (pioglitazone), potential increase in MI (rosiglitazone)

Alpha-glucosidase inhibitors - Delays intestinal glucose absorption

  • Acarbose (Precose), miglitol (Glyset)
  • GI side effects, three times a day dosing

Meglitinides - stimulates pancreatic beta-cell insulin release

  • Repaglinide (Prandin) and Nateglinide (Starlix)
  • Side effects: May cause hypoglycemia

GLP-1 Agonists - lowers blood sugar by mimicking incretin - causes insulin secretion and decreased glucagon and delays gastric emptying

  • Exenatide (Bydureon, Byetta), dulaglutide (Trulicity), semaglutide (Ozempic), liraglutide (Victoza, Saxenda)
  • Side effects: Requires injection, frequent GI side effects, caution if gastroparesis
  • Benefits: Weight loss, reduced CV mortality (semaglutide, liraglutide) in patients with CVD

DPP-4 Inhibitors - dipetpidylpetase inhibition - inhibits degradation of GLP-1 so more circulating GLP-1

  • Sitagliptin (Januvia), Saxagliptin (Onglyza)
  • Side effects: expensive, possible increased risk of heart failure with saxagliptin

SGLT2 Inhibitor - SGLT2 inhibition lowers renal glucose threshold which results in increased urinary glucose excretion

  • Canagliflozin (Invokana or Sulisent)
  • Side effects: Vulvovaginal candidiasis, urinary tract infections, bone fractures, lower limb amputations, acute kidney injury, DKA, long-term safety not established
  • Benefits: Weight loss , reduction in systolic blood pressure, reduced cardiovascular mortality in patients with established CVD

Insulin – add if HbA1C > 9

Follow Up: Annual- ophthalmologist visit, urine microalbumin

Complications – neuropathy (most common), retinopathy (leading cause of blindness), nephropathy

Normal fasting glucose is between 70 and 100

Diagnosis of DM is made by one of the following:

  • Random blood glucose level of > 200 mg/dL AND diabetic symptoms
  • 2 separate fasting (8 hours) glucose levels of > 126 mg/dL
  • 2-hour plasma glucose of > 200 on an oral glucose tolerance test (3-hour GTT is the gold standard in GDM)
  • Hemoglobin A1c of > 6.5%

Diagnostic criteria for prediabetes

  • A1C 5.7 - 6.4
  • Fasting glucose 100 - 125
  • 2-hour oral glucose tolerance test 140-199

Glucose goals and basic management

  • A1C < 7.0 % check every 3 months if not controlled and 2x per year if controlled
  • Preprandial glucose 80-110 (60-90 if pregnant)
  • Postprandial blood glucose goal (1.5 - 2 hours after meal) is < 140
  • Annual dilated eye exams, ACEI if microalbuminuria, annual foot examination
  • Blood pressure should be maintained at < 130/80
  • New statin guidelines: recommend statins in persons with diabetes mellitus who are 40 to 75 years of age with LDL-C levels of 70 to 189 mg per dL but without clinical ASCVD (see guidelines)
Picmonic Picmonic
IM_DawnPhenomenon_V1.5_ The dawn phenomenon is the presence of hyperglycemia upon awakening. The increase in blood glucose is caused by increased hormone production in the early morning hours. Between the hours 2AM-6AM, the body naturally increases production of growth hormone and cortisol. Treatment involves changing the patient's current insulin regimen. The patient may have their current administration times changed, be given a long-acting insulin in the evening, or be given an insulin pump. Since insulin affects blood glucose levels, the patient's glucose levels should be closely monitored particularly between 2AM-6AM. Instruct the patient to limit carbohydrates before bedtime to avoid spikes in blood sugar during the night.

Dawn Phenomenon Picmonic

IM_MED_DKAS&S_v1.3_ Diabetic ketoacidosis (DKA) is a medical emergency and complication of diabetes. Patients have increased insulin requirements, which leads to a shortage. As a response, the body begins burning excess fat (and fatty acids), causing ketone body buildup. Lab values seen in DKA include blood sugars above 250 mg/dL, and anion gap metabolic acidosis with pH below 7.3 and bicarbonate below 18. Patients will also show present plasma ketones. Due to an extracellular shift, patients may be hyperkalemic.

_DM_Diabetic_Glomerulonephropathy_v1.6_ Diabetic glomerulonephropathy is the kidney disease seen in patients with significantly progressed diabetes. There is damage to the kidney due to nonenzymatic glycosylation of the basement membrane which alters the permeability of arterioles and glomeruli and results in nephrotic syndrome. Patients will have increased GFR due to preferential efferent sclerosis, mesangial expansion due to hyperfiltration pressure, and will ultimately enter kidney failure if glucose levels are not controlled.

Diabetic Glomerulonephropathy Picmonic

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