Hypothalamus/Pituitary Relationships and Biofeedback Flashcards
Pituitary tumors
Often put pressure on the optic nerves causing visual problems, dizziness
Posterior pituitary
Supraoptic nucleus SON - ADH
Paraventricular nucleus PVN - Oxytocin
Anterior pituitary secretions
ACTH TSH FSH LH GH Prolactin girls like acting trashy for prom
Hypothalamus direct/indirect control of pituitary
Directly releases hormones to the anterior pituitary via portal system - both neural and endocrine connection
Releases hormones on posterior pituitary solely via neural connection
Primary, secondary, tertiary endocrine disorders
Primary- low/high hormone levels due to defect in peripheral endocrine organ
Secondary- low/high hormone levels due to defect in pituitary
Tertiary- low/high hormone levels due to defect in hypothalamus
Anterior pituitary targets what organs
Gonads (hypothalamic-pituitary-gonad HPG axes etc..)
Liver
Thyroid
Adrenal
(also a hypothalamic-pituitary-prolactin axes)
Acromegaly
Excessive soft tissue, cartilage and bone in face
Prolonged and excessive secretion of growth hormone
Before puberty-causes gigantism (long bone growth) before closure of bone epiphysis
After puberty- causes acromegaly (deep organ/cartilage growth) after close of bone epiphysis
Growth hormone
Produced by somatotropes–> somatotropin (GH)
Somatostatin is growth hormone inhibiting factor GHIH
GH receptor GHR linked to JAK-STAT
Signals liver to produce IGF-1 (somatomedin)
Inhibited by somatostatin and IGF-1
Stimulated by fasting/hunger (grehlin) and hypoglycemia
Regulation of GH release
Increased GH leads to decreased GHRH
Increased IGF-1 leads to decreased GH and increased GHIH
High carb/low protein effect on GH release
High carb stimulates GH production but low protein will inhibit it
Lower carb intake and blood glucose + higher protein intake will lead to GH/IGF production and peripheral metabolism shifts to lipids for energy, hepatic gluconeogenesis is stimulated
Diagnosing gigantism/acromegaly
Elevated serum GH and IGF-1
AND failure to suppress GH production in response to an oral load of glucose (very high sensitivity test)
Pituitary enlargement on MRI
GH/IGF secretion timing
GH levels fluctuate throughout day, while IGF levels remain constant
High during sleep, peaks with exercise
Sleep disturbances can perturb GH secretion
GH is secreted throughout life
GH deficiency
Lower secretion of GHRH (due to hypothalamic dysfunction)
Lower GH secretion
Failure to generate somatomedins
GH or somatomedin resistance
Prolactin (PRL) release
Synthesized by lactotropes
Secretion begins 5th week of pregnancy
PRL UNDER TONIC INHIBITION BY HYPOTHALAMIC DOPAMINE
Primary action is to stimulate/maintain lactation
Suppresses LH and FSH to decrease reproductive function and suppress sexual drive
Prolactin regulation
PRL inhibits dopamine release from hypothalamus so that pituitary cannot be inhibited from making prolactin
Estrogen from pregnancy stimulates prolactin
Prolactinoma
Pituitary adenoma secreting prolactin (most common type)
Decreased FSH/LH due to hypopituitarism causes what
Women- hypogonadism, menstrual irregularity
Men- Infertility, hypogonadism, reduced sperm count
Hypopituitarism
Decreased: GH FSH/LH TSH ACTH ADH
Oxytocin actions
Milk ejection, stimulated by suckling, but also sight, sound or smell of infant
Production stimulated by dilation of cervix or orgasm, causes uterine contractions
Pitocin induces labor
Zona glomerulosa (adrenal gland) releases
Mineralcorticoid- Aldosterone
Zona reticularis and zona fasciculata release
Glucocorticoids and Androgens
Epinephrine vs norepinephrine area of action
NE- at target cell near point of release
E- at distant target cell
PNMT upregulated by what
Cortisol
Pheochromocytoma
Benign, unilateral adrenal tumor
Catecholamines secreted by these tumors stimulate both alpha and beta adrenergic receptors
17a enzyme deficiency
Increased ACTH, BP
Decreased cortisol, K+
Decreased androstenedione in labwork
Undescended testes, lack of secondary sexual characteristics
21b enzyme deficiency
Decreased ACTH, cortisol, BP
Increased K+
Increased renin activity and 17-hydroxy-progesterone in labs
11b enzyme deficiency
Decreased aldosterone, cortisol and K+
Increased BP
Decreased renin activity
Addisons disease
Primary adrenal insufficiency
Primary deficiency of cortisol and aldosterone
Hypotension, hyponatremia, decreased blood Na
Weakness, weight loss, hyperpigmentation
Primary hyperaldosteronism
Excess secretion of aldosterone
Hypertension, hypokalemia, low plasma renin, low K+
CRH and hyperpigmentation
CRH–>ACTH–> activates melanocytes to produce melanin
Cushings syndrome vs disease
Cushings syndrome is high levels of cortisol caused by adrenal tumor
Cushings disease is high levels of ACTH and cortisol caused by pituitary tumor/ectopic ACTH secreting tumor
Dexamethasone high dose distinguishes if increased cortisol is caused by pituitary tumor or ACTH secreting ectopic tumor.
Low dose dexa just tells you if you have CS or not
Dexamethasone causes feedback inhibition of pituitary to inhibit ACTH release
