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PANCE > Hematology (4%) > Flashcards

Hematology (4%) Flashcards

1
Q

Acute Lymphocytic Leukemia (ALL)

A

Most common childhood cancer (ALL kids have cancer)
ALL = Anemia, lumps, limp
Bone marrow biopsy = > 20% lymphoblasts
CNS prophylaxis with intrathecal methotrexate

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2
Q

Acute Myeloid Leukemia (AML)

A

Middle aged
Acute Promyelocytic Leukemia (APL) = most common subtype
Bone marrow biopsy = > 20% myeloblasts

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3
Q

Acute Promyelocytic Leukemia (APL)

A 
Auer rods (A-rod plays in the big APL)
Treatment = chemo PLUS Vitamin A
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4
Q

Chronic Lymphocytic Leukemia (CLL)

A 
Older adults (70 yr)
Smudge cells (CLL --> Crushed Little Lymphocytes)
IF asymptomatic --> observe
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5
Q

Chronic Myeloid Leukemia (CML)

A

Phl chromosome = 9 –> 22 translocation
Treatment = tyrosine kinase inhibitors (Imatinib)

Tyrone is a country music lover (CML) and went to concert in Philadelphia on 9-22.

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6
Q

Thrombotic Thrombocytopenic Purpura (TTP)

A 
Severe deficiency of ADAMTS13 --> increase in vWF
FAT RN (fever, anemia, thrombocytopenia, renal failure, neurological symptoms)
Treatment = plasma exchange
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7
Q

Disseminated Intravascular Coagulation (DIC)

A

DDIC = D dimer elevated, dripping (oozing), ill, clots
Increased PT/PTT
Increased D dimer
Decreased fibrinogen

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8
Q

Hemolytic Uremic Syndrome (HUS)

A

HUSS = hamburger, urinary symptoms, shitting, school-aged
E. coli 0157:H7
Elevated serum creatinine

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9
Q

Immune Thrombocytopenic Purpura (ITP)

A 
More common in females (20-40 yo)
Autoantibodies against platelets
Children = after viral infection
Adult = chronic
Diagnostics = isolated thrombocytopenia, + direct Coombs, NO schistocytes
Treatment = steroids, IVIG
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10
Q

Heparin Induced Thrombocytopenia (HIT)

A

Heparin exposure in last 5-10 days
Thrombosis
Thrombocytopenia –> 50% decrease after heparin initiation
Treatment = STOP heparin and START non-heparin anticoagulation (Argatroban)

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11
Q

Low Molecular Weight Heparin

A

Anything that ends in -PARIN

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12
Q

Three Types of Anemia

A

Microcytic (MCV < 80)
Normocytic (MCV 80-100)
Macocytic (MCV > 100)

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13
Q

Etiologies of Microcytic Anemia

A

TICS

  • Thalessemia
  • Iron deficiency
  • Chronic disease
  • Sideroblastic
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14
Q

Etiologies of Normocytic Anemia

A

Chronic disease
Sickle cell
G6PD deficiency
Hereditary spherocytosis

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15
Q

Etiologies of Microcytic Anemia

A

Vitamin B12 deficiency

Folate deficiency

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16
Q

Ferritin

A

Stored iron

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17
Q

Transferrin (TIBC)

A

Binds to and transports iron

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18
Q

HgA

A

Primary global in adults

2 alpha + 2 beta chains

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19
Q

Iron Deficiency Anemia

A

Most common cause of anemia
Etiologies = blood loss and decreased intake/absorption
Diagnostics = decreased iron, decreased ferritin, increased TIBC

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20
Q

Sideroblastic

A 
Accumulation of iron in the mitochondria
Diagnostics = iron increased, ferritin decreased, TIBC decreased
Ringed sideroblasts (SIDE of the O is BLASTed with iron)
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21
Q

Thalessemia

A

Abnormality in global production
Alpha or Beta
Diagnostics = hemoglobin electrophoresis

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22
Q

Alpha Thalessemia

A

1 deletion = asymptomatic
2 deletions = mild anemia
3 deletions = severe anemia (transfusion dependent), HbH
4 deletions = hydros fetalis (incompatible with life), Hb Barts

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23
Q

Beta Thalssemia

A

Minor (1 deletion) or major (2 deletions)

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24
Q

Beta Thalessemia Minor

A

Mild anemia

Usually asymptomatic

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25
Q

Beta Thalessemia Major

A 
Severe anemia
Extramedullary hematopoiesis
Frontal bossing
Hair on end appearance on skull x-ray
Chipmunk facies
Diagnostics = Increased HgA2, HbF

Beta fish are the BOSS and their fins have hair on end appearance

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26
Q

Anemia of Chronic Disease

A

Microcytic OR normocytic
Etiologies = RA, CKD, IBD, DM, malignancy
Diagnostics = iron decreased, ferritin increased, TIBC decreased

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27
Q

Sickle Cell

A

Most common in African Americans
Pathophysiology = valine replaces glutamic acid
(VAL kicks butt with her big GLUTS)
Diagnostics = hemoglobin electrophoresis –> HbS, decreased HgA
Treatment = hydroxyurea (for prevention)

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28
Q

G6PD Deficiency

A

Pathophysiology = decreased G6PD = no conversion of NADP to NADPH
Symptoms present under stress (G5PD):
- Green at the gills (infection)
- Fava beans
- Primaquine
- Dapsone
X-linked recessive
Diagnostics = peripheral smear –> Heinz bodies, bite cells
(STRESS makes me eat BITES of fries with HEINZ ketchup)

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29
Q

Hereditary Spherocytosis

A

Pathophysiology = dysfunctional RBC skeleton proteins –> increased fragility of RBCs and alteration of biconcave to sphere-shaped RBCs
Clinical presentation = splenomegaly, jaundice
Diagnostics = MCHC elevated (36+), EMA binding > osmotic fragility

30
Q

Vitamin B12 Deficiency

A

Pernicious anemia = most common cause
Clinical presentation = neurological symptoms
Diagnostics = MMA increased (you must B12 to watch MMA)

31
Q

Pernicious Anemia

A

Autoimmune destruction of gastric parietal cells
Problem with parietal cells = problem with intrinsic factor (IF)
IF responsible for transporting vitamin B12

32
Q

Folate Deficiency

A

Etiologies = diet (chronic alcoholics, elderly) and pregnancy
Clinical presentation = NO neurological symptoms
Diagnostics = MMA normal

33
Q

Hemophilia A

A

Factor VIII deficiency
Male
PTT prolonged
Treatment = DDAVP and factor VIII infusions

34
Q

Hemophilia B

A 
Factor IX deficiency
Male
PTT prolonged
Factor IX infusions
NO DDAVP*
35
Q

von Willebrand Disease

A

Most common inherited bleeding disorder
Decrease in quality/quantity of vWF
Clinical presentation = mucocutaneous bleeding, excessive bruising
Treatment = DDAVP, vWF concentrates

36
Q

Factor V Leiden

A

Most common cause of inheritable hypercoaguable state
Single point mutation in factor V
Clinical presentation = VTE, miscarriages
Treatment = anticoagulation

37
Q

Protein C and S Deficiency

A

Protein S and C –> Stop Clots
Deficiency = hypercoaguable state
Clinical presentation = VTE, warfarin-induced necrosis
Treatment = anticoagulation, protein C concentrate

38
Q

Common Pathway

A

Factors I, II, V, X

39
Q

Extrinsic Pathway

A

Factors III, VII

PT (play tennis outside)

40
Q

Intrinsic Pathway

A

Factors VII, IX, XI, XII

PTT (play table tennis inside)

41
Q

Hodgkin Lymphoma (6 B’s)

A 
B cell malignancy
B symptoms
Bound in place (contiguous spread - better prognosis)
Binucleated cells (Reed-Sternberg)
Bimodal age distribution
eBv infection
42
Q

Most common Hodgkin Lymphoma

A

Nodular sclerosing (70%)

43
Q

Hodgkin Lymphoma Treatment

A

Chemo/radiation (ABVD)

44
Q

Non Hodgkin Lymphoma

A 
ABSENCE of Reed-Sternberg Cells
Extranodal involvement (poor prognosis)
45
Q

Most Common Extranodal Site for Non Hodgkin Lymphoma

A

GI tract

46
Q

Non Hodgkin Lymphoma Treatment

A

Chemo/radiation (R-CHOP)

47
Q

Most common type of Non Hodgkin Lymphoma

A

Diffuse Large B Cell

48
Q

Burkitt’s Lymphoma

A

Starry sky appearance
EBV
Jaw/facial bone tumor
Endemic Africa

Guy holding a control bar while kite surfing at night on the coast of Africa when Jaws appears.

49
Q

Lymphoma Diagnostics

A

Excisional biopsy

PET/CT scan

50
Q

Multiple Myeloma - Pathophysiology

A

Proliferation of a single clone of plasma cell (IgG, IgA)

51
Q

Multiple Myeloma - Risk Factors

A

> 65 yo
African American
Men

52
Q

Multiple Myeloma - Clinical Presentation

A

BREAK

  • Bone pain
  • Recurrent infections
  • Elevated Ca++
  • Anemia
  • Kidney injury

CRAB

  • Ca++ elevated
  • Renal impairment
  • Anemia
  • Bone pain
53
Q

Multiple Myeloma - Diagnostics

A

Serum protein electrophoresis –> monoclonal spike protein
Urine protein electrophoresis –> Bence-Jones proteins
Skull x-ray –> “punched out” lytic lesions
Bone marrow aspiration –> plasmacytosis (> 10%)

54
Q

Multiple Myeloma - Treatment

A

Autologous stem cell transplant

55
Q

Polycythemia Vera - Pathophysiology

A

Overproduction of all 3 myeloid stem cell lines (primarily RBCs)
JAK2 mutation

56
Q

Polycythemia Vera - Risk Factors

A

50-60 yo

Men

57
Q

Polycythemia Vera - Clinical Presentation

A

Pruritus –> especially after hot shower/bath
Hepatosplenomegaly
Facial flushing

58
Q

Polycythemia Vera - Diagnostics

A

3 major or 2 minor plus 1 major

Major:

  • Increased RBC mass
  • Bone marrow biopsy –> hypercellularity
  • Presence of JAK2 mutation

Minor:

  • Decreased serum EPO
  • Increased leukocyte alkaline phosphatase
  • Normal O2 sat
  • Iron deficiency
  • Increased granulocytes, WBCs, platelets, B12
59
Q

Polycythemia Vera - Treatment

A

Phlebotomy
Low dose aspirin
IF high risk = hydroxyurea, ruxolitinib

60
Q

Myelodysplastic Syndrome (MDS)

A

Preleukemic disorder
Abnormal differentiation of cells of the myeloid cell line
> 65 yo
Clinical presentation = asymptomatic pancytopenia
Diagnostics:
- CBC with peripheral smear –> decrease in 1+ myeloid cell line
- Bone marrow biopsy –> dysplastic, increased myeloblasts with < 20% pseudo-pelter-Huet cells

61
Q

Leukopenia

A

Decreased WBCs
Agranulocytosis –> may be caused by methimazole
Causes = viruses, chemo, steroids, SLE, clozapine
CBC = WBC > 3.7, neutropenia, ANC < 1.5
Treatment = discontinue causative agent

62
Q

Hereditary Hemochromatosis

A

Excess iron deposition in heart, liver, pancreas, endocrine organs
C282Y HFE
Decreased hepcidin = Increased intestinal iron absorption
Clinical presentation = bronze/metallic skin
Diagnosis = liver biopsy, increased hemosiderin
Treatment = phlebotomy

63
Q

Autoimmune Hemolytic Anemia

A

Increased destruction of erythrocytes due to presence of anti-erythrocyte antibodies (AEA)
Clinical presentation = asymptomatic, fatigue, SOB, pallor, jaundice
Treatment = corticosteroids, Ig/splenectomy if refractory

64
Q

Autoimmune Hemolytic Anemia - Diagnostics

A 
Decreased Hgb, Hct
Increased reticulocytes
Increased LDH
Decreased haptoglobin
Increased indirect bilirubin
\+ direct Coombs
65
Q

Lead Poisoning - Pathophysiology

A

Acquired sideroblastic anemia

< 6 yo

66
Q

Lead Poisoning - Clinical Presentation

A

Neurologic:

  • Ataxia
  • Fatigue
  • Learning disabilities
  • Difficulty concentrating
  • Peripheral neuropathy (wrist/foot drop)

GI:
- Lead colic –> intermittent abdominal pain, V, loss of appetite, constipation

67
Q

Lead Poisoning - Diagnostics

A

Serum lead > 10 mcg/dL
Peripheral smear –> microcytic hypo chromic anemia, basophilic stippling
Bone marrow biopsy –> ringed sideroblasts
X-rays –> lead lines

68
Q

Lead Poisoning - Treatment

A 
Removal of source
IF moderate (45-69 mcg/dL) --> succiner
69
Q

Hemolytic Anemias - Diagnostics

A 
Increased reticulocyte count
Increased LDH
Increased indirect bilirubin
Decreased haptoglobin
Decreased Hct, Hgb
70
Q

Pernicious Anemia

A 
Pathophysiology = autoantibodies against intrinsic factor
Diagnostics = + schilling test, MCV > 100, hyperhsegmented neutrophils, decreased IF, decreased parietal cell antibodies
Treatment = B12 IM monthly

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