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.

RoundsRx

Dashboard

Overview

Recent

Rotations

Quick Reference

Antibiotic Guide Analgesia Guide Sedation Guide Bowel Regimen Electrolyte Replacement Pain Management & Conversions Drug Interactions Anticoag Reversal IV Fluid Guide Inotropes Guide Vasopressors Insulin Guide Code Blue & Rapid Response Procedures Guide ECG Interpretation Lab Interpretation Radiology Quick Ref GCS Pocket Card Admission Orders & I-PASS Landmark Trials

Tools

💎 Clinical Pearls 🧠 Pimp Me Quiz 🧮 Clinical Calculators 📰 What's New 🎓 Intern Survival Guide ✅ Rounding Checklists 🩺 Procedure Guides ⚡ Electrolyte Replacement 💧 IV Fluids Guide 🩸 Transfusion Guide 💓 ECG Pattern Guide 🧪 Lab Interpretation Guide 📱 QR Poster 🔗 Resources 🎙️ Channels & Podcasts 🎮 Medical Games 🏛️ Famous Cases 🎬 Media Library

ℹ️ About

Available offline

Endocrine

Hyperthyroidism / Graves' Disease

Graves' = most common cause of hyperthyroidism. TSI-mediated thyroid stimulation. Treatment: thionamides, RAI, or surgery. Know when each is preferred.

🔍 Overview

Overview

Hyperthyroidism = excessive thyroid hormone production/release. Causes: Graves' disease (70-80% -autoimmune, TSI stimulates TSH receptor), toxic multinodular goiter (elderly, autonomous nodules), toxic adenoma (single hot nodule), thyroiditis (subacute/painless -transient release of preformed hormone, NOT overproduction), exogenous thyroid hormone, iodine-induced (Jod-Basedow). Graves' has unique extra-thyroidal features: Graves' ophthalmopathy (proptosis, lid lag, diplopia -25-50%), pretibial myxedema (localized dermopathy), thyroid acropachy (digital clubbing). Symptoms: anxiety, tremor, weight loss, heat intolerance, palpitations (AF in 10-15%), diarrhea, menstrual irregularity, hyperreflexia.

🧪 Workup

Workup

TSH -suppressed (< 0.1 mIU/L). Most sensitive initial test.
Free T4 + Free T3 -both elevated in overt hyperthyroidism. T3 thyrotoxicosis: suppressed TSH + normal FT4 + elevated FT3 (early Graves' or toxic nodule).
TSI (thyroid-stimulating immunoglobulins) or TRAb (TSH receptor antibodies) -positive in Graves'. Specific. Can be used to confirm diagnosis without RAIU in pregnancy or when RAIU unavailable.
Radioactive iodine uptake (RAIU) -differentiates causes:
- Diffusely elevated = Graves'
- Focal hot nodule (suppressed rest) = toxic adenoma
- Patchy = toxic multinodular goiter
- Low/absent uptake = thyroiditis (preformed hormone release, not production), exogenous, or iodine excess
ESR/CRP -elevated in subacute (de Quervain) thyroiditis (painful + elevated inflammatory markers)
CBC -baseline before starting thionamides (agranulocytosis risk)
LFTs -baseline before thionamides (PTU → hepatotoxicity)
ECG -atrial fibrillation (10-15% of hyperthyroid patients). Often rate-controlled with beta-blockers alone.
Thyroid ultrasound -if nodule palpated or RAIU shows focal uptake. Evaluate for suspicious features.

🚨 Management

Management

Beta-blocker (ALL patients, symptom control): Propranolol 20-40 mg TID-QID (preferred -also blocks T4→T3 conversion) or atenolol 50-100 mg daily. Continue until euthyroid.
Graves' disease -3 treatment options:

Thyroiditis: Self-limited (4-8 weeks). Beta-blockers only. NSAIDs or prednisone for pain (subacute). Thionamides are USELESS (no new hormone being made -just release of preformed).

Monitoring

💊 Medications

Medications

Drug	Dose	Route	Notes
Methimazole (Tapazole)	10-30 mg daily → titrate	PO	First-line thionamide. Once daily dosing. Agranulocytosis (0.2-0.5%) -check CBC if fever/sore throat. Teratogenic in 1st trimester. ATA, 2016
PTU (propylthiouracil)	100-200 mg TID	PO	ONLY for: 1st trimester pregnancy, thyroid storm, methimazole allergy. TID dosing. FDA black box: severe hepatotoxicity (fulminant liver failure). Also blocks T4→T3.
Propranolol	20-40 mg TID-QID	PO	Symptom control. Also blocks peripheral T4→T3 conversion. Use in ALL hyperthyroid patients.
Radioactive iodine (I-131)	Per nuclear medicine calculation	PO	Definitive. Causes permanent hypothyroidism (expected outcome). Avoid pregnancy × 6 months after. Worsen ophthalmopathy → prednisone cover.
SSKI (saturated KI)	1-2 drops TID	PO	Wolff-Chaikoff effect -acute iodine load transiently blocks thyroid hormone release. Pre-op preparation for thyroidectomy. Give AFTER thionamide established.
Cholestyramine	4g TID	PO	Adjunct -binds thyroid hormone in gut, reduces enterohepatic recirculation. Used in severe thyrotoxicosis.

🏥 Rounds

Pimp Questions

❓ Why is methimazole preferred over PTU?

Methimazole advantages: once-daily dosing (vs TID for PTU), lower hepatotoxicity risk, more consistent pharmacokinetics, no FDA black box warning. PTU is preferred ONLY in: (1) first trimester pregnancy (methimazole causes aplasia cutis + choanal atresia), (2) thyroid storm (PTU also blocks T4→T3 conversion), (3) methimazole allergy/intolerance. After first trimester, switch back to methimazole. ATA, 2016

❓ How does RAIU differentiate causes of thyrotoxicosis?

High uptake (diffuse) = Graves'. High uptake (focal) = toxic adenoma or toxic MNG. Low/absent uptake = thyroiditis (preformed hormone leaking from damaged gland -no new synthesis), exogenous thyroid hormone, or iodine excess. This is the key test because treatment differs fundamentally: thionamides work for Graves'/toxic nodules (blocking new synthesis) but are useless in thyroiditis (nothing being synthesized).

❓ Why can RAI worsen Graves' ophthalmopathy?

RAI-induced thyroid destruction releases thyroid antigens that cross-react with orbital tissue (TSH receptor is expressed in orbital fibroblasts). This triggers an immune flare targeting the orbits → worsening inflammation, proptosis, diplopia. Risk is highest in smokers and those with pre-existing active ophthalmopathy. Prevention: prednisone 0.3-0.5 mg/kg starting the day of RAI × 4-6 weeks taper in moderate-risk patients. Avoid RAI entirely in moderate-severe active ophthalmopathy.

❓ What is the most feared side effect of thionamides and how do you screen for it?

Agranulocytosis (ANC < 500) -incidence 0.2-0.5%, usually within first 90 days. Can be fatal if not recognized. DO NOT do routine CBC monitoring (too insensitive, can develop rapidly between checks). Instead: educate the patient to present immediately for fever, sore throat, or mouth sores → get STAT CBC. If ANC < 500 → stop thionamide permanently, admit, broad-spectrum antibiotics, G-CSF, switch to non-thionamide therapy (RAI or surgery).

❓ How do you manage hyperthyroidism in pregnancy?

First trimester: PTU (methimazole is teratogenic). Second/third trimester: switch to methimazole (PTU hepatotoxicity risk). Use the lowest effective dose -aim for FT4 at upper limit of normal (mild maternal hyperthyroidism is safer than fetal hypothyroidism from overtreatment). RAI is absolutely contraindicated in pregnancy (ablates fetal thyroid). Check TSI/TRAb in third trimester -if elevated, neonatal hyperthyroidism possible. ATA, 2016

Sample Presentation

Ms. Patel is a 32-year-old woman with 3 months of 15 lb weight loss despite increased appetite, palpitations, tremor, anxiety, and heat intolerance. Exam: HR 108, diffusely enlarged thyroid with bruit, lid lag, mild proptosis bilateral, fine tremor. Labs: TSH < 0.01, FT4 4.8 (elevated), FT3 12 (elevated), TSI positive. RAIU: diffusely elevated at 65% (normal 10-30%).

Key Points: Classic Graves' disease -suppressed TSH, elevated FT4/FT3, positive TSI, diffusely elevated RAIU. Start propranolol for symptoms. Discuss 3 treatment options. Methimazole 20 mg daily for 12-18 month trial is reasonable first-line (32-year-old who may want pregnancy). Check CBC + LFTs baseline. Ophthalmology referral for proptosis.

TFTs (TSH + FT4) q4-6 weeks during thionamide titration. TSH may remain suppressed for months -use FT4 to guide dose adjustments initially.
CBC -if fever or sore throat on thionamides (agranulocytosis: ANC < 500). Get STAT CBC. Incidence 0.2-0.5%, usually within first 90 days.
LFTs -baseline + periodic on PTU. Discontinue if transaminases > 3× ULN. PTU hepatotoxicity can be fulminant.
TSI/TRAb -if monitoring for remission after thionamide trial. Persistently elevated = high relapse risk. Check before stopping thionamide at 12-18 months.
Post-RAI: TFTs q4-6 weeks × 6 months. Hypothyroidism typically develops by 6-12 weeks. Start levothyroxine when TSH rises.
Post-thyroidectomy: Check calcium q6h × 48h (hypoparathyroidism risk). Start levothyroxine. Check TSH at 6 weeks.
Ophthalmopathy assessment -active inflammation = orbital CT/MRI, refer ophthalmology. IV methylprednisolone for moderate-severe active orbitopathy [EUGOGO].

Monitoring

📋 Summary

Summary

Diagnosis

TSH suppressed + FT4/FT3 high. TSI/TRAb for Graves'. RAIU differentiates all causes.

Graves' Rx

Methimazole 12-18 mo trial (40% remission), RAI (definitive), or surgery.

Thyroiditis

Low RAIU. Self-limited. Beta-blockers only. Thionamides are useless.

Pregnancy

PTU in 1st trimester → methimazole after. Lowest dose. No RAI ever.

Emergency

Agranulocytosis: fever + sore throat → STAT CBC → stop thionamide → admit.

Pearl

RAI worsens ophthalmopathy (give prednisone cover). Propranolol also blocks T4→T3.

📄 One Pager

One-Pager

Hyperthyroidism

Graves', Toxic Nodule, Thyroiditis

RAIU Pattern

Diffuse high = Graves'. Focal hot = toxic adenoma. Patchy = MNG. Low = thyroiditis/exogenous/iodine.

Treatment Choice

Methimazole first-line (12-18 mo). RAI if definitive needed (causes hypothyroidism). Surgery for large goiter/nodule/ophthalmopathy. Thyroiditis: beta-blockers only.

Trials

ATA Hyperthyroidism Guidelines 2016 · EUGOGO (ophthalmopathy management)