Objektif pengajaran

1) Menyatakan definisi anemia.

2) Menyatakan klasifikasi anemia
3) Menyatakan etiologi anemia.
4) Menerangkan patofisiologi anemia.
5) Menyatakan manifestasi klinikal anemia.
6) Menyatakan penyiasatan yang dilakukan dalam kes
anemia.
7) Menyatakan diagnosis perbezaan anemia.
8) Menghuraikan pengendalian kes anemia.
9) Menyatakan komplikasi anemia.
10) Menerangkan pendidikan kesihatan kepada pesakit
anemia.
11) Menyatakan prognosis anemia.
Definisi
 Keadaan di mana terdapat kekurangan
atau kadar konsentrasi hemoglobin (sel
darah merah) dalam darah periferi bawah
paras normal mengikut umur dan jantina.

 Kekurangan jumlah pigmen hemoglobin

yang membawa oksigen dalam darah.
Kamus jururawat
Definisi WHO
 Blood hemoglobin (Hb)
concentration < 13g/dL or
hematocrit (Hct) < 39% in adult
males.
 Blood hemoglobin (Hb)
concentration < 12g/dL or
hematocrit (Hct) < 37% in adult
females.
Klasifikasi
1. Mengikut morfologi sel darah merah
(cytometric)
2. Mengikut kepada kadar penghasilan dan
kemusnahan sel darah merah
(erythrokinetic)
3. Mengikut punca anemia pada peringkat
molekul (biochemical or molecular)
Cytometric
 Berdasarkan kepada size SDM yang
diperiksa dibawah mikroskop.
 Saiz – Mean Corpuscular Volume (MCV)
 Konsentrasi Hb per SDM - Mean
Corpuscular Hemoglobin Concentration
(MCHC)
 Jumlah Hb per SDM – Mean Cell
Hemoglobin (MCH)
Klasifikasi Cytometric
a) Normochromic, Normocytic Anemia
b) Hypochromic, Microcytic Anemia
c) Normochromic, Microcytic Anemia
Normochromic, Normocytic
Anemia
 Normal MCHC & MCV
 Penyebab;
◦ Anemia penyakit kronik – cth penyakit sepsis,
tumor
◦ Anemia hemolitik – cth - perolehan akibat
prosthetic cardiac valve
◦ Anemia pendarahan akut – cth kes trauma,
bleeding PV (abortion)
Normocytic, normochromic
anemia
Hypochromic, Microcytic Anemia
 Paras MCHC & MCV rendah
 Penyebab;
◦ Anemia kekurangan zat besi (Iron deficiency
Anemia)
◦ Thalassemia
◦ Keracunan lead
Hypochromic, Microcytic Anemia
Normochromic, Macrocytic Anemia
 Paras MCHC & MCV tinggi
 Penyebab;
◦ Kekurangan Vit B12 (Vit B12 deficiency)
◦ Kekurangan Folate (Folate deficiency)
Macrocyte
Micrositic, normochromic anemia
 Renal disease (erythropoietin loss)
Microcytosis
Klasifikasi Erythrokinetic
 Berdasarkan kepada kadar pertukaran
SDM;
◦ Meningkat – dalam kes hemolisis SDM atau
pendarahan
◦ Sum-sum merah tulang bertindakbalas dan
hasilkan banyak SDM yang tidak matang dan
dibebaskan ke peredaran darah.
Klasifikasi Molekular
 Berdasarkan kegagalan penghasilan SDM
normal akibat kekurangan faktor yang
perlu dalam pembentukan SDM.
Jenis Anemia
a) Iron deficiency anemia.
◦ Kurang elemen zat besi.
◦ Sum-sum merah tulang gagal menghasilkan
SDM yang cukup akibat kurang zat besi untuk
hasilkan hemoglobin.
b) Vitamin deficiency anemias.
◦ Elemen spt folate & vitamin B-12 amat
diperlukan untuk hasilkan SDM yang normal.
◦ Biasanya disebabkan pengambilan diet yang
kurang bahan diatas.
Jenis Anemia
c. Anemia of chronic disease.
◦ Contoh penyakit kronik spt kanser, HIV/AIDS,
rheumatoid arthritis, Crohn's disease &
penyakit inflammatori kronik — boleh
mengganggu penghasilan SDM dan
menyebabkan anemia. Kegagalan ginjal juga
menyebabkan anemia.
Jenis Anemia
d. Aplastic anemia.
◦ Jarang berlaku dan merupakan anemia yang
boleh menyebabkan kematian
◦ Kurang kemampuan sum-sum merah tulang
untuk hasilkan SDM.
◦ Penyebab – jangkitan virus spt hepatitis,
keturunan (Fanconi’s anemia), leukemia,
myeloma, lymphoma, carcinoma, myelofibrosis,
ubatan & penyakit autoimmune.
Jenis Anemia
e. Hemolytic anemia.
◦ SDM dimusnahkan lebih awal dari masanya
dan sum-sum merah tidak sempat untuk
menggantikan jumlah SDM yang musnah.
◦ Penyebab - G6PD deficiency, sickle cell,
malaria, hyperspleenism, prosthetic heart
valve, warm antibody & cold antibody etc.
Jenis Anemia
f. Sickle cell anemia.
◦ Diwarisi
◦ Disebabkan oleh hemoglobin yang tidak
normal yang menyebabkan SDM berbentuk
sabit (sickle).
◦ SDM sabit akan musnah lebih awal dari
masanya dan menyebabkan pengurangan SDM
kronik.
Jenis Anemia
 Lain-lain jenis anemia.
◦ Thalassemia yang disebabkan oleh
keabnormalan pembentukan rantaian
hemoglobin.
Etiologi
 3 punca asas
1. Peningkatan Kerosakan / kemusnahan sel
darah merah
2. Kehilangan darah
3. Penghasilan sel darah merah baru tidak
mencukupi.
Patofisiologi
I. Gangguan kematangan SDM
a) Gangguan sintesis hemoglobin –
 kecacatan kematangan sitoplasma – sel SDM kecil &
pucat.
 Disebabkan kurang bekalan zat besi (iron deficiency
anemia), kurang penghasilan globin (thalassemia) atau
idiopatik (sideroblastic anemia)
b) Replikasi DNA yang lambat –
 kecacatan kematangan nukleus – sel SDM besar.
 Disebabkan kurang folate & vit B12, terdedah kepada
toksik (methotrexate atau agen kemoterapi),
kecacatan intrinsik kematangan sum-sum merah
(refractory anemia & myelodysplasia)
Patofisiologi
II. Kehilangan darah (pendarahan)
◦ Trauma
◦ Pendarahan GIT
◦ Menorrhagia, gross hematuria
◦ Kecederaan spleen, hepar
◦ Kepatahan pelvik
Patofisiologi
III. Hemolisis SDM
◦ Kecacatan intrasel SDM –
hemoglobinopathies, sickle cell, thalassemia.
◦ Kekurangan enzim glucose-6-phosphate
dehydrogenase (G6PD) – hemolisis SDM
dengan ubatan spt chloroquine, sulfonamides
◦ Sel sabit (sickle)
◦ Keabnormalan mambran – spurr cell,
hereditary spherocytosis, hereditary
elliptocytosis
Patofisiologi
III. Hemolisis SDM (sbgn)
◦ Immunohemolytic anemia;
a. Warm antibody (IgG) – idiopatik, SLE, leukemia,
ubatan (penicilline, methyldopa, quinine)
b. Cold antibody (IgM) – infeksi mycoplasma,
mononucleosis, lymphoma.
◦ Trauma mekanikal – injap jantung prosthetic, DIC,
penolakan buah pinggang, thrombotic
thrombocytic purpura.
◦ Kesan toksik secara terus – malaria, toksin
clostridium welchi, toxoplasmosis
◦ Hypersplenism
Manifestasi Klinikal
1. Boleh bermula secara akut atau kronik
2. Persembahan am spt:
◦ Pucat (pallor) – cardinal sign
◦ lemah, letih lesu, edema, kulit kering
3. Sistem kardiovaskular spt:
◦ Palpitasi, dispnea, sakit angina, takikardia
sinus, ―Ejection systolic murmur‖,
kardiomegali
4. Sistem alimentari spt:
◦ Anoreksia, heart burn, lidah (glossitis atau
kudis), splenomegali, hepatomegali
Manifestasi Klinikal
5. Sistem saraf pusat spt:
◦ Dizziness, Giddiness, Tingling
sensation(kebas), insomnia, dimness of vision,
pelupa, kurang konsentrasi.
6. Sistem Pembiakan spt:
◦ Amenorrhea, Menorrhagia, Abortion
7. Kuku – Koilonychia
8. Rambut - nipis
Pallor
Koilonichia
Glossitis
Hepatospleenomegaly
 Investigasi
1. Full Blood Count- mengesan anemia,
thrombositopenia dan jangkitan
2. Full Blood Picture- kesan morfologi sel
darah
3. MCV- kesan jumlah sel darah merah
4. MCHC- kesan isipadu sel darah merah
5. Serum vit B12- kesan vit B12 dlm darah
6. Serum Ferritin - <15g/L
7. Total Iron Binding Capacity (TIBC) -
>380g/dL
8. Serum Iron (SI) - <50g/dL
7. Bone marrow aspiration – for FBC &
FBP
8. Direct Coomb’s Test – kesan IgG
(Hemolitik Anemia)
9. Gastric analysis – Mengesan ahidrokloria
10. Serum Bilirubin – Mengesan jaundis
11. Renal Profile – Mengesan fungsi ginjal
Nilai normal FBC

Lelaki Wanita

Red cell count 4.4-6.1 4.2-5.4

Hg (g/dl) 13.0-18.0 11.5-16.5
Haematocrit
0.40-0.54 0.37-0.47
(pcv)
Erythrocyte Indices
a) Mean Corpuscular Volume (MCV) –
mengukur purata isipadu SDM. Normal
= 80 – 94 fL
b) Red Cell Distribution Width (RDW) –
normal = 11.5 – 14.5%
c) Mean Corpuscular Hemoglobin (MCH)
– normal = 27 – 31 pg
d) Mean Corpuscular Hemoglobin
Concentration (MCHC) – normal = 32
– 36 g/dL
 Nilai FBC bagi kes Anemia
Iron Macrocytic
Deficiency Anaemia
Red cell count 4.9 2.7
Hg (g/dl) 10.4 10.4
Haematocrit
0.35 0.32
(pcv)
Intepretasi Ujian Darah (MCV)
Diagnosis Perbezaan
 Aplastic Anemia
 Hemolytic Anemia
 Iron Deficiency Anemia
 Megaloblastic Anemia
 Pernicious Anemia
 Sickle Cell Anemia
 Thalassemia, Alpha
 Thalassemia, Beta
Pengendalian kes
1. Rawatan umum:
◦ Bagi kes anemia akut dan teruk - transfusi
darah packed cell bagi kes teruk (Hb%
rendah dan Hct < 25%).
◦ Bagi kes anemia kronik tidak perlu transfusi
darah jika pesakit masih dapat menunjukkan
simptomatik anemia dan rawatan ubatan
telah diberikan.
Pengendalian kes
2. Rawatan spesifik:
◦ rawatan punca – henti pendarahan
◦ terapi zat besi- untuk ↑ penghasilan RBC
 Tab. Ferrous Sulfat 300mg TDS
 I.V dextran-zat besi 100-200mg BD
 IM imferon 2-5 ml harian
 Transfusi darah bagi kes teruk (Hb% rendah atau
Hct < 25%).
◦ Masalah kekurangan Folate
 1mg PO qd.
Pengendalian kes
 Masalah Kekurangan Vit B12
◦ IM Vit B12 100g qd selama 1/52
◦ Kemudian IM Vit B12 100 - 1000g setiap
bulan atau 2 mg oral crystaline Vit B12 setiap
hari
 Anemia penyakit kronik
◦ Rawat punca
◦ Kegagalan renal – beri recombinant human
erythropoietin 50 – 150U/kg 3 kali seminggu.
Pengendalian kes
 Anemia Sickle Cell
◦ Hydroxyurea 10 – 30mg/kg secara oral setiap
hari .
◦ Rawat jangkitan pada peringkat awal
◦ Asid Folik
◦ Painful crises – beri oksigen, analgesik, infusi
intravena dan hipertransfusi.
◦ Allogenic bone marrow transplant
Pengendalian kes
 Thalasemia
◦ Tranfusi darah untuk kekalkan Hb > 9g/dL
◦ Asid Folik
◦ Deferoximine chelation – elak terlebih Fe
◦ Spleenectomy
◦ Allogenic bone marrow transplant
 Anemia Aplastik
◦ Antithymocyte globulin + cyclosporin
◦ bone marrow transplant (pesakit muda)
Pengendalian kes
 Autoimmune hemolysis
◦ Glucocorticoid
◦ Immunosupressive agent
◦ Danazol
◦ Plasmaparesis
◦ Rituximab
 G6PD Deficiency
◦ Elakkan ubatan yang menyebabkan hemolisis
SDM
Drugs and substances should be
avoided by G6PD deficient individual
Drugs and substances (group) Examples
Anti malarial drugs Primaquin
Sulphonamides Sulphacetamid, Sulphametoxazole,
Sulphanilamid, Sulphapyridin
Sulphones Thiazolesulfone, Dapsone
Other sulphur-containing drugs Glibenclamide
Nitrofurans Nitrofurantoin(Furadantin)
Other drugs Toluidin blue, Trinitrotoluene(TNT),
Urate oxidase, Phenylhydrazine,
Furazolidone (Furoxone), Methylene
Blue, Nalidixic acid, Niridazole,
Phenazopyridine, Isobutyl Nitrite,
Acetanilide, Aspirin
Other substances Naphthalene, Moth balls, High-dose of
vitamin K or ascorbic acid
Food substance Fava beans
3. Rawatan simptomatik
◦ sedation utk rehat dan tenangkan pesakit
◦ Vitamin B Kompleks
◦ Losyen atau krim utk kulit kering
4. Penjagaan kejururawatan
◦ Rehat atas katil
◦ Mengawal tekanan darah, nadi, kadar
pernafasan dan suhu badan
◦ Diet – tinggi protein dan kalori
◦ Kebersihan diri.
Komplikasi
1. Kegagalan Jantung
2. Tumbesaran Terbantut
3. Pertahanan badan rendah (mudah
dijangkiti)
Pendidikan Kesihatan
1. Mengambil ubat mengikut arahan doktor
2. Datang untuk rawatan susulan
ditetapkan
3. Makanan berzat – terutama zat besi dan
folic acid
4. Rehat secukupnya
5. Amalkan cara hidup sihat
MAKANAN KAYA DENGAN
ZAT BESI
 ground beef,
 clams,
 spinach,
 lentils,
 baked potato with skin,
 sunflower seeds,
 and cashews.
Prognosis
 Usually, the prognosis depends on the underlying cause of the anemia.
However, the severity of the anemia, its etiology, and the rapidity with
which it develops can each play a significant role in the prognosis. Similarly,
the age of the patient and the existence of other comorbid conditions
influence outcome.
 Bleeding from esophageal varices
◦ Approximately 30% of patients with cirrhosis die from variceal bleeding. Patients with
Child class C liver disease have a 50% mortality rate. The rate of rebleeding in
medically treated patients is in excess of 70%.[10]
 Sickle cell anemia
◦ Patients who are homozygous (Hgb SS) have the worst prognosis, because they tend
to have more frequent crises. Patients who are heterozygous (Hgb AS) have sickle cell
traits, and they have crises only under extreme conditions.
 Thalassemias
◦ Patients who are homozygous for beta thalassemia (Cooley anemia or thalassemia
major) have a worse prognosis than do patients with any of the other thalassemias
(thalassemia intermedia and thalassemia minor). These few years have witnessed
groundbreaking advancements in the treatment of thalassemias, especially with iron
chelation therapies, allowing thalassemia patients to live well into adulthood.[9] Patients
who are heterozygous for beta thalassemia have mild microcytic anemia that is not
clinically significant.
 Aplastic anemia
◦ Chances of survival are poorer for patients with idiosyncratic aplasia caused by
chloramphenicol and viral hepatitis and better when paroxysmal nocturnal
hemoglobinuria or anti-insecticides are the probable etiology. The prognosis for
idiopathic aplasia lies between these 2 extremes, with an untreated mortality rate of
approximately 60-70% within 2 years after diagnosis.
◦ The 2-year fatality rate for severe aplastic anemia is 70% without bone marrow
transplantation or a response to immunosuppressive therapy.
 Hyperplasia
◦ Among patients with a hyperplastic bone marrow and decreased production of RBCs,
one group has an excellent prognosis, and the other is unresponsive, refractory to
therapy, and has a relatively poor prognosis. The former includes patients with
disorders of relative bone marrow failure due to nutritional deficiency in whom
proper treatment with vitamin B-12, folic acid, or iron leads to a correction of anemia
once the appropriate etiology is established. Drugs acting as an antifolic antagonist or
inhibitor of DNA synthesis can produce similar effects.
◦ Certain patients with marrow hyperplasia (see the image below) may have refractory
anemia for years, but some of the group eventually develop acute myelogenous
leukemia.
 Other conditions
◦ In ectopic pregnancy, the prognosis with prompt
management is excellent, with a mortality rate of about 1-
2%.
◦ In patients with hemophilia, about 15% of them eventually
develop inhibitors to factor VIII and may die from bleeding
complications.
◦ Patients with idiopathic thrombocytic purpura (ITP)
usually respond to immunosuppression or splenectomy
and have an excellent prognosis.
◦ Approximately 80-90% of patients who have TTP and
undergo plasmapheresis recover completely.
◦ Hemolytic-uremic syndrome carries a significant morbidity
and mortality if untreated. As many as 40% of those
affected die, and as many as 80% develop renal
insufficiency.
Sekian
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