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562 Cards in this Set
- Front
- Back
|
the only endocrine gland that stores its hormones
|
thryoid gland
|
|
|
the thyroid gland receives_______ blood / min
|
80-120 ml
|
|
|
parafollicular cells secrete:
|
calcitonin
|
|
|
calcitonin's function:
|
reduce calcium concentration in body fluids when level is elevated
|
|
|
a follicle is:
|
a sac of stored hormones (colloid) surrounded by follicle cells that produce it
|
|
|
how many layers of follicle cells in a follicle:
|
1 layer
|
|
|
where a parafollicular cells located?
|
in between follicles
|
|
|
triiodothyronine is known as:
|
T3
|
|
|
tetraiodothyronine is known as
|
T4
|
|
|
what do T3 and T4 bind with?
|
intracellular nuclear receptor molecules
|
|
|
what does T3 and T4 do?
|
it initiates new protein synthesis, increases rate of glucose, fat and protein metabolism , and may increase body temp.
|
|
|
normal growth of many tissues is dependent on?
|
T3 and T4
|
|
|
which is the predominant thryoid hormone; T3 or T4?
|
T4
|
|
|
which is more potent; T3 or T4?
|
T3
|
|
|
what do tissues do to T4?
|
they convert it to T3
|
|
|
what is TGB
|
thyroglobulin
|
|
|
what is the process of formation thryoid hormone?
|
iodide trapped by follicular cells-->synthesis of thyroglobulin-->release of TGB into colloid-->iodination of tyrosine in colloid-->form T3 & T4 by combining T1 & T2-->uptake & digest TGB in follicle cells--> secrete T3 &T4 into blood
|
|
|
what type of molecule is thyroglobulin?
|
a large glycoprotein
|
|
|
process of making TGB
|
synthesized in rER, glycosylated in golgi, packaged in secretory vesicles, released on apical side into colloid
|
|
|
TGB has a large number of?
|
tyrosine residues
|
|
|
what happens to tyrosine residues in TGB?
|
they are iodinated to form hormones
|
|
|
what is an iodide trap?
|
a Na/ I active symporter on the basal side
|
|
|
what stimulates activity in the iodide trap
|
TSH
|
|
|
what is the electron acceptor in the oxidation of I- to I2
|
hydrogen peroxide
|
|
|
what enzyme catalyzes the oxidation of I- to I2?
|
thyroid peroxidase
|
|
|
what is organification of iodine?
|
Iodine combines w/ tyrosine on TG to form monoiodotyrosine (MIT) and diiodotyrosine (DIT) which remains attached to TG until the thryoid gland is stimulated to secrete it. In the presence of thyroid peroxidase
|
|
|
what catalyzes the organification of iodine
|
thryoid peroxidase
|
|
|
how is T4 formed
|
2 DIT couple to form T4---catalyzed by thyroid peroxidase
|
|
|
how is T3 formed
|
1 DIT and 1 MIT couple to form T3 - catalyzed by thyroid peroxidase
|
|
|
what catalyzes coupling reactions?
|
thyroid peroxidase
|
|
|
where does TSH come from
|
the pituitary
|
|
|
what hormone stimulates the thyroid gland?
|
TSH (from the pituitary)
|
|
|
how is TGB moved out of the thyroid gland?
|
it is pinocytosed as part of the colloid, and pinocytic vesicles fuse with lysosomes
|
|
|
how is hydrolysis involved with MIT, DIT, T3 and T4
|
it is used in the recycling process for all of them
|
|
|
what is the function of thryoid deiodinase?
|
it removes Iodine form MIT and DIT
|
|
|
what happens to Iodine after it is hydrolyzed by thyroid deiodinase?
|
it is recycled/reused
|
|
|
what happens to tyrosine after hydrolysis by thryoid deiodinase?
|
it is used in the synthesis of TGB
|
|
|
how does T3 and T4 circulate in the plasma?
|
either free or bound to TBG
|
|
|
what is TBG
|
thyroid binding globulin
|
|
|
what enzyme converts T3 and T4
|
tissue iodinases
|
|
|
what inhibits thyroid peroxidase
|
propylthiouracil (PTU)
|
|
|
what does PTU do?
|
it inhibits thyroid peroxidase and all of its steps (oxidation, organification and coupling)
|
|
|
when clinically would a person take PTU
|
if they have hyperthyroidism
|
|
|
what does T3 and T4 regulate?
|
metabolic rate, synthesis of protein, breakdown of fats, use of glucose for ATP production---is calorigenic
|
|
|
what are the functions of calcitonin?
|
it builds bone and stops reabsorption of bone----lowers blood Ca2+levels
|
|
|
what is the action of T3 on growth?
|
leads to growth formation and bone maturation
|
|
|
what is T3's effect on the CNS
|
causes CNS maturation
|
|
|
what is the effect of T3 on BMR?
|
increased Na+, K+,ATPase, increase O2 consumption, heat production, & BMR
|
|
|
what is the effect of T3 on metabolism
|
increases glucose absorption, glycogenolysis, gluconeogenesis, lipolysis, protein synthesis and degradation
|
|
|
what is the effect of T3 on cardiovascular?
|
increases cardiac output
|
|
|
calorigenic effect of thyroid hormones are:
|
increase O2 consumption in all tissues, except brain, testes, uterus,lymph nodes, spleen and pituitary
|
|
|
cretinism is due to:
|
low thyroid hormones levels in a fetus
|
|
|
CNS effects of thryoid hormones:
|
development of the CNS
|
|
|
what does Catecholamine do?
|
increases synthesis of beta andrenergic receptors leading to increase in cardiac output
|
|
|
what is the purpose of beta andrenergic receptors?
|
they increase the hearts responsiveness to epinephrine
|
|
|
what effect does thyroid hormone have on the heart?
|
it affects the type of myosin present (alpha myoglobin heavy chains w/ higher ATPase activity
|
|
|
what effect does thyroid hormone have cholesterol metabolism?
|
lowers the cholesterol in plasma
|
|
|
what effect does thyroid hormones have on the respiratory system?
|
increases respiratory rate and minute ventilation
|
|
|
control of T3 & T4 is regulated by:
|
negative feedback
|
|
|
low blood levels of T3, T4 or low metabolism stimulate the release of:
|
TRH
|
|
|
elevated T3 inhibits the release of:
|
TRH and TSH
|
|
|
TRH goes from the hypothalamus to the:
|
anterior pituitary gland
|
|
|
TRH stimulates the release of:
|
TSH by thyrotrophs
|
|
|
TSH released into blood stimulates
|
thyroid follicular cells
|
|
|
low blood level of hormones stimulate:
|
the hypothalamus
|
|
|
increased BMR is a symptom of
|
hyperthyroidism
|
|
|
sudden unexpected weight loss is a sign of
|
hyperthyroidism
|
|
|
a negative nitrogen balance is a sign of:
|
hyperthyroidism
|
|
|
increased heat production is a symptom of:
|
hyperthyroidism
|
|
|
constant sweating is a sign of:
|
hyperthyroidism
|
|
|
increased cardiac output is a symptom of:
|
hyperthyroidism
|
|
|
dyspnea is a symptom of
|
hyperthyroidism
|
|
|
tremors and muscle weakness are a symptom of
|
hyperthyroidism
|
|
|
exopthalmos is a symptom of
|
hyperthyroidism
|
|
|
goiter is a symptom of
|
hyperthyroidism or hypothyroidism
|
|
|
graves disease is caused by
|
hyperthyroidism
|
|
|
thyroid neoplasia is a symptom of
|
hyperthyroidism
|
|
|
excess TSH secretion is a sign of
|
hyperthyroidism
|
|
|
propylthiouracil is used to treat
|
hyperthyroidism
|
|
|
thyroidectomy is used to treat
|
hyperthyroidism
|
|
|
beta andrenergic blocking agents are used to treat:
|
hyperthyroidism
|
|
|
decreased BMR is a symptom of
|
hypothyroidism
|
|
|
sudden weight gain is a sign of
|
hypothyroidism
|
|
|
positive nitrogen balance is a sign of:
|
hypothyroidism
|
|
|
decreased heat production is a sign of
|
hypothyroidism
|
|
|
cold sensitivity is a sign of
|
hypothyroidism
|
|
|
decreased cardiac output is a sign of
|
hypothyroidism
|
|
|
hypoventilation is a sign of
|
hypothyroidism
|
|
|
lethargy and mental slowness are a symptom of
|
hypothyroidism
|
|
|
drooping eyelids are a sign of
|
hypothyroidism
|
|
|
myxedema is a sign of
|
hypothyroidism
|
|
|
growth retardation is a sign of
|
hypothyroidism
|
|
|
perinatal mental retardation is a sign of
|
hypothyroidism
|
|
|
hashimoto's thyroiditis is a disease caused by:
|
hypothyroidism
|
|
|
surgery for hypothryoidism can cause
|
hypothyroidism
|
|
|
iodine deficiency can cause
|
hypothyroidism
|
|
|
congenital cretinism is a sign of
|
hypothyroidism
|
|
|
decreased TSH or TRH is a sign of
|
hypothyroidism
|
|
|
a decrease in TRH or TSH is a sign of
|
hypothyroidism
|
|
|
if there is a defect in the anterior pituitary TSH levels will be:
|
increased
|
|
|
if primary defect is in the thyroid gland then TSH levels will be
|
increased
|
|
|
if the defect is in the hypothalamus or anterior pituitary TSH levels will be
|
decreased
|
|
|
if a person is hyper-reflexic they may have:
|
hyperthyroidism
|
|
|
if a person has insomnia, they may have
|
hyperthyroidism
|
|
|
soft smooth hair and skin can be a sign of
|
hyperthyroidism
|
|
|
increased iodide uptake can be a sign of
|
hyperthryoidism
|
|
|
weak, sluggish, flabby muscles can be a sign of:
|
hypothyroidism
|
|
|
coarse hair, and rough dry skin can be a sign of:
|
hypothyroidism
|
|
|
Goiter is due to:
|
thyroid overstimulation by TSH
|
|
|
what is the pineal gland made of:
|
consists of pinealocytes and neuroglia
|
|
|
what is responsible for setting the "biological clock"
|
melatonin
|
|
|
what is the treatment for jet lag and SAD
|
bright light
|
|
|
what is the pineal gland a part of:
|
the epithalamus
|
|
|
what is the function of melatonin?
|
it enhances sleep
|
|
|
what is the precursor to melatonin?
|
secretonin
|
|
|
what influence does melatonin have on reproduction?
|
it can decrease GnRH from the hypothalamus, inhibiting reproductive function
|
|
|
what is the function of arginine?
|
regulates function of reproductive system in some animals
|
|
|
what is the effect of norepinephrine on melatonin
|
it inhibits its secretion
|
|
|
what stimulates the pineal gland
|
norepinephrine from the superior cervical ganglion
|
|
|
what happens in darkness?
|
lack of norepinephrine stimulates melatonin
|
|
|
what happens in light
|
norepinephrine inhibits melatonin secretion
|
|
|
what is a circadian cycle?
|
an internal clock with an intrinsic 24-25 hour cycle
|
|
|
where is the circadian clock at in the brain?
|
in the suprachiasmatic nucleus
|
|
|
what is SAD?
|
depression that occurs during the winter months when the day length is short
|
|
|
what causes SAD?
|
the overproduction of melatonin
|
|
|
how do you treat SAD and Jet lag?
|
exposure to artifical light or sunlightwhere are the parathyroid glands
|
|
|
what do principal (chief) cells do?
|
they produce parathyroid hormone
|
|
|
what are the 2 types of cells in the parathyroid gland
|
principal and oxyphil cells
|
|
|
what does the oxyphil cells do?
|
the function is unknown
|
|
|
what are the major functions of the parathyroid gland?
|
it is the major regulator of Ca2+, Mg2+, and HPO4
|
|
|
what does PTH do to calcium?
|
it raises blood Ca2+ levels
|
|
|
what does the PTH do to osteoclasts?
|
it increases their activity
|
|
|
how does PTH affect the kidneys?
|
it increases reabsorption of Ca2+, promotes formation of calcitrol (vitamin D3)
|
|
|
how does PTH affect HPO4
|
it inhibits the reabsorption of it
|
|
|
what does calcitrol do?
|
it causes absorption of Ca2+ and Mg2+ by the intestinal tract
|
|
|
what does negative feedback influence?
|
it is directly on the secretion of hormones, does not involve the pituitary
|
|
|
what is the overall effect of PTH on bones
|
it stimulates osteoclast to degrade bone, which results in bone resorption, increase in Ca2+ and HPO4-in the blood
|
|
|
what is the effect of PTH on the GI?
|
it is an indirect effect, calcitrol increases interstitial absorption of Ca2+, Mg 2+, and HPO4-
|
|
|
cause of hypothyroidism
|
accidental removal during thyroidectomy
|
|
|
what are the symptoms hypothryoidsim
|
hypocalcemia, normal bone structure, increased neuromuscular excitability (tetany, larygnospasm, & death from asphyxiation can result), flaccid heart muscle (cardiac arrythmia may develop) and diarrhea
|
|
|
what are the causes of hyperparathyroidism?
|
adenomas of the parathyroid gland, hyperplasia of the parathyroid and carcinomas
|
|
|
what are the symptoms of hyperparathyroidism?
|
hypercalcemia or normal blood Ca2+ levels, CaCO3- deposited throughout the body (renal tubules, lungs, blood vessels, gastric mucosa especially), Bones weaken, neuromuscular system less excitable, weak muscles, increased force of cardiac contraction @ high blood Ca2+ levels----can lead to cardiac arrest, constipation
|
|
|
what % of cells produce digestive enzymes
|
99%
|
|
|
what cells produce hormones
|
islet cells
|
|
|
are the islets endocrine or exocrine
|
endocrine
|
|
|
what do exocrine cells surround?
|
a ducts
|
|
|
what are endocrine cells near?
|
capillaries
|
|
|
what do alpha cells secrete?
|
glucagon
|
|
|
what do beta cells secrete?
|
insulin
|
|
|
what do delta cells secrete?
|
somatostatin
|
|
|
what do F-cells secrete?
|
pancreatic polypeptide
|
|
|
how would you test for hormone levels
|
radioimmuno assays
|
|
|
how many islet cells are there in the pancreas?
|
1 to 2 million
|
|
|
what % of the islet cells are alpha cells, and what do they produce
|
20% and glucagon
|
|
|
what % of the islet cells are beta cells, and what do they produce?
|
70% and insulin
|
|
|
what % of the islet cells are delta cells and what do they produce?
|
5% and somatostatin
|
|
|
what is the effect of insulin on muscle?
|
promotes glucose uptake and metabolism, insulin increases permeability to glucose
|
|
|
is skeletal muscle more or less permeable to muscle during exercise?
|
more permeable
|
|
|
if there is excess glucose in a muscle fiber, what does insulin do?
|
it promotes storage of glucose as glycogen
|
|
|
what is the effect of insulin on the liver?
|
it promotes glucose uptake, storage and use
|
|
|
what does insulin do to phosphorylase in the liver?
|
it inactivates it
|
|
|
what effect does insulin have on glycogen synthase in the liver?
|
increases its activity (need to make glycogen)
|
|
|
what is the effect on glucokinase in the liver?
|
increases its activity - need to phosphorylate glucose to trap it in the cell and maintain the concentration gradient
|
|
|
if the liver glyogen stores are full and there is extra glucose left over what will the liver do?
|
it will begin converting glucose into fatty acids and triglycerides
|
|
|
as the insulin levels decrease between meals, what happens to phosphorylase?
|
it increases activity and begins splitting glycogen back into glucose
|
|
|
as insulin levels fall between meals what happens to glucose phosphatase?
|
it is activated, it will dephosphorylate glucose so that it can leave the liver and go to other parts of the body
|
|
|
what is the effect of insulin on the brain?
|
none, the brain cells are always permeable to glucose irrespective of insulin
|
|
|
how does insulin effect lipid metabolism?
|
it promotes fat synthesis and storage
|
|
|
what will glucose be converted to on its way to becoming a fatty acid?
|
glucose -->pyruvate-->acetyl CoA--> fatty acid
|
|
|
what carries Fatty acids from the liver to adipocytes?
|
VLDL
|
|
|
what is the effect of insulin on adipose capillaries?
|
it activates lipoprotein lipase
|
|
|
what is the function of lipoprotein lipase?
|
it breaks down the triglycerides for absorption by the adipocyte
|
|
|
inside of an adipocyte, what is the effect of insulin?
|
it inhibits lipases to prevent fat catabolism, and induces the formation of glycerol phosphate
|
|
|
what will happen if there is a lack of insulin?
|
lipolysis of stored FA and release of FFA by activating hormone sensitive lipase, increased cholesterol and phospholipid production (can lead to arteriosclerosis) and excess acetoacetic acid production for synthesis of ketone bodies
|
|
|
what is the effect of insulin on protein metabolism?
|
stimulates AA uptake by tissues, increases protein translation from mRNA, regulates gene expression, inhibits protein catabolism, decreases gluconeogenesis, interacts synergistically with growth hormone
|
|
|
what effect does a lack on insulin have on protein metabolism?
|
it leads to protein degradation and increase in AA's in blood plasma
|
|
|
what are the factors that stimulate insulin secretion?
|
increased glucose, amino acid, fatty acid, and keto acid concentrations, glucagon, growth hormone, cortisol, GIP, potassium, vagal stimulation (acetylcholine), sulfonylurea drugs, and obesity
|
|
|
what factors inhibit insulin secretion?
|
decreased blood glucose, fasting, exercise, somatostatin, alpha-adrenergic agonists, diazoxide
|
|
|
the only endocrine gland that stores its hormones
|
thryoid gland
|
|
|
the thyroid gland receives_______ blood / min
|
80-120 ml
|
|
|
parafollicular cells secrete:
|
calcitonin
|
|
|
calcitonin's function:
|
reduce calcium concentration in body fluids when level is elevated
|
|
|
a follicle is:
|
a sac of stored hormones (colloid) surrounded by follicle cells that produce it
|
|
|
how many layers of follicle cells in a follicle:
|
1 layer
|
|
|
where a parafollicular cells located?
|
in between follicles
|
|
|
triiodothyronine is known as:
|
T3
|
|
|
tetraiodothyronine is known as
|
T4
|
|
|
what do T3 and T4 bind with?
|
intracellular nuclear receptor molecules
|
|
|
what does T3 and T4 do?
|
it initiates new protein synthesis, increases rate of glucose, fat and protein metabolism , and may increase body temp.
|
|
|
normal growth of many tissues is dependent on?
|
T3 and T4
|
|
|
which is the predominant thryoid hormone; T3 or T4?
|
T4
|
|
|
which is more potent; T3 or T4?
|
T3
|
|
|
what do tissues do to T4?
|
they convert it to T3
|
|
|
what is TGB
|
thyroglobulin
|
|
|
what is the process of formation thryoid hormone?
|
iodide trapped by follicular cells-->synthesis of thyroglobulin-->release of TGB into colloid-->iodination of tyrosine in colloid-->form T3 & T4 by combining T1 & T2-->uptake & digest TGB in follicle cells--> secrete T3 &T4 into blood
|
|
|
what type of molecule is thyroglobulin?
|
a large glycoprotein
|
|
|
process of making TGB
|
synthesized in rER, glycosylated in golgi, packaged in secretory vesicles, released on apical side into colloid
|
|
|
TGB has a large number of?
|
tyrosine residues
|
|
|
what happens to tyrosine residues in TGB?
|
they are iodinated to form hormones
|
|
|
what is an iodide trap?
|
a Na/ I active symporter on the basal side
|
|
|
what stimulates activity in the iodide trap
|
TSH
|
|
|
what is the electron acceptor in the oxidation of I- to I2
|
hydrogen peroxide
|
|
|
what enzyme catalyzes the oxidation of I- to I2?
|
thyroid peroxidase
|
|
|
what is organification of iodine?
|
Iodine combines w/ tyrosine on TG to form monoiodotyrosine (MIT) and diiodotyrosine (DIT) which remains attached to TG until the thryoid gland is stimulated to secrete it. In the presence of thyroid peroxidase
|
|
|
what catalyzes the organification of iodine
|
thryoid peroxidase
|
|
|
how is T4 formed
|
2 DIT couple to form T4---catalyzed by thyroid peroxidase
|
|
|
how is T3 formed
|
1 DIT and 1 MIT couple to form T3 - catalyzed by thyroid peroxidase
|
|
|
what catalyzes coupling reactions?
|
thyroid peroxidase
|
|
|
where does TSH come from
|
the anterior pituitary
|
|
|
what hormone stimulates the thyroid gland?
|
TSH (from the pituitary)
|
|
|
how is TGB moved out of the thyroid gland?
|
it is pinocytosed as part of the colloid, and pinocytic vesicles fuse with lysosomes
|
|
|
how is hydrolysis involved with MIT, DIT, T3 and T4
|
it is used in the recycling process for all of them
|
|
|
what is the function of thryoid deiodinase?
|
it removes Iodine form MIT and DIT
|
|
|
what happens to Iodine after it is hydrolyzed by thyroid deiodinase?
|
it is recycled/reused
|
|
|
what happens to tyrosine after hydrolysis by thryoid deiodinase?
|
it is used in the synthesis of TGB
|
|
|
how does T3 and T4 circulate in the plasma?
|
either free or bound to TBG
|
|
|
what is TBG
|
thyroid binding globulin
|
|
|
what enzyme converts T3 and T4
|
tissue iodinases
|
|
|
what inhibits thyroid peroxidase
|
propylthiouracil (PTU)
|
|
|
what does PTU do?
|
it inhibits thyroid peroxidase and all of its steps (oxidation, organification and coupling)
|
|
|
when clinically would a person take PTU
|
if they have hyperthyroidism
|
|
|
what does T3 and T4 regulate?
|
metabolic rate, synthesis of protein, breakdown of fats, use of glucose for ATP production---is calorigenic
|
|
|
what are the functions of calcitonin?
|
it builds bone and stops reabsorption of bone----lowers blood Ca2+levels
|
|
|
what is the action of T3 on growth?
|
leads to growth formation and bone maturation
|
|
|
what is T3's effect on the CNS
|
causes CNS maturation
|
|
|
what is the effect of T3 on BMR?
|
increased Na+, K+,ATPase, increase O2 consumption, heat production, & BMR
|
|
|
what is the effect of T3 on metabolism
|
increases glucose absorption, glycogenolysis, gluconeogenesis, lipolysis, protein synthesis and degradation
|
|
|
what is the effect of T3 on cardiovascular?
|
increases cardiac output
|
|
|
calorigenic effect of thyroid hormones are:
|
increase O2 consumption in all tissues, except brain, testes, uterus,lymph nodes, spleen and pituitary
|
|
|
cretinism is due to:
|
low thyroid hormones levels in a fetus
|
|
|
CNS effects of thryoid hormones:
|
development of the CNS
|
|
|
what does Catecholamine do?
|
increases synthesis of beta andrenergic receptors leading to increase in cardiac output
|
|
|
what is the purpose of beta andrenergic receptors?
|
they increase the hearts responsiveness to epinephrine
|
|
|
what effect does thyroid hormone have on the heart?
|
it affects the type of myosin present (alpha myoglobin heavy chains w/ higher ATPase activity
|
|
|
what effect does thyroid hormone have cholesterol metabolism?
|
lowers the cholesterol in plasma
|
|
|
what effect does thyroid hormones have on the respiratory system?
|
increases respiratory rate and minute ventilation
|
|
|
control of T3 & T4 is regulated by:
|
negative feedback
|
|
|
low blood levels of T3, T4 or low metabolism stimulate the release of:
|
TRH
|
|
|
elevated T3 inhibits the release of:
|
TRH and TSH
|
|
|
TRH goes from the hypothalamus to the:
|
anterior pituitary gland
|
|
|
TRH stimulates the release of:
|
TSH by thyrotrophs
|
|
|
TSH released into blood stimulates
|
thyroid follicular cells
|
|
|
low blood level of hormones stimulate:
|
the hypothalamus
|
|
|
increased BMR is a symptom of
|
hyperthyroidism
|
|
|
sudden unexpected weight loss is a sign of
|
hyperthyroidism
|
|
|
a negative nitrogen balance is a sign of:
|
hyperthyroidism
|
|
|
increased heat production is a symptom of:
|
hyperthyroidism
|
|
|
constant sweating is a sign of:
|
hyperthyroidism
|
|
|
increased cardiac output is a symptom of:
|
hyperthyroidism
|
|
|
dyspnea is a symptom of
|
hyperthyroidism
|
|
|
tremors and muscle weakness are a symptom of
|
hyperthyroidism
|
|
|
exopthalmos is a symptom of
|
hyperthyroidism
|
|
|
goiter is a symptom of
|
hyperthyroidism or hypothyroidism
|
|
|
graves disease is caused by
|
hyperthyroidism
|
|
|
thyroid neoplasia is a symptom of
|
hyperthyroidism
|
|
|
excess TSH secretion is a sign of
|
hyperthyroidism
|
|
|
propylthiouracil is used to treat
|
hyperthyroidism
|
|
|
thyroidectomy is used to treat
|
hyperthyroidism
|
|
|
beta andrenergic blocking agents are used to treat:
|
hyperthyroidism
|
|
|
decreased BMR is a symptom of
|
hypothyroidism
|
|
|
sudden weight gain is a sign of
|
hypothyroidism
|
|
|
positive nitrogen balance is a sign of:
|
hypothyroidism
|
|
|
decreased heat production is a sign of
|
hypothyroidism
|
|
|
cold sensitivity is a sign of
|
hypothyroidism
|
|
|
decreased cardiac output is a sign of
|
hypothyroidism
|
|
|
hypoventilation is a sign of
|
hypothyroidism
|
|
|
lethargy and mental slowness are a symptom of
|
hypothyroidism
|
|
|
drooping eyelids are a sign of
|
hypothyroidism
|
|
|
myxedema is a sign of
|
hypothyroidism
|
|
|
growth retardation is a sign of
|
hypothyroidism
|
|
|
perinatal mental retardation is a sign of
|
hypothyroidism
|
|
|
hashimoto's thyroiditis is a disease caused by:
|
hypothyroidism
|
|
|
surgery for hypothryoidism can cause
|
hypothyroidism
|
|
|
iodine deficiency can cause
|
hypothyroidism
|
|
|
congenital cretinism is a sign of
|
hypothyroidism
|
|
|
decreased TSH or TRH is a sign of
|
hypothyroidism
|
|
|
a decrease in TRH or TSH is a sign of
|
hypothyroidism
|
|
|
if there is a defect in the anterior pituitary TSH levels will be:
|
increased
|
|
|
if primary defect is in the thyroid gland then TSH levels will be
|
increased
|
|
|
if the defect is in the hypothalamus or anterior pituitary TSH levels will be
|
decreased
|
|
|
if a person is hyper-reflexic they may have:
|
hyperthyroidism
|
|
|
if a person has insomnia, they may have
|
hyperthyroidism
|
|
|
soft smooth hair and skin can be a sign of
|
hyperthyroidism
|
|
|
increased iodide uptake can be a sign of
|
hyperthryoidism
|
|
|
weak, sluggish, flabby muscles can be a sign of:
|
hypothyroidism
|
|
|
coarse hair, and rough dry skin can be a sign of:
|
hypothyroidism
|
|
|
Goiter is due to:
|
thyroid overstimulation by TSH
|
|
|
what is the pineal gland made of:
|
consists of pinealocytes and neuroglia
|
|
|
what is responsible for setting the "biological clock"
|
melatonin
|
|
|
what is the treatment for jet lag and SAD
|
bright light
|
|
|
what is the pineal gland a part of:
|
the epithalamus
|
|
|
what is the function of melatonin?
|
it enhances sleep
|
|
|
what is the precursor to melatonin?
|
secretonin
|
|
|
what influence does melatonin have on reproduction?
|
it can decrease GnRH from the hypothalamus, inhibiting reproductive function
|
|
|
what is the function of arginine?
|
regulates function of reproductive system in some animals
|
|
|
what is the effect of norepinephrine on melatonin
|
it inhibits its secretion
|
|
|
what stimulates the pineal gland
|
norepinephrine from the superior cervical ganglion
|
|
|
what happens in darkness?
|
lack of norepinephrine stimulates melatonin
|
|
|
what happens in light
|
norepinephrine inhibits melatonin secretion
|
|
|
what is a circadian cycle?
|
an internal clock with an intrinsic 24-25 hour cycle
|
|
|
where is the circadian clock at in the brain?
|
in the suprachiasmatic nucleus
|
|
|
what is SAD?
|
depression that occurs during the winter months when the day length is short
|
|
|
what causes SAD?
|
the overproduction of melatonin
|
|
|
how do you treat SAD and Jet lag?
|
exposure to artifical light or sunlightwhere are the parathyroid glands
|
|
|
what do principal (chief) cells do?
|
they produce parathyroid hormone
|
|
|
what are the 2 types of cells in the parathyroid gland
|
principal and oxyphil cells
|
|
|
what does the oxyphil cells do?
|
the function is unknown
|
|
|
what are the major functions of the parathyroid gland?
|
it is the major regulator of Ca2+, Mg2+, and HPO4
|
|
|
what does PTH do to calcium?
|
it raises blood Ca2+ levels
|
|
|
what does the PTH do to osteoclasts?
|
it increases their activity
|
|
|
how does PTH affect the kidneys?
|
it increases reabsorption of Ca2+, promotes formation of calcitrol (vitamin D3)
|
|
|
how does PTH affect HPO4
|
it inhibits the reabsorption of it
|
|
|
what does calcitrol (Vit. D3) do?
|
it causes absorption of Ca2+ and Mg2+ by the intestinal tract
|
|
|
what does negative feedback influence?
|
it is directly on the secretion of hormones, does not involve the pituitary
|
|
|
what is the overall effect of PTH on bones
|
it stimulates osteoclast to degrade bone, which results in bone resorption, increase in Ca2+ and HPO4-in the blood
|
|
|
what is the effect of PTH on the GI?
|
it is an indirect effect, calcitrol increases interstitial absorption of Ca2+, Mg 2+, and HPO4-
|
|
|
cause of hypothyroidism
|
accidental removal during thyroidectomy
|
|
|
what are the symptoms hypothryoidsim
|
hypocalcemia, normal bone structure, increased neuromuscular excitability (tetany, larygnospasm, & death from asphyxiation can result), flaccid heart muscle (cardiac arrythmia may develop) and diarrhea
|
|
|
what are the causes of hyperparathyroidism?
|
adenomas of the parathyroid gland, hyperplasia of the parathyroid and carcinomas
|
|
|
what are the symptoms of hyperparathyroidism?
|
hypercalcemia or normal blood Ca2+ levels, CaCO3- deposited throughout the body (renal tubules, lungs, blood vessels, gastric mucosa especially), Bones weaken, neuromuscular system less excitable, weak muscles, increased force of cardiac contraction @ high blood Ca2+ levels----can lead to cardiac arrest, constipation
|
|
|
what % of cells produce digestive enzymes
|
99%
|
|
|
what cells produce hormones
|
islet cells
|
|
|
are the islets endocrine or exocrine
|
endocrine
|
|
|
what do exocrine cells surround?
|
a ducts
|
|
|
what are endocrine cells near?
|
capillaries
|
|
|
what do alpha cells secrete?
|
glucagon
|
|
|
what do beta cells secrete?
|
insulin
|
|
|
what do delta cells secrete?
|
somatostatin
|
|
|
what do F-cells secrete?
|
pancreatic polypeptide
|
|
|
how would you test for hormone levels
|
radioimmuno assays
|
|
|
how many islet cells are there in the pancreas?
|
1 to 2 million
|
|
|
what % of the islet cells are alpha cells, and what do they produce
|
20% and glucagon
|
|
|
what % of the islet cells are beta cells, and what do they produce?
|
70% and insulin
|
|
|
what % of the islet cells are delta cells and what do they produce?
|
5% and somatostatin
|
|
|
what is the effect of insulin on muscle?
|
promotes glucose uptake and metabolism, insulin increases permeability to glucose
|
|
|
is skeletal muscle more or less permeable to muscle during exercise?
|
more permeable
|
|
|
if there is excess glucose in a muscle fiber, what does insulin do?
|
it promotes storage of glucose as glycogen
|
|
|
what is the effect of insulin on the liver?
|
it promotes glucose uptake, storage and use
|
|
|
what does insulin do to phosphorylase in the liver?
|
it inactivates it
|
|
|
what effect does insulin have on glycogen synthase in the liver?
|
increases its activity (need to make glycogen)
|
|
|
what is the effect of insulin on glucokinase in the liver?
|
increases its activity - need to phosphorylate glucose to trap it in the cell and maintain the concentration gradient
|
|
|
if the liver glyogen stores are full and there is extra glucose left over what will the liver do?
|
it will begin converting glucose into fatty acids and triglycerides
|
|
|
as the insulin levels decrease between meals, what happens to phosphorylase?
|
it increases activity and begins splitting glycogen back into glucose
|
|
|
as insulin levels fall between meals what happens to glucose phosphatase?
|
it is activated, it will dephosphorylate glucose so that it can leave the liver and go to other parts of the body
|
|
|
what is the effect of insulin on the brain?
|
none, the brain cells are always permeable to glucose irrespective of insulin
|
|
|
how does insulin effect lipid metabolism?
|
it promotes fat synthesis and storage
|
|
|
what will glucose be converted to on its way to becoming a fatty acid?
|
glucose -->pyruvate-->acetyl CoA--> fatty acid
|
|
|
what carries Fatty acids from the liver to adipocytes?
|
VLDL
|
|
|
what is the effect of insulin on adipose capillaries?
|
it activates lipoprotein lipase
|
|
|
what is the function of lipoprotein lipase?
|
it breaks down the triglycerides for absorption by the adipocyte
|
|
|
inside of an adipocyte, what is the effect of insulin?
|
it inhibits lipases to prevent fat catabolism, and induces the formation of glycerol phosphate
|
|
|
what will happen if there is a lack of insulin?
|
lipolysis of stored FA and release of FFA by activating hormone sensitive lipase, increased cholesterol and phospholipid production (can lead to arteriosclerosis) and excess acetoacetic acid production for synthesis of ketone bodies
|
|
|
what is the effect of insulin on protein metabolism?
|
stimulates AA uptake by tissues, increases protein translation from mRNA, regulates gene expression, inhibits protein catabolism, decreases gluconeogenesis, interacts synergistically with growth hormone
|
|
|
what effect does a lack on insulin have on protein metabolism?
|
it leads to protein degradation and increase in AA's in blood plasma
|
|
|
what are the factors that stimulate insulin secretion?
|
increased glucose, amino acid, fatty acid, and keto acid concentrations, glucagon, growth hormone, cortisol, GIP, potassium, vagal stimulation (acetylcholine), sulfonylurea drugs, and obesity
|
|
|
what factors inhibit insulin secretion?
|
decreased blood glucose, fasting, exercise, somatostatin, alpha-adrenergic agonists, diazoxide
|
|
|
what effect will sympathetic stimulation have on insulin secretion?
|
it will inhibit insulin's secretion
|
|
|
increased epinephrine from the adrenal medulla will lead to?
|
inhibition of insulin secretion
|
|
|
what are the three major effects of glucagon?
|
1. breakdown of liver glycogen 2. increased gluconeogenesin in the liver 3. stimulates lipolysis
|
|
|
what effect does glucagon have on adenyl cyclase?
|
increased it activity which leads to an increase in cAMP, which leads to the release glycogen from the liver
|
|
|
what does phosphorylase A do to glycogen?
|
it splits it into glu-1-P, which is dephosphorylated and released from the liver as glucose
|
|
|
will secretion of glucagon lead to protein anabolism or catabolism
|
catabolism, via gluconeogenesis, to maintain constant blood glucose levels
|
|
|
what effect does glucagon have on lipases?
|
it increases their activtiy to mobilize FA's for energy and preserve glucose
|
|
|
what inhibits glucagon secretion?
|
insulin, somatostatin, free fatty acids, and ketones
|
|
|
what stimulates glucagon secretion?
|
fasting, decreased glucose concentration, increased AA concentration (especially arginine), CCK, beta-adrenergic agonists, acetylcholine
|
|
|
what factors inhibit glucagon secretion?
|
insulin, somatostatin, increased FA and ketoacid concentration
|
|
|
hyperglycemia will stimulate or inhibit glucagon?
|
inhibit
|
|
|
hypoglycemia will stimulate or inhibit insulin?
|
inhibit
|
|
|
hyperglycemia will stimulate or inhibit insulin?
|
stimulate
|
|
|
hypoglycemia will stimulate or inhibit glucagon?
|
stimulate
|
|
|
what are the target tissues for insulin?
|
liver, adipose tissue, muscle, satiety center in the hypothalamus
|
|
|
what is the target tissue for glucagon?
|
the liver
|
|
|
if you are looking to build muscle mass, which hormone is more important to stimulate, insulin or glucagon?
|
insulin
|
|
|
what is the function of somatostatin?
|
to decrease motility of the stomach, duodenum, gall bladder. It also decreases secretion and absorption in the GI
|
|
|
what effect does somatostatin have on glucose and insulin?
|
it inhibits them
|
|
|
insulin stimulates or inhibits somatostatin?
|
inhibits
|
|
|
glucagon stimulates or inhibits somatostatin?
|
stimulates
|
|
|
what causes diabtes mellitus?
|
inadequate secretion of insulin or inability of tissue to respond to insulin
|
|
|
what is the difference between type I and type II diabetes mellitus
|
Type I is insulin dependent, Type II in non-insulin dependent
|
|
|
if there is a decrease in insulin associated with diabetes mellitus where is the problem?
|
the beta cells are defective (potentially due to autoimmune disorders or viral infections)
|
|
|
if there is decreased insulin secretion then what problem will arise?
|
there will be very high levels of glucose in the blood
|
|
|
what are some clinical signs that one may have diabetes mellitus?
|
glucose in urine, dehydration (due to osmotic diuresis), polyurea (intra & extracellular dehydration), unquenchable thirst, ketoacidosis, protein breakdown
|
|
|
what are some secondary effects of diabetes mellitus?
|
hypertension and atherosclerosis
|
|
|
what is the treatment for Type I diabetes?
|
insulin therapy
|
|
|
what is the major issue with Type II daibetes
|
decreased sensitivity to insulin
|
|
|
what is the primary cause of Type II diabetes
|
obesity
|
|
|
does a patient with Type II have to be on insulin therapy?
|
no, many can be managed by diet, caloric restrictions
|
|
|
are there treaments other than insulin for type II diabetes?
|
yes, thiazolidinediones and metformin to increase insulin sensitivity and sufonylurease to increase insulin secretion
|
|
|
what is the function of pancreatic polypeptide?
|
it inhibits somatostatin secretion, gall bladder contraction and secretion of pancreatic digestive enzymes
|
|
|
what is the function of the thymus gland?
|
its secretions promote proliferation and maturation of T cells
|
|
|
what hormones are secreted by the thymus?
|
thymosin, thymic humoral factor, thymic factor, thymopoietin
|
|
|
what are eicosanoids?
|
they are local hormones secreted by all body cells
|
|
|
what are the two families of eicosanoids?
|
leukotrienes and prostaglandins
|
|
|
what do leukotrienes influence?
|
WBC's and inflammation
|
|
|
what do prostaglandins do?
|
they alter smooth muscle contraction, glandular secretion, blood flow, platelet function, nerve transmission, metabolism, etc.
|
|
|
what is the major function of prostaglandins?
|
control of vascular smooth muscle activity
|
|
|
what are the localized actions of PGE/F?
|
act on microcirculation & adjust local blood flow in response to changing metabolic requirements of the tissue
|
|
|
what is PGI
|
prostacyclins
|
|
|
what do prostacyclins do?
|
it is a potent inhibitor of platelet aggregation - maintains vascular flow
|
|
|
where are prostacyclins produced?
|
by the endothelium on the blood vessel walls
|
|
|
what is the role of thromboxanes?
|
may play a role in Ca+ ionophore to increase Ca, Ca may in turn regulate the changes in cellular shape needed for platelet aggregation
|
|
|
where are leukotrienes made?
|
in leukocytes
|
|
|
what is the function of leukotrienes?
|
the are potent vasoconstrictors, increase vascular permeability, induce inflammation or allergic response in sites of injury or invasion by foreign agents
|
|
|
how many hormones does the hypothalamus secrete that control the pituitary gland?
|
9 different releasing and inhibiting hormones
|
|
|
how does the hypothalamus control the pituitary gland?
|
through neurohormones and action potentials
|
|
|
where is the pituitary /hypophysis located?
|
in the sella turcica
|
|
|
what are the 2 parts of the pituitary gland
|
the anterior and posterior pituitary
|
|
|
what portion of the pituitary is the anterior portion
|
75%
|
|
|
what portion of the pituitary is the posterior portion
|
25%
|
|
|
what does the anterior pituitary develop from?
|
from the a depression in the roof of the mouth known as Rathke's pouch
|
|
|
what types of cells make up the pituitary glands?
|
neuroglial cells called pituicytes
|
|
|
what is the posterior pituitary called
|
neurohypophysis
|
|
|
what is the anterior pituitary called?
|
adenohypophysis
|
|
|
what are the 3 areas of the adenohypophysis?
|
pars distalis, pars intermedia, pars tuberalis
|
|
|
how do neurohormones get from the hypothalamus to the pituitary?
|
via the hypothalamohypophysial portal system
|
|
|
hormones of the posterior pituitary:
|
antidiurect hormone (ADH) and oxytocin
|
|
|
hormones of the anterior pituitary:
|
GH or somatotropin, TSH, ACTH, melanocyte stimulating hormone (MSH), luteinizing hormone (LH), follicle stimulating hormone (FSH), prolactin
|
|
|
what is HGH secreted by?
|
the somatotrophs of the anterior pituitary
|
|
|
what stimulates the secretion of HGH (somatotropin)?
|
GHRH (growth hormone releasing hormone)
|
|
|
what inhibits the secretion of HGH?
|
growth hormone inhibiting hormone (GHIH) aka somatostatin
|
|
|
what stimulates the secretion of TSH (thyrotropin)
|
thyrotropin releasing hormone (TRH)
|
|
|
what cells secrete TSH?
|
thyrotrophs
|
|
|
what inhibits the secretion of TSH?
|
GHIH
|
|
|
what cells secrete FSH?
|
gonadotrophs
|
|
|
what stimulates the secretion of FSH?
|
gonadotrophic releasing hormone (GnRH)
|
|
|
what cells secrete luteinizing hormone?
|
gonadotrophs
|
|
|
what stimulates the secretion of LH
|
GnRH
|
|
|
what stimulates the secretion of prolactin?
|
Proactin-releasing Hormone (PRH) & TRH
|
|
|
what inhibits prolactin secretion?
|
prolactin inhibiting hormone (PIH) which is dopamine
|
|
|
what cells secrete ACTH?
|
corticotrophs
|
|
|
what stimulates the secretion of ACTH?
|
corticotropin-releasing hormone (CRH)
|
|
|
what cells secrete melanoctye stimulating hormone?
|
corticotrophs
|
|
|
what stimulates the secretion of melanocyte stimulating hormone?
|
corticotropin releasing hormone (CRH)
|
|
|
what inhibits the secretion of melanocyte stimulating hormone?
|
Dopamine
|
|
|
what local effect does HGH have on cells?
|
it increased the cellular synthesis of insulin like growth factor ---will act locally or enter the blood
|
|
|
what are the target cells for HGH?
|
liver, skeletal muscle, cartilage and bone
|
|
|
what are the effects of HGH on cells?
|
increase cell growth & cell division, stimulates lipolysis, stimulates glycogenolysis and gluconeogenesis and retards the uptake of glucose by muscle so levels of glucose stay high to supply the brain
|
|
|
what is the effect of low blood sugar on the hypothalamus?
|
it stimulates the release of GHRH, which in turn caused the anterior pituitary to release more HGH, and more glycogen is broken down into glucose by liver cells
|
|
|
what is the effect of high blood sugar on the hypothalamus?
|
it stimulates the release of GHIH, which in turn inhibits the secretion from the anterior pituitary
|
|
|
what is a normal blood glucose level?
|
90mg/100ml
|
|
|
what are the stimulatory factors for HGH secretion?
|
decreased glucose conc., decreased FFA conc., arginine, fasting or starvation, hormones of puberty (estrogen, testosterone), exercise, stress, stage III and IV sleep, alpha-adrenergic agonists
|
|
|
what are the inhibitory factors for HGH?
|
increased glucose conc., increased FFA conc., obesity, senescence, somatostatin, somatomedins, GH, beta-adrenergic agonists, pregnancy
|
|
|
what are the diabetogenic effect of HGH
|
can lead to insulin resistance and glucose intolerance---raises blood glucose concentration, pancreas releases insulin continually, beta-cell burnout. This will eventually cause diabetes mellitus if no insulin activity can occur
|
|
|
what types of hormones are TSH, LH, & FSH?
|
they are glycoproteins
|
|
|
what is the function of FSH in females?
|
it initiates the formation of follicles within the ovary and stimulates follicle cells to secrete estrogen
|
|
|
what is the function of FSH in males?
|
it stimulates the production of sperm in the testes
|
|
|
what is the function of LH in females?
|
secretion of estrogen, ovulation of secondary oocyte from the ovary, formation of corpus luteum, secretion of progesterone
|
|
|
what is the function of LH in males?
|
it stimulates the interstitial cells of leydig to secrete testosterone
|
|
|
what is the function of prolactin?
|
under the right conditions it causes milk production, it stimulates breast development, lactogenesis and inhibits ovulation
|
|
|
how does suckling effect prolactin secretion?
|
it reduces the level of hypothalamic inhibition & prolactin levels rise as does milk production
|
|
|
what happens to prolactin when nursing ceases?
|
hypothalamic inhibition of prolactin increases and milk production slows
|
|
|
what does ACTH stimulate?
|
it stimulates cells of the adrenal cortex that produce glucocorticoids
|
|
|
What is the function of MSH?
|
it is not entirely certain, althoug it does increase skin pigmentation in frogs
|
|
|
what are the direct effects of IGF's?
|
promotes growth of body cells, protein synthesis, tissue repair, lipolysis, & inc. blood glucose levels
|
|
|
what hormones does the posterior pituitary (neurohypophysis) secrete?
|
it only secretes 2 neurohormones, ADH & oxytocin.
|
|
|
what does the posterior pituitary mainly consist of?
|
axon terminals of hypothalamic neurons
|
|
|
what are the target tissues of oxytocin?
|
the uterus and mammary glands
|
|
|
what are the functions of oxytocin?
|
it enhances uterine muscle contraction, suckling and crying stimulates milk ejection by causing muscle contraction in the mammary glands
|
|
|
is the secretion of oxytocin during childbirth a positive or negative feedback system?
|
it is a positive feedback system
|
|
|
what is another name for ADH
|
vasopressin
|
|
|
what are the functions of ADH?
|
decrease urine production, decrease sweating, increase BP
|
|
|
what are the regulatory factors of ADH
|
dehydration increases ADH, overhydration inhibits AHD
|
|
|
what does a lack of ADH cause?
|
diabetes insipidus
|
|
|
what is the adrenal medulla derived from?
|
ectoderm
|
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what are the two areas of the adrenal gland?
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the cortex and the medulla
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what are the zones of the adrenal cortex?
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the zona glomerulosa, zona fasciculata, zona reticularis
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what is secreted from the zona glomerulosa?
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it secretes mineralocorticoids, mainly aldosterone
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what is secreted from the zona fasciculata?
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it secretes glucocorticoids, mainly cortisol
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what is secreted by the zona reticularis?
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androgens, mainly DHEA
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what types of cells are in the adrenal medulla
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chromaffin cells
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what do the chromaffin cells in the medulla secrete?
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epinephrine and norepinephrine
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what type of molecules are epinephrine and norepinephrine?
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they are amino acid derivatives
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what are the target tissues for epinephrine and norepinephrine?
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heart, blood vessels,liver, fat cells
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what is the effect of epinephrine and norepinephrine on its target tissues
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increased cardiac output, inc. blood flow to sk. Muscle and the heart, inc. release of glucose & FA into blood
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what types of molecules are cortisol, aldosterone, and sex steroids?
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they cholesterol based steroids
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what are the target tissues for cortisol?
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nearly all tissues
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what is the effect of cortisol on its target tissues?
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increased protein and fat breakdown, inc. glucose production via gluconeogenesis, inhibition of the immune response
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what is the target tissue for aldosterone?
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the kidneys
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what is the effect of aldosterone on the kidneys?
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increased Na+ reabsorption, and K+ and H+ excretion
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what are the target tissues for androgens?
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it targets many tissues
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what is the effect of androgens their target tissues?
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minor importance in males, causes development of secondary sexual characteristics in females such as axillary and pubic hair
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what happens to DHEA (androgen secreted in zona reticularis)
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it is converted into other steroids
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what % of zona glomerulosa hormonal activity is influenced by aldosterone?
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95%
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what happens if there is a hypersecretion of aldosterone?
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high blood pressure caused by retention of Na+ and H2O in blood. May be a sign of a tumor causing aldosteronism
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what happens if the patient is dehydrated, has a Na+ deficiency, or there is a homorrhage?
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there will be decrease in blood volume & decreased in BP
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what % of zona fasciculata hormonal activity is due to cortisol?
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95%
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what hormone does the zona fasciculata secrete?
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cortisol, cortisone and corticosterone
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what are the effects of cortisol on its target tissues?
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inc. rate of protein metabolism, gluconeogenesis, lipolysis, resists stress by making nutrients available for ATP production, raises BP (vasoconstriction), anti-inflammatory effects, depresses immune response, diurnal fluctuations
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what are the anti-inflammatory effects of cortisol?
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reduces the release of histamine, decreases capillary permeability, depresses phagocytosis
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how do glucocorticoids affects target cells for epinephrine/norepinephrine?
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the receptor molecules decrease w/o enough glucocorticoids
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how does cortisol effect muscle mass?
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it maintains muscle function & decreases muscle mass
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what is the effect of cortisol on bone?
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it decreases bone formation & increases bone resorption
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what is the effect or cortisol on connective tissue?
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it decreased the amount of CT
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what is the effect of cortisol on a fetus?
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it facilitates maturation of a fetus
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what is the effect of cortisol on the kidneys?
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it increase glomerular filtration and free water clearance
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what is the effect of cortisol on the brain?
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it modulates emotional tone and wakefulness
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what is the effect of cortisol on CRH and ACTH?
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it inhibits them
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what type of regulation impacts glucocorticoids?
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negative feedback
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what are some of the effects of DHEA in females?
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increases libido, is the only source of postmenopausal estrogen, stimulates growth of pubic and axillary hair, contributes to growth spurt in puberty
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what is congenital adrenal hyperplasia?
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a genetic disorder, with defective cortisol synthesis, no negative feedback, high ACTH secretion by ant. Pituitary, enlargement of adrenal cortex, accumulation of cortisol precursors---some converted to testosterone ---leads to mascunlinzation
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what is the effect of congenital hyperplasia in females?
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causes beard growth and male distribution of body hair, deeper voice, atrophy of breasts, growth of clitoris (may resemble a penis)
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what is the effect of congenital hyperplasia in males?
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the effects may be masked by testosterone
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what are the clinical signs of addison's disease?
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hypoglycemia, anorexia, weakness, hypotension, hyperkalemia, metabolic acidosis, decreased pubic & axillary hair in females, hyperpigmentation
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how are the ACTH levels in a patient with addison's disease
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they are increased, due to the negative feedback effect of decreased cortisol
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what is the treatment for addision's disease?
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replacement of glucocorticoids and mineralocorticoids
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what is another name for addison's disease?
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primary adrenocortical insufficiency
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what are the clinical signs of cushings syndrome?
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hyperglycemia, muscle wasting, central obesity, round face, supraclavicular hump, osteoprorosis, striae, virilization of menstrual disorders in females, hypertension
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how are the ACTH levels in a patient with cushings syndrome?
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they are decreased, this is due to the negative feedback effect of increased cortisol
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what is the treatment for cushings syndrome?
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ketoconazole, metyrapone
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when a patient has cushing's disease are there any differnces b/t it and cushing's syndrome?
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yes, there is an increase in ACTH, although the symptoms are the same
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what is the treatment for cushing's disease?
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surgical removal of ACTH secreting tumor
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what are the symptoms of Conn's syndrome?
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hypertension, hypokalemia, metabolic acidosis, decreased renin levels
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what is the cause Conn's syndrome?
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an aldosterone secreting tumor
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what is the treament for Conn's syndrome?
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an aldosterone antagonist (such as spironolactone) or surgery
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what are the symptoms of a 21-beta hydroxylase deficiency
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virilization of females, early acceleration of linear growth, early appearance of pubic and axillary hair, symptoms of deficiency of glucocorticoids and mineralocorticoids
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how are the ACTH levels w/ Conn's syndrome?
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they are increased due to the negative feedback effect of decreased cortisol
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what is the treatment for Conn's syndrome?
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replacement of glucocorticoids and mineralocorticoids
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what are the symptoms of a 17-alpha-hydroxylase deficiency
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lack of pubic and axillary hair in females, symptoms of deficiency of glucocorticoids, symptoms of excess mineralocorticoids
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what are the ACTH levels w/ an 17-alpha-hydroxylase deficiency
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they are increased due to the negative feedback effect of decreased cortisol
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what is the treatment for 17-alpha-hydroxylase deficiency
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replacement of glucocorticoids and aldosterone agonists (spironolactone)
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what are the symptoms of hyposecretion of aldosterone
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hyponatremia, hyperkalemia, acidosis, low BP, tremors and tetany of muscles, polyuria
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what are the symptoms of hyposecretion of cortisol?
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hypoglycemia, depressed immune system, weight loss due to unused proteins and fats, loss of appetite, nausea, vomiting, increased skin pigmentation (by elevated ACTH)
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what are the symptoms of hyposecretion of androgens?
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in women, reduction of pubic and axillary hair
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what are the symptoms of hypersecretion of aldosterone?
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slight hypernatremia, hypokalemia, alkalosis, high BP, weakness of sk. Muscles, acidic urine
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what are the symptoms of hypersecretion of cortisol?
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hyperglycemia --leads to diabetes mellitus, depressed immune system, destruction of tissue proteins (muscle atrophy, osteoprorosis, weak capillaries, thin skin, impaired wound healing, mobilization and redistribution of fats, causes moon face, buffalo hump, and abdominal fat hump, euphoria and depression
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what are the effects of hypersecretion of androgens?
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in women, hirsuitism (excessive facial and body hair), acne, increased sex drive, regression of breast tissue, loss of regular menses
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how are cells in the adrenal medulla stimulated
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the chromaffin cells are stimulated by direct innervation from the sympathetic NS
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what is the name for the effects of epinephrine and norepinephrine?
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they are called sympathomimetic
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what are the effects of sympathimimetic hormones
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their effects mimc sympathetic NS, cause fight/flight behavior, reduce activity of organs not essential for physical activity, increase blood flow and metabolism of organs needed
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what neurotransmitter increases hormone secretion by the adrenal medulla?
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Acetylcholine
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what builds new bone?
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calcium moves in as osteoblast build new bone
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what breaks down bone?
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calcium moves out as osteoclasts break down bone
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what happens when osteoclast and osteoblast activity is equal?
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the movement of calcium in and out is equal
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what are some of the functions of Ca+
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nerve & muscle function, blood clotting, enzyme function in many biochemical rxn's
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at what level does blood calcium need to be maintained?
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9-11mg/100ml
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what can happen if calcium levels get out of homeostasis?
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cardiac arrest of too high, respiratory arrest of too low
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what are the 3 ways calcium exists in the human body?
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bound, non-ionized, & ionized
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what is bound calcium?
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it is in the plasma and is non-diffusable across capillaries
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what % of the body's calcium is bound?
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41%
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what is non-ionized calcium?
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it is bound anions-- it is diffusable across capillary beds
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what % of calcium if ionized?
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9%
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what % of calcium is ionized?
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50%
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what is important about ionized calcium?
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it is diffusable across capillary beds and is important in physiological controls
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what happens if there are elevated extracellular levels of calcium?
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it prevents membrane depolarization
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what happens if there are decreased extraceullar levels of Ca+
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it leads to spontaneous action potential generation
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what is the function of PTH?
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it increases Ca2+ extracellular levels and decreases extracellular phosphate levels, promotes the formation of active vitamin D
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what is the action of Vitamin D?
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it stimulates uptake of Ca2+ by the intestines
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what is the function of calcitonin?
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it decreases extracellular Ca2+ levels
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what is the active forms of vitamin D
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it is vitamin D3
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what does vitamin D stimulate?
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synthesis of Ca2+ binding protein in intestinal cells (maintains) Ca+ gradient, Ca-ATPase to pump it out of cells into capillaries
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what are the symptons of hypercalcemia?
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NS and neuromuscular reflexes are hyporeflexia, decreased muscle activity-lethargy, decreased QT interval, constipation, lack of appetitie, CaPO4 starts to precipitate at high Ca levels
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what are the symptoms of hypocalcemia?
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NS excitement, increased membrane permeability to Na+, depolarizing membrane to threshold, hyperreflexia, spontaneous twitching, muscle cramps, over-excitation may result in tetany, Chvostek sign, Trousseau sign
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what is the Chvostek sign?
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twitching of facial muscles elicited by tapping on facial nerve
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what is Trousseau sign?
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carpopedal spasm upon inflation of a blood pressure cuff
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what is the cause of hypophosphatemia?
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reduced absorption from the intestine associated w/ Vit. D deficiency and alcohol abuse
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what are the symtoms of hypophosphatemia?
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reduced rate of metabolism, reduced O2 transport, WBC function and blood clotting
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what are the causes of hyperphosphatemia?
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renal failure, tissue destruction w/ chemotherapy used to treat metastatic tumors, hyperparathyroidism (initially leads to inc. plamsa Ca2+ combined w/ reduced excretion of phosphate by the kidneys
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what are the symptoms of hyperphosphatemia?
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related to reduced plasma Ca2+ conc. due to CaPO4 deposited in tissues such as lungs, kidneys, & joints
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under normal circumstances, how are high levels of phosphate regulated?
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Blood Phosphate inc.-->PO4 levels exceed ability of kidneys to reabsorb from filtrate-->PO4 ions remain in filtrate-->eliminated in urine
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under normal circumstances, how are low levels of Phosphate regulated?
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Blood PO4- levels decrease-->PO4 ions decrease-->efficiency of phosphate ion reabsorption from filtrate in kidney inc.-->inc. PO4 ion reabsorption dec. phosphate ion loss in urine-->PO4 ion levels increase
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what do people w/ hyperparathyroidsim have?
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stones, bones and groans
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what is hypercalciurea?
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it is defined as excessive urinary excretion of calcium, more than 250mg per day in women and 275-300mg per day in men
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