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MP - Lecture 33
Blood
| Question | Answer |
|---|---|
| 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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