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First Aid 2014 > GI: 346 - 348 > Flashcards

GI: 346 - 348 Flashcards

1
Q

Which cells make intrinsic factor?

A

Parietal cells (stomach)

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2
Q

What is the main role of intrinsic factor?

A

Binding protein for B12

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3
Q

Where is B12 taken up?

A

Terminal ileum

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4
Q

What happens as a result of autoimmune destruction of parietal cells?

A

Chronic gastritis and pernicious anemia

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5
Q

Which cells produce gastric acid?

A

Parietal cells (stomach)

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6
Q

What is the main effect of gastric acid?

A

Decrease stomach pH

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7
Q

How is gastric acid regulated?

A

Increased by: histamine, ACh, gastrin

Decreased by: somatostatin, GIP, prostaglandin, secretin

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8
Q

What is a gastrinoma?

A

Gastrin-secreting tumor that causes high levels of acid secretion and ulcers refractory to medical therapy

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9
Q

Which cells produce pepsin?

A

Chief cells (stomach)

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10
Q

What is the main action of pepsin?

A

Protein digestion

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11
Q

How is pepsin regulated?

A

Increased by vagal stimulation and local acid

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12
Q

What is the inactive form of pepsin and how is it activated?

A

Pepsinogen, activated by H+

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13
Q

Which cells in the GI tract secrete HCO3-?

A

Mucosal cells (stomach, duodenum, salivary glands, pancreas) and Brunner glands (duodenum)

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14
Q

What is the main function of HCO3- in the GI tract?

A

Neutralizes acid

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15
Q

How is HCO3- regulated in the GI tract?

A

Increased by pancreatic and biliary secretion with secretin

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16
Q

Where do you find the HCO3-containing mucus?

A

Covers the gastric epithelium

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17
Q

What are the 3 secretory cells found in the duodenum?

A

I cells (CCK), S cells (secretin), and K cells (GIP)

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18
Q

What are 3 secretory cells found in the antrum?

A

D cells (somatostatin), mucous cells, G cells (GRP)

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19
Q

In which part of the stomach will you find parietal cells and chief cells?

A

Body

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20
Q

What is the main mechanism by which gastrin promotes acid secretion?

A

Exerts effects on enterochromaffin-like (ECL) cells leading to histamine release rather than through its direct effect on parietal cells

Histamine goes on to increase intracellular levels of cAMP in the parietal cell –> drives H-K ATPase

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21
Q

Does atropine completely block vagal stimulation of gastrin release? Why or why not?

A

No, it blocks parietal cells but does not affect vagal stimulation of G cells since G cells use GRP instead of ACh

22
Q

What does ACh bind on the gastric parietal cell?

A

M3 receptor

23
Q

What does histamine bind on the gastric parietal cell?

A

H2 receptor

24
Q

What does gastrin bind on the gastric parietal cell?

A

CCK-B receptor

25
Q

What are two enzymes/compounds that antagonize the effects of ACh, gastrin, and histamine in the parietal cell?

A
  1. Prostaglandins/misopristol

2. Somatostatin

26
Q

How do prostaglandins/misopristol and somatostatin exert their action on the parietal cell?

A

Via Gi protein to decrease the levels of cAMP

27
Q

What class of drugs can inhibit release of H+ from parietal cells?

A

Proton pump inhibitors

28
Q

Where are Brunner glands located?

A

Duodenal submucosa

29
Q

What is the main function of Brunner glands?

A

Secrete alkaline mucus

30
Q

What happens to Brunner glands in peptic ulcer disease?

A

Hypertrophy

31
Q

Describe the tonicity/content of pancreatic secretions relative to the flow rate.

A

Isotonic fluid

At low flow: high Cl
At high flow: high HCO3

32
Q

What are 4 enzymes that are secreted by the pancreas?

A
  1. Alpha amylase
  2. Lipase, phospholipase A, colipase
  3. Proteases
  4. Trypsinogen
33
Q

What is the main role of alpha-amylase?

A

Starch digestion

34
Q

Which pancreatic enzymes are important for fat digestion?

A

Lipase, phospholipase A, colipase

35
Q

Give 4 examples of proteases secreted by the pancreas?

A
  1. Trypsin
  2. Chymotrypsin
  3. Elastase
  4. Carboxypeptidases
36
Q

What form are pancreatic proteases secreted as?

A

Zymogens (proenzymes)

37
Q

Describe the role of trypsinogen.

A

Once it is converted to its active form (trypsin) it can activate all of the other proenzymes and also cleave additional trypsinogen molecules into active trypsin (positive feedback loop).

38
Q

How is trypsinogen initially converted to trypsin?

A

By enterokinase/enteropeptidase, a brush-border enzyme on the duodenal and jejunal mucosa

39
Q

What is the only form of carbohydrate that can be absorbed by enterocytes?

A

Monosaccharides (glucose, galactose, fructose)

40
Q

Describe the absorption of glucose, galactose, and fructose.

A

Glucose, galactose - taken up by SGLT1 (Na+ dependent)

Fructose - taken up by facilitated diffusion by GLUT5

All are transported to blood by GLUT2

41
Q

What is the D-xylose absorption test used for?

A

Distinguishes GI mucosal damage from other causes of malabsorption

42
Q

Where is iron absorbed and in what form?

A

Fe2+ in duodenum

43
Q

Where is folate absorbed?

A

Jejunum and ileum

44
Q

Where is B12 absorbed?

A

Terminal ileum along with bile acids (requires intrinsic factor)

45
Q

What are Peyer patches and where are they found?

A

Unencapsulated lymphoid tissue found in lamina propria and submucosa of ileum

46
Q

Which cells are found in Peyer patches?

A
  1. M cells - sample and present antigens to immune cells

2. B cells - stimulated in germinal centers differentiate into IgA secreting plasma cells

47
Q

What happens to the B cells that become IgA secreting plasma cells?

A

Reside in the lamina propria

48
Q

How is the IgA processed?

A

Receives protective secretory component and is then transported across epithelium to the gut to deal with intraluminal antigen

49
Q

What are the components of bile?

A
  1. Bile salts
  2. Phospholipids
  3. Cholesterol
  4. Bilirubin
  5. Water
  6. Irons
50
Q

Which enzyme catalyzes the rate-limiting step of bile synthesis?

A

Cholesterol 7alpha-hydroxylase

51
Q

What are bile salts?

A

Bile acids conjugated to glycine or taurine to make them water soluble

52
Q

What are 3 functions of bile?

A
  1. Digestion and absorption of lipids and fat-soluble vitamins
  2. Cholesterol excretion (body’s only means of eliminating cholesterol)
  3. Antimicrobial activity (via membrane disruption)

First Aid 2014 (24 decks)

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