Fluids And Electrolytes Flashcards

1
Q

Water transport

A

Water transport in the small intestine is passive and is ultimately dependent on the basolateral Na+/K+-ATPase that sets up the electrochemical gradient within the cell.

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2
Q

SODIUM TRANSPORT

A

occurs along the entire length of the intestine in
villous cells. The energy for this is derived from the basolateral Na+/K+ pump that moves Na+ out of the cell at the basolateral side. Membrane transport proteins of the epithelial cells couple the influx of Na+ to the secondary active transport of sugars, amino acids and other ions.

There are 4 types

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3
Q

Electrogenic transport of Na+

A

results in the net transfer of charge across the cell.

The basolateral pump puts out 3 Na+ for every 2 K+ that enter, creating a low intracellular Na+ concentration and a negative electrical potential difference across the membrane. Na+ then enters the
cell along its electrical and chemical gradient. The exit of Na+ from the cell is uphill, requires energy and conserves the electrochemical gradient.

In the upper intestine Na+ crosses the brush border membrane down an electrochemical gradient (in the jeunum this is enhanced by co-transport).

However, because Na+ absorption is active, it can occur against an electrochemical potential difference, as in the ileum where the net rate of Na+ absorption is smaller (only slightly stimulated by co-transport).

In the colon Na+ can be absorbed against an even larger electrochemical gradient.

Synthesis of the Na+ channels can be induced by aldosterone leading to increases in Na+ absorption and K+ secretion.

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4
Q

Substrate-coupled transport of Na+

A

is also rheogenic as the substrate is not usually charged.

Na+ absorption is highest in the jejunum where it is enhanced by co-transport with a number of water-soluble organic solutes. This includes hexose sugars, certain amino acids and water-
soluble vitamins. A carrier molecule in the brush border couples the entry of Na+ and the organic solute into the cell. The downhill movement of Na+ into the cell indirectly provides energy for the movement of the organic solute.

This process is also called secondary active transport. The organic solute exits the cell by a carrier-mediated facilitated diffusion.

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5
Q

Electro-neutral transport of Na+ with Cl-

A

Electro-neutral transport of Na+ results in no net transfer of charge across the membrane such as co-absorption of Na+ with Cl- via a common carrier (symport). (Na+ and Cl- enter through a symport/uniport channel).

The energy for chloride movement into the cell is provided by the downhill movement of Na+.

Cl- moves out of the cell down its electrochemical gradient.

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6
Q

Electro-neutral transport of Na+ with H+

A

Na+ movement may be coupled to the counter transport of H+ ions via an antiporter. This process is also electroneutral because there is no net alteration in the charge distribution across the cell membrane.

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7
Q

Cl- and HCO3- in jejunum

A

In the jejunum both C- and HCO3- are absorbed in large amounts.

In the upper small intestine Cl- absorption is rapid and mainly by diffusion (the Cl- ions move along the electrochemical gradient ‘following’ the sodium ions). HCO3- is secreted into duodenum in the pancreatic and biliary secretions, and must be reabsorbed.

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8
Q

Cl- and HCO3- in ileum

A

Cl- absorbed

HCO3- secreted

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9
Q

Cl- and HCO3- in colon

A

Cl- absorption occurs even in low luminal concentrations.

HCO3- is secreted in exchange for absorption of Cl- (active).

HCO3- can then neutralize acidic products of the colonic bacterial flora.

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10
Q

K+ transport in jejunum and ileum

A

Passive absorption when concentration rises due to water absorption.

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11
Q

K+ transport in colon

A

Secretion or absorption may occur.

Secreted when luminal concentration is below 15 mEq/1 (passive transport because lumen is negative).

Absorbed if luminal concentration is higher.

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12
Q

Intestinal secretion of Cl-

A

Cl- is secreted in small and large intestines by crypt cells.

2 Cl- ions are coupled to inward movement of Na+ and one K+ by a basolateral triporter that has no net charge (accumulated K+ exits cell via a basolateral K+ channel to maintain negative potential within cell).

Process of secretion is under neural stimulation and is stimulated by acetylcholine in small intestine (increases intracellular Ca+), and by VIP in the colon (elevates intracellular cAMP).

Prostaglandins inhibit gastric acid secretion but stimulate crypt cell Cl- secretion (via increase of intracellular cAMP).

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13
Q

Diarrhea

A

A major cause of death worldwide. An increase in stool weight occurs which may be associated with increased liquidity, stool frequency, urgency.

causes of diarrhea include:

  1. decreased absorptive surface area,
  2. Osmotic diarrhea
  3. secretory diarrhea
  4. HIV enteropathy
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14
Q

Decreased absorptive surface area diarrhea cause

A

due to infection and inflammation.

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15
Q

Osmotic diarrhea

A

due to presence of non-absorbable solutes e.g. lactose intolerance.

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16
Q

Secretory diarrhea

A

resulting from bacterial overgrowth in the intestinal lumen is the result of hypersecretion and increased motility. Transit time is decreased and the reabsorption of water is hindered. However, increased secretion and motility may be important in clearing bacteria from the mucosal surface e.g. CHOLERA: Bacterial toxin B-subunits bind to a mucosal surface ganglioside (GM1). The A subunit then penetrates the membrane and is cleaved into A1 and A2 subunits. A2 allows the A1 subunit to penetrate the cell where it causes ADP-ribose to be added to an arginine residue on the α subunit of GS, the G protein responsible for adenylate cyclase activation. The resulting increase in intracellular cAMP causes crypts cells to begin pumping
chloride ions into the intestinal lumen. Water follows these ions producing severe dehydration. Dehydration is exacerbated because in enterocytes the toxin-induced increase in intracellular cAMP blocks Na+-Cl- cotransport, thus reducing water absorption.

17
Q

Diarrhea associated with HIV enteropathy

A

immune system alterations produce cytokine release and stimulation of ion and water movement across the colonic epithelium. In addition, HIV-induced dysfunction of colonic ECL cells may lead to the increased release of hormones or paracrine
substances that can stimulate both motility and secretion. In addition diarrhea can be infectious diarrhea (viruses, bacteria), psychogenic, or drug related.

As the immune system becomes progressively weaker due to HIV infection cell-mediated immunity of the gastrointestinal tract is impaired leading to opportunistic infections by viral agents (such as cytomegalovirus), protozoa and/or mycobacteria.

18
Q

Gut-Associated Lymphoid Tissue

A

Consists of organized aggregates of lymphocytes called Peyer’s Patches and diffuse populations of immune cells in the lamina propia.

Acts as barrier between host and potentially harmful infections and toxic agents.

Also permits immunological tolerance to potentially immunogenic dietary substances and bacteria that are normally found in the large intestinal lumen.

19
Q

Controls of hunger and satiety

A

Hypothalamus controls hunger and satiety.
– lateral nuclei serve as a feeding center
– ventromedial nuclei serve as the satiety center
– paraventricular, dorsomedial, and arcuate nuclei also play
important roles

20
Q

Feeding modulation:

A

– higher centers (e.g. amygdala and prefrontal cortex)

– neurohumoral signals from the GI tract

21
Q

Incretins

A

Incretins are a type of gastrointestinal hormone that can cause an increase in amounts of insulin released from pancreas (islets of Langerhans beta cells), and decrease in glucagon release (islets of Langerhans alpha cells).

They slow rate of absorption of nutrients into bloodstream by decreasing gastric emptying.

Two main ones are glucagon-like peptide 1 (GLP1) and Gastric inhibitory peptide (GIP). These are inactivated by dipeptidylvpeptidase 4 (DPP-4).

22
Q

Obesity

A

Excess of body fat (BMI > 30kg/m2 or >25% and >35% of body fat in male or female, respectively).

Risk factors for obesity: 
- Sedentary lifestyle 
- Abnormal feeding behavior 
• environmental, social, psychological factors 
• childhood overnutrition 
• neurogenic abnormalities 
- Genetic factors