GI7-11 Flashcards

1
Q

Why do cystic fibrosis patients have diarrhea?

A

Nutrient malabsorption

CF patients also tend to have pancreatic insufficiency so they can not break food down into absorbable products. Treatment usually includes pancreatic enzyme supplementation.

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2
Q

True/False

Octreotide administration is first line treatment for cystic fibrosis?

A

False, ocretotide is a somatostatin analogue that would further decrease pancreatic function (endocrine and exocrine). This would aggravate a CF patient’s malabsorption and nutritional deficiencies.

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3
Q

A patient who was recently administered an anesthetic (halothane) for surgery is at risk for life threatening, drug-induced injury to which organ?

A

Liver

Drug-induced liver injury is common after administration of halothane. In the US halothane usage has been replaced with other inhaled anesthetics, but halothane is still the most commonly used inhaled anesthetic worldwide. Also, inhaled anesthetic hepatotoxicity is histologically indistinguishable from acute viral hepatitis.

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4
Q

What surgical technique might you use to detect the source of a right upper quadrant bleed?

A

Pringle maneuver MA: Squeeze the hepatoduodenal ligament to occlude the (1)proper hepatic artery (2) common bile duct and (3) portal vein

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5
Q

Treatment:

Carcinoid syndrome

A

Octreotide

Symptoms of Carcinoid syndrome include: (1) watery diarrhea & cramping (2) flushing (3) bronchospasm & (4) fibrous plaques on the heart valves (R>L)

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6
Q

Describe the position of the esophagus on a CT image of the chest.

A

The esophagus is in between the trachea and the vertebral bodies. It is generally collapsed with no visible lumen.

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7
Q

What is the most common hepatic lesion?

A

metastasis from another primary site (eg, breast, lung or colon)

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8
Q

Curling’s ulcers vs. Cushing’s ulcers

arises from intracranial injury; caused by direct vagal stimulation

A

Cushing’s ulcers

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9
Q

Curling’s ulcers vs. Cushing’s ulcers

ulcers that arise in the setting of severe trauma/burns

A

Curling’s ulcers

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10
Q

Diagnosis:

What imaging modality is used to diagnose toxic megacolon in ulcerative colitis?

A

Flat plain X-ray

Note, (1) barium contrast studies & (2) colonoscopy are contraindicated due to the risk of perforation.

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11
Q

Which ligment encloses the portal triad?

A

Hepatoduodenal ligament

This makes sense because the portal vein carries blood from the stomach (duodenum) to the liver (hepatic).

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12
Q

What three structures comprise the portal triad?

A

(1) Proper hepatic artery (2) Portal vien (3) Common bile duct

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13
Q

What type of gastrointestinal problem, although rare, can arise in a patient with mitral stenosis or left ventricular failure?

A

Cardiovascular dysphagia due to a dilated left atrium putting pressure on the esophagus.

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14
Q

Amatoxin poisoining arises acutely within 6-24 hours of poisonous mushroom ingestion. Patients present with: (1) abdominal pain (2) vomiting (3) severe, cholera-like diarrhea with blood or mucus. Confirmation can be obtained via urine testing for alpha-amanitin.

Which type of RNA synthesis is inhibited?

A

mRNA

Amatoxin strongly inhibits mRNA.

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15
Q

The lumen of this abdominal organ can be seen anterior to the IVC on the right side of the body in a CT image taken at level L2.

A

the second part of the duodenum

*You know you are looking at abdominal CT image at level L2 if you see the kidneys

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16
Q

These two veins merge to become the IVC at level L4.

A

Common iliac veins

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17
Q

What vessels can be found just anterior to the right half of the vertebral bodies in the abdomen?

A

IVC

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18
Q

What type of mutation is associated with familial hypercholesterolemia?

A

Frameshift mutations

19
Q

What are the abdominal watershed areas?

A
  1. Distal Colon
  2. Splenic flexure
20
Q

What is a watershed area?

A

A region susceptible to ischemia after infarction or hypotension.

21
Q

Which abdominal region lies between the distribution of the superior mesenteric and inferior mesenteric arteries?

A

Splenic flexure

22
Q

Which abdominal region lies between the areas supplied by the inferior mesenteric arteries and hypogastric arteries?

A

distal sigmoid colon

23
Q

Seven (7) risk factors for the formation of cholesterol gallstones

A
  1. Caucasian race
  2. Female sex hormones/OCP
  3. Malabsorption of bile acid (ileal disease or resection)
  4. Obesity/rapid weight loss
  5. Glucose intolerance
  6. Fibrates/octreotide/ceftriaxone
  7. Hypomobility of gall bladder (pregnancy, advanced age, fasting, Hypertriglyceridemia, prolonged TPN)
24
Q

Which category of drugs suppresses 7alpha-hydroxylase activity preventing the conversion of cholesterol into bile acid and increasing the risk for cholesterol gallstones?

A

Fibrates (bezafibrate, fenofibrate, ciprofibrate)

25
Q

Your patient has hyperbilirubinemia, but lacks any apparent signs of liver disease or hemolysis? How could you differentiate a diagnosis of Gilbert Syndrome from Dubin-Johnson syndrome?

A

Gilbert syndrome –> elevated unconjugated (indirect) bilirubinemia without signs of liver disease
Dubin-Johnson –>elevated conjugated (direct) bilirubinemia without signs of liver disease, direct bilirubin should be at least 50% of the bilirubin.

26
Q

Diagnosis:

Esophageal manometry: “disorganized non-peristaltic contractions”

A

Diffuse esophageal spasm (DES)

27
Q

Diagnosis:

Barium esophagogram: “corkscrew” esophagus

A

Diffuse esophageal spasm (DES)

28
Q

Clinical Manifestation:

  1. intermittent dysphagia
  2. chest pain not relieved by rest and not associated with exertion
A

Diffuse esophageal spasm (DES)

29
Q

What is the best next step in the workup of a patient with suspected diffuse esophageal spasm (DES)?

A

Cardiac workup

DES, is associated with chest pain that may mimic unstable angina. Any suspected with DES should have a cardiac work up to rule out any cardiac causes.

30
Q

Clinical Manifestation:

Intestinal malrotation

A
  1. Intestinal obstruction (due to adhesive bands compressing the duodenum) –> bilious vomiting; cecum fixed to the RUQ
  2. Midgut volvulus (intestinal ischemia) –> intestinal gangrene and perforation
31
Q

What is the next step in the management of patient with: (1) periodic diarrhea (2) weight loss and (3) foul-smelling, bulky & frothy stools

A

Stool sample collection and stain with the Sudan III stain

This patient may be experiencing malabsorption. The Sudan III stain identifies fecal fat and is used to screen for malabsorption.

32
Q

What stain is used to screen for malabsorption?

A

Sudan III stain

33
Q

Diagnosis:

Abdominal X-ray reveals air in the gallbladder in a patient with a long history of gallstones

A

Gallstone ileus

The stone is likely obstructing the ileocecal valve.

34
Q

Pathogenesis:

Gallstone ileus

A
  1. Cholecystenteric fistula is formed
  2. Gallstone >2.5cm is passed
  3. Gall stone causes obstruction at the ileocecal valve
35
Q

Which hepatobilliary disease is associated with animitochondrial antibodies?

A

Primary biliary cirrhosis

36
Q

Which hepatobilliary disease is histologically similar to graft versus host disease?

A

Primary biliary cirrhosis

Histological appearance: (1) granulomatous bile duct destruction (2) heavy lymphocyte-predominant portal tract infiltrate

37
Q

Colorectal carcinoma in IBD/sporadic colorectal carcinoma

  1. Affects younger patients
  2. Progress from flat and non-polyploid dysplasia
  3. Histologically appears mucinous/has signet morphology
  4. EARLY p53 mutations and LATE APC mutations
  5. Distributed withing the proximal colon
  6. Multifocal
A

Colorectal carcinoma in IBD

38
Q

Your patient has longstanding ulcerative colitis and inquires about her risk for colorectal cancer. What do you tell her?

A

Colorectal carcinoma typically develops after 10 years.
20 year CRC incidence=2.5%
30 year CRC incidence=7.6%
40 year CRC incidence=10.8%

39
Q

Mechanism of Action:

Pancreatic divisum

A

Failure of the ventral and dorsal pancreatic buds to fuse.

This is usually an asymptomatic disease, but may predispose patients to acute or recurrent pancreatitis.

40
Q

Mechanism of Action:

Annular pancreas

A

Abnormal migration of the ventral bud.

This leads to compression of the duodenal lumen, causing duodenal stenosis. Clinical symptoms include: (1) recurrent vomiting in a neonate

41
Q

Clinical Manifestation:

Advanaced Wilson Disease

A

Neuropsychiatric symptoms (i.e. Parkinsonian-like tremor, rigidity, ataxia, slurred speech, drooling, personality changes, depression, paranoia and catatonia)

42
Q

Diagnosis:

Advanced Wilson Disease in a patient with impaired balance and difficutly speaking (neuropsychiatric symptoms)

A

observation of Kayser-Fleischer rings on slit lamp examination

Almost all patients with neuropsychiatric involvement will also have the Kayser-Fleischer rings.

43
Q

Diagnosis:

One month after a positive PPD test, your patient presents with fever, anorexia and nausea.

A

This patient has been treated with Isoniazid.

Isoniazid is (1) neurotoxic and (2) hepatotoxic. 10-20% of patients develop acute mild hepatic dysfunction. A smaller percent develop frank hepatitis (nausea, anorexia, fever). Also, the neurotoxic side effects can be prevented by co-administering pyridoxine (vitamin B6).

44
Q

Diagnosis:

Your patient is intolerant to fructose. What deficiency does this patient lack? Which carbohydrates should be avoided?

A

Patient has an aldolase B deficiency. Avoid (1) fructose and (2) sucrose; glucose+fructose