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Gastrointestinal - step > Physiology > Flashcards

Physiology Flashcards

1
Q

source of gastrin

A

G cells in antrum of stomach and duodenum

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2
Q

source of somatostatin

A

D cells in pancreatic islets and gi mucosa

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3
Q

source of CCK

A

I cells in duodenum and jejunum

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4
Q

source of secretin

A

S cells in duodenum

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5
Q

source of GIP

A

K cells in duodenum and jejunum

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6
Q

source of motilin

A

small intestine

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7
Q

source of VIP

A

para ganglia in sphincters, gall bladder and small intestine

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8
Q

what cells found in duodenum and secreted what

A 
G cells  - gastrin
I cells - CCK
K cells - GIP
S cell - secretion
D cells - somatostatin
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9
Q

what cells found in jejunum and secrete what

A

I cells - CCK

K cells - GIP

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10
Q

function of gastrin

A

increased H secretion
growth of gastric mucosa
increased gastric motility

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11
Q

stimulation of gastrin

A

stomach distension
alkalinisation
amino acids/peptides
vagus

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12
Q

inhibition of gastrin

A

decreased pH < 1.5

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13
Q

what causes gastrin to increased pathologically

A

h pylori chronic atrophic gastritis
Zollinger Ellison syndrome
chronic PPI use

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14
Q

what are actions of somatostatin

A 
decreased H secretion
decreased pepsinogen secretion
decreased pancreatic fluid secretion
decreased intestinal fluid secretion
decreased gall bladder contraction
decreased insulin release
decreased glucagon release
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15
Q

what stimulats somatostatin

A

increased by acid

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16
Q

what decreases somatostatin

A

decreased by vagus

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17
Q

what is octreotide

A

somatostatin analogue

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18
Q

treatment for acromegaly

A

octreodtide

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19
Q

treatment for insulinoma

A

octreotide

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20
Q

treatment for carcinoid syndrome

A

octreotide

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21
Q

treatment for variceal bleeding

A

octreotide

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22
Q

what does CCK do

A

increase pancreatic secrtion
increases gall baldder contraction
decreases gastric emptying
increases spincter of oddi relazation

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23
Q

what stimulates CCK

A

fatty acids

amino acids

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24
Q

how does CCk cause pancreatic secretion

A

acts on neural M pathways to increased pancreatic secretions

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25
Q

what does secretin do?

A

increases pancreatic HCO3 secretion
decreases gastric acid secretion
increases bile secretion

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26
Q

what stimulates secretin

A

acid
fatty acids in lumen
NO PROTEIN

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27
Q

why is the action of secretin important

A

neutralized acid from the stomach to permit action of pancreatic enzymes

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28
Q

what does GIP stand for?

A

flucose-dependent insulinotropic peptide

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29
Q

what does GIP do?

A

decrease H secretion

increases insulin release - if oral, not IV

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30
Q

what stimulates GIP?

A

fatty acids
amino acids
oral glucose

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31
Q

what does motilin do?

A

produces migrating motor complexes

MMC

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32
Q

what stimulates motilin

A

increases in fast

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33
Q

what is a motilin receptor angonist

A

erythromycin

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34
Q

what is a drug that can be used to stimulate intestinal peristalsis and why?

A

erythromycin bc tis a motilin receptor agonist

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35
Q

what does VIP do?

A

increases intestinal water and electrolyte secetion
increase relaxation of intestinal smooth muscle and sphincters
~~think of clinical implications for VIPoma~~

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36
Q

what stimulates VIP?

A

distension

vagal

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37
Q

what inhibits VIP

A

adrenergic

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38
Q

copious watery diarrhea
hypokalemia
achlorhydria

A

VIPoma, non alpha, non beta islet cell tumor (VIP increases intestinal water and electrolyte secretion and realizes intestiona smooth muschle and spinhters.

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39
Q

what does NO do?

A

increased smooth muscle relaxation includint the LES

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40
Q

what pathology does the significance of NO relaxation of the LES exist in?

A

achalasia

bird beak

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41
Q

what hormones cause H secretion

A

gastrin
ach
histamine

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42
Q

what hormones cause decreased H secretion

A

somatostatin
secretin
GIP

43
Q

what hormones increased pancreatic secretion

A

CCk
secretin
GIP (insulin)

44
Q

what hormones decrease pancreatic secretion

A

somatostatin

45
Q

what hormones have an effect on smooth muscle?

A

gastrin - increases gastric motility
somatostatin - decreased gall bladder contraction
CCK - gall bladder contraction, decreased gastric emptying, increased sphincter of oddi relaxation, VIP - increased intestinal and water electrolye secretion and relaxation of intestinal smooth muscle and sphincters
NO: relaxation of spnihcters including LES

46
Q

what hormones are stimulated by aa/protein?

A

gastrin
CCK
NOT SECRETIN
GIP

47
Q

what hormones are stimulated by fatty acids

A

CCK
secretin
GIP

48
Q

what hormeones are stimulated by oral glucose and not IV glucose

A

GIP

49
Q

what hormones are stimulated by distension

A

VIP

gastrin

50
Q

what hormones are stimulated by vagus

A

gastrin

VIP

51
Q

where are parietal cells located

A

body/fundus of stmach

52
Q

what do parietal cells make?

A

HCL and intrinsic factor

53
Q

what causes parietal cell destruction

A

chronic gastriris

pernicious anemia

54
Q

what stimulates gastric acid production

A

stimulated by histamine, ach and gasrin

55
Q

what inhibits gastric acid prodcution

A

somatostatin
GIP
PG
secretin

56
Q

what is a gastrinoma

A

gastrin secreting tumor that causes high levels of acid and ulcers refractor to medical therapy (like PPI)

57
Q

where does pepsinogen come from

A

chief cells in the body

58
Q

where does pepsin come from

A

pepsinogen in an acid environment

59
Q

what stimulates pepsinogen relase

A

vafal stimulation

local acid

60
Q

where does HCO3 come from

A

mucosal cells @ fundus of stomach, duodenum, salivary galnds, pancreas and brunner glands in the duodeunm

61
Q

what stimulats HCO3 secretion?

A

increased when pancreatic and biliary secretinos increased

secretin

62
Q

how does gastrin exert effects on parietal cells

A

mostly indirectly through stimulation of ECL to produce histamine
also directly on pariental cells
ENDOCRINE

63
Q

list the receptors on parietal cells

A 
M3 receptor
CCKb
H2 receptor
SST receptor
PG receptor
64
Q

list the receptors that are Gi

A

PG receptor

SST receptor

65
Q

list the receptors that are Gs

A

h2 receptor

66
Q

list the receptors that are Gq

A

CCKb

M3 receptor

67
Q

what cause the alkaline tide

A

water and carbon dioxide form bicarb and hydrogen inside parietal cells. h is extruded from cell via HKATPase and HCOe goes to blood in exchange for CL that also leaves into the lumen to combine with H to fomr HCl.

68
Q

what else can act on the pg receptor

A

misoprostal - inhibits

69
Q

where do proton pump inhibitors work

A

on the HKATPase that’s shooting H out to stomach and K into cell.

70
Q

describe pancreatic secretions

A

isotonic always

71
Q

pancreatic secretions low flow

A

high Cl, normal Na (high), normal K (low)

72
Q

pancreatic secretions high flow

A

high HCO3, normal Na (high), normal K (low)

73
Q

what is role of alpha amylase

A

starch digestion

74
Q

how is alpha amylase secreted

A

in active form

75
Q

what are lipases for

A

fat digestion

76
Q

what are proteases for

A

protein digestion

77
Q

list the proteases

A

trypsin, chymotrypsin, elastase, carboxypeptidases

78
Q

how are proteases secreted

A

as zymogens that are activated in the duodenum by trypsin

79
Q

describe how tryspinosgen is crucial to protein digestion

A

gets activated by enterokinase/enteropeptidase a brush border enzyme of the duodenum and jejunum so it can become active trypsin to activate other zymogens/proteases

80
Q

where do you find enterokinase/enteropeptidase

A

brush border of duodenum and jejunum

81
Q

how are carbs absorbed?

A

as monosaccharides: glucose, galactose, fructose

82
Q

describe how monosaccs are absorbed at apical membrane

A

SGLT-1: Na dependent for glucose and galactonse

GLUT5: fructose, facilitated diffusion - cannot be absorbed vrs a concentration gradient

83
Q

how are monosaccs absorbed at basolateral membrane?

A

GLUT2 facilitated diffusion

84
Q

how do you distinguish GI mucosal damage from other causes of malabsorption

A

D-Xylose absorption test

85
Q

where is Fe absorbed

A

as Fe++ in the duodenum

86
Q

where is folate absorbed

A

in the small bowel

87
Q

where is B12 absorbed

A

terminal ileum with bile salts

needs IF

88
Q

describe histo and location of a peyers patch

A

unencapsulated lymphoid tissue in the lamina propria and submucosa of the ileum

89
Q

what is an M cell?

A

specialized epi cells that sample and present antigens to immune cells

90
Q

What happens when a moo is encountered in an M cell?

A

B cells are stimulated in germinal cenetres to differentiate into IgA secreting plasma celsl which ultimately reside in the lamina propria. Ig A gets protective secretory component and is transported across the epithelium to the gut to deal with the intraluminal antigen

91
Q

what makes up bile

A

bile salts (primary conjugated with glycein or turaine - water soluble), phospholipids, cholesterol, bilirubin, water, ions

92
Q

what is the rate limiting step in bile synthesis

A

cholesterol 7alpha hydroxylase

93
Q

who cares about bile

A

everyone

94
Q

why do we care about bile

A

digestion and absorption of lipids and fat soluble vits ADEK

cholesterol excretion

anti moo via membrane disruption

95
Q

what is bodys only way to get rid of cholesterol

A

bile (what about people without a gallbladder!! give them bile acids and watch their cholesterol and atherosclerosis!?)

96
Q

how does bile protect vrs moos?

A

membrane disruptionq

97
Q

list the steps in bilirubin form heme to poop and pee :)

A

@ RES: heme - hemeoxygenase - biliveridin - reductase - bilirubin
@ blood: unconjugated bilirubin - albumin
@ liver: OATP passive transport of unconjugated bilirubin – UDP glucoronosyl-transferase - conjugated bilirubin – MRP2 active transport
@ gut bacteria: conjugate bilirubin – urobilinogen
@ feces: stercobilin brown
@ circulation : urobilinogen 90% of 20% back to lvier and 10% of 20% to urobilin and urine

98
Q

which bilirubin is water soluble

A

direct/conjucated

CONSENANTS

99
Q

which bilirubin is water insoluble

A

insoluble - vowels

indirect/uncongucated

100
Q

vitamin D deficicency

A

rickets: bone pain and deformity
osteomalacia: bone pain and muscle weakness
hypocalcemia tetany
supplement breast milk

101
Q

vitamin E deficiency

A

hemolytic anemia, acanthocytosis
muscle weakness
posterior colomn and spinocerebellar tract demyelination

102
Q

vitamin A deficiency

A 
night blindness - nyctalopia
dry, scaly skin - xerosis cutis
corneal degeneration - keratomalacia
bitot spots on conjunctiva
immunosuppression
103
Q

vitamin K deficiency

A

neonatal hemorrhage with increased PT and aPTT and normal bleeding time
give injection at birth - not in breast milk

104
Q

what vitamin deficiencies can cause anemia

A

vitamin E - hemolytic
B12 - megaloblastic macrocytic anemia
B9 - megaloblastic macrocytic anemia
B6 - sideroblastic anemia due to impaired hemoglobin synthesis and iron excess.

Gastrointestinal - step (10 decks)

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