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84 Cards in this Set
- Front
- Back
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Blood consists of what?
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RBCs, WBS, platelets, and plasma
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The generation of blood cells is called?
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Hematopoiesis!
Embryo- in yolk sacs Fetus- spleen, liver, lymph nodes then moves to bone marrow of long bones- Adults- almost exclusively in bone marrow of cranium, pelvis, sternum |
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It all begins with the ___________ stem cell?
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(multi-potential hematopoietic stem cell), AKA
(hemocytoblast), AKA (pluripotent stem cell) |
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Multi-potential hematopoietic stem cells lead to the development of?
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common myeloid progenitor- leads to monocytes, the granulocytes, platelets, & erythrocytes.
& common lymphoid progenitor- leads to T-cell lymphocytes & B-cell lymphocytes |
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Erythrocytes are the oxygen carrying red blood cells.
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Both reticulocytes (immature RBC) and erythrocytes are functional and are released into the blood.
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Lymphoid cells are derived from common lymphoid progenitors. The lymphoid lineage is primarily composed of T-cells and B-cells.
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cornerstone of the adaptive immune system
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Myeloid cells, which include granulocytes, megakaryocytes (form platelets) and macrophages are derived from common myeloid progenitors.
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They are involved in such diverse roles as innate immunity, adaptive immunity, and blood clotting (platelets)
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Erythrocytes (RBCs)
Most abundant cells- |
Transport hemoglobin and therefore transport O2. develop bone marrow, live about 120 days; take the form of flexible biconcave disks, lack nucleus and cannot synthesize protein
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T-cells & B-cells
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B-lymphocytes provide for antibodies
T-lymphocytes provide for initiating immune response & effecting cell-mediated immunity. |
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Neutrophils
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55-65% of WBCs
primary pathogen fighting cell. when numbers are decreased infection is highly likely. granulocyte, short life. |
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Eosinophils
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1-3% of WBCs
help to control allergic response and fight parasites. granulocyte |
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Basophils
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0.3-0.5% WBCs
release heparin-a blood thinner; histamine- a vasodilator; and other inflammatory mediators. granulocyte |
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Monocytes
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3-8% of WBCs
differentiate into macrophages that enter tissues. largest WBC, circulating life of about 1-3 days before entering tissues where they can live for months even years. They destroy larger material, important in chronic inflammation. |
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Hypoxia
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body as a whole (generalized hypoxia) or a region of the body (tissue hypoxia) is deprived of adequate oxygen supply in high altitude, depressed respiratory drive, etc.
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Hypoxemia
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a state in which there is low levels of O2 in the blood such as may occur with anemias and will cause hypoxia.
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H & H
Is ? |
hematocrit & hemoglobin
globin: M - 14-16.5 g/dL F -12-15 g/dL crit: M - 40-50% F - 37-47% |
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Anemia
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condition where hemoglobin of blood is insufficient to meet demand of body-
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Anemia
Causes? |
bleeding, decrease in RBCs, higher number of immature RBCs, hemolysis, high altitude, menstruation, some meds, nutrition, autoimmune, surgery, injury, trauma, disease, kidney failure
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Iron Deficient Anemia
What? Nutritional based |
supply of iron is not adequate enough for optimal RBC formation
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Iron Deficient Anemia
Info- |
most common type in the world
poverty, women of childbearing age, children (nutrition) |
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Iron Deficient Anemia
Class? |
Microcytic-Hypochromic Anemia
RBCs are small, pale, MCV is decreased, MCH is decreased |
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Iron Deficient Anemia
Causes? |
related to excessive iron loss
by bleeding, meds that cause GI bleeds (aspirin, ibuprofen); decreased dietary intake (spinach, liver, raisins, malabsorption- some foods, decreased GI acid! |
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Iron Deficient Anemia
How it presents? |
develops gradual, fatigue, dyspnea, pallor, brittle nails, clubbing, smooth sore tongue, dizziness, states of hypoxia, PICA, Cheilosis
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Iron Deficient Anemia
Assessment? Treat by replacing iron stores- (stored in the liver attached to protein ferritin) |
H&P, SxS, O2, CBC, MCV (size of RBC), MCH, MCHC, occult bleeding test of GI,
24h Schilling test- does body absorb B12? |
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Pernicious Anemia
What? Nutrition based |
impaired cellular division and maturation d/t lack of B12 or inability to absorb B12. short life cycles d/t Defective DNA synthesis
develops slowly |
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Pernicious Anemia
Class? |
Macrocytic-Normochromic-Anemia
aKa megoblastic anemia RBCs are large, abnormal shape, hemoglobin is good increase MCV, increase MCH |
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Pernicious Anemia
Causes? |
inability to absorb B12 d/t nutrition, GI alterations, loss of intrinsic factor
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Pernicious Anemia
How it presents? |
pallor even jaundice, weakness, fatigue, diarrhea, beefy red tongue, paresthesias, impaired proprioception
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Pernicious Anemia
Assessment? Treat by B12 injection |
very similar to iron deficient anemia-
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Folic Acid Deficiency Anemia
What? Nutrition based |
impaired cell synthesis and maturation d/t lack of folic acid or inability to absorb
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Folic Acid Deficiency Anemia
Class? |
Macrocytic-Normochromic Anemia
aKa megaloblastic anemia RBCs large, possible abnormal shape, hemoglobin concentration good, increase MCV, increase MCH |
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Folic Acid Deficiency Anemia
Causes? |
inability to absorb d/t nutrition, alcoholics, anorexia, malabsorption, some meds
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Folic Acid Deficiency Anemia
How it presents? |
pallor, progressive weakness, fatigue, dyspnea, GI symptoms, increased HR possible
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Folic Acid Deficiency Anemia
Assessment? Treat by replacement of folic acid- |
basically the same as other anemia-
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Sickle Cell Anemia
What? Hemolytic based |
chronic condition where RBCs are elongated, rigid, and assume a crescent shape. reduces hemoglobin capacity-
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Sickle Cell Anemia
Class? |
Normocytic-Normochromic Anemia
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Sickle Cell Anemia
Causes? |
caused by autosomal genetic defect of hemoglobin S, a mutation in the beta chain of the hemoglobin molecule through a substitution of the amino acid valine for glutamine
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Sickle Cell Anemia
How it presents? |
pallor, jaundice d/t increased hemoglobin breakdown after increased hemolysis of RBCs, fatigue, pain, pain, pain especially in joints- priapism in men
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Sickle Cell Anemia
Assessment? |
pain management, assess joints, O2 related issues and SxS of decreased oxygenation
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Sickle Cell Anemia
Treatment? |
meds, hydration, rest, O2, pain meds, transfusion maybe needed
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Sickle Cell Crisis
What? |
extreme vessel occlusion that occurs as a result of the sickled cell shape coupled with hemolytic actions of the spleen, etc.
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Sickle Cell Anemia
Info- |
Hereditary
8% of African Americans are heterozygous for sickle cell 1% of African Americans are homozygous for sickle cell |
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Sickle Cell Crisis
Causes? |
low body temp, conditions of low O2, excessive exercise, kill respiratory drive, infection, stress, dehydration, acidosis
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Polycythemia Vera
What? |
a condition of increased number of circulating RBCs and hemoglobin.
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Polycythemia Vera
Class? |
Normocytic-Normochromic Anemia
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Polycythemia Vera
Primary or secondary |
Primary- autosomal, as bone marrow overproduces RBCs, WBCs and platelets
Secondary- most common forms: Abnormal increase in erythropoietin Abnormal levels of may be produced from exposure to high altitudes, systemic disorders, hypoventilation, long term smokers |
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Polycythemia Vera
Info- |
most common in Caucasian men of European Jewish Ancestry-
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Polycythemia Vera
How it presents? |
plethora of RBC, engorged retinal veins, hepatosplenomegaly, HA, hypertension, fatigue, dizziness, weakness, hypermetabolism, pruritis (itch or want to scratch)
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Polycythemia Vera
Treatment? |
taking blood from PT, decrease iron intake, teach smoke cessation, pain med, & comfort
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Infectious Mononucleosis
'kissing disease' |
an acute infection of the B lymphocytes caused by Epstein Barr virus
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Infectious Mononucleosis
info- |
most common in 15-35 yr old with peak @ 15-19. transmission from saliva, sneezing, close contact. not as catchable as common cold.
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Infectious Mononucleosis
How it presents? |
classic triad of symptoms fever, sore throat, and lymph node enlargement.
fatigue, increased WBCs |
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Infectious Mononucleosis
Treatment? |
rest, fluids, meds
NO ASPIRIN IN CHILDREN! |
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Leukemia
Acute- Chronic- |
malignant neoplasm of blood forming tissues of the bone marrow, spleen, and lymph tissues.
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Leukemia
Acute- Chronic- Characterized by? |
abnormal proliferation and accumulation of WBCs as a whole.
types are categorized by WBC affected and course of disease- |
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Leukemia
Acute-Info |
rapid onset,
progresses rapidly short clinical course left untreated death ensues in days |
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Leukemia - Acute
Acute Lymphocytic/Lymphoblastic Leukemia (ALL) |
immature lymphocyte proliferation-
most common in 2-10 yr old- can occur in older people- rapid onset- short clinical course- left untreated death ensues in days |
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Leukemia - Acute
Acute Myelogenous/Myelocytic Leukemia (AML) |
immature granulocytes proliferate and accumulate-
incidence increases with age > 50 most common acute form for adults- can effect RBCs, WBCs, Platelets can progress from MDS (a pre-leukemia)- |
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Leukemia
Chronic-Info |
insidious (subtle or stealthy) onset-
prolonged clinical course- asymptomatic early stage- life expectancy can be > 5 yr |
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Leukemia - Chronic
Chronic Lymphocytic Leukemia (CLL) |
abnormal and incompetent lymphocytes proliferate and accumulate-
gradual onset- more common in men- frequent in 50-70 yr old |
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Leukemia - Chronic
Chronic Myelogenous Leukemia (CML) |
uncontrolled proliferation of granulocytes and marked increase in blast cell circulation-
Philadelphia Chromosome- COMMON IN CHILDREN adults primary 30-50 yr old- gradual onset- |
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Leukemia
Acute- Chronic- How it presents? |
FATIGUE is chief complaint-
Fever is the sign for Dx infection- Leukopenia during chemo- signs of thrombocytopenia- anemia, SOB, wt loss, activity intolerances, bone/joint pain, HA, anorexia, splenomegaly- |
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Leukemia
Acute- Chronic- Assessment? |
pain in joint, spleen, liver-
nutrition, sign of bleeding of infection, CBC, H&H, PLT *must have biopsy for diagnosis* |
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Leukemia
Acute- Chronic- Treatment? |
pain meds, antiemetics, Chemo, bone marrow transport, biologics (kick start immune system)-
*protect from infection* oral care, hydration & nutrition |
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Lymphoma
Hodgkin's Lymphoma Non-Hodgkin's Lymphoma |
group of malignant neoplasms that affect the lymphatic system.
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Hodgkin's Lymphoma
Characterized by? |
Characterized by presence of Reed-Sternberg cells-
originates in one lymph node and spreads to others. can infiltrate other tissues. peaks in 2 age groups 15-35 & 50-70 often older Caucasian men no known cause just risks |
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Non-Hodgkin's Lymphoma
Characterized by? |
no known cause just risks-
often older Caucasian men 50-70 originates outside lymph system- lack of Reed-Sternberg cells- |
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Lymphoma
Hodgkin's Lymphoma Non-Hodgkin's Lymphoma How it presents? |
insidious onset, painless lymph node enlargement cervical, axillary, then on to the inguinal nodes.
More Advanced Stage: wt loss, night sweats, malaise, chills, pruritis, anorexia, renal failure- |
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Multiple Myeloma
What? |
a cancer of the plasma cell, it is an incurable but treatable disease.
mostly men 50-69 prominent in African Americans (2X) unknown cause- no cure |
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Multiple Myeloma
Characterized by? |
bone pain, Bence Jones proteins, increased blood viscosity
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Multiple Myeloma
How it presents? |
insidious onset, bone pain number 1 complaint, infection, osteoporosis, renal stones, hypercalcemia from bone destruction, GI distress, musculoskeletal disorders
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Multiple Myeloma
Assessments? |
pain, fractures, balance/gait, kidney function, CV function
No cure: manage pain, blood products |
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Thrombocytopenia
What? |
platelet count less than 100,000/mm3
ectopic causes unknown usually associated with other disease processes. |
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Thrombocytopenia
Treatment? Neumega!!! |
watch and teach for signs of bleeding and potential dangers-
monitor PLT counts, use caution with veinipunctures |
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Immune (Idiopathic) Thrombocytopenia Purpura (ITP)
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destruction of platelets is greatly accelerated. Platelets become coated with antibodies as a result of autoimmune response.
Acute : Common in children Chronic: Common in adults More prevalent in females age 20-40 |
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Secondary:
Immune (Idiopathic) Thrombocytopenia Purpura (ITP) |
Due to:
Medications, Spices Viral or bacterial infections Bone marrow disorders Chemo and radiation |
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Hemophilia
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Hereditary clotting factor disorders
Prolonged coagulation time X-linked recessive disorder Carried by females Disorder almost exclusively in males |
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Hemophilia A
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Deficiency in factor VIII
Deficiency is determined by first performing a PTT on client’s plasma |
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Hemophilia B (Christmas disease)
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Deficiency in factor IX
Vitamin dependent beta globulin Dependent on amount of thromboplastin |
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Hemophilia
Characterized by? |
prolonged bleeding
Spontaneous bleeding can occur Bleeding usually occurs in the joints |
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Hemophilia
Treatment? |
Replace deficient factor
Hemo A: Cryoprecipitate with factor VIII Hemo B: Plasma or factor IX concentrate NEVER GIVE ASPIRIN Joint bleeding: o Rest joint o Apply ice o Administer hemophilia factors |
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Disseminated Intravascular Coagulopathy (DIC)
What? |
abnormal response of clotting mechanisms
Clot process is accelerated and normal clotting substances become depleted |
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Disseminated Intravascular Coagulopathy (DIC)
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May become side effect in some forms of shock
Most common with septic shock Occurs secondary to other disorders |
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Disseminated Intravascular Coagulopathy (DIC)
Secondary causes? |
Sepsis, Shock, Malignancy
Liver disease, Metabolic disorders Circulatory disorders GYN conditions Spinal or brain injuries Transfusion reactions Immune disorders |
