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GI/Liver > Lec 3 > Flashcards

Lec 3 Flashcards

1
Q

During what stages of digestion is acid secreted?

A

cephalic, gastric, and intestinal phases

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2
Q

Where are chief and parietal cells located in gastric fundic gland?

A
  • chief cells near base

- parietal cells in middle below mucous neck cells

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3
Q

What substances are secreted by gastric fundic gland mucosa?

A

HCl
Pepsinogen
Intrinsic Factor

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4
Q

What is the function of the stomach?

A
  • mechanical churning
  • initiate protein/fat digestion
  • produce intrinsic factor for vit B12 absorption
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5
Q

What does “the stomach as two organs” mean?

A

1st organ = secretes stuff = fundus and body + cardia

2nd organ = antrum = mixes and grinds

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6
Q

What is motilin?

A

hormone made in duodenum
binds receptors on smooth muscle throughout gut and pro-motility

–> increases phase III contractions of migrating motor complex [MMC]

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7
Q

What is effect of erythromycin on GI?

A

motilin agonist –> increase contraction of bowel

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8
Q

What do stretch receptors on stomach act on?

A
  • increase secretion of gastrin by G cells
  • increase secretion of acid/pepsin
  • activate vagus
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9
Q

Where is histamine released from?

A

ECL cells in gastric fundus

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10
Q

What is action of histamine in GI?

A
  • binds H2 receptors on parietal cells

- stimulates parietal to secrete HCl

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11
Q

What causes histamine to be released by ECL cells?

A
  • ACh and gastrin
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12
Q

What is gastrin?

A

a hormone released by G cells in the antrum –> goes through bloodstream to reach parietal cells in stomach fundus

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13
Q

What is action of gastrin?

A

binds gastrin receptors [CCK-b} on parietal cells

stimulates parietal to secrete HCl

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14
Q

Where is gastrin released from?

A

G cells in gastric antrum

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15
Q

What is action of ACh in stomach?

A

released by vagus nerve and binds muscarinic M3 receptors on parietal cell

stimulates parietal cell to secrete acid
also stimulates ECL cell to release histamine

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16
Q

What causes parietal cell to release HCl?

A
  • ACh from vagus
  • gastrin from G cells
  • histamine from ECL cells
  • stretch
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17
Q

What are 2 effects of ACh on stomach?

A
  • stimulates parietal cells to release acid

- stimulates ECL to release histamine

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18
Q

What cells release somatostatin?

A

D cells in the antrum

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19
Q

When is somatostatin released?

A

D cells sense low pH –> causes them to release somatostatin

20
Q

What is action of somatostatin?

A
  • acts on G cells to inhibit gastrin release

- inhibits ECL cells and parietal cells directy

21
Q

Where is pepsinogen released from?

A

chief cells in the fundus

gets converted to pepsin in the acidic stomach

22
Q

How does acid get into the lumen of stomach?

A

in exchange for K through the H-K ATPase pump

23
Q

What makes up the mucus-bicarbonate barrier of stomach? What induces their secretion?

A
  • mucus secreted by surface epithelium
  • bicarbonate is within the mucus

their secretion is stimulated by prostaglandins

24
Q

What causes duodenal ulcers?

A

hypersecretion of acid

25
Q

What causes gastric ulcers?

A

disurption of mucus barriers [by NSAIDS, aspirin, etc]

26
Q

What are some things that cause peptic ulcer disease?

A
  • H pylori
  • NSAIDS, aspirin
  • stress [due to ischemia]
  • gastrinoma

cigarettes and alcohol may aggravate but are not independent risk factors

27
Q

Where does h pylori infect?

A

only colonizes gastric-type epithelium [not intestinal or squamous]

28
Q

WHat is use of h pylori urease?

A

protects the h pylori from the acid in gastric lumen

29
Q

What is the H pylori toxin that causes peptic ulcers?

A

CagA

30
Q

How are some common complications of h pylori?

A
  • gastritis
  • peptic ulcer
  • associated w/ gastric adenocarcinoma and lymphoma
31
Q

What are x mech of action by which H pylori injures the mucosa?

A
  • directly releases cytokines on epithelial cells
  • disrupts mucous layer by production of proteases
  • stimulates host pro-inflammatory cytokines
  • inhibits somatostatin by antral D cells –> thus more gastrin –> acid hypersecretion
32
Q

What is presentation of peptic ulcer disease?

A
  • pain [may be relieve by food, may bore into back]
  • bleeding [melena, hematemesis]
  • gastric outlet obstruction
  • perforation
  • penetration
33
Q

What is most common cause of acute infectious gastritis?

A

h pylori

34
Q

What causes non-infectious acute gastritis?

A

aspirin, NSAIDS

severe physical stress, radiation

35
Q

How do NSAIDS cause gastritis?

A

inhibit mucosal prostaglandin synthesis

36
Q

How does esophagus protect itself from acid?

A

LES excludes acid/pepsin from refluxing; esophageal motility keeps contents moving distally

37
Q

How does duodenum protect itself from acid?

A

neutralizes acid/pepsin with duodenal/pancreatic/biliary bicarbonate

38
Q

What are 3 basic types of treatment for peptic ulcer disease?

A
  • remove inciting agent
  • medication
  • surgery
39
Q

What medications are used for peptic ulcer disease?

A
  • antacids to neutralize acid
  • PPIs and H2 blcoekrs to block acid production
  • enhance prostaglandin production [sucralfate]
40
Q

How does a highly selective vagotomy work?

A
  • eliminate cholinergic stimulus to parietal cells
41
Q

How does an antrectomy work?

A

remove gastrin-producing area and the are most susceptible to ulcer

anatomosis either by Billroth I or Billroth II

42
Q

How does a subtotal gastrectomy work?

A

remove antrum and most of the body to the stomach; eliminates gastrin secretion and most of the parietal cells

43
Q

What is difference Billroth I and Billroth II?

A

Billroth I = hook up the duodenum to the fundus of the stomach; only works if top of duodenum is in good shape

Billroth II = hook up the middle of the duodenum to the fundus of the stomach; leaves the top of the duodenum but its kind of off to the side

44
Q

What happens if you leave some of the antrum during billroth surgery?

A

you will have G cells there making gastrin but they are no longer in contact with the lumen so don’t get turned off by low acid

its like having a gastrinoma –> get hypersecretion of acid.

45
Q

What are major causes of hypergastrinemia?

A
  • insufficient amount of luminal acid [due to destruction of parietal cells in pernicious anemia OR use of PPIs/H2 blockers]
  • overproduction of gastrin [antral G hyperplasia, retained antrum]
  • ectopic production of gastrin [gastrinoma]
46
Q

What is pernicious anemia?

A

autoimmune destruction of parietal cells leads to loss of acid secretion
anti parietal cell and anti IF antibodies

47
Q

What is zollinger-ellison?

A

gastrin producing neuroendocrinetumor n pancrea or duodenal wall

autonomously produces gastrin –> acid hypersecretion by parietal cells

GI/Liver (36 decks)

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