Blood Flashcards
Blood Functions
Transport
Acid-Base Balance
Protective
Plasma composition
Ions, nutrients, waste, respiratory gases, proteins
Separating Plasma Proteins
- Differential precipitation by salts
- Sedimentation in ultracentrifuge
- Electrophoretic mobility
- Immunological characteristics
Electrophoresis
Fractional method where particles move through gel on voltage gradient
a. molecular weight
b. charges of particles
Plasma Proteins
Made in liver
- Albumin
- Fibrinogen
- Golublins a, b
Lymphoid tissue
- Globulin y
Role of Plasma Proteins
Determines distribution of fluid between plasma + ISF compartments by controlling transcapillary movement
Colloidal Osmotic Pressure
Plasma proteins are not diffusible through the capillary wall so exert pressure to move fluid in
COP increases = water –> plasma
COP decreases = water –> ISF
Bulk flow
Change in hydrostatic pressure moving molecules
Starling Forces
Filtration
Osmotic Flow
Filtration
Pushes fluid out of capillaries
Colloidal Osmotic Pressure
Plasma proteins pull fluid into capillaries
Influences on COP
Albumin is the most common plasma protein = small and oval size makes COP rise
- Concentration in the plasma
- Molecular weight of protein
Factors in Transcapillary Dynamics
- Hydrostatic pressure
- COP
- Capillary permeability
- Lymphatic drainage
Edema
Accumulation of fluid in Interstitial spaces
Causes of Edema
Increased hydrostatic pressure
Lowered COP
Increased capillary permeability
Obstruction of lymphatic drainage
Role of Plasma Proteins
- Distribution between ISF and plasma
- Viscosity of plasma
- Buffering power of plasma (pH = 7.4)
Hematopoiesis
Production of blood cells
Erythropoiesis
Production of RBCs
Thrombopoiesis
Production of platelets
Leukopoiesis
Production of WBCs
Sites of Hematopoiesis
Prenatal
Flat bones of skull
Shoulder blades
Pelvis
Vertebrae
Sternum
Ribs
Epiphyseal site in long bones
Hematopoiesis Steps
Multipotential Stem Cells –> Committed Stem Cells –> Blood Cells
Cytokines promote growth
HGFs = proliferation + differentiation of blood cell precursors
Erythrocytes
Facilitate transport of respiratory gases between lungs
Erythrocyte Properties
Shape: Biconcave disk
No organelles
Lots of hemoglobin
Advantage of Biconcave Disk
- Maximal surface area (efficient diffusion)
- Lots of flexibility (squeeze through narrow capillaries)
Hemoglobin
Found in erythrocytes
Can bind to 4 O2 molecules
Oxygen links to polypeptide chains of heme and iron
Hb functions
- Transport O2 and CO2
- Act as buffer
Why is Hb inside RBCs and not in plasma?
i) Plasma viscosity
ii) Plasma COP
iii) Less loss via kidney
Factors influencing ability of Hb to bind to O2
- Temperature
- Ionic composition
- pH
- Intracellular enzyme concentration
RBC Precursors Differentiation
Start with Stem Cells –> Reticulocytes –> RBCs
1. Decrease in size
2. Lose nucleus
3. Accumulation of Hb
Erythropoietin
Glycoprotein hormone/ cytokine produced by kidney
Stimulus is Hypoxia
Erythropoiesis Cycle
- O2 supply decreases
- Increased release of erythropoietin
- Erythropoietin goes in plasma
- Bone marrow stimulated
- RBCs produced
- Oxygen levels increase
Testosterone
Increases release of erythropoietin
Increases sensitivity of RBC precursors
Estrogen has opposite effect
Destruction of RBCs
Life span: 120 days
Macrophages recognize old RBCs and engulf them
Jaundice
- Excessive Hemolysis
- Hepatic Damage
- Bile Duct Obstruction
Polycythemia
Relative: due to decreased plasma volume
Absolute: Physiological or Pathological
Increases blood viscosity = prone to blood clots
Physiological Causes of Polycythemia
- High altitudes
- Increased exercise
- Lung diseases (emphysema)
- Heavy smoking (high CO in blood)
Pathological Causes of Polycythemia
Tumours cause unregulated production of RBCs in bone marrow
Due to genetic mutation
Anemia
Decrease in oxygen carrying capacity of blood
Morphologic Description of cells
- Microcytic
- Normocytic
- Macrocytic
- Normochromic
- Hypochromic
Smaller cells (< 80)
Normal size cells (80 - 94)
Larger cells (> 94)
Normal amount of Hb
Decreased levels of Hb in RBCs
Etiological Classifications of Anemia
Diminished production
Ineffective Maturation
Survival Disorders
Diminished production Anemia
Aplastic anemia: caused by outside factor (radiation)
Stimulation failure: renal disease
Iron deficiency: not enough iron = less O2 carried
Ineffective Maturation
Deficiency in B12 or Folic Acid
- Intrinsic factor deficiency = pernicious anemia
Survival Disorders
Congenital: abnormal membrane structure, missing enzymes, abnormal Hb structure
Acquired: toxins, drugs, antibodies
Why do women have less RBCs
Lower muscle mass = don’t need as much oxygen
Menstrual loses
Hemostasis
Arrest of bleeding following vascular injury
a) Vasoconstriction
b) Platelet Plug
c) Clotting
Vasoconstriction
i) Nervous reflex
ii) Myogenic response, smooth muscle in vessel wall contracts
iii) Chemical vasoconstrictors
Platelet Response
- Adhesion
- Activation + release of cytokines
- Aggregation
- Consolidation
Platelet functions
Release vasoconstriction agents
Form platelet plug
Release clotting factors
Clot retraction
Stabilize endothelial integrity
Platelets
Bind to damaged area by collagen
Adhesion to cell membrane
Aggregation = change shape once connected to collagen
Thrombin promotes platelet plug
Prolonged Bleeding
Failure of blood vessel to constrict
Could be due to platelet deficiencies
a) Numerical: have less than normal
b) Functional: can’t perform their role
Aspirin
Inhibits the synthesis and release of TXA2
- No constriction
Clotting
Initiated by injury to blood vessel wall
Interaction of plasma proteins and clotting factors (enzymes or co-factors)
Presence of Ca2+ and phospholipid agents
Required Factors of Coagulation
Ca2+
Phospholipids
Protein plasma proteins
Clotting Factor Deficiencies
Congenital
Acquired: liver disease or vitamin K deficiency (involved in synthesis of prothrombin)
Control of coagulation
inhibitors and coagulants block reactions in pathway scheme
Clot Lysis (Fibrinolysis)
Plasminogen –> plasmin –> breaks fibrin into fibrin fragments
Inhibitors of platelet adhesion
Aspirin
Anticoagulant drugs
Coumadin: blocks synthesis of functional prothrombin
Heparin: promotes inhibition of thrombin activation and action
Thrombolytic drugs
Promote clot lysis
