Intro To Blood I & Ii (Foundations Exam 1)

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average adult blood volume

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5-6 liters

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blood contains:

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formed (cellular) and conformed elements

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cellular elements of blood

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- white blood cells, red blood cells, and platelets
-largely derived from bone marrow, lymph nodes, and thymus
-mature cells develop from a common progenitor cell (stem cell) in the bone marrow

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nonformed elements of blood

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- plasma that contains water, sugars, lipids, vitamins, minerals, electrolytes, and numerous proteins

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bone marrow structure

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- encased by cortical bone
- traversed by trabecular bone
- meshwork of thin-walled capillary-venous sinuses
- surrounding extracellular matrix, fat and hematopoietic compartment

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newly formed cells exit the marrow via...

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the sinusoids

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bone marrow function

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- site of production of RBCs, granulocytes, monocytes, platelets and early lymphocytes
- children --> all bones used for hematopoiesis
- adults --> restricted to central bones (ribs, vertebrae, pelvis, sternum, skull) and proximal portions of humerus and femur
- all cells develop from a common progenitor cell (stem cell)

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pluripotent stem cell

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gives rise to two types of multi potent progenitors
- common lymphoid stem cell
- common myeloid stem cell

-capacity for self-renewal

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common myeloid stem cell

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gives rise to committed cells which differentiate along either the granulocytic/monocytic, megakaryocytic, or erythroid pathways

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common lymphoid stem cells

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give rise to precursors of T-cells, B-cells, and natural killer cells

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5 types of white blood cells present in blood

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granulocytes (neutrophils, eosinophils, basophils) and mononuclear cells (lymphocytes and monocytes)

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granulocyte basic characteristics

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-based on staining characteristic of specific granules in cytoplasm
- single nucleus that is multi-lobed

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granulocytopoiesis

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- granulocytes develop by differentiation of myeloblasts
- increasing granularity and segmentation of nucleus

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why is it important to know the normal nuclear morphology of granulocytes?

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- etiology of patient's anemia
- certain vitamin deficiencies (B12 and folate) show hyper segmentation of neutrophil nuclear lobes in addition to anemia

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development of granulocytes

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- 10-14 days
- neutrophils last ~1 day in circulation
- 1-2 days in tissues

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resting state marrow produces:

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1-2 x 10^9 granulocytes/kg/day

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when are neutrophils released from marrow?

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at the band and segmented state under normal circumstances
- blood contains more segmented than banded forms

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clinical correlate of release of neutrophils

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during infection, inflammation, marrow disease, or other stressor, earlier neutrophil precursors are released ("left shift")
- if additional WBCs are needed, increased WBC production can be increased

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monocytopoiesis

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- monocytes are precursors to cells of mononuclear phagocytic system (resident macrophages

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mononuclear phagocyte system includes:

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connective tissue macrophages, alveolar macrophages, liver macrophages (Kupfer cells), microglial cells of CNS, Langerhans cells of the skin

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production of monocytes

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- 2-3 days (from stem cell to blood)
- circulate ~3 days
- last ~ 3 months in tissues (?)

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lymphocytopoiesis

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- multipotent lymphoid stem cells reside in bone marrow
- further education and differentiation occur in secondary lymphoid organs
T-cells --> thymus and spleen
B-cells --> lymph nodes and tonsils

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proliferative disorders

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increased WBC count
- expansion of leukocytes and further divided into neoplastic or reactive conditions

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leukopenia

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- decreased leukocyte count
- usually due to reduction in number of neutrophils (neutropenia) --> more susceptible to infections

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lymphopenia

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congenital immunodeficiencies, HIV, chemotherapy, autoimmune disorders, corticosteroid therapy, certain acute viral infections

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neutropenia

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Causes:
1. reduced production --> bone marrow infiltrate (leukemia, neoplasms, infections), vitamin deficiency, myelodysplasia
--clue: anemia and thrombocytopenia (decreased platelets) present
2. increased destruction --> drugs, autoimmune conditions, overwhelming infections

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leukocytosis

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increase in WBC count

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mechanisms of leukocytosis

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1. increased release from the marrow (infection)
2. decreased margination and extravasation (glucocorticoids, exercise)
3. increased numbers of marrow precursors (infection, inflammation, neoplasms)

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neutrophilic leukocytosis (neutrophilia)

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acute bacterial infections, non-infectious inflammation (tissue damage -->MI), corticosteroid therapy, certain malignancies (chronic myelogenous leukemia)

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eosinophilic leukocytosis (eosinophilia)

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allergic disorders (asthma, hay fever, etc.), parasitic infections, drug reactions, certain malignancies (myelogenous leukemia)

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basophilic leukocytosis (basophilia)

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rare, allergic disorders, infections, chronic myelogenous leukemia

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monocytosis

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chronic infections (tuberculosis), lupus, inflammatory bowel disease, monocytic leukemia

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lymphocytosis

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viral infections, tuberculosis, neoplasms

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erythrocytopoiesis

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- increasing hemoglobinization of cytoplasm and reduction in nuclear size
- driven by erythropoietin produced in kidneys

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production of RBCs

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- 7 days
- 120 days in circulation
- replace 1% of RBCs/day
- 2-4 x 10^9 RBCs produced/kg/day under steady state

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reticulocytes

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- young erythrocytes
- blood smear --> larger and more blue because they still contain ribosomal RNA

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in response to anemia, production of RBCs....

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- increased up to 8-fold
- peripheral blood may see increase in early RBCs (reticulocytes and even nucleated RBCs)

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red cell morphology

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- biconcave discs filled with hemoglobin
-nucleus is extruded during final state of development in bone marrow
- ~ 8 micrometers in diameter

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Red blood cell functions

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1. oxygen and carbon dioxide transport in blood
2. Acid balance

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Laboratory evaluations of RBCs

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- complete blood count (CBC) --> WBC, platelets, and RBC
- size and amount of hemoglobin
- normal person --> uniform size and shape

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mean cell volume (MCV)

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80-100 fL

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microcytic

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low MCVs

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macrocytic

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cells larger than normal (MCV)

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hemoglobin content evaluation

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- average per cell (mean cell hemoglobin)
- concentration (mean cell hemoglobin concentration)

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hypochromic

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cells with decreased content of hemoglobin

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anemia

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reduction of the number of red blood cells and/or hemoglobin content of blood --> reduction in oxygen transport capacity and organ hypoxia

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classification of anemia

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-underlying mechanism or according to alterations in RBC morphology and the hemoglobin content of RBC

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causes of anemia

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1. blood loss
2. increased rate of RBC destruction
3. impaired RBC production

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megakaryocytopoiesis

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- committed stem cell undergoes endomitotic division (nucleus divides but not cytoplasm)
-->large cell whose nucleus has multiple nuclear lobes
- straddle marrow sinusoidal discontinuities and shed fragments of cytoplasm -->fragments=platelets

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platelet production

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- 5-10 days
- survive 10 days in circulation

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which counter-regulatory mechanisms slow the formation of fibrin "cement"?

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protein C, protein S, antithrombin

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which counter-regulatory mechanisms break down clots?

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fibrinolysis --> plasminogen

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what is the site of synthesis of procoagulant, anticoagulant,and fibrinolytic proteins?

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liver

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coagulation cascade

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series of conversions of inactive enzymes to active enzymes that culminates in formation of insoluble protein fibrin
- intrinsic, extrinsic, and common pathways
- takes place on the phospholipid surface of activated platelets

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prothrombin time

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measures the extrinsic and common pathways
- the time to fibrin formation

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partial thromboplastin time

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measures intrinsic and common pathways

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antithrombin

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inactivates thrombin and other coagulation factors
--> inhibition of coagulation cascade and less fibrin formation

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activated protein C

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(cofactor Protein S)

--> cleave factors Va and VIIIa to inactive proteins
--> inhibit clotting

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tissue plasminogen activator (t-PA)

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synthesized by endothelial cells

--> promote fibrinolysis to clear fibrin deposits

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causes of bleeding disorders

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1. vessel walls
2. platelets
3. coagulation factors

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petechiae

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minute, pinpoint hemorrhage (1-2mm)
causes: thrombocytopenia and defective platelet function

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purpura

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(>3mm)
causes: vasculitis, increased vascular fragility, thrombocytopenia, defective platelet function,

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ecchymoses

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subcutaneous hemorrhage (>1-2cm)
causes: platelet defects (small) and coagulation factor deficiencies (larger)

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hemarthrosis

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deep tissue hematomas and bleeding into joints
causes: coagulation factor deficiencies

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mucosal bleeding

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(hematuria, menorrhagia, epistaxis)
causes: platelet disorders

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thrombocytopenia

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most common acquired bleeding disorder
causes:
1. decreased production: drugs, primary bone marrow disorders, vitamin deficiency, congenital disorders, infection (HIV)
2. accelerated destruction: more common --> destroyed by immune mediate or non-immune mediate/mechanical process

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Von Willebrand Disease (vWD)

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hemorrhagic disorder related to abnormalities in clotting factors
-->defect is in platelet adhesion to damaged endothelium
- one of the most common inherited diseases
- decrease in vWF production or function

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hallmark presentation of vWD

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platelet type bleeding
--> spontaneous mucocutaneous bleeding (epistaxis, menorrhagia, pupura, petechiae)

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consequences of vWD

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severe vWD
--> stability of FVIII is markedly reduced and may have bleeding similar to hemophilia

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laboratory findings of vWD

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normal platelet count
decreased vWF protein and/or function

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treatment of vWD

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- DDAVP (desmopressin) --> causes release of vWF and FVII from endothelial cells
- vWF concentrates

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Hemophilia A

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(FVIII deficiency)
- X-linked inherited

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clinical presentation of Hemophilia A

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easy bruising, hemorrhage after surgery/trauma, spontaneous hemorrhage into joints (hemarthrosis)

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hemarthrosis

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spontaneous bleeding into joints

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laboratory findings of hemophilia A

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prolonged aPTT and low factor VIII activity

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treatment of hemophilia A

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FVIII replacement

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size of basophil

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8-12 micrometers

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morphology of basophil

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- bilobed nucleus
- numerous large, dark purple granules stain with basic dye

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function of basophil

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- mast cell precursor (?)
- release vasoactive agents
- function similar to mast cells

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basophil
% of WBCs in blood?

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0-2%

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size of neutrophil

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10-14 micrometers

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morphology of neutrophil

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- multi-lobed (3-5 lobes)
three granule types:
1. primary granules (azurophilic)
2. secondary granules
3. tertiary granules

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primary granules (neutrophils)

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(azurophils)
microbicidal agents

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secondary granules (neutrophils)

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most numerous, light tan
- lysozyme, collagenase, complement activators

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tertiary granules (neutrophils)

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metalloproteinases

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function of neutrophils

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acute inflammatory response to tissue damage:
- secrete enzymes that degrade tissue
- ingest and destroy damaged tissue
-phagocytose and digest foreign substances (including microorganisms)

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neutrophil
% of WBCs?

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40-75%

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size of eosinophil

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12-14 micrometers

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morphology of eosinophils

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- multi-lobed (2-3 lobes)
-large, orange-red granules stain with eosin
- contain major basic protein, histaminase, collagenase

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function of eosinophils

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- allergic reactions
- parasitic infections
- chronic inflammation
- modulate local immune response by release cytokines
--> cause tissue damage

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eosinophils
% of WBCs

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0-5%

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size of lymphocyte

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6-30 micrometers

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morphology of lymphocytes

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- vary in size
- small lymphocytes --> common in blood
- round to slightly indented nucleus
- stain pale blue cytoplasm
natural killer cells are larger lymphocytes with granules

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function of lymphocytes

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T-cell --> cell mediated immunity
B- cell --> antibody production
NK cells --> kill virus infected cells, tumor cells

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lymphocytes
% of WBCs?

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15-50%

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size of monocyte

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18 micrometers

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morphology of monocyte

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- lobated nucleus (not segmented)
- abundant blue-gray cytoplasm with small azurophilic granules

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function of monocytes

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-differentiate into macrophages in tissues
- phagocytose bacteria, tissue debris, and other cells
- present antigen to T-cells

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monocytes
% of WBCs?

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0-12%