Endocrine System: Hypothalamus and Pituitary Gland Cascades

Endocrine signaling (neuronal connection) Start: hypothalamus End: Posterior Pituitary

1. Collection of cell bodies (nuclei) in the hypothalamus 2. Axon extends into the infundibulum into the posterior pituitary 3. Axon terminals in the poster pituitary release neurotransmitter 4. Neurotransmitter triggers the release of neurohormones into the blood and then out to the body

Oxytocin

1. Contraction of uterine smooth muscle during birth 2. Milk secretion from breast tissue 3. Bonding behaviors in both males and females (parental)

Testosterone and Estrogen

-stimulate growth in puberty -inhibition when prolonged exposure

Peptides released from the posterior pituitary

1. Anti-diuretic hormone (ADH aka vasopressin) 2. Oxytocin

6 major hypophysiotropic hormones

1. Corticotropin releasing hormone (CRH) 2. Thryotropin releasing hormone (TRH) 3. Growth hormone releasing hormone (GHRH) 4. Somatostatin (SST) 5. Gonadotropin releasing hormone (GnRH) 6. Dopamine (catecholamine) - 1 through 5 are peptides

Hypothyroidism cascade

1. Decrease in TH because of lack of iodide 2. Produces symptoms -no long loop negative feedback allows upper part of cascade to become unbalanced 3. TRH secretion in the hypothalamus increases 4. TSH secretion in the anterior pituitary increases

Functions of Adrenal Catecholamines in stress

1. Dilates respiratory airs and increases ventilation 2. reduces digestion and urine release 3. dilates blood vessels in the heart and skeletal muscle 4. mobilizes glucose (from liver) and fat from adipose tissue 5. Dilates pupil 6. Increase CNS alertness

3 gland cascade growth hormone

1. Hypo secretes GHRH (+) and SST(-) 2. Stimulates or inhibits release of GH in the somatotroph cells (40-50%) 3A. Liver secretes IGF-1 3B. Many organs and tissues create protein and facilitate carb and lipid metabolism

3 gland cascade (gonads)

1. Hypo secretes GnRH 2. Stimulates release of FSH and LH in the gonadotroph cells in the anterior pituitary 3. Target cells (gonads) 4A. germ cell development (sperm/ovum) 4B. secretion of estrogen/progesterone and testosterone

3 gland cascade thyroid hormone (general)

1. Hypo secretes TRH 2. Stimulates release of TSH in thyrotroph cells in the anterior pituitary 3. Thyroid hormone - secretes T3 and T4

3 gland cascade prolactine

1. Hypothalamus release dopamine and maybe TRH (+) 2. Inhibits release of prolactin in lactotroph cells in the anterior pituitary 3. Target cells in the breast which regulate breast development and milk production in women

3 gland cascade for cortisol

1. Hypothalamus releases CRH 2. Stimulates release of ACTH in the corticoptroph cells 3. Adrenal cortex secretes cortisol

Thyroid hormone cascade detailed

1. Hypothalamus secretes TRH -hypophysiotropin hormone 2. Thyrotroph cells in the anterior pituitary stimulate release of TSH 3. Thyroid gland releases T3 and T4, 4. Target cells for TH convert T4 to T3 5a. T3 and T4 go to anterior pituitary (no more TH) 5b. TH goes to hypothalamus (no more TRH)

3 gland cascade hypothalamus and anterior pituiatary

1. Hypothalamus secretion of hypophysiotrophic hormone 1 into the plasma (portal vessel) 2. Hormones arrive at cells in the anterior pituitary and triggers hormone 2 to be released into the plasma 3. Third endocrine gland secretes hormones 3 into the plasma and reaches target cells

Hormones for bone growth

1. IGF locally 2. Growth hormone globally (circulating)

Functions of Thyroid Hormone

1. Increase gene transcription and protein synthesis 2. Controls BMR and body temperature 3. Permissie of beta adrenergic receptors (catecholamines) EPI and NE 4. Development and function of fetal CNS 5. Permissive for overall growth and development

Functions of cortisol in stress

1. Metabolic effect 2. Bone resorption 3. Support sympathetic responses 4. Stimulates erythropoietin 5. Anti-inflammatory 6. psychological 7. inhibition of non essential functions

Physiological Levels of Cortisol (basal levels)

1. Metabolic effects 2. Permissive effect of adrenergic receptors in cardiovascular system 3. Anti inflammatory 4. Fetal/neonatal development

When does the brain get to max size

8 years old because of skull

Bone reabsportion cortisol (stress)

Calcium mobilization -repair bone breaks Long term effect: osteoporosis

What defines the adrenal cortex layers

Focus on primary secretion -enzymes define layers

Adrenal insufficiency (primary)

Hyposecretion of cortisol because something is wrong with the adrenal gland Causes: -Addison's disease -Destructive tumors -infection -Auto immune destruction

beta two adrenergic receptors

Norepinephrine arrives at the smooth muscle -relaxes and dilates blood vessel

Hypothyroidism and causes

Not enough secretion of thyroid hormone (below typical level) Causes: -damage to thyroid gland -lack of iodide in diet -auto immune thyroiditis (hashimoto's) destroy thyroid gland

Long loop negative feedback in Hypo and Anterior pituitary cascade

Out from the body into the brain -regulates secretion of hypothalamus hormones

Half of the cells in the anterior pituitary are dedicated to what type of cells?

Somatotroph cells -growth hormone

CRH effect on anterior pituitary

Stimulates secretion of ACTH

Graves disease

Stimulates the TSH receptors

Osteoblasts

build bone -come up into cartilage and covert it into bone

Chondrocytes

cell in growth plates -newer go through rapid mitosis at the top of the plate (hyperplasia) -older are enlarging bottom of growth plate and secrete cartilage (hypertrophy)

Two stages were we grow the most

early childhood (3-4) adolescents (12-16)

Goiter

enlarged thyroid gland Why? - trophic effect of TSH on follicular cells causing larger follicular cells -no production of T3 and T4 because of lack of iodide

Reinforces and supports sympathetic NS effects

epinephrine

Instant sympathetic response hormone

fight or flight response initiated by norepinephrine

epiphyseal plate

growth plate between epiphysis and shaft -bones get longer

Effect of prolonged stress on sympathetic response

high blood pressure

adrenal insufficiency (secondary)

hyposecretion of cortisol because something is wrong with the anterior pituitary and tropic hormone -low ACTH in plasma -high CRH

hypophysiotropic hormones

hypothalamic hormones that regulate secretion of hormones from the anterior pituitary gland -more or less secretion

Cortisol action in growth

inhibition of growth -stimulates protein catabolism (break down)

Follicles trap ____ for the synthesis of thyroid hormones

iodide

Shaft

middle column of long bone -bone marrow produce more RBC

Glucose sparing

other tissues switch to fatty acids or ketones for fuel, saving the glucose for the nervous system

When do reproductive organs mature?

puberty -part of adolescents

What is another name for IGF

somatomedin

GHRH effect on anterior pituitary

stimulates release of GH

TRH effect on anterior pituitary

stimulates release of TSH and maybe prolactin

GnRh effect on Anterior Pituitary

stimulates secretion of LH and FSH

Insulin growth actions

support building -stimulates protein synthesis -stimulates fetal growth

Colliod

thyroglobulin and thyroid hormone

Thyroxine (T4)

-90% of secretion -"storage pool" in blood -converted to T3 in target cells -4 iodines

Long loop negative feedback of IGF on what hormones

-GHRH and GH

Symptoms of hyperthyroidism

-High BMR and temp -decrease in weight (inappropriate) -nervous and insomnia -fight or flight (permissive of sympathetic NS) -exophthalmos (bulging of eyes)

Cortisol neonatal development (basal level)

-brain, intestines, lungs and glands -production of surfactant in later stages of gestation

What is necessary for growth

-good nutrition -freedom from chronic illness -freedom from chronic stress -sleep -normal host of hormones

Symptoms of adrenal insufficiency (primary and secondary)

-hypotension -hypoglycemia -high plasma ACTH

DHEA

-important in females -develops secondary sex characteristics

Hypothyroidism Symptoms

-low BMR and temp -fatigue -weight gain due to low BMR -weak pulse (permissive of sympathetic NS) -decrease cognitive function (CNS function)

Triiodothyronine (T3)

-most active, potent form -3 iodines

Endocrine Signaling Start: Hypothalamus End: Anterior Pituitary

1. Nuclei in the hypothalamus with axon terminals ending at a capillary bed #1 where hypophysiotropic hormones are released 2. These hormones travel through the portal vessel in the infundibulum 3. Portal vessel ends at the capillary bed #2 which feeds the blood to a collection of cells 4. The hormones are released onto collection of cells in the anterior pituitary 5. Triggers the release of hormones from the anterior pituitary 6. Anterior pituitary hormones then go out to the entire body via general venous circulation

Growth hormone detailed cascade

1. Stimulus (sleep, eustress, exercise) 2. Hypothalamus secretes GHRH -goes into portal vessel -arrives at somatotroph cells 3. somatotroph cells stimulate release of GH from the anterior pituitary 4. GH arrives at the growth plate and induces the secretion of IGF 5. IGF promotes bone growth and development

The hypothalamus regulates activity of ________ in the anterior pituitary and _______ release from posterior pituitary

1. cells 2. neurohormone

Major hormones influencing growth

1. growth hormone 2. insulin 3. thyroid hormone 4. testosterone and estrogen 5. cortisol

Regulation of cortisol secretion cascade (details)

1. hypothalamus secretes CRH -goes through portal vessel 2. Arrives at anterior pituitary corticotroph cells 3. Stimulates anterior pituitary to secrete of ACTH 4. ACTH arrives at the adrenal cortex at the zona fasciculata cells -stimulate secretion of cortisol -growth, health, and development of fasciculata cells 5. Cortisol enters body to target cells 6. Long loop negative feedback (body to hypo)

Hypersecretion of cortisol symptoms

1. osteoporosis 2. Hyperglycemia 3. immunosuppression 4. obesity of trunk and face yet wasting of arms and legs 5. unusual fat on back and shoulders

When do growth plates fuse

After prolonged exposure to sex steroids, estrogen, and testosterone

Adrenal Cortex Layers

All steroid hormone derived from cholesterol 1. zona glomerulosa (aldosterone) 2. zona fasciculata (cortisol) 3. zona reticularis (androgens; DHEA)

Short loop feedback in hypo and anterior pituitary cascade

Anterior Pituitary keeps the hypothalamus under control -Hypo doesn't secrete too much hormone

Graves Disease Cascade

Antibodies and tumors ignore negative feedback 1. TSH receptors stimulated by TSI antibodies -secretion of TH -size of gland increase (goiter) 2. Symptoms 3. Lots of negative feedback (concentration dependent) -decrease in TRH and TSH to try to combat the high [TH] 4. TSI ignore negative feedback and continue to stimulate TSH receptors and produce more TH

Thyroid Stimulating Immunoglobulins (TSI)

Antibodies mimic TSH and bind to TSH receptors on follicular cells -increase TH secretion and gland growth

Thyroid gland (bowtie) is composed of?

Colloid filled spheres enclosed by a single layer of follicular cells -thyroid follicle (lake) -follicular cells (shoreline)

How do you store hydrophobic (amine) thyroid hormone?

Conjugating it to thyroglobulin(protein) and putting it in the colloid lake

Adrenal Medulla NP and EPI %

EPI 80% neurohormone NP 20% neurohormone

Psychological effect of cortisol (stress)

Elevates mood -endorphins co-released with ACTH to inhibit pain

Epiphysis

End of long bone

Adrenal Gland

Endocrine gland on top of kidney Composed two regions -cortex outer layer (Cortisol) -medulla inner (EPI)

Negative Feedback in Endocrine System

Ensure proper levels of all hormones -regulation of hormone levels in a cascade

Short loop negative feedback of GH on what hormone

GH stays in the brain and effects GHRH in the hypothalamus

Thyroid hormone and hormone synthesis 11.9

Goal: Thyroid hormone to be released into the blood 1. TSH receptors on follicular cells 2. iodide is cotransported into follicular cell 3. Pendrin transports iodide into the colloid 4. Thyroglobulin (TG) made in follicular cell get exocytosed into colloid -enzymes in the colloid modify and convert the tyrosine residues of thyroglobulin into T3 and T4 (required iodide) 5. Endocytosis of colloid that has attached T3 and T4 6. Lysosomes enzymes release T3 and T4 from TG 7. Hydrophobic and easily diffused out of the cell into the blood vessels -TG gets recycled

Stimulation of erythropoietin by cortisol (stress)

Goes to long bone and makes you produce more bone marrow for more RBC's -helps with bleeding wounds long term effect: too many RBC (harder to pump)

Metabolic effect of cortisol (basal levels)

Liver glucose production between meals to cells alive

What happens when GH arrives at the growth plate

IGF is made and released right at the growth plate -direct cause of bone growth

Where is the portal vessel?

Infundibulum

Dopamine (DA) effect on Anterior Pituitary

Inhibits prolactin

Somatostatin (SST) effect on Anterior Pituitary

Inhibits secretion of GH

Metabolic effect of cortisol (stress)

Mobilize glucose, fatty acids, and amino acids -fuel and tissue repair -glucose sparing Long term: muscle loss and diabetes

Somatostatin (stops)

Negative feedback on growth hormone

Thyroid hormone actions on growth

Permissive for growth hormone secretion and actions -increase number of GH receptors Permissive of development of CNS

Permissive effect of cortisol (basal level)

Permissive of adrenergic receptors -maintain adequate blood pressure

Anti inflammatory basal level of cortisol

Prevents hyper response of the immune system Example: there is no inflammation and huge pain every time you get a cut or run into something

Cushing's syndrome (cortisol)

Primary hypersecreting tumor in adrenal cortex of the zona fasciculata cells -too much cortisol

Thyroglobulin

Protein that attaches to thyroid hormone -stored in thyroid follicle (lake) -Synthesized by follicular cells

Tropic Hormones

Regulate secretion of hormones

Cushing Disease

Secondary hypersecreting tumor in the anterior pituitary corticotroph cells - too much ACTH production leading to too much cortisol

Trophic Hormone

Secretion influences health, growth, and development in targets -All hormones are trophic

Hyperthyroidism

Secretion of TH above normal levels Causes: -tumors -graves disease

Beta-one adrenergic receptors

When norepinephrine arrives in cardiac muscle -increase heart rate -fight response

Anti-Duiretic Hormone (vasopressin or ADH)

Two main functions 1. water retention at the kidney 2. Constriction of smooth muscle in blood vessel (bloodpressure)

Anti inflammatory effects in cortisol (stress)

Used in transplanted organs in order to prevent rejection

median eminence

Visible swelling -1st capillary bed located here

Alpha-one adrenergic receptors

When norepinephrine arrives at the smooth muscle -constrics and contracts blood vessels