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MSC - F. Surgery Answers 2025

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Trauma or pressure (prolonged sitting)

Pathogenesis:

1.Primary epithelial pit forms in the midline.

2.Hair enters the pit, acting as a foreign body.

3.Leads to granulomatous inflammation or secondary infection.

4.May progress to:

o Acute abscess (fluctuant, tender swelling) o Chronic discharging sinus/fistula

o Secondary fistulous tracts, often lateral to midline

Clinical Features:

Midline dimpling or sinus openings

Intermittent purulent discharge

Pain and swelling, especially during acute flare-ups

Fever, malaise in abscess stage

Secondary tracts/fistulas laterally or in buttocks

Chronic form: thick-walled sinus with granulation tissue

Diagnosis:

Clinical diagnosis is often sufficient.

Primary pits in midline pathognomonic.

Digital rectal exam: to rule out rectal fistula (especially posterior crypt involvement).

Imaging (when needed):

o Fistulography: in recurrent or complex disease

o MRI/CT: to rule out presacral lesions or deep extension

Differential Diagnosis:

1.Rectal fistula (has internal opening in crypts)

2.Pararectal teratoid cyst

3.Posterior meningocele

4.Presacral teratoma

5.Sacrococcygeal osteomyelitis

Treatment:

Only surgical. Conservative measures are not curative. 1. Uncomplicated pilonidal sinus:

Elective surgery

o Excision of epithelial tract and all primary pits

o Midline or off-midline closure, or healing by secondary intention

oBascom technique or cleft lift for reduced recurrence

2.Acute inflammation (abscess):

Stage-dependent approach:

oLocalized infiltrate: Early radical excision if inflammation limited

o Abscess >3 cm: Drainage first, followed by interval excision

oAvoid blind closure – wound left open or marsupialized

3.Chronic/recurrent sinus with secondary tracts:

Planned radical excision of entire tract and fistulae

Fistulectomy and wide excision with secondary intention healing

4.Inflammatory remission:

Definitive surgery after ensuring no active infection

Remove tract, scar tissue, and epithelial remnants

Inflammatory bowel diseases

1. Ulcerative colitis: definition, pathogenesis, classification, clinical picture, diagnosis.

1. Ulcerative Colitis (UC)

Definition

Ulcerative colitis is a chronic, idiopathic inflammatory bowel disease (IBD) characterized by continuous, diffuse inflammation limited to the mucosa and submucosa of the colon and rectum. It typically begins in the rectum and extends proximally in a contiguous fashion.

2. Etiology and Pathogenesis

Etiology

Multifactorial and not fully understood. Includes:

Genetic predisposition (family clustering, HLA associations)

Immune dysregulation (autoantibodies, T-cell imbalance)

Environmental factors (Western diet, pollution)

Dysbiosis of gut flora

Psychological stress

NSAID or antibiotic use

Pathogenesis

Breakdown of epithelial barrier → increased permeability

Autoimmune activation → cytokine release (TNF-α, IL-1β)

Neutrophilic infiltration of mucosa → crypt abscesses and ulceration

Oxidative stress and hypoxia worsen inflammation

Chronicity leads to pseudopolyps, fibrosis, and risk of dysplasia/malignancy

3.Pathomorphology

Rectum always involved, proximal spread is continuous

Mucosa/submucosa only; full-thickness involvement suggests Crohn’s

Multiple ulcers, surrounded by edematous mucosa

Pseudopolyps due to regenerative changes

Goblet cell depletion, crypt distortion, crypt abscesses on biopsy

4.Classification

By Location:

Ulcerative proctitis – limited to rectum

Proctosigmoiditis

Left-sided colitis

Extensive or total colitis (pancolitis) By Clinical Course:

Acute

Chronic

Recurrent

By Severity:

Mild: <4 stools/day, minimal bleeding

Moderate: 4–6 stools/day, moderate bleeding

Severe: >6 bloody stools/day, systemic toxicity

Fulminant: >10 stools/day, rapid progression, risk of toxic megacolon

5.Clinical Features

Chronic bloody diarrhea with mucus

Tenesmus, urgency

Abdominal cramping (esp. left lower quadrant)

Fatigue, weight loss, fever

Extraintestinal manifestations:

o Joints: arthritis (pauciarticular)

o Skin: erythema nodosum, pyoderma gangrenosum o Eyes: uveitis, episcleritis

oHepatobiliary: primary sclerosing cholangitis

6.Diagnosis

Lab Tests:

CBC: anemia, leukocytosis

ESR/CRP: elevated

Electrolyte imbalance

pANCA: positive in ~60–70% of UC patients

Stool Studies:

Rule out infectious colitis (C. difficile, ova/parasites, culture)

Endoscopy (Gold Standard):

Colonoscopy: continuous erythema, friable mucosa, ulcers, pseudopolyps

Biopsy: goblet cell loss, crypt abscesses, basal plasmacytosis

Imaging:

Abdominal X-ray: look for toxic megacolon

Barium enema (rare): "lead-pipe colon" – loss of haustra

Ultrasound/CT: wall thickening, especially in complications

2. Conservative and surgical treatment of ulcerative colitis. Indications for biological therapy in inflammatory bowel diseases.

7.Differential Diagnosis

Crohn’s disease

Infectious colitis (bacillary/amebic dysentery)

Ischemic colitis

Colorectal cancer

Non-ulcerative colitis (IBS, microscopic colitis)

Tuberculosis

8.Treatment

A. Medical (Conservative) Treatment

1.First-Line Agents

5-ASA (aminosalicylates): mesalazine, sulfasalazine (esp. for mildmoderate cases)

Corticosteroids: Prednisolone 40–60 mg/day for moderate-severe flares o IV hydrocortisone for fulminant disease

Tapering after remission to avoid adrenal suppression

2.Immunomodulators (for steroid-dependence/resistance)

Azathioprine, 6-mercaptopurine

Methotrexate (less commonly used in UC than Crohn’s)

3.Biologic Therapy (Indications below)

4.Supportive Therapy

IV fluids, electrolytes

Blood products if bleeding/anemia

Metronidazole for superimposed infection

Nutritional support (low-fiber diet in flare)

Vitamin and iron supplementation

Antidiarrheals (cautiously)

9.Indications for Biological Therapy in IBD

(usually for moderate-to-severe or refractory disease)

Failure or intolerance to 5-ASA, steroids, or immunosuppressants

Steroid-dependent or steroid-refractory disease

Extraintestinal manifestations unresponsive to conventional therapy

High-risk of surgery

Induction and maintenance of remission

Examples:

Anti-TNF agents: infliximab, adalimumab, golimumab

Anti-integrin: vedolizumab

Anti-IL-12/23: ustekinumab

JAK inhibitors (e.g., tofacitinib) – oral small molecules

10.Surgical Treatment

Indications

Absolute:

Perforation

Toxic megacolon unresponsive to therapy

Massive/continuous hemorrhage

Dysplasia or adenocarcinoma

Relative:

Chronic, steroid-dependent or refractory disease

Severe/recurrent complications

Growth retardation in pediatric cases

Surgical Options

Subtotal colectomy with ileostomy (emergency)

Proctocolectomy with ileal pouch-anal anastomosis (IPAA) (elective)

Total proctocolectomy with end ileostomy

3.Complications of inflammatory bowel diseases.

Local:

Toxic megacolon

Perforation

Massive GI hemorrhage

Colonic strictures

Colorectal cancer

Systemic/Extraintestinal:

Arthritis

Uveitis

Skin lesions (e.g., erythema nodosum)

Hepatobiliary (e.g., PSC)

Venous thromboembolism

Osteoporosis

Concomitant:

Malnutrition

Infections due to immunosuppressive therapy

4.Crohn's disease: definition, pathogenesis, classification, clinic, diagnosis.

Crohn’s disease (Granulomatous colitis) is a chronic, idiopathic inflammatory bowel disease (IBD) that involves transmural inflammation of the GI tract, most commonly affecting the terminal ileum and proximal colon. It is segmental (skip lesions) and may result in fistulas, strictures, and granuloma formation.

Etiology and Pathogenesis

Unclear cause, likely multifactorial:

o Genetic predisposition (e.g., NOD2/CARD15 mutations)

o Environmental triggers (e.g., smoking, diet)

o Dysbiosis: Altered gut microbiota

oImmune dysregulation: Overactive immune response (Th1/Th17mediated), with autoantibody formation against gut antigens

oInfectious hypothesis (e.g., mycobacteria, chlamydia) has been proposed but not proven

Pathomorphology

Transmural inflammation

Non-caseating granulomas (in ~50% of biopsies)

Segmental, asymmetrical involvement — “skip lesions

Cobblestone mucosa due to linear ulcers and edema

Fissures, fistulas, and fibrotic strictures can develop

Classification

1. By location:

o Ileitis

o Ileocolitis (most common)

o Colitis

o Perianal disease

oGastroduodenal involvement (rare)

2.By behavior:

oInflammatory

o Stricturing

oPenetrating (fistulizing)

3.By disease course:

oAcute or chronic

o Remitting or progressive

Clinical Features

Chronic relapsing abdominal pain, especially right lower quadrant

Diarrhea, often non-bloody

Low-grade fever, malaise

Weight loss

Extraintestinal symptoms:

o Arthritis, uveitis, erythema nodosum, pyoderma gangrenosum

oHepatobiliary involvement (e.g., primary sclerosing cholangitis)

Perianal disease:

oAnal fissures (painless), skin tags, fistulas, abscesses

Complications