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PANCE > Hematology 3% > Flashcards

Hematology 3% Flashcards

1
Q

Multiple myeloma shows ____ RBCs.

A

Rouleaux formation d/t increase plasma proteins

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2
Q

B12 and Folate deficiency presents as (macro/micro)cytic anemia and ____.

A

MACROcytic anemia

hypersegmented neutrophils

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3
Q

Heinz bodies =

Seen in ____

A

denatured Hgb in cells

Thalassemias (alpha thalassemia intermedia)
G6PD Deficiency

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4
Q

Howell-Jolly Bodies seen in ____.

A

Splenectomized pts

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5
Q

Target cells seen in ___.

A

Sickle cell disease
Thalassemia
Hgb SC

Severe Fe deficiency
Asplenia
Liver disease

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6
Q

Echinocytes (a.k.a. ____) seen in ____ (3)

A

Burr cells

Uremia *
Pyruvate kinase deficiency
Hypophosphatemia

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7
Q

Acanthocytes (a.k.a. ___) seen in ____ (5)

A

Spur cells

Liver disease (ETOHic cirrhosis) 
Post splenectomy
Thalaseemia
Autoimmune Hemolytic Anemia
Renal Disease
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8
Q

Reticulocytosis =

Seen when ___

A

Immature RBC

Increased blood loss
Increased RBC destruction (hemolytic anemia)

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9
Q

Fe deficiency anemia
(increase/decrease) serum Fe
(increase/decrease) ferritin
(increase/decrease) TIBC

A

decrease serum Fe
decrease ferritin
INCREASE TIBC

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10
Q 
Anemia of Chronic Disease
(increase/decrease) serum Fe
(increase/decrease) ferritin
(increase/decrease) TIBC
(increase/decrease) Haptoglobin
(increase/decrease) CRP
(increase/decrease) Hepcidin
A
  • decrease serum Fe
  • INCREASE ferritin
  • DECREASE TIBC
  • Increase Haptoglobin = binds free hemoglobin reducing iron availability for microbes
  • Increase CRP
  • Increase Hepcidin = prevent iron release from macrophages –> reducing iron availability for microbes
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11
Q

Low reticulocytes seen in ____

A

Fe, B12, Folate deficiencies

Anemia of chronic disease

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12
Q

High reticulocytes seen in ____

A

Blood loss

Hemolytic anemias

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13
Q

Indirect hyperbilirubinemia is associated with ___.

Direct hyperbilirubinemia is associated with ___.

A

Indirect: Jaundice

Direct: dark urine b/c water soluable

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14
Q 
Hemolytic anemia:
(increase/decrease) reticulocytes
(increase/decrease) LDH
(increase/decrease) indirect bilirubin
(increase/decrease) haptoglobin
A

Increase reticulocytes
Increase LDH = enzyme in RBCs –> RBC destruction –> increase LDH
Increase indirect bilirubin
DECREASE Haptoglobin = increase RBC destruction –> increased free Hgb –> haptoglobin binds to free Hgb –> haptoglobin stores used up

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15
Q

Alpha Thalassemia:

Hgb ratio

A

Normal Hgb ratios of HgbA, A2 and F

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16
Q

Beta Thalassemia:

Hgb ratio

A

Decreased HgbA
Increased HgbA2
Increased HbgF

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17
Q

T/F: TTP and HUS can be distinguished via abnormal coag labs (prolonged PT and PTT).

A

False. Both have normal coags, can’t be distinguished via labs.

Prolonged PT and PTT seen in Disseminated Intravascular Coagulation (DIC)

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18
Q

TTP presentation

A 
Thrombocytopenia
Hemolytic anemia
Kidney damage 
Neuro sx**
Fevers**
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19
Q

HUS presentation

A

Thrombocytopenia
Hemolytic anemia
Kidney damage

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20
Q

“Dark urine worse in AM”

A

Paroxysmal nocturnal hemoglobinuria

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21
Q

Schilling test used to diagnose ____.

Other findings (3)

A

Pernicious Anemia (B12 deficiency)

+ Intrinsic factor ab
Parietal cell ab
Increased gastrin levels

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22
Q

B12 is absorbed in ____

Folate is absorbed in ___

A

B12: ileum
Folate: jejunum

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23
Q

Watch for signs of ____ when giving B12 replacement

A

HYPOkalemia

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24
Q

T/F: Folate deficiency causes pallor, glossitis, stomatitis and neurologic sx (peripheral neuropathy, spinal cord demyelination** and degeneration)

A

False. B12 causes neurological symptoms, NOT folate. Otherwise, both present similarly.

Neurologic sx of B12 deficiency: peripheral neuropathy, ataxia, weakness, vibratory, sensory and proprioception deficits, DECREASED DTR

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25
Q

T/F: Replacing folate in pts w/ B12 deficiency will correct anemia but worsen neuro sx.

A

True

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26
Q

Microcytic anemia w/ normal/increased Fe or no response to Fe tx =

A

Thalassemia

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27
Q

HgbA =
HgbA2 =
HgbF =

A

HgbA = aabb
HgbA2 = aadd
HgbF =aagg

a= alpha
b= beta
d= delta
g = gamma
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28
Q

What type of thalassemia?

  1. normal Hgb ratio
  2. Increased HgbA2, increased HgbF, decreased HgbA
  3. Increased HgbA2, increased HgbF (90%), little or no HgbA
A
  1. Alpha thalassemia (mior, intermedia, major)
  2. Beta thalassemia minor
  3. Beta thalassemia major (Cooley’s)
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29
Q

Hgb Barts seen in ___

A

alpha thalassemia major (Hydrops fetalis)
=gamma tetramers

Associated w/ stillbirth, or death soon after

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30
Q

Deferoxamine

A

Iron chelating agents

Tx of severe anemia, Apha/beta thalassemia major

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31
Q

Pts with beta-thalassemia major will become symptomatic at age ___.

A

6 months (when HgbF declines)

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32
Q

Plummer Vinson syndrome =

A

Dysphagia + esophageal webs + atrophic glossitis + Fe deficiency

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33
Q

Anemia of chronic disease: (macro/normo/micro)chromic (macro/normo/micro)cytic anemia

Tx:

A

Normochromic, normocytic anemia

Tx: Erythropoietin-alpha

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34
Q 
G6PD Deficiency:
Peripheral smear shows \_\_\_\_
Labs:
(increased/decreased) reticulocytes
(increased/decreased) (indirect/direct) bilirubin
(increased/decreased) haptoglobin
A

Schistocytes
Heinz bodies

Increased reticulocytes
Increased indirect bilirubin
Decreased haptoglobin

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35
Q

Sickle cell disease dx:
Hemoglobin electrophoresis
Peripheral smear

A

Increased HgbF, HgbS, NO HgbA

Target cells, sickled erythrocytes, Howell-Jolly bodies (functional asplenia)

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36
Q

Sickle cell disease tx:
Pain control
Severe pain crisis
Immunization against ___

A

Pain control:
IV hydration and oxygen 1st step in pain crisis
Hydroxyurea: SEVERE pain crisis

Immunize against: S. pneumococcus, H. Influenza B, N. Meningococcus
(SHiN)

37
Q

Do NOT give ____ in Sickle Cell Disease pain crisis.

A

Meperidine (Demerol)

May lead to seizures and renal failure

38
Q

Signs of Sickle cell disease present at age ____.
MC 1st presentation =
Aplastic crisis associated w/ ___.
Osteomyelitis MC caused by ___.

A

6 months
Dactylitis
Aplastic crisis: Parvovirus B-12
Osteomyelitis: Salmonella

39
Q

PTT measures ___ pathway. Involves ___ factors.

A

intrinsic and common pathway

Factors 1, 2, 5, 8, 9, 10, 11, 12

40
Q

Warfarin therapy causes prolonged (PT/PTT)

Heparin therapy causes prolonged (PT/PTT)

A

Warfarin: PT
Heparin: PTT

41
Q

PT measures ___ pathway. Involves ___ factors.

A

Extrinsic and common pathway

Factors 1, 2, 5, 7, 10

42
Q

DIC causes prolonged (PT/PTT)
Vit K deficiency causes prolonged (PT/PTT)
vWD causes prolonged (PT/PTT)
Hemophilia A/B causes prolonged (PT/PTT)

A

DIC causes prolonged PT AND PTT
Vit K deficiency causes prolonged PT
vWD causes prolonged PTT
Hemophilia A/B causes prolonged PTT

43
Q

Heparin overdose antidote =

Warfarin overdose antidote =

A

Heparin OD = Protamine sulfate

Warfarin OD = Vitamin K

44
Q

Antibody against ADAMTS13 seen in ____.
PT/PTT:

Tx:

A

Thrombotic Thrombocytopenic Purpura (TTP)

Normal PT/PTT

Tx: Plasmapheresis ***
Immunosuppression: steroids, cyclophosphamides

45
Q

Difference between TTP and HUS presentation

A

Kidney failure more common in HUS

Fever and neurologic sx (HA, CVA, AMS) in TTP, NOT HUS

46
Q

Suspect ___ if renal failure in children with diarrhea prodrome

A

Hemolytic Uremic Syndrome

HUS usually preceded by Enterohemorrhagic E. Coli 0157:H&, Shigella, or Salmonella gastroenteritis

47
Q

Platelet activation by exotoxins seen in ___.

PT/PTT:

A

Hemolytic Uremic Syndrome

Normal PT/PTT

48
Q

T/F: Antibiotics are useful in treatment of HUS.

A

False. May actual worsen condition d/t increased verotoxin release w/ cell lysis.

49
Q 
Disseminated Intravascular Coagulation (DIC) 
(increase/decrease) PTT
(increase/decrease) PT
(increase/decrease) INR
(increase/decrease) fibrinogen
A

Increase PTT/PT/INR
Decrease fibrinogen

Also increased D-dimer

50
Q

Tx of Disseminated Intravascular Coagulation

A

Fresh Frozen Plasma: if severe bleeding
Cryoprecipiate: replace fibrinogen
Platelet transfusion: ONLY if <20K

51
Q

T/F: Idiopathic (Autoimmune) Thromobocytopenic Purpura presents with mucocutaneous bleeding (purpura, bruises, petechiae, bullae) and splenomegaly.

A

False. NO splenomegaly

52
Q

Acute ITP seen in MC___

A

children/boys after viral infection –> self limited

53
Q

Tx of ITP

A

Children: observation +/- IVIG
Adults: Corticosteroids –> IVIG –> splenectomy if refractory

54
Q

T/F: Petechiae is commonly seen in Hemophilia A/B.

A

False. Not common in Hemophilia A/B. Common in Von Willebrand Disease.

55
Q

Von Willebrand Disease:
Bleeding time and PTT prolongation worsen with ___.

Gold standard dx:

A

worsen with aspirin

Decreased Ristocetin activity test: No platelet aggregation w/ Ristocetin

56
Q

Von Willebrand Disease:
Prolonged (PTT/PT)
(Does/does not) correct w/ mixing study.

A

PTT

DOES correct

57
Q

Tx of Type I Von Willebrand Disease
Mild:
Moderate:
Severe:

A

Mild: NO treatment
Moderate: DDAVP
Severe: Cryoprecipitate

58
Q

Reed sternberg cells is pathognomonic for ____.

A

Hodgkin’s Lymphoma

59
Q

T/F: Hodgkin lymphoma is more difficult to cure than Non-Hodgkin lymphoma.

A

False. Hodgkin lymphoma is highly curable compared to NHL.

60
Q

Hodgkin or Non-Hodgkin lymphoma:

  1. Upper body lymph nodes
  2. MC in >50 y/o
  3. Associated w/ clonal B-cell proliferation
  4. Extra nodal sites are common
A
  1. Upper body lymph nodes: HL
    Peripheral lymph nodes: NHL
  2. MC in >50 y/o: NHL
    Bimodal 20 y/o and > 50 y/o: HL
  3. Associated w/ clonal B-cell proliferation: HL
  4. Extra nodal sites are common: NHL
    Pel-Ebstein fevers: HL
61
Q

MC indolent Non-hodgkin lymphoma

A

Follicular: Not curable generally

62
Q

MC aggressive Non-hodgkin lymphoma

A

Diffuse Large B cell: curable w/ chemo

63
Q

Clinical manifestation of Multiple Myeloma

A 
"BREAK"
Bone pain
Recurrent infections
Elevated calcium
Anemia
Kidney Failure
64
Q

Increased risk of multiple myeloma seen in ___

A

> 65 y/o
African Americans
men

65
Q

Single clone of plasma cells, accumulate in bone marrow interrupting marrow’s normal cell production.

A

Multiple myeloma

Increased monoclonal Ab (esp IgG, IgA)

66
Q

Dx of Multiple Myeloma

A

Serum Protein Electrophoresis: monoclonal protein spike
Urine Protein Electrophoresis: Bence-Jones proteins

Rouleaux formation, Increased ESR
Skull xray: Punched out lesions

Bone scan NOT helpful

67
Q

Bence Jones proteins seen in ___

A

Multiple Myeloma

68
Q

Philadelphia Chromosome = translocation between chromosome ___, causing fusion gene ___.

Seen in ___.

A

9 and 22
gene bcr-abl

CML

69
Q

MC childhood leukemia malignancy

Bone marrow shows:

A

ALL

Hypercellular > 20% blasts

70
Q

Auer rods seen in ___

71
Q

MC form of leukemia in adults:

MC acute leukemia in adults:

A

MC form of leukemia in adults: CLL

MC acute leukemia in adults: AML

72
Q

Tumor lysis syndrome caused by ___.

Management:

A

chemotx initiation d/t large number of cells being destroyed
- Hyperuricemia, HyperK, HypoCa, HyperPhosphate, acute renal failure

Management: Allopurinol

73
Q

Acquired myeloproliferative d/o w/ overproduction of all 3 stem cell lines.

A

Polycythemia Vera

74
Q

Polycythemia Vera:
(increase/decrease) Hematocrit/RBC
(increase/decrease) erythropoietin levels
(increase/decrease) WBCs
(increase/decrease) Leukocyte alkaline phosphatase
(increase/decrease) B-12

A 
Increased Hematocrit/RBC
Decreased erythropoietin levels
Increased WBCs
Increased Leukocyte alkaline phosphatase
Increased B-12
75
Q

Polycythemia Vera tx

A

Phlebotomy**

Hydroxyurea

76
Q

Primary erythrocytosis is distinguished from secondary erythrocytosis by ____.

A

normal WBC/platelets in 2ry

Secondary d/t:
Hypoxia (ex COPD)
Pathologic (renal dz)
Reactive polycythemia (normal RBCs mass in setting of decreased plasma volume)

77
Q

C282Y HFE genotype seen in ____

A

hereditary hemochromatosis

78
Q 
Hereditary hemochromatosis
(increase/decrease) serum iron
(increase/decrease) serum transferrin saturation
(increase/decrease) ferritin
(increase/decrease) TIBC
A

INCREASED iron, transferrin, ferritin

NORMAL/DECREASED TIBC

79
Q

Gold standard of dx for hereditary hemochromatosis

Tx

A

Liver biopsy: increased liver parenchymal hemosiderin

Tx: Phlebotomy

80
Q

Coagulopathy of Advanced Liver Disease:
(increase/decrease) PT
(increase/decrease) albumin
(increase/decrease) PTT

Tx:

A

Increased PT
Decreased albumin
Increased PTT (in advanced disease)

Tx: Fresh Frozen Plasma

81
Q

T/F: Increased association w/ EBV seen in Non-Hodgkins Lymphoma

A

False. In Hodgkins Disease. Rare in most NHL.

82
Q

Antibodies against RBC’s surface causing increased RBC destruction by macrophages, spleen and complement

Dx:

A

Autoimmune Hemolytic Anemia

Dx:
+ Direct Coombs test
Cold agglutinin study
Peripheral smear: microspherocytes, polychromasia, agglutination of RBCs

83
Q

+ Coombs distinguishes ____

A

Autoimmune Hemolytic Anemia from Hereditary Spherocytosis

84
Q

Warm agglutinin =___ , causes ___. Etiology:
Cold agglutinin =___, causes ___. Etiology:

Seen in ___

A

Warm = IgG Ab –> SPLENIC macrophage RBC destruction via phagocytosis
Etiology: SLE*** MC (Autoimmune d/o)

Cold = IgM Ab –>INTRAVASCULAR complement-mediated RBC lysis, especially in COLD temperatures
Etiology: May follow infection (Mycoplasma, EBV)

Seen in Autoimmune Hemolytic Anemia

85
Q

Tx of Autoimmune Hemolytic Anemia

A

Warm: Steroids**, immunosuppressants, splenectomy (removes site of RBC destruction)

Cold: avoid cold exposure**, warm fluids. Rituximab

86
Q

Osmotic fragility test used to dx ____

Coombs test +/-
Peripheral smear:
(Hyper/normo/hypo)chromic (macro/normo/micro)cytosis

A

Hereditary spherocytosis

Coombs test negative
Smear: 80% spherocytes, HypERchromic MICROcytosis

87
Q

Hereditary spherocytosis:
Autosomal ___ intrinsic hemolytic anemia
Causes defect in ____ –> ____ and ___ –> Increased RBC hemolysis in ___.

A

Autosomal dominant

Defect in RBC membrane/cytoskeleton –> cell fragility and sphere-shaped RBCs –> hemolysis in SPLEEN

88
Q

Treatment of choice of Hereditary spherocytosis in severe disease

A

Splenectomy*

Folic acid not curative but helpful

89
Q

Von Willibrand disease will have increased ____.

A

Bleeding time

PTT

PANCE (20 decks)

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