ABIM Endocrinology cheat sheet

Diabetes diagnosis: A1c ≥6.5%, fasting plasma glucose ≥126 mg/dL, 2-hour plasma glucose ≥200 mg/dL during a 75-g OGTT, or random glucose ≥200 mg/dL with classic symptoms; confirmation is needed unless hyperglycemia is unequivocal.

A1c reflects approximately 3 months of glycemia; hemolysis, recent transfusion, iron deficiency, pregnancy, and some hemoglobinopathies can make A1c unreliable.

ADA glycemic target for most nonpregnant adults is A1c <7%; a less stringent target such as <8% may be appropriate with limited life expectancy, severe hypoglycemia risk, or advanced complications.

Metformin is first-line therapy for type 2 diabetes unless contraindicated; do not initiate at eGFR <45 mL/min/1.73 m2, stop at eGFR <30, and hold during acute illness or contrast exposure when AKI risk is high.

In type 2 diabetes with atherosclerotic cardiovascular disease, heart failure, or chronic kidney disease, use an SGLT2 inhibitor or GLP-1 receptor agonist with proven benefit independent of A1c and metformin.

DKA diagnosis requires ketosis and metabolic acidosis with pH <7.30 and bicarbonate <18 mEq/L; glucose may be below 250 mg/dL in euglycemic DKA, especially with SGLT2 inhibitors or pregnancy.

Hypoglycemia levels: level 1 is glucose <70 mg/dL, level 2 is <54 mg/dL, and level 3 is severe with altered mental status or physical inability to self-treat.

HHS shows glucose >600 mg/dL, effective osmolality >320 mOsm/kg, minimal ketosis, and profound dehydration; mortality is higher than in DKA.

BMI categories: underweight <18.5, normal 18.5–24.9, overweight 25–29.9, and obesity ≥30 kg/m2; obesity classes are 1 = 30–34.9, 2 = 35–39.9, and 3 = ≥40.

Weight loss of 5–10% improves glycemia, blood pressure, and lipids; weight loss of ≥10% can produce remission of type 2 diabetes in some patients.

Pharmacotherapy for obesity is considered at BMI ≥30, or ≥27 with a weight-related comorbidity, as an adjunct to lifestyle intervention.

High-intensity statin therapy lowers LDL cholesterol by ≥50%, while moderate-intensity therapy lowers LDL cholesterol by 30–49%; very-high-risk patients may need additional nonstatin therapy.

The Friedewald equation estimates LDL cholesterol as total cholesterol minus HDL cholesterol minus triglycerides divided by 5; it is unreliable when triglycerides exceed 400 mg/dL.

Non-HDL cholesterol equals total cholesterol minus HDL cholesterol and includes all atherogenic apoB-containing particles; it is useful when triglycerides are elevated.

Statin-associated muscle symptoms: measure CK if severe; rhabdomyolysis is CK >10 times the upper limit of normal with renal injury; otherwise rechallenge with a different statin or lower dose.

Metabolic surgery is recommended at BMI ≥40, or BMI ≥35 with a comorbidity, and may be considered at BMI ≥30 with type 2 diabetes.

Overt hypothyroidism is an elevated TSH with low free T4; levothyroxine dose is about 1.6 mcg/kg/day in young healthy adults, with lower starting doses in older adults or coronary disease.

Subclinical hypothyroidism is an elevated TSH with normal free T4; treatment is considered if TSH >10 mIU/L, symptoms are present, pregnancy is planned, or cardiovascular risk is increased; recheck TSH 6–8 weeks after dose changes.

Thyrotoxicosis shows suppressed TSH with elevated free T4 and/or T3; Graves disease typically has TSH receptor antibodies, diffuse goiter, and orbitopathy.

Radioactive iodine uptake distinguishes causes: high uptake occurs in Graves disease, toxic adenoma, and toxic multinodular goiter; low uptake occurs in thyroiditis or exogenous thyroid hormone.

Thyroid storm is supported by the Burch-Wartofsky score; treatment includes a beta blocker, a thionamide, iodine given after the thionamide, glucocorticoids, and supportive care.

Thyroid nodule evaluation uses TSH and ultrasound; FNA is guided by nodule size and suspicious ultrasound features; Bethesda categories IV–VI generally warrant surgery.

Medullary thyroid cancer arises from parafollicular C cells, secretes calcitonin, and is associated with RET mutations and MEN2; papillary and follicular cancers are differentiated thyroid cancers.

Amiodarone thyrotoxicosis: type 1 is iodine-induced excess synthesis, while type 2 is destructive thyroiditis; type 2 often responds to glucocorticoids and type 1 to antithyroid drugs.

Adrenal insufficiency testing: morning cortisol <3 mcg/dL strongly suggests deficiency and >15 mcg/dL makes it unlikely; cosyntropin stimulation peak cortisol <18 mcg/dL at 30–60 minutes confirms.

Primary adrenal insufficiency causes elevated ACTH, hyperpigmentation, hyperkalemia, and aldosterone deficiency; secondary adrenal insufficiency causes low ACTH and usually normal potassium.

Adrenal crisis: give hydrocortisone 100 mg IV immediately, then about 50 mg every 6 hours, with saline and glucose; use dexamethasone if cosyntropin testing is planned.

Primary aldosteronism screening uses the aldosterone-to-renin ratio in resistant hypertension, hypokalemia, or adrenal incidentaloma; confirm with saline suppression or captopril challenge, then adrenal vein sampling if surgery is considered.

Pheochromocytoma is screened with plasma free metanephrines or 24-hour urine fractionated metanephrines; alpha blockade must precede beta blockade, and genetic testing is offered for hereditary disease.

Cushing syndrome screening uses 1-mg overnight dexamethasone suppression, late-night salivary cortisol, or 24-hour urinary free cortisol; ACTH and imaging determine the subtype.

Prolactinoma is treated first-line with a dopamine agonist; acromegaly shows elevated IGF-1 and failure to suppress GH during an OGTT; transsphenoidal surgery is used for many functioning tumors.

Pituitary apoplexy causes sudden headache, visual field loss, ophthalmoplegia, and hypotension from acute hemorrhage or infarction; emergent glucocorticoids and neurosurgical evaluation are required.

PCOS Rotterdam criteria: two of oligo-ovulation or anovulation, clinical or biochemical hyperandrogenism, and polycystic ovaries; exclude thyroid disease, hyperprolactinemia, and nonclassic adrenal hyperplasia.

Menopause is diagnosed after 12 months of amenorrhea; FSH >30 IU/L and low estradiol support the diagnosis; hormone therapy is most effective for vasomotor symptoms and requires individualized risk assessment.

Male hypogonadism requires low morning total testosterone on two occasions; low LH and FSH indicate secondary hypogonadism, while elevated LH and FSH indicate primary testicular failure.

Klinefelter syndrome is 47,XXY with small firm testes, gynecomastia, infertility, elevated gonadotropins, and low testosterone; testosterone replacement improves virilization and bone density.

Central precocious puberty begins before age 8 in girls or age 9 in boys; GnRH stimulation confirms it, and a GnRH agonist slows progression and preserves adult height.

Turner syndrome is 45,X or mosaic and causes short stature and ovarian dysgenesis; estrogen replacement induces puberty, and monitoring includes aorta, blood pressure, thyroid, and bone health.

PCOS ovulation induction: letrozole is first-line and often produces higher live-birth rates than clomiphene; metformin may be added for insulin resistance, and gonadotropins or IVF are used for refractory cases.

Hypogonadotropic hypogonadism causes low LH, low FSH, and low testosterone or estradiol; Kallmann syndrome includes anosmia; gonadotropins or pulsatile GnRH can restore fertility.

Corrected calcium = measured calcium + 0.8 × (4.0 − albumin in g/dL); ionized calcium is preferred in critical illness or when albumin is unreliable.

Hypercalcemia with high or inappropriately normal PTH suggests primary hyperparathyroidism; suppressed PTH suggests malignancy, vitamin D excess, granulomatous disease, or thyrotoxicosis.

Primary hyperparathyroidism: surgery is indicated for symptoms, age <50, calcium >1 mg/dL above the upper limit, T-score ≤−2.5, renal stones, or GFR <60 mL/min/1.73 m2.

Hypocalcemia causes perioral numbness, tetany, Chvostek and Trousseau signs, and prolonged QT; symptomatic cases are treated with IV calcium gluconate and magnesium correction.

Osteoporosis is a DXA T-score ≤−2.5; low bone mass is a T-score between −1.0 and −2.5; FRAX estimates fracture risk, and treatment options include bisphosphonates, denosumab, and anabolic agents.

Denosumab discontinuation causes rebound bone loss and vertebral fractures; transition to a bisphosphonate or continue therapy if stopping is necessary.

Vitamin D deficiency is 25-hydroxyvitamin D <20 ng/mL and insufficiency is 20–29 ng/mL; replacement uses cholecalciferol or ergocalciferol, while activated vitamin D is used in CKD.

Paget disease of bone causes elevated alkaline phosphatase, bone pain, deformity, skull enlargement, and hearing loss; bisphosphonates treat symptoms and complications.