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GI part 2 > Digestion and absorption of fluids and electrolytes > Flashcards

Digestion and absorption of fluids and electrolytes Flashcards

1
Q

Net ion movement

A

Difference between movement:
From lumen into blood
From blood into lumen

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2
Q

Segmental heterogeneity

A

differences in transport along the length of the intestines

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3
Q

Surface heterogeneity

A

differences in transport from the top of a villus to bottom of a crypt

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4
Q

cellular heterogeneity

A

differences in transport mechanisms in different cells within the same villus/ crypt

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5
Q

Small intestine absorption and secretion

A

net absorption of Na, Cl, and K

net secretion of HCO-3

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6
Q

Large intestine absorption and secretion

A

Net absorption of Na and Cl

Net secretion of K and HCO-3

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7
Q

Intestinal epithelial cells are polar

A

contain an apical and basolateral surfaces

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8
Q

transcellular movement

A

solute crosses two membranes in series

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9
Q

Paracellular movement

A

solute moves passively between epithelial cells through tight junctions
mucosal resistance is dependent on paracellular resistance which is a function of tight junction permeability and depends on tight junction structure
Overall, resistance increases as you move away from the mouth
Overall, resistance increases as you move down the crypt

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10
Q

resistance changes in paracellular movement

A

Overall, resistance increases as you move away from the mouth
Overall, resistance increases as you move down the crypt

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11
Q

actions and examples of secretagogues

A 
Induce secretion 
Agonists
Increase second messengers
Bacterial toxins
Hormones and Neurotransmitters
Immune regulatory products
Laxatives
Bile acids
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12
Q

actions and examples of absorptagogues

A 
Induce absorption
neural, endocrine or paracrine factors
few agonists 
Mineralocorticoids
Glucocorticoids
Somatostatin
Norepinephrine
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13
Q

Osmotic diarrhea

A

Osmotic Diarrhea
Dietary component that is not absorbed
Ex. lactose intolerance

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14
Q

Secretory diarrhea

A

Secretion of fluid and electrolytes from the intestine
Induced by secretagogues
Enterotoxins from bacteria
Increase second messengers
Does not affect Na+ absorption, therefore, administration of Oral Rehydration Solution, enriched with Na+ and Glucose reverses secretory diarrhea

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15
Q

Sodium absorption

A

Most absorbed by:
Villous epithelium of small intestine
Surface epithelium of large intestine
Na,K-ATPase (pump)
All transcellular Na+ transport is mediated by this pump which moves Na+ across the basolateral membrane
Results in low intracellular Na+ concentrations
Gradient used as a driving force for Na+ entry and other molecules through the gradient, Na+ channels or coupled channels

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16
Q

Nutrient-coupled Na+ transport

A

Secondary active transport
Couples uphill movement of nutrients with downhill (energetically favorable) movement of Na+
Increases intracellular [Na+] which thereby increases Na+ being pumped across the basolateral membrane into blood
Electrogenic process
Makes lumen more negative which can be driving force for Cl-
Only type of Na+ transport not inhibited by cAMP or cAMP agonists
I.e. No Inhibition by E. coli or cholera enterotoxin

Glucose coupled Na+ transport
Na/glucose cotransporter SGLT1
Apical membrane transport

Amino acid coupled Na+ transport
Na/amino acid cotransporters
Apical membrane transport
Each specific for different classes of amino acids

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17
Q

What is the only type of Na transport not inhibited by cAMP or cAMP agonists?

A

nutrient-coupled

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18
Q

Na-H Exchanger (NHE3)

A

Couples Na+ uptake to proton (H+) extrusion into intestinal lumen
Increases intracellular pH
Decreases luminal pH
Stimulated by secretion of HCO-3 in the duodenum, pancreas and bile
Driven by intracellular [Na+]
Present throughout intestine
Present in proximal small intestine without Cl-HCO3 exchanger
Stimulated by [HCO-3] here alone

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19
Q

Electroneutral NaCl Absorption (NHE3)

A

Parallel apical membrane exchangers coupled through pH
- Na-H
- Cl-HCO3
Primary method of Na absorption between meals
Does not contribute to post meal absorption (nutrient coupled)
Ileum and throughout large intestine
Clinical relevance of NHE3:
Decreasing NaCl absorption important in pathogenesis of diarrhea
E. coli induced traveler’s diarrhea activates cAMP
Inhibited by
cAMP and cGMP
increasing intracellular calcium

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20
Q

Electrogenic Na Absorption (ENaC)

A

Epithelial Na+ channels on apical surface
Highly specific
Very distal colon where Na+ can be absorbed against large gradients
Important in Na+ conservation
Enhanced by aldosterone
Just like kidneys, an aldosterone responsive epithelial tissue
Dependent upon gradient created by Na-K pump on basolateral surface

21
Q

Chloride absorption is often coupled to

A

Often coupled to Na+ absorption through intracellular gradient

22
Q

Passive transport of chloride

A

Voltage dependent Cl- absorption
Cl- absorption is driven by either
Nutrient coupled Na+ absorption in the small intestine
Creates a lumen negative potential difference
Paracellular
Electrogenic Na+ absorption in the distal colon
Creates lumen negative potential difference
Remember: Both are dependent on Na-K pumps in the basolateral membrane.

23
Q

Active transport of chloride: CL-HCO3 Exchanger (DRA)

A 
Apical surface
One Cl- brought in from lumen and one HCO3- extruded from cell
Villous cells of ileum 
Surface epithelium of large intestine
DRA Exchanger
Down-regulated in adenoma
Congenital Cl- Diarrhea
24
Q

Congenital Cl- diarrhea

A 
absence of Cl-HCO3
extremely high [Cl-] in stool
high plasma [HCO3-]
Alkalotic
Cl- exchangers in blood cells and renal tubules unaffected ( different gene)
25
Q

Chloride secretion (CFTR)

A

Promotes Na+ secretion resulting in NaCl secretion
Important in the pathogenesis of diarrhea
Basal state of secretion is low or 0
Requires activation by secretagogues (Ca2+ or cAMP)
Requires 3 basolateral membrane transporters
Na-K pump
lowers intracellular [Na+]
driving force for Cl- entering through Na/K/Cl cotransporter
Na/K/Cl cotransporter
Increases intracellular [Cl-]
K+ channels
Apical membrane
Cystic fibrosis transmembrane regulator (CFTR)
Cl- channel

26
Q

K+ absorption happens where?

A

small intestine

27
Q

K+ passive transport

A

Solvent Drag
Paracellular
Pulled through tight junctions via the movement of water

28
Q

K+ Active transport

A 
only in distal colon
Transcellular
K+ homeostasis
Apical
H-K pump
Pumps H+ into lumen
Basolateral 
Na-K pump
29
Q

K+ secretion happens where?

A

large intestine

30
Q

Passive K+ secretion

A 
Passive K+ Secretion
Predominant route
Driven by negative lumen (-15 to -25 mV)
Paracellular
Most in distal colon
Dehydration
Results in aldosterone secretion
makes lumen negative (Na+ absorption) inducing passive K+ secretion
31
Q

Active K+ Secretion

A 
Throughout colon
Basally low
Activated by aldosterone and cAMP
Pump-leak model
Basolateral membrane
Na/K pump
Creates low intracellular [Na+] which drives the cotransporter
Na/K/Cl cotransporter
Brings in K+ for secretion and Na+ to drive pump
K+ Channel
Contributes to K+ recycling
Apical membrane
K+ Channel
32
Q

Calcium absorption: active

A

transcellular
Only in duodenum
Small surface area and high speed of flow reduces uptake
Villous Epithelial Cells
Under control of Vitamin D (Influences all steps, Induces synthesis of Calbindin)

33
Q

Process of calcium active absorption

A 
1) Uptake through Ca2+ Channels 
Moves across apical membrane
Driven by the electrochemical gradient
2) Binding to Calbindin
Intracellular, cytosolic protein which buffers Ca2+
3) Extrusion through Ca2+ Pumps and Na-Ca Exchanger
Moves across basolateral membrane
Into interstitial fluid
34
Q

Passive paracellular uptake of calcium absorption

A 
Higher concentration than active uptake
Not under the influence of Vitamin D
Throughout small intestine
Jejunum and Ileum
Enhanced by low plasma concentration
Lactation
35
Q

Iron exists as

A

Ferric (Fe3+)

Ferrous (Fe2+)

36
Q

Vitamin C

A

Ascorbic Acid (Vitamin C)

  • Complexes with Iron
  • Reduces Iron from ferric to ferrous
  • Increases absorption

note: vitamin c needs to be in the GI tract at the same time as the iron in order to be able to do this

37
Q

Iron dysregulation

A 
Results in:
Anemia
Iron depletion
Hemochromatosis
Iron overload
Hereditary Hemochromatosis (HH)
Body absorbs excess iron
Women less susceptible to damage due to menstruation
38
Q

Excess iron becoming toxic in liver

A 
Results in:
Cirrhosis
Hepatomas
Pancreatic Damage
Bronze pigmentation
Pituitary and Gonadal failure
Arthritis
Cardiomyopathy

Detection:
Elevated iron and transferrin saturation
Elevated ferritin
Liver biopsy

Treatment:
Remove blood from patient (phlebotomize) every few months to normalize iron and ferritin.

39
Q

Heme Iron

A

Absorbed more efficiently
Active Transcellular Transport Only:
- Occurs only in duodenum
- Binds brush border protein
- Endocytotic mechanism
Transported to cytoplasm
Heme oxygenase
Releases free Fe3+
Enterocyte reduces Fe3+ to Fe2+
Then handled the same as free iron (see below

40
Q

Nonheme Iron

A
  • Absorbed less efficiently
    Exists as either ferric or ferrous iron
    -Active Transcellular Transport Only
    Occurs only in duodenum
41
Q

Active transcellular iron transport: divalent metal transporter

A 
Cotransports Fe2+ and H+ into cytoplasm
Inward directed H+ gradient
Not specific for Iron
Many divalent metals including toxic (Cd2+, Pb2+)
Not Ferric iron
Ferric Reductase Dcytb
Reduces ferric iron to ferrous iron
Cytochrome
Apical extracellular surface
Required for uptake in DMT1
42
Q

Active transcellular iron transport: mobilferrin

A

binds Fe2+ in cytoplasm

Carries Fe2+ to the basolateral membrane

43
Q

Ferroportin transporter (FP1)

A

Translocates Fe2+ across basolateral membrane

44
Q

When Fe2+ reachs the interstitial fluid:

A

oxidized Fe2+ to Fe3+
Facilitates binding to
Transferrin
Carries through plasma

45
Q

When Fe3+ reaches the blood

A

Bound to transferrin

Stored in liver and reticuloendothelial system

46
Q

which ions are affectors of diarrhea

A

Na and Cl-

47
Q

Cholera mechanism of action

A 
Cholera toxin binds apical receptors on crypt cells.
Results in an increase of cAMP
Results in secretion of Cl- by CFTR
Na2+ and H2O follow Cl- into lumen
Na2+ absorption inhibited by cAMP
Result: Secretory Diarrhea
48
Q

Oral rehydration solution

A

on the fact that nutrient coupled-Na2+ absorption is not inhibited by cAMP stimulating secretagogues.
Therefore, increasing glucose and/or amino acid concentrations in the lumen increases Na2+ reuptake.
This increases intracellular [Na+] which is necessary for Na,K-ATPase function.
Na,K-ATPase function is necessary for K+ and Cl- absorption as well.
Solution contains varying concentrations of glucose, Na2+, Cl- and HCO3-
Reverses dehydration and metabolic acidosis which were significant causes of mortality in the past.
Direct result of research in nutrient coupled-Na2+ absorption.

GI part 2 (16 decks)

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