GI: Small and large intestine Flashcards

1
Q

How do you initially manage someone with chronic diarrhea, >50 yo and <50 yo?

A

Patients older than 50 years should undergo colonoscopy to screen for colorectal cancer. Patients younger than 50 years should also have colonoscopy if features of inflammatory bowel disease are present. Any patient undergoing colonoscopy to evaluate diarrhea should have inspection of the terminal ileum (to assess for Crohn disease) and random biopsies of the colonic mucosa (to assess for microscopic colitis). Sigmoidoscopy is not recommended in most patients because it does not evaluate the proximal colon or terminal ileum.

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2
Q

In evaluation of diarrhea, if colonoscopy is negative what test do you go for next?

A

A 48- to 72-hour stool collection with analysis of fat content measures the amount of diarrhea and steatorrhea.

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3
Q

What fat excretion is diagnostic of steatorrhea? What diagnoses could this be?

A

Normal fat excretion is less than 7 g/d (in patients consuming 100 g/d of fat); however, this may be increased nonspecifically by any diarrheal disorder to 12 to 14 g/d. Fat excretion above 14 g/d is diagnostic of steatorrhea. Patients with steatorrhea should undergo evaluation for small-bowel mucosal disorders (celiac disease, Whipple disease), small intestinal bacterial overgrowth (SIBO), and pancreatic insufficiency.

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4
Q

What if a fat test of diarrhea demonstrates that it has no steatorrhea? Then what?

A

In patients with true diarrhea but without steatorrhea, measurement of stool electrolytes can be helpful to categorize the diarrhea so that more targeted testing can later be performed. Measurement of fecal sodium and potassium allows calculation of the osmotic gap, as follows:

290 – (2 × [stool sodium + stool potassium])

> 100 mOsm/kg (100 mmol/kg): Osmotic diarrhea
<50 mOsm/kg (50 mmol/kg), the diarrhea is secretory rather than osmotic.

50 and 100 mOsm/kg (50 and 100 mmol/kg) is equivocal

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5
Q

What is the stool osmotic gap? How is it used?

A

It helps separate out secretory diarrhea from osmotic diarrhea.

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6
Q

What is the differential for malabsorption/steatorrhea?

A

1) Celiac Disease
2) Small Intestinal Bacterial Overgrowth
3) Short Bowel Syndrome
4) Carbohydrate malabsorption

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7
Q

What is celiac disease?

A

Celiac disease is a chronic inflammatory enteropathy caused by an immune-mediated reaction to gluten and gliadins, proteins that are present in wheat and other grains.

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8
Q

How do you diagnose celiac disease? What are the serological makers?

A

The diagnosis of celiac disease requires positive serologic markers and a compatible small-bowel biopsy.

IgA tissue transglutaminase (tTG) antibodies and endomysial antibodies (EMA) are sensitive and specific serologic markers; testing for these should be done while the patient is consuming gluten.

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9
Q

What are the histological findings of celiac disease?

A

The classic findings on small-bowel histology are intraepithelial lymphocytosis, crypt elongation, and villous blunting

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10
Q

What is a lab abnormality that gives a clue to SIBO?

A

A clue to the diagnosis of SIBO is the combination of vitamin B12 deficiency (due to bacterial consumption) and an elevated serum folate level (due to bacterial production).

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11
Q

What are common causes of SIBO?

A

Diabetes, gastric bypass surgery

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12
Q

What is short bowel syndrome?

A

Short-bowel syndrome (SBS) arises when a large portion of the small intestine is resected or diseased. Causes of SBS are massive resection or bowel dysfunction related to ischemia, radiation enteropathy, Crohn disease, or trauma.

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13
Q

How much healthy intestine that remains causes short bowel?

A

Short-bowel syndrome arises when a large portion of the small intestine is resected or diseased; it typically does not occur until less than 200 cm of healthy small intestine remains.

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14
Q

How does ulcerative colitis present?

A

UC typically presents with bloody diarrhea and abdominal discomfort, the severity of which is related to the extent and severity of inflammation. Because UC typically involves the rectum, tenesmus, urgency, rectal pain, and fecal incontinence are common. Fever and weight loss are uncommon and suggest severe disease.

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15
Q

What is the distribution of ulcerative colitis?

A

The distribution of UC is generally divided into proctitis (involving the rectum only), left-sided colitis (inflammation does not extend beyond the splenic flexure), and pancolitis (inflammation extends above the splenic flexure).

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16
Q

How does Crohn’s disease present?

A

Common symptoms of CD are abdominal pain, diarrhea, and weight loss; fever and overt gastrointestinal bleeding are less common than is typically seen in UC.

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17
Q

What does the mucosa look like in Crohn’s disease? What is it’s distribution?

A

Additionally, unlike UC, the transmural inflammation seen in CD may predispose to fistula formation. Given the variable distribution of inflammation in CD, the symptoms can vary considerably between patients. Thirty percent of patients have isolated small-bowel disease, 40% have ileocolonic inflammation, and 25% have isolated colonic disease. The other 5% of patients have isolated upper gastrointestinal or perianal manifestations. Symptoms correlate with disease location.

*Ulcerative colitis extends throughout, Crohn’s can be certain discreet locations

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18
Q

What lab abnormalities suggest severe UC or Crohn’s?

A

y. Leukocytosis, anemia, hypoalbuminemia, and vitamin deficiencies indicate more severe disease. The erythrocyte sedimentation rate and C-reactive protein levels are often elevated; if so, these levels can be monitored as signs of response to therapy and subsequent disease flare.

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19
Q

What are the extra intestinal manifestations of UC and Crohn’s

A

Extraintestinal manifestations (EIMs) are found in approximately 10% of patients with IBD. The most common EIMs are oral aphthous ulcers, arthralgia, and back pain (indicating ankylosing spondylitis or sacroiliitis). Eye symptoms (redness, pain, swelling) may be due to uveitis, scleritis, or other causes of ocular inflammation and warrant immediate examination by an ophthalmologist. Skin manifestations are common and include pyoderma gangrenosum and erythema nodosum . Liver involvement can also be seen, most commonly in the form of primary sclerosing cholangitis.

20
Q

How do you diagnose UC and Crohn’s disease?

A

Because the symptoms of inflammatory bowel disease are nonspecific, visualization of the gastrointestinal tract, often by colonoscopy and biopsy of the colon and ileum, is required to make the diagnosis.
Patients with Crohn disease often need repeat imaging, raising concern about cumulative doses of diagnostic ionizing radiation; therefore, imaging should be used only when the results affect management, and modalities that do not use radiation (ultrasound, MRI) should be used in place of CT scanning whenever possible.

21
Q

For people with UC and Crohn’s disease, how often should colon cancer surveillance occur?

A

Patients with long-standing colitis associated with inflammatory bowel disease are at increased risk for colon cancer and should undergo surveillance colonoscopy every 1 to 2 years beginning after 8 to 10 years of disease.

22
Q

Treatment of Ulcerative Colitis:

  • Mild to Moderate
  • Severe
A

MILD TO MODERATE UC:
-First line: 5-ASA—Sulfasalazine may cause folate deficiency, and supplementation is recommended.

SEVERE UC:
-oral glucocorticoids (budesonide) and if responds, then taper over 2-4 months while transitioning to a maintenance medication (AZA, 6-MP, or a biologic agent) Patients with glucocorticoid-responsive disease are often treated with AZA or 6-MP for maintenance.

Patients whose symptoms do not respond to glucocorticoids are treated with cyclosporine, a biologic agent, or colectomy. Cyclosporine is effective for avoiding colectomy in the short term in most patients.

23
Q

Treatment of Crohn’s Disease

A

MILD TO MODERATE: start with glucocorticoids, either prednisone or budesonide

SEVERE: Patients with more severe disease are treated with a biologic agent. The three anti-TNF agents that are FDA approved for CD are infliximab, adalimumab, and certolizumab.

REFRACTORY DISEASE: Natalizumab is a monoclonal antibody that interferes with leukocyte migration out of the bloodstream by blocking α4 integrin. It is effective for induction and maintenance of remission in CD that has failed to respond to other medications

24
Q

What is microscopic colitis? How often does it happen and to whom?

A

Microscopic colitis (MC) accounts for 10% to 15% of patients with chronic, watery diarrhea. In contrast to IBD, MC is more common in older persons and does not cause endoscopically visible inflammation.

25
Q

What are some common meds that can cause microscopic colitis?

A

NSAIDs PPIs

26
Q

How is microscopic colitis diagnosed?

A

The diagnosis of MC is made by histologic evaluation of colonic biopsies; the classic finding is intraepithelial lymphocytosis (>20 intraepithelial lymphocytes per 100 epithelial cells). In collagenous colitis, the increase in intraepithelial lymphocytes may be less pronounced than in lymphocytic colitis, and the main histologic feature is thickening of the subepithelial collagen band (usually >10 µm).

27
Q

How is microscopic colitis managed?

A

Therapy for MC is based on symptom severity:

  • Any potentially causative medication should be stopped if possible.
  • Mild disease, antidiarrheal therapy such as loperamide or diphenoxylate can be used.
  • Moderate disease, bismuth subsalicylate may be beneficial.
  • Severe cases or those that do not respond to antidiarrheal agents or bismuth, budesonide is the treatment of choice.
28
Q

How is chronic constipation defined?

A

Constipation is classified as acute or chronic; it is also classified as secondary or functional. Chronic constipation is characterized by the regular presence of symptoms for a minimum of 3 months, with symptom onset at least 6 months prior to diagnosis.

29
Q

How is constipation initially managed if no red flag symptoms are present?

A

Initial lifestyle and dietary measures that should be pursued are increased physical activity and increased dietary fiber.

30
Q

Describe the different types of laxatives

A

SURFACTANTS: docusate sodium or docusate calcium are weak laxatives with an excellent safety profile. As such, they are most appropriate for very mild, intermittent constipation.

OSMOTIC: laxatives include magnesium hydroxide, lactulose, sorbitol, and polyethylene glycol (PEG) 3350; clinical trials have demonstrated the superiority and safety of PEG.

STIMULANT: laxatives include anthraquinone, senna, and the diphenylmethanes bisacodyl and sodium picosulfate. The stimulants are the fastest-acting agents (8-12 hours) and are most effective for acute exacerbations of constipation as well as slow-transit constipation.

31
Q

What do you use if constipation doesn’t respond to laxatives?

A

When constipation symptoms do not respond to fiber supplementation or osmotic and stimulatory laxative therapy, prosecretory agents, including the chloride channel activator LUBIPROSTONE and the guanylate cyclase-C activator LINACLOTIDE, are available by prescription.

32
Q

Management of IBS?

A

A strong clinician-patient relationship should be established using a patient-centered approach that is focused on effective patient and clinician communication. This can be achieved by using open-ended questions, actively listening to the patient, and showing empathy during patient encounters.

Given the growing role of presumed food intolerances in IBS symptoms (more than half of patients report symptom onset following meals), dietary interventions are growing in popularity. Although RCTs are lacking, dietary interventions may include the avoidance of trigger foods (caffeine, carbonated beverages, or fatty foods), increased dietary fiber, and various elimination diets that restrict gluten, lactose, fructose, or FODMAPs (Fermentable Oligosaccharides, Disaccharides, Monosaccharides, And Polyols).

33
Q

What medications have demonstrated efficacy for IBS-C?

A

Lubiprostone and linaclotide have demonstrated safety and efficacy in treating the global symptoms of IBS-C in high-quality RCTs.

34
Q

Medications to use for IBS-D?

A

The antispasmodic agents hyoscyamine and dicyclomine are used for the short-term treatment of abdominal pain in IBS-D or IBS-C, although they can cause constipation. The antidiarrheal agent loperamide is safe and is only effective for the bowel symptoms associated with IBS-D

35
Q

What are symptoms of diverticulitis? How is it diagnosed?

A

Symptoms of diverticulitis include abdominal pain, fever, and altered bowel habits (typically diarrhea).
If clinical features are highly suggestive of diverticulitis, imaging studies are unnecessary.

36
Q

What is occlusive mesenteric ischemia?

A

Embolism to the mesenteric arteries causes 50% of cases of AMI and usually involves the superior mesenteric artery (SMA). Emboli are usually of cardiac origin and are due to atrial fibrillation or left ventricle thrombus.

37
Q

What is nonocculsive mesenteric ischemia?

A

Nonocclusive mesenteric ischemia is caused by decreased mesenteric perfusion in low-flow states such as heart failure, sepsis, profound hypotension, or hypovolemia. It may also occur with use of vasoactive medications (vasopressors, ergots, triptans, cocaine, digitalis).

38
Q

What are some lab abnormalities observed in someone with acute mesenteric ischemia that has progressed?

A

Early in AMI, laboratory studies may be normal. Leukocytosis, hemoconcentration, anion gap metabolic acidosis, and elevations in lactate dehydrogenase and/or amylase levels may be seen as disease progresses.

39
Q

What is the standard for diagnosis of acute mesenteric ischemia

A

CT angiography is considered the standard for diagnosis of AMI because it is fast, noninvasive, widely available, and has a high sensitivity and specificity for diagnosing AMI and excluding other causes of pain.

40
Q

How is acute mesenteric ischemia managed?

A

Treatment consists of volume resuscitation, correction of acidosis and electrolyte imbalances, broad-spectrum antimicrobial agents, nasogastric decompression, and discontinuation of medications associated with vasoconstriction. Surgery is indicated for patients with peritoneal signs or for those in whom there is a high index of concern for AMI despite negative imaging studies. Necrotic bowel should be resected. Embolectomy or, in the case of thrombosis, thrombectomy and surgical revascularization or endovascular stenting of the underlying atherosclerotic lesion should be performed.

41
Q

What is the most common cause of chronic mesenteric ischemia? What are the symptoms?

A

Chronic mesenteric ischemia is almost always associated with atherosclerotic disease.
Symptoms of chronic mesenteric ischemia consist of postprandial pain within 60 minutes after meals, which results in fear of eating and weight loss.

42
Q

What is the treatment for chronic mesenteric ischemia?

A

Surgical revascularization is the most durable treatment for chronic mesenteric ischemia. Periprocedural morbidity and mortality are lower with endovascular stenting, which may be indicated for select patients.

43
Q

What is the first line treatment for internal and external hemorrhoids?

A

Initial treatment of hemorrhoids consists of dietary and lifestyle modifications to soften bowel movements and avoid constipation, straining, and prolonged time on the toilet.

44
Q

How are anal fissures managed?

A

Most acute anal fissures heal spontaneously; sitz baths, fiber or stool softeners, topical anesthetics, or anti-inflammatory ointments may provide symptomatic relief.

45
Q

What is the cause of anal cancer?

A

Anal carcinoma is a rare but increasing cause of cancer and accounts for approximately 2% of gastrointestinal cancers. Most anal cancers are squamous cell carcinomas and are associated with human papillomavirus (HPV) infection, particularly HPV 16 and HPV 18.

46
Q

What are risk factors for anal cancer?

A

Risk factors for anal cancer include HPV infection; sexually transmitted infections; multiple sex partners; men having sex with men; receptive anal intercourse; history of vaginal, cervical, or vulvar cancer; smoking; immunosuppression due to hematologic malignancy; solid organ transplantation; or HIV infection.

47
Q

How do most people with anal cancer present?

A

Most patients with anal cancer present with a perianal lesion or mass associated with rectal bleeding or anal discomfort.