5 Written Questions
5 Matching Questions
- ***Specific mechanism of ADH action. ADH helps reabsorb water, but how? Draw a diagram of this pathway. What's the key receptor to remember here?
2. Embryonic development
4. How hypothalamus sends signals to it
5. How blood supplies it
for anterior and posterior pituitary
- Growth of long bones - general sentence
- Negative feedback between hypothalamus, pituitary, and peripheral gland
1. Ultrashort loop definition
2. Short loop definition
3. Long loop definition
- Insulin secretion peaks after x to promote uptake, anabolism
- a Insulin secretion peaks after glucose absorption to promote uptake, anabolism
- b Big picture - Hypothalamus makes Xreleasing hormone that tells pituitary to make Xtropic hormone that tells peripheral gland to make X.
1. Ultra short loop : When high levels of a hormone negatively regulate the hormone itself. High X releasing hormone will negatively regulate production of X releasing hormone
2. Short loop: When the product of one hormone negatively regulates the hormone itself. For example, X tropic hormone is stimulated by X releasing hormone. High levels of X tropic hormone will inhibit release of X releasing hormone.
3. Long loop: when the final hormone produced can regulate most stages of the pathway. So hormone X will negatively regulate X tropic hormone at pituitary, negatively regulate X releasing hormone at hypothalamus, and can positively stimulate a hypothetical X inhibiting hormone.
- c 1. ENDOCRINE cells (5 types) for antpit (different hormones), vs. Nervous tissue for postpit
2. Outpocketing of oral cavity endothelium (Rathke's pouch)
for antpit while Downward extension of brain for postpit.
3. Growth (GH), Metabolism (TSH), Reproduction (FSH, LH), Milk production (PRL) for antpit.
H20 balance (ADH), milk production, labour (OCT) for postpit.
4. Hormonal signals via portal from median eminence for antpit, nerve signals for postpit
5. Venous portal veins from median eminence for antpit, arterial blood feeding terminal axons for postpit.
Cartilage (chondrocytes) is replaced with bone.
5 Multiple Choice Questions
- It's an important factor, but don't forget
Other factors in growth:
Freedom from chronic disease or environmental stress
Normal Hormonal Milieu
- 1. Increase
- Since the sella turcica forms a bony caudal border for the pituitary gland, a pituitary tumor can extend only upward in the rostral direction. This can result in compression of the optic chiasm, which lies on top of the pituitary, enveloping the pituitary stalk. Compression of the optic chiasm can lead to bitemporal hemianopsia, and, when there is no relevant trauma, this clinical finding is pathognomonic for a pituitary tumor.
- 1.Acromegaly - sustained GH secretion due to somatotroph tumor
Diagnose if person still has elevated GH even when given tons of glucose or IGF - which negatively regulates GH production
Treat with surgery or somatostatin analogues
2. Dwarfism - Too little secretion of GH, can be treatable and/or cured with GH treatment. If you have dwarfism with elevated GH: then you have impaired insulin or IGF
3. Panhypopituitarism: anterior pituitary is f'd up. Can be a side complication of acromegaly where a tumor grows inside - but it can destroy the gland too and impair anterior pituitary function
5 True/False Questions
What's different about locations for synthesis, storage, and release between postpit and antpit hormones? → Antpit = Hormones synthesized and stored in anterior pituitary itself (5 cell types synthesize the 6 hormones)
-Release of hormones regulated primarily by hypothalamic hormone release (+ or -) and feedback regulation from target gland hormones
Postpit - Oxytocin and Vasopressin are synthesized in the PVN and SON hypothalamic nuclei
-These hormones travel down and are stored in terminal axons in the posterior pituitary
-Action potentials initiated in hypothalamic nuclei trigger release of hormones into venous bloodstream
*****Essay question on exam - We see how GH counterbalances the effects of insulin, but GH can't function without insulin. Why is this? What role does insulin play that is critical for GH growth signalling to occur? → You need to remember the IGF/IGFBP pathway for this one.
IGF= insulin like growth factor
IGFBP = insulin like growth factor binding protein
GH stimulates IGF (aka somatomedins), but IGF remains bound to IGFBP when insulin concentration low. This helps prevent overaction of GH if no insulin.
However, when insulin is high, this tells the body to switch from insulin to GH signaling. It does this because rise in insulin inhibits IGFBP formation in liver. Thus GH will stimulate IGF synthesis, and high insulin will decrease IGFBP synthesis - so you get some free floaty IGF's hanging around. These IGF's go and bind to receptors and initiate growth signaling response.
Thus, insulin is the key to inhibiting IGFBP which blocks GH signaling.
1. Does it increase during pregnancy?
2. What maintains elevated prolactin?
3. Negatively regulates this hormone
4. What is the main function of prolactin? → 1. yes, 20 fold elevation
3. Prolactin negatively regulates dopamine
4. Stimulate original differentiation of breast tissue, expansion during pregnancy, and milk production
What important about low pressure in hypothalamic hypophyseal portal system? → growth hormone
Production of large amounts of dilute urine →
Cartilage (chondrocytes) is replaced with bone.