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Lab Dx Final Exam Review

moon
LAB Dx Lecture
FINAL EXAM STUDY OBJECTIVES
FALL TERM 2008

1. Know definitions of: all “-osis,” and “-penia” terms, leukoeryothroblastic reaction, and leukamoid reaction. Know the causes of leukoeryothroblastic reactions.
--osis = too many (panic high for WBC's: 30,000)
--WBC’s increase dt infx, leukemia, stress, inflam
--penia = not enough (panic low for WBC's: 500)
--WBC's decrease dt overwhelming infx, marrow aplasia/failure/infiltration, autoimmune, drugs
--leukemoid rxn = non-leukemic WBC count over 50,000, or a differential count with more than 5% metas or earlier, LAP is high (in leukemia LAP is low)
--leukemoid rxn assoc w/: severe bact infx, severe toxic states ie burns, marrow replacement by a tumor, severe hemolytic anemia, mbdt normal BM response to trauma, stress, metabolic dz, drugs, inflammation, connective tissue disease, or malignancy, 2º to secretion of CSF, often associated with immaturity of other cell lines Lab ↑ Leukocyte alkaline phosphatase which is ↓ or absent in leukemia, 'left shift' of myeloid series–↑ bands, metamyelocytes, myelocytes, plasma cells, plasmacytoid lymphocytes, toxic granulation, Döhle inclusion bodies, vacuolization–which implies intracellular bacterial phagocytosis
--leukoerythroblastic rxn = An ↑ in the peripheral blood of immature & nucleated RBCs, ie normoblasts, and immature granulocytes, metamyelocytes and bands
--causes of LER = metastatic cancer, hematopoietic malignancy (PCV, leukemia, myeloid metaplasia, mets), hemolytic anemia, Gaucher's disease, polytrauma, BM infiltration by various processes, including infection–eg, fungal, viral, TB, sarcoidosis, histiocytosis, hypoxia; one third of Pts with LER have no known underlying disease

2. Know details of WBC differential staining & counting.
--wright stain = a mix of methylene blue and eosin red dyes
--wright stain: turns nucleic acids blue by binding to basic dye, turns cytoplasm & some graules pink-red-orange dt binding acidic dye (granules in: neutrophils turn lavendar, eos turn orange/red, basos turn blue/black)
--absolute vs relative counting: if neuts are 30% of differential, and pt has 15,000 WBC's total, absolute neut count is 15,000 x .30 = 4500, relative counts are reported as percentages.
--a pt can have low relative counts but normal absolute counts, or other variations

3. Know Neutrophilic causes of: shift to the left, toxic granulation, hypersegmentation
--shift to left: usudt bact infx, also: idiopathic, metastatic cancer, hematopoietic malignancy, hemolytic anemia, Gaucher's disease, polytrauma, BM infiltration by various processes, including infection–eg, fungal, viral, TB, sarcoidosis, histiocytosis, hypoxia
--toxic granulation: dark purple granules in neuts cytoplasm mbdt severe infx, burns
--hypersegmentation: seen in macrocytic anemia dt B12/folate deficiency

???4. Know atypical lymphs, plasma cells, abnormal lymphocyte phenotype
--atypical lymphs: seen in viral infx eg: mono, nucleus fills whole cell because virus has taken over machinery to make its own DNA
--atypical plasma cells: see perinuclear clear zone "eccentric nucleus", cytoplasm is blue dt acid from RNA
--abnormal lymphocyte phenotype: ??? T cells, B cells and NK's.....hairy lymph pic,

5. Know WBC “pools” response to infections: early….late
--BMP = bone marrow pool = getting ready
--CGP = circulating granulocyte pool = in PB
--MGP = marginal granulocyte pool = at infection site
--normal for circulating count to decrease early in infx because of margination, later the marrow production catches up and numbers increase
--early: WBCs in circ adhere to BV wall and diapedese, migrate to infx, stims BM to make more WBCs (WBC count is low at this time)
--next: BM releases all available WBC's incl immature ones (bands increase), granulocyte pool is increased but WBC is normal or ‘masked neutrophilia’
Late infection:
--circulating pool and marginal pool equalize, WBC increases- Left shift (bands in periphery)
--recovery, BM slows, WBC's decrease, left shift gone

6. Know significance of abnormal platelet count
decreased: PLT dt hypersplenism, hemorrhage
increased: CML (50% malig w/ incr PLT), PCV, post-splenectomy

Platelet counts:
<20,000 Petechiae and ecchymosis, risk of hemorrhage
<40,000 Prolonged bleeding (w. surgery), hemorrhage is rare
<50,000 panic!
--140 K to 400 K/mm3 Normal
<150,000 Thrombocytopenia
>400,000 Thrombocytosis
>1,000,000 panic! Thrombocytothemia??

**Platelets & basophilic granules carry serotonin.

7. Have a general idea of the normal ranges for total WBC counts & differentials in adults & children. Know how viral & bacterial illnesses can affect these parameters.
--WBC totals: normal range 5,000-10,000 absolute
--neuts: 2,500-8,000 abs, 55-70%
--lymphs: 1,000-4,000 abs, 20-40%, elevates w/ viral infx, also pertussis
--monos: 100-700, 2-8%, increase w/ chronic bact infx and TB
--eos: 50-500, 1-4%, elevates w/ parasitic infx or allergy
--basos: 25-100, 0-2%, elevates w/ some kind of leukemia--CML, early?
--never let monkeys eat bananas
--WBC normals: Adult: 5,000-10,000 per mm3, Child: <2 yrs: 6,200-17,000, Newborn: 9,000-30,000

8. Know the functions of the various types of WBCs.
--NEUTROPHILS: granulocyte; primary defense against microbial invasion; capable of phagocytosis; production stimulated by bacterial infx, inflam, trauma, granules contain LAP.
--LYMPHOCYTES: agranulocyte; help fight infx (some bacterial and viral); 3 types: T cells (mature in thymus) B cells (mature in BM; produce ABs) NK (natural killer cells).
--MONOCYTES: agranulocyte; phagocytic-->bacteria; remove necrotic debris from blood; increase in some viral infx, chronic bacterial, TB.
--EOSINOPHILS: granulocyte; granules contain 4 proteins to help eliminate parasites; incr w/ parasitic infx, allergic, asthma, hay fever; decrease with cortisol excess.
--BASOPHILS: granulocyte; aka mast cells in tissues; phagocytose immune complexes, degranulate during allergic reactions (releasing histamine, heparin and serotonin).

9. Know the components of Wright’s stain and the basis of the staining reactions.
--methylene blue, basic, binds w/ acids (nucleic esp)
--eosin red, acid thus binds with basics (in granules & cytoplasm mostly)

10. Understand the difference between relative and absolute white blood cell counts, how they are determined/calculated, and the clinical merits of each. Know how to calculate the ABS count.
--reported differential % x WBC total gives cell type ABS, useful to understand levels of one cell when the totals are out of normal ranges

11. Know the general changes that occur as WBCs mature and the stages of granulocyte maturation.
--blast-pro-cyte-meta-band-seg, blast-pro-cyte-meta-band-seg
--myeloblast-->promyelocyte-->myeolocyte-->meta-->band-->seg-->hyperseg
--general: cell shrinks, nucleoli shrink, nucleus shrinks and either disappears or becomes more segmented, turns from blue to red (or just less blue)

12. Be familiar with the clinical significance of neutrophils with abnormal nuclear segmentation.
--hyperseg = 6+ lobes: B12/folate deficient, "shift to right"
--bands = nucleus indented less than 1/2: immature so hyperproliferation dt hemolysis, hypoxia, malignancy, etc, also seen in acute bact infx and w/ toxic granulation

13. Know the constituents that can be found in the granules of the three granulocytic WBCs.
--neut granules contain leukocyte alkaline phosphatase (LAP), LAP stain discriminates leukemoid rxn from leukemia: low LAP means leukemia, high LAP means leukemoid
--eos: granules contain: peroxidase, MBP, esoinophil cationic prot, eosinophil-derived neurotox
--basos: granules contain: heparin, histamine and serotonin
--neuts: granules contain: leukocyte alkaline phosphatase (LAP), and also (not on test): lactoferrin, cathelicidin, myeloperoxidase, bactericidal/permeability increasing protein (BPI), Defensins, serine proteases neutrophil elastase and cathepsin G, cathepsin, gelatinase
--toxic granules: dark purple and peppery in cytoplasm, sign of severe infx or burn--are these the toxic debris that has been phagocitized??

14. How and why do NRBCs affect the total WBC count?
--automated cell counters count NRBCs as WBCs
--NRBC's are not hemolyzed by reagents
--Corrected WBC = (Original WBC Count X 100) / (NRBC + 100)

15. Know the normal ratio of CD4:CD8 T-lymphocyte counts.
--CD4:CD8 should be one or higher, only gets lower in immun compromise

16. Be able to recognize a leukemoid reaction and evaluate its clinical significance. Know the test that can be used to DDx leukemoid reactions from leukemia.
--leukemoid = WBC's over 50,000 no leukemia, or lots of bands (left shift)
--LAP stain tells the difference, high LAP-->leukemoid, low lap-->leukemia (CML)

17. Know the life span of platelets, where they originate from, and be aware of the normal range in adults. Know how the spleen (or lack thereof) can affect the platelet count.
--no spleen-->high platelets, hyperactive spleen-->low platelets
--lifespan: 7-10 days
--from: megakaryocytes in BM
--normal: 140,000 to 440,000 in adults

18. Patients with abnormal platelet counts are at risk for _________________.
--hemorrhage or thrombus formation
--thrombocythemia = over 1,000,000
--thrombocytosis = over 400,000
--thrombocytopenia = under 150,000
--or so =-]

19. Know the factors that may interfere with platelet counts and MPVs.
--increase: high elevation, strenuous exercise, estrogen
--decrease: EDTA (PLTs clump around WBC's), natural clumping, pre-menstrual, drugs
--MPV >10fl: Idiopathic Thrombocytopenic Purpura, Bernard-Soulier Disease, May-Hegglin Anomaly
--MPV <6 fl: Aplastic Anemia, Wiskott-Aldrich Syndrome, Thrombocytopenia-absent radii (TAR Syndrome), Storage Pool Disease

ITP = IDIOPATHIC THROMBOCYTOPENIC PURPURA
--purpura = dz causing subcu bleeding
--Most common Thrombocytopenia cause in children
--Peak onset between ages 2 to 4 years
--IgG Antibody develops against platelet membrane antigen
--Acute follows Viral Exanthem or viral Infection, occurs in otherwise healthy patients
--Chronic Insidious onset in patient with immune disorder more common in teenage girls
--S/Sx: Purpura, Mild Splenomegaly in 5 to 10% of cases
--Absent signs: fever, lethargy, pallor or weight loss, bone or joint pain, LAD, hepatomegaly
--LABs: Platelet Count drops rapidly
--Tx: Corticosteroids, Splenectomy in refractory cases
--splenectomy: Safe and effective, mb preferred in younger patients, Gadenstatter (2002) Am J Surg 184:606

20. Know the potential clinical significance of an “unexpected” increased platelet count.
--50% chance it is a malignancy (CML)
--also mbdt: PVC, acute infx, splenectomy, RA, IDA, primary thrombocytosis

??? 21. What does the MPV tell you regarding BM function in thrombocytopenic patients?
--MPV = mean platelet volume
--In thrombocytopenia with normal functioning marrow, large immature platelets are released in attempt to maintain normal function (ex: hypersplenism)
--in thrombocytopenia with a suppressed bone marrow the platelets that are released are small (ex: chemo)
--MPV >10fl: Idiopathic Thrombocytopenic Purpura, Bernard-Soulier Disease, May-Hegglin Anomaly
--MPV <6 fl: Aplastic Anemia, Wiskott-Aldrich Syndrome, Thrombocytopenia-absent radii (TAR Syndrome), Storage Pool Disease

22. Know the diseases that are classified as myeloproliferative disorders, the related unifying concepts, and the definition for each disorder.
--myeloproliferative disorder caused by clonal expansion of pleuripotent stem cell resulting in abnormal production of erythroid, myeloid and megakaryocytic precursors in the bone marrow
--PCV = Polycythemia Vera: a myeloproliferative disorder of unknown cause characterized by increased hemoglobin concentration and increased RBC mass, more in males, age 60 average
--Myelofibrosis: bone marrow becomes fibrotic, splenomegaly, normo/normochromic anemia with Dacrocytes, Myeloid metaplasia = Extramedullary hematopoiesis
--Essential Thrombocythemia: PLT counts >500,000 in absence of other myeloproliferative disorders, seen in 50-70 yo, BM megakaryocyte hyperplasia, hemorrhagic OR thrombotic tendency.
--CML = chronic myelogenous leukemia, overproduction from myelogenous stem cell, 20% of all leukemias, both sexes affected, common btw ages of 20-50, rare in childhood, poor prognosis

23. Know when to consider polycythemia vera in your diagnosis.
--HCT is above 52% in males or 47% in females
--HGB over 16% in males or 14% in females/blacks
--panmyelosis
--splenomegaly

24. Know the major and minor diagnostic criteria for polycythemia vera.
MAJOR? MINOR? Hmmmmmm.
--HCT and HGB as above
--increased uric acid levels dt increased nucleic acid turnover
--low or undetectable EPO
--immature WBC’s, RBC’s with marked anisocytosis and poikilocytosis
--eliptocytes and dacrocytes
--neutrophils with abnormal morphology may be seen
--thrombocytosis
--expanded blood volume & hyperviscosity-->tissue hypoxia, vessel thrombosis
--weakness, headache, light-headedness, visual disturbances, fatigue, dyspnea
--bleeding diathesis (epistaxis)
--pruritus
--face mb red
--retinal veins engorged
--hepatomegaly frequent
--Splenomegaly in > 75% of patients
--RBC count > 6,000,000 /mm3
--BM usu hypercellular (all cell lines)
--RBC survival time decreases in 25% --> anemia and myelofibrosis
--O2 content of blood increased, but o2 sat decreased
--Raynaud’s phenomenon
--chronic-->increased cardiac output & increased capillary beds-->decrease tissue hypoxia

25. Know the differential diagnosis for the three classes of polycythemia.
RELATIVE = Due to low plasma volume: dehydration, burns, diuretics.
SECONDARY = “Reactive Polycythemia”: Hypoxia, seen with smoking, high altitude, lung disease.
PRIMARY = Polycythemia Vera: “Malignant” hematologic disorder, not self-limiting, Tx: phlebotomy, anti-neoplastic drugs

26. Know the peripheral blood picture for polycythemia vera.
--immature WBCs
--immature RBCs
--marked anisocytosis and poikilocytosis: microcytes, elliptocytes, and
--dacrocytes
--neutrophilia with abnormal morphology (what abn???)
--thrombocytosis with abnormal morphology & function: hemorrhage OR thrombosis

27. Be able to define myeloid metaplasia and know when it might occur.
--mm = extramedullary hematopoeisis: blood cells made in liver and spleen when bone marrow isn't functioning dt myelofibrosis or other ???, most in pts age 50-70

28. Be able to define myelofibrosis
-- = Fibrosis of bone marrow-->splenomegaly, normo/normo anemia, myeloid metaplasia

29. How does the peripheral blood picture vary between polycythemia vera and myelofibrosis?
--PCV: too many immature RBC's and wBC's, abnormal thrombocytes, thrombocytosis and abn neuts
--PCV: marked anisocytosis and poikilocytosis incl dacrocytes
--Myelofibrosis: normocytic anemia, mild poikilocytosis, thrombocytopenia

30.How would you distinguish between essential (1o) thrombocythemia and the other myeloproliferative disorders? Myeloprolif post
--only PLT's increased
--no dacrocytes or other fancy stuff

31. Know the clinical presentation and CBC picture for myelodysplastic syndrome, and know when to consider that as a diagnosis.
--fatigue, weakness, anorexia, weight loss, abdominal fullness
--bleeding & infections
--macrocytic anemia
--anisocytosis
--thrombocytopenia
--variations in PLT size
--WBCs may be N/H/L
--poss monocytosis and up to 5% blasts in PB
--post on MDS and leukemia
--MDS considered "pre-leukemic"-->ANLL (acute nonlymphocytic leukemia)/AML (acute myelogenous leukemia)
--A heterogenous group of disorders that result in ineffective hematopoiesis.
--proliferation of abnormal clones of hematopoietic cells in bone marrow-->cytopenias-->extramedullary hematopoiesis-->hepato- & splenomegaly
--BM mb normal or hypercellular
--BM contains < 30% blasts
--S/Sx: fatigue, weakness, anorexia, wt loss, may bleed easily and have increased infx
--LABS: macrocytic anemia with anisocytosis, thrombocytopenia with variations in PLT size
--WBCs mb N/H/L, may see MONOcytosis and up to 5% blasts in PB

32. Know the general classifications for leukemia and the characteristic age incidence and diagnostic features for each type of leukemia.
--ALL: kids, lymphoblasts, anemia 90%, thrombocytopenia 80%
--AML: mostly adults, auer rods, poor prog, anemia and thrombocytopenia in 90%
--CLL: little old man, lymphs stay over 5,000
--CML: commonest in adults 20-50, philadelphia 95%, PLT's high 60%, ABS eos & basos high

33. Know the characteristic features of Hodgkin’s and non-Hodgkin’s lymphomas and how to diagnose each type. Know the changes one might see in a CBC.
--Hodge: reed-sternberg cells in LN Bx, low-med neutrophilia, low lymphs early and worsening, incr eos 20%, mb thrombocytosis, incr ESR & LAP = active dz, two age peaks: 15-34 and 60+, spreads to contig LN's, pain after alc, fever, night sweat, pruritis early
--NONHodge: Anemia 33 % early, most laster, non-contig spread, leukemic phase in 20-40%, Dx by LN Bx only

34. Know the lab findings for multiple myeloma and for Waldenstrom’s macroglobulinemia. How would you DDx multiple myeloma from Waldenstrom’s macroglobulinemia? How can these diseases affect other body systems?
--on plasma cell dyscrasias
--MultMyeloma: plasma cell tumor in BM-->too much monoclonal Ig (can be G, A, D, E) or light chains (Bence Jones in urine 40%)(light chain indic higher bone lytic lesions, hypercalcemia & renal failure)
--MM Labs: Anemia, normocytic, normochromic, high ESR, normal WBC's & PLT's, incr Ca+ 33%, IgG 55%, IgA 20%, "M protein" 80%,
--MM S/Sx: bone pain (back, thorax), renal failure, & recurrent bacterial infections most common. Mb pathological fractures in vertebrae (leading to sudden change in height), and anemia.

--Waldenstroms: Clonal expansion of plasma cells-->IgM, Raynaud’s, Recurrent bact infx
--Wald Labs: mod anemia, high ESR, low leuk, relative high lymph, rel low PLT, mb Cryoglobulins, rheumatoid factor, and cold agglutinins, Relative serum viscosity is usually 4.0 (normal 1.4-1.8) due to increased proteins
--Wald Sx: most ASx, mb Sx of hyperviscosity (Raynaud’s), fatigue, bleeding from skin and mucous membranes, weakness, visual disturbances, headaches

--tell apart:
--MM has BJ's in urine, IgG or A, no anemia, high Ca+, bone pain & fx
--Wald has low PLT, IgM, mod anemia, may bleed, mb ASx

35. Know how to evaluate CBC results to initially classify anemia, and be familiar with the various causes of each type of anemia.
--yes'm

36. Know why a normal ferritin level may not necessarily exclude iron deficiency.
--many diseases, such as malignancy, liver disease and inflammatory diseases, cause a rise in ferritin independent of iron stores
--Normal levels does not exclude iron deficiency
--Falsely elevated in patients with chronic disease states
--Acts as acute phase reactant prot (incr 1-2 days after onset of acute, peaks @ 3-5 days)
OTHER ON FERRITIN
--Ferritin is the major iron-storage protein, primarily found in the liver.
--Good indicator of available iron stores in the body in healthy person
--1 ng/mL serum ferritin = about 8 mg of stored iron
--Levels below 10-12 mg/dL = diagnostic for Iron Deficiency Anemia (IDA)
--Serum Ferritin: Males 40-340 ng/mL, Females 14-150 ng/mL
--Levels rise persistently in males and post-menopausal females
--Severe protein depletion can decrease levels (take aa's to make other stuff, starvation?)

37. Know the effects of stress, hemolytic anemia, & neoplasia on serum iron levels.
--stress-->decrease
--hemolysis-->increase
--neoplasia-->increase
--serum iron changes daily and is not a good reference for diagnosing anemia
--Serum iron = measurement of the iron bound to transferrin
--levels fall between depletion of iron stores and development of anemia
--IDA pts have normal serum iron 10-15 % of the time (ferritin better test)
--severe stress decreases serum values 65%, recover to normal over the following week
--normal: Males: 65-175 picograms/dL
--normal: Females: 50-170 picograms/dL
--Interferers: transfusions, high iron meal or supplements, Hemolytic dz, Drugs
--Increase: Hemosiderosis or hemochromatosis, Iron poisoning, Hemolytic anemia
Massive blood transfusions, Liver disease, Lead toxicity
--Decrease: Diet deficient, Chronic blood loss, Malabsorption, Pregnancy – late, Iron Deficiency Anemia, Neoplasia

38. Know what TIBC measures. Know the effect of polycythemia vera, cirrhosis, hypoproteinemia, and hemolytic anemia on TIBC.
--TIBC measures transferrin in blood, ie: how much free iron transport capacity?
---PCV-->increased TIBC
--cirrhosis, hypoprot, hemolysis-->lower TIBC

39. Know the stages of iron deficiency anemia and their labs.
Example: In full-blown iron deficiency, the CBC will show microcytic hypochromic anemia, incr RDW, and possibly thrombocytosis; “iron studies” will show decreased serum iron, increased TIBC, decreased % saturation, and decreased ferritin.
--SUMMARY: marrow iron depleted-->hypochromic-->microytic
--BM depleted first
--begins to go hypochromic
--tissue stores pilfered to maintain MCHC, same level of hypochromicity while tissue depletes
--MCV falls last, at this stage RBC's have most of the FE in body, tissue is depleted
--RDW will increase whenever a high Fe meal is consumed and the body has Fe to make some regular sized RBC's: blood is priority

40. Know how to distinguish iron deficiency anemia from thalassemia.
BOTH
--micro hypo anemia
THAL
--*increased ferritin and serum Fe
--*increased retics
--*increased % saturation
--normal FEP (free erythrocyte protoporphyrin is precursor to HGB, needs Fe)
--normal or low TIBC
--basophilic stippling
--↑ RDW with abn shaped RBC’s
--HGBE normal
--mentzer index = MCV/RBC: under 13 thal over 13 IDA
IDA
--*decreased ferritin
--high FEP (precursor to HGB, needs Fe so high when no Fe to make HGB)
--increased TIBC (no Fe available so busses for transport are empty)
--decreased % sat
ANOTHER MICROHYPO
--pyridoxine (B6) deficiency
--needed for synthesis of gamma-ALA for heme synthesis
--commonly acquired dt TB tx

41. What are the peripheral blood smear characteristics of thalassemia? Be aware of the “normal” globin chain configurations of the 3 main types of hemoglobin. In general, what type of hemoglobin electrophoresis patterns would you see in alpha thalassemia and beta thalassemia?
--electrophoresis pattern in alpha: ??? sub gamma or beta for alpha
--electrophoresis pattern in beta: ??? sub delta, gamma, or beta2 for beta
TYPES OF HEMOGLOBIN BY GLOBIN CHAIN ARRANGEMENT
--alpha2beta2 is HGB type A1, and is 97% of normal adult HGB
--alpha2delta2 is type A1, 2%
--alpha2gamma2 is type F, 1% (fetal hemoglobin, main type during fetal & neonatal periods
--alpha2betaS2 is type S, sickle cell-->hemolytic anemia
--gamma4 (Bart's)
--beta4
SMEAR
--basophilic stippling in beta major, also targets and NRBC's
--↑ RDW with abn shaped RBC’s
--increased retics

42. Know the various types of anemia that can be caused by nutritional deficiencies.
--Megaloblastic anemia is due to B12/folate deficiencies.
--Vitamin B6 (pyridoxine) causes microcytic hypochromic anemia.
--IDA

43. Know how the peripheral blood picture can differ between megaloblastic anemia and macrocytic anemia.

First of all, megaloblastic is a type, in fact it is the prevalent type, of macrocytic anemia. Megaloblastic anemia is caused by deficiencies in DNA synthesis, usually secondary to B12/folate deficiency or chemotherapy. The largest macrocytes (MCV over 105) fall into this category. Megaloblastic anemia will show increased bilirubin dt hemolysis, ovalocytes, hypersegs, Howell-jolly bodies, and possibly low serum folate (not best folate measure). Non-megaloblastic macrocytic anemia is any macrocytic anemia in which DNA synthesis is unimpaired, and will be only slightly macrocytic (MCV barely over 100) or normocytic. Non-megaloblastic macrocytosis are most often assoc with alcoholism and liver dz, and may also be associated with increased reticulocytes with or without anemia. It may be an early sign of pernicious anemia. Spurious macrocytosis can result from laboratory artifacts. Cold agglutinins, severe hyperglycemia, and marked leukocytosis can lead to an incorrect high MCV value. Care is needed so that these situations do not lead to a fruitless search for a disorder known to cause macrocytic anemia.

megaloblastic: MCV>105, incr bili, ovals, hypersegs, Howell-jolly bodies
macrocytic: MCV>100, may have no other abnormality, may see round RBC’s, Target cells with liver dz and alcoholism (this independent of B12/folate deficiency)

44. Know the common laboratory features of megaloblastic anemia
--incr bili dt hemolysis
--macro-ovalocytes
--Howell-Jolly bodies
--hypersegmented neutrophils
--MCV over 105
--increased RDW
--mb pancytopenia in severe cases

45. What test would be most useful in documenting a “production deficit” anemia?
--"production deficit = aplastic, so BM biopsy

46. Know the lab features and test patterns for aplastic anemia.
--normocytic normochromic anemia
--decreased platelets
--increased risk of infection
--panctyopenia
--NO retics
--↑ serum iron
--assoc w/ chronic/systemic dz or hypoplastic marrow
--hypothyroidism-->anemia in 30-50% of patients
--CBC of peripheral blood and get a count which would likely reveal pancytopenia
--look for toxins: benzene, others that injure marrow?

47. Know the type of anemia you would likely see in G6PD deficiency, the conditions under which the anemia is most likely to occur, and what you might see on the peripheral blood smear.
--normo-normo
--decreased platelets
--increased risk of infection
--also pancytopenia
--NO retics
--elevated serum iron
--G6PD-->ATP deficient-->decreased flex, increased oxidative damage to RBCs-->intravascular hemolytic anemia
--triggers: aspirin, sulfa or antimalarials or fava beans

48. Be familiar with the differences between intravascular and extravascular hemolysis and know which anemias are categorized as such.
--extravascular: the spleen removes RBC's dt sickle cell anemia, hereditary spherocytosis (HS)
--intravascular: RBC's lysed by 1) mechanical trauma (mech heart valves, physical trauma such as marathon running, bongo drumming, malignant HTN) 2) immunologic: antibody fixation, auto- or allo- (idiopathic, mismatched blood transfusion, SLE, infx trigger, lymphoma, CLL) 3) toxic injury to RBC's (microangiopathic or infectious) (malaria, clostridium, septic shock-->disseminated intravascular coagulopathy [DIC]) 4) enzymopathy (G6PD)

49. Know the characteristic changes in the CBC of an individual with hereditary spherocytosis, and the specific lab tests used to diagnosis that disorder.
--decreased MCV
--decreased HGB
--hemolysis: increased bilirubin
--splenomegaly
--TESTS: osmotic fragility test
--increased MCHC, increased MCH
--increased retics

50. Be familiar with the anemias that are caused by antigen-antibody reactions.
WARM AUTOIMMUNE HEMOLYTIC ANEMIA
--IgG, binds at 37 degrees, idiopathic/SLE/RA/CA, mb fatal
COLD AIHA
--IgM below 37, Raynaud's
PCH = paroxysmal cold hemoglobinuria
--rare, assoc w/ measles, mono, chicken pox,
--IgG-->RBC's sensitive at cold temp-->hemolysis
PNH = PAROXYSMAL NOCTURNAL HEMOGLOBINURIA =
--complement induced
IMMUNE (not auto-) HEMOLYSIS
--ETIO: incompatible blood transfusions
--fetal maternal incompatibility
DRUG INDUCED: antibodies against drug cross react with RBC membrane

51. What tests can you order to confirm PNH and PCH?
--PNH--HAM'S test (being replaced by flow cytometry), also sucrose lysis test
--PCH--look for IgG in blood (ANA?)

52. What do all autoimmune hemolytic anemias (AIHA) have in common?
--antibodies opsonize person's own cells
--autoimmune hemolytic anemias (AIHA) have common autoantibodies to RBC antigens-->immune mediated hemolysis-->anemia

53. What is the primary purpose, indications for doing a Pap smear?
--purpose: to notice abnormalities in cervical tissue before cancer develops
--indications for pap: 1) onset of sex or 18 yo+, 2) minimum: annual for 3 consecutive yrs to establish basline 3) post hysterectomy, 4) hx of DES (diethyl stilbestro) exposure-->clear-cell vaginal ca and trouble getting preg 5) followup for dysplasia, 6) prenatal
--up to 25% false negative

54. What is the most critical area to sample when you are collecting a Pap smear?
--transformation zone (squamous-columnar junction)

??? 55. What are the minimal requirements for conventional and thin-prep Pap smear adequacy?
conventional:
--getting enough cells
--fixing cells before they dry
thin prep:
--getting enough cells
--get cells in liquid before they dry
interesting tips site: http://web2.airmail.net/uthman/pap_tips.html

56. Know the correlations between Pap smear cytological abnormalities and biopsy-obtained histopathological abnormalities.(WHO and Bethesda)

Comparison of WHO and Bethesda:
WHO Histopathologic Terms Bethesda Cytology Terms
CIN 1/ Mild Dysplasia LSIL [lower 1/3rd cervical epithelium]
CIN 2/ Moderate Dysplasia HSIL [middle 1/3rdepithelium]
CIN 3 / Severe Dysplasia HSIL [>2/3rd epithelium]
CIN 3 / Carcinoma in Situ HSIL [full thickness]

57. Know the organisms that may be detected on a Pap smear.
--HPV (papillomas)
--gardnerella (clue cells)
--actinomyces

The Hybrid Capture II assay is a specialized Human Papilloma Virus test that can provide qualitative detection of 18 (of the 100) types of HPV. This test can differentiate between low-risk HPV types and high/intermediate HPV risk types. However, it cannot determine the specific HPV type present. The “wave of the future” is PCR, polymerase chain detection, which can perform HPV DNA testing for high-risk HPV types. This will enable identification of individual HPV strains.

HPV Strain Linked to
6/11/42/43/44 Low risk
6 &11 benign lesions -> condylomata accuminata & mild dysplasia
16 & 18 most commonly associated with CIN & CIS
**HPV-16 causes 50% of cervical cancers**


58. What is the optimal time for collecting a Pap smear?
--day 14

The optimal time to collect a Pap smear is the week following cessation of menses, in the Proliferative phase, i.e. 2 weeks after the start of the menses, day 14.

59. Know the clinical significance of the maturation index.
--three types of cell maturity, parabasal (low est, atrophic vaginitis if dominant), intermed (prog exposure), superficial (most mature dt most est)

1st a little background: The sex hormones estrogen, progesterone & androgens cause maturation in squamous cells that can be detected by cytological exam.
MI is a ratio of 3 major cell types shed from the squamous epithelium. It’s expressed as a percentage of parabasal cells, intermediate cells, & superficial cells. Parabasal cells are the least mature cells having not been affected by estrogen or progesterone. Intermediate cells display mild maturation, having been affected by progesterone, and superficial cells display the most maturity, having been affected by estrogen. A predominance of parabasal cells indicates an absence of estrogen stimulation & superficial cells indicates estrogen stimulation. Intermediate cells have little clinical usefulness.
MI provides a sample (taken during a pap smear) that is easily analyzed to detect hormonal changes in the vagina that are age-appropriate or an early sign of possible hormonal related dz processes. Samples are taken with a gentle scrape along the lateral wall of the upper vagina at the level of the cervix.
MIs are useful for evaluating hormonal fct, evaluating cellular composition of the surface layers of vaginal tissue which reflects the balance of estrogen & progesterones effects on this tissue, & diagnosing conditions that produce abnormal hormonal balance (pituitary gland dysfunction, ovarian dysfunction, & hormone secreting tumors).
MIs can detect the beginnings of endometrial CA in menopausal women, & have been used to screen vaginal adenosis & clear cell carcinoma in women who were exposed in utero to diethylstilbestrol (DES), a synthetic estrogen.
So, MI
• Is used to evaluate hormones -> reflects Estrogen & Progesterone balance
• Is obtained by sampling the lateral vaginal wall
• Helps dx conditions of hormonal imbalance including: pituitary & ovarian dysfunction, menopause, & feminizing or virilizing tumors
• In menopausal women with predominately basal cells = “atrophic vaginitis”


60. Know the indications for and the clinical significance of sputum cytology.
Indications:
--abn chest X-ray, productive cough & negative bronchoscopy
--bronchoscopy & lung biopsy used more often now
Clinical sig:
--trachea, bronchus & lung malignancies
--benign cellular changes due to infx, toxins, viral pneumonitis.
--eos in asthma

61. Know the indications for and the clinical significance of urine cytology.
Indications:
--suspected CA
--suspect inflam dz of kidney, ureters, bladder, or urethra, viral (CMV)
--screen pops at risk for bladder cancer -> smokers, aniline dye workers, pts tx’d for GU CA
Clinical sig:
--GU inflam: epithelial hyperplasia, atypical cells, RBCs, WBCs
--Indication of virus: (CMV-->cytomegalic cell inclusions), measles(inclusion bodies)

62. Know the indications for and the clinical significance of nipple discharge cytology.
Indications:
--lactation w/o preg, esp if unilateral
--lact sometimes with perimenopause and OCP's w/o pathology, less worrisome if bilateral
--about 3% of breast CA & 10% of benign breast lesions cause lactation
--usu limited to patients w/o palpable breast masses or other evidence of possible breast CA
Clinical sig:
--ID B9 mastitis (subareolar abscess) or intraductal papilloma
--ID malignant conditions: intraductal CA or intracystic infiltrating CA

63. Know the indications for cervical biopsy.
Indications for biopsy:
--unexplained postcoital bleeding, hx of HPV, abn PAP
--LSIL, ASC-US, or AIS

64. Know the indications, potential complications, contraindications for endometrial biopsy.
Indications:
--DUB
--dx endometrial CA
--ID Est/Prog balance
--ovarian dysfx: perimenopause, amenorrhea, infertility
Complications:
--perforation of uterus
--excessive uterine bleeding
--interference w/ preg
--infx
Contraindications:
--vaginal or cervical infx
--preg
--inability to visualize cervix

65. Know when skin biopsy is contra-indicated.
Contraindicated:
--When you think it's cancer: refer to specialist, do not disturb
Indications:
--any growth that cannot be ID's as B9 on gross examination, moles w/ assym, irreg border, irreg color, large diam, changes/itches
--??? THESE RECOMMENDATIONS ARE CONTRADICTORY: Don't biopsy if you think it could be cancer, instead, biopsy if you're not sure it's benign. Uh huh.

66. What symptoms might cause you to suspect that your patient has kidney stones?
S/sx:
--sudden onset of pain in abdomen, back, groin, side
--hematuria, dysuria
--fever, chills
--vomiting
--urine foul smelling w/ struvite stones
--80% of stones are calcium oxalate

67. Know the most accurate diagnostic technique for gallstones.
--ultrasound
--usu made of cholesterol

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