Problem-Based Learning (PBL)

Tutorial 2
Scenario B Miss A
Group 10

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

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 +++

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 3940 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 bodys 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

2. PROBLEM IDENTIFICATION
1. Chief complain Whole body swelling which had been more prominent since 2 weeks before admission

2. General complaint Swelling was started when she woke up around the eyelids Swelling eventually developed to the whole body Urine was less than usual Since 1 year ago, frequently had tenderness around her joints especially at fingers joints, came and feded on its own Moderate fever which sometimes came an dfaded on its own Hair was easily fallen Stomatitis was often found without prominent cause Face was reddish especially at cheek if it was directly shone upon sunlight Consumed analgesics but so far had not gotten better

3. Physical examination General condition severely sick Sensorium compos mentis HR : 100 x/min, regular RR : 28 x/min, rapid and deep Blood pressure : 170/100 mmHg

4. Specific conditions Anasarca edema Stomatitis Ascites

5. Laboratory Examination 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 urinary protein +++

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 As 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 As complain? 17) What is the normal condition of all Miss As 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?

4. HYPOTHESIS

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

5. LEARNING ISSUE
1. Immune system 2. Urinary system 3. Interpretation 4. Auto imun 5. Hypersensitivity 6. SLE 7. Signs and symptoms 8. Analgesics

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 bodys 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 bodys 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.

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 lungsterritories 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 bodys fluids. Antibodies ambush foreign antigens circulating in the bloodstream. They are powerless, however, to penetrate cells. The job of attacking target cellseither cells that have been infected by viruses or cells that have been distorted by canceris 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 fluidstears, saliva, and the secretions of the respiratory and digestive tractsguarding 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 cellsperform 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 systems 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 persons 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. 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

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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 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 : 1.0 1.6 g/24hours or 15 25 mg/kgBB/24hours : 3 5.5 g/dl

Creatinin Albumin

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Cholestrol

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 persons immune system to weakened or inactivated forms of bacteria and viruses that can no longer cause disease, so that the persons 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.

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What are autoimmune disorders? 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 bodys 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 19

preserve organ function. New treatments and a greater understanding of autoimmune disorders are being researched. Patients should talk to their doctors and to any specialists they are referred to about their treatment options.

Systemic Autoimmune Diseases

Localized Autoimmune Diseases

Rheumatoid arthritis (RA) and Type 1 Diabetes Mellitus (pancreas Juvenile RA (JRA) (joints; less islets) commonly lung, skin) Lupus [Systemic (skin, Lupus Hashimoto's thyroiditis, Graves'

Erythematosus]

joints, disease (thyroid)

kidneys, heart, brain, red blood cells, other) Scleroderma (skin, intestine, less Celiac commonly lung) Sjogren's syndrome disease, Crohn's disease,

Ulcerative colitis (GI tract) (salivary Multiple sclerosis*

glands, tear glands, joints) Goodpasture's syndrome (lungs, Addison's disease (adrenal) kidneys) Wegener's granulomatosis (blood Primary biliary cirrhosis, Sclerosing vessels, sinuses, lungs, kidneys) cholangitis, (liver) Polymyalgia Rheumatica (large Temporal muscle groups) Arteritis / Giant Cell Autoimmune hepatitis

Arteritis (arteries of the head and neck)

Guillain-Barre syndrome (nervous system)

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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tissues and organs). Autoimmune disease can affect many parts of your body, like your nerves, muscles, endocrine system (system that directs your bodys 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 or chain of the FcRIII receptor (CD16) on mast cells, but remains largely unperturbed in complementdeficient mice, showing the primary importance of FcRIII 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 710 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 FcRIII 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 bloodgas 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.

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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, proteinuria, an an elevated active serum urinary creatinine, sediment,

hypoalbuminemia,

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

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Criterion 1. Malar rash

Definition / examples Fixed erythema over the malar eminences, tending to spare the nasolabial folds

2. Discoid rash 3. Photosensitivity 4. Oral ulvers 5. Arthritis 6. Serositis

Erythematosus raised patches, may scar Skin rash as a result of unusual reaction to sunlight Usually painless Non-erosive : Jaccouds arthropathy a. Pleuritis pleuritic pain, pleural rub, pleural Pericarditis ECG changes, rub, pericardial

effusion b.

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 patients 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 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

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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 antigenantibody complexes can suppress the bodys 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 diseases 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 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 26

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. Raynauds 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, lowgrade 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. 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 27

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 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 28

 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 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

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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 Sjogrens 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 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

30

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. Nonsteroidal 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. 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.

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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. 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

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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 isnt 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.

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, 33

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 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 34

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 antiinflammatory 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 doctor the maximum allowable dose of acetaminophen and any other guidelines for its use.

35

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 for the development of tolerance to adverse effects (for example, respiratory depression). According to eMedicine, "Some people with intense pain get such

36

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 ureteric or biliary spasm muscle rigidity

37

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 Hormonal Factors B cell proliferation

Environmental factors T cells

B cell differentiation

Autoantibody production Tissue Deposition Inflammation Products Prostaglandis Leukotriences Complement Breakdown products (C3a, C3b, and C5a) 1. Antilymphocytic 2. Antinuclear 3. Other

+ Ag

Specific Syndromes 1. CNS involvement 2. Thrombocytopenia 3. Anemia 4. Prolonged PTT 5. Nephritis

Sure SLE ( 4 symptoms)

<4 symptoms, maybe SLE

Terapi

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REFERENSI Guyton & Hall. 2006. Buku Ajar Fisiologi Kedokteran Edisi 9. EGC : Jakarta. Kamus Kedokteran Dorland. 2006. EGC : Jakarta. Price, Sylvia A. and Wilson. 2006. 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) Joestikespkjs 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-puspitasar9078&PHPSESSID=735f99a341908093de36c5a6ffbdf67c http://books.google.co.id/books?id=a_AxzerWAs8C&pg=PA145&lpg=PA145&dq=a nalgesic+pada+lupus&source=bl&ots=dteHb_I8Ek&sig=1oTqGiw2oYQyJrNMb0Y9 Patofisiologi Konsep Klinis Proses-Proses

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eOXoVIc&hl=id&ei=n41MSozrDoWKsgPM6f2mBQ&sa=X&oi=book_result&ct=re sult&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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