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MSS - GI Exam 1 > Exam 1 Choudhury Review > Flashcards

Exam 1 Choudhury Review Flashcards

1
Q

smooth muscle

A

one nucleus
unstriated
dense bodies present**
no troponin

has calmodulin

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2
Q

mechanical connections

A

dense bodies

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3
Q

electrical connections

A

gap junctions

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4
Q

varicosities

A

axon swelling at each contact point

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5
Q

smooth muscle innervation

A

both S and PS

lots of receptors for NT and hormones

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6
Q

multi unit smooth m.

A

one nerve to each nerve cell

-finer motor control

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7
Q

single unit smooth m.

A

one nerve to many muscle cells
-in visceral smooth m.
coordinated contraction

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8
Q

graded slow wave

A

action potential possible

-not always cause AP

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9
Q

interstitial cells of cajal

A

pacemaker of GI
-between long and circular muscles of muscularis externa layer

generate slow wave potentials

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10
Q

slow wave potential

A

oscillation without contraction or reaching threshold

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11
Q

depolarization of GI tract

A

slow Ca channels with slow inactivation

always ongoing cycle of contraction**

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12
Q

action potential spike

A

Ca influx and K eflux

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13
Q

3 major pathways to increase Ca

A

both extracellular and intracellular Ca

Ca rushes in from extracellular
binds to SR and releases intracellular Ca (CICR)

1 voltage gated
2 SR (voltage independent)
3 store-operated Ca channels (SOCs)
-also voltage independent

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14
Q

pharmacomechanical coupling

A

hormones and neurotransmitters can initiate increased Ca via G-protein coupled receptors (voltage independent)

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15
Q

Ca2+ excitation contraction coupling

A

phosphorylation of myosin in thick filament

  • uses less ATP
  • sustained contraction
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16
Q

Ca2+ binding calmodulin

A

forms CaM - activates MLCK
MLCK phosphorylates myosin

increased ATPase activity

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17
Q

latch state

A

maintain tension of smooth m. without fatigue

-low ATP consumption

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18
Q

intrinsic nerves in GI?

A

submucosal and myenteric

S and PS innervation

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19
Q

GI hormones

A

gastrin, secretin, CCK, GIP

-paracrines - somatostatin and histamine

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20
Q

extrinsic neves in GI?

A

autonomic nerves

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21
Q

Ach

A

parasympathetic

increased causes:
salvation, lacrimation, urination, contraction, GIT motility, defecation

decreased causes:
dry mouth, urine retention, constipation

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22
Q

increased parasympathetic activity

A

promote digestive and absorptive processes

increases motility and secretions

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23
Q

4 GI regulatory mechanisms

A

autonomic smooth m.
extrinsic nerves
intrinsic nerve plexuses
GI hormones

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24
Q

sympathetic innervation of GI

A

promotes decreased motility and secretion, increased sphincter constriction

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25
Q

enteric nervous system

A

divisions of ANS
-PS and S to GI tract

intrinsic neural control

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26
Q

myenteric plexus

A

auerbachs - between long and circ muscle layers of muscularis externa

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27
Q

submucusal plexus

A

meissners - submucosa

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28
Q

auerbachs plexus

A

motility of GI smooth muscle

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29
Q

meissners plexus

A

secretion and blood flow

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30
Q

all GI hormones?

A

peptides

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31
Q

classification of GI hormones

A

endocrine
paracrine
neurocrine

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32
Q

5 GI peptide hormones

A 
secretin
gastrin
CCK
GIP
motilin
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33
Q

candidate GI peptide hormones

A

pancreatic polypeptide
neurotensin
substance P

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34
Q

secretin

A

increased acid HCl is stimulus

increases pancreatic bicarbonate secretion

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35
Q

gastrin

A

increased by histamine

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36
Q

CCK

A

increased pancreatic enzyme secretion

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37
Q

GIP

A

inhibits gastrin secretion

-increases insulin release

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38
Q

motilin

A

increases upper GI mobility (during fasting)

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39
Q

gastrin secretion

A

after a meal

  • increase in gastric acid secretion
  • antrum and duodenum
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40
Q

duodenum/jejunum secretions

A

secretin, CCK, GIP, motilin

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41
Q

histamine

A

paracrine

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42
Q

AcH

A

non-peptide neurocrine

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43
Q

natures antacid

A

secretin

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44
Q

secretin affects

A

released response to decreased pH

more pancreas and liver bicarbonate
decreased gastric emptying
increased pancreas growth
decreased gastrin release

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45
Q

gastrin affects

A

from G cells in gastric mucosa, duodenum and pancreas

-increased in response to high protein, Ca, decaf, wine

increases parietal cell HCl secretion directly and through histamine (from ECL cells)

increased gastric mobility
increased acid has negative feedback
increased GI mucosa growth

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46
Q

inhibitors of gastrin release

A

secretin and glucagon

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47
Q

CCK affects

A 
released duodenum and jejunum
increased response to protein and fats
increased gallbladder contractions - increased bile
increases pancreatic bicarbonate
increases pancreatic growth
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48
Q

GIP affects

A

insulinotropic hormone
increased response to fat, protein, and GLUCOSE

decreases gastrin
increases insulin

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49
Q

motilin affects

A

every 90 seconds

in upper small intestine due to fasting or acid/fat

MMC

increased gastric and upper GI mobility

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50
Q

CCK vs. gastrin?

A

can activate eachothers receptors

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51
Q

enteroglucagon affects

A

increased with fat

pancreatic alpha cells
increase insulin and gastric secretion

delay gastric emptying

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52
Q

pancreatic polypeptide affects

A

increased with protein, fat, glucose

decreased pancreatic bicarb/enzymes

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53
Q

peptide YY

A

increased with fat

decrease gastric secretion and emptying
decrease intestine mobility

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54
Q

substance P

A

increase intestinal motlity and gallbladder contraction

neurocrine

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55
Q

neurotensin

A

increases glycogenolysis and decreased insulin and increase glucagon

neurocrine

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56
Q

VIP

A

relax intestine smooth m. and vascular smooth m.

vasodilates - NO

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57
Q

bomberin

A

vagal stimulation

increases gastrin

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58
Q

enkephalin

A

increased opiate receptors and sphincter contractions

treat diarrhea***

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59
Q

somatostatin affects

A

decrease gastrin and decrease acid

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60
Q

histamine

A

ECL cells
increase with gastrin

increase parietal cell HCl secretion

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61
Q

H2 receptor blocker

A

antacid

-blocks histamine receptors on parietal cells

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62
Q

zollinger ellison syndrome

A

non-beta cell tumor of pancreas or duodenum

increased gastrin
-ulcers, diarrhea, hypokalemia

aka gastrinoma

need high protein meal, IV Ca and secretin infusion

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63
Q

pancreatic cholera

A

increased VIP
-cancer of pancreatic islet cells

increase diarrhea

give fluids and electrolytes

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64
Q

saliva

A

hypotonic (active process)

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65
Q

alpha amylase

A

not essential

-alpha 1-4 bonds of carbs

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66
Q

salivary regulation?

A

rate only affected by neuronal

hormonal affects composition

67
Q

can you taste protein?

A

no

68
Q

lysozyme

A

antibacterial

69
Q

lactoferrin

A

chelates iron (antimicrobial)

70
Q

lactoperoxidase

A

antibacterial

71
Q

glycoprotein of IgA

A

against virus/bacteria

72
Q

EGF/NGF

A

mucosal growth

73
Q

kollikrein

A

activate bradykinin

increased blood flow to glands

74
Q

bicarbonate

A

no tooth decay

neutralizes acid

75
Q

salivon

A

functional unit secreting saliva

76
Q

reabsorption in salivon?

A

reabsorb Na and Cl

secrete K and HCO3

77
Q

plasma

A

high Na Cl

low K HCO3

78
Q

low rate saliva

A

hypotonic and high K

79
Q

high rate saliva

A

increased osmolality, increased HCO3-, alkaline, and increased Na

80
Q

Na reabsorption

A

apical - Na enters ENaCs epithelial sodium channels

basolateral - actively pumped out Na/K ATPase

81
Q

Cl- reabsorption

A

apical - Cl enters Cl HCO3- exchanger

basolateral - Cl- exits through Cl- channels

82
Q

HCO3 secretion

A

Cl HCO3- exchanger

83
Q

H2O in salivon

A

cannot be reabsorbed

-tight junctions

84
Q

K secretion

A

Na K ATPase

85
Q

content of saliva in acini

A

H2O, Na, Cl, K, HCO3, amylase

86
Q

hormonal control of saliva

A

ADH and aldosterone

regulate composition

87
Q

sympathetic saliva control

A

alpha beta receptors

88
Q

parasympathetic saliva control

A

M3 receptors

89
Q

increased activity saliva

A

smell, taste, sound, sight, spicy sour

90
Q

decreased activity saliva

A

sleep, fear, ANTI-DEPRESSANT, dehydration, fatigue

91
Q

drooling

A

increased nervous stimulation

treat with anticholinergics or remove sublingual gland

92
Q

xerostomia

A

dry mouth with decreased saliva production

drugs, radiation, autoimmune

93
Q

sjogrens syndrome

A

dry moth AND DRY EYES

  • glandular atrophy
  • also affects lacrimal glands
94
Q

digoxin

A

increased Ca and K in saliva

95
Q

addisions

A

increased Na in saliva

96
Q

cushings

A

primary aldosteronism
decreased Na in saliva

NaCl is zero**

97
Q

parkinsons

A

increased saliva

98
Q

stomach secretions

A

proximal - HCl, pepsinogen, intrinsic factor, mucus, bicarb, water

distal - gastrin, somatostatin

99
Q

intrinsic factor

A

for Vit B12 absorption in ileum
-aka cobalumine

needed to survive**

100
Q

chief cells

A

pepsinogen and renin

101
Q

ECL cells

A

histamine

102
Q

G cells

A

gastrin

103
Q

D cells

A

somatostatin

104
Q

oxyntic gland

A

fundus and body of stomach
-parietal cells
-peptic (chief) cells
mucous cells

105
Q

parietal cells

A

HCl and intrinsic factor

106
Q

pyloric gland

A

antrum and pylorus

-G cells and mucous cells

107
Q

stomach mucosa

A

regenerated every 3 days

108
Q

non parietal cell secretion

A

low rate
high Na and Cl
low H and K

109
Q

parietal cell secretion

A

after a meal
high rate

high H and Cl
low Na and K

110
Q

alkaline tide

A

venous blood leaving GI is alkaline

because bicarb dumped to blood and H+ goes to stomach (H/K ATPase)

111
Q

direct affects on parietal cells

A

AcH from vagus to M3 receptors
histamine from ECL cells to H2 receptors
gastrin from G cells to CCK receptors

all increase acid secretion

112
Q

indirect affects on parietal cells

A

AcH to M3 receptors on ECL causes histamine release

gastrin on CCK receptors on ECL causes histamine release

histamine then acts on parietal cells to increase acid secretion

113
Q

cephalic phase

A

in head 30%

via vagus

114
Q

gastric phase

A

in stomach 50-60%

food distending gastric mucosa

115
Q

intestinal phase

A

in intestine 10%

peptides in duodenum

116
Q

acid release

A

AcH - neuronal
gastrin - hormonal
histamine - paracrine

117
Q

somatostatin

A

inhibits G cells from producing gastrin

118
Q

GIP

A

inhibits gastrin and acid secretion from parietal cells

119
Q

secretin

A

decreases both gastrin and acid

nature antacid

120
Q

3 duodenum hormones inhibiting acid secretion

A

secretin
GIP
CCK

121
Q

secretin

A

too much acid food in duodenum

122
Q

CCK

A

too much fat/protein

  • increased pancreatic secretion
  • increased gallbladder contraction
123
Q

vagotomy

A

cut vagus nerve
inhibit gastric acid secretion
used to treat peptic ulcers

selective - cutting vagal nerves to parietal cells only

124
Q

pepsinogen

A

secreted by chief cells

stimulated by ACh, histamine, gastrin/CCK

125
Q

intrinsic factor

A

from parietal cells

necessary for absorption of vitamin B12

126
Q

vitamin B12

A

needs intrinsic factor to bind to cubulin

127
Q

mucus secretion

A

by surface cells

forms layer with bicarbonate
no acid damage to mucosa

128
Q

if acid to gastric epithelium

A

destroys mast cells - histamine

results in inflammation

129
Q

agents damaging mucosal damage

A

alcohol
salicylates
h pylori
bile acids

130
Q

ulcer formation

A

h pylori, NSAIDs (COX-1 inhibitor), stress

131
Q

aspirin

A

weak acid - easily absorbed in low pH of stomach

breaks protective mucosal barrier

132
Q

peptic ulcer disease

A 
gastric ulcer
duodenal ulcer (much more)
133
Q

h pylori infection

A

gastric ulcer disease

134
Q

gastrinoma

A

cancer of stomach

  • aka zollinger ellison syndrome
  • increased gastrin secretion

results in gastric ulcer disease

135
Q

gastrinoma

A

gastrin levels initially high

136
Q

atrophic gastritis

A

lack parietal cells

lower levels of gastrin initially

137
Q

h pylori

A

gram negative bacteria

damages mucosal barrier layer

138
Q

H2 receptor blockers

A

rantidine
cimentidine

decreases histamine activation of parietal cells
-increased gastric pH

139
Q

proton pump inhibitor

A

omeparazole

makes it more alkaline (increases gastric pH)

140
Q

antibiotics

A

clarithromycin

cymoxicillin

141
Q

side effects of PPIs

A

pneumonia
C difficle growth
osteoporosis

142
Q

dicyclomine

A

AcH inhibitor

-not very good

143
Q

acinar cells of pancreas

A

pancreatic enzymes

144
Q

ductal cells of pancreas

A

aqueous NaHCO3 solution

145
Q

pancreas innervation?

A

inhibited by S

stimulated by PS

146
Q

stimulated ductal cells of pancreas

A

secretin - in response to too much acid

147
Q

major protease in pancreatic juice

A

trypsinogen

148
Q

stimulates acinar cells of pancreas

A

CCK, ACh, secretin, VIP

all increase Ca
-activation of protein kinases increases acinar cell secretion

CCK directly and indirectly (PNS cholinergic paths)

149
Q

acinar fluid

A

isotonic

150
Q

ACh and CCK

A

stimulate NaCl secretion

phosphorylates ion channels

151
Q

secretin mechanism

A

duct cells

secretin generates electrical gradient favoring NaHCO3 cotransport

152
Q

lipase

A

triglyceride digestion

necessary for survival

153
Q

amylase

A

starch, glycogen digestion

154
Q

trypsin

A

protein digestion

155
Q

procolipase

A

move bile salts from fat particles

-makes way for lipase to come and break down the triglycerides

156
Q

trypsin inhibitors

A

in acinar and ductal cells to protect mucosa

157
Q

enterokinase

A

activates trypsinogen to trypsin

located in brush border of duodenal mucosal

158
Q

CCK release

A

stored in I cells

releasing peptide and monitor peptide
-stimulate CCK release

GRP and ACh stimulate monitor peptide release

these signaling molecules are peptide - so they will get digested and stops CCK release

159
Q

secretin release

A

from S cells in duodenal mucosa

acid stimulates ductal cells

160
Q

achlorhydric

A

cannot secrete gastric acid

no stimulus for secretin release
-results in duodenal ulcer

161
Q

potentiation on acinar cells

A

CCK and VIP result in even larger increase

162
Q

steatorrhea

A

fat in stool
early sign of pancreatic dysfunction
-due to low pancreatic lipase release

163
Q

pancreatitis

A

enzymes of pancreas eat itself

could be:
cancer
alcohol
gallstone obstruction

MSS - GI Exam 1 (11 decks)

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