Small Bowel Pathology Video

Small bowel pathology includes:

• Duodenal atresia
• Meckel diverticulum
• Volvulus
• Intussusception
• Small bowel infarction
• Lactose intolerance
• Celiac disease
• Tropical sprue
• Whipple disease
• Abetalipoproteinemia
• Neuroendocrine tumor
• Acute appendicitis

Duodenal Atresia

Duodenal atresia is due to a congenital failure of duodenum to canalize.

Imaging will classically show a double bubble sign in duodenal atresia.

Duodenal atresia is linked to Down syndrome.

Clinical features of duodenal atresia include:

• Polyhydramnios
• Stomach distension and a duodenal loop that is blind (the “double bubble” indication)
• Bilious vomiting

Meckel Diverticulum

Meckel diverticulum is when the gut wall’s three layers are all outpouched (true diverticulum).

Meckel diverticulum occurs because of the failure of the vitelline duct to involute.

Meckel diverticulum is associated with the rule of twos:

• 2% of the population
• 2% are symptomatic
• 2 years old or younger
• 2:1 male to female ratio
• 2 feet proximal to the ileocecal valve
• 2 inches long
• 2 types of mucosal lining

Volvulus

Volvulus is twisting of bowel along its mesentery.

Volvulus can lead to obstruction and disruption of the blood supply with infarction (mesenteric ischemia).

Common locations of volvulus are:

• Sigmoid colon (elderly)
• Cecum (young adults)

Intussusception

Intussusception is telescoping of the proximal portion of the bowel into the distal portion.

Peristalsis pulls the telescoped segment forward, which causes blockage and interruption of the blood supply with infarction.

In children, lymphoid hyperplasia is the most common cause of intussusception.

Intussusception typically occurs in the terminal ileum, resulting in intussusception into the cecum.

The most prevalent cause of intussusception in adults is a tumor.

Small Bowel Infarction

Small bowel damage from ischemia can be very serious.

Transmural infarction presents with thrombosis/embolism of the superior mesenteric artery or thrombosis of the mesenteric vein.

Mucosal infarction presents with marked hypotension.

Features of small bowel infarction include:

• Abdominal pain
• Bloody diarrhea
• Decreased bowel sounds

Lactose Intolerance

Reduction in the lactase enzyme’s activity, which is located at the brush boundary of enterocytes.

Lactase typically breaks down lactose into glucose and galactose.

By consuming milk products undigested lactose is osmotically active and causes stomach distension and diarrhea.

Lactose deficiency can be congenital (rare autosomal recessive disorder) or acquired (usually occurs in late childhood).

Temporary deficiency of lactose is visible after small bowel infection (lactase is highly susceptible to injury).

Celiac Disease

Celiac disease is an immune-mediated damage of small bowel villi because of gluten exposure.

Celiac disease is linked to HLA-DQ2 and HLA-DQ8.

Wheat and other cereals contain the protein gluten, whose pathogenic component is gliadin.

Tissue transglutaminase deamidates gliadin after it has been absorbed (TTG).

Antigen-presenting cells use MHC class I to present deaminated gliadin.

Tissue injury is mediated by helper T lymphocytes.

Clinical presentation of celiac disease includes:

• Bloating
• Diarrhea
• Undernutrition
• Small, herpes-like vesicles can be visible on skin called dermatitis herpetiformis 

Symptoms of celiac disease resolve with a gluten-free diet.

Laboratory findings of celiac disease include:

• IgA antibodies against endomysium
• Tissue transglutaminase (tTG)
• Gliadin

They are also present and are helpful for diagnosing people with IgA deficiency (higher incidence of IgA deficiency is visible in celiac disease).

Histology of celiac disease shows:

• IgA deposition at the tips of dermal papillae
• Villi are flattened, crypts are hyperplastic, and there are more intraepithelial lymphocytes, according to a duodenal biopsy

The jejunum and ileum are less affected than the duodenum, which has the most obvious damage.

Complications of celiac disease include:

• Small bowel carcinoma
• T-cell lymphoma

Tropical Sprue

Tropical sprue is damage to small bowel villi because of an unknown organism, leading to malabsorption.

Comparable to celiac disease, but can only be seen in tropical areas such as the Caribbean.

Tropical sprue occurs after infectious diarrhea and is treated with antibiotics.

The jejunum and ileum are most typically affected, and secondary vitamin B₁₂ or folate insufficiency may result.

The duodenum is less frequently affected by tropical sprue.

Whipple Disease

Whipple disease is a systemic tissue injury characterized by Tropheryma Whipplei (formerly called Tropheryma Whippelii) organisms.

Organisms that have partially been killed are found in macrophage lysosomes (positive for PAS).

The small bowel lamina propria is the classic site of involvement.

Macrophages compress lacteals.

Chylomicrons can’t be moved from enterocytes to lymphatics.

Whipple disease leads to fat malabsorption and steatorrhea.

Other usual sites of involvement of Whipple disease include:

• Synovium of joints causing arthritis
• Cardiac valves
• Central nervous system
• Lymph nodes

Abetalipoproteinemia

Apolipoproteins B-48 and B-100 deficiency are autosomal recessive conditions that can cause abetalipoproteinemia.

Clinical features of abetalipoproteinemia include:

• Malabsorption because of defective chylomicron formation (needs B-48)
• Absent plasma VLDL and LDL (need B-100)

Neuroendocrine Tumor

Neuroendocrine tumor is also known as carcinoid tumor.

Neuroendocrine tumors are malignant proliferations of neuroendocrine cells.

Neuroendocrine tumors are positive for CD56, synaptophysin, chromogranin.

Neuroendocrine tumors can occur anywhere in the gut, with the small bowel being the most typical place.

Neuroendocrine tumors typically begin as small nodules that resembles a submucosal polyp.

Neuroendocrine tumors frequently secrete serotonin.

Serotonin is released into the bloodstream through the portal vein and converted to 5-HIAA by the liver monoamine oxidase (MAO).

The urine contains excretion of 5-HIAA.

Serotonin can bypass liver metabolism when a carcinoid tumor spreads to the liver.

Carcinoid syndrome and carcinoid heart disease are caused by serotonin being released into the hepatic vein and leaking into the systemic circulation via hepato-systemic shunts.

Symptoms of carcinoid syndrome include:

• Bronchitis
• Diarrhea
• Skin flushing

These symptoms of carcinoid syndrome can be brought on by:

• Eating cured meats
• Alcohol consumption (i.e. red wine)
• Mental stress

Due to the presence of monoamine oxidase, which metabolizes serotonin in the lung, left-sided valvular lesions are not visible.

Carcinoid syndrome is characterized by right-sided valvular fibrosis (increased collagen) that causes tricuspid regurgitation and pulmonary valve stenosis.

Acute Appendicitis

Acute appendicitis is due to acute inflammation of the appendix.

Acute appendicitis is the most prevalent cause of acute abdomen.

Acute appendicitis is commonly associated with a fecalith or lymphoid hyperplasia that is obstructing the appendix.

Clinical features of acute appendicitis include:

• Periumbilical pain
• Fever
• Nausea
• Pain subsequently localizes to the right lower quadrant (McBurney point)
• Guarding and rebound tenderness are symptoms of peritonitis, which occurs as a result of rupture

Complications of acute appendicitis like periappendiceal abscess are frequent.