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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
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.
Pale Anemia
Fatigue Anemia
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