Hematology Flashcards
MCH =
10(hgb/rbc)
MCHC =
100(hgb/hct)
MCV =
10(hct/rbc)
normal wbc
5-10 x 10^3
normal rbc
male: 4-5 x 10^6
female: 3-4 x 10^6
normal hgb
male: 13.5 - 17.5 g/dL
female: 12 - 15.5 g/dL
normal hct
male: 40-55%
female: 36-48%
normal MCV
80-100
normal MCH
27-31
normal MCHC
32-36%
>= 40% is impossible
normal rdw
11-15%
normal plt
150-400 x 10^3
falsely increased hgb
turbidity in channel
↑↑ wbc
icterus
lipemia
effects of ↑↑ lymphs on indices
falsely ↑ rbc and therefore hct, MCV, RDW
iron profile in IDA
↓ ferritin
↓ serum FE
↓ % saturation
↑ transferrin
↑ TIBC
↑ rbc + ↓ H&H
sign of thalassemia
MCV in the 50s/60s
sign of thalassemia
3 reasons for target cells
thalassemia
hemoglobinopathy
liver disease
many targets
poik
↓↓ hgb A
↑ hgb F, A2
↓↓ H&H
Beta thal major
few targets
slightly ↓ hgb A
↑ hgb A2
↓ or N H&H
Beta thal minor
anemia prevalent in Mediterranean pop
thalassemia
— genes control beta chain genes
— genes control alpha chain genes
2
4
no alpha chains
Hgb Barts
hydrops fetalis
4 𝛄 chains hook together
hgb Bart
4 𝛅 chains hook together
hgb H
alpha + delta chains
hgb A2
alpha + gamma chains
hgb F
globin precipitates associated with hgb H
Heinz bodies
A2 cannot help to compensate in ——– thal
beta/delta
beta + delta fusion gene
Hgb Lepore
↑ retics
RPI >3
schistocytes
↓ H&H
hemolytic anemia
hemolytic anemia chemistry results
hemolysis
hemoglobinuria
↑ bilirubin
↑ LDH
↓ haptoglobin
↑ urobilinogen
sodium dithionite
sodium metabisulfite
sickle solubility reagents
alkaline hgb electrophoresis pattern
+
A
F
S D G L
C E O A2
=
acid hgb electrophoresis pattern
+
C
S
A
F
=
Cooley’s anemia
Beta thal major
Ab causing pernicious anemia
anti-IF
anti-parietal cell
Schilling’s test
for missing intrinsic factor
CNS sx only occur in ——- deficiency as a cause of anemia
B12
(not folate)
Dx hereditary spherocytosis
osmotic fragility ↑
defect in this membrane protein responsible for hereditary spherocytosis, ovalocytosis, etc
spectrin
tx for hereditary spherocytosis
splenectomy
cells are lysing mainly in the splenic environment
in EBV, we see ——- cells as reactive/atypical on the smear
T-cells
responding to the infection of B-cells
detects heterophile antibody
rapid monotest
rapid mono = reflex
EBV serology
lymphocytosis + smudge cells
CLL
CLL is usually a —– cell leukemia
B
CD19
CD20
CD21
CD5
CLL
B-cell leukemia; CD5 indicates malignancy
complications of CLL
infections
hypogammaglobulinemia
AIHA
blast crisis → ALL or AML
ZAP70
poor prognosis
TRAP stain
Hairy cell lymphoma
dry tap
myelofibrosis
hairy cell
CD11c
CD103
hairy cell
starry sky, vacuolated lymphs
endemic in Africa
jaw masses
Burkitt’s lymphoma
CD10 in ALL
CALLA
good prognosis
only seen in myeloid leukemia
auer rods
leukoerythroblastosis
CML
myelofibrosis
Philadelphia chromosome
CML
t9;22
CML
(Philadelpha - BCR/ABL)
LAP stain
↑ in infection
↓ in CML
normal in myelofibrosis
left shift
no ↑ in eos and basos
hypocellular BM
EMH
myelofibrosis
reticulin stain
myelofibrosis
↑ promyelocytes
double nuclei in pros
APML
bundles of auer rods
APML
t15;17
RARA
APML
emergent situation due to potential for DIC
treat with retinoic acid
APML
childhood leukemia
ALL
TdT +
population of young lymphs; lymphocytic leukemia
PAS +
T-cells & young erythroids
monitor ALL children for…
involvement of CNS
CD45
pan-leukocyte marker
CD34
blast marker
MCHC >40%
↑ MCV
↓ rbc
accurate hgb
cold agglutinin
causes anti-i cold agglutinin
EBV
causes anti-I cold agglutinin
Mycoplasma pneumoniae
MPNs
- CML
- polycythemia vera
- essential thrombocytosis
- myelofibrosis
JAK2
↓ EPO
PV
hypoxia
↑ EPO
secondary polycythemia
↓ plasma volume
↑ hct
relative polycythemia
both an MDS and an MPN
CMML
pancytopenia
hypercellular BM
myelodysplastic syndromes
↑ lysozyme
tissue/gum involvement
CMML
microcytic anemias
- IDA
- ACD
- thalassemia
- sideroblastic
lead poisoning or porphyria cause ———- anemia
sideroblastic
normocytic anemias
hemolytic
aplastic
mechanical hemolytic anemia as RBCs pass through small clots
DIC
HUS
TTP
macrocytic anemias
pernicious
folic acid def
myelodysplasia
liver disease/alcoholism
aplastic (some)
mechanisms of ACD
- increased hepcidin blocks release of Fe
- cytokines inhibit EPO
- cytokines inhibit erythropoiesis
- shortened RBC survival (overactive macros)
age 20-50
hemolytic anemia
renal dysfunction
thrombocytopenia
severe CNS sx
fever
TTP
age <5
hemolytic anemia
acute renal failure
thrombocytopenia
mild CNS sx
HUS
generates ATP
EM pathway
protects rbc from oxidative damage by glutathione reduction and NADPH production
hexose monophosphate pathway
(PPP)
keeps Fe in 2+ (ferrous) state
methemoglobin reductase pathway
methemoglobin
has Fe3+ (ferric)
generates 2,3-DPG
Rapoport-Luebering shunt
replaces O2 when hgb releases it
2,3-DPG
O2 curve shift to the left
LUNG environment
↑ pH
↓ pCO2
↓ 2,3-DPG
increased affinity for O2
O2 curve shift to the right
MUSCLE environment
↓ pH
↑ pCO2
↑ 2,3-DPG
decreased affinity for O2
del(5q)
good prognosis for MDS