Endocrine System Flashcards
What are the functions of the major endocrine glands? and what hormones do they secrete?
Hypothalamus: (neurocrine) controls pituitary endocrine secretions. It is part of the CNS and acts as an interface between the brain and endocrine system
ADH, oxytocin, and regulatory hormones
Pituitary: controls other endocrine glands and also affects peripheral tissues. contains both neural and endocrine tissues and receives both types of signals from the hypo.
anterior pituitary: ACTH, TSH, GH, PRL, FSH, LH, MSH
posterior pituitary: oxytocin and ADH
Pineal: controls circadian rhythm
melatonin
Thyroid: metabolic rate and growth
T3, T4 and calcitonin
Parathryoid: calcium and phosphorous homeostasis
PTH
Pancreatic Islets of Langerhans: metabolism and energy balance
insulin and glucagon
Adrenal (cortex and medulla): stress response, mineral balance and metabolism
cortex: aldosterone, cortisol, corticosterone, androgens
medulla: epinephrine and norepinephrine
Ovaries and Testies: maturation and development, sexual function, pregnancy
testes: androgens and inhibin
ovaries: estrogen, inhibin and progestins
What are the four major categories of the chemical nature of hormones? How are they made?
- peptide: They are encoded by a specific gene and then synthesized using normal protein synthesis machinery. They undergo lost of post-translational mechanisms. They are stored in secretory vesicles and secreted when needed. DNA –> mRNA –> proprehormone –> prehormone –> hormone + peptides are released
- steroid: They are made by changes to cholesterol. They are not stored but released immediately into ECF.
- thyroid: They are made from the tyrosine residues of proteins that are stored in the colloids of the thyroid. They are released upon proteolysis of the colloid proteins.
- catecholamines: They are synthesized from amino acids and are stored in secretory vesicles and secreted when needed.
How are hormones secreted from a secretory vesicle?
There will be a stimulus and that stimulus will cause an increase in intracellular Ca2+ or cAMP. That will cause the secretory vesicle to associate with the cytoskleton and it will translocate to the plasma membrane. At the plasma membrane, the vesicle will fuse and this fusion results in the release of hormones to the ECF.
How are short term and long term effects carried out by hormones?
Short term effects: Protein function alteration usually phosphorylation
Long term effects: gene expression modification
Which hormones are water soluble? Which are not? How are the non-water soluble hormones carried and what are the advantage (4) of this mechanism?
Water soluble: catecholamines and peptide hormones
Lipophylic: steroid and thyroid hormones. They are carried via plasma binding proteins. There are two types:
1. Specific Binding Proteins that have a high affinity for a specific hormone. (i.e. Thyronine Binding Globulin)
2. Non-specific low affinity binding proteins that are present in larger amounts and bind large quantities of nonspecific hormones (i.e. albumin)
Advantages:
1. Distribution: goes everywhere in the body and not just lipid environments
2. Protection: from degradation and excretion thereby increasing the half-life
3. Steadiness: prevents fluctuations since these hormones usually involve gene modification this is necessary
4. Reserve: creates a reservoir in the blood
What determines half life? What are four things that determine that? What is the half life and response time for steroids/ thyroids, catecholamines and peptides?
The rate of elimination determines half life. Rate of elimination is determined by: 1. Rate of reuptake 2. Metabolic degradation 3. Internalization 4. Excretion, usually via urine
Thyroids: 1/2: days and response: days
Steroids: 1/2: hours and response: hours to days
Peptides: 1/2: minutes and response: minutes to hours
Catecholamines: 1/2: seconds and response: sec or less
What is the importance of receptors? What are the two things that determine cellular response?
Receptors decide which cells respond to which hormone. Two things that determine cellular response to a hormone dose is number and affinity of receptors
What is threshold, sensitivity and maximal response when considering a hormone dose response curve? What causes shifts of the curve?
Threshold: hormone dose giving the lowest possible response.
Sensitivity: hormone dose that is necessary to elicit half a maximum response
Maximal response: hormone dose that elicits the largest possible effect
Shifts of the curve caused by
- changes in responsiveness: this is caused by down regulation of the receptor and decreased intracellular signaling pathway.
- changes in sensitivity: down regulation of the receptor and decreased affinity for the hormone. This is usually caused by prolonged exposure to the hormone
What are three ways the hypothalamus exerts control over the endocrine system?
- Hypothalamus secretes hormones that release secondary hormones from endocrine cells of the anterior pituitary gland.
- Hypothalamic neurons release hormones into the blood of the posterior pituitary
- It has neuronal control of the endocrine cells of the adrenal medulla.
What is the importance of the hypothalmic/pituitary relationship? What are the endocrine functions of it?
It allows a brain/ endocrine interface. Its endocrine functions are the creation of a master gland that receives sensory and peripheral inputs and it also has direct endocrine actions on peripheral tissues.
Describe the anatomy of the pituitary gland and how does it relate to the hypothalamus?
Posterior pituitary (neurohypophysis): contains axons from the neuronal cell bodies that are located in the hypothalamus. These axons contain nerve terminals that release hormones into the blood.
Anterior pituitary (adenohypophysis): contain endocrine cells that are indirectly controlled by neuroendocrine signals from the hypothalamus that are released into the median eminence. There they go into the portal vein and into the anterior pituitary where they will stimulate the release/ inhibition of secondary hormones which will be released into the general circulation and act on peripheral target tissues.
What are neurohormones? What are the two major ones that we know and what do they do?
Neurohormones are pituitary hormones released from nerve terminals originating in the hypothalamus.
The two major neurohormones are ADH (vasopressin) and oxytocin. ADH is involved in fluid regulation by changing water retention in the kidneys. Oxytocin is involved in uterine contraction and breast milk ejection from a lactating mammary gland.
How is ADH regulated? What can a deficiency in ADH cause?
When you have an increase in plasma osmolarity, that will cause you to be thirsty which will increase your water content and dilute your plasma OR it will cause you to increase ADH secretion which causes you to retain water in your kidneys and this causes a dilution of plasma as well. Once your plasma osmolarity is increased you are no longer thirsty and you are not secreting ADH.
A deficiency of ADH causes diabetes insipidus. This is usually caused by problems with the hypothalamus neurons, usually caused by trauma or disease. Failure to secrete sufficient vasopressin causes you to urinate a lot because you lose a lot of water. Since your body does not want you to hyperosmolarity or volume depletion, you have to constantly drink water. Treatment is administration of ADH.
What causes oxytocin release?
Oxytocin is released by the suckling of an infant on a breast. This causes oxytocin release which causes contraction of the glands in the breast which causes milk secretion.
Oxytocin is also released by uterine contractions and cervical distension. Oxytocin is released and enhances uterine contraction. After childbirth, oxytocin is involved in the involution of the uterus.
Describe the function and anatomy of releasing and inhibiting hormones. What is the mechanism of secretion/ synthesis?
These are hormones that are derived from neurons in the hypothalamus and released into the median eminence where they are taken up by portal veins and transported to the anterior pituitary. There is a high concentration in the anterior pituitary.
Releasing hormones: They act on the plasma membrane to cause the exocytosis of specific hormones from the endocrine cells of the hypothalamus.
Inhibiting hormones: reduce the synthesis and secretion of pituitary hormones at their target cells
Name the 6 hypothalmic hormones, their target cells and their effects.
GHIH (aka somatostatin) acts on somatotrophs and thyrotrophs to decrease GH and TSH.
- GH increases body size and IGF.
- TSH is involved in thyroid hormone secretion and thyroid enlargement.
GHRH acts on somatotrophs to increase GH.
CRH acts on corticotrophs to increase ACTH.
- ACTH is involved in hormone secretion and cell growth in the adrenal cortex.
GnRH acts on gonadotroph to increase FSH and LH.
- FSH (males) is involved in spermatogenesis and (females) is involved in ovarian follicle growth and estrogen secretion.
- LH (females) is involved in ovulation and luetinization and (males) testosterone secretion.
TRH acts on the thryotroph and mammotroph to increase TSH and PRL.
- PRL is involved in milk production
PIF (aka dopamine) acts on the mammotroph to decrease PRL.
Describe feedback of the pituitary hormones. Describe (in detail growth hormone feedback).
Pituitary hormones act on their target endocrine organ and the hormone that is released by that organ goes back and inhibits the hypothalamus and pituitary gland.
Growth hormone is involved in body growth in kids and the regulation of metabolism in adults. It is regulated by GHIH and GHRH from the hypothalamus. GH stimulates the secretion of somatomedin from the liver. Somatomedin is involved in muscle, bone and organ growth. The effect of IGF opposes insulin (so it is diabetogenic) because it also prevent glucose uptake and stimulates lipolysis. Somatomedin also exerts negative feedback on GH secretion by inhibiting GHRH secretion and promoting GHIH secretion by the hypothalamus.
What is the role of androgens, growth hormone and thyroid hormone in growth in children (0-20)?
Thyroid hormone is most active during the first few years of life and slowly declines.
Growth hormone is active throughout childhood.
Androgens are involved during growth spurts.
What happens when GH secretion goes wrong? What about when you have a pituitary tumor?
When GH secretion goes wrong you have have pituitary dwarfisim or gigantism. These indivudals are normal aside from size and usually there is not fatality except for one rare case where the man got so big that the cardiovascular system could not keep up with his size (approx. 9ft)
A pituitary tumor could cause acromegaly. There is an increase in somatotroph and it won’t stop secreting GH. There is a widening of the bones, coarser facial features, growth of hands and feet, overdevelopment of neck muscles and an occurrence of diabetes. Treatment is removal of the tumor or give GHIH (aka somatostatin).
Describe the regulation of prolactin and what prolactin does.
Prolactin stimulates breast development and milk secretion. PRL levels increase during pregnancy. Hypothalmic regulation is mainly through PRF (dopamine). TRH is minor comparatively. There is negative feedback and it is also stimulated by estrogen.
Describe the structure of the thyroid gland. Talk about the thyroid hormones, including rT3. .
The thyroid gland has follicular cells and C cells. Follicular cells are filled with colloid and make T3 and T4 and C cells secrete calcitonin.
Thyroid hormones are made from tyrosine residues that become iodinated. Primary product of the thyroid gland is T4 and it is iondinated at 3,5,3’5’. T3 is also a product (minor) and it is iodinated at 3’,3,5 and rT3 is the inactive form at it is iondinated at 3’,5’,3,5.
What is the importance of iodine?
Iodine is an element that is essential to the thyroid gland to make T3 and T4. Intake = ouput. The necessary amount is about 150ug and the typical US diet gets about 500ug. Unused iodine is simply released in the urine.
Describe the synthesis and release of thyroid hormones.
- Transport of iodine into the follicular cell is done via the Na/I symport, which is secondary active transport. After the I is in the follicular cell, it diffuses into the colloid via simple diffusion.
- Thyroglobulin (has a lot of tyrosine residues) is made in the ER of the follicular cell and it is transported into the colloid via the acinus that the cell makes for it. It is secreted with TPO (thyroid peroxidase) which is used for a variety of different functions.
- TPO catalyzes the oxidation of iodide into iodine and also iodizes thyroglobulin. This occurs in a step wise fashion with 3 first and then 5. It is also involved in coupling the DIT and MIT molecules that it made before so T3 and T4 are made but thyroglobulin is still attached.
- Now there is follicular reuptake of the colloid via endocytosis. The colloid fuses with lysozomes which intiate proteolytic degradation of thyroglobulin and release T3 and T4.
- T3 and T4 (mostly T4) are released into the blood and extra residues of DIT and MIT are degraded by iodotyrosine deiodinase (which is dependent on selenium) and the released iodine is used for new synthesis.
How do you process T4 hormones? Why is T3 more potent?
You process it by using either 5-deiodinase or 5’-deiodinase to make it either T3 or rT3. T3 is more potent because it is more soluble (so less bound to plasma proteins) and has a higher affinity for the receptor. However, the have the same cellular function.
Why does albumin carry so much T3 if it has a low affinity ?
There is so much albumin that even though it has a low affinity, it still carries quite a bit of T3. The majority of thyroid hormones are carried by thyroxine binding globulin which has a very high affinity for them.
Describe the homeostatic regulation of the thyroid gland. How does TSH, temp and iodine affect the gland?
T3 and T4 provide negative feedback to the hypothalamus so it will stop producing TRH (which stimulated release of TSH from the pituitary) when T3 and T4 levels are high.
TSH affects the gland
- increasing release of T3 and T4
- stimulating proteolysis of thyroglobulin
- increasing iodide uptake
- increasing follicular cell height
- increasing endocytosis of the colloid
- increasing rate of coupling and iodinazation
When there is low temperature, that causes the hypothalamus to increase TRH because it is a thermoregulator.
When there is iodine deficiency, it limits thyroid hormone synthesis.
What are the cellular and organismal effects of thyroid hormone?
Cellular: increase the synthesis of certain proteins
Organsimal:
— Childhood: bone growth, closure of epiphyseal plates, GH secretion, brain development (especially cerebral cortex), proper formation of the choclea
— Adulthood: basal metabolic rate, increase heat production, enhance sensitivity to catecholamines
What are the causes and effects of hypothyroidism in children?
Causes can be maternal iodine deficiency, fetal congenital abnormalities, or maternal antithyroid antibodies that go and attack the fetal thyroid gland. Hypothyroidism during pre and postnatal times can have severe effects including cretinism, which is deaf-muteness, dwarfism and mental retardation.
Remember if the thyroid deficiency is fetal in origin, then prenatally, you can compensate with the mothers T3 and T4 and after birth you can compensate with subsequent treatment and allow normal development.
