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GI > GI PHysio > Flashcards

GI PHysio Flashcards

1
Q

Endocrine hormones

A

released into circulation and reach all tissues

i.e. secretin, gastrin, CCK, GIP and motilin

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2
Q

Paracrine

A

released from endocrine cells and diffuse through extracellur space to target
i.e. histamine

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3
Q

Neurocrine

A

GI peptides located in nn. acting as neurotransmitters.

i.e. ACh

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4
Q

Secretin

A

“natures antacid”
stimulus: released from duodenal mucosa by HCl when pH falls below 4.5
site: released from duodenal mucosa
actions: stimulates pancreatic and liver bicarb. secretion, inhibits gastric emptying
inhibits gastrin release

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5
Q

Gastrin

A

Stimulus: distension due to food
Site of release: G cells in gastric mucosa, duodenum, and pancreas
Action: stimulates release of HCl by pareital cells of stomach via release of histamine from ECL cells
- aids in gastric motility
- acid feeds back to inhibit gastrin release, also inhibited by secretin and glucagon release

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6
Q

CCK (cholecystokinin)

A

Stimulus: proteins and fat in duodenum
Site of release: mucosal cells of small intestine and duodenum
Actions: stimulates gallbladder contractions to release bile for fat digestion and pancreatic bicarb. release

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7
Q

Gastric inhibatory peptide (GIP)

A

stimulus: glucose, fat, protein
site of release: intestinal mucosa
action: inhibits gastric secretions and stimulates insulin release

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8
Q

Motilin

A

stimulus: cyclical release every 90 minutes under neural control during periods of fasting or presence of acid/fat in duodenum
site of release: upper small intestine
action: stimulates gastric motility and upper GI motility via the interdigestive migrating myoelectric complex (MMC)

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9
Q

gastrin CCK interaction

A
  • they can both activate each others receptors b/c they have similar chemical structures
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10
Q

Enteroglucagon

A

similar to secretin

  • release stimulated by fat
  • releases insulin, inhibits gastric secretion and delays gastric emptyig
  • pancreatic alpha cells
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11
Q

Pancreatic polypeptide

A
  • polypeptide isolated from insulin
  • release stimulated by protein, fat, glucose
  • inhibits pancreatic bicarb. and enzyme secretion
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12
Q

Peptide YY

A

release stimulated by fat

inhibits gastric secretion and emptying as well as intestinal motility

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13
Q

Nuerocrine peptides

A

substance P, neurotensin, VIP, bombesin, enkephalins

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14
Q

substance P

A

stimulates intestinal motility and gallbladder contraction

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15
Q

neurotensin

A

increases blood glucose by stimulation of glycogenolysis. inhibits release of insulin

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16
Q

VIP

A

mediates relaxation of intestinal smooth muscle and vasodilates SM via NO

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17
Q

Bombesin

A

like GRP - released by vagal stimulation with resulting release of gastrin

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18
Q

Enkephalins

A

opiates slow intestinal motility and is used to treat diarrhea

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19
Q

Paracrine peptides

A

somatostatin, histamine,

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20
Q

somatostatin

A

found in gastric duodenal mucosa and pancreas

inhibits gastrin release and gastric acid secretion

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21
Q

histamine

A

produced by ECL cells

  • released by gastrin, stimulate acid secretion from parietal cells
  • potentiates action of gastrin and ACh on acid secretion
  • binds with H2 receptors
22
Q

Gastrinoma/Zollinger-Ellison Syndrome

A

tumor of pancreas/duodenum
continually release gastrin into blood
results in peptic ulcers, diarrhea, steatorrhea, hypokalemia

23
Q

Pancreatic Cholera

A
  • watery diarrhea syndrome
  • overproduction of VIP due to pancreatic islet cell tumor
  • results in signifiant intestinal secretion of fluid and electrolytes with production of copious diarrhea
  • frequently lethal due to large volume of fluid lost
24
Q

what do parietal cells secrete?

A

HCl: activates pepsinogen to pepsin (this is stimulated after a meal by gastrin and histamine)

IF –> absorbs vit B12

25
Q

Chief/zymogenic cells

A

Peptic cells: secretes pepsinogen/zymogens

26
Q

Oxyntic glands of stomach

A

located in fudus/body

Parietal, peptid, mucous cells

27
Q

Pyloric glands

A

G cell and mucous cells

28
Q

G cells

A

secrete gastrin: stimulates HCl and pepsinogen release (too much gastrin, drops pH and increases pepsin resulting in ulcers)

29
Q

Alkaline tide

A

H+ is pumped out into gastric lumen via H+/K+ ATPase

Cl- is pumped into parietal cells and gastric lumen via HCO3-/Cl- co transporter, thus directly after eating the blood becomes alkaline

30
Q

M3 Receptors;

A

respond to ACh secreted from Vagus n.

results in neuronal stimulation of parietal cells –> increased HCl secretion

31
Q

H2 receptors

A

histamine secreted from ECL cells stimulates parietal cells, thus increasing HCl secretion. Paracrine stimulation

32
Q

CCK receptor

A

Gastrin is secreted from G cells, works on CCK receptors. stimulates parietal cells and thus increases HCl. this is hormonal

33
Q

Somatostatin

A

inhibits G cell release of gastrin, inhibits parietal cell release of HCl

34
Q

Gastric inhibitory peptide

A

inhibits parietal cells in duodenum and jejunum

35
Q

secretin

A

inhibits gastrin
“natures anacid”
HCO3- release in duodenum

36
Q

phases of secretion

A
  1. cephalic: reflex sends impulses to medulla oblongata stimulating vagus n.
  2. gastric phase: food distends gastric mucosa: stimulates vagus and ENS
  3. Intestinal phase: peptides in duodenum stimulate gastrin secretion
    - secretin released when pH is too low in duodenum, results in HCO3- release
    CCK: released when fatty food in duodenum, results in bile release
37
Q

Vagotomy

A

cutting of vagus n. to inhibit gastric acid secretion

used to treat peptic ulcers

38
Q

Pepsinogen

A

secretion activated by vagus n. via Ach.
secreted by Chief cells
Is converted to enzyme Pepsin via HCl.

39
Q

Pernicious anemia

A

results from absence of IF, no B12 absorption, resulting in defective erythrocyte production

40
Q

Components of mucous?

A

HCO3- in mucous. results in acid being neutralized

  • If H+ penetrates cells, destroys mast cells, histamine is released, more H+ released resulting in further damage.
  • damage can be caused by alcohol, H. pylori, bile acids
41
Q

Peptic ucler disease

A

often asscoated with H. pylori
- acid and pepsin break through mucosal barrier, stimulates mast cells to release histamine, results in parietal cells releasing more HCl

  • can include gastric ulcer disease or duodenal ulcer disease
42
Q

gastric ulcer disease

A
  • assoc. with H. pylori
  • gastrinoma: too much release of gastrin
  • prob. with pepsin staying active too long
43
Q

Duodenal ulcer disease

A

increased acid secretion in gastric region
increased pepsin activation
pancreatitis: decreased HCO3- secretion

44
Q

Pentagastrin

A

has similar effect to gastrin, used to challenge people with peptic ulcer problems.
gastrinoma/duodenal ulcer –> gastric is already elevated, won’t go up much further

45
Q

Gastrinoma/Zollinger-Ellison Syndrom

A

increased gastrin secretion, at rest and after meals

- results in gastric ulcers

46
Q

Atrophic gastritis

A

H. pylori infection, results in increased gastric acid

47
Q

Pernicious anemia

A

Abs produced against parietal cells, results in decreased H+, no gastrin produced, no B12 absorption

48
Q

Omeprazole/Priolosec

A

proton pump inhibitor
decreases H+ release
used to treat peptic ulcers
can results in pneumonia, C. diff growth, osteoporosis.

49
Q

Xerostomia

A

dry mouth only
absence of saliva production
resulting from drugs, radiation, AI disease

50
Q

Sjoren’s syndrome

A

dry mouth and no tears
AI targets salivary and lacrimal glands
difficulty chewing, swallowing, speech and dental problems

51
Q

ductal cells?

A

reabsorb Na+, Cl- ; secrete K+ HCO3- in saliva
results in hypotonic saliva
via NA/K+ ATPase and Cl-/HCO3- exchanger

52
Q

how is saliva controlled?

A

only through ANS
PS: Ach –>M3 receptors –> fluid secretion
stimulated by smell, taste, sound site, chewing
inhibited by : sleep, fear, antidepreesant meds

GI (12 decks)

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