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Acid base balance a a Prof. H yder M. Abduln bi Homeostasis Normal plasma pH is 7.35 — 7. 45 ( 7.4 ) p from the German language potens = power And H = hydrogen pH means power of hydrogen Acidosis Physiological state of abnormal low plasma pH ( less than 7.35 ) Alkalosis Physiological state o...

Acid base balance a a Prof. H yder M. Abduln bi Homeostasis Normal plasma pH is 7.35 — 7. 45 ( 7.4 ) p from the German language potens = power And H = hydrogen pH means power of hydrogen Acidosis Physiological state of abnormal low plasma pH ( less than 7.35 ) Alkalosis Physiological state of abnormal high plasma pH ( more than 7.45 ) Buffering A chemical system that correct any change in Hydrogen ion concentration in case of increase acid or increase base of the plasma First line in buffering is Bicarbonate and Non bicarbonate ( Hb, protein, phosphate) It act by binding or releasing Hydrogen Carbonic acid— bicacarbonate buffer system Most body cells ( muscle ) generate CO2 CO2 is converted to carbonic acid ( binding to H2O ) ( H2CO3 ) fi Carbonic acid Sparkling zzy water Hemoglobin buffer system Hydrogen ions can also buffered by hemoglobin It help major changes in pH when PCO2 is increasing or decreasing By taking or releasing hydrogen By same role of carbonic acid equation Respiratory acid-base control Is the second line of buffer system . When chemical buffers alone cannot prevent changed in pH of plasma Respiration is the second line of defence By eliminating or releasing CO2 Renal acid base control The kidneys are the third line of defence against changes in body pH By excretion or secretion of bicarbonate and by Retention or excretion of hydrogen Four basic types of imbalance 1. Metabolic acidosis 2. Metabolic alkalosis 3. Respiratory acidosis 4. Respiratory alkalosis Metabolic acidosis Causes if metabolic acidosis Lactic acidosis Ketoacidosis —- diabetes Alcohol Starvation Renal failure Alcohol Compensation of metabolic acidosis Buffering by HCO3 Buffering by Hb Hyperventilation—- reduce CO2 Symptoms of metabolic acidosis Hyperventilation Lethargy Disorientation Stupor Muscle twitching Coma Metabolic alkalosis Causes Metabolic alkalosis Milk alkali syndrome Vomiting Gastric aspiration Diuretics Compensation of metabolic alkalosis Respiratory— hypoventilation CO2 increase so increase binding to H2O and thus increase H2CO3 formations and so increase H level ( H2CO3—H+HCO3) Symptoms of metabolic alkalosis Arrhythmia Decrease cerebral blood low— Confusion f Hypoventilation— pulmonary micro arelactasis Respiratory acidosis Causes Respiratory acidosis Increase PCO2 —- Decrease pH Drugs—- opiates, sedatives, Anesthesia Obesity Neurological disease— tetanus, botulism, high cord lesion Airway obstruction—- COPD, laryngospasm, aspiration Lung disease— empyema, pneumothora Chest wall conditions —kyphoscoliosis, spondylitis, obesity Compensation Buffering HCO3 Renal buffering —- acidi ication of f urine and bicarbonate retention Symptoms Tachypnea CO2 narcosis —- disorientation, confusion, headache,lethargy Skin warm, lushed and sweaty f Coma Respiratory alkalosis Causes Respiratory alkalosis Decrease CO2 in blood (Hyperventilation ) Pain Anxiety High altitude Mechanical ventilation Base excess and base de icit Base excess The amount of acid to added for each liter of blood to return its pH to 7.4 at PCO2 40 mmHg ( normal PCO2 level 35-45mmHg) Base de icit The amount of base ( bicarbonate ) added to restore serum bicarbonate f f to 25mEq/L at PCO2 40 mmHg ( normal level 22-28mEq/L) Base access ( alkaline)( pH high )——- give normal saline ( acidic) f Base de icit ( acidic)( pH low) —- give bicarbonate Using arterial blood Blood gas analyzer Coagulopathy and blood dyscrasia a a Prof. H yder M. Abduln bi Hemostasis The process to keep blood clot free And to form clot at site of injury Factors responsible for hemostasis 1. Vascular endothelium 2. Platelets 3. Clotting factors ( coagulation cascade ) 4. Fibrinolytic system Vascular endothelium Form the interior lining of blood vessel It prevent thrombosis by preventing attachment of blood cells and clotting factors It prevent platelets from interacting with collagen in the sub endothelial area It produce vasoconstictive, vasodilators, procoagulant ( phospholipid) and Fibrinolytic proteins. Stages of Hemostasis 1. Vasoconstriction 2. Platelet plug formation 3. Coagulation of blood Vasoconstriction The blood vessel constricts and decrease blood loss When blood vessel is cut, the endothelium is damaged and collagen is exposed This will activate platelets to secrete serotonin and other vasoconstrictive substances that cause constriction of blood vessel reducing blood loss Platelet plug formation Platelets will run to the site of ijury and aggregate to form a loose clot ( plug) that stop bleeding Coagulation of blood By an intrinsic and extrinsic pathways that cause activation of clotting system in a cascade manner where one factor activation lead to activation of subsequent factor until prothrombin is activated to thrombin f f Thrombin will activate ibrinogen to ibrin Activation of clotting factors Occur by two pathways 1. Intrinsic pathway— through an intrinsic substances secreted by injured vascular endothelium and exposure of collagen 2. Extrinsic pathway —- where the stimulation of clotting activation occur because of thromboplastin secreted by the injured tissue ff Domino e ect Common pathway start at factor X activation and here both Ca which is factor 5 is needed Vit K is needed in all the steps of clotting activation Vitamin K absorption needs lipid because it is fat soluble Vitamin Lipid needs bile for absorption Obtructive jaundice there will be Vitamin K de iciency—- f Leading to bleeding It is better to add some olive oil to green vegetables salad which are rich with Vitamin K for better absorption Fibrin is a long and branched protein threads attached to the loose platelet plug like a mesh or net Making a strong clot preventing further blood loss completely Fibrinolysis When blood vessel healed Plasminogen on the surface of the ibrin clot and endothelial cells will be activated into plasmin which f f lyse the ibrin clot Coagulopathy Disorders of Hemostasis due to1. De iciency or Inadequate function of platelets 2. De iciency of clotting factors 3. Excessive ibrinolysis f f f 4. Vessel wall defect Platelets defect Thrombocytopenia Example—- immune thrombocytopenic purpura Decrease bone marrow production Increase platelets destruction Uremia Clinical features Petechi Purpura Echymoses Epistaxis Gum bleeding Coagulation defect Hemophylia A Massive blood transfusion Hemophylia B Anticoagulant drugs Von Willebrands disease. Liver disease. f Vit K de iciency. DIC ( dissaminated Intravascular Coagulation) Von willebrands disease Is a genetic disease It’s action is as a adhesive protein that help platelets adhere to vascular endothelium And also as protein carrier for factor VIII ( anti hemophilic Factor) Clinical features Mainly super icial bleeding Bruising Hematuria Epistaxis Menorrhagia Gum bleeding Hematemesis f Rarely deep tissue bleeding Hemophilia Genetic disease ( male affected, female carrier) Either Hemophilia A (. De iciency of factor VIII j Or Hemophilia B. ( de iciency of factor IX ) called f f Christmas factor Clinical features Deep tissue bleeding ( 80-90%)—- hemarthrosis hematoma ( subcutaneous or intramuscular) Super icial bleeding —— mucocutaneous bleeding Nasal mucosa, GIT mucosa f Heavy bleeding after small cutb Disseminated intravascular coagulation ( DIC) It is a thrombo-hemorrhagic disorder Where there is rapid consumption of platelets and clotting factors leading to thrombosis Consumption of platelets and clotting factors make the blood out of any coagulation mechanism leading to bleeding Causes Severe infection Malignancy Obstetric complications— septic abortion Dead fetus Massive tissue injury —- extensive surgery Severe burn Massive trauma ( crush injury) Snake bite Clinical features Multiple organ failure due to micro thrombi Bleeding every where both internal and external Cell, cell injury and necrosis Prof. HAYDER M. ABDULNABI • Cell is the basic structural and functional unit of the body • Structure of the cell • Plasma membrane • Nucleus • Cytoplasm • Plasma membrane • Tow layers of lipid with protein molecule oating in between fl • Maintain shape • Protect the cell • Regulate in and out passage of substances • Maintains homeostasis fi • Nucleus • Contain nucleolus • Network of chromatin bers -DNA- chromosomes during cell division • Control all activities of the cell • Nucleolus synthesizes RNA to constitute ribosomes • Store hereditary information in genes • Cytoplasm • Jelly like material -80%water - contains organelles • • Golgi body • Formed of sacs, one end near the ER and the other end near the cell membrane • packing and delivering materials in side the cell by vesicles • Produce lysosomes • Endoplasmic reticulum• Network of tubules and vesicls- connected from one side to the nuclear membrane and from the other side to the cytoplasmic wall • Two types- smooth and rough ( ribosomes ) • Produce proteins, lipid, in liver detoxify poisons and drugs • Lysosomes • Spherical sacs lled fi with hydrolytic enzymes- destroy invaders like bacteria and viruses- detroy worn out organelles • Mitochondria • Small rods -synthesize energy rich compound ATP for all vital activities of the cell • CELL INJURY • Occur when the cell is exposed to to a severe stress-no longer able to adapt • Disruption of one or more of cellular components • TYPES OF CELL INJURY • Reversable- the morphological and structural changes are reversable if the damaging stimulus is removed • Irreversable- a state when the cell can not recover- deathtwo types • Necrosis and Apoptosis • CAUSES OF CELL INJURY • 1- Hypoxia ( oxygen debrivatiin )- Ischemia, anemia • 2- Physical agents- trauma, radiation, burn • 3- Chemical agents- poisons, alcohol, drugs • 4- microbiological agentsbacteria, parasites • 5- Immunological reactionautoimmune diseases • 6- Aging ( programmed process) • 7- nutritional- starvation, fi vitamin de ciency • MECHANISM OF CELL INJURY • Injurious agent cause cell injury by a ecting • 1- cell membrane • 2- aerobic respiration ff • 3- synthesis of enzymes • 4- genetic apparatus • Irreversible changes a ect- in • FATE OF CELL INJURY • Reversablil changes a ect ff ff cytoplasm and its. Components- nucleos still viable addition, mitochondria and cell membrane • FREE RADICALS • Unpaired electron in their outer orbit-chain of reactions- absorption of radiant energy, oxidation of cell components • Chemical(CCL4), irradiation, high O2 tention, aging • Cause- lipid oxidation, protein oxidation, DNA damage • Types of necrosis • 1. Coagulative- from sudden cessation of blood ow- heart, kidney, • 2 liquifection necrosis- ischemic or bacterial infection- by powerful enzymesabscess • 3. Caseous necrosis- cheesy- both coagulative and liquifection • 4. Fat necrosis- pancreatitis- lipase enzyme split fat that combine with calciumchalky white ( saponi cation) fl fi fi • 5. Fibrinoid necrosis- brin deposition( plasma protein)- immunological diseases • APOPTOSIS • Programmed cell death • The cell will die with out spelling it’s contents to outside cell membraneshrink and phagocytosed by scavengers • Important in destroying cells infected with viruses, or cells with damaged DNA, or cancer cells • Physiological apoptosisembryogenesis- post lactation breast atrophy Thank you