Endocrinology II Flashcards
Where is the ligand-receptor interactions found
Immune-, GI-, endocrine and neural systems
The values of the scatchqrd analysis
Bmax: no of binding sites: x axis intersection
Kd: affinity of interaction, lower number = stronger bond, slope of graph
Feedback mechanism
Neuro-immuno-endocrine regulation
- info from cns and immune system to hypothslamus to respond in “hormone language”
Membrane receptors: ion channel receptors
Acrtylcholine: na+, voltage gated channel (trigger action pot.), muscle/neural cells
Glutamate: neural+glial cells, Mg2+ as antagonist
Anion receptors: inhibitory synapses in cns: GABA mediated
IC enzyme receptors
Eg insulin, growth hormone receptors
Autophosphorylation
(Direct phosph. -> other substance is needed for the phosph)
G protein structure
3 subunits:
Alpha bind GDP -> then bind beta and gamma subunits - these bind the ic side of receptor -> alpha changes GDP for GTP
—> Gs or Gi
The parvocellular area of the thalamus consists of
Ventromedial nucleus
Dorsomedial nucleus
Infundibular nucleus
The magnocellular area of the thalamus consists of
Supraoptic nucleus
Paraventricular nucleus
What are the motor proteins used in axon transport called, what is this type of transport called?
(To transport up/down axon)
ATP IS USED - found and synthesized in both axon and neural body
Kinesin - from soma to synapse direction
Dynein - residues back to soma
Microtubular transport - direction of tp depends on polarity of transported substance as the microtubulr fibre is polar
Stimulating and releasing hormones
The hypothalamus produces releasing hormones and the pituitary produces stimulating hormones
The 4 inhibiting factors of the parvocellular area of the thalamus
Dopamine and Somatostatin are the most important
GABA - general
VIP - indirect effect, specific action
Origin of neuro- and adenohypophysis
Neurohypophysis - ectodermal glandular nervous tissue
Adenohypophysis - endodermal glandular tissue
Name the 6 hormones of the adenohypophysis according to their function as gonadotropic or metabotropic hormones
Metabotropic hormones: GH, ACTH, TSH ( prod. In groups in AH)
Gonadotropic hormones: PRL, FSH, LH (sporadicslly profuced everywhere)
Name the adenohypophyseal hormones according to if they are acidophils/basophils
Acidophils: GH, PRL
Basophils: TSH, ACTH
Half life is determined by
The syalic acid content of the hormone
What is the precursor of ACTH called?
POMC - pre-proopiomelanocortin
- incr. Bw and function against high stress
ACTH functions on the cortex adrenal hormones in what way
By incr. IC cAMP –> pkA –> cholesterol cleaving, steroid hormone synthesis (adrenocortical hormones)
ACTH functions
Melanocyte stimulation –> pigmentation
Incr. Production of adrenocortical hormones –> circadian rythm, menstrual cycle, long term stress symptoms
GH produced by
Acidophils in the adenohypophysis
GH fluctation
Pulsating release
High levels at night
Shifting btw incr/decr gh levels
GH’s indirect on the liver
stimulate activation of thyroid hormones
simulate synthesis of IGF’s aka somatotropin
- prod in response to gh, in liver to promote growth
why cant IGF exert an effect on insulin receptors
bc. Insulin-like Growth Factor is bound to a protein in the plasma even though it is water soluble
the two receptors of ADH and their function
AQP1: in vascular smooth muscle to induce contraction which increases the blood pressure
AQP2: in nephron of kidneys -> decrease osmolarity
types of MSH and their origin
alpha MSH: from ACTH
Beta MSH – formed by beta lipotropin
Gamma MSH – cleaved from the N – terminal of POMC
pigment granules; resting state vs. “activated” state
- how does the granules travel around the cell?
no color: granules around nucleus
color: granules are scattered throughout cell
travel along microtubules of cell
short description of melatonine synthesis
Light stimulation through the optic nerve -> suprachiasmatic nucleus ->spinal chord -> cervical ganglion -> CP(corpus pineale) -> norepinephrine release stimulates NAT (N-acetyl transferase) which is a key enzyme in melatonin synth. (transform serotonin -> N-acetylserotonin, which them is turned into melatonin)
pineal gland innervation
not directily connected to the CNS - innervated by postganglionic sympathetic nerve fibres
pineal gland origin and cell types
glial cells, pinealocytes
ectodermal structure of diencephalon
deiodinases
activativation and deactivation of thyroid hormones
basic structure of thyroid hormones
thyronine frame built by condensing 2 tyrosine frames
iodine found on C3 and C5 of inner and outer rings
name the thyroid hormones
T4 - thyroxine
T3 - triiodothyronine
rT3 - reverse triiodothyronine (reg. steps)
T4 is carried by which carrier proteins
TBG - thyroid binding globulin (also bind T3)
Albumin - also bind some T3
TBPA - thyroid-binding pre-albumin
transit time
the uptake by tissues of thyroid hormones - how long the tissues are in contact with passing amount of blood
long and short transit time where
long: liver: both bound and non-bound hormones are taken up 5sec
short: brain: 1 sec, free hormone conc determine hormonal supply
where does the thyroid hormones not have any effect in oxidative processes
brain, gonads, lymphatic organs and smooth muscle
metamorphosis
development after birth/hatching
- TH needed
TH in nervous system development
myelinization and create synaptic connections btw hormones
these hormones are needed for normal development
insulin, GH, TH
goiter
thyroid enlargement due to cell enlargement (hypertrophy) or cell proliferation(hyperplasia)
wolff-chiakoff effect
accumulation of iodine in the thyroid -> decr. hormone production
endemic goiter
high TSH levels -> bigger thyroid -> goiter
adrenal gland origin
cortex: mesoderm
medulla: ectoderm
adrenal gland hormone synthesis from what compound
LDL from plasma -> cholesterol -> steroid hormones
androgenic steroids
a type of adrenal hormone
- male sexual hormone produces mostly in testis and adrenal cortex, in lesser extent by ovary and placenta
estrogen steroids
a adrenal hormone, female sexual hormone produced in ovary, adrenal cortex, testis and placenta
corticosterone dominates over cortisol in
rat, rabbit and pidgeon
cortisol and corticosterone occur in equal conc in
dog and cattle
lacking glucocorticoids
Na⁺ loss -> decr. blood volume
K⁺ increase -> cardiac weakness
Incr. Capillary permeability -> edema develops
Muscular weakness
Water poisoning
AC overprod
lymph tissue degrades
no of eosinophil and basophil cells decrease
AC removal/destruction
lymphoid hyperplasia (cell proliferation)
GAS
(stress stimuli leads to) general adaptation syndrome
the 4 phases of stress
- initial stage: ACTH, Cannons reaction(F or F)
- stage of resistance: glucocorticoids
- stage of exhaustion or 4. stage of adaptive disorders
the 4 regulaters of mineralocorticoids
- incr. K⁺ -> incr aldosterone prod
- renin-angiotensin system activation -> ald. prod.
- decr. Na⁺ content, but conc remain the same
- ACTH - permissive effect, only needed for mineralocorticoids (aldosterone) to show its full effect, aldosterone synth will not be terminated if deficiency of ACTH
function of aldosterone
reabs of Na⁺ and secretion of K⁺
prod of transporters
catecholamines are produced where
epinephrine: adrenal medulla only
NE/dopamine: anywhere in tthe nervous system
synthesis of adrenaline
Phenylalanine -> tyrosine -> DOPA -> Dopamine -> Norepinephrine -> epinephrine
inactivation of catecholamines
MAO and COMT can degrade them
alpha1(pre) and alpha2(postsynaptic) receptors: hormone re-uptake
sympathetic-adrenal system
most important regulatory system of CO
NE stimulates which receptors
alpha1 and beta1
E stimulates which receptors
beta2, alpha1
dopamine acts on which receptors
D1 and D2
