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
