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26 Cards in this Set
- Front
- Back
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Adrenal gland cortex
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zona glomerulosa- aldosterone
zona fasiculata- cortisol zona reticularis- androgens |
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adrenal medulla
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catecholamines
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regulation of adrenal steroid release
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1. negative feedback loop
2. circadian rhythms |
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cortisol concentration is highest...
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in the morning
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What is the precursor for the biosynthesis of the adrenal hormones?
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cholesterol
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How is the release of cortisol regulated?
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circadian rhythm
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MOA of glucocorticoids
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1. glucocorticoid receptor is widely distributed
2. ligand binds to the cytosolic receptor 3. ligand/receptor complex translocates to the nucleus and binds to DNA 4. DNA transcription is activated |
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In general, all glucocorticoids:
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1. promote normal intermediary metabolism
2. increase resistance to stress 3. Alter blood cell levels in plasma 4. have anti-inflammatory action 5. affect other components of the endocrine system |
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effects of cortisol on carb metabolism
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1. increases blood glucose
2. increases gluconeogenesis 3. decreases use of glucose by cells |
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effects of cortisol on lipid metabolism
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1, increase blood fatty acid concentration
2. increase lipid breakdown in adipose tissue to fatty acids as energy source |
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effects of cortisol on protein metabolism
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1. increase blood amino acids
2. decrease AA entry into extrahepatic cells 3. increase protein brekdown in extrahepatic tissues 4. increase liver protein synthesis 5. increase conversion of AA to glucose in liver cells |
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What is the MOA of glucocorticoids at the cellular level and in the inflammatory response?
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cytosolic receptors bind and make proteins
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What is the effect of glucocorticoids in the liver and extrahepatic tissues?
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increases protein breakdown and protein synthesis, increases conversion of AA to glucose in liver cells
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Pharmacokinetics
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90% cortisol is bound to plasma proteins
synthetic corticosteroids are bound by albumin remaining 10% is free liver inactivation and renal excretion half-life of steroids may increase dramatically in individuals with hepatic dysfunction |
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short acting
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cortisone- t1/2=30 min, B1/2=8-12h
hydrociortisone- t1/2=80-116 min, B1/2=8-12 h |
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intermediate acting
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ALL HAVE BIOLOGICAL HALF LIFE OF 18-36 HOURS
prednisone - t1/2=60 min prenisolone- t1/2 =115-212 min triamcinilone- t1/2= 200+minutes methylprednisolone- t1/2=78-188 min |
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long-acting
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dexamethasone- t1/2=110-210 min
bethamethasone- t1/2=300+ min Biological t1/2 =36-54 hrs. |
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How much cortisol is bound to proteins and why is this important?
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90%, pretty much inactive
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What is the difference between the plasma and biological half life?
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Bio is longer
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Explain how a glucocorticoid may have mineralocorticoid characteristics.
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Aldosterone---salty water retention
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Anti-inflammatory effects of glucocorticoids
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1. inflammatory diseases
skin diseases arthritis, bursitis, tenosynovitis IBD 2. respiratory diseases (asthma, COPD) 3. rheumatoid disorderd and collagen diseases rheumatoid arthritis, lupus |
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inhibition of the immune system (glucocorticoids)
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1. autoimmune diseases
2. organ transplants 3. allegic conditions |
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other therapeutic effects
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1. replacement therapy (Addison's disease)
2. cerebral edema 3. premature delivery 4. eye injury (inhibit fibrosis) |
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Adverse effects
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1. osteoperosis
2. cataracts 3. hyperglycemia 4. decreased resistance to infection 5.Fluid and electrolyte imbalance 6. peptic ulcer disease 7. redistribution of body fat 8. loss of muscle mass 9. adrenal supression (Addison's disease) |
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Cushing syndrome
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etiology:
1. overproduction or adminiwtration 2. pituitary oversecretion of ACTH 3. Adrenal cortex tumor 4. ectopic secretion dermatologic effects 1. easy bruising, skin atrophy and thinning 2. acne 3. hirsutism |
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Addison's Disease
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primary adrenal insufficiency
1. autoimmune 2. tuberculosis 3. surgical removal secondary adrenal insuffieicncy 1. ACTH deficiency 2. glucocorticoid therapy symptoms 1. chronic fatigue 2. muscle weakness 3. loss of appetite 4. weight loss treatment 1. replacement therapy |
