Diarrhoea is a decreased stool consistency and increased frequency. It can be acute or chronic. the fundamental problem is the loss of fluid from
In diarrhoea you lose lots of fluid. This is because your body tries to clear the whatever is in your GI tract out of it, through excretion.
Mechanisms of diarrhoea.
Some mechanisms by which diarrhoea is produced are:
- Osmotic (keep it there; this is where secretions are not absorbed)
- Secretory (increased secretions)
- Inflammatory (mucosal inflammation)
- Motility (high motility means that there is far less time for secretion)
Cholera example
Cholera is a well understood organism which leads to diarrhoea which is why we are looking at it. It is a sticky bacteria which is needed for persistence in the GI lumen. Cholera produced diarrhoea by binding to the epithelial cell and and secreting a toxin which triggers cAMP which increases secretion.
Small intestine
Colon
The colon normally exchanges Na for K and Cl for HCO3. In secretory diarrhoea we see increased Na+ and Cl- in the colon and therefore higher rates of exchange. You will take Na+ and Cl- into the body and secrete K+ and HCO3- in their place into the lumen. This means people suffering from secretory diarrhoea will be acidotic and hypokalaemic. This will bump up resp rate and heart rate.
Treatment
Have to add volume via osmotic fluid. In epidemic you may need to give oral rehydration and with this give sugar and salt which uses the na+glu cotransporter to get water into the body.
Wrap up.
Study tasks
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Describe small intestine secretions including the mechanisms of secretion. How are these secretory processes changed by cholera infection?
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Describe the mechanisms of absorption of ions, low molecular weight substances and water from the small intestine.
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Describe absorption/secretion in the large intestine (colon). What changes) in these processes will there be in a person with cholera? What effect will flow rate / transit time of this fluid have on colonic absorption?
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Describe motility patterns in the small and large intestine. How will the increased volume of luminal fluid in this person affect motility?
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Describe and explain the changes in plasma biochemistry and acid-base status (concentrations of Na, K, CI, urea, haematocrit and arterial HCO3, pH, PCO2) that you might expect to see in this person.
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Summarise the mechanism by which cholera infection / toxin causes diarrhoea.
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How should this patient be managed? What is the physiological basis behind the composition of oral rehydration?
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What happens to this person’s body overall during this illness? i.e. what are the consequences with respect to ECF volume and circulation? What CVS changes/compensations would there be as the illness progressed? How does this person’s volume/CVS status compare with that of a person who is simply not drinking any water?