Endocrinology, Diabetes, Thyroid, Adrenal, Calcium/Phosphate Disorders & Cardiology

What is the pathophysiology of Type 1 diabetes?

Autoimmune destruction of pancreatic beta cells → absolute insulin deficiency.

What is the pathophysiology of Type 2 diabetes?

Insulin resistance + relative insulin deficiency.

What is the diagnostic criteria for diabetes using fasting plasma glucose (FPG)?

Fasting plasma glucose ≥126 mg/dL.

What is the diagnostic criteria for diabetes using HbA1c?

HbA1c ≥6.5%.

What is the diagnostic criteria for diabetes using oral glucose tolerance test (OGTT)?

2-hour plasma glucose ≥200 mg/dL.

What is the normal fasting glucose level?

70-99 mg/dL.

What is the normal HbA1c level?

What are examples of rapid-acting insulin?

Lispro, Aspart, Glulisine.

What is an example of short-acting insulin?

Regular insulin.

What is an example of intermediate-acting insulin?

NPH.

What are examples of long-acting insulin?

Glargine, Detemir, Degludec.

What is the mechanism of action (MOA) of Metformin?

Decreases hepatic glucose production; improves insulin sensitivity.

What are the adverse effects (AE) of Metformin?

GI upset, lactic acidosis (rare), B12 deficiency.

What is the MOA of Sulfonylureas?

Stimulates insulin release from pancreatic beta cells.

What are the AE of Sulfonylureas?

Hypoglycemia, weight gain.

What is the MOA of TZD (pioglitazone)?

PPAR-γ agonist → ↑ insulin sensitivity.

What are the AE of TZD?

Weight gain, edema, heart failure risk, fracture risk.

What are examples of DPP-4 inhibitors?

Sitagliptin, saxagliptin, linagliptin.

What is the MOA of DPP-4 inhibitors?

Prevent breakdown of incretins → ↑ insulin, ↓ glucagon.

What are the AE of DPP-4 inhibitors?

Generally well tolerated; rare pancreatitis.

What are examples of GLP-1 receptor agonists?

Liraglutide, semaglutide, exenatide.

What is the MOA of GLP-1 receptor agonists?

↑ insulin, ↓ glucagon, slow gastric emptying, ↑ satiety.

What are the AE of GLP-1 receptor agonists?

Nausea, vomiting, weight loss; risk of pancreatitis.

What are examples of SGLT2 inhibitors?

Empagliflozin, dapagliflozin, canagliflozin.

What is the MOA of SGLT2 inhibitors?

Inhibit glucose reabsorption in proximal tubule → glycosuria.

What are the AE of SGLT2 inhibitors?

Genital infections, UTIs, euglycemic DKA, volume depletion.

What is the insulin regimen for type 1 diabetes?

Basal-bolus (long-acting + rapid-acting with meals).

What is the Dawn phenomenon?

Morning hyperglycemia due to nocturnal GH/cortisol surge.

What is the Somogyi effect?

Rebound hyperglycemia after nocturnal hypoglycemia.

What are the symptoms of hypoglycemia?

Sweating, tremor, palpitations, confusion, seizures.

What are the lab findings in primary hypothyroidism?

↑ TSH, ↓ free T4.

What are the lab findings in primary hyperthyroidism?

↓ TSH, ↑ free T4/T3.

What is the hallmark antibody in Hashimoto's thyroiditis?

Anti-TPO, anti-thyroglobulin.

What is the hallmark antibody in Graves' disease?

TSI (thyroid-stimulating immunoglobulin).

What is the treatment for hypothyroidism?

Levothyroxine.

What are the dosing considerations for Levothyroxine?

Start low in elderly/CAD; titrate based on TSH.

What are the treatment options for hyperthyroidism?

Methimazole, PTU, radioactive iodine, surgery.

When is PTU preferred over Methimazole?

PTU in 1st trimester; methimazole preferred otherwise.

What are the AE of Methimazole/PTU?

Hepatotoxicity (PTU), agranulocytosis, rash.

What is the treatment for thyroid storm?

Beta-blocker + antithyroid + supportive care ± steroids.

What is the treatment for myxedema coma?

IV levothyroxine, supportive care, warming, treat precipitating cause.

What is the treatment for Graves' ophthalmopathy?

Steroids, selenium, sometimes surgery.

What is a contraindication for radioactive iodine?

Pregnancy, breastfeeding.

What are the symptoms of hypothyroidism?

Fatigue, cold intolerance, constipation, bradycardia, weight gain.

What are the symptoms of hyperthyroidism?

Heat intolerance, tachycardia, weight loss, tremor, diarrhea.

What are the lab findings in primary adrenal insufficiency (Addison's)?

↑ ACTH, ↓ cortisol, ↓ aldosterone, hyponatremia, hyperkalemia.

What are the lab findings in secondary adrenal insufficiency?

↓ ACTH, ↓ cortisol, aldosterone usually normal.

What is the presentation of an acute adrenal crisis?

Hypotension, shock, hyponatremia, hyperkalemia, hypoglycemia.

What is the treatment for adrenal crisis?

IV hydrocortisone + fluids + treat underlying cause.

What are the lab findings in Cushing's syndrome?

↑ cortisol; ACTH dependent or independent.

What is the difference between Cushing's disease and syndrome?

Disease = pituitary ACTH ↑; Syndrome = any cortisol excess.

What is the first-line test for Cushing's syndrome?

24-hour urine free cortisol or late-night salivary cortisol.

What are the lab findings in primary hyperaldosteronism?

↑ aldosterone, ↓ renin → hypokalemia, hypertension.

What is the treatment for hyperaldosteronism?

Spironolactone/eplerenone, surgery if adenoma.

What is the classic triad of symptoms for pheochromocytoma?

Headache, sweating, palpitations.

How is pheochromocytoma diagnosed?

↑ plasma free metanephrines or 24-hour urine catecholamines.

What is the pre-operative treatment for pheochromocytoma?

Alpha-blocker first, then beta-blocker.

What is the most common type of congenital adrenal hyperplasia?

21-hydroxylase deficiency.

What is the presentation of 21-hydroxylase deficiency?

Salt wasting, virilization, ambiguous genitalia in females.

What is the presentation of 11β-hydroxylase deficiency?

Hypertension, virilization, low renin.

What are the lab findings in primary hyperparathyroidism?

↑ PTH, ↑ Ca²⁺, ↓/normal phosphate.

What are the lab findings in secondary hyperparathyroidism?

↑ PTH, ↓/normal Ca²⁺, ↑ phosphate (CKD).

What are the lab findings in hypoparathyroidism?

↓ PTH, ↓ Ca²⁺, ↑ phosphate.

What are the lab findings in vitamin D deficiency?

↓ 25(OH)D, ↓/normal Ca²⁺, ↑ PTH.

What is the treatment for osteoporosis?

Bisphosphonates, denosumab, lifestyle, calcium + vitamin D.

What is the MOA of bisphosphonates?

Inhibit osteoclast-mediated bone resorption.

What are the AE of bisphosphonates?

Esophagitis, osteonecrosis of jaw, atypical femur fracture.

What is the MOA of denosumab?

RANKL inhibitor → ↓ osteoclast activity.

What are the AE of denosumab?

Hypocalcemia, osteonecrosis of jaw.

What is the MOA of calcitonin?

Inhibits osteoclasts → ↓ serum Ca²⁺.

What is the treatment for Paget's disease of bone?

Bisphosphonates, calcitonin if intolerant.

What are the symptoms of hypercalcemia?

Stones, bones, groans, psychiatric overtones.

What are the symptoms of hypocalcemia?

Tetany, Chvostek/ Trousseau signs, seizures.

What is Trousseau sign?

Carpal spasm with BP cuff inflation → hypocalcemia.

What is Chvostek sign?

Facial twitching when tapping facial nerve → hypocalcemia.

What is the formula for calcium correction for albumin?

Corrected Ca = measured Ca + 0.8*(4 - albumin).

What are examples of phosphate binders?

Sevelamer, calcium acetate.

What are the lab findings in rickets?

↓ Ca²⁺, ↓ phosphate, ↑ ALP, ↑ PTH.

What are the lab findings in osteomalacia?

Similar to rickets in adults; bone pain, fractures.

What is an example of a calcimimetic?

Cinacalcet → ↑ sensitivity of CaSR → ↓ PTH.

What are the causes of hyperphosphatemia?

CKD, hypoparathyroidism, excessive intake.

What are the causes of hypophosphatemia?

Malabsorption, vitamin D deficiency, refeeding syndrome.

What is the key difference between osteoporosis and osteomalacia?

Osteoporosis = bone density loss; osteomalacia = defective mineralization.

In which conditions is alkaline phosphatase elevated?

Bone turnover: Paget's, osteomalacia, healing fractures; liver disease.

What are the primary prevention strategies for osteoporosis?

Weight-bearing exercise, adequate calcium & vitamin D, avoid smoking/alcohol.

What is the normal serum sodium level?

135-145 mEq/L.

What defines hyponatremia?

Na⁺ <135 mEq/L.

What defines hypernatremia?

Na⁺ >145 mEq/L.

What are the causes of hypovolemic hyponatremia?

GI losses, diuretics, renal losses.

What are the causes of euvolemic hyponatremia?

SIADH, hypothyroidism, adrenal insufficiency.

What are the causes of hypervolemic hyponatremia?

CHF, cirrhosis, nephrotic syndrome.

What are the symptoms of hyponatremia?

Nausea, headache, confusion, seizures, coma.

What is the treatment for severe symptomatic hyponatremia?

Hypertonic saline (3%) cautiously, correct ≤8-10 mEq/L/day.

What are the symptoms of hypernatremia?

Thirst, lethargy, weakness, seizures, coma.

What is the treatment for hypernatremia?

Free water replacement; correct slowly to avoid cerebral edema.

What is the normal serum potassium level?

3.5-5.0 mEq/L.

What are the causes of hypokalemia?

Diuretics, GI losses, alkalosis, insulin, β-agonists.

What are the causes of hyperkalemia?

AKI/CKD, K⁺ supplements, medications (ACEi, ARB, K-sparing diuretics), acidosis.

What are the symptoms of hypokalemia?

Weakness, cramps, arrhythmias, U waves on ECG.

What are the symptoms of hyperkalemia?

Muscle weakness, peaked T waves, arrhythmias.