PATHOLOGY CHANTING BY DR.

PARAS
☆ CELL ADAPTATION

1. HYPERTROPHY =

•
↑ CELL SIZE
example → PHYSIOLOGICAL • UTERUS DURING PREGNANCY
•
BREAST DURING LACTATION
→ PATHOLOGICAL •
LVH

2. HYPERPLASIA =
↑ CELL NUMBER
•

EXAMPLE → PHYSIOLOGICAL • BREAST DURING

Beg 4
.

→ PATHOLOGICAL •
Puberty HORMONES
Ab ↑IN
.

↳ ↑ ANDROGEN → BPM
↳ ↑ ESTROGEN → Endometrial Ca .

3. ATROPHY =

•
& Cell size & Number

4. METAPLASIA =

•
⑥ cell is
replaced by another ⑨ cell
EXAMPLE → •

Squamous metaplasia -
SEEN IN Smokers
COLUMNAR METAPLASIA BARRED
→
esophagus
•
.

sq replaced columnar cells

by
→ .

→ HALLMARK = GOBLET CELL .

→ STAIN USED = ALVAN BLUE/ MUG CARMINE

☆ CELL INJURY

1. REVERSIBLE CELL INJURY

•
EARLIEST ION INVOLVED → Nat
• MOST IMP . MORPHOLOGICAL FEATURE → SWELLING
• ONLY PYKNOSIS IS SEEN

2. IRREVERSIBLE CELL INJURY

•
EARLIEST 10N INVOLVED → Can
•
MYLEIN FIGURES SEEN
•
LARGE AMORPUS DENSITY SEEN
• PYKNOSIS
KART ORRMEXIS
KARYOLYSIS
SEEN ON -
Light microscopy .

3. OXIDATIVE STRESS

• ↑ FREE RADICAL → OXIDATIVE STRESS

•
MOST POTENT FREE RADICAL → HYDROXYL RADICAL

Concequence FREE RADICAL INJURY

•
OF =

↳ PROTEIN MISFOLDING
↳ DAMAGE TO DNA

• BRAIN IS PROTECTED FROM FREE RADICAL INJURY

BY SOD -1
Csupera oxide Dismutase ☐ -
 /

CELL DEATH

1. NECROSIS → ALWAYS PATHOLOGICAL

→ 1nF . Ant
→ DENATURATION OF PROTEAN & ENZYMATIC
DIGESTION OF CELL 'S SEEN
TYPES
D- ◦COAGULATIVE NECROSIS
→ me TYPE OF NECROSIS
→ OCCURS IN SOLID ORGANS → HEART SPLEEN , KIDNEYetc
,

EXCEPT BRAIN
→ CONSIDERED AS DRY GANGRENE

B. LIQUEFACTIVE NECROSIS
→ SEEN IN BRAIN
→ WET GANGRENE

c. CASEOUS NECROSIS
→ SEEN IN TB
,
SYPHILIS
,
HISTOPLASMOSIS
CHEESE LIKE is seen
→ App .
.
D) FAT NECROSIS
→ CHALKY WHITE DEPOSITS ARE SEEN
→ SEEN IN PANCREAS OMENTUM MES ENTRY BREAST
, , ,

E> FIBRINOID NECROSIS

→ SEEN IN TYPE 11/111
HYPERSENST / V74 Rxn .

→ SEEN IN VESSEL WALL

→ PINK FIBRIN LIKE Dpp SEEN . .

DX OF NECROSIS =

2. APOPTOSIS → PROGRAMMED CELL DEATH

→ CAN BE PATHOLOGICAL OR PHYSIOLOGICAL
→ EARLIEST FEATURE → CELL SHRINK
→ MOST characteristic
featureNt
→ CHROMATIN CONDENSATION
→ INFLAMMATION -

→ APOPTOTIC BODIES ARE SEEN

 → ENZYMES INVOLVED IN APOPTOSIS
/ CASPASES
◦
→ INITIATOR 8,9 , -

10
EXECUTIONER 3,6 , 7
-

2. ENDONUCLEASE → DNA breakdown → STEPLADDER PATTERN

→ FACTORS IN APOPTOSIS
1. PRO APOPTOTIC FACTOR → BAX , BAK
2. ANTI-APOPTOTIC → BCL-2 a
BCL -
XL MCL -
I
,
3. SENSORS → BIM
,
BID BAD g
NOXA PUMA
, ,

3. NECRO PTOSIS
→ NECROSIS + APOPTOSIS
→ CASPASE INDEPENDENT

4- PYRO PTOSIS
'

→ FEVER 1- INFLAMMATION
 A

☆ CALCIFICATION =

DYSTROPHIC METASTATIC
•
SEEN DEAD TISSUE
•

SEEN IN LIVING
•
Serum eat ⑨ •
Serum ca2t↑

☆ PIGMENTS =

EXOGENOUS ENDOGENOUS

→ TATTOO → MELANIN
→ HEMOSIDERIN
→ LIPOFUSCIN
aka → WEAR TEAR
Pigment
☆ INFLAMMATION =

ACUTE CHRONIC
•
SHORT DURATION • LONG DURATION
•
NEUTROPHIL ← cells →
•
MONOCYTES
LYMPHOCYTE
* CARDINAL SIGN OF INFLAMMATION MACROPHAGE
•
RUBOR REDNESS
-

•
CALOR -
HEAT BY -
CELSUS
•
DOLOR -
PAIN
•
TUMOR -
SWELLING
• FUNCTIOLAESA BY -
VIRCHOW
 ACUTE INFLAMMATION

VASCULAR EVENTS CELLULAR EVENTS

↓ ↓
VASODILATION ROLING •
E-SELECTIN
↓ •
P SELECTIN
-

AVASCULAR PERMEABILITY ↓
↓ ADHESION •
I-
CAM

STASIS •
V -
CAM
↓ &
MIGRATION TRANSMIGRATION •
PECAN -
D
•
CD 31
↓
CHEMOTAXIS
•
Csa
•
LTBY
↓ •
12-8
OPSONISATION
•
C3b cub • Csb
,

Zghgg
•

PHAGOCYTOSIS
☆ GIANT CELLS

I. LANGHANS GIANT CELLS

→ SEEN IN -
TB

2. ASCHOFF GIANT CELL

→ RHEUMATIC HEART DISEASE

3. REED STERNBERG CELL

→ HODGKIN a LYMPHOMA

4. WARTH IN FINKEDLY GIANT CELL

→ MEASLES

5. ASTEROID BODIES
→ SARCOIDOSIS

6. SCHAU MAN BODIES

→ SARCOIDOSIS
 HISTAMINE VASODILATION
]
• •

PAF[Platelet BRONCHO CONSTRICTION

ActivatingFactory
• •

SEROTONIN
]
• •
VASOCONSTRICTION
•
PGFL

NITRIC OXIDE
] VASODILATION
• •

• PGDZ

•
1-✗ Az •
VASOCONSTRICTION
• A PLATELET AGGERICRATION
'

•
PqIz • VASODILATION
AGGERIGATION
.

• ↓ PLATELET

•
PG Ez • FEVER
• PAIN

•
STRONGEST / POTENT B. C =
LTCY
•
MAC =
Cs , 6,798,9
•
HYPERTROPHIC SCAR HELIO DS
→ COLOUR DARKER
→ COLOUR SAME AS THAN SKIN
'

SKIN
→ LOCATION =ANYWNR{
→
LOCATION -

P / NNA
STERNUM
SHOULDER
☆ GRANULOMA =

• CASEATING GRANULOMA
→ TB
→ SYPHILIS
→ HISTOPLASMOSIS

• NON CASEATING GRANULOMA

→ SARCOIDOSIS

•
PALISA DING GRANULOMA
→ WEGENER 'S GRANULOMATOSIS

•
STELLATE GRANULOMA
→ CAT SCRATCH DISEASE
☆ HYPERSENSITIVITY =

1. TYPE -
I =
ALLERGY
EXAMPLE -
ASTHMA ALLERGY ANAPHYLAXIS
, ,

2. TYPE -1T = BLOOD RELATED

EXAMPLE -

MY MYSTHENIA GRAVIS
BLOOD BLOOD TRANSFUSION
GROUP GOOD PASTURE
SYNDROME
IS IMMUNE THROMBOCYTOPENIC PURPURA
Rh Rh INCOMPATIBILITY
Positive PERNKOUS ANEMIA

3. TYPE # =
IMMUNE COMPLEX MEDIATED
EXAMPLE -_ S → SIE
H → HENOCH SCHELIN PURPURA
A ARTHUS RXN
→
R → RHEUMATOID ARTHRITIS
P → POLY ARTHRITIS NODOSA
→ TYPE # LEPRA REACTION

4. TYPE # =
DELAYED TYPE
→ TYPE I LEPRA RXN
☆ TYPES OF GRAFT

AUTO → SELF GRAFT

ISO → IDENTICAL TWINS
Allo → SAME SPECIES
XENO → DIFF RENT SPECIES

→ HYPER ACUTE GRAFT REJECTION → MIN -

hrs
→ ACUTE GRAFT REJECTION → DAY 's -
WEEKS
→ CHRONIC GRAFT REJECTION → MONTH .
-
YEAR'S

•
B- CELLS PRODUCED
ARE IN BNR MATURE / NBM
•
T-CELLS ARE PRODUCED IN BNI & MATURE IN
thymus

PRESENT
MAC I
Ag To C.D8 1- cells
• -
=

I PRESENT cells
Ag TO CDU
•
mm -
= 1- .
☆ TYPES OF CELLS

PERMANENT STABLE LABILE

•
NON -
DIVIDING ◦
DIVIDE WHEN NEED ◦
RAPIDLY DIVIDING
◦
LEFT CELL CYCLE °
Go PHASE °
91 PHASE

☆ REPAIR =

DEPOSITION / FORMATION OF GRANULATION TISSUE

•

•
HALLMARK OF GRANULATION NEOVASCULARIZATION

☆ WOUND HEALING =

1° INTENTION 2° INTENTION
•
WOUND IS CLEAN •
WOUND IS INFECTED

•
NO LOSS OF TISSUE • TISSUE LOSS + nt .

☆ IMP STEPS .

• 0 hrs - BLOOD CLOT

• 0 -24ms -

NEUTROPHILS
• DAY 3 - •
NEUTROPHILS = MACROPHAGE
•
GRANULATION TISSUE Appears
• DAYS - • ↑ GRANULATION
①
↑ NEOVASCUEARISATION
• DAY 14 - •
maximum COLLAGEN
•
DAY 28 -
•
SCARFORMATION
 •
CARCINOMA → BLOOD
•
SARCOMA → LYMPHATIC

* NEOPLASIA =

BENIGN MALIGNANT
→ SUFIX = OMA → SUFFIX = CARCINOMA
SARCOMA
→ AN APLASIA → -
nt AN APLASIA → + nt
→

→ SLOWECY GROWING → RAPIDLY GROWING

→ METASTASIS Nt - → METASTASIS tht
→ LOCAL INVASION nt -
→ LOCAL INVASION tht

↓
EXCEPTION = MALAGNANCY THAT END WITH OMA
•
MELANOMA
•
LYMPHOMA
•
CHLOROMA
•
SEMI NOMA

EXCEPTION = MALAGNANCY THAT DO NOT METASTASIZE

•
BASAL CELL CARCINOMA
•
GLIOMA

* POINTER TO DX CANCER →

KERATIN PEARLS
↳
Sq .
CELL CARCINOMA

ABNORMAL GLANDS
↳ ADENOCARCINOMA
☆ CELL CYCLE

◦
MOST RADIOSENSTNE PHASE Gam
◦
MOST RADIO RESISTANT PHASE S

◦
MOST RADIOSENSTNE CELL LYMPHOCYTE
◦
MOST RADIO RESISTANT CELL PLATELET

☆ TUMOR SUPPRESSOR GENES CTSG]

TSG CHROMOSOME TUMOR

Rb 139/14 •
RETINOBLASTOMA
BRCA -
I 17 •
BREAST CANCER
•
OVARIAN CANCER
BREA -2 13 •
BREAST CANCER
•
PROSTATE CANCER

NFI 17 •
NEUROFIBROMAS

NFL 22 •
SCHWANOMA

WT-14W -1-2 11 •
WILM 'S TUMOR

VHL 3 •
CLEAR CELL RCC

STK PEUTZ JEGHER

11 •

Syn .
☆ MARKER 'S
Imp .
TUMOR

•
PSA •
PROSTATE CANCER
CALCITONIN MEDULLARY CARCINOMA
of THYROID
• •

•
hCG •
CHORIOCARCINOMA
•
AFP •
HEPATOCELLULAR CARCINOMA
• CA 19-9 • PANCREATIC CANCER
•
Ca 125 •
OVARIAN CANCER
•
ca 15-3 •
BREAST CANCER
• CATECHOLAMINES •
PHEOCHROMOCYTOMA
☆ VASCULITIS
I LARGE VESSEL VASCULITIS
1. TEMPORAL ARTERITIS / GIANT CELL ARTERITIS
2. TAKAYASU ARTERITIS

II MEDIUM VESSEL VASCULITIS

1. PAN [ POLY ARTERITIS NODOSA] Paras Ki
2. KAWASAKI DISEASE Kawa SAKI
3. BUERGERS DISEASE BIKE

HI SMALL VESSEL VASCULITIS

1. MPA E ]
microscopic Polyangiitis
MY
2. WEGENER 'S GRANULOMATOSIS WAY to
3. CSS [ CHRUG STRAUS SYNDROME]
cnn-NDIGARM.tl
. HSH [ HENOCH SCHOLEIN PURPURA] H c)
• P -
ANCA tht PN
C- CHURG STRAUSS SYNDROME
M -

MICROSCOPIC POLYANGIITIS

• c- ANCA + nt IN
WECENER 'S GRANULOMATOSIS

☆ DX -
OF VASCULITIS -
Ab / BIOPSY
☆ RX OF ALL VASCULITIS -
STEROID
EXCEPT 1. BUERGER'S DISEASE → STOP SMOKING
2. KAWASAKI DISEASE IN →
Ig
-
.

3- WEGNERS GRANULOMATOSIS → CYCLOPHOSPHAMINE

☆ TEMPORAL ARTERITIS / GIANT CELL ARTERITIS

CIF •
FACIAL PAIN
•
PAIN IN CHEWING / MASTICATION
•
HEAD ACHE
•
POLY MYALGIA

DX TEMPORAL ARTERY BIOPSY

RX STEROIDS → BY RULE OF 60
FEMALE > 60 Years
•

•
ESR 760
• Rx
60mg PREDNISOLONE

☆ PAN CPOLY ARTERITIS NODOSA ]

•
CONDITION OCCUR DUE TO INFLAMMATION
•
TYPE III HSN .

INVOLVE MULTIPLE ORGAN Except LUNG

•

•
DX -
BIOPSY
•
Rx -
STEROID

☆ KAWASAKI DISEASE
Rx Pcm
It / ANTAGONIST -
ANAKINRA

IVIG
a- Toc >
* CHROG STRAUSS SYNDROME -

·
ASSOCIATED WITH ASTUMA/SODNOPUILIA
IgE may
·

DX-P-ANCA
RX-STEROIDS

* UENOCH SCUONLEN PURPURA

· mC VASCULITIS IN CHILDREN
Associated T NEPHROPATHX
IgA
·

CIFPALPABLE PURPLE RASH +n

UEMATURE A
·

DXCLINICAL SYMPTOMS
RX SELE LIMITING (90%)
·
CoW DOSE STRON XIDAYS ·
STRAWBERRY GUM

* WECENERS GRANULOMATOSIS
DX-C-ANCA
DOC-CYCLOPHOSPHAMIDE

* BURGERS DISEASE/ TUROMBO

ANGITIS OBLITTERANS

4/0 XOUNG MALE SMOER

·

·
ARTERX -> NEIN- NERVE
NEVER LXMPHATICS
RX -.
STOP SMOKING
· AMPUTATION
 LIVER
A
TYPE HEPATITIS
Hep
→ me OF
- -

→ me TYPE OF HEPATITIS in CHILDREN Hep A

-
-

B
→ MC TYPE OF CHRONIC
POTENTIAL CAUSE OF CHRONIC HEPATITIS
HEPATITIS -

Hep -

→ MOST -

Hep -
C

TYPE ACUTE HEPATITIS IN ADULT

HOPE
→ MC OF -

HEPATITIS ASSOCIATED c- PREG

→ mc
HepE
-
.

ACUTE VIRAL HEPATITIS CHRONIC VIRAL HEPATITIS

•
< Gmonth • >6 month
HIP *
HIP •
BRIDGING FIBROSIS
•
GROUND GLASS HEPATOCYTE
•
$
.

* MARKER 'S B
OF
Hep .

HBsAg VIRUS ENTRY

-

HBCAG NOT DETETED

_

HBEAG VIRUS REPLICATION __ Infectivity 've

_

ANTHBCAB
[ Igm ACUTE
-

Anti HBEAb -
IgG
END
-

OF
CHRONIC
INFECTIVITY
Anti HBSAB -

CURED
 Rx OF
Hep . B → TENOFOVIR
ENTECAVIR
LAMIVUDINE

Rx → LEDIPASVIR
OF
Hepc SOFUSBVLUVIR

☆ BILIARY TRACT DISORDER

I. 1° BILIARY CIRRHOSIS
•
AMA the [ ANTI MITOCHONDRIAL Abo]
-

•
Rx -
VRSODEOXYCHOLIC ACID
• TOC -

LIVER TRANSPLANT

2. 2° BILIARY CIRRHOSIS
•
CAUSE
-

OBSTRUCTION
Rx TREAT THE CAUSE
_

3. 1° SCLEROSING CHOLANGITIS
• P ANCA
-
the
•
Rx -
URSODEOXYCHOLIC ACID
•
Toc -
LIVER TRANSPLANT
 HEMATOLOGY
•
MC TYPE OF BLOOD GROUP -

ABO
•
LEAST COMMON TYPE -
BOMBAY PHENOTYPE
•
SAFEST BLOOD FOR TRANSFUSION -
CROSS MATCHED
• UNIVERSAL DONAR 0 -

•
UNIVERSAL RECIEPENT AB -

☆ PRETRANSFUSION TESTING
HIV , Hep B , Hep C g
SYPHILIS ,
MALARIA E

BLOOD
& &

PRBCC-14:c] PLATELET RICH PLASMA

ACUTE BLOOD LOSS
•

L >
•
Hb 27 Csever Anemia) PLATLETCROOMTEMPD FFP [-18°C]
•
THROMBOCYTOPENIA •
AFIBRINOGEN
•
WARFARIN TOXICITY
• BT NOTES =

WARMING BODY HEAT

'

◦
PRIOR C-
◦
6-8 drops / min
↓
◦
↑ RATE by
10-14
drops /min
◦
IN CASE OF ANY HYPERSENSTIVITY STOP B.T
Rx
Inj AVIL
.

Irj DEXAMETHASONE
.

◦ IN CASE OF HYPOTENSION
Rx Epinephrine
 I

☆ WBC DISORDERS =

NEOPLASTIC CELLS

BLOOD LYMPH NODES

LEUKEMIAS LYMPHOMA

MYELOID LYMPHOID HODGKIN'D NON-HODGKIN'S

ACUTE CHRONIC ACUTE CHRONIC

AML CML ALL CLL

☆ HODGKIN 'S LYMPHOMA

ETIOLOGY -
EBSTEIN BARR VIRUS ASSOCIATED
↓
PRODUCE LATENT MEMBRANE PROTEIN - I
[ ACTIVATE NF KB PATHWAY]
↓
-

↑ CELL PROLIFERATION
↓ + nt

HODGKIN 'S LYMPHOMA .

GF : • PEL EBSTEIN FEVER NIGHT SWEAT g WEIGHT LOSS

,
•
PAIN # CERVICAL LYMPHNODE ENLARGEMENT
•
SYMPTOM WORSEN WITH ALCOHOL .
•
Mp → 9-

☆ TYPES

•
LYMPHOCYTE RICH
LACUNAR VARIENT •
LYMPHOCYTE POOR worst
Prog .

•
EMPTY SPACE AROUND POPCORN VARIENT •
MIXED CELLULARITY Me
type INDIA
•
SEEN IN ODULAR
•
SEEN IN CNLPH D • NODULAR SCLEROSIS me in WORLD

SCLEROSING 11:L .

☒ ◦ DULAR ↳YMPHOCYTE •
LYMPHOCYTE Predominant Best Prog .

ERE DOMINANT A. I RX A - -
ADRIAMYCIN
B-
BLEOMYCIN
V -
VINBLASTINE
D- DACARBAZINE

☆ NON-HODGKIN'S LYMPHOMA
B- CELL ASSOCIATED TUMOR MARKER -
CDIG ,
CD 20

1. FOLLICULAR CELL LYMPHOMA → → cells

ARE

B- CELL LYMPHOMA
Arranged in FOLLICLES
•

•
d- ( 14,18)
BCL-2 OVEREXPRESSION
gene
•

2. BURKITT LYMPHOMA •
ON LYMPH NODE
•d- ( 8,147 BIOPSY →
C- MYC GENE OVEREXPRESSION
• STARRY SKY

Cfp JAW SWELLING

• + NT
App .

3. DLBCL DIFFUSE LARGE

-
B CELL LYMPHOMA
• MC TYPE & DANGEROUS TYPE c- WORST PROGNOSIS
• MYC -

TRANSLOCATION
 4. MANTLE CELL LYMPHOMA

•
SEEN IN ELDERLY [ MALE > FEMALE]
•
d- ( 11,14)
• ↑ EXPRESSION OF CYCLIN D, GENE

cleared
LYMPH NODE BIOPSY → small
lymphocytes
•

→ noisy all .

5. HAIRY CELL LYMPHOMA

DX -
• TRAP + vecspd STAIN]
.

CTARTARATE RESISTANT ACID PHOSPHATASE]

Hb , TLC , PLATELETS
•
& -

Bm BIOPSY -
HONEYCOMB / FRIED EGG
-
APPERANCE .

Rx CLADRIBINE
-

•
T-CELL ASSOCIATED

1. ADULT T-Cell LEUKEMIA 2- MYCOSIS FUNGOIDESISEZARY SYNDROME

→ BY HTLV -

A → NOT A FVNGAL INFECTION

]
IMMAN T-cell leukemia virus →

→ FLOWER CELLS
 O
O
3. ANAPLASTIC LARGE T-CELL LYMPHOMA
Pathogenesis ALK GENE MUTATION
- ON CHROMOSOME
2p
HIP -
HALLMARK CELLS

•
Imp CLASSIFICATION FOR LYMPHOMA REAL CLASSIFICATION
- -

•
STAGING METHOD Ann AARBOR METHOD -

•
RX OF NON HODGKIN 'S LYMPHOMA
R -

RITUXIMAB
C-
CYCLOPHOSPHAMIDE
H
RUBIANO
HYDROXYDUANO
-

ONCOVINC VINCRISTINE)
-

p -

PREDNISOLONE

☆ MYELOID DISORDER 'S

1. CML
•
CIF → HEPATOSPLENOMEGALY
• d- ( 9:22) : PHILADELPHIA CHROMOSOME
&
ABL
↓
-

Bergere Active

TYROSINE KINASE -

ACTIVE -
TO BLOCK -
Doc
-

IMATINIB
↓ Hb ⑨
'

LAB DX - • -

CANCER • TLC MMM

•
PLATELET COUNT↑↑
TOC -

BMT •
MYELOID LINEAGE CELL ↑↑
GARDEN PARTY APPERANC SEEN
Bm .

Biopsy →
2. AML
•
INTRACYTOPLASMIC RODS
AUER RODS
→

•
DYE -
MPOCMYELO PEROXIDASE]
SUDAN BLACK
•
TYPES -
MC TYPE -
M2
MOST SIGNIFICANT Ms → d- ( 15 ; 17)
GINGWAL INFILTRATE Ms

Rx -
BMT

3. CLL
• CLL → RICHTER TRANSFORMATION → DLBCL ( most severe)
•
me -
ADULT / ELDERLY
•
Ayw → AIHA [ AUTOIMMUNE HEMOLYTIC ANEMIA]

•
HPE : SMUDGE / PARACHUTE / BASKET cell

•
Doc -
FLUDRABINE
•
PERIODIC FOLLOWUP I -2yd -
PET SCAN -

4. ALL RXV -

VINCRISTINE
A
◦
me IN CHILDREN _

ASPARAGINASE
• Ll -
Mc P -

PREDNISONE
• 23 -
WORST PROGNOSIS 0 -
DOXORUBICIN
DOWN SYNDROME
•

afw
Txoc -
BONE MARROW
TRANSPLANT
☆ HEMATOPOIESIS =

• 3ʳᵈ WEEK OF INTRAUTERINE LIFE YOLK SAC

• 3ʳᵈ MONTH OF INTRAUTERINE LIFE LIVER
•
4M MONTH OF INTRAUTERINE LIFE B. MILNER
JUST BIRTH BONE MARROW
•
BEFORE

☆ HEMATOPOIETIC STEM CELL

LYMPHOBLAST MYELOBLAST

•
T-LYMPHOCYTES •
ERYTHROBLAST → RBC
•
B- LYMPHOCYTES •
MEGAKARYOBLAST →
PLATELET
• NA -
CELLS •
MYELOBLAST → NEUTROPHILS
EOSINOPHILS
BASOPHILS
•
MONO BLAST → MONOCYTE → MACROPHAGE

☆ IRON DEFICIENCY ANEMIA

•
me TYPE OF ANEMIA
• IRON IN BLOOD TRANSFERRIN
=

•
IRON IS STORED IN BODY =
FERRITIN
•
IRON IS ABSORBED IN DUODENUM via DMT -
 DX Hb ↓ ↑
TIBC Total Iron
Binding capacity ↑
-
-
-

Erythro proto porphyrin

Mcv ↓
FEP -
Free
SERUM Iron ↓
SERUM FERMIN ↓

CAUSE DIETRY def

-

EXCESS BLOOD LOSS -

TRAUMA etc

RSMEAR → •

microcytic Hypochromia cells

Pencil cells
shape
•

special Feature KOKO NYCHA

•
→

•
CHEILOSIS
Rx →
IF Hb < 7- = RRBC
If Hb > 7- =
ORAL →
Ferrers sulphate
I. ✓ →
Ferrers SUCROSE / CARBOXY MALTOSE
☆ SIDEROBLASTIC ANEMIA -

DX -
5. IRON ↑ ☆ A.SMEAR →

5. FERRITIN ↑
Basophilic stripling
•

MCV &
TIABC ↓

CAUSE -
◦
LEAD POISONING .

◦ IRON OVERLOAD
Rx • BMT
 ☆ AOCD -
ANEMIA OF CHRONIC DS -

CHRONIC Info
↓
•
MACROPHAGE → HEPCID.IN
↳ Lock Iron within stores .

DX → 5. FERMIN ↑
5. IRON ↓ Rx -

Treat the cause

men ↓
TIBC &

☆ THALASSEMIA =

•
B- THALA SEMI A
•
B- CHAIN DEFECT
TYPES
•

•
MINOR -
NO SYMPTOM -
No RX NEEDED
.

INTERMEDIATE MILD TO MOD SYMP B.1- 3-6 month

every
• -
. -

SEVERE SYMP month

MAJOR BT
every
• -
-

• DX -

• MCV ↓
• MCI C MENTZER INDEX = 273 crew cut
App
RBC
•
P .
SMEAR =
•

4F

CHIPMUNK
FACE
☆ SCA -
SICKLE CELL ANEMIA

GLUTAMIC ACID → VALINE at 6th POSITION

OF B- GLOBIN CHAIN
psmear
CIF •
JUNDKE .

r
•
GALLSTONE
◦ BONE PAIN
•
AUTO SPLENECTOMY
SICKLE CELL RBC
DX -
MCV -
n RX BT
46 - &

☆ SPLENECTOMY

AUTOSPLENECTOMY → SICKLE CELL ANEMIA

[ PLANNED → 4. SPMEROCYTOSIS ORK spherical

→ H ELLIPTOCYTOSIS
. 0 Apelike .

Ai HACAuto immune
→
hemolytic Anemia]
POST SPLENECTOMY → HOWELL JOLLY BODIES seen
 ☆ GGPD DEFICIENCY ANEMIA

•
✗ LR
•
GGPD def .
→ RBC at OXIDATIVE DAMAGE
GF •
No
Sym . at BIRTH / REST
↑ SYMPTOMS
•

STRSS

DX -
◦
Mcv -

⑨
◦ AS meas →
•

HEINZ BODIES
• BITE CELLS →

☆ AINA -
AUTOIMMUNE HEMOLYTIC ANEMIA

•
Associated c- CLL
DX -

COOMB TEST
Rx -

STEROID
↓

Ivan
↓
SPLENECTOMY

☆ MEGALOBLBSTIC ANEMIA
CAUSE
e. MCC -
DEFICIENCY
•
V14 B12
•
PERNICIOUS ANEMIA
PANCREATITIS
•

IMMERSLAND
•
GRESBOCK Synd .
 MEGALOBLASTIC ANEMIA

☆ FOLIC ACID DEFICIENCY ☆ B- 12 DEFICIENCY Anemia .

> 100 Mcv > 100

tntcmc)
tnt
F- IGLU test
Neurological
TEST
Defect SHILLING TEST

☆ APLASTIC ANEMIA •
• •

•
•

•
FAT cell
•
, , ,
•
•
• •
• •

•
APLASTIC ANEMIA → HSC LOST HSC
• B. m BIOPSY → ONLY FAT CELL

•
DX - RBC ↓ Rx -
◦
BMT
WBE ↓ •
BT
PLATELETS ↓ ◦ NRDC -
DARBOPOITIN
EPOITIN
•
↑ PLATELET ELTROMPOPAG
•
↑ WBC FILGRASTIN & SARGRAMUSTIN