Blood and Body Fluids - Students - Pharmacy - University of Jordan - PDF

Ph.Physiology 1 / rst semester 2024, [Nov 4, 2024 at 2:36 PM] 9 ‫🔹تسجيل املحاضرة‬ Body Fluids & Blood 1(Slide 21 ) ✅ 😁 ( ‫🔹في شرح ملحاضرة اليوم نزله الدكتور على التيمز )فيديو‬ : ‫هي اللينك للفيديو‬ https:// sjo.sharepoint.com/sites/PharmacyPhysiology1FirstSemester2024-2025/Shared%20Documents/ G...

Ph.Physiology 1 / rst semester 2024, [Nov 4, 2024 at 2:36 PM] 9 ‫🔹تسجيل املحاضرة‬ Body Fluids & Blood 1(Slide 21 ) ✅ 😁 ( ‫🔹في شرح ملحاضرة اليوم نزله الدكتور على التيمز )فيديو‬ : ‫هي اللينك للفيديو‬ https:// sjo.sharepoint.com/sites/PharmacyPhysiology1FirstSemester2024-2025/Shared%20Documents/ General/Recordings/L1-%20Blood%20and%20Body%20 uids-%20Pharmacy%201-%20Physiology- Body Fluids & Blood %20Faisal%20Mohammed-20241104_122824-Meeting%20Recording.mp4?web=1 Ph.Physiology 1 / rst semester 2024, [Nov 6, 2024 at 7:04 PM] 10 ‫🔹تسجيل املحاضرة‬ 🔹 Body Fluids & Blood part 2 (slide 52) ✅ : (‫🔹رابط املحاضرة )فيديو‬ https:// sjo.sharepoint.com/sites/PharmacyPhysiology1FirstSemester2024-2025/Shared%20Documents/ General/Recordings/L2-%20Blood%20physiology%201-%20Pharmacy- %20Faisal%20Mohammed-20241106_122939-Meeting%20Recording.mp4? 1000mL 1012 5 1110 11mm 1031 1000 0000 1034 1032 0mpig University of Jordan cnpermm 1 5miN  IT 5 10 3L 1061002 Litted 5 109 mL Em Objectives Saying  To determine the composition of body fluid compartments  To list the components of blood  To discuss the functions of plasma and determine its relative volume  To discuss the RBC formation, functions and fate  To determine the WBC types, its relative percentage and their functions  To discuss the functions of platelets in blood coagulation  To follow blood coagulation pathways  To discuss blood groupings and realize its important University of Jordan 2 University of Jordan 3 Sam stable G University of Jordan 4 as A WP.WS IS sw assis  250 400 He highlosomosity i 6 AT paw caterer 6  Movement of water between compartments g kid ◼ Normally, cells neither shrink or swell because intracellular and interstitial fluids have the same osmolarity So  Increasing osmolarity of interstitial fluid draws water out of cells and cells shrink  Decreasing osmolarity of interstitial fluid causes cells to swell ◼ Changes in osmolarity most often result from changes in balance Na+ concentration mo heei.gg IIgiit ◼ Water intoxication – drinking water faster than the kidneys can excrete it oftled  Can lead to convulsions, coma or death University of Jordan 5 Electrolytes in body fluids  Ions form when electrolytes dissolve ad dissociate  4 general functions ◼ Control osmosis of water between body fluid compartments ◼ Help maintain the acid-base balance ◼ Carry electrical current ◼ Serve as cofactors is 100morethan University of Jordan 6 Concentrations in body fluids Change one milliequivalent is equal to one millimole ,The milliequivalent unit incorporates both the ion concentration and the charge on the ions ◼ Concentration of ions typically expressed in milliequivalents per liter (mEq/liter)  Na00 + or Cl- number of mEq/liter = mmol/liter 0  Ca 40 2+ or HPO 2- number of mEq/liter = 2 x mmol/liter Kharge TO a plasmand 1st main◼ Chief difference between 2 ECF compartments (plasma and interstitial fluid) is plasma contains many more protein anions  Largely responsible for blood colloid osmotic pressure University of Jordan 7 mW ICF differs considerably from ECF  ECF most abundant cation is Na +, anion is Cl-  ICF most abundant cation is K +, anion are proteins and phosphates (HPO42-)  Na+ /K+ pumps play major role in keeping K+ E high inside cells and Na+ high outside cell 5b Resting w University of Jordan 8 Sodium Na + ◼ Most abundant cation in ECF ◼ 90% of extracellular cations I Plays pivotal role in fluid and electrolyte balance 0 because it ◼ 0 account for almost half of the osmolarity of ECF dartolyk in FCF wos.is of was a main soure I is_ad so it's normally in e.de of osmoticpressure University of Jordan 9 Chloride Cl - octtoinside 5 ◼ Most prevalent anions in ECF ◼ Moves relatively easily between ECF and ICF because most plasma membranes contain Cl- leakage channels and antiporters Go Active ◼ Can help balance levels of anions in different fluids Ei University of Jordan 10 Potassium K + ◼ Most abundant cations in ICF ◼ Key role in establishing resting membrane potential in neurons and muscle fibers ◼ Also helps maintain normal ICF fluid volume osmosis Helps regulate pH of body fluids when exchanged for H+ ◼ EE ◼ Controlled by aldosterone – stimulates principal cells in renal collecting ducts to secrete excess K+ University of Jordan 11  Bicarbonate - HCO3gga ppgggggggngggggggg systemic Second most prevalent extracellular anion ◼ Co2thno H2CQ ◼ Concentration increases in blood passing through systemic capillaries picking up carbon dioxide HE  Carbon dioxide combines with water to form carbonic PIT acid which dissociates In m  Drops in pulmonary capillaries when carbon dioxide exhaled 4s BETA ◼ Chloride shift helps maintain correct balance of anions in ECF and ICF __ ◼ Kidneys are main regulators of blood HCO3-  Can form and release HCO3- when low or excrete excess University of Jordan 12  T1 stimulus pHto H exhaler Co2 420 bacon HOT L out tomahasanightoughamachand F h l 4900mL of blood 70 70 4900 ML 319g Is 710mL 4.920 Blood volume  O d 1 1 28 d g ofPer blood volume 70 gx avarage F m blood relativetothebodyweight Blood water Eww 48 a_  Liquid connective tissue  3 general functions mL 1. Transportation G e ◼ Gases, nutrients, hormones, waste products 216 2. Regulation ◼ pH, body temperature, osmotic pressure coolliod 3. Protection he defines Bloodbleeding ◼ Clotting, white blood e cells, proteins crieviruss University of Jordan 13 Components of Blood ◼ Blood plasma – water liquid extracellular matrix patch (primarily proteins)  91.5% water, 8.5% solutes  Hepatocytes synthesize most plasma proteins ▪ Albumins, fibrinogen, antibodies  Other solutes include electrolytes, nutrients, enzymes, hormones, gases and waste products ◼ Formed elements – cells and cell fragments  Red blood cells (RBCs)  White blood cells (WBCs) Platelets Cothrombosis  University of Jordan 14  PY.is o o r r o T a University of Jordan 15  I. Blood composing  Blood composing: plasma + blood cells Essex  Hematocrit: (packed cell gggercentefnnwuioe p volume –PCV) blood cells occupies the percentage of total blood volume. normal value male: 40-50% bUSI o female: 37-48% newborn: 55%  d X1 mj 100mL Composition of Blood 7 89 ofproteinper 10 74f  Plasma: F gprd.lt 100 mL 7 89 protein ◼ Straw-colored liquid.  Consists of H20 and dissolved solutes. 1 ▪ Ions, metabolites, hormones, antibodies. 9 ▪ Na+ is the major solute of the plasma.  Plasma proteins: ◼ Constitute 7-8 grams/100 ml of plasma.  Albumin: (M.Wt 68000 Dalton) ▪ Accounts for 60-80% of plasma proteins (4.5 gm/dl) 0 ▪ Provides the colloid osmotic pressure needed to draw H20 from interstitial fluid to capillaries. ▪ Maintains blood pressure ▪ Transport of lipid soluble hormones IIII ▪ Nutrition University of Jordan 17  Composition of the Blood (continued)  Plasma proteins (continued): ◼ Globulins (2.5 gm/dl of plasma) (M.Wt 240000 daltons)  α globulin: ▪ Transport lipids and fat soluble vitamins. β globulin: t  ▪ Transport lipids and fat soluble vitamins.  γ globulin: (immunoglobulins) ▪ Antibodies that function in immunity.  Fibrinogen (0.5 gm/dl of plasma) (M.Wt. 500000 daltons) ◼ Constitutes 4% of plasma proteins. ◼ Important clotting factor. iiiit  Converted into fibrin during the clotting process. c University of Jordan 18  - Composition of the Blood (continued)  Function of plasma protein: (1) transportation, (2) nutrition, (3) forming colloid osmotic pressure, (4) coagulation and anticoagulation, (5) pH value buffer, (6) immunity (globulin)  Serum: ◼ Fluid from clotted blood.  Does not contain fibrinogen. E 5  Plasma volume: fibint fp Es ◼ Number of regulatory mechanisms in the body maintain homeostasis of plasma volume. University of Jordan 19 Formed Elements of Blood University of Jordan 20 THANK YOU  Body Fluids & Blood Lecture 2 Bone marrow development during a life : At a birth most of bone marrow is red and actively produced blood cells ,at child grow the red marrow is present in long bones and at bones ,bone growth increased hematopoietic demand to body growth , after a puberty much of the bone marrow in long bone converts to yellow marrow which is less active in blood cells production and red bone marrow remains active only in the at bonen to produce a blood cells for the University of Jordan 23 body  III.Blood Cells Blood cells are erythrocyte (red blood cell, RBC), leukocyte (white blood cell, WBC) and thrombocyte (platelet, P). 0 biogenesure smear  3 Formation of Blood Cells  Negative feedback systems regulate the total number of RBCs and platelets in circulation constant hemostosis  Abundance of WBC types based of response to invading pathogens or foreign antigens  Hemopoiesis or hemotopoiesis  Red bone marrow primary site Matto stem cells have the ability to develop into  Pluripotent many different types of cells Flat bones: sternum, scapula. These bones are contain a red bone marrow This type of bone marrow contains hematopoietic stem cells,which are the University of Jordan 25 stem cells for blood cells  E Hemopoietic process called stemcell became Pluripotent differentiated it can blood doesn'tgive o thapa type a single of cell Jarrow S presents  macro 7 0ᵗʰ Omegapiate Granuli 00 bonemarrow d.lk University of Jordan 27 Formation of Blood Cells  Pluripotent stem cells produce G ◼ Myeloid stem cells  Give rise to red blood cells, platelets, monocytes, neutrophils, eosinophils and basophils Gar◼ Lymphoid stem cells give rise to  Lymphocytes  Hemopoietic growth factors regulate differentiation and mon er proliferation Regulation protein ◼ Erythropoietin – RBCs stimulate Etein RBCs ◼ Thrombopoietin – platelets ◼ Colony-stimulating factors (CSFs) and interleukins – WBCs Q formation University of Jordan 28 meg GM Leukopoiesis  Cytokines stimulate different types and stages of WBC production.  Multipotent growth factor-1, interleukin-1, and interleukin-3: ◼ Stimulate development of different types of WBC cells.  Granulocyte-colony stimulating factor (G-CSF): ◼ Stimulates development of neutrophils. Magophagec  Granulocyte-monocyte colony stimulating factor (GM- CSF): Eso 00 University of Jordan o o ◼ Simulates development of monocytes and eosinophils. 29  5mi 1mm 5,1 1 180 Erythrocyte Physiology 5 106 18 5000m.ME per EL LL T 5e1t m Shape and number of red blood cells (RBC) soggy  Shape of RBC: like biconcave disc SMPad Its diameter is about 7~8 µm, peripheral thickness about 2.5 µm, central thickness about 1 µm and cubage about 90 µm3. 106mm IL 52 100 a  11 bloodt hatta Erythrocytes costs 5M 3516mm  Flattened biconcave discs.  Provide increased surface area through which gas can diffuse.  Lack nuclei and mitochondria. ◼ Half-life ~ 120 days.  Each RBC contains 280 million hemoglobin with 4 heme chains (contain iron).  Removed from circulation by phagocytic cells in liver, spleen, and bone marrow. University of Jordan 31  Functions of RBC Functions of RBC  RBC can be used for transportation of O2 and CO2 in the blood.  RBC can be served as pH buffer. are e ring porphyrin 1  Life and breakage of RBC  Life-span: 120 days, about 4 months, each RBC circulates 27 km averagely in vessels, short life-span for aged RBC T  soe lymphatic node, Breakage: places are liver, spleen and and after breakage, Hb released from RBC immediately combine with plasma α2-globulin (Hb y touched protein) which is taken in by liver for iron reuse. TB fe plasmaprote Line  Hb, very toxic if it get into blood, normally, it can be metabolized into bile pigment in liver.  O B plasma 2 protein 1 hemolysis exit t livr azgloubn.hemologsisc cl cwalgnI8 Blood Cells and Platelets hypotonic University of Jordan 34 Hematopoiesis  Undifferentiated cells gradually differentiate to become stem cells, that form blood cells.  Occurs in myeloid tissue (bone marrow of long f bones) and lymphoid tissue.  2 types of hematopoiesis: ◼ Erythropoiesis:  Formation of RBCs. ◼ Leukopoiesis:  Formation of WBCs. University of Jordan 35 Erythropoiesis  Active process. 3 BC 13 ◼ 2.5 million RBCs are produced every second. productionofRBC  Primary regulator is erythropoietin. protein Regulk ◼ Binds to membrane receptors of cells that will become erythroblasts. 2 ◼ Erythroblasts transform into normoblasts. To withoutnucleus ◼ Normoblasts lose their nuclei to become reticulocytes. ◼ Reticulocytes change into mature RBCs.  Stimulates cell division.  Old RBCs are destroyed in spleen and liver. ◼ Iron recycled back to myeloid tissue to be reused in hemoglobin production.  Need iron, vitamin B12 and folic acid for synthesis. University of Jordan 36  either Forfunction or for production carry 02 tronqi.ba Low0 IxiaRBCs kidnecerthropr.net Red Blood Cells/ Erythrocytes  Contain oxygen-carrying protein hemoglobin  Production = destruction with at least 2 million new RBCs per second  Biconcave disc – increases surface area  Strong, flexible plasma membrane  Glycolipids in plasma membrane responsible for ABO and Rh blood groups  Lack nucleus and other organelles ◼ No mitochondria – doesn’t use oxygen University of Jordan 37 Hemoglobin u ◼ Globin – 4 polypeptide chains ◼ Heme in each of 4 chains ◼ Iron ion can combine reversibly with one oxygen molecule ◼ Also transports 23% of total carbon dioxide  Combines with amino acids of globin ◼ Nitric oxide (NO) binds to hemoglobin  Releases NO causing vasodilation to improve blood flow and oxygen delivery University of Jordan 38 Shapes of RBC and Hemoglobin chain 4 globin ring pherophri 4 gerras University of Jordan 39 Red Blood Cells  RBC life cycle ◼ Live only about 120 days ◼ Cannot synthesize new components – no nucleus ◼ Ruptured red blood cells removed from circulation and destroyed by fixed phagocytic macrophages in spleen and liver a ◼ Breakdown products recycled  Globin’s amino acids reused  Iron reused forhemoglobin synthesis.tk  Non-iron heme ends as yellow pigment urobilin in urine We EaIf or brown pigment stercobilin in feces Bilirubin inRBCs _É University of Jordan Urobilin Sip IT is DID 40 urine c  smallamountlc Formation and Destruction of RBC’s Circulation for about 120 days 3 7 Amino Reused for protein synthesis Fe3+ Transferrin bonemarro vesyntles.is Globinprotein acids For 4 6 RBCs 5 Fe3+ 2 Heme Felt Jferic Transferrin Ferritin Fe3+ + Bilirubin Globin 9 + Biliverdin Liver Vitamin B12 1 Red blood cell Bilirubin 11 10 + 5 death and Erythopoietin Small phagocytosis Kidney intestine Bilirubin 8 Erythropoiesis in 13 12 red bone marrow Urobilin Macrophage in Urobilinogen Bacteria Key: c Stercobilin I spleen, liver, or red bone marrow in blood Large 14 in bile ofatid Urine Feces intestine ox on Billi bddd winskintaundc University of Jordan 41 so pigment  B a d 9 feb F How s Reduction doublebon singlebond yghment Erythropoiesis ◼ Starts in red bone marrow Got with proerythroblast ◼ a Cell near the end of 2 development ejects nucleus Ovidiu and becomes a reticulocytespikes Develop into mature RBC I ◼ within 1-2 days ◼ Negative feedback balances horror production with destruction 0ᵗQ ◼ Controlled condition is amount of oxygen delivery to tissues ◼ Hypoxia stimulates release of erythropoietin Can University of Jordan 42 991rem  Feedback Regulation of Erythropoiesis - regulated by renal oxygen content. o - Erythropoietin, a glycoprotein hormone, is produced by renal cells in response to a decreased renal blood O2 content. - Erythropoietin stimulates erythrocyte production in the red bone marrow.  Erythrocyte Disorders Anemia is a condition in which the blood has an abnormally low oxygen- carrying capacity. Common causes of anemia include: at 1) an insufficient number of red blood cells 2) decreased hemoglobin content 3) abnormal hemoglobin Two such examples are Thalassemias and Sickle-cell anemia, which are caused by genetic defects. Low chain carrier  Erythrocyte Disorders - 2 bonemarro Polycythemia primary RBC caused by hyperactive of Livesin ahighplace pressure or secondary person hypoxia 1 Egg is an abnormal excess of erythrocytes t hypoxia said assay i an gait ftp.w 02 erthroph REED that increases the viscosity of the blood, causing it to sludge or flow sluggishly. by 8 55 caused smokin Common causes of polycythemia include: p 1) Bone marrow cancer 2) A response to reduced availability of oxygen as at high altitudes THANK YOU Body Fluids & Blood Lecture 3 University of Jordan 49  material should Ifyou want to study the genetic you WBCs has a neukens use a WBCs Not RBCs because without Nucleus but RBCs Moot test type of a test Karyotype genetic WBCs Thegeneralfunction of Defenseagainst bacteria infection gtiig pathogens uiruse.by or Antibody Normal range of the Number for WBCs 42ohm RBG 5M.to y.parm w Reminder because it works Ifection it remains around few hours without that maybe around 3days shortlifespan the presence of ha.ae Infection Leukocytosis the number of WBCs ÑTToo Lessthan 4000 Leukopenia someone has an increase 18,000 synopolInsils appendix  Entail case weJust determin which types ofcells are increased GTechinque DLC differential Leukocyte Count Measure the Number 8 typeof was cellsinside your body 010 µ I spreading staining Total Number by device Multiple it by each percentage of each WBCs types 18,000 Total 851 Neutrophils Normal 50751 s this is the type that increase in patent blood So we directly know thetype finfection is bacterialinfetion because the NPfunction is generalytodfns oin.esspicaly againstbacteriainfe acute bacterial 251 GEoctin Such as theTonsillite drugfor bacetrial Antibiotics Core indicates the importance to knowthetype cause  core 11 181000 Lymphocytes Normal 20 301 i ioaons s so 0 501 bacetr drugforviralnothkutrohia.EE Antibiotic  Leukocytes astudy Contain nuclei and mitochondria.  TWIT  Move in amoeboid fashion. Eisited new ◼ Can squeeze one through capillary walls (diapedesis).towardtissue  Almost invisible, so named after their staining properties. ◼ Granular leukocytes: dye Is  Help detoxify foreign substances. ▪ Release heparin. 0 ◼ Agranular leukocytes:  Phagocytic. t ▪ Produce antibodies. of pento University of Jordan amoebridmonment 50  94 eze thrg the app and towardthe infectionLoutation Lodiapedesis soon o o Neutral aye t WBCS f eosinophils Neutrophile basophils Lovethe Neutral it  41 95 White Blood Cells/ Leukocytes   Have nuclei Do not contain hemoglobin comparedwith RBC  Granular or agranular based on ooo staining highlighting large conspicuous granules e  Granular leukocytes ◼ Neutrophils, eosinophils, basophils  Agranular leukocytes ◼ Lymphocytes and monocytes OFWBC Leukeyscytosis ofwp.sc 50 701 Neatorphile indecake of infection Esophile 2 4 Basoph cis eleakopegiqgiit monocycle 2 81 University of Jordan 51 Lymphan  todetermin thetype Differential leukocytecount and Number ofeachtype sodeterminthety.pe of infection Sutibleday or DY so It PCV EEany 900 To 18000 701 abnorr oooo DLC Types of White Blood Cells granula Agranular University of Jordan o 6 53 109 109 10  Tom Leukocyte Physiology battle Classification and numbers of Leukocyte Number of Leukocyte (white blood cells, WBC): (4.0~11)×109/L Classification: It is granulocyte (neutrophil, eosinophil, basophil), and agranular (monocyte and lymphocyte). Functions of WBCs ◼ Usually live a few days ◼ Except for lymphocytes – live for months or years ◼ Far less numerous than RBCs ◼ Leukocytosis is a normal protective response to invaders, strenuous exercise, anesthesia and surgery ◼ Leukopenia is never beneficial ◼ General function to combat invaders by phagocytosis or immune responses for lead Top University of Jordan duttible 55  Lymphocyets important forimmunity For ex given accine Someone was viruse 0 jactive body formed against Antibody Foreign body this antigenTbreakingitdown Antigen and our memory cell creating thehuman synthesis by Lympocytes memorisethis pathogen it so it doesn't cause so when the real pathogen on adilease act a teacher for viruse enters yourbody the the immune system to response memory cell directly recognise it for the real pathogens as active your immunesystem to aforeign Toit protect get rid for this disease the diseased yonagainst Lumphocytes elati body produced in Lyndon 4kcal killthe ᵈ besides the production n bothtypes act bomerrow a cs remains for month Lepta cytotoxicdrug so it forcancertreatmen.cc emothvapy or year  I sh.by diapedesis Rolling sticking squeezing Flowoutsidethe m cappetal Emigration of WBCs ahem closer from baceter Many WBCs leave the sitWBCsteen  bind and bloodstream directylationthe  Emigration (formerly diapedesis) a its  Roll along endothelium  Stick to and then squeeze between endothelial cells  Precise signals vary for different types of WBCs Ffi.ro sedacrtivchemical these chemical attract the WBCby University of Jordan 56 porcesscalled contain  s a 1 9 bdy bacteria releasachemical refepht WBCs c faccinfection chronicinfectif  Neutrophils and macrophages are active phagocytes omgowaeir.tt ◼ Attracted by chemotaxis  Neutrophils respond most quickly to tissue damage tt by bacteria 20bn lowamm f.tt Ulcer ◼ Uses lysozymes, strong oxidants, defensins  Monocytes take longer to arrive but arrive in larger numbers and destroy more microbes candestroy to D i up ◼ Enlarge and differentiate into macrophages bacteria Iff University of Jordan monocyte infet deff57 WBCs phagocytosis monocytes magrophaa  O pg y Ma P9 1 9 instati Neutrophils phaykytos WBCs E laik.IE  Basophila leave capillaries and release granules head containing heparin, histamine and serotonin, at sites of inflammation Antidepressant f We ◼ Intensify inflammatory reaction we ◼ Involved in hypersensitivity reactions (allergies)  Eosinophils leave capillaries and enter tissue fluid 2 ◼ Release histaminase, phagocytize antigen-antibody C complexes and effective against certain parasitic worms FEtangIJ.TT ova paraeTsottstoleifeas rm ÉÉ allergic Antigen Antibody complex basophilis University of Jordan 58  Cle L Physiological Characteristics and Functions of WBC emegration Terminology  Diapedisis: Metamorphosed WBCs pass through vessel wall getting into interstitial fluid.  Chemotaxis: It is a process that ofttimes WBC WBCs shift to some chemical 08 Diapedisis material (metabolic production, antigen-antibody complex, bacteria, toxin, etc).  Phagocytosis: It is a process that WBCs enclose and engulf exotic Blood or extraneous material, and use Vessel intracellular enzyme digesting them. Metamorphose  Physiological Characteristics and Functions of WBC i ①Neutrophil (50%-70%)  Another name, polymorphonuclear, PMN, 6~8 h in the vessels, diapedisis, chemotaxis and phagocytosis (using its hydrolyzed __ enzyme)  Tus L2mÑop Function: It plays a very important role in nonspecific cellular immunity system which is against pathogenic microorganism, such as bacteria, virus, parasite, etc.  Clinic relation: Number of neutrophil greatly increase occurring in acute inflammation and earlier time of chronic inflammation. Tousix appedit monocyte number decrease of neutrophil will result in poor  c Physiological Characteristics and Functions of WBC ② Eosinophil (2-4%) Circadian changes: Its number is lower in the morning and higher at night. Function: b antigagyti.ba 1. It limits and modulates the effects of basophil on fast e allergic reaction. C 2. It is involved in immune reaction against worm with opsonization. re Clinic relation: Its number increase when person suffers from parasite infection or allergic reaction.  Wxs seyleosinpD.it is SW I Physiological Characteristics and Functions of WBC 9 79difficulty contraction in bronchi narrowforbranin causing a weezing and a inbreathing ③ Basophil (0.5-1%) ◆ Circulatory time: 12 hours ◆ Basogranules contain heparin, histamine, chemotactic I factors and chronic reactive material for allergic reaction. c ◆ Function: It is also involved in allergic reaction. a 1. Heparin serves as lipase cobase and speeds up fatty decomposition. 2. Histamine and chronic reactive material increase permeability of capillary and contract bronchia smooth muscle, and result in allergic reaction such as measles, asthma. 3 We ME fo. 3. Eosinophil chemotactic factor A released by basophil can attract eosinophil collection and modify eosinophil function.  19 grit gale Physiological Characteristics and Functions of WBC ④ Monocyte (5-10%) Its body is large, diameter about 15~30 µm without granule Function: 0 poor 1. It contains many nonspecific lipase and displays the powerful phagocytosis. canelgaltto100bactria 2. As soon as monocytes get into tissue from blood , it change name called macrophage activating monocyte- macrophage activeform macrophages system to release many cytokins, such as colony stimulating factor (CSF), IL-1, IL-3, IL-6, TNFα, INF-α,β ,etc. 3. Cytokins induced by monocyte may modulate other cells growth. 4. Monocyte- macrophage system plays a very important role in specific immune responsive induction and regulation. infection  Chr c d mustolgan Physiological Characteristics tons ofbactera and Functions of WBC ⑤ Lymphocyte (20-30%) 2types ⚫ Classification: It can cliff be separated into T- Lymphocyte Lymphodnor and Let B- Lymphocyte. by thymus gland ⚫ Function: 1. Lymphocytes serve as a nuclear role in immune responsive reaction. wanna a É Lets Immun.gbt 2. T- Lymphocytes involved in cellular immunity. proyo.g 3. B- Lymphocytes involved in humoral immunity. fif ⚫ Clinic relation: Numbers increase of lymphocytes occur in acuteinfection chronic inflammation and late time of infection. of reduce achilder own adult  them go f thymland and emproy of some shrink dringthe Lymphocytes person becomeolder see  Lymphocytes are the major soldiers of the immune system ◼ B cells – destroying bacteria and inactivating their toxins byama t.IE ◼ T cells – attack viruses, fungi, transplanted cells, cancer cells and some bacteria ◼ Natural Killer (NK) cells – attack a wide variety of I infectious microbes and certain tumor cells Too University of Jordan 65  Acquired immunodeficiency syndrome augia o which one of the Lympocytes type is t.IT abnormal v t Immunodefi TgeD_ Humman Varne caused the AIDS Hey Our body are constantly trying to produce a tumor cell but Natural Killers kill this cells In case Tentthis tumor cell cancer this maybe our body produce this cells in way beyond because the capacity of the Lds to kill it oraybet because the abnormality falls Leukocytes are deployed in the infected areas outside blood vessels via 3 steps. 1) Margination 2) Diapedesis OFF 3) Chemotaxis Blood Capillary  Leukocytes are deployed in the infected areas outside blood vessels via 3 steps. rayighese 1) Margination WBCS slow down by cell adhesion molecules cells In secreted by endothelial __ Endothelial thebloodvessel WBCs movetoward Walls endothelium preparingtodiffuse out ofthe blood tothesiteofinfection Blood Capillary  slowdown infection endothelia cellgdksiguryyl.ae bindwithWBC then WBCScausing to roll ar Long thevessel wall 2) Diapedesis: Is Leukocytes slip out of the capillary blood vessels. Fa infection 5 55 age 0 the endothelium site to bloodstream Blood Capillary  3) Chemotaxis: WBCS Gather in large numbers at areas of tissue damage and infection by following the chemical trail of an molecules released by damaged cells or v pub other leukocytes É FIT 11 Blood Capillary  www.ywdwBCshaess EJ.FI a at Ps chemotactic Phagocytosis I f Destroy foreign substances or dead cells Blood Capillary  Leukocyte Disorders Normal Leukocyte Count: 4,000 – 11,000/l Leukopenia: < 4,000/l normal leukocytes Leukocytosis: > 11,000/l normal leukocytes i l 200.0 15 Leukopenia is one major side effect of chemotherapy. A thodimminuityayxot.tt  extraorginarry of Leukemia Leukocytes - Leukemia refers to a group of cancerous conditions of white blood cells. - I Descendants of a single stem cell in red bone I marrow tend to remain unspecialized and mitotic, and suppress or impair normal bone marrow function. Fr.IT - extraordinarily high number of abnormal e (cancerous) leukocytes ___g Is THANK YOU  Body Fluids & Blood Lecture 4 Notactually tell it's afragment ofcell platelet University of Jordan 74  Platelets thromobcytes are fragments of cells and are classified as a formed elements alongwith RBCs 8WBCs Egakaryocytes release small fragment of theircytoplasm intobloodstream and these fragment become platelts bowgow It's Zack a nuchi but it contains a store ADP serotonin andthromboxaneA2 granules a typeof prostaglandin which are cride for their main function in stopping bleeding blooddotting The process of stop bleeding called hemostasis Cicans to 5 anti ct civilised ydidiash.ws The Number 150,000 4001000 per ML pateint his platelts Number 50,000 is tooLow so thedoctor must not make a surgury because the patent body is exposed to bleeding So we must give the patoint platelts How RBCs live 120 day so if it was from 2weeks thrive No problem but the platelets have a short life span so if it available from 2weeksago they Lost it's function so wemustgive the patentfreshly blood which active in bloodclotting  g 46004 50000 Platelets (thrombocytes) TO  Smallest of formed elements. ◼ Are fragments of megakaryocytes. iii   ◼ Lack nuclei. Capable of amoeboid movement. Important in blood clotting: it iii Leo ◼ Constitute most of the mass of the clot. ◼ Release serotonin to vasoconstrict and reduce blood flow to area. Narrower for vessel  Secrete growth factors: ◼ Maintain the integrity of blood vessel wall. Survive 5-9 days. Ewood  University of Jordan 75 Platelets/ Thrombocytes mmyelodstemcd co  Myeloid stem cells develop eventually into a megakaryocyte  Splinters into 2000-3000 fragments platelets mm  Each fragment enclosed in a piece of plasma membrane  Disc-shaped with many vesicles but no nucleus  Help stop blood loss by forming platelet plug  Granules contain blood clot promoting chemicalsI  Short life span – 5-9 days University of Jordan 76 Normal Value and Function of Platelet 100,000mL 4001000mL  Normal value: 100×109 ~ 400×109, range from 6%~10% Normal changes: more number in the afternoon than in Ex  the morning, more in winter than in spring, more in the venous blood than capillary, after sport↑, pregnacy↑.  *Functions: 1. It maintains capillary endothelial cells smooth and integrated (repairing endothelium and providing nutrition). 2. It is involved in physiological hemostasis. stop bleeding  Platelet and clinic relation: i decrease of platelet, abnormal immune reaction, will results in hemorrhage or bleeding, purpuric symptom. was I  purpuric symptom hemorrhagebleeding purple or red spots on the resultby 7hdamage b odloss injuring skin causedbyhemorrhageunder in blood vessels severt the svin due to the Thrombocytopenia Low platelt sostagesofbmostas.is yn me Vascular spasm Damaged tissue released a chemical signal such as Serotonin or ThromboxaneA2 this chemical bind the wall of nessele so the smooth muscle in it's wall contract vasoconstriction this Narrow the blood vessel reducing blood flow and minimize blood Lost diameter d platelet plug formation platelets stick to the exposed collagen fiber in the damaged cell wall became activated by relasing a serothindthromboxan which recruit more platelet causing them to aggregation together making a plateletplug Blood clotting there're a 12 coagulation in our body Coagulation factor molt ofthem are proteins andthey are producedby alive some ofthem productionby the vitaminK this coagulation Lacto present in our body but in inactive form whenthe bleeding occur active to stop the bleeding  injury www.s I Hemostasis bcp attract collagen se.ro a8thra theplatelet into plaale  Sequence of responses that stops bleedingfound spicky  3 mechanisms reduce blood loss War 1. Vascular spasm 14.1 Smooth muscle in artery or arteriole walls contracts ◼ c 6 2. Platelet plug formation totagen ◼ Platelets stick to parts of damaged blood vessel, become activated and accumulate large numbers 3. Blood clotting (coagulation) University of Jordan 78  1) vascular spasms contracting Food Littleamount of with 3) blood clotting / 2) platelet plug formation coagulation collage platelths i but whentheinjury occurand shape can't movemetsoiteknst.ie to bind collagenfiber stars Platelet Plug Formation move platelet activation University of Jordan 80  Acrodgni.at 7prostglandin ThrombuxanA bond 20C14double Positivefeedback protaglanding 1 8 prowa prevent oEiii.is no Its clotting play aggregate Anticoagulant  clolls prevent Loplasma Blood Clotting 3. Blood clotting ◼ Serum is blood plasma cascade minus clotting proteins I ◼ Clotting – series of chemical reactions culminating in formation of fibrin threads i.F Eating sfinal Fdd ◼ Clotting (coagulation) byglass factors – Ca2+, several extrinsid f inactive enzymes, various molecules associated with platelets or released by Flid damaged tissues University of Jordan Plates 82 serum  M P Is 3 Stages of Clotting damagetissue outsideinjury 1. Extrinsic or intrinsic pathways lead to formation of prothrombinase enzym 2. Prothrombinase converts Eod prothrombin into thrombin 3. Thrombin converts fibrinogen (soluble) into fibrin (insoluble) forming the threads of the clot guy O University of Jordan O 83  Extrinsic damage in tissue outside this damaged tissue release a collagen IV activate v to release Cant activat faitor XI activated prothrombin Fibrin XA to rXI Stabelizing factor afeform thrombent LactivationFibrin loose hard net Fibrongan Fibrin This process contain a common Loosefibrin hard pathway between intesti benic fiber network water E Extensic is very fast Rapid itf.to Creation clots compared whith Intrestic because intrestic pathway has more steps companal with the extransic one Ca Factor IV in coagulation process inabsent ofseeds Castthe clotting cascade inhibit Calicum Chelating preventing of cast in bloodmake itcavaliable thritif was scia agent sedimentation powder I mail.ca Mayan's ftffssddg.eso PFG EDTA bind calicumchelating IM iculation IEEE factor  Pleven is a ably withoutsufficentCastthe cascade inhibit prentth bloodfromclotting Blood Coagulation snito 2Pathway 10 0 in'S'Ñ other feedback are vactor bleeding Pd shock death University of Jordan II 84  b Stabilizing odaddottingcascads Factor extracic intensic bloodreset collagen IO TTF FI with act Esx Jack c factor M Fix cast lycart IX as active care TF VI desprombined T prothrombin thrombin It Fbronga Erin so as actin Loose Fbrie stablizing Libion  Slow Rapid Blood Clotting xf0 ÑW k  Extrinsic pathway III Tba TFJJIIPI ◼ Fewer steps then intrinsic and occurs rapidly ◼ Tissue factor (TF) or thromboplastin leaks into the blood II from cells outside (extrinsic to) blood vessels and initiates formation of prothrombinase  Intrinsic pathway pfH2 it d ◼ More complex and slower than extrinsic _I ◼ Activators are either in direct contact with blood or contained within (intrinsic to) the blood ◼ Outside tissue damage not needed ◼ Also forms prothrombinase University of Jordan 85 Blood Clotting: Common pathway both atone ◼ Marked by formation of prothrombinase ◼ Prothrombinase with Ca2+ catalyzes conversion of prothrombin to thrombin ◼ Thrombin with Ca2+ converts soluble fibrinogen into insoluble fibrin ◼ Thrombin has 2 positive feedback effects Its  Accelerates formation of prothrombinase by product or  Thrombin activates platelets  Clot formation remains localized because fibrin absorbs thrombin and clotting factor concentrations are low Theabs callFetract Tanticoagulat University of Jordan 86  pre 1 c gulatio Blood Clotting  Function of platelets: ◼ Platelets normally repelled away from endothelial lining by prostacyclin (prostaglandin).  Do not want to clot normal vessels.  Damage to the endothelium wall: ◼ Exposes subendothelial tissue to the blood. me_ If the doctorgiven thepatent a drag inhibitthe LaborID bleeding continonly TTchristmasFactor University of Jordan 87  Blood Clotting (continued)  Platelet release reaction: ◼ Endothelial cells secrete von Willebrand factor to cause platelets to adhere to collagen. ◼ When platelets stick to collagen, they degranulate as platelet secretory granules: 0  Release ADP, serotonin and thromboxane A 2. platelet aggregation ▪ Serotonin and thromboxane A2 stimulate vasoconstriction. ▪ ADP and thromboxane A2 make other platelets “sticky.” ▪ Platelets adhere to collagen. ▪ Stimulates the platelet release reaction. activation  Produce platelet plug. ▪ Strengthened by University activationof Jordan of plasma clotting factors.88 Blood Clotting (continued)  Platelet plug strengthened by fibrin.  Clot reaction: ◼ Contraction of the platelet mass forms a more compact plug. ◼ Conversion of fibrinogen to fibrin occurs.  Conversion of fibrinogen to fibrin: ◼ Intrinsic Pathway: wf  Initiated by exposure of blood to a negatively charged surface (collagen). T.si ▪ This activates factor XII (protease), which activates other clotting factors.  Ca2+ and phospholipids convert prothrombin to thrombin. ▪ Thrombin converts fibrinogen IT to fibrin. ▪ Produces meshwork of insoluble fibrin polymers. University of Jordan 89  a Blood Clotting (continued)  Extrinsic pathway: interesting not ◼ Thromboplastin is not a part of the blood, so ssm aP called extrinsic pathway. factor ◼ Damaged tissue releases thromboplastin. plum  Thromboplastin initiates a short cut to from 2 donated formation of fibrin. cell Not EPF in invin plasminogen bijo aol.ba interting or activator pig 9 streptokinaseUniversity of Jordan Plffte clot 90  not less in 6 hor aft if I a nonce the strock infraction ofstrock Dissolution of Clots 12  Activated factor XII converts an inactive molecule into the active form (kallikrein). cc ◼ Kallikrein converts plasminogen to plasmin.  Plasmin is an enzyme that digests the fibrin. ◼ Clot dissolution occurs.  Anticoagulants: ◼ Heparin: 11 Injectiable ◼ Coumarin: corall 0  Activates antithrombin III. vitamin im  Inhibits cellular activation of vitamin K. (Vitamin K IM or dependent clotting factors are II, VIII and X). or 2 f if subcontents Drug University of Jordan 91  I without bacetria so formation fetus sterile pt of with isnot at much Breastfeeding the bacteria entertheirbody so they start form with so the doctor must inject the fetas the with immeditly afterthe pregnancy surgay I stop bleeding  Coagulation Disorders Thrombosis is the abnormal clotting of blood in an unbroken vessel. F Thrombus is a clot that attaches to the wall of blood vessel. Embolus is a clot that comes off the wall of blood vessel and travel in the blood stream. accaned ablooking Embolism is the blockage of blood flow by an IgEembolus that lodges in a small blood vessel. Infarction refers to cell death that results from embolism. Infarction is responsible for most strokes and heart attacks. related toheart myocardial Nubloodl  blood required ischem a brain Infraction first step Lung embolism Bleeding Disorders befor myocardial decrease in flow blood 1) Thrombocytopenia - the number of circulating platelets is deficient (