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GI test 2 > Digestion of Fluids and Electrolytes > Flashcards

Digestion of Fluids and Electrolytes Flashcards

1
Q

fluid movement through intestines

A

majority of fluid comes from secretions in the small and large intestines. Only 1/4 of fluid comes from food. The large intestine reabsorbs almost all of the fluid that it receives.

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2
Q

Small intestine

A

net absorption of Na+, Cl- and K+

net secretion of HCO3-

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3
Q

Large intestine

A

net absorption of Na+ and Cl-

Net secretion of K+ and HCO3-

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4
Q

epithelial cells: apical vs. basolateral surface?

A

apical surface: faces intestinal lumen (has Na+/glucose symporter)

basolateral surface: in contact with interstitium, adds solutes to lymph and blood. (through GLUT2, gradient established by Na+/K+ ATPase)

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5
Q

transcellular mvmt.

A
  • where solute moves across two membranes in series, by moving through the cell.
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6
Q

Paracellular movement

A
  • solute moves passively b/w epithelial cells through tight junctions
  • mucosal resistance is dependent on paracelllular resistance which is a function of tight junction permeability and depends on tight junction’s structure
  • resistance increases as you move away from the mouth - the distant colon results in the greatest resistance
  • as you move down into the crypts, the resistance is also increased
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7
Q

Secretagogues

A
  • molecule that induce secretion
  • agonists
  • increase second messengers
  • bacterial toxins and enterotoxins function in this way
  • can also be our own hormones and NT’s
  • can have immune regulatory products
  • laxatives (bile acids) can function in this way.
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8
Q

Absorptagogues

A
  • induce absorption, can be neural, endocrine, or paracrine.
  • generally they are mineralocorticoids or glucocorticoids.
  • we will focus on Somatostatin and NE
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9
Q

Ostmotic diarrhea

A

Dietary component that is not absorbed

ex. lactose induce and glucose/galactose induced
- dietay component in lumen is pulling water into lumen

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10
Q

Secretory Diarrhea

A
  • secretagogues induce the active secretion of fluids and electrolytes from the intestines

Example:

  • enterotoxins (released by bacteria) can increase 2nd messengers within cells and can modulate the absorption of ions which can effect the movmt of water and the secretion of ions, resulting in a watery stool
  • Does not affect Na+ absorption, therefore, administration of Oral Rehydration Solution, enriched with Na+ and Glucose reverses secretory diarrhea
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11
Q

Sodium

A
  • mostly absorbed by villous epithelium of small intestine and Surface epithelium of large intestine
  • absorbed via Na+/K+ ATPase pump:
    All transcellular Na+ transport is mediated by this pump which moves Na+ across the basolateral membrane (resulting in low intracellular sodium levels). 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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12
Q
  1. Nutrient coupled Na+ transport
A
  • transport of Na+ coupled with carbohydrates or AA transport into the cell (I.e. SGLT1)
  • 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: removing positive charges from lumen, to more negative, which can work as a driving force for Cl- transport into the cell.
  • SGLT1 transporter for glucose coupled Na+ transpot
  • AA coupled NA+ transport

* this process is not inhibited by cAMP, and thus not effected by bacteria*

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13
Q

Na-H Exchanger (NHE3)

A
  • couples Na+ uptake to proton H+ extrusion into intestinal lumen : Increases intracellular pH, moves Na+ into cell. Decreases luminal pH.
  • Stimulated by secretion of HCO-3 in the duodenum, pancreas and bile
  • Driven by intracellular [Na+] gradient
  • Present throughout intestine, a lot in jejunum
  • Present in proximal small intestine without Cl-HCO3 exchanger, Stimulated by [HCO-3] here alone

NHE1: housekeeping isoform to modulate intracellular pH, not an important player in mechanism of sodium absorption

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14
Q

Electroneutral NaCl absorption

A

Parallel apical membrane exchangers coupled through pH: Na-H, Cl-HCO3

  • primary method of sodium absorption in between meals: Na+ and Cl- brought into cell, H+/HCO3- extruded into the lumen
  • present in Ileum and throughout large intestines

Clinical relevance: bacterial enterotoxins modulate concentration of sodium and Cl- in lumen due to this transport. They increase cAMP and utilize cGMP - when they increase these second messengers they inhibit sodium/Cl- absorption by inhibiting the sodium-potassium ATPase function.

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15
Q

Electrogenic Na+ Absorption

A

“ENACS”: epithelial Na+ channels on apical surface: highly specific

  • very distal colon where Na+ can be absorbed against large concentration gradient (can be activated when need more Na+)
  • activated by Aldo (an absorptagogue)
  • Dependent upon gradient created by Na-K pump on basolateral surface
  • Important in Na+ conservation
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16
Q

Chloride Absorption: Passive transport

A
  • Often coupled to Na+ absorption through intracellular gradient.
  • Passive Transport: Voltage dependent Cl- OR paracellular absorption.

occurs in jejunum and distal portions of colon: the negative charge in the lumen induces the paracellular transport of Cl-. Can occur early in small intestine because of hight amount of Na+ absorbed here. Also can absorbed in passive manner through the voltage dependent channels. (but both methods are dependent on presence of Na+/K+ ATPase)

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17
Q

Active transport: CL-/HCO3 Exchanger

A
  • “DRAexchanger” - down-regulated in adenoma and colon cancer
  • Active transporter of Cl-
  • located on apical surface: one Cl- brought in and one HCO3- extruded
  • Basolateral transport via CIC-2 channel
  • Congenital Cl- Diarrhea: results from absence of this exchanger - causes high Cl- in stool and high plasma bicarb, thus they are alkalotic.
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18
Q

Cl- secretion

A
  • promotes Na+ secretion resulting in NaCl secretion –> important in pathogenesis of diarrhea
  • Basal state of secretion is low or 0- and requires activation by secretagogues
  • Basolateral players req’d: Na-K ATPase pump lowers intracellular sodium and driving force for Cl- to enter through N/K/Cl cotransporter. Allows for Na+ in and K+ in, Cl- follows. Then leaky K+ channel is reqd. so that K+ can leave the cell. If add Cl- transporter CFTR (on apical membrane), results in four necessary transporters to have this secretion.

CFTR allows Cl- to leave the cell and and be secreted into the lumen.
–> clinically relevant in Cystic fibrosis

19
Q

K+ absorption - less important

A
  • occurs in small intestine, and very distal colon
  • occurs through:
    1. passive transport through paracelllular route, being pulled through tight jucntions via the mvmt of water. (in small intestine)
    2. Also occurs through active transport in distal portions of colon - a means to rescue lost potassium - occurs through apical H+/K+ pump, which pumps H+ into lumen, and this requires the basolateral Na+/K+ ATPase
20
Q

Passive K+ Secretion - less important

A
  • occurs in large intestine only
  • driven by negative potential in the lumen through paracellular mvmtn.
  • during dehydration, aldosterone is an absorptagogue in Na+ absorption and the lumen turns more negative, resulting in K+ secretion and increased amount of K+ in stool.
  • overall results in net secretion of K+ in large intestine
21
Q

Active K+ secretion

A
  • occurs at a low level b/c is tightly regulated in colon
  • reqs 3 transporter in basolateral membrane: Na/K pump, Na/K/Cl- cotransporter and K+ channel
  • apical surface has K+ channel
22
Q

CA2+: active mechanism

A
  • taken in via active transcellular uptake : under the control of Vitamin D which induces the synthesis of Calbindin in the duodenum. Reqs. vitamin D because Calbindin must bind Ca2+ once it enters the cell in order to prevent it from acting as a signaling messenger intracellularly.
23
Q

Ca2+ absorption: active

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+ (necessary b/c it functions as a messenger)
3) Extrusion through Ca2+ Pumps and Na-Ca Exchanger: Moves across basolateral membrane and into interstitial fluid

24
Q

Passive paracellular uptake of Ca2+

A
  • changes in blood Ca2+ influence its paracellular uptake
  • Higher concentration than active uptake
  • Not under the influence of Vitamin D: it doesn’t enter cell thus doesn’t req. a chaperone
  • Occurs throughout small intestine: Jejunum and Ileum
  • Enhanced by low plasma concentration of Ca2+: Lactation - during lactation blood ca2+ levels fall as it is utilized which increases paracellular uptake
25
Q

Mg+ absorption

A

Active Transcellular Uptake: Only in Ileum

  • Independent of Vitamin D
  • Independent of Ca2+

Passive Paracellular Uptake

  • Throughout the small intestine: Duodenum and Jejunum
  • based on Mg+ concentration

Mg+ is reqd for production of PTH. Thus if have Mg+ deficiency will have low PTH which will decrease active Ca2+ transport resulting in active hypocalcemia

26
Q

Iron

A

Can exist in two forms:

  • Ferric (Fe3+) - found in foods, difficult to get to cell surface
  • Ferrous (Fe2+) - this is the form that can be taken up by the cell.
  • ascorbic acid (Vit C) - is important b/c it reduces iron from ferric to ferrous form: thus icnreases absorption of Fe2+
27
Q

Anemia

A

iron depletion

28
Q

Hemochromatosis

A

= iron overload
- Hereditary Hemochromatosis (HH): body absorbs excess iron - overtime the patient will have iron build up in end organs, and syptoms of disease will not be expressed for 30 years after. Women will show it even later due to menstruation

29
Q

Iron dysregulation

A
  • can accumulate in liver and pancreas
  • results in bronze pigmentation of skin
  • to detect: look at blood levels of iron, transferrin, ferritin and liver biopsy
  • treatment: remove blood from patient (phlebotomize) in order to normalize iron levels
Results in : 
Cirrhosis
Hepatomas
Pancreatic Damage
Bronze pigmentation
Pituitary and Gonadal failure
Arthritis
Cardiomyopathy
30
Q

Iron absorption: heme iron

A
  • can be absorbed on a heme via active transcellular transport
  • occurs only in duodenum via binding brush border protein
  • absorbed more efficiently in this way

Process:
Heme Fe2+ goes into cell. Heme oxygenase oxidizes the Fe2+ in heme, and then releases free Fe3+ in cell. Fe3+ is converted to Fe2+ by ferric reductase. Fe2+ then takes the nonheme pathway whereby it is transfered to mobilferrin. Fe2+ leaves the cell via ferroportin.

31
Q

nonheme irone

A

Absorbed less efficiently : Exists as either ferric or ferrous iron

Active Transcellular Transport Only: Occurs only in duodenum:

Ferric reductase Dcytb converts Ferric to ferrous form. DMT1 on apical membrane cotransports Fe2+ and H+ into cytoplasm. Fe2+ binds mobilferrin inside cell and transported to basolateral membrane. Binds FP1 at basolateral membrane and Fe2+ is transported outside of cell, converted back to Fe3+ and travels with transferrin in the blood.

Fe2+ and apoferritin result in ferritin (non-toxic storage in liver)

32
Q

DMT1

A

1) Divalent Metal Transporter (DMT1): on apical membrane
- Cotransports Fe2+ and H+ into cytoplasm: Inward directed H+ gradient
- Not specific for Iron: Many divalent metals including toxic (Cd2+, Pb2+), Not Ferric iron

33
Q

Ferric reductase Dcytb

A
  • Reduces ferric iron to ferrous iron: Cytochrome
  • Apical extracellular surface
  • Required for uptake in DMT1
34
Q

Mobilferrin

A
  • involved in active transcellular iron transport
  • binds Fe2+ in cytoplasm
  • carries Fe2+ to the basolateral membrane
35
Q

Ferroportin Transporter (FP1)

A
  • involved in active transcellular Iron transport

- translocates Fe2+ across basolateral membrane

36
Q

Active transcellular Iron transport

A
  1. DMT1 cotransports Fe2+ and H+ into cytoplasm
  2. Ferric reductase Dcytb reduces ferric iron to ferrous iron
  3. mobilferrin binds Fe2+ in cytoplasm and carries it to the basolateral membrane
  4. Ferroportin transporter (FP1) translocates Fe2+ across basolateral membrane
37
Q

Cholera enterotoxin induced Diarrhea

A
  • rice water = looks like rice due to mucous present in stool - (E. coli induced has presence of blood and not mucous)
  • lumenal concentration of Cl- will increase due to enterotoxin induced activation
  • Cl- secretion is activated by cAMP, Na+ is reduced by cAMP indirectly. resulting in increased NaCl in lumen, and also increased K+ in lumen –> great increase in water in lumen
38
Q

Mechanism of action of Cholera?

A
  1. Cholera toxin binds apical receptors on crypt cells.
  2. Results in an increase of cAMP
  3. Results in secretion of Cl- by CFTR
  4. Na2+ and H2O follow Cl- into lumen
  5. Na2+ absorption inhibited by cAMP

Result: Secretory Diarrhea

39
Q

Oral rehydration solution

A
  • should administer Glucose and Na+ at a very minimum for treatment
  • Relies 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.
40
Q

four types of apical Na+ transport?

A
  1. nutrient-coupled Na+ transport
  2. Na-H exchanger
  3. electroneutral NaCl absorption
  4. Electrogenic Na+ absorption
41
Q

3 types of Cl- absorption? one type of secretion?

A

absorption:
1. Active transport via Cl-HCO3 exchanger
2. Electroneutral NaCl abosorption
3. Passive transport through voltage dependent Cl- abosorption

secretion: through Na/K/Cl cotransporter ?

42
Q

Congenital Cl- Diarrhea

A

results from absence of Cl-HCO3- exchanger (DRA exchanger)

  • causes high Cl- in stool and high plasma bicarb, thus they are alkalotic
  • however, Cl- exchanger in blood cells and renal tubules remain unaffected, they are formed from a different gene.
43
Q

CFTR

A
  • clinically relevant to Cl- secretion
  • CFTR is implicated in Cystic Fibrosis, where this channel is absent and thus Cl- is not released from cell, thus mucus is thick and dries out which will inhibit nutrient absorption, exchange of gases, and can lead to weight loss in patients. Some patients might also express diarrhea because nothing will be being absorbed.
  • Cl- channel is responsive to cAMP (which is increased by bacteriotoxins), will activate a kinase resulting in active CFTR, and active Cl- secretion. If secreting Cl-, Na+ follows and H2O follows
44
Q

Ca2+ absorption

A
  • active transcellular uptake only takes place in duodenum. the small surface area and high speed of flow reduces uptake
  • villous epithelial cells under control of Vitamin D enhance absorption

GI test 2 (14 decks)

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