Presentation is loading. Please wait.

Presentation is loading. Please wait.

Blood Ch 19.

Similar presentations


Presentation on theme: "Blood Ch 19."— Presentation transcript:

1 Blood Ch 19

2 Blood Artery White blood cells Platelets Red blood cells

3 Function Blood Deliver O2 Remove metabolic wastes
Maintain temperature, pH, and fluid volume Protection from blood loss- platelets Prevent infection- antibodies and WBC Transport hormones

4 Blood Plasma-55% Buffy coat-<1% Formed elements-45%

5 Blood Plasma Components-55%
90% Water 8% Solutes: Proteins Albumin (60 %) Alpha and Beta Globulins Gamma Globulins fibrinogens Gas Electrolytes

6 Blood Plasma Components
Organic Nutrients Carbohydrates Amino Acids Lipids Vitamins Hormones Metabolic waste CO2 Urea

7 Buffy Coat- <1% Leukocytes Platelets

8 Formed Elements of the Blood-45%
Erythrocytes (red blood cells) Leukocytes (white blood cells) Platelets (thrombocytes)

9 Erythrocytes

10 Erythrocyte7.5m in dia ·   Anucleate- so can't reproduce; however, repro in red bone marrow ·   Hematopoiesis- production of RBC ·   Function- transport respiratory gases ·   Hemoglobin- quaternary structure, 2  chains and 2  chains ·   Lack mitochondria. Why? ·  1 RBC contains 280 million hemoglobin molecules ·   Men- 5 million cells/mm3 ·   Women- 4.5 million cells/mm3 ·   Life span days and then destroyed in spleen (RBC graveyard)

11 Hemoglobin

12 Hematopoiesis Hematopoiesis (hemopoiesis): blood cell formation
Occurs in red bone marrow of axial skeleton, girdles and proximal epiphyses of humerus and femur

13 Hematopoiesis Hemocytoblasts (hematopoietic stem cells)
Give rise to all formed elements Hormones and growth factors push the cell toward a specific pathway of blood cell development New blood cells enter blood sinusoids

14 Erythropoiesis Erythropoiesis: red blood cell production
A hemocytoblast is transformed into a proerythroblast Proerythroblasts develop into early erythroblasts

15 Erythropoiesis Phases in development
Ribosome synthesis Hemoglobin accumulation Ejection of the nucleus and formation of reticulocytes Reticulocytes then become mature erythrocytes

16 Developmental pathway
Stem cell Committed cell Developmental pathway Phase 1 Ribosome synthesis Phase 2 Hemoglobin accumulation Phase 3 Ejection of nucleus Proerythro- blast Early erythroblast Late erythroblast Reticulo- cyte Erythro- cyte Hemocytoblast Normoblast Figure 17.5

17 Regulation of Erythropoiesis
Too few RBCs leads to tissue hypoxia Too many RBCs increases blood viscosity Balance between RBC production and destruction depends on Hormonal controls Adequate supplies of iron, amino acids, and B vitamins

18 Hormonal Control of Erythropoiesis
Erythropoietin (EPO) Direct stimulus for erythropoiesis Released by the kidneys in response to hypoxia

19 Hormonal Control of Erythropoiesis
Causes of hypoxia Hemorrhage or increased RBC destruction reduces RBC numbers Insufficient hemoglobin (e.g., iron deficiency) Reduced availability of O2 (e.g., high altitudes)

20 Hormonal Control of Erythropoiesis
Effects of EPO More rapid maturation of committed bone marrow cells Increased circulating reticulocyte count in 1–2 days Testosterone also enhances EPO production, resulting in higher RBC counts in males

21 Formation & Destruction of RBCs

22

23 RBC Diseases Anemia- when blood has low O2 carrying capacity; insufficient RBC or iron deficiency. Factors that can cause anemia- exercise, B12 deficiency Polycythemia- excess of erythrocytes,  viscosity of blood; 8-11 million cells/mm3 Usually caused by cancer, tissue hypoxia, dehydration; however, naturally occurs at high elevations Blood doping- in athletesremove blood 2 days before event and then replace it; Epoetin;- banned by Olympics.

24 RBC Diseases Sickle-cell anemia-
HbS results from a change in just one of the 287 amino acids in the  chain in the globin molecule. Found in 1 out of 400 African Americans. Abnormal hemoglobin crystalizes when O2 content of blood is low, causing RBCs to become sickle-shaped. Homozygous for sickle-cell is deadly, but in malaria infested countries, the heterozygous condition is beneficial.

25 Genetics of Sickle Cell Anemia

26 Types of Leukocytes Granulocytes Neutrophils- 40-70% Eosinophils- 1-4%
4,000-11,000 cells/mm 3 Never let monkeys eat bananas Granulocytes Neutrophils % Eosinophils- 1-4% Basophils- <1% Agranulocytes Monocytes- 4-8% Lymphocytes %

27 Lymphocyte Eosinophil Basophil platelet Neutrophil Monocyte

28 eosinophil neutrophil monocyte RBC neutrophil monocyte lymphocyte lymphocyte basophil

29 ID WBC’s

30 Leukocyte Squeezing Through Capillary Wall
Diapedesis Leukocyte Squeezing Through Capillary Wall

31 WBC Diseases Mononucleosis Leukopenia Leukemias
Abnormally low WBC count—drug induced Leukemias Cancerous conditions involving WBCs Named according to the abnormal WBC clone involved Mononucleosis highly contagious viral disease caused by Epstein-Barr virus; excessive # of agranulocytes; fatigue, sore throat, recover in a few weeks

32 Platelets Small fragments of megakaryocytes
Formation is regulated by thrombopoietin Blue-staining outer region, purple granules Granules contain serotonin, Ca2+, enzymes, ADP, and platelet-derived growth factor (PDGF)

33 Developmental pathway
Stem cell Developmental pathway Hemocyto- blast Promegakaryocyte Megakaryoblast Megakaryocyte Platelets Figure 17.12

34 Hemostasis- stoppage of bleeding
Platelets: 250, ,000 cells/mm3 Tissue Damage Clotting Factors Platelet Plug

35 Hemostasis: Vessel injury 2. Vascular spasm 3. Platelet plug formation
4. Coagulation

36 Hemostasis (+ feedback)
Clotting Factors thromboplastin Prothrombin Thrombin Fibrinogen Fibrin Traps RBC & platelets Platelets release thromboplastin

37 Blood Clot RBC Platelet Fibrin thread

38 Disorders of Hemostasis
Thromboembolytic disorders: undesirable clot formation Bleeding disorders: abnormalities that prevent normal clot formation

39 Thromboembolytic Conditions
Thrombus: clot that develops and persists in an unbroken blood vessel May block circulation, leading to tissue death Embolus: a thrombus freely floating in the blood stream Pulmonary emboli impair the ability of the body to obtain oxygen Cerebral emboli can cause strokes

40 Thromboembolytic Conditions
Prevented by Aspirin Antiprostaglandin that inhibits thromboxane A2 Heparin Anticoagulant used clinically for pre- and postoperative cardiac care Warfarin Used for those prone to atrial fibrillation

41 Bleeding Disorders Thrombocytosis- too many platelets due to inflammation, infection or cancer Thrombocytopenia- too few platelets causes spontaneous bleeding due to suppression or destruction of bone marrow (e.g., malignancy, radiation) Platelet count <50,000/mm3 is diagnostic Treated with transfusion of concentrated platelets

42 Impaired liver function
Bleeding Disorders Impaired liver function Inability to synthesize procoagulants Causes include vitamin K deficiency, hepatitis, and cirrhosis Liver disease can also prevent the liver from producing bile, impairing fat and vitamin K absorption

43 Bleeding Disorders Hemophilias include several similar hereditary bleeding disorders Symptoms include prolonged bleeding, especially into joint cavities Treated with plasma transfusions and injection of missing factors

44 Hemophiliac- a sex-linked recessive trait, primarily carried by males (x chromosome)

45 Blood Types Type A Type B Type AB Type O

46 Blood Typing Blood type is based on the presence of 2 major antigens in RBC membranes-- A and B Blood type Antigen Antibody A A anti-B B B anti-A A & B AB no anti body Neither A or B O anti-A and anti-B Antigen- protein on the surface of a RBC membrane Antibody- proteins made by lymphocytes in plasma which are made in response to the presence of antigens. They attack foreign antigens, which result in clumping (agglutination)

47 ABO Blood Types b b Produces anti-B antibodies b Type A b b b b b

48 ABO Blood Types a a a Produces anti-A antibodies a Type B a a a a a a

49 ABO Blood Types Produces neither anti-A nor anti-B antibodies Type AB

50 Type O ABO Blood Types Produces both anti-A and anti-B antibodies b a

51 Rh Factor and Pregnancy
                                                                                                              RH+ indicates protein RH+ indicates protein RH- indicates no protein

52 Rh Factor and Pregnancy
Rh+ mother w/Rh- baby– no problem Rh- mother w/Rh+ baby– problem Rh- mother w/Rh- father– no problem Rh- mother w/Rh- baby-- no problem RhoGAM 28 weeks

53 Type AB- universal recipients Type O- universal donor Rh factor:
Rh factor: Rh+ 85% dominant in pop Rh- 15% recessive Blood Type Clumping Antibody A antigen A anti-A serum antibody anti-b B antigen B anti-B serum antibody anti-a AB antigen A & B anti A & B serum - O neither A or B no clumping w/ either anti A or B anti-a, anti-b

54 agglutinates with both sera)
Blood being tested Serum Anti-A Anti-B Type AB (contains agglutinogens A and B; agglutinates with both sera) RBCs Type A (contains agglutinogen A; agglutinates with anti-A) Type B (contains agglutinogen B; agglutinates with anti-B) Type O (contains no agglutinogens; does not agglutinate with either serum) Figure 17.16

55 Blood Type & Rh How Many Have It Frequency O Rh Positive 1 person in 3 37.4% Rh Negative 1 person in 15 6.6% A 35.7% 1 person in 16 6.3% B 1 person in 12 8.5% 1 person in 67 1.5% AB 1 person in 29 3.4% 1 person in 167 .6%

56 ABO Blood Types Phenotype Genotype O i i A I A I A or I A i B I B I B or I B i AB I A I B

57 Punnett square Type A and Type B cross IB i IA IAIB IAi IA IAIB IAi

58 INQUIRY What is an erythrocyte, leukocyte, and thrombocyte? What 2 things do red cells lack compared to white cells? What dietary component is needed for the production of red blood cells? The largest cells in the blood that leave the bloodstream to become macrophages are ____. In an acute infection, the white cell count would show as ______. Erythroblastosis fetalis , also known as hemolytic newborn disease, occurs in ____ mothers carrying ____ fetuses. What antigens and antibodies found on AB red cells? In a transfusion, what type blood can you give a type O person?


Download ppt "Blood Ch 19."

Similar presentations


Ads by Google