hematology

Badly discolored blood picture with very spiky cells. What caused this? - Slide not dry. Artifact.

-Burr cells (echinocytes) may be associated with uremia or pyruvate kinase deficiency -Crenated cells, that may be confused with true Burr cells/echinocytes, are frequent artifacts. They're caused by excess EDTA (underfilled collection tube), but may also be caused by a slow drying smear, drying in a humid environment, or an alkaline pH from glass slides. -True Burr cells (echinocytes)*** are less numerous -Corrective actions include making a new smear or re-collecting the sample, if possible

Labce notes about coag controls being out of range:

1. Document the abn results 2. Repeat the control that's out of range 3. If it's still out of range, prepare a new control, reagents, and also perform calibration 4. Once all controls are in range, run patient samples again

Pic of aggregation test.... Platelet aggregation... graph for ADP, epinephrine and collagen Graph of the platelet aggregation expressed in % transmittance for ADP, collagen and epinephrine -Result was 0% transmittance ACE. abnormal ADP, Collagen, and Epinephrine) Graph of ECA (Epinephrine, Collagen and ADP), two of them changed from 0 (either inc or dec), the other one is just 0. They will ask you which ones are normal/abnormal

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Siderotic granules: Prussian blue

Why? To verify that red cell inclusions contain iron, it is necessary to use an iron stain, such as Prussian blue. The iron-containing granules are called siderotic granules. Pappenheimer bodies are siderotic*** granules that are visible on a Wright-stained smear (from Labce) -may vary in size, seen in sideroblastic anemias and also Hemoglobinopathies

Hairy Cell plate, the picture looked blurry Test to identify Hairy cell leukemia? HCL large cells, CD markers: CD 11c, 19, 20, 22, 25, 103, FMC7

a. Atypical lymphocyte b. Hairy cell leukemia*** c. Normal lymphocyte -CT scan to look at enlarged spleen and/or lymph nodes -low RBCs, WBCs, and plts -pos TRAP stain- bright granular cytoplasmic positivity (acid phospatase rxn) -bone marrow biopsy to look for Hairy cells

Sample taken from indwelling catheter. Patient isn't on any anticoagulants yet. PT, aPTT and TT are way elevated: ***Heparin contamination (from catheter) Heparin contamination and mixing studies and TT/ fibrinogen time How do you know if the plasma used for PT has been contaminated with heparin? A. Test for PT B. Perform mixing studies (probably won't help because this is for detection of factor deficiencies and inhibitors) (more choices) idk

aPTT is particularly sensitive to heparin contamination Why is PT elevated? If it's heparin contamination, it should only affect the aPTT, TT, and fibrinogen (look at coag cascade flashcard)

1. PT, aPTT, and patient samples all run together were abnormally high- Choices: -CaCl2 added -Thromboplastin added by accident*** -Controls deterioration -Incubation temp. too low 2. Coagulation machine, controls and patient were run in duplicate. -Controls where normal -patient 1 PT normal aPTT abnormal -patient 2 PT abnormal aPTT normal a. CaCl2 b. Thromboplastin c. something about a light (chose this one, check) d. controls 3. Ran controls and PT was normal, aPTT was abnormal. Replaced controls and got same results. What should you do next? A) Change out the Recombiplastin B) Change out the CaCl2 reagents*** C) Rerun controls D) Run patient tests 4. PT and aPTT controls were abnormal QC repeated aPTT was normal what to do? Which reagents to replace? -(Recombiplastin*** and reagent diluent are for the PT test, not for the aPTT test. CaCl2 and Phospholipid are in two separate vials for the aPTT test)

aPTT reagents: Phospholipin and CaCl2 -for automated kits and come ready to use. PT reagents: Thromboplastin and Recombiplastin Details: PT controls are in range. aPTT controls are out. New controls produce the same results. Why? -CaCl2 may have been added to aPTT reagent accidentally. Change reagents and repeat. -CLIA violation to keep repeating test until it's in range

What does plasmin do?

-enzyme that degrades many blood plasma proteins, including fibrin clots. The degradation of fibrin is termed fibrinolysis Fibrinolysis: plasminogen activator release, conversion to plasmin, conversion of fibrin to FDP

Intrinsic factor is: Von Willebrand (8) When to do a Factor 8 assay- (intrinsic factor close to common pathway)? (Hemophilia A) -purpose is to determine the cause of prolonged or excessive bleeding -abnormal or excessive bleeding -easy bruising -heavy or prolonged menstrual periods -frequent gum bleeding -frequent nosebleeds -vitamin K deficiency -hemophilia -liver disease

-normal plt ct and function, normal PT, prolonged APTT

Thrombin time and why it would be increased or affected Anti-thrombin questions

-time between the addition of thrombin and the clot formation. Reptilase may be used -can be prolonged by heparin, fibrin degradation products (FDP), factor 13 deficiency, and fibrinogen deficiency or abnormality -Increased in hypofibrinogenemia (TT is less prolonged than the other disorders), dysfibrinogenemia (indefinitely prolonged), and afibrinogenemia (indefinitely prolonged) -antithrombin inactivates many enzymes (flashcards)

What is decreased in females who have their menstrual period? A. transferrin (also ferritin) (they will have inc TIBC bc of the inverse relationship)*** -this can also happen during pregnancy or chronic infection ? There was a question on what CBC (iron changes? Transferrin?) a young healthy woman on hormonal birth control (oral contraceptives) would have... (increased clotting factors?) (***increased serum Fe in women on hormonal birth control because periods are lighter. Also, ferritin will be high*** and TIBC and transferrin should be low) -low B6, B12, folic acid, and high homocysteine. Inc risk for thrombosis*** Girl with menorrhagia (heavy) and elevated APTT -a. DD b. ***afibrinogenemia c. Ristocetin (D-dimer isn't associated with heavy periods) (congenital afibrinogenemia can have abnormally heavy menstrual bleeding- menorrhagia) (Ristocetin is an antibiotic that causes thrombocytopenia and platelet agglutination. It's not used anymore)

A. Transferrin*** B. ALT C. Haptoglobin D. GGT

Lupus erythematosus What happen with complement? Decrease or increased, due to what....

C1q deficiency is the strongest genetic risk factor for SLE, although such deficiency is very rare Complement proteins (C3 and C4) are used up by the inflammation caused by lupus, which is why people with inflammation due to active lupus often have low complement levels Causes thrombosis: C3 (Complement proteins participate in venous thrombosis after ligation of the IVC. C3 has a role in activation of platelets) What's impaired on the RBCs in PCH? -Antibodies bind to RBCs. This allows complement to latch on. The antibodies destroy the RBCs as they move through the body. As the cells are destroyed, Hgb, is released into the blood and passed in the urine.

Absolute lymphocytosis-absolute lymphocyte count is: -in adults, more than 4000/ uL -in older children, more than 7000/ uL -in infants, more than 9000/ uL Relative lymphocytosis- higher proportion (more than 40%) of lymphs among the WBCs, however, absolute lymphocyte count (ALC) is normal (less than 4000/ uL) This is normal in children under age 2 Lympho(cyto)penia- < 1000/μL in adults or < 3000/μL in children < 2 yr

Causes: acute viral infections, such as mono, glandular fever, hepatitis, and CMV infection pertussis -some protozoal infections, such as toxoplasmosis and American trypanosomiasis (Chagas disease) -chronic intracellular bacterial infections such as TB or brucellosis -CLL or ALL Causes: age less than 2 years; acute viral infections; connective tissue diseases, thyrotoxicosis, Addison's disease, and splenomegaly with splenic sequestration of granulocytes Causes: AIDS, viral hepatitis, TB, and typhoid fever. -Autoimmune disorders such as lupus -Steroid therapy -Hodgkin's disease and aplastic anemia (defective stem cell production in aa) -Radiation and chemotherapy -protein undernutrition -can be inherited too

A result of CBC: inc WBC, the rest are normal. Platelets is 20. What is the blood picture?

Choices ranged from the normal or abnormal status of the FF (fibrinogen?), PT, PTT, Fibrinogen, D-Dimer (should be TTP because they are sick- WBC inc. With ITP, they aren't sick): All coag results should be normal, or slightly inc -Slightly inc values with TTP: aPTT, PT, fibrin monomer, FDP, D-dimer, schistocytes present (in ITP, all coag values are normal)

When using a butterfly for coag study- ***Draw and discard a waste light-blue top tube before the tube that will be used for coagulation studies. You don't have to fill it all the way up

Discard a blue top then use 2nd blue (waste tube is drawn first to remove the air in the tubing of the winged collection device. Once blood flows through the tubing, the waste tube can be removed and discarded. It does not need to be completely filled) Under-filling the tube changes the ratio of blood to anticoagulant. This can affect the accuracy of coagulation tests that are performed using this specimen

What it means to have a high platelet count? May-Hegglin- giant platelets, thrombocytopenia and hemolysis (seen in myeloproliferative disorders, stress platelets)- few granules, autosomal dominant, purpura, bleeding Bernard Soulier syndrome- The question is long but the main differentiation that caught my eye is "giant platelets". The rest of the choices are not in sync with the question. No May-Hegglin in the choices so I chose Bernard Soulier (has large plts and abnormal Ristocetin-induced aggregation)

Essential thrombocythemia (by overproduction from megakaryocytes in the bone marrow) Döhle leukocyte inclusions with giant platelets and macrothrombocytopenia, is a rare genetic disorder of the blood platelets that causes them to be abnormally large

High PT reason...

Factor 7 (right after 3 on the extrinsic pathway)

Plate of toxic granulation (seen with inflammatory conditions and infections)

Granulocyte cells seen on examination of the peripheral blood film of patients with inflammatory conditions. They are commonly found in patients with sepsis.

Sickle cell details: solubility test and then electrophoresis*** Sickle cell electrophoresis

Hemoglobin S is an abnormal Hgb created by a point mutation at the 6th position on the beta globin chain that results in replacement of glutamic acid by valine. It causes sickling of red cells under conditions of reduced O2 concentration. Hemoglobin electrophoresis- cellulose acetate pH 8.6 (usually the reflex test) - Crawl, Slow, Fast, Accelerated + from cathode (-) to anode (+) Interferences: glycated Hgb S elutes with Hgb A2 and may falsely inc the A2 result, which leads to a false suspicion of B-thalassemia

Blood EDTA given to the lab 6 hrs after draw will most effect...

I chose platelets (the count will decrease. EDTA prevents them from clumping) (WBC morphology will change minimally)

RBC: 3.9(Lipemic sample) 2.46 Hgb: 14 12.5 Hct: 36% 33% Question that gives a RBC count, Hgb, and HCT. I did the rule of 3 and found that the Hgb didn't meet the rule of 3 because it was too high CBC result, HCT did not match Hgb (Hbg x 3), what causes the false increase of Hgb? One of the choices is lipemia Given a table of values with normal HCT but low Hgb. The rule of 3 didn't match so I said lipemia was interfering. Automated instrument Hgb = 45 HCT = 33 The manual HCT done by techs is 33.5 What do you do? Check for lipemia*** bc it can falsely elevate (either Hgb or HCT, idk) on automated instruments Lipemia can interfere with optical methods. Use mechanical methods instead.

Lipemic specimen? I think I picked check for lipemia (elevates Hgb) HCT is not about 3x that of the Hgb (MCHC) is greater than 36. The scattergram will also be off. Also, the Hgb can be falsely increased after a meal. Hgb can be falsely decreased with in-vitro hemolysis

Multiple Myeloma and whether to test with a different type before confirmation- Bone marrow biopsy, IFE, and FISH? Picture of Rouleaux; the cause of this can be from the proliferation of (plasma cells-multiple myeloma) Multiple myeloma blood film pic

M protein blood test, M protein (Bence-Jones protein- light chains, inc in serum and urine) SSA and Protein urine test, then Immunoelectrophoresis (which will quantify it) Also, increased IgG or IgA monoclonal spike, gamma spike on SPEP Increased Calcium Ion Many lytic lesions causing bone pain Sheets of plasma cells in the bone marrow

18.3% (high) retic count. What do you do? (blood smear looks Howell bodies but I selected Heinz body staining) Histogram, they presented WBC, RBC and platelets. What is the cause of interference in the WBC? 2 yr old girl or 9 month old baby, normocytic, normochromic, normal WBC, normal plts, but retics is 0.1% a. Pure red cell aplasia*** b. Fanconi's anemia c. Aplastic anemia 3 y/o child has severe anemia w/ low RBC count of 1.7 x 10^6 ct. WBC and plt count are both normal. What is the diagnosis? Pure red cell aplasia*** (only red cell population is affected. RBC count doesn't fall that low in lead poisoning) Plate with RBC (hyperchromic, anisocytosis), Papp body inclusions (1-2/ RBC) in Wright. Patient has 18.5% of retics. ? Grainy picture of what looks like RBC agglutination/flocculation... What should you do next - I chose Heinz body stain (actually got this exact pic twice) HJ bodies use Wright and New Methylene Blue

Prepare Heinz body stain (retic and Heinz bodies are stained the same way)- could be a supravital like Brilliant Cresyl Blue, or New Methylene blue (supravital stain was an option, repeat retic was an option) a. ***nRBC I think b. Retics c. Platelet clot a. Pure red cell aplasia*** initially use Wright, but confirm Papp bodies with ***Prussian Blue

-What is RDW? (normal values and calculations too) -anisocytosis is identified from RDW and classified according to the MCV***

Red blood cell distribution width (RDW or RDW-CV or RCDW and RDW-SD) is a measure of the range of variation of red blood cell (RBC) volume that is reported as part of a standard complete blood count -inc RDW is anisocytosis: ref range is 12-15 -homogenous RBC population has a normal RDW -heterogenous RBC population has an inc RDW

Picture of Sideroblasts

Ringed sideroblasts characterizes sideroblastic anemia. Ring sideroblasts are named so because iron-laden mitochondria form a ring around the nucleus. It is a subtype of basophilic granules of the erythrocyte, but which can only be seen in bone marrow.

(Reactive) Monocytosis seen in what?

TB?*** (also, syphilis, malignancies) Infectious Mononucleosis? (lymphs would be high) Hypersensitivity? (Baso's in immediate hypersensitivity)

Beta Thalassemia major***- Cooley's anemia (most severe form of beta thalassemia) Alpha thalassemia = Hgb Bart/Major (other choices were Hgb D, sickle cell, etc) Alpha thalassemia: 3 deleted alpha genes: Hgb Bart (y4) present at birth and Hgb H has Heinz bodies (B4)

Thalassemia details: Adult Hgb (A) has 2 alpha and 2 beta chains. In thalassemia, there's deficient synthesis of either the alpha or beta chains. People with the disorder have low Hgb A, but high levels of the chain that is made. -Dacrocytes are seen in thalassemias -Black people, Mediterranean people, and Southeast Asians are more prone to the disorder Alpha: 1 mutated gene (- a, a a) Silent carrier, normal CBC 2 mutated genes (- a, - a) or (- -, a a) Alpha thal trait (or minor). Mild microcytic, hypochromic anemia 3 mutated genes (- -, - a) Hgb H disease (B4)- Heinz bodies -chronic hemolytic disease 4 mutated genes (- -, - -) Hydrops fetalis- (can't make alpha gene) nonviable fetus. It's rare. Severe anemia- stillborn -surviving children may have transfusion therapy and stem cell/bone marrow transplant -Hgb Bart's (y4) present at birth (ineffective at carrying oxygen) Beta: 1 mutated gene (B B, B -) Beta thalassemia minor (trait) -mild or no symptoms -one affected allele on chromosome 11 2 mutated genes (B -, B -) Beta thalassemia major -homozygous (Cooley's) -both alleles affected -Diagnosed in early childhood -Need transfusions -Jaundice, abdominal swelling, splenomegaly, growth retardation, skeletal abnormalities -microcytosis, hypochromia, poikilocytosis, anisocytosis, nRBCs 2 mutated genes (B B, B -) Beta thalassemia intermedia -mild symptoms -one or two affected alleles

Fibrinolytic assay- thrombin time Fibrinogen to Fibrin ***Thrombin: fibrinogen is converted at the wound into fibrin by the action of thrombin, a clotting enzyme

Thrombin time involves the addition of bovine or human thrombin to platelet poor plasma. It reflects the conversion of fibrinogen to fibrin but is also sensitive to the presence of inhibitors that may be present in the plasma e.g. heparin.

Lab results for TTP, ITP

Thrombotic Thrombocytopenic Purpura (TTP): -inc plt agg -neurological findings -fever -MAHA -renal failure -autoimmune disease in acquired TTP Immune Thrombocytopenic Purpura (ITP): -acute ITP usually occurs in children with viral infections, and it goes back to normal ITP- idiopathic thrombocytopenic purpura- excessive bruising and bleeding- low plts ITP has been associated with Helicobacter pylori infection Lab values: -low plt count -bone marrow will be normal because a low platelet count is caused by the destruction of platelets in the bloodstream and spleen— not by a problem with the bone marrow

Series of results of Hgb results for 5 consecutive days, results in Day 3 is high, the others are almost the same.

What is the reason? -machine malfunction -collected too early -specimen left standing too long*** (I think) could be from hemolysis

If PT and aPTT are inc what do you do next? -recollect with proper precautions to not contaminate (could be oral anticoagulants, Vit K def, or liver disease) (next choice would be to do LAC test)

good I think

Von Willebrand's disease results:

inherited, qualitative platelet disorder -inc bleeding -prolonged APTT -dec factor 8:C -dec VWF -***dec plt aggregation to ristocetin -***normal plt aggregation to ADP, epinephrine, and collagen

t15:17 (Retinoic Acid Receptor alpha gene) Peroxidase/Sudan Black indicates MPO/lipids: Myeloid Precursor Pos, Lymphoid Precursor Neg Cytogenic Anomaly in APL M3- t(15:17) (it's a chromosomal translocation)***

***APL (M3 type of AML) Auer rods. (pic of Auer rod)- can be on M2 too -MPO positive blasts are specific for (AML) -PAS block positivity is seen in (ALL), which has significance in absence of MPO positivity. -Diffuse or granular PAS positivity has no significance -MPO or Sudan black reactions are most useful in establishing the identity of AML and distinguishing it from ALL -DIC is associated with M3

Activated Protein C Resistance Test When to do PT (Coumadin/Warfarin therapy) Warfarin toxicity: administer Vit K Patient is on Coumadin/Warfarin therapy, what will be affected? What is the purpose of Protein C and S? Protein C- how aspirin affects test (prolonged, increased*** or unaffected?) -Protein C works similarly to aspirin. Not sure about the answer. Aspirin: inhibits cyclooxygenase (COX) -inhibits thromboxane formation that plts depend on

***Factor V Leiden Mutation -Resists the action of Protein C/S. People with unexplained or familial venous thromboembolisms (VTE) often have a resistance to activated Protein C. 95% of these people have a single point mutation in Factor V Leiden Warfarin recipients should undergo ***INR testing every 4 weeks. These people should have an INR of 2.0 to 3.0 for basic "blood-thinning" needs. For some who have a high risk of a blood clot, the INR needs to be higher - about 2.5 to 3.5*** Rapid decrease in protein C*** (they have to stop taking it temporarily to do the test) ***act as natural anticoagulant. Anticoagulant activity primarily through ***inactivation of coagulation factors 5a and 8a, which are required for factor 10 activation and thrombin generation. The catalytic activity of activated protein C (aPC) is greatly enhanced by the vitamin K-dependent cofactor protein S. Protein C is proteolytic

Order of draw

-Culture tube -Light blue, sodium citrate: D-dimer, fibrinogen -Red, serum: Bacteria and Viruses, some vitamins -Yellow, SST: Aldo, B12, ferritin -Green, Sodium/Lithium Heparin: CarboxyHgb, MethHgb, cytogenetics -Purple, EDTA: Everything else -Pink, Crossmatch (Thomas says it's also EDTA): Blood Groups -Gray, Fluoride Oxalate: Blood sugar, ethanol, lactate (Sodium Fluoride anticoagulant- prevents glycolysis)***

What deficiency Teardrop cells?

-DNA deficiency -Teardrop cells (Dacrocytes) are thought to form as a result of the removal of an inclusion from the cell as it moves through the spleen -This process is referred to as pitting. Since red cells are quite flexible and usually return to their normal shape following pitting, it has been theorized that in this case the membrane may have been stretched too far and thus cannot return to its original shape -Seen in extramedullary hematopoiesis, thalassemias, Pernicious anemia (dec B12)

DIC characteristics

-RBC fragments (schistocytes) -excessive and inappropriate fibrinolysis in response to excessive clotting -rapid dissolution clots leads to increase in fibrinolytic activity -acquired hemostasis disorder: -secondary to sepsis, obstetric complications, Ebola -consumption of: plts, Factors 1, 5, 8 -high levels of fibrinogen degradation product (FDP) and D-dimer -Possible Complications: Bleeding, Lack of blood flow to the arms, legs, or vital organs, Stroke

Codocytes seen in...

-Target cells, or codocytes, have an excess of cell membrane relative to cell volume -Hemoglobin E and beta thalassemia trait -Macrocytic target cells can be seen in ***(obstructive) liver disease, and microcytic target cells may be seen in thalassemia -Hemoglobin C and E disease -Following splenectomy -Artifact of slide preparation. Artifactual target cells are generally irregularly distributed on the slide

Hypersegmented neutrophils

-Vitamin B12 or folate deficiencies (megaloblastic anemia) -One of the earliest, most sensitive and specific signs of megaloblastic anemia (mainly caused by hypovitaminosis of vitamin B12 & folic acid) -Nuclear hypersegmentation of DNA in neutrophils strongly suggests megaloblastosis when associated with macro-ovalocytosis -Interruption of DNA synthesis- megaloblastic anemia

G6PD deficiency

-X-linked recessive enzyme deficiency -G6PD is required so your RBCs don't hemolyze -the deficiency can cause hemolytic anemia -fever, pain, dark urine -high in Africans, Mediterraneans

Picture of target cells with hemoglobin C crystals (bar-shaped). The WBC count was high on instrument 1 (method A), so a second instrument (method B) was used with a stronger lysing agent, and the WBC count was corrected Hemoglobin C disease Target cell blood smear, what is the effect of target cells on the instrument? Picture of sickle cell and target cells - which disease? -Hgb C disease***

-anti-lysing target cells are what increased the WBC count? RBCs containing hemoglobin C do not lyse normally (sickle cell diseases) Error in method A is on the lysing reagent (because target cells are hard to lyse) Normocytic, with frequent target cells***, spherocytes, and rarely, crystal-containing RBCs. nRBCs may be present. The RBCs do not sickle -Hard to lyse red cells include target cells -Unlysed red cells interfere in the ***WBC count & Differential measurements. (falsely high WBC) -Can perform a smear WBC estimate, run blood sample on another instrument, or perform a manual WBC count if available

Pelger-Huet anomaly - clinical significance Dissociation pseudo Pelger-Huet anomaly: (nuclear-cytoplasmic dissociation of maturation, pseudo-Pelger-Huet anomaly ring nuclei, and abnormal or absent granulation) Pseudo Pelger-Huet anomaly: Myeloproliferative disorders (can be associated with AIDS and AML)

-congenitally acquired condition of nuclear segmentation that has no clinical significance. If it's 70% P-H cells, it's probably homozygous -Pseudo Pelger-Huet cells are acquired abnormalities commonly seen in hematology/oncology practice and are markers of underlying disorders, such as myelodysplasia, myeloproliferative disease: (acute leukemia, certain drugs, and occasional acute infections)

Hemoglobinopathies- sickle cell solubility test and sources of error Picture of sickle cells - asked which reagent should be used to diagnose Protein solubility- Sodium dithionate and sickle cell (I chose severe anemia)

-cyanmethemoglobin reagent is used to detect the type of Hgb. Cloudy and turbid is SS. If Hgb is 10.7 and HCT is 0.22, dilute 1:2 w/ DI water, read it, then multiply by 2. -Hgb S and C can cause turbidity in the soln, but it can be cleared by diluting it. -cyanmethemoglobin -Protein-solubility screening method (Sickledex): Hgb D, S, C Harlem, C Georgetown, or Bart's could be present. These abnormal Hgbs are insoluble in dithionate, and the soln will be cloudy (can't see the black lines behind the tubes). Hgb A is soluble, and indicates a normal result. False pos results: nRBCs, erythrocytosis, leukocytosis, hyperlipidemia, hypergammaglobulinemia like multiple myeloma False neg results: Hgb S conc is less than 1 g/dL, usually in cases of high Hgb F (sickle cell screen not appropriate for infants 6 months old), total Hgb less than 6 g/dL, recent transfusion.

-Interpretation of blood smear with sickle cells -Interpretation of blood smear with polychromatophilic cells (presence of RNA) -when the bone marrow is stressed due to blood loss or other conditions, these cells are prematurely released into the blood

-low Hgb, low HCT, high WBC, high plt, low ESR, Hgb electrophoresis, Hgb solubility (turbid), iron deficiency -Slightly immature, non-nucleated red cells (reticulocyte stage) are blue-gray on Wright-stains from residual RNA. Stained with supravital (Heinz stains) -0.5-2.5% is normal for retic count

DIC lab results***

-low plts and fibrinogen*** -large plts and schistocytes -PT often prolonged with DIC as coagulation factors are consumed*** -aPTT may be prolonged*** -D-dimer - a test that detects a protein that results from clot break-down; it is often markedly elevated with DIC

Microangiopathic hemolytic anemia (MAHA) characteristics

-mechanism of MAHA is the formation of a fibrin mesh due to increased activation of the system of coagulation. The red blood cells are physically cut by these protein networks -anemia and schistocytes -increased serum bilirubin levels -Unconjugated hyperbilirubinemia above 15%

Mixing study details: (make chart of examples for this) -normal plasma contributes a sufficient concentration of clotting factors to "correct" for a factor deficiency -mixing study that corrects the aPTT is characteristic of factor deficiency (Danielle is correct) -mixing study that does not correct the aPTT indicates a factor inhibitor

-show correction for both the immediate and incubated PT/aPTT tests; the patient most likely has a factor deficiency (or multiple factor deficiencies) -show no correction in either the immediate or incubated PT/aPTT, the patient may have a coagulation inhibitor, most likely a lupus anticoagulant -show correction for the immediate PT/aPTT results, but no correction in the incubated PT/aPTT, the patient may have a slow-acting inhibitor such as anti-factor 8

Difference between traumatic tap & subarachnoid hemorrhage

-traumatic tap occurs if the needle inadvertently has entered an epidural vein during insertion -subarachnoid hemorrhage- A yellowish tinge to the CSF fluid is called xanthochromia, which is usually caused by RBC degeneration in the CSF

AML: M1- Myeloblast with minimal maturation M3- Acute Promyelocytic Leukemia (Auer rods) Slide of immature cells (Myelo, meta, looks like blasts) What test to confirm? a. Phil chromosome**** (for CML- shows mostly meta, myelo and segs) b. Sudan (black. Pos in AML- 20% blasts, inclusion bodies, neg in ALL-small homogenous blasts) c. Oil red d. PAS (neg or diffusely pos in AML, Pos in ALL- course grahules) Which leukemia + for Philadelphia? CML***

CML: older patients, left shift, Phil chromosome, inc serum uric acid and LDH from high cell turnover, eventually transforms into AML or ALL -Chronic phase: inc WBC, inc plt, dec RBC, <20% blasts (slight anemia) Low LAP -Accelerated phase: increasing WBC, >20% baso's -Blast phase: >20% blasts Myeloid Leukemia question that had indices <10% blasts -CML -Phil chromosome -left shift (immature neutrophils) -0 LAP -Phil chromosome t(9;22)*** AML: older patients, dec HCT, variable WBC, DIC common in AML, even more common in APL. Thrombocytopenia, petechiae, lethargy CLL: older patients, >55% small, mature lymphs (special lymphs), dec Hgb, dec plts -proliferation of B cells, basket/smudge cells Predominant cell type lineage in CLL- on common lymphoid progenitor cell line that goes to the ***B cells Leukemoid reaction: benign granulocytic proliferative response. Do NOT confuse with leukemia. WBCs look like leukemia cells. Neutrophil count very high (50 x 10^9/L), mostly immature cells, typically myelocytes. High LAP

Wright stain was too pink...what would you do? Picture of too pink and crenated RBCs with 1 granulocyte that has pink nucleus, what is the cause (should be on Wright stain)? ***it's too acidic and the RBCs take up too much eosin dye. Also, WBCs show poor detail when pH is decreased, coverslip was mounted before it was dry, and also, the stain was too acidic*** All of the above a. pH buffer b. ethanol fixing Blood smear was staining too Blue- reduce pH buffer* too Basic -too much blue causes prolonged stain time, inadequate washing, stain that's too alkaline (if a Heparin tube was used, the background is going to be too blue for diffs) A control blood smear was made that covered 60% of the slide. The red cells stained pink while white cells had their nuclei stain dark blue to light blue. The white cells were clustered at the tail end. A) Accept B) ***Reject - white cells clustered at tail (should cover at least half of the slide and be evenly distributed- prolonged storage on EDTA can cause this) C) Reject - Red cell color is incorrect

Choices: Increase pH...decrease pH...add more Wright stain.. -It's too acidic. Check with pH paper and correct pH; fresh methanol may be needed (pH needs to increase) Other possible solutions: -Increase staining time -Decrease duration of wash -Decrease stain time in red solution -Increase time in blue stain solution -Allow preparation to dry completely before mounting coverslip

MCV day 1: 78 MCV day 2: 77 MCV day 3: 76 MCV day 4: 62 Also, Hgb slowly dec. What is the reason? (It's shifting more and more to the left and showing more and more microcytes)

Wrong patient? (or Microcytic anemia may be caused by: iron deficiency, which can be caused by poor dietary intake of iron, menstrual bleeding, or gastrointestinal bleeding) -***Developing iron deficiency (from microcytic anemia) -interference due to lipemic sample -Sample from wrong patient

What causes a false increase in Sedimentation rate? ESR is increased, what is NOT a cause False decrease in ESR: sample more than 8 hours to be tested? (delay in setup)*** ESR falsely decreased: presence of Target cells impairs Rouleaux, which causes ESR to falsely decrease ESR falsely increased: severe anemia, tilting tube. True increase: inflammatory state Side note: excessive anticoagulant causes shrinkage of RBCs. The ESR is affected.

a) Tilting the tube*** (or vibration) b) Results reported in less than an hour ( I chose this since test is run for an hour) c) Sample run within 2 hours of collection d) Sample sitting for over 8 hours I picked macrocytes because macrocytes don't do Rouleaux. Other options were Rouleaux, increased globulins, inflammation

Case of a patient that had everything elevated and platelets super high, RBC, HCT. Primary PV In what condition do you find abnormally low (dec) EPO? Primary Polycythemia Vera (could also be from renal failure, anemias associated with: rheumatoid arthritis, AIDS, cancer, ulcerative colitis, sickle cell disease, and in premature neonates)

a. Polycythemia vera b. Polycythemia vera absolute c. Other types of PV that can't remember ***Primary Polycythemia Vera (a type of absolute Polycythemia)

2 mL of blood is collected in a 0.5 mL citrate tube. How is the PT (and APTT) affected? a. Dec because of the inadequate ratio b. ***Inc because of the inadequate ratio (4:1 blood to anticoagulant ratio. Too much citrate...clotting is prolonged. Heparin contamination?) c. Normal Patient with Hct 62%, the sodium citrate tube was centrifuged and noticed that the blood plasma ratio was low. What should the MLS do? a. take sample with more anticoagulant b. take sample with less anticoagulant*** c. take sample in heparin d. report -I chose report, the high Hct can be from a newborn sample or it can be a dehydrated patient -take sample with more anticoagulant*** Patient for coagulation study (citrate tube) has 67% HCT what would you do....Choices include 1. recollect with reduced anticoagulant*** 2. proceed with test 3. recollect with increased anticoagulant 4. recollect with heparin tube 57% Hematocrit is normal in: a. Male b. Female c. One year old (should be 29%-41%) d. Newborn*** (should be 45%-61% for 1 week old and it dec over time) Blood collected in EDTA tube, decreased ratio of plasma to cells. 68% HCT. What do you do? -Report result. (The patient was a baby, and they usually have high HCTs)

good

Charcot-Leyden crystals in stool: damaged eosinophil products -parasite infection related

good

Unfilled EDTA: dec microhematocrit

good

Inc plt and WBC- could be metabolic syndrome (if RBC high too, could be primary PV, or hemolytic anemia- high segs)

good I think

What does the RBC morphology look like with chronic hookworm infection that's been there for years? (interruption of nutrient acquisition bc the hookworm ingests and digests host blood, results in iron def or IDA)

microcytic, hypochromic

What happens to CO2, PCO2, and pH when blood is left around for an extended period of time?

pO2 and pH will increase (more basic) CO2 and pCO2 decreased