Endocrine Anatomy and Physiology Flashcards
what type of feedback regulation is endocrine function
most is negative and btwn many different points
-self limiting
ex. ant pituitary inhibits hypothalamus
horomes inhibit ant pituitary or hypothal
what is an example of positive feedback
LH induction of estrogen from ovaries which induces explosive LH surge
-estrogen or estradiol act on ant pituitary to promote more estrogen or estradiol
what does the hypothalamus release
releasing factors (vs inhibiting factors) which go into circulation to have an effect elsewhere
what is another name for the putuitary
where does it sit
aka hypophysis
master gland
sits in the hypophyseal fossa/sella turcica/ sphenoid
what kind of innervation does the pineal gland receive
what can happen if it englarges
sympathetic NS innervation
-it can compress the cerebral aqueduct if englarge=>leads to hydrocephaly which may effect eye movements
=>pretectal nuclei (upward gaze) and insterstituial nuclei (CN3) downward gaze
- goes through superchiasmic nucleus
- releases melatonin =>circadian rhythm
what does the thyroid gland release
C cells release what here
thyroid hormone
c cells here release calcitonin
what is the thymus gland involved in the production of
involved in the production of mature T-lymphocytes
-produces various growth factors
what hormone does the heart release
what does this promote
releases atrial natriuretic factor hormone
ANF promotes Na loss
-released when the atrium senses increased blood volume
-imp in bedridden people
in the lungs, what does ACE concert antiotensin to
angiotension 2
what do the adrenal glands release
aldosterone
what do the kidneys release
erythropoeitin and renin
what does the stomach release
gastrin
what do neuroendocrine cells in the small intestine release
neuroendocrine cells release gastric inhibitory peptide
what are the types of secretion here
- endocrine -acting on distant cells
ex. hormones - paracrine-acting on neighboring cells
ex. nitric oxide - autocrine-cells acting on themselves
- most notably in the immune system
what are the types of hormones in the endocrine system
aa
polypeptides
steroid
aa: what are norepinephrine and thyroxine derived from
what is melatonin derived from
- norepinephrine and thyroxine derived from tyrosine
- melatonin from tryptophan
polypeptides:
what are examples of glycoproteins
what are examples of growth hormones
what are examples of the secretin family
glyco: LH, FSH, TSH, hCG
growth hormones: GH, PRL, hPL
secretin: secretin, VIP, glucagon, GIP
what are steroids derived from
cholesterol
-aldosterone, cortisol, androgens estrogens
what are plasma transport proteins bound to
what are generally not
steroid and thyroid hormones
-aa and polypeptide hormones generally are not
what are polypeptide and protein hormone production synthesized as?
- what is signal peptide then cleaved to form?
- when is this proteolytically cleaved
preprohormone
- may contain sequences for several diff molec depending on where it is cleaved
- signal peptide is then cleaved to form prohormone
- prohormone proteolytically cleaved when its packaged into vesicles
what can POMC become
ACTH (adrenocorticotropic hormne) alpha MSH (melanocyte stim hormone) CLIP (corticotropin-like intermediate prot)
POMC is cleaved to ACTH
what does ACTH stimulate
what is an exmpale of a negative feedback here
ACTH stimulates the adrenal cortex to release its hormones
ex: if the adrenal cortex isn’t producing hormones properly, ACTH lvls may rise bc the end-product isn’t available to shut down ACTH production
ACTH cleaved to a-MSH and CLIP
a-MSH controls skin pigmentation, so an excess of ACTH (=>excess of a-MSH) has a symptom of skin darkness
what are the 2 parts of the anterior pituitary and what are they
- pars tuberalsis
- outer covering of pituitary stalk - pars distalis
- anterior lobe
what are the parts to the posterior pituitary
- median eminence of hypothalamus
- infundibular stalk
- infundibular process (post lobe)
what synthesize posterior pituitary hormones
hypothalamic neurons whose axons terminate in the posterior lobe synthesize post pituitary hormones
what are anterior pituitary hormones synthesized and secreted in reponse to
hypothalamic releasing hormones carried in the hypophyseal portal circulation
what does CRH (corticotropin-releasing hormone) stimulate
ACTH secretion by the ant pituitary
what does TRH (thyrotropin-releasing horm) stimulate
TSH secretion by the AP
what does GHRH (growth horm-releasing hormone) stimulate
stimulates GH secretion by the AP
what does LHRH (luteinizing hormone-releasing hormone) stimulte
stimulates LH and FSH secretion by the AP
what does ADH do
increases water reabsorption by collecting ducts in kidneys
-release induced by catecholamines, angiotension 2, reduced blood volume
increases aquaporin gene transcription and incorporation into kidney collecting duct membrane
what does oxytocin do
-what is this release induced by
stimulates smooth muscle contraction in breasts and uterus
-release induced by:
- sensory neurons in nipples
=> oxytocin stimulates myoepithelial cells in alveoli of mammary land
-stretch receptors in cervix during chidbirth
how do the monogamous prairie vole and promiscuous meadow vole differ in their distribution of oxytocin and vasopressin
monogamous have a higher density and distribution of oxytocin and vasopressin receptors in the brain
-the promiscuous ones have a much diff receptor distribution
what are the tropic hormones (basophils) of the anterior pituitary
ACTH: glucocorticoids, cortisol and corticosterone
TSH: T3 and T4 (thyroxine)
Gonadotropins: FSH-ovarian follicle development and spermatogenesis
LH-ovulation and luteinization of ovulated graafian follicle; stimulates estrogen and progesterone production by ovary and testosterone by leydig cells in testes
what are examples of non tropic hormones (acidophils) from the anterior pituitary
GH: stimulates growth during childhood
PRL: synthesis of milk during lactation
what does ACTH (adrenocorticotropic hormone) do
what is it a feedback regulator of
diurnal secretion regulated by corticotropin releasing hormone (CRH) and increased during stress
-feedback regulator of synthesis and secretion of glucocorticoids by zona fasciculata and reticularis of adrenal cortex
=>not a regulator of aldosterone secretion from zona glomerulosa
what is TR (thyrotropin releasing hormone) released w/
dirunal rythym
what is growth hormone secretion stimulated by
what is it inhibited by
- secretion stimulated by GHRH and thyroid hormones
- inhibited by somatostatin (SRIF)
what does GH stimulate
IGF-I, a mitogenic factor that mediates growth-promoting effects of GH
how is GH secreted
in short, pulsatile bursts day and night, but GF secretion is maximal at night
how does GF mediate effects
through JAK2 tyrosine kinase, which phosphorylates cytoplasmic and nuclear proteins
what happens when there is too much GH? too little?
too much: acromegaly
too ligght: pituitary dwarfism
what are some other functions of GF
- mobilizes triglycerides
- decrease glucose use by muscle and fat cells
- increases liver glucose production (anti-insultin actions, like glucocorticoids)
- increases protein synthesis in most organs
what does the thyroid gland produce
what does it regulate
T3 (triiodothyronin-4x more potent than T4) and T4 (thyroxine)
-regulates development and metabolic rate
what is colloid composed of
thyroglobulin (Tg), the storage form of thyroid hormones
- Tg where is forced into
- what occurs here
- what are the cells here entered through and exported by
- what is dietary iodide essential for
- Tg extruded into apical space where iodination occurs; iodine enters cells through sodium iodide symporter and is exported apically by pendrin
- dietary iodide essential for hormone synthesis
how many T4 and T3 do Tg contain
up to 30 T4 and a few T3s
-Tg is the storage form of T3/T4
how does the thyroid gland produce T3 and T4
- iodide symported (with Na) into follicular cells from blood
- pendrin exports iodide into lumen
- in the lumen Tg binds MIT, DIT, T3 and T4
- all the same molec, but with 1,2,3,4 iodides - macrophocytosis: a pseudopod form follicular cells grabs grab some Tg from thyroid colloid in the lumen when needed
- proteolysis occurs, liberating T3 and T4
what is thyroid hormone metabolism
reverse T3-an inactive metabolic byproduct
- T3 and T4 are active products
- a clinical measure of thyroid functions
what are the functions of thyroid hormone
critical role in CNS development, growth, and basal energy metabolism
what is a goiter
a diffuse or nodular enlargement of the thyroid gland
- what kind of receptors mediate thyroid effects
- what does thyroid hormore increase production of? what does this directly increase?
- what does TH promote?
- what rate does TH increase?
- what does TH stimulate
- type 2 receptors mediate by nuclear receptors that modulate gene transcriptions
- increases GH production
- directly increases synthesis of structural and enzymatic proteins in many tissues
- promotes growth/calcification of bone
- increases basal metabolic rate (BMR) by stimulating oxidative phosphorylation
- stimulates synthetic and degradative pathways of carb, lipid, and protein metabolism
what are the 3 zones that the cortex in the adrenal gland has?
what do they produce?
- zona glomerulosa
- produces aldosterone - zona fasciculata and 3. zona reticularis
- produce glucocorticoids, cortisol, corticosterone, androgen dehydroepiandrosterone
which zone of the cortex produces most of the androgen
reticularis
what is the medulla of the adrenal gland
what is it derived from
modified sympathetic ganglion
derived from neural crest
what is steroid hormone synthesis driven by
the availability of cholesterol
what is addison’s disease
glucocoritcoid and aldosterone deficiency due to infection or autoimmunity
what will generate free cholesterol
cholesterol esterases will generate free cholesterol (liberating it from cellular membranes)
what do StAR (steroidogenic acute regulatory protein) do?
moves cholesterol from the outer to inner mitochondrial membrane
-the rate-limiting step
what does ACTH promote
promotes activity of enzymes which cleave cholesterol and promote one of 3 interconnected pathways (mostly in smooth ER some in mit)
what are the 3 pathways that ACTH can promote
what are the end products of each
1. miteralocorticoid end product: aldosterone 2. glucocorticoid end product: cortisol 3. androgen end product: DHEA, A'Dione enzyme: 17 alpha-hydroxylase/17,20 lyase
what is the production of aldosterone stimulated by
what does it stimulate and increase?
- production stimulated by low bp, andiotension 2, and high extracellular potassium
- stimulates sodium reabsorption by distal convulted kidney tubles,
- increases water retention, increaes blood pressure, and increases secretion of potassium
what do glucocorticoids bind to? what do they stimulate? what do they inhibit? -what do they act as what do they protect the body during
- bind to glucocorticoid response elements in DNA
- stimulates gluconeogenesis
- stimualtes fat breakdown in adipose tissue
- inhibits glucose uptake
- acts an anti-inflammatory and immunosuppressive
- protects body in times of stress (keeps energy availble for the brain)
how do glucocorticoids stimulate gluconeogensise particularlyin the liver
-stimulates gluconeogenesis, (liver)
=> mobilizes aa from extrahepatic tissues to serve as substrates
how do glucocorticoids stimulate fat breakdown in adipose tissue
by using hormone-sensitive lipase
-the fatty acids released by lipolysis are used for production of energy in tissues like muscle, and the released glycerol provides another substrate for gluconeogenesis
how do glucocorticoids inhibit glucose uptake
by muscle and adipose tissue to converse glucose
what are the adrenal medullary hormones
what do they mediate
norepinephrine and epinephrine
- MORE EPINE released
- mediate fight or flight and metabolic response to hyperglycemia
what do the glucocorticoids in cortex catalyze
glucocorticoids in cortex catalyze methylatin of norepinephrine to produce epinephrine
how is norepinephrine changed to epinephrine
by methyl transferase (methylation of norepinephrine)
-in the cortex, glucocorticoids catalyze the conversion of norep to rep
L-tyrosine => L-DOPA => domapine => norepinephrine => ephinephrine
what are the cells in the islets of langerhans
what do they produce
alpha cells: produce glucagon -glucagon promotes glucose in the blood beta cells: produce insulin and amylin -amylin reduces glucagon release delta cells: produce somatostatin -somatostatin inhibits insulin, glucagon, GH and pancreatic polypeptide Fcells: produce pancreatic polypeptide -PP slows absorption of food, blunting the glucose response
what is the primary regulator of insulin secretion
glucose
is insulin response greater after oral of IV glusose
oral: factors (glucagon-like peptide, incretin-like gastin inhibitory polypeptide) are released by gut lining cells and promote insulin release
- enhance the effect of insulin for an equiv quantitiy of glucose
what is glucokinase
how does it act as a glucose sensory?
what causes the blockade of the ATP-dependent K channels
glucose sensor on beta cells which triggers insulin release
-by determining rate of glycolysis
-increase in cytosolic ATP causes blockade of ATP-dependent K channel
=> inhibits K efflex
=> target of sulfonylurea drugs
=>promotes depolarization (bc K efflux promotes repolarizatoin) and Ca influx
=>cells release insulin
what kind of Km does glucokinase have
low Km
lower than hexokinase
what uptake does insulin increase in cells
what does this reduce
what can this lead to
insulin increases K uptake into cells
- this reduces circulatory K levels (hypokalemia)
- severe hypokalemia can lead to fibrillation/death
what do insulin and glucagon do to... glucose fatty acids ketoacid amino acids K
glucose: insulin decrease, gluc increase fatty acids: insul decrease, gluc incr keotacid: insulin decre, gluc incr aa: insulcin decreases, gluc NO EFFECT K: insulin decreases, gluc NO EFFECT
how does insulin promote glucose updake in muscles and fat
by increasing GLUT4 on membrane
what is calcium and phosphate regulated by?
hormones of the kidneys and liver
what is calcium and phosphate obtained from? what determines their fate
-what are they absorbed by? how are they absorbed
diet: Gi tract, kidnys, and bones determine ultimate fate of each
- absorbed by small intestine by active transoprt and diffusion by active transport and diffusion
wehre is most calcium and phosphorus stored
99% ca stored in bones and teeth
86% phosphorus stored in bones nd teeth
what regulates calcium and phosphate
parathyroid hormone (PTH) calcitonin vit D3 (cholecalciferol)
what is PTH released from
what is it stimulated by?
what does this increase and decrease
what does this upregulate
PTH released from 3 paris of parathyroid glands
-stimulated by low plasma calcium
=> increases plasma calcium and decreases phosphate
-upregulates osteroCLAST activity (degrades bone)
what does calcitonin have the opp effect of? what is calcitonin released by what is it stimulated by what does this decrease what does it stimulate
opposite effect of PTH
released by parafollicular cells in thyroid
stimuated by high plasma calcium
decreases plasma calcium and phosphate
stimulates osteoBLAST activity (builds bone)
how do we obtain vit D?
what is this converted to?
what does this increase?
-from diet or sunlight effect on 7-dehydrocholesterol
=>converted in liver and kidneys to 1,25-dihydroxyvitamin D3 (calcitriol)
-1 is by liver enzymes
-25 is by kidney enzymes
-increases plasma calcium and phosphate
why is PTH involved in vit D3 processing?
what is PTH then inhitibed by
to increase Ca uptake
PTH is then inhibited by increased plasma levels of Ca
what is osteoporosis
reduction in total bone mass; equal loss of both mineral and ORGANIC MATRIX (collagen)
what are the causes of osteoporosis
- long term ca deficiency
- vit c deficiency; needed for collagen synthesis
- reduction in mechanical stress on bone-too much bed rest
- decline in estrogen at menopause
a decline in estrogen following menopause leads to osteoporosis, what are the 2 major reasons this happens
- estrogen inhibits osteoclastic factors (those promoting bone breakdown) released by T cells
- estrogen causes PTH effects on bone and enhances PTH effects on the kidneys
- active PTH => breakdown of bone
