BRS Physiology Flashcards

1
Q

layers of the GI tract

A
epithelial cell
Lamina propria
muscularis mucosae
submucosal plexus
circular muscle
myenteric plexus
longitudinal muscle
serosa

ELMS CMLS

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2
Q

vagus nerve innervates

A

stomach, upper large intestine, pancreas, esophagus

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3
Q

pelvic nerve innervates the

A

lower large intestine, rectum, anus

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4
Q

myenteric plexus (auerbach plexus)

A

motility of GI smooth muscle

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5
Q

submucosal (meissner plexus)

A

controls secretion and blood flow

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6
Q

actions of gastrin

A

stimulates H+ release by parietal cells

stimulates growth of gastric mucosa

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7
Q

gastrin secreted by what cells

A

G cells of the gastric antrum

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8
Q

stimuli for gastrin secretion

A

small peptides and amino acids in lumen of stomach
distension of stomach
vagal stimulation, mediated by GRP

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9
Q

inhibition of gastrin secretion

A

H+ in the lumen of the stomach: negative feedback

somatostatin: Gi

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10
Q

Actions of CCK

A

1) HCO3- release from pancreas potentiation with secretin
2) growth of Exocrine pancreas
3) pancreatic enzyme secretion
4) inhibits gastric emptying
5) contraction of the gallbladder and relaxation of sphincter of Oddi

HEPIC

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11
Q

cells that release CCK

A

released from I cells of duodenal and jejunal muscosa

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12
Q

stimuli for release of CCK

A

small peptides and amino acids
fatty acids and monoglycerides
(no triglycerides)

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13
Q

Secretin is homologous to ____

A

glucagon

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14
Q

actions of secretin

A

coordinate to reduce amount of H+ in the lumen of SI

1) stimulates pancreatic HCO3- secretion and increases growth of exocrine pancreas
2) stimulates HC)3- and H20 secretion by liver and increases bile production
3) inhibits H+ secretion by gastric parietal cells

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15
Q

secretin from what cells

A

S cells of duodenum

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16
Q

stimuli for secretin release

A

H+ in duodenum

Fatty acids in lumen of duodenum

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17
Q

GIP is homologous to

A

secretin and glucagon

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18
Q

actions of GIP

A

1) stimulates insulin release

2) inhibits H+ secretion by gastric parietal cells

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19
Q

Stimuli for release of GIP and where secreted

A

secreted by duodenum and jejunum
fat, protein, carbs,
FA,AA,oral glucose

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20
Q

GLP-1 action

A

binds pancreatic B-cells and stimulates insulin secretion

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21
Q

somatostatin inhibits what

is inhibited by?

A

1) inhibits release of all GI hormones, inhibits gastric H+ secretion
2) inhibited by vagal stimulation

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22
Q

histamine action

A

increases H+ secretion directly

potentions effects of gastrin and vagal stimulation

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23
Q

VIP homologous to?

A

secretin

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24
Q

VIP action

A

relaxation of GI smooth muscle including lower esophageal sphincter
stimulates pancreatic HCO3- section, inhibits gastric H+ secretion

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25
Q

GRP (bombesin) action and released from

A

released from vagus nerves that innervate G cells

stimulates gastrin release from G cells

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26
Q

Enkephalins secreted from

A

secreted from nerves in mucosa and SM of GI tract

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27
Q

enkephalins action

A

stimulate contraction of GI smooth muscle

inhibit intestinal secretion of fluid and electrolytes

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28
Q

Satiety center location

A

ventromedial nucleus of hypothalamus

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29
Q

feeding center

A

lateral hypothalamic area

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30
Q

anorexigenic neurons release

A

POMC and decrease appetite

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31
Q

orexigenic neurons release

A

neuropeptide Y and stimulate appetite

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32
Q

leptin

A

secreted by fat cells, decrease appetite

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33
Q

ghrelin

A

secreted by gastric cells, increase appetite

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34
Q

location of highest freq slow wave contraction and low

A

high is in duodenum

low is in stomach

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35
Q

achalasia

A

lower esophageal sphincter does not relax during swallowing and food accumulates in the esophagus

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36
Q

orad region of stomach

A

fundus and proximal body

contains oxyntic glands and responsible for receiveing ingested meal

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37
Q

caudad region of stomach

A

distal body and antrum

responsible for contactions that mix food and propel it into the duodenum

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38
Q

what is the regulator of contractions every 90 mintues even under fasting conditions

A

motilin

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39
Q

when is the rate of gastric emptying the fastes

A

when the stomach contents are isotonic

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40
Q

fat ___ gastric emptying by stimulating the release of ___

A

inhibits, CCK

41
Q

H+ in the duodenum ___ gastric emptying

A

inhibits

42
Q

segmetation contractions

A

mix intestinal contents with back and forth motion of chyme

43
Q

when food in the intestinal lumen is sensed by __ they release ___ which bind to __ and initiate the peristaltic relex

A

enterochromaffin cells, 5-HT, intrinsic primary afferent neurons (IPAN)

44
Q

gastroileal relex

A

mediated by extrinsic ANS and possibly gastrin

triggered by food in stomach

45
Q

where in the colon is most water absorbed

A

proximal colon

46
Q

initial starch digestion is done by what in saliva

A

a-amylase (ptyalin)

47
Q

initial triglyceride digestion is done by what in saliva

A

lingual lipase

48
Q

composition of saliva

A
high volume
high K+ and CO3-
low Na and Cl
hypotonic
a-amylase, lingual lipase, kalikrein
49
Q

at the lowest flow rate

A

lowest osmolarity, lowest Na+ and Cl- and HCO3-

highest K+ concentration

50
Q

at highest flow rate

A

composition of saliva is closest to that of plasma

51
Q

saliva is formed by 3 glands

A

parotid, submandibular, sublingual

52
Q

STRUCTURE OF GLAND:
Acinus
branching duct system
myoepithelial cells

A

acinus, secrete initial saliva
BDS, lined with columnar epithelial cells, modify saliva
myoepithelial cells, line acinua and initial ducts, contract and eject saliva into mouth

53
Q

ducts modify initial isotonic saliva
reabsorb
secrete

A

reabsorb Na+ and Cl-

secrete K+ and HCO3-

54
Q

aldosterone working on ducts

A

reabsorb Na+ and secrete K+

55
Q

why does saliva become hypotonic

A

ducts are relatively impermeable to water

56
Q

parasympathetic stimulation of saliva production

NT and receptor and second messenger

A

Ach binds muscarinic receptors on acinus and ductal cells

second messenger is IP3 and increased Ca2+

57
Q

what is an anticholinergic drug that inhibits production of saliva and causes dry mouth

A

atropine

58
Q

sympathetic stimulation of saliva production

NT and receptor and second messenger

A

NE binds B adrenergic receptors on acinar and cutal cells and the second messenger is cAMP

59
Q

what increases saliva production

A

food in mouth
smells
conditioned relex
nausea

60
Q

what decreases saliva production

A

sleep
dehydration
fear, anticholinergic drugs

61
Q

parietal cells secrete __ and _

where and resbsorb __

A

HCL and intrinsic factor

into lumen of stomach, absorb HCO3- into bloodstream

62
Q

in parietal cells how is H+ transported into the lumen of the stomach?

A

through the H+/K+ ATPase

Cl- is also transported into the lumen as well = HCl

63
Q

what drug inhibits the H+/K+ ATPase

A

omeprazole (proton pump inhibitor)

64
Q

what is the HCO3- that is reabsorbed in parietal cells exchanged for?

A

Cl-

65
Q

HCO3- is secreted in pancreatic secretions to neutralize H+ ions in SI
effect of vomiting

A

if vomiting occurs H+ never in SI and no HCO3- secretion causes metabolic alkalosis

66
Q

vagal stimulation of gastric H+ secretion:

Direct and indirect

A

Direct: vagus nerve innervates parietal cells with Ach binding M3 receptor and IP3 and increased Ca2+ cause release H+

indirect: vagus n innervates G cells of antrum with GRP which secrete gastrin, bind to CCKb receptor and stimulate release of H+ from parietal cells
- IP3 and ca2+

67
Q

atropine effect

A

anticholernergic drug blocks direct pathway of H+ secretion only

68
Q

gastrin stmiulates which cells

A

parietal–H+

enterochromaffin-like cells (ECL)—> histamine secretion—> H+ secretion

69
Q

Histamine action

A

released from ECL cells and binds H2 receptor on parietal cells, coupled to Gs protein, cAMP

70
Q

H2 receptor blocking drug

A

cimetidine

71
Q

inhibition of gastric H+ secretion

A

low pH of less than 3.0

somatostatin

72
Q

somatostatin direct and indirect pathways

A

direct: binds to receptor on parietal cell coupled to Gi, inhibits adenylyl cyclase and cAMP
- antogonist of histamine

Indirect: inhibits release of gastrin and histamine

73
Q

prostaglandins action

A

inhibit H+ secretion by Gi protein, inhibit adenylyl cyclase and decrease cAMP

74
Q

Peptic ulcer disease and damaging factors

A

ulcerative lesion of gastric or duodenal mucosa

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

75
Q

gastric ulcer

A

H+ secretion decreased bc secreted H+ leaks back through damaged gastric mucosa–> more gastrin levels increase
-cause is H. Pylori
converts urea to NH3 with urease so less acidic and can live here

76
Q

test for H. pylori

A

give person 13C-urea which is converted to 13CO2 by urease and measeured in expired air

H. Pylori have urease

77
Q

zollinger-ellison syndrome

A

gastrin secreting tumor of the pancreas causes increased H+ secretion, no negative feedback

78
Q

pancreatic secretion contains high concentration of what

A

HCO3-, also enzymes for digestion of protein, carbs, and fat

79
Q

pancreatic juice is characterized by

A

1) high volume
2) about same Na+ and K+ as plasma
3) higher HCO3- than plasma
4) lower Cl- concentration than plasma
5) isotonicity
6) pancreatic lipase, amylase, and proteases

80
Q

flow rate pancreas juice comp:

A
high = Na+ and HCO3- mainly, isotonic
low= Na+ and Cl- mainly, isotonic
81
Q

formation of pancreatic secretion

A

acinar cells secrete initial Na+ and Cl-

ductal cells reabsorb Cl- and secrete HCO3-

82
Q

secretin and pancreas and second messenger

A

acts on pancreatic ductal cells to increase HCO3- secretion
happens when H+ goes from stomach to duodenum
-cAMP is second messenger

83
Q

CCK and pancreas

A

acts on pancreatic acinar cells to increase enzyme secretion (amylase, lipase, proteases)
-potentiates effect of secretin on ductal cells to stimulate HCO3- secretion
second messengers are IP3 and increased CA2+

84
Q

Ach and pancreas

A

released in response to H+, small peptides, aa, FA in duod lumen
stimulates enzyme secretion by acinar cells
potentiates effect of secretin on HCO3- secretion

85
Q

a-amylases

A

hydroloze 1,4 glycosidic bonds in starch, yield maltose, maltotriose, and a-limit dextrins

86
Q

maltase, a-dectrinase, sucrase

A

in intestinal brush border hydrolyze oligosaccharides to glucose

87
Q

lactase degrades

A

lactose to glucose and galactose

88
Q

trehalase degrades

A

trehalose to glucose

89
Q

sucrase degrades

A

sucrose to glucose and fructose

90
Q

glucose and galactose from lumen to cells then cells to blood

A

1) SGLT 1 with Na+ down gradient and glucose uphill

2) GLUT2 from cell to blood

91
Q

fructose transport

A

exclusively by facilitated diffusion, cannot be absorbed against concentration gradient

92
Q

lactose intolerance

A

absence of brush border lactase so lactose cannot be converted to glucose and galactose for absorption
noabsorbed lactose and H2O remain in lumen and cause osmotic diarrhea

93
Q

endopeptidases

A

degrade proteins by hydrolyzing interior peptide bonds

94
Q

exopeptidases

A

hydrolyze one amino acid at a time from C terminus proteins and peptides

95
Q

pepsin

A

activated from pepsinogen by H+
optimal at pH between 1 and 3
if above 5 pepsin is denatured

96
Q

trypsinogen to trypsin by what enzyme

A

enterokinase

97
Q

what does trypsin work on

A

chymotrpsinogen, proelastase, and procarboxypeptidase A and B and also trypsinogen to make more trypsin

98
Q

free amino acid absorbtion

A

cotransported from lumen to intestinal cell with Na+, then aa to blood via facilitated diffusion

99
Q

dipeptide and tripeptide absorbtion

A

cotransported with H+ from lumen to cell

cyctoplasmic peptidases hydrolyze them to aas and then aas to blood via facilitated diffusion