Hematology Flashcards
(92 cards)
1
Q
What does a complete blood count tell you?
A
Number of blood cells, structure, function
2
Q
Hematocrit
A
Percent of RBC mass in 100 ml plasma volume. Decreased hematocrit: fluid overload/dilution
Increased hematocrit: dehydration
3
Q
Leukocytes
A
White blood cells; identify underlying conditions/infection
4
Q
Thrombocytes
A
Platelets; required for blood coagulation
5
Q
Erythrocyte ranges
A
Male: 4.2-5.4 x10^6/uL
Female: 3.6-5.0 x10^6/uL
Reticulocytes: 1-1.5% of total blood
6
Q
Hemoglobin ranges
A
Male: 14-16.5 g/dL
Female: 12-15 g/dL
7
Q
Hematocrit ranges
A
Male: 40-50%
Female: 37-47%
8
Q
RBC indices
A
Differentiate anemias by RBC size or color.
Iron deficiency: Small MCV (RBC size/volume); low MCHC (RBC concentration of Hgb); low MCH (red blood cell mass)
9
Q
Mean corpuscular volume (MCV)
A
85-100 fL
Microcytic anemia: Iron deficiency anemia
Macrocytic anemia: Pernicious anemia
10
Q
Mean corpuscular hemoglobin concentration (HCHC)
A
31-35 g/dL; RBC concentration of Hgb, which accounts for color (normochromic or hypochromic)
11
Q
Mean cell hemoglobin (MCH)
A
27-34 pg/cell; RBC mass (less useful in classifying anemia)
12
Q
Leukocyte range
A
4,500-10,000 uL or mm^3
Increased: Leukocytosis infection/systemic response
Decreased: Leukocytopenia; AIDS/HIV; risk for infections
13
Q
SEG; mature neutrophil (granulocyte/phagocyte) range
A
3,000-5,800 uL or mm^3
Immune defense against pathogens; increased seg during bacterial or fungal infections
14
Q
Immature neutrophils (band/granulocyte/phagocyte) range
A
150-400 uL or mm^3
Increase in bands, decrease in segs during systemic infection
15
Q
Eosinophil (granulocyte/phagocyte) range
A
50-250 uL or mm^3
Immune defense against allergens, asthma and parasites (histaminase that inactivates histamine); decreased inflammatory response
16
Q
Basophil (granulocyte/phagocyte) range
A
15-50 uL or mm^3
Allergic and hypersensitivity reaction mediators; histamine (vasodilator); heparin (anticoagulant)
17
Q
B-cell lymphocyte (agranulocyte) range
A
1,500-3,000 uL or mm^3 (10%)
Antibody plasma cells that recognize antigens; humoral mediated immunity; promote wound healing
18
Q
T-cell lymphocyte (agranulocyte) range
A
1,500-3,000 uL or mm^3 (80%)
From thymus; activates other immune system cells; cell mediated immunity
19
Q
Natural killer cell (agranulocyte) range
A
1,500-3,000 uL or mm^3 (10%)
Innate and natural immunity; destroys foreign cells and cancer cells
20
Q
Monocyte (agranulocyte) range
A
285-500 uL or mm^3
Moves from blood vessels to tissue and become macrophages; engulf bacteria/cell debride
21
Q
Macrophages (agranulocyte)
A
Immune response by activating lymphocytes; present antigen to T-cells
22
Q
Thrombocytes
A
Cell fragments; membrane without nucleus; cannot replicate; give platelets for lost platelets
23
Q
Platelet (PLT/thrombocyte) range
A
150,000-400,000 uL or mm^3
PLT adhesion forms bloodclots
24
Q
Bleeding time
A
2-7 minutes
*Prolonged in thrombocytopenia
25
Clotting time
8-12 minutes
*Prolonged in thrombocytopenia
26
Prothrombin time (PT)
12.7-15.4 seconds
Extrinsic clotting cascade; liver disease; impaired vitamin D production; measures Warfarin levels
27
Partial prothrombin time (PTT)
25-35 seconds
Measures intrinsic clotting cascade; prolonged in hemophilia A, B, and C; Von Willebrand's disease
28
International normalized ratio (INR)
Without anticoagulant therapy: 1
With anticoagulant therapy: 2-3
Measures extrinsic clotting potential. Preferred method to measure Warfarin levels.
29
Decreased hemoglobin abnormalities and CM
Anemia; blood loss
CM: Headaches, fatigue, lack or concentration, hemolysis (release of bilirubin leads to jaundice)
30
Increased hemoglobin abnormalities and CM
Smoking, high altitude, hypoxia
CM: Flush skin, fatigue, dizziness, headaches, vision changes
31
Decreased hematocrit abnormalities and CM
Dilution, pregnancy
CM: Fatigue, weakness, pallor, SOB, headaches
32
Increased hematocrit abnormalities and CM
Dehydration
CM: Decreased heat tolerance, excess sweating, weakness, fatigue, bloody stool, dehydration
33
Decreased WBC abnormalities and CM
Leukocytopenia
CM: Body aches, fever, chills, headaches, prone to infections
34
Increased WBC abnormalities and CM
Leukocytosis
CM: Fatigue, fever, lightheadedness, pallor, SOB, infection, systemic inflammation
35
Decreased platelets abnormalities and CM
Thrombocytopenia
CM: Fatigue, purpura, rash, petechiae, prolonged bleeding, nose bleeds, blood in urine/stool
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Increased platelets abnormalities and CM
Thrombocythemia
CM: Erythromelalgia (burning sensation), numbness in extremities, headache, weakness, vision changes, high index of suspicion for cancer
37
Clotting cascade factors
Intrinsic: Unfractionated heparin binds with active antithrombin; XII, XI, IX+VIII, X+V, II, I (fibrin)
Extrinsic: III (tissue factor), VII, X+V, II, I (fibrin)
38
Location of clotting cascade
Intrinsic: Endothelial lining (inside blood vessels)
Extrinsic: Tissue (outside of blood vessels)
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Time of clotting cascade pathway
Intrinsic: Slow
Extrinsic: Fast
40
Pharmacology
Intrinsic: Heparin inhibits; binds with antithrombin III then inhibits thrombin, Xa, Ixa, fibrin. IV route for high molecular weight, SQ for low molecular weight.
Fast acting and prevents the formation of new clots and inhibits existing clots from enlarging.
Extrinsic: Warfarin/Coumadin/Jantoven; inhibits II, VII, IX & X (stops producing fibrin). Oral route. Vitamin K antagonist, delayed onset to work, prevents new clotting factors from forming (fibrin). Avoid during pregnancies!
41
Antidote to clotting cascade
Intrinsic: Protamine sulfate
Extrinsic: Vitamin K
42
Serum monitor for clotting cascade
Intrinsic: Activated PTT; therapeutic range 60-80 seconds
Extrinsic: PT; INR therapeutic range 2-3
43
Reason for treatment of clotting cascade
Intrinsic and extrinsic: DVT, pulmonary embolism, prosthetic heart valves, myocardial infarction, cancer
44
Diet for clotting cascade treatment
Intrinsic: Garlic, onions, ginger, cannabis, papaya, mango, tobacco
Extrinsic: Limit green leafy vegetables, green tea, cranberries
45
What are the five stages of hemostasis (blood clotting)?
Initial injury
1. Vascular constriction
2. Formation of the platelet plug (primary hemostatic)
3. Blood coagulation (clotting cascade; secondary hemostatic)
4. Formation of blood clot
5. Clot retraction (clot dissolution)
Wound heals
46
What happens during stage 1 hemostasis?
Vessel constriction (endothelin 1) happens within one minute; neural reflexes and humoral factors are released from platelets and traumatized tissue,
Platelets release calcium and thromboxane A2 which is a vasoconstrictor responsible for vasospasms. Coagulation happens.
47
What happens during stage 2 hemostasis?
Platelets encounter damaged vessel wall. They change from smooth disks to spiny spheres. Adhesion requires von Willebrand Factor.
Degranulation and alpha & delta granule occur after platelet adhesion.
48
What happens during stage 3 hemostasis?
Coagulation cascade; conversion of soluble plasma protein fibrinogen into insoluble fibrin strands create meshwork to form blood clots.
Intrinsic and extrinsic coagulation pathways (prothrombin to thrombin and fibrinogen to fibrin)
Antithrombin III inactivates coagulation factors which protects uncontrolled thrombus formation on endothelial surface.
49
Describe intrinsic pathway hemostasis
Slow process caused by severe injury. Factor XII (Hageman) activated by blood in contact with collagen within the injured vessel, creating a clot in 1-6 minutes. Diagnosed by partial thromboplastin time (aPTT). Interventions include Heparin (IV), low molecular Heparin (SQ) and protamine sulfate (Heparin antidote).
50
Describe extrinsic pathway hemostasis
Rapid process caused by not as severe injury. Activated when blood encounters tissue extract. Clot is created in 15 seconds. Tissue factors thromboplastin and Factor III are released. Prothrombin time (PT) or international normalized ratio (INR) used for diagnosis. Interventions are Coumadin/Warfarin and vitamin K (antidote).
51
Clot retraction hemostasis
Occurs 20-60 minutes after clot forms. Serum is squeezed from clot to join edge of broken vessel. Platelets help with clot retraction (many required).
52
Clot dissolution hemostasis
Begins shortly after formation. Fibrinolysis strands of clots dissolve and plasminogen converts to plasmin. Outcome: Fibrin stabilizes clot and plasmin digests fibrin strands.
53
Which electrolyte is essential for the clotting cascade to work?
Calcium (Factor IV)
Not required for step 1 or 2, but all other steps of clotting process.
54
Thrombocytopenia etiology and clinical manifestations
Etiology: Decreased platelet number and production, increased platelet destruction; spontaneous bleeding in small vessels (mucus membrane & skin); ITP; TTP (fever & renal failure); drug-induced; impaired platelet function (due to uremia or VWD).
CM: Rash, petechiae, purpura, bruising, ecchymosis, hematomas, hematuria, hemarthroses
55
Thrombocytopenia diagnosis & PIE
Diagnosis: Med Hx and assessment; normal platelet range; circulating platelets <100,000 microL (<50,000 is prone to bruising and bleeding, spontaneous bleeding with <20,000)
Plan: Treat underlying causes
Interventions: Give platelets; plasmapheresis, medicine reconciliation, soft bristle toothbrush, closed toe shoes, antipyretics.
Evaluation: Platelet range 150,000-400,000 uL
56
Von Willebrand Disease etiology and clinical manifestations
Etiology: Decreased platelets adhesion & aggregation
Autosomal dominant disorders-Type 1 (mild), Type 2 (mild/moderate), Type 3 (severe/rare)
CM: Spontaneous bleeding (nose, gums, GI; hemoptysis, blood/tarry stool), excessive menstrual flow, excessive/prolonged bleeding with normal platelet count post surgery/dental work.
57
Von Willebrand Disease diagnosis and PIE
Diagnosis: Med Hx & assessment, genetic test
Plan: Correct underlying causes
Interventions: Routine treatment unnecessary for mild bleeding; Factor VIII, vWF complex, and desmopressin acetate (only useful for type 1); NO ASPIRIN
Evaluation: No bleeding
58
Hemophilia A & B etiology and clinical manifestations
Etiology: Sex-linked recessive disorder, hemophilia A is Factor VIII deficient, hemophilia B is Factor IX deficient and a spontaneous gene mutation.
CM: Spontaneous bleeding (soft tissue, GI, joints)
59
Hemophilia A & B diagnosis and PIE
Diagnosis: Med Hx & assessment, genetic test
Plan: Correct underlying causes, genetic counseling
Interventions: Prevent traumatic injuries; administer Factor VIII for type A and IX & DDVAP for type B (also avoid aspirin and NSAIDS)
Evaluation: No bleeding
60
Disseminated intravascular coagulation etiology
Widespread coagulation and bleeding in vascular compartments. Complication from other conditions. Starts with massive activation of coagulation sequence where there is unregulated production of thrombin that leads to the systemic formation of fibrin which decreases anticoagulants. Microthrombi cause occlusion, ischemia, and MODS. Clot formation consumes coagulating proteins and platelets, plasmin breaks down fibrin and acts as an anticoagulant (increases D-dimer). Extrinsic pathway activates by tissue trauma/obstetric disorders; intrinsic pathway activate by endothelial damage/Factor XII
61
DIC clinical manifestations, and DPIE
CM: Petechiae, purpura, puncture site oozing, severe hemorrhage, uncontrollable postpartum bleeding
Diagnosis: Med Hx & assessment, increased PTT, PT & D-dimer (serum fibrin degradation products).
Plan: Correct underlying causes
Interventions: Supportive care, blood product administration,
Evaluation: No bleeding or clots
62
DIC can be the result of
Tissue trauma, vascular endothelial injury, or sepsis (can be contributing factor)
63
Erythropoiesis
RBC life cycle: 120 days
Formation starts in bone marrow for adults (pelvis, rubs, sternum). Erythroblasts come from myeloid stem cells. Erythrocyte (immature) to reticulocyte to erythrocyte (mature, requires erythropoietin).
Erythropoietin hormone is stimulated by hypoxia or anemia. Requires iron, protein, vitamins B12,6 and folic acid
64
Destruction and elimination of RBC
RBC are 3 mm in diameter while micro blood vessels are 8 mm in diameter. Eventually they lose elasticity and become trapped in the liver and spleen. Heme is broken down into bilirubin (pigment). Globin is recycled for protein synthesis and iron is recycled to form new hemoglobin within bone marrow
65
Unconjugated bilirubin
Accumulates in blood, fat soluble, jaundice seen in sclera and skin
66
Conjugated bilirubin
Removed from blood by liver, water soluble, excreted in bile and urine (pigment)
67
Anemia ADPIE
CM: Hemorrhage, pallor from decrease Hgb, tachycardia, fatigue, palpitations
Diagnosis: Med Hx and assessment, decreased RBC, Hgb levels <8 g/dL
Plan: Correct underlying causes
Interventions: Blood transfusion, iron supplements, nutrition consult
Evaluation: RBC within normal range
68
Iron deficiency anemia ADPIE
Can come from menstruation, pregnancy, inadequate Fe intake, excessive aspirin & NSAID intake
CM: Pallor, smooth tongue, mouth lesions, dysphagia, tachycardia, waxy/pallor brittle hair & nails, spoon-shaped fingernails, pica
Diagnosis: Stool occult blood test, decreased hemoglobin & Fe & ferritin, colonoscopy
Plan: Correct underlying causes
Interventions: Stop the bleed, oral supplements, iron therapy, vitamin C to increase Fe absorption
Evaluation: Normal iron levels (8-24 umol/L)
69
Megaloblastic anemia (pernicious and folate deficiency)
Impaired DNA synthesis results in enlarged RBC (MCV >100 fL) due to impaired maturation and division. RBC produced are abnormally large due to excess cytoplasmic growth and structural proteins
70
Pernicious anemia ADPIE
Etiology: Vitamin B12 deficiency from strict veg. diet
CM: Jaundice, atrophic gastritis, neurologic syndrome (symmetric paresthesia and hands and feet, demyelination of dorsal and lateral spinal cord columns, loss of senses, spastic ataxia
Diagnosis: Med Hx & assessment; increased MCV, decreased B12; Schilling test; low folic acid level
Plan: Correct underlying causes
Interventions: Discontinue ETOH, vitamin B12 supplements
Evaluation: RBC in normal range
71
Folate deficiency ADPIE
Etiology: Malnutrition, GI disorders, celiac disease, ETOH abuse, anti-epileptic medications
CM: Jaundice, GI disturbances
Diagnosis: Med Hx and assessment, decreased folic acid
Plan: Correct underlying causes, avoid methotrexate (cancer therapy; inhibits conversion of folic acid)
Interventions: Folate supplements, dietary counseling (increased meat, eggs, and green leafy vegetables)
Evaluation: RBC in normal range
Plan:
72
Aplastic anemia etiology and CM
Etiology: Disorder of pluripotential bone marrow stem cells; life-threatening, pancytopenia (decreased RBC, WBC, & platelets). Unknown mechanism of underlying pathogenesis; failure of bone marrow to replace aging RBC that are destroyed.
CM: Fatigue, pallor, petechiae, ecchymosis, epistaxis, gingivitis, GI bleeding
73
Aplastic anemia DPIE
Diagnosis: Med Hx & assessment (identifying toxic agent exposure), CBC serum smear (pancytopenia), decreased serum leukocytes and neutrophils.
Plan: Correct underlying causes
Interventions: Remove toxic exposure, hematopoietic stem cell replacement, immunosuppressive therapy, infection control RBC transfusion, platelet and clotting factors infusion
Evaluation: CBC within normal range
74
Sickle cell anemia etiology
Recessive inherited disorder; HbS sickles when deoxygenated or hypoxia, may return to normal shape when oxygenated in lung. With repeated deoxygenation events, the cell remains sickled. Chronic hemolytic anemia, sickle cells are poor carriers of O2 molecules, sickle shape leads to vascular occlusion and ischemia. Fragile RBCs break down in spleen, leading to a high infection risk.
75
Lifespan and prevalence of sickle cell anemia
Life span of sickle cell: 20 days
8% of AA population is heterozygous for sickle cell trait. 0.1-0.2 of AA population is homozygous for disease. In parts of Africa where malaria is endemic, gene frequency approaches 30% of population because of its protective mechanism against mosquitoes.
76
Sickle cell anemia ADPIE
CM: Jaundice, chest pain, cough, fever (prone to infection), neurological changes (stroke, transient ischemic attack, cerebral bleed), vision impairments
Diagnosis: Med Hx & assessment, genetic test, chest x-ray for pulmonary infiltrate
Plan: No cure
Interventions: Oxygenation, hydration, pain management, blood transfusion, genetic counseling, stem cell transplant, maintain immunizations, hydroxyurea
Evaluation: Pain free
77
What supplement should be taken for pernicious anemia?
Cobalamin (B12) supplements
78
Hodgkin lymphoma etiology
Good prognosis with bimodal age distribution (15-40, >55). Lymphoma with abnormal atypical mononuclear tumor cells (Reed Sternberg). Unknown etiology; possible carcinogen/virus/genetic mechanism exposure; arises in a single node or chain of nodes. Spreads first to lymphoid tissue.
79
Non-Hodgkin lymphoma etiology
Poor prognosis. Originates from lymphocytes. Spreads in unpredictable fashion (B-cell is most common lymphoma, T-cell, NK cell). Unknown etiology; possible carcinogen/virus/genetic mechanism exposure.
80
Hodgkin lymphoma ADPIE
CM: Painless lymphadenopathy. Single, initial lymph node involvement above level of diaphragm. Group of nodes can be affected too. Fever, chills, night sweats, weight loss
Diagnosis: Med Hx & assessment, hallmark biopsy analysis (Reed-Sternberg cell), mediastinal masses on CXR/CT scan
Plan: Prepare for lymph biopsy, infection control
Interventions: Chemotherapy, radiation therapy
Evaluation: Staging is of great clinical importance; above/below diaphragm; disseminated
81
Non-Hodgkin lymphoma ADPIE
CM: Painless lymphadenopathy; local; systemic (retroperitoneum, mesentery, pelvis); fever, drenching night sweats, weight loss
Diagnosis: Med Hx & assessment, hallmark on biopsy analysis (No Reed-Sternberg cells), mediastinal masses on CXR/CT scan
Plan: Prepare for lymph biopsy, infection control
Interventions: Radiation therapy, chemotherapy
Evaluation: Stage of disease; clinical status of client
82
What is leukemia?
Malignant neoplasm of cells that originate from hematopoietic precursor cells. Leukemic cells spill into blood. Term first used by Dr. Rudolf Virchow. Normal RBC/WBC ratio is 333/1 but this is inverse for leukemia.
Leukemia increases neoplasm, unregulated and proliferating immature WBCs.
83
Leukocytosis
Increased WBCs (sign of infection response/inflammation)
84
Leukemia etiology and risk factors
Etiology: Unknown, but high incidence for people exposed to high levels of ionized radiation
Risk factors: Genetics, immune disorders, ionized radiation/carcinogenic agents
85
Acute lymphocytic leukemia (ALL)
75% of children leukemia
86
Chronic lymphocytic leukemia (CLL)
Common among adults (38%), malignancy of B-cells, fatal disease
87
Acute myelocytic leukemia (AML)
Common among adults (30%)
88
Chronic myelocytic leukemia (CML)
Typically affects older adults, spontaneous chromosome mutation, disorder of pluripotent hematopoietic progenitor cells
89
Leukopenia
Decrease in absolute number of leukocytes in serum. Affects specifically neutrophils. Critical role in host/defense mechanism against infections
90
Neutropenia
Decreased number of neutrophils, increased risk for infections, absolute neutrophil count (ANC) and duration influence severity of infection
91
Agranulocytosis
Absence of neutrophils
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How do you calculate ANC and what is its normal range?
ANC = Segs + Bands x WBC/100
Normal ANC: 1,000/uL
*Client placed on neutropenic precautions if ANC<500/uL
