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Step 3 > HEMATOLOGY > Flashcards

HEMATOLOGY Flashcards

1
Q

Anemia

  1. MCV
  2. MCHC
A
  1. micro-, normo-, macrocytic

2. indication of Hb synthesis; hyper-, hypo, normochromic

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2
Q

Macrocytic Anemia

  1. B12 deficiency
  2. folate deficiency
  3. diag
  4. how are homocysteine and methylmalonic acid levels interpreted
  5. what is the best test to confirm B12 deficiency after + result
  6. treatment
A

macrocytic anemia: extravastcular hemolyis occurs in the liver & spleen

low reticulocyte count
“ineffective erythropoiesis” RBCs destroyed as soon as leave BM

  1. peripheral neuropathy, smooth/shiny tongue, diarrhea
  2. no neuro probs
  3. CBC with smear-hypersegmented neutrophils & oval cells.
    B12 and folate levels.
  4. homocysteine levels go up with both B12 and folate deficiency. METHYLMALONIC LEVELS GO UP WHEN THERE IS A B12 DEFICIENCY ONLY
  5. anti parietal cell antibodies and anti-intrinsic factor antibodies (pernicious anemia)
  6. replacement. watch out for low K when replacing B12. hypokalemia results following the uptake of K by newly forming RBCs.
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3
Q
  1. drugs that cause megaloblastic anemia
  2. drugs that block GI absorption
  3. action of metformin and B12
A

purine and pyrimidine modulators: azathioprine, mycophenolate, fludarabine, hydroxyurea, MTX, trimethprim

  1. drugs that block GI absorption: EtOH, nitrofurantoin, estrogen, phenytoin
  2. metformin blocks B12 absorption
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4
Q

Hemolytic Anemia

  1. presentation
  2. diag
A
  1. sudden onset weakness and fatigue
  2. low haptoglobin,
    high: bili, retic, LDH,
    spherocytes

LDH & retic count improve first

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5
Q

Sickle Cell Anemia

  1. fever
  2. pain crisis treatment
  3. when is it time for exchange transfusion? goal?
  4. sudden drop in hematocrit
  5. parvo treatment?
  6. what meds should SCD pt be d/c with
A
  1. fever + SCD =antibiotics immediately ! emergent
  2. O2, NS hydration, pain meds
  3. brain: stroke

eye: visual disturbance from retinal infarct
lung: pulm infarct, plueritic pain and abnormal CXR
penis: priapism from infarction of prostatic plexus of veins
goal: HbS 30-40%
4. parvovirus B19 or folate deficiency. SCD pts should all be on folate replacement . if pt already on folate replacement then cause is parvovirus B19 (invades BM, halts production). PCR for parvo DNA most accurate.

  1. transfusions and IV Ig
  2. folate replacement, pneumococcal vaccine, HU if more than 4 crises/year
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6
Q 
Sickle Cell (SC) Disease 
1. what disturbance is typical
A
  1. freq visual disturbance, renal probs: hematuria, isosthenuria, UTI
    no pain crises !

no specific treatment.

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7
Q

Sickle Cell Trait

A

may have hematuria and concentrating defect. with hypoxia (scuba diving) splenic vein thrombosis could occur

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8
Q

Autoimmune Hemolysis

A

hx of other autoimmune dx or meds like penicillin, alpha methyl dopa, quinine, self drugs

diag: high: indirect bili, LDH, retic count. Low haptoglobin. spherocytes on smear.

most accurate test Coombs test–>”warm antibodies” = IgG

treatment: steroids . IVIG . if recurrent splenectomy.

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9
Q

Cold Induced Hemolysis (Cold Agglutinins)

  1. clues
  2. diag
  3. treatment
A
  1. hx of mycoplasma or EBV
  2. coombs negative, complement +
  3. rituximab. steroid, IVIG, splenectomy don’t work.
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10
Q

G6PD Deficiency

  1. presentation, clues in hx
  2. diagnosis
  3. treatment
A

presentation:
- sudden onset hemolysis
- can be X-linked
- most common form of oxidant stress to cause acute hemolysis with G6PD deficiency is infection
- oxidizing drugs: sulfa meds, primaquine, dapsone
- fava bean ingestion

    • heinz body test (Hz bodies are collections of oxidized, precipitated Hb embedded in red cell membrane)

-bite cells appear when pieces of red cell membrane get removed by spleen

most accurate test: G6PD levels (after 2 months). a normal G6PD level immediately after an episode of hemolysis doesn’t exclude G6PD deficiency. on the day of hemolysis the most deficient cells have been destroyed and the G6PD levels are normal

  1. avoid oxidant stress
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11
Q

Pyruvate Kinase Deficiency

A

presents the same way G6PD deficiency in terms of hemolysis. not provoked by medications or fava beans

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12
Q

Hereditary Spherocytosis

A

=genetic loss of ankyrin & spectrin in red cell membrane.

presents with:

  • recurrent episodes of hemolysis
  • splenomegaly
  • bilirubin gallstones
  • elevated MCHC

diag: eosin-5-maleimide (more accurate than osmotic fragility)
treatment: splenectomy will prevent hemolysis

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13
Q

Hemolytic Uremic Syndrome

Thrombotic Thrombocytopenic Purpura

A 
HUS (look for hx of E. Coli 0157:H7)
diagnose based on "ART"
Autoimmune hemolysis- intravascular
Renal- increased BUN and Cr
Thrombocytopenia
TTP (ticlopidine can cause)
diagnose based on "FAT RN" 
Fever
Autoimmune hemolysis- intravascular 
Thrombocytopenia 
Renal- increased BUN and Cr
Neurological issues

ADAMTS-13 is down in TTP

treatment: 
some resolve on their own
if severe, then plasmapheresis 
NO STEROIDS
NO ANTIBIOTICS - WILL WORSEN IN ECOLI HUS
NO PLTS- WILL MAKE HUS/TTP WORSE

mechanism HUS/TTP
ADAMTS-13 = enzyme that breaks down von Willebrands factor to release PLTs from one another. when VWF isn’t dissolve, the PLTs from abnormally prolonged that serve as a barrier. TBCs the run into these stands break down and are destroyed

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14
Q

Paroxysmal Nocturnal Hemoglobinuria

A

presents with:
pancytopenia
recurrent dark urine (especially in the morning)

can transform into aplastic anemia or AML

diag: CD55 and CD59 antibody (decay accelerating factor)
treatment: prednisone. if severe eculizumab

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15
Q

HELLP

A

hemolysis
elevated liver enzyemes
low PLTS

normal coag (PT and PTT) unlike DIC 
deliver baby
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16
Q

Methemoglobinemia

A

presents with shortness of breath for no clear reason and normal CXR
blood is locked in an oxidized state that cant pick up O2

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17
Q
  1. Transfusion Related Lung injury (TRALI)
  2. IgA deficiency
  3. ABO incompatibility
  4. Minor blood group incompatibility
  5. febrile nonhemolytic reactions
A
  1. presents with acute shortness of breath from antibodies in the donor blood against recipient WBCs
  2. presents with anaphylaxis. in the future, use blood donations from an IgA deficient donor or washed red cells
  3. presents with acute symptoms of hemolysis while transfusion is occurring
  4. minor blood group incompatibility to Kell, Duffy, Lewis or Kidd antigens or Rh incompatibility presents with delayed jaundice . no specific therapy
  5. small rise in temp. no therapy needed. reaction is against donor white cell antigens. prevented by using filtered blood transfusions in the future to remove the white cell antigens
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18
Q 
Acute Leukemia 
1. presentation 
2. diag test
AML
PML
3. treatment 
AML
M3, PML
ALL
A
  1. pancytopenia. fatigue, bleeding, infection
    functional immunodeficiency
    high WBC–>sludging of brain, eyes, lungs
  2. blasts on peripheral smear
    - cytogenetic abnormalities
    - Auer rods-AML
    - M3, PML associated with DIC
  3. AML: idarubicin/daunorubicin & cytosine arabinoside
    M3, PML: All trans retinoic acid (ATRA)
    ALL: intrathecal MTX
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19
Q

Myelodysplasia

  1. presentation
  2. diag test
  3. treatment
A
  1. presentation: elderly pts w/ pancytopenia, high MCV, low retic count & macroovalocytes, normal B12
    - mild slowly progressive preleukemia syndrome
    - most pts die of infection/bleeding
  2. diag test
    smear: Pelger-Huet cell (neutrophil with 2 lobes)

3.treatment
supportive, prn transfusions
can give azacitadine (increases survival), decitabine, lenalidomide

20
Q

Chronic Myelogenous Leukemia

  1. presentation
  2. diag test
  3. treatment
A
  1. presentation: high WBC predominantly neutrophils, splenomegaly
    untreated CML has highest risk transformation to acute leukemia
  2. diag test
    - high neutrophils, low LAP
    - Philadelphia chrom by PCR blood or BCR/ABL by FISH

3.treatment
1st: imatinib
BMT curative but not first line

21
Q

Chronic Lymphocytic Leukemia

  1. presentation
  2. diag test
  3. treatment
A
  1. presentation
    pts >50 yrs with high WBC described as “normal appearing lymphocytes.” often asymptomatic
  2. diag test
  3. peripheral blood smear: smudge cells

3.treatment: based on stage
0-1 no tx
if more advanced then fludarabine (extends survival) + rituximab

22
Q

Hairy Cell Leukemia

  1. presentation
  2. diag test
  3. treatment
A
  1. presentation
    pancytopenia, massive splenomegaly, middle age pts
  2. diag test
    hairy cells on smear & immunophenotyping on flow

3.treatment:cladribine

23
Q

Myelofibrosis

A

presents same as hairy cell leukemia with normal TRAP
diag: tear drop cell on smear
treatment: fibrosis of BM, JAK2mutation
BMT curative
if cant do BMT then lenalidomide, thalidomide

24
Q

Polycythemia Vera

  1. presentation
  2. diag test
  3. treatment
A
  1. presentation:
    headache, blurred vision, dizziness, fatigue, splenomegaly, pruritus (after hot shower b/c histamine released from basophils)
2. diag test
CBC: super high hematocrit
JAK stat mutation 
high B12
high LAP
3.treatment
phlebotomy
hydroxyurea
daily aspirin 
anagrelide if thrombocythemia
25
Q

Essential Thrombocythemia

  1. presentation
  2. diag test
  3. treatment
A
  1. presentation:
    headache, visual disturbance, pain in hands
    common cause of death: bleeding, thrombosis
  2. diag test
    JAK stat mutation
    really high PLTs

3.treatment
hydroxyurea to lower PLT count
anagrelide
daily aspirin

26
Q

Multiple Myeloma

  1. presentation
  2. diag test
  3. treatment
A
  1. presentation: bone pain from fracture caused by normal use. prone to renal failure, infection
  2. diag test: get BM biopsy
    a. skeletal survey: osteolytic lesions
    b. serum protein gel electrophor: high Ig’s (usually IgG)
    c. urine protein elctrophor: bence jones proteins
    d. peripheral smear: “rouleaux” of RBCs. MPV high b/c sticking together
    e. high Ca levels
    f. beta2 micoglobulin level is prognostic indicator
    g. BUN, Cr in case renal insuff

3.treatment
a. melphalan & steroids
can add thalidomide, lenalidomide, bortezomib
BMT most effective for pts <70yrs with adv dx

27
Q

Monoclonal Gammopathy of unknown Significance

  1. presentation
  2. diag test
  3. treatment
A
  1. presentation: pt >70yrs, elevated IgG
  2. diag test: SPEP shows asymptomatic elevation of IgG
  3. treatment: none
28
Q

Waldenstroms Macroglobulinemia

  1. presentation
  2. diag test
  3. treatment
A
  1. presentation
    hyperviscosity with IgM overproduction, blurry vision, confusion, headache, enlarged nodes and spleen
  2. diag test: serum viscosity really high, high IgM on SPEP

3.treatment
a.plasmapheresis if symptomatic
if need more then fludarabine, chlorambucil, rituximab

29
Q

Aplastic Anemia

  1. presentation
  2. diag test
  3. treatment
A
  1. presentation: pancytopenia
    can be caused by Hep B and Hep C
  2. diag test: pancytopenia
  3. treatment: no cytogenetic abnormalities
    a. if pt is <50 then BMT
    b. if BMT not possible, then antithymocyte globulin & cyclosporine
30
Q

Lymphoma

  1. presentation
  2. diag test
  3. treatment
A
  1. presentation: big lymph nodes
    HD: usually begins at neck and spreads out
    NHL: usually presents widespread dx,”B” symptoms
2. diag test: 
step 1: 
excisional lymph node biopsy
NO NEEDLE BIOPSY
HD: reed-Sternberg cells

step 2: determine stage with CXR, contrast CT (chest, abd, pelvis, head), BM biopsy
NO LYMPHANGIOGRAM OR EXPLORATORY LAP ABD

  1. treatment
    HD: ABVD
    (Adriamycin, bleomycin, vinblastine, dacarbazine)

NHL: CHOP
cyclophosphamide, hydroxyadriamycin, oncovin, prednisone
add rituximab (check for Hep B) if anti=CD20 antigen +

31
Q

Chemo Induced Nausea

1. 5HT inhibitors

A
  1. ondansteron (don’t give if prolong QT on EKG)
  2. glucocorticoids
  3. neurokinin- antagonists
  4. dopamine antagonists–phenothiazines and metoclopramide
  5. anticholinergic: chlorpromazine, prochlorperazine (will worse dementia)
32
Q

Von Willebrands Disease

  1. presentation
  2. diag test
  3. treatment
A
  1. presentation:
    superficial bleeding from mucosal surfaces from PLT dysfunction (epistaxis, petechiae)
  2. diag test
    ristocetin cofactor assay and von Willebrands factor
  3. Treatment
    1st line: desmopressin/DDAVP
    2nd: Factor VIII
    if both fail recombinant VWF
33
Q

Idiopathic Thrombocytopenic Purpura

A

presentation:
PLT type bleeding
PLTs <10,000-30,000

diag: (diagnosis of exclusion)
smear shows big PLTs
sonogram: normal spleen size found in ITP
BM: high # megakaryocytes
antibodies to glycoprotein IIb/IIIa receptor

treatment:
prednisone
IVIG admin if PLTs <20,000
chronic ITP: romiplstin, eltrombopag (stimulate megakaryocytes. they’re erythropoietin analogs)

34
Q

Uremia Induced PLT dysfunction

  1. presentation
  2. diag test
  3. treatment
A

uremia prevents PLT degranulation
presentation
PLT-like bleeding in pt w/ renal failure & norm PLT count

diag test
ristocetin test and VWF levels will be normal

treatment
1st: desmopressin (ddavp), dialysis, estrogen

35
Q

Thrombocytopenia

treatment

A

PLT>50,000 –no treatment
PLT<50,000 & minor bleeding–prednisone
PLT<10,000-20,000 & serious bleeding–IVIG or rhogam
recurrent episodes–splenectomy
no response to splenectomy–romiplastin, eltrombopag

36
Q

Factor VIII

  1. presentation
  2. diag test
  3. treatment
A
  1. presentation: joint bleeding or hematoma in little boy
  2. diag test: mixing study, then specific factor level
    3.treatment:
    severe deficiency -Factor VII replacement
    minor deficiency–DDAVP
37
Q

Factor IX

  1. presentation
  2. diag test
  3. treatment
A
  1. presentation: joint bleeding or hematoma
  2. diag test: mixing study, then specific factor level
  3. treatment: Factor IX replacement
38
Q

Factor XI

  1. presentation
  2. diag test
  3. treatment
A
  1. presentation: rare bleeding with trauma or surgery
  2. diag test: mixing study, then specific factor level
  3. treatment: fresh frozen plasma with bleeding episodes
39
Q

Factor XII

  1. presentation
  2. diag test
  3. treatment
A
  1. presentation: no bleeding
  2. diag test: mixing study, then specific factor level
  3. treatment: no treatment necessary
40
Q

What reverses warfarin toxicity

A

prothrombin complex concentrate (pcc)
pcc has all the vit K dependent factors (II, VII, IX, X, C, S)
works faster than vitamin K or fresh frozen plasma

41
Q

Heparin induced thrombocytopenia

A

presentation:
allergic rxn involving at least 50% drop in PLTs a few days after the start of heparin
Thrombosis most common clinical manifestation

diag:
PLT factor 4 antibodies or
heparin induced, antiPLT antibodies

treatment: stop heparin & use foundaparinux or a NOAC

42
Q

Antiphospholipid Syndrome (lupus anticoagulant/cardiolipin antibodies)

A 
presentation: 
venous/arterial thrombosis
high aPTT with normal PT 
spontaneous abortion 
false + VDRL

diag: mixing study, then russel viper venom test us most accurate for lupus anticoagulant
treatment: heparin followed by warfarin

43
Q

Protein C Deficiency

A

skin necrosis with warfarin use
venous thrombosis

diag: protein C level
treatment: heparin followed by warfarin

44
Q

Factor V leiden

A

most common cause of thrombophilia, venous thrombosis

diag: factor V mutation test
treatment: heparin followed by warfarin

(functionally a protein C deficiency. if factor V is mutated protein C wont inhibit it)

45
Q

Antithrombin deficiency

A

no change in the aPTT with a bolus of IV heparin
venous thrombosis

diag: antithrombin III levels
treatment: large amts of heparin or direct thrombin inhibitor followed by warfarin

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