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FHB GI > 52 Digestion/Absorption > Flashcards

52 Digestion/Absorption Flashcards

1
Q

Define digestion.

Where does most of it occur in the small intestine?

A

The process by which ingested food is broken down chemically into absorbable molecules.
- Duodenum

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2
Q

Define absorption.

Where does most of it occur in the small intestine?

A

The movement of nutrients, water and electrolytes from the lumen of the intestine into blood.
- Jejunum

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3
Q

What are the 2 general cellular pw’s of absorption?

A

Cellular and paracellular (tight junctions) paths

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4
Q

Where does most carbohydrate absorption occur?

A

Most in duodenum, followed by jejunum and then ileum.

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5
Q

Where does most Ca2+ absorption occur in the GI tract?
Folate?
Iron?

A
  • Ca2+: Duodenum, but also some in jejunum and ileum.
  • Folate: Duodenum
  • Iron: Duodenum
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6
Q

Where does most bile acid recycling occur in the GI tract?

A

Distal ileum, some in colon and jejunum, and least in duodenum.

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7
Q

Carbs constitute __% of the typical american diet.

A

50%

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8
Q

What types of carbs are typically ingested?

A

Polysaccharides, disaccharides, and very little amount of monosaccharides.

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9
Q

Which of the following can be absorbed through intestinal epithelial cells? Polysacchs, disacchs, monosacchs.

A 
Monosaccharides only
(Thus all ingested carbs must be digested to monosacchs to be absorbed thru the intestine)
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10
Q

A major dietary carbohydrate is starch – a mixture of both straight and branched-chain polymers of ________.

A

glucose

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11
Q

What are the straight chain polymers of glucose (found in starch) called?

A

amylose

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12
Q

What are the branched chain polymers of glucose (found in starch) called?

A

amylopectin

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13
Q

What 3 disaccharides are found in our food?

A

Trehalose, sucrose, lactose

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14
Q

What 2 molecules are linked together in trehalose?

What breaks down trehalose?

A

2x glucose

- Trehalase

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15
Q

What 2 molecules are linked together in sucrose?

What breaks down sucrose?

A

glucose + fructose

- Sucrase

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16
Q

What 2 molecules are linked together in lactose?

What breaks down lactose?

A

glucose + galactose

- Lactase

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17
Q

What type of linkage is found in cellulose? Why is this important?

A

Beta-1,4 (we can’t break it down)

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18
Q

Where is alpha amylase found?

What does it hydrolyze? (what alpha bonds remain?)

A
  • Saliva and pancreatic secretions

- Breaks down alpha-1,4 (alpha-1,6 bonds remain)

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19
Q

How far down the GI tract does salivary alpha amylase go before being inactivated?

A

Esophagus (inactivated at low pH of stomach)

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20
Q

Pancreatic amylase (most significant) digests internal alpha-1,4-bonds in starch, yielding a mixture of mainly what 3 lengths of sugars?

A

Disaccharides, trisaccharides and oligosaccharides.

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21
Q

Give an e.g. of an oligosaccharide breakdown product of amylopectin.
E.g of a trisaccharide? Disaccharide?

A
  • Oligo: alpha-limit dextrin (from amylopectin)
  • Tri: maltotriose (3x glucose)
  • Di: maltose (2x glucose)
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22
Q

After starch digestion into alpha-limit dextrins, maltotriose, and maltose by alpha amylase (mostly via pancreas), these disaccharides are further digested to monosaccharides by what 3 enzymes? Where are they found?

A
  • Alpha-dextrinase AKA isomaltase (breaks down alpha-1,6 branches), maltase and sucrase. (break down to glucose)
  • Brush border
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23
Q

What are the 3 end products of carb digestion that can be absorbed by intestinal epithelial cells?

A

Glucose, galactose, fructose

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24
Q

*How is glucose absorbed across the apical intestinal epithelial cell membrane?
What other molecule is transported this way?

A

SGLT1, a sodium/glc active transporter (against both gradients)
- Galactose as well

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25
Q

*In what way are glucose and galactose transported across the basilar membranes of intestinal epithelial cells?

A

Facilitated diffusion via GLUT2

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26
Q

*How does fructose get across the intestinal epithelial cell apical membrane?
Basilar membrane?

A
  • Apical: Facilitated diffusion (GLUT5)

- Basilar: Facilitated diffusion (GLUT2)

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27
Q

Define lactose intolerance.
How prevalent is it?
What is the major symptom?
Tx?

A

Definition: Lack or deficiency of lactase in the brush border- lactose is not digested to glucose and galactose. Reflects a nl developmental decline in the expression of lactase by enterocytes.

  • Present in 50% of adult and higher in some pops (Asians).
  • Sx: Diarrhea (ingested lactose remains undigested and unabsorbed in the intestinal lumen, leading to water retention and thus *osmotic diarrhea)
  • Tx: Some benefit from taking bacterially derived lactase enzyme in a tablet form.
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28
Q

What is congenital lactose intolerance?

Tx?

A

Lack of jejunal lactase (rare, serious).

- Tx: Replace lactose with a sucrose or fructose diet to avoid diarrhea.

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29
Q

A defect in the SGLT1 transporter would cause what molecules to not be absorbed?
What is the name of the condition?
Sx?
Tx?

A
  • glucose, galactose
  • Glucose-galactose mal-absorption
  • Sx: diarrhea
  • Tx: Fructose diet
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30
Q

What are the 7 essential AA’s that must be obtained from the diet? (do we have to memorize?)

A

Val, Leu, Ile, Phe, Try, Thr, Met

“Valerie Lu is phoning translations through Mexico”

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31
Q

Protein digestion starts in the stomach with the action of ______________.

A

Pepsin

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32
Q

Protein digestion is completed (after the stomach) via proteases released from ________________ and ________________.

A
  • Pancreas

- Brush border of small intestine

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33
Q

What are some e.g.’s of endopeptidases?

A

Pepsin, trypsin, chymotrypsin, elastase

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34
Q

What is a common e.g. of an exopeptidases?

What end of the polypeptide does it break down?

A

Carboxypeptidase A and B

- C-terminal end

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35
Q

Recall: what cells secrete pepsinogen in response to protein?

A

Gastric chief cells

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36
Q

*What activates pepsinogen to pepsin?

A

Low pH

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37
Q

*How and where is pepsin inactivated?

A

Once it reaches high pH of duodenum (via pancreatic HCO3-)

38
Q

What are the protein breakdown products of pepsin?

Is pepsin essential for protein digestion?

A
  • A mixture of intact ptn, large peptides, and very little free AAs
  • No
39
Q

Name the 5 major pancreatic proteases (in their inactive precursor form).

A
  1. Trypsinogen
  2. Chymotrypsinogen
  3. Proelastase
  4. Procarboxypeptidase A
  5. Procarboxypeptidase B
40
Q

*Pancreatic trypsinogen is converted to trypsin via what enzyme?
Where is this enzyme found?

A
  • Enterokinase

- Brush border epithelial cells

41
Q

*Chymotrypsinogen, proelastase, and procarboxypeptidase A + B are conveted to their active form via what molecule?
What else does this molecule convert?

A

Trypsin

- Also converts some trypsinogen to trypsin

42
Q

The 5 major proteases break down proteins into…

A

AAs, di- and tri-peptides and oligo-peptides.

43
Q

How large can peptides be and still be absorbable?

A

Tripeptides or smaller are absorbable

44
Q

*What 2 transport proteins move AA’s (and di/tri-peptides) transported across the apical membrane of intestinal epithelial cells?

A
  • Cotransported passively w/Na+

- Cotransported passively w/H+

45
Q

*How do AA’s leave through the basilar membrane of intestinal epithelial cells?

A

Facilitated diffusion (like carbs)

46
Q

*Inside the cell, most of the peptides are hydrolyzed to amino acids by ________________.

A

Cytosolic peptidases

47
Q

What is clinically relevant regarding peptide xport into epithelial cells?

A

Peptide transporters uptake some drugs

48
Q

If someone has a disorder where they can’t absorb single AA’s, are they doomed?

A

No, because can partially compensate w/di-/tripeptides + cytosolic peptidase.
- Trypsinogen deficiency: rare and serious. Tx: Diet of partially hydrolyzed proteins.

49
Q

What is cystinuria?

A

Transporter for dibasic amino acids (cystine, lysine, arginine, ornithine) is absent in small intestine and kidney, so there’s low or no absorption of these in intestine or kidney.
- The intestinal defect results in failure to absorb amino acids – excreted in feces. The renal defect results in increased excretion (hence cystinuria)

50
Q

*Name the 4 major categories of lipids in the diet?

A
  1. Triglycerides (major pool) – most of these have long-chain FAs esterified to glycerol backbone.
  2. Phospholipids
  3. Cholesterol
  4. Vitamins A, D, E and K (not lipids but fat soluble)
51
Q

Why can’t lipids be digested similarly to carbs and proteins?

A

Lipid in a fatty meal floats on the surface of gastric contents, limiting the area of interface b/w aqueous and lipid phases. Thus access to lipolytic enzymes are restricted (enzymes are soluble in aqueous phase).

52
Q

How does emulsification help in the digestion of lipids?

A

Mixing/churning into fine droplets greatly increases SA for digestive enzymes to act

53
Q

In the stomach, lipid droplets are emulsified by _________________.
In the small intestine, the primary emulsifying agent is _________________.

A
  • dietary proteins (lipid digestion begins here)

- bile

54
Q

Recall: what cells release gastric lipase?

A

Chief cells (as well as pepsinogen)

55
Q

What % of lipid digestion occurs in the stomach?

Is it required?

A

10%

- no, *more important that the stomach empty chyme slowly to allow for pancreatic enzyme action (recall: CCK)

56
Q

*Bile acids together with ____________ and products of lipid digestion surround and emulsify dietary lipids.

A

Lysolecithin

57
Q

Name the 3 three important lipolytic enzymes (that can work at neutral pH) in pancreatic juice.

A
  • Pancreatic lipase
  • Phospholipase A2
  • Cholesterol ester hydrolase
58
Q

*Describe the action of pancreatic lipase.

A

Hydrolyzes triglycerides to monoglyceride + fatty acids.

59
Q

*In the presence of bile acids, pancreatic lipase is inactivated unless this cofactor binds to both ____________ (name the enzyme/cofactor) and the bile acid.

A

Colipase

60
Q

*Describe the action of phospholipase A2.

What activates it?

A

Hydrolyzes phospholipids such as those present in cell membranes to lysolecithin + fatty acids.
- Trypsin activates it

61
Q

*Describe the action of cholesterol ester hydrolase.

A

Hydrolyzes cholesterol ester to free cholesterol + fatty acids. (Also hydrolyzes ester linkages of triglycerides, producing glycerol).

62
Q

Which products of lipid digestion are soluble in the intestinal lumen in mixed micelles?
What is the water-soluble exception?

A

Monoglycerides, fatty acids, cholesterol, lysolecithin

- Exception: glycerol

63
Q

Core of a micelle contains the products of lipid digestion – the exterior is lined with ___________________.

A

Amphipathic (both hydrophilic and hydrophobic face) bile salts

  • The hydrophilic portion of the bile salts dissolves in the aqueous solution of intestinal lumen, shielding the hydrophobic regions of lipolytic products, solubilizing the lipids in micellar core.
64
Q

*What form does digested lipid have to be in to traverse the apical intestinal epithelial membrane?
How does it get across?

A

Must be released from micelles (micelle doesn’t enter cell)

- Diffusion

65
Q

What happens to lipid digestion products once they enter the epithelial cell?

A

They are re-esterified with free FAs on the sER to form triglycerides, cholesterol esters, and phospholipids.

66
Q

*The re-esterified lipids are packaged with apoproteins to form ______________.

A

Chylomicrons

67
Q

Describe the structure of a chylomicron. (not sure if important)

A

Have triglycerides and cholesterol at the core, phospholipids and apoproteins on the outside.

68
Q

How do chylomicrons get back to the bloodstream?

A

Exocytosis, but so large that they travel in lymphatics (rather than bv’s) to get to thoracic duct and into bloodstream

69
Q

Is pancreatic insufficiency related to exocrine or endocrine dysfunction?
What are some dz’s that fall under the umbrella of pancreatic insufficiency?
What’s a fatty symptom of this defect?

A
  • Exocrine
  • Chronic pancreatitis; CF
  • Steatorrhea (fat in stool)
70
Q

*What are the 2 ways pH can become to low in the small intestine, causing pancreatic enzymes to be disabled?

A
  1. Gastric parietal cells secrete excessive H+ (Zollinger-Ellison syndrome)
  2. Pancreas doesn’t secrete enough HCO3- to neutralize acidic chyme.
71
Q

What is a possible dangerous problem during ileal resection, w/r/t bile salts?

A

Enterohepatic circulation of bile is interrupted – bile is lost in feces.

72
Q

What is abetalipoproteinemia?

What is the problem on the cellular level?

A

Failure to synthesize Apo B – chylomicrons are either not formed or are unable to be transported into lymph.

73
Q

Name all of the ways that fluid can get into the GI tract.

A

Small intestine, pancreatic juice/bile, gastric juice, saliva, and diet (all relatively even amounts)

74
Q

What are the 2 parts of the GI tract that absorb water?

Which does more?

A 
Small intestine (majority) and colon.
(only 100-200 mL excreted in stool)
75
Q

What are the 2 broad cellular mechanisms by which water can be reabsorbed in the small intestine?
What about the colon?

A

Paracellularly and transcellularly

- Colon: only absorbs transcellularly (due to tighter junctions)

76
Q

What part of the small intestine is the major site of Na+ reabsorption?

A

Jejunum

77
Q

Recall: What are the 3 ways by which Na+ enters the apical side of GI epithelial cells?

A
  1. Na+/monosaccharide cotransporters
  2. Na+/AA cotransporters
  3. Na+/H+ exchanger
78
Q

What additional transporters does the ileum have that the jejunum does not?

A

Cl-/HCO3- exchanger in apical membrane

- Also has a Cl- xporter (instead of HCO3- xporter) in the basolateral membrane

79
Q

*In the ________ (J/I), there is net absorption of NaCl and in the ________ (J/I) there is net absorption of NaHCO3.

A

Ileum
Jejunum
(both absorb Na+)

80
Q

Generally, how do the crypt epithelial cells of the intestines differ from the villi cells in terms of secretion/absorption?

A
  • Crypt cells: mostly secrete fluid and electrolytes

- Villi cells: mostly absorb fluid and electrolytes

81
Q

*Besides NKP, what other major transporter is found on the basolateral membrane of intestinal epithelial cells?
What Cl- protein is found in the apical membrane?

A

Na+ -K+ -2Cl- cotransporter (*brings them all into cell from basolateral side)
- Cl- channel

82
Q

In the small intestine, the Cl- channels of the apical membrane are usually closed. How are these channels activated?
What occurs when the channels open, secretion of Cl- or absorption?

A

Activated by hormones and NTs such as ACh, VIP (-> AC, cAMP second msger)
- *Cl- secretion

83
Q

*How does Cholera lead to severe diarrhea?

A

Cholera toxin comes in from gut, activates adenylyl cyclase to high degree (normally activated via hormones/ACh/VIP) - fluid (via Cl-) secretion by the crypts overwhelms the absorptive capacity of villus cells, causing life-threatening diarrhea.

84
Q

Differentiate osmotic diarrhea from secretory diarrhea.

A
  • Osmotic Diarrhea: Caused by the presence of non-absorbable solutes in the intestinal lumen.
  • Secretory Diarrhea: Caused by excessive secretion of fluid by crypt cells.
85
Q

Would cholera cause osmotic or secretory diarrhea?

A

Secretory (fluid excessively secreted due to overactive Cl- excretion

86
Q

Would lactase deficiency cause osmotic or secretory diarrhea?

A

Osmotic (lactose not digested to glucose and galactose, thus retaining water; bacteria can make it worse by digesting the lactose into more osmotically active forms)

87
Q

*Ca2+, absorbed in small intestine, depends on the active form of what vitamin for its absorption?
How does this help Ca2+ get into cell?

A

Active vitamin D (1,25-dihydroxycholecalciferol, 1,25-DHCC)

- Induces formation of calbindin D-28K

88
Q

How does Ca2+ get across apical intestinal cell membrane?

Basolateral?

A
  • Diffuses in w/calbindin D-28K (requires 1,25-DHCC for its formation)
  • Ca2+ ATPase
89
Q

Inadequate Ca2+ absorption causes what dz in children?

What about adults?

A
  • Rickets (kids)

- Osteomalacia (adults)

90
Q

How is vit B12 released from food in the stomach?

What then binds the B12?

A

Pepsin

- R proteins

91
Q

*How what happens to vit B12 in the small intestine (what 2 things bind to it)?
Which part of the small intestine absorbed it?

A
  1. R proteins degraded by pancreatic proteases
  2. B12 xfered to IF (secreted by gastric parietal cells)
    - Ileum
92
Q

*During a gastrectomy, parietal cells are lost. How could this lead to a dz of vit B12 absorption?
What is the dz called?

A

No parietal cells -> no IF -> no B12 absorption

- Pernicious anemia

FHB GI (10 decks)

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