Cell Injury PATHWAYS of INJURY

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GENERAL PATHOLOGY Cell Injury PATHWAYS OF INJURY HYPOXIC INJURY Interference with Energy Production Direct Damage to membranes DR. M. TARIQ JAVED Professor Department of Pathology, Faculty of Veterinary Science, University of Agriculture, Faisalabad, Pakistan. Web: https://sites.goocities.ws/mtjaved 1 2 Hypoxic Injury 1. INTERFERENCE WITH ENERGY PRODUCTION hypoxia decreased O2 at the cell anoxia complete lack of O2 Hypoxic Injury Hypoxemia decreased O2 in the blood ischemia reduced blood supply to the tissue leads to hypoxia 3 4 1 Hypoxaemia Ischaemia Too little oxygen in the blood Occlusion of the blood vessels Too little oxygen in the air Failure of the heart to pump Failure to properly ventilate the lungs enough blood Failure of the lungs to properly oxygenate the blood Failure of the heart to pump enough blood through the lungs Tremendously increased dead space (i.e., pulmonary thromboembolus) 5 6 Haemoglobin problems Failure of the Cells to Utilize (anaemic hypoxia) Oxygen (cytochromes) Inadequate circulating red cell mass (histotoxic hypoxia) (anaemia) Inability of haemoglobin to carry the • Cyanide poisoning oxygen (carbon monoxide poisoning) • Rotenone poisoning High affinity haemoglobin that will not • Dinitrophenol poisoning give up their oxygen to the tissues (methemoglobinemia) 7 8 2 Cell Deprived of oxygen Interrupts oxidative metabolism Depletion of Energy Sources (Glucose) Decreased Energy in the cell Na/K pump failure 9 10 11 3 13 14 Biochemical “point of no return”: Inability to restore mitochondrial function phospholipase activation mitochondrial permeability increases Plasma membrane defects-contributing factors phospholipase activation degradation of membrane phospholipids lipid degradation products membrane detergent effect Ca2+ proteases cytoskeletal degradation membrane detachment 16 15 4 3 R’s of success: Respect for self, Respect for others Responsibility for all your actions 17 18 19 5.

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Module G: Oxygen Transport • Oxygen Transport Studies • Tissue Hypoxia • Cyanosis • Polycythemia
Topics to Cover • Oxygen Transport • Oxygen Dissociation Curve Module G: Oxygen Transport • Oxygen Transport Studies • Tissue Hypoxia • Cyanosis • Polycythemia Oxygen Transport Dissolved Oxygen • As oxygen diffuses across the A-C membrane, it • Oxygen is carried from the lungs to the dissolves into the plasma and remains in that tissues in two different fashions: fashion until it reaches the tissue. • Oxygen Dissolved in the blood plasma (PO ) 2 • Expressed as a partial pressure - PO2 • Oxygen Combined with Hemoglobin (SO2) • Normal arterial level = 80-100 mm hg • Normal venous level = 35 – 45 mm hg • The quantity of oxygen dissolves is a function of Henry’s law. •At 37 C 0.003 ml of oxygen will dissolve in 100 ml of blood. (Henry’s Law) • At 100 mm hg PaO2, the amount of dissolved oxygen is 0.3 ml O2/100 ml blood (0.3 vol%). Combined Oxygen • Dissolved oxygen is inadequate for metabolic needs. • Need a substance which will bind to oxygen and carry it, BUT will release it when needed. • Voila! Hemoglobin! • Miracle #2…As we’ll see later, hemoglobin also carries carbon dioxide and is a key buffer of [H+]. 1 Hemoglobin chains • Each RBC contains approximately 280 million molecules of hemoglobin chains • Adult Hemoglobin (Hb A) consists of • 4 Heme Groups – Primarily iron in the Fe+2 (ferrous) state. Heme • 4 Globulin – 4 amino acid chains (2 & 2 ) Units • One heme group binds with one of the amino acid chains and oxygen binds with the iron in the heme group in a reversible way. +2 O2 + Fe FeO2 (Oxyhemoglobin) FERROUS Hemoglobin & the RBC • “Normal” hemoglobin level • 15 g/dl (men) & 13-14 g/dl (women) - Malley •15 +1.5 g/dl (men) & 13.5 + 1.5 g/dl (women) – Egan •15 +2 (men) & 14 + 2 (women) - Easy • Why do women have less? • The hemoglobin molecule resides in the erythrocyte and is responsible for giving the blood its red color.
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Mitochondrial Dysfunction After Severe Tbi: a New Translational Target?
-Edición provisional- MITOCHONDRIAL DYSFUNCTION AFTER SEVERE TBI: A NEW TRANSLATIONAL TARGET? Juan Sahuquillo, MD, PhD1, Marian Vidal-Jorge2, Angela Sánchez-Guerrero2 Department of Neurosurgery1, Neurotraumatology and Neurosurgery Research Unit2 Vall d’Hebron University Hospital Universitat Autònoma de Barcelona, Barcelona, Spain Significant advances in the treatment of TBI have been limited by a lack of knowledge of the biochemical, cellular and molecular changes involved in its pathophysiology. These obstacles have been overcome to a certain degree by new monitoring tools —cerebral microdialysis (MD) and monitoring of partial pressure of oxygen in the brain (PtiO2)— that have allowed clinicians to explore the metabolic disturbances of the injured brain with unprecedented detail. The data gathered by these monitoring tools in the past two decades has provided an opportunity to take a second look at the pathophysiology of TBI, motivating clinical researchers to redefine some of the unchallenged traditional concepts. The hypothesis that mitochondrial dysfunction is at the core of many acute metabolic disorders observed in acute TBI is one of the old concepts that deserves a second look and is the focus of this chapter. New neuromonitoring techniques, including PtiO2 and MD monitoring, are widely used in neurocritical care units, allowing for the quasi-continuous profiling of brain oxygen supply and brain metabolism [1, 2]. Data provided by these tools have cast doubt on the predominant role of ischemia in the pathophysiology of TBI. Many studies have found that the injured brain may experience severe alterations of energetic metabolism in the presence of CBF and oxygen supply well above the ischemic range[3-5].
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Neurological Disorders & Epilepsy Journal Special Issue Article “Brain Hypoxia” Letter Seizures Induces Hypoxia and Hypoxia Induces Seizures. A Perverse Relationship that Increases the Risk of SUDEP Jerónimo Auzmendi1,2 and Alberto Lazarowski1* 1Department of Clinical Biochemistry, University of Buenos Aires, Argentina 2National Council for Scientific and Technical Research (CONICET), Argentina ARTICLE INFO LETTER “He uttered a cry and was seen to be rubbing his hands together. His pulse was Received Date: October 11, 2020 Accepted Date: October 25, 2020 immediately examined for but was not palpable” [1]. Published Date: October 28, 2020 Hypoxia is a biological stimulus capable of promoting both rescue and survival KEYWORDS mechanisms, as well as triggering a sequence of irreversible events that lead to death of cell, tissue and even individual. Brain and heart functions depend critically on Seizures adequate energy supply and they are highly susceptible to hypoxic conditions. Hypoxia SUDEP Adequate oxygen supply is needed for the brain and heart to metabolize glucose as its major energy source. But how many type of hypoxia we know, and how much Copyright: © 2020 Alberto severe is the hypoxic condition, when more than one type of hypoxia are Lazarowski, et al., Neurological simultaneously acting? Four types of hypoxia are distinguished in medicine: α- the Disorders & Epilepsy Journal. This is an open access article distributed under hypoxemic hypoxia, due to a decrease in the amount of breathable oxygen or the Creative Commons Attribution cardiopulmonary failure, b- the anemic hypoxia related with decreased amount of License, which permits unrestricted use, functional hemoglobin, c- the stagnant hypoxia, secondary to reduced or unevenly distribution, and reproduction in any medium, provided the original work is distributed flow of blood distribution to the tissues, and mainly result from heart properly cited.
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Effects of Aqueous Extract of Kuding Leaves on Cyanide- Induced Toxicity and Packed Cell Volume (PCV)
Article Number: 3518D12 A Paper Presented at the WANNPRES 9th Sub-Regional Scientific Meeting, University of Nigeria, Nsukka, Enugu State, Nigeria. 30th May – 2nd June, 2018 Copyright ©2018 Author(s) retain the copyright of this article Conference Proceedings http://www.proceedings.academicjournals.org/ Full Length Research Paper Effects of aqueous extract of kuding leaves on cyanide- induced toxicity and packed cell volume (PCV) Obiajulu Christian Ezeigwe1*, Christopher Onyemeziri Alisa2 and Josephine Ezekwesili-Ofili1 1Department of Applied Biochemistry, Faculty of Biosciences, Nnamdi Azikiwe University, Awka, Anambra State, Nigeria. 2Department of Chemistry, Federal University of Technology, Owerri, Imo State, Nigeria. Cyanide poisoning occurs when a living organism is exposed to a compound that produces cyanide ions (CN−) when dissolved in water. Kuding leaves are Chinese leaves used for weight control. Aqueous extract of kuding leaves was assessed for its effect on cyanide-induced toxicity and packed cell volume (PCV) in Wistar rats. Group A was administered 1% Tween-80 at 5 ml/kg. Group B was not induced but received 400 mg/kg body weight of the extract only, Group C received 3 mg/kg of cyanide without treatment, Group D received 200 mg/kg of the extract, Group E received 300 mg/kg of the extract, and Group F received 400 mg/kg of the extract. PCV was determined using automated haematology analyzer (Mindray-BC-28000). A significant reduction (p>0.05) in weight was observed for the group that received only 400 mg/kg body weight of the extract and the group that received only 3 mg/kg body weight of cyanide for two weeks when compared with the control group.
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Cyanide Poisoning After Bitter Almond Ingestion
CASE REPORTS continue therapy with cholestyramine after many years of administration. ABBREVIATIONS USED IN TEXT REFERENCES A-ao2 = alveolar-arterial difference in oxygen CVP=central venous pressure 1. Riely C, Collier E, Jensen P, et al: Arteriohepatic dysplasia: A benign syndrome of intrahepatic cholestasis with multiple organ Flo2=fraction of inspired oxygen involvement. Ann Intern Med 91:520-527, Oct 1979 PCWP=pulmonary capillary wedge pressure 2. Watson DH, Miller V: Arteriohepatic dysplasia. Arch Dis Child 48:459-466, Jun 1973 Qs/Qt=right-to-left intrapulmonary shunt 3. Alagille D, Odievre M, Gautier M, et al: Hepatic ductular SEM =standard error of the mean hypoplasia associated with characteristic facies, vertebral malfor- T/2 = cyanide half-life in blood mations, retarded physical, mental and sexual development and cardiac murmur. J Pediatr 86:63-71, Jan 1975 4. Alagille D, Habib EC, Thomassin N: L'atr6sie des voies bili- aires intrah6patiques avec voies biliaries extrahepatiques permeables chez l'enfant. Journees Paris Pediatr pp 301-318, 1969 poisoning, Graham and colleagues2 noted the 5. Alagille D, Thomassin N: L'atresie des voies biliares intra- h6patiques avec voies biliaires extrahepatiques permeables chez paucity of cases in which cyanide blood levels had l'enfant. Rev Med Chir Mal Foie 45:93-104, 1970 been reported. They further questioned the effi- 6. Greenwood RJ, Rosenthal A, Crocker A, et al: Syndrome of intrahepatic biliary dysgenesis and cardiovascular malformations. cacy and safety of the traditional therapy of Pediatrics 58:243-247, Aug 1976 7. Henriksen M, Langmark F, Sorland S, et al: Hereditary intravenous sodium nitrite and sodium thiosulfate.
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Cyanide-Induced Cytochrome A,A3 Oxidation-Reduction Responses in Rat Brain in Vivo
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Acute Hydrogen Sulfide Poisoning in a Dairy Farmer
Clinical Toxicology (2007) 45, 420–423 Copyright © Informa Healthcare ISSN: 1556-3650 print / 1556-9519 online DOI: 10.1080/15563650601118010 CASELCLT REPORT Acute hydrogen sulfide poisoning in a dairy farmer GREGGAcute hydrogen sulfide poisoning GERASIMON, M.D.1, STEVEN BENNETT, M.D., FCCP2, JEFFREY MUSSER, DO3, and JOHN RINARD, DO4 1Major, Medical Corps, U.S. Army, Internal Medicine, Womack Army Medical Center, Fort Bragg, North Carolina, USA 2Major, Medical Corps, U.S. Army, Pulmonary and Critical Care Medicine, Madigan Army Medical Center, Tacoma, Washington, USA 3Major, Medical Corps, U.S. Army, Critical Care Medicine, Madigan Army Medical Center, Tacoma, Washington, USA 4Captain, Medical Corps, U.S. Army, Internal Medicine, Madigan Army Medical Center, Tacoma, Washington, USA Introduction. Hydrogen sulfide is a lipid-soluble gas produced in occupational settings and from decaying organic matter. We present a 36- year-old man who developed acute respiratory arrest from hydrogen sulfide poisoning while performing work as a dairy farmer. Case report. The subject entered a poorly ventilated tank containing degrading eggs and, within seconds, collapsed. Coworkers were able to extract him within minutes but he was apneic. He was intubated by emergency medical services and subsequently managed with supportive care in the intensive care unit. Upon admission, a powerful rotten egg scent was noted and a hydrogen sulfide poisoning was suspected. Serum analysis for the presence of thiosulfate confirmed the diagnosis. Nitrite therapy was not administered as the subject arrived outside of the therapeutic window of effectiveness and showed evidence of excellent oxygenation. His examinations following arrival were consistent with an anoxic brain injury which slowly improved several months after the incident with intensive neuro-rehabilitation.
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Hypoxia , Asphyxia , and Cyanosis
ﺼﺩﻕﺼﺩﻕ ﺍﺍﷲﷲ ﺍﻟﻌﺍﻟﻌﻅﻅﻴﻡﻴﻡ ﺍﺍﻻﻻﺴﺴﺭﺍﺀﺭﺍﺀ ﺍﻴﺔﺍﻴﺔ 5588 HHypypoxoxiaia ,, AAsspphhyxyxiaia ,, anandd CCyanosiyanosiss HypHypoxiaoxia Def: •• Hypoxiaxia means O2 deficiency at tissue level resulting from disturbance in respiratory processes. •Hypoxemia → ↓ O2 content and PO2 in arterial blood. •• Remember:ber: •• Respiration is the process of transport of atmospheric oxygen to tissues and carbon dioxide from tissues to atmosphere. •• It is divided into 3 divisions;s; I- External Respiration •Pulmonary ventilation •Gas exchange II- Intermediate respiration: •Transport of gases by blood III - Internal Respiration Oxidation of food with release of energy HypHypoxiaoxia Types: It can be divided into: 1) Disturbance in external respiration → Hypoxic hypoxia 2) Disturbance in respiratory function of the blood → •Anaemic hypoxia •Stagnant hypoxia 3) Disturbance in internal respiration → Histotoxic hypoxia. Types and Causes of Hypoxia Hypoxic hypoxia Anaemic hypoxia Stagnant hypoxia histotoxic hypoxia Def., Hypoxia results from Hypoxia results from Hypoxia results from Hypoxia is due to defective oxygenation of deficiency of Hb in reduced tissue defect in internal arterial blood. amount or functions. perfusion respiration 1) ed PO2 in the 1)All types of anaemia 1)General: 1) Cyanide poisoning: Causes ↓ atmospheric air as in high 2)CO poisoning i. Shock. Cyanide blocks more altitude or breathing O2 3) MetHb ii.Congestive heart than 40 enzyme poor mixtures e.g. in 4) Sulph Hb failure. systems mainly mines. iii. Polythycemia. cytochrome oxidase 2) Ventilation defect: 2) Local: system. i. Obstructive disease e.g. Obstruction of blood 2) Alcoholic obstruction of the airway . vessels either from poisoning: ii. Restrictive disease e.g. inside by thrombus and Alcohol blocks pulmonary fibrosis . emboli or from outside.
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Hypoxia and Cyanosis Respiratory Block
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American Osteopathic College of Occupational and Preventive
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Toxicological Profile for Cyanide
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