Cortisol, Thyroid hormones, PTH, Growth of hard and soft tissue

calcitonin and calcitriol, grothw (integrative nature)

hormone.
*Hormones involved
* Main function
* synergism
* Cat or anab?
* permissiveness
* triggers
* Bone anatomy
* Response levels
* what is trabecular bone
* co-secretions
* what is the epiphysegeal plate
*Biosynthesis levels
* cells involved in bone
* Biosynthesis mechanism dynamicity
* chemical nature * why is bone a unique
biomaterial
* how is it carried in plasma
` * what gives bones tensile
* Receptor location
strength
* pathologies
* synergism
Calcium regulation
* permissiveness
* main hormones
*antagonistic molecules
* organs involved
* Inhibitors
* Calcium functions
* tissues that depend on the
* what organs are involved in
hormones
vitamin-D activation
* independent tissues
* calcium vs phosphate
* feedback reg regulation

* integrative nature * what happens if phosphate is

high and calcium is high?
* extra
* what is osteoporosis
* what is osteogenesis
imperfecta
*Calcium distribution
Extra
* what is permisivenes, and synergism
 Cortisol
* Main function
Prevent hypoglycemia
Mimics glucagon and
epinephrine functions
* Cat or anab?
catabolic
* triggers
low plasma glucose
stress
* Response levels
Systemic :
Increases glucose levels
in plasma
Breakdown of proteins
(muscle)
Lipolysis (increases Tg)
(adipose tissue)
Can increases blood
pressure
Can suppress immune
system
Stimulates bone
breakdown
Mood, memory and
learning
Negative calcium balance
Decreases
intestinal
absorption
Increases renal
excretion
Too much can cause
Diabetes
Hypertension
Immunosuppressio
n
Skinny arms and
legs due to tissue
loss
Osteoporosis
Acne
Cellular and molecular:
Activates enzymes that
increase catabolic
behavior
Glycogenolysis
Lipolysis
Protein breakdown
blocks cytokines release
and macrophages
communication $%#$
inhibits inflammation
gluconeogenesis
* co-secretions
N/A
*where is it synthesize: organ,
tissue and type of cell
Organ: adrenal cortex
Tissue: zona fasciculate
(glucocorticoids)
* synthesis and mechanism:
From cholesterol and on
demand
* chemical nature
 steroid destroys adrenal
cortex
* how is it carried in plasma
* Prohormone
corticoid-globulin binding
protein %%^$ Pro-opio-melano-corticotropin
Alpha-MSH
* where are the receptors located ACTH
in the cell Other peptides
cytosolic and nuclear * synergism
* pathologies Glucagon and epinephrine
due to too much or too little * permissiveness
cortisol.
Could be primary (AC) or Glucagon and epinephrine
secondary (HYP) or (PIT)
*antagonistic molecules
Cushings disease
(hypercortisolism) * Inhibitors
Symptomps
Tissue wasting * tissues that depend on the
Moon face hormones
Mood changes Liver
Osteoporosis Muscle
Immunity issues Addipose tissue
At risk of
Immune system
diabetes(hyperglyc
emia) * independent tissues
Causes
Tumor on (AC or N/A
PIT) * feedback reg
Iatrogenic
Addisons disease CRH(HYP)---ACTH(PIT)---
(hypocortisolism) cortisol(AC)
Symptoms Cortisol negatively feeds back
Hypoglycemia to pituitary gland and
Skin looks tan hypothalamus
Skin ACTH short loop feedback to
hyperpigmentation HYP.
due to alpha-MSH
Too much * integrative nature
androgen secretion
(see figure for
details) *Extra
Causes
Immune system CRH and urocortin play a role in
Lowering food intake
attacks and
immunity
 Mood Significance of
POMC endorphins in stress
B-endorphins, alpha-MSH, response?
ACTH.

Thyroid Hormones
* Main function Increases body
metabolism and T (A)
Metabolism long term
Ceullular
Increase O2 consumption Incr enzymatic activity
(thermogenesis) Incr enzyme production
Normal development Incr thermogenesis
Nervous system Causes mithocondria
Skeletal system uncoupling
Regulates tissue growth Modulates the 3 main
Sexual maturation macromolecules
* Cat or anab metabolism.
Glucose Oxidation
Adults
Catabolic
* co-secretions
Children
anabolic T3 andT4
* triggers *where is it synthesize: organ, tissue
and type of cell
Tonic
Organ
* Response levels
Thyroid gland
Systemic (Adults and children Tissue
response differ) Thyroid Follicles
Filled with colloid
 Glycoprotein Could be primary or secondary
micture Graves disease
Cell ( Hyperthyroidism)
Follicular cells play a role Symptoms
Mainly affects
Nervous
system
Heart
Metabolism
* synthesis mechanism Incr protein
catabolism (muscle
See figure for details weakness)
Iodine goes into cell and then Incr nervous
colloid space system excitability
Thyroglobulin (manufactured in Incr HR
follicular cells) goes to colloid Exopthalmus
Tyrosine combines with iodine (bulging eye balls)
to form MIT Sensitive too heat
MIT reacts again with iodine to Too much
form DIT thermogenesis
MIT+DIT= T3 Causes
DIT+DIT= T4 Immune problems
Both T3 and T$ connect to (Thyroid-
thyroglobulin and enter cell by stimulating
endocytosis immunoglobulins)
Overstimulat
Then in cell the dissociate from
e thyroid
globulin
Does not
And leave cell
obey
* chemical nature feedback
regulation
Made of 2-tyrosines + iodines Too much
Lypophilic secretion
Amine derived Goiter
develops
* how is it carried in plasma
Tumors (PIT or
Thyroxine binding globulin THYR)
Hypothyroidism
* where are the receptors located in Symptoms
the cell Low met rate
Sensitive to cold
Cytosolic and nuclear
Low internal heat
* pathologies Low prot synthesis
(ADULTS)
Too much TH or too little Brittle nails
Both HYPO and HYPER cause Thining of hair
GOITER Myoxema
 Slow bone and * permissiveness
tissue growth
To GH and Insulin
(KIDS)
Bradychardia *antagonistic molecules
Slow reflexes
CRETINISM N/A
Decreases
* Inhibitors
hormone secretion
in infancy N/A
Decrease mental
capabilities * tissues that depend on the hormones
Stunned growth
Many tissues
Causes * independent tissues
Low iodine
(primary) N/A
Treatment
* feedback reg
Hyperthyroidism
Destroy TRH(HYP)---TSH(PIT)---T3+T4--
gland using [Deiodinase]--T3
radioactive T3 is active form
iodine T4 is more abundant
Remove Both T3 and T4 negatively
surgically feedback (SL and LL)
Hypothyroidism
Give TH * integrative nature
* extra

Not necessary to live

But is necessary for quality of
* synergism life not for quantity
Thyroid gland is made up of two
N/A
cells

PTH
* Main function Catabolic to bone
Increase calcium levels in * triggers
plasma
Low calcium levels in plasma
* Cat or anab?
* systemic and tissue, cellular ,and * chemical nature
molecular response
Peptide
Systemic
Increase calcium levels * how is it carried in plasma
Breaksdown bone Dissolves in plasma
Increases intestine
calcium permeability * where are the receptors located in
indirectly by stimulating the cell
kidneys to activate
Membrane surface
calcitriol.
Increase renal * pathologies
reabsorption in distal
nepron Too much can cause
Increases Phosphate osteoporosis
excretion by reducing
* synergism
reabsorption
Cellular and molecular * permissiveness
Incr VitD synthesis
Incr renal absorption of *antagonistic molecules
calcium * Inhibitors
Incr renal excretion of
phosphate * tissues that depend on the hormones
Notice that calcium and
Directly
phosphate actions are
Kidney
regulate in opposite Bone
directions
Indirectly
Stimulates osteoclast
intestine
Incr bone readsorption
* independent tissues

* co-secretions
* feedback reg
*where is it synthesize: organ, tissue
and type of cell low calcium---(ca-sensitive-R
sense it), PTH---incr calcium
Organ calcium feeds back negatively
PTH gland, behing to CASR.
thyroid gland
Tissue and cell
4 cells at the back of
* integrative nature
thyroid
activates calcitriol
* synthesis mechanism
involved in calcium regulation
and phosphate
* extra
 Para Thyroid Gland is necessary
to live, but Thyroid is not
Calcitroil (1,25dihydroxycholeocalciferol)
incr intestinal transport of
calcium
* Main function
incr renal reabsorption of
Increase calcium levels calcium
Promotes phosphate helps mobilize calcium
reabsorption out of bones
promotes phosphate
* Cat or anab? reabsorption
* triggers * co-secretions
Low calcium levels in plasma *where is it synthesize: organ, tissue
High PTH and type of cell
prolactin
complex synthesis mechanism
* systemic and tissue, and cellular and involving: many organs skin,
molecular response liver and kidneys
see figure for details
systemic
PTH stimulates kidneys to
incr calcium levels in
activate VIT-D3
plasma
incr permeability in
intestine

* synthesis mechanism

See figure for details

Skin activates VIT-D, then liver processs it sends it to kidney where it
becomes vit-D3 (simplified version)
 * synergism
* permissiveness
* chemical nature *antagonistic molecules

steroid * Inhibitors

* how is it carried in plasma * tissues that depend on the hormones

bound to plasma protein intestine

Bone
* where are the receptors located in Kidney
the cell
* independent tissues
not mention ,but probably
cytosolic * feedback reg

* pathologies
 high calcium, inhibits PTH works in conjunction with PTH
production which in turns
* extra
inhibits kidney from activate
VIT-D to VIT-D3
* integrative nature
Calcitonin

* Main function

stop bone reabsorption

decrease calcium in plasma
increase kidney calcium * synthesis mechanism
excretion * chemical nature

peptide
* Cat or anab?
* how is it carried in plasma
Anabolic to bone
dissolved in plasma
* triggers
* where are the receptors located in
High calcium levels in plasma the cell
* systemic and tissue, cellular ,and * pathologies
molecular response
* synergism
Systemic
Stops bone breakdown * permissiveness
Increase calcium
*antagonistic molecules
excretion in kidney
* Inhibitors
* co-secretions
* tissues that depend on the hormones
*where is it synthesize: organ, tissue
and type of cell * independent tissues

Organ * feedback reg

Thyroid gland
* integrative nature
Tissue and cells
C-cells * extra

Growth Hormone
* Main function tissue growth
 * plasma transport
* Cat or anab? Half dissolved, half bound to
plasma protein
Anabolic
* receptor location
* triggers
membrane receptor
Tonic
tyrosine activity
Circadian rythims
Other hormones
Stress
* pathologies
Circulating nutrients
too much or too little
* response levels
results depend on age
Systemic Dwarfism (Children)
Soft tissue growth Severe deficiency of GH
Bone and cartilage in childhood
growth Acromegaly (Adults)
Increase plasma glucose Adults with severe
Incr Protein synthesis secretion of GH
Incr lipolysis Height does not increase
Cellular Cartilage and soft tissue
Transcription of proteins continue growing
Cell division Lengthening of jaw
Induce hypertrophy Growth of hand and feet
Induce hyperplasia Giantism (Children)
Oversecretion of GH in
* co-secretions children
GH acts as a trophic hormone in * synergism
the liver
Liver secretes INSULIN-LIKE- * permissiveness
GROWTH-FACTOR
Thyroid hormones, insulin, sex
*Biosynthesis hormones play a permissive role
AT PUBERTY.
Organ
Pitutitary gland *antagonistic molecules
* Inhibitors

* synthesis mechanism Somatostatin. Secreted by

hypothalamus
Preprohormone----
prohormone----vesicle storage + * tissues that depend on the
enzymes---cleavage and release hormones

* chemical nature Non-endocrine and endocrine

cells
peptide liver
* independent tissues * integrative nature
* feedback reg Require for Growth
Acts in conjunction with thyroid
(GHRH or Somatostatin)[HYP]---
hormone, insulin and sex
GH[PIT]---(Liver+other tissue)---
hormones
IGF[LIV]+soft and hard tissue
growth * extra
IGF act as negative feedback
(short and long loop)
 Growth and bone
*Hormones involved

Thyroid-H, GH, Insulin, Sex H

For long-bone growth GH, insulin growth factors, and sex-H are the most
important
* synergism
* permissiveness

TH, Insulin, and Sex-H are permissive to GH

* Bone anatomy

Chemical composition
Mineral part
Calcium phosphate (hydroxyapatite)
Structure
Epiphysis
Diaphysis
Epiphyseal plate (longitudinal growth)
Marrow cavity

* what is trabecular bone

Spongy bone
* what is the epiphyseal plate

Site of linear bone growth

In Adults it closes, so no more linear growth occurs

* cells involved in bone dynamicity

Osteoblast
Osteoclast
Chondrocytes
Osteocytes (inactive osteoblasts)

* why is bone a unique biomaterial

Piezoelectric
Mineralize phase + collagenous phase gives unique mechanical properties
High tensile strength
Respond to stress
Dynamic nature

* what gives bones tensile strength

Collagen

Calcium regulation

* main hormones

PTH
Calcitroil
Calcitonin

* organs involved

Bone
Kidneys
Intestines

* Calcium functions

Signaling (vesicle secretion, neurotransmitter release)

Intracellular cement that holds together tight junctions (cadherins)
Cofactor in coagulation cascade
Affect neuronal excitability
 Hypocalcemia
Nervous system become hyperexcitable
Why? Sodium becomes more permeable
Tetany can occur
Hypercalcemia
Depresses neuromuscular activity

* what organs are involved in vitamin-D activation

Skin
Liver
kidneys

* calcium vs phosphate regulation

Control by PTH
Opposite directions
Calcium is retained
Phosphate is excreted

* what happens if phosphate is high and calcium is high?

Calcium stones might form

* what is osteoporosis

Bone resorption exceeds bone deposition

Metabolic disorder
Common in women, due to lowering of estrogen levels in menopause
Treatments
Bisphophonates
Poison osteoclast
dynamic nature of bone is disrupted
more fractures can develop if chronic ingestion of
bisphosphonates
Causes
Low calcium intake
Genes
Hormonal imbalances (too much PTH)
Smoking
menopause

* what is osteogenesis imperfecta

Brittle bone
 Disruption in the production of collagen
Make defective collagen
Genetic disease

* Calcium distribution

ECM
Bone (largest reservoir) and teeth
ECF
Half is bound to plasma proteins
Other half is freely ionized
cofactor in coagulation cascade
Role in smooth and myorcdium contraction
neurtrasnmitter
cement in tight junctions
ICF
Endoplasmic Reticulum
What is hyerphosphatemia
High phosphate levels in blood
Due to precipitation with calcium, plasma calcium levels get lowered
(hypocalcemina)
Hypocalcemia cause incr sodium permeability in neurons
Hyperexcitability of nervous system
Tetany of respiratory muscles can occur
Asphyxiation can occur
Poteintial cause could be
Renal insufficiency