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Gen.Exam.Review > Ch6. GI > Flashcards

Ch6. GI Flashcards

1
Q

What is the difference between circular muscle vs longitudinal muscle in the GI tract?

A

circular muscle contraction– causes a decrease in diameter of the lumen

Longitudinal muscle– contraction causes shortening of a segment of GI

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2
Q

What make up the enteric nervous system of the GI tract?

A

submucosal plexus (Meissner plexus) an dmyenteric plexus

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3
Q

The extrinsic innervation of the GI tract has (parasymp/symp) efferent fibers carried from the

A

brain stem and spinal cord to the GI tract

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4
Q

The extrinsic innervation of the GI tract has (parasymp/symp) afferent fibers carry what information?

A

sensory info from chemo receptors and mechanoreceptors in the GIT to the brain stem and spinal cord

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5
Q

Parasympathetic nervous system is usually excitatory or inhibitory on the funcitons of the GIT

A

excitatory

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6
Q

The parasympathetic nervous system innervation of the GIT is carried by what nerves?

A

vagus & pelvic nerves

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7
Q

Where do preganglionic parasympathetic fibers synapse where in the GIT?

A

myenteric and submucosal plexuses

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8
Q

The sympathetic nervous system is typically excitatory or inhibitory on the functions of the GIT?

A

inhibitory

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9
Q

Where do sympathetic nerves orginate in what portion of the spinal cord?

A

between T8 and 12

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10
Q

what is the function of myenteric plexus (Auerbach plexus)?

A

controls the motility of the GI smooth muscle

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11
Q

what is the function of the submucosal plexus (Meissner plexus)

A

primarily secretion and blood flow
**receives info from chemoreceptors & mechanoreceptors in the GI tract

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12
Q

Site of secretion: Gastrin

A

G cells of stomach

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13
Q

Site of secretion: CCK

A

I cells of duodenum and jejunum

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14
Q

Site of secretion: secretin

A

S cells of duodenum

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15
Q

Site of secretion: GIP

A

duodenum & jejunum

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16
Q

What is the stimulus for secretion of Gastrin?

A

-small peptides & amino acids
-distention of the stomach
-vagus (via GRP)
-inhibited by H in stomach
-inhibited by somatostatin

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17
Q

What is the stimulus for secretion of CCK?

A

small peptides & fatty acids (monoglycerides; triglycerides cannot cross intestinal cell membranes)

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18
Q

What is the stimulus for secretion of secretin?

A

-H in duodenum
-fatty acids in duodenum

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19
Q

What is the stimulus for secretion of GIP?

A

fatty acids, amino acids and oral glucose

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20
Q

GI hormone, what is the action of: Gastrin

A

INC Gastric H secretion
stimulates growth of gastric mucosa

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21
Q

GI hormone, what is the action of: CCK

A

-stims contraction of gallbladder and relaxation of sphincter of Oddi
-INC pancreatic enzyme and HCO3 secretion
-INC growth of exocrine pancreas/gallbladder
-inhibits gastric emptying

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22
Q

GI hormone, what is the action of: secretin

A

INC pancreatic HCO3 secretion
INC biliary HCO3 secretion
DEC gastric H secretion

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23
Q

GI hormone, what is the action of: GIP

A

INC insulin secretion
DEC Gastric H secretion

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24
Q

Gastrin works on what cells of the GI tract?

A

gastric parietal cells

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25
Q

What cells secrete gastrin?

A

G cells of the gastric antrum
**in response to a meal

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26
Q

What is the most potent stimuli for secretion of gastrin?

A

pheylalanine
tryptophan

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27
Q

What are mechanisms that inhibit gastrin secretion?

A

-H in the lumen of the stomach (negative feeback control)
-somatostatin

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28
Q

CCK is released from what cells of the duodenal and jejunal mucosa?

A

I cells

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29
Q

Secretin is released from what cells of the duodenum?

A

S cells

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30
Q

MOA of motilin

A

INC GI motility and is involved in interdigestive myoelectric complexes

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31
Q

MOA of pancreatic peptide

A

inhibits pancreatic secretions

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32
Q

MOA of glucagon-like peptide (GLP-1)

A

binds pancreatic Beta-cells and sitmulates insulien secretion

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33
Q

MOA leptin

A

decreases appetite

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34
Q

MOA Ghrelin

A

increases appetite

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35
Q

What are the GI paracrines?

A

somatostatin
histamine

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36
Q

Somatostatin is secreted by cells throughout the GI tract in response to

A

H in the lumen

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37
Q

Somatostatin secretion is inhibited by

A

vagal stimulation

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38
Q

MOA of somatostatin

A

inhibits release of all GI hormones
and
inhibits gastric H secretion

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39
Q

Histamine is secreted by what cells of the gastric mucosa?

A

Mast cells

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40
Q

What is the effect of histamine on the GI tract?

A

increases gastric H secretion
**directly potentiates the effects of gastrin & vagal stimulation

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41
Q

What are Neurocrines of the GI tract?

A

synthesized in neurons of the GI tract, moved by axonal transport down the axons & released by action potentials in the nerves
–> neurocrines then diffuse across teh synaptic cleft to a target cell

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42
Q

List the GI neurocrines

A

vasoactive intestinal peptide (VIP)
neuropeptide Y
nitric oxide (NO)
GRP (bombesin)
enkephalins

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43
Q

Vasoactive intestinal peptide (VIP) is released from neurons in what part of the GI tract?

A

mucosa & smooth muscle

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44
Q

what is the effect of vasoactive intestinal peptide (VIP)?

A

produces relaxation of GI smooth muscle, including the lower esophageal sphincter

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45
Q

What is the MOA of vasoactive intestinal peptide (VIP)?

A

stimulates pancreatic HCO3 secretion and inhibits gastric H secretion
**resembles secretin

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46
Q

GRP (Bombesin) is released from where?

A

vagus nerves tha tinnervate the G cells

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47
Q

GRP (bombesin) MOA

A

stimulates gastrin release from G cells

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48
Q

What are the actions of enkephalins?

A

-stimulate contraction of GI smooth muscle (particularly lower esophageal, pyloric & ileocecal sphincters)
-inhibit intestinal secretion of fluid & electrolytes

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49
Q

Where is the satiety center located?

A

-inhibits appetite
**located in the ventromedial nucleus of the hypothalamus

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50
Q

Where do the oscillating membrane potentials in GI smooth muscle originate?

A

interstitial cells of cajal
**serves as the pacemaker for GI smooth mm
**not action potentials

51
Q

What is the mechanism of slow wave production in the GI smooth muscle?

A

-cyclic opening of Ca channels (depolarization) followed by opening of K channels (repolarization)

52
Q

What initiates the vagovagal reflex?

A

distention of the stomach

53
Q

The rate of gastric emptying is fastest when?

A

-when stomach contents are isotonic

54
Q

When is gastric emptying inhibited?

A

-hypertonic or hypotonic
-fat (by stim CCK)
-H in the duodenum

55
Q

Food in the intestinal lumen is sensed by enterochromaffin cells, which release what hormone?

A

serotonin (5-HT)

56
Q

Describe the gastroileal reflex

A

presence of food in the stomach triggers increased peristalsis in the ileum & relaxation of the ileocecal sphincter
**intestinal contents are delivered to large intestine

57
Q

Describe the gastrocolic reflux

A

presence of food in the stomach increases motility in the colon & increases frequency of mass movements

58
Q

What neuronal functions mediate the gastrocolic reflex?

A

-rapid parasympathetic component– initiated when stomach is stretched by food
-slower, hormonal component mediated by CCK & gastrin

59
Q

What are the functions of saliva?

A

-initial starch digestion by alpha-amylase and initial triglyeride digestion by lingual lipase
-lubrication of ingested food by mucus
-protection of mouth & esophagus by dilution and buffering of ingested food

60
Q

The composition of saliva is characterized by:

A

-high volume
-high K and HCO3 concentrations
-low Na and Cl concentrations
-hypotonicity
-presence of alpha-amylase, lingual lipase & kallikrein

61
Q

What stimulates gastric secretion?

A

gastrin
parasympathetic nervous system
histamine

62
Q

Pancreatic secretion is stimulated by:

A

secretin
CCK (potentiates secretin)
Parasympathetic nervous system
CCK

63
Q

What stimulates bile secretion?

A

-CCK (causes contraction of gallbladder and relaxation of sphincter of Oddi)
-Parasympathetic nervous system (causes contraction of gall bladder)

64
Q

Initially saliva has the same concentration as plasma, which part of the salivary duct produces this?

A

acinus

65
Q

Where is saliva modified and how is it modified (from initial concentrations)?

A

-the ducts
–> reabsorb Na and Cl
–> secrete K and HCO3

66
Q

What is the effect of aldosterone on saliva?

A

-acts on ductal cells
- increases reabsorption of Na and secretion of K (analagous to the actions on renal distal tubule)

67
Q

Parasympathetic stimulation of saliva glands increased transport via what cranial nerves?

A

CN VII & IX

68
Q

What do the parietal cells secrete?

A

HCL & intrinsic factor

69
Q

What hormones stimulate parietal cells?

A

-gastrin
-vagal stimulation (ACh)
-histamine

70
Q

Chief cells secrete what?

A

pepsinogen (converted to pepsin at low pH)

71
Q

What stimulate chief cells?

A

vagal stimulation (ACh)

72
Q

What do G cells of the stomach produce?

A

gastrin

73
Q

What stimulates G cells for secretion?

A

vagal stimulation (via GRP)
small peptides

74
Q

What inhibits G cell secretion?

A

somatostatin
H in stomach (via stimulation of somatostatin release)

75
Q

Mucous production in the cells is stimulated by?

A

vagal stimulation (ACh)

76
Q

What cells are produced by the body (fundus) of the stomach?

A

parietal cells
chief cells

77
Q

what cells are produced by the antrum of the stomach?

A

G cells
mucous cells

78
Q

What are the steps in which the parietal cells secrete HCL in the stomach?

A
  1. parietal cells, CO2 & water converted to H and HCO3, catalyzed by carbonic anhydrase
  2. H secreted into the lumen of the stomach by H-K pump (H,K AtPase)
  3. HCO3 produced in cells absorbed into the bloodstream in exhcange for CL (CL-HCO3 exchange); pH of blood increases (alkaline tide)
79
Q

omeprazole MOA

A

proton pump inhibitor
**inhibits H, K ATPase and blocks blocks H secretion

80
Q

Gastrin stimulates H secretion by interacting with…

A

CCK on the parietal cells

81
Q

Histamine stimulates H secretion by activating what receptors on parietal cells?

A

H2 receptors

82
Q

What is the second messenger for histamine?

A

cAMP

83
Q

What hormones work to stimulate H secretion?

A

-histamine potentiates the actions of ACh and gastrin
-AcH potentiates the actions of histamine & gastrin

84
Q

What work as negative feed back mechanisms, for inhibition of gastric H secretion?

A

low pH of stomach (inhibits gastrin secretion)
somatostatin
prostaglandins

85
Q

What is the mechanism by which prostaglandins inhibit gastric H+ secretion?

A

-activate Gi proteins, inhibiting adenylyl cyclase & dec cAMP levels

86
Q

What is the direct pathway by which somatostatin inhibits gastric H secretion?

A

-binds receptors on parietal cells, Gi protein, thus inhibiting adnylyl cyclase & decreasing cAMP levels

87
Q

What is the indirect pathway by which somatostatin inhibits gastric H secretion?

A

inhibits the release of gastrin and histamine, thus decreasing H secretion indirectly

88
Q

Pancreatic secretion has higher concentration of what electrolyte?

A

HCO3
**has lower Cl concen than plasma

89
Q

Acinar cells produce the pancreatic secretion, then how do ductal cells modify pancreatic secretion?

A

-secreting HCO3 and absorbing Cl via CL-HCO3 exchange

90
Q

What is the secondary messenger for secretin?

A

cAMP

91
Q

What is the effect of CCK on pancreatic acinar cells?

A

increase enzyme secretion (amylase, lipases, proteases)

92
Q

CCK potentiates the effect of what on pancreatic ductal cells?

A

secretin on ductal cells to stimulate HCO3- secretion

93
Q

What are the second messengers of CCK?

A

IP3 and increased intracellular Ca

94
Q

What are the contents of bile?

A

bile salts
phospholipids
cholesterol
bile pigments (bilirubin)

95
Q

How do bile salts aid in intestinal digestion and absorption of lipids?

A

By emulsifying them and solubilizing them in micelles

96
Q

What is the effect of CCK on the gall bladder?

A

-contraction of the gall bladder & relaxation of the sphincter of Oddi

97
Q

Where are bile acids reabsorbed to recirculate bile acids to the liver?

A

terminal ileum
**via Na-bile acid cotransporter

98
Q

How are carbohydrates absorbed in the small intestine?

A

via monosaccharides (glucose, galactose, fructose) via Na-dependent cotransport (glucose, galactose) and facilitated diffusion (fructose)

99
Q

How are proteins absorbed in the small intestine?

A

amino acids, dipeptides, tripeptides via Na-depednent cotransport (aa) and H-dependent cotransport (di & tri-peptides)

100
Q

How are lipids absorbed in the small intestine?

A

to fatty acids, monoglycerides and cholesterol via micelles form with bile salts in intestinal lumen
–>diffusion of fatty acids, monocglycerides and cholesterol into cell
–>re-esterification in cell to triglycerides & phospholipids and chylomicrons form in cell and are transferred to lymph

101
Q

How is vitamin B12 absorbed in the small intestine and ileum?

A

SI: Na-dependent cotransport
ileum: intrinsic factor- Vit B12 complex

102
Q

How is calcium absorbed in the small intestine?

A

Vit D dependent (calbindin D-28K)

103
Q

How is Fe absorbed in the small intestine?

A

-Fe3+ is reduced to Fe2+
- binds to apoferritin in cell

104
Q

when Fe is absorbed from small intestine, it circulates in blood bound to?

A

transferrin

105
Q

pancreatic proteases (trypsin, chymotrypsin, etc), are secreted in inactive forms that are activated in the small intestine as follows:

A
  1. trypsinogen is activated to trypsin by brush border enzyme: enterokinase
  2. trypsin then converts chymotrypsinogen, proelastase and procarboxypeptidase A and B to active forms
106
Q

What is the effect of lipids on gastric emptying?

A

slows b/c CCK slows gastric emptying

107
Q

What is the effect of pancreatic lipases on the lilpids?

A

hydrolyze lipids to fatty acids, monoglycerides, cholesterol & lysolecithin

108
Q

List pancreatic enzymes

A

pancreatic lipase
cholesterol est hydrolase
phospholipase A2

109
Q

How are chylomicrons transported out of the intestinal cells

A

by exocytosis

110
Q

lack of what protein leads to the inability to transport chylomicrons out of the intestineal cells

A

apoprotein B

111
Q

Potassium is absorbed in what part of the GIT and secreted in what part of the GIT?

A

absorbed: SI
secreted: colon

112
Q

In diarrhea why do we see hypokalemia?

A

K secretion by the colon is increased b/c of flow rate-depedent mechanism similar to renal distal tubule

113
Q

Where are the secretory vs absorptive mechanisms located in the small intestine?

A

secretory: crypts
absorptive: villi

114
Q

list fat soluble vitamins

A

A, D, E and K
**incorporated into micelles and absorbed along with other lipids

115
Q

How are water soluble vitamins absorbed?

A

Na-dependent cotrnasport emchanisms

116
Q

absorption of vitamin B12 in the ileum requires what?

A

intrinsic factor
**secreted by the stomach

117
Q

The absorption of calcium is dependent on what?

A

adequate amounts of active form of vitamin D, 1,25 dihydroxycholecalciferol

118
Q

How is iron absorbed?

A

as heme iron (iron bound to hemoglobin or myoglobin) or as free Fe2+

119
Q

bilirubin is carried in circulation bound to?

A

albumin

120
Q

IN the liver, wha tis bilirubin conjugated with

A

glucronic acid via the enzyme UDP glucuronyl transferase

121
Q

Where is conjugated bilirubin excreted?

A

** in urine and bile

122
Q

In the intestine, conjugated bilirubin is converted to

A

urobilinogen
**returned to the liver via enterohepatic circulation
–urobilin and stercobilin secreted in feces

123
Q

In the liver describe phase 1 and 2 reactions

A

phase I: catalyzed by cytochrome p450 enzymes, followed by
phase II: conjugate substances

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