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LAPORAN PRATIKUM EVIDENCE BASED MEDICINE

KELOMPOK 24 D Ghozi Natul Isral Melati Asri Vekky Tria Novanda Larissa Ardelia Ulva Desti Wahyuni Muhammad Iqbal Dinda Putri Amir Husnul Khotimah (10313110) Amwal Halil ( Ranisha Arulrajah (1010314011)

DOSEN PEMBIMBING : dr. Darwin Amir UNIVERSITAS ANDALAS 2010

Scenario
A 26-years-old account consulted her general practitioner with the complaint of increasing tiredness and fatique over a 6-week period accompanied by a weight loss of about 8 kg. The symptoms had started after a particularly severe upper respiratory infection accompanied by an intensely sore throat, cough and muscle aches and pains. At first the symptoms were tolerable but, on return to work, she found that by mid-morning she was exhausted. Any form of physical exertion was difficult and followed by severe fatique. She had taken two weeks off work and had rested but had found that the lack of energy and concentration did not improve. Six months previously she had had a period of disturbed sleep characterized by waking at 2-3 a.m. this had followed the break-up of four-year relationship, and had been associated with feelings of tiredness and loss of appetite. She had gradually recovered without treatment although she had depressed. Four years previously she had had an iron deficiency anemia attributed to menorrhagia. this had responded to oral iron. She had been taking an oral contraceptive since that time. on examination she was 5'7'' and weighed 50 kg. She looked tired. BP 90/65. P 66 regular she was not clinically anaemic. There was no lymph node enlargement. There was no abnormalities in the heart, lungs or abdomen. The optic fundi and CNS examination were abnormal.

Skenario
Seorang yang berusia 26 tahun, mengkonsultasikan hasil pemeriksaan umumnya dengan keluhan meningkatnya rasa lelah dan keletihan selama 6 minggu periode diikuti dengan turunnya berat badan sebanyak 8 kg. gejala dimulai setelah infeksi saluran perenapasan atas diikuti dengan nyeri pada kerongkongan, batuk, serta sakit otot dan nyeri. Pertama-tama gejala dapat dikendalikan, tapi saat mulai bekerja, di tengah tengah pekerjaan dia kehabisan tenaga. Dia sudah berhenti bekerja selama dua minggu dan beristirahat tetapi, kekurangan energi dan susah berkonsentrasi. Enam bulan sebelumnya dia mengalami gangguan pada karakteristik periode tidur dengan terbangun pada jam 2-3 dini hari, ini diawali dengan berhentinya hubungan yang telah berjalan selama empat tahun yang diikuti dengan persaan lelah dan kehilangan selera. Dia biasanya menghiraukan tanpa berkonsultasi dengan dokter umumnya. ia perlahanlahan pulih tanpa pengobatan meskipun ia depresi. empat tahun sebelumnya dia mengalami anemia deficiency besi yang disebabkan menoragia. Ini telah diobati oleh oral iron. dia sudah memakai kontrasepsi oral sejak saat itu. pada pemeriksaan dia 5'7'' dan berat 50 kg. Ia tampak lelah. BP 90/65. P 66 biasa dia tidak klinis anemia. Tidak ada pembesaran kelenjar getah bening. Tidak ada kelainan pada jantung, paru-paru atau perut. pemeriksaan mata dan pemeriksaan Sistem Saraf Pusat normal.

Step 1 Define Problem mampu mengetahui masalah (penyakit) yang sedang dihadapi pasien dan mengubah masalah tersebut menjadi pertanyaan yang dapat dijawab. Pertanyaan klinik yang relevan dapat di jawab dengan mengandung unsur : 1. Patient (Pasien) A 26-years-old account consulted her general practitioner… Seorang yang berusia 26 tahun, mengkonsultasikan hasil pemeriksaan umumnya… She had gradually recovered without treatment although she had depressed. ia perlahan-lahan pulih tanpa pengobatan meskipun ia depresi. Dengan gejala : a. empat tahun yang lalu pasien mengalami anemi defisiensi besi diikuti dengan menorrhagia. b. sejak saat itu dia mengonsumsi kontrasepsi oral c. pasien berkonsultasi kepada dokter dengan keluhan peningkatan keletihan dan rasa lelah selama lebih dari 6 minngu disertai penurunan berat badan sebanyak 8 kg.uan d. gejala dimulai setelah pasien mengalami infeksi saluran pernapasan atas disertai nyeri tenggorokan, batuk, dan nyeri otot dan beberapa sakit. e. beberapa aktivitas fisik sulit dilakukan dan diikuti dengan kelelahan yang parah. f. pasien memutuskan untuk cuti kerja untuk beristirahat, namun energy dan konsentrasinya tidak ada peningkatan g. karena permasalahan pribadi pasien mengalami gangguan tidur serta sering terbangun di pagi hari diikuti dengan rasa lelah dan hilangnya selera makan. h. pasien berangsur-angsur membaik tanpa pengobatan. i. dokter menyimpulkan pasien mengalami depresi ringan j. dalam pemeriksaan, pasien terlihat kurus, tensinya rendah (BP 90/65),nadinya secara klinis dia tidak terkena anemia k. tidak ada pembesaran kelenjar getah bening l. tidak ada gangguan jantung, paru, dan perut. m. pemeriksaan sisem saraf pusat dan mata normal ,

3. COMPARISON Terapi pengobatan menorrhagia : 1. Suplemen zat besi 2. Kontrasepsi oral 3. Suntikan hormone 4. Obat-obatan yang membantu penghambatan keluar darah

Terdapat beberapa jenis klasifikasi dari anemia. Micrositik hipokronik yaitu kekurangan zat besi (fe). Anemia aplastik 3. balita.STEP 2 Tracking down the information sources needed Medical literature which can assist in providing answers to the question raised in clinical practice is broadly scattered. Makrositik normokromik ( megaloblastik) yaitu kurang asam folat dan vitamin B12  anemia aplastik . family medicine journals and government reports. remaja). antara lain: 1. Anemia defisiensi ini masih dapat dibagi lagi menjadi beberapa klasifikasi secara morfologis. Anemia defisiensi 2. Anemia defisiensi besi ini dapat disebabkan oleh: masukan besi kurang atau rendah : makanan kurang mengandung besi. pengeluaran yang berlebihan ( diare ) kebutuhan yang meningkat kebutuhan yang meningkat ini biasanya terjadi pada : masa pertumbuhan (seperti pada bayi. Anemia Hemolitik 4. wanita pada masa menstruasi. journals. penyerapan kurang baik. Anemia Pasca perdarahan mari kita coba bahas satu persatu klasifikasi dari enemia menurut etiologinya. klasifikasi anemia berdasarkan etiologi atau penyebabnya dibagi menjadi 1. wanita hamil dan menyusui. piridoksin atau tembag. pengeluaran berlebihan ( infeksi cacing dan lain sebagianya) 2.  Anemia defisiensi anemia defisiensi yaitu anemia yang disebabkan oleh karena kekurangan bahan baku pembuat sel darah atau kekurangan salah satu atau beberapa bahan yang diperuntukkan untuk pematangan eritrosit.

ulkus peptikum. anemia is typically defined as hemoglobin level of less than 13.anemia aplastik adalah anemia yang disebabkan oleh karena rusaknya sumsum tulang. obat. radiasi. For men. obat. epistaksis What is anemia? Anemia is a medical condition in which the red blood cell count or hemoglobin is less than normal.0 gram/100ml. perdarahan kronis seperti pada orang cacingan. infeksi. sitostatika. berdasarkan penyebab hemolisenya dapat dibagi lagi menjadi: 1. didapat : bahan kimia. idiopatik  anemia pasca perdarahan anemia pasca perdarahan ini adalah terjadi akibat kehilangan darah baik secar cepat atau perlahan lahan anemia perdarahan ini dapat di klasifikasikan laagi menjadi : 1. aplasia yang mengenai sistem trombopoetik yang disebuat amegakariostatik trombositopenik purpura (ITP) penyebab dari anemia aplastik ini diantaranya adalah : • • faktor kongenital faktor didapat: diataranya karena bahan kimia. Perdarahan acut seperti karena kecelakaan. These definitions may vary slightly depending on the source and the laboratory reference used. infeksi dan idiopatik  Anemia Hemolitik Anemia hemolitik adalah anemia yang disebabkan karena terjadinya penghancuran darah sehingga umur dari eritrosit pendek ( umur eritrosit normalnya 100 sampai 120 hari). . klasifikasi dari anemia aplastik : 1. aplasia yang mengenai fratnulopoetik yang disebut agranulositosis 3. alergen. gangguan enzim dari tubuh. kongenital : faktor dari eritrosit sendiri. hemagloblastoma 2.5 gram/100ml and in women as hemoglobin of less than 12. operasi besar 2. The normal level of hemoglobin is generally different in males and females. aplasia yang mengenai sistem eritropoetik 2.

. by a loss or destruction of blood. especially the MCV. then it is called a macrocytic anemia (large cell volume). Looking at each of the components of a complete blood count (CBC). If the MCV is low (less than 80). by a decrease in production of red blood cell or hemoglobin. 2. or 2. 3. Anemia is caused essentially through two basic pathways. the anemia is categorized as microcytic anemia (low cell volume). As more common classifications of anemia (low hemoglobin) is based on the MCV. Anemia is either caused: 1. it is called a normocytic anemia (normal cell volume). a physician can gather clues as what may be the most common reason for anemia. If the MCV is in the normal range (80-100). or the volume of individual red blood cells.What causes anemia? Any process that can disrupt the normal life span of a red blood cell may cause anemia. 1. If the MCV is high. Red blood cells are made in the bone marrow. Normal life span of a red blood cell is typically around 120 days.

Can not enough iron cause anemia? Absolutely! This is because iron is major component of hemoglobin and essential for its proper function. Anemia that is due to low iron levels is called iron deficiency anemia. Iron deficiency it is a very common cause of anemia. Motrin). What about acute (sudden) blood loss as a cause of anemia? . This is generally without any major symptoms as the blood loss is relatively small and temporary. iron deficiency anemia is most often due to a diet lacking iron. Stomach ulcer bleeding that may or may no be induced by medications even very common over-the-counter drugs as aspirin and ibuprofen (Advil. Chronic blood loss due to any reason is the main cause of low iron level in the body as it depletes the body's iron stores to compensate for the ongoing loss of iron. For instance. Iron deficiency anemia can also be due to small repeated l bleeding. iron deficiency anemia usually presents with low mean corpuscular volume (microcytic anemia) in addition to low hemoglobin. In infants and young children. Women are more likely than men to have iron deficiency anemia because of the loss of blood each month through normal menstruation. for instance from colon cancer or from stomach ulcers. Interpretation of CBC may lead to clues to suggest this type of anemia.

This type of anemia could happen in people who are unable to absorb vitamin B12 from their intestines due to a number of reasons: o o strict vegetarians who may not be taking adequate vitamin supplements. along with folate. Certain chemotherapy for cancers can also cause damage to the bone marrow and decrease red blood cell production. o • For example. resulting in anemia. Finally. o o o • • • Another common cause of anemia is called anemia of chronic disease. This type of anemia could result in severe symptoms and consequences if not addressed promptly. What are other causes of anemia? Some of the most common causes include: • Vitamin B12 deficiency may cause pernicious anemia. leafy vegetables. • There can be rupture of red blood cells (hemolytic anemia) due to antibodies clinging to the surface of the red cells (for example. Some medications can cause anemia in a variety of ways. This could typically occur in individuals with long-standing chronic diseases. or cancers of the bone marrow (such as leukemia or multiple myeloma) can cause the bone marrow to inadequately produce red blood cells. resulting in anemia. This typically causes macrocytic (large cell volume) anemia. Human immunodeficiency virus (HIV) and acquired immune deficiency syndrome (AIDS) can cause anemia. patients with kidney failure may lack the hormone necessary to stimulate normal red blood cell production by the bone marrow. and also long-term heavy alcohol use. Folate deficiency can be the culprit of anemia. This may also be caused by inadequate absorption. cancers that spread (metastasize) to the bone marrow.Acute blood loss from internal bleeding (as from a bleeding ulcer) or external bleeding (as from trauma) can produce anemia in an amazingly short span of time. A wide assortment of bone marrow diseases can cause anemia. . or long-term alcoholics. hemolytic disease of the newborn and in many other conditions). Vitamin B12. Certain infections may involve the bone marrow and result in bone marrow impairment and anemia. underconsumption of green. is a involved in making the heme molecule that is an integral part of hemoglobin.

In fact. It is worth noting that if anemia is longstanding (chronic anemia). if the anemia occurs rapidly (acute anemia). appear pale. Additional symptoms may include: • • • hair loss. How is anemia diagnosed? . Depending on the degree of the genetic abnormality.Can anemia be hereditary? Yes. and become short of breath. Hereditary disorders can shorten the life-span of the red blood cell and lead to anemia (for example. and worsening of heart problems. moderate. hereditary anemias may cause mild. or severe anemia. the patient may experience significant symptoms relatively quickly. some of these anemias are so mild that they are not noticeable and are incidentally revealed during a routine blood work. malaise (general sense of feeling unwell). fatigue easily. Others with anemia may feel: • • • • • tired. On the other hand. anemia may be genetic. alpha thalassemia and beta thalassemia). some may be too severe to be compatible with life and may result in death of the fetus (unborn infant). On the other hand. the body may adjust to low oxygen levels and the individual may not feel different unless the anemia becomes severe. develop palpitations (feeling of heart racing). sickle cell anemia). What are the symptoms of anemia? Some patients with anemia have no symptoms. Hereditary disorders can also cause anemia by impairing the production of hemoglobin (for example.

CBC analysis was performed by a physician or a laboratory technician by viewing a glass slide prepared from a blood sample under a microscope. Hemoglobin 4. a fraction of one millionth of a liter. White blood cell (WBC) count 5. too. and the hemoglobin. and color of red blood cells. there is often a low red blood cell count and a low hematocrit. Platelet count Only the first three of these tests: the red blood cell (RBC) count. much of this work is often automated and done by machines. shape. Differential blood count (the "diff") 6.5 is abnormal in men less than 12. Hematocrit 3. What is a complete blood cell (CBC) count? A CBC is a test for counting and examining the different types of cells in the blood. or normal. What is the hematocrit? The hematocrit is specifically a measure of how much of the blood is made of red cells.0 in women. When there is a low hemoglobin level. Units of MCV are reported in femtoliters. too low. Six component measurements make up a CBC test: 1. which basically measures the average volume of red blood cells in a blood sample. This is important in distinguishing the causes of anemia. CBC test may be ordered by a physician as a part of routine general check-up and screening or based on clinical signs and symptoms that may suggest anemia or other blood abnormalities. The hematocrit is a very convenient way to determine whether the red blood cell count is too high. Additionally. Traditionally. Other useful clues to causes of anemia that are reported in a CBC are the size. are relevant to the diagnosis of anemia. Reference ranges are slightly different from one source to another. The hematocrit is a measure of the proportion of blood that is composed of the red blood cells. What does a low hemoglobin level mean? Low hemoglobin is called anemia. . mean corpuscular volume (MCV) is also often reported in a CBC. Today. the hematocrit.Anemia is usually detected or at least confirmed by a complete blood cell (CBC) count. but typically hemoglobin of less than 13. Red blood cell (RBC) count 2.

anemia as a result of blood loss from a stomach ulcer should begin with medications to heal the ulcer. The proportion of the tube that consists of RBCs is then measured. Epogen) may be used to stimulate bone marrow red blood cell production. Sometimes iron supplements will also be needed to correct iron deficiency. How is anemia treated? The treatment of the anemia varies greatly. http://www. surgery is often necessary to remove a colon cancer that is causing chronic blood loss and anemia. In certain patients with bone marrow disease (or bone marrow damage from chemotherapy) or patients with kidney failure. First. Vitamin B12 injections will be necessary for patients suffering from pernicious anemia or other causes of B12 deficiency. epoetin alfa (Procrit.medicinenet.How is hematocrit determined? The RBCs in the sample of blood are packed down by spinning the tube in a centrifuge under prescribed conditions. For example. the underlying cause of the anemia should be identified and corrected. In severe anemia. then it should be discontinued under the direction of the prescribing doctor.com/anemia Anemia Classification and external resources . The hematocrit is 45. blood transfusions may be necessary. Likewise. If a medication is thought to be the culprit. Let's say that it is 45%.

also spelled anaemia and anæmia. There are two major approaches: the "kinetic" approach which involves evaluating production. ICD-10 ICD-9 DiseasesDB MedlinePlus eMedicine MeSH D50. Anemia can be classified in a variety of ways. anemia leads to hypoxia (lack of oxygen) in organs. meaning lack of blood) is a decrease in normal number of red blood cells (RBCs) or less than the normal quantity of hemoglobin in the blood.[3] and the "morphologic" approach which groups anemia by red blood cell . to mention a few. destruction and loss. 280-285 663 000560 med/132 emerg/808 emerg/734 D000740 Anemia (pronounced /əˈniːmiə/. it can include decreased oxygen-binding ability of each hemoglobin molecule due to deformity or lack in numerical development as in some other types of hemoglobin deficiency.The pale hand of a woman with severe anemia (right) in comparison to the normal hand of her husband (left). and discernible clinical spectra. underlying etiologic mechanisms. Because hemoglobin (found inside RBCs) normally carries oxygen from the lungs to the tissues.-D64. The three main classes of anemia include excessive blood loss (acutely such as a hemorrhage or chronically through low-volume loss). based on the morphology of RBCs.[1][2] However. from Ancient Greek ἀναιμία anaimia. varying degrees of anemia can have a wide range of clinical consequences. Because all human cells depend on oxygen for survival. There are several kinds of anemia. produced by a variety of underlying causes. excessive blood cell destruction (hemolysis) or deficient red blood cell production (ineffective hematopoiesis). Anemia is the most common disorder of the blood.

g. On examination. general malaise and sometimes poor concentration. Most commonly. focusing early on the question of production may allow the clinician to more rapidly expose cases where multiple causes of anemia coexist. In very severe anemia. Pica. paper. The patient may have symptoms related to this. They may also report shortness of breath. and cardiac enlargement. the consumption of non-food based items such as dirt. people with anemia report non-specific symptoms of a feeling of weakness. The morphologic approach uses a quickly available and cheap lab test as its starting point (the MCV). There may be signs of specific causes of anemia. koilonychia (in iron deficiency). The signs and symptoms can be related to the anemia itself. On the other hand. dyspnea. grass. there may be signs of a hyperdynamic circulation: a fast heart rate (tachycardia). In severe anemia. bone deformities (found in thalassaemia major) or leg ulcers (seen in sickle cell disease). the signs exhibited may include pallor (pale skin. intermittent claudication of the legs. angina (if preexisting heart disease is present). and symptoms can be minor or vague.size. on exertion. the body may compensate for the lack of oxygen carrying capability of the blood by increasing cardiac output. jaundice (when anemia results from abnormal break down of red blood cells — in hemolytic anemia). may be a symptom of iron deficiency. although it occurs often in those who have normal levels of hemoglobin. There may be signs of heart failure. or fatigue. • Signs and symptoms Main symptoms that may appear in anemia Anemia goes undetermined in many people. and symptoms of heart failure. ice. mucosal linings and nail beds) but this is not a reliable sign. e. and hair.. . wax. or the underlying cause. flow murmurs. such as palpitations.

Generally. and is sometimes a necessity in regions of the world where automated analysis is less accessible. vague bruises.0 Hb threshold (mmol/l) 6. Restless legs syndrome is more common in those with iron deficiency anemia. MCH and MCHC) to be calculated.5 12. Apart from reporting the number of red blood cells and the hemoglobin level. increased sweating. Examination of a stained blood smear using a microscope can also be helpful. four parameters (RBC count.6206 mmol/L)[citation needed] Age or gender group Children (0. WHO's Hemoglobin thresholds used to define anemia[5] (1 g/dL = 0. MCV and RDW) are measured. which is an important tool in distinguishing between the causes of anemia. non-pregnant (>15yrs) Hb threshold (g/dl) 11.0 11.Chronic anemia may result in behavioral disturbances in children as a direct result of impaired neurological development in infants. and compared to values adjusted for age and sex. the automatic counters also measure the size of the red blood cells by flow cytometry. vomiting. allowing others (hematocrit.8 7. clinicians request complete blood counts in the first batch of blood tests in the diagnosis of an anemia.4 7. and blood in stool. hemoglobin concentration.4 .5–5. and reduced scholastic performance in children of school age. chronic heartburn. Some counters estimate hematocrit from direct measurements.1 7. Diagnosis Peripheral blood smear microscopy of a patient with iron-deficiency anemia. Less common symptoms may include swelling of the legs or arms. In modern counters.0 yrs) Children (5–12 yrs) Teens (12–15 yrs) Women.0 12.

radiographic findings. If the degree of anemia is significant. Even where the source of blood loss is obvious. If an automated count is not available. or clinical signs of bleeding. In manual examination. elevated LDH suggesting cell destruction. serum iron. Clinical signs of loss or destruction include abnormal peripheral blood smear with signs of hemolysis. hemoglobin electrophoresis.0 13. and at what rate. serum creatinine). When the diagnosis remains difficult. evaluation of erythropoiesis can help assess whether the bone marrow will be able to compensate for the loss. or frank bleeding. even a "normal" reticulocyte count actually may reflect an inadequate response. activity of the bone marrow can also be gauged qualitatively by subtle changes in the numbers and the morphology of young RBCs by examination under a microscope. serum vitamin B12. pregnant Men (>15yrs) 11. renal function tests (e. particularly the blood reticulocyte (precursor of mature RBCs) count. destruction or loss The "kinetic" approach to anemia yields what many argue is the most clinically relevant classification of anemia. Production vs.8 8.g. The reticulocyte production index is a calculation of the ratio between the level of anemia and the extent to which the reticulocyte count has risen in response. transferrin. RBC folate level. When the cause is not obvious. and the "kinetic" approach to anemia. This then yields the classification of defects by decreased RBC production versus increased RBC destruction and/or loss. The following is a simplified schematic of this approach: . a bone marrow examination allows direct examination of the precursors to red cells. a reticulocyte count can be done manually following special staining of the blood film.1 SSSReticulocyte counts. clinicians use other tests: ESR.0 6. Newly formed RBCs are usually slightly larger than older RBCs and show polychromasia. A reticulocyte count is a quantitative measure of the bone marrow's production of new red blood cells. This classification depends on evaluation of several hematological parameters. in part because some automatic counters now have the capacity to include reticulocyte counts. such as guiaic-positive stool. ferritin. have become more common than in the past in the large medical centers of the United States and some other wealthy nations.Women.

Reticulocyte production index shows appropriate response to anemia = ongoing hemolysis or blood loss without RBC production problem.Anemia Reticulocyte production index shows inadequate production response to anemia. No clinical Clinical findings Clinical findings and normal .

chronic gastric bleeding with B12 and folate deficiency. In clinical workup. the MCV will be one of the first pieces of information available. with superimposed or related hemolysis or blood loss. if they are normal size (80–100 fl). Here is a schematic representation of how to consider anemia with MCV as the starting point: Anemia . anemia is classified by the size of red blood cells. The size is reflected in the mean corpuscular volume (MCV).findings consistent with hemolysis or blood loss: pure disorder of production. and if they are larger than normal (over 100 fl). sickle cell anemia with superimposed iron deficiency. Macrocytic anemia (MCV>100) Normocytic anemia (80<MCV<100) Microcytic anemia (MCV<80) * For instance. normal MCV and hemolysis or loss may be seen in bone marrow failure or anemia of chronic disease. this is either done automatically or on microscopic examination of a peripheral blood smear. If the cells are smaller than normal (under 80 fl). normocytic. the anemia is said to be microcytic. ** Confirm by repeating reticulocyte count: ongoing combination of low reticulocyte production index. and other instances of anemia with more than one cause. Red blood cell size In the morphological approach. so even among clinicians who consider the "kinetic" approach more useful philosophically. morphology will remain an important element of classification and diagnosis. the anemia is classified as macrocytic. production*. a microcytic anemia is often the result of iron deficiency. and abnormal MCV= acute hemolysis or loss MCV: hemolysis or without adequate time for bone loss and chronic marrow production to disorder of compensate**. for instance. This scheme quickly exposes some of the most common causes of anemia.

abnormal white blood cells may point to a cause in the bone marrow. and beta-thalassemia HbE syndrome HbC syndrome and various other unstable hemoglobin diseases • Sideroblastic defect o o o Hereditary sideroblastic anemia Acquired sideroblastic anemia. for example. Microcytic anemia Main article: Microcytic anemia Microcytic anemia is primarily a result of hemoglobin synthesis failure/insufficiency. including lead toxicity Reversible sideroblastic anemia .Macrocytic anemia (MCV>100) Normocytic anemia (MCV 80– 100) Microcytic anemia (MCV<80) High reticulocyte count Low reticulocyte count Other characteristics visible on the peripheral smear may provide valuable clues about a more specific diagnosis. which could be caused by several etiologies: • Heme synthesis defect o Iron deficiency anemia o Anemia of chronic disease (more commonly presenting as normocytic anemia) • Globin synthesis defect o o o o alpha-.

amebiasis. Other types of Liver Disease can also cause macrocytosis.Iron deficiency anemia is the most common type of anemia overall and it has many causes. folic acid (or both). leading to reduced vitamin B12/folate absorption. compared with only 2% of adult men. the most common cause of macrocytic anemia. Therefore one must always be aware of anemia following this procedure. • • • Hypothyroidism Alcoholism commonly causes a macrocytosis. Intrinsic factor is required to absorb vitamin B12 from food. • • Iron deficiency anemia is caused by insufficient dietary intake or absorption of iron to replace losses from menstruation or losses due to diseases. RBCs often appear hypochromic (paler than usual) and microcytic (smaller than usual) when viewed with a microscope. Studies[who?] have shown that iron deficiency without anemia causes poor school performance and lower IQ in teenage girls. A lack of intrinsic factor may arise from an autoimmune condition targeting the parietal cells (atrophic gastritis) that produce intrinsic factor or against intrinsic factor itself. Worldwide. The principal cause of iron deficiency anemia in premenopausal women is blood lost during menses. is due to a deficiency of either vitamin B12. while B12 deficiency does.[7] • Macrocytic anemia Main article: Macrocytic anemia • Megaloblastic anemia. upper endoscopy and lower endoscopy should be performed to identify bleeding lesions.[6] Iron is an essential part of hemoglobin. These lead to poor absorption of vitamin B12. 20% of all women of childbearing age have iron deficiency anemia. although not specifically anemia. the most common cause of iron deficiency anemia is parasitic infestation (hookworm. o Pernicious anemia is caused by a lack of intrinsic factor. schistosomiasis and whipworm). and other drugs that inhibit DNA replication. In men and post-menopausal women the chances are higher that bleeding from the gastrointestinal tract could be due to colon polyp or colorectal cancer. o Macrocytic anemia can also be caused by removal of the functional portion of the stomach. and low iron levels result in decreased incorporation of hemoglobin into red blood cells. In the United States. Iron deficiency is the most prevalent deficiency state on a worldwide basis. Folate deficiency normally does not produce neurological symptoms. such as during gastric bypass surgery. Methotrexate. Deficiency in folate and/or vitamin B12 can be due either to inadequate intake or insufficient absorption. Iron deficiency is sometimes the cause of abnormal fissuring of the angular (corner) sections of the lips (angular stomatitis). zidovudine. . Iron deficiency anemia can also be due to bleeding lesions of the gastrointestinal tract. Faecal occult blood testing.

which result in restricted cell division of the progenitor cells. red tongue and glossitis. e. There are many causes of Heinz body anemia. The treatment for vitamin B12-deficient anemia was first devised by William Murphy who bled dogs to make them anemic and then fed them various substances to see what (if anything) would make them healthy again. Evidence for multiple causes appears with an elevated RBC distribution width (RDW).. but the red blood cell size (Mean corpuscular volume) remains normal. for example in alcoholism.[9] Normocytic anemia Main article: Normocytic anemia Normocytic anemia occurs when the overall hemoglobin levels are always decreased.[8] Other features may include a smooth. Heinz body anemia Heinz bodies form in the cytoplasm of RBCs and appear like small dark dots under the microscope.g. and some forms can be drug induced. It can be triggered in dogs by ingesting onions or zinc. The cause of megaloblastic anemia is primarily a failure of DNA synthesis with preserved RNA synthesis.Macrocytic anemia can be further divided into "megaloblastic anemia" or "non-megaloblastic macrocytic anemia". which suggests a wider-than-normal range of red cell sizes.e. All three shared the 1934 Nobel Prize in Medicine. due to hookworm infestation leading to deficiency of both iron and vitamin B12 or folic acid [10] or following a blood transfusion more than one abnormality of red cell indices may be seen. there is unimpaired DNA globin synthesis. macrocytic hypochromic. . He discovered that ingesting large amounts of liver seemed to cure the disease. Causes include: • • • • Acute blood loss Anemia of chronic disease Aplastic anemia (bone marrow failure) Hemolytic anemia Dimorphic anemia When two causes of anemia act simultaneously. It is triggered in cats by eating onions[11] or acetaminophen (paracetamol). The nonmegaloblastic macrocytic anemias have different etiologies (i. In addition to the non-specific symptoms of anemia. and in horses by ingesting dry red maple leaves. George Minot and George Whipple then set about to chemically isolate the curative substance and ultimately were able to isolate the vitamin B12 from the liver. specific features of vitamin B12 deficiency include peripheral neuropathy and subacute combined degeneration of the cord with resulting balance difficulties from posterior column spinal cord pathology. The megaloblastic anemias often present with neutrophil hypersegmentation (6–10 lobes).) which occur.

[13] As with vitamin B12.[13] affecting all kinds of blood cells.[13] by insufficient erythropoietin production Anemia of endocrine disorders o o • Disturbance of proliferation and maturation of erythroblasts o Pernicious anemia[13] is a form of megaloblastic anemia due to vitamin B12 deficiency dependent on impaired absorption of vitamin B12. It generally occurs in premature infants at 2 to 6 weeks of age. it causes megaloblastic anemia Anemia of prematurity. o Pure red cell aplasia[13] o Aplastic anemia. iron deficiency. Several of these may interplay to eventually cause anemia. causing deficient globin synthesis[13] Anemia of renal failure[13] (also causing stem cell dysfunction) o o o o o • Other mechanisms of impaired RBC production o Myelophthisic anemia[13] or Myelophthisis is a severe type of anemia resulting from the replacement of bone marrow by other materials. Indeed. blood loss and fluid overload (hypervolemia). by diminished erythropoietin response to declining hematocrit levels.Causes Broadly. Fanconi anemia is a hereditary disorder or defect featuring aplastic anemia and various other abnormalities. Myelodysplastic syndrome[13] o . resulting in deficient heme synthesis[13] thalassemias. but this usually doesn't cause any lasting symptoms unless a relatively impaired RBC production develops because of iron deficiency. Anemia of renal failure. causes of anemia may be classified as impaired red blood cell (RBC) production. such as malignant tumors or granulomas. the most common cause of anemia is blood loss. increased RBC destruction (hemolytic anemias).[12] Impaired RBC production • Disturbance of proliferation and differentiation of stem cells. combined with blood loss from laboratory testing. Anemia of folic acid deficiency.

causing the erythrocytes to be sequestered and destroyed by the spleen.[13] causing defects in membrane lipids Enzyme deficiencies   Pyruvate kinase and hexokinase deficiencies. or a malignancy.[13] another defect in membrane skeleton proteins Abetalipoproteinemia. that is.[13] causing defect glycolysis Glucose-6-phosphate dehydrogenase deficiency and glutathione synthetase deficiency. are hereditary genetic disorders. o o o Hereditary elliptocytosis.o anemia of chronic inflammation[13] Increased RBC destruction Further information: Hemolytic anemia Anemias of increased red blood cell destruction are generally classified as hemolytic anemias. It is the most common of the autoimmune hemolytic diseases. except paroxysmal nocturnal hemoglobinuria.[13] causing increased oxidative stress o Hemoglobinopathies   Sickle cell anemia[13] Hemoglobinopathies causing unstable hemoglobins[13] o • paroxysmal nocturnal hemoglobinuria[13] Extrinsic (extracorpuscular) abnormalities o Antibody-mediated  Warm autoimmune hemolytic anemia is an anemia caused by autoimmune attack against red blood cells. such as chronic lymphocytic leukemia (CLL)[16][16] .[13] where there the red blood cells have defects that cause premature destruction. primarily by IgG. These are generally featuring jaundice and elevated LDH levels. • Intrinsic (intracorpuscular) abnormalities.[15] It can be idiopathic. All of these.[14] o Hereditary spherocytosis[13] is a hereditary defect that results in defects in the RBC cell membrane. drug-associated or secondary to another disease such as systemic lupus erythematosus. without any known cause.

combined with insufficient RBC production. causing acute blood loss Gastrointestinal tract lesions. or ferrous gluconate. Mild to moderate iron deficiency anemia is treated by oral iron supplementation with ferrous sulfate. It can be idiopathic[17] or result from an underlying condition. Trauma[13] or surgery. Rh disease. Cold agglutinin hemolytic anemia is primarily mediated by IgM. it is very common to experience stomach upset and/or darkening of the feces. When taking iron supplements. Iron deficiency from nutritional causes is rare in non-menstruating adults (men and postmenopausal women). . The diagnosis of iron deficiency mandates a search for potential sources of loss such as gastrointestinal bleeding from ulcers or colon cancer.[13] one of the causes of hemolytic disease of the newborn Transfusion reaction to blood transfusions[13]   o Mechanical trauma to red cells  Microangiopathic hemolytic anemias.[18] Anemia of pregnancy is anemia that is induced by blood volume expansion experienced in pregnancy.[13] also generally causing chronic blood loss Fluid overload Fluid overload (hypervolemia) causes decreased hemoglobin concentration and apparent anemia: • • General causes of hypervolemia include excessive sodium or fluid intake. including thrombotic thrombocytopenic purpura and disseminated intravascular coagulation[13] Infections. ferrous fumarate. The stomach upset can be alleviated by taking the iron with food. this decreases the amount of iron absorbed. Treatments There are many different treatments for anemia and they depend on severity and cause. sodium or water retention and fluid shift into the intravascular space. Vitamin C aids in the body's ability to absorb iron. including malaria[13] heart surgery   Blood loss • • • • Anemia of prematurity from frequent blood sampling for laboratory testing.[13] causing a rather chronic blood loss Gynecologic disturbances. however. so taking oral iron supplements with orange juice is of benefit.

[23][24] Hyperbaric oxygen Treatment of exceptional blood loss (anemia) is recognized as an indication for hyperbaric oxygen (HBO) by the Undersea and Hyperbaric Medical Society. to the recent improvements in blood banking and transfusion techniques. anemia associated with chemotherapy. at least in part. Four randomized controlled clinical trials have been conducted to evaluate aggressive versus conservative transfusion strategies in critically-ill patients. or with ongoing blood loss. The physiological principle that reduction of oxygen delivery associated with anemia leads to adverse clinical outcomes is balanced by the finding that transfusion does not necessarily mitigate these adverse clinical outcomes.Vitamin supplements given orally (folic acid) or subcutaneously (vitamin B-12) will replace specific deficiencies.[25] In 2002. Blood transfusions Doctors attempt to avoid blood transfusion in general. or anemia associated with renal disease. transfusions of donated blood are often lifesaving. at least two retrospective studies have shown increases in adverse clinical outcomes in critically ill patients that underwent more aggressive transfusion strategies. Van Meter reviewed the publications surrounding the use of HBO in severe anemia and found that all publications report a positive result. acute bleeding.[25][26] The use of HBO is indicated when oxygen delivery to tissue is not sufficient in patients who cannot be transfused for medical or religious reasons. In severe cases of anemia.[19][20][21][22] In addition.[citation needed] Transfusion of the stable but anemic hospitalized patient has been the subject of numerous clinical trials.[25] The beliefs of some religions (ex: Jehovah's Witnesses) may prohibit the receipt of transfused blood products. In severe. to stimulate red cell production. Improvements in battlefield casualty survival is attributable. In anemia of chronic disease. HBO may be used for medical reasons when threat of blood product incompatibility or concern for transmissible disease are factors.[27] See also • • Human iron metabolism List of circulatory system conditions . a blood transfusion may be necessary. epoetin alfa. some clinicians prescribe recombinant erythropoietin. since multiple lines of evidence point to increased adverse patient clinical outcomes with more intensive transfusion strategies. All four of these studies failed to find a benefit with more aggressive transfusion strategies.

delta) · Sickle-cell disease/trait · HPFH Hereditary Hemolytic (mostly Normo-) membrane: Hereditary spherocytosis (Minkowski-Chauffard syndrome) · Hereditary elliptocytosis (Ovalocytosis) · Hereditary stomatocytosis Red blood cells Acquired Autoimmune (WAHA. HK) hemoglobinopathy: Thalassemia (alpha.74. beta. CAD.Pathology: hematology · hematologic diseases of RBCs and megakaryocytes / MEP (D5069. PCH . TI. 280-287) ↑Polycythemia Polycythemia vera ↓Anem Nutritional ia Micro-: Iron deficiency anemia (Plummer-Vinson syndrome Macro-: Megaloblastic anemia (Pernicious anemia) enzymopathy: G6PD · glycolysis (PK.

Purpura n/ fulminans) · autoimmune (Antiphospholipid) coagulopat hy/ bleeding diathesis ↓ Nonthrombocytopenic purpura: Henoch-Schönlein purpura ↑ Thrombocytopenia Thrombocytopenic purpura: ITP (Evans syndrome) · TM (TTP) and purpura Heparin-induced thrombocytopenia · May-Hegglin anomaly .membrane (PNH) MAHA · TM (HUS) Drug-induced autoimmune · Drug-induced nonautoimmune Hemolytic disease of the newborn Hereditary: Fanconi anemia · Diamond–Blackfan anemia Aplastic (mostly Normo-) Acquired: PRCA · Sideroblastic anemia · Myelophthisic Blood tests MCV (Normocytic. Macrocytic) · MCHC (Normochromic Hypochromic) Other Methemoglobinemia · Sulfhemoglobinemia · Reticulocytopenia Thrombocytosis Essential thrombocytosis primary: Antithrombin III deficiency · Protein C deficiency/Activated protein C resistance/Protein S Coagulatio Hypercoagulabilitydeficiency/Factor V Leiden · Hyperprothrombinemia acquired: DIC (Congenital afibrinogenemia. Microcytic.

the brain is protected by the skull.[1] • Development . Gray platelet syndrome) Clotting factor Hemophilia (A/VIII.wikipedia.org/wiki/Anemia" Categories: Hematology | Anemias | Blood disorders | Hematopathology M: MYL drug (B1/2/3+5+6). heme. btst http://en. btst Retrieved from "http://en. It contains the majority of the nervous system and consists of the brain and the spinal cord. all multicellular animals except sponges and radially symmetric animals such as jellyfish. and both are enclosed in the meninges. In vertebrates. rbmg/mogr/tumr.org/wiki/Anemia Central nervous system The central nervous system (CNS) is the part of the nervous system that integrates the information that it receives from. C/XI) • Von Willebrand disease • Hypoprothrombinemia/II · XIII cell/phys (coag. Together with the peripheral nervous system. The CNS is contained within the dorsal cavity. all parts of the bodies of bilaterian animals—that is. gran) sysi/epon.wikipedia. as well as the retina. with the brain in the cranial cavity and the spinal cord in the spinal cavity. B/IX. while the spinal cord is protected by the vertebrae. it has a fundamental role in the control of behavior. and coordinates the activity of.Platelet function adhesion (Bernard-Soulier syndrome) · aggregation (Glanzmann's thrombasthenia) · platelet storage pool deficiency (Hermansky-Pudlak syndrome.

and its cavity forms the third ventricle. Hippocampus. the hippocampus and the neocortex. and ultimately meet. This tube initially differentiates into three vesicles (pockets): the prosencephalon at the front. Lateral . Basal ganglia. the rhombencephalon. As the vertebrate grows. The telencephalon differentiates into. Amygdala. between the mesencephalon and the spinal cord. the ectodermal wall of which forms the rudiment of the nervous system. Neocortex. the mesencephalon. pretectum. and the rhombencephalon divides into the metencephalon and myelencephalon. (By six weeks in the human embryo) the prosencephalon then divides further into the telencephalon and diencephalon. The tectum. hypothalamus. The metencephalon becomes. Diencephalon elaborations include the subthalamus. and. among other things. and their cavities develop into the fourth ventricle. these vesicles differentiate further still.Development of the neural tube Main article: Neuroanatomy During early development of the vertebrate embryo. the myelencephalon forms the medulla oblongata. and its cavity becomes the first and second ventricles. the pons and the cerebellum. and its cavity grows into the mesencephalic duct (cerebral aqueduct). cerebral peduncle and other structures develop out of the mesencephalon. transforming the groove into a closed tube. the striatum. among other things. a longitudinal groove on the neural plate gradually deepens as ridges on either side of the groove (the neural folds) become elevated. Brain regions of a 4 week old human embryo Central nervous Brain Prosencephalon Telencephalon system Rhinencephalon. thalamus and epithalamus.

[4] Like planarians. members of the phylum Platyhelminthes (flatworms). Pretectum. Thalamus. Mesencephalic duct Metencephalon Rhombencephalon Myelencephalon Spinal cord Evolution Main article: Brain See also: Encephalization and Archicortex Pons. Hypothalamus. and longitudinal nerve cords form the CNS. the laterally projecting nerves form the PNS. Subthalamus. A molecular study found that more than 95% of the 116 genes involved in the nervous system of planarians. clearly defined delineation of a nervous system into a central nervous system (CNS) and a peripheral nervous system (PNS). also exist in humans. consisting of two fused anterior ganglia. though more complex than those of planarians. Cerebellum Medulla oblongata Mesencephalon Brain stem The central nervous system (2) is a combination of the brain (1) and the spinal cord (3). vertebrates have a distinct CNS and PNS.ventricles Diencephalon Epithalamus. . which includes genes related to the CNS. Pituitary gland.[2] [3] Their primitive brain. Third ventricle Tectum. Cerebral peduncle. Pineal gland. have the simplest. Planarians.

had no children and was not a frequent attender at the surgery. The major trend that can be observed is towards a progressive telencephalisation: the telencephalon of reptiles is only an appendix to the large olfactory bulb. the allometric study of brain size among different species shows a striking continuity from rats to whales.gyri and sulci . serta retina. SSP yang terkandung di dalam rongga punggung. outermost part of the cerebral cortex known as the neocortex. Indeed. She worked long and irregular hours for an IT company. Ini berisi sebagian dari sistem saraf dan terdiri dari otak dan sumsum tulang belakang. opossums. amphibians. The area of the neocortex of mice is only about 1/100 that of monkeys. dengan otak dalam rongga tengkorak dan sumsum tulang belakang di rongga tulang belakang. She occasionally drank alcohol and had a BMI of 29. She had attended because she wantedablood test. [1] Mrs Smith was a 43-year-old housewife who was generally well and healthy but led a stressful life. and that of monkeys is only about 1/10 that of humans. otak dilindungi oleh tengkorak. .[5] In addition. Mammals – which appear in the fossil record after the first fishes. In the human brain. the size and complexity of the neocortex increased over time. ia memiliki peranan penting dalam kontrol perilaku. Mrs Smith attended the surgery complaining of feeling tired all the time for about three months. She woke up in the morning still feeling tired and not refreshed. rats lack convolutions in their neocortex (possibly also because rats are small mammals). and allows us to complete the knowledge about the evolution of the CNS obtained through cranial endocasts. semua hewan multisel kecuali spons dan binatang radial simetris seperti ubur-ubur. dan mengkoordinasikan kegiatan. dan keduanya tertutup di meninges.[6] Within placental mammals. sedangkan sumsum tulang belakang dilindungi oleh tulang belakang. whereas cats have a moderate degree of convolutions.[5] Sistem saraf pusat (SSP) adalah bagian dari sistem saraf yang mengintegrasikan informasi yang diterimanya dari.The basic pattern of the CNS is highly conserved throughout the different species of vertebrates and during evolution. and Tasmanian devils) lack the convolutions . She was divorced but in a stable relationship. the telencephalon covers most of the diencephalon and the mesencephalon. Bersama dengan sistem saraf perifer. while in mammals it makes up most of the volume of the CNS. She had been diagnosed with irritable bowel syndrome but was not on regular medication. and reptiles – are the only vertebrates to possess the evolutionarily recent. koalas. and humans have quite extensive convolutions. I asked her if her lifestyle could have been contributing to her symptoms and she agreed that it was a possibility.found in the neocortex of most placental mammals (eutherians). wombats.[5] The neocortex of monotremes (the duck-billed platypus and several species of spiny anteaters) and of marsupials (such as kangaroos. semua bagian tubuh hewan bilaterian-yaitu. Pada vertebrata.

At that point the penny dropped that Mrs Smith probably had coeliac disease. The rest ofher blood tests were normal. She was told not to start a gluten-free dietuntil advised by the specialists when the diagnosis was confirmed. including U&Es. I explained it was likely that she had coeliac disease. She denied taking OTC medications and I really had drawn ablank on the cause ofher anaemia. There wasnothingsignificantin the history and physical examination was unremarkable. I finally asked about family history of illnesses and the only thingshe could think of was that a cousin had an allergy to food. She had no obvious blood loss. When she then came to see me. The rest. Food on prescription Subsequently. I gave her a patient information leaflet oncoeliac disease. I added that she would have a small bowel biopsy via endoscopy to obtain definitive histological diagnosis. so I suggested that she make an appointment to see the nurse for a cervical smear. IUD check and some routine blood tests.Ienteredallherprescription foodproductsontoherrecordso she could have a repeat prescription. Mrs Smith said she thought it was to gluten. which included B12 and folate.I asked if she had any blood tests in mind and she said no but felt as if she needed a check-up. ferritin. Mrs Smith attended surgery a few days later and I delved deeper into the history. were normal. I commenced her on ferrous sulphate after she attended for some further blood tests. Mrs Smith saw a dietitian to find appropriate foods for prescription and commenced on a gluten-free diet. but the ferritin was low. Unsurprisingly. Iron deficiency Her blood tests came through a few days later. This also had the contact details of the organisation Coeliac UK. her MCV was 75fL and a blood film suggested iron deficiency. calcium and anti-tissue transglutaminase antibodies. LFTs and TFTs. and I referred her to the local coeliac service to confirm the diagnosis.3g/dL. I noticed that her cervical smear was overdue and she needed an IUD check. she had an IUD in place and had had no periods for about two years. She had the characteristic changes of coeliac disease in her small bowel biopsy. This is important asblood tests are sometimes misleading. Of interest was that her Hb was 9. and it was normal. . She had a DXA scan to exclude osteoporosis. these antibodies were positive (as were the endomysial antibodies) and I saw her the following week.

The feelings of . eat. you’re exhausted all the time. However. Understanding Depression SIGNS. it may be depression. She was reassured bythefactthattheoutlook is good when there is good compliance with agluten-free diet. and apathetic." the lows of depression make it tough to function and enjoy life like you once did. Many people use the word “depression” to explain these kinds of feelings. She had found the patient information leaflethelpful. and just getting through the day can be overwhelming. interfering with your ability to work. Learning about depression— including its signs. they feel lifeless. and have fun. and treatment—is the first step to overcoming the problem. setbacks. But when emptiness and despair take hold and won't go away. More than just the temporary "blues. But first. and disappointments. as recommended by NICE. Some people describe depression as “living in a black hole” or having a feeling of impending doom. Sadness is a normal reaction to life’s struggles. depression is different from normal sadness in that it engulfs your dayto-day life. some depressed people don't feel sad at all—instead. CAUSES AND HELP Feeling down from time to time is a normal part of life. She later told me that none ofher relatives had tested positive. but depression is much more than just sadness. In Mrs Smith's family. sleep.I saw her a month later. study. things may feel hopeless. causes. empty. I suggested that first-degree relatives might want to be screened by offering them serological testing. Hobbies and friends don’t interest you like they used to. only her and her cousin with the food allergy had coeliac disease. you need to understand depression. SYMPTOMS. What is depression? We all go through ups and downs in our mood. symptoms. When you’re depressed. Whatever the symptoms. but with help and support youcan get better.

restless. or oversleeping (also known as hypersomnia). It’s important to remember that these symptoms can be part of life’s normal lows. as if they have a death wish (e. tying up loose ends) Saying things like “Everyone would be better off without me” or “I want out. and the longer they’ve lasted—the more likely it is that you’re dealing with depression. aching muscles. Feeling agitated. the stronger they are. Your tolerance level is low. especially waking in the early hours of the morning. everything and everyone gets on your nerves.g.” A sudden switch from being extremely depressed to acting calm and happy. It's not just a warning sign that the person is thinking about suicide: it's a cry for help. Feeling fatigued. or remembering things. The deep despair and hopelessness that goes along with depression can make suicide feel like the only way to escape the pain. Self-loathing. Trouble focusing. Loss of energy. But the more symptoms you have.helplessness. Your whole body may feel heavy. Sleep changes. An increase in physical complaints such as headaches. pastimes. When these symptoms are overwhelming and disabling. You’ve lost your ability to feel joy and pleasure. and stomach pain. A bleak outlook—nothing will ever get better and there’s nothing you can do to improve your situation. Significant weight loss or weight gain—a change of more than 5% of body weight in a month. Either insomnia. with little. if any. Irritability or restlessness. Unexplained aches and pains. Depression and suicide Depression is a major risk factor for suicide. . but there are some common signs and symptoms. Common signs and symptoms of depression          Feelings of helplessness and hopelessness. that's when it's time to seek help. Loss of interest in daily activities. and worthlessness are intense and unrelenting. Concentration problems. sluggish. Signs and symptoms of depression Depression varies from person to person. hopelessness. back pain. so take any suicidal talk or behavior seriously. speeding through red lights) Calling or visiting people to say goodbye Getting affairs in order (giving away prized possessions. or sex. Strong feelings of worthlessness or guilt. or on edge. Appetite or weight changes. and even small tasks are exhausting or take longer to complete. making decisions. Warning signs of suicide include:         Talking about killing or harming one’s self Expressing strong feelings of hopelessness or being trapped An unusual preoccupation with death or dying Acting recklessly. You harshly criticize yourself for perceived faults and mistakes. Thoughts of death or suicide are a serious symptom of depression. relief. No interest in former hobbies. and physically drained. social activities.

5-4.If you think a friend or family member is considering suicide. Haemoglobin. kadar haemoglobin biasanya kurang dari 13. Karena sel ini dapat (gr/dl) 11 12 13 12 11 . Proses ini berjalan dari sel induk yang dikenal dengan sel pluripoten yang dapat membagi secara terus-menerus dan yang anak selnya membentuk tipe sel yang khusus.5 juta/mm3 dan pada wanita 3.5 Kelompok Anak Dewasa Umur 6 bulan s/d 6 tahun 6 tahun s/d 14 tahun Laki-laki Wanita Wanita hamil Eritrosit. Talking openly about suicidal thoughts and feelings can save a life. Filed under: Uncategorized | Defenisi Anemia didefinisikan sebagai berkurangnya kadar darah. Walaupun nilai normal dapat bervariasi antara laboratorium.5-5.5 gr/dl pada pria dewasa dan kurang dari 11. 2010. Normal eritrosit pada pria 4. Anemia Defisiensi Besi Posted on April 2. dan Zat Besi Setiap orang memproduksi sekitar 1012 (sel darah merah) baru tiap hari melalui proses eritropoeisis yang kompleks dan teratur dengan baik.5 juta/mm3.5 gr/dl pada wanita dewasa. express your concern and seek professional help immediately. Berikut ini merupakan tabel batas normal kadar haemoglobin dalam darah . bediferensiasi secara ireversibel.

Gower2. bikonkaf. Sel ini adalah retikulosit yang akan segera kehilangan poliribosomnya dan menjadi sel darah merah yang matang (eritrosit). Setiap sel darah merah mengandung sekitar 640 juta molekul haemoglobin dan setiap molekul haemoglobin dewasa normal (Hb A) terdiri atas 4 rantai polipeptida α2β2 masing-masing dengan gugus haemnya sendiri. Tahap selanjutnya eritroblas basofilik dengan basofilik sitoplasma yang kuat dan suatu nukleus yang padat tanpa memperlihatkan nukleolus. monosit. kelompok β. dimasukkan ke dalam suatu lapisan tipis sitoplasma. Sel pertama yang dikenali adalah proeritroblas yang merupakan sel yang besar dengan kromatin yang longgar berikatan dan anak inti jelas kelihatan dan sitoplasma basofilik. eritroblas basofilik. Lalu kemudian terbentuk eritoroblas polikromatofilik yang ditandai dengan timbulnya beberapa warna karena sitoplasma mulai dipenuhi oleh . haemoglobin. Produksi eritropoeitin meningkat pada anemia. Gen untuk rantai globin ini terdapat dalam 2 kelompok. Pada janin dan embrio. eritrosit. nukleus terus memadat dan tidak ada sitoplasma basofil yang terlihat. γ. ζ paada kromosom 16. Enam puluh lima persen haemoglobin disintesis dalam eritroblas dan 35% pada stadium retikulosit5. ε pada kromosom 11 dan kelompok α. haemoglobin Gower 1. pergeseran utama dari haemoglobin janin ke dewasa terjadi 3-6 bulan setelah lahir. Fungsi utama sel darah merah adalah mengangkut oksigen ke jaringan dan mengembalikan karbondioksida dari jaringan ke paru-paru. Eritropoeitin merangsang eritropoiesis dengan meningkatkan sel progenitor yang terikat untuk erotropoiesis6. badan kecil. menghasilkan suatu sitoplasma asidofilik uniformis yang disebut dengan eritroblas ortokromatofilik. darah dewasa normal juga berisi jumlah kecil dua haemoglobin lain. tidak dapat melepaskan oksigen secara normal. jika karena sebab metabolik atau struktural. δ.000. Sel induk multipotent akan berdiferensiasi menjadi sel-sel progenitor atau prekusor yang dalam mana karakteristik morfologi berdiferensiasi untuk pertama kali dan akan mengarah kepada sel-sel yang akan dibentuk selanjutnya5. Keduanya disebut sebagai sel induk multipotent. Untuk mencapai pertukaran gas ini. Pada suatu saat. sel ini akan melahirkan suatu seri tonjolan sitoplasma dan mendorong nukleusnya. Berat molekul HbA adalah 68. retikulosit eritroblas ortoklromatofilik (normoblas) dan eritrosit. Sel matang adalah sel yang telah berdiferensiasi mencapai tahap dimana sel telah dapat melaksanakan fungsinya. maka sel ini disebut sebagai sel induk pluripoten. Diferensiasi eritrosit meliputi pembentukan proeritroblas.menghasilkan semua tipe sel darah. Pada tahap berikutnya. Hb F dan Hb A2 yang juga mengandung rantai α tetapi rantai γ dan rantai δ masing-masing sebagai pengganti β5. Eritropoiesis diatur oleh hormon eritropoeitin. Sel ini akan berdiferensiasi menjadi satu turunan sel yang akan menjadi limfosit (sel-sel limfoid) dan turunan yang lain membentuk sel-sel mieloid yang berkembang di sumsum tulang(granulosit. eritroblas polikromatofilik. Proses pematangan adalah sintesis dan pembentukan sebuah enukleasi. sel darah merah mengandung protein khusus. yaitu eritrosit6. Hormon ini adalah suatu polipeptide. megakariosit). . Normalnya 90 % hormon ini dihasilkan di sel interstitial peritubular ginjal dan 10 % di hati dan tempat lain. Portland dan fetal banyak terdapat pada berbagai stadium.

sebagai alat angkut elektron di dalam sel dan sebagai bagian terpadu berbagai reaksi enzim di dalam jaringan tubuh. Kemudian tetramer empat rantai globin dengan masing-masing gugus haem. Agar dapat diabsorbsi. Besi mempunyai fungsi esensial dalam tubuh : sebagai alat angkut oksigen dari paru-paru ke jaringan tubuh. • Asam organik Seperti vitamin C sangat membantu penyerapan besi non haem dengan merubah bentuk feri menjadi bentuk fero yang mudah diserap selain itu vitamin C membentuk gugus besi. Semakin besar transferin darah membawa besi ke sumsum tulang untuk membuat 7. Di dalam mukosa besi dapat membentuk feritin sebagai simpanan besi sementara dalam sel7. Sebagian besar besi dalam bentuk feri direduksi menjadi fero. Absorpsi terjadi di bagian atas usus halus (duodenum) dengan bantuan alat bantu protein khusus yaitu protein transferin dan feritin. Piridoksal fosfat (vit B6) adalah koenzim untuk reaksi ini yang dirangsang oleh eritropoetin dan dihambat olah haem. Hal ini terjadi dalam suasana asam di dalam lambung dengan adanya HCl dan vitamin C yang terdapat di dalam makanan. Faktor-faktor yang mempengaruhi absorpsi besi: • Bentuk besi Besi-haem yang merupakan bagian dari haemoglobin dan mioglobin yang terdapat pada daging hewan dapat diserap 2 kali lipat dari pada besi non haem. Penyebaran besi dari sel mukosa ke sel tubuh bergantung pada simpanan besi dalam tubuh dan diatur oleh jumlah dan tingkat kejenuhan transferin. Besi dalam makanan terdapat dalam bentuk besi haem seperti terdapat dalam haemoglobin dan myoglobin makanan hewani dan besi non haem dalam makanan nabati. gula dan asam amino yang mengandung sulfur. . Taraf absorbsi besi diatur oleh mukosa saluran cerna yang ditentukan oleh kebutuhan tubuh7. Tranferin terdapat dalam dua bentuk. Sebelum diabsorpsi. di dalam lambung besi dibebaskan dari ikatan organik seperti protein. Akhirnya protoporfirin bergabung dengan besi untuk membentuk haem yang masing-masing molekulnya bergabung dengan rantai globin yang terbuat pada poliribosom. dari mukosa besi akan diangkut oleh transferin reseptor ke semua jaringan tubuh. Bila besi tidak dibutuhkan reseptor transferin berada dalam keadaan jenuh dan hanya sedikit besi diserap dalam mukosa dan sebaliknya.Sintesis haem terjadi banyak dalam mitokondria oleh sederet reaksi biokimia yang dimulai dengan kondensasi glisin dan suksinil koenzim A dibawah aksi enzim kunci delat-amino laevulinic acid (ALA)-sintetase yang membataasi kecepatan.askorbat yang tetap larut pada pH yang lebih tinggi dalam duodenum. Transferin mukosa mengangkat besi dari saluran cerna ke dalam sel mukosa dan sebaliknya.haemnya sendiri terbentuk dalam ‘kantong’ untuk membangun molekul haemogobin5. Besi non haem diionisasi oleh asam lambung dan direduksi menjadi fero dan dilarutkan dalam cairan pelarut seperti asam askorbat. Besi merupakan mineral mikro yang paling banyak dalam tubuh manusia yaitu sebanyak 3-5 gram di dalam manusia dewasa. besi non haem harus berada dalam bentuk terlarut.

Defisiensi besi . Yang termasuk golongan ini adalah : 1.• Asam fitat dan asam oksalat dalam sayuran. absorpsi besi non haem meningkat 10 kali dan besi haem 2 kali. Anemia mikrositik disebabkan : 1.1. • Kebutuhan tubuh akan besi berpengaruh besar terhadap absorbsi besi. sehingga anemia dapat kita klasifikasikan sebagai berikut : 1. Anemia megaloblastik. dan vitamin.1. Tahap kedua terlihat dengan habisnya simpanan besi dan meningkatnya protoporfirin (prekursor haem).2. seperti protein. tahap pertama terjadi bila simpanan besi berkurang yang terlihat penurunan feritin dalam plasma hingga 12 µg per L yang dikompensasi dengan kemampuan mengikat besi total atau TIBC. • Keasaman lambung Kekurangan asam klorida di dalam lambung atau penggunaan obat-obat bersifat basa dapat mengalami absorpsi lambung.2.7 Klasifikasi Banyak hal-hal yang dapat menimbulkan berkurangnya jumlah sel darah merah tersebut. Tahap ketiga terjadi anemia gizi besi dimana kadar haemoglobin turun di bawah normal dan eritrosit berbentuk hipokromik mikrositik. mineral-mineral. besi. Bila tubuh kekurangan atau kebutuhannya meningkat. Anemia defisiensi yaitu anemia disebabkan gangguan pembentukan haemoglobin akibat kurangnya bahan-bahan yang diperlukan.1. Selain itu dapat juga terjadi karena pendarahan akibat cacingan atau luka dan penyakit gastro intestinal.1. • Tanin Merupakan polifenol dan terdapat dalam teh dan kopi yang juga menghambat absorpsi besi dengan cara mengikatnya. disebabkan : 1. 1. Kalsium dosis tinggi berupa suplemen juga dapat menghambat absorpsi besi namun mekanismenya belum diketahui.2.7 Kehilangan besi dapat terjadi karena konsumsi makanan yang kurang seimbang atau gangguan absorpsi besi.1. Kekurangan besi terjadi dalam 3 tahap. Zat ini menghambat penyerapan besi karena mengikat besi. Defisiensi asam folat (citroforum factor) atau malabsorpsi Defisiensi vitamin B12 atau malabsorpsi 1.

• • Pembentukan antibodi yang aktif misal pada Autoimun hemolitik anemia idiopatik Drug induced . baik oleh karena pengaruh faktor-faktor dari luar eritrosit seperti infeksi.2. 3. Anemia karena penyakit ginjal menahun 2. inflamasi.2.1. dan lain-lain. • • 3.1. parasit.1. keracunan. ketidakcocokan golongan darah pada transfusi darah ataupun faktor-faktor bawaan (intrinsik). obat-obatan.2.1.1. Antibodi didapat secara pasif misal pada haemolitik disease of the new born.3. Hb E dan lain-lain.1.2. intoksikasi obat-obatan atau bahan logam.1. akibat rhesus isoimunisasi maupun A atau B isoimunisasi 3. Faktor Ekstrinsik (Ekstraselluler). • • • Kelainan struktur eritrosit Sferositosis herediter Elliptositosis hemolitik Paroksimal nokturnal haemoglobinuria Kelainan enzim (haemolitik anemia non sferositik) Defisiensi piruvat kinase Defisiensi heksokinase Kelainan sintesa Thallasemia Haemoglobin abnormal seperti Hb S. Yang termasuk kedalam golongan ini adalah : 3.3. Rusaknya pabrik sel darah ini dapat ditimbulkan oleh berbagai sebab seperti infeksi berat. Gangguan-gangguan imunologi disebabkan: 3.4. Anemia hemolitik yaitu anemia disebabkan proses hemolitik.3. Keracunan timah hitam Keadaan lain yaitu : Anemia karena infeksi.1. radiasi. 1. • • 3.2.2. Anemia aplastik yaitu anemia disebabkan rusaknya pabrik sel darah (sumsum tulang).2. Hb C. Faktor Intrinsik (Intrasellular): 3. baik sendiri maupun kombinasi 3. Hb D. atau proses keganasan 1. 1.

5. bisa berupa: • • Trombositopenia (Trobocytopenic Purpura) Trombopatia (tromboasthenia) 4. Kelainan/gangguan trombosit.4. Kelainan/gangguan kompartemen pembekuan misal: • • • • Hemofilia A Hemofilia B Von Willibrand DIC (Disseminated Intravaskular Coagulation) 4. Anemia pasca pendarahan yaitu anemia yang disebabkan karena pendarahan.3. Kelainan/gangguan kompartemen fibrinolisis akibat: • Sekunder dari penyakit hati5 Etiologi Anemia pada Remaja Putri Anemia dapat terjadi karena : . Yang termasuk kedalam golongan ini adalah: 4.1. Kelainan/ gangguan kompartemen pembuluh darah.2. Kelainan/ gangguan kompartemen jaringan • • Pada kekurangan vitamin C (scurvy) Pada keadaan lain yang jarang yaitu Sindrome Ehler Danlos dan Pseudoxanthoma elasticum 4. misal: • • • • • • Teleangiektasi hemorhagika herediter Pseudohemofilia (variant von Willibrand) Purpura Henoch schoelein Lupus eritematosus sistemik Syndrome Waterhouse Friedrichsen (karena meningokoksemia) Kekurangan vitamin C atau scorbut 4.• Simtomatik seperti pada malaria 4.

lesu. yang walaupun kaya akan zat besi.• Defisiensi zat gizi yang berperan dalam eritropoesis. Pada masa pertumbuhan seperti pada remaja. Kurangnya asupan vitamin C (scurvy). berupa badan lemah. Kecacingan (terutama cacing tambang). • Meningkatnya kebutuhan tubuh akan zat besi. stomatitis angularis. Gejala umum anemia yang disebut sebagai sindrom anemia (anemic syndrome). fungsi kognitif yang buruk. tetapi mungkin berkaitan dengan berkurangnya besi dalam enzim yang mengandung besi. 2. Pada anak. cepat lelah. seperti zat besi. Sejalan dengan berkembangnya keadaan ini. ayam). dan penurunan perkembangan psikomotor. • Meningkatnya pengeluaran zat besi dari tubuh. Diagnosis Gejala Klinis Jika terjadi defisiensi besi. Menurunkan kemampuan dan konsentrasi belajar. serta telinga berdenging. Kebutuhan normal pada remaja putri adalah 14-25 mg/hari.5mg/hari. bergerigi atau kuku sendok (kolonikia). Infeksi cacing tambang menyebabkan perdarahan pada dinding usus. meskipun sedikit tetapi terjadi terus menerus yang mengakibatkan hilangnya darah atau zat besi. defisiensi besi sangat bermakna karena dapat menyebabkan timbulnya iritablitas. Penyebab terjadinya perubahan sel epitel tidak jelas. disphagia akibat adanya selaput faring(sindrom Paterson-Kelly atau Plummer-Vinson) dan keinginan makan yang tidak biasa (oika). asam folat. namun hanya sedikit yang bisa diserap dengan baik oleh usus. hati. Makanan nabati (dari tumbuh-tumbuhan) misalnya sayuran hijau tua. . Mengganggu pertumbuhan sehingga tinggi badan tidak mencapai optimal. vitamin B6 dan vitamin E.7 Akibat anemia pada remaja putri :3 1. Perdarahan atau kehilangan darah pada waktu haid berarti mengeluarkan zat besi yang ada dalam darah rata-rata sebanyak 0. cadangan retikulo endotel (hemosiderin dan feritin) habis seluruhnya sebelum timbul anemia. Makanan yang kaya akan kandungan zat besi adalah : makanan yang berasal dari hewani (seperti ikan. Menurunkan kemampuan fisik.vitamin B12. 3. mata berkunang-kunang. kuku rapuh. daging. kebutuhan tubuh akan zat besi meningkat tajam. pasien dapat mengalami gejala dan tanda umum anemia dan mengalami glositis yang tidak nyeri. yang dapat meningkatkan absorbsi zat besi.

Pada hapusan darah tepi menunjukkan anemia hipokromik mikrositer pada anemia defisiensi besi dan makrositik megaloblastosis pada defisiensi asam folat dan vitamin B12. emia. • • • • Diagnosis Banding • Thallasemia (khususnya thallasemia minor) : o Hb A2 meningkat o o Feritin serum dan timbunan Fe tidak turun Anemia karena infeksi menahun :  biasanya anemia normokromik normositik. pada anemia aplastik.• • Irritabilitas dan anoreksia merupakan gejala yang khas pada kasus-kasus yang lanjut. Bila diberi pengobatan maka perobahan gejala ini nampak walaupun perbaikan hematologis belum bermakna. Kadang-kadang terjadi anemia hipokromik mikrositik Feritin serum dan timbunan Fe tidak turun Keracunan timah hitam (Pb)     terdapat gejala lain keracunan P Anemia sideroblastik : .TIBC meningkat. menurun pada anemia aplastik dan normal pada anemia defisiensi besi dengan hemosiderin menurun hingga menghilang. Serum feritin : jika kurang dari 10 µg/l. Pada anemia defisiensi besi. retikulosit normal atau menurun. Sumsum tulang : marrow sellularity meningkat pada anemia hemolitik. koilonichia. ikterus pada anemia hemolitik. uria. saturasi sering 15% atau kurang. pika pada anemia defisiensi besi. Pada . MCV menurun. Atropi papil lidah. angular cheilitis. dimana hal ini menunjukkan defisiensi besi pada jaringan. MCHC menurun. Free Erithrocyte Protoporphyrin (FEP) meningkat. Retikulositosis.5 Pemeriksaan laboratorium • • • • • Penurunan kadar haemoglobin mulai dari ringan sampai berat. Pansitopenia.

10 Suplementasi TTD (Tablet Tambah Darah) pada remaja putri dilakukan secara mandiri dengan dosis 1 tablet seminggu sekali minimal selama 16 minggu. untuk memperbanyak asupan asam folat dan vitamin B-12 yang banyak terdapat di hati. 10 • Suportif Makanan gizi seimbang terutama yang mengandung kadar besi tinggi yang bersumber dari hewani (limfa. Asam askorbat 100 mg/15 mg besi elemental (untuk meningkatkan absorbsi besi).10 Langkah Promotif/Preventif Upaya penanggulangan AKB diprioritaskan pada kelompok rawan yaitu BALITA. sarden. 10 . Anemia aplastik dapat diterapi dengan transplantasi sumsum tulang. wanita usia subur termasuk remaja putri dan pekerja wanita. separuh dari deficit dikoreksi pada minggu IV-V dan mencapai level normal pada bulan IIIV. respon yang diharapkan yaitu : Retikulositosis pada minggu I-II. memenuhi kebutuhan zat besi pada masa pertumbuhan cepat. Anemia berat memerlukan tindakan transfusi darah terutama pada kasus akut Kalau penyebabnya adalah infeksi seperti cacingan. anak usia sekolah. kecuali jika perdarahan masih terus berlangsung. dan kacang-kacangan. kopi. meningkatnya konsentrasi pada minggu IIIIV. 10 Terapi yang dilakukan pada Anemia Defisiensi Besi lebih disukai melalui oral. telur.25 mg asam folat dalam setiap Sulfat Ferous 200 mg. ibu hamil dan menyusui. terdapat ring sideroblastik pada pemeriksaan sumsum tulang 9 Terapi • Medikamentosa Pemberian preparat besi (ferosulfat/ferofumarat/feroglukonat) dosis 4-6 mg besi elemental/kg BB/hari dibagi dalam 3 dosis.9 Pengobatan anemia yang efektif adalah dengan mengatasi penyebabnya. daging) dan nabati (bayam. diberikan di antara waktu makan.5-2 jam setelah makan. sayuran berwarna hijau tua. Preparat besi ini diberikan sampai 2-3 bulan setelah kadar normal. 10 Pada anemia gizi maka harus diperbaiki pola makannya dengan memperbanyak konsumsi makanan yang kaya zat besi. hati. disarankan mengkonsumsi teh. kacang-kacangan). Satu tablet ini berisi 60 mg zat besi dan 0. Upaya pencegahan efektif untuk menanggulangi AKB adalah dengan pola hidup sehat dan upaya-upaya pengendalian faktor penyebab dan predisposisi terjadinya AKB yaitu berupa penyuluhan kesehatan. maka diberi antihelmintik. seperti daging merah. ikan. hati. Disarankan pula . infeksi kronis/berulang pemberantasan penyakit cacing dan fortifikasi besi. cokelat atau susu 1. keju. dan dianjurkan minum 1 tablet setiap hari selama masa haid/menstruasi. Agar zat besi dapat diabsorbsi optimal.

keganasan.10 Terapi parenteral.Terapi oral • • • • Diet yang mengandung zat besi Garam Besi Oral (Sulfas Ferossus).Folat). keracunan timbal). seperti inflamasi. dosis diturunkan atau preparat besi oralnya diganti. Sementara menstruasi yang berlangsung lebih dari 7 hari disebut sebagai hipermenorrea. penyakit ginjal. As. diare. konsentrasi menurun. pirosis. atau diagnosis penyakit yang salah (Thallasemia. Menoragia merupakan suatu kelainan menstruasi dimana perdarahan menstruasi lebih dari 80ml/hari pada siklus yang normal. penyakit hepar. konstipasi. Respon terapi yang gagal : preparat oral yang salah (tablet salut enterik. indikasinya adalah : • • • • Malabsorbsi Intoleransi terhadap preparat besi oral Pada kebutuhan yang besar yang tidak dapat diberikan secara oral Pasien yang tidak kooperatif atau tidak dapat dipantau secara rutin Contoh preparat : Iron Dextran Lama pemberian terapi : Agar simpanan besi tercukupi. Menstruasi yang berlangsung berkepanjangan dengan jumlah darah yang terlalu banyak untuk dikeluarkan setiap harinya dapat menyebabkan tubuh kehilangan terlalu banyak darah sehingga memicu terjadinya anemia. Jarang digunakan secara rutin. besi yang tidak larut dan dosis kurang). sakit kepala. MENORAGIA Siklus menstruasi yang normal berlangsung antara 21-35 hari. Terapi definitif dibutuhkan jika tetap terjadi perdarahan. merupakan yang paling aman dan murah Jangan memberi antasida atau agen penghambat produksi asam bersamaan dengan makanan Beberapa pasien mungkin tidak dapat mentoleransi dengan gejala seperti demam. adanya penyakit defisiensi lain (Vitamin B12. jari tangan dan kaki menjadi kebas. adanya penyakit yang mempengaruhi eritropoietik. Untuk mengatasinya. depresi. lama terapi yang tidak adekuat. Penderita menoragia dapat mengalami beberapa gejala seperti: • pasien perlu mengganti pembalut hampir setiap jam selama beberapa hari berturut-turut . dan metallic taste. mudah lelah. selama 2-8 hari dengan jumlah darah haid sekitar 25-80 ml/hari. perdarahan tidak terkonrol. terapi oral dilanjutkan selama 2-3 bulan setelah level normal. Gejala-gejala yang timbul akibat anemia diantaranya adalah napas menjadi lebih pendek.infeksi. dll.

dll Disfungsi organ yang menyebabkan terjadinya menoragia seperti gagal hepar atau gagal ginjal. kegemukan. mudah lelah.• • • • perlunya mengganti pembalut di malam hari atau pembalut ganda di malam hari menstruasi berlangsung lebih dari 7 hari darah menstruasi dapat berupa gumpalan-gumpalan darah terdapat tanda-tanda anemia. hiperplasia endometrium. tumor pituitari. obatobatan anti-inflamasidan obat-obatan antikoagulan Pengobatan Pengobatan menorrhagia sangat tergantung kepada penyebabnya. menorrhagia juga dapat diterapi dengan pemberian hormon dari luar. obat-obatan kemoterapi. diantaranya: a. pemeriksaan USG. Menorrhagia yang terjadi akibat adanya mioma dapat diterapi dengan melakukan terapi . polip endometrium. tes pap smear. seperti napas lebih pendek. kekurangan protrombin. siklus anovulasi. Kelainan hormon endokrin misal akibat kelainan kelenjar tiroid dan kelenjar adrenal. kurang konsentrasi. dll. pucat. Terapi zat besi perlu diberikan untuk periode waktu tertentu untuk menggantikan cadangan zat besi dalam tubuh. kanker dinding rahim dan lain sebagainya. Kelainan anatomi rahim seperti adanya mioma uteri. dan lain sebagainya. hormon steroid. dll c. misal : akibat von willebrand disease. Iatrogenik : misal akibat pemakaian IUD. adanya kelainan organik : • • • infeksi saluran reporduksi kelainan koagulasi. Untuk memastikan penyebabnya. biopsi dinding rahim. Sindrome Polikistik Ovarium (PCOS). maka zat besi perlu diberikan untuk menormalkan jumlah hemoglobin darah. d. b. Jika menoragia diikuti oleh adanya anemia. terutama untuk menorrhagia yang disebabkan oleh gangguan keseimbangan hormonal. idiopatik trombositopenia purpura (ITP). Penyakit hati kronik dapat menyebabkan gangguan dalam menghasilkan faktor pembekuan darah dan menurunkan hormon estrogen. Selain itu. dokter akan melakukan beberapa pemeriksaan seperti pemeriksaan darah. Terapi hormonal yang diberikan iasanya berupa obat kontrasepsi kombinasi atau pill kontrasepsi yang hanya mengandung progesteron. Penyebab Timbulnya perdarahan yang berlebihan saat terjadinya menstruasi (menorragia) dapat terjadi akibat beberapa hal.

hormonal atau dengan pengangkatan mioma dalam rahim baik dengan kuretase ataupun dengan tindakan operasi. ^ MedicineNet. References 1.com --> Definition of Anemia Last Editorial Review: 12/9/2000 8:31:00 AM .

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