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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CoreQuick Reference

Lab Interpretation

What's actually important in the CBC, BMP, LFTs, and coags -not just the reference ranges, but what the abnormalities mean clinically and what to do about them.

📐 Classic Fishbone Diagrams

BMP Fishbone

AG = Na⁺ − (Cl⁻ + HCO₃⁻) | Normal: 8–12 | BUN:Cr > 20:1 → pre-renal AKI

CBC Fishbone

Transfuse: Hgb < 7 (most) | < 8 (ACS) | Plt < 10K (prophylactic) | < 50K (procedure)

CMP = BMP + Hepatic Panel

BMP (8 values): Na⁺, K⁺, Cl⁻, HCO₃⁻, BUN, Cr, Glucose, Ca²⁺
CMP adds (6 more): Albumin, Total protein, AST, ALT, ALP, Total bilirubin
When to order CMP over BMP: New admission, liver disease, medications with hepatotoxicity, TPN, unexplained AMS, jaundice

🔬 CBC

Lab	Normal	High	Low	Clinical Action
WBC	4.5–11 K	Leukocytosis: infection (#1), steroids (demargination), stress, leukemia, medication	Leukopenia: sepsis (bad sign -WBC consumed), chemo, bone marrow failure, SLE, viral	Leukocytosis + fever → blood cultures + workup. Neutropenia (ANC < 500) + fever → cefepime within 60 min.
Hgb/Hct	M: 14–17 F: 12–16	Polycythemia vera, dehydration (hemoconcentration), chronic hypoxia	Anemia: classify by MCV. Microcytic (iron def, thalassemia), normocytic (chronic disease, AKI, bleeding), macrocytic (B12/folate, EtOH, MDS)	Transfuse if Hgb < 7 (most patients) or < 8 (ACS). Reticulocyte count to assess production.
Platelets	150–400 K	Reactive (infection, inflammation, iron deficiency, splenectomy). Essential thrombocythemia if > 450K persistent.	Thrombocytopenia: ↓ production (chemo, EtOH, MDS), ↑ destruction (ITP, TTP, HIT, DIC), sequestration (splenomegaly), dilutional (massive resuscitation)	If new drop → review meds (heparin → 4T score for HIT). < 50K → hold anticoagulation. < 10K → transfuse (unless TTP/HIT).

🔬 BMP / CMP

Lab	Normal	Key Abnormalities	Quick Action
Na⁺	136–145	Low: see Hyponatremia. High: free water deficit (dehydration, DI, inadequate access to water).	Correct ≤ 8–10 mEq/L per 24h in either direction.
K⁺	3.5–5.0	High: AKI, ACEi/ARB, spironolactone, rhabdo, hemolysis (pseudohyperK), acidosis. Low: diuretics, GI losses, renal wasting.	K⁺ > 6 + ECG changes → calcium first, then insulin/D50. See Hyperkalemia. Always check Mg.
HCO₃ / CO₂	22–28	Low: metabolic acidosis (calculate AG). High: metabolic alkalosis or chronic respiratory acidosis compensation.	Low HCO₃ → calculate anion gap → if elevated, calculate delta-delta. See Acid-Base.
BUN / Cr	BUN 7–20 Cr 0.7–1.3	↑ BUN/Cr > 20:1: pre-renal (dehydration, HF, GI bleed). ↑ BUN + Cr proportionally: intrinsic renal (ATN). Cr trend matters more than absolute value.	Compare to baseline. Rising Cr → hold nephrotoxins (NSAIDs, ACEi, contrast), check volume status, UA, FENa.
Glucose	70–100 (fasting)	High: DM, steroids, stress response, DKA. Low: insulin excess, sulfonylurea, liver failure, sepsis, adrenal insufficiency, alcohol.	< 70 → D50 1 amp IV + recheck in 15 min. > 300 → check ketones + anion gap (DKA?).
Calcium	8.5–10.5 (total) 1.1–1.3 (ionized)	Always correct for albumin or check ionized. See Hypercalcemia.	High Ca → check PTH. Low iCa → check Mg, PO₄, PTH, vitamin D.

🔬 Liver Function Tests

Pattern	AST/ALT	Alk Phos / GGT	Bilirubin	Think
Hepatocellular	↑↑↑ (AST/ALT > 10× ULN)	Mildly ↑	Variable	Viral hepatitis, drug-induced (acetaminophen -check level + NAC), ischemic hepatitis ("shock liver"), autoimmune hepatitis, Wilson disease
Cholestatic	Mildly ↑	↑↑↑	↑↑	Bile duct obstruction (stone, mass, stricture) → RUQ US first. Intrahepatic: PBC, PSC, drug-induced, infiltrative. GGT confirms hepatic origin of alk phos.
Mixed	↑↑	↑↑	↑	Drug-induced, granulomatous hepatitis
AST > ALT (> 2:1)	Ratio > 2:1			Alcoholic hepatitis (classic ratio). Also: cirrhosis, Wilson disease, rhabdomyolysis (AST from muscle -check CK).

"LFTs" is a misnomer. AST, ALT, and alk phos measure liver INJURY, not function. True liver FUNCTION markers: albumin (synthesis), INR (clotting factor synthesis), bilirubin (conjugation/excretion). A patient with normal AST/ALT but INR of 3 and albumin of 2 has severe liver dysfunction.

🔬 Coags, Inflammatory Markers & More

Lab	Normal	Clinical Meaning
PT / INR	PT 11–13.5s INR 0.9–1.1	Extrinsic pathway (factors VII, X, V, II, fibrinogen). Elevated: warfarin, liver disease, DIC, vitamin K deficiency. INR is the standardized version of PT.
aPTT	25–35s	Intrinsic pathway (XII, XI, IX, VIII). Elevated: heparin (therapeutic monitoring), hemophilia (VIII or IX deficiency), lupus anticoagulant (paradoxically prolonged but prothrombotic), DIC.
Fibrinogen	200–400 mg/dL	Low: DIC (consumed), liver failure. High: acute phase reactant (inflammation). Most specific lab for DIC severity. Critical value < 100 → give cryoprecipitate.
D-dimer	< 500 ng/mL	Sensitive but NOT specific. Elevated in PE, DVT, DIC, surgery, pregnancy, cancer, infection, trauma -basically any hospitalized patient. Useful to RULE OUT PE/DVT when low pretest probability (Wells ≤ 4).
Lactate	< 2.0 mmol/L	↑: tissue hypoperfusion (sepsis, shock -Type A) or impaired clearance (liver failure, metformin -Type B). Lactate > 4 in sepsis → mortality > 30%. Trend is more important than single value.
Procalcitonin	< 0.1 ng/mL	< 0.25: bacterial infection unlikely. > 0.5: likely bacterial. Useful for: antibiotic de-escalation in pneumonia/sepsis (if procal drops > 80% → safe to stop abx). NOT reliable in: immunocompromised, post-surgery, burns, pancreatitis.
ESR	M: 0–22 F: 0–29	Non-specific inflammation. Very high (> 100): infection (endocarditis, osteomyelitis), autoimmune (SLE, PMR/GCA), malignancy (myeloma). Slow to rise and slow to fall. SLE flare: ↑ ESR + normal CRP.
CRP	< 3 mg/L	Faster marker of inflammation than ESR. Rises within 6h, peaks 48h. Good for tracking treatment response. CRP elevated in SLE = think infection, not flare.
Troponin (hs-TnI)	Varies by assay	Myocardial injury. NOT specific for MI -elevated in: PE, HF, sepsis, CKD (chronic elevation), myocarditis, takotsubo, cardioversion. Trend matters: rise-and-fall pattern = acute injury. Stable low-level = chronic (CKD, HF).
BNP / NT-proBNP	BNP < 100 NT-proBNP < 300	Rule out HF: BNP < 100 or NT-proBNP < 300 makes HF very unlikely. Falsely low: obesity (adipose tissue clears BNP). Falsely high: Afib, PE, CKD, age.