Phys review Flashcards
hormones secreted from hypothalamus
TRH CRH GnRH somatostatin dopamine
ant pituitary hormones
released from portal circulation TSH FSH LH ACTH MSH GH Prolactin
post pituitary hormones
released directly from neurons
oxytocin
ADH
thyroid hormones
T3
T4
calcitonin
parathyroid hormones
PTH
pancreas hormones
insulin
glucagon
adrenal medulla hormones
NE
Epi
kidney hormones
renin
vit D
adrenal Cx hromones
cortisol
aldosterone
adrenal androgens
testes hormones
testosterone
ovaries hormones
E2
progesterone
corpus luteum
estradiol
progesterone
Placenta
HCG
E3
progesterone
HPL
example of positive feedback loop
E2 on anterior pituitary midcycle
lipid soluble hormone receptors
inside cell
usually in nucleus
lipid soluble hormone action
TF -> new proteins
lipid soluble hormone storage
synthesized as needed
exception T3 and T4
lipid soluble hormone plasma transport
attached to proteins
exception adrenal androgens
lipid soluble hormone half life
long due tprportional to affinity for carrier
water soluble hormone receptor
outer surface of cell
water soluble hormone action
second messangers
water soluble hormone storage
stored in vesicles
sometimes prohormone stored
water soluble hormone plasma transport
dissolved unbound
water soluble hormone half life
short proportional to MW
tertiary condition ex
hypothalamic failure
TRH, TSH, and T3/4 ALL low
secondary condition ex
pituitary failure
high TRH low TSH and T3/4
primary thyroid conditions ex
thyroiditis
graves
thyroiditis
TRH and TSH high
T3/4 low
graves
low TRH and TSH
high T3/4
mutation in hormone receptor
all preceding signaling molecules will be elevated
nuclei of post pituitary
SON (supraoptic nuclei)
PVN (paraventricular nuclei)
ADH
maintain normal osmolality of body fluids
releases in response to increased serum osmolality (and decreased BP)
increases number of aquaporins in distal tubule to increase water resorption
induces contraction of vascular smooth mm
Oxytocin
milk letdown
uterine contraction
receptor for ADH
V2 on basolateral membrane of collecting duct
DI
Dx confirmed by dehydration stimulus with inability to concentrate urine
plasma osmolality in DI
neurogenic normal/high
nephrogenic normal/high
urine osmolality in DI
neurogenic low
nephrogenic low
plasma ADH
neurogenic low
nephrogenic normal-high
urine osmolality after water deprivation
no change
plasma ASH after water deprivation
neurogenic no change
nephrogenic high
urine osmolality after ADH administation
neurogenic high
nephrogenic no change
factors which stimulate GH
decrease glucose concentration decreased FFAs arginine fasting/starvation hormones of puberty (E,T) EXERCISE STRESS STAGE III/IV sleep alpha-adrenergic agonisits
factors which inhibit GH
increased glucose concentration increased FFAs obesity senesence somatostatin somatomedins GH beta-adrenerigc agonists pregnancy
overall affects of GH
diabetogenic effect
increased protein synthesis and organ growth (IGF-I)
increased linear growth (IGF-I)
diabetogenic effect of GH
causes insulin resistance decreased glucose uptake increased blood glucose increased lipolysis increased blood insulin levels
increased protein synthesis and organ growth
IGF-I
increased aa uptake
increased DNA, RNA, and protein synthesis
increased lean body mass and organ size
increased linear growth
IGF-I
altered cartilage metabolism
factors which stimulate prolactin
pregnancy (due to estrogen) breast-feeding sleep stress TRH Dopamine antagonists
factors which inhibit prolactin
dopamine
bromocriptine (dopamine agonist)
somatostatin
prolactin
GnRH
pulsatile release prevents downregulation of its receptors
constant infusion will cause a decrease in LH and FSH
T3/4 synthesis
- synthesis of TG and exocytosis to follicular lumen
- transport of I into cell via Na cotransport
- oxidation of I via peroxidase
- organification of I into MIT and DIT ( inhibited by PTU)
- coupling rxn (DIT+DIT = T4 DIT + MIT = T3)
endocytosis of TG
-proteolysis of iodinated TG -> T3/4 - MIT and DIT and TG recycled
transport of T3/4
circulate bound to TBG and to lesser extend albumin and TTR
- 98% of T4 bound
- 5% of T3 bound
T3
more active thyroid hormone b/c 10x higher affinity for TR
ratio of T4:T3 is 10:1
tissues contain deiodinases to convert T4 -> T3
people without
normal TH levels
T4 5-12ug/dL
T3 70-190ng/dL
factors which stimulate TH
TSH
Thyroid stimulating immunoglobulins
increased TBG levels (pregnancy)
factors which inhibit TH
I deficiency
deiodinase deficiency
excessive I intake (Wolff-Cahikoff effect)
Perchlorate (thiocyanate) inhibit NA/I cotransporter
PTU (inhibits peroxidase)
decreased TGB levels (liver disease)
TH effects on growth
growth formation
bone maturation
TH effects on CNS
maturation of CNS
TH effects on BMR
increased Na/K ATPase
increased O2 consumption
increased heat production
TH effects on metabolism
increased glucose absorption
increased glycogenolysis
increased gluconeogenesis
TH effects on CV
increased CO
thyrotoxicosis
graves disease factitious thyrotoxicosis toxic adenoma toxic nodular goiter pituitary overproduction of TSH granulomatous thyroiditis subacute lymphocytic thyroiditis
graves disease
autoimmune thyroid disease
.5% of population
factitious thryotoxicosis
exogenous thyroid hormone with gland atrophy and low TG
toxic adeoma
aka hot nodule
overproduction of TH by nodule with low TSH and gland atrophy surrounding nodule
toxic nodular goiter
multiple nodules
pituitary overproduction of TSH
rare
granulomatous thyroidtiis
aka subacutre thyroiditis
viral etiology with painful gland
hyperthyroidism -> euthyroidism -> hypothyrodism -> euthyroidism
subacute lymphocytic thyroiditis
aka silent thyroiditis
believed to be autoimmune
non-tender gland transient
example is postpartum thyroiditis
primary hypothyroidsim
hashimotos 5-10% of population
T cell mediated, but Abs can also be present
radioactive ablation of thyroid
zona glomerulosa
aldosterone
controlled by Ang II and K
zona fasciulata
cortisol
controlled by ACTH
zona reticularis
androgens
controlled by ACTH
medulla
Epi
controlled by ANS
factors which stimulate cortisol
decreased blood cortisol sleep-wake transition stress, surgery, trauma hypoglacemia psychiatric disturbances ADH alpha-adrenergic agonists beta-adrenergic antagonisits serotonin
factors which inhibit cortisol secretion
increased cortisol
opioids
somatostatin
factors which stimulate aldosterone secretion
angiotensin II
ACTH
high plasma K
actions of glucocorticoids
increased gluconeogenesis increased proteolysis increased lipolysis decrease glucose utilization decrease insulin sensitivity
actions of mineralcortiocoids
increased Na reabsoprtion
increased K secretion
increased H secretion
actions of adrenal androgens
females: stimulate growth of pubic and axillary hair and stimulate libido
males: same as testosterone
acute cortisol effects
mobilize glucose
optimize adrenergic R fnx to increase CO
helps provide energy for inflammatory and immune response, but also protects from damage of unregulated inflammation
acute cortisol on liver
increased glycogenolysis
increased gluconeogenesis
acute cortisol on skeletal mm
increased proteolysis
decreased protein synthesis
increased glycogenolysis
decreased glut-4 mediated glucose uptake
acute cortisol on adipose tissue
increase lipolysis
decreased lipogeneis
decreaed glut-4 mediated glucose uptake
chronic cortisol on CNS
increased appetite
chronic cortisol on liver
increased hepatic glycogen synthesis
chronic cortisol on skeletal m
increased proteolysis
decreaed GLUT-4 mediated glucose uptake
chronic cortisol in adipose tissue
decrease lipolysis
increased TG synthesis
increased preadipocyte to adipocyte differentiation
decreased GLUT 4 mediated glucose uptake
chronic cortisol effects
promote localized obesity (abdominal, neck, face)
mm wasting and weakness
glucose intolerance
acute cortisol and other hormones
decreased insulin/glucagon ratio
increased Epi and NE
chronic cortisol and other hormones
increased insulin/glucagon ratio
decreased epi and NE
addison disease
primary adrenocortical insufficiency
addisons clinical
hypoglycemia anorexia, weight loss, nausea vomiting weakness hypotension hyperkalemia metabolic acidosis decreaed pubic and axillary hair in females hyperpigmentation
addisons ACTH
increased sue to decreased cortisol
addisons Tx
replacement of glucocorticoids and mineralcorticoids
cushings syndrome
primary adrenal hyperplasia
cushings syndrome clinical
hyperglycemia
mm wasting
central obesity
round face, supraclavicular fat, buffalo hump
striae
virilzation and menstrual disorders in females
HTN
cushings syndrome ACTH
decreased due to neg feedback of increased cortisol
cushings syndrome Tx
ketoconazole
metyrapone
cushings disease
excess ACTH
cushings diseases ACTH
increased
cushings diseases clinical
same as cushing syndrome
cushings diseases Tx
surgical removal or ACTH secreting tumor
Conn syndrome
aldosterone secreting tumor
Conn clinical
HTN
hypokalemia
metabolic alkalosis
decreased renin levels
conn Tx
aldosterone antagonists
surgery
21 beta-hydroxylase deficiency clincal
virilization of femailes
early acceleration of linear growth
early appearance of pubic hair and axillary hair
symptoms of deficiency of glucocorticioids and mineralcorticoids
21 beta-hydroxylase deficiency ACTH
increased due decreased cortisol
21 beta-hydroxylase deficiency Tx
replacement of glucocortiocoids and mineralcorticoids
17 alpha hyroxylase deficiency clinical
lack of pubic and axillary hair in females
symptoms of deficiency of glucocortiocoids
symptoms of deficiency of glucocorticoids
symptoms of excess mineralcorticoids
17 alpha hyroxylase deficiency ACTH
increased
17 alpha hyroxylase deficiency Tx
replacement of glucocorticoids aldosterone antagonists (spironolactone)
Glucose R on brain
GLUT3
glucose R on liver
GLUT2
glucose R on mm
GLUT4
Glucose R on adipose tissue
GLUT4
beta cells of pancreas
insulin
alpha cells of pancreas
glucagon
delta cells of pancreas
somatostatin
actions of insulin
increase glucose uptake increase glycogen formation decrease glycogenolysis decrease gluconeogenesis increases protein synthesis increases fat deposition decreases lipolysis increases K uptake
factors which stimulate insulin
increased glucose increased aa increased FA and ketoacids glucagon cortisol GIP K vagal stimulation Ach sulfonylurea drugs obesity
factors which inhibit insulin
decreased glucose fasting exercise somatostatin alpha-adrenergic agonists diazoxide
actions of glucagon
increased glycogenolysis
increases gluconeogenesis
increased lipolysis
increased ketoacid formation
factors which stimulate glucagon
fasting decreased glucose concentration increased aa concentration beta-adrenergic agonists Ach
factors which inhibit glucagon
insulin
somatostatin
increased FA and ketoacid concentration
effects of glucagon on blood
increases glucose, FA, and ketoacids concentrations
high insulin:glucagon ratio
favors anabolic rxns
low insulin: glucagon ratio
favors catabolic rxns
normal Ca levels
8.5-10.5 mg/dL
symptoms of hypocalcemia
twitching, mm cramps, tingling, numbness
symptoms of hypercalcemia
constipation, polyuria, polydipsia, lethargy, coma, death
Free Ca
50%
45% bound to albumin (kicked off by H)
5% complexed
free PO4
84%
hormones which control Ca
PTH
vit D
calcitonin
organs which control C
skeleton
kidney
intestines
CaSR
Ca sensor R
7 membrnae G-protein coupled R
senses extracellular Ca-ionized Ca
R found on parathyroid cells, parafollicular cells, and renal tubular cells
fnx of PTH
- triggers Ca and PO4 resopriton from bone
- promotes Ca resorption from kidney
- promotes PO4 excretion from kidney
- increases vit D production in kidney
functions of vit D
bone remodeling
Ca absorption from gut
renal resorption of Ca and PO4
PTH binds to osteoblasts
osteoblasts release RANKL (IL6) which binds to RANK on osteoclasts to stimulate bone resorption
OPG
soluble receptor for RANKL to inhibit activation of osteoclasts
loss of RANKL
increases bone density
osteopetrosis
loss of OPG
decreases bone density
osteoporosis
severe vit D deficiency
0-10
moderate vit D deficiency
10-20
mild vit D deficiency
20-30
normal vit D
> 30
90% of hypercalcemias due to
primary hyperparathyroidism (increased PTH)
or
hypercalcemia of malignancy
other causes of hypercalcemia
granulomatous disease vit D toxicity vit A toxicity hyperthyroidism thiazide diuretics milk-alkali syndrome immobilization adrenal insufficiency adrenal insufficiency acute renal failure familial hypocalciuric hypercalcemia
familial hypocalciuric hypercalcemia
heteozygous inactivating mutation in CaSR
increased PTH and serum Ca
causes of hypocalcemia
vit D deficiency hypoparathyroidism pseudohypoparathyroidism hypomagnesmia renal failure liver failure acute pancreatitis hypoporteinemia
pseudohypoparathyroidism
genetic condition causing resistance to PTH