test one week two Flashcards Preview

endocrine repro > test one week two > Flashcards

Flashcards in test one week two Deck (88):

how do hypothalamic hormones reach the posterior pituitary?

Hypothalamic hormones reach the posterior pituitary via neurons;
hypothalamic hormones are stored here.


how do hypothalamic-hypophysiotrophic hormones reach the anterior pituitary?

Hypothalamic-hypophysiotrophic hormones reach the anterior pituitary
via the hypothalamohypophyseal portal system; hypothalamic hormones
regulate synthesis & secretion of anterior pituitary hormones.


where is oxytocin synthesized and by what cells?

hypothalamus by magnocellular neurons within the paraventricular nucleus
Neuropeptide of 9 amino acids:


physiological actions of oxytocin

Oxytocin stimulates contraction of myoepithelial cells within breast tissue
-Specific effect on target cells:
Binds to G-protein receptors on the surface of myoepithelial cells, triggering a g-protein linked phospholipase C pathway, and increased intracellular Ca++. (Gq/11 pathway)
-Causes milk ejection
-Suckling of a nursing baby stimulates tactile receptors within the nipple, which is relayed back to the spinal cord and to the magnocellular neurons of the hypothalamus.
-Other sensory inputs may trigger the milk ejection reflex.
-Positive feedback: increased pressure and stretch of cervix, increased oxytocin
-Oxytocin stimulates contraction of uterine smooth muscle


synthetic oxytocin uses

-Augments labor: faster harder, always with amniotomy (AROM)
-Controls postpartum hemorrhage

Used in management of incomplete spontaneous abortion (incomplete miscarriage)


other oxytocin actions:

linked to sex, monogomy, mother baby pairing


ADH is synthesized where by what?

in the hypothalamus by magnocellular neurons of the supraoptic nucleus


physiological actions of ADH

Stimulates water retention by the collecting ducts of the nephrons of the kidney
-Specific effect on target cells:
Binds to G-protein receptors on the surface of collecting duct cells, triggering a g-protein linked adenylate cyclase pathway
Aquaporins are inserted into the apical membrane of collecting duct cells
-Without ADH, filtrate from nephrons stays dilute and produce a urine that is high in volume and low in solute concentration (up to 20 L/day)
-With ADH, filtrate from nephrons becomes concentrated, and urine is low in volume and high in solute concentration (1.5-2 L/day)
-Diabetes insipidus NOT MELLITUS
Neurogenic (central): ADH not produced (secreting tissue problem)
Nephrogenic (renal): ADH does not stimulate (target tissue problem)


primary endocrine disorder:

Primary disorders: malfunction with bottom level glands (thyroid, adrenal cortex, gonads)


secondary endocrine disorder

Secondary disorders: malfunction of pituitary hormones (TSH, ACTH, LH, FSH)


tertiary endocrine disorder

Tertiary disorders: malfunction of hypothalamic hormones (TRH, CRH, GnRH, GHRH, somatostatin, dopamine)
Growth hormone and prolactin do not follow this same terminology


how is hormone secretion of the hypothalamus-pituitary gland axis controlled?

via negative feedback loops


what inhibits TSH secretion?

GHIH (SS Somatostatin)


TRH stimulates and inhibits what

stimulates release of TSH and prolactin (PRL) but inhibits GnRH


consequences of a GH ademnoma

could cause a rise in GHIH (SS), which then inhibits TSH and then causes a drop in T4


prolactin physiological actions and secretion control?

primarily controlled by negative feedback by PIH (Dopamine)
Prolactin is the only purely non-tropic hormone of the A.P.

Prolactin stimulates the growth and development of the mammary gland and production of milk by mammary epithelial cells by causing:
Amino acid and glucose absorption
Milk protein production (β-caseins and α-lactalbumin)
Lactose and fat (triacylglycerol) synthesis


GH physiological actions

GH is both tropic (via the liver) and non-tropic (directly affecting) on bone, cartilage, and muscle
Adipose: stimulates release of FFA

Skeletal: stimulates AA absorption and protein synthesis

Liver: stimulates IGF and glucose secretion

GH secretion increased during childhood, peaks during puberty, and slowly declines during adulthood

Clinically relevant: use of GH to decrease body fat; historically the abuse of anabolic steroids by athletes/actors is combined with GH


what controls T3 T4 production and release?

controlled by tsh and trh


t3 t4 actions?

Thyroid hormone exists primarily as T4 (tetraiodothyronine or thyroxine) in the blood, but is converted to T3 (triiodothyronine) in peripheral tissues.
Thyroid hormone increases O2 use in mitochondria.

Major determinant in basal metabolic rate, oxygen consumption, and energy use throughout the body

Thyroid hormone has both inotropic and chronotropic effects on the heart
-Heart: Chronotropic and inotropic

Muscle: Stimulates protein catabolism

Adipose tissue: Stimulates fat catabolism

Nervous: Promotes neural development

Skeletal: Promotes normal development

GI: Stimulates carbohydrate (glucose) absorption

Throughout body: Simulates oxygen consumption in many tissues


what pathways do LH and FSH use to effect testes and ovaries?



what cells are the primary target of LH?

LH primarily targets theca cells of the ovaries and Leydig cells of the testes


what is the primary target of FSH?

FSH primarily targets Granulosa cells of the ovaries and Sertoli cells of the testes


what controls secretion of acth from the anterior pituitary



ACTH physiologic role?

ACTH causes the adrenal cortex to secrete a number of corticoids (21 C steroids), including:
Primarily: glucocorticoids (cortisol and corticosterone)
Secondarily: Mineralocorticoids (aldosterone and deoxycorticosterone). Aldosterone secretion is primarily controlled by renin-angiotensin pathway

These steroids from the adrenal cortex are 21 C steroids and are not functionally related to androgens (19 C) and estrogens (18 C)

Corticoids play roles in
Regulating glucose, protein, and fat metabolism in the body
Regulating Na+ treatment by the kidneys
Suppressing the immune system


adenomas of the anterior pituitary typical cause what kind of hormone pathology and how many cells involved?

excess hormone production usually only affecting one cell type


most common cause of anterior pituitary hormone deficiency?

head trauma


over-excretion of prolactin (PRL) can lead to what symptoms

PRL hypersecretion can effect sexual development/regulation/fertility
because PRL inhibits GnRH


TSH receptor type

GPCR increases camp in cell


describe the starvation reflex and its significance

T3 levels collapse while there is an increase in RT3 levels this lowers BMR /rt3 has no biological effect


graves disease pathology

autoimmune body makes antibodies that mimic the action of tsh by binding their receptors causing hyperthyroidism and goiter
hot/weight loss/ high metabolic rate/possible physchosis
Low tsh levels and trh levels/ high t4


iodine deficiency pathology

hypothyroidism low metabolic rate low t4 high trh and tsh /cold weight gain slow reflexes


which genes lead to gonadal differentiation into testes?

SRY gene activation


which gene leads to gonadal development into ovaries?

Wnt 4


what does the epididymis and ductus defrons, tubules come from?

mesenephros (wolfian ducts)


what does the fallopian tubes come from



What cells make sperm and egg?

Primordial germ cells induce gonad formation. If they don’t migrate to reach primitive gonads, the gonads fail to differentiate into testis or ovaries.


what do primordial germ cells arise from?

epiblast not until germ cells populate genital ridge do you start to see differenciation


what is the embrological origin of gonads and kidneys

intermediate mesoderm


what cells secrete testosterone?

leydig cells of Testes produce testosterone which signals differentiation of internal and external genitalia


what does the tunica albuginea come from?

primitive cortex of the kidney while the medulla becomes the rest of the testes


what does the ductos defrons come from

mesenephric duct


what is a hypospadias and what causes it?

Cause: urethral folds fail to fuse on ventral surface of penis


what are two remnants of the paramesonephric (mullerian) duct in males?

appendix testies and prostatic utricle


what is the cause of : Epispadia?

Defective migration of the genital tubercle primordii to the cloacal membrane resulting in malformation of genital tubercle; penile urethra opens on dorsum of penis


what is the cause of an indirect hernia?

failure of processus vaginalis to close around deep inguinal ring


what is a hydrocyle and what causes it?

excessive production of serous fluid within tunica vaginalis accumaltion of fluid in scrotum


what is a chrypochordism and what causes it?

failure of testes to descend into scrotum during development


cause of main internal femal genitalia defects?

failure of the paremenephric duxts to merge


Klinefelter syndrome pathology

47, XXY; male
Caused by nondisjunction
Testes form, but are infertile (aspermatogenesis) due to low testosterone levels
Impaired sexual maturation


turner syndrome pathology?

45, XO
Cause: Nondisjunction
Results in: Gonadal dysgenesis; streak gonads
Because ovaries are not required for internal and external genitalia formation: female external and internal genitalia (except ovaries) are normal.
Lack of secondary sex trait development at puberty (because no ovaries = no estrogen).
Also present: Short-stature, broad chest, short neck; lymphedema of hands and feet; amenorrhea


swyer syndrome pathology

46, XY
Cause: Point mutation of SRY gene; defective TDF protein.
Results in: Gonadal dysgenesis; streak gonads.
Because ovaries are not required for internal and external genitalia formation: female external and internal genitalia (except ovaries) are normal.
Lack of secondary sex trait development at puberty (because no ovaries = no estrogen).
Also present: Amenorrhea


True Hermaphroditism cause?

transloaction of y chromosome onto x have both ovarian and testicular tissue



46, XX
Cause: Congenital adrenal hyperplasia
Ovaries form (due to absence of TDF; 2 normal X chromosomes)
Internal reproductive organs usually female
Masculinization of external genitalia (due to timing of increased adrogens from adrenal gland).



46, XY
Testes form (normal SRY gene; normal TDF)
CAUSE: Insufficient androgen production and AMH from testes (hypogonadism)
External and internal genitalia female (due to absence of testosterone and AMH)



Testes form due to normal functioning Y chromosome
AMH and testosterone production is normal (testes are normal)
CAUSE: Lack of androgen receptors expression on reproductive tissues (tissues are not responsive to testosterone)
Mesonephric duct degenerates (due to testosterone insensitivity); no male internal reproductive viscera.
Paramesonephric ducts degenerate (due to presence of AMH); no female internal reproductive viscera.
Female external genitalia (because these will form in the absence of hormonal input); Vagina is short and blind-ending  (no uterus)


blood supply to posterior pituitary

inferior hypophyseal artery


blood supply to anterior pituitary

supplied by superior hypophyseal artery


CRH can cross talk to what hormone?



TRH can cross talk to stimulate what



what kind of receptor is IGF-1



what factors stimulate GH release

Deep sleep fasting hypoglycemia, stress


what factors inhibit GH release?

obesity hyperglycemia, hypothyrodism


what factors inhibit IGF?

malnutrition/actute illness/


GH actions

Diabetogenic effect- causes insulin resistance
↓ glucose uptake
↑ blood glucose levels
↑ lipolysis
↑ blood insulin levels
Increased protein synthesis and organ growth (through the actions of IGF-I)
↑ amino acid uptake
↑ DNA, RNA, protein synthesis
↑ lean body mass and organ size
Increased linear growth (through the actions of IGF-I)
Altered cartilage metabolism


embryological origins of adrenal medulla?

neuroectodermal (neural crest cells) tissue


embryological origin of adrenal cortex

mesodermal tissue


what stimulates the sythesis of L-DOPA



What enzyme converts norepi to epi?

PNMT cortisol increases the activity of PNMT


what is Vanillylmandelic
acid (in urine) used to measure

catecholomine status


where are glucocorticoids mainly coming from?

zona fasiculata of the adrenal cortex?


where are mineralcorticoids coming from?

zona glomerulosa


where are adrenal adrogens coming from mainly

zona reticularis


what can stimulate adosterone release?

ANG II, increased K concentration, ACTH all use different pathways so they can influence aldosterone independently


what are the primary actions of cortisol?

acts on liver fat muscle to increase Plasma glucose: gluconeogenesis, AA metabolism and lipolysis  hyperglycemia
Bone: bone metabolism to reduce density
skin and viscera=wasting of fat tissue
Hematopoietic and lymph tissue= reduce immune response and inflammation


what kind of receptor is acth?

gPCR coupled to adenlyly cyclase


what triggers the release and production of nor epi and epi

nuerons trigger the release but acth controls how much is made


few factors that increase acth release

ADH, alpha adrenergic agonists, beta adrenergic antagonist


cushings disease pathology

pituitary adenoma causes excess acth which primarily effects cortisol release causing wasting in the arms and bruiding and hump fat deposit


addisons deisease

primary adrenal insufficiency HIGH ACTH but low cortisol because adrenal gland non responsive


thyroiditis patho

inflammation of the thyroid gland can lead to t3 t4 release leading to thyrotoxicosis but is not a case of hyperthyroidism
Subacute lymphocytic thyroiditis (silent or painless thyroiditis) (believed to be autoimmune in etiology) with non-tender gland- transient
Example is postpartum thyroiditis
cycle: Hyperthyroidism→ euthyroidism→ hypothyroidism→ euthyroidism


hashimotos pathology

hypothyrodism relatated to T cell-mediated but antibodies can also be present (α-TPO) Autoantibodies against thyroglobulin and thyroid peroxidase, TSH receptor, and iodine transporter,Classical presentation: goiter, skin change, peripheral edema, constipation, headache, fatigue, and anovulation
TSH and TRH ↑ but T3 and T4 ↓
Treatment: replacement therapy with levothyroxine (T4)
inflammation of the thryroid glnad


sheehans syndrome

postpartum pituitary gland necrosis, is hypopituitarism (decreased functioning of the pituitary gland), caused by ischemic necrosis due to blood loss and hypovolemic shock during and after childbirth.



tumor of chromaffin tissue results in excess catecholyamine produciton leads to headachs sweating, hypertension, palpitations


17 alpha hydroxylase is responsible for the conversion of what? if a person is missing 17-alpha hydroxylate what will they be deficient in?

pregnenelone to progesterone and pregnenelone to 17-alpha hydroxy pregnenelone
-without can' produduce DHEA or Cortisol.... necessarary for the conversion of cortisterone to cortisol


if deficient in 21-hydroxylase what happens?

can't convert progesterone into deoxycorticosterone which means no aldosterone and no cortisol but still have DHEA


deficiency in 11 beta hydroxylase

no aldosterone or cortsol but still have 21 hydroxylase so still can produce deoxycortsione


cushings disease vs cushings syndrome

acth dependent is called cushings disease/ actch independent is called cushings syndrome


CRH can cross talk and activate what

ADH which can lead to hyponatremia due to excessive water retention