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MP - Lecture 33


MP – Lecture 33 Blood Cells
Types of blood cells: Erythrocytes, thrombocytes (platelets), and leukocytes
Types of leukocytes: Granulocytes (neutrophil, eosinophil, and basophil) and agranulocytes (monocytes and lymphocytes)
Blood centrifugation Important method in diagnostics, a non-invasive method that determines blood abnormalities
Hematocrit Measurement of formed elements in blood
Blood count Number of each type of blood cell per cubic millimeter
Differential count Number of each type of WBC expressed as a percentage of total WBC
Major determinant of hematocrit (and blood overall): Red blood cells (largest abundance by far)
Formed elements of blood Erythrocytes, leukocytes, and thrombocytes
Plasma proteins of blood Albumin, fibrinogen, and globulins
Serum Supernatant remainder after blood has been allowed to clot
Formed elements makes up ___% of blood volume. 45%
Plasma fluid makes up ___% of blood volume. 55%
Lower values of hematocrit indicate disorders such as: Anemia or chronic hemorrhage
Albumin (source) Liver
Albumin (function) Maintain colloid osmotic pressure and transport certain insoluble metabolites
α- and β-globulin (source) Liver
α- and β-globulin (function) Transport metal ions, protein bound lipids, and lipid-soluble vitamins
γ-globulin (source) Plasma cells
γ-globulin (function) Antibodies of immune defense
Clotting proteins (source) Liver/platelets
Clotting proteins (function) Formation of fibrin threads (blood clotting)
Complement proteins, C1 – C9 (source) Liver
Complement proteins, C1 – C9 (function) Host defense, destruction of microorganisms and initiate inflammation
Chylomicrons (source) Intestinal epithelial cells
Chylomicrons (function) Transport triglycerides to liver
Very low density proteins (source) Liver
Very low density proteins (function) Transport triglycerides from liver to body cells
Low density proteins (source) Liver
Low density proteins (function) Transport cholesterol from liver to body cells
Erythrocyte count (no./mm ³) 4.5 – 5.5 x 10^6
Erythrocyte diameter (μm) 7 – 8
Erythrocyte lifespan 120 days
Platelet count (no./mm ³) 1.5 – 4 x 10^5
Platelet diameter (μm) 2 – 5
Platelet lifespan 7 – 12 days
Leukocyte count (no./mm ³) 5 – 9 x 10^3
Neutrophil differential count 50 – 70%
Neutrophil diameter (μm) 10 – 12
Neutrophil lifespan Hours to days
Eosinophil differential count 1 – 3%
Eosinophil diameter (μm) 10 – 12
Eosinophil lifespan 8 – 12 days
Basophil differential count 0.5 – 1%
Basophil diameter (μm) 10 – 12
Basophil lifespan Very long
Lymphocyte differential count 20 – 40%
Lymphocyte diameter (μm) 7 – 12
Lymphocyte lifespan Months to years
Monocyte differential count 1 – 6%
Monocyte diameter (μm) 9 – 12
Monocyte lifespan Months
Most abundant to least abundant leukocyte Neutrophil (70%) > Lymphocyte (20%) > Monocyte (6%) > Eosinophil (3%) > Basophil (1%) [Never Let Monkeys Eat Bananas]
Basis for sickle cell anemia is: Single amino acid mutation (Val instead of Glu)
Sickle call pathology Sickle shaped RBC are more rigid and unable to easily move through small capillaries, collecting and blocking vasculature
Iron deficiency anemia (cause) Impaired Hb production due to low Fe intake, chronic blood loss, or increase Fe demand
Iron deficiency anemia (RBC morphology) Small RBC with large area of central pallor (microcytic-hypochromic anemia)
Iron deficiency anemia (clinical features) Pallor, brittle nails, oral lesions, and GE symptoms
Pernicious anemia (cause) Impaired production of RBC due to vitamin B12 deficiency because of deficient intrinsic factor synthesis
Pernicious anemia (RBC morphology) Large, abnormal RBC precursors in bone marrow and blood (megaloblastic anemia)
Pernicious anemia (clinical features) Weakness, bilateral tingling and numbness in hands and feet, red painful tongue, and sub-acute degeneration of posterior and lateral spinal columns
Sickle cell anemia (cause) Production of abnormal HbS cells due to β-chain mutation at one amino acid (autosomal recessive with heterozygotes usually asymptomatic)
Sickle cell anemia (RBC morphology) Fragile misshaped (sickle) RBCs with decreased lifetime
Sickle cell anemia (clinical features) Join and abdominal pain, increased bilirubin levels, lower extremity ulcers, and increased risk of Salmonella osteomyelitis
Hereditary spherocytosis (cause) Mutation in spectrin causing defective RBC membrane (autosomal dominant)
Hereditary spherocytosis (RBC morphology) Fragile round hyperchromic RBC sensitive to lysis
Hereditary spherocytosis (clinical features) Jaundice and splenomegaly
β-thalassemia (cause) Various mutations in β-chain of Hb (autosomal recessive with heterozygotes mild or asymptomatic)
β-thalassemia (RBC morphology) Small pale RBC with decreased lifetime
β-thalassemia (clinical features) Splenomegaly and bone deformities
Function of platelets Physically plug damaged vasculature, secrete vasculature repair factors, and blood clotting
Platelet discoid morphology maintained by: Actin filaments encircling periphery of platelet
Granulomere Inner portion of platelet containing various types of granules, lysozomes, clotting proteins, and glycogen
Blood clotting process 1) Platelets produce thromboplastin, 2) Thromboplastin converts prothrombin to thrombin, 3) Thrombin converts fibrinogen to fibrin, 4) Fibrin monomers polymerize to form fibrin threads, 5) Fibrin threads trap platelets and RBCs to form clot
Thrombocytopenia Reduced number of platelets, normal breakage of vasculature resulting in discoloration
T cells (primary function) Destruction of cells bearing intracellular antigens (T-cytotoxic) and secretion of cytokines that regulate intensity and duration of immune responses (T-helper)
B cells (primary function) Clearance of extracellular antigens by secreted antibodies and presenting exogenous antigens to T-helper cells
Natural killer cells (primary function) Antigen-specific and nonspecific cytotoxicity for tumor cells and virus-infected cells
Neutrophils (primary function) Release inflammatory mediators and nonspecific phagocytosis and destruction of bacteria
Eosinophils (primary function) Defense against parasitic organism
Basophils (primary function) Release of mediators in certain allergic reactions
Mast cells (primary function) Release mediators in certain allergic reactions
Macrophages (primary function) Nonspecific phagocytosis of exogenous antigens, dead host cells, cellular debris, and bacteria, and antigen presentation for T-helper cells
Dendritic cells (primary function) Antigen presentation (efficient) for T-helper cells
Neutrophil (nuclear shape); 3 to 5 lobes
Neutrophil (granules) Many azurophilic granules, small dusty rose granules
Neutrophil (phagocytic activity) High bacterial
Eosinophil (nuclear shape) Bi-lobed
Eosinophil (granules) Few azurophilic granules, large red/orange specific granules
Eosinophil (phagocytic activity) Moderate, antigen-antibody complex
Basophil (nuclear shape) Irregular
Basophil (granules) Few azurophilic, large dark blue to black specific granules
Basophil (phagocytic activity) None
Neutrophil phagocytosis forms: H2O2
Eosinophil’s specific granules are: Lysosomes with crystalline core
Basophil degranulation induced by: Allergens, releasing histamine
Inefficient phagocytosis by neutrophils can lead to: Re-releasing bacteria and pathogens upon neutrophil death
Response to allergens is by: Basophils and mast cells
Mechanism of immediate type I hypersensitivity reactions 1)Secreted IgE produced after first exposure to allergen binds to mast cells and basophils, 2) Subsequent exposure to allergen, receptor-bound IgE induces degranulation to effect various processes
Histamine and serotonin (hypersensitivity reaction) Increase vascular permeability and smooth muscle contraction
Chemotactic factors (hypersensitivity release reaction) Increase attraction of eosinophils and neutrophils
Platelet-activating factor (hypersensitivity release reaction) Increase platelet aggregation and degranulation, and increase pulmonary smooth muscle contraction
Heparin (hypersensitivity release reaction) Decrease blood clotting
Degranulation releases various factors inducing: Localized allergic symptoms or systemic anaphylaxis
After release reaction, mast cells: Synthesize and release prostaglandins and leukotrienes to mediate late-phase reaction
Prostaglandin (hypersensitivity late-phase reaction) Increase vasodilation and pulmonary smooth muscle contraction
Leukotrienes (hypersensitivity late-phase reaction) Slow reactive substance of anaphylaxis, increases bronchoconstriction, mucus production, and vascular permeability
Phagocytosis by macrophage Engulfed material is degraded by lysozymes with most products exocytosed, but antigenic peptides that interact with MHCII molecules move to cell surface for T-helper cells
Created by: emyang



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