Endocrine System Intro Flashcards

1
Q

Definition of Endocrine System

A
  • INTEGRATES + CONTROLS ORGAN FUNCTION
    • VIA CHEMICAL/HORMONAL SECRETION from CELLS, TISSUE, GLANDS
    • CARRIED IN THE BLOOD to TARGET ORGANS = DISTAL from site of hormone synthesis, where target organ activity INFLUENCED○ FAST/SLOW RESPONSE
    • ENDOCRINE SYSTEM + NERVOUS SYSTEM = COMMUNICATES + CONTROLS ALL BODY FUNCTIONS
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2
Q

Different -crine Chemicals

A

Paracrine - act local to site of synthesis + don’t travel to distal sites

Autocrine - act on/in same cell that synthesises hormone

Exocrine - released from exocrine glands via ducts to external environment, incl. GIT

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3
Q

Endocrine Communication

A
  • HORMONES TRAVEL IN BLOOD TO TARGET ORGANS/TISSUES
    • THEY DETECT HORMONES BY PRESENCE OF SPECIFIC RECEPTORS (for that chemical on/in the cells)
    • Cannot respond to hormone if there are no receptors
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4
Q

Neural Communication

A
  • SIMILAR TO ENDOCRINE SYSTEM, BUT NEUROTRANSMITTER WORKS LOCALLY W/I SYNAPTIC CLEFT
    • ENDOCRINE + NERVOUS SYSTEMS CO-OPERATE INTIMATELY = PROVIDES FURTHER CONTROL, esp. for LONG-TERM PHENOMENA (e.g. growth)
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5
Q

Neuroendocrine Communication

A
  • ENDOCRINE + NERVOUS SYSTEMS COMBINE
    • NERVES RELEASE HORMONES = ENTERS BLOOD + TRAVEL TO TARGET CELLS
    • ALL HORMONES CIRCULATE THROUGH BLOOD, but RESPONSE to HORMONE IS SPECIFIC AS ONLY TARGET CELLS HAVE RECEPTORS FOR HORMONE
    • THE SAME HORMONE CAN HAVE MANY DIFF. EFFECTS IN DIFF. TARGET CELLS VIA DIFF. RECEPTORS EXPRESSED
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6
Q

Endocrine Systems

A

ENDOCRINE FUNCTION IN VARIOUS PHSYIOLOGICAL SYSTEMS:

* REPRODUCTIVE
* RENAL
* GI

& IS A DIFFUSE SYSTEM OF GLANDS:

* THYROID GLAND
* ADRENAL GLAND
* PITUITARY GLAND
* HYPOTHALAMUS
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7
Q

Features of Endocrine Hormone

A

Produced by a cell or group of cells

Secreted from those cells into the blood

Transported via the blood to distant targets

Exert their effects at very low concentrations (act in the range 10-9 -10-12 M)

Act by binding to receptors on target tissues

Have their action terminated, often via negative feedback loops.

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8
Q

Classification of Endocrine Hormones

A

Protein/Peptide Hormones (made from chains of amino acids)

Amine Hormones (made mainly from tyrosine, except melatonin - made from tryptophan)

Steroid Hormones (made from cholesterol)

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9
Q

Peptide Hormones (how are they made, stored, transported in the blood)

A
  • SYNTHESISED AS PREPROHORMONE BEFORE REQ.
    • CLEAVED into PROHORMONE + STORED IN VESICLES UNTIL REQ.
    • H2O soluble = no need for carrier proteins
    1. INITIAL PEPTIDE HORMONE is produced by RIBOSOMES = LARGE + INACTIVE PREPROHORMONE (may contain 1/multiple copies of active hormone)
    2. Then CLEAVED INTO PROHORMONES in ENDOPLASMIC RETICULUM (smaller + inactive proteins)
    3. PROHORMONES PACKAGED INTO VESICLES IN GOLGI APPARATUS W/ PROTEOLYTIC ENZYMES
    4. PROTEOLYTIC ENZYMES BREAK DOWN PROHORMONE = ACTIVE HORMONE + OTHER FRAGMENTS
    5. ACTIVE HORMONE + FRAGMENTS STORED IN VESICLES in ENDOCRINE CELLS UNTIL RELEASE TRIGGERED = THEN VESICLE CONTENTS RELEASED INTO PLASMA (CO-SECRETION)
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10
Q

Mechanism of Action of Peptide Hormones

A

Cannot diffuse into cell as lipophobic = bind to membrane bound receptors on target cell

• BINDING = FAST BIOLOGICAL RESPONSE (secs - mins)

	○ MODULATES G PROTEIN COUPLED RECEPTORS/TYROSINE KINASE LINKED SIGNALLING PATHWAYS

GCPR = activates 2nd messenger system and/or ion channels = modifies existing proteins = rapid response

Tyrosine Kinase Linked Receptor = alters gene expression - slower + longer lasting activity

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11
Q

Amine Hormones (how are they made, stored, transported in blood)

A

Made in advance & stored

2 types of amine hormones (from tyrosine):

Catecholamines = dopamine, norepinephrine, epinephrine; similar mechanism of action to peptide hormones (hydrophilic)

Thyroid Hormones = thyroxine (T4), Triiodothronine (T3); similar mechanism of action to steroid hormones (lipophilic)

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12
Q

Steroid Hormones (how are they made, stored, transported in blood)

A

• SYNTHESISED DIRECTLY AS NEEDED = NOT STORED

	○ Cannot store as steroid hormones v. lipophilic = cannot be retained w/i lipid membranes

	○ Once synthesised = diffuse across membrane into ISF & into blood

• POORLY H2O SOLUBLE = TRANSPORTED BOUND TO CARRIER PROTEINS e.g. ALBUMIN

	○ STABILISES TRANSPORT THROUGH PLASMA + PROTECTS THEM FROM ENZYMATIC DEGRADATION (increases half-life)
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13
Q

Which Organs are Steroid Hormones Produced by & Why Do They Produce Different Versions of Steroid Hormones?

A

Gonads (testes & ovaries) = sex steroids

Placenta = hCG, sex steroids

Kidney = Vitamin D3

Adrenal Cortex = corticosteroids

DIFF. CELLS HAVE DIFF. ENZYMES = SYNTHESISE DIFF. DERIVATIVE OF CHOLESTEROL - this is why excess steroid hormones can have crossover effects

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14
Q

Physiological Activity of Steroid Hormones (how much of circulating steroid hormones actually have an effect)

A
  • SMALL AMOUNT OF UNBOUND FREE STEROID/THYROID HORMONE IN PLASMA
    • ONLY FREE HORMONE CAN DIFFUSE ACROSS CAPILLARY WALLS + CAUSE ACTION○ FREE HORMONE : HORMONE-PROTEIN COMPLEX = much MORE IN FAVOUR of BOUND/COMPLEXED HORMONE
    • In health = USUALLY LVLS OF FREE HORMONE CONSTANT, but AS FREE HORMONE TAKEN UP = MORE HORMONE RELEASED BY CARRIERS
      ○ FREE HORMONE + COMPLEXED HORMONE = TOTAL PLASMA [HORMONE]
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15
Q

Affecting Hormone Secretion

A

○ MOST ENDOCRINE PATHWAYS = SECRETION RESPONSIVE TO -VE FEEDBACK REFLEXES (e.g. parthyroid hormone secretion decreases w/ increasing plasma [Ca2+])

	○ SOME ENDOCRINE PATHWAYS ALSO RESPOND TO NEURAL FEEDBACK LOOPS (e.g. adrenaline; stimuli activates generalised symp. discharge & symp. fibres to adrenal medulla, not so much -ve feedback loop as hormone secretion decreased when stimuli goes)

	○ SOME HORMONE SECRETION SUBJECT TO MULTIPLE CONTROL MECHANISMS (e.g. insulin - plasma [glucose], ANS activity, food presence in gut, additional hormones like glucagon)
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16
Q

Other Factors Impacting Endocrine Function (disruption of hormonal lvls)

A

• [NORMAL PLASMA HORMONE] DISRUPTED = HOMEOSTATIC RERSPONSES INITIATED TO REDUCE IMPACT ON END FUNCTION

	○ PROLONGED EXPOSURE TO LOW HORMONE [HORMONE]PLASMA = UP-REGULATION of RECEPTOR NO. = INCREASED TISSUE SENSITIVITY TO HORMONE

	○ PROLOGED EXPOSURE TO HIGH HORMONE [HORMONE]PLASMA = DOWN-REGULATION of RECEPTOR NO. = DECREASED TISSUE SENSITIVITY TO HORMONE

	○ This can affect HORMONE'S OWN RECEPTORS + RECEPTORS FOR OTHER HORMONES = PERMISSIVE/ANTAGONISTIC EFFECTS
17
Q

Permissive Effects

A

PRESENCE OF ONE HORMONE ENHANCED EFFECT OF ANOTHER e.g. thyroid hormone increased epinephrine receptors, allowing epinephrine to have greater effect on lipolysis

18
Q

Antagonistic Effects

A

PRESENCE OF ONE HORMONE REDUCES EFFECT OF ANOTHER e.g. growth hormone impairs response to insulin by reducing insulin receptors

19
Q

Why are clinical lvls of hormones have to be analysed carefully?

A
  • MOST HORMONES RELEASED IN SHORT BURSTS = CONC. VARIES WIDELY = THEREFORE, SINGLE VALUE POSS. MISLEADING
    • 24HR MONITORING MAY BE REQ. TO GIVE TRUE PICTURE