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GI/Liver > Physiology > Flashcards

Physiology Flashcards

1
Q

What are the major dietary monosaccharide carbs?

A

glucose, galactose, fructose

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2
Q

What are the disaccharides and their compositions?

A

sucrose: glucose + fructose a(1-4)maltose: glucose + glucose a(1-4)lactose: glucose + galactose b(1-4)

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3
Q

What are the complex carbs and their compositions?

A

amylose: (glucose)n linear a(1-4)amylopectin: (glucose)n linear a(1-4) with a(1-6) branchescellulose, not digestible: (glucose)n linear a(1-4)

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4
Q

What enzymes does the salivary glands secrete?

A

alpha-amylase (endoglycosidase); releases maltose, maltotriose, maltotetrose and a-limit dextrins but not glucose

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5
Q

What enzyme does the pancreas secrete?

A

similar to salivary a-amylase in action but diff gene product

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6
Q

What are made by enterocytes (surface-expressed, not secreted)?

A

isomaltase (endoglycosidase), disaccharidases (sucrase, maltase, lactase)

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7
Q

How do endoglycosidases inc efficiency of amylose and amylopectin digestion?

A

produce many substrates for maltase and isomaltase

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8
Q

What happens in lactose-intolerant individuals?

A

don’t have neutral B-galactosidase (lactase) –> it is non-absorbable, osmotically active solute

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9
Q

Why do only enterocytes (not the pancreas) express oligosaccharidases and disaccharidases?

A

converting to monosaccharides would multiple osmolarity so limiting hydrolysis to the absorptive surface minimizes the impact on chyme osmolarity

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10
Q

How do enterocytes extract glucose from chyme efficiently?

A

SGLT (Na-dependent glucose transporter) uses PE in Na+ electrochemical potential difference across the apical membrane to carry glucose from chyme into enterocytes against a steep concentration difference- 1/2 from [Na+] diff and 1/2 from voltage diff- GLUT2 - glucose diffuse from enterocyte to interstitial fluid and circulation

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11
Q

Why does digesting protein require a lot of metabolic E?

A

it is hard to solubilize non-covalent intermolecular bonds –> need mechanical E and acid - need E to secrete acid and HCO3-

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12
Q

What are the pancreatic proteases?

A

endopeptidases: trypsin, chymotrypsin, elastasesexopeptidases: carboxypeptidase A, carboxypeptidase B

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13
Q

Why are the pancreatic proteases secreted as zymogens?

A

Prevents them from destroying each other and the pancreas- N-terminal peptide sequence is inhibitory

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14
Q

How are the zymogens activated?

A

Enterokinase on the enterocyte absorptive surface converts trypsinogen to catalytically-active trypsin, which activates the other zymogens

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15
Q

Where are there Na-coupled transporters and what kind?

A

Na+ coupled transports for neutral L-a amino acids across apical membraneNa+ independent transporters for basal-lateral membrane transporteralso Na+ coupled amino acid transporters on basal-lateral membrane for enterocyte protein synthesis during fasting

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16
Q

Why does dipeptide absorption require Na+?

A

Dipeptide transporter is a H+ coupled co-transporter. There is a large voltage diff across apical membrane creates electrochemical diff that drive H+ from chyme to cytosol. Na+/H+ uses Na+ electrochemical potential to pump back into chyme

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17
Q

What are the major amino acid malabsorption syndrome?

A

prolinuria (iminoglycinuria): proline, hydroxyproline and glycinecystinuria: cystein, lysine, arginine

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18
Q

Why does prolinuria include such structurally diff amino acids?

A

Rotational motion excludes other amino acids except glycine from the narrow binding site for proline and hydroxyproline

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19
Q

Why are lipase, colipase and bile salts necessary?

A

Lipids are so poorly soluble in H2O that small concentrations.- Hydrolyze TG into bile salt micelles

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20
Q

What does pancreatic lipase make from TG?

A

2 free FA molecules, 1 2-monoglyceride

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21
Q

How do free FA accelerate TG hydrolysis?

A

free FA are amphipilic –> help saponofication by amplifying the surface area of lipid-H2O interface

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22
Q

Ho do diglycerides and free FA go from enterocytes to circulation?

A

Re-esterified to TG in lumen of ER –> combine with apolipoprotein to make VLDL –> exocytosed across basal-lateral PM –> lacteals to superior VC

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23
Q

How are bile salts recycled?

A

depleted bile sale micelles go within chyme to terminal ileum –> Na+ coupled transporters to enterocytes –> hepatic protal vein to liver –> bile salts in gall bladder secrete to duodenum

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24
Q

Why is gallbladder prone to stone formation?

A

secretion of bile salts accompanied by large V of NaCl-rich solution, when too much cholesterol then complex with Ca+ into crystals

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25
Q

saliva fxn

A

lubricate, cleanse, maintain teeth, oral microbial flora; release flavora-amylase - hydrolyze starch partiallylingual lipase - hydrolyze lipids partially

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26
Q

pancreatic juice fxn

A

neutralize gastric aciddigestive enzymes: a-amylase, proteases, lipase

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27
Q

bile fxn

A

neutralize gastric acidbile salts for lipid absorption

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28
Q

bile fxn

A

neutralize gastric acid, bile salts for lipid absorption

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29
Q

how do gastric surface epithelial cells use HCO3- to protect themselves from gastric acid?

A

gastric mucus layer slows flux of H+ from lumen to cells and slows flux of HCO3 from cells to lumen

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30
Q

What receptor do gastrointestinal epithelial cells use

A

G-protein coupled Receptors

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31
Q

How do M3Ach, Gastrin and CCK R work?

A

Gaq/Ga11 bind and activate phospholipase CB –> hydrolyze PIP2 -> release IP3, DAG, Ca2+

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32
Q

How do b-Adrenergic Receptor
Histamine (H2) Receptor
Secretin Receptor
VIP Receptor work?

A

Gas binds adenylel cyclase and converts ATP to cAMP

33
Q

How do a1-adrenergic R elevate cytosolic Ca2+?

A

Gai binds and acitvates ADP-ribosyl cyclase –> conver NAD to cADP-R –> bind ER ryanodine R

34
Q

what hormone is made in stomach?

A

Gastrin

35
Q

What are the stimulate for gastrin release?

A

neural signals: gastrin-releasing peptide, Ach
distention
amino acids and peptides

36
Q

Gastric target cells and response?

A

Gastric parietal cells - increases acid secretion

gastric smooth muscle - inc motility

37
Q

What hormones are made in the small intestine?

A

gastric inhibitory peptide (GIP), cholecytokinin (CCK), secretin

38
Q

What stimulates GIP release?

A

fatty acids, monosaccharides

39
Q

what are the target cells and response for GIP?

A

gastric parietal secretion - inhibits acid secretion

pancreatic islets - potentiates insulin secretory response to glucose

40
Q

What is the stimuli for CCK release?

A

amino acids, FA

41
Q

What are the major target cells and response to CCK?

A

pancreatic acini - enzyme and NaCl secretion
pancreatic ducts - potentiate bicarb secretory response to secretin
hepatic ducts - potentiate bicarb secretory response to secretin
gallbladder - contraction
gastric smooth muscle - decreases gastric emptying

42
Q

What is the stimuli for secretin release?

A

acid

43
Q

What are the target cells and response for secretin?

A

pancreatic ducts - bicarb secretion
hepatic ducts - bicarb secretion
pancreatic acini - potentiate enzyme and NaCL secretory response to CCK
stomach - decrease emptying and acid secretion

44
Q

What roles of symp and parasymp signals play in control of salivary gland fxn?

A

symp - activate secretory vesicle exocytosis: protein secretion
parasymp - activate ion transporters (Na+, Cl-, h2o, some HCO3-)

45
Q

What is the impact of parasymp on gastric motor and secretory fxns?

A

motility - mixing and empyting
gastrin release
acid release

46
Q

where are G cells most abundant

A

pyloric region

47
Q

where are oxyntic (parietal) cells most abundant

A

corpus

48
Q

How is the stomach divided?

A

Top is for receptive relaxation - HCI - and bottom for peristalsis - gastrin (mixing and emptying)

49
Q

role of enterochromaffin-like cells (ECL cells)

A

gastric simulates ECL cells to release histamine –> activates H2 R on oxyntic cells to stimulate acid secretion

50
Q

What slows gastric emptying?

A

duodenal chyme - any deviation from isotonicity
CCK
GIP inhibits gastric acid secretion (not needed for carb, lipid)

51
Q

How is pancreatic secretion controlled?

A

parasymp signals and CCK - inc Na, Cl-, H2O secretion, exocytosis, zymogen and hydrolase
secretin - inc ductal Na+, HCO3-, H2O secretion

52
Q

What happens during the cephalic phase?

A

signals: sight, though, smell of food; taste food, chewing/swallowing
elicit parasym to salivary glands, stomach, pancreas

53
Q

What happens during gastric phase?

A

signals: activate mechanoRs, G cell amino acid Rs
response: inc parasymp signalling to stomach, gastric motor and secretion

54
Q

What happens during intestinal phase?

A

signals: activate mechanoR, osmoRs, enteroendocrine cells
response: inc parasymp signal to pancreas; mix and propulsion
- coordinate gastric emptying with intestinal processing
- coordinate gastric acid secretion with need
- neutralize acid
- deliver pancreatic hydrolases and zymogens and bile salts

55
Q

Why do relatively small decreases in fluid absorbed or increased secreted fluid cause large changes in fluid excreted in stool?

A

volume absorbed - 70-100X the volume excreted

volume secreted - 60-80X the volume secreted

56
Q

Why does small intestine’s leakiness make it susceptible to osmotic diarrhea?

A

allow NaCl to flow into fluid and water follows

57
Q

how does bile salt-dependent fluid secretion in the liver work?

A

tight junctions between hepatocytes are leaky

58
Q

Why is the epithelial leakiness necessary for efficient Na+ coupled substrate absorption in the small intestine?

A

voltage drop across the apical membrane as large (negative) as possible so more substrate absorption
- leakiness allows Na+ to flow back from interstitial fluid to chyme

59
Q

How is Cl- absorption coupled to Na+ - coupled substrate absorption?

A

there are large unidirectional fluxes of Na and Cl

- net amt Cl- absorbed = net amt Na+ absorbed

60
Q

How does small intestine absorb NaCl independently of substrates for Na+ - coupled substrate absorption?

A

Na/H exchanger and Cl/HCO3 exchanger in apical membrane

K/Cl basal-lateral membrane - Cl- from cytosol to interstitial fluid

61
Q

How does the small intestine absorb fluid when osmolarity of chyme is equal to osmolarity of the plasma?

A

Most of basolateral PM surface area faces lateral intercellular space –> accumulate solutes to increase osm of fluid

  • H2O flows into lateral intercellular space
  • nutrients, Na, Cl diffuse through BM to reach plasma
  • local osmosis forces H2O out of lateral space to circulation
62
Q

How does the large intestine absorb NaCl and H2O efficiently?

A

epithelial cells use Na/H and Cl/HCO3 exchangers to transport Na and Cl from chyme to cytosol

  • ENaC and CFTR to transport
  • tight junctions prevent Na and Cl from diffusing back to chyme
  • H2O absorbed isosmotically
63
Q

How does the large intestine secrete K+ and HCO3?

A
  • apical K+ channels (to chyme)

- apical CFTR - HCO3 to chyme

64
Q

Why does the V of stool excreted impact the body’s K+ and HCO3- pH balance?

A

concentrations in stool are constant

- excessive fluid excretion = excessive excretion of K+ and HCO3- –> hypok+, metabolic acidosis

65
Q

How does cholera toxin influence fluid secretion in intestinal crypts?

A

Active subunit catalyzes ADP-ribosylation of Gas –> active state

  • make cAMP –> activate PKA –> activate apical CFTR and basolateral NaCl influx
  • secrete NaCl and H2O
66
Q

How does cholera toxin influence fluid absorption in intestinal villi?

A

PKA inactivates apical Na/H exchangers, blocking substrate independent NaCl absorption and so can’t reabsorb H2O at villi

67
Q

How does oral rehydration therapy work?

A

PKA doesn’t inactivate Na+ coupled mechanisms so can use high glucose to drive Na and Cl absorption –> H2O absorbed

68
Q

What heterotrimeric GTP-binding proteins do CCK R and MAchR couple to?

A

Gaq and Ga11

69
Q

What are the signaling effectors of CCK R and MAchR?

A

Gaq and Ga11 - phospholipase cB –>PIP2 –> IP3 and DAG

70
Q

What are the second messengers for CCK and MAchR?

A

IP3 –> Ca+ –> Ca+ calmodulin-dependent kinase

DAG + Ca+ –> protein kinase C

71
Q

What are the steps for secretory vesicle exocytosis?

A

docking and fusion - TSNARES and VSNARES
exocytosis - apical microfilament network around vesicle - activate myosin-like motors
recycled through endosome and TGN

72
Q

Why does cytosolic Ca2+ oscillate?

A

When Gaq and Ga11 are inactive then Ca2+ is pumped out of cytosol back into ER and interstitial fluid

73
Q

Why do Ca oscillations stop during supramaximal stimulation?

A

Gaq and Ga11 bound to GTP active forms constant present

74
Q

Why do only some GCPR agonists cause supramaximal stimulation?

A

Ach is short-lived because hydrolyzed by Achesterase

CCK not rapidly degraded

75
Q

What is the mechanism in acute hemorrhagic pancreatitis?

A

cathepsins (lysosomal proteases) accumulate in same vacuoles as pancreatic zymogens –> activate then proteases destroy vacuole and cell

76
Q

What are the lysosomal hydrolases?

A

procathepsins (proteases), prophospholipases, glycohydrolases

77
Q

How do the lysosomal hydrolases traffic to lysosomes?

A

because recycling between prelysosome, late endosome and early endosome, some procathepsins get activated in prelysosome are carried back to earlier compartments

78
Q

What happens when lysosomal hydrolase traffic to late endosome is blockaded?

A

catalytically active cathepsins activate procathepsins

GI/Liver (4 decks)

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