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GI > Digestion and Absorption of Carbohydrates and Proteins > Flashcards

Digestion and Absorption of Carbohydrates and Proteins Flashcards

1
Q

What are the three classes of carbohydrates?

A

Monosaccharides (monomers)

Oligosaccharides (short polymers)

Polysaccharides (long polymers)

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2
Q

Fiber, pectin and cellulose are examples of?

A

Indigestible polysaccharides

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3
Q

What are the polysaccharides we can digest? (4)

A
  1. Starch
  2. Glycogen
  3. Amylose
  4. Amylopectin
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4
Q

What percent of dietary carbs in western society is from starch? Where is it primarily derived from?

A

45-60%

Primarily from plants

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5
Q

What is the primary source of dietary glycogen?

A

Animals

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6
Q

What type of structure of polysaccharide is amylose?

A

Straight

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7
Q

What type of polysaccharide structure does amylopectin have?

A

Branched

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8
Q

Identify the polymers

A
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9
Q

What are the two dietary oligosaccharides?

A

Sucrose and Lactose

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10
Q

What are the two dietary monosaccharides?

A

Glucose and Fructose

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11
Q

What kind of carbohydrates can the intestine absorb?

A

Monosaccharides

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12
Q

What are the two steps of carbohydrate digestion?

A
  1. Intraluminal hydrolisis
  2. Membrane digestion
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13
Q

What are the two types of amylases that participate in intraluminal hydrolysis of carbs?

In what form are these secreted?

A

Alpha-Amylases

  1. Salivary Amylase
  2. Pancreatic Amylase

Secreted in enzymatically active form

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14
Q

What does salivary amylase do? What inactivates it?

A

Initiates starch digestion

Inactivated by gastric acid

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15
Q

What does pancreatic Alpha amylase do?

A

Completes starch digestion in the lumen of the small intestine

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16
Q

What stimulates the secretion of pancreatic alpha amylase?

A

Cholecystokinin (CCK)

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17
Q

Pancreatic alpha-amylase cannot digest all linkages and the product is oligosaccharides. What structural components are ndigestible?

A

Terminal linkages and branch points

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18
Q

What is responsible for the membrane digestion?

Where does this happen?

Where does it definitely and specifically not happen?

A

Brush border oligosaccharidases

Mostly in the proximal jejunum.

Does not happen in the large intestine

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19
Q

What are the brush border oligosaccharidases? (3)

A
  1. Lactase
  2. Glucoamylase
  3. Sucrase-isomaltase
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20
Q

What is the action of lactase? When/how does expression change in humans?

A
  • Digests lactose into glucose and galactose
  • Expression decreases after weaning in the infant
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21
Q

What is glucoamylase also known as?

A

Maltase

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22
Q

Sucrase-isomaltase is two enzymes, what does it cleave?

A

•Cleaves sucrose and splits branch points

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23
Q

How is lactase downregulation determined? What can excess downregulation lead to?

A

Hereditarily determined

Lactase deficiency or Lactose intolerance

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24
Q

What are the symptoms of lactase deficiency/lactose intolerance?

A

–cramps
–diarrhea
–flatus

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25
Q

What are the symptoms of lactose intolerance determined by?

A
  1. Rate of peristalsis and gastric emptying
  2. Colonic bacteria
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26
Q

Colonic bacteria can metabolize undigested lactose into what? How do these contribute to the symptoms of lactose intolerance?

A

Short chain fatty acids (induces osmotic diarrhea)

CO2 (contributes to flatulence)

H2

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27
Q

What monosaccharides are readily absorbed by the small intestine?

A
  1. Glucose
  2. Galactose
  3. Fructose
28
Q

What are the two apical membrane transporters?

A
  1. Na/glucose transporter (SGLT1)
  2. GLUT5
29
Q

What does the Na/glucose transporter (SGLT1) do? What kind of transport is it? How is it driven?

A
  • Responsible for glucose and galactose uptake
  • Secondary Active transcellular
  • Driven by intracellular [Na+] via Na,K-ATPase
30
Q

What is GLUT5 responsible for? Where would we find it in the small intestine? How does it work?

A
  • Responsible for fructose uptake
  • In jejunum
  • Facilitated diffusion
31
Q

What is the basolateral membrane transporter?

32
Q

What does GLUT2 do? How does it do it?

A
  • Responsible for the transport of all three monosaccharides into interstitium
  • Facilitated diffusion
33
Q

What causes glucose-galactose malabsorption?

A

–Single aa substitutions in SGLT1
•Inhibits uptake of glucose and galactose via SGLT1

34
Q

What does glucose-galactose malabsorption result in?

How do you treat?

A
  • Diarrhea due to reduced Na+ absorption via SGLT1
  • Eliminate glucose, galactose and lactose from diet
35
Q

How must proteins be broken down to be useable?

A

–Proteins must first be digested into oligopeptides and amino acids to be absorbed

36
Q

What are the pathways by which protein digestion is accomplished?

A
  1. Luminal proteases (3 different paths)
  2. Brush border proteases
37
Q

Luminal proteases secreted by the stomach and pancrease break down protein into?

A

Peptides and a.a.’s

38
Q

Brush border proteases hydrolyze peptides into?

39
Q

general luminal proteases of path 3 and 4 hydrolyze peptides into oligopeptides. What cell type takes these up? What does it do with them?

A

Enterocyte

Path 3 - hydrolyzes intracellularly to a.a.’s

Path 4 - oligopeptides moved directly to interstitium

40
Q

What do endopeptidases have affinity for? What do they produce?

A

Bonds adjacent to specific a.a.’s

Products are oligopeptides

41
Q

What do exopeptidases hydrolyze? What are the products?

A

Bonds adjacent to amino or carboxy terminus

products are single a.a.’s

42
Q

How are gastric proteases secreted?

A

proenzymes

43
Q

What cells secrete pepsinogen?

A

Chief cells

44
Q

What activates pepsinogen?

A

pH of 1.8 to 3.5, activated to pepsin

45
Q

What kind of peptidase is pepsin?

A

endopeptidase

46
Q

Pancreatic proteases are secreted as proenzymes. What are the five types?

A
  1. Trypsinogen
  2. Chymotrpsinogen
  3. proelastase
  4. procarboxypeptidase A
  5. procarboxypeptidase B
47
Q

What activates trypsinogen?

A

Jejunal brush border enzyme activates to trypsin, which can autoactivate tryspinogen and other pancreatic proteases

48
Q

What activates chymotrypsinogen? What kind of peptidase is it?

A

Activated by trypsin

Endopeptidase

49
Q

What activates proelastase? What kind of peptidase is it?

A

Trypsin

Endopeptidase

50
Q

What activates procarboxypeptidases A and B? What kind of peptidase are these?

A

Trypsin

Exopeptidases

51
Q

Why are there such large numbers of brush border peptidases? (Trust me, there are)

A

–Large numbers of them because each peptidase recognizes only some peptide bonds

52
Q

Cytoplasmic peptidases work on what?

A

smaller dipeptides and tripeptides

53
Q

What does the PepT1 transporter do?

A

moves oligopeptides

54
Q

In adults, how is whole protein that is endocytosed degraded?

A

In lysosome

55
Q

Where are M cells found?

A

Peyer’s patches

56
Q

What are M cells specialized for?

A

protein uptake

57
Q

What do M cells do with proteins?

A
  1. Package them as antigens in clathrin coated pits
  2. present to immunocompetent cells at the basolateral membrane
58
Q

What percent of absorbed protein enters the blood as single a.a.’s?

A

more than 90%

59
Q

How is the PepT1-H+/oligopeptide cotransporter driven?

A

Actively - driven by a H+ and Na+ gradient

60
Q

There are at least 7 identified transporters of single amino acids in the apical membrane, how are these divided?

What does each division do?

A

–Divided into those driven by Na/K pump and Na+ independent

»Na+ dependent: neutral aa
»Na+ independent: basic aa and cysteine

61
Q

There are at least five basolateral membrane protein transporters. Describe them

A

–3 for exit
»Na+ independent

–2 for entrance
»Na+ dependent
»For enterocyte nutrition and growth

62
Q

Hartnup disease is an autosomal recessive hereditary disorder. What is the defect in? What are the symptoms?

How do we treat?

A
  • Defect is in apical transport of neutral a.a.
  • Symptoms include
    • Pellagra
    • cerebellar ataxia
    • psychiatric abnormalities
  • No treatment (due to normal oligopeptide absorption)
63
Q

Cystinuria is an autosomal recessive hereditary disorder, what is the defect in?

What are the symptoms?

How do we treat?

A
  • Defect in apical transport of basic a.a. and cysteine
  • kidney stones
  • no treatment due to normal oligopeptide absorption
64
Q
  • A 16 d/o girl was admitted to the newborn outpatient clinic with diarrhea, poor feeding, fever and moaning. She was born at 35 gestational weeks after an uneventful pregnancy with a birth weight of 2600 g. She was fed with breast milk soon after the birth and her initial neonatal period were uneventful.
  • Watery and profuse diarrhea (15 to 20 times/day and approximately 150 ml/kg) developed within one week after birth. Fever and moaning was then noted three days before the admission. On admission, she was ill looking and had the signs of dehydration including lethargy, confusion, tachypnea and hypotension. Arterial blood gas analysis showed severe metabolic acidosis. Urine analysis was normal.
  • The patient was treated with appropriate intravenous fluid and biochemical parameters improved without any complication. However, watery diarrhea and hypernatremic dehydration recurred after the infant was re-fed with breast milk. At this time, she was fed with lactose and fructose free, glucose as carbohydrate content, but diarrhea did not improve.
  • Stool pH was 6, and stool sugar testing was positive. No fat droplet was detected in stool examination. Stool osmolarity was compatible with osmotic diarrhea.

•The physician’s next step in diagnosis should be to administer:
A.Fructose Tolerance Test
B.Glucose Tolerance Test
C.Oral Rehydration Solution
D.Reduced Na+ Diet
E.Sudan III Test

GI (26 decks)

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