Hypothalamus and Pituitary ☺️ Flashcards

1
Q

Describe the basic structure of the HP axis

A

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

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2
Q

Female hormone negative feedback system

Male hormone negative feedback system

A

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

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3
Q

GH

  • function
  • source
  • regulation and release pattern
A

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)
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4
Q

PRL

  • function
  • release

Hyperprolactinemia

  • risk factors
  • presentation in men, women
  • management
A

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

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5
Q

Excess GH

  • causes
  • presentation
  • management
A

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

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6
Q

Insufficient GH

  • presentation
  • management
A

Dwarfism
GH deficiency after epiphyseal fusion

Before epipheaseal fusion
-recombinant hGH/hIGF -somatropin/mecasemin

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7
Q

PP hormones

  • release and regulation
  • functions
A

SO, PV nuclei
ADH - hyperosmolarity
-ANG2, SNS => VC, fluid uptake

OXY - uterine contracts, milk ejection, social behaviour
-labour, lactation

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8
Q

What are the 4 types of hormone deficiency

A

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

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9
Q

What are the 2 key principles of hormone replacement

A

Replace the hormones that are required

Recognize diurnal patterns of release

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10
Q

Pituitary adenomas

  • different presentations
  • investigations
  • management
A

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

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