Salvation and gastric Function Flashcards by Sarah Rachel

pathway of GI hormones

produced in GI endocrine cells, portal circulation, pass through liver, systemic circulation to target cells

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target cells of gastrin

parietal cells in stomach

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3 main GI paracrines

somatostatin,
histamine,
serotonin

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act locally on same tissue that secretes them

paracrines

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produced by enterochromaffic cells in intestine in response to distension; excites ENS to increase motility and secretions

serotinin (paracrine)

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produced by D cells; inhibits pancreatic and gastric secretions/motility; endocrine and paracrine

somatostatin

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released by EC-like cells in the stomach; stimulates HCl secretion via H2 receptors

histamine

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synthesized in neurons in GI tract; released following AP

neurocrines

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ACh, norepi, VIP, GRP (gastrin releasing peptide), substance P

neurocrines

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released from G-cells in stomach in response to food, distension, vagus; increases HCl secretion by parietal cells; stimulates growth of gastric mucosa

Gastrin

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secreted by I-cells in mucosa of duodenum and jejunum in response to facts and proteins/peptides/amino acids; increases gall bladder contraction; increases pancreatic enzymes (trypsin, chymotrypsin, lipases, amylases) and bicarb; inhibits gastric emptying

CCK

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secreted by S cells in mucosa of duodenum in response to acidic chyme from stomach; increases bicarb and fluid secretion by pancreas; decreases gastrin and gastric acid secretion; inhibits gastric emptying

Secretin

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trypsin, chymotrypsin, lipases, amylases

pancreatic enzymes

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secreted by M cells in mucosa of duodenum and jejunum during fasting period; promotes contraction of distal stomach and intestines to clear

Motilin

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secreted by K cells in mucosa of duodenum and jejunum in response to fat and carbs; act on pancreas to stimulate insulin secretion; inhibits HCl secretion by parietal cells

GIP (glucose-dependent insulinomic peptide)

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digestion starts in mouth

carbs, fats

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digestions starts in stomach

proteins

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what are and are not digested in stomach

are: proteins, lipids

are not: carbs

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pancreatic enzyme; digestion of proteins in intestine

chymotrypsin

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pancreatic enzyme; digestion of lipids in intestine

lipase

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pancreatic enzyme; digestion of carbs in intestine

amylase

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brush border disaccharidases and dipeptidases complete digestion of carbs and proteins respectively

membrane digestion

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lysozyme, IgA-binding protein

in saliva to reduce bacterial growth

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ptyalin; denatured below pH 4

salivary amylase

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progressive, chronic autoimmune disease which destroys salivary and lacrimal glands

Sjogren syndrome

dry mouth; dental caries and halitosis due to bacterial overgrowth

Xerostromia

secrete serous (watery) substance rich in a-amylase; secrete 25% of saliva each day

acinar cells of parotid gland

produce sero-mucous product rich in mucin glycoproteins; produce 75% of daily saliva

acinar cells of submandibular (70%) and sublingual (5%) glands

high flow rates - saliva is

like plasma

low flow rates - saliva is

hypotonic

flow in duct cells for saliva

Na and Cl out, K and HCO3 into saliva

only humoral agent to affect salivation; stimulates Na reabsorption and K secretion by salivary glands

aldosterone

are salivary duct cells permeable to water

no - tight junctions

what cells secrete lingual lipase

von ebner's cells

otic and submandibular ganglia

stimulated by parasympathetics via salivary nucleus of medulla

otic ganglion stimulates

parotid gland via Ach

submandibular ganglion stimnulates

submandibular gland via Ach

parotid and submandibular glands cause increased

salivary secretion via effects on acinar secretion and vasodilation

parotid and submandibular glands increase salivation via

acinar secretion, vasodilation

activated by salivary glands; causes production of bradykinin for vasodilation

kallikrein

how does bradykinin cause vasodilation

increased capillary hydrostatic P, increased capillary filtration, supplies fluid for secretion

PNS vs SNS effect on salivary flow

PNS - sustained increase | SNS - transient, smaller increase

where is the appetite area of brain

near parasym centers of anterior hypothalamus

where does appetite area of brain get its signals from

cerebral cortex or amygdala

mucous neck cells of oxyntic glands

secrete mucous

peptic/chief cells of oxyntic glands

secrete pepsinogen and gastric lipase

parietal/oxyntic cells of oxyntic glands

secrete HCl and intrinsic factor

what happens when parietal cells are destroyed

achlorhydria - lack of stomach acid secretion, pernicious anemia from lack of intrinsic factor

in body of stomach; empty secretory products via ducts into lumen; duct openings are called pits; contain parietal and chief cells

oxyntic glands

in antrum of stomach; deeper pits than oxyntic glands; contain G cells and mucous cells

pyloric glands

contain G cells (secrete gastrin) and D cells (secrete somatostatin)

pyloric glands

what do cardiac glands secrete

mucous

lack pepsin

digest meats poorly - can't digest collagen

condition for spontaneous conversion of pepsinogen to pepsin

pH < 3-5

HCO3-, mucous, prostaglandins, mucosal blood flow, GFs

protective of gastric mucosa

H+, pepsin, H. pylori, NSAIDs, stress, smoking, alcohol

damaging factors of gastric mucosa

if H+ penetrates into gastric epithelium

- damages mast cells which release histamine, inflammatory response - if severe blood flow decreases and cells are damaged

erosive gastritis

NSAIDs inhibit prostaglandin synthesis

stimulates HCO3- release in stomach

prostaglandin

enzyme for CO2 combining with H2O

carbonic anhydrase

where does a strong solution of HCl form in HCl secretion

canaliculus

driving force for HCl secretion

H+-K+ ATPase in lumenal membrane of stomach

alkaline tide

HCO3- is absorbed form the cell into the blood at the basolateral membrane via a Cl/HCO3 exchanger

target of drugs for GERD or ulcers

H+/K+ ATPase

vomiting center

medulla oblongata

where is the chemoreceptor which can stimulate vomiting

4th ventricle of brain

how does histamine stimulate acid secretion

acts on adjacent parietal cells

how does the vagus stimulate acid secretion

directly and indirectly

how does gastrin stimulate acid secretion

acts directly on parietal cells, | also acts indirectly via stimulation of histamine release

how does insulin stimulate acid secretion

acts directly on parietal cells to stimulate histamine secretion

how does somatostatin inhibit acid secretion

paracrine manner on parietal cells and G cells (inhibits gastrin)

how does GIP inhibit acid secretion

acts directly on parietal cells

how does secretin inhibit acid secretion

acts on G cells to suppress gastrin

atropine

inhibits Ach

Cimetidine

H2 receptor antagonist, | inhibits histamine

omeprazole, prilosec

proton pump inhibitors

direct and indirect stimulation of HCl secretion

direct - vagus (via Ach receptors) | indirect - gastrin

how does the vagus stimulate gastrin release

vagus releases gastrin releasing peptide (GRP) onto G cells

the vagus has direct stimulation in the cephalic phase on HCl release via

Ach receptor on parietal cells

the vagus has indirect stimulation in the cephalic phase on HCl release via

GRP on G cells which then release Gastrin

cephalic phase stimuli

smell, taste, conditioning

gastrin phase stimuli

distention, distention of antrum, amino acids/peptides

major inhibitiory mech of HCl secretion (factor; direct/indirect)

somatostatin - direct and indirect

HCl is needed for activation of

pepsinogen

histamine is released from

ECL cells

in the stomach, the vagus directly stimulates

- parietal cells (via Ach) = direct - ECL cells (increased histamine) - D cells (decreased somatostatin)

lumenal H+ directly stimulates D cells, somatostatin inhibits gastrin, reduce acid secretion

negative feedback

products of protein digestion directly stimulate G cells, gastrin stimulates acid secretion

positive feedback

pepsinogen is secreted from

oxyntic glands of the stomach

xerostomia, or antichonlinergics, would cause what change in Cl and K content in saliva

deacreased flow rate - more time to diffuse - Cl decreases - K increases

is gastrin inhibitory peptide (GIP) found in the lumen of the stomach?

no - intestines only

HCl, lipase, mucous, and intrinsic factor are all secreted

directly into lumen of stomach

where does most carb digestion occur

duodenum

RLS in acid secretion

proton pump

effect of vagotomy on cephalic phase acid secretion

wipes it out

Digestion of ___ is impaired to the greatest extent in patients with achlorhydria (failure of HCl secretion by stomach)

protein

Salvation and gastric Function Flashcards

(96 cards)