NCCPA™ PANCE Endocrine System Blueprint diabetes mellitus type I and type II (PEARLS)
Diabetes mellitus type 1 | Patient will present as → a young patient with weight loss, increased thirst, and urination. The patient has felt tired and nauseous. On examination her weight is below the 5th percentile, she looks thin, and her skin is pale. her blood pressure is 100/70 and her pulse is 104 bpm. Her respirations are deep at a rate of 28 breaths/minute. Her breath smells fruity Etiology: Autoimmune- HLA-DR3/4/O antibodies. Islet cell antibodies Presentation of Type I DM:
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
Somogyi effect: Nocturnal hypoglycemia followed by rebound hyperglycemia due to a surge in growth hormone
Check 3 am blood sugar!
Insulin waning: a progressive rise in glucose from bedtime to morning DKA: Fruity breath, weight loss, rapid respirations, hypotension
Diagnosis of DM is made by one of the following:
Insulin and C-peptide levels – low or inappropriately normal fasting C-peptide and insulin levels with concomitant hyperglycemia
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
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Diabetes Mellitus Type 2 | ReelDx Virtual Rounds (Diabetes Mellitus Type 2)Patient will present as → a 35-year-old Mexican American male complaining of increased thirst, frequent urination, hunger, fatigue, and blurred vision random finger stick blood glucose is 225. Diagnosis: random glucose > 200 x two or fasting glucose > 126 x two, A1c of > 6.5% Diabetes Medications: Metformin - decreases hepatic glucose production and peripheral glucose utilization, decreases intestinal glucose absorption (these are reasons it leads to weight loss)
Sulfonylureas - stimulates pancreatic beta-cell insulin release (insulin secretagogue)
Thiazolidinediones - increases insulin sensitivity in peripheral receptor site adipose and muscle has no effect on pancreatic beta cells
Alpha-glucosidase inhibitors - Delays intestinal glucose absorption
Meglitinides - stimulates pancreatic beta-cell insulin release
GLP-1 Agonists - lowers blood sugar by mimicking incretin - causes insulin secretion and decreased glucagon and delays gastric emptying
DPP-4 Inhibitors - dipetpidylpetase inhibition - inhibits degradation of GLP-1 so more circulating GLP-1
SGLT2 Inhibitor - SGLT2 inhibition lowers renal glucose threshold which results in increased urinary glucose excretion
Insulin – add if HbA1C > 9 Follow Up: Annual- ophthalmologist visit, urine microalbumin Complications – neuropathy (most common), retinopathy (the leading cause of blindness), nephropathy Normal fasting glucose is between 70 and 100 Diagnosis of DM is made by one of the following:
Diagnostic criteria for prediabetes
Glucose goals and basic management
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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.
Play Video + QuizDiabetic ketoacidosis (DKA)
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.
Diabetic Ketoacidosis (DKA) Treatment | Play Video + Quiz |
Diabetic Ketoacidosis (DKA) Signs and Symptoms | Play Video + Quiz |
Diabetic Ketoacidosis (DKA) Diagnosis and Labs | Play Video + Quiz |
Diabetic glomerulonephropathy
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.
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