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Phgy 210 > endocrinology lecture 1 and 2 > Flashcards

endocrinology lecture 1 and 2 Flashcards

1
Q

What does endocrine signaling involve?
What is an important endocrine gland, what is an example of their target site?

A

-involves hormone secretion into the blood by an endocrine gland
-anterior pituitary gland releases LH and FSH (follicle stimulating hormone) into the blood which transports to gonads (cells of ovary and testes)
-gonads produce steroid hormones, estrogen (female) and androgens (male)

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2
Q

Where does neuroendocrine stimulus usually go, what is the source?
-what can dopamine be?

A

-source of hormones are nerve cells
-stimulus goes to hypothalmus, then anterior pituitary
-dopamine can be a neurotrasmitter or hormone

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3
Q

paracrine signaling vs autocrine signaling?

A

-paracrine signaling is when cell releases a signaling substance to a nearby cell
-autocrine is when the cell is talking to itself, it releases hormones and also expresses receptor on its own cell

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4
Q

What are the 6 steps of communication by hormones?

A
  1. synthesis
  2. release of hormone
  3. transport to target site by bloodstream
  4. detection
  5. change in cellular metabolism
  6. removal of hormone
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5
Q

Where does hypothalmic pituitary signaling occur?
Where does it go from?

A

-via blood vessels of the pituitary stalk
-from hypothalmus to anterior pituitary, hypothalamic neurohormones either inhibit of activate one of the 6 type of hormone producing cells in anterior pituitary

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6
Q

What are protein hormones produced by?
Where does synthesis of the proteins occur?
What does the rough ER do?
What does golgi apparatus do?
What do vesicles do?

A

pre-pro proteins
-on ribosomes, prepro hormones
-turns prepro hormones into prohormones
-golgi packages prehormone into hormone and other peptides
-vesicles do storage of hormone

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7
Q

What are the main steroids?

A

Cortisol, aldosterone, testosterone, and estradiol
-also vitamin D and progesterone

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8
Q

What are the 3 thyroid hormones?
What are the levels of each hormone?
What is different about the third one?

A

T4 (90%) and T3 (9%) which are thyroid hormones, and rT3 (0.9%) which does not bind to thyroid hormones

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9
Q

What is special about the mechanism of the hormone receptor?
how can the receptors be regulated?

A

-it has a lock and key mechanism, which means the hormone has a structure complementary to receptor
-can be regulated by increasing or decreasing the hormone activity and/or synthesis

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10
Q

What are 3 mechanisms by which a hormone can exert effects on target cells?

A
  1. direct effects on function at the cell membrane
  2. intracellular effects mediated by 2nd messenger systems
  3. intracellular effects mediated by genomic or nuclear action
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11
Q

What is example of direct effect vs 2nd messenger system and genomic/nuclear action of hormones?

A
  1. direct effect- a target binds to receptor
    2.you have a first messenger than binds to receptor then an inactive protein turns into an active protein leading to a biological effect
  2. genomic signaling is by nuclear receptors which include receptors for steroid hormones, leading to an altered functional response
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12
Q

What is the feedback mechansim for hormone secretion?
What is an example?

A

-it is negative feedback mechanism
Ex. Ca++ acts in negative feedback loop to regulate plasma calcium levels

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13
Q

What are the 2 different tissues in the pituitary gland?

A
  1. anterior pituitary is endocrine tissue
    2.posterior pituitary is neuronal tissue
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14
Q

Anterior pituitary hormones from hypothalmus:
What does GnRH release (gonadotropin releasing hormone)?
What does GHRH release?
What does somatostatin release?
What does TRH release (thyrotropin releasing hormone)
What does cortiocotropin releasing hormone release (CRH)?

A

-FSH and LH which fo to gonads
-growth hormone which goes to live and other organs
-growth hormone and TSH (thyroid stimulating hormone)
-TSH (thryoid) and prolactin (breasts)
-ACTH which goes to adrenal cortex (adrenocortiotropin hormone)

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15
Q

What are the posterior pituitary hormones?
What are their circulating half lives?
What do the supraoptic nucleus and paraventricular nucleus produce respectively?

A

-arginine vasopressin and oxytocin which control smooth muscle
tone
-1-3 minutes
-vasopressin (or ADH) and oxytocin

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16
Q

What are the anterior pituitary targeting hormones?
Which hormone is not produced by pre-pro peptide?

A

-TRH, GnRH, somatostatin, GRH, PIH, and CRH
-PIH (prolactin inhbitng hormone) is not gene encoded, it is a derivative of free tyrosine

17
Q

What is oxytocin responsible for in the body in females?

A

child birth-causes uterine contraction
milk ejection
behavioral effects-reduces anxioty and enhances bonding

18
Q

what does oxytocin do in the body for males?

A

-ejaculation
-behavioral effects-reduces anxiety and enchances bonding

19
Q

What components are in the thyroid gland?
What is the synthesis under the control of?
In what gender is it larger in, what amount is needed for healthy thyroid state?

A

thyroglobin which contaisn hormones T4 and T3
-under the control of TSH of pituitary gland
-larger in females than males
-need 3g to maintain healthy state

20
Q

How are thyroid cells able to trap iodide/transport it?

A

thyroid follicular cells are able to trap iodide and transport it across the cells against the chemical gradient (active transport)

21
Q

How does iodine help form thyroid hormones T4 and T3?
What regulated formation of T3 and T4

A

-iodine is used for iodination of tyrosine residue of thyroglobulin to form monoiodotyrosine (MIT) and diiodotyrosine (DIT)
-for T4 coupling of 2 DIT form T4 while coupling of one MIT which one DIT forms T3
-formation is increased by TSH

22
Q

What regulates synthesis + control of TSH?
What happens when T3 and T4 levels increase/
What receptors does TSH interact with/

A

TRH controls that (thyrotropin releasing hormone)
-they exert negative feedback on hypothalamic and pituitary levels to decrease release of TRH and TSH
-interacts with specific receptors located on follicular cells, leading to increased production of T4 and T3

23
Q

What happens to T3 and T4 if iodine supply is deficient?
What can stimulation of thyroid cells lead to?

A

-the synthesis of T3 and T4 decreases which causes TSH production to increase and thyroid follicular cells to be constantly stimulated
-can lead to a goiter

24
Q

What is it called when a thyroid is unable to synthesize active thyroid hormones due to iodine defiency?

A

-non toxic goiter (doesnt produce thyroid hormones no matter how large it is)

25
Q

What does increase thyroid hormone release do to calorigenesis in most cells, like cardiac output, oxygenation, and rate of breathing?

A

-it increases all of those thing by increasing rate and strength of contractions, increase oxygenation in blood, increase number of RBC in circulation

26
Q

How does increased thyroid effect carb metabolism?
-effect on lipid turnover?

A

-promtes glycogen formation in liver, and increased glucose uptake in adipose tissue+muscle
-increased lipid synthesis, increased lipid metabolizaition, increased lipid oxidation

27
Q

How does thyroid hormne effect protein metabolism and growth?

A

-Stimulates protein synthesis
-promotes neural branching and myelination of nerves
-promotes development and muturation of nervous system
-stimulates GH secretion, bone growth, and liver IGF-I production

28
Q

What increases Basal metabolic rate (BMR)?

A

-T4 and T3 since they have effect on carbs, lipids, and proteins, which increases need for O2

29
Q

How does thyroid effect CNS?

A

-required for normal brain development, and for synthesis of nerve growth factor

30
Q

Which actions of thyroid hormone are dependent and independet of protein synthesis?

A

-T3 and T4 entering target nucleus to bind to cognate receptor and alter transcription of genes is dependent on synthesis of protein
-hormones inducing interaction with plasma membrane and mitochondira is independent of protein synthesis, not blocked by inhibitors
-T3/T4 increasing uptake of amino acids at plasma membrane is independent of protein synthesis

31
Q

What is too much or too little thryoid hormone called?

A

-too little=hypothyroidism ( low levels of thyroid hormones)
-too much-hyperthyroidism (high levels of thyroid hormones)

32
Q

What are the 4 types of hypothyroidism?

A
  1. primary hypothyroidism (inability to synthesize active thyroid hormone)
    2.secondary hypothyroidism (at level of pituitary, little stimulation of TSH)
  2. tertiary hypothroidism (at level of hypothalamus, little to no synthesis of TRH (thyrotropin releasing hormone)
  3. infantile hypothyroidism (absence of thyroid gland at birth
33
Q

What is primary hypothyroidism caused by?

A

-atrophy of thyroid
-autoimmune thyroiditis-destruction of anitbodies against cellular components of thyroid (hashimotos disease)
-goiterois hypothyroidism (block of T3 and T4 synthesis)

34
Q

What can infantile hypothyroidism lead to?

A

-decreased growth and mental development, can develop dwarfism or cretinism (mental retardation)

35
Q

What are the 3 types of hyperthyroidism?

A
  1. primary hyperthyroidism-at level of thyroid gland
    2.secondary hyperthyroidism- at level of anterior pituitary gland, no negative feedback from increased T3/T4 levels to synthesize TSH
    3.tertiary hyperthyroidism- at level of hypothalamus- no negative feedback of high T3/T4 to decrease synthesis of thyrotropin releasing hormone (TRH)
36
Q

What are the causes of hyperthyroidism, what does constant stimulation lead to in primary thyroidism?

A
  1. toxic diffuse goiter, graves disease which is an autoimmune disease characterized by LATS (long acting thyroid stimulator), mimics T3 and T4 action
    -constant stimulation of LATS causes a goiter to create a toxic goiter
    2.thyroid cancer-synthesizing thyroid hormone independent of TSH
37
Q

What are treatments for hyperthyroidism?

A
  1. can do surgery +replacment therapy
    2.adminitration of radioactive iodide (destroys thyroid follicles)
    3.antithyroid drug like propylthiouracil (blocks addition of iodine to thyroiglobulin)

Phgy 210 (24 decks)

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