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A & P final > Gastrointestinal Physiology > Flashcards

Gastrointestinal Physiology Flashcards

1
Q

what does uveitis correlate with

A

gut inflammation (ex. crohn’s disease)

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2
Q

why is the gut important to optometry

A

in the sense of nutrition’s effect on the eye

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3
Q

what is digestion

A

mechanical and chemical breakdown of food into molecular constituents

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4
Q

absorption of nutrients goes from the digestive tract lumen to the….

A

blood and lymph

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5
Q

what is motility

A

mixing of food for digestion and absoption

propulsion of food through digestive tract (GI tract)

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6
Q

what is taste

A

chemical sensitivity to food

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7
Q

what are the different organs that have associated lymphatic tissues (ALTs)

A

gut ALT (GALT)
mucosal (MALT)
conjunctive (CALT)

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8
Q

what are peyer’s patches

wehre is the highest concentration

A

aggregates of immune cells in the gut

highest concentration in the distal ileum

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9
Q

what cells are meant to prevent food allergies

A

certain cells which line the gut are meant to prevent food allergies

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10
Q

from which development layer are the myenteric plexus and meissner’ plexus derived

A

neural crest

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11
Q

why does a gut have “a nervous system unto itself”

A

it operates w/o much input from the CNS

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12
Q

where is the myenteric (Auerbach’s) plexus located

A

btwn circular and longitudinal muscle layers

-part of muscalaris externa

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13
Q

where is the meissner’s plexus

A

just inside the inner circular layer of muscle

-part of submucosa

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14
Q

what are the accessory organ

A

liver
gall bladder
exocrine pancreas

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15
Q

what are the componenets of the small intestine

A

duodenum
jejunum
illeum

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16
Q

what are the components to the large intest

A 
cecum
ascending colon 
transverse colon
descending colon 
sigmoid colon
rectum 
anus
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17
Q

what is the epithelium of the mucosa used for

A

secretion and absorption

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18
Q

what are the components to mucosa

A

epithelium
lamina propria
muscularis mucosa

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19
Q

what are the components of the muscularis externa

A

inner circular/outer longitudinal

auerbach’s (myenteric) plexus

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20
Q

what does the muscularis mucosa do

A

contract fairly continuous

gently agitates surface ep, allowing for “enhanced contact” btwn epithelium and food in the lumen

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21
Q

any neuron outside of the CNS is _____ derived

everything else is ____ Derived

A

neural crest

neural tube

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22
Q

how do the layers of the histological organization go from inner to outer

A 
epithelial cells
lamina propira
muscularis mucosa
mucosa
submucosa
muscularis externa
serosa
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23
Q

what are smooth muscle cells linked by
what does this allow for
what do most gut muscles act as

A

gap junctions
allows for electrical syncitium
most gut muscles act as unitary muscles

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24
Q

what kind of cells are interstitial cells of cajal

what are they produced by

A

pacemaker cells

produced by inactivation and activation of Na-K-ATPase

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25
Q

electrical slow waves are everywhere, what plays an important role in this

A

ca influx plays an important role in action potential mediation

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26
Q

what produce muscle contraction
the magnitude is proportional to what
caused by an influx of what

A

spike potentials

  • magnutude proportional to spike #
  • caused by influx of Ca
  • number of spikes is influenced by various nts
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27
Q

what are insterstial cells of cajal produced by

A

inactivation and activation of Na-K-ATPase

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28
Q

electrical slow waves may trigger action potentials, what channel mediates this?

what can happen when these are used to treat cardiovascular disorders?

A

L-type Ca channels

-diordered GI motility may be side effect of treating cardiovascular disorders w/ L-type channel blockers

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29
Q

what is the enteric NS

-what kind of neurons can it control

A

extension of CNS that controls GI tract independently of CNS control
-controls more than a million neurons: sensory, motor, interneuron

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30
Q

what are the 3 patterns of GI motility

A
  1. propulsion
  2. trituration
  3. mixing
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31
Q

what is propulsion?

how does this help push food along in one direction

A

movement of ingested food, liquids, GI secretions and sloughed cells
peristalsis: alternating contraction/relaxation of smooth circular and longitudinal muscles

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32
Q

what is emesis

A

technical term for vomiting

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33
Q

what is trituration

  • where does this take place
  • once complete, where does the food leave through
A

crushing and griding of food in the stomach

  • crashing together of waves moving in opp directions in the stomach
  • takes place in the ANTRUM with the pylorus closed (retropulsion)
  • once complete, leaves through the opened pylorus
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34
Q

what is mixing

A

blending various secretions (pancreatic, biliary, intestinal) w/ nutrients

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35
Q

what are the 2 gastroenteric reflexes and what do they do

what are gastroenteric reflexes

A

gastroilial: empties the terminal portion of the ileum
gastrocolic: movements in colon
- distension of the stomach initiates reflex that increases the rates of peristalsis and secretion along the small intestine

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36
Q

what is the rectoanal reflex

what muscle does this

A

when rectum is distended, there is reflex relaxation of internal anal sphincter
-puborectalis muscle of the pelvic floor (tail wagging)

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37
Q

what muscle is the puborectalis a part of

A

part of levator ani muscle

-when it relaxes, defacation occurs

38
Q

what is hirschsprung’s dieaese

A

congenital blockage of the large intestine due to improper muscle movement in the colon
-nerves of the myenteric and meissner’s plexi haven’t migrated into the right positions to stimulate the appropriate msucles for propulsion

39
Q

congenital megacolon is associated w/ waht

A

down syndrome 10% of pts

40
Q

what is the current theory of hirschsprung’s disease

A

may be caused by failed migration of colonic ganglion cells during gestation
-most cases not familial

41
Q

in hirschsprung’s what causes the bowel and abdomen to swell

A

intestinal contesnts build up behind the blockage, causing the bowel and abdomen to swell
-if the condition if severe, the newborn may fail to pass stool and may vomit

42
Q

what is the salivary gland secretion regulated by

what is its baseline secretion

A

parasympathetic nervous system
30 ml/hr
-needed even when not eating, for dental health

43
Q

how does salivary gland secretion lubricate food

A

acinar cells in the glands produce the more watery components of secretions

44
Q

salivary gland secretion begins digestion, how?

  • what does amylase break polysaccharides into
  • what does lingual lipase break down triglycerides to
A

carb and fat digestion begins in the mouth

  • amylase breaks down polysaccharides to oligosaccharides and maltose
  • lingual lipase: breaks down triglycerides to fatty acids and glycerol
45
Q

salivary gland secretion has an immune function, what is involved

A

IgA is the secreted immunoglobulin
-salivary glands, mammary glands, lacrimal glands, lining of GI and respiratory tracts
Lysozyme and lactoferrin: antibacterial enzymes
-lysozome breaks down bacterial cell walls

46
Q

what does epidermal growth factor do to salivary gland secretion

A

promotes healing of the mucosa in the mouth and stomach

prevents and heals ulcers

47
Q

saliva is hypotonic, what are the ions

A

higher K and HCO
-pumped into the acinar duct lumen (saliva)
-aldosterone stimulates K removal from tissue and into the lumen
low Na and Cl
-pumped out of saliva
-water can’t follow Na out bc of the properties of the duct cells
chloride shift
-cl leaves in exchange for HCO3
-keeps saliva relatively basic
-neutralizes stray stomach acid/protects the bottom of the esophagus

48
Q

in gastric secretion, the stomach absorbs water and lipid soluble substances, what are they

A

alcohol, glucose, aa, medium chain fatty acids, drugs

49
Q

gastric secretion prepares _____ for digestion

A

chyme (food slurry)

50
Q

oxyntic glands are in the fundus and corpus (body) of the stomach and parietal cells in the glands secrete _____

  • this and vit _____ are required for ______
  • what results ffrom poor absorption of this vit
A

intrinsic factor and HCl

  • intrinsic factor complexes w/ vit B12 and is required for B12 absorption in the distal ileum
  • pernicious anemia results from poor B12 absorption
51
Q

histamine acts on parietal cells to promote _____

A

acid production

-binds to parietal H2 receptors

52
Q

chief cells produce ____ and _____

what do these do

A

gastric lipase and pepsinogen

  • gastric lipase continues fat digestion
  • pepsin digests proteins and is derived from pepsinogen+acid
53
Q

pyloric glands are in the antrum and pyloric regions, what kind of cells are here and what do they do

A

neuroendocrine cells: release hormones that act in the gut

  • G cells: in antrum, release gastrin (hormone that stimulates acid production)
  • parasympathetic innervation by vagus to parietal cells promotes acid release
  • D cells: produce somatostatin and inhibits gastrin secretion
54
Q

what are the 4 ways to promote stomach acid production

A
  1. G cells release gastrin which acts on parietal cells
  2. parasympathetic innervation of parietal cells (via acetylcholine)
  3. parasym stimulation of G cells => #1
  4. histamine secreting stomach cells release hisatmine, which binds to H2 receptors, which cause parietal cells to promote acid production
55
Q

carbonic anhydrase in parietal cells results in generation of what

A

H and HCO3
H is pumped out in exchange for K, this involves ATPase
-Cl follows H out to form HCl in the stomach

56
Q

chloride ions are brought into the cells via ______

what is the movement of cells

A

chloride shift

  • cl in from the blood, HCO3 out
  • btwn blood and parietal cells
  • an “alkaline tide” into the blood (thought to protect cells from the acid on the other side)
57
Q

what is zollinger-ellison syndrome caused by

what can this lead to

A

cuased by gastrin secreting tumor of the pancrease; leads to peptic ulcers (most actually in duodenum)

58
Q

what kind of drugs retulates stomach acid secretion

A
  1. H2 receptor blockers
    - ex. zantac, pepcid, cimetidine (tagamet)
  2. Ach/Muscarinic blockers
    - ex. atropine
  3. proton pump inhibitors
    - block H/K ATPase
    ex. omeprazole (prilosec)
59
Q

proton pump inhibitor use is linked w/ increased susceptibility to bacterial infections, how

A

reduce the acidity/effectiveness of stomach acid in destroying pathogens

60
Q

what are the 3 phases of stimulation of acid secretion after ingesting a meal

A
  1. cephalic
    - thinking about food gets things going
    - via vagus stim of parietal and G cells
  2. gastric
    - due to physical distension (by food entry)
    - mediated by local reflexes
  3. intestinal
    - stimulated by aa in the blood
61
Q

what stimulates secretion

what inhibits secretion

A

stim: vagal stimulation, histamine, and gastrin
inhibits: chyme in duodenum; directly and via gastric inhibitory peptide (GIP) and secretin produced in duodenum

62
Q

once you’re in the duodenum, material will come into contact w/ pancreatic secretions, how

A

secretions via sphincter of oddi

63
Q

what pH do pancreatic enzymes work best at

A

neutral pH

  • pancreatic secretions have the same osmolarity of plasma (more basic)
  • neutralize acidic chyme
64
Q

what do acinar cells release

A

some ions and enzymes

-small volume containing Na and Cl ions and enzymes

65
Q

ductal cells are like the stomach acid secreting cells in reverse, an “acid tide”
-what kind of system does this use? what occurs

A 
antiporter system, fueled by entry of Cl from the lumen into the cell 
-exchanged for HCO3 
-no ATPase involvement in this antiport 
Na/K antiport btwn duct cell and blood
-Na to blood
-K to the cell
-uses NA/K ATPase
66
Q 
where is the cystic fibrosis transmembrane conductance reulator located at? 
what does it secrete?
-what does it allow re-entry of 
waht do mutations in the gene cause? 
what are the signe?
A
  • located on the luminal side of the membrane
  • secrete Cl ions out of the cells
  • allows re-entry of Cl to fuel antiport for the acid tide
  • mutattions in this gene cause cystic fibrosis
  • signs: salty tasting skin, poor growth and weight gain, thick and sticky mucus, frequent chest infections, coughing, shortness of breath
67
Q

how does secretin and VIP retulate pancreatic secretion

A

secretin and VIP: secreted by endocrine cells in the duodenum in response to acid

  • acts on ductal cells to increase HCO3 secretion to neutralize chyme
  • responsible for water and electrolytes
68
Q

how does CCK regulate pancreatic secretion

A

acts on gallbladder and pancrease

stimulates bile, enzymes, etc

69
Q

pancreatic acinar cells secrete ____ which break down nearly anything
why can pancreatitis be deadly?

A

enzymes

  • very unpredictable
  • massive enzyme release
  • local breakdown in the post body wall
70
Q

what is bile composed of

A

bile salts, pigments (bilirubin), cholesterol, phospholipids, proteins

71
Q

what is bile produced by
where is it concentrated in
can a person live w/o a gallbladder?
what stimulates gallbladder contraction

A

hepatocytes and concentrated in the gallbladder

  • a person can live w/o a gallbladder, but has to be more attentive of fat intake
  • CCK stimulates gallbladder contraction
72
Q

what are the functions of biliary secretion

A
  1. absorption of lipids (bile acids)
    - cholic and deoxycholic acids
    - forms micelles to digest lipids
    - reabsorbed in the distal ileum
  2. excretion of cholesterol and bilirubin
73
Q

what is jaundice

A

certain liver diseases interfere w/ normal production and discharge of bile
-pigments deposit in sclera, skin, tissues, some fluids=> yellowish pigmentation

74
Q

bilirubin is a major component of bile pigments

-breakdown product of what?

A

breakdown product of Hb

75
Q

how do CCK and secretin work in regulation of bile production

A

CCK: release stimulated by presence of fatty acids or aa

  • causes contraction of gall bladder and indirectly relaxes spincter of oddi (like vagus nerve)
    secretin: release from intestinal mucosa stimulated by presence of acid
  • stimulates bicarbonate production by bile duct cells (like pancreatic duct cells)
  • this is how bile contributes to neutralization of acid in duodenum
76
Q

when do gallstones form

A

form when bile has too little bile salts or too much cholesterol or billirubin

77
Q

how does gastrin stimulate bile secretion

A

directly and indirectly by increasing acid production

78
Q

what do steroids do to bile secretion

A

inhibit

79
Q

what are some other fucntions of the liver

A
  1. plasma protein secretion
    - anything ending in “inogen”
  2. nutrient store formation
  3. metabolite conversion
  4. detoxification
    - cytochrome P450: breaks down toxic molec
    - converts ammonia to urea
80
Q

in carbohydrates where does digestion start

  • what does this form
  • what does the brush border membrane break down
  • what does glucose and galactose absoroption depend on
A

starts w/ salivary amylase, then pancreatic amylase

  • forms disaccharides and oligosaccharides
  • brush border membrane breaks down disaccharides
  • glucose and galactose absorption depends on Na dependent carrier (fructose uptake by facilititate transport)
81
Q

where does protein digestion start
pepsinogen is converted to ______ in stomach
trypsinogen to ______
-what is this converted by

A
  • starts in stomach, then small intestine
  • pepsinogen converted to pepsin in stomach
  • trypsinogen to trypsin
  • converted by enteropeptidase
  • trypsin activates other enzymes
82
Q

essential fatty acids are _______

-omega 3 and omega 6 have what kind of bond at

A

unsaturated

double bond at 6 and 3 from the end of the molec

83
Q

which omega 3’s are essential for normal development of vision of newborns

A

eicosapentaenoic (EPA) and docosahexaenoic (DHA)

84
Q

where does digestion of lipids start in

using what kind of cells

A

starts in mouth w/ lingual lipase, followed by stomach w/ acid lipase (chief cells)

85
Q

pancreatic lipase forms ____ and ____ to be stored in adipocytes

A

monoglyceride and 2 fatty acids

86
Q

phosphlipase digests _____

cholesterol esterase breaks down ____

A

phospholipids

cholesterol

87
Q

how do bile salts emulsify fats

A

by forming micelles which enhance delivery to, and absorption by, brush border

88
Q

what do micelles transport

what do they prodivde for digestion of lipids

A
  • transport poorly soluble monoglycerides and fatty acids

- provide increased surface area for digestion of lipids in the micelles

89
Q

the gut secretes chylomicrons and VLDLs

  • where are the absorbed fats reassembled
  • how are they packaged for easier transport
  • transported out of the gut via what
A

in the enterocyte (lining cells of the gut)

  • packaged into chylomicrons for easier transport
  • transported out of the gut via the lymphatic system
90
Q

what are the fat soluble vitamins

-how are they absorbed

A

A, D, E, K

-absorbed passively and incorporated into chylomicrosn

91
Q

iron is an important component of heme and also participant in many enzymatic rxns
-how is it transported in the blood

A

iron is actively transported in the blood via transferrin after being converted to ferritin by binding w/ apoferritin

A & P final (8 decks)

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