Endocrine Flashcards
Negative Feedback
- probably the most important monitoring system to see if we have enough
- can only say we don’t need it anymore; it cannot help an organ that is over producing
Example: Low TSH but high T3 & T4
when we have decreases or increases in both, then we have a problem and we must determine the problem
(possible adenoma or hypothalmic issue)
TRH is the mothership messenger that tells the anterior pituitary which says, OK, we need to send messengers to the thyroid because we don’t have enough, then TSH goes out; TSH is underboss: is is the messenger that goes to the thyroid that ways we need more T3 or T4;
They thyroid is the metabolic gas pedal we have increased metabolic activity, AA, etc with Less, we have let up in the gas pedal
Negative Feedback
Thyroid: They hypothalmus releases thyrotropin releasing hormone TRH. TRH causes the release of TSH (thyrotropin). TSH released from the anterior pituitary targets the thyroid gland and stimulates the release of T4 and some T3. Most of T3 is converted in teh periphery. So when there is low circulating thyroid hormones, we would expect that if the negative feedback loop is working, that there would be a high level of TSH in the blood but a low actual thyroid hormone
Hormone effects:
direct effects
&
permissive effects
hormone regulation
up-regulation
down regulation
Direct Effects
I am releasing a hormone and it is going to have “THIS” activity
-Ex: T4 increases metabolic activity in a lot of things
Perissive effects
Ex: cortisol sensitizes the tissue to epinephrine and norepinephrine
-giving a medication will: more sensitive to
and will make things more potent because of the potentiation of things
UP REGULATION
- low numbers of hormones increase the number of receptors per cell
- Lipid controlling drugs work this way:
if only a little bt, receptors will up regulate because the body needs it
-initially sweep a lot of cholesterol out of the system and the liver freaks out because it needs cholesterol to make bile and hormones, especially gonadal hormones and it aus I ned more cholesterol and I don’thave it; so it upregulates hepatocytes that pull LDL out of the system, and with lipid-controlling meds the liver never catches up so the amount of availability on the system is way down because the lier is pulling it out to create what it needs
Down Regulation
High concentrations decrease the number of receptors
- when there are too many hormones in concentration, we have down regulation to say we don’t need anymore and the hormones float out in circulation
- EX: insulin sensitivity:
whenever there are a loss of hormones floating around, either the upper end or too many, cells begin to say “I don’t need that much” ad they down regulate the receptors and it leaves more of that hormone out in circulation just sitting wround. Because a person is diabetic, he has a very high circulating level of glucose, there is a ton if gluose, there is a ton of insulin and hyperinsulinemia makes the tissues sy”Woah, I don’t need that much”, so the tissues actually become less sensitive to the insulin and glusoce molecule together and they take up less of it which exacerbates the problem; we know that people who have diabetes, their insulin sensitivity is a pajor part of the problem
Hypothyroidism
expected:
High TSH, low T3 and T4
Hyperthyroidism
Low TSH, High T3 and T4
Hypothalmic Pituuitary axis
They Hypothalmic-Pituitary axis is the basis for the neuro-endocrine system. They hypothatmus and the pituitary make up the basis for this system, which includes the feedback mechanisms. When the hypothalmus targets the pituitary with particular releasing factors, it causes the release of others that then target distant organs. When those distant organs relese their hormones, catecholamine and other substances, therei presence in the blood or their actions provide negative feedbck reducing subsequent messengers and secretion. This is the Basis for HPA.
Hypothalmic -Pituitary Axis
reason why many of the decadron-type drugs for 54321
-y giving ehn a glucocorticoid, creating a false negative feedback loop (exogenous); hypothalmus is saying “I have a lot of cortisol in the system, what do I need to send?”
ACTH
They Hypothalmus
Pituitary
and target hormones
AXIS
Goes down in line:
Hypothalmus to pituitary to target hormones
Posterior Pituitary
(neurohpyohysys)
stores and releases oxytocin and ADH
(both produced in they hypothalmus and stored in the posterior pituitary)
Anterior Pituitary
(adenohypophysis)
stores multiple hormones including the trophic hormones
Any hormones labeled trophic or tropic:
targets another endocrin hormone
b endorphins
these hormones form a complex with other substances (they are ligands) to bind with other opiod receptors
b lipotropin
Melanocyte stimulating hormone (MSH)
stimulate the production and release of skin pigments from the melanocytes
FSH
stimulates egg maturation and sperm production. When low in women, it tends to cause amenorrhea. If low in men, loss of facial hair, decreaed libido and erectile dysfunction
Prolactin
(luteotrophic hormone…VERY close to lutotropic)
Doesn’t have a known particular releasing factor, but it does have an inhibiting factor in the hypothalmus (most likely dopamine)
It is presumed that there is a releasing factor, but it hasn’t been isolated. Prolactin is also produced in other tissues in the body. Stiulates lactation and normal sexual function.
Supresses ovaian function
Lutenizing hormone (LH)
Lutotropin
- increases the production and release of teroid hormones. -Surge in women releasing egg at ovulation
- defiency in women may cuse wt gain, heavy period, insomnia, irritibility
low in men-reduced testosterone
Growth Hormone (GH)
(somatotropin)
Bone and muscle growth, release of insulin-like factors from the liver
Adrenocorticotrophic hormone (ACTH)
The “Stress” messenger: stimulated the release of glucocorticoids (cortison which increases protein and CHO metabolism, increes anti-inflammatory factors and causes gluconeogenesis (the reason BS elevated when on steroids) and mineralocorticoid (aldosterone) and causes reabsorption of sodium
Hyper/hypo thyroidism
Primary:
dysfunction or disease of the thyroid gland
Hyper/hypo thyroidism
Thyrotoxicisis aka hyperthyroidism
Graves Disease
Most common cause of hypothyroidism
Pretibial myxedema
- auto-immune driven
- body creates antibodies to thyroid itself; diseases they thyroid and creates an over production of thyroid)
Hyperthyroidism resulting from nodular thyroid disease
Goiter
