Endocrine-2 Flashcards
tropic hormones refers to
hormones released by the ant pit
hypothalamic hormones
trh, crh, gnrh, ghrh, prl inhibitory, somatostatin
trh
causes ant pit to release tsh
crh
stimulates release of acth
gnrh
stimulates release of lh & fsh
ghrh
stimulates release of gh
prl inhibitory
inhibits release of prl
somatostatin
inhibits release of gh & digestive hormone
endocrine axes
end products feed back to inhibit regulators of own secretion
castration results in an increase of __ BECAUSE you wouldn’t produce
lh & fsh secretion; testosterone
if person can’t produce thyroid hormone, their tsh & trh levels are
HIGH
secretion of acth inhibited by
corticosteroids
describe thyroid axes
trh -> tsh -> th -> feedback inhibits tsh & trh
can corticosteroids be stopped abruptly? why?
no. body can’t tell difference between drug taken & cortisol it produces; body thinks cortisol levels are high -> shuts off prod of acth & crh
glucocorticoids suppress the
hypothalamus & ant pit
why must you taper person off drugs slowly
to give axes time to start producing acth & crh again
abruptly withdrawing drug can be fatal because
aldosterone can’t be released w/o presence of acth
adrenal medulla
modified sympathetic ganglion
adrenal cortex
endocrine tissue
adrenal medulla releases __ in response to
epi & norepi; sns
adrenal cortex releases __ in response to
aldosterone, cortisol, & weak androgens; ant pit producing acth
all hormones produced in the adrenal cortex are __ hormones; derived from __
steroid hormones; cholesterol
cortisol is a __ hormone
stress
why is cortisol considered a stress hormone
it tries to make nutrients available so you have energy source
cortisol disorders
cushing’s syndrome & addison’s disease
cause of cushing’s syndrome
over secretion of acth from ant pit or too much hormone produced from adrenal cortex
effect of cushing’s syndrome
changes in carbohydrate & protein metabolism
result of cushing’s syndrome
- cortisol elevates blood sugar -> hyperglycemia
- defect in metabolism -> abnormal fat deposition, moon face, etc.
- muscle breakdown & muscle weakness
cause of addison’s disease
inadequate secretion of glucocorticoids (cortisol) & mineralcorticoids (aldosterone)
why can addison’s disease be fatal?
lack of aldosterone production which is essential for life
main effect of addison’s disease
darkening of skin (bc trying to prof a lot of acth = producing msh)
cushing’s disease mimics someone who is on
high dose of prednisone
symptoms: euphoria, psychotic, poor wound healing, bruising, prone to infection
cushing’s syndrome
why is it bad to place cortisol near bone frequently
cortisol stimulates osteoclast activity -> lead to osteoporosis
adrenal medulla releasing epi & norepi is similar to that of the NS however it
lasts longer (put straight into bloodstream)
adrenal medullary tumor (pheochromocytoma) symptoms
epi & norepi high, hr high, high bp, blood sug, nervousness, digestive probs, glycosuria, thin
stress releases
cortisol
why does increased stress increase illness
glucocorticoids inhibit immune responses
chronically elevated cortisol ->
atrophy of hippocampus (defects in learning & memory)
glucocorticoids (stress hormone) stimulate
catabolism
catabolism
breakdown
ex of catabolism
protein -> amino acids
anabolism
building
why do glucocorticoids stimulate catabolism
they try to provide nutrients to be used as energy sources
gluconeogenesis
production of glucose from non-carbohydrate sources
what do glucocorticoids stimulate to provide nutrients
gluconeogenesis, fat & protein breakdown, elevation of blood sugar, & opposition of insulin effects
stress complicates diabetes tx? why?
t; stress -> glucocorticoids -> aggravate insulin resistance
spherical hollow sacs
follicles
follicles lines with __ that secrete __
follicular cells; thyroxine
protein rich fluid inside thyroid follicles
colloid
where is thyroid hormone stored
w/in colloid
parafollicular cells secrete
calcitonin
calcitonin
lowers blood calcium
pth
increases blood calcium
what does thyroid hormone do?
increases bmr
as a result of an increase of bmr ->
o2 consumption (generates heat), thyroid hormone secretion (in cold weather), hr + force of contraction, & resp rate ALL RAISED
what else does thyroid hormone do?
stimulates appetite, accelerates breakdown of macromolecules, & for NS maturation
which hormone if not produced in infancy can affect brain development
thyroid hormone
person with too much thyroid hormone is
thin, gittery, hr racing, high bp, sweating, constantly hungry
person with too little thyroid hormone
overweight, tired, lethargic, cold
calcitonin secreted by
parafollicular cells of thyroid
calcitonin lowers blood calcium levels by
inhibiting osteoclast activity & by stimulating renal calcium excretion
iodine deficiency goiter cause
inadequate thyroid hormone produced
iodine deficiency goiter results in
increased tsh -> but since don’t have thyroid hormone = hypertrophy of gland
grave’s disease caused by
autoantibodies against thyroid gland
grave’s disease results in
hypertrophy & toxic goiter or thyrotoxicosis
mechanism of grave’s disease
autoantibodies look like tsh -> bind to tsh receptor -> stimulate thyroid hormone & gland growth
what determines if they have goiter
whether tsh receptor is being stimulated or not
iodine deficiency stimulated by
tsh
grave’s disease stimulated by
antibodies
grave’s disease: patient also develops
exopthalmia (antib’s bind to recep’s behind orbits->eyes bulge)
grave’s disease: patient actual tsh levels very
LOW (tsh stops bc have tons of thyr horm)
grave’s disease: patient bmr & bp
high
hypothyroidism in adults aka
myxedema
hypothyroidism in adults can also result in
swelling of hands & feet
hypothyroidism in children aka
cretinism
pth raises blood calcium by
- stimulating osteoclast activity
- prod. vit d
- increasing renal reabsorption of ca
pancreas is a mixed gland
t
islets are __ structures
endocrine
alpha cells ->
beta cells ->
glucagon
insulin
insulin secreted in response to a
rise in plasma glucose
insulin binds receptors in target cells ->
results in translocation of glucose transporters -> glucose taken up by ADIPOSE tissue -> stimulates glycogen prod -> fat deposition -> storage of hormone
insulin effects
- inhibits lipolysis
- induces prod of fat-forming enzymes
- inhibits protein breakdown
ketogenesis
when you use FATS as energy source -> prod ketones
testosterone produced by
interstitial cells of leydig
ovarian follicles release
estrogen
estrogen produced by
granulosa cells
cells that surround developing oocyte
granulosa cells
what converts testosterone to estrogen
aromatase
you must have __ to make estrogen
testosterone
progesterone produced by
corpus luteum
keeps uterine lining in tact to continue pregnancy
placenta
placenta releases
estrogen & progesterone
insulin rises during __ state
absorptive (following a meal) aka postprandial phase
insulin falls during __ state
postabsorbative (fasting)
hormonal regulation of metabolism primarily via
plasma glucose levels & amino acid levels
if can’t use glucose as energy source & must use fat breakdown you produce __ as a biproduct
ketoacids
result of ketoacids accumulating
ketoacidosis
ketoacidosis usually only occurs in
untreated type 1 diabetes
high blood glucose stimulates insulin to get
stored
glucagon stimulated by
fall in blood glucose
glucagon inhibited by
rise in blood glucose
glucagon increases blood glucose during
fasting
type 1 diabetes you do produce insulin
f; don’t
type 1 diabetes __ cells not functional
beta
type 1 diabetes tx
give insulin
insulin overproduction type __
2 diabetes
cause of type 2 diabetes
either cells aren’t responding OR down regulating receptors; have insulin resistance
can end up w/ islet cell failure -> islet cells can’t produce insulin (BIG PROBLEM) -> characteristic of
type 2 diabetes
patients w/ type2 diabetes usually develop keto acids
f; rarely bc have insulin working to some degree so ARE pulling in some glucose
are beta cells functional in type 2 diabetes
yes
type2 tx
diet & exercise
what is the hallmark of glycosuria
hyperglycemia
the word diabetes refers to
freq urination
the word mellitus refers to
honeyed/sweet
which type of diabetes is insulin dependent
1
what gets used up trying to neutralize ketoacids
bicarb buffers
ketone bodies & glycosuria results in
osmotic diuresis
osmotic diureses ->
severe dehydration -> severe electrolyte disturbances & acidosis -> comma & death
loss of insulin sensitivity/ insulin resistance characteristic of
type2
down regulation of receptors or loss of receptor sensitivity, down regulation of glucose transporters characteristics of
type2
in the early stages of type2, patient produces normal-slightly elevated insulin
t
type2 has a gradual progression
t
what up-regulates glucose transporters on skeletal m
exercise
if lifestyle modification alone can’t control type2 ->
oral hypoglycemic agents added
what do oral hypoglycemic agents do
help body use glucose
oral hypoglycemic agents only work well with
diet & exercise
why are insulin levels high in patient w pre diabetes
body not responding to insulin so puts more out to get a response
obesity kills more than smoking & drinking combined
t
what happens over time if body not responding to insulin & keeps putting more out to get a response
islet cells can get exhausted & stop producing insulin
catecholamines
epi & norepi
catecholamines stimulate
glycogenolysis, release of glucose from liver, lypolysis
glucocorticoids promote
lypolysis, ketogenesis, gluconeogenesis, & protein breakdown
what does thyroxine do
increases bmr
what promotes heat generation which is important to cold adaptation
thyroxine
why is cornoary art disease associated w type 2
high blood sugar causes tears in endothel -> makes it easier for lipids to deposit
what condition goes hand in hand with type 2
dyslipidemia
gucocorticoids cause protein synthesis to go
down
glucocorticoids cause blood glucose, glycogen, & gluconeogenesis to go
up
the skeleton is a huge __ & __ reservoir
ca & phosphate
bone resorption done by
osteoclasts
bone resorption returns __ & __ to blood
ca & phosphate
what stimulates osteoclast apoptosis
estrogen
why are women more prone to osteoporosis after menopause
estrogen stimulates osteoclast apoptosis
what increases absorption of ca & phosphate from gut
vit d
what must be present for pth to stimulate osteoclast activity
vit d
bone remodeling important for
stress adaptation
__ is secreted in response to low blood ca
pth
how does pth raise blood calcium
- stimulating osteoclast activity
- increasing renal reabsorption while inhibiting phosphate reabsorption
- increasing formation of vit d
regulators of pth
- ca levels
- vit d levels
- glucocorticoids
vit d production beings in the
skin
vit d is protective against certain cancers
t
raises plasma concentrations of ca & phosphate
vit d
how does vit d raises plasma concentrations of ca & phosphate
by increasing intestinal reabsorption of ca & phosphate & from gut & by being permissive to osteoclast activity
vit d results in increased
pth
vit d results in low
plasma phosphate
vit d decreased by
elevated plasma phosphate
pth stimulates excretion of __ so that the net effect is an increase in blood ca
phosphate
osteoblast
bone forming
widow’s hump a result of
spinal compression
breakdown occurs faster than formation
t
__ is inhibited when ca levels are high
pth
elevation in vit d levels will inhibit
pth
glucocorticoids stimulate pth production
t
glucocorticoids cause osteoporosis
t; bc pth stimulates osteoclast activity
sunlight far more protective at increasing vit d
t
how does pth cause the production of vit d
pth stimulates kidneys to perform last hydroxylation for active form of vit d
what does vit d do
raises plasma concentrations of ca & phosphate
vit d promotes osteoclast activity
f; in order to pth to stim osteoclast activity, vit d must be present
