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 painpain 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.Antacidmedicines that neutralize stomach acid.

3.Rheumatoid arthritischronic autoimmune disease that causes inflammation and deformity of the joints

4.NSAIDA nonsteroidal anti-inflammatory drug, such as aspirin or ibuprofen.

5.Lymphadenopathyabnormal enlargement of the lymph nodes, usually associated with disease.

6.CheilitisInflammation of the lips.

7.Koilonychiasmeans "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 volumeThe average volume of red cells in erythrocyte indices, calculated from the hematocrit and the red blood cell count.

9.Anisocytosiserythrocytes showing abnormal variations in size

10.Hypochrome microcyterthe color of the erythrocyte is less and the size is small

11.PoikilocytosisA condition in which erythrocytes are distorted in shape.

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.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 iron- deficiency 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

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

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.

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)

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

7. Laboratory examination 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

RDW = 17 %◦ Normal = 11,6 – 14,6%◦ Interpretation = increase the size variations of cell

Anisocytosis◦ Interpretation = reticulocytosis, blood transfuse

Hyperchrome microcyter◦ Interpretation = decrease hemoglobin concentration

Poikilocytosis◦ Interpretation = leukemia, sel sabit, hemolisis microangiopaty

Serum iron = 8 mg/dl◦ Normal = 50 – 150 mg / dl◦ Interpretation = iron deficiency, infection chronic

Iron binding capacity = 450 mg/dl◦ Normal = 240 – 360 mg/ dl◦ Interpretation = iron deficiency and pregnancy

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

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

Peripheral smear

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

RBCs

RBC distribution width (RDW)

↑ ↑ ↑ Normal

Serum iron

Serum iron: iron-binding capacity

↓:↑ ↓:↓ ↑:Normal ↓:↓

% Saturation of transferring < 10 0 > 50 > 10

Serum ferritin

(Normal, 30–300 ng/mL) < 12 No data available > 400 30–400

Bone marrow

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

1:1–1:2 1:1–1:2 1:1–5:1 1:1–1:2

Marrow iron Absent Present ↑ Present

Ringed sideroblasts Absent Absent Present Absent

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

9. Working DiagnosisIron deficiency: 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.

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.

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.

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:

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

Pemberian preparat besi untuk mengganti kekurangan besi dalam tubuh :

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

◦ 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 x 3

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

◦ 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 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.

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

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

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. PrognosisIron 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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