Hematology

Hypoproliferative Anemia

Hyperproliferative Anemia

Microcytic Anemia

Normocytic Anemia

Macrocytic Anemia

Thalassemia

Alpha Thalassemia

Beta Thalassemia

Iron Deficiency Anemia

Anemia of Chronic Disease

Sideroblastic Anemia

B12 Deficiency

Folate Deficiency

Pure Red Cell Aplasia

Aplastic Anemia

Hemolytic Anemias

Hereditary Spherocytosis

Paroxysmal Nocturnal Hemoglobinuria

Glucose 6 Phosphate Dehydrogenase Deficiency

Sickle Cell Disorders

Autoimmune Hemolytic Anemia

Cold Agglutinin Disease

Neutropenia

Polycythemia Vera (PCV)

Thrombocytosis

Myelofibrosis

Myelodysplastic Syndrome

Multiple Myeloma

Monoclonal Gammopathy of Unknown Significance (MGUS)

Waldenström’s Macroglobulinemia

Chronic Lymphocytic Leukemia

Chronic Myelogenous Leukemia

Acute Lymphoblastic Leukemia

Acute Myelogenous Leukemia

Hodgkin's Lymphoma

Non-Hodgkin's Lymphoma

Infectious Mononucleosis

Ehrlichiosis

Histoplasmosis

Acute Thrombocytopenia

Idiopathic (Immune) Thrombocytopenic Purpura

Heparin Induced Thrombocytopenia

Thrombotic Thrombocytopenic Purpura

Hemolytic Uremic Syndrome

Coagulation: prolonged PT

Liver Disease (prolonged PT)

Vitamin K deficiency (prolonged PT)

Coagulation: prolonged aPTT

von Willebrand Disease

Glanzmanns thrombasthenia

Bernard-Soulier

Acquired Thrombopathy

Prothrombin 20210A Mutation

anticoagulation disorders

Disseminated Intravascular Coagulation

Hemophilia A

Hemophilia B

Reticulocyte count will be low (<2%)

Reticulocyte count will be high (>3%)

seen primarily in southeast Asian, Mediterranean or African descent

seen primarily in Mediterranean (Italian, Greek) and less often in Asians and Africans

fatigue, dyspnea on exertion, tachycardia, nail changes, dysphagia, pica ; microcytic/hypochromic as iron stores depleted

mild to moderate anemia; initially normocytic and moves to mild microcytic hypochromic due to defect in moving iron into RBCs

may have enlarged spleen or liver; mild to moderate anemia

glossitis, anorexia, diarrhea, peripheral neuropathy

malnourished appearing, diarrhea, cheilosis, glossitis, NO neurological symptoms; alcohol is most common precipitator due to impaired hepatic function

severe anemic symptoms

any age; pancytopenia; fatigue, weakness, excess bleeding/bruising, petechiae, purpura, pallor

anemia may not be apparent until RBC life span becomes shortened to approx 20 days

anemia, splenomegaly, jaundice; pigment type gallstones may be present; maybe chronic leg ulcers

episodic hemolytic anemia will cause Fe deficiency as well; venous thrombosis; deficient hematopoiesis causing pancytopenia; reddish-brown urine

episodic hemolysis often triggered by oxidative stress (infections, toxins or drugs); no splenomegaly; no chronic hemolytic anemia

pallor, jaundice, splenomegaly, leg ulcers, pigment gallstones, priapism; vascular occlusion leading to infarction

anemia can be rapid onset and severe

mottled or numb fingers/toes; anemia is rarely severe

stomatitis (ulcers in mouth); fever sometimes; severe infections such as septicemia, pneumonia and cellulitis may occur

dyspnea, headaches, visual disturbances, tinnitus, pruritus, thromboses; PE shows retinal-vein occlusion, ruddy cyanosis and splenomegaly

rare in children, slight female predominance; approx 1/3 or pts asymptomatic at diagnosis; 2/3 of pts report vasomotor symptoms or complications from thrombosis or bleeding

early stages asymptomatic; later stages: general malaise, weight loss, splenomegaly or splenic infarction (LUQ pain); hepatomegaly in 50% of pts

asymptomatic; abnormal blood counts during routine screening; if symptomatic: fatigue, bleeding, recurrent infections, fever, splenomegaly, pallor

fatigue/anemia, recurrent infections, lytic lesions predisposing pts to bone pain, pathologic fractures and hypercalcemia, kidney failure, hyperviscosity of blood;

probable precursor to multiple myeloma

fatigue, hyperviscosity syndrome (nausea, vertigo, visual, mucosal or GI bleeding); weight loss, headache, cold hypersensitivity, peripheral neuropathy, hepatomegaly, splenomegaly, engorged retinal veins

male 2: female 1; 25% asymptomatic at diagnosis; fatgue, drenching night sweats, weight loss, frequent and/or persistent infections, lymphadenopathy (80%), skin infections/shingles less common

young to middle age adults; phily chromosome present in over 95% of cases; bcr-abl is another way of diagnosing CML; fever with no infection, bone pain, LUQ pain due to enlarged spleen, fatigue, weakness, night sweats, bleeding and brushing, petechiae

pts acutely sick over days/weeks, not months; primarily children's disease; can affect T or B cells; malaise, fatigue, fever, bleeding gums, lympadenopathy, splenomegaly, petechiae, weight loss, meningitis, lethargy, anorexia, dyspnea

similar to ALL; pancytopenia with circulating blasts, bone marrow with >20% blasts; peripheral smears showing WBC with Auer Rods; hepatomegaly, splenomegaly, elevated erythrocyte sedimentation rate

median age of onset is mid 50s; male 5: female 1; fatique, abd discomfort from splenomegaly

enlargement of lymphoid tissue, spleen, liver; painless cervical, supraclavicular, and mediastinal lymphadenopathy; constitutional/b symptoms (fever, drenching night sweats, weight loss); shortness of breath common with mediastinal mass

Three grades: indolent (slow growing); intermediate (aggressive, mix of small to large cells); high grade (very aggressive); lymphadenopathy persistent and painless, isolated or difuse; B symtpoms; occasional ab pain, vomiting, bleeding, edema

usually in immunocompromised pts; organism in neutrophils and monocytes on Wright-Giemsa stained blood film; organism in macrophages on bone marrow smear

nose bleeds, gum bleeds, bruising, menorrhagia, petechia

same as acute (no systemic illness, spleen normal); common in childhood, starts with viral infection and have it intermittently throughout life; adult form is chronic

heparin for 4-10 days (if plt count drops more by half or more than assume HIT); inflammation/necrosis at subcutaneous sites, limb asymmetry, cool/pulseless extremities; arterial or venous thrombosis

mental status changes and symptoms correlating to end-organ damage (fever +/- mild renal insufficiency); associated with some meds; rare disease, but really sick; most prevalent in young women

renal failure; no mental status changes; most common in infants, children and pregnant women

hepatic coagulopathy

bruises easily, increased bleeding after minor procedures (dental), menorrhagia*

can act in concert with smoking, birth control pills/hormone replacement

anti-phospholipid (recurrent thromboses, 2nd trimester miscarriages, thrombocytopenia, valvular heart disease, migraines)

excessive thrombosis + bleeding (bc using up clotting products), organ dysfunction, shock, death; can get subacute DIC (Trousseau's syndrome) - see recurrent superficial cloting and DVTs

spontaneous hemarthroses

MCV < 80

MCV 80-100

MCV > 100

A Thal trait: HgB electrophoresis shows no increase in HgB A2 or F, no HgB H; usually diagnosed via exclusion; Hgb H: peripheral smear abnormal, high retic count b/c hemolysis is occuring and body is trying to keep up with rate of destruction

Thal major: severe anemia, marrow expansion causes bony deformities, growth retardations, hepato-splenomegaly (HSM), iron overload, predom Hgb F;

Thal intermedia: can have bone abnormalities and HSM, iron overload, 10% HgbA2 and the rest is HgbF; Thal minor: Hgb can be 3g/dL below normal, smear can show basophilic stippling

look at stool to rule out occult blood loss; classically microcytic, although Hgb will drop before MCV; abnormal iron indices, low ferritin, absent marrow iron, abnormal peripheral blood smear(anisocytosis),

plts may be increased; (serum iron < 30, TIBC > 400, % sat < 10, ferritin < 15, marrow iron 0); RDW high; serum iron and ferritin low b/c used up stores

microcytic or normocytic morphology; retic count usually normal; serum iron and TIBC may be low, ferritin is normal or elevated; marrow iron stores normal;

LOW EPO LEVEL (bone marrow is sluggish because the pt has an underlying disease); MCV not as low as iron deficiency

MCV usually low normal or high; serum iron high; diagnosed by bone marrow showing ringed sideroblasts

RBCs are macrocytic with MCV 110-140; anemia may be severe w/coexisting thrombocytopenia and leukopenia; peripehral smear may show hypersegmented neutrophils;

decreased retic count; B12 levels <100pg/ml in symptomatic pts; elevated methylmalonic acid (indicator of deficiency at tissue level); Schilling's test

macrocytic; similar to B12 deficiency (MCV high); RBC folate levels less than 150ng/mL; RBC folate is better than serum folate

reticulocytes low or absent, morphology normal, WBC and plts not affected, bone marrow is normocellular

decreased retic count; morphology and MCV usually normal, but hematopoietic progenitor and precursor cells are less than 1% normal levels; bone marrow is hypocellular but no abnormal cells are seen

haptoglobin levels low; LDH often elevated; hemoglobinuria; elevated indirect bilirubin; elevated retic count; stable or falling Hgb

loss of central pallor in RBCs; anemia usually microcytic and mild to moderate or absent (bone marrow is usually able to compensate); reticulocytosis is present; indirect bili may be elevated; Coombs test negative

flow cytometry assays demonstrating absence of CD59 Ab; anemia is variable, usually normocytic unless Fe deficiency present; episodic hemolysis is intravascular so will find hemoglobinuria

peripheral smear shows bite cells and Heinz bodies; reticulocytosis and increased bili during acute hemolytic episode; enzyme assays for G6PD will be low during an acute crisis

chronic hemolytic anemia, very low Hgb around 7-10g/dL; sicked cells in peripheral smear (5-50% of total RBCs); reticulocytosis; nucleated RBCs; leukocytosis and thrombocytosis; indirect bili is high; hemoglobin electrophoresis

positive Coombs test; severe anemia (Hgb 6-10g/dL); elevated retic count; peripheral smear shows spherocytes and nucleated RBCs; elevated indirect bili; 10% may have concurrent immune thrombocytopenia

mild reticulocytosis; see spherocytes in peripheral smear; coombs test positive for complement; positive fold agglutinin test

neutrophil count lower than 1500/mcL; calculate absolute neutrophil count (ANC) (the lower the ANC the greater the risk for serious, life-threatening infections)

increased number of RBCs/Hgb and perhaps increase in other cell types (but not as great as increase in RBCs); splenomegaly, systolic hypertension, engorged retinal veins;

positive JAK-2 serum test in 74-97% of pts (use to confirm dx); peripheral blood often appears microcytic with or without iron deficiency

Physical exam often unremarkable but sometimes: splenomegaly, hepatomegaly, leukocytosis, erythrocytosis, mild anemia; occasional immature precursor cells and/or large plts in peripheral smear; increased number of megakaryocytes in bmbx

plt count very high (over 600,000);

fibrosis in bone marrow (difficult to aspirate), giant plts, teardrop poikilocytosis in advanced cases, nucleated RBCs (hematopoietic precursors) may be found in peripheral blood;

hypercellular bone marrow with reticulin or collagen fibrosis; WBC counts usually increased but highly variable; plt counts initially may be high, normal or decreased

SPEP IgG moderately elevated

IgM spike (monoclonal antibody spike); anemia; plasmacytic lymphocytes on bmbx; differentiated from MGUS by the presence of bone marrow infiltration; serum viscosity; bone radiographs normal; low RBCs, low plts, high SPEP

lymphocytosis (WBC > 20,000); anemia, thrombocytopenia, peripheral blood with mature small lymphocytes and smudge cells; hepatomegaly, splenomegaly, lymphadenopathy; coexpression of CD19 and CD5; hypogammaglobulinemia

transition from low grade lymphoma/CLL to a high grade/aggressive lymphoma

B-symptoms:

most common presentation of non-Hodgkin’s lymphoma (could also be Hodgkin Disease or CLL)

Reed-Sternberg cells

Ringed sideroblasts or 5q- syndrome

Teardrop cells

Elevated HGB/HCT

Test to confirm a suspected diagnosis if CBC abnormal

Important chemo side effects:

Monoclonal IgM paraprotein

Rouleaux

Lytic lesions

Urinary Bence-Jones proteins or Serum M-spike proteins

Philadelphia Chromosome (bcr/abl gene rearrangement)

Imatinib (Gleevec & ST1571), oral chemo

Blasts + Pancytopenia (decreased WBC, RBC, and plts)

Auer Rods in WBCs =

Most common leukemia in children

Most common occurring leukemia

Smudge cells

Collective term for all physiologic mechanisms the body uses to protect itself from blood loss. Constant balance of maintaining blood in the fluid state & stopping bleeding from injured sites

failure to maintain hemostasis

failure to maintain fluidity

4 Major Systems Involved in hemostasis

released, enhancing coagulation cascade & secondary (stable) hemostatic plug formation.

potent stimulator of platelet aggregation & vasoconstriction

Intrinsic pathway: Factors

Extrinsic pathway: Factors

Common pathway: Factors

mild: no treatment; transfusion support; splenectomy; transplant; iron chelation therapy

Hgb H: splenectomy may be helpful, folic acid to help with stability of RBC membrane

Thal major: transfusions, splenectomy, iron chelation, allogeneic bone marrrow transplant for cure

evaluate and treat blood loss; oral iron supplements; encourage stool softeners; parenteral iron

EPO injections + iron helpful for certain patients, but usually inadequate to maintain Hgb; transfusions are effective but multiple transfusions can generally cause problems down the road

Deferoxamine (Desferal used at home, administered via IV or SQ for 12-16hrs/day; ascorbic acid (vit C) increases iron excretion used with deferoxamine (initiated 1-2 mos after chelator); deferasirox (Exjade) is an oral iron chelator but $$$

Anemia: morphology rel to MCV

Diff Dx for micro anemia

Anemia: RBC production problem (vs destruction prob) distinguished by:

Formula: corrected retic

Hypoproliferative anemia due to:

Hyperproliferative anemia due to:

Degrees of thalassemia dz

Thal: Hgb-H dz labs

Beta thal types

Tx for Hgb H dz

Tx for beta thal major

Most common cause of anemia worldwide

Causes of Fe def anemia

Tx for Fe def anemia

Anemia of chronic dz

Enzyme disorder: adequate Fe but can't get it into Hgb; Fe accumulates in ?

Sideroblastic findings

Tx: Sideroblastic anemia

Macrocytic anemias

Causes of B12 def

S/S = Glossitis, periph neuropathy (Stocking-glove paresthesias); MCV 110-140; low retic, hyperseg PMNs, high methylmalonic a.

Tx B12 def

B12 def vs folic acid def

Causes folic acid def

Folic acid def findings

PRCA is contracted:

Autoimmune dx mediated by T lymphocytes or (rarely) IgG antibody against erythroid precursors

Poss causes include thymoma, solid tumors, SLE, RA, HIV/hep, phenytoin

PRCA findings

PRCA Tx

Due to BM failure (injury or suppression); pancytopenia

Causes of aplastic anemia

Aplastic anemia findings

Aplastic anemia: diff dx from: 1-MDS; 2-hairy cell; 3-normo

Aplastic anemia tx

Aplastic anemia prognosis

Hemo anemias: intrinsic vs extrinsic

Reticulocytosis may reflect:

Hemo anemia lab findings

Distinguishing Etiology of Hemolysis

Due to spectrin pro in cytoskeleton

Triad: anemia, splenomegaly and jaundice

Pigment type gallstones; chronic leg ulcers

Hereditary spherocytosis findings

Hereditary spherocytosis tx

Acquired stem cell disorder making RBC membrane prone to lysis by complement

PNH findings

Episodic hemolytic anemia; Venous thrombosis; Deficient hematopoiesis -> pancytopenia ... indicate:

PNH labs

In PNH, increased risk of:

PNH tx

Episodic hemolytic anemia related to oxidative stress (hereditary)

G6PD def prevalence

Stress triggers of G6PD def

G6PD def findings

G6PD def tx

Autosomal recessive disorder in which abnormal Hgb leads to chronic hemolysis

In sickle cell dz, rate of sickling depends on:

Sickle cell prevalence

S/S = Pallor, jaundice, splenomegaly, leg ulcers, pigment gallstones, priapism

2 RBC conditions w/pigment gallstones

Sickle cell: vascular occlusion leading to infarction

Sickle cell labs

Sickle cell tx

SSA longterm issues

Acquired disorder which IgG autoantibody formed that binds to RBC membrane

AIHA: ___% are idiopathic; seen in ___

AIHA findings

AIHA tx

Acquired hemolytic anemia due to IgM autoantibody

Cold agglutinin dz causes

Cold agglutinin dz findings

Cold agglutinin dz tx

Defn neutropenia

Absolute Neutrophil count formula

Neutropenia findings

Neutropenia tx

Anemia: no hepatosplenomegaly

Anemia: No neuro S/S

Aplastic anemia S/S

Reticulocytosis

Neg Coombs

Pos Coombs

Heinz bodies

Low retic

Evans syndrome

Anagrelide may be used for:

Cytoreductive tx

Engorged retinal veins

Causes of vessel wall dz

Causes of thrombocytopenia (decrease in plt numbers)

Causes of decreased plt function

Examples of plt dz

ITP dx is...

ITP findings

ITP tx

2 types of HIT

HIT mechanism

HIT PMH

HIT labs

HIT tx

Dz = increase in ultra-high molecular weight multimers of von Willebrand Factor

TTP causes:

H&P for TTP

TTP labs

micro-angiopathic hemolytic anemia (MAHA)

TTP tx

HUS: mental status changes?

HUS findings

HUS tx

Extrinsic & intrinsic coag pathways converge to form:

PT measures:

PT is sensitive to (1) & normal range is (2)

aPTT measures:

aPTT normal range

Cause of prolonged PT:

Very rare causes of prolonged PT

Common pathway defs will prolong:

All clotting factors (x FVIII) made in:

fx of liver dz on coag

MOA: warfarin tx on high PT

Vitamin K is a necessary co-factor in the g-glutamyl carboxylation of:

MOA: vit K def on high PT

Situations in which vit K def is seen:

Causes of prolonged aPTT:

Deficiencies in HMWK, PK, and FXII are assoc w/which bleeding problems?

Clotting factor def assoc w/Jewish ancestry

FVIII def AKA = ? Prevalence = ?

FIX Deficiency AKA = ? Prevalence = ?

FVIII, FIX Deficiency: percentages assoc w/bleeding/severity

Hx includes hemarthrosis, bleeding into joints, and/or x-linked FH of probs

FVIII/FIX def findings

FVIII/FIX def tx

Prolonged aPTT; doesn't correct w/mixing study

FVIII Inhibitor

FVIII Inhibitor

Treatment to Eradicate FVIII Inhibitor:

von W Dz usu presents w/PT/aPTT = ?

Most common bleeding disorder, at a prevalence of ?

limited to mucocutaneous bleeding

Fns of vW factor

vW Dz lab data

vW Dz tx (for mild Forms):

vW Dz tx (for Severe Bleeding/Surgery):

Coagulation dz: causes elevated levels of prothrombin; leads to a modest increase in hypercoagulability, (2-fold)

Second most common inherited cause of hyper-coaguability

Prothrombin 20210A Mutation: concomitant risk factors

Fibrinolysis/Anti-coagulant Disorders usu present as:

Antithrombin activity is markedly stimulated by:

Antithrombin def is manifested by:

Protein C or Protein S Def: Predisposition to:

Uncommon causes of venous thromboses

Activated Protein C Resistance AKA:

Dz: mutation makes it resistant to inactivation by Activated Protein C

Most common hereditary hyper-coagulable state; mainly ltd to ?

Factor V Leiden: Heterozygous state increases risk of thrombosis up to:

Factor V Leiden: Homozygous state increases risk:

Auto-antibody that interferes with the natural anti-coagulant system

Anti-Phospholipid Syndrome presents with:

Recurrent arterial or venous thromboses; 2nd trimester miscarriages; Thrombocytopenia; Valvular heart dz; suggests ?

Anti-Phospholipid Syndrome: Lab Data:

Anti-Phospholipid Syndrome: tx

Condition in which circulating plasma (which contains the clotting factors), turns into serum

DIC: presentation

Acral ischemia

Hx pos for Heparin, Tacrolimus, Ticlopidine may point to:

Signs of hemorrhage in DIC

CBC for pt w/DIC

DIC labs:

DIC tx

DIC tx (if bleeding, or surg needed)

Defn Hemorrhage:

Defn Thrombosis:

Steps in forming the primary hemostatic plug:

Platelet Release involves:

thromboxane A2 is:

visible end product of coagulation =

fibrin is digested by

Normal BT is

Single best indication of functional platelet deficiency

BT prolonged when:

Adult ITP

Most common drug causing ITP

Dz’s causing ITP

TTP findings

Dx sim to TTP but w/o neuro S/S

AutoAb to ADAMTS13 seen in:

TTP tx:

HUS tx & prognosis

Trousseau’s syndrome

DIC labs

DIC tx

most common congenital disorder of hemostasis

von Willebrand’s FH

von W defect is in:

vWF is synthesized in:

Fn of vWF:

vWF is carrier protein for:

vWF labs

vW dz Rx

Glanzmann’s

Glanzmann’s tx

Liver = site of prodn of all clotting factors except:

Thrombopathies

Tx for liver dz/thrombocytopenia

Bernard-Soulier Syndrome

Platelet aggregation abnormal with ristocetin, which corrects with the addition of normal platelets, in:

Causes of acquired thrombopathy

Defn Thrombopathy (Qualitative)

Subacute DIC (Trousseau’s syndrome): will see:

___ pathway initiates coag process; then _____ pathway enhances _____ formation in clot

First factors to be affected in hepatic dysfunction

natural anticoagulants

causes of vit K def

Most common drug induced form of thrombocytopenia

HIT occurs when?

HIT involves:

Confirm HIT with:

Unlike PTT, PT tests for

PT monitors:

PT/PTT ref ranges

PTT monitors:

Heparin tx PTT range

Fibrinogen unique to:

Factor Xa to monitor:

Hereditary hypercoag states

Hemophilia A

Most common severe bleeding disorder

Hemophilia B

Lupus Anticoagulant

Most frequent cause of hereditary thrombophilia

Diff btw hep & LMWH

D-Dimer

Protein C def pts

Type I HIT:

Type II HIT:

ACT

Distinguish liver dz coagulopathy from vit K def

Deficiency allows unopposed conversion of fibrinogen to fibrin

Virchow's Triad

Pathophysiologic Basis for Myeloproliferative Disorders

True increase in RBC mass

Relative increase in RBC mass

Conditions causing secondary P. vera

P. vera: incidence/prevalence

P. vera S/S

Hallmark of P. vera =

P. vera H & H

Condition w/thrombosis; splenomegaly; Plethora; systolic hypertension; engorged retinal veins

P. vera lab data

P. vera mgmt

P. vera mgmt

P. vera prognosis

Causes of Reactive (Secondary) Thrombocytosis

Causes of Reactive (Secondary) Thrombocytosis

Thrombocytosis S/S

Thrombocytosis findings

Thrombocytosis Mgmt

Thrombocytosis Prognosis

Disorder in which bone marrow is replaced with scar tissue, leading to anemia

Myelofibrosis findings

Myelofibrosis peak incidence & survival

Cause of Myelofibrosis

JAK-2 mutations may be associated with:

Increased bone marrow production of megakaryocytes leads to increased peripheral platelet count

Myelofibrosis S/S

Myelofibrosis findings

Myelofibrosis mgmt

Acquired clonal disorders of the hematopoietic stem cell

______ cytopenias affect one or more cell lines (RBC, WBC, and/or PLTs)

Dz occurs when blood cells do not develop into mature cells, but rather stay in an immature stage within the BM

Some chromosomal abnormalities (5q – loss of part of the long arm of chromosome 5); “pre-leukemia”

MDS: risk factors include exposure to:

MDS pts

MDS Labs

MDS CBC

MDS: >20% blasts in BM indicates:

Blasts in BM <20%; Pelger-Huet cells (bi-lobed neutrophils) seen in:

MDS BM shows:

MDS Mgmt

MDS: Allogeneic BM txplt may cure ?? % of pts

Cornerstone for tx of MDS

MDS prognosis

Risk of transformation to leukemia depends on:

Etiology of multiple myeloma; assoc with:

Replacement of normal bone marrow by plasma cells leads to bone marrow failure

Lytic lesions predisposing patients to bone pain, pathologic fractures, and hypercalcemia

Multiple myeloma S/S

Multiple myeloma findings

Multiple myeloma classic triad:

Important to differentiate btw multiple myeloma and:

Multiple myeloma evaluation

Part of eval for multiple myeloma (if elevated = very poor outcome)

Thalidomide may be part of tx for:

Multiple myeloma mgmt

Multiple myeloma Prognosis:

MGUS prevalence

What MGUS looks like

Malignancy of B lymphocytes

Waldenström’s Macroglobulinemia causes overproduction of:

Median age of onset is 64 yrs

Waldenström’s S/S

Fatigue, cold hypersensitivity, peripheral neuropathy, engorged retinal veins may indicate:

Hallmark of Waldenstrom:

Waldenström’s Macroglobulinemia Findings

Waldenström’s is differentiated from MGUS by:

Waldenström’s Macroglobulinemia mgmt

Most commonly occurring leukemia

CLL Mgmt

CLL prevalence

Characterized by clonal proliferation and accumulation of mature-appearing B lymphocytes (95 % of cases) in blood and lymphoid tissue; clonal malignancy of B lymphs

CLL S/S

CLL findings

RAI Staging System used for:

CLL growth

Lymphocytosis, WBCs >20,000/µL = hallmark of:

RAI Stage 0

RAI Stage 1

RAI Stage 2

RAI Stage 3

RAI Stage 4

Blast crisis

CML will likely transform to:

Primarily disease of children

?? % of ALL pts are children (usually 3 -7 yo)

Accounts for 10-20% of acute adult leukemia

CML mgmt

3 phases of CML (defined by # blasts in marrow)

Slowly progressing dz: too many WBCs made in BM (esp myeloid cells)

CML prevalence

Philadelphia chromosome present in ??% of CML cases

_____ can trigger Philadelphia chromosome

CML S/S

CML findings

CML tx goal:

Type of leukemia = immature, abnormal cells in BM (>20%) and blood (>10%) & in liver, spleen, lymph nodes

ALL prognosis

ALL & AML S/S

ALL & AML labs

AML: median age at onset:

AML: 5 year survival:

Hyperleukocytosis

ALL mgmt

Chemo phases for ALL

AML Etiology

AML findings

AML mgmt

Hairy Cell leukemia prevalence

Hairy Cell leukemia presentation

Hairy Cell leukemia tx

Dz’s tx’d w/tumor lysis

Hallmark of Hairy Cell leukemia

Hodgkin Dz

Non-Hodgkin Dz

Group of cancers w/enlarged lymphoid tissue, spleen, liver, & Reed-Sternberg cells

Hodgkin Dz prevalence

_____ found in 40 – 50% of Hodgkin dz cases

Reed-Sternberg cells

Hodgkin Dz mechm of spread in pt

Hodgkin Dz S/S

Hodgkin Dz findings

Hodgkin Dz diagnostics

Hodgkin Dz Stage I:

Hodgkin Dz Stage II:

Hodgkin Dz Stage III:

Hodgkin Dz Stage IV:

Hodgkin Dz mgmt: Stage I and IIa:

Hodgkin Dz mgmt: Stage IIb:

Hodgkin Dz mgmt: Stage III:

Hodgkin Dz mgmt: Stage IV:

Hodgkin Dz: Five year survival rate:

Hodgkin Dz: if relapse:

Hodgkin Dz mgmt

5th most common malignancy in US

NHL prevalence

Dz: arise from cells in Lymphoid tissue (90% of cases are derived from B-lympocytes)

3 Grades of NHL

NHL S/S

NHL findings

NHL staging

NHL mgmt

NHL tx depends on:

Role of surgery in NHL

Mgmt of Low Grade NHL

Mgmt of Intermediate Grade NHL

Mgmt of High Grade Lymphoma ((Large B-Cell Lymphoma)

Lymphoblastic lymphomas are treated with:

Oncologic emergencies

Can affect T or B lymphocytes

Type of HL that accounts for 80% of HL cases

Bulky lymphadenopathy seen in:

Only curative tx for MDS

Smudge cells

Serum viscosity 1.4-1.8 xH2O visc

Next-door dz

Pancytopenia

Giant plts & teardrop poik

Drenching night sweats

B-symptoms

Lymphadenopathy (in 80%)

Skin infxn/shingles

RAI staging is for

Lytic lesions

Smudge cells

Serum viscosity 1.4-1.8 xH2O visc

Next-door dz

Pancytopenia

Giant plts & teardrop poik

Drenching night sweats

B-symptoms

Lymphadenopathy (in 80%)

Skin infxn/shingles

RAI staging is for

Lytic lesions

Auer rods

Dohle bodies

Toxic gran

Hyperseg

Vacuoles

BM aspirate

LAP

Meningitis

Fried egg

Hypercellular bone marrow with reticulin or collagen fibrosis

Preleukemia

Immunoproliferative dz

Plts in leukemias

Immunologic phenotypes = Common; Early B lineage; T cell

M0-M7 phenotypes

Coexpression of CD19, CD5

Hypogammaglobulinemia

Anemia seen in leukemias

Isolated lymphocytosis

Lymphocyte pleomorphism; heterophile Ab

Clustered bacteria in vacuoles in WBCs; low plts; leukopenia w/left shift; Rising Ab immunofluorescence titer

Histoplasmosis CBC

Engorged retinal veins

Normocytic

Normochromic

RDW

Anisocytosis

Poikilocytosis

Hematopoiesis

Erythropoiesis

Granulopoiesis

Erythropoietin

Blood Indices

MCV

MCH

MCHC

Blood

Capillaries