Intro to Endo Hormones [TRH] Flashcards

1
Q

What is endocrinology?

A

study of hormones secreted by endocrine glands, tissues and cells

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2
Q

What are the 3 types of hormones?

A
  1. peptide protein
  2. lipid
  3. non-peptide amino acid based
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3
Q

What is the cirulatory half life of hormones determined by?

A

metabolic modifications of the free (unbounded) hormone into inactive products by the liver and kidney

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4
Q

name 5 key facts about hormones and receptor interactions?

A
  1. free hormone binds free R to form complexes
  2. H-R binding is reversible
  3. R’s are saturable
  4. both H & R have varying levels of specificity
  5. H-R binding activates 2nd messengers +/- transcription in target cells
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5
Q

How is hormone activity terminated in the target cell?

A

H-R membrane complexes are endocytosed & degraded by proteosome and/or lysosome

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6
Q

What is the hierarchy of the endocrine system?

A
  1. hypothalamus
  2. pituitary gland

+/- 3rd endocrine gland

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7
Q

What are the releasing hormones secreted by the hypothalamus?

What are the inhibitory H’s secreted by the hypothalamus?

A

releasing:

  • GnRH
  • CRH
  • TRH
  • GHRH

inhibitory:

  • somatostatin
  • dopamine
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8
Q

what are the 2 major fxns of the hypothalamus?

A
  1. integrator of homeostatic & reproductive signals
  2. H secretion that regul8s ant. pituitary prodxn & secretion

(some neurons of hypoT extend into post. pit to release H there too)

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9
Q

name the parts of the pituitary gland?

A
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10
Q

HOw does the hypoT control the post. pit?

What is the advantage of this?

A

hypoT neurons extend into the post. pit and produce/release oxytocin & ADH

  • H’s are released into post. pit & immediately enter general circulation

***advantage: target cells see stimulatory H very fast!!

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11
Q

Describe the basic outline/pathway of H travel thru the Hypophyseal portal system [ant. pit]

A

HypoT secrete H [releasing or inhibitory] into hypoT-hypophyseal portal system

  • portals bathe ant. pit cells w/ H –> binds
  • ant. pit cells release their H’s –> act on 3rd endocrine gland [this doesnt always happen]
  • 3rd endo H acts on target cells
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12
Q

What is the MC method of regulating H secretion?

What is the other RARE method?

A

Negative feedback: MC

-limits amt of H released

POsitive feedback: rare

-reinforcing “snowball’ effect–> more H secreted!

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13
Q

How are peptide H’s usually produced [in what form]?

A

usually produced as a proH–>needs to be cleaved/activated

ex: proinsulin–> insulin & C-peptide

other ex’s: TSH, LH, FSH

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14
Q

What are 2 types of lipid derived H’s?

A
  1. Eicosanoids [PGE]
  2. Steroid H’s [estrogen]
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15
Q

What 3 subclasses of H’s are formed from amino-acid derived H’s?

A
  1. thyroid H’s [T4]
  2. Catecholamines [Epi]
  3. tryptophan derivitives [melatonin]
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16
Q

How are steroid H’s synthesized & secreted?

How do steroid H’s traverse cell membranes?

A

Derived from cholesterol [lipid]–>NOT H20 soluble

  • enzyme in SER & golgi convert to final product
  • produced & secreted W/O storage!
  • bound to carrier/transport proteins in serum
  • free H [released from carrier] enters target cell

**they get thru cell membranes via moving down their [] gradients

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17
Q

What is significantly unique about Eicosanoid H’s?

What 3 classes of enzymes produce eicosanoid H’s?

A

*They are biologically active lipid mediators*

enzymes:

  • COx-1 & 2–> PG’s & TXA’s
  • Lipoxygenase–> LTE’s
  • cypP450 mono-oxygenases–> epoxides
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18
Q

Where do eicosanoids tend to work?

A

tend to occur @ low levels & work locally

and signal thru GPCR [transmembrane]

***note: they are drug targets!!!

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19
Q

Catecholamines are synthesized and stored how?

which other class of H’s are they most similar to?

A

**similar to protein H –> bind GPCR

synth/store:

  • prduced in neurons
  • pkged in vesicles for release on demand
20
Q

Thyroid H’s are synthesized and stored how?

Which other class of H’s are they most similar to?

A

**similar to steroids–> bind R’s of nuclear superfamily

Synth/store:

  • synth on protein backbone
  • processed in lysosomes
  • produxn is controlled by enzyme activity and Iodine availability
  • secretion is based on diffusion down [] gradient
21
Q

What downregulates H signaling [general]?

2 main ones

A
  • decrease R #
  • increase degradation of H in cells
22
Q

What upregulates H’s [general]?

2 main things

A
  • increase R #
  • decrease degradation of H in cells
23
Q

Protein H’s bind what type of R?

A

Protein H’s bind protein R’s on th target cell membrane [cuz cant go thru em]

  • R may be tyrosine kinase–> signals passed via phosphorylation cascade
  • protein H-R binding may activate 1+ 2nd messenger signaling network
    • Gproteins, adenylate cyclase, IP3, Ca/calmodulin etc.
24
Q

3 ways Gproteins transduce signal cascades

A
  1. stimulate adenylate cyclase –> makes cAMP
  2. increase cytoplasmic Ca++ (released from intracellular stores)
  3. activate PLC –>makes DAG & IP3
    • DAG–> induces PKC activity
    • IP3–> induces Ca++ release from ER
25
Q

What are most protein H R’s coupled with?

A

Gs-alpha stimulatory subunit!!!

  • GS-alpha is part of ayB subunit–. ultimately activates cAMP
  • cAMP activates PKA
  • PKA phosphorylates downstream targets
26
Q

What is the action of ADH?

A

promotes water retention by the kidneys

-via V2 cells of post.pit

27
Q

What is GHRH’s action?

A

stimulates synthesis & release of GH

-somatotroph cells of ant.pit

28
Q

What is CRH’s action?

what cells are involved in it’s release?

A
  • stimulates synth & release of ACTH
  • cells: ant. pit
29
Q

What is ACTH’s action?

what cells are involved in it’s release?

A
  • stimulates synth & release of cortisol
    • released via zona fasiculata of adrenal cortex in kidneys
30
Q

What is TSH’s action?

what cells are involved in it’s release?

A
  • stimulates synth & release of majority of T4
    • via thyroid gland
31
Q

What is LH’s action?

A
  • stimulates follicular maturation & ovulation in women
  • stimulates testosterone prodxn & spermatogenesis in males
32
Q

What is FSH’s action?

what cells are involved in it’s release?

A
  • stimulates follicular development in women
  • spermatogenesis in males
33
Q

What is PTH’s action?

what cells are involved in it’s release?

A
  • increases blood Ca++ levels
    • via PTH1 R in kidneys & bones OR
    • via PTH2 R in CNS & bones & kidneys
34
Q

What is calcitonin’s action?

what cells are involved in it’s release?

A
  • decreases blood Ca++ levels
    • via calcitonin R in intestines, bones, kidneys and brain
35
Q

What is glucagon’s action?

what cells are involved in it’s release?

A
  • stimulates glycogen breakdown in liver
36
Q

What is hCG’s action?

A
  • promotes cellular differentiation & is potentially involved in apoptosis
37
Q

What is Epi’s action?

what cells are involved in it’s release?

A
  • stimulates glycogenolysis
    • released from adrenal medulla [fasting st8 or stressful situation]
38
Q

What H’s work thru Nuclear R Superfamilies?

A
  • steroid & thyroid H’s
  • some lipid H’s

***these NRS’s are transcription factors!!

39
Q

Describe Steroid R signaling

A
40
Q

What is homodimerization of steroid H-R complexes necessary for?

A

needed for DNA binding at specific Hormone-Response-Elements [HRE’s]

41
Q

What do we need to know about nuclear superfamilies?

A

–Thyroid supplementation targets T3R
–Glucocorticoid therapies targets GR
–Type II Diabetes treatment targets PPAR
–Vitamin D responses due to VDR
–Progesterone therapy during pregnancy targets PGR

42
Q

What/how does the body get rid of H?

A
  • liver/kidney degradation of circulating H
    • carrier proteins protect & extend half lives of H’s
  • urinary or biliary excretion [depends on H20 solubility]
  • cell uptake & degradation following R signaling
43
Q

In what pattern are hypothalamic H’s secreted?

why?

A

PULSATILE!!! [circadian rhythm]

  • prevents desensitization of downstream R’s
44
Q

What do these terms mean in relation to H activity?

  • additive or synergistic
  • permissive
  • antagonistic
A
  • additive/synergistic: multiple H’s can have larger effect
  • permissive: some H’s allow other H to exert its full effect
  • antagonistic: diminish effect of other H’s
45
Q

How long does it take to respond to protein H’s versus steroid H’s?

A

proteins: minutes after binding R
steroids: slow, hours after R binding