Presentation on theme: "IN THE NAME OF GOD. Side effects from glucocorticoids are mostly seen with oral and injectable glucocorticoids, but can be seen with inhaled and topical."— Presentation transcript:
Side effects from glucocorticoids are mostly seen with oral and injectable glucocorticoids, but can be seen with inhaled and topical steroids at higher doses. glucocorticoid toxicity is related to both the average dose and cumulative duration of use.
moon face buffalo hump central obesity Truncal and peripheral adipocytes vary in sensitivity to the glucocorticoid facilitated lipolytic effect—that is, the peripheral adipocytes are more sensitive to this effect than the central adipocytes.
Cataract Glaucoma Exophthalmos Swelling of lids and ocular muscle
The pathogenesis is multifactorial,involving increased peripheral vascular sensitivity to adrenergic agonists, increased hepatic production of angiotensinogen (renin substrate), and activation of renal mineralocorticoid receptors.
Glucocorticoids increase hepatic glucose production (in part by increasing substrate availability through proteolysis and lipolysis); they also induce insulin resistance and hyperinsulinemia and inhibit glucose transport into the cells. New-onset diabetes occurs in patients with underlying impaired glucose tolerance or subclinical diabetes.
Serum lipids, both triglycerides and cholesterol, may be increased during corticosteroid therapy.
There was no increased incidence of PUD in those taking corticosteroids alone but there was an increased risk in those taking non- steroidal anti-inflammatory drugs. when a patient is prescribed corticosteroid treatment who has risk factors for PUD such as a past history of PUD; smoking; high alcohol intake; or receiving ulcerogenic drugs(NSAIDS ) should be given a prophylactic agent for GI bleeding.
Polycythemia is a feature of Cushing’s syndrome but does not appear to be a feature of corticosteroid therapy.
The total white blood count is increased in patients on corticosteroids. The various classes of white blood cells are affected in the following ways: Polymorphonuclear leucocytes increased Lymphocytes decreased; T cells are reduced to a greater extent than B cells although immunoglobulin synthesis is also decreased Monocytes decreased Eosinophils decreased
Steroids act in multiple ways to inhibit the immune system and so their use is associated with an increased susceptibility to infection.
Corticosteroid use is associated with sodium and water retention; this can be reduced by recommending a low salt diet.
The greatest rate of bone loss occurs in the first 6 months and is thought to continue at a lower rate for as long as steroids are used. Bone loss is greatest in trabecular (cancellous) bone, which is more metabolically active but also occurs in cortical bone.
Reduced osteoblast activity resulting in reduced bone formation Increased bone resorption due to increased osteoclast activity Reduced intestinal absorption of calcium and phosphate Reduced renal reabsorption of calcium Secondary hyperparathyroidism Reduced sex hormones
A substantial increase in fracture risk can occur within 3-6 months of steroid treatment. If steroids are discontinued, bone improves substantially after 6-24 months. It seems that bone loss is related to the dose of glucocorticoids.
During corticosteroid use there is a reduction in muscle protein synthesis and protein catabolism; therefore, muscle weakness and loss of bulk can occur. In its extreme form a steroid myopathy may develop, affecting the proximal muscles in upper and lower extremities.
Osteonecrosis (avascular necrosis) is a serious complication of corticosteroid.The risk increases with both dose and duration of treatment but it is not possible to predict who will be affected. The femoral head is most frequently involved but other large joints may be affected. Joint pain and stiffness are the earliest symptoms.
Psychosis has been reported and usually develops within 2 weeks of starting treatment, particularly with doses of >40 mg/day prednisolone. Symptoms respond to tapering of the corticosteroids, usually within 3 weeks.
Exogenous glucocorticoids can lead to HPA suppression and secondary adrenal insufficiency (isolated glucocorticoid deficiency with normal aldosterone secretion). The abrupt cessation, or too rapid withdrawal, may cause symptoms of AI.
Any patient with Cushingoid appearance Any one who has received more than 20 mg prednisone daily (or equivalent) for more than 3 weeks Any one who has received an evening dose of prednisone (even physiologic) for more than 3 weeks
No need for testing, and these patients should be treated like any patient with secondary AI by giving stress dose of glucocorticoids perioperatively.
Any patient who has received any dose of glucocorticoids for less than 3 weeks Any patient on less than 5 mg prednisone, provided that it is not taken in the evening Alternate glucocorticoid therapy
We try to limit the adverse effects of glucocorticoids by the following steps: Use of the lowest dose of glucocorticoids for the shortest period of time needed to achieve the treatment goals Treatment of those pre-existing comorbid conditions that may increase risk when glucocorticoids are required Monitoring of patients under treatment for adverse effects that may benefit from additional intervention
Pre-existing conditions or risk factors for adverse effects that should be assessed or treated when glucocorticoids are to be instituted include : Diabetes mellitus Hyperlipidemia Hypertension Heart failure
Glaucoma and Cataract Low bone density or Osteoporosis Peptic ulcer disease Use of non-steroidal anti-inflammatory drugs Presence of infection
During treatment with glucocorticoids and depending upon individual risk factors such as dose and duration of glucocorticoids usage,other medications being used,and comorbidities,particular attention should be given to Body weight Blood pressure Heart failure and peripheral edema Serum lipid Diabetes or glucose intolerance Glaucoma Fracture risk