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Physiology > GI Deck 1 > Flashcards

GI Deck 1 Flashcards

1
Q

2 functions of the GI system

A

1- absorb nutrients/electrolytes/H20

2- excrete waste

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2
Q

4 basic properties that underly 2 functions

A

1- motility
2- secretion
3- digestion
4- absorption

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3
Q

what is the cephalic phase?

A

activation of the GI tract in readiness for a meal (idea of food, smell, sight, sound)

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4
Q

which cranial nerves carry the impulse to activate salivary secretion?

A

CN 7 & 9 (facial and glossopharyngeal)

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5
Q

what is the pathway from sensory input to readiness of GI tract?

A

sensory input -> cortex/hypothalamus -> lower pons/upper medulla -> DMN of vagus activates parasympathetics -> increase salivary secretion (7&9), gastric secretion, pancreatic secretion, etc.

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6
Q

what is the oral phase?

A

same as the cephalic, but food is present in the mouth

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7
Q

what do you add with the oral response?

A
  • chemoreceptors in tastebuds & mechanoreceptors in mouth & pharynx
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8
Q

what is xerostomia?

A
  • dry mouth which reduces the pH in oral cavity, causing tooth decay, difficulty swallowing, esophageal errosion
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9
Q

what is the purpose of chewing?

A
  • break down food into tiny particles
  • mix with enzymes (amylases, lipases)
  • mixing with mucin to lubricate
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10
Q

what are the main muscles of chewing and what are they innervated by?

A

temporalis, masseter, pterygoids

innervated by mandibular branch of trigeminal

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11
Q

where do GI secretions come from (3 locations)?

A

1) glands associated (salivary, pancreas, liver)
2) gut wall (Brunner’s) - mostly mucus/bicarb
3) intestinal mucosa

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12
Q

what are secretions elicited by? which systems can they come from?

A

secreatogogues; can be endocrine, paracrine, neurocrine

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13
Q

3 pairs of major salivary glands

A

1) parotid
2) submandibular
3) sublingual

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14
Q

3 types of secretion cells and how they stain

A

serous (dark), mucous (light), mixed

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15
Q

which gland is primarily serous?

A

parotid

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16
Q

which gland is primarily mucous?

A

sublingual

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17
Q

which gland is mixed?

A

submandibular

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18
Q

what are the units of secretion?

A

acini cells

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19
Q

what are demilunes?

A

in a mixed group of secretion cells, mucous cells swell and push serous cells into caps

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20
Q

What are myoepithelial cells?

A

present around acini cells and intercalated ducts; contain actin & myosin to contract and expel saliva forward

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21
Q

what are the 3 functions of saliva?

A

lubrication
protection
initial digestion

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22
Q

what does the composition of saliva depend on?

A

the rate of secretion & flow

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23
Q

how is saliva compared to the composition of blood? due to which ions?

A
  • hypotonic

- because Na/Cl are low in saliva

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24
Q

3 transporters of the luminal side of acinus cell

A

Na/H antiporter, Cl/Bicarb antiporter, H/K antiporter (also have Na/K pump on blood side)

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25
Q

what is the net result of acinus cells?

A
  • net absorption of Na/Cl; (net secretion of bicarb & K+)
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26
Q

at highest flow rate, (4 mL/min) what does saliva look like?

A
  • less time for modification, looks similar to plasma but is still hypotonic
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27
Q

how is bicarb altered with flow rate? how does it compare to other secretions?

A

secrete more bicarb with flow, (normal pattern is less- secrete less K+)

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28
Q

what are the ways in which acinar cell secretion is regulated?

A

neural (symp and PARASYMP)

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29
Q

which CN does PS use to regulate acini cells? which neurotransmiters?

A

CN 7 & 9

Ach acting on muscarinic receptors, increasing IP3/Ca, increasing saliva

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30
Q

where does sympathetic regulation for the acini cells come from?

A

T1-T3/superior cervical ganglion

Ne acting on Beta adrenergics, increasing cAMP and increasing salavia

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31
Q

3 increases stimulation of salivary cells causes

A

1) saliva production
2) bicarb & enzyme secretion
3) contraction of myoepithelial cells

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32
Q

what does atropine block?

A

PS muscarinic receptors, decreasing saliva production

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33
Q

during which phase is swallowing voluntary?

A

short segment in oral phase

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34
Q

where is the regulatory swallowing center?

A

medulla & lower pons

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35
Q

what are the steps of the swallowing reflex?

A

stretch receptors near opening of pharynx - medulla/ower pons - respiratory center/ motor CNs to pharynx&upper esophagus / vagus to esophagus

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36
Q

what are the 3 phase of swallowing?

A

oral, pharyngeal, esophageal

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37
Q

what are the 2 functions of the UES and LES?

A
  • propel food from pharynx to stomach

- protect airway & esophagus from acid reflux

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38
Q

how many waves of peristalsis do you have?

A

1* peristalsis - doesn’t clear entire bolus to stomach

2* peristalsis- under control of enteric NS, caused by distention of esophagus

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39
Q

what is receptive relaxation? which NTs cause it?

A

when orad stomach & LES relax at the same time; VIP and NO

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40
Q

which molecule causes the LES to relax?

A

VIP

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41
Q

what is greater- intraesophageal pressure or abdominal pressure?

A

abdominal pressure- hard to keep air & acid out of esophagus

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42
Q

what is LES resting tone like?

A

pressure is higher than esophagus or orad stomach

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43
Q

what thick layer of cells protects esophagus and anal canal from friction?

A

stratified squamous epithelium

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44
Q

what is GERD, and during chronic GERD what disappears?

A

gastroesophageal reflux disaease; LES tone is not enough, stratified squamous epithelium disappears

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45
Q

what factor is known to cause GERD?

A

increase in intrabdominal pressure- pregnancy and obesity

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46
Q

what is a hiatal hernial and in what population do you find them?

A

muscular problem, stomach sneaks through esophageal hiatus into diaphragm; found in older patients

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47
Q

what is achalasia?

A

SM does not have normal peristalsis & LES does not relax; myenteric plexus is lost

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48
Q

what can you use to treat achalasia temporarily?

A
  • use atropine
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49
Q

What are the two types motility in the small intestine and which neural systems do they use?

A

Segmental (enteric NS)

Peristaltic (Ach/Substance P/VIP/NO)

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50
Q

What is the MMC and what is it stimulated by?

A

Migrating motor complex
Every 90 minutes get periodic contraction
Stimulated by motilin

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51
Q

major functions of gastric phase

A
  • storage
  • motor activity
  • secrete IF
  • secrete H+ (kills stuff & activates pepsin)
  • secrete mucus & bicarb (simple columnar)
  • secrete water
52
Q

what is the essential factor of gastric secretion?

A

intrinsic factor (required to absorb B12)

53
Q

how is the gastric phase regulated?

A
  • neural (extrinsic and ENS)
  • paracrine (histamine)
  • endocrine (gastrin, somatostatin)
54
Q

Which region prevents reflux, causes burping, accepts food? what is it closest to?

A
  • cardia region

- closest to LES

55
Q

In which region are most of the secretory cells?

A

fundus

56
Q

In which region are the g-cells?

A

antrum

57
Q

What are the 3 regions based on glandular tissue of gastric mucosa?

A
  • small cardiac
  • oxynitic/parietal (fundus)
  • pyloric (antrum)
58
Q

6 types of secretory cells in fundus/antrum

A 
1- parietal/oxynitic cells (HCl/IF)
2- Mucous neck cells
3- peptic/chief cells (pepsinogens)
4- ECL cells (histamine)
5- D cells (somatostatin)
6- G cells
59
Q

what makes up gastric juice?

A

HCl, pepsinogen, bicarb, mucus, IF

60
Q

net secretion in stomach? net absorption?

A

secretion- HCl

absorption- bicarb

61
Q

pathway for gastric secretion of acid

A

extrinsic efferents of vagus- intrinsic nerves that innervate parietal cells, ECL cells, g-cells

62
Q

neurocrine, endocrine & paracrine regulators of gastric acid secretion

A

neurocrine- Ach,
endocrine- gastrin
paracrine- histamine

63
Q

What percent of HCl is secreted during the cephalic/oral phases vs. gastric phase

A

30% vs 60%

64
Q

5 pathways for HCl secretion during gastric phase?

A 
1- direct- vagal on parietal cells
2- indirect- vagus - GRP- etc. 
3- indirect- Ach/gastrin(?) on ECLs
4- vagovagal (distention of stomach)
5- small peptides & AAs
65
Q

what is negative feedback on HCl pathway stimulated by and where?

A

low pH (<3) in antrum

66
Q

direct and indirect effects of somatostatin

A

direct- SS antagonizes cAMP

indirect- SS inhibits ECL & g-cells

67
Q

motility division of stomach

A

orad- thin walled

caudad- thick walled

68
Q

GD junction functions

A

1) filter
2) controls rate of emptying
3) prevents reflux

69
Q

gastric vs duodenal ulcer

A

gastric- NOT HIGH ACID; have something wrong with mucosal barrier (e.g. H. pylori)
duodenal- have high H+ (damaged pancreas, high stomach secretions)

70
Q

what is Zollinger-Ellison syndrome? what 2 things does it cause?

A
  • gastrin secreting tumor in pancreas

- increased H+ secretion, increased parietal cell mass

71
Q

which electrolytes are high and which are low in saliva?

A

high K+, bicarb

low Na, Cl

72
Q

6 changes that represent the intestinal phase of the response to the meal

A

(1) increased pancreatic secretion
(2) increased gallbladder contraction
(3) relaxation of the sphincter of Oddi
(4) regulation of gastric emptying
(5) inhibition of gastric acid secretion
(6) interruption of the migrating motor complex (MMC).

73
Q

4 things that must happen for gastric emptying

A

1) increase in tone in proximal stomach
2) increased antral contraction strength
3) forced opening of the pylorus
4) inhibition of duodenum

74
Q

what is the vagal pathway that inhibits gastric emptying?

A

H+/hyperosmolarity act on vagal afferents - activates vagal efferents to decrease the strength of antral contractions, contract pylorus, and decrease proximal gastric motility

75
Q

two major factors that contribute to the inhibition/slowing of gastric emptying?

A
  • presence of fat in duodenum

- presence of H+ in duodenum

76
Q

what mediates the effect of fat on slowing gastric emptying?

A
  • CCK secreted in the presence of FAs

- causes pylorus contraction, regulates gallbladder contraction, relaxation of sphincter of Oddi, pancreatic secretion

77
Q

what mediates the effect of H+ on slowing gastric emptying?

A
  • reflexes in enteric NS
  • H+ receptors in duodenal mucosa - relay info to myenteric plexus & smooth muscle
  • results in ample neutralization by pancreatic bicarb
78
Q

what part of the pancreas has significant contributions towards the digestion process?

A

EXOcrine pancreas

  • 90% of pancreas volume
  • secretes enzymatic and aqueous components
79
Q

what are the two components of pancreatic secretion, and what are the two cells they are secreted by?

A

aqueous (high bicarb) - centroacinar & ductal cells

enzymatic- acinar cells

80
Q

3 things that secrete bicarb to maintain neutral pH in duodenum so pancreatic enzymes can be active

A

1) pancreas ductal cells *** largest contributor
2) duodenal surface epithelial cells
3) biliary ductules

81
Q

what are the main effector arms of the pH regulatory system? which hormone are they acted upon by?

A

ducts

secretin - stimulates secretion of bicarb (& negative feedback)

82
Q

which cycle does low pH in duodenum signal?

A

low pH in duodenum- stimulates S cells in intestinal epithelium- secretin is released- secretin stimulates secretion of bicarb- negative feedback on low pH

83
Q

what does secretin increase in ductal cells? what does this product do?

A
  • increases cAMP which opens CFTR Cl- channels so Cl- is spilled into lumen
84
Q

what does an elevation of Cl in the lumen stimulate?

A

Cl reabsorption and bicarb secretion (antiporter)

85
Q

what are the two sources for bicarbonate?

A
  • absorbed across basolateral membrane via NBC-1 symporter (Na dependent!!)
  • carbonic anhydrase breaking down H20 & CO2 intracellularly (extrudes proton into pancreas venous blood)
86
Q

net result of pancreatic ductal secretion

A

secrete bicarb into lumen

absorb H+, acidify pancreatic venous blood

87
Q

what is mutated in cystic fibrosis? what problem does this cause in the pancreas?

A

CFTR, decreases ductal secretion, precipitates enzymes in duct & destroys gland

88
Q

if you administer secretin, what should happen? which disorder is this altered in?

A
  • ductal cells should produce bicarb

- Zollinger-Ellison, gastric-like cells in pancreas that respond to secretin by releasing gastrin

89
Q

what stimulates CCK release from I cells in small intestinal epithelium?

A

1) FAs & AAs binding to I cells
2) FAs & AAs binding to paracrine cells that release CCK-RP
3) Neural stimulation of pancreas releasing monitor peptide

90
Q

2 ways CCK stimulates pancreatic acinar secretion

A

1) binding to CCK1 receptors on acinar cells (endocrine)

2) paracrine effect stimulates neural reflex, causing vagovagal reflex in pancreas, releasing Ach, GRP, & VIP

91
Q

How do CCK, Ach, and GRP act?

A

mobilize intracellular Ca2+, causes fusion of zymogen granules & exocytosis

92
Q

how does trypsin inhibit pancreatic secretion in absence of protein

A
  • trypsin can bind to protein, CCK-RP & messenger peptide and degrades what it binds
  • with low protein, it degrades CCK-RP and messenger peptides, don’t get release of CCK to stimulate exocytosis of vesicles
93
Q

what are pancreatic proteases activated by?

A

trypsin

94
Q

what is pancreatitis (inflammation of pancreas) caused by?

A

premature activation of proteases by trypsin

95
Q

what activates trypsinogen to trypsin and where?

A
  • enterokinase as a brush border enzyme in the small intestine
96
Q

pathways for stimulation of pancreatic secretion (cephalic, gastric, intestinal)

A
  • cephalic- thought of food- vagal/enteric nerves
  • gastric- stomach distension- vagovagal
  • intestinal
  • low pH- secretin
  • peptides- CCK
  • distension- enteropancreatic reflexes
  • CCK sensory enteric neurons- vagovagal
97
Q

what is the ASBT and where is it found?

A

apical sodium bile transporter, found in terminal ileum, recycles 90-95% of bile when lipid absorption is complete

98
Q

what is the majority of our diet?

A

50% carbs, mostly polysaccharides

99
Q

what can be absorbed through the intestinal epithelium?

A

carbs- 3 monosaccharides (GFG)
proteins- AAs, di & tripeptides
fats- cholesterol, monoglycerides, lysolecithin, fatty acids

100
Q

what is trehalose broken down into and by what?

A

2 glucose molecules by trehalase

101
Q

what is sucrose broken down into and by what?

A

glucose & fructose by sucrase

102
Q

what is lactose broken down into and by what?

A

glucose & galactose by lactase

103
Q

what is the most significant enzyme to break down starch and what does it break down? what can it not digest?

A
  • pancreatic alpha amylase
  • only hydrolyzes alpha 1,4 linkages (straight chains)
  • can not digest beta 1,4 linkage (cellulose)
104
Q

what are the products of alpha amylase and their enzymes?

A

maltose (maltase), maltotriose (sucrase), alpha-dextrins (alpha-dextrinose)

105
Q

how are carbohydrates transported across the apical membrane?

A
  • SGLT1- symporter w/ Na for gulcose & galactose, is 2* active
  • GLUT5- fructose
106
Q

how are carbohydrates transported across the basolateral membrane?

A

Glut2- passive, does glucose/galactose/fructose

107
Q

where does protein digestion start and with which peptide? what does it give?

A

stomach, pepsin; gives intact proteins and large peptides

108
Q

what are 5 major pancreatic proteases secreted as inactive precursors/what are their active forms?

A 
trypsinogen/trypsin
chymotrypsinogen/chymotrypsin
proelastase/elastase
procarboxypeptidase A/carboxypeptidase A
procarboxypeptidase B/carboxypeptidase B
109
Q

what are the two classes the 5 major pancreatic proteases secreted as inactive precursors are divided into?

A

endopeptidases - hydrolyze interior peptide bonds (pepsin, trypsin, chymotrypsin, elastase)
&
exopeptidase- hydrolyze one amino acid at a time from C-terminal end (carboxypeptidase A&B)

110
Q

how are AAs, dipeptides & tripeptides absorbed?

A

AAs- w/ Na symporter (and Na/K ATPase on bl side)
Di/tripeptides- with H+ symporter (broken down with peptidase inside cell)

AAs leave via facilitated diffusion

111
Q

what is the major supply of lipids in the diet? what is it broken down into and by which enzymes?

A

triglycerides

  • monoglycerides & 2 FAs
  • lingual, gastric & pancreatic lipases
112
Q

what is used for emulsification in the stomach & small intestine? what are the emulsifications called in the SI?

A

stomach- dietary proteins

SI- bile acids & lysolecthin (caused micelles)

113
Q

what are the 3 major pancreatic lipolytic enzymes that work at a neutral pH?

A

pancreatic lipase
phospholipase A2
cholesterol ester hydrolase

114
Q

which cofactor is important to prevent bile acids from inhibiting phospholipase activity?

A

colipase

115
Q

what are the 5 steps of lipid absorption?

A

1) lipids are released from micelles at the apical membrane
2) lipid digestion products are re-esterified with free fatty acids
3) products packaged with apoproteins to form chylomicrons
4) chylomicrons are secreted by exocytosis
5) chylomicrons are transported by lymphatic capillaries

116
Q

what is a phospholipid broken down into and by which enzyme?

A

lysolecithin & FA

by phospholipase A2

117
Q

what is the main way in which water is reabsorbed in the small intestine?

A

paracellularly via leaky tight junctions

118
Q

what is the major site for Na reabsorption in SI? using which transporters? what is it absorbed with in this region?

A

jejenum
SGLT, AAs, Na/H+ exchanger
absorbed with bicarb

119
Q

in addition to the 3 Na transporters, what does the ileum also have?

A

bicarb/Cl exchanger with basolateral Cl transporter

120
Q

in the small intestine, which cells are responsible for absorption? secretion?

A

absorption- brush border epithelial cells

secretion- crypts

121
Q

what does cholera do?

A

causes the overproduction of cAMP, stimulating the CFTR Cl- channel and causing the secretion of water > water absorption

122
Q

what are the two types of diarrhea and examples of things that cause them?

A

osmotic- lactose intolerance

secretory- cholera, e. coli

123
Q

what do you have on the basolateral side of intestinal crypt cell?

A
  • Na/K+ ATPase
  • Na/K/2Cl- cotransporter
  • receptor for hormones/neurotransmitters that activates cAMP to open CFTRs
124
Q

what is required for Ca2+ absorption? what does it induce?

A

active form of vitamin D (1,25 dihydroxycholecaliferol)

induces synthesis of calbindin D-28K to bind Ca2+ in cell

125
Q

what is required for B12 absorption? where does it occur, and by which mechanism?

A

intrinsic factor, ileum, cotransport with IF

Physiology (22 decks)

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