05b: Intestinal Absorption Flashcards

1
Q

T/F: Absorption of CHO, proteins, and fats is complete in upper half of small intestine.

A

True

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2
Q

The distal 1/3 of intestine is essential for absorption of:

A

Vit B12-IF complex and bile salts

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3
Q

T/F: Most water, vit/minerals absorbed in distal half of small intestine.

A

False - proximal half

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4
Q

Tight junctions throughout intestine exhibit variable permeability to (X) compounds. Where along intestine are these junctions more/less leaky?

A

X = water and ions;

More leaky at proximal small intestine and grow tighter gradually toward colon

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5
Q

The transepithelial potential difference in intestine/colon is positive on (luminal/ISF) side. Would you expect this difference to be greater in small intestine or colon?

A

ISF;

Colon (less permeable tight junctions)

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6
Q

Brunner’s glands in (X) part of GI tract secrete (acidic/neutral/alkaline) and (serous/mucous) fluid that likely serves (Y) function.

A

X = duodenum (submucosa)
Alkaline
Mucous
Y = protective

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7
Q

Most CHO we consume is in the form of (mono/di/poly)-saccharides. Which of these forms of CHO can be absorbed in small intestine?

A

Polysaccharides/starch (60%);

Only monosaccharides!

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8
Q

The enzymes that can breakdown poly/di-saccharides into monosaccharides come from/reside in (X). List some of these enzymes.

A

X = anchored in luminal membrane of enterocytes;

  1. Maltase and isomaltase
  2. Lactase
  3. Sucrase
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9
Q

T/F: Enzymes on enterocytes that break down CHO to monosaccharides all have specific substrates.

A

False - some hydrolyze more than one substrate

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10
Q

T/F: Lactase can only hydrolyze lactose.

A

True

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11
Q

T/F: Sucrase can only hydrolyze sucrose.

A

False - but sucrose can only be hydrolyzed by sucrase

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12
Q

Following normal meal, most ingested CHO is digested/absorbed in (first/middle/last) (X)% of small intestine.

A

First;

X = 20

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13
Q

Which monosaccharides share common mechanism of transport into enterocytes? Which mechanism is that?

A

Glucose and galactose;

Na-dependent co-transport (via SGLT1 carrier)

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14
Q

T/F: Glucose, galactose, and fructose compete for the same apical carrier in small intestine.

A

False - only glucose and galactose do

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15
Q

Apical uptake of fructose in small intestine is via (X) (carrier/channel) and is dependent on (ATP/Na).

A

X = GLUT5 carrier

Neither

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16
Q

Intestinal absorption: Basolateral exit of (X) monosaccharides is (up/down)-hill via (Y) (transporter/channel).

A

X = glucose, galactose, fructose
Downhill
Y = GLUT2 (facilitated transporter)

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17
Q

Some evidence shows that tight junction permeability (increases/decreases) following activation of SGLT1 transport, which is responsible for (X). What’s the function of this?

A

Increases;
X = apical transport of glucose and galactose

Allows paracellular absorption of glucose if its luminal concentration is high

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18
Q

In glucose-galactose malabsorption syndrome, (X) transport system is not functioning. What’s fed to infants with this disorder?

A

X = SGLT1 (Na-dependent, brush border sugar transport system);

Fructose

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19
Q

Oral sugar tolerance test: if patient is intolerance, (X) symptom will ensue and sugar will appear in (blood/feces).

A

X = diarrhea

Feces

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20
Q

T/F: Most protein absorption takes place in ileum.

A

False - nearly completely absorbed by the time it’s traversed the jejunum

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21
Q

T/F: Intact proteins and large peptides cannot be absorbed in intestine.

A

False - only in minute amounts via receptor-mediated endocytosis

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22
Q

T/F: Any protein leaving the stomach is in the form of peptides since no enzyme can break them down to AA.

A

False - pepsin can reduce small amount into AA/peptides

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23
Q

T/F: Small peptides are significantly more concentrated than single AAs in intestinal lumen.

A

True (about 3-4x)

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24
Q

T/F: The rate of AAs exceeds the rate of di-peptides/tri-peptides.

A

False - vice versa

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25
Q

AA transporters in small intestine are classified according to which characteristics?

A
  1. Specificity for groups of AA (neutral, acidic, etc)

2. Na- dependent/independent

26
Q

PepT1 is a(n) (X)-dependent transport system for (Y).

A
X = proton
Y = small (di/tri)-peptides
27
Q

In addition to the transporters, diffusion across (apical/basolateral) membrane is possible for small, (X) AAs.

A

Basolateral;

X = hydrophobic

28
Q

Hereditary disorders involving malfunctioning AA transporters are likely recognized by (presence/absence) of AAs in (blood/urine/feces). Why?

A

Presence;
Urine;

AA transporters defective in enterocytes also found (and defective) in renal tubule

29
Q

T/F: In AA absorption defects, malnutrition does not ensue since AAs can be absorbed in di/tri-peptide form.

A

True

30
Q

With daily ingestion of (X) volume water and GI secretion of (Y) volume fluid, how much fluid does intestine absorb each day?

A
X = 2L
Y = 7L

9 L absorbed

31
Q

List the key locations in GI tract where significant water reabsorption takes place.

A

Jejunum and (to lesser extent) ileum

32
Q

Intestinal water absorption is secondary to (X) (secretion/reabsorption). This phenomenon is referred to as (Y).

A
X = Na reabsorption
Y = standing osmotic gradient
33
Q

T/F: Water absorption in GI tract takes place only minimally through aquaporins and moreso through tight junctions.

A

False - NO aquaporins found as of yet

34
Q

List the location in GI tract where Na reabsorption rate is highest. Where along tract does Na absorption not occur?

A

Jejunum;

Na absorbed along the entire length of intestine

35
Q

Na transport across (luminal/basolateral) membrane requires Na/K ATPase in (X) part of intestine. Why is the ATPase needed?

A

Basolateral;
X = all

Na exiting is against its electrochemical potential difference (ISF is more positive than lumen)

36
Q

ENaC, aka (X), is (transporter/channel/ATPase) found in (apical/basolateral) membrane of (Y) part of GI tract. It’s responsible for:

A

X = epithelial Na channel
Apical;
Y = colon

Na absorption into colonic cells

37
Q

Na transport in colon, via (X) mechanism, is stimulated by (Y) hormone/NT.

A
X = ENaC (channel)
Y = aldosterone
38
Q

Any left-over HCO3 in intestinal lumen is reabsorbed in (X) location and involves the (secretion/absorption) of (Y).

A

X = jejunum
Secretion;
Y = H+ (to form CO2 that diffuses across membrane)

39
Q

T/F: During intestinal reabsorption of HCO3, the molecule absorbed from lumen is technically a different one than that secreted into blood.

A

True - enters cell as CO2 and then carbonic anhydrase does its thing within cell to form H and (new) HCO3

40
Q

T/F: From jejunum onward, HCO3 is only up for reabsorption.

A

False - colon normally secretes HCO3 in exchange for Cl

41
Q

Colon (secretes/absorbs) HCO3 via (trans/para)-cellular mechanism.

A

Secretes;

Transcellular (HCO3/Cl exchange)

42
Q

Large paracellular absorption of Cl occurs in (X) part of GI tract. It’s driven by:

A

X = jejunum

Electrical potential difference (set up by Na absorption)

43
Q

Feces is typically (neutral/alkaline/acidic) and has relatively high concentration of (X) ion.

A

Alkaline;

X = K

44
Q

In small intestine, K is usually (absorbed/secreted). What’s the mechanism and driving force?

A

Absorbed (lumen to blood);

Paracellular diffusion; lots of water reabsorbed raises K conc in lumen

45
Q

In the colon, K is normally (absorbed/secreted) in (para/trans)-cellular manner.

A

Secreted;

Both

46
Q

In disease like cholera, the toxin (activates/inhibits) (X), leading to increased intestinal (absorption/secretion) and (Y) symptom.

A
Activates;
X = AC (irreversibly)
Massive secretion (of electrolytes and water);
Y = diarrhea
47
Q

Mechanism for Ca absorption in intestine depends on level of (X). What are the two potential mechanisms?

A

X = intake;

  1. Paracellular (ileum; adequate intake)
  2. Transcellular (duodenum; low intake)
48
Q

Transcellular absorption of Ca: entry into cell is (uphill/downhill) via (X) (channel/transporter/ATPase).

A

Downhill;

X = Ca channel (TRPV 6)

49
Q

T/F: Ca absorption in small intestine depends on voltage-sensitive Ca channel (TRPV 6).

A

False - it’s voltage-insensitive

50
Q

Transcellular absorption of Ca: which step is rate-limiting? This step requires (X).

A

Intracellular diffusion;

X = calbindin (Ca-binding protein)

51
Q

Transcellular absorption of Ca: exit from basolateral membrane involves (X) (channel/transporter/ATPase).

A

X = Ca ATPase and Na/Ca exchange

52
Q

How does Vitamin D play role in enhancing (X) mineral (absorption/secretion)?

A

X = Ca absorption;

Increase synthesis of calbindin and Ca ATPase

53
Q

(X) absorption is tightly regulated because it can have deleterious effects. Further, it’s sequestered by proteins: (Y) in plasma and (Z) in cells.

A
X = Fe
Y = transferrin
Z = ferritin
54
Q

Most Fe absorption takes place in (X) portion of GI tract, where (Y) enzyme on surface of cells makes it more soluble by:

A
X = upper duodenum
Y = ferrireductase (on brush border)

Reducing Fe3+ to Fe2+ (more soluble)

55
Q

Fe absorption: Free (ferrous/ferric) ion crosses apical membrane via (X).

A

Ferrous;

X = Divalent Metal Transporter (DMT1)

56
Q

Fe absorption: some (ferrous/ferric) ions can be absorbed while bound to (X). How are they freed intracellularly?

A

Ferrous;
X = heme

Heme oxygenase frees ion

57
Q

Fe that is lost in the feces is (free/bound). Elaborate.

A

Bound to ferritin;

This binding occurs in enterocytes and is near irreversible

58
Q

Calbindin is to Ca what (X) is to Fe.

A

X = mobilferrin

59
Q

Fe absorption: upon exit through basolateral membrane via (X), Fe undergoes which changes for transport into blood?

A

X = ferroportin

Oxidized to ferric ion (via ferroxidase) and incorporated into plasma transferrin

60
Q

Apoferritin, produced by (X) cells, (increases/decreases) when Fe stores are abundant.

A

X = mucosal

Increases (binds more Fe so more Fe lost in feces)

61
Q

(X) is a peptide released by liver that (increases/decreases) Fe absorption via which mechanism?

A

X = hepcidin
Decreases;

Initiates internalization/degradation of basolat ferroportin transporter

62
Q

List the three main mechanisms that regulate Fe absorption.

A
  1. Apoferritin levels
  2. Hepcidin
  3. Hypoxia inducible transcription factor