Some Skin Manifestations in Hypoparathyroidism
Total Page:16
File Type:pdf, Size:1020Kb

Load more
Recommended publications
-
Impetigo Herpetiformis: a Case Report
Perinatal Journal • Vol: 13, Issue: 4/December 2005 227 Impetigo Herpetiformis: A Case Report ‹ncim Bezircio¤lu1, Merve Biçer1, Levent Karc›1, Füsun Özder2, Ali Balo¤lu1 1First Clinic of Gynecology and Obstetrics, 2Clinics of Dermatology, Atatürk Training and Research Hospital, ‹zmir Abstract Objective: Impetigo herpetiformis is a rare and potentially life-threatening pustular dermatosis affecting mainly pregnant women. We report here a case of impetigo herpetiformis which occured in twenty-ninth week of pregnancy. Case: A 32 year old gravida 2, para1 pregnant woman who was referred to our institution because of congestive heart failure, gestational diabetes mellitus and oligohidroamnios in 27th gestational age was hospitalized. Eruptive pustular lesions which appeared in 29th week of the gestation has spread her entire body. Her pustular cultures were negative. A punch skin biopsy from a pustule on the trunk made the diagnosis of impetigo herpetiformis. The patient who developed spontaneous uterine contractions was treated with betamethazone and tocolysis. The patient who did not respond to this treatment was taken to delivery at 30 weeks of gestation.The newborn showed no skin lesions after birth. The skin lesions of the mother improved in the second postpartum week. Conclusion: The rates of maternal mortality and fetal mortality and morbidity due to placental insufficiency are increased in impetigo herpetiformis. To reduce the mortality and morbidity rates the antenatal management of impetigo herpetiformis should be organized with a multidisciplinary approach. Keywords: Impetigo herpetiformis, generalized pustular psoriasis. Impetigo herpetiformis: Bir olgu sunumu Amaç: ‹mpetigo herpetiformis gebelerde görülen yaflam› riske edebilen nadir bir püstüler dermatozdur. Bu çal›flmada 29.gebe- lik haftas›nda ortaya ç›kan impetigo herpetiformis olgusu sunulmufltur. -
Epileptic Seizure, As the First Symptom of Hypoparathyroidism in Children, Does Not Require Antiepileptic Drugs
Childs Nerv Syst DOI 10.1007/s00381-016-3264-2 ORIGINAL PAPER Epileptic seizure, as the first symptom of hypoparathyroidism in children, does not require antiepileptic drugs Meng-Jia Liu1 & Jiu-Wei Li2 & Xiu-Yu Shi1 & Lin-Yan Hu1 & Li-Ping Zou1,3 Received: 28 May 2016 /Accepted: 3 October 2016 # The Author(s) 2016. This article is published with open access at Springerlink.com Abstract Introduction Objective Patients with hypoparathyroidism exhibit metabol- ic disorders (hypocalcemia) and brain structural abnormalities Epileptic seizure occurs when a burst of electrical impulses in (brain calcifications). Currently, studies have determined the brain exceeds the normal limits. Its manifestation can vary whether antiepileptic drug (AED) treatment is required for from uncontrolled jerking movement (tonic–clonic seizure) to epileptic seizures in children with hypoparathyroidism. momentary loss of awareness (absence seizure). These im- Method This study aims to evaluate the data of two medical pulses spread to adjacent areas in the brain and create an un- centers in Beijing based on the diagnosis of epileptic seizures controlled storm of electrical activity. Brain diseases character- as the first symptom of hypoparathyroidism in children. ized by enduring predisposition to generate epileptic seizures Result A total of 42 patients were included and assigned into are collectively called epilepsy. According to pathogenesis, ep- AED and non-AED treatment groups in a 1:2 matched case– ilepsy can be classified into six categories: metabolic, structural, control study. Results show that the seizure outcome after inherited, immunologic, inflammatory, and idiopathic. 1 year of AED treatment is not significantly different from Hypoparathyroidism is an endocrine disease that results that of the control. -
ICD-9 Diagnosis Codes Effective 10/1/2011 (V29.0) Source: Centers for Medicare and Medicaid Services
ICD-9 Diagnosis Codes effective 10/1/2011 (v29.0) Source: Centers for Medicare and Medicaid Services 0010 Cholera d/t vib cholerae 00801 Int inf e coli entrpath 01086 Prim prg TB NEC-oth test 0011 Cholera d/t vib el tor 00802 Int inf e coli entrtoxgn 01090 Primary TB NOS-unspec 0019 Cholera NOS 00803 Int inf e coli entrnvsv 01091 Primary TB NOS-no exam 0020 Typhoid fever 00804 Int inf e coli entrhmrg 01092 Primary TB NOS-exam unkn 0021 Paratyphoid fever a 00809 Int inf e coli spcf NEC 01093 Primary TB NOS-micro dx 0022 Paratyphoid fever b 0081 Arizona enteritis 01094 Primary TB NOS-cult dx 0023 Paratyphoid fever c 0082 Aerobacter enteritis 01095 Primary TB NOS-histo dx 0029 Paratyphoid fever NOS 0083 Proteus enteritis 01096 Primary TB NOS-oth test 0030 Salmonella enteritis 00841 Staphylococc enteritis 01100 TB lung infiltr-unspec 0031 Salmonella septicemia 00842 Pseudomonas enteritis 01101 TB lung infiltr-no exam 00320 Local salmonella inf NOS 00843 Int infec campylobacter 01102 TB lung infiltr-exm unkn 00321 Salmonella meningitis 00844 Int inf yrsnia entrcltca 01103 TB lung infiltr-micro dx 00322 Salmonella pneumonia 00845 Int inf clstrdium dfcile 01104 TB lung infiltr-cult dx 00323 Salmonella arthritis 00846 Intes infec oth anerobes 01105 TB lung infiltr-histo dx 00324 Salmonella osteomyelitis 00847 Int inf oth grm neg bctr 01106 TB lung infiltr-oth test 00329 Local salmonella inf NEC 00849 Bacterial enteritis NEC 01110 TB lung nodular-unspec 0038 Salmonella infection NEC 0085 Bacterial enteritis NOS 01111 TB lung nodular-no exam 0039 -
C.O.E. Continuing Education Curriculum Coordinator
CONTINUING EDUCATION All Rights Reserved. Materials may not be copied, edited, reproduced, distributed, imitated in any way without written permission from C.O. E. Continuing Education. The course provided was prepared by C.O.E. Continuing Education Curriculum Coordinator. It is not meant to provide medical, legal or C.O.E. professional services advice. If necessary, it is recommended that you consult a medical, legal or professional services expert licensed in your state. Page 1 of 199 Click Here To Take Test Now (Complete the Reading Material first then click on the Take Test Now Button to start the test. Test is at the bottom of this page) 5 hr. Nail Structure and Growth & TCSG Health and Safety Outline Why Study Nail Structure and Growth? • The Natural Nail • Nail Anatomy • Nail Growth • Know Your Nails Objectives After completing this section, you should be able to: C.O.E.• Describe CONTINUING the structure and composition of nails. EDUCATION • Discuss how nails grow. • Identify diseases and disorders of the nail All Rights Reserved. Materials may not be copied, edited, reproduced, distributed, imitated in any way without written permission from C.O. E. Continuing Education. The course provided was prepared by C.O.E. Continuing Education Curriculum Coordinator. It is not meant to provide medical, legal or professional services advice. If necessary, it is recommended that you consult a medical, legal or professional services expert licensed in your state. 1 CONTINUING EDUCATION All Rights Reserved. Materials may not be copied, edited, reproduced, distributed, imitated in any way without written permission from C.O. -
Continuous Rhpth (1–34) Treatment in Chronic Hypoparathyroidism
ID: 20-0009 -20-0009 C T Fuss and others Continuous rhPTH (1-34) in ID: 20-0009; May 2020 hypoparathyroidism DOI: 10.1530/EDM-20-0009 Continuous rhPTH (1–34) treatment in chronic hypoparathyroidism Carmina Teresa Fuss1, Stephanie Burger-Stritt1, Silke Horn1, Ann-Cathrin Koschker1, Kathrin Frey1, Almuth Meyer2 and Stefanie Hahner1 Correspondence should be addressed 1Division of Endocrinology and Diabetology, Department of Medicine I, University Hospital Würzburg, Würzburg, to S Hahner Germany and 2Division of Endocrinology and Diabetology, Department of Internal Medicine, Helios Klinikum Erfurt, Email Erfurt, Germany [email protected] Summary Standard treatment of hypoparathyroidism consists of supplementation of calcium and vitamin D analogues, which does not fully restore calcium homeostasis. In some patients, hypoparathyroidism is refractory to standard treatment with persistent low serum calcium levels and associated clinical complications. Here, we report on three patients (58-year-oldmale,52-year-oldfemale,and48-year-oldfemale)sufferingfromseveretreatment-refractorypostsurgical hypoparathyroidism. Two patients had persistent hypocalcemia despite oral treatment with up to 4 µg calcitriol and up to 4 g calcium per day necessitating additional i.v. administration of calcium gluconate 2–3 times per week, whereas the third patient presented with high frequencies of hypocalcemic and treatment-associated hypercalcemic episodes. S.c. administration of rhPTH (1–34) twice daily (40 µg/day) or rhPTH (1–84) (100 µg/day) only temporarily increased serum calcium levels but did not lead to long-term stabilization. In all three cases, treatment with rhPTH (1–34) as continuous s.c. infusion via insulin pump was initiated. Normalization of serum calcium and serum phosphate levels was observed within 1 week at daily 1–34 parathyroid hormone doses of 15 µg to 29.4 µg. -
Guide to Learning in Maternal-Fetal Medicine
GUIDE TO LEARNING IN MATERNAL-FETAL MEDICINE First in Women’s Health The Division of Maternal-Fetal Medicine of The American Board of Obstetrics and Gynecology, Inc. 2915 Vine Street Dallas, TX 75204 Direct questions to: ABOG Fellowship Department 214.871.1619 (Main Line) 214.721.7526 (Fellowship Line) 214.871.1943 (Fax) [email protected] www.abog.org Revised 4/2018 1 TABLE OF CONTENTS I. INTRODUCTION ........................................................................................................................ 3 II. DEFINITION OF A MATERNAL-FETAL MEDICINE SUBSPECIALIST .................................... 3 III. OBJECTIVES ............................................................................................................................ 3 IV. GENERAL CONSIDERATIONS ................................................................................................ 3 V. ENDOCRINOLOGY OF PREGNANCY ..................................................................................... 4 VI. PHYSIOLOGY ........................................................................................................................... 6 VII. BIOCHEMISTRY ........................................................................................................................ 9 VIII. PHARMACOLOGY .................................................................................................................... 9 IX. PATHOLOGY ......................................................................................................................... -
Quick Guide to Laboratory Values
March 2021 www.nursingcenter.com Quick Guide to Laboratory Values Use this convenient cheat-sheet to help you monitor laboratory values related to fluid and electrolyte status. Remember, normal value ranges may vary according to techniques used in different laboratories. SERUM ELECTROLYTES Electrolyte Nursing Considerations (Range) Calcium (Ca2+) Hypocalcemia 8.5-10.5 mg/dL • Signs and symptoms o Seizures, neuromuscular irritability or tetany (may include paresthesia, bronchospasm, laryngospasm, carpopedal spasm [Trousseau’s sign], Chvostek’s sign [facial muscle contractions elicited by tapping facial nerve on ipsilateral side], tingling sensations of the fingers, mouth, and feet, increased deep tendon reflexes [DTRs]), bleeding abnormalities o ECG changes may include prolonged QT interval and arrythmias. • Implement seizure precautions and close monitoring of respiratory status. Hypercalcemia • Signs and symptoms o Lethargy, confusion, nausea, vomiting, anorexia, constipation, muscle weakness, depressed DTRs • Monitor cardiac rate and rhythm. • Increase mobilization, provide adequate hydration either with IV fluids or encouragement of oral intake. • Watch for digitalis toxicity. Chloride (Cl-) Hypochloremia 97-107 mEq/L • Signs and symptoms o Muscle spasms, alkalosis, and depressed respirations • May be precipitated or exacerbated by GI losses (vomiting, diarrhea). Hyperchloremia • Monitor for acidosis. Magnesium (Mg2+) Hypomagnesemia 1.8-3 mg/dL • Signs and symptoms o Cardiac/ventricular arrhythmias, laryngeal stridor/spasm, neuromuscular -
E464ac551ab13f3547a4f8129a8
Revista6Vol88ingles_Layout 1 1/8/14 12:02 PM Página 1022 1022 COMMUNICATION s Perception of brittle nails in dermatologic patients: a cross-sectional study* Percepção de unhas frágeis entre pacientes dermatológicas: um estudo transversal Giulio Cesar Gequelim1 Cynthia Yone Kubota1 Sarah Sanches2 Daniela Dranka1 Marcelo Murilo Mejia1 Fernando Mitsuo Sumiya1 Juliano Vilaverde Schmitt3 DOI: http://dx.doi.org/10.1590/abd1806-4841.20132327 Abstract: Brittle Nails Syndrome is characterized by fragility of the nail plate, affecting 27% of women. We eval- uated dermatology patients in a cross-sectional study about perception of nail fragility. One hundred and thirty- eight women were included, with median age of 36.5 years. Nail examination showed changes in 57% and 49% reported nail fragility. The first three fingernails were the most affected. Onychoschizia was related to ony- chophagia (OR = 3.29), housework (OR = 2.95) and water contact (OR = 2.44). Onychorrhexis had the strongest association with nail fragility perception (OR = 17.89). The fragility was more perceived by those who were black, of mixed race and atopic, and was associated with depressed mood. Keywords: Asthma; Depression; Nail diseases; Race or ethnic group distribution; Risk factors Resumo: A síndrome das unhas frágeis caracteriza-se por fragilidade da lâmina ungueal, acometendo 27% das mulheres. Realizamos estudo transversal com pacientes dermatológicas sobre a percepção de fragilidade ungueal. Avaliamos 138 pacientes com idade mediana de 36,5 anos. Ao exame, 57% apresentavam alterações e 49% relatavam fragilidade ungueal. Os três primeiros dedos das mãos foram os mais acometidos. A onicosquizia associou-se com onicofagia (OR = 3,29), trabalhos domésticos (OR = 2,95) e contato com água (OR = 2,44). -
Code Description
Code Description 0061 Chronic intestinal amebiasis without mention of abscess 0062 Amebic nondysenteric colitis 0063 Amebic liver abscess 0064 Amebic lung abscess 00642 West Nile fever with other neurologic manifestation 00649 West Nile fever with other complications 0065 Amebic brain abscess 0066 Amebic skin ulceration 0068 Amebic infection of other sites 0069 Amebiasis, unspecified 0070 Other protozoal intestinal diseases, balantidiasis (Infection by Balantidium coli) 0071 Other protozoal intestinal diseases, giardiasis 0072 Other protozoal intestinal diseases, coccidiosis 0073 Other protozoal intestinal diseases, trichomoniasis 0074 Other protozoal intestinal diseases, cryptosporidiosis 0075 Other protozoal intestional disease cyclosporiasis 0078 Other specified protozoal intestinal diseases 0079 Unspecified protozoal intestinal disease 01000 Primary tuberculous infection, unspecified 01001 Primary tuberculous infection bacteriological or histological examination not done 01002 Primary tuberculous infection, bacteriological or histological examination results unknown 01003 Primary tuberculous infection, tubercle bacilli found by microscopy 01004 Primary tuberculous infection, tubercle bacilli found by bacterial culture 01005 Primary tuberculous infection, tubercle bacilli confirmed histolgically 01006 Primary tuberculous infection, tubercle bacilli found by other methods 01010 Tuberculous pleurisy in primary progressive tuberculosis unspecified 01011 Tuberculous pleurisy bacteriological or histological examination not done 01012 Tuberculous -
Fluid & Electrolytes Fluid Balance Sodium 135-145 Meq/L
11/24/2009 Fluid & Electrolytes The Basics Fluid Balance Sodium 135‐145 meq/L • Imbalances typically associated with parallel changes in osmolality • Plays a major role in – ECF volume and concenttitration – Generation and transmission of nerve impulses – Acid–base balance 1 11/24/2009 Hypernatremia • Elevated serum sodium occurring with water loss or sodium gain • Causes hyperosmolality leading to cellular dehydration • Primary protection is thirst from hypothalamus Differential Assessment of ECF Volume Hypernatremia • Manifestations – Thirst, lethargy, agitation, seizures, and coma • Impaired LOC • Produced by clinical states – Central or nephrogenic diabetes insipidus – Serum sodium levels must be reduced gradually to avoid cerebral edema 2 11/24/2009 Nursing Management Nursing Diagnoses • Potential complication: seizures and coma leading to irreversible brain damage • Management • Treat undliderlying cause • If oral fluids cannot be ingested, IV solution of 5% dextrose in water or hypotonic saline • Diuretics Hyponatremia • Results from loss of sodium‐containing fluids or from water excess • Manifestations – CfiConfusion, nausea, vomiting, seizures, and coma Nursing Management Nursing Diagnoses • Risk for injury • Potential complication: severe neurologic changes • Management • Abnormal fluid loss – Fluid replacement with sodium‐containing solution • Caused by water excess – Fluid restriction is needed • Severe symptoms (seizures) – Give small amount of IV hypertonic saline solution (3% NaCl) 3 11/24/2009 Potassium 3.5‐5.5 meq/L • -
Hypoparathyroidism, Sensorineural
Joseph et al. BMC Endocrine Disorders (2019) 19:111 https://doi.org/10.1186/s12902-019-0438-4 CASE REPORT Open Access Hypoparathyroidism, Sensorineural deafness and renal disease (Barakat syndrome) caused by a reduced gene dosage in GATA3: a case report and review of literature Anne D. D. Joseph1* , Nirmala D. Sirisena2, Thirunavukarasu Kumanan1, Vathualan Sujanitha1, Veronika Strelow3, Raina Yamamoto3, Stefan Wieczorek3 and Vajira H. W. Dissanayake2 Abstract Background: Barakat syndrome is an autosomal dominant rare genetic disease caused by haploinsufficiency of the GATA binding protein 3 (GATA3) gene. It is also known as HDR syndrome, and is characterized by varying degrees of hypoparathyroidism, sensorineural deafness and renal disease. This is the first report of a heterozygous GATA3 whole gene deletion causing HDR syndrome in a Sri Lankan family. Case presentation: A 13-year-old boy with an acute febrile illness, hypocalcaemia and bilateral carpopedal spasm was referred for evaluation. A past medical history of treatment for persistent hypocalcaemic symptoms since the age of 7 months was obtained. Biochemical investigations showed persistent low serum corrected calcium levels with hyperphosphataemia, hypomagnesaemia, low parathyroid hormone levels, hypercalciuria, and low total 25-hydroxy vitamin D levels. His renal functions and renal sonography were normal. Audiometry showed bilateral moderate to severe sensorineural hearing loss. On screening, his mother was also found to have asymptomatic hypocalcaemia, hypomagnesaemia, hyperphosphataemia, hypercalciuria and low total 25-hydroxy vitamin D levels. She had impaired renal functions and chronic parenchymal changes in the renal scan. Audiometry showed bilateral profound sensorineural hearing loss. Genetic analysis using multiplex-ligation dependent probe amplification showed a reduced gene dosage for GATA3 that is consistent with a heterozygous whole gene deletion in both the child and mother. -
Hyperemesis Gravidarum with Paraparesis and Tetany
Open Access Case Report DOI: 10.7759/cureus.17014 Hyperemesis Gravidarum With Paraparesis and Tetany Jyotsnaa Muralitharan 1 , Vijayakumar Nagarajan 1 , Umarani Ravichandran 1 1. Internal Medicine, Rajah Muthiah Medical College & Hospital, Chidambaram, IND Corresponding author: Jyotsnaa Muralitharan, [email protected] Abstract Subacute-onset muscle weakness can result from channelopathies, inflammatory myopathies, thyroid dysfunction, hypoparathyroidism, vitamin D deficiency, and dyselectrolytemias like hypokalemia, hypocalcemia, and hypomagnesemia. We report a curious and extremely rare case of a 29-year-old woman with hyperemesis gravidarum presenting with disabling muscle weakness involving her lower limbs and trunk, and concurrent features of tetany. Following voluminous vomiting over the last two months, she presented with history of weakness of her lower limbs of 14 days duration, resulting in difficulty in her getting out of bed or walking unassisted. On examination, she was hypotensive (80/60 mmHg) and tachycardic (110 bpm), with flaccid weakness of her lower limbs (proximal weakness more than distal weakness - power of 1/5 at the hips bilaterally, and 3/5 at the knees and ankles bilaterally) and diminished deep tendon reflexes. She also had positive Trousseau’s sign and Chvostek’s sign. Interestingly, she also had thinned-out bluish sclerae, a high-arched palate, short stature, and bilateral conductive hearing loss. Laboratory evaluation revealed anemia, hyponatremia, hypokalemia, hypomagnesemia, hypochloremia, hypophosphatemia, and low vitamin D levels. Electrocardiogram showed prolonged QT interval. Her thyroid function test and parathyroid levels were normal. With parenteral replenishment of the electrolytes and vitamin D, her power improved and she was discharged on oral supplements. Thus, this case report demonstrates the importance of aggressive, early, and adequate management of hyperemesis gravidarum to prevent dyselectrolytemia-associated paraparesis.