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Kaplan: GI system > GI secretions: gastric, pancreatic and drugs for peptic ulcer disease > Flashcards

GI secretions: gastric, pancreatic and drugs for peptic ulcer disease Flashcards

1
Q

What are the gastric secretory products?

A

HCl; intrinsic factor; pepsinogen; gastrin; mucus

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2
Q

What, where and stimulus of HCl secretion?

A

pareital cells;
body/fundus of stomach;
=>gastrin; ACh (from vagus); histamine

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3
Q

What, where and stimulus of intrinsic factor secretion?

A

pareital cells;
body/fundus of stomach;
=>gastrin; ACh (from vagus); histamine

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4
Q

What, where and stimulus of pepsinogen secretion?

A

chief cells;
body/fundus of stomach;
=> ACh (from vagus); gastrin; HCl

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5
Q

What, where and stimulus of gastrin secretion?

A

G cells;
Antrum;
=> small peptides/amino acids; vagus (via GRP); stomach distension

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6
Q

What, where and stimulus of mucus secretion?

A

mucous cells;
entire stomach;
ACh (from vagina)

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7
Q

inhibitors of HCl and intrinsic factor?

A
  • Low pH inhibits (by inhibiting gastrin)
  • prostaglandins
  • chyme in duodenum (via GIP and secretin)
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8
Q

inhibitors of pepsinogen

A

H+ (via somatostatin)

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9
Q

inhibitors of gastrin

A

H+ (via somatostatin)

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10
Q

action of mucus

A

forms gel on mucosa to protect mucosa from HCl and pepsin;

traps HCO3 to helps neutralize acid

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11
Q

action of gastrin

A
  • increase HCl secretion (parietal cells)
  • increase pepsinogen secretion (chief cells)
  • increase histamine secretion by ECL cells
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12
Q

action of pepsinogen

A
  • Digests up to 20% of proteins

- converted to pepsin w/ low pH and pepsin (autocatalytic)

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13
Q

action of intrinsic factor

A
  • necessary for VITAMIN B12 absorption by ileum;

- forms complex w/ vitamin B12

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14
Q

action of HCl

A
  • kills pathogens

- activates pepsinogen to pepsin

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15
Q

What are the 3 primary triggers of H+ secretion?

A
  • ACh (from vagus) => M3 muscarinic receptor
  • Histamine => H2 histamine receptor
  • Gastrin => unidentified receptor
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16
Q

Describe the 3 steps in gastric H+ secretion

A

1) parietal cell=> CO2, H2O converted to H+ and HCO3 via carbonic anhydrase
2) H+ secreted into lumen of stomach by H-K ATPase => Cl- is secreted w/ H+
3) HCO3 absorbed into bloodstream in exchange for Cl-

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17
Q

What is alkaline tide?

A

after meal=> enough H+ secreated to raise pH of systemic blood and turn urine alkaline => alkaline tide

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18
Q

3 phases of gastric secretion

A

cephalic, gastric, intestinal phases

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19
Q

how does cephalic phase of gastric secretion occur?

A

“senses” increase gastric secretion via PANS => 30% responsible for H+ secretion

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20
Q

how does gastric phase of gastric secretion occur?

A

-food in stomach increases secretion;
-proteins, peptides, alcohol, caffeine cause *gastrin release
-gastric distention initiates vagovagal reflexes
=>60% of acid secretion

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21
Q

how does intestinal phase of gastric secretion occur?

A

-protein digestion products in duodenum stimulate gastrin secretion;
-absorbed amino acids act to stimulate H+ by parietal cells
=>less than 10% of acid secretion due to meal

22
Q

What are the drug classes for peptic ulcer disease?

A

antacids;
H2 antagonists; PPI;
mucosal protective agents; antibiotics

23
Q

primary antacid agents

A

MgOH; AlOH; CaOH

24
Q

What are the effects of antacids?

A

Mg=> laxative effect

AlOH=> constipating effect

25
Q

Agents of H2 antagonists?

A

*cimetidine;

ranitidine; famotidine; nizatidine

26
Q

How does cimetidine work and what type of physio effects are associated?

A

inhibits hepatic drug metabolizing enzymes

antiandrogen effects

27
Q

Agents of PPI

A

*omeprazole

lansoprazole; esomeprazole; pantoprazole; rabeprazole

28
Q

How do PPI work?

A

irreversibly inactivate H-K ATPase => block H+ secretion

29
Q

What disease do PPI work well in?

A

PUD, ZE syndrome; GERD

30
Q

mucosal protective agents

A
  • Sucralfate

- misoprostol

31
Q

action of sucralfate

A

polymerizes in stomach and forms protective coating over ulcer beds

32
Q

when is misoprostol used?

A

PGE1 derivative used for peptic ulcers caused by NSAIDs

33
Q

What and why are the antibiotics used in peptic ulcer disease?

A

macrolides; metronidazole; tetracyclines

=> treat H. pylori

34
Q

What are the exocrine secretions of pancreas caused by?

A

acinar cells and ductal cells

35
Q

How do acinar cells produce exocrine secretions?

A

contain numerous enzyme-containing granules in cytoplasm

36
Q

how do ductal cells produce exocrine secretions?

A

secrete HCO3

37
Q

How do exocrine secretions reach duodenum?

A

pancreatic duct

38
Q

What is the fxn of HCO3 in duodenum?

A
  • neutralizes HCl in chyme entering stoamch

- deactivates pepsin

39
Q

What causes an increase in HCO3 production?

A

H+ entering duodenum
*=> S cells secrete secretin
=> secretin acts on pancreatic ductal cells to increase HCO3 production

40
Q

What enzyme is responsible for HCO3 production? and where does this occur?

A

ductal cells contain *carbonic anhydrase

41
Q

How does HCO3 get into the blood?

A

exchange for Cl-

42
Q

If a person goes and eats a lot of Gus’s fried chicken, what is responsible for this digestion?

A

*CCK released by I cells in response to meals w/ small peptides, amino acids and fatty acids
=> stimulate pancreatic enzyme secretion

43
Q

What is the role of ACh in pancreatic enzymes?

A

via vagovagal reflexes=> stimulates enzyme secretion; potentiates action of secretin

44
Q

What provides protection of pancreatic acinar cells against self-digestion?

A
  • proteolytic enzymes are secreted as inactive precursors

* produce enzyme inhibitors

45
Q

What is the role of enzyme inhibitor production wrt protection of acinar cells?

A

inactivate trace amounts of active enzyme formed w/in

46
Q

What is the role of proteolytic enzymes being secreted as inactive precursors for acinar cell protection?

A

these enzymes get activated in gut lumen

47
Q

What are pancreatic enzymes that are not pro-enzymes so acinar cells are not protected?

A

ribonucleases; amylase; lipase

48
Q

What are the proteases of pancreas and associated reaction catalyzed?

A

trypsin=> proteins to peptides;
chymotrypsin=> proteins to peptides;
carboxypeptidase => peptides to amino acids

49
Q

What are the polysacchardases of pancreas and associated reaction catalyzed?

A

amylase => starch/glycogen to maltose, maltotriose, alpha-limit dextrins

50
Q

What are the lipases of pancreas and associated reaction catalyzed?

A
  • phospholipases A & B=> phospholipids to phosphoate, FA, glycerol
  • esterases=> cholesterol esters to free cholesterol and FA
  • TAG lipases=> Triglycerides to FA and monoglycerides
51
Q

What are the nucleases of pancreas and associated reaction catalyzed?

A
  • ribonuclease=> RNA to ribonucleotides

* deoxyribonuclease=> DNA to doxyribonucleotides

Kaplan: GI system (11 decks)

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