Symptoms signs ;

-
pallor

III.
'

"b :
-
THR) Pulse T Respiration rate
,

If
n i n e.

-
n cave named )

symptoms prominent PETTITTE -

Hemic muumuus ( systolic murmur : Mr . As )

①MMf-g
severe anemia confusion
Angina ,
-

: CHF ,

* low
Og supply due to tr or Below normal red cell mass

# Anemia can be klagsified Based on color & size

↳
Color :
prrmo chromatic , Hypo chromatic
↳ site :
Milroy tic Normocytic Macwcytio

And
, ,

Classification Based on
morphology f- I Based on
underlying pathophysiological mechanisms

1-
t t
-

#
v =
V
Micro lytic
Normocytic Macwcytic -
-

CT Mcu) V
Hypochromia Hmat) Nurmoohwmic Normoonwmic
-
-

accelerated RBC loss / Impaired RBL Production

#
anemia
#
anemia Destruction -

L#
Most common

① Defeciency ④ Acute Blood loss / Hemorrhage ① Folate Defective

Deficiency stem cells
=

Iron

?E¥!II!I!s→He
v

IIe:& of Blood 1085

-

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nihil! I.
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③ ② anemia
Brpefeaenykobaiamine)
-

eases
Hemolytic anemia Abnormal puikrahinormaiureaninof rises
Ied : chronic Blood loss #

)
#I
(Increased
T Hb Bereakdown products
DCS the km of RBC
*

③ lead ③ anemia of chronic Dieases 44-

Bilirubin )
-

Bone Marrow
replacement leukemias (Bone cancer )
poisoning
=
ron .
.

, ,
.

#
↳
Bt
chronic inflammation
Bug underlyin cause
④ Thalassemia other causes

µ
-

X (usually Hereditary )
Intravascular
-
Extravascular Extvisnudshiitn be Intrinsic cause Chronic Blood acute Blood
* Defector action of RBCs - -

/ Hemorrhage
By phagocytes in the spleen
I 085 1085
-

① Mechanicals * seen
Turbos that
① Ima ①Membrane defect →
Hereditary spuerocytosis
A) Defective Values -

B) Microvascular thrombi → DIC les 1) Autoimmune disease ② Enzyme Defect → G -

le PD
-

deficiency
-

c) Heat 2)
② Im¥cs Drug
A)
Hereditary spnerocytus.is Associated
③ Hemoglobin defect fhigfdaess.me?asdisease
runs

At risk for Iron

deficiency anemia * At risk for Hypothermia
→
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anemia

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blood gradual * Associated w/ ( TEPO ) erythropoietin
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* chronic loss loss of Iron →
compensatory From spleen
Attur * Associated
w/ splenomegaly
↳
parasites malaria
4) Hyper SpheerisM
→

✓ hw "" t B) Toxin production ( uostridia)

teticulocytvsis ( T RBCs plasma)

im¥ncy Underproduction of RBCs in

t
Mechanical RBC lysis car twheel RBC lysis
Vascular Based Destruction
spleen Destruction
*
Micwcytic Hypochromia anemia * Normocytic Nvrmo chromatic anemia

serum glycoprotein
( thet birds to Free
hemoglobin)))
THB in circulation

Hemolytic
#
anemia labs "

① peripheral Blood smears : Normochromrc d Novouocytir anemia

w/ polychromes ia t nucleated RBCs

② Bone Marrow : if Done ; erythroid hyperplasia

③ plasma serum :

A Bilirubin :
Tuncoujugated
B LD # : T

tr
C Hayato globin Revel :
or Absent

D Free hemoglobin levels : T ( in intravascular hemolysis)

① Urine :

Hem¥si¥wra , hemoglobin uutattntravascu.ee -

hemolysis)

F- Macwoytre I Milroy tic ,

F- hyper chromatic , f- hypo

chromatic

F- spherules
-

F- Anisooytusis
 Based on
underlying pathophysiological mechanisms

v
# u v

Destruction accelerated RBC loss / Impaired RBL Production

- -

/
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V
÷
-

→ -

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Ttb Breakdown products
*iron Bilirubin )
-

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.
.

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.

t t
I
fl¢
( Usually acquired ) (usually Hereditary )
y
v
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-

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Chronic Blood
- -
*

① Mechanical RBCs to
MPkt# Mtm SPE -

① Immune mediated Damage : acute Blood

Injury
:

ieFeeevavesnouawwu.ua * seen in RBCs that a re :

#uueDiwDqaowatell , ①Membrane defect →
Heveditavyspherocytosis
. ÷¥÷÷÷÷÷ } µ± ¥÷÷÷÷ / Hemorrhage
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loss
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loss
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a can
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-

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↳
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-

acuteness :
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,
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mic ayagyy.SI?aIIyYej9YYin-xGapo:at=sHignenumwus-
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parasites ( malaria)
sickle cell anemia C
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anemonesis
-

Intracellular
-

: -

→ Gb PD A lower enzyme levels Intermittent hemolysis

.cl#Aumgga.y!
( Beslan
-

IgM
after
- ' " acute
( ma ages Bite
-

toxin production ( dog # diag

-

Being exposed to
; )
-

A, and
agglutinin type y,¥y.gg?yn,,,,;.g..,*nam, , aµ¥eea*, * no pig ,, of hypo voyeur ,q
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gradual depletion w/ compensatory

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blood loss
② NonatedDamge
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roses
: .

1) n e I n i 3
③ Hemoglobin defect → sickle cell disease
,
A) Valve prosthesis Artificial & NdIt ↳

off
-

:
valve

III.III.Ya?'÷Y depletion ( Iron reticulatus is

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B)
.

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anglo pathic hemolytic
Micro anemia 1% Hbf
As ( seed trait) Black American
→ Heterozygotes sickle
-
partial Miurvascwcav obstruction
§ Pnrtechvn
against Falciparum Malaria infection

p
-

DIC malignant hypertension FTP / HUS , sickle cell

-

, → repeated oxygenation of Deoxygenate aon (sickle fun)

-
→ Membrane
Damage crisis

recycling SLE
,
Disseminated cancer
thrombosis
Iron -
march
www.msn.ra
Complication : small vessel
RBCs # Normocyffu nrormo chromatic anemia

2) Infections Thalassemia>
( Binds Hemoglobin in Blluod)
,

to Free - malaria
T

#
schistuytes
:

t*
Microcytil Hypo chronic anemia od # Iron defect ency
-
-

3) chemicals
-

4) Hyper spienism
' -

④paroxismal
-

Nocturnal hemoglobinvial PNH)

Defeat
Acquired

Hemolytic
=
anemia labs :

① peripheral Blood smears : Normochromrc d

Novonocytir anemia

w/ polychromes ia t nucleated RBCs

② Bone Marrow : if Done ; erythroid hyperplasia

③ plasma serum :

A Bilirubin :
Tuncoujugated
B LD # : T

tr
C Hayato globin Revel :
or Absent

D Free hemoglobin levels : T ( in intravascular hemolysis)

① Urine : Hevesi durra

, hemoglobin uutalintravasculeu hemolysis)
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 Lecture 14 & 16- RBC disorders
Anemia
#RBC
RBC Destruction Impaired production
/
-

/ t s
g-
I
-

1 -t
Hemolyticanemi# it:P:::'m:: i'Eisemann /
1) short life
span V
v '

chronic
.am.

-
J macrocyti-clmega-obe.tk
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Acute Hemorrhage Normochwmic cytic Nomo anemia

Loss
Low Hb low Mcv low MCH TA RD W I , TBIC T

(A cute
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, ,

Blood loss )
comms
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chronic
Blood loss in western

Defective DNA
synthesis
*
dft ① Iron
Deficiency
'

Folate :
Most children a pregnant want
W
Bp Defecieucy common in -

- or
.

- a neural products ; absorbed in Duodenum

*
Peripheral Blood MCV I Hepa din inhibits uptake of Iron From Gut
-

smear > too f- L

- -

retiudocytes
:

triage)
-

, ( secreted by liver www.T Hepatic Irons

At risk for Iron

deficiency anemia At Hypothermia
,

* risk for Hyper segmented Neutrophils ( 25 Lobes)

, ② Anemia of chronic Disease
risk of Patients may
¥ No hypo Vole Mig have
cytupeuia r

(t
pan t trunk
ferritin TB Ic t

transferring
INHAVAS(
* Bone Marrow
#p Hepadmit Eytnrutioiten
, ,

) hematopoiesis large Hb ,

Hyper cellular

HEMOLYSIS
: ( ineffective

€XtfqWhyCale✓
cells rise WBC
,
ncgakeryvuyfees
:
, , ,

* chronic blood loss gradual loss of Iron → * Associated w/

compensatory CT Epo ) erythropoietin From spleen ✓ ↳V * Folate $ Biz Needed For synthesis of Thyroid alate ( DNA molecule)
③ Sideroblastic anemia

↳ -

# H E MO(y SI S
culocytvsis ( T RBCs plasma)
im¥ncy Underproduction of RBCs teh
-

in
④
① Blztdefeciency / terminal DX low Hb pancyfopenra TT Mex Thalassemia
'

: Distal ileum ileum absuubsnm

hypochromia Miro cytic
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:
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✓ , large

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-
*
Biz Diet Biz Birds to heptucovvin until it reaches Duodenum
Myeloma on

Mechanical to RBCs
Compliment (Immune causes) to RBCs
injury * caused by defects that TRBC Destruction Tltuuosciusnwue i
Free swum :
cause bwheve releases the Biz Hapto
pancreatic
From Corvin
proteases .

- - by the phagocytosis Associated w/ splenomegaly ) Knelling test

spleen Biz

Micwcytic Hypochromia Nvrmo chromatic

bird to Intrinsic Factor ( secreted 8
-

Normocytic
then
via by gastric parietal
: cells

anemia anemia
( Non Immune causes ) paruxysmalnoctuvnalttemogluobinuriaf.PH#
and travels to Distal ileum 4 taken up
by Enterocytes visa IF receptor

D
Biz
.

Rare
acquired genetic
then
transported into blood to to body ) Laren Uta

④RBCMembrahedefect.it#erdarypmruWsis:Intrinsivcau
* clonal stem cell disorder :
periodic hemolysis go
-
* Mutation in
Phosphatidylinositol glycan class A ( PIG A) carrier
protein Trans cobalamin
gene
-

X linked mutation
AD mutation of cytoskeleton
-

I)
Etiology proteins Ankyrin Band Band 4.2 d spectrin
: 3

① Cardiac
:

Values Artificial
, ,
* PIGA ,
: value Mure affected is
responsible for
synthesizing glycosyl phosphatidylinositol C# PI)
-
¥
Etiology of Vitamin ( cobalamin)
Defecting
Bp
:

* GPI is
responsible For
anchoring
* Northern European population
then
surface membrane
proteins on
hematopoietic
BTO PW theft L Valves cells such
RBC Life span ① 4
Dietary intake : Biz Found in animal vreleatlpruolucts
days
Blood
group antigens , adhesion molecules compliment repeating prose.us * 10 12
as : a -
, :
I

TI) Pathogenesis
② angry pathic hemolytic
regulating compliment
3 GPI mutated
Micro
for
proteins
* that
responsible are
↳ gfnzf
anemia
CD 55
TIL I!fib*aYmaPIIIwf of RBC Membrane → loss of small fragments during normal shearing in blood vegans

]
Decay accelerating Mutation cytoskeletal proteins - reduced stability
I

1
Factor
'

in
②
-
:

# Occurs after a
partial Microvascular obstruction z membrane inhibitor reactive lysis : CD 59
the
Body clears them out
Blood circulation → RBCs become spherical (spherucytosis) → unable to travel
through splenic
sinusoids → splenic Macrophages ImmpairedGIabbn ;

Ktutrauascwlev Hemolysis ) ( Most cause of 4312 Defect Auto Immune

eng )
:
3 pernicious anemia common
-

c8 Binding protein
Phagouytosed Destroy Anemia &
splenomegaly
-

RBCs →
#
Seen in : ① DIC ( Crohn's Disease)
Disease that
*
symptoms .
. -

Malabsorption syndromes Destroys the

② F) Anemia Fatigue
Malignant hypertension clinical features gnathic mucosa
Dyspnea
III) Tx :
:
,

: GI surgery stomach or ileum

-

Hemoglobinaria ( parietal cell)

1) Supportive
2) -

③ Hug YTTP
3) Pancntupenia →
Aplastic anemia ① Anemia :
A- Asymptomatic
⑤) Mild to moderate Anemia
→
25%

Most
-

Fish Tapeworm infestation :

Di phyllo both r u i n Calum
4) Thrombosis :
→ common

2)
Splenectomy
c) corrects the anemia but
① ③
dlt platelet Dysfunction severe anemia → @ Bir th ; minority :
↳ pro thrombotic state Gyenettc
→

g Lf
D. Borders

④ Jaundice
Lead cause of Death of this
Disease
-

5) # Tun
Sphevucyfrsis
Mutations
conjugated hyper will genes responsame fu absorption
renal

⑤
bilirubinm i n
persist
:

insufficiency in
-

; or
metabolism of
Disseminated cancers caused
By chronic hemoglobinaura

③splenomegaly
Bez
* D Coombs t) test
# peripheral Diagnosis
:
:
Schistocytvsis ( RBC w/ varying )
shapes
:
Htt

clmicopathologicalkatuve.SI/)Di#HdY
2) Aplastic Anemia
Blood helmet cells
leg Burrows
'

, , triangle cells 3)
refractory anemia ① Anemia symptoms .
.
Dyspnea , pallor , Fatigue
HD unexplained thrombosis 1) Fm Hx ② Mild
w/ eytopenia ✓✓ of anemia
jaundice

③ Malarial Infections 5)
hemolysis
CBC : Anemia or
pan cylvpenra
2) use for anemia

3) Evidence of hemolysis
③
Beefy
④ CNS
tongue
symptoms
-

!
-

Angelo blast cells in

oropharyngeal tongue
Bae helps w/ Narwhal myelination
4) Pe r i o d s :

6) Evidence of intravascular hemolysis Hemoglobinvia

: Heuosrderiruvia
A) nurmocyfic nor mo chromic ( MCV 80 MCHC n 30% )
Degeneration of
NO :
, :
0 Dorsal & lateral tracts of CNS
-

7) old Test 's : ①

, : No motor or
sensory
sucrose hemolysis test ② Ham's acid test B) spherucytcs
, ② Para Limb
c) Polychromatic cells
paresis , sensory ataxia
,
lower pasrasthesra
8) I nucleated RBCs
Flow cytometry : absence of CD 55 slob 59
D) Howell Jolly bodies → if patient had
splenectomy
-

* TX
Immunosuppression 5) TMCHC
"

or Bone marrow
transplant
6) test It )
Osmotic
fragility
7) Coombs Test t )

③Cold Antibody IHA Il) Rikers ④ Folate vegetabalks

:

green leafy do sorbed pwxihel

:

#
aplastic hemolytic anemia
,
i. je sire
Infections w/ Parvovirus can cause or

w/ ¢
-

↳ Prevents RBC
Destruction

⑦ coldAgglutnintypeftg.tt ) ⑨ coldttemolysintype (IgG) Alcoholics t intake

got veggies , Tumors
,( piss invented , pregnancy Drug 's :
Methotrexate
Fingertips)
( ,
* IgM Abs Bind to RBCs in peripheral circulation
* IgG
,
)
)
auto antibodies against RBCs which
@htt cancer
@ < 30°C
(Inactive At Body Temp 37k
'
-

②
patients w/ causes Paroxysmal cold
Hemoglobin Wia
IgG)
This
type produced
Warm antibody I HA (
* is in :

①Infections :
A)
Mycoplasma : ie M )
r * Does not cause
agglutination like IgM -

B) EBV But activates direct RBC lysis via

compliment * Most common IHA Extrinsic Defect
c) HIN
,

D) CM " *
fixes # 10 Idiopathic soy
IgG compliment cold peripheries & upon
-

in ! .

E) Influenza It Intravascular hemolysis & # 20 1) Autoimmune Disease

'
SLEE
rewarming causes : -

② Neoplasm : A) B -

cell lymphoma Hemoglobinvia 2) B cell

-

neoplasms : CLL , lymphomas

* to autoimmune phenomenons 3) Drug rxn :
Methyldope penicillin
)
,
*
Complication patients develop Raynaud phenomenon ( peripheral
: aero
cyanosis * 2¥ post viral Infections → children ! !
against RB#IgI ( active @ 370 Body Temp)
#
dlt Stfdgrg in Peripheral capillaries antibody
complication :
-

paroxysmal coed
Hemoglobin urea
,

Intravascular ↳ Antibody coated RBCs removed

hemolysis by spleen
-

*
IgM Abs stimulate :( cleave E3 ) & release Csb to cops in Tze
the
IgM coated RBC which is then Destroyed ( removed in spleen 4¥ can
transform into Sphevocytes dft partial removal of RBC membrane

( Extravascular hemolysis) Extrinsic

, * chronic Mild anemia & Moderate splenomegaly : Asymptomatic
* activates Compliment system
* 1)
TI .

supportive treatment & remove underlying offending agent

÷÷q.....
2) Immunosuppression :
corticosteroids
-

③EeotG6PDHB ③ Hemoglobin defect → sickle cell disease

,
( HBA is replaced w/ Hbs )
NIt
-

t.on.ca#ffI7InI'I E.ssIsI: : :'

In:3
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967 . HbA (a 22532)
ein~aian.xr.m.es "

1%
A) Gb PD At Variant
HBF K£82) A ( seed trait) Black American
high hemolytic Hbs
level anemia sickle
Heterozygotes
s
No §
enzyme
: -
:

X -

Hot ) .

B) Gb PD A- * Pntechm Malaria infection

lower enzyme levels acute Intermittent of hemolytic against Facliciparum
⇐

Variant : =

episodes anemia
sickle cell
+ repeated oxygenation & Deoxygenate aon (sickle fun)
Membrane
Damage crisis
-

↳ Black Americans >

-

; normal enzyme activity but decreased half Life -

C) Gb PD M ( Mediterranean) variant rial au a Complication small vessel thrombosis ( Btc they clump together
)
fypomfalciparum
:
Most severe variant ; Middle East natural selection
protection
-
: :

- , * Abnormal RBC 's undergo Intravascular & Extravascular Hemolysis area moderate -

T *
D) G le PD B variant riskfactorsthatcantriggevsickleceucvis.is#
normal
type
:

l )
: Infectious
24 Dehydration
II )
Pa¥¥q .
Acidosis

[ hemoglobin
Gb deficient to levels of oxidative stress Oxidation of SH of denatured Hb 4) exposure cold environments
high
→
PD RBCs exposed on chairs →
precipitation to
groups
are on

(
5)
RBC membrane Heinz bodies Hypoxia
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④
items

>A ) if Membrane Intravascular Hemolysis

* damage is severe

B) if
wafgymwtoeaspjeyengapndwnqeffars.at?ihTar
Rbi

",
membrane moderate -
damage is

m . .. The Hen .
Bodies (inclusion) Bite cells hemolysis,

III ) clinicalpresentahvh :
Patterns of Hemolysis

A) Acute intravascular hemolysis :

2.3 days after exposed to oxidant stress :
1) Infections
2) ingested drugs : Antimalarial s (prima
quire) ,
sulfonamides

3) ingested foods fava : beans

B) Neonatal jaundice
c) Chronic low -

grade hemolytic anemia

↳ No environ me

II ) Diagnosisllabfihdlhgs
A) Clinical History of patient
&
B) CBC :
signs of Anemia Hemolysis
c) Peripheral Blood smear : D Nur mo chromic Nurmucyh c
-

anemia
-

2) Heinz Bodies
3) polychromatic cells I nucleated RBCs

4) Bite cells

D) Gile PD 3 months after to avoid false

Assay : Needs to be done an
episode Negative
 i÷
Chronic Blood

At risk for Iron

deficiency anemia * At risk for Hypothermia
* no risk of hypo vote Mia

blood gradual loss of Iron → * Associated w/ CT EPO ) erythropoietin

* chronic loss
compensatory From spleen

↳
culocytvsis ( T RBCs plasma)
im#ncy Underproduction of RBCs teh
-

in

T¥uHypomwmiWa NormocyticNvrmochwmaticanemi
 Lecture 16: RBC disorders 2

I
÷ hemuglob.in#
Hemoglubinupathyimutatiminglvbingeneespwductimo

:÷:i÷÷i÷÷ I
isicklecehdiseo.se

.In÷÷÷÷i
:÷i ÷ ÷ ÷ ÷÷÷÷i÷÷:i÷ :÷÷i ÷ i÷i: ÷:i÷i:÷÷
④RBCMembranedefecti-iarypmruuois.Intrinsiua.ie
I)
Etiology
AD mutation of cytoskeleton
proteins Ankyrin Bands Band 4.2 a spectrin ③EMmkfect-TGPDAYiwidaweinimt.ro#
:[ II.Aa *sj In
:
NuHomi "
II.Ibs
¥7,3 !
: * "
, , ,

Northern European population

.
* B. globin gene
XR Males Hbf 12282)
I)
EtiVaan
→ it
:
.

RBC Life span

days
* ,
: lo - 12
A) G6PD Variant high hemolytic
TI) enzyme level No anemia
IEh.LU#ants:Heveditay
: -

pathogenesis X
B) Gb PD A
-

acute Intermittent of hemolytic At Hbs Iss) :(

←

Variant : lower enzyme levels episodes anemia )

-

Homozygotes
=
blood sickle cell anemia
normal
loss of small fragments during
-

shearing in

] PItmamamn.am
Mutation of RBC Membrane →
in cytoskeletal proteins - reduced stability f
-
↳ loot Natural selection in africa :

↳ Black Americans
.

sinusoids i normal emme activity but dlltehkd half life

splenic Macrophages
-

Blood circulation RBCs spherical (spherucytosis) B) Hbs ( As) t )

→
→ become → unable to travel
through splenic sickle cell trait
-

Heterozygotes ; Black Americans loot )

C) rial au a
.

Gb PD M ( Mediterranean) variant
fypomfalciparum)z
↳ 40 '
Most severe variant ; Middle East natural selection
protection
- -

: :
,
c) HBA ( AA )
Phagouytosed Destroy splenomegaly Normal wild
-

RBCs →
Anemia & :
type
y
D) G6PD_B variant :
normal
type
I) pathogenesis
III) clinical features : Tx :
) Supportive ) During deuxygenahvn Hbs
aggregate & polymer ite to each other → assemble spindles / sickies
t
into Neadhe deforms RBCs shape

Path0PhWN↳gy-
into
t I molecules like →

① Anemia
shape
-

sicking is reversible durian

,
a) Asymptomatic →
25% ↳

[ hemoglobin
B) mad to moderate anemia most Gb deficient
PD RBCs exposed to
high levels of Oxidative stress → Oxidation of SH on chairs →
precipitation of denatured Hb ↳ But repeated irrecusable sicking dit membrane damage
groups
→ common are on
sicking causes
2)
Splenectomy Riffa]
c) severe anemia → @ Bir th ; minority : corrects the anemia but RBC Heim bodies
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④ Jaundice causes

gygiean
,

# Tun
conjugated hyper Sphevucyfvsis will
,
bilirubinm i n
persist
:

>A) if Membrane Intravascular Hemolysis

damage is severe

:÷÷i÷÷÷i:÷÷i :÷ ÷ ÷ ÷ ÷
*
paruxysmalnoctuvnalttemogluobinurial.PH#
Rare
acquired genetic clonal stem cell disorder :
periodic hemolysis
VI)
:÷ :i÷ :÷i ÷:i÷ :÷i:÷ i÷:÷ ÷ ÷ ÷ VII ) iT
A) sudden / acute anemia
triggered By
4
types
.

* ( PIG A)
"

Mutation in
:

Phosphatidylinositol glycan class A -

gene
m m

1) infections ( H influenza pneumonia)

X linked Mutation strep
'

,
.
-

2) Dehydration
3) exposure to cold
* PIG A 4) hypoxia
is
responsible For
synthesizing glycosyl phosphatidylinositol (# pp) 8) Acidosis
* GPI is
responsible For
anchoring surface membrane proteins on
hematopoietic
cells such Blood
group antigens adhesion molecules d compliment
as :
, ,
regulatory proteins
-

3 GPI for
regulating compliment mutated
*
proteins responsible that
-

are -

amp '' m"

Decay accelerating CD 55 'T
,hg inhibitthey
]
' - Factor :
-

, are absent
CD 59
membrane inhibitor reactive 48 is
-

z the clears them out

Body
3 C8 KIutravascwl.eu Hemolysis )
Binding protein

VIII)
sumptuous
Diagnosis to lab findings
* :

-
#

1) Anemia :
Fatigue Dyspnea ,

2) Hemoglobinuric
1) Fm Hx of sickle cell disease
3) pancytupenia →
Aplastic anemia
II, CBC of hemolytic
signs anemia
'

4) Thrombosis
-
:

dlt platelet Dysfunction 3) Peripheral A ) sick led

↳ pro thrombotic state Blood shape RBCs
→ :

Lead cause of Death of this

Disease B ) polychromatic I a nucleated RBCs
45) renal in
suffect c) Howell Jolly only after auto
splenectomy

[
ency ;
-
Bodies :

caused
By chronic hemoglobinuvtq
4)
Confirmatory test : ps ← Gold standard
*
Dis :
)
l
Coombs t) test knkeeamnmia-Hbs.tt bet Hba
-

Tn
Hbst , Hbft , Hb At

2) Aplastic
-
sickle cell trait
Anemia -

5) test ? test
3)
Screening Sicking
:
Mixing patients Blood w/ Oxygen consuming agent ( meta bisulfite)
-

iducesi okay
-

refractory anemia

HD unexplained thrombosis
w/ eytopenia or

5) CBC
hemolysis
: Anemia or
pan cylvpenra
E) Treatment
-
XI) clinical outcome
-
course
6) Evidence
A) Supportive Measures Analgesics ( Pain ) renovation Blood transfusions
A) p, is w/ Css) got survival to soy
y yo
:

intravascular zoyyo ,
,

of I survival
hemolysis Hemoglobin go
,

: uria Hewosrdennuria
.
to
,
B) Folic acid
7) old Test 's : ① sucrose hemolysis test
,
② Haris acid test suppliant B) infections is the common cause of Death in children <
5410 W/ SCD

c) Penicillin prophylaxis for auto splenectomies patients

c) Adults organ failure ( kidneys)
-

8)
:

Flow cytometry : absence of CD 55 & CD 59

D) Hydroxy Unea = increase CHBFI d inhibit Hbs
polymerization ( sicking) D) Vaso Occlusive complications
-

occur if recurrent : Acute chest syndrome , stroke , kidney Damage

* "
Immunosuppression
"

or Bone marrow
transplant E) Bone Marrow transplant
#
 Lecture 16: RBC disorders 2

* Reduced
synthesis of Noemi x-or-B.qha.ms =
t [ Hb ] -
-

Milwcyticttypochwmah.CI f- INCH
,
t MCHC

↳ T RBC Extravascular Hemolysis Extravascular hemolysis anemia pattern

aggregate # inclusion Bodies damage
=
-

* Common in : Mediterranean , Afrran ,

& Asian
populations dit protection From P Falciparum
.

2 chromosome KH
genes on
:

Definition Reduced of normal B globin

synthesis chains
w/ Unimpaired chain production
-
: -

b
TT t chains
globin
-

I)
Etiology :
2B globin genes
-
(alleles)

A) Bt thalassemia I B. chain promotor region Mutation

synthesis
: =

B) PO thalassemia :
No B chain
-

production =
Mutation in
spire site or chain termination

I)

ctinB.thalassemi.am#r:CB4Bo,Bt/Bt,BYBI
)
icaltsthalassemiasyndwmesl
↳ transfusion
Severe
dependent anemia (soon after Birth)

WT WT
z )
s.thalassemiamimoltraiti.CO/Bwoiyw,?tb#
↳ Mild
Asymptomatic anemia

3) s.thalassemiaintermediai.CA/Bt,B4B0,Bt/B,B#wty
WT o

↳
Moderately severe anemia ; Does not
require regular transfusion

III) B. thalassemia Major clinic pathology

/
I #

A) Clinic M After he months of Birth

-

→
:
severe anemia

B) HE Ht )
:3
leg 1dL
-
-

c) pain :

1) reduWi→ impaired Hb production

↳
Miuwcytic hypochromia anemia

2) excessofunpairedtghob.in#speriptate
↳
reduced life / survival of RBCs & RBC precursors dlt cell membrane

damage
↳ Results in :
-

1) Hepato splenomegaly :
dit Extravascular Hemolysis

:÷÷÷÷÷÷÷÷:÷:÷÷÷÷÷÷:÷÷÷÷:÷÷::
"
÷ ÷ ÷ :÷ ÷ ÷ ÷ ÷ ÷
"

D Family
" ". . "

History ( TRDW)
2) CBC for anemia : b [ Hb]
variable cell sizes
. . . .
-

3) Evidence of Extravascular Hemolysis Canisocytvsis)

4) peripheral & Variable cell shapes
Blind r ) Milky tic Hypuohwmik
)
smear :
( poi kilo miosis)
2) Anisopuikilocytvs is
Many target cells
-

minor →

3) Polychromatic cells I am cheated RBCs

major →
5) Hb electrophoresis :

1) Absent or severe I Hb A
2) T Hbf levels

Hb Az T -
- or normal
 Lecture 18 : Not Done

÷÷i:*"'÷i÷fi÷f÷÷÷÷÷÷÷
÷÷÷÷
÷÷÷÷÷
Disease
-

(IgG ) ( IgM) (IgG )

-

Most common t of hemolytic toy 701 Paroxysmal cold Hemoglobinvria ( occurs )

cold temperatures
type immuno anemia causes
-

when
person
-

in
-
. .

Clinical per es earththey of Anemia Moderate

chronic mild symptoms $
splenomegaly
-

signs 4
symptoms
-

Morphology
-

Labinvegtigovns
(t )
Labium : Direct Coombs test (t ) : 1) Direct Coombs test ( Antiglobin Test -
DAT) (t ) LabWs ! Direct Coombs test
labmvesltgahmsi A) peripheral blood smear :
Schistocytosis : Burr cells helmet cells
, ,
triangle cells
→
Patients RBCs incubated w/ IgM IgG , compliment

↳b In Vey
are or or
,

tightmy
↳ Positive test
aggluhnanm

e) indirect Coombs test ( indirect Anti globin Test IDAT)

-

:÷:i÷÷÷÷÷÷÷
÷÷i÷÷÷÷÷÷
.in

⇐301)
1) Antibodies ( IgG )
pathogenesis 3¥ ! .ru?oCsarephagvmti2e by Macrophages 1) Petz is
coat RBCs @ peripheral circulation @ ⇐0°C pathogenesis in the cold peripheral circulation direct lysis
to RBC membrane
agglutinates $
they via
binds →
IgM
: - : -

in : -

; cause
,. ,

Pq thru gym8 IS
M
spleen ( Histiocytes) Extravascular Hemolysis fixes compliment rapidly ; As blood recirculates & warms up → Compliment Mediated compliment → Intravascular Hemolysis upon rewarming of
Blood
= -

Hemolysis by spleen → Extravascular

hemolysis
partial removal of RBC transforms them into
Spheruuytts ( Raynauds phenomenon)
-

Membrane
studying
-

blood
of in capillaries oytaggluhnahm causes aero cyanosis

risk factors

Tx ! Do not
really need treatment

Complicating /
But

↳ A)
Supportive
& removal of
offending agent

tf lathe ht s B) Immunosuppression

additional

notes
 ( t RBC count)

÷÷ii÷i÷
i÷ :i÷÷÷/
i÷÷÷÷÷÷
Disease

B12 Defect ency Folate AKA Anemia of chronic inflammation

-

Impaired DNA
synthesis deficiency -

Impaired DNA
synthesis :

( cobalamin) Distal ileum proximal jejunum

- -

A)
1) Symptoms of Anemia :
fatigue , pallor , Dyspnea . . . . . 1) Symptoms of Anemia :
fatigue , pallor , Dyspnea . . - - -

signs : l ) pallor , Dry 1 rough skin B) Sew : 1) Anemia :

Clinical p eregentaHuff
2)
Atrophic glossitis Fatigue , SOB , palpitations
wi loss of tungue papillae
2) Mild jaundice 2) Mild jaundice 2) Pica & ice
3) koilonychia (spoon Nails) craving

Signs & Sy f 4) Angular

ping strong
omits 3) restless

[
asrgyue.am ,
leg syndrome
3) Beefy tongue 3) Beefy tongue 4) Plummer Vinson
w/ EDA
-

syndromic :

1) Dysphagia
4) CNS symptoms 4)
combined
( B12 involved in
myelination of Neurons) : NO CNS
Symptoms 2) Esophageal
3) IDA
web

Subacute degeneration : para paresis, sensory ataxia , lower Limb paresthesia

-

1) Boreham 1) Hyper cellularity

: But not effective
hematopeisis

My ✓ N U If
2) Megalomanic RBCs * WB " 1) Miuwcytic hypochromia

p q

Malabsorption syndromes
:
:'i÷÷÷÷÷÷i÷ :i÷ ÷'÷:i ÷:i÷ :÷ ÷'i ÷÷ii÷ i ÷ ÷ ÷: i ÷ ÷ ÷ :÷÷i÷÷÷÷÷
infancy
-
Fish tape worm *

c) .hn/yyyeodaynDIsyrndbmthat
Gemmy affect any factors involved absorbing B12
= Disseminated cancer

Very rare
-

People taking Dungy Folate types : Methotrexate th meth oprim

-
-
,

NUcba§§_
For of
pathogenesis
:
coenzyme synthesis Thymidine
Defect
inadequate DNA
synthesis
→
Defective
ency
-
-

Pfe thro 8 IS maturation

glum
w/ normal mRNA gprotein synthesis
Nuclear 1 cytoplasmic asynohwny

£" " " ""

t
)

µ
Haha:X
f
!gyine )
(Coba
-

1) strict 1) Pregnant women

vegans
✓I S K FALINVS 2) pernicious anemia →
parents will present w/ chronic 21 Malignant 1 Metastatic humors
atrophic gastritis

3) infants

TX !
retiunwcyte response improvementsdays after TX : * Must rule Biz
deficiency *
Comfy
intent
/
B" 'm → out
-

Yy (ayy my
injection
-

give ¥m
1st and then folic acid replacement
↳ can be depleted if given folate
only

µ LfIme Uf f degeneration ( Cns

complications : severe combined sxs)

additional
t
f
t T
notes
 WBCDtsorde.rs

Too Few WBC - →

Too
#

# many WBL

¢ I
µ \
pathuqenesrsotwlxmalignenci.es/ymphOpeniA
:§"im"
Neutropenia ①
chromosomal translocations & oncogenes

¥¥YNsis
myeloid leukemia ( Nhl)
- -
② Inherited Down's syndrome
genetic Disorders

NwPksthleh#Ys (Malignancies)
: → Acute

'
Mut'

÷! !!!:!÷÷¥÷÷÷÷
' '
* Reduced lymphocyte count * reduced neutrophil count caused
; By :

¥÷ ÷ ÷ :
/ \ / \
④ Immune
→ Dysregulation SLE

Neutrophil
:

* seen in
following settings 1 Disease : N - Got -
:
NeutrophilIia ⑤
Langone :
radium , chemotherapy
¢ -
30 T .

1) advanced HIV infection E- SY .

* reduced to ineffective Accelerated Dystmehmrr ① Acute inflammation V
B ly Production consumption of Neutrophils
-

infections )
-

:
pyrogenic Bacteria
Fungal ( candide
.

leukemia
,

) (BP Tissue MI
lymphoma
[
-

z autoimmune Diseases Damage Burns , trauma swarms

"

on tender
, -

lymph node
enlargement (painless,
Deposition
"
of Antibodies chemicals rheumatoid
Neoplasia involving Bone Marrow
""
aYEudIMk
-

or :
Gout ar thritis *
, *
Neoplasia, in lymph nodes or
-

4% extra nodal
symptoms based on site of
that nodal
bohtuflhiaipanmbpem.at
are extra

②
masses
* A
3) ④ Acute
hemorrhage malignancy
Acute viral infections ④ Aplastic Anemia :
suppression of myeloid precursor sternums Autoimmune or
Drug mediated destruction :
ie, SLE & Rheumatoid Arthritis

£ I q€##
Fever untiukudrd weight loss
③ /MectNh2 tumors night sweats ,
-

Malignancy extensive
: ,

4) ②Drug ② Splenomegaly # DO hle Bodies 9 toxic

Drug induced Induced granulation histology of Neutrophils
:
: in
of committed precursors
sequestration of Blood cells
:
-

suppression
up
↳ " "to - -

Eosinophilic Eosinophilia ACUTE chWhr

chemo →
""
③
Megaloblastic anemia Myelodysplastic syndromes ③
:
overwhelming infection consumption
↳
:
Increased
anergy
,
* Precursor cells * differentiated / Mature
-
- - '

ineffective gr-anulopoe.is
steroid
therapy Precursor * differentiated / Mature
predominate cells
predominate
④ granulomas ①
Allergies * cells
'

&
Malignancies asthma , hay fever
:
( space
occupying )
:
Bone marrow infiltration

② Skin Diseases Bohus

pinphigoid Predominate cells
predominate
pemphigus Vulgaris
:

,
Devmitidis Heupetiforms
⑤ Kosman syndrome ,
: Rare inherited disorders
③ parasites :
malaria

Cyclic Neutropenia
④ Allergic Drug rxns :

⑤
Malign anus
:

Hodgkin lymphomas ,
T -

cell
Lymphoma
⑥
Mighty!Ysi"I
;7mY¥]] collagen vascular Diseases : Vasculitis ( Chung strauss vasculitis )
#
Agranulocytosis :
severe
Neutropenia ( <
500 Celyn)
=
can lead to life threatening infections
- underlying infection

÷ i÷ ÷ ÷ ÷ ÷ ÷:÷÷÷÷÷÷÷÷i÷÷÷÷÷÷ ↳ iet Many usually

marrow
,
immune -
:÷÷÷:*
mediated , By suppression
.""

of
.

precursors
① Chronic Infections : TB ricketts rusts Bacterial endocarditis Malaria
, , ,

②
collagen Vascular Diseases i SLE ,
Marfan
syndrome
C? )

③ Inflammatory Brwel Diseases

'

Ulcerative colitis
'

→
ReachVelymphocyt0 :
B -

caus sitcoms

① Disorders chronic inflammation

w/
:

② Viral infections :
EBU
, Hep A ,
CMV ,
infectious mononucleosis

I
③ Borditeka Pertussis Infection ( whooping
cough)
:

↳ * this the
only Bacteria that cause lymphocytosis all ,

others cause Neutrophil ia

 Blood Neoplasms
✓ n
Myeloid lymphoid neoplasm
/ I ↳
Acute leukemia,
-

Myeloid
( Acute) Mature
! chronic clinical

e- Myelodysplastic syndrome Early precursor Neoplasm History)

chronic
Myulopolifurahue Neoplasms
neoplasms
Acutetlymphoblastic / )
lymphoma IAU)
Hudgins non-Hodgkin
L b
F- Cell B. cell
All ALL
'

HAW) ( BAH)

(B. cell lymphomas)

 NHL translocations : t 114 -18)
Lymphoma
Follicular lymphoma BCL 2 ( 18) Ig 114) #
Neoplasia in lymph nodes or
-

, ,

t ( 8 ; 14) Burkitt lymphoma masses that are extra model

§
\
K ( Ili 8)

#
Lymphoma ( MALtome) / Extranodal Marginal
( Have
l Malt Zone
lymphoma -

thi )
( Ht) reed Sternberg cells) →
" " ""
-

TP " " " "

14 mantle cell
lymphoma

(
( Do not have reed
) non
It's

Hodgkins lymphoma Hodqkiuslyvuphovras

-

siernbuvgceus -
*
Painless rubbery enlargement of I more
or
lymph Nodes ( LN) ; Become painful when
drinking ALCOHOL

#
* B -

symptoms lsystemic symptoms : Fever , weight loss Night sweets

,

÷¥%÷"
*±"
" "" " " "
""
"

µ
"" "

tendency
signals causing = IT inflemuetuy polifuvatim of lymphocytes

Premphoio #Matnve(peviphereDB-ce ✓ CD Lot , 45T , 15

15435,45
-

30
-
-
:
,
CD:

Neuptesms Neoplasm -

#
pariah classical
-

① Acute lymphoblastic leukemia / Lymphoma ① Diffuse large B cell ( DcBeck) ⑤ BwkiHshmphumaLB#

lymphoma
-

* 13 cell Neoplasm curable in children &

Young adults Tx :
High Dose of
aggressive
-

( #LL)
j older people Bad prognosis
#* curable if treated early Moderate , agreesNe
;
chemotherapy
# Associated EBU Epstein
A) Most lymphoma
of EBV induced
:
Barr virus
common Adult 604/0 w/ 3
types Burkitt lymphoma
:
median =

, Godchildren
T
[
* ① Endemic
BL → loot EBU African
B) 1¥
=

Etiology
.

De 2%7
.

novo

*
: , most common

A⑥wfe rapid Onset of Symptoms :

affec ted EBV associated
② = 15-1

③ Iii!!! Infiniti.IE#
.

CBC btw 2% transformation of

grade tumor
:
Wo a low ; Follicular lymphoma a small B cell
-

lymphomas
••

J
, - -
Her Er n associated
→
parents ar t
C)
Be .

Rapidly
,

/
BM
replacement symptoms Cytopeuias , Dune pain
←

enlarging lymph node mass

-
:
or Masses
-
Extranodal Masses
-

Lymphnod enlargement I organomegaly ( liver spleen) ,

: GET, skin ,
Wald eyer 's ring * Clinical features
#
:

Histology patient will come in to clinic

wfoBM.sywnptowr.es#-Biochem:Myelo during stage I II

-

Children
=
-
Presence of
w/ scanty basophil cytoplasm
blast cells ice
: BM d PB or
,
B Fever weight
-

Symptom loss $
-

peroxidase Black C-) PAS Ct) es !

Night
& sudan
, , , sweats

/ ImmuuoeyB##
Cytogenetics
8paL
-

:
presence of translocations deletions , and/or
, hyper plvidy ( African)
-
Flow cytometry Marker for lymphoblasts = Tdtt I
# Associated w/ Down's syndrome after 5 yo D) CD IOI 19T 20T -
* Tumor of
Jaw 4 Facial Bones
# Abdominal
pain , w/ Mass
*
presents w/ symptoms
/
-

→ Involving Distal Ileum

* Treatment of ALL
* spreads to
/ of the
underlying
immunotherapy K Rituximab)
Bp
,$to
other sites
literacy
3 E) TX
phases
:
intensive chemo d anti CD -20
'

:
(testes , wavy , kidney) ascites Immunodeficiency

/
,

/
remission Induction * Areas where malaria
again
]*tef
!
.EE?p7YheiYIi:Ij/
is
Twee
-

-
consolidation therapy phases also included
② Follicular lymph✓) Ma (FL)
High

:÷:÷ i÷ ÷ ÷ ÷ ÷ :÷÷ ÷i ÷ ÷ ÷ ÷:*: ÷

maintenance
-

therapy -

- Bone Marrow
transplant ( only if pxreplases) * Indolent lymphoma ( slow growing ,
Incurable ,
40% Can Form into D LBL L

A) originates From Germinal center of B- cells in lymphnudes

:*
lot 19T 20T in *
B) Adults yo ; CD
:
; so -
60 , , .

.. . c) t ( 1448 ) : fusion of Poche-2118 ) onto Ig H locus ( 14)

".. which inhibits apoptosis
# allows
overexpression of BCL 2 gene
-

(pro
gene)
-
survival . "
.

D) Painless Lymphadenopathy canbe localized or

generalized

⑥ Hairy cell leukemia

-
:

40% cell May look like CML (Chunn myeloid leukemia )

: cells with Fine hair like cytoplasmic
Hepato splenomegaly Frequently involved ( liver &
spleen)
-
-
,
:

projections
-
-

# Iindoleut
BMinuuwemeut-CBvnepo.in
comes to clinic @ Uncommon
-

stage IT w/
* old males MSF ( 4 it ) BRAE Mntahus Here .net#rreonire
)

#
;
- E ) Morphology :
-
nodular ( 75¥ )
,
or Diffuse ( LST ) .

growth pattern of Germinal center ,

f
-

f
Centrobytes
Hq E E : small cleaved cells w/o Nucleoli
*
Amie 's :# No lymph Node Involvement #
=
:: isn't:÷÷::c:::::÷::::::÷: www..us -
BM symtoms :
Bone Pain , Pancytupenia
V
pancytopeuia Infections

[ Bleeding
BCL -2 :

T
-

high
,
level of Bu ( Gc)
B cell Steg Mg
2 expression within Geuhenal center
-

H( g
-

cell ALL Haitian

'

ALL Abdominis M&m 'm "

-
-

splenomegaly spleen Tcnvowemut

-
: :

Liver involvement
Hepatomegally
-

Morphology
#
*

(T
.

ALL) (B
① PB :

Eine thymus
.

③
Wenders d pale Blue cytoplasm w/
cells
w/ round
kidney shaped

ALL)
.

or

leukemia/
,
=

Chenier
) lymphocytic
-

Balls, Brain , B- one

-
thread

stage Description
-

like or web -
like extensions
,
② small
lymphocyte Infiltrates w/
"
BM cell
( Mature B cells
-

cytoplasm > ( Fried egg

abundant pale
)
- - " -
appear
an
-
Bone Mevww Fibrosis The of
: cause
Dry Tap during Bone Merrow Aspiration

①
* Thymic enlargement
44
Imeaiasn
Svc syndrome
-

nai mass ① I
genetic abnormalities
smalllymphocyhzlymphomejc.LI/S# ③
spleen Beefy
⑨ CD 20T 25T :
:

,
appearance

,
Ho ,
103
-

DH red
pulp infiltration
, spuenomegany
Halima "
I Single lymph node
region or
single extra -

lymphatic organ Is ite

# Indolent , Incurable : COD (cause of Death:) : progressive cytopenia → Infection ,

Bleeding =

* CD : at '5ytE let ,yt8t # Testicular

enlargement * Both of these are the game except to which the extent of Peripheral Blood ( PB)
1. Very specific For hairy cell !
IT 2 More Node of
lymph Diaphragm
- or side
,
regions
, on Sammie

⑤ TRAP stain HD -
is involved i

Monoc⑧I
-

* t ( 9 ,-22) : Bad prognosis Syco Teens * adults

* CNS
symptoms
or
j :
headaches Blurred vision
, , A) anytime PB : > sooo
- a lymphocyte cells 1mL
=
CLL & DM (Bone marrow) involvement 2 or more
lymph Node
regions on Both
#
sides of
Diaphragm
±
spleen

svuoniinyidphooyfe
-

Vomiting
-

B) BB <
1mL Enlarged lymphnodes ( LN )
⑦ PIASMALB-ce.tl/Nloplh8MS-i
anytime :
-
cell's = su t
-

lot , 19+20,25 * Cline 1) Early Diagnosis Incidental Associated

w/ Bone # Multiple I
finding Dissimilated
* CD : CBC involvement
:
-
:
on of or More extra lymphatic organs or tissues

2) pain
* t ( 12,21) : Good prognosis ; children 2- to y lo hates : -

generalized lymphadenopathy *
-

Hepato splenomegaly (50-604) Group plasma of B -

cell
Neoplasms that secrete Monoclonal
A Added to #
# =
stage if none of B- symptoms are
present
]→ Spherocytes ImMunus
Some
developer Autoimmune ( which
Pax's of
( tumor used
-

can

-
or
Fragments Immunoglobulins can be as
) or
Hemolytic anemia or Autoimmune Thrombocytopenia markers

*
Immunoglobulins Blood called M proteins B
Hypo ammoglobal hernia Ig 's Infections in
-
-

B Fever sweats
weight Night
-

symptoms
-

: :
loss ,
-

Mature T / N K cell
*
,

#
µ
o -

Eventually panoytupeuia Bk BM replacement Immunoglobulins 1h Wine called : Bence Jones -

Bodies ( monoclonal Ig light chains xork )

* Types of plasma Neoplasms
fMulhpleµyewma→Igc#*
Been :

it:'m ! En!! !!:L!.IT?oYetIIY5m:epwemu..ysn.uumpurm

Iet stage IA THIRD
*mwpuowgymro smudge cells (in all our

. ②solitary plasmacytoma →
IgG
3) LN ! Diffuse replacement (Malave) lymphocytes ③Walden Shrm Macro
globule uremia
-

→ IgM
- by small round

④ Flow
cytometry CD : St , 19T , zot 23T 43T ④ Heavy Heavy chains ( Fragment of Ig )
TX?
:
,
chain Disease →

Radiation
,

Is I Multi
-

) 1- Amyloidosis light chains ( Atnmyloidosts)

( Mature
drug chemotherapy
→
-
B cells
-

But can 't Become plasma aus -

⑥ Mono lual Gawk

opathy of Undetermined significance (MGUS)
buy agnessired
* All T-cells # Compg CawkofD⑧D)
:

⑦ MUltiplemye.hn#MM)
: IF Panwetopenia
are → Infections
, Bleeding
#*
* Transformation into aggressive careers
i-PYYympuuoy.fr leukemia( PLL)
:
2070 Usually good prognosis
- & S
year survival rate
depends on
stage
65-70410 MSF
-

* Median age

Very Bad
Africans
prognosis DLB CL (5- toy) ,q
- . ,

* plasma (
Bones Axial : vertebrae 8k$11)
cell
Neoplasm involving Multiple > ribs >
90-1 IA IA 504
-

:
stage #A #B
stage
-
.
:
or

FU H L s
,
# GO % B cells * Most common M -

protein ( serum) :
IgG 160%) & IgA sometimes C2o%)

④ Extra Nodal Marginal Zone lymphoma

are -

# TX :
Alkylating agent , Young ( Homo ) BMT (
Bone marrow transplant)
¥ Complications longterm 20 Acute lung
May develop
- :
survivors cancers
Myeloid leukemia
:
or cancer
*
# UM dft Bone destruction or
10 Y T cells & I N Roell
si:
Bone pain : Fractures
-
.
.
② cytopenia :
dit Bone replacement

:MALTLymphumaorMALTom#
AKA ③ Hypercalcemia t
: dit Brune resorption causing lytic
lesions in Bone
* Indolent I
:: :ae:g%fYEmYI¥a,
er :
dit
* small Mature lymphocytes Most Found extra Nodal Mucosa
commonly in areas &
⑤ DH
* f- ( 11:18)
hey 20
Hypercalcemia , Bence jones
19T , snot
i.

CD : proteins,
,
amyloid Deposition
* Causes :
chronic infection : H pylvvyi
. in stomach ( gastritis) ⑥ oregano Meg ally : LN
, spleen , liver
, lungs -_ if late
#
or stage
Auto Immune Dteases : Hashimoto's thyroiditis Sjorgen's , syndrome ,
SIE # X -

Ray :
"

lytic lesions
"
in axial bones (Vertebrae > ribs> skull ) dlt

H chronic Iuhammehm Bone resorption

* .

pylori causes rxns → Dense lymphoid aggregates can evolved

into Marginal zone

lymphoma (mu) # Diagnosis For MM Clonal DM 210% Plus I often following
:
;
,
=

# Other sites : (Hashimoto's 1) Hypercalcemia , renal

insufficiency Anemia BITE lesions
salivary & thyroid glands auto-immune inflammation thyroiditis ) lytic
at lesions , ,

f) Malignant
- - "

Biomarkers :
-

I boy BM clonal plasma

.
cells
-

$1 Focal lytic lesion on MRI

I 100
* seminar Light
-

chain

Usually breathed for

lung period of time But eventually spreads to other
-
Mucosal sites
Lecture 27- blood & lymph infection-1