Flashcards Internal Medicine EOR: Endocrine (2026) (Smarty PANCE) | Quizlet

What is Adrenal Insufficiency?

A disorder of inadequate cortisol production, either from adrenal gland destruction (primary/Addison disease) or deficient ACTH stimulation (secondary).

What distinguishes primary from secondary adrenal insufficiency on labs and exam?

Primary (Addison): low cortisol with HIGH ACTH, plus hyperpigmentation, hyperkalemia, and hyponatremia; Secondary: low cortisol with LOW ACTH, no hyperpigmentation, and usually normal potassium.

What is the most common cause of primary adrenal insufficiency in developed countries?

Autoimmune adrenalitis (autoimmune destruction of the adrenal cortex).

What is the diagnostic test of choice for adrenal insufficiency?

Cosyntropin (ACTH) stimulation test — a subnormal cortisol response confirms the diagnosis; an early-morning cortisol can screen.

How is adrenal (Addisonian) crisis managed emergently?

Immediate IV hydrocortisone, aggressive IV fluids (normal saline with dextrose), and correction of electrolytes; do not delay steroids for testing.

Why is hydrocortisone preferred over dexamethasone in acute adrenal crisis when diagnosis is uncertain?

Hydrocortisone provides both glucocorticoid and mineralocorticoid activity, but dexamethasone can be used first if a cosyntropin test is planned because it does not interfere with the cortisol assay.

What chronic maintenance therapy is required in primary adrenal insufficiency?

Glucocorticoid replacement (hydrocortisone or prednisone) PLUS mineralocorticoid replacement (fludrocortisone); patients need stress-dose steroids during illness.

What is Hyperaldosteronism?

Excess aldosterone production causing sodium retention, potassium loss, and hypertension, most often from a unilateral adrenal adenoma (Conn syndrome) or bilateral adrenal hyperplasia.

What is the classic lab triad of primary hyperaldosteronism?

Hypertension, hypokalemia, and metabolic alkalosis (though many patients are normokalemic).

What is the initial screening test for primary hyperaldosteronism?

Plasma aldosterone-to-renin ratio (ARR) — a high aldosterone with suppressed renin suggests the diagnosis.

What confirmatory test follows a positive aldosterone-to-renin ratio?

An aldosterone suppression test (oral salt loading or IV saline infusion) showing failure to suppress aldosterone.

How is the subtype of primary hyperaldosteronism localized?

Adrenal CT followed by adrenal venous sampling to distinguish a unilateral adenoma from bilateral hyperplasia.

What is the treatment for a unilateral aldosterone-producing adenoma versus bilateral hyperplasia?

Unilateral adenoma: laparoscopic adrenalectomy; Bilateral hyperplasia: mineralocorticoid receptor antagonist (spironolactone or eplerenone).

What is Hypercortisolism (Cushing Syndrome)?

A state of chronic glucocorticoid excess producing central obesity, skin changes, hypertension, and metabolic disturbances.

What is the most common overall cause of Cushing syndrome?

Exogenous (iatrogenic) glucocorticoid use; the most common endogenous cause is a pituitary ACTH-secreting adenoma (Cushing disease).

What are the classic clinical features of Cushing syndrome?

Central obesity, moon facies, dorsocervical fat pad (buffalo hump), purple abdominal striae, proximal muscle weakness, easy bruising, hypertension, and hyperglycemia.

What are the first-line screening tests for Cushing syndrome?

Late-night salivary cortisol, 24-hour urinary free cortisol, or low-dose (1 mg overnight) dexamethasone suppression test.

How does ACTH level help differentiate the cause of Cushing syndrome?

Low/suppressed ACTH indicates an adrenal source; normal-to-high ACTH indicates ACTH-dependent disease (pituitary adenoma or ectopic ACTH).

How does the high-dose dexamethasone suppression test distinguish Cushing disease from ectopic ACTH?

Cortisol suppresses with high-dose dexamethasone in pituitary Cushing disease but fails to suppress with ectopic ACTH production.

What is the definitive treatment for Cushing disease (pituitary adenoma)?

Transsphenoidal resection of the pituitary adenoma.

What is Pheochromocytoma?

A catecholamine-secreting tumor of the adrenal medulla chromaffin cells causing episodic or sustained hypertension.

What is the classic symptom triad of pheochromocytoma?

Episodic headache, palpitations, and diaphoresis (often with paroxysmal hypertension).

What is the "rule of 10s" for pheochromocytoma?

Roughly 10% bilateral, 10% extra-adrenal, 10% malignant, 10% familial, and 10% in children.

What is the best initial biochemical test for pheochromocytoma?

Plasma free metanephrines or 24-hour urine metanephrines and catecholamines.

What is the critical sequence of medical management before pheochromocytoma surgery?

Alpha-blockade FIRST (phenoxybenzamine) to control blood pressure, THEN beta-blockade if needed; giving beta-blockers first risks unopposed alpha stimulation and hypertensive crisis.

What is the definitive treatment for pheochromocytoma?

Surgical resection (adrenalectomy) after adequate alpha-adrenergic blockade.

What is Diabetes Mellitus Type 1?

An autoimmune destruction of pancreatic beta cells leading to absolute insulin deficiency, typically presenting in children or young adults.

How does type 1 diabetes typically present?

Acute onset of polyuria, polydipsia, polyphagia, and weight loss, sometimes with diabetic ketoacidosis as the first presentation.

What antibodies and labs support a diagnosis of type 1 diabetes?

Positive GAD-65, islet cell, and insulin autoantibodies, with low C-peptide reflecting absent endogenous insulin.

What are the diagnostic glucose criteria for diabetes mellitus?

Fasting glucose ≥126 mg/dL, A1c ≥6.5%, random glucose ≥200 mg/dL with symptoms, or 2-hour OGTT ≥200 mg/dL.

What is the cornerstone of type 1 diabetes management?

Lifelong insulin therapy, typically basal-bolus regimens or insulin pump, with carbohydrate counting and glucose monitoring.

What is the recommended A1c goal for most adults with diabetes?

Generally

What is Diabetes Mellitus Type 2?

A disorder of insulin resistance with relative insulin deficiency, strongly associated with obesity and metabolic syndrome.

What is the first-line pharmacologic agent for type 2 diabetes?

Metformin, combined with lifestyle modification, unless contraindicated.

Which diabetes medication classes provide cardiovascular and renal benefit?

GLP-1 receptor agonists (cardiovascular benefit, weight loss) and SGLT2 inhibitors (cardiovascular, heart failure, and renal protection).

What is the main contraindication and risk concern with metformin?

Avoid in significant renal impairment (eGFR

What screening is recommended for diabetic complications?

Annual dilated eye exam, urine albumin-to-creatinine ratio, comprehensive foot exam, and lipid monitoring.

What blood pressure and statin recommendations apply to most patients with diabetes?

Target BP generally

What is Diabetic Ketoacidosis (DKA)?

An acute hyperglycemic emergency from insulin deficiency causing hyperglycemia, ketosis, and anion-gap metabolic acidosis, most often in type 1 diabetes.

What is the classic biochemical triad of DKA?

Hyperglycemia (usually >250 mg/dL), anion-gap metabolic acidosis (pH

What are common precipitants of DKA?

Infection, insulin nonadherence or omission, new-onset diabetes, myocardial infarction, and certain medications.

What are the cornerstones of DKA management?

Aggressive IV fluid resuscitation, IV insulin infusion, and careful potassium repletion while monitoring electrolytes and the anion gap.

Why must potassium be checked before starting insulin in DKA?

Insulin drives potassium intracellularly; if serum potassium is low (

When should dextrose be added to fluids during DKA treatment?

When glucose falls to approximately 200 mg/dL, add dextrose to allow continued insulin infusion until the anion gap closes and ketoacidosis resolves.

What is Hyperosmolar Hyperglycemic Syndrome (HHS)?

A hyperglycemic emergency of type 2 diabetes marked by severe hyperglycemia, profound dehydration, and hyperosmolality with minimal or no ketoacidosis.

How does HHS differ from DKA biochemically?

HHS has much higher glucose (often >600 mg/dL) and serum osmolality (>320 mOsm/kg) with little to no ketosis and no significant acidosis, unlike DKA.

What is the typical clinical presentation of HHS?

Profound dehydration and altered mental status that develops gradually over days, often in elderly type 2 diabetics.

What is the cornerstone of HHS treatment?

Aggressive IV fluid resuscitation is the priority, followed by insulin and potassium repletion with close electrolyte monitoring.

Why does HHS carry a higher mortality than DKA?

It typically affects older patients with more comorbidities and causes more severe dehydration and hyperosmolality.

What is Hyperparathyroidism?

Excess parathyroid hormone (PTH) secretion leading to hypercalcemia (primary) or a compensatory response to hypocalcemia (secondary).

What is the most common cause of primary hyperparathyroidism?

A single parathyroid adenoma.

What is the classic clinical mnemonic for hypercalcemia symptoms?

"Stones, bones, abdominal groans, and psychiatric moans" — kidney stones, bone pain, constipation/abdominal pain, and depression/confusion.

What are the characteristic labs in primary hyperparathyroidism?

Elevated calcium with an inappropriately high or normal PTH, often with low phosphate.

What is the most common cause of hypercalcemia in hospitalized patients (the key differential)?

Malignancy — in malignancy-related hypercalcemia, PTH is suppressed, helping distinguish it from hyperparathyroidism.

What is the definitive treatment for symptomatic primary hyperparathyroidism?

Parathyroidectomy.

How is acute severe hypercalcemia managed?

Aggressive IV normal saline hydration first, followed by bisphosphonates and calcitonin for rapid lowering.

What is Hypoparathyroidism?

Deficient parathyroid hormone secretion leading to hypocalcemia and hyperphosphatemia.

What is the most common cause of hypoparathyroidism?

Iatrogenic injury or removal of the parathyroid glands during thyroid or neck surgery.

What are the classic signs of hypocalcemia on physical exam?

Chvostek sign (facial twitch on tapping the facial nerve) and Trousseau sign (carpal spasm with blood pressure cuff inflation).

What symptoms result from the hypocalcemia of hypoparathyroidism?

Perioral and distal paresthesias, muscle cramps, tetany, and in severe cases seizures or laryngospasm.

What ECG change is associated with hypocalcemia?

Prolonged QT interval.

What is the treatment for hypoparathyroidism?

Calcium supplementation and active vitamin D (calcitriol); severe symptomatic hypocalcemia requires IV calcium gluconate.

What is Hyperthyroidism / Thyroid Storm?

A state of thyroid hormone excess; thyroid storm is its life-threatening, decompensated extreme with fever, tachycardia, and altered mental status.

What is the most common cause of hyperthyroidism?

Graves disease, an autoimmune disorder caused by thyroid-stimulating immunoglobulins.

What are the characteristic labs and unique exam findings of Graves disease?

Low TSH with high free T4/T3, positive TSI antibodies, plus exophthalmos and pretibial myxedema unique to Graves.

What is the classic clinical presentation of hyperthyroidism?

Weight loss, heat intolerance, palpitations, tremor, anxiety, diarrhea, and warm moist skin.

What is the pharmacologic management of thyroid storm?

Beta-blocker (propranolol) for symptoms, a thionamide (PTU preferred in storm), iodine given AFTER the thionamide, and glucocorticoids.

Why must iodine be given after the thionamide in thyroid storm?

Giving iodine before blocking synthesis could provide substrate for new hormone production; the thionamide blocks synthesis first, then iodine blocks release.

What are the definitive treatment options for hyperthyroidism?

Radioactive iodine ablation, antithyroid drugs (methimazole), or thyroidectomy.

What is Hypothyroidism / Myxedema Coma?

A deficiency of thyroid hormone; myxedema coma is its severe, decompensated form with hypothermia, altered mental status, and cardiovascular collapse.

What is the most common cause of hypothyroidism in iodine-sufficient regions?

Hashimoto (chronic autoimmune) thyroiditis.

What labs confirm primary hypothyroidism?

Elevated TSH with low free T4; positive anti-TPO antibodies support Hashimoto thyroiditis.

What are the classic clinical features of hypothyroidism?

Fatigue, cold intolerance, weight gain, constipation, dry skin, bradycardia, and delayed relaxation of deep tendon reflexes.

What is the treatment of hypothyroidism?

Levothyroxine, titrated to normalize TSH.

How is myxedema coma managed?

IV levothyroxine (with consideration of T3), IV glucocorticoids (until adrenal insufficiency is excluded), and supportive care including warming and ventilatory support.

What is Thyroiditis?

Inflammation of the thyroid gland that can cause transient hyperthyroidism, hypothyroidism, or both, depending on the cause and phase.

What is the classic course of subacute (de Quervain) thyroiditis?

A painful, tender thyroid following a viral upper respiratory infection, with a triphasic course of hyperthyroidism, then hypothyroidism, then recovery.

How is the hyperthyroid phase of thyroiditis distinguished from Graves disease?

Thyroiditis shows LOW radioactive iodine uptake (hormone leak from damaged cells), whereas Graves shows HIGH diffuse uptake.

What is postpartum thyroiditis?

Transient autoimmune thyroid inflammation within a year of delivery, often with a hyperthyroid phase followed by hypothyroidism, frequently anti-TPO positive.

What is the treatment of the painful hyperthyroid phase of subacute thyroiditis?

Symptom control with NSAIDs (or corticosteroids if severe) and beta-blockers for hyperthyroid symptoms; antithyroid drugs are not effective.

What is a Thyroid Nodule?

A discrete lesion within the thyroid gland that may be benign or malignant and is evaluated for cancer risk.

What is the first step in evaluating a thyroid nodule?

Check a TSH and obtain a thyroid ultrasound.

What does the TSH result direct in nodule workup?

If TSH is low, obtain a radioactive iodine uptake scan to assess for a hyperfunctioning ("hot") nodule; if TSH is normal or high, proceed based on ultrasound characteristics.

Which thyroid nodules require fine-needle aspiration biopsy?

Nodules with suspicious ultrasound features or those above size thresholds based on risk; "hot" (hyperfunctioning) nodules are rarely malignant and usually do not need biopsy.

What is the most common type of thyroid cancer?

Papillary thyroid carcinoma, which has the best prognosis.

What ultrasound features raise concern for thyroid malignancy?

Microcalcifications, irregular margins, marked hypoechogenicity, taller-than-wide shape, and abnormal cervical lymph nodes.

What is a Goiter?

An enlargement of the thyroid gland, which may be diffuse or nodular and associated with normal, increased, or decreased thyroid function.

What is the most common cause of goiter worldwide?

Iodine deficiency.

What symptoms can a large goiter cause from local compression?

Dysphagia, dyspnea, hoarseness, and a positive Pemberton sign (facial congestion when raising the arms).

What is the initial workup of a goiter?

Thyroid function tests (TSH) and thyroid ultrasound to assess size, nodularity, and function.

What is a toxic multinodular goiter?

A goiter with multiple autonomously functioning nodules producing excess thyroid hormone, causing hyperthyroidism.

What is Acromegaly?

A disorder of growth hormone excess in adults, almost always from a pituitary somatotroph adenoma, causing soft tissue and bony overgrowth.

What are the classic clinical features of acromegaly?

Enlarging hands and feet, coarsening facial features, frontal bossing, prognathism, macroglossia, and excessive sweating.

What is the best initial screening test for acromegaly?

Serum IGF-1 level (random GH is unreliable due to pulsatile secretion).

What is the confirmatory test for acromegaly?

Oral glucose tolerance test showing failure of growth hormone to suppress.

What imaging follows biochemical confirmation of acromegaly?

Pituitary MRI to identify the adenoma.

What is the first-line treatment for acromegaly?

Transsphenoidal surgical resection of the pituitary adenoma; somatostatin analogs (octreotide) are used when surgery is incomplete or not feasible.

What is a Pituitary Adenoma (Prolactinoma)?

A benign pituitary tumor; a prolactinoma is the most common type and secretes excess prolactin.

How does a prolactinoma present in women versus men?

Women: amenorrhea, galactorrhea, and infertility; Men: decreased libido, erectile dysfunction, and sometimes mass effect symptoms because they present later.

What mass-effect symptom is classic for a large pituitary adenoma?

Bitemporal hemianopsia from compression of the optic chiasm.