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GI Flashcards

1
Q

Define cirrhosis.

A

chronic liver disease characterized by fibrosis replacing hepatocytes, disruption of the liver architecture, and widespread nodules in the liver

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2
Q

What are the downstream effects due to disruption of the normal liver architecture by cirrhosis?

A
  • decreased blood flow through the liver with subsequent hypertension in portal circulation
  • hepatocellular failure that leads to impairment of biochemical functions
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3
Q

Describe the pathogenesis of portal hypertension in those with cirrhosis.

A

fibrosis contributes to a disruption of the normal liver architecture, which reduces blood flow through the liver, leading to hypertension in portal circulation

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4
Q

What are the possible causes of cirrhosis?

A
  • alcoholic liver disease is the most common cause
  • chronic hepatitis B and C are the second
  • drugs such as acetaminophen toxicity
  • autoimmune hepatitis
  • primary or secondary biliary cirrhosis
  • hemochromatosis or Wilson’s disease
  • hepatic congestion secondary to right-sided heart failure or pericarditis
  • a1-antitrypsin deficiency
  • hepatic venoocclusive disease after bone marrow transplantation
  • nonalcoholic steatohepatitis
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5
Q

What is the gold standard for diagnosing cirrhosis?

A

liver biopsy

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6
Q

What are the classic signs of chronic liver disease?

A
  • ascites
  • varices
  • gynecomastia or testicular atrophy
  • palmar erythema and spider angiomas
  • hemorrhoids
  • caput medusa
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7
Q

What procedure is used to reduce portal hypertension?

A

trans jugular intrahepatic portal-systemic shunt (TIPS)

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8
Q

What is the most life-threatening complication of portal hypertension?

A

bleeding secondary to esophagogastric varices

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9
Q

Describe the presentation and treatment of esophagogastric varices.

A
  • clinical features include hematemesis, melon, hematochezia, and exacerbation of hepatic encephalopathy
  • prophylaxis with nonselective B-blockers
  • bleeding is best treated with hemodynamic stabilization (fluids) followed by IV antibiotics, 3-5 days of octreotide, and an emergent upper GI endoscopy
  • endoscopic ligation is preferred over endoscopic sclerotherapy
  • IV vasopressin can be a substitute for octreotide because it causes vasoconstriction of mesenteric vessels, reducing portal pressure
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10
Q

Why is endoscopic vatical ligation preferred over endoscopic sclerotherapy of esophageal varices?

A

because the rebleed rate is considerably lower in patients who receive ligation

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11
Q

What causes ascites in those with liver disease?

A

portal hypertension and hypoalbuminemia

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12
Q

Describe the clinical presentation and treatment of ascites.

A
  • presents with abdominal distention, shifting dullness, and a fluid wave
  • treated with bed rest, low-sodium diet, and diuretics
  • therapeutic paracentesis can be used for those with tense ascites, shortness of breath, or early satiety
  • followed by TIPS to relieve portal hypertension
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13
Q

What is the differential diagnosis for ascites and how can we differentiate between these causes?

A
  • the differential includes cirrhosis and portal hypertension, CHG, chronic renal disease, fluid overload, tuberculous peritonitis, malignancy, hypoalbuminemia, impaired liver inactivation of aldosterone
  • a diagnostic paracentesis is performed and the serum-ascites albumin gradient is measured
  • a difference of more than 1.1 g/dL is suggestive of portal hypertension while a difference less than that suggests another cause
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14
Q

Describe hepatic encephalopathy, including precipitating factors, clinical features, and treatment.

A
  • it is a cognitive dysfunction caused by a build up of ammonia in those with chronic liver disease
  • precipitated by alkalosis, hypokalemia, sedating drugs, GI bleeding, systemic infection, or hypovolemia
  • presents with decreased mental function, confusion, poor concentration, asterisks, rigidity and hyperreflexia, and fetter hepaticus (musty odor of breath)
  • treat with lactulose to prevent absorption of ammonia form the GI tract, rifaximin to kill bowel flora and halt ammonia production, or protein-restricted diet
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15
Q

List the complications of liver failure.

A

AC, 9H

  • ascites
  • coagulopathy
  • hypoalbuminemia
  • portal hypertension
  • hyperammonemia
  • hepatic encephalopathy
  • hepatorenal syndrome
  • hypoglycemia
  • hyperbilirubinemia/jaundice
  • hyperestrinism
  • HCC
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16
Q

Describe hepatorenal syndrome including definition, clinical features, and treatment.

A
  • it is a progressive renal failure in advanced liver disease secondary to renal hypo perfusion resulting from vasoconstriction of renal vessels
  • precipitated in many cases by infection or diuretics
  • presents with azotemia, oliguria, hyponatremia, hypotension, and low urine sodium
  • does not respond to volume expansion and liver transplantation is the only cure
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17
Q

Describe SBP including the typical agents, clinical features, method for diagnosis, and treatment.

A
  • it is an infection of the ascitic fluid, usually by E. coli, Klebsiella, or S. pneumoniae
  • usually presents as fever, change in mental status, abdominal pain, vomiting, and rebound tenderness in those with known ascites
  • diagnosed based on a paracentesis with a finding of more than 250 PMNs or 500 WBCs; very often culture negative
  • treat with broad-spectrum antibiotic therapy and improvement should be seen in 1-2 days
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18
Q

Why do those with liver failure experience hyperestrinism?

A

because they have reduced hepatic catabolism of estrogens

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19
Q

Hyperestrinism has what manifestations in those with liver failure?

A
  • spider angiomas
  • palmar erythema
  • gynecomastia
  • testicular atrophy
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20
Q

What is unique about the coagulopathy caused by liver disease? What is the preferred treatment?

A

the PT is prolonged and vitamin K is an ineffective treatment because the liver cannot utilize it; instead, patients must be given fresh frozen plasma

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21
Q

Cirrhosis

A
  • chronic liver disease characterized by fibrosis replacing hepatocytes, disrupted architecture, and widespread nodules
  • most often caused by alcoholic liver disease or chronic hepatitis B or C; other causes include autoimmune, drugs, a1-antitrypsin deficiency, right-sided heart failure
  • classic signs include ascites, varices, gynecomastia, testicular atrophy, palmar erythema, spider angiomas, hemorrhoids, caput medusa
  • complications include ascites, coagulopathy, hepatorenal syndrome, hyperestrinism, hyperammonemia, hypoalbuminemia, portal hypertension, hepatic encephalopathy, hypoglycemia, hyperbilirubinemia, and HCC
  • treat varices prophylactically with beta-blockers and symptomatically with fluids, octreotide, and endoscopy
  • use the serum-ascites albumin gradient (>1.1) to determine if it is secondary to portal hypertension and treat with sodium restriction and diuretics
  • treat hepatic encephalopathy with lactulose, rifaximin, and protein-restricted diet
  • diagnose SBP with a paracentesis showing more than 250 PMNs and treat with broad spectrum antibiotics covering E. coli, Klebsiella, and S. pneumoniae
  • treat coagulopathy with FFP
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22
Q

What is the most common type of colorectal cancer?

A

an endoluminal adenocarcinoma arising from the mucosa

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23
Q

Describe the various methods available to screen for colorectal cancer?

A
  • fecal occult blood testing has poor sensitivity and specificity, but a positive result should be followed by a colonoscopy
  • colonoscopy is the most sensitive and specific test
  • flexible sigmoidoscopy is an imaging technique that can reach the area where 50-70% of polyps and cancers arise
  • barium enema evaluates the entire colon and is often complementary to a flexible sigmoidoscopy
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24
Q

What is the most significant tumor marker for colorectal carcinoma and what is its utility?

A

CEA is not a good screening test but can be used for monitoring response to treatment and to monitor for recurrence

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25
Q

What is the most common site of metastasis for colorectal carcinoma?

A

the liver via the portal circulation

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26
Q

When does colorectal cancer screening begin?

A

typically at age 50, but if a family member has colon cancer, it should begin at age 40 or 10 years before the age of onset in that family member

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27
Q

Hyperplastic Colonic Polyps

A
  • the most common type of colonic polyp
  • they form due to hyperplasia of glands
  • have a “serrated” appearance on microscopy
  • they have no malignant potential but cannot be differentiated from adenomatous polyps on colonoscopy so are typically removed
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28
Q

Juvenile Polyps

A
  • a sporadic, hamartomatous, benign polyp
  • usually arises in children younger than 10
  • tends to prolapse and bleed because they are highly vascular, so they are typically removed
  • increase the risk for carcinoma
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29
Q

What are pseudopolyps?

A

an inflammatory colorectal polyp associated with ulcerative colitis

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30
Q

Adenomatous Colonic Polyps

A
  • a neoplastic proliferation of glands
  • benign but premalignant and may progress to adenocarcinoma via the adenoma-carcinoma sequence
  • most have tubular histology, which has a small risk of malignancy, but may be villous which carry a greater risk
  • other characteristics that increase the risk for progression are size greater than 2 cm and sessile growth
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31
Q

What is the goal of a colonoscopy?

A

to remove all adenomatous colonic polyps

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32
Q

What characteristics of an adenomatous colonic polyp increase the risk for malignant progression?

A
  • size greater than 2 cm
  • villous histology rather than tubular
  • presence of atypical cells
  • sessile architecture rather than pedunculated
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33
Q

What are the most significant risk factors for colorectal carcinoma?

A
  • age over 50
  • personal history of adenomatous polyps or prior CRC
  • inflammatory bowel disease; UC more than Crohns
  • family history of a first degree relative with CRC
  • polyposis syndromes including FAP, HNPCC, Gardner syndrome, Turcot syndrome, Peutz-Jeghers, familial juvenile polyposis coli
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34
Q

Describe the following polyposis syndromes:

  • familial adenomatous polyposis
  • hereditary nonpolyposis CRC
  • Gardner syndrome
  • Turcot syndrome
  • Peutz-Jeghers
A
  • FAP: an autosomal dominant mutation in the APC tumor suppressor which leads to the formation of hundreds of adenomatous polyps and eventually CRC
  • HNPCC: aka Lynch syndrome, it is a microsatellite instability brought on by a DNA mismatch repair enzyme defect and increases the risk of colorectal without adenomatous polyps, ovarian, and endometrial carcinoma
  • Garder syndrome: a variant of FAP characterized by polyps, osteomas, dental abnormalities, benign soft tissue tumors, demoed tumors, and sebaceous cysts
  • Turcot syndrome: a variant of FAP characterized by polyps plus cerebellar medulloblastoma or glioblastoma multiform
  • Peutz-Jeghers: an autosomal dominant condition characterized by multiple hamartomatous, benign polyps throughout the GI tract with hyperpigmentation of the lips, oral mucosa, and genital skin in addition to increased risk of gynecological and breast cancers
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35
Q

Hereditary Nonpolyposis Colorectal Carcinoma

A
  • aka Lynch syndrome, the typical example of microsatellite instability
  • an inherited mutation in a DNA mismatch repair enzyme increases the risk for colorectal, ovarian, and endometrial carcinoma
  • in such cases, colorectal carcinoma tends to arise de novo rather than from an adenomatous polyp and at a relatively early age on the right-side
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36
Q

Familial Adenomatous Polyposis

A
  • an autosomal dominant disorder characterized by 100s or 1000s of adenomatous colonic polyps
  • due to an inherited APC mutation on chromosome 5 (a tumor suppressor gene involve in the adenoma-carcinoma sequence)
  • colon and rectum are removed prophylactically; otherwise, almost all patients develop carcinoma by age 40
  • associated with CRC on the left-side of the colon
  • Gardner syndrome is a subpopulation of FAP with fibromatosis and osteomas
  • Turcot syndrome is a subpopulation of FAP with CNS tumors
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37
Q

What is Gardner syndrome?

A

a syndrome including familial adenomatous polyposis (APC mutation), fibromatosis, osteoma, dental abnormalities, demoed tumors, and sebaceous cysts

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38
Q

What is Turcot syndrome?

A

a syndrome of familial adenomatous polyposis (APC mutation) and CNS tumors like cerebellar medulloblastoma and glioblastoma multiforme

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39
Q

Peutz-Jeghers Syndrome

A
  • an autosomal dominant syndrome of multiple hamartomatous, benign polyps throughout the GI tract with hyperpigmentation of the lips, oral mucosa, and genital skin
  • increases the risk for colorectal, breast, and gynecologic cancer
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40
Q

Colorectal Carcinoma

A
  • adenoma-carcinoma sequence tends to be at work in cancer on the left and microsatellite instability on the right
  • right-sided usually grow as a raised lesion with occult blood or melena, iron-deficiency anemia, no change in bowel habits, and vague or RLQ pain
  • left-sided carcinoma tends to grow as a napkin-ring lesion with decreased stool caliber, alternating constipation/diarrhea, hematochezia, and LLQ pain
  • rectal tend to present with hematochezia, tenesmus, and a feeling of incomplete evacuation of stool
  • most commonly spreads to the liver
  • CEA is an important tumor marker, useful for assessing treatment response and detecting recurrence but not for screening
  • after surgery, surveillance typically includes annual CXR or CT for 5 years, colonoscopy at 1 year and then every 3 years, and CEA monitoring every 3-6 months
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41
Q

Compare and contrast the presentation of right-sided and left-sided colonic carcinomas.

A
  • both tend to be characterized by abdominal pain due to partial obstruction or peritoneal dissemination, weight loss, and some form of blood in the stool
  • left-sided tend to grow as napkin-ring lesions with decreased stool caliber, signs of obstruction, alternating constipation/diarrhea, and hematochezia
  • right-sided tend to present with occult blood in the stool or melena, iron deficiency anemia, weakness, and RLQ mass
  • in short, left to to obstruct while right tend to bleed
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42
Q

What is the typical presentation of rectal cancer?

A
  • hematochezia is the most common symptom
  • tenesmus
  • feeling of incomplete evacuation of stool due to the rectal mass
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43
Q

What is the typical protocol for surveillance of recurrence in those with colorectal cancer?

A
  • CXR or CT abdomen/pelvis annually for 5 years
  • colonoscopy at 1 year post-op and then every 3 years
  • CEA level every 3-6 months
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44
Q

Diverticulosis

A
  • an out pouching of mucosa and submucosa through the muscularis propria (false diverticulum)
  • risk factors are those that are related to wall stress: constipation, straining, low-fiber diet, and age
  • they arise where the vase recta transverse the muscularis propria because this is a weak point in the wall; and most often in the sigmoid colon
  • usually asymptomatic but may cause present with LLQ discomfort, bloating, constipation or diarrhea
  • diagnosed based on barium enema
  • treat with high-fiber foods or psyllium to reduce wall stress
  • may be complicated by painless renal bleeding, which usually stops spontaneously, or diverticulitis
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45
Q

Diverticulitis

A
  • due to feces becoming impacted in a diverticulum, which then causes erosion and microperforation
  • presents with LLQ pain, fever, and leukocytosis
  • may be complicated by abscess formation, colovesical fistula, obstruction due to chronic inflammation and thickening of the bowel wall, or free colonic perforation and peritonitis
  • diagnosed with CT abdomen and pelvis with oral and IV contrast, which may reveal swollen, edematous bowel wall or an abscess; note that barium enema and colonoscopy are contraindicated due to the risk of perforation
  • manage with 7-10 days of IV antibiotics, bowel rest, and IVF; resection recommended for recurrent episodes
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46
Q

How is diverticulitis diagnosed?

A

with a CT scan of the abdomen and pelvis with oral and IV contrast; barium enema and colonoscopy are contraindicated because of the risk of perforation

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47
Q

What is the typical presentation and treatment for angiodysplasia of the colon?

A

these AV malformations are a common cause of lower GI bleeding but the bleeding usually stops spontaneously and only rarely requires colonoscopies coagulation

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48
Q

What are the four primary causes of acute mesenteric ischemia and how do they differ in presentation?

A
  • embolic: symptoms are more sudden and painful
  • arterial thrombosis: symptoms are more gradual and less severe
  • nonexclusive ischemia: typically occurs in critically ill patients
  • venous thrombosis: symptoms may be present for several days or weeks with gradual worsening
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49
Q

Acute Mesenteric Ischemia

A
  • a compromised blood supply, usually involving the SMA
  • can be due to an arterial embolism (rapid onset and severe), arterial thrombosis (history of atherosclerotic disease with more gradual and less severe presentation), non-occlusive (splanchnic vasoconstriction secondary to low cardiac output seen in critically ill elderly patients), or venous thrombosis
  • presents with severe abdominal pain disproportionate to physical findings, anorexia, vomiting, mild GI bleeding
  • if bowel becomes infarcted, signs include tachypnea, lactic acidosis, fever, and altered mental status
  • may be complicated by peritonitis, sepsis, or shock
  • the diagnosis is made by mesenteric angiography; may see thumbprinting on barium enema due to thickened edematous mucosal folds
  • treat with IV fluids and broad spectrum antibiotics plus direct intra-arterial infuse of the vasodilator papaverine during arteriography for arterial causes or heparin for venous thrombosis
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50
Q

Chronic Mesenteric Ischemia

A
  • caused by atherosclerosis occlusive disease of main mesenteric vessels like the SMA
  • presents with abdominal angina characterized as a dull, typically postprandial, pain and weight loss
  • diagnosed with mesenteric arteriography
  • treated with surgical revascularization
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51
Q

Ogilvie Syndrome

A
  • a syndrome of signs, symptoms, and radiographic evidence of large bowel obstruction without mechanical obstruction
  • causes include recent surgery or trauma, serious medical illness like sepsis or malignancy, and medications like narcotics, anticholinergics, etc.
  • treat with IV fluids, electrolyte repletion, decompression with gentle enemas or NG suction
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52
Q

Pseudomembrane Colitis

A
  • aka, antibiotic-associated colitis, it is an overgrowth of C. difficile with toxin production
  • can occur with almost any antibiotic but clindamycin, ampicillin, and cephalosporins are most common
  • symptoms of profuse watery diarrhea and crampy abdominal pain usually may begin within 6 weeks of antibiotic usage
  • may be complicated by toxic megacolon with a risk for perforation
  • diagnosed based on C. difficile toxin assay and abdominal radiograph to evaluate for toxic megacolon; leukocytosis is supportive; flexible sigmoidoscopy is the most rapid test but is invasive and rarely used
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53
Q

Which antibiotics are most commonly associated with C. diff?

A

ampicillin, clindamycin, and cephalosporins

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54
Q

Colonic Volvulus

A
  • a twisting of the bowel along it’s mesentery, resulting in obstruction and vascular compromise
  • most commonly in the sigmoid colon for adult populations and in the cecum in pediatric patients
  • presents with acute onset of colicky abdominal pain, obstipation, abdominal distention, anorexia, n/v
  • sigmoidoscopy is the preferred test for sigmoid volvulus as it is both diagnostic and therapeutic
  • other tests: an omega loop sign on plain film indicates sigmoid volvulus, a coffee bean sign indicates a cecal volvulus, and a barium enema shows a bird’s beak sign at the point of twisting
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55
Q

What are the omega loop and coffee bean signs?

A
  • omega loop is a bent inner-tube shape seen on plain abdominal films indicative of sigmoid volvulus
  • coffee bean sign is a large air-fluid levels in the RLQ on plain abdominal films indicative of cecal volvulus
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56
Q

Which is more sensitive and specific of liver damage, ALT or AST?

A

ALT is more sensitive and specific

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57
Q

What is the hallmark lab finding indicative of alcoholic hepatitis?

A

an AST to ALT ratio greater than 2

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58
Q

What should low/normal, mildly, moderately, and severely elevated aminotransferases suggest to you about liver pathology?

A
  • low/normal: cirrhosis or metastatic liver disease
  • mild: think of chronic viral or acute alcoholic hepatitis
  • moderate: think acute viral hepatitis
  • severely: think extensive hepatic necrosis secondary to ischemia and shock liver, acetaminophen toxicity, or severe viral hepatitis
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59
Q

How elevated would you expect aminotransferases to be in someone with cirrhosis?

A

both cirrhosis and metastatic liver disease typically have normal or low liver transaminases because the number of healthy functioning hepatocytes i markedly reduced

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60
Q

What are possible causes of a rise in ALT or AST levels in asymptomatic patients?

A

A-I

  • Autoimmune hepatitis
  • hepatitis B
  • hepatitis C
  • Drugs or toxins
  • Ethanol
  • Fatty liver
  • Growths (tumors)
  • Hemodynamic disorders (e.g. CHF)
  • Iron (hemochromatosis), copper (Wilson disease), or AAT deficiency
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61
Q

What would cause a decrease in albumin levels?

A

chronic liver disease, nephrotic syndrome, malnutrition, and inflammatory states

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62
Q

Is the PT or PTT affected by chronic liver disease?

A

PT

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63
Q

What hepatic pathology causes an elevated alkaline phosphatase? What test should you perform to improve the specificity for hepatic pathology?

A
  • measure the gamma-glutamyl-transferase level, which should be elevated if ALK-P
  • if both are elevated, it suggests an obstruction to bile flow in some part of the biliary tree
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64
Q

What does the presence of HBsAg in an individual indicate?

A

it is the first serologic marker to rise in those with an HBV infection and it is indicative of present infection, either acute or chronic

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65
Q

What does the presence of HBeAg or HBV DNA in an individual indicate?

A
  • it is a marker of infectiousness, so it is positive during the acute phase and can be positive or negative during the chronic phase
  • it is absent in all other phases
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66
Q

What do IgM and IgG against HBc indicate in an individual being assessed for hepatitis?

A
  • IgM is seen only in the acute and window stages early in infection
  • IgG is seen in the later phases (chronic infection or resolution)
  • importantly no such antibodies are seen in individuals who have only been immunized and not exposed to HBV
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67
Q

What does the presence of antibodies to HBs indicate in an individual being assessed for hepatitis?

A

it is protective and as such, is seen in those with resolved past infection and who have been immunized

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68
Q

What is the typical presentation of Wilson disease?

A
  • liver disease including acute hepatitis, cirrhosis, and fulminant hepatic failure
  • Kayser-Fleischer rings, which don’t impact ivision
  • extrapyrmidal signs and psychiatric disturbances
  • renal involvement leading to aminoaciduria and nephrocalcinosis
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69
Q

Wilson Disease

A
  • an autosomal recessive disease of copper metabolism
  • ATP7B mutation impairs incarnation into ceruloplasmin and excretion into bile; instead, copper accumulates in the liver and leaks out as hepatocytes die
  • presents between 5-35 years old with liver disease, Kayser-Fleischer rings, extrapyramidal signs, psychiatric disturbances, hemolytic anemia, aminoaciduria, and nephrocalcinosis
  • diagnosis is made based on decreased serum ceruloplasmin levels and a liver biopsy which demonstrates elevated copper concentration
  • treat with d-penicillamine which removes removes excess copper and with zinc which prevents uptake of dietary copper
70
Q

Hemochromatosis

A
  • an autosomal recessive defect in iron metabolism
  • excessive iron absorption from the intestine leads to accumulation in the liver, pancreas, heart, joints, skin, etc. and eventually leads to fibrosis secondary to hydroxyl free radical formation
  • presents after age 40 with signs of liver disease, restrictive cardiomyopathy presenting as CHF or arrhythmias, bronze diabetes, arthritis, hypogonadism, and hypothyroidism
  • the diagnosis is made based on elevated serum iron, serum ferritin, and iron saturation; decreased TIBC, and liver biopsy showing elevated iron concentration
  • treat with repeated phlebotomies
  • HCC is a common cause of death in these patients
71
Q

Hepatocellular Adenoma

A
  • a benign liver tumor
  • risk factors are OCP use, female gender, pregnancy and anabolic steroid use as they respond to estrogen
  • presents with RUQ pain or fullness
  • has very little malignant potential but may rupture leading to hemoperitoneum and hemorrhage
  • diagnosed based on CT, ultrasound, or hepatic arteriography
  • discontinue OCP use and surgically resect tumors larger than 5 cm that do not regress after stopping
72
Q

Cavernous Hemangiomas

A
  • the most common type of benign liver tumor
  • typically small and asymptomatic, but during pregnancy or use of OCPs it may enlarge to produce RUQ pain and mass effect
  • may be complicated by rupture with hemorrhage, obstructive jaundice, coagulopathy, CHF secondary to large AV shunt, and gastric outlet obstruction
  • diagnose with a CT as biopsy is contraindicated by the risk for hemorrhage
73
Q

Hepatocellular Carcinoma

A
  • a malignant tumor of hepatocytes
  • risk factors include chronic hepatitis, cirrhosis (secondary to alcohol, nonalcoholic fatty liver disease, hemochromatosis, Wilson disease, A1AT deficiency), aflatoxin or vinyl chloride exposure, hepatic adenoma, and glycogen storage disease
  • symptoms include painful hepatomegaly, weight loss, anorexia, fatigue, portal HTN, ascites, jaundice, and splenomegaly
  • primarily complication is Budd-Chiari syndrome (liver infarction secondary to hepatic vein obstruction)
  • diagnosed based on liver biopsy
  • AFP is a useful screening tool and is helpful in monitoring the response to therapy
  • treat with resection or transplantation if possible; otherwise transcatheter arterial chemoembolization, radio frequency ablation, or selective internal radiation
74
Q

Hemobilia

A
  • refers to blood draining into the duodenum via the common bile duct from a source anywhere along the liver, biliary tract, or ampullary region
  • most often caused by trauma, surgery, tumors, or papillary thyroid carcinoma
  • presents with GI bleeding in the form of melena or hematemesis, jaundice, and RUQ pain
  • arteriogram is diagnostic or an upper GI endoscopy will show blood coming out of the ampulla of Vater
75
Q

Hydatid Liver Cyst

A
  • a liver infection with the tapeworm Echinococcus granulosus, typically in the right lobe of the liver
  • may cause RUQ and rupture into the peritoneal cavity causing fatal anaphylactic shock
  • treat with resection followed by mebendazole
76
Q

Pyogenic Liver Abscess

A
  • usually caused by a biliary tract obstruction which reduces bile flow and allows bacterial proliferation; may also be caused by a GI infection with spread via the portal venous system or by penetrating liver trauma
  • etiologic agent is usually E. coli, Klebsiella, Proteus, Enterococcus, or anaerobes
  • presents with fever, malaise, anorexia, weight loss, n/v, RUQ pain, and jaundice; they appear very ill
  • diagnosed based on elevated LFTs and an US or CT
  • treat with percutaneous drainage and IV antibiotics
77
Q

Entamoeba histolytica Infection

A
  • an amebic liver abscess
  • most common in men, particularly homosexual men
  • presents with fever, RUQ pain, n/v, hepatomegaly, and diarrhea
  • LFTs are typically elevated and serologic testing is diagnostic; stool antigen test is not very sensitive
  • treat with therapeutic aspiration and IV metronidazole
78
Q

Budd-Chiari Syndrome

A
  • liver infarction secondary to occlusion of hepatic venous outflow which leads to congestion and microvascular ischemia
  • secondary to hyper coagulable states, myeloproliferative disorders, pregnancy, hepatocellular carcinoma, chronic inflammatory states, and idiopathic
  • most cases are indolent with gradual development of hepatomegaly, ascites, RUQ pain, jaundice, and vatical bleeding
  • diagnose with a hepatic venogram; serum ascites albumin gradient more than 1.1 supports the diagnosis
  • treat with balloon angioplasty with stent placement in the IVC
79
Q

What are the three major causes of jaundice?

A
  • hemolysis
  • liver disease
  • biliary obstruction
80
Q

Describe bilirubin metabolism.

A
  • protoporphyrin is reduced to unconjugated bilirubin
  • water-insoluble UCB is transported to the liver via albumin where it is conjugated with glucuronate by uridine glucuronyl transferase (UGT) in hepatocytes
  • CB is water soluble and excreted in bile
  • in the bile gut bacteria metabolize CB to urobilinogen
  • most urobilinogen is oxidized and excreted in the feces as stercobilin, giving stool it’s brown color
  • some urobilinogen enters enterohepatic circulation and is reabsorbed
  • the rest is excreted in urine as urobilin, giving it a yellow color
81
Q

When does hyperbilirubinemia typically become evident as jaundice?

A

once total bilirubin exceeds 2 mg/dL

82
Q

What kind of hyperbilirubinemia is associated with dark urine?

A

conjugated bilirubin is water soluble so in direct hyperbilirubinemia it can be excreted in the urine, causing it to be darker

83
Q

List causes of direct hyperbilirubinemia.

A 
decreased intrahepatic excretion of bilirub
- hepatocellular disease (viral or alcoholic hepatitis, cirrhosis)
- Dubin Johnson syndrome
- primary biliary cirrhosis
- primary sclerosis cholangitis
extra hepatic biliary obstruction
- gallstones
- carcinoma of the head of the pancreas
- cholangiocarcinoma
- extrahepatic biliary atresia
84
Q

Gilbert Syndrome

A
  • an autosomal dominant condition characterized by mildly diminished UGT activity
  • results in a mild elevation of UCB during times of stress
  • not normally significant clinically but may cause mild jaundice
  • the mild version of Crigler-Najjar syndrome
85
Q

Crigler-Najjar Syndrome

A
  • the absence of UGT, which leads to extremely high levels of unconjugated bilirubin in the blood
  • often leads to Kernicterus in the early days of life
  • treatment involves plasmapheresis and phototherapy, but is usually fatal
86
Q

Dubin Johnson Syndrome

A
  • a deficiency of the bilirubin canalicular transport protein required for hepatocytes to move CB into the canaliculi
  • results in elevated conjugated bilirubin in the blood
  • the liver becomes pitch black but otherwise this is not clinically significant; it is often an incidental finding during surgery
  • Rotor syndrome is similar but lacks liver discoloration
87
Q

Obstructive Jaundice

A
  • biliary tract obstruction due to gallstones, carcinoma, parasites, or liver fluke leading to jaundice
  • the obstruction prevents conjugated bilirubin from entering the GI tract, so it leaks into the blood instead
  • urine will be dark with bilirubin rather than urobilinogen and urine urobilinogen will be low and stools pale
  • there is pruritus due to an increase in plasma bile acids, hypercholesterolemia with xanthomas, and steatorrhea with malabsorption of fat-soluble vitamins
  • labs show elevated direct (CB) bilirubin, reduced urine urobilinogen, and an increase in alkaline phosphatase
88
Q

Describe how the jaundice caused by viral hepatitis compares to other causes of jaundice.

A
  • arises because inflammation disrupts hepatocytes and small bile ductules
  • contributes to an increase in both conjugated bilirubin and unconjugated bilirubin because less bilirubin is conjugated and that which is doesn’t leave via the GI tract, instead it leaks into the blood
  • urine is dark due to an increase in urine bilirubin, but urine urobilinogen is normal or decreased
89
Q

What is a common drug that induces cholelithiasis?

A

cholestyramine because it binds bile and inhibits reabsorption, reducing the bile content of the gallbladder, reducing solubility of cholesterol and bilirubin

90
Q

Cholelithiasis

A
  • can be either cholesterol or pigmented stones
  • can be cholesterol (associated with metabolic syndrome and elevated estrogen states), brown pigmented (associated with biliary tract infection), or black pigmented (associated with hemolysis or alcoholic cirrhosis)
  • the cardinal symptom is biliary colic, pain located in the RUQ or epigastrium that is worse after eating and at night and may radiate to the right subscapula
  • may be complicated by cholecystitis with prolonged obstruction, choledocholithiasis, gallstone ileus, or malignancy
  • diagnosed with RUQ ultrasound
  • treat with elective cholecystectomy if recurrent
91
Q

What is the difference between cholesterol, brown pigmented, and black pigmented gall stones?

A
  • cholesterol tend to be yellow and are associated with obesity, diabetes, hyperlipidemia, multiple pregnancies, OCP use, and Crohn disease
  • brown pigmented stones are usually found in bile ducts and are the result of biliary tract infection
  • black pigmented stones are usually found in the gallbladder and are associated with hemolysis or alcoholic cirrhosis
92
Q

What is Boas sign?

A

referred right sub scapular pain of biliary colic

93
Q

Acute Cholecystitis

A
  • acute inflammation of the gallbladder wall secondary to obstruction of the cystic duct (not infectious)
  • presents with constant pain in the RUQ or epigastrium which may radiate to the right shoulder or scapula, nausea, vomiting, anorexia, fever, Murphy sign, and leukocytosis
  • may be complicated by perforation of the gallbladder or by cholecystoenteric fistula with gallstone ileus
  • diagnose with RUQ ultrasound that finds thickened gallbladder wall, pericholecystic fluid, distended gallbladder, and the presence of stones
  • CT is better for evaluating for the complications of acute cholecystitis and a radionuclide HIDA scan can be used when ultrasound is inconclusive
  • treat with IVF, bowel rest, IV antibiotics, analgesics, and correction of any electrolyte abnormalities; cholecystectomy is often required and should be performed in the first 24 hours
94
Q

What is Murphy’s sign?

A

inspiratory arrest during deep palpation of the RUQ in those with acute cholecystitis

95
Q

What is a HIDA test?

A
  • a radionuclide scan of the gallbladder

- a positive HIDA scan means the gallbladder is not visualized and is diagnostic for acute cholecystitis

96
Q

What are signs of a biliary tract obstruction?

A
  • elevated ALK-P and GGT
  • direct hyperbilirubinemia
  • jaudice
  • pruritus
  • clay-colored stools and dark urine
97
Q

Acalculous Cholecysitis

A
  • acute cholecystitis without stones obstructing the cystic duct
  • usually idiopathic and seen in patients with severe underlying illness
  • presents with constant pain in the RUQ or epigastrium which may radiate to the right shoulder or scapula, nausea, vomiting, anorexia, fever, Murphy sign, and leukocytosis
  • treat with emergent cholecystectomy
98
Q

Choledocholithiasis

A
  • a gallstone in the common bile duct
  • classified as primary if it originated in the CBD, and these tend to be pigmented stones, or secondary if it originated int the gallbladder an then passed into the CBD, which tend to be cholesterol or mixed stones
  • presents with RUQ or epigastric pain that may radiate to the right shoulder or subscapula, jaundice, hyperbilirubinemia, and elevated ALK-P
  • RUQ is the initial study but has low sensitivity for stones in the CBD so an ERCP may be necessary and it can be therapeutic
  • treat with ERCP with sphincterotomy and stone extraction with stent placement
99
Q

What is the difference between cholelithiasis and choledocholithiasis?

A
  • cholithiasis is a stone in the gallbladder, which tends to be asymptomatic or to present with biliary colic alone
  • choledocholithiasis is a stone in the common bile duct, which tends to present with biliary colic and obstructive jaundice
  • cholithiasis can be diagnosed by ultrasound but choledocholithiasis often requires ERCP
  • cholithiasis rarely requires treatment while choledocholithiasis requires removal via ERCP with sphincterotomy and stent placement
100
Q

What is gallstone ileum?

A

when a gallstone enters the bowel lumen via a cholecystoenteric fistula and gets stuck in the terminal ileum where it causes a small bowel obstruction

101
Q

Cholangitis

A
  • an infection of the biliary tract
102
Q

What is the difference between cholecystitis and cholangitis?

A
  • cholecystitis is an inflammation of the gallbladder wall due to cholelithiasis and resulting obstruction
  • cholangitis is an infection of the biliary tract secondary to obstruction which leads to biliary stasis and bacterial overgrowth
103
Q

Cholangitis

A
  • an infection of the biliary tract secondary to obstruction which leads to biliary stasis and bacterial overgrowth
  • usually caused by choledocholithiasis but may also be due to pancreatic or biliary neoplasm, post-op strictures, or invasive procedures like an ERCP
  • presents with Charcot’s triad of RUQ pain, jaundice, and fever or Reynolds pentad which also includes septic shock and altered mental status
  • the most significant complication is hepatic abscess
  • RUQ ultrasound is the initial study and is supported by findings of hyperbilirubinemia, leukocytosis, and mild elevation of serum transaminases
  • cholangiography should not be performed during the acute phase but should be performed after the patient has been afebrile for 48 hours to evaluate the underlying cause
  • treat with IV antibiotics and IV fluids, then decompress the CBD with PTC, ERCP, or laparotomy
104
Q

What is a porcelain gallbladder?

A

intramural calcification of the gallbladder wall, which must be treated with a prophylactic cholecystectomy as most will eventually develop cancer of the gallbladder

105
Q

Define cholecystitis, cholangitis, primary sclerosing cholangitis, and primary biliary cirrhosis.

A
  • cholecystitis: an inflammation of the gallbladder wall secondary to obstruction
  • cholangitis: an infection of the biliary tract secondary to obstruction, stasis, and bacterial overgrowth
  • primary sclerosing cholangitis: a chronic, idiopathic, progressive thickening of the intrahepatic or extrahepatic bile duct walls leading to cirrhosis
  • primary biliary cirrhosis: an autoimmune, chronic, progressive destruction of intrahepatic bile ducts with portal inflammation and scarring that may progress to cirrhosis
106
Q

Primary Sclerosing Cholangitis

A
  • a chronic, idiopathic, progressive thickening of the intrahepatic or extrahepatic bile duct walls
  • strongly associated with ulcerative colitis
  • presents with obstructive jaundice, pruritus, fatigue, malaise, and weight loss
  • may be complicated by cirrhosis, portal hypertension, and liver failure or by cholangiocarcinoma
  • ERCP or PTC is used for diagnosis and will show bead-like dilatations and strictures; cholestatic LFTs support the diagnosis
  • the only curative treatment is liver transplantation; otherwise, use ERCP with stent placement and cholestyramine for symptomatic relief
107
Q

Primary Biliary Cirrhosis

A
  • an autoimmune, chronic progressive liver disease characterized by destruction of intrahepatic bile ducts with portal inflammation and scarring
  • presents with fatigue, pruritus, jaundice, RUQ discomfort, xanthomata and xanthelasmata, osteoporosis
  • may be complicated by cirrhosis and liver failure
  • diagnose with cholestatic LFTs and positive antimitochondrial antibodies confirmed by liver biopsy; cholesterol, HDL, and IgM are all likely elevated
  • treat with cholestyramine for pruritus; calcium, vitamin D, and bisphosphanates for osteoporosis, ursodeoxycholic acid to slow progression; and transplant for cure
108
Q

What are antimitochondrial antibodies indicative of?

A

primary biliary cirrhosis

109
Q

Ulcerative colitis is strongly associated with what gallbladder pathology?

A

primary sclerosing cholangitis

110
Q

Compare and contrast primary sclerosing cholangitis with primary biliary cirrhosis.

A
  • primary sclerosing cholangitis is an intra- and extra-hepatic bile duct thickening and lumen narrowing which is more common in men, is strongly associated with UC, is diagnosed by ERCP which shows bead-like dilations, and is treated with liver transplantation
  • primary biliary cirrhosis is intrahepatic bile duct destruction, which is more common in women, has no association with IBD, is characterized by the presence of antimitochondrial antibodies, is diagnosed by liver biopsy, and is treated with ursodeoxycholic acid followed by liver transplantation
111
Q

What is secondary biliary cirrhosis?

A
  • a chronic progressive, cholestatic liver disease characterized by destruction of intrahepatic bile ducts with portal inflammation and scarring
  • secondary to long-standing mechanical obstruction, sclerosing cholangitis, cystic fibrosis, or biliary atresia
112
Q

What is the major risk factor for cholangiocarcinoma?

A

primary sclerosing cholangitis

113
Q

What are the three classifications of cholangiocarcinoma?

A

based on location

  • intrahepatic
  • proximal third of the CBD, these are most common
  • distal extrahepatic: these are most likely resectable
114
Q

Cholangiocarcinoma

A
  • an adenocarcinoma of the intrahepatic or extrahepatic bile ducts
  • classified as intrahepatic, proximal third of the CBD which are most common, or distal extrahepatic which are most likely to be resectable
  • the strongest risk factor is primary sclerosing cholangitis
  • presents with obstructive jaundice and weight loss
  • diagnosed by cholangiography
  • treat with resection if possible; otherwise, use chemotherapy, stenting, and biliary drainage
115
Q

Choledochal Cyst

A
  • a cystic dilatation of the biliary tree
  • presents with epigastric pain, jaundice, fever, and RUQ mass
  • complicated by cholangiocarcinoma, hepatic abscess, recurrent cholangitis or pancreatitis, rupture, or biliary obstruction
  • ERCP provides a definitive diagnosis but ultrasound often suffices
  • treat with surgery
116
Q

What is biliary dyskinesia and how is it diagnosed?

A
  • it is a motor dysfunction of the sphincter of Oddi which leads to recurrent episodes of biliary colic without evidence of gallstones
  • the diagnosis is made by a HIDA scan in which the radionuclide is followed by IV CCK; this will demonstrate a diminished ejection fraction from the gallbladder
  • treat with laparoscopic cholecystectomy and endoscopic sphincterotomy
117
Q

Acute Appendicitis

A
  • caused by an obstruction of the appendix by hyperplasia of lymphoid tissue, a fecalith, or foreign body
  • this obstruction can ultimately cause distention followed by ischemia, infarction, necrosis, perforation, and peritonitis
  • presents with sharp abdominal pain that migrates from the epigastrium toward McBurney’s point, anorexia, n/v, rebound, guarding, fever, Rovsing sign, Psoas sign, and obturator sign
  • a clinical diagnosis that can be supported by CT or US
  • treat with laparoscopic appendectomy
118
Q

Describe the rovsing, psoas, and obturator signs of appendicitis.

A
  • rovsing: deep palpation of the LLQ causes referred pain in the RLQ
  • psoas: RLQ pain when the right thigh is extended as the patient lies on the left side
  • obturator: pain in the RLQ when flexed right thigh is internally rotated when patient is supine
119
Q

What is a carcinoid tumor?

A
  • a malignant proliferation of neuroendocrine cells, which often secrete serotonin
  • secreted serotonin is metabolized by liver MAO into 5-HIAA, so they are asymptomatic until they metastasize to the liver
  • once metastasized they produce carcinoid syndrome (including bronchospasm, diarrhea, and flushing of the skin) and carcinoid heart disease (right-sided valvular fibrosis leading to tricupsid regurgitation and pulmonary valve stenosis)
  • contain neurosecretory granules and are thus chromogranin positive; 5-HIAA levels are elevated in urine
120
Q

Acute Pancreatitis

A
  • inflammation and hemorrhage of the pancreas due to premature activation of trypsin and autodigestion
  • most commonly due to (“I GET SMASH”): idiopathic, gallstones, ethanol, trauma, scorpion stings, mumps/malignancy, autoimmune, steroids, hyperlipidemia/hypercalcemia or rupture of a posterior duodenal ulcer
  • presents with steady, dull, epigastric pain radiating to the back; n/v; low grade fever, tachycardia, hypotension, and leukocytosis
  • hemorrhagic pancreatitis is indicated by blood tracking along fascial planes: grey turner sign (flank ecchymoses), cullen sign (periumbilical ecchymoses), and fox sign (inguinal ligament ecchymosis)
  • CT is the most accurate test; serum lipase and amylase are elevated, LFTs may be elevated if caused by a gallstone, hyperglycemia, leukocytosis, hypoxemia, hypocalcemia
  • complications include shock, pancreatic pseudocyst, pancreatic abscess formation, or DIC/ARDS (enzymes enter blood)
  • treat with bowel rest, IVF, and pain control (don’t use morphine as this increases sphincter of Oddi tone)
121
Q

Chronic Pancreatitis

A
  • a persistent inflammation of the pancreas with fibroses and alterations of pancreatic ducts, which impairs both exocrine and endocrine functioning
  • the most common cause is chronic alcoholism
  • presents with severe epigastric pain radiating to the back exacerbated by alcohol or eating and accompanied by n/v, weight loss, steatorrhea, and diabetes
  • chronic epigastric pain and calcifications on CT is diagnostic; notably, serum amylase and lipase aren’t elevated
  • treat with analgesics, bowel rest, pancreatic enzymes given with H2 blockers, insulin, alcohol abstinence, and frequent small-volume low-fat meals
122
Q

Why are pancreatic enzymes with H2 blockers given to those with pancreatitis?

A

the enzymes inhibit CCK release, which rests the pancreas, and the H2 blockers inhibit gastric acid secretion to prevent the degradation of the pancreatic enzymes

123
Q

How does pancreatic carcinoma in the head/neck differ from that arising in the body/tail?

A
  • in the head, you’re more likely to have obstructive jaundice with pale stools and a palpable gallbladder
  • in the tail, you’re more likely to have very late secondary diabetes without obesity
124
Q

Pancreatic Adenocarcinoma

A
  • an adenocarcinoma arising from the pancreatic ducts
  • risk factors include smoking and chronic pancreatitis
  • presents with epigastric abdominal pain, weight loss, obstructive jaundice with pale stools and palpable gall bladder (when arising in the head of the pancreas), secondary diabetes mellitus (when arising in the body or tail), pancreatitis and migratory thrombophlebitis
  • ERCP is the most sensitive test but CT is preferred
  • CA 19-9 is a better tumor marker than CEA
  • requires resection but PTC or ERCP with stent placement can be palliative
125
Q

What is an aortoenteric fistula?

A

a rare cause of GI bleeding in patients with a history of aortic graft surgery two have a small GI bleed of the duodenum before a massive, fatal hemorrhage hours to weeks later

126
Q

How do we define upper and lower GI bleeding?

A

the dividing line is the ligament of Treitz in the duodenum

127
Q

What are the most common causes of upper and lower GI bleeding?

A 
upper:
- PUD
- reflux esophagitis
- esophageal and gastric varices
- Mallory-Weiss tear
- hemobilia
- aortoenteric fistula
- neoplasma
- AV malformations
lower:
- diverticulosis and angiodysplasia make up most cases
- IBD, CRC, adenomatous polyps, hemorrhoids, and anal fissures make up most other causes
128
Q

What does coffee ground emesis suggest?

A

it suggests an upper GI bleed with a slow rate of bleeding

129
Q

What is melena?

A

black, tarry, liquid, foul-smelling stool caused by the degradation of hemoglobin by colonic bacteria and suggestive of an upper GI bleed

130
Q

What signs of GI bleeding suggest an upper GI bleed and which suggest a lower GI bleed?

A
  • hematemesis, coffee ground emesis, and melena suggest an upper GI bleed
  • hematochezia suggests a lower GI bleed (or a very briskly bleeding upper GI bleed)
  • occult blood can be from anywhere along the GI tract
131
Q

Why is the BUN/Cr ratio important when evaluating a GI bleed?

A

it can help you localize the bleed because an elevated ratio is suggestive of an upper GI bleed

132
Q

If you suspect a lower GI bleed, what should your first step be?

A

to exclude an upper GI bleed

133
Q

What is the most accurate diagnostic test to evaluate an upper GI bleed? What is often the initial test?

A
  • the most accurate, and possibly therapeutic, is an upper endoscopy
  • NG tube placement is often the initial procedure, however, because you can quickly evaluate the aspirate to distinguish an upper from a lower GI bleed
134
Q

What tests should be order in patients with the following:

  • hematemesis
  • hematochezia
  • melena
  • occult blood
A
  • hematemesis: an upper endoscopy
  • hematochezia: rule out an anorectal cause with DRE then perform a colonoscopy
  • melena: an upper endoscopy first followed by a colonoscopy if no source is found
  • occult blood: colonoscopy first followed by an upper endoscopy if no source is found
135
Q

What are the indications for surgery in those with a GI bleed?

A
  • hemodynamic instability that hasn’t responded to treatment or who have an ongoing transfusion requirement beyond 5 units in the first 4-6 hours
  • severe initial or recurrent bleeding
  • bleeding for more than 24 hours
  • an ulcer with a visible vessel at the base
136
Q

Achalasia

A
  • an acquired motor disorder characterized by an inability of the LES to completely relax and by abnormal peristalsis
  • most cases are idiopathic and result from damage to ganglion cells in the myenteric plexus; adenocarcinoma of the proximal stomach and Chagas disease are possible causes
  • presents with dysphagia equal for solids and liquids (patient may twist their body, extend their neck, or walk around to force food into the stomach), regurgitation, chest pain, weight loss, recurrent pulmonary complications, and putrid breath
  • barium swallow shows the bird’s beak sign and manometry confirms the diagnosis
  • treatment options include antimuscarinic agents, sublingual nitroglycerin, long-acting nitrates, and CCBs; injection of botulinum toxin into the LES; forceful dilation with pneumatic balloon; or Heller myotomy
137
Q

Esophageal Cancer

A
  • either adenocarcinoma (more common in the West) or squamous cell carcinoma (more common worldwide)
  • adenocarcinoma refers to a proliferation of glands, and arises from pre-existing Barrett esophagus in the lower third of the esophagus
  • squamous cell carcinoma arises in the upper and middle thirds of the esophagus in response to irritation; risk factors include alcohol, tobacco, very hot tea, achalasia, esophageal web, and esophageal injury
  • both present late and thus have a poor prognosis
  • symptoms include progressive dysphagia (solids then liquids), weight loss, anorexia, pain, and hematemesis
  • squamous cell often presents with hoarse voice and cough as well due to involvement of the recurrent laryngeal nerve and trachea, respectively
  • diagnose with barium swallow followed by an upper endoscopy with biopsy and brush cytology; a transesophageal ultrasound helps determine the depth of penetration for staging
138
Q

What is the difference between adenocarcinoma and squamous cell carcinoma of the esophagus?

A
  • either adenocarcinoma (more common in the West) or squamous cell carcinoma (more common worldwide)
  • adenocarcinoma refers to a proliferation of glands, and arises from pre-existing Barrett esophagus in the lower third of the esophagus
  • squamous cell carcinoma arises in the upper and middle thirds of the esophagus in response to irritation; risk factors include alcohol, tobacco, very hot tea, achalasia, esophageal web, and esophageal injury
  • they share many symptoms like dysphagia and odynophagia but SCC is also more likely to involve the recurrent laryngeal nerve and trachea leading to hoarseness and cough
139
Q

Diffuse Esophageal Spasm

A
  • a non-peristaltic, spontaneous contraction of the esophageal body with normal sphincter function
  • presents with non cardiac chest pain that may mimic angina and may even radiate to the jaw, arms, or back along with dysphagia but regurgitation is rare
  • upper GI barium swallow will show a corkscrew esophagus and esophageal manometry is diagnostic
  • treat with nitrates and calcium channel blockers
140
Q

Esophageal Hernias

A
  • can be either a sliding hiatal hernia or a paraesophageal hiatal hernia depending on whether the gastroesophageal junction herniates or not
  • presents with heartburn, chest pain, and dysphagia
  • sliding may be complicated by GERD, reflux esophagitis, and aspiration; paraesophageal may be complicated by obstruction, hemorrhage, or strangulation
  • diagnose with barium upper GI series and upper endoscopy
  • treat sliding medically with antacids, small meals, and elevation of the head after meals; treat paraesophageal surgically
141
Q

Mallory-Weiss Syndrome

A
  • a longitudinal laceration of the mucosa at the gastroesophageal junction caused by severe vomiting
  • most often seen in alcoholics and bulimics
  • presents with painful hematemsis
  • diagnose with upper endoscopy
  • risk of Boerhaave syndrome with rupture of esophagus leading to air in the mediastinum and subcutaneous emphysema
  • rarely requires surgery to stop the bleeding but acid suppression is used after to promote healing
142
Q

What is the difference between Mallory-Weiss and Boerhaave syndrome?

A

Mallory-Weiss is a tear of the esophageal mucosa while Boerhaave is a rupture of the entire wall

143
Q

Plummer-Vinson Syndrome

A
  • a syndrome of upper esophageal web, iron deficiency anemia, koilonychia, and atrophic oral mucosa
  • considered a premalignant lesions for squamous cell carcinoma of the esophagus
  • treat with esophageal dilatation and correct any nutritional deficiencies
144
Q

Schatzki Ring

A
  • a circumferential ring (i.e. web) in the lower esophagus that is accompanied by a sliding hiatal hernia
  • usually due to ingestion of alkali, acids, bleach, or detergents in a suicide attempt
  • may cause dysphagia or stricture formation and increases the risk for esophageal cancer
145
Q

Zenker Diverticulum

A
  • a false pharyngoesophageal diverticulum
  • caused by failure of the cricopharyngeal muscle to relax during swallowing, which increases intraluminal pressure and causes an out pouching of mucosa through Killian triangle between the tyropharyngeal and cricopharyngeal parts of the inferior pharyngeal constrictor
  • results in dysphagia, obstruction, gurgling, aspiration, foul breath, and a neck mass
146
Q

What is a traction diverticula?

A
  • an esophageal diverticula located in the midpoint of the esophagus near the tracheal bifurcation
  • caused by traction from contagious mediastinal inflammation and adenopathy in the case of pulmonary TB
147
Q

What is a epiphrenic diverticula?

A

an esophageal diverticula found in the lower third of the esophagus associated with spastic esophageal dysmotility or achalasia

148
Q

What is the most important prognostic factor in those with esophageal perforation?

A

the amount of time between perforation and surgery (should be less than 24 hours)

149
Q

Esophageal Perforation

A
  • caused by blunt trauma, forceful vomiting, mechanical tubes or instruments
  • presents with severe retrosternal pain, tachycardia, hypotension, tachypnea, dyspnea, fever, and a mediastinal crunch produced by the heart beating against air-filled tissues
  • diagnose with contrast esophagram; a CXR usually shows air in the mediastinum
  • IVF, NPO, antibiotics, and H2 blockers may suffice in stable patients with small perforations, otherwise surgery should be performed within 24 hours
150
Q

What are the three most common causes of peptic ulcer disease?

A

H. pylori infection, chronic NSAID use, and acid hypersecretory states such as Zollinger-Ellison syndrome

151
Q

Gastric Ulcer

A
  • a solitary mucosal ulcer, most often in the lesser curvature of the antrum
  • less common than a duodenal ulcer
  • usually due to H. pylori but may also be caused by use of NSAIDs or bile reflux
  • presents with epigastric pain that worsens with meals because acid production increases
  • rupture carries a risk of bleeding from the left gastric artery
  • can be caused by intestinal type gastric carcinoma, in which case they tend to be larger and irregular with heaped up margins
152
Q

Duodenal Ulcer

A
  • a solitary mucosal ulcer
  • more common than a gastric ulcer
  • most cases are due to H. pylori but a few are due to a gastrinoma (ZE syndrome)
  • presents with epigastric pain that improves with meals since the duodenum preps for the meal by increasing protective measures
  • diagnose using endoscopic biopsy, which shows hypertrophy of Brunner glands
  • anterior wall is more commonly affected but in the posterior duodenal, rupture is more likely
  • rupture leads to hemorrhage of the gastroduodenal artery or acute pancreatitis and you may see free air under the diaphragm with referred pain to the shoulder via the phrenic nerve
  • almost never malignant (in contrast to gastric ulcers)
153
Q

How does a duodenal ulcer compare to a gastric ulcer?

A
  • duodenal are more common
  • duodenal are more often caused by H. pylori
  • both present with epigastric pain but that associated with duodenal ulcers gets better with meals and that associated with gastric ulcers get worse with meals
  • rupture of a duodenal ulcer is likely to cause bleeding of the gastroduodenal artery while rupture of a gastric ulcer is likely to cause bleeding of the left gastric artery
  • duodenal ulcers are almost never malignant but gastric ulcers can be caused by intestinal type gastric carcinoma
154
Q

What does triple and quadruple therapy consist of for H. pylori and when should each be used?

A
  • triple therapy includes a PPI, amoxicillin, and clarithromycin to be used for initial therapy
  • quad therapy includes a PPI, bismuth subsalicylate, metronidazole, and tetracycline to be used for retreatment
155
Q

What roles do sucralfate and misoprostol play in the treatment of peptic ulcer disease?

A
  • sucralfate facilitate ulcer healing but must be taken frequently, is costly, and can cause GI upset
  • misoprostol reduces the risk for ulcer formation associated with NSAID therapy but has the same disadvantages
156
Q

Acute Gastritis

A
  • acidic damage to the stomach mucosa due to an imbalance between acidity and mucosal defenses
  • risk factors include: severe burn (hypovolemia leads to decreased blood supply), NSAIDs (reduced prostaglandin production), heavy alcohol consumption, chemotherapy, increased intracranial pressure (stimulates vagus leading to acid production), and shock (reduced blood flow)
  • the result is superficial inflammation, erosion, or ulcer
  • presents with epigastric pain
  • treat with acid suppression and cessation of NSAIDs; consider upper GI endoscopy, ultrasound to rule out gallstones, and H. pylori test if symptoms don’t resolve in 4-8 weeks of treatment
157
Q

Chronic H. pylori Gastritis

A
  • more common than chronic autoimmune gastritis
  • H. pylori ureases and proteases weaken mucosal defenses, particularly in the antrum, and contribute to mucosal inflammation
  • presents with epigastric abdominal pain
  • increases risk for ulceration, intestinal type gastric adenocarcinoma, and MALT lymphoma
  • treat with triply therapy (PPI, amoxicillin/metronidazole, and clarithromycin)
  • confirm eradiaction with negative urea breath test and lack of stool antigen
  • treatment resolves ulcers and reverses intestinal metaplasia
158
Q

Intestinal Type Gastric Carcinoma

A
  • an adenocarcinoma
  • presents as a large, irregular ulcer with heaped up margins, most often in the lesser curvature of the antrum
  • risk factors include intestinal metaplasia (with goblet cells) due to chronic gastritis, nitrosamines in smoked foods, and type A blood group
  • symptoms arise late with weight loss, abdominal pain, anemia, and early satiety
  • may present with acanthosis nigricans or Leser-Trelat sign
  • spread is to the left supraclavicular node known as Virchow’s node
  • most likely to metastasize to the liver but may metastasize to the periumbilical region, known as a Sister Mary Joseph nodule
159
Q

Diffuse Type Gastric Carcinoma

A
  • an adenocarcinoma
  • characterized by signet ring cells that diffusely infiltrate the gastric wall along with desmoplasia that results in thickening of the stomach wall known as linitis plastica
  • not associated with H. pylori, intestinal metaplasia, or nitrosamines
  • symptoms arise late and include weight loss, abdominal pain, anemia, and early satiety
  • may present with acanthosis nigricans or Leser-Trelat sign
  • spread is to the left supraclavicular node known as Virchow’s node
  • most likely to metastasize to the liver but may metastasize to the ovaries bilaterally, which is known as a Krukenburg tumor
160
Q

What is a Blumer’s shelf?

A

metastatic gastric carcinoma to the pelvic cut-de-sac, which can be palpated on rectal exam

161
Q

What is a Sister Mary Joseph node?

A

metastatic gastric carcinoma to the periumbilical lymph node

162
Q

What is Virchow’s node?

A

metastatic gastric carcinoma to the supraclavicular fossa nodes

163
Q

What is an irish node?

A

metastatic gastric carcinoma to the left axillary adenopathy

164
Q

Small Bowel Obstruction

A
  • can be classified as partial vs. complete, closed vs. open loop, and proximal vs. distal
  • obstruction may be due to adhesion, incarcerated hernia, malignancy, intussusception, Crohn disease, SMA syndrome
  • obstruction leads to distention, causing reflex vomiting, increased intestinal secretion proximal to the point of obstruction, and decreased absorption; this contributes to a hypochloremic, hypokalemic, metabolic alkalosis and dehdyration
  • presents with cramping abdominal pain, nausea, vomiting that may be feculent, obstipation, and abdominal distention
  • abdominal films show dilated loops of small bowel, air-fluid levels proximal to the point of obstruction, and minimal gas in the colon; barium enema can diagnose colonic obstruction; and an upper GI series may be necessary if those are inconclusive
  • treat with fluids, potassium, gastric decompression, antibiotics, and surgery if indicated
165
Q

What is a closed loop small bowel obstruction?

A

one in which the lumen is occluded at two points by an adhesive band or hernia ring

166
Q

What is different about the clinical presentation of a proximal small bowel obstruction compared to a distal one?

A
  • proximal present with frequent vomiting, severe pain, and minimal abdominal distention
  • distal present with less vomiting and greater abdominal distention
167
Q

Paralytic Ileus

A
  • a decrease or absence of peristalsis without mechanical obstruction
  • may be due to medications including narcotics and anticholinergics, a post-operative state, spinal cord injury, shock, metabolic disorder, or peritonitis
  • abdominal films show a uniform distribution of gas in the small bowel, colon, and rectum
  • treat with IVF, NPO, correction of electrolytes, and NG suction
168
Q

Celiac Disease

A
  • a CD4 mediated damage of the small bowel villi due to gluten exposure, and in particular the component gliadin
  • strongly associated with HLA-DQ2 and HLA-DQ8
  • presents in children with abdominal distention, diarrhea, and failure to thrive or in adults with chronic diarrhea and bloating
  • fat malabsorption may contribute to vitamin D deficiency and osteoporosis, vitamin K deficiency and easy bleeding, and B12/folate deficiency and megaloblastic anemia
  • small, herpes-like vesicles may arise on the skin, known as dermatitis herpetiformis, due to IgA deposition at the tips of dermal papillae
  • associated with IgA deficiency but labs find IgA or IgG against endomysium, tTG, or gliadin
  • biopsy reveals flattened villi, hyperplasia of crypts, and increased intraepithelial lymphocytes in the duodenum
  • small bowel carcinoma and T-cell lymphoma are late complications that often presents as refractory disease despite good dietary control
169
Q

Whipple Disease

A
  • systemic tissue damaged characterized by macrophages loaded with partially destroyed Tropheryma whippelii in lysosomes
  • most often affects the small bowel propria in which case macrophages compress lacteals, preventing the absorption of chylomicrons and contributing to fat malabsorption and steatorrhea
  • presents with weight loss, diarrhea, joint pain, arthritis
  • organism is intracellular gram positive and stains PAS positive in foamy macrophages
  • requiers 1-2 years of antibiotic therapy
170
Q

Tropical Sprue

A
  • damage to small bowel villi due to an unknown organism found in tropical regions, causing malabsorption
  • arises after infectious diarrhea and responds to antibiotics plus folic acid
  • damage is most prominent in the jejunum and ileum
171
Q

Crohn Disease

A
  • a form of inflammatory bowel disease mediated by Th1
  • affects the full thickness of the wall, forming knife-like fissures
  • can affect anywhere in the GI tract with skip lesions, but the terminal ileum is most common and colon is least
  • presents with right lower quadrant pain, non-bloody diarrhea, malabsorption and weight loss, n/v, fever, erythema nodosum, and arthritis
  • complications include fistulae, anorectal disease, small bowel obstruction, cholelithiasis, calcium oxalate nephrolithiasis, growth retardation, and aphthous ulcers
  • grossly, there is cobblestoning of the mucosa, creeping fat, and stricture as healing involves myofibroblasts
  • histology reveals noncaseating granulomas and lymphoid aggregates
  • treat with sulfasalazine, which is converted to 5-ASA and blocks prostaglandin release; metronidazole, systemic corticosteroids, azathioprine, bile acid sequestrates cholestyramine or colestipol, infliximab, or adalimumab
172
Q

Ulcerative Colitis

A
  • a form of inflammatory bowel disease mediated by Th2
  • affects the mucosal and submucosa only, forming ulcers
  • begins in the rectum and extends proximally in a continuous manner, limited to the colon
  • presents with hematochezia, LLQ pain, frequent but small bowel movements, and tenesmus
  • may be complicated by iron deficiency anemia, strictures, colorectal cancer, primary sclerosing cholangitis, cholangiocarcinoma, toxic megacolon and perforation, pyoderma gangrenous, and ankylosing spondylitis
  • grossly, there are pseudopolyps and a loss of haustra, known as the “lead pipe” sign
  • histology reveals crypt abscesses with neutrophils
  • sulfasalazine, which is converted to 5-ASA and blocks prostaglandin release, is the mainstay of treatment with systemic corticosteroids for acute exacerbations
  • colectomy is curative

IM (13 decks)

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