Digestion and Absorption of Carbohydrates and Proteins Flashcards Preview

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Flashcards in Digestion and Absorption of Carbohydrates and Proteins Deck (65):
1

What are the three classes of carbohydrates?

Monosaccharides (monomers)

Oligosaccharides (short polymers)

Polysaccharides (long polymers)

2

Fiber, pectin and cellulose are examples of?

Indigestible polysaccharides

3

What are the polysaccharides we can digest? (4)

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

4

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

45-60%

Primarily from plants

5

What is the primary source of dietary glycogen?

Animals

6

What type of structure of polysaccharide is amylose?

Straight

7

What type of polysaccharide structure does amylopectin have?

Branched

8

Identify the polymers

9

What are the two dietary oligosaccharides?

Sucrose and Lactose

10

What are the two dietary monosaccharides?

Glucose and Fructose

11

What kind of carbohydrates can the intestine absorb?

Monosaccharides 

12

What are the two steps of carbohydrate digestion?

  1. Intraluminal hydrolisis
  2. Membrane digestion

13

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

In what form are these secreted?


Alpha-Amylases

  1. Salivary Amylase
  2. Pancreatic Amylase
     

Secreted in enzymatically active form

14

What does salivary amylase do?  What inactivates it?

Initiates starch digestion

Inactivated by gastric acid

15

What does pancreatic Alpha amylase do?  

Completes starch digestion in the lumen of the small intestine

16

What stimulates the secretion of pancreatic alpha amylase?

Cholecystokinin (CCK)

17

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

Terminal linkages and branch points

18

What is responsible for the membrane digestion?  

Where does this happen?

Where does it definitely and specifically not happen?

Brush border oligosaccharidases

Mostly in the proximal jejunum.

Does not happen in the large intestine

19

What are the brush border oligosaccharidases?  (3)

  1. Lactase
  2. Glucoamylase
  3. Sucrase-isomaltase

20

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


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

21

What is glucoamylase also known as?

Maltase

22

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


•Cleaves sucrose and splits branch points
 

23

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

Hereditarily determined

Lactase deficiency or Lactose intolerance

24

What are the symptoms of lactase deficiency/lactose intolerance?


–cramps
–diarrhea
–flatus 
 

25

What are the symptoms of lactose intolerance determined by?

  1. Rate of peristalsis and gastric emptying
  2. Colonic bacteria

26

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

Short chain fatty acids (induces osmotic diarrhea)

CO2 (contributes to flatulence)

H2 

27

What monosaccharides are readily absorbed by the small intestine?

  1. Glucose
  2. Galactose
  3. Fructose

28

What are the two apical membrane transporters?

  1. Na/glucose transporter (SGLT1)
  2. GLUT5
     

29

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


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

30

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

•Responsible for fructose uptake
•In jejunum
•Facilitated diffusion
 

31

What is the basolateral membrane transporter?

GLUT2

32

What does GLUT2 do?  How does it do it?


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

33

What causes glucose-galactose malabsorption?


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

34

What does glucose-galactose malabsorption result in?  

How do you treat?

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

35

How must proteins be broken down to be useable?


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

36

What are the pathways by which protein digestion is accomplished?

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

37

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

Peptides and a.a.'s

38

Brush border proteases hydrolyze peptides into?

a.a.'s

39

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

Enterocyte

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

Path 4 - oligopeptides moved directly to interstitium

40

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

Bonds adjacent to specific a.a.'s

Products are oligopeptides

41

What do exopeptidases hydrolyze?  What are the products?

Bonds adjacent to amino or carboxy terminus

products are single a.a.'s

42

How are gastric proteases secreted?

proenzymes

43

What cells secrete pepsinogen?

Chief cells

44

What activates pepsinogen?

pH of 1.8 to 3.5, activated to pepsin

45

What kind of peptidase is pepsin?

endopeptidase

46

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

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

47

What activates trypsinogen?

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

48

What activates chymotrypsinogen?  What kind of peptidase is it?

Activated by trypsin

Endopeptidase

49

What activates proelastase?  What kind of peptidase is it?

Trypsin

Endopeptidase

50

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

Trypsin

Exopeptidases

51

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


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

52

Cytoplasmic peptidases work on what?

smaller dipeptides and tripeptides

53

What does the PepT1 transporter do?

moves oligopeptides

54

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

In lysosome

55

Where are M cells found?

Peyer's patches

56

What are M cells specialized for?

protein uptake

57

What do M cells do with proteins?

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

58

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

more than 90%

59

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

Actively - driven by a H+ and Na+ gradient

60

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

What does each division do?


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


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

61

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


–3 for exit
»Na+ independent


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

62

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

How do we treat?

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

63

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

What are the symptoms?

How do we treat?

  • Defect in apical transport of basic a.a. and cysteine
  • kidney stones
  • no treatment due to normal oligopeptide absorption

64


•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
 

 

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