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LOGO

LOGO Gangguan Eritrosit: Anemia dr. Bastiana SpPK
LOGO Gangguan Eritrosit: Anemia dr. Bastiana SpPK

Gangguan Eritrosit: Anemia

dr. Bastiana SpPK

Gangguan Eritrosit

Gangguan Eritrosit LOGO Anemia Polisitemia www.themegallery.com Company Logo

LOGO

Anemia Polisitemia
Anemia
Polisitemia
Gangguan Eritrosit LOGO Anemia Polisitemia www.themegallery.com Company Logo

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ANEMIA

Definisi Anemia:

ANEMIA Definisi Anemia: LOGO ✓ Sindroma klinis yang disebabkan penurunan massa eritrosit total dalam tubuh. ✓

LOGO

Sindroma klinis yang disebabkan penurunan massa eritrosit total dalam tubuh.

Keadaan dimana massa eritrosit dan atau massa hemoglobin tidak dapat memenuhi fungsinya untuk menyediakan oksigen bagi jaringan tubuh

Penurunan di bawah normal kadar Hb, hitung eritrosit, dan hematokrit

tubuh ✓ Penurunan di bawah normal kadar Hb, hitung eritrosit, dan hematokrit www.themegallery.com Company Logo

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ANEMIA

Penurunan Hb dan Hct : < batas bawah 95% interval referens dari kelompok usia, jenis
Penurunan Hb dan Hct :
< batas bawah 95% interval referens
dari kelompok usia, jenis kelamin
dan lokasi geografis (ketinggian)
Hb<12-14 g/dl ; (Hct <36-41%),
Hb<7g/dl ! symptom (+)
Akut: hipovolumia (pucat,
ggn penglihatan, syncope, tachycardia) ;
Kronis: tissue hypoxia (fatique, dyspnea,
Headache, angina)
tachycardia) ; Kronis: tissue hypoxia (fatique, dyspnea, Headache, angina) www.themegallery.com LOGO Anemia Company Logo

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tachycardia) ; Kronis: tissue hypoxia (fatique, dyspnea, Headache, angina) www.themegallery.com LOGO Anemia Company Logo

LOGO

Anemia
Anemia

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ANEMIA symptoms / syndrome

ANEMIA → symptoms / syndrome LOGO Hb ↓ PCV ↓ Hypoxia → Otak , Otot RBC

LOGO

Hb ↓ PCV ↓ Hypoxia → Otak , Otot RBC ↓ Kompensasi :
Hb ↓
PCV ↓
Hypoxia
→ Otak , Otot
RBC ↓
Kompensasi :

- heart rate tachycardia flow rate cardiomegaly heart failure - blood flow priority (pallor) - RBC 2,3-DPG content O2 dissoc.curve

shift to the right O2 release to the tissues .

5

2,3-DPG content ↑ → O2 dissoc.curve 
 shift to the right → O2 release to the

Klasifikasi Anemia

Klasifikasi Anemia LOGO Berdasarkan patofisiologi: I. Kegagalan produksi sel darah merah: A. Gangguan sel induk

LOGO

Berdasarkan patofisiologi:

I. Kegagalan produksi sel darah merah:

A. Gangguan sel induk hematopoesis

! Anemia Aplastik

B. Gangguan sintesis DNA

! Anemia Megaloblastik

C. Gangguan sintesis Hemoglobin (Hb)

! Anemia Defisiensi Besi, Thalasemia

D. Gangguan sintesis eritropoetin

! Anemia karena GGK

Defisiensi Besi, Thalasemia D. Gangguan sintesis eritropoetin ! Anemia karena GGK www.themegallery.com Company Logo

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Lanjutan…

anemia

berdasarkan patofisiologi

Lanjutan… anemia berdasarkan patofisiologi LOGO E. Gangguan karena mekanisme lain: ! Anemia karena penyakit kronis, !

LOGO

E. Gangguan karena mekanisme lain:

! Anemia karena penyakit kronis,

! anemia sideroblastik ! Anemia karena infiltrasi sumsum tulang

II. Peningkatan destruksi sel darah merah:

! Anemia Hemolitik

III. Kehilangan darah (Blood Loss) ! Anemia karena perdarahan akut

! Anemia Hemolitik III. Kehilangan darah (Blood Loss) ! Anemia karena perdarahan akut www.themegallery.com Company Logo

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Anemia

Anemia LOGO Anemia berdasarkan morfologi ❖ Anemia sec. morfologi eritrosit, dilihat dari: - ukuran dan warna

LOGO

Anemia berdasarkan morfologi

Anemia sec. morfologi eritrosit, dilihat dari:

- ukuran dan warna di bawah mikroskop atau

- indeks eritrosit (MCV, MCH, dan MCHC)

- Kriteria Ukuran (size): Normositik, Mikrositik, Makrositik

- Kriteria Warna (pucat): Normokromik, Hipokromik

Normositik, Mikrositik, Makrositik - Kriteria Warna (pucat): Normokromik, Hipokromik www.themegallery.com Company Logo

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Cara Mengetahui Ukuran eritrosit:

Cara Mengetahui Ukuran eritrosit : LOGO * membandingkan dengan inti sel limfosit kecil (di bawah mikroskop)

LOGO

* membandingkan dengan inti sel limfosit kecil (di bawah mikroskop) :

ukuran sama = normositik

lebih kecil

lebih besar = makrositik

= mikrositik

* Menghitung MCV (Mean Cell Volume) MCV= PCV/Ery X 10 (fL) (1 fL=10 -12 L= 1µm 3 ) N : dewasa = 80-100 fL , di bawah 1 thn = 76- 86 fL MCV : normositik , mikrositik, makrositik

* Eritrosit dengan variasi ukuran yang abnormal! anisositosis

= 76- 86 fL MCV : normositik , mikrositik, makrositik * Eritrosit dengan variasi ukuran yang

9

Bandingkan ukuran sel eritrosit dengan inti limfosit

Bandingkan ukuran sel eritrosit dengan inti limfosit LOGO 10

LOGO

Bandingkan ukuran sel eritrosit dengan inti limfosit LOGO 10
Bandingkan ukuran sel eritrosit dengan inti limfosit LOGO 10

10

LOGO 11

LOGO

LOGO 11
LOGO 11

11

Perhatikan Warna sel eritrosit :

Perhatikan Warna sel eritrosit : LOGO - Bandingkan diameter central pallor(CP) dengan diameter sel eritrosit tersebut

LOGO

- Bandingkan diameter central pallor(CP) dengan diameter sel eritrosit tersebut .

- Normal, bentuk sel eritrosit adalah seperti cakram bikonkaf (biconcave disk) pada hapusan darah tepi terlihat bulat, Ø 7-8 µ dengan area central pallor di bagian tengah

7-8 µ 
 dengan area central pallor di bagian tengah CP ≤ 1/3 Ø Eri =

CP 1/3 Ø Eri = normokromik

CP>

½ Ø Eri = hipokromik

12

Eritrosit dengan central palor (CP)

Eritrosit dengan central palor (CP) LOGO Bandingkan diameter CP dengan diameter sel eritrosit 13

LOGO

Bandingkan diameter CP dengan diameter sel eritrosit

Eritrosit dengan central palor (CP) LOGO Bandingkan diameter CP dengan diameter sel eritrosit 13
Eritrosit dengan central palor (CP) LOGO Bandingkan diameter CP dengan diameter sel eritrosit 13

13

LOGO - Warna, dapat diketahui juga dari MCH (Mean Cell Hb) MCH= Hb/RBC x 10

LOGO

- Warna, dapat diketahui juga dari MCH (Mean Cell Hb) MCH= Hb/RBC x 10 (pg) Dewasa: MCH=27-32 pg, Anak-anak: MCH=23-31 pg (1pg=10 -12 g=1µµg)

MCH normal

MCH < normal hipokromik

normokromik

- MCHC (Mean Cell Hb Concentration) :

MCHC=Hb/PCV x 100 (g/dL)

Normal: MCHC = 32-36 g/dL

hipokromik → normokromik - MCHC (Mean Cell Hb Concentration) : MCHC=Hb/PCV x 100 (g/dL) Normal: MCHC

14

Klasifikasi Anemia secara morfologi

Klasifikasi Anemia secara morfologi LOGO 1. Anemia Hipokromik-Mikrositik. 2. Anemia Normokromik-Normositik Anemia

LOGO

1. Anemia Hipokromik-Mikrositik.
1. Anemia Hipokromik-Mikrositik.
secara morfologi LOGO 1. Anemia Hipokromik-Mikrositik. 2. Anemia Normokromik-Normositik Anemia Makrositik 3.
2.
2.

Anemia Normokromik-Normositik

Anemia Makrositik 3.
Anemia Makrositik
3.
1. Anemia Hipokromik-Mikrositik. 2. Anemia Normokromik-Normositik Anemia Makrositik 3. www.themegallery.com Company Logo

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Anemia hipokromik- mikrositik

Anemia

normokromik-

 

normositik

1 Contoh: - Anemia defisiensi Fe - Thalasemia - Anemia akibat Penyakit Kronik - Anemia
1
Contoh:
- Anemia
defisiensi Fe
- Thalasemia
- Anemia akibat
Penyakit Kronik
- Anemia
sideroblastik

MCV <80 fl; MCH <27 pg

- Anemia sideroblastik MCV <80 fl; MCH <27 pg www.themegallery.com 2 Contoh: - Anemia pasca perdarahan

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2 Contoh: - Anemia pasca perdarahan akut - Anemia aplastik - Anemia hemolitik - Anemia
2
Contoh:
- Anemia pasca
perdarahan akut
- Anemia aplastik
- Anemia hemolitik
- Anemia akibat
penyakit kronik
- Anemia pada GGK
- Anemia pada
mielofibrosis
- dll

MCV

80 -95 fl

MCH

27-34 pg

mielofibrosis - dll MCV 80 -95 fl MCH 27-34 pg LOGO Anemia makrositik 3 A. Megaloblastik,

LOGO

Anemia makrositik

3 A. Megaloblastik, contoh: - Anemia defisiensi Folat, - Anemia defisiensi vitamin B12 B. Nonmegaloblastik
3
A. Megaloblastik,
contoh:
- Anemia defisiensi
Folat,
- Anemia defisiensi
vitamin B12
B. Nonmegaloblastik
contoh:
- Anemia pd peny.
Hati kronis
- Anemia pd
hipotiroid, dll

MCV > 95 fl

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Hipokromik-Mikrositik

Hipokromik-Mikrositik LOGO 17

LOGO

Hipokromik-Mikrositik LOGO 17
Hipokromik-Mikrositik LOGO 17

17

Normokronik-normositik

Normokronik-normositik LOGO 18

LOGO

Normokronik-normositik LOGO 18
Normokronik-normositik LOGO 18

18

Makrositik

Makrositik LOGO ✓ makrosit-oval 
 (Anemia megaloblastik ditandai oleh makrosit oval ini) 19

LOGO

makrosit-oval (Anemia megaloblastik ditandai oleh makrosit oval ini)

Makrositik LOGO ✓ makrosit-oval 
 (Anemia megaloblastik ditandai oleh makrosit oval ini) 19
Makrositik LOGO ✓ makrosit-oval 
 (Anemia megaloblastik ditandai oleh makrosit oval ini) 19

19

Pendekatan diagnostik Anemia:

Anamnesis:

Pendekatan diagnostik Anemia: ❖ Anamnesis : 
 LOGO onset /bleeding tendency / routine medicinal / occupation

LOGO

onset /bleeding tendency / routine medicinal / occupation / hobby / travel history / family / diet / GI symptoms / menstruation cycle / history of previous pregnancy-delivery / alcohol consumption , etc

Pemeriksaan fisik :

conjunctiva & lips (pallor) / mouth (cheilosis) / tongue (glossitis) / gum / nails (koilonychia) , hair (signa de bandera, alopecia) , jaundice , petechiae , liver & spleen , lymphenodes ,rectal / vaginal toucher , feet (ulcer,arthritis)

, jaundice , petechiae , liver & spleen , lymphenodes ,rectal / vaginal toucher , feet

20

LOGO ❖ Pemeriksaan Laboratorium - CBC (complete blood count ) → to confirm anemia (Hb,

LOGO

Pemeriksaan Laboratorium

- CBC (complete blood count ) to confirm

anemia (Hb, PCV, RBC) & the type of anemia (MCV; MCH; MCHC), RDW

- Reticulocyte count reflects marrow’s responses .

- PBS : to look for the RBCs’ shape and any abnormalities of RBCs besides the other blood cell lines

- Iron status ( Serum Iron ,TIBC, % Transferrin saturation , Iron storage )

- Blood chemistry ( direct/total bilirubin,LDH and stool examination for occult blood test , etc) . PBS: Pheripheral blood smear

( direct/total bilirubin,LDH 
 and stool examination for occult blood test , etc) . PBS: Pheripheral

21

Lanjutan…. Pendekatan Doagnostik…

Lanjutan…. Pendekatan Doagnostik… LOGO - Radiological examinations ( Chest X-ray, 
 USG , MRI ) -

LOGO

- Radiological examinations ( Chest X-ray, USG , MRI )

- Cardiological examinations (EKG,Treadmill, Echocardiography)

Notes ! :

- First confirm Anemia ( Hb , PCV , RBC )

- Classify the anemia (MCV, MCH, MCHC)

- Causes of anemia

22

LOGO 23
LOGO 23
LOGO 23

LOGO

23

LOGO 24
LOGO 24

LOGO

LOGO 24

24

Anemia Hipokromik-Mikrositik

Anemia Hipokromik-Mikrositik LOGO - Setiap kondisi yang menimbulkan gangguan sintesis Hb ! gambaran hipokromik

LOGO

- Setiap kondisi yang menimbulkan gangguan sintesis Hb ! gambaran hipokromik mikrositik

- Anemia Defisiensi Besi ! penyebab tersering dari anemia Hipokromik-Mikrositik

- Perhatikan penyebab lain (DD=diff diagnosis) sebelum mendiagnosis Anemia def. besi, spt:

- anemia akibat penyakit kronis

- Thalasemia

- anemia Sideroblastik, dll

sebelum mendiagnosis Anemia def. besi, spt: - anemia akibat penyakit kronis - Thalasemia - anemia Sideroblastik,

25

LOGO 26
LOGO 26

LOGO

LOGO 26

26

ANEMIA DEFISIENSI BESI

Definisi:

ANEMIA DEFISIENSI BESI ❖ Definisi: LOGO Anemia yang timbul akibat kosongnya cadangan besi tubuh ! besi

LOGO

Anemia yang timbul akibat kosongnya cadangan besi

tubuh! besi utk eritropoeisis

Anemia def. Fe, ditandai dgn:

! besi utk eritropoeisis ❖ Anemia def. Fe, ditandai dgn: ! pembentukan Hb - anemia hipokromik

! pembentukan Hb

- anemia hipokromik mikrositik

- besi serum

- TIBC (Total Iron Binding Capacity)

- Saturasi transferin

- Feritin serum

Iron Binding Capacity) - Saturasi transferin - Feritin serum - Pengecatan Besi sumsum tulang negatif -
Iron Binding Capacity) - Saturasi transferin - Feritin serum - Pengecatan Besi sumsum tulang negatif -
Iron Binding Capacity) - Saturasi transferin - Feritin serum - Pengecatan Besi sumsum tulang negatif -
Iron Binding Capacity) - Saturasi transferin - Feritin serum - Pengecatan Besi sumsum tulang negatif -
Iron Binding Capacity) - Saturasi transferin - Feritin serum - Pengecatan Besi sumsum tulang negatif -

- Pengecatan Besi sumsum tulang negatif

- Respon terhadap pengobatan dengan preparat Fe

- Pengecatan Besi sumsum tulang negatif - Respon terhadap pengobatan dengan preparat Fe www.themegallery.com Company Logo

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LOGO www.themegallery.com Company Logo

LOGO

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Faktor Penyebab (Etiologi)

Faktor Penyebab (Etiologi) LOGO I. Keseimbangan negatif Fe (Negative Iron balance): 
 - Asupan Fe ↓

LOGO

I. Keseimbangan negatif Fe (Negative Iron balance):- Asupan Fe

(inadequate diet , impaired absorption)

- Fe loss

(GI bleeding, excessive menstrual flow, bleeding diathesis)

- demands

(infancy, pregnancy, lactation)

↑ (GI bleeding, excessive menstrual flow, bleeding diathesis) 
 - ↑ demands (infancy, pregnancy, lactation) 29

29

Lanjutan….Faktor Penyebab

Lanjutan….Faktor Penyebab LOGO II. Inadequate presentation to erythroid precursors: 
 - atransferrinemia 
 - Anti

LOGO

II. Inadequate presentation to erythroid precursors:

- atransferrinemia

- Anti TrfR Ab

III. Abnormal Fe balance :

- Aceruloplasminemia

- Autosomal dominant hemochromatosis ( mutations in ferroportin )

Fe balance : 
 - Aceruloplasminemia 
 - Autosomal dominant hemochromatosis 
 ( mutations in ferroportin

30

Patogenesis desifisiensi Fe

Patogenesis desifisiensi Fe LOGO ❖ 3 pathogenetic factors: 
 - Impaired Hb synthesis (consequence of reduced

LOGO

3 pathogenetic factors: - Impaired Hb synthesis (consequence of

reduced Fe supply) Transferin saturation< 16% ! inadequate Fe-supply to marrow Hb contents of RBC ↓ → hypochromic & microcytosis

- Generalized defect in cellular proliferation

- Fe-deficient oxidative damage to the red cell’s membrane RBC deformability ↓ → RBC viability ↓→ RBC destruction especially in spleen reduced RBC survival

deformability ↓ → RBC viability ↓→ RBC destruction ↑ especially in spleen → reduced RBC survival

31

Status besi tubuh:

Status besi tubuh: LOGO ❖ Serum Iron = SI ❖ Total Iron Binding Capacity (TIBC) ❖

LOGO

Serum Iron = SI

Total Iron Binding Capacity (TIBC)

% Transferrin Saturation = SI/TIBCx100%

Simpanan besi (Iron storage):

- Hemosiderin produk degradasi feritin yang tidak

larut dalam air mayoritas tdd aggregat kristal ferric

oxyhydroxide, FeOOH (di Hepar danSutuldideteksi dengan biopsi/aspirasi dan pengecatan besi (prosedur invasif)

- Ferritin kompleks garam Fe3+dan apoferitin yang

larut dalam air, dengan jumlah yang sangat kecil di serum.

(dideteksi dengan metode imunoasai)

apoferitin yang larut dalam air, dengan jumlah yang sangat kecil di serum. 
 (dideteksi dengan metode

32

LOGO ❖ Kandungan besi tubuh = 35-50 mg/kgBB: ±80% 20% - Fe fungsional, sebagai heme-Iron

LOGO

Kandungan besi tubuh = 35-50 mg/kgBB:

±80%

20%

- Fe fungsional, sebagai heme-Iron (65% Hb, myoglobin, enzim heme : cytochrom-C,A,A3,B, catalase , peroxidase) - Non-heme-Fe (sebagian kecil) - simpanan besi / Iron storage (ferritin,

hemosiderin) hanya ± 15% pada wanita 0.2% - circulating (terikat padaTransferrin)

besi / Iron storage (ferritin, hemosiderin) hanya ± 15% pada wanita 0.2% - circulating (terikat padaTransferrin)

33

Iron Cycle in the body :

Iron Cycle in the body : LOGO ❖ Fe-diet → as heme-Fe (Hb, myoglobin, 
 enzyme-Fe),

LOGO

Fe-diet as heme-Fe (Hb, myoglobin, enzyme-Fe), 5-35% adsorbed from animal/meat sources , adsorbed easily . as non-heme-Fe (vegetables , legumes), 90% of diet-Fe but only 2-20% of it absorbed depends on the iron-status and the ratio of Enhancer:Inhibitor

but 
 only 2-20% of it absorbed → 
 depends on the iron-status and 
 the

34

LOGO Enhancers (zat yang menstimulasi 
 penyerapan (absorbsi) : 
 Ascorbate, Cytrate, organic acids /

LOGO

Enhancers (zat yang menstimulasi penyerapan (absorbsi) :Ascorbate, Cytrate, organic acids / other amino acids , by reducing Fe 3+ to Fe 2+ .

Inhibitors (zat yang menghambat absorbsi) :

Carbonate, Phytate, Tannins, Phosphate, Oxalat chelate Non-heme-Fe unabsorbable

absorbsi) : 
 Carbonate, Phytate, Tannins, Phosphate, 
 Oxalat chelate Non-heme-Fe → unabsorbable 
 35

35

LOGO ❖ Bahan makanan yang menghambat absorbsi besi non heme ( Non-heme Iron ) :

LOGO

Bahan makanan yang menghambat absorbsi besi non heme (Non-heme Iron) :

- Phytate (dari legumes, sayuran)

- Tannin & Polyphenol (dari teh, kopi, wine, coklat )

- Phosphate/phosphoprotein dari kuning telur

- Minerals (Ca, Zn, Cd) - Tetracycline yang bereaksi dengan Fe menghambat absorbsi

dari kuning telur - Minerals (Ca, Zn, Cd) - Tetracycline yang bereaksi dengan Fe → menghambat

36

Siklus Fe dalam tubuh :

Siklus Fe dalam tubuh : LOGO Diet’s Iron → duodenum / proximal jejunum . 
 


LOGO

Diet’s Iron duodenum / proximal jejunum .

Iron from gut released into circulation , bound to transferin distributed to body’s organ / tissues( to bone marrow as a part of heme / Hb ) circulate inside red blood cells with blood flow

organ / tissues( to bone marrow as a part of heme / Hb ) → circulate

37

The development of IDA

The development of IDA LOGO • Stage-1 (prelatent Fe-deficient): 
 - progressive loss of storage-Fe 


LOGO

Stage-1 (prelatent Fe-deficient):

- progressive loss of storage-Fe

- body’s Fe reserve is still sufficient to maintain both the transport and functional compartment , so RBC development is still normal .

- peripheral blood picture is normal , no symptoms of anemia , but ferritin is .

*IDA= Iron Deficiency Anemia

peripheral blood picture is normal , no 
 symptoms of anemia , but ferritin is ↓

38

LOGO * Stage-2 (latent Fe-deficient) 
 - Exhaustion of storage-Fe , RBC 
 production is

LOGO

* Stage-2 (latent Fe-deficient)

- Exhaustion of storage-Fe , RBC production is still normal , Ferritin ↓↓

- Circulating-Fe (SI) begin , Transf- Receptor .

* Stage-3 (Fe-Deficiency Anemia)

- Stadium of Iron Deficiency Anemia

begin ↓ , Transf- 
 Receptor ↑ . * Stage-3 (Fe-Deficiency Anemia) 
 - Stadium of

39

LOGO Stage-1 Stage-2 Stage-3 (prelatent) (latent) (IDA) Marrow ↓ ( - ) ( - )

LOGO

Stage-1 Stage-2 Stage-3 (prelatent) (latent) (IDA) Marrow ↓ ( - ) ( - ) Ferritin
Stage-1
Stage-2
Stage-3
(prelatent)
(latent)
(IDA)
Marrow
( - )
( - )
Ferritin
<12ug/L
<12ug/L
Transf-Sat
N
<16%
<16%
sTrfR
N
Retic Hb 

content
N
Hb
N
N
<
MCV
N
N
<
N <16% <16% sTrfR N ↑ ↑ Retic Hb 
 content N ↓ ↓ Hb N

40

LOGO Symptoms Morphology SI - TIBC Ferritin Anemia I D A Hypo – Micro SI↓

LOGO

Symptoms Morphology SI - TIBC Ferritin Anemia I D A Hypo – Micro SI↓ -
Symptoms
Morphology
SI - TIBC
Ferritin
Anemia
I D A
Hypo –
Micro
SI↓ -
TIBC ↑
↓↓
Anemia
A.C D
Hypo –
Micro
SI ↓ -
N/ ↑
TIBC ↓ /
N
I D A Hypo – Micro SI↓ - TIBC ↑ ↓↓ Anemia A.C D Hypo –

41

Pendekatan Diagnostik Anemia Defisiensi Fe

Pendekatan Diagnostik Anemia Defisiensi Fe 
 LOGO 1. Anamnesis – pola menstruasi, kehamilan / 
 persalinan,

LOGO

1. Anamnesis – pola menstruasi, kehamilan / persalinan, tendensi perdarahan, penyakit kronis, diet, pekerjaan, riwayat bepergian

2. Pemeriksaan fisik – sistematik dari seluruh permukaan tubuh sampai ke organ dalam ( hati, limpa, kelenjar getah bening (lymphnodes)

– sistematik dari seluruh permukaan tubuh sampai ke organ dalam ( hati, limpa, kelenjar getah bening

42

LOGO 3. Laboratorium- Hema (DL, LED, Hapusan darah tepi, Retikulosit) - Serum (SI,TIBC,Ferritin, Bilirubin) -

LOGO

3. Laboratorium- Hema (DL, LED, Hapusan darah tepi, Retikulosit)

- Serum (SI,TIBC,Ferritin, Bilirubin)

- BMA (Bone Marrow Aspiration)

- Pemeriksaan Urine dan tinja

4. Penunjang - Radiology (EKG, USG) - Endoscopy

Bilirubin) - BMA (Bone Marrow Aspiration) - Pemeriksaan Urine dan tinja 4. Penunjang - Radiology (EKG,

43

LOGO S I TIBC Normal N N (1/3 mol.Trsf) I D A ↓ ↑ An.of
LOGO
S I
TIBC
Normal
N
N
(1/3 mol.Trsf)
I D A
An.of Chronic
Disease
N
/ ↓
Fe Overload
↑↑
N
/ ↑
Normal N N (1/3 mol.Trsf) I D A ↓ ↑ An.of Chronic Disease ↓ N /

44

Pemeriksaan Lab. Anemia def. Fe

Pemeriksaan Lab. Anemia def. Fe LOGO 1. CBC – confirm Anemia & find hypochromic microcytic picture

LOGO

1. CBC – confirm Anemia & find hypochromic microcytic picture from BSE and Red Cells Indices ( Hb, PCV ,MCV , MCH , MCHC)

2. SI

Fe 2+ released from Transferrin + ferrozine

(chromagen) measured colored complex TIBC – serum + excess FeCl2 to fill all Transferrin-binding sites the excess Fe is fixed by Mg- carbonate Fe-saturated Transferrin is measured with Ferrozine (= TIBC)

the excess Fe is fixed by Mg- 
 carbonate → Fe-saturated Transferrin is 
 measured with

45

LOGO % Saturasi Transferrin = SI/TIBC X 100% Erythropoeisis impaired when % Tf.Sat < 15%

LOGO

% Saturasi Transferrin = SI/TIBC X 100% Erythropoeisis impaired when % Tf.Sat < 15%

3. Ferritin Serum :

Serum Ferritin level ~ Fe-storage Ferritin <15 ug/L Definitive Fe-Deficient N/Ferritin in IDA , if :

- impaired liver function ( damaged hepatocyte), hemolysis, inflammation / infection / malignancy ( Ferritin = acute-phase protein )

hepatocyte), hemolysis, inflammation / infection / 
 malignancy ( Ferritin = acute-phase 
 protein ) 46

46

4. Transferrin Serum :

4. Transferrin Serum : LOGO measured by immunodiffusion methode Normal value : 2-4 g/L 5. Bone

LOGO

measured by immunodiffusion methode Normal value : 2-4 g/L

5. Bone Marrow’s Aspirate evaluation :

( using Perls or Prussian Blue stain )

methode Normal value : 2-4 g/L 5. Bone Marrow’s Aspirate evaluation : ( using Perls or

47

Anemia of Chronic Infection

Anemia of Chronic In fection LOGO ❖ Gejala klinis miripdengan anemia def.Fe ❖ Gambaran lab. hematologi

LOGO

Anemia of Chronic In fection LOGO ❖ Gejala klinis miripdengan anemia def.Fe ❖ Gambaran lab. hematologi

Gejala klinis miripdengan anemia def.Fe

Gambaran lab. hematologi = Anemia def. Fe (An.Hypo-Micro, MCV, MCH , SI ) , tapi TIBC N/ and Ferritin N/ )

Pathogenesis :

) , tapi TIBC N/ ↓ and Ferritin N/ ↑ ) ❖ Pathogenesis : 
 Fe

Fe storage

) , tapi TIBC N/ ↓ and Ferritin N/ ↑ ) ❖ Pathogenesis : 
 Fe

//

Transferrin

Tissues / RES

48

Penyebab menurunnya ‘circulating Fe’ :

Penyebab menurunnya ‘circulating Fe’ : LOGO 1. Impairment of Fe release from 
 macrophage in competing

LOGO

1. Impairment of Fe release from macrophage in competing with

lactoferrin, phagocyte’s product , even

storage-Fe is still enough .

2. Inadequate EPO Respons towards

anemia (effects of cytokine production by macrophage) .

still enough . 2. Inadequate EPO Respons towards 
 anemia (effects of cytokine production by 


49

Diagnosis Anemia akibat penyakit kronis:

Diagnosis Anemia akibat penyakit kronis: LOGO ❖ lab hematologi: 
 - Anemia hipokromik mikrositik 
 -

LOGO

lab hematologi: - Anemia hipokromik mikrositik

- SI , TIBC /N , Ferritin N/( jika Ferritin , ! An. Def.Fe )

- Inflamasi / infeksi (+) : CRP and LED

Problem: IDA with inflammation ferritin (falsely diagnosed as ACD) ; it can be differentiated by sTfR exam (serum transferrin receptor) that in IDA but normal in ACD .

as ACD) ; it can be differentiated by sTfR exam (serum transferrin receptor) that ↑ in

50

Anemia Sideroblastik

Anemia Sideroblastik LOGO ❖ Defek pada sintesis Heme → akumulasi Fe di mitochondria → degenerasi Fe

LOGO

Anemia Sideroblastik LOGO ❖ Defek pada sintesis Heme → akumulasi Fe di mitochondria → degenerasi Fe

Defek pada sintesis Heme akumulasi Fe di mitochondria degenerasi Fe granula Fe di sekitar inti normoblast, membentuk struktur spt cincin {paling jelas terlihat dengan pengecatan Perl (Perls’ stain) } Ringed Sideroblast (karakteristik anemia Sideroblastik)

Sideroblast bisa dijumpai secara normal di sutul

} → Ringed Sideroblast (karakteristik anemia Sideroblastik) ❖ Sideroblast bisa dijumpai secara normal di sutul 51

51

LOGO Sideroblast and Ringed Sideroblast ( in Sideroblastic Anemia ) 52

LOGO

Sideroblast and Ringed Sideroblast ( in Sideroblastic Anemia )

LOGO Sideroblast and Ringed Sideroblast ( in Sideroblastic Anemia ) 52
LOGO Sideroblast and Ringed Sideroblast ( in Sideroblastic Anemia ) 52

52

53 LOGO
53 LOGO

53

53 LOGO

LOGO

LOGO ❖ Classification of Sideroblastic Anemia 1. Hereditary : X-linked, defect in heme- synthesis enzyme

LOGO

Classification of Sideroblastic Anemia

1. Hereditary : X-linked, defect in heme- synthesis enzyme pathway

Fe absorption ↑ → % of Transferrin saturation and Ferritin level

in heme- synthesis enzyme pathway 
 Fe absorption ↑ → % of Transferrin saturation and Ferritin

54

2. Acquired :

- Primary :

2. Acquired : 
 - Primary : 
 LOGO Stem cell clonal mutations(MDS = MyeloDysplastic Syndromes
2. Acquired : 
 - Primary : 
 LOGO Stem cell clonal mutations(MDS = MyeloDysplastic Syndromes

LOGO

Stem cell clonal mutations(MDS = MyeloDysplastic Syndromes , RA-RS) Normochromic-macrocytic anemia . Marrow : erythroid hyperplasia with dysplastic or megaloblastic appearance - ringed sideroblast in normoblast .

. Marrow : erythroid hyperplasia with dysplastic or megaloblastic appearance - ringed sideroblast in normoblast .

55

-

- Secondary;

- - Secondary; LOGO Abnormal metabolism of Vit.B6 (alcoholism, malabsorption) , impairment of heme synthesis (

LOGO

Abnormal metabolism of Vit.B6 (alcoholism, malabsorption) , impairment of heme synthesis ( Pb intoxication) , Rhematoid Arthritis , or An.megaloblastik .

Usually related to myeloproliferative diseases ( AML, Myelofibrosis, Polycythemia or another types of MDS )

. Usually related to myeloproliferative diseases ( AML, Myelofibrosis, Polycythemia or another types of MDS )

56

Macrocytic Anemia

Macrocytic Anemia LOGO - Non-Megaloblastic Macrocytic Anemia : ❖ Reticulocytosis ❖ Liver disease / Alcoholism ❖

LOGO

- Non-Megaloblastic Macrocytic Anemia :

Reticulocytosis

Liver disease / Alcoholism

Myelodysplastic Syndrome

Erythroleukemia (FAB-M6)

- Megaloblastic Macrocytic Anemia

disease / Alcoholism ❖ Myelodysplastic Syndrome ❖ Erythroleukemia (FAB-M6) - Megaloblastic Macrocytic Anemia 57

57

Megaloblastic Macrocytic Anemia

Megaloblastic Macrocytic Anemia 
 LOGO macrocyte = erythrocyte with MCV > normal . macrocyte/microcyte depend on

LOGO

macrocyte = erythrocyte with MCV > normal . macrocyte/microcyte depend on the balance between nuclei & cytoplasmic maturation .

(nuclear dividing stopped when intracellular Hb production reach a proper level ) . If nuclear maturation delayed ( in DNA synthesis’s defect ) or cytoplasmic maturation ( increase of EPO’s activities ) critical level of Hb achieved earlier Macrocyte

↑ ( increase of EPO’s activities ) → critical level of 
 Hb achieved earlier →

58

LOGO Megaloblast = bigger than normal normoblast . 
 Megaloblastic changes = increased size of

LOGO

Megaloblast = bigger than normal normoblast .Megaloblastic changes = increased size of hemopoietic precursor cells in bone marrow ( not only in normoblast !)

Primary defect : Defect of DNA synthesis ( altered almost all active cells / organs i.e :

hemopoietic tissue, epithelial cells , mucous cells, etc )

synthesis ( altered almost all active cells / organs i.e : hemopoietic tissue, epithelial cells ,

59

LOGO ❖ Etiology of DNA synthesis defect : 
 
 deficiency of vit.B12 and folic

LOGO

Etiology of DNA synthesis defect :

deficiency of vit.B12 and folic acid maturation dysharmony between nuclei & cytoplasm (delayed nuclei maturation) increased cels (megaloblastic changes) marrow’s ineffective erythropoiesis intramedullary hemolysis total/indirect Bili and LDH .

→ marrow’s ineffective erythropoiesis → intramedullary hemolysis → total/indirect Bili and LDH ↑ . 60

60

LOGO ❖ Deficiency of Folic acid: 
 
 - - - Inadequate diet 
 (intake

LOGO

Deficiency of Folic acid:

LOGO ❖ Deficiency of Folic acid: 
 
 - - - Inadequate diet 
 (intake <

-

-

-

Inadequate diet (intake < / demand in pregnancy - lactation , child’s growth / malabsorption in tropical sprue / bowel resection / small intestine inflammation )

Drug’s effect (anti-epilepsi)

FA loss (dialysis)

61

LOGO ❖ Deficiency of Folic acid: 
 
 - - - Inadequate diet 
 (intake

LOGO

Deficiency of Folic acid:

LOGO ❖ Deficiency of Folic acid: 
 
 - - - Inadequate diet 
 (intake <

-

-

-

Inadequate diet (intake < / demand in pregnancy - lactation , child’s growth / malabsorption in tropical sprue / bowel resection / small intestine inflammation )

Drug’s effect (anti-epilepsi)

FA loss (dialysis)

62

LOGO ❖ Deficiency of Vit.B12: 
 
 - Inadequate diet : 
 Intake < in

LOGO

Deficiency of Vit.B12:

- Inadequate diet : Intake < in vegetarians , demand , impaired absorption caused by decreased Intrinsic Factor ( gastrectomy , pernicious anemia ) Malabsorption (bowel infection , worms / blind loop syndr )


 ( gastrectomy , pernicious anemia ) 
 Malabsorption (bowel infection , worms 
 / blind

63

VITAMIN B12

ASAM FOLAT

VITAMIN B12 ASAM FOLAT LOGO -Food from animal products -Heat stabile -Storage : enough for 3

LOGO

-Food from animal products -Heat stabile -Storage : enough for 3 yrs -Relatively low needs (only 1% of folate requirements)

-Limited sources (vegetable , fruits) -Heat labile -Storage enough only for 3 mths -Higher folate needs

CAUSE OF DEFICIENCY

CAUSE OF DEFICIENCY

-Vegetarian (seldom) -Impaired Intrinsic Factor (pernicious anemia) -Gastrectomy -Atropic Gastritis -Anticonvulsant, alcoholism

-Nutrition (alcoholism, goat’s milk diet) -Prematurity -Hemodyalisis -Bowel resection -Pregnancy -Anticonvulsant , MTX

64

goat’s 
 milk diet) -Prematurity -Hemodyalisis -Bowel resection -Pregnancy -Anticonvulsant , MTX 
 64 


LOGO Pathogenesis of Megaloblastic Anemia : ❖ Megaloblastic changes ❖ atrophy of tongue papilla &

LOGO

Pathogenesis of Megaloblastic Anemia :

Megaloblastic changes atrophy of tongue papilla & mucosal GI glossitis , gastritis, nausea , constipation. B12 defic demyelinisation of spinal cord & peripheral nerve loss of foot’s balance / sensory (Neuropatia) FA defic hyperhomocysteinemia thrombosis and vascular occlusion .

balance / sensory (Neuropatia) ❖ FA defic → hyperhomocysteinemia → thrombosis and vascular occlusion . 65

65

B12 Metabolism

B12 Metabolism LOGO ❖ Vit.B12 → purine & pyrimidin synthesis → 
 synthesis DNA & RNA

LOGO

Vit.B12 purine & pyrimidin synthesis synthesis DNA & RNA mitosis and maturation

Vit.B12 made from microbiological source because plants do not produce B12 ( meat , liver, eggs and milk are rich of Vit B12 ).

Vit.B12 content in the daily diet is 5-3ug , daily requirement of B12 is 1-3 ug, and B12 body’s storage is 2-5 mg (enough for 3 yrs)

in the daily diet is 5-3ug , daily requirement of B12 is 1-3 ug, and B12

66

LOGO Vit.B12 absorption ❖ B12 diet → in gaster bind by IF (Intrinsic Factor) produced

LOGO

Vit.B12 absorption

B12 diet in gaster bind by IF (Intrinsic Factor) produced by parietal cells IF-B12 complex ileum : B12 absorbed , IF freed into the lumen

impaired IF : gastrectomy/gastritis/ Auto-Ab-antiIF or Auto-Ab-antiparietal) no absorption of B12

impaired DNA synthesis Achlorhydria)

(Pernicious Anemia with

Pernicious Anemia = autoimmune disease auto-Ab to parietal cells (Anti-IF or Anti-Parietal)

Anemia with ❖ Pernicious Anemia = autoimmune disease → auto-Ab to parietal cells (Anti-IF or Anti-Parietal)

67

LOGO Hematological pictures of Megaloblastic Anemia ❖ Bone Marrow : - megaloblastosis - ineffective erythropoiesis

LOGO

Hematological pictures of Megaloblastic Anemia

Bone Marrow :

- megaloblastosis

- ineffective erythropoiesis

Peripheral blood :

- Oval macrocytosis

- Hypersegmented neutrophil ( five 5-lobed cells or one 6-lobed cell) or the mean lobes of 100 neutrophils is > 3.4

neutrophil ( five 5-lobed 
 cells or one 6-lobed cell) or the mean lobes of 100

68

Megaloblastic Anemia

Megaloblastic Anemia LOGO ! find oval-Macrocyte cell and hypersegmenteneutrophil . 69

LOGO

! find oval-Macrocyte cell and hypersegmenteneutrophil .

Megaloblastic Anemia LOGO ! find oval-Macrocyte cell and hypersegmenteneutrophil . 69
Megaloblastic Anemia LOGO ! find oval-Macrocyte cell and hypersegmenteneutrophil . 69

69

Diagnosis of Megaloblastic Anemia

Screening :

Diagnosis of Megaloblastic Anemia ❖ Screening : 
 LOGO - CBC , Neutrophil’s lobe count 


LOGO

- CBC , Neutrophil’s lobe count

- Serum Indirect Bilirubin , LDH (lactate dehydrogenase)

Spesific tests :- Bone Marrow Aspiration: megaloblastosis &

megaloblastic changes, erythropoietic activitiy ( ineffective erythropoiesis)

- Folate & Vit.B12 assay

- Gastric juice analysis

- Schilling Tests - Antibody Assay


 - Folate & Vit.B12 assay 
 - Gastric juice analysis 
 - Schilling Tests 


70

Anemia Hemolitik

Anemia Hemolitik LOGO ❖ Anemia hemolitik: anemia yang disebabkan oleh proses hemolitik. ❖ Hemolisis: pemecahan

LOGO

Anemia hemolitik: anemia yang disebabkan oleh proses hemolitik.

Hemolisis: pemecahan eritrosit sebelum waktunya (sebelum masa hidup rerata eritrosit, yaitu 120 hari). (Proses pemecahan eri karena sdh waktunya! senescence=penuaan)

Hemolisis dapat terjadi di dalam pembuluh darah (hemolisis intravaskular) dan di luar pembuluh darah (hemolisis ekstravaskular).

darah (hemolisis intravaskular) dan di luar pembuluh darah (hemolisis ekstravaskular). www.themegallery.com Company Logo

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HEMOLYTIC ANEMIA

HEMOLYTIC ANEMIA LOGO ❖ Normal red cell’s survival = 110-120 days → destructed by macrophage in

LOGO

Normal red cell’s survival = 110-120 days destructed by macrophage in marrow and spleen .When the survival are shortened EPO production is stimulated (compensated) no Hb changes anemia (–) . If the destruction is acute or chronic with very shortened life of red cells , there will no compensation anemia (+) .

destruction is acute or chronic with very shortened life of red cells , there will no

72

Definition of Hemolytic Anemia :

Definition of Hemolytic Anemia : LOGO ❖ anemia caused by shortened red cell’s survival as a

LOGO

anemia caused by shortened red cell’s survival as a result of excessive uncompensated destruction of red cells .

Hemolytic process = every process of red cells destruction with still / without compensated by bone marrow anemia is not always present .

process of red cells destruction with still / without compensated by bone marrow → anemia is

73

- Compensation ability of bone marrow :

- Compensation ability of bone marrow : LOGO ❖ Ability to ↑ red cells production (

LOGO

Ability to red cells production ( 6-8 x normal )

:

-

survival shorten ½ → production 2x

-

survival shorten ¼ → production 4x

-

survival shorten 1/6 production 6x

-

survival shorten 1/8 production 8x

of production 6-8 x is maksimum . If red cells live only 20 days anemia (+).

production ↑ 8x 
 ↑ of production 6-8 x is maksimum . ❖ If red cells

74

LOGO Diagnostic approach in Hemolytic Anemia : 1. Confirm anemia (Hb/PCV/RBC) 
 an acute case

LOGO

Diagnostic approach in Hemolytic Anemia :

1. Confirm anemia (Hb/PCV/RBC)an acute case usually acquired , and chronic case is mostly hereditary .

2. To find the signs of hemolytic process .

3. Extra or Intravascular ?

4. Hereditary or acquired ?

5. The cause of hemolysis episodes .

of hemolytic process . 3. Extra or Intravascular ? 4. Hereditary or acquired ? 5. The

75

The signs of Hemolytic process :

The signs of Hemolytic process : LOGO 1. Increased of red cells destruction - Unconjug.bilirubin serum

LOGO

1. Increased of red cells destruction

- Unconjug.bilirubin serum ↑ → jaundice

- Urobilinogenuria

- Hb-uria sign of intravascular hemolysis

- Abdom.pain splenomegaly, spleen infarction

- Leg’s Ulcer intrinsic defect of erythrocyte

- Haptoglobin serum ↓↓ /neg intravascular hemolisys .

→ intrinsic defect of erythrocyte 
 - Haptoglobin serum ↓↓ /neg → intravascular 
 hemolisys .

76

LOGO 2.Destruksi eritrosit : - Microspherocyte, Fragmentocyte, Poikilocyte - Erythrocyte Osmotic Fragility ↑ -

LOGO

2.Destruksi eritrosit :

- Microspherocyte, Fragmentocyte, Poikilocyte

- Erythrocyte Osmotic Fragility

- Positive Autohemolysis test

- Shortened of red cells’ survival

3. Tanda Peningkatan Eritropoisis:

- Reticulocytosis

- Normoblastosis

- Erythropoietic Hyperplasia in bone marrow

3. Tanda Peningkatan Eritropoisis: - Reticulocytosis - Normoblastosis - Erythropoietic Hyperplasia in bone marrow 77

77

LOGO 78

LOGO

LOGO 78
LOGO 78

78

LOGO 79

LOGO

LOGO 79
LOGO 79

79

LOGO 80

LOGO

LOGO 80
LOGO 80

80

LOGO 81

LOGO

LOGO 81
LOGO 81

81

Hemolisis Ekstra vaskular

Hemolisis Ekstra vaskular LOGO ❖ Hemolisis ekstravaskular lebih sering dijumpai dibandingkan hemolisis intravaskular

LOGO

Hemolisis ekstravaskular lebih sering dijumpai dibandingkan hemolisis intravaskular

Hemolisis terjadi di sel makrofag dari sistem retikuloendothelial (RES) terutama pada Lien, hepar dan sutul karena sel ini mengandung enzim heme oksigenase

Lisis terjadi karena kerusakan membran eritrosit (misal Akibat reaksi Ag-Ab; presipitasi hb di sitoplasma, menurunnya fleksibilitas eri,dll)

kerusakan membran eritrosit (misal Akibat reaksi Ag-Ab; presipitasi hb di sitoplasma, menurunnya fleksibilitas eri,dll)
LOGO 83
LOGO 83

LOGO

LOGO 83

83

LOGO 84
LOGO 84

LOGO

LOGO 84

84

LOGO 85

LOGO

LOGO 85

85

LOGO 85

Klasifikasi Anemia Hemolitik

Klasifikasi Anemia Hemolitik LOGO Dibagi atas 2 golongan besar, yaitu: 1. Anemia hemolitik karena faktor di

LOGO

Dibagi atas 2 golongan besar, yaitu:

1. Anemia hemolitik karena faktor di dalam eritrosit sendiri (gangguan intra korpuskuler) 2. Anemia hemolitik karena faktor di luar eritrosit (gangguan ekstra korpuskular)

2. Anemia hemolitik karena faktor di luar eritrosit (gangguan ekstra korpuskular ) www.themegallery.com Company Logo

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lanjutan….Klasifikasi anemia hemolitik :

lanjutan….Klasifikasi anemia hemolitik : LOGO 1. Gangguan intra korpuskular (Hereditary Hemolytic Anemia ) 
 -

LOGO

1. Gangguan intra korpuskular (Hereditary Hemolytic Anemia )

-

Membrane abnormality (hereditary spherocytosis , hereditary ovalocytosis )

-

defect of globin chain (Thalassemia, Hb-

pathia)

-

enzyme defect ( G-6PD deficiency , PK-deficiency)

of globin chain (Thalassemia, Hb- 
 pathia) - enzyme defect ( G-6PD deficiency , PK- 


87

Hereditary Spherocytosis :

Hereditary Spherocytosis : LOGO 88

LOGO

Hereditary Spherocytosis : LOGO 88
Hereditary Spherocytosis : LOGO 88

88

Hereditary Ovalocytosis :

Hereditary Ovalocytosis : LOGO 89

LOGO

Hereditary Ovalocytosis : LOGO 89
Hereditary Ovalocytosis : LOGO 89

89

LOGO Lanjutan……klasifikasi anemia hemolitik 2. Gangguan ekstrakorpuskular (Acquired Hemolytic Anemia): 
 - physical

LOGO

Lanjutan……klasifikasi anemia hemolitik

2. Gangguan ekstrakorpuskular (Acquired Hemolytic Anemia):

- physical / chemical substances

- infections (bacteria, parasites, viruses, fungi)

- mechanical trauma (prostetic heart valves)

- Immune mechanism (Alloimmune / Autoimmune / Drug-Induced HA)

- mechanical trauma (prostetic heart valves) 
 - Immune mechanism (Alloimmune / 
 Autoimmune / Drug-Induced

90

LOGO - Hereditary Spherocytosis : ❖ autosomal dominant ❖ Spherocytosis, decreased membrane surface area relative
LOGO - Hereditary Spherocytosis : ❖ autosomal dominant ❖ Spherocytosis, decreased membrane surface area relative

LOGO

- Hereditary Spherocytosis :

autosomal dominant

Spherocytosis, decreased membrane surface area relative to cell volume osmotic fragility test (OFT)among the family member .

The primary lesion is caused by membrane protein defects ( of spectrin) cytoskeleton instability .

60% - chronic anemia , jaundice, splenomegaly, 20% without hemolysis / splenomegaly . Bilirubin excretion ,causing bilestone in USG.

91

Thalassemia :

Defect of 1 or more globin-chain synthesis (the amount = quantitatively) :

globin-chain synthesis (the amount = quantitatively) : 
 LOGO - deficiency of α globin-chain → α

LOGO

- deficiency of α globin-chain → α-thalassemia

- deficiency of β globin-chain → β -thalassemia

- deficiency of δβ globin-chain → δβ -thalassemia

the primary defects in Hb-pathia is in the globin amino acids structure (qualitatively)

→ δβ -thalassemia the primary defects in Hb-pathia is in the globin amino acids structure (qualitatively)

92

LOGO 93

LOGO

LOGO 93
LOGO 93

93

LOGO 94

LOGO

LOGO 94
LOGO 94

94

α-Thalassemia

α -Thalassemia LOGO ❖ α -Thalassemia = is caused by the impairment of α -globin chain

LOGO

α-Thalassemia = is caused by the impairment of α-globin chain production/synthesis .

α-globin chain synthesis is directed by 2 pairs of α-gene (4 locus α-gen) depending of the number of defected locus 3 types of α-Thalassemia ( α-thal trait , HbH Disease, and HbBart’s Hydrops Fetalis)

of defected locus → 3 types of α -Thalassemia ( α -thal trait , HbH Disease,

95

Clinical consequences in α-Thalassemia

Clinical consequences in α -Thalassemia LOGO ❖ Deficiency of α -globin chain → excess of β

LOGO

Deficiency of α-globin chain excess of β , γ chain since fetal life to form β 4-tetramers (HbH) or γ 4-tetramers (HbBart) .

Defect of 1-2 α-Gen = α-trait (clinically good)

Defect of 3 α-Gen = HbH disease ( Hb 10-11 g/ dl) excess of β -chain to form β 4- tetramers (HbH) as intracellular inclusion detected by BCB-stain .

excess of β -chain → to form β 4- tetramers (HbH) as intracellular inclusion → detected

96

HbH-inclusion ( β 4) in HbH Disease as shown in staining (compare with reticulocyte)

BCB LOGO
BCB
LOGO
HbH-inclusion ( β 4) in HbH Disease as shown in staining (compare with reticulocyte) BCB LOGO
HbH-inclusion ( β 4) in HbH Disease as shown in staining (compare with reticulocyte) BCB LOGO

97

LOGO ❖ Defect of 4 α -gene (HbBarts’hydrops fetalis) → clinically severe , stillborn baby

LOGO

Defect of 4 α-gene (HbBarts’hydrops fetalis) clinically severe , stillborn baby with hydrops fetalis ( severe hypoxia ) .HbBarts = γ 4-tetramers (excess of γ-chains that unable to form HbF ) .

HbBarts and HbH inclusions precipitated in red cell’s membrane mechanical trapping in spleen macrophagic phagocytosis hemolysis .

in red cell’s membrane → mechanical trapping in spleen → macrophagic phagocytosis → hemolysis . 98

98

99 LOGO
99 LOGO

99

99 LOGO

LOGO

LOGO 100
LOGO 100

LOGO

LOGO 100

100

- β -Thalassemia

- β -Thalassemia LOGO ❖ Clinically consequences in β -Thalassemia : 
   - No problems

LOGO

Clinically consequences in β -Thalassemia :

 

-

No problems during fetal life because HbF synthesis is normally produced (normal α and γ chains)

-

When HbA is dominantly needed , the

clinically problems exist as incapability to synthesize HbA ( α2 β 2) excess of α-chain compensated of δ and γ production HbA2 (in β -Thalassemia minor) and HbF (in

β -Thalassemia mayor)

γ production → HbA2 
 ↑ (in β -Thalassemia minor) and HbF ↑ (in 
 β

101

Β-Thalassemia mayor :

Β -Thalassemia mayor : LOGO - severe anemia → repeated transfusion is oftenly needed → Fe

LOGO

- severe anemia repeated transfusion is oftenly needed Fe ↑↑ → hemochromatosis

- chronic ineffective erythropoiesis

medullary hypertrophy in childhood facial malformation:

* Frontal bossing

* Maxillary hypertrophy

* Hypertelorism (mongoloid’s eye)

facial 
 malformation: 
 * Frontal bossing 
 * Maxillary hypertrophy 
 * Hypertelorism (mongoloid’s eye)

102

- β -chain deletion forms :

- β -chain deletion forms : LOGO ❖ β 0 -Thalassemia : no β -chain production.

LOGO

β 0 -Thalassemia : no β -chain production. β + Thalassemia : β -chain production << in heterozygous case : medium severein homozygous : severe (Cooley’s anemia)


 << 
 in heterozygous case : medium severe 
 in homozygous : severe ( Cooley’s

103

LOGO 104

LOGO

LOGO 104
LOGO 104

104

Laboratory Diagnosis in Thalassemia

Laboratory Diagnosis in Thalassemia LOGO 1. CBC, Peripheral Blood Smear 2. Hb-Electrophoresis : in Celulose-Acetat (pH

LOGO

1. CBC, Peripheral Blood Smear

2. Hb-Electrophoresis : in Celulose-Acetat (pH 8.4) for thalassemia and Hb-pathia screening Using hemolysate formed bands of different types of Hb ( normal : bands A, F, and A2 , measured densitometrically)

hemolysate → formed bands of different types of Hb ( normal : bands A, F, and

105

106 LOGO
106 LOGO

106

106 LOGO

LOGO

Lanjutan…

Lab

diagnosis in thalasemia

Lanjutan… Lab diagnosis in thalasemia LOGO 3 . HbA2 mesurement to diagnose β -Thalassemia trait using

LOGO

3. HbA2 mesurement to diagnose β -Thalassemia trait using anion-exchange resin column chromatography

in both HbELP and chromatography , HbC, HbE and HbO can interrupt the conclusion because of the same band location with HbA2 .

4. HbF determination : - Alkali Denaturation Test - Acid-elution (Kleihauer) test - RID or ELISA methods

HbF determination : 
 - Alkali Denaturation Test 
 - Acid-elution (Kleihauer) test - RID or

107

LOGO 5. HbH Inclusion detection : 
 - Supravital staining using Brilliant 
 Cresyl Blue

LOGO

5. HbH Inclusion detection :

-

Supravital staining using Brilliant Cresyl Blue (BCB) or NewMethylene Blue (NMB)

-

HbH inclusion seen as dispersed blue- green granules in red cells (compare with reticulocyte as a filament)

-

in HbH disease : HbH inclusion +++

-

in Thalassemia- α-trait : HbH inclusion + in 1: 10000 eritrosit .

disease : HbH inclusion +++ 
 - in Thalassemia- α -trait : HbH inclusion + 


108

Defisiensi G-6PD

Defisiensi G-6PD 
 LOGO - Oxidant → produce H2O2 → oxidizing 
 Hb’s free sulfhydryl →

LOGO

- Oxidant produce H2O2 oxidizing Hb’s free sulfhydryl to form Sulf-Hb aggregates that precipitated as Heinz Bodies destructed in spleen .

- Oxidant / Sulf-Hb are controlled by Reduced Glutathione (GSH)

Bodies → destructed in spleen . 
 
 - Oxidant / Sulf-Hb are controlled by 


109

110 LOGO
110 LOGO

110

110 LOGO

LOGO

- X-linked, ± 300 variants .

❖ - X-linked, ± 300 variants . 
 LOGO normal G-6PD genes : - type B

LOGO

normal G-6PD genes : - type B (GdB) - type A (GdA) - Abnormal enzyme types :

1. GdA– (type A–)

2. Gd-Mediterranean (GdMed)

3. Gd-Canton : many in Asia

- G-6PD deficient red cells are resistent to Plasmodium Falciparum .


 3. Gd-Canton : many in Asia 
 - G-6PD deficient red cells are resistent 


111

-

- 
 Substances causing lysis in G-6PD deficiency : 1. Antimalaria 2. Sulfonamides 3. Vit.K, Vit.C

Substances causing lysis in G-6PD deficiency :

1. Antimalaria

2. Sulfonamides

3. Vit.K, Vit.C

4. Lung Infection

(virus,bacteria)

5. Antipyreticum

6. Fava beans7. Naphtalene 8. Uremia 9. Antibiotics (Penicilline , streptomycine

112

6. Fava beans 
 7. Naphtalene 8. Uremia 
 9. Antibiotics 
 (Penicilline , 
 streptomycine

LOGO

LOGO ❖ The highest G-6PD activity is in 
 reticulocyte . ❖ G-6PD screening test

LOGO

The highest G-6PD activity is in reticulocyte . G-6PD screening test :

is in 
 reticulocyte . ❖ G-6PD screening test : 
 
 Test’s principle : 


Test’s principle :

G-6P + NADP

G-6PD

113

❖ G-6PD screening test : 
 
 Test’s principle : 
 G-6P + NADP G-6PD 


6-PG + NADPH UV

(fluorescence)

Acquired Hemolytic Anemia :

Acquired Hemolytic Anemia : 
 
 LOGO - Secondary Hemolytic Anemia caused by 
 infection /

LOGO

- Secondary Hemolytic Anemia caused by infection / systemic disorders :

Malignancy – Autoimmune-reacted hemolysis , microangiopathy or hypersplenisme , appearing Anemia of chronic disease, bleeding tendencies, and marrow’s suppression

or hypersplenisme , appearing Anemia of chronic disease, bleeding tendencies, and marrow’s suppression 
 114

114

LOGO ❖ Disseminated Intravascular Coagulation (DIC): 
 Systemic intravascular coagulation → fibrin deposit

LOGO

Disseminated Intravascular Coagulation (DIC): Systemic intravascular coagulation fibrin deposit intravascularly / endothelial damage (microangiopathyi) caused by sepsis red cells destruction .

Chronic Liver Disease : hemolysis caused by hypersplenism .

Chronic Renal Disease: hemolysis caused by microangiopathy

Disease : hemolysis caused by hypersplenism . 
 ❖ Chronic Renal Disease: hemolysis caused by microangiopathy

115

Acquired Hemolytic Anemia (extracorpusc.)

Acquired Hemolytic Anemia (extracorpusc.) 
 LOGO Immune Hemolytic Anemia ❖ Red cell membrane-bound Ab hemolysis .

LOGO

Immune Hemolytic Anemia

Red cell membrane-bound Ab hemolysis . The speed & hemolysis location depend on IgG or IgM, and the ability to activate complement . Optimal temperature to bind Ab : 37 0 C – Warm-IgG-Type <30 0 C – Cold-IgG-Type

. ❖ Optimal temperature to bind Ab : 
 37 0 C – Warm-IgG-Type 
 <30

116

Lanjutan….acquired hemolytic anemia

Lanjutan….acquired hemolytic anemia LOGO ❖ Cell+IgG → destructed by spleen 
 Cell+IgM → enhance the

LOGO

Cell+IgG destructed by spleenCell+IgM enhance the activation of complement’s cascade intravascular hemolysis

Immune destruction often cause minimally membrane damage shape change into spherocyte .

hemolysis 
 ❖ Immune destruction often cause minimally membrane damage → shape change into spherocyte .

117

LOGO ❖ Immune Hemolytic Anemia classification : 
 
 1. Alloimmune : Transfusion Rx ,

LOGO

Immune Hemolytic Anemia classification :


 1. Alloimmune : Transfusion Rx , Hemolytic 
 Disease of the Newborn (HDN) 

1. Alloimmune : Transfusion Rx , Hemolytic 

Disease of the Newborn (HDN) 

2. Autoimmune : Warm/Cold AIHA, 

Paroxysmal Cold Hb-uria (PCH)


3. Drug-induced HA : penicilline type, aldomet, and stibophen type .

Paroxysmal Cold Hb-uria (PCH)
 
 3. Drug-induced HA : penicilline type, 
 aldomet, and stibophen type

118

LOGO Hemolytic Disease of the Newborn (HDN) – 
 Rh-neg mother , with Rh-Pos fetus
LOGO Hemolytic Disease of the Newborn (HDN) – 
 Rh-neg mother , with Rh-Pos fetus

LOGO

Hemolytic Disease of the Newborn (HDN) –

Rh-neg mother , with Rh-Pos fetus , during I and second pregnancy

LOGO Hemolytic Disease of the Newborn (HDN) – 
 Rh-neg mother , with Rh-Pos fetus ,

119

Antiglobulin Tests (Coombs) :

Antiglobulin Tests (Coombs) : LOGO ❖ Direct Coombs Test (Direct Antiglobulin Test/ DAT) = Ab detection

LOGO

Direct Coombs Test (Direct Antiglobulin Test/ DAT) = Ab detection test (IgG and or C3d / complement-bound red cells) .

Indirect Coombs Test = test for serum free Ab .

DAT usually positive in AIHA (.

red cells) . 
 
 Indirect Coombs Test = test for serum free Ab . 


120

Drug-Induced hemolytic anemia :

Drug-Induced hemolytic anemia : LOGO ❖ Penicilline type : drug as hapten binds red cell membrane

LOGO

Penicilline type : drug as hapten binds red cell membrane antigenic stimulate Ab production against Drug in drug-red cell complex

Ab production against Drug in drug-red cell complex Phenacetin/Quinidin type : Drug (hapten) adsorbed protein

Phenacetin/Quinidin type : Drug (hapten) adsorbed protein stimulated-Ab binds drug-protein complex activate complement red cell lysis.

Aldomet type : drug change red cell membrane’s structure detected as foreign cell Autoantibody production .

type : drug change red cell membrane’s structure → detected as foreign cell → Autoantibody production

121

LOGO 122

LOGO

LOGO 122
LOGO 122

122

Aplastic (Hypoplastic?) Anemia

Aplastic (Hypoplastic?) Anemia LOGO ❖ Severe & fatal Anemia because of ↓ red cells/ leucocytes/platelet

LOGO

Severe & fatal Anemia because of red cells/ leucocytes/platelet production (pancytopenia) caused by Stem Cells impairment (radiation, chemicals, drugs, or genetic matters)

Marrow aplasia / hypoplasia-causing

matters) 
 ❖ Marrow aplasia / hypoplasia-causing substances cytostatics (6-MP, 
 busulfan), arsen,

substances

cytostatics (6-MP, busulfan), arsen, chloramphenicol, anticonvulsant (phenytoin), analgetic (phenylbutazone) , DDT, etc

- radiation , benzene,

123

LOGO Symptoms & Lab.appearance of Aplastic Anemia ❖ fatigue, palpitation, infections, bleeding tendency ❖ Lab

LOGO

Symptoms & Lab.appearance of Aplastic Anemia

fatigue, palpitation, infections, bleeding tendency

Lab : - pancytopenia - normochromic normocytic - ‘dry-tap’ marrow , hypocellularity

Prognosis : - bad especially for < 40 yrs old patients marrow transplantation .

❖ Prognosis : 
 - bad especially for < 40 yrs old patients → 
 marrow

124

- Treatment for Aplastic Anemia :

- Treatment for Aplastic Anemia : LOGO 1. Avoid every toxic material 2. Avoid infections /

LOGO

1. Avoid every toxic material

2. Avoid infections / bleeding tendency

3. Use Washed-Erythrocyte if transfusion is needed or Plat.Concentrate (PC) for any profuse bleeding ( give corticosteroid if bleeding is minimal)

4. Marrow stimulants (androgenic hormon )

5. Marrow Transplantation

( give corticosteroid if bleeding is minimal) 4. Marrow stimulants (androgenic hormon ) 5. Marrow Transplantation

125

POLISITEMIA (ERITROSITOSIS)

POLISITEMIA 
 (ERITROSITOSIS) LOGO ❖ Peningkatan patologis massa eritrosit ❖ massa eritrosit normal : ( sea

LOGO

Peningkatan patologis massa eritrosit

massa eritrosit normal : (sea level)

- o : 26 - 32 ml / kg BB

- o

normal : ( sea level ) - o : 26 - 32 ml / kg BB

: 23 - 29 ml / kg BB

level ) - o : 26 - 32 ml / kg BB - o : 23

eritrositosis : massa eritrosit > normal ( PCV : o >51% ; o >48% )

32 ml / kg BB - o : 23 - 29 ml / kg BB ❖

Klasifikasi :

I. Primer (Otonomik)

• Klasifikasi : I. Primer (Otonomik) LOGO A. Polisitemia Vera B. Eritrositosis Murni (Eritremia) II. Sekunder

LOGO

A. Polisitemia Vera

B. Eritrositosis Murni (Eritremia)

II. Sekunder

A. Fisiologis (Oksigenasi Jaringan

)
)

B. Non-fisiologis (Oksigenasi Jaringan N)

III. Eritrositosis Relatif

Sekunder A. Fisiologis ( Oksigenasi Jaringan ) B. Non-fisiologis ( Oksigenasi Jaringan N ) III. Eritrositosis

ERYTHROCYTOSIS - DIAGNOSTIC TESTS

ERYTHROCYTOSIS - DIAGNOSTIC TESTS LOGO • Complete Blood Count • Bone Marrow examination • Arterial Blood

LOGO

Complete Blood Count

Bone Marrow examination

Arterial Blood Gas analysis

Leukocyte Alkaline Phosphatase

P 5O

IVP or renal ultrasound

Liver ultrasound or CT scan

Erythropoietin level

Erythroid progenitor assay

Sleep apnea evaluation

• Liver ultrasound or CT scan • Erythropoietin level • Erythroid progenitor assay • Sleep apnea

POLISITEMIA VERA

Proliferasi

klonal

neoplastik

sel

POLISITEMIA VERA • Proliferasi klonal neoplastik sel LOGO progenitor hematopoitik pluripoten • Kriteria diagnosis

LOGO

progenitor hematopoitik pluripoten

Kriteria diagnosis P.V. :

Kategori A

1.Massa eritrosit:

Lk > 36 ml / kgBB (PCV > 54%) Pr > 32 ml / kg
Lk
> 36 ml / kgBB (PCV > 54%)
Pr
> 32 ml / kg BB (PCV > 51%)
2. Saturasi oksigen
3. Splenomegali
> 92%

Kategori B

Kategori B LOGO 1. Trombositosis (> 400.000 / µ l) 2. Lekositosis (> 12.000 / µ

LOGO

1. Trombositosis (> 400.000 / µl)

2. Lekositosis (> 12.000 / µl)

3. Skor LAP

4. B12 serum > 900 pg/ml

/ µ l) 3. Skor LAP ↑ 4. B12 serum > 900 pg/ml • Diagnosis PV

• Diagnosis PV

A1 + A2 +

+
+
+
+

A3

+
+

bila :

+
+

atau

A1 + A2 + dan 2 dari kategori B

+
+
+
+
+
+
LOGO PRIMARY “PURE” ERYTHROCYTOSIS ( ERYTHREMIA ) • peningkatan massa eritrosit murni • tidak ada

LOGO

PRIMARY “PURE” ERYTHROCYTOSIS ( ERYTHREMIA )

• peningkatan massa eritrosit murni

• tidak ada penyebab eritrositosis sekunder

• kadar eritropoitin normal atau rendah

• mungkin akibat mutasi gene reseptor eritropoitin progenitor eritroid jadi lebih sensitif terhadap eritropoitin.

• mungkin akibat mutasi gene reseptor eritropoitin → progenitor eritroid jadi lebih sensitif terhadap eritropoitin.

II. ERITROSITOSIS SEKUNDER

• Merupakan

respons

terhadap

keadaan

SEKUNDER • Merupakan respons terhadap keadaan LOGO lain yang bersifat : - fisiologis : akibat oksigenasi

LOGO

lain

yang bersifat :

- fisiologis : akibat oksigenasi jaringan yang

- non fisiologis : tanpa penurunan oksigenasi jaringan

yang bersifat : - fisiologis : akibat oksigenasi jaringan yang ↓ - non fisiologis : tanpa
LOGO III. ERITROSITOSIS RELATIF • Sindroma Gaisbock • Stress erythrocytosis • Pseudo erythrocytosis - Massa

LOGO

III. ERITROSITOSIS RELATIF

• Sindroma Gaisbock

• Stress erythrocytosis

• Pseudo erythrocytosis

- Massa eritrosit tinggi normal - Volume plasma rendah

Gaisbock • Stress erythrocytosis • Pseudo erythrocytosis - Massa eritrosit tinggi normal - Volume plasma rendah

LOGO

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SOAL LATIHAN :

SOAL LATIHAN : LOGO 1. Nyonya Ana, usia 40 tahun, MRS (Masuk Rumah Sakit) dengan keluhan

LOGO

1. Nyonya Ana, usia 40 tahun, MRS (Masuk Rumah Sakit) dengan keluhan pusing, dan badan terasa lemah. Pemeriksaan fisik:

KU lemah, Tensi: 100/60 mmHg, Nadi:90 x/menit, RR: 20 x/menit, suhu:37˚C. Kepala/Leher: anemia (+), tidak dijumpai ikterus, dyspnea dan sianosis, Thorak/Cor dan Abdomen :dalam batas normal (dbn). Extremitas: dbn. Hasil laboratorium: Hb 8 g/dl, RBC 3,20 x 10 12 /L, Hematokrit 24 %, MCV 75 fl, MCH 25 pg, MCHC 33 g/dl. Jika anda adalah dokter jaga di RS tersebut, dari data yang ada, kemungkinan diagnosis pasien tersebut adalah:

A. Anemia normokromik-normositik

B. Anemia hipokromik-mikrositik

C. Anemia makrositik

D. Anemia makrositik-megaloblastik

E. Anemia makrositik-non megaloblastik

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Lanjutan …

soal

latihan

Lanjutan … soal latihan LOGO 2. Dari kasus ny. Ana, 40 tahun tersebut, diagnosis diferensial untuk

LOGO

2. Dari kasus ny. Ana, 40 tahun tersebut, diagnosis diferensial untuk penyebab anemianya adalah:

A. Anemia defisiensi folat, anemia defisiensi Vitamin B12,

B. Anemia karena perdarahan akut, anemia aplastik

C. Anemia defisiensi besi, thalasemia, anemia sideroblastik

D. Anemia hemolitik, anemia pada penyakit mielofibrosis

E. Anemia pada penyakit liver, anemia pada penyakit hipotiroid

penyakit mielofibrosis E. Anemia pada penyakit liver, anemia pada penyakit hipotiroid www.themegallery.com Company Logo

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Lanjutan …

soal latihan

Lanjutan … soal latihan LOGO 3. Dari soal kasus Ny. Ana, 40 tahun tersebut, langkah pemeriksaan

LOGO

3. Dari soal kasus Ny. Ana, 40 tahun tersebut, langkah pemeriksaan laboratorium selanjutnya yang perlu dilakukan untuk konfirmasi diagnosis adalah:

A. pemeriksaan bilirubin, haptoglobin, hitung retikulosit

B. Serum Iron, TIBC dan Feritin

C. Pemeriksaan B12 dan asam folat dalam darah

D. Pemeriksaan T3, T4 dan TSH

E. Pemeriksaan Aspirasi sumsum tulang

folat dalam darah D. Pemeriksaan T3, T4 dan TSH E. Pemeriksaan Aspirasi sumsum tulang www.themegallery.com Company

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CLINICAL CASE

CLINICAL CASE LOGO A 35-year-old man complains of chronic physical fatigue, which began 3-4 weeks ago.

LOGO

A 35-year-old man complains of chronic physical fatigue, which began 3-4 weeks ago. He said he felt tired all of the time even through his occupation as a software developer was mentally but not physically demanding. He breathed comfortably at rest but, when he exerted himself, he experienced difficulty in breathing and had hard time catching his breath. He also complained of „more than usual” mental fatigue, confessing an increasing inability to concentrate and focus his attention on tasks at hands. Colleagues noticed his pallor and his inattentiveness at brainstorming sessions and suggested he reschedule his annual physical examination for an earlier date. He complained of vague abdominal pain and sense of abdominal fullness. His appetite was depressed, and he thought perhaps his physical and mental symptoms were caused by poor diet. However, attempts to increase eating resulted in nausea. His stools, he said, were sometimes loose and tarry. Eventually, increased heart palpitations and chest pain made him seek medical advice

said, were sometimes loose and tarry. Eventually, increased heart palpitations and chest pain made him seek
LOGO Laboratory findings revealed the following:   Laboratory test Patient Normal RBC (red blood cell

LOGO

Laboratory findings revealed the following:

 

Laboratory test

Patient

Normal

RBC (red blood cell count)

3.5 T/L

4.5-6.0 T/L

HCT (hematocrit ratio)

28%

40-52%

Hb (hemoglobin)

8.0g/dL

13-17g/dL

MCV (mean corpuscular volume)

70fL

78-95fL

MCH (mean corpuscular hemoglobin)

22.8pg

29pg

MCHC (mean corpuscular hemoglobin concentration)

28%

34%

MCH (mean corpuscular hemoglobin) 22.8pg 29pg MCHC (mean corpuscular hemoglobin concentration) 28% 34%

QUESTIONS

QUESTIONS LOGO Case history questions: 1. What general medical condition is suggested by the person’s symptoms?

LOGO

Case history questions:

1. What general medical condition is suggested by the person’s symptoms?

2. What fundamental change in function of blood related to the red blood cells could simultaneously affect the function of several systems (cardiovascular, respiratory, gastrointestinal, and others)?

3. What specific diagnosis is supported by the laboratory findings?

4. How could the stool be related to the laboratory findings?

diagnosis is supported by the laboratory findings? 4. How could the stool be related to the

ANSWER

1. Answers: Anemia

ANSWER 1. Answers: Anemia LOGO 2. A reduction in oxygen-carrying capacity of the blood and thus

LOGO

2. A reduction in oxygen-carrying capacity of the blood and thus a reduction in the delivery of oxygen to various body tissues

3. An iron defficiency anemia

4. Most cases of iron-defficiency anemia result from internal blood loss. Dark, tarry loose stools suggest bleeding from the gastrointestinal tract and warrant further tests to determine the exact cause

tarry loose stools suggest bleeding from the gastrointestinal tract and warrant further tests to determine the

LOGO

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