Steroid Side Effects Mnemonic

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  • Side Effects of Steroids – “5 S”
  • Glucocorticoids Pharmacology Video Tutorial - MADE EASY
  • Steroid side effects | Medical Mnemonics
  • Top Extremely Important Pharmacology Mnemonics - DrugsBank
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  • Corticosteroid Mnemonics in Pharmacology for Medical and Dental Professional Exams ,Session 1

    Side Effects of Steroids – “5 S”

    steroid side effects mnemonic Glucocorticoids GC are a class of steroid hormones that bind to the glucocorticoid receptor GRwhich is present in almost every vertebrate animal cell. This video tutorial on Glucocorticoids Pharmacology has been provided by: Glucocorticoids bind to the cytosolic glucocorticoid receptor GRa type nuclear receptor that is activated by ligand binding. After a hormone binds to the corresponding receptor, the newly formed complex translocates itself into the cell nucleus, where it binds to glucocorticoid response elements GRE in the promoter region of the target genes resulting in the regulation steroid side effects mnemonic gene expression. This process is commonly referred to as transcriptional activation, or transactivation. The proteins encoded by these up-regulated genes have a wide range of effects, including, for example:. The opposite mechanism is called transcriptional steroid side effects mnemonic, haldol im peak time transrepression.

    Glucocorticoids Pharmacology Video Tutorial - MADE EASY

    steroid side effects mnemonic

    Synthetic glucocorticoids mimic the effects of cortisol , a steroid hormone produced by the zona fasciculata, the middle region of the adrenal cortex.

    Elevated blood levels of ACTH in turn stimulate the synthesis of cortisol by the adrenal gland Chrousos, ; Wikipedia: It also affects many other body functions that would be nonessential or detrimental in a stressful situation, one of which is the suppression of inflammatory responses.

    The powerful suppressive effect of cortisol-like glucocorticoids on the immune system is frequently exploited in the treatment of numerous inflammatory disorders resulting from over-activity of the immune system, ranging from asthma to ulcerative colitis Chrousos, Mechanism of action of glucocorticoids. The majority of effects produced by glucocorticoids result from initial steroid binding to intracellular glucocorticoid receptors followed by translocation to the nucleus and changes in gene transcription.

    In their steroid-free unbound state, intracellular glucocorticoid receptors GR are bound to stabilizing proteins that include heat-shock protein 90 Hsp90 and immunophilin. The unbound form of the receptor is not capable of affecting gene transcription.

    Binding of steroid initiates a conformational change that results in an exchange of chaperone proteins, which permits attachment of the steroid-GR complex to the dynein protein trafficking pathway. This results in translocation of the steroid-GR complex from the cytoplasm into the nucleus Wikipedia: Once in the nucleus, the steroid-GR complex dimerizes and binds to glucocorticoid response elements GRE associated with the regulatory region of glucocorticoid-sensitive genes.

    Binding of the glucocorticoid-GR dimer either represses, or stimulates the transcription of sensitive genes, resulting in changes in synthesis of mRNA, followed by changes in protein synthesis. These steps are necessary for producing most cellular responses to glucocorticoids, and typically take hours to days to develop.

    Both a reduction in the synthesis of inflammatory cytokines , as well as upregulation in the synthesis of annexin A1 are known to play important roles in mediating the antiinflammatory and immunomodulatory effects of glucocorticoids. As illustrated at the top left, in some situations glucocorticoids are able to produce more rapid responses by binding to membrane-associated receptors and exerting effects that do not involve changes in gene regulation. These non-genomic mechanisms remain poorly understood.

    Neutrophil migration through the vasculature to sites of inflammation is markedly reduced. This effect, combined with an enhanced release of cells from the bone marrow, and reduced neutrophil apoptosis, causes the WBC count to increase Chatham, Cortisol is released during times of stress to supply glucose as an energy substrate to organs facing stressful conditions.

    Stress responses that increase cortisol release include vigorous exercise, psychological stress or fear, acute trauma, surgery, pain, severe infection and hypoglycemia. Cortisol's effects to elevate blood glucose are important in maintaining energy homeostasis during the stress response, and ensure that critical organs such as the brain continue to receive nutrients at a time when they are most needed for survival.

    Chronically elevated glucocorticoids can produce a dramatic redistribution of body fat. The redistribution of fat is believed to result from different sensitivities of peripheral vs truncal fat cells to:. The mechanisms remain poorly understood.

    Administration of glucocorticoids results in diverse changes to different types of white blood cells. Examples of commonly used synthetic compounds include:.

    Therapeutically, glucocorticoids are usually given at doses that produce minimal mineralocorticoid stimulation in order to avoid the side effects associated with activation of this pathway e. This enzyme exists in two isoforms that catalyze opposing conversions of cortisone to cortisol.

    The type 1 isozyme, which is expressed in the liver, converts inactive cortisone to cortisol. Cortisol can interact with both glucocorticoid GR and mineralocorticoid MR receptors.

    In contrast, the type 2 isoform converts active cortisol to inactive cortisone. This significantly reduces the effects of circulating cortisol on the mineralocorticoid receptors expressed in the collecting duct of the kidney, and minimizes the mineralocorticoid effect of normal levels of cortisol on the cells of the distal collecting duct.

    However, enzymatic inactivation can become saturated at extremely high levels of cortisol such as in Cushing's disease , resulting in the development of sodium retention, fluid retention and hypertension. Type 2 HSD is also expressed by the placenta, which inactivates maternal cortisol before it reaches the fetus.

    A similar inactivation process also occurs for prednisolone. This is not true for some other synthetic glucocorticoids such as dexamethasone, that are not similarly affected by this enzyme. The major therapeutic effects top and side effects bottom produced by glucocorticoids. Many of the side effects are reversible when glucocorticoid treatment is discontinued. Adapted from Buttgereit et al, Side Effects highlighted in red are irreversible typically requiring surgical replacement.

    Symptoms of Cushing's Syndrome, or chronic systemic effects of elevated glucocorticoids. Secondary adrenal insufficiency caused by chronic glucocorticoid GC therapy. Chronic treatment with glucocorticoids will reduce pituitary release of ACTH, which over a time period of weeks to months can result in progressive atrophy of cortisol producing cells in the adrenal gland top right.

    When a patient takes a glucocorticoid for treatment of an illness, the presence of the cortisol-like medication will suppress the release of ACTH by the pituitary Figure 5, top right. Because the cortisol-producing cells of the adrenal gland zona fasciculata depend on ACTH stimulation for normal homeostasis, a reduction in ACTH release for any significant time e. Adrenal atrophy reduces the ability of the adrenal gland to produce normal levels of cortisol when therapy with a glucocorticoid such as prednisone is discontinued.

    Several weeks of exogenous glucocorticoid therapy are typically required for development of adrenal insufficiency Salvatori, ; Chrousos, Longer-acting glucocorticoids, and higher doses of systemic glucocorticoids vs topical or inhaled formulations have been associated with a higher risk of developing adrenal suppression.

    There are no current evidence-based guidelines regarding the optimal method for discontinuing glucocorticoid therapy, although gradual tapering of dosages over a period of weeks to months, prior to complete discontinuation, is recommended to allow time for recovery of the hypothalamic-pituitary-adrenal axis Liu et al, The signs and symptoms of secondary adrenal insufficiency that result from a sudden withdrawal of glucocorticoids in the presence of HPA axis suppression are typically similar to those seen with Addison's disease, but don't include changes in skin pigmentation because ACTH secretion is not increased , or significant electrolyte disturbances because aldosterone is regulated by the renin-angiotensin system rather than ACTH Nieman Hydrocortisone given twice or three times per day is commonly preferred for the treatment of adrenal insufficiency because its short half-life allows it to more closely mimic the normal circadian rhythm for cortisol.

    Includes both glucocorticoids e. Naturally occurring glucocorticoids are part of the feedback mechanism the body utilizes to reduce immune activity inflammation.

    Exogenous glucocorticoids synthetic or natural are used to treat diseases caused by an overactive immune system e. Glucocorticoids are distinguished from mineralocorticoids and sex steroids that have different receptors, target cells and effects. Aldosterone is the most important endogenous mineralocorticoid. Aldosterone is produced in the zona glomerulosa region of the adrenal cortex.

    Because of it comes from a zone of the adrenal cortex, it is also considered a type of corticosteroid. Aldosterone's physiological role is essential in maintenance of adequate fluid volume needed for normal cardiac output and arterial blood pressure. Without adequate levels of mineralocorticoids, diminished cardiac output can result in fatal shock.

    In contrast, elevated levels of aldosterone associated with long term stimulation of the Renin-Angiotensin-Aldosterone-System RAAS is involved in the development of vascular remodeling and systolic heart failure. For more information see the section on mineralocorticoid pharmacology.

    Glucocorticoids exert a majority of their effects by altering gene expression Figure 1. Diffusion of glucocorticoids across cell membranes where they bind to cytoplasmic glucocorticoid receptors GRs. Inactive forms of GRs form complexes with other chaperone proteins that maintain the conformation of the receptor.

    Two of the major chaperone proteins are heat-shock protein 90, and immunophilin. Steroid binding to GRs results in a conformational change in the GR receptor, an exchange of chaperone proteins immunophilin is exchanged for HSp52 , and attachment of the activated receptor to a dynein motor protein and cytoskeleton, that results in translocation of the activated GR to the nucleus.

    Activated GRs dimerize and bind to specific DNA sequences within the regulatory regions of affected genes. GREs provide specificity to the effects of glucocorticoids on gene transcription.

    Metabolic effects of glucocorticoids generally are mediated primarily by transcriptional activation. Rapid non-genomic effects of glucocorticoids have been identified, but the mechanisms responsible remain poorly understood Boldizsar et al, ; Lee et al, Non-genomic effects of glucocorticoids appear to be mediated by a combination of hormone sensitive membrane-bound and cytoplasmic receptors Lee et al, Annexin A1 previously named lipocortin-1 was the first characterized member of the annexin superfamily.

    Its major effects are summarized in Figure 1. The mechanisms involved in elevating blood glucose include: Increased gluconeogenesis glucose formation. The redistribution of fat is believed to result from different sensitivities of peripheral vs truncal fat cells to: Examples of commonly used synthetic compounds include: Prednisone has a high ratio of glucocorticoid vs mineralocorticoid activity, which is desirable for use as an anti-inflammatory and immunosuppressant agent where effects on sodium and water balance are undesirable.

    Prednisone is a prodrug that has no biologic activity until it is converted by hepatic metabolism to prednisolone the active metabolite. Metabolic conversion may be impaired with hepatic dysfunction. The active metabolite of prednisone. This protects the fetus from high levels of these glucocorticoids. In contrast, this enzyme does not have the same inactivating effect on some other synthetic glucocorticoids such as dexamethasone. At recommended doses, it is essentially free of glucocorticoid activity.

    Duration of action is hrs. It is used in the treatment of Addison's disease in which cells of the zona glomerulosa region of the adrenal cortex that produce aldosterone have been destroyed. Inhibition of bone deposition. Avascular Necrosis of Femur Head Animal studies indicate GC-induced increased levels of serum lipids result in both increased formation of microemboli in the arteries supplying bone, and fat-related blockage of venous flow from bone.

    N ecrosis, avascular necrosis of the femoral head. Boldizsar F et al Emerging pathways of non-genomic glucocorticoid GC signalling in T cells.

    Buttgereit F et al Greenspan's Basic and Clinical Endocrinology. Glucocorticoid-induced avascular bone necrosis: Glucocorticoid effects on the immune system. Basic and Clinical Pharmacology. Girol AP et al J Immunology

    Steroid side effects | Medical Mnemonics

    steroid side effects mnemonic

    Top Extremely Important Pharmacology Mnemonics - DrugsBank

    steroid side effects mnemonic

    Mnemonics Related to Side Effects..!!

    steroid side effects mnemonic