TUTORIAL REPORT

SCENARIO E BLOCK 7

TEAM 2
Tutor : dr. Mitayani, M.Si., Med

Members :

Permata Puspasyari (702017010)

Ahmad Al Akbar Purja (702017062)
Taris Ade Sulistiani (702020002)
Wulan Putri Utami (702020017)
Luthfi Abiyyu Mahfuzh (702020021)
Assyifa Antonia (702020029)
Uly Andesja Yuvita (702020034)
Wulan Aristi (702020045)
Zakia Salsabila (702020068)
Rahma Syifa Aulia (702020069)
Bimo Rizki Priambudi (702020108)

MEDICAL FACULTY
MUHAMMADIYAH PALEMBANG UNIVERSITY
2020/2021
 PREFACE

First of all, thanks to Almighty God, Allah SWT who has given His bless to the
writers to finish this tutorial report with title “Scenario E Tutorial Report Block 7”.
Shalawat and Salam are always given to our great prophet, prophet Muhammad SAW
and his family, friends, and followers until the end of the time.
The writers realize that this report are far from perfection. Therefore we hope
for the critic and suggestion that will help for improvement in the future. To finish this
report, the writers got so many help, guidance, and suggestion. In this chance, the
writers want to express our respect and thanks to:
1. Allah SWT, who has given the writers’s health and His blessness.
2. Both parents, who always give us their any kind of support
3. dr. Mitayani, M.Si.,Med as tutor
4. Fellow friends of Medical Faculty Muhammadiyah Palembang University
Class ’20.
5. All parties involved in making this tutorial report..
Hopefully Allah SWT give us reward for the good deeds to all people who write
and help in this tutorial report. Last, hopefully this tutorial report will be beneficial for
us and science development. May Allah SWT always protect us. Aamiin.

Palembang, July 14th 2021

Writers

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 TABLE OF CONTENTS

PREFACE ..................................................................................................................... ii

CHAPTER I .................................................................................................................. 1

PRELIMINARY ........................................................................................................... 1

1.1 Background ............................................................................................................. 1

1.2 Purpose and Objective ............................................................................................ 1

CHAPTER II................................................................................................................. 2

DISCUSSION ............................................................................................................... 2

2.1. Tutorial Data .......................................................................................................... 2

2.2. Case ........................................................................................................................ 3

2.3 Terms of clarification............................................................................................. 4

2.4 Identification of problem ..................................................................................... 4

2.5 Priority of problem............................................................................................... 5

2.6 Analysis of problem ............................................................................................. 6

2.7 Conclusion ........................................................................................................... 37

2.8 Conceptual framework ........................................................................................ 38

BIBLIOGRAPHY ....................................................................................................... 39

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 CHAPTER I

PRELIMINARY

1.1 Background
Tutorial is one of the Problem Based Learning (PBL) which is done by
discussing in small groups guided by tutors using problem scenarios as triggers.
This tutorial aims to facilitate students to learn actively, efficiently, and relevant
to the problems they face. Through this tutorial process can trigger curiosity and
critical thinking in students. The tutorial also encourages students to be more
involved and responsible for their own learning process .

In this tutorial there are stages in solving a case scenario. Thus, the problems
formulated should potentially develop an understanding of the interrelationships
of basic science, biomedics, clinical and humanities in a clinical problem. In
addition, it is also hoped that the problem formulation can trigger students to think
critically, be able to analyze and draw hypotheses.

In this tutorial process also requires the prior knowledge principle, which is
prior knowledge or knowledge before reading from any source. Thus, prio
knowledge can build the spirit of thinking and be able to know the initial abilities
possessed, so that it will continue to be triggered to study existing problems.

1.2 Purpose and Objective

The purpose and objectives of this case study tutorial report are:

1. As a tutorial group task report that is part of learning system at the Faculty
of Medicine, University of Muhammadiyah Palembang
2. Can resolve the case given in the scenario with the method of analysis and
learning of group discussion
3. The achievement of the objectives of the tutorial learning method

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 CHAPTER II
DISCUSSION

2.1. Tutorial Data

Tutor : dr. Mitayani, M.Si., Med

Moderator : Wulan Aristi

Desk Secretary : Bimo Rizki Priambudi

Board Secretary : Zakia Salsabila

Member : 1. Permata Puspasyari

2. Akhmad Al Akbar Purja
3. Taris Ade Sulistiani
4. Wulan Putri Utami
5. Luthfi Abiyyu Mahfuzh
6. Assyifa Antonia
7. Uly Andesja Yuvita
8. Rahma Syifa Aulia
Date and Time : Wednesday, July 14th 2021
13:00 – 15.30

Regulations:

1. All tutorial members must issue opinions

2. Raise your hand when submitting an argument

3. Mention the name when expressing an opinion

4. Polite and full of manners in expressing opinions

5. Permission when going out of the room

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2.2. Case
Skenario E Blok VII Batch 2020

“Blushing Cheeks ”
Miss C, a 23 years old woman, came to RSMP with the main complaint of
joint pain since 2 months ago. She also complains of frequent intermittent fevers.
The fever decreased when taking paracetamol and relapsed 2-3 times per month.
She went to primary health centre, and it is said that she had typhoid fever and was
then referred to the RSMP.
Since 6 months ago, She often complains of hair loss, thrush on the roof of
the mouth that are not painful. Two months ago, a red patch appeared on the cheek
area and became red when exposed to the sun. There is no family history of this
disease.

Physical Examination :
General appearance: looks mildly sick, sensorium: compos mentis,
Vital Sign: Respiratory rate 20x/m, Pulse rate : 80x/mt, temp 37.4° C, blood
pressure : 120/80 mmHg.
Specific examination :
Head : alopecia (+), pale palpebra conjungtive (-), icteric sklera (-), Face : malar
rash (+), mouth : ulceration on the palate (+).
Nech: enlargement of the lymph node (-)
Cor/pulmo: within normal limit
Abdoment : hepar and lien were not palpable
Ekstremity : wrist and feett: swelling/redness (+), warm (+)

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 Laboratory Examination
Blood test : Hb: 11,7 gr/dL, Eritrocyte 4.5x106/uL, Leucocyte: 6000/uL,
Trombocyte 178.000/uL, diff count 0/2/2/51/34/11. Ht 34 vol%, reticulocyte 0,5
%, LED : 100 mm/hour,
Urinalysis : within normal limit.

2.3 Terms of clarification

No Terms Meaning
Pain that body temperature to be higher than
1 Fever
usual (KBBI, 2017)
2 Alopecia Absence of hair on the skin that normally grows
Analgesics and antipyretics which have an
3 Paracetamol effect similar to aspirin but only slightly have an
inflammatory effect
Analgesics and antipyretics which have an
4 Relapsed effect similar to aspirin but only slightly have an
inflammatory effect
Erythrocyte sedimentation rate (ESR),the speed
5 LED of red blood cells settles in the rest tube in units
of mm/hour
Appear in the skin covering the nose and
6 Malar Rash surrounding areas on the cheeks to form a
butterfly pattern
A serious , sometimes fatal bacterial infection
7 Thypoid transmitted by water, milk or other foods that is
contaminated by salmonella typhi
Is painful area on the outside of the body or on
8 Ulceration the surface of an organ inside the body that may
bleed or produce a poisonous substances
9 Urinalysis Urine Analysis

2.4 Identification of problem

1. Miss C, a 23 years old woman, came to RSMP with the main complaint of
joint pain since 2 months ago. She also complains of frequent intermittent
fevers. The fever decreased when taking paracetamol and relapsed 2-3 times

4
 per month. She went to primary health centre, and it is said that she had
typhoid fever and was then referred to the RSMP.
2. Since 6 months ago, She often complains of hair loss, thrush on the roof of the
mouth that are not painful. Two months ago, a red patch appeared on the
cheek area and became red when exposed to the sun. There is no family
history of this disease.
3. Physical Examination :
General appearance: looks mildly sick, sensorium: compos mentis,
Vital Sign: Respiratory rate 20x/m, Pulse rate : 80x/mt, temp 37.4° C, blood
pressure : 120/80 mmHg.
Specific examination :
Head : alopecia (+), pale palpebra conjungtive (-), icteric sklera (-), Face : malar
rash (+), mouth : ulceration on the palate (+).
Nech: enlargement of the lymph node (-)
Cor/pulmo: within normal limit
Abdoment : hepar and lien were not palpable
Ekstremity : wrist and feett: swelling/redness (+), warm (+)

4. Laboratory Examination
Blood test : Hb: 11,7 gr/dL, Eritrocyte 4.5x106/uL, Leucocyte: 6000/uL,
Trombocyte 178.000/uL, diff count 0/2/2/51/34/11. Ht 34 vol%, reticulocyte
0,5 %, LED : 100 mm/hour,
Urinalysis : within normal limit.

2.5 Priority of problem

Number 2, reason : because Miss C has some symptoms that have not healed for
months so that should get more attention

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2.6 Analysis of problem
1. Miss C, a 23 years old woman, came to RSMP with the main complaint of joint
pain since 2 months ago. She also complains of frequent intermittent fevers. The
fever decreased when taking paracetamol and relapsed 2-3 times per month. She
went to primary health centre, and it is said that she had typhoid fever and was
then referred to the RSMP.
a. What is the meaning miss C came to RSMP with the main complaint of
joint pain since 2 months ago. She also complains of frequent intermittent
fevers ?
This means that the joint pain experienced by Miss. C may occur due to
the accumulation of antigen-antibody complexes that trigger the formation
of complement that attracts phagocytes and triggers the inflammatory
process. Meanwhile, fever occurs due to the body's response to
inflammation, resulting in the release of endogenous pyrogens (IL-1, IL-6,
prostaglandins, tumor necrosis factor (TNF)) and an increase in thermostart
in the hypothalamus. And also it can be interpreted as Miss.C complaints
of joint pain since 2 months ago and she also complains of frequent
intermittent fevers are she may experince SLE, Rheumatoid arthritis,
rheumatic olimyalgia, gouty arthritis, Osteoarthritis, and others (Tarigan,
2015).

b. What classification of fever ?

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.

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 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.
7. Pel Ebstein Fever : In Pel Ebstein fever there is a fever with a fever-
free period for 3-4 days, then the body temperature rises again for 7-
10 days. This type of fever is found in infections mononucleosis.
8. Low grade fever : Low grade fever is said when the body temperature
does not exceed 37.8°C throughout the day and increases at night.
Types of fever like found in tuberculosis patients. This type is also
called constant or continuous because the body temperature is not too
high (low grade) and hasn't changed much for over 24 hours.
9. Prolonged fever: Fever that lasts more than 14 days
10. Chronic fever : Fever that lasts more than a month to a year. (Zein,
2012)

c. How pathophysiology of thphoid fever ?

Salmonella typhi bacteria with food or drink enter the body through the
mouth. At the time of passing through the gaster with an much acid, many
bacteria die. Bacteria that are still alive will reach the small intestine,
attaches to mucosal cells and then invades and penetrates the intestinal wall
to be precise in the ileum and jejunum. M cells, the epithelial cells lining
Peyer's patches are the survival and multiplication of Salmonella typhi.
Bacteria reach the follicle Small intestinal lymph causes ulcers on the
intestinal mucosa. Ulcers can cause intestinal bleeding and perforation.
Then follow the flow to the lymph nodes mesenteric and some even pass
through the systemic circulation to the reticulo tissue Endothelial system

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 (RES) in the liver and spleen. After the incubation period, Salmonella
Typhi leaves their habitat through the thoracic duct into the circulation
systemically reaches the liver, spleen, bone marrow, gallbladder and
Peyer's patches from the terminal ileum. Bacterial excretion in bile can re-
invade the intestinal wall or incurred through fees. Endotoxins trigger
macrophages in the liver, spleen, intestinal and mesenteric lymphoid glands
to release sales locally causes necrosis of bowel or liver cells and
systematically causes clinical symptoms of typhoid fever. (Cita, 2011)

d. What is the anatomy and physiology in this case ?

A joint is a point where two bones make contact. Joints can be classified
either histologically on the dominant type of connective tissue functionally
based on the amount of movement permitted. Histologically the three joints

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in the body are fibrous, cartilaginous, and synovial. Functionally the three
types of joints are synarthrosis (immovable), amphiarthrosis (slightly
moveable), and diarthrosis (freely moveable). The two classification
schemes correlate: synarthroses are fibrous, amphiarthroses are
cartilaginous, and diarthroses are synovial. (Marieb et.al, 2014)

Fibrous Joint
A fibrous joint is a fixed joint where fibrous tissue comprised primarily
of collagen connects bones. Fibrous joints are usually immoveable
(synarthroses) and have no joint cavity. They are subdivided further into
sutures, gomphoses, and syndesmoses. (Marieb et.al, 2014)
Sutures are immobile joints in the cranium. The plate-like bones of the
skull are slightly mobile at birth because of the connective tissue between
them, termed fontanelles. This initial flexibility allows the infant’s head to
get through the birth canal at delivery and permits the enlargement of the
brain after birth. As the skull enlarges, the fontanelles reduce to a narrow
layer of fibrous connective tissue, called Sharpey’s fibers, that suture the
bony plates together. Eventually, cranial sutures ossify- the two adjacent
plates fuse to form one bone; this fusion is termed synostosis.
Gomphoses are the immobile joints between the teeth and their sockets in
the mandible and maxillae. The periodontal ligament is the fibrous tissue
that connects the tooth to the socket. (Marieb et.al, 2014)
Syndesmoses are slightly movable joints (amphiarthroses). In
syndesmosis joints, the two bones are held together by an interosseous
membrane. For example, the tibia connects to the fibula, forming the
middle tibiofibular joint, and the ulna attaches to the radius, forming the
middle radio-ulnar joint. (Marieb et.al, 2014)

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Cartilaginous Joint
In cartilaginous joints, the bones attach by hyaline cartilage or
fibrocartilage. Depending on the type of cartilage involved, the joints
further classify as primary and secondary cartilaginous joints. (Marieb et.al,
2014)
Primary cartilaginous joints, also known as synchondroses, only involve
hyaline cartilage. These joints may be slightly mobile (amphiarthroses) or
immobile (synarthroses). The joint between the epiphysis and diaphysis of
growing long bones is an example. (Marieb et.al, 2014)
The secondary cartilaginous joint, also known as symphysis, may
involve either hyaline or fibrocartilage. These joints are slightly mobile
(amphiarthroses). A classic example is the pubic symphysis. (Marieb et.al,
2014)

Synovial Joint
Synovial joints are freely mobile (diarthroses) and are considered the
main functional joints of the body. Its joint cavity characterizes the synovial
joint. The cavity is surrounded by the articular capsule, which is fibrous
connective tissue that is attached to each participating bone just beyond its
articulating surface. The joint cavity contains synovial fluid, secreted by
the synovial membrane (synovium), which lines the articular capsule.
Hyaline cartilage forms the articular cartilage, covering the entire
articulating surface of each bone. The articular cartilage and the synovial
membrane are continuous. Some synovial joints also have associated
fibrocartilage, such as menisci, between articulating bones. (Marieb et.al,
2014)
Synovial joints are often further classified by the type of movements
they permit. There are six such classifications: hinge (elbow), saddle
(carpometacarpal joint), planar (acromioclavicular joint), pivot

10
(atlantoaxial joint), condyloid (metacarpophalangeal joint), and ball and
socket (hip joint). (Marieb et.al, 2014)

Skin Anatomy and Physiology

The skin is a protective barrier that has vital functions such as:
protection against conditions outside the environment both from physical
and chemical effects, as well as preventing excess water loss from the body
and as thermoregulation. The protective function of the skin is to protect
the body from fluid loss electrolytes, mechanical trauma and ultraviolet
radiation, as a barrier to invasion pathogenic microorganisms, respond to
stimuli of touch, pain and heat because there are many nerve endings, where
nutrients and water are stored Can be used when there is a decrease in blood
volume and the site of occurrence metabolism of vitamin D
(Perdanakusuma, 2007).
Skin function :
1. Skin as body temperature regulator
2. Skin as a protector and body filter
3. Skin maintains body moisture
4. The skin as a sensitive nervous system.

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 The skin consists of two different layers, the outer layer is the epidermis
which is the epithelial layer and the inner layer is the dermis which is the a
layer of connective tissue.
a. Epidermis
The epidermis is the outermost layer of the skin which consists of stratified
epithelium horned, containing malonocytes, Langerhans and Merkel cells.
Thick Epidermis varies in various places on the body, is thickest on the
palms of the hands and feet. The thickness of the epidermis is only about
5% of the thickness skin. The epidermis consists of five layers (from the
top to the deepest) namely the stratum corneum, stratum lucidum, stratum
granulosum, stratum spinosum and stratum basale (stratum Germinatum)
(Perdanakusuma, 2007).
b. Dermis
The dermis is composed of cells in various shapes and conditions, the
dermis composed mainly of collagen and elastin fibers. Thickened collagen
fibers and collagen synthesis decreases with age. While elastin fibers
continue to increase and thicken, the elastin content of human skin It
increases about 5 times from fetus to adult. In old age, collagen will cross
each other in large numbers and the elastic fibers will be reduced This
causes the skin to lose its elasticity and look wrinkled (Perdanakusuma,
2007). The dermis contains hair follicles, hair papillae, sweat glands, sweat
ducts, sebaceous glands, hair-bearing muscles, blood vessels and nerve
endings and some of the fat fibers found in the fat layer under the skin
(Tranggono and Latifah, 2007).
c. Subcutaneous
The subcutaneous layer is the layer below the dermis which consists of fat
layer. This layer contains connective tissue that connects the skin loosely
with the underlying tissue. The amount and size varies according to the area

12
 of the body and the nutritional state of the individual. Function to support
supply blood to the dermis for regeneration (Perdanakusuma, 2007).

e. What is the relation between age and gender in this case ?

Based on the results of research that has been done, it shows that there
are more women with SLE (92.9%) than men (7.1%). It is suspected that
the hormones estrogen and prolactin, which are more abundant in women,
can activate polyclonal B cells, resulting in excessive autoantibody
production in SLE patients. (Istiqomah et all, 2018)
Age range 21-30 years, because the incidence of SLE is more common
in patients in the reproductive period, where hormonal factors result in
excessive production of autoantibodies in SLE patients. (Istiqomah et all,
2018)
According to the Center for Disease Control (CDC), lupus
primarily occurs in women approximately four to twelve women for
every man, and more frequently occurring inthe childbearing years for
females. The CDC states, "Blacks (and probably Hispanics, Asians,and
Native Americans) are affected more than whites. People with a family
history of SLE or other autoimmune diseases are at slightly higher risk
for developing SLE" ("Systemic", 2015, p.1). Even with these
concentrations of who is affected by lupus it truly can affect any
gender,race, ethnicity, and age.

f. How pathophisiolgy of joint pain ?

Hypersensitivity Reaction Type III → Autoimmune Disease →
Erythematosous Systemic Lupus → Blood Circulation Disorders →
Damage Inflammatory → Tissue in Joints → Joint Pain. (Suntoko, 2017)

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g. What is the etiology of thypoid fever ?
Typhoid is caused by Salmonella typhi, which is a gram-negative enteric
bacterium in the form of a bacillus and is pathogenic to humans. This
disease is easily transferred from one person to another who does not
maintain personal and environmental hygiene, namely direct transmission
if these bacteria are present in the feces, urine or vomit of the patient and
can transmit it to others and indirectly through food or drink. Salmonella
typhi plays a role in local inflammatory processes in tissues where bacteria
breed and stimulates the synthesis and release of pyrogens and leukocytes
in inflamed tissues resulting in fever. This typhoid disease has a close
relationship with the environment, especially in an environment where the
supply of drinking water does not meet the health requirements and poor
sanitation in the environment. The factors that influence the spread of
typhoid are air pollution, general sanitation, water quality, temperature,
population density, poverty and others.(Ardiaria, 2019)
The main causative agent of typhoid fever is Salmonella typhi and
Salmonella paratyphi, both are members of the Enterobacteriaceae family.
Salmonella is a genus[2] that has two species Salmonella enterica serovar
and enteritidis classified through extensive analysis by multiplex
quantitative polymerase chain reaction (PCR).[3] Both Salmonella typhi
and Salmonella paratyphi (A, B, C) are Salmonella enterica serotypes.
Nontyphoidal salmonella (NTS) is more typical in children and is mostly
limited to gastroenteritis.
Salmonella is transmitted by the fecal-oral route through contaminated
water, undercooked foods, fomites of infected patients, and is more
common in areas with overcrowding, social chaos, and poor sanitation. It
is only transmitted from an infected person to another person, as humans
are its only host. Major sources of salmonella are poultry, eggs, and rarely
turtles. In one study done on the distribution of salmonella isolates by

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 whole-genome sequencing in chicken slaughterhouses in China, 57% of
samples were positive.
Normal flora of the gut is protective against the infection. The use of
antibiotics such as streptomycin destroys the normal flora, which heightens
its invasion. Malnutrition decreases normal gut flora and thus increases the
susceptibility to this infection as well. Hence, the use of broadspectrum
antibiotics and poor nutrition amplify the incidence of typhoid fever.
(Bhandari et.al, 2020)

h. What is etiology of joint pain ?

Any general body infection: joint pains may be caused by any general
body infection, especially a flu-like illness with high temperature (fever).
Many joints feel painful, or there may be a feeling of pain 'all over' or in all
joints. (Michael et.al, 2016)
Osteoarthritis (OA): the most common form of arthritis in the UK. This
is a joint pain caused by a 'wear and tear' of the joint. It may be most
noticeable at first in just one joint, such as the hip or knee, but as time goes
on usually affects several joints. As well as the hip, knee and hands, the
many joints in the spine are often affected. See the separate leaflet called
Osteoarthritis. (Michael et.al, 2016)
Rheumatoid arthritis (RA): causes inflammation, pain, and swelling of
joints. Painful and stiff joints are often worse in the morning in people with
RA. Persistent inflammation over time can damage affected joints. The
severity can vary from mild to severe. See the separate leaflet called
Rheumatoid Arthritis. (Michael et.al, 2016)
Gout: causes attacks of painful inflammation in one or more joints. The
pain of a gout attack can be severe. Gout often first occurs in just one joint,
most commonly the big toe, but may go on to affect other joints. See the
separate leaflet called Gout. (Michael et.al, 2016)

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 Fibromyalgia: causes pains and tenderness in many areas of the body,
as well as tiredness and other symptoms. See the separate leaflet called
Fibromyalgia. (Michael et.al, 2016)
The main cause of joint pain is still unknown certainly. Usually a
combination of genetic, environmental, hormonal and reproductive system
factors. But the biggest trigger factor is infection factors such as bacteria,
microplasma and viruses. There are several theories put forward as the
cause of joint pain, namely:
a. Immunity mechanisms.
Joint pain sufferers have autoantibodies in their serum, known as
rheumatoid factor. Antibodynya is an antimagic globulin (IgM) factor that
reacts to changes in IgG titers greater than 1:100, usually associated with
vasculitis and poor prognosis.
b. Metabolic factors.
Metabolic factors in the body are closely related to the autoimmune
process.
c. Genetic factors and environmental trigger factors.
Joint pain is associated with genetic markers. Also with environmental
problems, housing problems and poor and humid arrangements also trigger
joint pain.
d. Age factor.
Degeneration of body organs causes the elderly to be vulnerable to both
acute and chronic diseases (Michael, et all , 2016).

i. What is the meaning The fever decreased when taking paracetamol and
relapsed 2-3 times per month ?
Because paracetamol as analgesic and antipyretic in the body where this
drug only relieves the symptoms of pain and inflammation related to the
disease symptomatic so that if the antibody is disturbed then fever can re-
arise or relapse. (Wilmana et.al, 2016)

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j. How epidemiology in case ?
The incidence of SLE varies among ethnic groups and by geographic
location, sex, and age. The reported prevalence of SLE in the general
population is approximately 20 to 150 cases per 100,000 persons.4–6

Geography
A report submitted by the National Arthritis Data Working Group
estimated that SLA affects 250,000 Americans.41 The prevalence of SLE
in the U.S. demonstrates a distinct elevation among Asian, Afro-American,
Afro-Caribbean, and Hispanic-Americans compared with Americans of
Eastern European descent.42,43 For example, the prevalence of SLE
among Caucasian patients in Rochester, Minn., is approximately 40 cases
per 100,000 persons, compared with Hispanic patients in Nogales, Arizona,
where the rate is 100 cases per 100,000 persons.44,45
Black persons in Africa have a much lower incidence of SLE than
African-Americans in the U.S.46 The incidence of SLE in various
populations (e.g., urban versus rural areas) is also a topic in need of further
investigation. Epidemiologic data utilizing lupus registries point to the need
for larger, population-based studies with a large patient base. Such data are
currently lacking because of potential obstacles, such as differing case
definitions, small-source populations, and varying demographic group
targets 47. (Ardiaria, 2019)

Sex and Age

SLE is more common in women, particularly those of child-bearing age.
This increased incidence may be attributed to hormones, namely estrogen,
as studies have shown women who had an early menarche or who used oral
contraceptives or hormonal therapies had an increased risk of SLE.48,49

17
 The lower risk in men is similar to that in prepubertal or postmenopausal
women. Klinefelter’s syndrome, which features an extra X chromosome in
males, is linked to an elevated incidence of SLE, thereby providing further
support for the association between SLE and a possible hormonal
pathogenesis. (Ardiaria, 2019)

k. How farmakodimanic of paracetamol ?

The cyclooxygenase (COX) enzyme has several isoforms. The best
known are COX-1 and COX-2. Although both have similar characteristics
and catalyze the same reactions, there are differences in their effects.
COX-1 is an enzyme that is expressed by almost all tissues in the body,
including platelets, and has a role in the production of prostaglandins
involved in gastric protection, platelet aggregation, autoregulation of renal
blood flow, and initiation of parturition. Meanwhile, COX-2 plays an
important role in the inflammatory process by activating inflammatory
cytokines. COX-2 is also highly expressed in the kidney and produces
prostacyclin which plays a role in renal homeostasis.
Activation of COX-1 and COX-2 was influenced by arachidonic acid
levels. When arachidonic acid levels are low, prostaglandins will be formed
mainly from COX-2, while when arachidonic acid levels are high,
prostaglandins will be formed mainly from COX-1. This level of
arachidonic acid also affects the action of paracetamol. Low levels have a
potent effect on paracetamol and high levels will inhibit the action of
paracetamol.
Paracetamol has analgesic and antipyretic effects equivalent to NSAIDs.
As an analgesic, paracetamol inhibits prostaglandins by acting as a
substrate in the COX-1 and COX-2 enzyme peroxidase cycle and inhibits
peroxynitrite which is an activator of the COX enzyme. As an antipyretic,

18
 paracetamol inhibits the increase in the concentration of prostaglandins in
the central nervous system and cerebrospinal fluid caused by pyrogens.
The clinical effect of paracetamol can be seen within an hour after
administration. In some studies it was found that paracetamol can reduce
temperature by 1oC after one hour of administration.
Paracetamol is not as effective as NSAIDs in relieving pain in acute arthritis
because it cannot reduce prostaglandin levels in synovial fluid. Compared
with NSAIDs, paracetamol has less side effects to the gastrointestinal
system. Therefore paracetamol can be used to reduce pain in patients with
a history of peptic ulcer. (Katzung, 2016)

l. How farmakokinetik of paracetamol ?

Pharmacokinetics of paracetamol are quite good with high
bioavailability.
a. Absorption
Paracetamol is well absorbed in the small intestine through passive
transport in oral administration. Provision of food will slightly slow
absorption of paracetamol. In rectal administration, there are variations in
peak concentrations in plasma and the time needed to reach peak
concentrations in plasma is longer (Moriarty C, 2014).
b. Distribution
After oral administration, peak concentrations in plasma will be achieved
within 10 – 60 minutes on regular tablets and 60 - 120 minutes for slow-
release tablets. The average concentration in plasma is 2.1 μg / mL in 6
hours and the levels are only detected in small amounts after 8 hours.
Paracetamol has a half-life of 1-3 hours. Paracetamol has high
bioavailability. About 25% of paracetamol in the blood is bound by protein
(Moriarty C, 2014).

19
c. Metabolism
Paracetamol metabolism is mainly in the liver through the process of
glucoronidation and sulfation into non-toxic conjugates. A small portion of
paracetamol is also oxidized via the cytochrome P450 enzyme into a toxic
metabolite in the form of N-acetyl-p-benzo-quinone imine (NAPQI).
Under normal conditions, NAPQI will be conjugated by glutathione to
cysteine and the mercapturic acid conjugate. When given large doses or
with glutathione deficiency, NAPQI cannot be detoxified and causes acute
liver necrosis (Moriarty C, 2014).
d. Elimination
About 85% of paracetamol is excreted in conjugated form and is free in
urine within 24 hours. In oral paracetamol, excretion through the renal takes
place at a rate of 0.16 - 0.2 mL / min / kg. This elimination will be reduced
in individuals age > 65 years or with kidney disorders. Aside from the
kidneys, around 2.6% will be excreted via biliary. Paracetamol can also be
excreted by hemodialysis (Moriarty C, 2014).
Paracetamol is rapidly and completely absorbed from the
gastrointestinal tract.The highest concentration in plasma is reached within
half an hour and plasma half-life of 1-3 hours. This drug is spread
throughout the body fluids Binding of this drug to plasma proteins is
variable, only 20%-50% is possible bound to concentrations found during
acute intoxication. After dose therapeutically, 90%-100% of the drug is
found in the urine during the first day, especially after hepatic conjugation
with glucuronic acid (about 60%), -acid sulfate (about 35%), or cysteine
(about 3%), small amounts of metabolites hydroxylation and deacetylation
have also been detected. A small amount of paracetamol undergoes a
cytochrome P450-mediated N hydroxylation process which form N-acetyl-
benzoquinoneimine, which is an intermediate very reactive. These
metabolites react with the sulfhydryl groups of glutathione. However, after

20
 ingestion of large doses of paracetamol, these metabolites are formed in the
amounts sufficient to remove hepatic glutathione. (Kusuma, 2013)

m. What are the side effect of the drug paracetamol ?

In general, acetaminophen (the active ingredient contained in
Paracetamol) is well-tolerated when administered in therapeutic doses. The
most commonly reported adverse reactions have included nausea,
vomiting, constipation. Injection site pain and injection site reaction have
been reported with the IV product. (Ennis et.al, 2016)
Few if any drugs come without side effects, and paracetamol is no
different. Below we’ve listed common side effects of paracetamol, most of
which are rare and mild, with one notable exception:
a. an allergic reaction, which can cause a rash and swelling
b. flushing, low blood pressure and a fast heartbeat – this can sometimes
happen when paracetamol is given in hospital into a vein in your arm
c. blood disorders, such as thrombocytopenia (low number of platelet
cells) and leukopenia (low number of white blood cells)
d. liver and kidney damage, if you take too much (overdose) – this can be
fatal in severe cases
The most likely side effect that can occur from taking paracetamol is
liver and kidney damage when you take too much. For this reason, it’s
essential to stick to the guidelines and recommendations strictly: always
leave at least four hours in between doses, and never take more than 4
grams of paracetamol in 24 hours (4 dosages of 1g).

Hepatic
Common (1% to 10%): Increased aspartate aminotransferase
Rare (less than 0.1%): Increased hepatic transaminases
Frequency not reported: Liver failure[Ref]

21
Gastrointestinal
Very common (10% or more): Nausea (up to 34%), Vomiting (up to 15%)
Common (1% to 10%): Abdominal pain, diarrhea, constipation, dyspepsia,
enlarged abdomen
Frequency not reported: Dry mouth[Ref]
Hypersensitivity
Postmarketing reports: Anaphylaxis, hypersensitivity reactions[Ref]
Hematologic
Common (1% to 10%): Anemia, postoperative hemorrhage
Very rare (less than 0.01%): Thrombocytopenia, leucopenia,
neutropenia[Ref]
Dermatologic
Common (1% to 10%): Rash, pruritus
Rare (less than 0.1%): Serious skin reactions such as acute generalized
exanthematous pustulosis, Stevens-Johnson syndrome, and toxic epidermal
necrolysis
Very rare (less than 0.01%): Pemphigoid reaction, pustular rash, Lyell
syndrome[Ref]
Respiratory
Common (1% to 10%): Dyspnea, abnormal breath sounds, pulmonary
edema, hypoxia, pleural effusion, stridor, wheezing, coughing[Ref]
Cardiovascular
Common (1% to 10%): Peripheral edema, hypertension, hypotension,
tachycardia, chest pain[Ref]
Metabolic
Common (1% to 10%): Hypokalemia, hyperglycemia[Ref]
Nervous system
Common (1% to 10%): Headache, dizziness
Frequency not reported: Dystonia

22
 Musculoskeletal
Common (1% to 10%): Muscle spasms, trismus
Psychiatric
Common (1% to 10%): Insomnia, anxiety
Genitourinary
Common (1% to 10%): Oliguria
Local
Common (1% to 10%): Infusion site pain, injection site reactions
Ocular
Common (1% to 10%): Periorbital edema
Other
Common (1% to 10%): Pyrexia, fatigue
Rare (0.01% to 0.1%): Malaise (Ennis et.al, 2016)

n. What is contraindication of paracetamol ?

Contraindications: IV severe hepatic impairment or severe active liver
disease. (Twycross, 2013)

o. What is indication of paracetamol ?

Paracetamol (acetaminophen) is the most commonly used drug in the
world, with a long record of use in acute and chronic pain. In recent years,
the benefits of paracetamol use in chronic conditions has been question,
notably in the areas of osteoarthritis and lower back pain. And, the effect
of chronic therapeutic dose paracetamol use on the liver and GI system in
general is less clear. (McCrae et.al, 2018)

p. What about pathophysiology of fever in this case ?

Trigger factor (enviromental factors and hormonal factors) → APC Actived
→ Stimulation of white blood cells (monocytes, lymphocytes and
neuritfils) by exogenous pyrogens in the form of toxins, inflammatory

23
 mediators or imun reactions → then the cells will deliver chemicals known
as endogenous pyrogens → so that endogenous and exogenous pyrogens
will stimulate endothelium hypothalamus to form prostaglandins →
prostaglandins that have been formed will increase the thermostat
benchmark at the center of thermolegulation of the hypothalamus → then
the hypothalamus will gapper temperatures lower than the new benchmark
temperature → so this triggers a mechanism to increase heat for
compentation. (Setiati et.al, 2014)

2. Since 6 months ago, She often complains of hair loss, thrush on the roof of the
mouth that are not painful. Two months ago, a red patch appeared on the cheek
area and became red when exposed to the sun. There is no family history of
this disease.
a. What is the meaning Since 6 months ago, She often complains of hair loss,
thrush on the roof of the mouth that are not painful ?
Miss C has systemic lupus erythematosus (SLE). Because based on
complaints felt by miss A refers to the criteria or symptoms of mild SLE.
SLE Criteria:
1. Mouth Ulceration
2. Photosensitivity
3. Peripheral Neuropathy
4. Malar rash
5. artritisnonerosif
6. Pleuroperikarditis
Fever that is felt miss C is a common manifestation of SLE in systemic
autoimmune disorders which are usually found constitutional abnormalities
such as: fatigue, fever, and decreased appetite (Setiati et.al, 2014).

24
b. What is the meaning Two months ago, a red patch appeared on the cheek
area and became red when exposed to the sun ?
This means that Ms. C 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, 2019).
Rash on the face is considered the clinical manifestation that most
directs the diagnosis of SLE, where the rash is in the form of a butterfly rush
(butterfly rush) in the form of slightly edematous erythema on the nose and
cheeks. On parts of the body that are exposed to the sun, skin rashes can
occur due to hypersensitivity. This photosensitivity occurs because UV light
causes apoptosis in the skin, normally these apoptotic cells are immediately
removed, but in SLE there is a defect in the apoptotic clearance system so
that these cells trigger an immune response (Tarigan, 2017).

c. What is the correlation between main complain and additional complaint in

this scenario ?
The correlation that Ms. C experienced clinical manifestations of
Systemic Lupus Erythematosus (SLE) disease,and complaints felt by miss
C refers to the criteria or symptoms of SLE.
SLE Criteria:
· Mouth Ulceration
· Photosensitivity
· Malar rash (Najirman, 2019).

25
d. How the pathophysiology of red patch ?
The redness that occurs is due to the inflammatory process. Very
inflammatory process closely related to the immune system. Broadly
speaking, the body's immunity is divided into 2 namely the
innate/nonspecific immune system and the acquired/specific immune
system. Non-specific will attack all incoming antigens, while the specific is
the next defense which selects the incoming antigen. When an antigen enters
the body, phagocytic specialists (macrophages and neutrophils) will
phagocytize the antigen. This is coincides with the release of histamine by
mast cells in tissue areas the damaged one. This released histamine makes
blood vessels vasodilate to Increases blood flow to the infected area. In
addition, histamine also makes capillary permeability increases so that
plasma proteins that should remain in the in the blood vessels will easily
come out into the tissue. This causes the skin reddish color due to
inflammation. (Pardiansyah, 2015)

e. What is pathophysiology of hair loss in this case ?

The mechanism of non-scarring alopecia in SLE still remains to be
discovered. Cutaneous LE results from a combination of genetic
predisposition, ultraviolet radiation, recruitment of T cells and a plethora
of chemokines and cytokines. Involvement of hair follicles may share a
similar pathophysiology, further complicated by the dynamic nature of hair
cycle. We speculate that a high level of proinflammatory cytokines and an
aggregation of immune cells during SLE exacerbations may negatively
affect the hair growth cycle. Type I IFN plays an important
proinflammatory role in both cutaneous and systemic LE. Although the
inhibition of anagen phase and premature hair shedding are primarily
linked to IFN-γ, increasing evidence suggests that IFN-α may also have a
similar effect on hair follicles. Reduction of follicular density in the absence
of other scarring signs on histopathology may demonstrate a

26
 biphasic pattern of alopecia in SLE, where the early process has no scarring,
but follicular dropouts become apparent later. Persistently active SLE may
impair the follicular stem cell functions, leading to exhaustion of their
proliferative capacity and subsequent permanent follicular degeneration.
(Chanprapaph et.al, 2019)

Hair loss is alopecia

Environment factors → cells apoptosis occurs → Secrete nuclear antigen →
complex antigen antibodies(nuclear antigen-Anti nuclear antigen) →
deposit in inflammatory body tissues → inflammatory skin layer
→alopecia. (Umborowati, 2013)

f. What is etiology of hair loss ?

The hallmark finding in cicatricial alopecias is fibrosis of the follicular
structure, which is appreciated clinically as obscured follicular openings on
the scalp. The scarring process usually begins with the inflammatory cells
infiltrating the follicular bulge, a contiguous part of the outer root sheath
located at the insertion point for the arrector pili muscle. This marks the
bottom of the permanent portion of hair follicles and is also where the
epidermal hair stem cells are located. Once replacement by fibrous tissue is
established, hair loss is permanent and irreversible. Scarring alopecias are
usually either (1) primary, in which the hair follicle is the main target of
inflammation; or (2) secondary, if a separate disease process causes
destruction of the nearby follicular structure. In 2001, the North American
Hair Research Society proposed a classification scheme for the primary
scarring alopecias based on the predominant inflammatory cell type on 39
histology (lymphocytic, neutrophilic, mixed, non-specific). Scalp DLE
serves as a model for studying the processes leading to primary lymphocytic
cicatricial alopecias (Concha and Werth, 2018).

27
 Alopecia is caused by the immune system attacking hair follicles
(autoimmune diseases). This condition causes the discharge of pro-
inflammatory cytokines andchemokin. then cause a cessation of hair
production. As a result, the hair becomes hair loss and eventually becomes
bald. Until now it is not known the exact cause why the immune system
attacks and damages the hair follicles. However, the condition is thought to
be triggered by viral infections, trauma, hormonal changes, and physical or
psychic stress.

g. What the menaing of There is no family history of this disease ?

The causes of systemic lupus erythematosus are unknown, however,
combination of genetic factor (some gene interaction, family history),
hormonal (women in productive age, estrogen and prolactin suspected
influenced) and environtment (Psychology stress, UV light, Polution,
Cigarrette’s smoke, drugs, chemical agent) suspected to cause SLE
(Fitzpatrick dkk, 2018).
From the statement, family history can be excluded as the factors of SLE in
Ms. C

h. How the pathophysiology of thrush on the roof of the mouth ?

Trush on the roof of the mouth is ulceration mouth
Environment factors → cells apoptosis process → Secrete nuclear antigen
→ complex antigen antibodies (nuclear antigen-Anti nuclear antigen) →
deposit in the tissues of body → inflammatory lessions of ulceration.
(Cappello, 2019)

28
i. What is the possible disease cause by red patch appeared on the cheek area
and became red when exposed to the sun ?
Because Lupus was first described as a dermatologic condition.
Cutaneous manifestations of SLE comprise four diagnostic criteria and
multiple other clues to a potential diagnosis of lupus (1). The first is malar
rash, which is characterized by an erythematous rash over the cheeks and
nasal bridge. It lasts from days to weeks and is occasionally painful or
pruritic. The second feature is photosensitivity, which may be elicited from
patients who are asked if they have any unusual rash or symptom
exacerbation after sun exposure. The third feature may be discoid rash.
Discoid lesions often also develop in sun-exposed areas but are plaque like
in character, with follicular plugging and scarring. They may be part of
systemic lupus or may represent discoid lupus without organ involvement,
which is a separate diagnostic entity. Alopecia is the fourth and often less-
specific cutaneous feature of SLE. It often affects the temporal regions or
creates a patch like pattern of hair loss. Other cutaneous manifestations
related to but not specific to SLE include Raynaud phenomenon, livedo
reticularis, panniculitis (lupus profundus), bullous lesions, vasculitic
purpura, telangiectasias, and urticaria (2). Diagnosis of lupus panniculitis
was considered on clinical and histopathological grounds. Between 70 and
80% of patients develop skin lesions during the course of disease.
Approximately 20% of them have skin lesions as an initial presentation. The
pathognomonic lupus or butterfly rash across the nose occurs in only 30%
of patients with SLE. The acute lupus rash may be present elsewhere.
Discoid or disc-shaped skin lesions, pathognomonic for discoid lupus, can
manifest also in SLE. Photosensitivity rash can appear even after mild sun
exposure (3). Livedo reticularis, a reddish purple rash, is usually present in
patients with severe vasculitis or in individuals with elevated APL. Alopecia
with patchy or diffuse loss of hair with scalp scarring is another skin

29
 manifestation. Raynaud's phenomenon can cause bluish discoloration of
digits and blanching of the skin. (Cojocaru, 2011)

3. Physical Examination :
General appearance: looks mildly sick, sensorium: compos mentis, Vital Sign:
Respiratory rate 20x/m, Pulse rate : 80x/mt, temp 37.4° C, blood pressure :
120/80 mmHg.
Specific examination :
Head : alopecia (+), pale palpebra conjungtive (-), icteric sklera (-), Face : malar
rash (+), mouth : ulceration on the palate (+).
Nech: enlargement of the lymph node (-)
Cor/pulmo: within normal limit
Abdoment : hepar and lien were not palpable
Ekstremity : wrist and feett: swelling/redness (+), warm (+)

a. What is the interpretasion of physical examination ?

Physical Examination Results Interpretasion

Alopecia (+) Abnormal

Head Konjungtiva Pale and palpebral (-) Normal
Icteric Sklera (-) Normal
Face Malar rash (+) Abnormal
Mouth Ulceration on the palate (+) Abnormal
Neck Enlargement of the lymph noda (-) Normal
Cor/Pulmo Within normal limit Normal
Abdoment Hepar were not palpable Normal
Wrist and feet :
Extreminity Swelling redness (+) Abnormal
Warm (+) Abnormal

30
 b. How abnormal mechanism physical examination ?
1. Malar rash (+)
Autoantibodies sent by plasma cells → sent in blood → antigens of the
patient's body. Autoantibodies that are released by antigens released in the
blood → apoptosis → make antigen-antobody complexes. Autoantibodies
→ activate the inflammatory system → organ damage → skin (most at risk
of sun damage or UV rays) → face (malar rash). (Uva, 2012)

2. Ulceration on the palate (+)

Environmental factors (in the case probably by exposure to UV rays by the
Sun) → impaired immune regulation system → activates T and B cells →
abnormal T-suppressor cell function → increased auto antibody production
→ damage to mucous tissue in the mouth → Ulceration. (Uva, 2012)

4. Laboratory Examination
Blood test : Hb: 11,7 gr/dL, Eritrocyte 4.5x106/uL, Leucocyte: 6000/uL,
Trombocyte 178.000/uL, diff count 0/2/2/51/34/11. Ht 34 vol%, reticulocyte
0,5 %, LED : 100 mm/hour, Urinalysis : within normal limit.
a. What is the interpretasion of laboratory examination ?
Pemeriksaan
Normal Pada Kasus Interpretasi
Laboratorium
Darah Rutin
Hb 13,8-17,2 gr/dL 11,7 gr/dL Anemia
Erytrocite 4,3-5,6 x 106/uL 4,5X106/uL Normal
Trombosit 150.000-400.000/mm3 178.000/mm3 Normal
Leukosit 4.000-11.000/mm3 6000/mm3 Normal

31
 Basofil : 0-1
Eosinofil : 1-6
Rod Neutrophils : 3-5
Shift to the
Diff count Segmented 0/2/2/51/34/11
right
Neutrophils : 40-70
Limfosit : 35-45
Monosit : 2-10

Hematocrit 37-43 % 34 vol% Decrease

Retikulosit 0.5-1,5 % 0,5 % Normal
LED < 15 mm/hour 100 mm/hour Increase
Urinalisa
Within normal
Urin Within normal limit Normal
limit

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).

5. Additional examination
Given during second tutorial:
immunological serum examination: C3 : 40 mg/dL , C4 : 45 mg/dl, Anti ds-
DNA : 332 IU/ml , ANA : > 1: 1000.
a. What is the interpretasion of additional examination ?

C3 : 40 mg/dL Abnormal 80-177 mg/Dl

C4 : 45 mg/dL Normal 12-48 mg/Dl
Anti ds-DNA : 332 IU/ml Abnormal
ANA : > 1 : 1000 Abnormal (positif)

32
6. How to diagnosis in this case ?
• From anamnesis and Physical Examination
Correct diagnosis of SLE is very important, so that this disease can be treated
properly. The following criteria for SLE diagnosis are according to the revised
1997 ACR. This classification consists of 11 criteria where the diagnosis must
meet 4 of the 11 criteria that occur at the same time or with a gap period.
1. Malar rash
2. Discoid rash
3. photosensitivity
4. Serositis
5. Neurological disorders
6. Hematologic Disorders
7. Immunological disorders
8. Antibodi antinuclear Positif (ANA)
9. Arttritis
10. Renal impairment
11. ulceration
• So from 11 SLE diagnosis, in case Miss C have 5 diagnosis from thats
complain,Physical Examination, and Laboratory Examination such as
malar rash, photosensitivity, ANA positif, artritis, and ulceration. If 4 or
more of the above criteria are met, the diagnosis of SLE has a sensitivity of
85% and a specificity of 95%. Meanwhile, if there are only 3 criteria and
one of them is a positive ANA, it is very likely that SLE disease and
diagnosis depends on clinical observation. (Perhimpunan Reumatologi
Indonesia, 2011)

7. What is differential diagnosis in this case ?

• Systemic Lupus Erythematous (SLE)
• Undifferentiated connective tissue disease

33
 • Sjögren's Syndrome
• Antiphospholipid antibody syndrome (APS)
• Fibromialgia (ANA positive)
• Idiopathic thrombocytopenic purpura
• Lupus is drug-induced
• Early rheumatoid arthritis
• Vasculitis (Perhimpunan Reumatologi Indonesia, 2011)

8. What is working diagnosis in this case ?

Systemic Lupus Erythematous et causa autoimmune disease

9. What is the treatment in this case ?

Education → Patients should always be reminded not to be too much exposed
to sunlight, high doses of corticosteroids, cytotoxic drugs. Pregnancy
management, contraindications for pregnancy, eg antimalarials or
cyclophosphamide.

Rehabilitation → Broadly speaking, rehabilitation objectives, indications and

techniques involve:
Break, Physical therapy, Therapy with modalitiesorthotic.

Medicine → Corticosteroids are used as the mainstay of treatment in patients

with SLE. Although associated with the emergence of many reports of side
effects, corticosteroids remain the drug that is widely used as anti-inflammatory
and immunosuppressive.10,22 SLE patients with organ involvement are usually
given corticosteroids to suppress inflammation so that there is no further organ
damage. Corticosteroids better than NSAIDs in reducing inflammation,
especially internal organs. Corticosteroids can be given orally, injected directly

34
 into the joint or intravenously (Tarigan, 2017). Prednisone < 10 mg/day or
equivalent ( Sudoyo, 2009). (Indonesian Rheumatology Association, 2012)

Topical glucocorticoids for rash → chloroquine base 4 mg/kg/bb (2500-

500mg/day) with an eye examination note at the time of initial administration
and continued for 3 months while hydroxychloroquine dose 5-6.5 mg/kg/bb
(200-400 mg/day) and eye check every 6-12 months ( Sudoyo, 2009).

10. What is the complications in this case ?

1. Retinal toxicity
2. End-stage renal disease
3. Neuropsychiatric and neurocognitive dysfunction
4. Shrinking lung syndrome
5. Gonadal dysfunction
6. Glucorticoid-induced side effects
7. Osteonecrosis
8. Osteoporosis
9. Coronary Artery Disease
10. Phlebothrombosis and pulmonary embolism (Mukherjee, 2006)

11. What is the prognosis in this case ?

Quo ad vitam : Dubia ad bonam
Quo ad functionam : Dubia ad bonam
Quo ad sanationam : Dubia ad malam

12. What is the SKDU in this case ?

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

35
 most appropriate referral for subsequent patient management. Doctor graduates
are also able to follow up after returning from referral.

13. What is the Islamic values in this case ?

• Islamic point: Q.S. Al-Baqarah 155-156
َ‫صبِ ِريْن‬ ِ ِۗ ‫اْل ْنفُ ِس َوالث َّ َم ٰر‬
ِّ َ‫ت َوب‬
ّٰ ‫ش ِِر ال‬ َ ْ ‫اْل ْم َوا ِل َو‬
َ ْ َ‫ص ِ ِّمن‬
ٍ ‫ع َونَ ْق‬ ْ ْ َ ِ‫ َولَنَ ْبلُ َونَّ ُك ْم ب‬.
ِ ‫ش ْيءٍ ِ ِّمنَ الخ َْوفِ َوال ُج ْو‬
Which means : And We shall surely test you with a little fear and
hunger, and lack of wealth, lives, and fruits. And give glad tidings to the
patient." (Q.S. Al-Baqarah: 155)
Conclusion : In this case, SLE is a systemic disease that means it affects
multiple organs. This can cause stress for patients because of the pain
they feel. And Allah hopes that it will come upon them, that is good
news because we belong to God, and indeed to Him we will return.
• HR. Abu Dawud dari Abu Darda
Hadith narrated by Abu Dawud, from Abu Darda, the Messenger of
Allah said: "Verily, Allah has sent down disease" and medicine, and He
has made for every (illness) there is a cure, so seek treatment and do not
use things that are unlawful.” (HR. Abu Dawud).
Conclusion: Rasulullah SAW gave very valuable information for us.
That every disease suffered by humans there is a cure. This is of course
very important, especially for those who are experiencing a disaster in
the form of illness, mild or severe, so that they remain optimistic,
patient, pray, and continue to try to recover from their illness.
• HR Bukhari
From Abu Hurairah radhiyallahu 'anhu, from the Prophet , he said:
“Allah has not sent down the disease but has also sent down the cure”
Conclusion: God is good, who gives medicine for all diseases. Diseases
for which a cure has not yet been found are only caused by the
limitations of the human mind which has not been able to find them. Do

36
 not despair of Allah's mercy if a calamity befalls you. Keep believing in
Allah, and keep trying and asking for the best.

2.7 Conclusion
Miss C, 20 years old is having joint pain, malar rash, alopecia, ulceration, she is
suffering of systemic lupus erythematosus (SLE) caused by autoimmune problem.

37
 2.8 Conceptual framework

Environment Factors Hormonal Factors

Stimulated Autoimmune to Formed

Systemic Lupus Erythematosus

(Autoimmune)

Attack on Multiple Organs

Damage on the skin Damage in musculoskeletal Inflamation

Malar rash, photosensitivity,

Joint Pain Fever
alopecia

38
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