Surgical MCQ Answers - Verified from Schwartz, Harrison's & Doherty

Q1 (Page 1) - Upper GI Bleeding: Initial Investigation

• Schwartz's Principles of Surgery, 11e - EGD is the preferred initial investigation for upper GI bleeding
• Washington Manual of Medical Therapeutics - "EGD, with high diagnostic accuracy and therapeutic capability, is the preferred investigative test in upper GI bleeding"

Q2 (Page 2) - Pancreatitis: Non-Alcoholic Causes

• I - Idiopathic
• G - Gallstones (most common overall cause)
• E - Ethanol (alcohol)
• T - Trauma
• S - Steroids
• M - Mumps / Malignancy
• A - Autoimmune
• S - Scorpion sting
• H - Hypercalcemia / Hypertriglyceridemia (TG >1000 mg/dL)
• E - ERCP
• D - Drugs

Q3 (Page 2/3) - Obstructing Left-Sided Colorectal Cancer in Elderly/Unstable Patient

• Primary anastomosis carries high risk of anastomotic leak in an unprepared, obstructed bowel
• Hartmann's procedure (resection + end colostomy) is safer - allows definitive cancer resection while avoiding anastomosis in a high-risk setting
• Colostomy can be reversed later once patient is stable
• Schwartz's Principles of Surgery supports Hartmann's as the standard approach in this scenario

Q4 (Page 3) - Bowel Obstruction Diagnosis

• Schwartz's Surgery - CT scan is the preferred imaging for bowel obstruction; plain X-ray is initial screening

Q5 (Page 4) - Spontaneous Bacterial Peritonitis (SBP): Most Common Organism

• E. coli (~37%) - most common single organism
• Klebsiella pneumoniae (~17%)
• Streptococcus pneumoniae (~12%)
• Gram-negatives account for ~70% of cases

• Schwartz's Principles of Surgery, 11e - "The first line of empiric treatment is with a third-generation cephalosporin because the majority of cases are caused by aerobic gram-negative microbes such as E. coli"

Q6 (Page 4) - Rectal Prolapse: Classic Presentation

• Full-thickness rectal prolapse = concentric rings of mucosa, all bowel wall layers protrude, appears with straining
• Prolapsed hemorrhoids = radial folds (not concentric), separated by sulci

• Current Surgical Therapy, 14e - "Full thickness rectal prolapse appears as concentric rings..."
• Berek & Novak's Gynecology - "Full thickness (all layers) come through the anus as concentric rings"

Q7/Q8 (Page 5) - Adenomatous Polyp and Carcinoma Relationship

• A. A villous growth pattern RARELY leads to carcinoma - FALSE (villous has the HIGHEST malignant potential)
• B. The propensity for neoplastic transformation is related to size - TRUE
• C. Adenomas are rare in areas of low cancer incidence - TRUE (adenoma-carcinoma sequence is established)
• D. Adenomas and adenocarcinomas share the same anatomic location - TRUE
• E. Immature cells are found higher than normal in the crypts - TRUE (this is the pathologic hallmark)

1. Size (especially >1 cm - high risk; >2 cm = ~40% risk)
2. Histology (villous > tubulovillous > tubular)
3. Degree of dysplasia

Q9 (Page 6) - Diverticulitis: Clinical Diagnosis

1. LLQ pain/tenderness
2. Fever with leukocytosis
3. ± Palpable mass (inflamed diverticular phlegmon or abscess)

• Goldman-Cecil Medicine - "Physical examination typically reveals LLQ tenderness, sometimes with localized guarding or a palpable mass. Rebound tenderness suggests free perforation."

Q10 (Page 10) - Best Test for H. pylori Detection (Cost + Accuracy)

• A. Serology (antibody test) - Cannot distinguish active from past infection; positive even after eradication; less accurate
• C. Endoscopic biopsy - Invasive, expensive, requires endoscopy
• D. Endoscopic rapid urease test - Also invasive, requires endoscopy

• Non-invasive
• High sensitivity (~95%) and specificity (~96%)
• Detects ACTIVE infection (not past)
• Cost-effective
• Can confirm eradication after treatment
• Harrison's Principles of Internal Medicine, 22e - "Three types of studies routinely used include serologic testing, the 13C-urea breath test, and the fecal H. pylori antigen test"
• Robbins Basic Pathology - "This high-sensitivity, high-specificity test may be used for diagnosis of H. pylori infection"

Q11 (Page 11) - Colorectal Cancer Screening in Family History

• Average risk: begin at age 45 (or 50 by older guidelines)
• First-degree relative with CRC or advanced adenoma: Start at age 40 OR 10 years before the youngest relative's diagnosis age, whichever comes first
• Thompson & Thompson Genetics in Medicine - "first-degree relative with colon cancer...triggers initiation of colon cancer screening by colonoscopy at age 40, or 10 years before the earliest diagnosis"
• Schwartz's Surgery - "rises to 12% if one first-degree relative is affected"

Q12 (Page 12) - Gardner's Syndrome

• Osteomas (skull, mandible, long bones)
• Desmoid tumors (mesenteric/retroperitoneal - most dangerous)
• Epidermoid/sebaceous cysts (skin)
• Supernumerary/impacted teeth
• Congenital hypertrophy of retinal pigment epithelium (CHRPE)
• Gastric/duodenal polyps

Q13 (Page 13) - Malignant Polyp on Endoscopy

• Favorable histology (well-differentiated, no lymphovascular invasion, clear margins >2mm, no sessile/sm3): Endoscopic resection may be curative
• Unfavorable histology (poorly differentiated, lymphovascular invasion, positive/close margins, sm3 invasion): Surgical resection required regardless of apparent gross clearance

Q14/Q15 (Page 15) - Coagulopathy Management Before Surgery

• FFP provides immediate coagulation factor replacement (all factors) - rapid reversal
• Vitamin K provides sustained reversal (works over hours by enabling hepatic factor synthesis)
• Together they stabilize coagulation before invasive intervention

Q16 (Page 16) - Peritonitis/Adhesions and Steroids

Q17 (Page 17) - Columns of Morgagni Location

• Columns of Morgagni = longitudinal mucosal folds in the anal canal, located above the dentate line (in the transitional/columnar zone)
• Dentate line = junction between columnar epithelium (above) and squamous epithelium (below)
• Above dentate line: Columns of Morgagni, internal hemorrhoids, visceral innervation (painless)
• Below dentate line: External hemorrhoids, somatic innervation (painful), squamous epithelium

Q18 (Page 18) - Thrombosed External Hemorrhoid Management

• If < 72 hours from onset and severe pain: Surgical excision (not just incision and drainage) under local anesthesia - excision of the entire thrombosed hemorrhoid gives definitive relief and prevents recurrence
• If > 72 hours or symptoms improving: Conservative management (sitz baths, stool softeners, analgesics, topical agents)

Q18b (Page 18) - Anal Melanoma Features

1. Aggressive behavior (poor prognosis, early hematogenous spread)
2. S-100 protein positivity (melanocytic marker) + HMB-45 positive
3. Wide local excision is the surgical approach (abdominoperineal resection does not improve survival over WLE)

Q20 (Page 20) - Most Common Bacteria in SBP (Revisited)

Summary Table

Answer: B. Bowel Wall Perforation

Step-by-Step Analysis of All Clues

Features suggesting peritonitis/infection in a cirrhotic patient:

The Decisive Finding: Free Air Under the Diaphragm

"Chest and abdominal radiography should be performed when patients have abdominal pain to exclude free air, which signals a perforation (Fig. 137-2). Free air under the diaphragm on an upright chest film suggests the presence of a bowel perforation and associated peritonitis."

• Harrison's Principles of Internal Medicine, 22e, Chapter 137

Why NOT Spontaneous Bacterial Peritonitis (Option C)?

"The diagnosis of PBP is not easy. It depends on the exclusion of a primary intraabdominal source of infection... No specific radiographic studies are helpful in the diagnosis of PBP. A plain film of the abdomen would be expected to show ascites."

"In PBP, a single organism is typically isolated; anaerobes are found less frequently in PBP than in secondary peritonitis, in which a mixed flora including anaerobes is the rule. In fact, if PBP is suspected and multiple organisms including anaerobes are recovered from the peritoneal fluid, the diagnosis must be reconsidered and a source of secondary peritonitis sought."

The Runyon Criteria (distinguishing SBP from secondary peritonitis)

• Glucose = 69 mg/dL (blood glucose, not ascitic) and Lactate = 36 mg/dL (elevated, suggesting ischemia/perforation)
• LDH = 200 mU/mL (elevated) - consistent with perforation
• These values + free air = secondary peritonitis from perforation

Why Not the Other Options?

• A. Acute pancreatitis - Does NOT cause free air under the diaphragm; presents with epigastric pain, elevated amylase/lipase
• D. Gastric ulcer - A non-perforated gastric ulcer would NOT produce free air; only a PERFORATED gastric ulcer would (which falls under bowel/viscus perforation, option B)
• E. Non-ruptured duodenal ulcer - Explicitly non-ruptured = no free air; incompatible with this presentation

Final Answer: B. Bowel Wall Perforation

Runyon Criteria: Differentiating SBP from Secondary Peritonitis

Background: Why This Distinction Matters

• SBP → IV antibiotics alone (third-generation cephalosporin); NO surgery
• Secondary peritonitis → Surgery (source control) + antibiotics; delay = death

The Three Runyon Criteria (Ascitic Fluid Parameters)

"Secondary peritonitis is suggested by an ascitic glucose level <50 mg/dL, an ascitic LDH level higher than the serum LDH level, and the detection of multiple pathogens on ascitic fluid culture."

• Harrison's Principles of Internal Medicine, 22e (Ch. 53)

"Determining peritoneal fluid total protein, LDH, glucose, and alkaline phosphatase levels, as well as fluid Gram stain, assist in distinguishing SBP from other causes of peritonitis."

• Rosen's Emergency Medicine

Extended Runyon Criteria (Full Box 76.2 Parameters)

Microbiology: A Critical Additional Clue

"In PBP, a single organism is typically isolated; anaerobes are found less frequently in PBP than in secondary peritonitis, in which a mixed flora including anaerobes is the rule. In fact, if PBP is suspected and multiple organisms including anaerobes are recovered from the peritoneal fluid, the diagnosis must be reconsidered and a source of secondary peritonitis sought."

Why Each Cutoff Makes Pathophysiological Sense

Total Protein >1 g/dL

• In SBP, the cirrhotic liver produces low-protein ascites (typically <1 g/dL) because damaged sinusoids lose protein-retaining capacity
• Bowel perforation floods the peritoneum with protein-rich bowel contents, raising ascitic protein dramatically
• Also: ascitic protein <1.5 g/dL is itself a risk factor for developing SBP (low opsonic activity)

LDH > serum LDH

• LDH is released by necrotic/ischemic tissue and dying neutrophils
• In secondary peritonitis from a perforation, massive tissue destruction and bacterial load raise ascitic LDH above serum levels
• In SBP, bacterial burden is low (translocation, not perforation), so LDH remains proportionate to serum

Glucose <50 mg/dL

• Bacteria and leukocytes consume glucose rapidly
• In secondary peritonitis, the enormous bacterial load (polymicrobial bowel contents) outstrips glucose supply
• In SBP, the lower bacterial burden results in minimal glucose consumption, so levels stay near normal (>50 mg/dL)

Complete Diagnostic Framework for Ascitic Fluid

Step 1 — PMN Count
  PMN ≥250/mL → Bacterial peritonitis (SBP vs Secondary)
  PMN <250/mL → Bacterascites or non-infected ascites

Step 2 — Apply Runyon Criteria (if PMN ≥250)
  ≥2 of 3 met (protein >1, LDH > serum, glucose <50)?
    YES → SECONDARY PERITONITIS → SURGICAL source control
    NO  → SBP → IV antibiotics, NO surgery

Step 3 — Confirm with cultures
  Monomicrobial → SBP
  Polymicrobial with anaerobes → Secondary peritonitis

Step 4 — Imaging
  Free air on X-ray/CT → Secondary peritonitis (perforation confirmed)

Applied to the Previous Question

Summary Card

Runyon Criteria - 2 of 3 = Secondary Peritonitis:

1. Ascitic protein >1 g/dL
2. Ascitic LDH > upper limit of serum normal
3. Ascitic glucose <50 mg/dL

Plus: polymicrobial culture, gram stain positive for multiple organisms

Imaging: free air = perforation = surgery

"Start screening 10 years before the youngest case in the family or at age 40 — whichever is earlier."

Applying the Guideline to This Patient

Why the Other Options Are Wrong

• A. Colonoscopy starting at age 38 - Wrong. Screening should have started at age 28. Waiting until 38 means waiting 2 more years when he is already overdue.
• B. Sigmoidoscopy starting at age 40 - Wrong on two counts: wrong modality (colonoscopy, not sigmoidoscopy, is the gold standard for high-risk patients) and wrong age (40 is too late here).
• C. Tetanus booster every 5 years - Completely irrelevant; standard interval is every 10 years.
• E. Hepatitis B screening - Irrelevant to this clinical scenario.

Answer: D. Colonoscopy soon

Answer: D. A fluoroquinolone plus imipenem

Full Clinical Analysis

What is actually happening here?

Why Pseudomonas Coverage is Mandatory

1. Structural lung disease (bronchiectasis, COPD)
2. Corticosteroid therapy (>10 mg/day prednisone equivalent)
3. Broad-spectrum antibiotic use in prior 3 months
4. Hospital/ICU setting
5. Malnutrition/immunosuppression

• Maximize bactericidal activity
• Prevent emergence of resistance
• Provide synergistic killing

Why Option D (Fluoroquinolone + Imipenem) is Correct

Imipenem (carbapenem)

• Covers gram-positive, gram-negative including Pseudomonas, anaerobes
• Broadest spectrum beta-lactam available
• Antipseudomonal carbapenem - acts on cell wall (beta-lactam mechanism)

Fluoroquinolone (ciprofloxacin)

• Antipseudomonal fluoroquinolone - acts on DNA gyrase/topoisomerase IV
• Different mechanism of action from imipenem
• Dual antipseudomonal coverage from two different drug classes = synergy + resistance prevention

Why Each Other Option is Wrong

A. Fluoroquinolone + clindamycin

• Clindamycin covers anaerobes and gram-positives (MRSA, Streptococci)
• It has NO activity against Pseudomonas or gram-negative rods
• This combination leaves the most dangerous pathogen uncovered
• WRONG

B. Aminoglycoside + TMP-SMX

• TMP-SMX covers Pneumocystis jirovecii (PCP) and some gram-negatives
• While PCP is a steroid complication worth considering, the presentation here (multilobar infiltrates, acute respiratory failure, leukocytosis, fever after 1 week hospitalization) is more consistent with bacterial HAP than PCP (PCP typically has bilateral interstitial/ground-glass pattern, lower LDH threshold, subacute onset)
• This regimen does NOT provide reliable antipseudomonal coverage
• Aminoglycosides are nephrotoxic and used only as part of broader combination, not as monotherapy backbone
• WRONG (and also an unusual combination clinically)

C. Antipseudomonal penicillin alone

• e.g., piperacillin-tazobactam or ticarcillin
• This does cover Pseudomonas, but it is monotherapy
• In a severely immunocompromised, intubated patient with high Pseudomonas risk, monotherapy is inadequate - resistance can emerge rapidly
• Guidelines recommend dual coverage for this scenario
• WRONG - insufficient for severity of illness

E. Fluoroquinolone alone

• Monotherapy with a single agent
• While fluoroquinolones (ciprofloxacin) do cover Pseudomonas, single-agent therapy is insufficient for severe HAP/VAP in immunocompromised patients
• Risk of fluoroquinolone resistance in Pseudomonas is well-established; monotherapy can lead to breakthrough resistance within days
• WRONG - monotherapy inappropriate for this severity

Additional Consideration: Could This Be PCP?

Final Answer: D. Fluoroquinolone + Imipenem