SYSTEMIC LUPUS ERTHYMATOSUS

(SLE)

1
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

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 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.

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 TABLE OF CONTENTS

Client’s Profile 1

Hospitalization History 2

Literature of Illness 6

I. History 6
II. Anatomy and Physiology 6
III. Signs and Symptoms/ Clinical Manifestation 10
IV. Pathophysiology/Causes 11
V. Diagnostic Tests 13
VI. Management and Treatment 14
VII. Prognosis 16
VIII. Epidemiology 17
IX. Pictures 19

Drug Study 20

Discussion and Analysis 29

Conclusion 38

Summary 39

Appendices 40

I. Client’s Picture and Documentation Picture 40

II. Client’s Authorization Letter 42
III. Client’s Discharge Summary 43
IV. Client’s Laboratory Test Results 44

Reference 45

Student’s Curriculum Vitae 46

CLIENT’S PROFILE

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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

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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

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 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

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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

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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

I. HISTORY

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 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)

II. 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

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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

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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.

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 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)

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 III. 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

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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

IV. 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),

15
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)

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 V. 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.

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  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.

VI. 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

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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

19
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.

VII. 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

20
considered warranted especially for cancers affecting the immune system. SLE is

considered incurable, but highly treatable.

VIII. 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.

21
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 [Link] 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

22
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).

IX. PICTURES RELATED TO CLIENT’S ILLNESS

Fig. 3. - Malar rash Fig. 5. Acute diffuse cutaneous lupus

Fig. 4– Periungual erythema and nailfold Fig.6. Subacute cutaneous lupus

vasculitis

23
erythematosus Fig.7. Facial discoid lupus rash with a
malar distribution. Note the erythema
(indicating disease activity), keratin
plugged follicles, and dermal atrophy.

24
 Drug Study

NAME OF DRUG DOSAGE,FR MECHANSIM I N D I C AT I O C O N T R A I N D I C AT I ADVERSE NURSING

AND EQUENCY OFACTION N ON REACTION RESPONSIBILITIES
CLASSIFICATIO AND ROUTE
N

GENERIC NAME: - 10 Inhibits the Alone or with Hypersensitivity. CNS: Monitor blood
Amlodipine mg/t transport of other agents blood pressure less headache, pressure and pulse
BRAND NAME: ab calcium into in the than , 90 mmHg. dizziness, before therapy
Norvasc - OD myocardial and management Use cautiously in fatigue, during dose titration,
CLASSIFICATIO - Per vascular smooth of sever hepatic CV: and periodically
N: Orem muscle cells hypertension impairment history peripheral during
Therapeutic: resulting in the angina of aortic Stenosis edema, therapy. Monitor ECG
Anti- inhibition of pectoris and angina, during prolonged
hypertensive excitation vasospastic brachycardi therapy. Monitor
Pharmacologic: 'contraction angina a, intake and output
Calcium coupling and hypotensio ratios and daily)
channel subsequent n, eight. Assess for
blockers contraction. Therap palpitations signs of CHF
eutic effects: GI: gingival (peripheral edema,
systemic hyperplasia rales/crackles,
vasodilation , nausea dyspnea weight gain
resulting in the DERM: and jugular venous
decreased blood flushing distention
pressure. Coronary *Lab test
vasodilation considerations: Total
resulting in serum calcium is not
decreased affected by calcium
frequency and channel blockers.
severity attacks of
angina
SOURCE: Davi’s Drug Study Guide for Nurses (11th edition). [Link]
NAME OF DOSAGE MECHANSIM I N D I C AT I O N C O N T RA I N D ADVERSE REACTION/ SIDE NURSING
DRUG AND ,FREQUE OFACTION I C AT I O N EFFECT RESPONSIBILITIES
CLASSIFIC NCY
ATION AND
ROUTE
Ranitidine Route: Competitivel •Short-term Contraindicate •CNS: headache, malaise, assessment:
Hydrochlor Oral y inhibits the treatment of active d with allergy dizziness, somnolence, 1. History: allergy to
ide Dosage: action of duodenal ulcer to ranitidine, insomnia, vertigo ranitidine, impaired
Brand 50mg histamine at • Short-term lactation Use • CV: tachycardia, bradycardia renal or hepatic
Name: Timing: the H2 treatment cautiously with • Dermatologic: rash, function, lactation,
Zantac OD receptors of active, benign impaired renal alopecia pregnancy.
Classificatio of the gastric ulcer or hepatic • GI: constipation, diarrhea, 2. Physical: skin lesions,
n: Anti-ulcer parietal cells •Maintenance function, nausea and vomiting, orientation, affect liver
of the therapy for pregnancy abdominal pain, hepatitis evaluation, abdominal
stomach, duodenal ulcer at •Hematologic:leucopenia,gr examination, normal
Inhibiting basal reduced dosage. anulocytopenia,thrombocyto output, renal function
gastric acid • Short-term penia,pancytopenia tests, CBC
secretion and treatment for Interventions:
gastric acid GERD 1. Administer oral
secretion .•Pathologic drug with meals
that is hypersecretory and at bedtime
stimulated by conditions 2. Decrease doses in
food, insulin, • Treatment of renal and liver
histamine, erosive esophagitis failure.
cholinergic •Treatment [Link] concurrent
agonists, of heartburn, acid antacid therapy to
gastrin and indigestion, relieve
pentagastrin

Published by: Harvey Banag. [Link]

NAME OF DOSAGE,FR MECHANSIM I N D I C AT I O N C O N T RA I N ADVERSE REACTION NURSINGRESPONSIBILITIES
DRUG AND EQUENCY OFACTION D I C AT I O N
CLASSIFICATI AND ROUTE
ON
Dosage: Rapid-acting Treatment of History of CNS:He a da c he 1. Observe patients
Generic 40mg potent edema hypersensitiv GI:Nausea, receiving
Name: Route: Per sulfonamide associated with ety to Vomiting, oral and parenteral drug carefully;
Furosemide Orem "loop" CHF, furosemide or gastric burning, closely
Brand Name: Frequency: diuretic and cirrhosis of liver, sulphonamid anorexia, monitor BP and vital signs.
Lasiz Every antihypertensiv and es; increasing diarrhea, Sudden death from cardiac
8 hours e with kidney disease, oliguria, constipation, arrest
Classification pharmacologic including anuria, fluid abdominal has been reported.
: effects nephrotic and cramping, acute 2. Monitor BP during
and uses syndrome. May electrolyte pancreatitis, periods of
Electrolytic almost be depletion jaundice. diuresis and through
and water identical to used for states; CV:Postural period of
balance those of management of hepatic coma Hypotension, dosage adjustment.
agent; Loop ethacrynic hypertension, dizziness with 3. Observe older adults
diuretic acid. Exact alone Patients who excessive closely
mode of action or in combination are pregnant, diuresis, acute during period of brisk
not with lactating hypotensive diuresis.
clearly defined; other episodes, Report symptoms to
decreases antihypertensive circulatory physician.
renal agents, and for collapse. 4. Lab tests: Obtain
vascular treatment of frequent
resistance hypercalcemia. blood count, serum and
and may Has urine
increase been used electrolytes, CO2, BUN,
renal blood concomitantly blood
flow. with sugar, and uric acid values
mannitol for during
treatment of first few months of therapy
 severe and
cerebral edema, periodically thereafter.
particularly in 5. Monitor for signs and
meningitis. symptoms of hypokalemia

Published by Reisha Fungo. [Link]

NAME OF DRUG DOSAGE, MECHANSI I N D I C AT I O N C O N T RA I N ADVERSE NURSINGRESPONSIBILITIES

AND FREQUE M OFACTION D I C AT I O N REACTION
CLASSIFICATIO NCY AND
N ROUTE
Ciprofloxacin 500 mg Bactericidal Ciprofloxacin is used in Ciprofloxacin CNS: Question for history
Twice a : interferes the treatment of chronic is Headache, of hypersensitivity to
Classification: day with bacterial prostatitis. It is contraindicat dizziness, Ciprofloxacin or
Antibacterial: bacterial also used in the ed in persons ataxia, Quinolones
Fluoroquinolon DNA treatment of skin or skin with a history hallucination 2. May be given
e replication structure, GI tract, bone of hypersensi CV: without regards to meals.
insusceptibl or joint; lower tivity to arrhythmias, Preferred dosing time 2
e bacteria respiratory tract, and ciprofloxacin, angina hours after meals.
preventing urinary tract infections. any member EENT: dry 3. Do not administer
cell Ciprofloxacin is also of the eye, eye antacids within 2hours
production used in the treatment quinolone pain of Ciprofloxacin.
of chancroid. class GI: nausea, 4. Encourage
Ciprofloxacin is also of antimicrobi diarrhea, dry c r a n b e r r y juice or
used in the treatment al mouth, citrus fruits.
of infectious diarrhea, agents, or abdominal 5. Evaluate food
uncomplicated any of the pain tolerance.
gonorrhea, empiric product GU: renal 6. Determine pat tern
treatment of febrile components. failure of bowel activity.
neutropenia, and acute Other: fever, 7. Check for
sinusitis. It can also be rash, d i z z i n e s s , headache,
used for conjunctival hypersensiti visual difficulties, and
keratitis, vity tremors.
keratoconjunctivitis, 8. Observe therapeutic
corneal ulcers, response.
blepharitis,
dacrocystitis,
blepharoconjunctivitis
Published by Tony Daniel M. Gurbuxani. [Link]

NAME OF DOSAGE,F MECHANSIM I N D I C AT I O N C O N T RA I N D I C A ADVERSE REACTION NURSINGRESPONSIBILIT

DRUG AND REQUENCY OFACTION TION IES
CLASSIFICATI AND
ON ROUTE
Prednisone Dose: Interactions Supress Contraindications/ CNS: depression, Assess patient for
Classificatio 5 mg with other inflammation warnings/interactio euphoria, signs of adrenal
n: Route: patient drugs, and the ns CV: hypertension insufficiency
Systemic PO OTC or herbal normal Contraindicated in GI: anorexia, (hypotension, weight
corticosteroi Time/freq medicines immune respo pt’s w/ Active nausea, loss, weakness,
ds uency: QD (ask patient nse. Used untreated Derm: acne, nausea, vomiting,
specifically) systemically infections, decreased wound anorexia, lethargy,
Phenytoin and locally in a known alcohol, healing, confusion,
increases wide variety of bisulfite, or ecchymoses, restlessness) before
metabolism, chronic tartrazine fragility, and periodically
may diseases hypersensitivity hirsutism, petechia during therapy
decrease including: or intolerance, e, Endo: adrenal
effectiveness Inflammatory Administration suppression, MS:
Medication (COPD of live virus muscle wasting,
Anti- vaccines. osteoporosis,Misc:
inflammation Use cautiously in cushingoid
of airways pt’s w/Chronic appearance (moon
treatment (will lead face, buffalo hump)
to adrenal
suppression; use
lowest possible
dose for shortest
period of time)

Published by Cassie.. [Link]

NAME OF DRUG DOSAGE MECHANSIM I N D I C AT I O N C O N T RA I N D I C ADVERSE NURSINGRESPONSIBILITIES
AND ,FREQUE OFACTION AT I O N REACTION
CLASSIFICATION NCY AND
ROUTE
FOLIC ACID 4g Vitamin B Folate deficiency, Folic acid alone Reportedly Assessment & Drug
(VITAMIN B PO complex macrocytic for pernicious nontoxic. Effects
9 QD essential anemia, and anemia or other Slight •
, for nucleoprotei megaloblastic vitamin B flushing and Obtain a careful history of
PTEROYLGLUTAMI n synthesis and anemias 12 feeling of dietary intake and drug
C ACID)(fol'ic) maintenance associated with deficiency states; warmth and alcohol usage prior to
of normal malabsorption normocytic, following IV start of therapy. Drugs
Classifications erythropoiesis. syndromes, refractory, administrati reported to cause folate
Vitamin B Acts against alcoholism, prima aplastic, or on. deficiency include oral
9 folic acid ry liver disease, undiagnosed contraceptives, alcohol,
deficiency that inadequate anemia barbiturates,
impairs dietary intake, methotrexate, phenytoin,
thymidylate pregnancy, primidone, and
synthesis and infancy, and trimethoprim. Folate
results childhood deficiency may also result
in production of from renal dialysis.
defective DNA •
that leads to Keep physician informed
megaloblast of patient’s response to
formation and therapy.
arrest of bone •
marrow Monitor patients
maturation. on phenytoin
for subtherapeutic plasma
levels.

Published by:[Link]
NAME OF DOSAG MECHANSIM I N D I C AT C O N T RA I N D I C A ADVERSE NURSINGRESPONSIBILITIES
DRUG AND E,FREQ OFACTION ION TION REACTION
CLASSIFICATI UENCY
ON AND
ROUTE
Fe SO4 PO:300 Action: •Preventio Contraindicated in: GI: ASSESSMENT:
Classificatio mg2- • n and •Primary constipation, Assess nutritional status and dietary
n: 4timesd An essential treatment hemochromatosis dark stools, history to determine possible cause
Therapeutic: aily mineral found of iron diarrhea, of anemia and need for patient teaching.
Antianemics in hemoglobin, deficiency •hemolytic anemias epigastric pain, Assess for bowel function for
Pharmacologic myoglobin, and anemia and other anemias GI: bleeding constipation or diarrhea .Notify
: Iron many enzymes not due to iron physician or other health care
supplements • deficiency professional and use appropriate
Parenteral iron • nursing measures and should these
enters the some products occur.
blood stream contain alcohol, IMPLEMENTATION:
and organs tartrazine, or Oral preparations are most effectively
of the reticulo sulfites and should absorbed if administered 1 hour before
endothelial be avoided or 2 hours after meals. If gastric
system (liver, inpatients with irritation occurs, administer with
spleen, bone known intolerance or meals. Take tablets and capsules with
marrow),where hypersensitivity afull glass of water or juice. Do not
iron is • crush or chew enteric – coated tablets
separated out Concurrent oral iron and do not open capsules.
and becomes therapy HEALTH TEACHING:
part of iron Encourage patient tocomply with
stores. medicationregimen.
• Take missed doses as soonas
Prevention/treat remembered within 12hours; otherwise,
ment of iron return toregular dosing schedule. Donot
 deficiency as double doses.
its therapeutic
effect.

Published by Nelle Agni. [Link]

NAME OF DOSAG MECHANSIM I N D I C AT I O N C O N T RA I N D I C A ADVERSE NURSINGRESPONSIBILITIES

DRUG E,FREQ OFACTION TION REACTION
AND UENCY
CLASSIFIC AND
ATION ROUTE
NaHCO3 650 Increases Tr e a t m e n Hypoventilation, Hypernatr Obtain patient history including
(sodium mg plasma t o f metabo hypocalcemia, emia and drug history and
bicarbona TID bicarbonate, lic acidosis, incre a se se rum serum os any hypersensitivity.
te) Oral neutralizes promotion osmolarity, molarity, Assess respiratory and pulse rate,
Rout gastric acid o f gastric, further i n a l l s i t paravenous rhythm, depth, lung sounds and
Classificat e which forms systemic a uationsw h e r e administrati notify the physician.
ion: water, sodium n d urine s o d i u m intake ons may Assess for carbon dioxide in GI
Fluids, chloride, carbon alkalinization must berestri l e a d t tract, may lead to perforation if
Electrolyt dioxide, and in c t e d l i k e cardia o t i s s ulcer is severe.
e, Blood raises blood pH. t h e c a s e cinsufficiency,ede u e Test and monitor urine pH, urinary
Products, o f intoxicati mahypertension,ec necrosis. output, during beginning
And on lampsia,s e v e r e treatment.
Hematolo w i t h w k i d n e y insufficie If patient has oedematous
gical e a k ncy tendency, notify physician.
Drugs organic acids 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
Published by Sheena Kristine.[Link]
NAME OF DOSAGE,F MECHANSIM I N D I C ATI O CONTRAINDIC ADVERSE NURSINGRESPONSIBIL
DRUG AND REQUENC OFACTION N ATI O N REACTION ITIES
CLASSIFICA Y AND
TION ROUTE
CaCO3 Decreases total Antacid, Hypocalcaemia, bone Constipation, > administer as antacid1
Calcium DOSAGE: acid load of GI calcium tremors, severe renal flatulence, diarrhea, hr after meal and at bed
carbonate 350mg tract. Increase supplement, failure, hypersensitivity renal dysfunction, acid time>administer as
Adult:1- esophageal osteoporosis rebound supplement 1½ hrs after
2capsules Sphincter tone meal and at
daily bedtime>advice pt to
increase fluids to 2L unless
contraindicated
[Link]
 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, 11 th 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 Remarks

(NCCLS)
Albumin 2.8 g/dL 3.8-5.0 Lower
Coagulation: 21. 10 sec 10- 13.50 ~14 Slower

Prothrombin time
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 Main Problem Manifestations Medical Nursing
Factors Management Intervention

G-genetic Dysfunctional SKINS- butterfly STEROIDS- P-psychological

A-autoimmune immune rash Suppress support
V-viral factor system JOINTS- Arthritis inflammation A- administer
E-exposure and produces KIDNEY- and immune medications
intake of antibodies protenuria and reaction L- lifetime
medications against the hematuria PLASMA monitoring and
body cells HEART- EXCHANGE lifestyle changes
The antibodies pericarditis THERAPY- M- monitor for
attack multiple BRAIN- psychosis, remove the seizure
organs: seizures and circulating development
SKIN, depression antibodies
JOINTS,
KIDNEY,
HEART,
BRAIN

APPENDICES

I. 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
[Link] Hospital

II. CLIENT’S AUTHORIZATION LETTER

File Attached
To Hard Copy
III. CLIENT’S DISCHARGES SUMMARY

File Attached
To Hard Copy
IV. CLIENT’S LABORATORY TEST RESULTS

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, 6 th 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 [Link]

Organization of Teratology Information Specialists - [Link].

Medscape Author: Christie M Bartels, MD, MS; Chief Editor: Herbert S Diamond, MD –

[Link]

[Link]
 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