Endocrinology

 
 

 
 

 
 

 
 
 
 
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endocrine glandsanterior pituitary, posterior pituitary, thyroid, parathyroid pancreas, adrenal cortex, adrenal medulla, ovaries, testes
receptorintegral membrane protein that receives hormones
target cell has how many receptors for a particular hormone?2000-100,000
down-regulationwhen a hormone is present in excess the number of target cell receptors may decrease
steroidslipids that are derived from cholesterol. These are lipid soluble and will thus cross the plasma membrane and enter cells rapidly. Estrogens, progesterone, testosterone, aldosterone, cortisol
biogenic aminessynthesized by modifying amino acids; T3 and T4, epinephrine, histamine, serotonin
peptides and proteinsthese hormones consist of chains of 3 to 200 amino acids. Oxytocin, ADH, Insulin, parathyroid hormone, calcitonin, CCK and gastrin
how are most hormones transported in the blood?carrier proteins
master glandanterior pituitary, now known to be controlled by the hypothalamus. has structure of an endocrine gland
seven hormones of anterior pituitarygrowth hormone GH, Adrenocorticotripic hormone ACTH, Thyroid stimulating hormone TSH, prolactin PRL, follicle stimulating hormone FSH, luteinizing hormone LH, melanocyte stimulating hormone MSH
two hormones of posterior pituitaryantidiuretic hormone ADH, oxytocin
the hypothalamus makes hormones for which pituitaryposterior
the hypothalamus transports hormones down the axons of the neurosecretory cells for which pituitaryposterior
which pituitary is controlled by substances made in the hypothalamusanterior
releasing or inhibitory hormoneshypothalamic substances which regulate the anterior pituitary; CRH stimulates ACTH; TRH stimulates TSH and a little prolactin; GnRH or LHRH stimulates FSH and LH; GIH or somatostatin inhibits GH
Growth HormoneGH or somatotropin; stimulates the uptake of amino acids into cells; stims growth of long bones and soft tissues; closure of epiphyseal cartilage stops growth of long bones-puberty (sex hormones)
pituitary adenoma causesacromegaly and gigantism
gigantism & acromegalygigantism-excess GH before puberty; acromegaly-excess GH in adults
symptoms of acromegaly/gigantismovergrowth of bone, particularly of the skull and mandible; nose thickened and puffy, large ears, large tongue, large hands, increased sweating, fatigue, and weight gain
Pituitary Dwarfismlack of GH or GRH before puberty; may also be caused by hypothalamic-pituitary tumor; symptoms-small body, normal proportions; mild obesity w/ lack of appetite
How to diagnose pituitary dwarfisminadequate rise in serum GH after provocative stimulus such as Arginine infusion, oral levodopa, or clonidine
Prolactinstimulates the production of milk; promotes breast development in pregnancy
Thyroid stimulating hormone- TSHpromotes and maintains growth and development of the thyroid gland and stimulates it to secrete thyroxine (T4) and triidothyronine (T3)
Follicle Stimulating Hormone FSHstimulates growth and develpment of the follicle to maturity, stims the follicle to secrete estrogens, stimulates testicular growth, enhances production of androgen-binding protein in the Sertoli cells (this increases the conentratino of testosterone near
Luteinizing hormone LHacts with FSH in the development of the follicle, promotes ovulation, responsible for the formation of the corpus luteum, stims corpus luteum to produce estrogen and progesterone, stims production of testosterone by the interstitial cells in males
Adrenocorticotropin ACTH or corticotropinPromotes and maintains normal growth and development of the adrenal cortex and stims the secretion of the glucocorticoids (cortisol); also affects the secretion of the androgens and the mineralcorticoids (aldosterone). ACTH is a polypeptide that is 39 a
osteoblast activitystimulated by GH
epiphyseal cartilagestimulates by GH; makes space for bone formation
somatomedinsGH exerts growth-promoting effects indirectly by stimulating somatomedins; somatomedin IGF is an insulin-like growth factor
GH does not act directly on its target cells to bring aboutcell division, enhanced protein sythesis, or bone growth
where is IGF-I madeliver mostly
production of IGF-I is controlled bynutritional status, age, and tissue specific factors
what closes the epiphyseal plate?sex hormones among other things
hormones of the posterior pituitaryoxytocin and ADH (vasopressin)
where are posterior pituitary hormones synthesizedin the hypothalamus and then transported intracellularly to the posterior pituitary from which they are released
oxytocin functionsstimulate milk secretion and strong uterine contractions
milk secretion physiologyoxytocin causes contraction of myoepithelial cells surrounding mammary alveoli (women not secreting enough milk are given an oxytocin nasal spray)
uterine contraction physiologyoxytocin alters transmembrane ionic currents in myometrial smooth muscle cells to produce sustained uterine contractions. Sensitivity to oxytocin of uterine muscle increases during pregnancy.
diabetes insipiduslack of ADH (often due to damage to the pituitary or the hypothalamus. loss of 75% of ADH secretory neurons is necessary before polyuria is evident)
Alcohol's effect on ADHdecrease release of
Narcotics effect on ADHincrease release of
symptoms of lack of ADHpolyuria, polydipsia, dehydration, fever, dry tongue, delirium
where are catecholamine hormones secretedadrenal medulla; these are epinephrine and norepinephrine (these supplement the action of the sympathetic nervous system)
what does the adrenal cortex secrete in generalcorticosteroids
chromaffin cells do whatsecrete catecholamines in the adrenal medulla
corticosteroid hormones of the adrenal cortexmineralocorticoids, glucocorticoids, and gonadocorticoids
three zones of adrenal cortexzona glomerulosa, zona fasciculata, zona reticularis
other name for mineralcorticoidsaldosterone
other name for glucocorticoidscortisol (hydrocortisone)
other name for gonadocorticoidssex hormones
action of mineralcorticoids (aldosterone)regulate the concentration of extracellular electrolytes, especially sodium and potassium, water balance
regulation of mineralcorticoids (aldosterone)renin-angiotensin system (angiotensin II)
action of glucocorticoids (cortisol)influence the metabolism of carbohydrates, proteins, and fats; promote vasoconstriction; anti-inflammatory; decrease antibody production
regulation of glucocorticoids (cortisol)ACTH from the adenohypophysis of the pituitary gland in response to stress
action of gonadocorticoids (sex hormones)supplement the sex hormones from the gonads
addison's diseaseinadequte secretion of glucocorticoids and mineralcorticoids which results in hypoglycemia, na+ and K+ impalance, dehydration, hypotension, weight loss, and general weakness
cushing syndromehypersecretion of corticosteroids generally caused by a tumor of the adrenal cortex or by oversecretion of ACTH by the pituitary. Symptoms are puffy face, hyperglycemia, hypertension, decreased antibodies, and muscle weakness
adrenogenital syndromealteration of enzymes required to produce mineralcorticoids and glucocorticoids, results in an increase in the production of sex hormones. symptoms: masculinization of females, facial and body hair, acne, paleness, increased muscularity, atrophy of breas
what does the thyroid gland producethyroxine (T4) and triiodothyronine (T3), and calcitonin
physical structure of thyroidtwo laterla lobes interconnected by an isthmus (neck area)
histological structure of thyroidspherical sacs called thyroid follicles. Humans have about one million follicles. Each follicle is lined with principal cells which synthesize T3 and T4 and contain a protein-rich fluid called colloid. Between the follicles are perifollicular cells whi
action of triiodothyronine and thyroxineregulate metabolism; increase rate of protein synthesis; increase rate of energy release from carbs; regulate growth; stimulate maturity of nervous system; regulate body temp
regulation of T3 and T4hypothalamus and release of TSH from adenohypophysis of the pituitary gland
Action of Calcitonin (thyrocalcitonin)lowers blood calcium by inhibiting the release of calcium from bone tissue
regulation of calcitonincalcium levels in the blood
cretinisminsufficient secretion of T4 and T3 in infants and children. Stunted growth, thickened facial features, large protruding tongue, abnormal bone growth, mental retardation, decreased metabolic rate, general lethargy. Treat with T3 and T4
myxedemainsufficient secretion of T4 and T3 in adults. Weight gain, slow pulse, dry brittle hair, decreased basal metabolic rate, lack of energy, sensation of coldness, diminished perspiration, weakness. treat with T3 and T4
goitera pathological enlargment of the thyroid gland due to insufficient iodine intake. Take iodine.
graves' disease (thyroxicosis)excessive secretion of T4 and T3. Loss of weight, rapid pulse, warm, moist skin, increased appetite, increased basal metabolic rate, tremor, goiter, exophthalmos (bulging eyes); muscular weakness. Treatment: surgical removal of a portion of thyroid gland,
what percent of calcium is in crystalline form99%
lf the non crystalline calcium, what percent is in cells and what percent is in extracellular fluidof 1%, .9% is inside the cells and .01% is in the extracellular fluid
parafollicular or C cellsproduce calcitonin in the thyroid gland; lower the blood calcium and phosphates by: 1. decreasing bone resorption by inhibiting the activity of osteoclasts 2. stimulating urinary excretion of calcium and phosphate by inhibiting their reabsorption in the k
parathyroid glandsfour small glands attached to the posterior surface of the thyroid glands. Principal or chief cells in the parathyroid glands secrete parathyroid hormone (PTH) or parathormone.
what happens in the absence of PTHdeath in a few days from hypocalcemia
functions of PTH (parthormone)stimulates the activity of osteoclasts to reabsorb bone (remove Ca++ from bones), stims the kidneys to reabsorb ca++ from the filtrate, promotes the formation of 1,25 dihydroxyvitamin D3
1, 25 dihydroxyvitamin D3 functionhelps raise the plasma calcium and phosphate levels by stimulating 1. intestinal absorption of Ca++ and Phosphate 2. reabsorption of Ca++ from bones 3. renal absorption of ca++ and phosphate so that less is excreted in the urine
hyperparathyroidismusually caused by a tumor in one of the parathyroid glands. Is characterized by hypercalcemia- muscle weakness, neurological disorders, decreased alertness, poor memory
hypoparathyroidismused to be caused by removal of parathyroids during thyroid surgury. Could lead to death. Other symptoms- hypocalcemia, increased neuromuscular excitability
endocrine gland in the pancreasislets of langerhans (clusters of cells); alpha cells secrete glucogon, beta cells secrete insulin
Glucogonelevates blood glucose by stimulating glycogenolysis in the liver, this helps the body maintain sufficient blood glucose levels during fasting and starvation
Insulinpromotes the cells to take up glucose; some tissue do not require insulin for glucose uptake (brain, kidney, intestinal, and red blood cells); stimulates glycolysis; lowers blood glucose levels
diabetes mellitusinsulin deficiency
genetic factors in diabetes mellituspredisposition of diabetes is inherited, the genetic factors are complex (on chromosome 6), over 20% of the relatives of diabetic patients have abnormal glucose tolerance curves
other possible causes (not hereditary) of diabetes mellitusenvironmental chemicals and drugs, infectious agents (mumps virus, rubella, pancreatitis), autoimmune events (antibodies damage the beta cells, anti-insulin receptor antibodies
two types of diabetes mellitustype I-insulin-dependent (juvenile onset), type II-noninsulin-dependent (maturity onset)
type I insulin-dependent (juvenile onset) diabetes mellitusrequires insulin injections (there is no insulin being secreted), often severe and complicated by ketoacidosis, onset usualy in youth but may occur at any age
type II noninsulin-dependent (maturity onset) diabetes mellitus90-95% of diabetes, injections not required, patient usually obese, may use oral hypoglycemic drugs to stimulate insulin release from beta cells, insulin resistance is a factor for 60-80% of patients with type II diabetes
how to diagnose diabetes mellitusoral glucose tolerance test; oral administration of 1.75 g/Kg of glucose after at least 3 days on a 300 g carbohydrate diet
symptoms of diabetes mellitusglycosuria, polyuria (glucose acts as an osmotic diuretic), polydipsia, hyperglycemia, weakness, loss of weight, acetone breath (ketoacidosis), acetone in the urine
increased risk of infection due to diabetes mellitusfactors that increase infection 1. pathogens proliferate rapidly b/c of excess glucose 2. hypoxia-glycosylated hemoglobin in RBC's impedes the release of O2 3. decreased blood flow to infected area b/c of vascular damage 4. white blood cells have impaired
insulin excess results ininsulin shock (hyperinsulinism)
gestational diabetes mellitus (GDM)refers to diabetes that occurs during pregnancy (in 1 to 14% of pregnancies) and then disappears following delivery
GLUT4transporter that moves glucose across the membrane