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ABIM > GI > Flashcards

GI Flashcards

1
Q

Cholestatic LFT+IBD

A

PSC

PSC Ddx:

  1. secondary causes of sclerosing cholangitis and
  2. IgG4-associated cholangitis/autoimmune pancreatitis.
  3. PSC-autoimmune hepatitis overlap syndrome

PSC should be considered in patients with a cholestatic pattern of liver test abnormalities (particularly an elevated alkaline phosphatase), especially those with underlying inflammatory bowel disease.

DxMethod: cholangiography characteristic bile duct changes (multifocal strictures, segmental dilations) and excluding secondary causes of sclerosing cholangitis.

A percutaneous liver biopsy may support the diagnosis of PSC, but it is rarely diagnostic. In patients with characteristic findings on cholangiography, a liver biopsy is typically not required. However, liver biopsy is required for patients with suspected small duct PSC or if other conditions such as an overlap syndrome with autoimmune hepatitis are suspected.

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2
Q

% of long term NSAID users who develop significant GI bleed or ulcer perforation

A

2 to 4%

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3
Q

% of patients who have varices at time of diagnosis of cirrrhosis

A

50%

Gastroesophageal varices are present in almost half of patients with cirrhosis at the time of diagnosis, with the highest rate among patients with Child–Turcotte–Pugh (hereinafter called Child) class B or C disease

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4
Q

% of patients with GERD undergoing endoscopy who have Barrett

A

14

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5
Q

Abdominal pain out of proportion + new onset atrial fibrillation

A

CT Angiogram

The CT scan should be performed without oral contrast, which can obscure the mesenteric vessels, obscure bowel wall enhancement, and can lead to a delay of the diagnosis. The origins of the celiac axis and superior mesenteric artery should also be evaluated for the presence of calcification that indicates an underlying atherosclerotic process as a possible etiology for mesenteric ischemia.

This patient presents with new-onset atrial fibrillation, as well as acute abdominal pain with an unremarkable abdominal examination. This is concerning for mesenteric ischemia, which in this case could have been caused by an embolic event. The most appropriate initial study for the diagnosis of mesenteric ischemia would be CT angiography (Answer C), which would facilitate identification of vessel occlusions that could be causing this patient’s symptoms. The classic description of mesenteric ischemia is the presence of marked abdominal pain with relatively benign findings on abdominal exam—“pain out of proportion to exam.”

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6
Q

Achalasia: pathogenesis

A

progressive degeneration of ganglion cells in the myenteric plexus

  1. Progressive degeneration of ganglion cells in the myenteric plexus leading to failure of relaxation of LES + loss of peristalsis in the distal esophagus.
  2. The etiology of primary or idiopathic achalasia is unknown.
  3. Secondary achalasia is due to diseases that cause esophageal motor abnormalities similar or identical to those of primary achalasia.
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7
Q

Bacterial-overgrowth-syndrome.Causes

A
  1. Small bowel stasis:
    1. Diverticula, surgery
    2. Motility problems: eg scleroderma
  2. Entero-colic fistula:
    1. Crohn
    2. Resection of ileocecal valve
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8
Q

Bacterial-overgrowth-syndrome.Rx

A
  1. Broad-spectrum antibiotics (ciprofloxacin, rifaxamin) x 2 to 3 weeks
  2. Nutrition deficiency support
  3. Fix underlying problems
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9
Q

Barrett: Mx parameters

A
  1. Non-dysplastic: Endocopic surveillance, biopsy, PPI
  2. Low grade dysplasia: Endoscopic eradication
  3. High grade dysplasia: Endoscopic eradication
  4. EAC: surgery

Endoscopic eradication: resection + ablation

Our approach to endoscopic eradication therapy is to perform endoscopic resection of any visible mucosal irregularities, followed by RFA to ablate the remaining metaplastic epithelium. (See ‘Endoscopic resection’ above and ‘Endoscopic ablative therapies’ above.)

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10
Q

Barrett: DxCriteria

A
  1. columnar epithelium in distal esophagus.
  2. Histology: intestinal metaplasia

The endoscopist must document that columnar epithelium lines the distal esophagus.

•Histologic examination of biopsy specimens from that columnar epithelium must reveal specialized intestinal metaplasia

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11
Q

Barrett: Risk factors

A
  1. White ethnicity
  2. Age
  3. Central obesity
  4. Long GERD

Factors known to increase the risk for Barrett’s esophagus include white ethnicity, older age, obesity (especially central obesity), and long duration of GERD symptoms.

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12
Q

Barrett, nondysplastic: risk of adenocarcinoma

A

0.1 to 0.4% annually

  1. Risk of esophageal adenocarcinoma in patients with nondysplastic Barrett is ~ 0.1 to 0.4 percent annually
  2. RR: 30
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13
Q

Bile-acid-diarrhea.Causes

A

Bile acids are absorbed in the ileum. Diseases that affect the ileum (i.e., Crohn disease) or where the ileum has been resected will cause bile acid diarrhea.

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14
Q

Bile-acid-diarrhea.types

A
  1. Bile acid diarrhea: liver can compensate, cholestyramine sensitive.
  2. Fatty acid diarrhea: steatorrhea, cholestyramine resistant; try low fat diet
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15
Q

Bleeding.Mx

Stable patient; GI bleed over; negative upper and lower endoscopy. Next step?

A

Video capsule endoscopy

  1. suspected small bowel bleeding
  2. suspected Crohn disease
  3. assess mucosal healing
  4. detect small bowel tumors.
  5. detect small bowel injury associated with NSAIDs
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16
Q

Bleeding

Commonest cause of small bowel bleeding?

A

Angioectasia

Associated with AS

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17
Q

Homozygosity for the C282Y genotype

A

Classical HH

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18
Q

Cancer associated with Plummer-Vinson

A

Squamous Cell

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19
Q

Candida esophagitis: Rx

A

Fluconazole

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20
Q

Ceftriaxone: why should it be given in varceal bleeding?

A

20% have positive blood cultures and SBP

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21
Q

Celiac-disease.Serology.BestTest

A
  1. IgA endomysial antibody (IgA EMA)
  2. IgA tissue transglutaminase antibody (IgA tTG)
  3. ●IgG tissue transglutaminase antibody (IgG tTG)
  4. ●IgA deamidated gliadin peptide (IgA DGP)
  5. ●IgG deamidated gliadin peptide (IgG DGP)

Serum IgA endomysial and tissue transglutaminase antibody testing have the highest diagnostic accuracy. The IgA and IgG antigliadin antibody (AGA) tests have lower diagnostic accuracy with frequent false positive results as compared with IgA tTG and IgA DGP assays and are therefore no longer recommended for initial diagnostic evaluation or screening [2]. However, the newer anti-deamidated gliadin peptide (DGP) assays described above show high diagnostic accuracy. IgA EMA, IgA tTG, IgA DGP and IgG DGP levels fall with treatment; as a result, these assays can be used as a noninvasive means of monitoring the response to a gluten-free diet. (See ‘Monitoring adherence and response to gluten-free diet’ below.)

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22
Q

Celiac-Sprue.also-known-as

A

Gluen sensitive enteropathy

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23
Q

Celiac-sprue.associations

A
  1. Dermatitis herpetiformis
  2. Autoimmune disorders

Dermatitis herpetiformis is characterized by intensely itchy, chronic papulovesicular eruptions, usually distributed symmetrically on extensor surfaces (buttocks, back of neck, scalp, elbows, knees, back, hairline, groin, or face).[1]:616[9][12] The blisters vary in size from very small up to 1 cm across.

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24
Q

Celiac-Sprue.DDx

A

IBS

Diagnosis is often delayed for many years after the onset of symptoms

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25
Q

Celiac-sprue.micronutrient-loss

A

Iron, calcium, Vitamin D

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26
Q

Celiac-Sprue.pathology

A

Flattened villi of the proximal small bowel

Prevalence: 1: 200

(HLA) DQ2 or DQ8

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27
Q

Celiac-sprue.refractory-to-rx

A

The possibility of early-onset small bowel lymphoma should be considered in refractory cases

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28
Q

Celiac-sprue.Rx

A

Life-long gluten free diet

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29
Q

Celiac-sprue.screening

A

Osteoporosis

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30
Q

Celiac-sprue.testing

A
  1. Antiendomysial antibody is an IgA antibody that is 85% to 98% sensitive and 97% to 100% specific
  2. Tissue transglutaminase (tTG) antibody is an IgA antibody that is 90% to 98% sensitive and 95% to 97% specific
  3. Antigliadin antibody (immunoglobulin G [IgG] and IgA) has lower sensitivity and specificity
  4. If there is a high suspicion of disease but negative antibodies, check total IgA concentration to rule out IgA deficiency. In these cases, an IgG-based assay (serum IgG tTG antibody) can be used or upper endoscopy with biopsies.
  5. Diagnostic: small bowel biopsy, which demonstrates flattened or blunted villi and increased lymphocytes
  6. Gold standard: repeat endoscopy with biopsies after gluten-free diet. These should show resolution. Rarely performed nowadays, with the diagnosis made by serology,
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31
Q

Child-Pugh

A
  1. Encephalopathy
  2. Ascites
  3. Bilirubin
  4. albumin
  5. INR

None (1 point)

Grade 1: Altered mood/confusion (2 points)

Grade 2: Inappropriate behavior, impending stupor, somnolence (2 points)

Grade 3: Markedly confused, stuporous but arousable (3 points)

Grade 4: Comatose/unresponsive (3 points)

Ascites

Absent (1 point)

Slight (2 points)

Moderate (3 points)

Bilirubin

< 34.2 mcmol/L (1 point)

34.2-51.3 mcmol/L (2 points)

> 51.3 mcmol/L (3 points)

Albumin

> 35 g/L (1 point)

28-35 g/L (2 points)

< 28 g/L (3 points)

Prothrombin time prolongation

Less than 4 seconds above control/INR < 1.7 (1 point)

4-6 seconds above control/INR 1.7-2.3 (2 points)

More than 6 seconds above control/INR > 2.3 (3 points)

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32
Q

Chronic NSAID use: Indxn for ulcer prophylaxis

A
  1. 2 or more risk factors
  2. History of complicated ulcer

Misoprostol or PPI

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33
Q

Cirrhosis: DxCriteria

A
  1. Exam: (small liver, splenomegaly, telengectasia)
  2. Labs: poor synthetic function, pancytopenia
  3. USG findings
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34
Q

Colonoscopic screening interval after finding polyps

A
  1. Family history, pathology, size and number
  2. If more than 10: repeat in 1 to 3 years
  3. if 3 to 10 small, low risk: 3 years.
  4. if big (> 10 mm), 3 years
  5. If If 1 to 2, tubular adenoma, no villous component: 5 years
  6. Small, hyperplastic: sigmoid, rectum: 10 years
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35
Q

Copper chelating agent used in Wilson’s

A

Penicillamine

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36
Q

Crohn.disease-sites

A
  1. 80% : distal ileum
  2. 50%: ileum + colon
  3. Small number: upper GI
  4. 30%: perianal disease
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37
Q

A 25-year-old man comes to your office because he has diarrhea. Four months ago, he had an exploratory laparotomy for a small bowel obstruction. He was found to have 30 cm of distal ileal Crohn disease, which was resected with ileocolonic continuity re-created. He received therapy with antibiotics during an uneventful perioperative period. Shortly after beginning a normal diet and despite feeling well otherwise, he began to have six to eight watery bowel movements daily, which have not resolved. Most bowel movements occur after breakfast. He has had no fever, bloating, hematochezia, nocturnal diarrhea, or weight loss. He has not traveled abroad. Physical examination of the abdomen is normal except for a well-healed, midline scar. Results of complete blood count, biochemical profile, and examination of the stool for leukocytes are negative. What would be the best initial therapeutic intervention?

Corticosteroids

Metronidazole

Cholestyramine

Sulfasalazine

Codeine sulfate

A

Common and challenging problem of recurrent diarrhea after the initial operation. Possible causes include recurrent Crohn disease, partial obstruction caused by adhesions with or without bacterial overgrowth, antibiotic-associated diarrhea, and either bile-salt diarrhea or malabsorption secondary to the ileal resection.

It would be unusual, but not impossible, for Crohn disease to recur within 1 month of a resection. Signs of inflammation (e.g., leukocytosis, blood or leukocytes in the stool, fever) or obstruction (e.g., bloating, distention, postprandial pain, weight loss) are absent. Thus empirical therapy with either corticosteroids or sulfasalazine is incorrect.

The persistence of diarrhea for 4 months without systemic symptoms or fever and the absence of leukocytes in the stool make antibiotic-associated colitis extremely unlikely.

Operations for cancer, inflammatory bowel disease, and intestinal infarction can lead to resection of varying lengths of ileum. The pathophysiologic consequences of the resection depend on the length of the ileum resected. Normally, more than 95% of bile acids secreted into the intestine are reabsorbed and recirculated to the liver.

Resection of a short segment of the ileum leads to malabsorption of conjugated bile acids, resulting in secretory diarrhea. Typically, bile-salt diarrhea is watery, may not start until a normal diet is resumed after surgery, is precipitated by a meal (most commonly breakfast, when a large quantity of bile is stored in the gallbladder), and does not lead to weight loss.

In bile-salt diarrhea: cholestyramine, can dramatically reduce troublesome watery diarrhea.

With ileal resections of about 100 cm or more, the liver synthesis of bile acids cannot keep up with the colonic losses; the concentration of bile acids in the duodenum falls, and steatorrhea develops.

It should be expected, however, that such a patient with steatorrhea would lose weight and not maintain weight as in this case.

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38
Q

Dysphagia: FirstStudy

A

Barium swallow

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39
Q

Esophageal webs and rings: Sx

A

Solid food dysphage

  1. thin, delicate structures that partially occlude the lumen.
  2. Rings: distal esophagus. Typically: mucosal
  3. Schatzki rings: commonest; mucosal structures at the squamocolumnar junction that are smooth and thin, and are evident radiographically either at the junction between the esophagus and stomach or within a sliding hiatal hernia.
  4. Web refers to a thin mucosal fold that protrudes into the lumen and is covered with squamous epithelium.
  5. Usually: anteriorly in the cervical esophagus, causing focal narrowing in the postcricoid area.
  6. Esophageal rings and webs characteristically cause solid food dysphagia, particularly evident with meat or bread.
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40
Q

Evidence for screening for Barrett

A

Weak

  1. It has been proposed that patients with GERD symptoms should be screened endoscopically for Barrett.
  2. Expert suggestion: if multiple risk factors for esophageal adenocarcinoma then screening.
  3. Evidence supporting this recommendation is weak
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41
Q

GE Varices: pathogenesis

A

Portal hypertension is the cause

Portal hypertension in cirrhosis is caused by:

  1. increased resistance to portal flow:
    1. structural (distortion of liver vascular architecture by fibrosis and regenerative nodules)
    2. dynamic (increased hepatic vascular tone due to endothelial dysfunction and decreased nitric oxide bioavailability)
  2. Increased portal venous blood inflow.
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42
Q

GERD: DDx

A
  1. gastroparesis,
  2. gastrinoma (rare),
  3. gallbladder dysfunction,
  4. eosinophilic esophagitis
  5. Angina
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43
Q

Elderly patient with at low risk for GI bleeding: RxStrategy for reducing risk of bleeding

A

Lowest possible NSAID dose

No need for PPI

Definition of low risk: none of the following

  1. Age > 65
    • anticoagulant or antiplatelet
  3. History of uncomplicated ulcers
  4. High dose NSAID
44
Q

GI.IBD.disease-activity-measurement

A
  1. Crohn’s disease activity index (CDAI)
  2. Harvey-Bradshaw index of Crohn’s disease activity
45
Q

Hemodynamic instability + ongoing lower GI bleeding: Mx steps

A
  1. EGD first because source is upper in 15-20% of patients with hematochezia and is safer.
  2. Abdominal angiography next if (1) fails.
  3. Diagnostic colonoscopy in 8-12 hours AFTER stabilization.
46
Q

Hepatology.DILI

Pattern of liver injury in amoxicillin induced DILI

A

Markedly cholestatic

47
Q

HH: LabCriteria

A
  1. transferrin saturation > 45 percent +
  2. serum ferritin > 200 ng/mL in men and > 150 ng/mL in women
  3. C282Y homozygosity

The diagnosis of HH is suspected in the patient with the above signs and symptoms and a transferrin saturation greater than 45 percent and serum ferritin greater than 200 ng/mL in men and greater than 150 ng/mL in women. Classical HH is confirmed when genetic testing reveals homozygosity for the C282Y genotype. Clinical manifestations of iron overload appear to be uncommon in patients who are heterozygous or compound heterozygous for the C282Y or H63D mutations.

48
Q

IBD.age-distribution

A

Bimodal: 15 to 25 years, 50 to 80 years

49
Q

IBD.colon-cancer-risk

A

2 to 5%

Screen: 8 to 10 years after Dx, then every 1 to 2 years

50
Q

IBD.Crohns.Ddx

A
  1. IBS
  2. UC
  3. Infection
  4. Others:

Because of its segmental nature of CD, a variety of diseases are in the Ddx. These include:

  1. appendicitis,
  2. diverticulitis,
  3. ischemic colitis, and a
  4. perforating or obstructing carcinoma.
  5. Lymphoma, chronic ischemia, endometriosis, and carcinoid can all give a radiologic and clinical picture that is easily confused with CD of the small bowel.
51
Q

IBD.Crohns.DxMethodology

A

endoscopic Fx or imaging Fx in a patient with a compatible clinical history

52
Q

IBD.Crohns.WorkUp.Initial-Imaging

A

MR Enterography

  1. Colonoscopy with intubation of the terminal ileum : ileocolonic CD.
  2. Magnetic resonance enterography as the initial test to evaluate the small intestine.
  3. Wireless capsule endoscopy may also be useful for detecting small bowel involvement.
  4. Although several serologic markers for CD are commercially available, the accuracy remains unclear.
53
Q

IBD.Crohns.WorkUp.Sequence

A

Colonoscopy first with predominant diarrhea, while imaging studies first for those presenting with abdominal pain.

54
Q

IBD.Rx

A
  1. Mild: 5-ASA
  2. Moderate, severe: steroids (eg budenoside)
  3. Steroid-resistant, steroid-dependent: Immunosuppressants
    1. Azathioprine, 6-MP, methotrexate (Crohn’s)
    2. Biologics: Anti–tumor necrosis factor (TNF) therapies
55
Q

IBD.Rx.anti-TNF-agents

A

infliximab, adalimumab, and certolizumab pegol

All are effective in treatment of luminal Crohn disease Fibrostenotic Crohn disease without active inflammation are unlikely to benefit.

Patients who are intolerant to one anti-TNF agent may tolerate a different agent

56
Q

IBD.Rx.anti-TNF-Rx.BeforeStart

A

Rule out TB

57
Q

IBD.Rx.other-biologics

A
  • Anti-integrin antibodies
  1. Vedolizumab
  2. Natalizumab
  • Anti-IL-12/23 antibody: Ustekinumab
58
Q

IBD.serology

A
  1. Anti–Saccharomyces cerevisiae: sensitivity: 80%
  2. p-ANCA: sensitivity: 60%
59
Q

IBS.DDx

A

If constipation is severe, rule out:

  1. hypothyroidism,
  2. hyperparathyroidism,
  3. diverticulosis,
  4. anorectal dysfunction, and
  5. malignancy
60
Q

IBS.Rx

A
  1. Constipation predominant: Tegaserod, a 5-hydroxytryptamine receptor 4 partial agonist
  2. Diarrhea predominant: Alosetron, a 5-hydroxytryptamine receptor 3 agonist, modulates visceral afferent activity from the GI tract

Interesting SideFx profiles: Tegaerod: increased incidence of ischemic cardiovascular events; Alosetron: apparent increased incidence of ischemic colitis

61
Q

A 56-year-old white male complains of intermittent dysphagia for the past 3 months, particularly with the ingestion of meat. He has no difficulties swallowing liquids. He has no history of smoking, uses no medications, and has had no weight loss. What test would be best to evaluate him?

A

Barium swallow

Dx: Schatzki

62
Q

Intestinal.Malabsorption.Carbohydrate

Stool pH

A

pH < 6

carbohydrate malabsorption, stool pH is acidic (pH <6) due to bacterial fermentation of unabsorbed carbohydrate such as lactose.

63
Q

LGIB: indixn for angiography

A

Massive, uncontrolled bleed

  1. Once an upper GI bleeding source is excluded,
  2. colonoscopy is examination of choice.
  3. Mesenteric angiography with or without preceding radionuclide scanning or CT angiography, depending on institutional expertise, is appropriate in the small subset of patients with massive bleeding that cannot be stabilized for colonoscopy
64
Q

Malabsorption.Distal-bowel.micronutrients-lost

A

Vitamins ADEK, B12

65
Q

Malabsorption.Proximal-bowel.Micronutrients-lost

A

Iron, calcium, folate

66
Q

Microscopic-colitis.DxMethod

A

Biopsy

Colonoscopy: biopsy from both right and left colon; looks grossly normal.

67
Q

Microscopic-colitis.Rx

A
  1. Stop causal drug (eg. NSAID)
  2. Rx1: Budenoside
  3. Rx2: 5-Asa drug
  4. Cholestyramine
68
Q

Microscopic-colitis.types-and-prevalence

A
  1. Collagenous
  2. Lymphocytic

10% of chronic diarrheas

DxClue: Celiac sprue not responsive to diet

69
Q

NAFL vs NASH

A

NAFL: steatosis, no inflammation

NASH: steatosis + inflammation

that histologically is indistinguishable from alcoholic steatohepatitis

70
Q

NASH related cirrhosis: screening

A

HCC

Patients with NASH-related cirrhosis should undergo screening for hepatocellular carcinoma.

71
Q

Oral-candidiasis

Ddx

A

Oral lichen planus

72
Q

Pancreatitis+Obstructive jaundice

AST = 115 U/L (reference range, 20-48 U/L)

ALT = 108 U/L (reference range, 10-40 U/L)

Alkaline phosphatase = 688 U/L (reference range, 50-120 U/L)

Total bilirubin = 9.8 mg/dL (reference range, 0.3-1.2 mg/dL)

CT of the abdomen reveals a diffusely enlarged pancreas with a hypodense lesion at the head of the pancreas and nondilated pancreatic duct, as well as intrahepatic and extrahepatic ductal dilations. CA 19-9 concentration is 49 U/mL (reference range 0-35 U/mL). Endoscopic retrograde cholangiopancreatography reveals a long stricture of the distal common bile duct. During endoscopic ultrasonography, the 3-cm heterogenous mass at the head of the pancreas is biopsied. Pathology is negative for malignancy and demonstrates lymphoplasmacytic infiltrate.

A

IgG4 autoimmune pancreatitis

autoimmune pancreatitis (type 1) with concomitant immunoglobulin G4 (IgG4)–associated sclerosing cholangitis. Biliary strictures in IgG4-associated cholangitis are intrapancreatic, proximal extrahepatic, and/or intrahepatic. Autoimmune pancreatitis falls into the spectrum of IgG4-related disease, which has been described in virtually every organ system outside of the pancreaticobiliary system. The International Consensus Diagnostic Criteria for type 1 autoimmune pancreatitis is 5-fold: supportive radiographic findings (diffuse or “sausage-like” pancreatic fullness, with or without a pancreatic mass), elevated serum IgG4 levels (greater than 2 times the upper normal limit), consistent pancreatic histology (lymphoplasmacytic infiltrate, storiform fibrosis, >10 cells per high-power field, positive for IgG4), extrapancreatic disease (such as the proximal biliary strictures in this patient), and corticosteroid responsiveness.

73
Q

Patient with recent intra-abdominal infection+ SxSy of bowel ischemia

A

Mesenteric venous thrombosis

74
Q

Patients with cirrhosis and GI bleeding should receive prophylactic

A

ceftriaxone

75
Q

postprandial abdominal pain, weight loss, and sometimes an abdominal bruit

. It is four times more prevalent in women compared with men

A

Celiac artery compression syndrome

Recurrent abdominal pain related to compression of the celiac artery by the median arcuate ligament.

AKA Dunbar syndrome.

●A definitive diagnosis of celiac artery compression syndrome requires vascular imaging to confirm compression of the celiac artery by the median arcuate ligament (duplex ultrasound combined with advanced vascular imaging), preferably with respiratory maneuvers

76
Q

PPI: important drug interaction

A

Reduce clopidogrel efficacy

Other SideFx:

  1. Increased infections
  2. Hypomagnesemia
  3. Reduced bone density
77
Q

Roux-En-Y: Indixn

A
  1. BMI > 40
  2. BMI > 35 + serious complication such as DM2
78
Q

SBP: Ascites fluid polymorph count

A

> 250

79
Q

SBP: Rx

A

Antibiotics, albumin

80
Q

Sliding vs paraesophageal hernia

A
  1. GES status:
    1. mobile GES + stomach “slides” up is sliding up
    2. GES fixed, fundus slides past esophagus: paraesophageal.

Schematically:

Schematic diagram of different types of hiatus hernia. Green is the esophagus, red is the stomach, purple is the diaphragm, blue is the HIS-angle. A is the normal anatomy, B is a pre-stage, C is a sliding hiatal hernia, and D is a paraesophageal (rolling) type.

81
Q

Small intestine bacterial overgrowth. Test?

A

Hydrogen breath

82
Q

Transfusion threshold in upper GI bleeding

A

7

Current guidelines call for a target hemoglobin level of 7 g/dL or greater in most patients with upper gastrointestinal bleeding to lower the risk of rebleeding.

83
Q

Tropical-Sprue

A
  1. Hx: Chronic-diarrhea after tropical visit
  2. Pathology: Similar to Celiac sprue
  3. Folate deficiency
  4. Non-responsive to gluten-free diet
  5. Rx: Tetracycline, folate
84
Q

Two screening tests for SxSy cirrhosis and portal hypertension

A
  1. EGD (to look for varices).
  2. Ultrasound (to look for HCC) q6month
85
Q

Uncontrolled LGIB: why not blind segmental colonic resection?

A
  1. 75% re-bleed rate.
  2. Mortality rate: 50%
86
Q

Utility of Child-Turcott-Pugh in variceal bleeding

A

Helps predict risk of re-bleeding

The 6-week mortality with each episode: 15 to 20%,

ranging from 0% among patients with Child class A disease to approximately 30% among patients with Child class C disease.10-12

87
Q

Unexplained abnormalities in liver function, chronic liver disease, cirrhosis

●Cardiac enlargement with or without heart failure or conduction defects

●Diabetes mellitus

●Hypogonadism, with decreased libido and impotence in men

●Skin hyperpigmentation

●Unexplained fatigue

●Arthropathy, especially involving the second and third metacarpophalangeal joints

●Positive family history of iron overload

A

Suspect HH

88
Q

Active Variceal bleeding: MxStrategy

A
  1. Resuscitation,
  2. prevention and treatment of complications,
  3. treatment of bleeding
89
Q

Varices: MxStrategy

A
  1. Primary prophylaxis to prevent a first episode of variceal hemorrhage,
  2. treatment of the acute bleeding episode, and
  3. Secondary prophylaxis (prevention of recurrent variceal hemorrhage).

Rather like MI

90
Q

Varices: risk factors for bleeing

A
  1. Size
  2. Red wale marks
  3. Advanced liver disease
91
Q

What impairs endoscopic visualization of this structure?

A

Schatzki ring

Esophageal rings are most clearly identified on barium esophagram. Cannot be well visualized unless the lower esophagus is widely distended. The ring appears as a thin membrane with a concentric smooth contour that projects into the lumen.

92
Q

Which vitamin should be avoided in hereditary hemochromatosis?

A

Vitamin C

93
Q

Whipple-disease.cause

A

Tropheryma whippelii

Gram +ve bacillus

94
Q

Whipple.Dx

A

PAS-+ve macrophages, usually small bowel

95
Q

Whipple.Rx

A

Bactrim x 1 year

96
Q

Why avoid EtOH in HH?

A
  1. Increased iron absorption
  2. Red wine: high iron?!
  3. Cirrhosis
  4. HCC

Ethanol can increase iron absorption, and some red wines contain relatively high concentrations of iron [52].

●Consumption of more than 60 g of alcohol per day (the amount contained in approximately four glasses of wine or beer) was associated with a ninefold increase in the likelihood of developing cirrhosis in a cohort of 224 C282Y homozygous patients with documented iron overload [53]. The risk was increased with alcohol consumption of as little as 40 g per day.

Patients in the high alcohol intake group also had a higher incidence of hepatocellular carcinoma, and developed cirrhosis at a lower mean hepatic iron concentration and at a younger age than those with lesser alcohol consumption. A

97
Q

Screening patients with cirrhosis for hepatocellular carcinoma every _ months with ultrasonography. Lesions larger than _ cm on ultrasonography are highly suggestive of hepatocellular carcinoma, and guidelines suggest 4-phase CT or contrast-enhanced MRI.

A

Screening patients with cirrhosis for hepatocellular carcinoma every 6 months with ultrasonography. Lesions larger than 1 cm on ultrasonography are highly suggestive of hepatocellular carcinoma, and guidelines suggest performing confirmatory testing with 4-phase CT or contrast-enhanced MRI.

98
Q

Hepato-biliary: Gilbert’s

Why do patients with Gilbert’s become transiently jaundiced after acute illnesses?

A
  1. We assume that the acute illness causes hemolysis.
  2. Hemolysis will lead to bilirubin over-production.
  3. The error in Gilbert’s syndrome is an incomplete ability to conjugate bilirubin.
  4. Unconjugated bilirubin accumulates leading to the apperance of jaundice.

Gilbert’s: defect in the promotor of the gene for uridine diphosphoglucuronate-glucuronosyltransferase 1A1, which is responsible for the conjugation of bilirubin with glucuronic acid.

99
Q

Hepato-biliary: Conjugated vs Unconjugated

% of circulating bilirubin which is unconjugated

A

96%

100
Q

Hepato-biliary: Unconjugated hyperbilirubinemia:

Mechanism

Meta: Rationale

A
  1. Hemolysis leads to the production of bilirubin.
  2. In order to be excreted in bile, bilirubin needs to be made water soluble, which is achieved by conjugating it to glucuronic acid.
  3. Bilirubin overproduction exceeds the liver’s capacity to conjugate the bilirubin, causing unconjugated hyperbilirubinemia.
101
Q

Hepato-biliary: LFT interpretation:

Normal values of AST, ALT and Alkaline phosphatase

A

Less than 35

30 < [AlkPhos] < 120

102
Q
A
103
Q

Pancreas: pancreatic cyst: less than 3 cm, incidentally detected: follow up

A

MRI in one year

for cysts > 3cm or have dilated main duct or solid component: EUS FNA

For patients who do not have an indication for resection based on cross-sectional imaging alone, we pursue additional evaluation with endoscopic ultrasound with fine-needle aspiration in cysts >1.5 cm in size and for lesions with worrisome features (solid component within the cyst, main pancreatic duct >0.5 cm in size, symptoms related to the cyst, family history of pancreatic cancer).

●Many pancreatic cysts can be followed with surveillance imaging (algorithm 1).

104
Q

Radiation proctitis: Rx

A

First: sucralfate enema, Second: argon laser

105
Q

Pancreas divisum: Incidental: Rx

A

Observation

Asymptomatic patients in whom pancreas divisum is incidentally found on abdominal imaging (eg, computed tomography scan or magnetic resonance cholangiopancreatogram) and have no abnormality of the pancreas or clinical history of pancreatitis require no additional evaluation or treatment of pancreas divisum. (See ‘Asymptomatic patients’ above.)

●In patients with pancreas divisum and mild or infrequent bouts of pain, we suggest conservative management rather than treatment of the minor papilla narrowing associated with pancreas divisum (Grade 2B). (See ‘Patients with minimal/infrequent symptoms’ above.)

●Patients with pancreas divisum and recurrent pancreatobiliary-type pain, acute pancreatitis, or chronic pancreatitis associated with clinically significant disability require pancreatic imaging and an evaluation of the underlying etiology. We suggest minor papilla therapy for patients with two or more bouts of acute pancreatitis or one bout of severe acute pancreatitis if no other etiology is found and if there is evidence of dorsal duct dilation on pancreatic imaging (Grade 2B). (See ‘Patients with recurrent/severe symptoms’ above.)

●While endoscopic and surgical sphincterotomy have not been compared directly, they appear to have comparable success rates and rates of restenosis. The choice of therapy should be guided by the patients’ comorbidities, preference, and local institutional expertise. Success rates vary based on the clinical presentation and may be higher in patients with idiopathic recurrent acute pancreatitis as compared with those with chronic pancreatitis or chronic abdominal pain. (See ‘Choice of therapy’ above and ‘Surgery’ above and ‘Endoscopic therapy’ above.)

106
Q

FAP + 100 polyps: Rx

A

Colectomy

107
Q

Ulcerative colitis: Erythema nodosum: Implies

A

Increased disease activity

Consider prednisone

ABIM (36 decks)

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