Blood Cells Flashcards
Types of blood cells
Erythrocytes: RBC
Thrombocytes: Platelets
Leukocytes: WBC
RBC characteristics
Diameter: 7.2 micrometers
Lifespan: 120 days
Number: 5x10^6/microL (most common)
Bi-concave shape
Platelets Characteristics
Diameter: 2-3 micrometers
Lifespan: 7-8 days
Number 250,000-400,000/microL
WBC Characteristics
Diameter: 10-18 micrometers
Lifespan: hours or years
Number: 8,000-10,000/microL
What is Hematopoiesis
Formation of blood cells derived from multipotential (pluripotential) hematopoietic stem cells.
What is Erythopoiesis
Production of RBC
What is Thrombopoiesis
Production of Platelets
What is Leukopoiesis
Production of WBC
General Pattern of Hematopoiesis
Division:
Pluripotential stem cells replicates
Differentiation:
Stem cells commits to certain blood cell type
What are Cytokines
Proteins/peptides released by a cell that affect growth/development of another cell.
What are Hematopoietic Growth Factors
Cytokines influencing blood cell precursors
Prenatal Sites of Hematopoiesis
Yolk sac: first 3 months
Liver and spleen: after 1 month and up to 9 months
Bone marrow: After 3 months and for rest of life
Postnatal sites of Hematopoiesis
Axial skeleton: for whole life, in flat bones of skull, shoulder blades, sternum, vertebrae, ribs, pelvis
Distal Long bones: ends after 30 years
(in epiphysis of long bones)
Function of RBC
Transport respiratory gasses
Advantage of Biconcave shape in RBC
Allows Maximal surface area + minimal diffusion distance
increase permeability
high flexibility: can squeeze through capillaries
What is CBC
Complete blood count: RBC, WBC, platelet, Hematocrit, [Hb]
Cell size terms for RBC
Normocytic: 7 micrometers
Microcytic: smaller than 7 micrometers
Macrocytic: larger than 7 micrometers
Cell shape terms for RBC
Sickle Cell: irregular form, cannot travel correctly
Spherocyte: non biconcave, travel is harder, less flexible
How is # of RBC balanced
Rate of production = Rate of destruction of RBC = 2x10^6/s
RBC composition
Water
Lipids, proteins, ions
33% Hb
no organelles: no nucleus, no mitochondria
Roles of Enzymes in RBC
Glycolytic Enzymes: generate energy anaerobically (without O2)
Carbonic Anhydrase: CO2 transport
Structure of Hemoglobin
Four Heme chains and a Globin center
How many molecules of O2 can bind to a Hb molecule, and how many Fe2+
4 O2 molecules and 4 Fe2+ ions
Effect of Hb on O2 solubility
O2 alone in plasma has very low solubility : 0.3 ml O2/100 ml plasma
With Hb, solubility is high: 20 ml O2/100 ml blood
Effect of O2 on blood color
Hb saturated with O2 = bright red
O2 leaves Hb = dark red
Why have Hb in RBC instead of dissolved in plasma
Plasma viscosity would increase
Plasma COP would increase
Hb would be lost via kidney (same size as Albumin which is lost through kidneys)
Factors affecting binding/release of O2 to Hb
Temperature
Ionic composition
pH
pCO2
intracellular enzyme concentration
Describe RBC precursor Proliferation
first 3-5 days, erythropoietin acts on Pluripotential hematopoietic stem cells
division and differentiation occur
cells decreases in size
during last 24h cells are Reticulocytes with a nucleus but they lose it.
Hb accumulates in cell
What is erythropoietin
Type of glycoprotein hormone/cytokine responsible for growth of RBC
Produced by Kidney
Released by stimulus from Hypoxia
Factors determining # of RBC
O2 requirements: training requires more RBC to have better O2 intake
O2 Availability: At high altitude, O2 is more scarce, so more RBC to retain more O2
what is Hypoxia
Decreased RBC count from lack of O2 in environment or additional need for O2 in tissues
Explain negative feedback of Erythropoiesis
Kidney senses Hypoxia and releases Erythropoietin
Erythropoietin reaches plasma and stimulates committed RBC precursors in Bone Marrow
RBC # increases
Oxygen levels in plasma increase
Increased O2 is detected by kidney which stops further release of erythropoietin
Hormonal effects on erythropoietin
Testosterone: increases release of erythropoietin and sensitivity of RBC precursors to Erythropoietin (males have more RBC than females)
Estrogen: opposite effect
Classification and Etiology of Anemia: Diminished Production, Abnormality at site of production (bone marrow)
Aplastic (Hypoplastic anemia)
Etiology: unknown exposure to radiation chemicals or drugs
Class. normocytic, normochromic
What happens to old RBC when they die
Recognized and removed by Macrophages in liver and spleen
What happens to RBC components when it is destroyed
Hb : Heme and Bilirubin pigment are sent to waste through liver and after to the intestinal tract
Globin : goes back into amino acid pool
Fe: Transferrin moves Fe for recycling and ferritin stores it in liver, spleen and gut
Characteristics of Bilirubin
Pigment giving yellow color to plasma
Must be at 1mg/dL concentration
If more it causes jaundice
Causes of jaundice
Excessive hemolysis: high digestion of RBC = more waste
Liver damage: less Bilirubin goes to waste
Higher concentration than 1mg/dL
Bile duct obstruction: bilirubin does not reach intestinal tract and cannot be evacuated in feces (waste is sent to blood)
What is polycythemia
Production of RBC > Destruction RBC
Ex: Ht = 70% instead of normal 45%
What is Anemia
Production of RBC < Destruction RBC
Decrease in oxygen carrying capacity of blood
Ex: Ht = 30% instead of normal 45%
Hb content is lower
Relative polycythemia
Due to decreased plasma volume
Absolute Polycythemia
May be physiological or pathological
Physiological Polycythemia
Secondary effect due to high O2 needs or lower availability
Indirect increase of RBC due to
High altitude
Increased physical activity
Chronic lung disease
Heavy smoking
Pathological Polycythemia
Direct cause of RBC increase
Primary effect due to
Tumors of cells producing EPO
Unregulated RBC Production by bone marrow
Problems of polycythemia
Increases blood viscosity
Slow blood flow leads to blood clots
Anemia : morphological
Shape: RBC are normocytic microcytic or macrocytic
Color: hypochromic hyperchromic or normochromic
Classifications of Anemia
Morphological: shape and color
+
etiologic :
diminished production,
ineffective maturation,
increased RBC destruction/ reduced survival
Classification and etiology of Anemia for diminished production from inadequate stimulus
Stimulation failure anemia
etiology: renal disease (less EPO prod.)
Class. Normocytic Normochromic
Classification and etiology of Anemia for diminished production from inadequate raw materials
Iron deficiency Anemia (most common)
etiology: increased required Fe or inadequate supply of Fe
Class. Microcytic, Hypochromic
What happens to Fe during RBC destruction
25 mg Fe/day is released
24 mg Fe/day is recycled
1 mg Fe/day is lost
Requirement difference of Fe in diet for males and females
males require 1mg Fe/day
Females during menstruations require 2 mg Fe/day since 25mg Fe/month is lost in menstruations
Classification and etiology for anemia from ineffective maturation
Maturation failure anemia
etiology: deficiencies of Vitamin B12 and folic acid (for DNA synthesis)
inadequate supply of Fe
Class. Macrocytic, Normochromic
Classification and etiology for anemia from Increased RBC destruction/reduced survival
Hemolytic Anemia, can be with jaundice
Etiology: congenital, acquired (toxins, drugs, antibodies)
Class. Abnormal RBC membrane structure: less flexible, fragile
Abnormal enzyme systems
Abnormal Hb structure = sickle cell
What is Hemorrhage
Blood loss
external or internal
What is Hematoma
accumulation of blood inside tissues
What is Hemostasis
Arrest of bleeding after vascular injury
Overlapping mechanisms of Hemostasis
Primary Hemostasis
Secondary Hemostasis
What is primary Hemostasis
Within few seconds
Platelets respond to block bleedings
Vascular response: vasoconstriction
What is secondary Hemostasis
Takes a few minutes
Clot formation
by coagulation factors activated by thrombin
Hemostasis general steps
Vasoconstriction
Platelet Plug formation
Blood Clot Formation
What is vasoconstriction
Smooth muscle cells of vessel wall contract when injury happens
opposed endothelial cells stick together, so less blood can go through
What is Platelet response
Platelet group to the site of damaged blood vessel and plug
(White Thrombus)
Platelet Structure
2-4 micrometer diameter, no nucleus
contains many granules with factors for vasoconstriction, platelet aggregation, clotting, growth,
microtubules, mitochondria, sER
live 7-10 days
produced at every site of Hematopoiesis
Hematopoiesis of Platelets
Pluripotential cells become Myeloid stem cell
Thrombopoietin from liver Differentiates into Megakaryocyte
Steps of Platelet Plug Formation (4)
Adhesion
Activation and release of Cytokines
Aggregation
Consolidation (white thrombus formed)
Platelet functions
Release vasoconstricting agents/cytokines
forma platelet plug (white thrombus)
Release clotting factors
Participate in clot retraction
Maintenance of endothelial integrity
What is clotting
After injury to blood vessel, sequential activation and interaction of a group of plasma proteins/clotting factors in presence of Ca++ and phospholipid agents
Clotting Pathways
Extrinsic pathway
Intrinsic pathway
both depend on Ca++, phospholipids and protein factors
both make prothrombinase pathway: male thrombin
Extrinsic pathway
takes 15-20 secs
Tissue phospholipids, plasma factors and Ca++ produce Thrombin
Thrombin activates fibrinogen which results in fibrin being created (Red thrombus)
Intrinsic Pathway
takes 3-6 min
damage to blood vessel activates plasma factors, Ca++ and PF3 to do prothrombinase
Thrombin is produced and it activates fibrinogen => fibrin => blood clot
Positive feedback in prothrombinase
extrinsic pathway produces small amount of thrombin
Thrombin activates intrinsic pathway and more thrombin is produced
What regulates clotting
Inhibitors of platelet adhesion
Anticoagulants (block reactions of coagulation scheme)
What is Thrombolysis
Clot lysis is the destruction of clot of prevention from adhesion
How does Clot Lysis happen
Intrinsic/extrinsic proactivators activate Plasminogen activator
Plasminogen is activated and becomes plasmin
Plasmin blocks Fibrin from becoming fragments to clot
What are inhibitors of platelet adhesion
Aspirin prevent platelets from closing blood vessels.
used to prevent heart attacks: blood clots inside vessels
Anticoagulant Drugs do what
Interfere with clot formation
Coumarin blocks synthesis of Prothrombin
Heparin inhibits thrombin activation
Thrombolytic drugs do what
Promote clot Lysis
