GI Week 3 Flashcards

1
Q

What are the two types of gastric adenocarcinoma? Identify the following pictures.

A

ANSWER: The two types are Intestinal (Left) and Gastric (Right) type. Intestinal type forms glands while diffuse type does not. “Signet ring” cells are also associated with the diffuse type of gastric adenocarcinoma.

Lecture: Pathology of Gastric Disorders

Objective 3: Explain the pathobiology of stomach cancer and understand the definition of early stage gastric cancer and familial gastric cancer.

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2
Q

At higher flow rates, salivary composition goes from isotonic to increased concentrations of what ions?

A

At higher salivary flow rates, there is increased amounts of Na+, HCO3-, and Cl-, while K+ levels decrease.

Lecture: Salivary Gland and Stomach Secretion

Objective 1: Describe how acinar secretions are modified by duct cells to produce the final salivary fluid that enters the buccal cavity.

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3
Q

Determine whether the following are factors which stimulate the release of secretin and CCK.

  1. Fat
  2. Bicarbonate
  3. Glucose
  4. Amino Acids
  5. Acid
A

Fat stimulates release of secretin and CCK

Bicarbonate is released when CCK stimulates the pancreatic acinar cells

Glucose does not stimulate the release of secretin or CCK.

Amino acids stimulate release of CCK

Acid stimulates release of both secretin and CCK.

Lecture: Stomach & Exocrine Pancreas Secretion

Objective 14: List the stimuli that release secretin and CCK and explain the route by which these regulatory peptides stimulate the pancreas.

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4
Q

What is the mechanism by which H.pylori infection affects post-prandial acid secretion?

A

The bacterium H.pylori preferentially damages D-cells in the stomach which are responsible for somatostatin secretion. With lower levels of somatostatin inhibition, gastrin secretion is increased, stimulating more post-prandial acid secretion.

Lecture: Peptic Ulcer Disease and H. pylori

Objective 1: Recognize the interplay between acid secretion and H. pylori infection in the pathogenesis of peptic ulcer.

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5
Q

A patient comes to you with numbness and tingling in her fingers as well as difficulties with memory. Her CBC shows megaloblastic anemia. What vitamin deficiency should you treat her for?

A

You should treat her for B12 deficiency! Treatment with Folate (B9) may mask her symptoms without preventing further neurological damage.

Lecture: Nutrition

Objective 3: Be able to identify characteristic signs and symptoms of deficiencies of vitamins such as thiamine, riboflavin, niacin, folate, B12, vitamin C, iron, zinc, and the fat soluble vitamins A, D &E.

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6
Q

How does the SGLT1 transporter in the drive water absorption in the small intestine?

A

SGLT1 is a co-transporter for Na+ and glucose. As these are transported into the cell, water follows the change in tonicity.

Lecture: Water and Electrolyte Absorption

Objective 3: Describe the location and mechanisms that mediate the intestinal trans-epithelial movement of water, the major electrolytes, iron, and calcium.

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7
Q

Identify the disorder demonstrated by this specimen.

A

ANSWER: This is an example of Crohn’s disease. Notice the “cobblestoning” as well as the narrowing of the lumen. Other features that can be seen in this disease are serpiginous “skip” lesions and non-caseating granulomas.

Lecture: Pathology of Small Intestine Disorders

Objective 2: Describe morphologic features and complications of Crohn’s disease.

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8
Q

High extraction drugs are considered _______ -limited while low extraction drugs are limited by ­­­______ and ________.

A

High extraction drugs are flow-limited and insensitive to intrinsic hepatic metabolism while low extraction drugs are limited by hepatic metabolism and protein binding.

Lecture: Absorption and Metabolism/Pharmacology Review

Objective 3: Apply core concepts of pharmacology to understand nuances of drug therapy in the setting of gastrointestinal and hepatobiliary disorders.

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9
Q

Your patient has had several days of bloody diarrhea. Upon questioning his prior dietary habits, you learn he ate some chicken that also caused other family members to fall sick with diarrhea. Gram-stain of his stool reveals a curved Gram-negative rod. What is the likely etiology of his diarrhea? Is this inflammatory or non-inflammatory diarrhea? What is a rare complication of this infection?

A

He likely has a Campylobacter jejuni infection causing inflammatory diarrhea (demonstrated by the blood in his stool). A rare complication is Guillain-Barre syndrome which is characterized by ascending paralysis.

Lecture: Microbial Pathogens of the GI Tract

Objective 2: You should learn the properties and virulence determinants of the bacteria, viruses, and parasites that infect the gastrointestinal tract.

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10
Q

You are experimenting with a substance secreted by some intestinal crypt cells. You find that they have antibacterial properties. What substance could this be? What cells release it?

A

These could be defensins, lysozyme, PLA2, or REG3 proteins released by Paneth cells which are found at the bottom of intestinal crypts. These are antimicrobial peptides.

Lecture: Mucosal Immunity

Objective 1: Be able to identify unique anatomical aspects of the gut mucosal immune system.

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11
Q

What test could you order to determine if a patient’s foul-smelling, greasy stool is due to pancreatic insufficiency?

A

Fecal elastase <100 ug/g will help you assess exocrine pancreatic function.

Lecture: Clinical Features of Malabsorption

Objective 3: Describe how pancreatic insufficiency can cause steatorrhea and how it is diagnosed.

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