Endocrine - DI, DM I & II 04/13/2016: Review of Endocrine Pancreas: Endocrine and Exocrine Gland Alpha Cells
Endocrine - DI, DM I & II 04/13/2016: Review of Endocrine Pancreas: Endocrine and Exocrine Gland Alpha Cells
Endocrine - DI, DM I & II 04/13/2016: Review of Endocrine Pancreas: Endocrine and Exocrine Gland Alpha Cells
04/13/2016
o Hypoxia
o Pathogens proliferated rapidly due to increased glucose in
body fluid
o Decreased blood supply due to vascular changes
o Suppressed immune response
Diabetes insipidus (DI): disorder of insufficient ADH activity, leading
to polyuria and polydipsia
Two forms:
o Neurogenic DI caused by insufficient ADH secretion when any
lesion of hypothalamus, pituitary stalk, or posterior pituitary
interferes w/ADH syntheses
Hereditary disorders that affect ADH genes; closed head
injuries
o Nephrogenic DI: caused by inadequate response of renal
tubules to ADH, which is usually acquired (related to drugs
[loop diuretics, general anesthetics] that damage the renal
tubules or inhibit generation of cAMP) or hereditary disorders
that result in structural changes to the pituitary gland
Often confused w/ pathogenic polydipsia, caused by chronic
ingestion of large quantities of fluid that was out the renal
medullary concentration gradient
o Resolves w/decreased fluid ingestion
Pathophysiology: partial to total inability to concentrate urine
o Insufficient ADH causes excretion of large volumes of dilute
urine, leading to ^ plasma osmolality (urine output of 12L/day to 8-12L/day)
o Dehydration develops; serum hypernatremia and
hyperosmolality
Manifestations: polyuria, nocturia, continuous thirst, polydipsia
o large bladder capacity and hydronephrosis
o Neurogenic = abrupt onset; Nephrogenic = gradual onset
Eval & Treatment: distinguished from other polyuric states;
o Low urine specific gravity & osmolality; hypernatremia;
continued diuresis despite serum sodium >145 mEq/L
o Psychogenic differentiated from Nephrogenic based on plasma
ADH levels
ADH low in psychogenic; normal to high in Nephrogenic
o Treatment: ADH replacement therapy; intranasal
administration of synthetic vasopressin analog DDAV