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93 Cards in this Set

  • Front
  • Back
Virtually all colorectal tumors arise from [what type of benign tumor].
adenomas. The majority of endoluminal adenocarcinomas arise from the mucosa. p114
Colon cancer screening begins at age _____. If one fmaily member has colon cancer begin at age ____ or ___ years before age of onset of family member.
50; 40; 10
p114
What is the most sensitive and specific test for colorectal cancer screening?
A. fecal occult blood testing
B. digital rectal examination
C. colonoscopy
D. flexible sigmoidoscopy
E. barium enema
F. Carcinoembryonic antigen (CEA)
C. colonoscopy!

CEA is NOT useful for screening but is useful for baseline and recurrence surveillance. And it does have prognostic significance: Patients with preop CEA > 5 ng/mL have a worse prognosis overall.
p114
What is the most common site of distant spread hematogenously of colorectal cancer?
liver since portal circulation to the liver is next in line! Also common is lumbar /vertebral veins to lungs. Other patterns of spread are direct extension (circumferentially and then thru the bowel wall to later invade other abdominoperineal organs) and lymphatic, and transperitoneal and intraluminal.
p114
Inflammatory bowel disease (both ulcerative colitis and Crohn's dz) pose an increased risk for colorectal cancer but which poses more of a risk?
UC poses > risk than Crohn's dz.
p115
What kind of dietary factors increase risk of colorectal cancer?
high fat, low-fiber diets are associated with higher risk of CRC
p115
Which major polyposis syndrome is described:
Autosomal dominant dz characterized by hundreds of adenomatous polyps in the colon. Colon is always involved and the duodenum is involved in 90% of the cases. Polyps can also form in the stomach, jejunum, and ileum. Risk of CRC is 100% by third or fourth decade of life. Prophylactic colectomy is usually recommended.

A. Familial adenomatous polyposis
B. Gardner's syndrome
C. Turcot's syndrome
D. Peutz-Jeghers
E. Familial juvenile polyposis coli
F. Hereditary nonpolyposis CRC- Lynch syndrome I
G. Hereditary nonpolyposis CRC- Lynch syndrome II
A. Familial adenomatous polyposis
p115
Which major polyposis syndrome is described:
Polyps plus osteomas (boney outgrowths), dental abnormalities, benign soft tissue tumors, desmoid tumors (rare fibrous aggressive tumors) and sebaceous cysts. Risk of colorectal cancer is 100% by age 40.

A. Familial adenomatous polyposis
B. Gardner's syndrome
C. Turcot's syndrome
D. Peutz-Jeghers
E. Familial juvenile polyposis coli
F. Hereditary nonpolyposis CRC- Lynch syndrome I
G. Hereditary nonpolyposis CRC- Lynch syndrome II
B. Gardner's syndrome
p115
Which major polyposis syndrome is described:
Autosomal recessive. Polyps plus cerebellar medulloblastoma or glioblastoma multiforme.

A. Familial adenomatous polyposis
B. Gardner's syndrome
C. Turcot's syndrome
D. Peutz-Jeghers
E. Familial juvenile polyposis coli
F. Hereditary nonpolyposis CRC- Lynch syndrome I
G. Hereditary nonpolyposis CRC- Lynch syndrome II
C. Turcot's syndrome
p115
Which major polyposis syndrome is described:
Single or multiple hamartomas that are scattered thru entire GI tract. Pigmented spots around lips ,oral mucosa, face, genitalia and palmar surfaces. Unlike adenomas, hamartomas have very low malignant potential. Intussusception of GI bleeding can occur though.

A. Familial adenomatous polyposis
B. Gardner's syndrome
C. Turcot's syndrome
D. Peutz-Jeghers
E. Familial juvenile polyposis coli
F. Hereditary nonpolyposis CRC- Lynch syndrome I
G. Hereditary nonpolyposis CRC- Lynch syndrome II
D. Peutz-Jeghers
p115
Which major polyposis syndrome is described:
Without adenamtous polposis, early onset colorectal cancer; absence of antecedent multiple polyposis
A. Familial adenomatous polyposis
B. Gardner's syndrome
C. Turcot's syndrome
D. Peutz-Jeghers
E. Familial juvenile polyposis coli
F. Hereditary nonpolyposis CRC- Lynch syndrome I
G.Hereditary nonpolyposis CRC- Lynch syndrome II
F. Hereditary nonpolyposis CRC- Lynch syndrome I
p115
Which major polyposis syndrome is described:
without adenomatous polyposis. Early onset of colorectal cancer; absence of antecedent mulitple polyposis plus increased number and early occurence of other cancers (female genital tract, skin, stomach, pancreas, brain, breast, biliary, etc.)

A. Familial adenomatous polyposis
B. Gardner's syndrome
C. Turcot's syndrome
D. Peutz0Jeghers
E. Familial juvenile polyposis coli
F. Hereditary nonpolyposis CRC- Lynch syndrome I
G. Hereditary nonpolyposis CRC- Lynch syndrome II
G. Hereditary nonpolyposis CRC- Lynch syndrome II
p115
What are some common symptoms of colorectal cancer?
melena (black tarry feces), hematochezia (fresh blood in stool), abdominal pain, change in bowel habits, or unexplained iron deficiency anemia are common. As is weight loss.

CRC is the most common cause of large bowel obstruction in adults.
p115
___________ is the most common cause of large bowel obstruction in adults.

A. Colonic polyps
B. Colorectal cancer
C. Diverticulosis
D. Pseudomembranous colitis
B. Colorectal cancer
p115
Colorectal cancer signs and symptoms might be based on specific location of the tumor! For example, obstruction on [ left / right ] side is unusual because of the larger luminal diameter, allowing for large tumor growth to go undetected. Instead, the triad of anemia, weakness and mass at site can be present. On the other hand, the [ left / right ] side has a small luminal diameter so signs of obstruction are more common as are change in bowel habits and hematochezia.
RIGHT SIDE: larger luminal diameter, allows for large tumor growth to go undetected. Anemia, weakness and mass at site can be present.

LEFT SIDE: small luminal diameter so signs of obstruction are more common as are changes in bowel habits and hematochezia.
p116
True or False:
Radiation therapy is indicated in rectal cancer treatment but not colon cancer treatment.
Vrai
p116
Which liver function test is more sensitive nad specific for liver damage: ALT or AST?
ALT!

The two usually have a similar increase though in alcoholic hepatitis, AST-ALT ratio can be 2+:1!

If ALT:AST mildly elevated (low hundreds), think of chronic viral hepatitis or acute alcoholic hepatitis.
If moderately elevated (high hundreds to thousands), think acute viral hepatitis.
If severely elevated (>10k), extensive hepatic necrosis has occurred such as ischemia, liver shock due to prolonged hypotension or circulatory collapse, acetaminophen toxicity, severe viral hepatitis.

Note that liver transaminases are often nromal or even lw in patients with cirrhosis or metastatic liver dz b/c the # of healthy functioning hepatocytes is markedly reduced.
p132
If ALT: AST is mildly elevated [what would that be numerically?], think of chronic viral hepatitis or acute alcoholic hepatitis.

If moderately elevated [what would that number be?], think acute viral hepatitis.

If severely elevated [what would that number be?], extensive hepatic necrosis has occurred such as ischemia, liver shock due to prolonged hypotension or circulatory collapse, acetaminophen toxicity, severe viral hepatitis.
If ALT: AST is mildly elevated (low hundreds), think of chronic viral hepatitis or acute alcoholic hepatitis.
If moderately elevated (high hundreds to thousands), think acute viral hepatitis.
p132

If severely elevated (>10k), extensive hepatic necrosis has occurred such as ischemia, liver shock due to prolonged hypotension or circulatory collapse, acetaminophen toxicity, severe viral hepatitis.

Note that liver transaminases are often normal or even low in patients with cirrhosis or metastatic liver dz b/c the # of healthy functioning hepatocytes is markedly reduced.

p132
Alkaline phosphatase is NOT specific to the liver but is also found in what other places? (3) So when is it elevated?
bone, gut and placenta

So is elevated when there is obstruction to the bile flow (ex. cholestasis) in any part of the biliary tree. If levels are elevated, measure the GGT (Gamma glutamyl transferase) level to ensure the elevation is hepatic in origin (rather than bone or intestinal). If the GGT is elevated, this strongly suggests a hepatic origin.
p.132
Alkaline phosphatase elevation can be due to other things besides liver dysfunction. What other lab value can be measured such that if both Alk phos and this other lab value are elevated, then hepatic origin is strongly suggested as supposed to if the other level is normal but ALK-P is elevated, then consider bone disease.
The other lab value to measure is GGT, or gamma glutamyl transferase
p133
True or False:
Prothrombin time is not prolonged until most of the liver's synthetic capacity is lost, which corresponds to advanced liver disease.
TRUE
p133
There are three types of gallstones: cholesterol stones, pigment stones, mixed stones. Which are associated with
A. hemolysis
B. alcoholic cirrhosis
C. obesity
D. diabetes
E. hyperlipidemia
F. biliary tract infection
A. hemolysis - pigment stones (black)
B. alcoholic cirrhosis- pigment stones (black)
C. obesity - cholesterol stones (yellow or green)
D. diabetes - cholesterol stones (yellow or green)
E. hyperlipidemia - cholesterol stones (yellow or green)
F. biliary tract infection - pigment stones (brown)
p132
There are three types of gallstones: cholesterol stones, pigment stones, mixed stones. Which accounts for the majority of stones?
Mixed stones - have components of both cholesterol and pigment stones!
Most cases of gallstones are asymptomatic though biliary colic is the cardinal symptoms if there are some. Pain occurs as the gallbladder contracts against the obstruction. What are symptoms?
Pain is typically located int eh RUQ or epigastrum and may be mild, moderate or severe. Patients classically report pain after eating and at night. Boas's sign is referred R subscapular pain of biliary colic.
p133
Differentiate between cholecystitis and choledocholithiasis.
Cholecystitis pain is usually due to gallbladder wall inflammation (which is due to obstruction of the cystic duct). Choledocholithiasis just refers to gallstones in the duct, but not necessarily inflammation of the ducts.
p133
What are the following signs and what are they indicative of?
A. Boas's sign
B. Murphy's sign
A. Boas's sign - the referred R subscapular pain of biliary colic, as seen in cholelithiasis (stones in the gallbladder)
B. Murphy's sign - inspiratory arrest durring deep palpation of the RUQ, pathognomonic for cholecystitis
p133/4
Pain of acute cholecystitis persists for [ several days / several hours ] whereas pain of biliary colic (cardinal symptom of cholelithiasis) lasts for [ several days / several hours ] .
Pain of acute cholecystitis lasts SEVERAL DAYS ;
pain of biliary colic lasts SEVERAL HOURS.
p 133
True or False:
Obstruction of the cystic duct (NOT infection) induces acute inflammation of the gallbladder wall.
TRUE!
p134
What are some symptoms (4) and signs (6) of acute cholecystitis?
Symptoms: pain in RUQ or epigastrum that might radiate to R shoulder or scapula ; Nausea, Vomiting, Anorexia

Signs: RUQ tenderness, rebound tenderness in RUQ, Murphy's sign, hypoactive bowel sounds, low grade fever, leukocytosis.
p134
What does a "positive HIDA scan" indicate?

hint: with respect to the gallbladder
Radionuclide scan = HIDA.

Is used when ultrasound is inconclusive. Its sensitivity and specificity parallel that of ultrasound. If HIDA scan is normal, acute cholecystitis can be ruled out. A POSITIVE HIDA SCAN MEANS THAT THE GALLBLADDER IS NOT VISUALIZED! If gallbladder is not visualized 4 hours after injection, diagnosis of acute cholecystitis is confirmed. p134
What is the treatment for acute cholecystitis?
1.Pt should be admitted. Conservative measures include hydration with IV fluids, bowel rest (NPO), IV antibiotics, analgesics, correction of electrolyte abnormalities.
2. Surgery : Cholecystectomy is indicated in most patients with symptomatic gallstones. Early cholecystectomy (within first 24-48 hours) is preferred. Recurrence rate with nonsurgical treatment is ~70%! Timing of surgery depends on severity of symptoms and patient's risk assessment for surgery, but in most patients, early cholecystectomy is preferred.
p.134
What is acalculous cholecystitis?
Acute cholecystitis WITHOUT STONES obstructing the cystic duct. Usually idiopathic and seen in pts with severe underlying illness (possibly ass with dehydration, ischemia, burns, severe trauma, and post-op state). Emergency cholecystectomy is treatment of choice or if too ill for surgery, percutaneous drainage of the gallbladder with cholecystostomy. p134
TRUE OR FALSE:
Pts with common bile duct stones (choledocholithiasis) can be asymptomatic for years. However, unlike patietns with cholelithiasis, where biliary colic can lead to acute cholecystitis, the onset of symptoms in choledocholithiasis can signal the development of life-threatening complications like cholangitis and acute pancreatitis.
TRUE TRUE TRUE

p135
What is Charcot's triad and what is it indicative of?
Charcot's triad: fever, RUQ pain, jaundice. Classic triad present in cholangitis in 50-70% of cases.

Also note:
Reynold's pentad = Charcot's triad (RUQ pain, jaundice, fever) + septic shock + altered mental status. Indicative of cholangitis.
p136
What is Reynold's pentad and what is it indicative of?
Reynold's pentad = Charcot's triad (RUQ pain, jaundice, fever) + septic shock + altered mental status. Indicative of cholangitis.
p136
What is the most dreaded and serious complication of acute cholangitis?
HEPATIC ABSCESS p136
What are carcinomas of the gallbladder associated with (3)?
Gallstones, cholecystoenteric fistula, porcelain bladder
p136
This condition is a chronic idiopathic progressive dz of intrahepatic or extrahepatic bile ducts characterized by thickening of bile duct wallas and narrowing of their lumens leading to cirrhosis, portal hypertension and liver failure. There is a strong association with Ulcerative Colitis. Complications are cholangiocarcinoma, recurrent bouts of cholangitis.

A. Acute cholecystitis.
B. Carcinoma of gallbladder
C. Primary biliary cirrhosis
D. Primary sclerosing cholangitis
D. Primary sclerosing cholangitis
p136

No curative treatment other than liver transplantation. Use cholestyramine for symptomatic relief (to decrease pruritis).
This condition is a chronic and progressive cholestatic liver disease characterized by destruction of intrahepatic bile ducts with portal inflammation and scarring. It is a slowly progressive dz with variable course that can progress to cirrhosis and end stage liver failure. It is an autoimmune dz and most commonly seen in middle aged women.

A. Primary biliary cirrhosis
B. Primary sclerosing cholangitis
A. Primary biliary cirrhosis

Cholestatic LFTs (Alk-phosphatase will be increased), POSITIVE ANTIMITOCHONDRIAL ANTIBODIES (AMAs) found in 90-95% of patients. Elevated cholesterol, HDL. Elevated immunoglobulin M.

Do a LIVER BIOPSY to confirm diagnosis! And abdominal U/S or CT scan to rule out biliary obstruction.
p137
What is the treatment for primary biliary cirrhosis?
This condition is a chronic and progressive cholestatic liver disease characterized by destruction of intrahepatic bile ducts with portal inflammation and scarring due to an autoimmune process. It is a slowly progressive dz with variable course that can progress to cirrhosis and end stage liver failure. Most commonly seen in middle aged women.

That said, treatment is :
Symptomatic for pruritis (cholestyramine), osteoporosis (calcium, bisphosphonates, Vit D). Ursodeoxycholic acid (a hydrophilic bile acid) can slow progression of the disease.
Liver transplantation is the only curative treatment available though. :(

p137
Dark urine and clay-colored stools. Think of what condition?
Obstructive jaundice aka biliary tract obstruction. Associated with gallstones, pancreatic carcinoma, cholangiocarcinoma, parasites, and liver fluke. See on lab findings increased CB, decreased urine urobilinogen and increased alk phos.
p119 in pathoma and peppered in the GI Step Up chap
What are the risk factors to perforation of the appendix in acute appendicitis?
Delay in treatment (>24 hours), and extremes of age (infants and elderly). Signs of appendiceal rupture include: high fevere, tachycardia, marked leukocytosis, peritoneal signs, toxic appearance.
p139
True or False:
Appendicitis is unlikely if pt has abdominal pain, N/V, but is hungry.
TRUE!

Anorexia is ALWAYS present. If pt is hungry, it is unlikely appendicitis.
p139
Where is McBurney's point and when would maximal tenderness be noted here?
McBurney's point = two thirds the distance from the umbilicus to the R anterior superior iliac spine. In acute appendicitis!
p139
Differentiate between :
A. Rosving's sign
B. Psoas sign
C. Obturator sign
A. Rosving's sign - Deep palpation in LLQ causes referred pain in RLQ
B. Psoas sign - RLQ pain when R thigh is extended as patient lies on L side OR RLQ pain when pt tries to flex the R hip against resistance you apply
C. Obturator sign - pain in RLQ when flexed R thigh is internally rotated when patient is supine.
p139
Match the "sign" ( Obturator, Psoas, Rosving's) to its description:
A. RLQ pain when R thigh is extended as patient lies on L side OR RLQ pain when pt tries to flex the R hip against resistance you apply
B. Deep palpation in LLQ causes referred pain in RLQ
C. pain in RLQ when flexed R thigh is internally rotated when patient is supine.
A. Psoas sign - RLQ pain when R thigh is extended as patient lies on L side OR RLQ pain when pt tries to flex the R hip against resistance you apply
B. Rosving's - Deep palpation in LLQ causes referred pain in RLQ
C. Obturator sign - pain in RLQ when flexed R thigh is internally rotated when patient is supine.
p139
Acute appendicitis is a clinical diagnosis but if diagnosis is uncertain or if atypical presentation, what imaging studies can be helpful?
CT scan (98-100% sensitivity) or ultrasounds (90% sensitivity).
p139
Cutaneous flushing, diarrhea, sweating, wheezing, abdominal pain and heart valve dysfunction are all manifestations of excess serotonin secretion caused by what condition that originates from neuroendocrine cells and whose most common site is the appendix?
Carcinoid syndrome = excess serotonin secretion due to carcinoid tumor.
p139
Most cases of acute pancreatitis are due to what two things (70-80%)? What is the most common cause for chronic pancreatitis?
Alcohol abuse and gallstones (40% each).
p140

Other causes: Post-ERCP, viral infections (mumps, Coxackievirus B), drugs (sulfonamides, thiazide diuretics, furosemide, estrogens, HIV meds), post op complications, scorpion bites, pancreatic CA, hypertriglyceridemia and hypercalcemia, uremia, blunt abdominal trauma.

Chronic pancreatitis common cause is alcoholism (>80% of cases). p142
Pt has known alcohol abuse history (and admits to it currently), and has abdominal pain in epigastric region that radiates to the back and described as steady, dull and severe and worse when supine and after meals. Also reports N/V and anorexia. What does this pt likely have?
Acute pancreatitis.
p140
Differentiate between :
A. Boa's sign
B. Cullen's sign
C. Fox's sign
D. Grey Turner's sign
E. Obturator sign
F. Psoas sign
G. Rosving's sign
A. Boa's sign - indicative of cholelithiasis. Is referred R subscapular pain of biliary colic

These are ecchymoses seen in acute hemmorhagic pancreatitis:
B. Cullen's sign - periumbilical ecchymosis
C. Fox's sign - ecchymosis of inguinal ligament
D. Grey Turner's sign - flank ecchymosis

These are seen in acute appendicitis:
E. Obturator sign - pain in RLQ when pt's flexed knee and hip are internally rotated with pt supine
F. Psoas sign - RLQ pain when R thigh is extended as patient lies on L side OR RLQ pain when pt tries to flex the R hip against resistance you apply
G. Rosving's sign - Deep palpation in LLQ causes referred pain in RLQ
p139-140, 133
What is a better test for acute pancreatitis:
serum amyalse or serum lipase?
serum lipase is better as it is more specific for pancreatitis than amylase.
p140

Diagnosis of acute pancreatitits is usually amde based on clinical presentation. Lab studies are supportive, and CT scan is confirmatory.
The hypocalcemia that results from acute pancreatitis is due to what?
Fat saponification! As fat necrosis binds calcium!
p140
What is the treatment for pts with mild pancreatitis? What about severe pancreatitis?
Mild pancreatitis: bowel rest (NPO), IV fluids, pain control (fentanyl or meperidine preferred over morphine since morphine causes an increase in sphincter of Oddi pressure).

Severe pancreatitis: admit to ICU. Enteral nutrition in first 72 hours recommeneded thru nasojejunal tube. If severe pancreatitis has not resolved in a few days, then do TPN.

Ranson's criteria is used to determine severity. 3+ criteria met should --> ICU!
p142 (see p 140 for Ranson's criteria)
The combination of chronic epigastric pain and ________ on plain abdominal films is diagnostic for chronic pancreatitis. The classic triad of ____, _______, and [the first blank above] is also diagnostic.
Chronic epigastric pain and calcifications.

steatorrhea, diabetes mellitus, and pancreatic calcification
p142
True or False:
Serum amylase and lipase levels are not elevated in acute pancreatitis.
FALSE.

In acute pancreatitis, serum amylase and lipase levels are indeed elevated . Note, though that serum lipase is more specific to look at for pancreatitis than amylase.

It is only in CHRONIC PANCREATITIS where the serum amylase and serum lipase levels are not elevated.
p142
What are the risk factors for pancreatic CA?
CIGARETTE SMOKING is the most clearly established risk!

Others are: chronic pancreatitis, diabetes, heavy alcohol use, exposure to chemicals like benzidine and b-napthylamine.
p144
With what diseases are the following tumor markers used?
A. CEA (2)
B. CA 19-9
C. AFP
A. CEA : Colon cancer and pancreatic cancer
B. CA 19-9 : Pancreatic cancer
C. AFP : Hepatocellular Carcinoma
p144, 116, 127
Differentiate between :
A. Boa's sign
B. Cullen's sign
C. Fox's sign
D. Grey Turner's sign
E. Obturator sign
F. Psoas sign
G. Rosving's sign
A. Boa's sign - indicative of cholelithiasis. Is referred R subscapular pain of biliary colic

These are ecchymoses seen in acute hemmorhagic pancreatitis:
B. Cullen's sign - periumbilical ecchymosis
C. Fox's sign - ecchymosis of inguinal ligament
D. Grey Turner's sign - flank ecchymosis

These are seen in acute appendicitis:
E. Obturator sign - pain in RLQ when pt's flexed knee and hip are internally rotated with pt supine
F. Psoas sign - RLQ pain when R thigh is extended as patient lies on L side OR RLQ pain when pt tries to flex the R hip against resistance you apply
G. Rosving's sign - Deep palpation in LLQ causes referred pain in RLQ
p139-140, 133
Whipple's procedure is the only hope for a cure for this condition but only a minority of pts with this condition have resectable tumors and the prognosis is grim even after resection with a 5 year survival rate of 10%.
Pancreatic cancer
p144
A lower GI bleed (or positive occult blood test of stool) in patients over 40 is _____________ until proven otherwise.
colon cancer
p145
Upper GI bleeding causes are (10, name a few of em). Lower GI bleeding causes are (8, name a few of em).
Upper GI bleeding causes:
- peptic ulcer dz (duodenal ulcer in 25% of cases, gastric ulcer in 20%, gastritis in 25%)
- reflux esophagitis
- esophageal varices
- gastric varices
- gastric erosions, dodenitis
- Mallory-Weiss tear
- Hemobilia
- Dieulafoy's vascular malformation (submucosal dilated arterial lesions that can cause massive GI bleeding)
- aortoenteric fistulas
- neoplasms

Lower GI bleeding causes:
- diverticulosis (40%, usually painless)
- angiodysplasias (40%)
- IBD (UC, Crohn's)
- colorectal CA
- colorectal adenomatous polyps
- ischemic colitis
- hemorrhoids, anal fissures
- small intestinal bleeding
p145
Define the types of GI bleeding and if it suggests lower or upper GI bleeding:
A. "coffee ground" emesis
B. hematemesis
C. hematochezia
D. melena
E. occult blood in stool
A. "coffee ground" emesis: suggests upper GI bleeding as well as lower rate of bleeding (in comparison to frank hematemesis)
B. hematemesis: vomiting blood. Suggests upper GI bleeding. Indicates moderate to severe bleeding that may be ongoing.
C. hematochezia: bright red blood per rectum. Lower GI source, typically of L colon or rectum)
D. melena: black, tarry, liquid, foul-smelling stool. Caused by degradation of Hgb by bacteria in colon; presence of melena indicates blood has remained in GI tract for several hours. The further the bleeding site from rectum, the more likely melena will occur. Melena suggests UPPER GI bleeding 90% of the time. Note that dark stools can also result from bismuth, iron, spinach, charcoal and licorice.
E. occult blood in stool : source of bleeding is anywhere along GI tract
p145
What test(s) do you order with each bleeding type:
A. hematemesis
B. hematochezia
C. melena
D. occult blood
A. hematemesis: vomiting blood, thus an upper GI endoscopy is the initial test
B. hematochezia: bright red blood per rectum. First rule out anorectal cause (hemorrhoids). Colonoscopy should be the initial test b/c colon cancer is hte main concern in pts 50+.
C. melena: dark tarry liquidy foul smelling stool. Upper endoscopy is the initial test b/c bleeding site most likely in upper GI tract. But order a colonoscopy if no bleeding site is identified from the endoscopy.
D. occult blood: colonoscopy is the initial test in most cases (colon cancer is the main concern). Order an upper endoscopy if no bleeding site is identified from the colonoscopy
p146
BUN-Cr ratio is elevated with [bleeding where] if patient has no renal insufficiency.
UPPER GI BLEEDING
p146
Esophageal cancer has two pathologic types: squamous cell carcinoma and adenocarcinoma. Which...
A. has risk factors of alcohol and tobacco use, HPV, achalasia, and nasopharyngeal carcinoma
B. has risk factors of GERD and Barrett's esophagus
C. has higher incidence in African American men
D. is more common in Caucasians and men
E. is more common in distal third of the esophagus/ gastroesophageal junction
A. has risk factors of alcohol and tobacco use, HPV, achalasia, and nasopharyngeal carcinoma = SCC
B. has risk factors of GERD and Barrett's esophagus = ADENOCARCINOMA
C. has higher incidence in African American men = SCC
D. is more common in Caucasians and men = ADENOCARCINOMA
E. is more common in distal third of the esophagus/ gastroesophageal junction = ADENOCARCINOMA
p148
What are the two most common features of esophageal cancer (no matter the pathologic type)?
A. Anorexia
B. Aspiration pneumonia
C. Dysphagia
D. Hematemesis
E. Hoarsness of voice
F. Odynophagia
G. Tracheoesophageal or bronchoesophageal fistula
H. Weight loss
C. Dysphagia
H. Weight loss

are the two most common clinical features of esophageal cancer. The others listed are also clinical features. (dysphagia most common)
p148
What are the various common causes of achalasia both in the US (2) and worldwide (1)?
In US: idiopathic and then adenocarcinoma of proximal stomach.

Worldwide, Chagas dz.

p149
With [ achalasia / esophageal cancer ], there is equal difficulty swallowing solids and liquids whereas in [ achalasia / esophageal cancer ], there is greater dysphagia for solids than for liquids.
With ACHALASIA equal difficulty with solids and liquids; with ESOPHAGEAL CANCER there is more difficulty with solids.

p149
What study confirms the diagnosis of achalasia?
A. barium swallow yielding "bird's beak"
B. manometry
C. upper GI endoscopy
B. manometry - will reveal failure of LES relaxation and aperistalsis of esophageal body

p149
True or False:
Patients with achalasia have a sevenfold increase in risk of esophageal cancer.
TRUE. There is a 10% chance of developing esophageal CA 15 to 25 years after the initial diagnosis of achalasia. Usually the CA will be squamous cell type. Thus, perform surveillance esophagoscopy to detect the tumor at an early stage!
p149
An upper GI barium swallow that reveals "corkscrew esophagus" is seen in 50% of people with this condition. What are clinical features of this condition?
This is diffuse esophageal spasm. There can be noncardiac chest pain that mimics angina and may radiate to the jaw, arms, and back. Dysphagia is common though regurgitation is NOT.
p151
With regards to the esophageal hiatal hernias, differentiate between type 1 (sliding) and type 2 (paraesophageal) hernias in terms of their definitions and how to treat em.
Type 1 (sliding) : 90% of cases. Both GE junction and portion of stomach herniate into the thorax thru the esophageal hiatus (GE junction is ABOVE diaphragm). Treat medically with antacids, small meals and elevation of the head after meals. Consider surgery if no response to the therapy or if esophagitis evident.

Type 2 (paraesophageal): <5% of cases. Stomach herniates thru esophageal hiatus and into the thorax but GE junction does not and remains BELOW the diaphragm. Uncommon hernia can become strangulated!! Treat with elective surgery due to risk of obstruction, hemmorhage, incarceration and strangulation.

p151
Differentiate between Mallory-Weiss syndrome and Boerhaave's syndrome as both involve tears in the upper GI tract.
Mallory-Weiss syndrome: MUCOSAL tear at or just below the gastroesophageal junction as result of forceful wretching or vomiting.

Boerhaave's syndrome: TRANSMURAL (causing esophageal perforation) tear
p152
True or False:
Most cases of Mallory-Weiss syndrome stops bleeding without any treatment.
TRUE

remember, Mallory-Weiss tear is a mUCOSAL tear (not transmucosal) at the gastroesophageal junction.

p152
Circumferential ring in the lower esophagus that is always accompanied by a sliding hiatal hernia is called:
A. Boerhaave's syndrome
B. Mallory-Weiss syndrome
C. Plummer-Vinson Syndrome
D. Schatzki's ring
E. Zenker's diverticulum
Circumferential ring in the loewr esophagus that is always accompanied by a sliding hiatal hernia is called....... D. Schatzki's ring

Usually asymptomatic but mild dysphagia can be present. Usually due to ingestion of alkali, acids, bleach or detergents (as in suicide attempts).
p152
Compare and contrast duodenal versus gastric ulcers with regards to:
A. which is more likely to have Helicobacter pylori infection
B. which has low and which has high malignant potential
C. which occurs in younger (<40) versus older (40+) pts
D. which has a risk factor of smoking
E. which has a risk factor of NSAIDs
F. which has eating usually relieving pain and which doesn't have the relief with eating
G. which is nocturnal pain more common in
A. which is more likely to have Helicobacter pylori infection : DUODENAL
B. which has low and which has high malignant potential: DUODENAL LOW, GASTRIC HIGH
C. which occurs in younger (<40) versus older (40+) pts: YOUNGER IS DUODENAL, OLDER IS GASTRIC
D. which has a risk factor of smoking: GASTRIC
E. which has a risk factor of NSAIDs: DUODENAL
F. which has eating usually relieving pain and which doesn't have the relief with eating : RELIEF WITH FOOD IS DUODENAL, NOT GASTRIC
G. which is nocturnal pain more common in: DUODENAL
p154
For diagnosis of H.pylori infection, what breath test do you do?
Urease detection via urea breath test. Sensitivity and specificity > 95%. Documents active infections and helps to assess results of antibiotic therapy.
p155
Eradicate H. pylori with...
A. Triple therapy (PPI + 2 antibitoics)
B. Quadruple therapy (PPI + bismuth + 2 antibiotics)
C. Misoprostol
D. Sulcrafate
A. Triple therapy (PPI + 2 antibitoics) if initial therapy, for 2 weeks
B. Quadruple therapy (PPI + bismuth + 2 antibiotics) if recurrent therapy, for 1 week
p.155

Note: Misoprostol reduces risk for ulcer formation ass with NSAID therapy but is costly and commonly causes GI SE. Sucralfate facilitates ulcer healing but is also costly and can cause GI upset
What is the most common cause of chronic gastritis?
A. NSAID usage
B. H.pylori infection
C. alcohol abuse
D. heavy cigarette smoking
E. caffeine consumption
B. H.pylori infection
p157
True or False:
Dehydration is a key event in small bowel obstruction.
TRUE

Intestinal distention causes reflex vomiting, increased intestinal secretion proximal to the point of obstruction, and decreased absorption. This leads to hypochloremia, hypokalemia, and metabolic alkalosis. The resulting hypovolemia leads to systemic findings such as tachycardia, hypotension, tachypnea, AMS and oliguria.
p159
What are some manifestations of strangulated bowel in small bowel obstruction? (8)
- fever
- severe and continuous pain
- hematemesis
- shock
- gas in the bowel wall or portal vein
- abdominal free air
- peritoneal signs
-increased lactic acid --> acidosis

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When peristalsis is decreased or absent but no mechanical obstruction is present, what condition is present? What is the treatment?
Paralytic ileus.

This resolves with time or when cause is addressed medically.

Treatment involves IV fluids, NPO, correction of electrolyte imbalances (ESPECIALLY HYPOKALEMIA), nasogastric suction if necessary, and placement of a long tube if persistent.
p160
What is characterized by hypersensitivity to gluten in wheat products and results on weight loss, abdominal distention, bloating, diarrhea?
Celiac sprue
p160
[ Celiac dz / Chron's dz / Ulcerative colitis ] is a chronic transmural inflammatory dz that can affect ANY part of the GI tract (mouth to anus) but most commonly involves the small bowel (terminal ileum specifically). Can involve skip lesions.
Crohn's dz

p161
Clinical features of this inflammatory bowel dz includes: diarrhea without blood, malabsorption and weight loss, RLQ pain, N/V, fever, malaise, and extraintestinal manifestations in 15-20% of cases: uveitis, arthritis, ankylosing spoindylitis, erythema nodosum, pyoderma gangrenosum, aphthous oral ulcers, cholelithiasis, nephrolithiasis.
Crohn's dz
p 161
What is the treatment for Crohn's dz? (1st, 2nd, 3rd line)
1st: Sulfasalazine. It's active compound 5-ASA (mesalamine) is released in the colon and blocks prostaglandin release and serves to reduce inflammation.
2nd: If no response to sulfasalazine, then metronidazole.
3rd: If no response to metronidazole, then systemic corticosteroids via prednisone.

Surgery eventually required in most patients (indications: SBO, fistulae, disabiling disease, perforation or abscess).
p162
[ Celiac dz / Chron's dz / Ulcerative colitis ] is a chronic inflammatory dz of the colon or rectal mucosa. Involves the rectum in all cases and can involve the colon partially or entirely. Small bowel usually not involved. NO skip lesions. Inflammation is NOT transmural but instead just limited to the mucosa and submucosa.
Ulcerative colitis.
p163
Clinical features for this inflammatory bowel condition are: hematochezia, abdominal pain, frequent but small bowel movements, tenesmus, and extraintestinal symptoms (Jaundice, uveitis, arthritis, skin lesions, etc.)
Ulcerative colitis
p163
If considering diagnosis of ulcerative colitis, what initial studies should you do and why?
- Stool cultures for C diff, ova and parasites to rule out infectious diarrhea.
- fecal leukocytes (though keep in mind WBCs can appear in UC, ischemic colitis, or infectious diarrhea)
- colonoscopy to assess extent of dz and presence of complications
p163
Colon cancer, sclerosing cholangitis and choalngiocarcinoma risk are all higher with [ Celiac dz / Chron's dz / ulcerative colitis ].
Ulcerative colitis!
p163
What is the leading cause of death in ulcerative colitis (affects <5% of pts)?
A. colon CA
B. sclerosing cholangitis
C. cholangiocarcinoma
D. toxic megacolon
D. toxic megacolon
p164
Which irritable bowel disease can be cured with surgery: Crohn's dz or ulcerative colitis?
Ulcerative colitis! Do a total colectomy!
Can be treated with medical therapy (sulfasalazine, immunosuppresants) but indications for surgery include: severe debilitating dz, refractory dz, toxic megacolon, hemorrhage, perforation, fulminant exacerbation that does NOT respond to steroids, evidence of colon CA, growth failure or failure to thrive in children, systemic complications.
p165