Stress Hormones

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Last updated 8:09 PM on 10/5/26
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23 Terms

1
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How does GH promote tissue growth?

It increases amino-acid uptake and protein synthesis, supporting growth—especially in muscle and bone.

It also stimulates liver production of IGF-1/somatomedins, which mediate many growth effects.

2
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What organs are sensitive to GH?

The skeletal muscles and bones

3
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How do these muscles explain a growth spurt?

When sex hormones rise during puberty, that causes an increase in GH which supports growth hence we have a growth spurt.

4
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What effect does GH have on fatty acids?

Gh will mobilise fatty acids as energy substrates and stumulate muscle cells to use fatty acids as energy substrates.

5
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When does GH secretion increase?

  • Sleep, especially at night

  • Exercise

  • Fasting

  • Stress

  • Puberty


6
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What stimulates and inhibits GH release?

Hypothalamic GHRH/GRH stimulates release from the anterior pituitary; somatostatin/GH-IH inhibits it.

7
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GRH, when is this high?

The circardian rythm modulates its release and it will be high during the night.

8
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How is GH controlled by negative feedback?

IGF-1/somatomedins inhibit further GH secretion through feedback to the pituitary and hypothalamus. High blood glucose also suppresses GH release.


9
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How does dwarfism occur?

  • GH deficiency but also by bone deformations (pituitary dwarfism → short stature and normal body proportions)

  • May also have a psycological cause.


10
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The HPA Axis Regulation

  • The stimulus is stress and the circadian rhythm modulates CRH release.

  • CRM + AVP causes ACTH release and work synergistically


11
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Cortisol production in adrenal glands in HPA Axis and negative feedback.

Adrenal gland in kidney release cortisol. The primary function of the cortisol is to convert long-term energy substrates into readily available substrates like glucose.

Negative feedback will occur at the pituitary, hypothalamus and hippocampus.

12
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What kinds of croticoids do the adrenals secrete?

  • Glucocorticoids release is stimulated by ACTH in response to stress

  • Mineralocorticoids (aldosterone) release is stimulated by angiotensin II in response to low blood volume and promotes reabsorption of sodium and water and secretion of potassium in the kidneys.


13
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What are the different corticosteroid receptors?

  • Mineralcorticoid Receptor: high affinity and high expression in limbic structures

  • Glucocorticoid Receptor: low affinity, wiely expressed, inhibits CRH and VP gene expression.

  • Co-expression in hippocamus: detection of cortisol level.


14
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What is stress?

  • Any condition that disrupts homeostasis

  • Which results in:

    • specific stress response (homeostatic adjustments like body temperature)

    • generalised stress response (activation of HPA axis upon prolonged stress states)

    • psychological stress often in a alearned condition towards psycological stressors that do not cause an immediate disruption of homeostatis

    • psycological stress results in emotional states like anxiety, fear, frustration or depression.


15
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What is the generalised stress response?

Stress → adrenaline first → cortisol/other hormones for prolonged stress → exhaustion if stress persists.

16
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Addisons and Cushings disease

  • Addison’s disease: too little cortisol → fatigue, muscle weakness, poor stress tolerance.

  • Cushing’s disease/syndrome: too much cortisol → protein and fat breakdown, central/upper-body fat accumulation, thin limbs


17
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The HPT axis regulation and stimulus

The primary stimulus is low body temoerature and the circadian rhythm modulates TRH release, which is high at night.


18
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Primary function of thyroid glands and negative feedback?

  • Fuc=nction is to increasee oxygen consumption and metabolic heat production

  • Negative feedback occurs at pituitary and hypothalamus


19
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Thyroid biosynthesis

T4 is mainly released by the thyroid, but T3 is the more active form. T4 is converted to T3 in tissues such as liver and kidney. Thyroid hormone increases oxygen consumption, ATP turnover, metabolic rate, and heat production.

20
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How do thyroid hormone receptors regulate gene expression?

Thyroid hormone receptors are intracellular members of the steroid-receptor family. They form heterodimers with retinoid X receptors (RXR) and bind DNA even without T3.

When T3 binds the receptor, transcription of target genes is activated especially genes encoding enzymes involved in energy use and ATP production.

21
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What are the causes, symptoms, and treatment of hypothyroidism (myxoedema)?

  • Hypothyroidism results from too little thyroid hormone, commonly due to autoimmune thyroid destruction (primary hypothyroidism) or insufficient TSH release (secondary hypothyroidism).

  • It causes low metabolic rate, cold intolerance, fatigue, muscle weakness, low body temperature, and depression.

  • Treatment is thyroid-hormone replacement, usually levothyroxine


22
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What are the causes, symptoms, and treatment of Graves’ disease?

Graves’ disease is an autoimmune cause of hyperthyroidism in which the thyroid is overactive.

It causes high metabolic rate, heat intolerance, weight loss, restlessness, goitre, and often protruding eyes.

Treatment may use radioactive iodine or surgery, followed by thyroid-hormone replacement when needed

23
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Why are thyroid hormones essential during early fetal brain development?

Before approximately pregnancy week 17, fetal brain development depends strongly on maternal T4.

Insufficient maternal thyroid hormone can impair synapse formation, myelination, and axonal transport, causing severe neurodevelopmental impairment.

Adequate maternal iodine intake supports thyroid-hormone synthesis and prevention.