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-YieldRheumatology

Dermatomyositis & Polymyositis

Inflammatory myopathies causing proximal muscle weakness. DM has characteristic skin findings (heliotrope rash, Gottron papules). Elevated CK. Associated with malignancy (DM). EMG and muscle biopsy confirm diagnosis. Steroids first-line.

🔍 Overview

Dermatomyositis vs Polymyositis

Feature	Dermatomyositis	Polymyositis
Skin findings	Heliotrope rash (purple eyelid discoloration), Gottron papules (papules over MCP/PIP/knuckles), V-sign, shawl sign, mechanic's hands	None
Muscle weakness	Proximal, symmetric, progressive	Proximal, symmetric, progressive
Histology	Perimysial inflammation, perifascicular atrophy	Endomysial inflammation, CD8+ T cells invading fibers
Malignancy	Strong association -screen for ovarian, lung, breast, GI, lymphoma	Weaker association
Antibodies	Anti-Mi-2, anti-MDA5, anti-TIF1-γ (malignancy-associated)	Anti-Jo-1 (antisynthetase syndrome: ILD, arthritis, mechanic's hands)

DM in adults requires age-appropriate malignancy screening. Anti-TIF1-γ antibody is specifically associated with malignancy-associated DM. Screen with CT chest/abdomen/pelvis, mammogram, colonoscopy, and pelvic exam.

Inclusion Body Myositis (IBM)

Feature	Inclusion Body Myositis
Age	>50 years. Most common inflammatory myopathy in elderly.
Pattern	ASYMMETRIC, distal + proximal. Finger flexors, wrist flexors, quadriceps ("Can't grip, can't walk").
CK	Mildly elevated or normal
Key feature	Does NOT respond to immunosuppression (unlike DM/PM)
Histology	Endomysial inflammation + rimmed vacuoles + amyloid deposits
Treatment	No effective treatment. PT/OT. IVIG may help swallowing.

Skin Findings in Detail (Dermatomyositis)

Heliotrope rash: Purple/lilac discoloration of eyelids, often with periorbital edema. Pathognomonic for DM.
Gottron papules: Erythematous/violaceous papules over MCP, PIP, DIP joints and knuckles. Pathognomonic.
Gottron sign: Flat erythematous patches over elbows, knees, medial malleoli.
V-sign: Erythema over anterior neck/chest in V-distribution.
Shawl sign: Erythema over upper back and shoulders.
Mechanic's hands: Rough, cracked, hyperkeratotic skin on radial side of fingers. Associated with antisynthetase syndrome.
Holster sign: Erythema over lateral thighs.
Periungual erythema: Dilated nailfold capillaries.
Calcinosis cutis: Calcium deposits under skin, more common in juvenile DM.

Mnemonic: HELIOGRAMS

Heliotrope rash, Erythema (V-sign), Limbs (Gottron), Interstitial lung disease, Other autoimmune, Gottron papules, Raynaud, Arthritis, Mechanic's hands, Shawl sign

🚨 Management

Treatment

First-line: Prednisone (Deltasone) 1 mg/kg/day × 4–6 weeks, then taper
Steroid-sparing: Methotrexate (Trexall) or Azathioprine (Imuran)
Refractory: Rituximab (Rituxan), IVIG, Mycophenolate (CellCept)
ILD management: If antisynthetase syndrome -mycophenolate, rituximab, or cyclophosphamide
Physical therapy -maintain function during and after treatment
Malignancy screening -age-appropriate, especially in DM

📋 Case 1, Classic Dermatomyositis

Patient: 42F presents with progressive proximal weakness × 2 months, cannot climb stairs or lift arms overhead. Purple discoloration of eyelids, papules over knuckles. CK 8,500.

Action:

Classic dermatomyositis. Heliotrope rash + Gottron papules + proximal weakness + elevated CK.
Order: Myositis-specific antibodies (including anti-TIF1-γ), EMG, MRI thighs, age-appropriate malignancy screening.
Start prednisone 1 mg/kg/day.
Anti-TIF1-γ positivity → intensive cancer screening: CT chest/abdomen/pelvis, mammogram, colonoscopy, pelvic exam.
PFTs at baseline for ILD screening.

📋 Case 2, Antisynthetase Syndrome with ILD

Patient: 58F with DM, anti-Jo-1 positive. Develops progressive dyspnea, dry cough. PFTs show restrictive pattern. HRCT: ground-glass opacities, NSIP pattern.

Diagnosis: Antisynthetase syndrome with ILD.

Action:

ILD is the main driver of mortality in antisynthetase syndrome -not the myopathy.
Treatment: Steroids + mycophenolate or rituximab for ILD.
Avoid methotrexate (can cause drug-induced ILD).
Serial PFTs q3–6 months to monitor progression.
Look for other features: mechanic's hands, Raynaud, arthritis, fever.

📋 Case 3, Inclusion Body Myositis

Patient: 72M with 2-year history of progressive difficulty opening jars, frequent falls. Asymmetric weakness, finger flexor weakness, quadriceps atrophy. CK 450 (mildly elevated). Failed 6-month trial of prednisone.

Biopsy: Rimmed vacuoles.

Diagnosis: Inclusion body myositis.

Action:

No effective immunosuppressive treatment -IBM does not respond to steroids, MTX, or azathioprine.
PT/OT for functional maintenance and fall prevention.
Swallowing evaluation -dysphagia is common. IVIG may help swallowing.
Key distinguishing features: age >50, asymmetric, distal involvement (finger flexors), quadriceps atrophy, failed immunosuppression, rimmed vacuoles on biopsy.

🧪 Workup

CK -elevated (usually > 10× normal). Primary marker of muscle damage.
Aldolase -elevated (more specific for muscle, also elevated)
Myositis-specific antibodies -Anti-Jo-1, anti-Mi-2, anti-MDA5, anti-SRP, anti-TIF1-γ
EMG -myopathic pattern (short, small, polyphasic motor units, fibrillation potentials)
MRI of thighs -STIR sequences show edema in affected muscles. Can guide biopsy site.
Muscle biopsy -gold standard for diagnosis and classification
PFTs -ILD screening (anti-Jo-1)
Malignancy screening -CT, mammogram, colonoscopy

💊 Medications

Drug	Dose	Role
Prednisone (Deltasone)	1 mg/kg/day	First-line. Taper over months once CK normalizes and strength improves.
Methotrexate (Trexall)	15–25 mg weekly	Steroid-sparing. Give with folic acid. Avoid in ILD (can cause drug-induced ILD).
Azathioprine (Imuran)	2–3 mg/kg/day	Steroid-sparing alternative. Check TPMT.
IVIG	2 g/kg over 2–5 days monthly	Refractory cases, especially DM
Rituximab (Rituxan)	375 mg/m² × 4 weekly	Refractory myositis, antisynthetase-associated ILD

📋 On Rounds

Pimp Questions

How do you distinguish myositis from steroid myopathy during treatment?

This is a critical clinical challenge. Both cause proximal weakness. Myositis flare: CK is elevated/rising, inflammatory markers up. Steroid myopathy: CK is NORMAL, no inflammatory markers. Steroid myopathy is painless. If CK is normal but weakness persists/worsens, consider reducing steroids. If CK is rising, the myositis is active and steroids may need to be increased or a steroid-sparing agent added.

What is antisynthetase syndrome?

A clinical syndrome associated with anti-aminoacyl-tRNA synthetase antibodies (most commonly anti-Jo-1). Features: (1) ILD (interstitial lung disease -often the dominant and most life-threatening feature), (2) Inflammatory myopathy, (3) Mechanic's hands (cracked, rough skin on palms/fingers), (4) Arthritis, (5) Raynaud phenomenon, (6) Fever. ILD drives prognosis -PFTs and CT chest are essential at diagnosis.

How do you differentiate DM/PM from inclusion body myositis?

IBM: age >50, ASYMMETRIC weakness (unlike DM/PM which is symmetric), involves DISTAL muscles (finger flexors, wrist flexors -"can't make a fist"), quadriceps atrophy ("falls going downstairs"), CK only mildly elevated or normal, does NOT respond to steroids or immunosuppression. Biopsy: rimmed vacuoles + amyloid. Most common inflammatory myopathy in elderly men.

What antibody is most associated with cancer in dermatomyositis?

Anti-TIF1-γ (anti-p155/140). This antibody has the strongest association with malignancy-associated DM. Patients with anti-TIF1-γ need intensive cancer screening: CT chest/abdomen/pelvis, mammogram, colonoscopy, pelvic exam, and age-appropriate screening. Some guidelines recommend repeating screening annually for 3–5 years.

⚡ Summary

DM vs PM

DM: heliotrope rash, Gottron papules, malignancy association. PM: no skin findings, endomysial CD8+ cells.

Key Lab

CK elevated (often >10× normal). Aldolase also elevated. Myositis-specific antibodies.

Diagnosis

EMG (myopathic pattern), MRI thighs (edema on STIR), muscle biopsy (gold standard).

Treatment

Prednisone 1mg/kg first-line. Steroid-sparing: MTX or azathioprine. Refractory: rituximab, IVIG.

Malignancy

DM strongly associated. Anti-TIF1-γ = malignancy-associated. Screen: CT, mammogram, colonoscopy.

Antisynthetase

Anti-Jo-1. ILD + myopathy + mechanic's hands + arthritis. ILD drives prognosis.