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How does glucose normally pass from the intestinal lumen into the blood? 30 %

Introduction

Sugar is absorbed in the form of monosaccharides by specific brush border membrane carriers which are in close functional proximity to the brush border digestive hydrolases.The collective brush borders of the epithelial sheet on the intestine form a barrier in which sugars have to pass therefore separating digestive function of the lumen from the cells making up the epithelium, brush border enzymes are involved in the terminal process of the digestion of carbohydrates maltase, which hydrolyses maltose into glucose, sucrase which hydrolyses sucrose into glucose and fructose lactase which hydrolyses lactose into glucose and galactose in essence changing poly and disaccharides into monosaccharide’s ready for absorption. The brush border membrane is composed of fatty chains of phospholipids which acts as a barrier to large molecules like hexoses i.e.

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glucose, galactose and fructose. Sherwood, L (2010).

This is overcome by them meeting specific requirements to enable them to bind to membrane transport carriers. Glucose and galactose membrane transport carriers have two binding sites on the brush border membrane. This transport carrier requires Na+ to be co transported with the sugar, this sodium dependant carrier enables against the gradient transport by coupling to the fluctuating trancellular movement of sodium at the brush border membrane and achieves an against the gradient accumulation of sugar at the expense of the “downhill” flux of Na+ energy in the form of ATP is put into a sodium pump to enable it to work. Sherwood, L (2010).

The main apical transporter for active glucose uptake in small intestinal epithelial cells is the sodium-dependent glucose co transporter (SGLT). SGLT-1 unidirectionally mediates glucose absorption from the intestinal lumen into epithelial cells. SGLT-1 co transports glucose and sodium. The transporter is initially facing into the lumen and is capable of binding sodium but not glucose. Sodium binds and induces a conformational change that opens the glucose-binding pocket. The transporter then reorients in the membrane such that the pockets holding sodium and glucose are moved inside the cell. Sodium dissociates into the cytoplasm due to the conformal change which occurs causing glucose binding to destabilize and dissociate into the cytoplasm. This transcellular pathway is powered by a downhill gradient of Na+ across the apical membrane, maintained by the basolateral Na+/K+ GLUT2 in the basolateral membrane. Debajyoti Das (2005).

The GLUT-2 transports glucose, providing a common exit pathway into the blood. Fructose is transported across the apical membrane by a specific facilitative transporter, GLUT5. (GLUT5)is a facilitative transporter not an active transport system. The basolateral transporter GLUT-2 facilitates diffusive transport of intracellular glucose into the interstitium and bloodstream. Debajyoti Das (2005).

How would Dioralyte benefit the child(20%)

Dioralyte is given as part of the treatment for severe dehydration and is a form of treatment known as Oral Rehydration Therapy (ORT). It is used for rehydration because simply giving a saline solution (water plus Na+) by mouth would have no beneficial effect due to the normal mechanism by which Na+ is absorbed by the healthy intestinal wall is impaired in the diarrhoeal state and if the Na+ is not absorbed neither can the water be absorbed. Excess Na+ in the lumen of the intestine would actually be counterproductive and causes increased secretion of water so the diarrhoea worsens. U, Desselberger (2003).

Dioralyte would benefit the child because glucose is added to the dioralyte solution the glucose molecules are absorbed through the intestinal wall unaffected by the diarrhoeal disease state and in conjunction sodium is carried through by a co-transport coupling mechanism. This occurs in a 1:1 ratio, one molecule of glucose co-transporting one sodium ion (Na+) with potassium being passively absorbed. Therefore sodium transport coupled to glucose transport in small intestine enables more efficient absorption of fluids and salts. Glucose should be close to equivalent with the Na+ content. Dioralyte takes advantage of this so therefore contains both glucose and sodium molecules. U, Desselberger (2003).

Further to this dioralyte contains electrolytes because electrolyte imbalance and fluid loss also causes metabolic acidosis. Acidosis is corrected by the addition of bicarbonate or another base such as citrate which diorlyte contains so as to help neutralise the acidosis that occurs in the blood. U, Desselberger (2003).

Potassium passively absorbed. passive water uptake This characteristic has been used for the development of oral rehydration therapy to manage hypersecretory diarrheal disease sodium is also lost. The body’s store of sodium (in the form of sodium ions Na+) is almost entirely in solution in body fluids.In some parts of the world, cholera is endemic. How would the symptoms of cholera compare with those of viral enteritis(20%)

Cholera is an intestinal infection caused by the ingestion of the Vibrio Cholera bacterium and the symptoms usually last 3 to 5 days. It has a host of symptoms divided into three stages, stage 1 is commonly known as the diarrheal stage which consists of watery diarrhea, vomiting, muscle cramps and rice water stools. These are the first initial symptoms with the muscle cramp being due to a loss of fluid and electrolytes from the body, due to the persistent loss of water through vomiting and diarhea this leads to severe dehydration which then causes a host of new symptoms hence stage 2. William, C (2009).

Due to the intense diarrhea stage two is known as the dehydration stage. In this stage the symptoms consist of dehydration, cold skin, sunken eyes, thirst, faint pulse, voice changes by becoming higher pitched, reduced urine, muscle cramps, shock can set in because of the tremendous physical pressure the body is under leading to muscle weakness. Once the cholera has left the body it will no longer be producing the toxin which causes so many symptoms in the body. The next stage the body has to go through is known as the recovery stage. William, C (2009).

Stage three is known as the recovery stage, the person may continue to experience mild or extreme diarhea, due to the huge levels of dehydration there is a large loss of sodium, chloride, potassium and bicarbonate which leads to an electrolyte imbalance.

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The person will also experience intense thirst coupled with reduced urination, hypotension, hypokalemia, acidosis and potential kidney failure. William, C (2009).

The symptoms of gastroenteritis are very similar to cholera as the definition of gastro enteritis is inflammation of the gastro intestinal tract involving the stomach and small intestine. In effect cholera causes a severe case of gastro enteritis and therefore the symptoms are very similar for both illnesses. The sufferer can feel nausea, vomiting diarrhea, abdominal pain, dehydration which leads to muscle cramps and muscular aches and therefore weakness in strength, loss of appetite, fainting, weakness, abdominal pain, fever additional to this is the suffering of a headache. The condition is usually of acute onset and will usually last six days. U, Desselberger (2003).

Overall the difference in symptoms between cholera and gastro enteritis are very small, the most significant difference in symptoms is that in gastro enteritis the person will experience a fever. Gastro enteritis is the symptom of the disease and is defined as an inflammation of the stomach and small intestine. The inflammation is caused most often by an infection from some viruses which produce toxins which then lead to an inflammation of the intestine. So it is important to realise that when comparing the symptoms of cholera with viral enteritis that viral enteritis is the symptom not the cause of the disease and in itself is not a virus or bacteria unlike the virus cholera. U, Desselberger (2003).

Describe the molecular mechanism of action of cholera toxin. (30%)

Inactivates GTP ase function of G protein coupled receptors in intestinal cells.

Each cholera toxin molecule is composed of 5 B binding subunits and one A active subunit, the b sub units bind to the intestinal epithelial cells of the internal mucosa, the a active subunit then enters the intestinal mucosa via endocytosis and catalyses the transfer of an ADP-ribose from NAD to the ? subunit of a G protein. Chadhuri, K (2009).

This stimulates production of the enzyme adenylate cyclise into an irreversible activation and an increase in intracellular cAMP concentration which is responsible for the production of cyclic AMP. The modified G protein is no longer able to switch off adenylate cyclise cAMP and is produced constitutively at a 100 fold increase in the production of cAMP This converts the G-protein into a permanently active state, so it sends a never-ending signal. Chadhuri, K (2009).

Increased levels of cAMP result in disruption of the active transport of electrolytes across the cell membrane, in the gut epithelial cell cAMP level influences ion transport this hinders fluid absorption, leading to fluid secretion into the small intestine. The high levels of cAMP cause ion channels in the cell membrane of the crypt cells at the base of the villi in the small intestine to open, resulting in uncontrolled secretion of H2O, Na+, K+, Cl–, and HCO3– into the lumen of the small intestine resulting in rapid dehydration due to the osmotic and electrical gradients caused by the loss of Cl-. Ramamurthy, T (2011).

The high cAMP levels also inhibit the uptake of Na+ ions into the cells at the top of the villi, with the result that Na+ and Cl? ions accumulate in the lumen. Water moves out of the epithelial cells into the lumen by osmosis due to the concentration gradient created by the high cAMP levels, and both water and electrolytes are lost from the body as the copious electrolytes including Na+ follow the osmotic and electric gradients created by the excretion of Cl–. It is this removal of water and electrolytes that cause the diarrhea and dehydration seen in the disease. Ramamurthy, T (2011).

Bibliography.

Chadhuri, K (2009). Cholera Toxins. 3rd ed. Germany: Springer.

Debajyoti, D (2005). BIOCHEMISTRY. 12th ed. America: ACADEMIC PUBLISHERS.

Desselberger, U (2003). Viral gastroenteritis . Amsterdam: ELSEVIER

Ramamurthy, T (2011). Epidemiological and Molecular Aspects on Cholera. 3rd ed. New York: Springer.

Sherwood, L (2010). Human physiology: from cells to systems. 7th ed. CANADA: Yolando Cossia

William, C (2009). Cholera. 2nd ed. New york: Info Base Publishing

References.

How does glucose normally pass from the intestinal lumen into the blood30 %

Sherwood, L (2010). Human physiology: from cells to systems. 7th ed. CANADA: Yolando Cossia. Page 73-75.

Sherwood, L (2010). Human physiology: from cells to systems. 7th ed. CANADA: Yolando Cossia. Page 73-75.

Debajyoti Das (2005). BIOCHEMISTRY. 12th ed. America: ACADEMIC PUBLISHERS. p341-342.

Debajyoti Das (2005). BIOCHEMISTRY. 12th ed. America: ACADEMIC PUBLISHERS. p341-342.

How would Dioralyte benefit the child?

U, Desselberger (2003). Viral gastroenteritis . Amsterdam: ELSEVIER. p94-96

U, Desselberger (2003). Viral gastroenteritis . Amsterdam: ELSEVIER. p94-96

In some parts of the world, cholera is endemic. How would the symptoms of cholera compare with those of viral enteritis(20%)

William, C (2009). Cholera. 2nd ed. New york: Info Base Publishing. p57-59

William, C (2009). Cholera. 2nd ed. New york: Info Base Publishing. p59-61

William, C (2009). Cholera. 2nd ed. New york: Info Base Publishing. p-61-62

Desselberger, U (2003). Viral gastroenteritis. Amsterdam: ELSEVIER. p94-96

Desselberger, U (2003). Viral gastroenteritis. Amsterdam: ELSEVIER. p94-96

Describe the molecular mechanism of action of cholera toxin. (30%)

Chadhuri, K (2009). Cholera Toxins. 3rd ed. Germany: Springer. p105-114

Chadhuri, K (2009). Cholera Toxins. 3rd ed. Germany: Springer. p185-197

Ramamurthy, T (2011). Epidemiological and Molecular Aspects on Cholera . 3rd ed. New York: Springer. p105-114.

Ramamurthy, T (2011). Epidemiological and Molecular Aspects on Cholera . 3rd ed. New York: Springer. p105-114.

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