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GIGU Midterm > Digestion and Absorption in the GI Tract > Flashcards

Digestion and Absorption in the GI Tract Flashcards

1
Q

What causes lactose intolerance?

A

when the brush border lactase enzyme activity is deficient or absent, which results in undigested and unabsorbed lactose

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2
Q

what happens when lactose is unabsorbed?

A

it is converted to SCFAs and hydrogen gas in the SI; it remains in the lumen

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3
Q

how do you get osmotic diarrhea with lactose intolerance?

A

the lactose remains in the lumen and holds H20 in the lumen as well and that is what causes the osmotic diarrhea

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4
Q

what does the lactose ferments into?

A

methane and H+ gas

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5
Q

what breaks down starches in the mouth?

A

salivary amylase

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6
Q

what is starch broken down into?

A

maltose and then the maltose is broken into glucose

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7
Q

where does most of the starch breakdown occur?

A

in the small intestine

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8
Q

what breaks down the starch in the small intestine?

A

pancreatic amylase

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9
Q

the lumen surface of the small intestine is arranged in longitudinal folds known as what?

A

folds of Kerckring

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10
Q

where are villi longest?

A

in the duodenum

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11
Q

what is lactose normally broken down into?

A

glucose and galactose

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12
Q

how does glucose and galactose get into the epithelial cell of the SI duodenum from the lumen?

A

through the SGLT1 co-transporter- secondary active transporter

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13
Q

how does fructose get into the epithelial cells of the SI duodenum?

A

through the GLUT5 transporter- facilitated diffusion

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14
Q

how does glucose, galactose, and fructose get into the blood?

A

GLUT2 transporter (facilitated transport)

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15
Q

what could be used to reduce glucose absorption into the epithelial cell?

A

sotagliflozin

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16
Q

how can you test for a carbohydrate assimilation disorder (global)?

A

you can administer D-xylose- it should be in the urine; if you have an absorption issue and you aren’t absorbing the sugars, the d-xylose will not be absorbed- it will go through the SI and end up in the feces

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17
Q

how can you test for a specific sugar enzyme deficiency?

A

you can use a hydrogen breath test

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18
Q

what are the five protein assimilation disorders we discussed?

A

chronic pancreatitis, congenital trypsin absence, cystinuria, hartnup disease, and cystic fibrosis

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19
Q

what does chronic pancreatitis lead to?

A

deficiency of pancreatic enzymes (lack of proteases e.g. trypsinogen)

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20
Q

what does congenital trypsin absence lead to?

A

the absence of all pancreatic enzymes

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21
Q

why does congenital trypsin absence lead to the absence of all pancreatic enzymes?

A

pancreatic enzymes are secreted as zymogens and activated by either enterokinase (aka TRYPSINOGEN) or trypsin itself

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22
Q

what is defected in cystinuria?

A

SLC3A1 or SLC7A9

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23
Q

what is a sign of cystinuria?

A

AA secreted into the feces or urine

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24
Q

what are three important symptoms of hartnup disease?

A

3 Ds: diarrhea, dermatitis, and dementia

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25
Q

what results will you see with Hartnup’s disease?

A

they will have urinary excretion of tryptophan

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26
Q

what are some CFTR mutations associated with?

A

loss of HCO3- secretion; therefore they can’t move enzymes from the ducts, acute or chronic pancreatitis

27
Q

what are the brush border enzymes that break down proteins?

A

aminopolypeptidase and dipeptidases

28
Q

how are amino acids transported into the epithelial cell of the small intestine from the lumen?

A

Na+-AA cotransporter

29
Q

how are dipeptides and tripeptides transported into the epithelial cell of the small intestine from the lumen?

A

H+ dependent cotransporter

30
Q

once inside the epithelial cell of the small intestine, what happens to most of the di-/tri- peptides?

A

they are hydrolyzed to amino acids by peptidase

31
Q

how do the amino acids get out of the epithelial cell of the small intestine into the blood?

A

via facilitated diffusion (separate for each amino acid)

32
Q

what does celiac sprue/ disease lead to?

A

the destruction of small intestine villi (atrophy) and hyperplasia of the intestinal crypts

33
Q

what are the common malabsorption deficiencies associated with celiac’s?

A

folate, iron, calcium, and vitamins A B12 and D

34
Q

what is tropical sprue and what is it caused by?

A

it is a loss or decreased number of intestinal epithelial cells; intestinal infection

35
Q

what are the nutritional deficiencies associated with tropical sprue?

A

folate and vitamin B12

36
Q

what is the major symptom of tropical sprue?

A

diarrhea

37
Q

how do you treat tropical sprue?

A

tetracycline and folate for 6 months

38
Q

what is the digestion of lipids complicated by?

A

their insolubility

39
Q

what is the effect of CCK on the stomach?

A

it inhibits gastric emptying

40
Q

where does most of the digestion of lipids occur?

A

in the small intestine

41
Q

what is pancreatic lipase inactivated by?

A

by bile salts

42
Q

what is needed to reactivate the pancreatic lipase?

A

colipase (which is activated by trypsin)

43
Q

once the fatty acids are are emulsified by the micelle, how do they get into the epithelial cell of the small intestine from the apical membrane?

A

there is diffusion of the micellar content across the apical membrane

44
Q

what happens to the products of lipid digestion once inside the intestinal epithelial cells?

A

they are reesterified

45
Q

Inside the epithelial cells of the small intestine, what are the reesterified lipids packaged with and what do these form?

A

they are packaged with apoproteins and form chylomicrons

46
Q

failure to synthesize Apo B leads to what?

A

abetalipoproteinemia, aka no lipid absorption

47
Q

what happens to the chylomicrons?

A

they are exocytosed into the lymphatics

48
Q

problems anywhere along the path of lipid digestion/absorption leads to what?

A

steatorrhea

49
Q

What could lead to problems with lipid digestion/absorption? associated with pancreatic enzyme secretion

A

pancreatitis, pancreatic insufficiency, or zollinger-ellison syndrome (improper acidity in the duodenum contents)

50
Q

what are two main causes of SIBO?

A

too little gastric secretion and small intestine dysmotility

51
Q

what effect does SIBO have on bile salts?

A

they deconjugate them, so they will not be able to emulsify lipids/micelle formation, leads to lipid digestion/absorption issues

52
Q

how can you diagnose SIBO?

A

use a breath test and test for methane and hydrogen

53
Q

what are the water-soluble vitamins?

A

b vitamins and vitamin C

54
Q

when does intrinsic factor bind to the vitamin b12?

A

not until the small intestine (ileum)

55
Q

what are the symptoms of a vitamin B12 deficiency?

A

pernicious anemia, weakness, and nerve conductance issues

56
Q

what is the common cause of pernicious anemia?

A

atrophic gastritis

57
Q

what does vitamin d deficiency result in?

A

inadequate calcium absorption

58
Q

how does Fe2+ get out of the enterocyte/ where is the regulation at?

A

through ferroportin

59
Q

what is the absorption like in the jejunum?

A

lots of sodium is absorbed

60
Q

what is the absorption like in the ileum?

A

sodium is absorbed and HCO3- is secreted

61
Q

what is the absorption/secretion like in the colon?

A

Na absorption and K secretion

62
Q

what is the effect of cholera?

A

it increases cAMP, which results in increased Cl- secretion

63
Q

in cholera, what does the resulting Cl- secretion accompanied by?

A

secretion of Na+ and H20

64
Q

what does cholera lead to?

A

massive secretory diarrhea–> look for chloride

GIGU Midterm (19 decks)

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