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Hematology Flashcards

1
Q

What ethnicity most commonly has hemophilia C?

A

Ashkenazi Jews

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2
Q

What is the function of vWF?

A

facilitates attachment and aggregation of platelets, forming a plug

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3
Q

What is the inheritance pattern of hemophilia A? B?

A 
A = XLR
B = XLR
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4
Q

What is the MOA of heparin?

A

activates antithrombin

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5
Q

What is the MOA of argatroban, bivalirudin, and dabigatran?

A

Direct thrombin inhibitors (factor II)

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6
Q

What is MOA of aminocaproic acid?

A

Inhibits tPA

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7
Q

What is the MAO of tPA and other thrombolytics?

A

Inhibition of the conversion of plasminogen to plasmin

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8
Q

What does PTT measure? PT?

A 
PTT = intrinsic
PT = extrinsic
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9
Q

Which is prolonged PT or PTT with hemophilia A? B?

A

Both PTT

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10
Q

Describe the mixing study for screening for hemophilia?

A

Add in normal blood to patient’s blood. If blood clots, (since factors are now present), this strongly suggests hemophilia

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11
Q

What factor levels indicate the need for an immediate transfusion of platelets for hemophilia? What about for DDAVP?

A

Less than 1%

More than 5% = DDAVP

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12
Q

What is the inheritance pattern of vWF disease?

A

AD

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13
Q

What is the most common inherited bleeding disorder?

A

vWF disease

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14
Q

What factor levels are decreased in vWF disease?

A

VIII

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15
Q

What is the result of a ristocetin cofactor assay with vWF disease?

A

Decreased

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16
Q

What is the treatment for vWF disease?

A

DDAVP

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17
Q

What will coagulation studies show with vWF disease?

A

Increased bleedings time (from platelet dysfunction) and increased PTT (from loss of factor VIII)

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18
Q

What is the pathophysiology of HIT (heparin induced thrombocytopenia)

A

Administration of heparin induces the body to form antibodies to platelets, causing a paradoxical hypercoagulable state

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19
Q

What is antiphospholipid antibody syndrome associated with?

A

SLE

RA

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20
Q

Hospitalized patient on a heparin drip who develops thrombocytopenia should be suspicious for what disorder?

A

HIT

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21
Q

What is the treatment for HIT?

A
  • D/c heparin

- Start argatroban or lepirudin

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22
Q

What must women with factor V leiden avoid?

A

OCPs

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23
Q

What is the pathophysiology DIC?

A

Deposition of fibrin in small blood vessels, leading to activation of the coag pathways, causing thrombosis and end-organ damage

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24
Q

What is the acute presentation of DIC?

A
  • Bleeding from venipuncture sites

- Ecchymoses and petechiae

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25
Q

What is the chronic presentation of DIC?

A
  • Bruising and bleeding
  • thrombophlebitis
  • Renal dysfunction
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26
Q

What is the treatment of DIC?

A

Transfuse RBCs, platelets, and manage shock

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27
Q

What is the major difference between DIC and liver disease in terms of coag results?

A

Unlike liver disease, factor VIII is depressed

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28
Q

What is the pathophysiology of thrombotic thrombocytopenic purpura (TTP)?

A

Deficiency of vWF enzyme (ADAMS-13) results in abnormally large vWF multimers, that aggregate platelets and crease platelet microthrombi

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29
Q

What are the five major s/sx of TTP?

A
  • Thrombocytopenia
  • microangiopathic hemolytic anemia
  • Neurological changes
  • Impaired renal function
  • Fever
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30
Q

What will a PBS show with TTP?

A

Schistocytes

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31
Q

What is the pathophysiology of HUS?

A

E.coli O157:H7 infection causes renal dysfunction, resulting in uremia and thus platelet dysfunction.

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32
Q

What is the treatment of TTP?

A

Plasma exchange

Steroids

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33
Q

Why are platelet transfusions contraindicated in TTP?

A

Additional platelets will be consumed and further the activation cascade

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34
Q

What is the pathophysiology of idiopathic thrombocytopenic purpura?

A

IgG antibodies form against the patient’s platelets, cause splenic destruction

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35
Q

What diseases are associated with ITP?

A

SLE
HIV
CA
HCV

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36
Q

What is the usual presentation of ITP?

A

Asymptomatic

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37
Q

What is the acute presentation of ITP?

A

Abrupt onset of hemorrhagic complications following a viral illness

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38
Q

What is the chronic presentation of ITP?

A

Insidious onset of symptoms or incidental thrombocytopenia

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39
Q

True or false: ITP is a diagnosis of exclusion

A

True

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40
Q

What is the treatment for ITP?

A

If platelets more than 30,000, nothing

If not, then corticosteroids or IVIG

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41
Q

What is the treatment for symptomatic ITP when pharmacotherapy fails?

A

Splenectomy

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42
Q

What are the PE findings of Fe deficiency anemia?

A

Glossitis
Cheilosis
Koilonychia

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43
Q

What is the role of ferritin?

A

Stores of Fe in the body

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44
Q

What does a large RDW indicate?

A

Irregular erythropoiesis

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45
Q

What is the treatment for Fe deficiency anemia?

A

Replace Fe orally for 4-6 months.

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46
Q

What are the four major causes of microcytic anemias?

A
  • Fe deficiency
  • Thalassemias
  • Chronic disease
  • Sideroblastic anemia
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47
Q

What happens to ferritin levels in anemia of chronic disease?

A

Goes up, but serum Fe stores go down

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48
Q

What happens to TIBC in anemia of chronic disease?

A

Decreases

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49
Q

What happens to TIBC in Fe deficiency anemia?

A

Increases

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50
Q

What happens to RDW with Fe deficiency anemia vs anemia of chronic disease?

A

Increases with Fe deficient

Normal with ACD

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51
Q

What happens to serum transferrin receptors with Fe deficiency anemia vs anemia of chronic disease?

A

Increase with Fe deficiency

Normal in ACD

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52
Q

What are the drugs/chemicals that can cause sideroblastic anemia?

A
  • INH
  • Amphenicol
  • Pb
  • EtOH
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53
Q

What is the pathophysiology of sideroblastic anemia?

A

Inhibition of heme synthesis causes build up of Fe around the nucleus of cells

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54
Q

How can you differentiate folate vs B12 deficiency?

A

Folate deficiency will have only elevated homocysteine, whereas B12 has both elevated levels of homocysteine, and methylmalonic acid

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55
Q

What are the bone marrow findings of megaloblastic anemias?

A

Hypersegmented PMNs

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56
Q

What are the steps of the Schilling test?

A

measures the absorption of cobalamin via ingestion of radiolabeled cobalamin with and without intrinsic factor. The patient is given an unlabeled B12 IM shot to saturate B12 receptors in the liver and an oral challenge of radiolabeled B12. The radiolabeled B12 will pass into the urine if properly absorbed

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57
Q

What is the fish tapeworm notorious for causing B12 deficiency?

A

Diphyllobothrium latum

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58
Q

What is the function of haptoglobin, and what happens to levels of it with hemolytic anemia?

A

Binds free Fe in the blood.

Decreased levels in hemolytic anemia 2/2 binding of now free Fe

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59
Q

What are the PBS findings of G6PD deficiency?

A

Bite cells

Heinz bodies

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60
Q

What is the pathogenesis of PNH?

A

PNH is a deficiency in GPI-anchor molecules that keep CD55/CD59 attached to cells, resulting in hemolysis by complement.

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61
Q

What is the best diagnostic modality to detect PNH?

A

CD55/CD59 flow cytometry

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62
Q

What is the pathogenesis of hereditary spherocytosis?

A

Autosomal dominant defect or deficiency in spectrin or ankyrin,

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63
Q

What is the best diagnostic modality to detect hereditary spherocytosis?

A

Osmotic fragility test

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64
Q

What type of anemia is had with hereditary spherocytosis?

A

Extravascular hemolytic anemia

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65
Q

What is the treatment for hereditary spherocytosis?

A

Splenectomy

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66
Q

What is the inheritance pattern of sickle cell disease?

A

AR

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67
Q

What are the three major vaccinations that should be given prophylactically to asplenic patients?

A

Pneumovax
HiB
Meningococcal

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68
Q

What extremity findings may be present in children with sickle cell disease?

A

dactylitis

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69
Q

What organ dysfunction can be caused by sickle cell?

A

Autosplenectomy
Renal
Lungs

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70
Q

What is acute chest syndrome?

A

a vaso-occlusive crisis of the pulmonary vasculature commonly seen in patients with sickle cell anemia. This condition commonly manifests with pulmonary infiltrate on a chest x-ray, and is preceded by a lung infection

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71
Q

What virus classically causes an aplastic crisis with sickle cell disease?

A

Parvovirus B19

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72
Q

What is the treatment for acute chest syndrome?

A

Abx

Blood transfusion

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73
Q

What are the PBS findings associated with sickle cell? (2)

A
  • Sickle cells

- Howell-Jolly bodies (purple inclusion bodies)

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74
Q

What is the reasoning behind using hydroxyurea in sickle cell disease?

A

Increases HbF production, leading to less sickling

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75
Q

What antibody type is associated with warm and cold hemolytic anemia respectively?

A 
Warm = IgG
Cold = IgM
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76
Q

What can cause warm autoimmune hemolytic anemia?

A

SLE

CLL

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77
Q

What can cause cold autoimmune hemolytic anemia?

A

Mycoplasma pneumoniae

Mono

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78
Q

What is the diagnostic modality of choice for autoimmune hemolytic anemia?

A

Direct coomb’s test

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79
Q

What is the treatment for severe warm autoimmune hemolytic anemia?

A

Steroids

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80
Q

What is the MOA of rituximab?

A

Anti-CD20 antibody

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81
Q

Both AIHA and hereditary spherocytosis can present with spherocytes and positive osmotic fragility tests, but only (____) will have a ⊕ direct Coombs test.

A

AHIA

82
Q

Which has four and which two genes: beta or alpha parts of Hb?

A 
Alpha = 4
Beta = 2
83
Q

What ethnicities usually develop thalassemias?

A

African
Middle eastern
Asians

84
Q

What will Fe studies show with thalassemias?

A

Normal

85
Q

What is the drug given to patients who require chronic transfusions to prevent cardiomyopathy?

A

Deferoxamine

86
Q

What is the treatment for beta thalassemia major and HbH disease?

A

Chronic transfusions

87
Q

What is the usual presentation of 0/4 alpha globin?

A

Hydrops fetalis

88
Q

What is HbH disease?

A

1/4 alpha globin genes

Patients have chronic hemolysis, with increased reticulocyte counts, as well as skeletal changes

89
Q

What is alpha thalassemia trait?

A

2/4 alpha genes

Usually asymptomatic

90
Q

What is the presentation of 3/4 alpha globin genes?

A

Silent carrier

91
Q

What is the genetic change that causes polycythemia major?

A

JAK2 mutation (Y-kinase)

92
Q

What happens to EPO with PCV?

A

Decreased

93
Q

What is the treatment for PCV?

A

Hydroxyurea and IFN

94
Q

What is the telltale sign of porphyria?

A

Pink urine

95
Q

What are the 5 Ps of AIP?

A
  • Painful abdomen
  • Port wine urine
  • Polyneuropathy
  • Psych
  • Precipitated by drugs
96
Q

What is the best way to diagnose AIP? (2)

A

Urine plasma and porphyrin levels

Specific mutated enzyme assay

97
Q

What is the treatment for an acute attack of AIP?

A

High dose glucose to decrease heme synthesis during attacks (negative feedback)

98
Q

What is the pathophysiology of febrile nonhemolytic transfusion reaction?

A

Cytokine formation during storage of blood

99
Q

What is the pathophysiology of allergic transfusion reaction?

A

AB formation against donor proteins

100
Q

What is the pathophysiology of hemolytic transfusion reaction?

A

Preformed antibodies against donor erythrocytes

101
Q

What is the presentation of febrile nonhemolytic transfusion reaction?

A

Fever, chills, and malaise 1-6 hours post transfusion

102
Q

What is the presentation of allergic transfusion reaction?

A

Prominent urticaria

103
Q

What is the presentation of hemolytic transfusion reaction?

A

Anaphylaxis

104
Q

What is the treatment for hemolytic transfusion reaction?

A

IVFs

105
Q

What is the treatment for febrile nonhemolytic transfusion reaction?

A

acetaminophen

106
Q

What is the treatment for allergic transfusion reaction?

A

Antihistamines

107
Q

What are auer rods, and in which diseases are they seen?

A

Crystallized myeloblastic protein (MPO)

AML

108
Q

What is the most common childhood malignancy?

A

ALL

109
Q

What is the usual presentation of ALL?

A

Rapid onset of anemia, thrombocytopenia etc

110
Q

What are the usual PE findings of ALL?

A

HSM

Bleeding ums

111
Q

What is the treatment to prevent renal damage from AML (besides adequate hydration)?

A

allopurinol

Rasburicase

112
Q

What, generally, is CLL?

A

A malignant proliferation of crappy lymphocytes

113
Q

What are the usual s/sx of CLL?

A

B symptoms
Infections
HSM

114
Q

Smudge cells are seen in which malignancy?

A

CLL

115
Q

Which have MPO: myeloblasts or lymphoblasts?

A

Myeloblasts

116
Q

Which has prominent nucleoli, and which have inconspicuous: myeloblasts vs lymphoblasts?

A

prominent in myeloblasts

Inconspicuous in lymphoblasts

117
Q

What are the sequale of infiltration of bone marrow from CLL?

A
  • Granulocytopenia
  • Thrombocytopenia
  • Hypogammaglobulinemia
118
Q

What is the treatment for CLL? Prognosis?

A

Fludarabine and chlorambucil

Used to alleviate symptoms.

119
Q

What are the usual s/sx of CML?

A

Anemia
Splenomegaly
B symptoms

120
Q

What are the three phases of CML?

A
  1. Chronic (several years)
  2. Accelerated (transition)
  3. Blast crisis (acute leukemia phase, few months left)
121
Q

What is the translocation the produces CML?

A

t(9;22)

122
Q

What is the treatment for CML?

A

imatinib

123
Q

What are the granulocytes?

A

PMNs
Eosinophils
Basophils

124
Q

What is the usual age of presentation for: ALL?

A

Less than 13

125
Q

What is the usual age of presentation for: AML?

A

13-40 years

126
Q

What is the usual age of presentation for: CML?

A

40-60

127
Q

What is the usual age of presentation for: CLL?

A

60+

128
Q

How can you differentiate a leukemoid reaction from CML?

A

LAP is high is leukemoid reaction

LAP is low in CML

129
Q

What is hairy cell leukemia?

A

Malignant proliferation of B cells

130
Q

What protein does hairy cell leukemia usually produce?

A

TRAP

131
Q

What is the treatment for hairy cell leukemia?

A

Cladribine

132
Q

What is the characteristics cell fro HL? What are the CD markers for this?

A

Reed-sternberg cells

CD15 and CD30

133
Q

What cell line is usually involved with NHL?

A

Mainly B cell, but sometimes T cells

134
Q

What is the difference between NHL and HL in terms of presentation?

A

HL = Many peripheral nodes involved

NHL = Single group of localized nodes spread contiguously

135
Q

What is the age distribution for NHL?

A

65-75 year olds

136
Q

What is the age distribution for HL?

A

Bimodal

137
Q

What is the infectious associated for HL and NHL?

A 
HL = EBV
NHL = HIV, autoimmune
138
Q

What is the natural history of follicular lymphoma?

A

Indolent course

Painless waxing and waning adenopathy

139
Q

What is the natural h/o diffuse large B cell lymphoma?

A

Intermediate grade

Single rapidly growin mass

140
Q

What is the treatment regimen for diffuse large B cell lymphoma? Prognosis?

A

R-CHOP

Good prognosis

141
Q

What are the histological characteristics of Burkitt’s lymphoma?

A

“Starry sky”

142
Q

What infection is associated with Burkitt’s lymphoma?

A

EBV

143
Q

What is the CD marker that is positive in Mantle cell lymphoma?

A

CD5 (although it is a B cell lymphoma)

144
Q

What is the natural history of adult T cell lymphoma?

A

HIgh grade–can progress to ALL

145
Q

What is the viral etiology of adult T cell lymphoma?

A

HTLV

146
Q

What is mycosis fungoides / sezary syndrome?

A

T cell lymphoma of the skin, that presents with cutaneous lesions and pruritus

147
Q

Skin bx of mycosis fungoides usually shows what?

A

Cerebriform lymphoid cells

148
Q

What is the gold standard for diagnosing lymphomas?

A

Excisional lymph node bx

149
Q

What is the treatment for lymphomas in general?

A

if low grade, palliative

If high, aggressive

150
Q

HL is generally a B or T cell malignancy?

A

B cell

151
Q

Above what anatomical landmark do HLs usually present?

A

Above the diaphragm

152
Q

What are the Pel-Ebstein fevers associated with HL?

A

Alternating febrile/nonfebrile fevers that last 1-2 weeks

153
Q

What are the three major factors of staging for HL?

A
  • Number of lymph nodes
  • Presence of B symptoms
  • If above and below diaphragm are involved
154
Q

What subtype of HL has the best prognosis?

A

Lymphocyte predominant

155
Q

What causes the hypercalcemia associated with MM?

A

Osteoclast activation with resulting lytic bone lesions

156
Q

Why are patients with MM immunocompromised?

A

Shoddy, monoclonal IgG and/or IgA production

157
Q

What are the characteristic findings of a serum protein electrophoresis?

A

Monoclonal spike

158
Q

What is the classic PBS findings with MM?

A

Rouleaux formation

159
Q

What happens to the total protein:albumin ratio with MM?

A

Increased

160
Q

What are the characteristics urinary findings in MM?

A

Bence jones proteins

161
Q

What is the treatment for young patients with MM?

A

Autologous bone marrow transplant

162
Q

What is the treatment for old patients with MM?

A

Melphalan (oral alkylating agent) and prednisone

163
Q

What causes adult fanconi syndrome?

A

MM damaging renal tubules

164
Q

M protein spike = ?

A

Waldenstrom’s macroglobulinemia

165
Q

What, generally, is Waldenstrom’s macroglobulinemia?

A

Clonal disorder of B cells that leads to a malignant monoclonal gammopathy–INcreased levels of IgM

166
Q

What are the hemodynamic changes that can occur with Waldenstrom’s macroglobulinemia?

A

Hyperviscosity syndrome

167
Q

What are the usual s/sx of Waldenstrom’s macroglobulinemia?

A
  • Raynaud phenomenon
  • Neuro problems
  • Blurred vision 2/2 engorged blood vessels
168
Q

What can MGUS progress to?

A

Waldenstrom’s

MM

169
Q

What is the dolg standard for diagnosing Waldenstrom’s macroglobulinemia? What will this show?

A

Bone marrow bx

Dutcher bodies (PAS+ IgM deposits around the nucleus)

170
Q

What is the treatment for Waldenstrom’s?

A

Chemo for the underlying malignancy

Plasmapheresis to remove excess immunoglobin

171
Q

What is the cause of AL amyloidosis?

A

Plasma cell dyscrasia with deposition of monoclonal light chain fragments

172
Q

What is the cause of AA amyloidosis?

A

Deposition of the acute phase reactant serum amyloid A

e.g. chronic inflammatory diseases

173
Q

What is the cause of dialysis related amyloidosis?

A

Beta-2 microglobulin deposits

174
Q

What is the cause of Heritable amyloidosis?

A

Deposition of abnormal gene products (prealbumin)

175
Q

What is the senile-systemic amyloidosis?

A

Deposition of otherwise normal transthyretin

176
Q

What are the the three major organs that are affected by amyloidosis?

A

Kidneys
Heart
Liver

177
Q

What is the diagnostic test of choice for amyloidosis?

A

Bx with congo red stain

178
Q

What is the treatment for primary amyloidosis?

A

Experimental chemo

autologous stem cell transplant

179
Q

What is the technical definition of neutropenia?

A

ANC less than 1500

180
Q

What is the most common cause of neutropenia?

A

infections followed by drugs

181
Q

What is the usual presentation of chronic neutropenia?

A

Recurrent sinusitis
Gingivitis
Perianal infections

182
Q

What lab tests should be ordered in the work up of neutropenia?

A

ANA levels

183
Q

What is the treatment for neutropenia?

A

ABx
G-CSF
IVIG

184
Q

What is the treatment for neutropenic fever?

A

Broad spectrum abx–cefepime

185
Q

What are the components of the NAACP mnemonic for eosinophilia?

A
  • Neoplasm
  • Allergies
  • Asthma
  • Collagen vascular dz
  • Parasites
186
Q

CSF analysis showing eosinophilia is suggestive of what?

A

of a drug reaction or infection with coccidioidomycosis or a helminth.

187
Q

Hematuria + eosinophilia may be ?

A

Schistosomiasis

188
Q

What is a syngeneic transplant?

A

From identical twin

189
Q

What is the cause of GVHD?

A

Minor histocompatibility complex antigens

190
Q

What are the s/sx of GVHD?

A
  • Skin changes
  • Cholestatic liver dysfunction
  • obstructive lung path
191
Q

Down syndrome patients are predisposed to what neoplastic process?

A

ALL

192
Q

What condition is associated with SCC and BCC of the skin?

A

Xeroderma pigmentosum

193
Q

What condition is associated with malignant melanomas?

A

Multiple dysplastic nevi

194
Q

What cancer is associated with chronic atrophic gastritis?

A

Gastric adenocarcinoma

195
Q

What cancer is associated with ulcerative colitis?

A

Colonic adenocarcinoma

196
Q

What cancer is associated with tuberous sclerosis?

A

AStrocytoma and cardiac rhabdomyomas

197
Q

What cancer is associated with Paget’s disease of the bone?

A

osteosarcoma and fibrosarcoma

198
Q

What cancer is associated with Plummer vinson syndrome?

A

SCC of the esophagus

199
Q

What cancer is associated with autoimmune disease?

A

Malignant thymomas

200
Q

What is the treatment for an acute transplant rejection?

A
  • Corticosteroids
  • Antilymphocyte abs
  • Tacrolimus

A1 (32 decks)

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