Histology Flashcards

1
Q

What faulty sphincter is responsible for the symptoms of GERD?

A

Lower Esophageal Sphincter pressure is absent or with transient LES relaxation.

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2
Q

Which layer of tissue is damaged by GERD? What is the consequence of this damage?

A

Esophageal superficial squamous epithelium. Stimulates the basal cell layer to proliferate –> hyperplasia.

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3
Q

What does GERD backflow consist of?

A

Gastric acid, pepsin and bile

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4
Q

What is Barrett’s esophagus? What are these patients at risk for developing?

A

Chronic gastric acid reflux (chronic GERD) causes change from stratified squamous to columnar. Patients are prone to develop adenocarcinomas (cancer that starts within the mucus glands of an organ).

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5
Q

Gastrin adenomas of the pancreas is a symptom of _______. This leads to uncontrolled _______ output and subsequent severe ulcerations.

A

Zollinger-Ellison syndrome. HCl output.

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6
Q

What is the relationship between helicobacter pylori and gastric acid? This bacteria is the major contributor to the pathogenisis of __________.

A

Unlike most other enteric organisms, H. pylori colonizes gastric mucous. Causes peptic and duodenal ulcer disease (PUD). Also causes chronic superficial gastritis.

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7
Q

Peptic Ulcer Disease is aggravated by NSAIDS because …? Hint: Cox-1, Cox-2 and prostaglandins

A

COX-1 inhibition by NSAIDS results in decreased prostaglandin synthesis which results in impaired gastric mucosal defense and repair mechanisms.

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8
Q

Prostglandins stimulate ____ and ______ from surface epithelial cells, which helps protect the lining of the stomach.

A

Mucus and bicarbonate

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9
Q

Prostaglandins also help epithelial cells with ______ and _____ ; this process is mediated by growth factors such as _______.

A

Proliferation and regeneration. Growth factors include: TGF-B, EGF, HGF and trefoil factors (in stomach TTF1 and TFF2).

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10
Q

A rare autosomal recessive disease with severe intractable diarrhea and malabsorption in neonates.

Hint: Brush border atrophy with accumulation of lysosomal granules and microvillus inclusions without crypt hypertrophy or immune cell filtrate.

A

Microvillus Inclusion Disease

This disease is always fatal unless treated with parenteral nutrition and intestinal transplants.

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