endocrine Flashcards
Mechanisms of Hormone Alterations
Inappropriate Amounts of Hormone Delivered to Target Cell
Inappropriate Response by Target Cell
Inadequate Hormone Synthesis
1.Inadequate quantity of hormone precursors
2.Secretory cell unable to convert precursors to active hormone
1.Decrease in the number of receptors
2.Impaired receptor function
3.Presence of antibodies against specific receptors
Failure of Feedback Systems
Dysfunctional or Ectopic Hormones Intracellular Disorders
1.Inadequate biologically free hormone
2.Hormone degraded at an altered rate
3.Circulating inhibitors
4.Ectopic production of hormones
1.Inadequate synthesis of a second messenger
2.Intracellular enzymes or proteins are altered
Dysfunctional Delivery System
1.Inadequate blood supply
2.Inadequate carrier proteins
alteration in hypothalamus
The most common cause of apparent hypothalamic dysfunction is interruption of the pituitary stalk. Such interruptions prevent hypothalamic hormones from reaching the pituitary gland
syndrome of inappropriate ADH secretion (SIADH)
ADH release in the absence of normal physiologic stimuli from the pituitary gland cause water retention. fluid is reabsorbed in the kidney therefore dilutional hyponatremia, high urine osmolarity, high urine sodium concentration.
symptoms of SIADH
related to hyponatremia
- thirst, fatigue, dulled sensorium
-vomiting, abd cramps
-lethargy, confusion, muscle twitching
related to water retention
-weight gain but peripheral edema is absent
Diagnosis and management
of SIADH
(1) serum hypoosmolality and hyponatremia,
2) urine hyperosmolarity (i.e., urine osmolality is greater than expected for the concomitant serum osmolality)
(3) the absence of conditions that can alter volume status (e.g., adrenal or thyroid dysfunction, congestive heart failure, or renal insufficiency)
correct hyponatremia
characteristic of Diabetes Insipidus
insufficient ADH activity, leading to polyuria (frequent urination) and polydipsia (frequent drinking)
Neurologic Diabetes Insipidus ( central DI)
insufficient ADH secretion
due to lesion of the hypothalamus, pituitary stalk, or posterior pituitary interferes with ADH synthesis, transport, or release.
Traumatic brain injury
immunological
hereditary
Nephrogenic DI
inadequate response of the renal tubules to ADH.
disease damage the renal tubules.
Drugs that induce reversible form of nephrogenic DI
lithium carbonate, colchicine, amphotericin B, loop diuretics, general anesthetics, and demeclocycline.
Diseases that causes Nephrogenic DI
pyelonephritis, amyloidosis, destructive uropathies, and polycystic kidney disease.
Diabetes Insipidus
partial to total inability to concentrate urine. Insufficient ADH activity causes excretion of large volumes of dilute urine, leading to increased plasma osmolality, serum hypernatremia
diagnostic and management of DI
polyuria, polydipsia, hypernatremia
low urine specific gravity (<1.010), low urine osmolality (<200mOsm/kg),
high serum osmolality (300mOsm or more depending on water intake),
ontinued diuresis despite a serum sodium level of 145mEq/L or greater.
The diagnosis of DI
-two-step water deprivation testing in which urine output is maintained despite dehydration.
compare and contrast SIADH and DI
Hypopituitarism
absence of one or more anterior pituitary hormones or the complete failure of all anterior pituitary hormone functions.
common cause of hypopituitarism
Pituitary infarction
(due to significant blood loss or hypovolemic shock.) lead to tissue damage, fibrosis
space-occupying lesions include pituitary adenomas or aneurysms, which can enlarge and compress the pituitary gland.
traumatic brain injury,
removal or destruction of the gland
infections (e.g., meningitis, syphilis, tuberculosis),
autoimmune hypophysitis,
drugs (e.g., bexarotene, carbamazepine, ipilimumab).
mutation of the prophet of pituitary transcription factor (PROP-1) gene,
hormone release by the anterior pituitary gland
FLAT PeG
FH
LH
ACTH
TSH
Prolactin
GH
Most common autoimmune Hypothyroid condition
Hashimoto thyroiditis
autoimmune
thyroid infiltration of T lymphocytes and follicular destruction
Primary hyperthyroidism
results from thyroid gland dysfunction
Graves disease,
toxic multinodular goiter, toxic thyroid adenoma.
Graves disease
B cell-mediated type 2 hypersensitivity reaction,
immune system produces antibodies - thyroid-stimulating immunoglobulins (TSI) or thyroid receptor antibodies (TRAb). bind to and activate TSH receptors on the surface of thyroid cells
leads to the stimulation and enlargement of the thyroid gland and excessive production of thyroid hormones (hyperthyroidism).
T cells infiltrate also observed in the the thyroid gland due to overall immune response.
difference btw Graves disease,
toxic multinodular goiter, toxic thyroid adenoma.
Toxic multinodular goiter occurs when there are several hyperfunctioning nodules leading to hyperthyroidism. Unlike Graves disease, there is absence of an autoimmune stimulus. If only one big nodule is hyperfunctioning, it is termed toxic adenoma.
GH and the anterior pituitary gland
Controlled by hypothalamic release of GHRH and growth inhibiting hormone (somatostatin). Ant pit release small pulsatile amount of GH each day.
GH acts on the Liver stimulates production of insulin-like growth factor 1 that promotes cell metabolism
GH acts on the muscle inc protein synthesis
GH slows carb utilization inc blood glucose and insulin
GH acts on the growth plate of the bones, inc osteoblast and growth
Hypoglycemia and increased concentration of amino acids in the blood stimulates GH release
ACTH and the anterior pituitary gland.
Regulate the release of hormones by the anterior adrenal gland.
in response to signals from the hypothalamus CRH
ACTH stimulates the release of
Glucocorticoid - cortisol ,antiinflammatory, metabolic effect
Mineralocorticoids - aldosterone, influence electrolyte and fluid balance
(physiological, psychological stress) Hypoxia, hypoglycemia, hyperthermia, exercise, and cortisol insufficiency stimulate the release of ACTH
Cushing disease
Cushing disease refers to excess endogenous secretion of ACTH
Overproduction ACTH by a primary pituitary adenoma (most common and can occur at any age)
Ectopic secreting ACTH by a nonpituitary tumor, such as a small cell carcinoma of the lung (more common in older adults)
ACTH dependent - high ACTH low CRH
Over secretion of cortisol due to Adrenal gland tumor
ACTH independent - low CRH low ACTH
Cushing Syndrome
Cushing syndrome (chronic hypercortisolism) refers to the clinical manifestations resulting from chronic exposure to excess cortisol regardless of cause.
primary cause by exogenous glucocortioid medication
Breast Cancer
