midterm physio deck 1 Flashcards
FSH negative feedback
has a set point from the hypothalamus when level falls –> hypothalamus released pituitary FSH which acts on ovaries to enhance steroid production –> back to set pointestrogen and progesterone give feedback to the hypothalamus and pituitary to inhibit FSH secretion
two amine hormones?
norepi and epi (catecholamines)
7 protein peptide hormones
prolactinADHadrenocorticotropinTRH (thyrotropin releasing hormone)inhibinsomatomedinschorionic gonadotropin (HCG)
ribosomal vs enzymatic hormone synthesis
ribosomal –> protein hormones; 1 large precursor –> posttranslational cleavagesenzymatic –> amine, iodothyronine and steroid hormones; direct synthesis
what hormones circulate free (not bound to carrier)?
protein and amine hormones
what hormones need to be bound to carriers in circulation?
iodothyronines and steroids (insoluble)
where are carrier proteins made?
liver
site of hormone action for1) protein and amine hormones2) iodothyronine and steroid hormones
1) cell surface (more receptors = more responsiveness)2) cytosol and nucleus
what kind of receptor does insulin and growth factors use?
tryosine kinase
cell surface g protein mechanism
amine or protein hormone binds –> conformational change –> GTP binds to regulatory protein –> activation of adenylate cyclase (ATP –> cAMP)
mechanism of cell surface receptor linked to phospholipase c
hormone binds –> enzyme PLC is activated by g protein and splits membrane PIP2 (phosphatdyl inositol 45 bisphosphate) into IP3 and DG (diacylglycerol)–DG activated protein kinase c (PKC) –> phosphorylates proteins–IP3 stimulates ca release from ER –> ca is a tertiary messenger for enzymes
steroid hormone mechanism
lipid soluble and dissolves through lipid bilayer –> binds to cytosol and nuclear intracellular receptors –> form dimers –> dimers go to nucleus and bind chromatin-promoter elements –> enaple expression or repression of that genesteroid hormones directly regulate transcription
thyroid hormone mechanism
act in nucleus to regulate DNA expressionthyroxine (T4) is the precursor for the active t3(triiodothyronine)t4 is activated to t3 by a deiodinase enzymet3 then diffuses into nucleus and binds chromatin receptors
pituitary divisions
adenohypophysis = anterior—-pars tuberalis, pars distalis(anterior), and pars intermedianeurohypophysis = posterior—-pars nervosa infundibulum = neural stalk
pituitary comes from 2 embryonic sources =at 11 weeks, ?
neural ectoderm and upward growth from oral cavityat 11 weeks it is cradled by the sphenoid in the sella turcica
hormones from the adenohypophysis (anterior pituitary) =
FLAT PGFSHLHACTHTSHprolactinGH
three types of cells in the adenohypophysis
basophilsacidophils chromophobes
basophils secrete?
secrete FSH, LH, ACTH, TSH (FLAT)thyrotrophs –> TSHgonadotrophs –> FSH and LHcorticotrophs –> ACTH, B endorphin and B lipotrophin
acidophils secrete?
prolactin, GH and APGlactotrophs –> prolactinsomatotrophs –> GH
chromophobes
are degranulated, precursor, or apoptotic cells
does pituitary have a vascular system?
yes, capillaries are fenestrated with diaphragms
TRH
made by hypothalamus and works on thryotroph to make TSH –> thyroid hormones do negative feedback on thyrotrophs and hypothalamus neuroendocrine cells
dopamine vs prolactin
dopamine inhibits prolactin productionsucking and estrogen decrease dopamine release
intermediate lobe of pituitary releases…
MSH (appetite regulation)opioids (endorphin, dynorphin)POMC (pro-opiomelanocortin)
POMC
pro-opiomelanocortinthe precursor to ACTH, alpha-MSH, B-MSH, gamma MSH, and B endorphin
Pars nervosa and its products
posterior lobe (neurohypophysis)—major nuclei are above the gland and contain neurosecretory cells –> their projections enter the pars nervosaocytocin - contraction of SM ADH (vasopressin)
what is synthesized in the pineal body?
melatonin
melatonin synthesis
tryptophan–> 5-hydroxytryptophan –> serotonin –> N-acetylserotonin –> melatonin
sympathetic innervation of the pineal gland (pineal pathway)
light –> eye –> suprachiasmatic nucleus –> sympathetic central pathway –> superior cervical ganglion –> pineal gland
effects of melatonin
increased secretion at night–CNS and liver metabolismtargets are retina, CNS, and pituitaryeffects on circadian rhythm, reproduction, aging, and disease
hormones secreted by the posterior pituitary (neurophypophysis) are synthesized where?
in neurosecretory cells of the hypothalamus –> then transported down axons via the neurohypophyseal tract for storage and release in the pars nervosa
neurosecretory cells
cell bodies in the hypothalamus and the axon terminals in the neurohypophysis (where the secretory granules are)
5 mechanisms for regulating fluid and electrolyte balance
ADH –> promotes renal water conservationthirstrenin-agiotensin-aldosterone (salt and volume)atrial natriuretic hormonesodium appetite
ADH mechanism
bind to cell surface receptor –> activate adenylate cyclase –> increased cyclic AMP –>increased permeability of nephron to water = resorption of water
when body hydration goes down, adh secretion goes
up
ADH pressor effect
when released in large amounts, ADH has a pressor effect (vaspressin)vasoconstriction that increases BP, venous return, and cardiac output
osmoreceptors are located in the
supraoptic and paraventricular nuclei of the anterior hypothalamus
volume receptors are located in the?role?
left atrium and pulmonary veinsthey relay signals back to the anterior hypothalamic nuclei
thirst center is located in the
hypothalamus
2 most important factors regulating ADH secretion are
1- the osmolality of the plasma around the osmoreceptors2 - the effective blood volume around the volume receptors
increase in plasma osmolality –>
increased thirst/ADH secretion
ADH and ocytocin biosynthesis
separate precursors in granules from hypothalamus travel down neurohypophyseal tract –> during transport posttranslational processing occurs w enzymatic cleavages –> mature granules are stored in the nerve terminals in the pars nervosa in Herring bodiesdepolarization releases contents + neurophysin (unknown effect) into blood–ACh is stimulatory; norepi is inhibitory
ADH and oxytocin in circulation: by carrier or free?
circulate free; t1/2=15 mininactivated by proteolytic enzymes in liver/kidney/blood
diabetes insipidus
H20 disorder due to low or lack of ADH or inability of ADH to work –> causes polyuria and polydipsia–permanent DI is due to damage to hypothalamus, median eminence or upper stalk
neurohypophyseal DI
partial or complete lack of ADH (hypothalamic issue)—renal water loss = water depletion from all fluid compartments –> hypovolemia, serum hyperosmolality, and hypernatremiahyperosmolality activates thirst –> polydipsia** if thirst center is also damaged –> adypsia/hypodipsia = dangerous depletion
treatment for neurohypophyseal DI
super active ADH analog–if partial lack – ADH replacement, DDAVP(desamino D arginine vasopressin)
nephrogenic DI
lack of ADH action because distal nephron wont respond to ADH***exogenous ADH cannot reinstate water balance, unlike the other type of DI (neurohypophyseal)treatment
psychogenic polydipsia
compulsve water drinking = impaired thirst mechanismdilution of body fluids –> serum hypoosmolality and hyponatremia = suppressed ADHin absence of ADH, lots of dilute urine to normalize osmolalitycan cause washout effect if excessive intake is prolonged –> kidneys unable to concentrate urine***polydipsia PRECEDES polyuriatreat with sustained water restriction!!
SIADH
syndrome of inappropriate ADH(schwartz barry syndrome)inapropriately high ADH secretion due to changed set point (hypothalamic) or exogenous ADH (tumor) or faulty receptors–> water retention, dilutional hyponatremia, rise in ecvand inappropriate concentrated urineincreased renal blood flow = decreased renin secretion –> decreased aldosterone –> increased Na excretionstretched atrium can release natriuretic factor –> increased Na excretion –> hyponatremia
SIADH treatment
reduce water intake, remove cause, suppress ADH (dilantin) and inhibit ADH (lithium receptor antagonist)
actions of oxytocin
lactation and parturition (induces labor)
sheehan syndrome
pituitary infarction (loss of anterior) due to circulatory collapse from hemorrhage at parturition–during pregnancy blood supply doesnt expand as the gland does–hemorrhage cuts supply –> necrosis and infarction
pituitary tumors cause vision issues because
they impinge on the optic chiasm
neurohypophysis is derived from?adenohypophysis is derived from?
N- diencephalon (neural)/infundibulumA- rathkes pouch (ectoderm from oral cavity)
thyroid formation
from endoderm and neural crest (parafollicular cells from ultimobranchial body)moves from foramen cecum down to location**if the path isnt obliterated, there can by thyroglossal cysts left over
the kidneys ascend until
they contact the suprarenal glands in the 9th week
fetal cortex of suprarenal gland
fetal cortex is functional until the 2nd post-natal month when it starts regressing; the remaining definitive cortex becomes organized into three layers seen in the adult
pancreas formation
from two budsthe dorsal and ventral buds fusetip of ventral becomes the uncinate process
endocrine cells in the testes
leydig cells produce testosteronesertoli cells secrete MIF (mullerian inhibiting factor) and inhibin
endocrine cells of the ovary
follicular cells produce estrogenluteal cells produce progesterone
embryologic origin of pituitary:anteriorintermediateposterior
a and i = ectoderm of the oral cavity/rathkes pouch p = ectoderm of neural tube
embryologic origin of pineal gland and thyroid
pineal = ectoderm/neural tubethyroid–follicular cells = endoderm, foramen cecum–parafollicular cells = neural crest, ultimobranchial body
embryologic origin of the parathyroidsuperiorinferior
s= endoderm of 4th pharyngeal pouchi = endoderm of 3rd pharyngeal pouch
suprarenal cortex is fromsuprarenal medulla is from
SC - mesodermSM = neural crest
ovary and testis are from
gonad, mesoderm
