lecture 4 Flashcards by benno Brennan

Adrenal cortex features

Stimulates by stress response
Produces steroid hormones derived from steroids (corticosteroids)
Regulation of Na+ and K+ and fluid volume

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Zones of the cortex

Glomerulosa = aldosterone
Fasciculata = cortisol ( and androgens)
R = androgens
medulla

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Medulla hormones

Adrenaline and noradrenaline

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Cortisol

Stress hormone
Secreted from zone fasciculate
Release controlled by CRH/ACTH

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Circadian rhythms and CRH

CRH secretion synchronised with sleep/wake cycle

Stress induced secretion of CRH increases glucocorticoid/cortisol secretion and overrides rhythms

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Actions of cortisol/glucocorticoid

provides fuel
protects CVS
depresses inflammation and immune responses

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Metabolism - how is it regulated using cortisol .. LOW BLOOD GLUCOSE

Insulin decreases
Glucagon increases 
Growth hormone increases 
Cortisol increases 
Hunger increases
release of fats from white fat

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Cortisol effect on CVS

Increases contractility and force of contraction
Increases peripheral resistance
Increases effects of noradrenaline and adrenaline
Increases number of angiotensin receptors

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Hypertension and cortisol

Common In Cushings

Excess cortisol

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Hypotension and cortisol

Common in Addisons

Deficit of cortisol

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Cortisol - inflammatory and immune response

Antiiflammaory and immunosuppressive

Inhibits secretion of cytokines, histamine release, proliferation of immune cells and synthesis of antibodies

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Therapeutic use of glucocorticoids ( cortisol )

reduce inflammation

damp down immune responses

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How is cortisol regulated

Hypothalamus releases CRH via portal hypophyseal circulation
Anterior pituitary releases ACTH via systemic circulation
Adrenal cortex ( cortisol)

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Feedback control of cortisol

Time of day ( shift work) - circadian rhythm
Negative feedback
Positive feedback - physical and emotional

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AVP =

ADH

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Aldosterone main function

main role is to regulate salt and water in the body, thus having an effect on blood pressure.

Aldosteorne is secreted from

Adrenal gland - glomerulosa zona

How is aldosterone released

Low Na stimulates renin release in kidney
Renin cleaves angiotensinogen to Ang I
Ang I converted to Ang II

Aldosterone stimulates..

Na-K ATPase in collecting ducts
Na reabsorbed from filtrate
K secreted into filtrate
Water retention

Corticosteroid receptors

Steroids fat soluble

Cytosolic receptors

Glucocorticoid receptors - CORTISOL
Mineralocorticoid receptors - ALDOSTERONE

paths to disregulation fo cortisol

Primary = adrenal cortex - cortisol/aldosterone 
Secondary = Anterior pituitary( ACTH)
Tertiary = hypothalamus ( CRH)

Too little cortisol - primary deficit

Failure of adrenal cortex to secrete cortisol
Loss of negative feedback on CRH and ACTH secretion
CRH and ACTH increase

Too little cortisol - secondary deficit

Failure of pituitary to secrete ACTH
Loss of negative feedback
CRH high but ACTH low
Atrophy of adrenal cortex

Symptoms of Addisons ( too little cortisol )

Hypotension 
Hypoglycemia 
Hyponatremia 
Hypovolumia 
Hyperpigamnetation 
Hyperkalaemia

Hyperkaeamia

High K+ Suggests lack of aldosterone

Main causes of Addisons

Autoimmune destruction of adrenal cortical cells = primary Chronic glucocorticoid treatment = secondary Infection Drugs that inhibit cytochrome p450 Cortisol resistance

Treatment ( urgent ) for addisonian crisis

High dose IV Fludrocortisone - mineralocorticoid ( primary) Glucocorticoid and fluids Need to restore blood volume, pressure and sugar

Cushings disease symptoms

Muscle wasting High blood sugar Fat deposition Hypertension

Cushings disease

ACTH high Stimulastes MR Raises blood volume,blood pressure and Na

Excess cortisol effects

Reduces inflammation - asthma, IBS, Supresses immune system - MS Atrophy of zone fascicula ( cortex)

Cushings treatment

Remove or destroy abdnormal source of ACTH/cortisol

Why shouldn't steroids be stopped suddenly

treatment will reduce ACTH secretion via negative feedback Low ACTH = atrophy of cortex Tapering off= ACTH can rise, growth of cortex is stimulated

What is aldosterone release controlled by

Ang II

Addisons crisis

``` Circulatory collapse Hypoglycaemia Nausea and vomiting Weakness Depression and fatigue ```