SCENARIO E BLOCK 7 TUTORIAL

“Puffy Cheek”

Tutor : dr. Vina Pramayastri

GROUP 6

1. Rizqi Athalia 702019072

2. Rifka Arifin 702019030

3. Muhammad Fuad Arifin Fachrozi 702019046

4. Laoura Angelita Ekawantri 702019047

5. Mareta Aulia 702019053

6. Lidya Zalfa Nabila 702019063

7. Destya Kurnia Putri 702019086

8. Fadhilah Jasmine Shahab 702019094

9. Raphaelano Naufal Permono 702019099

10. Tsaqif Novindra Putra 702019101

11. M. Abidinsyah 702016020

FACULTY OF MEDICINE

MUHAMMADIYAH UNIVERSITY OF PALEMBANG

2019/2020
 CHAPTER I

INTRODUCTION

1.1. Background

Immune system or immune system is the ability of the body to fight

infections, eliminating the work of toxins and other virulent factors that are
antigenic and immunogenic. Antigen itself is a substance or compound that
can stimulate the formation of antibodies. Antigen can be proteins, fats,
polysaccharides, nucleic acids, Lipopolysaccharides, lipoproteins and others.
While it is antigenic is the nature of a compound that is able to stimulate the
formation of specific antibodies to the compound. Speaking of endurance, we
often hear immunogen which is a compound that can stimulate the formation
of immunity/immunity, and Immunogenic properties is a compound that can
stimulate the formation of specific antibodies that are protective and
increased cellular immunity. If the immune system is weakened, the ability to
protect the body is also reduced, so that pathogens, including viruses can
grow and thrive in the body (Siswanto, et al., 2013).

On this occasion, a case study tutorial of scenario A which presents cases

that related to autoimmunity.

Miss A, a 20 years old woman, came to emergency department of Type

A Hospital a chief complaint of being weak and easily tired since 2 weeks
ago accompanied by dizziness, especially when standing. Ms. A also
complains that the urine is like a darkly colored tea and discomfort in the
right upper abdomen. Ms. A went to the type C hospital for treatment, and
being told that she had anemia so she was referred to Type A Hospital for
hematological examination, immunological examination and further
management.

Since 6 months ago, Ms. A often complains of fever that is not too high,
tend to disappear and appear all by itself, accompanied by joint pain,
especially in the wrists and legs, hair loss, thrush on the palate that is not
painful. Two months ago Miss A cheeks appeared reddish and turned red
when exposed to sunlight. Ms. A has already been treated at the puskesmas
and given paracetamol when fever and also given ibuprofen if joint pain
appear, but these complaints still often appear. Family history of the same
complain were denied.

Physical Examination :

General appearance: looks mildly sick, sensorium: compos mentis,

Vital Sign: Respiratory rate 24x/m, Pulse rate : 100x/mt, temp 37.4° C,
blood pressure : 120/80 mmHg.

Specific examination :

Head : alopecia (+), pale konjungtive and palpebra (+), icteric sklera (+),
Face : malar rash (+), mouth : ulceration on the palate (+).

Nech: enlargement of the lymph node (-)

Cor/pulmo: within normal limit

Abdoment : hepar were palpable 2 finger below the arcus costae, lien were
palpable at S2

Ekstremity : wrist and foot: edema (-), redness (-), warm

Laboratory Examination

Blood test : Hb: 5,7 gr/dL, Eritrocyte 177x104/uL, Lekocyte: 2000/uL,

Trombocyte 78.000/uL, diff count0/2/2/51/34/11. Ht 16 vol%, retikulocyte

2,5%, LED : 100 mm/hour,

Blood chemistry: Bilirubin direct 1.1 g/dL, bilirubin indirect: 2,6 g/d

Urinalysis : within normal limit

Morphological examination of RBC: normochrom normositer

1.2. Purpose

The purpose of this case study tutorial report are:

1. As a group task report which is a competency-based curriculum learning

system in the medical facultyof Muhammadiyah Palembang.
2. Can solve cases given in a scenario by group analysis and learning
methods
3. The purpose of the tutotiral learning method is reached.
 CHAPTER II

DISCUSSION

2.1 Data Tutorial

Tutor : dr. Vina Pramayastri
Moderator : Rizqi Athalia
Table Secretary : Lidya Zalfa Nabila
Board Secretary : Raphaelano Naufal Permono

Tuesday, June 2nd 2020

(13.00 – 16.00 p.m)
Thrursday, April 4th 2020
(13.00 – 16.00 p.m)
The rule of tutorial :

1. Deactivate the phone or condition the phone silence.

2. Raise your hand when going to argument
3. Get permission when going out of the room
4. It is prohibited to bring food or eat in the room during the discussion in
progress
2.2 Scenario E

“Puffy Cheek”
Miss A, a 20 years old woman, came to emergency department of Type A
Hospital a chief complaint of being weak and easily tired since 2 weeks ago
accompanied by dizziness, especially when standing. Ms. A also complains
that the urine is like a darkly colored tea and discomfort in the right upper
abdomen. Ms. A went to the type C hospital for treatment, and being told that
she had anemia so she was referred to Type A Hospital for hematological
examination, immunological examination and further management.
Since 6 months ago, Ms. A often complains of fever that is not too high,
tend to disappear and appear all by itself, accompanied by joint pain,
especially in the wrists and legs, hair loss, thrush on the palate that is not
painful. Two months ago Miss A cheeks appeared reddish and turned red
when exposed to sunlight. Ms. A has already been treated at the puskesmas
and given paracetamol when fever and also given ibuprofen if joint pain
appear, but these complaints still often appear. Family history of the same
complain were denied.
Physical Examination :
General appearance: looks mildly sick, sensorium: compos mentis,
Vital Sign: Respiratory rate 24x/m, Pulse rate : 100x/mt, temp 37.4° C, blood
pressure : 120/80 mmHg.
Specific examination :
Head : alopecia (+), pale konjungtive and palpebra (+), icteric sklera (+), Face
: malar rash (+), mouth : ulceration on the palate (+).
Nech: enlargement of the lymph node (-)
Cor/pulmo: within normal limit
Abdoment : hepar were palpable 2 finger below the arcus costae, lien were
palpable at S2
Ekstremity : wrist and foot: edema (-), redness (-), warm
Laboratory Examination
 Blood test :Hb: 5,7 gr/dL, Eritrocyte 177x104/uL, Lekocyte: 2000/uL,
Trombocyte 78.000/uL, diff count 0/2/2/51/34/11. Ht16 vol%, retikulocyte
2,5 %, LED : 100 mm/hour,
Blood chemistry: Bilirubin direct 1.1 g/dL, bilirubin indirect: 2,6 g/dL
Urinalysis : within normal limit
Morphological examination of RBC: normochrom normositer

2.3 Terms of Clarfication

NO Clarifications Meaning
1. Dizziness The sensation of disturbed feelings
oscillating and the feeling of movement in
the head, dizziness, imbalance (Dorland)
2. Fever Increased body temperature above normal
(Dorland)
3. Anemia Reduced number of red blood cells
(Dorland)
4. Alopecia Absence of hair on the skin that normally
grows (Dorland)
5. Eritrocyte Red blood cells (Dorland)
6. Paracetamol Analgesics and antipyretics which have an
effect similar to aspirin but only slightly
have an inflammatory effect (Dorland)
7. Palpebra Eyelid (Dorland)
8. Edema Abnormal fluid collection in the body's
intercellular space (Dorland)
9. Leukocyte White blood cells, colorless cells that are
able to move ameboidically, with the main
function of which is to protect the body
from microorganisms (Dorland)
10. Ibuprofen Nonsteroid anti-inflammantory drugs used
 in treatment of rheumatic, fever,
osteoarthritis, rheumatoid arthritis,
inflamation of rheumatism and other
neurons and vascular headache (Dorland)
11. Thrombocytes Pieces of blood or which have an irregular
shape and do not have a nucleus (Dorland)
12. Reticulocyte Young erythrocytes that show basophilic
reticulum in vital staining (Dorland)
13. LED Erythrocyte sedimentation rate (ESR), the
speed of red blood cells settles in the test
tube in units of mm / hour (Dorland)
14. Urinalysis Urine analysis (Dorland)

2.4 Problems Identification

1. Miss A, a 20 years old woman, came to emergency department of Type A
Hospital a chief complaint of being weak and easily tired since 2 weeks
ago accompanied by dizziness, especially when standing. Ms. A also
complains that the urine is like a darkly colored tea and discomfort in the
right upper abdomen.
2. Ms. A went to the type C hospital for treatment, and being told that she
had anemia so she was referred to Type A Hospital for hematological
examination, immunological examination and further management.
3. Since 6 months ago, Ms. A often complains of fever that is not too high,
tend to disappear and appear all by itself, accompanied by joint pain,
especially in the wrists and legs, hair loss, thrush on the palate that is not
painful. Two months ago Miss A cheeks appeared reddish and turned red
when exposed to sunlight.
4. Ms. A has already been treated at the puskesmas and given paracetamol
when fever and also given ibuprofen if joint pain appear, but these
complaints still often appear. Family history of the same complain were
denied.
5. Physical Examination :
 General appearance: looks mildly sick, sensorium: compos mentis,
Vital Sign: Respiratory rate 24x/m, Pulse rate : 100x/mt, temp 37.4° C,
blood pressure: 120/80 mmHg.
Specific examination :
Head : alopecia (+), pale konjungtive and palpebra (+), icteric sklera (+),
Face : malar rash (+), mouth : ulceration on the palate (+).
Nech: enlargement of the lymph node (-)
Cor/pulmo: within normal limit
Abdoment : hepar were palpable 2 finger below the arcus costae, lien were
palpable at S2
Ekstremity : wrist and foot: edema (-), redness (-), warm
6. Laboratory Examination :
Blood test : Hb: 5,7 gr/dL, Eritrocyte 177x104/uL, Lekocyte: 2000/uL,
Trombocyte 78.000/uL, diff count 0/2/2/51/34/11. Ht 16 vol%,
retikulocyte 2,5 %, LED : 100 mm/hour,
Blood chemistry: Bilirubin direct 1.1 g/dL, bilirubin indirect: 2,6 g/dL
Urinalysis : within normal limit
Morphological examination of RBC: normochrom normositer

2. 5 Problem Priority
The priority problem is number 3, because Miss A has some
symptoms that have not healed for months so that should get more
attention

2.6 Problems Analysis

1. Miss A, a 20 years old woman, came to emergency department of Type A
Hospital a chief complaint of being weak and easily tired since 2 weeks
ago accompanied by dizziness, especially when standing. Ms. A also
complains that the urine is like a darkly colored tea and discomfort in the
right upper abdomen.
a) What the meaning of Miss A, a 20 years old woman, came to emergency
department of Type A Hospital a chief complaint of being weak and
 easily tired since 2 weeks ago accompanied by dizziness, especially
when standing?
This means that experience symptoms of anemia due to chronic illness
experienced by patients. Common symptoms of anemia include
weakness, lethargy, fatigue, dizzy eyes, and ringing in the ears,
conjunctiva and pale nails (Bakta, IM, 2014).
b) What is the anatomy and fisiology in this case?

Bickley, Lynn S. 2009.

Anatomy
1. Right lobe of liver, gall blodder, partiallyhepatic duodenal colon,
part of the right kidney and right middle glands.
2. Pyloric gaster, duodenum, pancreas and part of hepar
3. Gaster, spleen, the caudal portion of the pancread, flexura colon
lienalis, the proximal part of the left kidney and the left middle
gland
4. Colon ascenden, distal part of the right kidney, party duodenal,
and jejunum
5. Omentum, mesenterium, bottom of the duodenum, jejenum,
ileum
6. Colon ascenden, distal part of the left kidney, partly jejenum and
ileum.
7. Sekum, appendix, distal ileum, and right ureteral
8. Ileum, vesica urinaria, uterus
9. Colon sigmoid, left ureters and ovarium
 (Tortora, 2016).

Physiology

Urinary system

To produce urine, nephrons and the renal duct has three basic
processes :

1. Glomerular filtration
In first step of urine filtration, water and the majority of the
solutes in plasma flows. Penetrating the glomerular capillary
walls. Where water and solutes are filtered and move into the
glomerular capsules and then kidney tubule (Tortora, 2016).
2. Reabsorption of tubules
As the filtration fluid flows through renal tubules and
through the ducts on the kidney. Tubular cells reabsorption
of about 99% of water and many important solutes other.
Water and solutes return to blood as blood flows through
peritubulus capillaries and recta vesa. Reabsorption means
the inclusion of new materials to in the body, such as
occuring the gastrointestinal tract (Tortora, 2016).
3. Secretion tubules
When filtration fluid flows through the tubule renal and
kidney duct cells, renal tubular cells and ductus of other
substances, such as residual substances, medicines, and
excess ions into the liquid. Secretion of tubular secretions a
material from the blood (Tortora, 2016).
c) What the meaning Ms. A also complains that the urine is like a darkly
colored tea and discomfort in the right upper abdomen?
The meaning urine likely collored tea is because bilirubin levels increase
and discomfort in the right upper abdomen because hepatomegali
(Sherwood, 2018).
d) What are the classification of urine colors?
 Cleveland Clinic. 2013.

Red urine

• Medications: Rifampicin, Warfarin, Phenazopyridine,

Ibuprofen, Deferoxamine, Hydroxocobalamine
• Foods: beets, carrots, blackberries.
• Intravascular hemolysis: G6PD deficiency, Sickle cell
anaemia, Thalassemia, Transfusion reaction.
• Other medical conditions: Porphyria, Nut cracker syndrome,
Nephrolithiasis, BPH, Urinary bladder malignancy, Prostrate
malignancy.
• Other conditions: contamination (menstruation), factitious
disorder.

Orange urine

• Medications (in addition to causes of red urine): Isoniazid,

Riboflavin.

Brown urine
 • Acetaminophen overdose, Metastatic melanoma.

Black urine

• Medications: Metronidazole, Nitrofurantoin, Sorbitol, Cresol,

Intramuscular iron.
• Medical conditions: Alkaptonuria, Metastatic melanoma.

White urine:

• Mineral sediments: hyperoxaluria, hypercalciuria,

phosphaturia.
• Medical conditions: Chyluria (filariasis, lymphatic fistula),
Pyuria, Urinary tuberculosis, Proteinuria.

Blue and green urine:

• Medications: Methylene blue, Promethazine, Cimetidine,

Propofol, Metoclopramide, Amitryptyline, Indomethacin,
Tetrahydronapthalene.
• Other conditions: Herbicide ingestion, pseudomonas UTI,
bile pigments in urine, Hartnup disease, Blue diaper
syndrome (Andrizal, 2018).
e) What is the etiology of the case?
SLE is a multifactorial disease with unknown exact etiology, however,
several genetic, immunological, endocrine, and environmental factors
play a role in the etiopathogenesis of SLE (A. Angel et all, 2020).
f) What is the pathofisiology of tired and dizziness?
Environmental factors > cell apoptosis Process > Secrete nuclear antigen
> complex antigen antibody (nuclear antigen-Anti nuclear antigen) >
Attack specific cells such as erythrocytes > solving erythrocytes >
solving Hb > Hb levels decreased > Oxygen supply in the body is
reduced > weak, easily tired and dizziness when standing (Guyton,
2016).
g) How epidimiology in case?
Still not getting definite data about the prevalence of SLE in
Indonesia. In the US, the most reliable number is 0.05 - 0.1% of
participation, but different figures are obtained in various reports. Some
races, such as blacks, Native American ancestry, and blacks, are at
higher risk for SLE and can cure more severe illnesses. The prevalence
of SLE worldwide is no different from reports from the US; this disease
seems to be more commonly found in China, in Southeast Asia, and
among black breeds in the Caribbean but rarely found in blacks in
Africa. SLE rarely occurs at prepubertal age but often begins at the
second updated age; some studios show the peak of these two new cases
in about 50 years. Gender distribution is quite clear; SLE develops in
women of childbearing age about ten times that of men of the same age.
At a younger age, women are three to four times more often than men.
At an older age, put off women and men is In accordance with the
theory that says SLE is more often in the female sex, this case is also
female. In accordance with the studio which said the second peak of
SLE at the age of around 50, this case was taken 48 years (Cervera, dkk,
2009).
h) How pathophysiology of urine like a darkly colored tea?
Antierythrocyte antibodies that damage the erythrocytes in SLE
patients, so that it will deconstruct the erythrocytes and break down the
hemoglobin that will enter into the reticuloendothelial system, then
increase the levels of bilirubin that affects the patient's urine color.
Environmental factors (in the case probably by exposure to UV rays by
the Sun) - > the process of cell apoptosis -> release antinuclear antigen -
> complex antigen- antibodies -> the destruction of specific cells ->
erythrocytes -> breakage of Hb increase -> the formation of indirect
bilirubin and direct increased -> urobilinogen in the kidneys merating ->
urine like a darkly colored tea (Ratnadi, dkk, 2015).
i) How the pathophysiology of being weak?
 Increased of Hemolisis → Decreased of Red Bloods and Hemoglobin
(Anemia Condition) → Hipoxemia → Tissue Hipoxia → Being Weak
(Huether, dkk, 2017).
j) What are the possible cause of discomfort in the right upper abdomen?
It's abdominal pain in 25% cases SLE, likely accompanied nausea
(infrequent vomiting) and diarrhoea. The symptoms quickly dissipate if
the system's disorder gets adequity treatment. The resulting pain may be
caused by sterile peritonitis or arteritis of tiny blood vessels the
mesenterium and the intestines resulting in ulcerative bowel. Arteritis
can also cause pancreatitis (Albar, 2010).
2. Ms. A went to the type C hospital for treatment, and being told that she
had anemia so she was referred to Type A Hospital for hematological
examination, immunological examination and further management.
a) How many types of anemia? and how about this case?
Anemia in SLE patients Can be an immune or non immune disease .
1. Anemia which is a non immune disease
Anemia in Chronic disease : is a decrease in Hb levels
secondary to chronic disease (chronic inflammation, infection
or malignancy) and is the most common co-morbidity in
chronic. Disease . The serum iron concentration decreases and
the total iron binding capacity is unchanged or slightly low.
Also found a decrease in iron saturation in transferrin.
Iron deficiency : is a lack of iron to form hemoglobin,
hemoglobin insufficiency
Sideroblastic anemia: dysfunction of iron absorption by
erythroblasts and defects in porphyrin and heme synthesis.
Anemia secondary to other disease ex: Sickle cell anemia
Sickle cell anemia is abnormal hemoglobin synthesis,
abnormal cell forms with susceptibility to damage, lysis, and
phagocytosis.
Anemia in kidney disease
Drug induced anemia
 2. Immune- mediated anemia in SLE patients is Autoimmune
hemolytic anemia (AHA) is a cause of anemia in 5-19% of
SLE patients. Several clinical syndromes occur, each
mediated by different autoantibodies (IgG or lIgM) that attack
red blood cells. As a result, red blood cells are damaged more
quickly so that the number decreases in circulation.
Autoimmune hemolytic anemia usually develops gradually in
most patients, but sometimes it can also develop rapidly so that
a progressive hemolytic crisis occurs.Autoimmune hemolytic
anemia can be associated with anticardiolipin antibodies, or it
can be part of the antiphospholipid syndrome, which is
associated with antiphospholipid antibodies, thrombosis,
thrombocytopenia and recurrent miscarriage.
Aplastic anemia: inadequate erythropoiesis. Caused by a
decrease in stem cell proliferation
Pernicious anemia: vitamin Bz deficiency, DNA and RNA
synthesis in abnormal erythroblasts; premature cell death.
caused by cognitive deficiency or can be from instrimtive
factors (IF), genetic disorders of DNA synthesis
Drug induced hemolytic Anemia
Pure red cell aplasia (IPDL, 2014).
b) What is the classification of hospital?
Hospital classification based on regulation of the Minister of Health of
Republic of Indonesia No. 340/Menkes/Per/III/2010, the hospital can
fulfill the requirements of ownership, type of service, and class.
1. Based on ownership. Hospitals include government hospitals
(central, provincial, and district), STATE-owned hospitals (ABRI),
and hospitals with private owned (BUMS) or overseas hospitals
(PMA).
2. By service type. Included in this type are general hospitals,
psychiatric hospitals, and specialty hospitals (e.g. heart, mother and
child hospitals, eye hospitals, etc.).
 3. By class. The hospital based on its class is distinguished from A
class A, B (education and non-educational) hospital, class C, class D.
1. A-class general hospital, is a general hospital that has a wide and
subspecialty medical facilities and capabilities.
2. B-class General Hospital, is a general hospital that has the facilities
and medical service capability of at least eleven species and limited
subspecialty.
3. C-class General Hospital, is a general hospital that has the facilities
and capabilities of basic specialist medical care.
4. D-class General Hospital, is a general hospital that has basic
medical facilities and capabilities (Permenkes, 2010).
c) What the meaning of Ms. A went to the type C hospital for treatment,
and being told that she had anemia so she was referred to Type A
Hospital for hematological examination, immunological examination
and further management?
Means that she is going to have further examination of blood, blood-
forming organs and blood diseases for hematological data, and
structure and function of the immune system, the immune response,
immune-based disorders as well as immunological methods of
analysis for immunological data because in type C hospital such
examination cannot be done so type C hospital referred her to type A
hospital to get said examination (Ivana, 2009).
d) How to do hematological examination and immunological
examination?
Routine hematological examination consists of several types of
examination. Hemoglobin, the number of leukocytes, the number of
erythrocytes, hematocrit value, platelet count. Examination complete
blood has used a tool Automatic Hematology Analyzer. Inspection
with an automated tool will get results very quickly. To guarantee the
accuracy and accuracy of laboratory tests, it is necessary to control
quality. Quality control (QC) is a process or stage in the procedure
carried out to evaluate the testing process, with the aim of verifying
 that the quality system is running properly and is carried out with the
aim of ensuring laboratory inspection results, knowing and resolving
irregularities, and knowing the source of deviations (Jemani, 2019).
e) What are the anemia risk factors?
The main risk factors for iron deficiency anemia are low iron intake,
poor absorption of iron, and periods of life when iron requirements are
high such as during growth, pregnancy, and breastfeeding. Other
nutritional deficiencies such as vitamins A, B12, folate, riboflavin,
and copper (Cu) and the presence of acute diseases and chronic
infections such as malaria, cancer, tuberculosis, and HIV can also
increase the risk of anemia (Silalahio, 2016).
f) What is pathophysiology anemia?
Premature destruction of RBCs can occur intravascularly or
extravascularly in the reticuloendothelial system, although the latter is
more common. The primary extravascular mechanism is sequestration
and phagocytosis due to poor RBC deformability (i.e., the inability to
change shape enough to pass through the spleen). Antibody-mediated
hemolysis results in phagocytosis or complement-mediated
destruction, and can occur intravascularly or extravascularly. The
intravascular mechanisms include direct cellular destruction,
fragmentation, and oxidation. Direct cellular destruction is caused by
toxins, trauma, or lysis. Fragmentation hemolysis occurs when
extrinsic factors produce shearing and rupture of RBCs. Oxidative
hemolysis occurs when the protective mechanisms of the cells are
overwhelmed (Philips, dkk, 2018).
g) What is the relationship of the main complaint with additional
complaint?
The meaning is miss. A has a symptom of SLE in which the main
complaint is weak and easily tired accompanied by dizziness (anemia
hemolitik) and additional complaint such as the urine is like darkly
colored tea and discomfort in the right upper abdomen,fever, joint
 pain, thrush on the palate, and malar rash, this symptom can be used to
make it easier to diagnose the patient's illness (George, dkk, 2012).
h) What is etiology of anemia?
Hemolytic anemia : Hemolytic anemia (HA) is divided into
extravascular and intravascular causes.
Extravascular hemolysis: red cells are prematurely removed from
the circulation by the liver and spleen. This accounts for a majority of
cases of HA

o Hemoglobinopathies (sickle cell, thalassemias)

o Enzyemopathies (G6PD deficiency, pyruvate kinase deficiency)

o Membrane defects (hereditary spherocytosis, hereditary

elliptocytosis)

o Drug-induced

Intravascular hemolysis: red cells lyse within the circulation, and is

less common.

o PNH

o AIHA

o Transfusion reactions

o MAHA

o DIC

o Infections

o Snake bites/venom

(Turner.J et all, 2020)

i) What is the epidemiology of anemia?

Anemia is a major health problem in society that is often found
throughout the world, especially in developing countries like
Indonesia. This disorder is a cause of chronic disability that has a
 major impact on health, economic and social welfare conditions. The
world's population with anemia is around 30% or 2.20 billion people,
with most of them living in the tropics. The prevalence of anemia
globally is around 51%.
The Republic of Indonesia Ministry of Health (2013) shows that the
national prevalence of anemia in all age groups is 21.70%. The
prevalence of anemia in women is relatively higher (23.90%)
compared to men (18.40%). The prevalence of anemia based on
location of residence shows that living in rural areas has a higher
percentage (22.80%) than living in urban areas (20.60%), while the
prevalence of anemia in women aged 15 years or older is 22.70%
(Priyanto, 2018).
3. Since 6 months ago, Ms. A often complains of fever that is not too high,
tend to disappear and appear all by itself, accompanied by joint pain,
especially in the wrists and legs, hair loss, thrush on the palate that is not
painful. Two months ago Miss A cheeks appeared reddish and turned red
when exposed to sunlight.
a) What classification of fever, in case?
1. Septic Fever: fever whose temperature never reaches normal,
high at night and drops to above normal levels in the morning.
2. Heptic fever: fever which reaches normal temperature.
3. Remitten fever: (in the case) fever which body temperature
can drop every day but never reach normal temperatures, the
temperature difference is 2 degrees Celsius.
4. Intermittent fever: a fever whose body temperature drops to
normal levels for several hours a day.
5. Continuous fever: fever whose temperature varies throughout
the day does not differ by more than 1 degree.
6. Cyclic fever: fever which rises in body temperature for several
days followed by a fever free period for several days which is
then followed by an increase in body temperature as before
(IPDL, 2014).
b) What the meaning Since 6 months ago, Ms. A often complains of
fever that is not too high, tend to disappear and appear all by itself,
accompanied by joint pain, especially in the wrists and legs, hair loss,
thrush on the palate that is not painful?
Miss A has systemic lupus erythematosus (SLE). Because based on
complaints felt by miss A refers to the criteria or symptoms of SLE.
SLE Criteria:
1. Mouth Ulceration
2. Photosensitivity
3. Peripheral Neuropathy
4. Malar rash
5. artritisnonerosif
6. Pleuroperikarditis
Fever that is felt miss A is a common manifestation of SLE in
systemic autoimmune disorders which are usually found constitutional
abnormalities such as: fatigue, fever, and decreased appetite (Setiati,
dkk, 2014).
c) What is the meaning of miss a cheeks appeared reddish and turned red
when exposed to sunlight?
This means that Ms. A experienced clinical manifestations of
Systemic Lupus Erythematosus (SLE) disease. Skin manifestation is
one of the most common symptoms found in patients with LES of
about 25%, which can be found at every stage of the disease. One
manifestation of the skin is Subacute Cutaneous Lupus Erythematosus
(SCLE). Patients with SCLE are usually photosensitive and ultra
Violet (UV) radiation can induce and / or exacerbate skin
manifestations (Najirman, Fajriansyah, 2019).
d) What are the possible causes of reddish and turned red when exposed
to sunlight?
Exposure to the sun may bring on lupus skin lesions or trigger an
internal response in susceptible people. It can be a photosensitivity
reaction, an inflammation triggered by sunlight reporting because the
 immune system of patients with difficulty recovering skin cells
demaged by UV (Ultraviolet) (Ferri, 2018).
e) What is the pathophysiology of fever in this case?
SLE is included in warm autoimmune hemolytic anemia, so this
type of anemia is caused by the body's production of antibodies
against erythrocytes themselves. This disorder is characterized by a
direct antiglobulin test / DAT or often known as the Coomb's Test
which is positive, and is distinguished into warm and cold types
depending on whether the antibody reacts more strongly with
erythrocytes at 37C or 40C (Hoffbrand, dkk, 2016).
In the body there are cd55 and cd59 antigens that function as
barriers in the mechanism of erythrocyte destruction, now in SLE
patients there is IgG in the body which causes decreased expression of
the cd55 and cd59 genes, eritrosi susceptibility to lysis, then
progressive erythrocyte destruction -> autoimmune hemolytic anemia
(Oktafany, 2017).
Anemia is one of the hematological manifestations of SLE that
occurs due to suppression of erythropoiesis by the presence of chronic
inflammation. The severity of anemia often reflects the underlying
conditions, including SLE. The lower the hemoglobin (Hb) level,
usually the more severe the underlying disease (Putu, dkk, 2016).
f) What is the pathophysiology of joint pain?
C fibers and A-gamma aferent nerve fibers that channel the pain
impluses into the spinal cord in the dorsal nerve roots. The fiber split
while entering the corda and then again blend in the kornu dorsalis
(posterior) spinal cord.
From kornu dorsalis, pain impluses are sent to neurons that transmit
information to the opposite side of the spinal cord medulla in the
anterior commision and then fused in the anterolateralist tractus.
Which rises to the thalamus and other brain, so that the pain arises
(Hartwig, dkk, 2006).
g) What is causes the joint paint?
 Joint pain occurs due to buildup antigen-antibody complex that
provokes formation of complement that attracts phagocytes and
triggers the inflamation process (Tarigan, 2015).
4. Ms. A has already been treated at the puskesmas and given paracetamol
when fever and also given ibuprofen if joint pain appear, but these
complaints still often appear. Family history of the same complain were
denied.
a) What are the uses of paracetamol and ibuprofen?
Paracetamol
In Indonesia ,the use of paracetamol as an analgesic and antipyretic
,has replaced the use of salicylates .As another analgesic ,paracetamol
should not be given too long because it might cause analgesic
nephropathy .if the therapeutic does does not provide benefits, usually
a larger dose does not help.Because it hardly irritates the stomach
paracetamol is often combined with AINS for analgesic effects
(Sulistia, 2016).
Ibuprofen
A common goal in the development of pain and inflammation
medicines has been the creation of compounds that have the ability to
treat inflammation, fever, and pain without disrupting other
physiological functions. General pain relievers, such as aspirin and
ibuprofen, inhibit both COX-1 and COX-2. A medication's
specificaction toward COX-1 versus COX-2 determines the potential
for adverse side effects. Medications with greater specificity toward
COX-1 will have greater potential for producing adverse side effects.
By deactivating COX-1, nonselective pain relievers increase the
chance of undesirable side effects, especially digestive problems such
as stomach ulcers and gastrointestinal bleeding. COX-2 inhibitors,
such as Vioxx and Celebrex, selectively deactivate COX-2 and do not
aff ect COX-1 at prescribed dosages. COX-2 inhibitors are widely
prescribed for arthritis and pain relief. In 2004, the Food and Drug
Administration (FDA) announced that an increased risk of heart attack
 and stroke was associated with certain COX-2 inhibitors. This led to
warning labels and voluntary removal of products from the market by
drug producers; for example, Merck took Vioxx off the market in
2004. Although ibuprofen inhibits both COX-1 and COX-2, it has
several times the specificity toward COX-2 compared to aspirin,
producing fewer gastrointestinal side effects.
A selective cyclooxygenase inhibitor (IC50=14.9uM). Inhibits PGH
synthase-1 and PGH synthase-2 with comparable potency, Cyclo-
oxygenase inhibitor; analgesic; anti-inflammatory, Antibiotic
(Chemical book, 2020).
b) How pharmacodynamics and pharmacokinetics of paracetamol?
Paracetamol
Phenol amino derivatives are fenasetin and acetaminophen.
Acetaminophen (paracetamol) is a fenasetin metabolite with the same
antipyretic effect and has been used since 1893. Antipyretic effect is
caused by the Aminobenzen group. Acetaminophen in Indonesia is
better known as paracetamol. Paracetamol is antipyretic and analgesic
but the anti-inflammatory properties are weak once. Paracetamol is a
non-narcotic analgesic drug that has a way of inhibiting the synthesis
of prostaglandins especially in the central nervous system (CNS).
Pharmacodynamics
The analgesic effect of paracetamol is to eliminate or reduce mild to
moderate pain. Paracetamol lowers body temperature with suspected
mechanisms based on central effects. The inflammatory effect is very
weak, therefore paracetamol is not used as an antireumatic. The
inability of paracetamol to provide an anti-inflammatory effect itself
may be related to the fact that paracetamol is simply an inhibitor of a
weak cyclooxygenase in the presence of high concentrations of
peroxide found in inflammatory lesions. Paracetamol is a weak
inhibitory biosynthesis of prostaglandins. The effects of irritation,
erosion, and gastric bleeding are not seen in these drugs, as well as
respiratory disorders and alkaline acid balances.
 Pharmacokinetics
Paracetamol is rapidly and perfectly absorbed through the
gastrointestinal tract. The highest concentrations in plasma are
achieved within half an hour and the half-life of plasma between 1-3
hours. The drug is spread throughout the body fluids. The binding of
these drugs to plasma proteins varies, only 20%-50% which may be
bound to concentrations found during acute intoxication. After a
therapeutic dose, 90%-100% of the drug is found in urine during the
first day, especially after the hepatic conjugation with glukoronic acid
(about 60%), sulfuric acid (about 35%), or cysteine (about 3%), a
small number of metabolites of hydroxylation and Deaseillation has
also been detected. A small portion of paracetamol is subjected to an
N-hydroxylation process that is interlaced by cytochrome P450 which
forms N-acetyl-benzokuinoneimin, which is a highly reactive
compound between. This metabolite reacts with the Sulfhydryl group
in Glutation. However, after ingesti paracetamol large doses, this
metabolite is formed in adequate amounts to remove hepatic
glutathione (Katzung, 2016).
c) How pharmacodynamics and pharmacokinetics of ibuprofen?
The pharmacokinetics of ibuprofen in terms of absorption,
metabolism, distribution, and drug elimination.
1. Absorption
Ibuprofen is quickly absorbed, after oral consumption.
Bioavailability of the drug is 80%. Ibuprofen lysine, or
ibuprofen salt is absorbed faster than ibuprofen acid. The peak
concentration of ibuprofen lysine, or ibuprofen salt is about 45
minutes, while ibuprofen acid is about 90 minutes. The peak
concentration of ibuprofen in serum generally lasts for about
1-2 hours. Bioavailability of the drug is hardly influenced by
food. There is also no interference with ibuprofen absorption,
if given together with antacids, both containing aluminum
hydroxide and magnesium hydroxide.
 2. Metabolism
Ibuprofen is rapidly metabolized in the liver, producing
metabolites such as propionic acid phenyl hydroxymethyl
propyl, and propionic acid phenyl carboxypropyl.
3. Distribution
Ibuprofen is distributed throughout all body tissues, mainly
concentrated in synovial fluid. The presence of ibuprofen
drugs in synovial fluid is longer than in plasma. This drug is
bound to proteins around 90‒99%, especially with albumin.
4. Elimination
The half-life of drugs in serum is around 1.8 to 2 hours.
Complete ibuprofen excretion in 24 hours, after the last dose.
About 45% ‒79% of the dose of the drug absorbed orally, is
found in urine, in the form of metabolites, while the free or
conjugated form of ibuprofen is about 1% and 14%,
respectively(Rainsford K.D, 2012).

Pharmacodynamics
1. In general, ibuprofen's work as an anti-inflammatory, analgesic
and antipyretic is by inhibiting prostanoids production
pathways, such as prostaglandin E2 (PGE2) and prostaglandin
I2 (PGI2), which are responsible for triggering pain,
inflammation and fever. Ibuprofen inhibits the activity of the
cyclooxygenase I and II enzymes, thus reducing the formation
of prostaglandin and thromboxane precursors. Furthermore,
there will be a decrease of prostaglandin synthesis, by the
enzyme prostaglandin synthase.
2. Specifically, the mechanism of action of ibuprofen as an anti-
inflammatory is through multiple modes of action:
1. Prevents the accumulation and adhesion of leukocytes such
as neutrophils, polymorphonuclear, and macrophage
monocytes in inflammatory tissue
 2. Inhibits the production and action of inflammatory
leukocytes such as leukotriene B4, nitric oxide, interleukin-1
3. Reduction of afferent pathways and efferent mediation of
pain.

The mechanism of action of ibuprofen as an antipyretic

consists of two actions, namely controlling the production of
leucocyte-derived interleukin-1 and other peptide components from
endogenous pyrogens, and directly inhibiting the production of
endogenous pyrogens or interleukin-1 prostaglandin E2 (PGE2),
which is induced by the hypothalamus.

Pain control by ibuprofen involves several different

mechanisms, but related to each other. The action of ibuprofen
inhibits the production of prostaglandins and nitric oxide, which
act as afferent impulses in peripheral pain and spino-thalamic
transmission. In addition, ibuprofen can stimulate the production of
endogenous anandamide analgesics, which are cannabinoid-like
analgesics, by inhibiting enzymes that hydrolyze these substances
into arachidonic acid (Rainsford K.D, 2012).
d) What is the meaning about family history of the same complaint were
denied?
The meaning of the disease experienced by miss.A is not a hereditary
disease because it is found miss.A family does not experience the
same complain like miss.A. it is known that SLE is caused by
interactions between gene susceptibility (including HLA-DRB1, IRF5,
STAT4, HLA-A1, DR3, and B8 alleles), hormonal influences, and
environmental factors. The interaction of these three factors will
cause an abnormal immune response (Maidhof, dkk, 2012).
e) What would happened to ms a body if she had given paracetamol
when fever and also given ibuprofen?
a. Paracetamol
 Giving Paracetamol when a fever can reduce body temperature. the
analgesic effect of Paracetamol & prenasetin is similar to salicylate.
can reduce pain The effects of paracetamol & center such as
salicylates.

b. Ibuprofen
Ibuprofen is an antipyretic analgesic drug and a non-steroidal anti-
inflammatory drug. as an analgesic, this drug is effective against &
other pain (FK UI, 2019).
5. Physical Examination :
General appearance: looks mildly sick, sensorium: compos mentis,
Vital Sign: Respiratory rate 24x/m, Pulse rate : 100x/mt, temp 37.4° C,
blood pressure: 120/80 mmHg.
Specific examination :
Head : alopecia (+), pale konjungtive and palpebra (+), icteric sklera (+),
Face : malar rash (+), mouth : ulceration on the palate (+).
Nech: enlargement of the lymph node (-)
Cor/pulmo: within normal limit
Abdoment : hepar were palpable 2 finger below the arcus costae, lien were
palpable at S2
Ekstremity : wrist and foot: edema (-), redness (-), warm
a) What are the interpretations in the case?
Physical Examination Results Normal Value Interpretation

Composmentisawareness Compos Mentis Normal

Blood Pressure 120/80 mmHg 120/80 mm/Hg Normal

Respiratory speed24 x / minute 16-24x/menit Normal

Temperature 37.4 degrees C 6.5-37.2 36,5-37,2degrees Fever

degrees C C (Hyperthermia)
Pulse 100 x/Minute 60-100 x/Minute Normal

Special circumstances :
Physical Examination Results Interpretasion

Head Alopecia ( + ) Abnormal

Konjungtiva Pale and Abnormal

palpebral (+)

Icteric Sklera (+) Abnormal

Face Malar rash (+) Abnormal

Mouth Uleration on the palate (+) Abnormal

Neck Enlargement of the lymph Normal

noda (-)

Cor/ Pulmo Within normal limit Normal

Abdoment Hepar were palpable 2 finger Abnormal

below the arcus costae,lien
were palpable at S2

Ekstremity Wrist and foot

Edema (-) Normal

Redness (-) Normal

Warm Normal

(Price, Wilson, 2013)

 b) How abnormal mechanism of physical examination?
1. Hb breakdown → bilirubin increase → urine darkly collored
tea (Guyton, 2016).
2. Hb breakdown → improvement of reticuloendothelial system
→ hepatomegaly and splenomegaly (Guyton, 2016).
3. Environment factors → cells apoptosis → antigen → complex
antigen antibodies → deposit in the tissues of body →
inflammatory lessions of ulceration membrans in palate mole
(Guyton, 2016).
4. Environment factors → cells apoptosis → antigen → complex
antigen antibodies → deposit in inflammatory body tissues →
inflammatory skin layer → alopecia and malar rash (Guyton,
2016).
6. Laboratory Examination :
Blood test : Hb: 5,7 gr/dL, Eritrocyte 177x104/uL, Lekocyte: 2000/uL,
Trombocyte 78.000/uL, diff count 0/2/2/51/34/11. Ht 16 vol%,
retikulocyte 2,5 %, LED : 100 mm/hour,
Blood chemistry: Bilirubin direct 1.1 g/dL, bilirubin indirect: 2,6 g/dL
Urinalysis : within normal limit
Morphological examination of RBC: normochrom normositer
a) How is the interpretation of laboratory examination?
No. Pemeriksaan Normal Pada Kasus Interpretasi
Lab
1. Hb Lk : 14-16 5,7 gr/dL Abnormal
Pr : 12-14 (Anemia)
2. Ht 37-43% 16% Abnormal
3. Leukosit 4000- 2000/mm3 Abnormal
11.000/mm3 (Leukopenia)
4. Diff Count Basofil: 0-1 0/2/2/51/34/34/ Eosinofil ↓
Eosinofil: 1-6 11 N. batang ↓
N. batang: 3-5 Monosit ↑
 N. segmen: 40-
70
Limfosit: 30-45
Monosit:2-10
5. Trombosit 150.000- 78.000/mm3 Abnormal
400.000/mm3 (trombositopenia)

6. Erytrocite 4,3-5,6 x 106 117 x 104 /uL erythrocytopenia

/uL
7. LED Pr: <15 mm/jam 100 mm/jam Abnormal ↑
Lk: <10
mm/jam
8. Urinalisis within normal within normal Normal
limit limit
9 Bilirubin 0,1-1,0 mg/dL 1,1 mg/dL Abnormal ↑
direct
10 Bilirubin 0,1 - 0,3 mg/dL 2,6 mg/dL Abnormal ↑
Indirect
11. Normochrom Normochrom anemia of acute
normosister normosister disease
12. Retikulosit 0,5-1,5% 2,5% Retikositosis

(Price, Wilson, 2013)

b) How abnormal mechanism of laboratory examination?

Environmental Factor - The process of cell apoptosis - Secrete
antinuclear antigen - antigen antibodicomple - destruction of specific
cells - erythrocytes decreases - solving hb- hb levels decreases-
increased bilirubin formation- indirect bilirubin increases (Guyton,
2016).
c) Additional examination :
Immunological serum examination: C3 : 40 mg/dL , C4 : 45 mg/dl,
Anti ds-DNA : 532,5 IU/ml , ANA : > 1: 1000. Tes Coombs direk (+),
indirek (+).
Means : Coomb test is a test for patients with hemolytic anemia. in
this case, positive test results. It’s mean ms. A positive hemolytic
anemia.
C3 and C4 Defiiency, Anti ds-DNA (+), Coomb direct (+) indirect
(+).
From all the examination, Miss A can be ascertained suffering from
systemic lupus erythematosus (SLE).
Coomb test
Complement on the surface of red blood cells where sensitization has
occurred invivo. Anti human globulin reagent is added to washed red
blood cells agglutination shows a positive test. Indirect Coombs Test
(Indirect Coombs Test / ICT) is used to search the presence of
irregular (incomplete) antibodies in the serum. Coating is done first
normal erythrocytes in group O (or erythrocytes in the appropriate
class with examined serum) with known serum or suspect containing
barrier antibodies. The next step is to prove the existence of these
antibodies by using Coombs Serum (Kemenkes, 2018).
ANA
Antinuclear antibodies / ANA contains 2 (two) main components
autoantibodies, the first autoantibodies group against DNA and
histones; second is group autoantibodies against an extractable nuclear
antigens (ENA), including anti-Sm, anti-RNP, Ro /SSA or La / SSB,
Scl-70, histidyl-tRNA synthetase (Jo-1) and PM-1, respectively
different sensitivity and specificity based on the underlying disease
ANA can be speckled, homogeneous, peripheral, nucleolar, and
estimated centromere pattern related to certain rheumatic diseases.
Homogeneous and peripheral patterns show antibodies to histone /
dsDNA / chromatin cells. Nucleolar and centromere patterns have a
correlation with scleroderma. Check the ANA pattern requires
competence of laboratory personnel. Checking for ANA patterns is
not a checking definitive to determine a disease and no further checks
are needed for detect more specific autoantibodies. (Birtane, 2012).
C3, C4
Low complement levels, especially C3, C4, and CH50 (complement
total hemolytic), important for diagnosis and monitoring of disease
activity. Low levels of C4 can represent disease activity, but can also
describe partial production deficiencies, while C3 is low describe
complement activation. Cerebrospinal fluid can show pleiocytosis and
increased levels protein, and P antiribosomal antibodies and
antineutrons can be found though serum levels are negative (Rahman,
Isenberg, 2008).
Anti ds-DNA
Antinuclear antibodies (ANAs) directed against a variety of
macromolecules occur in extraordinarily high frequency in systemic
rheumatic diseases. Many rheumatic diseases are characterized by the
presence of one or more of these ANAs. Therefore, the identification
of the specific antibody is useful in the detection and diagnosis of the
disease.1 Anti-dsDNA is present in 50-70% of patients with SLE.2,3
Circulating DNA/anti-DNA immune complexes are considered to play
a part in the pathogenesis of SLE.3 The presence of anti-dsDNA is
one of the diagnostic criteria for SLE.4 IgG antibodies to dsDNA are
considered clinically most useful for the diagnosis and management of
SLE.5-10 Antibodies to single stranded DNA (ssDNA) and IgM
antibodies to dsDNA are found in a number of other connective
diseases, liver diseases, as well as in some normal individuals.11,12
Accurate detection of anti-dsDNA is important in the diagnosis and
management of SLE. EIA tests for anti-dsDNA have demonstrated
greater sensitivity than standard IFA and RIA tests allowing for
improved detection of low titer antibodies to dsDNA (DAI, 2008).
7. How to diagnosis the case?

1. This classification consists of 11 criteria where the diagnosis must meet 4

out of 11 criteria that occur simultaneously or with a time period.
2. Modification of this criterion was conducted in 1997.
3. If there are 4 or more criteria above, SLE diagnosis has 85% sensitivity
and 95% specificity. Whereas if only 3 criteria and one of them ANA
positive, then very likely SLE and diagnosis relies on clinical observation.
If the ANA test result is negative, then it may not be SLE. If only a
 positive ANA test and other clinical manifestations do not exist, then it is
not necessarily SLE, and long-term observation is required (IPDL, 2014).
8. What is differential diagnosis in the case?
Some of the diseases or conditions below often confuse diagnosis due to
similar clinical features or similar laboratory tests
a. Undifferentiated connective tissue disease
b. Sjögren's Syndrome
c. Antiphospholipid antibody syndrome (APS)
d. Fibromialgia (ANA positive)
e. Idiopathic thrombocytopenic purpura
f. Lupus is drug-induced
g. Early rheumatoid arthritis
h. Vasculitis
(Perhimpunan reumatologi indonesia, 2011).
9. What is additional examination in the case?
Necessary supporting examination for Diagnosis and Monitoring
1. Hemoglobin, Lecocytes, Count cell types, blood erythrocyte
sedimentation rate (LED)
2. Routine and microscopic urine, the 24-hour frequency of proteins,
and when the urine is exacluinine.
3. Blood chemistry (ureum, creatinine, liver function, lipid profile)
4. PT, aPTT on the antiphospholipid syndrome
5. Serology of ANA, anti-dsDNA, complement (C3, C4))
6. Photo Plain Thorax

* Examination is only for early diagnosis, not required for monitoring.

* Every 3-6 months when stable. Every 3-6 months in patients with
active kidney disease. ANA, antinuclear antibodies; PT/PTT,
prothrombin time/partial thromboplastin time (Perhimpunan
Reumatologi Indonesia, 2011).

10. What us the working diagnosis in the case?

SLE ( Systemic lupus erithematosus) serious level.
 Sistemik Lupus Eritomatous Kulit (Butterfly Rush) .
Tarigan, NS. 2015.

Annegret, dkk. 2015.

11. How is the treatment in the case?
There are types and dosages of drugs used in SLE :
Type Dosage
OAINS Depending on OAINS
Kortikosteroid Depending on the degree of SLE
Klorokuin 250 mg/day (3,5-4 mg/kg weight/day)
Hidroklorokuin 200-400 mg/day
Azatioprin 50-150 mg/day. Dose divided 1-3,
depending on body weight
Siklofosfamid Per oral : 50-150 mg
Metotreksat 7.5-20 mg/weeks
Siklosporin A 2,5-5 mg/kg weight, 100-400 mg/days.
Depending on body weight
Mikofenolate mofetil 1000-2000 mg in 2 doses.
(IPDL, 2014).

Non Pharmacology

1. Education / Counseling

Basically, SLE patients need correct information and support

from the surrounding area with the intention to be able to live
independently. Need to be explained about the course of the disease
and its complexity. Patients need knowledge of physical activity
problems, reducing or preventing recurrence including protecting the
skin from sun exposure (ultraviolet) by wearing sunscreen,
umbrellas, or hats; do the exercises in an integrated manner. Patients
must pay attention if they have an infection. It is necessary to
regulate the diet so that osteoporosis is not overweight or
dyslepidemia occurs. Information is needed to monitor various organ
functions, both related to disease activity or due to drug use. Family
education is directed at cutting psychological stigma due to families
with SLE, providing information on the need for excessive family
support. This is so that patients with SLE can be understood by their
families and be able to be independent in their daily lives

2. Rehabilitation Program
 There are various modalities that can be given to patients with
SLE depending on the aims and objectives of this program. One
important thing is understanding the decrease in muscle mass to 30%
if patients with SLE are left in an immobility condition for more than
2 weeks. Besides the decrease in muscle strength will occur around
1-5% per day in conditions of immobility. Various exercises are
needed to maintain joint stability Physical modalities such as
administration of heat and cold.

Needed to reduce pain relieve the behavior of muscle spasms.

Also other modalities such as TENS provide substantial benefits to
patients with muscle pain or stiffness Broadly speaking, the
objectives, indications and technical implementation of the
rehabilitation program involve the following purposes, namely: Rest,
Physical Therapy, Therapy with Modality, Ortotic, etc (IPDL, 2014).

12. What is the complication in the case?

Answer :
• Retinal toxicity
• End-stage renal disease
• Neuropsychiatric and neurocognitive dysfunction
• Shrinking lung syndrome
• Gonadal dysfunction
• Glucorticoid-induced side effects
• Osteonecrosis
• Osteoporosis
• Coronary Artery Disease
• Phlebothrombosis and pulmonary embolism

(Mukherjee, 2006).

13. What is prognosis in the case?

Although current treatment of lupus has improved survival dramatically,
prolonged and complete remission— defined as 5 years without clinical
 and laboratory evidence of active disease and on no treatment—has
remained elusive for most patients. The incidence of flare is estimated to
0.65 per patient-year of follow-up. Moreover, a significant number of
patients (10–20% in tertiary referral centres) do not respond adequately to
immunosuppressive therapies (George, dkk, 2012).
14. SKDU?
3A. not an emergency
Doctor graduates are able to make clinical diagnoses and provide
preliminary therapy in non-emergency situations. doctor graduates are able
to determine the most appropriate referral for subsequent patient
management. Doctor graduates are also able to follow up after returning
from referral (KKI, 2019).
15. What is Islamic point of view?
"And give good tidings to those who are patient, (that is) those who,
when afflicted by disaster, say ill Innalillahi wa innailaihi roji’un. ' They
are the ones who have the perfect blessing and grace from their Lord, and
they are the people who are guided. " (Surat al-Baqarah: 155-157).
Hadith: "Indeed, a great reward is obtained through great trials as well. If
Allah loves someone, then Allah will give a trial to him, whoever is
pleased (accepts it) then Allah will respect him and whoever is angry
(accepts it) then Allah is angry with him. " (HR. At Tarmizi).

2.7 Conclusion
Miss. A, a 20 years old women, is having malar rash, photosensitivity, anemia,
leukopenia, trombositopenia, bilirubinemia, she is suffering of systemic lupus
erythematosus (SLE) caused by autoantibodies problem.
2.8 Scema of Synthetis

Environment Factors

Immune Dysregulation
Hipersensitivity Type 3

APC Actived

APC Actives CD4+ T-

Cells in lymphatic nodes

B-Cells produce plasma cells

Plasma cells produce

antibodies (autoantibodies)

SLE (Systemic Lupus Erytmathosus)

Discoid Rash Malar Rash ANA Positive Hemolytic

Anemia
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