Splenomegaly By Dr Bashir Ahmed Dar Associate Professor Medicine Chinkipora Sopore Kashmir Email [email protected]

8/14/2019 Splenomegaly By Dr Bashir Ahmed Dar Associate Professor Medicine Chinkipora Sopore Kashmir Email [email protected]

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SPLENOMEGALY

By Dr Bashir Ahmed DarBy Dr Bashir Ahmed Dar

Associate Professor MedicineAssociate Professor Medicine

Chinkipora Sopore KashmirChinkipora Sopore Kashmir

Email [email protected] [email protected]


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Slight enlargement just palpable (less

than 5 cm) Infections acute,subacute and chronicInfections acute,subacute and chronic

SLESLE

Rheumatoid arthritisRheumatoid arthritis

AmyloidosisAmyloidosis


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Moderate enlargement (to

umbilicus) LymphomasLymphomas

LeukaemiasLeukaemias

Congestive splenomegalyCongestive splenomegaly Haemolytic anaemiasHaemolytic anaemias

Polycythaemia VeraPolycythaemia Vera

ITPITP Myelodysplastic disordersMyelodysplastic disorders


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Marked enlargement (more than

8 cm or below umbilicus) MyelofibrosisMyelofibrosis

Hairy cell leukaemiaHairy cell leukaemia

Tropical splenomegalyTropical splenomegaly Kala azarKala azar

Thalassaemia majorThalassaemia major

Gauchers diseaseGauchers disease Feltys syndromeFeltys syndrome


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Infective causes of splenomegaly

Acute causesAcute causes

Infectious mononucleosisInfectious mononucleosis

TyphoidTyphoid BrucellosisBrucellosis

Infective hepatitisInfective hepatitis

ToxoplasmosisToxoplasmosis TyphusTyphus

SepticaemiaSepticaemia


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Infective causes of splenomegaly

Subacute and chronic causesSubacute and chronic causes

Bacterial endocarditisBacterial endocarditis

TuberculosisTuberculosis

BrucellosisBrucellosis SyphilisSyphilis

HistoplasmosisHistoplasmosis

MalariaMalaria

Kala azarKala azar

HydatidHydatid

TrypanosomiasisTrypanosomiasis


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Massive splenomegaly


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Rheumatoid arthritis (Feltys

syndrome)

Comprises ofComprises of

Arthritis,Splenomegaly,LeucopeniaArthritis,Splenomegaly,Leucopenia


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Features of Feltys syndrome

Arthritis,splenomegaly,leucopeniaArthritis,splenomegaly,leucopenia

Extra-Articular ManifestationsExtra-Articular Manifestations

rheumatoid nodules (76%)rheumatoid nodules (76%)

weight loss (68%)weight loss (68%) Sjogren's Syndrome (56%)Sjogren's Syndrome (56%)

lymphadenopathy (34%)lymphadenopathy (34%)

leg ulcers (25%)leg ulcers (25%)

pleuritis (19%)pleuritis (19%)

skin pigmentation (17%)skin pigmentation (17%) neuropathy (peripheral) -17%neuropathy (peripheral) -17%

episcleritis (8%)episcleritis (8%)

others: pericarditisothers: pericarditis


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Investigations Felty's syndrome

high Rf titre in 98%high Rf titre in 98%

ANA in 67%ANA in 67%

elevated ESR, immunoglobulins, circulatingelevated ESR, immunoglobulins, circulatingimmune complexesimmune complexes

positive LE cell test in 33%positive LE cell test in 33%

decreased complement levelsdecreased complement levels elevated transaminases and alkalineelevated transaminases and alkaline

phosphatase in 25-50%phosphatase in 25-50%


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Tropical Splenomegaly

In tropical areas massive splenomegalyIn tropical areas massive splenomegaly

often seenoften seen

Areas like Uganda,Nigeria,new guinea andAreas like Uganda,Nigeria,new guinea and

other parts of Africaother parts of Africa

The evidence suggests a relationshipThe evidence suggests a relationship

between malaria and tropical splenomegalybetween malaria and tropical splenomegaly Rarely occurs in malarial free areasRarely occurs in malarial free areas


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Tropical Splenomegaly

Malarial parasite are not routinely seen in bloodMalarial parasite are not routinely seen in bloodfilms of ptsfilms of pts

The disorder usually presents in young adult lifeThe disorder usually presents in young adult lifebut may occur in childrenbut may occur in children

The diagnosis is usually made by exclusion ofThe diagnosis is usually made by exclusion ofother causesother causes

There may also be 10 fold increase polyclonal igMThere may also be 10 fold increase polyclonal igMconcentration in serum of which small portionconcentration in serum of which small portionrepresents malarial antibodies liver may also showrepresents malarial antibodies liver may also showlymphocytic infiltrationlymphocytic infiltration


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Kala azar (leishmaniasis)

Visceral leishmaniasisVisceral leishmaniasis

Cutaneous leishmaniasisCutaneous leishmaniasis

Mucocutaneous leishmaniasis (espundia)Mucocutaneous leishmaniasis (espundia)

Diffuse Cutaneous leishmaniasisDiffuse Cutaneous leishmaniasis


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kala azar, black fever, sandflydisease, Dum-Dum fever and

espundia.

SYNONYMS


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in the familyTrypanosomatidae

In the genus Leishmania


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EstimatesAll over world except

Not found in South-east Asia

350 million people at risk12 million people infected / year

There are 59,000 deaths / year


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Incubation 1 week to monthsIncubation 1 week to months

Having (many reservoirs)Having (many reservoirs)

No direct person to person transmissionNo direct person to person transmission Spontaneous healing can happen (cutaneousSpontaneous healing can happen (cutaneous

form) in months to yearsform) in months to years

No vaccineNo vaccine

Some Facts


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LEISHMANIASIS or KALA-AZAR

It is the result of the infection with oneIt is the result of the infection with oneof the species of protozoa (leishmania).of the species of protozoa (leishmania).

Conveyed by:Conveyed by:

Sandflies (Phlebotomus).Sandflies (Phlebotomus).

Visceral LeishmaniasisVisceral Leishmaniasis: L. donovani: L. donovani

MucocutaneousMucocutaneous : L. Braziliensis: L. Braziliensis


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L i h i


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Have specific reservoirs

Leishmania

Parasites


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Rodents

Sloths


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VectorsPhlebotomine Sand Flies

20 t 40 d


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20 to 40 days

30to70eggs

hatch

1to2weeks

4 instars

diapauses in 4th instar

pupald

evelop

ment

5-10

day

s

adults crepuscular

and nocturnal


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Opossum

Armadillo


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Visceral LeishmaniasisVisceral Leishmaniasis::

L. donovaniL. donovaniMucocutaneousMucocutaneous

L. BraziliensisL. Braziliensis


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Cutaneous : L. tropica majorL. tropica minor

New World : L. BrazilienL. Mexicana

Oldworld


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PATHOLOGY

L. donovani parasitizes theL. donovani parasitizes the reticu. endoth.reticu. endoth.cellscells

Great proliferation of macrophageGreat proliferation of macrophage

Cells result:Cells result: Liver spleenLiver spleen enlarg.enlarg.

The red bone marrow extendThe red bone marrow extend..


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Leishmania: an obligate intracellular

protozoan parasite (2-6 m in diameter)

parasi

tophor

ous

vacuol

esof

macro

phages


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Promastigotes in Sand Fly gut

and in Culture Media

(about1

5-30

m

by2

-3m

),


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Amastigote in macrophage

TheThe

amostigotes ofamostigotes of

differentdifferent

species arespecies arevery similar onvery similar on

lightlight

microscopy.microscopy.

CLINICAL PICTURE


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CLINICAL PICTURE

early stages is not easy for diagnose.early stages is not easy for diagnose.

There is no constantThere is no constant physical signs.physical signs.

Changes in the blood pictureChanges in the blood pictureparticularlyparticularly Leucopenia.Leucopenia.

Outstanding physical sign is theOutstanding physical sign is theenlargement of the spleen 3 cm. aenlargement of the spleen 3 cm. a month.month.

LiLiver : enlarged spleen + liver are: enlarged spleen + liver are


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LiverLiver : enlarged spleen + liver are: enlarged spleen + liver are

neither tender nor painful.neither tender nor painful.

SometimesSometimes: Jaundice = prognost.: Jaundice = prognost.

SignificanceSignificance

EnlargedEnlarged : Lymph node, could be: Lymph node, could be

but its not a feature of thebut its not a feature of the

disease.disease.

WastingWasting : Emaciated pat with a: Emaciated pat with a

protuberantprotuberant


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Abdomen ( liver + spleenAbdomen ( liver + spleenenlarged)enlarged)

FeverFever : Without subjective symptoms: Without subjective symptomsof fever no delirium.of fever no delirium.

SometimesSometimes: there is no fever: there is no fever

SkinSkin : dry, rough. The natural: dry, rough. The naturalpigmentation of the skin overpigmentation of the skin overthe bone and around thethe bone and around the

mouth is deepened. (Kalamouth is deepened. (Kala

azar??)azar??)


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Clinical Forms of Leishmaniasis

Cutaneous

Mucocutaneous

DiffuseCutaneous

Visceral


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Cutaneous form


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Wet lesion by L.major

L. majoroccurs most commonlyin rural areas, causing moist,

ulcerative lesions which may beextensive and sometimes involvethe epithelium of lips and nose.

These are thecommonest types of

lesion caused by L.major.

Prominent rolled edgeof the lesions is the bestarea to demonstrate theparasites


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Lymphatic spread ofL.major

The ink marks indicate a lineof subcutaneous nodulesalong the lymphatic, passingproximally from the lesion on

the lower part of this mansarm.

The nodules usually resolvewithout complications whenthe primary lesin heals with

or without specific therapy.


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Clinical Forms

of

Leishmaniasis


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Simple dry lesion by L.tropica

dry, usually self-healing lesions,

Generally single

Urban area inNorth Africa andthe Middle East tothe former USSR,Afghanistan,western states ofIndia

The lesions

frequently containvery largenumbers ofparasites.


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Leishmaniasis recidivans

Infection with L. tropica maybecome very chronic, with ahyperallergic reaction leading tolupus-like lesions such as seen in

this child. Amastigotes may be very difficult to

find in the lesions.


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Mucocutaneous lesion by L.aethiopica

In addition to simplecutaneous lesionsdue to infection withL. aethiopica, otherforms are seen inthe Ethiopian

highlands whererock hyraxes are thereservoirs. It has notyet beenascertained whetherthe mucocutaneous

condition seen hereis due to this oranother species ofLeishmania.


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Chicleros ulcer by L.mexicana

Forest workersForest workers

collecting gum fromcollecting gum from

wild chicle treeswild chicle trees

commonly sleepcommonly sleep

near the forest floornear the forest floorand are bitten onand are bitten on

exposed parts of theexposed parts of the

head by vectors.head by vectors.

Ulcers leading toUlcers leading to

erosion of theerosion of theauricular cartilage.auricular cartilage.


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Lymphatic spread of

L. mexicana

As noted for L. major,lymphatic spread mayalso occur with NewWorld species.

This patient wasinfected with L.guyanensis the agentof Pian bois. In suchinfections the

lymphatic nodules mayulcerate.


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Pharyngeal involvement

Ulceration often extends to the pharynx and soft palate,and the first symptoms may be related to tissue destructionin this area.

This man had the scar of a large ulcer which had apparentlyhealed on his leg some 30 years before.


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PKDLPost Kalazar Dermal Leishmaniasis


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Visceral form


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Clinical picture of kala-azar in Kenya

Increasingenlargement ofthe spleen andliver is acharacteristicfeature while, indark-complexionedsubjects,deepening skinpigmentation is

seen-hence thesynonym kala-azar, the blacksickness.

A generalized lymphadenopathy is common in Africankala-azar; the parasite in this area is considered to be inthe L. donovani complex.


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Diagnosis

Demonstration of Parasite from aspirateDemonstration of Parasite from aspirate

- lymph node- lymph node

; inguinal LN, sensitivity 60%; inguinal LN, sensitivity 60%

- bone marrow- bone marrow

; iliac crest, sensitivity 70%; iliac crest, sensitivity 70%- spleen; sensitivity 95~99%- spleen; sensitivity 95~99%

- liverliver

PB smear (HIV infected patient)PB smear (HIV infected patient)

SerologySerology- a- avoid the necessity for the more invasive procedurevoid the necessity for the more invasive procedure- direct agglutination test- direct agglutination test

PCRPCR


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Iliac crest aspiration of bone marrow

The most directmeans ofdiagnosis of kala-azar is thedetection ofamastigotes inbone-marrow,spleen or blood;the organisms arerecognized indried smears of

material stainedwith aRomanowsky stainby theircharacteristicmorphology.


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L. infantum in macrophage from bone marrow

While typically found in macrophages as shown here,While typically found in macrophages as shown here,isolated extracellular amastigotes from disrupted hostisolated extracellular amastigotes from disrupted host

cells are commonly seen in such preparations.cells are commonly seen in such preparations.


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Amastigotes in macrophage fromskin

The diagnosis isconfirmed bydemonstraingamastigotes insmear made

from thecutaneouslesions.


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Punch biopsy

A piece of tissuemay be removedunder localanesthetic with adisposable skin

punch forhistology, cultureand the directdemonstration ofamastigotes.


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Parasitised macrophage in skinsection

Manyparasitisedmacrophagescan be seen inthis section

from an acutelesion caused byL. major.

DIAGNOSIS


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DIAGNOSIS1.1. Needle aspirationNeedle aspiration

Bone sternum liver, spleenBone sternum liver, spleenHistology cultureHistology culture

L. donovani bodyL. donovani body

2.2. a.a. LeucopeniaLeucopenia:: Neutropenia Neutropenia relative mononucleosis.relative mononucleosis.

b.b. Progressive fall with the red cellProgressive fall with the red cell

countcount

Formalin gel (aldehydeForm

alin gel (aldehyde)

)


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g ( yg ( y ))

2 drops formalin + 2 ml serum2 drops formalin + 2 ml serum

After 20 min, white ringAfter 20 min, white ring

5.5. Complement fixation and fluorescentComplement fixation and fluorescent

False positive trypanosomal infectionFalse positive trypanosomal infection

The complement fixationThe complement fixation early positive early positive

negative after cure. Sometimes + or lung. Othernegative after cure. Sometimes + or lung. Other

diseases.diseases.


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6.6. Fluorescent antibodyFluorescent antibody

IV + V:IV + V: In trypanosomal infectionIn trypanosomal infection

Skin test (Montenegro)Skin test(Montenegro)

Delayed hypersensitivity reactionDelayed hypersensitivity reaction

0.2 ml. suspension0.2 ml. suspension


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TREATMENT AntimonialAntimonial

i.i. Urea, stibamine, pentavalen + antmonyiaUrea, stibamine, pentavalen + antmonyia

I.V. daily or every 2 daysI.V. daily or every 2 days

6 10 dose6 10 dose

First 100 mg then 200 then 250First 100 mg then 200 then 250

Total dose 2 5 g. adultTotal dose 2 5 g. adult

Side EffectSide Effect:: Nausea, vomiting, joint pain,Nausea, vomiting, joint pain,

Abdominal pain, diarrheaAbdominal pain, diarrhea

C t i di tiContraindication: Li d kidLiver and kidney


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ContraindicationContraindication:: Liver and kidneyLiver and kidney

failurefailure

ii.ii. Sodium stibogluconate (PentostamSodium stibogluconate (Pentostam)) I.M. 600 mg total daily for 6-10 daysI.M. 600 mg total daily for 6-10 days

Repeated after 14 days; if neededRepeated after 14 days; if needed

Side effectSide effect::Anaphylactic shockAnaphylactic shock

7.7. Diamidiem Diamidiem

Pentamidine isothionatePentamidine isothionate

Dose 3 -4 mg / kg / BW total 300 mgDose 3 -4 mg / kg / BW total 300 mg

Side effectSide effect:: HypoglycemiaHypoglycemia


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Treatment

Sodium stibogluconateSodium stibogluconate

Pentavalent antimony (SbPentavalent antimony (Sb+5+5))


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demonstration of amastigotes(L. donovani bodies)demonstration of amastigotes(L. donovani bodies)

intracellular form is usually 2-4 micron consists ofintracellular form is usually 2-4 micron consists ofnucleus and is rod like with a homogeneous massnucleus and is rod like with a homogeneous mass

of cytoplasm,while the extracelluar or culture formof cytoplasm,while the extracelluar or culture form

is14-20 microns in length 1.5 to 3.5 breadthis14-20 microns in length 1.5 to 3.5 breadth

L. donovani bodyL. donovani body


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Myelofibrosis or myelosclerosis

Fibrosis and collagen formation in marrowFibrosis and collagen formation in marrow

Primary developing in polycythemia veraPrimary developing in polycythemia vera

Secondary in TB,secondarySecondary in TB,secondarycarcinoma,hodgkins disease,leukaemia,andcarcinoma,hodgkins disease,leukaemia,and

variety of other conditions.variety of other conditions.

Myeloid metaplasia ,spleenomegalyMyeloid metaplasia ,spleenomegalyhepatomaegaly etc etchepatomaegaly etc etc


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GAUCHERS DISEASE


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History

Discovered by Philippe Gaucher, a medicalDiscovered by Philippe Gaucher, a medical

student in Paris, in 1882.student in Paris, in 1882.

He was studying a woman with an enlargedHe was studying a woman with an enlarged

spleenspleen


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DefinitionDefinition

Gaucher's (go-SHAYZ) disease occursGaucher's (go-SHAYZ) disease occurs

when certain harmful fatty substanceswhen certain harmful fatty substancesbuild to excessive levels in your liver,build to excessive levels in your liver,

spleen, lungs, bone marrow and, lessspleen, lungs, bone marrow and, less

commonly, your brain. Thiscommonly, your brain. This

accumulation of fatty material in tissuesaccumulation of fatty material in tissuesinterferes with the normal functioning ofinterferes with the normal functioning of

organs, and may cause organorgans, and may cause organ

enlargement and bone pain.enlargement and bone pain.


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Gaucher's disease results from anGaucher's disease results from an

enzyme deficiency, and sometimes theenzyme deficiency, and sometimes the

term "glucocerebrosidase deficiency" isterm "glucocerebrosidase deficiency" is

used to describe this condition.used to describe this condition.

Gaucher's disease is most common inGaucher's disease is most common in

Eastern and Central EuropeanEastern and Central European

(Ashkenazi) Jews. It can occur at any(Ashkenazi) Jews. It can occur at anyage in life, and affects males andage in life, and affects males and

females approximately equally.females approximately equally.


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What Is It?

Gauchers DiseaseGauchers Disease- rare inherited metabolic- rare inherited metabolicdisease or disorder ; due deficiency or lack of andisease or disorder ; due deficiency or lack of anenzyme calledenzyme called GlucocereborsidaseGlucocereborsidase

Results in an accumulation ofResults in an accumulation ofglucocerebrosideglucocerebrosidewithin cells in various body tissues ( spleen, liver,within cells in various body tissues ( spleen, liver,

bone marrow, and skeleton)bone marrow, and skeleton)

Severity of the disease can vary and thus diseaseSeverity of the disease can vary and thus diseasedivided into following typesdivided into following types


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TYPE 1

Most common and can begin at any ageMost common and can begin at any age

1 in 10,0001 in 10,000 Patients are bruised very easilyPatients are bruised very easily

Fatigued due to anemiaFatigued due to anemia

Lung and kidney injuriesLung and kidney injuries

Weakening of the skeletonWeakening of the skeleton


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TYPE 1 (continued)

Victims have a shortened life-spanVictims have a shortened life-span

Usually die from clots and pneumoniaUsually die from clots and pneumonia


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TYPE 2

Rarest of all the typesRarest of all the types

Appears during the first few months of lifeAppears during the first few months of lifein a babyin a baby

Great brain damage mental retardationGreat brain damage mental retardation


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TYPE 2 (continued)

Loss of muscle controlLoss of muscle control

Enlargement of liver and spleenEnlargement of liver and spleen

Nervous system fails to function wellNervous system fails to function well

Patients usually die by age 2Patients usually die by age 2


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TYPE 3

Begins in childhoodBegins in childhood

Liver and spleen enlargementLiver and spleen enlargement

Causes bone marrow and damages theCauses bone marrow and damages thecentral nervous systemcentral nervous system

Mental retardation is quite commonMental retardation is quite common

Usually die around the ages 15-30Usually die around the ages 15-30


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Symptoms (continued)

Muscle weaknessMuscle weakness

Poor coordinationPoor coordination

SeizuresSeizures


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How Do You Get It?

Acquired if both parents of the disease areAcquired if both parents of the disease are

carrierscarriers

A victim receives an abnormal form of theA victim receives an abnormal form of thegenes- agenes- a Gaucher GeneGaucher Gene from both parentsfrom both parents

CarrierCarrier- person with one normal gene and- person with one normal gene and

one Gaucher Gene ( a carrier will not showone Gaucher Gene ( a carrier will not showsigns of the disease)signs of the disease)


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If 2 Carriers Have Children

There is a one in four chance of aThere is a one in four chance of a

child inheriting the diseasechild inheriting the disease


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Who Has It?

10,000 to 20,000 Americans10,000 to 20,000 Americans

High rate found in the Ahkenazi JewishHigh rate found in the Ahkenazi Jewish

population-1 out of 500-1000 birthspopulation-1 out of 500-1000 births Types 2 & 3 are found in 1 out of 50,000-Types 2 & 3 are found in 1 out of 50,000-

100,000 births100,000 births

Type 3-mainly found in people of northernType 3-mainly found in people of northernSwedish AncestrySwedish Ancestry


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Prevention

No real preventionNo real prevention

Genetic Counseling is recommended forGenetic Counseling is recommended for

parents with a family history of the diseaseparents with a family history of the disease


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Treatments

NoNo CURECURE

Enzyme replacement therapy-injections ofEnzyme replacement therapy-injections of

the enzymethe enzyme Result: decrease liver and spleen sizeResult: decrease liver and spleen size

reduce skeletal abnormalitiesreduce skeletal abnormalities

restores normal growth &restores normal growth &developmentdevelopment

restores well being of the patientrestores well being of the patient


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Hairy cell leukaemia

Hairy cell leukaemia is an uncommonHairy cell leukaemia is an uncommon

disorder of middle and late adult life.disorder of middle and late adult life.

Characterized by the presence in boneCharacterized by the presence in bonemarrow,spleen,and peripheral blood ofmarrow,spleen,and peripheral blood of

abnormal mononuclear cells with hairyabnormal mononuclear cells with hairy

cytoplasmic projections and best detectedcytoplasmic projections and best detectedby phase contrast microscopy.by phase contrast microscopy.


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Males affected more than femalesMales affected more than females

Marked by splenomegaly , howeverMarked by splenomegaly , however

lymphadenopathy is unusuallymphadenopathy is unusual Splenectomy is usually regarded asSplenectomy is usually regarded as

treatment of choicetreatment of choice

Long term use of injections of alphaLong term use of injections of alphainterferon cause regression of hairy cellsinterferon cause regression of hairy cells


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Hairy cell leukemia is actually a mature BHairy cell leukemia is actually a mature B

cell neoplasm. It is usually classified as acell neoplasm. It is usually classified as a

sub-type of chronic lymphoid leukemia forsub-type of chronic lymphoid leukemia forconvenience. It is uncommon, representingconvenience. It is uncommon, representing

about 2% of all leukemias, or less than aabout 2% of all leukemias, or less than a

total of 2000 new cases diagnosed each yeartotal of 2000 new cases diagnosed each year

in the North America and Western Europein the North America and Western Europe

combined.combined.


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Originally known as histiocytic leukemia,Originally known as histiocytic leukemia,

malignant reticulosis, or lymphoidmalignant reticulosis, or lymphoid

myelofibrosis in publications dating back tomyelofibrosis in publications dating back tothe 1920s, this disease was formally namedthe 1920s, this disease was formally named

leukemic reticuloendotheliosisleukemic reticuloendotheliosis


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SymptomsSymptoms

In hairy cell leukemia, the broken "hairy cells"In hairy cell leukemia, the broken "hairy cells"build up in the bone marrow, which means that thebuild up in the bone marrow, which means that thebone marrow has difficulty producing enoughbone marrow has difficulty producing enoughnormal cells: white blood cells to fight infections,normal cells: white blood cells to fight infections,red blood cells to carry oxygen, and platelets tored blood cells to carry oxygen, and platelets to

stop bleeding. Consequently, patients usuallystop bleeding. Consequently, patients usuallypresent with infection, anemia-related fatigue,present with infection, anemia-related fatigue,and/or easy bleeding.and/or easy bleeding.

H t l i Di d C i


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Hematologic Disorders Causing

Massive Splenomegaly Polycythemia VeraPolycythemia Vera Multiple MyelomaMultiple Myeloma

POEMS SyndromePOEMS Syndrome

Waldenstrm's MacroglobulinemiaWaldenstrm's Macroglobulinemia

chronic lymphocytic leukemiachronic lymphocytic leukemia

non-Hodgkin lymphomanon-Hodgkin lymphoma

chronic myelocytic leukemiachronic myelocytic leukemia malaria (hyper-reactive malarialmalaria (hyper-reactive malarial

splenomegaly)splenomegaly)

Documents

Splenomegaly By Dr Bashir Ahmed Dar Associate Professor Medicine Chinkipora Sopore Kashmir Email [email protected]