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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ℹ️ About

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Autoimmune Hepatitis

Chronic liver inflammation from immune-mediated destruction. Predominantly young women. Type 1 (ANA/ASMA+) is most common. AST/ALT can exceed 1000 in acute flares. High relapse rate if treatment stopped. Elevated IgG is the hallmark serologic finding.

🔍 Overview

Overview

Autoimmune hepatitis (AIH) is a chronic inflammatory liver disease caused by loss of immune tolerance to hepatocytes. It predominantly affects young women (female:male ratio 4:1) but can occur at any age. Can present as acute hepatitis (AST/ALT often >1000) or chronic liver disease with insidious progression to cirrhosis. Associated with other autoimmune conditions (thyroiditis, UC, RA, celiac).

Types

Type 1 (80%) -ANA and/or anti-smooth muscle antibody (ASMA) positive. Adults predominantly. Most common worldwide.
Type 2 -Anti-liver-kidney microsomal antibody (anti-LKM1) positive. More common in children. Tends to be more severe.

🚨 Management

Induction

Standard induction: Prednisone 40-60 mg daily, tapering over 4-8 weeks to 5-10 mg daily, PLUS Azathioprine (Imuran) 50 mg daily at week 2, uptitrated to 1-2 mg/kg.
Alternative: Budesonide (Entocort) 9 mg daily -first-pass hepatic metabolism means fewer systemic side effects. BUT: do NOT use in cirrhotic patients (portosystemic shunts bypass first-pass metabolism, negating the benefit). Manns, Gastroenterology 2010

Maintenance

Azathioprine monotherapy (1-2 mg/kg daily) once steroids are tapered. Aim to maintain on the lowest effective azathioprine dose. Relapse rate is 80-90% if treatment is stopped -most patients need lifelong therapy.

TPMT Testing

Check TPMT before starting azathioprine -homozygous TPMT deficiency causes fatal myelosuppression. Heterozygous patients need dose reduction. Also monitor CBC regularly on azathioprine (q2 weeks for first 2 months, then q3 months).

🧪 Workup

Diagnostic Workup

AST/ALT -often markedly elevated (>1000 in acute flares). Hepatocellular pattern.
IgG levels -elevated IgG is the hallmark. Polyclonal hypergammaglobulinemia.
ANA -positive in Type 1 (not specific for AIH)
ASMA (anti-smooth muscle antibody) -more specific for Type 1 AIH
Anti-LKM1 -diagnostic of Type 2 AIH
Liver biopsy -interface hepatitis (lymphoplasmacytic infiltrate at the portal-parenchymal junction) is classic. May show bridging necrosis in severe cases.
Rule out other causes:
- Viral hepatitis -Hep A IgM, HBsAg, anti-HBc, anti-HCV, Hep E IgM
- Drug-induced liver injury -thorough medication history
- Wilson disease -ceruloplasmin (especially in patients <40)
Simplified AIH Scoring System -uses ANA/SMA titers, IgG levels, liver histology, and exclusion of viral hepatitis. Score >=7 = definite AIH.

💊 Medications

Medications

Drug	Dose	Route	Notes
Prednisone INDUCTION	40-60 mg daily, taper to 5-10 mg over 4-8 weeks	PO	Standard induction. Monitor glucose, BP, bone density on prolonged use.
Azathioprine (Imuran) MAINTENANCE	50 mg daily initially, uptitrate to 1-2 mg/kg	PO	Check TPMT BEFORE starting. Fatal myelosuppression if homozygous deficient. Monitor CBC q2 weeks x 2 months, then q3 months. AASLD 2020
Budesonide (Entocort)	9 mg daily (3 mg TID)	PO	Alternative to prednisone. First-pass metabolism = fewer systemic effects. Do NOT use in cirrhosis.
Mycophenolate (CellCept)	1-2 g daily	PO	Second-line for azathioprine-intolerant patients. Teratogenic -avoid in pregnancy.
Tacrolimus (Prograf)	1-6 mg daily (target trough 3-5 ng/mL)	PO	Salvage therapy for refractory AIH. Monitor trough levels and renal function.

🏥 Rounds

Pimp Questions

❓ Why can't you use budesonide in cirrhotic patients with AIH?

Budesonide has high first-pass hepatic metabolism -normally 90% is cleared by the liver, so systemic exposure is minimal. In cirrhosis, portosystemic shunts bypass the liver, so budesonide enters systemic circulation at high levels -losing its advantage over prednisone and causing full systemic steroid side effects. Use prednisone instead.

❓ What is the most important lab to distinguish AIH from other causes of hepatitis?

IgG level. Elevated IgG (polyclonal hypergammaglobulinemia) is the hallmark of AIH and is part of the simplified diagnostic criteria. While ANA and ASMA are useful, they are not specific -ANA can be positive in many conditions. IgG elevation combined with autoantibodies and interface hepatitis on biopsy is the diagnostic triad.

❓ Why must you check TPMT before starting azathioprine?

Azathioprine is metabolized by thiopurine methyltransferase (TPMT). Patients with homozygous TPMT deficiency (~0.3% of population) accumulate toxic metabolites causing fatal myelosuppression -severe pancytopenia. Heterozygous patients (~10%) need dose reduction. Testing prevents a completely preventable catastrophic drug reaction.

❓ What happens when you try to stop AIH treatment?

The relapse rate is 80-90% when treatment is withdrawn, even after achieving biochemical remission. Most patients require lifelong immunosuppression with low-dose azathioprine. Consider attempting withdrawal only after: (1) sustained biochemical remission for >2 years, (2) confirmed histologic remission on repeat biopsy, and (3) very close follow-up with labs q2-4 weeks after stopping.

Clinical Examples

📋 Case 1, Classic Type 1 AIH Presentation

Patient: 32F with 3 weeks of fatigue, jaundice, RUQ pain. AST 1180, ALT 1420, T. bili 7.6, INR 1.2. IgG 3400 (markedly elevated). ANA 1:320, ASMA 1:160. Viral hepatitis negative. Biopsy: interface hepatitis with plasma cells.

Key findings: Type 1 AIH (ANA/ASMA positive). Simplified AIH score ≥ 7 = definite. Interface hepatitis with lymphoplasmacytic infiltrate is the hallmark histologic finding.

Management:

Prednisone 40-60 mg daily (or budesonide 9 mg daily if non-cirrhotic), expect ALT improvement within 2 weeks
Add azathioprine 50 mg daily after 2 weeks → titrate to 1-2 mg/kg (check TPMT first!)
Goal: biochemical remission (normal ALT + IgG) within 6-12 months
Taper prednisone slowly over 3-6 months → maintain on azathioprine monotherapy
Relapse rate 80-90% if treatment stopped, most patients need lifelong azathioprine

Teaching point: AIH responds dramatically to steroids, if ALT does not improve within 2 weeks, reconsider the diagnosis. The combination of prednisone + azathioprine allows faster steroid taper and fewer steroid side effects.

📋 Case 2, Acute Severe AIH (Fulminant Presentation)

Patient: 24F with 1 week of rapidly worsening jaundice, confusion. AST 2800, ALT 3200, T. bili 18, INR 3.8, albumin 2.4. IgG 4200. ANA 1:640. Developing hepatic encephalopathy grade II.

Key findings: Acute severe AIH with impending liver failure (INR > 1.5 + encephalopathy = acute liver failure criteria). Must decide quickly: steroids or transplant listing.

Management:

Methylprednisolone 60 mg IV daily, trial of steroids for 7 days maximum
If improving (bilirubin decreasing, INR improving by day 7): continue steroids, add azathioprine
If NOT improving or worsening: list for emergent liver transplant (MELD exception)
LILLE score or similar at day 7 to objectively assess steroid response
ICU monitoring, lactulose for encephalopathy, FFP only if actively bleeding (don't mask INR trend)

Teaching point: Acute severe AIH gets a 7-day steroid trial, this is both diagnostic and therapeutic. If no response, proceeding with steroids delays transplant listing. The key is having a clear timeline and objective response criteria before starting.

📋 Case 3, AIH Flare on Azathioprine (Non-Compliance)

Patient: 40F with known AIH in remission on azathioprine 150 mg daily. Stopped taking it 3 months ago (felt well). Now AST 680, ALT 820, IgG 2800, bilirubin 4.2. Previously well-controlled.

Key findings: AIH flare from medication non-compliance. This is the most common reason for relapse. Predictable, 80-90% relapse when therapy is withdrawn.

Management:

Restart prednisone 30-40 mg daily (re-induce remission)
Restart azathioprine at previous effective dose (150 mg daily)
Taper prednisone once ALT normalizing → maintain azathioprine indefinitely
Counsel: AIH requires lifelong therapy in most patients. Stopping medication risks flare → fibrosis progression
Repeat liver biopsy if concern for interval fibrosis progression from uncontrolled inflammation

Teaching point: Each untreated flare accelerates fibrosis. Patients who relapse after stopping therapy should generally never attempt withdrawal again, the risk-benefit clearly favors lifelong low-dose azathioprine over recurrent flares and progressive liver damage.

Sample Presentation

Ms. Patel is a 28-year-old woman with no significant past medical history presenting with 2 weeks of fatigue, jaundice, and RUQ discomfort. Labs: AST 1,240, ALT 1,580, total bilirubin 8.4, INR 1.3, albumin 3.2. IgG markedly elevated at 3,200 (normal <1600). ANA 1:320, ASMA 1:160. Hepatitis A, B, C, E serologies negative. Ceruloplasmin normal. Liver biopsy: interface hepatitis with lymphoplasmacytic infiltrate. Simplified AIH score: 8 (definite AIH).

Key Points: Classic Type 1 AIH in a young woman -markedly elevated transaminases, elevated IgG, positive ANA/ASMA, interface hepatitis on biopsy. Check TPMT, start prednisone 60 mg daily, add azathioprine 50 mg at week 2. Monitor for steroid side effects. Counsel that lifelong therapy is likely needed (80-90% relapse rate if stopped).

Monitoring

LFTs (AST/ALT) -q2-4 weeks during induction, then q3 months on maintenance. Goal: normalization of transaminases.
IgG level -normalize with successful treatment. Useful marker of disease activity.
CBC -monitor for azathioprine myelosuppression. q2 weeks for first 2 months, then q3 months.
TPMT result -must have before starting azathioprine.
Liver biopsy -consider repeat biopsy before treatment withdrawal to confirm histologic remission (biochemical remission does NOT guarantee histologic remission).
Hepatocellular carcinoma screening -if cirrhosis present, standard HCC screening (ultrasound + AFP q6 months).
Bone density -DEXA if prolonged steroid use.

📋 Summary

Summary

Hallmark

Elevated IgG + autoantibodies (ANA, ASMA, anti-LKM1) + interface hepatitis on biopsy

Types

Type 1: ANA/ASMA+ (80%, adults). Type 2: anti-LKM1+ (children, more severe).

Treatment

Prednisone 40-60 mg + azathioprine 1-2 mg/kg. Check TPMT first!

Maintenance

Azathioprine monotherapy. Lifelong in most. 80-90% relapse if stopped.

Budesonide

Alternative to prednisone. Do NOT use in cirrhosis (portosystemic shunts).

Danger

TPMT deficiency + azathioprine = fatal myelosuppression. Always test first.