Ans. C: Acute pancreatitisHypoalbuminemia is the most common cause of hypocalcemia and is due to cirrhosis, nephrosis, malnutrition, burns, chronic illness, and sepsis.Hypomagnesemia causes end-organ resistance to PTH and inhibits the hypocalcemic feedback loop through unceain mechanisms. Causes of hypomagnesemia include pancreatitis, aminoglycoside treatment, amphotericin B, loop diuretics, alcoholism, and malnutrition.Hyperphosphatemia may be seen in critical illness and in patients who have ingested phosphate-containing enemas. Phosphate binds calcium avidly, causing acute hypocalcemia.Multifactorial causes are probably the most clinically relevant hypocalcemic emergencies include the following:- Acute pancreatitis: Free fatty acids chelate calcium, causing saponification in the retroperitoneum.- Rhabdomyolysis: Increased phosphates from creatine phosphokinase (CPK) and other anions (i.e., lactate, bicarbonate) chelate calcium.- Sepsis can cause hypocalcemia through many mechanisms.- Toxic shock syndrome can cause hypocalcemia.High calcitonin levels cause low calcium.- Malignancy: Osteoblastic metastases (e.g., breast cancer, prostate cancer) and tumor lysis syndrome may cause hypocalcemia (by differing mechanisms).- Hepatic or renal insufficiency: Calciuresis, hypomagnesemia, hypoalbuminemia, and low active vitamin D levels may contribute to poor calcium homeostasis.- Infiltrative disease: Sarcoidosis, tuberculosis, and hemochromatosis may infiltrate the parathyroids, causing dysfunction.-- Toxicologic causes include hydrofluoric acid burn or ingestion.Enhanced protein binding and anion chelation- Protein binding is enhanced by elevated pH and free fatty acid release in high catecholamine states.Anion chelation is seen in high phosphate states (e.g., renal failure, rhabdomyolysis, mesenteric ischemia, oraladministration of phosphate-containing enemas); high citrate states (e.g., massive blood transfusion, radiocontrastdyes); and high bicarbonate, lactate, and oxalate levels.Medication effects- Proton pump inhibitors (PPIs) reduce gastric acid production resulting in reduced calcium absorption.- Selective serotonin inhibitors can have a calcium antagonistic effect on smooth muscle, paicularly vascular endothelium.- Calcitonin and bisphosphonates cause chelation and end-organ inhibition.- Phenobarbital and phenytoin enhance vitamin D catabolism and decrease calcium resorption in the gut.Foscarnet complexes with calcium.Fluoride, paicularly hydrofluoric acid, chelates calcium avidly and causes profound hypocalcemia. Ethylene glycol complexes with calcium.Estrogen inhibits bone resorption.Cimetidine decreases gastric pH, slowing fat breakdown, which is necessary to complex calcium for gut absorption.Aluminum and alcohol suppress PTH.Gadolinium-based contrast material can falsely lower serum calcium levels and should be considered if levels are drawn sholy after magnetic resonance imaging.Postsurgical effectsParathyroid adenoma resection causes a transient hypocalcemia due to end-organ PTH resistance in the first postoperative day.Pancreatectomy prevents calcium absorption in the duodenum and the jejunum by eliminating necessary enzymes.Small bowel syndrome causes hypocalcemia by reducing the surface available to absorb fatty acids and calcium.PTH deficiency/resistanceInfiltrative diseases include Wilson disease and metastatic cancer.Pseudohypoparathyroidism is due to PTH resistance and has many forms, most notably Albright disease. Renal failure can result in a variety of endocrine disorders, occasionally including hypocalcemia.Vitamin D deficiency/resistance- Rickets may be due to lack of vitamin D or end-organ receptor resistance.- Hepatorenal disease: The liver and the kidney provide intermediary enzymes to form active 1,25 (OH)2 D.