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Hematology RC Editable > Lab/Morphology > Flashcards

Lab/Morphology Flashcards

1
Q

Morphological and clinical features of Alder Reilly

A

Pathophys: Lack lysome enzyme needed to degrade mucopolysaccharides
Clinical presentation: dysmorphism, skeletal dysplasia, HSM, corneal opacities

Morphology: azurophilic cytoplasmic inclusions in ALL leukocytes (including lymphocytes) of patient with accumulated mucopolysaccharidosis
-NEVER has dhole bodies

Alder…ALL WBCs
reiLLy … lacks lysozyme

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2
Q

Morphological and clinical features of Chediak Higashi

A

Pathophys: fusion of primary and secondary lysosomal granules leading to poor fxn in killing phagocytized bacteria

Clinical presentation: partial oculocutaneous albinism, recurrent infections, neuropathy, photophobia, nystagmus, HSM, pancytopenia, LAN, Increased risk of EBV-linked lymphomas

Morphology: Giant azurophilic (or grey) granules within granulocytes (neutrophils, eosinophils).

HiGashi…all grans

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3
Q

Morphological features of MYH9 disorder

A

Giant platelets and Dohle-like bodies in neutrophils (also seen in monos, other granulocyte and lymphocytes)

Seen in all forms except Epstein.

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4
Q

Conditions with pseudo-pelgerization

A

MDS
AML
CMML
Drug effect (Tac)

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5
Q

Forward scatter

A

Size

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6
Q

Side scatter

A

Granularity

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7
Q

Antigens that make up Rh

A

C,D, E, c, e

Clinically Significant

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8
Q

Antigens that make up Kell

A

K,k, Kpa,Kpb, Jsa,Jsb

Clinically Significant

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9
Q

Antigens that make up Duffy

A

Fya, Fyb

Clinically Significant

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10
Q

Antigens that make up Kidd

A

Jka, Jkb

Clinically Significant

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11
Q

Antigens that make up Lewis

A

Lea,Leb

Clinically Insignificant

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12
Q

Antigens that make up MNS

A

M,N,S,s,U

Clinically Significant=S,s,U
Clinically Insignificant-M,N

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13
Q

Antigens that make up I

A

i,I

Clinically Insignificant

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14
Q

Antigens that make up Iutheran

A

Lua,Lub

Clinically Insignificant

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15
Q

Antigens that make up XG

A

Xga, Xgb

Clinically Insignificant

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16
Q

Define a Bethesda unit

A

The amount of inhibitor that will neutralize 50% of 1U of factor VIII:C in normal plasma after incubation for 120 mins at 37 degrees.

Reciprocal of the dilution of patient plasma that inhibits 50% of FVIII activity in an equal volume of normal plasma

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17
Q

What is on the Y and X axes of a Kaplan-Meier Survival Curve?

A 
X = time
Y = percent survival
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18
Q

Causes of megablastosis

A
  1. Vitamin B12 def
  2. Folate def
  3. Copper deficiency
  4. Drugs: HU, MTX, phenytoin Azathioprine, HIV drugs
  5. MDS
  6. Parvovirus B19
  7. Congenital Dyserythropoeitic Anemia
  8. Inherited pyrimidine synthesis disorders: orotic aciduria
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19
Q

Causes of ringed sideroblasts

A 
MDS-RS
Congenital RS
Alcohol
Drugs (Isoniazid, chloramphenicol, linezolid)
Hypothermia
Copper deficiency
Lead poisoning
Zn excess

5 iron granules per erythroid precursor, Take up ⅓ of nucleus. Prussian blue stain!

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20
Q

How do epigenetic drugs work? What are a few examples?

A

Epigenetic drugs work by regulating chromatin. The 2 major components of chromatin are DNA and histone proteins.

Epigenetic drugs work by:

  1. DNA methylation
  2. Histone acetylation and methylation

Examples:
HDAC inhibitors: Vorinostat (CTCL), Panobinostat (MM), Romidepsin (CTCL)
Hypomethylating agents: AZA, decitabine

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21
Q

Diagnostic criteria of TRALI

A

Acute onset (during or within 6 hours of transfusion)
Hypoxemia* (PaO2/FiO2 ≤300 or SpO2 <90% on room air or other clinical evidence of hypoxemia)
Bilateral infiltrates on frontal CXR
No evidence of circulatory overload/left atrial hypertension
No pre-existing ALI/ARDS before transfusion

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22
Q

Mechanism of TRALI (two-hit hypothesis)

A
  1. Neutrophil sequestration and priming – The first hit involves neutrophil sequestration and priming (sensitive neutrophils) in the lung microvasculature, due to recipient factors such as endothelial injury.
  2. Neutrophil activation – The second hit is activation of recipient neutrophils by a factor in the blood product. Activation is associated with the release from neutrophils of cytokines, reactive oxygen species, oxidases, and proteases that damage the pulmonary capillary endothelium

MOST COMMON ANTIBODY: HNA-3a

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23
Q

Most common antibody involved in TRALI

A

MOST COMMON ANTIBODY: HNA-3a

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24
Q

Ways to minimize TRALI

A
  1. Not using female plasma for FFP (just for fractionated products)
  2. Using male plasma to resuspend platelets
  3. Only males or nulliparous F for apheresis plasma/platelet collections
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25
Q

Causes of plt refractoriness

A 
Common:
Alloimmunization
ABO mismatch
Sepsis/Infection
DIC
ITP
Active bleeding
Splenomegaly
Fever

Less Common:
HSCT

26
Q

Name 3 causes of cytopenias that are a result of transfusion of blood products

A

Transfusion related Graft vs host disease
Acute Hemolytic Transfusion Reaction
Delayed Hemolytic Transfusion Reaction
Post-transfusion Purpura
Hyperhemolysis in SCD
Transfusion related alloimmune thrombocytopenia
Transfusion-related alloimmune neutropenia
Bacterial sepsis

27
Q 
What stain is used to detect the following:
Iron granules:
Heinz bodies (Hb):
Hemoglobin H (Hb): 
Pappenheimer bodies:
Ringed sideroblasts:
A

Iron granules: Prussian Blue Stain
Heinz bodies (Hb): Supravital stain = Brilliant Cresyl blue or methylene blue
Hemoglobin H (Hb): Supravital stain = Brilliant Cresyl Blue Staining
Pappenheimer bodies: Perl’s Prussian blue (seen on Wright-Geimsa stain)
Ringed sideroblasts: Prussian Blue

“if it starts with an H = Hb = brilliant cresyl blue”

28
Q

Heinz body- What is it? 3 causes.

A

Denatured hemoglobin
Causes: oxidant induced hemolysis, G6PD, NADPH def, liver disease, hyposplenism

unstable Hb, methemoglobin, Thal

29
Q

Howell-Jolly body- What is it? 3 causes.

A

Unedited nuclear fragment (DNA)

Causes: hyposplenism, asplenism (surgical removal or SCD), severe hemolytic anemia.

30
Q

Basophilic stippling- What is it? 3 causes.

A

Aggregates of clumped up RNA/ribosomes
Causes: lead poisoning, thalassemia, MDS, sideroblastic anemia, B12/folate deficiency, HbSS, CDA

P5NT def

31
Q

Pappenheimer body- What is it? 3 causes.

A

Iron inclusions

Causes: sideroblastic anemia, MDS, thalassemia, megaloblastic anemia, hemolytic anemia, CDA, post-splenectomy states

32
Q

Describe the 3 steps of PCR and how they work

A

Denaturing: Separate the DNA strand of interest via heating (strand separation)

Annealing: Primers are then added to anneal to the opposite DNA strands of the desired target sequence (primer hybridization)

Extension: Complementary strand is then synthesized (strand synthesis) Using a polymerase

This cycle of denaturing, annealing and extension ensures exponential amplification of the target sequence by using the amplified sequences of the previous cycle as a new template

33
Q

Based on retrospective studies, what is the optimal ratio of transfusion of blood products in massive hemorrhage from trauma?

A

RBC:FFP:Plt = 1:1:1

NB: JAMA 2015 RCT:
No difference in 1:1:1 vs 1:1:2 (Plasma:Plt:RBC) at 24h or 30d mortality

34
Q

How does a Coulter counter work? (or what is the principle that allows it to work)

A

Electrical Impedance:
particles pulled through an orifice concurrent with an electric current, produce a change in impedance that is proportional to the volume of the particle traversing the orifice.

35
Q

3 causes of dyspnea post transfusion beside infectious complications

A
  1. TACO
  2. TRALI
  3. HEMOLYSIS (AHTR)
  4. Anaphylaxis
36
Q

Explain how the Kleihauer test works to detect hb F

A

When fetal cell screen is positive, the Kleihauer-Betke test is used to quantify the amount of FMH
Unlike Rosette test, KBT is specific for fetal red cells regardless of their Rh type:
Blood smear is prepared from maternal sample
Expose to acid buffer
Fetal Hemoglobin resists acid elution → Fetal cells are intact and adult cells (senstive to acid) appear as ghosts
2000 red cell are counted and the percentage of fetal to maternal cells is calculated

37
Q

Reasons for a false positive Kleihauer-Betke

A

HPFH, Sickler on HU, thalassemias

38
Q

Explain the Rosette Test (Fetal cell screen):

A

Maternal blood is incubated with anti-D, resulting in antibody coating any Rh-positive fetal cells present in the maternal circulation.

Rh positive indicator cells are added, and they will form a rosette around fetal cells that are coated with anti-D.

39
Q

Target cells

  1. Mechanism of formation
  2. 4 causes
A
  1. Target cells form via increased surface area to volume ratio (target caused by redundant cell membrane).
    Increased SA:volume:
    ●Decreased cell volume–>hemoglobinopathies + IDA
    ●Increased cell membrane–> obstructive liver disease.
2. Causes: 
Iron def 
Thalassemia 
Liver disease (esp obstructive)
Post splenectomy
  • can withstand osmotic lysis
40
Q

Causes of Echinocytes

A
  1. KidnEeeY failure
  2. Liver failure
  3. Artifact
  4. Hemoglobin C/D/E
41
Q

Causes of Achanthocytes

A
  1. Liver disease
  2. Abetaliproteinemia
  3. McLeod phenotype (reduced surface kell)
  4. (Rh-null) - neuroacanthocyotosis (extravascular hemolysis, chorea, dementia) + HSM, myopathy and cardiomyopathy.
42
Q

Causes of spurious elevated platelet count

A
  1. Severe microcytosis (IDA or microspherocytes seen in burns)
  2. RBC fragmentation (Brisk MAHA)
  3. Cryoglobulins
  4. Cytoplasmic Debris from Nucleated Cells (Seen in DLBCL, monoblastic leukemia)
  5. Lipid micelle interference (post-pranial sampling, TPN)
  6. Microorganisms (fungi, bacteria)
  7. Hemoglobin H disease
43
Q

What does Reptilase Time test?

A

-Assesses the final step in fibrinogen conversion to fibrin
Reptilase is resistant to antithrombin III so it is not prolonged in samples containing DTIs, or heparin, whereas TT will be prolonged.

-Similar to thrombin time but utilize a different activator (Reptilase from snake) that cleaves the fibrinogen to fibrin
Principles: Reptilase is added to platelet poor plasma and the clotting time measured. The test requires no added phospholipid or calcium.

44
Q

In a patient with a prolonged Thrombin Time but normal Reptilase Time, what does this suggest?

A

Heparin or a direct thrombin inhibitor.

45
Q

What are four components of the PTT reagent?

A
  1. Phospholipids
  2. Calcium
  3. Platelet poor plasma
  4. Surface activator (kaolin, micronized silica, celite, ellagic acid)
46
Q

What are components of the PT reagent?

A
  1. Platelet poor plasma
  2. Tissue factor (containing phospholipid) called thromboplastin.
  3. Calcium
47
Q

Differences between hairy cell and SMZL in peripheral blood pathology?

A
  1. Hair-like fine cytoplasmic projections circumferential in HCL versus bipolar villous projections in SMZL
  2. Kidney bean shaped nucleus in HCL (uniform sizes vs. biphasic in SMZL)
  3. Monocytopenia in HCL
  4. Replaces red pulp of spleen (SMZL replaces white pulp)
48
Q

How do acanthocytes form in liver disease?

A

acanthocyte formation is a 2-step process:

1) transfer of free cholesterol from abnormal plasma lipoproteins into the RBC membrane
2) remodeling of abnormally shaped erythrocytes by the spleen.

49
Q

The peripheral blood smear in pyrimidine- 5′-nucleotidase deficiency shows what?

A

red cells with coarse basophilic stippling

50
Q

2 reasons for false negative lupus anticoagulant?

A
  1. Poorly centrifuged plasma (becomes platelet rich)

2. Acute VTE-may be consumed in acute event, suggest testing 3-6 weeks after VTE.

51
Q

In pts with APLA the INR may be elevated at baseline making the INR unreliable for Warfarin monitoring. What test can be used instead?

A

Chromogenic FX assay.

Correlate with POC INR monitoring q4-6 months to ensure INR is accurate.

52
Q

What are the 3 measured (not calculated) RBC parameters when using an automated analyzer?

A
  1. RBC
  2. MCV or Hct (depending on machine used)
  3. Hemoglobin
53
Q

2 causes of spurious elevated and decreased RBC count.

A

Increased

  1. Hyperleukocytosis
  2. Giant plts

Decreased

  1. Hemolysis
  2. Cryoglobulins
  3. RBC aggultinins

Hemoglobin measurements can be elevated artifactually by increased sample turbidity because of leukocytosis, paraproteinemia, carboxyhemoglobinemia, hyperbilirubinemia, or hyperlipidemia.

54
Q

How do you calculate hematocrit?

A

hematocrit = MCV (10−15 L) × RBC count (1012/L) × 100.

55
Q

What are 3 benefits of using the Anti-XA assay over the PTT to monitor UFH?

A
  1. a shorter time to a therapeutic result
  2. less variability resulting in decreased dosage changes and ordered tests
  3. no confounding from factor deficiencies, LACs, contact factor def, or acute phase reactants
  4. limited interferences from common biologic substances.
56
Q

APLA pt has a prolonged INR. What is one potential cause. If you want to start the pt on Warfarin, what other parameter could you use to monitor therapeutic effect?

A
  • LAC can cause reagent-dependent prolongations of PT results.
  • Acquired factor II deficiency due to a non-neutralizing prothrombin auto-ab that increases the clearance rate
  • Can use chromogenic factor X activity (not chromogenic anti-Xa) as an alternative to the INR (not widely available)
  • Or measure II, VII, X activity. If not affects by LAC, can you use suppression of factor activity to monitor Warfarin.
57
Q

What are 5 pre-analytic variables that may affect plt aggregomatry results?

A
  1. Low plt count (Need PRP, plt 200-400)
  2. Drugs (ASA, SSRI, etc.)
  3. Temperature (room temp)
  4. pH (physiologic)
  5. Food (high chylomicrons can interfere)
  6. Fibrinogen level (need fibrinogen to aggregate)
58
Q

3 causes of a prolonged dVVT?

A
  1. Presence of lupus anticoagulant
  2. Heparin levels greater than 1.0U/mL
  3. DTI (Direct thrombin inhibitor)
  4. Common pathway factor deficiencies
  5. Presence of factor inhibitors II, V or X
59
Q

What are 3 ways to overcome a positive antibody screen for a pt treated with Daratumuab?

A

i) standard blood bank techniques including dithiothreitol and enzymatic treatment of reagent cells, using reagent red blood cells negative for CD38
ii) blocking CD38 antigens on reagent or donor cells
iii) neutralization of anti-CD38 antibody in patient plasma prior to testing
iv) extended antigen typing of patient red blood cells in conjunction with provision of phenotypically matched units for transfusion

60
Q

What are 4 drugs classes that can interfere with transfusion lab testing?

A
  1. Dara–> anti CD-38
  2. Fludarabine, AIHA
  3. CD-47- used in AML
  4. PD-1, PDL1 inhibitors-DAT + AIHA case reportable
61
Q

What is the difference between partial D and weak D?

A

Partial D: Forward type as Rh (+), because they express D proteins that are chimeric in nature and are made up of pieces of CE.
Ramifications is that they may develop antibodies if given Rh(+) blood → HDFN, DHTR, etc
Need to be transfused Rh(-) blood, can serve as donors for Rh(+)
When pregnant, need to be given Rh(D)-immunoglobulin
(African and caucasian)

Weak D: Forward type as Rh(-), because they express such low levels of D protein
Can be transfused Rh(+) blood, can serve as donors for Rh (+)
Problem with Donors who are Rh (-) must have extended testing and can sensitize recipient Rh-
When pregnant, do not need to be given Rh(D)-immunoglobulin
(Caucasian)

62
Q

What are two morphologic features of prolymphocytes?

A
  1. Small to medium sized lymphocytes
  2. Non grandular basophilic cytoplasm
  3. Round,oval or irregular nuclei
  4. Visible nucleus
  5. Cytoplasmic protrusions or blebs

Hematology RC Editable (28 decks)

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