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Celiac Disease (Gluten-Sensitive Enteropathy) 1. Background Definition: An autoimmune-mediated intestinal disorder triggered by dietary gluten (wheat, barley, rye) in genetically susceptible individuals. Pathophysiology: Ingestion of gluten → immune response against tissue transglutaminase (tTG) → villous atrophy and crypt hyperplasia in the small intestine → malabsorption. Genetics: Strongly associated with HLA-DQ2 and HLA-DQ8 alleles. Epidemiology: Affects ~1% of the population; higher prevalence in Northern European ancestry and patients with autoimmune diseases (type 1 diabetes, autoimmune thyroiditis). Complications: Malnutrition, iron-deficiency anemia, osteoporosis, infertility, dermatitis herpetiformis, and increased risk of intestinal T-cell lymphoma. 2. History Symptoms (classic form): Chronic diarrhea, steatorrhea, weight loss, abdominal bloating, and fatigue. Atypical/non-GI manifestations: Iron-deficiency anemia, osteoporosis, neuropathy, short stature, delayed puberty, infertility. Dermatologic: Dermatitis herpetiformis — pruritic papulovesicular rash on extensor surfaces. Onset: May appear in childhood or adulthood; often improves when gluten is avoided. Risk factors: Family history, autoimmune diseases, selective IgA deficiency. 3. Exam Findings May be normal in mild cases. Signs of malabsorption: pallor (anemia), glossitis, muscle wasting, or peripheral edema (hypoproteinemia). Rash consistent with dermatitis herpetiformis (elbows, knees, buttocks). 4. Making the Diagnosis Initial test: Serologic testing — tissue transglutaminase IgA (tTG-IgA) and total IgA (to rule out IgA deficiency). Confirmatory test (gold standard): Small bowel biopsy via upper endoscopy showing villous atrophy, crypt hyperplasia, and intraepithelial lymphocytosis. If IgA deficient: Use IgG-based tests (deamidated gliadin peptide IgG or tTG-IgG). HLA typing (DQ2/DQ8): Negative result effectively rules out celiac disease (useful if diagnosis uncertain). Note: Patients must be consuming gluten before testing to avoid false negatives. 5. Management A. Dietary Strict lifelong gluten-free diet (avoid wheat, barley, rye). Nutritional counseling and monitoring for deficiencies (iron, folate, B12, vitamin D, calcium). B. Medical Dermatitis herpetiformis: Dapsone for symptomatic relief, plus gluten-free diet. Treat associated deficiencies (iron, folate, vitamin D, calcium). C. Monitoring Follow-up tTG-IgA titers to assess dietary adherence. Bone density screening (osteoporosis risk). Rare refractory cases may require corticosteroids or immunosuppressants.   Question A 29-year-old woman with chronic diarrhea, bloating, and weight loss undergoes upper endoscopy after positive celiac serology. Duodenal biopsies are obtained. Which of the following histologic findings is most characteristic of this patient’s disease?

Vitamin B12 (Cobalamin) Deficiency 1. Background Definition: Deficiency of vitamin B12, leading to impaired DNA synthesis and abnormal myelin formation, resulting in megaloblastic anemia and neurologic dysfunction. Physiology: B12 obtained from animal products. Absorbed in the terminal ileum after binding to intrinsic factor (from gastric parietal cells). Stored in the liver; body reserves last 3–5 years. Functions: Cofactor for DNA synthesis (thymidylate synthase). Necessary for conversion of homocysteine → methionine and methylmalonyl-CoA → succinyl-CoA. 2. Etiology Mechanism Examples Inadequate intake Strict vegan diet (rare) Malabsorption (most common) Pernicious anemia (autoimmune loss of intrinsic factor), gastric bypass, atrophic gastritis Ileal disease/resection Crohn disease, ileal resection Competition Fish tapeworm (Diphyllobothrium latum) Medication effects Metformin, proton pump inhibitors, H2 blockers (decrease absorption) 3. History Onset: Insidious; symptoms develop over months to years. Constitutional: Fatigue, weakness, pallor. GI: Glossitis (smooth, sore tongue), anorexia, mild diarrhea. Neurologic: Peripheral neuropathy: Paresthesias, numbness, ataxia. Posterior column involvement: Impaired vibration and position sense, positive Romberg. Lateral corticospinal tract involvement: Spasticity, weakness. Cognitive or psychiatric changes in severe deficiency (“megaloblastic madness”). 4. Exam Findings General: Pallor, mild jaundice (from ineffective erythropoiesis). Neuro: Decreased vibration/position sense, gait ataxia, weakness, hyperreflexia. Tongue: Smooth, beefy red (atrophic glossitis). If pernicious anemia: May have other autoimmune findings (vitiligo, thyroid disease). 5. Making the Diagnosis A. Laboratory Findings Test Findings CBC Macrocytic anemia (MCV >100 fL) Peripheral smear Hypersegmented neutrophils Reticulocyte count Low Serum B12 Decreased (

Small Bowel Obstruction (SBO) 1. Background Definition: Partial or complete blockage of the small intestine that prevents normal passage of intestinal contents. Pathophysiology: Mechanical obstruction (most common): physical blockage of the lumen. Functional obstruction (ileus): failure of peristalsis without physical blockage. Leads to proximal dilation, fluid sequestration, electrolyte imbalance, and risk of bowel ischemia if untreated. Common causes: Adhesions from prior abdominal surgery (most common). Hernias (second most common, esp. worldwide). Neoplasms, Crohn disease, intussusception, volvulus, or foreign bodies. Complications: Bowel ischemia, perforation, sepsis, hypovolemia. 2. History Symptoms: Colicky abdominal pain, nausea/vomiting, abdominal distension, obstipation (no flatus or stool). Pain often intermittent and crampy; vomiting more prominent with proximal obstruction. History clues: Prior abdominal surgery → adhesions. Hernia bulge → incarceration or strangulation. Weight loss, anemia → malignancy. Red flags: Persistent pain, fever, or peritoneal signs suggesting ischemia or strangulation. 3. Exam Findings Inspection: Distension, visible peristalsis (late). Auscultation: Early: High-pitched “tinkling” bowel sounds. Late: Absent sounds (suggests ischemia or necrosis). Palpation: Tenderness, possible hernia, rebound/guarding if peritonitis. Rectal exam: May show empty rectum or occult blood. 4. Making the Diagnosis Gold standard imaging: CT abdomen and pelvis with IV contrast — identifies level of obstruction, cause, and complications (ischemia, perforation). Initial test: Abdominal X-ray (upright and supine) — shows dilated loops of small bowel, air-fluid levels, and absence of colonic gas. Laboratory findings: Hemoconcentration or elevated hematocrit (dehydration). Leukocytosis (infection or ischemia). Electrolyte abnormalities (hypochloremic, hypokalemic metabolic alkalosis). Strangulation signs: Fever, tachycardia, leukocytosis, continuous pain, metabolic acidosis. 5. Management A. Initial Stabilization NPO (bowel rest). IV fluids and electrolyte correction. Nasogastric tube decompression for vomiting or distension. Monitor for signs of ischemia or perforation. B. Definitive Management Partial/simple SBO: Conservative management (IV fluids, NG decompression, serial exams). Complete or complicated SBO (strangulation, perforation, peritonitis): Emergency surgical intervention. Adhesive disease: Laparoscopic adhesiolysis if nonoperative measures fail. Hernia-related: Urgent repair after decompression. C. Prevention / Follow-up Early ambulation post-surgery to reduce adhesion formation. Treat underlying causes (hernia repair, tumor resection, Crohn management).  

Mesenteric Ischemia 1. Background Definition: Intestinal hypoperfusion leading to ischemia and necrosis of the bowel wall; can be acute or chronic. Pathophysiology: Acute mesenteric ischemia (AMI): Sudden loss of blood flow to small intestine. Causes: Arterial embolism (most common; often from atrial fibrillation or MI). Arterial thrombosis (atherosclerotic plaque). Venous thrombosis (hypercoagulable states). Nonocclusive ischemia (low flow states—shock, vasopressors). Chronic mesenteric ischemia (CMI): Atherosclerotic narrowing of mesenteric arteries leading to postprandial pain (“intestinal angina”) and weight loss. Epidemiology: AMI is uncommon but carries high mortality (~60%). CMI seen in older adults with diffuse atherosclerosis. 2. History Acute: Severe, sudden-onset abdominal pain that is disproportionate to physical findings. Nausea, vomiting, diarrhea, or occult GI bleeding. May have atrial fibrillation, recent MI, or heart failure. Chronic: Recurrent, dull epigastric pain occurring 30–60 minutes after meals. Fear of eating → weight loss. Risk factors: Embolic disease (A-fib, valvular disease). Atherosclerosis (coronary, carotid, peripheral). Hypotension, dehydration, hypercoagulable disorders. 3. Exam Findings Acute: Abdomen may be soft or mildly tender early, with pain out of proportion to findings. Later: peritonitis (guarding, rebound) if infarction occurs. Possible tachycardia, hypotension, or signs of shock. Chronic: Bruit over epigastrium or abdomen. Weight loss, signs of malnutrition. 4. Making the Diagnosis Gold standard: CT angiography (CTA) — best initial and confirmatory test; shows arterial occlusion, bowel wall thickening, or pneumatosis intestinalis. Laboratory clues: Elevated lactate (due to anaerobic metabolism). Leukocytosis, metabolic acidosis. Other modalities: Mesenteric angiography (definitive but invasive). Duplex ultrasound for chronic disease (shows stenosis). Plain X-ray: May show thumbprinting or pneumatosis intestinalis (late finding). 5. Management A. Acute Mesenteric Ischemia Immediate resuscitation: IV fluids, broad-spectrum antibiotics, bowel rest, and correction of arrhythmia or hypotension. Definitive treatment: Embolic: Emergent surgical embolectomy or endovascular thrombolysis/stenting. Thrombotic: Surgical revascularization or bypass. Nonocclusive: Treat underlying shock; reduce vasopressors. Necrotic bowel: Resection required. B. Chronic Mesenteric Ischemia Definitive: Endovascular angioplasty/stenting or surgical bypass of affected vessels. Supportive: Risk factor modification (stop smoking, control lipids, manage atherosclerosis). Question A 72-year-old man with a history of atrial fibrillation presents with sudden, severe abdominal pain that began 2 hours ago. He describes the pain as diffuse and constant. On examination, he appears uncomfortable and mildly diaphoretic. His abdomen is soft with minimal tenderness and no rebound or guarding. Laboratory results show: WBC count: 17,000/µL Lactate: 5.2 mmol/L (normal

Which of the following is an advantage of L1 regularization?

Match the letter of the correct answer with the cavity.

Which term means weakness affecting one side of the body?

Which term means the surgical repair of a nerve?

Which term refers to a condition in which there is diminished skeletal muscle tone?

Which term means the study of the functions of the body structure?