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I now have strong textbook content from Goldman-Cecil, Katzung, and Washington Manual. Let me compile the comprehensive Step 3 high-yield guide for Cardiology & Pulmonology.

Step 3 High-Yield: Cardiology & Pulmonology

CARDIOLOGY

1. Heart Failure (HFrEF vs HFpEF)

Know the difference immediately:

Feature	HFrEF (Systolic)	HFpEF (Diastolic)
EF	< 40%	≥ 50% (preserved)
CO	Decreased	Decreased
Diuretics	First-line if edema	Use cautiously
ACEi/ARB	Reduce mortality	May help (reduce LVH)
Beta-blockers	Reduce mortality	Useful for rate/BP
Aldosterone antagonists	Reduce mortality	May be useful
Digoxin	May reduce symptoms	Little/no role
CCBs	No/small benefit	Useful (rate, BP)
SGLT2 inhibitors	Reduce mortality	Beneficial

Stages (ACC/AHA):

Stage A: Risk factors only (HTN, DM) - no structural disease → control risk factors
Stage B: Structural disease, no symptoms → ACEi/ARBs
Stage C: Symptoms present → full medical therapy
Stage D: Refractory → advanced therapies (LVAD, transplant)

Drug hierarchy for HFrEF (mortality benefit):

ACE inhibitor (or ARB if ACEi-intolerant) - first-line
Beta-blocker (carvedilol, metoprolol succinate, bisoprolol)
Aldosterone antagonist (spironolactone/eplerenone) - moderate/severe HF
ARNI (sacubitril/valsartan) - replaces ACEi in stable patients
SGLT2 inhibitor (dapagliflozin/empagliflozin) - reduces hospitalizations + mortality
Ivabradine - if HR ≥ 70 on max beta-blocker
Loop diuretic (furosemide) - symptom relief if edema (NO mortality benefit alone)

Pitfalls Step 3 loves:

Do NOT combine ACEi + ARB (hyperkalemia, renal failure)
Do NOT use ACEi/ARB if K+ > 5.5 or SCr > 3.0
Hypokalemia from loop diuretics + digoxin = deadly arrhythmias
Spironolactone contraindicated if GFR < 30

2. Atrial Fibrillation

Classify first:

New-onset < 48 hrs vs. > 48 hrs (or unknown duration) - this drives your approach
Paroxysmal vs. Persistent vs. Long-standing persistent vs. Permanent

Hemodynamically unstable → immediate synchronized cardioversion (don't delay for anticoagulation)

Hemodynamically stable → two decisions:

A. Rate vs. Rhythm Control:

Rate control preferred for most chronic AF patients (AFFIRM trial)
Rhythm control preferred for: symptomatic AF, HFrEF with AF (ablation preferred over drugs)
Rate control target: resting HR < 80 bpm
Rate control drugs: beta-blockers or CCBs (diltiazem, verapamil); digoxin for sedentary patients or HFrEF

B. Anticoagulation (stroke prevention): Use CHA₂DS₂-VASc score:

0 (male) / 1 (female) = no anticoagulation
1 (male) = consider
≥ 2 (male) / ≥ 3 (female) = anticoagulate

DOACs preferred over warfarin (except mechanical valves, rheumatic AF - use warfarin for those)

DOACs: apixaban, rivaroxaban, dabigatran, edoxaban

Cardioversion rules:

AF < 48 hrs: can cardiovert immediately (anticoagulate for 4 weeks after)
AF > 48 hrs or unknown: anticoagulate for 3 weeks before → cardiovert → continue 4 weeks after (or do TEE to rule out LA thrombus first)

3. ACS (STEMI vs. NSTEMI/UA)

STEMI:

Reperfusion is everything: Primary PCI within 90 min (door-to-balloon) if available
Fibrinolysis if PCI not available within 120 min
Give: aspirin + P2Y12 inhibitor (ticagrelor or clopidogrel) + anticoagulant (heparin)

NSTEMI/UA:

High-risk features: dynamic ST changes, troponin rise, TIMI ≥ 3, hemodynamic instability → early invasive strategy (cath within 24-48 hrs)
Low-risk: conservative management

Universal Post-ACS medications (all patients, indefinitely):

Aspirin 81 mg
Beta-blocker (start when stable)
ACE inhibitor (especially if EF < 40%, DM, HTN)
Statin (high-intensity: atorvastatin 40-80 mg)
P2Y12 inhibitor × 12 months (ticagrelor preferred over clopidogrel)

4. Hypertensive Urgency vs. Emergency

	Urgency	Emergency
BP	Severely elevated	Severely elevated
End-organ damage	None	Present
Treatment	Oral agents, lower BP over 24-48 hrs	IV agents, lower MAP by ~25% in 1st hour

Target: lower MAP by 25% in first hour (not to normal!) - overly rapid reduction causes ischemic stroke

IV agents for emergency: labetalol, nicardipine, clevidipine, hydralazine (pregnancy), sodium nitroprusside (use cautiously - cyanide toxicity)

Special cases:

Aortic dissection: labetalol (rate + pressure control together)
Ischemic stroke with tPA candidate: treat BP only if > 185/110
Pre-eclampsia: labetalol, hydralazine, nifedipine

5. Cardiac Arrhythmias (Quick Reference)

Finding	Diagnosis	Treatment
Wide complex tachycardia, no pulse	VF	Immediate defibrillation
Pulseless VT	VF protocol	Defibrillation + epinephrine
Stable wide complex tachycardia	VT	Amiodarone IV; if unstable → sync cardioversion
SVT (narrow, regular)	AVNRT most common	Vagal maneuvers → adenosine
Narrow irregular	AF	Rate/rhythm control per above
Long QT → torsades	TdP	Stop offending drug; Mg sulfate IV; do NOT use amiodarone
Complete heart block (3rd degree)	AV block	Atropine → transcutaneous pacing → permanent pacemaker

Wolff-Parkinson-White (WPW): delta wave, short PR, wide QRS. If AF develops → DO NOT give AV nodal blockers (adenosine, verapamil, digoxin) - will preferentially conduct through accessory pathway → VF → death. Use procainamide or cardioversion.

PULMONOLOGY

6. Pulmonary Embolism

Risk stratification drives treatment:

High-risk (massive PE): hypotension (SBP < 90), shock, cardiac arrest
Intermediate-risk (submassive): normotensive but RV dysfunction + elevated troponin/BNP
Low-risk: none of the above

Diagnosis:

Wells score first:
- Low probability → D-dimer (if negative, PE ruled out)
- Moderate/High probability → CT pulmonary angiogram (gold standard)
V/Q scan: for contrast allergy or renal failure
ECG findings: S1Q3T3, sinus tachycardia (most common), T-wave inversions V1-V4, RBBB
Echo: RV dilation/hypokinesis, elevated TV regurgitation jet velocity
BNP + troponin: elevated in submassive/massive (prognostic, not diagnostic)

Treatment:

Anticoagulation - start immediately, even before confirmatory test if high clinical suspicion
Preferred agents: LMWH (enoxaparin) → bridge to DOAC or warfarin. DOACs now preferred (rivaroxaban, apixaban can be used directly without heparin bridge)
ESRD/dialysis: unfractionated heparin (UFH) preferred over LMWH
Duration:
- Provoked (reversible risk factor): 3 months
- Unprovoked / cancer: indefinite (cancer: LMWH or edoxaban)

Fibrinolytics (tPA):

Indicated for massive PE (hemodynamic compromise) with no absolute contraindications
Absolute contraindications: prior hemorrhagic stroke, active bleeding, intracranial surgery/trauma within 3 weeks, GI bleed within 1 month
Not routine in submassive PE (increases major bleeding/stroke)

IVC filter: when anticoagulation is absolutely contraindicated

7. COPD Exacerbation

Triggers: viral URI (most common), bacterial infection (H. flu, S. pneumo, Moraxella), air pollution

Work-up: O₂ sat, ABG, ECG, CXR (to rule out pneumothorax, pneumonia, CHF)

Treatment (Washington Manual):

Drug	Dose
Albuterol (SABA)	MDI 2-4 puffs q1-4h OR nebulizer 2.5 mg q1-4h
Ipratropium (anticholinergic)	MDI 2 puffs q4h OR neb 0.5 mg q4h
Prednisone	40 mg/day x 5 days (equivalent to longer courses)
Antibiotics	3-7 days (see below)

Antibiotics: give if increased dyspnea + increased sputum volume + purulent sputum (2/3 Anthonisen criteria)

No risk factors: macrolide, 2nd-3rd gen cephalosporin, doxycycline, TMP-SMX
Risk factors present (age > 65, FEV1 < 50%, >3 exacerbations/yr, cardiac comorbidity): antipseudomonal fluoroquinolone or beta-lactam

Oxygen target: 88-92% saturation (not 100% - hypercapnic drive risk). Use Venturi mask for precise delivery.

NIV (BiPAP): preferred over intubation for moderate-severe exacerbation with hypercapnia + pH 7.25-7.35

ICU criteria: need for invasive MV, hemodynamic instability, mental status changes, severe hypoxemia/hypercapnia/acidosis not responding to NIV

8. Asthma (Acute Exacerbation)

Severity guides treatment:

Mild-Moderate: SABA (albuterol) q20 min x 3, +/- ipratropium, O₂ to keep SpO₂ ≥ 92%
Severe: Add systemic corticosteroids (methylprednisolone IV or prednisone PO) + continuous albuterol + ipratropium
Life-threatening/near-fatal: magnesium sulfate IV, consider heliox, prepare for intubation

Step-up therapy (chronic):

SABA prn only
SABA + low-dose ICS
Low-dose ICS + LABA
Medium-dose ICS + LABA
High-dose ICS + LABA
Add oral corticosteroids, biologics (omalizumab for allergic, dupilumab for eosinophilic)

LABA monotherapy is contraindicated (without ICS - increases asthma mortality)

9. Pneumonia (Community vs. Hospital)

CAP - CURB-65 score (1 point each):

Confusion, Urea > 19, RR ≥ 30, BP < 90/60, Age ≥ 65
0-1: outpatient; 2: admit; ≥ 3: ICU consideration

CAP outpatient treatment:

Healthy, no recent antibiotics: amoxicillin OR doxycycline OR azithromycin
Comorbidities: respiratory fluoroquinolone (levofloxacin/moxifloxacin) OR beta-lactam + macrolide

CAP inpatient (non-ICU): beta-lactam + macrolide OR respiratory FQ

CAP ICU: beta-lactam + azithromycin OR beta-lactam + FQ

HAP/VAP (≥ 48 hrs after admission): cover MRSA + Pseudomonas

Vancomycin or linezolid (MRSA) + antipseudomonal beta-lactam (piperacillin-tazobactam, cefepime) +/- aminoglycoside

Atypical pathogens: Mycoplasma (young adults, "walking pneumonia" - treat with macrolide or doxycycline), Legionella (water exposure, GI symptoms, hyponatremia - treat with FQ or azithromycin), Chlamydophila

10. Pleural Effusion

Transudate vs. Exudate (Light's Criteria - any one = exudate):

Pleural fluid protein / serum protein > 0.5
Pleural fluid LDH / serum LDH > 0.6
Pleural fluid LDH > 2/3 upper limit of serum LDH normal

Transudates: CHF (most common - bilateral), cirrhosis, nephrotic syndrome, hypothyroidism, PE Exudates: pneumonia/parapneumonic, malignancy, TB, pancreatitis, rheumatoid arthritis, PE

Additional pleural studies:

pH < 7.2 = complicated parapneumonic → drain (chest tube)
Glucose < 60 = complicated/empyema
Bloody: malignancy, PE, trauma
Amylase high: pancreatitis or esophageal rupture
ADA high: TB

BONUS: High-Yield Numbers to Memorize

Value	Context
EF < 40%	HFrEF (systolic dysfunction)
EF ≥ 50%	HFpEF (diastolic dysfunction)
Door-to-balloon < 90 min	STEMI primary PCI
Lytic within 120 min if no PCI	STEMI fibrinolysis cutoff
MAP reduction 25% in 1st hour	Hypertensive emergency
SpO₂ target 88-92%	COPD exacerbation (not higher)
O₂ sat ≥ 92%	Asthma target
Wells + D-dimer	PE low probability workup
PE provoked → 3 months AC	Standard duration
CHA₂DS₂-VASc ≥ 2 (male)	AF anticoagulation threshold
CURB-65 ≥ 3	Consider ICU for CAP

Sources: Goldman-Cecil Medicine; Washington Manual of Medical Therapeutics; Katzung's Basic & Clinical Pharmacology, 16e; Fuster and Hurst's The Heart, 15e; Murray & Nadel's Textbook of Respiratory Medicine.

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Step 3 High-Yield: GI & Hepatology

1. Cirrhosis - Complications and Scoring

Child-Pugh Score (5 parameters, 1-3 pts each)

Parameter	1 pt	2 pts	3 pts
Bilirubin (mg/dL)	< 2	2-3	> 3
Albumin (g/dL)	> 3.5	2.8-3.5	< 2.8
PT/INR	INR < 1.7	1.7-2.3	> 2.3
Ascites	None	Mild	Moderate/severe
Encephalopathy	None	Grade 1-2	Grade 3-4

Class A = 5-6 pts (compensated, good prognosis)
Class B = 7-9 pts (decompensated - threshold for transplant listing)
Class C = 10-15 pts (worst prognosis)

MELD Score (now MELD-Na)

Formula uses: INR + bilirubin + creatinine + Na

Used to prioritize liver transplant waitlist in the US (UNOS)
Superior to Child-Pugh for predicting short-term mortality
MELD ≥ 15: transplant benefit outweighs risk

Step 3 pearl: MELD replaced Child-Pugh for transplant allocation. Know both scoring systems and when each is used.

2. Ascites

SAAG (Serum-Ascites Albumin Gradient) = serum albumin - ascitic albumin

SAAG ≥ 1.1 g/dL (High gradient = Portal HTN)	SAAG < 1.1 g/dL (Low gradient = No portal HTN)
Cirrhosis (most common)	Nephrotic syndrome
Alcoholic hepatitis	Peritoneal carcinomatosis
CHF	Tuberculous peritonitis
Budd-Chiari syndrome	Pancreatic ascites
Portal vein thrombosis	Chylous ascites

Memory trick: SAAG ≥ 1.1 = portal hypertension is the cause. SAAG < 1.1 = not portal HTN.

Ascitic fluid always order:

Cell count (PMN > 250 = SBP)
Albumin (for SAAG)
Total protein
Culture/gram stain

Ascites management:

Na restriction (2 g/day) + fluid restriction
Diuretics: spironolactone (first-line) ± furosemide (ratio 100 mg:40 mg to maintain K+)
Refractory ascites: large-volume paracentesis (LVP) + albumin infusion (8 g/L of fluid removed)
TIPS: for recurrent refractory ascites not responding to the above

3. Spontaneous Bacterial Peritonitis (SBP)

Diagnosis: ascitic fluid PMN (neutrophils) > 250 cells/mL - treat empirically even if culture negative

Common organisms: E. coli, Klebsiella, S. pneumoniae (gram-negatives dominate)

Treatment:

Empiric: cefotaxime (3rd-gen cephalosporin) IV x 5 days, OR oral fluoroquinolone (ciprofloxacin/norfloxacin) for mild cases
Add IV albumin (1.5 g/kg on day 1, 1 g/kg on day 3) → prevents hepatorenal syndrome

Prophylaxis (SBP prevention):

Primary: norfloxacin if ascitic protein < 1.5 g/dL + renal impairment or Child-Pugh ≥ 9
Secondary (after first SBP episode): indefinite norfloxacin or ciprofloxacin

Tip: Secondary peritonitis (surgical) has glucose < 50, LDH > serum, protein > 1 g/dL, polymicrobial culture - needs surgery.

4. Variceal Bleeding

Step-by-step management (all simultaneous):

Resuscitate: 2 large-bore IVs, type and crossmatch, target Hgb 7-8 g/dL (restrictive transfusion policy)
Octreotide IV (somatostatin analogue) - reduces portal pressure; start immediately, continue 3-5 days
Prophylactic antibiotics (ceftriaxone IV or ciprofloxacin) - reduces SBP risk and mortality
Urgent EGD within 12 hours - variceal band ligation (preferred) or sclerotherapy
PPI - high-dose IV (treat concomitant peptic ulcer disease)
Failed endoscopy: Sengstaken-Blakemore tube (balloon tamponade) as bridge → TIPS

Rescue therapy: TIPS (transjugular intrahepatic portosystemic shunt) - if endoscopy fails or rebleeding

Primary prophylaxis (prevent first bleed):

Non-selective beta-blockers (propranolol, nadolol, carvedilol) for medium/large varices
OR endoscopic band ligation if beta-blockers not tolerated

Secondary prophylaxis (prevent rebleed):

Non-selective beta-blockers + band ligation (combination better than either alone)

5. Hepatic Encephalopathy

Precipitants (know all - "THE CRAP" mnemonic):

Toxins/drugs (opiates, benzodiazepines, sedatives)
Hemorrhage (GI bleed - blood is protein load)
Electrolyte disturbance (hypokalemia, alkalosis)
Constipation
Renal failure (uremia)
Alcohol
Portosystemic shunt
Infection/SBP

Mechanism: Ammonia + aromatic amino acids → increased GABA stimulation → encephalopathy (Note: ammonia level does NOT correlate with severity)

Grades:

Grade 1: personality change, sleep disturbance
Grade 2: confusion, lethargy, asterixis (flapping tremor - best clinical sign)
Grade 3: stupor, incomprehensible speech
Grade 4: coma

Treatment:

Identify and treat precipitant (most important step)
Lactulose 15-45 mL PO BID-QID → titrate to 3-5 soft stools/day (first-line)
- Acute episode: 30 mL q1-2h initially, then taper
- Can give as enema (300 mL in 700 mL water) if can't tolerate oral
Rifaximin 550 mg PO BID - add if no improvement with lactulose, or for maintenance to reduce hospitalizations
Protein restriction is NOT recommended long-term (worsens malnutrition); prefer branched-chain amino acids

6. Hepatorenal Syndrome (HRS)

Type 1 (now called AKI-HRS): Rapidly progressive (creatinine doubles to > 2.5 in < 2 weeks) - precipitated by SBP, GI bleed, sepsis - high mortality

Type 2 (now CKD-HRS): Slowly progressive, associated with refractory ascites

Diagnosis of exclusion - rule out: hypovolemia (give fluid challenge), nephrotoxins, obstruction, intrinsic renal disease

Treatment:

Vasoconstrictors + albumin:
- Midodrine (alpha-agonist) + octreotide (inhibits vasodilation) + IV albumin - preferred in outpatient/non-ICU
- Norepinephrine + albumin - ICU setting
- Terlipressin + albumin - most evidence-based (not widely available in US)
Definitive treatment: liver transplantation
Dialysis/RRT: bridge to transplant only

Preventive: Give IV albumin with large-volume paracentesis and with SBP treatment (prevents HRS)

7. Peptic Ulcer Disease (PUD)

Causes: H. pylori (60-70% of duodenal ulcers) and NSAIDs are responsible for most cases

H. pylori testing:

Active ulcer: urea breath test, stool antigen test (non-invasive); biopsy via endoscopy (gold standard)
Serology (IgG): does NOT confirm active infection, only exposure
Test all patients with active PUD, history of PUD, or MALT lymphoma

H. pylori eradication regimens:

Standard triple therapy (7-14 days): PPI + amoxicillin + clarithromycin (avoid if >15% local clarithromycin resistance)
Quadruple therapy (10-14 days): PPI + bismuth + metronidazole + tetracycline (preferred if penicillin allergy or high clarithromycin resistance)
Concomitant therapy: PPI + amoxicillin + clarithromycin + metronidazole

Confirm eradication ≥ 4 weeks after treatment: urea breath test or stool antigen (NOT serology - stays positive after eradication)

NSAID-induced ulcers:

Stop NSAID if possible
PPI for treatment and prevention
If must continue NSAID: add PPI (or misoprostol, less tolerated)
COX-2 inhibitor reduces GI risk but NOT cardiovascular risk

Complications of PUD:

Bleeding: endoscopy with epinephrine injection + thermal coagulation; PPI IV bolus then drip; repeat endoscopy if rebleeding
Perforation: free air on imaging → emergent surgery
Gastric outlet obstruction: endoscopy for dilation ± surgery

8. Acute Pancreatitis

Common causes: Gallstones (#1), Alcohol (#2), then Hypertriglycerides (> 1000 mg/dL), ERCP, drugs, trauma, hypercalcemia, idiopathic

Diagnosis: 2 of 3 criteria:

Typical abdominal pain (epigastric, radiating to back)
Lipase (or amylase) ≥ 3x upper limit of normal
Characteristic imaging (CT/MRI)

Severity scoring - Ranson's Criteria (48 hrs):

On admission:

Age > 55
WBC > 16,000
Glucose > 200
LDH > 350
AST > 250

At 48 hours:

Hematocrit drop > 10%
BUN rise > 5
Ca < 8 mg/dL
PaO₂ < 60 mmHg
Base deficit > 4
Fluid sequestration > 6L

< 3 criteria = mild; ≥ 3 = severe; ≥ 6 = ~50% mortality

Also use: BISAP score (BUN > 25, Impaired mental status, SIRS, Age > 60, Pleural effusion) - calculable within 24 hrs

Management (all supportive):

Aggressive IV fluid resuscitation (Lactated Ringer's preferred over NS - reduces SIRS) - 250-500 mL/hr initially
NPO initially; early enteral nutrition preferred (NG tube) over TPN once tolerated
Pain control (IV opioids)
No role for routine antibiotics unless infected necrosis suspected
ERCP: only if gallstone pancreatitis + cholangitis or persistent biliary obstruction (within 24-48 hrs)

Complications:

Pseudocyst: wait 4-6 weeks; drain if symptomatic (endoscopic preferred)
Infected necrosis: CT-guided needle aspiration to confirm → antibiotics (imipenem or meropenem) → necrosectomy if no improvement
Hemorrhagic pancreatitis: Grey Turner sign (flank ecchymosis), Cullen sign (periumbilical ecchymosis)

9. Inflammatory Bowel Disease (IBD)

Crohn's Disease vs. Ulcerative Colitis

Feature	Crohn's	Ulcerative Colitis
Location	Any GI tract (mouth to anus)	Colon only (rectum always involved)
Pattern	Skip lesions, transmural	Continuous, mucosal only
Histology	Non-caseating granulomas	Crypt abscesses, no granulomas
Endoscopy	Cobblestone, linear ulcers	Pseudopolyps, loss of haustra
Perianal disease	Common	Rare
Fistulas/abscesses	Yes	No
Smoking	Worsens Crohn's	Protective in UC
Toxic megacolon	Rare	Classic complication
Colon cancer risk	Slightly increased	Significantly increased

Treatment Approach (both diseases - step-up):

Mild-Moderate: 5-ASA agents (mesalamine) - UC especially; sulfasalazine
Moderate-Severe flare: Corticosteroids (prednisone, budesonide)
Maintenance / Steroid-sparing: Azathioprine, 6-mercaptopurine (slow onset, check TPMT before dosing), methotrexate (Crohn's)
Biologic therapy (moderate-severe or steroid-dependent):
- Anti-TNF: infliximab, adalimumab (both CD and UC)
- Anti-integrins: vedolizumab (gut-selective, fewer systemic effects)
- Anti-IL-12/23: ustekinumab (Crohn's)
- JAK inhibitors: tofacitinib (UC)
Surgery: UC - total colectomy is curative; Crohn's - surgery for complications (strictures, abscesses, fistulas), NOT curative

Extraintestinal manifestations (parallel vs. independent of bowel disease):

Parallel (follow disease activity): peripheral arthritis, erythema nodosum, episcleritis
Independent: ankylosing spondylitis, primary sclerosing cholangitis (PSC - strongly associated with UC), pyoderma gangrenosum, uveitis

PSC (Primary Sclerosing Cholangitis):

Strongly associated with UC (not Crohn's)
Elevated alkaline phosphatase (out of proportion), "beading" of bile ducts on MRCP/ERCP
Increased risk of cholangiocarcinoma
No effective medical treatment; liver transplant is definitive

10. Hepatocellular Carcinoma (HCC)

Risk factors: Cirrhosis (any cause), HBV (even without cirrhosis), HCV, alcoholic cirrhosis, NAFLD/NASH, hemochromatosis, alpha-1 antitrypsin deficiency, aflatoxin exposure

Surveillance: Ultrasound every 6 months for all cirrhotic patients; add AFP optionally

For HBV: start surveillance after age 40 even without cirrhosis

Diagnosis: Nodule > 1 cm in cirrhotic liver with typical imaging features (arterial enhancement + portal/venous washout on triple-phase CT or MRI) = HCC (no biopsy needed)

Treatment by stage:

Resectable, non-cirrhotic: hepatic resection
Cirrhotic, within Milan criteria (single nodule ≤ 5 cm OR ≤ 3 nodules each ≤ 3 cm, no vascular invasion): liver transplantation
Intermediate (unresectable, no vascular invasion): TACE (transarterial chemoembolization)
Advanced (vascular invasion/metastasis): sorafenib or lenvatinib (systemic)

11. Viral Hepatitis Fast Facts

Virus	Transmission	Chronicity	Marker	Treatment
HAV	Fecal-oral	Never	Anti-HAV IgM (acute)	Supportive
HBV	Blood/sexual/vertical	5-10% adults; 90% neonates	HBsAg (active), Anti-HBs (immune), HBeAg (replication)	Tenofovir, entecavir
HCV	Blood (IV drug use #1)	70-85%	Anti-HCV, confirm RNA	DAAs (sofosbuvir-based) - >95% cure
HDV	Blood (co-infects with HBV)	Only with HBV	Anti-HDV	Prevent with HBV vaccine
HEV	Fecal-oral	Rarely	Anti-HEV IgM	Supportive; ribavirin if immunocompromised

HBV serology interpretation:

HBsAg	Anti-HBs	Anti-HBc	Interpretation
+	-	+ (IgM)	Acute HBV
+	-	+ (IgG)	Chronic HBV
-	+	+ (IgG)	Past infection, recovered, immune
-	+	-	Vaccinated (no natural infection)
-	-	+ (IgG)	Window period or resolved infection

HCV: Treat ALL patients with chronic HCV regardless of fibrosis stage. DAAs (direct-acting antivirals): ledipasvir/sofosbuvir, glecaprevir/pibrentasvir - cure rate > 95%

12. Drug-Induced Liver Injury (DILI) - High-Yield

Drug	Pattern
Acetaminophen	Centrilobular necrosis; toxic > 4 g/day (lower in alcoholics); treat with N-acetylcysteine
INH (isoniazid)	Hepatocellular; risk increases with age + alcohol
Amoxicillin-clavulanate	Cholestatic (most common drug-induced cholestasis)
Statins	Mild transaminase elevation (usually benign); rare hepatitis
Methotrexate	Hepatic fibrosis with long-term use
Valproate	Hepatotoxicity (especially children)
Halothane	Massive hepatic necrosis (rare, re-exposure)

Acetaminophen overdose: Use Rumack-Matthew nomogram (serum level at 4 hrs vs. time) → NAC if level in toxic range. NAC works even up to 24 hrs after ingestion.

BONUS: High-Yield Numbers for GI & Hepatology

Value	Meaning
PMN > 250/mL in ascites	SBP (treat empirically)
SAAG ≥ 1.1 g/dL	Portal hypertension
MELD ≥ 15	Transplant benefit exceeds risk
Milan criteria: ≤ 5 cm single or ≤ 3 nodules each ≤ 3 cm	HCC transplant eligibility
HCC surveillance every 6 months	Ultrasound ± AFP
Lipase ≥ 3x ULN	Pancreatitis diagnosis
Ranson's ≥ 3	Severe pancreatitis
Hgb transfusion target 7-8 in GI bleed	Restrictive strategy reduces mortality
Octreotide + antibiotics + EGD within 12 hrs	Variceal bleed standard of care
Lactulose goal	3-5 soft stools/day
Rifaximin 550 mg BID	Hepatic encephalopathy maintenance

Sources: Harrison's Principles of Internal Medicine 22e; Washington Manual of Medical Therapeutics; Yamada's Textbook of Gastroenterology 7e; Mulholland & Greenfield's Surgery 7e; Schwartz's Principles of Surgery 11e; Sleisenger & Fordtran's GI and Liver Disease

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Step 3 High-Yield: Nephrology & Electrolytes

1. Acute Kidney Injury (AKI) - The Three-Category Approach

Classify First: Prerenal vs. Intrinsic vs. Postrenal

Finding	Prerenal	Intrinsic (ATN)	Postrenal
BUN:Cr ratio	> 20:1	< 10-15:1	Variable
FENa	< 1%	> 2%	Variable
Urine Na	< 20 mEq/L	> 40 mEq/L	Variable
Urine osm	> 500 mOsm/kg	< 350 mOsm/kg	Variable
Urine sediment	Bland (hyaline casts)	Muddy brown granular casts	Variable
Response to fluids	Yes (creatinine improves)	No	No

Key caveat: FENa < 1% also occurs in contrast nephropathy, myoglobinuria, early obstruction, and glomerulonephritis - it is NOT exclusive to prerenal.

Muddy brown granular casts = ATN (acute tubular necrosis) - pathognomonic

Causes by Category:

Prerenal: Hypovolemia (bleeding, vomiting, diarrhea, burns), CHF, cirrhosis, sepsis, NSAIDs (decrease prostaglandin-mediated afferent dilation), ACEi/ARB (decrease efferent constriction)

Intrinsic renal:

Glomerular: glomerulonephritis, vasculitis
Tubular: ATN (ischemic or nephrotoxic - aminoglycosides, contrast, cisplatin, myoglobin, hemoglobin)
Interstitial: acute interstitial nephritis (AIN) - drug-induced (NSAIDs, penicillins, PPIs), infection, sarcoid → WBC casts + eosinophiluria
Vascular: renal artery stenosis/thrombosis, TTP/HUS

Postrenal (obstruction): BPH (#1 in older men), kidney stones, cervical/prostate cancer, neurogenic bladder → ultrasound shows hydronephrosis

AKI Management:

Find and treat the cause
Volume resuscitation for prerenal (IVF) - Lactated Ringer's preferred over NS
Relieve obstruction for postrenal (catheter, nephrostomy)
Stop nephrotoxins
Monitor electrolytes (K+, bicarb), fluid balance, and urinary output
Dialysis indications: AEIOU - Acidosis (pH < 7.1), Electrolyte (refractory hyperK+), Intoxication (methanol, ethylene glycol, salicylates, lithium), fluid Overload (refractory), Uremia (encephalopathy, pericarditis, bleeding)

2. Chronic Kidney Disease (CKD)

KDIGO Staging by GFR (CKD-EPI equation):

Stage	GFR (mL/min/1.73m²)	Description
G1	≥ 90	Normal/high - kidney damage markers present
G2	60-89	Mildly decreased
G3a	45-59	Mild-moderately decreased
G3b	30-44	Moderate-severely decreased
G4	15-29	Severely decreased
G5	< 15	Kidney failure (ESKD)

CKD requires: GFR < 60 OR kidney damage markers (albuminuria, abnormal urinary sediment, structural/biopsy abnormality) for > 3 months

CKD Complications and Management:

Complication	When	Treatment
Hypertension	All stages	ACEi/ARB (first-line - also reduces proteinuria)
Proteinuria	All stages	ACEi/ARB (target < 500 mg/day)
Metabolic acidosis	GFR < 30	NaHCO₃ supplementation (target bicarb ≥ 22)
Hyperkalemia	GFR < 30-45	Dietary restriction, patiromer, sodium zirconium cyclosilicate
Anemia	GFR < 30-45	Iron first (check ferritin/TSAT), then erythropoiesis-stimulating agents (ESAs: epoetin, darbepoetin) - target Hgb 10-11 g/dL
Renal osteodystrophy	GFR < 30	Phosphate restriction + binders (calcium carbonate, sevelamer); active vitamin D (calcitriol); correct secondary hyperPTH
Secondary hyperPTH	GFR < 30	Calcitriol, cinacalcet (calcimimetic)
Dyslipidemia	All stages	Statin therapy

ACEi/ARB in CKD: Allow Cr rise up to 30% above baseline. If greater → rule out renal artery stenosis. Contraindicated in bilateral renal artery stenosis.

Referral to nephrology: GFR < 30 or rapidly declining GFR

3. Glomerular Disease - Nephrotic vs. Nephritic

The Core Distinction:

Feature	Nephrotic Syndrome	Nephritic Syndrome
Proteinuria	> 3.5 g/day (massive)	< 3.5 g/day (non-nephrotic)
Hematuria	Absent or minimal	Present (RBC casts - pathognomonic)
Edema	Severe (hypoalbuminemia)	Mild to moderate
Hypertension	Variable	Yes (Na retention)
GFR/Cr	Usually normal initially	Reduced
Complement	Usually normal	Low (in many)

Nephrotic Causes - "The Big 4":

Disease	Key Association	Biopsy Finding	Treatment
Minimal Change Disease (MCD)	Children (#1 cause), NSAIDs, Hodgkin lymphoma	Normal on LM; effacement on EM	Prednisone (excellent response)
Focal Segmental Glomerulosclerosis (FSGS)	Black adults, HIV, heroin, obesity, reflux	Focal sclerosis on LM	Prednisone; resistant → tacrolimus/cyclosporine
Membranous Nephropathy (MN)	Adults (#1 idiopathic cause), HBV, solid tumors, SLE, NSAIDs	"Spike and dome" on EM	Cyclophosphamide + steroid; anti-PLA₂R Ab positive in primary
Diabetic Nephropathy	DM > 10-15 yrs	Kimmelstiel-Wilson nodules	ACEi/ARB; SGLT2 inhibitors; tight glucose/BP control

Nephrotic syndrome complications:

Hypercoagulable state → renal vein thrombosis, DVT, PE (loss of antithrombin III)
Hyperlipidemia + lipiduria (fatty casts, oval fat bodies, Maltese cross)
Susceptibility to infections (loss of immunoglobulins) - especially encapsulated organisms

Nephritic Causes - "The RAPId GNs":

Disease	Key Clues	Complement	Antibody
Postinfectious GN	1-3 wks after strep pharyngitis or impetigo; "lumpy-bumpy" subepithelial humps	Low C3	ASO titer
IgA nephropathy (Berger disease)	Synpharyngitic hematuria (during URI, not 2 weeks later); adults; most common GN worldwide	Normal	Mesangial IgA deposits
Lupus nephritis	Young women, SLE, class III/IV most severe	Low C3/C4	ANA, anti-dsDNA, anti-Sm
MPGN	HCV, cryoglobulins, tram-track pattern	Low C3	Variable
ANCA vasculitis (pauci-immune GN)	Granulomatosis with polyangiitis (c-ANCA/PR3), microscopic polyangiitis (p-ANCA/MPO)	Normal	c-ANCA or p-ANCA
Anti-GBM disease (Goodpasture)	Pulmonary-renal syndrome; hemoptysis + hematuria	Normal	Anti-GBM (anti-type IV collagen)

Rapidly Progressive GN (RPGN): Crescents on biopsy; weeks to months to ESRD without treatment → treat urgently with IV methylprednisolone + cyclophosphamide (or rituximab for ANCA)

Complement levels to memorize:

Low C3, Normal C4: Post-strep GN, C3 glomerulopathy
Low C3 and C4: SLE, MPGN, cryoglobulinemia, subacute bacterial endocarditis
Normal C3 and C4: IgA nephropathy, ANCA vasculitis, anti-GBM disease

4. Hyponatremia (Na < 135)

Step-by-Step Approach:

Step 1 - Check serum osmolality:

Hypertonic (> 295): hyperglycemia (for every 100 mg/dL rise in glucose → Na drops ~1.6 mEq/L), mannitol
Isotonic (285-295): pseudohyponatremia (hyperlipidemia, hyperproteinemia)
Hypotonic (< 285): true hyponatremia → proceed to Step 2

Step 2 - Assess volume status:

Volume Status	Urine Na	Cause
Hypovolemic	< 20 mEq/L	Extrarenal loss (vomiting, diarrhea, third-spacing)
Hypovolemic	> 20 mEq/L	Renal loss (diuretics, Addison's, cerebral salt wasting)
Euvolemic	> 20 mEq/L	SIADH, hypothyroidism, psychogenic polydipsia
Hypervolemic	< 20 mEq/L	CHF, cirrhosis, nephrotic syndrome
Hypervolemic	> 20 mEq/L	AKI, CKD

SIADH - Must Know:

Causes: CNS disease, pulmonary disease (pneumonia, TB, small cell lung cancer - #1 tumor), pain, nausea, drugs (SSRIs, carbamazepine, cyclophosphamide, vincristine, oxytocin, NSAIDs, chlorpropamide)

Diagnostic criteria: Hypo-osmolar hyponatremia, Urine osm > 100, Urine Na > 40, euvolemic, no diuretic use, normal thyroid/adrenal function

Treatment by severity:

Asymptomatic/mild: fluid restriction (600-1000 mL/day) - first-line for SIADH
Moderate symptoms: fluid restriction + salt tabs; demeclocycline (chronic SIADH)
Severe symptoms (seizures, coma): 3% hypertonic saline IV
- Correct Na by no more than 6-8 mEq/L in 24 hrs (max 10-12 mEq/L/24 hrs)
- Overcorrection → osmotic demyelination syndrome (ODS)/central pontine myelinolysis → irreversible quadriplegia, dysarthria, dysphagia
Vaptans (tolvaptan, conivaptan): V2-receptor antagonists for euvolemic/hypervolemic hyponatremia; avoid in liver disease

Hypovolemic hyponatremia: Isotonic saline (NS) 0.9% to restore volume

5. Hyperkalemia (K+ > 5.5)

Causes:

Decreased renal excretion: AKI, CKD, Addison's, Type 4 RTA (hypoaldosteronism - most common RTA in adults, especially diabetics)
Drugs: ACEi, ARBs, K+-sparing diuretics (spironolactone, amiloride, triamterene), NSAIDs, TMP-SMX, heparin
Shift out of cells: acidosis (metabolic), rhabdomyolysis, tumor lysis, beta-blockers, digoxin toxicity, succinylcholine
Pseudohyperkalemia: hemolysis of sample, thrombocytosis, leukocytosis

ECG Changes (in order of severity):

Peaked T waves (earliest)
Prolonged PR interval
Widened QRS
Sine wave pattern
Ventricular fibrillation / asystole

Treatment (memorize the sequence - "C-BIG-K-Drop"):

Drug	Dose	Mechanism	Onset	Duration
Calcium gluconate 10%	10 mL IV over 2-3 min; repeat in 5-10 min if no change	Stabilizes myocardial membrane	1-3 min	30-60 min
Insulin + Glucose	10-20 units regular insulin + 25-50 g glucose IV	Shifts K+ into cells	15-30 min	4-6 hrs
Sodium bicarbonate	IV isotonic solution (3 amps NaHCO₃ in 1L D5W)	Shifts K+ into cells (if metabolic acidosis)	30-60 min	Hours
Albuterol (nebulized)	10-20 mg nebulized over 30-60 min	Beta₂ → shifts K+ into cells	30 min	2-4 hrs
Patiromer / SZC	Patiromer 8.4 g PO daily	GI K+ binder (removes K+)	Hours	Chronic use
Kayexalate (sodium polystyrene)	15-60 g PO	GI K+ exchange (less predictable, risk bowel necrosis)	Hours	-
Furosemide	IV	Kaliuresis (if adequate renal function)	30-60 min	-
Dialysis	Emergent hemodialysis	Removes K+	Rapid	-

Calcium gluconate does NOT lower K+ - it only stabilizes the myocardium. Always follow it immediately with agents that shift or remove K+.

6. Acid-Base Disorders

Systematic Approach (Step 3 loves mixed disorders):

pH: < 7.35 = acidosis; > 7.45 = alkalosis
Primary process: PCO₂ ↑ = respiratory acidosis; PCO₂ ↓ = respiratory alkalosis; HCO₃ ↓ = metabolic acidosis; HCO₃ ↑ = metabolic alkalosis
Compensation: (expected vs. actual - if not matching, mixed disorder)
Anion gap (for metabolic acidosis): Na - (Cl + HCO₃); normal = 8-12 mEq/L (correct for albumin: add 2.5 for every 1 g/dL albumin below 4)

Compensation Rules:

Disorder	Expected Compensation
Metabolic acidosis	PCO₂ = (1.5 × HCO₃) + 8 ± 2 (Winter's formula)
Metabolic alkalosis	PCO₂ increases 0.7 mmHg per 1 mEq/L rise in HCO₃
Respiratory acidosis (acute)	HCO₃ rises 1 mEq/L per 10 mmHg rise in PCO₂
Respiratory acidosis (chronic)	HCO₃ rises 3.5 mEq/L per 10 mmHg rise in PCO₂
Respiratory alkalosis (acute)	HCO₃ falls 2 mEq/L per 10 mmHg fall in PCO₂
Respiratory alkalosis (chronic)	HCO₃ falls 5 mEq/L per 10 mmHg fall in PCO₂

High Anion Gap Metabolic Acidosis - "MUDPILES" or "GOLDMARK":

Mnemonic	Cause
M	Methanol
U	Uremia
D	DKA / starvation ketoacidosis
P	Propylene glycol / Paraldehyde
I	INH / Iron
L	Lactic acidosis (Type A: tissue hypoxia; Type B: metformin, liver failure, seizures)
E	Ethylene glycol
S	Salicylates

Normal Anion Gap (Hyperchloremic) Metabolic Acidosis:

GI bicarbonate loss: diarrhea (#1), fistulas, ileostomy
Renal: Renal tubular acidosis (RTA)
Saline excess (dilutional)

Renal Tubular Acidosis (RTA) - Rapid Review:

Type	Defect	Urine pH	K+	Common Causes
Type 1 (Distal)	Can't secrete H+ distally	> 5.5 (alkaline)	Low (hypokalemia)	Sjögren's, SLE, amphotericin B, myeloma; leads to nephrolithiasis (calcium phosphate stones)
Type 2 (Proximal)	Can't reabsorb HCO₃	< 5.5 (acid)	Low (hypokalemia)	Fanconi syndrome, multiple myeloma, Wilson's, acetazolamide, tenofovir; associated with rickets
Type 4	Hypoaldosteronism → can't excrete K+	< 5.5 (acid)	High (hyperkalemia)	Diabetic nephropathy (#1), ACEi/ARBs, NSAIDs, adrenal insufficiency, TMP-SMX

Memory trick: Type 4 RTA = the ONLY RTA with hyperkalemia. Most common in diabetics.

7. Hypercalcemia

Causes by PTH Level:

PTH high (primary hyperparathyroidism - most common overall):

Parathyroid adenoma (85%), hyperplasia (10-15%), carcinoma (rare)
Labs: High Ca, Low phosphate, High PTH, High urine Ca
Symptoms: "Bones, Stones, Groans, Psychic Moans"

PTH low (malignancy - most common in hospitalized patients):

Osteolytic metastases (breast, lung, myeloma - direct bone destruction)
Humoral hypercalcemia of malignancy (PTHrP): squamous cell lung, renal cell, breast, bladder
Other: Vitamin D toxicity, granulomatous disease (sarcoid, TB - 1α-hydroxylase in macrophages), thiazide diuretics

Treatment:

Severity	Treatment
Mild (< 12 mg/dL), asymptomatic	Hydration, treat underlying cause
Moderate-Severe (> 12-14 mg/dL)	Aggressive IV NS (volume expansion promotes calciuresis - first and most important step)
After hydration	Furosemide only after adequate hydration (forces calciuresis) - NOT before
Persistent	IV bisphosphonates (zoledronic acid, pamidronate) - lasts weeks-months
Malignancy-related	Denosumab (RANK-L inhibitor), calcitonin (rapid onset, tachyphylaxis)
Life-threatening/renal failure	Hemodialysis
Granulomatous/lymphoma	Steroids (inhibit 1α-hydroxylase)

Key Step 3 trap: Do NOT give furosemide before adequate IV fluid resuscitation - will worsen volume depletion and hypercalcemia.

8. Hypokalemia (K+ < 3.5)

Causes:

GI losses: Vomiting (metabolic alkalosis), diarrhea (metabolic acidosis)
Renal losses: Loop/thiazide diuretics, hyperaldosteronism (Conn's syndrome), Cushing's, hypomagnesemia (always check Mg²+ in refractory hypoK+), RTA types 1 and 2, Bartter/Gitelman syndromes
Cellular shift: Insulin, beta-agonists (albuterol), alkalosis, refeeding syndrome, hypokalemic periodic paralysis

ECG Changes:

Flattened/inverted T waves
Prominent U waves (after T wave in V2-V3) - most specific
Prolonged QU interval
Risk of digoxin toxicity (hypoK+ potentiates digoxin)

Treatment:

Mild (3.0-3.5): Oral potassium replacement (KCl preferred)
Severe (< 3.0 or symptomatic): IV KCl - max 10-20 mEq/hr via peripheral IV; 40 mEq/hr via central
Always replace magnesium - hypoMg causes refractory hypoK+ (Mg required for K+ reabsorption in thick ascending limb)

9. Key Urine Sediment Findings

Finding	Diagnosis
Muddy brown granular casts	ATN (ischemic or toxic)
RBC casts	Glomerulonephritis (pathognomonic)
WBC casts	Pyelonephritis, acute interstitial nephritis
Waxy/broad casts	Advanced CKD (wide tubules)
Hyaline casts	Normal or dehydration/prerenal
Fatty casts, oval fat bodies, Maltese cross (polarized light)	Nephrotic syndrome
Eosinophiluria	Acute interstitial nephritis (also renal cholesterol emboli)

BONUS: High-Yield Numbers to Memorize

Value	Meaning
BUN:Cr > 20:1	Prerenal AKI
FENa < 1%	Prerenal (or early obstruction, GN, contrast)
FENa > 2%	ATN (intrinsic renal)
Urine protein > 3.5 g/day	Nephrotic syndrome
RBC casts	Nephritic/GN
GFR < 60 for > 3 months	CKD by definition
Na correction max 6-8 mEq/L/24 hrs	Prevents osmotic demyelination
Hyperkalemia + peaked T waves	Give calcium gluconate first
Anion gap > 12	High-gap metabolic acidosis
Type 4 RTA + hyperkalemia	Diabetic nephropathy / ACEi use
Ca > 12 mg/dL acute	Aggressive IV NS first
Hypokalemia + refractory	Check and replete magnesium

Sources: Washington Manual of Medical Therapeutics; Goldman-Cecil Medicine; Comprehensive Clinical Nephrology 7e; Brenner & Rector's The Kidney; Harrison's Principles of Internal Medicine 22e; Morgan & Mikhail's Clinical Anesthesiology 7e

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