Alteration in Hormone Regulation Flashcards
Cell surface receptor–associated disorders.
(1) a decrease in the number of receptors, leading to decreased or defective hormone-receptor binding
(2) impairment of receptor function, resulting in insensitivity to the hormone
(3) presence of antibodies against specific receptors that either reduce available binding sites or mimic hormone action suppressing or exaggerating the target cell response
(4) unusual expression of receptor function, as occurs in some tumor cells.
Intracellular disorders.
involve acquired defects in post-receptor signaling cascades or inadequate synthesis of a second messenger needed to transduce the hormonal signal into intracellular events
most common cause of hypothalamic dysfunction
interruption of the pituitary stalk
caused by destructive lesions, rupture after a head injury, surgical transection, or tumor.
Diseases of the posterior pituitary usually cause
abnormal secretion of antidiuretic hormone (ADH, arginine vasopressin)
An excess amount of this hormone results in water retention and a hypoosmolar state,
a deficiency in the amount or response to ADH results in serum hyperosmolarity
Syndrome of inappropriate antidiuretic hormone (SIADH) secretion
characterized by high levels of ADH in the absence of normal physiologic stimuli for its release
A common cause of SIADH
ectopic production of ADH by tumors, such as small cell carcinoma of the duodenum, stomach, and pancreas; cancers of the bladder, prostate, and endometrium; lymphomas; and sarcomas.
cause of SIADH, especially in the elderly
hypoglycemic medications (e.g., chlorpropamide), antidepressants, antipsychotics, narcotics, general anesthetics, chemotherapeutic agents, nonsteroidal anti-inflammatory drugs, and synthetic ADH
(These drugs either stimulate ADH release, enhance the physiologic effects of ADH, or have a biologic action similar to that of ADH)
Pathophysiology of SIADH
ADH increases renal collecting duct permeability to water resulting in an expansion of extracellular fluid volume
leads to:
dilutional hyponatremia (low serum sodium concentration)
hypoosmolarity
urine that is inappropriately concentrated with respect to serum osmolarity, because water is reabsorbed that normally would be excreted.
signs/symptoms SIADH
thirst, impaired taste, anorexia, dyspnea on exertion, fatigue, and dulled sensorium (drop of serum sodium 140 to 130 mEq/L)
gastrointestinal symptoms, including vomiting and abdominal cramps, weight gain from water retention, even with nausea and vomiting (drop in serum sodium from 130 to 120 mEq/L)
confusion, lethargy, muscle twitching, and seizures; severe and sometimes irreversible neurologic damage (serum sodium levels less than 110 to 115 mEq/L)
correction of any underlying causal problems and fluid restriction
treatment of SIADH
Manifestations of SIADH
(1) serum hypoosmolality (<280 mOsm/kg) and hyponatremia (serum sodium level <135 mEq/L)
(2) urine hyperosmolarity (i.e., the osmolality of the urine is always higher than the concurrent serum osmolality)
(3) urine sodium excretion that matches sodium intake
(4) normal renal, adrenal, and thyroid function
(5) absence of conditions that can alter volume status
Diabetes Insipidus
insufficiency of ADH, leading to polyuria (frequent urination) and polydipsia (frequent drinking).
Neurogenic or central Diabetes Insipidus (DI)
caused by insufficient secretion of ADH.
abrupt onset
a well-recognized complication of traumatic brain injury or pituitary surgery
neurogenic diabetes insipidus (DI)
lesion of the hypothalamus, pituitary stalk, or posterior pituitary interferes with ADH synthesis, transport, or release
cause of neurogenic DI
Nephrogenic Diabetes Insipidus (DI)
inadequate response of the renal tubules to ADH
can be genetic or acquired
Slow onset
pyelonephritis, amyloidosis, destructive uropathies, polycystic disease, and intrinsic renal disease
lead to nephrogenic DI
lithium carbonate, colchicines, amphotericin B, loop diuretics, general anesthetics (such as methoxyflurane), and demeclocycline.1
drugs that can cause nephrogenic DI
Pathophysiology of DI
partial to total inability to concentrate urine
Insufficient ADH activity causes the excretion of large volumes of dilute urine, leading to increased plasma osmolality
thirst is stimulated
dehydration develops rapidly without ongoing fluid replacement
If the individual with DI cannot conserve as much water as is lost in the urine, serum hypernatremia and hyperosmolality occur
signs/symptoms of DI
polyuria, nocturia, continuous thirst, and polydipsia
The criteria for the diagnosis of DI include
polyuria
polydipsia
low urine specific gravity (<1.010)
low urine osmolality (<200 mOsm/kg)
hypernatremia
high serum osmolality (300 mOsm or more depending on adequate water intake)
continued diuresis despite a serum sodium level of 145 mEq/L or greater.
water deprivation with measurement of serum osmolarity and plasma ADH levels
diagnostic test for DI
no decrease in urine volume or increase in urine osmolality
patient with DI who is undergoing water depravation for diagnosis of DI
Neurogenic DI can be differentiated from nephrogenic DI
measuring the response to administered desmopressin:
Neurogenic DI will respond with an increased ability to concentrate the urine
Nephrogenic DI will not respond.
Treatment for nephrogenic DI
fluid replacement using oral or intravenous routes
Treatment for neurogenic DI
intravascular or, more commonly, oral or intranasal administration of the synthetic vasopressin analog DDAVP (desmopressin)
Management of nephrogenic DI
treatment of any reversible underlying disorders
discontinuation of etiologic medications
correction of associated electrolyte disorders
