INTRODUCTION

Cerebrovascular disease is a group of brain dysfunctions related to disease of

the blood vessels supplying the brain. Hypertension is the most important cause; it
damages the blood vessel lining, endothelium, exposing the underlying collagen where
platelets aggregate to initiate a repairing process which is not always complete and
perfect. Sustained hypertension permanently changes the architecture of the blood
vessels making them narrow, stiff, deformed, uneven and more vulnerable to fluctuations
in blood
pressure.
A stroke is caused by the interruption of the blood supply to the brain, usually
because a blood vessel bursts or is blocked by a clot. This cuts off the supply of oxygen
and nutrients, causing damage to the brain tissue. Strokes can be classified into two
major categories: ischemic and hemorrhagic. This study focuses on hemorrhagic stroke
per se.
Hemorrhagic strokes are primarily caused by intracranial or subarachnoid
hemorrhage. The bleeding most probably occur in the brain tissue, the ventricles or/and
in the subarachnoid space. Primary intracerebral hemorrhage from a spontaneous
rupture of small vessels is caused chiefly by uncontrolled hypertension. Subarachnoid
hemorrhage, on the other hand, results from a ruptured intracranial aneurysm. In elderly
patients, a common cause of intracerebral hemorrhage is cerebral amyloid angiopathy
hich involves damage caused by deposit of beta-amyloid protein in the small and
medium-sized blood vessels of the brain.
The most common symptom of a stroke is sudden weakness or numbness of the
face, arm or leg, most often on one side of the body. Other symptoms include:
confusion, difficulty speaking or understanding speech; difficulty seeing with one or both
eyes; difficulty walking, dizziness, loss of balance or coordination; severe headache with
no known cause; fainting or unconsciousness.
Patients who survive the acute phase of care usually have more severe deficits
and a longer recovery time compared to those who suffered from ischemic stroke.
Cerbrovascular diseases end millions of lives every year. Stroke survivors have
to adapt to a life with restrictions in activities of daily living as a consequence of
cerebrovascular disease. Many surviving stroke patients will often depend on other
people’s continuous support to survive.
In many of our hospital duties, CVD was observed to be one of the most
prevalent cases in the ward. Thus, it is just justifiable that we are to gain extra-
knowledge on this particular disease. Knowing the possible medical interventions and
nursing care to be given to such clients will enable us to give optimum care to our future
clients with the same condition.

II. Assessment Tool:

I. GENERAL INFORMATION

NAME: Corsenito Josol Lasco AGE: 50-years-old

BIRTHDAY: March 5, 1960 BIRTHPLACE: Tagbilaran, Bohol

SEX: Male RELIGION: Kristohanon

ADDRESS: Butuan, Agusan del Norte

INFORMANT: Wife

ADMISSION:

Date: August 20, 2010 TIME: 2:00 AM

CHIEF COMPLAINT UPON ADMISSION: slurred speech, facial drooping,

 lost of consiusness

DIAGNOSIS/IMPRESSION: Cerebrovascular Disease, Hemorrhagic Stroke

History of Past Illness:

The client has no history of any major disease conditions aside from his already
known hypertension. He had more so gone through episodes of fever, cough and colds
in the latter years.

History of present Illness:

In the morning of August 19, 2010, the patient had an onset of sudden slurring of
speech, facial drooping and then lost of consciousness. He was immediately brought to
Butuan District hospital and was then eventually referred to Northern Mindanao Medical
Center last August 20, 2010 around 2am due to the same complaints.

Family Health-Illness History:

The patient is a father of 7 children (21, 19, 18, 16, 14, 1 and 10 years old) of
which all are on a good health condition as stated by the wife who in all fairness seems
to be in a good health and has no complaints regarding her health. Hypertension, as
told by Mrs. Lasco, was observed to be a prevalent condition in the patient’s kin on his
mother’s side.

Vital signs:

The patient has the following vital signs during Assessment day last August 23, 2010,
of: BP: 150/100mmHg, PR: 85bpm, RR: 28cpm, T: 36.8c and 02 sat of 96%

And on the second day of Assessment last August 24, 2010 of: BP: 150/100mmHg, PR:
84bpm RR: 24cpm, T: 26.7c and 02 sat of 97%

Cognitive-Perception (while confined):

His wife said that he speaks bolanon because he was born at bohol. He was not able to
answers our questions because he was unconscious upon the assessment.

Role-Relationship Pattern (while confined)

He’s married for almost 10 years already. He He is the bread winner of their
family and he is able to support their needs. They where very worried on the condition
of their father.

Nutrition-Metabolic Pattern (while confined)

The patient is on NGT feeding with 2,100 kcal/day with aspiration precaution
CHO260, CHM105, fat 70grams. There were no reports of vomiting and has a weight
loss of 50%.

Elimination pattern (hospitalization)

The patient defecates daily. He was on an indwelling catheter.

Activities of daily living (ADL)

The patient is a farmer. Thus, the kind of work he does involves a lot of physically
challenging activities. This then serves as his daily exercise.

Activities Tolerance-Exercise pattern (while confined)

As the patient was suffering from hemiparesia, he is intolerant in doing exercises.

Values – Belief Pattern

He is Roman Catholic together with their children but his wife is a member of another
religious affiliation “kristohanon”. Still they have a strong faith in God.
Physical Assessment
1st day of assessment 2nd day of assessment

Head
Facial Movements Symmetrical Symmetrical

Fontanels Closed Closed

Hair Fine Fine

Scalp Clean Clean

Eyes
Lids Symmetrical Symmetrical

Periorbital Region Intact/full Intact/full

Conjunctiva Pink Pink

Sclera Icteric icteric

Reaction to light R- Brisk R- Brisk

L- Brisk L- Brisk

Reaction to Uniform constriction / Uniform constriction /

accommodation Convergence Convergence

Nose
Septum Midline Midline

Mucosa Pinkish Pinkish

Patency Both patent Both patent

Gross Smell Normal/symmetrical Normal/symmetrical

Sinuses Non-tender Non-tender

Ears
External Pinnae Normoset; Symmetrical Normoset; Symmetrical

Tympanic Membrane Intact Intact

Gross Hearing Not assessed normal

Orientation Not assessed Oriented

Appropriate not asessed Cooperative;

behavior/communication Responsive

Level of Consciousness unconscious drowsy

Emotional State Not asessed Calm

Skin
General Color Pallor Pallor

Texture Smooth Smooth

Turgor Firm Firm

Temperature Cool Cool

Moisture Dry Dry

Mouth
Lips Pallor Pallor

Mucosa Pinkish Pinkish

Tongue Midline Midline

Teeth Dentures Dentures

Gums Pinkish Pinkish

Neck
Trachea Midline Midline

Thyroids Non-palpable Non-palpable

Others Left sided weakness Left sided weakness

Pharynx
Uvula Midline Midline

Tonsils Not Inflamed Not Inflamed

Posterior Pharynx Not Inflamed Not Inflamed

Mucosa Pinkish Pinkish

Abdomen
Configuration Symmetrical Symmetrical

Bowel Sounds Normoactive Normoactive

Percussion Tympanitic Tympanitic

Back and Extremities

Range of Motion Decreased at left side Decreased at left side

Muscle tone and Weakness at left side Weakness at left side

strength

Spine Kyphosis kyphosis

Cardiovascular Status
Precordial Area Flat Flat

Peripheral Pulses Weak, pulse Weak, pulse

Capillary Refill 4 seconds 4 seconds

Respiratory Status
Breathing Pattern Tachypnea tachypnea

Shape of Chest AP:1 L:2 AP:1 L:2

Lung Expansion Symmetrical Symmetrical

Vocal/Tactile Fremitus Symmetrical Symmetrical

Percussion Resonant Resonant

Breath Sounds rhonchi rhonchi

Cough Non-productive Non-productive

Reproductive Status
Prostate Normal normal

Penis No discharge No discharge

Scrotum Equal; nontender Equal; nontender

LABORATORY RESULTS
Urinalysis

Date: August 28, 2010

Color: Yellow Protein: (-)

pH: 7.0 Mucous Threads: few
Clarity: clear Pus cells (WBC): 1-2
Odor: --- RBC: 2-3
SpGr: 1.010 Bacteria: ---
Glucose: (-)

Urinalysis

Date: August 27, 2010

Color: Yellow Protein: trace

pH: 6.6 Mucous Threads: few
Clarity: hazy Pus cells (WBC): plenty
Odor: --- RBC: plenty
SpGr: 1.030 Bacteria: ---
Glucose: (-)

August 28, 2010

HEMATOLOGY RESULTS

LABORATORY
EXAM RESULT NORMAL VALUE INTERPRETATION

W.B.C. 5.0 5.0 – 10.0 10^3/UL Within normal range

RBC 8.6 4.2 – 5.4 10^6/UL Increased number of RBCs indicates

pulmonary diseases
Hgb 10.4 12.0 – 16.0 Decreased tissue perfusion
10^6/UL
Hct 31.7 37.0 – 47.0% Less than normal ; dehydration, anemia
include vitamin or mineral deficiencies,
recent bleeding and malignancies.
MCV 90.6 82.0 – 98.0 fl Within normal range

MCH 29.7 27.0 – 31.0 fg Within normal range

MCHC 32.8 31.5 – 35.0 g/dL Within normal range

RDW-CV 13.6 12.0 – 17.0% Within normal range

PDW 9.9 9.0 – 16.0 Within normal range

MDV 9.1 8.0 – 12.0 Within normal range

Differential Count
Laboratory Result Normal value Interpretation
Exam
Lymphocyte 25.8 17.4-48.2 Within normal range
(%)
Neutrophils (%) 62.6 43.4-76.2 Within normal range
Monocytes (%) 10.3 4.5-10.5 Within normal range
Eosinophils (%) 1.3 1.0-3.0 Within normal range
Basophils (%) 0.0 0.0-2.0 Within normal range
Platelets 262 10^3/uL 150-400 Within normal range

August 28, 2010

Blood Sugar 108.2 60-110

Creatinine 1.02 0.60-1.30
BUN 37.6 4.5-23.5
potassium 4.0 3.4-5.4
sodium 142.6 134.0-149.0

August 22, 2010

ARTERIAL BLOOD GAS
Ph 7.363 7.35-7.45
pcO2 26.3 35-45mmHg
pO2 112 80-105mmHg
HCO3 15.0 22-26mEq/L
BE ecf -10 -2 to +3 mEq/L
O2 sat 98% 95-98%

CT Scan Report
August 25, 2010

Result:

Multiple axial tomographic sections of the head from the skull base to vertex without
contrast obtained revealing the following:

There is faint hyperdense collection in the right basal ganglia 3.0 x 5.5 x 2.3 cm
(approximately 20 ml) with perilesional edema. There is effacement of the right lateral
ventricles with associated shift of the midline structures by about1.0 cm to the left. The
right sylvian tissue is likewise effaced, Mild mass effect is noted in the right side
midbrain and pons.

Hypodense focus is noted in the left frontal periventricular region. Tiny

hypodensities are seen in the right centrum semiovale and in the posterior lining of the
left internal capsule.

The posterior fossa structures are unremarkable.

There is layering density in the sphenoid sinuses. The rest of the paranasal
sinuses are well aerated.
 Opacities are seen in the mastoid air cells, bilaterally. The orbits and sella are
unremarkable. The visualized osseous structures are unremarkable.

Impression:
Acute to Subacute hemorrhage, right basal ganglia
Subfalcinc herniation to the left
Ischemic infarction, left frontal perixeventricular
Lacunar infarction, right centrum semiovale and posterior of the left
Sphenoid sinusitis
Mastoiditis, bilateral

III. Anatomy and Physiology

A. Narrative:

Renal System Anatomy and Physiology

Kidneys
 The kidneys regulate the volume and concentration of fluids in the body by

producing urine. Urine is produced in a process called glomerular filtration, which is the

removal of waste products, minerals, and water from the blood. The kidneys maintain

the volume and concentration of urine by filtering waste products and reabsorbing

useful substances and water from the blood.

The kidneys also perform the following functions:

• Detoxify harmful substances (e.g., free radicals, drugs)

• Increase the absorption of calcium by producing calcitriol (form of vitamin D)

• Produce erythropoietin (hormone that stimulates red blood cell production in the

bone marrow)

• Secrete renin (hormone that regulates blood pressure and electrolyte balance)

The kidneys are a pair of bean-shaped organs located below the ribs near the middle of

the back. They are protected by three layers of connective tissue: the renal fascia

(fibrous membrane) surrounds the kidney and binds the organ to the abdominal wall;

the adipose capsule (layer of fat) cushions the kidney; and the renal capsule (fibrous

sac) surrounds the kidney and protects it from trauma and infection.

Renal Artery

The renal artery enters the kidney and the renal vein emerges from the kidney at an
indentation in the middle of the organ called the hilum. The renal artery supplies oxygen

and blood to the kidney. Blood flows from the kidney through the renal vein after waste

products have been removed.

Formation and Elimination of Urine

The formation of urine occurs in the basic units of the kidney, called nephrons. Each

human kidney contains over 1 million nephrons. Nephrons consist of a network of

capillaries (called a glomerulus), a renal tubule, and a membrane that surrounds the

glomerulus and functions as a filter (called Bowman's capsule). The glomeruli are

where urine production begins. Urine formation occurs in the renal tubules, which

travel from the outer tissue of the kidney (called the cortex), to the inner tissue (called

the medulla), and return to the cortex.

Extensions of the cortex project into the medulla and divide the tissue into renal

pyramids. The renal pyramids extend into funnel-like extensions (called calyces), where

the collection of urine occurs. Minor calyces merge to form major calyces and major

calyces merge to form the renal pelvis, the upper portion of the ureter.

Each section of the renal tubule performs a different function. As the tube leads away

from Bowman's capsule into the cortex, it forms the proximal convoluted (highly coiled)

tubule. In this section, waste products and toxic substances (e.g., ammonia, nicotine)

are forced out of the blood through a permeable membrane and useful substances

(e.g., glucose, amino acids, vitamins, minerals) are reabsorbed.

Urine then travels through the loop of Henle, a long U-shaped extension of the proximal

convoluted tubule. It consists of a descending limb and an ascending limb. Some

sections of the loop are permeable to water and impermeable to substances in the urine

(e.g., salt, ammonia), and some sections are impermeable to water and permeable to

other substances.
The next section is the distal convoluted tubule. Normally, this section is water

permeable. Substances that remain in the urine are reabsorbed, increasing the

concentration of the urine. After passing through the distal convoluted tubule, the urine

consists almost entirely of waste products. Most of the water and other useful

substances have been reabsorbed.

Next, urine enters the collecting tubule. Urine from several nephrons empties into each

collecting tubule. These tubules form the calyces, and the calyces form the renal pelvis

(upper portion of the ureter). Urine travels from the kidneys through the ureters to the

bladder, where it is stored until it is eliminated from the body through the urethra.

PATHOPHYSIOLOGY OF LUPUS NEPHRITIS

Narrative

The pathophysiology of SLE and LN is a complex process, involving at least one

environmental stimulus acting on a genetically susceptible host. Many environmental

factors, including infectious diseases, estrogens, heavy metals, silica dust, and tobacco

smoke, have been implicated as increasing the risks for developing SLE (Cooper et al.,

1998). LN is a glomerular inflammatory process that frequently manifests as proteinuria,

hematuria, azotemia, hypertension, or urine sediment consisting of red blood cell casts,

waxy casts, and cellular debris, or any combination of these. However, asymptomatic

proteinuria and hematuria are frequent initial manifestations that are often overlooked or

misinterpreted upon physical examination. LN frequently is not diagnosed until the

nephrotic syndrome emerges. Renal insufficiency is a frequent outcome, but it generally

is not an early manifestation because unaffected nephrons often compensate for

damage to injured nephrons (Greenberg, 1998).

A brief review of glomerular structure is necessary before discussing the LN process

(see Figure 1). The glomerulus is actually a tuft of capillaries consisting of three layers

of cells. The innermost layer of fenestrated (porous) endothelial cells is adjacent to the

middle negatively charged glomerular basement membrane, the primary barrier to

filtration. Negatively charged substances, such as most plasma proteins including

albumin, cannot normally filter through the glomerular basement membrane. Positively

charged and neutral substances may filter easily, depending on their molecular size and

shape. The outer capillary wall, also adjacent to the glomerular basement membrane, is

composed of podocytes, a type of epithelial cells. A Bowman's capsule surrounds each

glomerular tuft. Mesangial cells between the glomerular capillaries connect them to

each other (Greenberg, 1998).

SLE is characterized by the production of autoantibodies and the deposition of immune

complexes (Mohan & Datta, 1995). Autoantibodies occur in response to and interact

with a host's own tissues and are recognized as foreign by the host's immune system.

Immune complexes, which can circulate in the blood or precipitate in tissues, are

aggregations that always include antigen and antibody and may also include

complement proteins. Activated complement proteins are destructive to cells identified

and marked by antibodies as foreign (Greenberg, 1998; Sim, 1993).

The first discernible abnormality of SLE is hyperactivity of B lymphocytes as a result of

either intrinsic B lymphocyte defects or defects in helper T lymphocytes (CD4 cells) that

regulate B lymphocyte function. The excessive activation of B lymphocytes, by factors

such as viruses, bacteria, nucleic acids, and estrogens, results in production of

autoantibodies with subsequent immune complex formation (Cooper et al., 1998). In

SLE, B lymphocytes spontaneously secrete increased amounts of antibodies. Thus,

abnormal B lymphocytes can contribute negatively to an already taxed or deficient

immunologic system, transforming SLE from an inactive to an active stares. Many of the

autoantibodies produced react with a multitude of subcellular antigens, including

double-stranded DNA (dsDNA, i.e., native DNA that has two helical strands of nucleic

acids bound together), ribonucleoprotein (RNP, i.e., a combination of RNA and protein),

phospholipids, and other nuclear and cytoplasmic proteins (Mohan & Datta, 1995).

Activated B lymphocytes direct humoral immune responses. Antibody deposition in itself

is not sufficient to induce renal injury. However, when antibodies bind with antigens and

form immune complexes, leukocyte infiltration and glomerular cell proliferation are

initiated and the complement protein cascade is activated (Greenberg, 1998; Sim 1993).

Glomerular injury is then induced either by recruitment of inflammatory cells (e.g.,

neutrophils, monocytes, macrophages) to the site or production of oxidants, proteases,

prostaglandins, and cytokines. These substances alter the permeability and structure of

the glomemlar basement membrane. The net result of these changes is proteinuria

(Greenberg, 1998; Pollak & Pirani, 1997).The chronic deposition and formation of

immune complexes are primary mediators in the pathogenesis of vascular, glomerular,

mesangial, tubule, and interstitial immune deposits. Glomemlar capillaries are

particularly predisposed to deposition of immune complexes. Immune complex

deposition in glomerular capillaries is influenced by the following: rate of glomerular

blood flow; the efficiency of systemic phagocyte clearance of immune complexes; the

rate of immune complex production; the size and charge of immune complexes; the

strength with which immune complexes are bound; and glomerular capillary

hemodynamic factors such as hydraulic pressure, basement membrane permeability,

and previous glomerular damage (Mohan & Datta, 1995).

Normally, B and T lymphocyte clones that can potentially react against the host's own

body cells are deleted through apoptosis (i.e., programmed cell death) (Fournie & Druet,

1996). SLE patients have abnormal apoptosis such that the life span of activated B cells

is prolonged, and autoantibody levels are increased. Increased numbers of

autoantibodies are then available for the production of greater amounts of immune

complexes. Glomerular mesangial cells provide the predominant means for removing

immune complexes by phagocytosis. However, immune complex deposition and

endocapillary hypercellularity (i.e., proliferation of native cells or infiltration of tissue by

neutrophils, monocytes, T lymphocytes, and platelets) negatively affect the

mesangium's ability to rid the kidneys of immune complex deposits (Berden, 1997;

Greenberg, 1998).

The emergence of anti-dsDNA antibodies is the hallmark of SLE and marks the final

common pathway through which various causative mechanisms can act to induce renal

damage. Anti-dsDNA antibodies can induce organ damage by targeting antigens directly

or indirectly by first forming immune complexes with nucleosomes (complexes of

histone in cell nuclei) and then being deposited onto negatively charged sites (e.g.,

glomerular basement membrane) (Mohan & Datta, 1995). Berden (1997) theorizes that

because systemically-released nucleosomes are the primary targets of autoantibodies,

they can contribute to the evolution of tissue lesions, the production of anti-dsDNA

antibodies, and the induction of autoimmunity. These are the changes that account for

the myriad clinical manifestations possible with SLE.

Qualitative and quantitative changes in nucleosomes may be a consequence of

disturbed apoptosis. First, greater numbers of nucleosomes are released into the

circulation as more cells are destroyed (Berden, 1997). Second, toxic oxygen radicals

present in the circulation as a result of complement activation can structurally alter

nucleosomes (Sim, 1993). Third, the nucleosomal structural alterations have the

potential to transform helper T lymphocytes in such a way that they cannot distinguish

self from non-self antibodies (Berden, 1997). Loss of self-tolerance by helper T

lymphocytes can then lead to B lymphocyte hyperactivity and the cascade of events

characteristic of SLE.

Thrombi occur frequently in active LN. Endothelial cell damage activates the
coagulation system and thrombi formation. Platelets also are involved in the

development of lesions through their association with fibrin in the formation of clots.

Circulating coagulant (anti-phospholipid antibodies) and abnormal fibrinolysis are

present in patients exhibiting systemic venous and arteriolar thrombi as well as

glomerular capillary thrombi.

The World Health Organization (WHO) has described a classification system with six

categories of renal pathology with SLE. The categories are characterized by

inflammation, cellular proliferation, and membrane thickening. Late in the course of

SLE, sclerosis of blood vessels or fibrosis of tissues may be seen. Physical properties

of deposited antibodies or immune complexes, dynamics of tissue deposition and

clearance, cytokines, and genetically determined differences in host reactivity are

responsible for differences in pathology observed in SLE and for the factors responsible

for disease progression (Cameron, 1999).

Schematic Diagram:
DRUG STUDY

NURSING
DRUG ORDER MECHANISM OF INDICATIONS CONTRAINDICATIONS ADVERSE EFFECTS OF RESPONSIBILITIES/
(Generic name, brand ACTION THE DRUG PRECAUTIONS
name, classification,
dosage, route,
frequency)

Generic Name: inhibits cell-wall Prophylaxis against Hypersensitivity to Diarrhea Missed dose should be

Ceftriaxone synthesis, infection secondary to cephalosporins, serious Nausea taken as soon as

promoting osmotic depressed immune hypersensitivity to Vomiting possible unless almost

Classification: instability; usually system due to SLE penicillins. Cramps time for next dose

anti-infective ; bactericidal Pseudolithiasis

third generation Rashes Advise patient to report

cephalosporin Urticaria sign of superinfection and

Hemolytic anemia allergy

Dosage: 1gm Phlebitis at IV site Advise patient to notify

Route: IVTT Allergic reactions health care provider if

Frequency: q 24h including anaphylaxis and fever and diarrhea

serum sickness develops

DRUG STUDY
NURSING
DRUG ORDER MECHANISM OF CONTRAINDICATIONS ADVERSE EFFECTS RESPONSIBILITIES/
(Generic name, brand ACTION OF THE DRUG PRECAUTIONS
name, classification, INDICATIONS
dosage, route,
frequency)
Block the conversion of
• Monitor vital signs as
Generic Name: angiotensin I to Alone or with other Hypersensitivity. Dizziness, Fatigue
suggested and necessary
Perindopril vasoconstrictor agents in the Cross sensitivty Headache, Insomnia • Caution patient to avoid salt

Angiotensin II. ACE management of among other ACE Weakness, Cough substitutes or foods containing
high levels of Potassium or
Classification: also inactivates the hypertension inhibitors may occur. Hypotension
sodium unless directed by
Antihypertensives; vasodilator bradykinin Pregnancy and Angina pectoris health care professional

ACE inhibitors and other vasodilatory angioedema Tachycardia • Caution patient to change
positions slowly to minimize
prostaglandins. ACE Taste disturbances
hypotension, particularly after
Dosage: 10gm ; 1 tab inhibitors also increase Anorexia initial dose

Route: po plasma rennin levels Diarrhea ; Nausea • Encourage patient to comply

with additional interventions
Frequency: OD and reduce aldosterone Proteinuria
for hypertension
levels. Net result is Hyperkalemia • May cause dizziness, safety
systemic vasodilation Angioedema; fever precautions should be
observed
DRUG STUDY

NURSING RESPONSIBILITIES/
DRUG ORDER MECHANISM OF CONTRAINDICATIONS ADVERSE PRECAUTIONS
(Generic name, brand ACTION EFFECTS OF
name, classification, INDICATIONS THE DRUG
dosage, route,
frequency)
• Monitor vital signs as

Generic Name: Inhibits the transport of Alone or with Hypersensitivity Dizziness, Fatigue suggested and necessary
• Monitor intake and output
Amlodipine calcium into myocardial other agents in Blood Pressure of Headache,
• Caution patient to avoid salt
smooth muscle cells, the management <90 mmHg Nausea, peripheral substitutes or foods containing
Classification: resulting in inhibition of of hypertension edema, angina, high levels of Potassium or
sodium unless directed by health
Antihypertensives; excitation-contraction bradycardia,
care professional
calcium channel coupling and hypotension, • Encourage patient to comply
blockers subsequent contraction. palpitations, with additional interventions for
hypertension
Systemic vasodilation gingival
• May cause dizziness, safety
Dosage: 10mg resulting in decreased hyperplasia, precautions should be observed
Route: po blood pressure flushing • Caution to wear protective
clothing and use of sunscreen to
Frequency: OD
prevent photosensitivity
reactions
DRUG STUDY

NURSING
DRUG ORDER MECHANISM OF CONTRAINDICATIONS ADVERSE EFFECTS OF RESPONSIBILITIES/
(Generic name, brand ACTION THE DRUG PRECAUTIONS
INDICATIONS
name, classification,
dosage, route,
frequency)

• Assess fluid status

Generic Name: Inhibits the reabsorption of Edema due
Furosemide sodium and chloride from
the loop of Henle and
Classification: distal renal tubule.
Loop diuretics Increases renal excretion
of water, sodium, chloride,
Dosage: 40mg magnesium, hydrogen and
Route: IVTT calcium. May have renal
Frequency: q12 and peripheral
vasodilatory effects.
Hypersensitivity Dizziness, encephalopathy,
• Monitor intake and output
Headache, insomnia,
to renal Cross sensitivity with • Monitor vital signs
nervousness, hearing loss,
disease. thiazides and • Caution patient to change
tinitinus, hypotension,
positions slowly to minimize
hypertension sulfonamides will constipation, diarrhea, dry
orthostatic hypotension
mouth, dyspepsia, nausea,
occur. Pre-existing
• Encourage patient to comply
vomiting, excessive
electrolyte with additional interventions
urination, hyperglycemia,
for hypertension
imbalance, hepatic dehydration, hypochloremia,
hypokalemia, • May cause dizziness, safety
coma, or anuria.
hypomagnesemia, precautions should be
observed
hyponatremia, hypovolemia,
metabolic alkalosis, • Caution to wear protective

hyperurecemia, increased clothing and use of sunscreen

Effectiveness persists in
BU, muscle cramos, to prevent photosensitivity
impaired renal function. reactions
myalgia
DRUG STUDY
NURSING RESPONSIBILITIES/
DRUG ORDER MECHANISM OF CONTRAINDICATIONS ADVERSE EFFECTS OF PRECAUTIONS
(Generic name, brand ACTION THE DRUG
name, classification, INDICATIONS
dosage, route,
frequency)

• Assess fluid balance and signs

Generic Name: Acts as an Management of Metabolic or respiratory Edema, flatulence,
of acidosis
gastric distention,
Sodium bicarbonate alkallanizing agent metabolic alkalosis. Hypocalcemia • Monitor urine pH
metabolic alkalosis,
by releasing acidosis As an antidote for • Administer with a full glass of
hypernatremia,
water
Classification: carbonate ions ingesting strong acid hypokaemia, sodium and
• Missed dose should be taken
water retention, tetany
Anti-ulcer ; minerals as soon as possible unless
alkalanizing agent Severe abdominal pain of almost time for next dose
• Advise patient to not take milk
unknown cause
products concurrently with this
Dosage: 2 tabs
medication. This may rsult to
Route: po renal calculi
• Monitor serum electrolyte levels
Frequency: t.i.d.
• Review symptoms of lectrolyte
imbalance and advise patient to
notify health care provider if
these symptoms occurs
DRUG STUDY
NURSING
DRUG ORDER MECHANISM OF ACTION CONTRAINDICATIONS ADVERSE EFFECTS OF RESPONSIBILITIES/
(Generic name, brand THE DRUG PRECAUTIONS
INDICATIONS
name, classification,
dosage, route,
frequency)

Generic Name: Essential for nervous,
Calcium carbonate muscular and skeletal
systems. Maintain cell
Treatment Hypercalcemia. CNS: tingling sensations, • Double check that you are
giving the correct form of
and Renal calculi. CV: mild drop in blood
calcium; resuscitation cart
prevention of Venticular fibrillation. pressure, vasodilation, may contain both calcium

Classification: membrane and capillary hypocalcemia bradycardia, cardiac arrest gluconate and calcium
chloride
Mineral or electrolyte permeability. Act as an with rapid IV injection
• Monitor calcium levels
replacements and activator in the transmission GI: irritation, constipation, frequently

supplements of nerve impulses and chalky taste, hemorrhage, • Report abnormalities

• Review methods of
contraction of the cardiac, nausea, vomiting, thirst and
preventing constipatient and
Dosage: 1 tab skeletal and smooth abdominal pain endorse his to patient as his
Route: po muscle. Essential for bone GU: polyuria, renal calculi medication may cause
constipation
Frequency: t.i.d. formation and blood Metabolic: hypercalcemia
• Encourage to have adequate
coagulant.
vitamin D intake
• Avoid milk products
DRUG STUDY

NURSING
DRUG ORDER MECHANISM OF CONTRAINDICATIONS ADVERSE EFFECTS OF RESPONSIBILITIES/
(Generic name, brand ACTION THE DRUG PRECAUTIONS
name, classification, INDICATIONS
dosage, route,
frequency)

Generic Name: Supress inflammation Autoimmune Active untreated Depression, euphoria, • Monitor vital signs
• Monitor intake and output
Hydrocortisone and the normal disorder – infection. Lactation. hypertension, anorexia,
• Stress importance of proper
immune response Systemic Lupus Tartrazine acne, decreased wound hygiene such as
Classification: Erythematosus hypersensitivity or healing, ecchymoses, handwashing
• Maintain a clean environment
corticosteroid intolerance. fragility, hirsutism,
to prevent infection
petechiae, adrenal

Dosage: 100 mg sufficiency, muscle wasting,

Route: IVTT osteoprosis, adrenal

Frequency: q6h suppresion, cushingoid

appearance, increased

susceptibility to infection,

headache

NURSING CARE PLAN

 ASSESSMENT DATA GOALS AND NURSING INTERVENTIONS AND EVALUATION
(Subjective & Objective Cues) NURSING DIAGNOSIS OBJECTIVES RATIONALE
(Problem and Etiology)
*Assess pain characteristics for
Subjective: Acute Pain related to Following 8-hours of baseline data Goals were met. The
biological injuring agents nursing intervention, * Observe or monitor signs and client was able to
“sakit akong koto-koto.” As secondary to disease client will be able to: symptoms associated with pain, verbalize and
verbalized by the client condition of systemic lupus such as BP, heart rate, temperature, understand other ways
erythematosus a. Report relief from color and moisture of skin, of being relieved from
Objective: pain with a scale restlessness, and ability to focus. pain. She was able to
of 3/10 Some people deny the experience of demonstrate proper
Facial grimace b. Verbalize non- pain when it is present. Attention to breathing techniques
pharmacologic associated signs may help the nurse to facilitate relaxation.
Muscle guarding methods that in evaluating pain.
provide relief * Eliminate additional stressors or Pain scale: 3/10
restlessness c. Demonstrate use sources of discomfort whenever
of relaxation skills possible.
Pain Scale: 7/10 and diversional * Provide rest periods to facilitate
activities comfort, sleep, and relaxation.
1. Nonpharmacological methods
include the following:
o Distraction techniques Heighten
one’s concentration upon
nonpainful stimuli to decrease one’s
awareness and experience of pain.
Some methods are breathing
modifications and nerve stimulation.
o Relaxation exercises Techniques
are used to bring about a state of
physical and mental awareness and
tranquility. The goal of these
techniques is to reduce tension,
subsequently reducing pain.

ASSESSMENT DATA
(Subjective & Objective Cues)
Subjective:
“manglagom juhd nah siya
pagtusukan sa dagom para
magkuha ug dugo…” As
verbalized by the client
Objective:
Hematomas on punctured sites
Skin crusts / unhealed wound on
lower extremities
Skin discolorations
NURSING CARE PLAN
GOALS AND NURSING INTERVENTIONS AND EVALUATION
NURSING DIAGNOSIS OBJECTIVES RATIONALE
(Problem and Etiology)
Impaired skin integrity After 8-hours of nursing Goals were met. The
related to immunological interventions, client will o Encourage implementation and patient demonstrated
deficit secondary to lupus be able to: posting of a turning schedule, understanding on her
nphritis restricting time in one position to 2 course of treatment
• Participate in hours or less and customizing the
prevention measures schedule to patient’s routine and
and treatment program caregiver’s needs.
• Verbalize
understanding on the * Encourage ambulation if patient is
process and overt able.
symptoms of the
disease * Clean, dry, and moisturize skin,
especially over bony prominences,
twice daily or as indicated by
incontinence or sweating.
• Encourage adequate nutrition
and hydration:
• Instruct on proper wound care
and application of pressure
right after puncture or
withdrawal of blood sample

ASSESSMENT DATA
(Subjective & Objective Cues)
Subjective:
“sige lang ko ug ihi pero
ginagmay ra…” As verbalized
by the client
Objective:
Urine output = 50-100 cc
NURSING DIAGNOSIS
(Problem and Etiology)
Impaired urinary elimination
related to disruptive function
of the kidneys secondary to
lupus nephritis
NURSING CARE PLAN
GOALS AND NURSING INTERVENTIONS AND EVALUATION
OBJECTIVES RATIONALE
Documented urine color
After 8-hours of nursing and characteristic, intake Goals were met. The
interventions, client will and output, and pt daily client was able to
be able to: weight. Reported any verbalized
changes for Observed voiding understanding on her
• Verbalize pattern fro Urine characteristics condition and how she
understanding of help notifying diagnosis can help to alleviate it.
condition
• Specify causative Discuss with patient the nature of
factors her condition

ASSESSMENT DATA
(Subjective & Objective Cues)
Subjective:
“manglagom juhd nah siya
pagtusukan sa dagom para
magkuha ug dugo…” As
verbalized by the client
Objective:
Hematomas on punctured sites
Skin crusts / unhealed wound on
lower extremities
Skin discolorations
NURSING CARE PLAN
GOALS AND NURSING INTERVENTIONS AND EVALUATION
NURSING DIAGNOSIS OBJECTIVES RATIONALE
(Problem and Etiology)
Impaired skin integrity After 8-hours of nursing Goals were met. The
related to immunological interventions, client will client was able to
deficit secondary to lupus be able to: verbalize and
nephritis understand other ways
• Participate in of being relieved from
prevention measures pain. She was able to
and treatment program demonstrate proper
• Verbalize breathing techniques
understanding on the to facilitate relaxation.
process and overt
symptoms of the Pain scale: 3/10
disease
VII. Discharge Planning
M (Medications) - Follow strict compliance to the medications as prescribed by the
attending physician following the right medication, dosage, time
and route.
- Provide a well organized plan for administering and taking in of
medication.

E (Exercise) - Expose the self to the sun because sunlight provide natural
source of vitamin D, for only short periods, beginning with 3-5
minutes the first day, a little more the next day, and so on up to 15-
20 minutes at a time.
- Short walks are encouraged but not to the extent of fatigue

T (Treatment) - Seek medical attention if any unusualities happens.

H (Hygiene) - Self-care must be done to promote proper hygiene and well-

being. Daily bathing is necessary

O (Outpatient) - Plan a follow-up visit one week after being discharged or if there
are any frequent recurrences of abdominal pain and other problems

D (Diet) - Diet as tolerated. A full diet is required with provision and

adherence to a healthy diet/ eating of nutritious foodd

S (Spirituality) - Strengthen spirituality by allowing the significant others to spend

time in prayer.
- Go to church every Sunday
 Learning Experience

This rotation was awesome. I learned a lot and I’m very happy about the
things that happened during the rotation. I felt as if I was able to really help other
people, the patent and the watchers. The experience enabled me to realize the realities
of life. I felt very fortunate of the things that I have.

Furthermore, I am very contented with everything. More than contented

even, of the learning I had on this rotation. This case study had made me realize the
importance of punctuality and the trouble of procrastination. I’ll do better soon. Mistakes
does not have to end as is, we learn from it. It would make us realize how we should do
better next time.
XII. Bibliography

Deglin, J.H and Vallerand, A.H. David’s drug Guide for Nurses. 10th ed. F.A. Davis
company. Philadelphia, Pennsylvania. 2003.

Black, Joyce E. et al. Medical-Surgical Nursing: Clinical Management for Continuity of

Care. 5th ed. Merriam Webster Bookstore, Inc. Philippines. 1997.

Doenges, Marilynn E. et al. Nursing Care Plans: Guidelines for Individualizing Patient
Care. 6th ed. F.A. Davis Company. Bangkok, Thailand. 2002.

Smeltzer, Suzanne E. et al. Textbook of Medical Surgical Nursing. 10th ed. Lippincot
Williams & Wilkins. Springhouse. 2004.

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