physio endocrine test.txt

autocrine and paracrine

Endocrine and Neurocrine

cAMP and Ca²⁺

SNS

Iodide

T

• 1) humoral
• 2) neuronal
• 3) hormonal

• When the blood concentration of a specific hormone product either increases or decreases
• The hormone will then do the inverse to counteract the imbalance

Low Ca causes more PTH to be produced

fright - SNS firing - Adrenal medulla release of catecholamines

• CRH from hypo
• ACTH from Pituitary gland
• Cortisol from Adrenal gland

• hydrophilic = cell membrane receptor
• hydrophobic = nuclear membrane receptor

• Guanylate cyclase - cGMP
• Adenylyl cyclase - cAMP
• PLC - IP³⁺/Ca²⁺

SRE recepetor

• A/B, C, D, E, F
• Hormone binds E
• DNA binds C at zinc fingers

Negative

• 1) oxytocin
• 2) Na deplorization
• 3) Estrogen

• Autologous: regulates own receptors
• Heterologous: regulates another cell's receptors

Sum of parts is greater than each part itself

One hormone affects how another hormone reacts, but it does not add to its affect

Hormone A reduces effects of Hormone B

• 1) underproduction
• 2) overproduction
• 3) sensitivity

• Ant.: Neurocrine (inside) then Endocrine (exit)
• Post.: Neurocrine

• Ant: Gut
• Post: brain, neural tissue

ACTH, TSH, FSH, LH

GH, PRL

• Release thyroid from thyroid gland
• growth of thyroid gland

• Activate adrenal gland
• Release androgen and cortisol

• females: follicular dev. for egg locations
• males: sperm production

• females: ovulation, secretion of estrogen and progesterone
• Males: testosterone secretion

Growth and metabolism

• females: Increase milk production
• males: LH receptors

Neurophysins

• 4 Neurophysins (NP)
• 5 ADH (AVP)

• Water retention
• Plasma volume restoration
• decrease plasma osmolarity

decreases

• Milk letdown
• uterine contractions

Oxytocin increases ANP release (since we want to lower blood pressure)

• sign: dilute urine
• Cause: lack of ADH (neurogenic or nephrogenic)

• Hypo: loss of one or more anterior pituitary hormone (ACTH, LH, FSH, LSH, GH, PRL)
• Pan: Loss of all anterior pituitary hormone

GH-binding protein *

*not necessary b/c it is a hydrophilic peptide but since it is so important and critical it is nice to increase the half life

Sleep, especially at the beginning

• False
• * Higher in children than adults

• Somatomedins (somatostatin, IGF)
• GHRH (short loop)
• GH (Long loop)

low insulin

T, active when FFA are low to isolate fat

• Anabolic
• * helps build muscle

GH causes insulin resistance b/c it inhibits glucose uptake by insulin

• ANP decreases
• Renin increases
• ** increase ECF volume

glucagon and cortisol

insulin

Linear bone growth

T

• F
• * Occurs b/c of high glucose level on carbs and the increase in insulin. That will inhbit GH and IGF-1

Increases to block effects of insulin and can cause type II diabetes

• acromegaly: GH increased after puberty
• gigantism: GH increased before puberty

• Growth
• Maturation
• Metabolism
• Heat production
• energy mobilization

Parafollicular (P or C) cells

• Hypo: colloid not absorbed
• Hyper: colloid absorbed, removed

• 1) Iodide uptake: from food via Na channel (uptake tyrosine from blood as well)
• 2) Incorporation: bring iodide and tyrosine together (via oxidation and organification)
• 3) Coupling: Bring tyrosines together to form Thyroid
• 4) Diffusion: Release thyroid finto blood

TSH

• ** Oxidation **
• Pendrin moves Iodide to the apical membrane once inside the thyroid gland

• ** organification **
• Once Iodide is at the apical membrane, it is incorporated with Tyrosine

• Inhibit the amount of Iodine incorporation by mainly blocking Na/I channels
• Allows thyriod to settle to normal levels

Couple Tyrosines (Mono and Di) to form T4 and T3

To activate Colloid endocytosis into follicular cells so T4 and T3 can be released in the blood

Thyroid Deiodinase

Type 2

• TRH
• TSH
• Dopamine
• Somatostatin
• T3 (and some T4)

• Brain
• Gonads
• Spleen

CNS development

• TSH increases
• **Occurs b/c of lack of negative feedback from T3

Treat hypothyroidism

• decrease coupling
• decrease oxidation
• decrease Na/I pump uptake

• decrease coupling
• decrease oxidation
• decrease T4-T3 conversion via Thyroid deiodinase

Early AM (start to increase during sleep)

• maintain BP: Alpha-1 receptor
• Anti-inflammation: Block IL-2
• Antagonize Vit. D function: Inhibit Calcium reabsorption, demineralize b one
• CNS: emotion, decrease REM, more awake
• Fetal dev.: surfactant, GI tract

• Low ECF
• High Potassium

All three zones of cortex not producing (no cortisol, no aldosterone, no androgens)

• Syndrome: ACTH low, Cortisol high
• Disease: ACTH high

• Dex is an artificial Cortisol
• In Cushing's syndrome, there is not ACTH to inhibit so Cortisol levels stay the same
• In Cushing's disease, there is high ACTH so dex acts like extra Cortisol and will inhibit Cortisol and ACTH production

• ACTH secreting tumor some where else in body
• No treatment can decrease Cortisol or ACTH production

Aldosterone secreting tumor

• Spironolactone to inhibit Aldo
• Remove tumor

Too much androgen (DEHA and Androstenedione)

NE

Epi

Overproducing adrenal medulla causing abundance of Catecholamines

• abundance: insulin
• starvation: glucagon (secreted with cortisol)

• Beta = insulin
• Alpha = Glucagon
• Delta = Somatostatin

C-Protein (b/c of long half life and short half-life of insulin)

2