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Neuro > Neurohormones > Flashcards

Neurohormones Flashcards

1
Q

what are neurohormones?

A

produced by specialised nerve cells called neurosecretory cells and released into the blood rather than the synaptic space

  • diffuse out of capillaries and act on receptors
  • can have an effect on cells some distance away
  • can act as neurotransmitters or autocrine/paracrine messengers
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2
Q

a small amount of hormone released from a neurones can have what kind of effect?

A

a widespread effect all around the body

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3
Q

Nervous system (Neuron point to point communication) vs Endocrine (Neurohormone communication)

A

ENDOCRINE SYSTEM

  • Mediators travel within blood vessels
  • Utilises chemical mediators (hormones)
  • Slow communication
  • Effects can be long-lasting

NERVOUS SYSTEM

  • Signalling along nerve fibres
  • Transmission of electrical impulses
  • Fast communication
  • Effects are generally short-acting
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4
Q

name 3 types of hormones

A
  1. peptides/proteins
    - can be synthesised in a large precursor
    - can be post-transcriptionally modified
  2. amino acid derivatives
    - tyrosine derived
    - neurotransmitter that can also act as a hormone
  3. steroid hormones
    - derived from cholesterol
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5
Q

principal endocrine organs

A
  • hypothalamus
  • pituitary gland
  • thyroid gland
  • parathyroid gland
  • adrenal gland
  • pancreas
  • ovary
  • testes
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6
Q

anterior and posterior pituitary

A
  • there are neurons which basically project from the hypothalamus and release neurohormones directly in the portal system, and they are transported to the anterior pituitary, where they bind to receptors and cause a different neurohormones to be released into circulation
  • magnocellular neurons project from the hypothalamus directly to the posterior pituitary
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7
Q

different endocrine rhythms

A
  • circadian - 24 hr clock, GH, cortisol (cortisol levels highest in the morning)
  • pulsatile - periodicity longer than 24 hrs gonadotrophins
  • infradian - periodicity less than 24 hrs menstrual cycle
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8
Q

key nuclei involved with neurosecretory cells

A

medial pre-optic, the arcuate and the paraventricular nuclei

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9
Q

what causes cortisol release?

A

CRH, a peptide released directly in the capillary system, is transported to anterior pituitary and causes ACTH release. ACTH travels to adrenal cortex and induce the release of cortisol.

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10
Q

what causes thyroxin release?

A

TRH induces release of TSH from the anterior pituitary. TSH acts on thyroids and induces release of thyroxin.

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11
Q

what does the posterior pituitary release?

A

VP and oxytocin from magnocellular neurons

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12
Q

what are Parvocellular neurosecretory cells?

A
  • smallneuronsin the hypothalamic
  • axons of these cells project to themedian eminence, at the base of the brain, where the nerve terminals release peptides thehypothalamo-pituitary portal system
  • peptides carried to anterior pituitarygland, where they regulate the secretion of hormones into the systemic circulation
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13
Q

what is another name for growth hormone release inhibiting hormone? and what is its effect?

A

somatostatin

-inhibits GH release, VIP, glucagon, insulin, TSH

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14
Q

list the specialised cells of the anterior pit and their role?

A

gonadotroph cells - control LH/FSH secretion
somatotroph cells - control GH secretion
corticotroph cells - control ACTH secretion
thyrotroph cells - control TSH secretion
lactotroph cells - control prolactin secretion

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15
Q

ACTH

A

ACTH is derived from POMC

  • stress activates hypothalamic neurones to release CRH, stimulating pituitary corticotrophs to release ACTH
  • ACTH stimulates cortisol production from adrenal cortex, glucocorticoids and sex hormone production from zona fasiculata
  • Cortisol will induce a negative feedback effect, acting on cortisol receptors in the pituitary/hyp inhibiting CRH or ACTH release
  • There is a problem is cortisol is higher for a prolonged period of time eg. periods of chronic stress/repetitive exposure to stressful stimuli (eg. abuse)
  • as the HPA is hyperstimulated, which will lead to high levels of basal cortisol levels, leading to depression/anxiety disorders
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16
Q

TSH regulation

A

TRH - hypothalamus
portal system
TSH - pituitary

TSH acts on TSH receptors in the thyroid to release T3 and T4. T3 is more potent, deiodinase enzyme converts T4 to T3

huge surge of thyroxin = negative feedback - thyroxin receptors in the pituitary and hypothalamus inhibit TSH/TRH release

17
Q

prolactin

A

release by lactotrophs in anterior pit

  • increased in pregnancy and lactation
  • increases milk production
  • under the control of dopamine - released from the hypothalamus directly into blood circulation, and it inhibits prolactin release
18
Q

where are VP and oxytocin synthesised and released?

A

supraoptic and para ventricular nuclei in the hypothalamus, released in posterior pit

19
Q

Kidneys and hypothalamus

A

thirst
kidney starts releasing renin - cleaves angiotensinogen into Ang I.
Ang I converted into ang II, which causes vasoconstriction
Ang II acts on the subfornicular organ in the brain, giving a signal to release vasopressin from the pituitary (Subfornical organ projects to vasopressin cells in lateral hyp)

VP will induce thirst but will also act on the kidney to induce water retention

20
Q

mechanisms of action of peptide hormones?

A

eg. GH
peptide binding leads to receptor dimerisation, tyrosine kinase recruitment
-causes phosphorylation of target proteins, induce secondary messenger systems

21
Q

mechanisms of action of GPCR’s?

A
  • can be gs/gi/gq coupled
  • GTP exchange for GDP
  • gi/gs - stimulate or inhibit AC, cAMP, PKA. eg. TSH, ACTH
  • gq - phospholipase C, PIP2- DAG and IP3, eg. oxytocin and GnRH
22
Q

mechanisms of action of nuclear/cytoplasmic receptors?

A

eg. cortisol acts on nuclear receptors

cortisol has gets inside the cell because it’s lipophilic), binds to the nuclear receptor and translocates into the nucleus
-once inside the nucleus, the complex will bind to DNA to increase gene expression

23
Q

what does a pituitary adenoma cause?

A
  • too much GH - gigantism and acromegaly
  • hypogonadism
  • loss of visual field
  • too much ACTH, XS cortisol secretion, Cushings syndrome
  • hypopituitarism
  • too much PRL
24
Q

hypothyroidism

A
  • too little thyroid hormone
  • most common cause is Hashimoto’s disease
  • autoimmune disease where immune system makes antibodies to the thyroid
  • can cause mental retardation,
    slow growth, cold hands and feet, and lack
    of energy
25
Q

hyperthyroidism

A
  • graves’ disease, autoimmune disease
  • antibodies attack the thyroid gland and mimic
    TSH so the gland make too much thyroid hormone
  • occurs in women (20 – 50 with a family history of thyroid disease)
  • goitre (enlarged thyroid gland)
    -difficulty breathing and sleeping, anxiety, irritability, fatigue
  • rapid/irregular heartbeat, trembling fingers
  • pregnant women with uncontrolled Graves’ disease have greater risk of miscarriage, premature birth, and babies with low birth weight
  • Graves’ ophthalmopathy occurs if untreated, bulging eyes
26
Q

Adrenal insufficiency

A

Addison’s disease
-most common cause of primary AI is
autoimmune
-symptoms: fatigue, muscle weakness, decreased appetite, and weight loss, nausea, vomiting, and diarrhea, muscle and joint pain, low blood pressure, dizziness, low blood glucose, sweating, darkened skin on the face, neck, and back of the hands and irregular menstruation

27
Q

excessive adrenal secretion

A

Cushing’s syndrome
-results from excess cortisol secretion

exogenous cushing’s syndrome occurs in:
-Patients taking cortisol-like medications such as Prednisone for treatment of inflammatory
disorders eg asthma and Rheumatoid arthritis
or after organ transplant

  • can occur with pituitary tumors the produce too much ACTH (Cushing’s disease)
  • signs and symptoms of Cushing’s syndrome include: Weight gain, rounded face and extra fat on the upper back and above the clavicles, diabetes, hypertension, osteoporosis, muscle loss and weakness, thin, fragile skin that bruises easily, purple-red stretch marks, facial hair in women, irregular menstruation
28
Q

what are the effects of VP?

A

anti-diuretic effect

  • acts on the kidney inducing water retention
  • anti-diuretic effect
  • vasoconstrictive effect, increasing BP

– good when you are thirsty, dehydrated or when you have low BP

29
Q

what are the effects of oxytocin?

A

released in response to suckling, cervical dilation or oestrogen

  • acts on oxytocin receptors on the uterus, inducing and regulating uterine contractions
  • act on mamillary glands to induce milk ejection
  • POSITIVE FEEDBACK

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