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HemeOnc Flashcards

1
Q

CD14

A

Macrophage

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2
Q

Histaminase and arylsulfatase

A

Eosinophils

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3
Q

Hypersegmented neutrophil

A

B12/folate deficient

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4
Q

Heparin and histamine

A

Basophils, Mast cells

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5
Q

vWF receptor

Fibrinogen receptor

A

vWF: Gp1b

Fibrinogen: gpIIb/gpIIIa

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6
Q

CD34

A

Bone marrow stem cell

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7
Q

CD19/CD20

A

B cell

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8
Q

CD3/CD4

A

TH1/TH2

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9
Q

CD3/CD8

A

Cytotoxic t cell

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10
Q

Hemophilia A vs Hemophilia B

A

A- Factor VIII def

B - Factor IX def

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11
Q

Factors that vitamin K deficiency affects

A

II, VII, IX, X, protein C, protein S

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12
Q

Epoxide reductase

A

Reduces Vitamin K so it is active

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13
Q

Factors antithrombin inhibits

A

II, VII, IX, X, XI, XII

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14
Q

gpIb deficiency affects?

gpIIb/gpIIIa defiency affects?

A

gpIb - affects adhesion

gpIIb/gpIIIa - affects aggregation

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15
Q

Clopidogrel/Ticlopidine affect?

A

gpIIb/gpIIIa -> Decreased aggregation

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16
Q

Abciximab affects

A

gpIIb/gpIIIa

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17
Q

What affect do polycythemia and CHF have on ESR?

A

Decrease ESR

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18
Q

G6PD deficiency leads to what microsopic changes?

A

Heinz bodies, Bite cells

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19
Q

Asplenia leads to what microscopic change?

A

Howell Jolly bodies

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20
Q

What is the cause of hemolytic uremic syndrome?

A

E. coli O157:H57 from beef

Toxin damages endothelial cells -> leads to Hemolytic Uremic syndrome

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21
Q

Abnormal ristocetin test

And therapy

A

Looks at vWF disease

Therapy: Desmopressin will increase vWF release from Weibel Palade bodies in endothelial cells

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22
Q

What enzyme activates vitamin K? What acts on this enzyme to inhibit?

A

Vitamin K - Activated by epoxide reductase

K then gamma carboxylates to activate II, VII, IX, X, C, S

Inhibited epoxide reductase by warfarin

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23
Q

What do endothelial cells produce to decrease thrombosis?

A

PGI2

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24
Q

Function of thrombin

A

Converts fibrinogen to fibrin

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25
Q

What does DIC affect?

A

Activates the coagulation cascade

26
Q

What is the function of tPa?

A

Activates plasminogen to plasmin which breaks down fibrin clots and decreases clotting factors

27
Q

How can fibrinolysis disorder be distinguished from DIC?

A

DIC - low platelet count, and increased D Dimers

Fibrinolysis disorder -> Increased plasmin which affects fibrin and clotting factors but no change in platelets and no elevation of D dimers

28
Q

How do endothelial cells prevent thrombosis?

A

Release tPa, which activates plasmin to cleave fibrin and clotting factors

Prostacyclin (PGI2), and NO release

heparin like molecules to increase antithrombin III

29
Q

What effect does homocysteine have?

What can cause an elevation in this?

A

endothelial damage is caused by elevated homocysteine

Caused by decreased B12/folate levels -> Decreased homocysteine to methionine

Or caused by decreased homocysteine to cystathionine

30
Q

What hb levels define anemia in males and females?

A

Males < 13.5

Females < 12.5

31
Q

Esophageal web, glossitis, beefy red tongue, iron def anemia

A

plummer vinson syndrome

32
Q

People with thalassemia are protected against what?

A

Plasmodium falciparum malaria

33
Q

What are the types of alpha thalassemia?

A

1 mutation - asymptomatic

2 mutations - cis: asian -> can pass to offspring
trans: african

Three genes: HbH formation

Four genes: Hydrops fetalis and Hb Barts

34
Q

What are the forms of B thalassemia to know?

A

Chromosome 11 (alpha thal is 16)

B/B+: relatively minor, target cells seen and HbA2 increases (alpha2/delta2)

B0/B0 -> increased HbF increased HbA2

Crewcut appearance, extramedullary hematopoiesis

inc. risk of parvovirus B19

35
Q

What population has increased risk of parvovirus B19 aplastic crisis?

A

B thalassemia major

36
Q

B12 or folate deficiency leads to a buildup of what substance that damages endothelial cells leading to coagulation?

A

Homocysteine

37
Q

Where is folate absorbed in the body?

A

Jejunum

38
Q

Where and how is B12 absorbed?

A

Terminal ileum via intrinsic factor formed by gastric parietal cells

39
Q

What lab finding is specific to Folate deficiency?

A

Normal methylmalonic acid

40
Q

What step is impaired in B12 deficiency?

What are the clinical findings?

A

B12 deficiency: Excess methylmalonic acid

Dec. conversion of methylmalonic acid to succinyl coA

CLinical findings: Spinal cord degeneration -> afects posterior column and lateral corticospinal tract

41
Q

What is the first step that should be done in assessing a normocytic anemia?

A

Take the reticulocyte count and multiply by the hematocrit/45

> 3% is good

<3% means there is a problem making blood cells

42
Q

How can extravascular vs intravascular normocytic anemias be distinguished?

A

Extravascular - Jaundice due to increased unconjugated bilirubin via protoporphyrin breakdown from Hb via splenic macrophages

Intravascular normocytic anemia - Hemosidenuria due to increased hemoglobin breakdown and iron absorption in the renal tubules, and decreased haptoglobin which binds the hemoglobin in the blood from RBC breakdown

43
Q

What causes spherocytosis?

A

Defect of cytoskeletal proteins

44
Q

Osmotic fragility test

A

Hereditary spherocytosis

45
Q

What biochemical substitution is found in sickle cell anemia?

A

Replace glutamic acid with valine

46
Q

When is dactylytis seen?

What about acute chest syndrome with vasoocclusion in pulmonary microcirculation?

A

Dactylytis - Children with sickle cell anemia

Acute chest syndrome - Adults with sickle cell (similar to CHF)

47
Q

What is the major complication of sickle cell TRAIT?

A

Eventual inability to concentrate urine as sickling occurs in renal medulla

48
Q

What is the biochemical change in hemoglobin C?

A

Replacement with lysine (lyCine) and HbC crystals

49
Q

What marker distinguishes immature left shift leukocytes?

A

Decreased CD16 Fc receptor

50
Q

What cell line is increased in CML?

A

t(9:21)

Basophils

51
Q

What kind of cells undergo hyperplasia in infectious mononucleosis?

Where are they located?

A

T cells

Paracortex

White pulp of spleen -> Periarterial lymphatic sheath

52
Q

What initial screening test is done to check for EBV mononucleosis?

What if it is negative?

What secondary test is performed to confirm?

A

Monospot test

Negative -> CMV

Secondary test -> EBV viral capsid test

53
Q

What do ALL cells have positive nuclear staining for?

A

Tdt -> DNA polymerase

B cells - CD 10/19/20

T cells - CD2 to CD8!!! not CD10!!

54
Q

What group is most at risk for ALL?

A

Down syndrome children AFTER the age of 5 years

55
Q

What translocation is a marker for good prognosis in ALL? What is poor?

A

Good - t(12:21)

Poor - t(9:22)

56
Q

What is seen in AML in terms of cytoplasmic staining?

A

Auer rods

MPO (myeloperoxidase)

57
Q

What is the translocation in Acute Promyelocytic Leukemia?

A

t(15:17)

retinoic acid

58
Q

Down syndrome before age 5

A

acute megakaryoblastic leukemia

59
Q

CD 5 CD 20 and smudge cells

A

CLL

60
Q

TRAP with dry tap bone marrow w/ accumulation in red pulp of spleen

Treatment?

A

Hairy cell leukemia

2-CDA -> adenosine deaminase inhibitor

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