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116 Cards in this Set

  • Front
  • Back
name 7 steroids
glucocorticoids
estrogen
testosterone
progesterone
aldosterone
vitamin D
thyroid hormone!!
t/f: the alpha subunit of the G protein has the GDP/GTP
true

(the stimulatory/inhibitory activity of G proteins resides in alpha subunit)

if stimulatory--> activates ac-->inc cAMP
phosphodiesterase?
enzyme that degrades cAMP

(inhibited by caffiene)
what's the IP3 mechanism?
hormone binds receptor,

via a G protein, activates phospolipase C

phospholipase C liberates DAG and IP3 from membrane lipids

IP3 inc Ca
DAG + Ca activatesPKC

physiologic actions
TSH, LH, and FSH have what in common?
their alpha subunits are identical

their beta ones are different
POMC gives rise to.....
ACTH
MSH (melanocyte stimu hormone)
beta-lipotropin
beta-endorphin
somatomedins=
IGF

(insulin-growth factor.
it's receptor has tyrosine kinase activity...just like insulin!)
growth hormone ___glucose uptake
decreases (GH is diabetogenic)


does it decrease glucose uptake of fat cells and increase of muscle?

(check this...)
GH ___lipolysis
GH inc lipolysis
GH ___protein synthesis
increases
GH deficiency can be caused by

(4 things)
1) dec GHRH (hyp)
2) dec GH (ap)
3) failure to generate IGF in the liver
4)GH receptor deficiency
GH excess can be treated by
octreotride (somatostatin analog)

somatostatatin dec GH
GHRH inc GH
actions of prolactin

4 functions---on milk, breast, males, GnRH
-milk production (casien, lactalbumin)
-stimulates, with estrogen, breast development

-inhibits GnRH synthesis/release
(it's the natural birth control....! its so cool)

-inhibits spermatogenesis (by dec GnRH)
prolactin excess causes
1)galactorrhea
2) failure to ovulate and amenorrhea (bc it inhibits GnRH secretion)
what stimulates prolactin release?
TRH (thyrotropin releasing hormone)
what can treat prolactin excess?
a dopamine agonist like bromocriptine
ADH and oxytocin are made where?
in hyothalamic nuclei, packaged in secretory granules with thier respective neurophysins
ADH made in which nuclei
supraoptic nuclei
actions of ADH on
V1
V2 receptors
V1--constricition of vascular s muslce
V2--water permeability
oxytocin made in...
paraventricular nuclei
oxytocin causes...

(2 things)
ejection of milk from the breast, when stimulated by suckling (via contraction of myoepithelial cells...milk goes from alveoli to ducts to infant)

-contraction of the uterus

(oxytocin can be used to induce labor and reduce postpartum bleeding)
what increases oxytocin release
sucking (main)
dilation of the cervix and orgasm
thiocyanate & perchlorate anions

inhibit what?
iodine pump
5' iodinase _____
converts T4 to T3 (takes an iodine atom out)
peroxidase does what?
basically catalalyzes most of the rxns leading to T4, T3 productions
what inhibits peroxidase
propylthiouracil (in follicular cell membrane)
what's the Wolff-Chaikoff effect?
high levels of iodine inhibit the iodine pump,--> dec thyroid hormone production
T/F more t3 is produced, which is the more active form
more T4 is produced! but yeah, T3 is the more active one
describe organification of I2
1) TYROSINE added onto thyroglobulin on the ribosomes of the thryoid follicular cells

2) thryoglobulin is packaged into secretary vescieles on the Golgi apparatus and then goes into the follicular lumen

3) on its way there (at the interface of the cell and the lumen), the tyrosine residues of thyroglobulin react with I2 to form DIT and MIT (monoiodoTYROSINE, and diiodoTRYOSINE)

DIT + DIT =T4
DIT + MIT = T3

(they couple, while attached to thyroglobulin)
how are thryoid hormones released?
1) TSH stimulates the cell
2) iodinated thyroglobulin is taken from LUMEN back into CELL

3) in the cell, the lysosomal enzymes digest the thyroglobulin, releasing the T4, T3 into circulation
chronic levels of high TSH cause----
thyroid hypertrophy (goiter)
what inhibits TSH secretion---> T3 or T4?
T3 (by downregulating TRH receptors in the ap)
thyroid hormone affects growth by--------
thyroid hormones work synergistically with GH and somatomedins (IGF) to inc bone formation

in deficiency: bone age is less then chron age

you NEED thryoid hormone to get adult stature
thyroid h affects CNS by____
maturation of CNS absolutely dependent on thyroid hormone during prenatal period...otherwise, there's irreversible mental retardation


(that's why neonatal screening of hypothyroidism is mandatory!!)
thyroid h effects on autonomic n system
has many actions as symp n system bc

1) upregulates B1 adrenergic receptors in the heart

---> inc HR and SV--> in CO
thyroid hormone affects BMR:
increases synthesis of Na, K, ATPase

O2 consumption and BMR are increased by thyroid hormone in all tissues except brain, gonads, and spleen
overall of thyroid effect is catabolic

t/f
true
(inc lipolysis, glycogenolysis, glucose, protein degradation)

both protein synthesis and deg are inc but deg is inc more than synthesis
where is androstenedione converted to testosterone?
testes
19 carbon steriods have what kind of activity
androgenic

(DHEA, androstenedione)


(adrenal androgens have a ketone group on C17, an are excreted as 17-ketosteroids in the urine)
18 carbon steriods have___
estrogenic activity!
oxidation of the A ring (aromatization) to produce estrogens occurs WHERE?
ovary, placenta
what's the deal with the dexamethasone suppresion test?
figures out where exactly the increase of ACTH is coming from


its a synthetic glucocorticoid that's able to inhibit ACTH secretion (just like cortisol does)

normal: the dexamethasone inhibits ACTH release (see dec in ACTH)

ACTH-secreting tumor:

low-dose of dexamethasone doesn't inhibit cortisol release

but high-dose does


if adrenal corticol tumors: neither low or high dose of dexamethasone does anything
cortisol is essential for response to-----
STRESS
in what ways does cortisol stimulate gluconeogenesis?
(3)
1) inc protein catabolism
2)dec glucose utilization and insulin sensitivity
3) inc lipolysis..which provides glycerol to the liver for gluconeogenesis
antiflammatory effects of cortisol?
1) inc LIPOCORTIN which inhibits PHOSPHOLIPASE A2, which liberates arachidonate from membrane phospholipids...ARACHIDONATE is the precursor for prostaglandins and leukotrienes which are nec for the inflammatory response



also, cortisol inhibit proliferation of T-CELLS
and inhibit production of IL-2

also, cortisol inhibits release of histamine and serotonin from mast cells and platelets
cortisol on blood pressure?
upregulates alpha-1 receptors on arterioles, increasing vasoconstrictor effect of norepinephrine

cortisol excess--> arterial pressure inc
primary adrenocortical insufficiency aka
Addison's disease

primary insufficiency of adrenal cortex (usually, autoimmune destruction of adrenal cortex)
secondary adrenocortical insufficiency caused by
primary deficiency of ACTH
adrenocortical excess =
Cushing's disorder!
(there dec ACTH due to neg feedback)

(most commonly caused by pharmacologic doses of glucocorticoids)


Cushing's disease: when caused by overproduction of ACTH
Conn's syndrome is
hyperaldosteronism

(caused by aldosterone-secreting tumor)
21B hydroxylase deficiency
decreased cortisol and aldosterone

inc adrenal androgens
17 -alpha hydroxylase deficiency
dec cortisol and androgens

inc aldosterone

lack of pubic and axillary hair (which depend on adrenal androgens) in women
what stimulates glucagon secretion?
low blood glucose
where does glucagon act?
liver + adipose tissue+muscle
what does glucagon do?
1) increases glycogenolysis
2) inc gluconeogenesis...by dec production of Fructose 2, 6 biphosphate, decreasing phosphofructokinase activity



Increases KETOACID and FATTY ACID conc in blood
1) inc lipolysis
2) the acetyl coA produced from fatty acid degradation -->ketoacids
glucagon _____ urea production
increases

amino acids are used for gluconeogenesis-->and the resulting amino groups are incoporated in urea
insulin is packaged along with
C-peptide
insulin acts on
liver, adipose, muscle
how does insulin decrease blood glucose?
1) inc glucose uptake (via inc glucose transporters)
2) inc glycogen synthesis (and inhibit glycogenolysis)
3) dec gluconeogenesis (by inc fructose 2, 6 biphosphate...increasing phosphofructokinase activity...substrate diverted from glucose formation)
insulin _____blood FA and ketoacid
decreases!
adipose: stimualates fat deposition, and inhibits lipolysis

no ketoacid increase (bc fat is not being degraded...no acetyl CoA....no KA)
insulin _____ blood amino acid
decreases!!
stimulates aa uptake, protein synthesis,
insulin is catabolic

t/f
false! anabolic
primary vs central hypothyroidism
primary: TSH high, thyroid hormones low

central: both TSH + thyroid hormone low
bone classifications of
1) appearance
2) histogenesis
3) bone tissue/marrow
4) collagen organization
Appearance:
Long, flat, cuboidal

Histogenesis: Endochondral vs. intramembranous ossification

Bone tissue/marrow: Compact (cortical) vs. trabecular (cancellous)

Collagen organization: Woven (primary) vs.lamellar (secondary)
what inhibits RANKL on osteoblasts?
osteoprotegrin
Osteoporosis -
bone resorption exceeds bone formation
Osteopetrosis –
defective bone resorption
Osteomalacia –
defective mineralization
Paget’s disease –
disorganized bone resorption and formation
common sites of osteoporitic fractures
vertebrae, hip bone, wrist
1 alpha hydroxylase is stimulated by_____ , & inhibited by _______
PTH and hypophosphatemia


1,25 Vitamin D (neg feedback)
pathogenesis of osteomalacia
Vitamin D deficiency-->
dec calcium absorption-->
dec serum calcium-->
inc PTH-->
osteoclastic bone resorption --> release of calcium into circulation-->
blood level normalizes-->
Loss of bone mineral !!
you'll see _____mineralized osteoid in osteomalacia
dec
Paget's disease
defective resorption + formation
Disease of osteoclast (overactive)
Osteoblast abnormalities
Localized areas
High bone turnover
where is the C-peptide cleaved from proinsulin
ER
where does pre-proinsulin--> pro-insulin?
ER
how does blood glucose stimulate insulin secretion?
1) glucose goes through GLUT2
2) inc ATP synthesis
3) ATP-sensitive K+ channels open (Kir6,2)
4) depolarization
5) voltage sensitive Ca+ channels open
6) inc Ca+ in cell
7) exocytosis of insulin
t/f both parasymp + symp stimulate glucagon release
true!
t/f symp inhibits insulin release and parasymp stimulates insulin release
true!
what inhibits both insulin + glucagon?
somatostatin
t/f the brain relies on insulin for glucose uptake
false!
Normoglycemia
FPG <110 mg/dL
2-hr PG <140 mg/dL
Diabetes, glucose cutoff
FPG ≥126 mg/dL (fasting)
2-hr PG ≥200 mg/dL
Type II diabetes
Relative insulin deficiency and/or insulin resistance
what corresponds to the first peak of insulin release after glucose injection?
the insulin that's in the granules is released

second phase: insulin is being made
how do you get dehydration + electrolyte losses in diabetes?
inc glucose acts as an osmotic diuretic--> loss of hypotonic fluids--> dehydration

osmotic diuretic-->electrolyte depletion
Pit-1 gives rise to __________
thyrotrophs
lactotrophs
somatotrophs
Russell-Silver Syndrome
imprinting abnormality:

Intrauterine growth retardation
Poor postnatal growth
symptoms of GH deficiency

6
Marked short stature
Growth failure
Hypoglycemia in infancy
Central distrubution of body fat
Delayed bone age
Low serum IGF-1 and IGFBP-3
choose one: intrinsic tallness, advanced growth, accelerated growth

BA= CA normal growth rate
intrinsic tallness


Familial nl variant
Marfans
choose one: intrinsic tallness, advanced growth, accelerated growth

BA =HA normal growth rate
advanced growth


Constitutional normal
Obesity
Hyperthyroidism
Infant giants
choose one: intrinsic tallness, advanced growth, accelerated growth

BA > HA increased growth rate
accelerated growth

(GH excess, sexual precocity)


this doesn't seem intuitive...right yiuka? (that BA > HA??)...its right though. i checked on the lecture
what are the components of the pituitary gland?
adenohypophysis (epithelial)
neurohypophysis (neural)
any increase in size of pituitary will cause ___________ bc expansion will only happen in 1 direction
dizziness, vision problems

(will affect optic n)
3 types of diabetes insipidus?
neurogenic (low ADH)
nephrogenic (ADH resistance)
psychogenic (compulsive water drinkers)
the ap's blood is _________ blood coming from the hypothalamus
venous
colloid?
newly synthesized thyroid hormone attached to thyroglobulin
how do we treat precocious puberty?
by treating with GnRH (negative feedback)
cortisol is not absolutely necessary for life as long as ______________ is being produced
corticosterone
cortisol effect on bone formation?
dec synthesis of Type 1 collagen
dec osteoblast production
dec intestinal calcium absorption

overall: dec bone formation!
for females, adrenal androgens are the _________ androgens and responsible for __________
major

pubic and axillary hair and for libido
renin is ________ in Conn's syndrome?
low

(high aldosterone levels--->negative feedback)
in 17-alpha hydroxylase insufficiency, is aldosterone high or low?
low!

why? bc both deoxycorticosterone and corticosterone are high....which have mineralocortical activity....negative feedback-->aldosterone is low!

(the renin-angiotensin system controls aldosterone levels)
why is oral glucose a more powerful stimulant for insulin secretion than intravenous glucose?
stimulates secretion of GI hormone, GIP (which has an independent stimulatory effect on glucose)
what's responsible for the insulin resistance of obesity and Type II diabetes?
downregulation of insulin receptors
insulin _________ K+ uptake in cells by increasing activity of the ___________

why does it do this?
increases uptake

Na+K+ ATPase

insulin is protecting against an inc in serum K+ (maybe because K+ is released when glucose stimulates insulin secretion in B cells...?)
Sertoli cells are to ___________ in female
Leydig cells are to ___________in female
granulosa cells
theca cells
primary spermatocytes become __________ after Meiosis 1 and then become ______________ after Meosis II
secondary spermatocytes

spermatids

primary spermatocytes (diploid 4N)
secondary spermatocytes (haploid 2N)
spermatids (haploid 1N)
spermatozoa (after loss of cytoplasm + flagella)
_____________ form tight junctions with each other to form the blood testes barrier
Sertoli cells
seminiferous tubules-->_________> vas deferens---> urethra
epididymus
why do seminal vesicles secrete prostaglandins with the sperm?
1) react with cervical mucosa to make it more penetrable by sperm

2) induce peristaltic contractions in female reproductive tract to propel sperm?
primary spermatocytes (______ 4N)
secondary spermatocytes (_____ 2N)
spermatids (haploid 1N)
spermatozoa (after loss of cytoplasm + flagella)
diploid

haploid
what happens during capacitation?
takes 4-6 hrs
--inhibitory factors in the seminal fluid are washed free
--cholesterol is withdrawn from the sperm membran
--Ca+2 influx into sperm inc motility
--acrosomal membrane fuses with the outer sperm membrane
what don't Leydig cells have that prevents them from making gluco-and mineralo-corticoids?
21b and 11b hydroxylase
what do Leydig cells have that allow them to make testosterone from androstenedione?
17b hydroxysteroid dehydrogenase
98% of testosterone is bound to ________ + ____________
sex-steroid binding globulin + albumin