REINVENT THE WAY YOU LEARN WITH
BY DR PRIYANKA
Patho
DR. PRIYANKA
SACHDEV
MASTERCHART DR. PRIYANKA
SACHDEV
HEMOLYTIC ANEMIAS
Paroxysmal Nocturnal
Hereditary Spherocytosis G6PD Deficiency Anemia
Hemoglobinuria (PNH)
Introduction AD XR Acquired intrinsic defect in RBC
membrane
Pathogenesis: Mutation in Ankyrin > Band 3 G6PD absent Mutation in PIG-A gene
> Spectrin > Band 4.2
Oxidant stress
RBC become spherocytes Glycosyl Phosphotidyl Inositol
(GPI) not synthesized
NADPH not generated in HMP
trapped in spleen pathway
CD55, CD59 absent on RBC
Extravascular hemolysis Oxidised Glutathione not
converted to reduced
Glutathione RBC sensitive to complement-
mediated lysis during
sleep/acidosis
RBC not protected from
oxidant injury
Intravascular hemolysis
Extravascular +
Intravascular hemolysis
Lab Diagnosis 1 PS Spherocytes 1 PS Heinz Bodies 1 Ham Test
& Bite Cells
2.
2 Osmotic Fragility Test
2 Flow Cytometry
Fragility
Bimodal RBC
Heinz bodies on
supravital stain
Bite cell
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MASTERCHART DR. PRIYANKA
SACHDEV
HEMOLYTIC ANEMIAS
Autoimmune Hemolytic Anemia (AIHA) Sickle Cell Anemia (SCA) Thalassemia
Types
Introduction
Warm Cold Qualitative abnormality of Quantitative abnormality of
globin chain synthesis globin chain synthesis
Ab react at 37°C Ab react at 0-4°C
HbA ( 𝝰 2 β 2 )
Pathogenesis: Ab formed against RBC Ag 2 Types
β-globin gene mutation (Ch 11)
Ab attach to RBC
α Thal β Thal
Single point mutation at 6th position
Warm Cold Glutamic acid replaced by valine Deletion of α chain gene
(ch 16)
Ab coated RBC Activates HbS
Pass through spleen Complement (MAC) Point mutation of β chain
gene (ch 11)
Deoxy Hb Sickled RBC
Extravascular Intravascular
hemolysis hemolysis
Polymerization to Splenic
form elongated rods Sequestration
Sickle-shaped RBC Phagocytosis
abnormally sticky
Extravascular
Vaso - occlusion hemolysis
Lab Diagnosis 1.
1 PS Spherocytes 11. PS Sickle Cells, Howell- 1
1. PS Microcytic Hypochromic
Jolly Bodies RBC, Target Cells
2.2 Osmotic Fragility fragility
2
2. Coombs Test 22. Hb Electrophoresis
1 band
Ask Doubt
3 NES TROF test +
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MASTERCHART DR. PRIYANKA
SACHDEV
ANEMIAS DUE TO ↓ RBC PRODUCTION
Iron Deficiency Anemia (IDA) Sideroblastic Anemia Anemia of Chronic Disease (AOCD)
Introduction MC anemia in world and India Inability to incorporate iron into Hb Anemia secondary to chronic disease
Dietary lack Erythroblast
Chronic disease
Pathogenesis:
absorption
↓ Iron
Mitochondrial enzyme defect
requirement Proinflammatory cytokines
Blood loss
Ferritin is utilised for Hb Iron cannot be converted to heme
synthesis ↓ Erythropoietin ↑ Hepcidin
Iron accumulate into mitochondria of
Once Ferritin also erythroblast Reduced iron transfer
Defective
depleted from storage pool to
Erythropoisis
Erythroid Precursor
Hb synthesis Ringed Sideroblast
Abnormal (Microcytic, iron storage
Sideroblastic
hypochromic) RBC
Anemia AOCD
Formed
IDA
Lab Diagnosis 1 PS Microcytic hypochromic 1 PS Microcytic hypochromic RBC 11. PS Normocytic Normochromic
RBC, Target cell
22. BM Micronormoblast 2
2. BM Ringed Sideroblast 2 BM iron
Ask Doubt
3 Transferrin sat 3
3. Transferrin sat 3 Transferrin sat
4 TIBC 4
4. TIBC 4 TIBC
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MASTERCHART DR. PRIYANKA
SACHDEV
ANEMIAS DUE TO ↓ RBC PRODUCTION
Megabloblastic Anemia Pernecious Anemia Aplastic Anemia
Introduction Imparied DNA Synthesis Special type of Megaloblastic Anemia Pancytopenia
Pathogenesis: ↓ vit B12 or ↓ folic acid Auto Ab against gastric Parietal cells Aplasia of Bone Marrow
↓ DNA synthesis ↓ in HSC (Hematopoietic stem
Intrinsic factor absent cells)
Defective Nucleus Maturation ↓ in all 3 blood cells
Vit B12 not absorbed
Nucleus Maturation lags behind
cytoplastic maturation ↓ RBC ↓ WBC ↓ Platelet
Vit B12 deficiency
Megaloblast and Macrocytes Anemia Leucopenia Thrombocytopenia
Pernecious Anemia
Megaloblastic Anemia
Pancytopenia
Lab Diagnosis 1.1 PS Macrocytes, Howel-Jolly 1
1. Schilling test 1.1 BM Dry tap
body, Basophilic stippling,
Carbot ving, Hypersegmented
neutrophils
22. BM Megloblastic
Ask Doubt
33. Schilling test
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MASTERCHART DR. PRIYANKA
SACHDEV
LEUKEMIAS
CML AML ALL CLL
MC Age > 50 years 15 - 40 years Children 60 years
Pathogenesis -
t(9;22) / ABL - BCR 2 types
t(8;21) Del 13q
translocation ->
t(15;17) Del 11q
Philadelphia
Pre B cell ALL Pre T cell ALL Del 17p
Chromosome inv(16)
PAX5, EBF mutation Trisomy 12q
Hypodiploidy
NOTCH 1
Hyperdiploidy
mutation
t(9;22)
Classification Chronic phase Blast < 10% 1. FAB M0, M1, M2, M3, 1. FAB L1, L2, L3
Accelarate phase Blast 10-19% M4, M5, M6, M7
Blast phase Blast > 20%
Lab Diagnosis 1.1 PS Immature mycloid 1. 1 PS Myeloblast 1 1. PS Lymphoblast 11. PS Mature Small Lymphocytes
precursors (Myeloblast,
Promyelocytc, Myelocyte,
Metamyelocyte, Band forms)
MPO + PAS +
Sudan Black + Immunophenotyping CD19,
2 Cytochemistry NAP 2 Cytochemistry 2 Cytochemistry 2
CD20, CD23, CD5
score ↓ NSE + Acid Phosphatase +
Treatment 1. Target therapy Imitinib 1. Chemotherapy cytosine 1. Chemotherapy Vincristine + 1. Palliative and symptomatic t/t
arabinoside + Anthracyclines Prednisolone + Anthracyclines
2. BM transplant + 6 Thioguanine L- asparginase
APML (M3) Tretinoin
2. BM transplant 2. BM transplant
Index to assess prognosis of CML Good prognosis
Progress Criteria Good Bad
Age <40 years
M2, M3, M4 forms of AML
Sokal index 1. Age 2-10 years <2 years; >10 years
Blast cell with Auer rods
a) Age TLC < 25 x 10⁹/L
b) Platelet count t (15;17), t (8;21), inv 16 2. Gender Female Male
c) Spleen size Leukemia without preceding
d) Circulating blasts MDS 3. Race White Black
e) Cytogenetic changes
Bad prognosis
4. CNS, mediastinum, Absent Present
Ask Doubt Age <2 years or >55 years testicular
M0, M6, M7 forms of AML involvement
Hasford system
Complex karyotypes
a) Age TLC > 100 x 10⁹/L
b) Platelet count
5. Peripheral blood <100000 >100000
Deletions 5q, 7q
blast count
c) Spleen size AML with preceding MDS or
d) Circulating blasts anticancer drug exposure
e) Basophils and
6. Cytogenetics a. Hyperdiploidy a. Hypodiploidy (<50
(>50 chromosomes) chromosomes)
eosinophils
b. t (8:14)
b. Trisomy 4, 7, 10
c. t (1:19)
c. t (9:12) and t d. t (9:22)
PATHOLOGY 5 9321001103 (12:21) e. t (4:11)
MASTERCHART DR. PRIYANKA
SACHDEV
HODGKIN’S LYMPHOMA
Classical Non Classical
Nodular Sclerosis Mixed Cellularity Lymphcyte rich Lymphocyte depleted Lymphocyte Predominant
MC type in MC type in Associated
MC
world India with HIV
Gender M=F M>F M>F M>F M>F
Age Adolescent Biophasic (young and Old age Old age Young age
>55 years
Lacunar type Classical type Classical type Pleomorphic LH (Popcorn)
type type
RS cell
Histo-
pathology
CD 15+ CD 15+ CD 15+ CD 15+ CD 15-
IHC CD 30+ CD 30+ CD 30+ CD 30+ CD 30-
CD 20+
Bcl 6+
Association No Yes Yes Yes No
with EBV
Prognosis Excellent Very Good Good Poor Excellent
Ask Doubt
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MASTERCHART DR. PRIYANKA
SACHDEV
NON-HODGKIN’S LYMPHOMA (NHL)
Diffuse Large B cell Follicular Lymphoma Burkitt lymphoma Hairy cell leukemia
lymphoma ( DLBCL)
Introduction -MC NHL - Arise from germinal - Very aggressive but - Excellent prognosis
centre chemosensitive
-Worse prognosis - Chemosensitive
- Tumour lysis syndrome
Age 60 years Middle age Children or young 55 years
adults
Pathogenesis -t(14;18) - t(14;18) - t(8;14) BRAF
-BCL - 6 multation mutation
Lab Diagnosis 1 LN biopsy → large 1 LN biopsy → Centrocytes 1 LN biopsy → starry 1 PS → Hairy cells
cleaved cell in diffuse and centroblasts sky pattern
pattern
2 Bm biospy → Dry tap or
Honey comb
appearance
Immunophenotype CD 10 CD 10 CD 10 CD 19
CD 19 CD 19 CD 19 CD 20
CD 20 CD 20 CD 20 Surface Ig
BCL - 6 BCL - 6 CD IIc
BCL 6
BCL - 2 Surface IgM CD 25
Surface Ig CD 103
Ask Doubt
Annexin A1
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