Published on March 1, 2014
Topic Glucocorticoid Presented by : Abdul Qahar buneri AWKUM (Buner Campus)
Glucocorticoid action physiological and pharmacological action • Physiological action Small doses correct the metabolic abnormalities in part directly, in part by permitting other reactions to occur : Permissive action - the requirement for g.to be present for catecholamines to exert their effects (pressor response, bronchodilation)
Physiological action • Intermediary metabolism: Increased protein catabolism Increased hepatic glycogenesis (glycogen synthesis) and glyconeogenesis decreased utilisation of glucose by muscle • resistance to „Stress“
Physiological action Hyperglycemia, catabolic and antianabolic Hyperglycemia effects G.increase serum glucose concentrations (gluconeogenesis) (and thus stimulates insulin release) and inhibits the uptake of glucose by muscle cells. The increased insulin secretion stimulates lipogenesis. All contributes to maintenance of an adequate supply to the brain
Pharmacological action At high doses: Antiinflammatory (acute and chronic inflammation) Immunosuppressive Antiallergic Antiproliferative
Antiinflammatory action G.dramaticaly reduce the manifestation of inflammation due to their profound effects on the concentration, distribution, and function of peripheral leukocytes and to their suppressive effects on the inflammatory cytokines and chemokines, and on the mediators of inflammation. The concentrations of neutrophils in the circulation increases while the lymphocytes (T and B cells), monocytes, eosinophils and basophils decrease. The changes are maximal in 6 hours and are dissipitated in 24 h after a high (pharmacological) dose. Function of tissue macrophages is inhibited. G.cause vasoconstriction,and decrease capillary permeability by reducing the amount of histamine released by mast cells.
Doses physiological/pharmacological • Cortisol secretion in a healthy human Daily secretion at rest: 20-40 mg secretion in stress: >100 mg Cortisol 10-30 mg/day in two or three decreasing doses 15-10-5 mg (15-10 mg , 10-5 mg) Synthetic corticosteroids that are long-acting and devoid of saltretaining activity should not be used.
IRDC and surfactant • a lipid surface-tension-lowering agent is a mixture of dipalmitoylphosphatidylcholine, other lipids, and proteins the fluid lining the alveoli. If the surface tension is not kept low when the alveoli become smaller during expiration, they collapse - atelectasis. S. also helps to prevent pulmonary edema. S is produced by type II alveolar epithelial cells and is important at birth.The lungs remain collapsed until birth.After birth, the infant makes several movements and the lung expands. S. keeps them from collapsing again. S.deficiency is an important cause of infant respiratory distress syndrome (IRDS) that develops in infants born before their surfactant system is functional.
IRDC and surfactant • Therapy: Surfactant preparations derived from bovine lungs and synthetic surfactant for use by inhalation are used profylactically at birth to decrease the severity of IRDS but not the incidence of chronic lung disease in suvivors. Maturation of surfactant in the lungs is accelerated by glucocorticoid hormones. The lungs are rich in glucocorticoid receptors. Betamethasone 12 mg i.m Patchy atelectasis is also associated with s. deficiency in adults who have gone cardiac surgery involving use of a pump oxygenator and interruption of the pulmonary circulation. Abnormalities that develop following occlusion of a main bronchus, occlusion of one pulmonary artery…..ARDS
Glucocorticoid excess (pharmacol. • • • • • • • therapy)-cont. Cushing´s syndrome Osteoporosis, mental disorders Adrenal insufficiency Diabetes resistant to insulin but rarely develops ketoacidosis Peptic ulcers (occasionaly observed even after only a few days of treatment) Wound healing is impaired Bacterial and mycotic infections may be masked
Glucocorticoid excess Subcapsular posterior cataracta, increased intraocular pressure, glaucoma Growth retardation in children
Glucocorticoid excess Cushing´s syndrome Patients protein-depleted as a result of excess protein catabolism. The skin and subcutaneous tissue are thin, muscles are poorly developed. Wounds heal poorly, and minor injuries are caused. Body fat is redistributed in a characteristic way. The extremities are thin, but fat collects in the abdominal wall, face and upper back („buffalo hump“). The subdermal tissues rupture to form prominent reddish-purple striae. Moon face. Hyperglycemia (gluconeogenesis+decreased peripheral utilization of glucose---insulin-resistant DM About 85% of patients are hypertensive (deoxycorticosteron secretion is increased ---- steroid diabetes
Glucocorticoid excess Osteoporosis, mental disorders • A loss of bone mass for decreasing bone formation and increasing bone resorption leads eventually to collapse of vertebral bodies and other fractures. • Mental aberrations ranging from increased appetite, insomnia and euphoria to frank toxic psychosis
Glucocorticoid excess Adrenal suppression Free glucocorticoid inhibits ACTH and the degree of pituitary secretion inhibition is proportionate to the circulating glucocorticoid concentration. • The dangers involved when prolonged treatment with anti-inflammatory doses of G. is stopped deserve emphasis. Not only is the adrenal atrophic and unresponsive after such treatment but the pituitary may be unable to secrete normal amount of ACTH for as long as a month.The cause of the deficiency is presumably diminished ACTH synthesis.
Glucocorticoid excess Adrenal suppression When is this mechanism manifested during longterm therapy? if dosing is suddenly withdrawn What is the risk? adrenal insufficiency Prevention? Slow withdrawal of therapy with antiinflammatory dosing, At time of minor stress the patient should be given supplementary therapy (twofold dose increases for 24-48 hours) or severe stress (up to 200 mg of cortisol or 50 mg of Prednisone for 48-72 hours)- such accidental trauma or major surgery.
Glucocorticoid excess Therapy with steroids with mineralocorticoid effects in addition to glucocorticoid effects: sodium and fluid retention, loss of potassiumIn patients with normal cardiovascular and renal functions , this leads to a hypokalemic, hypochloremic alkalosis and eventually a rise in blood pressure. In patients with hypoproteinemia, renal disease, or liver disease- edema may occur In patients with heart disease: heart failure
Glucocorticoids by abdul qahar. Endocrine hypertension By Abdul Qahar. Modern synthetic theory of organic evolution shared by abdul qahar buneri.
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