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Pathophysiology of Diabetes Insipidus: DX: Serum ADH

There are two main types of diabetes insipidus: neurogenic and nephrogenic. Neurogenic diabetes insipidus is caused by a deficiency of antidiuretic hormone (ADH) secretion by the pituitary gland. Without ADH, the kidneys are unable to concentrate urine, resulting in excessive urine production and thirst. Nephrogenic diabetes insipidus is caused by kidney insensitivity to ADH despite normal secretion. This prevents water reabsorption in the collecting ducts of the kidneys, also causing excessive urine production and thirst. Both types result in an inability to concentrate urine and regulate water levels in the body.
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0% found this document useful (0 votes)
113 views3 pages

Pathophysiology of Diabetes Insipidus: DX: Serum ADH

There are two main types of diabetes insipidus: neurogenic and nephrogenic. Neurogenic diabetes insipidus is caused by a deficiency of antidiuretic hormone (ADH) secretion by the pituitary gland. Without ADH, the kidneys are unable to concentrate urine, resulting in excessive urine production and thirst. Nephrogenic diabetes insipidus is caused by kidney insensitivity to ADH despite normal secretion. This prevents water reabsorption in the collecting ducts of the kidneys, also causing excessive urine production and thirst. Both types result in an inability to concentrate urine and regulate water levels in the body.
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PATHOPHYSIOLOGY

OF DIABETES INSIPIDUS

Neurogenic Diabetes
Nephrogenic Diabetes
Insipidus
Insipidus


Predisposing Factors Predisposing Factors Precipitating Factors

Precipitating Factors
Pituitary hypogenesis Male Sickle cell disease

Trauma to pituitary stalk
• AVP-neurophysin Genetic- mutation in the Drugs such as demeclocyline, lithium,
AVPR2 gene, encoding aminoglycosides
Hypothalamic/ Pituitary
• Wolfram syndrome the renal vasopressin V2
Surgery receptor Pyelonephritis

Tumors, Ischemia, Viral X-linked recessive Electrolyte imbalance


encephalitis and meningitis

Renal insensitivity to the effect of
vasopressin

Deficient or absent excretion of ADH
Dx: Serum ADH


V1 and V2 receptors in the kidneys are not stimulated



No activation of adenyl cyclase and cyclic AMP (second
messenger)


Aquapourin 2, which is a water Aquaporins 3 & 4 is the water channels
channel membrane protein that
located in the basolateral membrane not
responds through the action of altered by ADH. Water reabsorption is
cAMP is deactivated. not altered there

Collecting tubules fail to increase


Water reabsorption does not occur in the luminal membrane water permeability



Dx: Water Deprivation
Test
Excretion of an increased Decreased body Rise in plasma osmolality
Desmopressin volume of dilute urine water Thiazide
diuretics

Indomethacin

Decreased urine Thirst mechanism is stimulated
specific gravity

Increase in water uptake Polydipsia


Osmolality of body fluid stabilizes at a new higher level that approximates the

osmotic threshold for thirst

Serum Na
Hypernatremia Dehydration

Fatigue Polyuria

Hypotension Dry Mucus Membranes


References: http://books.google.com.ph/books?id=VQSSnC-
csvoC&pg=PT87&dq=central+diabetes+insipidus
http://books.google.com.ph/books?id=aRIh19rGY7QC&pg=PT521&dq=neurogenic+diabetes+insipid
us+PATHOPHYSIOLOGY

http://books.google.com.ph/books?id=6gezJTHaAVMC&pg=PA44&dq=neurogenic+diabetes+insipid
us+pathophysiology

http://www.mdconsult.com/books/

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