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About This Presentation

Blood Anatomy and Physiology


Slide Content

BLOOD ANATOMY AND PHYSIOLOGY

BLOOD Connective tissue Formed elements- Erythrocytes (Red blood cells) Leukocytes (White blood cells) Thrombocytes (Platelets)

BLOOD Extracellular matrix Plasma

FUNCTIONS OF BLOOD Transportation: Primary function of blood is to delivery oxygen and nutrients to and remove wastes from body cells Defense: Many types of WBCs protect the body from external threats Platelets help to protect the body from further fluid loss

CHARACTERISTICS OF BLOOD Freshly oxygenated blood is bright red Deoxygenated blood is darker red Color is dependent on hemoglobin Viscous (5x more than water) Sticky to touch Normal temp is about 100.4F pH is about 7.4

CHARACTERISTICS OF BLOOD Males: average 5-6 liters of blood Females: average 4-5 liters of blood

BLOOD PLASMA Composed primarily of water (92%) Straw colored 7% is made of plasma proteins

BLOOD PLASMA Albumin - most abundant Manufactured by the liver Plays a role in maintaining osmotic pressure and water balance between blood and tissues

BLOOD PLASMA Globulins- most are involved with the immune system Fibrinogen - involved with clotting

BLOOD PLASMA Other plasma solutes (1% of plasma) Electrolytes (sodium, potassium, calcium) Dissolved gases (oxygen, carbon dioxide, nitrogen) Various nutrients (vitamins, lipids, glucose, amino acids, metabolic wastes)

PRODUCTION OF THE FORMED ELEMENTS Lifespan is very brief Body must form new blood cells and platelets quickly and continuously When you donate blood- plasma is replaced within 24 hours, but takes 4-6 weeks to replace blood cells

PRODUCTION OF THE FORMED ELEMENTS Hematopoiesis - production of the blood cells After birth, most hematopoiesis occurs in the red bone marrow Red bone marrow- connective tissue within the spaces of cancellous bone

PRODUCTION OF THE FORMED ELEMENTS Extramedullary hematopoiesis- hematopoiesis outside of the medullary cavity of adult bones; liver and spleen have the ability to generate the formed elements Occurs in situations like bone cancer where the marrow is destroyed, causing hematopoiesis to fail

PRODUCTION OF THE FORMED ELEMENTS All formed elements arise from stem cells of the red bone marrow Hemopoietic stem cell (hemocytoblast)- all the formed elements of blood originate from this specific type of cell

HEMOPOIETIC GROWTH FACTORS Erythropoietin (EPO)- glycoprotein hormone secreted by the kidneys in response to low oxygen levels Prompts production of red blood cells Why might athletes use synthetic EPO as a performance enhancer? Thrombopoietin- produced by the liver and kidneys, triggers the development of megakaryocytes into platelets

HEMOPOIETIC GROWTH FACTORS

BONE MARROW ASPIRATION Bone marrow aspiration (biopsy)- a diagnostic test of a sample of red bone marrow

BONE MARROW TRANSPLANT Bone marrow transplant- donor’s healthy bone marrow (and its stem cells) replaces the faulty bone marrow of a patient First necessary to destroy the patient’s own diseased marrow through radiation or chemotherapy

ERYTHROCYTES- RED BLOOD CELLS Most common formed element Males - about 5.4 million erythrocytes per microliter of blood Females- about 4.8 million erythrocytes per microliter of blood

ERYTHROCYTES Primary function of erythrocytes: Pick up inhaled oxygen from the lungs and transport it to the body’s tissues Pick up some carbon dioxide waste at the tissues and transport it to the lungs for exhalation

ERYTHROCYTES- SHAPE AND STRUCTURE As erythrocyte matures in red bone marrow, loses its nucleus and most other organelles Reticulocyte - immature erythrocyte Usually 1-2% of the erythrocyte count Rely on anaerobic respiration- they don’t consume oxygen that they’re transporting

ERYTHROCYTE- SHAPE AND STRUCTURE Biconcave disks More interior space for the presence of hemoglobin Provides more surface area for gas exchange

HEMOGLOBIN Large molecule made up of protein and iron Four folded chains of a protein called globin Red pigment molecule called heme (contains an ion of iron) Each iron ion in heme can bind to one oxygen Each hemoglobin can transport 4 oxygen

HEMOGLOBIN An individual erythrocyte may contain about 300 million hemoglobin molecules So…one erythrocyte can transport up to 1.2 billion oxygen molecules

HEMATOCRIT Measures the percentage of erythrocytes in a blood sample Males 42-52% Females 37-47% Performed by spinning the blood sample in a centrifuge Heavier elements separate from the lighter, liquid plasma Erythrocytes settle at the bottom

HEMATOCRIT Volume of erythrocytes after centrifugation is also called packed cell volume (PCV) Typically, about 45% of a sample is erythrocytes Buffy coat – leukocytes and platelets in a centrifuged sample

OXYGENATION TO TISSUES Percent saturation- hemoglobin sites occupies by oxygen in a patient’s blood Normal pulse oximeter readings range 95-100%

ERYTHROCYTES Normal life span of an erythrocyte- 120 days Worn out cells removed by phagocytic cell called macrophage (located primarily in liver, spleen, bone marrow)

LEUKOCYTES- WHITE BLOOD CELLS Major component of the body’s defenses against disease Protect the body against invading microorganisms and body cells with mutated DNA, and they clean up debris Far less numerous than RBCs

LEUKOCYTES True cells- possess a nucleus and organelles Normal value 4,000-11,000 per microliter of blood Life span ranges from few days to few hours

LEUKOCYTES- MOVEMENT Erythrocytes stay within the blood vessels, but leukocytes can move! They move to tissues to perform their defensive functions Blood is just a highway for leukocytes to get where they need to go

LEUKOCYTES- MOVEMENT Diapedesis - process by which WBCs squeeze through adjacent cells in a blood vessel to perform their defensive functions

LEUKOCYTES- MOVEMENT How do the leukocytes know where they need to go? Chemotaxis- injured or infected cells emit a “911” call which attracts more leukocytes to the site

CLASSIFICATION OF LEUKOCYTES Two Groups: Granulocytes Agranulocytes

CLASSIFICATION OF LEUKOCYTES-GRANULOCYTES Neutrophils 50-70% of total WBCs Rapid responders to infection site Phagocytic to bacteria

CLASSIFICATION OF LEUKOCYTES Eosinophils Capable of phagocytosis About 2-4% of WBCs Respond to allergies, parasitic worm infections, and some autoimmune diseases

CLASSIFICATION OF LEUKOCYTES Basophils Least common WBCs Intensify the inflammatory response Granules release histamine- contribute to itch and inflammation And heparin- opposes blood clotting

CLASSIFICATION OF LEUKOCYTES -AGRANULOCYTES Lymphocytes Only formed element of blood that arises from lymphoid stem cells Form initially in bone marrow but further development occurs in lymphatic tissue Second most common type of leukocyte

CLASSIFICATION OF LEUKOCYTES T lymphocytes/B lymphocytes play prominent roles in defending the body against specific pathogens High counts characteristic of viral infections as well as some types of cancer

CLASSIFICATION OF LEUKOCYTES Monocytes Originate from myeloid stem cells 2-8% of total WBCs Macrophages are monocytes that have left the circulation Phagocytize debris, foreign particles, old erythrocytes

NEVER LET MONKEYS EAT BANANAS- MOST TO LEAST WBCS N……Neutrophils L…..Lymphocytes M….Monocytes E….Eosinophils B….Basophils

PLATELETS Not actually a cell but rather a fragment of the cytoplasm of a cell called a megakaryocyte 150,000-450,000 per microliter of blood Critical to hemostasis

HEMOSTASIS Three major steps to the process: 1) Vascular spasm 2) Formation of a platelet plug 3) Coagulation Blood usually clots in 3-6 minutes

HEMOSTASIS- VASCULAR SPASM When a vessel is punctured, or the wall is damaged, vascular spasm occur Smooth muscle in the walls of the vessel contracts dramatically Believed to be triggered by chemicals called endothelins Lasts about 30 mins (can last up to 4 hrs)

HEMOSTASIS- FORMATION OF THE PLATELET PLUG Platelets normally float free in the plasma Now, they encounter the rupture area Begin to clump together Become spiked and sticky Assisted by glycoprotein called vonWillebrand factor

HEMOSTASIS- FORMATION OF THE PLATELET PLUG Helps to stabilize the growing platelet plug Platelets release chemicals that help with homeostasis including serotonin Platelet plug can temporarily seal a small opening in a blood vessel Buys the body more time while more durable repairs are being made

HEMOSTASIS- COAGULATION CASCADE Coagulation - formation of a blood clot Chemicals called clotting factors prompt reactions that activate still more coagulation factors Damaged tissue and platelets release enzyme thromboplastin Thromboplastin + (required) Ca+ ions and proteins form prothrombin activator

HEMOSTASIS- COAGULATION CASCADE Prothrombin activator (requires Ca+ ions) converts Prothrombin to thrombin Prothrombin is a plasma protein produced by the liver Thrombin catalyzes the reaction that fragments fibrinogen to fibrin

HEMOSTASIS- COAGULATION CASCADE Fibrinogen - soluble plasma protein that is converted to insoluble fibrin Fibrin - an insoluble protein that forms long threads like a net This is what forms the clot

CLOTTING FACTORS Multiple clotting factors are involved in the coagulation process Most are formed in the liver Vitamin K is required for the synthesis of many of these Calcium is also needed for coagulation

HEMOSTASIS Thrombus- unwanted blood clot, can stay stationary or break free and travel Embolus - blood clot that breaks free and travels Fibrinolysis - gradual degradation of the clot

HEMOSTASIS Stabilized clot is acted upon by contractile proteins within the platelets As proteins contract, they pull on the fibrin threads, which brings together the edges of the clot tighter together Also wrings out the clot a small amount of fluid called serum (blood plasma without clotting factors)

BLOOD TYPING Blood transfusions in humans were very risky procedures until the discovery of the major human blood groups by Karl Landsteiner Austrian physician Discovered in 1900

BLOOD TYPING Antigens- substances that the body does not recognize as belonging to the “self” Trigger a defensive response from the leukocytes of the immune system

BLOOD TYPING Agglutination - mismatched red blood cells clump together (different than clotting!) These clumps of RBCs block small blood vessels and deprive the body of oxygen As the clumps are degraded (hemolysis)

ABO BLOOD TYPES

ABO BLOOD GROUPS Two antigens A and B Glycoproteins Type A- antigen A on RBC membrane Type B- antigen B on RBC membrane Type AB- antigens A and B on RBC membrane Type O- neither A or B antigen ABO blood types are genetically determined

RH FACTOR Rh blood group is classified according to the presence or absence of a second erythrocyte antigen identified as Rh Antigen D is clinically significant Rh has two alleles (+is dominant) 85% of Americans are Rh+

RH FACTOR- PUNNETT SQUARES + + - +- +- - +- +- + - + ++ +- - +- --

ABO BLOOD GROUPS Universal recipient AB+ Universal donor O-

ABO BLOOD GROUPS Blood type is genetically determined A and B antigen molecules on the surface of RBCs are produced by two different enzymes

ABO BLOOD GROUPS These two enzymes are encoded by different versions, or alleles, of the same gene: A and B The A and B alleles code for enzymes that produce the type A and B antigens A 3rd version of this gene, the O allele codes for a protein that isn’t functional and doesn’t produce surface molecules

BLOOD GENOTYPES AND PHENOTYPES

PUNNETT SQUARES A woman with type A blood (genotype AA) is married to a man with type B blood (genotype BB) What blood types might their future children have? A A B AB AB B AB AB

PUNNETT SQUARES A man has type B blood (genotype BO), and his wife has type A blood (genotype AO) What blood types might their future kids have? A O B AB BO O AO OO

Disorders of the blood

ERYTHROBLASTOSIS FETALIS Occurs in Rh – mothers with the birth of an Rh + baby Problems are rare in first pregnancy, since the baby’s Rh+ cells rarely cross the placenta But, during or immediately after birth, the Rh- mother can be exposed to the baby’s Rh + cells

ERYTHROBLASTOSIS FETALIS After exposure, the mother’s immune system begins to generate anti-Rh antibodies If the mother conceives another Rh+ baby (second pregnancy) the Rh antibodies she has produced can cross the placenta into the fetal bloodstream and destroy the fetal RBCs

ERYTHROBLASTOSIS FETALIS May cause anemia in mild cases, but can be so severe that without treatment, the fetus may die in the womb

ERYTHROBLASTOSIS FETALIS RhoGAM is a drug that can temporarily prevent the development of Rh antibodies in the Rh- mother

ERYTHROBLASTOSIS FETALIS Will keep fetus from developing this serious disease RhoGAM antibodies destroy any fetal Rh+ erythrocytes that may cross the placental border

ERYTHROBLASTOSIS FETALIS RhoGAM is normally given to Rh- mothers during weeks 26-28 of pregnancy and within 72 hours of birth Very effective in preventing this disease

ERYTHROBLASTOSIS FETALIS If mom is Rh+…not a problem If dad is Rh-…not a problem But if mom is Rh-, doctors will still treat Rh- mom with RhoGAM because they will assume that the dad is Rh+ to be on the safe side

DISORDERS OF THE ERYTHROCYTES Hypoxemia- low blood oxygen Normal range 95-100% Polycythemia- hematocrit (volume % of RBCs) is elevated Polycythemia vera – rare blood cancer in which the bone marrow produces too many erythrocytes

DISORDERS OF THE ERYTHROCYTES Anemia- general term, number of RBCs or hemoglobin is deficient Three major types: Caused by blood loss Caused by faulty or decreased RBC production Caused by excessive destruction of RBCs

DISORDERS OF THE ERYTHROCYTES Iron deficiency anemia- most common type Amount of available iron is insufficient to allow production of sufficient heme Common when there is a deficiency of iron in the diet (teens, children, vegans, vegetarians) Can also be caused by either an inability to absorb and transport iron, or slow chronic bleeding

DISORDERS OF THE ERYTHROCYTES Sickle cell anemia- Genetic disorder Caused by production of an abnormal type of hemoglobin (hemoglobin S) Causes erythrocytes to be sickle shaped

DISORDERS OF THE ERYTHROCYTES Abnormally shaped cells can become lodged in narrow capillaries Blocking blood flow to tissues Can cause joint issues, delayed growth, blindness, strokes

DISORDERS OF THE ERYTHROCYTES SS- normal, no disease Ss- carrier, may pass disease on to offspring ss- disease

DISORDERS OF THE ERYTHROCYTES Deep vein thrombosis (DVT)- blood clot forms in one of the veins, usually legs Swelling, redness, warmth Sometimes no symptoms Never rub a suspected DVT!

DISORDERS OF THE ERYTHROCYTES Pulmonary Embolism- blood clot travels and gets wedged in an artery of the lung Often comes from a DVT

DISORDERS OF THE ERYTHROCYTES Shortness of breath, chest pain If not treated promptly, made lead to sudden death Need to break up clot with anticoagulants

DISORDERS OF THE ERYTHROCYTES Carbon monoxide poisoning- CO is a colorless, odorless gas found in car exhaust fumes and tobacco smoke Combines with hemoglobin just like oxygen but does not let go

DISORDERS OF THE ERYTHROCYTES Hemoglobin molecules are not available to carry oxygen to the tissues and the human suffocates. Carbon monoxide poisoning is often fatal but can be treated by giving the patient pure oxygen that slowly replaces the CO

DISORDERS OF THE ERYTHROCYTES

DISORDERS OF THE LEUKOCYTES Leukocytosis - excessive production of leukocytes Sometimes due to infection In other cases, cells are immature and are ineffective

DISORDERS OF THE LEUKOCYTES Leukopenia- too few leukocytes are produced

DISORDERS OF THE LEUKOCYTES Leukemia- cancer involving an abundance of WBCs Chronic leukemia- mature leukocytes accumulate and fail to die Acute leukemia- overproduction of young, immature leukocytes Cells do not function properly

DISORDERS OF THE LEUKOCYTES LEUKEMIA

DISORDERS OF THE LEUKOCYTES

DISORDERS OF THE LEUKOCYTES Lymphoma - cancer in which masses of malignant T and/or B lymphocytes collect in lymph nodes, the spleen, the liver and other tissues Malignant leukocytes don’t function properly Vulnerable to infection

DISORDERS OF THE LEUKOCYTES

DISORDERS OF THE PLATELETS Thrombocytosis - condition in which there are too many platelets May trigger formation of unwanted blood clots

DISORDERS OF THE PLATELETS Thrombocytopenia- insufficient number of platelets Blood may not clot properly Excessive bleeding may result

DISORDERS OF THE PLATELETS Petechiae- small red or purple spots on the skin Caused by a minor bleed from broken capillary blood vessels

HEMOPHILIA- “BLEEDER’S DISEASE” Hemophilia A- most common 80% of cases Unable to make enough factor VIII Hemophilia B- 20% of cases Deficiency of factor IX

HEMOPHILIA Missing a clotting factor, blood doesn’t clot properly Caused by an inherited X linked recessive trait, with the defective gene located on the X chromosome

HEMOPHILIA Females have two X chromosomes, so if the factor VIII gene (Hemophilia A) on one chromosome doesn’t work, the gene on the other chromosome can do the job of making enough factor VIII Males only have one X chromosome

HEMOPHILIA FEMALES XHXH- normal female, no disease XHXh- carrier, can pass disease on to her offspring XhXh- female has disease

HEMOPHILIA MALES XHY- normal male, no disease XhY- male with disease MALES will NOT be carriers

PUNNETT SQUARES A normal woman (XHXH) and her husband who has hemophilia (XhY) are considering having children. They would like to know the odds of their sons and daughters having hemophilia. What would you tell them? XH XH Xh XHXh XHXh Y XHY XHY

PUNNETT SQUARES If a female is a carrier for hemophilia (XHXh) and is married to a man with hemophilia (XhY), what is the probability that she will have a daughter with hemophilia? XH Xh Xh XHXh XhXh Y XHY XhY

DISORDERS OF THE PLATELETS Von Willebrand disease- missing von Willebrand factor (helps platelets clump together)
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