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ADRENALINE INSUFFICIENCY PRESENTED BY: DR APEKSHA INAMDAR MODERATED BY: DR DANIEL MABEN.
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CONTENTS Introduction Anatomy Function Disorders Aetiology Pathophysiology & complications Clinical presentation Laboratory findings Medical management Dental management Conclusion References
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INTRODUCTION Third potentially life threatening situation but readily treatable. First recognized by Addison in 1844 Least likely to occur in dental office Incidence-0.3-1% in 100000
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ANATOMY 6 to 8g Endocrine glands Located bilaterally at the superior pole of each kidney. Outer cortex and an inner medulla. The adrenal medulla functions as a sympathetic ganglion and secretes catecholamines, primarily epinephrine Adrenal cortex secretes several steroid hormones
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Every day about 10-20mg of hydrocortisone and 0.125mg of aldosterone is secreted
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Dental management of the medically compromised patient by Donald A Falace and James Little Everyday about 0.125mg of aldosterone is secreted
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ADRENOCORTICAL DISORDERS Adrenocortical hyperfunction may lead to release of excessive: glucocorticoids (Cushing disease) mineralocorticoids (Conn syndrome or hyperaldosteronism) androgens (congenital adrenal hyperplasia) Adrenocortical hypofunction may lead to the depletion of: glucocorticoids (Addison's disease) mineralocorticoids (hypoaldosteronism)
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CUSHING'S SYNDROME Excess circulating corticosteroids Cause : Tumors of pituitary / adrenal gland Administration of glucocorticosteroids for treatment of various medical problems. Normal daily secretory rate of cortisol = 20mg/day
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Conn’s syndrome Primary hyperaldosteronism = Arises from adrenal cortex as benign tumour/ hyperplasia Secondary hyperaldosteronism = activation of renin-angiotensin. Clinical features: Hypokalaemia Metabolic alkalosis Polyuria Mucle cramps & weakness Hypertension polydypsia
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CORTICOSTEROID S IMPORTANCE OF CORTICOSTEROIDS Corticosteroids -effect on the vascular system (blood vessels, heart) and liver during episodes of physiologic stress Mineralocorticoids --maintaining blood pressure Norepinephrine -rise in mean blood pressure (does not cause vasodilation)-peripheral resistance increase- due alpha action Epinephrine - rise in systolic and fall in diastolic –peripheral resistance increases- due to beta action Glucocorticoids promote gluconeogenesis and glycogen deposition in the liver and inhibit peripheral utilization of glucose resulting in increased blood glucose levels
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Clinical indications of glucocorticoid usage in nonadrenal disorders Han S. Clinical pharmacology review for primary health care providers: II. Steroids. Translational and Clinical Pharmacology. 2015 Jun 1;23(1):15-20.
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ADRENALINE INSUFFICIENCY Acute adrenal insufficiency is a life threatening state caused by insufficient level of cortisol which is a hormone produced and released by adrenal gland. ETIOLOGY PRIMARY AISECONDARY AI ONSET ACUTE AICHRONIC AI AI = ADRENAL INSUFFICIENCY
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CAUSES Sudden withdrawal of long term steroid therapy Stress either physiological or psychological Autoimmune adrenalitis After bilateral adrenalectomy Tuberculosis, AIDS, metastatic diseases Sudden destruction of pituitary gland-secondary Lesions of hypothalamus-tertiary Adrenal gland injured through trauma, hemorrhage infection, thrombosis, Causes of adrenal insufficiency Patients on systemic corticost eroids Adrenal disorders Hypopitu itarism TraumaAddison’ s disease SurgeryPost- adrenale ctomy General anaesthe sia Waterho use- Frederic hsen syndrom e Infection / inflamm ation Congenit al adrenal hyperpla sia
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Predisposing factors for adrenaline insufficiency Sudden withdrawal of steroid hormones in a patient suffering from Addison’s disease Sudden withdrawal of steroid hormones in a patient with normal adrenal cortices After stress, physiological or psychological After bilateral adrenelectomy After sudden destruction of pituitary gland After injury to both adrenal gland
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Pathophysiolo gy Patient with Primary adrenal insufficiency:-{Addison) Hypofunctioning adrenal cortex Cannot produce blood levels of corticosteroids And cannot respond to increase or decrease blood levels of ACTH So patient under stress or non-stressful situation cannot increase cortisol levels Acute adrenal insufficiency develops
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Receiving glucocorticosteroid therapy for non endocrine related disease Total amount of endogenous and exogenous steroids determines blood levels of cortisol Adrenal cortex daily-20mg +exogenous dose-50mg Causes elevation of glucocorticosteroid in blood Inhibit ACTH Inhibit adrenal cortex to secrete cortisol Patient with normal adrenal cortex{secondary}
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As glucocorticosteroid therapy continues ability of adrenal glands to produce endogenous glucocorticoids decreases If exogenous therapy is abruptly stopped ACTH and endogenous steroids may prove deficient Adrenal cortex cannot produce required cortisol levels Any stressful situation may provoke acute adrenal insufficiency
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Addison’s disease Primary adrenal insufficiency
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Return to Normal Functioning depends upon 1.WHICH corticosteroid was given -20 mg Hydocortisone = 5 mg Prednisolone = 0.75 dexamethasone -Patients with Addisons disease require 15- 25 mg of hydrocortisone in 2 divided doses i.e. 2/3 in morning & 1/3 in evening -But patients suffering from diseases such as arthritis receive 10 mg Prednisolone equivalent to 50 mg of Hydrocortisone 2.DOSE of exogenous corticosteroid administered 3.DURATION of treatment – any patient receiving glucocorticoids for 2 weeks or more 4.How FREQUENTLY glucocorticoids were given 5.ROUTE of administration topical & intra articular injections do NOT suppress adrenal cortex
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Rule of “Two” Adreno Cortical Insufficiency may be suspected in a patient who has received glucocorticoids 1.In a dose of 20 mg or more of cortisone or its equivalent. 2.Oral or parenteral steroids for 2 weeks or more 3.Above two within 2 years of dental treatment
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Diagnosi s 1)ACTH (cosyntropin) stimulation test 2)Estimation of serum cortisol levels-low 3)Checking fasting blood sugar levels-low 4)Serum potassium levels-high 5)Serum sodium levels-low
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1)Electrolyte disturbance a)Hyponatremia b)Hyperkalemia c)Hypercalcemia d)Hypoglycemia 2)Anemia 3)Azotemia 4)Eosinophilia LABORATORY FINDING
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