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Hematology Flashcards

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USMLE® Step 1 flashcards
1
Q

Burkitt Lymphoma

genetic abnormality

main features - endemic form vs. non

biopsy

A

t(8;14) puts c-myc with Ig promoter

jaw tumor + LAP in Africans due to EBV

(non-endemic can be abdominal tumor w/ rapid doubling + spontaneous tumor lysis)

biopsy shows “starry sky” of macrophages + apoptotic bodies among many lymphocytes; malig B-lymphos have vacuolated cytoplasm

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2
Q

Follicular Lymphoma

translocation
biopsy
presentation

A

t(14;18) puts Ig promoter with BCL-2

composed of small-cleaved “centrocytes” with larger uncleaved “centroblasts”; low mag biopsy is highly packed B-cell follicles without normal nodal architecture

pts are middle-age with painless, fluctuating LAP or abd. pain with abdominal masses

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3
Q

Eosinophilic (M4Eo subtype) AML

A

inv(16)

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4
Q

CML

translocation
special histo

chronic stable presentation

A

t(9;22) BCR-ABL fusion protein

NO AUER RODS bc cells are more mature!
many different precursor cell types (not just blasts)

present with non-specific symptoms in chronic stable phase

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5
Q

APML

translocation?
presentation (2)?
tx?

A

t(15;17) puts RARA with PML; see Auer rods in promyelocytes

presents with DIC +/- fever via low WBCs

tx with ATRA (induces PML/RARA degradation + stimulates maturation)

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6
Q

mantle cell lymphoma

translocation

A

t(11;14) puts cyclin D1 near Ig heavy chain; cyclin D1 promotes G1 to S transition

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7
Q

Diffuse Large B-cell lymphoma

epidemiology
presentation

A

1 NHL

rapid growing nodal (neck, abd, mediastinum) or extranodal symptomatic mass; commonly in tonsils or GI tract

systemic B symptoms common

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8
Q

Acute Lymphoblastic Leukemia

epidemiology
5 s/s

A

1 kid leukemia; composed of pre-B (CD19/10) or pre-Ts (CD1/2/5)

LAP, HSmegaly, fever, bleeding + bone pain

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9
Q

Hairy Cell Leukemia

in whom? 2 s/s and one absent sx

histo + special staining positivity

A

splenomegaly + pancytopenia in older men; no LAP!

hairy cells and TRAP+

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10
Q

Mycosis fungoides

cell type? histo feature?

derma description?

A

cutaneous T-cell lymphoma

CD4+ cells infiltrate dermis/epidermis > Pautrier microabscesses

plaques on trunk/butt look like eczema/psoriasis; may see generalized erythema / erythroderma

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11
Q

LAP score

what is it? what does it indicate? other ways (1 main, 3 minor) to differentiate the 2 conditions LAP score differentiates

A

Leukocyte Alkaline Phosphatase

normal or increased in LEUKEMOID REACTION

decreased in CML

Dohle bodies - basophilic PERIPHERAL granules in neutrophils of leukemoid reaction (rER ribosomes), or pt with burns or myelodysplasia

Other signs of leukemoid reaction:

Increased bands (left shift)
Toxic granulation - cytoplasmic granules in neutros
Cytoplasmic vacuoles

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12
Q

Leukemoid Reaction

what is it? differential?

A

benign leukocytosis (>50,000) due to severe infection, hemorrhage, solid tumor or acute hemolysis

marrow is hypercellular to normal; see INCREASED BANDS and early mature neutrophil precursors (myelocytes, etc.)

high LAP score
Dohle bodies - peripheral basophilic rER in neutros
Cytoplasmic vacuoles - in neutros
Toxic granulation - in neutros

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13
Q

Hereditary Spherocytosis

inheritance + mutations?

smear?

manifestations (3)?

A

AD mutation of spectrin/ankyrin

some (not all… unless homozygous I guess) RBCs ~2/3 diameter of normal and lack central pallor

hemolytic anemia, jaundice and splenomegaly

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14
Q

Hereditary Spherocytosis

Labs? (3)
Complications + associations? (2)
Tx?

A

Labs - high MCHC, negative coombs, increased osmotic fragility

Complications - pigmented gallstones, aplastic crises via parvovirus B19

tx is splenectomy

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15
Q

Inherited Hypercoagulability

2 MCCs

A

Leiden Factor V - #1 MCC, Va is protein C resistant (no change to aPTT on addition of activated protein C)

Prothrombin mutations

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16
Q

Autoimmune Hypercoagulability

MCC

main serum finding + 3 clinical findings

2 labs

A

antiphospholipid antibody syndrome

lupus anticoagulant / anticardiolipin Abs plus 1+ of following:
venous thromboembolism
arterial thromboembolism
FREQUENT FETAL LOSS

prolonged aPTT + thrombocytopenia

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17
Q

Lead Poisoning

epidem?
s/s? (6 general, 1 special)
smear?
biochem? 2 enzymes

A

kids eat paint chips; adults are miners/industrial workers (eg, battery manufacturing) who inhale lead

adults - weakness, abd. pain + constipation

if severe - HA, cognitive sx, peripheral neuropathy

signs - blue “LEAD LINES” at gingivodental junction

smear - basophilic stippling (rRNA) with hypochromic microcytic anemia

d-ALA dehydratase and ferrochelatase inhibition > poor iron incorporation into heme > low Hb

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18
Q

Polycythemia Vera

mutation + result?

labs? (3)

complications, s/s? (1 GI, 1 MSK, 1 vascular, 1 abdominal, 2 derma)

A

JAK2 mutation (V617F; Val > Phe)

makes stem cells more sensitive to growth factors (EPO, TPO)

labs - increased RBC mass, plasma volume, low EPO (may have high platelets, WBCs)

may have:

thrombosis (viscous blood)
peptic ulcers + pruritus (basophils > histamine)
gout (high turnover)

red (“ruddy”) face
splenomegaly

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19
Q

Main signs for multiple myeloma (4)

others? (3)

A 
elderly patient with...
osteolytic lesions
hypercalcemia
anemia
acute kidney injury
(CRAB = calcium, renal, anemia, bone)

also…
constipation (via high Ca)
fatigue
recurrent infections

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20
Q

What is “myeloma kidney”?

pathogenesis?

labs? (3)

A

light chain cast nephropathy - intact Igs can’t pass glomerulus, but light chains (kappa + lambda) can > combine with Tamm-Horsfall proteins to form obstructive casts > tubular rupture

DIPSTICK negative for protein (for albumin only)
spot / 24-hr TURBIDIMETRY positive for protein
urine ELECTROPHORESIS shows light chains

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21
Q

Sometimes dipstick is positive for protein in myeloma patient. Why?

A

Monoclonal Immunoglobulin Deposition Disease

intact Ig or heavy/light chains deposit in glomerulus and cause NEPHROTIC SYNDROME; then albumin and intact Igs will be found in urine

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22
Q

AML

cell type + features (2)?

epidem?

WHO crit?

A

myeloblast cells; large nucleus, little cytoplasm, AUER RODS with PEROXIDASE positivity

mostly >65 pts with signs of pancytopenia

WHO - at least 20% blasts in marrow (peripheral WBCs median 15,000 at dx)

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23
Q

large CD19 and CD10+ cells in periphery in kid

dx?

A

precursor B-ALL

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24
Q

large CD1, CD2, and CD5+ cells in periphery in kid

dx?

A

precursor T-ALL

variable CD1a expression
CDs 2, 3, 4, 5, 7 and 8 are expressed (T cell markers)

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25
Q

Mature B Cell Leukemia

other names?
cells?
CDs?

A

chronic lymphocytic leukemia -or- small lymphocytic leukemia

small, round, monomorphic B cells in blood, marrow + nodes

CD19 and CD5 (a T cell marker!)

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26
Q

Primary Myelofibrosis

primary pathogenesis?
result?

A

clonal MEGAKARYOCYTES secrete TGF-BETA > stimulates fibroblasts in marrow to produce collagen > marrow fibrosis

HSCs migrate to liver + spleen > EXTRAMEDULLARY HEMATOPOIESIS

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27
Q

Primary Myelofibrosis

manifestations (5)?

think systemic, GI, hematologic and biopsy

A
  1. severe fatigue
  2. hepatomegaly with MASSIVE SPLENOMEGALY (can compress stomach and cause GI sx)
  3. at least 1 CYTOPENIA
  4. “Teardrop cells” aka dacrocytes (rbc damage in spleen or fibrotic marrow)
  5. DRY TAP on marrow aspiration; must biopsy marrow
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28
Q

Primary Myelofibrosis

risks?
histo?

A

risks - chemical exposure (toluene, benzene)

histo - hypocellular marrow and significant fibrosis with atypical megakaryocytes (biopsy only… tap usually dry)

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29
Q

Smear findings in beta thalassemia

2 main things; 5 extra

A
  1. hypochromic microcytic anemia (MCV <80)
  2. increased central pallor

“anisopoikilocytosis” varied shape and size

target cells, teardrop cells, nucleated precursors

basophilic stippling

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30
Q

what happens with alpha chains in beta thalassemia?

consequences (2)?

A

unpaired alpha chains precipitate in RBCs

damage membrane > precursor death > ineffective erythropoiesis

lysis of circulating cells > extravascular hemolysis

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31
Q

Pathogenesis of bone lesions in MM

A

IL-1 (activates osteoclasts) and IL-6 from neoplastic cells leads to resorption and OSTEOPENIA

(pain, fractures and “punched out” lesions on xray

hypercalcemia > fatigue, confusion, constipation)

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32
Q

Hyperimmunoglobulinemia in MM

causes what in blood (2)?
labs (2)?

A

rouleaux on peripheral smear
increased ESR

M protein in serum
M spike on electrophoresis

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33
Q

accumulation of light chains throughout body in MM

name?
microscopy?
organs affected (4)?

A

AL amyloidosis

eosinophilic extracellular deposits on light micro
CONGO stain > “apple green” birefringence

mainly KIDNEY, also heart, tongue and nervous system

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34
Q

Reed-Sternberg cells are derived from what?

A

germinal center B cells

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35
Q

Thrombotic Thrombocytopenic Purpura

pathophys

A

low ADAMTS13 (either acquired auto-Ab or hereditary)

uncleaved vWF > platelet trapping > microvascular thrombosis and microangiopathic hemolytic anemia

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36
Q

Thrombotic Thrombocytopenic Purpura

clinical features

A

microangiopathic HEMOLYSIS with SCHISTOCYTES
THROMBOCYTOPENIA with normal PT/aPTT

sometimes:
renal failure
neurologic sx (ex: lacunar infarct with focal pure sensory loss)
FEVER

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37
Q

TTP

treatment (3)

A

plasma exchange
steroids
rituximab

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38
Q

Idiopathic Aplastic Anemia

2 general pathomechanisms

3 classes of causes with examples

A

either direct TOXIC insult or T-CELL RESPONSE against precursors

  1. Toxins - gasoline, tobacco smoke
  2. Drugs - CHEMo, CARbamazepine
  3. Viruses - hepatitis, EBV

(gas goes in CARS; tobacco smoke contains CHEMicals)

39
Q

Inherited cause of aplastic anemia?

musculoskeletal changes? (2)
increases risk of? (2)

A

Fanconi anemia

short stature + no thumbs

risk of malignancy (MDS and AML)

40
Q

Sideroblastic Anemia

MCCs

(5 things w/ examples)

A 
alcohol abuse
copper or B6 deficiency 
meds - isoniazid, chloramphenicol, linezolid
myelodysplastic syndrome
X-linked form - d-ALA synthase defic.
41
Q

mechanism of isoniazid or B6 defic. sideroblastic anemia

A

INH inhibits PYRIDOXINE PHOSPHOKINASE, normally converts pyridoxine to to pyr-5-phosphate

pyr-5-P is a d-ALA SYNTHASE cofactor in heme synth

42
Q

sideroblastic anemia

peripheral smear (2)
stain
A
  • microcytic hypochromic anemia
  • ringed sideroblasts - iron granules accumulate around nucleus

Prussian blue stain

43
Q

reticulocyte appearance on peripheral smear

A

slightly larger and BLUER with WRIGHT-GIEMSA than RBC

blue due to retention of RIBOSOMAL RNA in a reticular network in the cytoplasm

44
Q

Howell Jolly bodies

what are they?

A

DNA remnants in reticulocytes

seen in splenectomy or low spleen function (normally removed by spleen)

45
Q

What are Pappenheimer bodies?

A

ferritin aggregates in RBCs / reticulocytes

seen in sideroblastic anemia

46
Q

Hematological signs of CML

general and more specific, 4 points overall

A
  • elevated WBCs with increased precursor forms
  • decreased LAP score
  • “myelocytic bulge” - predominance of myelocytes as opposed to more mature metamyelocytes
  • absolute BASOPHILIA and/or EOSINOPHILIA
47
Q

Pure Red Cell Aplasia

what causes it? 
2 causes (1 has 2 disease examples)

what 2 tests can help determine cause

A

inhibition of erythrocytic precursors by IgG AUTOANTIBODIES or CYTOTOXIC T CELLS

  1. immune dysfunction - THYMOMA (IgG auto-Abs; thymoma removal sometimes cures aplasia) and LYMPHOCYTIC LEUKEMIA (self-reactive CD8+)
  2. PARVO B19 can also cause it

all prca patients should have CHEST CT for thymoma and ANTI-B19 IgM serum test

48
Q

Hodgkin lymphoma

epidemiology (2 groups)?
main presenting sx?

A

BIMODAL AGE dist (peak in 20s and 60s)

  • NONTENDER lymphadenopathy (or incidental LAP on routine chest cxr)
  • B symptoms - fever, night sweat, weight loss
49
Q

Hodgkin lymphoma

dx (smear? cbc? definitive?)

A

peripheral smear + cbc usually normal

NODE BIOPSY is definitive dx - REED-STERNBERG CELLS with lymphos, histiocytes and eosinophils

50
Q

Differential: vW disease vs. hemophilia vs. ITP

A

vWD - skin + mucosa bleeding (epistaxis, heavy period, gingival, GI) since childhood; labs show only increased bleeding time + aPTT (factor VIII)

hemophilia - DEEPER bleeding into joints/muscles, GI + urinary tract; labs show high aPTT (intrinsic path)

ITP - EPISODIC bleeding that is MUCOCUTANEOUS with purpura, petechia + epistaxis; labs show low PLTs and high bleeding time

51
Q

Hemophilia A or B

lab characteristics?

A

prolonged aPTT only

(normal PT, BT and PLTs)

deficiency factor VIII or IX (intrinsic path)

52
Q

vW disease

lab characteristics?

A

prolonged aPTT and bleeding time

(normal PT and PLTs; aPTT can be normal)

aggregation studies can be normal

platelet can’t bind collagen properly due to impaired bridging via vWF (Gp1b), plus vWF doesnt protect factor VIII

53
Q

DIC

lab characteristics

A

prolonged BT, PT, aPTT and low PLTs

consumptive coagulopathy uses up all factors + platelets

54
Q

How does chronic kidney disease affect hemostasis?

labs?

A

Uremia-induced platelet dysfunction (toxins impair platelet agg + adhesion)

Prolonged BT

normal PT, aPTT and PLTs

55
Q

Heparin use

lab characteristics

A

prolonged aPTT only (low plts only if HIT)

normal PT, BT, and PLTs

only affects thrombin and factor X

56
Q

Warfarin use

lab characteristics

A

prolonged PT, minimal prolongation of aPTT

normal BT and PLTs

affects factors II, VII, IX and X

57
Q

Factor XIII deficiency

factor XIII function? s/s? labs?

A

a rare AR disease with DELAYED, recurrent bleeds after trauma, surgery

factor XIII is a transglutaminase that cross-links fibrin polymers to stabilize them; it’s a later process in clot stabilization so effects are delayed

normal bleeding time, PT and aPTT

58
Q

What are dysfibrinogenemias?

labs?

A

inherited abnormalities in fibrinogen

can cause excessive bleeding -OR- thrombophilia

alter THROMBIN TIME (TT), as well as PT and aPTT

bleeding time is normal

59
Q

Idiopathic Thrombocytopenic Purpura:

pathophys, labs, s/s

A

GpIIb/IIIa auto-Ab

thrombocytopenia (only peripheral smear abnormality); NO fever; PT, aPTT normal

spontaneous bleeding uncommon (unless PLT <10,000)

60
Q

Thrombotic Thrombocytopenic Purpura:

pathophys, labs, s/s

A

ADAMTS12 auto-Ab causes activation of platelets by long vWF polymers

don’t bleed usually; fibrinogen, PT and aPTT normal

61
Q

TTP-HUS

pentad

A
  1. fever
  2. neurological sx - progressive lethargy
  3. renal failure
  4. anemia
  5. thrombocytopenia

in setting of antecedent GI illness

62
Q

Beta Thalassemia Minor

what kind of anemia? what kind of cells on smear? what kind of hemoglobin is high?

A

microcytic hypochromic

increased HbA2 (alpha2delta2) and sometimes high HbF

poikilocytes including SPHEROCYTES and TARGET CELLS

but pt is ASYMPTOMATIC bc this is “minor” variant

63
Q

Beta Thalassemia

generally what do the mutations affect?

A

mutations affecting transcription, processing and translation of mRNA for beta-globin

usually aberrant splicing or premature chain termination during translation

sometimes pt mutation prevent RNA polymerase from binding promoter

64
Q

How does beta thalassemia result in hemolysis?

A

insoluble ALPHA CHAIN TETRAMERS precipitate in RBCs and cause membrane instability

65
Q

Most common cause of extramedullary hematopoiesis?

A

severe chronic hemolytic anemia

as in beta thalassemia, etc.

66
Q

what non-hematological complication is common in patients with extramedullary hematopoiesis?

A

Skeletal abnormalities (expanding mass of progenitor cells in marrow thins cortex + impairs growth)

  • Pathologic fractures
  • Maxillary overgrowth
  • Frontal bossing
67
Q

JAK2

what is it and what does it do?

mutations cause what? (3)

A

a CYTOPLASMIC (non-receptor) TYR KINASE

activates the STAT pathway (“signal transducers and activators of transcription”)

Polycythemia vera
Essential thrombocytosis
Primary myelofibrosis

68
Q

JAK2 inhibitor for tx of primary myelofibrosis

A

ruxolitinib

69
Q

Peripheral smear finding in CHRONIC LYMPHOCYTIC LEUKEMIA

A

smudge cells

70
Q

Daily prophylaxis with WHAT ANTIBIOTIC can prevent INFECTION WITH WHAT in a sickle cell pt?

A

penicillin prevents Strep pneumo (and other gram+, but encapsulated are most important in sickle cell)

71
Q

Causes of sideroblastic anemia

1 genetic (enzyme?)
1 acquired
6 reversible

A

X-linked ALA synthase defect

Myelodysplastic Syndrome

  1. Alcohol - MCC
  2. B6 defic. (pyridoxine)
  3. Pb poisoning
  4. Chloramphenicol
  5. Isoniazid
  6. Cu deficiency
72
Q

Tx of sideroblastic anemia

A

B6

cofactor for ALA synthase

73
Q

Skeletal / x-ray findings in BETA THALASSEMIA MAJOR

Other finding related to hematopoietic issues?

A
  1. “crew cut” on skull xray due to MARROW EXPANSION
  2. chipmunk facies

extramed. hpoiesis > HSM

74
Q

When does BETA THALASSEMIA MAJOR present and why?

A

after abt 6 months of life, because HbF (alpha2gamma2) is high until then, then is replaced by HbA2 (alpha2delta2)

75
Q

Alpha Thalassemia

genetics?

certain kind of genetic change specific to one population + certain kind specific to another

A

α-globin DELETIONS lead to decreased α-globin synth

the CIS deletions (on same chromosome) occur in ASIANS

the TRANS deletions (on diff. chroms.) occur in AFRICANS

76
Q

What is the disease and number of globin genes deleted in an asymptomatic carrier for alpha thalassemia?

A

α-thalassemia “minima”

no anemia, just a silent carrier

(αα / α–) only one α-globin gene deleted

77
Q

What is the deletion situation in a person with alpha thalassemia minor? And clinical sx?

A

either TRANS (α–/α–) or CIS (αα/– –)

mild microcytic hypochromic
cis deletion can be worse for offspring

78
Q

What is Hemoglobin H disease?

genetics? clinical situation?

A

(– –/α –) 3 α globin genes deleted

excess beta-globin forms beta4 Hb called Hb H

moderate to severe microcytic hypochromic

79
Q

What is Hemoglobin Barts disease?

genetics? clinical situation?

A

(– –/– –) ALL four globin genes deleted

excess gamma-globin forms gamma4 Hb

HYDROPS FETALIS, incompat with life

80
Q

what is the treatment for beta thalassemia major?

what can this cause?

A

frequent transfusions

can cause secondary hemochromatosis

81
Q

General difference in bleeding tendencies in…

coagulopathy vs. platelet defects

A

coagulopathy - DEEP TISSUE bleeding (joints, muscle, subcutis)

platelet - MUCOCUTANEOUS bleeding (epistaxis, petechiae)

82
Q

Transfusion of PACKED RBCs

tx what 2 conditions?

raise what 2 parameters?

A

tx acute blood loss and severe anemia

raise Hb and O2 carrying capacity

83
Q

In platelet transfusion…

how much does each “unit” of plts raise PLT levels approximately?

A

~ 5000/mm3/unit

84
Q

3 conditions in which FFP or prothrombin complex concentrate is used

A
  1. DIC
  2. Cirrhosis
  3. immediate anticoagulation reversal (ie rat poison or warfarin OD)
85
Q

Difference between

FFP
vs.
Prothrombin complex concentrate

A

FFP - all coag factors and plasma proteins

PCC - factors II, VII, IX and X plus proteins C/S

86
Q

What does CRYOPRECIPITATE contain and what does it treat?

A

fibrinogen (factor I)
factor VIII
factor XIII
vWF

tx deficiencies of fibrinogen and factor VIII (incl. vW disease)

87
Q

What are the 5 risks of blood transfusion?

think of what blood contains, what blood product containers contain, and blood aging for hints to 3

A
  1. Infection (low risk)
  2. Transfusion reactions (low with proper type)
  3. Secondary hemochromatosis via Fe overload
  4. HYPOCALCEMIA - via citrate chelation
  5. HYPERKALEMIA - via rbc lysis in old blood
88
Q

Mutations in CHRONIC MYELOMONOCYTIC LEUKEMIA

note: myeloMONOCYTIC not just myelogenous

A

PDGF-R mutations

89
Q

Anemia in chronic liver disease

Type?
Peripheral smear?
Severity?

A

usually NORMO- or slightly MACROCYTIC and MILD (Hb of 10-11 g/dL)

TARGET cells in spear

(microcytic only in <25% of chronic liver disease anemias)

90
Q

If a patient has microcytic hypochromic anemia, but no uterine bleeding, dark stools or visible stool blood…

what is the most likely cause of anemia?

A

still IDA despite the lack of noticed blood

still need to do an occult blood test, check ferritin, maybe colonoscopy (especially if older)

(key here is that the lack of blood seen does NOT rule out some GI blood loss somewhere)

91
Q

Polycythemia vera

dx and tx

A
  • low EPO and cytogenetics (JAK2 mut.)

- phlebotomy (target Hct <45%)

92
Q

2 tumors OTHER THAN RENAL that can secrete EPO?

A

cerebellar hemangioblastoma

uterine fibroids (leiomyoma)

93
Q

Difference in peripheral smear of someone with generally increased serum proteins vs. specifically COLD AGGLUTININS?

A

general serum protein increase > ROULEAUX (stacked RBCs)

cold agglutinins > CLUMPED rbcs

94
Q

Diff btwn multiple myeloma and Waldenstrom macroglobulinemia

A

MM - either IgG or IgA increased; plus CRAB sx

Waldenstrom - IgM is increased causing a HYPERVISCOSITY syndrome (blurred vision, Raynaud)

(remember… MM already has Ms… Waldenstrom needs Ms)

*USMLE* (28 decks)

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