37: Hypothalamic/Pituitary Relations Flashcards
Neurohypophysis vs adenohypophysis
Neuro: posterior pituitary
Adeno: anterior pituitary
How is the posterior pituitary connected to the hypothalamus?
Post pit is a collection of axons whose cell bodies are in the hypothalamus
Two nuclei of the posterior pituitary
SON (supraoptic nulcei) and PVN (paraventricular nuclei)
Two neuropeptides secreted by the posterior pituitary
ADH, oxytocin
How does ant pit communicate with hypothalamus
Neurally and hormonally
Connection between hypothalamus and pituitary gland and what’s inside it
Hypophyseal stalk, holds the hypothalamic-hypophyseal portal blood vessels
What can pituitary tumors cause?
Pressure on optic nerves -> visual issues and dizziness
Primary, secondary, and tertiary endocrine disorders regarding the HPA axis
Primary: targets peripheral gland
Secondary: targets pituitary
Tertiary: targets hypothalamus
GH fluctuation during the day
Peaks with exercise and sleep
GH fluctuation throughout lifetime
Peak at puberty, moderate amount as an adult, almost none in senescence
Things that stimulate GH production
- Fasting/hunger/starvation
- Hypoglycemia
- Puberty hormones
- Exercise
- Sleep
- Stress
Fed state influence on GH
Carbs and proteins -> GH produced -> liver produces IGF-1
What is stimulated by GH in fed state?
Lipolysis, mitogenesis, differentiation of cells, synthesis of DNA/RNA/proteins
GH action in low protein state
GH is inhibited -> no IGF-1 from liver
What happens in low protein state?
Lipogenesis, carb storage, weight gain
What happens with GH in a low carb state?
GH levels increase -> IGF-1 is produced
What is stimulated by a low carb state?
Lipolysis, ketogenic metabolism, diabetogenic state
Diabetogenic state
Insulin sensitivity - increased blood glucose causes insulin resistance, so there is decreased glucose uptake and utilization by target tissues -> increased blood insulin levels
Causes of gigantism vs acromegaly
Gigantism: excess GH before closure of bone epiphyses
Acromegaly: excess GH after closure of bone epiphyses
What occurs in acromegaly?
Promotion of growth of deep organs, bones, and cartilage
Hormonal cause of gigantism
IGF-1 stimulates long bone growth
GH insensitivity
GH receptors on liver are non-functional -> less IGF-1 -> less negative feedback on GH -> lots of GH produced
Secondary deficiency of the HPGH axis: levels of GH and IGF-1
Low GH and low IGF-1
Tertiary deficiency of the HPGH axis: GHRH, GH, and IGF-1 amounts
All three are low
