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BECOM II Exam 4 > GI Physiology > Flashcards

GI Physiology Flashcards

1
Q

what is the function of the muscularis mucosae?

A

controls the secretion of the gut, not contraction

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2
Q

2 plexuses of enteric nervous system

A
  1. myenteric (Auerbach) plexus - b/w inner and out muscularis layers; gut contraction (peristalsis)
  2. meissner plexus - in submucosa that controls secretions; not found in esophagus
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3
Q

function of gap junctions in GI

A

for muscle contraction

  • degree of peristalsis has to be controlled (not all contracted at once)
  • act as functional syncytium
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4
Q

function of interstitial cells of Cajal

A

pacemaker cells of smooth muscle (auto rhythm)

-found in enteric nervous system

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5
Q

contraction of the muscular fibers

A

circular contraction
-reduces lumen diameter & contracts behind bolus to propel it forward
longitudinal contraction
-reduces length but increase lumen size ahead of bolus

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6
Q

what stimulates the circular fibers?

A

pacemaker (Cajal) cells and incoming neurons

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7
Q

what stimulates longitudinal fibers?

A

excitatory musculomotor neurons

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8
Q

role of Ca2+ in GI

A
  • coupling of muscle contractions

- depolarization along w/ Na+ (action potentials)

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9
Q

spontaneous vs. non-spontaneous contractions

A

stomach and intestine –> spontaneous, contract w/o stimulus, peristalsis default
esophagus and gallbladder –> non spontaneous, need stimulus for contraction

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10
Q

what are the 2 ways Ca2+ can be released in the GI?

A
  1. electromechanical coupling - skeletal and smooth muscle, depolarization release of Ca2+
  2. pharmacomechanical coupling - only smooth muscles, intracellular signaling to release Ca2+ from stores
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11
Q

function of slow waves

A
  • not strong enough to cause contraction - minor depolarization
  • amplitude determines whether spikes will occur
  • spikes cannot exceed slow waves
  • slow waves 1st –> AP spikes next
  • different frequencies in different sections of GI
  • generated by Cajal cells
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12
Q

action (spike) potential roles

A

have to happen on top of slow waves

  • higher amplitude of slow waves –> more AP
  • longer duration (slow)
  • use Ca2+ and Na+ channels to initiate
  • L-type channels for Ca2+
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13
Q

what happens if you block the L-channels?

A

disrupt GI motility –> constipation

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14
Q

changes in the resting membrane potential

A
  • parasympathetic stimulation - more depolarization, increase excitability for contraction
  • sympathetic stimulation - hyperpolarization, weaker slow waves
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15
Q

4 neural control mechanisms of GI

A
  1. enteric nervous system - function on own, peristalsis
  2. paravertebral sympathetic chain - response directly on tissues or on ENS indirectly
  3. CNS in brain stem and spinal cord
  4. cortical areas in brain
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16
Q

parasympathetic innervation of gut

A

cell bodies in brain stem and sacral region –> efferent motor signals

  • vagus nerve (motor and sensory fibers) innervate upper GI
  • sacral plexus innervates lower GI
  • have inhibitory and stimulatory efferent fibers
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17
Q

sympathetic nervous system on the gut

A
  • reduces blood flow, motility, and secretion

- increases contractions at sphincters but reduces them everywhere else –> paralytic ileus after surgery

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18
Q

afferent sensory fibers from gut

A

stimulated by irritation, distention, chemicals

-send signals to ENS, brain stem, or spinal cord

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19
Q

GI reflexes

A
  1. ENS - function even w/o vagus nerve stimulation
  2. paravertebral ganglion - gastrocolic, enterogastric, colonileal
  3. spinal cord or brainstem -vagovagal, pain, defecation
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20
Q

what is the vagovagal reflex?

A

relaxes/dilates stomach in response to incoming food

  • vagus nucleus and NTS motor activity in brainstem (where vagal afferents synapse)
  • efferents synapse with ENS (inhibitory or stimulatory)
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21
Q

efferent fibers of vagus nerve

A

synapse with ENS

  • inhibitory and stimulatory to musculature
  • stimulatory only to secretory
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22
Q

function of enteric nervous system

A

mini brain of the gut

-contain myenteric and meissner plexuses

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23
Q

myenteric (Auerbach) plexus

A

b/w longitudinal and circular muscle fibers

  • controls motility
  • excitatory or inhibitory neurons (does not always cause contraction)
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24
Q

submucosal (meissner) plexus

A

control secretion and absorption

  • integrates sensory info.
  • communicates with myenteric
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25
Q

2 types of ENS neurons

A
  1. afterhyperpolarization neurons (AH type)
    - long lasting hyperpolarization –> hard to get depolarization
    - mostly in Auerbach
    - cAMP 2nd messengers
  2. S type neurons
    - fast depolarization and repolarization
    - more reliant on Na+ channels and more susceptible to channel blockers
    - IP3 and Ca2+ as 2nd messengers
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26
Q

function of metabotropic receptors

A

slow EPSP

  • excitatory musculomotor neuron –> prolonged contraction
  • inhibitory musculomotor neuron –> prolonged relaxation
  • activated by NTs, histamine, and hormones
  • EPSP in secretomotor cells will always cause secretion (no inhibitory neurons)
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27
Q

function of ionotropic receptors

A

fast EPSP

  • fast depolarization
  • mediated by ACh
  • has ion channels
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28
Q

slow IPSP

A

hyperpolarizing effect –> suppresses excitability

  • opiods –> constipation
  • NE & somatostatin –> reduce secretion & act on Meissner
  • Galanin –> act on Auerbach
  • adenosine
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29
Q

presynaptic inhibition

A

negative feedback on presynaptic neuron by the NTs released

  • CCK, ATP, histamine, NE, ACh
  • histamine binds to H3 to inhibit fast EPSPs
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30
Q

presynaptic facilitation

A

stimulate presynaptic neuron to increase NT release

-prokinetic drugs used to increase gut motility by increasing NT release

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31
Q

what are the main excitatory NTs from the musculomotor neurons?

A

ACh and substance P

-cell bodies in myenteric plexus

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32
Q

what are the main excitatory NTs from the secretomotor neurons?

A

ACh and VIP

-cell bodies in submucosal plexus

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33
Q

what happens with hyperactivity of secretomotor neurons by histamine?

A

binds to H2 receptors increasing EPSP –> diarrhea

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34
Q

what happens when you suppress the secretomotor activity by opioids?

A

constipation

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35
Q

enteric inhibitory musculomotor neuron

A

hyperpolarizing potential –> prevent depolarization

  • ATP, VIP, and NO important inhibitory NTs
  • inhibit circular muscle layer
  • determines force and direction of contraction
  • inhibiting the inhibitor causes tonic contraction
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36
Q

what is the function of GRP?

A

NT that stimulates the release of gastrin

-atropine blocks the muscarinic but not GRP synapse

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37
Q

what is the main function of GIP?

A

insulin release for heads up signal during food intake

-stimulated by ingestion of carbs mainly

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38
Q

vasodilators of splanchnic circulation

A

CCK, VIP, gastrin, secretin, kinins, NO, adenosine

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39
Q

countercurrent blood flow in intestinal villi

A

tip of villi hypoxic normally

-long term constriction –> necrotic villi –> shock –> inhibit absorption

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40
Q

different contractions when moving bolus

A
  • segment behind bolus - contract circular muscle & longitudinal (propulsive segment)
  • segment ahead of bolus - contract longitudinal & relax circular
  • PNS –> stronger contractions
  • SNS –> weaker contractions
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41
Q

what is peristalsis initiated by?

A

ENS - segment distention or brush stimulation

  • propagation by synaptic gates
  • can close transmission gates to inhibit long term peristalsis –> inhibit depolarization waves
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42
Q

function of pro kinetic drugs

A

presynaptic facilitation –> more gate opening –> increase propulsion
-given to diabetic patients

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43
Q

what can inhibition of peristaltic gates cause?

A

paralytic ileus

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44
Q

lower esophageal sphincter

A

prevent stomach acid entry

-problems –> heart burn, barrett esophagus

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45
Q

pyloric sphincter

A

problems –> bile reflux –> gastritis and ulcers

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46
Q

sphincter of Oddi

A

pancreatic and GB juice enter duodenum

-problems –> bacterial overgrowth, bloating, ab pain

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47
Q

ileocolonic (ileocecal) sphincter

A

prevent retrograde flow from cecum into ileum

-problems –> fecal incontinence

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48
Q

deglutition

A

swallowing –> maintained by center in midbrain to control pharyngeal muscles
-brain injury –> peristalsis but no swallowing

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49
Q

role of primary peristalsis

A

presence of food starts swallowing –> contract circular muscles as pharyngeal junction to propel food
-no change in esophagus length

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50
Q

role of secondary peristalsis

A

triggered by failure of primary to push food into stomach

-stronger wave

51
Q

esophageal achalasia

A

loss of LES inhibition

-no inhibitory neurons and food cannot pass due to constriction

52
Q

motor of antral (pyloric) pump

A

initiated by interstitial cells of Cajal - stimulation moves slow waves to spike waves –> contraction
-slow AP to gastroduodenal junction (3 contractions per min.)

53
Q

leading vs. trailing contractions

A
  • leading contraction (initial depolarization by rising AP) causes contraction of pyloric sphincter
  • trailing contraction (plateau phase) causes stronger contraction - almost complete closure of pylorus
  • waves keep coming –> retrograde flow of chime
54
Q

regulation of antral contractions

A

myogenic function - ACh release from the vagus nerve can make it stronger but not required

  • Gastrin stimulates
  • VIP and NE decrease plateau phase and contractions
55
Q

2 functions of gastric reservoir

A
  1. accommodation of arriving meal

2. contraction to maintain compressive force to push food to antral pump

56
Q

adaptive and receptive relaxation

A
  • receptive - during swallowing (no food yet)
  • adaptive - accommodating food already in stomach
  • both vagovagal reflex –> afferent and efferent components –> inhibit so they can relax for incoming food
57
Q

feedback relaxation

A

presence of nutrients in small intestine inhibit stomach contractions

58
Q

rate of gastric emptying

A

determined by type of meal and duodenum

  • high gastric volume and isotonic –> faster
  • high acidity and calories –> slower
59
Q

role of migrating motor complex (MMC)

A

start when digestion and absorption are complete

  • inhibited by vagus nerve –> increase function with vagotomy
  • clean out debris from small intestine
  • failure of MMC to function –> bacteria entry and overgrowth in colon
60
Q

small intestine digestive motor

A

MMC replaced by digestive mobility after meal

  • segmentation and mixing to mix enzymes with chime
  • not same thing as peristalsis
61
Q

large intestine motility

A
  • adaptive relaxation - cecum relaxation for food entry from ileum
  • distended cecum slows down ileum
62
Q

function of transverse colon

A

store feces and chime

  • dehydration
  • complete segmentation to increase surface area and water absorption (haustrations)
63
Q

gastrocolic reflex

A

empties stomach to prepare for incoming food which pushed food out of large intestine

64
Q

fecal passage

A

somatic control

  • distention of rectum –> rectoanal reflex (relaxation of internal anal sphincter) which is ENS reflex
  • constipation if you inhibit rectoanal reflex
65
Q

what is lost during bilateral vagotomy?

A

gastric adaptive and receptive reflex

66
Q

salivary secretion is stimulated by what?

A

SNS and PNS, not hormones

67
Q

what is the enzyme in saliva?

A

amylase

  • breaks down carbs
  • gives taste
68
Q

salivon

A

functional unit of salivary glands

  • acinus cells –> secrete enzymes from zymogen granules
  • secrete mucous and bicarb
  • reabsorb Na+ & secrete K+
  • high Na+ in saliva with excess saliva
69
Q

regulation of salivary secretion

A
  • PNS increase salivation directly or indirectly through bradykinin vasodilation
  • SNS - short lives, viscous, less secretion of saliva
  • mineralcorticoids and ADH (Na+ absorption, K+ secretion)
70
Q

gastric secretion

A
  1. pyloric glands - G cells secrete gastrin
  2. oxyntic (gastric) glands - parietal (HCl, IF), endocrine (somatostatin), chief (pepsinogen)
    -both glands contain mucous cells
    D cells –> secrete somatostatin
71
Q

function of gastrin

A

increase gut motility and acid secretion

  • release stimulated by gastrin releasing peptide from vagus, not ACh like most
  • AAs also increase gastric acid secretion
72
Q

importance of intrinsic factor

A

from parietal cells

  • B12 absorption
  • inflammation of ileum –> pernicious anemia
73
Q

how do you inhibit gastric acid secretion?

A
  • proton pump inhibitors –> cemetidine and rantidine
  • somatostatin
  • secretin
  • enterogastrins
  • GIP
74
Q

regulation of the pancreas

A
  • ACh –> increase enzyme secretion, but not bicarb
  • Secretin –> stimulate bicarb secretion; VIP partial agonist
  • CCK –> stimulate enzyme production; Gastrin partial agonist
75
Q

small intestine secretions

A
  1. Brunner’s glands
    - stimulated by irritant, vagus, secretin
    - secrete mucous and bicarb to neutralize stomach acid
  2. crypts of Lieberkuhn
    - mucous, water, and bicarb secretion
    - has digestive enzymes
    - contain stem and paneth cells
76
Q

function of bicarb in large intestine

A

protect against acid and fermentation

-can have water and bicarb loss with irritation such as diarrhea

77
Q

function of bile

A
  • bile salts emulsify fats into micelles for digestion
  • bile salts from cholesterol
  • bile pigments from bilirubin
  • a lot of bicarb found in bile
78
Q

what enzyme converts cholesterol to primary bile acids?

A

cytochrome P450

-secreted by the liver stored in the gallbladder

79
Q

how is bile conjugated?

A

-bacteria form the deconjugated bile salts and the liver conjugates the bile (glyco, tauro) for better emulsification

80
Q

where are the bile salts recycled?

A

distal ileum after absorption of fats takes place

81
Q

role of CCK in duodenum

A

contract gallbladder to release bile into duodenum

82
Q

role of secretin in duodenum

A

from S cells in duodenum

  • increase bicarb production in pancreas and liver
  • bile salt independent flow
83
Q

what do bile acids/salts have to be tightly controlled?

A

potential toxicity

  • gastritis if it leaks into stomach
  • release more bile when eating bc GB is contracted and it is recycled back through enterohepatic circulation
84
Q

what is the role of gastrin on bile release?

A
  • directly increase bile production by liver

- increase acid –> increase secretin –> bile production indirectly

85
Q

why is bile salt pores located in distal ileum?

A

special pores for bile recycling

  • fat is already absorbed at this time, don’t need bile salts anymore
  • bacteria also located here to deconjugate the bile forming secondary bile salts
86
Q

recycling mechanisms for bile salts

A
  1. diffusion
  2. carrier transport
  3. deconjugation
  4. dehydroxylation
87
Q

how do you get bilirubin in the liver?

A

biliverdin from Hb of broken down RBCs –> albumin takes it to liver –> liver removes it from albumin recirculating it

88
Q

why does urine have yellowish color?

A

bilirubin is conjugated making it more water soluble to enter bile –> absorbed by small intestine and converted to urobilinogen which is absorbed by kidney

89
Q

where does most of food absorption take place?

A

in the jejunum and ileum

-bile salts in terminal ileum

90
Q

what molecule is needed for most reabsorption?

A

Na+

91
Q

what is the function of dietary fibers?

A

not reabsorbed

  • soften stool –> prevent colon cancer (less inflammation)
  • bind to bile salts –> indirect way to lower cholesterol
92
Q

salivary amylase/ptylalin

A
  • gives taste
  • works in neutral or alkaline pH
  • not needed for life
93
Q

pancreatic alpha amylase

A
  • needed for life
  • work in neutral pH
  • break down starch to maltose
  • only break into disaccharides
94
Q

what 3 monosaccharides are absorbed at intestine?

A

galactose, glucose, fructose

  • galactose & glucose –> need Na+ and SGTL1
  • fructose –> no Na+ nor SGTL1
95
Q

disaccharidases

A

break disaccharides into monosaccharides

  • supplied by brush border of intestine
  • lactase or sucrase deficiency –> diarrhea
  • congenital or acquired (Chron’s)
96
Q

fat digestive enzymes in small intestine

A
  1. lingual lipase - taste
  2. gastric lipase - break down milk fat
  3. pancreatic lipase - important, breaks TAGs only
  4. colipase - better interaction of fat & lipase; inhibit bile salts
  5. PLA2 - breaks phospholipids
  6. cholesterol esterase - break cholesterol
97
Q

role of bile salts in absorption

A

emulsification of fats for better absorption

-poorly absorbed in jejunum

98
Q

ezitimibe

A

inhibits cholesterol transporter in intestine –> lowering levels

99
Q

lipid handling in enterocytes

A
  • long chain FA –> form PL, TAGs
  • cholesterol –> form cholesterol esters (cholesterol acyltransferase)
  • chylomicrons - transport fat
  • VLDL - transport cholesterol via lymph
  • medium/short chain FAs enter directly to blood
100
Q

steatorrhea

A

fatty stool from pancreatic or bile deficiency

-poor fat soluble vit. absorption

101
Q

abetalipoproteinemia

A

no Apo B –> no chylomicrons or VLDL –> poor fat absorption

102
Q

pancreatic endopeptidases

A
  • trypsin
  • chymotrypsin
  • elastase
103
Q

pancreatic exopeptidases

A
  • carboxypeptidase A –> attack aliphatic or aromatic C terminus
  • carboxypeptidase B –> attack basic C terminus
104
Q

disorders of protein absorption

A
  • Hartnup - defective carrier for Trp
  • cystinuria - defective carrier for cysteine
  • treat with dipeptides –> absorbed in blood then broken down
105
Q

retinol (vit. A)

A
  • fat soluble
  • passive absorbed in intestine –> chylomicron –> stored in liver
  • deficient –> night blindness, skin lesions
106
Q

vitamin D

A
  • fat soluble
  • passive absorption in intestine –> chylomicron
  • deficient –> rickets, osteomalacia
107
Q

vitamin E

A
  • fat soluble
  • absorbed with lipoproteins and RBCs
  • deficient –> fragile RBCs
108
Q

vitamin K

A
  • fat soluble
  • absorbed by chylomicrons stored in liver
  • needed for synthesis of coagulation factors
  • deficiency –> bleeding disorders
109
Q

vitamin C (ascorbic acid)

A
  • absorbed in distal ileum

- deficiency –> scurvy

110
Q

vitamin B1 (thiamine)

A
  • absorbed in jejunum

- deficiency –> beriberi

111
Q

vitamin B2 (riboflavin)

A
  • absorbed in proximal intestine (jejunum)

- deficiency –> anorexia, impaired growth, nervous system

112
Q

niacin

A
  • absorbed in small intestine
  • lowers cholesterol
  • deficiency –> anorexia, indigestion, muscle weakness, skin eruptions, PELLAGRA
113
Q

vitamin B6 (pyridoxine)

A
  • absorbed in small intestine

- deficiency –> anemia, CNS effects

114
Q

biotin

A
  • absorbed in small intestine

- coenzyme for carboxylase & decarboxylase enzymes

115
Q

folic acid

A
  • absorbed all over intestine
  • deficiency –> megaloblastic anemia, lesions, poor growth
  • needed for pregnant women 1st 3 month
116
Q

vitamin B12 (cobalamin)

A
  • absorbed in distal ileum by intrinsic factor (from parietal cells in stomach)
  • pernicious anemia without
117
Q

NaCl absorption in jejunum

A
  • ingest hypotonic fluid
  • basolateral Na+/K+ ATPase
  • Na+ in, H+ out
  • carbonic anhydrase in lumen produces water (absorbed) and CO2 (diffuses) –> carbonic anhydrase in enterocyte makes H+ (back to lumen) and bicarb (absorbed)
  • paracellular Cl-
  • acidosis if lose too much bicarb
118
Q

NaCl absorption in ileum

A
  • basolateral Na+/K+ ATPase
  • Cl-/bicarb exchanger necessary for Na+/H+ exchanger to function
  • Cl- in, bicarb out
  • Na+ in, H+ out
  • still reclaim bicarb with water and CO2 conversion in lumen
119
Q

K+ absorption/secretion

A 
small intestine --> paracellularly 
large intestine (colon) 
-high K+ in lumen --> absorb 
-low K+ in lumen --> secrete 
-increase BK channels by bacteria or shear flow --> hypokalemia (ex. diarrhea induced)
120
Q

Ca++ absorption

A

tightly regulated

  • TRPV5,6 bring Ca++ in –> transported by calbindin –> basolateral ATP pump and Na+/Ca++ exchanger for absorption
  • Vit. D increase channels, calbindin, and pumps
121
Q

iron absorption

A

2 forms

  • heme (animals/humans) –> faster absorption
  • nonheme (plants) –> pH dependent (slow absorption at neutral or alkaline) forming precipitates
122
Q

iron absorption - transporters

A
  • heme iron –> absorbed by facilitated transport
  • nonheme iron –> absorbed by DMT-1
  • ferritin for storage, transferrin in blood for transport
  • Ca++ decreases absorption
  • vit. C increase absorption
123
Q

H2O absorption

A

hypertonic meal –> water secretion in jejunum –> water absorption in ileum, colon
hypotonic meal –> water secretion in jejunum –> water absorption in jejunum, ileum

BECOM II Exam 4 (10 decks)

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