2.RBC and Hemoglobin.pptx123456700000001

Pathology of Blood , immunology 1234567 ,talk about RBCs and Hemoglobin that preasnt in blood componte.77788fgftrbkjjiuuhvcdsewuipo[l,,nccvxctipiiuuyyr6897644121esmppopogfseewtyggcddseweq2q579-0-oojlmmvzdlp09u7565yi7544wrfjhgdgvjkiu765yttewuuo,mnnmmkp-00977uhjjhnjdjrt8g3vwdwcxkjsdvyyemnvvppdjjewknbzxfsw276jr;[d[nbcijhgdjiwhenfjfgeufuefjjefejhgwhduyyyyywjvhxcxxxxxfYSQTRWY1WUIIUUUYYYQKDSNNMCVCZCXXXRQEWR25454545452UYEHKYU097886798YNSMFKDFJKNJJDHFFHHRGHJRJGHJHJGHJG,JURGUGUTGTRUTRGFV VHDIEUFUEURUYRTUIRHJJIIJKHGUUUYUKGJKDHSGWEWRREWRWYIWROIIYOS MNXKJDJSDGFUSKJFJDDJKFJJGDG...,,UUERYTURTUIRUIUYYUHUTREYYDEWQ23568875344DFHL[PKJ,VSAWQWE2`235DCZS8IDIUYYTTFCGDTYTUTTFGFPITJMGJVFRIRORJLKFMKVLRPRIPRDMNDVSTEWREYRIPT9RIU46487453746583KFMMVNVLFPPR]R;RLC,M.XNOFY845374280508OFKKJRFKTUOEPOIOIFJJKJJHTDRDRER3213223RESFCGCXXFDZHGLK;PIP;M,NNVVCN.,;P[98754312`32`RWSDAE JGFTIIUOKJJFGIUFDGDKJGIGJGHJFYFUYUTUFNJYUDU656452`2`2`5UKVNKVJOF08IU8UKBTLOIUYTFVBNMPTRFGHJKLLKJGFCVNMMNVC OIUREWERTYUIOP[;LKJHGFWERTYUIOP[CVBNM,.RTYUIOP.,NVTL.LLKDJLJSDLKFNHJTKJKJJKLLIUTYREOLMMCXAWQ245UPORT;F,.DCMNJOI9IOKMMNBVCRY4556987099076553423457YIUJK.,.,.MLM,;JOIUUUUGRIUUOITYILVGXFDRDEWQ324557896745431656385IK,ND,NM XXVUGIGEIURK JGULD BIUIOOTIJIYJIRYIOIORI.UGIRUGTORIOIYKJSJGIYRIUHGKJRHHYIUIRHUREIRJURUIFOIRUTOE8TEIT98885839873OIREKJHVKKJVKJHGJUGEUW3RY3WYIRWIURUEWFEFJSFKJGFYRYE347627836534JKVNVVKFOITOTJRM.,MP863123579KMNVCW22345DDZAQETIL.,.L;/./;;LKJHCGFTYYUYIYI;LL,.,KKUILO8098590-9PLK,KJHYYU7TIP0O=-0=09UOJKJGFDTRE4YUDTRRYU7UOUKJHV,CK.OOOIYIRTORIT9534567890LFCSRTYUIODPFLEF,DMNCVMIUYTRERE6IEOERP765EWDFNM.LSOFDOIRIJLDCKJZNLUOYJJ6J6RLTKUOU7I6564RTFYYKMMDFJKKDJGRIEIUYTUEWYTP98WUOIJDKVNBLKFLES756789OLKJMIIUREUTOIERTISRGKJDKZNKNFVJFISERYT87W4968495UOLRMJNIU64WQAQ1``1298098766IKSMOIUYTRETYLS,C,CDLI9876545678L,X,O876545678L,C,C.X,MNVCVBNMLsjDIUWOEIOEWI5ERTYUIO;L,MSZCKASLCYUTUAYDEIUYTRE5678OIKJ,MCNJKJKJSDIFUEFNNNVCNDZU76R5RTYUIJKNM,MC,SDKFKEFUIFJKALKFAHEUYTRTYUIKJMD,CMMDVJCKUSUIEFTYUYEUITRR76890OILEKF,M,,CMD,LEAOIT4ET467890-ODLKM,C,MDKDXJVUIYTREWRTYUIO,MC N,KSFKJAIEUEATEO[E]OAEFL,DC.,DSZ;P]F[;REG[PRPRPGM,VND;KFOIAEPOEYTPIOEALKKIUYTREWYUE;LF.DV,DX XJLJGOIYEATWP94874W067-4609834T4OTUIE4-43-=34-[PTJKGFD.UHIWYIOJNDNVDHFYUE8WQ98R3472642134567IUFKJSDCOIUYTREETYUEWURIEHFNESXCVBNMLIWEPOIRPOWQOWR4OQOKMLIUYIUHJKGIIPOKHKJFSKLKFGLTTKJDTSJGSJGNMSMFMFVMCMKZDJAFIAEFAS;IJFHAKJDNVN VGFREHJKJKBKHJDRTE544244OIUGFKNCFCTD6IIJ, JVZ;OGS9E09W498Q42=43UQLKRMWFVSCaK.//ZG1`12345678IFEOJESAKNFKDSJCDIUYTRESAKSJ;SCMNBVCXZNXLCERTYUIOP[ELF,DDLKJHGFDSFFUAD[POIUYTREOIALZSKDLKJ;R;PRPOIRT9WE80949875872654324567SLF.,C.X, .;LKCSZOJF;IDZ;LKJJJJIYUDSX ,;USDYUO;KLD.,XZ.,C XZC ,CMV/.DLKYTREEYTUAUI;OLKJM,IUJCXNM.,KLIEOD;L.,/;;PO65RFDCJKIK,.LIUHRERTYIKJL,,MVZNBDV,J.LKJDLIATRIUE4IUTEALDNMLIFO9Q87T0Q97876543214356LKMNDBVCXCVBNM,;LLKJTRERTYUP'AE;SLMFDC87WOIUELKJDM;IHJ5TRFDMOGHKKJHUYUYTRDUHKJLKFJSOIUGOSARLIJALKDFIUSYFEAEUOWUYR7QW48TOEIFUYFCGHJKM,NBVLISUEFIEIRTIORDJLKDVBKDSZFIRGIHUGYUGRHKGVJDFGIETK4TN GNDUVHSIURGOIDUYTRTYGHUIJKMNNBDKZKHDGDIUEIUESZIFKKJKYDUFH.

1. RBC and Hemoglobin Dr. Sarah yousif MBBS.MSc

2. Characteristics of mature red cells: Count: male: 4.5–6.3 millions/mm 3 female: 4.–5.5 millions/mm 3 Biconcave shape: Increases surface area Increases flexibility Has no nucleus or organelles

3. Characteristics of red cells Average volume (MCV): ~80 femtoliter Macrocyte high MCV Microcyte :low MCV Contains haemoglobin: Each cell contains ~30 picogram of HB (MCH) Live for 120 days Destruction mainly in the spleen by macrophages

4. Regulation of production The hormone erythropoietin produced by the kidney is the main stimulus for the bone marrow Production of erythropoietin is stimulated by hypoxia ( O 2 )

5. Haemoglobin

6. Average concentration: male: 14-18 g/dl female: 12-16 g/dl Structure: globin + haem Globin part: Four polypeptide chains: 2 α chains 2 β chains The haem : Porphyrin ring + iron

7. Oxygen is transported bound to iron Iron in haem is in reduced state (ferrous, Fe ++ ) Oxidized iron can not bind O 2

8. Because O2 is poorly soluble in the plasma, 98.5% of the O2 carried in the blood is bound to hemoglobin

9. Therefore, hemoglobin plays the key role in: O2 transport Contributing significantly to CO2 transport The pH-buffering capacity of blood.

10. Red blood cells contain no nucleus or organelles. During the cell’s development these structures are extruded to make room for more hemoglobin Thus, an RBC is mainly a plasma membrane–enclosed sac full of hemoglobin.

11. ERYTHROCYTE ENZYMES a few crucial, nonrenewable enzymes remain within a mature erythrocyte: glycolytic enzymes and carbonic anhydrase. The glycolytic enzymes are necessary for generating the energy needed to fuel the active transport mechanisms involved in maintaining proper ionic concentrations within the cell. Ironically, even though erythrocytes are the vehicles for transporting O2 to all other tissues of the body, for energy production they themselves cannot use the O2 they are carrying. Lacking the mitochondria that house the enzymes for oxidative phosphorylation, erythrocytes must rely entirely on glycolysis for ATP formation

12. The other important enzyme within RBCs, carbonic anhydrase , is critical in CO2 transport. T is enzyme catalyzes a key reaction that leads to the conversion of metabolically produced CO2 into bicarbonate ion (HCO 3–), which is the primary form in which CO2 is transported in the blood. Thus, erythrocytes contribute to CO2 transport in two ways—by means of its carriage on hemoglobin and its carbonic anhydrase–induced conversion to HCO3

13. Types of haemoglobin Haemoglobin A: The normal haemoglobin in adults Haemoglobin F (2 α chains and 2 γ chains : found in foetus Has higher affinity for O 2 than Hb A (importance?) Oxyhaemoglobin : Hb bound to O 2 Bright red colour Deoxyhaemoglobin : Hb without O 2 ,blue colour

14. Methaemoglobin : haemoglobin with oxidized iron Can not transport O 2 Normal concentration in the blood less than 1% of total Hb The red cells have an antioxidant system Concentration in the blood may increase on exposure to strong oxidants

15. Abnormal haemoglobins Haemoglobin S: A genetic disorder In the β chain the amino acid valine has replaced glutamic acid The changes may involve one chain or both chains Haemoglobin S is less soluble and may precipitate inside the cells This change the cell to sickle shape Sickle cells live for short time causing haemolytic anaemia : sickle cell anaemia

16. Thalasaemia Genetic disorder The number of the globin chains is less May affect the α chains or the β chains The cells live for short time causing anaemia

17. ERYTHROCYTES’ SHORT LIFE SPAN The price erythrocytes pay for their generous content of hemoglobin to the exclusion of the usual specialized intracellular machinery is a short life span. Without DNA, RNA, and ribosomes, red blood cells cannot synthesize proteins for cell repair, growth, and division or for renewing enzyme supplies. Equipped only with initial supplies synthesized before they extrude their nucleus and organelles, RBCs survive an average of only 120 days, in contrast to nerve and muscle cells, which last a person’s entire life. During its short life span of four months, each erythrocyte travels about 700 miles as it circulates through the vasculature.

18. Haemoglobin breakdown Red cells live for 120 days Destruction is mainly in the spleen Fate of haemoglobin: Globin chains are broken down to amino acids which are re-utilized . Iron is transported by protein transferrin to bone marrow and liver.

19. Porphyrin ring is converted to bilirubin Normal concentration in blood 1mg/100 ml Bilirubin is a yellow pigment, water insoluble Carried by the albumin to the liver In the liver: Converted to water soluble by conjugation with glucuronic acid Bilirubin then excreted by the liver in the bile into the small intestine

20. In the intestine: Bilirubin is converted by intestinal bacteria to urobilinogen ( stercobilinogen ) Most of urobilinogen is reabsorbed from the terminal ileum into the blood circulate back to liver and reexcreted ( enterohepatic circulation) Some excreted in urine Stercobilin excreted in faeces gives the faeces its characteristic colour

21. Jaundice Yellow colouration of the sclera and mucous membranes Results from high concentration of bilirubin ≥2mg/100ml

22. : Prehepatic jaundice: Excessive destruction of the red cells: Production of more bilirubin than the ability of the liver to excrete Eg . Malaria Spherocytosis Hepatic jaundic : Diseases of the liver so it can not conjugate and excrete normally produced bilirubin Eg Viral hepatitis

23. Post hepatic jaundice (obstructive jaundice): Obstruction of the bile ducts Eg : Gall stones tumours

24. Nutritional factors for normal red cells production Certain factors must be present in the diet in adequate amounts for the bone marrow to produce normal red cells with normal concentration of haemoglobin Examples: Iron Vitamins Proteins

25. Iron Enters in the formation of haemoglobin Total amount in the body: 4 grams mainly in the blood (65%) It binds and transport O 2 The binding is oxygenation not oxidation

26. Dietary sources: Mainly meat, vegetable, fruits Iron absorption: In the upper small intestine Only 10% of ingested iron is absorbed Factors help absorption Gastric HCL Vitamin C

27. Factors inhibit iron absorption: Phytates: in plants Daily requirement: Iron loss from the body vey small Males about 1 mg/day Females about 2 mg/day(why?)

28. To replace the loss: Males need 10 mg/day Females need 20 mg/day Pregnant ladies are routinely given iron supplements? Iron transported in blood bound to transferrin Excess iron is stored in liver in the form of ferritin

29. Iron deficiency: Inadequate intake Chronic blood loss Consequences: Iron deficiency anaemia : the red cells are small ( microcytic ) Contains less amount of haemoglobin (low MCH):pale Microcytic hypochromic anaemia

30. Folic acid: Water soluble vitamin Required for DNA synthesis Needed for blood cell formation and maturation Sources: green vegetables Dietary requirement: 100-300 microgram/day stored in the body in small amounts Higher amounts needed for pregnant women

31. Consequences of deficiency: Less number of cells Large size of cells Macrocytic anaemia Deficiency of folic acid during pregnancy may cause developmental abnormalities for the baby: neural tube defect Women are advised to take folic acid in preparation for pregnancy and during pregnancy

32. Vitamin B 12: Water soluble vitamin Sources: foods of animal origin (not found in plants) Dietary requirements: 1-2 micrograms/day Stored in the liver ~ 2-3 mg Absorption: Needs intrinsic factor secreted by the gastric parietal cells Absorption from terminal ileum

33. Deficiency of B 12 is commonly due to failure of absorption eg : Pernicious anaemia : damage of the gastric parietal cells by autoantibodies Consequences of deficiency: Macrocytic anaemia Demyelination of the neurons

34. The various causes of anemia can be grouped into six categories: Nutritional anemia( iron deficiency anemia ) Pernicious anemia( inability to absorb enough ingested vitamin B12 from the digestive tract) Aplastic anemia is caused by failure of the bone marrow to produce enough RBCs Renal anemia may result from kidney disease Hemorrhagic anemia is caused by losing a lot of blood. Hemolytic anemia (Hemolysis, the rupture of RBCs, occurs either because otherwise normal cells are induced to rupture by external factors, as in the invasion of RBCs by malaria parasites, or because the cells are defective, as in sickle cell disease

35. Polycythemia, in contrast to anemia, is characterized by too many circulating RBCs and an elevated hematocrit There are two general types of polycythemia, depending on the circumstances that trigger the excess RBC production: primary polycythemia and secondary polycythemia.