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Hypertensive Encephalopathy As the Initial Manifestation of Cushing's
The Journal of Medical Research 2016; 2(6): 144-145 Case Report Hypertensive encephalopathy as the initial manifestation JMR 2016; 2(6): 144-145 November- December of Cushing’s syndrome ISSN: 2395-7565 © 2016, All rights reserved Alagoma Iyagba*1, Arthur Onwuchekwa1 www.medicinearticle.com 1 Department of Internal Medicine, University of Port Harcourt Teaching Hospital, Port Harcourt, Rivers State, Nigeria Abstract A 65-year old lady was rushed into the accident and emergency department with a two-day history sudden onset severe generalized throbbing headache associated with restlessness, irritability, irrational talk, projectile vomiting and loss of consciousness of three hours duration. On examination, she had moon face, buffalo hump, and truncal obesity with body mass index was 45.84kg/m2. Her blood pressure was 190/120 mmHg. Serum cortisol done at 0800 hrs the next day was elevated with a value of 511 ng/ml. 1 mg overnight dexamethasone was 148 ng/ml. The diagnosis of hypertension secondary to Cushing’s syndrome should be strongly considered in any hypertensive obese patients regardless of age with typical ‘cushingoid facies’. An assessment of serum cortisol in such patients would be beneficial in diagnosing this condition and optimizing treatment outcomes. Keywords: Cushing’s, Hypertension, Encephalopathy. INTRODUCTION Cushing’s syndrome is the constellation of a large group of signs and symptoms resulting from prolonged pathologic hypercortisolism caused by excessive adrenocorticotropic hormone (ACTH) secretion by tumors in the pituitary gland or elsewhere, or by ACTH-independent cortisol secretion from adrenal tumors[1]. It is one of the endocrine causes of hypertension with profound cardiovascular and neurological effects. -
PATIENT FACT SHEET (Deltasone)
Prednisone PATIENT FACT SHEET (Deltasone) Prednisone (Deltasone) is part of a potent class of inflammatory conditions, including redness, anti-inflammatory agents, known as corticosteroids, swelling and pain. Prednisone is used to treat which are used to control inflammation of the rheumatoid arthritis, lupus, vasculitis, and many joints and organs. It is often used to treat a variety of other inflammatory diseases. WHAT IS IT? Dosing of prednisone varies widely depending on tablets take effect about 6 hours after taking the the state of the disease being treated. Doses used dose. Prednisone stops working soon after stopping in rheumatoid arthritis are commonly 5-10mg daily, the medication. If you have been taking prednisone while doses needed in lupus and vasculitis are often regularly for longer than 2 weeks, do not stop it 80mg daily, or sometimes higher. Prednisone usually suddenly. Instead, you should discuss a tapering HOW TO achieves its effect within 1-2 hours. The delayed release schedule with your physician. TAKE IT Most side effects are related to the dose administered medications, there is an increased risk of infection when and duration of treatment, so the goal is to use it at combining prednisone with other medications that the lowest effective dose for the shortest period of time affect your immune system. Additionally, when taking necessary. Some potential side effects include easy prednisone with NSAIDs (such as naproxen or ibuprofen), bruising, osteoporosis (or weakened bones), diabetes, there can be an increased risk of stomach ulcers. Make hypertension, weight gain, cataracts, glaucoma, and sure to review all of your medications with your physician SIDE a bone disorder called avascular necrosis. -
Celestone Syrup Page 1 Nda 14-215/S-009, 015
CELESTONE SYRUP PAGE 1 NDA 14-215/S-009, 015 CELESTONE® betamethasone syrup, USP DESCRIPTION CELESTONE Syrup, for oral administration, contains 0.6 mg betamethasone in each 5 mL. The inactive ingredients for CELESTONE Syrup include: alcohol (less than 1%), citric acid, FD&C Red No. 40, FD&C Yellow No. 6, flavors, propylene glycol, sodium benzoate, sodium chloride, sorbitol, sugar, and water. The formula for betamethasone is C22H29F05 and it has a molecular weight of 392.47. Chemically, it is 9-fluoro-11β,17,21-trihydroxy-16β-methylpregna-1,4-diene-3,20-dione and has the following structure: (Add structure) Betamethasone is a white to practically white, odorless crystalline powder. It melts at about 240°C with some decomposition. Betamethasone is sparingly soluble in acetone, alcohol, dioxane, and methanol; very slightly soluble in chloroform and ether; and is insoluble in water. CLINICAL PHARMACOLOGY Glucocorticoids, naturally occurring and synthetic, are adrenocortical steroids that are readily absorbed from the gastrointestinal tract. Naturally occurring glucocorticoids (hydrocortisone and cortisone), which also have salt- retaining properties, are used as replacement therapy in adrenocortical deficiency states. Their synthetic analogs, such as betamethasone, are primarily used for their anti-inflammatory effects in disorders of many organ systems. A derivative of prednisolone, betamethasone has a 16β methyl group that enhances the anti-inflammatory action of the molecule and reduces the sodium- and water-retaining properties of the fluorine atom bound at carbon 9. INDICATIONS AND USAGE Allergic states: Control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment in asthma, atopic dermatitis, contact dermatitis, drug hypersensitivity reactions, perennial or seasonal allergic rhinitis, serum sickness. -
Steroid Use in Prednisone Allergy Abby Shuck, Pharmd Candidate
Steroid Use in Prednisone Allergy Abby Shuck, PharmD candidate 2015 University of Findlay If a patient has an allergy to prednisone and methylprednisolone, what (if any) other corticosteroid can the patient use to avoid an allergic reaction? Corticosteroids very rarely cause allergic reactions in patients that receive them. Since corticosteroids are typically used to treat severe allergic reactions and anaphylaxis, it seems unlikely that these drugs could actually induce an allergic reaction of their own. However, between 0.5-5% of people have reported any sort of reaction to a corticosteroid that they have received.1 Corticosteroids can cause anything from minor skin irritations to full blown anaphylactic shock. Worsening of allergic symptoms during corticosteroid treatment may not always mean that the patient has failed treatment, although it may appear to be so.2,3 There are essentially four classes of corticosteroids: Class A, hydrocortisone-type, Class B, triamcinolone acetonide type, Class C, betamethasone type, and Class D, hydrocortisone-17-butyrate and clobetasone-17-butyrate type. Major* corticosteroids in Class A include cortisone, hydrocortisone, methylprednisolone, prednisolone, and prednisone. Major* corticosteroids in Class B include budesonide, fluocinolone, and triamcinolone. Major* corticosteroids in Class C include beclomethasone and dexamethasone. Finally, major* corticosteroids in Class D include betamethasone, fluticasone, and mometasone.4,5 Class D was later subdivided into Class D1 and D2 depending on the presence or 5,6 absence of a C16 methyl substitution and/or halogenation on C9 of the steroid B-ring. It is often hard to determine what exactly a patient is allergic to if they experience a reaction to a corticosteroid. -
Differential Effects of Hydrocortisone, Prednisone, And
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Springer - Publisher Connector Nebesio et al. International Journal of Pediatric Endocrinology (2016) 2016:17 DOI 10.1186/s13633-016-0035-5 RESEARCH Open Access Differential effects of hydrocortisone, prednisone, and dexamethasone on hormonal and pharmacokinetic profiles: a pilot study in children with congenital adrenal hyperplasia Todd D. Nebesio1*, Jamie L. Renbarger2,3, Zeina M. Nabhan1, Sydney E. Ross2, James E. Slaven4, Lang Li5, Emily C. Walvoord1 and Erica A. Eugster1 Abstract Background: Little is known about the comparative effects of different glucocorticoids on the adrenal and growth hormone (GH) axes in children with congenital adrenal hyperplasia (CAH). We sought to compare the effects of hydrocortisone (HC), prednisone (PDN), and dexamethasone (DEX) in children with classic CAH and to investigate a potential role of pharmacogenetics. Methods: Subjects were randomly assigned to three sequential 6-week courses of HC, PDN, and DEX, each followed by evaluation of adrenal hormones, IGF-1, GH, and body mass index (BMI). Single nucleotide polymorphism (SNP) analysis of genes in the glucocorticoid pathway was also performed. Results: Nine prepubertal subjects aged 8.1 ± 2.3 years completed the study. Mean ACTH, androstenedione, and 17-hydroxyprogesterone (17-OHP) values were lower following the DEX arm of the study than after subjects received HC (p ≤ 0.016) or PDN (p ≤ 0.002). 17-OHP was also lower after HC than PDN (p < 0.001). There was no difference in IGF-1, GH, or change in BMI. SNP analysis revealed significant associations between hormone concentrations, pharmacokinetic parameters, and variants in several glucocorticoid pathway genes (ABCB1, NR3C1, IP013, GLCCI1). -
Chapter 13. Secondary Hypertension
Hypertension Research (2014) 37, 349–361 & 2014 The Japanese Society of Hypertension All rights reserved 0916-9636/14 www.nature.com/hr GUIDELINES (JSH 2014) Chapter 13. Secondary hypertension Hypertension Research (2014) 37, 349–361; doi:10.1038/hr.2014.16 OVERVIEW AND SCREENING approximately 5–10% of hypertensive patients,984,985 and it is the most Hypertension related to a specific etiology is termed secondary frequent in endocrine hypertension. In addition, frequent etiological hypertension, markedly differing from essential hypertension, of factors for secondary hypertension include renal parenchymal hyper- which the etiology cannot be identified, in the condition and tension and renovascular hypertension. A study reported that sleep therapeutic strategies. Secondary hypertension is often resistant hyper- apnea syndrome was the most frequent factor for secondary hyper- tension, for which a target blood pressure is difficult to achieve by tension.517 The number of patients with secondary hypertension standard treatment. However, blood pressure can be effectively may further increase with the widespread diagnosis of sleep apnea reduced by identifying its etiology and treating the condition. There- syndrome. fore, it is important to suspect secondary hypertension and reach an Generally, the presence of severe or resistant hypertension, juvenile appropriate diagnosis. hypertension and the rapid onset of hypertension suggest the possi- Frequent etiological factors for secondary hypertension include bility of secondary hypertension. In such hypertensive patients, a close renal parenchymal hypertension, primary aldosteronism (PA), reno- inquiry on medical history, medical examination and adequate vascular hypertension and sleep apnea syndrome. Renal parenchymal examinations must be performed, considering the possibility of hypertension is caused by glomerular diseases, such as chronic secondary hypertension. -
Inhaled Budesonide and Prednisone Led to Similar Rates of Asthma Relapse After Emergency Department Discharge
Evid Based Med: first published as 10.1136/ebm.5.5.139 on 1 September 2000. Downloaded from Inhaled budesonide and prednisone led to similar rates of asthma relapse after emergency department discharge FitzGerald JM, Shragge D, Haddon J, et al. A randomized, controlled trial of high dose, inhaled budesonide versus oral prednisone in patients discharged from the emergency department following an acute asthma exacerbation. Can Respir J 2000 Jan/Feb;7:61–7. QUESTION: In patients who are discharged from the emergency department after a severe acute asthma attack, do high doses of prednisone and inhaled budesonide lead to similar rates of asthma relapse? Design Inhaled budesonide v prednisone in patients discharged from the emergency department after ‡ Randomised (unclear allocation concealment*), blinded a severe acute exacerbation of asthma {clinicians, patients, outcome assessors, and statisti- Outcomes at cians}†,* controlled trial with 7–10 day follow up. 7 to 10 days Budesonide Prednisone RRR (95% CI) NNT (CI) Setting Relapse rate 10% 12% 15% (−94 to 63) Not significant 3 university affiliated urban emergency departments in ‡Abbreviations defined in glossary; RRR, NNT, and CI calculated from data in article. Canada. Patients 185 patients who were 15–70 years of age, had an acute asthma exacerbation, were well enough to be discharged (postbronchodilator FEV1 > 50% of predicted normal rate), and were able to use Turbuhaler correctly. Exclusion criteria included chronic obstructive pulmonary disease, intolerance to systemic glucocorticosteroids, peptic ulcer COMMENTARY disease, active tuberculosis, fungal infection, type 1 diabetes mellitus, moderate to severe hypertension, preg- A particular strength of the study by FitzGerald et al is that it nancy, lactation, or no effective contraception use (for had sufficient power to assess whether the 2 interventions women of childbearing age). -
HEMADY (Dexamethasone Tablets), for Oral Use Chronic Use
HIGHLIGHTS OF PRESCRIBING INFORMATION These highlights do not include all the information needed to use • Gastrointestinal Perforation: Avoid use in active or latent peptic ulcers, HEMADYTM safely and effectively. See full prescribing information for diverticulitis, fresh intestinal anastomoses, and nonspecific ulcerative HEMADY. colitis, since they may increase the risk of a perforation. (5.7) • Osteoporosis: Increased risk; monitor for changes in bone density with HEMADY (dexamethasone tablets), for oral use chronic use. (5.8) Initial U.S. Approval: 1958 • Behavioral and Mood Disturbances: May include euphoria, insomnia, mood swings, personality changes, severe depression, and psychosis. --------------------------- INDICATIONS AND USAGE ------------------------- Monitor for signs and symptoms and manage promptly. (5.10) HEMADY is a corticosteroid indicated in combination with other anti • Kaposi’s Sarcoma: Kaposi’s sarcoma has been reported to occur in patients myeloma products for the treatment of adults with multiple myeloma. (1) receiving corticosteroid therapy, most often for chronic conditions. (5.11) • Embryo-Fetal Toxicity: Can cause fetal harm. Advise females of ----------------------- DOSAGE AND ADMINISTRATION --------------------- reproductive potential of the potential risk to a fetus. (5.13, 8.1) Recommended Dosage: 20 mg or 40 mg orally once daily, on specific days depending on the protocol regimen. (2) ------------------------------ ADVERSE REACTIONS ---------------------------- The most common adverse reactions are -
Inhaled and Oral Corticosteroids
Inhaled and Oral Corticosteroids Corticosteroids (steroids) are medicines that are used to treat many chronic diseases. Corticosteroids are very good at reducing inflammation (swelling) and mucus production in the airways of the lungs. They also help other quick-relief medicines work better. The steroids (corticosteroids) used to treat asthma and other chronic lung diseases are not the same as anabolic steroids, used illegally by some athletes for bodybuilding. Corticosteroids do not affect the liver or cause sterility. Does the Body Make Steroids? Corticosteroids are similar to cortisol, a hormone produced by the adrenal glands in the body. Cortisol is one of the body's own natural steroids. Cortisol is essential for life and well being. During stress, our bodies produce extra cortisol to keep us from becoming very sick. Normally the adrenal glands release cortisol into the blood stream every morning. The brain monitors this amount and regulates the adrenal function. It cannot tell the difference between its own natural cortisone and that of steroid medicines. Therefore, when a person takes high doses of steroids over a long time, the brain may decrease or stop cortisol production. This is called adrenal supression. Health care providers generally decrease a steroid dosage slowly to allow the adrenal gland to recover and produce cortisol at a normal level again. If you have been on steroids long- term do not stop taking them suddenly. Follow your doctor’s prescription. What are Some Steroid Medicines? Steroid medicines are available as nasal sprays, metered- dose-inhalers (inhaled steroids), oral forms (pills or syrups), injections into the muscle (shots) and intravenous (IV) solutions. -
Pharmacologic Characteristics of Corticosteroids 대한신경집중치료학회
REVIEW J Neurocrit Care 2017;10(2):53-59 https://doi.org/10.18700/jnc.170035 eISSN 2508-1349 Pharmacologic Characteristics of Corticosteroids 대한신경집중치료학회 Sophie Samuel, PharmD1, Thuy Nguyen, PharmD1, H. Alex Choi, MD2 1Department of Pharmacy, Memorial Hermann Texas Medical Center, Houston, TX; 2Department of Neurosurgery and Neurology, The University of Texas Medical School at Houston, Houston, TX, USA Corticosteroids (CSs) are used frequently in the neurocritical care unit mainly for their anti- Received December 7, 2017 inflammatory and immunosuppressive effects. Despite their broad use, limited evidence Revised December 7, 2017 exists for their efficacy in diseases confronted in the neurocritical care setting. There are Accepted December 17, 2017 considerable safety concerns associated with administering these drugs and should be limited Corresponding Author: to specific conditions in which their benefits outweigh the risks. The application of CSs in H. Alex Choi, MD neurologic diseases, range from traumatic head and spinal cord injuries to central nervous Department of Pharmacy, Memorial system infections. Based on animal studies, it is speculated that the benefit of CSs therapy Hermann Texas Medical Center, 6411 in brain and spinal cord, include neuroprotection from free radicals, specifically when given Fannin Street, Houston, TX 77030, at a higher supraphysiologic doses. Regardless of these advantages and promising results in USA animal studies, clinical trials have failed to show a significant benefit of CSs administration Tel: +1-713-500-6128 on neurologic outcomes or mortality in patients with head and acute spinal injuries. This Fax: +1-713-500-0665 article reviews various chemical structures between natural and synthetic steroids, discuss its E-mail: [email protected] pharmacokinetic and pharmacodynamic profiles, and describe their use in clinical practice. -
Cholesterol (Precursor of Steroid Hormones)
Unit IV – Problem 5 – Biochemistry: Biosynthesis of Steroid Hormones & Steroid Hormone Receptor - Cholesterol (precursor of steroid hormones): It is composed of 27 carbons with four rings and a hydroxyl group (-OH) attached at carbon 3 and is found in cell membrane (why?) → to regulate membrane fluidity and permeability. Cholesterol from diet will be packaged in chylomicrons (in the gut) to be transported into lymph and then into plasma. Cholesterol is synthesized de novo (from scratch) in the cytosol of the liver. - Steroid Hormones: The rate-limiting irreversible step in steroid hormone synthesis is represented by the conversion of cholesterol into pregnenolone (which contains 21 carbons) via the enzyme desmolase. How to name steroids? 21 carbons: pregnanes (pregnenolone). 19 carbons: androstanes (testosterone). 18 carbons: estranges (estrogen). - Classes of steroid hormones: Mineralocorticoids: from zona glomerulosa of adrenal cortex. Glucocorticoids: from zona fasciculate of adrenal cortex. Androgens: from testes and zona reticularis of adrenal cortex. Estrogens and progestogens: from ovaries and placenta. - Synthesis of steroid hormones: Enzyme Sex Mineralocorticoids Cortisol Labs Presentation deficiency hormones XY: Hypertension, 17α- pseudohermaphroditism ↑ ↓ ↓ hypokalemia and hydroxylase XX: lack secondary ↓DHT sexual development Hypotension, Infancy: salt wasting; hyperkalemia, ↑ 21- childhood precocious ↓ ↓ ↑ renin activity and ↑ hydroxylase puberty; XX: 17- virilization hydroxyprogesterone ↓ aldosterone, ↑ 11- 11β- Hypertension (low deoxycorticosterone ↓ ↑ XX: virilization hydroxylase renin) (results in ↑ BP) - Glucocorticoids (natural): Synthesized in zona fasciculate of adrenal cortex. Regulated by: Corticotrophin-releasing hormone (CRH) which is secreted from the hypothalamus and then stimulating the anterior pituitary gland to produce adrenocorticotropic hormone (ACTH) which in turn will enhance the synthesis of cortisol from zona fasciculata. Functions of cortisol (BIG FIB): ↑ Blood pressure. -
Cushings Disease
put together by Alex Yartsev: Sorry if i used your images or data and forgot to reference you. Tell me who you are. [email protected] Cushings Disease History of Presenting Illness - weight gain, BUFFALO HUMP with supraclav fat pads, moon face, central obesity - purple stretch marks , HEADACHE, POLYURIA, NOCTURIA, GALACTORHHOEA? - easy bruising , Changes in pigmentation?? DARKER? Acanthisis Nigricans? - skin thinning . It can only be ACTH SECRETING ADENOMA!! - irregular menses hirsutism . - difficulty climbing stairs, getting out of a low chair, and raising their arms. - Depression CUSHINGOID FEATURES WITH HIRSUITISM AND - cognitive dysfunction VIRILISATION? BUT NO PIGMENT CHANGES?? - emotional lability Think about an ADRENAL CARCINOMA!! - bone disease (fractures) - STOMACH ULCERS from corticosteroid excess - Appetite Gain! ACUTELY cortisol excess causes EUPHORIA - Exacerbation of diabetes CHRONICALLY cortisol excess causes DEPRESSION - Hypokalemia (weakness ) - hypernatremia ELECTROLYTES ALL WRONG? MUCH ACNE, FLORID HYPERTENSION, OEDEMA, HIGH GLUCOSE, …BUT : NO FAT REDISTRIBUTION? ACUTE ONSET? Sounds like an ECTOPIC NEOPLASTIC SOURCE Differential Diagnoses - Hypothalamic disease (too much CRH) - Primary Cushing Disease (ACTH-secreting pituitary adenoma) - Adrenal cortisol-secreting adenoma - Ectopic Neoplastic Source of cortisol eg. lung cancer ( disease of decrepit old men) - Use + Abuse of corticosteroid medication - Hypercortisolism secondary to alcoholism - Depression - Hypothyroidism ~ADRENAL CRISIS~ - Hypoadrenalism