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Blood Cardiovascular review The main transport system Consists of the heart and the blood vessels through which the blood flows in the body Three types of blood vessels which blood flows: arteries, veins, and capillaries Function of the blood
- Transportation: Hormones, CO2 and wastes, O2 and nutrients
- Protection: clot formation against infection
- Regulation: PH, Body temperature, fluid volume Composition of Blood Characteristics Scarlet = O2 rich, Dark red =O2 poor More dense, viscous than water PH 7.35-7.45, temperature 38C 8% body weight (5-6 liters in males, 4-5 liters in females) Components The ONLY fluid tissues in the body Erythrocytes (RBCs) Leucocytes (WBCs) Platelets Image is blood once centrifuged Blood Plasma 55% of whole blood 90% water Composition of Plasma *TABLE Water Electrolytes Plasma proteins (Albumin, Globulins, Fibrinogen) Nonprotein nitrogenous substances Nutrients (organic) Respiratory gases Hormones
Which protein contribute most for plasma osmotic pressure? Albumin is the plasma protein that contributes most to plasma osmotic pressure (specifically colloid osmotic/oncotic pressure). As the most abundant plasma protein (60% of total protein), it maintains fluid balance by holding water inside blood vessels, preventing edema. Summary of Formed Elements ** Leukocytes Only formed element that is a complete cell Function in defense against diseases , <1% of total blood volume Granulocytes contain visible cytoplasmic granules, phagocytic Agranulocytes lack visible cytoplasmic granules Types
Formation of all blood cells; red cells, white cells, and platelets—from hematopoietic stem cells, primarily within the red bone marrow The Reticular CT contains: immature blood cells, macrophages, fat cells, reticular cells Hemocytoblasts = stem cells for all formed elements = cells become committed Erythropoiesis Erythrocyte (RBC) formation Stages explained begins when a hematopoietic stem cell descendant called a myeloid stem cell transforms into a proerythroblast proerythroblasts give rise to basophilic erythroblasts that produce huge numbers of ribosomes cells divide many times during first two phases Hemoglobin is synthesized and iron accumulates as the basophilic erythroblast transforms into polychromatic erythroblast then orthochromatic erythroblast orthochromatic ejects its nucleus = Reticulocyte (young rbc w clumps of ribosomes) because nucleus ejected, shape collapses into a biconcave shape and becomes a true erythrocyte process takes 15 days to get to reticulocyte then 2 days to finally become mature erythrocyte after ribosomes are degraded by intracellular enzymes Reticulocyte vs Erythrocyte
o Reticulocyte = immature red blood cells released from bone marrow, and contains some RNA residual = bursting of hemoglobin o Erythrocyte = fully mature red blood cells = no nucleus = biconcave = carries oxygen and carbon dioxide Hormonal Control of Erythropoiesis Erythropoietin (EPO) – Glycoprotein produced in the Kidneys There’s always some EPO circulating the blood More EPO would be released by the kidneys if a patient was hypoxic Blood oxygen levels can drop by; excessive bleeding, insufficient Hb per RBC (as in iron deficiency), reduced availability of oxygen at high altitude or during pneumonia Athletes & EPO abuse EPO ↑ hematocrit from 45% to 65%, ↑ stamina & performance ↑ blood viscosity + dehydration during race can clotting, stroke or heart failure Testosterone also enhances the Kidney’s production of EPO which could be responsible for high RBC count and hemoglobin levels we see in males Blood viscosity increases due to elevated red blood cell count (polycythemia), dehydration, high plasma protein levels (e.g., fibrinogen, immunoglobulins), reduced red blood cell flexibility, and smoking. Dietary Requirement Materials required for erythropoiesis: Amino acids, lipids, and carbohydrates Iron: available from diet o 65% of the iron in hemoglobin the rest in liver, spleen, and bone marrow o Free ions = toxic so iron is bound to proteins o Iron is stored in cells as ferritin & hemosiderin o Iron Is transported in blood by being bound to protein transferrin Vitamin B12 and folic acid are needed for DNA synthesis of rapidly dividing cells like RBC’s Life Cycle of RBC Life span = 100-120 days Old RBCs become fragile b/c they get trapped and break apart in smaller circulatory channels, especially those in the spleen. That’s why the spleen is called “RBC graveyard”
Polycythemia vera: Bone marrow cancer leading to excess RBCs Hematocrit may go as high as 80% (more RBCs dividing then usual) Treatment: therapeutic phlebotomy (blood draw) Secondary polycythemia: caused by any condition that stimulates EPO production (like low O2 levels at high altitude or medication) Abnormal excess of RBCs = high blood viscosity sluggish blood flow Platelets Cytoplasmic fragments of megakaryocytes Anucleate Blue stained outer region Purple-stained granules contain serotonin, Ca2, enzymes, ADP, & platelet-derived growth factor (PDGF) – Act in clotting process Normal 150,000-400,000 platelets/ml of blood Life span = 10 days Location of Platelets Formation Bone: megakaryocytes send cytoplasmic projections into red bone marrow capillaries (sinusoids) = breaks off into platelets Lungs: large megakaryocyte fragments or whole ones enter marrow travel to the lungs and get trapped in smaller pulmonary capillaries = fragment into more platelets accounts for more than half of the platelets in circulation Hemostasis Process of blood stoppage after blood vessel injury Requires clotting factor & substance released by platelets & injured tissues Steps:
- Vascular spasm
- Platelet plug formation
- Coaugulation (blood clotting) Vascular Clotting Vasoconstriction of vessel in response to damage Its purpose is to reduce blood loss, allowing time for steps 1 & 2 to occur Triggered by: damage to vascular smooth muscles chemicals from endothelial cells & platelets Pain receptor reflexes Most effective in smaller blood vessels Platelet Plug formation Normally conditions: o platelets don’t stick to each other or endothelial cells o nitric oxide (NO) & prostacyclin (PGI2) secreted by endothelial cells act to prevent platelet aggregation ensures that clotting only happens where and when its needed o Intact endothelial cells release nitric oxide and prostacyclin. Both chemicals prevent platelet aggregation (clumping) in undamaged tissue and restrict aggregation to the site of injury. o ** if platelets aggregated consistently without injury it would lead to pathologic thrombosis, vessel occlusion, ad infarction (stroke, heart attack) When vessels are damage: o Platelets stick to exposed collagen fibers o Von Willebrand factors help to stabilize platelet-collagen adhesion o Platelet becomes activated swells becomes spikes and stickier and then releases chemical messengers Adenosine diphosphate (ADP ) = cases more platelet aggregation by allowing them to stick to the area Serotonin & thromboxane A2 = promote vascular spasm & spasm aggregation o More platelets aggregate = release more chemicals = aggregates even more platelets = positive feedback loop Coagulation
Phase 3: Pathway to the fibrin mesh Thrombin converts soluble fibrinogen fibrin which forms fibrin polymer = causes plasma to become a gel-like trap catching formed element Thrombin (and Ca2+) activates XIII ( fibrin stabilizing factor) = crosslinks fibrin strands to fibrin mesh = structural clot further strengthens and stabilizes clot Clot formation complete in 3-6 minutes post injury Anticoagulants Substances that inhibit clotting Clot formation depends on balance between procoagulants and anticoagulants They dominate to prevent clotting (except in area of damage) Clot Retraction & Fibrinolysis Clot retraction – actin and myosin platelets contract within 30-60 mins = pulls on fibrin strands, squeezes serum from clot = draws ruptured blood vessel edges together Repair – platelet derived growth factors stimulate division of smooth muscle cells & fibroblast to rebuild wall of vascular endothelial growth factor (VEGF) = stimulates endothelial cells to multiply and restore the lining Fibrinolysis – process of clot removal after completed repair Begins within 2 days and continues serval days after until clot is dissolved Plasminogen converted to plasmin by tissuePlaminogenActivator, XIIa, thrombin Limiting Clot Growth or Formation
Fibrin
XIIa Thrombin
Plasmin
(active enzyme)
Endothelial cells
tPA
Fibrin
degrades
Plasminogen
(inactive
precursor)
Factors limiting normal clot growth Ø Mechanisms limiting clot size: Swift removal and dilution of clotting factors Inhibition of activated clotting factors Ø Clot forms thrombin, which is bound to fibrin threads, limiting size of clot Antithrombin III (plasma protein) inactivates unbound thrombin Heparin inhibits thrombin by enhancing activity of anithrombin III Factors preventing undesirable clotting Platelets not clinging to smooth, intact endothelial lining of blood vessel Endothelial cells secrete antithrombic substances: nitric oxide & prostacyclin Contact activation – clot coming in contact with blood flowing normally Hemostasis Disorder Thromboembolic conditions Ø Thrombi and emboli Thrombus = clot that develops and persists in unbroken vessel Embolus= thrombus freely floating in blood stream Embolism= embolus obstructing a vessel Ø Anticoagulant drugs: used to prevent undesirable clotting Bleeding disorders Ø Thrombocytopenia: deficient number of circulating platelets Ø Impaired liver function: unable to synthesize clotting factors Ø Hemophilia: hereditary bleeding disorders Disseminated Intravascular coagulation (DIC) Ø Widespread clotting in unbroken vessels, followed by severe bleeding o Petechiae occurs due to wide spread hemorrhage (platelet deficiency or dysfunction) Blood transfusion Cardiovascular system lowers the impacts of blood loss by:
- Reducing volume to affect blood vessels
- Making more RBCs Body compensates blood loss to a certain extend 15-30% blood loss = pale and weak 30% blood loss = potential fatal severe shock Whole blood transfusion = For substantial blood loss Packed red blood cells (PRBCs) for anemia
Rh Blood Groups 52 Rh antigens or Rh factors ( C,D,E, c, e are common) Rh+ indicates the presence of D antigen (85% Americans have Rh+) = means that their RBCs carry the D antigen; People (15%) that don’t carry D antigen = Rh- (negative) Anti-Rh antibodies do not spontaneously form in Rh- o It forms when Rh- person receives Rh+ blood, o Rh- mom is carrying a Rh+ fetus Second exposure (second birth) results in typical transfusion reaction Hemolytic disease of newborn – erythroblastosis fetalis Occurs in Rh- mom with Rh+ fetus o 1 st^ pregnancy = mom Rh- is exposed to Rh+ baby, baby born healthy, but mom makes anti-Rh antibodies o 2 nd^ pregnancy = mom’s anti-Rh crosses placenta and destroys RBCs of Rh+ baby – baby treated with prebirth transfusion and transfusions after birth RhoGAM serum that contains anti-Rh antibody can prevent Rh- from becoming sensitized Transfusion Reactions Occurs when mismatched blood is infused Problem: recipient’s plasma antibodies attack donor’s RBC RBCs first agglutinate and clog small vessels RBC’s then rupture and Hb is released into blood stream Results o Diminished oxygen-carrying capacity o Decreased blood flow to blood vessel o Kidney failure Symptoms: fever, chills, low blood pressure, rapid heartbeat, nausea, vomiting Treatment: prevent kidney damage with fluids and diuretics to wash out hemoglobin Blood Typing Blood is mixed with antibodies against common antigens o If antigen is present, clumping of RBCs will occur Blood is typed for ABO, and for Rh factor in this manner Cross matching: typing between specific donor & recipient Mix recipient’s serum with donor’s RBCs Mix donor’s serum with receipt’s RBCs Developmental Aspects of Blood
Blood cells develop from collections of mesenchymal cells called blood islands Fetal blood cells form in yolk sac, liver, and spleen The fetus forms hemoglobin F, which has higher affinity for O 2 than hemoglobin A formed after birth Red bone marrow is primary a hematopoietic area by seventh month Blood diseases of aging Chronic leukemias, anemias, clotting disorders Usually precipitated by disorders of heart, blood vessels, or immune system
Life Cycle of RBC
Blood Clotting Factors
Clot formation – Intrinsic & Extrinsic Pathways
Definitions Hematocrit (Hct) - is a blood test measuring the percentage of total blood volume composed of red blood cells. It is a key component of
Go over Blood typing and transfusion Where and what loops does homeostasis have with circulatory system.. with different organs especially kidney, and liver
