Gastro Physiology Flashcards

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
Q

distal body & antrum (caudad has a much thicker wall & more forceful contractions); retropulsion propels gastric contents back into stomach for further mixing

A

Caudal region

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26
Q

Migrating myoelectric complexes

A

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

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27
Q

Neurocrins from PNS - name 3

A

VIP, enkephalins, motilin

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28
Q

2 kinds of contractions in small intestine

A

segmentation: mixing chyme w/o forward movement & peristaltic – forward movement

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29
Q

Orad contraction involves 2 compounds?

A

ACh and Substance P

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30
Q

Caudal relaxation involves 2 compounds?

A

VIP and NO

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31
Q

gastrocolic reflex

A

distention of the stomach increases frequency of mass movement sin the large intestine

32
Q

parotid glands

A

serous cells – aqueous fluid

33
Q

Kallikrein

A

involved in synthesis of bradykinin, a potent vasodilator; during periods of high saliva flow, increase in bradykinin increases bloodflow

34
Q

4 components of gastric juices

A

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
Q

oxyntic glands

A

Body of the stomach contains oxyntic glands, which empty their secretory products into the lumen of the stomach

36
Q

oxyntic cells

A

parietal cells, secrete IF and HCl

37
Q

3 phases of gastric HCl secretion

A

cephalic (anticipation) - 30%
gastric - 60%
intestinal - 10%
inhibited by a low pH

38
Q

Prostaglandins in stomach?

A

increase secretion of both mucus and bicarb, thereby enhancing the protective barrier

39
Q

chief cells

A

peptic cells, secrete pepsinogen

40
Q

G cells

A

secrete gastrin into bloodstream

41
Q

Mucus neck cells secrete

A

mucus, bicarb, pepsinogen

42
Q

Acinar cells of pancreatic exocrine tissue?

A

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
Q

Centroacinar cells & ductal cells

A

secrete aqueous HCO3  initially isotonic (stimulus for the aqueous secretions is the presence of H+ ions)

44
Q

CCK secretion by?
Note:
Intestinal phase of pancreatic secretion: CCK receptors on acinar cells, most important stimulus for the enzymatic secretions

A

I cells secrete CCK due to presence of small peptides (tryptophan, phenylalanine, methionine) & fatty acids / Ach stimulates enzyme secretion by vagovagal reflexes

45
Q

Major stimulus for aqueous secretion?

A

Secretin from the S cells of the duodenum in response to low pH in the duodenum
Aqueous secretions contain bicarb

46
Q

Primary Bile Acids

A

(made by hepatocytes): Cholic Acid & Chenodeoxycholic Acid

47
Q

Secondary Bile Acids

A

(dehydroxylated by intestinal bacteria) Deoxycholic Acid & Lithocholic Acid

48
Q

Conjugation of Bile Acids to bile salts (makes them more water soluble)?? how?

A

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
Q

major bile pigment?

A

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
Q

Formation of urobilinogen

A

Some bilirubin glucoronide is decongugated & reduced to urobilinogen by intestinal bacteria, some excreted, some reabsorbed

51
Q

Rate limiting step in bile acid synthesis

A

cholesterol 7-alpha hydroxylase

52
Q

-alpha-amylase role? formation of 3 dissaccharides?

A

digests the 1,4 glycosidic binds in starch leading to formation of 3 dissacharides =
alpha-limit dextrins
maltose
maltotriose

53
Q

intestinal brushborder enzymes

A

alpha-dextrinase, maltase, sucrase

54
Q

3 monosaccharides

A

glucose, galactose, fructose

55
Q

Trehalose

A

2 glucose

56
Q

Lactose

A

glucose, galactose

57
Q

Sucrose

A

Fructose

Glucose

58
Q

glucose & galactose transport

A

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
Q

Fructose transport

A

facilitated diffusion

60
Q

Exopeptidases

A

hydrolyze one amino acid at a time from the C-terminal

61
Q

Endopeptidases

A

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
Q

Pancreatic Lipase

A

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
Q

Choleserol ester hydrolase

A

cholesterol ester  cholesterol + FA

64
Q

Phospholipase A2

A

Phospholipid  Lysolecithin & FA

65
Q

Water Soluble Vitamins

A

B1, B2, B12, C, biotin, nicotinic acid, pantothenic acid – sodium dependent transport in small intestine w/ exception of B12 (cobalamin) – requires intrinsic factor

66
Q

Fat Soluble Vitamins

A

diffuse across apical membrane & are incorporated into chylomicrons

67
Q

B12 absorption

A

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
Q

Calcium absorption

A

depends on 1,25 dihydroxycholecalciferol, which induces synthesis of Vit D-dependent Ca2+ binding protein (calbindin D-28K) in intestinal epithelial cells

69
Q

Iron absorption

A

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
Q

Jejunum electrolyte absorption

A

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
Q

Ilium electrolyte absorption

A

also contains a Cl-HCO3 exchange on apical surface (secretes bicarb into the lumen)  net absorption of NaCl

72
Q

Colon electrolyte absorption

A

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
Q

Sucrose

A

Fructose (needs fructokinase, aldo B)

glucose

74
Q

lactose

A

galactose, glucose

75
Q

maltose

A

2 glucose