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Gastro Physiology Flashcards

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1
Q

Gastric mucosa 3 layers

A

Mucuosal consists of epithelial cells (absorptive & secretory functions), lamina propia (conncetive tissue, blood/ lymph vessels), muscalaris mucosae (smooth muscles)

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2
Q

Gastric Submucosa

A

collagen, elastin, most of the blood vessels & the submucosal plexus (Meissner’s

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3
Q

Gastric hormones (4)

A

released from endocrine cells (free cells or clusters spread over large areas but not concentrated in glands) of GI into portal circulation, pass thru liver to systemic circulation & target cells in the GI (gastrin, CCK, secretin, GIP)

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4
Q

Gastric paracrine

A

peptides that act a short distance from where they are released; only paracrine is somatostatin which inhibits actions throughout GI (histamine acts locally but it is not a peptide)

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5
Q

from cholinergic neurons: contract smooth muscle in wall & relax sphincters, increase salivary, gastric, pancreatic secretion

A

Ach

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6
Q

from adrenergic neurons: relax smooth msucle in wall and contract sphincter, increases salivary secretion

A

NE

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7
Q

NT that increases gastric secretion

A

GRP

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8
Q

from neurons of mucosa & smooth muscle: contraction of smooth muscle, decreases intestinal secretion

A

Enkephalin (opiates)

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9
Q

neurons of mucosa and smooth muscle, relaxes smooth muscle, decreases intestinal secretion

A

Neuropeptide Y

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10
Q

cosecreted with Ach, contracts smooth muscle increasing salivary secretion

A

Substance P

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11
Q

Gastrin - 2 types

A

little gastrin (G-17 secreted by G cells in atrum in response to food & G34 between meals – both come from different biosynthetic pathways); the C-terminal tetrapeptide is minimal fragment necessary for activity (1/6 as active as the entire gastrin molecule); functions to increase H+ secretion and growth of gastric mucosa (small peptides and amino acids in stomach (esp. aromatics like tryptophan and phenylalanine), distention of stomach, vagal stimulation through GRP causes release; inhibited by low gastric acid pH

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12
Q

CCK

A

promotes fat digestion & absorption; has the same C-terminal as gastrin & therefore some gastrin activity (but you need the C-terminal heptapeptide); secreted by the I cells of the duodenal and jejunal mucosa; response to presence of monoglycerides/ FFAs but NOT TAGS, and to small peptides (fat & protein stimuli) 5 actions: increases secretion of pancreatic enzymes, bicarb, inhibits gastric emptying, stimulates gall bladder contraction & also relaxation of the sphincter fo Oddi, stimualtes growth of exocrine gall bladder and pancreas

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13
Q

Secretin

A

needs the entire molecule to be active; from the S cells of the duodenum in reponse to H+ and DDAs in the lumen; pancreatic lipases function optimally at pH of 6-8 and are inactivated at pH < 3; secretin inhibits the effect of gastrin

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14
Q

Gastrin Inhibitory Peptide (GIP)

A

from cells of duodenal and jejunal mucosa in response to all 3 nutrients (carbs, peptides, fats), stimulates insulin secretion

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15
Q

motilin

A

from upper duodenum during fasting states; initiates the gastrointestinal motility- the interdigestive myoelectric complexes at 90 minute intervals

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16
Q

pancreatic polypeptide

A

response to nutrients fat, protein, carbs to inhibit pancreatic secretion of bicarb and enzymes

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17
Q

Frequency of slow waves along GI tract

A

stomach with the lowest rate, duodenum with the highest rate; frequency of waves is not influenced by hormones (but the APs/ contractions are influenced)

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18
Q

Origin of slow waves (pacemaker?)

A

interstitial cells of Cajal in the myenteric plexus

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19
Q

Phases of swallowing

A

oral (tongue pushes food to pharynx w/ high density of somatosensory receptors to initiate involuntary swallowing reflex in medulla)

pharyngeal (pharynx  upper esophageal sphincter opens by swallowing reflex and inhibit breathing), esophageal by reflexes)

esophageal phase (primary peristaltic wave coordinated by swallowing reflex, but if food not cleared, a secondary peristaltic wave is initiated by distention of the esophagus (mediated by the enteric NS)

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20
Q

Lower esophageal sphincter opens by

A

by vagal N, which is petidergic and releases VIP to relax LES

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21
Q

Receptive Relaxation

A

VIP also relaxes the orad region of the stomach

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22
Q

Esophagus intrathoracic location (only the LES is in the abdomen), intraesophageal pressure is loess than atm P & lower than abdominal pressure  problem of keeping air out and no GERD resolved w/ …?

A

upper and lower esophageal sphincters

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23
Q

The thickness of the stomach muscle wall increases …

A

distally

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24
Q

fundus, proximal body of stomach; receptive relaxation (vagovagal reflex - VIP) increases the volume to accommodate up to 1.5L food

A

Orad region

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25
distal body & antrum (caudad has a much thicker wall & more forceful contractions); retropulsion propels gastric contents back into stomach for further mixing
Caudal region
26
Migrating myoelectric complexes
at 90 minute intervals function to clear the stomach (3-4 min interval frequency), PNS (gastrin & motilin as well) increases APs and SNS (secretin, GIP) decrease APs
27
Neurocrins from PNS - name 3
VIP, enkephalins, motilin
28
2 kinds of contractions in small intestine
segmentation: mixing chyme w/o forward movement & peristaltic – forward movement
29
Orad contraction involves 2 compounds?
ACh and Substance P
30
Caudal relaxation involves 2 compounds?
VIP and NO
31
gastrocolic reflex
distention of the stomach increases frequency of mass movement sin the large intestine
32
parotid glands
serous cells – aqueous fluid
33
Kallikrein
involved in synthesis of bradykinin, a potent vasodilator; during periods of high saliva flow, increase in bradykinin increases bloodflow
34
4 components of gastric juices
Pepsinogen - pepsin by low pH to digest proteins HCl - lowers pH to activate pepsin IF - B12 absorption Mucus protects against corrosive effects of HCl
35
oxyntic glands
Body of the stomach contains oxyntic glands, which empty their secretory products into the lumen of the stomach
36
oxyntic cells
parietal cells, secrete IF and HCl
37
3 phases of gastric HCl secretion
cephalic (anticipation) - 30% gastric - 60% intestinal - 10% inhibited by a low pH
38
Prostaglandins in stomach?
increase secretion of both mucus and bicarb, thereby enhancing the protective barrier
39
chief cells
peptic cells, secrete pepsinogen
40
G cells
secrete gastrin into bloodstream
41
Mucus neck cells secrete
mucus, bicarb, pepsinogen
42
Acinar cells of pancreatic exocrine tissue?
secrete enzymes (amylase and lipase are secreted as active enzymes); pancreatic proteases are inactive & made active in the duodenum; the stimulus for the enzyme secretion is the presence of peptides in the duodenum
43
Centroacinar cells & ductal cells
secrete aqueous HCO3  initially isotonic (stimulus for the aqueous secretions is the presence of H+ ions)
44
CCK secretion by? Note: Intestinal phase of pancreatic secretion: CCK receptors on acinar cells, most important stimulus for the enzymatic secretions
I cells secrete CCK due to presence of small peptides (tryptophan, phenylalanine, methionine) & fatty acids / Ach stimulates enzyme secretion by vagovagal reflexes
45
Major stimulus for aqueous secretion?
Secretin from the S cells of the duodenum in response to low pH in the duodenum Aqueous secretions contain bicarb
46
Primary Bile Acids
(made by hepatocytes): Cholic Acid & Chenodeoxycholic Acid
47
Secondary Bile Acids
(dehydroxylated by intestinal bacteria) Deoxycholic Acid & Lithocholic Acid
48
Conjugation of Bile Acids to bile salts (makes them more water soluble)?? how?
the liver conjugates bile acids with amino acids, glycine & taurine to form bile salts, this changes the pKs of bile acids  more water soluble (lower pKas allow them to be ionized at a pH of 3-5)
49
major bile pigment?
Bilirubin – byproduct of hemoglobin metabolism, the major bile pigment; cells of the reticuloendothelial system degrade hemoglobin, yielding bilirubin, which is carried in the blood bound to hemoglobin -The liver extracts bilirubin from blood & conjugates it to glucoronic acid to form bilirubin glucuronide, which is secreted into bile & excreted in feces
50
Formation of urobilinogen
Some bilirubin glucoronide is decongugated & reduced to urobilinogen by intestinal bacteria, some excreted, some reabsorbed
51
Rate limiting step in bile acid synthesis
cholesterol 7-alpha hydroxylase
52
-alpha-amylase role? formation of 3 dissaccharides?
digests the 1,4 glycosidic binds in starch leading to formation of 3 dissacharides = alpha-limit dextrins maltose maltotriose
53
intestinal brushborder enzymes
alpha-dextrinase, maltase, sucrase
54
3 monosaccharides
glucose, galactose, fructose
55
Trehalose
2 glucose
56
Lactose
glucose, galactose
57
Sucrose
Fructose | Glucose
58
glucose & galactose transport
Glucose & galactose are cotransported w/ sodium into epithelial cells (secondary active transport – uses the electrical gradient created by the Na-K ATPase on the basolateral surface
59
Fructose transport
facilitated diffusion
60
Exopeptidases
hydrolyze one amino acid at a time from the C-terminal
61
Endopeptidases
interior peptide bond of proteins, includes in the stomach, pepsin, and in the small intestine: tryptin, chymotrypsin, elastase, carboxypeptidase A, carboxypeptidase B (all of these proteases are activated by trypsin (which is activated by enterokinase in the brush border)
62
Pancreatic Lipase
triglyceride > Monoglyceride + 2 FAs Pancreatic lipase is inactivated by bile acids, but to solve this problem it is secreted w/ colipase, activated in intestinal luman by trypsin, displaces the bile acids from interphase so lipase can function
63
Choleserol ester hydrolase
cholesterol ester  cholesterol + FA
64
Phospholipase A2
Phospholipid  Lysolecithin & FA
65
Water Soluble Vitamins
B1, B2, B12, C, biotin, nicotinic acid, pantothenic acid – sodium dependent transport in small intestine w/ exception of B12 (cobalamin) – requires intrinsic factor
66
Fat Soluble Vitamins
diffuse across apical membrane & are incorporated into chylomicrons
67
B12 absorption
Free salivary B12 binds R protein, IF is secreted by gastric parietal cells, pancreatic proteases degrade the R protein, absorbed by specific transporters in the ilium
68
Calcium absorption
depends on 1,25 dihydroxycholecalciferol, which induces synthesis of Vit D-dependent Ca2+ binding protein (calbindin D-28K) in intestinal epithelial cells
69
Iron absorption
Iron is absorbed across the apical surface by intestinal epithelial surface as free iron or as heme iron; inside the cells, heme iron is digested by lysosomal enzymes to release free iron, which binds apoferritin & is transported across to blood bound to beta-globulin called transferrin (takes from SI to liver to bone marrow)
70
Jejunum electrolyte absorption
Jejunum – major site for sodium reabsorption; ~ early proximal tubule of the kidney (sodium enters cell, coupled w/ glucose / galactose; H+ secreted into the lumen & bicarb into blood  net absorption of NaHCO3
71
Ilium electrolyte absorption
also contains a Cl-HCO3 exchange on apical surface (secretes bicarb into the lumen)  net absorption of NaCl
72
Colon electrolyte absorption
similar to principle cells of the collecting duct of the kidneys; sodium channels (and chloride channels) – increased by aldosterone, secretes potassium into the lumen; increased flow rate in colon increases channel activity (can lead to potassium wasting)
73
Sucrose
Fructose (needs fructokinase, aldo B) | glucose
74
lactose
galactose, glucose
75
maltose
2 glucose

Gastroenterology (5 decks)

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