When to intubate in GCS?

GCS ≤ 8 requires intubation for airway protection. The patient cannot protect their own airway at this level of consciousness. Motor score is the most prognostically important component.

What is the best initial fluid for sepsis resuscitation?

Lactated Ringer's (LR) is the preferred resuscitation fluid. The SMART trial (2018) showed balanced crystalloids reduced death, new renal failure, and persistent renal dysfunction compared to normal saline.

When to start vasopressors in septic shock?

Start norepinephrine (first-line vasopressor) if MAP remains < 65 mmHg after initial 30 mL/kg crystalloid resuscitation, or earlier if patient is profoundly hypotensive. Do not delay pressors to complete full fluid resuscitation.

Why can serum uric acid be normal during acute gout?

During acute inflammation, IL-6 increases renal urate excretion and redistributes urate from plasma to tissues. Up to 40% of acute gout flares have normal serum uric acid. Joint aspiration with polarized microscopy is needed for definitive diagnosis.

How do you distinguish lupus flare from infection in SLE?

Key clues: CRP is low/normal in flare but elevated in infection. Complement (C3/C4) drops in flare but is normal/elevated in infection. Procalcitonin is elevated in bacterial infection but normal in flare. Anti-dsDNA rises in flare, stable in infection.

What is the difference between DKA and HHS?

DKA features acidosis (pH 600), hyperosmolality (> 320), and minimal ketosis -typically in Type 2 DM. DKA requires insulin drip; HHS requires aggressive fluid resuscitation first.

When to give tPA in acute ischemic stroke?

IV alteplase (tPA) can be given within 4.5 hours of last known well time in eligible patients. CT head must rule out hemorrhage first. For large vessel occlusion, mechanical thrombectomy can be performed up to 24 hours with favorable imaging.

What antibiotics for community-acquired pneumonia?

Inpatient non-ICU: ceftriaxone + azithromycin. ICU: ceftriaxone + azithromycin (add vancomycin if MRSA risk). Outpatient healthy: amoxicillin. Outpatient with comorbidities: augmentin + azithromycin or respiratory fluoroquinolone. Duration: 5 days if clinically stable for 48 hours.

How to interpret iron studies?

Iron deficiency: low ferritin (< 30), high TIBC, low iron, low transferrin saturation (< 20%). Anemia of chronic disease: normal/high ferritin (acute phase reactant), low TIBC, low iron. A ferritin of 50-100 in an inflamed patient may still represent iron deficiency.

What is the correction rate for hyponatremia?

Correct sodium no more than 8 mEq/L in 24 hours to avoid osmotic demyelination syndrome (ODS). For symptomatic severe hyponatremia with seizures, give 3% hypertonic saline 100-150 mL bolus over 10-20 minutes. If overcorrected, use D5W + DDAVP rescue protocol.

When to start antibiotics in meningitis?

Within 30-60 minutes. Do NOT delay antibiotics for LP or CT. Draw blood cultures, start empiric antibiotics (vancomycin + ceftriaxone ± ampicillin if > 50 or immunocompromised), then perform LP when possible. Dexamethasone should be given before or with the first antibiotic dose.

DOACs vs warfarin in antiphospholipid syndrome?

DOACs are contraindicated in APS. The TRAPS trial (2018) showed rivaroxaban was inferior to warfarin with more thrombotic events in triple-positive APS patients. Warfarin with INR target 2-3 is the standard for APS, indefinitely.

How to manage scleroderma renal crisis?

ACE inhibitors (captopril) are life-saving -start immediately and titrate aggressively. Do NOT hold for rising creatinine. Steroids > 15 mg prednisone per day precipitate scleroderma renal crisis. ARBs are NOT a substitute -evidence is only for ACEi.

What are the 4 pillars of heart failure treatment?

Guideline-directed medical therapy (GDMT) for HFrEF: (1) ARNI or ACEi/ARB, (2) beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) MRA (spironolactone or eplerenone), (4) SGLT2 inhibitor (dapagliflozin or empagliflozin). All four should be initiated and titrated to target doses.

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High-YieldEndocrine

Hypoparathyroidism

Low PTH → hypocalcemia + hyperphosphatemia. Most common cause: post-thyroidectomy/parathyroidectomy. Chvostek and Trousseau signs. Treat with calcium + calcitriol. Monitor for QTc prolongation and seizures.

🔍 Overview

Pathophysiology

PTH maintains serum calcium by: (1) increasing renal Ca²⁺ reabsorption, (2) stimulating osteoclasts (bone resorption), (3) activating vitamin D (1,25-dihydroxy) in the kidney → ↑ intestinal Ca²⁺ absorption. Loss of PTH → low calcium, high phosphate.

Etiology

Cause	Details
Post-surgical (#1)	After thyroidectomy or parathyroidectomy -parathyroid glands damaged/removed
Autoimmune	Autoimmune polyendocrine syndrome type 1 (APS-1)
Hypomagnesemia	Mg < 1.0 → impaired PTH secretion AND PTH resistance. Fix Mg first!
Infiltrative	Hemochromatosis, Wilson disease, metastatic cancer
DiGeorge syndrome	22q11 deletion -absent parathyroids + thymic aplasia

Always check magnesium in hypocalcemia. Hypomagnesemia causes functional hypoparathyroidism -PTH cannot be secreted or act properly. Calcium will NOT correct until magnesium is repleted.

Causes of Hypoparathyroidism

Cause	Mechanism	Key Feature
Post-surgical (most common)	Parathyroid glands damaged or removed during thyroidectomy/parathyroidectomy	Hypocalcemia within 24–72h post-op; may be transient or permanent
Autoimmune	Autoimmune destruction of parathyroid glands (APS-1: AIRE gene mutation)	Associated with mucocutaneous candidiasis, adrenal insufficiency
DiGeorge syndrome	22q11.2 deletion → absent/hypoplastic parathyroids	Congenital: cardiac defects, thymic aplasia, characteristic facies
Hypomagnesemia (functional)	Mg < 1.0 → impaired PTH secretion AND end-organ PTH resistance	PTH is low despite low calcium; calcium won't correct until Mg repleted
Infiltrative (hemochromatosis, Wilson)	Iron/copper deposition in parathyroid glands destroys tissue	Look for liver disease, skin changes; check ferritin, ceruloplasmin

Mnemonic -CHVOSTEK for Signs of Hypocalcemia:
Chvostek sign (facial twitch on tapping) · Hyperreflexia · Vitals (prolonged QT interval) · Obtundation/seizures · Spasm (Trousseau sign -carpopedal spasm) · Tetany · Excitability (neuromuscular irritability) · Kidney stones (chronic hypercalciuria → nephrocalcinosis)

🚨 Management

Acute Symptomatic Hypocalcemia

Calcium gluconate 1–2g IV over 10–20 min (preferred over CaCl for peripheral IV -less tissue necrosis)
Follow with continuous infusion: 0.5–1.5 mg/kg/hr of elemental calcium
Correct magnesium if low -MgSO₄ 2g IV
Continuous telemetry -monitor QTc

Chronic Management

Calcium Carbonate (Tums) 1–3g elemental calcium daily in divided doses
Calcitriol (Rocaltrol) 0.25–2 mcg daily -active vitamin D (PTH normally activates vitamin D; without PTH, must give active form)
Natpara (recombinant PTH) -for refractory cases not controlled with calcium/calcitriol

Acute vs Chronic Management

Setting	Treatment	Details
Acute	IV Calcium Gluconate	1–2g IV over 10 min; preferred for peripheral IV (less tissue necrosis)
	Continuous calcium drip	0.5–1.5 mg/kg/hr elemental calcium; titrate to ionized Ca q4–6h
	Cardiac monitoring	Continuous telemetry -prolonged QTc → torsades risk; correct Mg simultaneously
Chronic	Calcitriol (Rocaltrol)	0.25–2 mcg daily -active vitamin D (bypasses PTH-dependent activation)
	Calcium Carbonate (Tums)	1–3g elemental calcium daily in divided doses with food
	Thiazide diuretics	Reduce urinary calcium excretion → prevent nephrocalcinosis/kidney stones
	Natpara (recombinant PTH)	PTH replacement for refractory cases; reduces calcium/calcitriol requirements

🧪 Workup

Serum calcium -low (correct for albumin: add 0.8 per 1g albumin below 4)
Ionized calcium -most accurate
PTH -low or inappropriately normal (confirms hypoparathyroidism)
Phosphate -elevated (PTH normally promotes PO₄ excretion)
Magnesium -check in ALL hypocalcemia. Low Mg → functional hypoPTH
25-OH vitamin D -rule out deficiency (common confounder)
ECG -prolonged QTc

💊 Medications

Drug	Dose	Purpose
Calcium Gluconate	1–2g IV over 10–20 min	Acute symptomatic hypocalcemia -peripheral IV safe
Calcium Chloride	1g IV	3× more elemental Ca than gluconate -central line only (tissue necrosis risk)
Calcitriol (Rocaltrol)	0.25–2 mcg daily	Active vitamin D -replaces PTH-dependent activation
Calcium Carbonate (Tums)	500–1500 mg elemental Ca TID	Chronic oral replacement. Take with food (needs acid for absorption).
Magnesium Sulfate	2–4g IV	Correct hypomagnesemia FIRST -calcium won't correct otherwise

📋 On Rounds

Pimp Questions

Why must you check magnesium before treating hypocalcemia?

Magnesium is essential for both PTH secretion and PTH action at target organs. When Mg is < 1.0 mg/dL: (1) PTH secretion is impaired (despite low calcium, PTH remains low), (2) PTH receptors are resistant. Giving calcium without fixing magnesium is futile -the body cannot maintain calcium homeostasis. Always check and correct Mg first in any hypocalcemia.

📋 Case 1, Post-Thyroidectomy Hypocalcemia

Patient: 54F, post-op day 1 from total thyroidectomy for papillary thyroid carcinoma. Reports perioral tingling and fingertip numbness.

Exam: Chvostek sign positive (facial twitch on tapping). Trousseau sign positive. HR 88, BP 118/72.

Labs: Total Ca 6.8 mg/dL (low), ionized Ca 0.82 mmol/L (low), PO₄ 5.2 (high), PTH < 5 pg/mL (low), Mg 2.0 (normal).

ECG: Prolonged QTc at 510 ms.

Management:

Calcium gluconate 2g IV over 10 min → symptoms improve within minutes
Start continuous calcium drip at 1 mg/kg/hr elemental calcium
Continuous telemetry for QTc monitoring
Begin Calcitriol (Rocaltrol) 0.5 mcg BID + oral calcium carbonate 1g TID
Check ionized Ca q4–6h; taper IV calcium as oral takes effect
Counsel patient: may need lifelong calcium + calcitriol if parathyroids do not recover

Key lesson: Post-thyroidectomy hypocalcemia is the #1 cause of hypoparathyroidism. Always monitor calcium in the first 24–72h post-op. Symptomatic patients need IV calcium urgently.

📋 Case 2, DiGeorge Syndrome with Seizure

Patient: 8-month-old male with known 22q11.2 deletion (DiGeorge syndrome), history of tetralogy of Fallot repair. Presents with generalized tonic-clonic seizure lasting 2 minutes.

Labs: Ionized Ca 0.7 mmol/L (critically low), total Ca 5.9 mg/dL, PO₄ 7.1 (high), PTH < 3 pg/mL, Mg 1.8 (normal).

Management:

IV calcium gluconate 100 mg/kg (max 2g) slow push over 10 min with cardiac monitoring
Seizure resolves with calcium correction
Start Calcitriol (Rocaltrol) 0.25 mcg daily + oral calcium supplements
Immunology consult (thymic aplasia → T-cell deficiency)
Lifelong calcium and calcitriol replacement -absent parathyroids will not recover

Key lesson: DiGeorge syndrome = absent parathyroids + thymic aplasia. Seizures in DiGeorge should trigger immediate calcium check. These patients need lifelong replacement -no chance of parathyroid recovery.

📋 Case 3, Chronic Hypoparathyroidism with Nephrocalcinosis

Patient: 62F with chronic hypoparathyroidism (post-thyroidectomy 8 years ago), on calcitriol 1 mcg BID + calcium carbonate 1.5g TID. Presents with flank pain. CT shows bilateral nephrocalcinosis.

Labs: Total Ca 9.2 (normal on replacement), 24h urine Ca 420 mg (elevated, normal < 300), creatinine 1.4 (baseline 0.9), PO₄ 4.8.

Problem: Without PTH, kidneys cannot reabsorb calcium → chronic hypercalciuria → nephrocalcinosis → renal damage despite normal serum calcium.

Management:

Add hydrochlorothiazide 25 mg daily -thiazide diuretics enhance renal calcium reabsorption, reducing urinary calcium
Reduce calcitriol dose to 0.5 mcg BID (lower target serum Ca to low-normal 8.0–8.5)
Consider Natpara (recombinant PTH) -PTH replacement restores physiologic calcium handling, reduces urinary calcium
Low-sodium diet (Na increases urinary Ca excretion)
Nephrology consult for CKD management
Monitor 24h urine calcium q3–6 months, renal US annually

Key lesson: Chronic hypoparathyroidism management is a balancing act. Aim for low-normal serum Ca to minimize urinary calcium losses. Thiazides and PTH replacement (Natpara) are key tools for preventing nephrocalcinosis.

⚡ Summary

#1 Cause

Post-thyroidectomy/parathyroidectomy. Iatrogenic parathyroid removal/damage.

Lab Pattern

↓ Ca, ↓ PTH, ↑ PO₄. Always check Mg -low Mg causes functional hypoPTH.

Acute Rx

Calcium gluconate 1-2g IV (peripheral safe). CaCl via central only. Telemetry for QTc.

Chronic Rx

Oral calcium carbonate + calcitriol (active vitamin D -bypasses need for PTH activation).

Fix Mg First

Mg < 1.0 → impaired PTH secretion AND resistance. Calcium won't correct without Mg.

Monitoring

Ionized Ca, QTc (torsades risk), 24h urine Ca (nephrocalcinosis), renal US annually.