Hematology Flashcards
Ave no of RBCs per cubic mm
Ave of hemoglobin
- 2 Men
- 7 Women
15g per 100ml
Each gram of hemoglobin is capable of combining with approximatelt
1.34 mm of oxygen
Multiple proteins that promote growth
Growth inducers
Causes one type of stem cell to differentiate one or more steps toward the final type of adult cell
Differentiation inducers
Factors that affect inducer production in Rbc
Exposure of body to low level of oxygen in a prolonged period of time
Differentiation
Production of greatly increased erythrocytes
Principal factor that stimulates RBC production
EPO
90% of EPO formed in
kidneys and the rest liver
Cells that produce EPO
Fibroblast like interstitial cells surrounding tubules in renal cortex and outer medulla
Renal epithelial cell
Essential to synthesis of DNA
Lack of both result in maturarion failure
Deficiency -> megaloblast
Vitamin B12
Folic acid
Inability to absorb Vitamin B12 from GIT
Because of atrophic gastric mucosa
Pernicious anemia
Parietal cell secrete
Glycoprotein called IF binding tightly with B12 and protects vitamin from digestion by GI enzymes
Hemoglobin formation starts in
proerythroblast stage -> reticulocyte stage
Bind together loosely to form entire Hgb molecule
Four hgb molecules
Most important feature ability to bind loosely and reversibly oxygen
total average quantity of iron
4-5 grams
65% hgb
4-% myoglobin
1% various heme
Intestinal enterocyte iron absorption
1-2mg/day
Iron is stored i
Liver parenchyma as iron-ferritin complex
Secretion during infection or inflammation
Hepcidin
After significant hemorrhage
Replaces the plasma 1-3 days
3-4 weeks for RBCs to return to normal levels
Blood loss anemia
Non functioning bone marrow
Exposure to gamma radiation, toxic chemicals (insecticide, benzene), autoimmune disorders SLE
blood transfusion or bone marrow transplants
Aplastic anemia
Lack of B12, folic acid, intrinsic factor
Slow reproduction of erythrocytes in bone marrow
Large odd shaped cells megaloblast
Megalobastic anemia
fragile rbc that rupture as they pass capillary
Number is normal but life span is short
Sickle cell anemia by abnormal composition of globin chain of hemoglobin HgbS precipitating in long crystals
Hemolytic anemia
Number of RBCs in circulation inc due to hypoxia or genetic aberation
Polcythemia
Physiologic - living in high altitude, cardiac failure
Genetic aberration - HCT 60-70 JAK 2 mutation, increased viscosity of blood
Life span of lymphocyte
Months to years
Mobile units of protective system of the body
Formed in BM and lymph tissue and transported in the blood to areas of inflammation
Five types in the blood
Leukocytes
Protect body via process of phagocytosis
Granulocyte
Monocytep
Granulocyte and monocytes are products of
Myelocytic lineage
Lymphocytes are products of
lymphocytic lineage
Life span of granulocyte
4-5 h in circulating blood
4-5d in tissues
Monocyte life span
10-12 h before they enter tissues and become macrophages
Enter cells and become tissue mac via
Neutrophils
Macrophages
Amoeboid chemotaxis
Factors that inc chance of phagocytosis
Rough surface
No protective protein coat
Foreign particle
Phagocytosis is
highly selective
First line of defense against invasion
Macrophages
Second line of defense in inflamed tissue
Neutrophil
neutrophilia
Third wave of inflamed tissue
Third line of defense
Second macrophage invasion
Predominant leukocyte
Fourth line of defense
Greatly increased production of
Granulocytes and monocytes
Factors involved in feedback control of mac and neutrophil response
Formed by mac and T cells
TNF IL-1 GMCSF GCSF MCSF
Combination of necrotic tissue, dead neutrophils, dead mac and tissue fluid
Pus
Produced in large numbers in persons with parasitic infection
Eosinophils
Eosinophils release
hydrolytic enzymes ROS larvicidal polypeptides called MBP detoxify some of inflammation inducing substances released by mass cells and basophils and destroy allergen-antibody complex
Circulating mast cells
IgE antibodies have propensity to become attached to mast and this cell
Basophils
Basophils and mast cells release
Histamine
Bradykinin
Serotonin
Lymph node or lymphogenous tissue
Lymphogenous leukemia
Produced by BM and many extramedullary organs
Myelogenous
Leukemic cells are usually
nonfunctional
Almost all leukemias spread to
Spleen, LN, liver and other regions that have rich blood supply
cause metabolic destruction
Antibody-antigen complex activates the
Classical pathway
Ability to resist organisms or toxins that damage tissues of the body
Immunity
Phagocytosis of bacteria
Destruction of pathogen by acidic secretion
Digestive enzyme of GIT
resistance of skin to invasion
Certain chemicals in blood that attach to foreign org or toxin
Innate immunity
Ability to develop powerful protective mechanism against specific invading agent
Acquired immunity
Development of circulating antibodies
Humoral
B cell immunity
Formation of large numbers of activated lymphocytes specifically designed to destroy foreign agent
Cell mediated
T cell immunity
Initiates development of immunity at least 8000 kilodaltons
Antigen
Smaller substances that attach to proteins
Haptens
Responsible for acquired immunity
LN, spleen, submucosal areas of GIT and bone marrow
T and B lymphocytes
Lymphocytes
Where T lymphoctes are preprocessed
Thymus
Removal of thymus eliminates
Cell mediated immunity
Subsequent exposure to same antigen causes more rapid response due to
Memory cell
Antibodies are
Gamma globulin proteins called immunoglobulin
Five general classes of antibodies
IgM IgA IgG IgD IgE
Most numerous
75%
IgG
Antibodies act by directly attacking the invader
Agglutination
Precipitation
Neutralization
Lysis
System of about 20 proteins normally present in the plasma that can be activated by antigen-antibody reaction
Complement
Stimulate phagocytosis both by
Neutrophils
Mac
Complement:
Phagocytosis by neutrophil and mac
Rupture of cell membrane of bacteria and other invading organism
Agglutination
Structure of viruses
T helper cells secrete
IL 2,3,4,5,6
Forms protein mediators called lymphokines
T helper cells
Secrete hole forming proteins called perforins
Cytotoxic t cells by direct attack
Regulates activity of other cells so excessive immune reactions do not occur
Supressor T cells
Failure of tolerance mechanism
Autoimmune diseases
Develop during processing of T lymphocytes in thymus and B lymphocytes in bone marrow
Tolerance
Continuous exposure to self antigen in fetus is thought to cause self reacting t and b lymphocytes to become
Destroyed
Caused by activated T cells
Skin eruption, edema or asthmatic attack
Allergy and hypersensitivity
Caused by IgE antibodies called reagins
Allergy
How many HLA antigens are present over human cell
6
Antigens
Cause blood transfusion reactions
Agglutinogen
Gamma globulin of IgM and IgG
Agglutinins
Entry into body of small numbers of group A and B antigens in food and through contact with bacteria
If blood samples are mismatched so that anti A or anti B plasma agglutinins are mixed with RBCs containing A or B agglutinogens -> RBCs agglutinate into clumps
Most lethal effects of transfusion
Renal failure
Spontaneous occurence of agglutinin almost never happens
Individual must first be expsosed to an Rh antigen usually through transfusion of blood or pregnancy
anti-Rh agglutinin develop and reach maximum concentration within about 2-4 months
Rh blood types
Progressive agglutination and subsequent phagocytosis of RBCs
Erythroblastosis fetalis
Transplantation of tissue or whole organ from one part of the body to another
Autograft
All cells in transplanted organ contain virtually same antigen
Survive indefinitelt if provided with an adequate blood supply
Identical twin
Transplantation of one organ from one identical twin to another
Isograft
One human being to another
Immune reaction almost always occur
Graft die within 1-5 weeks after transplantation unless specific therapy is given to prevent the immune reaction
Allograft
Transplantation of organ from one species to a different species
Xenograft
Tx: cyclosphorine, tacrolimus
Most impt antigens in graft rejection
More than 150 types of HLA but only 6 are present on cell surface of any one person
Impossible for two individuals with exception of identical twins to have the same six HLA
present on WBC and cells of tissue
HLA antigen complex of antigen
Prevention of graft rejection
Glucocorticoid hormone IL-2
Azathioprine toxic to lymphoid block formation of t cell
Cyclosporine and tacrolimus inhibit formation of T helper and blocks t cell mediated reaction
Immunosupressive antibody therapy anti IL2 receptor antibodies
Clotting factor part of extrinsic pathway
7
Precention of blood loss
Hemostasis
Hemostasis steps
Vascular spasm -constriction TXA2
Formation of platelet plug -release ADP and TXA2
Formation of blood clot - 15-20 seconds (severe) and within 1-2 minutes (minor)
Within 3-6 mins: entire opening or broken end of vessel filled with clot
After 20 mins to 1 hourclot retracts
Growth of fibrous or scar tissue
Extrinsic pathway
Trauma to vascular or extravascular tissue
Release of tissue thromboplastin, phospholipid, lipoprotein complex
Reacts with Factor 7
Activates factor 10 in presence of calcium ions
Common pathway via factor 10
Intrinsic pathway
After trauma to blood vessel or exposure of blood vessel to collagen
Factor 12 or Hageman factor forms activated factor 12
Then releases phospholipids and platelet factor 3
Activates factor 12 acts on factor 11
Activated factor 11 acts on factor 9
Activated factor 9 works with factor 8, PF3, ca and phospholipid ions activating common pathway
Most important factors for prevention of clotting in normal vascular system
Smoothness of endothelium
Layer of glycocalyx on endothelium
Thrombomodulin binding thrombin
Most important anticoagulants in blood
Fibrin thread
Alpha globulin: antithrombin III
Removes thrombin from circulation
Heparin
Conditions that cause excessive bleeding in humans
Vitamin K deficiency 1972 2-prothrombin, protein C
Hemophilia
Thrombocytopenia
Roughened endothelial surface or sluggish blood flow
Thromboembolic conditions
Virchow’s triad
Venous stasis
Activation of blood coagulation
Vein damage
Extracted from several animal tissues
Therapeutic dose: 0.5 to 1 mg/kg
Inc clotting time from 6 mins to 30 mins or longer
Antidote
Heparin
Protamine sulfate
Heparin inc effetiveness of
Antithrombin III
Competes with Vitamin K for active site
Coumarin/warfarin