What elements of the physical exam are important for you to focus on in an outpatient with type 2 diabetes?

Elevated blood sugar damages the walls of blood vessels (from capillaries to arteries) and nerves. The physical exam in patients with type 2 diabetes should focus on uncovering findings that suggest that microvascular/macrovascular or neurologic complications have occurred. Microvascular damage can be apparent in the capillaries in the retina (retinopathy), glomeruli (nephropathy), and nerves (both sensory and autonomic; neuropathy). Fundoscopy should be attempted, though this is best accomplished with a dilated exam by an eye-care professional. Although nephropathy is difficult to assess on exam, lower extremity edema suggesting low oncotic pressure from glomerular protein loss can be a clue. Neuropathy should be assessed annually by performing a detailed exam of the foot. Vibration sense should be tested using a 128 Hz tuning fork on the big toe. A monofilament should be pressed against multiple areas on the plantar surface of the foot until it bends to test pressure sensation. A safety pin or broken tongue depressor should be used to test two-point discriminant sensation. Finally, ankle and patellar reflexes should be tested. Visual inspection of the feet should be performed to assess for areas of ulceration that a patient with decreased sensation may not feel. Open ulcers are a major risk factor for the development of infections in diabetics such as cellulitis and osteomyelitis. The toenails should be inspected for onychomycosis (as evidenced by yellow discoloration and hypertrophied nail matrix) and the interdigital areas assessed for tinea pedis (which can manifest as dry, cracked skin). Both conditions can create portals of entry for bacteria that can lead to cellulitis. Dorsalis pedis and posterior tibialis pulses should be assessed for strength and symmetry as diminished pulses are a macrovascular manifestation of diabetes.

What are some secondary causes of diabetes and how can the physical exam be helpful in diagnosing them?

Type 2 diabetes is responsible for approximately 90% of the cases of diabetes. The remaining 10% of cases are type 1 diabetes (mostly patients who are teenagers or younger) and secondary forms. The disease process in type 2 diabetes starts with tissue resistance to insulin (the hormone responsible for allowing cells to uptake and metabolize glucose) due to dietary and genetic factors. As a result of less glucose available inside the cells to utilize, pancreatic beta cells continue to increase the production of insulin and the liver continues to produce glucose (via gluconeogenesis). If diabetes goes untreated for long enough, the pancreatic beta cells can “burn out” and lose their synthetic ability altogether.

Insulin resistance and the ensuing elevated circulating levels of both glucose and insulin are responsible for a number of historical and physical findings. Insulin resistance and the decreased uptake of glucose into cells for use in cellular metabolism is responsible for the patient’s fatigue and weight loss. Elevated levels of insulin are responsible for acanthosis nigricans, the hyperpigmented velvety rash your patient has on his neck. Elevated levels of blood glucose are responsible for increasing the osmolality of his blood leading to increased urination (osmotic diuresis), increased thirst, and dehydration and can also result in blurry vision due to swelling of the lens.

Though the etiology is different, secondary forms of diabetes can present in a similar fashion. Patients with recurrent pancreatitis can develop diabetes owing to beta cell destruction and pancreatic fibrosis. These patients have recurrent bouts of epigastric abdominal pain associated with nausea and vomiting, but sometimes patients can develop chronic, painless pancreatitis. The most common causes of pancreatitis include frequent alcohol use, medications, and elevated triglyceride levels. Therefore, a thorough review of the patient’s social habits and medications is warranted. Hemochromatosis is an inherited disorder of increased iron absorption leading to iron deposition in the liver, pancreas, heart, joints, and skin. It can also be acquired via frequent blood transfusions. A patient presenting with darkened skin (due to iron deposition), joint pain, and new onset diabetes should prompt one to think of this disease, also known as “bronze diabetes.”

Several endocrine conditions can cause secondary diabetes as well. Diabetes can be the first sign of acromegaly (caused by a growth hormone–secreting pituitary tumor) in approximately 5% of cases. However, the disease usually presents in adults with frontal bossing; enlargement of the tongue, lips, and nose; and occasionally carpal tunnel syndrome. Cushing’s syndrome (in which excess cortisol stimulates the production of glucose leading to hyperinsulinemia) presents with a number of physical exam findings including proximal muscle weakness, central adiposity, a “buffalo hump,” and purple striae on the abdomen that appear as stretch marks. Cushing’s syndrome is caused by an adrenocorticotropic hormone (ACTH)–secreting tumor or exogenous glucocorticoids, so again, a thorough review of medications is always warranted. Lastly, pheochromocytoma is a rare tumor that secretes dopamine, epinephrine, and norepinephrine (all of which can stimulate glucose production) and presents with severe episodic hypertension, palpitations, sweating, flushing, and sometimes arrhythmia.

Finally, medications such as thiazide diuretics and beta blockers have been associated with the development of diabetes, though these medications are sometimes necessary to control blood pressure and other conditions frequently encountered in diabetics. Pentamidine, an antiparasitic medication used as prophylaxis or treatment for pneumocystis pneumonia in patients with acquired immune deficiency syndrome (AIDS), has been associated with insulin-dependent diabetes after its use. The atypical antipsychotics are also strongly correlated with the development of the metabolic syndrome and type 2 diabetes mellitus.