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ANATOMY AND PHYSIOLOGY of ADRENAL GLANDS AND SIADH & DI
ANATOMY AND PHYSIOLOGY of ADRENAL GLANDS AND SIADH & DI
ANATOMY AND PHYSIOLOGY of ADRENAL GLANDS AND SIADH & DI
1. Water equilibrium.
Hypersecretion of T3 and T4 = Grave’s disease, Dopamine is used to treat shock. It dilates the
goiter, arteries, elevates systolic blood pressure, increases
cardiac output, and increases urinary output.
SECRETIONS OF THE PARATHYROID GLAND…
Epinephrine is also called adrenalin. It elevates
The two pairs of parathyroid glands are located on systolic blood pressure, increases heart rate and
the dorsal or back side of the thyroid gland. They cardiac output, speeds up the release of glucose
secrete parathyroid (PTH) which plays a role in the from the liver… giving a spurt of energy, dilates the
metabolism of phosphorus. Too little results in bronchial tubes and relaxes airways, and dilates
cramping; too much results in osteoporosis or the pupils to see more clearly. It is often used to
kidney stones. counteract an allergic reaction.
The thymus gland has two lobes, and is part of the When serum osmolality increases, your body
lymphatic system. It is a ductless gland, and releases ADH. This keeps water from leaving in the
secretes thymosin. This is necessary for the urine, and it increases the amount of water in the
Thymus’ normal production of T cells for the blood. The ADH helps restore serum osmolality to
immune system. normal levels. If you drink too much water, the
concentration of chemicals in your blood
decreases.
DI and SIADH
Serum Osmo below 280 mOsm/L
Brain Regulation = water excess
Neuroscience patients must be continually Too much water for the amount of
assessed and monitored for their response solute
to therapy
To maintain plasma or serum osmo within range,
Early detection is critical to the protection free water intake and excretion must balance
and integrity of the brain
When serum osmolality decreases, your
Normal Brain Regulation body stops releasing ADH. This increases
the amount of water in your urine. It keeps
TBW accounts for 60% of body weight too much water from building up in your
body (overhydration).
20% ECF
Antidiuretic Hormone (ADH): balances Na
40% ICF and water in body and controls water
conservation
Fluid shifts can occur depending on
concentrations of solutes in ICF and ECF Changes in pressure of ECF triggers release
of ADH from pituitary gland
Na and K are principle determinants in
fluid shifts Release is coordinated with activity of the
thirst center- regulates intake
Osmolarity: amount of solute in fluid
(urine, blood) ADH binds with receptor sites of the
collecting duct in kidney resulting in
The unit of osmotic concentration is
increased free-water resorption
the osmole. the number of moles of solute
ADH causes vasoconstriction
Causes of DI
Head Trauma
Diabetes Insipidus Post-operative (hypophysectomy, pituitary
Disordered regulation of water balance due to tumor)
impaired urinary concentrating ability secondary to Brain Tumors
inadequate secretion of ADH or resistance to ADH. CNS Infection (meningitis, abcess)
Increased ICP
Four Types of DI: Idiopathic - denoting any disease or
Central/Neurogenic (CDI)
condition which arises spontaneously or for
=rare disorder of water homeostasis secondary to
which the cause is unknown.
deficient synthesis or secretion of arginine
ICH- intracerebral brain hemorrhage
vasopressin peptide (AVP) from the hypothalamo–
Stroke
neurohypophyseal system (HNS) in response to
Hypoxia
osmotic stimulation.
Medications (Dilantin, clonidine, alcohol)
Nephrogenic (NDI)- Damage to hypothalamus or posterior
=is an inability to concentrate urine due to pituitary
impaired renal tubule response to vasopressin
(ADH), which leads to excretion of large Diabetes Insipidus (DI) Clinical Signs!
amounts of dilute urine
Dehydration! Excessive loss of water from
Dipsogenic body tissue and imbalance of essential
= damage in thirst regulating center electrolytes (Na, K, Cl)
Polydipsia (excessive thirst)
Gestational Polyuria (excessive amount of urine)
=It occurs only during pregnancy when an Low specific gravity (1.001 to 1.005)
enzyme made by the placenta destroys ADH in Serum hyperosmolality and hypernatremia
the mother. Primary polydipsia. Also known as
dipsogenic diabetes insipidus, this condition can Investigate the following for DI
cause production of large amounts of diluted urine Unquenchable thirst
from drinking excessive amounts of fluids Polydipsia
Polyuria (hourly urine output > 200 mls)
Pathophysiology of DI Unexplained weight loss
Urinary frequency
Nocturia
Dry skin/poor skin turgor
Tachycardia and hypotension
Inability to respond to the increased thirst Water Deprivation Test
stimulus and compensate for the excessive • After baseline measurement of: weight,
polyuria ADH, plasma sodium, and urine/plasma
Hypernatremia that becomes severe and is osmolality, the patient is deprived of fluids
manifested by- confusion, irritability, under strict medical supervision
stupor, coma and neuromuscular • Frequent (q2h) monitoring of plasma and
hyperactivity progressing to seizures. urine osmolality follows.
Elderly • The test is generally terminated when
Unconscious/intubated plasma osmolality is >295 mOsm/kg or the
patient loses ≥3.5% of initial body weight.
Labs and Diagnostics for DI • DI is confirmed if the plasma osmolality is
Serum calcium >295 mOsm/kg and the urine osmolality is
Glucose <500 mOsm/kg.
Creatinine
Potassium Nephrogenic DI vs Neurogenic DI
Urea level DDAVP Challenge
Check urine osmolality 1-2hrs after
The following may also be indicated: 1mcg SQ DDAVP
If little or no change: likely
24hr urine collection to quantitative NDI or dipsogenic DI
polyuria If significant increase in
CT/MRI urine osmolality, likely CDI
rule out pituitary causes, Abbreviation for “1-desamino-8-d-arginine
metastases, hemorrhage, vasopressin.” DDAVP is a synthetic version
neuronal damage, cerebral of antidiuretic hormone (ADH) originally
tumors. developed to treat diabetes insipidus. .
Radioimmunoassy: to measure Desmopressin
5 units vasopressin IV
circulating ADH concentrations
Measure osmolality
A significant increase (>50%) in
urine osmolality after administration
of ADH is indicative of CDI
Treatment of DI
Lab Results for diagnosis of DI Correct the underlying cause and maintain
adequate fluid replacement.
DI Therapy varies with the degree and type
of DI present or suspected.
IVF may be necessary to correct
hypernatremia; avoid rapid replacement
Free water restriction
After assessing fluid status and serum
sodium level, treat both dehydration and
hypernatremia
For chronic neurogenic DI- require
hormonal replacement therapy: DDAVP
(nasal vasopressin)
Consultation with an endocrinologist is
Diagnosis of DI should be considered in any strongly recommended
person producing large volumes of dilute urine
Treatment for Nephrogenic DI Central Pontine Myelinolysis: brain cell
Removal of the underlying cause/offending drug dysfunction caused by destruction of the
DDAVP usually ineffective myelin sheath covering nerve cells in
Thiazide diuretic (HCTZ) is first line brainstem
treatment Na levels rise too fast or corrected too
Adequate hydration quickly
Low-sodium diet + thiazide diuretics to s/s: (not necessarily immediate)
induce mild sodium depletion. Acute paralysis
Indomethacin may also be useful to reduce Dyschagia
urine volume. Dysarthria