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Random boards stuff > Heme > Flashcards

Heme Flashcards

1
Q

How do you tell the difference btw CML and leukemoid?

A

Look similar b/c increase WBC with early cells

  • -alkaline phosphatase is decreased in CML
  • -Need t(9,22) cytogenics to diagnose CML
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2
Q

pre-surg prophylax against DVT

A

low molecular weight heparin. helps antithrombin III

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3
Q

What do you use if u can’t use heparin

A

Direct thrombin inhibitors

  • -Argatroban
  • -Lepirudin
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4
Q

epstein barr causes which malignancy

A

Burkett’s lymphoma. Will showa high Ki-67 (proliferation index0

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5
Q

High AFP in a pregnant woman

A

Neural tube defect

–Can also be yolk sac tumor

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6
Q

Cladribine mechanism

A

purine analog that is incorporated into DNA causing strands to break.

Resistant to adenosine deaminase

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7
Q

Indication cladribine

A

hairy cell leukemia

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8
Q

Purine analogs

A

6-thiopurine
fludarabine
cladribine

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9
Q

Pyrimidine analogs

A

5-FU
capecitabine
cytarabine
gemcitabine

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10
Q

Factor V leiden factor pts at risk for

A

DVT–>pulmonary thromboembolism
cerebral vein thrombosis
pregnancy loss

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11
Q

Why remove spleen from SCD pts

A

At risk for splenic infarction

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12
Q

What causes heparin induced thrombocytopenia?

A

Antibodies to heparin. Results in paradoxical thrombosis or bleeding. More common with unfractionated (high molecular weight) heparin

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13
Q

What are the direct thrombin inhibitors?

A

hirudin, lepirudin and argatroban

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14
Q

AML translocation

A

t(8,21)

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15
Q

Acute promyelocytic leukemia (AML variant) translocation

A

t(15,17). Will look similar to AML but with more promyelocytes (Large, basophilic nucleus)

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16
Q

Burkitt lymphoma translocation

A

t(8,14)

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17
Q

CML translocation

A

t(9,22)

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18
Q

Mantle cell translocation

A

t(11,14)

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19
Q

CLL genetics

A

13q deletion

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20
Q

Describe the APL mechanism

A

Transfer of retinoic acid receptor alpha to the PML gene. Fusion of two gene products occurs

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21
Q

Side effect of dauno/doxorubicin

A

irreversible dose-dependent cardiotoxicity

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22
Q

Which drugs cause bone marrow suppression?

A

chloramphenicol, ziduvine, phenylbutazone

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23
Q

Which drugs cause liver necrosis?

A

acetaminophen and halothane

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24
Q

Which drugs cause pulmonary fibrosis?

A

Busulfan and bleomycin

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25
Q

Pure red cell aplasia–what do you need to look our for

A

rare severe hypoplasia of marrow erythroid elements. Associated with thymoma, lymphocytic leukemia, and Parvo B19

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26
Q

c-myc

A

Burkitt lymphoma. Chromosome 8

–It’s a transcription activator of apoptosis and differentiation

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27
Q

what does t(11,14) do?

A

mantle cell on chromosome 11

  • More Cyclin D1
  • Increased G1-S
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28
Q

Bcl-2

A

follicular lymphoma
t(14,18)
chromosome 18
inhibits apoptosis

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29
Q

BCR-ABL

A

inhibits apoptosis

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30
Q

t(14,18)

A

follicular lymphoma

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31
Q

pathophys of follicular

A

Bcl2 overexpression

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32
Q

ristocetin aggregation test

A

measures vWF dependent platelet aggregation. Activates GP Ib-IX receptors so they can bind to vWF.

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33
Q

Does vWF cause changes in PT or PTT?

A

Yes–PTT (carries factor VIII)

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34
Q

Hageman factor XII

A

No clotting problems but prolonged PTT

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35
Q

glanzmann thrombasthenia testing

A

response to adenosine diphosphate (ADP), epinephrine, and collagen are decreased
–ristocetin normal

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36
Q

STARY SKY APPEARANCE

A

BURKITT LYMPHOMA

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37
Q

CLOSELY PACKED LYMPH NODE FOLLICLES

A

FOLLICULAR LYMPHOMA

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38
Q

large sheets of lymphocytes with large nuclei

A

Large B cell lymphoma

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39
Q

BLASTS

A

AML OR ALL

–ALL in kids more likely and usually B Cell rather than T cell

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40
Q

Blasts in a kid presenting with a mediastinal mass causing SVC syndrome or stridor

A

T cell ALL

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41
Q

B12 deficiency signs

A

elevated methylmalonic acid AND homocysteine

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42
Q

Folate deficiency signs

A

elevated homocystein

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43
Q

How to prevent hemorrhagic cystitis with chemotherapy?

A

hydration and mesna, which binds acrolein, a toxic metabolite

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44
Q

What membrane protein allows RBCs to carry CO2?

A

Chloride HCO3 antiporter

  • -accounts for the chloride shift. HCO3 enters, CL- leaves in tissues
  • -chloride levels low in venous blood
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45
Q

1/3 of platelet pool is stored in

A

the spleen

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46
Q

platelets contain what granules

A

alpha granules

dense granules

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47
Q

alpha granules

A

vWF

Fibrinogen

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48
Q

delta granules

A

ADP, calcium

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49
Q

lifespan of a platelet

A

8-10 days

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50
Q

granulocytes

A

neutrophil, eosinmophil, basophil

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51
Q

mononuclear cells

A

monocytes, lymphocytes

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52
Q

Normal neutrophil count

A

50-60

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53
Q

Normal lymphocyte count

A

25-33

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54
Q

hypersegmented poly

A

vitamin B12/folate deficiency

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55
Q

neutrophil granules

A 
alkaline phosphatase
collagenase
lysozyme
lactoferrin
azurophilic granules
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56
Q

azurophilic granules

A

acid phosphatase
peroxidase
B-glucuronidase

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57
Q

produces histaminase and arylsulfatase

A

eosinophils

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58
Q

causes of eosinophilia

A 
neoplastic
asthma
alelrgic
collagen vascular disease
parasites
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59
Q

basophils release

A

heparin
histamine
leukotrienes

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60
Q

drug: prevents mast cell degran

A

cromolynsodium

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61
Q

mast cells release

A

histamine
heparin
eosinophil chemotaxis

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62
Q

bradykinin activates

A

vasodilation
permeability
pain

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63
Q

other action of XIIa

A

activates kallikrein from prekallikrein

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64
Q

kallidrein

A

HMWK–>bradykinin

plasminogen–>plasmin

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65
Q

action of plasmin

A

degrades fibrin

activates complement cascade

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66
Q

hemophilia A

A

deficiency factor VIII

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67
Q

hemophilia B

A

deficiency factor IX

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68
Q

warfarin inhibits

A

epoxide reductase (reduces vitamin K)

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69
Q

Protein C

A

works with protein S to cleave and inactivate Va and VIIIa

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70
Q

what activates protein C?

A

thrombomodulin

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71
Q

antithrombin inactivates

A

II,VII,IX, X, XI, XII

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72
Q

what activates antithrombin?

A

heparin

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73
Q

what starts coagulation cascade?

A

platelet release of ADP and Ca2+

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74
Q

What induces GpIIb/IIIa expression?

A

ADP binding

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75
Q

anti-aggregation factors

A

PGI2 (prostacyclin)

NO

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76
Q

Ticlopidine and clopidogrel mechanism

A

inhibits ADP induced expression of GpIIb/IIIa

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77
Q

what cell expresses thrombomodulin?

A

Protein C

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78
Q

what do endothelial cells produce?

A

vWF
thromboplastin
tPA
PGI2

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79
Q

Acute phase reactants in plasma cause

A

RBC aggregation

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80
Q

Increase ESR

A

autoimmune dz
neoplasms
GI disease
pregnancy/infection

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81
Q

decrease ESR

A 
sickle cell anemia
CHF
microcytosis
low fibrinogen
polycythemia
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82
Q

Acanthocyte

A

liver disease

abetalipoproteinemia

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83
Q

basophilic stippling

A

thalassemias
anemia of chronic disease
lead poisoning

Baste the tail

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84
Q

elliptocyte

A

hereditary elliptocytosis

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85
Q

bite cell

A

G6PD deficiency

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86
Q

macro-ovalocyte

A

megaloblastic anemia, marrow failure

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87
Q

ringed sideroblasts

A

excess iron storage

–sideroblastic anemia

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88
Q

schistocyte

A

DIC
TTP/HUS
traumatic hemolysis

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89
Q

TTP

A

thrombocytic thrombocytopenia purpura

  • -blood clots in all the small vessels
  • -thrombocytopenia (purpura)
  • -MAHA–schistocytes
  • -neuro sx
  • -kidney failure
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90
Q

spherocyte

A

hereditary spherocytosis

autoimmune hemolysis

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91
Q

teardrop cell

A

bone marrow infiltration

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92
Q

target cell

A

HbC
Asplenia
Liver dz
Thallassemia

HALT don’t shoot the TARGET

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93
Q

heinz bodies

A

G6PD,

–Similar appearance in alpha-thalassemia

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94
Q

howell jolly bodies

A

asplenia

napthlalene (moth ball) ingestion

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95
Q

RBC smear in iron deficiency

A

microcytosis

hypochromia

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96
Q

plummer vinson syndrome

A 
iron deficiency anemia
esophageal webs
atrophic glossitis (smooth tongue)
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97
Q

y4 Hb in pt with hydrops fetalis

A

4 gene deletion of alpha thalassemia

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98
Q

Very little alpha globin with Beta globin tetramers

A

HgbH disease

  • -caused by only one functional alpha gene
  • -anemia
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99
Q

1-2 gene deletion of alpha chain

A

no significant sx

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100
Q

cis deletion of alpha thalassemia more common in

A

azns

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101
Q

trans deletion of alpha thalassemia more common in

A

africans

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102
Q

beta thalassemia prevalent in

A

mediterranean population

103
Q

increase in HbA2 (over 3.5%) in asymptomatic pt

A

beta thalassemia minor

104
Q

chipmunk face, crew cut on skull Xray

–severe anemia requiring blood transfusions

A

beta thalassemia major (homozygote)

105
Q

hemoglobin in beta thalassemia major

A

HbF (a2, y2)

106
Q

blood smear in beta thalassemia major

A 
anisocytosis
poikilocytosis
microcytosis
hypochromia
schistocytes
107
Q

house with chipped paint

A

lead poisoning

108
Q

first line tx for LEAD

A

Dimercaprol and EDTA

109
Q

tx for lead poisoning in a kid

A

succimer

110
Q

sx of lead poisoning

A
  1. lead lines on gingivae
  2. encephalopathy, erythrocyte basophilic stippling
  3. abdominal pain, sideroblastic anemia
  4. drops of wrist and foot
111
Q

pt with anemia
increased iron, ferritin, normal TIBC
hereditary cause

A

hereditary sideroblastic anemia

112
Q

reversible causes of sideroblastic anemia

A

alcohol, lead, isoniazid

113
Q

tx hereditary sideroblastic anemia

A

pyridoxine B6

114
Q

cause hereditary sideroblastic anemia

A

d-ALA synthase defect

115
Q

inheritance of sideroblastic anemia

A

X linked

116
Q

causes of microcytic anemia

A 
iron deficiency
ACD
thalassemias
lead poisoning
sideroblastic anemia
117
Q

causes of normocytic nonhemolytic anemia

A

ACD
aplastic anemia
chronic kidney disease

118
Q

macrocytic megaloblastic anemia

A

folate deficiency
b12
orotic aciduria

119
Q

nonmegaloblastic macrocytic anemia

A

liver dz
alcoholism
reticulocytosis

120
Q

anemia

  • -normal MMA
  • -increased homocysteine
A

folate deficiency

121
Q

anemia

  • -increased homocysteine
  • -increased MMA
A

B12 deficiency

122
Q

causes of B12 deficiency

A

diphyllobothrium latum
–crohn’s
vegans
PPIs

123
Q

signs of subacute combined degeneration

A

peripheral neuropathy
loss of vibration and proprioception
spasticity (loss of lateral corticospinal)
dementia

124
Q

treatment for orotic aciduria

A

uridine monophosphate

125
Q

which drugs cause macrocytic anemia?

A

5-FU, AZT, hydroxyurea. these all interfere with DNA synthesis, but NO megaloblastic RBCs

126
Q

anemia

  • -decreased haptoglobin
  • -increased LDH
  • -hemoblogin in urine
A

intravascular hemolysis

127
Q

anemia

–increased LDH and high unconjugated bili

A

extravascular hemolysis. Means you’re losing RBCs through spleen clearance, not lysis in vessels

128
Q

findings in anemia of chronic dz

A
  1. increased hepcidin
  2. ferritin
  3. decreased TIBC
  4. decreased iron
129
Q

cause of aplastic anemia

A
  1. radiation, benzene, chloramphenicol, alkylatin agents
  2. viral: parvo, EBV, HIV, HCV
  3. fanconi’s
  4. autoimmune
130
Q

fanconi’s

A

proximal renal tubules[1] of the kidney in which glucose, amino acids, uric acid, phosphate and bicarbonate are passed into the urine

131
Q

dry bone marrow type showing hypocellular marrow with fatty infiltration

A

aplastic anemia

132
Q

signs of aplastic anemia

A

pancytopenia

133
Q

positive osmotic fragility test

A

hereditary spherocytosis

134
Q

hereditary spherocytosis prone to asplastic crisis from infection by

A

parvo B19

135
Q

back pain with hemoglobinuria days later. Heiz bodies and bite cells

A

G6PD

136
Q

G6PD: intravascular or extravascular hemolysis?

A

mostly extravascular

137
Q

hemolytic anemia in newborn

A

pyruvate kinase deficiency

–low ATP=rigid RBCs

138
Q

HbC cause

A

glutamic acid to lysine mutation at residue 6.

139
Q

hemolytic anemia, pancytopenia, and venous thrombosis

–CD55/59 negative RBCs on flow

A

Paroxysmal nocturnal hemoglobinuria

–increased complement-mediated RBC lysis

140
Q

how do you get PNH?

A

acquired mutation in stem cell

–loss of GPI anchor or decay accelerating factor (protect RBC from complement

141
Q

tx PNH

A

eculizumab

142
Q

crew cut on skull x ray with severe anemia and sudden vasoocclusive crises

A

sickle cell

143
Q

mutation in sickle cell

A

Substitution of glutamic acid with valine at position 6

144
Q

SCD child suddenly showing howell jolly bodies

A

autosplenectomy

145
Q

kidney problems in SCD

A

renal papillary necrosis

146
Q

tx sickle ell

A

hydroxyurea or bone marrow transplant

147
Q

warm agglutinin type of antibody

A

IgG

148
Q

cold agglutinin type of antibody

A

IgM

149
Q

Warm agglutinin seen in

A

chronic anemia with

SLE, CLL, drugs

150
Q

cold agglutinin seen in

A

chronic anemia with

  • mycoplasma pneumonia
  • mono
  • CLL
151
Q

pathophys MAHA

A

RBCs damaged b/c of narrow vessel lumen

152
Q

cause of MAHA

A

DIC
TTP-HUS
SLE
Malignant HTN

153
Q

macroangiopathic anemia

A

mechanical destruction RBC (valves, aortic stenosis)

–schistocytes

154
Q

iron lab values in hemochromatosis

A

increased serum iron
increased ferritin
decreased TIBC
increased transferrin saturation

155
Q

pregnancy/OCP iron tests

A

increased transferrin
decreased transferrin saturation
normal iron and ferritin

156
Q

steps in heme synthesis

A
  1. glycine+succinylCoa
  2. d-ALA
  3. Porphobilinogen
  4. HMB
  5. Uroporphyrinogen
  6. coproporphytingoen
  7. protoporphyrin
  8. heme
157
Q

dALA synthase requires what vitamin

A

b6

158
Q

lead poisoning blocks

A

d-ALA dehydratase

ferrochelatase

159
Q

sideroblastic anemia is a defect in

A

d-ALA synthase

160
Q

Acute intermittent porphyria is a block in

A

porphobilinogen deaminase

161
Q

Porphyria cutanea tarda is a block in

A

uroporphyringen decarboxylase

162
Q

accumulated protoporph and dALA

A

lead poisoning

163
Q

accumulated porphobilinogen dALA and uroporphyrin (tea colored urine)

A

acute intermittent porphyria

164
Q

battery/ammunition/radiator factory worker

A

lead poisoning

165
Q 
painful abdomen
port wine urine
polyneuropathy
psych disturbances
precipitated by drugs
A

acute intermittent porphyria

166
Q

tx AIP

A

glucose and heme–inhibit ALA synthase

167
Q

blistering photosensitivity with uroporphyrin in the urine

A

porphyria cutanea tarda

168
Q

defect in porphyria cutanea tarda

A

uroporphyrinogen decarboxylase

169
Q

PT tests

A

extrinsic pathway (I, II, V, VII, X)

170
Q

PTT tests

A

intrinsic pathway (everything but VII and XIII)

171
Q

clotting results in hemophilia

A

Increased PTT (factor VIII and IX)

172
Q

clotting results in vitamin K deficiency

A

Increased PT, PTT

173
Q

bernard soulier labs

A

decreased PC

increased BT

174
Q

glanzmann’s labs

A

increased BT

no change in PC

175
Q

blood smear shows no platelet clumping

A

glanzmanns

176
Q

cause idiopathic thrombocytopenic purpura

A

anti-GpIIb/IIIa antibodies

–spleen consumes platelet/antibody complex

177
Q

labs in ITP

A

decreased platelets
increased BT
increased megakaryocytes

178
Q

TTP cause

A

deficiency of ADAMTS13

–cannot separate vWF multipers causing platelet aggregation and thrombosis

179
Q

labs in TTP

A

decrased PC
Increased BT
schistocytes
increased LDH

180
Q

tx vWF

A

DDAVP

181
Q

labs vWF

A

increased BT

–if severe, increased PTT

182
Q

inheritance vWF

A

autosomal dominant

183
Q

DIC labs

A
  1. low PC
  2. high BT, PT, PTT
  3. Schisto
  4. D dimers
  5. low fibrinogen
  6. low factor V and VIII
184
Q

mutation in prothrombin gene mutation

A

3’ untranslated region=more prothrombin

185
Q

pt has no increase in PTT after heparin administration

A

antithrombin deficiency

186
Q

pt has thrombotic skin necrosis with hemorrhage after warfrin

A

protein C or S deficiency.

–cannot inactivate factors V and VIII

187
Q

what is contained in cryoprecipitate?

A 
fibrinogen
factor VIII
factor XIII
vWF
fibronectin
188
Q

serum changes with blood transfusions

A

hypocalcemia

hyperkalemia

189
Q

leukemoid rxn labs

A

increased WBC with left shift

INCREASED leukocyte alkaline phosphatase

190
Q

CML labs

A

increased WBC with left shift

DECREASED leukocyte alk phos

191
Q

typical spread of hodgkin’s

A

localized

  • single group of nodes
  • spreads contiguously
192
Q

typical spread non-hodgkin’s

A

multiple peripheral nodes

  • extranodal involvement
  • does not spread through blood
193
Q

strongest prognostic indicator in hodgkins

A

stage

194
Q

hodgkin’s associated with

A

EBV

195
Q

non-hodgkin’s associated with

A

HIV/immunosuppression

196
Q

hodgkin age group

A

young adulhood and over 55 years. usually men

197
Q

non-hodgkins age group

A

20-40 years

198
Q

B symptoms more common in hodgkins or non-hodgkins

A

hodgkins

199
Q

Reed sternberg cells are positive for

A

CD30 and CD15

200
Q

Most common form of hodgkin’s

A

nodular sclerosing

201
Q

prognosis of nodular sclerosing

A

good. prognosis with lymphocyte mixed/depleted is poor

202
Q

t(8,14)

A

burkitt’s

203
Q

cmyc

A

burkitt’s

204
Q

endemic form of burkitt’s in africa

A

jaw lesion

205
Q

sporadic burkitt’s

A

pelvis/abdomen

206
Q

most common adult NHL

A

diffuse large B cell

207
Q

t(11,14)

A

mantle cell

208
Q

cyclin D1

A

mantle cell

209
Q

t(14,18)

A

follicular

210
Q

bcl02

A

follicular

211
Q

which NHLs can be seen in children

A

classically burkitt’s

20% of diffuse large B cell lymphomas

212
Q

CD5+ NHL

A

mantle cell

213
Q

prognosis follicular lymphoma

A

difficult to cure

–indolent course

214
Q

prognosis mantle cell

A

poor

215
Q

adult T cell lymphoma caused by

A

HTLV-1

216
Q

sx: adult T cell lymphoma

A

cutaneous lesions

217
Q

adult t cell lymphoma affects people from

A

Japan
west africa
caribbean

218
Q

cutaneous patches/nodules with CD4+ cells

A

mycosis fungoides/sezary

219
Q

rouleaux formation

A

multiple myeloma

220
Q

histology multiple myeloma

A

plasma cells with clock face chromatin–lots of em

–intracytoplasmic inclusions, white

221
Q

waldenstrom’s macroglobulinemia

A

M spike without lytic bone lesions

222
Q

Risk of MM in MGUS

A

1-2% per year

223
Q

ALL affects what age group

A

less than 15 years

224
Q

mediastinal mass

A

T cell ALL

225
Q

tdT and CALLA positive

A

ALL

226
Q

Which ALL has the best prognosis?

A

t(12, 21)

227
Q

smudge cells

A

small lymphocytic lymphoma/chronic lymphocytic leukemia

228
Q

SLL and CLL typically affect what age group

A

> 60 years

229
Q

presentation of SLL/CLL

A

asymptomatic. autoimmune hemolytic anemia

230
Q

TRAP positive

A

hairy cell leukemia

231
Q

tx: hairy cell leukemia

A

Cladribin

232
Q

t(15,17)

A

M3 type AML

233
Q

median age of AML

A

65

234
Q

auer rods

A

AML

235
Q

Common presentation of M3 AML

A

DIC

236
Q

tx: M3 AML

A

all trans retinoic acid

237
Q

CML age group

A

30-60

238
Q

t(9,22)

A

CML

239
Q

blood mear in CML

A

increased neutrophil
metamyelocytes
basophils
splenomegaly

240
Q

CML can transform to

A

AML/ALL (blast crisis)

241
Q

AMl-M3 subtype also known as

A

acute promyelocytic leukemia

242
Q

peroxidase positive cytoplasmic inclusions

A

auer rods

243
Q

child with lytic bone lesions and skin rash. cells show lots of birbeck granules on EM

A

langerhans histiocytosis

244
Q

pathophysiology of langerhans histiocytosis

A

functionally immature dendritic cells cannot stimulate T lymphocytes.

245
Q

Cells in langerhans histiocytosis express

A

S-100 and CD1a

246
Q

JAK2 positive

A

myeloproliferative disorder
-polycythemia vera
essential thrombocytosis
myelofibrosis

247
Q

RBC, WBC, platelets in polycythemia vera

A

All increased

248
Q

RBC, WBC, platelets in essential thrombocytosis

A

platelets increased

249
Q

RBC, WBC, platelets in myelofibrosis

A

Low RBC. variable wbc and platelets

250
Q

RBC, WBC, platelets in CML

A

low RBC lots of WBC and platelets

251
Q

Lymphoid lineage

A

B cells
T cells
NK cells

252
Q

relative polycythemia

A

decreased plasma volume (dehydration)

253
Q

appropriate polycythemia

A

increased RBC 2ndary to O2 saturation

254
Q

inappropriate absolute

A

increased RBC mass caused by

  1. RCC, wilms’ tumor
  2. HCC
  3. Hydronephrosis
  4. OR ectopic EPO

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