Summary

This document provides an overview of the endocrine system, focusing on adrenal glands, their hormones, effects, and disorders. It covers various aspects, including the structure and function of adrenal glands, the impact of cortisol, and related diseases. It also addresses the consequences of adrenal gland dysfunction.

Full Transcript

Endocrine Disorders of Adrenal Glands Adrenal Glands: are endocrine glands that produce a variety of hormones. They are found above the kidneys. Each gland has an outer cortex which produces steroid hormones and an inner medulla. The gland secretes the following hormones...

Endocrine Disorders of Adrenal Glands Adrenal Glands: are endocrine glands that produce a variety of hormones. They are found above the kidneys. Each gland has an outer cortex which produces steroid hormones and an inner medulla. The gland secretes the following hormones: Epinephrine (adrenaline). from the medulla Norepinephrine (noradrenaline). Glucocorticoids (cortisol) Mineralocorticoids (aldosterone). from the cortex Sex hormones. Pituitary adrenal axis. Pituitary adrenal axis that regulates the secretions of the adrenal cortex is composed of the hypothalamic hormone Corticotropin Releasing Hormone(CRH), the pituitary hormone Adrenocorticotropic Hormone (ACTH) and adrenal cortex hormone (cortisol mainly). Secretion of cortisol from adrenal cortex is directly dependent on ACTH level. Blood levels of cortisol show a peak in the morning and decline to a minimum by evening. This diurnal variation of cortisol is disrupted by changing sleep-wake patterns. Adrenal gland secrete 15-30 mg cortisol daily, under stress the cortisol level may reach 300 mg. 1 Effects of cortisol: Increase blood glucose level (Increase gluconeogenesis) Control carbohydrate, protein and fat metabolism Increase higher function of the brain as memory, concentration, and intellectual performance. Increase production of RBCs Decrease fibroblastic activity Inhibit osteoblasts and decrease bone formation Decrease numbers of eosinophils, basophils, monocytes and lymphocytes Anti-inflammatory and anti-allergic effect Decrease capillary permeability Decrease release of inflammatory mediators Stabilization of lysosomal membrane Disorders of Adrenal Glands 1- Adrenal cortex insufficiency Etiology 1. Congenital. 2. Acquired which is either A. Primarily: Addison’s disease. B. Secondary: To pituitary insufficiency. To exogenous steroid therapy. A- Primarily adrenal cortex insufficiency: Addison’s disease Definition: It is adrenal cortex insufficiency (atrophy) leading to failure of cortisol and aldosterone secretion. 2 Etiology Autoimmune disease: Due to circulating antibodies against adrenal cortex. Tuberculosis. Hemorrhage. Histoplasmosis. Malignancy. Clinical features ❖ Manifestations related to low level of aldosterone. 1. Sodium and water depletion. 2. Reduced extracellular volume and hypotension. 3. Retained potassium and hydrogen ions. 4. Hyperkalemia and acidosis. ❖ Manifestations related to low level of cortisol. 1. Stimulation of pituitary gland leads to increase level of: ACTH. 2. Melanocyte stimulation activity which → increase skin and 3. oral melanin pigmentation. 4. Hypoglycemia. 5. Weight loss, weakness. Addisonian crisis (adrenal crisis). Adisonian crisis --> ( adrenal crisis or acute adrenal insufficiency) Manifested by severe exacerbation of symptoms: hypotension, headache, dehydration, weakness, nausea, vomiting. Precipitated by factors that increase the body demand for cortisol such as surgery, stress, infection, trauma, GA. The patient may die if not treated immediately. Laboratory finding: Decreased: cortisol, sodium. Increased: ACTH, potassium. 3 B- Secondary adrenal cortex insufficiency: Patients on glucocorticoid therapy 1. Owing to their anti-inflammatory and immuno-suppressive action, they are prescribed for management of: Allergic diseases. Autoimmune diseases: LE, pemphigus vulgaris, etc… 2. They are prescribed as replacement therapy in patients with Addison’s disease. Complications of glucocorticoids therapy A. Adrenal cortex atrophy B. Exaggerated normal physiologic action A- Adrenal cortex atrophy The long term low dose steroid (10 mg prednisone for one month) or the short term high dose steroid results in adrenal cortex suppression (atrophy). Mechanism of adrenal atrophy 1. Adrenal cortex secretion is under the control of ACTH secreted by pituitary. 2. Exogenous steroid results in suppression of ACTH release in turn endogenous adrenal cortex secretion is suppressed and adrenal glands undergo atrophy. Patients with adrenal cortex atrophy cannot tolerate stress, surgery, GA, infection and trauma, so the patient suffers adrenal crisis. Causes of adrenal crisis 1- Adrenal insufficiency + Certain conditions Congenital adrenal insufficiency. Stress, GA, infection, Primary: Addison’s disease. surgery, trauma → Secondary: Adrenal crisis. Pituitary insufficiency Exogenous steroid. 2- Sudden withdrawal of exogenous steroid. 4 How to avoid adrenal atrophy? 1. Alternate day therapy: On the day off therapy, the adrenal pituitary axis is allowed to function and produce endogenous cortisol. 2. Single morning dose of exogenous steroid 1.5 hrs after arising. 3. Supplementary corticosteroid should be given before and during period of stress (GA, trauma,…). 4. Gradual withdrawal of steroid therapy to allow for the restoration of adrenal function. 5. Careful case history: patients who had steroid therapy during the last year (normal function of adrenal gland is restored within 9-12 months). B- Exaggerated normal physiologic action 1. Carbohydrate metabolism Impair glucose uptake and utilization by peripheral tissue. Increase gluconeogenesis. Thus, result in cortisol induced diabetes. 2. Lipid metabolism ❖ Increase fat deposition in Face → Moon face. Interscapular region → Buffallo hump. Abdomen → Pendulus abdomen. ❖ These features are related to fat redistribution rather than increase lipogenesis. 3. Protein metabolism Increase breakdown of proteins leading to: Muscular weakness. 4. Lymphoid atrophy leading to: Fulminating infection. Reactivation of latent infection. 5 6. Blood cells: Increase neutrophils, RBCs, platelets, decrease lymphocytes. 7. Blood pressure: hypertension. 8. Retardation of growth in children. 9. Increased intracranial pressure. 10.Euphoria or depression. 11.Osteoporosis: Due to negative calcium balance. 12.Peptic ulcer and hemorrhage. Question: what are the contraindications to corticosteroid treatment? Contraindications of corticosteroid therapy (Some indicated with caution) Diabetes Mellitus Osteoporosis Hypertension Viral infections Glaucoma TB Peptic ulcer Pregnancy and lactation Children Patients on anticoagulants 2- Adrenal Cortex Hyperfunction Etiology A. Cushing disease: due to pituitary gland adenoma → increase stimulation of adrenal cortex. B. Cushing syndrome: due to primary adrenal adenoma. C. Iatrogenic Cushing syndrome: due to exogenous corticosteroid therapy. Manifestations Patients have a round face due to muscle wasting and accumulation of fat (moon face). Buffalo hump due to fat accumulation in the dorsocervical area. Increasing abdominal fat with proximal muscle wasting in arms and legs. Lack of skin integrity with easy bruising and purple stiae. Surface capillaries become fragile, more susceptible to hematoma with mild trauma. Osteoporosis. 6 Oral manifestations Delayed growth and including dental structure. Patients considered to be immunocompromized more susceptible to infections (including oral candidiasis, recurrent herpes labialis, gingival and periodontal diseases. Impaired wound healing, Antibiotic coverage should be considered for dentoalveolar infections or any scheduled oral surgery. General rules For prescribed steroid 1. Weigh the favorable results expected against numerous side effects gained. 2. The combination of steroid with non steroid anti-inflammatory (NSAID) drugs or with other immuno-suppressive drugs may reduce the need for high steroid dose. 3. If the initial dose is effective, the dose should be reduced to the minimum effective dose. 4. Withdrawal of steroid should never be sudden, gradual withdrawal permit gradual regain of adrenal cortex activity and avoid the incidence of adrenal crisis. 5. Alternate day therapy or single daily dose is recommended to minimize adrenal atrophy. For dentists who deal with patients on steroid therapy. Patient with established severe adrenal insufficiency usually require premedication with oral or intramuscular corticosteroids before an invasive procedure Dosages must be agreed upon with the patient’s physician A frequent regimen is to double the daily dose of oral corticosteroid the day before and on the day of surgery GOOD LUCK A. Prof. Dr. Souzy Kamal Anwar 7

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