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USMLE Rx > Hematology > Flashcards

Hematology Flashcards

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USMLE® Step 1 flashcards
1
Q

In a patient with pernicious anemia, what would stage 1 and stage 2 of the schilling test show.

A

Stage 1 [just B12]- low urinary B12

Stage 2[B12 with intrinsic factor]- high urinary B12

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2
Q

What additionally additive is added in stage 3 and stage 4 of schilling test

A

stage 3- oral antibiotics

stage 4- pancreatic enzymes

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3
Q

What kind of anemia and RBC deformity is associated with ‘apple core’ lesions

A

apple core lesions on barium enema indicate colon lumen narrowing due to tumor- colon cancer
Anemia of chronic blood loss leading to iron deficiency anemia- microcytic cells

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4
Q

Which diseases show spherocyte deformities in RBCs

A

hereditary spherocytosis, G6PD Deficiency, thalassemias, autoimmune hemolytic anemias

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5
Q

Where are pappenheimer bodies found

A

sideroblastic anemia

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6
Q

In an infant which diseases would cause hypocellular bone marrow findings

A

Fanconi’s anemia, Diamond-blackfan anemia, Schwachman-Diamond syndrome

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7
Q

Where is B12 absorbed

A

Terminal ileum

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8
Q

What is the etiology, pathophysiology , sxs and complications of Fanconi’s Anemia

A

Etiology-genetic defect of DNA repair, sensitive to alkylating agents
pathophys- hereditary aplastic anemia. Associated with facial abnormalities, wide thumbs, pigmented skin
sxs- pancytopenia symptoms
Complications- high risk for AML in kids

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9
Q

What is diamond-blackfan syndrome

A

erythroid aplasia that causes macrocytIc anemia

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10
Q

Outline the journey of B12 from swallowing to absorption

A

Salive in mouth contains R-protein that binds to B12 and goes with it to duodenum. In duodenum, pancreatic enzymes release B12 from R-proteins and B12 binds to intrinsic factor. Intrinsic factor/B12 complex binds to ileal receptors

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11
Q

What is the difference between direct and indirect coomb’s test

A

Direct- anti-human immunoglobulin [coomb’s reagent] added to patient blood cells. If antibodies present, coomb’s reagent will bind and cause agglutination.
Indirect- coomb’s reagent added to patient serum and donor rbcs. This detects if there are unbound antibodies in patient serum.

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12
Q

Why does anemia of chronic disease occur

A

IL-6 release due to inflammatory mediators. Causes increased ferritin, hepcidin, decreased ferroportin
Decreased transferrin

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13
Q

What changes in pallor, MCHC do spherocytes have.

A

Spherocytes have no central pallor and increased MCHC

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14
Q

What are the morphological changes in RBC in G6PD deficiency

A

Supravital stain- heinz bodies

Wright-Giemsa stain- bite cells

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15
Q

What is leukocyte alkaline phosphatase [LAP] used for. What is LAP in acute and chronic myelogenous leukemias.

A

LAP is used to differentiate inflammatory process from AML and CML. LAP would be low in AML and CML

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16
Q

What is the etiology, pathophys, and complications of AML

A

Etiology- t[15;17]
Pathphys- myeloid progenitor cells proliferate in bone marrow. Auer rods seen inside peripheral myelogenous cells and are myeloperoxidase positive.
Complications- APL subset might cause DIC and microangiopathic hemolytic anemia.

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17
Q

Why is RDW increased in iron deficiency anemia

A

Because progressive iron deficiency causes decreased cell size as time goes on

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18
Q

In what diseases can microangiopathic hemolytic anemia occur [MAHA]

A

E.Coli causing TTP, leading to MAHA and HUS

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19
Q

What morphology does antibody-mediated destruction of RBCs show

A

Spherical RBCs [not schistocytes]

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20
Q

Which gene and enzyme deficiency can lead to paroxysmal nocturnal hemoglobinuria

A

PIGA gene leading to phosphotidylinositol glycosyltransferase

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21
Q

What would the RDW, MCHC, reticulocyte count in hereditary spherocytosis show.

A

increased RDW, Increased MCHC, increased reticulocyte count

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22
Q

Which conditions increase the risk of ALL in children.

A

Fanconi’s anemia, bloom syndrome, ataxia telegenctasia, neurofibromatosis type 1 and DOWN SYNDROME

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23
Q

What are the three main signs of leukemias

A

Anemia, thrombocytopenia, and neutropenia

also leukocytosis

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24
Q

In children that present with acute leukemia, what is the automatic diagnosis until presented otherwise.

A

ALL

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25
Q

What would the erythrocyte count and RDW be in mild thalassemias.

A

High RBC in mild thalassemia [which is very unusual]

normal RDW

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26
Q

Explain the etiology, morphology, pathophysiology and symptoms and complications for CLL.

A

Etiology-
Morphology- smudge cells with small, mature appearing neutrophils. High white blood cell count.
Pathophysiology-
Symptoms-
Complications- warm or cold autoimmune hemolytic anemia, infections due to hypogammaglobulinemia

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27
Q

What are the 2 hallmark findings of TTP

A

thrombocytopenia and MAHA

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28
Q

What are some common later in life complications of hereditary spherocytosis

A

bilirubin gallstones and cholecystitis

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29
Q

In what disease is rouleaux formation seen

A

Multiple myeloma and any disease with increased serum proteins

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30
Q

What happens to PT, aPTT and bleeding time in vWF deficiency

A

bleeding time and aPTT increase. PT remains normal

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31
Q

What is glanzmann syndrome and what happens to PT, aPTT and bleeding time in Glanzmann syndrome

A

platelet have defective gpIIb/gpIIIa so cannot aggregates. Increased bleeding time. Since it is platelet defect- normal aPTT and PT.

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32
Q

what is bernard-soulier syndrome and what happens to PT, aPTT and bleeding time in it.

A

Platelet defect in gpIb- so loss of platelet adhesion. High bleeding time, normal PT and aPTT

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33
Q

What is the triad of findings in plummer-vinson syndrome.

A

Atrophic glossitis, esophageal webs and iron deficiency anemia

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34
Q

What are patients with plummer vinson syndrome at a higher risk of developing.

A

Esophageal squamous cell carcinoma

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35
Q

What is hemoglobin oxidized to due to G6-PD deficiency and oxidative stress.

A

Methemoglobin

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36
Q

What are the bowel complications of burkitt’s lymphoma.

A

Intussussecption of ileum/cecum due to tumor and resulting bowel obstruction

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37
Q

How do you distinguish DIC from TTP and ITP

A

All have thrombocytopenia but only DIC will have elevated INR and TTP will have the classic FATRN pentad. ITP is diagnosis of exclusions

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38
Q

How do you distinguish toxin-producing bacterial infections from gram negative DIC.

A

toxin-producing bacteria will not have the widespread coagulation cascade activation like and will have normal INR/PT and aPTT. They will have thrombocytopenia like DIC but more likely to have hemolytic anemia [like HUS]

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39
Q

What can trigger an aplastic crisis in sickle cell patients.

A

Parvovirus B19.

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40
Q

What is the most common complication in those with sickle cell TRAIT.

A

microhematuria and isothenuria

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41
Q

Which factors does antithrombin III neutralize.

A

Factors IIa, IXa and Xa

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42
Q

What does factor XIIIa do.

A

Crosslinking of fibrin polymers.

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43
Q

Name some disorders which will have schistocytes on peripheral smear.

A

DIC, HELLP syndrome, TTP

44
Q

How do you distinguish autoimmune hemolytic anemia from hereditary spherocytosis.

A

Coomb’s test

45
Q

Name the complications of ALL.

A

DIC

46
Q

Why is there an ‘M’ spike in multiple myeloma.

A

Due to IgA or IgG presence causing an increase in gamma-globulin fraction.

47
Q

Which disease is indicated due to an absence of HbA1 but an increase in HbA2.

A

Beta-thalassemia major since HbA2 is a2g2

while HbA1 is a2b2 normal hemoglobin

48
Q

What does a leukocytosis with a marked thrombocytosis suggest.

A

Myeloproliferative disorder

49
Q

Why does HbH disease lead to hemolytic anemia.

A

HbH [Beta4] combines and forms insoluble tetramers and inclusion bodies in RBCs

50
Q

Name risk factors for non-hodgkin’s lymphoma

A

Immunosuppresion

51
Q

What is lupus anticoagulant.

A

Lupus anticoagulant is an IgM or IgG antibody found in SLE patients that can lead to acquired antiphospholipid antibody syndrome. It binds to platelet phospholipids, overactivating them and making them accessible to clotting factors—causes thrombosis. PTT and PT however will increase because less exogenous phospholipid will be available for these tests. It can cause recurrent miscarriages and false positive syphillis tests.

52
Q

What are the classic symptoms of B-cell lymphomass

A

Night sweats, weight loss, fevers

53
Q

Which leukemia are Down syndrome patients most likely to have before 5 years old. After 5 years old.

A

Before 5 years old- AML

After- ALL

54
Q

What are the classic symptoms of leukemia

A

easy bruising, anemia, thrombocytopenia, fatigue, weight loss, fever maybe

55
Q

Which leukemias have DIC as a complication

A

AML [especially M3/APML] and CML

56
Q

What does the BCR-ABL translocation in CML to.

A

produces a deregulated, constitutively active tyrosine kinase enzyme that leads to clonal overproduction of hematoepoetic myeloid stem cells

57
Q

If you’re looking at a histology slide of lots of immature granular cells, what are the main diagnosis

A

AML or CML

58
Q

What does a histology picture of CLL look like.

A

monomorphic, small and mature appearing lymphocytes

59
Q

What is proteinuria in the setting of Multiple myeloma called. What is the criterea

A

Bence-Jones proteinuria thanks to monoclonal free light chains produced by the malignant plasma cells. Must have great than 1 g of proteinuria in 24 hours

60
Q

Which viral infection is most likely to unmask hereditary spherocytosis.

A

Parvovirus B19

61
Q

What kind of RBCs would you see on histology of pyruvate kinase deficiency.

A

Burr cells or echinocytes

62
Q

A dry tap with PBS of tear drop cells points towards which diagnosis.

A

Myelofibrosis

63
Q

What are some genes associated with myelofibrosis.

A

JAK, TET2, CALR, MPL

64
Q

what is the translocation in follicular lymphoma.

A

t [14;18]

65
Q

What is the translocation and gene in AML

A

t[15;17] PML-RARA

66
Q

What is the gene and translocation marker in mantle cell lymphoma.

A

t [11;14] cyclin D1-Ig heavy chain

67
Q

Which two lymphomas share the CD5 marker.

A

DLBCL, SLL [CLL], Mantle cell lymphomas, Peripheral T cell lymphoma

68
Q

Which diseases can potentially transform into DLBCL

A

SLL/CLL, follicular lymphoma, Marginal zone lymphoma, Splenic maltoma, MALToma, lymphoplasmocytic lymphoma, nodular lymphocyte hodgkin’s predominant lymphoma

69
Q

Which area does the sporadic form of burkitt’s lymphoma usually involve.

A

Abdomen

70
Q

What would the bone marrow findings of hairy cell leukemia be.

A

Dry tap due to reticulin fibrosis

71
Q

What is Richter’s transformation.

A

Transformation of CLL/SLL into fast growing DLBCL [is it also transformation of other malignancies into DLBCL]

72
Q

What is the translocation in Ewing’s sarcoma. What is the classical histological feature in Ewing’s sarcoma.

A

t[11;22]; Onion skinning of bone diaphysis on Xray imaging.

73
Q

What is the pathogenesis, histology details of nodular sclerosing type hodgkin’s lymphoma.

A

Usually in young women, characterized by a type of Reed-sternberg cells called Lacunar Cells. Histological artifaction causes them to look like cells with clear spaces between each other. Classical finding is mediastinal lymphadenopathy.

74
Q

How does bcl2 causes antiapoptosis.

A

bcl2 and bcl-xl inhibit the activation and release of cyct c from mitochondria. So cyt c won’t bind APAF-1 and caspase cascade won’t be activated.

75
Q

Which leukemia is mostly likely to stain positive for tdt

A

ALL

76
Q

What are the CD markers for B-ALL.

A

CD 10, 19, 20

77
Q

What are the CD markers for T-ALL.

A

CD 2, 3, 4, 5, 7, 8

78
Q

What is the age distribution in hodgkin’s lymphoma.

A

Bimodal. Young people and people above 55.

79
Q

A patient with HIV presents with tumor containing spindle-shaped malignant cells. What is the likely malignancy.

A

Kaposi Sarcoma [HHV8]- neoplasm of endothelial cells

80
Q

Describe Kaposi sarcoma lesions.

A

Purple plaques or nodules.

81
Q

What are some symptoms seen in hypercalcemia patients.

A

Bone issues, constipation, nausea, abdominal pain, kidney stones, confusion, dimentia

82
Q

What is essential thrombocytosis.

A

Too much production of megakaryocytes that overproduce platelets. Risk progressing to leukemia.

83
Q

A patient presents with thrombocytopenia, increased BT, increased PT and increased aPTT. Also there is decreased fibrinogen. What is the process that is occurring.

A

DIC

84
Q

What treatment is useful for AML M3.

A

All trans-retinoic acid.

85
Q

Explain the genetic abnormality in acute promyelocytic leukemia.

A

Fusion protein that causes cell to not be responsive to retinoic acid, causing arrested maturation of cell at promyelocytic stage. This causes DIC.

86
Q

What is the common translocation in ALL.

A

t[12;21]

87
Q

What type of mutation occurs in duchenne’s muscular dystrophy.

A

Frameshift, X-linked mutation

88
Q

What is the septic inflammatory response syndrome [SIRS] criteria for severe sepsis.

A

Two of the follow conditions must be met-

  1. Temperature above 38 degrees or below 36 degrees
  2. HR more than 90/min
  3. abnormal WBC count
  4. RR more than 20/min or CO2 less than 32mmHg in arteries
89
Q

What is main concern in acute vs chronic DIC.

A

In acute DIC, like in sepsis, the main concern is bleeding.

In chronic DIC, like in cancer, the main concern is thrombosis

90
Q

What is the PT, aPTT, D-dimer, INR, fibrinogen level in DIC.

A

Increased INR, PT, aPTT, D-Dimer, decreased fibronigen

91
Q

What is the function of fibrinogen [factor I].

A

Gets converted into fibrin. Is backbone of the mature clot because it crosslinks platelet glycoprotein IIa and IIIb receptors.

92
Q

What are the two functions of vWF.

A
  1. bind collagen to platelets via glycoproteins.

2. carry factor VIII

93
Q

What is the Ristocetin aggregation test.

A

Ristocetin is an antibiotic that causes vWF in blood to bind to platelet receptor 1b, causing aggregation.
In vWF disease, the aggregation is reduced.

94
Q

Name some differences of clinical presentation in hemophila A/B and vWF disease.

A

vWF will show nosebleeds, menorrhagia, and primary hemostasis such as bleeding after invasive procedures.
Hemophilia will often show hemarthrosis and intracranial bleed [secondary hemostasis] and bleeding at a last time.

95
Q

What is the difference between primary and secondary hemostasis.

A

Primary Hemostasis- platelet plug due to bleeding and vascular injury.
Secondary Hemostasis- coagulation activation and fibrin clot- stabilization of platelet plug.

96
Q

What does protein C do.

A

Inactivates factor V and VIII

97
Q

What does LFA-1/CD18 deficiency do.

A

Reduced trafficking of leukocytes into tissues and their extravasation. This causes leukocyte adhesion deficiency and increased, recurring bacterial infections and delayed umbilical cord separation. LFA1 is a protein found on phagocytes.

98
Q

What happens in Bernard Soulier disease.

A

Deficiency of gb1b causing vWF to not bind to platelet resulting in impaired platelet adhesion. Platelet count decreases.

99
Q

How would you distinguish factor VIII deficiency from vWF deficiency.

A

Check bleeding time. BT is high in vWF but normal in factor VIII deficiency.

100
Q

Vitamin K deficiency can develop due to long term——–use

A

chronic antibiotic use

101
Q

Name some drugs that can cause ITP.

A

trimethoprim/sulfamethaxazole, acetominophen, heparin, quinine, vancomycin

102
Q

Howell-Jolly bodies are found in which conditions.

A

Any condition with splenic dysfunction and when patient undergo a splenectomy. Howell jolly bodies are nuclear remnants that would usually be removed by the spleen.

103
Q

What exactly does vWF do.

A

Is a ligand for platelet adhesion and carries factor VIII

104
Q

What is glanzmann thrombasthenia.

A

Defect in gpIIb/gpIIIa platelet receptors for fibrinogen, but normal platelet adhesion.

105
Q

How many days does it take for the vitamin k levels to stabilize in a newborn.

A

7-10 days

106
Q

What is the BT, PC, aPTT, PT in vitamin K deficiency.

A

Normal PC and BT, Increased aPTT and PT

107
Q

What do you suspect in a patient with an increased bleeding time but normal platelet count, normal aPTT, PT, D-dimers.

A

Qualitative platelet disorder like glanzmann or bernard-souliers

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