case-anemia hipoplasi.doc

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HYPOPLASTIC ANEMIA

Definition

Hypoplastic anemia is condition with decrease of erytrocyte, leucocyte and

trombocyte that caused by depression of bone marrow.

Etiology

a. Genetic factor

b. Drug and chemis material

It caused by hypersensitivitas or over dosis of drug : Chloramfenicol,

benzene, busulvan, cyclophosfamid.

c. Infection : hepatitis virus non A-nonB

d. Radiation

e. Immunologys

f. Anemia aplastic on other diseases

g. Idiopatic

Pathogenesis

There is no single pathogenetic mechanism in hypoplastic anemia. Stem cell

differentiated to erytropoetic, granulopoetic, trombopoetic, limpopoetic. The other

stem cell crack by active to new stem cell. Half of stem cell on dormant that can

differentiated to variety of system of hemopoetic.

Causes of Heart Failure

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It is importan not only to identify the underlying cause of heart disease, but

also the presipitating causes of it. Clinical manifestation of heart failure appear of

the first time in course of some acute disturbance that place additional load on

myocardium that chronically is excessive burdened. The presipitating caused are:

1. Infection

2. Anemia

3. Thyrotoxicosis and pregnancy

4. Arythmias

5. Rheumatic and other forms of myocarditis

6. Infective endocarditis

7. Physical,dietary, fluid, environmental,and emotional excesses

8. Sistemic hypertension

9. Myocardial infarction

10. Pulmonary embolism

Pathophysiology

Early in the various heart diseases, the conpensatory mechanism are adequate

to maintain a normal cardiac output and normal intracardiac pressure at rest and after

exercise. Hypertrophy may be recognized by physical examination

,electrocardiography, or echocardiography, and when ventricular dilatation occurs,

cardiac enlargement can be seen on the plain chest film. Compensated heart disease

becomes decompensated as ventricular volume and filling pressures of the

respective ventricle increases. This is known as diastolic dysfunction and can be the

primary cause of increased left ventricular filling pressure and pulmonary congestive

heart failure. Diastolic dysfunction is particularly common in elderly patients with

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hypertention and in patients with myocardial ischaemia due to the coronary heart

disease.

As the filling pressure increases, hydrostatic pressure exceeds colloid osmotic

pressure at the capillary level, and pulmonary venous congestion occurs. When the

limphatics can no longer adequately remove the excess fluid, interstitial and then

alveolar edema of the lung occurs, resulting in symptoms of left ventricular failure

with dyspnea, exertional cough, orthopnea, paroxysmal nocturnal dyspnea, and

pulmonary edema,. Raised venous pressure, hepatomegaly, dependent edema, and

ascites occur when failure involves the right ventricle.

Clinical Findings

Treatment

1. Transfusi

2. Kotikosteroid

3. Transplantation of bone marrow

4. Imunosupresive

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CASE REPORT

A male patient aged 36 years old was admitted to Internal Medicine

Department of RSUP Dr. M. Djamil Padang on December 3th, 2003 with:

Chief complain: Bleeding of gynggiva since 5 days before admitted in hospital

Present illness history:

Bleeding of gynggiva since 5 days before admitted in hospital, 3 glasses a

day

Bleeding of gynggiva was not causing by trauma

Bleeding gynggiva was often since 9 months ago, not too much

There is no bleeding on the other of body.

Fatique ,dizzy since 9 months ago, the patien cannot work normally.

Pale since 9 months ago.

Fever since 0ne month, not continue, not shivering, not sweating, not high

Appetite decreased since he got ill.

Nausea (-), vomite (-)

Mixturation and defecation were normal.

Previous illness history:

The patient never get typhus

The patient never get hepatitis

The patient never get radiation

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The patient never get drugs in long time

Familial Illness History:

His nephew get bleeding diseases and BMP positif (pastway)

Occupation and Socials Economics History:

- Farmer

Physical Examination

Vital Sign:

- General appearance : Moderetely ill

- level of consciousness : Composmentis cooperative

- blood pressure : 120/60 mmHg

- pulse rate : 99 x/menit

- respiratory : 28x/menit

- temperature : 38 0C

- cyanosis : (-)

- general edema : (-)

Skin:

- colour : brown,pale

- palpable temperature: febris

- icteric : (-)

- edema : (-)

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Lymph node : no enlargement

Head:

- Eye: conjungtiva was anemic, sclera was not ikteric

- Mouth : gynggiva was bleeding

Neck:

- Pharinx: no disturbance

- JVP : 5 -2 cmH2O

- No enlargement of lymph nodes and thyroid gland

- Tonsil : no enlargement

Chest :Normochest

Lungs:

Inspection :Symetric on static and dynamic. Respiratory tipe :

Thoracoabdominal

Palpation : Fremitus was the same on the right and left side

Percussion : Sonor both of lung

Auscultation : Vesikuler N, wheezing -, rales -

Heart:

Inspection : ictus was not visible

Palpation : ictus was palpable one finger medial of linea midclavicularis

sinistra 5 Th ICS

Percussion : Left: one fingers medial of LMCS 5 Th ICS

Right: Linea sternalis dextra

Upper: 2nd

ICS

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Auscultation : Pure, Reguller, M1>M2, A2>P2, murmur -, gallop -

Abdomen:

Inspection : no enlargement

Palpation : liver and spleen not palpable

Ballotement (-)

Percussion : timpany, shifting dullness (-)

Auscultation : peristaltic sound was normal

Back:

Inspection: simetric.

Palpation : pressure pain of Murphy angle (-)

Percution : Knock pressure of CVA (-)

Extrimities:

- physiological reflex : +/+ normal

- patologycal reflex : -/- normal

- swollen legs : (-)

- tremor : (-)

- sianotic fingers : (-)

- edema : (-)

Laboratory Finding (LF)

Blood : Hb : 2,7 gr%

Leucocyte : 1200/mm3

Trombosyte : 16.000/mm

Working Diagnosis:

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- Anemia Normocytic Normocrom ec Hypoplastic ec Idiopatic

Differencial Diagnosis

Anemia Normocytic normocrom ec Hypoplasia ec insecticide

Therapy:

- Bedrest, smooth food, high calories high protein

-IVFD NaCl 0,9 %

- Transfusi Trombosite

- Transfusi PRC

- Transamin 3x1

- Vit K 3x1

-Vit C 3x1

Planning examination:

- BMP

- Faal Hemostatic

FOLLOW UP

December 4rd 2003

A/: -fever (-)

- fatique (+)

- appetite decreased

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- Bleeding gynggiva (-)

PE/:- GA Conc BP PR RR T

Moderately ill Cmc 100/60 102x/i 24x/i 36,80 C

Eye : Conjungtiva was anemic

Laboratory Finding :

Hb : 2,5 mg% MCH : 32,4

Leukocite : 900 /mm MCV : 92,3

Ht : 7 % MCHC : 35,2

Trombocite : 69.000 /mm Bood peripheral appearance:

Eritrocite :0,8 juta /mm Pansitopenia

DC :0/0/1/56/36/7

Bilirubin Total : 7,2 mg % Albumin : 3,4 g%

Globulin : 3,8 g% SGOT :22 U/I

SGPT : 23 U/I Ureum : 30 mg%

Creatinin : 0,9 mg %

Urine :

Protein - Reduction

Urobilin + Bilirubin - Lecosite : 2-3

Feses :

Color : Yellow Consistensi :mole

Working Diagnosis:

Anemia Normocitic Normocrom ec Hypoplasia ec Idiopatic

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Therapy : continued

December 5 th 2003A/: -fever (-)

A/ - fatique (+)



-fever (-)

PE/:- GA LC BP PR RR T

Moderatelly ill CMC 110/60 100x/I 24x/I 37 0c

Conjungtiva : anemic

WD : same as before

Th/: continued

December 6rd 2003

A/ - fatique (+)



-fever (-)


Moderatelly ill CMC 120/70 100x/i 26x/i 360

Eye : Conjungtiva was anemic

Laboratory finding :

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Hb : 2,6 g% MCh :31,5

Leukosite : 800/mm MCV :92,3

Eritrosite : 0,82 million MCHC : 39,1

Ht : 8% Trombosite : 69.000/mm

Reticulosite : 3 % Blood peripheral appearance : normositic

normocrom,anisositosis

Wd : same as before

Th/: continued + Transfusi PRC 2 unit

December 8rd 2003

A/ - fatique (+)

- appetite normal

- bleeding gyngiva (-)

-fever (-)


Moderatelly ill CMC 110/70 90x/i 24x/i 36,10

Eye : Conjungtiva : anemic was decreased

Hb : post transfusi december 7 rd 2003 was 5,1 %

Wd : same as before

Therapy : continued + transfusi Trombosite 10 unit

December 9rd 2003

A/ - fatique (+)

- appetite normal

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-fever (-)


Moderatelly ill CMC 120/70 82x/i 24x/i 36,0


Laboratory finding :

Hb : 6,7 g% Blood peripheral appearance : normositic normocrom

LED : 135/-

Leukosite : 900/mm

DC : 0/0/4/36/57/3

December 10rd 2003

A/ - fatique (+)

- appetite normal


-fever (-)


Moderatelly ill CMC 120/60 99x/i 25x/i 370


Wd : Anewmia normositic normocrom ec hypoplasia ec idiopatic

Therapy : same as before

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December 11d 2003

A/ - fatique (+)

- fever (-)

- appetite normal



Moderatelly ill CMC 120/7 95/i 22/i 370


Skin : not pale

Wd : Anemia normositic normocrom ec hypoplasia ec idiopatic

Therapy : same as before

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DISCUSSION

From this case, the diagnosis conclude by anamnesis, physical examination

and suggested examination. In anamnesis we fuond bleeding ginggiva since 5 days

before admitted in hospital, fatique since 9 month ago, pale since 9 month ago,

nephew of patient get bleeding diseases too (pastaway), appetite decrease since he

got ill, hardly breath since 9 months ago, dizzy since 9 months ago.

From physical exanination we found conjungtiva was anemic, bleeding

ginggiva, skin was pale.

From laboratory we found eritorsite, leucosite, trombosite

decreased( pansitopenia), Hb decreased, Peripheral blood appearance was normositic

normocrom.

Based on data from ananesis, physical examination, laboratory finding, we

built up diagnose Anemia normosytic normocrom ec hipoplastic ec idiopatic.

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Case presentation

HYPOPLASTIC ANEMIA

Presentator :

RIKA LISISWANTI

99120006

Opponent :

BOI SAIDI

96120104

Moderator :

Prof. Dr. H. NUZIRWAN ACANG, Sp.PD-KH

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DEPARTEMENT OF INTERNAL MEDICINE

MEDICAL FACULTY OF ANDALAS UNIVERSITY

PADANG

2003

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case-anemia hipoplasi.doc

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