Exam 4 Flashcards
the anterior pituitary originates from
Rathke’s pouch which is an embryonic invagination of the pharyngeal epithelium
*ectodermal tissue
the posterior pituitary originates from
a neural tissue outgrowth fro the hypothalamus
*neurally derived
characteristics of hypothalamic releasing hormones (6)
- secreted in pulsatile manner
- Associated w/ plasma membrane receptors and promote increase in intracellular 2nd messengers
- stimulate release of stored hormones of the AP
- stimulate synthesis of AP hormones
- required for maintence of target cells
- has autocrine effects (exhibit trophic influences over cells they regulate)
how does the vascular system of the pituitary contribute its functions
it is highly vascularized (2 capillary networks) which creates a high resistance of blood flow (ie. slow), therefore even though the releasing hormones secreted by the hypothalamus are in low concentrations, they will be concentrated by the slow flow, and will strongly affect the anterior pituitary
examples of hypothalamic releasing hormones
- TRH
- GnRH
- CRH
- GHRH
- GHIH aka Somatostatin
- PIF
- PRF (dopamine)
*all are peptides except PIP which is dopamine
Cell types of the Anterior Pituitary and their products
- Somatotropes- GH
- Corticotropes- ACTH
- Thyrotropes- TSH
- Gonadotropes- LH and FSH
- Mammotroph/Lactotropes- PRL
Hormones secreted by Anterior pituitary
- GH
- ACTH
- TSH
- PRL
- FSH and LH
promotes growth of the entire body by affecting protein formation, cell multiplication and cell differentiation
Growth hormone
Controls the secretion of some of the adrenocortical hormones, which affect the metabolism of glucose, proteins, and fat
Adrenocorticotropin (ACTH)
Controls the rate of secretion of thyroxine T4 and triiodothyronine T3 by the thyroid gland, these hormones control rates of most intracellular chemical reactions in the body
TSH
promotes mammary gland development and milk production
Prolactin
promotes mammary gland development and milk production
FSH and LH
Secretion from the posterior pituitary is controlled by
nerve signals that start in the hypothalamus
Secretion by the anterior pituitary is controlled by
hormones called hypothalamic releasing and hypothalamic inhibitory hormones/factors that are secreted by the hypothalamus and are conducted to the anterior pituitary through small blood vessels called hypothalamic hypophysial portal vessels.
LHRH is secreted in low amounts from hypothalamus –> LH or FSH from the AP are much greater.
How is such a small amount influencing the release?
vasculature!! capillary network–> venous structures –> capillary network –> SERIES resistance –> high R –> sluggish blood flow is why such small amounts of hormone has such a big effect !
Regulation of hormone release from pituitary
- Ultrashort loop inhibition (autocrine inhibition)- hypothalamus releasing hormone has a neg .effect on hypothalamus
- Short loop inhibition- Ant. pituitary secretes a trophic hormone that has a neg. effect on hypothalamus
- Long loop inhibition- trophic hormone effects target cell which releases another hormone that has a neg. effect on hypothalamus and AP hormone
*hypothalamic endocrine axis!
hormones secreted by posterior pituitary
- ADH aka vasopressin
2. oxytocin
controls the rate of water excretion into the urine
ADH
helps express milk from the glands of the breast to the nipples and helps in the delivery of the baby at the end of gestation.
oxytocin
major hormones of the adrenal cortex (types of corticosteroids)
1. Glucocorticoids (cortisol, corticosterone) 2. Mineralocorticoids (aldosterone) 3. Sex steroids (17-keto steroids) (androgens and estrogens)
affect the electrolytes (the minerals) of the ECF, especially sodium and potassium
Mineralocorticoids
affect blood glucose concentration. They also affect protein and fat metabolism
Glucocorticoids
*essential for life
what hormones are secreted from the different parts of the adrenal cortex and medullat
Zona Glomerulosa- Aldosterone
Zona fasciculata- glucocorticoids and sex steroids
Zona reticularis- sex steroids
medulla- epi and norepi
**All Cortex parts are stimulated by ACTH!
describe how Cortical atrophy and hypertrophy occur
atrophy- caused by hypophysectomy bc it loses ACTH
Hypertrophy- caused by increase in ACTH. ( stress–> hypothalamus stimulated ==> + CRH –> + pituitary–> increase in ACTH release
*ACTH regulates adrenal cortex maintenance
ACTH and cortisol levels increase on a diurnal rhythm, when are levels highest
rise at 4 am and peak around 7-8AM
*as you approach sleep/wake cycle, ACT and correspondingly cortisol increases
all steroids are derived from
cholesterol
describe the synthesis of steroids
ACTH binds to Gs receptor–> + PKA–> phosphrorylation–> + CEH **RLS
LDL mediates receptor mediated endocytosis –> LDLs are made of 50% cholesterol in ester form –> + CEH breaks down cholesterol esters to yield free cholesterol **RLS –> enters ER–> synthesis of steroid hormones in mito
**ACTH is literally driving the availability of free cholesterol to engage in biosynthetic activity!!!!
describe congenital adrenal hyperplasia (CAH)
it is a consequence of an enzyme in the cortisol production pathway being almost non-existant. So the person lacks the enzyme machinery to engage in cortisol production. This leads to a back up of ACTH and a hyperplastic adrenal gland
what is the dexamethasone suppression test
This test evaluates the integrity of the hypothalamus, pituitary, adrenal gland axis.
-Dexa is a powerful glucocorticoid given orally at night that raises glucocorticoid levels in the system. This negatively influences ACTH release and ultimately the release of cortisol
ACTH impacts all aspects of steroid hormone synthesis. What are its impacts
Immediate: (via phosphorylation of CEH via PKA)–> increase cholesterol transport to mito and more bind to p450= enhanced production of steriods by a number of hydroxylases
Subsequent: increase in LDL receptors and gene transcription
Longterm: (via insluin like growth factors)–> increases the size and number of cells in the adrenal cortex
what stimulates aldosterone secretion
angiotensin II
decrease in ECF volume (decrease BP)–> renin release from kidneys–> cleaves angiotensinogen from liver–> angiotensin I–> cleaved by ACE from lungs–> angiotensin II–> stimulates aldosterone release from zona glomerulosa
how is cortisol transported to its target
- binds primarily to transcortin- 80% (has the highest affinity for cortisol)
- overflow cortisol binds to albumin (15%) (lower affinity for cortisol)
- Free cortisol in ECF that can associate with receptors
This is our most important mineralocorticoid it is a K+ secretor Na+ keeper- lipophilic substance so it crosses membrane! Receptor is in cytoplasm or in nucleus
aldosterone
aldosterone is regulated by
angiotensin II
Plasma Na+ reduction (causes increase in aldosterone)
Plasma K+ increase (cause increase in aldosterone)
ACTH - weak but still promotes
our most important glucocorticoid
cortisol
what are the effects of increased AA in the ECF due to increased cortisol?
AA undergo transamination (utilization) in the liver to produce TCA cycle intermediates (can then be used to promote gluconeogensis, glycogen synthesis, and urea cycle activity–> see an increase in BUN via deamination)
cortisols diabetogenic results
- hyperglycemic, ketogenic, lypolytic
- increase in FFA
- increase in plasma AA–> increase in BUN
How does cortisol effect insulin
- shifts the curve to the right
- requires more insulin to drive the same level activity bc cortisol desensitized cells to insulin
how does cortisol affect the immune system and inflammation
- blocks NO production = decreased vasodilation
- blocks platelet activation factors= decreased permeability
- inhibits phospholipase which produces Arachidonic acid= decreased inflammation
- blocks interleukin production of T and B cells
- Blocks macrophage production of interleukins= increased fever
what are the effects of aldosterone
- increase Na+ reabsorption and passive movement of water with it (increase in [Na+] in plasma)
- increase in K+ secretion
- increase in ECF volume
- increase in BP
*results in more concentrated urine
describe the biosynthesis of catecholamines
-occurs in adrenal medulla
Tyrosine–>Dopa (via tyrosine hydroxylase **RLS)–> Dopamine–> norepi (via dopamine beta-hydroxylase)–> Epi (via PMNT)
Tyrosine hydroxylase and dopamine beta-hydroxylase are (+) by ACTH and sympathetic stimulation
PMNT is stimulated by cortisol
Cushing’s can be caused by
- Adenomas of the anterior pituitary that secrete large amounts of ACTH which then causes adrenal hyperplasia and excess cortisol.
- Abnormal function of the hypothalamus that causes high levels of corticotropin releasing hormone CRH which stimulates excess ACTH
- Ectopic secretion of ACTH by a tumor elsewhere in the body like an abdominal carcinoma
- Adenoma of the adrenal cortex