small bowel diseases Flashcards

1
Q

When does diarrhea occur?

A

• When small bowel output exceeds colonic absorptive capacity

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2
Q

What tests do you use with watery diarrhea to get a differential diagnosis?

A
• Osmotitic vs. secratory
	• Get the stool osmotic gap
	• Stool osm gap = 290- 2(stool Na + stool K)
		○ If gap> 50mOsm THIS IS OSMOTIC
			§ Lactose intolerance
			§ Sorbitol
			§ Fructose
			§ Magnesium containing laxatives
		○ If gap < 50mOsm THIS IS SECRETORY
			§ Bacterial toxins
			§ Neuroendocrine tumors (gastrinoma, VIPoma, Carcinoid
			§ Bile salt (like terminal ileal resection)
			§ Stimulant laxatives
			§ Motility disorders (diabetes, IBS)
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3
Q

What are the 4 different overall types of diarrhea?

A
  • Watery
    • Steatorrhea
    • Inflammatory/exudative (often bloody)
    • Functional (IBS)
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4
Q

What is steatorrhea?

A
• Fecal fat positive diarrhea
	• Can be malabsorption OR maldigestion
	• Malabsorption
		○ Celiac
		○ Whipple's disease
			§ Whipple diseaseis a systemicdiseasemost likely caused by a gram-positive bacterium, Tropheryma whippelii.[1,2]Although the first descriptions of the disorder described a malabsorption syndrome with small intestine involvement, thediseasealso affects the joints, central nervous system, and cardiovascular system
		○ Small bowel bacterial overgrowth
		○ Short gut from surgery
	• Maldigestion
	• Pancreatic insufficiency
	• Biliary obstruction
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5
Q

What might cause inflammatory or exudative diarrhea?

A
• Chrohn's disease
	• Ischemia
	• Invasive infections (colon)
		○ C difficile
		○ EHEC
		○ Amebiasis
		○ Shigella
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6
Q

When do you classify a watery diarrhea as functional?

A
  • When there is nothing else going on
    • This is a diagnosis of exclusion
    • Usually watery diarrhea here
    • Think IBS
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7
Q

Steatorrhea is a manifestation of what?

A

• Dysfunctional lipid absorption in some capacity
• Decreased pancreatic and biliary secretions
• Abnormal enterocyte processing
• Lymphatic obstruction
What does Pancreatic Insufficiency have to do with diarrhea?
• Lack of ability to absorb fats and proteins can cause an oily foul-smelling diarrhea called steatorrhea
• steatorrhea occurs because of the decreased activity of lipase and colipase, leading to lipid maldigestions

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8
Q

Describe Small intestinal Bacterial Overgrowth

A

• There is always normal flora in the proximal small intestine
○ Lactobacilli
○ Enterococci
○ Gram positive aerobes
○ Facultative anaerobes
• Overgrowth occurs in conditions of hypomotility
○ Scleroderma, diabetes
• Partial intestinal obstruction, bowel diverticula and decreased gastric acid secretion also contribute to bacterial overgrowth states.
• Too much bacteria in the lumen means food doesn’t get onto the enterocyte surface
○ Also inactivate bile acids, catabolize disaccharidases in microvilli and reduce effectiveness of enterokinases
• Overgrowth inhibits bowel motility as well

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9
Q

How Liver Disease lead to steatorrhea?

A

• Fewer hepatocytes and decreased function of the stragglers
• Leads to decreased bile formation
• Bile is necessary for lipid absorption through the forming of micelles.
• No lipid absorption, fatty stools
How might Gastric Disorders cause steatorrhea?
• The bile salts that emulsify the fatty foods get mixed into the chyme in the stomach
• If there is stomach damage or a motility issue that mixing gets less and less efficient, leading eventually to malabsorption of fats

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10
Q

What are the clinical manifestations of small bowel bacterial overgrowth?

A

• Diarrhea, steatorrhea, abdominal pain, flatulence, bloating and weight loss
• Eventually certain vitamin deficiencies are seen
○ A, D, E and B12
• B12 is because anaerobic bacteria utilize and deplete B12 from the lumen before the enterocytes absorb it
• Serum folate levels are normal or HIGH due to bacterial production of folate
○ One example of an inappropriate normal
○ This is also helpful for ruling out tropical sprue in which B12 and folate deficiency are co-occuring

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11
Q

What are the five categories of disease that can adversely affect and even destroy the absorptive surface area of the small intestine?

A
• Intestinal inflammation and villus flattening
	• Ulceration
	• Ischemia
	• Infiltration
	• Other
		○ Bypass
		○ Extensive small intestine resection
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12
Q

How does celiac sprue ablate the absorptive surface of the small intestine?

A

• Also known as celiac disease or gluten-sensitive enteropathy
• Inflammatory disease of small intestine, occurring because of an immune response to peptides of gluten
○ Wheat, rye, barley and oats
• Characterized by loss of villi due to the presence of increased intraepithelial lymphocytes
• Also characterized by crypt hyperplasia leading to malabsorption
• It’s the infilration of lymphocytes and the crypt hyperplasia that poof up the villi so much they get flattened out, look like mesas and lose a good portion of their absorptive capacity

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13
Q

How does celiac sprue present clinically?

A

• Symptoms of malabsorption-steatorrhea
○ Diarrhea, weight loss, bloating and abdominal pain
○ Degree of malabsorption may predict the severity of mucosal involvement
○ Carbohydrate, fat, and protein malabsorption occur because of villus destruction
*ADEK are the fat-soluble vitamin deficiencies
○ Celiac disease affects the proximal small intestine so malabsorption of iron and folate are included

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14
Q

What tests must you order to make the celiac sprue dx?

A
• Intestinal biopsy
		○ See villous flattening, intraepithelial lymphocytes and crypt hyperplasia
	• Serologic tests 
		○ anti-endomysial antibodies (IgA)
			§ 90% sensitive, 99% specific
		○ Anti-tissue transglutaminases (tTg)
			§ 90% sensitive, 99% specific
		○ Anti-gliadin IgA and IgG antibodies
			§ Sensitive, not specific
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15
Q

How do patients manage celiac sprue?

A
  • Lifelong gluten free diet
    • Adherence can reverse the villous flattening in weaks
    • Also reduces autoantibody titers
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16
Q

What is tropical sprue?

A

• Unknown etiology, but suspected to involve bacterial toxins or colonization of a particular bacteria that leads to symptoms very much like celiac sprue
• This is not a gluten-sensitive disease and doesn’t make the antibodies to the gluten items like celiac sprue
• However, the villous flattening is very similar, just patchy
• Symptoms can arrive YEARS after travel to the tropics
○ SE asia, caribbean and india
• Classic presentation is magaloblastic anemia due to vitamin B12 and folate deficiency accompanied by diarrhea
• Treat with a really long antibiotic course. Huh. And B12 and folate replacement

17
Q

What is the classic presentation of tropical sprue?

A
  • Classic presentation is magaloblastic anemia due to vitamin B12 and folate deficiency accompanied by diarrhea (in a person who has traveled to SE asia, caribbean or to india
    • Treat with a really long antibiotic course. Huh. And B12 and folate replacement
18
Q

A patient presents with GI symptoms but also fever, joint pain, and even some neurological symptoms. Worried, you check heart and lungs and see some abnormalities there. What disease might affect all these organ systems?

A

• Whipple’s disease (tropheryma whippelii)
• GI, fever, joint pain
• Neurologic symptoms
• Thirty percent have cardiac and pulmonary involvement
• Small intestine biopsy - villous blunting along with infiltration of lamina propria
○ Large PAS-positive staining macrophages filled with organism
• Treat with prolongued course of antibiotics

19
Q

What do we need to know about small bowel malignancy?

A

• It’s extremely rare to have a primary tumor of the small intestine
○ Less than 2% of all GI tumors
• Of these, adenocarcinoma, then carcinoid, sarcoma and lymphoma are the tumor types in order of percentage

20
Q

How is the colon divided from proximal to distal?

A
  • Ileocecal valve
    • Cecum
    • Ascending colon
    • Hepatic flexure
    • Transverse colon
    • Splenic flexure
    • Descending colon
    • Sigmoid colon
    • Rectum
    • anus
21
Q

Duodenal atresia (pathology important)

A
  • congenital failure of duodenum to canalize, associated with down syndrome
  • clinical features = polyhydramnios, distention of stomach and blind loop of duodenum (double buble sign on radiology), bilious vomiting
22
Q

Meckel diverticulum (pathology important)

A
  • outpouching of all three layers of bowel wall, thus a true diverticulum
  • arises due to failure of the vitelline duct to involute
  • Remember the rule of 2’s (seen in 2% of population, 2 inches long and located in small bowel within 2 feet of ileocecal valve, CAN (but usually doesnt’) present during first 2 years of life with bleeding, volvulus, intussusception, obstruction)
23
Q

Volvulus (pathology important)

A

twisting of bowel alon it’s mesentery

  • results in obstruction and disruption of the blood supply with INFARCTION
  • most common locations are sigmoid colon in old people and cecum in young adults
  • ischemic bowel picture, and risks for perforation increase with the worse the ischemia gets.
24
Q

Intussusception (pathology important)

A

Telescoping of proximal segment of bowel forward into distal segment

  • pulled forward by peristalsis, resulting in obstruction and disruption of blood supply with infarction (think of it as a herniation, but within the bowel itself)
  • starts giving you an ischemic bowel picture with added bonus of inflammatory destruction of the bowel itself.