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Pathogenesis of Dehydration Related to Endocrine System, Results in…
Pathogenesis of Dehydration Related to Endocrine System
Adrenal failure
Adrenocorticotrophic hormone (ACTH) decrease at hypothalamus.
The hormone then travel through blood reach adrenal cortex receptor
When less hormone reach adrenal cortex receptor reduce in production of adrenal hormone which is all three hormones which is Glucocorticoids, Adrogens and Mineralocorticoid.
Mineralocorticoid is important water retention and absorption will reduce sodium and metabolism therefore lead to dehydration
The primary mineralocorticoid is aldosterone, therefore the reduce of aldosterone. With the reduce of aldosterone there will be decrease of salt and water reabsorption into the bloodstream from kidney, thereby decrease blood volume, low blood pressure as well as increase potassium levels in the blood.
Diabetes insipidus
Central diabetes insipidus
- cause partial or complete absence of vasopressin secretion by hypothalamus
Nephrogenic diabetes mellitus
- cause resistance of vasopressin at the level of nephrons due to vasopressin receptor or aquaporin-2 protein abnormalities
Excessive free water excretion
Polyuria, polydipsia
Dehydration, hypernatremia if inadequate water intake to compensate for loss of water
Hyperplasia of parathyroid gland
If there is a hyperplasia of the parathyroid gland, there will be an increased in secretion of parathormone. This increases the mobilization of calcium from bone
This would make the bones to be fragike and easily broken
If the fractured bone cuts any blood vessels causing haemorrhage; leading to hypovolemic shock.
The loss blood must be compensated in order for normal blood circulation. Therefore the heart undergoes hypertrophy due to the increase in work load.
In order to compensate the hypovolemic shock, more water is retained leading to dehydrstion state.
This also could cause fractiure of teeth because it is getting fragile as well
When pulp is exposed, the sensory nerves are directly exposed as well. This cause severe pain to the animal. The animal wouldn’t be able to drink or eat because of the highly sensitive trigeminal nerve which branches into maxillary and mandibular nerve.
The inability to eat or drink due to pain leads to dehydration
Cushing’s Disease
Disease of pituitary gland
Excessive secretion of adrenocorticotropin hormone (ACTH)
ACTH travels to the adrenal glands via the bloodstream
ACTH stimulating effect on aldosterone
Increase in aldosterone production from adrenal gland
High aldosterone levels can lead to low potassium levels
Low potassium levels cause excessive thirst and frequent urination
Excessive water loss from body leading to dehydration
Hyperthyroidism
Results in dilatation of blood vessels of peripheral circulation
The dilatation of blood vessels leading to reduction of peripheral resistance. Therefore the renal artery hypotension in turns stimulate the Juxtaglomerular cells (JG cells) of the kidney to release a proteolytic enzyme known as renin
When renin is released into the blood, it acts upon a circulating angiotensinogen that undergoes proteolytic cleavage to form angiotensin I.
Vascular endothelium, particularly in the lung, has an enzyme known as Angiotensin Converting Enzyme (ACE) convert angiotensin I into angiotensin II.
This angiotensin II has function in increase the cardiac output.
The increase of blood flow through the body results in increase in glomerular filtration rate.
The increase in the hyrostatic pressure within the afferent arteriole causes more renal blood flow into gromerulus capillaries.
High amount of the plasma components then are filtered from the glomerular capillaries across the glomerular filtration barrier into the urinary space within Bowman capsule.
This increased amount of ultrafiltrate flows through the tubular system as tubular fluid and later excreted as urine in high amount. The animal with hyperthyroidism therefore shows clinical signs of polyuria and polydipsia due to the kidney unable to conserve water
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Disorder of Pancreatic Islet Cells
Pancreatitis, immune destruction of
β cells, inherited disorders and amyloidosis
Destroys both exocrine &
endocrine pancreatic tissue
Type I diabetes mellitus
Deficiency of insulin production and
secretion by islet β cells
Decreased movement of glucose into insulin-sensitive cells (particularly hepatocytes, adipocytes, skeletal myocytes)
Increase in hepatic glucose production and hyperglycemia
Hepatomegaly
Increase in blood sugar level
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Down regulation of insulin receptors, insulin receptor antagonism, obesity
Type II diabetes mellitus
Failure of target cells to
respond to insulin
Increase in glucagon secretion
Promotes hepatic gluconeogenesis & fatty acid oxidation
Hyperglycemia and ketoacidosis
Results in hypofunction of pancreatic islet cells