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312 Cards in this Set
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What is 12 - 20 um, N:C ratio 8:1 has royal blue cytoplasm, FINE chromatin, 1 - 2 nucleoli. Normally CONFINED in the BM
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Pronormoblast or rubriblast
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What is 10 - 15 m, N:C ration 6:1. Chromatin is COARSER, with slightly visible PARACHROMATIN, nuc usually NOT VISIBLE. Normally CONFINED in the BM
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Basophilic normoblast or prorubicyte
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What is 10 - 12 um, N:C ratio 4:1. Cytoplasm is POLYCHROMATOPHILIC due to HGB production. Chrom is CLUMPED with distinct areas of PARACHROMATIN. LAST stage to DIVIDE. Normally CONFINED in the BM
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Polychromatic normoblast or rubricyte
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What is 8 - 10 um, N:C 1:2, nucleus is PYKNOTIC. LAST NUCLEATED stage, normally CONFINED in the BM
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Orthochromic normoblast or metaubricyte
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What is 7 - 10 um, POLYCHROMATOPHILIC, NO NUCLEUS, reticulocyte with SUPERVITAL STAIN. 0.5 - 2& of RBCS in adult peripheral blood
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Polychromatophilic erythrocyte (reticulocyte) or diffusely basophilic erythrocyte (retic)
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What is 7 - 8 um, BICONCAVE disc. reddish-pink cytoplasam with area of central pallor one third the diameter of the cell
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mature erythrocyte
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What is it called when erythrocytes stain differently various shade of blue pink etc
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polychromomatophilic
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What is the function of Erythrocyte where is it site of production & what is it life span?
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O2 transport, BM & 120 days
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What is the function of Granulocytes where is it site of production & what is it life span?
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defense against bacterial infection, BM & 9 - 10 days
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What is the function of Lymphocytes where is it site of production & what is it life span?
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cellular & hummoral immunity, lymphoid tissue (B lymphs 1 - 5 days & T lymps 60 - 530 days)
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Which Acute Nonlymphocytic Leukemia (ANLL) is described as: having undifferentited blasts - that are common in adults
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acute myelogenos without maturation AML (M0)
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Which Acute Nonlymphocytic Leukemia (ANLL) is described as: PO of MYELOBLASTS with mim maturation, some promyelocytes may be present, AUER RODS may be present, PSEUDO PELGER HUET anomaly may be present - that are common in adults
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acute myelogenous with mim maturation AML (M1)
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Which Acute Nonlymphocytic Leukemia (ANLL) is described as: MYELOBLAST PO, some maturation to or beyond promyelocyte stage. AUER RODs are common, most COMMON type of acute myelogenous leukemia
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acute myelogenous with maturation AML (M2)
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Which Acute Nonlymphocytic Leukemia (ANLL) is described as: the PROMYELOCYTE is the PO cell. myeloblasts & myelocytes may be present. AUER RODS are common, high incidence of DIC. uncommon type
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acute promyelocytic APL (M3)
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Which Acute Nonlymphocytic Leukemia (ANLL) is described as: earl myelogenous cells PO with approx 20% MONOCYTIC cells, blasts may have indented & convoluted nuclei, AUER RODS may be present, PSEUDO PELGER HUET anomaly may be present, SECOND most common type
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acute myelomonocytic AMML (M4)
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Which Acute Nonlymphocytic Leukemia (ANLL) is described as: having M5a has a PO of MONOBLASTS. M5b has promonocytes & monocytes as well. uncommon type
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acute monocytic AMoL (M5)
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Which Acute Nonlymphocytic Leukemia (ANLL) is described as: Erythroblats with MEGALOBLASTOID changes & other dysplastic features, MYELOBLASTS & PROMYELOCYTES, AUER RODS may be present
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acute erythroleukemia (Di Gugliolmo syndrom) EL (M6)
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Which Acute Nonlymphocytic Leukemia (ANLL) is described as: proliferation of MEGAKARYOBLASTS & ATYPICAL MEAGAKAROCYTES. megakaryocytic fragments may be seen in the peripheral blood. uncommon type
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acute megakrayoblastic MegL (M7)
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What is the term for rapidly progessive disease w/ abnormal expansion of immature cells & blasts
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acute leuk
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What is the term for slowly progessive with abnormal expansion of mature cells
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chronic leuk
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What is the leukemia at the genetic aspect
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its a mutation & altered expression of ONCOGENES & TUMORS suppress genes
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Myeloid encompasses 4 types of leuk, what are they
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granulocytic, monocytic, megakaraocytic & erythrocytic
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Define AML
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cancer of the blood & myeloid line of WBCs & BM, rapid progression & affect IMMATURE blood cells rather than mature cells
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Of the three different Acute Lymphoblastic Leukemia (ALL) which is uniform population of small LYMPHOBLASTS w/ scanty cytoplasm, round nuc with occ CLEFTING, homo chromatin, inconspicuous nuc. children
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L1 - small cell homogeneous)
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Of the three different Acute Lymphoblastic Leukemia (ALL) which is heterogeneous population of large PLEMORPHIC LYMPHOBLASTS with nuclear clefting & INDENTION. older children & adults
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L2 - large cell heterogeneous
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Of the three different Acute Lymphoblastic Leukemia (ALL) which is uniform population of relatively LARGE LYMPHOBLASTS with DEEPLY basophilic cytoplasm, VACUOLES & round to oval nuc WITHOUT indentations - secondary to BURKITT's LYMPHOMA
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L3 - Burkitt type
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Under the five immunologic marker classification of ALL, which has <5% of ALL. corresponds to FAB type L3
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B cell ALL
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Under the five immunologic marker classification of ALL, which has 10 - 15% of ALL. most are FAB type L1
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Pre-B cell ALL
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Under the five immunologic marker classification of ALL, which has 85% of childhood ALL & 75% of adult ALL. FAB type L1 or L2. Highest remission rate
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Pro-B cell ALL
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Under the five immunologic marker classification of ALL, which has 15% of ALL. FAB type L1 or L2. POOR PROGNOSIS
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T-cell ALL
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What is it called when lymphoid leuk & lymphomas are a clonal proliferation of lymphoid cells that have been "frozen" at a given stage of maturation typically retaining some features of their normally differentiated counterpart
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lymphocyte ontogeny
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Where is the B cell developed
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in the BM (larsa eqvnt tissue)
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Where is the T cell developed
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in the thymus
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With Chronic Lymphoproliferative disorders, what are the characteristics of Chronic lymphocytic leuk (CLL)
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1. common in adults
2. B-CLL is most common 3. lymphocytosis w/ relatively mature lymphocytes 4. smudge cells 5. may be acc by: anemia, thrombocytopenia & prodtx of autoantibodies (autoimmune hemolytic anemia or idiopathic thrombocytopeia purpura - low platelet count for unknown cause related to antibodies vs platelets |
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With Chronic Lymphoproliferative disorders, what are the characteristics of Hairy cell leuk
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1. scant to abundant, AGRANULAR, light grayish blue cytoplasm, with IRREGULAR HAIR like PROJECTIONS.
2. round to oval nuc with loose chromatin 3. PANCYTOPENIA 4. when lymphocytes become malignant & proliferates |
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Which Chronic Myeloproliferative Disorders (CMPD) is described with marked LEUKOCYTOSIS with an increase in MATURE & IMMATURE cells of the granulocytic series. THROMBOCYTOSIS is common, PHILADELPHIA chromosome may be found in malignant cells. Anemia
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chronic myelogenous leukemia (CML) or chronic granulocytic leukemia
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Which Chronic Myeloproliferative Disorders (CMPD) is described with BM FIBROSIS, extramedullary hematopoiesis, all stages of MYELOID maturation in peripheral blood, including immature EOS & BASOs, NUCLEATED RBCs, TEARDROP RBCS & defective PLATELETS
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agnogenic myeloid metaplasia (AMM) or idiopathic myelogibrosis. myelofibrosis with myeloid metaplasia
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Which Chronic Myeloproliferative Disorders (CMPD) is described with increased in ALL CELLULAR BM elements, increase H&H, increased leukocyte alkaline phosphatase (LAP)
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POLYCYTHEMIA VERA (PV) aka primary polycythemia, erythremia
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Which Chronic Myeloproliferative Disorders (CMPD) is described with platelets >1000 x 10 9/L, marked platelet anisocytosis, ocassional megakaryocyte fragments
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essential thrombocythemia (ET) (platelets norm range: 150 - 450)
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With Hematopoesis, give the period & age where this site(s) develop in the blood islands of yolk sac,
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mesoblastic - embyro @ 3rd - 12 th week of gestation
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With Hematopoesis, give the period & age where this site(s) develop in the liver, spleen, thymus, lymph nodes
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hepatic - fetus (beg @ 5th week of gestation)
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With Hematopoesis, give the period & age where this site(s) develop in the bone marrow
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myeloid - beg 5th MONTH of gestation & continuing throughout adult hood
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Notes: Mesoblastic
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primitive erythroblasts produce embryonic HGB ( gower I, gower II, portland)
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Notes: Hepatic
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the LIVER is the primary site of RBC production until the 6th month & may continue to produce blood cells to a lesser degree until 1 - 2 weeks after birth, in adult the liver & spleen may be reactivated for RBC production if the BM fails to keep up with the demand (EXTRAMEDULLARY HEMATOPOIESIS). the spleen, thymus, & lymph nods produce lymphocytes throughout life
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Notes: Myeloid
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by 3 weeks of age, the BM is the ONLY normal site of RBC production, in child all marrow is active. in adult, FAT fills the SHAFTs of the long bones & only active hematopoietic sites are in the PELVIS, VERTEBRAE, RIBS, STERUM, SKULL, & PROXIMAL EXTREMITIES of the long bones. fatty marrow may be reactivated to compensate for anemia
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whats the cause of megaloblastic
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vitamin B12 or folic acid deficiency
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what the cause of iron deficiency
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deficiency of iron
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whats a good example of megaloblastic
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pernicious anemia
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whats a good example of iron deficiency
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iron deficiency anemia
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whats are the characteristics of megablastic
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- macrocytic/normochromic anemia
- oval macrocytes, hypersegment neutrophils - (increase megaloblast in BM, macro oval in blood) - increase serum ions - increase serum bili - ineffective erythropoiesis (decrease retics) |
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whats are the characteristics of iron deficiency
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microcytic, hypochromic rbcs
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explain the nuclear & cytoplasm development in megaloblastic
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NUCLEAR maturation lags behind cytoplasmic maturation, cell grow larger without dividing - defective NUC maturation cause by impaired DNA sythz
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explain the nuclear & cytoplasm development in iron deficiency
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CYTOPLASMIC maturation lags behind nuclear maturation due to deficiency in iron needed for HGB sythz
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whats the main cause of Vit B12 deficiency is
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pernicious anemia that LACK INTRINSIC FACTOR - glycoprotein needed for absorption of VIT B12
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Define pernicious anemia
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a form of megaloblastic anemia due to vita b12 deficiency cause by IMPAIRED ABSORPTION of vit b12
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What are the Schiling test results for pernicious anemia
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Part 1 - abnormal
Part 2 - corrected |
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Troubleshooting Wright stained blood, what would be the cause of this problem: necrobiotic WBCS
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blood more than 5 hours old
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Troubleshooting Wright stained blood, what would be the cause of this problem: rouleaux
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delay in spreading blood, smear too thick, increased proteins (multiple myeloma)
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Troubleshooting Wright stained blood, what would be the cause of this problem:created RBCS
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slow drying, humidity, blowing on slide, blood more than 5 hours old
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Troubleshooting Wright stained blood, what would be the cause of this problem: moth eaten (laked) rbcs
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water in stain, humidity, blowing on slide to dry
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Troubleshooting Wright stained blood, what would be the cause of this problem: rbcs appear small, stacked & without central palor, wbcs are distorted
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too far into smear
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Troubleshooting Wright stained blood, what would be the cause of this problem: rbcs appear large, flat no central parlor
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too closed to the feathered edge
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define thalassemia
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genetic defect result in REDUCE rate of sythz of one of the globin chains that make up HGB
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what is the molecular strx for HGB A
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two ALPHA & two BETA
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what is the molecular strx for HGB A2
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two ALPHA & two DELTA
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what is the molecular strx for HGB F
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two ALPHA & two GAMMA
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what is the molecular strx for HGB S
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VALINE sub for glutamic acid in 6th position of beta chain
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what is the molecular strx for HGB C (autosomal recessive disorder that cause mild hemolytic anemia)
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LYSIN sub for glutamic acid in 6th position of beta chain (protects against MALARIA)
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What is HGB F function
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main O2 transport for protein (for babies)
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What does HGB S do to the RBCs
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abnormal HGB cause distorted RBCs = fragile + prone to rupture cz anemia
- sickle cell can block BV tissue & organ damage & pain |
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What are the adult reference ranges for A, A2, & F
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A = 97 %
A2 = 2 % F = 1% |
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What are the newborn reference ranges for A, A2, & F
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A = 20%
A2 = 2 % F = 80% |
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This HGB derivative cause IRON to be oxidized FERRIC (Fe3+) state, usually acquired from exposure to oxidant, rarely inherited
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methemoglobin
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What are the effect of methemoglobin with O2
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can not bind O2, cynaosis, possible death - HENIZ bodies, treated with METHYLENE BLUE
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This HGB derivative cause sulfur bound to heme, acquired from exposure to drugs & chemicals
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sulfhemoglobin
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what are the effects of sulfhemoglobin in O2
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O2 afinity, 1/1000th normal, cyanosis - this can not be converted back to normal HGB, NOT DETECTED in cyamethemoglobin method
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This HGB derivative cause carbon monoxide bound to heme
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carboxyhemoglobin
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what are the effect of carboxyhemoglobin in O2
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reduced O2 to tissue, can be fatal - the affinity of HGB for Co is 200x that for O2 skin turns CHERY RED
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Troubleshooting the Wright Stain blood smear - what is the possible cause of drop of blood too large, spreader slide held at too high an angle, spreading too quickly, polycythemia
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smear too thick
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Troubleshooting the Wright Stain blood smear - what is the possible cause of drop of blood too large
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smear too long
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Troubleshooting the Wright Stain blood smear - what is the possible cause of drop of blood too small, spreader slide not high enough angle, spreading too slowly, anemia
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smear too thin
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Troubleshooting the Wright Stain blood smear - what is the possible cause of drop of blood too small
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smear too short
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Troubleshooting the Wright Stain blood smear - what is the possible cause of change in angle of spreader slide during spreading, spreading too slowl
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wavy smear
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Troubleshooting the Wright Stain blood smear - what is the possible cause of dirt slide, increased lipids
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holes in slides
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Troubleshooting the Wright Stain blood smear - what is the possible cause of dirty or chipped spreader slide
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tails of blood beyond feathered edge
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Troubleshooting the Wright Stain blood smear - what is the possible cause of uncleaned spreader slide edge, delay in spreading drop of blood, not spreading entire drop of blood, spreading before drop has completely flowed along spreader slide, pressure on spreader slide, pushing spreader slide too slowly, bullet shaped smear, can result in false lymphocytosis
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large WBCs pushed to side & feathered edge
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Troubleshooting the Wright Stain blood smear - what is the possible cause of smear not completely dried before staining, inadequate fixation
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thick part of smear flake off during staining
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Troubleshooting the Wright Stain blood smear - what is the possible cause of overstaining, inadequate washing, slide stained after 1 week, increased proteins
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blue appearance macroscopically
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Troubleshooting the Wright Stain blood smear - what is the possible cause of RBC agglutination
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grainy appearance macroscopically
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Troubleshooting the Wright Stain blood smear - what is the possible cause of increase WBC or platelets
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blue specks at feathered edge
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Troubleshooting the Wright Stain blood smear - what is the possible cause of overwashing, understaining, bad stain
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faded, washed out appearance macroscopically
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Troubleshooting the Wright Stain blood smear - what is the possible cause of inadequate washing, unfiltered stain, uncleaned slides, drying during staining
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precipitate
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Troubleshooting the Wright Stain blood smear - what is the possible cause of platelet clumped at feathered edge, inadequate buffering, pH too acidic
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no platelet seen
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Troubleshooting the Wright Stain blood smear - what is the possible cause of platelet satellitosis due to EDTA, make smear directly from fingerstick to avoid artifact due to anticoag
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platelet surrounding neurtophils
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Troubleshooting the Wright Stain blood smear - what is the possible cause of overstaining, inadequate washing, stain or buffered too alkaline (pH >6.8), film too thick, smear too old, protein abnormality, heparin, very high WBCS with many blasts
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bluish rbcs
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Troubleshooting the Wright Stain blood smear - what is the possible cause of understaining, overwashing, stain or buffer too acid (pH<6.4)
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red appearance macroscopically, bright red RBCs, pale nuclei in WBCS
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What etiology does iron deficiency have
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inadequate iron for HGB sythz
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What etiology does siderblastic anemia have
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emz defect in heme
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What etiology does anemia of chronic disease have
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defective iron utilization
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What etiology does beta thalassemia minor (b) have
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decrease production of beta chain (heterozygous)
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What etiology does beta thalassemia MAJOR (Cooley's anemia) have
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decrease in production in beta chain (homozygous)
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What etiology does pernicious anemia have
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reduced intrinsic factor secondary to gastric atrophy, deficiency in vit b12 impairs DNA sythz
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what classification is iron deficiency
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microcytic, hypochromic
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what classification is sideroblastic anemia
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microcytic, hypochromic
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what classification is anemia of chronic disease
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usually normocytic, normochromic one fourth to one third may be microcytic, hypochromic
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what classification is beta thalassemia minor
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microcytic, hypochromic
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what classification is beta thalassemia mahor
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microcytic, hypochromic
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what classification is pernicious anemia
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MACROCYTIC
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what anemia is describe as having: macro-ovalocytes, normal teardrops, hypersegmentation with LOW wbcs & LOW platelets
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pernicious anemia
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what anemia is describe as having: marked aniso & poik, hypochromic microcytes, targe calls, ovalocytes, nucleated RBCS, basophillic stippling
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beta thalassemia major (cooley's anemia)
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what anemia is describe as having: aniso, poikm hyprochromic microcytes, target cells, basophillic stippling
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beta thalassemia minor (B)
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what anemia is describe as having: normal or hypochromic microcytic RBCs
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anemia of chronic disease
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what anemia is describe as having: dimorphic RBCs, pappenheimer bodies, basophillic stippling
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sideroblastic anemia
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what anemia is describe as having: aniso, poik, hyperchromic microcytes
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iron defncy
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what is ferritin
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protein inside cell that STORES FE+ for later use, its the body current STORAGE for iron
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What is LD test for and where is it found
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isoEMZ converts PYRUVIC ACID 2 LACTIC ACID, found in the liver, kidney, straited muscles, myocardium tend to accumulate when organ/tissue is diseased or injured
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what is the etiology of sickel cell anemia (ss)
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inheritance of sickel cell gene from BOTH parents, sub of VALINE for glutamic acid on the 6th position of the beta chain
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what is the etiology of sickel cell trait (as)
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inheritance of sickle gene from ONE parent
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what is the etiology of HGB C disease (cc)
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inheritance of gene for HGB C from BOTH parents. LYSINE is sub for glutamic acid in the 6th position of the beta chain
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CL
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what is the etiology of HGB C trait (ac)
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inheritance of gene for HGB C from ONE parent
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what is the etiology of SC disease
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inheritance of ONE sickel cell gene and one HGB C gene
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what is the etiology of hereditart spherocytosis
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defect of cell membrane
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which anemia would have blood smear of aniso, poik, slight hypochromasia, many target cells, fragmented cells, folded cells ("pocketbook cells"), occasional HGB C crystals, occasional microspherocytes
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HGB C disease
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which anemia would have blood smear of many target cells
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HGB C trait
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which anemia would have blood smear of target cells, pocketbook cells, occasional SC crystal ("gloves")
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SC disease (SC)
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which anemia would have blood smear of varying degree of anio, poik, polychromasia & spherocytes,
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hereditary spherocytosis
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which anemia would have blood smear of polychromasia, spherocytes, nucleated RBCs
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autoimmune hemolytic anemia
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which anemia would have blood smear of aniso, poik, sickel cells, fragmented cells, target cells, nucleated RBCs, spherocytes, Howell Jolly bodies, basophilic stippling, siderotic granules, polychromasia
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sick cell anemia (SS)
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which anemia would have blood smear of occasional target cells, no sickle cells unless hypoxic (when body does not receive enough O2)
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sickle cell trait (as)
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name the 5 anemias that would give results as "normal" on HGB electrophoresis hint (HIS-PA)
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1. iron defncy
2. sideroblastic anemia 3. anemia of chronic disease 4. pernicious anemia 5. hereditar spherocytosis |
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which anemias that would give results on HGB electrophoresis of >90 % C, <7 % F, no A
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HGB C disease (cc)
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which anemias that would give results on HGB electrophoresis of 50 - 60 % A, 30 - 40 % C
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HGB C trait (ac)
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which anemias that would give results on HGB electrophoresis of equal amounts of C and S, normal to 7% F, no A
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SC disease (sc)
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which anemias that would give results on HGB electrophoresis of >80% S, 1 - 20% F, 2 - 4.5% A2, no A
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sickle cell anemia (ss)
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which anemias that would give results on HGB electrophoresis of 50 - 65% A, 35 - 45% S, normal F, normal to slightly increased A2
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sickel cell trait (as)
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difference cause of anemia can be caused
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nutritx defncy, blood loss, increase or decrease destruction of production of rbcs, infection, toxicity, heredity & acquired defects
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define haptoglobin
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protein attached to FREE HGB in blood, this form a complex that is rapidly cleared out of the circulation by LIVER for destruction & recycling
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which anemias that would give results on HGB electrophoresis of >90% A, 3.5 - 7% A2, F may be slight increased
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beta thalassemia minor
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which anemias that would give results on HGB electrophoresis of little or no A, up to 98% F
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beta thalassemia MAHOR (cooley's anemia)
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define trasferrin
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protein for iron delivery & binding (liver)
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what is TIBC
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measure transferrin capacity in blood that can be saturated (how much transferrin can CARRY)
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what is the method of measuring HGB
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cyanmethemoglobin
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define erythropoietin
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produced in the KIDNEY & increase in state of anemia
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anemia can be classified by
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normocytic/normochromic
microcytic/hypochromic macrocytic/normochromic |
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retics can be stained with what kind of stain
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methylene blue & briliant cresyl blue
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Sickel cell anemia & trait, hemoglobin C disease & trait is classified as hemoglobinpathy or thalassemia
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hemoglobinpathy
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beta thalassemia major & minor is classified as hemoglobinpathy or thalassemia
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thalassemia
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which HGB disorder is due to ALTERATION in globin chains
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hemoglobinpathy
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which HGB disorder is due to REDUCE/ABSENT synthesis of normal chain
|
thalassemia
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this abnormality is associated with: QUALITATIVE abnormality, abn in AMINO acid sequence of globin chain, but not in AMOUNT in globin produced
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hemoglobinpathy
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this abnormality is associated with: QUANTITATE abnormality, amion acid sequence of globin chains is NORMAL , but there is UNDERPRODUCTION of one or more globin chains
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thalassemia
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describe the blood smear of the rbcs for Acute Blood Loss
|
normocytic, normochromic
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describe the blood smear of the rbcs for Chronic Blood Loss
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microcytic, hypochromic (due to iron defncy)
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name the stage for granulocytic maturation of the following: 15-20 um, small amount of dark blue cytoplasm, usually NO granules, nuc has DELICATE chromatin with nucleoli
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myeloblast
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name the stage for granulocytic maturation of the following: sim to myeloblast but has PRIMARY (secondary) granules
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promyelocyte
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name the stage for granulocytic maturation of the following: presence of SECONDARY (specific) granules (eos, bas, neut) last stage to DIVIDE
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myelocyte
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name the stage for granulocytic maturation of the following: nucleus begins to INDENT
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metamyelocyte
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name the stage for granulocytic maturation of the following: nuclear indentation is more than half
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band
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name the stage for granulocytic maturation of the following: 2 - 5 nuclear lobes connected by thin strands of chromatin
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segmented neutrophil
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which leukocyte abnormalities is described when: presence of IMMATURE GRANULOCYTES in the peripheral blood
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shift to the left (ex: bacterial infection, inflammation)
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which leukocyte abnormalities is described when: DARK STAINING granules in cytoplasm of NEUTROPHILS
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toxic granulation (ex: infection, inflammation)
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which leukocyte abnormalities is described when: LIGHT BLUE PATCHES in cytoplasm of neutrophils
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dohle bodies (ex: infection, burns)
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which leukocyte abnormalities is described when: PHAGOCYTIC VACUOLES in cytoplasm of neutrophils
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vauolizations (ex: septicemia, drugs, toxins, radiation)
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which leukocyte abnormalities is described when: more than 5% of seg neut with 5 lobed nuclei or any with more than five lobes
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hypersegmentation (ex one of the first stages of pernicious anemia)
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which leukocyte abnormalities is described when: most neut have ROUND or BILOBED nuclei
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pelger-huet anomaly (ex: inherited disorder, no clinical effect, may be misinterpret as a shift to the left)
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which leukocyte abnormalities is described when: RED NEEDLES in cytoplasm of leukemic MYELOBLAST & MONOBLASTS
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auer rods (ex: nonlymphocytic leukemia)
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which leukocyte abnormalities is described when: one or more - large size, elongated or indented nuc, immaure chrom, increase parachromatin, nucleoli, increased cytoplasm, dark blue to very pale cytoplasm, peripheral basophilia, scalloped edges due to cytoplasm being indented by adjacent rbcs, frothy appearance, many azurophilic granules
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variant lymphocytes/atypical or reactive (ex: viral infection - IM, CMV)
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what is the role of the SPLEEN
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helps cleanse blood from bacteria & viruses
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which disorder is myeloproliferative disorder of unknown cause characterized by increase in TOTAL BLOOD VOLUME, viscocity, typically acc by nosebleed, headache, dizziness, itchy skin, reddish complextn, enlargement of spleen
|
polycythemia vera (pv)
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which of the abnormal leukocytes would be seen if there is: bacterial infection, inflammation, hemorrhage, hemolysis, stress
|
neutrophilia (increase neut)
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which of the abnormal leukocytes would be seen if there is: acute infection, antibodies, drugs, chemicals, radiation
|
neutropenia (decrease neut)
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which of the abnormal leukocytes would be seen if there is: IM, CMV, whooping cough, acute infectious lymphocytosis
|
lymphocytosis (increase lymphs)
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which of the abnormal leukocytes would be seen if there is: convalescence from viral infection, chronic infections, TB, subacute bacterial endocarditis, PA infections, Rickettisal infections
|
monocytosis (increase mono)
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which of the abnormal leukocytes would be seen if there is: allergies, skin disease, PA infections
|
eosinophilia (increase eos)
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which of the abnormal leukocytes would be seen if there is: chronic myelogenous leukemia (CML), PV
|
basophilia (increase baso)
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RBC Inclusion - which inclusion is described: aggregation of RNA (ribosomes), with multiple irregular purple inclusion EVENLY distributed throughout cell
|
basophillic stippling
|
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RBC Inclusion - which inclusion is described: round, purple, 1 - 2um in diamtere, usually ONLY ONE per cell - nuclear remnants (DNA)
|
howell jolly bodies
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RBC Inclusion - which inclusion is described: reddish purple RINGS or FIGURE 8, may be part of mitotic spindle, remnant of microtubules or fragments of nuclear membrane
|
cabot rings
|
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RBC Inclusion - which inclusion is described: small purpish blue granules, vary in size, shape number, usually at periphery in clusters
|
pappenheimer bodies
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RBC Inclusion - which condition is described: exposure to lead, accerate or abn HGB sythz, thalassemia
|
basophilic stippling
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RBC Inclusion - which inclusion is described: postplenectomy, thalassemia, hemolytic & megaoblastic anemia, sickle cell anemia
|
howell jolly bodies
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RBC Inclusion - which inclusion is described: pernicious anemia, thalassemia, postsplenectomy, lead poisoning
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cabot rings
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RBC Inclusion - which inclusion is described: sideroblastic anemia, postsplenectomy, thalassemia, sickle cell anemia, hemochromatosis
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papperheimer bodies
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RBC Inclusion - what is the significance of coarser, exposure to lead, fine young RBCs
|
basophillic stippling
|
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RBC Inclusion - what is the significance of usually putted by spleen, seen with accelerated or abnormal erythropoiesis
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howell jolly bodies
|
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RBC Inclusion - what is the significance of rapid blood regeneration, abn erythropoiesis
|
cabot rings
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RBC Inclusion - what is the significance of faulty iron utilization
|
pappenheimer bodies
|
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RBC Inclusion - what is the description of following inclusion: blue granules of varying sizes & shape that are caused by aggregates of iron particles
|
sideroric grandules
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RBC Inclusion - what is the significance of blue staining network that has residual RNA (ribosomes)
|
reticulocytes
|
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RBC Inclusion - what is the significance of round blue inclusions, varying sizes, close to cell membrane, may be more than one that are preciitated, oxidized, denatured HGB
|
heniz bodies
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RBC Inclusion - what is the inclusion would have the seen with the following conditions: sideroblastic anemia, postsplenectomy, thalassemia, sickle cell anemia, hemochromatosis
|
siderotic granules
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RBC Inclusion - what is the inclusion would have the seen with the following conditions: hemolytic anemia, blood loss, following treatment for iron defncy or megaloblastic anemia
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reticulocytes
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RBC Inclusion - what is the inclusion would have the seen with the following conditions: G^PD defncy, unstable hHGB, chemical injury to RBCs, drug induced hemolytic anemia
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heniz bodies
|
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|
define hemachromatosis
|
(hereditary) caused body to absorb TOO MUCH Fe+ from the FOOD you eat = excess iron store in your organs esp liver & pancreas
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what RBC Morphology is seen in: many anemias
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anisocytosis
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what RBC Morphology is seen in: vit B12 defncy, folic acid defncy, pernicious anemia, hemolytic anemia, cirrhossi, alcoholism, NORMAL in NEWBORNS
|
macrocytes
|
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what RBC Morphology is seen in: iron defncy anemia, thalasemia
|
microcytes
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what RBC Morphology is seen in: seen in anemias (besides aniso)
|
poikilocytosis
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what RBC Morphology is seen in: hereditary ovalocytosis, various anemias
|
elliptocytes/ovalocytes (oval or pencil shaped)
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|
|
what RBC Morphology is seen in: osmotic balance, if seen in most cell in thin part of smear, don't report, probably artifact due to excess anticoag or slow drying
|
created RBCs (round cell with KNOBBY UNIFORM PROJECTIONS/SCALLOPED shaped)
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|
|
what RBC Morphology is seen in: damage to RBC membrane, ureamia (blood in UA), carcinoma of stomach, bleeding peptic/gastric ulcers
|
burr cells (echinocytes) - round cell with SPINY UNEVEN spaced PROJECTIONs
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|
|
what RBC Morphology is seen in: damage to RBC membrane, alcoholic cirrhosis, postspectomy, abetalipoproteinemia (disorder that interfere with normal absorbtx of fat & fat soluble vit from food)
|
acanthocytes (SHRUKEN cells with IRREGULAR spiny projections - fingerlike)
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|
|
|
define hyperchromic anemia
|
increase HGB with REDUCTION of RBC ex: pernicious anemia - severe hyperchromic anemia
|
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what RBC Morphology is seen in: fragments of RBCs, seen with DIC, hemolysis, artificial heart valves, burns, microangiopathic hemolytic anemia
|
schistocytes (RBCs fragments, helmets triangular cells)
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|
|
|
what RBC Morphology is seen in: microangiopathic hemolytic anemia, pulmonary emboli in sickle cell anemia
|
blister cells (RBCs with one or more vacuoles)
|
|
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|
what RBC Morphology is seen in: sickle cell anemia
|
sickle cells (drepanocytes) - crescent S or C shaped, boat shaped, oat shaped
|
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|
what RBC Morphology is seen in: HGB C disease
|
HGB C crystals - blunt, six sided, dark staining projections, "bar of gold", washington monument (note: LYSINE sub on glumatic acid - & protects vs MALARIA)
|
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|
|
what RBC Morphology is seen in: myelofibrosis (BM undergoes fibrosis), various anemias
|
teardrop (dacryocytes)
|
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|
what RBC Morphology is seen in: ion defncy anemia, thalassemia
|
hypochromia (central pallor greater than one third cell diameter)
|
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|
|
what RBC Morphology is seen in: dimophric anemia, post transfusion
|
ansiochromia (mixture of normchromic & hypochromic rbcs)
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|
|
|
define myelofibrosis
|
disorder of BM resulting replacement of increase fibrosis CT in marrow
|
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|
|
what is fibrin & where is it made
|
made from FIBRINOGEN that helps plug/clot mesh for wound site, produced in the LIVER
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|
what RBC Morphology is seen in: 1. young RBCs, rectis with supervital stain, sign of active erythropoiesis, 2. 1 - 2 % in normal adults
3. increase with acute blood loss, 4. hemolytic anemia 5. following treatment for iron defncy or pernicious anemia |
polychromasia (bluish gray color)
|
|
|
|
what RBC Morphology is seen in:
1. hemoglobinopathies, 2. thalassemia 3. alocholism 4. postspectomy 5. may be artificat if observed in only one part of smear |
target cells (codocytes) aka bull's eyes or mexican hat
|
|
|
|
what RBC Morphology is seen in:
1. hereditary stomatocytosis, 2. hereditary spherocytosis, 3. thalassemia 4. alcoholic cirrhosis 5. Rh null disease 6. may be artificat in parts of smear that are too thick or think |
stomatocytes (rbc with SLITLIKE central pallor)
|
|
|
|
what RBC Morphology is seen in:
1. damaged rbcs membrane 2. hereditary sphereocytosis 3. autoAB 4. burns 5. hemoglobinopathies 6. hemolysis 7. ABO hemolytic dz of newborn 8. incompat blood tranfxn 9. transfused of stored blood 10. a few are normal due to aging of rbcs |
spherocytes (small dark stainng rbcs without central pallor)
|
|
|
|
what RBC Morphology is seen in:
1. SERUM PROTEIN abnormality ex: increase globulins or fibrinogen 2. seen in multiple myeloma & macroglobulinemia 3. may be artifact due to dela in spreading drop of blood or smear too thick |
rouleaux (rbcs resemble stack coins)
|
|
|
|
what RBC Morphology is seen in: autoAB & cold agglutinin
|
agglutination (rbc in irregular clumps)
|
|
|
|
define cold aggltn disease
|
autoimmune disease increase concentration circulating ANTIBODIES direct against RBCs at COLD TEMP
|
|
|
|
what are some characteristics of CDA (4 examples)
|
1. type of autoimmune hemolytic anemia
2. cold aggltn are made in BM, increase levels occurs when immune malfunctx 3. body mistakes it as foreign & sets up autoimmune response = prematurely killing RBCs (HEMOLYSIS) 4. are IGM |
|
|
|
with ESR what happens to the the values if sources of errors were : inaccurate timing
|
ESR could be increase or decrease
|
|
|
|
with ESR what happens to the the values if sources of errors were : pat has anemia
|
change in RBC: plasma ratio favors ROULEAUX formation, INCREASE esr
|
|
|
|
with ESR what happens to the the values if sources of errors were : polycythemia
|
INCREASE viscosity, DECREASE esr
|
|
|
|
with ESR what happens to the the values if sources of errors were : anisocytosis
|
cells dont rouleaux as readily, DECREASE esr
|
|
|
|
with ESR what happens to the the values if sources of errors were : poikilocytosis
|
cells dont rouleaux as readily, DECREASE esr
|
|
|
|
with ESR what happens to the the values if sources of errors were : agglutinated RBCs
|
agglutinates settles faster, INCREASE esr
|
|
|
|
with ESR what happens to the the values if sources of errors were : marcocytosis
|
LARGE cells settle FASTER, INCREASE esr
|
|
|
|
with ESR what happens to the the values if sources of errors were : microcytosis
|
SMALL cells settle more SLOWLY, DECREASE esr
|
|
|
|
with ESR what happens to the the values if sources of errors were : increased fibrinogen or globulins
|
FAVORS rouleaux formation , INCREASE esr
|
|
|
|
what are 7 source of errors that may cause INCREASE in ESR values
|
temp, tilt, rouleaux formation, aggltn rbcs, macrocytosis, increase fibrin & globins
|
|
|
|
with ESR what happens to the the values if sources of errors were : excess anticoag
|
RBCs SHRINK, DECREASE esr
|
|
|
|
with ESR what happens to the the values if sources of errors were : hemolysis
|
rbcs colum is decreased, DECREASE esr
|
|
|
|
with ESR what happens to the the values if sources of errors were : sp at rm temp more than 4 hours
|
rbcs SWELL, DECREASE esr
|
|
|
|
with ESR what happens to the the values if sources of errors were : rm temp below 22 - 27c
|
cells settle MORE SLOWLY, DECREASE esr
|
|
|
|
with ESR what happens to the the values if sources of errors were : rm temp above 22 - 27c
|
cells settle FASTER, INCREASE ESR
|
|
|
|
with ESR what happens to the the values if sources of errors were : tilted tube
|
INCREASE esr, a 3 degree angle from vertical can accelerate esr by 30%
|
|
|
|
with ESR what happens to the the values if sources of errors were : inclusion of buffy coat in reading
|
DECREASE esr
|
|
|
|
with ESR what happens to the the values if sources of errors were : inaccurate reading in scale
|
increase/decrease esr
|
|
|
|
with ESR what happens to the the values if sources of errors were : bubbles in column
|
DECREASE esr
|
|
|
|
what does ESR measure
|
amount of settling of RBCs in column of anticoag whole blood (mx: globlin & fibrinogen)
|
|
|
|
why do we test ESR
|
its an nonspecific indicator of inflammation, increase in acute & chronic infections, rheumatic fever, rheumatoid arthritis, myocardial infaraction, TB, subacute bacterial endocarditis
|
|
|
|
what method do we use for ESR
|
wintrobe & westergreen - westergreen is preferred, longer column increase sensitivity
|
|
|
|
Hemo special stains: this stain detects RNA, used for retic counts
|
new methylene blue
|
|
|
|
Hemo special stains: this stain detects iron, used for siderocytes
|
prussian blue
|
|
|
|
Hemo special stains: this stain detects peroxidase found in primary granules & auer rods
|
peroxidase (myeloperoxidase)
|
|
|
|
Hemo special stains: this stain detects LIPIDS in primary & secondary granules of granulocytes
|
suddan black
|
|
|
|
Hemo special stains: this stain detects esterase in primary granules if myeloid cells
|
napthold asd chloroactate esterase
|
|
|
|
Hemo special stains: this stain detects nospecific esterase in monocyte precusors
|
a-napthyl acetate esterase or a-napthyl butyrate esterase (strong positive in monocytic cells, inhibited by addition of sodium fluoride)
|
|
|
|
Hemo special stains: this stain detects esterase emz in myeloid & monocytic cells
|
combined esterase (use to eva the ratio of myelocytic & monocytic cells on smear based on different color staining
|
|
|
|
Hemo special stains: this stain detects primitive lymphoid cells
|
TdT - activity is elevated in L1 & L2
|
|
|
|
Hemo special stains: this stain detects GLYCOGEN
|
periodic acid schiff (PAS) - rbc precursors in erythroleukemia stain intensely, normal rbc & rbc precusor are negative, large coarse clumpts in lymphoblats in ALL
|
|
|
|
define erythroleukemia
|
malignant disorder marked by proliferation of erythroblastic & myeloblastic tissue & later stages of leukemia
|
|
|
|
Hemo special stains: this stain detects TARTRATE resistant acid phosphatase
|
tartrate resistant acid phosphatase - ID hairy cell leukemia
|
|
|
|
Hemo special stains: this stain detects alkaline phosphatase in bands & seg neutro
|
leukocyte alkaline phosphatase - INCREASED in leukemia reaction & PV.
DECREASE in CML score 100 seg netro & bands from 0-4+ and total normal 20 -100 |
|
|
|
Plasma Cell Disorders: which disorder is described as: MALIGNANT PLASMA cells in marrow, rare abn plasma cell on peripheral smear
1. normocytic, normochromic anemia 2. rouleaux on blood smear 3. INCREASE esr, due to increase in GLOBULINS 4. M spike on serum protein electrophoresis (monoclonal gammopathy) 5. may have BENCE JONES proteinuria 6. LYTIC BONE dz |
multiple myeloma
|
|
|
|
Plasma Cell Disorders: which disorder is described as: ABN plasma cell in peripheral blood (>2 x 10 9/L)
1. PANCYTOPENIA 2. rouleaux 3. monoclonal gammopathy |
plasma cell leukemia
|
|
|
|
Plasma Cell Disorders: which disorder is described as: monoclonal gammopathy due to INCREASE in IGM
1. rare plasmacytoid lymphocytes or plasma cells on smear 2. rouleaux 3. may have BJ in urine & CRYGLOBULINs |
WALDENSTROM's macroglobulinemia
|
|
|
|
which disorder has anemia characterized by DEFECTIVE FUNCTIONS of the blood forming organs (BM) & is caused by TOXIC agents, idiopathic (spanstaneously/unknown)
|
aplastic anemia
|
|
|
|
define PANCYTOPENIA
|
abnormal reduction of: RBCs, WBCs & platelets
|
|
|
|
SOE - what would cause the following error on manual HGB test: value is increased because of turbidity (higher absorbance), use patient plasma in reagent to blank
|
lipemia
|
|
|
|
why do we test ESR
|
its an nonspecific indicator of inflammation, increase in acute & chronic infections, rheumatic fever, rheumatoid arthritis, myocardial infaraction, TB, subacute bacterial endocarditis
|
|
|
|
what method do we use for ESR
|
wintrobe & westergreen - westergreen is preferred, longer column increase sensitivity
|
|
|
|
Hemo special stains: this stain detects RNA, used for retic counts
|
new methylene blue
|
|
|
|
Hemo special stains: this stain detects iron, used for siderocytes
|
prussian blue
|
|
|
|
Hemo special stains: this stain detects peroxidase found in primary granules & auer rods
|
peroxidase (myeloperoxidase)
|
|
|
|
Hemo special stains: this stain detects LIPIDS in primary & secondary granules of granulocytes
|
suddan black
|
|
|
|
Hemo special stains: this stain detects esterase in primary granules if myeloid cells
|
napthold asd chloroactate esterase
|
|
|
|
Hemo special stains: this stain detects nospecific esterase in monocyte precusors
|
a-napthyl acetate esterase or a-napthyl butyrate esterase (strong positive in monocytic cells, inhibited by addition of sodium fluoride)
|
|
|
|
Hemo special stains: this stain detects esterase emz in myeloid & monocytic cells
|
combined esterase (use to eva the ratio of myelocytic & monocytic cells on smear based on different color staining
|
|
|
|
Hemo special stains: this stain detects primitive lymphoid cells
|
TdT - activity is elevated in L1 & L2
|
|
|
|
Hemo special stains: this stain detects GLYCOGEN
|
periodic acid schiff (PAS) - rbc precursors in erythroleukemia stain intensely, normal rbc & rbc precusor are negative, large coarse clumpts in lymphoblats in ALL
|
|
|
|
define erythroleukemia
|
malignant disorder marked by proliferation of erythroblastic & myeloblastic tissue & later stages of leukemia
|
|
|
|
Hemo special stains: this stain detects TARTRATE resistant acid phosphatase
|
tartrate resistant acid phosphatase - ID hairy cell leukemia
|
|
|
|
Hemo special stains: this stain detects alkaline phosphatase in bands & seg neutro
|
leukocyte alkaline phosphatase - INCREASED in leukemia reaction & PV.
DECREASE in CML score 100 seg netro & bands from 0-4+ and total normal 20 -100 |
|
|
|
Plasma Cell Disorders: which disorder is described as: MALIGNANT PLASMA cells in marrow, rare abn plasma cell on peripheral smear
1. normocytic, normochromic anemia 2. rouleaux on blood smear 3. INCREASE esr, due to increase in GLOBULINS 4. M spike on serum protein electrophoresis (monoclonal gammopathy) 5. may have BENCE JONES proteinuria 6. LYTIC BONE dz |
multiple myeloma
|
|
|
|
Plasma Cell Disorders: which disorder is described as: ABN plasma cell in peripheral blood (>2 x 10 9/L)
1. PANCYTOPENIA 2. rouleaux 3. monoclonal gammopathy |
plasma cell leukemia
|
|
|
|
Plasma Cell Disorders: which disorder is described as: monoclonal gammopathy due to INCREASE in IGM
1. rare plasmacytoid lymphocytes or plasma cells on smear 2. rouleaux 3. may have BJ in urine & CRYGLOBULINs |
WALDENSTROM's macroglobulinemia
|
|
|
|
which disorder has anemia characterized by DEFECTIVE FUNCTIONS of the blood forming organs (BM) & is caused by TOXIC agents, idiopathic (spanstaneously/unknown)
|
aplastic anemia
|
|
|
|
define PANCYTOPENIA
|
abnormal reduction of: RBCs, WBCs & platelets
|
|
|
|
SOE - what should you do if your manual HGB test is: LIPEMIA
|
values is increased because of turbidity (higher absorbance), use patient plasma in reagent to blank
|
|
|
|
SOE - what should you do/expect if your manual HGB test is: WBC>30 x 10 9/L
|
value is increased because of turbidity (higher absorbance), centrifuge reactions tube & read absorbance of supernatant
|
|
|
|
SOE - what should you do/expect if your manual HGB test is: HGB S or C
|
cells are resistant to lysis, values is increased because of turbidity, dilute mixture 1:2 with distilled water, reread, multiple results x2
|
|
|
|
SOE - what should you do/expect if your manual HCT test is: tourniquet left on too long
|
INCREASE due to hemoconcentration
|
|
|
|
SOE - what should you do/expect if your manual HCT test is: has excess anticoagulant
|
DECREASE due to SHRINKAGE of RBCS
|
|
|
|
SOE - what should you do/expect if your manual HCT test is: hemolysis
|
DECREASE due to DESTRUCTION of RBCs
|
|
|
|
SOE - what should you do/expect if your manual HCT test is: insufficient mixing
|
could be high/lower, depending on portion sampled
|
|
|
|
SOE - what should you do/expect if your manual HCT test is: inadequate time or speed of centrifugation
|
DECREASE value due to insufficient packing of cells
|
|
|
|
SOE - what should you do/expect if your manual HCT test is: inclusion of buffy coat in reading
|
INCREASE value
|
|
|
|
SOE - what should you do/expect if your manual HCT test is: parallax error
|
failure to look straight down when reading result, could increase/decrease value
|
|
|
|
SOE - what should you do/expect if your manual HCT test is:incorrect use of hematocrit reader
|
could be high/lower depending on error
|
|
|
|
SOE - what should you do/expect if your manual HCT test is: poikilocytosis
|
INCREASE, due to trapped plasma
|
|
|
|
SOE - what should you do/expect if your manual RETIC test is:refractive artifacts
|
INCREASE value, RNA disappears when out of focus
|
|
|
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SOE - what should you do/expect if your manual RETIC test is: other inclusions
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pappenheimer bodies, howell jolly bodies, heniz bodies are seen with SUPERVITAL stain, differentiate by other stains
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SOE - what should you do/expect if your Tube Solubility Test for HGB S test is: lipemia
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FALSE + due to turbidity
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SOE - what should you do/expect if your Tube Solubility Test for HGB S test is: leukocytosis
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FALSE + due to turbidity
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SOE - what should you do/expect if your Tube Solubility Test for HGB S test is: polycythemia
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FALSE +
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SOE - what should you do/expect if your Tube Solubility Test for HGB S test is: increased globulins
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FALSE + due to turbidity
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SOE - what should you do/expect if your Tube Solubility Test for HGB S test is: blood from infant less than 6 months old
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FALSE NEGATIVE, due to predominance of HGB F
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SOE - what should you do/expect if your Tube Solubility Test for HGB S test is: recent transfusion
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FALSE NEGATIVE
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SOE - what should you do/expect if your Tube Solubility Test for HGB S test is: HGB less than 7 g/dL
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FALSE NEGATIVE (nr: 14 - 18, 12 - 16 g/dL)
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In manual WBCs count, what is used to lyse the RBCs and what are WBCs counted on?
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acetic acid is used as diluet to lyse RBCs, WBCs are counted on Neubauer hemacytometer, nucleated RBCs cant be distinguished from WBCS
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what is used in eosinphil count & what kind of special hemacytometer is used to count cells
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PHLOXINE stains eos red. cells are counted with a larger volume than Neubauer chamber (Fuchs-Rosenthal or Speirs Levy)
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what is the procedure for reading a hemotocrit
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packed cell volume, microhematocrit tubes are centrifuged @10,000 rpm for 5 mins, the ratio of the volume occupied by the RBCs to the volume of WB is determined, values may be slightly higher than automated HCT due to trapped plasma
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what method is used to measure HEMOGLOBIN and describe the oxidization of K+ cyanide to K+ ferricyanide to methemoglobin
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1. cyanmethoglobin method
2. K+ cyanide & K+ ferricyanide reagent (Drabkins) 3. K+ ferricyanide OX ferrous ions ---> ferric ions = METHEMGLOBIN 4. methemglobin reacts with CYANIDE ions forming = CYANMETHEMOGLOBIN 5. read #540 nm 6. mz all HGB except sulfHGB |
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what does the sugar water test (sucrose hemolysis)
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screening for paroxysmal noctural HGBuria (PNH), sucrose provides a medium to low ionic stregth that promotes the binding of the complement, PNH RBCs are complement sensitive & lyse, normal RBCs are unaffected
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what does the ham test (acid serum test) for
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confirm of PNH, serum is acidified, which activates complement, PNH RBCs lyses, normal rbcs are unaffected
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what does hemoglobin A2 by microcolumn test for
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screening test for BETA THALASSEMIA MINOR (increase HGB A2)
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what is paroxysmal noctural HGBuria (PNH)
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form of hemolytic anemia characterized by abn strong response to action of COMPLEMENT, by acute episodes of hemolysis esp @ nite with hGBuria noted upon urination after waking
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what is used in solubility test for sickling hemoglobin
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sickling HGB produce turbid solution when mized with SODIUM DI-THIO-NITE. screen test only, not specific for HGB S, does not diff from AS or SS, confirmed with HGB electrophoresis
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what does osmotic fragility test for
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measure the ABILITY of the RBCs to take UP WATER without LYSING, RBCS are incubated w/ various concentration of NaCl, the amount of hemolysis is determined by reading the absorbance of the SUPERNANT from each tube
1. normal = hemolysis begin @ 0.45% & complete @ 0.30% 2. increased in HEREFITARY SPHEROCYTOSIS 3. DECREASE w/ target cells, sickle cell anemia, iron defncy anemia, thalassemia |
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what is LE prep test for
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outdated test for diagnosis of lupus erythematosus, antinuclear antibody in patient's serum digests nucleus of damaged WBCs, when is then phagocytized by neutrophil or monocyte (lupus = inflamed connective tissue disorder)
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what is the procedure for malaria smears
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examine thin & thick smears, thick smears concentrates parasites & is used to screen, it is not fixed, so RBCs lyse making detection easier. thin smear must be examined to speciate.
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