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
2
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.
3
TABLE OF CONTENTS
Client’s Profile
1
Hospitalization History
2
Literature of Illness
6
I.
II.
III.
IV.
V.
VI.
VII.
VIII.
IX.
6
6
10
11
13
14
16
17
19
History
Anatomy and Physiology
Signs and Symptoms/ Clinical Manifestation
Pathophysiology/Causes
Diagnostic Tests
Management and Treatment
Prognosis
Epidemiology
Pictures
Drug Study
20
Discussion and Analysis
29
Conclusion
38
Summary
39
Appendices
40
I.
II.
III.
IV.
Client’s Picture and Documentation Picture
Client’s Authorization Letter
Client’s Discharge Summary
Client’s Laboratory Test Results
40
42
43
44
Reference
45
Student’s Curriculum Vitae
46
CLIENT’S PROFILE
4
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
5
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
6

Final Diagnosis:
Nausea
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
7
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
8
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
9
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
10
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
11
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 endstage 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.
12
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)
13
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
14
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)
16
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), antiSmith (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.
17

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
18
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 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
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.
vasculitis
23
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.
24
Drug Study
NAME OF DRUG
AND
CLASSIFICATIO
N
GENERIC NAME:
Amlodipine
BRAND NAME:
Norvasc
CLASSIFICATIO
N:
Therapeutic:
Antihypertensive
Pharmacologic:
Calcium
channel
blockers
DOSAGE,FR
EQUENCY
AND ROUTE
-
10
mg/t
ab
OD
Per
Orem
MECHANSIM
OFACTION
I N D I C AT I O
N
C O N T R A I N D I C AT I
ON
Inhibits the
Alone or with Hypersensitivity.
transport of
other agents blood pressure less
calcium into
in the
than , 90 mmHg.
myocardial and
management Use cautiously in
vascular smooth
of
sever hepatic
muscle cells
hypertension impairment history
resulting in the
angina
of aortic Stenosis
inhibition of
pectoris and
excitation
vasospastic
'contraction
angina
coupling and
subsequent
contraction. Therap
eutic effects:
systemic
vasodilation
resulting in the
decreased blood
pressure. Coronary
vasodilation
resulting in
decreased
frequency and
severity attacks of
angina
SOURCE: Davi’s Drug Study Guide for Nurses (11th edition). http://www.scribd.com
ADVERSE
REACTION
NURSING
RESPONSIBILITIES
CNS:
headache,
dizziness,
fatigue,
CV:
peripheral
edema,
angina,
brachycardi
a,
hypotensio
n,
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.
NAME OF
DRUG AND
CLASSIFIC
ATION
Ranitidine
Hydrochlor
ide
Brand
Name:
Zantac
Classificatio
n: Anti-ulcer
DOSAGE
,FREQUE
NCY
AND
ROUTE
Route:
Oral
Dosage:
50mg
Timing:
OD
MECHANSIM
OFACTION
I N D I C AT I O N
C O N T RA I N D
I C AT I O N
ADVERSE REACTION/ SIDE
EFFECT
NURSING
RESPONSIBILITIES
Competitivel
y 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,
Contraindicate
d 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,gr
anulocytopenia,thrombocyto
penia,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:
1. Administer oral
drug with meals
and at bedtime
2. Decrease doses in
renal and liver
failure.
3.Provide concurrent
antacid therapy to
relieve
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NAME OF
DRUG AND
CLASSIFICATI
ON
Generic
Name:
Furosemide
Brand Name:
Lasiz
Classification
:
Electrolytic
and water
balance
agent; Loop
diuretic
DOSAGE,FR
EQUENCY
AND ROUTE
MECHANSIM
OFACTION
I N D I C AT I O N
C O N T RA I N
D I C AT I O N
ADVERSE REACTION
NURSINGRESPONSIBILITIES
Dosage:
40mg
Route: Per
Orem
Frequency:
Every
8 hours
Rapid-acting
potent
sulfonamide
"loop"
diuretic and
antihypertensiv
e 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
History of
hypersensitiv
ety to
furosemide or
sulphonamid
es; increasing
oliguria,
anuria, fluid
and
electrolyte
depletion
states;
hepatic coma
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
Patients who
are pregnant,
lactating
severe
cerebral edema,
particularly in
meningitis.
and
periodically thereafter.
5. Monitor for signs and
symptoms of hypokalemia
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NAME OF DRUG
AND
CLASSIFICATIO
N
DOSAGE,
FREQUE
NCY AND
ROUTE
MECHANSI
M OFACTION
I N D I C AT I O N
C O N T RA I N
D I C AT I O N
ADVERSE
REACTION
NURSINGRESPONSIBILITIES
Ciprofloxacin
Ciprofloxacin is used in
the treatment of chronic
Classification:
bacterial prostatitis. It is
Antibacterial:
also used in the
Fluoroquinolon
treatment of skin or skin
e
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
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NAME OF
500 mg
Twice a
day
Bactericidal
: interferes
with
bacterial
DNA
replication
insusceptibl
e bacteria
preventing
cell
production
DOSAGE,F
MECHANSIM
I N D I C AT I O N
Ciprofloxacin
is
contraindicat
ed in persons
with a history
of hypersensi
tivity to
ciprofloxacin,
any member
of the
quinolone
class
of antimicrobi
al
agents, or
any of the
product
components.
C O N T RA I N D I C A
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,
hypersensiti
vity
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
c r a n b e r r y juice or
citrus fruits.
5. Evaluate food
tolerance.
6. Determine pat tern
of bowel activity.
7. Check for
d i z z i n e s s , headache,
visual difficulties, and
tremors.
8. Observe therapeutic
response.
ADVERSE REACTION
NURSINGRESPONSIBILIT
DRUG AND
CLASSIFICATI
ON
Prednisone
Classificatio
n:
Systemic
corticosteroi
ds
REQUENCY
AND
ROUTE
Dose:
5 mg
Route:
PO
Time/freq
uency: QD
OFACTION
Interactions
with other
patient drugs,
OTC or herbal
medicines
(ask patient
specifically)
Phenytoin
increases
metabolism,
may
decrease
effectiveness
Medication
Antiinflammation
of airways
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TION
Supress
inflammation
and the
normal
immune respo
nse. Used
systemically
and locally in a
wide variety of
chronic
diseases
including:
Inflammatory
(COPD
Contraindications/
warnings/interactio
ns
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)
IES
CNS: depression,
euphoria,
CV: hypertension
GI: anorexia,
nausea,
Derm: acne,
decreased wound
healing,
ecchymoses,
fragility,
hirsutism, petechia
e, 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
NAME OF DRUG
AND
CLASSIFICATION
FOLIC ACID
(VITAMIN B
9
,
PTEROYLGLUTAMI
C ACID)(fol'ic)
Classifications
Vitamin B
9
DOSAGE
,FREQUE
NCY AND
ROUTE
4g
PO
QD
MECHANSIM
OFACTION
I N D I C AT I O N
C O N T RA I N D I C
AT I O N
ADVERSE
REACTION
NURSINGRESPONSIBILITIES
Vitamin B
complex
essential
for nucleoprotei
n 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, prima
ry 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
administrati
on.
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
CLASSIFICATI
ON
Fe SO4
Classificatio
n:
Therapeutic:
Antianemics
Pharmacologic
: Iron
supplements
DOSAG
E,FREQ
UENCY
AND
ROUTE
PO:300
mg24timesd
aily
MECHANSIM
OFACTION
I N D I C AT
ION
C O N T RA I N D I C A
TION
ADVERSE
REACTION
NURSINGRESPONSIBILITIES
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/treat
ment of iron
•Preventio
n and
treatment
of iron
deficiency
anemia
Contraindicated in:
•Primary
hemochromatosis
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
•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
deficiency as
its therapeutic
effect.
double doses.
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NAME OF
DRUG
AND
CLASSIFIC
ATION
DOSAG
E,FREQ
UENCY
AND
ROUTE
MECHANSIM
OFACTION
I N D I C AT I O N
C O N T RA I N D I C A
TION
ADVERSE
REACTION
NURSINGRESPONSIBILITIES
NaHCO3
(sodium
bicarbona
te)
Classificat
ion:
Fluids,
Electrolyt
e, Blood
Products,
And
Hematolo
gical
Drugs
650
mg
TID
Oral
Rout
e
Increases
plasma
bicarbonate,
neutralizes
gastric acid
which forms
water, sodium
chloride, carbon
dioxide, and
raises blood pH.
Tr e a t m e n
t o f metabo
lic acidosis,
promotion
o f gastric,
systemic a
n d urine
alkalinization
in
t h e c a s e
o f intoxicati
on
w i t h
w
e a k
organic acids
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Hypoventilation,
hypocalcemia,
incre a se se rum
osmolarity,
further i n a l l s i t
uationsw h e r e
s o d i u m intake
must berestri
c t e d l i k e cardia
cinsufficiency,ede
mahypertension,ec
lampsia,s e v e r e
k i d n e y insufficie
ncy
Hypernatr
emia and
serum os
molarity,
paravenous
administrati
ons may
l e a d
t
o
t i s s
u e
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
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
CaCO3
ROUTE
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
daily
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
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
M 0.40-0.52 F 0.36-0.48
DIFFERENT COUNT
NEUTROPHILS
0.60
0.50 -0.70
LYMPHOCYTES
0.16
0.20- 0.40
MONOCYTES
EOSINOPHILS
0.06
0.02-0.06
0.18
BASOPHILS
0.00
ESR
150
0.02-0.05
0.005-0.01
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
Creatinine
Reference
April 30, 2013
21.10
0.6-2.0 mg/dl
May 6, 2013
22.15
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
Albumin
Coagulation:
2.8 g/dL
21. 10 sec
(NCCLS)
3.8-5.0
10- 13.50 ~14
Lower
Slower
Prothrombin time
Potassium
Hemoglobin
Hematocrit
WBC
Lymphocyte
Band
Eosinophil
Monocyte
Platelet count
7.8 p nmol/L
67 L
0.20 L
22.55 H
0.04 L
0.00 L
0.00
0.03 L
122 L
3.5-5.3
117-140
0.34-0.44
5.0-15.0
0.20-0.50
0.02-0.05
0.00-0.01
0.08-0.14
150-390
Higher
Lower
Lower
Higher
Lower
Lower
Baseline
Lower
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 SLELupus 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
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
Nursing
Intervention
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
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 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