3 Blood Flashcards
Circulation of blood
O2 exchange in cap beds
Systemic: O2 released CO2 picked up
Lungs: O2 picked up, CO2 released
Whole blood (8% of total)
Plasma 55% Elements 45%
Whole blood –> Formed elements are (number per L)
Platelets 150,000-400,000
WBCs 5000-10,000
RBCs 4.8-5.4 mil
Whole blood –> WBC –>
Neutrophils 60-70% Lymphocytes 20-25% Monocytes 3-8% Eosinophils 2-4% Basophils 0.5-1.0%
Whole blood –> Blood plasma is made of
7% protein
- 5% water
- 5% other
Blood plasma –> protein
Albumins 54%
Globulins 38%
Fibrinogen 7%
Blood plasma –> other solutes (the 1%)
Lytes, nutrients, gases, reg substances, waste products
Vital stats of blood
pH 7.35 to 7.45
M 5-6L
F 4-5L
Functions of blood
TRANSPORTATION: O2, CO2, nutrients, wastes, hormones, immunoglobulins
REGULATION: cooling by heat loss, buffers -pH, constant volume
PROTECTION - clots, WBCs and immunoglobulins
Hemopoisesis
Blood cell production in red bone marrow which occurs after birth
Red bone marrow is
Highly vascularized connective tissue located in microscopic spaces between trabeculae of spongy bone in:
Bones of axial skeleton, pectoral and pelvic girdles and proximal epiphyses of the humerus and femur.
Eryhtropoietin
Regulates differentiation and proliferation of RBCS. EPO from kidneys
Thrombopoietin (liver)
Makes platelets
Cytokines
Made in red bone marrow, leukocytes, macrophages, fibroblasts and endothelial cells.
Cytokines act locally to stimulate and regulate cells involved in nonspecific defence (phagocytosis) and immune response
RBC anatomy
7 micrometers in diameter
Biconcave disc shaped
No nucleus
Hematocrit is
Percentage of RBC in blood volume
Males 40-50 (average 47)%
Females 38-46 (average 42)%
Hemoglobin values men
135-180 grams/litre or
13.5 to 18.0 g/dl
Each RBC has 280 million molecules of hemoglobin
Hemoglobin values females
120-160 grams/litres or
12.0 - 16.0 g/dl
Each RBC has 280 million molecules of hemoglobin
Hemaglobin has
Beta polypeptide chains and alpha polypeptide chains
Why is vulcan blood green
Copper is the mineral of their O2 transport protein
Function of eryhtrocytes
Transport O2 using hemoglobin
Forms of hemoglobin
Oxyhemoglobin (hemoglobin with oxygen bound, bright red)
Deoxyhemoglobin (without oxygen, dark red)
Carbaminohemoglobin (Hb-CO2)
Production of RBCs
Kidneys sense low O2, increase EPO, proerythroblasts in red bone marrow mature more quickly into reticulocytes, more reticulocytes enter circulating blood, large number of RBCs enter circulation which increases oxygen delivery to tissues and homeostasis is returned
How long do RBCs live for
120 days
Pluripotent stem cells
Pluripotent stem cells turn into myeloid (RBC/WBC) or Lymphoid (T, B and NK cells)
A progenitor cell decides which precursor cell it will turn into, the precursor then becomes the active cell
E.G Pluripotent to CFU-E (colony-forming erythrocyte, the progenitor cell) to proerythroblast to reticulocyte (which ejects nucleus) to RBC
Dietary requirements for normal RBCs
IRON for hemoglobin synthesis
B12 for cell division
FOLIC ACID for cell division
Anemia definition
Reduced O2 carrying capacity of blood, caused by reduction of RBCs or reduction of hemoglobin in RBCs
Reduced RBC number causes
Hemorrhagic - obvi a bleed dumdum
Hemolytic - rupture of RBC
Aplastic - destruction of bone marrow leads to decreased erythropoiesis
Causes of reduced Hb
Iron deficiency (most common) from lack of intake, lack of absorption, or chronic blood loss Pernicious anemia from low B12 or low intrinsic factor
Intrinsic factor
Glycoprotein produced by parietal cells of stomach necessary for B12 (cobalamin) absorption in the ileum or small intenstine
Polycythemia
Increased in number of RBC causing thick and viscous blood in response to low PaO2 (COPD, high altitudes)
Poons notes say “hematocrit increases (80%)”
Porphyria
Vampires
Rare genetic disorder causing defective Hb, pts have light sensitivity where light can blister/scar or cause rashes (photodermatitis)
Garlic consumption exacerbates condition
Causes retraction of gums which exposes roots of teeth
Leukocyte nucleus shape
Nucleated shape depends on type of WBC
Leukocyte movement
Have the ability to leave blood and vessels to move into tissue, via diapedesis
5 types of leukocytes (I think)
Eosinphil, basophil, neutrophil, monocyte, macrophage
Leukocyte ranges
4X10^9/L - 10X10^9/L
Leukocyte sites of production
Red bone marrow, lymphatic tissue nodes, nodules, spleen) and macrophages/lymphocytes at site of inflammation
Leukocytes life span/function
10 hrs (PMNs) to 15 years (lymphocytes) Function is immunite (innate and adaptive)
Phagocytosis done by
Neutrophils (PMNs) and macro
Specific immunity by
Lmyphocytes - NK cells
T cells; B cells –> plasma cells –> antibodies
Platelet formation
Fragments of cytoplasm that break off from megakaryocytes in red bone marrow and enter blood stream (thrombocytes)
Platelet function
Blood clotting (chemical mediators) Platelet plug formation
Thrombocytopenia
Condition of decreased platelets
Leads to bleeding
Thrombocytosis
Too many platelets, possibly after a spleenectomy
Hemostasis (stoppage of blood flow) requires
Vascular spasm
Platelet plug formation
Blood coagulation
Enzymes in platelet plug formation
ADP, ATP, Ca2+, serotonin, thromboxane A2 (prostaglandin)
fibrin stabilizing factor
PDGF (proliferation of vascular endothelial cells, smooth muscle fibers and fibroblasts)
Platelet plug formation
Platelets adhere to cells which activates them. They extend projections that enable them to interact with one another and liberate their vesicles (ADP, thromoboxane A2 cause vasoconstriction, ADP makes other platelets sticky) and then fibrin causes platelet plug to stick in place.
Overview of clotting
12 clotting factors and a stabilizing (#13)
4 produced in the liver
4 need calcium
4 need vitamin K
Extrinisic/intrinsic have different ways of getting to prothrombinase but then its the same
Prothrombinase
Start of common pathway
Converts prothrombin (in liver) to thrombin (an enzyme) which converts soluble fibrinogen into fibrin
Fibrinogen also made in liver
Extrinsic pathway
Thromboplastin (also called tissue factor) leaks into cells from OUTSIDE vessels (trauma).
When Ca2+ present, TF makes clotting factor X, which combines with factor V (also needs Ca2+) to form prothrombinase
Intrinsic pathway
For when endothelial cells inside vessels get injured
Lipids release phospholipids when damaged by trauma.
Contact with collagen fibres activates XII which eventually activates X which then combines with V to make prothrombinase
*phospholipids (plus Ca2+) or blood and collagen activate 10
Common pathway
Prothrombinase and Ca2+ catalyze converson of prothrombin to thrombin.
Thrombin plus Ca2+ converts fibrinogen to loose fibrin threads which are insoluble. Thrombin also activates XIII (strengthens and stabilizes fibrin threads into sturdy clot)
Plasma contains some XIII which is also released from RBCs trapped in clots
Thrombin plus V accelerate formation of prothrombin (positive feedback)
Thrombin activates platelets which reinforces their aggregation and they release phospholipids (Ca2+ make X)
Vitamin K clotting
May have deficiencies if fat absorption (lack of gallbladder function) is altered.
Responsible for II (prothrombin) VII, IX and X
Two mechanism of clot removal
Fibrinolytic system
natural inhibitors and anticoagulants
Fibrinolytic system
Dissolves clots at site of damage once damaged vessel is repaired
Plasminogen (in clot) activated by plasmin which dissolves clot (fibrinolysis)
Drugs that do this are streptokinase, t-PA (tissue plasminogen activator)
Natural inhibitors and anticoagulants
Neutralize clotting factors
Antithrombin, heparin, coumarin
Drugs that do this are coumadin and ASA
Prevents vasoconstriction and platelet aggregation
Thrombosis definition
Clot formation in intact blood vessel (thrombus)
Embolus defontion
clot that dislodges and is transported in blood
Hemophilia
Hereditary disease with a deficiency of a clotting factor, bleeding may occur spontaneously or after minor injury
ABO system
A has A antigen
Neither antigen is type O
You have antibodies for whatever antigen you DONT have
Factors are IgM so they don’t cross placenta barrier (too fat mike) and produced a few months after birth
Rh
Antigen present is Rh+ but Rh- doesn’t usually have antibodies until exposed to Rh+ blood
Rh pregnancies
Hemolytic disease of the newborn (HDN) can occur if Rh+ blood from previous transfusion or previous births has gotten into mothers blood stream. If fetus is Rh+ a shot of RhoGAM (anti-RH antibodies) to prevent this which binds to Rh in fetus and inactivate it
