USMLE Step 2 CK endocrinology & diabetes questions

Prediabetes is defined as fasting plasma glucose 100-125 mg/dL, 2-hour OGTT glucose 140-199 mg/dL, or HbA1c 5.7-6.4%. This patient's fasting glucose values (118 and 121 mg/dL) and HbA1c of 6.3% both fall within the prediabetes range, and none of his values meet diagnostic thresholds for diabetes (fasting ≥126 mg/dL, 2-hour OGTT ≥200 mg/dL, HbA1c ≥6.5%, or random glucose ≥200 mg/dL with symptoms). Diagnosis requires two abnormal results, which he has, but both fall short of the diabetic cutoff. He should be counseled on lifestyle modification and considered for metformin if additional risk factors are present.

• A. His fasting glucose and HbA1c values are both below the diagnostic thresholds for diabetes.
• B. Diabetes insipidus involves impaired water handling with normal glucose, not elevated glucose or HbA1c.
• D. This diagnosis applies only during pregnancy and is not relevant here.
• E. His values exceed the normal range (fasting <100 mg/dL, HbA1c <5.7%).

The USPSTF recommends screening for prediabetes and type 2 diabetes in adults aged 35-70 years who have overweight or obesity (BMI ≥25 kg/m2, or ≥23 kg/m2 in Asian American individuals). This patient is 39 years old with a BMI of 29 kg/m2, meeting both the age and weight criteria, so screening is indicated now rather than waiting. Screening can be done with fasting plasma glucose, HbA1c, or an OGTT. Waiting for symptoms would miss the asymptomatic window during which early detection improves outcomes.

• A. The BMI threshold for screening eligibility is 25 kg/m2, not 35 kg/m2.
• B. Screening for type 2 diabetes is not contingent on pregnancy status.
• D. Waiting for symptoms defeats the purpose of screening asymptomatic at-risk adults.
• E. Age 45 is not the threshold; screening begins at age 35 in adults with overweight or obesity.

In the two-step approach to gestational diabetes screening, a 50-g glucose challenge test is performed first; a 1-hour value above the institutional threshold (commonly 130, 135, or 140 mg/dL) is abnormal and requires a confirmatory 100-g 3-hour OGTT. The diagnosis of gestational diabetes is made only if two or more of the four OGTT values (fasting, 1-hour, 2-hour, 3-hour) meet or exceed the Carpenter-Coustan criteria. A single abnormal screening value is not sufficient to diagnose gestational diabetes or start treatment. HbA1c is not used for gestational diabetes diagnosis because pregnancy alters red cell turnover and glucose dynamics.

• A. HbA1c is unreliable in pregnancy and is not part of the gestational diabetes diagnostic algorithm.
• B. Repeating the screening test is not standard practice after an abnormal result; the confirmatory OGTT should be performed instead.
• C. A fasting glucose alone does not provide the diagnostic criteria needed for gestational diabetes.
• E. A single abnormal screening test value is not diagnostic; confirmatory testing with the 100-g OGTT is required.

Metformin remains first-line pharmacotherapy for most patients with type 2 diabetes because of its efficacy, low hypoglycemia risk, weight neutrality, and long safety record, and it is safe at this patient's eGFR of 82 mL/min/1.73m2. Metformin is contraindicated when eGFR falls below 30 mL/min/1.73m2 and should be used with caution or dose-reduced between 30-45 mL/min/1.73m2 due to the risk of lactic acidosis from reduced renal clearance. Sulfonylureas like glyburide carry higher hypoglycemia risk and are not first-line. Insulin is reserved for more severe hyperglycemia or when oral agents fail.

• A. Glyburide carries a higher risk of hypoglycemia and weight gain and is not first-line therapy.
• B. Repaglinide has a short duration of action, requires dosing with each meal, and carries hypoglycemia risk, making it a less preferred initial choice.
• C. Pioglitazone can cause fluid retention and weight gain and is not preferred as initial monotherapy.
• D. Insulin is not first-line for a patient with only mildly elevated HbA1c and no contraindication to oral agents.

In patients with type 2 diabetes and established atherosclerotic cardiovascular disease, GLP-1 receptor agonists such as semaglutide are preferred add-on therapy because they reduce major adverse cardiovascular events and also promote significant weight loss, benefiting this patient's obesity. GLP-1 agonists work by enhancing glucose-dependent insulin secretion, suppressing glucagon, slowing gastric emptying, and promoting satiety. Sulfonylureas and thiazolidinediones lack proven cardiovascular benefit and the latter can worsen weight gain and fluid retention. DPP-4 inhibitors are weight-neutral and have not shown cardiovascular benefit comparable to GLP-1 agonists.

• A. Sitagliptin is weight-neutral and has not shown the cardiovascular risk reduction seen with GLP-1 receptor agonists.
• B. Glipizide has no proven cardiovascular benefit and can cause weight gain and hypoglycemia.
• C. Acarbose has modest glycemic efficacy and gastrointestinal side effects, with no cardiovascular benefit demonstrated.
• D. Pioglitazone causes fluid retention and weight gain, which is undesirable in a patient with cardiovascular disease and obesity.

SGLT2 inhibitors such as empagliflozin reduce hospitalization for heart failure and slow progression of chronic kidney disease in patients with type 2 diabetes, making them the preferred add-on in a patient with both heart failure and reduced eGFR. They act by inhibiting glucose and sodium reabsorption in the proximal tubule, producing natriuresis and modest glycemic improvement, and remain effective and indicated even as eGFR declines to levels below 60 mL/min/1.73m2. Pioglitazone is contraindicated in heart failure because it causes fluid retention and can worsen cardiac decompensation. Sulfonylureas and insulin do not provide the cardiorenal protection demonstrated with SGLT2 inhibitors in this population.

• A. Glyburide offers no cardiorenal benefit and carries hypoglycemia risk.
• B. Pioglitazone is contraindicated in heart failure due to fluid retention and risk of worsening cardiac decompensation.
• D. Nateglinide has a short duration of action and no demonstrated cardiorenal protective effect.
• E. Insulin NPH does not provide the heart failure or renal protective benefits shown with SGLT2 inhibitors and is not first-line here.

Sulfonylureas such as glipizide stimulate insulin secretion from pancreatic beta cells independent of glucose levels, which can cause hypoglycemia, especially in elderly patients or those with irregular meals. The resulting insulin-driven anabolic effect, along with defensive eating to prevent hypoglycemia, commonly leads to weight gain. This combination of hypoglycemia and weight gain is a classic adverse effect profile of sulfonylureas, distinguishing them from weight-neutral or weight-reducing agents.

• A. Metformin does not cause hypoglycemia and is typically weight-neutral or associated with modest weight loss.
• C. Acarbose delays carbohydrate absorption and does not cause hypoglycemia or weight gain.
• D. Sitagliptin, a DPP-4 inhibitor, has a low risk of hypoglycemia and is weight-neutral.
• E. Empagliflozin, an SGLT2 inhibitor, promotes weight loss and has a low risk of hypoglycemia as monotherapy.

SGLT2 inhibitors such as empagliflozin can cause euglycemic diabetic ketoacidosis, particularly in the setting of surgery, fasting, or reduced caloric intake, because the drug promotes continued glucosuria and relative insulinopenia-driven ketogenesis even when serum glucose is only mildly elevated or normal. Patients present with an anion gap metabolic acidosis and significant ketonemia despite glucose levels below the typical DKA threshold of 250 mg/dL. Current guidance recommends holding SGLT2 inhibitors before scheduled surgery and in any acute illness with poor oral intake to prevent this complication.

• B. There is no history of significant alcohol use to support alcoholic ketoacidosis.
• C. Hyperosmolar hyperglycemic state requires markedly elevated glucose, typically above 600 mg/dL, with minimal ketosis.
• D. Starvation ketosis causes mild ketosis without severe acidosis or a pH this low.
• E. Metformin-associated lactic acidosis presents with an elevated lactate level rather than prominent ketonemia.

Long-term metformin use impairs calcium-dependent absorption of the vitamin B12-intrinsic factor complex in the terminal ileum, leading to vitamin B12 deficiency in up to 10-30% of chronic users. Vitamin B12 deficiency can cause a peripheral neuropathy that mimics diabetic peripheral neuropathy, so measuring serum B12 is an appropriate next step before attributing new neuropathic symptoms solely to diabetes. Current guidelines recommend periodic monitoring of vitamin B12 levels in patients on long-term metformin therapy.

• A. Switching to a sulfonylurea is unnecessary since his glycemic control is excellent and does not evaluate the new neuropathy.
• B. Starting gabapentin treats symptoms without addressing a potentially reversible underlying cause.
• C. Nerve conduction studies are not the next step before excluding a readily treatable cause such as B12 deficiency.
• D. Increasing the metformin dose would worsen B12 malabsorption and does not address his well-controlled glucose.

Elevated pre-lunch glucose with normal fasting, pre-dinner, and bedtime values indicates inadequate glycemic control specifically after breakfast, which is corrected by the rapid-acting insulin given before that meal. Increasing the breakfast dose of insulin lispro targets the postprandial rise without affecting the already well-controlled fasting glucose or other mealtime values. Basal-bolus regimens are adjusted by matching each insulin dose to the glucose excursion it is intended to control, so isolated pre-lunch hyperglycemia points to the breakfast bolus.

• A. Pre-dinner glucose is already well controlled, so increasing the dinner lispro dose is not indicated.
• B. A second glargine dose is unnecessary when fasting glucose is already at goal and the problem is isolated to one time point.
• D. Fasting glucose is at goal, so increasing basal glargine would risk nocturnal or early morning hypoglycemia without fixing the pre-lunch spike.
• E. Switching to regular insulin would not address the specific postprandial pattern and regular insulin has a slower onset, worsening control after breakfast.

Thiazolidinediones such as pioglitazone activate PPAR-gamma receptors, which increases renal sodium and water reabsorption and leads to fluid retention, plasma volume expansion, and peripheral edema. This fluid retention can precipitate or worsen heart failure, so thiazolidinediones are contraindicated in patients with New York Heart Association class II-IV heart failure. In contrast, SGLT2 inhibitors are preferred in patients with diabetes and heart failure because they reduce hospitalization for heart failure.

• A. Glipizide does not cause fluid retention and is not contraindicated in heart failure.
• B. Insulin does not cause significant fluid retention through a PPAR-gamma mechanism and is safe in heart failure.
• C. Sitagliptin has no established mechanism of significant fluid retention and is generally safe in heart failure, though saxagliptin has shown some increased risk.
• D. Empagliflozin is favored in heart failure because it reduces heart failure hospitalizations and cardiovascular mortality.

Hyperosmolar hyperglycemic state is characterized by severe hyperglycemia, usually above 600 mg/dL, markedly elevated serum osmolality above 320 mOsm/kg, and altered mental status, typically without significant ketosis or a widened anion gap because residual insulin secretion suppresses lipolysis and ketogenesis. This patient's near-normal bicarbonate, normal anion gap, and negative ketones distinguish her from diabetic ketoacidosis, in which ketosis and a high anion gap metabolic acidosis predominate. HHS classically occurs in older patients with type 2 diabetes who have an inciting illness and inadequate fluid intake, leading to profound dehydration.

• B. Diabetic ketoacidosis would show a significant anion gap, low bicarbonate, and positive serum or urine ketones, none of which are present here.
• C. Uremic encephalopathy would require significant renal failure with elevated BUN and creatinine, which are not described here.
• D. Lactic acidosis would present with an elevated anion gap and low bicarbonate, which this patient does not have.
• E. Alcoholic ketoacidosis requires a history of alcohol use and would show ketosis, which is absent in this patient.

The first step in managing diabetic ketoacidosis is aggressive isotonic saline infusion to restore intravascular volume and correct the severe dehydration typical of DKA, which also helps lower glucose and improve tissue perfusion. Insulin therapy should not be started until volume resuscitation is underway and the serum potassium level is known, because insulin drives potassium intracellularly and can precipitate life-threatening hypokalemia if the starting potassium is low, as in this patient at 3.1 mEq/L. Potassium repletion should begin before or concurrently with insulin when the potassium level is below 3.3 mEq/L, but fluids are given first.

• A. Subcutaneous insulin has unpredictable absorption in the setting of poor perfusion and is not appropriate; intravenous insulin is used only after initial fluid resuscitation.
• B. Starting insulin before adequate fluid resuscitation and before addressing this low potassium level risks precipitating severe hypokalemia and arrhythmia.
• D. Sodium bicarbonate is not routinely recommended in DKA except in cases of severe acidosis with pH below 6.9, and fluids take priority.
• E. Potassium repletion is important given the level of 3.1 mEq/L, but isotonic fluids should be initiated first to begin restoring perfusion and renal potassium handling.

Once serum glucose falls to approximately 200 mg/dL during DKA treatment, dextrose should be added to the intravenous fluids, typically as D5 normal saline or D5 half-normal saline, while continuing the insulin infusion at a rate sufficient to resolve the ketoacidosis. This approach prevents hypoglycemia while allowing insulin to continue clearing ketones and closing the anion gap, since the anion gap of 14 mEq/L and bicarbonate of 16 mEq/L indicate the acidosis has not yet resolved. Insulin should not be stopped or reduced without adding dextrose, because premature discontinuation risks recurrent ketosis before resolution criteria are met.

• B. Stopping the insulin infusion before the acidosis has resolved risks rebound ketogenesis and worsening DKA.
• C. A dextrose bolus would cause a rapid glucose spike and is not the standard approach; dextrose should be added to the maintenance infusion instead.
• D. Reducing the insulin rate without adding dextrose does not address the resolving but still active ketoacidosis and risks undertreating it.
• E. Transitioning to subcutaneous insulin is appropriate only once the anion gap has closed, bicarbonate has normalized, and the patient is able to eat, not at this point.

This patient has symptomatic hypoglycemia with altered mental status and an unsafe swallow, so oral therapy is contraindicated due to aspiration risk. Because intravenous access is already established, IV dextrose (commonly D50W, 25 g) is the fastest and most appropriate route to rapidly correct severe hypoglycemia. Glucagon is reserved for situations without IV access. Repeat glucose should be checked after treatment to confirm resolution and guide further monitoring.

• A. Oral glucose risks aspiration in a patient with altered mental status who cannot safely swallow.
• B. Intramuscular glucagon is appropriate when IV access is unavailable, not when it is already established.
• D. Cortisol testing does not address the immediate life-threatening hypoglycemia and delays treatment.
• E. Insulin would worsen hypoglycemia and is contraindicated.

Current guidelines (ADA) recommend annual screening for diabetic nephropathy starting at the time of diagnosis in type 2 diabetes using a spot urine albumin-to-creatinine ratio (UACR), because it is simple, accurate, and does not require timed collection. An elevated UACR (≥30 mg/g) on at least two of three samples over 3-6 months indicates albuminuria and the need for further management. Estimated GFR should be measured concurrently but does not substitute for albuminuria screening. Early detection allows institution of renin-angiotensin system blockade to slow progression.

• B. Renal ultrasound is not indicated for routine nephropathy screening in diabetes.
• C. A 24-hour urine collection is more cumbersome and not needed for routine annual screening when a spot UACR suffices.
• D. Cystatin C is not the standard screening test for diabetic nephropathy.
• E. Nephrology referral is premature before any screening test has been obtained.

The comprehensive annual diabetic foot examination includes monofilament testing (typically with a 10-gram Semmes-Weinstein monofilament) to assess for loss of protective sensation, a key risk factor for ulceration. This simple bedside test, combined with inspection for deformities, skin changes, and pulse palpation, identifies patients at high risk who need more frequent foot care, patient education, and possibly specialized footwear. Nerve conduction studies and vascular imaging are not part of routine annual screening unless specific abnormalities are found. Early identification of sensory loss allows preventive measures before ulcers develop.

• A. Podiatry referral is not needed as a first step when no abnormalities have yet been identified on screening.
• B. Ankle-brachial index is used to evaluate for peripheral arterial disease, not to screen for loss of protective sensation.
• D. Doppler ultrasound is not a routine screening tool for diabetic foot risk assessment.
• E. Nerve conduction studies are not part of routine annual screening and are reserved for atypical or diagnostically unclear neuropathy.

Primary hypothyroidism is characterized by elevated TSH and low free T4, reflecting failure of the thyroid gland itself with loss of negative feedback leading to compensatory pituitary TSH elevation. This pattern, combined with the classic symptoms of fatigue, cold intolerance, weight gain, and delayed reflex relaxation, confirms the diagnosis. Secondary hypothyroidism would show a low or inappropriately normal TSH with low free T4 due to pituitary or hypothalamic failure. The most common cause of primary hypothyroidism in iodine-sufficient regions like the US is Hashimoto thyroiditis.

• A. Sick euthyroid syndrome typically shows low or normal TSH with variable T4/T3 levels in the setting of acute systemic illness, which does not fit this presentation.
• B. Secondary hypothyroidism shows low or inappropriately normal TSH with low free T4, not an elevated TSH as seen here.
• D. Subclinical hypothyroidism shows elevated TSH with a normal free T4, not a low free T4 as in this patient.
• E. Thyroid hormone resistance typically shows elevated TSH and elevated, not low, free T4 levels.

Calcium carbonate, iron salts, and antacids form insoluble complexes with levothyroxine in the gut, reducing its absorption by up to 30%. Levothyroxine should be taken on an empty stomach, typically 30-60 minutes before breakfast, and divalent cation supplements should be separated by at least 4 hours. Taking levothyroxine with food, especially calcium- or iron-containing products, lowers bioavailability and can lead to under-treatment despite an adequate prescribed dose. Switching the levothyroxine formulation does not address the absorption interaction.

• A. Switching to liothyronine does not eliminate the calcium-binding interaction and is not standard first-line therapy.
• C. Levothyroxine is best absorbed on an empty stomach, not with food at bedtime.
• D. Food, particularly calcium- and iron-containing foods, decreases levothyroxine absorption rather than improving it.
• E. Taking them together significantly reduces levothyroxine absorption due to chelation by calcium.

Graves disease is an autoimmune disorder caused by TSH receptor-stimulating antibodies that diffusely activate the thyroid gland, producing suppressed TSH, elevated free T4, diffusely increased radioactive iodine uptake, and often extrathyroidal features such as proptosis from orbital inflammation. The combination of a diffuse non-tender goiter, ophthalmopathy, and diffuse uptake on scan is classic for Graves disease rather than a nodular process. Toxic multinodular goiter would show patchy, heterogeneous uptake, and subacute thyroiditis would show low, not elevated, uptake due to follicular destruction.

• B. Struma ovarii is ectopic thyroid tissue in an ovarian teratoma and would show suppressed, not increased, uptake in the neck.
• C. Toxic multinodular goiter shows patchy, heterogeneous uptake corresponding to multiple autonomous nodules, not diffuse uptake.
• D. Subacute thyroiditis causes thyrotoxicosis with low, not elevated, radioactive iodine uptake due to follicular cell destruction.
• E. A TSH-secreting pituitary adenoma would present with an elevated or inappropriately normal TSH, not a suppressed one.

On a thyroid radioiodine uptake scan, toxic multinodular goiter characteristically shows a patchy pattern with multiple autonomously functioning nodules taking up tracer avidly while the surrounding normal thyroid tissue is suppressed due to low TSH. This patchy, heterogeneous pattern distinguishes it from a toxic adenoma, which shows a single focal hot nodule with suppression of the rest of the gland, and from Graves disease, which shows diffuse homogeneous uptake. Recognizing the scan pattern helps guide treatment, such as radioactive iodine ablation targeted to the hyperfunctioning areas.

• A. Diffuse homogeneous uptake is characteristic of Graves disease, not toxic multinodular goiter.
• B. A single focal hot nodule with suppression of the rest of the gland describes a toxic adenoma, not multinodular goiter.
• C. Absent uptake throughout the gland suggests thyroiditis or exogenous thyroid hormone use, not a hyperfunctioning nodular process.
• E. Uniformly decreased uptake in a normal-sized gland is inconsistent with a multinodular hyperfunctioning goiter.

Propylthiouracil is preferred over methimazole during the first trimester of pregnancy because methimazole is associated with a rare but characteristic embryopathy, including aplasia cutis and choanal or esophageal atresia, when exposure occurs during organogenesis. Propylthiouracil carries a small risk of hepatotoxicity, so therapy is typically switched to methimazole after the first trimester once organogenesis is complete. Radioactive iodine is contraindicated in pregnancy because it crosses the placenta and can ablate the fetal thyroid, and surgery is reserved for specific situations such as drug intolerance or very large goiters.

• A. Radioactive iodine is contraindicated in pregnancy due to placental transfer and risk to the fetal thyroid.
• C. Methimazole use in the first trimester carries a risk of embryopathy including aplasia cutis and choanal atresia.
• D. Potassium iodide monotherapy is not standard long-term management of Graves disease in pregnancy.
• E. Thyroidectomy is not first-line therapy and is reserved for special circumstances such as drug intolerance.

Agranulocytosis is a rare but serious idiosyncratic adverse effect of thionamides, presenting with fever and sore throat due to severe neutropenia, typically with an absolute neutrophil count below 500/mm3. The offending drug must be stopped immediately, and the patient should receive supportive care, broad-spectrum antibiotics if infection is suspected, and close monitoring, since continuing or substituting another thionamide risks cross-reactivity and further marrow suppression. Switching to propylthiouracil is inappropriate because agranulocytosis is a class effect that can recur with any thionamide.

• A. Continuing or increasing methimazole in the setting of agranulocytosis risks worsening neutropenia and life-threatening infection.
• B. Antibiotics alone without stopping the causative drug do not address the underlying marrow suppression.
• D. Growth factor support may be considered in severe cases but methimazole must be discontinued first, not continued.
• E. Agranulocytosis is a class effect of thionamides, so switching to propylthiouracil risks recurrence.

Subacute (de Quervain) thyroiditis typically follows a viral upper respiratory illness and presents with a painful, tender goiter, elevated inflammatory markers such as ESR, and a transient thyrotoxic phase caused by release of preformed hormone from damaged follicles. The radioactive iodine uptake is characteristically low during this phase because follicular destruction impairs new hormone synthesis, distinguishing it from Graves disease, which shows elevated diffuse uptake. The thyrotoxic phase is self-limited and often followed by a transient hypothyroid phase before recovery.

• A. Hashimoto thyroiditis is usually painless and presents with hypothyroidism rather than an acute painful thyrotoxic phase.
• C. Graves disease would show elevated, not decreased, radioactive iodine uptake, and the thyroid is typically non-tender.
• D. Toxic adenoma shows a focal hot nodule on uptake scan, not diffusely decreased uptake, and is not typically painful.
• E. Acute suppurative thyroiditis presents with high fever, marked tenderness, and signs of bacterial infection such as abscess, not a viral prodrome with low uptake thyrotoxicosis.

Postpartum thyroiditis is a destructive lymphocytic thyroiditis causing release of preformed hormone, which produces a thyrotoxic phase with low radioactive iodine uptake because the gland is not synthesizing new hormone. This contrasts with Graves disease, where thyroid-stimulating immunoglobulins drive diffuse increased uptake. The absence of orbitopathy, bruit, or a personal history of autoimmune thyroid disease, combined with the postpartum timing, favors a destructive process. Management is usually supportive (beta-blockers) since the thyrotoxic phase is self-limited and often followed by a hypothyroid phase.

• B. Elevated TSI is characteristic of Graves disease, not postpartum thyroiditis.
• C. Diffuse increased uptake indicates Graves disease with active new hormone synthesis.
• D. Thyroglobulin antibodies can be positive in both conditions and do not distinguish the uptake pattern.
• E. A cold nodule suggests a focal lesion, not the diffuse destructive process of postpartum thyroiditis.

Papillary thyroid carcinoma confirmed on cytology, particularly for tumors larger than 1-4 cm or with concerning sonographic features, is treated with surgical resection, typically total or near-total thyroidectomy, with lobectomy an option for small, low-risk unifocal tumors. Surgery allows accurate staging, treatment of the primary tumor, and consideration of adjuvant radioactive iodine when indicated. Levothyroxine suppression alone and radiation therapy are not substitutes for definitive surgical treatment. Radioactive iodine ablation is used after surgery, not as monotherapy.

• A. External beam radiation is not first-line therapy for differentiated thyroid cancer.
• C. A definitive cytologic diagnosis of carcinoma does not require repeat biopsy before treatment.
• D. Radioactive iodine is used as adjuvant therapy after thyroidectomy, not as a substitute for surgery.
• E. Medical suppression alone does not treat the malignancy and is not an alternative to surgery.

Medullary thyroid carcinoma arises from calcitonin-secreting parafollicular C cells and is markedly elevated calcitonin along with carcinoembryonic antigen, as in this patient. The family history of thyroid cancer and pheochromocytoma strongly suggests multiple endocrine neoplasia type 2, an autosomal dominant syndrome caused by RET proto-oncogene mutations. Flushing and diarrhea can occur from tumor secretion of vasoactive peptides. All patients with confirmed medullary thyroid carcinoma should undergo RET genetic testing and screening for pheochromocytoma and hyperparathyroidism.

• A. Anaplastic carcinoma presents with rapidly enlarging, invasive masses in older patients, not elevated calcitonin.
• B. Papillary carcinoma does not secrete calcitonin and is not associated with MEN2.
• C. Follicular carcinoma arises from follicular cells and does not cause calcitonin elevation.
• E. Hashimoto thyroiditis causes diffuse goiter with antibody elevation, not elevated calcitonin or a dominant nodule.

Dopamine agonists, particularly cabergoline, are first-line therapy for prolactinomas because dopamine normally inhibits prolactin secretion, and these drugs effectively shrink tumor size and normalize prolactin levels in most patients. Cabergoline is preferred over bromocriptine due to greater efficacy and better tolerability. Surgery is reserved for patients who do not respond to or cannot tolerate dopamine agonists, or who have acute visual compromise. Radiation is used only when medical and surgical therapy fail.

• A. Radiation therapy is a later option after medical and surgical treatment fail.
• B. Octreotide is used for somatotroph or thyrotroph adenomas, not prolactinomas.
• C. Levothyroxine treats hypothyroidism and does not address the prolactin-secreting tumor.
• E. Surgery is reserved for dopamine agonist-resistant or intolerant cases, not first-line therapy.

Insulin-like growth factor 1 (IGF-1) reflects integrated growth hormone secretion over time and is the best initial screening test when acromegaly is clinically suspected, since growth hormone is secreted in a pulsatile fashion and random levels are unreliable. If IGF-1 is elevated, the diagnosis is confirmed with an oral glucose tolerance test, where failure of growth hormone to suppress below 1 ng/mL confirms autonomous secretion. Pituitary MRI is then obtained to localize the adenoma once the biochemical diagnosis is established.

• A. MRI is used for localization after biochemical confirmation, not as the initial test.
• B. Urinary free cortisol screens for Cushing syndrome, not acromegaly.
• C. Random growth hormone levels fluctuate throughout the day and are unreliable for screening.
• D. This confirmatory test is performed after an elevated IGF-1 level, not as the first step.

Bitemporal hemianopsia results from compression of the crossing nasal retinal fibers at the optic chiasm, most commonly caused by a pituitary macroadenoma. MRI of the brain with fine cuts through the sella is the most accurate imaging modality for visualizing pituitary and suprasellar masses and their relationship to the optic chiasm. CT can detect larger lesions but is inferior to MRI for soft tissue detail in this region. Once an adenoma is identified, further workup includes hormonal evaluation for both hypersecretion and hypopituitarism.

• A. Carotid ultrasound evaluates carotid artery stenosis, unrelated to chiasmal compression.
• B. Lumbar puncture evaluates intracranial pressure and is not indicated for this visual field pattern.
• D. Visual evoked potentials assess optic nerve conduction, not structural causes of the defect.
• E. CT angiography is used to evaluate vascular pathology, not soft tissue pituitary lesions.

Failure to concentrate urine despite water deprivation and a rising plasma osmolality, followed by a greater than 50% increase in urine osmolality after desmopressin administration, indicates a deficiency of endogenous antidiuretic hormone that corrects with exogenous hormone replacement, confirming central diabetes insipidus. In nephrogenic diabetes insipidus, the kidneys are unresponsive to antidiuretic hormone, so urine osmolality would not rise significantly after desmopressin. Primary polydipsia is excluded by the inability to concentrate urine despite an appropriately elevated plasma osmolality, which indicates true inability to retain water rather than excessive intake alone.

• A. SIADH causes hyponatremia with inappropriately concentrated urine, not hypernatremia with dilute urine.
• B. Osmotic diuresis from hyperglycemia is excluded by the normal serum glucose level.
• C. Nephrogenic DI would show minimal urine osmolality increase after desmopressin due to renal resistance to ADH.
• E. Primary polydipsia typically shows a smaller rise in plasma osmolality and some urine concentration during water deprivation.

Sheehan syndrome is postpartum pituitary necrosis caused by severe obstetric hemorrhage and hypotension, which compromises blood flow to the physiologically enlarged, hyperemic pituitary gland during pregnancy. It presents with failure of lactation (prolactin deficiency), followed by variable combinations of hypothyroidism, adrenal insufficiency, and amenorrhea, and can present acutely with headache and visual field defects from pituitary swelling or infarction. The combination of failed lactation, hypotension, hyponatremia, hypoglycemia, and low cortisol after a hemorrhagic delivery strongly supports this diagnosis. Hormone replacement (glucocorticoids first, then thyroid hormone) is required.

• A. Lymphocytic hypophysitis typically occurs late in pregnancy or postpartum without a preceding hemorrhagic/hypotensive event and is autoimmune in origin.
• B. Cerebral venous sinus thrombosis causes headache and can occur postpartum, but does not explain failed lactation or the hypopituitary hormone pattern.
• D. Prolactinoma with hemorrhage (pituitary apoplexy from a tumor) would be expected to show elevated, not absent, prolactin-related milk production and is unrelated to the hemorrhagic delivery history.
• E. Craniopharyngioma is a slow-growing tumor, not an acute postpartum event tied to hemorrhage.

This patient's hyperpigmentation, hyponatremia, hyperkalemia, orthostatic hypotension, and low morning cortisol suggest primary adrenal insufficiency (Addison disease). The cosyntropin (synthetic ACTH) stimulation test is the gold-standard confirmatory test: serum cortisol is measured before and 30-60 minutes after administration of synthetic ACTH, and failure of cortisol to rise appropriately (peak less than 18-20 µg/dL) confirms adrenal insufficiency. A plasma ACTH level helps distinguish primary from secondary disease but does not by itself confirm the diagnosis of adrenal insufficiency. Hyperpigmentation specifically points to primary disease, since elevated ACTH and related peptides stimulate melanocytes.

• A. An isolated ACTH level helps localize primary versus secondary disease but cannot confirm the diagnosis without a stimulation test.
• B. The dexamethasone suppression test is used to diagnose Cushing syndrome, not adrenal insufficiency.
• D. 24-hour urine free cortisol screens for cortisol excess (Cushing syndrome), not deficiency.
• E. The insulin tolerance test assesses growth hormone and ACTH reserve in suspected hypothalamic-pituitary disease, not first-line for primary adrenal insufficiency, and carries hypoglycemia risk.

A low or inappropriately normal ACTH level in the setting of low cortisol localizes the defect to the pituitary or hypothalamus (secondary adrenal insufficiency), since an intact pituitary should respond to low cortisol with a markedly elevated ACTH. The sellar mass causing compression of ACTH-secreting corticotrophs explains the low ACTH and secondary cortisol deficiency. Potassium is typically normal in secondary adrenal insufficiency because aldosterone secretion, which is regulated by the renin-angiotensin system rather than ACTH, is preserved. The absence of hyperpigmentation also argues against primary disease, since ACTH and related peptides are not elevated.

• A. Primary adrenal insufficiency would show an elevated, not suppressed, ACTH level due to loss of cortisol negative feedback.
• B. Congenital adrenal hyperplasia presents in infancy or childhood and would show elevated, not low, ACTH.
• D. Adrenal hemorrhage causing primary insufficiency would also elevate ACTH, not suppress it.
• E. Ectopic ACTH secretion causes markedly elevated ACTH and hypercortisolism (Cushing syndrome), not cortisol deficiency.

This patient with known adrenal insufficiency presents with shock, fever, and altered mental status consistent with acute adrenal crisis, precipitated by an intercurrent illness and inability to take oral steroids. Adrenal crisis is a medical emergency with significant mortality if untreated, so empiric intravenous hydrocortisone must be given immediately along with aggressive fluid resuscitation, without waiting for confirmatory laboratory results. A random cortisol level can be drawn before the hydrocortisone dose if feasible, but treatment should never be delayed for test results in a patient this unstable. Delaying treatment to perform stimulation testing or imaging risks death from cardiovascular collapse.

• A. Fludrocortisone has primarily mineralocorticoid activity and is not the agent of choice in acute crisis; stress-dose hydrocortisone provides both glucocorticoid and some mineralocorticoid effect.
• B. The cosyntropin stimulation test is a diagnostic test for undiagnosed adrenal insufficiency, not appropriate during an acute crisis in a known Addison disease patient, and treatment must not be delayed for it.
• C. Imaging has no role in the acute management of adrenal crisis and would dangerously delay life-saving treatment.
• E. Waiting for laboratory confirmation in a patient with hemodynamic instability risks fatal delay in treatment.

This patient's central obesity, violaceous striae, proximal myopathy, hypertension, and hyperglycemia are classic features of Cushing syndrome, and screening is required before determining the cause. The overnight low-dose (1 mg) dexamethasone suppression test, 24-hour urinary free cortisol, or late-night salivary cortisol are the recommended initial screening tests; failure of cortisol to suppress below 1.8 µg/dL after dexamethasone supports the diagnosis. Only after biochemical confirmation of hypercortisolism should further tests be used to localize the source (ACTH level, high-dose suppression testing, or imaging). Ordering localization tests before confirming the syndrome risks misdiagnosis and unnecessary imaging.

• A. Plasma ACTH is used to determine the cause (ACTH-dependent vs independent) only after Cushing syndrome has been biochemically confirmed.
• B. Adrenal imaging should only follow biochemical confirmation and ACTH-based localization, since incidental adrenal masses are common and nonspecific.
• D. The high-dose dexamethasone suppression test is used to distinguish pituitary from ectopic ACTH sources once ACTH-dependent Cushing syndrome is established, not for initial screening.
• E. Petrosal sinus sampling is an invasive localization test reserved for equivocal cases of suspected pituitary Cushing disease after the diagnosis is confirmed.

An elevated ACTH level confirms ACTH-dependent Cushing syndrome, narrowing the differential to a pituitary corticotroph adenoma (Cushing disease) or an ectopic ACTH-secreting tumor. Suppression of cortisol by more than 50% with high-dose dexamethasone indicates that the source retains some responsiveness to negative feedback, which is characteristic of a pituitary adenoma; ectopic ACTH-secreting tumors typically fail to suppress because they lack the glucocorticoid receptor feedback regulation seen in normal corticotrophs. This pattern should prompt pituitary MRI to localize a corticotroph adenoma. If no suppression occurred, an ectopic source and chest/abdominal imaging would be pursued instead.

• B. An adrenal adenoma causes ACTH-independent Cushing syndrome with a suppressed ACTH level, not elevated ACTH as seen here.
• C. Ectopic ACTH sources like small cell lung carcinoma typically fail to suppress with high-dose dexamethasone due to autonomous ACTH secretion.
• D. Bilateral adrenal hyperplasia causing primary cortisol excess would suppress ACTH, not elevate it.
• E. Exogenous glucocorticoid use suppresses endogenous ACTH and would not produce an elevated ACTH level or this suppression pattern.

Prolonged glucocorticoid therapy (typically more than 3 weeks at supraphysiologic doses) suppresses the hypothalamic-pituitary-adrenal axis, and abrupt discontinuation can precipitate adrenal crisis because endogenous cortisol production has not yet recovered. The appropriate approach is a gradual, progressive taper of the glucocorticoid dose over weeks to months, allowing the HPA axis time to recover, with close monitoring for symptoms of adrenal insufficiency during the taper. In some cases, once the dose approaches physiologic replacement levels, a morning cortisol level or cosyntropin stimulation test can help confirm HPA axis recovery before complete discontinuation. Patient education about stress dosing during illness is also important during this period.

• A. Fludrocortisone is a mineralocorticoid, not appropriate for glucocorticoid replacement or HPA axis recovery during a steroid taper.
• B. Switching to a single stress dose of IV hydrocortisone does not address the need for gradual withdrawal and HPA axis recovery.
• C. Abrupt cessation after prolonged glucocorticoid use risks adrenal crisis due to HPA axis suppression and unrecovered endogenous cortisol production.
• E. Weekly cosyntropin testing is not the standard approach to withdrawal management and is unnecessarily invasive as the primary strategy; testing may be used later to confirm recovery, not to guide the entire taper.

Resistant hypertension with unprovoked or diuretic-induced hypokalemia is a classic presentation of primary hyperaldosteronism, and the plasma aldosterone-to-renin ratio is the recommended screening test per the Endocrine Society guideline. A high ratio with an elevated aldosterone suggests autonomous aldosterone production and prompts confirmatory testing (e.g., oral sodium loading or saline infusion test). Adrenal imaging and venous sampling are used only after biochemical confirmation, to localize a source once the diagnosis is established. Interfering medications such as diuretics and ACE inhibitors should be withdrawn when feasible before testing to avoid false results.

• A. Adrenal CT is a localization study performed after a positive screening and confirmatory test, not the first step.
• B. This is a Cushing syndrome test and is not indicated for this clinical picture.
• C. This evaluates for Cushing syndrome, which does not fit this hypokalemic hypertensive presentation as well as aldosteronism.
• D. Adrenal venous sampling is used for subtype localization after the diagnosis is biochemically confirmed, not for initial screening.

Before resection of a pheochromocytoma, patients require alpha-adrenergic blockade (commonly phenoxybenzamine or a selective alpha-1 blocker) for at least 7-14 days to control blood pressure and allow volume expansion, followed by beta-blockade if needed for reflex tachycardia. Giving a beta-blocker before alpha-blockade is established leaves alpha-1 receptors unopposed by vasodilation, causing a hypertensive crisis from unopposed alpha-mediated vasoconstriction. Adequate preoperative blockade reduces the risk of intraoperative hypertensive crisis and postoperative hypotension from catecholamine withdrawal. Calcium channel blockers are sometimes used as adjuncts but are not the standard sole preoperative agent.

• A. Beta-blockade alone does not address the vasoconstriction mediated by alpha-1 receptors and is not standard monotherapy.
• C. Resection without adequate adrenergic blockade risks life-threatening intraoperative hypertensive crisis.
• D. Starting a beta-blocker before alpha-blockade can precipitate a hypertensive crisis due to unopposed alpha-adrenergic vasoconstriction.
• E. Calcium channel blockers may be adjunctive but are not the primary or sole recommended preoperative therapy.

Guidelines for asymptomatic primary hyperparathyroidism recommend parathyroidectomy when any of several criteria are met: serum calcium more than 1 mg/dL above the upper limit of normal, creatinine clearance less than 60 mL/min, T-score ≤ -2.5 at any site or a prior fragility fracture, 24-hour urine calcium > 400 mg with elevated stone risk, or age younger than 50 years. This patient's T-score of -2.7 meets the skeletal criterion for surgery, making parathyroidectomy the appropriate next step regardless of the absence of symptoms. Surgery is curative and the only intervention affecting disease course rather than just monitoring biochemical markers. Medical therapy and surveillance are reserved for patients who do not meet surgical criteria or who decline or cannot undergo surgery.

• A. Cinacalcet lowers calcium medically but does not address the underlying disease or bone loss and is reserved for patients unfit for or declining surgery.
• C. Vitamin D supplementation alone does not address the parathyroid adenoma or surgical indication present here.
• D. Monitoring alone is appropriate only when surgical criteria are not met; this patient's T-score meets the threshold for intervention.
• E. Bisphosphonates can help bone density but do not treat the underlying parathyroid pathology and are not first-line when surgical criteria are met.

Humoral hypercalcemia of malignancy is most commonly caused by squamous cell carcinoma (classically of the lung) secreting PTHrP, which binds PTH receptors in bone and kidney to stimulate osteoclastic bone resorption and renal calcium reabsorption, producing severe hypercalcemia with a suppressed PTH. The suppressed intact PTH here distinguishes this from primary hyperparathyroidism, and the elevated PTHrP confirms the humoral mechanism rather than direct bony invasion. Ectopic calcitriol production is the mechanism in lymphoma, and osteolytic metastases cause hypercalcemia through local cytokine-mediated bone destruction rather than a systemic humoral factor; in this vignette, a solitary mass with elevated PTHrP best fits humoral hypercalcemia of malignancy rather than diffuse metastatic osteolysis.

• B. This granulomatous mechanism occurs in sarcoidosis or tuberculosis, not in squamous cell carcinoma with elevated PTHrP.
• C. A suppressed PTH of 8 pg/mL excludes autonomous PTH secretion from a parathyroid adenoma.
• D. This mechanism applies to local osteolytic hypercalcemia from diffuse bone metastases (e.g., multiple myeloma, breast cancer), not to elevated PTHrP with a suppressed PTH.
• E. Ectopic calcitriol (1,25-dihydroxyvitamin D) production is characteristic of lymphoma, not squamous cell lung cancer, and would raise calcitriol rather than PTHrP.

The first step in severe symptomatic hypercalcemia is aggressive isotonic saline hydration to correct volume depletion (common from vomiting and hypercalciuria-induced nephrogenic diabetes insipidus) and to promote renal calcium excretion. Calcitonin is added next because it acts within hours to lower calcium through inhibition of osteoclastic resorption, serving as a bridge while slower-acting agents take effect. Bisphosphonates such as zoledronic acid have a delayed onset (2-4 days) and are given after initial volume repletion, often alongside or after calcitonin, to produce a more durable reduction in calcium. Hemodialysis is reserved for severe hypercalcemia with renal failure or heart failure precluding aggressive fluids, and glucocorticoids are used mainly for hypercalcemia from granulomatous disease or certain lymphomas, not solid tumor-related hypercalcemia.

• A. Dialysis is reserved for cases with renal failure or fluid overload precluding saline, not as a first step in this patient.
• B. Calcitonin is typically added after or along with fluids once volume status is being addressed, not before fluid resuscitation.
• C. Bisphosphonates have a delayed onset of action and are given after volume repletion, not as the immediate first step.
• E. Glucocorticoids are useful for granulomatous or lymphoma-related hypercalcemia, not as initial therapy for malignancy-associated hypercalcemia from a solid tumor.

Inadvertent removal or devascularization of the parathyroid glands during total thyroidectomy can cause acute hypoparathyroidism, leading to hypocalcemia within the first 24-48 hours postoperatively. The findings described, facial twitching with tapping over the facial nerve (Chvostek sign) and carpal spasm with sustained blood pressure cuff inflation (Trousseau sign), reflect neuromuscular irritability from low ionized calcium. Perioral and digital paresthesias are classic early symptoms of hypocalcemia. Confirmation requires a serum calcium and PTH level, and treatment involves calcium and vitamin D (calcitriol) supplementation.

• B. Thyroid storm presents with fever, tachycardia, and altered mental status from thyrotoxicosis, not Chvostek and Trousseau signs.
• C. While hypomagnesemia can cause similar signs, the clinical context of recent thyroidectomy makes postsurgical hypoparathyroidism far more likely than an unrelated cause.
• D. A hematoma causes neck swelling and airway compromise, not these neuromuscular findings.
• E. Recurrent laryngeal nerve injury causes hoarseness or voice changes, not tetany or the signs described.

A T-score of -2.5 or lower at the femoral neck, total hip, or lumbar spine establishes a diagnosis of osteoporosis, independent of FRAX score, and is itself an indication to begin pharmacologic therapy. Oral bisphosphonates such as alendronate are first-line therapy for postmenopausal osteoporosis because they reduce vertebral and hip fracture risk, are effective, and are low cost. FRAX scoring is used to guide treatment decisions in patients with osteopenia (T-score between -1.0 and -2.5), not in those who already meet the T-score threshold for osteoporosis. Calcium and vitamin D supplementation alone is inadequate once osteoporosis is diagnosed. Raloxifene is a second-line option, generally reserved for patients who cannot tolerate bisphosphonates or who have a predominant concern for vertebral fracture and breast cancer risk reduction.

• A. FRAX is used for treatment decisions in osteopenia, not when the T-score already confirms osteoporosis.
• B. A T-score of -2.7 already meets the diagnostic threshold for osteoporosis; delaying treatment with repeat imaging is unnecessary.
• C. Raloxifene is a second-line agent, not first-line therapy for postmenopausal osteoporosis.
• E. Calcium and vitamin D alone do not adequately treat established osteoporosis.

Osteonecrosis of the jaw is a recognized adverse effect of long-term bisphosphonate therapy, particularly after invasive dental procedures such as extractions, due to suppressed bone turnover and impaired healing in the jaw, which has a high rate of bone remodeling and is exposed to oral flora. Risk increases with longer duration of therapy, typically beyond 3-5 years. Atypical femur fractures, another long-term bisphosphonate complication, occur in the subtrochanteric or diaphyseal femur after low-energy trauma rather than causing avascular necrosis of the femoral head. Vertebral fractures are a consequence of untreated osteoporosis, not a bisphosphonate adverse effect. Bisphosphonates do not typically cause hypocalcemia or esophageal stricture; reflux esophagitis is a known risk, but stricture requiring dilation is not a classic complication.

• A. Vertebral compression fractures result from untreated osteoporosis, not from bisphosphonate therapy itself.
• C. Bisphosphonates can cause transient hypocalcemia at initiation in severe vitamin D deficiency, not specifically around dental procedures after years of use.
• D. Avascular necrosis of the femoral head is not a recognized bisphosphonate complication; atypical femur fractures occur in the subtrochanteric or diaphyseal region instead.
• E. Esophagitis, not stricture requiring dilation, is the recognized upper gastrointestinal complication of oral bisphosphonates.

Statin-associated myopathy presents with symmetric muscle aching, often in large proximal muscle groups, with elevated creatine kinase, typically occurring within weeks of starting or increasing the dose of a statin. A creatine kinase level several-fold above the upper limit of normal (here, more than 4 times normal) with symptoms warrants discontinuation of the statin and close follow-up with repeat creatine kinase measurement to confirm resolution and rule out rhabdomyolysis. Continuing the same dose risks progression to rhabdomyolysis and renal injury. Fibrates are not an appropriate substitute and actually increase myopathy risk when combined with statins; they are not first-line for ASCVD risk reduction. Muscle biopsy is unnecessary for straightforward statin myopathy. Myalgia with a significantly elevated creatine kinase is clinically significant and should not be dismissed.

• A. A creatine kinase of 850 U/L (over 4 times the upper limit of normal) with symptoms is clinically significant and requires action, not just reassurance.
• B. Fibrates are not indicated here and do not address ASCVD risk reduction in the way statins do; they also increase myopathy risk if combined with a statin later.
• C. Continuing the statin with a creatine kinase this elevated risks progression to rhabdomyolysis.
• E. Muscle biopsy is not needed when the clinical and laboratory picture is consistent with statin-induced myopathy.

This patient meets the Rotterdam criteria for polycystic ovary syndrome, which requires at least 2 of the following 3 features after exclusion of other causes: oligo-ovulation or anovulation (menstrual cycles longer than 35 days), clinical or biochemical hyperandrogenism (hirsutism, here increased terminal hair in a male pattern distribution), and polycystic ovarian morphology on ultrasound (12 or more follicles measuring 2-9 mm or increased ovarian volume greater than 10 mL). This patient has all three features, and secondary causes such as congenital adrenal hyperplasia, hyperprolactinemia, and thyroid dysfunction have been excluded with normal 17-hydroxyprogesterone, prolactin, and TSH. Congenital adrenal hyperplasia is excluded by a normal 17-hydroxyprogesterone level. Hypothalamic amenorrhea typically occurs with low body weight or excessive exercise and presents with low gonadotropins, not hyperandrogenism or polycystic ovaries. Primary ovarian insufficiency presents with amenorrhea and elevated FSH in women under 40, not oligomenorrhea with hyperandrogenism.

• A. Hypothalamic amenorrhea is associated with low body weight or excessive exercise and low gonadotropins, not hyperandrogenism or polycystic-appearing ovaries.
• C. An androgen-secreting tumor typically causes rapidly progressive, severe virilization (e.g., clitoromegaly, voice deepening), which is not described here.
• D. Congenital adrenal hyperplasia is excluded by the normal 17-hydroxyprogesterone level.
• E. Primary ovarian insufficiency presents with amenorrhea and elevated FSH, not with hyperandrogenism and oligomenorrhea.

Metabolic syndrome is diagnosed when 3 or more of the following 5 criteria are met: waist circumference greater than 88 cm (35 in) in women or greater than 102 cm (40 in) in men, triglycerides 150 mg/dL or higher, HDL cholesterol less than 50 mg/dL in women (less than 40 mg/dL in men), blood pressure 130/85 mm Hg or higher (or on treatment for hypertension), and fasting glucose 100 mg/dL or higher (or on treatment for hyperglycemia). This patient meets 5 of 5 criteria: waist circumference 92 cm exceeds the 88 cm threshold for women, triglycerides of 165 mg/dL exceed 150 mg/dL, HDL of 42 mg/dL is below the 50 mg/dL threshold for women, blood pressure of 134/86 mm Hg exceeds 130/85 mm Hg, and fasting glucose of 108 mg/dL exceeds 100 mg/dL. Metabolic syndrome identifies patients at increased risk for type 2 diabetes and cardiovascular disease, warranting lifestyle intervention.

• B. Her waist circumference of 92 cm exceeds the 88 cm threshold for women and counts as an abnormal criterion.
• C. She actually meets all 5 criteria, not just one, far exceeding the minimum of 3 required for diagnosis.
• D. Her blood pressure of 134/86 mm Hg exceeds the 130/85 mm Hg threshold and counts as an abnormal criterion.
• E. Her fasting glucose of 108 mg/dL exceeds the 100 mg/dL threshold and counts as an abnormal criterion.