Endocrine Disorders (Exam 3) Flashcards
How doe endocrine glands get their jobs done?
by secreting or releasing hormones into the blood
hormone
molecule that acts as a message to convey information
what kind of responses do hormones give off?
slower, long acting responses
do hormones affect all cells/tissues?
why?
NO!
they reach all parts of the body, but only target certain cells that have receptors to the hormone
where are receptors for water soluble hormones found?
on the surface of the target cell, on the plasma membrane
water soluble hormone examples
polypeptides
catchecholamines
lipid soluble hormones examples
steroids
thyroids
where are lipid soluble hormones found?
in the nucleus
water soluble hormone receptors are coupled to
various second messenger systems which mediate the action of the hormone in the cell
changes evoked by the actions of secondary messengers are
usually rapid
three levels of integration for hormones
hypothalamus hormones
anterior pituitary hormones
endocrine targets and the hormones they secrete
hypothalamic hormones
regulate anterior pituitary trophic hormones that determine target gland secretion
What does the endocrine system regulate/control?
growth and development
male/female reproductive system
energy
level of salts/sugars in the blood
what are the organs that regulate the endocrine system (10)
pineal gland
hypothalamus
parathyroid glands
adrenal glands
kidneys
testes/ovaries
pancreas
thyroid gland
pituitary gland
the endocrine glands are located
all over the body
pituitary gland
master gland
regulates other endocrine glands
thyroid gland
metabolism, body heat, bone growth
parathyroids
use of calcium and phosphorus
hypothalamus
links NS to endocrine system
adrenal gland
responses to stress, metabolism, BP, salt balance
pancreas
blood sugar
ovaries
testes
eggs and female characteristics
sperm and male characteristics
a molecule is only a _____________ when described in the context of its role in an ________________ system
hormone
endocrine communication
GH solubility
and hypothalamic releasing factor
lipid soluble
GHRH (stimulates)
somatostatin (inhibits)
ACTH solubility
and hypothalamic releasing factor
water soluble
CRH (stimulates)
FSH solubility
and hypothalamic releasing factor
lipid soluble
GnRH (stimulates)
LH solubility
and hypothalamic releasing factor
water soluble
GnRH (stimulates)
TSH solubility
and hypothalamic releasing factor
lipid soluble
TRH (stimulates)
PRL solubility
and hypothalamic releasing factor
water soluble
DA (inhibits)
TRH (stimulates)
hormones in the hypothalamus
PRH
PIH (dopamine)
TRH
CRH
GHRH
GHIH
GnRH
hormones in the anterior pituitary
prolactin
TSH
ACTH
GH
FSH
LH
what regulates hypothalamic and pituitary hormones?
peripheral hormones feedback
adrenal cortex
responsible for secretion of mineralocorticoids, glucocorticoids and androgens
mineralcorticoids
aldosterone
maintains sodium and fluid balance
glucocorticoids
cortisol
provide the body with the materials needed for energy
androgens
testosterone
hyper secretion can cause masculinizing characteristics
regulation of the adrenal hormones is accomplished through
adrenocorticotropic hormone (ACTH)
aldosterone secretion is primarily accomplished through
RAAS
11 beta hydroxylase defect
second most common enzyme defect
excessive production of 11-deoxycorticosterone which in high concentrations in an effective mineralcorticosteroid
aldosterone and cortisol production is greatly decreased
administration of glucocorticoids shuts down _____________ production by inhibiting ______________
androgen
ACTH secretion
Congenital Adrenal Hyperplasia
genital abnormalities due to deficiencies of the adrenal gland and caused by 21-hydroxylase defects
complications of chronic exogenous corticosteroid use
suppressed or quiescent HPA axis
Zona fasciculata atrophy
decreased CRH and ACTH secretion
full recovery of endogenous cortisol secretion may require up to ___________
why?
18 months following steroid withdrawal
ACTH has to act for an extended time to restore normal synthetic capacity of adrenal cortex
Cortisol production lags behind restoration of ACTH secretion
posterior pituitary
composed mainly of cells called “pituicytes” which act as packing and supporting cells
stores and releases hormones into the close capillaries. Hormones produced in the hypothalamus
where are posterior pituitary hormones produced?
in the hypothalamic nuclei
ADH - supraoptic nucleus, 1/6 in PV nuclei
Oxytocin - paraventricular nucleus, 1/6 in S nuclei
which hormones does the posterior pituitary release?
antidiuretic hormone/arginine vasopressin
oxytocin
anti diuretic hormone
decreases the amount of water lost at the kidneys and elevates BP
increased blood osmolarity or decreased blood volume are sensed in the _________________ and increase ___________ secretion
brain or cortex
vasopressin
diabetes insipidus
hypo-osmotic polyuria secondary to abnormal synthesis, regulation or renal action of antidiuretic hormone
blocked ADH production
central diabetes insipidus vs nephrogenic diabetes insipidus
central - vasopressin deficiency
nephrogenic - vasopressin resistance
oxytocin
stimulates contractile cells in mammary glands
stimulates smooth muscle cells in uterus
stimulates myoepithelial cells of breast to contract
oxytocin is responsible for the _________ of milk
ejection
factors inhibiting release of oxytocin
emotions - stress, fright
drugs and alcohol
factors stimulating release of oxytocin
suckling
emotions - sight/sound of a baby’s cry
dilation of cervix
myometrial sensitivity to OT increased by ____________ concentration of which is high in _____________
estrogen
pregnancy at the end of pregnancy
what hormone stimulates prolactin secretion?
which one inhibits it?
stimulates - thyrotropin releasing hormone
inhibits - dopamine
hyperprolactinemia
abnormally high levels of prolactin in the blood
caused by a benign tumor in the pituitary gland
OT/PRL axis
PRL stimulates development/growth of mammary glands and milk production during pregnancy
OT causes muscle contraction to expel milk in the breast
secondary hyper secretion due to hypothalamic problem
CRH levels - high
ACTH levels - high
Cortisol levels - high
secondary hyper secretion due tov pituitary problem
CRH levels - low
ACTH levels - high
cortisol levels - high
primary hyper secretion due to problem with adrenal cortex
CRH levels - low
ACTH levels - low
cortisol levels - high
adrenocortical primary insufficiency
Addisons disease
autoimmune destruction of the adrenal cortex –> acute adrenal crisis
characteristics of Addisons disease
low glucocorticoids, androgen, and mineralocorticoids
low cortisol - hypoglycemia
low aldosterone - hypotension, hyperkalemia
high ACTH secretion
adrenocortical secondary insufficiency
caused by deficiency of ACTH
Cushing’s syndrome/disease characteristics
high cortisol - hyperglycemia, poor wound healing, central obesity, HTN
high androgen - virilization of women
aldosterone-secreting tumor (Conn’s syndrome) characteristics
high sodium reabsorption - HTN
high potassium secretion - hypokalemia
adrenocortical excess examples
Cushings syndrome/disease
Aldosterone secreting hormone (Conn’s syndrome)
Addison’s disease leads to ________________ due to uninhibited ________________ from anterior pituitary
hyperpigmentation
ACTH release
symptoms of Addison’s disease
muscle weakness and fatigue
hypotension
n/v, weight loss, diarrhea
hair loss
hypoglycemia
addison’s disease occurs when a person is exposed to
major stresses such as trauma, infection, surgery or major illness
waterhouse-friderichesen syndrome
one or both adrenal glands stop working from severe infection
stop producing cortisol
Cushings syndrome
hyper secretion of cortisol from adrenal cortex
Cushings Disease
hyper secretion of ACTH –> increased release of both cortisol and androgenic hormones
symptoms of adrenocortical excess
purple striae
moon face with upper body obesity
growth hormone is produced in the
anterior pituitary
Liver can synthesize __________________ to help regulate growth
Insulin-like GF-1
growth hormone increases
lean growth by increasing rates of muscle protein synthesis and decreasing degredation
GH increases _____________ of fatty acids from _____________
lipolysis
adipocytes
using IGF-1, GH increases
chondrocyte proliferation and osteoblast activity in bone
the plasma concentration of GH
changes with age
(decreases exponentially)
why is plasma measurement of GH problematic?
pulsatile release and short half life of GH
GH is highest during
strenuous exercise and during sleep
dwarfism
due to panhypopituitarism during childhood
correct proportions but development is slow
does someone with dwarfism go through puberty?
No
if there is only growth hormone deficiency in dwarfism then
sexual maturity occurs
african pygmy
form of dwarfism
rate of growth hormone secretion is normal/high
inability to form IGF-1
giantism cause
acidophilic tumors of anterior pituitary before puberty
giantism
body tissue grow rapidly
hyperglycemia
acromegaly cause
acidophilic tumor after puberty
acromegaly
bones, soft tissues become thicker
enlargement of organs
kyphosis
metabolic effects of GH on protein metabolism
increase protein synthesis
reduces breakdown of cell proteins by decreasing catabolism of protein
metabolic effects of GH on fat metabolism
increases the concentration of fatty acids
metabolic effects of GH on glucose metabolism
increase of the blood glucose concentration
(dec uptake of glucose and glucose utilization)
low glucose stimulates the release of
GHRH (growth hormone releasing hormone)
GHRH ________ release of GH which works to ______________
increases
raise blood glucose levels to normal
high blood glucose stimulates the release of
GHIH (growth hormone inhibiting hormone)
GHIH __________ release of GH which works to ______________
inhibits
lower blood glucose levels to normal
high protein intake leads to
increased GH, somatomedin and insulin –> no change in caloric storage
high carbohydrate intake leads to
decreased GH, inc insulin, no change somatomedin –> inc caloric storage
fasting leads to
inc GH, dec somatomedin and insulin –> inc caloric mobilization
if there is an increase in somatomedin, there is
an increase in protein synthesis and growth
(direct relationship)
two important thyroid hormones
thyroxine (T4)
triiodothyronine (T3)
the difference between T3 and T4 is that
T3 has 3 iodines and T4 has 4 iodines
Thyroid hormone is synthesized by
tyrosine
enzyme that helps in TH synthesis
thyroid peroxidase
TH synthesis
tyrosine –> MIT or DIT –> T3 or T4
T4 is converted to T3 by
deiodinase
which isoform of deiodinase converts T4 to reverse T3?
D3 (sometimes D1)
which isoform of deiodinase converts T4 to T3?
D1 and D2
major actions of thyroid hormones
increase basal metabolic rates
maintenance of body temp
stimulates rate of cellular respiration
necessary for normal growth and maturation
when T3/T4 are decreased, the basal metabolic rate ______________ and carbohydrate metabolism __________
decreases
decreases (gluconeogenesis/glycogenolysis)
when T3/T4 are increased, the basal metabolic rate ______________ and carbohydrate metabolism __________
increases
increases (gluconeogenesis/glycogenolysis)
where are thyroid hormones made
the thyroid gland duh!
size of the thyroid gland depends on
age
sex
physiological condition (pregnancy/lactation)
which TH is secreted more?
T4 (100 mcg/day) —- T3 is only 6!
almost all of T4 is
converted to T3 in tissues
colloid
pink staining proteinaceous material in thyroid follicle
thyroglobulin (TBG)
stores thyroid hormones
when the thyroid gland is inactive
follicles are large
when the thyroid gland is active
follicles are small
thyroid homeostasis
release of TRH -> release of TSH –> release T3 and T4 in follicles –> normal body temperature
the half life of TRH is ___________
the half life of TSH is ______________
the thyroid hormone half life is ____________
5 min
1 hour
1-7 days
thyroid stimulating hormone is a __________ while thyrotropin releasing hormone is a _____________
glycoprotein
tripeptide
untreated hypothyroidism can contribute to
hypertension
dyslipidemia
infertility
cognitive impairment
neuromuscular dysfuntion
two most common causes of hypothyroidism
hashimotos thyroiditis (developed)
iodine deficiency (developing countries)
who is more affected in hypothyroidism?
women
symptoms of hypothyroidism
SLUGGISH
sleepiness
loss of memory
unusually dry skin
goiter
gradual personality
increase in weight
sensitivity to cold
hair loss
endemic goiter
in iodine insufficient area
sporadic goiter
in iodine sufficient area
how is hypothyroidism related to goiters?
dec TH –> inc TSH –> TSH acts on thyroid –> increases blood flow -> stimulates follicular cells and inc colloid production
Wolff-Chaikoff effect
plasma iodide levels are extremely high (15-20X)
Primary hypothyroidism
insufficient functioning of thyroid gland
impaired TH synthesis
drug mediated inhibition of TH production involved
thionamide
amiodarone
lithium
severe conditions of primary hypothyroidism is called __________
extreme?
myxedema
myxedema coma
Hashimoto’s Thyroiditis
immune system attacks the thyroid gland causing inflammation
autoimmune
secondary hypothyroidism
insufficient secretion of TSH
tertiary hypothyroidism
insufficient secretion of TRH
thyroid resistant syndrome
organs not responding to T4 and T3
reduced binding affinity for T3 at TR beta
diagnostic test for checking thyroid hormones
anti-TPO antibody test
Allan Herndon Dudley Syndrome
X linked mental retardation
manifest with truncal hypotonia, poor head control
mutation in MCT8 (transports TH to neurons)
Allan Herndon Dudley syndrome results in
high levels of serum T3, low levels of T4 and normal levels of TSH
Hyperthyroidism key symptoms
apparent bulging of the eyes
rapid heartbeat
nervous excitability
primary hyperthyroidism
graves disease (autoimmune - mimics effect of TSH)
graves disease
excessive production of TH
enlarged thyroid gland
exophthalmic goiter
99% of calcium is in
the bone and teeth
after the 3rd decade of life,
bone resorption exceeds bone accretion/formation
can calcium be synthesized
nope
calcium balance
intake = output
positive calcium balance
intake > output
occurs during growth
negative calcium balance
intake < output
leads to osteoporosis
nondiffusable plasma calcium
40%
bound to albumin
diffusible plasma calcium
60%
salt form (50% - ionized, 9% complexed)
what form of calcium is active
ionized calcium
acidosis decreases protein binding resulting in
increased free calcium levels
alkalosis promotes increased protein binding which
decreases free calcium levels
bone
67% - inorganic hydroxyapatite
33% - organic osteoid
majority of organic calcium in the bone is
type I collagen
if free calcium is too low it can lead to
neural hyper excitability
if free calcium is too high it can lead to
neuronal depression
control points for calcium
absorption in intestines
excretion in urine
temp storage in bone
active control of calcium
vitamin d3
PTH
calcitonin
skeletal loading
phosphate metabolism
majority is in the bone
kidneys and bones are primary sites of regulation
two forms of inorganic phosphate
ECF
ICF
calcium phosphate has
limited solubility
solubility product for calcium phosphate
ion calcium x phosphate ion concentration
(constant = 1.36 x 10^-26)
if the product of the two ions is greater than SP,
you would expect precipitation of calcium phosphate
the regulation of plasma calcium levels are critical for
normal cell function
neural transmission
membrane stability
bone structure
blood coagulation
intracellular signaling
the regulation of plasma calcium relies on
interactions with PTH
dietary vitamin D
calcitonin synthesized in the C cells of thyroid gland
major sites of regulation for calcium
bone
kidney
intestine
how is calcium regulated in the bone?
vitamin D increases bone reabsorption with a resulting increase of calcium into circulation
how is calcium regulated in the kidney?
PTH promotes calcium reabsorption and phosphate excretion
PTH stimulates the formation of
active form of vitamin D
how is calcium regulated in the intestine?
vitamin D increases absorption of dietary calcium and facilitates renal reabsorption of filtered calcium
three ways homeostatic regulation returns blood calcium to normal when it is low
kidney saves calcium
digestive tract absorbs calcium (inc PTH)
bones release calcium (dec calcitonin)
three ways homeostatic regulation returns blood calcium to normal when it is high
kidneys excrete more calcium
digestive tract absorbs less calcium (dec PTH)
bones take up calcium (inc calcitonin)
vitamin D
steroid hormone when active
has both dietary and endogenous precursors
vitamin D2
ergocalciferol
from plants from ergosterol
vitamin D3
cholecalciferol
UV rays from precursor 7-dehydrocholesterol in skin
vitamin D promotes
intestinal absorption of calcium
vitamin D causes synthesis of
calcium binding and related facilitated transport
it takes ____________ to get a fully developed response from vitamin D
a couple of days
vitamin D works with
PTH to cause calcium absorption from bone
principal target of vitamin D and what happens there
intestine
stimulates calcium and phosphorus absorption
second major target of vitamin D and what happens there
bone
provides calcium and phosphate to initiate crystallization of bone osteoid
does vitamin D effects the immune system?
if so, how?
yes
promotes differentiation of monocyte precursors to monocytes and macrophages
what happens in the kidney due to vitamin D?
increases renal tubular reabsorption of both calcium and phosphate
vitamin D deficiencies due to
insufficient dietary intake of vitamin D
inadequate exposure to light
renal and liver disease
severe bone dimineralization
vitamin D deficiency due to renal and liver disease
inadequate conversion to 25-cholecalciferol and 1,25 - dihydroxycholecalciferol
vitamin D deficiency due to severe bone demineralization
osteomalacia
rickets
PTH release is increased by
hypocalcemia
hyperphosphatemia
catecholamines
PTH release is suppressed by
hypercalcemia
vitamin D
severe hypomangesemia
primary hyperparathyroidism
excessive production and release of PTH by PT glands
secondary hyperparathyroidism
defect is outside the PT
primary hyperparathyroidism examples
chief cell adenoma
PT hyperplasia
PT carcinoma
secondary hyperparathyroidism examples
severe calcium and vitamin D deficiency
CKD
primary hypoparathyroidism
too little PTH secretion
secondary hypoparathyroidism
decreased end organ responsiveness to PTH
digeorge syndrome
genetic disorder, low PTH
low blood calcium and high phosphorus
endocrine disorders result from
hormone deficiency
hormone excess
hormone resistance
endocrine disruptors
exogenous substance that changes endocrine function and causes adverse effects at the level of the organism, its progeny, or population
diethylstilbestrol (DES)
endocrine disruptor
interrupts the estrogen pathway
used to prevent miscarriages, but would lead to daughters of mothers that took this having them instead
why would the same hormone have different effects on target cells?
different receptors for the same hormone
different hormones for the same receptor
different hormones may have the same effects on target cells if
the same receptors for different hormones, leading to target gene expression
why would the same hormone have different effects on target cells?
different receptors for the same hormone
different signal transduction pathways