Case Study: Systemic Lupus Erythematosus: Lupus Nephritis

51











SYSTEMIC LUPUS ERTHYMATOSUS
(SLE)


A CASE STUDY REPORT OF A 33-YEAR-OLD FEMALE WITH SYSTEMIC LUPUS ERYTHEMATOSUS


A Case Study Report Presented to the
College of Arts and Sciences
Caraga State University


Prof. Adelita Nakila Toledo
Adviser


Mary Coleen L. Diango



October 2014
ACKNOWLEDGEMENT

Special thanks to Dr. Licayan for giving us such opportunity to access the medical records of some patients with autoimmune diseases in the city hospital (Butuan Medical Center, Butuan City). I would like to extend my sincerest thanks to Madeline Logroño for the financial support and to Mateo Diango for the guidance to the said area or vicinity of the patient. And also, for the cooperation of Mr. Ellan Mantasa for giving significant information about her spouse illness or disease. Thanks to the medical staff of Manuel J. Santos Hospital (Butuan City) for the medical information of Ms. Tiempo. To Mrs. Condrada Galagar Tiempo- mother of Joann Tiempo and Leah Mae Tiempo (sister) for authorizing me to access her daughter's medical records in M.J. Santos Hospital. To my sister Lorraine Diane Diango R.N, who patiently explained the medical terms and processes.
This paper will not be made possible without the presence of mentioned references in the paper. To the organization and authors, thank you.


TABLE OF CONTENTS
Client's Profile 1
Hospitalization History 2
Literature of Illness 6
History 6
Anatomy and Physiology 6
Signs and Symptoms/ Clinical Manifestation 10
Pathophysiology/Causes 11
Diagnostic Tests 13
Management and Treatment 14
Prognosis 16
Epidemiology 17
Pictures 19
Drug Study 20
Discussion and Analysis 29
Conclusion 38
Summary 39
Appendices 40
Client's Picture and Documentation Picture 40
Client's Authorization Letter 42
Client's Discharge Summary 43
Client's Laboratory Test Results 44
Reference 45
Student's Curriculum Vitae 46

CLIENT'S PROFILE

Client's Name: Ms. Jo Ann Galagar Tiempo
Age: 33 years old
Date of Birth: April 24, 1980
Place of Birth: Santa Cruz, Butuan City
Blood Type: B+
Work: None, Housewife
Religion: Roman Catholic
Address: P-1 Manila de Bugabos, Butuan City
Parents: Mr. Anatalio Tiempo
Mrs. Condrada Galagar
Spouse: Ellan Mantasa
Number of Children: Alive: 2 Dead: 1
Date of Death: May 28, 2013
Place of Death: Manuel J. Santos, 554 Montilla Boulevard, Butuan City

Hospitalization History
Hospital Admitted: Butuan Medical Center, Butuan City
Chief Complaints:
Admitting Diagnosis: Bipedal Edema
Final Diagnosis: Chronic Kidney Disease due to Lupus Nephritis
Connective Tissue Disease – Lupus Systemic Erythematosus
Client's History: As per noted * Pulmonary Tuberculosis
* Convulsion History
* Miscarriage (2012)
Admission Date: April 30, 2013
Admission Time: 5:00 pm
Discharge Date: May 8, 2013
Discharge Time: 4:30 pm
Attending Physician: Dr. De Vera, Francisco
Co/Mngt: Dr. Limcangco, Ponciano
Dr. Lagrito
Dr. De Castro
Radiologist: Jonathan M. Tahud, M.D., DPBR
Pathologist: Ponciano S. Limcangco, M.D.,
Hospital Admitted: Manuel J. Santos, Montilla Boulevard, Butuan City
Chief Complaints:
Admitting Diagnosis: Difficulty in Breathing
Nausea
Final Diagnosis: End Stage Renal Disease

Client's History: Note progress: Facial and Bipedal edema, Pallor, SOB,
Nausea, Vomiting, Fever, Allergy
Admission Date: May 25, 2013
Admission Time: NA
Discharge Date: NA
Discharge Time: NA
Attending Physician: Dr. Sy, Rafael B.
Surgeon: Dr. Hipol III, Rodrigo
Radiologist: Gerardo Tan Remandaban, M.D., DPBR
Pathologist: Edgardo B. Abadino M.D., FPSP

Joann Galagar Tiempo, a 33-year old lady lived in P-1 Manila de Bugabus together with her spouse Ellan Mantasa, she was born on April 24, 1980 at Santa Cruz, Butuan City. Their way of living is through farming. She was admitted at Butuan Medical Center on April 30, 2013 under admitting physician, Dr. de Vera. Prior to admission her spouse says that the patient complains about her discomfort, itchiness and difficulty in urination. Ambulatory brought by her first degree cousin in the hospital due to her yellowish discoloration (jaundice) of the skin with chief complaints of discomfort due to back itchiness, bipedal edema, shortness of breathing and abdominal pain. The patient experienced episode of discomfort and pain for the past one year. One month prior to her hospitalization or admission, noticed itchiness and redness of the face. The final diagnoses for the patient's case are Chronic Kidney Disease related to Lupus Nephritis, Connective Tissue Disease namely Systemic Lupus Erythematosus and Anemia (subject for blood transfusion). According to her spouse, the patient experienced convulsion in her younger age and also lung problem in her teenage years during her stay in Ozamiz City, indeed her medical history states that she has Pulmonary Tuberculosis and has a history of miscarriage.
During her admission, she was seen and examined by Dr. de Vera, orders and medicines were prescribed with some test like CBC, BT. While Creatinine test, ESR and chest x-ray were requested and her vital signs was monitored. She was given some medication such as ranitidine 50 mg and 5 mg prednisone, on her first day of admission. On the second day furosemide was given after transfusion, NaHCO3 650mg, CaCO3 500mg, ciprofloxacin 500 mg and were advised for dialysis. On the third day, she was given amlodipine 10 mg/tab, the following day; more blood transfusion was followed up. On the fifth day, she was advised to wear masked all the time and the day after, permitted to go home per request, prescribed with folic acid + FeSO4, NaHCO3 650 mg, CaCO3, and prednisone 5 mg.
Patient was then admitted in Manuel J. Santos Hospital, after the local election in May 25, 2013 when she experienced burning and intensive pain in the abdominal region and lower back (lumbar region) (source: Ellan Mantasa). The patient's admission complaints were nausea and difficulty of urination. Her history noted the progressive facial and bipedal edema, pallor, shortness of breathing, nausea, vomiting and allergy. The initial vital signs of the patient was; temperature: 38 °C , BP: 170/ 100 with noted swollen right leg and decrease of breath sounds. Further intervention was done like she was prescribed or advised to catheterization and dialysis.











LITERATURE OF ILLNESS
HISTORY
The term 'lupus' (Latin for 'wolf') was first used during the Middle Ages to describe erosive skin lesions evocative of a 'wolf's bite'. In 1846 the Viennese physician Ferdinand von Hebra (1816–1880) introduced the butterfly metaphor to describe the malar rash. He also used the term 'lupus erythematosus' and published the first illustrations in his Atlas of Skin Diseases in 1856. Lupus was first recognized as a systemic disease with visceral manifestations by Moriz Kaposi (1837–1902). The systemic form was further established by Osler in Baltimore and Jadassohn in Vienna. Other important milestones include the description of the false positive test for syphilis in SLE by Reinhart and Hauck from Germany (1909); the description of the endocarditis lesions in SLE by Libman and Sacks in New York (1923); the description of the glomerular changes by Baehr (1935), and the use of the term 'diffuse connective tissue disease' by Klemperer, Pollack and Baehr (1941). The beginning of the modern era in SLE was the discovery of the 'LE' cell by Hargraves, Richmond and Morton at the Mayo Clinic in 1948. (Bertsias et al., 2012)

ANATOMY & PHYSIOLOGY
Systemic Lupus Erythematosus (SLE) is a chronic, inflammatory autoimmune collagen disease resulting from disturbed immune regulation that causes an exaggerated production of autoantibodies (Johnson et al., 2008). Systemic lupus erythematosus (SLE) is a chronic disease that causes inflammation in connective tissues, such as cartilage and the lining of blood vessels, which provide strength and flexibility to structures throughout the body. The signs and symptoms of SLE vary among affected individuals, and can involve many organs and systems, including the skin, joints, kidneys, lungs, central nervous system, and blood-forming (hematopoietic) system. SLE is one of a large group of conditions called autoimmune disorders that occur when the immune system attacks the body's own tissues and organs (Genetics Home Reference, June 2014).
Lupus is a chronic (long-term) disease that causes inflammation — pain and swelling. Most patients feel fatigue and have rashes, arthritis (painful and swollen joints) and fever. The immune system is the body's defense system. When healthy, it protects the body by making antibodies (blood proteins) that attack foreign germs and cancers. With lupus, the immune system misfires. Instead of producing protective antibodies, an autoimmune disease begins and makes "autoantibodies," which attack the patient's own tissues. Doctors sometimes refer to this as a "loss of self-tolerance." As the attack goes on, other immune cells join the fight. This leads to inflammation and abnormal blood vessels (vasculitis). These antibodies then end up in cells in organs, where they damage those tissues.
A Lupus complication includes kidney failure. Your two kidneys are part of your renal system, which also includes two ureters, the bladder, and the urethra. As the primary organs of the renal system, your kidneys are responsible for:
Maintaining the correct amount and type of body fluids
Removing waste products and toxic substances
Regulating the hormones (chemical messengers) that help control blood pressure and blood volume
Lupus Nephritis
Inflammation of the nephrons, the structures within the kidneys that filter the blood, is called glomerulonephritis, or nephritis. Lupus nephritis is the term used when lupus causes inflammation in your kidneys, making them unable to properly remove waste from your blood or control the amount of fluids in your body. Abnormal levels of waste can build up in the blood, and edema (swelling) can develop. Left untreated, nephritis can lead to scarring and permanent damage to the kidneys and possibly end-stage renal disease (ESRD). People with ESRD need regular filtering of their body's waste done by a machine (dialysis) or a kidney transplant so that at least one kidney is working properly.
Lupus nephritis most often develops within the first five years after the symptoms of lupus start. It usually affects people between 20 and 40. In the early stages of lupus nephritis, there are very few signs that anything is wrong. Often the first symptoms of lupus nephritis are weight gain and puffiness in your feet, ankles, legs, hands, and/or eyelids. This swelling often becomes worse throughout the day. Also, your urine may be foamy or frothy, or have a red color. The first signs of lupus nephritis often show up in clinical laboratory tests on the urine.

Fig.1. Anatomy of kidney affected with SLE- Lupus Nephritis


Fig. 2: Comparison: A. Normal Nephron and Glomeruli structure, B. SLE-Lupus Nephritis affected kidney (Nephron and Glomeruli)
CLINICAL MANIFESTATION
Onset is insidious or acute. SLE can go undiagnosed for many years. The clinical course is one of the exacerbations and remissions. Multisystem features include nephritis, cardiopulmonary disease, rashes and more indirect evidence of systemic inflammation. According to the genetics home reference of US National Library of Medicine, SLE may first appear as extreme tiredness (fatigue), a vague feeling of discomfort or illness (malaise), fever, and weight loss. There are manifestations in different systems of the body. In musculoskeletal system: arthralgias and arthritis (synovitis) are common presenting features. Joint swelling, tenderness, and pain on movement are common, accompanied by morning stiffness. In integumentary system: several different types are seen (e.g, [SCLE] subacte cutaneous lupus erythematosus - causes sores after being out in the sun, [DLE] discoid lupus erythematosus- causes a rash that doesn't go away (Medline Plus, August 2014)). A butterfly rash across the bridge of the nose and cheeks occurs in fewer than half of the patients and may be a precursor to systemic involvement. Lesions worsen during exacerbations (flares) and may be provoked by sunlight or artificial ultraviolet light. Oral ulcers may involve buccal mucosa or hard palate. In cardiovascular system: Pericarditis is the most common clinical cardiac manifestation. Popular, erythematosus and pulpuric lesions may occur on the fingertips, elbows, toes and may progress extensor surfaces of forearms or lateral sides of hands and may progress to necrosis. Other systemic manifestations: Pleuritis or pleural effusions may occur, lymphadenopathy occurs in half of all SLE patients and renal involvement (glomeruli) may lead to systemic hypertension. SLE has varied and frequent neuropsychiatric presentations, generally demonstrated by subtle changes in behavior or cognitive ability. Depression and psychosis are common (Johnson et al., 2008).
Some people with lupus often have features that are not specific to lupus. These include fever, fatigue, weight loss, blood clots and hair loss in spots or around the hairline. They may also have heartburn, stomach pain, and poor circulation to the fingers and toes. Pregnant women can have miscarriages (OTIS, 2010). Renal malfunction may occur as a result of systemic complication (Lupus Nephritis).
Symptoms of Lupus Nephritis are the following:
Sudden and unexplained swelling, especially in the extremities (feet, ankles, legs, fingers, arms) or the eyes
Blood in the urine
Elevated blood pressure
Foamy appearance in urine
Increased urination, especially at night

PATHOPHYSIOLOGY/CAUSES
This disturbance is brought by some combination of genetic, hormonal (as evidence by the usual onset during the childbearing years), and environmental factors (sunlight, thermal burns). Certain medications, such as hydralazine (Apresoline), procinamide (Pronestyl), isoniazid, chlorpromazine (Thorazine), and some anticonvulsant, have been implicated in chemical-or drug induced SLE. In SLE, the increase in autoantibody production is thought to result from abnormal suppressor T-cell function, leading to immune complex deposition and tissue damage. Inflammation stimulates antigens, which in turn stimulate additional antibodies, and the cycle repeats (remissions and exacerbations) (Johnson et al., 2008).
Normal variations (polymorphisms) in many genes can affect the risk of developing SLE, and in most cases multiple genetic factors are thought to be involved. In rare cases, SLE is caused by mutations in single genes. Most of the genes associated with SLE are involved in immune system function, and variations in these genes likely affect proper targeting and control of the immune response. Sex hormones and a variety of environmental factors including viral infections, diet, stress, chemical exposures, and sunlight are also thought to play a role in triggering this complex disorder. About 10 percent of SLE cases are thought to be triggered by drug exposure, and more than 80 drugs that may be involved have been identified. In people with SLE, cells that have undergone self-destruction (apoptosis) because they are damaged or no longer needed are not cleared away properly. The relationship of this loss of function to the cause or features of SLE is unclear. Researchers suggest that these dead cells may release substances that cause the immune system to react inappropriately and attack the body's tissues, resulting in the signs and symptoms of SLE (Genetics Home Reference: US National Library for Medicine, June 2014)



DIAGNOSTIC TEST
According to the American College of Rheumatology (2013) the diagnostic test that can be done to the patients with SLE are: Abnormal blood tests; low blood cell counts: anemia, low white blood cells or low platelets, positive antinuclear antibody: referred to as ANA and present in nearly all patients with lupus certain antibodies that show an immune system problem: anti-double-strand DNA (called anti-dsDNA), anti-Smith (referred to as anti-Sm) or antiphospholipid antibodies, or a false-positive blood test for syphilis (meaning you do not really have this infection) .Lab tests. If your doctor suspects you have lupus from your symptoms, you will need a series of blood tests to confirm that you do have the disease. The most important blood screening test measures ANA, but you can have ANA and not have lupus. Therefore, if you have positive ANA, you may need more specific tests to prove the diagnosis. These blood tests include antibodies to anti-dsDNA and anti-Sm.
The presence of antiphospholipid antibodies can help doctors detect lupus. These antibodies signal a raised risk of certain complications such as miscarriage, difficulties with memory, or blood clots that may lead to stroke or lung injury. Doctors also may measure levels of certain complement proteins (a part of the immune system) in the blood, to help detect the disease and follow its progress. Diagnosis may require urine and blood tests as well as a kidney biopsy.
Urine test: Blood or protein in the urine is a sign of kidney damage.
Blood test: The kidneys remove waste materials like creatinine and urea from the blood. If the blood contains high levels of these substances, kidney function is declining. Your doctor should estimate your glomerular filtration rate based on your creatinine score.
Kidney biopsy: A biopsy is a procedure to obtain a tissue sample for examination with a microscope. To obtain a sample of your kidney tissue, your doctor will insert a long needle through the skin. Examining the tissue with a microscope can confirm the diagnosis of lupus nephritis and help to determine how far the disease has progressed.
MANAGEMENT/TREATMENT
There is no cure for lupus, and treatment can be a challenge. However, treatment has improved a great deal. Treatment depends on the type of symptoms you have and how serious they are. Patients with muscle or joint pain, fatigue, rashes and other problems that are not dangerous can receive "conservative" treatment. These options include nonsteroidal anti-inflammatory drugs — referred to as NSAIDs. Lupus is treated with drugs that block your body's immune system. Some of these are prednisone, azathioprine, cyclophosphamide or cyclosporine. A newer medication, belimumab, is a monloclonal antibody that is also available. Antimalarial drugs, such as hydroxychloroquine and chloroquine, can also be used to help control lupus.
Nonsteroidal anti-inflammatory drugs. NSAIDs decrease swelling, pain and fever. These drugs include ibuprofen (brand names Motrin, Advil) and naproxen (Naprosyn, Aleve). Some of these NSAIDs can cause serious side effects like stomach bleeding or kidney damage. Always check with your doctor before taking any medications that are over the counter (without a prescription) for your lupus. Antimalarial drugs. Patients with lupus also may receive an antimalarial medication such as hydroxychloroquine (Plaquenil). Though these drugs prevent and treat malaria, they also help relieve some lupus symptoms, such as fatigue, rashes, joint pain or mouth sores. They also may help prevent abnormal blood clotting.
Corticosteroids and immune suppressants are prescribed by doctors. Patients with serious or life-threatening problems such as kidney inflammation, lung or heart involvement, and central nervous system symptoms need more "aggressive" (stronger) treatment. This may include high-dose corticosteroids such as prednisone (Deltasone and others) and drugs that suppress the immune system. Immune suppressants include azathioprine (Imuran), cyclophosphamide (Cytoxan) and cyclosporine (Neoral, Sandimmune). Recently mycophenolate mofetil (CellCept) has been used to treat severe kidney disease in lupus—referred to as lupus nephritis. This exciting treatment advance occurred thanks to research studies in patients—called clinical trials. It provides hope that some of the other drugs that researchers are testing in patients will help lupus. It also underscores the need for patients with lupus to take part in studies.
Combination treatment: Health care providers may combine a few medications to control lupus and prevent tissue damage. Each treatment has risks and benefits. Most immune-suppressing medications, for instance, may cause major side effects. Side effects of these drugs may include a raised risk of infections as well as nausea, vomiting, hair loss, diarrhea, high blood pressure and osteoporosis (weak bones). Rheumatologists may lower the dose of a drug or stop a medicine because of side effects or when the disease goes into remission. As a result, it is important to receive careful and frequent health exams and lab tests to track your symptoms and change your treatment as needed. (American College of Rheumatology, 2013). If you develop kidney disease, you may need to eat less protein and sodium (salt). If you have high blood pressure, you should be sure to take the drugs prescribed to control your pressure. If you are overweight, losing weight may help to control your blood pressure.

PROGNOSIS
Systemic lupus erythematosus (SLE) carries a highly variable prognosis for individual patients. The natural history of SLE ranges from relatively benign disease to rapidly progressive and even fatal disease. SLE often waxes and wanes in affected individuals throughout life, and features of the disease vary greatly between individuals. The disease course is milder and survival rate higher in persons with isolated skin and musculoskeletal involvement than in those with renal disease and CNS disease. A consortium report of 298 SLE patients followed for 5.5 years noted falls in SLE Disease Activity Index 2000 (SLEDAI-2K) scores after the first year of clinical follow-up and gradual increases in cumulative mean Systemic Lupus International Collaborating Clinics (SLICC) damage index scores (Medscape by Christie Bartels, Feb. 2014).
As longevity of people with SLE increases, the likelihood of complications also increases in four areas: cardiovascular disease, infections, osteoporosis, and cancer.
Standard preventive measures and screening for related diseases may be necessary to deal with the increased risks, due to the side effects of medications. Extra vigilance is considered warranted especially for cancers affecting the immune system. SLE is considered incurable, but highly treatable.

EPIDEMIOLOGY
Prevalence rates in lupus are estimated to be as high as 51 per 100 000 people in the USA. The incidence of lupus has nearly tripled in the last 40 years, mainly due to improved diagnosis of mild disease. Estimated incidence rates in North America, South America, and Europe range from 2 to 8 per 100 000 per year. Women are affected nine times more frequently than men and African American and Latin American mestizos are affected much more frequently than Caucasians, and have higher disease morbidity. The disease appears to be more common in urban than rural areas. Sixty-five percent of patients with SLE have disease onset between the ages of 16 and 55 years, 20% present before age 16, and 15% after the age of 55 (Boumpas et al., 2012).
There are different prevalence rates for people of the same race in different areas of the world. The contrast between low reported rates of SLE in black women in Africa and high rates in black women in the United Kingdom suggests that there are environmental influences. In general, black women have a higher rate of SLE than women of any other race, followed by Asian women and then white women. In the United States, black women are 4 times more likely to have SLE than white women. A review of SLE across Asia-Pacific countries revealed considerable variation in prevalence and survival rates. For example, overall prevalence rates ranged from 4.3 to 45.3 per 100,000, and the overall incidence ranged from 0.9 to 3.1 per 100,000 per year. Moreover, Asians with SLE had higher rates of renal involvement than whites did, and cardiovascular involvement was a leading cause of death in Asians. More than 90% of cases of SLE occur in women, frequently starting at childbearing age. The use of exogenous hormones has been associated with lupus onset and flares, suggesting a role for hormonal factors in the pathogenesis of the disease. The risk of SLE development in men is similar to that in prepubertal or postmenopausal women. Interestingly, in men, SLE is more common in those with Klinefelter syndrome (ie, genotype XXY), further supporting a hormonal hypothesis. In fact, a study by Dillon et al found that men with Klinefelter syndrome had a more severe course of SLE than women but a less severe course than other men.
The female-to-male ratio peaks at 11:1 during the childbearing years. A correlation between age and incidence of SLE mirrors peak years of female sex hormone production. Onset of SLE is usually after puberty, typically in the 20s and 30s, with 20% of all cases diagnosed during the first 2 decades of life.Men with lupus tend to have less photosensitivity, more serositis, an older age at diagnosis, and a higher 1 year mortality compared to women. SLE tends to be milder in the elderly with lower incidence of malar rash, photosensitivity, purpura, alopecia, Raynaud's phenomenon, renal and central nervous system involvement, but greater prevalence of serositis, pulmonary involvement, sicca symptoms, and musculoskeletal manifestations (Bertsias and Cervera, 2012).
A review of the worldwide literature (predominantly North America, Europe, and Asia) found that the incidence of pediatric-onset SLE ranged from 0.36 to 2.5 per 100,000 per year and the prevalence ranged from 1.89 to 25.7 per 100,000. The prevalence of SLE is highest in women aged 14 to 64 years. SLE does not have an age predilection in males, although it should be noted that in older adults, the female-to-male ratio falls. This effect is likely due to loss of the estrogen effect in older females. (Medscape by Christie Bartels, Feb. 2014).

PICTURES RELATED TO CLIENT'S ILLNESS

Fig. 3. - Malar rash
Fig. 4– Periungual erythema and nailfold vasculitis
Fig. 5. Acute diffuse cutaneous lupus
Fig.6. Subacute cutaneous lupus erythematosus
Fig.7. Facial discoid lupus rash with a malar distribution. Note the erythema (indicating disease activity), keratin plugged follicles, and dermal atrophy.






Drug Study
NAME OF DRUG AND
CLASSIFICATION
DOSAGE,FREQUENCY AND ROUTE
MECHANSIM OFACTION
INDICATION
CONTRAINDICATION
ADVERSE REACTION
NURSING RESPONSIBILITIES
GENERIC NAME:
Amlodipine
BRAND NAME:
Norvasc
CLASSIFICATION:
Therapeutic: Anti-hypertensive Pharmacologic: Calcium channel blockers

10 mg/tab
OD
Per Orem

Inhibits the transport of calcium into myocardial and vascular smooth muscle cells resulting in the inhibition of excitation 'contraction coupling and subsequent contraction. Therapeutic effects: systemic vasodilation resulting in the decreased blood pressure. Coronary vasodilation resulting in decreased frequency and severity attacks of angina
Alone or with other agents in the management of hypertension angina pectoris and vasospastic angina
Hypersensitivity. blood pressure less than , 90 mmHg. Use cautiously in sever hepatic impairment history of aortic Stenosis
CNS: headache, dizziness, fatigue,
CV: peripheral edema, angina, brachycardia, hypotension, palpitations
GI: gingival hyperplasia, nausea
DERM: flushing
Monitor blood pressure and pulse before therapy during dose titration, and periodically during therapy. Monitor ECG during prolonged therapy. Monitor intake and output ratios and daily) eight. Assess for signs of CHF (peripheral edema, rales/crackles, dyspnea weight gain and jugular venous distention
*Lab test considerations: Total serum calcium is not affected by calcium channel blockers.
SOURCE: Davi's Drug Study Guide for Nurses (11th edition). http://www.scribd.com
NAME OF DRUG AND
CLASSIFICATION
DOSAGE,FREQUENCY AND ROUTE
MECHANSIM OFACTION
INDICATION
CONTRAINDICATION
ADVERSE REACTION/ SIDE EFFECT
NURSING RESPONSIBILITIES
Ranitidine Hydrochloride
Brand Name: Zantac
Classification: Anti-ulcer 
Route: Oral
Dosage: 50mg
Timing: OD
Competitively inhibits the action of histamine at the H2 receptors of the parietal cells of the stomach, Inhibiting basal gastric acid secretion and gastric acid secretion that is stimulated by food, insulin, histamine, cholinergic agonists, gastrin and pentagastrin
Short-term treatment of active duodenal ulcer
Short-term treatment of active, benign gastric ulcer
Maintenance therapy for duodenal ulcer at reduced dosage.
Short-term treatment for GERD
. Pathologic hypersecretory conditions
Treatment of erosive esophagitis
Treatment of heartburn, acid indigestion,
Contraindicated with allergy to ranitidine, lactation Use cautiously with impaired renal or hepatic function, pregnancy
CNS: headache, malaise, dizziness, somnolence, insomnia, vertigo
CV: tachycardia, bradycardia
Dermatologic: rash, alopecia
GI: constipation, diarrhea, nausea and vomiting, abdominal pain, hepatitis
Hematologic:leucopenia,granulocytopenia,thrombocytopenia,pancytopenia
assessment:
1. History: allergy to ranitidine, impaired renal or hepatic function, lactation, pregnancy.
2. Physical: skin lesions, orientation, affect liver evaluation, abdominal examination, normal output, renal function tests, CBC
Interventions:
Administer oral drug with meals and at bedtime
2. Decrease doses in renal and liver failure.
3.Provide concurrent antacid therapy to relieve
Published by: Harvey Banag. http://www.scribd.com

NAME OF DRUG AND
CLASSIFICATION
DOSAGE,FREQUENCY AND ROUTE
MECHANSIM OFACTION
INDICATION
CONTRAINDICATION
ADVERSE REACTION
NURSINGRESPONSIBILITIES
Generic Name:
Furosemide
Brand Name:
Lasiz
Classification:
Electrolytic and water
balance agent; Loop
diuretic

Dosage:
40mg
Route: Per Orem
Frequency: Every
8 hours

Rapid-acting potent
sulfonamide "loop"
diuretic and
antihypertensive with
pharmacologic effects
and uses almost
identical to those of
ethacrynic acid. Exact
mode of action not
clearly defined;
decreases renal
vascular resistance
and may increase
renal blood flow.
Treatment of edema associated with CHF,
cirrhosis of liver, and
kidney disease,
including nephrotic
syndrome. May be
used for
management of
hypertension, alone
or in combination with
other
antihypertensive
agents, and for
treatment of
hypercalcemia. Has
been used
concomitantly with
mannitol for
treatment of severe
cerebral edema,
particularly in
meningitis.

History of hypersensitivety to furosemide or
sulphonamides; increasing oliguria, anuria, fluid and
electrolyte depletion
states; hepatic coma

Patients who
are pregnant,
lactating

CNS:He a da c he
GI:Nausea,
Vomiting, oral and
gastric burning,
anorexia,
diarrhea,
constipation,
abdominal
cramping, acute
pancreatitis,
jaundice.
CV:Postural Hypotension,
dizziness with excessive
diuresis, acute
hypotensive
episodes,
circulatory
collapse.
1. Observe patients receiving
parenteral drug carefully; closely
monitor BP and vital signs.
Sudden death from cardiac arrest
has been reported.
2. Monitor BP during periods of
diuresis and through period of
dosage adjustment.
3. Observe older adults closely
during period of brisk diuresis.
Report symptoms to physician.
4. Lab tests: Obtain frequent
blood count, serum and urine
electrolytes, CO2, BUN, blood
sugar, and uric acid values during
first few months of therapy and
periodically thereafter.
5. Monitor for signs and
symptoms of hypokalemia
Published by Reisha Fungo. http://www.scribd.com

NAME OF DRUG AND
CLASSIFICATION
DOSAGE,FREQUENCY AND ROUTE
MECHANSIM OFACTION
INDICATION
CONTRAINDICATION
ADVERSE REACTION
NURSINGRESPONSIBILITIES
Ciprofloxacin

Classification:
Antibacterial: Fluoroquinolone
500 mg
Twice a day
Bactericidal: interferes with bacterial DNA replication insusceptible bacteria preventing cell production
Ciprofloxacin is used in the treatment of chronic bacterial prostatitis. It is also used in the treatment of skin or skin structure, GI tract, bone or joint; lower respiratory tract, and urinary tract infections. Ciprofloxacin is also used in the treatment of chancroid. Ciprofloxacin is also used in the treatment of infectious diarrhea, uncomplicated gonorrhea, empiric treatment of febrile neutropenia, and acute sinusitis. It can also be used for conjunctival keratitis, keratoconjunctivitis, corneal ulcers, blepharitis, dacrocystitis, blepharoconjunctivitis
Ciprofloxacin is contraindicated in persons with a history of hypersensitivity to ciprofloxacin, any member of the quinolone class of antimicrobial
agents, or any of the product components.
CNS: Headache, dizziness, ataxia, hallucination
CV: arrhythmias, angina
EENT: dry eye, eye pain
GI: nausea, diarrhea, dry mouth, abdominal pain
GU: renal failure Other: fever, rash,
hypersensitivity
Question for history of hypersensitivity to Ciprofloxacin or Quinolones
2. May be given without regards to meals. Preferred dosing time 2 hours after meals.
3. Do not administer antacids within 2hours of Ciprofloxacin.
4. Encourage cranberry juice or citrus fruits.
5. Evaluate food tolerance.
6. Determine pattern of bowel activity.
7. Check for dizziness, headache, visual difficulties, and tremors.
8. Observe therapeutic response.
Published by Tony Daniel M. Gurbuxani. http://www.scribd.com

NAME OF DRUG AND
CLASSIFICATION
DOSAGE,FREQUENCY AND ROUTE
MECHANSIM OFACTION
INDICATION
CONTRAINDICATION
ADVERSE REACTION
NURSINGRESPONSIBILITIES
Prednisone
Classification:
Systemic corticosteroids
Dose:
5 mg
Route:
PO
Time/frequency: QD
Interactions with other patient drugs, OTC or herbal medicines (ask patient specifically) Phenytoin increases metabolism, may decrease effectiveness
Medication
Anti-inflammation of airways
Supress inflammation and the normal immune response. Used systemically and locally in a wide variety of chronic diseases including: Inflammatory (COPD
Contraindications/warnings/interactions
Contraindicated in pt's w/ Active untreated infections, known alcohol,
 bisulfite, or tartrazine hypersensitivity or intolerance, Administration of live virus vaccines. Use cautiously in pt's w/Chronic treatment (will lead to adrenal suppression; use lowest possible dose for shortest period of time)

CNS: depression, euphoria,
CV: hypertension
GI: anorexia, nausea,
Derm: acne, decreased wound healing, ecchymoses, fragility, hirsutism, petechiae, Endo: adrenal suppression, MS: muscle wasting, osteoporosis,Misc: cushingoid appearance (moon face, buffalo hump)
Assess patient for signs of adrenal insufficiency (hypotension, weight loss, weakness, nausea, vomiting, anorexia, lethargy, confusion, restlessness) before and periodically during therapy
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NAME OF DRUG AND
CLASSIFICATION
DOSAGE,FREQUENCY AND ROUTE
MECHANSIM OFACTION
INDICATION
CONTRAINDICATION
ADVERSE REACTION
NURSINGRESPONSIBILITIES
FOLIC ACID
(VITAMIN B
9
,PTEROYLGLUTAMIC ACID)(fol'ic)

Classifications
Vitamin B
9

4 g
PO
QD

Vitamin B complex essential for nucleoprotein synthesis and maintenance of normal erythropoiesis. Acts against folic acid deficiency that impairs thymidylate synthesis and results in production of defective DNA that leads to megaloblast formation and arrest of bone marrow maturation.
Folate deficiency, macrocytic anemia, and megaloblastic anemias associated with malabsorption syndromes, alcoholism, primary liver disease, inadequate dietary intake, pregnancy, infancy, and childhood
Folic acid alone for pernicious anemia or other vitamin B
12
deficiency states; normocytic, refractory, aplastic, or undiagnosed anemia

Reportedly nontoxic. Slight flushing and feeling of warmth following IV administration.
Assessment & Drug Effects

Obtain a careful history of dietary intake and drug and alcohol usage prior to start of therapy. Drugs reported to cause folate deficiency include oral contraceptives, alcohol, barbiturates, methotrexate, phenytoin, primidone, and trimethoprim. Folate deficiency may also result from renal dialysis.

Keep physician informed of patient's response to therapy.

Monitor patients on phenytoin for subtherapeutic plasma levels.

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NAME OF DRUG AND
CLASSIFICATION
DOSAGE,FREQUENCY AND ROUTE
MECHANSIM OFACTION
INDICATION
CONTRAINDICATION
ADVERSE REACTION
NURSINGRESPONSIBILITIES
Fe SO4
Classification:
Therapeutic: Antianemics Pharmacologic: Iron supplements
PO:300 mg2-4timesdaily
Action:

An essential mineral found in hemoglobin, myoglobin, and many enzymes

Parenteral iron enters the blood stream and organs of the reticulo endothelial system (liver, spleen, bone marrow),where iron is separated out and becomes part of iron stores.

Prevention/treatment of iron deficiency as its therapeutic effect.

Prevention and treatment of iron deficiency anemia

Contraindicated in:
Primary hemochromatosis

hemolytic anemias and other anemias not due to iron deficiency

some products contain alcohol, tartrazine, or sulfites and should be avoided inpatients with known intolerance or hypersensitivity

Concurrent oral iron therapy

GI: constipation, dark stools, diarrhea, epigastric pain,
GI: bleeding
ASSESSMENT:
Assess nutritional status and dietary history to determine possible cause of anemia and need for patient teaching.
Assess for bowel function for constipation or diarrhea .Notify physician or other health care professional and use appropriate nursing measures and should these occur.
IMPLEMENTATION:
Oral preparations are most effectively absorbed if administered 1 hour before or 2 hours after meals. If gastric irritation occurs, administer with meals. Take tablets and capsules with afull glass of water or juice. Do not crush or chew enteric – coated tablets and do not open capsules.
HEALTH TEACHING:
Encourage patient tocomply with medicationregimen.
 Take missed doses as soonas remembered within 12hours; otherwise, return toregular dosing schedule. Donot double doses.

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NAME OF DRUG AND
CLASSIFICATION
DOSAGE,FREQUENCY AND ROUTE
MECHANSIM OFACTION
INDICATION
CONTRAINDICATION
ADVERSE REACTION
NURSINGRESPONSIBILITIES
NaHCO3
(sodium bicarbonate)

Classification: Fluids, Electrolyte, Blood Products, And Hematological
Drugs
650 mg
 TID Oral
Route

Increases plasma bicarbonate, neutralizes gastric acid which forms water, sodium chloride, carbon dioxide, and raises blood pH.
Treatment of metabolic acidosis, promotion of gastric, systemic and urine alkalinization in the case of intoxication with weak organic acids
Hypoventilation, hypocalcemia, increase serum osmolarity, further in all situationswhere sodiumintake must berestricted likecardiacinsufficiency,edemahypertension,eclampsia,severe kidneyinsufficiency
Hypernatremia and serum osmolarity, paravenous administrations may lead to tissue necrosis.
Obtain patient history including drug history and any hypersensitivity.
 Assess respiratory and pulse rate, rhythm, depth, lung sounds and notify the physician.
 Assess for carbon dioxide in GI tract, may lead to perforation if ulcer is severe.
Test and monitor urine pH, urinary output, during beginning treatment.
If patient has oedematous tendency, notify physician.
If patient is vomiting withhold medication and immediately inform the physician.
If the patient exhibits shortness of breath and hyperpnea, immediately inform the physician.
Inform physician if relief is not obtained or if the patient demonstrate any symptoms suggest bleeding, such as black tarry stools or coffee ground emesis.
Caution patient to immediately report to physician if symptoms such as nausea, vomiting and anorexia
occurs
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NAME OF DRUG AND
CLASSIFICATION
DOSAGE,FREQUENCY AND ROUTE
MECHANSIM OFACTION
INDICATION
CONTRAINDICATION
ADVERSE REACTION
NURSINGRESPONSIBILITIES
CaCO3
Calcium carbonate


DOSAGE: 350mg
Adult:1-2capsules daily

Decreases total acid load of GI tract. Increase esophageal Sphincter tone
Antacid, calcium supplement, osteoporosis
Hypocalcaemia, bone tremors, severe renal failure, hypersensitivity
Constipation, flatulence, diarrhea, renal dysfunction, acid rebound
> administer as antacid1 hr after meal and at bed time>administer as supplement 1½ hrs after meal and at bedtime>advice pt to increase fluids to 2L unless contraindicated
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Analysis and Discussion

Part I. Butuan Medical Center

Table 1: Hematology Result
Test
Result
Unit
Reference (NCCLS)
WBC
10.43
10^9/L
5.0-10.0
RBC
1.75
10^12/L
M 4.5-5.2 F 3.5-6.6
HEMOGLOBIN
48
G/L
M135-175 F 125-155
HEMATOCRIT
0.15

M 0.40-0.52 F 0.36-0.48
MCV
83.4
fL
82-92
MCH
27.4
Pg
27-32
MCHC
329
G/L
320 – 380
PLATELET
228
10^9/L
150- 400
DIFFERENT COUNT



NEUTROPHILS
0.60

0.50 -0.70
LYMPHOCYTES
0.16

0.20- 0.40
MONOCYTES
0.06

0.02-0.06

EOSINOPHILS
0.18

0.02-0.05
BASOPHILS
0.00

0.005-0.01
ESR
150
MM/HR
M 0-10 F 0-20
*Erythrocyte Sedimentation Rate (ESR) *mean corpuscular hemoglobin concentration (MCHC) * mean corpuscular volume (MCV) *Mean Corpuscular Hemoglobin concentration (MCH) * White Blood Cells (WBC) * Red Blood Cell (RBC).

A brief description of each of the measured parameters: WBC White Blood Count: A total count of the number of white cells per liter of blood. Increased in inflammation, infection and in dyscrasias (such as leukemia). Decreased: In various infections, bone marrow defects, drugs, etc. An examination of the features described below will indicate which of the white cell types is causing the general lowering. RBC Red Cell Count: A total count of the number of red cells per liter of blood. Increased in overproduction states of the marrow (polycythemia, chronic oxygen deprivation). Decreased in anemia. An examination of the red cell indices usually reveals the nature of the abnormality. Hemoglobin: The total amount of hemoglobin in the blood (irrespective of the number of cells containing the hemoglobin). Hematocrit: The total volume of the red cells in the blood. MCV Mean Corpuscular Volume is an indication of the size of the red cells. MCH Mean Corpuscular Hemoglobin is a measure of the amount of hemoglobin per red blood cell. MCHC Mean Corpuscular Hemoglobin Concentration is the amount of hemoglobin per liter of fluid in each cell. Lymphocytes The lymphocytes are the circulating immune response cells. Monocytes: Phagocytic (engulfing) white cells. Basophils: Phagocytic white cells. Platelets: The small cells which are intimately involved in coagulation and clot formation.
Upon the result of the Hematological test that was conducted last April 2013 the patient's result of ESR was noticeably five times high or above the normal range. An erythrocyte sedimentation rate test, measures the speed at which red blood cells settle to the bottom of an upright glass test tube. This measurement is important because when abnormal proteins are present in the blood, typically due to inflammation or infection, they cause red blood cells to clump together and sink more quickly, which results in a high ESR value. The ESR is useful in detecting inflammation in the body that may be caused by infection, some cancers, and certain autoimmune diseases. Thus, saying that the abnormally high ES rate is due to the said autoimmune disease (the SLE; Systemic Lupus Erythematosus). In relation, with the high ESR, the WBC was also slightly beyond the normal range. White blood cells are the mainstay of the immune system. Some white blood cells, known as macrophages, play a function in innate immunity by surrounding, ingesting, and destroying invading bacteria and other foreign organisms in a process called phagocytosis (literally, "cell eating"), which is part of the inflammatory reaction and in the patient's case is virtually seen by the presence of bipedal edema thus makes us conclude that the macrophages phagocytic role malfunctions which results in not recognizing which cell should and should not be eaten. Macrophages also play an important role in adaptive immunity in that they attach to invading antigens and deliver them to be destroyed by other components of the adaptive immune system. The eosinophil is also high, knowing that the eosinophil is attracted to sites of parasitic infections, antigen-antibody reactions and play a part in allergic reactions. These may implicate that something is wrong inside the body causing this eosinophils to increase in number and this may correlated with the ESR result (the abnormal increased of ES rate due to proteins).
Another abnormalities in the Hematologic test is that there is a drop of the RBC, Hemoglobin, Hematocrit (description above) which indicates that the patient is anemic which reduces the oxygen-carrying capability of blood and the patients history of pulmonary tuberculosis may have any connection with the said results. For us to understand the said results, red blood cells are composed predominantly of a protein and iron compound, called hemoglobin that captures oxygen molecules as the blood moves through the lungs, giving blood its red color. As blood passes through body tissues, hemoglobin then releases the oxygen to cells throughout the body, in relation with the patients hematology results of low RBC and hemoglobin, due to the incapability of the blood to transport oxygen, there is a deficiency of supply in oxygen thus making the cell inability or alter to function for the reason that oxygen plays an important role in the cellular respiration and manufacturing ATP (energy). Red blood cells are so packed with hemoglobin. Hemoglobin also takes up and releases nitric oxide, which plays an important role in regulating blood pressure. Due to lower count of the patient's RBC, she was advised and subjected to blood transfusion.
Table 2: Creatinine Level
Date
April 30, 2013
May 6, 2013
Creatinine
21.10
22.15
Reference
0.6-2.0 mg/dl
0.6-2.0 mg/dl

Serum creatinine levels and urinalysis are used in screening for renal involvement. Early detection allows for prompt treatment so that renal damage can be prevented (Smeltzer et al., 2008). Renal involvement may lead to hypertension, which also requires careful monitoring and management. As seen in the results that there is high level of creatinine which is related to the patient's nephritis (kidney inflammation caused by any infection).

The patient's spouse Mr. Ellan Mantasa as noted from his interview said that his partner mentioned that she has a history of convulsion in her childhood years. Theoretically speaking, her convulsion experience probably contributed her autoimmune disease if she has taken any anti-convulsant medicine. When Mrs. Condrada Tiempo was asked, that the patient during that year received medication but was not sure and forgot the said drug because that happens a long time ago. As it was noted in the book of Johnson (Brunner & Suddarths's Textbook of Medical-Surgical Nursing, 11th edition), that certain medications like anticonvulsants, have been implicated in chemical or drug that induced SLE. According to Mr. Ellan Mantasa, his partner (Joann Tiempo) has a history of lung problem when she's still working in Ozamis City in her teenage years but doesn't follow the proper medication due to financial problem; he also once said that her wife had trouble in her pregnancy leading to miscarriage of their child prior to her illness diagnosis. Lupus appears to increase the chance of miscarriage early in pregnancy. While studies vary, miscarriage rates with lupus have been reported to be up to 35% during the first trimester. A previous miscarriage, kidney disease, and the presence of specific antibodies (antiphospholipid) have been associated with a higher chance of miscarriage in women with lupus.
The final diagnoses of the patient were Chronic Kidney Disease due to Lupus Nephritis and Connective Tissue Disease – Lupus Systemic Erythematosus. The presence of Nephritis is the manifestation of the immune system complication. This may result to a further damage of the kidney that will lead for the advice for dialysis. The patient may not die because of her illness but because of the complications. The medication that was prescribed by the physicians may actually give cure to her said illness but may also give rise to another complication as brought by the side effects or contradictions of the drug.
Part II. Manuel J. Santos Hospital
Table 3: Laboratory Results
Test
Result Unit
Normal Range (NCCLS)
Remarks
Albumin
2.8 g/dL
3.8-5.0
Lower
Coagulation: Prothrombin time
21. 10 sec
10- 13.50 ~14
Slower
Potassium
7.8 p nmol/L
3.5-5.3
Higher
Hemoglobin
67 L
117-140
Lower
Hematocrit
0.20 L
0.34-0.44
Lower
WBC
22.55 H
5.0-15.0
Higher
Lymphocyte
0.04 L
0.20-0.50
Lower
Band
0.00 L
0.02-0.05
Lower
Eosinophil
0.00
0.00-0.01
Baseline
Monocyte
0.03 L
0.08-0.14
Lower
Platelet count
122 L
150-390
Lower

The decrease in albumin indicates kidney diseases or liver diseases. Albumin helps move many small molecules through the blood including bilirubin (yellow breakdown product of normal heme catabolism). Prothrombin time (PT) is a blood test that measures how long it takes blood to clot. A prothrombin time test can be used to check for bleeding problems. PT is also used to check whether medicine prevent blood clots is working. Blood clotting factors are needed for blood to clot (coagulation). Prothrombin, or factor II, is one of the clotting factors made by the liver. Due to the result of PT above, we can say that another organ is also affected other than the kidney.
Prothrombin time (PT) is measured to:
Find a cause for abnormal bleeding or bruising.
Check to see if blood-thinning medicine, such as warfarin (Coumadin), is working. If the test is done for this purpose, a PT may be done every day at first. When the correct dose of medicine is found, you will not need so many tests.
Check for low levels of blood clotting factors. The lack of some clotting factors can cause bleeding disorders such as hemophilia, which is passed in families (inherited).
Check for a low level of vitamin K. Vitamin K is needed to make prothrombin and other clotting factors.
Check if it is safe to do a procedure or surgery that might cause bleeding.
Check how well the liver is working. Prothrombin levels are checked along with other liver tests, such as aspartate aminotransferase and alanine aminotransferase.
Check to see if the body is using up its clotting factors so quickly that the blood can't clot and bleeding does not stop. This may mean the person has disseminated intravascular coagulation (DIC).
Potassium is both an electrolyte and a mineral. It helps keep the water (the amount of fluid inside and outside the body's cells) and electrolyte balance of the body. Potassium is also important in how nerves and muscles work. Abnormal potassium levels may cause symptoms such as muscle cramps or weakness, nausea, diarrhea, frequent, urination, dehydration, low blood pressure, confusion, irritability, paralysis, and changes in heart rhythm. A blood test to check potassium is done to:
Check levels in people being treated with medicines such as diuretics and for people having kidney dialysis.
Check to see whether treatment for too low or too high potassiumlevels is working.
Check people with high blood pressure who may have a problem with their kidneys or adrenal glands.

Joann Galagar Tiempo was pre-operatively diagnosed of Acute Renal Failure with transition to Chronic Renal Failure and was ordered to be subjected to dialysis. Dr. Hipol III, Rodrigo was the attending surgeon of the patient. Dr, Hipol III performed the operation using ultrasound to guide the Internal Jugular catheter placement. Dialysis is the artificial process of eliminating waste (diffusion) and unwanted water (ultrafiltration) from the blood. Our kidneys do this naturally. Some people, however, may have failed or damaged kidneys which cannot carry out the function properly - they may need dialysis. In other words, dialysis is the artificial replacement for lost kidney function (renal replacement therapy). Dialysis may be used for patients who have become ill and have acute kidney failure (temporary loss of kidney function), or for fairly stable patients who have permanently lost kidney function (stage 5 chronic kidney disease). Approximately 1,500 liters of blood are filtered by a healthy person's kidneys each day. We could not live if waste products were not removed from our kidneys. People whose kidneys either do not work properly or not at all experience a buildup of waste in their blood. Without dialysis the amount of waste products in the blood would increase and eventually reach levels that would cause coma and death. 
Internal jugular venous access (especially right-sided) is associated with a low rate of catheter malposition, and is commonly used in situations that require reliable tip positioning for immediate use, such as drug administration or transvenous pacing. Similarly, the direct route from the right internal jugular vein to the superior vena cava facilitates hemodialysis access and pulmonary artery catheter placement. The Ultrasound shows that the IJV catheter was noted in place, tip of which is directed towards the superior vena cava region.

Fig.8. the location of Internal Jugular Vein Catheterization

Conclusion
The SLE of Joann Tiempo develops a new complication which leads to Lupus Nephritis that targets and damages the functional and basic unit of the kidney and the filtering capability of the kidney was altered. Based on the analysis, the patients SLE- Lupus Nephritis can be partially determine with the presence of edema. The patient's edema manifested the bipedal inflammation (right leg: most affected part) and facial inflammation (right eye: most affected part). The laboratory result of Prothrombin time test resulted to reach at the abnormal rate thus saying that another complication of the liver was arising. Almost all of the laboratory results of the patient's remarks goes down or lowered which directly implicates that the patient's body in response to the illness was not proper or normal. The crucial stage of the patient's dialysis though may add few days of her life but the procedure cannot give any assurance of healing but only maintenance. The patient actually died due to the said complications of the acute to chronic renal failure which was considered as ESRD or the End-Stage-Renal Disease.
The monthly or yearly check up is very important for us to be aware of the possible illness, diseases or abnormalities in our body. Early detection of any illness may extend one's life together with proper medication or treatment and medical procedures. Life without money is lame but money without life is dead. For it was said that health is wealth.



Summary

Table 4. Systemic Lupus Erythematosus- Autoimmune Disease Summary
Etiologic Factors
Main Problem
Manifestations
Medical Management
Nursing Intervention
G-genetic
A-autoimmune
V-viral factor
E-exposure and intake of medications
Dysfunctional immune system produces antibodies against the body cells
The antibodies attack multiple organs:
SKIN, JOINTS, KIDNEY, HEART, BRAIN
SKINS- butterfly rash
JOINTS- Arthritis
KIDNEY- protenuria and hematuria
HEART- pericarditis
BRAIN- psychosis, seizures and depression
STEROIDS-
Suppress inflammation and immune reaction
PLASMA EXCHANGE THERAPY- remove the circulating antibodies
P-psychological support
A- administer medications
L- lifetime monitoring and lifestyle changes
M- monitor for seizure development





APPENDICES
CLIENT'S PICTURE AND DOCUMENTATION PICTURE



Fig.9. Way to the patient's place or vicinity. The main road of San Vicente if travelled straightly will lead you to Dulag, Butuan City. A motorcycle terminal is noticeable between the way to Tungao and Santa Cruz. The way to Santa Cruz will lead to Manila de Bugabus.

Fig. 10. Ellan Mantasa residency. P-1 Manila de Bugabus.

Fig. 11. Photos during interview and the patient's images during her admission in M.J.Santos Hospital

CLIENT'S AUTHORIZATION LETTER
File Attached To Hard Copy

File Attached To Hard Copy
CLIENT'S DISCHARGES SUMMARY

File Attached To Hard Copy

File Attached To Hard Copy
CLIENT'S LABORATORY TEST RESULTS

File Attached To Hard Copy

File Attached To Hard Copy
Reference

Book
Johnson, J.Y, 2008," Handbook for Brunner's and Suddarth's Medical- Surgical Nursing, 11th edition" p.739-742
Smeltzer, S., Bare, B., Hinkle, J., Cheever, K., 2008, "Brunner's and Suddarth's Textbook of Medical- Surgical Nursing, 11th" v2.p.1909, 1910.
Porth, C, M. and Kuhert, M.P. Pathophysiology: Concepts of Altered Health States, 6th edition, Philadelphia: Lippincott, Williams and Wilkins, 2003.
Pondang, R, M. and Pondang, J.A, P. Nursing Red Book, 2nd edition, 2012
PDF and Website
American College of Rheumatology www.rheumatology.org
Organization of Teratology Information Specialists - www.OTISpregnancy.org.
Medscape Author: Christie M Bartels, MD, MS; Chief Editor: Herbert S Diamond, MD –
http://www.lifelabs.com/Lifelabs_BC/Patients/MedicalConditions/Hematology http://emedicine.medscape.com/article/


Curriculum Vitae

Name: Mary Coleen L. Diango
Home Address: P-11 Mahaba, Florida, Butuan City
Birth Date: February 16, 1994
Birth Place: P-3 Florida, Butuan City
Parents: Mr. Mateo Diango
Mrs. Madeline Logroṅo
Siblings: Anthony Stephen L. Diango,
Lorraine Diane L. Diango,
Verlyn Jay L. Diango
Educational Background
Primary Education: Mariana L. Pineda Memorial Elementary School, Butuan City
Honor Received: 7th Honor
Secondary Education: Florida National High School, Butuan City
Honor Received: Salutatorian, Journalist of the Year
Tertiary Education: Caraga State University, Main Campus
Program: Bachelor of Science in Biology