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Catabolism
breaking down of complex materials (enzymes)
Anabolism
building of complex materials (enzymes)
Pure endocrine glands
pituitary
thyroid
parathyroid
thymus
adrenals
pineal
Mixed endocrine/exocrine
pancreas
gonads
exocrine released via ducts
Hormones
chemical substances secreted by cells into blood
delay producing effects from seconds to hours
prolonged effects
amino-acid based or steroid hormones
blood levels controlled by negative feedback systems
Humoral stimuli
tropic hormones
secretion of hormones in direct response to changing blood levels of ions and nutrients
declining blood Ca2+ concentration stimulates parathyroid glands to secrete PTH (parathyroid hormone)
Nervous system modulation
modifies the stimulation of endocrine glands and their negative feedback mechanisms
can override normal endocrine controls
Hypothalamus
controls pituitary gland
Pituitary gland
secretes 8 hormones, most control other hormones
adenohypophysis (anterior lobe)
neurohypophysis (posterior lobe)
Adenohypophysis
anterior lobe of pituitary (glandular)
hypophyseal portal system: vascular connection between hypothalamus and adenohypophysis
Neurohypophysis
posterior lobe of pituitary (neural)
hypothalamic hypophyseal tract: collection of axons from hypothalamus to neurohypophysis
Adenohypophysis hormones
growth hormone (GH)
prolactin (PRL)
tropic hormones:
thyroid-stimulating hormone (TSH)
adrenocorticotropic hormone (ACTH)
follicle-stimulating hormone (FSH)
luteinizing hormone (LH)
Neurohypophysis hormones
antidiuretic hormone (ADH or vasopressin)
oxytocin
Growth hormone (GH)
stimulates protein synthesis & use of fats for fuel, greatest effect of bone and skeletal muscle
too much GH in childhood leads to gigantism or acromegaly in adults
too little GH in childhood leads to pituitary dwarfism
Prolactin (PRL)
in females: stimulate breast development, milk production, blood level rise towards end of pregnancy
in males: stimulate testosterone production
Thyroid stimulating hormone (TSH)
stimulates thyroid gland
rising blood levels of TH act of pituitary and hypothalamus to block release of TSH
Adrenocorticotropic hormone (ACTH)
stimulates adrenal cortex to release corticosteroids
triggered by hypothalamic corticotropin-releasing hormone (CRH) determined by hypothalamus
fever, hypoglycemia, and stressors triggers release of CRH
Gonadotropins
regulate function of ovaries and testes (estrogen and testosterone production)
triggered by hypothalamic gonadotropic-releasing hormone (GnRH) during/after puberty
FSH
LH
Follicle-stimulating hormone (FSH)
regulate function of the ovaries and testes (estrogen and testosterone production)
stimulates gamete (egg or sperm) production/ maturation
Luteinizing hormone (LH)
regulate function of the ovaries and testes (estrogen and testosterone production)
causes ovulation (turns the follicle into a corpus luteum in females)
in males, stimulates testosterone production
Oxytocin
stimulates smooth muscle contraction in breasts (milk ejection) and uterus (labor)
synthetic and natural oxytocic drugs are used to induce or hasten labor (pitocin)
Antidiuretic hormone (ADH)
regulates water volume and blood pressure
directly affects water reabsorption (prevents urine formation)
synthesized in hypothalamus
alcohol can inhibit ADH release and cause copious urine output and dehydration (morning-after dry mouth)
Hypersecretion of ADH
too much water retained
edema, headache and disorientation
Hyposecretion of ADH
diabetes insipidus
excess urine output that’s not sweet (like diabetes mellitus)
polyuria and polydipsia
Thyroid gland
largest endocrine gland
produces 2 hormones
thyroid hormone (TH)
calcitonin (thyrocalcitonin)
Thyroid hormone (TH)
T3 - triiodothyronine
T4 - thyroxine (common): glucose oxidation, regulate BMR, heat production, effect heart and nervous system
Calcitonin (thyrocalcitonin)
decreases blood calcium by stimulating calcium salt deposit in bones
antagonistic to parathyroid hormone
Hyperthyroidism
glucose oxidation (weight loss and muscle wasting)
increased BMR (increased appetite, weight loss)
increased heat production (increased body temp and heat tolerance)
rapid heart rate (cardiovascular system)
irritability, restless, insomnia (nervous system)
Hypothyroidism
common cause: lack of iodine
glucose oxidation (decreased metabolism, stored as fat)
decreased BMR (decreased appetite, weight gain)
decreased heat production (decreased body temp, cold tolerance)
low heart rate (cardiovascular system)
mental dullness, depression (nervous system)
Parathyroid hormone (PTH)
increases available calcium in blood by:
releasing calcium from bone
cause kidneys to reabsorb more calcium and less phosphate
stimulate kidneys to convert vitamin D to calcitriol: increase calcium absorption from food)
produced by chief cells
Hyposecretion of PTH
causes neural excitability, can lead to:
tetany- prolonged muscle spasms which can lead to respiratory paralysis
Hypersecretion of PTH
causes bone deformation, softening and spontaneous fractures
Adrenal cortex
synthesizes and released steroid hormones called corticosteroids
basic template for all steroid hormones: cholesterol
mineralocorticoids
glucocorticoids
gonadocorticoids
Mineralocorticoids
mainly aldosterone
regulate Na+ reabsorption in tubules, indirectly regulate water reabsorption as “water follows the solute”
Glucocorticoids
mainly cortisone, corticosterone and hydrocortisone (cortisol)
increase blood glucose levels
Gonadocorticoids
mainly androgens
male sex hormones which are converted to testosterone or estrogen after release
source of estrogen post menopause
Adrenal medulla
releases epinephrine (80%) and norepinephrine (20%)
neural stimuli: blood glucose levels rise, blood vessels to constrict, heart beat faster, blood flow increase to heart and skeletal muscle
Pancreas
glucagon
insulin
Glucagon
stimulated by low blood glucose levels (hypoglycemia)
major target is liver: promotes degradation of stored glycogen to release glucose into blood
hypoglycemia caused by too much insulin (anxiety, nervousness, tremors, weakness and coma)
Insulin
stimulated by high blood glucose levels (hyperglycemia)
lowers blood glucose levels by: enhancing transport glucose into body cells, triggering enzymatic activity in cells that catalyzes the oxidation of glucose for ATP production, promoting liver to make glycogen
Diabetes mellitus (DM)
caused by hyposecretion of insulin (type I) or ineffective insulin receptors (type II)
inability of cells to use glucose and loss of glucose in urine
3 cardinal signs: polyuria, polydipsia, polyphagia
Type I diabetes mellitus
autoimmune, beta-cell destruction, NO insulin formed
must get insulin injections, lack of insulin causes DKA
Type II diabetes mellitus
enough insulin, receptors not responding adequately
patients generally obese and sedentary
weight loss, healthy diet and exercise can return person to normal
Gonads
females - ovaries: estrogen and progesterone
males - testes: testosterone
Estrogen
development of breasts and maturation of reproductive organs
work with progesterone in cyclin changes in uterine lining and preparation of mammary glands for lactation
Progesterone
maintains uterine lining in quiescent state during pregnancy and works with estrogen
Testosterone
initiates maturation of reproduction organs, secondary characteristics and libido
Thymus and Pineal gland
thymus: hormones direct maturation and specialization of T-cells (thymosin and thymopoietin)
pineal (epiphysis cerebri): produces melatonin (inhibit precocious sexual maturation, creates drowsiness)