Problem-Based Learning (PBL)

Tutorial 2

Scenario B “Miss A”

Group 10

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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

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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 +++

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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

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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%

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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 +++

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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?

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4. HYPOTHESIS

Miss A, 20 years old suffered SLE due to autoimmune disorder

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5. LEARNING ISSUE

1. Immune system

2. Urinary system

3. Interpretation

4. Auto imun

5. Hypersensitivity

6. SLE

7. Signs and symptoms

8. Analgesics

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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.

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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

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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.

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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.

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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.

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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

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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

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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

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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 :

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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?

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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

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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

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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

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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

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Guyton & Hall. 2006. Buku Ajar Fisiologi Kedokteran Edisi 9. EGC : Jakarta.

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Price, Sylvia A. and Wilson. 2006. Patofisiologi Konsep Klinis Proses-Proses

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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/.

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