GI 08 Flashcards

1
Q

Absorption

A

mvt of nutrients, water, and electrolytes from intestinal lumen to blood (paracellularly or cellularly)

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2
Q

How are carbohydrates ingested (saccharide types)

A

Poly, mono, and disaccharides

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3
Q

What kinds of saccharides are absorbed through intestinal lumen

A

Monosaccharides (esp. glucose, fructose, galactose)

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4
Q

What is the major dietary carbohydrate, and what does this mean?

A

Starch - mix of straight and branched chain polymers of glucose

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5
Q

Major 4 disaccharides in food

A

Trehalose, sucrose, maltose, and lactose

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6
Q

Maltose

A

2 glucose

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7
Q

sucrose

A

glucose and fructose

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8
Q

lactose

A

glucose and galactose

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9
Q

Monosaccharies in our diet are mainly (3)

A

glucose, fructose, galactose

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10
Q

Cellulose

A

Glucose linkage that we cannot break (b1,4 linkage) - excreted or used for bacteria in gut

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11
Q

where does digestion of carbs begin

A

mouth - salivary amylase (breaks a1,4-linkage)

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12
Q

What happens to salivary amylase in stomach

A

shit gets fucked (no worky)

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13
Q

pancreatic amylase

A

most significant amylase in digestion, digests a1,4-bonds and gives mixture of disaccharides, trisaccharides, and oligosaccharides - alpha-limit dextins, maltose, and maltotriose must break them down further, and then down more by a-dextrinase (isomaltase), maltase, and sucrase to get glucose which can be absorbed by intestinal epithelium

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14
Q

Do disaccharies require amylase igestion

A

no

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15
Q

Where are the enzymes for carbohydrate digestion

A

brush border epthelium

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16
Q

How do we bring monosaccharides into the cell

A

SGLT1- Glucose and galactose, share a ride with Na
GLUT5 (for fructose)
requires atp

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17
Q

how do we get monosaccharides across into the blood

A

GLUT2 (glucose, galactose, fructose) - this is facilitated diffusion

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18
Q

Lactose intolerance

A

Lack/deficiency in lactase in brush border

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19
Q

result of lactose intolerance

A

osmotic diarrhea because sugar holds onto water and you poop it out

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20
Q

Congenital lactose intolerance

A

Lack of jejunal lactase - rare and serious, replace lactose with sucrose or fructose diet

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21
Q

Glucose-galactose malabsorption

A

Mutation of SGLT1 leads to inability to absorb these - can result in severe diarrhea and thus dehydration and other consequences - fructose only diet is recommended

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22
Q

Essential amino acids

A

Cannot be synthesized by body; must be obtained in diet

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23
Q

Where does protein digestion start

A

Stomach (pepsin)

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24
Q

Where is protein digestion completed, and how?

A

Small intestine with pancreatic and brush-border proteases (endopeptidases and exopeptidases)

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25
Q

endopeptidase

A

hydrolyzes the interior peptide bonds of proteins (pepsin, trypsin, chymotrypsin, elastase)

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26
Q

Exopeptiases

A

hydrolyze one amino acid at a time from C terminal ends of proteins and peptides (carboxypeptidases A and B)

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27
Q

Is pepsin active in the small intestine

A

no (high pH will inactivate it and small intestine should have pancreatic HCO3-)

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28
Q

Is pepsin essential for protein digestion in a healthy individual

A

no

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29
Q

Where are proteases that act in small intestine

A

Brush border and secreted from pancreas

30
Q

5 major pancreatic proteases that are secreted as zymogens

A
Trypsinogen
chymotrypsinogen
proelastase
procarboxypeptidase A
Procarboxypeptidase B
31
Q

What is the first step in protein digestion in the intestine

A

activate trypsinogen to trypsin by enterokinase (located on brush border)

32
Q

What enzyme catalyzes the conversion of inactive intestinal precursors to active enzymes

A

trypsin - it also autocatalyzes any remaining trypsinogen to active trypsin

33
Q

What are the absorbable kinds of protein digestion products

A

amino acids, dipeptides, tripeptides
Oligopeptides are not absorbable - they must be hydrolyzed by brush border proteases to yield smaller absorbable molecules

34
Q

Products of the 5 pancreatic proteases

A

amino acids, dipeptides, tripeptides, and oligopeptides

35
Q

How do we get amino acids, dipeptides, and tripeptides from GI lumen to blood

A

There are AA transporters that will transpot a specific kind of amino acid (ex, neutral, basic whatever) from lumen - these will sometimes take up drugs (clinically relevant). Inside the cell, peptides will be hydrolyzed into amino acids by cytosolic peptidases, nd amino acids exit cell via facilitated diffusion on blood side

36
Q

Cystinurea

A

Transporter for dibasic amino acids (cystine, lysine, arginine, ornithine) is absent in small intestine and kidney, so no or low absorption of these happens in SI / kidney. This results in failure to absorb them and they are excreted in feces

37
Q

Major categories of lipid in diet (3)

A

Triglycerides, phospholipids, cholesterol

There are also many vitamins that ae along for the ride

38
Q

fat soluble vitamins

A

A, D, E, K

39
Q

What problem do we face when digesting lipids

A

lipids and water hate each other so we need to make them kiss to give lipolytic enzymes access

40
Q

Emulsification

A

the mixing action of stomach and small intestine churns dietary lipids into a suspension of fine droplets, this greatly increases surface area for digestion enzymes (also, bile salts are considered emulsifiers)

41
Q

In stomach, what emulsifies lipids

A

dietary proteins

42
Q

in small intestine, what emulsifies lipids

A

bile acids

43
Q

Where does lipid digestion start

A

There is a lingual lipase, but she says stomach

Gastric lipase is released by chief cells nd hydrolyzes about 10% of dietry triglycerides

44
Q

Major contribution of stomach in lipid digestion

A

Slow emptying into the small intestine, which allows adequate time for pancreatic enzyme action

45
Q

What hormone is released when dietary lipids enter the small intestine and what is the result

A

CCK - this will slow down gastric emptying to give time for these fats to be broken down

46
Q

Where does most lipid digestion occur

A

small intestine

47
Q

What are the 3 lipolytic enzymes that work at neutral pH that are released from the pancreas

A

pancreatic lipase
phospholipase A2
cholesterol ester hydrolase

48
Q

What is colipase?

A

Cofactor that keeps pancreatic lipase active even when it interacts with bile acids - binds to both and anchors lipase to fat droplet even when bile acids are present

49
Q

What activates phospholipase A2

A

trypsin

50
Q

What is the one FA product that is not going to be part of micelles

A

Glycerol (this is water soluble)

51
Q

Structure of micelle

A

Products of lipid digestion (monoglycerides, FAs, cholesterol, lysolecithin) are solublized in intestinal lumen in mixed micelles (notice no glycerol, this is water soluble). The core of a micelle has the products of this digestion - exterior is lined with amphipathic bile salts. The hydrophilic portion of bile salts dissolves in aqueous solution of intestinal lumen and shields the hydrohobic region - solubilizes the lipids in the micelle core

52
Q

Micelles get into brush border epithelium – how?

A

Diffusion - but its more like the membranes mingle and the lipids are yeeted inside because the micelle itself does not get in. Bile salts are left in intestinal lumen to be reabsorbed in ileum, and inside the cell lipid digestion products are re-esterified with FFAs on smooth endoplasmic reticulum to form TGs, cholesterol ester, and phospholipids, then repackaged as a chylomicron with apoproteins (like ApoB) and sent out into the lymph system

53
Q

can chylomicrons get into blood capillaries

A

nope must go through lymph system

54
Q

Where are chylomicrons going to join the blood

A

when lymph is yeeted into the thoracic duct that empties lymph to vena cava

55
Q

Where is most sodium reabsorbed

A

Jejunum - water will follow

56
Q

Transporters of sodium + other electrolytes and water in jejunum

A

Sodium + sugar / AA transporter and Na/H exchanger bring Na in, NKA helps Na leave

Also, bicarbonate is absorbed here from CA activity
Net absorption: NaHCO3

57
Q

Transporters of sodium + other electrolytes and water in ileum

A

Na + sugar / AA trnsporters, Na/H exchanger will bring sodium in from GI, and NKA will let it leave into blood.

Cl is absorbed here instead of HCO3
Net absorption: NaCl

58
Q

Crypts (secrete / absorb) fluid and electrolytes

A

Secrete

59
Q

Lining of villi cells (secrete / absorb) electrolytes and fluid

A

absorb

60
Q

Apical membrane of crypt cells has what kind of anion channel

A

chloride

61
Q

basolateral membrane of crypt cells have what 2 transporters

A

NKA, Na/K/Cl-

62
Q

Net change in water in crypts is (loss from body, absorption into body)

A

loss / secretion

63
Q

Cholera impact on water

A

adenylyl cyclase will be highlly activated in crypt cells and lead to fluid secretion by crypt that overwhelms absorptive capacity of villus

64
Q

Are chloride channels in apical membranes of crypt cells usually open?

A

No they are usually closed, but will open because of neurotransmitters like Ach after sensing chyme in small intestine

65
Q

Osmotic diarrhea

A

Diarrhea caused by presence of nonabsorbable solutes in intestinal lumen (ex. someone shitting their brains out after having ice cream if they’re lactose intolerant)

66
Q

Secretory diarrhea

A

like cholera, this is caused by excessive secretion of fluid by crypt cells (major cause is overgrowpth of enterohepatic bacteria like cholera or E coli)

67
Q

Calcium absorption

A

Actively absorbed in small intestine but requires active form of vitamin D, which needs the vitamin D dependent calcium binding protein calbindin D-28K

68
Q

How does calcium get into cell on luminal side

A

diffusion down electrochemical gradient

69
Q

how is calcium absorbed into blood

A

Out a calcium ATP-ase

70
Q

How do we absorb vitamin B12

A

B12 is released by food from pepsin in stomach. In stomach it binds to R proteins which will stabilize it.
In stomach, parietal cells create intrinsic factor.
In duodenum, pancreatic proteases degrade R proteins and B12 is transfered to intrinsic factors.
These B12-intrinsic factors are absorbed by a specific transport mechanism in ileum - without B12 absorption you get pernicious anemia