Haematology- Dr Suchanda Mam Flashcards
Stained PBF info ?
Morphology of RBC
morphology of WBC
Mop=rphology of plateelt
differential count of WBC
relative no of P
parasite `
uses of PBF ?
🔬 Peripheral Blood Film (PBF) Uses
1️⃣ Anemia Dx → Microcytic (IDA, Thal), Macrocytic (B12, Folate), Normocytic (ACD, Hemolysis)
2️⃣ Hemolysis → Schistocytes (MAHA, DIC), Spherocytes (HS, AIHA), Heinz bodies (G6PD), Bite cells
3️⃣ Infections → Malaria (Plasmodium), Babesia, Trypanosoma
4️⃣ Leukemia/Lymphoma → Blast cells (AML, ALL), Smudge cells (CLL), Auer rods (AML)
5️⃣ Platelet Disorders → Thrombocytopenia (ITP, TTP), Giant platelets (Bernard-Soulier)
6️⃣ Parasites → Microfilaria, Malaria, Leishmania
⚠ Gold standard for malaria, hemolysis, leukemia
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immature WBC series ?
🔬 Immature WBC Precursors (Myeloid & Lymphoid Series)
🦠 Myeloid Lineage (Granulocytes & Monocytes)
1️⃣ Myeloblast → Earliest myeloid precursor (AML if excess)
2️⃣ Promyelocyte → Auer rods in AML M3 (APL)
3️⃣ Myelocyte → Last stage to divide, seen in leukemoid rxn
4️⃣ Metamyelocyte → Bean-shaped nucleus, ↑ in infections
5️⃣ Band cell → Shift to left (bacterial infections, CML)
6️⃣ Mature Neutrophil, Eosinophil, Basophil, Monocyte
🦠 Lymphoid Lineage (Lymphocytes)
1️⃣ Lymphoblast → ALL (CD10+, TdT+)
2️⃣ Prolymphocyte → Seen in CLL (Smudge cells)
3️⃣ Mature B & T Lymphocytes
⚠ Leukemia? Excess of immature cells (blasts) in PBF
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Immature series of RBC
🔬 Immature Forms of RBCs (Erythropoiesis)
1️⃣ Proerythroblast → Earliest RBC precursor (Large nucleus, basophilic cytoplasm)
2️⃣ Basophilic Erythroblast → Deep blue cytoplasm (⬆️ RNA for Hb synthesis)
3️⃣ Polychromatophilic Erythroblast → Mixed blue-pink cytoplasm (Hb accumulation)
4️⃣ Orthochromatophilic Erythroblast → Small nucleus, pink cytoplasm (Hb-rich)
5️⃣ Reticulocyte → No nucleus, still RNA+ (⬆️ in hemolysis, blood loss, anemia recovery)
6️⃣ Mature RBC → Biconcave, No nucleus, fully functional
⚠ Reticulocytosis = Marker of Active Erythropoiesis (Hemolysis, Blood Loss, Recovery)
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Hypersegmented N ?
> 5% N have 5 lobes
Hypersegmented N where ?
IDA
Megaloblastic A
myeloproliferative d
chronic renal failure
in which power of microscope hypersegmented Neutrophils are seen ?
✔ 40x (High Power Field - HPF) → Initial screening
✔ 100x (Oil Immersion Lens) → Detailed morphology, confirmation
LD body where ?
WBC monocyte
which stain in PBF <
leishman stain
parasite site ?
RBC - plasmodium
WBC - LD
Plasma- brugia malayi , WB , trypnosoma
Leishman stain composition?
eosin methyline blue
methyl alchohol
WBC pipette use <
total count of WBC P eosinophil spermatozoa , cells in CSF URINE
RBC pipette use ?
total count of RBC WBC P
RBC p e koto time dilute ?
blood taken - 0.5
diluting fluid upto - 101
RBC will be diluted 200 times
- 1
- 101
100 times
0.5-1-100 mark in shaft
Hb pipette use <
total count of all
WBC pipette identify ?
white bead - for well mixing of b;lood
site of blood collection ?
🔬 Sites of Blood Collection
1️⃣ Venous Blood (Most Common)
✔ Median Cubital Vein → Preferred site (Easy access, low complications)
✔ Cephalic Vein → Alternative, used in obese patients
✔ Basilic Vein → Less preferred (Close to nerves & artery)
✔ Dorsal Hand Veins → Used if arm veins unavailable
2️⃣ Arterial Blood (For ABG)
✔ Radial Artery → Preferred for ABG (Allen’s test first)
✔ Brachial Artery → Risky (Deep, near nerve)
✔ Femoral Artery → Used in emergencies
3️⃣ Capillary Blood (Finger/Heel Stick)
✔ Finger Prick → Glucose, Hb, Blood Smear
✔ Heel Prick (Neonates) → Newborn screening, Bilirubin
⚠ Site selection depends on purpose & patient condition
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neubaurer counting chaamber uise ?
🔬 Neubauer Counting Chamber Uses
1️⃣ 🔴 RBC Count → Polycythemia, Anemia
2️⃣ ⚪ WBC Count → Leukocytosis, Leukopenia
3️⃣ 🩸 Platelet Count → Thrombocytopenia, Thrombocytosis
4️⃣ 🦠 CSF Cell Count → Meningitis (Bacterial ⬆️ PMNs, Viral ⬆️ Lymphocytes)
5️⃣ 🩺 Sperm Count (Semen Analysis) → Infertility Workup
6️⃣ 💧 Body Fluid Cell Count → Pleural, Peritoneal, Synovial Fluid
⚠ Manual Method, Gold Standard for Low-Count Samples
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dilution in WBC pipette ?
0.5
11
20
1
11
10
best method of Hb coutn .
CyanMetHaemoglobin method
why spreader slide is not placed on the blood drop /
🔬 Why Spreader Slide is NOT Placed on Blood Drop Directly?
✔ Prevents excessive absorption → Avoids thick smears
✔ Ensures smooth spreading → Uniform monolayer of cells
✔ Prevents cell distortion → Maintains morphology of RBCs, WBCs, Platelets
✔ Avoids clumping → Better differentiation of WBCs
⚠ Correct Method → Touch blood drop at 30-45° angle & push smoothly
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,method of Hb estimation ?
by measurement of iron content + color
sahlis Hb miter
CyanMetHaemoglobin method
oxy Hb method
alkaline hematin method
acid alkali methos
sahlis Hb miter with color matching bpox <
acid hematin method - Qualitative method
Estimation of Hb
why best ?
acurate result
colour permanant
reaction is rapid
all forms of Hb found - except HbS
ESR dec ?
polycythemia
sickel cell anemia
congestive cardiac failurte
dehydration
stain of PBF
chotoboi 2
preparation of PBF
Chotoboi 2
30% blast cell <
acute Leukaemia
Fragmented RBC <
T
ITP
DIC
haemolytic anemia
Target cells ?
HITS
haemoglobinopathies
IDA
T
post-splenectomy
liver D
ESR def ?
rate at which sedimentation take place in 1st hour
pencil cells ?
IDA
schistocytes ??
🔬 Examples of Conditions with Schistocytes:
1️⃣ 🔴 DIC (Disseminated Intravascular Coagulation) → ⬆️ PT, ⬆️ APTT, ⬇️ Platelets, ⬆️ D-Dimer
2️⃣ ⚡ TTP (Thrombotic Thrombocytopenic Purpura) → Pentad: Fever, MAHA, Thrombocytopenia, Renal failure, Neuro Sx
3️⃣ 💥 HUS (Hemolytic Uremic Syndrome) → Triad: MAHA, Thrombocytopenia, AKI (E. coli O157:H7)
4️⃣ 🩸 HELLP Syndrome → Hemolysis, Elevated Liver Enzymes, Low Platelets (Pregnancy)
5️⃣ 🔧 Mechanical Hemolysis → Prosthetic heart valves, Aortic stenosis
⚠ Peripheral Smear → Confirm Schistocytes in all cases
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size & shape abnormal of RBC ?
size - anisocytosis
shape - poikilocytosis
normal RBC shape ?
round + biconcave
name of anisopoikilocytic cells ?
Anisopoikilocytic cells include:
🔬 Schistocytes (fragmented RBCs)
🔬 Acanthocytes (spur cells)
🔬 Echinocytes (burr cells)
🔬 Target cells (codocytes)
🔬 Teardrop cells (dacrocytes)
🔬 Sickle cells (drepanocytes)
🔬 Elliptocytes
🔬 Spherocytes
🔬 Bite cells (degmacytes)
🔬 Helmet cells (keratocytes)
Seen in conditions like hemolytic anemias, liver disease, thalassemia, and microangiopathies.
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size normal RBC <
normocytic
T confirmatory?
Hb electrophoresis
high ESR cause <
TB
MM
RA
SLE
RF
MI
pregnancy’
nephrotic syndrome
MM ?
neoplastic proliferation of Plasma cell that infiltrate in BM
anticoagulant name ?
3.8% Na citrate
EDTA
heparin
paul hellar mixture
K oxalate
ESR e Blood : anticoagulant?
4:1
IDA confirmatory ?
iron profile
why 4:1 ?
mimics physiological plasma conc
ensure uniform erythrocyte suspension without clotting
accurate measurement of sedimentation rate
BM of IDA <
C- EH
M/E - Dec
E - EH
G - N
M - N
PBF findings of IDA <
WBC + P = N
RBC -= M+H+A+P + T + P
blood bank anticoagulant + T ?
Storage of Blood Components and its Significance |
In blood banking, CPDA-1, a citrate-phosphate-dextrose-adenine solution, is commonly used as an anticoagulant and preservative, while stored blood components should be kept at a temperature between 2 and 4°C.
citrate based A
sideroblast ki ?
they are
erythroblast with prussian blue +
iron granules in their cytoplasm
sideroblastic anemia confirmatory?
bnone marrow
Plasma cell origin ?
B cell
What type of disorder is T ?
microcytic hypochromic
Hb disorder ‘
quantitative
PCV value <
male 0.4-0.54 L/ 1L blood
female 0.37-0.47 L /L
PCV >?
V Of RBC in relation to that of the whole blood
PCV + ?
polycythemia vera
dehydration
COPD
chronic heart disease
PCV dec ?
Anemia
overhydration
MCV +
macrocytic
megaloblastic
RCI ?
MCV - 76-96 fl
MCH - 27-32 pg
MCHC - 31-35 gm/dl
at birth Hb ?
23 gm/dl
reticulocytosis cause and def ?
- Hemolytic Anemia
- Blood Loss
- Treatment of Anemia
- Hemorrhage
- Bone Marrow Recovery
- High Altitude
Reticulocytosis is a condition characterized by an increased number of reticulocytes in the bloodstream. Reticulocytes are immature red blood cells (RBCs) that are released from the bone marrow into the blood. They typically mature into fully functional RBCs within 1-2 days. A higher-than-normal reticulocyte count indicates that the bone marrow is producing and releasing more red blood cells than usual.
MCV -?
Microcytic
IDA
T
breakdown products of Hb ?
As the name implies, hemoglobin first breaks down into heme and globin. Globin is the protein component whose amino acids either get recycled or degraded. The heme, however, is what we’re interested in here because it breaks down into iron and bilirubin.
Hbf at birth >? %
60-95%
male Hb <
14-18 gm/dl
children Hb>
11.5-14.5
female Hb <
11.5-16.5 gm/dl
O2 affinity of HbF ?
HbF dosenot bind to 2,3-DPG-dihydrooxy-phosphoglycerate
fetal RBC pick up O2 at lower PO2
chains of Hb >
4 globin chain
2 alpha’
2 beta
4 ferrous iron
apoferritin ?
combine with Fe3+ - form ferritin for storage
inc in Fe overload
causes of eosniophilia ?
allergic disease
helminthic infection
loefflers syndrome
pulmonary eosinophilia
pathological blood loss
- Gastrointestinal Bleeding
- Gynecological Causes
- Trauma or Injury
- Surgical Complications
- Coagulation Disorders
- Medications
- Infections
- Cancer
- Vascular Abnormalities
- Renal Causes
- Liver Disease
- Thrombocytopenia
PCV & ESR ?
inversely proportionate
same as surface area
Iron content stain ?
pearl prussian blue
LS ? other name <
Löffler syndrome is a form of eosinophilic pulmonary disease characterized by absent or mild respiratory symptoms (most often dry cough), fleeting migratory pulmonary opacities, and peripheral blood eosinophilia.
T classify ?
349
transferrin ?
Fe3+ transporter in plasma
inc in IDA
haemoglobinopathies ? def
348
storage form of Fe ?
ferrintin
haemosiderin
RCi in megaloblastic anemia ?
MCV MCH +++
MCHC - N
macrocytosis cause ?>
megaloblastic anemia
liver disease
‘alchholism
reticulocytosis
hypothyroidism
evidence of haemolysis <
bilirubin
urobillinogen
HbA valo na kharap >
good
as O2 transport by binding with 2,3-BPG
bad when glycated/mutated -HbA1C - hyperglycemia
def HA ?
excess RBC destruction
short lifespan of RBC
T def ?
348
classify HA ?
intrinsic/ intracospuscular
membrane - hereditory ellipotocytosis + so=pherocytosis ‘
Hbdefect - T scikle cell ane mia
extrinsic / extracorpuscular
immune mediated
non-immune mediated
fish tape organism ?
diphyllobothriuum latum
Beta T major other name ?
cooleys anemia
stab form in megaloblastic anemia <
granulopoeisisn e
metamyelocyte stage - giant stab form
pernicius anemia ?
Another name for pernicious anemia is Addison’s anemia or Biermer’s anemia. It is a type of vitamin B12 deficiency anemia caused by the inability to absorb vitamin B12 due to a lack of intrinsic factor, a protein produced by the stomach.
lymphocytosis cause ?
IM
mumps
rubella
TB
peryusis
neutrophiulia cause <
acute - appendicits - tonsilitis
pyelonephritis’
bacterial pneumonia
schilling test what type of V-B12
radioactive V-B12 absorption test
features of VB12 deficiency ?
macrocytic megaloblastic anemia
glossitis
peripheral neurophaty
subacute combined degeneratiuon of spinal cord
b12 bindnwith <>
IF
VB12 in body >
mehtylcobalamine
adenosylcobalamine
PNH ?
acquired defect in red cell membrane
characterized by chronic haemolytic anemia
which factor in paroxymal nocturnal haemoglobinuria <>
decay accelering factor - DAF
Hb electrophoresis of T >
352
TEST for T <
Hb electrophoresis
WBC count in B t ?
N/ mild leukocytosis
15-40*10^9/L
heinz body ?
HA
T
Drug induiced HA drug name ><
primaquine
chloroquine
fansider
aspirine
co-trimoxazole
probenecid
chloramphenicol
sickle cell anemia ?
355
production of an abnormal Hb - Hb-S
who are resistant & prone to SCA ?
Prone to Sickle Cell Anemia:
1. Individuals with Sickle Cell Trait (HbAS):
- One normal hemoglobin gene (HbA) and one sickle hemoglobin gene (HbS).
- They are carriers and can pass the gene to their offspring but usually do not show symptoms.
-
Individuals with Sickle Cell Disease (HbSS):
- Inherit two sickle hemoglobin genes (HbS) from both parents.
- They develop the full-blown disease with symptoms like anemia, pain crises, and organ damage.
-
Populations with High Malaria Prevalence:
- People of African, Mediterranean, Middle Eastern, and Indian descent.
- The sickle cell trait provides some resistance to malaria, leading to higher prevalence in these regions.
Resistant to Sickle Cell Anemia:
1. Individuals with Normal Hemoglobin (HbAA):
- Inherit two normal hemoglobin genes (HbA) and do not carry the sickle cell gene.
- They are not at risk of developing sickle cell anemia or passing it on.
-
Populations with Low Malaria Prevalence:
- Regions where malaria is rare (e.g., Northern Europe, East Asia).
- The sickle cell gene is less common in these populations due to the lack of selective pressure from malaria.
Key Note:
- Sickle cell trait (HbAS) provides partial resistance to malaria, which is why the gene persists in malaria-endemic regions.
- Sickle cell disease (HbSS) occurs when two carriers (HbAS) have a child, with a 25% chance of the child having the disease.
alpha T type ?
silent carrier
A-T trait
Hb-H
Hb-Barts hydrops fetalis
Haemoglobinopathies vs T ?
352
CBC of T ?
351
Dose anemia occur in sickle cell trait form ?
No, anemia does not typically occur in individuals with sickle cell trait (HbAS). Sickle cell trait is a heterozygous condition where a person inherits one normal hemoglobin gene (HbA) and one sickle hemoglobin gene (HbS).
Key Points:
1. Normal Hemoglobin Levels:
- Individuals with sickle cell trait usually have normal or near-normal hemoglobin levels.
- They do not experience the chronic anemia seen in sickle cell disease (HbSS).
-
Mild Symptoms:
- Most people with sickle cell trait are asymptomatic.
- In rare cases, symptoms like mild anemia or pain may occur under extreme conditions (e.g., severe dehydration, high altitude, or intense physical exertion).
-
Difference from Sickle Cell Disease:
- In sickle cell disease (HbSS), the abnormal hemoglobin (HbS) causes chronic hemolysis and anemia.
- In sickle cell trait, the presence of normal hemoglobin (HbA) prevents significant sickling and anemia under normal circumstances.
Conclusion:
Sickle cell trait does not cause chronic anemia. However, in rare and extreme situations, mild anemia or other symptoms may occur.
AT Hb-H <
HbH 2-4%
HbF 10% -
SCA type ?
SC trait
SS disease homogenous
B T major < %
HbA - 0-50%
HbF - 50-98%
beta +
??
reduction of synthesis of beta chain
BT minor ? %
HbA2 – 4-10%
HbF - 1-5 %
intravascular vs extravascular HA ?
384
Membrane defect identification test ?
osmotic fragility test
388
autoimmune HA type ?
warm AB
cold AB
Warm AB vs Cold AB ?
382
A T ? HB - bARTS %
HbB 100%
beta o
??
complete absence of synthesis of beta chain
HbE which D >
HbE d
T hb ?
352
PBF of SCA ?
356
Sickling test ?
356
1 drop blood + 1 drop 2% Na meta-bisulphite solution on microscopic slide
cover slip
1-4 hr stand in room
microscope
pancytopenia def
376
Is sickle cell anemic reversible or irreversible /
irreversible due to genetic nature
which drug ?
chloramphenicol
Aplastic anemia cause ?
373
causes of P ?
377
aplastic anemia PBF ?
375
Aplastic anemia >
375
hemorrhagic disorders ?
432
blood grouping system ?
ABO
Rh
M & N
kell
kidd
duffy
lewis
colton
452
dry tape ?
failure of aspirate any material at all
causes of dry tap ?
technical cause
TB
leukaemia
lymphoma
MM
myelofibrosis
myeloproliuferarive d
hodgkins d
hairy cell leukarmia
HA VS SCA in terms of osmotic fragility test ?
OFT inc in HA
dec in SCA
blood rap <
aspiration of blood without bone marrow particles
blood tap «_space;cause <
faulty technique
hypoplastic/aplastic marrow
Bone marrow indication /
307
BT + CT both inc ?
DIC
vWD
ITP - PBF ?
439
ITP - Mrrow findings ?
439
+
+
N
N
+
haemophilia ?
443
bone marrow composition ?
CT
reticulin fibrils
reticular cells
fat cells
nerve fibers
macrophages
blood vessels
305
DIC def ?
448
obsterical cause of DIC ?
abortion
amniotic fluid embolism
abruptio placentae `
o Group er ATg & AB /
Atg - O
AB - Anti-A & B
ABO blood groupin g type ?
453
AB
A
B
O
AB of AB group ?
NIL
pathological effects of sickling - answer in short ?
HA
sickle cell crisis
vaso-occlusive crisis
aplastic crisis
haemolutic crisis
ulcer of lower leg
hand foot syndrom,e
splenic squestration
356
thrombocytosis cause ?
441
hemorrhage
‘trauma
infection
IDA
malignancy
splenectomy
PRV
myelofibrosis
myelodysplastic syndrome
When female affetced in H <>
Turners syn drome
affected F * carrier M
lionization of normal X chromosom e
BM findings of AA ?
375
leuco-erythroblastic blood picture ?
414
why F carrier in H >
defective gene present in chromosome X
erytroblastosis fetalis all ?
461
thrombocytopenia cause /
437
aplastic anemia vs subleukamic leukamie ?
415
koto % pt of CML Philadelphia?
90%
bone ,marrow aspiration instruments
trephine - surgical - needle
cnnula trocer
306
hazards of blood transfusion ?
458
M:E of AA .
normal
define Leukaemia /
396
Lab Dx of CML ?
407
Classify L ?
396
lymphoblast myeloblast ?
402
FAB - AL /
398
Lab Dx of AML >
400
ALL vs AML ?
401
ALL e ki ki cell .
401
PAS stain ?
402
TC DC of WBC in ALL ?
In ALL:
- TC: High (leukocytosis) or low (leukopenia).
- DC:
- Increased lymphoblasts (>20%).
- Decreased neutrophils (neutropenia) and normal lymphocytes (lymphopenia).
- Anemia and thrombocytopenia common.
ALL CGL age >
ALL - children - 2-4
CGL- 30-60
classify CML ?
Chronic Myeloid Leukemia (CML) is classified into three phases based on disease progression:
-
Chronic Phase:
- Most patients are diagnosed in this phase.
- Mild or no symptoms.
- <10% blasts in blood or bone marrow.
- Responsive to treatment.
-
Accelerated Phase:
- Disease progression with worsening symptoms.
- 10–19% blasts in blood or bone marrow.
- Increased basophils (>20%).
- Resistance to treatment.
-
Blast Phase (Blast Crisis):
- Resembles acute leukemia.
- ≥20% blasts in blood or bone marrow.
- Poor prognosis, rapid progression.
Key Note:
- Progression from chronic → accelerated → blast phase indicates worsening disease.
BLastic crisis features ?
410
CGL e TC DC of WBC >
In CGL (CML):
- TC: Markedly elevated WBCs (>100,000/µL).
- DC:
- Increased granulocytes (neutrophils, basophils, eosinophils).
- <10% blasts (chronic phase), 10–19% (accelerated), ≥20% (blast crisis).
- Anemia and thrombocytosis common.
myeloproliferaive <
417
myelodysplastic ?
411
immunoproliferative d ?
422
MM def /
424
labv Dx of MM ,.
424
BJ protein /
425
features 3 of MM <
426
Paraprotein example /
423
paraproteinemia def ?
423
PRV all /
419
other name of wintrobe ESR tube ?
The Wintrobe ESR tube is also known as the Wintrobe tube or Wintrobe hematocrit tube. It is a narrow, graduated glass tube used for both erythrocyte sedimentation rate (ESR) measurement and hematocrit determination.
confirmatory of megaloblastic anemia /
bone marrow
why hematocrit is called so ?
The term hematocrit comes from the Greek words:
- “Haima” (αἷμα): meaning blood.
- “Krites” (κριτής): meaning judge or to separate.
Why it’s called hematocrit:
- The hematocrit measures the volume percentage of red blood cells (RBCs) in whole blood after centrifugation.
- It essentially separates and judges the proportion of RBCs in the blood, hence the name hematocrit.
why anemia occurs in megaloblastic anemia ?
In megaloblastic anemia, anemia occurs due to:
- Impaired DNA synthesis (vitamin B12/folate deficiency).
- Ineffective erythropoiesis: Large, immature RBCs (megaloblasts) are destroyed in bone marrow.
- Macrocytic RBCs: Fewer, shorter-lived RBCs enter circulation.
leukamoid reaction e ki L thakbe >
NO
Identify all instrument Bone marrow examination a ki ki dekh Blood tap, dry tap ki? Jodi blood tap hoy amra ki kori? D/b megaloblastic anemia and pernicious anemia How u will identity them Procedure of shilling test Radioactive ta kon route a dei?kno dei? Neutrophilia, ecslophilia def+ casuse Megaloblastic anemia BMF.
Schilling test - orally - Radioactive VB12
megaloblastic vs pernicious ?
schilling test <
neutrophilia def ?
N - >7500 /mm3
eosinophilia def >q
> 700 cells/mm3 in Peripheral blood
leukocytosis - neutrophilia
same
v-B12 deficiency cause ?
360
factors of ESR
323
PBF of megaloblastic anemia >
10000000000000000000%%%
RBC - macrocytosis oval macrocyte - A-P - megaloblast - howel jolly body
WBC - neutropenic - hypersegmenetd N
P - Thrombocytopenia
composition of paul heller mixture /
phenol - 2.5%
nitric oxide - 0.5%
distilled water
which one of paul heller help in systemic disease <
nitric acid
d of CNS & kidney
proteuinuria
stain of cytopahtological and histopthological <
C - Pap
H - H & E
Characters of megaloblast ?
large cell
cytoplasm - abundant
round RBC
maturation arrested
nucleus - stippled apperance
howell jolly body
369
megaloblastic anemia cause ?
morphological classification basic ?
red cell size’
degree of Hb
MCV MCH MCHC
Anemia def ?
dec below normal limit
of Hb conc erythrocyte count / hematocrit
M:E inc when ?
CML
AA
infection
inflammation
chronic anemia
M:E dec ?
IDA
T
megaloblastic anemia
hemolytic anemia n
hypochromia ?
central pallor > 1/3
why pernicious anemia ?
dec VB12 absoprtion
why vitmain b12 absoprtion less
no Intrinsic factor
autoimmune destruction of gastric parietal cell
parietal cell theke asa IF - bind korbe na B12 er sathe
no absoprtion in ileium
complete absent of peptide chain ?
AT major - hydrops fetalis Hb barts
B T major
complain of H patient >
bleeding in joint cavity
cause of prolobged BT ?
Leukaemia
prolonged CT ?
H
DIC
vWD
Which L has normal platelet count ?
CLL
ALL predominant cell & %
lymphoblast
>20%
AML cell ?
myeloblast
>20%
all heamatological d confirmatory tets
bone marrow
CBC
Difference between 2 polycythemia ?
419
platelet countin CML ?
407
Predominant cell of all leukaemia ?
The predominant cell type in each type of leukemia is as follows:
-
Acute Lymphoblastic Leukemia (ALL):
- Lymphoblasts (immature lymphocytes, usually B-cell or T-cell precursors).
-
Acute Myeloid Leukemia (AML):
- Myeloblasts (immature myeloid cells).
-
Chronic Lymphocytic Leukemia (CLL):
- Mature B-lymphocytes (small, mature-looking lymphocytes).
-
Chronic Myeloid Leukemia (CML):
- Granulocytes (neutrophils, basophils, eosinophils) and their precursors (myelocytes, metamyelocytes).
-
Hairy Cell Leukemia:
- Abnormal B-lymphocytes with “hairy” projections.
Key Note:
- ALL and AML involve immature cells (blasts).
- CLL and CML involve more mature cells.
which Amino acid is dec in SCA <
Glutamic acid
347 as HbS
replced by lysine
advice given to a SCA pt ?
Advice for a Sickle Cell Anemia Patient
Patients with sickle cell anemia (SCA) need lifelong care to prevent complications and improve quality of life. Here’s the essential advice:
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- Prevent Pain and Sickle Cell Crises
✅ Stay Hydrated – Drink plenty of water to prevent dehydration, which can trigger sickling.
✅ Avoid Extreme Temperatures – Cold and heat can worsen sickling and cause pain crises.
✅ Manage Stress – Emotional and physical stress can trigger a crisis.
✅ Avoid High Altitudes – Low oxygen levels can increase sickling risk (e.g., air travel, mountains).
✅ Exercise in Moderation – Avoid overexertion; take breaks and stay hydrated.
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- Prevent Infections
✅ Vaccinations: Pneumococcal, meningococcal, Hib, flu, and COVID-19 vaccines are essential.
✅ Daily Penicillin (if recommended): For children up to 5 years to prevent infections.
✅ Seek Immediate Care for Fever (≥38°C/100.4°F): Infections can be life-threatening.
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- Medication & Treatment
✅ Hydroxyurea: Reduces sickling and pain crises by increasing HbF (fetal hemoglobin).
✅ Folic Acid Supplements: Helps RBC production.
✅ Pain Management: Use acetaminophen, NSAIDs, or opioids (if prescribed) for crises.
✅ Blood Transfusions: For severe anemia or stroke prevention.
✅ Bone Marrow Transplant (Curative Option): Recommended for severe cases in young patients.
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- Lifestyle & Regular Checkups
✅ Regular Doctor Visits – Monitor anemia, organ function, and complications.
✅ Healthy Diet – Balanced nutrition with folate-rich foods.
✅ Avoid Smoking & Alcohol – These worsen sickling and organ damage.
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- Watch for Serious Complications
⚠️ Severe Pain Crisis – May need IV fluids and pain medications.
⚠️ Stroke Symptoms – Weakness, speech issues, vision loss → Seek emergency care.
⚠️ Acute Chest Syndrome – Fever, chest pain, breathing difficulty → Medical Emergency!
⚠️ Priapism (Prolonged Painful Erection) – Can cause permanent damage.
Would you like more details on treatment options or crisis management?
D/B megaloblastic a & Pernicoius anemia /
Megaloblastic Anemia vs. Pernicious Anemia
Summary:
- Megaloblastic anemia is a general term for anemia caused by B12 or folate deficiency.
- Pernicious anemia is a specific type of megaloblastic anemia caused by autoimmune loss of intrinsic factor.v
Feature | Megaloblastic Anemia | Pernicious Anemia |
|—————————|————————————————–|———————————————|
| Definition | Anemia due to impaired DNA synthesis (vitamin B12 or folate deficiency). | A type of megaloblastic anemia caused by vitamin B12 deficiency due to lack of intrinsic factor. |
| Cause | - Vitamin B12 deficiency (dietary, malabsorption).<br></br>- Folate deficiency. | Autoimmune destruction of parietal cells in the stomach, leading to lack of intrinsic factor. |
| Intrinsic Factor | Not directly involved. | Intrinsic factor is absent or non-functional. |
| Gastric Involvement | None. | Autoimmune gastritis damages parietal cells. |
| Symptoms | - Fatigue, weakness.<br></br>- Macrocytic RBCs.<br></br>- Neurological symptoms (if B12 deficient). | Same as megaloblastic anemia + neurological symptoms (e.g., paresthesia, ataxia). |
| Treatment | - Vitamin B12 or folate supplementation. | Lifelong vitamin B12 injections (oral B12 ineffective due to lack of intrinsic factor). |
| Key Note | Broader term; includes all causes of B12/folate deficiency. | A specific cause of vitamin B12 deficiency. |
why neurological deficiency in vit-B12 ?
isomerization of methyl malonyl co-enzyme A to succinyl co-enzyme A is depenedent on VB12
Dec VB12 = NO isomerization = inc methyl malonic acid
incorporation of abnormal FA into neuronal lipids
myelin breakdown
neurological breakdown
folate deficiency M/A
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what is howell jolly body ?
Howell-Jolly bodies are small, round, dark-purple inclusions found in red blood cells (RBCs). They are nuclear remnants (DNA fragments) that persist after the nucleus is expelled during normal RBC maturation.
Key Features:
1. Appearance:
- Small, dense, round inclusions.
- Visible on a peripheral blood smear stained with Wright or Giemsa stain.
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Causes:
- Hyposplenism or asplenia (e.g., surgical removal of the spleen, sickle cell disease, or functional hyposplenism).
- Megaloblastic anemia.
- Hemolytic anemia.
- Post-chemotherapy or bone marrow transplantation.
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Significance:
- Indicates impaired spleen function (spleen normally removes nuclear remnants from RBCs).
- Seen in conditions where the spleen is absent or not functioning properly.
Clinical Relevance:
- Presence of Howell-Jolly bodies suggests splenic dysfunction and may indicate underlying conditions like sickle cell disease, post-splenectomy state, or autoimmune diseases.
13.32025
12.22AM
ALL complain ?
- gum bleeding
- bruises
- cervical lymphadenopathy
- fever
- sore throat
- epistaxis
- rash
- severe anemia
- body ache
- spleen palpable
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13.3.2025
5.35 PM
