Soft Tissue Calcification and Ossification
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Calcinosis Cutis
Dermatology Online Journal UC Davis Calcinosis cutis: A rare feature of adult dermatomyositis Inês Machado Moreira Lobo, Susana Machado, Marta Teixeira, Manuela Selores Dermatology Online Journal 14 (1): 10 Department of Dermatology, Hospital Geral de Santo António, Porto, Portugal. [email protected] Abstract Dermatomyositis is an idiopathic inflammatory myopathy with characteristic cutaneous manifestations. We describe a case of a 55- year-old woman with dermatomyositis who presented with dystrophic calcinosis resistant to medical treatment. Dermatomyositis is an idiopathic inflammatory myopathy with characteristic cutaneous manifestations, including heliotrope rash, Gottron papules, periungual telangiectasias, photodistributed erythema, poikiloderma, and alopecia. Although heliotrope rash and Gottron papules are specific cutaneous features, calcinosis of the skin or muscles is unusual in adults with dermatomyositis. However, it may occur in up to 40 percent of children or adolescents [1]. Calcinosis cutis is the deposition of insoluble calcium salts in the skin. Calcinosis cutis may be divided into four categories according to the pathogenesis as follows: dystrophic, metastatic, idiopathic, and iatrogenic. In connective tissue diseases, calcinosis is mostly of the dystrophic type and it seems to be a localized process rather than an imbalance of calcium homeostasis. Calcium deposits may be intracutaneous, subcutaneous, fascial, or intramuscular. Clinical synopsis A 55-year-old woman was referred for evaluation because of multiple, firm nodules of the lateral hips since 1994. At that time, dermatomyositis was diagnosed based on cutaneous, muscular and pulmonary involvement. The nodules, gradually enlarging since 1999, have begun to cause incapacitation pain and many exude a yellowish material suggestive of calcium. She denied an inciting traumatic event. -
Calciphylaxis with Normal Renal and Parathyroid Function Not As Rare As Previously Believed
OBSERVATION Calciphylaxis With Normal Renal and Parathyroid Function Not as Rare as Previously Believed Andrew H. Kalajian, MD; Paula S. Malhotra, MD; Jeffrey P. Callen, MD; Lynn P. Parker, MD Background: Calciphylaxis is a life-threatening form of previously reported cases of nontraditional calciphylaxis metastatic calcification-induced microvascular occlusion identified the following patient characteristics that high- syndrome. Although traditionally observed in patients with light clinical situations potentially predisposing to calci- end-stage renal disease and/or hyperparathyroidism, the phylaxis: hypoalbuminemia, malignant neoplasm, sys- development of calciphylaxis in “nontraditional” pa- temic corticosteroid use, anticoagulation with warfarin tients having both normal renal and parathyroid func- sodium or phenprocoumon, chemotherapy, systemic in- tion has been reported. However, to date there has been flammation, hepatic cirrhosis, protein C or S deficiency, no collective analysis identifying common patient char- obesity, rapid weight loss, and infection. acteristics potentially predisposing to the development of calciphylaxis in nontraditional patients. Conclusions: Calciphylaxis is becoming increasingly common in patients with normal renal and parathyroid Observations: A 58-year-old woman with endometrial function. The observations from this study may assist der- carcinoma developed extensive calciphylaxis despite the matologists in the rapid diagnosis and prompt initiation presence of normal renal and parathyroid function. -
Electrolyte Disorders in Cancer Patients: a Systematic Review
Berardi et al. J Cancer Metastasis Treat 2019;5:79 Journal of Cancer DOI: 10.20517/2394-4722.2019.008 Metastasis and Treatment Review Open Access Electrolyte disorders in cancer patients: a systematic review Rossana Berardi, Mariangela Torniai, Edoardo Lenci, Federica Pecci, Francesca Morgese, Silvia Rinaldi Clinica Oncologica, Università Politecnica delle Marche, Azienda Ospedaliero-Universitaria Ospedali Riuniti Umberto I - GM Lancisi - G Salesi, Ancona 60126, Italy. Correspondence to: Prof. Rossana Berardi, Clinica Oncologica, Università Politecnica delle Marche, Azienda Ospedaliero- Universitaria Ospedali Riuniti di Ancona, Via Conca 71, Ancona 60126, Italy. E-mail: [email protected] How to cite this article: Berardi R, Torniai M, Lenci E, Pecci F, Morgese F, Rinaldi S. Electrolyte disorders in cancer patients: a systematic review. J Cancer Metastasis Treat 2019;5:79. http://dx.doi.org/10.20517/2394-4722.2019.008 Received: 26 Apr 2019 First Decision: 26 Jul 2019 Revised: 20 Nov 2019 Accepted: 20 Nov 2019 Published: 9 Dec 2019 Science Editor: Stephen J. Ralph Copy Editor: Jing-Wen Zhang Production Editor: Jing Yu Abstract Electrolyte disorders are very common complications in cancer patients. They might be associated to a worsening outcome, influencing quality of life, possibility to receive anticancer drugs, and conditioning survival. In fact, they might provoke important morbidity, with dysfunction of multiple organs and rarely causing life-threatening conditions. Moreover, recent studies showed that they might worsen cancer patients’ outcome, while a prompt correction seems to have a positive impact. Furthermore, there is evidence of a correlation between electrolyte alterations and poorer performance status, delays in therapy commencement and continuation, and negative treatment outcomes. -
Section XI Extraskeletal (Ectopic) Calcification and Ossification
Section XI Extraskeletal (Ectopic) Calcification and Ossification Michael P. Whyte Division of Bone and Mineral Diseases, Washington University School of Medicine at Barnes-Jewish Hospital and Center for Metabolic Bone Disease and Molecular Research, Shriners Hospitals for Children, St. Louis, Missouri INTRODUCTION somewhat higher value because they have greater serum phos- phate concentrations compared with adults. However, this is A significant number and variety of disorders cause extraskel- not well established.(5) etal deposition of calcium and phosphate (Table 1). In some, The material that comprises metastatic calcification may be mineral is precipitated as amorphous calcium phosphate or as amorphous calcium phosphate initially, but hydroxyapatite is crystals of hydroxyapatite; in others, osseous tissue is formed. deposited soon after.(2) The anatomic pattern of deposition The pathogenesis of ectopic mineralization is generally attrib- varies somewhat between hypercalcemia and hyperphos- uted to one of three mechanisms (Table 1). First, a supranormal phatemia, but occurs irrespective of the specific underlying “calcium-phosphate solubility product” in extracellular fluid condition or mechanism for the disturbed mineral homeostasis. can cause metastatic calcification. Second, mineral may be Additionally, there is a predilection for certain tissues. deposited as dystrophic calcification into metabolically im- Hypercalcemia is typically associated with mineral deposits paired or dead tissue despite normal serum levels of calcium in the kidneys, lungs, and fundus of the stomach. In these and phosphate. Third, ectopic ossification (or true bone forma- “acid-secreting” organs, a local alkaline milieu may account tion) occurs in a few disorders for which the pathogenesis is for the calcium deposition. In addition, the media of large becoming increasingly understood. -
Fluid and Electrolyte Balance
Fluid and Electrolyte Balance Done By: Faisal S. AlGhamdi Abdullah Almousa Total Body Fluids and fluids compartment: 60% in male of Total body weight 55% in female 2/3 (65%) of TBW is intracellular (ICF) 1/3 (35%) extracellular water – 25 % interstitial fluid (ISF) – 5 - 7 % in plasma (IVF intravascular fluid) – 1- 2 % in transcellular fluids – CSF, intraocular fluids, serous membranes, and in GI, respiratory and urinary tracts (third space) • Fluid compartments are separated by membranes that are freely permeable to water. • Movement of fluids due to: – Hydrostatic pressure (Fluid) – Osmotic/Oncotic pressure (tissue) In Hydrostatic pressure: As the pressure increase as the movement of fluid outside increase In Osmotic pressure: As the pressure increase as the absorption of fluid increase. Fluid balance: • Neutral balance: input = output • Positive balance: input > output • Negative balance: input < output (+ve lead to edema, and -ve lead to dehydration) Daily input should = Daily output Most of water intake in Beverages Most of water output in Urine Electrolytes: Cations – positively charged ions . Na+, K+ , Ca++, H+ Anions – negatively charged ions - - 3- . Cl , HCO3 , PO4 Intracellular fluid space: • 40% of body weight • Largest proportion is in skeletal muscle • Larger percentage of water is Intracellular in males (large muscle mass) • Cations = Potassium & Magnesium • Anions = Phosphates and Proteins Extracellular fluid space: • 20% of body weight • Interstitial 15%, Plasma 5% • Cations = Sodium • Anions = Chloride and Bicarbonate Homeostasis: • Maintained by Ion transport, Water movement and Kidney function. • Tonicity Isotonic, Hypertonic and Hypotonic (the difference btw tonicity and osmolarity that tonicity is concentration of solutions in relation to adjacent compartments *like concentration of plasma compared to interstitial space*, but osmolarity take the compartment on it’s own) Movement of body fluids: “ Where Na goes, H2O follows” Diffusion – movement of particles down a concentration gradient. -
T PATHOLOGIC CALCIFICATION Deposition of Calcium Salts In
t PATHOLOGIC CALCIFICATION Deposition of calcium salts in tissues other than osteoid or enamel is called pathologic or heterotopic calcification. Two distinct types of pathologic calcification are recognised: Dystrophic calcification, which is characterised by deposition of calcium salts in dead or degenerated tissues with normal calcium metabolism and normal serum calcium levels. Dystrophic calcification may occur due to 2 types of causes: ● Calcification in dead tissue ● Calcification of degenerated tissue Metastatic calcification, on the other hand, occurs in apparently normal tissues and is associated with deranged calcium metabolism and hypercalcaemia. Since metastatic calcification occurs in normal tissues due to hypercalcaemia, its causes would include one of the following two conditions: ● Excessive mobilisation of calcium from the bone. ● Excessive absorption of calcium from the gut. Pathogenesis of Dystrophic Calcification The process of dystrophic calcification has been likened to the formation of normal hydroxyapatite in the bone involving 2 phases: ● Initiation and propagation: Initiation is the phase in which precipitates of calcium phosphate begin to accumulate intracellularly in the mitochondria, or extracellularly in membrane-bound vesicles. Propagation is the phase in which minerals deposited in the initiation phase are propagated to form mineral crystals. Pathogenesis of metastatic calcification Metastatic calcification occurs due to excessive binding of inorganic phosphate ions with calcium ions, which are elevated due to underlying metabolic derangement. This leads to formation of precipitates of calcium phosphate at the preferential sites. Metastatic calcification is reversible upon correction of underlying metabolic disorder. GANGRENE Gangrene is a form of necrosis of tissue with superadded putrefaction. The type of necrosis is usually coagulative due to ischaemia (e.g. -
Parenteral Nutrition Primer: Balance Acid-Base, Fluid and Electrolytes
Parenteral Nutrition Primer: Balancing Acid-Base, Fluids and Electrolytes Phil Ayers, PharmD, BCNSP, FASHP Todd W. Canada, PharmD, BCNSP, FASHP, FTSHP Michael Kraft, PharmD, BCNSP Gordon S. Sacks, Pharm.D., BCNSP, FCCP Disclosure . The program chair and presenters for this continuing education activity have reported no relevant financial relationships, except: . Phil Ayers - ASPEN: Board Member/Advisory Panel; B Braun: Consultant; Baxter: Consultant; Fresenius Kabi: Consultant; Janssen: Consultant; Mallinckrodt: Consultant . Todd Canada - Fresenius Kabi: Board Member/Advisory Panel, Consultant, Speaker's Bureau • Michael Kraft - Rockwell Medical: Consultant; Fresenius Kabi: Advisory Board; B. Braun: Advisory Board; Takeda Pharmaceuticals: Speaker’s Bureau (spouse) . Gordon Sacks - Grant Support: Fresenius Kabi Sodium Disorders and Fluid Balance Gordon S. Sacks, Pharm.D., BCNSP Professor and Department Head Department of Pharmacy Practice Harrison School of Pharmacy Auburn University Learning Objectives Upon completion of this session, the learner will be able to: 1. Differentiate between hypovolemic, euvolemic, and hypervolemic hyponatremia 2. Recommend appropriate changes in nutrition support formulations when hyponatremia occurs 3. Identify drug-induced causes of hypo- and hypernatremia No sodium for you! Presentation Outline . Overview of sodium and water . Dehydration vs. Volume Depletion . Water requirements & Equations . Hyponatremia • Hypotonic o Hypovolemic o Euvolemic o Hypervolemic . Hypernatremia • Hypovolemic • Euvolemic • Hypervolemic Sodium and Fluid Balance . Helpful hint: total body sodium determines volume status, not sodium status . Examples of this concept • Hypervolemic – too much volume • Hypovolemic – too little volume • Euvolemic – normal volume Water Distribution . Total body water content varies from 50-70% of body weight • Dependent on lean body mass: fat ratio o Fat water content is ~10% compared to ~75% for muscle mass . -
Osteochondrosis – Primary Epiphyseal (Articular/Subchondral) Lesion Can Heal Or Can Progress
60 120 180 1 distal humeral condyles 2 medial epicondyle 3 proximal radial epiphysis 4 anconeal process Lab Ret study N=1018 . Normal . Affected . Total 688 (67.6%) . Total 330 (32.4%) . Male 230 (62.2%) . Male 140 (37.8%) . Female 458 (70.7%) . Female 190 (29.3%) Affected dogs N=330 1affected site - 250 (75.7%) 2 affected sites - 68 (20.6%) 3 affected sites - 12 (3.6%) immature skeletal diseases denis novak technique for skeletal radiography tissue < 12 cm “non-grid” (“table-top”) technique “high detail” system radiation safety diagnosis X – rays examination Ultrasound CT bilateral lesions - clinical signs ? unilateral present > one type of lesion 2ry arthrosis Common Osteochondrosis – primary epiphyseal (articular/subchondral) lesion can heal or can progress Osteochondritis dissecans – free articular fragment will progress Arthrosis Osteochondrosis talus / tarsus Lumbosacral OCD Lumbosacral OCD Inflammatory diseases Panosteitis – non infectious Hypertrophic osteodystrophy (HOD) – perhaps infectious Osteomyelitis - infectious Panosteitis New medullary bone Polyostotic Multiple lesions in one bone Symmetrical or nonsymmetrical Sclerotic pattern B I L A T E R A L periosteal new bone forms with chronicity Cross sections of a tibia different locations Hypertrophic osteodystrophy (HOD) Dogs are systemically ill, febrile, anorectic, reluctant to walk most will recover Radiographic changes of HOD . Polyostotic . Metaphyseal . Symmetrical . Changes of lesion Early Mid Late lytic “plates” in acute case HOD - 4 m ret – lesions are present -
Hyperostosis Corticalis Infantalis (Caffey's Disease)* J
754 S.A. TYDSKRIF VIR GENEESKU DE 14 Junie 1969 HYPEROSTOSIS CORTICALIS INFANTALIS (CAFFEY'S DISEASE)* J. M. WAGNER, M.B., B.CH., M.R.e.p., Senior Paediatrician, Edenvale Hospital, AND A. SoLOMON, M.B., B.CH., DIP.MED., D.M.R.(D.), Radiologist, Pneumoconiosis Research Unit, CSIR, Baragwanath Hospital, Johannesburg Infantile cortical hyperostosis is a disorder affecting the skeleton and some of its contiguous fascias and muscles. It is suggested that infantile cortical hyperostosis is a pre natal collagen disease.' The early stage is of acute inflammation and loss of the periosteal and subperiosteal definition. There is a fibrous and osteoblastic reaction and overlying tissue including muscle is involved. No bacteria are seen. Later, there is subperiosteal new lamellar bone formation. The peri osteum is thickened and hyperplastic and the overlying soft tissues are oedematous and sections show round-cell infiltration. The subacute phase re-establishes periosteum as an entity. The later remodelling stage removes the extraperipheral bone from within, resulting in dilatation of the medullary cavity. There is evidence to suggest that infantile cortical hyper ostosis had been recognized in 1930.' Caffey and Silver man first described the disease in 1946." Smyth et al.' also recorded cases in 1946. Altogether 102 cases have been reported, Sidbury and Sidbury' contributing 69 reports and Holrnan' describing 33 cases. Infantile cortical hyper ostosis has been described in Negroes but seems rare in the South African Bantu. CASE REPORT The patient, a 3-year-old Bantu male, had a normal birth weight. Two siblings were in good health. The mother stated that the child's jaw was swollen and that he had Fig. -
PATHOPHYSIOLOGY UNIT-1 .Basic Principles of Cell Injury And
B.PHARMACY2nd SEMESTER SUBJECT: PATHOPHYSIOLOGY UNIT-1 .Basic Principles of Cell Injury and Adaptation Cell Injury: Introduction • Cell injury is defined as a variety of stresses a cell encounters as a result of changes in its internal and external environment. • The cellular response to stress may vary and depends upon the following: – The type of cell and tissue involved. – Extent and type of cell injury. ETIOLOGY OF CELL INJURY: 1. Genetic causes • Developmental defects: Errors in morphogenesis • Cytogenetic (Karyotypic) defects: chromosomal abnormalities • Single-gene defects: Mendelian disorders • Multifactorial inheritance disorders. 2. Acquired causes • Hypoxia and ischaemia • Physical agents • Chemical agents and drugs • Microbial agents • Immunologic agents • Nutritional derangements • Aging • Psychogenic diseases • Iatrogenic factors • Idiopathic diseases. 2.1. Oxygen deprivation: HYPOXIA Ischemia (loss of blood supply). Inadequate oxygenation (cardio respiratory failure). Loss of oxygen carrying capacity of the blood (anemia or CO poisoning). 2.2. PHYSICAL AGENTS: Trauma Heat Cold Radiation Electric shock 2.3. CHEMICAL AGENTS AND DRUGS: Endogenous products: urea, glucose Exogenous agents Therapeutic drugs: hormones Nontherapeutic agents: lead or alcohol. 2.4. INFECTIOUS AGENTS: Viruses Rickettsiae Bacteria Fungi Parasites 2.5. Abnormal immunological reactions: The immune process is normally protective but in certain circumstances the reaction may become deranged. Hypersensitivity to various substances can lead to anaphylaxis or to more localized lesions such as asthma. In other circumstances the immune process may act against the body cells – autoimmunity. 2.6. Nutritional imbalances: Protein-calorie deficiencies are the most examples of nutrition deficiencies. Vitamins deficiency. Excess in nutrition are important causes of morbidity and mortality. Excess calories and diet rich in animal fat are now strongly implicated in the development of atherosclerosis. -
Calcinosis Cutis,Calcinosis Circumscripta,And “Mille Feuille
Calcinosis Cutis, Calcinosis Circumscripta, and “Mille Feuille” Lesions James Yi-Chien Lin, DVM MS; Han-Ju Tsai, DVM MS; Kau-Shen Hsu, DVM; Fun-In Wang, DVM PhD Skin and subcutaneous lesions of 2 cases with natural occurring Cushing’s disease and 1 case with calcinosis circumscripta were compared. Case 1 was typical of osteoma cutis, containing somewhat regularly arranged discrete ossification foci in the mid and deep dermis. Case 2 had layers of “mille feuille”, yellowish to white gritty chalky substances diffusely scattered in the sub- cutis, seen histologically as disseminatedly scattered light purple crystalloid and blue granular mineral salts. Lesions stained orange red with Alizarin Red S indicated the presence of calcium ions. Discrete ossification foci in the deep dermis and early multifocal collagenolysis with mine- ralization were also noted. Case 3 was typical of calcinosis circumscripta, seen grossly as yel- lowish chalky substance in both dermis and subcutis, and histologically as lakes of well- circumscribed light purple crystals and granular deep blue mineral salts. Case 2 had features of calcinosis cutis such as ossification foci and early multifocal collagenolysis. Case 2 also had “mille feuille” that was histologically similar to those mineral salts in case 3, but was not circum- scribed, and was not exactly calcinosis universalis. The component in case 1 was most likely hydroxyapatite Ca10(PO4)6(OH)2; the “mille feuille” of case 2 was most likely “calcium soap” after panniculitis and fat necrosis; and that in case 3 was most likely calcium phosphate CaPO4. Lo- cal factors, such as fluid exudation reflecting how well the inflammation was controlled clinically, may influence the wound healing, and thus the outcome of lesions. -
Sir, Metastatic Calcification in the Eye Is Often Seen in the Cornea and the Interpalpebral Conjunctiva. in Hypercalcaemic Subje
804 LETTERS TO THE JOURNAL References described in the sclera.1 Rarely has calcium been 1 1. Schepens CL, Acosta F. Scleral implants: an historical detected in the uvea. There have been few previous perspective. Surv OphthalmoI1991;35:447-53. case reports of patient with clinically evident 2. Wizina RA. Removal of solid silicone rubber explants choroidal calcification following hypercalcaemia due after retinal detachment surgery. Am J Ophthalmol to primary hyperparathyroidism 2. We present the 1983;95:495-7. clinical and investigative findings of a patient who 3. Deutsch J, Aggarwal RK, Eagling EM. Removal of had been treated for primary hyperparathyroidism · scleral explant elements: a 10-year retrospective study. and who was found some years later to have Eye 1992;6:570-3. choroidal calcification. 4. Delaney WV, Tomisi PF, Hampton GR, et al. Complications of scleral buckling procedures. Arch OphthalmoI1987;105:702-3. Case Report A 60-year-old woman with a complex medical history was referred to the eye clinic in September 1991. She Sir, was diagnosed with infiltrating carcinoma of the Choroidal Calcification in Primary Hyperpara breast in January 1991. She had a right mastectomy thyroidism and axillary clearance in February 1991 and was Metastatic calcificationin the eye is often seen in the subsequently placed on tamoxifen 20 mg daily. cornea and the interpalpebral conjunctiva. In Visual deterioration on the right prompted referral hypercalcaemic subjects calcium has also been for examination for uveal metastases. Fig. 1. Fundus photographs showing the creamy-white to yellow-orange lesions representing areas of choroidal calcification: Top left, right superior vessel arcades; bottom left, right temporal vessel arcades; top right, left superior vessel arcades; bottom right, left inferotemporal vessel arcade.