honors anatomy & physiology. act together to coordinate body’s activities both: use...
TRANSCRIPT
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THE ENDOCRINE
SYSTEMHonors Anatomy & Physiology
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ENDOCRINE VS NERVOUSSYSTEM
act together to coordinate body’s activities both:
use chemical messengers to communicate cell to cell
major function: homeostasis endocrine: slower response time
hormones transported thru circulatory system target cells (any cell with hormone receptor)
anywhere in body nervous: quicker conduction of signals
neurotransmitters act on cells close by
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GLANDS
Endocrine Exocrine
no ducts secretions released
and diffuse into blood capillaries
have ducts secretions released
onto surface example: sweat
glands, salivary glands
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2 TYPES OF HORMONES
Peptide Steroid
bind to protein receptors in cell membranes (do not enter cell)
receptor-hormone activate enzyme in cytoplasm series of reactions result in cell response
enter cell & bind to receptor in cytoplasm or nucleus
Activates transcription of gene protein produced
generally action slower than peptide hormone
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ENDOCRINE SYSTEM
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HYPOTHALAMUS part of brain secretes
“releasing” hormones that act on pituitary gland
axons that store the 2 posterior pituitary hormones end there
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PITUITARY GLAND 2 lobes: posterior & anterior
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NEGATIVE FEEDBACK INHIBITION
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THYROID GLAND stimulated by TSH secretes thyroxin (T4) and
triiodothyronine (T3) (-) feedback inhibition
both have similar effects on target cells
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HYPOTHYROIDISM Thyroid produces too little hormone several causes: Hashimoto’s
autoimmune/ lack of Iodine in diet goiter (enlargement of thyroid due to increased TSH stimulation
Symptoms:Adults: lethargy, weight gain, anovulatory
cycles Infants:cretinism: dwarfism, low IQ, failure
to reach sexual maturity
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GOITER
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HYPERTHYROIDISM excessive secretion of thyroid hormones
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PARATHYROID GLANDS 4 small glands embedded in posterior
surface of thyroid gland secrete: parathyroid hormone (PTH)
regulated by serum Ca++ levels actions:1. stimulates removal of Ca++ from bone2. increases kidney tubules reabsorption of
Ca++3. activates vit D which enhances Ca++
absorption from food
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THYMUS upper thorax,
posterior to sternum largest in infants,
decreases as we age produces: thymosin –
programs T cells
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ADRENAL GLAND
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ADRENAL CORTEX outer layer produces 2 kinds of steroid hormones1. Glucocorticoids
major 1 – cortisol: reduces swelling by inhibiting immune
system/ raises serum glucose (stimulates liver to make glucose from proteins or lipids
2. Mineralocorticoids major 1- aldosterone acts on kidney to promote absorption of
Na+ & excretion of K+
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PANCREAS1. Insulin
protein reduces blood glucose by increasing entry
of glucose into cells/making glycogen in hepatocytes
regulated by blood glucose levels
2. Glucagon protein raises blood glucose by acting on
glycogen stores in liver regulated by blood glucose levels
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TESTES paired oval organs suspended in scrotum site of:
spermatogenesis production of androgens:1. Testosterone major one made by interstitial cells/stimulated by FSH
& LH produces male 2◦ sex characteristics in
puberty promotes growth & maturation of
reproductive system organs increases libido
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OVARIES paired, almond-shaped organs in pelvic
cavity produce ova release: estrogens & progesterone begin functioning in puberty in response
to anterior pituitary gonadotrophins
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ESTROGENS Estrone &Estradiol made by follicle
where ova is maturing stimulate:
development of 2◦ sex characteristics work with progesterone to prepare
uterine lining for implantation help maintain pregnancy & prepare
breasts to lactate(those estrogens made in placenta)
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PROGESTERONE made &secreted by corpus luteum acts with estrogen to prepare uterine
lining for implantation quiets uterine muscle during early
pregnancy helps prepare breasts for lactation
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PLACENTA produces hCG (human Chorionic
Gonadotropin)stimulates corpus luteum of ovary to
continue producing estrogens and progesterone so lining of uterus does not slough off (like in menstruation)
turns pregnancy tests +by 3rd mo pregnancy placenta produces
estrogen & progesterone (ovaries become inactive rest of pregnancy)
also produces hPL (human placental lactogen) works w/E & P in preparing breasts for lactation
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PITUITARY DISORDERS
AnteriorPituitary
PosteriorPituitary
Giantism: hypersecretion hCG
during chidhood abnl increse in length
of long bones hypersecretion hCG
in adulthood acromegaly (epiphyseal plates sealed) see thickening of bones of hands, face & thickening of skin on brow
Diabetes Insipidus:
defects in ADH excrete large
volumes of urine dehydration & thirst (bed-wetting in children)
can die w/in 2 days from the dehydration
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THYROID GLAND DISORDERS Hypothyroidism: Cretinism: congenital hypothyroidism
severe mental retardation if not tx’d
most states require testing new borns
Myxedema:adultshallmark:edema of facial tissues, slow HR, low body temp, sensitivity to cold, dry skin & hair, muscle weakness
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CRETINISM & MYXEDEMA
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THYROID GLAND DISORDERS Graves Disease most common form of
hypothyroidism 7 – 10 x more common in females autoimmune disorder:
autoantibodies that mimic TSH causes thyroid to grow & make thyroid hormones
signs: enlarged thyroid, exophthalmos
tx: surgical excision of all or part of thyroid or use of antithyroid drugs to block synthesis of hormones
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GRAVES DISEASE
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GOITER enlarged thyroid could be associated with hypo- or
hyperthyroidism, or euthyroidism (normal level of hormones) seen when intake of iodine too low
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ADRENAL GLAND DISORDERS Cushing’s Syndrome: hypersecretion of cortisol caused by tumors that secrete
cortisol (in adrenal cortex)ACTH stimulates more cortisol production in adrenal cortex
muscle wasting spindly arms & legs, “moon” face, “buffalo hump” red face
~80% have hypertension
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CUSHING’S SYNDROME
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ADRENAL GLAND DISORDERS Addison’s Disease: hyposecretion of glucocorticoids &
aldosterone most are autoimmune: antibodies
cause adrenal cortex destruction or block binding of ACTH to its receptors
TB can destroy adrenal cortex symptoms: (after 90% of cortex
destroyed) mental lethargy, anorexia, N/V, wt loss, hypotension, hypoglycemia, muscular weakness
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PANCREATIC ISLET DISORDERS Diabetes mellitus: (honey-
sweetened) inabillity to use or produce insulin 4th leading cause death in USA blood glucose levels high glucosuria 3 polys: polyuria, polydipsia,
polyphagi
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DIABETES MELLITUS Type 1: autoimmune abys destroy beta
cells mostly develops <20 yrs old most common in northern European
heritage cells starved for glucose so switch to
breaking down fatty acids ketone production ketoacidosis untx’d death
transport of lipids from adipocytes plaque formation in walls of arteries = atherosclerosis
excess glucose attaches to proteins in lens catarracts
small vessel disease: blindness, kidney failure, amputation of toes legs, impotence
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DIABETES MELLITUS TREATMENT self-monitoring of blood glucose
levels injections of insulin Diet:
45 – 50% carbohydrates<30% fats
Exercise
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TYPE 2 DIABETES non-insulin-dependent diabetes
(NIDDM) more common (90% of all cases) typically occurs in obese people > 35
yrs old#s children diagnosed increasing
many control it with diet, exercise, wt loss
oral hypoglycemic drugsstimulates secretion of insulin from beta
cells