Lopez Review Flashcards
Adenylyl cyclase mechanism
E.g. ACTH, LH, FSH, TSH, glucagon
Phospholipase C mechanism
E.g. GnRH, TRH, GHRH,
hormone-receptor complex works as a transcription factor that regulates the rate of transcription of a gene
E.g. thyroid hormones, glucocorticoids, aldosterone, estrogen, testosterone bind to receptor intracellularly and then bind to the SRE site on the DNA
The connections between the hypothalamus & anterior lobe are
The connections between the hypothalamus & anterior lobe are both neural & endocrine!
The connections between the hypothalamus and the posterior pituitary is
neural
1° endocrine disorder:
1° endocrine disorder: low or high levels of hormone due to defect in the peripheral endocrine gland
2° endocrine disorder:
.2° endocrine disorder: low or high levels of hormone due to defect in the pituitary gland
3° endocrine disorder:
3° endocrine disorder: low or high levels of hormone due to defect in the hypothalamus
what is the target of somatostatin?
somatotrophs in the AP, inhibits GH release
what is the target of GHRH?
somatrophs in the AP–> causes release of GH
what is the target of PIF?
lactotrophs. dopamine (PIF) decreases prolactin release
what is the target of TRH?
thyrotrophs in the AP normally; thyrotrophs AND lactotrophs when it is abnormally elevated
when is growth hormone highest and lowest?
adolescence it is highest; adulthood it is lowest
Somatomedins
insulin like growth factor (IGF-1): secreted by target tissues in response to growth hormone: negatively inhibits AP release of GR and positively stimulate hypothalamus to release the somatostatin to inhibit GH release from the AP
Growth hormone effects
- Diabetogenic effects
- increase in blood glucose concentration) • C
- insulin resistance by decreasing glucose uptake & utilization by target tissues
- increases lipolysis in adipose tissue
- Results in an increase of blood insulin
- increased protein synthesis & organ growth
- increased uptake of a.a •
- Stimulates synthesis of DNA, RNA, & protein
- Mediated by somatomedins (IGF-1)
- linear growth
- Stimulates synthesis of DNA, RNA, & protein
- Mediated by somatomedins (IGF-1)
- increases metabolism in cartilage-forming cells & chondrocytes proliferation
…..an important of determinant of GH, IGF-1, & insulin levels
nutritional status: fasting DECREASES somatomedin
- GH deficiency occurs with
- decreased secretion of GHRH due to hypothalamic dysfunction
- decreased growth hormone secretion 1° deficiency (lack of somatomedin feedback)
- GH or somatomedin resistance caused by deficiency of receptors
hyperprolactinemia: feedback system
prolactin negative feedbacks to the hypothalamus and suppresses GnRH (no LH or FSH), inhibits itself by stimulating dopamine release.
……neurons have cell bodies primarily in the supraoptic nuclei of the hypothalamus
ADH neurons have cell bodies primarily in the supraoptic nuclei of the hypothalamus
….. neurons have cell bodies primarily in the paraventricular nuclei of the hypothalamus
oxytocin neurons have cell bodies primarily in the paraventricular nuclei of the hypothalamus
Secretion of ADH is most sensitive to
Secretion of ADH is most sensitive to plasma osmolarity changes! An increase of only 1% in the osmolarity will increase ADH secretion
ADH triggers and receptors
what receptors do they act on in the body?
V1 receptors in blood vessels; V2 receptors in the kidneys
triggers: think the “big 3” one for each letter in ADH
- decreased blood pressure on barroreceptors in the cardiac and aortic receptors
- decreased stretch receptors stimulation in the atria
- increased osmolarity
- increased Plasma osmolarity (above 280 mOsm)
- DECREASED Blood pressure
- DECREASED Blood volume
- increased Angiotensin II
- Sympathetic stimulation
- Dehydration
three common trigger points for ADH
1) cardiac and aortic baroreceptors
2) aortic stretch receptors
3) mOsm receptors via interneurons
causes of decreased ADH
- primary polydipsia: Hypothalamus
* Primary stimulation of thirst osmoreceptors (Primary polydipsia) - Central DI
* decreased ADH from a problem in the hypothalamus or pituitary - Nephrogenic DI
* resistance to ADH caused by renal damage, sickle cell anemia, or drugs such as lithium
botton line: if ADH increases after administration of desmopressin
if ADH increases with desmopressin, it is either normal or nephrogenic
Hypoosmolarity fails to inhibit ADH release
SIADH
causes of SIADH
- SCC –> ADH secretion
- Lymphoma
- adrenal insufficiency
- CNS tumor
- brain damage
SIADH symptoms: above Na 120 and below Na 120
above is asymptomatic; below –> vomiting, lethargy, anorexia, confusion, headach, extensor plantar response
17 alpha deficiency
substrates shunted away from cortisol and androgen production and into mineralcorticoid production –> increased aldosterone
CRH regulation
- stress + FB, circadian rhythm +/-
- cortisol NFB on both pit and hyptothal
whenever ACTH is high, what do you get
high cortisol and hyperpigmentation
what is the substrate directly responsible for stimualting aldosterone release?
angiotensin II
alpha, beta, delta cells: secretory products and location
alpha- glucagon, peripheries
beta- insulin, central
delta- somatostatin, between alpha and beta cells
+ and - feedback between insulin, glucagon, and somatostatin
glucagon +fb –> insulin released
insulin -fb–> decreases glucagon release
somatostatin -fb–> decreases insulin and glucagon
Sulfonylurea drugs (e.g. tolbutamide, glyburide)
Sulfonylurea drugs (e.g. tolbutamide, glyburide)
- promotes the closing of ATP-dependent K (potassium inward rectifier)
- increases insulin secretion; used in the treatment of type II diabetes mellitus
accumulation of what molecule closes the inward rectifier K channel, triggering depolarization and inward Ca2+ influx–> releasing insulin?
ATP
+ stimulus for insulin; - fb decreasing insulin release
FF, aa’s, glucose, glucagon, K+, cotisol, GIP, vegal stim (ACh), sulfonylurea drugs, obesity
decreasing blood glucose, fasting exercise, somatostatin, alpha adreneric agonist, diazoxide
adipocytes as an endocrine tissue: what does it secrete, and how does it contribute to DM?
adipokines, FFs (increase insulin release, inflammation –> insulin resistance
convert mmol/l blood glucose into mg/dl
multiple mmol/L x 18 –> mg/dl
CaSR how it works
Gq and Gi inhibit PTH hormone and PTH gene in the presence of high calcium stimulation; when not stimulated the inhibition is released (i think); when inhibition is released, PTH is produced and released. Vit D (1, 25) also inhibits PTH production but stimulated CaSR synthesis and release
