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Endocrine Signaling and Systems > Endocrine signalling > Flashcards

Endocrine signalling Flashcards

1
Q

What are some functions of exocrine glands?

A
  • Ductless
  • release hormones into surrounding fluid
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2
Q

What are some functions of endocrine glands?

A
  • Ducts
  • substances (non-hormonal) travel along these to a surface
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3
Q

What are neurohormones?

A

Hormone produced by nerve cells and secreted into the circulation

–e.g. vasopressin or noradrenaline

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4
Q

What factors stimulate hormone release?

A

HORMONAL:

stim. from other hormones (tropic ‘nourishing’ hormones)

NEURAL:

stim. from nerve fibres

HUMORAL:

level of substances in blood (e.g. ions)

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5
Q

What does hormone interaction with target cells depend on?

A

– Amount of hormone (circulating in blood)

– Bond affinity (betw. R and hormone)

– # of R’s (for hormone)

Up-regulation

Down -regulation

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6
Q

What is up-regulation?

A

Target cells form MORE R’s in response to hormone

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7
Q

What is down-regulation?

A

Target cells LOSE R’s in response to hormone

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8
Q

What are the 3 types of hormone combinations that can influence the response at target cells?

A

Permissiveness

Synergism

Antagonism

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9
Q

What is permissiveness?

A

A hormone must be present to permit another hormones effects

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10
Q

What is synergism?

A

Combination of hormones produces an effect greater than sum of separate effects

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11
Q

What is antagonism?

A

A hormone decreases effectiveness of another hormone

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12
Q
A
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13
Q

What is (primary and secondary) endocrine dysfunction?

A

Result of abnormal hormone plasma concentrations (rates of secretion)

Primary - abnormality within gland

Secondary - gland normal, but too little/much stim.

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14
Q

How is endocrine dysfunction normally treated?

A

Medications

(may replace hormones or cause atropy of target gland)

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15
Q

What causes endocrine dysfunction?

A

Causes can be complex!

–Downregulation of R’s (e.g. hyperinsulinemia)

–Problems with signal transduction (testicular feminisation syndrome)

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16
Q

What are the 3 main types of hormones, and where are they derived from?

A

PEPTIDES

(derived from chains of a.a.’s)

AMINES

(derived from a.a’s tyrosine & tryptophan)

STEROIDS

(derived from cholesterol)

17
Q

What are the 4 main characteristics of peptide hormones?

A

(Most common type of hormone)

–short half-life (only a few mins)

– Lipophobic (hydrophillic) –> transported freely in blood but can’t cross cell mem. [can’t diffuse into target cell])

– Stored in secretory vesciles!

(synthesised as prehormone (ER))

(modified to prohormone (Golgi))

(hormone release via secretory vesciles (regulated or not))

–effects usually very rapid

–cAMP or phosphoinositol are common 2nd messenger systems

–2nd messenger cascades lead to cascades & signal amplification

18
Q

What is signal amplification?

A

R-ligand complex activates an amplifier enzyme

THUS, results in a single signal molecule turning on many 2nd messengers

These signals regulate cellular activity:

  • enzymes
  • R’s
  • transporters
  • genes
  • protein synth.

etc.

19
Q

What are amine hormones?

A

–Small

–1-­‐2 a.a’s, benzene ring and an OH group.

Tyrosine → Catecholamine/Thyroid Hormones

Tryptophan → Melatonin

20
Q

What 2 classes of amine can be derived from Tyrosine?

A

CATECHOLAMINES

THYROID HORMONE

21
Q

What are the characteristics of catecholamines?

A

‘LIKE’ PEPTIDES!

[E.g. Dopamine

Noradrenaline

Adrenaline]

– Hydrophilic

–bound to carrier proteins (half)

–R’s @ cell surface

–activates 2nd messengers

–half-life a few mins

22
Q

What are the characteristics of thyroid hormones?

A

‘LIKE’ STEROIDS!

[E.g. T4, T3]

– Hydrophobic

–bound to carrier proteins

–intracellular R’s

–activates genes

–half-life a few days

23
Q

What are steroid hormones?

A

Lipids synth. (as needed) in smooth ER of gonads, adrenals & placenta

– derived from cholesterol (lipophilic/hydrophobic)

Enzymes in mitochondria and ER of tissues convert cholesterol into all other steroid hormones & intermediates

–for transport, needs to be BOUND to carrier proteins (extends half-life!)

– R’s are in CYTOPLASM, NUCLEUS or MEMBRANE

–effects target cells INTRACELLULARLY by activating target genes for protein synth.!

24
Q

How is cholesterol synthesised?

A

–Within cell (from acetate)

–Held in stores (lipid droplets)

–Taken up from plasma in low density lipoproteins (containing cholesterol)

Endocrine Signaling and Systems (7 decks)

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