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Problem-Based Learning (PBL)
Tutorial 2
Scenario B “Miss A”
Group 10
0
Table Content
Table Content ....................................................................................................... 1
Profile ................................................................................................................... 2
Scenario ................................................................................................................ 3
Content
1. Term Clarification .................................................................................... 4
2. Problem Identification .............................................................................. 5
3. Problem Analyze ...................................................................................... 7
4. Hipothesis ................................................................................................ 8
5. Learning Issue .......................................................................................... 9
6. Synthesis .................................................................................................. 10
Referensi .............................................................................................................. 41
1
SCENARIO
Miss A, aged 20 years, came to emergency room with chief complain of whole
body swelling which had been more prominent since 2 weeks before admission.
Swelling was started when she woke up around the eyelids. This swelling eventually
developed to the whole body. Urine was less than usual. She had no complaint about
defecation one year ago, patient frequently had tenderness came and faded on its own.
The patient also complained about moderate fever which sometimes came and faded
on its own. Her hair was easily fallen. Stomatitis was often found without prominent
cause. Her face was reddish especially at cheek if it was directly whone upon sunlight.
Miss A had consumed analgesics whenever she had these complaints but so
far had not gotten better.
Physical examination : General condition → severely sick. Sensorium →
compos mentis
HR : 100 x/min, regular; RR : 28 x/min, rapid and deep; temperature : 37.5
°C; Blood pressure : 170/100 mmHg
Specific conditions : anasarca edema, stomatitis, ascites, and edema at
extremities were found
Hb : 9.5 gr%, WBC : 8000/mm3, ESR : 105 mm/hour, ureum 138 mg/dl,
creatinine 3.2 mg/dl, albumin 2.5 g/dl, cholesterol 268 mg/dl, triglycerid 235 mg/dl,
and urinary protein +++
2
CONTENT
1. TERM CLARIFICATION
1. Swelling = an abnormal enlargement of a part of the body, typically as a result
of an accumulation of fluid
2. Eyelids = each of the upper and lower folds of skin that cover the eye when
closed
3. Albumin = a simple form of protein that is soluble in water and coagulable by
heat, such as that found in egg white, milk, and (in particular) blood serum
4. Stomatitis = inflammation of the mucous membrane of the mouth
5. Moderate fever = a temperature between 102° F - 103° F or 39–40 °C
6. Tenderness = pain or discomfort when an affected area is touched
7. Reddish = face is easy red cause of UV
8. Analgesics = any member of the diverse group of drugs used to relieve pain
(achieve analgesia)
9. Anasarca edema = also known as "extreme generalized edema" is a medical
condition characterised by widespread swelling of the skin due to effusion of
fluid into the extracellular space
10. Edema = swelling that is caused by fluid trapped in your body’s tissues
11. Compos mentis = fully aware
12. Ascites = the accumulation of fluid in the peritoneal cavity, causing abdominal
swelling
13. Ureum =
14. Creatinine = a compound formed in protein metabolism and present in much
living tissue. It is involved in the supply of energy for muscular contraction. A
guanidine derivative, usually present as a phosphate, chemical formula :
C4H9N3O2
15. Triglycerid = an ester formed from glycerol and three fatty acid groups.
Triglycerid are the main constituents of natural fats and oils, and high
concentrations in the blood indicate an elevated risk of stroke
16. Urinary protein = urin yang mengandung protein
3
2. PROBLEM IDENTIFICATION
1. Chief complain
J Whole body swelling which had been more prominent since 2 weeks
before admission
2. General complaint
J Swelling was started when she woke up around the eyelids
J Swelling eventually developed to the whole body
J Urine was less than usual
J Since 1 year ago, frequently had tenderness around her joints
especially at fingers joints, came and feded on its own
J Moderate fever which sometimes came an dfaded on its own
J Hair was easily fallen
J Stomatitis was often found without prominent cause
J Face was reddish especially at cheek if it was directly shone upon
sunlight
J Consumed analgesics but so far had not gotten better
3. Physical examination
J General condition → severely sick
J Sensorium → compos mentis
J HR : 100 x/min, regular
J RR : 28 x/min, rapid and deep
J Blood pressure : 170/100 mmHg
4. Specific conditions
J Anasarca edema
J Stomatitis
J Ascites
5. Laboratory Examination
J Hb : 9.5 gr%
4
J WBC : 8000/mm3
J ESR : 105 mm/hour
J Ureum : 138 mg/dl
J creatinine 3.2 mg/dl
J albumin 2.5 g/dl
J cholesterol 268 mg/dl
J triglycerid 235 mg/dl
J urinary protein +++
5
3. PROBLEM ANALYSIS
1) What are the mechanisms of all complain?
2) What causes of all complain?
3) Why was the swelling started around the eyelids when she woke up?
4) Why the swelling spreat from the eyelids to whole of body?
5) What is the pathogenesis of all Miss A’s complain?
6) Why the fever which sometimes came and faded?
7) Why did stomatitis occur without any prominent cause?
8) Why Miss A had consumed analgesics had not gotten better?
9) What is differential diagnosis?
10) What is complication of SLE?
11) What is prevention of SLE?
12) What is prognosis of SLE?
13) Apakah penyakit ini bisa kambuh? Bagaimana mencegah kambuh?
14) Why was the urine less than usual?
15) What are the correlation between all of complain with all of complain?
16) What are the effects of all Miss A’s complain?
17) What is the normal condition of all Miss A’s complain?
18) Why the tenderness just happen around her joints especially at fingers joints?
19) Why the tenderness came and faded on its own?
20) What is the correlation between whole body swelling and tenderness?
21) Why was her hair easily fall?
22) What is the intrepretation of the lab examination? What is the treatment for
Miss A?
6
4. HYPOTHESIS
Miss A, 20 years old suffered SLE due to autoimmune disorder
7
5. LEARNING ISSUE
1. Immune system
2. Urinary system
3. Interpretation
4. Auto imun
5. Hypersensitivity
6. SLE
7. Signs and symptoms
8. Analgesics
8
6. SYNTHESIS
1. Immune system
a. The Structure of the Immune System
The organs of the immune system are positioned throughout the body. They
are called lymphoid organs because they are home to lymphocytes, small
white blood cells that are the key players in the immune system. Bone
marrow, the soft tissue in the hollow center of bones, is the ultimate source of
all blood cells, including lymphocytes. The thymus is a lymphoid organ that
lies behind the breastbone. Lymphocytes known as T lymphocytes or T cells
(“T” stands for “thymus”) mature in the thymus and then migrate to other
tissues. B lymphocytes, also known as B cells, become activated and mature
into plasma cells, which make and release antibodies.
Lymph nodes, which are located in many parts of the body, are lymphoid
tissues that contain numerous specialized structures.
o T cells from the thymus concentrate in the paracortex
o B cells develop in and around the germinal centers.
o Plasma cells occur in the medulla.
Lymphocytes can travel throughout the body using the blood vessels. The cells
can also travel through a system of lymphatic vessels that closely parallels the
body’s veins and arteries.
Cells and fluids are exchanged between blood and lymphatic vessels, enabling
the lymphatic system to monitor the body for invading microbes. The
lymphatic vessels carry lymph, a clear fluid that bathes the body’s tissues.
Small, bean-shaped lymph nodes are laced along the lymphatic vessels, with
clusters in the neck, armpits, abdomen, and groin. Each lymph node contains
specialized compartments where immune cells congregate, and where they can
encounter antigens.
Immune cells, microbes, and foreign antigens enter the lymph nodes via
incoming lymphatic vessels or the lymph nodes’ tiny blood vessels. All
lymphocytes exit lymph nodes through outgoing lymphatic vessels. Once in
the bloodstream, lymphocytes are transported to tissues throughout the body.
9
They patroleverywhere for foreign antigens, then gradually drift back into the
lymphatic system to begin the cycle all over again.
The spleen is a flattened organ at the upper left of the abdomen. Like the
lymph nodes, the spleen contains specialized compartments where immune
cells gather and work. The spleen serves as a meeting ground where immune
defenses confront antigens.
Other clumps of lymphoid tissue are found in many parts of the body,
especially in the linings of the digestive tract, airways, and lungs—territories
that serve as gateways to the body. These tissues include the tonsils, adenoids,
and appendix.
b. Immune Cells and Their Products
The immune system stockpiles a huge arsenal of cells, not only lymphocytes
but also cell-devouring phagocytes and their relatives. Some immune cells
take on all intruders, whereas others are trained on highly specific targets. To
work effectively, most immune cells need the cooperation of their comrades.
Sometimes immune cells communicate by direct physical contact, and
sometimes they communicate releasing chemical messengers.
The immune system stores just a few of each kind of the different cells needed
to recognize millions of possible enemies. When an antigen first appears, the
few immune cells that can respond to it multiply into a full-scale army of cells.
After their job is done, the immune cells fade away, leaving sentries behind to
watch for future attacks.
c. B Cells
B cells and T cells are the main types of lymphocytes. B cells work chiefly by
secreting substances called antibodies into the body’s fluids. Antibodies
ambush foreign antigens circulating in the bloodstream. They are powerless,
however, to penetrate cells. The job of attacking target cells—either cells that
have been infected by viruses or cells that have been distorted by cancer—is
left to T cells or other immune cells (described below).
Each B cell is programmed to make one specific antibody. For example, one B
cell will make an antibody that blocks a virus that causes the common cold,
while another produces an antibody that attacks a bacterium that
causespneumonia. When a B cell encounters the kind of antigen that triggers it
10
to become active, it gives rise to many large cells known as plasma cells,
which produce antibodies.
o Immunoglobulin G, or IgG, is a kind of antibody that works efficiently
to coat microbes, speeding their uptake by other cells in the immune
system.
o IgM is very effective at killing bacteria.
o IgA concentrates in body fluids—tears, saliva, and the secretions of the
respiratory and digestive tracts—guarding the entrances to the body.
o IgE, whose natural job probably is to protect against parasitic
infections, is responsible for the symptoms of allergy.
d. T Cells
Unlike B cells, T cells do not recognize free-floating antigens. Rather, their
surfaces contain specialized antibody-like receptors that see fragments of
antigens on the surfaces of infected or cancerous cells. T cells contribute to
immune defenses in two major ways: some direct and regulate immune
responses, whereas others directly attack infected or cancerous cells.
Helper T cells, or Th cells, coordinate immune responses by communicating
with other cells. Some stimulate nearby B cells to produce antibodies, others
call in microbe-gobbling cells called phagocytes, and still others activate other
T cells.
Cytotoxic T lymphocytes (CTLs)—also called killer T cells—perform a
different function. These cells directly attack other cells carrying certain
foreign or abnormal molecules on their surfaces. CTLs are especially useful
for attacking viruses because viruses often hide from other parts of the
immune system while they grow inside infected cells. CTLs recognize small
fragments of these viruses peeking out from the cell membrane and launch an
attack to kill the infected cell.
e. Autoimmune Diseases
Sometimes the immune system’s recognition apparatus breaks down, and the
body begins to manufacture T cells and antibodies directed against self
antigens in its own cells and tissues. As a result, healthy cells and tissues are
destroyed, which leaves the person’s body unable to perform important
functions.
11
Misguided T cells and autoantibodies, as they are known, contribute to many
autoimmune diseases. For instance, T cells that attack certain kinds of cells in
the pancreas contribute to a form of diabetes, whereas an autoantibody known
as rheumatoid factor is common in people with rheumatoid arthritis. People
with systemic lupus erythematosus (SLE) have antibodies to many types of
their own cells and cell components. SLE patients can develop a severe rash,
serious kidney inflammation, and disorders of other important tissues and
organs.
No one knows exactly what causes an autoimmune disease, but multiple
factors are likely to be involved. These include elements in the environment,
such as viruses, certain drugs, and sunlight, all of which may damage or alter
normal body cells. Hormones are suspected of playing a role because most
autoimmune diseases are far more common in women than in men. Heredity,
too, seems to be important. Many people with autoimmune diseases have
characteristic types of self-marker molecules.
f. Immune Complex Diseases
Immune complexes are clusters of interlocking antigens and antibodies.
Normally, immune complexes are rapidly removed from the bloodstream.
Sometimes, however, they continue to circulate and eventually become
trapped in the tissues of the kidneys, lungs, skin, joints, or blood vessels.
There, they set off reactions with complement that lead to inflammation and
tissue damage. Immune complexes work their mischief in many diseases.
These include malaria and viral hepatitis, as well as many autoimmune
diseases.
g. Immune Deficiency Disorders
When the immune system is missing one or more of its parts, the result is an
immune deficiency disorder. These disorders can be inherited, acquired
through infection, or produced as a side effect by drugs such as those used to
treat people with cancer or those who have received transplants.
Temporary immune deficiencies can develop in the wake of common virus
infections, including influenza, infectious mononucleosis, and measles.
Immune responses can also be depressed by blood transfusions, surgery,
malnutrition, smoking, and stress.
12
Some children are born with poorly functioning immune systems. Some have
flaws in the B cell system and cannot produce antibodies. Others, whose
thymus is either missing or small and abnormal, lack T cells. Very rarely,
infants are born lacking all of the major immune defenses.
2. Urinary system
The urinary system (also called excretory system or the genitourinary system)
is the organ system that produces, stores, and eliminates urine. In humans it
includes two kidneys, two ureters, the bladder, and the urethra. The analogous
organ in invertebrates is the nephridium.
Control of Urine Volume
Our urine is produced not only in order to eliminate many of the cellular waste
products, but also to control both the amount and the composition of the
extracellular fluid in the body. Controlling the amount of water and chemicals
in the body is essential to life, and our body does so by producing various
amounts of urine so that we can either excrete the "extra" water and chemicals
(mainly sodium) or conserve the water and chemicals when they are in short
supply. Therefore, the volume of urine that we excrete everyday is a reflection
of how much extracellular fluid and sodium our bodies have to spare. The
kidney tubule regulation of the salt and water in our bodies is the most
important factor in determining urine volume. Too much water and salt in our
bodies is dangerous and too little water and salt in our bodies is dangerous.
Therefore, the level of water and salts excreted in urine - the urine volume - is
adjusted to the needs of the body. As a general rule, however, and under
optimum conditions, the body produces urine at a rate of about 1 ml/min.
Physiology
a) Kidney
The kidneys are bean shaped organs, which lie in the abdomen,
retroperitoneal to the organs of digestion, around or just below the
ribcage and close to the lumbar spine. The organ is about the size of a
human fist and is surrounded by what is called Peri-nephric fat, and
situated on the superior pole of each kidney is an adrenal gland. The
kidneys receive their blood supply of 1.25 L/min (25% of the cardiac
output) from the renal arteries which are fed by the Abdominal aorta.
13
This is important because the kidneys' main role is to filter water
soluble waste products from the blood. The other attachment of the
kidneys are at their functional endpoints the ureters, which lies more
medial and runs down to the [Trigone of urinary bladder]
The right kidney lies at a slightly lower level than the left kidney (due
to the bulk of the right lobe of the liver), and the lower pole can be
palpated in the right lumbar region at the end of deep inspiration in a
person with poorly developed abdominal muscles. Each kidney moves
about 1 inch (2.5 cm) in a vertical direction during full respiratory
movement of the diaphragm. The normal left kidney, which is higher
than the right kidney, is not palpable.
Location and Description
The two kidneys function to excrete most of the waste products of
metabolism. They play a major role in controlling the water and
electrolyte balance within the body and maintaining the acid-base
balance of the blood. The waste products leave the kidneys as urine,
which passes down the ureters to the urinary bladder, located within
the pelvis. The urine leaves the body in the urethra.
The kidneys are reddish-brown and lie behind the pentoneum high up
on the posterior abdominal wall, largely under cover of the costal
margin (Fig. 5-42). The right kidney lies slightly lower than the left
kidney because of the large size of the right lobe of the liver. With
contraction of the diaphragm during respiration, both kidneys move
downward in a vertical direction by as much as 1 inch (2.5 cm). On the
medial concave border of each kidney is a vertical slit, which is
bounded by thick lips of renal substance and is called the hilum (Fig.
5-43). The hilum extends into a large cavity called the renal sinus. The
hilum transmits, from the front backward, the renal vein, two branches
of the renal artery the ureter, and the third branch of the renal artery
(VA.U.A.). Lymph vessels and sympathetic fibers also pass through
the hilum.
Coverings
The kidneys have the following coverings
14
1. Fibrous capsule: This surrounds the kidney and is closely applied to its outer surface.
2. Perirenal fat: This covers the fibrous capsule.3. Renal fascia: This is a condensation of connective tissue that
lies outside the perirenal fat and encloses the kidneys and suprarenal glands; it is continuous laterally with the fascia transversalis.
4. Pararenal fat: This lies external to the renal fascia and is often in large quantity It forms part of the retroperitoneal fat.
The perirenal fat, renal fascia, and pararenal fat support the kidney and hold them in position on the posterior abdominal wall.
On the anterior abdominal wall the hilum of each kidney lies on the
transpyloric plane, about 3 fingerbreadths from the midline. On the
back, the kidneys extend from the twelfth thoracic spine to the third
lumbar spine, and the hili are opposite the first lumbar vertebra
The kidneys perform a number of tasks, such as: concentrating urine,
regulating electrolytes, and maintaining acid-base homeostasis. The
kidney excretes and re-absorbs electrolytes (e.g. sodium, potassium
and calcium) under the influence of local and systemic hormones. pH
balance is regulated by the excretion of bound acids and ammonium
ions. In addition, they remove urea, a nitrogenous waste product from
the metabolism of amino acids. The end point is a hyperosmolar
solution carrying waste for storage in the bladder prior to urination.
Humans produce about 2.9 liters of urine over 24 hours, although this
amount may vary according to circumstances. Because the rate of
filtration at the kidney is proportional to the glomerular filtration rate,
which is in turn related to the blood flow through the kidney, changes
in body fluid status can affect kidney function. Hormones exogenous
and endogenous to the kidney alter the amount of blood flowing
through the glomerulus. Some medications interfere directly or
indirectly with urine production. Diuretics achieve this by altering the
amount of absorbed or excreted electrolytes or osmalites, which causes
a diuresis
15
b) Urethra
The endpoint of the urinary system is the urethra. Typically the
urethra in humans is colonised by acommensal bacteri below the
external urethral sphincter. The urethra emerges from the end of the
penis in males and between the clitoris and the vagina nalga females.
The renal pelvis (pelvis of the ureter) is the funnel- shaped expanded
upper end of the ureter. It lies within the hilum of the kidney and
receives the major calyces. The ureter emerges from the hilum of the
kidney and runs vertically downward behind the parietal pentoneum
(adherent to it) on the psoas muscle, which separates it from the tips of
the transverse processes of the lumbar vertebrae. It enters the pelvis by
crossing the bifurcation of the common iliac artery in front of the
sacroiliac joint. The ureter then runs down the lateral wall of the pelvis
to the region of the ischial spine and turns forward to enter the lateral
angle of the bladder.
Urinary Bladder
Location and Description
The urinary bladder is situated immediately behind the pubic bones
within the pelvis. It is a receptacle for the storage of urine and in the
adult has a maximum capacity of about 500 ml. The bladder has a
strong muscular wall. Its shape and relations vary according to the
amount of urine that it contains. The empty bladder in the adult lies
entirely within the pelvis; as the bladder fills, its superior wall rises up
into the hypogastric region. In the young child the empty bladder
projects above the pelvic inlet; later, when the pelvic cavity enlarges,
the bladder sinks into the pelvis to take up the adult position.
The empty bladder is pyramidal in shape, having an apex, a base, and a
superior and two inferolateral surfaces; it also has a neck.
The urinary bladder is situated immediately behind the pubic bones
within the pelvis. It is a receptacle for the storage of urine and in the
adult has a maximum capacity of about 500 ml. The bladder has a
strong muscular wall. Its shape and relations vary according to the
amount of urine that it contains. The empty bladder in the adult lies
entirely within the pelvis; as the bladder fills, its superior wall rises up
16
into the hypogastric region. In the young child the empty bladder
projects above the pelvic inlet; later, when the pelvic cavity enlarges,
the bladder sinks into the pelvis to take up the adult position.
The empty bladder is pyramidal in shape, having an apex, a base, and a
superior and two inferolateral surfaces; it also has a neck.
3. Interpretation
Hb
Adult men = 14 – 18 gr/dl
Adult women = 12 - 16 gr/dl
Old men = 12.4 – 14.9 gr/dl
Old women = 11.7 – 13.8 gr/dl
WBC (white blood count)
Basofil = 0 – 2%
Eosinofil = 1 – 5%
Limfosit = 15 – 40%
Monosit = 1 – 8%
Neutrofil = 38 – 70%
Total = 4500 – 10000/micrometer
ESR = Erythrocyte Sedimentation Rate
Men < 50 years old = < 15mm/hour
Men > 50 years old = < 20mm/hour
Result = - congestive heart failure
- low plasma
Trigliserida :
20 – 29 years old = 10 – 140 mg/dl
30 – 39 years old = 20 – 150 mg/dl
Creatinin : 1.0 – 1.6 g/24hours or 15 – 25 mg/kgBB/24hours
Albumin : 3 – 5.5 g/dl
Cholestrol :
17
20 – 29 years old = 120 – 240 mg/dl
30 – 39 years old = 140 – 270 mg/dl
4. Autoimmune
What is the immune system?
The immune system is the body's means of protection against microorganisms
and other "foreign" substances. It is composed of two major parts. One
component, B lymphocytes, produces antibodies, proteins that attack "foreign"
substances and cause them to be removed from the body; this is sometimes
called the humoral immune system. The other component consists of special
white blood cells called T lymphocytes, which can attack "foreign" substances
directly; this is sometimes called the cellular immune system. It takes time for
both components of the immune system to develop. T lymphocytes become
protective, and antibodies are developed after a person is exposed to specific
"foreign" threats. Over a lifetime, the immune system develops an extensive
library of identified substances and microorganisms that are cataloged as
“threat” or “not threat.” Vaccinations utilize this process to add to the library.
They expose a person’s immune system to weakened or inactivated forms of
bacteria and viruses that can no longer cause disease, so that the person’s
immune system will recognize them and create antibodies that will be ready to
protect against the infectious forms of these microorganisms if the person
comes in contact with them in the future.
Normally, the immune system can distinguish between “self” and “not self”
and only attacks those tissues that it recognizes as “not self.” This is usually
the desired response, but not always. When a person is given an organ
transplant, the immune system will correctly recognize the new organ as “not
self” (unless it is from an identical twin) and will attack it in a process called
rejection. To prevent rejection, the transplant patient must take drugs that
reduce the activity of the immune system (immunosuppressants) for the rest of
his life.
What are autoimmune disorders?
18
Autoimmune disorders are diseases caused by the body producing an
inappropriate immune response against its own tissues. Sometimes the
immune system will cease to recognize one or more of the body’s normal
constituents as “self” and will create autoantibodies – antibodies that attack its
own cells, tissues, and/or organs. This causes inflammation and damage and it
leads to autoimmune disorders.
The cause of autoimmune diseases is unknown, but it appears that there is an
inherited predisposition to develop autoimmune disease in many cases. In a
few types of autoimmune disease (such as rheumatic fever), a bacteria or virus
triggers an immune response, and the antibodies or T-cells attack normal cells
because they have some part of their structure that resembles a part of the
structure of the infecting microorganism.
Autoimmune disorders fall into two general types: those that damage many
organs (systemic autoimmune diseases) and those where only a single organ or
tissue is directly damaged by the autoimmune process (localized). However,
the distinctions become blurred as the effect of localized autoimmune
disorders frequently extends beyond the targeted tissues, indirectly affecting
other body organs and systems. Some of the most common types of
autoimmune disorders include
In some cases, the antibodies may not be directed at a specific tissue or organ;
for example, antiphospholipid antibodies can react with clotting proteins in the
blood, leading to formation of blood clots within the blood vessels
(thrombosis).
Autoimmune disorders are diagnosed, evaluated, and monitored through a
combination of autoantibody blood tests, blood tests to measure inflammation
and organ function, clinical presentation, and through non-laboratory
examinations such as X-rays. There is currently no cure for autoimmune
disorders, although in rare cases they may disappear on their own. Many
people may experience flare-ups and temporary remissions in symptoms,
others chronic symptoms or a progressive worsening. Treatment of
autoimmune disorders is tailored to the individual and may change over time.
The goal is to relieve symptoms, minimize organ and tissue damage, and
preserve organ function. New treatments and a greater understanding of
19
autoimmune disorders are being researched. Patients should talk to their
doctors and to any specialists they are referred to about their treatment
options.
What are autoimmune diseases?
Our bodies have an immune system that protects us from disease and
infection. But if you have an autoimmune disease, your immune system
attacks itself by mistake, and you can get sick. Autoimmune diseases can
affect connective tissue in your body (the tissue which binds together body
20
Systemic Autoimmune Diseases Localized Autoimmune Diseases
Rheumatoid arthritis (RA) and
Juvenile RA (JRA) (joints; less
commonly lung, skin)
Type 1 Diabetes Mellitus (pancreas
islets)
Lupus [Systemic Lupus
Erythematosus] (skin, joints,
kidneys, heart, brain, red blood
cells, other)
Hashimoto's thyroiditis, Graves'
disease (thyroid)
Scleroderma (skin, intestine, less
commonly lung)
Celiac disease, Crohn's disease,
Ulcerative colitis (GI tract)
Sjogren's syndrome (salivary
glands, tear glands, joints)
Multiple sclerosis*
Goodpasture's syndrome (lungs,
kidneys)
Addison's disease (adrenal)
Wegener's granulomatosis (blood
vessels, sinuses, lungs, kidneys)
Primary biliary cirrhosis, Sclerosing
cholangitis, Autoimmune hepatitis
(liver)
Polymyalgia Rheumatica (large
muscle groups)
Temporal Arteritis / Giant Cell
Arteritis (arteries of the head and
neck)
Guillain-Barre syndrome (nervous
system)
tissues and organs). Autoimmune disease can affect many parts of your body,
like your nerves, muscles, endocrine system (system that directs your body’s
hormones and other chemicals), and digestive system.
Who is at risk for getting autoimmune diseases?
Most autoimmune diseases occur in women, and most often during their
childbearing years. Some of these diseases also affect African American,
American Indian, and Latina women more than white women. These diseases
tend to run in families, so your genes, along with the way your immune system
responds to certain triggers or things in the environment, affect your chances
of getting one of these diseases. If you think you may have an autoimmune
disease, ask your family members if they have had symptoms like yours. The
good news is that if you have an autoimmune disease, there are things you can
do to feel better!
5. Hypersensitivity type III
Systemic disease caused by immune complex formation can follow the
administration of large quantities of poorly catabolized antigens.
Type III hypersensitivity reactions can arise with soluble antigens. The
pathology is caused by the deposition of antigen:antibody aggregates or
immune complexes at certain tissue sites. Immune complexes are generated in
all antibody responses but their pathogenic potential is determined, in part, by
their size and the amount, affinity, and isotype of the responding antibody.
Larger aggregates fix complement and are readily cleared from the circulation
by the mononuclear phagocytic system. The small complexes that form at
antigen excess, however, tend to deposit in blood vessel walls. There they can
ligate Fc receptors on leukocytes, leading to leukocyte activation and tissue
injury.
A local type III hypersensitivity reaction can be triggered in the skin of
sensitized individuals who possess IgG antibodies against the sensitizing
antigen. When antigen is injected into the skin, circulating IgG antibody that
has diffused into the tissues forms immune complexes locally. The immune
complexes bind Fc receptors on mast cells and other leukocytes, which creates
21
a local inflammatory response with increased vascular permeability. The
enhanced vascular permeability allows fluid and cells, especially
polymorphonuclear leukocytes, to enter the site from the local vessels. This
reaction is called an Arthus reaction. The immune complexes also activate
complement, releasing C5a, which contributes to the inflammatory reaction by
ligating C5a receptors on leukocytes (see Sections 2-12 and 6-16). This causes
their activation and chemotactic attraction to the site of inflammation. The
Arthus reaction is absent in mice lacking the α or γ chain of the FcγRIII
receptor (CD16) on mast cells, but remains largely unperturbed in
complementdeficient mice, showing the primary importance of FcγRIII in
triggering inflammatory responses via immune complexes.
A systemic type III hypersensitivity reaction, known as serum sickness, can
result from the injection of large quantities of a poorly catabolized foreign
antigen. This illness was so named because it frequently followed the
administration of therapeutic horse antiserum. In the preantibiotic era,
antiserum made by immunizing horses was often used to treat pneumococcal
pneumonia; the specific anti-pneumococcal antibodies in the horse serum
would help the patient to clear the infection. In much the same way, antivenin
(serum from horses immunized with snake venoms) is still used today as a
source of neutralizing antibodies to treat people suffering from the bites of
poisonous snakes.
Serum sickness occurs 7–10 days after the injection of the horse serum, an
interval that corresponds to the time required to mount a primary immune
response that switches from IgM to IgG antibody against the foreign antigens
in horse serum. The clinical features of serum sickness are chills, fever, rash,
arthritis, and sometimes glomerulonephritis. Urticaria is a prominent feature of
the rash, implying a role for histamine derived from mast-cell degranulation.
In this case the mast-cell degranulation is triggered by the ligation of
cellsurface FcγRIII by IgG-containing immune complexes.
The onset of disease coincides with the development of antibodies against the
abundant soluble proteins in the foreign serum; these antibodies form immune
complexes with their antigens throughout the body. These immune complexes
22
fix complement and can bind to and activate leukocytes bearing Fc and
complement receptors; these in turn cause widespread tissue injury. The
formation of immune complexes causes clearance of the foreign antigen and
so serum sickness is usually a self-limiting disease. Serum sickness after a
second dose of antigen follows the kinetics of a secondary antibody response
and the onset of disease occurs typically within a day or two. Serum sickness
is nowadays seen after the use of anti-lymphocyte globulin, employed as an
immunosuppressive agent in transplant recipients, and also, rarely, after the
administration of streptokinase, a bacterial enzyme that is used as a
thrombolytic agent to treat patients with a myocardial infarction or heart
attack.
A similar type of immunopathological response is seen in two other situations
in which antigen persists. The first is when an adaptive antibody response fails
to clear an infectious agent, for example in subacute bacterial endocarditis or
chronic viral hepatitis. In this situation, the multiplying bacteria or viruses are
continuously generating new antigen in the presence of a persistent antibody
response that fails to eliminate the organism. Immune complex disease ensues,
with injury to small blood vessels in many tissues and organs, including the
skin, kidneys, and nerves. Immune complexes also form in autoimmune
diseases such as systemic lupus erythematosus where, because the antigen
persists, the deposition of immune complexes continues, and serious disease
can result.
Some inhaled allergens provoke IgG rather than IgE antibody responses,
perhaps because they are present at relatively high levels in inhaled air. When
a person is reexposed to high doses of such inhaled antigens, immune
complexes form in the alveolar wall of the lung. This leads to the
accumulation of fluid, protein, and cells in the alveolar wall, slowing blood-
gas interchange and compromising lung function. This type of reaction occurs
in certain occupations such as farming, where there is repeated exposure to
hay dust or mold spores. The disease that results is therefore called farmer's
lung. If exposure to antigen is sustained, the alveolar membranes can become
permanently damaged.
23
6. SLE
a. Definition
Systemic lupus erythematosus (SLE) is a chronic inflammatory disease
of unknown cause that can affect the skin, joints, kidneys, lungs,
nervous system, serous membranes, and/or other organs of the body.
Immunologic abnormalities, especially the production of a number of
antinuclear antibodies, are another prominent feature of the disease.
b. Clinical course
The clinical course of SLE is variable and may be characterized by
periods of remissions and chronic or acute relapses. Women, especially
in their 20s and 30s, are affected more frequently than men.
Patients with SLE are subject to myriad symptoms, complaints, and
inflammatory involvement that can affect virtually every organ. The
most common pattern is a mixture of constitutional complaints with
skin, musculoskeletal, mild hematologic, and serologic involvement.
However, some patients have predominately hematologic, renal, or
central nervous system manifestations. The pattern that dominates
during the first few years of illness tends to prevail subsequently.
c. Diagnosis
The diagnosis of SLE is straightforward in a patient who presents with
several compatible clinical features and has supportive laboratory
studies. A good example is a young woman who presents with
complaints of fatigue, arthralgia, and pleuritic chest pain, who is found
to have hypertension, a malar rash, a pleural friction rub, several tender
and swollen joints, and mild peripheral edema. Laboratory testing may
reveal leukopenia, anemia, an elevated serum creatinine,
hypoalbuminemia, proteinuria, an active urinary sediment,
hypocomplementemia, a positive Coombs test, and positive tests for
antinuclear antibodies, including those to double stranded DNA and
the Smith (Sm) antigen.
A person is said to have SLE if he or she meets any 4 of these 11
criteria simultaneously or in succession
Criterion Definition / examples
24
1. Malar rash Fixed erythema over the malar eminences,
tending to spare the nasolabial folds
2. Discoid rash Erythematosus raised patches, may scar
3. Photosensitivity Skin rash as a result of unusual reaction to
sunlight
4. Oral ulvers Usually painless
5. Arthritis Non-erosive : Jaccoud’s arthropathy
6. Serositis a. Pleuritis – pleuritic pain, pleural rub, pleural
effusion
b. Pericarditis – ECG changes, rub, pericardial
effusion
7. Renal disorder a. Proteinuria (> 3 + or 0.5 g/day)
b. Cellular casts in urine
8. Neurological disorder a. Seizures
b. Psychosis
9. Haematological disorder a. Haemolytic anaemia
b. Leukopaenia
c. Lymphopaenia
d. Thrombocytopaenia
10. Immunological disorder a. Anti-DNA antibodies
b. Anti-Sm antibodies
c. Anti-phospholipid antibodies
11. Anti-nuclear antibody Exclude drug causes
The following tests will aid in diagnosis of lupus by examining the
status of the patient’s immune system :
i. The anti-nuclear antibody test determines if the person has
autoantibodies that react with components in cell nuclei.
Almost all lupus patients will have a positive reaction to this
test
ii. The anti-DNA antibody test determines if the patient has
antibodies to DNA
25
iii. The anti-Sm antibody test looks for antibodies to a protein.
While many lupus patients do not have anti-Sm antibodies, they
are rarely found in people without lupus
iv. Tests for the presence of immune complexes (the combination
of antibodies and teh substances with which they react) in the
blood are valuable, both for diagnosing and monitoring the
disease.
v. An analysis of the serum complement level, which
d. Causes and incidence
The exact cause of SLE remains a mystery, but evidence points to
interrelated immunologic, environmental, hormonal, and genetic
factors. Autoimmunity is thought to be the prime causative
mechanism. In autoimmunity, the body produces antibodies against its
own cells such as the antinuclear antibody. The formed antigen-
antibody complexes can suppress the body’s normal immunity and
damage tissues. Patients with SLE produce antibodies against many
different tissue components, such as red blood cells (RBCs),
neutrophils, platelets, lymphocytes, or almost any organ or tissue in the
body.
Certain predisposing factors may make a person susceptible to SLE.
Physical or mental stress, streptococcal or viral infections, exposure to
sunlight or ultraviolet light, immunization, pregnancy, and abnormal
estrogen metabolism may all affect this disease’s development.
SLE may also be triggered or aggravated by treatment with certain
drugs — for example, procainamide, hydralazine, anticonvulsants and,
less commonly, penicillins, sulfa drugs, and hormonal contraceptives.
SLE strikes 8 times more females than men, increasing to 15 times
more during childbearing years. It occurs worldwide but is most
prevalent among Asians and Blacks.
e. Signs and symptoms
The onset of SLE may be acute or insidious and produces no
characteristic clinical pattern. However, its symptoms commonly
include fever, weight loss, malaise, and fatigue as well as rashes and
26
polyarthralgia. SLE may involve every organ system. In 90% of
patients, joint involvement is similar to that in rheumatoid arthritis.
Skin lesions are most commonly erythematous rashes in areas exposed
to light. The classic butterfly rash over the nose and cheeks occurs in
fewer than 50% of the patients. (See < /span>Butterfly rash.)
Ultraviolet rays often provoke or aggravate skin eruptions. Vasculitis
can develop (especially in the digits), possibly leading to infarctive
lesions, necrotic leg ulcers, or digital gangrene. Raynaud’s
phenomenon appears in about 20% of patients. Patchy alopecia and
painless ulcers of the mucous membranes are common.
Constitutional symptoms of SLE include aching, malaise, fatigue, low-
grade or spiking fever, chills, anorexia, and weight loss. Lymph node
enlargement (diffuse or local, and nontender), abdominal pain, nausea,
vomiting, diarrhea, and constipation may occur. Females may
experience irregular menstrual periods or amenorrhea during the active
phase of SLE.
About 50% of SLE patients develop signs of cardiopulmonary
abnormalities, such as pleuritis, pericarditis, and dyspnea. Myocarditis,
endocarditis, tachycardia, parenchymal infiltrates, and pneumonitis
may occur. Renal effects may include hematuria, proteinuria, urine
sediment, and cellular casts, which may progress to total kidney
failure. Urinary tract infections may result from heightened
susceptibility to infection. Seizure disorders and mental dysfunction
may indicate neurologic damage. Central nervous system (CNS)
involvement may produce emotional instability, psychosis, and organic
mental syndrome. Headaches, irritability, and depression are common.
f. Pathogenesis
The clinical heterogeneity of this disease is mirrored by its complex
aetiopathogenesis. Twin studies initally indicated the importance of
genetic factors, and genome screening has highlighted a number of
potential loci of interest. In the susceptible individual, disease may
result from a variety of environmental triggers including exposure to
sunlight, drugs and infections, particularly with Epstein-Barr virus.
27
Even within one patient, lupus flares can result from different
precipitants at different times.
Despite extensive work, the precise pathological mechanisms of SLE
are still not fully understood. The majority of patieents have elevated
levels of autoantibodies, directed in particular against nuclear
components such as nucleosomes, DNA, and histones, and it is
generally accepted that at least some of these have a directly
pathogenic role, either by precipitating as immune complexes in target
organs or by cross-reacting with other functionally relevant antigens,
the presence and persistence of these autoantibodies indicate an
abnormality in tolerance, which results from a combination of
abnormal handling of autoantigens following apoptosis, and deranged
function of T and B lymphocytes
g. Differential Diagnosis
The list of possible differential diagnoses is broad, and will vary with
the presentation of each case. The non-specific clinical features of
widespread pain and fatigue mean that in some cases fibromyalgia an
other chronic pain syndromes may be appropriate differentials. Indeed,
it is important to note that firomalgia and SLE can co-exist in the same
patient.
A number of patients will present with a cluster of feature suggestive
of an autoimmune rheumatic disease, though at inital presentation the
final diagnosis appears unclear. A proportion of these
“undifferentiated” patients will go on to develop full blown SLE, or
other diseases such as systemic sclerosis
Some malignancies, particularly lymphoma and leukaemia, which are
relevant to this agegroup, can present with a similar clinical picture.
Similarly, there is significant overlap with the presentation of some
infections, notably, tuberculosis, HIV/AIDS and bacterial endocarditis.
In view of the immunosuppressive nature of the required drugs, it is
clearly crucial to exclude underlying infection vefore starting treatment
for SLE.
h. Clinical manifestations
28
J Constitutional symptoms such as fatique, weight loss and fever are
not life threatening, but have a significant impact on quality of life.
Patients with SLE describe overwhelming fatigue and unsatisfying
sleep, though the extent to which this tiredness relates directly to
lupus disease activity remains controversial
J Renal disease affects about 3-$ of patients with SLE, and remains
the most dangerous life-threatening complication. Patients who will
develop lupus nephritis most commonly do so within the first few
years of their disease. As renal involvement is often asymptomatic
particularly iniatially, regular urinalysis and blood pressure
monitoring is crucial. Renal involvement is characterized by
proteinuria (> 0.5 g/24hours), and/or red cell casts, and early
referral for renal biopsy is generally advocated. The histological
calassification of lupus nephritis under the auspices of the
International Society of Nephrology and the Renal Pathology
Society. Lupus Nephritis classes I – V describe mesangial (I and
II), proliferative (III and IV) or membranous (V) lesions, and each
biopsy may have features of more than one class of disease.
Classes III and IV are subdivided further depending on the activity
or chronicity of the abnormalities seen. Class VI is reserved for
widespread sclerotic disease. The renal biopsy findings are used to
assess prognosis and guide management. Response to treatment
can be assessed using serial urine protein / creatinine ratios, in
addition to other more general measures of disease activity.
Class I Minimal mesangial lupus nephritis
Normal on light microscopy. Mesangial immune deposits on
immunofluorescence
Class II Mesangial proliferative lupus nephritis
Mesangial hypercellularity or matrix expansion, with mesangial immune
deposits on immunofluorescence
Class II Focal lupus nephritis
Glomerulonephritis involving <50% of glomeruli, typically with
29
subendothelial immune deposits
Class IV Diffuse lupus nephritis
Glomerulonephritis involving >50% of glomeruli, typically with
subendothelial immune deposits. Can be segemental or global
Class V Membranous lupus nephritis
Global or segemental sub-epithelial immune deposits
Class VI Advanced sclerotic lupus nephritis
>90% of glomeruli globally sclerosed without residual activity
i. Laboratory findings
Over 90% of patients with SLE have positive anti-nuclear antibodies
(ANA). Significant titres are accepted to be of 1:80 or greater. ANA
although sensitive, is far from specific for SLE. A positive ANA is also
seen in many other illnesses including systemic sclerosis and
polymositis, as well as some chronic infections. All patients should be
screened for extractable nuclear antigens (ENA). Different ENAs are
associated with different disease manifestations – for instance, anti-Sm
is associated with renal involvement, and anti-Ro with secondary
Sjogren’s syndrome.
Antibodies to double-stranded DNA (dsDNA), and more recently to
nucleosomes (though this test is not commonly available in most
routine labs) are more specific for SLE, and anti-dsDNA titres are also
predictive of renal involvement. Moreover the titres of these antibodies
fluctuate with disease activity and therefore serial testing is a useful
monitoring tool. Typically, a disease flare is accompanied by a rising
titre of dsDNA antibodies and erythrocyte sedimentation rate (ESR),
and falling complement and lymphocyte count. The C-reactive protein
(CRP), unlike the ESR, does not usually rise with disease activity
unless there is arthritis or serositis, and a raised CRP in a patient with
SLE must always make you consider infection.
j. Treatment
30
SLE is a relapsing and remitting disease, and treatment aims are
threefold : managing acute periods of potentially life-threatening ill
health, minimizing the risk of flares during periods of relative stability,
and controlling the less life-threatening, but often incapacitating day to
day symptoms. Our limited understanding of the precise pathogenesis
of SLE means that the majority of treatments are still broadly
immunosuppressive in action, and hence carry a significant risk of
adverse effects.
At the milder end of the spectrum, hydroxychloroquine is commonly
used. This is effective for skin disease, joint pain and fatigue. Non-
steroidal anti-inflammatory drugs are also useful for arthralgia and
arthritis, though more aggressive treatment with methotrexate may be
required. Low dose oral steroids or intramuscular injections of depot
steroid preparations are sometimes used for mild disease, but
immunosuppressive therapies and high dose steroids are generally
reserved for major organ involvement.
Lupus nehphritis remains the complication which carries with it the
biggest risk of death or long term morbidity. Combining high dose
corticosteroids with cyclophosphamide was the gold standard in the
management of proliferative lupus nephritis for many years. Although
efficacious, this regimen is limited by signifcant toxicity. Both agents
are immunosuppressive. In addition, corticosteroids are associated with
a whole host of adverse effects including osteoporosis and weight gain,
and cyclophosphamide can cause haemorrhagic cystitis and infertility.
More recently, the classic regimen of monthly boluses of 1g
cyclophosphamide for 6 months, followed by once every three months
for the next 2 years, has been modified by some groups, who instead
advocate the use of “low-dose” cyclophosphamide (6 fortnightly pulses
of 500mg). Following remission induction azathioprine is commonly
used for maintenance therapy. Mycophenolate mofetil has been added
to the repertoire of drugs used for the treatment of lupus nephritis. This
is now used commonly as maintenance therapy following
cyclophosphamide, and its use in the induction phase has been adopted
in some centres.
31
Similarly, immunosuppressive treaments, such as cyclophosphamide
and azathioprine, are also used for central nervous system involvement
and rarely, serositis, and haematological disease. Furthermore,
persistent autoimmune thrombocytopenia sometimes reuires
immunoglobulin.
In an attempt to improve management, biological therapies are being
developed, which target specific cells or molecules within the
abnormally functioning immune system. For example, the depletion of
B cells using rituximab, an anti-CD20 monoclonal antibody previously
used in the treatment of B cell lymphomas, is now being used in
patients with severe disease which has not reponded to conventional
treatments.
k. Prognosis
Despite significant advances in treatment over the last decade, SLE
still caries a significant risk of mortality and long term morbidity. A
European study of 1000 patients with SLE, demonstrated a 10 year
survival probability of 92% overall, reduced to 88% in those who
presented with nephropathy. Mean age at death was 44, but varied
widely from 18 – 81 years.
Cause of death varies with disease duration. In one cohort, renal lupus
accounted for the biggest number of deaths in those with less than 5
years of disease, whereas vascular disease was the most important
factor in the group who died later in the disease course.
As mentioned previously, we are becoming increasingly aware of the
impact that premature atherosclerosis is having on the long term
prognosis of lupus patients who survive the early years of illness. Aas
we develop better immune targeted therapies, optimizing the
management of these longer term complications will become
increasingly important.
7. Signs and symptoms
Symptoms may come and go. The times when a person is having symptoms
are called flares, which can range from mild to severe. New symptoms may
appear at any time.
32
The physician will look for symptoms such as Malar rash, Discoid rash,
sensitivity to light, skin reactions to exposure to sun, a rash over the cheeks
and nose, raised red patches, ulcers of the mouth an nose, arthritis, serositis,
pleuritis, pericarditis, Hemolytic anemia, leucopenia, seizures, renal disorder
and psychosis or depression. At least four of these problems must be occurring
or have occurred, not necessarily simultaneously, to get a Lupus diagnosis.
a. Swelling
Swelling involves the enlargement of organs, skin, or other body
structures. It is caused by excessive buildup of fluid in the tissues. This
buildup can lead to a rapid increase in weight over a short period of
time (days to weeks).
Swelling can occur throughout the body (generalized) or it may be
limited to a specific part of the body (localized).
b. Urine less than usual
Cause of glomerular isn’t working well
c. Tenderness
Tenderness same sympthom with aedema
d. Moderate fever
Fever with no known cause
e. Hair was easily fallen
Terlihat kelainan kulit spesifik berupa bercak malar menyerupai kupu
– kupu di muka dan eritema umum yang meonjol. Pasien menjadi
fotosensitif dan LES kambuh bila terjemur sinar matahari cukup lama.
Kulit yang terkena sinar matahari menunjukkan kelainan subakut yang
bersifat rekurens, berupa bercak menonjol kemerahan, dan meanhun.
Terdapat kelainan kulit menahun berupa bercak diskoid yang bermula
sebagai eritema papul atau plak bersisik. Sisik ini menebal dan melekat
disertai hipopigmentasi sentral. Terutama terjadi di daerah yang
terkena sinar matahari dan dapat menimbulkan kebotakan di kepala.
33
f. Stomatitis
Stomatitis is an inflammation of the mucous lining of any of the
structures in the mouth, which may involve the cheeks, gums, tongue,
lips, throat, and roof or floor of the mouth. The inflammation can be
caused by conditions in the mouth itself, such as poor oral hygiene,
poorly fitted dentures, or from mouth burns from hot food or drinks, or
by conditions that affect the entire body, such as medications, allergic
reactions, radiation therapy, or infections.
Pathophysiology
Severe iron deficiency anemia can lead to stomatitis. Iron is necessary
for the upregulation of transcriptional elements for cell replication and
repair. Lack of iron can cause the genetic downregulation of these
elements, leading to ineffective repair and regeneration of epithelial
cells, especially in the mouth and lips.
When it also involves an inflammation of the gingiva, it is called
gingivostomatitis.
g. reddish face
Sinar ultra violet mengurangi supresi imun sehingga terapi menjadi
kurang efektif, sehingga LES kambuh atau bertambah berat. Ini
disebabkan sel kulit mengeluarkan sitokin dan prostaglandin sehingga
terjadi inflamasi di tempat tersebut maupun secara sistemik melalui
peredaran di pembuluh darah.
h. Consumed analgesics but so far had not gotten better
Obat tertentu dalam persentase dosis kecil pada pasien tertentu dan
diminum dalam jangka waktu tertentu membuat kerja obat tidak
berfungsi secara optimal.
Sakit kepala lupus, seperti juga migrain pada umumnya, ditangani
dengan analgesic (penghilang rasa sakit) seperti Fiorinal, suntikan
sumatripan (Imitrex), antiradang seperti (Naprosyn, Aleve), dan
vasoconstrictor seperti campuran ergot (DHE-45, Migranal, Cafergot)
yang digunakan untuk serangan akut, sementara beta-blocker, tricyclic
34
antidepressant. Atau calcium channel blocker memberi pencegahan
dan kadang – kadang bisa dikonsumsi dalam jangka panjang. Sakit
kepala lupus, bagaimanapun, berbeda dengan migrain pada umumnya,
karena para pasien bisa merespons secara drastis terhadap percobaan
dua puluh sampai enam puluh miligram prednisone per hari selama 1
minggu, yang kadang – kadang berguna bagi para penderita migrain.
Pengidap lupus yang mengalami sakit kepala tetapi tidak membaik
oleh pengobatan rutin sebaiknya mendapat perawatan neurologis atau
bisa juga disebabkan karena rendahnya dosis yang diberikan.
8. Analgesics
analgesics are a class of drugs used to relieve pain. The pain relief induced by
analgesics occurs either by blocking pain signals going to the brain or by
interfering with the brain's interpretation of the signals, without producing
anesthesia or loss of consciousness. There are basically two kinds of
analgesics: non-narcotics and narcotics.
It should be noted that some references include aspirin and other non-steroidal
anti-inflammatory drugs (NSAIDS) in the class of analgesics, because they
have some analgesic properties. Aspirin and NSAIDS primarily have an anti-
inflammatory effect, as opposed to being solely analgesic.
i. Non-Narcotic Analgesics
Acetaminophen is the most commonly used over-the-counter, non-narcotic
analgesic. Acetaminophen is a popular pain-reliever because it is both
effective for mild to moderate pain relief and relatively inexpensive. It
must be emphasized though that the safety of acetaminophen is tied to
proper use of the drug (use according to specific prescribing instructions).
If acetaminophen is not used according to the directions on the label,
serious side effects and possible fatal consequences can occur. For
example, taking more than 4000 mg/day or using it longterm can increase
the risk of liver damage. The risk of liver damage with acetaminophen use
is also increased by ingesting alcohol. Make sure you discuss with your
35
doctor the maximum allowable dose of acetaminophen and any other
guidelines for its use.
Many people do not realize that acetaminophen is found in more than 600
over-the-counter drugs. It can be found in combination with other active
ingredients in many cold, sinus, and cough medications. The cumulative
effect of acetaminophen must be considered if you are talking multiple
drugs which contain acetaminophen.
How can acetaminophen damage the liver? Acetaminophen changes into
metabolites which are eliminated from the body. By taking more than the
recommended maximum daily dose of acetaminophen, more toxic
metabolites are produced than can be eliminated.
ii. Narcotic Analgesics
There are two types of narcotic analgesics: the opiates and the opioids
(derivatives of opiates). Opiates are the alkaloids found in opium (a white
liquid extract of unripe seeds of the poppy plant).
Opioids are any medication which bind to opioid receptors in the central
nervous system or gastointestinal tract. According to Wikipedia, there are
four broad classes of opioids:
Endogenous opioid peptides (produced in the body: endorphins,
dynorphins, enkephalins)
Opium alkaloids (morphine, codeine, thebaine)
Semi-synthetic opioids (heroin, oxycodone, hydrocodone,
dihydrocodeine, hydromorphone, oxymorphone, nicomorphine)
Fully synthetic opioids (pethidine or Demerol, methadone, fentanyl,
propoxyphene, pentazocine, buprenorphine, butorphanol, tramadol,
and more)
Opioids are used in medicine as strong analgesics, for relief of severe or
chronic pain. Interestingly, there is no upper limit for the dosage of opioids
used to achieve pain relief, but the dose must be increased gradually to allow
36
for the development of tolerance to adverse effects (for example, respiratory
depression). According to eMedicine, "Some people with intense pain get such
high doses that the same dose would be fatal if taken by someone who was not
suffering from pain"
There have been debates over the addictive potential of opioids vs. the benefit
of their analgesic properties for treating non-malignant chronic pain, such as
chronic arthritis. Some experts believe opioids can be taken safely for years
with minimal risk of addiction or toxic side effects. The enhanced quality of
life which opioids may provide the patient must be considered.
Side Effects / Adverse Reactions of Opioids
Common side effects and adverse reactions:
nausea
vomiting
drowsiness
dry mouth
miosis (contraction of the pupil)
orthostatic hypotension (blood pressure lowers upon sudden standing)
urinary retention
constipation and/or fecal impaction
Less common side effects and adverse reactions:
confusion
hallucinations
delirium
hives
itch
hypothermia
bradycardia (slow heart rate)
tachycardia (rapid heart rate)
raised intracranial pressure
37
ureteric or biliary spasm
muscle rigidity
flushing
Most severe side effects and adverse reactions:
respiratory depression
fatal overdose
More Information on Specific Analgesics :
Acetaminophen (Tylenol)
Codeine (Tylenol #2,3,4)
Darvocet (Propoxyphene/Acetaminophen)
Darvon (Propoxyphene)
Duragesic (Fentanyl Patch)
Hydromorphone (Palladone, Dilaudid)
Morphine (MSContin, Oramorph)
Oxycodone (OxyContin, Roxicodone)
Percocet (Oxycodone/Acetaminophen)
Percodan (Oxycodone/Aspirin)
Talwin NX (Pentazocine/Naloxone)
Ultracet (Tramadol/Acetaminophen)
Ultram (Tramadol)
Vicodin (Hydrocodone/Acetaminophen)
38
Genetic factor Environmental factors
Hormonal Factors
Tissue Deposition
Autoantibody production
T cells
1. Antilymphocytic2. Antinuclear3. Other
B cell differentiation
+ Ag
B cell proliferation
Specific Syndromes1. CNS involvement2. Thrombocytopenia3. Anemia4. Prolonged PTT5. Nephritis
Inflammation ProductsProstaglandisLeukotriencesComplementBreakdown products (C3a, C3b, and C5a)
Sure SLE(≥ 4 symptoms)
<4 symptoms,maybe SLE
Terapi
39
REFERENSI
Guyton & Hall. 2006. Buku Ajar Fisiologi Kedokteran Edisi 9. EGC : Jakarta.
Kamus Kedokteran Dorland. 2006. EGC : Jakarta.
Price, Sylvia A. and Wilson. 2006. Patofisiologi Konsep Klinis Proses-Proses
Penyakit Volume 1 dan 2. EGC : Jakarta.
Robbins, Cotrans, and Kumar. 1995. Buku Saku Dasar Patologi Penyakit. edisi 5.
EGC : Jakarta.
Jawetz. 2007. Mikrobiologi KedokteranStaf pengajar. EGC : Jakarta
Harrison's Principles of Internal Medicine, McGraw-Hill, edited by Eugene
Braunwald, et. al., 2001.
http://en.wikipedia.org/wiki/lupus
"tenderness." Etymology. Oxford English Dictionary. http://dictionary.oed.com/.
Systemic Lupus Erytematosus (SLE) « Joestikespkj’s Blog.html
U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES NATIONAL
INSTITUTES OF HEALTH . National Institute of Allergy and Infectious Diseases
NIH Publication No. 07-5423 September 2007. Immunesystem.pdf.
www.niaid.nih.gov
http://www.scribd.com/doc/10454981/Concept-Mapping-SLE
http://joestikespkj.wordpress.com/2009/03/11/systemic-lupus-erytematosus-sle/
http://www.adln.lib.unair.ac.id/go.php?id=gdlhub-gdl-s1-2008-puspitasar-
9078&PHPSESSID=735f99a341908093de36c5a6ffbdf67c
40
http://books.google.co.id/books?
id=a_AxzerWAs8C&pg=PA145&lpg=PA145&dq=analgesic+pada+lupus&source=bl
&ots=dteHb_I8Ek&sig=1oTqGiw2oYQyJrNMb0Y9eOXoVIc&hl=id&ei=n41MSozr
DoWKsgPM6f2mBQ&sa=X&oi=book_result&ct=result&resnum=3
http://www.skincosmos.com/id/systemic-lupus-erythematosus/
Marie A. Chisholm-Burns, Marie A. Chisholm, Barbara G. Wells, Terry L.
Schwinghammer, Patrick M. Malone, Jill M. Kolesar, John C. Rotschafer. 2008.
Pharmacotherapy Principles & Practice. USA. Handbook : booksgoogle
http://www.sap.com/industries/healthcare/pdf/BWP_SB_Patient_Management.pdf
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