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Cortisol Unmask Diabetes Insipidus

Arginine Vasopressin-independent Mechanism Of Impaired Water Excretion In A Patient With Sarcoidosis Complicated By Central Diabetes Insipidus And Glucocorticoid Deficiency

Arginine Vasopressin-independent Mechanism Of Impaired Water Excretion In A Patient With Sarcoidosis Complicated By Central Diabetes Insipidus And Glucocorticoid Deficiency

Arginine Vasopressin-Independent Mechanism of Impaired Water Excretion in a Patient with Sarcoidosis Complicated by Central Diabetes Insipidus and Glucocorticoid Deficiency 1Department of Internal Medicine, Osaka City Sumiyoshi Hospital, 1-2-16, Higashikagaya, Suminoeku, Osaka City, Osaka 559-0012, Japan 2Department of Internal Medicine, Osaka City Juso Hospital, Osaka 532-0034, Japan 3Department of Endocrinology and Metabolism, Osaka City General Hospital, Osaka 534-0021, Japan 4Department of Pathology, Osaka City General Hospital, Osaka 534-0021, Japan Received 13 February 2011; Accepted 7 June 2011 Copyright 2011 Katsunobu Yoshioka et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. A 28-year-old man was admitted to our hospital because of reduced livido and increased fatigability. Four months before admission, he noticed polyuria, which was gradually relieved by admission. Magnetic resonance imaging revealed enhancing lesion centrally in the pituitary stalk. Biopsy from the skin revealed noncaseating granuloma composed of epithelioid cells, and a diagnosis of sarcoidosis was made. Although plasma arginine vasopressin (AVP) was undetectable after administration of hypertonic saline, urinary output was within normal range (1.5 to 2.2 L/day). The urine osmolality became above plasma levels during the hypertonic saline test. Hormonal provocative tests revealed partial glucocorticoid deficiency. Soon after the glucocorticoid therapy was begun, moderate polyuria (from 3.54.0 liters daily) occurred. At this time, plasma AVP was undetectable, and urine osmolality was consistently below plasma levels durin Continue reading >>

Unmasking Of Partial Diabetes Insipidus During Stress But Not Maintenance Dosing Of Glucocorticoids In An Infant With Septo-optic Dysplasia

Unmasking Of Partial Diabetes Insipidus During Stress But Not Maintenance Dosing Of Glucocorticoids In An Infant With Septo-optic Dysplasia

Unmasking of Partial Diabetes Insipidus during Stress but Not Maintenance Dosing of Glucocorticoids in an Infant with Septo-Optic Dysplasia 1Division of Pediatric Endocrine, Department of Pediatrics, University of North Carolina, Chapel Hill, NC 27599, USA Received 2010 Nov 15; Revised 2011 Feb 24; Accepted 2011 Feb 26. Copyright 2011 Copyright 2011 Mala Puri et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. This article has been cited by other articles in PMC. Background. It is well acknowledged that glucocorticoid (GC) replacement can unmask diabetes insipidus (DI) in subjects with hypopituitarism. Objective. To increase the awareness and monitoring for transient and symptomatic DI in children with partial hypopituitarism during periods in which increased GC needs are required. Methods/Case. A 2-month-old female infant with septo-optic dysplasia (SOD; on thyroid and maintenance GC replacement therapy at 8 mg/m2/day) developed transient DI during 2 separate episodes of stress (one hypothermia, one febrile) when stress dosing of GC (25 mg/m2/day) was instituted. Conclusion. Children not diagnosed with DI during initial evaluation for hypopituitarism may benefit from rescreening of serum sodium levels during acute periods of stress that demand "stress" GC dosing. This will permit treatment and/or increased vigilance for ensuing permanent DI. Septo-optic dysplasia (SOD) is a malformation syndrome in which at least 50% of children have associated hypopituitarism [ 1 , 2 ]. This condition includes agenesis of the septum pellucidum, hypoplasia, or aplasia of the optic nerves and chiasm that results in var Continue reading >>

Development Of Hypernatremia After Glucocorticoid Administration: Unmasking Central Diabetes Insipidus In A Patient With Newly Diagnosed Central Hypocortisolism

Development Of Hypernatremia After Glucocorticoid Administration: Unmasking Central Diabetes Insipidus In A Patient With Newly Diagnosed Central Hypocortisolism

Abstract: Background: Patients with intra-cerebral metastases frequently receive glucocorticoids, particularly in the presence of peri-lesional vasogenic cerebral oedema. We present a case of presumptive lung carcinoma with cerebral metastases in whom central diabetes insipidus (CDI) was unmasked after glucocorticoid administration and correction of undiagnosed central hypocortisolism. Clinical Case: A 71-year-old lady with a past history of bronchial asthma was admitted to the Neurosurgery department for lethargy, poor oral intake, functional decline and progressive confusion on a background of visual blurring for a number of months. Imaging studies of the brain with CT and MRI revealed a suprasellar mass and multiple intracerebral hypodensities associated with perilesional oedema suggestive of metastases. On admission, the patient was clinically dehydrated and had mild hyponatremia (serum sodium 130 mmol/L, reference interval (RI) 134-144 mmol/L). Her early morning serum cortisol was low at 147 nmol/L (RI 240-618 nmol/L). Thyroid function test was normal. The patient was rehydrated with 0.9% saline drip and sent for contrast-enhanced CT thorax, abdomen and pelvis which showed findings consistent with a primary lung malignancy and normal bilateral adrenal glands. In view of her history of asthma, hypocortisolemia and intracerebral metastases, intravenous hydrocortisone was initiated shortly before her scans and switched to dexamethasone subsequently. Soon after glucocorticoid administration, the patient was noted to become polyuric, with serum sodium and osmolality rising up to 163 mmol/L and 355 mOsm/kg (RI 275-305 mOsm/kg) respectively on the third day. The paired urine osmolality was also inappropriately dilute (392 mOsm/kg) despite the high serum osmolality. The En Continue reading >>

Coexistence Of Central And Nephrogenic Diabetes Insipidus In A Preterm Infant

Coexistence Of Central And Nephrogenic Diabetes Insipidus In A Preterm Infant

Coexistence of Central and Nephrogenic Diabetes Insipidus in a Preterm Infant Michel-Macas Carolina1, Cordero-Gonzlez Guadalupe2 1Neonatology Fellow, Instituto Nacional de Perinatologa, Mxico; 2Neonatal Intensive Care Unit, Instituto Nacional de Perinatologa, Mxico. Background: Diabetes insipidus (DI) is a rare cause of hypernatremia in preterm newborns. Common causes of central DI include intra-ventricular hemorrhage, congenital infection and midline defects. Nephrogenic DI (NDI) is less frequent and can be caused by nephrocalcinosis. Case Report: We hereby report 665 gram female infant born at 27 weeks gestation with central DI and treated with desmopressin. The infant presented again with hypernatremia and showed a poor response to desmopressin. The finding of nephrocalcinosis oriented us to a nephrogenic component of DI. Conclusion: Although nephrogenic diabetes insipidus is the less frequent form of DI, preterm newborns present many risk factors for developing nephrocalcinosis (prolonged ventilation, diuretic therapy, dexamethasone, hypercalcemia) and NDI as a result. In a preterm newborn with CDI, a nephrogenic component must be suspected in the set of decreasing response to DDAVP. Diabetes Insipidus, Diuretics, Hypernatremia, Infant, Nephrocalcinosis. Endocrinal disorders are commonly associated with premature, low birth weight and small size for gestational age sick infants in neonatal intensive care unit (NICU) [ 1 ]. Diabetes insipidus (DI) is characterized by the inability to concentrate urine secondary to vasopressin deficiency or to vasopressin resistance resulting in polyuria and hypernatremia. Diagnosis of NDI is rarely made in very low birth weight (VLBW) and preterm infants since hypernatremic dehydration, high urine output, reduced ability to excrete Continue reading >>

Neurosarcoidosis-associated Central Diabetes Insipidus Masked By Adrenal Insufficiency

Neurosarcoidosis-associated Central Diabetes Insipidus Masked By Adrenal Insufficiency

Central diabetes insipidus (CDI) is an infrequent complication of neurosarcoidosis (NS). Its presentation may be masked by adrenal insufficiency (AI) and uncovered by subsequent steroid replacement. A 45-year-old woman with a history of NS presented 2 weeks after abrupt cessation of prednisone with nausea, vomiting, decreased oral intake and confusion. She was diagnosed with secondary AI and intravenous hydrocortisone was promptly begun. Over the next few days, however, the patient developed severe thirst and polyuria exceeding 6 L of urine per day, accompanied by hypernatraemia and hypo-osmolar urine. She was presumed to have CDI due to NS, and intranasal desmopressin was administered. This eventually normalised her urine output and serum sodium. The patient was discharged improved on intranasal desmopressin and oral prednisone. AI may mask the manifestation of CDI because low serum cortisol impairs renal-free water clearance. Steroid replacement reverses this process and unmasks an underlying CDI. The full text of all Editor's Choice articles and summaries of every article are free without registration The full text of Images in ... articles are free to registered users Only fellows can access the full text of case reports (apart from Editor's Choice) - become a fellow today, or encourage your institution to, so that together we can grow and develop this resource Don't forget to sign up for content alerts so you keep up to date with all the case reports as they are published, and let us know what you think by commenting on the Editor's blog Continue reading >>

Payperview: Osmoregulation Of Plasma Vasopressin In Three Cases With Adrenal Insufficiency Of Diverse Etiologies - Karger Publishers

Payperview: Osmoregulation Of Plasma Vasopressin In Three Cases With Adrenal Insufficiency Of Diverse Etiologies - Karger Publishers

Osmoregulation of Plasma Vasopressin in Three Cases with Adrenal Insufficiency of Diverse Etiologies Iwasaki Y.a Kondo K.a Hasegawa H.b Oiso Y.a I have read the Karger Terms and Conditions and agree. Neurohypophyseal function was studied by hypertonic saline infusion with plasma vasopressin measurement in 3 patients with adrenal insufficiency before and after cortisol replacement. Although each patient had different causes of adrenal insufficiency, all showed impaired water excretion before replacement. The first patient with isolated adrenocorticotropin deficiency had marked hyponatremia and inappropriate vasopressin secretion which was normalized after replacement, indicating vasopressin hypersecretion during hypoadrenocorticism. The second patient had combined anterior and posterior pituitary deficiency due to postpartum hypopituitarism and showed completely absent vasopressin secretion, with her polyuria being masked before cortisol replacement, suggesting a vasopressin-independent intrarenal mechanism of antidiuresis. The third patient with panhypopituitarism due to a pituitary tumor also had preexisting diabetes insipidus with defective vasopressin secretion. In this case, however, plasma vasopressin was found to be elevated when adrenal insufficiency and hyponatremia subsequently developed. Together, these results indicate that vasopressin hypersecretion does occur during adrenal insufficiency, but that the accompanying urinary diluting defect may be attributable either to vasopressin-dependent or to vasopressin-independent mechanisms. Continue reading >>

Cortisol Deficiency

Cortisol Deficiency

- granulomatous disease (eg sarcoid, TB, eosinophilic granuloma, Wegener's) necrosis or bleeding into pituitary macroadenoma surgery for lesions in region of hypothalamus, pituitary or midbrain Cortisol deficiency due to hypothalamic or midbrain lesions is more likely tobe asociated with diabetes insipidus than cortisol deficiency due to pituitarylesions. Only features which distinguish primary from secondary form are associated features of failure of pituitary function other than ACTH in the secondary type and endocrine pigmentation and features of associated diseases in the primary type. Addisonian pigmentation useful when present but often absent in auto-immune cases - characteristically seen in palmar creases , other skin creases, exposed areas, scars and buccal mucosa . May be associated vitiligo Weight loss - cmst symptom of cortisol insufficiency Non-specific abdo pain, often severe and colicky Shock and hypotension (Addisonian crisis - may be ppt. by intercurrent disease or infection) Acute cortisol deficiency results in muscle cramps, myalgia with unexplained fever, shock and hypotension. Secondary hypoadrenalism results in reproductive failure, +/- skin thickening, accentuation of tendency to hypoglycaemia (GH deficiency). Secondary hypothyroidism is a late feature. - consider diagnosis in presence of unexplained catecholamine-resistanthypotension, especially if the patient has hyperpigmentation, vitiligo, pallor,scanty axillary and pubic hair, hyponatraemia, or hyperkalaemia - possibility of spontaneous adrenal insufficiency due to adrenal haemorrhage oradrenal vein thrombosis must be considered in patients with upper abdominal orloin pain, abdominal rigidity, vomiting, confusion, and arterial hypotension - raised urea - most consistent biochemical abnormali Continue reading >>

2016 Endocrine Society Guidelines: Central Adrenal Insufficiency

2016 Endocrine Society Guidelines: Central Adrenal Insufficiency

We suggest measuring serum cortisol levels at 89 am as the first-line test for diagnosing central adrenal insufficiency. We recommend against using a random cortisol level to diagnose AI. We suggest that a cortisol level <3 g/dL is indicative of adrenal insufficiency and a cortisol level >15 g/dL likely excludes an AI diagnosis. We suggest performing a corticotropin stimulation test when morning cortisol values are between 3-15 g/dL to diagnose AI. Peak cortisol levels <18.1 g/dL at 30 or 60 minutes indicate AI. We suggest that clinicians perform biochemical testing for the hypothalamic-pituitary-adrenal (HPA) axis at least 1824 hours after the last hydrocortisone (HC) dose or longer for synthetic glucocorticoids (GC). We recommend using hydrocortisone, usually 1520 mg total daily dose in single or divided doses. Patients using divided doses should take the highest dose in the morning at awakening and the second in the afternoon (two-dose regime) or the second and third at lunch and late afternoon, respectively (three-dose regime). We suggest using longer-acting glucocorticoids in selected cases (eg, non-availability, poor compliance, convenience). We recommend that clinicians teach all patients with adrenal insufficiency regarding stress-dose and emergency GC administration and instruct them to obtain an emergency card/bracelet/necklace regarding AI and an emergency kit containing injectable high-dose GC. We recommend against using fludrocortisone in patients with central adrenal insufficiency. We recommend that clinicians treat patients with suspected adrenal crisis (AC) due to secondary AI with an immediate parenteral injection of 50100 mg hydrocortisone. We suggest evaluating central hypothyroid patients for adrenal insufficiency before starting LT4 therapy. If thi Continue reading >>

Life-threatening Hypernatremia In A Case Of Diabetes Insipidus/panhypopituitarism

Life-threatening Hypernatremia In A Case Of Diabetes Insipidus/panhypopituitarism

Life-Threatening Hypernatremia In A Case Of Diabetes Insipidus/Panhypopituitarism Author links open overlay panel EkamolTantisattamo Thomas B.Francis Open Access funded by The Korean Society of Nephrology Management of diabetes insipidus (DI) accompanied by panhypopituitarism requires understanding of the relationships between ADH and thyroid/glucocorticoid tone. Low thyroid/glucocorticoid tone decreases free water clearance which protects against DI and may lead to hyponatremia while high thyroid/glucocorticoid tone may unmask DI and facilitate hypernatremia. A 31 year-old man with DI/panhypopituitarism was stable until his levothyroxine was incorrectly lowered based on TSH levels. He became hypothyroid and was hospitalized 3 times over 1 month for recurring altered mental status and mild hyponatremia. DDAVP was repeatedly held with rapid onset of polyuria resulting severe hypernatremia. On the last admission, he presented with altered mental status from sepsis. Serum sodium was 135mmol/l. He was made NPO and treated with stress dose hydrocortisone and fludrocortisone. DDAVP was held for the mild hyponatremia. Serum sodium rapidly elevated to 168mmol/l after only 12 hours. DDAVP was restarted with liberalization of diet to unlimited free water access causing rapid downward sodium correction. Hypernatremia almost always results from iatrogenic causes. In our case, holding DDAVP for hyponatremia resulted in rapid onset of hypernatremia and volume depletion. Stress dose glucocorticoids further unmasked DI. Thirst and free access to water which typically protects patients with un-replaced DI were not operational due to his NPO status which contributed to the rapid rise in serum sodium. Water balance is controlled by thyroid, glucocorticoid, and principally ADH working at Continue reading >>

Volume 5, Chapter 37. Disorders Of The Adrenal Cortex

Volume 5, Chapter 37. Disorders Of The Adrenal Cortex

Congenital adrenal hyperplasia (CAH) is a group of common inborn errorsof metabolism that are transmitted as autosomal-recessive traits. 1 , 2 These enzymatic deficiencies cause impaired cortisol production as a resultof their intermediary role in the steroidogenic pathway that convertscholesterol to cortisol. When cortisol production is decreased, thelevel of adrenocorticotropic hormone (ACTH) rises because of the absenceof negative feedback. 3 Because the body attempts to maintain normal cortisol levels, there isoverproduction and accumulation of cortisol precursors proximal to theenzymatic block. These precursors are shunted toward the productionof C19 androgens (androstenedione and testosterone ), leading to the clinicalmanifestations of virilization and hirsutism. The 21-hydroxylase (21-OH) and 11-hydroxylase enzymes also are used in the mineralocorticoidpathways whose end product is aldosterone. When the enzyme is defectivein this pathway, patients cannot conserve sodium. This conditionleads to the salt-wasting form of the disease. Patients with the classic neonatal forms have sexual ambiguity, progressivevirilization, and sometimes salt loss or hypertension. These conditionsrequire life-long medical management 4 and often surgical reconstruction of the deformed genitalia. 5 The nonclassic (asymptomatic) and late-onset (usually pubertal) formsare more common than the classic presentation. The most common form ofclassic CAH is 21-hydroxylase deficiency (CAH21), which accounts for 95% of the cases of CAH. The next most common formsare 3-hydroxysteroid dehydrogenase deficiency (CAH3-HSD) and 11-hydroxylase deficiency (CAH11). 2 In CAH21, the abnormality is in the 21-OH enzyme (P45021), blocking the conversion of hydroxyprogesterone (17OHP) to 11-deoxycortisol (compo Continue reading >>

Unmasking Of Diabetes Insipidus With Steroid Treatment

Unmasking Of Diabetes Insipidus With Steroid Treatment

Unmasking of diabetes insipidus with steroid treatment Adeel Ghaffar, Barbara McGowan, George Tharakan, Nehal Narayan, Rebecca Cox, Emma Hatfield & Karim Meeran Endocrine Unit, Department of Investigative Medicine, Imperial College Healthcare trust, 6th floor, Commonwealth Building, Hammersmith Hospital, London, UK. A 36-year-old man was referred to the neurologists for leg weakness and pain, fatigue and lethargy for 2 years. Sarcoidosis was diagnosed 6 years previously, on the basis of uveitis, lower motor neurone facial palsy, hilar lymphadenopathy and transbronchial biopsy. Prednisolone had been discontinued 3 years prior to his current presentation. His blood pressure was 99/71. Examination was otherwise unremarkable. His ACE was 109 U/l (1070). His TSH was 1.29 mU/l., with a free T4 of 5.9 pmol/l. Cortisol was 56 nmol/l. Prolactin was 818 mU/l (75375 mU/l). LH and FSH were undetectable. Testosterone was very low at 0.3 nmol/l. GH was 0.5 U/l. IGF-1 was 9 nmol/l (1364). Other bloods, and an LP were unremarkable. MRI of brain and spine showed thickening and contrast enhancement around the pituitary infundibulum and hypothalamus. Peak cortisol on SST was 450 nmol/l. He was commenced on hydrocortisone 10 mg, 5 mg, 5 mg, and thyroxine 50 mcg. He was given 1 g methylprednisolone daily for 3 days. He complained of polyuria and polydipsia. His serum osmolality was 302 mOsmol/kg. Concurrent urinary osmolality was 119 mOsmol/kg. A formal water deprivation test was performed. Continue reading >>

Unmasking Of Central Diabetes Insipidus In A Patient After Steroid Treatment

Unmasking Of Central Diabetes Insipidus In A Patient After Steroid Treatment

SESSION TYPE: Critical Care Student/Resident Case Report Posters IPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PMINTRODUCTION: Central diabetes insipidus is a condition characterized by excretion of large volumes of dilute urine secondary to either a deficiency in the production or release of arginine vasopressin. Glucocorticoids are necessary for the kidneys to excrete salt free water. Symptoms of central diabetes insipidus may be masked by concomitant ACTH deficiency. Polyuria may appear when corticosteroid replacement is instituted. We present a case of a woman who developed shock and was given dexamethasone for secondary adrenal insufficiency subsequently unmasking diabetes insipidus.CASE PRESENTATION: A 40-year-old Caucasian female with a remote history of pituitary surgery, presented with a 2-month history of recurrent vomiting, diarrhea and generalized weakness. Physical examination demonstrated drowsiness, tachycardia and hypotension. Initial labs revealed hyponatremia of 130 mmol/dl, hypokalemia 3.1mmol/dl, urine specific gravity of 1.030 and normal renal function. She was started on normal saline boluses but subsequently required vasopressors for refractory shock. Her work up included a serum cortisol which was found to be very low at 0.9 mcg/dl (normal cortisol level 5-25 mcg/dl). Cosyntropin stimulation test was positive for secondary adrenal insufficiency, and dexamethasone was initiated. The patient's symptoms resolved, however she subsequently developed polyuria. Further workup now revealed a low urine osmolality of 209 mOsmol/kg, plasma osmolality of 307 mOsmol/kg and hypernatremia of 149 mmol/dl. She was started on desmopressin for a new diagnosis of central diabetes insipidus. The patient improved and was discharged home on dexamethason Continue reading >>

Unmasking Other Pituitary Deficits During Growth Hormone Replacement Therapy - Em|consulte

Unmasking Other Pituitary Deficits During Growth Hormone Replacement Therapy - Em|consulte

Unmasking other pituitary deficits during growth hormone replacement therapy Department ofMedical Sciences, University ofMilan, Endocrine andMetabolic Unit, Fondazione Ospedale Maggiore Policlinico IRCCS, Milan, Italy Hypothalamic-pituitary system represents a complex neuroendocrine unit that exerts its influence on the whole organism, by stimulating the target endocrine glands. In turn, the feedback of peripheral hormones strictly controls hypothalamic-pituitary activity. In particular, the growth hormone-insulin-like growth factor I (GH-IGF-I axis) plays an important role in modulating other hypothalamic-pituitary axes. There are complex relationships between the GH system and the hypothalamus-pituitary-thyroid (HPT) axis. The reported effects of rhGH administration on thyroid status of patients with growth hormone deficiency (GHD) have been remarkably divergent. Studies on the effects of long-term rhGH replacement treatment in GHD children have described either unchanged [ 3 Click here to see the Library ] serum T3 levels. Transient changes in serum thyroid hormone levels have also been found in GHD children receiving GH [ 30 WyattDT, GesundheitN, ShermanB. Changes in thyroid hormone levels during growth hormone therapy in initially euthyroid patients: lack of need for thyroxin supplementation. J Clin Endocrinol Metab 1998;83:3493-3497. Click here to see the Library ], whereas no changes have been recorded in a placebo-controlled double-blind trial of GH therapy in non-GHD short children [ 20 RoseSR, LeongGM, YvanowskiJA, et al. Thyroid function in non-growth hormone-deficient short children during a placebo-controlled double blind trial of recombinant growth hormone therapy. J Clin Endocrinol Metab 1995;80:320-324. Click here to see the Library ]. As far as GHD adu Continue reading >>

Hypocortisolism Flashcards | Quizlet

Hypocortisolism Flashcards | Quizlet

Potency - Hydrocort : pred : dexa = 40 : 10 : 1 (10mg = 2mg = 0.25mg) Why is hydrocortisone preferred for replacement in adrenal insufficiency? 1) most potent in mineralocorticoid action 2) ~100% bioavailable (20mg/day vs 5mg pred vs 0.5mg dexa) 3) shortest-acting, which is useful for titration to physiologic secretion, and for omitting dose during follow-up SST Primary hypocortisolism - in secondary, the zona glomerulosa continues to secrete aldosterone under the influence of the RAAS Caveats to hydrocortisone replacement for adrenal insufficiency Should follow pt's diurnal rhythm rather than clock time i.e. upon waking for shift workers =/= morning If pt is hypothyroid as well, give hydrocort before thyroxine How should the pt with adrenal insufficiency being started on hydrocortisone replacement be monitored for DI? Detailed Hx for S&S of glucocorticoid over/underreplacement, need for self-adj of stress doses Carry medik awas card identifying steroid treatment at all times, including contact detail of GP/endocrinologist. Inform any doctors or dentists of your condition and dose of steroids. Morning tablet should be taken before getting out of bed Emergency hydrocortisone injection kit on standby with competent caregiver Sick day rules for pts on steroid replacement If mild illness (URTI) with no fever, continue same dose. If febrile, requiring bedrest or Abx, double usual dose and see GP. If diarrhea/vomiting and unable to take orally, inject IM and visit ED stat. Endocrine: Weight gain, worsening glycaemic control/new-onset DM Psychiatric: Confusion, irritability, suicidal thoughts CVS: Oedema, HTN, electrolyte abnormalities Skin: Skin thinning, delayed wound healing Continue reading >>

Hypopituitarism

Hypopituitarism

Are You Sure the Patient Has Hypopituitarism? Hypopituitarism is defined as partial or complete deficiency in one or more of the hormones produced by the anterior pituitary gland (ACTH, TSH, FSH, LH, GH, prolactin) or posterior pituitary (ADH, oxytocin). Panhypopituitarism refers to decreased production of all of the pituitary hormones of the anterior pituitary (adenohypophysis) with or without deficiency of posterior pituitary (neurohypophysis) function. The clinical manifestations seen in patients with deficiencies of pituitary hormones that control target glands (ACTH, TSH, and gonadotropins) are generally those of primary deficiencies of target gland hormones, with a few important exceptions. The presentation and clinical manifestations of hypopituitarism may vary and are determined by the following factors: Which of the pituitary hormones are affected? The severity of the deficiency of each affected hormone The acuity and duration of hormone deficiencies Patients who have hypopituitarism due to a pituitary tumor or parasellar mass lesion may have symptoms of headache and visual field defects. In diseases which can affect the whole anterior pituitary the order in which loss of anterior hormone production occurs is often predictable. In most cases, secretion of GH, FSH, and LH decreases before declines in TSH and ACTH levels are observed. Therefore the earliest clinical presentation in children may be growth delay, and in adults hypogonadism. Exceptions to this rule are not uncommon and isolated pituitary hormone deficiencies, though rare, do occur. Prolactin deficiency is rare and suggests near total destruction of the anterior pituitary gland, such as can be seen with pituitary apoplexy. It should be noted that the most common causes of anterior pituitary failure Continue reading >>

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