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IHO > Week 3 friday > Flashcards

Week 3 friday Flashcards

1
Q

bone marrow aspiration

A

only collects bone marrow

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2
Q

bone marrow biopsy

A

collects bone marrow AND bone

Jamshidi needle is used

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3
Q

type of myeloid leukemia

A

acute and chronic

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4
Q

type of lymphoid leukemia

A 
acute lymphoblastic leukemia
chronic "
Hodgkins lymphoma
non "
MM
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5
Q

acute leukemia pathphys
AML
ALL (lymphoblastic)

A

prolif of IMMATURE myeloid or lymph in bone marrow
Caused: clonal expanion and maturation failure form genetic defect that arrets in BLAST PHASE
Causes crowding and hurts other cell lines

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6
Q

findings in acute leukemia

A

sudden onset
bone marrow failure (fatigue, infetion, bleeding)
bone pain
organ infiltration

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7
Q

lab findings in acute leukemia

A

IMMATURE blast cells
leukocytosis
anemia
thromobocytopenia

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8
Q

Acute myeloid leukemia (must know)

A

bone marrow prolif, think BLAST
20% is cutoff
bad prognosis

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9
Q

3 ways to check if leukemia is myeloid in origin

A

auer rods, dysgranulopoeisis (no granules), and cytochemistry

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10
Q

Auer rods

A

ONLY found in malignant myeloid ells

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11
Q

AML-M0 must know

A

increase blast (20% min)
need marker identification (need to use flo cyt)
myeloid peroxidase negative

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12
Q

AML - M1 must know

A

increase in blast cells.
NO maturation
auer rods
myeloid peroxidase POSITIVE

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13
Q

AML-M2 must know

A

increase in blasts
maturing neutro
t(8,21) in some cases (genetic abnormality)

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14
Q

AML - M3 must konw

A 
increase in PROMYELOCYTES
faggot cells (bunch of auer rods)
dic disseminated intravascular coagulation
t(15:17) found in ALL cases (better prognosis)
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15
Q

dic disseminated intravascular coagulation

A

form clots all over body from granulation stimulated coag system
use it all up and then bleed out
NEED SPECIAL TREATMENT FOR THESE PATIENTS

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16
Q

faggot cell

A

diagnosis for acute promyelocyte leukemia

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17
Q

AML m4 must know

A 
incrase myeloblast
incrase monocyte
extramedullary TUMOR masses
-found often in CNS
(inv16) genetic abnormality in SOME
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18
Q

AML M5 must know

A

increase MONOCYTES
Non specific esterase POSITIVE
M5A M5B
extramedullary tumor masses

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19
Q

extramedullary tumor masses found in?

A

AML M5 AND AML M4

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20
Q

AML m6

A

increase erythroblast
incraese myeloblast
DYSERTHROPOIESIS

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21
Q

AML M7 must know

A

incrase MEGAKARYOBLAST
myeloid peroxidase negative
need markers

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22
Q

myeloid peroxidase positive and negative?

A

negative in M0 and M7

positive in M1

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23
Q

non specific esterase positive in?

A

AML M5

24
Q

AML with t(15,17)

A

give all trans retinoic acid to help overcome maturation block

25
Q

genetic abnormalities 11q23

A

monocytic component

BAD PROGNOSIS

26
Q

AML with FLT3 mutation

A

mutation of tyrosine kinase
found in .3 of all AML cases
monocytic cells
POOR PROGNOSIS

27
Q

Poor prognosis mutations

A

FLT-3
11q23
(5,7) which is in multilineage dysplasia

28
Q

therpay related AML

A

alkylating agents!
busulfan, etoposide
very hard to treat

29
Q

better aml prognosis

A

8,21, inv16 and 15,17

30
Q

myelodysplastic syndrome

A

abnormal stem cells
dysmyelopoiesis
incrase blasts

31
Q

characteristics of MDS

A

megaloblastic nuclie in RBC. also fragmentation (dyserythropoeisis) MACROCYTIC
neutrophils hypogran and hyposeg (dysgranulopoeiss)
megakaryocytes are small and non-lobed (dysplastic megakaryocyte)

32
Q

treatment for MDS

A

low grade : support and follow

high grade: BE AGGRESSIVE

33
Q

Acute lymphoblastic leukemia must know

A

prolif of lympoid blast in blood and marrow
more common in children
good prognosis

34
Q

how to classify ALL

A

immunophenotyping for B vs T
termindal deoxy transferase (found in both)
Tcell ang in T, and Tcell antigen in B
19,20 and 21 cd markers specific for b cell

35
Q

prognosis of ALL

A

worse in T lymphoblastic

better if blymphoblastic leukemia

36
Q

T-lymphoblastic leukemia must know

A

teenage males with mediastinal mass
high WBC
BAD PROGNOSIS

37
Q

smudge cells

A

more common in lympo blood smears (more fragile)

38
Q

b lymphoblastic must know

acute lympoblastic leukemia

A

several subtypes
Rarely, Ph+
tdt +
most common in CHILDREN

39
Q

Prognosis for acute lymphoblastic leukemia

A

T is bad
age 1-10 is good
wbc below 50k is good
hyperdiploidy found in cytogenetics is GOOD

40
Q

treatment for acute lympoblastic leukemia

A

chemo _ bone marrow transplant

many children are cured

41
Q

anopheles mosquito

A

carries plamodia

42
Q

plasmodium trophozoites

A

MOST COMMON FORM FOUND IN CELLS INFECTED WITH PLASMODIUM

43
Q

p vivax

A

enlarged cells with schuffner dots

44
Q

p ovale microscope

A

enlarged cells with schuffners dots

45
Q

p malaria microscope

A

rosette arrangement of the merozoites

46
Q

p falciparum

A

high parasite burden
severe anemia
multiorgan symptoms
HIGH FATALITY RATE

47
Q

most common plasmodium?

A

vivax and falciparum (most deadly)

48
Q

plasmodium replase?

A

vivax and ovale

49
Q

sporozoites enter blood stream from mosquito and go where?

A

LIVER IS FIRST where it forms SCHIZONTS

takes minutes to hour

50
Q

Schizonts

A

the little baby replicates of plasmodium found in cell

51
Q

merozoites

A

plasmodium form that leaves liver and infects RBC

leaves rbc to infect others as well

52
Q

microscope of falciparum

A

lots of trophzoite rings

banana shaped gametocyte

53
Q

p falciparum is bad because?

A

forms rosettes that bind to endothelium (clump of RBC surrounding infected cell)
stops blood flow and leads to cerebral ischemia in children
stimulates cytokines tnf, infgamma and il1
suppress rbc production

54
Q

What cells shows little knobs?

A

ones infected with falciparum

knobs bind to ligands on endothelial cells

55
Q

fever in plasmodiu

A

falciparum is everyday
vivax and ovale every 48 hours (3rd day)
malariea is quartan, 72 hours, every 4th day

56
Q

host resistance to plasmodium?

A

any disease with RBC alteration
- sickle cell, thal, 66pd, rbc antigens
populations can develop this over time if live in areas where disease is active

57
Q

p falciparum resistance to immune?

A

antigenic variation!

changes Pfemp expressoin making it hard to fight off

IHO (9 decks)

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