Dathophysiology
Rapid Revision KROKI
Minna Mamik
@ Medic Mukul
,Minna Mamik
Anemia
colour Index
>Hereditary hemolytic Anemia (mutation present
=
0.9-1.0
Hypockcomic Anemia Membrane
defects Ameditary Spherocytosis Minkonsky
2
1. -> c
shaffered Syndr
Normocytic Anemia Based on MCV N 00-100f1
=
2.
Enzyme Deficiency ->
G-G-PD
deficiency
Hyperchromic Anemia ~ Mean Capusatan Volume
Hexokinase deficiency
>Hypochromic Anemia -
CI o.q or less than do MCV 3.
Hemoglobinonopathics-> Sickle all Anemiaz
Glutamate repla
Oh
Thalassemia
MiocoCytic Anemia
-> peripheral
newio-
by Valine
pathy
I
S-Sideroblastic Anemia -t Bs (Basophilic
Stippling Seen)
Extravascular Micovas
-- Icon
deficiency Anemia (Nail brittleness & Hainloss)
hemolysis -
spleen hemolysi
stick to b
CoutRBC)
-
T- Thalassemia (blood doesn't
make Hb) vessels
autosomal
enoughinherited
zeccesive
A -
Anemia of Chronic Disease (such as Kidney Diseasel Hereditary Sphereocytosis -
Autosomal
(membranopadty)
Dominant
L- Lead
H ↳due do membrane protein defect
poisining
GSphere talenen ↳ Spectzin, Anchyzin, Band cell
(SAB)
& ↳Extravascular
>Namocydic Anemia MCV 80-100 cl 0.9-1.0 hemolysis
=
-
GGPD deficiency Anemia x-linked Recessive ⑭P
Aplastic Anemia
(bylomyledenBoneMaaree
·
-
G-6 -
P
chronic Renal Failure ↳Accumulation of H202 (fee Radical)
exhe-sp
·
in Risc x
↓
-
·
Anemia of Chronic Disease
Hemolysis oxidative stress 6-phosphog
·
Hemoytic Anemia
↓
during ↓
conate
RBC Destruction Ab Denaturation
↓ ↓
Anemia
>Macrocytic -
MCV> 100 & CI> 1.0 intzavascular
Deoxygenated pencipatation
hemolysis of Hb
L- Liver Dysfunction (Heinz bodies)
Neural ↓
A -
Hypothyzoidism Tube
↑ Defect pass through spleen &
(Dueto VitBiz/Badef) Destroyed by splenic Macoph
M
-Megaloblastic Anemia >Factas
causing hemoysis ↓
↳ Howel Bodies in
GGPD
Jolly seen
Cell formed
c -
Cytotoxic drug - chronic infections
Anti malarial
Bite
↓
-
Drugs like
Extravascular hemolysis
-Fava beans
poikilocydosis -
change in shape of RBC (pp) Note;GGPD, Sickle cellAnemia & Thalassemia
(pizal
Anisocytosis -
Change in Size of RBC (2a) protective against plasmodium
Cresistand to malaria)
Pecusa of RBC ->
Rediculocytes (NON -
Nucleated)
>Autoimmune
Hemoydic Anemia
type
Periphera) finding
Smean
hypersensitivity
It reaction
nemia Microse Andibodies proteins
Due do
against RBC membrane
- ->
>Macrocytic Anemia -
Macco cells
Spherocytes - in
Hereditarysphereocytosis, Microangiopathic hemolytic Anemia
(NO Centralpallor)
Syndrome (Hus)
↳
autoimmune
hemoydic An. Hemoyhic Uzemic
↳ Thrombodic
>Polychromasia ->
Hemoydic Anemia
Thompocytopenia purpura
↳ Disseminated Intravascular
> Bite cell ->
Glucose -
6.phosphate Deh.
Coagulation
Heinz Bodies. Deficiency Anemia
↳ composed of
We See
Schistocyte/helmet/Fragmental RBC
denaturated Hb
percipated >paraoxymal Noctural
Hemoglobinuria
>Schistocyte/ helmet I Microangiopathic Hemolytic ↳
Only Amhemolytic Anemia
Anemia
Fragmented RBC ↳ More
hemoglobin (Abrucial
Cell & inThalassemia ↳ (HRBC)
>Target Pancytopenia
↳ Microcytic
Basophillic Stripping hypochromic ↳
erythroctes
t &↑ Ab
Red Cells
↳ MCC Fe
of death=
overload due to repeated Transfusion
, Minna Mamik
Leukemia - Cancer of blood-faring dissue Acute
Myeloid Leukemia
(including bone Marrow &
lymphatic System)
<15-45
yes
Hemadopoiesis -> Formation of Blood Cells . Gum
hyperplasia/Bleeding
↳ liver BR & Liver, Bone Marow)
Coagulation (DIC)
(yolk sac -Disseminated Inteavascular
ardweek 3rdmoth 4th month just before
Birth
Hemapoltic Stem Cell >Chronic Leukemia -
Neoplastic peration of Mature
Common Myeloid Common' lymphoid Circulating lymphocytes, characterised
Drogenita peogenita. by high WBC Count
I
I T -
&
B-lymphocytes
>Erythoblast-> RBC & Chronic Myeloid leukemia
>Megakaryoblast platelets ->
NK cells
↳
Eldery people
*ByodMaromslauk
>Myeloblast >Massive
hepatosphenomegaly Seen
↳ of
Neutrophils Babeseen
.
cytoplasm -
>changed chromosome -
22 (philadelphia chromosome
·
Eosinophils -
Binudeate/spectac shaped Nuclei >↑ No. of all
mydoid linege cell (Madue Myeloid)
granules in Cytoplasm
Brick Red
·
Basophils
-4
Basophils 1 Both are absent in Reactive
z
large Bluish geanues in
cytoplasm
which obscure the nucleus -
tcanslocation Neutrophilic Leukocytosis (*nautzophil
9 h&22nd CLeukemoid Reaction)
t
>Monoblast ->
Monocytes-largestcell, kidney shaped nucleus,
Agranulates (donthave granules)
Chronic
lymphoid leukemia Goyrs)
↳ Neoplasticproliferation of mature
monocytes
B-cell
I Agranulogy en
↳ Blood Smear -> 4
lymphocytus
Normal level CD34 -
MackerfaMSC) Smudge & Botkin
Cells
WBC -> 3 9x109/L hematopoletic stem cell
↳ of lymph
-
6x10/ Involvement node leads togeneralised
RBC
-
=
4 -
lymphadenopathy (Small lymphocytic leukemia)
(cancuous/abnormall cells)
Neoplastic lessions of WBCs
can become
leukemia L
can become
>
Lymphoma Acte Chronic
↓
Involvement of Bone Mariow/ More Systemic/c
Blast > 30% >pediferation of
mature cell
Smeal Tissue Involvement
Periphezal >WBC <50x10"/ >WBC<50x109/
↓
of
like lymphnode/spediferation
Lympho-&Ryeloblast
>promyelocytes
Spleen
Leukemia
>Acute
Mariow/Peripheral
Lymphoma
↳ 30% blasts in Bone Blood
lymphogranulo-
Lymphoblasts Mycoblasts Hodgkin's lymphoma metosis
Non-Hodgkin's lymphoma
-Smallen in Size
-Langen in Size 1) Bimodal age distribution 1) Can Occur at
any age
-Geanules present
(15-20 yes, elders)
>No Granules 2) Generalised lymphadeno-
Guical,
padhy
Ave Mods abscent & Auns mods present 2) lymphadenopathy
(Hall mark of Ryeloblasts)
>Coarse/dumped Chromatin Contagious Spread
3) 3)
Non-Contagions spread
>Open up/Homogenous
Chromatin 4) Reed-Sterberg
aka
alls pt.
Acute
lymphoid leukemia -
ALL owl's
eyes cells
>MC Cancer in Children (2-9yrs)
>t Number of NBC - ↑ infections Lymphogzanulomadosis one of lymphadenopathy disease
st
platelets 2 Reed -
Steenberg cells
Idepatosplenomegaly 3 Necrosis in Immune
Ozgans
· TdttVe (RackenfaAll) 4
parphyzidic Spleen
Rapid Revision KROKI
Minna Mamik
@ Medic Mukul
,Minna Mamik
Anemia
colour Index
>Hereditary hemolytic Anemia (mutation present
=
0.9-1.0
Hypockcomic Anemia Membrane
defects Ameditary Spherocytosis Minkonsky
2
1. -> c
shaffered Syndr
Normocytic Anemia Based on MCV N 00-100f1
=
2.
Enzyme Deficiency ->
G-G-PD
deficiency
Hyperchromic Anemia ~ Mean Capusatan Volume
Hexokinase deficiency
>Hypochromic Anemia -
CI o.q or less than do MCV 3.
Hemoglobinonopathics-> Sickle all Anemiaz
Glutamate repla
Oh
Thalassemia
MiocoCytic Anemia
-> peripheral
newio-
by Valine
pathy
I
S-Sideroblastic Anemia -t Bs (Basophilic
Stippling Seen)
Extravascular Micovas
-- Icon
deficiency Anemia (Nail brittleness & Hainloss)
hemolysis -
spleen hemolysi
stick to b
CoutRBC)
-
T- Thalassemia (blood doesn't
make Hb) vessels
autosomal
enoughinherited
zeccesive
A -
Anemia of Chronic Disease (such as Kidney Diseasel Hereditary Sphereocytosis -
Autosomal
(membranopadty)
Dominant
L- Lead
H ↳due do membrane protein defect
poisining
GSphere talenen ↳ Spectzin, Anchyzin, Band cell
(SAB)
& ↳Extravascular
>Namocydic Anemia MCV 80-100 cl 0.9-1.0 hemolysis
=
-
GGPD deficiency Anemia x-linked Recessive ⑭P
Aplastic Anemia
(bylomyledenBoneMaaree
·
-
G-6 -
P
chronic Renal Failure ↳Accumulation of H202 (fee Radical)
exhe-sp
·
in Risc x
↓
-
·
Anemia of Chronic Disease
Hemolysis oxidative stress 6-phosphog
·
Hemoytic Anemia
↓
during ↓
conate
RBC Destruction Ab Denaturation
↓ ↓
Anemia
>Macrocytic -
MCV> 100 & CI> 1.0 intzavascular
Deoxygenated pencipatation
hemolysis of Hb
L- Liver Dysfunction (Heinz bodies)
Neural ↓
A -
Hypothyzoidism Tube
↑ Defect pass through spleen &
(Dueto VitBiz/Badef) Destroyed by splenic Macoph
M
-Megaloblastic Anemia >Factas
causing hemoysis ↓
↳ Howel Bodies in
GGPD
Jolly seen
Cell formed
c -
Cytotoxic drug - chronic infections
Anti malarial
Bite
↓
-
Drugs like
Extravascular hemolysis
-Fava beans
poikilocydosis -
change in shape of RBC (pp) Note;GGPD, Sickle cellAnemia & Thalassemia
(pizal
Anisocytosis -
Change in Size of RBC (2a) protective against plasmodium
Cresistand to malaria)
Pecusa of RBC ->
Rediculocytes (NON -
Nucleated)
>Autoimmune
Hemoydic Anemia
type
Periphera) finding
Smean
hypersensitivity
It reaction
nemia Microse Andibodies proteins
Due do
against RBC membrane
- ->
>Macrocytic Anemia -
Macco cells
Spherocytes - in
Hereditarysphereocytosis, Microangiopathic hemolytic Anemia
(NO Centralpallor)
Syndrome (Hus)
↳
autoimmune
hemoydic An. Hemoyhic Uzemic
↳ Thrombodic
>Polychromasia ->
Hemoydic Anemia
Thompocytopenia purpura
↳ Disseminated Intravascular
> Bite cell ->
Glucose -
6.phosphate Deh.
Coagulation
Heinz Bodies. Deficiency Anemia
↳ composed of
We See
Schistocyte/helmet/Fragmental RBC
denaturated Hb
percipated >paraoxymal Noctural
Hemoglobinuria
>Schistocyte/ helmet I Microangiopathic Hemolytic ↳
Only Amhemolytic Anemia
Anemia
Fragmented RBC ↳ More
hemoglobin (Abrucial
Cell & inThalassemia ↳ (HRBC)
>Target Pancytopenia
↳ Microcytic
Basophillic Stripping hypochromic ↳
erythroctes
t &↑ Ab
Red Cells
↳ MCC Fe
of death=
overload due to repeated Transfusion
, Minna Mamik
Leukemia - Cancer of blood-faring dissue Acute
Myeloid Leukemia
(including bone Marrow &
lymphatic System)
<15-45
yes
Hemadopoiesis -> Formation of Blood Cells . Gum
hyperplasia/Bleeding
↳ liver BR & Liver, Bone Marow)
Coagulation (DIC)
(yolk sac -Disseminated Inteavascular
ardweek 3rdmoth 4th month just before
Birth
Hemapoltic Stem Cell >Chronic Leukemia -
Neoplastic peration of Mature
Common Myeloid Common' lymphoid Circulating lymphocytes, characterised
Drogenita peogenita. by high WBC Count
I
I T -
&
B-lymphocytes
>Erythoblast-> RBC & Chronic Myeloid leukemia
>Megakaryoblast platelets ->
NK cells
↳
Eldery people
*ByodMaromslauk
>Myeloblast >Massive
hepatosphenomegaly Seen
↳ of
Neutrophils Babeseen
.
cytoplasm -
>changed chromosome -
22 (philadelphia chromosome
·
Eosinophils -
Binudeate/spectac shaped Nuclei >↑ No. of all
mydoid linege cell (Madue Myeloid)
granules in Cytoplasm
Brick Red
·
Basophils
-4
Basophils 1 Both are absent in Reactive
z
large Bluish geanues in
cytoplasm
which obscure the nucleus -
tcanslocation Neutrophilic Leukocytosis (*nautzophil
9 h&22nd CLeukemoid Reaction)
t
>Monoblast ->
Monocytes-largestcell, kidney shaped nucleus,
Agranulates (donthave granules)
Chronic
lymphoid leukemia Goyrs)
↳ Neoplasticproliferation of mature
monocytes
B-cell
I Agranulogy en
↳ Blood Smear -> 4
lymphocytus
Normal level CD34 -
MackerfaMSC) Smudge & Botkin
Cells
WBC -> 3 9x109/L hematopoletic stem cell
↳ of lymph
-
6x10/ Involvement node leads togeneralised
RBC
-
=
4 -
lymphadenopathy (Small lymphocytic leukemia)
(cancuous/abnormall cells)
Neoplastic lessions of WBCs
can become
leukemia L
can become
>
Lymphoma Acte Chronic
↓
Involvement of Bone Mariow/ More Systemic/c
Blast > 30% >pediferation of
mature cell
Smeal Tissue Involvement
Periphezal >WBC <50x10"/ >WBC<50x109/
↓
of
like lymphnode/spediferation
Lympho-&Ryeloblast
>promyelocytes
Spleen
Leukemia
>Acute
Mariow/Peripheral
Lymphoma
↳ 30% blasts in Bone Blood
lymphogranulo-
Lymphoblasts Mycoblasts Hodgkin's lymphoma metosis
Non-Hodgkin's lymphoma
-Smallen in Size
-Langen in Size 1) Bimodal age distribution 1) Can Occur at
any age
-Geanules present
(15-20 yes, elders)
>No Granules 2) Generalised lymphadeno-
Guical,
padhy
Ave Mods abscent & Auns mods present 2) lymphadenopathy
(Hall mark of Ryeloblasts)
>Coarse/dumped Chromatin Contagious Spread
3) 3)
Non-Contagions spread
>Open up/Homogenous
Chromatin 4) Reed-Sterberg
aka
alls pt.
Acute
lymphoid leukemia -
ALL owl's
eyes cells
>MC Cancer in Children (2-9yrs)
>t Number of NBC - ↑ infections Lymphogzanulomadosis one of lymphadenopathy disease
st
platelets 2 Reed -
Steenberg cells
Idepatosplenomegaly 3 Necrosis in Immune
Ozgans
· TdttVe (RackenfaAll) 4
parphyzidic Spleen
