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FAQ's

How long does the VIVIT dissection last?

The post mortem experience is 5 hours long, split into 2 parts.

How many people can participate in one VIVIT dissection?

There is 150 tickets available for each session. This is a comfortable number that can engage with the experience given the AV equipment installed.

Is the anatomy human?

No. The anatomy is of swine origin. Identical in size and structure -once harvested the samples are moved into VIVIT. VIVIT is a life size synthetic cadaver which is dissected for the audience to teach the structure and function of the human body.

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Anti-diuretic Hormone


Syndrome of inappropriate antidiuretic hormone (SIADH) and diabetes insipidus are opposites of each other and all depend on the same hormone antidiuretic hormone (ADH). Normally ADH is produced in the hypothalamus and then stored in the posterior pituitary gland ready to be released. ADH also known as vasopressin works on the kidneys, specifically in the distal convoluted tubule and the collecting ducts of the nephrons. It increases the amount of aquaporins within the nephron allowing more water to be reabsorbed out of the urine. This results in a decrease in volume and therefore an increase in osmolarity (concentration) of the urine that is being excreted. The reabsorbed water from the aquaporins enters the circulation where it causes a reduction in plasma osmolarity (becomes more dilute). This reduction in osmolarity is detected by the hypothalamus and ADH production is inhibited.

The more ADH, the more aquaporins and therefore more water reabsorption; this is what happens in SIADH. In SIADH negative feedback system where the reduced plasma osmolarity causes a reduction in ADH production doesn’t function. This can be due to ADH being produced elsewhere in the body such as a small cell lung cancer sometimes is able to produce ADH, certain drugs such as antidepressants, infections, and damage to the brain (meningitis, subarachnoid haemorrhage) can also cause SIADH. This dilution of the plasma that is seen in SIADH causes a reduction in the sodium concentration due to dilution. This hyponatraemia can cause symptoms like nausea and vomiting to the extremes of muscle cramps, seizures and even coma. Management of these patients is done through tackling these two problems, so fluid is restricted and sodium is replaced. Don’t forget the underlying cause still needs to be treated otherwise it would turn into a vicious cycle.

Diabetes insipidus on the other hand is where the opposite effects occur, there is too little aquaporins in the nephrons of the kidney so not enough water is reabsorbed, leading to very dilute and copious amounts of urine, usually over 3 litres a day. It presents with similar symptoms of diabetes mellitus (where insulin is affected), polydipsia (increased thirst) and polyuria (increased urination) due to this excess loss of fluids. This loss of fluids causes dehydration, a more concentrated circulatory system so the patient often presents with hypernatraemia (increase sodium in the blood). There are two types of diabetes insipidus: cranial and nephrogenic. Cranial refers to a problem within the brain and the production of ADH, not enough ADH = not enough aquaporins. Nephrogenic is where there is ADH being produced however the kidneys don’t respond to this appropriately and they subsequently don’t increase the number of aquaporins in response to the ADH. These two types can be differentiated by whats called a water deprivation test. This is where the patient is deprived of fluid for 8 hours and urine osmolarity checked, if this is still low then diabetes insipidus is diagnosed, as dehydration would usually cause and increased concentration of urine. However, to differentiate between cranial and nephrogenic a ADH analogue is given, desmopressin. The urine osmolarity is then checked again, if a cranial cause the urine osmolarity will have increased showing that there was a lack of ADH not that the patient’s kidneys did not respond to ADH. Nephrogenic cause is indicated by still very dilute urine, showing that the kidneys didn’t respond to ADH and increase the amount of aquaporins absorbing water out of the urine. Cranial diabetes insipidus is treated by just replacing this ADH using desmopressin, whereas nephrogenic type is treated using thiazide diuretics, as these drugs inhibit the reabsorption of sodium from the urine decreasing the amount of sodium in the blood.

So in a patient with concentrated urine and hyponatraemia, think could this be SIADH. Patient with dilute polyuria and hypernatraemia, could this be diabetes insipidus?



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