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.
 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 Sideroblastic Iron Iron Reutilization
Deficiency Utilization
Peripheral smear
Microcytosis (M) vs M>H M>H M > H , may be M>H
hypochromia (H) normocytic
Polychromatophilic targeted Absent Absent Present Absent
cells
Stippled RBCs Absent Absent Present Absent
RBCs
RBC distribution width (RDW) ↑ ↑ ↑ Normal

Serum iron
Serum iron: iron-binding ↓:↑ ↓:↓ ↑:Normal ↓:↓
capacity
% 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, 1:1–1:2 1:1–1:2 1:1–5:1 1:1–1:2
1:3–1:5)
Marrow iron Absent Present ↑ Present
Ringed sideroblasts Absent Absent Present Absent
> = more common than; ↑ = increased; ↓ = decreased.
9. Working Diagnosis
Iron 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
x3
 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. 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.
THANK YOU
Questions so far??????