GI secretions Flashcards

1
Q

Secretin

A

nature’s antacid
released from duodenal mucosa by HCl causes pH falls below 4.5

stimulates pancreatic and liver bicarb, stimulates pancreatic growth, inhibit gastric emptying, inhibits gastrin

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2
Q

Gastrin

A

released from G cells in gastric mucosa, duo, pancreas in response to proteins, distention, nerves, Ca, decaf coffee, wine

stimulates HCl from stomach via Hist (indirect) or can stimulate the Parietal cells directly

aids in gastric motility, stim GI mucosal growth
inhibited by acid, secretin, glucagon

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3
Q

CCK

A

released from mucosal cells of the SI and the duodenum by proteins and fat
stimulates GB contractions to release bile
sim pancreatic bicarb
stimulates pancreatic growth

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4
Q

GIP

A

released from intestinal mucosa in response to Glu, fat and protein
inhibits gastric secretions and stimulates insulin release

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5
Q

motilin

A

released cyclically (/90min) from the SI under neural control during periods of fasting or in presence of acid or fat in duo

stimulates gastric motility, GI motility via the interdigestive migrating myoelectric complex

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6
Q

Enteroglucagon

A

formed in the pancreatic a cells
stimulated by fat
causes insulin release, inhibits gastric secretion, delays gastric emptying

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7
Q

Pancreatic polypeptide

A

isolated from insulin
stimulated by protein, fat, glucose
inhibits pancreatic bircarb and enzyme secretion

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8
Q

Substance P

A

stimulates intestinal motility and GB contraction

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9
Q

VIP

A

mediates relaxation of intestinal smooth muscle and vascular smooth muscle (VD) via NO

stim pancreatic and intestinal secretion
inhibits gastric secretion
n

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10
Q

Somatostatin

A

from gastric, duodenal mucosa and pancreas
inhibits gastrin release and gastric acid secretion
paracrine

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11
Q

Histamine

A
produced in ECL cells 
stimulated by gastrin 
stimulates acid secretion from parietal cells, increases gastrin and ACh activity 
basis for H2 R blockers 
paracrine
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12
Q

salivary bicarb

A

minimizes tooth decay***

neutralizes refluxed gastric acid (heart burn)

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13
Q

Neuronal regulation of salivary glands

A

ANS regulate the flow
SNS stim secretion: alpha and beta receptors
PSNS stim secretion (dominant) M3R

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14
Q

Hormonal control of salivary glands

A

ADH and ald modify composition of saliva by decreasing its Na conc and increasing K conc

Kallikrein—>bradykinin–>VD—>increases blood flow—>increased salivary secretion

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15
Q

what inhibits saliva secretion

A

sleep, fear, antidepressants, dehydration, fatigue

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16
Q

Xerostomia

A

dry mouth due to absence of saliva production (drugs, radiation AI DISEASE)
Buccal infection
dry mouth ONLY

17
Q

Sjogren syndrome

A

AI process targets salivary AND LACRIMAL GLANDS

difficulty chewing, swallowing, and speech, poor dentition

18
Q

digitoxin therapy

A

increases Ca and K in saliva

19
Q

Parietal cells (oxyntic)

A

body and fundus

secrete HCl and IF (needed for B12 abs)

20
Q

Chief (Peptic) cells

A

secrete pepsinogen, zymogens—>converted into pepsin

21
Q

Mucous cells

A
secrete mucous (thick and thin) (highest up)
located in the body as well as the antrum an pyloric regions
22
Q

G cells

A

secrete gastrin—>stimulates parietal cells—>HCl and pepsinogen
located in the antrum and pyloric regions

23
Q

alkaline tide

A

the release of H+ by parietal cells is balanced by their release of HCO3- into the blood, making the venous blood leaving the gut highly alkaline

24
Q

Causes of Gastric Ulcer formation

A

Occurs in the gastric mucosa
from increased acid secretion
**gastrinoma or Zolliner-Ellison syndrome—>inc gastrin
Pepsin remains active for too long
failure of mucosal defense (NSAIDS, H. Pylori)

25
Q

Duodenal Ulcer

A

occurs in the duodenum
more common
from increased acid secretion in the gastric region
pepsin remains active for too long
decreased bicarb secretion from pancreas (pancreatitis)

26
Q

Gastrinoma or zollinger-ellison syndrome

A

pancreatic islet cell adenoma—>increased gastrin—>increased gastric acid secretion—>gastric and or duodenal ulcer due to increased acid and pepsin activity

no change in acid after gastrin challenge (acid already maxed out)

27
Q

Pernicious anemia

A

AI condition in which antibodies act against parietal cells and/or IF—>decreased H+ and somatostatin—> decreased inhibition of gastrin, but still no H+

lack of IF= no B12 reabs =no RBC formation

Acid output is always 0 even after gastrin challenge

28
Q

Pentagastrin

A

used to evaluate gastric function
under normal conditions you see a large increase in acid output after giving it

-people with duodenal ulcers will also have a large increase in acid output

no change in pt with gastric ulcer (gastrinoma) or pernicious anemia)

29
Q

H. pylori activity

A

colonizes mucus layer
releases urase which damages epithelial cells
causes inflammation, mucosal degradation and cell death

30
Q

PPI’s and s/e

A

inhibit the H/K+ exchanger
decrease H+ release—>increased gastric pH

s/e are Pneumonia (due to increased pH, which is better for bacteria growth)
C. Diff growth in gut
Osteoporosis
Duodenal ulcer

31
Q

Steatorrhea

A

fat in stool
early sign of pancreatic dysfunction
indicates reduced pancreatic enzyme and bicarb secretion

32
Q

alcoholism and pancreatitis

A

ETOH damages the liver causing TGs and Ca to enter the blood which damage pancreatic tissue (activation of pancreatic enzymes which start to autodigest)
chronic condition

33
Q

Cephalic phase of gastric acid secretion

A

30% of total gastric acid secretion
conditioned reflexes
ACh acts on parietal cells and ECL

34
Q

Gastric phase of gastric acid secretion

A
food distends gastric mucosa
50-60%
vagus and ENS reflexes activated 
increases acid and pepsinogen secretion 
increased gastrin release
35
Q

Intestinal phase of gastric acid secretion

A

peptide in duo stimulate gastrin
acidic chyme inhibits impulses from the MO and decrease vagal stimulation, decrease acid secretion
release of Secretin, GIP and CCK

activation of pancreatic enzymes: highest rate of release at this point in time

inhibits release of food from the stomach so that you can take care of the food already in the duodenum