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MD4001 Week 9 > 1. The hypothalamus-pituitary axis (Slide 15 onwards) > Flashcards

1. The hypothalamus-pituitary axis (Slide 15 onwards) Flashcards

1
Q

What are the neurohormones controlling the secretions of ant pit?

A

TH
CRH
GHRH (or somatotrophin releasing hormone)
GnRH ( aka FSH-RH and LH-RH)
Prolactin Releasing Factor (LRF)
Prolactin release inhibiting factor (aka Dopamine)

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2
Q

Neurohormones released from post pituitary into systemic circulation?

A

Vasopressin aka ADH

Oxytocin

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3
Q

Two groups of ant pituitary release?

A

Trophic hormones (primary actions on other endocrine glands)

Hormones acting on peripheral target cells

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4
Q

What are the trophic hormones of anterior pit?

A
  1. Thyrotropin/ Thyroid-stimulating hormone (TSH)
  2. Corticotropin /Adrenocorticotropic hormone (ACTH)
  3. Gonadotrophins
    - Luteinising Hormone (LH)
    - Follicle-stimulating hormone (FSH)
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5
Q

What are the ant pit hormones acting on peripheral target cells?

A
  1. Somatotropin / Growth hormone (GH)
  2. Prolacton (PL)

3 α, β and γ Melanotropin / Melanocyte-stimulating hormone (MSH)

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6
Q

Pre-cursor protein for corticotropin?

A

POMC (Pro-opiomelanocortin)

Also a precursor for many other end products depending on cell/enzyme. i.e. common precursor

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7
Q

**beta sub-unit gives hormone ________

A

**beta sub-unit gives hormone specificity

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8
Q 
What cells secrete:
TSH
ACTH
LH/FSH
GH
PL
MSH
A

TSH: Thyrotrophs, basophils

ACTH: Corticotrophs, basophils

LH/FSH: Gonadotrophs, basophils

GH: Somatotrophs, acidophils

PL: Lactoptrophs or mammotrophs, acidophils

MSH: Melanotrophs, basophils

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9
Q

Mechanisms controlled growth hormone release

A
  1. Neurosecretory cells in the arcuate nucleus secrete GH-releasing hormone that reaches the somatotrophs via the hypophyseal portal blood supply
  2. Cells in the periventricular region release somatostatin (a hormone that is a potent inhibitor of GH secretion) into portal blood supply
  3. . GHRH causes somatotrophs to synthesise and release GH
  4. Somatostatin inhibits the release the GH by somatotrophs

Somatostatin&raquo_space;» GHRH

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10
Q

What is the feedback inhibition of GH release?

A
  1. GH stimulates secretion of IGF-1 (insulin-like growth factor) from peripheral target tissues (at liver)
  2. IGF-1 then direct;y inhibits GH release by suppressing the somatotrophs
  3. GH inhiibts its own secretion via “short-loop” feedback on somatotrophs
  4. IGF-1 indirectly GH release by increasing secretion of somatostatin from nuclei in the periventricular region
  5. IGF-1 indirectly inhibts GH release by suppressing GHRH release fro the arcuate nucleus in the hypothalamus
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11
Q

Change in GH during 24hrs?

A

Circadian rhythm shows highest peaks between midnight and 4am (i.e. sleep onset)

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12
Q

Release for the hormones from the anterior pit show _______ rhythms

A

Release for the hormones from the anterior pit show circadian rhythms

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13
Q

Physiological actions of GH?

A
  1. Direct anti-insulin
    • increased lypolysis in adipose tissue
    • increased blood glucose
    (both due to decreased glucose uptake in muscle and adipose tissue; antagonised by insulin release)
  2. Indirect actions (igf-1 release from liver)
    • increased cartilage formation and bone growth
    • increased general protein synthesis and cell growth/division

Physiological consequences
• increased linear growth and lean body mass. Vital importance for normal post-natal development and rapid growth through puberty. Maintenance of protein synthesis and tissue functions in adults

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14
Q

Pathologies associated with GH?

A
  1. GH DEFICIENCY
    • Dwarfism in children due to predictable effects on linear bone growth and decreased availability of lipids and glucose for energy
  2. GH EXCESS - ACROMEGALY (often due to pituitary adenoma)
    Before Puberty…
    • GIGANTISM due to excess stimulation of epiphyseal plates
    After Puberty (no stimulation of linear growth due to fusion of epiphyses)…
    • PERIOSTEAL bone growth causing enlarged hand, jaw and foot size
    • Soft Mssue growth leading to enlargement of the tongue and coarsening of facial features
    • Insulin resistance and glucose intolerance (diabetes)
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15
Q

Treatment of GH deficiency and excess?

A

GH deficiency: Human GH

GH excess: Synthetic long-acting somatostatin (e.g. octreotide) with varying success

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16
Q

Physical signs of giantism

A
  • Hand and feet gradual enlargement
  • Rapid growth
  • Soft tissue swelling
  • Skin tags (wart-like)
  • Muscle weakness/fatigue
  • Skin changes (i.e. thickenings, oilliness, acne)
  • Hirsutism
  • Coarsening of facial features
17
Q

Other symptoms of giantism

A
  • Arthralgia (joint pain) 75%
  • Amenorrhea (72%)
  • Hyperhidrosis (++ perspiration)
  • Sleep apnea
  • Headaches
18
Q

Action of GnRH

A 
GnRH from hypothalamus
--> FSH and LH from Ant pit
-->
1. Germ cell develop,ment
-Gonads to secrete hormones
Men: Testosterone
Women: Estrogen and progesterone
19
Q

Action of TRH (thyroid releasing hormone)

A

TRH from hypothalamus

  • -> TSH from Ant Pit
  • -> Action on thyroid
  • Secretes thyroizine (T4) and triiodothyronine (T3)
20
Q

Action of DA (Dopamine)

A

DA release from hypothalamus

  • -> Prolactin release from ant pituitary
  • -> Action on breast tissue
  • Breast development
  • Milk production
21
Q

Action of CRH (corticotropin releasing hormone)

A

Release of CRH from hypothalamus

  • -> ACTH release from anterior pituitary
  • -> Action on adrenal cortex
  • Secrete cortisol
22
Q

Action of GHRH (Growth Hormone Release hormone) and SS (somatostatin)?

A

Release of GHRH and SS from the hypothalamus

  • -> GH release from the anterior pituitary
  • ->
    1. LIVER AND OTHER CELLS
  • Secrete insulin-like growth factor 1 (IGF-1)
    2. MOST ORGANS AND TISSUES
  • Promotes protein synthesis, carbohydrate and lipid metabolism
23
Q

-PROWhat is the cellular processing of AVP (ADH)?

A

147 long peptide, broken down to give of;

  • Signal peptide
  • VP
  • Neurophysin II
  • Glycopeptide (undergoes degeneration)
24
Q

What is the cellular processing of oxytoxin?

A

106 long peptide, breakdown to:

  • OT
  • Neurophysin I (after processing)
25
Q

Where are AVP (ADH) synthesised?

A

In neuroscretory cells within the supra-optic nucleus (SON) and paraventricular nucleus (PVN)

26
Q

PVN?

A

Periventricular nucleus

27
Q

SON?

A

Supra-optic nucleus

28
Q

Cause of ADH release?

A
  1. Increase in blood osmolariy –> Detected by brain osmoreceptors
  2. Decrease in blood volume –> detected by volume receptors in carotid artery, aorta and left atrium
  3. RAAS –> Release of Angiotensin II
29
Q

ADH deficiency ??

Cause?

A

In diabetes insipidus, AVP fails to properly regulate your body’s level of water, and allows too much urine to be produced and passed from your body.

There are two main types of diabetes insipidus:

  1. cranial diabetes insipidus – where the body doesn’t produce enough AVP, so excessive amounts of water are lost in large amounts of urine
  2. nephrogenic diabetes insipidus – where AVP is produced at the right levels but, for a variety of reasons, the kidneys don’t respond to it in the normal way.
30
Q

Where is oxytocin produced?

A

In hypothalamus neurones in the supra-optic nucleus (SON) and paraventricular nucleus (PVN)

31
Q

Oxytocin:
Bound to glycoprotein it is carried in the axons to the post pit where it is stored in vesicles in the expanded axons
Neurosecretion is controlled directly by nervous impulses from the hypothalamus

A

Oxytocin:
Bound to glycoprotein it is carried in the axons to the _____ pit where it is stored in vesicles in the expanded axons
Neurosecretion is controlled directly by nervous impulses from the ______

32
Q

Hypothalamic control of milk production and ejection, what is the role of prolactin and oxytocin??

A
  1. Suckling stimulus travels from breast, through the spinal cord to the hypothalamus
  2. Neurons from the spinal cord inhibit DA release from the arcuate nucleus. The decreased level of DA removes the inhibition that DA normally produces on lactotrophs in the anterior pituitary, leading to prolactin release.
    Prolactin stimulates milk production in the breast
  3. Neurons from the spinal cord also stimulate the production and release of oxytocin from the PVN (paraventricular nucleus) and SON (supraoptic nucleus).
    Oxytocin is released in the posterior pituitary and then into systemic blood –> Breast and myoepithelial cell
  4. Neurons from the spinal cord inhibit neurones in the arcuate nucleus and the preoptic area of the hypothalamus, causing a fall in GnRH production. The reduced stimulation of the gonadotrophs inhibits the ovarian cycle.
33
Q 
Pineal gland:
Location?
Connected to the hypothalamus?
In darkness...
Regulates??
"brain sand"?
A

Position: Lies in the midline in the posterior part of the roof of the 3rd ventricle

Pinealocytes have neural connections with the hypothalamus

In darkness (not sleep) the pineal secretes melatonin (from tryptophan)

Regulates:
1. Circadian rhythms (melatonin has an hypnotic effect)
2. Reproductive processes including the onset of puberty in humans
3 Effects on aging and regulation of the immune system

Brain sand? Accumulates calcium phosphate with time… ‘brain sand’ visible in the midline on X rays and other scans

MD4001 Week 9 (12 decks)

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