Intro to Blood Flashcards
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blood in stool
LO #1: Describe the components of blood.
cellular: WBC, RBC, platelets, derived from bone marrow, lymph nodes and thymus
non-cellular aka plasma: sugars, lipids, vitamins, minerals, electrolytes and numerous proteins (enzymes, hormones, antibodies, blood clotting factors)
LO #2: Describe the morphologic features that characterize differentiation of marrow precursors cells to the mature cells seen in the blood and the approximate time this process takes for platelets, RBCs, and neutrophils.
All cells in the bone marrow develop from a common progenitor
cell, or stem cell. This pluripotent stem cell has the capacity for selfrenewal and can give rise to all mature cells of the blood and immune
organs (this is why it is called pluripotent). This pluripotent stem cell
gives rise to two types of multipotent progenitors, the common
lymphoid and the common myeloid stem cell.
platelets: 5-10 days
neutrophils: 10-14 days
RBC: 7 days
leukocytes
white blood cells
- neutrophils
- lymphocytes
- monocytes
- eosinophils
- basophils
neutrophils
10-14 days to mature
40-75%
acute inflammatory response - secrete enzymes that degrade tissue, ingest and destroy damaged tissue and phagocytose and digest foreign substances, including microorganisms
lymphocytes
15-50% main functional cells of the immune system T-Cells B-Cells NK Cells
monocytes
0-12%
travel from bone marrow to tissues where they differentiate into phagocytes of the mononuclear phagocyte system, phagocytose bacteria, tissue debris and other cells
present antigen to T-Cells
eosinophils
0-5%
associated with allergic reactions, parasitic infections and chronic inflammation
modulate local immune response by release of cytokines and interleukins
basophils
0-2%
functionally related to mast cells of connective tissue
mast cell precursor
release vasoactive agents when stimulated
leukocytosis
(- cyto = cell, -osis = increased) – increase in the
WBC count. The causes are numerous, but 3 general mechanisms
are known: 1) increased release from the marrow (Ex: infection), 2)
decreased margination and extravasation (glucocorticoids, exercise)
and 3) increased numbers of marrow precursors (infection,
inflammation, neoplasms). Leukocytosis can be further classified
based on which WBC is increased:
a. Neutrophilic leukocytosis (neutrophilia): acute bacterial
infections, non-infectious inflammation (ex: tissue damage such
as a myocardial infarction), corticosteroid therapy, neoplasms
(chronic myelogenous leukemia)
b. Eosinophilic leukocytosis (eosinophilia): allergic disorders
(asthma, hay fever, allergic skin diseases), parasitic infections,
drug reactions, neoplasms (chronic myelogenous leukemia)
c. Basophilic leukocytosis (basophilia): reactive basophilia is
not a common finding. Basophilia can be seen in allergic
disorders, infections, inflammation, and neoplasms (chronic
myelogenous leukemia)
d. Monocytosis: acute and chronic infections (tuberculosis),
collagen vascular disorders (lupus), inflammatory bowel
disease, neoplasms (monocytic leukemia)
e. Lymphocytosis: viral infections, tuberculosis, neoplasms
(chronic lymphocytic leukemia is most common cause of
neoplastic lymphocytosis)
leukopenia
Leukopenia (-penia = deficiency) – decreased leukocyte count.
This can occur in a variety of settings and usually is due to a reduction
in the number of neutrophils (neutropenia), with lymphopenia being
less common. Individuals with leukopenia are more susceptible to
infections.
a. Lymphopenia – Causes: congenital immunodeficiencies,
HIV, chemotherapy, autoimmune disorders, corticosteroids,
certain acute viral infections
INTRODUCTION TO BLOOD
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b. Neutropenia – 1) Reduced production: any condition in
which the bone marrow is infiltrated (leukemia, other
neoplasms, infections), vitamin deficiency, and myelodysplasia.
A clue to these disorders is that anemia and thrombocytopenia
(decreased platelets) may also be present. 2) Increased
destruction: Drugs, autoimmune conditions, overwhelming
infections. (This general scheme for classifying cytopenia(s) will
also be used when evaluating anemia and thrombocytopenia.)
left shift of granulocytes
Left shift or blood shift is an increase in the number of immature leukocytes in the peripheral blood, particularly neutrophil band cells. Indicates infection, hypoxia, shock
anemia
a reduction of the number of red blood cells and/or
hemoglobin content. Leads to a reduction in oxygen transport
capacity and organ hypoxia.
• Classified according to underlying mechanism or according
to alterations in RBC morphology, including the size of the RBC
(MCV) and the hemoglobin content of the RBC (MCHC).
• Many causes are known: 1) Blood loss, 2) Increased rate of
RBC destruction and 3) Impaired RBC production
hemostasis system
= blood; -stasis = a condition of balance, static
Hemostasis results from a highly regulated set of complex events
with 2 main functions:
1. Rapid formation of a clot to stop bleeding from a damaged
vessel (vessel wall, platelets, coagulation cascade)
2. Prevent out of control clot formation (counter-regulatory
mechanisms)
Hemostasis involves four general components:
1. Vessel wall: After initial damage to a vessel, there is a brief period of vasoconstriction that reduces the amount of blood flowing to the area.
2. Platelets: Damage to the endothelium exposes collagen, which is normally
hidden from the blood. Circulating von Willebrand factor (vWF) binds to
this collagen. Platelets then adhere to vWF to form an initial hemostatic
plug.
3. Coagulation cascade (Secondary hemostasis): This activates platelets and they release granule contents.
These granule contents recruit additional platelets to the site and play
a role in the coagulation cascade. During damage to the vessel wall,
tissue factor (TF) is also exposed to the circulation. TF, along with the
activated platelets, initiate the coagulation cascade (refer to Figure 4-6,
Robbins Pathologic Basis of Disease, 9th Ed), which results in the
formation of insoluble fibrin, a “cement” that holds the platelets
together into a stable hemostatic plug.
4. Counter-regulatory mechanisms: In order to limit the hemostatic
response to the site of vascular injury and to limit the final size of the
clot, counter-regulatory mechanisms are set into motion. The counterregulatory proteins slow formation of fibrin and limit the clot to the site
of vascular damage (protein C, protein S and antithrombin). In addition,
fibrinolysis acts to limit the size of the clot and contributes to clot
dissolution.
Primary Hemostasis Disorders
Petechiae – minute, pinpoint hemorrhage (1-2mm)
o Thrombocytopenia and defective platelet function
• Purpura (>3mm)
o Similar causes as petechiae
o Also, vasculitis and increased vascular fragility
Ecchymoses or subcutaneous hemorrhage (>1-2 cm)
o Platelet defects (small)
• Mucosal bleeding (hematuria, menorrhagia, epistaxis) is more common in platelet disorders
platelet disorders, mucocutaneous, immediate bleeding
