Unit 5: Week 3 Flashcards

1
Q

What is a stimulus for a hormone?

A

Blood levels of hormones are managed by negative feedback loops.

An external or internal stimulus or low level of hormone can trigger the release of more hormones to correct an imbalance or reach equilibrium.

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2
Q

What is hormonal stimuli?

A

It’s the most common stimuli.

The endocrine gland is stimulated by tropic hormones. Hormones of the anterior pituitary gland are stimulated by tropic releasing and inhibiting hormones from the hypothalamus.

Different groups of neurosecretory cells produce different hormones. This leads to further release of tropic hormones from the pituitary gland for further hormonal stimulation.

This acts in negative feedback to inhibit the release of tropic hormones from the anterior pituitary and hypothalamus.

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3
Q

What is humoral stimuli?

A

Changing levels of extracellular fluid triggers hormonal release. Parathyroid hormone, calcitonin (thyroid gland) and insulin remain on humoral stimuli. Beta eyelid cells in pancreas.

  1. Blood calcium levels are picked up by receptors in the parathyroid gland which secrete parathyroid hormone
  2. This activates osteolsastic reabsorbtion of bone minerals and increased calcium levels in the blood.
  3. PTH has a further effect on kidneys and small intestine to decrease calcium excretion and increase calcium absorption, promoted by active vitamin D (calcitriol)(converted from vitamin d in the liver).
  4. The rise in calcium levels in the blood removes the stimulus and acts as a negative feedback loop on the parathyroid gland to inhibit PTH secretion.
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4
Q

What is neural stimuli?

A

Nerve impulses stimulate hormone release.
An example is that glands are under control of the sympathetic nervous system.

In response to short term stressors, the amygolia sends distress signals to the hypothalamus which in turn activates the sympathetic branch of the ANS.

The pre synaptic neuron doesn’t terminate at the chain ganglia and instead passes directly and synapses with chromafin cells in the medulla to release catecholamines norepinephrine and epinephrine.

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5
Q

What are some examples of posterior pituitary neurons being triggers by neural stimuli?

A

The magnocellular cell in the PVN secretes oxytocin/ADH.

These are packaged into vesicles and sent down on an unmyelinated axon to be secreted from axon terminals in the posterior pituitary gland.

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6
Q

How does positive feedback work in childbirth?

A
  1. Baby moves deeper into birth canal and stretches cervix.
  2. Nerve impluses are sent to the hypothalimus via neruons.
  3. Hypothalamus sends impulses to posterior pituitary, where oxytocin is stored.
  4. Oxytocin released into the blood to stimulate uterine muscle. The uterus contracts which results in the baby moving further down and causing more stretch stimuli.
  5. At birth, stretching of the cervix lessens and positive feedback cycle is broken.
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7
Q

What does antidiuretic hormone do?

A

Hypothalamic nuclei produce ADH.

Osmoreceptors detect high blood osmolarity and stimulate the posterior pituitary to release ADH into the blood.

ADH acts via the second messenger system on the collecting ducts and the distal convoluted tubule of the nephron. Acting on vasopressin 2 receptors to produce aquaphorin 2, to increase water permeability and increase water reabsorbtion.

This increases blood volume and decreases blood osmolarity closer to isotonic and acts as a negative feedback.

ADH can also stimulate vasoconstriction by binding on vasopressin 1 receptors on the surface of smooth muscle. Thirst is also stimulated by osmoreceptors in the hypothalamus picking up blood osmolarity levels.

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8
Q

What is the short term stress response?

A

Hypothalamus sends signals to the cell bodies of the preganglionic sympathetic fibres in the thoracolumbar portion of the spine. Presynaptic neurones pass through the chain ganglia and synapse directly with chromafin cells in an intramural ganglion. Astarcholin stimulates chromafin cells to convert tyrosine into epi/noraepi. Epi goes to the liver and binds with receptors to cause glycogenlysis (converting glycogen to glucose) and gluconeogenesis (glucose is formed from non-carbohydrates precurses eg glycerol, amino acids, lactic acids).

NorEpi can also go to the heart and interact with receptors to increase myogenic impulses of the SA node which increases heart rate and strength of contraction.

they both interact with blood vessels to cause vasoconstriction in the gut, kidneys and bladder, and vasodilation in the liver, skeletal muscle, brain and bronchials.

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9
Q

What is the long term stress response?

A

Long term stressors can be fever, hunger, stress. Neurosecretary cells release CRH. The hypothalamus releases CRH which stimulates the anterior pituitary to release ACTH.

ACTH is a weak stimulator for the zone glomerulosa, but a strong stimulator for the zone faciculaca (via the second messenger system). Cortisol is released which is a lipid soluble hormone, so it passes through the cell membrane of muscle tissue and acts on intercellular receptor (hormone receptor complex traves to the nucleus and stimulates cromatin to alter gene expression) to synthasise proteases, to release amino acids by cleaving protein bonds.

Similar process occurs in bone and adapose tissue which results in trygliceride being cleaved into fatty acids and glycerol. The liver uses these to undergo gluconeogenesis.

Cortisol increases sensitivity of adonergic receptors to increase the effects of epi/norepi. The cortisol stimulates the liver to undergo glycogenesis (store glucose and glycogen) but due to the overall effect of increased sensitivity of adonergic receptors there’s more glucose in the system. Cortisol inhibits the immune system from producing inflammatory cytoclines.

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