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BIOL 2420 > GI physiology > Flashcards

GI physiology Flashcards

1
Q

what are the 5 functions of the GI system?

A

1) motility: deglutition, peristalsis, mass movements
2) secretion: mucus, water (8L a day), enzymes
3) digestion: mechancial (physical changin, breaking down), chemical (enzymes)
4) absorption: transytosis
5) barrier function (not talked about in this text)

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2
Q

classify the 4 main functions of the GI system into the areas they happen

A

digestion and motility (into blood): lumen of the digestive tract

secretion (into blood, lumen, and wall) and absorption (into blood): wall between lumen and ISF

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3
Q

list in which order food will be processed from ingestion to excretion starting at the mouth (a.k.a the alimentary canal)

A
  • mouth
  • esophagus
  • stomach
  • small intestine (duodenum (80-100 cm), jejunum (4m), ileum (80cm))
  • caecum (appendix)
  • large intestine (formation of feces)
  • rectum (stores feces)
  • anus
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4
Q

what are the accessory organs of the alimentary canal

A
  • liver (produces bile, important for lipid digestion)
  • gall bladder (non-essential, stores biles and [] it)
  • pancreas (important for digestive enzymes - empties into duodenum)
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5
Q

what starts mechanical digestion?

A

the mouth (mastication)

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6
Q

place the following layers of the GI tract in order from inner most membrane to outer most

a) muscularis
b) mucosa
c) serosa
d) submucosa

A

b, d, a, c

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7
Q

tissue layers of GI tract: mucosa

A
  • single epithelium layer of cells
  • lamina propria - which contains blood vessels and nerves
  • muscularis mucosae (muscle of the esophagus)
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8
Q

tissue layers of GI tract: submucosa

A

Submucosal plexus

  • network of neurons (part of the ANS)
  • parasympathetic (rest and digest) and sympathetic (fight or flight)
  • more neurons in gut than in out brain
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9
Q

tissue layer of GI tract: muscularis

A
  • circular muscle which controls the diameter
  • myenteric plexus - controls 2 layers for coordinated controlled movement

-primarily comprised of 2 layers EXCEPT for in the stomach

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10
Q

tissue layers of the GI tract: serosa

A
  • outer layer
  • peritoneum (lining of abdominal cavity)
  • anchors the tube to the body wall
  • mesothelium (visceral peritoneum)
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11
Q

what type of involuntary control do we have in our intestinal musculature?

A

-skeletal muscle - swallowing (voluntary at the beginning then becomes involuntary) and clinching (only 10% under voluntary control)

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12
Q

the musculature in the intestinal tract is mostly under _____ control

A

involuntary

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13
Q

what are the 7 sphincters of the GI tract

A

1) upper esophageal
2) lower esophageal (prevents stomach contents from coming back up)
3) pyloric (doorway out of stomach)
4) ileocecal
5) colorectal (functional)6
6) internal anal
7) external anal (voluntary)

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14
Q

how does smooth muscle differ from skeletal muscle in terms of actin and myosin?

A

there is more actin and less myosin

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15
Q

how does smooth muscle differ from skeletal muscle in terms of structure

A
  • no sarcomeres
  • dense bodies (contain actin, comparable to Z lines in skeletal muscle)
  • contraction is calmodulin-dependent

fig 12.25

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16
Q

explain smooth muscle contraction simply, as a review

A

1) high Ca++ binds and activates Ca+ calmodulin complex
2) this complex phosphorylates MLCK
3) MLCK phosphorylates myosin, placing it in the cocked position
4) cross bridge formation

1) when Ca++ levels are low, Ca+/calmodulin compelx unbinds
2) myosin phosphatase removes phosphate from myosin
3) cross-bridge releases

fig 12.26

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17
Q

only when MLCK is phosphorylated, will the smooth muscle contract

true or false?

A

true

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18
Q

what are the 4 GI movements?

A

1) segmentation
2) peristaltic waves
3) migrating motor complexes (MMCs)
4) gastric movements

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19
Q

GI movements: segmentation

A
  • active contraction
  • not used to push food down length of the tube, very MINOR CONTRIBUTION to motility
  • main purpose is to mix contents by squeezing back and forth to push materials back and forth
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20
Q

GI movements: peristaltic waves

A
  • weak but repetitive movements
  • constrictions are 1 cm or less
  • very short and weak which causes nice even flow
  • can get intestinal issues if this is not working properly
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21
Q

GI movements: migrating motor complexes (MMCs)

A
  • strong and long contractions
  • a single MMC can move the entire length of the gut starting at the stomach (gets things out in a hurry)
  • MMC starts at the stomach and squeezes small intestine to get rid of its contents - keeps intestine clean and clear
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22
Q

GI movements: gastric movements

A
  • third muscle layer
  • churning motion
  • this helps liquefy contents
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23
Q

myenteric plexus - def.

A

the major nerve supply to the gastrointestinal tract and controls GI tract motility. According to preclinical studies, 30% of myenteric plexus’ neurons are enteric sensory neurons, thus Auerbach’s plexus has also a sensory component
-sensory, motor, and interneurons

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24
Q

what are the excitatory functions of the myenteric plexus

A
  • muscle tone
  • contraction intensity (used to control strength of contraction)
  • contraction rate (speed or frequency)
  • peristaltic velocity
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25
Q

what are the inhibitory functions of the myenteric plexus?

A
  • sphincter tone (necessary if we want more material to move)
  • back flow (sometimes it is necessary for material to go backwards)
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26
Q

most of the functions of the gut are controlled locally

true or false?

A

true

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27
Q

slow waves in the GI tract are created by which type of cells?

A

undulating changes in ICCs (interstitial cells of cajal which are pacemaker cells)

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28
Q

explain the intrinsic control of GI function

A
  • resting membrane potential is not stable
  • interstitial cells of cajal (ICCs) (pacemaker cells) reach threshold with variable K+ permeability
  • spike potentials are produced with an influx of Ca++ (reach threshold) (mechanoreceptors, chemoreceptors)
  • this leads to greater depolarization (gap junctions and summation), higher frequency (because of greater depolarization), stronger contraction (because of high frequency)
  • hyperpolarization prevents excitation (inhibits potentials generated by ICCs) (relaxation)

fig 21.4a

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29
Q

explain the 3 modes of extrinsic control of GI function

A
  • independent function
  • extrinsic coordination controlled by myenteric plexus

1) ANS
- parasympathetic - promotes intestinal functions (acetylcholine)
- sympathetic - norepinephrine (causes hyperpolarization)
2) hormones
3) cognitive and emotional control
- ex: getting angry produces more stomach acid

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30
Q

gastrointestinal reflexes: intragut communication

A
  • different organs need to communicate with each other

- stomach talks to small intestine and large intestine and vice versa

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31
Q

what kinds of stimuli sends signals to begin gastrointestinal reflexes?

A

-a few examples:

distention, chemicals, irritants

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32
Q

gastrointestinal reflexes: proximal to distal reflexes

A
  • new contents

- ex: stomach telling small intestine food is coming to get ready

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33
Q

gastrointestinal reflexes: distal to proximal reflexes

A
  • old contents
  • ex: large intestine telling small intestine that it is already full
  • THESE REFLEXES OVERRIDES PROXIMAL TO DISTAL REFLEXES
  • or else stomach would just keep pushing food through
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34
Q

increased motility in the gut leads to what?

A
  • increased MMCs (need to get rid of contents in small intestine if you have an infection for example)
  • ex: diarrhea
  • serve as a protective mechanism
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35
Q

what are the two major symptoms of disturbed motility in the gut

A

constipation and diarrhea

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36
Q

decreased motility in the gut leads to what?

A
  • material stays in the gut for too long, too much water is reabsorbed, leads to constipation
  • consequences include: distention, perforation (too much stretch, leads to tearing), and death
  • Chagas disease (destroys the enteric nervous system, all control dissapears, large intestine is completely filled with material)
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37
Q

what is the emetic centre?

A

the centre in the medulla that receives cues from blood hormones, visual cues, motion, or stomach contents that initiates vomiting

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38
Q

how can excess vomiting be dangerous? how can we control this?

A
  • excess vomiting can lead to a pH imbalance, body chemistry become alkaline (because of decreased acidic content from stomach)
  • disturbances in pH can be fatal
  • to control this, we take antiemetics (emetic system)
  • drug that stops vomiting
  • but, we need to know what is causing the vomiting otherwise we can’t treat it because not every treatment works for every cause
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39
Q

throughout the GI tract ___L of fluids are secreted daily

A

7

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40
Q

what are the sources of fluids are secreted in the GI tract?

A
  • saliva
  • gastric juice
  • bile
  • pancreatic juice
  • small intestinal secretions

fig 21.3

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41
Q

what are 3 functions of fluid secretion by the GI tract?

A
  • liquefaction
  • lubrication
  • digestion
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42
Q

what is the major organ of absorption

A

small intestine

-approximately 7500 mL gets absorbed by small intestine and 1400 mL by large intestine

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43
Q

how much saliva is secreted per day

A

approximately 1.5 L (1500 mL)

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44
Q

what are the 4 functions of saliva secretion

A

1) moistening
2) lubrication
- mucin (mucus protein)
3) defence
- lyzosome - breaks down cell walls of certain bacteria
- IgA - immunoglobulin A - antibody
4) digestion
- salivary amylase (breaks down amylose, a.k.a. starch)

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45
Q

how is the secretion of saliva controlled? (3 ways)

A

1) tactile stimulation
- ex: food in mouth promotes salivation
2) cognitive stimulation
- thinking about food
3) autonomic NS
- parasympathetic (increases salivation) and sympathetic (decreases salivation) innervation

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46
Q

gastric secretion occurs in the _______

A

gastric pits which contain gastric glands

-these go deep down into tissue of the stomach

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47
Q

what are the two types of mucus cells in the gastric pits?

A

1) surface mucus cells: mucus-producing cells which cover the inside of the stomach, protecting it from the corrosive nature of gastric acid. These cells line the gastric mucosa
2) mucus neck cells: found in the necks of gastric pits

fig 21.9a

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48
Q

in gastric secretion, acid (HCL) is released into the stomach by ______ cells

A

parietal cells

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49
Q

what is the role of a chief cell?

A

The gastric chief cell (also known as a zymogenic cell or peptic cell) is a cell in the stomach that releases pepsinogen and chymosin. Pepsinogen is activated into the digestive enzyme pepsin when it comes in contact with acid produced by gastric parietal cells

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50
Q

name 3 hormones involved in gastric secretion and their functions

A

1) enterochromaffin-like (ECL) cells - produce histamine
2) G cells - produce gastrin
3) D cells - produce somatostatin

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51
Q

what are chaperone cells in gastric secretion?

A
  • a.k.a. parietal cells
  • these bind to something until it is able to get absorbed
  • ex: intrinsic factor binds to B12 and prevents acid from breaking it down before it is absorbed
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52
Q

how much gastric juice is secreted/day?

A

approximately 2500 mL

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53
Q

what are the 3 functions of gastric acid secretion?

A

1) bacteriocidal role (kils bacteria) - many bacteria we eat survive this
2) digestion or proteins
- acid hydrolysis: non-enzymatic breakage of peptide bond
- denaturation
3) digestion of bone (not as important for us as we don’t eat too much bone)

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54
Q

what would happen if too much gastric acid was secreted?

A
  • peptic ulcer disease (too much acid leads to stomach lesions)
  • gastrointestinal reflux disease (GERD) (too much acid in stomach can cause acid reflux that can splash up through lower esophageal sphincter)
  • alkaline tide
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55
Q

what is an alkaline tide?

A

refers to a condition, normally encountered after eating a meal, where during the production of hydrochloric acid by parietal cells in the stomach, the parietal cells secrete bicarbonate ions across their basolateral membranes and into the blood, causing a temporary increase in pH

  • cause by too much gastric acid secretion
  • more acid in the stomach = more pressure for protons to go back into ISF, but at the same time we are increasing the buffering in ISF from formation of barbonic acid through HCO3-/Cl- pump

fig 21.9c

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56
Q

what is the difference in pH from the ISF to the stomach?

A
  • pH of 1 in the stomach and about 7.4 in the ISF
  • this is about 1 million times greater in the stomach which is only separated by a single layer of cells which creates a gradient, explaining why H+ leaks through
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57
Q

what are the 3 phases involved in the control of stomach secretions?

A

1) cephalic phase
2) gastric phase
3) intestinal phase

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58
Q

what controls the cephalic phase of stomach secretions?

A

-control comes from the brain - vagus nerve stimulates enteric nervous system

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59
Q

the cephalic phase of stomach secretion causes direct stimulation of which types of cells?

A

1) parietal cells which promote acid production
2) G cells which release gastrin
- responsible for acid secretion - HCL and pepsinogen secretion
3) ECL-cells which release histamine
- promotes acid secretion by parietal cells

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60
Q

what controls the gastric phase of stomach secretion?

A

the presence of luminal contents

-there are baroreceptors (detect pressure) and chemoreceptors (detect lipids) here which detect luminal contents

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61
Q

the gastric phase of stomach secretion stimulates which type of cells?

A

1) goblet cells (stimulate mucus production for lubrication, protection of gastric epithelium)
2) parietal cells (increase acid production)
3) G-Cells (increase acid production)
4) Chief cells (pepsinogen production)

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62
Q

what happens during the gastric phase of stomach secretions when the pH gets under 2?

A
  • there is a negative feedback response
  • D-Cells are stimulated and release somatostatin (this has an inhibitory effect, shuts down the production of acid)

fig 21.10

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63
Q

which cell involved in the control of stomach secretions is not innervated by the submucosal plexus? what stimulates this cell?

A

D cells, these cells are stimulated by the negative feedback loop caused by too much acid secretion

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64
Q

the intestinal phase of stomach secretion control is triggered by what?

A

duodenal pH

  • there are no longer contents in the stomach at this point
  • contents from the stomach have a low pH when they reach the duodenum
  • also triggered by duodenal lipids
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65
Q

what is stimulated by the intestinal phase of stomach secretion control?

A
  • secretin (parietal cells, chief cells) - these inhibit stomach secretion
  • gastric inhibitory peptide (strong inhibition)
  • cholecysokinin (CCK) (lesser inhibition)
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66
Q

what is the name for a molecule that increases secretion

A

a secretagogue

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67
Q

what are the secretagogues that promote gastric acid secretion

A
  • acetylcholine (released by vagus nerve)
  • gastrin
  • histamine
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68
Q

what is the name for a molecule that decreases secretion

A

anti-secretagogue

69
Q

what are the anti-secretagogues that decrease gastric acid secretion

A
  • PGE2 (prostoglandin 2) (product of arachadonic acid and metabolism - produced by enzyme COX)
  • norepinephrine
70
Q

there are two major therapeutic targets for reducing acid secretion in the stomach in cases where excess acid is present. What are they?

A

1) histamine (H2) blockers - Tagamet, Zantac, Pepcid
- histamine is a secretagogue, these prevent secretagogue effects
- reversible competition

2) proton pump inhibitors - Prilosec, Prevacid
- H+/K+ exchange pump
- irreversible binding

71
Q

what does NSAID stand for

A

non steroidal anti-inflammatory drugs

72
Q

what are 3 examples of common NSAIDs

A

ibuprofen, naproxen, aspirin

73
Q

NSAIDs work by inhibiting which enzyme?

A

COX

74
Q

COX-1

A
  • releases small amounts of prostoglandin, regulates gastric secretion
  • effective antisecretagogue, prevents too much acid secretion
  • ALWAYS WORKING
75
Q

COX-2

A
  • inducible form, it is NOT ALWAYS ON, gets turned on during inflammation
  • produced large amounts of prostoglandin E2 (inflammation hurts, this is why NSAIDs work to alleviate pain
76
Q

what happens if we take NSAIDs too often?

A

-taking them every once in a while is okay, but when we start taking them regularly, we are reducing the protective effects in the stomach

77
Q

what can happen if we inhibit both COX enzymes?

A

gastropathy

78
Q

1st generation NSAIDs

A
  • NON-SPECIFIC
  • these block ALL COX enzymes
  • cox - 1 is constitutive - good for protection
  • cox - 2 is inducible - during inflammation
79
Q

both cox enzymes (1 and 2) work through which type of second messenger system?

A

Ca++ dependent second messenger systems

80
Q

2nd generation NSAIDs

A
  • these are selective
  • ex: Celecoxib, Refocoxib
  • these inhibit COX - 2 ONLY (inflammatory)
81
Q

what is dangerous about ONLY inhibiting the cox-2 enzyme? (2nd generation NSAIDs)

A
  • this leads to undesirable effects

- Vioxx often led to heart attacks (up to 140 000 in one year)

82
Q

NO modified NSAIDs

A
  • experimental drugs that have been modified to reduce the risks
  • these are non selective
  • nitric oxide is released when NSAID is ingested - at low doses, NO causes vasodilation
  • more blood flow gets to the stomach, this effectively washes away any backflow from protons, dilutes it
83
Q

H2S modified NSAIDs

A
  • hydrogen sulfide releasing NSAID
  • non specific
  • example of this is naproxen
  • low doses of H2S reduces inflammation, preventing damage to tissue
  • prevents the problem before it even starts - damaged tissue causes inflammation
84
Q

endocrine pancreas

A
  • where pancreatic islets are found

- cells that produce insulin, cells that produce glucagon

85
Q

exocrine pancreas

A
  • where pancreatic duct is found
  • stuff accumulates in pancreatic duct, drains pancreas
  • this leads to the duodenum

fig 21.14a

86
Q

how much pancreatic juice is secreted daily? what are the two components of this juice?

A

about 1500 ml/day

-there is an aqueous component and an enzyme component

87
Q

aqueous component of pancreatic juice

A

comprised of:

  • Na+
  • bicarbonate (most important part; buffers pH) (carbonic anhydrase (ca))
  • Cl-/HCO3- exchanger (HCO3- pumped into lumen)
  • water

bicarbonate, Na+, and Cl- all get pumped into lumen, which is then followed by water

fig 21.14c

88
Q

enzymatic component of pancreatic juice

A

comprised of:

  • proteolytic zymogens
  • pancreatic amylase (breaks down starch)
  • pancreatic lipases (breaks down lipids)

-these are all stimulated by other signals - aqueous and enzymatic components can be controlled separately by different stimuli

fig 21.14c

89
Q

which channel is affected in individuals with cystic fibrosis?

A

the CTFR channel in exocrine pancreas

-this is what pumps Cl- into lumen of pancreas or intestine

90
Q

how is pancreatic secretion controlled?

A

vagus nerve

  • parasympathetic stimulation - - ACh
  • the enzymatic component of juice mostly triggers this (more than the aqueous component)
  • sympathetic (NE)
  • leads to inhibition of secretion
91
Q

how do fatty acids control decretion in the duodenum?

A
  • food in the lumen of the duodenum release enzymes (CCK) to break down food
  • CCK slows gastric motility, slowing gastric emptying, regulating how much content can bet into the duodenum
  • a.k.a. decreases gastric emptying

-this happens as the stomach is emptying

THIS IS THE ENZYMATIC COMPONENT

92
Q

how does acidic chyme in the duodenum control pancreatic secretion?

A
  • release of secretin - (AQUEOUS COMPONENT)
  • decreases gastric emptying
  • stimulates release of aqueous component, to buffer acid
  • this happens as the stomach is emptying
93
Q

Liver: Bile

A
  • there is a continual production of this (about 5000ml/day)
  • good for neutralization - bicarbonate
  • emulsification by bile salts (taking lipids and trying to solubilize them, don’t want lipids in our food to separate from aqueous component cause we can’t digest them)
94
Q

Liver: Gallbladder

A
  • stored and concentrates bile (from 5 to 15 x)
  • approximately 30-60 ml of time (which is 15 x the concentration as when it was produced)
  • BILE IS STORED HERE and concentrated here
  • when the gallbladder is too full, it empties into small intestine (otherwise it is released as necessary)
95
Q

what is the liver’s main blood supply?

A

hepatic artery and poral vein

96
Q

what controls liver secretion?

A
  • cholescystokinin (CCK) (chol -= bile, cyst = to move)
  • triggered by fats in the duodenum
  • this play a big role in gallbladder emptying, lipids in the duodenum stimulate the released of bile
  • Secretin, stimulated by acidic chyme (releases bile)
  • stimulates bicarbonate rich bile production (buffer)

fig 21.15

97
Q

the small intestine is made up of ____ cells that either go to the bottom of the crypts or the top of the villi

A

stem

98
Q

Small intestine architecture: villi

A
  • these are mature cells = enterocytes (MAIN SITE OF ABSORPTION)
  • goblet cells (stimulate mucus secretion)
99
Q

small intestine architecture: crypts (of Lieberkhun)

A
  • these are immature cells
  • this is the site of SECRETION
  • secrete about 1500 ml/day
  • each villa may have 4-6 crypts surrounding it
  • good site for bacteria (warm, moist) so flushing action washes away bacteria (daugher stem cells have either bacteriocidal (kills bacteria) or bacteriostatic (stops bacteria form growing) roles

-THIS CELL IS DIFFERENT FROM CELLS OF VILLI AND HAS DIFFERENT FUNCTIONS

fig 21.11

100
Q

look at fig 21.13

A

review of small intestine secretion

101
Q

small intestine secretion control

A
  • LOCAL distention (largest factor)
  • ONLY when food is present

-secretin and CCK also help increase intestinal secretion (but have a very minor role)

  • secretagogues - large factor increasing secretion
  • inflammation in small intestine will increase secretion in this area
  • infection increases secretion (cholera toxin - prostoglandins; increased cAMP [] or Ca++ [])

-increased secretion is another cause of diarrhea (watery stool)

102
Q

cholera

A
  • bacteria
  • vibrio cholerae is found in contaminated water/food
  • world wide distribution
  • causes severe gastroenteritis in children (from powdered milk mixed with contaminated water, severe diarrhea, dehydration, and death - can lose 23 L a day in diarrhea)
  • cholera toxin activates adenylyl cyclase (increases cAMP production, Cl- secretion, and everything else which follows)
103
Q

what are the effects of the cholera toxin?

A

1) increased Cl- secretion
- leads to an increase in Na+ and water secretion
2) hypersecretion causes SEVERE dehydration (rather secrete 23000 ml a day)
3) absorption is NOT AFFECTED
- you can treat this with oral rehydration therapy (ORT)
- as long as intake of water is larger than output
- drinking salty solution (gatorade), having salt in water helps us absorb it
4) cystic fibrosis is often correlated with cholera
- CFDR PUMP DOES NOT WORK (mentioned before)
- increases in cAMP, has nowhere to go

104
Q

what are the components of the large intestine?

A

1) deep crypts of Lieberkuhn (go down into lamina propria)
2) goblet cells - large cells that produce mucus (good for lubrication and as an adhesive medium (conversion of chyme into feces, solidifying contents)

105
Q

how is the large intestine controlled?

A

1) tactile stimulation
- local distention - by baroreceptors
2) parasympathetic NS (increases production)
3) some emotions (stress)
- leads to mucoid diarrhea
- chronic stress has secretagogue effects (largely affecting goblet cells) - increases mucus production in diarrhea

106
Q

what is the major difference betweent he structures of the small intestine and the large intestine?

A

they are very similar, bu the large intestine does not have villi

107
Q

where is most of the absorption done in the GI tract?

A

small intestine - huge surface area

108
Q

which two things increase the surface area of the small intestine?

A

massive surface area due to:

  • villi: increases SA by 10x
  • microvilli: which have a brush border and increase SA by 50x

**remember that absorption happens in villi and not in crypts (secretion)
fig 21.1f

109
Q

what are the two modes of digestion

A

1) mechanical - for macro-molecules that are too large to be absorbed (chewing - separates food into paste, this happens in mouth and stomach)
2) chemical
- 2 forms in the stomach (acid hydrolysis - breakage of pepetide bonds; enzymatic - bulk of digestion)
- this gets food small enough for absorption

110
Q

where are the 3 areas of absorption?

A

1) stomach - alcohol and aspirin are absorbed here, these effects are quicker
2) small intestine - main site of absorption
3) large intestine - minimal absorption

absorption is classified as getting material into epithelial cells (from lumen of gut into cytoplasm)

111
Q

what is our microbiome?

A

ecosystem of microbiome in important for our health (helps prevent certain diseases - arthritis, asthma)
-our microbiome is largely the result of being born naturally - babies born via C-section do not have this - more susceptible to these diseases

112
Q

define “transport” into circulation

A
  • from cytoplasm into ISF

- get nutrients from our gut that go into blood

113
Q

what is the hepatic portal system?

A

blood that leaves intestine, and does not go directly to heart (could potentially be high in compounds that are not wanted/dangerous) - so it is detoxified before it goes to the heart
-goes to the liver first to detoxify things you may have ingested

114
Q

in enzymatic digestions from the mouth to the small intestine, what are the digestive enzymes?

A
  • salivary glands (salivary amylase)
  • gastric pits (gastric enzymes - in gastric juice) - gastric amylase, different isoforms in different environments, optimal = pH of 2 in stomach
  • exocrine pancreas (pancreatic amylase)
  • liver (bile salts - lipid digestion)
  • intestinal microbiome

-brush border enzymes - tethered epithelial enzymes - # proportional to surface area

115
Q

dietary carbohydrates (CHOs) make up approximately ____% of calories in a human diet

A

50

116
Q

what are complex carbohydrates that we ingest?

A

Polysaccharides

  • starch (amylose or amylopectin) - long linear chain held together by glycocidic linkages
  • glycogen - long chain of glucose with branched polymers (more complex)
  • cellulose (humans cannot digest, prevents stool from getting too hard because water has to stay with this)
117
Q

what are the simple carbohydrates that we ingest?

A

dissacharides

  • sucrose
  • lactose
  • maltose

monosaccharides
-glucose
-fructose
0galactose

118
Q

what is sucrose?

A

glucose + fructose

119
Q

what is lactose?

A

glucose + galactose

120
Q

what is maltose?

A

glucose + glucose

121
Q

what is glucose?

A

6 member ring

122
Q

what is fructose?

A

5 member ring

123
Q

what is galactose?

A

6 member ring

124
Q

monosaccharides and disaccharides are the only absorbable carbohydrates

true or false?

A

false, monosaccharides are the only absorbable carbohydrates, the others need to be broken down first

125
Q

what are the 3 types of luminal amylases? how do they differ in what they do?

A
  • salivary amylase
  • gastric amylase
  • pancreatic amylase
  • the effect is the same for each
  • amylase takes amylose or glycogen and breaks it down to maltose, sucrose, or lactose
126
Q

where are brush border enzymes found?

A

small intestine

127
Q

brush border enzymes

A
  • final step in digestion of dietary carbohydrates and proteins
  • small intestine enterocytes
  • disaccharidases (breaks down disaccharides)
  • sucrase-isomaltase (sucrase, maltase) - breaks down sucrose and maltose
  • lactase (breaks down lactose)
128
Q

when the lactase enzyme is turned _____ one is lactose intolerant

A

off

129
Q

carbohydrate absorption and transport includes which types of carbohydrates?

A

monosaccharides only

130
Q

on the apical membrane, we find SGLT-1 channels, what do these do?

A
  • sodium glucose linked co-transporter
  • brings both glucose and Na+ from lumen into cell, powered by Na+/K+ ATPase (gradient)
  • SGLT1 is a secondary ACTIVE transporter for glucose or galactose
131
Q

on the apical membrane, we find GLUT-5 channels, what do these do?

A
  • transport of fructose (FACILITATED DIFFUSION)
  • down gradient
  • this does not transport glucose
132
Q

on the basolateral membrane, we find GLUT-2 transporters, what do these do?

A
  • facilitated diffusion of ALL monosaccharides across basolateral membrane
  • once in ISF, they get picked up by capillaries
  • normally, there is not a lot of fructose or galactose in our blood (mostly only in hepatic portal system - links liver and intestinal tract)
133
Q

why isn’t there a lot of galactose or fructose in our blood?

A
  • this is mostly found in hepatic portal system, and these are converted into glucose, or
  • stored as glycogen (by the liver), or
  • converted to lipids

-lipids are high energy molecules - more efficient energy storage - THIS ALL HAPPENS IN THE LIVER

fig 12.17b

134
Q

why do we have different mechanisms for carbohydrate absorption? (diffusion and active transport)

A
  • normal blood glucose [] is 4-7
  • cytoplasmic [] is 10
  • luminal [] ranges from 1-40
  • this varies depending on what and when you eat
  • if absorption was by diffusion, you would be losing the energy you’re trying to get because shortly after a meal, [] would be high in lumen of the intestine but between meals, glucose would be higher in cell, so instead of going into the blood, glucose would diffuse back into the lumen
  • SGLT1 can only move glucose INTO the cell
135
Q

glucose is absorbed via secondary active transport because of the varying concentrations throughout the day, but why isn’t fructose absorbed via this mechanism?

A
  • fructose still moves by facilitated diffusion because there is such a small amount so it doesn’t make a difference
  • it is rapidly converted into glucose most of the time so its [] is essentially 0

-facilitated transporter (GLUT-5) depends on the [] gradient

136
Q

protein digestion: mechanical digestion

A
  • mastication - starts in the mouth, separating proteins while chewing
  • separates proteins to gastric juice and saliva can start working on food
  • proteins are denatures in the stomach because of the low pH
137
Q

protein digestion: acid hydrolysis

A
  • activation of pepsinogen - this breaks peptide bonds randomly, NOT SELECTIVELY
  • transformation into polypeptides
  • pepsinogen is broken down into pepsin (by acid in stomach) - active proteolytic enzyme
138
Q

protein digestion: enzymatic digestion

A
  • breakage of peptide bonds
  • because of the pH (2-3)
  • this makes up about 10-20% of digestion
  • end result: shorter polypeptides, not usually single amino acids
139
Q

what are the 3 endopeptidases involved in protein digestion

A

1) pepsin - cleaves pepsinogen
2) trypsin - cleaves trypsinogen
3) chymotrypsin - cleaves chymotrypsinogen

140
Q

endopeptidases break down polypeptides into amino acids

true or false?

A

false, endopeptidases break polypeptides down into smaller peptides, not individual amino aicds

-this cleaves part of the chain that is INSIDE

141
Q

exopeptidase

A
  • breaks down polypeptides

- takes an amino acid group off the SIDE of the chain, shortening the polypeptide by 1 AA

142
Q

what are two exopeptidases

A
  • aminopeptidase

- carboxypeptidase

143
Q

what is the end result of the work from an endopeptidase, and exopeptidase?

A

endo - cleaves in the middle of the polypeptide chain, end result: two smaller polypeptides

exo - cleave 1 amino acid terminus off the end of the polypeptide chain, end result: one single amino acid and diemrs, trimers, etc.

144
Q

what are the different modes in which proteins can be absorbed?

A

1) for trimers, can be absorbed through tripeptide H+ channels
- same thing for dimers (dipeptides) - tripeptides and dipeptides are both LINKED WITH H+ ABSORPTION

2) amino acids - linked with Na+ absorption (Na+ linked co-transporter)
3) basolateral transporters - type specific

4) transcytosis - this is for small peptides, which are carried across the cell intact
- this is good for surveillance because once something is broken down, cannot tell what it was

THESE ARE ALL SECONDARY ACTIVE TRANSPORTERS

fig 21.18c

145
Q

what is the most common lipid in the body

A

tryglycerides

146
Q

_____ fats are comprised of all single bonds, and are solid at room temperature

A

saturated

147
Q

______ fats are comprised of double bonds between carbon atoms, and are liquid at room temperature (kinked)

A

unsaturated

148
Q

which enzymes aid in lipid digestion?

A

1) salivary lipase (short lived)
- different isoforms produced by different glands
2) gastric lipase (minor contribution)
- largely to do with surface area

lipases can only act on the surface of the lipid droplets, this makes up about 10% of digestion - little activity for enzymes

149
Q

what is the process whereby we transform LIPIDS into SOLUBLE molecules?

A

emulsification

  • bile salts from the gallbladder increase the solubility of lipids by surrounding them
  • pancreatic lipase turns lipids in monoglycerides and free fatty acids
  • these get surrounded by bile salts and become micelles - increases surface area - more room for digestion
  • monoglycerides diffuse across the membrane and are transformed back into tryglycerides in the smooth ER (where the primary role is lipid synthesis)
  • cholimicrons
150
Q

what are cholimicrons?

A
  • lipoproteins (HDL and LDL)
  • cholymicrons are too big to be absorbed into blood stream, so they get absorbed by lacteal cells (lymphatic system) and eventually return in the blood

fig 21.9d

151
Q

_____ lipoprotein has a high [] of protein and a low [] of lipids

A

high density

152
Q

_______ lipoprotein has a low [] of protein and a high density of lipids

A

low density

153
Q

how much water is secreted per day? how much do we consume?

A
  • 7L/day PLUS consumption

- we are supposed to consume about 2L, so this adds up to 9L/day, where most of the water is reabsorbed

154
Q

where is most water reabsorbed?

A

small intestine (92% - 7.5L) via osmosis

155
Q

how much water does the large intestine absorb?

A
  • 6-7% (1400mL)

- aids in feces transformation

156
Q

what happens when there is poor water uptake in the large intestine?

A

watery stool - diarrhea

157
Q

what happens if there is too much water uptake in large intestine?

A

-hard stool - constipation

158
Q

is water absorption in the gut an active or passive transport?

A

-glucose,, Na+, fructose, AAs, K+, etc are all being transported from lumen to ISF, so water follows passively through osmosis

159
Q

what are the three parts that make up the tight junctions in the gut

A

1) contractile cytoskeletal elements
- made up of filaments including actin, myosin light chain - which forms a ring around the perimeter (perijunctional actomyosin ring), when ring contract, diameter gets smaller

2) cytoplasmic complex - ZO-1 (zonula occudens), proteins to link elements (bridging proteins) near the membrane

3) integral membrane proteins - forms junction between adjacent cells
- claudins and occulins - these vary from loose to tight claudins/occulins to form either loose or tight junctions

these junctions are highly regulated

160
Q

what is Giardia?

A
  • when the barrier function in the gut is altered

- the most common intestinal parasite - world wide prevalence of 8% and up to 100% in some areas

161
Q

what is giardiasis? what are some symptoms?

A
  • the most common water borne disease - beaver fever
  • most cattle and wild animals have this
  • mild to severe diarrhea for 1 to 2 weeks, then you get better
162
Q

how is giardiasis transmitted to other organisms?

A

fecal-oral transmission
-zoonosis - process by which humans can be infected by animals

  • when the parasite gets into large intestine, forms a cyst because it is no longer a suitable environment
  • become more resilient, allows them to be passed in feces and get ingested by other host
  • 1 cyst is enough to establish an infection
163
Q

explain how giardia disrupts the cytoskeleton

A
  • reorganization of the cytoskeleton (actin and ZO-1)
  • myosin light chain kinase activation (calmodulin dependent, but here it is a parasite-dependent increase in paracellular permeability)

-healthy cells have more actin near perimeter of cells (perijunctional actomyosin ring) and ZO-1 is where it should be

  • in infected cells, ZO-1 is more dispersed, tight junctions are being stretched and cells, separated, cell is dying in response to being infected
  • actin proteins are aggregated, pulled into nucleus - leaving the perimeter where they should be associated with tight junctions
164
Q

what happens after the barrier function is compromised because of giardiasis?

A
  • decreased digestion
  • reduced absorption
  • diffuse microvillus shortening (reduced surface area)
  • pathology occurs shorter AFTER barrier dysfunction
165
Q

pathophysiology of giardiasis: microvillus brush border injury

A
  • this is diffuse, not only where the parasite is sitting
  • all microvilli shrink (some are completely gone) - fewer and less dense
  • this leads to up to 60% loss of surface area
  • leads to maldigestion and malabsorption diarrhea
  • crypt hyperplasia - hypersecretion
  • crypts get deeper, leads to more secretion, we don’t absorbed water AND we are dumping more water in
  • this brush border injury is HOST DERIVED (immune system)
166
Q

explain how the pathophysiology of giardia is “host derived”

A
  • CD8+ T-lymphocytes - shorten microvilli
  • T-cell deficient mice with giardiasis
  • the shortening of microvilli comes from T cells, mice without T cells did not get shortening

CD4+ T-cells - helper cells

  • good for parasite clearance
  • in T-cell defficient mice, the infection lasts a long time
167
Q

____ are cytotoxic T cells and ____ are helper T cells

A

CD8+, CD4+

168
Q

would a mouse injected with purified CD4+ T cells coming from another mouse infected with giardiasis develop giardiasis?

A

-no, the disease would not spread - no CD8+ cells present

169
Q

would a mouse injected with purified CD8+ T-cells coming from another mouse infected with giardiasis develop giardiasis?

A

-yes, this leads to disease state

BIOL 2420 (5 decks)

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