week 3 Flashcards
magnocellular vs parvocellular neurons
magnocellular (in PVN and SON): oxytocin, vasopression
parvocellular: CRH, TRH, GHRH, GHIH, DA, GnRH/LHRH, PRH
** IN THE HYPOTHALAMUS
posterior vs anterior pituatiary
posterior: oxytocin, vasopressin
anterior: ACTH, TSH, FSH/LH , GH , PrL
most loops are negative feedback but 1 is postiive
oxytocin
GH made from
and stimulates release of what
somatotrophs in the anterior pituitary
insulin like growth factor IGF1
stimulated by hypoglucemia, dopamine, arginine, GHRH(hypothalamus) and grhelin
GH is inhibited by
somatostatin/ GHIH
i.e. hyperglycemia
and IFG-1
GH receptor
class 1 cytokine receptor
GH for
bone growth longitudinal
acromegaly (also cancer, GNG and insulin resistance, vision if tumor big, cardio)
and
gigantism (before puberty and epiphyseal long bone fuse)
prolactin is made from
lactotrophs
make milk and mammary gland
stimulate prolactin
suckling and estrogen GnRH, serotonin, oxytocin
inhibit prolactin
dopamine, somatostatin, GABA
4 types of hormon
glucocorticoids (cortisol) (blood sugar and stress)
mineralocorticoids (aldosterone) - (water salt balance)
catecholamines (NE and E)
which part of adrenal glands for the hormoens
cortex= cortisol and aldosterone
medulla- NE And E
adrenal medulla is made freom vs adrenal cortex
medulla (NE and E) neural crest cells (“SNS”)
cortex (cortisol and aldosterone) is mesoderm
adnrenal medulla hormone and PNS or SNS
SNS and NE and E
hormones in adrenal cortex and what its derived freom
mesoderm
zona glomerulosa- aldosterone
zona fasiculata- cortisol
zona reticularis- androgens
adrenal medulla vs adnreal cortex derived
medulla- neural crest cells (SNS)
cortex- medulla
HPA axis
hypothalamus to anterior pituitary to target gland
i.e. hypothalamus has TRH to AP has TSH to target T3 T3 in thyroid
what in the anterior pituitary to make cortisol
CRH (hypthal) –> ACTH (AP)
mineralcortioicd regulated by
- Secretion of angiotensin II
- Serum K+ levels
steroid hormones (cortisol, aldosterone, estrogen, testosterone) are made from
cholesterol (then enzymes to convert to homrone)
made on demand bc lipid soluble (hydrophobic) can cross cell membrane via simple diffusion
how to get cholesterol
from LDL then use * Cholesteryl ester hydrolase (CEH) removes the fatty acid
in the inner mitochondrial membrane what helps to get cholesterol in
Steroidogenic acute regulatory protein (StAR)
what does cholesterol turn into in inner mitochondrial memrbane
pregnenlone
bow to get pregnenolone to become cortsiol
lots of rxn via : side-chain cleavage enzyme (SCC)
* This is the rate limiting step of the synthesis pathway
steps of make cortsiol
LdL to cholesterol with cholesterol ester hydorlase (CEH)
then into inner mitochondria membrane via STAR
then become pregnenolone
: side-chain cleavage enzyme (SCC) to turn into cortisol
* This is the rate limiting step of the synthesis pathway
ACTH upregulates cortisol production (steroidogensis)
▪ Increased LDL receptor expression
▪ Increased activity of CEH and StAR
▪ Increased activity of the side chain cleavage enzymes
CRH and ACTH regulation
via circadian and SCN and melatonin and stress
synthesis of mineralocorticoids (aldosterone)
same as cortisol but when gets to corticosterone use aldosterone synthase enzyme to convert to aldosterone
this is done in zona glomerulosa
unlike cortisol in zona fasciulata
RAAS system regulates aldosterone
decreased perfusion to kidney the release renin then ANGIO II to vasoconstrict and make aldosterone and absorption Na+ and secrete. K+
aldosterone
▪ Decreased potassium reabsorption from the GI tract
▪ Increased activity of the sodium/potassium pump in many
cells
▪ Increased sodium reabsorption and increased potassium
secretion from the kidney
how is cortisol carried in circulation
cortsiol via cortisol binding protein
aldosterone is unbound
what needs to happen to cortsiol and aldosterone by the liver before being excreted by the kidneys
glucuronidation makes the hydrophobic steroid hormones more polar & therefore more easily excreted by the kidney
- Eliminated forms of cortisol are known as 17-hydroxycorticosteroids
- Aldosterone as 18-glucuronide
catecholamine (NE and E) are made form
tyrosine –> DOPA –> dopamine –> NE–> E
how does cortsiol convert NE to E
sympathetic stimulation
PMNT enzyme
catabolism of catecholimees
NE –> noremetaneprhine
E –> metanephrine
via COMT
then via MAO into vanillylmandelic acid (VMA)
excrete in urine
tertiary secondary and primary endocrine disroder
territory at hypothalamus
secondary at pituaitary
primary at final organ
cushings syndrome and most common cause
hypercortisol (mostly from iatreogenic/ meds)
Cushing disease
ACTH procucing microadenoma
secondary - high cortisol
adrenal labs
dexametahaone syppresion test
Addisons vs cushings
cushing- too much cortsiol form secondary
addisons- primary adrenal insufficiency
addison
Chronic primary Adrenal Insufficiency
not enough cortsiol, aldosterone and androgen
primary hyperaldosteronism/ conn syndrome
- Causes sodium retention and potassium excretion * Resulting in hypertension and hypokalemia
congenital adrenal hyperplasia
cant make cortisol
Most common enzyme deficiency: 21-Hydroxylase
accumulate progesterone –> ambiguous genatlia
chromaffin cells in adnreal medulla for
NE and E (catecholameins)
