A. HYPOTHALAMUS AND PITUITARY Flashcards
what is the anterior pituitary also known as
adenohypophysis (Adeno = gland)
what is the appearance of the anterior pituitary
vascularised
what is the posterior pituitary also known as
neurohypophysis
what is the appearance of the posterior pituitary
neural
what is in close proximity with the pituitary gland
optic chiasm (where optic nerves cross) and the carvenous sinus (with cranial nerves)
characteristics of pituitary tumours
- called adenomas
- benign and don’t spread
- slow growing (years)
what are the consequences of pituitary gland tumours due to the mass pressure on surrounding structures
- increased intracranial pressure causing headaches
- compression of optic nerves/chiasm causing visual field defects
- compression on cavernous sinus causing cranial nerve palsies (partial paralysis of nerves which supply eye, ear etc)
what are the consequences of pituitary gland tumours due to effects on hormones
- over-production of a pituitary hormone due to tumour arising from hormone-secreting pituitary cells
- inadequate production of other remaining hormones due to tumour mass causing compression of other pituitary cells
pathway of hormones for anterior pituitary
- cell bodies and neurones secrete hypothalamic-releasing factors (hormones)
- they pass along portal vessels to reach capillary bed in anterior pituitary
- control secretion of hormones from specific endocrine cells of anterior pituitary into circulation
pathway of hormones for posterior pituitary
- cell bodies of paraventricular and supraoptic nuclei secrete hypothalamic-releasing factors (hormones)
- neurones carry oxytocin and vasopressin (ADH) down axon fibres to posterior pituitary
- stored and released here
what is the endocrine axis
Interactions between hypothalamus, pituitary gland and peripheral endocrine glands, with feedback regulation of hormone secretion, to maintain physiological homeostasis
what kind of hormones are hypothalamus and anterior pituitary hormones
tropic (ie affect activity of an endocrine gland)
what are the hormones of the anterior pituitary
- growth hormone (somatotropin) secreted by specific endocrine cells (eg - somatotroph cells secrete GH)
- prolactin
- adrenocorticotropic hormone (ACTH) (corticotropin)
- thyroid-stimulating hormone (TSH) (thyrotropin)
- luteinising hormone: gonadotropin
- follicle-stimulating hormone (FSH): gonadotropin
*a different specific endocrine cells secrete each of these
gonadotrophin pathway
- GnRH in hypothalamus
- releases LH and FSH in anterior pituitary
- stimulatory effect (+) on LH and FSH
- affects gonads (peripheral endocrine gland)
- sex hormones produced
growth hormone pathway
- GHRH in hypothalamus
- releases GH in anterior pituitary
- stimulatory effect (+) on GH
- GH affects liver (peripheral endocrine gland)
- IGF-1 produced (insulin-like growth factor 1)
thyroid-stimulating hormone pathway
- TRH (thyrotropin-releasing hormone) in hypothalamus
- releases TSH in anterior pituitary
- stimulatory effect (+) on TSH
- TSH affects thyroid (peripheral endocrine gland)
- thyroid hormones produced
- has a stimulatory effect on prolactin production aswell
somatostatin (a GH) pathway
inhibitory effect on GH and TSH
prolactin pathway
- dopamine in hypothalamus
- releases prolactin in anterior pituitary
- inhibitory effect on prolactin
- affects breast tissue (exocrine gland - therefore prolactin isn’t a tropic hormone)
ACTH pathway
- CRH in hypothalamus (also CRF - factor)
- releases ACTH in anterior pituitary
- stimulatory effect on ACTH
- ACTH affects adrenal cortex (peripheral endocrine gland)
- cortisol produced
what effects does GH have
- linear growth (ie long bones)
- effects on metabolism
- effects via GH receptor on target cells
what is the direct action of GH
metabolism - has anti-insulin effects (ie - diabetogenic) as increases blood glucose
how does GH increase blood glucose
Muscle:
- increases amino acid uptake
- increased protein synthesis
- decreases glucose uptake
Adipose tissue
- increases lipolysis
- decreases glucose uptake
Liver:
- increases gluconeogenesis
what is the indirect action of GH
promotes growth (IGF-1)
how does GH promote growth
- stimulates release of growth factors (ie: IGF-I, IGF-II - somatomedins) from liver and other cell types
- growth is via action of IGF-I on cells
- promotes growth of soft tissue (increase cell size - hypertrophy and cell number - hyperplasia)
- promotes skeletal growth (length and thickness)
what can a deficiency in GH cause (hypopituitarism)
stunted growth in children (pituitary dwarfism - proportional dwarfism) and deficiency in adult
non-specific symptoms of GHD in adults
- Psychological changes
- Malaise, excessive tiredness, anxiety and depression
- Osteoporosis
- Poor muscular tone, decrease in lean body mass
- Impaired hair growth
- Increase in adipose tissue (especially around the waist)
treatment of GHD
- in the past, from human cadaver pituitaries
- now, recombinant HGH licensed in UK
- used in sport?
what can an excess in GH cause
accelerated growth in children (gigantism) and acromegaly in adults
what causes excessive GH
- GH-secreting pituitary tumour
treatment of excess GH
- surgery or radiotherapy
- inhibit GH release with somatostatin analogues (eg - octreotide)
- some tumours respond to dopamine receptor agonists (eg - bromocriptine) as they acquire expression of dopamine receptors
- resistance to above: use pegvisomant which is highly selective GH receptor antagonist
symptoms of excess GH in adults
- Coarsening of facial features (look older) due to increased thickening of bone, cartilage and soft tissue development
- Enlarged hands and feet
- Headaches, vision disturbance due to GH tumour
- Sleep apnoea, general tiredness due to enlargement of body tissue
- Hypertension, cardiomegaly due to enlargement of heart
- Glucose intolerance (diabetes) as GH increases blood glucose
what effects does prolactin have
- stimulates mammary glands to produce milk (lactation)
- promotes growth and development of the breasts
- high prolactin concentrations inhibit GnRH release
what type of hormone is prolactin
trophic - promotes growth and tissue integrity
what causes hyperprolactinaemia
prolactinoma - non-cancerous tumor of the pituitary gland
symptoms of hyperprolactinaemia
- loss of fertility/libido as inhibits GnRHs
- galactorrhoea (in non-pregnant) f>m
- gynaecomastia: benign development of breast tissue (m>f)
treatment for hyperprolactinaemia
- dopamine receptor agonists (Eg - cabergoline, bromocriptine) which inhibit prolactin secretion and shrink the tumour
- surgery/radiotherapy for tumours resistant to drug therapy
what are the 2 hormones of the posterior pituitary
- vasopressin AVP or aka ADH: pituitary gland releases AVP when the amount of water in the body becomes too low
- oxytocin
- love hormones for attachment?
(stored in axon terminals)
what is AVP/ADH release stimulated by
- increase in body fluid osmolality
- fall in blood volume/pressure (also angiotensin II, nausea, acute stress)
treatment of excess AVP/AHD
- blood vessels: vasoconstrictors (eg - vasopressin) via V1 receptors (at higher AVP concs)
- kidney: to increase permeability and hence reabsorption of water via V2 receptors block ADH action using V2 receptor antagonists (tolvaptan)
what can a deficiency of AVP/ADH cause
diabetes insipidus
1. pituitary DI
- excretion of large volumes of dilute urine (polyuria and hence polydipsia)
- use desmopressin (analogue of ADH)
- nephrogenic DI
- lack of response in collecting tubes to ADH (polyuria and hence polydipsia)
- use diuretics (thiazide-like diuretics)
*You just need to increase the amount of water you drink to compensate for the fluid lost through urination sometimes
what can an excess of AVP/ADH cause
syndrome of inappropriate ADH secretion (SIADH)
- retention of water so small volume of urine, highly concentrated
- hyponatraemia (due to dilution effect)
when is oxytocin released
- produced in males and females
- stimulated release by suckling and by cervical stimulation (parturition)
what effects does oxytocin have
- stimulates milk let-down and hence expression of breast milk
- contraction of uterine smooth muscle
- parental/reproductive behaviour, social bonding
clinical use of oxytocin
induction/enhancement of labour
