Endocrine, nervous and immune systems work together to regulate responses to internal
and external environment
Hormone release is regulated
... [Show More] by:
o Chemical factors (BGL, Ca levels)
o Endocrine factors (cortisol)
o Neural control- ANS stimulates
Negative feedback- MOST COMMON, occurs when a changing chemical, neural or
endocrine response DECREASES synthesis and secretion of hormone
Positive feedback occurs when a neural, chemical, or endocrine response INCREASES
synthesis and secretion of hormone.
o Also occurs when increased hormone level further increases synthesis and
secretion of that same hormone
o Ex- cyclic rise of estradiol levels
Hormone receptors of target cells have 2 functions
o Recognize and bind with high affinity to their particular hormones
o Initiate signal to appropriate intracellular effectors
o The sensitivity or affinity of the target cell to a particular hormone is r/t the
concentration of receptors for cell- more receptors= more sensitive to stimulating
effects of hormone
High concentrations of hormone decrease the number or affinity of receptors per cell=
DOWNREGULATION
o The cell can adjust its sensitivity to the concentration of signaling hormone
o Receptors on plasma membrane are continuously synthesized and degraded so
changes in receptor concentration may occur within hours
Thyrotoxicosis
Condition that results from any cause of an increased amt of TH levels
HYPERthyroidsm= form of thyrotoxicosis which excess amts of TH are secreted
Thyrotoxicosis and hyperthyroidism used interchangeably
More prevalent in women and iodine-deficient geographical areas
Diseases that cause primary hyperthyroidism= Graves’ disease, toxic multinodular goiter,
toxic adenoma
Secondary- less common and caused by TSH-secreting pituitary adenomas
S/S are attributable to metabolic effects of increased circulating levels of TH
o Increased metabolic rate with heat INTOLERANCE
o Thin hair, exophthalmos, normal or enlarged thyroid (goiter), tachycardia (HF),
wt loss, diarrhea, N/V, warm skin, sweaty palms, hyperreflexia, pretibial
myxedema, restlessness, insomnia, fatigue, tremor
Treatment= antithyroid drug therapy, radioactive iodine, surgery. Major complication of
hyperthyroidism tx= hypothyroidism
Thyrotoxic crisis (Thyroid Storm)
Rare but dangerous worsening of thyrotoxic state
Death can occur in 48 hrs without treatment
Spontaneous, occurs in individuals who have undiagnosed or partially treated severe
hyperthyroidism and are subjected to excessive stress from other causes (infection, pulm
& CV disease, trauma, burns, seizures, surgery, OB complications, emotional distress,
dialysis)
S/S caused by sudden release of T4 and T3 exceeding metabolic demands
S/S= hyperthermia, tachycardia esp. atrial dysrhythmias, high-output HF, agitation,
delirium, N/V/D
Tx= drugs that block TH synthesis, betablockers for CV symptoms, corticosteroids,
iodine
Hypothyroidism
Results from deficient production of TH- most common d/o of thyroid fn
More common in women and elderly- primary =99% of all cases
S/S= low basal metabolic rate- cold intolerance, lethargy, tiredness, low body temp,
bradycardia, diastolic HTN. Decrease in TH can lead to excessive TSH production
goiter
Diagnosis is made by measurement of increased TSH and decreased TH
Hormone replacement with levothyroxine is treatment
Hypoparathyroidism
Abnormally low PTH levels
Most commonly caused by damage to or removal of parathyroid glands during thyroid
surgery
Occurs because of the anatomic proximity of parathyroid glands to the thyroid
Also assoc. with genetic syndromes, including familial hypoparathyroidism and
DiGeorge syndrome
Pathophys- a lack of circulating PTH causes depressed serum Ca levels and increased
phosphate levels
o In absence of PTH, reabsorption of Ca from bone and regulation of Ca
reabsorption by renal tubules is increased causing decreased renal phosphate
excretion hyperphosphatemia
S/S= perioral numbness, paresthesia, tingling, tetany, hyperreflexia, tonic-clonic seizures
Cushing’s Syndrome
Disorder of adrenal cortex
Syndrome refers to clinical manifestations resulting from chronic exposure to excess
endogenous cortisol, more common in women
Disease refers to excess endogenous secretion of ACTH (Corticotropin)
ACTH-dependent hypercortisolism results from overproduction of pituitary ACTH by
pituitary adenoma
Cushing-like syndrome may develop as a side effect of long-term use of glucocorticoids
Pathophys- excess ACTH stimulates excess production of cortisol loss of feedback
control of ACTH secretion [Show Less]