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RED - Endocrine Pharmacology & Therapeutics > E6 - Hypothalamus & pituitary > Flashcards

E6 - Hypothalamus & pituitary Flashcards

1
Q

What is the clinical relevance of pituitary tumours?

A
  • Most common cause of pituitary disease (adenomas)
  • Mostly benign/slow-growing (years)
  • Cause problems as pressure on surrounding structures (due to location); greater intra-cranial pressure, close to optic nerve = headaches/visual disturbances
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2
Q

What problems can pituitary tumours cause?

A
  • Over-production of a pituitary hormone (hypersecretion)
  • Inadequate production of other remaining hormones (squeezing/squashing other pituitary cells; hyposecretion)
  • Local effects on anatomically-related structures (e.g. visual disturbances, headaches; greater intra-cranial pressure)
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3
Q

What is hypopituitarism?

A

Inadequate secretion of pituitary gland hormones causing dwarfism in children and premature aging in adults

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4
Q

What is the relationship between the hypothalamus and the anterior pituitary with regards to cell bodies etc?

A
  • Cell bodies located in the hypothalamus: arcuate, ventromedial and preoptic nuclei, give signal for hormone synthesis at anterior pituitary
  • Releasing factors pass along portal vessels to reach the capillary bed of the anterior pituitary
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5
Q

What is the relationship between the hypothalamus and the posterior pituitary with regards to cell bodies etc?

A
  • Cell bodies of the paraventricular (PVN) and supraoptic (SON) nuclei located in the hypothalamus - site of hormone synthesis ‘neuro’
  • Hormones oxytocin and vasopressin respectively stored in the axon terminus of the posterior pituitary before release
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6
Q

Where is growth hormone synthesised, what does it do (briefly) and where does it act?

A
  • Synthethised in somatotrophs in the anterior pituitary
  • Has a major role in growth & development (particularly linear growth; elongation of long bones) + affects metabolism
  • Acts via GH receptor on target cells
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7
Q

What does the hormone prolactin do?

A
  • Stimulates mammary glands to produce milk (lactation) and promotes growth & development of breasts
  • Inhibits GnRH release
  • Synthesised in lactotrophs (/mammo-)
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8
Q

What does ACTH do?

A
  • Adrenocorticotropic hormone
  • Stimulates synthesis/release of cortisol
  • Synthesised from a very large precursor glycoprotein known as pro-opiomelanocortin (POMC)
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9
Q

What does TSH do?

A
  • Thyroid-stimulating hormone

- Stimulates synthesis and release of thyroid hormones

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10
Q

What is LH (luteinizing hormone)?

A
  • Stimulates steroid hormone synthesis (e.g. testosterone)

- Causes ovulation/formation of corpus luteum

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11
Q

What is FSH?

A
  • Stimulates follicular development (ovaries) and spermatogenesis (testes)
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12
Q

Which anterior pituitary hormones are single-chain polypeptides with disulfide bonds?

A
  • Somatotropes(trophs) e.g. somatotropin (growth hormone, GH)
  • Lactotropes(trophs) e.g. prolactin
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13
Q

Which anterior pituitary hormone is a small peptide?

A

Corticotrope(trophs) e.g. corticotropin (adrenocorticotropic hormone, ACTH)

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14
Q

Which anterior pituitary hormones are glycoproteins with 2 subunits?

A
  • Thyrotropes(trophs) e.g. thyrotropin (thyroid stimulating hormone, TSH)
  • Gonadotropes(trophs) e.g. LH, FSH
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15
Q

What is the difference between tropic and trophic?

A
  • Tropic: ‘turning’; affecting activity of an endocrine gland
  • Trophic: ‘feed, grow’; promoting growth, tissue integrity
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16
Q

Describe the OG endocrine axis.

A
  • Hypothalamus:
    Releasing hormone
    +/- Anterior pituitary:
    Tropic hormone (short -ve feedback to hypothalamus)
    + Peripheral endocrine glands
    Peripheral hormone (long -ve feedback to ant pit. and hypo.)
    + Target cell response (some -ve feedback to hypo.)
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17
Q

What effect does hypothalamic stimulation usually have on the anterior pituitary and which hormone is the exception?

A
  • Hypothalamus usually exerts stimulatory influence on the anterior pituitary (e.g. on LH/FSH, GH, TSH, ACTH)
  • Prolactin is the exception; under major inhibitory influence (from dopamine from hypothalamus) unless stimulated by TRH
18
Q

What are the direct actions of growth hormone (somatotropin)?

A

On metabolism:

  • Increases lipolysis (catabolic; triglycerides broken down to fatty acid + glycerol)
  • Increased AA uptake and protein synthesis (anabolic)
  • Increased hepatic glucose output (gluconeogenesis) & decreased glucose uptake (fat/adipose, skeletal muscle)

Anti-insulin (diabetogenic; counter-regulatory to insulin)

  • NET effect, shift of fuel source from CHOs to fats
  • GH elevates blood glucose; secondary cause of diabetes
19
Q

What are the indirect actions of growth hormone (somatotropin)?

A

Promotes growth:
- Stimulates release of growth factors such as IGF-I (insulin-like GF) & II (somatomedins) from liver (and other cell types)

20
Q

How does growth hormone stimulate growth and what are the processes that are stimulated?

A

Growth is via the action of IGF-I on cells:
- Stimulate protein synthesis, increase cell size (hypertrophy) increasing lean body mass
- Stimulate cell division, increase cell number (hyperplasia) increasing size of individual organs
- Promotes skeletal growth (increasing linear growth = height)
(Not about fat accumulation)

21
Q

How is GH release controlled?

Hint: re. endocrine axis

A
  • Environmental stimuli: sleep, stress, exercise
  • Nutrient stimuli: decrease glucose, decrease [FFA], increased [AA]
    HYPOTHALAMUS
    + GHRH/ - SST (somatostatin)
    ANTERIOR PITUITARY
    + GH > direct effect on metabolism
    > Short feedback loop to hypothalamus
    LIVER/OTHER TISSUES
    + Somatomedins (e.g. IGF-I) > indirect effect increasing growth
    > Long feedback loop to Liver + Hypothalamus
22
Q

What is the pattern of GH secretion throughout the day/throughout life?

A

Day:
- 70% of total daily GH released during sleep (pulsatile release)

Life:

  • Mean daily secretions are high during childhood reaching a peak at puberty
  • Fall to lower concentrations in adulthood
  • Fall in GH in later life partially responsible for some signs of aging
23
Q

What can occur as a result of GH (growth hormone) deficiency?

A
  • Stunted growth in children (pituitary dwarfism; no long bone development)
  • Deficiencies in adulthood:
    > psychological changes,
    > malaise, excessive tiredness, anxiety, depression
    > osteoporosis
    > poor muscular tone, decrease in lean body mass
    > impaired hair growth
    > increase in adipose tissue

Normally signs associated with old age.

24
Q

How is GH deficiency treated?

A

Recombinant human growth hormone (anabolic effects abused in sport)

25
Q

What is the result of excess growth hormone?

A
  • Gigantism (accelerated growth in children)

- Acromegaly (adults)

26
Q

What are some of the common characteristics of acromegaly?

A
  • Coarsening of facial features (enlarged jaw/brow/chin etc.)
  • Enlarged hands and feet (soft tissue expansion; bone growth on existing growth and not long bone growth like gigantism)
  • Headaches, visual disturbances (pituitary tumour pressure)
  • Sleep apnoea, general tiredness
  • Hypertension, cardiomegaly (enlarged heart)
  • Glucose intolerance (DM)
27
Q

What most often causes excess growth hormone release and how is it treated?

A
  • Most often due to GH-secreting tumour

Treatment:

  • Surgery/radiotherapy
  • Or inhibit GH release with somatostatin analogues
  • Some tumours respond to dopamine receptor agonists (some GH-adenomas acquire dopamine receptor expression)
28
Q

What is the net result of prolactin inhibiting GnRH release?

A
  • Inhibiting GnRH release means breastfeeding women have no menstrual cycle; aiding lactation
29
Q

What is the result of excess prolactin and what is it caused by?

A
  • Hyperprolactinaemia

- Cause: prolactinoma (pituitary tumour making too much prolactin)

30
Q

What are the symptoms of hyperprolactinaemia and how is it treated?

A

Symptoms:

  • Loss of fertility/libido (inhibited GnRH = inhibited menstruation)
  • Galactorrhoea (dilute, milky discharge)

Treatment:

  • Dopamine receptor agonists; inhibit prolactin secretion and shrink tumour
  • Surgery/radiotherapy considered when prolactinoma resistant to drug therapy
31
Q

What the main hormones released at the posterior pituitary?

A
  • (Arginine) Vasopressin (AVP;ADH)
  • Oxytocin
  • Made in cell bodies in the hypothalamus (supraoptic/paraventricular nuclei), travel down axons and stored at the end (axon termini) until release
32
Q

What is vasopressin release triggered by?

A

Stimulated by:

  • increase in body fluid osmolality (osmotic control)
  • fall in blood volume/pressure (haemodynamic control)
  • (acute) stress
33
Q

What are the actions of vasopressin (ADH)?

A
  • Blood vessels: vasoconstriction, via V1 receptors (high [AVP])
  • Kidney: DCT and CD see increased permeability via insertion of aquaporins (via V2 receptors)
  • Stimulates ACTH release
34
Q

What disease state is as a result of vasopressin deficiency?

A

Diabetes insipidus (different from DM):

  • Pituitary DI
  • Nephrogenic DI
35
Q

What does pituitary diabetes insipidus entail and how is it treated?

A

Inadequate release of AVP (ADH) results in:

  • Polyuria (large volumes of dilute urine excreted)
  • Resulting polydipsia (dehydrated thus thirsty)

Treatment:
- Desmopressin (synthetic ADH analogue, has no vasoconstrictor activity)

36
Q

What does nephrogenic diabetes insipidus entail and how is it treated?

A

As a result of:

  • Inadequate response in collecting ducts to ADH
  • Results in polyuria and resulting polydipsia as Pituitary DI

Treatment:
- Diuretics

37
Q

What disease state is as a result of vasopressin excess?

A

Syndrome of inappropriate ADH secretion (SIADH):

  • Retention of water = small urine volume, highly concentrated (even with fluid excess)
  • Hyponatraemia (due to dilutional effect; not Na+ depletion)
38
Q

How is SIADH treated?

A
  • Treat underlying cause (CNS pathologies, malignancy, CHS drugs; isn’t a tumour of posterior pituitary though)
  • Restrict water intake
  • If ineffective, block ADH action in kidney using V2 receptor antagonist
39
Q

How is oxytocin release stimulated and how is it regulated?

A
  • Stimulated by suckling and cervical stimulation (parturition; giving birth)
  • Release is via positive feedback control
40
Q

What are the actions of the posterior pituitary hormone oxytocin?

A
  • Stimulate ‘milk let-down’, expression of breast milk
  • Uterine smooth muscle contraction
  • Maternal behaviour/social behaviour/social bonding

RED - Endocrine Pharmacology & Therapeutics (7 decks)

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