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Download PG Medical 2nd Year Pathology Anemia Handwritten Notes

Download PG Medical ( Post Graduate Medical degree) 2nd Year Pathology Anemia Handwritten Notes

This post was last modified on 02 August 2021

Medical PG Handwritten Notes 1st Year, 2nd Year, 3rd Year and 4th Year (Study Material)


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Anaemia

Stem Cells

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CFU-E

Hb Ist appears

-EINT, Special Stains

Bro-erythroblast (paronoamoblast)

(Pronarmblast)

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Noumoblast

Early Normoblast - Basophilic

Hb detected. Intermediate - Polychaematophilic

Routine stains

Late - Oathochromatic.

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Nucleus Removed

Reticulocytes - (non nucleated)

RBC maturation

PB Time. 48hrs

Reticulocytes - Reticulum like structure

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Ribosomal RNA proteins

can be stained by Romanowsky stain (Routine stain)

1) Giemsa 3) Jenner stain

2) Leishmann 4) Weight stain.

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Supervital stain - specific staining

Best stain - New methylene Blue > Brilliant Cresyl Blue.

Use of Romanowsky stain -

-Reticulocytes

-Howell - Jolly Bodies

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-Basophilic stippling

-Cabot Ring

Heinzy Bodies- never stained by Romanowsky stain..!!

-methyl violet/Crystal violet stain!

Reticulocyte < Peripheral Blood

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Bone marrow

NR- 0.5 to 1.5/ TR- Hemolytic anaemia.

VR- aplastic anaemia.

Nutritional anaemia(Fe, Vit B12)

In megloblastic anaemia mild Hemolysis, can also - Jaundice,

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splenomegaly, Nu. RBC

B.m: Hypercellular

M/E- Ratio Reversal (normal M/E = 3/1)

Erythroblastic Hyperplasia.

B12

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Folic acid

No DNA Synthesis nonuclear maturation.

Apoptosis (nucleated RBC)

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Infants Anterior Tibia lateral parts

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child/adults- Posterior iliac Crest

Obesity - Anterior iliac Crest

Hemolytic Anaemia

Hereditary Spherocytosis - AD/AR.

RBC membrane protein defect

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a) Spectrin-m/abundant, m/emutation elliptocytosis.

b) Ankyrin - m/c mutant in spherocytosis

c) Band-3 (Anion Transport Protein)

d) Protein 42- Palladin.

e) Glycophorin (not associated with HS)

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a-Spectrin mutation: Coagulate Severitary

RBC-Biconcave, Spectrin-actin interaction.

Actin

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Glycophorin > Band 3

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Glycophorin A > B > C > D:

RBC-7.5µm dia.

- Central pallor-1/3rd of diameter of RBC.

Hypochromic-CP->1/2 of dia of RBC.

Function- Provide flexibility/deformability to RBC.

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mutation

No flexibility

damaged membrane

Surface area

Micro spherocytes (Smaller, no Central pallor)

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Spleen (extravascular Hemolysis)

B- Splenectomy, But even after splenectomy, Spherocytes persists HS

Hemolytic Anaemia mild to moderate Severe.

Jaundice

pigmented gallstones

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Reticulocytes 15-7 days (Transient)

Aplastic crisis

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Screening Test

RBC isotonic 0.9/ NaCl.

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Hemolysis start at 0.5% (0.48%)

Hemolysis Completed 0.3%

Hereditary Spherocytosis

Hemolysis - >0.5% (osmotic fragility)

G6PD deficiency)- XLR

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m/c a/w - Bacterial infections

m/c Drug - primaquine > Rapson.

Java beans (favism)

malaria protective - P. falciparum

enzyme def Hb-pathies

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G6PD deficiency Thalassemia

Pyruvate kinase deficiency HbC.

Sickle cell carrier

Duffy DR. P. vivax

negative Protective against

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NO DR P. vivax.

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NADP

NADPH

No Reducing agent Reduced glutathione.

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Denatured globin chains Heinz cells.

Bite cells.

Paroxysmal Nocturnal Hemoglobinuria.

Urine Sample must be collected in morning

Ist void

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mid stream

5-10%-Congenital.

Somatic mutation in stem cell - Phosphatidyl Inositol.

coded by pian Glycosyl - A gene. mutation

Anchorprotein.

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Complement Regulatory Protein

1) CD-59 - Membrane inhibitor of Reactive lysis

2) CD. 55 - Decay accelerating factor.

3) - Co Binding protein

M/Imutation: GPI-AP.

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Amongst, complementary Regulatory protein- CD59.

PB Pancytopenia + Hemolytic Ant Thrombosis. / - Triad

m/c Cause of death Hepatic Vein thrombosis

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PEV

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Pathogenesis- Acidic PH

Activate complement

C5-9 (MAC) generally RBC

protected against MAC

Damage to RBC by CRP

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Scanning- Intravascular Hemolysis

HAMS test, m/I

Sucrose lysis Test.

Confirm Flow Cytometry

PNH Aplastic anaemia

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MTDS Acute Leukaemia

Pre leukeamic Condition - PNH, MTDS, aplastic anemia

Autoimmune Hemolytic Anaemia - AIHA

Warm Cold

m/c Type Warm agglutinin Hemolysin

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IgM IgG

Ig G1. Syphilis, mycoplasma Donath

m/c dus OLL Viral infections. Landsteiner Ab

AI disorders - SLE (against P-Ag)

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Cold type

Drugs- Penicillin Paroxysomal

cold Hemoglobinuria.

a-methyl Dops m/c associated with viral infection

m/c- Spherocytosis * IgG P.Ag

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RBC

AIHA. activate complement.

Hemolysis

Coombs Test

Direct Indirect

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Ab in Abs HDN in

Surface of. in Serum: maternal Sample.

RBC Cross matching

Nousein unexpected Ab

AIHA Non-Immunogenic (in Rare blood

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MAHA groups)

Drug induced.

-ITP (IgG platelets)

Hemolytic disease of newborn.

Coombs Test-ve: Aplastic Anemia.

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mismatch Blood Transfusion.

in Recipient.

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Embryonic Hb (Weeks 10L)

Gower I Zeta-2 Epsilon-2.

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2) Gower II a2 e2

3) Portland I Zeta2 e2

4) Portland II Zeta2 ?2.

Sweeks

HbF a2 ?2

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HbA a2 ß2 [HbA2 a2 d2]-minor.

Hb pathies Quantitative

Qualitative / a, ß (Quantity reduced)

Sickle cell anaemia. a-a thallassemia,

ß. chain. ß-chain ß thallasemia.

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6th position

glutamic Valine

[polar]-ve neutral

Insoluble

-Solubility is altered

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-Stability-normal.

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ß-thallasemia

Point mutation.

missense

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Point mutation

nonsense

Partially accepted missense a-thallasemia-Deletion.

point mutation. -loss of a chain

a-thallasemia- aa/aa

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1a gene deletion : aa/a- : Courier

2a gene deletion: a-/a-; aa/--: Trait

3a gene deletion: a-/-- Hbz

4a gene deletion- --/-- Hb Bartz - Hydrops fetales.

ß-thallasemia.

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Q. [21/F: Hb-59% unit of BT; Hepato splenomegaly]

T.major, T.minor, T.trait, AIHA

1) T. major: Codey A/mediterranean Anaemia.

Hb-<3g%

multiple units of BT. Iron overload.

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CHF m/c COD

Usual-to years

Rarely reach and decade

Confam: HPL chromatography Hb. electrophoresis

HbF To confirm

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HbA-96% HbF-30-90/

HbF-<2%.

HbA2-3.5%

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Thalassemia

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Pediatric

Hb->7g/

upto occasional Blood Transfusion

pediatric.

Adult Transfusion dependent anemias.

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HPLC - HbF (10-30/):

3) Thalassemia minor: Pediatric/adult

9-11g%

No.H/o blood transfusion

Both HbF HbA2

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electrophoresis

HbF- (1.1-41)-nodiagnostic

HbA2-4-8/-bondiagnostic.

P. B Microcytic Hypochromic anaemia

hoal Timinos.

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RDW-11.5-14.5

anisocytosis

Mentzer index MCV <13 13

RBC Count

NESTROF - Best Screening method for thalassemia

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Normal

0.3/

normally Hemolysis Complete

No lines seen

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Hemolysis-not complete

RBC membrane Stable.

Thalassemia

Sickle cell Anaemia

Hemolysis osmotic

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not complete fragility

Able to view lines

0.3% - Hemolysis complete

RBC-dissolved.

Normal

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HbE

Hbs Slow movement

Cathode(-) Anode (+)

HbA -ve faster.

2 Bands Carrier - Hbs + HbA

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only 1 Band Disease

sunder Hypoxia, Sickle cells express adhesion

molecule.

1) Vasoo.cclusive-m/c.clinical picture

CRSs hand foot Syndrome

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b) acute chest syndrome

(respiration) Not Jusemble

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3) fish mouth vertebra

M/C Cause of DIT in Sickle Cell Salmonella infections

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4) Autosplenectomy.

PB- Diserythrocytesis.

nuclear Remnants - Howell Jolly Bodies

1) splenectomy

Aplastic Crisis Parvarus megaloblastic anaemia

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III) Sequestration Crisis- most dangerous,

life threatening cuses

Large volume of RBC dumped within Spleen.

Dacute Painful splenic enlargement.

ii) Hypovolemia - Shock (within 4hrs)

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patient-dye

medical emagency

Hemosiderin+ Ca2+ Fibrotic Tissue

Gamma Gandy Bodies

1) SCA

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2) CNTL

3) Liver aucheus

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1) most important factor HbS concentration

In cauter - HbA polymerization, prevents Sickling.

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1) Fetal Hb-Sickling

Reach to adult-level (<2%)-6months.

4. year old hay episodic. HP/Jaundice since birth

- Least-likely-Sickle.cellanaemia.

ii) HBC Anaemia / Hbsc disease

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Sickling; Hbc Removes water & Sodium from

all. FHbscendentation - Sickling

katuves of Hat - 1) padifovative retinopathy

2) Bone infarction.

Screening- Sodium metabisulphite.

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2) Sodium dithionate.

HPLC> electrophoresis.

Megaloblastic disease

1) Vit-B-12

ii) Folic - Av.

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Ab against intrinsic factor of Castle (Parietal alls)

Pernicious Ab against

anaemia Fundus

Adenocarcinoma in pernicious - Fundus

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Macrocytosis

most charecteristic

microcytosis

Macrocytosis MCV 100L

diameter of RBC - >9µm.

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Microcytic MCV <80L

diameter of RBC <6µm

met specific - Hyper Segmented neutrophils

Neutrophil Globes of neutrophil <<<

75 lobes ->15 / neutrophils: 102

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dyserythrocytesis.

1) Howell-Jolly Bodies:

ii) Fine Basophilic stippling

iii) Cabot Ring Figure of 8

Target Cells

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Sickle cell Anaemia

Iron deficiency Anaemia

Thalassemia frost Megaloblastic Anaemia.

charecteristic)

MCV > 100L

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MCHC 33-37 g/dl

H.ST, megaloblastic-normal. (not charecteristic

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m/c presentation fatigability, iron

Latent Iron deficiency Anaemia- Iron Stores without

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Anemia

Hb within normal limits

Fe-absorped-Fe 2+.

SI proximal duodenum

Storage RES - BNT, liver, spleen.

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Fe3+ B.N Peripheral Blood.

Serum ferritin/Storage Iron.

Hepcidin - master Regulator of iron metabolism

1) Iron absorption

2) Iron mobilization from storage sites

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Fe 2+

Apex

DMTT-1

DMTT-non specific

Transporter,

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all divalent metal ions

Hephaestin Basal Hepcidin

Fe2+

Fe 3+

Fe Transferrin

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Carries.

Ferritin

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Lab findings

earliest

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i) Serum ferritin - most Sensitive

11) Transferrin

TIBC - normal 300-400µg/dl

Anemia of chronic disease

iv) Saturation of Transferrin (N: 22-50%

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IDA-<16/)

v) Hepcidin-

IDA with inflammation/infection

Serum ferritin (Acute phase Reactant)

gold standard Bone marrow Biopsy)- with spacial

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Stain (Peils Prussian blue)

for iron stores.

11) Transferrin Receptors -

TR

TR

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TR

TR

blood

Serum Transferrin Ratio with log index of ferritin>

Serum Transferrin Receptor > Serum ferritin

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Best investigation to diff- IDA & ACA:

1) Bone marrow with Special Stains

2) Serum Transferrin Recepts.

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