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Block 3; Week 3 Michelle > Ward II > Flashcards

Ward II Flashcards

1
Q

What are the 3 ways in which the SI has such a large surface area?

A
  1. Circular concentric Kirkring folds 3X
  2. Intestinal Villi 30X
  3. Each enterocyte on the villi has microvilli (brush border) 600X
    Whoa!!
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2
Q

What is an important thing that is associated w/ the brush border of intestinal enterocytes?

A

glycocalyx
this is the location for numerous enzymes that break down proteins & carbs in their final stages before absorption.
Its a perfect location right next to where they will be absorbed…otherwise all the little breakdown products could create an osmotic gradient & diarrhea.

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3
Q

What is each villus equipped with? Why is this so important?

A

its own blood & lymphatic supply (Lacteal)…this ensures optimal removal of peptides, AA, sugars, & fats.

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4
Q

What is segmentation & why is it important in the small intestine?

A

It is contraction of the circular muscles of the small intestine so that chyme is moved back & forth & gets max exposure to digestive enzymes.
There is a gradient of the segmentation contractions…highest frequency in duodenum & lowest frequency in ileum. After all, we need the chyme to move downwards.

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5
Q

T/F Cellulose is a carb that can be broken down in the human GI system.

A

False. Can’t be broken down in human GI.

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6
Q

What are the 3 major sources of carbs in food?

A
  1. Disaccharides: sucrose, lactose etc
  2. polysaccharides: starches
  3. Other: amylose, glycogen, alcohol, lactic acid
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7
Q

What is the first thing to initiate carb breakdown?

A

mastication & salivary secretions

includes oral amylase: 3-5% of carb hydrolysis

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8
Q

Does hydrolysis of carbs happen in the stomach?

A

YES

30-40-% of starch hydrolysis happens here after like an hour…it is broken down into maltose

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9
Q

Do pancreatic secretions contribute to hydrolysis of carbs?

A

Of course! Glad you asked…
alpha amylase is secreted by the pancreas, more powerful than oral amylase…
hydrolyzes carbs & produces maltose, maltotriose, & alpha-limited dextrins.

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10
Q

Where does the final breakdown of carbs before absorption happen? Why is this important?

A

It occurs @ the brush border (microvilli on enterocytes of villi). Here there are a bunch of enzymes…right next to transporters for glucose & galactose.
Important to absorb as soon as broken down:
prevents osmotic gradient–>diarrhea
prevents feedback inhibition of the breakdown

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11
Q

What are the 4 important enzymes that are on the brush border of the SI? Which of these are capable of being upregulated?

A

Lactase:
turns lactose–>glucose + galactose
alpha-dextrinase: non-specific dextrin enzyme
Sucrase: sucrose–>glucose + fructose
Maltase: maltose–>2 glucose
**sucrase & maltase can both be up-regulated.

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12
Q

Describe in detail how glucose is absorbed @ the brush border.

A

SGLT1 is a cotransporter @ the brush border that uses the energy of sodium going down its conc’n gradient to absorb glucose. Thus, glucose & Na+ go into the enterocyte. A Na+/K+ pump on the basolateral side of the enterocyte pumps Na+ out. Glucose is transported out of the enterocyte by a basolateral transporter, Glut 2.

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13
Q

Describe in detail how galactose is absorbed @ the brush border.

A

SGLT1 is a cotransporter @ the brush border that uses the energy of sodium going down its conc’n gradient to absorb galactose. Thus, galactose & Na+ go into the enterocyte. A Na+/K+ pump on the basolateral side of the enterocyte pumps Na+ out. Galactose is transported out of the enterocyte by a basolateral transporter, Glut 2. “

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14
Q

Describe in detail how fructose in absorbed @ the brush border.

A

Glut 5 is a transporter on the apical side of the enterocyte @ the brush border. It takes fructose into the enterocyte. Glut 2 allows fructose to leave the enterocyte on the basolateral side.

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15
Q

What percentage of caucasians have a lactose intolerance–lactase deficiency?
Of Jews, Arabs, American Indians?
Of Blacks, orientals, eskimos?

A

10% Caucasians
60% of Jews, Arabs, American Indians
70-95% of Blacks, Orientals, Eskimos

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16
Q

What causes the diarrhea & flatulence experienced w/ patients who are lactose intolerant?

A

the lactose can’t be absorbed & some of the lactose is broken down into lactic acid by intestinal bacteria
These 2 factors create an osmotic diarrhea.
Also, the intestinal bacteria breaking down lactose into lactic acid produces gas. Thus, the flatulence.

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17
Q

How can you test for lactase deficiency?

A

Fasting
A bunch of lactose
test blood levels for glucose. If lactose can’t be broken down to produce glucose & galactose…then you won’t find glucose in the blood at higher levels.

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18
Q

Why are dietary fibers important?

A

They help to add to the bulkiness of stool & reduce their transit time.

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19
Q

What’s the problem with longer transit time of feces?

A

Well, I’m glad you asked…Carcinogenic bile acids cause colonic cancer. An example of carcinogenic bile acids is lithocholic acid. This is formed by the deconjugation of chendeoxycholic acid by luminal bacteria. When you reduce transit time you reduce the formation of these acids. You reduce the risk of colon cancer. Yay for dietary fiber!

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20
Q

Proteins have to be digested before they are absorbed…with one exception? What is it?

A

gamma globulins in mother’s milk eaten by newborns…directly absorbed w/o digestion

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21
Q

What are 3 main sources of the protein our body deals with?

A
  1. Food
  2. Protein that is sloughed off by intestinal mucosa
  3. enzymatic proteins that are secreted
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22
Q

Are all of the pancreatic enzymes that are secreted into the intestine digested & excreted in feces?

A

NO

most are absorbed by pinocytosis & recycled to the pancreas

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23
Q

Where is most of the protein absorbed in the GI? How much of the absorbed protein is AA? How much of it is short peptides?

A

It is absorbed in the SI, usually absorbed in the jejunum.
AA: 30-40%
Short Peptides: 60-70%

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24
Q

What are the 3 types of protein transport?

A

Neutral AA: absorbed @ large conc’n
Basic AA: actively absorbed at small conc’n
Acidic AA: metabolized prior to absorption

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25
Q

What types of enzymes first break down proteins?

A

pancreatic proteases: trypsin & chymotrypsin & carboxypeptidase

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26
Q

What types of enzymes break down proteins @ the brush border?

A

carboxypeptidase
aminopeptidase
dipeptidase

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27
Q

What type of transport gets peptides & free AA into enterocytes? What type of transport gets it from the enterocytes into the bloodstream?

A

AA—> Cell: Active transport

Cell–>Blood: facilitated diffusion

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28
Q

How is trypsinogen (released by the pancreas) activated? What does it do once it’s activated?

A

Enterokinase is a brush border enzyme in the duodenum. It activates trypsinogen to trypsin. Trypsin then activates a bunch of pancreatic enzymes, including trypsinogen!! Way to give back, buddy. : )

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29
Q

What are endopeptidases? What are 3 examples? What do they specifically break down?

A

Endopeptidases are enzymes that break down interior peptide bonds of proteins
Trypsin: targets ones w/ basic C terminal ends
Chymotrypsin: targets ones w/ aromatic C-terminal ends
Elastase: targets ones w/ neutral C-terminal ends

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30
Q

What are exopeptidases? What are 2 examples? What do they specifically break down?

A

Exopeptidases are enzymes that break down exterior peptide bonds.
Carboxypeptidase A: targets ones w/ aromatic & neutral C-terminal ends.
Carboxypeptidase B: targets ones w/ basic C-terminal ends

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31
Q

What do gastric pepsin & pancreatic peptidase do?

A

break proteins down into di & tripeptides

32
Q

free amino acid absorption into enterocytes is coupled w/ what? How about the absorption of di & tripeptides?

A

AA: coupled w/ sodium

Di & Tripeptides: proton coupled symporter called PEPT1

33
Q

What’s the deal w/ Celiac Sprue?

A

the wheat protein attacks the microvilli of the intestinal mucosa
these patients lack gluten hydroxyls to break down gluten…with this incomplete digestion–>toxic substances produced

34
Q

Why are cystic fibrosis & hereditary pancreatitis associated w/ bad protein absorption?

A

these diseases lead to a decrease in trypsin & thus poor absorption of protein

35
Q

What is cystinuria?

A

defective transport of cysteine in the proximal renal tubule & small bowel

36
Q

What is Hartnup disease?

A

hereditary condition

lack of a few active transporters that absorb neutral amino acids

37
Q

Dietary lipids include which 4 substances?

A

phospholipids
sterols
hydrocarbons
waxes

38
Q

Are lipids absorbed in the stomach?

A

NO, except for a few short chain fatty acids

39
Q

What is the role of CCK in the digestion & absorption of lipids?

A

CCK slows gastric motility
stimulates the pancreas to secrete lipase
causes gallbladder contraction & sphincter of Oddi relaxation so that bile is released

40
Q

Absorption of lipids depends on what 4 events?

A
  1. Secretion of Bile & lipase’s
  2. emulsification
  3. hydrolysis of ester linkages
  4. solubilization via bile salt micelles
41
Q

What is emulsification?

A

So the problem is that fat droplets like each other so much…they would just congregate among themselves & never open themselves up to degradation & absorption…thus emulsification is important. The fat droplets are suspended via lecithin, bile salts, fatty acids, & other stuff. It increases the surface area of the lipids so that hydrolysis can happen.

42
Q

Why is colipase, secreted by the pancreas, important?

A

b/c bile salts inhibit lipase from getting at the fat. Colipase is secreted by the pancreas & activated by trypsin & attaches the 2 together so that hydrolysis can occur.

43
Q

How are bile salts reabsorbed?

A

they are actively reabsorbed in the distal ileum & enter into enterohepatic circulation

44
Q

What is the importance of micelles?

A

They bring fats to the enterocytes to be absorbed.

45
Q

Describe what is absorbed & the process of triglyceride resynthesis.

A

fatty acids & monoglycerides are passive absorbed @ the brush border. These go to the SER & either via monoglyceride acylation (mainly) or phosphatadic acid from triglycerides. Then they go to the Golgi & protein is added. Some other stuff may be added & chylomicrons & VLDLs are formed . These are both lipoproteins. Via vesicles they are secreted into the lacteal of the villi & into the lymphatic system.

46
Q

What are the fat soluble vitamins?

A

Vitamin A
Vitamin D3
Vitamin E
Vitamin K

47
Q

What are the water soluble vitamins?

A 
Vitamin C
Vitamin B1
Vitamin B2
Vitamin B6
Biotin
Folic Acid
48
Q

Where is Vitamin A found? How is it absorbed? What happens to it after it is absorbed?

A

Vit A found in animals & beta carotene.
It is absorbed in the SI w/ the help of a micelle. It is converted into retinal ester & formed into a chylomicron. Then it ends up in the liver.

49
Q

What happens to Vitamin D3?

A

It is absorbed into the SI. In the blood, it binds to D binding protein & it is eventually stored in various organs.

50
Q

Where is Vitamin E found? How is it absorbed? Where does it eventually go?

A

vegetable oils
It is passively absorbed.
It circulates w/ lipoproteins & erythrocytes.

51
Q

What are the 2 main sources of Vitamin K? What is each broken down into & how are they absorbed?

A 
Source #1: green vegetables
broken down into phylloquinone
actively absorbed
Source #2: gut flora
broken down into menaquinones.
passively absorbed
52
Q

How is Vitamin C absorbed?

A

It is actively absorbed in the ileum.

53
Q

How is vitamin B1 absorbed @ low conc’n & high conc’n?

A

@ low conc’n: absorbed via active carrier mediated mechanism

@ high conc’n: passive diffusion

54
Q

How is vitamin B2 aka riboflavin absorbed?

A

It is actively absorbed in the proximal small intestine.

55
Q

How is Vitamin B6 absorbed?

A

by simple diffusion in the small intestine

56
Q

How is biotin aka Vitamin B7 absorbed?

A

by Na+ dependent active transport

@ high conc’n tho: passive diffusion

57
Q

Folic acid is usu found in the body as ____. At the brush border it is further broken down into______. It is then absorbed into the enterocyte via_____.

A

found in the body as: polyglutamyl conjugates
brush border broken down to monoglutamylfolate
enters the enterocyte via facilitated transport

58
Q

What are the 3 important uses of folic acid?

A

nucleic acid formation
RBC maturation
growth promotion

59
Q

A lack of Vitamin B12 can result in _____.

A

pernicious anemia

Yikes!!

60
Q

What is the journey of vitamin B12 from consumption to tissue deposition? Once upon a time…

A

The vitamin B12 is released from dietary protein via gastric acid & pepsin.
In the stomach it binds R protein (released by saliva).
In the SI (higher pH) binds more to IF protein (released by saliva). IF protein binds an ileal receptor. this allows the vitamin to be absorbed into the SI.
Once it is in the blood it binds transcobalamin II for delivery to tissues.

61
Q

Where are water & electrolytes absorbed in the GI?

A

Mainly SI

Also colon, but only 25% of its abilities are used! Sad. Underappreciated colon!

62
Q

So like 7-10L/day of fluid is processed thru the GI…how much of that is from drink & food?

A

2 L

the rest comes from stuff secreted in the body

63
Q

How is water absorbed in GI?

A

Basically:
Na+ transport is active
water & anions follow passively

64
Q

What are the 4 models for NaCl absorption in the SI?

A

(I) Movement via restricted diffusion though water filled channels.

(ii) Co-transport of Na+ with sugars/AA’s.
(iii) Co-transport of Na+ with Cl-.
(iv) Counter-transport of Na+ for H+.

65
Q

How is NaCl absorbed in the colon?

A

restricted diffusion under the control of aldosterone
cell jcns here are less leaky
Cl- moves down an electrochemical gradient as there is a positive charge on the basolateral side
Na+ absorbed via Na/Cl cotransport
& Na+ absorbed via countertransport w/ H+
other cotransport that was present in the SI is absent here…

66
Q

What is the 3 compartment model of fluid absorption?

A
  1. ions are moved into epithelial cells & into the blood. This creates an osmotic gradient.
  2. water moves via this osmotic gradient into the intercellular space.
  3. the hydrostatic pressure of the water building up in the intercellular space causes it to be absorbed into the capillaries
67
Q

What is hemochromatosis?

A

a disease of unregulated iron absorption & subsequent iron overload
impairs organ systems
leads to: cirrhosis, diabetes, cardiomyopathy

68
Q

T/F Calcium absorption is down its electrochemical gradient.

A

False. It is up its gradient.

69
Q

T/F There are binding proteins at the brush border that help in the absorption of Ca++.

A

TRUE

70
Q

Calcium levels in the enterocytes are minimized by what?

A

CaBP in ER & Golgi

71
Q

What are the 2 main categories of iron absorption?

A

Heme Iron

Non-heme iron

72
Q

How is heme iron absorbed?

A

The heme is taken up by endocytosis in the SI. Lysoenzymes in the enterocytes break it down into free iron that is secreted into the blood.

73
Q

How is non-heme iron absorbed?

A

The enterocytes release transferrin into the lumen.
Transferrin binds Iron & forms the Transferrin-Fe complex. This complex binds to the brush border via receptors. It is absorbed & the receptors are recycled. The complex is brought to the basolateral side & somehow absorbed into the blood.

74
Q

How is iron found in the blood?

A

Most often as Fe bound to transferrin.

Sometimes bound to apoferritin, forming ferritin. I think it’s harder to release Fe from there.

75
Q

What are the 2 regulatory mechanisms for iron levels in the body?

A
  1. the regulation of the brush border receptors for the transferrin-Fe complex
  2. the amount of ferritin found in the blood. It rises as iron levels in the blood rise. Maybe a way of keeping the iron locked up from tissues to prevent iron overload???

Block 3; Week 3 Michelle (9 decks)

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