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BLOOD CELLS

Blood – a type of connective tissue that performs 3 functions: 2 major components of blood:
transportation (of O2, nutrients, hormones, & waste), Plasma (55%) composed of water containing proteins, electrolytes, gases, nutrients, and waste.
regulation (of fluid, electrolyte, and acid/base balance), and Serum – plasma minus clotting factors.
protection (coagulation and infection control). Blood Cells (45%) RBCs, WBCs, and Platelets.

Hematopoiesis – blood cell production – via differentiation of Hematopoieitic Stem Cells – mediated by Colony Stimulating Factor
(Hematopoieitic) Stem Cells – (embryonic cells) non-differentiated immature blood cell found in bone marrow. Mature blood cells CANNOT undergo mitosis, therefore, ONE
DAUGHTER CELL ALWAYS REMAINS!!!!! (radiation can kill this)
Cells differentiate into 2 types (precursor cells): Myeloid (RBCs, most WBCs, Platelets) or Lymphoid (Lymphocytes)
Bone Marrow – the soft material that fills the central core of bones – 2 types: yellow and red, (red – actively produces blood cells), ALL blood cell types ORIGINATE in bone
marrow, some MATURE in other places in body (ex. T-cells mature in Thymus)
*Normal aging causes a ↓ in red bone marrow and # of stem cells (this results in a diminished ability to compensate for an acute or chronic illness)
CBC – the total count of RBCs (including Hgb and Hct), WBCs, and Platelets
Differential – a breakdown of all blood components and types of each including both mature (segmented) and immature (bands)
Pancytopenia – a marked decrease in all major blood components: RBCs, WBCs, and Platelets (Anemia, Infection, and Hemorrhage)

DEVELOPMENT/PROCESS OF DEATH OF A RED BLOOD CELL CLOT FORMATION


DIFFERENTIATION OF BLOOD CELLS
Facilitated by (CSF) Colony Stimulating Factor Erythrocyte (RBC) Vascular Phase
↓ vessels contract/blood flow decreases
Fragments ↓
↓ Platelet Phase
Hemoglobin platelets become sticky and accumulate
↓ ↓ platelet plug forms
Heme Globulin ↓
↓ ↓ ↓ Clotting/Coagulation Phase
Bilirubin Iron Amino Acids damaged cells release clotting factor
↓ ↓ ↓ ↓
Excreted Reused Reused prothrombin activator is formed
by liver ↓
along with prothrombin converts to thrombin
bile ↓
fibrinogen converts to fibrin

clot is formed
BLOOD CELLS/COMPONENTS
CELL TYPES or COMPONENTS NORM RANGE FUNCTION ↑ LEVELS IN ↓ LEVELS IN
(Hgb) Hemoglobin Polycythemia Normal Aging
RBCs A complex protein-iron compound Based on body mass. Transports O2 and CO2 to and from body cells. Hemoconcentation caused by: Anemias
Erythrocytes composed of : Can be used as an index of the oxygen-carrying capacity Dehydration Bleeding (GI, menstration)
Heme (iron & O2 binds to this) & M 14-18 of the blood. Hemorrhage
Primary Fx – Globulin (protein & CO2 binds to F 12-16 Also act as a buffer in Acid/Base balance. Hemodilution: ↑ Fluid Volume
this). Gives blood it’s red color. ↑ Hgb = ↑ MCH ↓ Hgb = ↓ MCH
Oxygen & CO2
(Hct) Hematocrit Typically 3X Hgb value Represents the % of RBCs in relation to total blood
Transportation Measurement of RBCs to total blood M 40-54% volume. SAME CONDITIONS AS Hgb SAME CONDITIONS AS Hgb
(120 day lifespan)
volume F 36-46%
Erythropoiesis – is the process of RBC production. Process influenced by/requires: protein, iron, folic acid, vitamins B12, B2, and B6. It is stimulated by hypoxia and controlled by erythropoietin (released by the kidneys).
Erythropoietin – a hormone synthesized and released by the kidneys need for RBC production (erythropoiesis).
Reticulocyte – an immature erythrocyte. Levels measure the rate at which new RBCs are released into circulation (can mature w/i 48 hours). Used to evaluate rate and amount of RBC production/bone marrow activity.
Hemolysis – destruction of RBCs. Monocytes and macrophages remove abnormal, defective, damaged, and old RBCs. Occurs in bone marrow, liver, and spleen. Process ↑ (indirect) bilirubin.
M: 1 - 15 mm/h erythrocyte sedimentation rate – non-specific but ↑ = (faster/heavy) found in acute and chronic inflammatory reactions due to aggregation of RBCs, malignancy, MI, end-stage
ESR
F: 1 - 20 mm/h renal disease, and with normal aging
RBC MCH mean corpuscular hemoglobin – measure of the amount of Hgb per RBC (normochromic – normal color or hypochromic – pale color (↓ Hgb per cell)
Indi- MCHC mean corpuscular hemoglobin concentration – measure of the amount of Hgb relative to the size of the RBC.
cies MCV mean corpuscular volume – measures size of RBCs (normocytic, microcytic, or macrocytic) ↑ in size with normal aging
Total 0.1 - 1.0 mg/dL total bilirubin is the total of both direct and indirect – nonspecific to liver function or RBC hemolysis
Bilirubin Direct 0.1 - 0.3 mg/dL direct bilirubin is r/t liver’s inability to excrete proper amount of bilirubin
Indirect 0.2 - 0.8 mg/dL indirect bilirubin is a measure of the degree of RBC hemolysis (destruction)
Release histamine, inflammatory response/allergic
Basophils 1%
reaction
Granulocytes aka
WBCs Polymorphonu- Eosinophils 3% Protect from parasites, limited phagocytosis
clear Leukocytes During infection,
Leukocytes Neutrophils 60%
shift-to-the-left is an ↑
Phagocytosis, 1st responders to inflammatory response elderly may have
in band (immature) cells
nd only a minimal ↑
Phagocytosis, 2 responders to inflammatory response,
Primary Fx – cellular immune response, in blood for short time then
in WBC due to
Protection Monocytes 6% diminished bone
migrate to tissues to become Macrophages (more
Agranulocytes aka marrow reserves
from Mononuclear
phagocytic than Monocytes, facilitate B&Tcell responses)
of granulocytes
Infection Humoral - antibody production, memory cells, mature in
Leukocytes B-cells
bone marrow
Lymphocytes 30%
Cell Mediated – immune response, memory cells, mature
T-cells
in Thymus Gland
Band – immature, differentiated WBCs
Segmented – mature, differentiated WBCs
Leukopenia – a total WBC count of less than 4000 (associated with bone marrow suppression and some types of Leukemia)
Neutropenia – a Neutrophil count of less than 1000/ severe is less than 500 (associated with bone marrow suppression and Leukemia)
Not technically “CELLS” RELATED LAB VALUES: Aid in blood CLOTTING Aging has no effect on platelet count.
PLATELETS PT – Prothrombin Time 12-15 seconds Must have adequate & available amounts which are ↑ in some plasma coagulation ↓ PTT with normal aging
Thrombocytes They are fragments of (Coumadin) metabolically and structurally sound for clotting to factors with normal aging
150,000-400,000 Megakaryocytes. PTT – occur.
(Heparin)
INR – Involved in homeostatis.
Primary Fx – By “plugging” any openings in capillary walls.
Blood Clotting/ Involved in clot shrinkage and retraction.
Coagulation
(5-9 day lifespan) Differentiated in bone marrow from
Megakaryocytes.
Thrombopoietin – a growth factor that acts on bone marrow to stimulate platelet production.
Normal Blood Clotting requires 3 components: vascular response (vasoconstriction), platelet response (aggregation & adhesion), and plasma clotting factors (coagulation factors – ex. Prothrombin, fibrinogen)
Thrombocytopenia – a platelet count of less than 100,000 (can cause bleeding); count less than 20,000 (can cause spontaneous hemorrhage)
ANEMIAS
Classification: Morphologic (cellular characteristics) based on size and color of RBCs Anemia is NOT a disease; it reflects a disease state.
Labs: MCH (color: normochromic or hypochromic) & Defined as: an abnormally low amount of circulating RBCs, hemoglobin
MCV (size: normocytic, microcytic, or macrocytic) concentration, or both.
Etiological (underlying cause) based on clinical conditions causing the anemia Resulting in: diminished oxygen-carrying capacity and delivery to tissues
Pathophysiologic (nature of RBC defect) Hypoproliferative or Hemolytic (this is how the powerpoints classify them) and organs (hypoxia).
Mild: (Hgb 10-14) most are asymptomatic, w/ co-morbidities or exercise: palpitations, dyspnea, diaphoresis Treatment: identify and treat cause
Moderate: (Hgb 6-10) ↑ cardiopulmonary symptoms with activity/may also experience when at rest Goal of Treatment: to restore and maintain adequate tissue oxygenation.
Severe: (Hgb < 6) many clinical manifestations involving multiple body systems (smooth sore tongue, cheilosis (fissures in corners of lips)
HYPOPROLIFERATIVE ANEMIAS HEMOLYTIC ANEMIAS
meaning – a defect/decrease in the production of RBCs meaning – increased destruction of RBCs
APLASTIC ANEMIA IRON DEFICIENCY PERNICIOUS ANEMIA SICKLE CELL ANEMIA THALASSEMIA
TYPES/ (RARE) ANEMIA (Seen most often in the ELDERLY) (African Americans @ HIGH risk) (Mediterranean, Asians, & African
PATHO Immune Mediated Condition (Most COMMON anemia) Defective DNA Synthesis in RBCs Autosomal Recessive Disorder Americans @ HIGH risk)
Marrow Stem Cells Replaced w/Fat Inadequate Iron for Hgb Synthesis problem in erythropoiesis/maturation Defective Hgb Molecule Lacking or ↓ Globulin Protein =
↓ in ALL BLOOD CELLS Vit B12 or Intrinsic Factor Deficiency Defective Hgb Chain Synthesis
Idopathic (cause unknown) Dietary def (older adults-poor diet) Vitamin B12 deficiency HEREDITARY DISORDER HEREDITARY DISORDER
Drugs, Chemicals, or Radiation Malabsorption (Chrones disease) Lack of Intrinsic Factor (which is Irregularly (crescent) shaped RBCs Problems early in life – Dx in
(benzene, chloramphenicol) Menorrhagia (pre-menopausal & secreted in the stomach-needed for ↓ Hgb carrying capacity childhood
CAUSES
Infections pregnant) absorption) Sickle Cells die quickly
&RISK:
Bleeding (common in GI – ulcers, Other Causes: Absorption issues:
gastritis) Chrones, gastric bypass, gastritis,
alcoholism, heredity, Ileitis, diverticuli
DX PANCYTOPENIA - ↓ levels of: MCV, MCH, MCHC Schilling’s Test (pernicious specific)
TOOLS/ ↓ RBCs, all WBCs, & Platelets Iron Studies: Blood Tests:
LABS: TIBC Total Iron Binding Capacity B12/Folate
Serum Ferritin – stored Iron (Fe) MMA (methylmelonic acid)
Serum Iron – Homocysteine Levels
Fatigue, dyspnea, pallor, palpitations, Fatigue, dyspnea, pallor, palpitations, Fatigue, dyspnea, pallor, palpitations, Fatigue, dyspnea, pallor, Fatigue, dyspnea, pallor,
headache, confusion, ↑ sensitivity to cold headache, confusion, ↑ sensitivity to cold headache, confusion, ↑ sensitivity to cold palpitations, headache, confusion, ↑ palpitations, headache, confusion, ↑
PURPURA (red-purp bruising d/t sensitivity to cold sensitivity to cold
platelets) IF Severe – Glossitis - smooth, sore, red Glossitis
↓ in Hemtopoiesis -bld cell production tongue and Recurrent PAINFUL episodes r/t PALE MUCOUS MEMBRANES
S & S:
PANCYTOPENIA Cheilosis - fissues in corners Confusion/dementia, vertigo (loss of acute vaso-occlusion
Leads to: (ANT) of lips balance)
Anemia Hemolytic Crisis (can cause death)
↑ risk of ----- Neutropenia Anorexia, N&V, Abd pain, weakness, Treatment = HOP
infection ----- Thrombocytopenia ataxia, paresthesia of feet/hands Hydration
Bone Marrow Suppression Oxygenation
Can cause complete Marrow Failure Pain
ID & Stop causative agent (if known) ID & Stop causative agent (if known) Give Vitamin B12 IM monthly
BMT – Bone Marrow Transplant Increase Iron (Fe) rich foods (must be IM, oral will not be absorbed)
- Age UNDER 45 years Iron (Fe) supplement/replacement meds
TX:
- Must find MATCH - (HLA) (do not use enteric coated or suspended) (injection of) EPOGEN ???
- (HLA) human leukocyte antigen - Vitamin C is given to aid in the
Guard against bleeding & infection absorption of Iron (Fe) from 10-20%
Transfuse; Corticosteriods to 75% when taken with Vit. C!!
Stimulate bone marrow function (take with OJ or tomato juice)
Corticosteriods can cause: ↑ Iron (Fe) can cause: Staining at site INTERVENTIONS/TEACHING IN ALL ANEMIAS:
Agitation, weight gain, immune (teeth for po, Ztrack for injection), Initiate SAFETY Precautions r/t ↓ O2 to brain can cause issues: Ortho HTN risk, Syncope (dizziness, fainting)
TEACH suppression, hyperglycemia dark stools, heartburn, and constipation “Blood Healthy” Diet: ↑ Protein, Folic Acid (for RBC synthesis), Vit B2, B6, B12, and Iron.
PT: Elderly – give Cyclosporin & ATG Drink plenty of fluids Rest periods, meds (EPOGEN stimulates RBC production), Transfusions may be necessary (packed RBCs)
(horse) Good sources of dietary Iron (Fe): Give O2 to relieve headaches
dark green leafy veg, liver, red meat, Patients may experience Depression and/or Apathy
whole wheat or fortified breads, dried Anemia is NOT a normal sign of aging.
fruits, legumes, cereal, potatoes
LEUKEMIAS
LEUKEMIA: (WBC Cancer) Malignant hematological disorder characterized by a proliferation of immature WBCs (in bone marrow, lymph nodes, spleen) that infiltrate the bone marrow, peripheral blood, & other organs.
The controlling factors that regulate orderly differentiation and maturation are absent.
The proliferation and accumulation of the immature cells causes overcrowding and impairment of production of normal cell lines.
CLASSIFICATION: Acute or Chronic: rate of onset Myeloid or Lymphoid: type of leukemic WBC involved
ACUTE LEUKEMIAS CHRONIC LEUKEMIAS
WBC growth is arrested while IMMATURE – proliferation & expansion of primitive (BLAST cells) WBC growth arrested at a more mature phase/level of development. Cells APPEAR MATURE.
Leads to (anemia, granulocytopenia (neutropenia), thrombocytopenia) Can infiltrate other organs Leads to
Severe and Aggressive – Rapid Onset and Rapid Death if untreated. Onset is gradual but if untreated will result in Death.
(ALL) Acute Lymphocytic (AML) Acute Myelogenous (CLL) Chronic Lymphocytic (CML) Chronic Myelogenous
Lease common of the 4 Leukemias (ADULT - peak incidence at 60-70 yrs old) (predominant in men and at 50-70 yrs old) (peak incidence at 45 yrs old)
TYPES/ (MOST COMMON IN CHILDREN (<14 yrs.) Uncontrolled proliferation of Myeloblasts - the Production and accumulation of Excessive development of MATURE-
PATHO (precursors of GRANULOCYTES) this pushes FUNCTIONALLY INACTIVE, LONG- APPEARING NEOPLASTIC
Uncontrolled proliferation of Lymphoblasts out other (normal) hematopoietic cells. LIVED, MATURE-APPEARING GRANULOCYTES in the BM which also
-IMMATURE LYMPHOCYTES in BM Lymphocytes (Bcells) in BM which also infiltrate Spleen & Liver. Has 3 PHASES.
CAN CAUSE CNS MANIFESTATIONS infiltrate Spleen & Liver PHILADELPHIA CHROMOSOME present.
CAUSES There is generally no single causative agent in the development of Leukemia. Most result from a combination of factors: genetic (chromosomal changes), and environmental influences: (chemicals –benzene,
&RISK: hydrocarbons, cigarette smoke), cytotoxic chemotherapeutic drugs (alkylating agents), viruses, radiation (including radiologists), immunologic deficiencies, and co-morbidity/host susceptibility.
Peripheral Blood Tests show: Peripheral Blood Tests show: Peripheral Blood Tests show: Presence of PHILADELPHIA CHROMOSOME in
↓ RBCs, Hbg, Hct, platelets, ↓ normal or ↑ WBCs ↓ RBCs, Hbg, Hct, platelets, ↓ to ↑ WBCs w/blast Mild ↓ RBCs, Hbg, Hct, platelets, ↓ WBCs to cells in 90% of patients.
DX
*initially ↑ WBCs = BAD prognosis *initially ↑ WBCs = BAD prognosis <100,000 w/↑ in Lymphocytes Peripheral Blood Tests show:
TOOLS/
Bone Marrow Tests show: Bone Marrow Tests show: Bone Marrow Tests show: ↓ RBCs, Hbg, Hct, ↑ platelets initially leading to ↓ in
LABS:
very ↑ LymphoBlast cells in bone marrow very ↑ MyeloBlast cells in bone marrow very ↑ Lymphocytes in bone marrow platelets, WBC Diff = ↑ Neutrophils, normal
*Bone Marrow Suppression – can lead to Failure *Bone Marrow Suppression – can lead to Failure *Bone Marrow Suppression – can lead to Lymphocytes and Monocytes
Lymphoblasts may be present in cerebrospinal Failure Bone Marrow Tests show:
fluid (Leukemic Meningitis) 55-70% Neutrophils (neoplastic) = BMS
Diagnosis and Classification of Leukemias done through Peripheral Blood Tests (CBC w/diff) and Bone Marrow Examination. Morphologic, Histochemical, Immunologic, and Cytogenetic methods are used to identify
cell subtypes and the stage of development of leukemic cell populations. Lumbar Puncture (ALL in CNS) and CT scan are used to determine the presence of leukemic cells outside of the blood and bone marrow.
Abrupt: fever, bleeding Fatigue, weakness, headache, mouth sores, Usually NO SYMPTOMS Chronic Stable Phase: NO SYMPTOMS early on is
Insidious: weakness, fatigue, bleeding tendency minimal hepatosplenomegaly & Typically, dx when seeking tx for unrelated disease – progressing to fatigue, night sweats,
lymphadenopathy, sternal tenderness issue pallor, dyspnea, anemia, anorexia/wt. loss, and
Anemia, Granulocytopenia, anemia, bleeding (epistaxis-nose, gums, Later can exhibit: LYMPHADENOPATHY splenomegaly. Usually S&S well controlled w/tx
S & S/ Thrombocytopenia, Infections bruising) fever, infections (ex. CELLULITIS) (swollen lymph nodes throughout the body) (WBCs controlled) for 3-5 years but WILL progress
Compli- Leucostasis – leukemic blasts aggregate and chronic fatgue, anorexia, splenomegaly, to an
cations invade capillary walls causing rupture and hepatomegaly Accelerated Phase: S&S return lasting approx 1
bleeding. year then leading to the:
CLL = Large Lymph Nodes Blastic Phase (Blastic Crisis): Acute and
CNS MANIFESTIONS: Leukemic meningitis Aggressive TERMINAL phase – neoplastic cells
take over - may only live for 3-6 months.
Induction (combo) Therapy Drugs: COAP Induction (combo) Therapy Drugs: Allogeneic (from donor/umbilical cells)
*Cylclophosphamide all BM suppressors BMT Bone Marrow Transplant – ONLY
SE: pulmonary toxicity, hemorrhagic cystitis, *cytarabine (Ara-C, Cytosar) POTENTIAL CURE
BM suppression, anorexia, N&V, alopecia SE: anorexia, N&V, mucositis, liver dysfx, fever
*Oncovin / vincristine (cell cycle specific) *antitumor antibiotics – anthracyclines: Interferon – best non-BMT treatment – prolongs
SE: ↓ serum NA, numbness, loss of reflexes, (daunorubicin, doxorubicin (Andriamycin) survival
constipation, abd pain, alopecia (hair loss) SE: cardiac toxicity HF, N&V, mucositis,
TX: *arabinoside alopecia (hairloss) Intensive multi-drug CHEMO in BLASTIC (end)
*prednisone corticosteroid/anti-tumor properties Intensification Therapy Phase
SE: hyperglycemia, immuno-suppression, Consolidation Therapy
weight gain, agitation Maintenance Therapy – not as effective in
Intensification Therapy AML but given every 3-4 weeks.
Consolidation Therapy BMT Bone Marrow Transplant
Maintenance Therapy –given for 2-3 years.
Cranial Radiation Therapy
Intrathecal Methotrexate
BMT Bone Marrow Transplant
TREATMENTS:
Main treatment is CHEMO/COMBINATION THERAPY:
3 reasons for Combination Therapy:↓ drug resistance, Minimize any 1 drug toxicity (results in multiple milder SE), Interrupt cell at different stages
Not all are CURABLE but attaining REMISSION or disease control is usually realistic (Complete Remission – no evidence of disease, Partial Remission – lack of symptoms, normal blood smear but evidence of disease in
bone marrow). PROGNOSIS is directly related to ability to remain in remission; with each relapse it may be more difficult to achieve remission.

INDUCTION (chemo)THERAPY: Aggressive treatment with Cytotoxic Chemotherapy Drugs (severely depresses bone marrow/immune system). 70% of newly dx patients will achieve complete remission (must prevent
relapse w/additional tx) Nursing Interventions for Induction Therapy: focus on ANT – (anemia, neutropenia, thrombocytopenia), infection, and psychosocial support.
POST-INDUCTION (aka) POST-REMISSION (chemo)THERAPIES INCLUDE:
INTENSIFICATION THERAPY (high-dose therapy): Immediately following Induction Therapy, given for several months. Same drugs at a HIGHER dose.
CONSOLIDATION THERAPY: Started after REMISSION is achieved. Eliminates any remaining leukemic cells.
MAINTENANCE THERAPY: Lower dose of induction therapy drugs given to keep body leukemia free.

BMT/BONE MARROW TRANSPLANT:


MYELOMA/LYMPHOMAS
MULTIPLE MYELOMA
DEFINED AS An ultimately fatal malignancy affecting the plasma cells in the bone marrow.

“Myeloma” = tumor of the bone marrow


“Multiple” = more than one area affected.
ACTION and - Proliferating plasma cells ↓ bone marrow function and immunity and destroy
bone tissue.
CAUSES - Cause is unknown
DIAGNOSTIC Most (80%) are dx after the development of one of the complications below.
(20%) are dx via discovery of ↑ protein found in blood or M protein found in urine.
TOOLS
Dx based on: H&P, lab work, imaging studies (MRI), & bone marrow biopsy.

COMPLICA- Anemia (in 75% @ dx) caused by plasma cells inhibiting Hgb production in
marrow
TIONS/ - S&S: fatigue, weakness, SOB, dyspnea on exertion
Bone Pain (initial symptom in 50%) caused by ↑ in plasma cells causing fractures
SIGNS AND and/or osteo lesions which can lead to nerve compression.
SYMPTOMS - S&S: pain, paresthesia, sensory loss
Infection (a leading cause of death) depressed production or function of
immunoglobulins ↓ ability to fight infection
HYPERcalcemia (in 25%) malignant cells ↑ bone breakdown (osteolysis) causing
CA to leave bone and enter blood
- S&S: Early: fatigue, N&V, anorexia, polyuria, dry mucous membranes,
constipation. Late: dehydration, confusion, LOC, ↓ tendon reflexes, ECG changes,
orthostatic HTN, or hypercalcemic crisis – sudden ↑ in serum CA leading to renal
failure, coma, or death
Renal Dysfunction (a leading cause of death)
Triggered by: dehydration, infection, nephrotoxic agents, hypercalcemia, direct
myeloma involvement in the kidney
Hyperviscosity of the Blood occurs when excess serum protein ↑ blood thickness
and ↓ flow
- S&S: blurred vision, headache, drowsiness, confusion, irritability, SOB
TREATMENT

TEACHING/
NURSING
ONCOLOGY/CANCERS
BREAST COLORECTAL PROSTATE SKIN
DIAGNOSTIC
TOOLS:

SIGNS AND
SYMPTOMS:

TREATMENT:

TEACHING/
NURSING
IMPLICATIONS: