Pathogenic Mechanisms of Endocrine Disease in Domestic and Laboratory Animals
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Chapter 1 Cellular Reaction to Injury 3
Schneider_CH01-001-016.qxd 5/1/08 10:52 AM Page 1 chapter Cellular Reaction 1 to Injury I. ADAPTATION TO ENVIRONMENTAL STRESS A. Hypertrophy 1. Hypertrophy is an increase in the size of an organ or tissue due to an increase in the size of cells. 2. Other characteristics include an increase in protein synthesis and an increase in the size or number of intracellular organelles. 3. A cellular adaptation to increased workload results in hypertrophy, as exemplified by the increase in skeletal muscle mass associated with exercise and the enlargement of the left ventricle in hypertensive heart disease. B. Hyperplasia 1. Hyperplasia is an increase in the size of an organ or tissue caused by an increase in the number of cells. 2. It is exemplified by glandular proliferation in the breast during pregnancy. 3. In some cases, hyperplasia occurs together with hypertrophy. During pregnancy, uterine enlargement is caused by both hypertrophy and hyperplasia of the smooth muscle cells in the uterus. C. Aplasia 1. Aplasia is a failure of cell production. 2. During fetal development, aplasia results in agenesis, or absence of an organ due to failure of production. 3. Later in life, it can be caused by permanent loss of precursor cells in proliferative tissues, such as the bone marrow. D. Hypoplasia 1. Hypoplasia is a decrease in cell production that is less extreme than in aplasia. 2. It is seen in the partial lack of growth and maturation of gonadal structures in Turner syndrome and Klinefelter syndrome. E. Atrophy 1. Atrophy is a decrease in the size of an organ or tissue and results from a decrease in the mass of preexisting cells (Figure 1-1). -
Appendix 3.1 Birth Defects Descriptions for NBDPN Core, Recommended, and Extended Conditions Updated March 2017
Appendix 3.1 Birth Defects Descriptions for NBDPN Core, Recommended, and Extended Conditions Updated March 2017 Participating members of the Birth Defects Definitions Group: Lorenzo Botto (UT) John Carey (UT) Cynthia Cassell (CDC) Tiffany Colarusso (CDC) Janet Cragan (CDC) Marcia Feldkamp (UT) Jamie Frias (CDC) Angela Lin (MA) Cara Mai (CDC) Richard Olney (CDC) Carol Stanton (CO) Csaba Siffel (GA) Table of Contents LIST OF BIRTH DEFECTS ................................................................................................................................................. I DETAILED DESCRIPTIONS OF BIRTH DEFECTS ...................................................................................................... 1 FORMAT FOR BIRTH DEFECT DESCRIPTIONS ................................................................................................................................. 1 CENTRAL NERVOUS SYSTEM ....................................................................................................................................... 2 ANENCEPHALY ........................................................................................................................................................................ 2 ENCEPHALOCELE ..................................................................................................................................................................... 3 HOLOPROSENCEPHALY............................................................................................................................................................. -
Introduction to the Endocrine System: Mechanisms of Disease
Introduction to the Endocrine System: Mechanisms of Disease Mark J. Hoenerhoff, DVM, PhD, DACVP Associate Professor, In Vivo Animal Core Unit for Laboratory Animal Medicine University of Michigan Medical School 1.1 Lairmore and Rosol, Vet Pathol. 2008 May;45(3):285-286. 1.2 HORMONES CONTROL EVERYTHING!! 1.3 quora.com “CAPEN’S TEN LAWS” OF ENDOCRINE DISEASE 1. Primary Hyperfunction 2. Secondary Hyperfunction 3. Primary Hypofunction 4. Secondary Hypofunction 5. Endocrine Hyperactivity 2o to Other Organ Disease 6. Hypersecretion of Hormones by Non-endocrine Tumors 7. Endocrine Dysfunction due to Failure of Target Cell Response 8. Failure of Fetal Endocrine Function 9. Endocrine Dysfunction 2o to Abnormal Hormone Degradation 10. Syndromes of Iatrogenic Hormone Excess 1.4 Capen CC. Endocrine Glands. In: Maxie G, ed. Jubb, Kennedy & Palmer’s Pathology of Domestic Animals. 5th ed. Elsevier; 2007:325-326. Papadopoulos and Cleare, Nat Rev Endocrinol. 2011 Sept 27;8(1):22-32 1.5 Bassett and Williams, Bone. 2008 Sep;43(3):418-426. 1. PRIMARY HYPERFUNCTION OF ENDOCRINE ORGANS • Often result of functional neoplastic disease of endocrine gland • Autonomous secretion of hormones – DIRECT effect on target organ • Outpaces body’s ability to utilize and degrade hormone • Functional disturbance of hormone excess • Parathyroid chief cell tumors Hyperparathyroidism • Thyroid follicular tumors Hyperthyroidism 1.6 1. PRIMARY HYPERFUNCTION • Parathyroid tumors Hyperparathyroidism Parathyroid PTH Solar Arias et al, Open Vet J. 2016;6(3):165-171. 1.7 Bassett and Williams, Bone. 2008 Sep;43(3):418-426. 1. PRIMARY HYPERFUNCTION • Parathyroid tumors Hyperparathyroidism Parathyroid PTH https://ntp.niehs.nih.gov/nnl/index.htmSolar Arias et al, Open Vet J, 2016 1.7 Bassett and Williams, Bone. -
Intro to Pathology
Homeostasis • Maintenance of a steady state Adaptations • Reversible functional and structural responses to physiologic stress and some pathogenic stimuli • New altered “steady state” is achieved Adaptive responses • Hypertrophy • Altered demand (muscle . hyper = above, more activity) . trophe = nourishment, food • Altered stimulation • Hyperplasia (growth factors, . plastein = (v.) to form, to shape; hormones) (n.) growth, development • Altered nutrition • Dysplasia (including gas exchange) . dys = bad or disordered • Metaplasia . meta = change or beyond • Hypoplasia . hypo = below, less • Atrophy, Aplasia, Agenesis . a = without . nourishment, form, begining Cell death, the end result of progressive cell injury, is one of the most crucial events in the evolution of disease in any tissue or organ. It results from diverse causes, including ischemia (reduced blood flow), infection, and toxins. Cell death is also a normal and essential process in embryogenesis, the development of organs, and the maintenance of homeostasis. Two principal pathways of cell death, necrosis and apoptosis. Nutrient deprivation triggers an adaptive cellular response called autophagy that may also culminate in cell death. Adaptations • Hypertrophy • Hyperplasia • Atrophy • Metaplasia HYPERTROPHY Hypertrophy refers to an increase in the size of cells, resulting in an increase in the size of the organ No new cells, just larger cells. The increased size of the cells is due to the synthesis of more structural components of the cells usually proteins. Cells capable -
Type 1 Established Condition List
Part C of the IDEA and Family Education and Support Programs: Use of the Established Condition List for Type I Eligibility May 23, 2019 When determining Type I Eligibility for Part C of the IDEA and Family Education and Support Programs: 1. The Program providers use the Established Condition Statement as completed and signed by a physician or psychologist. 2. After receipt of the Statement, the Program providers' designated personnel will refer to this Established Condition List to determine if the child's condition is one that is identified as meeting Type I Established Condition criteria in the Montana. 3. If yes, the Program provider completes the multidisciplinary assessment (with written consent from the family) of the child's needs and family's concerns, priorities, and resources to enhance the development of the child for the development of the IFSP. 4. If no, the Program provider (with written consent from the family) moves toward establishing Type II Measured Delay eligibility (50% delay in one developmental domain or two or more 25% delays in developmental domains) using a multidisciplinary evaluation team that includes the family, the service coordinator, and at least one other discipline. 5. If yes, the child meets Type II Measured Delay eligibility, the Program provider completes (with written consent from the family) the multidisciplinary assessment of the child's needs and family's concerns, priorities, and resources to enhance the development of the child for the development of the IFSP. 6. If no, the family receives written notification of the eligibility decision and the Program provider shares more appropriate referrals with the family. -
Do We Really Understand the Difference Between Optic Nerve Hypoplasia and Atrophy?
DO WE REALLY UNDERSTAND THE DIFFERENCE BETWEEN OPTIC NERVE HYPOPLASIA AND ATROPHY? CREIG S. HOYT and WILLIAM V. GOOD San Francisco, California I. CHANGING CLINICAL PROFILE OF nerve have proven to be less useful especially in the most OPTIC NERVE HYPOPLASIA perplexing, subtle cases.12,13 Hypoplasia of the optic nerve is a developmental anomaly II. AETIOLOGY in which there is a subnormal number of axons within the No single aetiological factor has been identified in the affected nerve, although the mesodermal elements and pathogenesis of optic nerve hypoplasia.5 Genetic factors glial supporting tissue of the nerve are norma1.1,2 Though do not appear to be important as only a few rare cases have once considered rare,3,4 optic nerve hypoplasia is now been reported to be associated with autosomal reces appreciated to be a relatively common congenital anomaly sive14,15 or autosomal dominant16 inheritance. Optic nerve that may present with a wide spectrum of visual disabil hypoplasia may also be associated infrequently with tri ities.s Although it was once thought that this anomaly was somy-1817 and trisomy-21.1S Although in cattle it has been only compatible with very poor visual acuity it is now well clearly documented that mothers infected with a mucosal documented that it may occur even in the presence of virus are at risk of giving birth to calves with optic nerve normal visual acuity or subtle visual field changes.6,7 hypoplasia,19 the role of maternalinfection in human cases Optic nerve hypoplasia may occur as an isolated defect of optic nerve hypoplasia remains unclear.