Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI Fellowship > Small Intestine > Flashcards

Small Intestine Flashcards

1
Q

Where are 95% of bile acids absorbed?

A

The terminal ileum. Which absorbs 95% of bile acids through active bile acid transport into the portal circulation. Bile acids circulate back to the liver . Only 5% of bile acids are excreted in stool

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the main determinant of diarrhea after ileum resection?

A

The etiology of diarrhea after ileal resection depends on the length of the resected ileum. If less than 100cm of ileum resected, you can see mild bile acid malabsorption but if MRE than 100cm resected you will see SEVERE bile acid malabsorption.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How do the bile acids after ileum resection cause diarrhea?

A

The unabsorbed bile acids irritate the colonic mucosa resulting in secretory diarrhea (cholerheic diarrhea).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Why does a patient with ileum resection less than 100cm not develop steatorrhea (increase in fat excretion in the stools)?

A

The liver can compensate for the lost bile acids, and the total bile acid content in the enterohepatic circulation remains constant, therefore steatorrhea does not develop.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what type of treatment is best for patients with (bile acid) diarrhea after ileal resection of less than 100cm?

A

Bile acid sequestrants ( like cholestyramine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

For which group of patients with ileum resection (Less than 100cm resected vs MORE than 100cm resected) is Bile acid sequestrants ( like cholestyramine) beneficial? and which group is it harmful?

A
  1. Beneficial in pts with less than 100cm of ileum resected
  2. In pts with >100cm resected, cholestyramine will worsen symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why does a patient with ileum resection MORE than 100cm develop steatorrhea (increase in fat excretion in the stools)?

A

The liver can NOT compensate for the SIGNIFICANT lost of bile acids, and the total bile acid content in the enterohepatic circulation is DECREASED, leading to fat malabsorption and steatorrhea.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what type of treatment is best for patients with (bile acid) diarrhea after ileal resection more than 100cm?

A

Treat with low fat diet and anti-diarrheals. Consider medium chain fatty acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is meant by the term “ileal break”?

A

The ileum secretes Peptide YY in response to fat and other luminal nutrients. Peptide YY acts to slow upper GI motility. This negative feedback mechanism is referred to as the ileal break.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does loss of ileal break contribute to diarrhea after ileal resection?

A

Losing the ileal break can contribute to diarrhea in patients with ileal resection, because they no longer have the ileum to secrete peptide YY which slows down Upper GI motility.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

which clinical syndrome is associated with greasy, foul smelling diarrhea, weight loss, vitamins ADEK deficiencies?

A

Fat Malabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the 3 main causes of fat malabsoprtion?

A
  1. Exocrine insufficiency
  2. Small intestinal disease
  3. Bile acid deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

which two test can be used to prove a patient has fat malabsoprtion?

A
  1. Stool Sudan stain (abnormal if > 5fat globules/HPF)
  2. Fecal fat excretion (abnormal if 7g of fat/24 hours )- patients are told to eat >100g fat per day for the 3 days before the test)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what 4 labs tests can be used to investigate the etiology of fat malabsorption?

A
  1. Chem panel to rule out biliary obstruction & look for hepatic disease
  2. Tissue transglutaminase antibodies (TTG-IgA) for celiac disease
  3. Fecal elastase to test for pancreatic insufficiency
  4. D-Xylose test
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What types of conditions are suggested by an abnormal vs normal D-xylose test?

A
  1. An abnormal D-Xylose test suggests small intestinal mucosal disease
  2. Normal D-Xylose test suggests pancreatic or other non small bowel cause of steatorrhea.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are treatment options for fat malabsorption?

A

Depends on etiology, consider supplementation with medium chain fatty acids, and pancreatic enzyme replacement.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

which condition is associated with excessive loss of protein from the GI tract leading to hypoproteinemia and edema?

A

Protein losing enteropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

which clinical features include edema, ascites, pericardial or pleural effusion, anasarca, related to the GI tract (not liver)?

A

Protein losing enteropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the 2 categories of causes of protein losing enteropathy?

A
  1. GI mucosal disease (erosive or non-erosive disease can lead to protein loss form the surface epithelium
  2. Increased mucosal interstitial pressure due to lymphatic or venous outflow obstruction leading to protein leakage from the mucosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

In terms of GI Mucosal etiologies of protein losing enteropathy, what are the erosive causes?

A
  1. Severe gastritis
  2. Ulcerative jejuno-ileitis
  3. Infectious colitis/enteritis
  4. IBD
  5. GI ischemia
  6. acute graft vs host
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

In terms of GI Mucosal etiologies of protein losing enteropathy, what are the NON-erosive causes?

A
  1. Hypertrophic gastropathy (Menetriers)
  2. Celiac disease
  3. Whipple disease
  4. Eosinophilic gastroenteritis
  5. GI sarcoidosis, amyloidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

In terms of Increased intestinal pressure etiologies of protein losing enteropathy, what are the causes?

A
  1. Intestinal lymphangiectasis
  2. Heart disease (CHF, constrictive pericarditis, etc.)
  3. Severe portal HTN
  4. Mesenteric venous thrombosis
  5. Neoplastic involvement of mesenteric lymph nodes
  6. Mesenteric tuberculosis
  7. Retroperitoneal fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is the best method to diagnose/evaluate protein losing enteropathy?

A

Alpha 1 antitrypsin clearance (A1-AT): This is the best way to evaluate enteric protein loss. It requires a 24 hour stool collection because spot measurements are not reliable.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what makes an Alpha 1 antitrypsin clearance test to diagnose/evaluate protein losing enteropathy abnormal?

A

abnormal If Alpha 1 antitrypsin clearance >27ml/day in patients without diarrhea, and 56ml/day in patients with diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

In using an Alpha 1 antitrypsin clearance test to diagnose/evaluate protein losing enteropathy, why are PPIs recommended prior to testing?

A

Pepsin can degrade A1-AT that is lost from gastric mucosa, which can lead to false negative test result. Therefore PPI is recommended prior to doing the Alpha 1 antitrypsin clearance test especially if a gastric source of protein loss is suspected.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Does the Alpha 1 antitrypsin clearance test to diagnose/evaluate protein losing enteropathy help you tell the difference between GI mucosal disease and intestinal sources of protein loss?

A

No it does not, use the tech99m labeled albumin scintigraphy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what test is used to identify the source of site of protein loss in evaluating protein losing enteropathy?

A

the tech99m labeled albumin scintigraphy- the tech 99m labeled albumin is injected and serial images of the abdomen are obtained to identify the site of protein loss.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is the treatment for protein losing enteropathy?

A

Supportive care, treat underlying etiology, low fat high protein diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What diet is recommended in protein losing enteropathy?

A

Low fat, high protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

which 5 tests can be used To diagnose carbohydrate malabsorption?

A
  1. Fecal pH (less than 5.5 suggests carb malabsorption)
  2. Stool osmotic gap (>100)
  3. D-Xylose test
  4. Hydrogen breath test
  5. Lactose intolerance test
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what fecal ph suggests carbohydrate malabsorption?
(normal is 6.5 to 7.5)

A

pH (less than 5.5 suggests carb malabsorption (

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

how is the stool osmotic gap calculated?

A

290- (stool Na + stool K) x2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what does the D-xylose test for carb malabsorption test specifically?

A

test examines the ability of the small intestine to absorb the monosaccharide d-xylose, which does not require bile acids or pancreatic enzymes for absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

in what medical situation can you se a false positive D-Xylose test for carb malabsorption?

A

Renal dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

during what two situations can you see false positive results for the hydrogen breath test for carb malabsorption?

A
  1. SIBO
  2. pt taking antibiotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Which clinical syndrome is characterized by an increase in the number or change in the type of bacteria in the small intestine resulting in symptoms of excess gas formation and malabsorption?

A

SIBO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what IS THE normal bacteria density in the;
1. Stomach
2. Duodenum
3. Small Intestine
4. Colon

A
  1. 10^3
  2. 10^3
  3. 10^4 -10^7
  4. 10^10 to 10^13
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

which two bacteria form most of the proximal intestinal bacteria? which are mostly in colon?

A
  1. Streptococcus and Lactobacillus
  2. anaerobes (Bacteroid, Clostridum, Bifidobacterium)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the 7 anatomical risk factors for SIBO?

A
  1. blind small intestinal loop
  2. absence of ileocecal valve
  3. small intestinal diverticulae
  4. entero-enteric fistula
  5. intestinal strictures
  6. gastrocolic or jejenocolic fistula
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the MOTILITY related risk factors for SIBO?

A
  1. Diabetic autonomic neuropathy
  2. Scleroderma
  3. Amyloidosis
  4. Hypothyroidism
  5. Opioids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the ACID suppression risk factors for SIBO?

A
  1. Vagotomy
  2. Atrophic gastritis
  3. Achlorhydria
  4. PPI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What 2 labs abnormalities can be seen in patients with SIBO?

A
  1. Increased folate levels due to increased bacterial synthesis
  2. Decreased B12 levels due to increase bacterial usage of B12
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the Gold standard test to diagnose SIBO?

A

Gold standard: proximal jejunal aspirate of MORE than 10*3 colony forming units mL.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Aside from the proximal jejunal aspirate, what other diagnostic test can be used to diagnose SIBO?

A

Hydrogen breath test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How does Hydrogen breath test
work to diagnose SIBO?

A

Anaerobic bacteria ferment a test substrate (glucose 75g or lactulose 10g) producing hydrogen that is detected in breath samples.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What indicated a positive Hydrogen breath test for SIBO?

A

The test is positive or abnormal if there is a rise in the hydrogen concentration: (PPM: parts per million)
- More > 20 PPM within 2 hours after ingestion of lactulose.
- More > 12 PPM within 3 hours after ingestion of glucose.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

in doing a hydrogen breath test for SIBO, what would cause a late peak in hydrogen concentration?

A

Late peaks are due to colonic bacterial fermentation of the substrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what are the 2 main limitations to the hydrogen breath test for SIBO?

A
  1. Rapid absorption of glucose in the proximal small intestine may result in a false negative result.
  2. Rapid intestinal transit results in a false positive early peak of hydrogen due from colonic fermentation rather than SIBO
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

For patients with a positive Hydrogen breath test for SIBO what confirmatory or repeat testing should be considered?

A

It is recommended that in patients with a positive test, are considered for repeat testing with scintigraphy. This involves labelling the ingested meal with 99m Te-sulfur colloid. This radiolabeled meal is detected by nuclear scanning in the cecum to confirm the time the test med arrives to the colon. If the hydrogen peak occurs after the meal reaches the cecum, then this is due to colonic fermentation rather than SIBO.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Which clinical condition is assoc with excessive intestinal methane production by methanogenic Archaea (organisms that are not bacteria)?

A

Intestinal Methonogenic overgrowth (IMO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

In the intestine, what is the main methanogen ?

A

In the intestine, the main methanogen is Methanobrevibacter smithii

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what is the treatment for SIBO?

A

Antibiotics (Amoxicillin-clavulanic acid,
Doxycycline, metronidazole, ciprofloxacin, trimethoprim-sulfamethoxazole, Rifaximin. If SIBO is considered based on symptoms and risk factors, and if diagnostic tests are not available, it is reasonable to give a treatment trial for 7~10 days.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

which antibiotics can be used to treat SIBO? Which is the safest?

A

Amoxicillin-clavulanic acid 500/125 t.i.d.
Doxycycline 100 mg b.i.d., metronidazole 250-500 mg t.i.d., ciprofloxacin 500 mg b.i.d., trimethoprim-sulfamethoxazole 160/800 mg b.i.d.
* Rifaximin (400 or 550 mg t.i.d.) is the safest due to its low intestinal absorption

54
Q

Are probiotics recommended to treatment of SIBO?

A

Probiotics have not been found to consistently improve SIBO and are not recommended

55
Q

Can patients be given multiple courses of antibiotics for recurrent SIBO sxs?

A
  • Recurrence after treatment is common. Patients can be given repeated courses of antibiotics as needed for symptom control. Change the antibiotic type to decrease the rate of bacterial resistance.
56
Q

Clinical syndrome associated with malabsorption and intestinal failure resulting from the decrease in the normal intestinal length (or surface area) to < 30%, or 200 cm in adults?

A

Short bowel syndrome (SBS)

57
Q

What is the length the intestine has to be to be considered short bowel syndrome?

A

Less than 200cm or less than 30%

58
Q

How does colon play a role in short bowel syndrome?

A

The presence of the colon partially compensates for malabsorption by increasing its absorption of water and electrolytes.

59
Q

What are the most common causes of short bowel syndrome?

A

Common etiologies include mesenteric vascular events (SMA or SMV thrombosis), midgut volvulus, Crohn’s disease, trauma, and radiation enteritis, Post-operative short bowel syndrome

60
Q

In patients with short bowel syndrome, what are the 5 predictors of those who will need to be TPN dependent?

A

1 small bowel length less than 50-100cm
2 low plasma citrullin levels (citrullin is an amino acid produced by enterocytes)
3 absence of ileocecal valve
4 absence of an intact and functional colon
5 residual small bowel mucosal disease

61
Q

What are the two main complications of short bowel syndrome?

A
  1. D- lactic acidosis
  2. Hyperoxaluria
62
Q

In terms of complications of short bowel syndrome, how is D- lactic acidosis caused?

A

D- lactic is a rare neurologic syndrome that results from the accumulation of D-lactate in the serum of patients with short bowel syndrome.
The accumulation of D-lactate results from the increased delivery of carbohydrates to the colon, where they are metabolized by colonic bacteria to produce D-lactate.

63
Q

In terms of complications of short bowel syndrome, how is hyperoxaluria caused?

A

Hyperoxaluria results from the effect of steatorrhea on oxalate absorption. Normally calcium binds oxalate in the intestinal lumen and is excreted in stool. In patients with steatorrhea, calcium binds the unabsorbed fat, and oxalate binds sodium and is absorbed in the colon in higher amounts. Oxalate is excreted in the urine resulting in oxalate stones. In the absence of a functional colonic epithelium, oxalate is not absorbed and hyperoxaluria does not develop.

64
Q

what are the most common neurologic manifestations of short bowel syndrome associated D- lactic acidosis?

A

Neurologic manifestations: altered mentation, hallucinations, nystagmus, dysarthria, ataxia, weakness. ‘

65
Q

what is the treatment for short bowel syndrome associated D- lactic acidosis?

A

Treatment: withhold carbohydrate intake, give IVF and oral antibiotics (metronidazole, vancomycin).

66
Q

what is the best way to prevent short bowel syndrome associated D- lactic acidosis?

A

Prevention: limit simple sugars; provide complex carbohydrates in tube feeds.

67
Q

In terms of complications of short bowel syndrome, how is it managed with dieT?

A

Diet: encourage hyperphagia. Give elemental and low-fat diet. Add medium chain fatty acids.
Parenteral IVF and TPN. Micronutrient, vitamin, and mineral supplementation.

68
Q

In terms of complications of short bowel syndrome, how is it managed with medications??

A

Loperamide (2-4 mg every 8 hours).
Diphenoxylate with atropine (2.5-5 mg every 8 hours).
Tincture of opium (5-10 drops every 8 hours).
Clonidine (0.2 mg PO b.i.d. or transdermal patch).
Octreotide (50-100 mcg subq or IV b.i.d. or t.i.d.).
PPIs are given to inhibit excess gastric secretion.

69
Q

In terms of complications of short bowel syndrome, which two medications help to enhance bowel adaptation ??

A
    • Somatropin (orbrive) is recombinant growth hormone that is FDA approved for treatment of SBS. t has significant side effects (peripheral edema, arthralgia, carpal tunnel syndrome) and may lead to acute pancreatitis and impaired glucose tolerance. It is not widely used in clinical practice.
  2. Teduglutide (Gattex®)

FDA approved for the treatment of SBS. Glucagon like peptide 2 (GLP-2) is normally secreted from the L cells in the ileum and colon and improves intestinal adaptation and proliferation.
Teduglutide is a long acting GLP-2 analogue given as a subcutaneous injection that enhances the structural and functional integrity of the remaining intestine in SBS.”

70
Q

In terms of short bowel syndrome, what surgical option can be performed as part of the management/treatment?

A

1. Intestinal transplantation
short bowel syndrome is the most common indication for intestinal transplant. The 1-year patient survival after intestinal transplant is 90%. The 1-year graft survival is 75%. 12

71
Q

What is the most common indication for intestinal transplant?

A

short bowel syndrome

72
Q

which clinical condition associated with immune mediated enteropathy that results from hypersensitivity to gluten.?

A

Celiac disease

73
Q

what are the main 7 nutritional deficiencies seen in Celiac disease?

A

IDA, and nutritional deficiencies like vitamins A, D, E, K, B12 and folate deficiency.

74
Q

What is the main metabolic/systemic complications seen in patients with Celiac disease?

A

Metabolic bone disease (osteopenia, osteoporosis), hyposplenism, spontaneous abortion, infertility, chronic fatigue.

75
Q

In patients with celiac disease presenting with life threatening diarrhea, malabsorption, and severe metabolic derangements, what diagnosis should be considered?

A

”Celiac crisis”. This is a rare clinical presentation of celiac disease, which refers to life threatening diarrhea, malabsorption, and severe metabolic derangements caused severe edema in the small bowel.
Most patients with this condition do not have a pre-existing diagnosis of celiac disease.

76
Q

what work up should be done in patients in patients with idiopathic mild elevation of liver enzymes and possible gluten senstitivty?

A

Test for celiac disease in patients with idiopathic mild elevation of liver enzymes.

77
Q

Which autoimmune conditions are associated with celiac disease?

A

Autoimmune and connective tissue diseases: Type 1 DM, thyroiditis, Addison disease, Rheumatoid arthritis, Sjögren’s syndrome.

78
Q

Which hepatic conditions are associated with celiac disease?

A

Liver: Autoimmune hepatitis, primary biliary cholangitis, primary sclerosing cholangitis

79
Q

Which patient population has a six-fold increased risk of celiac disease?

A

Down syndrome patients have a sixfold increased risk of celiac disease.

80
Q

In Celiac patients, what dermatologic condition should be considered with in those with pruritic papules and vesicles on extensor surfaces?

A

Dermatitis herpetiformis presents as grouped pruritic papules and vesicles on extensor surfaces. It is seen in up to 25% of patients with celiac disease. Nearly 100% of patients with dermatitis herpetiformis have celiac disease. Skin biopsy with immunofluorescence shows granular IgA deposition at the dermoepidermal junction.

81
Q

How is celiac disease diagnosed?

A

The patient must be on gluten containing diet while performing the serologic testing and biopsies, otherwise the sensitivity of these tests will decrease.

  1. IgA-tissue transglutaminase antibody (IgA TTG)
    Sensitivity ~95%, specificity > 95%. This test is recommended as the first line test for celiac disease.
82
Q

Which test is recommended as the first line test for celiac disease?

A

IgA-tissue transglutaminase antibody (IgA TTG)

83
Q

In a patient with negative IgA TTG for celiac, but the suspicion for celiac is high, what test should be done next?

A

If there is a high suspicion for celiac disease in a patient with a negative IgA TTG, test for total IgA levels.
If total IgA levels are low, test for celiac disease using IgG-TTG, or IgG deamidated gladin peptides.
If antibodies are positive, then perform duodenal biopsies to confirm the diagnosis.

84
Q

In a patient with negative IgA TTG for celiac, but the suspicion for celiac is high, and the total IgA levels ARE LOW, what test should be done next?

A

If total IgA levels are low, test for celiac disease using IgG-TTG, or IgG deamidated gladin peptides. If antibodies are positive, then perform duodenal biopsies to confirm the diagnosis.

85
Q

Endoscopically, how can celiac disease be diagnosed?

A

perform duodenal biopsies to confirm the diagnosis.

86
Q

Aside from IgA-tissue transglutaminase antibody (IgA TTG) or IgG-TTG or IgG deamidated gladin peptides, what other tests can be used to diagnose celiac disease? Is this more or less sensitive than (IgA TTG) antibody?

A

Anti-endomysial antibodyies. These have a sensitivity 85-95%, specificity 95-97%, less than IGA TTG

87
Q

In diagnosing celiac disease, can you check antigliadin antibodies?

A

Antigliadin antibodies have low sensitivity and specificity (<80%) and are not recommended.

88
Q

These two alleles, HLA-DQ2 and HLA-DQ8, are strongly related to which GI disease?

A

Celiac disease is strongly related to HLA-DQ2 and HLA-DQ8 on chromosome 6.

89
Q

90% to 95% of patients with celiac disease have the which allele type?

A

90% to 95% of patients with celiac disease have the HLA-DQ2 allele, and the other 5% to 10% have the HLA-DQ8 allele.

90
Q

In patients with suspected celiac disease, what is the significance of a patient NOT having either the HLA-DQ2 or the HLA-DQ8 allele?

A

They dont have celiac. Absence of both alleles rules out the diagnosis of celiac disease (i.e, negative predictive value is ~100%)

91
Q

what endoscopic findings can be seen in patients with celiac disease?

A

Endoscopic findings in celias disease: mucosal fissuring, scalloping, nodularity, and loss of villi.
These findings have low sensitivity (50-60%).

92
Q

How should biopsies be obtained in patients with suspected celiac disease?

A

1. Always obtain mucosal biopsies, even if the duodenal mucosa appears normal.
2. Take four biopsies from the distal second portion, and 1-2 biopsies from the bulb.

93
Q

what part of the intestines is most commonly involved in celiac disease?

A

Most patients with celiac disease have duodenal involvement +/- jejunal patchy enteropathy, however, few patients (<5%) may have patchy jejunal enteropathy alone.

94
Q

which classification system is used to describe the spectrum of histologic changes in celiac disease?

A

Marsh classification system

95
Q

What is the treatment for patients with celiac disease?

A
  1. Refer to a dietician to start a gluten free diet
    2.
96
Q

which types of foods should be avoided in patients diagnosed with celiac disease?

A

Patients should avoid all wheat, barley, and rye. This food should not contain any ingredient that is any type of wheat, rye, barley, or crossbreds of these grains. It should contain less than 20 parts per million of gluten.

97
Q

which nutritional deficiencies can be seen and should be checked for in celiac patients?

A

Check for nutritional deficiencies (A, D, E, B12, folate, iron, copper, zinc) and supplement as necessary.

98
Q

which medication (not approved in the US) has been shown to reduce signs and symptoms of celiac disease better than gluten free diet?

A

Larazotide acetate, a novel oral peptide that modulates intestinal permeability through its effects on tight junctions

99
Q

how is non-responsive celiac disease defined?

A

Persistent symptoms, signs or laboratory abnormalities typical of celiac disease despite 6 to 12 months of dietary gluten avoidance. This is further divided into primary non response (no initial response to gluten free diet) or secondary response (recurrence after initial response).

100
Q

what is the first two steps in management of non responsive celiac disease?

A
  1. Confirm the diagnosis. Review prior serology and biopsy.
  2. Check for noncompliance with gluten free diet, which is the most common cause of non-responsive celiac disease.
101
Q

what is the most common cause of non-responsive celiac disease?

A

 noncompliance with gluten free diet

102
Q

what labs can be checked to see if a celiac patient who is not responding to gluten free diet is actually adhering to a gluten free diet? 

A

A negative TTG-IgA does not confirm strict adherence to a gluten free diet, as antibodies can revert to negative even with minimal diet adherence.

103
Q

In non-responsive celiac disease who had a normal biopsy, what should be done for mangement?

A
  1. Repeat endoscopy and biopsy. If the duodenal biopsy is normal, consider alternative or co-existing disease such as lactase deficiency, microscopic colitis, SIBO, irritable bowel syndrome or pancreatic insufficiency
  2. Perform a colonoscopy and biopsy if diarrhea is present.
  3. Consider capsule endoscopy to assess for complications
104
Q

How is Refractory (truly non-responsive) celiac disease defined?

A

symptomatic severe villous atrophy despite a confirmed gluten free diet of at least 6 months.

105
Q

what are the two types of refractory celiac disease ?

A

Refractory celiac disease is divided into two types:
1. Type 1 refractory celiac disease (less severe than type 2, with a five-year survival is ~90%.) Small intestinal biopsy shows normal (polyclonal) intraepithelial lymphocytes (IELs).

2. Type 2 refractory celiac disease (more severe disease with a five-year survival is less than 50%), Characterized by the presence of an abnormal clonal population of IELs. These can demonstrate loss of normal CD3 or CD8 expression.

106
Q

which is type 2 refractory celiac disease more concerning that type 1?

A

type 2 refractory celiac disease can progress to enteropathy-associated T-cell lymphoma, ulcerative jejuno-ileitis, or rarely to mesenteric lymph node cavitations.

107
Q

what are the treatment options for type 2 refractory celiac disease ?

A

Treatment options include glucocorticoids (prednisone, budesonide) and thiopurines.

108
Q

which condition is associated with ingestion of gluten leading to symptoms similar to celiac disease, but without celiac-specific antibodies and histologic features of villous atrophy.?

A

Non celiac gluten sensitivity (NCGS).

109
Q

which condition is associated with an allergy to wheat associated with the production of specific IgE antibodies.?

A

Wheat allergy

110
Q

which condition is associated with caused by Tropheryma whipplei, a gram-positive rod-shaped bacterium?

A

Whipple disease

111
Q

what is the most common symptoms of Whipple disease?

A

Abdominal pain, fever, arthralgias, diarrhea, weight loss, occult GI bleeding, Neurologic manifestations

112
Q

What two key Pathognomonic neurologic findings are seen in
patients with Whipple disease?

A
  1. Oculomasticatory myorhythmia (eye and jaw movement).
    2. nOculo-facial-skeletal myorhythmia (slow nystagmus with rhythmic jaw and skeletal movement).
113
Q

What endoscopic findings can be seen in patients with Whipple disease??

A

Upper endoscopy shows proximal intestinal edema and white patches that represent lipid collections.

114
Q

How should biopsies be taken in patients with Whipple disease??

A

Take multiple biopsies from the distal second or third portion of the duodenum

115
Q

These histologic findings are associated with which GI disease?

A

the diagnosis of Whipple disease is confirmed by demonstrating foamy macrophages in the lamina propria that are periodic acid-Schiff stain (PAS) positive. The positive PAS stain represents the large amount of glycoprotein in the cell wall of the T. whipplei organisms filling the macrophages.

116
Q

Foamy macrophages can be seen in small bowel biopsies in what two conditions in the GI tract?

A
  1. Whipple disease, we see foamy macrophages in the lamina propria that are periodic acid-Schiff stain (PAS) positive
  2. In common variable immunodeficiency, foamy macrophages can be seen in small bowel biopsies, but these are PAS negative.
117
Q

What is the treatment for Whipple disease ?

A
  1. Ceftriaxone for 10-14 days followed by oral TMP/SMX for 1 year.
    Alternative regimen: penicillinG for 10-14 days followed by oral TMP/SMX for 1 year
118
Q

What is the treatment for Whipple disease in sulfa-allergic patients?

A

Sulfa-allergic patients should receive ampicillin instead of TMP/SMX.

119
Q

what is The most common benign lesion in the small bowel?

A

The most common benign lesion in the small bowel is tubular adenoma.

120
Q

What 3 main risk factors for small intestinal adenocarcinoma?

A

Risk factors for small intestinal adenocarcinoma
1. Peutz-Jeghers syndrome
2. Familial adenomatous polyposis
3. Lynch syndrome

Other risk factors include celiac disease and Crohn’s disease.

121
Q

What 3 main risk factors for small intestinal lymphoma?

A

Prolonged immunosuppression, celiac disease, Crohn’s disease, radiation enteropathy.

122
Q

Patients with neurofibromatosis type 1 (von Recklinghausen disease) develop WHAT type of GI issues

A

Patients with neurofibromatosis type 1 (von Recklinghausen disease) develop multiple small intestinal gastrointestinal stromal tumor (GIST)

123
Q

WHAT is the most common type of GI lymphoma in the Middle East?

A

Immunoproliferative small intestinal disease (IPSID) also called Mediterranean lymphoma, or a -heavy chain disease

124
Q

what does Immunoproliferative small intestinal disease (IPSID) arise from ?

A

It arises from the mucosal associated lymphoid tissue (MALT).
IPSID is characterized by overproduction of a monoclonal immunoglobulin a -heavy chain.

125
Q

what lymphoma is characterized by chromosomal translocation t(11:14)?

A

MCL is characterized by the chromosomal translocation t(11:14), resulting in overexpression of cyclin D1.

126
Q

what lymphoma is characterized by chromosomal translocation (14: 18?

A

Follicular lymphoma is associated with chromosomal translocation 14: 18

127
Q

which lymphoma most commonly arises in terminal ileum and cecum?

A

Burkitt’s lymphoma

128
Q

which lymphoma is associated with type 2 refractory celiac disease?

A

Enteropathy-associated T-cell lymphoma (EATL)

129
Q

what is the overall EATL prognosis for patients with EATL?

A

EATL has a poor prognosis, with a median overall survival of 10 months.

130
Q

Which type of lymphoproliferative disease is caused by B cell proliferation due to Epstein-Barr virus (EBV) infection in chronic immunosuppression?

A

Post-transplant lymphoproliferative disease (PTLD)

131
Q

HOW does immunosuppression causes Post-transplant lymphoproliferative disease ?

A

Chronic immunosuppression and decreased t cell function prevents the normal elimination of EBV infected cells from the circulation. This allows for unchecked B cell proliferation leading to PTLD.

132
Q
A

GI Fellowship (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions