GI I Flashcards

1
Q

bolus

A

food ball made from saliva and chewing in mouth

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2
Q

what does the large intestine absorb?

A

fluid and electrolytes

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3
Q

liver blood supply

A

25% from celiac artery

75% from portal vein (drains from GI system)

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4
Q

how much blood pools in the liver

A

10%, 500mL

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5
Q

how much nutrients does the liver take (first pass)

A

1/3-1/2 of nutrients

not fat or suppositories

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6
Q

how is the GI wall organized?

A

inner layer is absorptive/secretory cells
submucosa: motility and endocrine responses
muscularis externa: motor innervation

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7
Q

what 3 elements are the control mechanism for GI functiin

A

hormonal
neuronal
myogenic

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8
Q

what are the 6 gastric hormones and their source?

A
gastrin- G cells (stom, duo)
CCK- I cells (duo, jej)
Secretin- S cells (duo, jej)
GLIP/GLP- K cells, L cells (duo, jej)
Motillin- M cells (duo, jej)
Somatostatin- D cells (pancreatic islets, GI mucosa)
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9
Q

what does gastrin do?

A

increases acid secretion, mucosa growth, motility

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10
Q

what does CCK do?

A

increase pancreatic bicarb, contraction of gallbladder/relax oddi
decrease gastric emptying

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11
Q

what does secretin do?

A

increases pancreatic and billiary bicarb secretion

decrease gastric acid secretion, growth of mucosa

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12
Q

what does GIP/GLIP do?

A

increases pancreatic insulin secretion

decrease gastric acid secretion

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13
Q

what does motillin do?

A

increases migrating motor complex during fasting

so no SIBO

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14
Q

what does somatostatin do/?

A

decrease gastric acid secretion
decrease pancreatic bicarb
decrease gallbladder contraction

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15
Q

does sym NS or para NS have direct connection with GI muscles and cells?

A

sym NS

for fight or flight response

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16
Q

what are the 3 enteric NT? fx?

A

Ach- parasym effects
VIP relax smooth muscle
GRP- increase gastrin secretion

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17
Q

are ICPs coupled to themselves or SMCs?

A

BOTH

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18
Q

what are the pacemakers in the GI system?

A

ICCs innervated by ENS
slow wave mechanism, contraction when threshold achieved (spike)
more spikes= larger contraction

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19
Q

what are the three things that control GI blood supply

A

arteriole control
ANS command
local events

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20
Q

what are the vasodilators for the GI arterioles?

A

NO
VIP
Ach
Substance P

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21
Q

when you are in shock what does that do to your absorption

A

ischemic villus (impaired)

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22
Q

what are the two local events that can change blood supply?

A

metabolic (changes in oxygen)

myogenic (stretch/tension)

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23
Q

what are the three things that make up peyers patch?

A

m cell- IGA secretions
SED (subepithelial dome) and SIGA secretion
TDA (thymus dependent area) t cells enzymes and secretions

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24
Q

what can radiation cause in GI?

A

low surface area (less absorbtion)

low goblet cell (less mucous)

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25
Q

does sympathetic or parasympathetic make saliva more protein rich?

A

sympathetic

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26
Q

when is the saliva more hypotonic?

A

low flow rates
155mEq
less basic

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27
Q

when is saliva less hypotonic?

A

high flow rates
220mEq
more basic (pH8)

28
Q

why does flow rate effect Na and Cl so much?

A

contact time

29
Q

why does flow rate effect HCO3 so much?

A

selectively stimulated by parasympathetics, levels at 2mL/min

30
Q

what are the key cells for gastric secretion

A
mucous (mucous)
parietal (Hcl, instinsic factor)
ECL (histamine)
chief cell (pepsinogen, gastric lypase)
D cell (somatostatin)
G cell (gastrin)
31
Q

what is imperitive for gastric secretions?

A

vagus innervation stimulates all

32
Q

what is the optimal pH for pepsin?

A

1.8-3.5pH

33
Q

what pH is pepsin REVERSIBLY inactivated?

A

at pH 5

34
Q

what pH is pepsin IRReversibly inactivated?

A

> pH7-8

35
Q

what is the vago-vagal reflex?

A

like you are eating a bAGEL:

stomach distension, vagel afferents send to CNS then vagal efferents increase digestion

36
Q

what 3 substances stimulate gastric acid (HCl) release?

A

Ach (vago vagal)
hormone gastrin ( two pathways)
local histamine release (ECL cells)

37
Q

what stimulates somatostatin?

A

H+ stimulate D cells to release SS and inhibit all 3 cells types G cell, ECL, parietal to stop gastric acid

38
Q

histamine receptor antagonism effect?

A

block histamine from ECL from binding to parietal cell

decrease gastric acid

39
Q

NSAIDs effect?

A

blocks prostaglandins and “inhibit the inhibitor”

increase gastric acid

40
Q

proton pump inhibitor effect?

A

blocks proton pump and decrease in acid

41
Q

what are the factors that protect the stomach from digesting itself?

A
mucins (gels)
trefoil factor family (stabilize mucosa)
bicarb
epithelial replacement
tight junctions
42
Q

what is the pH of pancreatic juice?

A

8.6, isotonic to plasma

43
Q

compare and contrast the composition of saliva vs pancreatic juices

A

see notes

44
Q

what breaks down protein, carbs and fat in pancreas?

A

protein- protease
carbs- amylase
fat- lipase/colipase

45
Q

why dont the pancreatic enzymes digest itself?

A

they are stored in inactive form

46
Q

what is secreted during oral glucose load

A

GIP

47
Q

what is inhibited in very acidic conditions (<1.5)

A

gastrin

48
Q

what 2 things cause bile to go into gallbladder?

A

hepatic secretion pressure

pressure from closure of oddi

49
Q

how is the bile concentrated?

A

Cl and bicard are pumped out with water

50
Q

what is the ideal bile:lectin:cholesterol ratio?

A

10:3:1

51
Q

why does the bile:lectin:cholestrol ratio matter?

A

to maintain solubility

increased cholesterol, decreased bile or lectin cause gallstones

52
Q

describe the process of gallbladder releasing bile

A

see chart

53
Q

what % of bile acid pool is reabsorbed in the ileum?

A

95%

54
Q

what absorbs bile in the ileum?

A

apical sodium dependent bile salt transporter

55
Q

describe the circulation of bile salts

A

see chart

56
Q

what percent of bile is lost in feces?

A

5%

57
Q

what are the 5 functions of the liver?

A
carb metabolism
synthesis of plasma proteins
synthesis of lipoproteins
immunity
inactivation of toxins
58
Q

what is the liver triad?

A

portal venule
portal arterioles
bile duct

59
Q

what does the liver do for immunity?

A

kupffer cells produce lymph

60
Q

what is kernicterus?

A

brain damage in children from the build up of bilirubin

61
Q

how is bilirubin made?

A

degredation of heme

62
Q

unconjugated bili

A

toxic

binds albumin, lipid soluble (enters cells)

63
Q

conjugated bili

A

non toxic
water soluble
bili glucuronide

64
Q

what does the liver do with bili?

A

uptakes and traps with Y&Z protein
conjugates with glucuronic acid
secrets through bile to SI

65
Q

where is bile exreted?

A

bile/gut 80% urobilinogen
liver 18% reuptakes
kidney 2% exretes as urine urobillnogen

66
Q

what does cirrhosis cause?

A

ascites