Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Gastrointestinal > GI Secretions + Hormones B&B > Flashcards

GI Secretions + Hormones B&B Flashcards

1
Q

which cells secrete hydrochloric acid and mucous + bicarbonate, respectively?

A

parietal cells - HCL

neck cells - mucous + bicarbonate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

describe the histological location and appearance of parietal cells vs chief cells of the stomach

A

both found in lamina propria (mucosal layer) of gastric glands

parietal cells appear eosinophilic (pink) and are more concentrated closer to the lumen (upper layers) - secrete HCl

chief cells appear basophilic (purple) and are more concentrated in basal (deeper) layers - secrete pepsin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are 3 ways by which the parietal cells are stimulated to secrete HCL?

A
  1. gastrin (direct): hormone from G cells of antrum (distal stomach), binds CCKb receptor on parietal cells
  2. gastrin (indirect): activates ECL cells (entero-chromaffin-like), which release histamine, which stimulates parietal cell secretion via H2 receptor
  3. vagus nerve: releases ACh to activate M3 receptors + releases gastrin-releasing peptide (GRP) which activates G cells, which stimulate parietal cell secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

in the direct pathway of stimulation, gastrin is secreted from the ___ cells and binds _____ receptor on parietal cells to stimulate acid secretion

A
  1. gastrin (direct): hormone from G cells of antrum (distal stomach), binds CCKb receptor on parietal cells
  2. gastrin (indirect): activates ECL cells (entero-chromaffin-like), which release histamine, which stimulates parietal cell secretion via H2
  3. vagus nerve: releases ACh to activate M3 receptors + releases gastrin-releasing peptide (GRP) which activates G cells, which stimulate parietal cell secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

in the indirect pathway of stimulation, gastrin is secreted from ___ cells and activates ECL cells, which mediate _____ release to cause acid secretion from parietal cells

A
  1. gastrin (direct): hormone from G cells of antrum (distal stomach), binds CCKb receptor on parietal cells
  2. gastrin (indirect): activates ECL cells (entero-chromaffin-like), which release histamine, which stimulates parietal cell secretion via H2 receptors
  3. vagus nerve: releases ACh to activate M3 receptors + releases gastrin-releasing peptide (GRP) which activates G cells, which stimulate parietal cell secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the 2 substances released from the vagus nerve that stimulate gastric acid secretion?

A
  1. ACh - activates M3 receptors
  2. gastrin-releasing peptide (GRP) - activates G cells (produce gastrin), which stimulate parietal cell acid secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

why can’t a patient with gastric ulcers be effectively treated with atropine?

A

atropine = muscarinic blocker, blunts parietal cell stimulation by ACh (secreted from vagus nerve)

however, the vagus nerve also releases gastrin-releasing peptide (GRP) which activates G cells to release gastrin

gastrin both directly (via CCKb receptor) and indirectly (via histamine release from ECL cells) stimulates acid secretion from parietal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

which cells release intrinsic factor, necessary for vitamin B12 absorption?

A

parietal cells - secrete HCl and intrinsic factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

explain the cause of the “alkaline tide” that occurs after meals

A

in the basal membrane of parietal cells, carbonic anhydrase converts H2O + CO2 —> HCO3- + H+

the H+ is secreted into the lumen of the stomach via an apical H+/K+ ATPase (anti-transporter) [Cl- is secreted via a separate channel]

the HCO3- leftover is secreted into the serum via a basal HCO3-/Cl- anti-transporter (where the Cl- comes from) —> increased bicarbonate in serum causes alkaline tide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how can urinary chloride be used to determine the cause of metabolic alkalosis?

A

will be LOW in vomiting because HCl is lost

will be HIGH in diuretic use because these drugs block NaCl reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

which 2 endogenous substances inhibit the secretion of H+ from parietal cells? what signaling pathway do the use?

A
  1. somatostatin
  2. prostaglandins

both decrease cAMP via Gi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

which 2nd messengers do the following stimulators and inhibitors of gastric acid secretion use?
a. ACh (via vagus)
b. gastrin (via G cells)
c. histamine (via ECL cells)
d. somatostatin
e. prostaglandins

A

via Gq —> IP3/Ca2+ (via PLC) = ACh and gastrin (both stimulators)

via Gs —> cAMP (via AC) = histamine (stimulator)

via Gi —> decrease cAMP = somatostatin and prostaglandins (both inhibitors)

[all the above are exerting effects on H+/K+ ATPase anti-transporter]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the stimulus for pepsin secretion, and from which cells is it secreted?

A

stimulus for release = vagus nerve

released from chief cells as pepsinogen, activated by H+ (pH 1-3) to pepsin

function = digests proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

where is gastrin secreted from, and how does it reach the parietal cells?

A

produced by G cells in the mucosa (lamina propria) of the antrum of the stomach (closest to pylorus/duodenum)

secreted into portal vein, travels via bloodstream to reach parietal cells (in lamina propria of body of stomach)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

3 effects of gastrin

A
  1. stimulates H+ secretion by parietal cells
  2. stimulates hypertrophy/hyperplasia of gastric mucosa.
  3. Increases gastric motility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

which 2 amino acids are potent stimulators of gastrin release?

A
  1. phenylalanine
  2. tryptophan
17
Q

where do gastrinomas occur? (2)

A

gastrin secreting tumors occurring in duodenum or pancreas (G cells found in fetal pancreas)

—> excessive acid secretion + hypertrophy/hyperplasia of mucosa
—> Zollinger-Ellison Syndrome: abdominal pain + chronic diarrhea

18
Q

what are the symptoms of Zollinger-Ellison Syndrome? (4)

A

occurs with gastrinomas (occur in duodenum or pancreas)

  1. abdominal pain (acidity)
  2. chronic diarrhea - acidity activates pancreatic enzymes and inhibits Na/H2O absorption in small intestines
  3. ulcers in distal duodenum (unusual location) - refractory to PPI therapy
  4. heartburn
19
Q

how can a secretin test be used to dx a gastrinoma?

A

normal G cells inhibited by secretin (hormone) - however, gastrinomas are stimulated by secretin, so gastrin levels will rise after administration

helps differentiate gastrinomas from other causes of high gastrin levels

20
Q

how are gastrinomas treated? (3)

A
  1. high dose PPI - omeprazole, lansoprazole, pantoprazole
  2. octreotide (somatostatin)
  3. surgical excision
21
Q

why does pernicious anemia cause a rise in gastrin levels?

A

pernicious anemia = autoimmune gastritis, loss of parietal cells which are responsible for absorption of vitamin B12 (intrinsic factor)

G cells produce gastrin to stimulate parietal cells —> Gastrin levels increase in an attempt to stimulate parietal cells to increase absorption of vitamin B12

22
Q

what are 4 effects of cholecystokinin?

A
  1. gallbladder contraction
  2. Pancreatic enzymes secretion from the I cells of the duodenum + jejunum
  3. relaxation of sphincter of Oddi
  4. inhibits gastric emptying (time for enzymes to work)
23
Q

what is the mechanism by which cholecystokinin stimulates the secretion of pancreatic enzymes?

A

Indirectly – there are CCK receptors on the vagus nerve, which releases acetylcholine —> stimulates pancreatic secretion

24
Q

What molecules stimulate the release of cholecystokinin? (2)

A
  1. fatty acids + monoglycerides (NOT triglycerides)
  2. amino acids

[CCK stimulates contraction of gallbladder + secretion of pancreatic enzymes]

25
Q

what stimulates the release of secretin and what is its role?

A

Released by S cells of duodenum in response to acid and fatty acids and duodenum —> raises pH in small intestine via bicarb secretion from pancreatic duct cells

also inhibits gastric acid secretion, increases bio production, and promotes pancreatic flow (water secreted with bicarbonate)

26
Q

What pharmalogical agent is used to treat bleeding varices before surgery?

A

varices = blood vessel in esophagus or stomach that occur with portal HTN or liver disease; bleeding can be fatal

octreotide (somatostatin) is administered to reduce splanchnic blood flow [inhibitory hormone to digestion] to decrease bleeding (then ultimately treated with surgery)

27
Q

what are four clinical uses for octreotide?

A

Octreotide = somatostatin

  1. Carcinoid syndrome - somatostatin receptors found on carcinoid tumors (release serotonin), can improve flushing and diarrhea
  2. Acromegaly - inhibits growth hormone secretion
  3. Gastrinoma/glucagonoma - inhibits hormone release
  4. Bleeding varices - decreases splanchnic blood flow
28
Q

What stimulates the release of GIP (GI hormone) and what are its effects?

A

GIP = glucose-dependent insulinotropic peptide —> stimulates insulin release from pancreas (also blunts H+ secretion)

released by K cells of duodenum/jejunum in response to glucose, fatty acids, and amino acids (only hormone stimulated in response to fats, proteins, and carbs)

29
Q

explain why oral glucose is metabolized faster than IV glucose

A

oral glucose stimulates the release of GIP (glucose dependent insulinotropic peptide), which stimulates insulin release from the pancreas

[IV glucose does not stimulate GIP release]

30
Q

what is the role of VIP (vasoactive intestinal peptide)?

A

neurocrine that causes relaxation of smooth muscle - important for relaxation of lower esophageal sphincter

also raises pH by stimulating pancreatic bicarb secretion (water follows, increasing flow in GI tract)

31
Q

what are the symptoms of a VIPoma (3), and why do these occur?

A

VIP (vasoactive intestinal peptide) relaxes smooth muscle and increases bicarb secretion from pancreas + inhibits gastric acid secretion

  1. watery (secretory) diarrhea - water follows bicarb, causes tea-colored, odorless diarrhea resembling cholera
  2. hypokalemia - from high volume diarrhea
  3. achlorhydria - absence of gastric acid
32
Q

Pt is a 44yo M presenting with complain of chronic, tea-colored, odorless diarrhea. They have also been having difficulty digesting food despite trying different diets. Labs show hypokalemia and endoscopic sample shows a high pH in the stomach. What is the dx?

A

dx = VIPoma —> VIP (vasoactive intestinal peptide) relaxes smooth muscle and increases bicarb secretion from pancreas + inhibits gastric acid secretion

  1. watery (secretory) diarrhea - water follows bicarb, causes tea-colored, odorless diarrhea resembling cholera
  2. hypokalemia - from high volume diarrhea
  3. achlorhydria - absence of gastric acid
33
Q

which antibiotic can treat a “frozen stomach” by binding/activating motilin receptors?

A

erythromycin

gastroparesis (frozen stomach/intestine) often occurs in diabetics

Gastrointestinal (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions