Diabetes mellitus (Type 2): Clinical sciences

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Diabetes mellitus (Type 2): Clinical sciences

Endocrine Midterm

Endocrine Midterm

Pituitary gland histology
Pituitary apoplexy
Pituitary adenoma
Hypopituitarism: Pathology review
Anatomy of the diencephalon
Sheehan syndrome
Hypopituitarism
Kallmann syndrome
Hypoprolactinemia
Hyperprolactinemia
Pituitary tumors: Pathology review
Thyroid and parathyroid gland histology
Parathyroid disorders and calcium imbalance: Pathology review
Anatomy of the thyroid and parathyroid glands
DiGeorge syndrome
Parathyroid hormone
Hypoparathyroidism
Thymic aplasia
Hyperparathyroidism
Hyperparathyroidism: Clinical sciences
Approach to hypocalcemia: Clinical sciences
Hyperphosphatemia
Hypercalcemia
Bone remodeling and repair
Hypomagnesemia
Approach to hypocalcemia (pediatrics): Clinical sciences
Thyroid nodules and thyroid cancer: Pathology review
Thyroid cancer
Thyroid nodules: Clinical sciences
Thyroid carcinoma: Clinical sciences
Thyroid hormones
Thyroid eye disease (NORD)
Thyroid storm
Hashimoto thyroiditis
Postpartum thyroiditis
Riedel thyroiditis
Hashimoto thyroiditis: Clinical sciences
Subacute granulomatous thyroiditis
Anatomy clinical correlates: Viscera of the neck
Approach to hypothyroidism: Clinical sciences
Approach to hyperthyroidism and thyrotoxicosis: Clinical sciences
Hyperthyroidism: Pathology review
Euthyroid sick syndrome
Hypothyroidism: Pathology review
Hypothyroidism
Graves disease: Clinical Sciences
Hyperthyroidism medications
Hypothyroidism medications
Thyroglossal duct cyst
Pancreas histology
Pancreatic cancer
Pancreatitis: Pathology review
Chronic pancreatitis
Approach to pancreatic masses: Clinical sciences
Acute pancreatitis
Pancreatic secretion
Insulins
Insulin
Hypoglycemics: Insulin secretagogues
Pancreatic neuroendocrine neoplasms
Approach to hypoglycemia: Clinical sciences
Diabetes mellitus: Pathology review
Growth hormone deficiency
Diabetes mellitus
Hypokalemia
Diabetes mellitus (Type 1): Clinical sciences
Diabetic ketoacidosis: Clinical sciences
Diabetes mellitus (pediatrics): Clinical sciences
Diabetes in pregnancy (GDM, T1DM, and T2DM): Clinical sciences
Approach to hyperkalemia: Clinical sciences
Diabetes mellitus (Type 2): Clinical sciences
Approach to hypoglycemia (pediatrics): Clinical sciences
Hunger and satiety
Approach to diabetes in pregnancy: Clinical sciences
Glucagon
Growth hormone and somatostatin
Somatostatin
Managing diabetes during the holidays: Information for patients and families
Diabetes insipidus and SIADH: Pathology review
Diabetic nephropathy
Gestational diabetes
Chronic kidney disease: Clinical sciences
Obesity and metabolic syndrome: Clinical sciences
Dyslipidemia: Clinical sciences
Miscellaneous hypoglycemics
Adrenal hormone synthesis inhibitors
Adrenal gland histology
Adrenal insufficiency: Pathology review
Congenital adrenal hyperplasia
Adrenal insufficiency: Clinical sciences
Adrenal masses: Pathology review
Primary adrenal insufficiency
Cushing syndrome
Pheochromocytoma: Clinical sciences
Glucocorticoids
Mineralocorticoids and mineralocorticoid antagonists
Cortisol
Cushing syndrome and Cushing disease: Clinical sciences
Endocrine system anatomy and physiology
Cushing syndrome and Cushing disease: Pathology review
Multiple endocrine neoplasia
Multiple endocrine neoplasia: Pathology review
Multiple endocrine neoplasia: Clinical sciences
Prolactinoma
Potassium sparing diuretics
Polycystic ovary syndrome (PCOS): Clinical sciences
Conn syndrome

Decision-Making Tree

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Diabetes mellitus is a condition where glucose can’t be properly moved from the blood into the cells. Now, there are two types of diabetes mellitus, type 1 and type 2, and the main difference between them is the underlying mechanism. Type 2 diabetes mellitus is most commonly seen in patients with obesity, when peripheral tissue becomes resistant to insulin, which is also known as insulin resistance.

Since tissues don’t respond as well to normal insulin levels, beta cells in the pancreas ramp up their insulin production. In order to have the same effect on peripheral tissue and therefore move glucose out of the blood, and into tissue cells. Over time, beta cells become dysfunctional and can no longer secrete sufficient insulin, which eventually results in impaired insulin secretion and high blood glucose levels. This can cause clinical manifestations ranging from prediabetes, diabetes mellitus, to severe life-threatening conditions, like hyperosmolar hyperglycemic state or HHS and diabetic ketoacidosis or DKA.

Now, if you suspect type 2 diabetes mellitus, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If the patient is unstable, stabilize the airway, breathing, and circulation. This means that you might need to intubate the patient. Next, obtain IV access and, if your patient is hypotensive, start IV fluids for volume resuscitation. Finally, put your patient on continuous vital sign monitoring, such as pulse oximetry, blood pressure, and heart rate.

Next, you want to know if your unstable patient with type 2 diabetes has HHS or, less frequently, DKA. Obtain a focused history and physical exam, and order labs, such as random blood glucose, serum osmolality, BMP, urinalysis, hemoglobin A1c, as well as ABG or VBG. Your patient might be too obtunded or confused to speak, so be sure to review the chart thoroughly and speak with caretakers to get an accurate history. Some patients have a known history of diabetes, while others might not. Next, history might reveal fatigue and headaches, as well as polydipsia and polyuria. Additionally, they might have symptoms of a precipitating illness, such as fever, or a history of recent infection or disruption to their diabetes treatment plan. On the other hand, physical exam might reveal a confused, somnolent patient with tachypnea, tachycardia, or hypotension. The mucous membranes are often dry.

Next, in HHS, lab results typically reveal a significantly elevated random blood glucose, often exceeding 600 milligrams per deciliter, and a high serum osmolality, usually greater than 320 milliosmoles per liter. On the other hand, BMP may reveal electrolyte abnormalities, such as hyponatremia and hypokalemia, as well as elevated BUN and creatinine. Finally, there will be an elevated hemoglobin A1c. On the other hand, in DKA, lab results typically reveal a significantly elevated random blood glucose, typically lower than in HHS, but exceeding 250 milligrams per deciliter, and a normal serum osmolality. BMP may reveal electrolyte abnormalities, such as hyponatremia and hypokalemia, as well as elevated BUN and creatinine. Next, urinalysis could show mild ketones. Finally, there will be an elevated hemoglobin A1c, and the ABG or VBG may reveal elevated anion gap metabolic acidosis.

Now, if the patient has enough of these findings, you can diagnose HHS or DKA. Management of these individuals includes IV fluid resuscitation to correct dehydration and hyperosmolality, as well as electrolyte repletion. Additionally, you can start an IV insulin drip, if needed, and don’t forget to treat any underlying or precipitating causes!

Now that we're done with unstable patients, let’s go back to the ABCDE assessment and discuss the stable ones. If your patient is stable, first obtain a focused history and physical examination. History often reveals symptoms such as unintentional weight loss, polydipsia, polyuria, and blurred vision. Additionally, the patient might report risk factors like a sedentary lifestyle with low physical activity, age greater than 45, a family history of type 2 diabetes mellitus, or a history of gestational diabetes.

Sometimes, the only symptom a patient might report is numbness or tingling of their extremities, indicating peripheral neuropathy. The physical exam typically reveals obesity, acanthosis nigricans, and diminished sensation to pinprick in the distal extremities. In addition, if you use a thin filament to press the sole, the patient might report decreased sensation. This is referred to as abnormal monofilament testing. At this point, you should suspect type 2 diabetes mellitus, and proceed with labs, such as hemoglobin A1c, a random blood glucose, a fasting blood glucose, and sometimes an oral glucose tolerance test, or OGTT for short.

Now lets look at the results of our labs to determine a diagnosis. Now, if the hemoglobin A1c is less than 5.7%, fasting blood glucose is less than 100 mg/dL, random blood glucose is less than 200 mg/dL, and blood glucose after the 2-hour OGTT is less than 140 mg/dL, then you should consider alternative diagnoses.

On the other hand, if the hemoglobin A1c is between 5.7% and 6.5%, fasting blood glucose is between 100 mg/dL and 126 mg/dL, random blood glucose is under 200 mg/dL, or blood glucose after the 2-hour OGTT is between 140 and 199, then the patient has prediabetes. In this case, encourage lifestyle modifications, such as a healthy diet and physical activity, to decrease the risk of developing type 2 diabetes mellitus. However, if your patient is at high risk for type 2 diabetes mellitus, consider adding an oral hypoglycemic, such as metformin. You should also repeat their diabetic screening tests yearly.

Sources

  1. "Cardiovascular Disease and Risk Management: Standards of Medical Care in Diabetes-2022" Diabetes Care (2022)
  2. "Management of hyperglycaemia in type 2 diabetes, 2022. A consensus report by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD)" Diabetologia (2022)
  3. "Screening for Prediabetes and Type 2 Diabetes: US Preventive Services Task Force Recommendation Statement" JAMA (2021)
  4. "Oral Pharmacologic Treatment of Type 2 Diabetes Mellitus: A Clinical Practice Guideline Update From the American College of Physicians" Ann Intern Med (2017)
  5. "Pathophysiology of Type 2 Diabetes Mellitus" Int J Mol Sci (2020)
  6. "Diabetes Mellitus Type 2" StatPearls Publishing (2023)