Hypothalamus and Pituitary ☺️ Flashcards
Describe the basic structure of the HP axis
Hypothalamus - SO, PV
-nuclei release releasing hormones into portal circulation => AP
Endocrine cells release trophic hormones into hypophyseal circulation => systemic circulation
Neural axons from hypothalamus release ADH, oxytocin directly into hypophyseal circulation in PP => systemic circulation
Pituitary in sella turcica in sphenoid
Pituitary next to optic chiasm
Female hormone negative feedback system
Male hormone negative feedback system
Hypothalamus GnRH => AP gonadotrophs
FSH => follicle dev => O, inhibin
LH => ovulation => corpus luteum => P
FSH => Sertoli cells (spermatogenesis) => Inhibin
LH => Leydig cells => T
Leydig stimulate Sertoli
GH
- function
- source
- regulation and release pattern
GHRH => somatotroph (most abundant cell in AP) => GH
Somatostatin => somatotroph => somatotropin => GH inhibition
Function
- growth of long bones until epiphyses fuse
- increase visceral size
- gluconeogenesis, lipolysis, protein synthesis
- cell growth
- stimulates IGF release from liver
Increases secretion
- pulsatile GHRH
- fasting (post prandial/drug induced hypoglycemia)
- exercise (tissue repair/AA infusion)
- sleep
Decreases secretion
- glucose
- somatostatin (increased by IGF)
PRL
- function
- release
Hyperprolactinemia
- risk factors
- presentation in men, women
- management
TRH => lactotrophs => PRL stimulation
Dopamine => lactotrophs => PRL inhibition
PRL inhibits GnRH
- breast dev in pregnancy
- milk prod postpartum
Female, childbearing age, MEN 1
Men - impotence, low libido, galactorrhea, gynecomastia
Women - amenorrhea, galactorrhea
D2 agonists - bromocriptine/cabergoline
Excess GH
- causes
- presentation
- management
Gigantism - hyperactive pituitary tumour, increased bone length before epiphyseal fusion
Acromegaly - hyperactive pituitary adenoma/ectopic GHRH/GH prod after epiphyseal fusion => loss of normal pulsatile release
- coarse facial features, spade hands, increased shoe size
- large tongue, interdental spaces
- sweat gland hypertrophy
Transphenoidal surgery - adenoma removal
Somatostatin analogues - octreotride/lanretide/pasireotide
D2 agonists - bromocriptine/cabergoline
Insufficient GH
- presentation
- management
Dwarfism
GH deficiency after epiphyseal fusion
Before epipheaseal fusion
-recombinant hGH/hIGF -somatropin/mecasemin
PP hormones
- release and regulation
- functions
SO, PV nuclei
ADH - hyperosmolarity
-ANG2, SNS => VC, fluid uptake
OXY - uterine contracts, milk ejection, social behaviour
-labour, lactation
What are the 4 types of hormone deficiency
Resistance
-target hormone receptor faulty
Primary
-endocrine gland cannot release target hormone
Secondary
-Pituitary can’t release trophic hormone
Tertiary
-Hypothalamus can’t release releasing hormones
What are the 2 key principles of hormone replacement
Replace the hormones that are required
Recognize diurnal patterns of release
Pituitary adenomas
- different presentations
- investigations
- management
Functional adenoma => hyperpituitarism
Non functional adenoma => hypopituitarism if it gets big enough
-low TSH => fatigue, weight gain
-low FSH, LH => decreased libido, menses
-low ACTH => thin hair, skin
Both lead to mass lesion
- bitemporal hemianopia => optic chiasm compressed
- headache => increased pressure
- hypopituitarism => pituitary compressed
Apoplexy => hypopituitary
CT =>suprasella mass
Hyper/hypo => measure trophic and target hormone
Insulin stress test to test pituitary response to hypoglycemia => normally GH, cortisol increases
Benign - watch and wait
Transphenoidal surgery, endocrine replacement
Radiotherapy
Inhibiting hormones for hyperactivity