CAMC Regional Medical Registration Examination Part 1

Administer intravenous hydrocortisone 100 mg stat bolus and initiate rapid infusion of 0.9% normal saline with 5% dextrose. This patient presents with acute Addisonian (adrenal) crisis superimposed on chronic primary adrenal insufficiency (Addison's disease), evidenced by preexisting mucocutaneous hyperpigmentation, severe refractory hypotension, abdominal pain simulating peritonitis, hyperkalemia (6.4 mmol/L), hyponatremia (122 mmol/L), normal-anion-gap metabolic acidosis (122 − 96 − 16 = 10 mmol/L), and hypoglycemia (2.8 mmol/L). In acute adrenal crisis, therapy must never be delayed for diagnostic procedures such as the ACTH stimulation test. Immediate life-saving management requires an intravenous bolus of hydrocortisone 100 mg stat, followed by 200 mg/24 hours (continuous IV infusion or 50 mg every 6 hours), coupled with rapid volume expansion using 0.9% normal saline with 5% dextrose. Saline with dextrose restores intravascular volume, corrects hyponatremia, and treats hypoglycemia. Fludrocortisone is unnecessary in the acute resuscitation phase because high-dose hydrocortisone provides maximal mineralocorticoid receptor binding.

Q: A 64-year-old male heavy smoker presents with progressive lethargy, confusion, constipation, and polyuria over the past 2 weeks. Physical examination reveals severe dehydration and dry oral mucosa. An electrocardiogram shows normal sinus rhythm with a markedly shortened QT interval (QTc 320 ms). Laboratory testing shows: serum sodium 140 mmol/L, serum potassium 3.8 mmol/L, serum creatinine 185 umol/L, total serum calcium 3.85 mmol/L (normal 2.15-2.55), serum albumin 30 g/L (corrected calcium 4.05 mmol/L), and serum phosphate 0.65 mmol/L. Intact parathyroid hormone (PTH) is suppressed at 4 pg/mL (normal 15-65), and serum PTHrP is markedly elevated. A chest radiograph demonstrates a 4 cm cavitating mass in the right upper lobe. What is the primary diagnosis and the most appropriate initial resuscitation strategy?

Humoral hypercalcemia of malignancy; aggressively hydrate with intravenous 0.9% normal saline at 200-300 mL/h, administer intravenous zoledronic acid, and add short-term subcutaneous calcitonin. This patient has severe hypercalcemia of malignancy (corrected calcium 4.05 mmol/L) secondary to Humoral Hypercalcemia of Malignancy (HHM) driven by tumor secretion of Parathyroid Hormone-related Protein (PTHrP) from a cavitating squamous cell bronchogenic carcinoma. The hallmark biochemical profile of HHM is severe hypercalcemia, low serum phosphate (0.65 mmol/L), and a suppressed intact PTH (< 10 pg/mL) with elevated PTHrP. The shortened QT interval on ECG is a classic manifestation of hypercalcemia. Emergency management requires a multimodal approach: (1) Aggressive volume resuscitation with 0.9% normal saline (initially about 200–300 mL/h, then adjusted to hydration, urine output and cardiac/renal status with overload monitoring) to reverse dehydration and restore renal calciuria; (2) Intravenous bisphosphonates (zoledronic acid 4 mg IV over 15 minutes) to potently inhibit osteoclastic bone resorption (effective after 48-72 hours); and (3) Subcutaneous or IM calcitonin (4-8 IU/kg every 12 hours) to provide rapid reduction of serum calcium within 2-4 hours as a bridge. Loop diuretics (furosemide) are strictly contraindicated until intravascular volume is fully re-expanded.

Q: A 44-year-old woman undergoes total thyroidectomy for multinodular goiter with compressive tracheal symptoms. Twenty-four hours postoperatively, she reports perioral numbness, tingling in her fingers and toes, and severe muscle cramps in both calves. On physical examination, tapping lightly over the facial nerve anterior to the ear elicits rapid twitching of the ipsilateral upper lip. Inflating a blood pressure cuff on her upper arm to 20 mmHg above systolic pressure precipitates painful carpal spasm with flexion of the wrist and adduction of the thumb within 90 seconds. An ECG reveals sinus rhythm with marked QT interval prolongation (QTc 510 ms). Stat laboratory tests reveal: corrected serum calcium 1.68 mmol/L (normal 2.15-2.55) and serum magnesium 0.52 mmol/L (normal 0.70-1.05). What is the most appropriate initial management step?

Administer 10 to 20 mL of 10% intravenous calcium gluconate diluted in 50 to 100 mL of 5% dextrose over 10 to 20 minutes, concurrently administering intravenous magnesium sulfate. This patient exhibits acute symptomatic hypocalcemia following total thyroidectomy (secondary to inadvertent parathyroid gland excision or ischemia), demonstrating classic Chvostek's and Trousseau's signs and marked ECG QT prolongation. Emergency management mandates immediate intravenous calcium gluconate 10% (10-20 mL diluted in 50-100 mL of 5% dextrose infused over 10-20 minutes with continuous cardiac monitoring). Calcium gluconate is preferred over calcium chloride because calcium chloride causes severe chemical thrombophlebitis and deep tissue necrosis if peripheral extravasation occurs. Concurrently, intravenous magnesium sulfate (1-2 g IV over 20 minutes) must be co-administered because hypomagnesemia (< 0.70 mmol/L) impairs both parathyroid hormone secretion and induces peripheral organ resistance to PTH; hypocalcemia is refractory to calcium therapy until the concurrent hypomagnesemia is fully corrected. Oral calcium and active vitamin D (calcitriol) are instituted as follow-up maintenance therapy.

Key Takeaways

Primary adrenal insufficiency (Addison's disease) destroys all three adrenal cortical zones, resulting in concurrent glucocorticoid and mineralocorticoid deficiency characterized by hyperpigmentation, severe hyponatremia, hyperkalemia, and non-anion gap metabolic acidosis.
Secondary adrenal insufficiency spares mineralocorticoid production because aldosterone is regulated by the renin-angiotensin-aldosterone system; hyperkalemia and cutaneous hyperpigmentation are characteristically absent.
Acute Addisonian crisis is an emergency shock state refractory to volume and vasopressors; immediate management with IV hydrocortisone 100 mg stat and 0.9% saline with 5% dextrose must never be delayed for diagnostic confirmation.
Cushing's syndrome screening requires at least two concordant positive tests (overnight 1 mg dexamethasone suppression test, 24-hour urinary free cortisol, or late-night salivary cortisol) before plasma ACTH measurement differentiates ACTH-dependent from ACTH-independent etiologies.
Severe hypercalcemia (corrected Ca > 3.5 mmol/L) produces ECG QT shortening and requires IV isotonic saline titrated to hydration, urine output and cardiac/renal status plus IV zoledronic acid, whereas acute symptomatic hypocalcemia produces QT prolongation and tetany requiring urgent 10% IV calcium gluconate and magnesium correction.

Last updated: November 2026

Adrenal Insufficiency: Primary vs. Secondary

Adrenal insufficiency develops when adrenal cortical hormone production fails to meet physiological demands. Differentiating primary adrenal insufficiency (Addison's disease) from secondary or tertiary adrenal failure is a foundational clinical skill that governs both diagnostic testing and long-term replacement therapy.

Primary Adrenal Insufficiency (Addison's Disease)

Primary adrenal failure involves progressive destruction or dysfunction of all three zones of the adrenal cortex:

Zona Glomerulosa Deficiency (Mineralocorticoid / Aldosterone): Loss of aldosterone impairs renal distal tubular sodium reabsorption and potassium/hydrogen ion excretion. This produces hypovolemia, postural hypotension, severe hyponatremia, hyperkalemia, and non-anion gap (normal anion gap) metabolic acidosis.
Zona Fasciculata Deficiency (Glucocorticoid / Cortisol): Cortisol deficiency causes anorexia, nausea, weight loss, generalized weakness, hypoglycemia, and unresponsiveness to vasopressors.
Zona Reticularis Deficiency (Androgens): Decreased DHEA-S leads to loss of axillary and pubic hair and reduced libido, most apparent in women.
Mucocutaneous Hyperpigmentation: The absence of negative feedback by cortisol triggers excessive hypothalamic CRH and anterior pituitary synthesis of pro-opiomelanocortin (POMC). Cleavage of POMC yields both adrenocorticotropic hormone (ACTH) and melanocyte-stimulating hormone (alpha-MSH), which stimulates melanocytes. Hyperpigmentation is most pronounced in sun-exposed areas, palmar skin creases, vermilion border of the lips, buccal mucosa, friction points (elbows, knees), and surgical scars.
Etiologies: Autoimmune adrenalitis (anti-21-hydroxylase antibodies) is a common cause of primary adrenal insufficiency. Other causes include infectious adrenalitis, including Mycobacterium tuberculosis (producing bilateral enlarged, calcified adrenal glands on CT), Histoplasma capsulatum, cytomegalovirus (CMV) in advanced HIV/AIDS, and bilateral adrenal hemorrhage (Waterhouse-Friderichsen syndrome associated with Neisseria meningitidis septicemia or antiphospholipid syndrome).

Secondary & Tertiary Adrenal Insufficiency

Secondary failure results from anterior pituitary ACTH deficiency (pituitary adenomas, Sheehan's postpartum pituitary necrosis, cranial irradiation), while tertiary failure results from hypothalamic CRH suppression. By far the most common cause in clinical practice is abrupt withdrawal of prolonged exogenous glucocorticoid therapy.

Critical Pathophysiological Distinction: In secondary/tertiary adrenal insufficiency, zona glomerulosa function is preserved because aldosterone secretion is regulated by the renin-angiotensin-aldosterone system (RAAS) and extracellular potassium, independent of ACTH. Consequently:
- No hyperkalemia is present (potassium is normal).
- No severe salt wasting or marked hypovolemia occurs.
- No hyperpigmentation develops (ACTH is low or inappropriately normal; skin often appears strikingly pale).

Diagnostic Evaluation & Acute Adrenal Crisis

Biochemical Diagnosis

Morning Serum Cortisol (08:00–09:00): Interpret with the assay and clinical context in stable patients. NICE modern-immunoassay guidance uses <150 nmol/L (~5.4 mcg/dL) as possible adrenal insufficiency requiring assessment, 150–300 nmol/L as indeterminate, and >300 nmol/L (~10.9 mcg/dL) as making insufficiency very unlikely. Follow local guidance for other assays; do not delay crisis treatment.
Short Synacthen (Cosyntropin) Test: Give 250 mcg synthetic ACTH IM or IV and measure cortisol at baseline and 30 and/or 60 minutes. Compare the peak with the laboratory's validated assay cutoff. 500 nmol/L (~18 mcg/dL) is a historical threshold; newer assays often use lower cutoffs. A universal 500–550 threshold can falsely label a normal response deficient.
Plasma ACTH: With confirmed cortisol deficiency, ACTH >2 times the assay upper reference limit supports primary adrenal insufficiency; low or inappropriately normal ACTH supports central failure. Interpret the stimulation test with specialist advice if recent central disease is suspected.

Acute Addisonian (Adrenal) Crisis

Adrenal crisis is a life-threatening medical emergency triggered by an acute physiological stressor (infection, surgery, trauma, acute gastroenteritis, or missed steroid doses) in a patient with pre-existing adrenal insufficiency.

Clinical Hallmarks: Severe, refractory hypotension and circulatory shock unresponsive to aggressive volume expansion and vasopressors; acute severe abdominal pain mimicking an acute surgical peritonitis; high spiking fevers; vomiting and diarrhea; profound hypoglycemia; and severe hyperkalemia with hyponatremia.
Emergency Resuscitation Protocol:
1. Immediate Glucocorticoid Replacement: Administer Intravenous Hydrocortisone 100 mg stat bolus, followed by 200 mg every 24 hours (50 mg IV every 6 hours or continuous IV infusion until clinical recovery, then taper with specialist advice). Clinical Mandate: Never delay hydrocortisone administration to perform diagnostic testing in a clinically unstable patient.
2. Mineralocorticoid Coverage: At doses >= 100 mg/day, hydrocortisone provides maximal mineralocorticoid receptor saturation; exogenous mineralocorticoid (fludrocortisone) is unnecessary in the acute crisis phase.
3. Aggressive Crystalloid Resuscitation: Infuse 0.9% Normal Saline with 5% Dextrose (1000 mL in the first hour, followed by 2 to 3 liters over the next 24 hours). This concurrently restores intravascular volume, corrects hyponatremia, and treats life-threatening hypoglycemia. Avoid potassium-containing fluids (such as Ringer's lactate).
4. Long-Term Maintenance: Once the patient is hemodynamically stable and eating, transition to oral Hydrocortisone (15 to 25 mg total daily dose, divided into 2 or 3 doses with the largest dose upon waking: e.g., 10 mg at 08:00, 5 mg at 12:00, 2.5 mg at 17:00) PLUS Fludrocortisone (0.05 to 0.2 mg once daily in the morning) for primary adrenal insufficiency. Counsel extensively on 'Sick Day Rules' (double the oral hydrocortisone dose for fevers > 38°C; triple dose for severe illness; carry a medical alert necklace and emergency injectable hydrocortisone 100 mg IM kit).

Cushing's Syndrome: Diagnostic Algorithm & Differential

Cushing's syndrome refers to the constellation of signs and symptoms caused by chronic glucocorticoid excess. Cushing's disease refers specifically to hypercortisolism caused by a pituitary ACTH-secreting corticotroph adenoma.

Clinical Manifestations

Facial rounding ('moon facies'), facial plethora, central truncal adiposity with supraclavicular and dorsocervical fat pads ('buffalo hump'), thinning of the skin, easy bruising, wide violaceous abdominal striae (> 1 cm in width), proximal muscle myopathy (difficulty climbing stairs or rising from a chair), secondary hypertension, impaired glucose tolerance or overt diabetes, osteoporosis, and neuropsychiatric changes (insomnia, depression, psychosis).

Diagnostic Algorithm for Hypercortisolism

Phase 1: Confirm Hypercortisolism (Exogenous Steroid Use Excluded First): Diagnosis requires at least two concordant abnormal screening tests:
1. Overnight 1 mg Dexamethasone Suppression Test (ODST): Administer 1 mg dexamethasone orally at 23:00; measure fasting serum cortisol at 08:00 the following morning. Normal is suppression of cortisol to < 50 nmol/L (< 1.8 mcg/dL). Failure to suppress indicates autonomous hypercortisolism.
2. 24-Hour Urinary Free Cortisol (UFC): Requires proper collection; levels > 3-fold above the upper limit of normal confirm hypercortisolism.
3. Late-Night Salivary Cortisol (measured at 23:00): Elevated levels demonstrate loss of the normal circadian nadir.
Phase 2: Establish ACTH-Dependence:
- Plasma ACTH < 5 pg/mL (Suppressed): ACTH-Independent Cushing's Syndrome. Autonomous adrenal production. Perform thin-slice contrast-enhanced Adrenal CT/MRI (differentiating unilateral benign adenoma, adrenocortical carcinoma, and bilateral nodular hyperplasia).
- Plasma ACTH > 15 to 20 pg/mL (Elevated or Inappropriately Normal): ACTH-Dependent Cushing's Syndrome.
Phase 3: Differentiate Pituitary vs. Ectopic ACTH Source:
- Cushing's Disease (Pituitary Adenoma, ~80% of ACTH-dependent): Retains partial negative feedback responsiveness. Serum cortisol suppresses by > 50% following a High-Dose (8 mg) Dexamethasone Suppression Test (HDDST) and exhibits exaggerated ACTH/cortisol surges following IV CRH administration. Pituitary MRI detects adenomas in 60-70%; Bilateral Inferior Petrosal Sinus Sampling (BIPSS) with CRH stimulation represents the definitive gold standard when MRI is negative or equivocal.
- Ectopic ACTH Secretion (~20% of ACTH-dependent): Typically caused by small cell lung carcinoma, bronchial carcinoid tumors, or pancreatic neuroendocrine neoplasms. Shows no cortisol suppression on high-dose dexamethasone and no response to CRH. Presents with severe hypokalemic metabolic alkalosis, profound muscle wasting, and hyperpigmentation.

Calcium Homeostasis: Hypercalcemia & Hypocalcemia

Extracellular calcium is tightly regulated within a narrow physiological range (corrected serum calcium 2.15 to 2.55 mmol/L [8.6 to 10.2 mg/dL]) by parathyroid hormone (PTH), 1,25-dihydroxyvitamin D (calcitriol), and calcitonin.

Hypercalcemia

More than 90% of all hypercalcemia cases are caused by either Primary Hyperparathyroidism or Hypercalcemia of Malignancy.

Primary Hyperparathyroidism: Most common in ambulatory outpatients. Solitary benign parathyroid adenoma (85%), multiglandular hyperplasia (15%), or parathyroid carcinoma (< 1%). Characterized by elevated or inappropriately normal PTH in the setting of hypercalcemia, low serum phosphate, hypercalciuria, and elevated 1,25-(OH)2D. Classically presents with 'bones, stones, abdominal groans, and psychic moans' (osteitis fibrosa cystica, nephrolithiasis, peptic ulcer, acute pancreatitis, depression).
Hypercalcemia of Malignancy: Most common in hospitalized patients. Driven by (1) Humoral hypercalcemia via tumor secretion of Parathyroid Hormone-related Protein (PTHrP) (squamous cell carcinomas of lung, head and neck, cervix, esophagus); (2) Osteolytic metastases (breast cancer, multiple myeloma); or (3) Ectopic production of 1,25-(OH)2D by lymphomas. Laboratory findings show hypercalcemia with a suppressed intact PTH (< 10 pg/mL).
ECG Features: Hypercalcemia causes shortening of the QT interval and widens the T-wave, predisposing to ventricular arrhythmias.
Emergency Treatment of Severe Hypercalcemia (Corrected Ca > 3.5 mmol/L [> 14 mg/dL]):
1. Aggressive Isotonic Saline Resuscitation: Start 0.9% NaCl at about 200–300 mL/hour in a volume-depleted adult, then adjust to hydration, urine output and cardiac/renal status while monitoring for overload. Volume replacement restores filtration and promotes urinary calcium excretion; the initial hourly rate is not a fixed 24-hour fluid prescription.
2. Intravenous Bisphosphonates: Administer Zoledronic Acid 4 mg IV over 15 minutes (or Pamidronate 60 to 90 mg IV over 2 to 4 hours). Highly potent osteoclast inhibitor; clinical onset is 48 to 72 hours, with peak calcium-lowering efficacy at 4 to 7 days. (Dose adjustment required in renal impairment).
3. Calcitonin: 4 to 8 IU/kg SC or IM every 12 hours. Provides rapid onset of action (lowers calcium within 2 to 4 hours by inhibiting osteoclasts and promoting renal excretion), acting as a bridging agent while awaiting bisphosphonate effect. Limitation: Tachyphylaxis develops after 48 hours due to receptor downregulation.
4. Glucocorticoids (Prednisone 40 to 60 mg daily): First-line for hypercalcemia mediated by calcitriol excess (sarcoidosis, tuberculosis, lymphoma).
5. Avoid Loop Diuretics: Furosemide is contraindicated until the patient is completely volume-resuscitated, and is reserved solely for managing iatrogenic fluid overload.

Hypocalcemia

Etiologies: Accidental removal or devascularization of parathyroid glands during total thyroidectomy (most common acute cause); severe hypomagnesemia (magnesium depletion inhibits PTH secretion and induces end-organ resistance to PTH; hypocalcemia is refractory to calcium until magnesium is corrected); vitamin D deficiency; acute pancreatitis (saponification of calcium in retroperitoneal fat); and chronic kidney disease.
Clinical Manifestations: Neuromuscular excitability, circumoral paresthesias, numbness of digits, muscle cramps, and laryngeal stridor/bronchospasm.
Physical Signs:
- Chvostek's Sign: Tapping over the facial nerve anterior to the ear tragus elicits ipsilateral twitching of the facial and lip muscles.
- Trousseau's Sign: Inflating a sphygmomanometer cuff to 20 mmHg above systolic BP for 3 minutes precipitates painful carpopedal spasm (flexion of the wrist and metacarpophalangeal joints, extension of interphalangeal joints, and adduction of the thumb ['main d'accoucheur']).
ECG Features: Prolongation of the QT interval (primarily ST-segment lengthening), predisposing to Torsades de Pointes and ventricular fibrillation.
Emergency Treatment of Acute Hypocalcemia:
- Administer Intravenous Calcium Gluconate 10% (10 to 20 mL [1 to 2 ampules] diluted in 50 to 100 mL 5% Dextrose over 10 to 20 minutes) with continuous ECG monitoring.
- Clinical Pearl: Calcium gluconate is preferred over calcium chloride because calcium chloride causes severe tissue necrosis and thrombophlebitis if extravasation occurs.
- Concurrent Hypomagnesemia: If serum magnesium is low (< 0.7 mmol/L), co-administer Intravenous Magnesium Sulfate 1 to 2 g over 20 minutes; calcium levels will not normalize until magnesium stores are replenished.

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Acute Adrenal Crisis & Severe Hypercalcemia Resuscitation Flowchart

Test Your Knowledge

A 36-year-old woman with a history of vitiligo is brought to the emergency department in a state of severe circulatory shock. Her family reports a 3-month history of fatigue, weight loss, anorexia, and hyperpigmentation of her gums and skin creases. Over the past 24 hours, she developed severe abdominal pain, persistent vomiting, and confusion. Physical examination reveals a lethargic, hypotensive woman with diffuse bronze skin and dark pigmentation over her palmar creases and vermilion border. Vital signs: BP 74/42 mmHg, HR 126 bpm, RR 22 breaths/min, temperature 38.6°C. Laboratory results demonstrate: serum sodium 122 mmol/L, serum potassium 6.4 mmol/L, serum chloride 96 mmol/L, serum bicarbonate 16 mmol/L, blood glucose 2.8 mmol/L, and serum creatinine 172 umol/L. What is the most appropriate immediate medical intervention?

Perform a 250 mcg ACTH stimulation test and withhold corticosteroids until the 60-minute serum cortisol is drawn

Administer intravenous hydrocortisone 100 mg stat bolus and initiate rapid infusion of 0.9% normal saline with 5% dextrose

Administer intravenous fludrocortisone 0.1 mg stat with 0.45% half-normal saline and insulin with dextrose for hyperkalemia

Administer high-dose intravenous dexamethasone 10 mg stat, initiate noradrenaline infusion, and schedule an urgent laparotomy for acute peritonitis

Test Your Knowledge

A 64-year-old male heavy smoker presents with progressive lethargy, confusion, constipation, and polyuria over the past 2 weeks. Physical examination reveals severe dehydration and dry oral mucosa. An electrocardiogram shows normal sinus rhythm with a markedly shortened QT interval (QTc 320 ms). Laboratory testing shows: serum sodium 140 mmol/L, serum potassium 3.8 mmol/L, serum creatinine 185 umol/L, total serum calcium 3.85 mmol/L (normal 2.15-2.55), serum albumin 30 g/L (corrected calcium 4.05 mmol/L), and serum phosphate 0.65 mmol/L. Intact parathyroid hormone (PTH) is suppressed at 4 pg/mL (normal 15-65), and serum PTHrP is markedly elevated. A chest radiograph demonstrates a 4 cm cavitating mass in the right upper lobe. What is the primary diagnosis and the most appropriate initial resuscitation strategy?

Primary hyperparathyroidism; initiate oral cinacalcet and administer intravenous furosemide 80 mg bolus prior to fluids

Sarcoidosis; administer intravenous methylprednisolone 1 g daily and initiate emergency hemodialysis

Humoral hypercalcemia of malignancy; aggressively hydrate with intravenous 0.9% normal saline at 200-300 mL/h, administer intravenous zoledronic acid, and add short-term subcutaneous calcitonin

Vitamin D intoxication; initiate high-dose ergocalciferol and infuse 5% dextrose in water at 50 mL/h

Test Your Knowledge

A 44-year-old woman undergoes total thyroidectomy for multinodular goiter with compressive tracheal symptoms. Twenty-four hours postoperatively, she reports perioral numbness, tingling in her fingers and toes, and severe muscle cramps in both calves. On physical examination, tapping lightly over the facial nerve anterior to the ear elicits rapid twitching of the ipsilateral upper lip. Inflating a blood pressure cuff on her upper arm to 20 mmHg above systolic pressure precipitates painful carpal spasm with flexion of the wrist and adduction of the thumb within 90 seconds. An ECG reveals sinus rhythm with marked QT interval prolongation (QTc 510 ms). Stat laboratory tests reveal: corrected serum calcium 1.68 mmol/L (normal 2.15-2.55) and serum magnesium 0.52 mmol/L (normal 0.70-1.05). What is the most appropriate initial management step?

Administer 10 to 20 mL of 10% intravenous calcium gluconate diluted in 50 to 100 mL of 5% dextrose over 10 to 20 minutes, concurrently administering intravenous magnesium sulfate

Administer 10 mL of 10% intravenous calcium chloride rapid push via a peripheral vein, withholding magnesium until oral medications resume

Administer high-dose oral calcium carbonate 2000 mg and oral calcitriol 1.0 mcg, withholding intravenous therapy to avoid hypercalcemia

Administer intravenous furosemide 40 mg to stimulate parathyroid hormone release, followed by intramuscular vitamin D3

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