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Internal Medicine > hematology > Flashcards

hematology Flashcards

1
Q

What is the typical presentation of ALL

A

CHILD + Lymphadenopathy + bone pain + bleeding + fever in a CHILD, bone marrow > 20% blasts in bone marrow

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2
Q

a 5 y/o child with lymphadenopathy, bone pain, bleeding, and fever. Bone marrow demonstrates > 20% lymphoblasts. What is the likely diagnosis

A

ALL

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3
Q

What is the peak age for ALL and how do you typically treat it

A

3-7 years old
Highly responsive to chemo

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4
Q

How does CLL typically present

A

Middle age patient, often asymptomatic (seen on blood tests), fatigue, lymphadenopathy, splenomegaly

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5
Q

a 60-year-old male complaining of fatigue. Blood tests demonstrate severe anemia, decreased neutrophil count, and small, abnormal B lymphocytes in the bone marrow (>30%) with levels at 90,000 per cubic millimeter. He has painless cervical lymphadenopathy and hepatosplenomegaly. What is the likely diagnosis

A

CLL

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6
Q

What is the most common leukemia in adults

A

CLL

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7
Q

What is the peak age for CLL

A

50

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8
Q

What will be seen on diagnostic lab tests for CLL

A

SMUDGE CELLS on peripheral smear, mature lymphocytes

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9
Q

How do you treat CLL

A

observation. If lymphocytes are > 100,000 or symptomatic -> treated with chemotherapy

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10
Q

a 52-year-old male who reports that he has been feeling very tired lately, and his wife thinks that he looks pale. You order a complete blood count, which shows: Hgb 8.5 g/dL (normal 13.5-17.5); WBC 1,200/microliter (normal 4,500 – 11,000); platelets 70,000/microliter (normal 150,000 – 400,000). The patient is referred for bone marrow biopsy, which shows myeloblasts with Auer rods. What is the likely diagnosis

A

AML

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11
Q

What are characteristic findings on bone marrow biopsies in someone with AML

A

Auer rods
Blasts
*Auer Rods and > 20% blasts seen in bone marrow

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12
Q

What are common CBC findings in someone with AML

A

Anemia, thrombocytopenia, neutropenia. Splenomegaly, gingival hyperplasia, and Leukostasis (WBC > 100,000)

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13
Q

What population is AML typically seen in

A

Adults >50y/o

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14
Q

a 49-year-old healthy male without complaints, but on a routine complete blood count (CBC) has markedly increased white blood cell count of 40,000 per uL (normal 4500 – 11,000). A peripheral blood smear demonstrates leukocytosis with myeloid cells present at various stages of differentiation, with more mature cells present at a greater percentage than less mature cells. The cytogenetic analysis is positive for the Philadelphia chromosome. What is the likely diagnosis

A

CML

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15
Q

When does CML typically present

A

70% asymptomatic until the patient has a blastic crisis

Adults >50

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16
Q

What are the diagnostic studies for CML

A

Strikingly Increased WBC count > 100,000 + hyperuricemia

Philadelphia chromosomes and splenomegaly

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17
Q

a 62-year-old male with a history of chronic kidney disease complaining of weight loss, fatigue, and weakness. Iron studies reveal decreased serum iron, increased ferritin, and decreased TIBC. The peripheral blood smear shows normochromic RBCs. What is the likely diagnosis

A

Anemia of chronic disease

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18
Q

When is anemia of chronic disease found

A

seen in chronic infection, chronic immune activation, and malignancy

  • often coupled with iron deficiency
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19
Q

How do you diagnose anemia of chronic disease

A

usually needs the presence of chronic infection, inflammation, cancer, microcytic/normocytic anemia, and values for serum transferrin receptor and serum ferritin that are between those typical for iron deficiency and sideroblastic anemia

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20
Q

What is sideroblastic anemia

A

a type of anemia that results from abnormal utilization of iron during erythropoiesis

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21
Q

What is seen in labs in those with anemia of chronic disease

A

normal or ↓ MCV, ↓ TIBC, ↑ Ferritin (high iron stores)

*Increased ferritin because it is not being transported to bone marrow

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22
Q

What is the most common cause of anemia of chronic disease

A

chronic renal failure and anemia from connective tissue disorder: RA, SLE, HIV, CA, cirrhosis, chronic infection

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23
Q

Why does renal failure lead to anemia

A

erythropoiesis impaired because of decreases in EPO production and marrow responsiveness to EPO

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24
Q

How can you treat (or manage) anemia of chronic disease

A

treat underlying disorder, recombinant EPO and iron supplements

*Treat with EPO analog (Epogen, Procrit) if Hgb <10 and stop when Hgb >11 d/t increased chance MI/stroke

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25
Q

What are the two main groups of clotting disorders that occur

A

Hemophilia
VWD

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26
Q

What is Hemophilia A

A

Low factor 8

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27
Q

What is hemophilia B

A

Low factor 9

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28
Q

What is VWD

A

missing protein for platelet function (doesn’t allow proper binding without the protein)

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29
Q

a 30-year-old woman with a recurrent history of nosebleeds and heavy menses. She recently read that taking a baby aspirin was good for the heart. However, ever since she started taking aspirin, she has been experiencing more and more nosebleeds. Her father and paternal uncle similarly have histories of prolonged nosebleeds. Labs show increased PTT, normal PT, and increased bleeding time. What is the likely diagnosis

A

VWD

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30
Q

What is the most common genetic bleeding disorder (autosomal dominant)

A

VWD

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31
Q

How can you differentiate vWF with hemophilia A when both are missing factor 8

A

You can differentiate this from hemophilia by lack of hemarthrosis, small amounts of superficial bleeding, common to have bleeding with minor injury and petechiae.

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32
Q

When there is a decrease in vWF, what clotting factor also get effected

A

factor 8

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33
Q

How do you treat vWD

A

DDAVP (desmopressin) or in cases of excessive bleeding a transfusion of concentrated blood clotting factors containing von Willebrand factor

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34
Q

a 3-year-old boy whose mom is concerned about his prolonged nosebleeds. Ever since he was about 2 years old, he has had multiple episodes of nosebleeds that stopped only after hours. On physical exam, his right elbow is slightly swollen and tender to palpation. There is a family history of unexplained bleeding in the patient’s maternal uncle. Lab results reveal increased PTT that corrects after mixing studies. Lateral radiograph of the knee shows swelling of the soft tissues from blood accumulation in the knee. What is the likely diagnosis

A

Hemophilia

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35
Q

What is the most common form of hemophilia

A

Hemophilia A (factor 8 deficiency)

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36
Q

What is another name for hemophilia B

A

Christmas disease

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37
Q

Who is more likely to be effected by hemophilia B

A

Males –> b/c it is autosomal recessive

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38
Q

With either hemophilia, what will be seen on assay

A

↑ PTT, normal PT and platelets, with ↓ Factor VIII or ↓ Factor IX on assay

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39
Q

How do you treat hemophilia

A

replacement of factor VIII or IX

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40
Q

a 20-year-old healthy male who was treated 4 days ago for an MRSA skin infection with sulfamethoxazole-trimethoprim (Bactrim). The infection is improving, but he is increasingly weak, and his sclera have turned yellow. Today, his hemoglobin is 11 g/ dL (13.5 to 18 g/ dL), and his MCV is 85 (80 to 100 fL); the corrected reticulocyte count is elevated, and he has increased indirect bilirubin and decreased haptoglobin. The peripheral smear demonstrates bite cells and Heinz bodies. What is the likely diagnosis

A

G6PD deficiency

41
Q

What are flare triggers for G6PD deficiency

A

Fava beans, antimalarials, sulfonamides

42
Q

What will be seen on smear with G6PD deficiency

A

Heinz bodies
bite cells

43
Q

Which nationalities are at highest risk for developing G6PD deficiency

A

African American
Middle Eastern
South Asian

44
Q

What is the treatment for G6PD deficiency

A

acute: blood transfusion
Maintenance: Avoid triggers

45
Q

What is virchows triad

A

Stasis
vessel injury
hyper coagulable state

46
Q

What are some hyper coagulable states

A

DIC
Polycythemia vera
HIT
antiphospholipid syndrome
TTP

47
Q

What are some acquired hyper coagulable states

A

malignancy (Trousseau’s syndrome), pregnancy,
nephrotic syndrome,
immobilization,
myeloproliferative disease
and Crohn disease

48
Q

What is the most common hyper coagulable deficiency

A

Factor V leiden

49
Q

What is factor V Leiden

A

procoagulant clotting factor – amplifies the production of thrombin → clot formation

Mutated factor V resistant to breakdown by activated Protein C - results in hypercoagulability

50
Q

How do you diagnose factor V Leiden

A

activated protein C resistance assay (factor V Leiden specific functional assay) - if positive, confirm with DNA testing. Normal PT/PTT

51
Q

How do you treat factor V Leiden

A

LMWH bridge to warfarin; long-term antithrombotic therapy not recommended

52
Q

What is protein C deficiency

A

vitamin K dependent anticoagulant liver protein that stimulates fibrinolysis and clot lysis (inactivates factor V and VIII) – potentiated by protein S

53
Q

How do you diagnose protein C deficiency

A

protein C/S functional assay: decreased protein C / S activity levels

54
Q

How do you treat protein C deficiency

A

heparin and oral anticoagulation for life

*At risk for skin necrosis w/ Warfarin

55
Q

What is Protein S deficiency

A

Protein S is a vitamin K-dependent glycoprotein. It serves as a cofactor for activated protein C, which inactivates procoagulant factors Va and VIIa, reducing thrombin generation

if there is a deficiency, thrombin generation will just continue without anything telling to to stop generating

56
Q

What does antithrombin III deficiency lead to

A

repetitive intrauterine fetal death (IUFD)

Associated with VTE; first episode 20-30 y/o

57
Q

How do you Treat antithrombin 3 deficiency

A

Asymptomatic pt requires anticoagulation only before surgical procedures

Pt with thrombotic events require high dose IV heparin then oral anticoagulation indefinitely

58
Q

What is antiphospholipid antibody syndrome

A

Autoantibodies react against platelet membranes, activating endothelial cells and platelets → complement-mediated thrombosis

often associated with SLE; characterized by thromboses and recurrent spontaneous abortions

59
Q

How do you diagnose antiphospholipid antibody syndrome

A

lupus anticoagulant, anticardiolipin, DRVVT test, prolonged PTT

60
Q

a 39-year-old female presents with concerns about sudden onset nosebleeds and a rash on her legs. She recalls a mild viral illness about three weeks ago. She is otherwise healthy and takes no regular medications. On examination, her oral mucosa is noted to have spontaneous bleeding, and her legs reveal widespread petechiae and a few larger purpura. Her abdomen is soft and nontender, and there is no palpable splenomegaly. Laboratory tests show a platelet count of 30,000/μL (normal 150,000 – 400,000/μL). The peripheral blood smear indicates a decreased number of platelets without clumping. The rest of her complete blood count, including white blood cell count and hemoglobin, is within the normal range. She is started on corticosteroids. What is the likely diagnosis

A

ITP

61
Q

What is ITP

A

Autoimmune reaction to platelets usually after a viral illness (ITP is insidious and chronic)

62
Q

How do you diagnose ITP

A

*Diagnosis of exclusion

Associated with HIV, HCV, SLE, CLL

CBC is normal except for low platelets. (+ Direct Coombs Test)

63
Q

How do you treat ITP

A

Children -> supportive care (IVIG for refractory cases)
Adults -> treat with Prednisone

64
Q

How do you treat iron deficiency anemia

A

*Ferrous sulfate 325mg
Six weeks to correct; six months to replete iron stores; recheck blood counts every 3 months x 1 year
Packed red blood cells when Hgb <8

65
Q

a 35-year-old female presents with fatigue, pallor, and restless legs syndrome. She has a history of heavy menstrual periods. Laboratory tests reveal microcytic, hypochromic anemia with low serum iron and ferritin levels. She is diagnosed with iron deficiency anemia and started on oral iron supplementation. Gynecological evaluation is recommended to address her menorrhagia. What is the likely diagnosis

A

Iron deficiency anemia

66
Q

What is Hodgkins lymphoma

A

painless lymphadenopathy + bimodal age distribution (15-35) and (>60)

67
Q

a 21-year-old male with fever, chills, and night sweats for 1 month. Exam reveals painless enlarged posterior cervical and supraclavicular lymph nodes bilaterally. CBC, HIV, and RPR are normal. Excisional biopsy of lymph node demonstrates Reed-Sternberg cells (owl-eye appearance), What is the likely diagnosis?

A

Hodgkins lymphoma

68
Q

What are common associated symptoms with Hodgkins lymphoma

A
  • Fever, chills, and night sweats for > 1 month.
  • usually localized single group of nodes
    **Associate with EBV (40% of patients)
69
Q

How do you diagnose and treat Hodgkins lymphoma

A

CXR - mediastinal adenopathy +Excisional biopsy of the lymph node shows Reed-Sternberg cells

TX: Chemotherapy, radiation therapy – is highly curable

70
Q

a 55-year-old male presents with a 3-month history of painless, progressive swelling in the left side of his neck. He also reports experiencing night sweats, unintentional weight loss of 10 pounds over the last two months, and a persistent feeling of tiredness. He has no significant past medical history and takes no regular medications. On examination, there is a firm, non-tender lymph node enlargement in the left cervical region. Additional similar nodes are palpable in the axillary and inguinal regions. A CT scan of the neck, chest, abdomen, and pelvis reveals widespread lymphadenopathy. What is the likely diagnosis

A

Non-hodkins lymphoma

71
Q

What are common associated symptoms to look for with non-hodgkins lymphoma

A

immunocompromised (HIV) patient with GI symptoms and painless peripheral lymphadenopathy

Non-contiguous, extranodal spread: GI and skin most common

*Fever/chill/night sweat NOT common

72
Q

how do you treat non-hodgkins lymphoma

A

Treat with rituximab, chemotherapy, radiation therapy

73
Q

a 67-year-old male with a history of recent fracture that occurred incidentally while he was walking and reports fatigue and back pain, along with general achiness and “pain in his bones.” While reviewing his chart, you note he has been treated for multiple infections recently. Recent lab work demonstrated hypercalcemia, increased β2 microglobulin, an increased BUN and Cr as well as a peripheral smear that demonstrated an abnormal stacking of RBCs. Serum protein electrophoresis reveals a monoclonal immunoglobulin spike (M protein), and Urine protein electrophoresis demonstrates Ig light chains (Bence Jones protein). A radiograph of the head demonstrates osteolytic lesions. What is the likely diagnosis

A

Multiple myeloma

74
Q

What is multiple myeloma

A

Cancer of monoclonal plasma cells; MC primary tumor of bone/bone marrow in pt > 50 yo

75
Q

What is the CRAB presentation and what disease is it associated with

A

multiple myeloma

Calcium elevation, renal failure, anemia, and bone lesions

76
Q

How is multiple myeloma diagnosed

A

Monoclonal proteinuria → Ig light chains (Bence Jones Protein)

Blood smear: Rouleaux formation (stacked RBCs)

Radiograph: X-ray showing lytic “punched-out” bone lesions of skull, spine, long bones

77
Q

What is the treatment for multiple myeloma

A

bone marrow transplant

78
Q

a 17-year-old African American male with known sickle cell disease presents with severe pain in his lower back and legs, a typical presentation of a vaso-occlusive crisis. He also reports a low-grade fever. On examination, he is in significant pain but has no signs of infection. He is admitted for pain management with intravenous opioids, hydration, and close monitoring for potential complications. What is the likely diagnosis

A

Sickle cell anemia

79
Q

What are the characteristic presentations of sickle cell anemia

A

African American, pain, family history of blood disorder, Hemoglobin electrophoresis: Hemoglobin S, Blood smear: Sickled RBCs, Howell-Jolly bodies, target cells

80
Q

how do you diagnose sickle cell anemia

A

(+) HgbS on hemoglobin electrophoresis → is definitive

81
Q

How do you treat sickle cell anemia

A

high flow O2, pain control during a crisis, supportive transfusion when Hgb <6

82
Q

What medication may help decrease the occurrence of sickle cell crisis

A

hydroxyurea

83
Q

a 5-year-old child of Southeast Asian descent presents with failure to thrive and severe anemia. The parents report a family history of a similar condition. Laboratory tests reveal microcytic anemia with target cells on the peripheral smear. Hemoglobin electrophoresis shows an elevated level of hemoglobin A2, consistent with beta-thalassemia. The child is referred to a pediatric hematologist for ongoing management, including regular blood transfusions and chelation therapy. What is the likely diagnosis

A

Thalassemia

84
Q

What is thalassemia

A

blood disorder passed down through families (inherited) in which the body makes an abnormal form or inadequate amount of hemoglobin. –>Microcytic hypochromic,

85
Q

What are the descriptors for beta thalassemia

A

-Most severe
- Hemoglobin A2 and F
- Mediterranean descent
- failure to thrive

86
Q

How do you treat beta thalassemia

A

transfusion dependent. iron chelation (deferoxamine)

87
Q

What are the descriptors for alpha thalassemia

A
  • Chinese and Southeast Asians
  • H disease
  • Hemoglobin Bart’s (hydrops fetalis)
88
Q

a 34-year-old woman who arrives at the ED with acute-onset fatigue, fever, palpitations, and blurry vision. On chart review, it is revealed that she was recently diagnosed with AIDS and was on multiple antiretroviral medications. On physical exam, her skin is mildly jaundiced. She has multiple purpuras over her extremities. A complete blood count is significant for a platelet count of 37,000/μL (normal 150,000 – 400,000/μL) and mild anemia. Her peripheral smear reveals schistocytes. She has a negative Coombs test. What is the likely diagnosis

A

TTP

89
Q

What is the difference between TTP and ITP

A

Different from ITP (ITP is insidious and chronic) from TTP, which is an acute febrile disease with multi-organ thrombosis (hence the name “thrombotic” thrombocytopenia)

90
Q

What causes TTP

A

After drugs: Quinidine, cyclosporine & pregnancy

Inhibition of ADAMTS13

91
Q

How will someone with TTP present

A

Purpura and “FAT RN”- Fever, Anemia, Thrombocytopenia, Renal failure, Neurological symptoms

92
Q

How do you treat TTP

A

steroids
plasmapheresis

93
Q

What is HUS

A

↓ Platelets + anemia + renal failure

94
Q

What is HUS associated with

A

E.coli and diarrheal illness in a child)

95
Q

What will the presentation be for HUS

A
  • severe kidney problems
  • will occur after E.Coli or shigella infection
96
Q

Which patient population will be highest risk for folate deficiency

A

alcoholics

97
Q

What is pathognomonic for folate deficiency

A

hypersegmented PMNs

98
Q

What folate agonists should be avoided in those with folate deficiency

A

bactrim, phenytoin, sulfasalazine

Internal Medicine (8 decks)

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