12. Digestion and Absorption in the Gastrointestinal Tract Flashcards

1
Q

Why are enterocytes susceptible to radiation and chemotherapy?

A

Because they have a turnover rate of only 3 to 6 days.

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2
Q

What is the major mechanism of uptake in the G.I. for protein and fats?

A

Pinocytosis.

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3
Q

What to essential molecules lose their ability to be absorbed s/p terminal ileum resection?

A

Vitamin B12.

Bile salts.

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4
Q

What does starch initially break down into?

A

Maltose and 3-9 polymers of glucose.

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5
Q

What do maltose and trehalose breakdown into?

A

Glucose + Glucose

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6
Q

What does lactose break down into?

A

Glucose + Galactose

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7
Q

What does sucrose break down into?

A

Glucose + Fructose

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8
Q

What transporter pulls glucose and galactose from the luminal side of the enterocytes?

A

SGLT1

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9
Q

What transporters are used to pump glucose, galactose, and fructose out of the basolateral side of the enterocyte into the blood?

A

GLUT2

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10
Q

Why does consumption of lactose by the lactose intolerant result in bloating and flatulence?

A

Because the lactose is instead fermented by the commensal flora of the G.I.

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11
Q

How much D-xylose must be present after five hours in order to be considered “normal absorption.”

A

4 g or more.

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12
Q

What is the method of absorption of D-xylose at the dose used in the D-xylose absorption test?

A

Passive absorption.

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13
Q

What portion of the digestion of proteins is not essential to maintain homeostasis?

A

The portion of protein digestion that occurs in the stomach. Namely, the activity of pepsin.

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14
Q

What enzymes are secreted by the pancreas to digest proteins?

A

Trypsin and chymotrypsin (enteropeptidases).

Carboxypeptidase A and carboxypeptidase B (exopeptidases).

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15
Q

Which of the proteolytic enzymes of the pancreas are responsible for breaking down large proteins into small polypeptides?

A

Trypsin and chymotrypsin (the endopeptidases).

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16
Q

What converts trypsinogen, chymotrypsinogen, proelastase, procarboxypeptidase A, and procarboxypeptidase B into their active forms?

A

Trypsin.

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17
Q

Besides trypsin, what converts trypsinogen into its active form?

A

Enterokinase from the brush border.

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18
Q

How do amino acids enter the enterocytes?

A

Via a Na+-amino acid transporter specific to the type of the amino acid (neutral, acidic, basic, imino).

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19
Q

What happens to dipeptides and tripeptides that enter the enterocytes?

A

They are either broken down by cytosolic peptidases and secreted as such, or they enter the portal system whole.

20
Q

How do amino acids exit the basolateral side of the enterocytes?

A

Via facilitated transport (not using sodium) with a transporter specific to the type of each amino acid (acidic, neutral, basic, imino).

21
Q

How will chronic pancreatitis or cystic fibrosis affect protein digestion?

A

It will cause deficiency of all pancreatic enzymes, including all of the proteases (trypsin, chymotrypsin, carboxypeptidase A & B) which are essential for the breakdown of proteins.

22
Q

What is the basic pathophysiology of cystinuria?

A

Defect or absence of the dibasic amino acid transporter. This results in a deficiency in the COAL amino acids (cystine, ornithine, arginine, lysine) in the body and their accumulation in the urine. Cystine then forms crystals, presenting like kidney stones.

23
Q

What is the basic pathophysiology of Hartnup disease?

A

Deficiency of pancreatic enzymes or defect in transporters of intestinal epithelial cells for neutral amino acids.

Presents like pellagra – dementia, diarrhea, dermatitis.

24
Q

How would cystic fibrosis result in steatorrhea?

A

Anything that creates an inability of the duodenum to increase the pH of the chyme will prevent the action of lipases, amylases, and peptidases.

Cystic fibrosis prevents the pancreas from releasing bicarbonate.

25
Q

What is the primary dietary form of fat?

A

Triglycerides.

26
Q

What serves to emulsify fats in the stomach?

A

Dietary proteins.

27
Q

What is the function of colipase?

A

Colipase binds to pancreatic lipase and displaces bile salts.

28
Q

Which fat digesting enzymes are secreted in their active form by the pancreas?

A

Pancreatic lipase.

Cholesterol ester hydrolyze.

29
Q

What enzyme is responsible for the breakdown of cholesterol esters?

What organ secretes it?

A

Cholesterol ester hydrolase.

The pancreas.

30
Q

How does cholecystokinin assist with the absorption of fats?

A

Delays gastric emptying, stimulates bile salt ejection, and indirectly increases the pH of the lumen via potentiating secretin.

31
Q

What pancreatic enzyme is responsible for phospholipid breakdown?

What other enzyme activates it?

A

Phospholipase A2.

Trypsin.

32
Q

What are the three lipases discussed in this class?

A

Lingual lipase.

Gastric lipase.

Pancreatic lipase.

33
Q

Why might small intestinal bacterial overgrowth (SIBO) interfere with fat digestion and absorption?

A

Small intestinal bacteria deconjugate bile salts. If this occurs too significantly fact cannot be absorbed properly.

34
Q

What are the two main causes of small intestinal bacterial overgrowth (SIBO)?

A

Increase intestinal pH due to diminished gastric secretions and small intestine dysmotility.

35
Q

What is “tropical sprue?”

A

A loss of or decreased the number of intestinal epithelial cells.

Reduced microvilli surface area causes a diminished lipid absorption – which causes steatorrhea as well as folate and vitamin B12 deficiency.

36
Q

What is caused by celiac sprue?

A

Destruction of small intestine villi.

Hyperplasia of the intestinal crypts.

Malabsorption of folate, iron, calcium, and vitamins A, B12, and D.

37
Q

How are most vitamins absorbed?

A

Via sodium dependent cotransport.

38
Q

What can be caused by small intestine bacterial overgrowth overall?

A

Pain, bloating, gas, diarrhea/constipation.

Malabsorption issues – steatorrhea and vitamin/mineral deficiency.

Improper lipase activity due to changes in pH.

39
Q

What is the diagnostic test for small intestine bacterial overgrowth (SIBO)?

A

Methane/hydrogen breath test.

40
Q

What is the function of vitamin B12?

A

Acts as a coenzyme for reducing ribonucleotides to deoxyribonucleotides.

Cofactor in folate coenzyme recycling.

Cofactor in nerve myelination.

41
Q

Besides resection or damage to the ileum, what two diseases can result in a vitamin B12 deficiency?

A

Atrophic gastritis and autoimmune metaplastic atrophic gastritis, both of which result in a decrease of functional intrinsic factor produced.

42
Q

What other nutrient does calcium absorption require to be effective?

A

Vitamin D (1,25 dihydroxycholecalciferol)

43
Q

What is transferrin, and how is it formed?

A

Transferrin is the absorbed form of free iron.
Apotransferrin in the bile enters the duodenum and binds free iron and hemoglobin. This forms transferrin which can then be absorbed into epithelial cells via pinocytosis.

44
Q

How does vitamin C play a role in iron absorption?

A

It is essential for ferric reductase, which reduces nonheme iron so it can be absorbed.

45
Q

What transports fructose on the apical and basolateral sides of enterocytes?

A

The apical side uses GLUT5 and of the basolateral side uses GLUT2.