Thesis(M Med(Neurology))--University of Limpopo(Medunsa Campus),2009. / 1 BACKGROUND (geophagia/pica) Pica is a tendency to ingest nonnutritive substances eg. chalk, paper, wood, coal etc. The American Psychiatric Association in its diagnostic and statistical Manual defines Pica as persistent eating of non-nutritive substances that is inappropriate for developmental level, occurs outside culturally sanctioned practice and, if observed during the course of another mental disorder, is sufficiently severe to warrant independent attention. The term pica comes from the Latin word magpie- a bird known for its indiscriminating eating habits. The deliberate consumption of earth, soil or clay is known as geophagia which is the commonest form of pica. Hippocrates is credited with the oldest description of this ancient practice. An ancient Roman textbook, De Medicina, compiled by Celsus during the rein of Emperor Tiberius (13 – 37 AD), mentions earth eating as one of the reasons for bad skin colour. It is a practice that continues to exist in modern times, the full extent however, remains unrealized most probably due to underreporting. Geophagia has been practiced at some stage, virtually world wide eg. America (north & south), Asia, Australia, Britain, India, various parts of Africa. The epidemiology however, is still unknown due to the lack of studies in this regard.

No description available.

Thesis--Wisconsin. / Includes bibliographical references (leaves 46-49).

No description available.

京都大学 / 0048 / 新制・課程博士 / 博士(社会健康医学) / 甲第22123号 / 社医博第98号 / 新制||社医||10(附属図書館) / 京都大学大学院医学研究科社会健康医学系専攻 / (主査)教授 中山 健夫, 教授 柳田 素子, 教授 長船 健二 / 学位規則第4条第1項該当 / Doctor of Public Health / Kyoto University / DFAM

by Albert Yan Wo Chan. / Thesis (M.D.)--Chinese University of Hong Kong, 1995. / Includes bibliographical references (leaves 203-242). / Chapter CHAPTER1 --- INTRODUCTION --- p.1 / Chapter 1.1 --- Brief History of thyroid diseases --- p.2 / Chapter 1.2 --- Thyrotoxicosis and muscle diseases --- p.7 / Chapter 1.2.1 --- Thyrotoxic myopathy --- p.8 / Chapter 1.2.2 --- Exophthalmic ophthalmoplegia (Grave's ophthalmopathy) --- p.10 / Chapter 1.2.3 --- Myasthenia gravis --- p.10 / Chapter 1.2.4 --- Thyrotoxic periodic paralysis (TPP) --- p.11 / Chapter 1.2.4.1 --- Overview --- p.11 / Chapter 1.2.4.2 --- Prevalence --- p.13 / Chapter 1.3 --- Periodic paralysis syndromes in the Chinese --- p.16 / Chapter 1.4 --- Potassium homeostasis in TPP --- p.19 / Chapter 1.5 --- Cellular potassium transport --- p.24 / Chapter 1.5.1 --- Role of the sodium pump --- p.24 / Chapter 1.5.2 --- Hormonal control of the sodium pump --- p.26 / Chapter 1.5.3 --- Molecular biology of the sodium pump --- p.27 / Chapter 1.5.4 --- Na-K-Cl transporter --- p.30 / Chapter 1.5.5 --- Summary --- p.32 / Chapter 1.6 --- Mechanism of paralysis --- p.33 / Chapter 1.7 --- Aetiology of TPP --- p.37 / Chapter 1.7.1 --- Genetic predisposition --- p.37 / Chapter 1.7.2 --- Possible membrane defect --- p.38 / Chapter 1.7.3 --- The central role of the sodium pump in the pathogenesis of TPP --- p.39 / Chapter 1.7.4 --- Environmental factor --- p.40 / Chapter 1.7.5 --- Summary --- p.40 / Chapter 1.8 --- Aims of the thesis --- p.41 / Chapter CHAPTER2 --- A PILOT STUDY ON THE PATHOPHYSIOLOGY OF TPP --- p.44 / Chapter 2.1 --- Aim --- p.45 / Chapter 2.2 --- Background --- p.45 / Chapter 2.2.1 --- The measurement of Na-K ATPase/ sodium pump activity --- p.45 / Chapter 2.2.2 --- In vitro decline in plasma potassium concentration --- p.48 / Chapter 2.2.3 --- Catecholamines --- p.49 / Chapter 2.3 --- Subjects & methods --- p.50 / Chapter 2.4 --- Results --- p.51 / Chapter 2.5 --- Discussion --- p.56 / Chapter 2.6 --- Conclusion --- p.58 / Chapter CHAPTER3 --- PLATELET NA-K ATPASE AS A TISSUE MARKER OF HYPERTHYROIDISM --- p.59 / Chapter 3.1 --- Aim --- p.60 / Chapter 3.2 --- Background --- p.60 / Chapter 3.2.1 --- Thyroid function tests (TFTs) --- p.60 / Chapter 3.2.2 --- TFTs vs tissue markers as an index of hyperthyroidism --- p.61 / Chapter 3.2.3 --- Sodium pump activity as a tissue marker and TPP --- p.63 / Chapter 3.2.4 --- Choice of tissue for sodium pump study --- p.64 / Chapter 3.2.5 --- Rationale behind the aim of study --- p.65 / Chapter 3.3 --- Subjects & methods --- p.68 / Chapter 3.3.1 --- Chemicals --- p.68 / Chapter 3.3.2 --- Subjects --- p.68 / Chapter 3.3.3 --- Plasma thyroid hormones analysis --- p.69 / Chapter 3.3.4 --- Determination of platelet Na-K ATPase activity --- p.71 / Chapter 3.3.4.1 --- Principle --- p.71 / Chapter 3.3.4.2 --- Preparation of platelets --- p.73 / Chapter 3.3.4.3 --- Preparation of platelet lysate --- p.73 / Chapter 3.3.4.4 --- Measurement of Na-K ATPase activity --- p.74 / Chapter 3.3.4.5 --- Measurement of Pi --- p.76 / Chapter 3.3.4.6 --- Measurement of protein --- p.78 / Chapter 3.4 --- Statistics & data handling --- p.80 / Chapter 3.5 --- Results --- p.81 / Chapter 3.5.1 --- Development of the platelet Na-K ATPase assay --- p.81 / Chapter 3.5.1.1 --- Introduction --- p.81 / Chapter 3.5.1.2 --- Effect of saponin concentration on the Na-K ATPase activity --- p.81 / Chapter 3.5.1.3 --- Linearity of the Na-K ATPase assay --- p.83 / Chapter 3.5.1.4 --- Imprecision of the Na-K ATPase assay --- p.83 / Chapter 3.5.1.5 --- Linearity of the Pi assay --- p.86 / Chapter 3.5.1.6 --- Linearity of the protein assay --- p.86 / Chapter 3.5.2 --- Thyroid function tests --- p.89 / Chapter 3.5.3 --- Platelet Na-K ATPase activity --- p.92 / Chapter 3.5.4 --- Correlation between thyroid hormones concentrations and platelet Na-K ATPase activity --- p.95 / Chapter 3.5.5 --- Correlation between age and platelet Na-K ATPase activity --- p.95 / Chapter 3.5.6 --- Performance of platelet ATPase as an indicator of hyperthyroidism --- p.99 / Chapter 3.6 --- Discussion --- p.102 / Chapter CHAPTER4 --- BASAL NA-K ATPASE ACTIVITY IN THYROTOXIC SUBJECTS WITH AND WITHOUT HYPOKALAEMIC PERIODIC PARALYSIS --- p.107 / Chapter 4.1 --- Aim --- p.108 / Chapter 4.2 --- Introduction --- p.108 / Chapter 4.2.1 --- Background --- p.108 / Chapter 4.2.2 --- Difficulties and limitations in TPP study --- p.109 / Chapter 4.3 --- Subjects & methods --- p.112 / Chapter 4.3.1 --- Platelet Na-K ATPase --- p.112 / Chapter 4.3.2 --- Rubidium loading test --- p.114 / Chapter 4.4 --- Statistics & data handling --- p.115 / Chapter 4.5 --- Results --- p.117 / Chapter 4.5.1 --- Platelet Na-K ATPase activity --- p.117 / Chapter 4.5.1a --- Thyrotoxic vs TPP --- p.121 / Chapter 4.5.1b --- Thyrotoxic vs euthyroid and TPP vs EuTPP --- p.124 / Chapter 4.5.1c --- Control vs euthyroid and EuTPP --- p.126 / Chapter 4.5.2 --- Rubidium loading test --- p.127 / Chapter 4.6 --- Discussion --- p.129 / Chapter 4.6.1 --- Clinical marker of TPP --- p.129 / Chapter 4.6.2 --- RBC/ lymphocyte sodium pump activity --- p.130 / Chapter 4.6.3 --- Platelet Na-K ATPase activity --- p.135 / Chapter CHAPTER5 --- VALIDATION OF THE ORAL GLUCOSE TOLERANCE TEST --- p.142 / Chapter 5.1 --- Aim --- p.143 / Chapter 5.2 --- Background --- p.143 / Chapter 5.2.1 --- Need for a validated protocol for OGTT --- p.143 / Chapter 5.2.2 --- Effectiveness of sodium fluoride as a preservative of glucose in blood sample --- p.144 / Chapter 5.2.3 --- Effect of delay in sample handling --- p.146 / Chapter 5.2.4 --- Ideal concentration of NaF --- p.147 / Chapter 5.2.5 --- D-mannose as a preservative of blood glucose --- p.147 / Chapter 5.2.6 --- Rationale behind the aim of study --- p.148 / Chapter 5.3 --- Subjects & methods --- p.149 / Chapter 5.3.1 --- Effectiveness of NaF --- p.149 / Chapter 5.3.2 --- Effect of delay in sample handling --- p.150 / Chapter 5.3.3 --- Ideal concentration of NaF --- p.151 / Chapter 5.3.4 --- Evaluation of D-mannose as a preservative of blood glucose --- p.151 / Chapter 5.4 --- Results and discussion --- p.153 / Chapter 5.4.1 --- Effectiveness of NaF --- p.153 / Chapter 5.4.2 --- Effect of delay in sample handling --- p.157 / Chapter 5.4.3 --- Ideal concentration of NaF --- p.159 / Chapter 5.4.4 --- D-mannose as a preservative of glucosein blood --- p.161 / Chapter 5.4.5 --- Summary --- p.167 / Chapter CHAPTER6 --- HYPERINSULINAEMIA AND NA-K ATPASE ACTIVITY IN TPP --- p.168 / Chapter 6.1 --- Aim --- p.169 / Chapter 6.2 --- Background --- p.169 / Chapter 6.2.1 --- "Insulin, hypokalaemia and sodium pump" --- p.169 / Chapter 6.2.2 --- Insulin and skeletal muscle membrane potential --- p.170 / Chapter 6.2.3 --- Potential role of insulin in the pathogenesis of TPP --- p.172 / Chapter 6.2.4 --- Hyperinsulinaemia and thyrotoxicosis --- p.173 / Chapter 6.2.5 --- TPP vs uncomplicating thyrotoxic patients --- p.173 / Chapter 6.2.6 --- Catecholamines and insulin secretion --- p.175 / Chapter 6.3 --- Subjects and methods --- p.177 / Chapter 6.4 --- Statistics and data handling --- p.179 / Chapter 6.5 --- Results --- p.180 / Chapter 6.6 --- Discussion --- p.187 / Chapter CHAPTER7 --- OVERALL DISCUSSION AND CONCLUSION --- p.192 / Chapter 7.1 --- General discussion --- p.193 / Chapter 7.2 --- Role of sodium pump in the pathogenesis of TPP --- p.196 / Chapter 7.3 --- Strategy for further study --- p.201 / Chapter 7.4 --- Conclusion --- p.202 / REFERENCES --- p.203 / APPENDIX --- p.239 / (Selected publications)

Prostate cancer is among the most common malignancies in males in the United States and adenocarcinoma accounts for 95% of all malignancies of prostate. Rarely prostate cancer can also present as small cell carcinoma. Pure small cell carcinoma is rare at time of initial diagnosis (<2%) however neuroendocrine differentiation into small cell carcinoma may emerge in men who have had previous treatment with ADT for prostate adenocarcinoma. These tumors, sometimes called treatment-related neuroendocrine prostate cancers or aggressive-variant prostate cancers, are increasingly recognized in the castration-resistant phases of disease progression. They account for less than 1% of all prostate cancers. A 73-year-old otherwise male had routine health screening in May 2018. Prostate specific antigen (PSA) level was elevated at 9.53 ng/mL. He had not had a screening PSA for at least two prior years but this was a significant change from prior levels. Patient was asymptomatic however the abnormal laboratory evaluation prompted consultation with Urology. Biopsy of prostate gland confirmed prostatic adenocarcinoma with Gleason's score of 5+ 4 = 9 with bilateral gland involvement. Imaging studies including CT scan of abdomen and pelvis, a bone scan and a PET scan showed no clear evidence of metastatic disease. Patient's clinical stage was determined to be IIIC with T2c N0 M0 disease. Patient began treatment with androgen deprivation therapy and received definitive radiation treatment with external bean radiation therapy from July to September 2018. PSA was 0.08 ng/ml at the end of radiation treatment. Patient did well for about 15 months, after which he had multiple hospital admissions for dyspnea, fluid retention and lower extremity edema. He was also found to have refractory hypokalemia. Patient underwent MRI brain which revealed numerous small enhancing calvarial and skull base lesions consistent with bony metastasis in the skull. Patient also underwent PET/CT scan which showed numerous thoracic spine bony lesions, numerous to count bony metastasis throughout the lumbar spine and pelvis, as well as multiple hepatic lesions. Patient underwent biopsy of right hepatic lobe lesion and pathology was consistent with small cell carcinoma with positive neuroendocrine markers including CD56, synaptophysin and TTF-1. Interestingly patient’s PSA was only 0.09ng/dL. Given refractory hypokalemia, paraneoplastic syndrome was suspected and further work-up was initiated. Serum cortisol levels were elevated at 119.6 mcg/dL (3.7-19.4) and ACTH level was 333 pg/mL (7.2 - 63.3). Aldosterone level was <1 ng/dL (0 - 30.0). Patient was diagnosed with paraneoplastic Cushing syndrome. Given aggressive nature of this small cell transformation, patient was started on treatment with systemic chemotherapy with Carboplatin/Etoposide during the hospital stay, with stabilization of potassium levels. Prostate small cell carcinoma poses a challenge for diagnosis and treatment. In contrast to adenocarcinoma of the prostate, serum prostate-specific antigen (PSA) is not predictive of disease severity, nor is it a useful tumor marker for monitoring progression or surveillance. Patients with prostate small cell cancer presents with more diverse symptoms than any other prostate cancer since it tends to metastasize early. Also paraneoplastic syndromes are more common in prostate small cell cancers as well.

No description available.

Malignant ventricular arrhythmias are a common cause of sudden cardiac death. Moderate therapeutic hypothermia (MTH) is routinely used in post-resuscitation care for anticipated neuroprotective effects. However, the safety of MTH in terms of the electrical stability of the heart has not been satisfactorily proved yet. Also, the increased sympathetic tone in patients with heart failure contributes to a higher incidence of malignant ventricular arrhythmias. The aim of this work was to verify the safety of MTH as regards the inducibility of ventricular fibrillation (VF) in the pig biomodel, especially in relation to spontaneous changes in the kalemia and QT interval. Furthermore, we assumed that renal denervation (RDN) could reduce the inducibility of VF. In the first part of the thesis, the extracorporeal cooling was introduced in fully anesthetized swine (n = 6) to provide MTH. Inducibility of VF was studied by programmed ventricular stimulation (8 basic stimuli with up to 4 extrastimuli) three times in each biomodel under the following conditions: during normothermia (NT), after reaching the core temperature 32 řC (HT) and after another 60 minutes of stable hypothermia (HT60). VF inducibility, effective ventricular refractory period (ERP), QTc interval, and potassium plasma level were measured. In...

VIPomas are rare pancreatic endocrine tumors (PETs), detected in 1 in 10 million people per year and usually present as a constellation of well-defined clinical features characterized by watery diarrhea, hypokalemia, and achlorhydria (WDHA). Theses tumors secrete an excess of vasoactive intestinal peptide (VIP) and are typically diagnosed only after they have metastasized liver, lymph nodes and lungs (60% to 80%). The diagnosis is confirmed by identifying hyper secretion of VIP in a setting of the localized pancreatic tumor. Symptomatic pancreatic VIPomas are usually solitary, more than 3 cm in diameter, and occur in the tail of pancreas in 75 percent of patients. We demonstrate a rare glimpse at an unusual small size of VIPoma at its earliest clinical presentation.