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C16 7-11 Flashcards

1
Q

What are the two major mechanisms of hormone action?

A

Water soluble hormones - Plasma membrane receptors/second messenger

Lipid soluble hormones - Intracellular receptors/direct gene activation

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2
Q

5 Steps in cyclic AMP signaling mechanism

A
  1. 1st messenger hormone binds to receptor on plasma membrane
  2. Receptor activates G proteins
    (hormone binding causes receptor to change shape allowing it to bind to inactive G protein, GDP is displaced by GTP turning it on)
  3. G protein activates adenylate cyclase
    (activated G protein binds to effector enzyme ac in the plasma membrane)
  4. Adenylate cyclase converts ATP to cyclic AMP
    (as long as the G protein is bound)
  5. cAMP activates protein kinases
    (cAMP diffuses throughout the cell triggering chemical reactions by activating protein kinases.
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3
Q

5 Steps in direct gene activation

A
  1. Steroid hormone diffuses through the plasma membrane and binds to an intracellular receptor.
  2. The receptor/hormone complex enter the nucleus.
  3. The receptor/hormone complex binds a hormone response element (a specific DNA sequence).
  4. Binding initiates transcription of the gene to mRNA.
  5. mRNA directs protein synthesis
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4
Q

What is a protein kinase?

A

Enzymes that phosphorylate (add a phosphate group to) various proteins many of which are other enzymes. Phosphorylation can either inhibit or activate proteins.

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5
Q

Explain the amplification or signal cascade of cyclic AMP.

A

Single hormone bound receptor can activate many G proteins AND when the activated G protein is bound to Adenylate cyclase, many ATP can be converted to cAMP AND a single kinase enzyme can catalyze hundreds of reactions.

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6
Q

What is the significance of phosphodiesterase?

A

Intracellular enzyme that Degrades cAMP.

Happens quickly and prevents the need for a extracellular control to stop the hormones activity.

Because of the amplification effect, most hormones need only be present briefly for results.

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7
Q

What are receptors made of (usually)?

A

Glycoproteins

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8
Q

What are the effects of hormones on target cells?

A 
Change membrane permeability, 
protein synthesis, 
enzymatic activity, 
secretory activity, 
mitosis.
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9
Q

What are the factors that effect target cell specificity?

A

Blood levels of hormone.
Number of hormone receptors.
Affinity of hormone and receptor (how perfect is the fit?) Interactions of other hormones.

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10
Q

Down regulation

A

Decrease in the number of receptors.

Can result from either a decrease in the number of receptors or decrease in binding affinity.

Basis for drug tolerance.

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11
Q

Up regulation

A

Increase in number of receptors.

Initial up-reg may be a cellular response to rising levels of hormones and then the cell may attemp to down regulate.

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12
Q

How is hormone release stimulated/regulated - (reflex mechanisms?)

A

Humoral, neural, hormonal.

Humoral - secretions in direct response to changing levels of of ions and nutrients in the blood/fluid
(ex. PTH in response to low blood calcium, ex2 Glucose, ex3 calcium).

Neural - nerve fibers stimulate release of hormones
(ex. Symp NS stimulates adrenal medulla to release NE/E, ex2 OXT).

Hormonal - response to hormones produced by other endocrine glands
(ex. hypothalamus regulating secretion of ant.pituitary hormones.)

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13
Q

What controls the release of hormones?

A

Neg feedback,

pos fb,

endocrine gland stimuli, (humoral/hormonal/neural)

nervous system modulation (NS always rules over endocrine)

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14
Q

What are the 3 types of interactions of different hormones acting on the same cell?

A

Permisiveness, synergism, antagonism

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15
Q

Permissiveness

A

When one hormone cannot exert its full effects without another hormone being present.

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16
Q

Synergism

A

More than one hormone produces the same effects at the target cell and their combined effects are amplified.

17
Q

Antagonism

A

One hormone opposes the action of another.

18
Q

How are different hormones transported?

A

Lipid soluble (steroid/thyroid/cacitriol) hormones do not dissolve in blood and require carrier molecules (usually water-soluble proteins from liver, they can be selective or non-selective.) albumin!!

Water soluble hormones circulate without carriers.

19
Q

What does the concentration of a circulating hormone reflect?

A
  1. its rate of release

2. the speed at which it is inactivated and removed from the body.

20
Q

Why does the half-life of hormones vary?

A

Different methods of removal. Some hormones are rapidly degraded by enzymes in their target cells. Others are removed from the blood by the kidneys or liver and the body excretes their breakdown products in urine.

21
Q

Half-life?

A

Length of time for a hormone’s blood level to decrease by half.

Shortest for water-soluble hormones (min to 1 hour), longer (days) for steroid hormones.

22
Q

3 benefits of transport protein?

A
  1. Makes hormone more water soluble
  2. Decreases elimination by liver/kidney (increases half life)
  3. Provides ready reserve of free (absorbable) hormone
23
Q

C+C H2O soluble Lipid soluble

Ex.
Loc
Mech
1/2
Trans
Result
A
  1. Example: Amino acid based/-TH Steroid based/+TH
  2. Location of receptor Plasma membrane Intracellular
  3. Mech of action 2nd messenger Direct gene activation
  4. Half Life Short Long
  5. Transport Dissolved in plasma Transport/carrier proteins
  6. End result of mech. of action Metabotropic/activates protein kinase Transcription/translation
24
Q

General patterns of hormone secretion? 3

A
  1. Tonic - only tweaked if environmental stressor (TH, temp change)
  2. Acute - short bursts (E/NE)
  3. Episodic - periodic (reproductive)
25
Q

Permissiveness examples?

A
  1. TH/Repro hormones - TH alone/no development, Repro alone/delayed development, TH & Repro = full development
  2. PRL/OXT - one can’t function without other
  3. Epi/TH - in lipolysis TH increases Beta 3 receptors
  4. Progesterone/Estrogen - Estrogen stimulation increases the number of progesterone receptors
26
Q

Synergism examples?

A
  1. Epi/Glucogon - E alone = 5 mg, Glu alone = 10mg, E +Glu = 22mg
  2. FSH/Testosterone - spermatogenesis
27
Q

Antagonism examples

A
  1. PTH/Calcitonin
  2. Insulin/Glucogen
  3. Progesterone inhibits uterine responsiveness to estrogen.
28
Q

Direct gene activation vs. 2nd messenger

A

DGA - Mrna

2nd messenger - cAMP, G protein, PIP2, faster

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