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FHB Exam 3 > GI: Digestion and Absorption > Flashcards

GI: Digestion and Absorption Flashcards

1
Q

Where do digestive enzymes originate?

A

salivary, pancreatic, gastric, intestinal brush border

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2
Q

Define digestion.

A

breaking down food into absorbable molecules via chemical and mechanical methods

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3
Q

Define absorption. What are the 2 methods of absorption?

A

absorption - movement of nutrients from the intestinal lumen into the bloodstream

  • transcellular
  • paracellular
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4
Q

Where are macromolecules most absorbed?

A

duodenum

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5
Q

Where are bile salts most absorbed?

A

ileum

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6
Q

What are the absorbable molecules of carbohydrate digestion?

A

monosaccharides:

  • glucose
  • fructose
  • galactose
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7
Q

What are the major dietary disaccharides?

A
  • trehalose
  • sucrose
  • lactose
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8
Q

What is trehalose?

A

glucose + glucose

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9
Q

What is sucrose?

A

glucose + fructose

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10
Q

What is lactose?

A

glucose + galactose

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11
Q

What happens to cellulose?

A
  • there is no endogenous enzyme to break down the B-1,4 chain linkages in cellulose
  • excreted as cellulose
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12
Q

What is the major dietary carbohydrate?

A

starch

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13
Q

What is starch?

A

made of a mixture of straight-chain and branched-chain polymers.

ex: amylose = straight chain
ex: amylopectin = branched chain

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14
Q

Describe the mechanism of starch digestion.

A
  1. salivary alpha-amylase begins the process, but is insignificant because once in the low gastric pH they are inactivated
  2. pancreatic amylase breaks down alpha-1,4 branch chains to create disaccharides, trisaccharides, and oligosaccharides from starch
    => alpha-dextrin
    => maltose
    => maltotriose
  3. intestinal brush border enzymes specific to each disaccharide breaks them down to glucose
    => alpha-destrinase
    => maltase
    => sucrase
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15
Q

Describe the enzymes involved in dietary disaccharide digestion.

A

trehalose => trehalase => glucose
sucrose => sucrase => glucose + fructose
lactose => lactase => glucose + galactose

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16
Q

Describe glucose absorption.

A
  1. SGLT1 actively transports Na+ and glucose into the cell

2. GLUT2 passively transports all monosaccharides across the basolateral membrane via facilitated diffusion

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17
Q

Describe galactose absorption.

A
  1. SGLT1

2. GLUT2

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18
Q

Describe fructose absorption.

A
  1. GLUT5 passively transports fructose into the cell via facilitated diffusion
  2. GLUT2
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19
Q

What is the cause, prevalence, and treatment for lactose intolerance?

A

Cause = lack or deficiency of brush border lactase enzyme leads to a buildup of lactose in the lumen, which is osmotically active and pulls water into the lumen => osmotic diarrhea

prevalence = 50% of adults, higher in Asians

Tx = exogenous lactase pills

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20
Q

What is the cause, prevalence, and treatment for congenital lactose intolerance?

A

cause = lack of jejunal lactase enzyme

prevalence = rare, serious

tx = avoid lactose; stick to a sucrose and fructose diet

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21
Q

What is the cause, prevalence, and treatment for glucose-galactose mal-absorption?

A

cause - mutated SGLT1 prevents absorption of glucose and galactose, causing a buildup of these monosaccharides in the lumen => osmotic diarrhea

prevalence = rare

tx = strict fructose diet to avoid buildup of glucose and galactose

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22
Q

What are the essential AAs?

A

FML WTH VIK

  • phenylalanine
  • methionine
  • leucine
  • tryptophan
  • threonine
  • histidine
  • valine
  • isoleucine
  • lysine
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23
Q

What are the 2 types of proteases?

A

endopeptidase - cleaves internal peptide bonds

exopeptidase - begins at the C-terminal and cleaves peptide bonds one by one

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24
Q

What are the endopeptidases?

A
  • trypsin
  • chymotrypsin
  • pepsin
  • elastase
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25
Q

What are the exopeptidases?

A
  • carboxypeptidase A

- carboxypeptidase B

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26
Q

What is the absorbable molecule of protein digestion?

A
  • free amino acids
  • dipeptides
  • tripeptides
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27
Q

Describe activation of pancreatic proteases.

A
  1. There are 5 pancreatic protease zymogens (chymotrypsinogen, trypsinogen, proelastase, procarboxypeptidase A, procarboxypeptidase B)
  2. enterokinase enzyme on the intestinal brush border activates trypsinogen to trypsin
  3. trypin activates all the other zymogens, including trypsinogen, to their active enzymes
28
Q

What is the mechanism for protein digestion?

A
  1. presence of a meal activates gastric chief cells to secrete pepsinogen
  2. acidic gastric pH activates pepsinogen to pepsin
  3. pepsin digests some proteins to large peptides
  4. once in the duodenum, pepsin is inactivated due to HCO3 neutralization of pH
  5. pancreatic enzymes further digest protein to free AAs, di-/tri-peptides, and oligopeptides
  6. oligopeptides are further digested by brush border enzymes
29
Q

Describe free AA absorption.

A
  1. Na+/AA symporters actively transport Na+ and free AAs into the cell
  2. AAs are transported across the basolateral membranes by facilitated diffusion
    NOTE: AA transporters on the apical membrane are specific to AA characteristics (basic, acidic, neutral, imino). Also, Na/AA symporters are only some of the AA transporters.
30
Q

Describe di-/tri-peptide absorption.

A
  1. H+/Peptide symporters actively transport H+ and peptides into the cell from the lumen
  2. cytosolic peptidase digests peptides into free amino acids
  3. AAs are transported across the basolateral membrane via facilitated diffusion
31
Q

What is the cause and treatment for single AA malabsorption?

A
  • body is unable to absorb a particular AA => deficiency
  • tx: diet should include peptides that have that particular AA so that the peptides can be absorbed and the AA released via cytosolic peptidase
32
Q

What is the cause and treatment for trypsinogen deficiency?

A
  • deficiency could be due to mutation => unable to digest proteins => protein malabsorption
  • Tx: diet provided of partially hydrolyzed proteins
33
Q

What is the cause of cystinuria?

A
  • lack of dibasic AA transporters on the apical membrane of intestines or kidney => cannot absorb cystine, lysine arginine, ornithine
    => deficiency of those AAs
  • if intestinal: buildup in lumen => excreted in feces
  • if renal: buildup in lumen => excreted in urine
34
Q

What are absorbable molecules of lipid digestion?

A
  • fatty acids
  • monoglycerides
  • cholesterol
  • lysolecithin
  • glycerol (but technically water soluble)
35
Q

What are typical dietary lipids?

A
  • triglycerides (3 FAs + glycerol backbone)
  • phospholipids
  • cholesterol
  • fat-soluble vitamins (not technically a lipid, but require lipids for digestion)
36
Q

What are the fat-soluble vitamins?

A

ADEK

37
Q

Define emulsification.

A

mixing lipids with aqueous solutions to create droplets around the lipids => increases SA for enzymes to reach the lipids

  • in the stomach = emulsified by proteins
  • in the intestine = emulsified by bile salts
38
Q

Why is emulsification needed for lipid digestion?

A

because lipids float on the gastric contents, while the enzymes are soluble in the aqueous phase of the chyme
- you need to mix them to increase the exposure of lipids to enzymes

39
Q

What lipolytic enzymes are found in pancreatic juice?

A
  • pancreatic lipase
  • phosopholipase A2
  • cholesterol ester hydrolase
40
Q

Describe the function of pancreatic lipase.

A
  • digest triglycerides => glyceride + FAs

- colipase binds to pancreatic lipase and bile salts to prevent inactivation

41
Q

Describe the function of phospholipase A2.

A
  • activated by trypsin

- digests phospholipids => lysolecithin + FAs

42
Q

Describe the function of cholesterol ester hydrolase.

A
  • digests cholesterol esters => free cholesterol + FA

- digests triglyceride esters => glycerol + FA

43
Q

Describe the mechanism of lipid digestion.

A
  1. gastric chief cells secrete gastric lipase, which digests about 10% of triglycerides
  2. chyme entering the duodenum activates secretion of CCK, which slows gastric emptying to allow adequate time for emulsification and lipid digestion
  3. bile salts and lipid products work to emulsify dietary lipids
  4. pancreatic juice enzymes break down lipids (see other flashcard)
  5. absorbable molecules (monoglycerides, cholesterol, lysolecithin, FA) are solubilized by amphipathic micelles
44
Q

Describe chylomicron structure.

A 
core = cholesterol esters and triglycerides
external = phospholipids and apoprotein
45
Q

What happens to micelles after they release their contents at the apical membrane?

A

dissociate

bile salts are reabsorbed in the ileum

46
Q

Describe the mechanism of lipid absorption

A
  1. micelles release lipid contents at the apical membrane
  2. once inside the cell, the smooth ER hydrolyzes/re-esterifies the products by adding on FAs to them
  3. the intracellular products are: triglycerides, cholesterol esters, and phospholipids
  4. these contents, along with apoproteins, are packaged into chylomicrons (secretory vesicles)
  5. chylomicrons are exocytosed and travel into the lymphatic circulation to the thoracic duct and then enter the bloodstream
47
Q

What is the cause of pancreatic insufficiency?

A
  • exocrine pancreas disease (pancreatitis, CF)
  • can’t make pancreatic enzymes
  • improper digestion of lipids
  • lipid buildup in the lumen retains water
    => steatorrhea
48
Q

What are the causes of duodenal acidity? What is the effect?

A

causes:

  • zollinger-ellison syndrome causes parietal cells to hypersecrete H+
  • pancreas doesn’t secrete enough HCO3 to neutralize chyme

effect: inactivation of pancreatic enzymes

49
Q

What are the cause and effect of bile salt deficiency?

A

cause: possible due to ileal resection, prevents bile salt reabsorption, bile lost in feces => not enough bile salts to form micelles
effect: can’t absorb lipids

50
Q

What is abetalipoproteinemia?

A
  • can’t synthesize apoprotein

- can’t form chylomicrons or chylomicrons can’t enter lymph

51
Q

What determines water absorption?

A

permeability of tight junctions:

  • intestine has leaky tight junctions => absorption paracellularly
  • colon has tight junctions => can’t absorb paracellularly, must be transcellular
52
Q

How much water is excreted through stool?

A

100-200 mL

hence, most water is absorbed

53
Q

What is the major site of sodium absorption?

A

jejunum

54
Q

What are the mechanisms of sodium absorption in the jejunum?

A

apical membrane:

  • SGLT transporters
  • Na/AA transporters
  • Na/H exchanger (fueled by carbonic anhydrase producing protons)

basolateral membrane:
- Na/K ATPase

55
Q

Where is the major site of chloride absorption?

A

ileum

56
Q

What are the mechanisms of chloride absorption in the ileum?

A

apical membrane:
- Cl/HCO3 exchanger

basolateral membrane:
- Cl transporter

57
Q

What are the mechanisms for NaCl secretion?

A

extrusion from the blood via basolateral Na/K/Cl cotransporter
for Na: paracellular from the blood => lumen
for Cl:
1. stimulated by ACh, VIP, hormones on basolateral receptors
2. adenylyl cyclase => cAMP
3. activates apical membrane Cl channel that secretes Cl

58
Q

What cells secrete NaCl? What happens to the secreted electrolytes?

A

intestinal crypt cells secrete NaCl

normally, villus cells absorb the electrolytes

59
Q

Describe what happens when cholera toxin is present.

A
  1. overstimulates adenylyl cyclase in crypt cells
  2. hypersecretion of Cl
  3. villus cells cannot keep up and there is a net secretion of electrolytes in the lumen
  4. osmotic diarrhea (life-threatening)
60
Q

What is the difference between osmotic and secretory diarrhea?

A
  • osmotic is due to non-absorbable molecules building up in the lumen
  • secretory is due to osmotically active molecules being secreted into the lumen (i.e. cholera, e. coli)
61
Q

Give 2 examples of osmotic diarrhea.

A
  • lactose intolerance leads to a buildup of lactose in the lumen, pulls water => intestinal bacteria may create more osmotically active lactose products
  • steatorrhea due to fat buildup holding on to water (unable to compact)
62
Q

What is the mechanism of calcium absorption?

A
  1. active vitamin D induces the synthesis of calbindin, Ca2+ binding protein
  2. Ca2+ diffuses into the cell
  3. binds to calbindin
  4. absorbed via basolateral Ca/ATPase pump
63
Q

What disorders arise from calcium malabsorption?

A

rickets

osteomalacia

64
Q

What is the mechanism of vitamin B-12 absorption?

A
  1. pepsin separates B12 from food
  2. B12 binds to R-protein
  3. pancreatic proteases in the duodenum degrade R protein
  4. B12 binds to IF
  5. binds to B12-IF receptor
65
Q

What happens to B12 absorption if you get a gastrectomy?

A

no gastric parietal cells = no IF
cannot absorb B12
tx: B12 injections

FHB Exam 3 (23 decks)

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