Download Cortisol (Hydrocortisone)

CORTISOL
(HYDROCORTISONE)
MICHAEL MONREAN
CORTISOL
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Cortisol is a steroid hormone derived from cholesterol.
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When used as a synthetic made drug it is referred to as
hydrocortisone.
Steroid hormones can be grouped into two classes
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1. Corticosteroids
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Produced in the adrenal cortex
2. Sex Steroids
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Produced in the gonads or placenta
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Cortisol is classified as a corticosteroid
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Within these two classes there are multiple types
depending on the receptors that the steroid binds to.
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Cortisol is thus classified as a glucocorticoid
GLUCOCORTICOID
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Glucocorticoid (GLUCOse + CORTex + sterOID)
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Named for their role in glucose metabolism, where they
are synthesized (adrenal cortex), and for their structure
Anti-inflammatory
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Allergy Suppressant
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Immune Suppressant
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Released in response to stressors or low blood glucose
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Best known for their temporary increase in energy
production from fight or flight response
Hypothalamopituitary adrenal (HPA) axis: Negative
Immune
Feedback
system:
External
altered
Stressors
Hypothalamus
CRH
Anterior
Pituitary Gland
(-)
Posterior
Pituitary Gland
ACTH
Glucocorticoids,
Adrenals Catecholamines,
etc..
Kidney
Muscle:
Net loss of amino
Acids (glucose)
Liver:
Deamination of
proteins into amino
acids,
gluconeogenesis
(glucose)
Fat Cells:
Free fatty
acid
mobilization
Heart rate:
Increased
STEROIDOGENESIS
CORTISOL
CHO
21
30
5
GLUCOCORTICOID
RECEPTOR
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Effect cell by binding to the GR
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When bound, activated GR complex upregulates the
expression of anti-inflammatory proteins in the nucleus
(transactivation)
Down regulates the expression of pro-inflammatory
proteins in the cytosol by preventing translocation of many
transcription factors from the cytosol into the nucleus
(transrepression)
-
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Allows/disallows gene expression of certain transcription
factors
Play an important role in pulmonary maturation during fetal
development  surfactant
EFFECTS OF
CORTISOL RELEASE
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Metabolic Response
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Cortisol stimulates gluconeogenesis and glycogenolysis in the
liver and the muscles.
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Deamination of proteins into amino acids
- Extreme conditions may lead to proteolysis
Glycogen to glucose and glucose-1-phosphate
Immune Response
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Prevents release of substances in the body causing
inflammation
-
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Treats conditions resulting from over activity of B-cell mediated
antibody response i.e. inflammatory diseases such as eczema,
rheumatoid arthritis, allergies
Prevents proliferation and growth of T-cells
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With large exposure can weaken the immune system
ADDITIONAL EFFECTS
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Cortisol reduces bone formation by reducing Ca2+ absorption
in the small intestine
- Long term exposure = possible osteoperosis
Down regulates formation of collagen
-
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Important connective tissue. Effected by deleterious effect of
immune system
Negative effect on wound healing
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Acts as a diuretic
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Effects electrolyte balance by increasing glomerular filtration rate
and plasma flow
- Consequently promotes potassium excretion and sodium
retention
Can effect memory retrieval and long term memory
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Works with adrenaline to produce emotional flash bulb memories
DIURNAL RELEASE
CYCLE
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There exists a normal release cycle in humans
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At highest levels early in the morning
At lowest levels 3-5 hours after sleep onset
Cycle believed to be regulated by light/dark cycle and
information sent to suprachiasmatic nuclei of the
hypothalamus via the retina.
-
Important to receive adequate sleep so as not to be
overexposed to higher cortisol levels
CORTISOL DISORDERS
Cushing’s Syndrome
- high corticosteroid levels in the blood
- changes in protein and carbohydrate metabolism
- buffalo hump or moon face
- free fatty acids mobilized to periphery
Addison’s Disease or Nelson’s Syndrome
- inadequate secretion of glucocorticoids
- hypoglycemia, Na+ and K+ imbalance, dehydration,
hypotension, rapid weight loss and general weakness
- tints or shades of deep amber or brown skin (due to the
stimulation of melanocytes from high ACTH secretion). This
results from inadequate negative feedback from low
glucocorticoid levels
- John F. Kennedy had Addison’s Disease