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Physiology > Exam 4 GI > Flashcards

Exam 4 GI Flashcards

1
Q

what are the segments of the GIT

A

the mouth, pharynx, esophagus, stomach, small and large intestines and the sphincters in between

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2
Q

what are the layers of the GIT

A

the serosa, longitudinal muscle, myenteric (Auerbach’s) nerve plexus, circular muscle, submucosa, submucosal (Meissner’s) plexus, muscular mucosa, mucosa and epithelial lining.

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3
Q

neural control is both intrinsic and extrinsic. what systems are associated with these

A

intrinsic, the enteric NS, which is made of the myenteric and submucosal plexus
extrinsic, the ANS, (PNS and SNS)

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4
Q

which stimulates and which inhibits with the use of what hormones

A

the SNS inhibits with NE and the PNS stimulates with ACh.

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5
Q

myenteric plexus is part of what NS, and where does it go from. between what layers is it found

A

enteric. goes from the esophagus to the anus. between the circular and longitudinal SM layers.

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6
Q

what is the function of the myenteric plexus. what are its stimulatory and inhibitory influences

A

to control GI motility.
stimulatory influences: increased tonic contraction (tone), increased contraction frequency and intensity (increased propulsion)
inhibitory influences: decreased sphincter tone (relaxation of the sphincters)

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7
Q

you need two things to pass food along. What two things does the myenteric plexus do to help food move along

A

increase the contraction and frequency of muscles, and also relax the sphincters.

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8
Q

what is the submucosal plexus location and function

A

between the esophagus to the anus. and it controls the local control (secretion, absorption, contraction of the muscularis mucosa)

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9
Q

why is the contraction of the muscularis mucosa important

A

this controls the SA of the epithelium, so this also determines the amount of absorption.

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10
Q

where do we get influence from the extrinsic NS of the GIT

A

the parasympathetic is from the cranial (vagal) nerves and the sacral nerves
the sympathetic is through the 4 plexus’s (superior cranial, celiac, superior and inferior mesenteric)

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11
Q

blood that courses through the gut, spleen and pancreas flow to the liver via the ___. in the liver, blood passes through the millions of minute liver sinusoids and finally leaves the liver via ___. this blood flow through the liver allows the reticuloendothelial cells to do what

A
  • portal vein
  • hepatic veins, then eventually to the vena cava
  • remove bacteria and other particulate matter. it filters the blood
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12
Q

after a meal, what happens to GI blood flow

A

increased 2-3x for 3-6 hours after a meal

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13
Q

what are some causes of activity induced blood flow

A 
vasodilation hormones (gastrin, secretin and CCK)
vasodilator kinins 
low O2, high aldosterone.
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14
Q

what I the nervous control of the GI blood flow. gives examples

A

PNS: increases gut activity, and increases blood flow
SNS: directly decreases blood flow, like during auto-regulatory escape, exercise and shock

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15
Q

why do you get cold after eating

A

in the extremities, you get cold because the blood is shunted away from the extremities to the gut

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16
Q

arterial and venous blood flow are in ___ directions. what does this mean for blood flow and the tips of the villi. what percent of blood is shunted this way

A

opposite. this allows most blood O2 to diffuse from the arterioles to the venules without the O2 being carried to the tip of the villi. 80%

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17
Q

what happens in diseases like circulatory shock to the blood flow in villi

A

the blood flow to the gut becomes curtailed, and the tips of the villi become O2 deficient, leading to ischemic death and disintegration which will lead to greatly diminished absorptive capacity.

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18
Q

all endocrines are hormones, and all hormones are

A

peptides.

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19
Q

where are these hormones released

A

into the blood, travel in the circulation to get to their destination

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20
Q

are all neurocrines (NT’s) peptides?

A

no, some are peptides, like VIP and others are not like ACh and NE.

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21
Q

how are neurocrines released

A

nerves release them and they travel to target cells

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22
Q

how are paracrines released and on what kinds of cells do they act

A

released by endocrine cells and diffuse to the target cells. they act on endocrine cells via positive and negative feedback

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23
Q

are paracrines peptides

A

some are like somatostatin and other are not like histamines

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24
Q

what are the two structurally related families of GI hormones

A

gastrin and CCK and then secretin, GIP, VIP and glucagon.

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25
Q

GIP

A

glucose dependent insulinotropic peptide

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26
Q

VIP`

A

vasoactive intestinal peptide

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27
Q

what does gastrin do when secreted

A

promotes H+ secretion by gastric parietal cells (1500x more potent then histamine)

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28
Q

what is the tropic activity of gastrin

A

stimulates the growth of the oxyntic mucosa of the stomach, the duodenal mucosa and the colon mucosa

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29
Q

why does surgical removal of the Antrum cause atrophy

A

because that is where the G-cells are located that release gastrin

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30
Q

what do patents with gastrin secreting tumors have

A

mucosal hyperplasia and hypertrophy

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31
Q

where is gastrin released from

A

from the G-cells in the Antrum and duodenum

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32
Q

what stimulates the release of gastrin

A
  • protein digestion products like small peptides and AA
  • nervous, physical distention
  • calcium, decaf coffee, wine
  • high pH (when gastrin is released, it releases H ions, which will lower the pH)
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33
Q

what inhibits the release of gastrin

A

acidification of the Antrum (when the pH is low, it is negative feedback to stop secreting gastrin)

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34
Q

response to a meal. within and between meals

A

with in a meal: large amount of G-17 are released from the Antrum, the small gastrin.
between meals, small amount of G-34 are released from the duodenum (big, secreted between meals)

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35
Q

Gastrinoma- Zollinger- Ellison Syndrome

A

gastrin secreting tumor, either in a non beta cell tumor of the pancreas (80%) or G-cell tumor in the duodenum (10-15%) continually secretes gastrin into the blood which will cause hyper secretion of acid. The increased parietal cell mass and stimulation of hyperplastic mucosa as well as the increased H secretion by parietal cells and hypertrophy of the gastric mucosa.

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36
Q

what are the symptoms of Gastrinoma- Zollinger- Ellison Syndrome

A

duodenal ulcers, diarrhea, steatorrhea, hypokalemia

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37
Q

Gastrinoma Summary

A

there is hyperglastrinemia, which causes an increase in parietal cell mass and acid secretion, which causes intestinal hyperacidity. This leads to peptic ulcers or a decrease in bile salts and a decrease in lipase activity (because lipase needs a high pH to work). the decrease in bile salts and the decrease in lipase activity will cause the diarrhea, steatorrhea and hypokalemia.

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38
Q

how do we get steatorrhea and hypokalemia from gastrinoma

A

steatorrhea, the low pH will inactivate the pancreatic lipase, which causes bile salts to precipitate.
hypokalemia results from the loss of GI secretions in the stool.

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39
Q

CCK. what does it do, where is it released from

A

cholecystokinin. promotes fat digestion and absorption. released from the I-cells in the duodenum and jejunum

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40
Q

what causes the release of CCK

A
  • fatty acids or monoglycerides (not TG)
  • peptides and single AA
  • acid (weak)
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41
Q

what are the 4 major actions of CCK

A
  1. emptying the gallbladder by contracting it and relaxing the sphincter of Oddi (contents can move from gallbladder to the intestines)
  2. secretion of pancreatic enzymes (potent stimulator) and HCO3 (weak stimulator)
  3. inhibits gastric emptying (gives more time to digest the fat)
  4. tropic effects (exocrine pancreas and gallbladder mucosa)
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42
Q

what is the principle stimuli for the delivery of pancreatic enzymes and bile to the small intestines

A

CCK

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43
Q

where is secretin released from, and what is its stimuli for release

A

from the S-cells of the duodenal mucosa and stimulus is acid in the duodenum (when the pH is below 4.5) and fatty acids int eh duodenum

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44
Q

what are the physiologic effects of “nature’s antacid” (secretin)

A
  • inhibits gastric acid secretion (enterogastrone)
  • stimulates pancreatic and bile bicarbonate secretion, needed for fat digestion
  • tropic effects of exocrine pancreas
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45
Q

what family is GIP (glucose-dependent insulinotropic peptide) a member of

A

secretin

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46
Q

what stimulates GIP (glucose-dependent insulinotropic peptide) release and from where

A

released from K-cells of duodenum and primal jejunum

any major nutrient and oral glucose, but not IV glucose (incretin)

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47
Q

what is the only GI hormones that is released in response to all major nutrients

A

GIP (glucose-dependent insulinotropic peptide)

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48
Q

what are the physiologic effects of GIP (glucose-dependent insulinotropic peptide)

A

stimulates the release of insulin (AKA gastric inhibitory peptide) and inhibits gastric acid secretion

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49
Q

motilin: where is it secreted from and what does it do

A

from the upper duodenum during fasting. will increase GI motility and initiates the inter digestive myoelectric complexes that occur in 90 min intervals

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50
Q

pancreatic polypeptide: where is it secreted from and what does it do

A

from the pancreas in response to the ingestion of PRO, CHO and lipids. inhibits pancreatic secretion of HCO3 and enzymes

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51
Q

enteroglucagon: where is it secreted from and what does it do

A

from the intestinal cells in response to a decrease in blood glucose concentration and stimulates the live to increase glycogenolysis (glycogen is broken down into gluc -1- phosphate) and gluconeogenesis (new glucose from non-CHO source)

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52
Q

glucagon-like peptide-1 (GLP-1): what is it produced from and where is it secreted by and what does it do

A

produced from proglucagon and secreted by L-cells of the small intestine. incretin

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53
Q

where are paracrines synthesized

A

in the endocrine cells of the GIT

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54
Q

do paracrines enter the systemic circulation

A

no, they act locally

55
Q

somatostatin. where is it secreted and in response to what. what does it do

A

from the D-cells of the GI mucosa in response to the lower pH (more acidic)also secreted by the hypothalamus and delta cells of the endocrine pancreas. it inhibits the secretion of GI hormones and inhibits gastric H+ secretion .

56
Q

histamine: where is it secreted, and what does it do

A

secreted by endocrine cells of the GI mucosa. along with gastrin and ACh (PNS), histamine stimulates the H+ secretion by gastric parietal cells.

57
Q

Neurocrines are ___ that are released by

A

neurotransmitters that are released by terminal nerve endings.

58
Q

examples of neurocrines

A

NE, ACh, VIP, GRP

59
Q

which is parasympathetic and which is sympathetic and what do they do to digestion. ACh and NE

A

ACh is PNS, and it increases digestion and contracts. NE is SNS and decreases digestion, and relaxes

60
Q

what does it mean when you say the GI smooth muscle is a syncytium

A

the larger areas of smooth muscle contract as a single unit, much like the heart.

61
Q

what is the purpose of gap junctions in the GI SM

A

to make it act like a syncytium became there are spaces for ions movement of low resistance, and they are between bundles of cells and layers of SM. There is a single AP propagation from cell to cell and it can spread within and between muscle layers. when one cell becomes depolarized, so do the others.

62
Q

what happens when circular muscle contracts

A

the diameter of the lumen decreases because of the smooth muscle contracting around it

63
Q

what happens when longitudinal muscle contracts

A

the segment decreases in length

64
Q

what are phasic and tonic contractions of the SM

A

phasic means they are periodic and have relaxation, and tonic means that there is a constant tone and no regular periods of relaxation

65
Q

what happens when a food bolus stretches the intestines

A

the SM circular contracts behind the bolus, pushing it forward and then the longitudinal will contract as well

66
Q

when the bolus is in the stomach and moves with gastric juices what is it called

A

chyme

67
Q

when the chyme passes through the small intestine to the large what is it called

A

feces

68
Q

what are slow waves

A

rhythmic changes int he membrane potential that are caused by variation of the sodium conductance. oscillating depolarization kinda like the SA node. these are not AP’s.

69
Q

what kind of cells make slow waves and what is it about their frequency

A

the interstitial cells of Cajal are the pacemaker cells that are in the myenteric plexus that make these slow waves. depending on where you are, they are about 3-12 waves per minute and this will dictate the maximum frequency of SM contraction. frequency RTS and is fixed

70
Q

what is the story with the amplitude of the slow waves. what happens with an increased amplitude

A

its variable. its affected by nervous and hormonal stimuli. an increased amplitude increases the spike potential frequency and increases the strength of the contraction

71
Q

what are spike potentials. when do they happen. what ion is responsible for contraction.

A

true AP’s. they happen with the slow waves reach the threshold (-40) and this causes the SM to contract. Ca.

72
Q

explain the frequency of spike potentials

A

they are affects by nervous and humoral control. an increase in frequency means an increase in contraction, but the increase in frequent does not increase the maximum frequency of contraction.

73
Q

describe the membrane potential. when it doesn’t reach threshold? when you have stimulation by stretch, ACh, PNS

A

slow waves don’t reach threshold, (-40) there are no spike. there are still constant periods of contraction and relaxation happening during resting state.
stimulation… threshold is met and a spike occurs.

74
Q

what does the SNS (NE) do to the spike potentials

A

it hyper polarizes the membrane and brings the resting membrane potential way down

75
Q

what is the relationship between electrical and mechanical activity

A

the mechanical always follows the electric (with a slight delay)

76
Q

what is the purpose of chewing

A

to break down cells and break apart ingested cellulose. you want to increase the SA of the food and decrease the particle size. you also want to mix the food with saliva

77
Q

what does saliva do

A

begins to digest starches (alpha amylase, lingual lipase) and lubricates the food for swallowing

78
Q

describe how swallowing works

A

its initiated voluntarily in the mouth and then there is an involuntary swallowing set in motion by the swallowing center int he medulla. There are three stages

79
Q

what are the three stages of swallowing

A
  1. oral phase (voluntary): initiates the swallowing process
  2. pharyngeal (involuntary): passage of food from the pharynx to the esophagus
  3. esophageal (involuntary); food from pharynx to stomach
80
Q

there are 4 steps of the esophageal phase, what are they

A
  1. the UES opens and the swallowing reflex allows food to travel from the pharynx to the esophagus. the UES will close to prevent reflux.
  2. the primary peristaltic contraction
    the LES opens and the orad region of the stomach relaxes (receptive relaxation) to facilitate moment of the bolus into the stomach
  3. secondary peristaltic wave, if the primary peristaltic contraction does not clear the bolus this happens
81
Q

what is the receptive relaxation

A

the orad of the stomach will relax as food comes towards to so it can enter the stomach. the third step of the epspoageal phase of swallowing

82
Q

what is primary peristalsis

A

the continuation of pharyngeal peristalsis, which is coordinated by the swallowing center of the medulla. Cannot occur after the vagotomy (striated muscle)

83
Q

what is secondary peristalsis

A

the stretch related afferent sensory input to the ENS and the swallowing center. Occurs after vagotomy

84
Q

what are some disorders of swallowing (dysphagia)

A

CVA/stroke: aspiration due to the UES and pharyngeal contractions not being coordinated. secondary peristalsis is still functional
muscular diseases: myasthenia gravis, polio, botulism
anesthesia: aspiration of stomach contents. food cannot leave because the sphincters. when the pressure is higher then the atmosphere, it wants to exit, prevented by UES. LES prevents it from going from stomach to esophagus. GERD is an example.

85
Q

where are the orad and caudad regions of the stomach

A

orad is the first third and the caudad is the last 2/3

86
Q

what prevents the gastric emptying from the stomach TO THE DUODENUM

A

the pyloris

87
Q

what is the function of the gastric smooth muscle

A

relax to accommodate food in the orad region (receptive relaxation)
in the caudad region, the SM will mix food with gastric juice (retropulsion)
it will also propel the chyme through the pyloris to the duodenum

88
Q

what happens as the meal empties

A

contractile activity and low amplitude contractions

89
Q

what is receptive relaxation

A

the vasovagal reflex where vagal afferent carry impulses to CNS and efferent away from CNS to stomach.

90
Q

what does gastric distensibility mean

A

CCk will increase and gastric emptying decreases, to give more time to digest Fat.

91
Q

what are four factors that increase gastric emptying

A
  1. increase the tone of the orad stomach
  2. forceful peristaltic contractions
  3. decrease the tone of the pyloris
  4. absence of segmental contractions in the intestines (like receptive relaxation)
92
Q

what are four factors that decrease gastric emptying when the receptors in the intestines are activated.

A
  1. relaxation of the orad stomach
  2. decreased forcible peristaltic contractions
  3. increase tone pyloric sphincter
  4. segmental contractions in the intestines (increase in P in the intestines, the harder it is to push food into the intestines)
93
Q

the activation of intestinal receptors does what to gastric emptying

A

it decreases it

94
Q

intestinal mucosa receptors are simulated by… and causes the triggering of…

A

high or low osmolarity, acid, fat, protein

triggers enterogastric reflex

95
Q

what happens with the enterogastric reflex

A

fat and protein release CCK which increases gastric distensibility and decreases gastric emptying
acid will decrease gastric emptying by intrinsic neural reflexes and the involvement of other homers will decrease gastric emptying

96
Q

how does small intestine motility contribute to digestion and absorption

A

it mixes the chyme with digestive enzymes, and circulation of chyme to achieve optimal exposure to mucosa, it also propels the chyme.

97
Q

where are slow waves more frequent, the stomach or the small intestine

A

the small intestine

98
Q

what are the two types of contractions in the small intestine and what are their functions

A

segmental contractions mix the chyme (circular- splits the bolus into two and allows mixing) and the peristaltic contractions propel the chyme (longitudinal).

99
Q

what are the functions of the large intestine SM

A

anything that is not absorbed I the small intestine enters the large intestine and is called feces. the large intestine SM ties the chyme and enhances fluid and electrolyte absorption through haustral contractions. and propels the feces for mass movements.

100
Q

what are haustral contractions

A

there are invaginations in the large intestine that contracts and causes movement helps to mix and propel

101
Q

where do mass movements occur and what is the function. how often do they happen

A

occur in the colon and canton to move feces over long distances, such as from the transverse colon to the sigmoid. occur 1-3 x/day.

102
Q

water absorption occurs in the _____ making fecal contents semisolid and increases the difficulty to move

A

distal colon

103
Q

mass movements lead to

A

bowel movements

104
Q

two reflexes associated with defecation

A

rectospinchteric and gastrocolic

105
Q

what is the rectospinchteric reflex

A

when the rectum fills with feces, the SM of the wall of the rectum contracts and the internal anal sphincter relaxes which is involuntary. but you won’t poop until the external anal sphincter relaxes which is voluntary

106
Q

what is the gastrocolic reflex

A

distention of the stomach by food ingestion increases the motility of the colon and the frequency of mass movements

107
Q

salivary glands have what appearance

A

a bunch of them looks like a bunch of grapes, but one singular one, an acinar, looks like a single grape.

108
Q

salivary glands are stimulated by both branches of the ___

A

ANS

109
Q

what is the difference between acinar cells and ductal cells

A

the acinar cells produce the primary secretion, similar to plasma (ptyalin, mucus, and ECF)

110
Q

the ductal cells do what

A

modify the primary secretion (Na, Cl, K, HCO3)

111
Q

the slower the rate of secretion, what will happen to the saliva

A

the slower the rate of secretion, the more the saliva will be modified and more time for the ductal cells to add stuff

112
Q

acinar cells make isotonic solutions. how do they do this

A

they pull Na in, then back out. The Cl follows, which makes an electrochemical gradient. Duct cells also release HCO3 and K into the saliva

113
Q

how does the PNS regulate saliva secretion

A

anything like conditioning, food, nausea and the smell of food increases the PNS and then secretes saliva.
things like dehydration, fear and sleep will decrease the PNS

114
Q

why is it good to brush your teeth before bed

A

to kill bacteria. when you sleep, less saliva is made and saliva helps us kill bacteria.

115
Q

what are the four main components of the gastric juice secreted by the gastric mucosa

A

HCL, pepsinogen, IF (to absorb B12), and mucus

116
Q

the body of the stomach contains oxyntic glands which contain what two cells, and what do they secrete

A
  1. parietal cells, secrete HCL and IF

2. chief cells: secrete pepsinogen

117
Q

the antrum of the stomach (last part of the stomach) contains pyloric glands which contain what two cells, and what do they secrete

A
  1. G-cells: secrete gastrin

2. mucus neck cells: secrete mucus, HCO3 and pepsinogen

118
Q

pepsinogen turns to what in response to a low pH? what does it do then

A

turns to pepsin and starts to digest PRO

119
Q

what are the three phases of gastric secretion

A
  1. cephalic phase (vagus): before you eat, visual, smell, increase gastric secretions.
  2. gastric phase: controlled by local reflexes, nervous secretory reflex, vagal, gastrin-histamine stimulation
  3. intestinal phase: when the chyme reaches the intestines, hormones.
120
Q

oxyntic glands have what kinds of cells, and what do they secrete

A

parietal (IF, HCl) and chief (pepsinogen)

121
Q

pyloric glands have what kinds of cells

A

G-cells (gastrin-not into the stomach, but into the circulation first) and mucus cells

122
Q

two phases of the regulation of HCl Secretion

A
  1. cephalic phase, 30%, smell, taste, conditioning through vagus nerve
  2. gastric, 60%, distension, AA and peptides.
123
Q

difference between gastric and duodenal ulcers

A

gastric, low H+ secretion with high gastrin levels, that hurts the gastric mucosa.
duodenal, high H+ levels and high gastrin

124
Q

are there high or low H+ concentrations in Zollinger Ellison syndrome. what does this mean

A

high, means that there is high gastrin (tumor levels)

125
Q

why does the stomach secrete mucus

A

for a protective barrier, to prevent cell erosion and death

126
Q

what are some damaging factors to mucus

A

H pylori, H+ and pepsin, NSAIDS, stress, smoking and alcohol

127
Q

what is peptic ulcer disease

A

starts with erosion of mucosa. it becomes a true ulcer when it goes down to tunica muscularis or even further down

128
Q

acid from the stomach releases ___ from the wall of the duodenum and fats and AA cause the release of___

A

secretin and CCK

129
Q

secretin causes

A

secretion of pancreatic fluid and bicarbonate

130
Q

CCK causes secretion of

A

enzymes

131
Q

describe bile secretion

A

the bile salts formed in the liver are stored int he gallbladder. when CCk is released in the presence of fat, the gallbladder contracts and the sphincter of Oddi relaxes, causing the contents of the gallbladder to go down the bile duct to the duodenum. At the ilium, the bile salts are reabsorbed through he portal circulation to the liver and recycled.

132
Q

what happens when you have too much bile or it stays too longs and solidifies

A

gallstones

133
Q

what are the four causes of gallstones

A
  1. too much absorption of water from the bile
  2. too much absorption of bile acids from bile
  3. too much cholesterol in the bile
  4. inflammation of the epithelium (not reabsorbed as well as you should, so cholesterol increases)
134
Q

what can cause gallstones, and what is a potential hazard to gallstones

A

high fat diets, like fast food. can block the bile duct.

Physiology (7 decks)

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