Week 3 friday Flashcards
bone marrow aspiration
only collects bone marrow
bone marrow biopsy
collects bone marrow AND bone
Jamshidi needle is used
type of myeloid leukemia
acute and chronic
type of lymphoid leukemia
acute lymphoblastic leukemia chronic " Hodgkins lymphoma non " MM
acute leukemia pathphys
AML
ALL (lymphoblastic)
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
findings in acute leukemia
sudden onset
bone marrow failure (fatigue, infetion, bleeding)
bone pain
organ infiltration
lab findings in acute leukemia
IMMATURE blast cells
leukocytosis
anemia
thromobocytopenia
Acute myeloid leukemia (must know)
bone marrow prolif, think BLAST
20% is cutoff
bad prognosis
3 ways to check if leukemia is myeloid in origin
auer rods, dysgranulopoeisis (no granules), and cytochemistry
Auer rods
ONLY found in malignant myeloid ells
AML-M0 must know
increase blast (20% min)
need marker identification (need to use flo cyt)
myeloid peroxidase negative
AML - M1 must know
increase in blast cells.
NO maturation
auer rods
myeloid peroxidase POSITIVE
AML-M2 must know
increase in blasts
maturing neutro
t(8,21) in some cases (genetic abnormality)
AML - M3 must konw
increase in PROMYELOCYTES faggot cells (bunch of auer rods) dic disseminated intravascular coagulation t(15:17) found in ALL cases (better prognosis)
dic disseminated intravascular coagulation
form clots all over body from granulation stimulated coag system
use it all up and then bleed out
NEED SPECIAL TREATMENT FOR THESE PATIENTS
faggot cell
diagnosis for acute promyelocyte leukemia
AML m4 must know
incrase myeloblast incrase monocyte extramedullary TUMOR masses -found often in CNS (inv16) genetic abnormality in SOME
AML M5 must know
increase MONOCYTES
Non specific esterase POSITIVE
M5A M5B
extramedullary tumor masses
extramedullary tumor masses found in?
AML M5 AND AML M4
AML m6
increase erythroblast
incraese myeloblast
DYSERTHROPOIESIS
AML M7 must know
incrase MEGAKARYOBLAST
myeloid peroxidase negative
need markers
myeloid peroxidase positive and negative?
negative in M0 and M7
positive in M1
non specific esterase positive in?
AML M5
AML with t(15,17)
give all trans retinoic acid to help overcome maturation block
genetic abnormalities 11q23
monocytic component
BAD PROGNOSIS
AML with FLT3 mutation
mutation of tyrosine kinase
found in .3 of all AML cases
monocytic cells
POOR PROGNOSIS
Poor prognosis mutations
FLT-3
11q23
(5,7) which is in multilineage dysplasia
therpay related AML
alkylating agents!
busulfan, etoposide
very hard to treat
better aml prognosis
8,21, inv16 and 15,17
myelodysplastic syndrome
abnormal stem cells
dysmyelopoiesis
incrase blasts
characteristics of MDS
megaloblastic nuclie in RBC. also fragmentation (dyserythropoeisis) MACROCYTIC
neutrophils hypogran and hyposeg (dysgranulopoeiss)
megakaryocytes are small and non-lobed (dysplastic megakaryocyte)
treatment for MDS
low grade : support and follow
high grade: BE AGGRESSIVE
Acute lymphoblastic leukemia must know
prolif of lympoid blast in blood and marrow
more common in children
good prognosis
how to classify ALL
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
prognosis of ALL
worse in T lymphoblastic
better if blymphoblastic leukemia
T-lymphoblastic leukemia must know
teenage males with mediastinal mass
high WBC
BAD PROGNOSIS
smudge cells
more common in lympo blood smears (more fragile)
b lymphoblastic must know
acute lympoblastic leukemia
several subtypes
Rarely, Ph+
tdt +
most common in CHILDREN
Prognosis for acute lymphoblastic leukemia
T is bad
age 1-10 is good
wbc below 50k is good
hyperdiploidy found in cytogenetics is GOOD
treatment for acute lympoblastic leukemia
chemo _ bone marrow transplant
many children are cured
anopheles mosquito
carries plamodia
plasmodium trophozoites
MOST COMMON FORM FOUND IN CELLS INFECTED WITH PLASMODIUM
p vivax
enlarged cells with schuffner dots
p ovale microscope
enlarged cells with schuffners dots
p malaria microscope
rosette arrangement of the merozoites
p falciparum
high parasite burden
severe anemia
multiorgan symptoms
HIGH FATALITY RATE
most common plasmodium?
vivax and falciparum (most deadly)
plasmodium replase?
vivax and ovale
sporozoites enter blood stream from mosquito and go where?
LIVER IS FIRST where it forms SCHIZONTS
takes minutes to hour
Schizonts
the little baby replicates of plasmodium found in cell
merozoites
plasmodium form that leaves liver and infects RBC
leaves rbc to infect others as well
microscope of falciparum
lots of trophzoite rings
banana shaped gametocyte
p falciparum is bad because?
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
What cells shows little knobs?
ones infected with falciparum
knobs bind to ligands on endothelial cells
fever in plasmodiu
falciparum is everyday
vivax and ovale every 48 hours (3rd day)
malariea is quartan, 72 hours, every 4th day
host resistance to plasmodium?
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
p falciparum resistance to immune?
antigenic variation!
changes Pfemp expressoin making it hard to fight off
