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Medical Physiology > Digestion and Absorption of Carbs, Proteins, and Lipids > Flashcards

Digestion and Absorption of Carbs, Proteins, and Lipids Flashcards

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USMLE® Step 1 flashcards
1
Q

example of soluble fiber

A

inulin – digested by symbiotic bacteria

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2
Q

example of insoluble fiber

A

psyllium husts — osmotically hold water to soften stool

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3
Q

where does digestion of carbs begin and end

A

in mouth by salivary amylase, ends in the SI by pancreatic amylase

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4
Q

what is transported from carbs?

A

monosaccharides (glucose, galactose, fructose) transported from lumen to intestinal epithelium via facilitated diffusion or active transport.

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5
Q

how are monosaccharides transported to blood?

A

facilitated diffusion

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6
Q

how are monosaccharides transported from lumen to intestinal epithelium?

A

facilitated diffusion and active transport

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7
Q

what are the disaccharides?

A

alpha dextrin, maltose, maltotriose, trehalose, lactose, sucrose

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8
Q

what is alpha dextrin broken down to

A

monosaccharide glucose by alpha dextrinase

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9
Q

what is maltose broken down to

A

glucose by maltase

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10
Q

what is maltotriose broken down to

A

glucose by sucrase

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11
Q

what is trehalose broken down to

A

glucose by trehalase

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12
Q

what is lactose broken down to

A

glucose and galactose by lactase

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13
Q

what is sucrose broken down to

A

glucose and fructose by sucrase

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14
Q

what are the only absorbable monomers

A

glucose, galactose, fructose

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15
Q

how are monosaccarides transported across SI epithelium?

A

secondary sodium/glucose symport, secondary sodium galactose symporter and facilitated diffusion fructose transporter – Na gradient created by Na/K ATPase

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16
Q

how are monosaccharides transported from SI epithelium to the blood?

A

facilitated diffusion of glucose, galactose, fructose

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17
Q

how can lactose intolerance develop?

A

deficiency of brush border enzyme lactase or defect in one of the monosaccharide transporters (glucose or galactose)

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18
Q

how does lactose act in the lumen?

A

as an osmole to hold water and cause diarrhea, then bacteria ferments it and produces lactic acid, methane and H2 gas

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19
Q

what is the hydrogen breath test

A

generalized test for food intolerance, measures H production in response to post-fasting ingestion of suspect foods

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20
Q

what are capable of producing H in humans?

A

only anaerobic bacteria in the colon are capable of producing H when exposed to unabsorbed CARBOHYDRATES (not proteins or fats)

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21
Q

steps of H breath test

A
  1. measure basal hydrogen in breath
  2. ingest 20-25mg of lactose (other other suspect food )
  3. measure breath H levels at 15, 30 and 60 min intervals over 2-3hours
  4. if breath hydrogen increases 20ppm over baseline, LACTOSE MALABSORBER
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22
Q

what defines a pt as a lactose malabsorber?

A

if H breath test increases breath H by 20ppm

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23
Q

how are proteins broken down?

A
  1. pepsin breaks them down to peptide fragments in the stomach
  2. pancreatic trypsin and chymotrypsin in the SI
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24
Q

how are peptide fragments broken down in to free AA?

A
  1. carboxypeptidase from pancreas
  2. aminopeptidase from intestinal epithelium
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25
Q

how do free AA leave lumen and enter epithelium?

A

secondary active transport

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26
Q

how do free amino acids leave the epithelium into the blood?

A

facilitated diffusion

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27
Q

how can small amounts of intact proteins enter ISF?

A

endo and exocytosis

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28
Q

what is the optimum pH of pancreatic proteases?

A

6.5

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29
Q

what converts trypsinogen to trypsin?

A

enteropeptidase

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30
Q

how is enteropeptidase produced?

A

in the crypts of lieberkuhn whenever food enters the duodenum from the stomach

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31
Q

why is trypsin important?

A

allows activation of other pancreatic enzymes that are secreted as inactive precursors

also initial trypsin production provides positive feedback for further trypsinogen conversion

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32
Q

what are endopeptidases and what do they do

A

trypsin and chymotrypsin, attack peptide bonds to form smaller fragments

33
Q

what are exopeptidases and what do they do

A

carboxypeptidases (A and D) hydrolyze the carboxy-terminal end of a peptide bond, removing a terminal AA

34
Q

how do exo and endopeptidases work together

A

act in concert generating 2-6AA peptide fragments as well as free AA. then further breakdown occurs by peptidases produced by intestinal mucosa.

35
Q

how much ATP do fatty acids make compared to carbs?

A

129 ATP vs 38 ATP

36
Q

what are the 4 lipids

A
  1. fatty acids
  2. triglycerides
  3. phospholipids
  4. cholesterol
37
Q

how are triglycerides broken down?

A

hydrolysis of TG by pancreatic lipase into monoglyceride and free fatty acids

38
Q

how does pancreatic lipase work?

A

clips fatty acids at positions 1 and 3 of the TG leaving 2 free fatty acids and 2 monoglycerides

39
Q

how are fats digested

A
  1. digested products and bile salts form amphipathic micelles.

micelles keep insolube products in soluble aggregates. (emulsification)

  1. pancreatic lipase and colipase act
  2. small amounts of insoluble products are released and absorbed by epithelial cells via diffusion
  3. FFA and monoglycerides recombine into triacylglycerols at the smooth ER, processed fruther in the golgi
  4. enter intersitial fluid as droplets called chylomicrons
  5. chylomicrons taken up by lacteals in the intestine for lymphatic/circulatory transport
40
Q

what is emulsification

A

large lipid droplets broken down into smaller droplets

41
Q

what drives emulsification

A

mechanical disruption (contractile activity of the GI tract) and emulsifying agents (amphipathic bile salts)

42
Q

what role do bile salts do in emulsification?

A

bile salt coating prevents re-coalescence as large aggregates/droplets are broken down into smaller and smaller droplets

43
Q

what is the point of emulsification?

A

increasing surface area for pancreatic lipase action (hydrolysis

44
Q

what does pancratic lipase breakdown of fats produce

A

a monoglyceride and 2 fatty acids

45
Q

why are triglyceride droplets covered in bile salts and phospholipids in the small intestine?

A

prevent adsorption of lipase

46
Q

how is activity of lipase restored?

A

binding of pancreatic coenzyme, colipase

is an amphipathic polypeptide, binds to bile salts and lipase (like a bridge!)

47
Q

what role do bile salts play in digestion of fats

A

bile salts increase surface area for attack by pancreatic lipase, prevents reaggregation of fat droplets.

DOES NOT BREAK DOWN THE FAT DROPLETS

48
Q

what is the problem that bile salts have and how is it solved

A

bile salt attachment block access of the enzyme to the lipid with the hydrophobic core of the small dropelets, so colipase binds to bile salts and lipase allowing acess to tri-and di-glycerides

49
Q

what provides mechanical disruption for emulsification?

A

contractile activity occuring in the lower portion of the stomach and small intestine, grinds and mixes luminal contents

50
Q

how are micelles formed

A

mechanical disruption–>bile emulsification–>lipase hydrolysis

51
Q

components of bile

A
  1. water
  2. cholesterol
  3. bile pigments
  4. anions of bile acids
  5. lecithin (phospholipids)
  6. bicarb and other ions
52
Q

what are the most important compounds in bile?

A

the anions — taurocholic acid (conjugate of cholic acid and taurine) and deoxycholic acid

53
Q

what do the bile acids look like?

A

amphipathic with hydrophilic and hydrophobic end.

hydrophobic end sits on surface of fat droplet with hydrophilic end facing the aqueous duodenal lumen

54
Q

describe primary bile acid to secondary bile acid

A

liver converts cholesterol to primary bile acid, then taurine or glycine is added to make conjugated bile acid. conjugated bile acid is secreted and colonic bacateria convert primary conjugatec bile acid to seconary bile acid by removing the amino acid.

55
Q

what are micelles loaded with?

A

lipid cleavage products

56
Q

what is the rate limiting step of absorption of lipids

A

diffusion of micelles thorugh the unstirred layer (fluid immediately surrounding the brush border)

57
Q

how do micelles travel into enterocytes?

A

diffusion gradient across unstirred layer favors the passive diffusion of lipid degradation products from micelles toward the brush border and into enterocytes

58
Q

what occurs when end products of fat degradation and micelle formation (free fatty acids and monoglyceride) diffuse into intestinal cell

A

reassemble into simple fat (TG) by the smooth ER, then transported to the golgi to package TG with cholesterol, lipoproteins, and other lipids into chylomicrons

59
Q

how are chylomicrons made

A

fats are degraded in the intestinal lumen into monoglycerides and free fatty acids, packaged into micelles. micelle products diffuse into intestinal cells., smooth ER reassembles into TG. golgi packages TG with cholesterol, lipoproteins, and other lipids into chylomicrons

60
Q

how do chylomicrons travel out of the enterocytes

A

packaged into vesicles for exocytosis, then diffuse into lacteals for transport through the lymphatic system (enter general circulation via thoracic duct)

61
Q

what do chylomicrons consist of?

A

triglycerides (85-92%)

phospholipids (6-12%)

cholesterol (1-3%)

proteins (1-2%)

62
Q

what do chylomicrons do

A

transport exogenous lipids to the liver, adipose, cardiac and skeletal muscle tissue where TG components are unloaded by lipoprotein lipase

63
Q

what allows triglycerides to be unloaded from chylomicrons in the tissues

A

lipoprotein lipase

64
Q

what happens with chylomicrons once they deliver TG?

A

remnants are taken up by the liver

65
Q

what do VLDL, IDL, and LDL do?

A

transport endogenous fats and cholesterol from liver to tissues

66
Q

what do HDL do?

A

transport endogenous cholesterol from tissues to liver

67
Q

what is optimal level of HDL for protection against heart diease?

A

more than 60mg/dL

68
Q

what heightens risk of heart disease in males?

A

less than 40mg/dL

69
Q

what heightens risk of heart disease in females?

A

less than 50mg/dl HDL

70
Q

what is HDL

A

high density lipoprotein, the smallest and densest lipoprotein due to high protein content.

71
Q

what can HDL do

A

remove cholesterol from arteries and transport it back to the liver for excretion or reutilization

72
Q

what LDL level corresponds to high risk of heart disease?

A

more than 200mg/dl LDL

73
Q

what LDL level corresponds to reduced risk for heart disease?

A

less than 100mg/dL

74
Q

how are VLDL made

A

assembled in the liver from cholesterol and apolipoproteins, and converted to LDL in the bloodstream

75
Q

what do chylomicrons do vs VLDL

A

chylomicrons transport dietary fats and cholesterol from intestines to tissues

VLDL transport endogenous fats and cholesterol from liver to tissues

76
Q

how is IDL made

A

degradation of VLDL, encircles various fatty acids to form 25-35nm water soluble particles

77
Q

what happens to IDL

A

cleared from plasma into the liver or further degraded to form LDL

78
Q

what can make LDL?

A

VLDL and IDL

79
Q

what are apolipoproteins

A

proteins that bind to and help solubilize hydrophobic lipids in the blood, and is a key risk marker for dyslipidemia, CV and neurodegenerative diseases

Medical Physiology (21 decks)

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