Iron Deficiency B2

By:

GROUP 2

A 60 year old male came to the clinic with chief complaint of weakness. He had prolonged symptoms of epigastric pain and need antacid for relieving it. He has suffered from rheumatoid arthritis since five years ago and always taken Non Steroidal Anti Inflammatory Drugs. ◦ Physical examination

 General appearance: pale,fatigue  HR:94x/minute,RR:24X/minute,Temperature:36,8’C,BP:110/60mmHg  Liver and spleen non palpable, No lymphadenopathy, Epigastric pain, Cheilitis positive, koilonychias positive

◦ Laboratory:

 Hb:5 g/dL, mean corpuscular volume (MCV) is 70 fL, MCH 25,MCHC 30%,RDW:17%  Blood semear: anisocytrosis, hypochrome microcyter, poikilocytosis  Fecal occult blood: positive  Serum iron = 8 mg/dl, Iron binding capacity = 450 mg/dl, Saturation = 1,1 %, Ferritin serum = 10 mg/L

1.Epigastric pain pain in the area of the abdomen, just below where lower ribs from both sides meet. It is located below the sternum, in the midline. 2.Antacid medicines that neutralize stomach acid. 3.Rheumatoid arthritis chronic autoimmune disease that causes inflammation and deformity of the joints 4.NSAID A nonsteroidal anti-inflammatory drug, such as aspirin or ibuprofen. 5.Lymphadenopathy abnormal enlargement of the lymph nodes, usually associated with disease. 6.Cheilitis Inflammation of the lips.

7.Koilonychias means "spoon nails." It refers to abnormally thin nails (usually of the hand) which have lost their convexity, becoming flat or even concave in shape. In a sense, koilonychia is the opposite of nail clubbing. 8.Mean corpuscular volume The average volume of red cells in erythrocyte indices, calculated from the hematocrit and the red blood cell count. 9.Anisocytosis erythrocytes showing abnormal variations in size 10.Hypochrome microcyter the color of the erythrocyte is less and the size is small 11.Poikilocytosis A condition in which erythrocytes are distorted in shape.

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A 60 year old male came to the clinic with chief complaint of weakness

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He had prolonged symptoms of epigastric pain and need antacid for relieving it. He has suffered from rheumatoid arthritis since five years ago and always taken Non Steroidal Anti Inflammatory Drugs.

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Physical examination

◦ General appearance: pale,fatigue ◦ HR:94x/minute,RR:24X/minute,Temperature:36,8’C, BP:110/60mmHg ◦ Liver and spleen non palpable, No lymphadenopathy, Epigastric pain, ◦ Cheilitis positive, koilonychias positive

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Laboratory:

◦ Hb:5 g/dL, mean corpuscular volume (MCV) is 70 fL, MCH 25, ◦ MCHC 30%,RDW:17% ◦ Blood semear: anisocytrosis, hypochrome microcyter, poikilocytosis ◦ Fecal occult blood: positive ◦ Serum iron = 8 mg/dl, Iron binding capacity = 450 mg/dl, Saturation = 1,1 %, Ferritin serum = 10 mg/L

1.What is the cause and mechanism of the weakness for this case? 2.What is the correlation of his weakness with his age? 3.What are the causes and mechanism of epigastric pain? 4.What is the effect of consuming NSAID since 5 years ago with his condition nowadays? 5.What is the correlation of NSAID with this case? 6.What is the Interpretation and mechanism of Physical Examination? 7.What is the interpretation and mechanism of laboratory examination? 8.What is the differential diagnosis of this case? 9.How to diagnose and the working diagnosis? 10. What is the management? 11. What is the complication? 12. How is the prevention?

A 60 year old male suffer from irondeficiency anemia due to GIT bleeding.

1.

Weakness

he used NSAID for 5 years to relieve his pain NSAIDs cause gastric erosions which can become ulcers. the ulcers may bleed (gastrointestinal bleeding) cause of epigastric pain used antacids to relieve his epigastric pain Reduced stomach acidity result in an impaired ability to digest and absorb certain nutrients, such as iron and the B vitamins Cause lack of function of the red blood cells, and the reduced ability of the red blood cells to carry iron to exercising muscles

weakness

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NSAIDs are associated with a number of adverse effects:

◦ inhibit biosynthesis of prostaglandin (inhibit cycloogenase enzyme Irreversible). ◦ prolong the bleeding time (inhibit aggregation of secunder erytrosit by inhibit synthesis of tromboksan) ◦ (this drugs work irreversibly, inhibit aggregation of trombocyte until 8 days.) ◦ Peptic Ulcer can happen if we give NSAID parenterally. ◦ Can lead to asymptomatic hepatitis. ◦ Hypersensitivity can occur after taking the medicine to nose polyp pt&asthma pt. ◦ cause gastric erosions which can become ulcers

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Action : ◦ NSAIDs cause a dual insult on the GIT:

 the acidic molecules directly irritate the gastric mucosa, and inhibition of COX-1 reduces the levels of protective prostaglandins.

◦ Risk of ulceration increases: with duration of therapy with higher doses.

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Antacid:

◦ Action mechanism:  buffer gastric acid, raising the pH to reduce acidity in the stomach. Other mechanisms may contribute, such as the effect of aluminum ions inhibiting smooth muscle cell contraction and delaying gastric emptying.

◦ Effect reduced stomach acidity:

Reduced stomach acidity result in an impaired ability to digest and absorb certain nutrients, such as iron and the B vitamins. the low pH of the stomach normally kills ingested bacteria, antacids increase the vulnerability to infection. also result in reduced bioavailability of some drugs. For example, the bioavailability of ketoconazole (antifungal) is reduced at high intragastric pH (low acid content)

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Weakness with age ◦ men lose a third of their muscle mass over their lifespan, and women lose somewhat less in the same period. The loss of strength and endurance can certainly be annoying and deflating to one's confidence and self-esteem. But it is possible to counter this tendency by paying attention to good nutrition and exercise. ◦ On the other hand, no matter how many preventive measures you may try, getting a little weaker or less active with age is inevitable. And the process may serve a useful purpose

6.

Physical Examination

Abnormal Condition

Cause

Pale

Anemia

Fatigue

Anemia

Epigastric Pain

Gastric Ulcer

Cheilitis

Iron Deficiency

Koilonychias

Iron Deficiency

Laboratory examination

7. 

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Hb = 5 g/dl

Normal = 14 – 18 g/dl Interpretation = anemia

MCV = 70 fL

Normal = 80 - 98 fl Interpretation = microcytic or the size of cell less than normal cell.

MCH = 25 pq

Normal = 26 – 32 pq Interpretation = hipochromic or the mean of hemoglobin less than normal cell.

MCHC = 30%

Normal = 32 – 36% Interpretation = decrease hemoglobin concentration

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RDW = 17 %

◦ Normal = 11,6 – 14,6% ◦ Interpretation = increase the size variations of cell

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Anisocytosis

◦ Interpretation = reticulocytosis, blood transfuse

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Hyperchrome microcyter

◦ Interpretation = decrease hemoglobin concentration

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Poikilocytosis

◦ Interpretation = leukemia, sel sabit, hemolisis microangiopaty

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Serum iron = 8 mg/dl

◦ Normal = 50 – 150 mg / dl ◦ Interpretation = iron deficiency, infection chronic

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Iron binding capacity = 450 mg/dl

◦ Normal = 240 – 360 mg/ dl ◦ Interpretation = iron deficiency and pregnancy

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Saturation = 1,1 % ◦ Normal = 20 – 45 % ◦ Interpretation = iron deficiency and chronic disease

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Ferritin serum = 10 mg/L ◦ Normal = 20 -250 mg/L ◦ Interpretation = iron deficiency

8. Differential Diagnosis for this case

Differential Diagnosis of Microcytic Anemia Due to Decreased RBC Production Diagnostic Criteria

Iron Deficiency

Iron-Transport Deficiency

Sideroblastic Iron Utilization

Iron Reutilization

Microcytosis (M) vs hypochromia (H)

M>H

M>H

M > H , may be normocytic

M>H

Polychromatophilic targeted cells

Absent

Absent

Present

Absent

Stippled RBCs

Absent

Absent

Present

Absent

↑

↑

Normal

Peripheral smear

RBCs RBC distribution width (RDW) ↑ Serum iron Serum iron: iron-binding capacity

↓:↑

↓:↓

↑:Normal

↓:↓

% Saturation of transferring

< 10

0

> 50

> 10

< 12

No data available

> 400

30–400

RBC:granulocyte ratio (normal, 1:1–1:2 1:3–1:5)

1:1–1:2

1:1–5:1

1:1–1:2

Marrow iron

Absent

Present

↑

Present

Ringed sideroblasts

Absent

Absent

Present

Absent

Serum ferritin (Normal, 30–300 ng/mL) Bone marrow

> = more common than; ↑ = increased; ↓ = decreased.

9. Working Diagnosis Iron deficiency: 

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most common cause of anemia and usually results from blood loss. Symptoms are usually nonspecific. RBCs tend to be microcytic and hypochromic, iron stores are low as shown by low serum ferritin and low serum iron levels with high serum total iron binding capacity. If the diagnosis is made, occult blood loss is suspected.

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Clinical

◦ History  While iron deficiency anemia is a laboratory diagnosis, a carefully obtained history can lead to its recognition. useful in establishing the etiology of the anemia and, perhaps, in estimating its duration. ◦ Diet A dietary history is important. Vegetarians are more likely to develop iron deficiency, unless their diet is supplemented with iron. ◦ Hemorrhage Patients report a history of bleeding from most orifices (hematuria, hematemesis, hemoptysis) before they develop chronic iron deficiency anemia; however, gastrointestinal bleeding may go unrecognized, and excessive menstrual losses may be overlooked.

◦ Symptoms Fatigue and diminished capability to perform hard labor are attributed to the lack of circulating hemoglobin occur out of proportion to the degree of anemia and probably are due to a depletion of proteins that require iron as a part of their structure. Increasing evidence suggests that deficiency or dysfunction of nonhemoglobin proteins has deleterious effects. These include muscle dysfunction, pagophagia, dysphagia with esophageal webbing, poor scholastic performance, altered resistance to infection, and altered behavior.

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Physical ◦ Anemia produces nonspecific pallor of the mucous membranes. ◦ A number of abnormalities of epithelial tissues are described in association with iron deficiency anemia. These include esophageal webbing, koilonychia, glossitis, angular stomatitis, and gastric atrophy. ◦ Splenomegaly may occur with severe, persistent, untreated iron deficiency anemia.

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Deficiency develops in stages: ◦ In the first stage, iron requirement exceeds intake, causing progressive depletion of bone marrow iron stores. ◦ As stores decrease, absorption of dietary iron increases in compensation. ◦ During later stages, deficiency impairs RBC synthesis, ultimately causing anemia. ◦ Severe and prolonged iron deficiency also may cause dysfunction of iron-containing cellular enzymes.

The staging Based on the chart above the patient in this case is already in stage 4 (late iron deficiency anemia).

10. Management Terapi kausal:

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tergantung penyebabnya, misalnya : pengobatan cacing tambang, pengobatan hemoroid, pengobatan menoragia.

Pemberian preparat besi untuk mengganti kekurangan besi dalam tubuh :

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Besi peroral : merupakan obat pilihan pertama karena efektif, murah dan aman.

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Besi parental :

 Efek samping lebih berbahaya, serta harganya lebih mahal. Indikasi, yaitu :    

Intoleransi oral berat Kepatuhan berobat berkurang Kolitis ulserativa Perlu peningkatan Hb secara cepat (misal preoperasi, hamil trisemester terakhir)

 Preparat yang tersedia : iron dextran complex, iron sorbitol citric acid complex.  Efek samping obat : reaksi anafilaksism flebitis, sakit kepala, flushing, mual, muntah, nyeri perut dan sinkop.

 Con`t ...  Dosis besi parental : harus dihitung dengan tepat karena besi berlebihan akan membahayakan pasien. Besarnya dosis dapat dihitung dengan rumus berikut ini : Kebutuhan besi (mg) = (15-Hb sekarang) x BB x3

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Pengobatan lain ◦ Diet : sebaiknya diberikan makanan bergizi dengan tinggi protein terutama yang berasal dari protein hewani ◦ Vitamin C : vitamin C diberikan 3 x 100 mg/ hari untuk meningkatkan absopsi tubuh

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Transfusi darah : anemia kekurangan besi jarang memerlukan transfusi darah. Indikasi pemberian transfusi darah pada anemia kekurangan besi adalah : Adanya penyakit jantung anermik dengan ancaman payah jantung  Anemia yang sangat simptomatik, misalnya anemia dengan gejala pusing yang mencolok  Penderita memerlukan peningkatan kadar hemoglobin yang cepat, seperti kehamilan trimester akhir atau preoperasi. 

11. Prevention 

Pendidikan kesehatan:

◦ Kesehatan lingkungan, misalnya tentang pemakaian jamban dan perbaikan lingkungan kerja, misalnya pemakaian alas kaki. ◦ Penyuluhan gizi : untuk mendorong konsumsi makanan yang membantu absorpsi besi

Pemberantasan infeksi cacing tambang sebagai sumber perdarahan kronik paling sering di daerah tropik Sumplemnetasi besi : terutama untuk segmen penduduk yang rentan seperti ibu hamil dan anak balita Fortifikasi bahan makanan dengan besi

12. Complications 

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Iron deficiency anemia diminishes work performance by forcing muscles to depend, to a greater extent than in healthy individuals, upon anaerobic metabolism. This is believed to be due to deficiency in iron-containing respiratory enzymes rather than anemia. Severe anemia due to any cause may produce hypoxemia and enhance the occurrence of coronary insufficiency and myocardial ischemia. Likewise, it can worsen the pulmonary status of patients with chronic pulmonary disease.

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Defects in structure and function of epithelial tissues may be observed in iron deficiency.

◦ Fingernails may become brittle or longitudinally ridged with development of koilonychia (spoon-shaped nails). ◦ The tongue may show atrophy of the lingual papillae and develop a glossy appearance. ◦ Angular stomatitis (koilonycias)may occur with fissures at the corners of the mouth. ◦ Dysphagia may occur with solid foods, with webbing of the mucosa at the junction of the hypopharynx and the esophagus (Plummer-Vinson syndrome); this has been associated with squamous cell carcinoma of the cricoid area. ◦ Atrophic gastritis occurs in iron deficiency with progressive loss of acid secretion, pepsin, and intrinsic factor and development of an antibody to gastric parietal cells. ◦ Blunted Small intestinal villi

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Cold intolerance develops in one fifth of patients with chronic iron deficiency anemia and is manifested by vasomotor disturbances, neurologic pain, or numbness and tingling

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Impaired immune function is reported in subjects who are iron deficient, and there are reports that these patients are prone to infection; however, evidence that this is directly due to iron deficiency is not convincing because of the presence of other factors.

13. Prognosis Iron deficiency anemia is an easily treated disorder with an excellent outcome; however, it may be caused by an underlying condition with a poor prognosis, such as neoplasia. Similarly, the prognosis may be altered by a comorbid condition such as coronary artery disease.

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Questions

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