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Linear / longitudinal mucosal tear at gastroesophageal junction? Potential complication risk?

Mallory-Weiss syndrome

risk of Boerhaave syndrome - transmural esophageal tear leading to air/fluid in mediatinum and subcutaneous emphysema (air bubbles in skin - crackles when pushed)

1

What does lactase deficiency do to stool osmotic gap and stool pH? Generally speaking, how is lactose tolerance tested?

Stool osmotic gap increases (gap is electrolytes vs. poorly absorbable substances like lactose)

Stool pH decreases (bacterial fermentation of lactose in gut lumen produces excess hydrogen/low pH and short-chain fatty acid products)

Lactose tolerance: pt given lactose, blood glucose monitored later

2

How many calories does metabolism of 1g protein produce? 1g carbohydrate? 1g fat?

1g protein or carbohydrate = 4cal energy

1g fat = 9cal energy

3

Where is pepsin made? How is it activated? What is its function and is it an essential function? Regulation?

made by chief cells of the stomach (located in body)

inactive pepsinogen cleaved to active pepsin in presence of H+/acid

functions to digest protein - NOT required for protein digestion
pancreatic proteases later degrades proteins further in the small intestine, so pepsin is not critical for protein digestion

regulated by vagal stimulation and pH (increased action)

4

Where in the stomach are parietal cells located? What do they produce?

Parietal cells in the body of the stomach

Produce:
1) intrinsic factor
2) gastric acid

5

How is gastric acid secretion regulated? What is the source of each of these regulatory factors? Which is most important?

Factors that increase gastric acid production:
- histamine (enterochromaffin-like cells stimulated by gastrin)
- ACh (vagus nerve)
- gastrin (G cells in the antrum of the stomach)

Histamine release from ECL cells is the most important mechanism!!

Factors that decrease gastric acid production:
- somatostatin (D cells of pancreatic islets and GI mucosa)
- GIP (glucose-dependent insulinotropic peptide or gastric inhibitory peptide; K cells of duodenum and jejunum)
- prostaglandin
- secretin (S cells of duodenum)

6

Where is cholecystokinin (CCK) made and secreted from? What does it do? How is it regulated?

made from I cells of the duodenum and jejunum

CCK acts on neural muscarinic pathways to cause pancreatic secretion:
- increases pancreatic secretion
- increases gallbladder contraction
- decreases gastric emptying
- increases sphincter of Oddi relaxation

CCK increased by fatty acids, amino acids

7

What is the function of secretin? Where is it made and how is it regulated?

- increases pancreatic HCO3- secretion
- decreases gastric acid secretion
- increases bile secretion

made in S cells of the duodenum
makes bicarb in response to increasing H+ concentrations in the duodenum
(also responds to fatty acids in the duodenum)

8

What acid-base disturbance is precipitated by ethanol intoxication?
Vomiting?
Prolonged diarrhea?
COPD or CNS depression?

Ethanol: causes lactic acidosis
(high anion gap metabolic acidosis)

Vomiting: loss of acidic gastric secretions
(metabolic alkalosis)

Prolonged diarrhea: loss of bicarbonate
(normal anion gap metabolic acidosis)

COPD or CNS depression: decreased respiration
(respiratory acidosis)

9

What is the mechanism of omeprazole?

Proton pump inhibitor (-prazole)

irreversibly inhibits H+/K+ ATPase in stomach parietal cells

10

Where is somatostatin made? What is its function?

D cells of the pancreatic islets and GI mucosa, antrum of stomach

Functions to decrease the production of all GI hormones (inhibitory and antigrowth hormone)
- decreases gastric acid and pepsinogen secretion
- decreases pancreatic and small intestine fluid secretion
- decreases gallbladder contraction
- decreases insulin and glucagon release

11

What is Zollinger-Ellison disease? What is it usually caused by? Associated syndrome?

intractable peptic ulcer disease
usually due to gastrinoma in pancreas or duodenum that causes high levels of acid secretion

gastrinoma of pancreas associated with MEN I

12

What does vasoactive intestinal peptide (VIP) do? Source?

increases water and electrolyte secretion
increases relaxation of intestinal smooth muscle and sphincters
inhibits gastric acid secretion

parasympathetic ganglia in sphincters, gallbladder, small intestine
pancreatic islet cells

13

What is a VIPoma? Symptoms? Treatment?

non-alpha, non-beta pancreatic islet cell tumor that secretes excess VIP

secretory diarrhea that does not have blood or pus and also fails to improve with dietary modification

WDHA syndrome
Watery Diarrhea
Hypokalemia
Achlorhydria

Treatment is somatostatin (inhibits all GI hormones, including VIP)

14

Hormone that increases HCO3 concentration? Released from? Most potent stimulator?

Secretin
from S cells of duodenum

ACID (HCl) is the most potent stimulus for secretin release.
Fatty acid in lumen also stimulates.

15

What effect would systemic mastocytosis have on the GI tract?

Increased histamine secretion from the abnormal proliferation of mast cells

Histamine increases gastric acid by parietal cells, leading to gastric hypersecretion.

16

What are the three phases of gastric acid secretion regulated by?

1) cephalic phase
mediated by cholinergic and vagal mechanisms, triggered by thought, sight, smell, taste of food

2) gastric phase
mediated by gastrin (histamine) and triggered by chemical stimulus of food and stomach distention

3) intestinal phase
initiated by protein-containing food in duodenum; unlike other phases DOWN-REGULATES gastric acid secretion after a meal by the release of peptide YY that binds ECL cells

17

What is diffuse esophageal spasm (DES)? What are the symptoms?

periodic, non-peristaltic contractions of the esophagus - uncoordinated contractions of several segments of the esophagus at the same time

Symptoms are intermittent dysphagia and occasional chest pain (mimics angina pectoris so need to have a cardiac work-up too)

18

What are the effects of gastrin on parietal cells?

1) increases gastric acid secretion
both directly (minor pathway) and via histamine release from ECL cells (major)

2) increases parietal cell mass (trophic effect)

19

How are pancreatic enzymes activated? How is premature activation prevented?

Pancreatic enzyme activation:
- enterokinase/enteropeptidase in duodenal lumen converts trypsinogen to trypsin
- trypsin activates inactive proenzymes/zymogens (including more molecules of trypsinogen) into their active forms

Prevention of premature activation:
- SPINK1 trypsin inhibitor that blocks activity of trypsin that gets prematurely activated in the pancreas
- Trypsin can act as its own inhibitor by cleaving other trypsin molecules
Both mechanisms prevent autodigestion of pancreatic tissue

20

Hereditary pancreatitis?

gene mutations that render trypsin insensitive to cleavage inactivation (most commonly from cleavage by trypsin itself) causes recurrent bouts of acute pancreatitis

21

Dysphagia and/or painful swallowing with endoscopy findings of hyperemia and ulcerations of esophageal mucosa? What organisms responsible? How to distinguish?

esophagitis

3 main causes of HIV-associated esophagitis:
- Candida (patches of adherent, grey/white pseudomembranes on erythematous mucosa; yeast cells and pseduohyphae mucosal invasion)
- CMV (linear ulceration; intranuclear and cytoplasmic inclusions)
- HSV-1 (small vesicles that evolve into "punched out" ulcers; eosinophilic intranuclear inclusions)

22

What is the main site of digestion? What is the main site of lipid absorption and what factor is necessary for this process? What does the ileum do?

Duodenum = main site of digestion

Jejunum = main site of lipid absorption; bile acids necessary for lipid absorption

Ileum = site of absorption of bile and vitamin B12

23

What is achalasia? Findings on barium swallow?

decreased esophageal body peristalsis and poor relaxation of the lower esophageal sphincter

Barium swallow shows dilated esophagus and bird's beak deformity

24

What causes acute pancreatitis?

either direct toxic insult (alcohol, iatrogenic, viruses, trauma, hypertriglyceridemia)
or
ischemia resulting from pancreatic ductal obstruction (gallstones)

leads to activation of trypsin inside pancreatic acinar cells by released lysosomal enzymes -- trypsin activates the rest of the zymogens