Endo Ii

Front 1

When is Melatonin made

Back 1

Melatonin

high at night
low at light

marked circadian syntheseis and secretion pattern driven by NE

Front 2

Melatonin

Synthesis from Tryptophan to Serotonin to Melatonin

Back 2

Tryptophan catalyzed by Tryptophan hydroxylas
catalyzed by aromatic aa decarboxylase
to serotonin
N-acetyltransferase activated by phosphorylation due to night time release of synaptic NE and beta receptor activation
2nd enzyme HIOMT is induced or activaed activity not circadian

Nacetyltransferase has hightest activity at night
Serotonin is converted at night to melatonin

Front 3

a

Back 3

May have membrane (rapid) and nuclear (slower) receptor mechanism

high affiningty GPCRs linked to cAMP

Physiological role is in sleep regulation ..promotes sleep

regulation of repro .. inhibits gonadotropin secretion... pineal distruction may cause premature puberty

Front 4

Describe Thyroid Autoregulation

Back 4

Thyroid Autoregulation occurs through plasma iodide ion concentrations at follicular plasma membrane

Increases in iodide intake decrease gland transport and hormone synthesis, and vice versa.

At high plasma iodide concentrations, gland iodide trapping drops precipitously (very high iodide dowes are used to shut down thyroid hormone prod in hyperthroid patients)

Front 5

Wolff-Chaikoff effect

Back 5

an effective means of rejecting excessively large quantities of iodide and preventing the thyrid from synthesizing large quantities of thyroid hormones

so if a person has hyperthyroidism giving high iodide will shut down the thyroid

Front 6

Tell me about TRH
where
how much
how is it regulated

Back 6

TRH
tripeptide
from prohormone in arcuate nucleus and median eminence
short half life (<5min)
low circulating levels

Hypothalamic TRH released into portal venous sys when plasma T4/T3 levels fall or suppressed when levels rise

Front 7

What is the fx of TRH

Back 7

TRH acts on its G protein-linked receptors on thyrotroph cell to stimulate TSH synthesis and release

secretion pulsatile and higher at night

Suppression of TSH by T4/T3 in pituitary is major site of negative FB loop

Front 8

TSH

Back 8

dimeric glycoprotein synthesized by pituitary thyrotroph cells
alpha subunit identical to FSH, LH and hCG
Beta subunit confers TSH biological activity

increases growth: DNA, RNA, Protein, Phospholipid, cell size, cell #, follicular formation.. chronic growth = goiter

Increases sythesis of hormone by trapping I, endocytosis of colloid, proteolysis of thyroglobin, increased glucose oxidation and NADPH generation.

Front 9

What causes Graves' disease

Back 9

Graves' dx (common hyperthyroid condition) is characterized by receptor antibodies that mimic TSH, hyperstimulating thyroid hormone production and growth of the thyroid gland (diffuse symmetrical hyperthyroid goiter)

Front 10

What are the underlying causes of goiters?

Back 10

see Vander

Front 11

What happens if iodide trapping is absent

Back 11

decreased thyroid uptake and salivary/blood ratio of radioactive iodide

Front 12

What happens if peroxidase is absent?

Back 12

increased early uptake of radioactive iodide, rapid discharge of perchlorate

Front 13

Deiodinase

Back 13

Increased uptake of radioactive iodide

excretion of mono and di iodotyrosines

Front 14

Coupling (organificiation)

Back 14

a

Front 15

What is the difference between steroid hormone receptors and thyroid hormone receptors?

Back 15

steroid hormones homodimerize
thyroid receptors bind to retinoic acid receptors
Vit A isomerizes .. these become ligands for a nuclear receptor

RXR dimerizes with thyroid hormone receptor forming a heterodimeric pair.

Front 16

Explain why albumin levels are important when assessing Ca2+ status

Back 16

Low total calcium in patient with no clinical sign of hypocalcemia and albumin is also low so free calcium is in normal range so no symptoms of hypocalcemia. Free calcium is the only active type of calcium

Front 17

Explain the physiological importance of thyroid hormones in overall development and metabolism

Back 17

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Front 18

Recognize structures of T4, T3 and reverse T3, and understand importance of dietary iodide and its thyroid gland uptake for their adequate biosynthesis.

Back 18

-

Front 19

Detail the HPT axis, including negative FB, and explain the role of TRH

Back 19

-

Front 20

Understand how TSH stimulates T3 and T4 biosynthesis in the thyroid follicle

Back 20

-

Front 21

Describe the role of thyroglobulin and thyroperoxidase in T3/T4 biosynthesis

Back 21

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Front 22

Clarify the importance and role of plasma proteins involved in thyroid hormone transport

Back 22

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Front 23

Be familiar with the similarities and differences between the thyroid hormone receptors and steroid hormone receptors

Back 23

-

Front 24

Explain how thyroid hormone receptors act to regulate gene TRXN , including the importance of retinoic acid and its receptors in this process

Back 24

-

Front 25

Relate the key effects of thyroid hormone/receptors on the physiology of specific organs

Back 25

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Front 26

Explain the clinical picture of hyperthyroidism and the importance of TSH assays

Back 26

-

Front 27

Explain the clinical picture of hypothyroidism, overt and subclinical, and the importance of TSH assays.

Back 27

-

Front 28

GH
where does it come from
what does it do
inhibited/stimulated

Back 28

from anterior pituitary
stimulates growth and metabolism
controlled by GHRH from hypothalamus
somatostatin from pancreas inhibits
excess in childhood = gigantism
excess in adulthood = acromegaly
deficiency in childhood = dwarfism

Front 29

PRL
where does it come from
what does it do
inhibited/stimulated

Back 29

from anterior pituitary
stimulates milk production in breasts that have been hormonally prepared during pregnancy
Inhibited by Dopamine
Minor stimulation by PRH from hypothalamus
Causes neg fb to hypothalamus to decreases GnRH

Front 30

TSH
where does it come from
what does it do
inhibited/stimulated

Back 30

TSH from ant. pituitary
is a glycoprotein that stimulates thyroid gland to absorb iodine
secretes T3/T4
stimulated by TRH from hypothalamus
inhibitied by T3/T4

Front 31

ACTH
where does it come from
what does it do
inhibited/stimulated

Back 31

ACTH from ant. pituitary
stimulates adrenal cortex to release corticoid and sex steroids
stimulated by CRH from hypothalamus
inhibited by negative feedback of glucocorticoids (cortisol)

Front 32

FSH
where does it come from
what does it do
inhibited/stimulated

Back 32

FSH from ant. pituitary is stimulated by GnRH from hypothalamus
FSH is inhibited by E or T

FSH in males
stimulates Sertoli cells to carry out spermatogenesis
stimulates seminiferous tubules

FSH in females
stimuates follicle growth
stimulates E secretion

Front 33

LH
where does it come from
what does it do
inhibited/stimulated

Back 33

LH in males
stimulates Leydig Cells to secrete T

LH in males
promotes ovulation
stimulates formation of corpus luteum and progesterone secretion

Front 34

ADH/Vasopressin
where does it come from
what does it do
inhibited/stimulated

Back 34

presses on blood vessels
causes constriction of arterioles and increase blood pressure
in kidney, stimulates water reabsorption, leading to increase blood pressure
stimulated by increase in plasma OSMOLARITY and decrease in plasma VOLUME sensed by osmoreceptors and baroreceptors.

Front 35

Aldosterone
where does it come from
what does it do
inhibited/stimulated

Back 35

produced by cells in the adrenal glomerulosa
stimulates active reabsorption of Na in distal convoluted tubule of kidney nephron -> water is passively reabsorbed
Excess Ald leads to water retention and high bp
Too low Ald leads to dehydration
controlled by renin angiotensis system not ACTH.
Hypoaldosterone is termed Addison's dx
has bodyguard 11β HSD to prevent cortisol acting on aldosterone receptors in kidney to prevent hypertension

Front 36

Cortisol
where does it come from
what does it do
inhibited/stimulated

Remember the zones of the adrenal gland from outer to inner: Zona Glomerulosa, Zona Fasciculata, Zona Reticularis

Back 36

cortisol is a glucocorticoid
from the zona fasciculata
is controlled by ACTH
antagonize insulin effects
increase blood glucose levels by:
1) breakdown of proteins into amino acids
2) conversion of amino acids into glucose (gluconeogenesis)
-decrease inflammatory response
-decrease allergic response

Front 37

Androstenedione
where does it come from
what does it do
inhibited/stimulated

Back 37

produced by cells in the zona reticularis
controlled by ACTH
can cause masculinization of women due to oversecretion of these adrenal adrogens.

Front 38

Epinephrine and Norepinephrine
where does it come from
what does it do
inhibited/stimulated

Back 38

Epinephrine and Norepinephrine
increases blood pressure
increases oxygen consumption
increases heart rate (tachycardia)
increases conversion of glycogen to glucose in blood by liver
vasodilation and dilation of pupils