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246 Cards in this Set

  • Front
  • Back
Amine hormones
Tyrosine derivatives

Thyroid Hormones, Epi, Norepi.
Anterior pituitary hormones (6)
GH, Prolactin, TSH, LH, FSH, ACTH.
POMC products
MSH (prod. in Int. lobe), beta lipotropin, beta endorphin, ACTH.
GH is homologous to what other hormones (2)?
Prolactin and human placental LACTOGEN.
GH increased by (6)
sleep, stress, hormones related to puberty, starvation, excercise, hypoglycemia.
GH decreased by (5)
somatostatin, somatomedins, oesity, hyperglycemia, pregnancy.
How does somatostatin inhibit GH secretion?
blocks anterior pituitary response to GHRH.
Somatomedins... name 2 places where and how they act...
produced as GH ACTS ON TARGET TISSUE.

inhibit secretion of GH by:
1. directly on AP (inhibit GH secretion).
2. indirectly on hypothalamus --> via stimulating SOMATOSTATIN.
Somatomedins also called...
IGF.. insulin like growth fators...
GH direct actions:
decrease glucose uptake (diabetogenic).

increase lipolysis

increase protein synth in muscle, increase lean body mass.

increase production of IGF/SOMATOMEDIN...
Actions of GH via IGF...
linear growth (pubertal growth spirt)

protein synth in muscle

protein synth in most organs.
Prolactin: what two processes does it stimulate??

What two processes does it inhibit??
lactogenesis, breast development with estrogen.

INHIBITS OVULATION (decrease GnRH)., INHIBIT spermatogenesis...
Prolactin secretion regulation (1 major stimulus, 2 major inhibitors...)
TRH - increases PRL secretion.
Dopamine - tonically inhibits PRL (e.g. PIF)
PRL inhibits its own secretion (stimulates hypothalmic dopamine release).
treat PRL excess with:
Bromocriptine (DOPAMINE AGONIST)....
PRL deficiency reason:
anterior pituitary destruction.
Excess PRL reason (2)
hypothalmic destruction (loose tonic dopamine inhibition).

PRL secreting tumors (prolactinomas).
Increase Prolactin secretion (factors).....6
Estrogen (pregnancy)
breast feeding
sleep
stress
TRH
dopamine antagonists.
Decrease PRL secretion (factors)... 3!!
Dopamine/Bromocriptine
Somatostatin
Prolactin (negative feedback via stimulus of dopamine).
ADH origin:
supraoptic nuclei of hypothalamus.
ADH actions (2)
1. increases H20 permeability of late distal tubules and CDs.
2. Constrict vascular smooth muscle (V1 receptor, IP3 mech).
Oxytocin origin
Paraventricular nuclei of hypo.
oxytocin action VERY GENERAL... 2 WORDS....
causes ejection of milk.
oxytocin secretion stimuli:
secretion stimuli: suckling (main), dilation of cervix, and orgasm...

NOTE SIGHT/SOUND OF INFANT CAN TRIGGER RELEASE without suckling...
Oxytocin mechanism of action (name 2 areas of action):
1. contract myoepi cells.
2. contract uterus (reduces postpartum bleeding), also induces labor.
Thyroglobulin synthesis from what?
Tyrosine
How does Iodide get into thyroid follicular cell?
I- pump... Na/I cotransport.
inhibitors of Iodide pump
thiocyanate, perchlorate (anions)...
Peroxidase actions in Thyroid Hormone production:
1. I- --> I2... (in mb).
2. I2 ---> DIT-TG-MIT. (organification)
3. Coupling reaction (forms T4 and/or T3).

NOTE .. .2 and 3 occur in the lumen of the follicle!!!.
TSH stimulates what steps in Thyroid hormone synthesis??
ALL OF THEM... (in SYNTHESIS)... therefore no breakdown etc???
Thyroid deiodinase... what does deficiency mimic??
Deiodinates leftover MIT and DIT... I2 released and reutilized.

Deficiency mimics I2 deficiency.
Wolff-Chaikoff effect
High levels of I- inhibit organification, and therefore inhibit synthesis of Thyroid Hormone.
Inhibitor of Thyroid Peroxidase
Propylthiouracil.
How are T3 and T4 transported in plasma?? what does it do??

What causes this to increase/decrease??
TBG - "buffers" free hormone.

Decreases with hepatic failure; total hormone decreases, but free hormone stays the same.

Increase with pregnancy (clinically euthroid too, because free hormone is buffered).
Thyroid hormone negative feedback mechanism:
via T3 --> downregulates TRH receptors on anterior pituitary.
Thryoid-stimulating immunoglobins/disease process...
IgG components.

Ab to TSH receptors on Thryoid gland, stimulate secretion.

Graves disease = high levels.
Graves disease hormone levels:
high circulating TH's.

low TSH.

TSIg's are high.
What hormones do thyroid hormones act synergistically with? What do they do together?
somatomedins

GH

promote bone fomration.
bone age with TH deficiency in development.
bone age is less than chronologic age... (WRT development, because it promotes fusion of growth plates).
how does Thryoid hormone act on the heart?

How is this used in treatment of hyperthyroidism?
upregulates beta1 receptors.

use beta blockers (propanolol) as adjunct therapy.
Where does TH NOT increase O2 utilization and BMR???
brain, gonads, spleen.
when do we see myxedema??
Hypothyroidism.
TSH levels in hypo vs hyper
hyper - decrease TSH.

hypo -
1.increase (if decreased feedback inhib because TH low)

2.decrease - if primary defect is in hypothalamus or anterior pituitary...
17 alpha hydroxylase knockout see lack in what? (3)
Cortisol
testosterone
E2
cholesterol desmolase - what does it do? What stimulates it? What do you lack if you don't have it? (4)
Cholesterol --> pregnenolone.

stimulated by ACTH.

Loose Aldosterone, Cortisol, testosterone, and E2.
Where does CRH origniate from?
Paraventricular nuclei of hypothalamus.
Cortisol feedback inhibition:
at AP and at Hypothalamus.
CRH second messenger; what is secreted when CRH binds?
cAMP

POMC
ACTH stimulates what two processes?
1. Cholesterol desmolase stimulation.
2. upregulates its own receptor.
Chronic ACTH elevation causes?
Adrenal cortex hypertrophy.
Dexamethasone supression test... what is it? what do we see with various pathologies?
synthetic glucocort.

NML - supresses ACTH with low level admin.

ACTH tumors (e.g. CUSHINGS DISEASE) - need high dose to inhibit ACTH/cortisol secretion.

Adrenal cortical tumors (PRIMARY ADRENAL HYPERPLASIA/CUSHINGS SYNDROME). - no supression.
What are three mechanisms that regulate aldosterone??
1. Tonic control by ACTH.
2. RAAS.
3. K+
What is the stimulus for RAAS?
decrease blood volume --> decrease renal perfusion pressure --> increase renin. etc.
Where does angiotensin II act to increase aldosterone??
aldosterone synthase.

adrenal glomerulosa.
What does Aldosterone do?
increases renal Na reabsorption, brings blood volume up

increases K+ secretion (correct hyperkalemia).
How do glucocorticoids stimulate GNG? (3)
1. increase protein catabolism in muscle.
2. decrease glucose utilization and insulin sensitivity - ADIPOSE.
3. increase lipolysis (glycerol to liver).
Glucocorticoid antiinflammatory mechanisms (3)
1. induce synthesis of lipocortin (PLA2 inhib... arach decrease... PG decrease).
2. Inihib IL2 production (T lymphocytes prolife INHIB).
3. Inhibit histamine and seratonin release (form PLATLETS and MAST CELLS).
Glucocorticoid Immunosupression/uses...
IL2 and T lympho inhibition.

use to prevent organ rejection.
What does cortisol do to alpha1?

What does this mean with cortisol deficiency??
upregulates alpha1 receptors in arterioles.

increased sensitivity to NE vasoconstrictor effects.

Deficiency = decreased pressure.
Addison's disease
primary adrenocort. deficiency, usually autoimmune cortex destruction.

decrease glucocort, mineralcort, and androgens prod in adrenals.
What does Addison's disease do to ACTH? What major indicator does this cause?
increases ACTH

hyperpigmentation (because MSH).
What does Addison's do to pubic and axillary hair in women?
decreases, because adrenal androgen deficiency.
What does Addison's do to ECF Volume and electrolytes?? (3)
DECREASED ALDOSTERONE: hypotension, hyerkalemia, metabolic acidosis.
Secondary adrenocortical deficiency

Name two sx that aren't present here that are present in primary adrenocortical deficiency/Addison's?
ACTH deficiency.

NO HYPERPIGMENTATION.

NO aldosterone sx.
Cushing's Disease. What happens to ACTH?
excess ACTH, via tumor.
Cushing's Syndrome. What happens to ACTH?
Primary adrenal hyperplasia.

increased aldosterone, cortisol, and adrenal androgens...

decreased ACTH.
Conn's Syndrome
Aldosterone secreting tumor.

Aldosterone sx.
21-betahydroxylase deficiency: what happens to cortisol, aldosterone, and androgens?? What happens to ACTH?
decrease cortisol and aldosterone.

increase androgens.

increased ACTH.
17-alpha-Hydroxylase deficiency: what happens to androgens, cortisol, and aldosterone?

What happens to ACTH?
decrease cortisol and adrenal androgens.

increase aldosterone.

increased ACTH.
What do adrenal androgens do in women?
cause growth of pubic and axillary hair at puberty.
Insulin decreases a lot of stuff in the blood. Name 5..
decreases:
glucose, AA, fatty acids, ketoacids, K+
Name 4 stimuli for Insulin secretion (aside from the "big 3").
Glucagon
GIP
GH
Cortisol
what is the mechanism for insulin reception. Glucagon?
Insulin - RTK.
glucagon - cAMP.
Glucagon INCREASES a lot of stuff in the blood. Name 3.
Increases:
glucose
FA
ketoacid
Name 4 stimuli of Glucagon secretion (leave out decrease in glucose)
amino acids
CCK
NE/epi
Ach
name 4 factors that decrease glucagon secretion:
insulin
somatostatin
FA, ketoacids.
How does glucose induce insulin secretion??
binds Glut2 receptor on beta panc.

inside beta, oxidized to ATP.

ATP CLOSES K channels --> depol.

depol opens Ca channels, stim secretion.
sulfonylurea drugs - what do they do?
stimulate insulin secretion by beta cells.

close K+ channels (act like ATP).
What happens to insulin receptors in starvation and obesity?
increased in starvation

decreased in obesity

BECAUSE insulin downregulates its own receptors...
What does insulin do to blood K concentration? Why?
decreases blood K.

stimulates K uptake in cells.
Calcium - binding in plasma... frequency...
40% bound to plasma proteins.

60% not bound; ultrafilterable.
Ultrafilterable Ca2+ includes...
1. complexed Ca2+ to anions
2. free, ionized Ca2+
what form of calcium is biologically active?
free, ionized Ca2+
Postive vs. negative Ca2+ balances:
postive - growing children, intestinal absorb exceeds urinary excrete.

negative - women in pregnancy/lactation. intestinal absorption less than secretion, deficit comes out of MATERNAL bones.
PTH - where is it secreted?
chief cells, parathyroid glands.
What stimulates PTH secretion? (2).
decreased plasma Ca2+

MILD increase in Mg2+... note major increase inhibits PTH secretion and causes hypoparathyroid sx).
What does PTH do to bone?
increases reabsorption/breakdown.
What does PTH do in the kidney (2)
1. decreases P reabsorption (increase urinary cAMP).

2. increases Ca2+ reabsorption.
What does PTH do in the intestine?
increases Ca2+ absorption VIA VITAMIN D ACTIVATION!!.
What is the overall serum effect of PTH?
increase Calcium

decrease phosphate.
What stimulates Vitamin D secretion (3)
decrease serum Calcium.
increase PTH (conversion).
decrease serum phosphate.
what does vitamin D do to bone/
increases resorption.
what does vitamin D do to the kidneys??
increase P reabsorb.

increase Ca reabsorb.
what does Vitamin d do in the intestine?
increase Calcium absorption (calbindin)

increase phosphate absorption.
What is the overall serum effect of Vitamin D?
increase calcium.

increase phosphate.
What stimulates calcitonin secretion?
increase serum calcium.
what does calcitonin do to bone??
decreases resorption
how does calcitonin act on the kidney and the intestine?
IT DOESN'T.
what is the overall serum effect of calcitonin?
decreases calcium... doesn't touch phosphate.???????
PTH second messenger at gland
cAMP.
Where in the kidney does PTH act to inhibit phosphate reabsorption??? what does this result in?
proximal tubule. Therefore increases phosphate excretion... this causes serum ionized Ca2+ to increase (increase active calcium).
PTH action on PT causes what in the urine?
cAMP.
Primary hyperparathyroidism... what happens to urine?

what happens to serum?

what happens to 1,25?
increase PTH via parathyroid adenoma usually.

phosphaturia, increase urinary cAMP.

serum calcium increase, serum phosphate decrease.

1,25 increases.
Humoral hypercalcemia of malignancy: what causes it?

What happens to serum Ca, P, and PTH?

What happens to urine?

what happens to 1,25 vitamin D?
PTH-rp (from malignancy)

increase calcium, decrease phosphate, decrease PTH (feedback inhib).

increase urinary phosphate excretion.

1,25 increases.
Surgical hypoparathyroidism:

What happens to PTH?

What happens to 1,25?

What happens to serum calcium and phosphate?
decrease PTH

decrease vitamin D

decrease serum Calcium

INCREASE serum phosphate.
What does PTH do to renal phosphate reabsorption?
inhibits it... therefore decreases plasma phosphate.
PseudoHYPO-PTH: what is it?

What happens to PTH levels?

What happens to Vitamin D?

What happens to serum calcium and phosphate?
Albright's hereditary osteodystrophy... DEFECTIVE Gs protein in KIDNEY AND BONE... causes resistance to PTH.

PTH increases, Vitamin D decrease.

Serum calcium decreases, serum phosphate increases.
Chronic renal failure - how does it cause secondary hyperparathyroidism?
Decreased GFR = P retention.

Phosphate complexes with Calcium, decreases biological activity.

Decreased Vitamin D synthesis by diseased renal tissue also decreases calcium that is active.

therefore, we have secondary hyperPTH.
Vitamin D deficiency: kids vs. adults.
Kids - rickets.
adults - osteomalacia.
What chemical is the common start of vitamin D active production?

How is it obtained?
cholecalciferol.

via Diet

via 7-dehydrocholesterol conversion (via UV light in skin).
Cholecalciferol conversions in Vitamin D metabolism..
1. Liver (to 25-OH).
2. Kidney (to 1,25 ACTIVE; and 24,25 INACTIVE).
In vitamin D metabolism, what stimulates 25-Oh to 1,25 ACTIVE in the kidneys?? (3) what enzyme is being acted on??
1. decrease free calcium.
2. increase PTH.
3. decrease phosphate.

via 1 alpha hydroxylase.
1-alpha hydroxylase:
stimulates active vitamin D production.
Where is calcitonin synthesized?
parafollicular cells (THYROID).
What two hormones do male testes secrete during development??
1. Testosterone - stimulates Wollfian duct development.
2. AMH - causes mullerian duct atrophy.
wollfian ducts - what stimulates them to develop and what do they become??
stimulated by testosterone from testes.

become male internal genital tract.
Mullerian ducts - what do they become (general)...
female internal genital tract.
What do female gonadal ovaries secrete during development? What does this result in?
Estrogen.

THEREFORE:
1. no testosterone (wollfian ducts dont develop).
2. no AMH (mullerian ducts are UNINHIBITED and can develop).
Leydig cells - what do they secrete? Why don't they secrete glucocorticoids or mineralcorticoids??
Testosterone.

don't have 21B-OHase or 11B-OHase.
What stimulates they Leydig cells to synth testosterone? Where does it act?? What is this analagous to??
LH.

acts on cholesterol desomlase.

analagous to ACTH action on desmolase in adnrenals.
What is testosterones "active form"?? Where is it made?? How??
DHT.
accessory organs (like prostate).
enzyme is 5-alpha-reductase.
Benign prostatic hyperplasia:

what causes it?
what can treat it?
1. too much DHT production in prostate.
2. tx with 5-alphareductase inhibitors (finasteride).
Male reproductive tract: where does FSH act?
what do these cells do?
what do these cells secrete?
Sertoli cells

spermatogenesis.

secrete INHIBIN w/ stimulus by FSH... inhibit ONLY FSH production in AP (not LH).
Male: where does LH act? What does it promote in these cells?

Where does the cell product act for negative feedback??
Leydig cells.

Testosterone synthesis.

Neg feedback at AP (inhibit LH, not FSH), AND at hypothalamus (inhibit GnRH).
How does testosterone reinforce spermatogenesis?
acts in paracrine mechanism (intratesticular) on Sertoli cells.

Reinforces effects of FSH.
Name 6 influences of testosterone in MALES
1. DIFFERENTIATION on epididymis, vas deferens, and seminal vesicles.
2. puberty growth spurt.
3. SPERMATOGENESIS (paracrine on sertoli).
4. deepening voice
5. increase muscle mass.
6. GROWTH of penis and seminal vessicles.
DHT influences: name 4
1. DIFFERENTIATION of penis, scrotum, and prostate (external + prostate differentiation).
2. male hair pattern.
3. sebaceous gland activity.
4. prostate growth.
Androgen insensitivity disorder: what do we see?
male without androgen receptors; therefore no DHT OR testosterone action...

"default" female external genitalia.

no internal female genital tract (because testes --> AMH).

increased testosterone levels.

inguinal testicles.
What initiates male and female puberty??
GnRH pulsatile onset.

increases FSH and LH.
FSH and LH lifespan variation (male and female):

childhood
puberty
senescence
childhood - lowest levels, FSH>LH.

puberty AND reproductive years, hormone levels increase, LH>FSH.

senescence... HIGHEST hormone levels, FSH>LH.
What 2 cells stimulate testosterone and estrogen production in females? How do they do it? What stimulates them?
Theca cells - stim w/ LH - prod. testosterone (UPREGULATE cholesterol DESMOLASE!!!)

granulosa cells - stim by FSH - have aromitase and take diffused testosterone ---> E2.
In the follicular phase of the menstrual cycle, what hormone is involved in feedback? Where does it act/what does it do?
Estrogen.

negative fback on AP.
In midcycle menstrual cycle, what hormone is involved in feedback? Where does it act/what does it do?
Estrogen.

postive; AP.
In the luteal phase of the menstrual cycle, what hormone is involved in feedback? Where does it act/what does it do?
Estrogen --> negative fback on AP.

Progesterone --> negative fback on hypothalamus.
What receptors does estrogen upregulate?? (3)
estrogen
progesterone
LH
what does estrogen do to prolactin??
stimulates synthesis during pregnancy.

BLOCKS action on breast during pregnancy...
Where does progesterone feedback in luteal phase??
blocks FSH and LH secretion via HYPOTHALAMIS GNRH INHIBITION.
What is progesterone's main action in the luteal phase??
maintains pregnancy via maintaining secretory activity of uterus.
Follicular phase:

1. days
2. LH and FSH receptors.
3. E2 levels? what does this do?
4. FSH and LH levels.
5. Progesterone levels.
1. 0-14.
2. LH and FSH receptors upregulated.
3. E2 levels increase, development of uterus.
4. progesterone levels remain low.
5. FSH and LH levels suppressed by E2 negative feedback on AP.
Ovulation:
when does it happen?
What causes LH surge?
What happens to E2 immediately after?
Cervical mucous?
ALWAYS 14 days before menses, regardless of cycle length.

LH Surge because burst in E2 and CHANGE TO POSITIVE FEEDBACK on AP...

E2 decreases right after ovulation, but then increase again in luteal phase.

more mucous, less viscous.
What does Corpus luteum synthesize?
estrogen

progesterone
What happens to endometrium in luteal phase?
increase vascularity and secratory activity to prep for fert. egg.
What happens to body temp. in luteal phase? Why?
increases.

progesterone acts on hypothalmic thermoreg. center.
When does luteal phase occur? What happens if there isn't any fertilization WRT hormones??
14-28.

no fert = CL regress = decrease estrogen and progesterone.
why does menses happen? What days of cycle?
CL degenerates.

estrogen and progesterone drops off.

0-4
What happens to estrogen and progesterone if pregnant?

What does this inhibit? What does this stimulate?
steady increase in progesterone and estrogen

inhibits ovulation (because inhibition of FSH and LH at both AP and Hypo)...

stimulates breast development.
What rescues the CL from regression in pregnancy? Where does it come from? How long does it operate?
HcG - stimulates CL continued estrogen and progesterone production.

Placenta.

peaks at week 9, then declines.
Second and third trimesters: where does progesterone and estrogen come from??
Progesterone from placenta.

Estrogen from interplay of fetal adrenal gland and placenta....

1 fetal adrenal synth DHEA-S
2 fetal liver hydroxylates DHEA-S
3 transfer to placenta, remove S and aromatize to estrogen TO MAKE E3... THEREFORE E3 INDICATES LIVER AND ADRENALS WORK!!!.
Human placental lactogen:
produced throughotu pregnancy.

similar actions to PRL and GH.
What does progesterone do to uterine contraction response through pregnancy???
increases threshold for uterine contraction (inhibits prematurity??)
What causes the uterus to be more sensitive to contratile stimuli near term??
estrogen:progesterone ratio increases.

less progesterone to "increase threshold"... therefore easier to contract uterus.
What does oxytocin do with respect to uterine contractions?
stimulates.

levels don't change right before partruition; only active AFTER is starts...
What happens to PRL during pregnancy?? Why?
increases steadily.

estrogen stimulates AP PRL production.
Why does lactation not occur during pregnancy??
estrogen and progesterone block PRL action on breast, even though production is increased.
What does suckling stimulate???
PRL AND Oxytocin secretion (recall oxytocin is the only one that increases via CNS/anticipation etc....)
What happens to ovulation during lactation? Give 2 reasons how.
supressed; PRL effects:
1. inhibits GnRH secretion at hypo... therefore decrease LH and FSH.
Antagonizes action of LH and FSH at OVARIES.
What does insulin do to stimulate glucose uptake by cells??
Stimulates Glut4 translocation to plasma membrane.
Where does glucose get taken up after a meal predominately??

How does this happen?
Liver

Glukokinase induced by insulin... keep G-6-P inside liver cells.
What hormones in the hypothalamus and pituitary glands use the Gq mechanism??
Oxytocin
Vasopressin (at V1 receptor)
Hypothalmic releasing factors.
Nuclear receptor superfamily... explain receptor structure:
N terminal - unique/varying sequence. Hormone independent regions.

DNA binding - 2 Zn fingers, 4 Cys each. Dimerization domain. Flanking region has nuclear localization sequence.

Cterm - hormone binding region; hormone-dependent activation domain.
Describe classical breakdown of nuclear receptor superfamily (categories). explain the differences...
1. vitamin D, retinoic acid, thyroid hormone--> these bind directly to DNA in absence of hormone. Corepressors bound without hormone, if hormone binds, then recruit coactivators.

2. steroids.
Where are hormone response elements located? Describe them.
on DNA.

6 nucleotides long.
Where do estrogen and androgen receptors bind their hormones?

What about glucocort and mineralcorts??
1. nucleus.

2. cytosol.
what types of receptors have chaperones? Name the chaperones. What happens when hormone binds?
Soluble receptors; Hsp90s etc.

Binding of hormone causes dissociation; this leads to exposure of nuclear localization sequences etc.
Name a receptor in the steriod receptor superfamily that can act as a transcription repressor when unbound? How does it work?
Glucocorticoid receptor.

Transcriptional repressor.
Name 6 hypothalmic/pituitary hormones that are coupled to Gs?
LH, FSH, TSH, ACTH, and Vasopressin V2.
Ectopic neoplastic hormone sources produce what kind of hormones usually?
Peptide hormones.
Where does the anterior pituitary develop from?

What about the posterior pituitary?
anterior - Rathke's pouch (outpouch of ORAL EPITHELIUM).

posterior - evagination of diencephalon.
Portal vessels in anterior pituitary blood supply.
Long portal vessels - 90% of bloood; from hypothalamus.

Short portal vessels - from posterior pituitary.
Glycoprotein family in anterior pituitary hormones. explain homology. What non-AP hormone is a member of this family?
FSH, LH, TSH

Each has alpha and beta subunit; beta is what's variable.

HcG - similar to LH.
Somatomammotropin family in AP. Structural homology?
GH, PRL

single chain polypeps with disulfide bonds; 50% homologous. HGH because GH is species specific.
primary cleavage products of POMC in anterior pituitary?
ACTH, Beta lipotropin.
What two hormones does GHIH inhibit?
TSH, GH.
What two hormones does TRH stimulate?
TSH
PRL
How are all anterior pituitary hormones released?
pulses. because hypothalmic hormones are pulsatile.
Pituitary Apoplexy... name a major cause of this.
acute infarct of pituitary gland. See in postpartum necrosis (Sheehan's syndrome), due to excessive blood loss in delivery.
ADH/Oxytocin homology - explain
strong structural homology

almost no biological overlap.

9 AA cyclics.
Why are ADH and Oxytocin very shortlived in circulation? (2 reasons).
1. peptides - circulate unbound.
2. very small (9AA), easily degraded.
What receptor and action does ADH have on renal JG cells?
V1; supresses renin release.
What does V1 ADH stimulation at renal glomerulus do?
mesangial contraction, decrease GFR.
What ADH receptor acts on the AP? What does it do?
V1; increases ACTH release.
What ADH receptor acts on renal collecting ducts? What does it do/
V2; increase H20 and urea permeability.
What ADH receptor acts on arterioles? What does it do?
V1; stimulates arteriolar constriction.

"V1 alpha 1"
V2 receptor sensitivity WRT ADH?
very high; small change in plasma osmolality required for ADH secretion.
V1 receptor sensitivity WRT ADH?
insensitive; hemmhorrage response.
What is the most important stimulus for increasing ADH secretion on an ongoing basis?
increased plasma osmolarity.
Where are osmosensitive cells located for the ADH response?
anterior hypothalamus

organum vasculosum.
ADH and volume maintenance via what 2 systems ... what pathway?
atrial stretch receptors

corotid and aortic arch baroreceptors.

both signal via an inhibitory vagal pathway to ADH (if volume too high).
Name four things that increase ADH secretion?
stressors, pain, opiates, barbituates.
Diabetes Insipidus WT ADH deficiency.... name the two types:
Nuerogenic - inadequate ADH production.

Nephrogenic - plenty of ADH, kidneys can't respond because receptor defect.
SIADH

2 sx.

2 reasons.
ADH hypersecretion without stimulus.

hypernatremia and low plasma osmolality.

tumor (lung), psych.
dx test - DI
fluid deprevation test; patient produces dilute urine even without fluid intake.
Central DI tx
desmopressin acetate (DDAVP)
Nephrogenic DI tx
thiazide diuretics - decrease plasma Na. Limit dietary Na.
What is the main regulator of the iodide trap?
TSH
Iodide pump activity is determined by what blood test? What is the normal range?
T/S ration... thyroid to serum ratio. NML = 30.
What are the half-lives of T3 and T4??
T3 --> one day.

T4 --> one week.
What is a goitrogen? Name 2. Name a food that can cause this.
blocks hormone production at one point or another, produces goiter.

examples - perchlorate, thiocyanate, CASSAVA = THIOCYANATE.
Name 3 plasma proteins that bind TH's and name their affinity and abundance...
TBG - high affinity, low abundance.

TBPA - intermediate affinity and abundance.

albumin - low affinity, high abundance.
What is the majority of T4 bound to? What is the majority of T3 bound to (tie between 2 binding proteins...)
T4 - TBG.

T3 -- TBG and Albumin (albumin 53%).
What does T3 resin uptake test show? How does it work?
TBG levels; measures uptake of T3 on synthetic resin.
What increases thyroid binding proteins (name 3).

What decreases thyroid binding proteins? (name 3)
1. estrogens, methadone, heroin.

2. glucocorticoids, androgens, salicylates.
What enzyme makes T3? What enzyme makes rT3? What enzyme increases following birth?
T3 via outer ring deiodinase.
rT3 via inner ring diodinase.

increase outer ring after birth.
What happens to T3 and rT3 in starvation?
increase rT3, decrease T3.
What happens to T3 and T4 in the cell? Where do they bind?
T4 converted to T3 so that levels inside cell are EQUAL.

bind in nucleus (both T3 and T4).
Periorbital myxedema versus general myxedema??
Graves disease - hyperTH = periorbital...

vs. general = hypoTH.
Primary Hypothyroid area of problem:
thyroid (TSH response low, TRH response high WRT TSH release).
Secondary Hypothyroid area of problem:
anterior pituitary ... because TSH response is normal, TRH response is low.
Tertiary hypothyroid area of problem:
hypothalamus. TSH and TRH responses are normal.
Thyroid storm - explain it, explain treatments (2):
hyperthyroids that get severe illness... really bad responses.. .sweating etc.

tx. with sodium iodide - actuely blocks RELEASE of already synth'd TH's... long term promotes synth.

beta block.
What is DHEA?
adrenal androgen.
metyrapone stimulation test
evaluates whether ACTH synthesis is adequate.

11beta hydorxylase inhibitor; therefore inhib. cortisol synthesis.... should thus timulate ACTH.
What is dextrameth test used to find?
ACTH secreting tumors.
Apparent mineralcorticoid excess: what enzyme deficiency causes it?

Why?
11Bhydroxysteroid dehydrogenase...

breaks down cortisol, so aldosterone can "control" its receptor... because both cortisol and aldosterone can bind it, and cortisol is produced at much higher levels.
11Bhydroxylase deficiency... what happens to cortisol, aldosterone, and androgens? What happens to BP?
decrease cortisol
decrease aldosterone
increase androgens
INCREASE DOC --> HYPERTENSION.
rate limiting enzymes of epinepherine synthesis?
1. Tyrosine hydroxylase (feedback inhibited).
2. PNMT (induced by cortisol).
principle urinary metabolites of catecholamines?
VMA
metanephrines.
beta2 receptor: sensitivity, vasculature... and receptor.
more sensitive to epi than NE.

vasodilate.

Gs
alpha1 receptor: sensitivity, vasculature, and receptor
Gq... SMC contract.
pheochromocytoma. Dx?
chromaffin tissue tumor (increase epi/NE)....

See increased urinary metabolites (VMA, metanepherine).
When does growth rate peak?
Mid-gestation.
IGFs are responsiblr for what two processes?
Bone growth.

Soft tissue growth.
Laron dwarfism: what is the underlying problem? What helped dx these patients?
1. GH receptor deficiency, thus high GH levels.
2. See low IGF-1 to dx, because tissues aren't responding to GH.
What 3 components do the seminal vesicles produce?
fructose, fibrinogen, PG.
What are 3 components of fluid from the prostate?
1. buffers.
2. clotting enzymes
3. fibrinolysin.
How many carbons do androgens have?
19
What hormone acts to induce pubertal changes in the male? What 2 other changes does it induce?
Testosterone.... causes hematocrit and LDL increases too.
What two hormones are required for spermatogenesis?
Testosterone and FSH. LH MAY BE REQUIRED.
What does inhibin do in males? What does activin do?
inhibin stimulates steroid production.

activin stimulates proliferation.
What is melatonin produced from. Where?
Seratonin; in pineal gland.
How do granulosa cells respond to LH surge?
They develop LH receptors just before ovulation.
Where do E1, E2, and E3 come from?
E1 - adrenal
E2 - ovaries
E3 - pregancy... (weakest)
What does inhibin do in females? what about activin?
inhibin - promotes steroidogenic actino of LH.

activin - promotes mitogenic action of FSH.
When after ovulation does fertilization occur? When does implantation occur? Why?
fertilization in ampulla at day 3.

delay until uterus becomes secretory/tract becomes progesterone dominated.

implant day 7-8.
In the fetus, what is responsible for stimulating testosterone production during period of sexual differentiation?
HcG!!! (NOT LH).
tx for anticipated RDS versus postpartum RDS...
anticipate - tx mother with glucocorticoids.

postpartum - tx with surfactant.
What glucose transporter is insulin independent? What one is insulin dependent?
Glut2 --> indep.

Glut4 --> insulin dependent.
Brush border enzymes involved in starch digestion:
alpha dextranase, maltase, sucrase, lactase, trehalase
trehalase
brush border enzyme

hyrdolizes trehalose to glucose.
What does amylase do in the gut?
starch --> alpha dextrins, maltotriose, and maltose.
Where is enterokinase located?
brush border.
Where is iron absorbed?
proximal small bowel. 2 forms of absoorption.... heme and nonheme...
describe signaling pathway for G. What other hormones use this pathway??
Jack/Stat path; shared by PRL and Cytokines...

Jack activates TF "Stats"... other paths activate MAP kinase, PLC, and PI3 kinase...
What are SMAD pathways associated with? What do they do??
TGFBeta.

form COMPLEXES and COMPLEX enters nucleus and acts as TF.
List enzyme deficiency basic results (WRT adrenal hormones) for 11,21,and 17
11 and 21 deficiency --> aldosterone and cortisol decrease.

17 deficiency --> cortisol and androgens decrease.
Glucophage
upregulates insulin receptors (metformin).
How does vitamin D promote calcium absorption in the duodenum?
promotes synthesis of CALBINDINS.