Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI Exam 1 > Biochemistry of the GI Tract > Flashcards

Biochemistry of the GI Tract Flashcards

1
Q

mouth - purpose and methods?

A
  • mastication increases surface area
  • saliva hydrates food stuffs
  • alpha-amylase begins breakdown of starch
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Stomach - purpose and methods?

A
  • acidic conditions denature proteins - proteins are difficult to breakdown! Need to get proteins ready for the enzymes!
  • secretion and activation of pepsin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Pancreas - purpose and methods?

A
  • secretes sodium bicarb to neutralize chyme

- secretes amylase, lipases, and peptidases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Liver and gallbladder - purpose and methods?

A

-synthesize and store bile acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Small intestine - purpose and methods?

A

-produces disaccharidases and peptidases to complete proteins and carb digestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

oral phase of carb digestion

A

-salivary alpha amylase hydrolyzes alpha 1,4-glycosidic bonds in starch and glycogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

intestinal phase of carb digestion:

A
  • pancreatic alpha-amylase continues hydrolysis of alpha1,4-glycosidic bonds into into glucose (mono), maltose (di) and maltotriose (trisaccharides)
  • oligosaccharidase, isomaltase and alpha-glucosidase complete breakdown into glucose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

maltose linkage?

A

alpha 1,4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

maltose breakdown yields?

A

2 glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

lactose linkage?

A

beta 1,4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

lactose breakdown yields?

A

glucose and galactose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

sucrose linkage?

A

alpha1-beta2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

sucrose breakdown yields?

A

glucose and fructose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is glucose taken up by intestinal epithelium?

What other nutrient does this method work for?

A
  • Na ATPase builds high sodium concentration in intestinal lumen
  • Na + glucose enter intestinal epithelium via SGLT1 transporter following Na gradient

-also works for Gal bc it is very similar structurally to Glu

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do we bring glucose from the intestinal epithelial cells into circulation?

A

-passive transport down gradient using GLUT2 transporter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do cells take up glucose?

How do sells make sure that they don’t loose the glucose that they take up? How do cells keep the glucose concentration steep?

A
  • steep concentration of Glucose used –> facilitated diffusion or other GLUT transporters
  • phosphorylate glucose as soon as it comes in — phosphorylation of glucose also allows the concentration gradient of glucose to remain high outside
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do intestinal epithelial cells take up fructose?

A

Use GLUT5 transporter - facilitated diffusion

NO Na GRADIENT USED

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does fructose get into the circulation from intestinal epithelial cells?

A

uses GLUT5 transporter - facilitated diffusion

19
Q

Where does fructose go after getting into circulation?

What happens to it next? WHy?

A
  • fructose goes to the LIVER
  • hepatocytes phosphorylate Fructose = keeps it from leaving cell and keep the concentration of fructose higher in circulation
20
Q

What is lactose intolerance?

What happens?

A
  • reduced ability to break down lactose
  • lactose is broken down by intestinal bacteria –> the 2 to 3 carbon metabolites draw water into intestines (diarrhea)
  • H2 and CO2 cause gas pain
21
Q

Diagnostic for lactose intolerance?

A

hydrogen breath test

administer lactose before the h breath test

22
Q

Protein digestion process:

A

1) Gastric enzymes - pepsin = denature protein
2) Pancreatic enzymes - trypsin, chymotrypsin, Elastase, carboxypeptidase = breakdown denatured protein into amino acids and oligopeptides
3a) (40%) amino acids taken up
3b) (60%) Brush border enzymes - endopeptidase, aminopeptidase, dipeptidiase = breakdown oligos into amino acids, dipeptides, and tripeptides

23
Q

zymogens are?

A

enzymes that need acidic conditions and/or proteolytic processing to activate an inactive precursor (zymogen)

24
Q

stomach zymogens?

A

-pepsinogen—>pepsin

25
Q

pancreas zymogens?

A
  • chymotrypsingen–>chymotrypsin
  • trypsinogen–>trypsin
  • procarboxypeptidases–> carboxypeptidases
  • proelastase–>elastase
26
Q

intestine zymogens?

A
  • ->aminopeptidase
  • ->dipeptidase
  • ->endopeptidase
27
Q

activation of zymogens starts with what signal on what cells??

What happens next?

A

cholecystokinin (CKK)

acts on pancreatic acinar cells and intestinal mucosal cells (relevant to this example- it does more)

the mucosal cell secretes enteropeptidases and the acinar cell secretes trypsinogen

trypsiogen activated to tyrpsin by the enteropeptidase

Trypsin then helps with more activation of trypsin. also activates chymotrypsin, proelastase, procarboxypeptidase

28
Q

master protease of zymogens?

A

trypsin

29
Q

Gastric phase- protein digestion:

A
  • HCl denatures proteins

- pepsinogen digests proteins into large fragments

30
Q

Intestinal phase - protein digestion:

A
  • pancreas synthesizes chymotrypsin, trypsin, carboxypeptidases A/B and elastase to break proteins into amino acids and oligopeptides
  • intestinal epithelium mades aminopeptidase, dipeptidase, and endopeptidase
31
Q

Pancreatic autodigestion - what happens and why?

A
  • protein digestion disorder
  • trypsinogen inhibitor (TI) prevents premature activation of trypsin in the pancreas
  • blockage of pancreatic duct or deficiency of TI results in autodigestion of the pancreas = pancreatitis
32
Q

trypsinogen inhibitor (TI) purpose?

A

prevents premature activation of trypsin in the pancreas

33
Q

Cystic fibrosis - what happens and why?

A
  • CFTR deficiency=thickened pancreatic mucous –> occluded ducts
  • secretion of pancreatic enzymes impaired in 80%
  • 10% develop pancreatitis
  • CF patients need oral enzyme supplements to help w/ malabsorption
34
Q

Celiac disease- what happens and why?

A
  • unidentified protease defect prevents complete degredation of gluten
  • small gluten fragments=toxic –> inflammatory reaction
35
Q

Amino acid uptake process-

1) which transporters?
2) locations for these transporters?

A

1) many amino acid transporters (SLC) that transport more than one amino acid - lots of back-up
2) intestines and also used in kidney for reuptake of amino acids

36
Q

Amino uptake disorders?

A

so much redundancy among SLC transporters that a mutation in one wont really hurt the system

-in the kidney this may affect kidney function

37
Q

Cystinuria:

-what is it? what happens?

A

-inefficient re-uptake of cystin (Cys-Cys) in the kidney

cystin crystals (poooor solubility) form in GU tract - does not sounds fun bc of obstruction and stones

38
Q

Hartnup disease-
what is it?
what happens?

A
  • defective uptake of neutral amino acids from intestine and kidney filtrate
  • can get deficiency of tryptophan –> needed for NAD synthesis = pellagra-like symptoms
39
Q

Problem with high protein intake?

A

liver ends up making a lot of urea!!

40
Q

Lipid digestion and uptake:

A
  • bile salts solubilize large lipid droplets
  • pancreatic lipase separates 2 FAs from triacylglycerol (TAG becomes MAC)
  • enterocytes take up lipid myceles and remake TAG
  • enterocytes pack lipids into ApoB48 chylomicrons
41
Q

Bile salts made where and derived from what precursor? secreted how?

A
  • made in liver from cholesterol

- secreted via the gall duct

42
Q

Purpose of bile salts?

A

solubilize lipids

43
Q

How much of secreted bile salts are recycles?

A

80% via intrahepatic circulation

44
Q

what breaks down the TAGs?

A

pancreatic lipase breaks it into 2 FAs and a monoacyl glycerol

GI Exam 1 (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions