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physiology > endocrine > Flashcards

endocrine Flashcards

1
Q

what are hormones?

A

are chemical messengers that are secreted from one cell, travel through the bloodstream and affect another cell in another part of the body.
- Used for homeostatic.

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2
Q

examples of the endocrine system at work.

A

Nutrient uptake
- Every time you eat your endocrine system are working to ensure your glucose is stable
Growth
- When to grow and how long, how much
Stress.
- Can’t have too much stress.

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3
Q

endocrine communication loop.

A

stimulus - hormone release into the blood - hormone binds to a receptor in a distant cell - distant cell responds to stimulus.
example- Stress (before an exam) -> adrenaline -> adernaine binds to specific heart cells -> in those heart cells it increases heartbeat

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4
Q

organs of the endocrine.

A

hypothalamus, pituitary gland, thyroid gland, adrenal glands, pancreas, pineal gland and parathyroid glands.

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5
Q

What are hormones made of?

A

Amino acids or cholesterol.
You eat building blocks for hormones. (eggs 26g proteins, 740mg cholesterol)

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6
Q

what makes a hormone know what to bind to?

A

Hormones ONLY bind to receptors specifically designed to receive it.
The receptors are only expressed in specific areas in the body. (square only goes to square)

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7
Q

what happens to hormones after use.

A
  • It is removed, broken down and recycled.
  • OR excreted in swear or urine.
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8
Q

what are pregnancy tests looking for?

A

detecting human chorionic gonadotrophin (hCG) in the urine.

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9
Q

how do lipid soluble hormones travel?

A

bound to carrier protein.

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10
Q

how do water-soluble hormones travel?

A

unbound/soluble.

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11
Q

chemical classification of water soluble hormones

A

some amines (catecholamines) , peptides and proteins.

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12
Q

chemical classification of lipid soluble hormones?

A

some amines (thyroid hormones) and steroids (cholesterol based).

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13
Q

receptors of water soluble hormones.

A

cell membrane. only bind to the outside of the cell.

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14
Q

receptors of lipid-soluble hormones.

A

intracellular. because the cell wall is made of lipids.

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15
Q

Action mechanism.
Water soluble

A

– activation of 2nd messengers to amplify hormone response. Remain outside the cell and the thing inside the cell to do the job.
Internal part amplifies the inside one.
Can make the response faster and bigger.

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16
Q

Action mechanism
Fat soluble

A

once it binds to the intrecellular receptor this enters the nucleas. to cause alteration of gene transcription (to make new proteins).

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17
Q

response time for lipid soluble hormones.

A

slow - hours to days.

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18
Q

response time for water soluble hormones.

A

fast.

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19
Q

what does the pituitary gland do?

A

master gland, all things that are important for survival. Connected to the brain through blood vessels and neurons

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20
Q

Posterior pituitary

A

Hypothalamus to posterior pituitary = axon connection
Posterior pituitary hormones made in hypothalamus
…travel down axons
…then stored in axon terminals
Action potentials cause hormone release from the nerve endings from posterior pituitary.

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21
Q

Anterior pituitary

A

Hypothalamus to anterior pituitary = blood vessel connection.
Releasing/inhibiting hormones made in hypothalamus
…travel in blood
…to affect anterior pituitary cells
…to release or inhibit release of anterior pituitary hormones
Two tired system.

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22
Q

posterior

A
  • Oxytocin
  • Anti-diuretic hormone neurons
    Release of OXT and ADH from pos pituitary
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23
Q

the stress axis.

A

Hypothalamus CRH -> Anterior pituitary (promote) ACTH -> peripheral target tissues adrenaline glad (cortisol).

24
Q

The thyroid hormone axis

A

Hypothalamus TRH-> Anterior pituitary (promote) TSH ->thyroid gland.

25
Q

Reproductive

A

Hypothalamus GnRH -> Anterior pituitary (promote) LH and FSH -> peripheral target tissues gonads estrogen, progesterone and testosterone.

26
Q

growth

A

Hypothalamus GHRH and GHIH -> Anterior pituitary (promote and inhibit) GH -> peripheral target tissues liver and other (cortisol).

27
Q

Prolactin axis – prolactin is persistently inhibited.

A

Hypothalamus DA -> Anterior pituitary (inhibit) PRL -> peripheral target tissues breast milk production.

28
Q

when do we have peak GHRH.

A

during deep sleep. then after exercise, and after 3 hours of a meal.

29
Q

GH growth effects.

A

GH stimulates protein synthesis in muscle. IGF-1 (from liver) stimulates the growth of bones, muscles and other tissues.

30
Q

GH metabolic effects

A

GH actions in the liver increase blood glucose. GH increases the breakdown adipose tissue to free fatty acids. Fuel mobilisation. Used to turned into glucose.

31
Q

how is GH regulated?

A

Negative Feedback Loop Both IGF-1 and GH inhibit the hormones that control their release. Produce something and then it comes to a certain level to then tell the body to stop. RED.
Growth Hormone Inhibiting Hormone (GHIH), AKA Somatostatin is stimulated by IGF-1 to inhibit downstream GH release. IGF-1 green.

32
Q

thyroid hormone.

A

Thyroid hormone controls cellular metabolism in every cell of your body Increases metabolic rate: the rate at which your body uses calories (energy)
Increases growth & development
Regulates heart rate
Regulates body temperature
Regulates muscle contraction.

33
Q

what is Hypothyroidism

A

decreased cellular metabolism

34
Q

Hyperthyroidism

A

increased cellular metabolism.

35
Q

thyroid hormone negative feedback loop.

A

TH inhibits both TRH and TSH release. Detected by cells, inhibiting release.
2. Removal of stimulus i.e. stop exercising.

36
Q

stress axis what is it imporatnt for?

A

Cortisol is important to survival during stress. Cortisol is a glucocorticoid.
The term glucocorticoid comes from the ability of cortisol to generate glucose in the liver from other body substrates.
It allows you to survive stress and fasting by mobilizing fuels.

37
Q

Glucocorticoid

A

regulates the amount of glucose available for your cells.

38
Q

what does cortisol target?

A

Muscle: Protein is broken down for fuel Less glucose uptake
Liver: More glucose is produced from fuels
Adipose Tissue: Fat is broken down for fuel Less glucose uptake.

39
Q

how is cortisol benefical or not benefical?

A

Beneficial: Fight or flight response to acute stress.
Not beneficial: Chronic, unmanaged stress. Breaks down muscle,

40
Q

negative feedback loop of stress.

A
  1. Negative Feedback Loop Both Cortisol and adrenocortcotrophin hormone(ACTH) inhibit the hormones that control their release.

2: Remove the stress stimulus

41
Q

four hormones of the integrated stress response.

A
  1. Cortisol 2. Anti-diruetic hormone (ADH) 3. Adrenaline (Epinephrine) 4. Noradrenaline (Norepinephrine)
42
Q

three systems of the integrated stress response.

A
  1. Indirect control through releasing hormones (CRH-ACTH-cortisol) 2. Direct release of hormone in posterior pituitary (ADH) 3. Direct control by nervous system (Adrenaline/Noradenaline)
43
Q

where does ADH come from?

A

Anti-Diuretic Hormone (ADH) neurons in the hypothalamus send their axons into the posterior pituitary gland. * ADH is released from nerve terminals in the posterior pituitary gland * ADH enters the bloodstream to reach distant target tissues

44
Q

targets of the ADH.

A

Kidneys
- Stimulate kidney cells to reabsorb water back into the blood * Increases blood volume * Increases blood pressure
Blood vessels
- Vasoconstriction * Increases blood pressure.

45
Q

what are the catecholamines.

A

Adrenaline (epinephrine) and Nor-adrenaline (Nor-epinephrine) are catecholamine hormones that are released from the adrenal medulla (middle of the adrenal gland). they have a fast response to stress. water-soluble hormones.

46
Q

how is catecholamines stimulised to release?

A
  • Catecholamine release is stimulated by neurons of the sympathetic nervous system (direct control by the nervous system).
  • Adrenaline and noradrenaline are secreted with stress and during exercise.
47
Q

Adreanline/Noradrenalone targets

A

Heart - Increase heart rate, increased strength of heart contraction
Blood vessels - Dilation and constriction of vessels to direct blood flow
Lungs - airway dilation.

48
Q

metabolic tragets of Adreanline/Noradrenalone.

A

Muscle: Glycogen breakdown for fuel
Adipose tissue: Fat is broken down for fuel
Liver: More glucose is produced from fuels, glycogen breakdown for fuel

49
Q

how adrenaline affects sport and exercise science.

A
  • Adrenaline binds to both alpha and beta catecholamine receptors
  • Receptors can drive different effects (e.g., adrenaline can cause vasoconstriction (alpha) or vasodilation (beta)
  • Drugs that block or enhance these receptors are banned in competitive sports.
50
Q

what are chemicals called that stimulate or increase the function of adrenergic receptors?

A

Called sympathomimetics because they cause similar effects to catecholamines (e.g. adrenaline).

51
Q

pancreas: insulin and glucagon.

A
  • High blood glucose stimulates insulin secretion from beta cells.
  • Low blood glucose stimulates glucagon secretion from alpha cells.
52
Q

what is Glycogenolysis

A

liberating glucose

53
Q

Gluconeogenesis

A

synthesizing glucose

54
Q

what does insulin secretion cause?

A

in the adipocytes and muscle - increase glucose uptake.
liver - cessation of glucose output; net glucose uptake.

55
Q

what does glucagon secretion cause?

A

liver - increase glycogenolysis.
increase gluconeogenesis
increase ketone synthetsis.

56
Q

difference in diabetes

A

Type 1 diabetes: a loss of beta cells in the pancreas leading to a deficiency in insulin.
Type 2 diabetes: due to insulin resistance or reduced insulin sensitivity.

physiology (11 decks)

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