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The Immune System functions as the bodys defense mechanism against invasion. But
when a bodys immune system attacks itself, it is probably having an autoimmune disease. The
individuals immune system attacks the healthy cells in the body by mistake instead of protecting
it from illness and infection. Systemic Lupus Erythematosus (SLE) is a chronic inflammatory
disease characterized by highly diverse clinical manifestations and the presence in the serum of
antibodies reacting with different cell nuclei components. The clinical course of the disease is
characterized by flares, periods of chronic disease, and periods of remissions (Pediatric
Nephrology Lippincott Williams and Wilkins, 2004).
Lupus Nephritis is a kidney inflammation and one of the most serious complications that
can result from SLE. Evidence suggests that 35% of adults in the United States show signs of
nephritis at the time of a lupus diagnosis and approximately 40% to 60% of people will develop
kidney involvement during the course of the disease. If not diagnosed and treated early enough,
lupus nephritis can lead to significant illness and sadly, even death.
According to the United States statistics as of April 2014, estimates of the prevalence of
clinical renal involvement in persons with SLE ranges from 30% to 90% in published studies.
The true prevalence of clinical lupus nephritis in persons with SLE is probably around 50%,
being higher in certain ethnic groups and in children. SLE is more common among women in the
third decade of their life and SLE Nephritis typically occurs in patients aged 20 to 40 years.
Children with SLE are at higher risk of renal disease than adults and tend to sustain more disease
damage secondary to more aggressive disease and treatment associated toxicity.
In the Philippines, it is estimated that 80% to 92% of the lupus population is female. The
prevalence trends also seem to exhibit variability based on geographic location. China and
Philippines show a greater incidence than Japan. The treatment for SLE Nephritis is almost the
same as from any other countries.
There were many organizations and foundations created for lupus patients. Locally, the
Lupus Foundation of Southern Mindanao, Inc. (LFSMI) was created starting with 41 members,
one of whom is Dr. Llewellyn Hao-Tanapo, an Internist and Rheumatologist, of Davao Doctors
Hospital. On September 21, 2000, the LFSMI was registered with Securities and Exchange
Commission (SEC), and the membership increased to 140 lupus patients.
SLE Nephritis is an interesting and quite complicated disease. The proponent conducted
this study to know and find out the probable cause of the clients occurrence of the said disease.
Knowing the fact that it is an autoimmune disease, the proponents never hesitated on choosing
this case with hopes that it would save and maintain the life integrity of the client and to other
Filipinos as well. Moreover, the importance of this study is recognized since it helps build the
proponents competence and skill in dealing such condition.
The proponent chose this case with high hopes that it would address the need of
information dissemination to the Filipinos on every corner of the country. We cannot deny the
fact that the country where majority of the population are living under the poverty line. With the
financial constraints, it has proved to be hard for the people to have access to education even to
the very basic health care facilities. With information and health teachings that will be given, it
would probably help every individual on how to deal with patients having this kind of disease.
Overall, by understanding SLE Nephritis, how it acts, what we can do to manage it, and
how to implement those actions, we can influence our patients future health tremendously, while
potentially improving their current life.
OBJECTIVES
General Objective:
Within 4 days of the patients stay at Pediatric Specialty Wing (PSW) Unit at Southern
Philippines Medical Center (SPMC) in Davao City, the proponent should be able to present a
comprehensive study on SLE Nephritis and understand the problem in order to develop adequate
knowledge and skills related to nursing procedures that will aid in the competency and
proficiency of the Nurses enrolled in the Degree of Master of Arts in Nursing at University of the
Visayas, Cebu City.
Specific Objectives:
The proponent also created certain aims that will help them in achieving their general
objectives. Within the 4 days of the patients stay at PSW Unit at SPMC in Davao City, the
proponent shall be able to:
I. Cognitive:
1. Identify the patients genogram;
2. Interpret the present developmental stage of the patient;
3. Comprehensively discuss the anatomy of the body systems involved;
4. Define the complete diagnosis that would explain the condition of our patient;
5. Determine the causative factors present to learn how the patient developed the illness;
6. Identify the signs and symptoms associated with the disease to grasp its cause;
7. Explain and trace the pathophysiology of Systemic Lupus Erythematosus;
8. Interpret the doctors orders by justifying the rationale;
9. Interpret laboratory findings;
10. Name and identify the proper dose, action, route, frequency, and nursing responsibilities
of each medication given to the patient;
11. Identify actual and potential nursing diagnosis;
12. Plan appropriate nursing interventions with patients condition to be able to provide
appropriate interventions and to render proper care; and
13. Evaluate the progress of clients condition and outcomes of care.
II. Psychomotor:
1. Display competence in performing the different procedures with the patient;
2. Gather pertinent data about the patient through detailed chart taking and interview;
3. Record the past and present health history of the patient;
4. Perform a comprehensive physical assessment on patient;
5. Render health teachings to the patient and her significant others to promote health; and
6. Implement plan of care with patient and significant others.
III. Affective:
1. Establish rapport with the patient and significant others;
2. Actively listen to the patient and significant others;
3. Attend to the needs and concerns of the patient genuinely;
4. Develop a caring, non-judgmental, and therapeutic attitude towards the patient and
significant others; and
5. Promote personal and professional growth of self and others.
PATIENT FROFILE
Name:
Jomueld
Age/Sex:
Address:
Birth Date:
Religion:
Iglesia Ni Cristo
Educational Attainment:
Kinder 1
Name of Father:
Bonifacio Jr.
Occupation:
Tricycle Driver
Educational Attainment:
Grade 6
Name of Mother:
Mary Ann
Occupation:
Housewife
Educational Attainment:
Date of Admission:
Admitting Diagnosis:
Department:
Pediatrics
immediately went to the clinic to seek for consultation and was prescribed with a medication that
she failed to remember the name.
Last February, he had an onset of relapsing fever for a week and as high as 40 degrees
Celsius. They consulted to Dr. Paredes, a Pediatrician, and were advised to submit their son for
CBC pc laboratory and the result showed an ongoing blood infection. They were prescribed with
Co-Amoxiclav suspension, an antibiotic, and Paracetamol syrup, an anti-pyretic, for fever and were
sent home. With no relief after one week, they consulted back to Dr. Paredes and the antibiotic was
shifted to Erythromycin suspension. Still with no relief after one week, they consulted another
physician in which they were asked to submit Jomueld for CBC pc and Urinalysis which revealed
with blood infection and Urinary Tract Infection (UTI). He was prescribed with Co-Amoxiclav
suspension and Paracetamol syrup and was asked to come back after two weeks of medication.
On the day of the follow-up check-up, Jomueld submitted urine specimen for repeat
Urinalysis and revealed no UTI and was asked to continue the antibiotic for another three days. Still
with no relief with his fever, his family finally went to Provincial Hospital in Mati City for further
evaluation under Dr. Jacob service and was asked to submit for an executive check-up. The CBC pc
result revealed still with blood infection, X-ray result was normal, Thyphidot was negative, and
Urinalysis revealed normal.
Last March, they were then referred to Southern Philippines Medical Center in Davao City
for further evaluation and management. On the way to the hospital, he experienced a 5-minute
seizure and as described by the mother, he suddenly went stiff and went unconscious.
In the Emergency Room of the SPMC, they were then admitted under the service of General
Pediatrics where they stayed for 32 days in the Pediatric General Wing (PGW) Unit with the
diagnosis of Benign Febrile Convulsion. Series of laboratory tests were done, serum Pro-calcitonin
test revealed high at 6.42, Typhidot was negative, WBC revealed high at 23.94 x10^3/ul,
Reticulocyte came low at 1.0, LDH as high as 1,515 u/L and serum Creatinine and Electrolytes were
normal.
The Pediatric Resident Physicians had hard time figuring out what the diagnosis of the
patient is. During his stay in the PGW Unit, his health was getting deteriorated according to his
mother wherein, he is too weak to walk, frequent sleepiness, paleness, cracked lips, mosquito bitelike rashes, and bleeding episodes such as hemoptysis and melena. His repeat CBC pc result
revealed that Hemoglobin was as low as 67 g/L and, thus, was given two units of packed RBC
blood transfusion. After two units of blood transfusion, the repeat Hemoglobin count was increased
to 97 g/L. Aside from his hematologic problem, the patient had also experienced joint pains,
difficulty of walking, relapsing moderate-grade fever and loss of appetite.
Midst April, Jomueld was then referred to the Hematology Service for evaluation and comanagement wherein his antibiotic was changed to Meropenem IV and ordered Diazepam for active
seizure. He was also requested to undergo ANA and Anti-dsDNA blood serology test which resulted
to negative ANA and positive Anti-dsDNA. With that result, he was then referred to Nephrology
Service and was transferred to Pediatric Specialty Wing (PSW) Unit for Methylprednisolone Pulse
Therapy. With these controlled previous signs and symptoms after pulse therapy such as decreased
joint swelling, resolved fever and increased in appetite and energy level, his diagnosis was changed
to SLE Nephritis.
After a month of stay in the PSW Unit, he was discharged in the institution with the
following home medications: Prednisone 20 mg/tablet two tablets to be taken once in every other
day, Azathioprine 50 mg/tablet one-half tablet once a day, Isoniazid 200mg/5ml syrup, to give five
milliliters once a day and lastly, Calcium Carbonate 500mg/tablet one tablet once a day.
End of July, Jomueld had an onset relapsing moderate-grade fever, in which her mother gave
him Paracetamol syrup with some relief. However, few days after his relapsing moderate-grade
fever he had an onset of five-minute grand-mal seizure and as described by the mother, had an
upward rolling of the eyes, stiffening of upper and lower extremities and increased in salivation.
Hence, this prompted admission to SPMC and with the initial impression of the Resident on duty
revealed Benign Febrile Convulsion, SLE Nephritis.
In the Emergency Room, Jomueld had an episode of epistaxis, seven times vomiting, and
high-grade fever. Vital Signs were taken and as followed: Blood Pressure 80/50mmHg, Pulse Rate
108bpm, Respiratory Rate 38cpm, and Temperature of 39 degrees Celsius. Initial laboratory results
revealed with normal Hemoglobin and WBC count and slightly low serum Calcium and
Magnesium. He was then given Paracetamol IVTT for fever, Odansetron IVTT for vomiting and
Tranexamic Acid IVTT for epistaxis. He was admitted back to the PSW Unit under the Nephrology
service and advised for pulse therapy with Methylprednisolone for three cycles and
Cyclophosphamide for one cycle. He was also prescribed with Cal-Mg tablet for correction of his
decreased serum Calcium and Magnesium. Repeat serum electrolytes and CBC pc were ordered and
both revealed with normal values.
After five days of stay in the PSW Unit, he was then discharged in the institution with the
following same home medications: Prednisone 20 mg/tablet two tablets to be taken once in every
other day, Azathioprine 50 mg/tablet one-half tablet once a day, Isoniazid 200mg/5ml syrup, to give
five milliliters once a day and lastly, Calcium Carbonate 500mg/tablet one tablet once a day.
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GENOGRAM
EDMUNDO Sr., 67
ERLINDA, 56
MARY ANN, 36
GABBY, 38
ALLAN, 37
GINO, 45
ALBERT, 24
JOMARYL, 6
JIMUELD, 5
JOMUELD, 5
LEGEND:
Hypertension
Bronchial Asthma
Bronchopneumonia
Deceased
Leukemia
BONIFACIO Jr., 43
JOVANI, 47
JOVENSON, 34
EDMUNDO Jr., 35
RENATA, 60
BONIFACIO Sr., 61
Pulmonary Tuberculosis
Vehicular Accident
Tetanus
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DEVELOPMENTAL DATA
Erik Erikson envisions life as a sequence of levels of achievement. Each stage signals a task
that must be achieved. The resolution can be complete, partial, or unsuccessful. He believes that the
greater achievement, the healthier the personality of the person. The developmental task can be
viewed as a series of crises and successful resolution of these crises is supportive to the persons
ego. Failure to achieve a task influences the persons ability to achieve the next task. He also
emphasizes that people must change and adapt their behavior to maintain control over their lives. In
this view, no stage in personality development can be bypassed, but people can become fixated at
one stage or regress to previous stage.
Jomueld, a five-year old patient, is considered to be in the late childhood according to
Eriksons Psychosocial Developmental Stages. This stage occurs during the preschool years,
between the ages of three and five. The central task in this stage is initiative versus guilt where
learning the degree of assertiveness and purpose influence the environment. The ability to evaluate
ones own behavior takes place. On the contrary, the indicators of negative resolution in this stage is
lack of confidence, pessimism, fear of wrong doing, over control and over restriction of own
activity takes place.
The patient exercised his initiative where he began to assert power and control over the
surroundings through directing play and other social interaction. As observed by the mother, the
child was able to interact regularly with his friends and classmates in school. He played happily
with other children and enjoyed lots of physical games as well as stories. He was full of confidence
in doing and exploring things especially in their activities. He can go to the toilet on his own, use
toilet paper properly and flush the toilet. He can also dress himself providing the fastenings are not
too difficult and able to feed himself with minimal supervision. Even at home, he loved to interact
with his siblings. Jumping, running and playing simple computer games were among of his
activities. Jomueld frequently asked many questions as his thirst for knowledge grows about the
world and why things happen and how that thing happens.
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At his age, Jomueld was able to identify his emotions. If he finds something funny, he
laughs. If something makes him feel sad or angry, he cries. When he does things that is not accepted
such as pushing or shouting and is reprimanded by his mother, he has the initiative to apologize. He
showed understanding of right and wrong.
The patient was able to achieve the task that Erikson identified in this stage which is
intimacy vs. guilt.
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PHYSICAL ASSESSMENT
General Appearance:
Affect and facial expression appropriate to situation. Speech is clear and comprehensible. He
is wearing a shirt and shorts, hair well combed and appears tidy. Vital Signs were taken prior the
examination and were as followed: Blood Pressure 90/60 mmHg, Cardiac Rate 107 bpm,
Respiratory Rate 24 cpm and Axillary Temperature 36.7 degrees Celsius.
Skin:
The color of the childs skin is evenly distributed and is warm to touch, soft, smooth over the
entire body with brown complexion. Skin with good turgor rapidly returns to its previous contour.
Head:
Hair is distributed evenly over the scalp, soft in texture, black in color and well combed and
no presence of dandruffs or lice noted. Fontanels are already closed. The head circumference is 50
centimeters and facial expression is symmetrical. Minimal abrasion noted at the left cheek.
Eyes:
No changes and problem in vision and he does not wear glasses. Sclera is white and clear,
conjunctiva color is pink and pupils are round, clear, and equal in size, equally brisk and reactive to
light at two millimeters in size. No abnormal pigmentations, hemorrhages or exudates noted. The
child has fine extraocular movement and able to follow objects without any difficulty.
Ears:
Both ears are clean and no discharges noted upon inspection. No changes in hearing, and
does not wear hearing aids.
Nose:
Pink in color and no discharges noted upon the time of examination, the septum is at
midline. No nasal flaring noted.
Mouth and Throat:
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Teeth are present and in good dentition, however there are some cavities noted upon
inspection, the tongue is in midline, pink in color, moist and there are no lesions. Gums and
mucosal membrane have no swelling, bleeding, or inflammation noted. Tonsils are normal and
noted to be at grade 2+. Positive gag reflex with no difficulty of swallowing noted.
Neck:
Active range of motion, normal flexion and extension, lateral rotation and tilting noted
without any difficulty. Trachea is midline and mobile. No lesions or masses noted upon palpation.
Chest:
The respiratory rate is 24 cycles per minute, regular in rhythm, unlabored and without the
use of accessory muscles noted. Chest expansion is equal with normal and clear breath sounds on
all areas upon auscultation. No lesions and any abnormalities noted.
Abdomen:
Abdomen is flat and soft, not distended, with bowel sounds of 3 times per minute. No
tenderness or masses noted upon palpation. No lesions observed.
Genital:
The patient is still not circumcised, no hypospadias or phimosis noted. No difficulty of
urination noted.
Upper and Lower Extremities:
Upper: Nails are pinkish in color, no signs of cyanosis or clubbing noted. Palms are pinkish
in color, with smooth texture. Range of motion is normal, has strong hand grip on both hands and
can both flex and extend without any difficulties, no pain on joints upon movements. No
deformities noted any difficulties in locomotion. Radial pulse is strong and not easily obliterated.
Lower: Toenails are pinkish in color. Range of Motion on both feet is normal and can flex
and extend without any deformities and no pain on joint movements. Minimal abrasions noted on
both feet but no discharges noted. No problem with walking and locomotion. Normal gait noted.
ANATOMY AND PHYSIOLOGY
15
immune
systems
and
are
two
functions.
The
as
well
as
parasitic
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MONOCYTES
Monocytes are agranular leukocytes that can form two types of cells:
1.
Macrophages
Monocytes respond slowly to infection and once present at the site of infection, develop into
macrophages. Macrophages are phagocytes able to consume pathogens, destroyed cells, and debris
by phagocytosis. As such, they have a role in both preventing infection as well as cleaning up the
aftermath of an infection.
2.
Dendritic cells
Monocytes also develop into dendritic cells in healthy tissues of the skin and mucous
membranes. Dendritic cells are responsible for the detection of pathogenic antigens which are used
to activate T cells and B cells.
GRANULAR LEUKOCYTES
1. Eosinophils
Eosinophils are granular leukocytes that reduce allergic inflammation and help the body
fight off parasites.
2. Basophils
Basophils are granular leukocytes that trigger inflammation by releasing the chemicals
heparin and histamine. Basophils are active in producing inflammation during allergic reactions and
parasitic infections.
3. Neutrophils
Neutrophils are granular leukocytes that act as the first responders to the site of an infection.
Neutrophils use chemotaxis to detect chemicals produced by infectious agents and quickly move to
the site of infection. Once there, neutrophils ingest the pathogens via phagocytosis and release
chemicals to trap and kill the pathogens.
Lymphoid stem cells produce T lymphocytes and B lymphocytes.
1. T LYMPHOCYTES
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T lymphocytes, also commonly known as T cells, are cells involved in fighting specific
pathogens in the body. T cells may act as helpers of other immune cells or attack pathogens directly.
After an infection, memory T cells persist in the body to provide a faster reaction to subsequent
infection by pathogens expressing the same antigen.
2. B LYMPHOCYTES
B lymphocytes, also commonly known as B cells, are also cells involved in fighting specific
pathogens in the body. Once B cells have been activated by contact with a pathogen, they form
plasma cells that produce antibodies. Antibodies then neutralize the pathogens until other immune
cells can destroy them. After an infection, memory B cells persist in the body to quickly produce
antibodies to subsequent infection by pathogens expressing the same antigen.
NATURAL KILLER CELLS
Natural killer cells, also known as NK cells, are lymphocytes that are able to respond to a
wide range of pathogens and cancerous cells. NK cells travel within the blood and are found in the
lymph nodes, spleen, and red bone marrow where they fight most types of infection.
LYMPH CAPILLARIES
As blood passes through the tissues of the body, it enters thin-walled capillaries to facilitate
diffusion of nutrients, gases, and wastes. Blood plasma also diffuses through the thin capillary walls
and penetrates into the spaces between the cells of the tissues. Some of this plasma diffuses back
into the blood of the capillaries, but a considerable portion becomes embedded in the tissues as
interstitial fluid. To prevent the accumulation of excess fluids, small dead-end vessels called
lymphatic capillaries extend into the tissues to absorb fluids and return them to circulation.
LYMPH
The interstitial fluid picked up by lymphatic capillaries is known as lymph. Lymph very
closely resembles the plasma found in the veins: it is a mixture of about 90% water and 10% solutes
such as proteins, cellular waste products, dissolved gases, and hormones. Lymph may also contain
bacterial cells that are picked up from diseased tissues and the white blood cells that fight these
pathogens. In late-stage cancer patients, lymph often contains cancerous cells that have
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metastasized from tumors and may form new tumors within the lymphatic system. A special type of
lymph, known as chyle, is produced in the digestive system as lymph absorbs triglycerides from the
intestinal villi. Due to the presence of triglycerides, chyle has a milky white coloration to it.
LYMPHATIC VESSELS
Lymphatic capillaries merge together into larger lymphatic vessels to carry lymph through
the body. The structure of lymphatic vessels closely resembles that of veins: they both have thin
walls and many check valves due to their shared function of carrying fluids under low pressure.
Lymph is transported through lymphatic vessels by the skeletal muscle pumpcontractions of
skeletal muscles constrict the vessels to push the fluid forward. Check valves prevent the fluid from
flowing back toward the lymphatic capillaries.
LYMPH NODES
Lymph nodes are small, kidney-shaped organs of the lymphatic system. There are several
hundred lymph nodes found mostly throughout the thorax and abdomen of the body with the highest
concentrations in the axillary (armpit) and inguinal (groin) regions. The outside of each lymph node
is made of a dense fibrous connective tissue capsule. Inside the capsule, the lymph node is filled
with reticular tissue containing many lymphocytes and macrophages. The lymph nodes function as
filters of lymph that enters from several afferent lymph vessels. The reticular fibers of the lymph
node act as a net to catch any debris or cells that are present in the lymph. Macrophages and
lymphocytes attack and kill any microbes caught in the reticular fibers. Efferent lymph vessels then
carry the filtered lymph out of the lymph node and towards the lymphatic ducts.
LYMPHATIC DUCTS
All of the lymphatic vessels of the body carry lymph toward the two lymphatic ducts: the
thoracic duct and the right lymphatic ducts. These ducts serve to return lymph back to the venous
blood supply so that it can be circulated as plasma.
1. Thoracic Duct
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The thoracic duct connects the lymphatic vessels of the legs, abdomen, left arm, and the left
side of the head, neck, and thorax to the left brachiocephalic vein.
2. Right Lymphatic Duct
The right lymphatic duct connects the lymphatic vessels of the right arm and the right side
of the head, neck, and thorax to the right brachiocephalic vein.
LYMPHATIC NODULES
Outside of the system of lymphatic vessels and lymph nodes, there are masses of nonencapsulated lymphatic tissue known as lymphatic nodules. The lymphatic nodules are associated
with the mucous membranes of the body, where they work to protect the body from pathogens
entering the body through open body cavities.
TONSILS
There are five tonsils in the body: two lingual, two palatine, and one pharyngeal. The lingual
tonsils are located at the posterior root of the tongue near the pharynx. The palatine tonsils are in the
posterior region of the mouth near the pharynx. The pharyngeal pharynx, also known as
the adenoid, is found in the nasopharynx at the posterior end of the nasal cavity. The tonsils contain
many T and B cells to protect the body from inhaled or ingested substances. The tonsils often
become inflamed in response to an infection.
PEYERS PATCHES
Peyers patches are small masses of lymphatic tissue found in the ileum of the small
intestine. Peyers patches contain T and B cells that monitor the contents of the intestinal lumen for
pathogens. Once the antigens of a pathogen are detected, the T and B cells spread and prepare the
body to fight a possible infection.
SPLEEN
The spleen is a flattened, oval-shaped organ located in the upper left quadrant of the
abdomen lateral to the stomach. The spleen is made up of a dense fibrous connective tissue capsule
filled with regions known as red and white pulp. Red pulp, which makes up most of the spleens
20
mass, is so named because it contains many sinuses that filter the blood. Red pulp contains reticular
tissues whose fibers filter worn out or damaged red blood cells from the blood. Macrophages in the
red pulp digest and recycle the hemoglobin of the captured red blood cells. The red pulp also stores
many platelets to be released in response to blood loss. White pulp is found within the red pulp
surrounding the arterioles of the spleen. It is made of lymphatic tissue and contains many T cells, B
cells, and macrophages to fight off infections.
THYMUS
The thymus is a small, triangular organ found just posterior to the sternum and anterior to
the heart. The thymus is mostly made of glandular epithelium and hematopoietic connective tissues.
The thymus produces and trains T cells during fetal development and childhood. T cells formed in
the thymus and red bone marrow mature, develop, and reproduce in the thymus throughout
childhood. The vast majority of T cells does not survive their training in the thymus and are
destroyed by macrophages. The surviving T cells spread throughout the body to the other lymphatic
tissues to fight infections. By the time a person reaches puberty, the immune system is mature and
the role of the thymus is diminished. After puberty, the inactive thymus is slowly replaced by
adipose tissue.
LYMPH CIRCULATION
One of the primary functions of the lymphatic system is the movement of interstitial fluid
from the tissues to the circulatory system. Like the veins of the circulatory system, lymphatic
capillaries and vessels move lymph with very little pressure to help with circulation. To help move
lymph towards the lymphatic ducts, there is a series of many one-way check valves found
throughout the lymphatic vessels. These check valves allow lymph to move toward the lymphatic
ducts and close when lymph attempts to flow away from the ducts. In the limbs, skeletal muscle
contraction squeezes the walls of lymphatic vessels to push lymph through the valves and towards
the thorax. In the trunk, the diaphragm pushes down into the abdomen during inhalation. This
increased abdominal pressure pushes lymph into the less pressurized thorax. The pressure gradient
reverses during exhalation, but the check valves prevent lymph from being pushed backwards.
TRANSPORT OF FATTY ACIDS
21
Another major function of the lymphatic system is the transportation of fatty acids from the
digestive system. The digestive system breaks large macromolecules of carbohydrates, proteins, and
lipids into smaller nutrients that can be absorbed through the villi of the intestinal wall. Most of
these nutrients are absorbed directly into the bloodstream, but most fatty acids, the building blocks
of fats, are absorbed through the lymphatic system.
In the villi of the small intestine are lymphatic capillaries called lacteals. Lacteals are able to
absorb fatty acids from the intestinal epithelium and transport them along with lymph. The fatty
acids turn the lymph into a white, milky substance called chyle. Chyle is transported through
lymphatic vessels to the thoracic duct where it enters the bloodstream and travels to the liver to be
metabolized.
TYPES OF IMMUNITY
The body employs many different types of immunity to protect itself from infection from a
seemingly endless supply of pathogens. These defenses may be external and prevent pathogens
from entering the body. Conversely, internal defenses fight pathogens that have already entered the
body. Among the internal defenses, some are specific to only one pathogen or may be innate and
defend against many pathogens. Some of these specific defenses can be acquired to preemptively
prevent an infection before a pathogen enters the body.
INNATE IMMUNITY
The body has many innate ways to defend itself against a broad spectrum of pathogens.
These defenses may be external or internal defenses. The internal defenses include fever,
inflammation, natural killer cells, and phagocytes.
EXTERNAL DEFENSES
The coverings and linings of the body constantly prevent infections before they begin by
barring pathogens from entering the body. Epidermal cells are constantly growing, dying, and
shedding to provide a renewed physical barrier to pathogens. Secretions like sebum, cerumen,
mucus, tears, and saliva are used to trap, move, and sometimes even kill bacteria that settle on or in
the body.
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Stomach acid acts as a chemical barrier to kill microbes found on food entering the body.
Urine and acidic vaginal secretions also help to kill and remove pathogens that attempt to enter the
body. Finally, the flora of naturally occurring beneficial bacteria that live on and in our bodies
provide a layer of protection from harmful microbes that would seek to colonize our bodies for
themselves.
INTERNAL DEFENSE
1. Fever
In response to an infection, the body may start a fever by raising its internal temperature out
of its normal homeostatic range. Fevers help to speed up the bodys response system to an infection
while at the same time slowing the reproduction of the pathogen.
2. Inflammation
The body may also start an inflammation in a region of the body to stop the spread of the
infection. Inflammations are the result of a localized vasodilation that allows extra blood to flow
into the infected region. The extra blood flow speeds the arrival of leukocytes to fight the infection.
The enlarged blood vessel allows fluid and cells to leak out of the blood vessel to cause swelling
and the movement of leukocytes into the tissue to fight the infection.
3. Natural Killer Cells
Natural killer (NK) cells are special lymphocytes that are able to recognize and kill virusinfected cells and tumor cells. NK cells check the surface markers on the surface of the bodys cells,
looking for cells that are lacking the correct number of markers due to disease. The NK cells then
kill these cells before they can spread infection or cancer.
4. Phagocytes
The term phagocyte means eating cell and refers to a group of cell types including
neutrophils and macrophages. A phagocyte engulfs pathogens with its cell membrane before using
digestive enzymes to kill and dissolve the cell into its chemical parts. Phagocytes are able to
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recognize and consume many different types of cells, including dead or damaged body cells.
CELL MEDIATED IMMUNITY
When a pathogen infects the body, it often encounters macrophages and dendritic cells of the
innate immune system. These cells can become antigen-presenting cells (APCs) by consuming and
processing pathogenic antigens. The APCs travel into the lymphatic system carrying these antigens
to be presented to the T cells and B cells of the specific immune system.
Inactive T cells are found in lymphatic tissue awaiting infection by a pathogen. Certain T
cells have antigen receptors that recognize the pathogen but do not reproduce until they are
triggered by an APC. The activated T cell begins reproducing very quickly to form an army of
active T cells that spread through the body and fight the pathogen. Cytotoxic T cells directly attach
to and kill pathogens and virus-infected cells using powerful toxins. Helper T cells assist in the
immune response by stimulating the response of B cells and macrophages.
After an infection has been fought off, memory T cells remain in the lymphatic tissue
waiting for a new infection by cells presenting the same antigen. The response by memory T cells to
the antigen is much faster than that of the inactive T cells that fought the first infection. The increase
in T cell reaction speed leads to immunitythe reintroduction of the same pathogen is fought off so
quickly that there are few or no symptoms. This immunity may last for years or even an entire
lifetime.
ANTIBODY-MEDIATED SPECIFIC IMMUNITY
During an infection, the APCs that travel to the lymphatic system to stimulate T cells also
stimulate B cells. B cells are lymphocytes that are found in lymphatic tissues of the body that
produce antibodies to fight pathogens (instead of traveling through the body themselves). Once a B
cell has been contacted by an APC, it processes the antigen to produce an MHC-antigen complex.
Helper T cells present in the lymphatic system bind to the MHC-antigen complex to stimulate the B
cell to become active. The active B cell begins to reproduce and produce two types of cells: plasma
cells and memory B cells.
1. Plasma cells
24
Urinary System
25
bladder,
and
urethra
26
bladder and are sealed at the point of entry to the bladder by the ureterovesical valves. These valves
prevent urine from flowing back towards the kidneys.
URINARY BLADDER
The urinary bladder is a sac-like hollow organ used for the storage of urine. The urinary
bladder is located along the bodys midline at the inferior end of the pelvis. Urine entering the
urinary bladder from the ureters slowly fills the hollow space of the bladder and stretches its elastic
walls. The walls of the bladder allow it to stretch to hold anywhere from 600 to 800 milliliters of
urine.
URETHRA
The urethra is the tube through which urine passes from the bladder to the exterior of the
body. The female urethra is around 2 inches long and ends inferior to the clitoris and superior to the
vaginal opening. In males, the urethra is around 8 to 10 inches long and ends at the tip of the penis.
The urethra is also an organ of the male reproductive system as it carries sperm out of the body
through the penis. The flow of urine through the urethra is controlled by the internal and external
urethral sphincter muscles. The internal urethral sphincter is made of smooth muscle and opens
involuntarily when the bladder reaches a certain set level of distention. The opening of the internal
sphincter results in the sensation of needing to urinate. The external urethral sphincter is made of
skeletal muscle and may be opened to allow urine to pass through the urethra or may be held closed
to delay urination.
MAINTENANCE OF HOMEOSTASIS
The kidneys maintain the homeostasis of several important internal conditions by controlling
the excretion of substances out of the body.
IONS
The kidney can control the excretion of potassium, sodium, calcium, magnesium, phosphate,
and chloride ions into urine. In cases where these ions reach a higher than normal concentration, the
kidneys can increase their excretion out of the body to return them to a normal level. Conversely,
27
the kidneys can conserve these ions when they are present in lower than normal levels by allowing
the ions to be reabsorbed into the blood during filtration.
pH
The kidneys monitor and regulate the levels of hydrogen ions (H+) and bicarbonate ions in
the blood to control blood pH. H+ ions are produced as a natural byproduct of the metabolism of
dietary proteins and accumulate in the blood over time. The kidneys excrete excess H+ ions into
urine for elimination from the body. The kidneys also conserve bicarbonate ions, which act as
important pH buffers in the blood.
OSMOLARITY
The cells of the body need to grow in an isotonic environment in order to maintain their
fluid and electrolyte balance. The kidneys maintain the bodys osmotic balance by controlling the
amount of water that is filtered out of the blood and excreted into urine. When a person consumes a
large amount of water, the kidneys reduce their reabsorption of water to allow the excess water to be
excreted in urine. This results in the production of dilute, watery urine. In the case of the body
being dehydrated the kidneys reabsorb as much water as possible back into the blood to produce
highly concentrated urine full of excreted ions and wastes. The changes in excretion of water are
controlled by antidiuretic hormone (ADH). ADH is produced in the hypothalamus and released by
the posterior pituitary gland to help the body retain water.
BLOOD PRESSURE
The kidneys monitor the bodys blood pressure to help maintain homeostasis. When blood
pressure is elevated, the kidneys can help to reduce blood pressure by reducing the volume of blood
in the body. The kidneys are able to reduce blood volume by reducing the reabsorption of water into
the blood and producing watery, dilute urine. When blood pressure becomes too low, the kidneys
can produce the enzyme renin to constrict blood vessels and produce concentrated urine, which
allows more water to remain in the blood.
28
FILTRATION
Inside each kidney are around a million tiny structures called nephrons. The nephron is the
functional unit of the kidney that filters blood to produce urine. Arterioles in the kidneys deliver
blood to a bundle of capillaries surrounded by a capsule called a glomerulus. As blood flows
through the glomerulus, much of the bloods plasma is pushed out of the capillaries and into the
capsule, leaving the blood cells and a small amount of plasma to continue flowing through the
capillaries. The liquid filtrate in the capsule flows through a series of tubules lined with filtering
cells and surrounded by capillaries. The cells surrounding the tubules selectively absorb water and
substances from the filtrate in the tubule and return it to the blood in the capillaries. At the same
time, waste products present in the blood are secreted into the filtrate. By the end of this process, the
filtrate in the tubule has become urine containing only water, waste products, and excess ions. The
blood exiting the capillaries has reabsorbed all of the nutrients along with most of the water and
ions that the body needs to function.
STORAGE AND EXCRETION OF WASTE
After urine has been produced by the kidneys, it is transported through the ureters to the urinary
bladder. The urinary bladder fills with urine and stores it until the body is ready for its excretion.
When the volume of the urinary bladder reaches anywhere from 150 to 400 milliliters, its walls
begin to stretch and stretch receptors in its walls send signals to the brain and spinal cord. These
signals result in the relaxation of the involuntary internal urethral sphincter and the sensation of
needing to urinate. Urination may be delayed as long as the bladder does not exceed its maximum
volume, but increasing nerve signals lead to greater discomfort and desire to urinate.
Urination is the process of releasing urine from the urinary bladder through the urethra and out
of the body. The process of urination begins when the muscles of the urethral sphincters relax,
allowing urine to pass through the urethra. At the same time that the sphincters relax, the smooth
muscle in the walls of the urinary bladder contract to expel urine from the bladder.
PRODUCTION OF HORMONES
The kidneys produce and interact with several hormones that are involved in the control of
systems outside of the urinary system.
29
CALCITROL
Calcitriol is the active form of vitamin D in the human body. It is produced by the kidneys
from precursor molecules produced by UV radiation striking the skin. Calcitriol works together with
parathyroid hormone (PTH) to raise the level of calcium ions in the bloodstream. When the level of
calcium ions in the blood drops below a threshold level, the parathyroid glands release PTH, which
in turn stimulates the kidneys to release calcitriol. Calcitriol promotes the small intestine to absorb
calcium from food and deposit it into the bloodstream. It also stimulates the osteoclasts of
the skeletal system to break down bone matrix to release calcium ions into the blood.
ERYTHROPOIETIN
Erythropoietin, also known as EPO, is a hormone that is produced by the kidneys to
stimulate the production of red blood cells. The kidneys monitor the condition of the blood that
passes through their capillaries, including the oxygen-carrying capacity of the blood. When the
blood becomes hypoxic, meaning that it is carrying deficient levels of oxygen, cells lining the
capillaries begin producing EPO and release it into the bloodstream. EPO travels through the blood
to the red bone marrow, where it stimulates hematopoietic cells to increase their rate of red blood
cell production. Red blood cells contain hemoglobin, which greatly increases the bloods oxygencarrying capacity and effectively ends the hypoxic conditions.
RENIN
Renin is not a hormone itself, but an enzyme that the kidneys produce to start the ReninAngiotensin Aldosterone System (RAAS). The RAAS increases blood volume and blood pressure
in response to low blood pressure, blood loss, or dehydration. Renin is released into the blood where
it catalyzes angiotensinogen from the liver into angiotensin I.
Angiotensin I is further catalyzed by another enzyme into Angiotensin II. Angiotensin II
stimulates several processes, including stimulating the adrenal cortex to produce the hormone
aldosterone. Aldosterone then changes the function of the kidneys to increase the reabsorption of
water and sodium ions into the blood, increasing blood volume and raising blood pressure. Negative
feedback from increased blood pressure finally turns off the RAAS to maintain healthy blood
pressure levels.
30
31
The evidence for a genetic susceptibility to SLE is based on familial aggregation. The
prevalence of SLE is estimated to be 2.6% to 3.5% in 1st-degree relatives of matched controls. No
single causal gene has been identified. Instead, multiple genes appear to influence a person's chance
of developing lupus when triggered by environmental factors. The most important genes are located
in the HLA region on chromosome 6, where mutations may occur randomly (de novo) or may be
inherited. HLA class I, class II, and class III are associated with SLE, but only classes I and II
contribute independently to increased risk of SLE (Pediatric Nephrology 5th Edition Lippincott
Williams and Wilkins, 2004).
Based on twin concordance studies, the induction of SLE requires more than genetic factors.
Environment, hormonal, toxic, and infectious factors have been proposed. The high degree of
homology between a small peptide sequence of the Epstein-Barr Virus (EBV) nuclear antigen-2 and
the SmD1 ribonucleoprotein, a target of autoantibodies in SLE patients, suggests that antibodies
elicited by the viral antigen may cross-react with SmD1. Thus, EBV may be causative factor in
SLE. Photosensitivity is a common feature of SLE, and the disease is aggravated by sun exposure in
40% to 70% of patients. Ultraviolet light induce apoptosis of keratinocytes, which may, in turn,
develop small surface blebs containing lupus autoantigens such as the Ro particle. Similarly, druginduce lupus such as chlorpromazine, procainamide, isoniazid, quinidine, phenytion, and
hydralazine are capable of inducing apoptosis. However, symptoms of drug-induced lupus generally
disappear once the medication that triggered the episode is stopped and is reversible condition
(Pediatric Nephrology 5th Edition Lippincott Williams and Wilkins, 2004).
The female predominance in SLE is particularly strong during childbearing ages, suggesting
that hormonal differences may contribute to the increased risk of the disease. Reduced androgen
levels and increased estradiol and prolactin exacerbate levels have been reported in SLE patients.
Moreover, whereas administration of androgens leads to improvement, estrogen and prolactin
exacerbate disease severity (Pediatric Nephrology 5th Edition Lippincott Williams and Wilkins,
2004).
SLE is often acute in onset and includes general symptoms of fever and fatigued associated
with cutaneous and articular symptoms. SLE may also begin with an isolated symptom such as a
32
hemolytic anemia, a nephritic syndrome with hematuria, chorea, or pericarditis. General symptoms,
particularly weight loss, anorexia, and asthenia, are virtually constant in SLE. Episodic fever is
frequent during acute phase of the disease or during infection. Pulmonary or urinary tract infections
are frequent during the course of SLE. Opportunistic infections may be life threatening. A number
of factors may favor a relapse of the disease, including exposure to UV light, infection, stress,
surgery or pregnancy (Pediatric Nephrology 5th Edition Lippincott Williams and Wilkins, 2004).
Arthralgia is the most common manifestation of SLE. Both large and small articulations,
especially of the hands, are affected, causing moderate pain and articular swelling. Arthritis is very
rarely deforming, and synovial fluid contains relatively few cells. Myalgia is less frequent,
Avascular osteonecrosis, which often affects femoral heads, may occur in the absence of treatment
with corticosteroids (Pediatric Nephrology 5th Edition Lippincott Williams and Wilkins, 2004).
The most classic skin lesion of SLE is the butterfly or malar rash over the cheeks and nose,
which is present in one-third of cases. The rash is often appears after sun exposure. Maculopapular
eruptions on the upper portion of the trunk as well as any areas exposed to light are the most
common. Popular lesion and squamous lesions on the trunk, face and palms of the hands can be
observed in the less severe cutaneous forms of the disease. Raynauds phenomena of the extremities
cause painful white marble-like lesions, leg ulcers, and periungual or finger-pad erythema.
Urticarial
eruptions
and
pigmentation
anomalies
are
sometimes
observed.
Cutaneous
photosensitivity is noted especially in white patients. Mucosal lesions, particularly in the forn of
oral ulcerations, are common. Alopecia is observed in some children, especially those with active
forms of the disease (Pediatric Nephrology 5th Edition Lippincott Williams and Wilkins, 2004).
Pulmonary involvement occurs in more than 75% of children. Pleuritis, observed in 40% of
children, is often asymptomatic or maybe present as thoracic pain. The pleural fluid is exudates,
containing a large number of neutrophils and lymphocytes. Anomalies in diaphragmatic function
have been reported and can be responsible or dyspnea. Pulmonary damage may be manifested as an
acute pneumonitis with thoracic pain, dyspnea, and fever. Pulmonary arterial hypertension is a rare
but severe problem that may be secondary to repeated pulmonary embolism. Acute pulmonary
hemorrhage during the acute phase of the disease or during infections may be life threatening.
33
34
The World Health Organization has divided lupus nephritis into five stages based on the
biopsy. This classification was defined in 1982 and revised in 1995. Class I is minimal mesangial
glomerulonephritis which is histologically normal on light microscopy but with mesangial deposits
on electron microscopy. It constitutes about 5% of cases of lupus nephritis. Renal failure is very rare
in this form. Class II is based on a finding of mesangial proliferative lupus nephritis. This form
typically responds completely to treatment with corticosteroids. It constitutes about 20% of cases.
Renal failure is rare in this form. Class III is focal proliferative nephritis and often successfully
responds to treatment with high doses of corticosteroids. It constitutes about 25% of cases. Renal
failure is uncommon in this form. Class IV is diffuse proliferative nephritis. This form is mainly
treated with corticosteroids and immunosuppressant drugs. It constitutes about 40% of cases. Renal
failure is common in this form. Class V is membranous nephritis and is characterized by extreme
edema and protein loss. It constitutes about 10% of cases. Renal failure is uncommon in this form.
35
36
37
38
39
40
41
42
43
NURSING THEORY
Florence Nightingales Environmental Theory
Nightingale believed that the environment was a major factor or component of nursing care.
She believed that the physical environment, when clean, can increase the chance of patients
recovering to the fullest. Nightingale identified different items that could help in the patients
recovery such as ventilation, warming, lighting, noise, bed and beddings, cleanliness of room and
walls, personal cleanliness and nutrition.
Factors
Pure fresh air
Rationale
Patient must be provided a fresh air during his hospital stay. This will
aid her fast recovery because inhaling fresh air helps her to feel calm
and comfortable. This feeling of calmness aids in fast recovery of the
Pure water
patient.
Must be given with pure and clean water in order for the patient to heal
faster. Pure water helps hydrate the patient. It also aids in correcting
Sufficient
supply
day. Having such foods would help our body to be strong which will
Cleanliness
Light
44
Henderson believed that the unique function of the nurse is to assist the individual, sick or
well, in the performance of those activities contributing to health or its recovery (or to a peaceful
death) that he would perform unaided if he had the necessary strength, will or knowledge. And to
do this in such a way as to help him gain independence as rapidly as possible (Henderson, 1991).
There are fourteen components based on human needs that make up nursing activities:
1. Breathe normally
Patients breathing pattern was normal. To maintain it, overcrowding environment was
controlled by limiting visitors.
2. Eat and drink adequately
Parents were encouraged to feed in small amounts frequently when patient refuses to eat.
3. Eliminate body wastes
Patient was advised to maintain cleanliness of peri-anal area after voiding or defecating.
4. Move and maintain desirable postures
Patient was not restricted in position. He maintained desirable positions and moved around.
5. Sleep and rest
Promoted and maintained a quiet environment for a sound sleep and rest.
6. Select suitable clothes
Encouraged the patient and parents to frequently change soiled or dirty clothes.
7. Maintain body temperature within normal range by adjusting clothing and modifying
environment
Temperature was maintained during hospitalization. Encouraged on wearing appropriate
clothes. Room was made well ventilated.
8. Keep the body clean and well groomed and protect the integument
Hygiene maintained. Routine care provided and taught parents about importance of hygiene.
9. Avoid dangers in the environment and avoid injuring others
Maintained a safe environment.
10. Communicate with others in expressing emotions, needs, fears, or opinions
Encouraged verbalization of feelings and listened to what the patient has to say.
11. Worship according to ones faith
45
46
Date
&
Cues
Need
Nursing Diagnosis
Objectives of Care
Nursing Interventions
Evaluation
Time
Objective:
3 PM
of seizure attacks
of convulsion.
GOAL MET
five minutes
convulsion
Patient was
visible
seizure
or specifically,
is
sign
previously
diagnosed with
understanding
Benign Febrile
individual
Convulsion
single
that
Body weakness
have
Febrile episodes
2014
at
7AM
Subjective:
Mother verbalized
usahay na mukalit
lang na siya mukirig,
seizure
hours span of
of prevention.
contribute
to the setting.
injury,
specifically, the
significant others
Hemoglobin
situation;
understanding
cells
of individual
oxygen.
human
is
that
levels
hemoglobin
H
causes,
3. Ascertain knowledge of
patients
Low
many
can
Within my 8
in
a able to:
29,
problem
in
body
of
the
may
behaviors,
a.) Verbalize
factors that
contribute to
risk
possibility of
factors
and interventions/safety
injury of the
47
result
to
seizure.
injury; and
During
episodes
convulsion,
as
enhance safety.
of
To promote safe
steps to correct
situation;
to 6. Discuss importance of
self monitoring of
b.) Demonstrate
conditions/ emotions.
behaviors,
to
Conditions/emotions
lifestyle changes
muscle spasms.
can contribute to
to reduce risk
occurrence of injury.
factors and
7. Provide an environment
protect patient
resting.
environment as
indicated to
enhance safety.
uncontrollable
surroundings.
7. Evaluate patients
response to violence in
surroundings.
May enhance disregard
P
48
c.) Modify
seizure/convulsion occurs.
bladder
distention
1.
11.
intake
and
accurately
49
Monitor
output
To
record
any
significant differences
2.
12.
Discuss
13.
Encourage
To
stimulate
and
facilitate voiding
4.
To help
muscles
relax
which
the
can
facilitate voiding
5.
15.
50
Assist
16.
patient
to
Encourage
keep
area
(genitals) clean
To prevent urinary tract
infection
7.
patient
16.
Encourage
to
verbalize
concerns
Open expression allow
patient
to
deal
problems
and
with
begin
solving it
8.
51
receive
DATE
CUES
NEED
TIME
NURSING
OBJECTIVE OF CARE
DIAGNOSIS
NURSING
EVALUATION
INTERVENTIONS
OBJECTIVE:
Drugs used:
Methylpredniso
related to
Immunosuprressive
Patients vital
Medications
infection such as an
signs remains in
elevation of temperature
normal range
T
O
B
E
R
30,
2014
@
3PM
lone therapy
Prednisone
Azathioprine
Cyclophospha
T
H
Systemic Lupus
GOAL MET
Erythematosus is an
spreading pathogens.
Results of
autoimmune disease,
2. Wearing gloves to
laboratory studies
indicate negative
in infection
Patient remains
foreign substances.
Immunosuppressive
possibility of transmitting
and symptoms of
medicines reduce
disease
infection.
inflammation and
system.
mide therapy
increase in production of
52
leukocytes by bone
marrow, usually in
response to bacterial
pathogens.
nosocomial infection
technique when
performing invasive
insertion
introducing pathogen to
the system
6. Assess IV site every 4
hours, noting the presence
of redness and warmth.
Change IV tubing every
72 hours or as indicated
by facility policy.
These measures prevent
53
nutritional intake.
promote healing
8. Assess the patient for
generalized sign and
symptoms of infection
Prompt detection of
infection helps minimize
complications.
Date
Cues
Need
Nursing Diagnosis
Objectives of Care
Nursing Interventions
54
Evaluation
&
Time
O
Objective:
Hyperthermia related to
Short Term
Independent:
Temp- 37.9
disease process
After 1 hour of
RR 28cpm
appropriate nursing
PR 135bpm
intervention the
accurate indication of
Flushed skin
patients temperature
core temperature.
Skin warm to
will decrease to
37.5oC.
B
E
R
29,
touch
Diagnosed with
1PM
alcohol.
Long Term
After 4 hours of
appropriate nursing
intervention the
shivering. Shivering
lawas sir,
makuyawan jud ko
range; with a
temperature of 36.5-
3. Remove excess
maghilanat siya,
magkombulsyon
80-100bpm and
baya ni
Subjective:
Mother verbalized
H
E
@
2 PM
GOAL MET
Within an hour of my
span of care, the
patients temperature
SLE Nephritis
2014
55
decreased to 37 C
RR 24cpm
PR 91bpm
Promote a well-
ventilated area to
patient.
4. Advise patient to
increase oral fluid
intake.
prevent elevated
temperature associated
with dehydration.
Reduce metabolic
demands/ oxygen
consumption.
6. Provide high-calorie
diet.
To meet increased
metabolic demands.
7. Educate and advise
support system to do
hot.
56
Dependent:
1. Provide antipyretic
medications as
indicated.
57
DAT
CUES
E
O
Objective:
NEE
DS
A
NURSING DIAGNOSIS
OBJECTIVE OF
INTERVENTIONS
CARE
After my 8 hour span
1. Establish rapport.
hemoglobin production
Nephritis
secondary to lupus
will be able to
cooperation.
EVALUATION
GOAL MET
58
Within my 8 hour
Febrile episodes
Lethargic
Muscle weakness
R
29,
2014
@
7
Subjective:
Medyo luya ning bataa sukad pag-admit
nephritis
participate in desired
2. Determine ability to
span of care my
activity at level of
participate in activities/
level of mobility.
participate in
recommended
1. Participation in
recommended
treatment program
experience troublesome
2. Tolerates activity of
3. Assess psychological
of motion exercises
with minimal
range of motion
assistance.
normally.
exercises.
of fatigue level.
pattern.
determining pattern/
timing of activity.
Helpful in
59
assistive devices.
To note the level of
activity the patient can
tolerate with or without
assistance.
6. Measure
physiological response
to activity such as
changes in blood
pressure or
heart/respiratory rate.
Abnormalities in vital
signs may indicate
intolerance.
7. Establish realistic
activity goals with
patients.
Enhances
commitment to
60
promoting optimal
outcomes.
8. Encourage patient to
do whatever possible.
Performing activities
uses muscles, helping to
maintain their function.
9. Provide environment
conducive to relief
fatigue.
Temperature and level
of humidity are known
to affect exhaustion.
10. Instruct patient or
significant others in
ways to monitor
responses to activity and
significant signs and
symptoms.
Indicates the need to
alter activity level.
11. Provide
61
supplemental oxygen as
indicated.
Presence of
anemia/hypoxemia
reduces oxygen
available for cellular
uptake and contributes
fatigue.
12. Assist patient to
identify appropriate
coping behaviors.
Promotes sense of
control and improves
self esteem.
62
MEDICAL MANAGEMENT
DATE/TIME
DOCTORS
RATIONALE
REMARKS
ORDER
October 29,
Please
admit
2014 @
Nephro ward
5:35 AM
significant
reduction
in
LDL
LABS:
CBC pc
baseline data.
are
general
laboratory
tests.
63
UA
the
urine,
which
can
indicate
kidney
involvement.
Creatinine
number
of
anti-rheumatic
Meds:
fluids.
To control Hyperthermia, administered as
Paracetamol
needed.
250mg/5mL,
DONE
give
5ml q4 PRN
Salbutamol 1 neb Q6 For
smooth
muscle
relaxation
and DONE
bronchodilation
Ampicillin 1gm q8
DONE
64
other day
Azathioprine
DONE
50mg/tab tab
Calcium Carbonate Helps to buffer acidity in the stomach.
DONE
500mg/tab 1 tab OD
Hold Ampicillin and
DONE
Salbutamol
Start
Methylprednisolone
days
D5Water to run in 4
hrs
Prehydration:
D5
0.3
NaCl
Cyclophosphamide
707mg
100cc
D5Water
Posthydration:
D5
0.3
NaCl
DONE
at
90cc/hr to run in
6hrs
DRUG STUDY
65
Generic Name
Azathioprine
Brand name
Classification
Mechanism of
Azasan, Imuran
Immunosuppressants
Azathioprine antagonizes purine metabolism and may inhibit synthesis of
Action
DNA, RNA, and proteins. It may also interfere with cellular metabolism and
inhibit mitosis. Its mechanism of action is likely due to incorporation of
thiopurine analogues into the DNA structure, causing chain termination and
Route, Dosage,
Frequency
Pharmacokinetics
cytotoxicity.
Azathioprine 50 mg tablet p.o once a day
Indication
66
Drug Interactions
Nursing
Responsibilities
67
Generic Name
Cyclophosphamide
Brand name
Classification
Mechanism of Action
Cytoxan
Anti-neoplastic
Cyclophosphamide is a drug that is used primarily for treating several types
of cancer. In order to work, cyclophosphamide first is converted by
the liver into two chemicals, acrolein and phosphoramide. Acrolein and
phosphoramide are the active compounds, and they slow the growth of
cancer cells by interfering with the actions of deoxyribonucleic acid (DNA)
within the cancerous cells. Unfortunately, normal cells also are affected,
68
and this results in serious side effects. In addition to slowing the growth of
cancerous cells, cyclophosphamide also suppresses the immune system and
Route, Dosage,
is referred to as immunosuppressive.
707mg + 100cc d5W
Frequency
Pharmacokinetics
Indication
up
to
25%
of
cyclophosphamide
excreted
unchanged.
Contraindication
Adverse Reactions
Causes kidney failure and may affect the heart and lungs
69
Drug Interactions
of blood.
Allopurinol (Zyloprim) enhances the ability of cyclophosphamide to
reduce production of blood cells from the bone marrow.
Nursing
Responsibilities
70
Use caution with sharp objects like safety razors or nail cutters and
avoid activities such as contact sports to lower the chance of getting cut,
bruised or injured.
Before having surgery, tell your doctor or dentist that you are using this
medication.
Caution is advised when using this drug in the elderly because they may
be more sensitive to its effects.
Caution is advised when using this drug in children because they may
be more sensitive to its effects, especially possible infertility later in
life.
This drug is not recommended for use during pregnancy. It may cause
harm to an unborn baby. Women of childbearing age and men should
use reliable form(s) of birth control during treatment with this drug and
for some period afterwards.
This drug passes into breast milk. Because of the potential risk to the
infant, breast-feeding while using this drug is not recommended.
Consult your doctor before breast-feeding.
71
Generic Name
Calcium Carbonate
Brand name
Classification
Mechanism of Action
Route, Dosage,
Frequency
Pharmacokinetics
Indication
Contraindication
72
Renal calculi
Hypophosphatemia
Hypercalcemia
Suspected digoxin toxicity
Adverse Reactions and upset stomach
vomiting
Side Effects
stomach pain
belching
constipation
dry mouth
increased urination
loss of appetite
metallic taste
Drug Interactions
Calcium carbonate can decrease the absorption of other drugs. Some
examples of affected drugs include tetracycline antibiotics (such as
doxycycline, minocycline), bisphosphonates (such as alendronate),
estramustine, iron, levothyroxine, pazopanib, strontium, quinolone
Nursing
Responsibilities
Client/Family Teaching:
1. Take as directed. Increase fluid intake and bulk in diet to prevent
constipation.
2. When used as a supplement take 1-1 hr after meals; as an
antacid take 1 hr after meals and at bedtime.
3. If using the gum, do not take more than 17 pieces/day of the 450
mg strength or more than 26 pieces/day of the 300 mg strength.
Do not take the maximum dose for more than 2 weeks.
73
Generic Name
Isoniazid
Brand name
Classification
Mechanism of Action
Niazid, Isotamine
Antitubercular
Interferes with lipid and nucleic acid metabolism of growing bacteria,
74
Route, Dosage,
Frequency
Pharmacokinetics
Indication
tuberculostatic agent.
Prophylaxis of tuberculosis in the following: HIV, close contacts with
those newly diagnosed with infectious tuberculosis, recent converters,
abnormal chest radiographs, IV drug users, those with increased risk of
tuberculosis, those less than 35 years of age with tuberculin skin test
reaction 10 mm or greater, and children less than 4 years of age if they
have greater than 10 mm induration from a purified protein derivative
Contraindication
Adverse Reactions
75
syndrome, arthralgia.
Al salts / Effect of isoniazid R/T GI tract absorption
Nursing
Responsibilities
76
77
Generic Name
Brand name
Methylprednisolone
Oral: Medrol
Route, Dosage,
Frequency
78
Pharmacokinetics
Indication
Contraindication
cord injury
Serious infections except septic shock or tuberculous meningitis; viral,
fungal and tubercular skin lesions; admin of live virus vaccines.
Preparations containing benzyl alcohol preservative are contraindicated
Adverse Reactions
in infants.
Edema, hypertension, arrhythmia;
transient leukocytosis;
Drug Interactions
79
Nursing
Responsibilities
Use caution with the 24-mg tablets marketed as Medrol; these contain
tartrazine, which may cause allergic reactions, especially in people who
are allergic to aspirin.
Do not to stop taking the oral drug without consulting your health care
provider.
80
Generic Name
Paracetamol
Brand name
Classification
Mechanism of Action
Biogesic
Antipyretic
Reduces fever by acting directly on the hypothalamic heat-regulating center
Route, Dosage,
Frequency
Pharmacokinetics
tract.
Distrubution: peak plasma concentrations occur about 10 to 60 minutes
after oral doses. Paracetamol is distributed into most body tissues. It
crosses the placenta and is present in breast milk. Plasma-protein
binding is negligible at usual therapeutic concentrations but increases
81
hours.
Analgesic-antipyretic in patients with aspirin allergy, hemostatic
fever
Unlabeled use: Prophylactic for children receiving DPT vaccination to
Contraindication
Adverse Reactions
pregnancy, lactation.
CNS: Headache
CV: Chest pain, dyspnea, myocardial damage when doses of 58 g/day
Indication
are ingested daily for several weeks or when doses of 4 g/day are
ingested for 1 yr
GI: Hepatic toxicity and failure, jaundice
GU: Acute kidney failure, renal tubular necrosis
Hematologic: Methemoglobinemiacyanosis; hemolytic anemia
hematuria, anuria; neutropenia, leukopenia, pancytopenia,
Drug Interactions
thrombocytopenia, hypoglycemia
Hypersensitivity: Rash, fever
Drug-drug
Nursing
Responsibilities
sulfinpyrazone
Possible delayed or decreased effectiveness with anticholinergics
Possible reduced absorption of acetaminophen with activated charcoal
Possible decreased effectiveness of zidovudine
Know the patients 10 rights.
Check the chart and the patient before administering medication.
82
inflammatory agent.
Avoid the use of other over-the-counter preparations. They may contain
acetaminophen, and serious overdosage can occur. If you need an over-
Generic Name
Prednisone
83
Brand name
Classification
Mechanism of Action
Rayos, Sterapred
Antiasthmatics, Corticosteroids
Glucocorticoids are naturally occurring hormones that prevent or
suppress inflammation and immune responses when administered at
pharmacological doses. At a molecular level, unbound glucocorticoids
readily cross cell membranes and bind with high affinity to specific
cytoplasmic receptors. This binding induces a response by modifying
transcription and, ultimately protein synthesis to achieve the steroid's
intended action. Such actions may include: inhibition of leukocyte
infiltration at the site of inflammation, interference in the function of
mediators of inflammatory response, and suppression of humoral
immune responses. Some of the net effects include reduction in edema
or scar tissue, as well as a general suppression in immune response.
The degree of clinical effect is normally related to the dose
administered. The anti-inflammatory actions of corticosteroids are
thought to involve phospholipase A2 inhibitory proteins, collectively
called lipocortins. Lipocortins, in turn, control the biosynthesis of
potent mediators of inflammation such as prostaglandins and
leukotrienes by inhibiting the release of the precursor molecule
arachidonic acid. Likewise, the numerous adverse effectsrelated to
corticosteroid use are usually related to the dose administered and the
Route, Dosage,
duration of therapy.
40 mg every other day p.o
Frequency
Pharmacokinetics
84
Contraindication
disease,
insulin
resistance
in
diabetes
mellitus,
persons.
Tuberculosis active or possibly latent is a contra-indication unless
adequate
amounts
of
suitable
anti-tubercular
drugs
are
by the physician.
It should be noted that prednisone has less tendency than many
corticosteroids to cause fluid retention and mineral imbalance but
Adverse Reactions
euphoria, depression
CV: Hypotension, shock, hypertension and CHF secondary to fluid
retention, thromboembolism, thrombophlebitis, fat embolism,
cardiac arrhythmias
85
hypocalcemia
Endocrine: Amenorrhea, irregular menses, growth retardation,
decreased carbohydrate tolerance, diabetes mellitus, cushingoid
state (long-term effect), increased blood sugar, increased serum
cholesterol, decreased T3 and T4 levels, HPA suppression with
therapy)
Hypersensitivity: Hypersensitivity or anaphylactoid reactions
Musculoskeletal: Muscle weakness, steroid myopathy, loss of
muscle mass, osteoporosis, spontaneous fractures (long-term
therapy)
Other: Immunosuppression, aggravation or masking of infections;
impaired wound healing; thin, fragile skin; petechiae, ecchymoses,
Drug Interactions
ketoconazole
Increased therapeutic and toxic effects of estrogens, including
hormonal contraceptives
Risk of severe deterioration of muscle strength in myasthenia
gravis patients who also are receiving ambenonium, edrophonium,
Nursing
Responsibilities
neostigmine, pyridostigmine
Decreased steroid blood levels with barbiturates, phenytoin,
rifampin
Decreased effectiveness of salicylates
Know the patients 10 rights.
Check the chart and the patient before administering medication.
Assess the patients condition before giving the medication to be
able to identify if there is a sudden reaction of the medication to
the patient.
Assess patients weight, reflexes and grip strength, affect and
orientation, pulse, BP, peripheral perfusion, adrenal insufficiency,
crackles/rales, dyspnea and cerebral edema.
86
corticosteroids.
Monitor intake and output of patient and daily weight.
Avoid exposure to infections.
Report unusual weight gain, swelling of the extremities, muscle
weakness, black or tarry stools, fever, prolonged sore throat, colds
or other infections, worsening of the disorder for which the drug is
being taken.
87
Basic Test
Rationale
Result
Clinical Significance
Nursing Interventions
Values
Hemoglobin To
29, 2014
measure
the
115.0
of
LOW
hemoglobin in the
blood,
which
Increased
vera
Acute
carrying
thermal
injury
Hemoconcent
It
also
response
blood
replacement
to
loss
Fluid
retention
Dehydration
therapy.
Recent
bleeding
severity of anemia
PRETEST:
-Identify the patient, and check the
Polycythemia
Decreased
Hemolysis
of red blood cells
the
the
Pregnancy
Hemorrhage
the syringe
COPD
Anemia
-Obtain
Cirrhosis of
the liver
Hyperthyroi
dism
for
ration
purpose
health
history
of
the
88
Hematocrit
0.40-0.52
To
measure
the
0.41
the
size
of
Addisons
disease
Recent
hemorrhage
Polycythemia Anemia
RBCs. It gives a
vera
Fluid overload
percentage of RBCs
Acute
Fluid retention
thermal
injury
Extreme
anemia., leukemia,
diet
decency,
other
physical
or
exertion
medical
Hemoconcent
condition
Cirrhosis
Hemolytic anemia
4.20-6.10
X10^6/uL
To
measure
the
4.20
different
condition
specimen
collection
takes
Lymphoma
the
patient
who
will
Polycytemia
Cirrhosis
COPD
Leukemia
Hypoxia
vera
Dehydration
RBC Count
Hemodilution
ration
COPD
Cigarette
nutritional supplements
and
pressure
of
the
tourniquet
-The patient may be seated or in the
supine position. The patients arm is
in extension, with easy access to the
antecubital fossa
DURING THE TEST:
-Ensure that the blood is not taken
89
WBC Count
To
assess
for
7.44
of NORMAL
Bacterial
Typhoid fever
5.0-10.0
presence
X10^6/uL
infection
and
Lymphoma
inflammation,
the
Leukemia
rubella, hepatitis)
as
WBC
differential
bone
Chronic
infection
Mumps
biopsy. It monitors
response
infection
to
intestines)
Tissue
radiation therapy
necrosis
(burns,
gangrene,
myocardial
infarction)
Varicella
55-75 %
To
monitor
hyponatremia
or
hypernatremia
indicating
fluid
excess or deficit.
Dengue fever
78
HIGH
Acute
Infection
Malaria
Pernicious anemia
chemotherapy and
Neutrophil
Viral
the venipuncture
-Ask the patient to open and close
hand a few times to help make the
Radiation
Antineoplastic
drugs
lupus POSTTEST:
erythematosus
Aplastic anemia
Chemotherapy
stops
Acute stress
Influenza
Eclampsia
Radiation therapy
Gout
90
An
Myelocytic
important
indicator
of
leukemia
infection
Viral infection
needed
Widespread
Rheumatoid
severe
arthritis
Rheumatic
fever
Thyroiditis
Lymphocytes To assess levels of
20-35%
lymphocyte
production.
test
19%
Trauma
Infectious
LOW
hepatitis
This
Cytomegalov
differentiates
irus infection
count.
Tuberculosis
WBC
Important to verify
bacterial
infection
or viral
Hodgkins
diseases
Systemic
lupus
erythematosus
Syphilis
Lymphocytic
Aplastic anemia
leukemia
HIV infection
Infectious
momonucleo
sis
procedure
-Check other signs of on infection
and inflammation such as redness,
swelling, heat, and pain in the
infected site
Military -Inform
physician
for
any
tuberculosis
unusualities in vital signs or the
Renal failure
patients condition
Terminal cancer
Thoracic
drainage
91
Monocytes
2-10
To assess levels of
monocytes.
Major NORMAL
Acute
infection
(bacterial,
It
viral)
regulates
Hairy
cell -Clarify
failure
answer
additional
leukemia
Bone
or
marrow others
-Tell patient
to
report
any
osmolarity of acid-
Tuberculosis
Aplastic anemia
Syphilis
Stress response to
increase in chronic
Ulcerative
infection
colitis
Myeloprolife
colon trauma
Shock
Burns
Cushings
syndrome
disease
Platelet
To assess levels of
Count
thrombocytes
150-400
which
are
X10^3/uL
cells
that
NORMAL
blood
are
involved in cellular
mechanisms
of
primary
homeostasis
313
that
Myeloprolife
rative disease
Autoimmune
disease
Polycythemia Chemotherapy
vera
Myelofibrosi
Thrombocytopeni
a
s
Iron
92
leads to formation
deficiency
of blood clots
anemia
Acute
or
chronic
infection
Inflammation
diseases
Chronic renal
Mean
Calculates
the
Corpuscular
weight
Hemoglobin
hemoglobin in the
25.7-32.20
average
pg
Mean
erythrocytes.
Measures
Corpuscular
average
Hemoglobin
concentration
or
Concentratio
percentage
of
n (MCHC)
hemoglobin in the
32.30-36.50
average erythrocyte
of
27.5
the NORMAL
the
33.4
NORMAL
disease
Heditary
spherocytosis
Heditary
spherocytosis
Iron
deficiency
anemia
Iron
deficiency
anemia
g/dl
93
URINE ANALYSIS
Date
Basic Test
Ordered
with Normal
October
Values
Appearance
29, 2014
Color
Rationale
Result
Clinical
Nursing Interventions
Significance
Some
medications
and
chemicals
are Clear
NORMAL
in
result.
Urine ranges from pale yellow to amber Dark
the
helps
NORMAL
diagnosis
evaluate
of
overall
renal function.
Specific
specific gravity
It is the measurement of the ability of the 1.03
Gravity
(1.005-1.03)
urine collection.
NORMAL
urine.
Presence of albumin is an indicator of Trace
kidney function.
A high urine pH may be due to kidney failure, 6.0
4.6-8
Instruct
to
collect
sample
preferably
NORMAL
94
a
on
Glucose
NORMAL
RBC
NORMAL
0-11 u/L
WBC
menstruation
The number of WBCs in urine sediment is 18
6-11 u/L
an
infection
or
HIGH
inflammation
vaginal secretions.
Normally in men and women, a few epithelial 7.0
0-11u/L
NORMAL
95
0-1u/L
NORMAL
0-111u/L
no microorganisms seen
in
the
NORMAL
urine
Basic
Tests Rationale
ordered
With Normal
October
Values
Creatinine
Result
33.52
Clinical Significance
Increased
Decreased
Nursing Interventions
Pretest:
96
29,
53.00-115.00 laboratory
2014
umol/L
test
LOW
used to evaluate
estimate
the
effectiveness
of
working well
dehydrated
filtration. It is an
acid
Obtain a history of
glomerular
amino
Iron
Myelofibrosis
and
waste product of
metabolism.
take
Calcium
2.40
medications.
Consumed
1.75-2.39
amount of calcium
HIGH
mmol/L
in the blood.
gastrointestinal,
result in decreased
genitourinary,
muscle mass.
hepatobiliary
Metastatic
Steomalacia
Pagets Disease
of
performed
nutrients
previously
tests
and
list
of
procedures.
Obtain
bone Vitamin
tumor
and
musculoskeletal
is
of albumin
of
patients cardiovascular,
sm
Hyperpathyroidis
list
Hypoparathyroidi
HIV/AIDS
too Malabsorption of
vitamin D
including
certain
much calcium or
complaints,
known allergies.
of meat
protein
patients
taking,
herbs,
deficiency
Magnesium
including
nutritional
supplements
and
nutraceuticals.
the
deficiency
practitioner
Kidney failure
97
and
Monitor
3.4-5.4
mmol/L
renal
metabolism.
4.40
Addisons disease
Potassium
To
disorders and to
Too
the
origin
Red
arrhythmias.
Magnesium is one
Magnesium
of
0.74-1.03
intracellular
mmol/L
cations
of
the
body.
It
is
the
m
much Not
major
measured
evaluate
electrolyte
disorders,
hypocalcemia,
to
1.09
HIGH
blood
Low
containing
antacids
There
are
fluid,
or
medication
dietary
the
patient.
diabetes
Long
food,
restrictions unless by
Uncontrolled
of
no
medical direction.
Hyperparathyroidi Gastrointestinal
disorders
sm
Dehydration
when
reviewing results.
intake
Hypothyroidism
magnesium
consideration
potassium on diet
cell Vomiting
Kidney failure
Use
enogh
destruction
Serum
Hyperaldosteronis
potassium on diet
of
deficiency
or Use of diuretics
acidosis
be
Chronic diarrhea
respiratory
endocrine
laboratory should
anemia
Metabolic
neuromuscular and
determine
tissue Iron
Kidney failure
evaluate
Liver disease
Myelofibrosis
may
term
have
discomfort
diuretic use
with
slight
the
or Prolonged
diarrhea
tourniquet.
98
hypokalemia, and
Severe burns
laxatives
acid-base
Sodium
imbalance.
To detect changes
approximately takes 5
135-145
problems
mmol/L
cushing syndrome
balance.
To
determine
electrolytes, acidbase
balance,
water
balance,
water intoxication,
and dehydration.
138
Adrenal
to 10 minutes.
like Dehydration,
morphine
and
to avoid unnecessary
SSRI
antidepressants
movement.
bicarbonate in diet
Use
Observe
standard
precautions
of
when
obtaining blood.
corticosteroids,
laxative, lithium,
Posttest:
and NSAIDS
Observe
venipuncture site for
bleeding or hematoma
formation.
Apply
pressure bandage.
Evaluate
test
99
B. POSSIBLE
Serology Blood Test
Anti-SM
Rationale
Nursing Intervention
Anti-Sm is an antibody directed against Sm, a specific protein Pretest:
found in the cell nucleus. The protein is found in up to 30% of
Obtain
history
of
patients
Antiphospholipid
known allergies.
Antibodies (APLs)
100
Anti-Ro
(SSA)
Anti-La(SSB)
used to help identify women with lupus that have certain risks
medical direction.
the
Inform
potentially
serious
problem
in
newborns.
the
the
patient
that
the
takes 5 to 10 minutes.
Intratest:
and
puncture
tourniquet.
needle
101
infection, the test is not diagnostic for lupus. Nor can it Posttest:
distinguish a lupus flare from an infection. Also, the level of
Complement
diagnostic of lupus.
ESR measures the speed of red blood cells moving toward the
Rate bottom of a test tube. When inflammation is present, blood
proteins stick together and fall and collect more quickly as
sediment. The more quickly the blood cells fall, the greater the
inflammation. ESR is used as a marker of inflammation.
Inflammation could indicate lupus activity. This test could be
used to monitor inflammation, which could indicate changes in
disease activity or response to treatment.
102
Test
Tissue
Rationale
A biopsy procedure involves removal of a small bit of
Nursing Intervention
Observe standard precautions when obtaining blood
Biopsies
Chest
ray
tissue.
medication is responsible.
X- An image of your chest may reveal abnormal shadows
that suggest fluid or inflammation in your lungs.
103
104
PROGNOSIS
CRITERIA
GOOD
FAIR
POOR
JUSTIFICATION
The patient is five years old. SLE in children is
uncommon but fatal. Most deaths in children with SLE
are the result of infection, nephritis, renal failure,
neurologic
disease,
or
pulmonary
hemorrhage.
Age
Onset
of
illness
Duration
illness
of
105
treatment
regimens,
in
particular
provided
by
the
nurses
regarding
refraining
individuals
are
vulnerable
to
106
Willingness
to
take
procedures
particularly
monitoring
through
immunosuppressant
medications
the
drugs.
frequent
blood
Their
laboratory
studies
and
socio-economic
Precipitating
factors
Predisposing
factors
107
age, genetics and race. The stakes are high for the
condition to occur as found out if the patient is between
three to five years old. Genetic implications arise from
having a twin brother. Studies show that having lupus
between twin siblings is high or having familial
tendencies in having twins in the family is commonly
associated to having autoimmune diseases. Since the
child patient is a Filipino, moreover an Asian. It is a
popular knowledge that Lupus is common to Asians or
having an Asian descent.
TOTAL
COMPUTATION
PROGNOSIS RATING
POOR
FAIR
GOOD
RESULT
TOTAL
Range
Poor = 1
1.00 - 1.69
Fair = 2
1.70 - 2.39
Good = 3
2.40 - 3.00
NARRATIVE PROGNOSIS
The overall prognosis of the patient based on the computed weigh among criteria is 2.00 and
its range falls under the fair prognosis. In the past, almost all diagnosed case of SLE and its
108
complications are categorically considered under poor prognosis. In todays advent of improving
and sophisticating advancements in medicine, particularly with regards to therapy and diagnostic
procedures whereby diseases such as SLE can be easily detected at early stages and therefore
provided with prompt medications. There are already promising specific therapy as a result of
continuous and rigid studies or researches. Tests are still being conducted to prove its efficacy and
effectiveness. Although at present there are already existing medicines that control or alleviate
conditions caused by flares of the diseases. It is much fortunate that patients are able to continue
with normal lives without much of the burden of disease and so it can be considered that quality of
life is restored. Compliance of the patient and or his family is vitally important. The treatment
process is long and could be overpowering, motivation is imperative thus they should look through
their situation as a binding factor and to strengthen them in facing not only this challenge but as
well others that may come.
DISCHARGE PLAN
Medications
Corticosteroids are used in all patients with clinically significant renal disease.
109
Immunosuppressive
agents,
particularly
cyclophosphamide,
azathioprine,
and
mycophenolate mofetil, are used in patients with aggressive renal lesions because they
improve the renal outcome. They may also be used in patients with inadequate response or
excessive toxicity to corticosteroids.
All patients with SLE who are on corticosteroids or who have arthritis are at increased risk
for osteopenia and its complications. Supplementation with vitamin D and calcium are
important tools for bone health in these patients. Of note, natural production of vitamin D
involves skin exposure to sun, which is discouraged in the SLE population, increasing the
risk of vitamin D deficiency.
Oral diazepam can reduce the risk of subsequent febrile seizures. Because it is intermittent,
this therapy probably has the fewest adverse effects. If preventing subsequent febrile
seizures is essential, this would be the treatment of choice.
Although it does not prevent simple febrile seizures, antipyretic therapy is desirable for
other reasons.
Can decrease number of subsequent febrile seizures when given with each febrile episode.
By increasing activity of GABA, a major inhibitory neurotransmitter, depresses all levels of
CNS, including limbic and reticular formation.
Exercise/Environment
110
Caution patients and/or their family that fatigue and stress have been associated with disease
flares.
Caution patients to avoid sunlight and to liberally apply waterproof sunblock every 2 hours
when exposed to the sun.
Treatment
The goal of therapy is to control disease manifestations, allowing the child to have a good
quality of life without major disease exacerbations, while preventing serious organ damage
that adversely affects function or life span. At the same time, the physician is challenged to
prevent intolerable adverse effects from the therapeutic regimen.
Before treatment, identify organ system involvement and exclude other possible diagnoses.
Many of the therapeutic options have serious adverse effects, contraindications, and drug
interactions. A high risk for infection, infertility, and future cardiovascular disease is noted.
The most important management tool in the treatment of systemic lupus erythematosus
(SLE) is meticulous and frequent reevaluation of patients.
Reevaluation includes clinical and laboratory evaluation, allowing prompt recognition and
treatment of disease flare that is essential to patient outcome.
HEALTH TEACHING
111
The patient and his or her family must have a thorough understanding of SLE, its potential
severity, and the complications of the disease and its therapy.
Treatment is difficult. The health providers and parents should expect issues, including
depression and noncompliance, to arise.
The best method for deterrence is to thoroughly educate the patient and family through
discussion, support groups, and literature.
Educate all patients with SLE with regard to the serious complications possible from poor
compliance, and infection. Poor compliance, in particular, is a significant prognostic factor.
Out-patient Referral
A Rheumatologist should be an integral part of the medical care team supporting the lupus
patient.
Other consultations depend on the type of organ involvement. Consider consultation with a
Nephrologist for severe end-organ disease.
Diet
Dietary restrictions are driven by the patients medical therapy. Most patients require a
Monitoring nontraditional remedies and food supplements is important, because they may
Alter metabolism of more traditional medications.
112
Systemic Lupus Erythematosus is a chronic disease that can affect a variety of different
body parts or organs. The human body is equipped with an internal immune surveillance system
which detects the presence of invading pathogens and other foreign elements that could be harmful
to the body. In some instance, a disorder may occur such as in the case of lupus and other
rheumatologic problems whereby the bodys immune system could not properly identify its real
enemy and produces antibodies which in this case it attacks its own thus causing damage within and
will manifest inflammation in different body parts or systems. Sometimes, on a rare occasion basis,
lupus nephritis can be the sole symptom of lupus. Childhood onset presents a few manifestations
thus arriving to a correct diagnosis more difficult. The hallmark signs and symptoms of lupus
nephritis are sometimes suggestive of other diseases as well. Perhaps the exact onset of the disease
on the patient can be traced back to an earlier period that there is already kidney involvement but
that would also be doubtful since progression of the disease can be erratic and rapid in progression.
Another complex problem is the management of lupus itself. The need to use both
immunosuppressants and corticosteroid suggests enormous caution on the part of the parents and
the child patient himself. Seemingly it will not only be the childs physical growth and development
that will be affected but as well as the psychological growth and development is at risk for
retardation due to several disease-imposed restrictions to impede normal functioning and living. He
can never be careless and reckless like other children. The family will be having a lot of difficulty
coping to the demands of their childs condition, there is a possibility that it will not only the patient
who will suffer physically and emotionally but it will be a burden to the whole family. Their
economic status can be a factor for the decline of survivability of the patient. Thus the condition of
the patient may have greater impact to their socioeconomic status. The real sacrifice is in the long
process of treatment which is almost a lifetime not until a real cure to this condition will be
available. Todays existing goals of therapy are usually directed to prevention of flares of lupus.
In a publication of the American Association of Kidney Patients, An update on Lupus
Nephritis, states that currently, the only way to truly confirm the most effective treatment of lupus
nephritis is to perform a kidney biopsy. If the urine and blood studies suggest this diagnosis, a
biopsy is used to confirm it and to determine the degree and severity of kidney involvement. This is
very important as it provides a guide as to what medicines may be required to treat it. In children (as
in adults), kidney biopsies are generally done in the hospital or outpatient surgery centre with
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general anaesthetic or conscious sedation. A biopsy needle is inserted through the skin of the back
and small pieces of the kidney tissue are removed. This tissue is then examined with a microscope
to see how much permanent (scar) or reversible damage has occurred. These findings are reported
based on the World Health Organization (WHO) classification system. Understanding the type of
lupus nephritis a child has helps in assessing the best treatment approach, and long term prognosis.
Another breakthrough is in the treatment regimens for lupus and lupus nephritis. Through research,
the understanding of how lupus nephritis occurs is slowly improving. This is leading to the
development of newer more specific medications for treatment of this condition. Bone marrow
transplant and plasmapheresis have also been utilized in very severe cases of lupus nephritis that
have not responded to conventional therapy. Occasionally, despite aggressive and long-term therapy,
children with lupus nephritis lose their kidney function. In this setting the patient is placed on either
hemodialysis or peritoneal dialysis until there is little or no evidence of lupus activity at which point
they are referred for kidney transplant. Lupus does not commonly recur in transplanted kidneys.
REFERENCE
http://emedicine.medscape.com/article/1008066-overview#aw2aab6b2b4
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https://www.aakp.org/education/resourcelibrary/dialysis-resources/item/an-update-on-lupusnephritis.html
http://emedicine.medscape.com/article/1176205-followup#a2651
http://www.medpagetoday.com/Rheumatology/Lupus/21556
http://www.mayoclinic.org/diseases-conditions/lupus/basics/risk-factors/con-20019676
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Surgical Nursing by Suzzane C. Smeltzer and Brenda G. Bare Vol.1
Pediatric Nephrology 5th Edition Lippincott Williams and Wilkins, 2004 Vol. 1
Black, J. M., & Hawks, J. H. (2009). Medical-Surgical Nursing: Clinical Management for
Positive Outcomes. 8th Edition. Missouri: Saunders.
Porth, C.M. (2005). Pathophysiology: Concepts of Altered Health States. 7th Edition. Lippincott
Williams & Wilkins.
Smeltzer, S. C., Bare, B. G., Hinkle, J. L., & Cheever, K. H. (2010). Brunner & Suddarths
Textbook of Medical-Surgical Nursing. 13th Edition. Volume 2. Philadelphia: Wolters Kluwer
Health/Lippincott Williams & Wilkins.
Black, J. M., & Hawks, J. H. (2009). Medical-Surgical Nursing: Clinical Management for
Positive Outcomes. 8th Edition. Missouri: Saunders.
Porth, C.M. (2005). Pathophysiology: Concepts of Altered Health States. 7th Edition.Lippincott
Williams & Wilkins
Smeltzer, S. C., Bare, B. G., Hinkle, J. L., & Cheever, K. H. (2010). Brunner & Suddarths
Textbook of Medical-Surgical Nursing. 13th Edition. Volume 2. Philadelphia: Wolters Kluwer
Health/Lippincott Williams & Wilkins.
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