DOCSLIB.ORG

Hypercalcemic Nephropathy in the Dog Ellen H

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Hypercalcemic Nephropathy in the Dog Ellen H Volume 47 | Issue 2 Article 9 1985 Hypercalcemic Nephropathy in the Dog Ellen H. Hikes Iowa State University Wallace B. Morrison Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/iowastate_veterinarian Part of the Nephrology Commons, and the Small or Companion Animal Medicine Commons Recommended Citation Hikes, Ellen H. and Morrison, Wallace B. (1985) "Hypercalcemic Nephropathy in the Dog," Iowa State University Veterinarian: Vol. 47 : Iss. 2 , Article 9. Available at: https://lib.dr.iastate.edu/iowastate_veterinarian/vol47/iss2/9 This Article is brought to you for free and open access by the Journals at Iowa State University Digital Repository. It has been accepted for inclusion in Iowa State University Veterinarian by an authorized editor of Iowa State University Digital Repository. For more information, please contact [email protected]. Hypercalcemic Nephropathy in the Dog Ellen B. Hikes, DVM· Wallace B. Morrison, DVM·· INTRODUCTION base status of the animal. Calcium is a functionally important ion and The ratio of ionized calcium to protein­ coenzyme in most all of the body systems. Be­ bound calcium is altered by fluctuations in sides its structural role in bone, calcium is in­ acid-base balance. Alkalosis decreases the per­ volved in muscle contraction, the blood coag­ centage of ionized calcium by increasing the ulation system, enzyme activity, nerve protein-bound fraction. Acidosis increases the impulse transmission, hormone release and percentage of ionized calcium.3.6·lI Approxi­ membrane permeability.I-3 Calcium metabo­ mately one-half of the calcium bound is to lism is regulated primarily by parathyroid protein, primarily albumin. Interpretation of hormone (PTH), calcitonin (CT), and vi­ total calcium depends on concurrent values tamin D (1,25-dihydroxycholecalciferol).1.1.4 for serum albumin and total protein. 9 A posi­ The release of these hormones is controlled by tive linear relationship exists between total the concentration of calcium in the plasma. 5 serum calcium and both serum total protein Exact regulation of calcium in extracellular and albumin. J.ll In order to obtain more fluid is necessary to maintain normal body complete information about serum ionized function. calcium concentration, a correction formula The skeleton contains approximately 99 for total serum calcium was derived on the percent of the body's calcium stores. Only one basis of serum concentrations of albumin and percent of the total calcium is found outside total protein. The formula for calculating total the skeleton and one-tenth of one percent in serum calcium based on albumin concentra­ the extracellular fluid. 4 •6 The extracellular tions is: pool of calcium is readily available for rapid Adjusted calcium (mg/dl) = exchange with intracellular stores.6 •7 Total Calcium (mg!dl)-Albumin (g/dl)+3.5 serum calcium (extra-cellular calcium) is The correction formula based on total serum present in three forms; protein-bound (50 %), protein concentration is: complexed (10%) and ionized calcium Adjusted calcium (mg/dl) = Calcium (mg! (40 % ).8 Ionized calcium is the biologically ac­ dl)-OA [Total Serum Protein (g/dl)] +3.3 tive fraction.6.9 In most cases, total serum cal­ The correction formulas account for the ef­ cium, not just ionized calcium, is measured fects of the quantity of protein,3.9 but not for due to the technical equipment required. the effects of acid-base fluctuations on protein­ Measurement of ionized calcium alone re­ binding of calcium. Calcium-adjustment for­ quires that blood be collected anaerobically mulas can determine whether hypocalcemia and analyzed soon after collection.3.l0 Ionized or a hypercalcemia are masked by abnormal calcium values usually parallel changes in to­ serum protein concentration.' Hypoproteine­ tal calcium. It is necessary to interpret total mia can decrease the measured calcium, and serum calcium results in the context of the hyperproteinemia will increase measured cal­ plasma albumin concentration and the acid- cium.6 As serum protein concentrations de­ crease, more calcium is ionized and then re­ moved from the serum by CT regulatory ·Dr. Hikes is a 1985 graduate of the College ofVeteri­ mechanisms. This results in an absolute de­ nary Medicine at Iowa State University. •• Dr. Morrison is an assistant professor of Veterinary crease in serum calcium. Albumin is the most Clinical Sciences at.Iowa State University. important calcium binder, binding approxi- 122 Iowa State University veterinarian mately 90 percent of the protein-bound cal­ PATHOGENESIS OF HYPERCALCEMIA cium. Therefore, it is more advantageous to Neoplasia is the most common cause of hy­ use the correcting formula based on albumin percalcemia in the dog, with lymphosarcoma rather than total protein. 3.6 the most commonly involved tumor. 5•10 Can­ The normal total serum calcium value for cer-associated hypercalcemia, formerly re­ the mature dog is approximately 10.0 mg/dl ferred to as pseudohyperparathyroidism, may (9.4-12.2 mg/dl) with variations due to diet be due to tumor metastases to the bone, con­ and analytical method.6.8·1o It is not unusual current parathyroid hyperplasia, or production to see young, rapidly growing dogs with val­ of bone-resorbing factors by neoplastic cells. 13 ues approaching 12.0 mg/dl. General values Hypercalcemia associated with tumors is usu­ for young dogs are approximately 11.1 ± 0.4 ally caused by a malignant tumor of non­ mg/dl (to.5 to 11.5 mg/dl).13 Older dogs parathyroid origin secreting a factor or factors (greater than eight years of age) may have which mimic the action of PTH.5 •6 •11.15 There normal serum calcium values of 9.0 mg/dl.s is no evidence radiographically or at necropsy There appears to be no breed- or sex-related of bone metastasis in this syndrome. Labora­ differences in total serum calcium concentra­ tory findings in cases of lymphosarcoma may tion. The total serum calcium concentration show hypercalcemia, normo- or hypophospha­ represents a balance between intestinal ab­ temia, azotemia, hypercalcinuria, hyperphos­ sorption, bone resorption and accretion, and phaturia, and hyposthenuria. 11 The changes in renal excretion and reabsorption. Hypercalce­ calcium and phosphorus result from the action mia exists when serum calcium levels rise of PTH-like substances, but these substances above the normal value of 12 mg/d1.4.5.10.11 are not inhibited by increases in serum cal­ Persistent hypercalcemia is indicated by in­ cium.1u5 It should be noted that it is impor­ creased serum calcium concentration on two tant to measure and interpret serum calcium or more consecutive determinations and may and phosphorus together, because their regula­ indicate the presence of parathyroid, renal or tion and control are interrelated.6 Studies have neoplastic disease.1.13•14 Table 1 lists the dif­ identified several hypercalcemic factors pro­ ferential diagnoses of symptomatic hyper­ duced by tumors: parathyroid hormone-like calcemia in order of most likely occur­ peptides,15 prostaglandin El,16 osteoclast-ac­ rence. 10.11•13 tivating factor15 and non-vitamin D sterols.4 The chemical substances produced by tumors and the mechanisms by which hypercalcemia is induced are apparently different for different types of tumors.11 Adenocarcinomas derived from apocrine glands of the anal sac are also an important cause of hypercalcemia in older fe­ male dOgs.6.10.17 Other neoplasms which may TABLE 1. be involved in this syndrome include testicular Differential Diagnosis interstitial cell tumors and carcinoma of the 1. Malignancy: Cancer-associated hypercalcemia mammary gland, stomach, thyroid and Lymphosarcoma lung.5.10.11.15 Adenocarcinoma (apocrine glands of the anal sac) Hypoadrenocorticism (canine Addison's dis­ Other (Multiple myeloma, mammary tumors) ease) results in hyperkalemia, hyponatremia 2. Hypoadrenocorticism and hypochloridemia due to decreased produc­ 3. Renal failure tion of glucocorticoids and mineralocorticoids. 4. Bone lesion In approximately 25 percent of the affected Metastatic Septic - bacterial or mycotic osteomyelitis dogs, hypercalcemia will also be seen.13 The Disuse osteoporosis severity of hypercalcemia is correlated with the 5. Hypervitaminosis D severity of hypoadrenocorticism. However, the Iatrogenic - diet hypercalcemia is usually mild, generally less Plants - Cestrum diumum 13 111 Solanum malacoxylon than 13.5 mg/dl. • The exact cause of the Trisetum jlavescens rise in calcium levels is unknown. Several 6. Primary hyperparathyroidism mechanisms have been proposed, and the most Adenoma likely explanation involves diminished renal Adenocarcinoma excretion of calcium due to increased tubular JiJI. 47, No. 2 123 reabsorption of calcium. IS Hypercalcemia as­ dogs with chronic renal failure, calcium levels sociated with hypoadrenocorticism usually of­ are 12.0 mg/dl or greater. IO The pathogenesis fers a good prognosis because it is corrected of hypercalcemia induced by primary renal dis­ following adequate corticosteroid therapy for ease is not fully understood, and several mech­ the hypoadrenocorticism. anisms have been proposed: a) decreased ex­ Primary and secondary bone tumors and cretion of calcium by the diseased kidney; b) septic osteomyelitis are uncommon causes of decreased renal tubular degradation of PTH; hypercalcemia in the dog, but are seen more c) PTH-induced hypercitricemia which in­ often in man as a mechanism of hypercalce­ creases complexed calcium; d) overcompensa­ mia. 19 Primary or secondary bone tumors may tion
Load more

Recommended publications
  • 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.
    [Show full text]
  • Soft Tissue Calcification and Ossification
    Soft Tissue Calcification and Ossification Soft-tissue Calcification Metastatic Calcification =deposit of calcium salts in previously normal tissue (1) as a result of elevation of Ca x P product above 60-70 (2) with normal Ca x P product after renal transplant Location:lung (alveolar septa, bronchial wall, vessel wall), kidney, gastric mucosa, heart, peripheral vessels Cause: (a)Skeletal deossification 1.1° HPT 2.Ectopic HPT production (lung / kidney tumor) 3.Renal osteodystrophy + 2° HPT 4.Hypoparathyroidism (b)Massive bone destruction 1.Widespread bone metastases 2.Plasma cell myeloma 3.Leukemia Dystrophic Calcification (c)Increased intestinal absorption =in presence of normal serum Ca + P levels secondary to local electrolyte / enzyme alterations in areas of tissue injury 1.Hypervitaminosis D Cause: 2.Milk-alkali syndrome (a)Metabolic disorder without hypercalcemia 3.Excess ingestion / IV administration of calcium salts 1.Renal osteodystrophy with 2° HPT 4.Prolonged immobilization 2.Hypoparathyroidism 5.Sarcoidosis 3.Pseudohypoparathyroidism (d)Idiopathic hypercalcemia 4.Pseudopseudohypoparathyroidism 5.Gout 6.Pseudogout = chondrocalcinosis 7.Ochronosis = alkaptonuria 8.Diabetes mellitus (b) Connective tissue disorder 1.Scleroderma 2.Dermatomyositis 3.Systemic lupus erythematosus (c)Trauma 1.Neuropathic calcifications 2.Frostbite 3.Myositis ossificans progressiva 4.Calcific tendinitis / bursitis (d)Infestation 1.Cysticercosis Generalized Calcinosis 2.Dracunculosis (guinea worm) (a)Collagen vascular disorders 3.Loiasis 1.Scleroderma
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • Understanding Calcinosis and Calciphylaxis
    PRACTICE DEVELOPMENT Understanding calcinosis and calciphylaxis KEY WORDS Calcinosis cutis is a rare cause of non-healing leg ulceration. There are many factors Calcinosis cutis that can delay the healing of venous leg ulceration and the deposition of calcium in Calciphylaxis the skin known as calcinosis cutis is one of these factors. There are five distinct forms: Warfarin-induced skin dystrophic calcification, metastatic calcification, idiopathic calcification, iatrogenic necrosis calcification and calciphylaxis. Warfarin skin necrosis has common clinical features with calciphylaxis and is therefore included in this article, which describes the types of calcinosis cutis, their clinical presentations and limited treatment options. The aim is to highlight these unusual causes and to assist healthcare professionals when faced with a non-healing ulcer. eg ulceration can be defined as a defect in neurotransmission and the blood coagulation the dermis located on the leg (Franks et al, pathway. At a cellular level, it is implicated in 2016). Leg ulceration is a significant clinical cell-to-cell communication (Walshe and Fairley, Lproblem with the majority attributing venous 1995). In the skin, it is specifically concerned with hypertension as the underlying disease process with keratinocyte proliferation, differentiation and venous leg ulceration affecting 1% of the population adhesion (Smith and Yamada, 2002). in the western world (Posnett et al, 2009). However, The level of serum calcium is closely there is a multitude of causative factors of leg ulcers, controlled by the parathyroid hormone. with the term leg ulcer purely signifying the clinical Regardless of this regulation, it is possible for manifestation and not the underlying aetiology.
    [Show full text]
  • A Case of Dystrophic Calcification in the Masseter Muscle Heon-Young Kim, Jung-Hyun Park* , Jun-Bum Lee and Sun-Jong Kim
    Kim et al. Maxillofacial Plastic and Reconstructive Surgery (2017) 39:31 Maxillofacial Plastic and DOI 10.1186/s40902-017-0130-4 Reconstructive Surgery CASEREPORT Open Access A case of dystrophic calcification in the masseter muscle Heon-Young Kim, Jung-Hyun Park* , Jun-Bum Lee and Sun-Jong Kim Abstract Background: Dystrophic calcification can occur in any soft tissue with the absence of a systemic mineral imbalance and is often associated with trauma, infection, or inflammation. It is easily found in the site of the heart and skeletal muscles and rarely appears in the head and neck area. Case report: We present a rare case of multiple calcified masses in the left masseter muscle of a 26-year-old female with a history of trauma in the area. In computed tomography, multiple radiopaque masses were observed inside the left masseter muscle and blood test results were normal. The calcified masses were diagnosed as dystrophic calcification and removed by surgery without any complications. Conclusion: Different types of calcifications may occur in the cheek area, and they need to be distinguished from dystrophic calcification. Thorough clinical examination and history taking is required together with blood testing and radiographic examinations. Keywords: Masseter muscle, Dystrophic calcification, Pathologic soft tissue calcification, Trauma Background the heart muscles and valves and rarely appears in the Pathologic soft tissue calcification of the cheek is an head and neck area [5]. Currently, there is no established uncommon condition. There are many different types protocol for its treatment. Some clinicians have recom- of calcifications, which includes dystrophic calcifica- mended observation, but others have suggested the tion, metastatic calcification, phleboliths, myositis surgical treatment case by case [6].
    [Show full text]
  • Siegenthaler, Differential Diagnosis in Internal Medicine (ISBN9783131421418), © 2007 Georg Thieme Verlag Index
    Index Notes: Please note that entries in bold and italics represent tables and figures respectively A parapharyngeal space, 479 acromegaly, 81, 82, 743−744 acute renal failure (ARF), 852−857 spleen, 151 hands, 90 angiography, 854 Abciximab, thrombocytopenia, teeth, 212 hypertension, 738 causes, 853 459 tuberculous paravertebral, skin changes, 66 classification, 852 abdomen 597−599 ACTH-dependent Cushing definition, 852 acute see acute abdomen absolute pupillary areflexia, 97 syndrome, 742 diagnostic procedure, 855−857 angina, mesenteric infarction, Abt−Letterer−Siwe disease, 445 ACTH-independent Cushing blood analysis, 856 266 Acanthamoeba infection, syndrome, 742−743 glomerular filtration rate, 855 blood vessels, polyarteritis meningitis, 135 Actinomyces infection see main laboratory nodosa, 179 acanthocytes actinomycosis investigations, 856 pain see abdominal pain liver cirrhosis, 398 Actinomyces israelii, 131 physical examination, physical examination, 30−31 urinary sediment analysis, 847, actinomycosis, 71, 526 855−856 pleural effusion, 248 848 neck swelling, 131 radiologic examinations, 857 ultrasound, secondary acanthocytosis, 417 activated partial thromboplastin renal biopsy, 857 hypertension, 733 acanthosis nigricans, 55, 55 time (aPTT), 452, 1052−1053 urinalysis, 856 abdominal organs, nervous accelerated junctional rhythms, acute abdomen, 257−259 differential diagnosis, 855, system, 256 719 causes, 257, 257−258 855−857 abdominal pain acetaminophen chronic renal failure, 861 acute tubular necrosis vs., acute, 257−273 analgesic
    [Show full text]
  • Calcinosis Cutis of Usual and Unusual Sites: an Eight Year Retro-Prospective Study in a Tertiary Teaching Hospital in Western Uttar Pradesh, India
    Original Research Article DOI: 10.18231/2394-6792.2017.0034 Calcinosis cutis of usual and unusual sites: An eight year retro-prospective study in a tertiary teaching hospital in Western Uttar Pradesh, India Alok Mohan1,*, Shruti Singh2, Veena K. Sharma3, Purva Sharma4, Swarn Kaur5 1,2Associate Professor, 3,5Professor, 4Junior Resident, Dept. of Pathology, 1,3,4Muzaffarnagar Medical College, Muzaffarnagar U.P., 2U.P. Rural Institute of Medical Sciences & Research, Saifai, U.P., 5Govt. Medical College, Khanpur lalan, Sonepat, Haryana *Corresponding Author: Email: [email protected] Abstract Introduction: Calcinosis cutis is characterized by deposition of calcium in the skin. Case reports of calcinosis cutis form a wonderful data in clinical and pathological literature. Aims and Objectives: The aim of the present study was to highlight the various clinicopathological aspects of calcinosis cutis lesions of various sites in our archives. Materials and Methods: We performed an analysis of clinicopathological features of all diagnosed cases of calcinosis cutis from our archives. This was a retro-prospective type of study for eight years i.e. from July 2008- June 2016. Observation and Results: In our study we studied 18 cases of calcinosis cutis from various sites. A few cases were unusual in terms of locations, size and presentation. Most common site was scrotum. Wide surgical excision was the treatment of choice. Histopathological diagnosis was rarely difficult. Histochemical Von Kossa staining was done in all cases for confirmation. Conclusion: The results from the present study displayed the various presentations, locations and variability on histopathological architecture, thus highlighting the various clinicopathological aspects of calcinosis cutis lesions.
    [Show full text]
  • PATHOLOGY MCQ 1) Hypertrophy A) Occurs After Partial Hepatectomy B
    PATHOLOGY MCQ 1) Hypertrophy a) occurs after partial hepatectomy b) increases function of an organ exponentionally c) is triggered by mechanical and trophic chemicals d) occurs after dennervation e) is usually pathological 2) All the following are features of apoptosis EXCEPT a) cell swelling b) chromatin condensation c) formation of cytoplasmic blebs d) lack of inflammation e) phagocytosis of apoptotic bodies 3) Dystrophic calcification a) is formed only in coagulative necrosis b) does not occur on heart valves c) rarely causes dysfunction d) is rarely found on mitochondria e) is formed by crystalline calcium phosphate mineral 4) Irreversible cell injury is characterised by a) dispertion of ribosomes b) cell swelling c) nuclear chromatin dumping d) lysosomal rupture e) cell membrane defects 5) Metaplasia a) can be caused by vitamin B12 deficiency b) preserves mucus secretion in the respiratory tract c) is typically an irreversible process d) is the process that occurs in Barrett’s oesophagitis e) is an increase in the number and size of cells in a tissue 6) Smooth endoplasmic reticulum a) is the site a cell steroid production b) is the site of cell protein synthesis c) d) e) is the site of cellular cytochrome oxidases 7) Pinocytosis a) adds to the cell membrane b) c) d) e) involves the uptake of soluble macromolecules 8) Examples of hyperplasia include a) b) c) d) glandular epithelium of pubertal breasts e) 9) Ribosomes a) have 3 subunits b) have 30% DNA c) synthesise haemoglobin d) e) 10) Which of the following is not associated with
    [Show full text]
  • Study Guide for Understanding Pathophysiology This Page Intentionally Left Blank Study Guide for Understanding Pathophysiology
    Study Guide for Understanding Pathophysiology This page intentionally left blank Study Guide for Understanding Pathophysiology Sue E. Huether, MSN, PhD Professor Emeritus College of Nursing University of Utah Salt Lake City, Utah Kathryn L. McCance, MSN, PhD Professor College of Nursing University of Utah Salt Lake City, Utah Section Editors Valentina L. Brashers, MD Professor Nursing and Attending Physician in Internal Medicine University of Virginia Health System Charlottesville, Virginia Neal S. Rote, PhD Academic Vice-Chair and Director of Research Department of Obstetrics and Gynecology University Hospitals of Cleveland; Professor of Reproductive Biology and Pathology Case School of Medicine Case Western Reserve University Cleveland, Ohio Prepared by Clayton F. Parkinson, PhD Professor Emeritus College of Health Sciences Weber State University Ogden, Utah 3251 Riverport Lane St. Louis, Missouri 63043 STUDY GUIDE FOR UNDERSTANDING PATHOPHYSIOLOGY, ISBN: 978-0-323-08489-5 5TH EDITION Copyright © 2012, 2008, 2004, 2000, 1996 by Mosby, an imprint of Elsevier Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein). Notices Knowledge and best practice in this field are constantly changing.
    [Show full text]