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GI2 > Digestion and Absorption > Flashcards

Digestion and Absorption Flashcards

1
Q

basis of absorption of the nutrients?

where does it occur mostly?

A

maximizing the amount of surface area in longitudinal folds called “folds of kerckring”

duodenum and then to the jejunum but less and less as it goes along

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2
Q

What is the brush border?

A

site of activity of digestive enzymes.

if it’s going to be absorbed it needs to make it through the unstirred layer as well as through the brush border.
so its a barrier that must be transversed to be absorbed.

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3
Q

What are enterocytes?

turnover rate? what is this good for?

A

enterocytes (epithelial cells)= digestion, absorption, and secretion…

3-6 days

susceptible to irradiation and chemo

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4
Q

What are goblet cells?

Paneth cells?

A

mucus producing

part of mucosal defenses against infection –> there on the brush border that destroy bacteria or produce inflammatory response to prevent anything from coming over.

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5
Q

What are the routes of passage into enterocytes?

4 ways

A

Pinocytosis –> reach out and pinch off some plasma membrane so the contents in the lumen can be pulled in.

this is the major uptake of PROTEIN AND FATS!

passive diffusion through pores

facilitated diffusion and active transport by membrane transporters

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6
Q

What are the different barriers that solutes have to move through from lumen to blood?

A

unstirred layer of fluid (stagnant, along the brush border.. not necessarily has a function)

glycocalyx

apical membrane

cytoplasm of the cell

basolateral membrane

basement membrane

wall of blood capillary/wall of lymphatic vessel.

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7
Q

What happens ff we remove the ileum? what about for adaptability?

what if there are genetic abnormalities?

A

bile acids and vitamin B12 are going to be problems here! you can adapt but still its hard

you’re pretty much screwed.. loss of adaptability. (lactase deficiency)..

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8
Q

What are the primary sugars?

A

sucrose, lactose, starch

they make it to the stomach.. starch becomes maltose, and then both the starch and maltose can move on down.

when the starch keeps moving down to the duodenum it’ll be made heavily into maltose by pancreatic amylase

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9
Q

What are the secondary sugars?

A

stuff from the food industry.

sorbitol

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10
Q

d-xylose.. what is it used for?

what is the levels you should see in the urine that is normal?

A

you can use this for absorption issues. absorbed by the small intestine but the body doesn’t know what to do with it so it’ll be excreted. so you know exactly what you put in and how much comes out.

it’s absorbed by both Na+ cotransporter (much like glucose and galactose) and by passive diffusion.

5 hours later you’re seeing how much made it into the urine.. if it’s more than 4 grams, you’re good.

less than 4? you have an absorptive problem.

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11
Q

what do we not have digestive enzymes for?

A

cellulose

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12
Q

What are the locations and what happens to breaking down carbohydrates?

what enzymes are in what?

A

starts in the mouth. salivary amylase breaks stuff down into manageable sugars.

pancreatic amylase in the small intestine breaks down more starch here into maltose.

the small intestine will also have brush border enzymes, maltase, sucrase, lactase and break them down into monosaccharides… glucose, fructose, and galactose!

These are what’s going to be absorbed.

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13
Q

Maltose breaks down to what?

Trehalose?

Lactose?

Sucrose?

A

glucose + glucose

glucose + glucose

glucose + galactose

glucose + Fructose

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14
Q

how is carbohydrate absorption happening?

where does galactose and glucose go to get into the epithelial cell of the small intestine?

what are they trying to block now in diabetic patients?

where does fructose go?

where are these transporters located?

A

you have the sodium potassium ATPase creating the gradient, but you have your glucose and galactose coming in via SGLT1… it does this by using the concentration gradient of Na as it’s being shoved out from the ATPase so it’s helping by going down its concentration gradient.

(SGLT1 is trying to be blocked!

Fructose comes in via GLUT5!

these are located on the luminal side!!

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15
Q

How do we get glucose, galactose, and fructose from the epithelial cell to the blood?

A

via Glut2 receptors (through facilitated diffusion)

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16
Q

Lactose intolerance is because of what?

what happens?

A

you’re missing this brush border enzyme Lactase!

remains in the lumen, holds H2O in the lumen, and you have OSMOTIC DIARRHEA happen.

huge amount of bloating, discomfort, diarrhea.

bacteria takes this leftover sugar and ferment it to methane production.

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17
Q

Does protein digestion take place in the mouth?

what happens when protein gets into the stomach, what are the different enzyme classes and how do they work?

A

any digestion of proteins in the mouth.. no!

you’re breaking down a big string of amino acids.

endopeptidases hydrolyze the interior bonds.. breaking the long strands of polypeptides to something more manageable for the exopeptidase.

exopeptidase hydrolyze one amino acid at the time from the carboxyl end!

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18
Q

What are examples of endopeptidases.. which one is made in the stomach? where are the other ones made?

A

Pepsin, trypsin, chymotrypsin, elastase

Pepsin

the rest in the pancreas in an inactive form!

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19
Q

what does CCK do to acinar cells?

A

tell it to make more enzymes for secretion

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20
Q

Stomach enzymatic breakdown only involves Pepsin… what pH is it activated?

how much protein breakdown is it doing?

if we lose pepsin, will we survive?

A

2-3

10-20%

yes, it’s not essential for protein digestion

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21
Q

Pancreas does what for protein breakdown?

what do we see that breaks stuff down into small polypeptides?

what from the pancreas breaks aa’s off of the polypeptide carboxyl ends?

A

mostly breaks down proteins into di- and tripeptides through trypsin, chymotrypsin, carboxypeptidase, and elastase.

trypsin and chymotrypsin break it d own to the polypeptides.

carboxypeptidase A and B cleaves the AA at the carboxyl ends.

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22
Q

in the small intestine, what enzymes are seen?

A

aminopolypeptidase, dipeptidases (some others)

amino acids then are absorbed into the enterocytes.

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23
Q

Recall that all of these enzymes (trypsinogen, chymotrypsinogen, proelastase, procarboxypeptidase A and B) are all in zymogen form.. what turns them into their functional selves?

how is it secreted?

A

Trypsin!!

it’s secreted in its inactive form, trypsinogen.. the enterokinase (brush border enzyme) that changes it to trypsin!

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24
Q

How are proteins absorbed into the epithelial cells?

how is the gradient maintained?

A

through 4 different co-transporters for each amino acid type… neutral, acidic, basic, Imino… these all use SODIUM AS SODIUM COTRANSPORTERS

just like the rest… Na/K ATPases

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25
Q

what’s good to know about proteins and amino acids into the enterocyte?

A

we don’t strictly take up amino acids.. we also take up dipeptides and tripeptides via pinocytosis and cotransporters.

H+ cotransporters!

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26
Q

What happens if there are dipeptides and tripeptides in the epithelial cells?

A

they can either diffuse out or they can be broken down by peptidases and shuttled out via the same property type amino acids that are on the lumen side.

27
Q

Chronic pancreatitis?

A

deficiency in pancreatic enzymes – lack of proteases (i.e. trypsinogen)

28
Q

Congenital Trypsin absence?

2 types of thought for this?

A

absence of trypsin.. all pancreatic enzymes are gone because you need trypsin to activate ALL zymogens!

there maybe trypsin, but maybe an absence of enterokinase.. so we have trypsinogen but it can never be made into trypsin.

29
Q

Cystinuria?

A

defect in or absence of Na/amino acid cotransporters.

di-basic AA transporter is absent so no cysteine, lysine, arginine, ornithine.

so these AAs are appearing in the feces and urine.

blood in the urine, cysteine crystals are present too

30
Q

Hartnup disease?

mnemonic?

what causes pellagra? what kind of deficiency? why is this deficient?

why do people present with neurological problems?

other notable symptoms?

A 
H
Autosomal
Recessive
Tryptophan
Neutral
nUetral
Pellegra (dementia, diarrhea, dermatitis)

niacin – precursor for serotonin, hence why neurological defects, and tryptophan is a necessary cofactor for niacin development!

cannot absorb neutral AA’s!

symptoms are red, scaly skin, photosensitivity, short stature.. high neutral AAs in the urine.

31
Q

Cystic fibrosis?

A

CFTR - regulated Cl channel is no longer helping to secrete bicarbonate so it can’t neutralize acid.. it disrupts the entire process and you can’t move enzymes from the ducts.. so it leads to acute and chronic pancreatitis.

you often see fat in the stool

32
Q

Why is fat digestion kind of strange?

what deals with it?

A

fat is insoluble. (triglycerides, diglyclerides, monoglycerides, fatty acids, cholesterol esters, phospholipids)

bile salts and lecithin emulsify fat products into micelles.

33
Q

How much fat is broken down in the stomach?

how is it broken down?

A

10%

lingual and gastric lipase

once we get down to the stomach, not much is happening.

34
Q

What happens to fat digestion in the small intestine?

what 3 enzymes are there?

A

Pancreatic lipase is secreted as an active enzyme.. but it needs Colipase (which is activated by trypisin) because it’s a coenzyme.

collapse binds to pancreatic lipase (and displaces bile salts in the process) in order to fully activate pancreatic lipase..

Cholesterol Ester Hydrolase catalyzes production of free cholesterol, and hydrolyzes triacylglycerides to glycerol

phospholipase A2 (secreted as proenzyme, activated by trypsin) –> phospholipid breakdown

35
Q

what keeps pancreatic lipase inactive?

A

bile salts without collapse

36
Q

Of the 3 enzymes in the small intestine used to digest lipids, which one needs to be activated by trypsin to work correctly?

A

Phospholipase A2

37
Q

how is fat absorbed into the enterocyte?

A

you take the things you’ve broken down by the lipases in the small intestine and package it into the micelles.

when it reaches the membrane there’s some pinocytosis and you leave behind the bile salts and we’re absorbing this stuff through passive diffusion.

38
Q

once the fats are in the enterocyte, then what happens?

A

you do re-esterification.. you put the fatty acids back together and package these chylomicrons

the chylomicrons are the circulatory transporters that are exocytosed into the lymphatics!

in order to package this, you have these proteins that identify what they are..

39
Q

What happens if you have ApoB?

A

abetalipoproteinemia.. which means no lipid absorption

everything backs up in the enterocyte. so you don’t have any absorption of the fats into the lipids!!

40
Q

Fat in the stools, fowl smelling stools, or what.. what are you thinking?

A

can’t absorb fat… steatorrhea

41
Q

What can cause problems with fat digestion? (diseases and problems)

A

Pancreatic insufficiency = can’t secrete pancreatic enzymes to digest and break down the fats

Zollinger Ellison Syndrome

Pancreatitis

42
Q

What is Zollinger ellison syndrome?

A

gastrin secreting tumor of pancreas.. increased amount of H+ secretion by gastric parietal.

too much acid doesn’t allow for proper activation of enzymes

43
Q

pancreatitis?

what happens?

A

trypsin (or other pancreatic enzymes) becomes activated and self-digest the pancreas.

impaired HCO3 and enzyme secretions

44
Q

what can cause deficits in the bile salts?

A

not making enough bile acids –> no micelle formation –> no solubilization of lipids that you’ve consumed

ileal resection –> loss of enterohepatic recirculation of bile salts

small intestinal bacterial overgrowth (SIBO) –> this interferes with bacteria because bacteria deconjugate the bile salts, impairing the micelle formation

severe overgrowth damages the mucosa

45
Q

how does SIBO happen?

A

too little gastric secretion and small intestine dysmotility

46
Q

What is tropical sprue?

what’s the cause?

what do you have a reduced number of?

what does this cause?

symptoms

A

loss or decreased number of intestinal epithelial cells…

so you have a lower microvilli surface area!

lipid absorption impaired due to loss of these cells (steatorrhea), also folate and vitamin B12 deficiency (also ADEK because they’re fat soluble and packaged too)

diarrhea

47
Q

What is Celiac Sprue (disease)

A

autoimmune disorder

antibodies develop against gluten component (gliadin)

leads to destruction of small intestine villi and hyperplasia of intestinal crypts.

folate, B12, calcium, ADEK stuff

48
Q

SIBO… how do they test for it?

one more time, why does it cause malabsorption

A

they do a breath test for methane and hydrogen because an overgrowth changes the composition in the gut… also it changes the pH in the which means less activity of lipase enzymes.

49
Q

Fat soluble vitamins?

water soluble vitamins?

A

ADEK

B + C

50
Q

b12 deficiency creates what?

why does it do that?

A

Pernicious Anemia

B12 is needed for development of red blood cells, so not having it will cause anemia (megaloblastic and microcytic anemia)

51
Q

what can cause vitamin B12

A

inflammation destroys parietal or an autoimmune attack on parietal cells

52
Q

What is Gastrectomy? what does this do to the parietal cells?

What about a gastric bypass?

A

loss of parietal cells (source of IF)

exclusion of the stomach, duodenum, and proximal jejunum which alters the absorption of vitamin B12

53
Q

take-home of calcium?

what helps shove calcium into the bloodstream from the intestines?

where is the main regulator found?

A

calcium absorption depends on the presence of Vitamin D!

calcitriol and parathyroid hormone facilitate the calcium and phosphate.

small intestine uses vitamin D-dependent Ca2+ binding protein CALBINDIN

if you have more levels of vitamin D, this protein will work better and help shove calcium into the enterocyte and into the blood stream.

54
Q

What are the vitamin D absorption deficiency?

explain the process of how Vitamin D is created and works the way it does because of how it’s created.

what happens if it doesn’t work?

A

Rickets or Osteomalacia (in adults)

lack of sunlight and diet.

vitamin D and then synthesizing it to 25-hydroxy vitamin D and then converting it to its active form in the kidney (so the liver and kidney are essential)…

so if you’re not getting enough in the diet or sun exposure you won’t have enough of the active form of vitamin D, which will reduce calcium absorption, which is why you get these disease.s.

55
Q

How is iron absorbed?

A

the liver secretes apotransferrin into the bile, and it enters the duodenum..

the apotransferrin binds with free iron and with hemoglobin (forming transferrin)

this then binds to receptors and the heme molecule goes through, processed through the lysosome, which shoots out reduced iron, which is shuttled out into the bloodstream and bind with transferrin to circulate.

free iron then can be converted by a reductase and absorbed through DMT1… and the iron in the enterocyte can be stored or taken into the circulation which then can be stored in the liver.

56
Q

what happens to free iron that makes it to the enterocytes?

what facilitates the process?

A

it can be absorbed

Vitamin C.

57
Q

where is calcium absorbed?

A

basically everywhere

58
Q

where is water absorbed usually?

A

the colon, almost exclusively

59
Q

flat mucosal surface (flattening of the villi).. what is it?

A

celiac sprue (celiac disease)

elevated stools.

60
Q

Celiac disease causes steatorrhea.. why?

A

reduced surface area available for absorption

61
Q

result of steatorrhea.. what kind of vitamins would be deficient?

A

A,D,E,K

62
Q

what is riboflavin?

niacin?

A

B2

B3

63
Q

impaired of what would be responsible for bruising?

A

Vitamin K = platelet

GI2 (20 decks)

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