EXAM #1: BIOCHEMISTRY OF THE GI TRACT Flashcards Preview

Gastrointestinal System > EXAM #1: BIOCHEMISTRY OF THE GI TRACT > Flashcards

Flashcards in EXAM #1: BIOCHEMISTRY OF THE GI TRACT Deck (66):
1

What enzymes are contained in the mouth that begin the breakdown of food?

1) Alpha-amylase
2) Lingual lipase

2

What is the function of alpha-amylase?

Breakdown of starch in the mouth

3

What is the function of lingual lipase?

Breakdown of TAGs in the mouth

4

What macronutrient is NOT brokendown in the mouth?

Protein

5

What are the components of gastric juice that breakdown food?

1) HCl
2) Pepsin

6

What is the inactive zymogen form of pepsin?

Pepsinogen

7

What converts pepsinogen into its active form?

Secretion of HCl that lowers the pH of the gastric juice

8

What are the three functions of HCl in the stomach?

1) Initial breakdown of protein
2) Activation of pepsinogen to pepsin
3) Kill microorganisms

9

What enzymes are produced by the pancreas?

Amylase
Lipase
Peptidase

10

In addition to enzymes, what else does the pancreas secrete?

NaCl
NaHCO3

11

What pancreatic enzyme is secreted in its active form?

Pancreatic alpha-amylase

12

What is the function of bile acids?

Emulsificaiton of aggregated lipids to make them more accessible for lipid digestion enzymes

13

What form must carbohydrates be absorbed in in the small intestine?

Monosaccharide

14

What are the common sources of glucose?

Honey
Fruit
Corn syrup

15

What are the common sources of fructose?

Honey
Fruit

16

What is the common source of sucrose?

Table sugar

17

What is amylose?

Plant carbohydrate/ starch with alpha 1,4 glycosidic bonds

18

What is amylopectin?

Plant carbohydrate/starch with alpha 1,4 glycosidic bonds AND alpha 1,6 branches

19

What is the specific molecular function of alpha-amylase?

Hydrolysis of non-terminal alpha-1,4 linkages

20

What is the function of pancreatic alpha-amylase?

Conversion of branched polysaccharides into oligosaccharide units in the small intestine

21

What are the end products of pancreatic alpha-amylase digestion?

1) Maltose
2) Maltotriose
3) alpha-limit dextrins

22

What is cellulose? Why can't humans breakdown cellulose?

Polysaccharide plant cell wall component with BETA 1,4 GLYCOSIDIC BONDS

****Humans don't have BETA 1,4 ENDOGLYOCSIDASES to breakdown cellulose

23

What is Chitin? Why can't humans breakdown Chitin?

Polymer of N-acetyl-glucosamine with Beta 1,4 Glycosidic bonds that we do not have the enzymes to breakdown

****Comes from fungi and arthropods*****

24

How are the oligosaccharides made by alpha-amylase broken down into monosaccharides?

Membrane bound glycosidases on the luminal side of small intestine enterocytes

25

What is lactose hydrolyzed into via lactase?

1) Glucose
2) Galactose

26

What is maltose hydrolyzed into via maltase?

2x Glucose

27

What is sucrose hydrolyzed to via sucrase/isomaltase?

1) Glucose
2) Fructose

28

What transporter transports glucose across the membrane of the enterocyte for absorption?

Na+/Glucose cotransporter SGLT1

29

What transporter transports fructose across the enterocyte membrane for absorption?

Facilitated diffusion transporter, GLUT5

30

What is the role of Na+/K+ ATPase pumps in the absorption of monosaccharides?

- Cotransporters use Na+ as the driving force
- Concentration gradient is maintained by Na+/K+ ATPase

31

Which monosaccharide transporter requires ATP? Which does NOT?

SGLT1= ATP
GLUT5= NO ATP

32

Once monosaccharides are in the enterocyte, how do they get into the circulation?

Facilitated diffusion transporter, GLUT2

33

Where does protein digestion begin? What enzyme?

Stomach via pepsin

34

What activates pepsinogen into pepsin?

Low pH from HCl secreted via parietal cells

35

What is the specific molecular function of pepsin?

Pepsin breaks proteins into large fragments

36

What happens to proteins in the small intestine?

Further breakdown into amino acids, dipeptides, and tripeptides

37

What pancreatic enzymes breakdown proteins in the small intestine?

Chymotrypsin
Trypsin
Carboxypeptidases
Elastase

38

What enzymes are produced by enterocytes of the small intestine to breakdown proteins?

Aminopeptidase
Dipeptidase
Endopeptidase

39

Which enzymes are zymogens, pancreatic proteases or small intestine proteases?

Pancreatic

40

What is the difference between an Endoprotease and an Exoprotease? Which pancreatic proteases are Endoproteases and which are Exoproteases?

Endoprotease= hydrolyze internal peptide bonds
- Trypsin
- Chymotrypsin
- Elastae

Exoprotease= hydrolyze only terminal peptide bonds
- CARBOXYPEPTIDASE

41

What enzyme in the small intestine enterocyte beings conversion of pancreatic zymogens to active proteases?

Enteropeptidase

42

What is the function of enteropeptiase?

Conversion of Trypsinogen to Trypsin

43

What is the general role of the pancreatic proteases? What is the follow-up role of the proteases produced by the small intestine enterocytes?

Pancreatic= large fragments into oligopeptides

Small intestine= oligopeptides into di/tripeptides and amino acids

44

Where does the further digestion of di/tripeptides occur?

Intracellularly i.e. in the enterocyte

45

What prevents Trypsin activation in the pancreas?

Trypsin inhibitor in the pancreas

46

What happens when pancreatic ducts are blocked i.e. how does this lead to acute pancreatitis?

Blocked ducts lead to an accumulation of Trypsinogen that overwhelms inactivating enzymes; activation occurs in the pancreas and leads to tissue damage

47

What disease of the pancreas is associated with CF?

Pancreatic insufficiency

48

How does CF lead to pancreatic insufficiency?

1) CFTR mutation= decreased Sodium Bicarboante
2) Dehydrates pancreatic juice/ thickens it
3) Thickened pancreatic juice reduces production of pancreatic digestive enzymes

49

What is the manifestation of pancreatic insufficiency?

Insufficient digestion of:
1) Lipids
2) Proteins
3) Carbohydrates

Plus symptoms excess FAT in the large intestine

50

Describe the etiology of Celiac Disease.

- Exact cause is unknown, but there is a peptidase defect
- Small peptides are present in the intestine that are toxic to mucosal cells
- Ingestion of gluten causes an inflammatory response

51

What transporter is present on the luminal membrane of the intestine and facilitate the uptake of amino acid, di and tripeptides?

SLC type transporters

52

What disease does a defect in SLC3A1/7A9 result in?

Cystinuria

53

Describe the etiology of Cystinuria.

- Defect in the amino acid transporter that catalyzes the reuptake of cystine in the kidney
- Cystine accumulates in the urine
- Cytine is insoluble and forms kidney stones

54

What do TAGs need to be digested into for uptake?

2x fatty acids
1x glycerol

55

What three enzymes facilitate TAG digestion? Which does the bulk of the work?

1) Lingual lipase
2) Gastric lipase
3) Pancreatic lipase*

*Pancreatic lipase does most of the digestion of lipids in the small intestine

56

What happens to lipids in the small intestine?

Emulsifiaction by bile acids to prevent the formation of large lipid droplets

57

What prevents pancreatic lipase from being denatured by bile acids?

Binding to colipase in the small intestine

58

What reaction is catalyzed by pancreatic lipase?

Hydrolysis of 2 fatty acids from TAG to form:
- Monoglycerol
- 2x fatty acids

59

Where are bile acids formed, stored, and secreted?

- Formed= liver from cholesterol
- Stored= gallbladder
- Secreted= duodenum

60

Where are bile acids reabsorbed for intrahepatic circulation/ recycling?

Ileum

61

What happens to fatty acids once they are absorbed into enterocytes?

Resynthesis to TAG in the endoplasmic reticulum

62

What happens to TAGs in the enterocyte, once they have been re-synthesized?

Packaging into Chylomicrons

63

What apolipoprotein facilitates the packacking of TAGs into chylomicrons?

Apo B-48

64

Where are chylomicrons secreted once formed in the enterocytes?

Lymphatic system

65

What is Steatorrhea?

Lipid malabsorption resulting in increased lipids in the feces

66

What are the causes Steatorrhea?

1) Disruption in delivery of bile acids to the duodenum
2) Compromised pancreas function e.g. CF
3) Defective intestinal mucosa
4) Products such a Olestra, a fat substitute that cannot be digested