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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 extraknowledge 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 BIRTHDAY: March 5, 1960 SEX: Male ADDRESS: Butuan, Agusan del Norte INFORMANT: Wife ADMISSION: Date: August 20, 2010 TIME: 2:00 AM AGE: 50-years-old BIRTHPLACE: Tagbilaran, Bohol RELIGION: Kristohanon

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

he is intolerant in doing exercises. Elimination pattern (hospitalization) The patient defecates daily.100 kcal/day with aspiration precaution CHO260. They where very worried on the condition of their father. .family and he is able to support their needs. This then serves as his daily exercise. fat 70grams. Thus. Activities Tolerance-Exercise pattern (while confined) As the patient was suffering from hemiparesia. Still they have a strong faith in God. There were no reports of vomiting and has a weight loss of 50%. Nutrition-Metabolic Pattern (while confined) The patient is on NGT feeding with 2. CHM105. Values – Belief Pattern He is Roman Catholic together with their children but his wife is a member of another religious affiliation “kristohanon”. He was on an indwelling catheter. Activities of daily living (ADL) The patient is a farmer. the kind of work he does involves a lot of physically challenging activities.

Midline Pinkish Both patent Normal/symmetrical Non-tender Midline Pinkish Both patent Normal/symmetrical Non-tender to Uniform constriction Convergence Symmetrical Intact/full Pink icteric R. Symmetrical Intact normal Oriented Cooperative.Brisk L.Physical Assessment 1st day of assessment Head Facial Movements Fontanels Hair Scalp Eyes Lids Periorbital Region Conjunctiva Sclera Reaction to light Symmetrical Intact/full Pink Icteric R.Brisk Reaction accommodation Nose Septum Mucosa Patency Gross Smell Sinuses Ears External Pinnae Tympanic Membrane Gross Hearing Orientation Appropriate Normoset.Brisk / Uniform constriction Convergence / Symmetrical Closed Fine Clean Symmetrical Closed Fine Clean 2nd day of assessment .Brisk L. Symmetrical Intact Not assessed Not assessed not asessed Normoset.

behavior/communication Level of Consciousness Emotional State Skin General Color Texture Turgor Temperature Moisture Mouth Lips Mucosa Tongue Teeth Gums Neck Trachea Thyroids Others Pharynx Uvula Tonsils Posterior Pharynx Mucosa Midline Not Inflamed Not Inflamed Pinkish Midline Non-palpable Left sided weakness Pallor Pinkish Midline Dentures Pinkish Pallor Smooth Firm Cool Dry unconscious Not asessed Responsive drowsy Calm Pallor Smooth Firm Cool Dry Pallor Pinkish Midline Dentures Pinkish Midline Non-palpable Left sided weakness Midline Not Inflamed Not Inflamed Pinkish Abdomen .

Configuration Bowel Sounds Percussion Back and Extremities Range of Motion Muscle strength Spine Cardiovascular Status Precordial Area Peripheral Pulses Capillary Refill Respiratory Status Breathing Pattern Shape of Chest Lung Expansion Vocal/Tactile Fremitus Percussion Breath Sounds Cough Reproductive Status Prostate Penis Scrotum tone Symmetrical Normoactive Tympanitic Symmetrical Normoactive Tympanitic Decreased at left side and Weakness at left side Decreased at left side Weakness at left side Kyphosis kyphosis Flat Weak. pulse 4 seconds Flat Weak. pulse 4 seconds Tachypnea AP:1 L:2 Symmetrical Symmetrical Resonant rhonchi Non-productive tachypnea AP:1 L:2 Symmetrical Symmetrical Resonant rhonchi Non-productive Normal No discharge Equal. nontender LABORATORY RESULTS . nontender normal No discharge Equal.

0 – 16. RBC Hgb Hct MCV MCH MCHC RDW-CV PDW MDV RESULT NORMAL VALUE 5.0 10^6/UL 37.9 9.4 31.0 – 16. dehydration.5 – 35. Within normal range Within normal range Within normal range Within normal range Within normal range Within normal range 5.Urinalysis Date: August 28.B.0 – 17.0% 9.6 10. 2010 Color: pH: Clarity: Odor: SpGr: Glucose: Urinalysis Date: August 27. recent bleeding and malignancies.0 8.0 – 10.030 (-) Protein: Mucous Threads: Pus cells (WBC): RBC: Bacteria: trace few plenty plenty --- INTERPRETATION Within normal range Increased number of RBCs indicates pulmonary diseases Decreased tissue perfusion Less than normal .7 32.8 13. 2010 Color: pH: Clarity: Odor: SpGr: Glucose: August 28.4 10^6/UL 12.0 fl 27.6 hazy --1. 2010 HEMATOLOGY RESULTS LABORATORY EXAM W.6 29.0 – 31.0 – 47.0 – 98.6 9.0% 82.0 10^3/UL 4.7 Yellow 7.0 fg 31.0 g/dL 12.2 – 5.0 90.0 – 12.1 Differential Count .010 (-) Protein: Mucous Threads: Pus cells (WBC): RBC: Bacteria: (-) few 1-2 2-3 --- Yellow 6.0 8. anemia include vitamin or mineral deficiencies.C.0 clear --1.

4-76. The rest of the paranasal sinuses are well aerated.0 150-400 Interpretation Within normal range Within normal range Within normal range Within normal range Within normal range Within normal range 108.5 3.2 43.0 0. 2010 Blood Sugar Creatinine BUN potassium sodium August 22.0 ARTERIAL BLOOD GAS Ph pcO2 pO2 HCO3 BE ecf O2 sat 7.2 4.363 26.0 -10 98% 7.35-7.2 1. 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 3.4-48.3 0.30 4.5 x 2.5-10. 2010 Result 25.5 1. Tiny hypodensities are seen in the right centrum semiovale and in the posterior lining of the left internal capsule.3 1.5-23.6 60-110 0.02 37.3 cm (approximately 20 ml) with perilesional edema.4-5.45 35-45mmHg 80-105mmHg 22-26mEq/L -2 to +3 mEq/L 95-98% CT Scan Report August 25. The posterior fossa structures are unremarkable.8 62.0 142.4 134.0-149. .0 cm to the left.0-2.0 262 10^3/uL Normal value 17.60-1. There is effacement of the right lateral ventricles with associated shift of the midline structures by about1.0-3.0 x 5. There is layering density in the sphenoid sinuses.6 10.6 4. Hypodense focus is noted in the left frontal periventricular region. The right sylvian tissue is likewise effaced.3 112 15.Laboratory Exam Lymphocyte (%) Neutrophils (%) Monocytes (%) Eosinophils (%) Basophils (%) Platelets August 28. Mild mass effect is noted in the right side midbrain and pons.

bilateral III. Anatomy and Physiology A. right centrum semiovale and posterior of the left Sphenoid sinusitis Mastoiditis. Narrative: Renal System Anatomy and Physiology Kidneys . left frontal perixeventricular Lacunar infarction.Opacities are seen in the mastoid air cells. Impression: Acute to Subacute hemorrhage. The orbits and sella are unremarkable. The visualized osseous structures are unremarkable. right basal ganglia Subfalcinc herniation to the left Ischemic infarction. bilaterally.

and the renal capsule (fibrous sac) surrounds the kidney and protects it from trauma and infection. The kidneys also perform the following functions: • • • Detoxify harmful substances (e.g.The kidneys regulate the volume and concentration of fluids in the body by producing urine.. 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 kidneys maintain the volume and concentration of urine by filtering waste products and reabsorbing useful substances and water from the blood. Renal Artery The renal artery enters the kidney and the renal vein emerges from the kidney at an . Urine is produced in a process called glomerular filtration. minerals. which is the removal of waste products. free radicals. and water from the blood. 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. the adipose capsule (layer of fat) cushions the kidney.

the upper portion of the ureter. Urine then travels through the loop of Henle.g. a renal tubule. The renal pyramids extend into funnel-like extensions (called calyces). Some sections of the loop are permeable to water and impermeable to substances in the urine (e. Urine formation occurs in the renal tubules. In this section. Each section of the renal tubule performs a different function. Nephrons consist of a network of capillaries (called a glomerulus). The renal artery supplies oxygen and blood to the kidney. to the inner tissue (called the medulla). Minor calyces merge to form major calyces and major calyces merge to form the renal pelvis. Formation and Elimination of Urine The formation of urine occurs in the basic units of the kidney. Blood flows from the kidney through the renal vein after waste products have been removed. ammonia). and some sections are impermeable to water and permeable to other substances. it forms the proximal convoluted (highly coiled) tubule. a long U-shaped extension of the proximal convoluted tubule. salt. It consists of a descending limb and an ascending limb. .g. nicotine) are forced out of the blood through a permeable membrane and useful substances (e. and return to the cortex. which travel from the outer tissue of the kidney (called the cortex).indentation in the middle of the organ called the hilum. vitamins. minerals) are reabsorbed. The glomeruli are where urine production begins. Each human kidney contains over 1 million nephrons.g. glucose. waste products and toxic substances (e. ammonia.. called nephrons. and a membrane that surrounds the glomerulus and functions as a filter (called Bowman's capsule).. where the collection of urine occurs.. Extensions of the cortex project into the medulla and divide the tissue into renal pyramids. As the tube leads away from Bowman's capsule into the cortex. amino acids.

However. or urine sediment consisting of red blood cell casts. Next. have been implicated as increasing the risks for developing SLE (Cooper et al. increasing the concentration of the urine. silica dust. hematuria. the urine consists almost entirely of waste products. estrogens. Urine from several nephrons empties into each collecting tubule. urine enters the collecting tubule. Normally. where it is stored until it is eliminated from the body through the urethra. Most of the water and other useful substances have been reabsorbed. or any combination of these. Many environmental factors. asymptomatic proteinuria and hematuria are frequent initial manifestations that are often overlooked or misinterpreted upon physical examination. and tobacco smoke. azotemia. heavy metals. involving at least one environmental stimulus acting on a genetically susceptible host. 1998). LN frequently is not diagnosed until the . LN is a glomerular inflammatory process that frequently manifests as proteinuria. waxy casts. After passing through the distal convoluted tubule. hypertension. Urine travels from the kidneys through the ureters to the bladder. These tubules form the calyces.The next section is the distal convoluted tubule. including infectious diseases. and the calyces form the renal pelvis (upper portion of the ureter). this section is water permeable. and cellular debris. Substances that remain in the urine are reabsorbed. PATHOPHYSIOLOGY OF LUPUS NEPHRITIS Narrative The pathophysiology of SLE and LN is a complex process..

and estrogens. In SLE. SLE is characterized by the production of autoantibodies and the deposition of immune complexes (Mohan & Datta. are aggregations that always include antigen and antibody and may also include complement proteins. Negatively charged substances. Thus. also adjacent to the glomerular basement membrane. A Bowman's capsule surrounds each glomerular tuft. but it generally is not an early manifestation because unaffected nephrons often compensate for damage to injured nephrons (Greenberg.. the primary barrier to filtration. Mesangial cells between the glomerular capillaries connect them to each other (Greenberg. 1998). depending on their molecular size and shape. such as most plasma proteins including albumin. . Activated complement proteins are destructive to cells identified and marked by antibodies as foreign (Greenberg. Positively charged and neutral substances may filter easily. nucleic acids. The outer capillary wall.nephrotic syndrome emerges. The excessive activation of B lymphocytes. B lymphocytes spontaneously secrete increased amounts of antibodies. 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. 1995). which can circulate in the blood or precipitate in tissues. results in production of autoantibodies with subsequent immune complex formation (Cooper et al. bacteria. 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. Renal insufficiency is a frequent outcome. Sim. 1993). a type of epithelial cells. Immune complexes. 1998). 1998). is composed of podocytes. by factors such as viruses. cannot normally filter through the glomerular basement membrane. Autoantibodies occur in response to and interact with a host's own tissues and are recognized as foreign by the host's immune system. 1998. The innermost layer of fenestrated (porous) endothelial cells is adjacent to the middle negatively charged glomerular basement membrane.

e. Many of the autoantibodies produced react with a multitude of subcellular antigens. The net result of these changes is proteinuria (Greenberg.. Immune complex deposition in glomerular capillaries is influenced by the following: rate of glomerular blood flow. Activated B lymphocytes direct humoral immune responses. However. Sim 1993). a combination of RNA and protein). glomerular.g. leukocyte infiltration and glomerular cell proliferation are initiated and the complement protein cascade is activated (Greenberg. the size and charge of immune complexes. 1997). i.e. Pollak & Pirani. prostaglandins. 1998. and glomerular capillary hemodynamic factors such as hydraulic pressure. the strength with which immune complexes are bound. Antibody deposition in itself is not sufficient to induce renal injury. monocytes. Glomerular injury is then induced either by recruitment of inflammatory cells (e. B and T lymphocyte clones that can potentially react against the host's own body cells are deleted through apoptosis (i. basement membrane permeability.The chronic deposition and formation of immune complexes are primary mediators in the pathogenesis of vascular. and previous glomerular damage (Mohan & Datta. mesangial. and autoantibody levels are increased.. 1996). ribonucleoprotein (RNP. 1995). Increased numbers of . neutrophils. 1998. proteases. Normally. when antibodies bind with antigens and form immune complexes. tubule. transforming SLE from an inactive to an active stares. 1995). programmed cell death) (Fournie & Druet. the efficiency of systemic phagocyte clearance of immune complexes. i. the rate of immune complex production. SLE patients have abnormal apoptosis such that the life span of activated B cells is prolonged. phospholipids. including double-stranded DNA (dsDNA. These substances alter the permeability and structure of the glomemlar basement membrane..abnormal B lymphocytes can contribute negatively to an already taxed or deficient immunologic system. native DNA that has two helical strands of nucleic acids bound together). Glomemlar capillaries are particularly predisposed to deposition of immune complexes.. macrophages) to the site or production of oxidants.e. and other nuclear and cytoplasmic proteins (Mohan & Datta. and interstitial immune deposits. and cytokines.

However.autoantibodies are then available for the production of greater amounts of immune complexes. 1995). 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. Loss of self-tolerance by helper T lymphocytes can then lead to B lymphocyte hyperactivity and the cascade of events characteristic of SLE. 1997. T lymphocytes. greater numbers of nucleosomes are released into the circulation as more cells are destroyed (Berden. the production of anti-dsDNA antibodies. Endothelial cell damage activates the . immune complex deposition and endocapillary hypercellularity (i. 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. Greenberg. and platelets) negatively affect the mesangium's ability to rid the kidneys of immune complex deposits (Berden. These are the changes that account for the myriad clinical manifestations possible with SLE. 1998). glomerular basement membrane) (Mohan & Datta.. 1997). Glomerular mesangial cells provide the predominant means for removing immune complexes by phagocytosis. Berden (1997) theorizes that because systemically-released nucleosomes are the primary targets of autoantibodies. First. toxic oxygen radicals present in the circulation as a result of complement activation can structurally alter nucleosomes (Sim. 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. 1997). proliferation of native cells or infiltration of tissue by neutrophils.e.g. Qualitative and quantitative changes in nucleosomes may be a consequence of disturbed apoptosis. 1993). monocytes. Third.. they can contribute to the evolution of tissue lesions. Thrombi occur frequently in active LN. and the induction of autoimmunity. Second.

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. The World Health Organization (WHO) has described a classification system with six categories of renal pathology with SLE. Circulating coagulant (anti-phospholipid antibodies) and abnormal fibrinolysis are present in patients exhibiting systemic venous and arteriolar thrombi as well as glomerular capillary thrombi. cellular proliferation. cytokines. and membrane thickening. sclerosis of blood vessels or fibrosis of tissues may be seen. Physical properties of deposited antibodies or immune complexes. 1999).coagulation system and thrombi formation. Schematic Diagram: . dynamics of tissue deposition and clearance. Late in the course of SLE. Platelets also are involved in the development of lesions through their association with fibrin in the formation of clots. The categories are characterized by inflammation.

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route. classification.DRUG STUDY DRUG ORDER (Generic name. Diarrhea Nausea Vomiting Cramps Pseudolithiasis Rashes Urticaria Hemolytic anemia Missed dose should be taken as soon as possible unless almost time for next dose Classification: anti-infective . usually bactericidal Advise patient to report sign of superinfection and allergy Advise patient to notify health care provider if Dosage: 1gm Route: IVTT Frequency: q 24h Phlebitis at IV site Allergic reactions including anaphylaxis and fever and diarrhea serum sickness develops . third generation cephalosporin instability. dosage. promoting osmotic Prophylaxis against infection secondary to depressed immune system due to SLE Hypersensitivity to cephalosporins. frequency) Generic Name: Ceftriaxone MECHANISM OF ACTION INDICATIONS CONTRAINDICATIONS ADVERSE EFFECTS OF THE DRUG NURSING RESPONSIBILITIES/ PRECAUTIONS inhibits cell-wall synthesis. serious hypersensitivity to penicillins. brand name.

particularly after initial dose • Encourage patient to comply with additional interventions for hypertension • May cause dizziness. 1 tab Route: po Frequency: OD inhibitors also increase plasma rennin levels and reduce aldosterone levels. safety precautions should be observed . ACE Classification: Antihypertensives. Fatigue Headache. ACE inhibitors also inactivates the vasodilator bradykinin and other vasodilatory prostaglandins. Cough Hypotension Angina pectoris Tachycardia Taste disturbances Anorexia Diarrhea . ACE Dosage: 10gm . Insomnia Weakness.DRUG STUDY DRUG ORDER (Generic name. fever • Monitor vital signs as suggested and necessary • Caution patient to avoid salt substitutes or foods containing high levels of Potassium or sodium unless directed by health care professional • Caution patient to change positions slowly to minimize hypotension. Nausea Proteinuria Hyperkalemia Angioedema. dosage. classification. Net result is systemic vasodilation Alone or with other agents in the management of hypertension Hypersensitivity. route. Cross sensitivty among other ACE inhibitors may occur. brand name. Pregnancy and angioedema Dizziness. frequency) Generic Name: Perindopril MECHANISM OF ACTION CONTRAINDICATIONS INDICATIONS ADVERSE EFFECTS OF THE DRUG NURSING RESPONSIBILITIES/ PRECAUTIONS Block the conversion of angiotensin I to vasoconstrictor Angiotensin II.

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

hypochloremia. nervousness. dosage. May have renal and peripheral vasodilatory effects. Headache. Increases renal excretion of water. Pre-existing electrolyte imbalance. hypotension. hypovolemia. nausea. insomnia. hepatic coma. tinitinus. hypomagnesemia. dyspepsia. sodium. excessive urination. Effectiveness persists in impaired renal function. encephalopathy. route. myalgia • Assess fluid status • Monitor intake and output • Monitor vital signs • Caution patient to change positions slowly to minimize orthostatic hypotension • Encourage patient to comply with additional interventions for hypertension • May cause dizziness. classification. Dosage: 40mg Route: IVTT Frequency: q12 magnesium. metabolic alkalosis. hearing loss. constipation. dehydration. or anuria.DRUG STUDY DRUG ORDER (Generic name. . hypertension Hypersensitivity Cross sensitivity with thiazides and sulfonamides will occur. hyponatremia. hydrogen and calcium. brand name. safety precautions should be observed • Caution to wear protective clothing and use of sunscreen to prevent photosensitivity reactions Classification: Loop diuretics distal renal tubule. muscle cramos. vomiting. diarrhea. hyperglycemia. chloride. hypokalemia. frequency) Generic Name: Furosemide MECHANISM OF ACTION CONTRAINDICATIONS INDICATIONS ADVERSE EFFECTS OF THE DRUG NURSING RESPONSIBILITIES/ PRECAUTIONS Inhibits the reabsorption of Edema due sodium and chloride from the loop of Henle and to renal disease. hyperurecemia. increased BU. dry mouth. Dizziness.

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

Renal calculi. Essential for bone formation and blood coagulant. route. CNS: tingling sensations. chalky taste. Act as an activator in the transmission of nerve impulses and contraction of the cardiac. vasodilation. cardiac arrest with rapid IV injection GI: irritation. . renal calculi Metabolic: hypercalcemia Classification: Mineral or electrolyte replacements and supplements membrane and capillary permeability. muscular and skeletal systems. bradycardia. frequency) Generic Name: Calcium carbonate MECHANISM OF ACTION INDICATIONS CONTRAINDICATIONS ADVERSE EFFECTS OF THE DRUG NURSING RESPONSIBILITIES/ PRECAUTIONS Essential for nervous. thirst and abdominal pain GU: polyuria.i. classification. CV: mild drop in blood • Double check that you are giving the correct form of calcium. Dosage: 1 tab Route: po Frequency: t. dosage. brand name. Maintain cell Treatment and prevention of hypocalcemia Hypercalcemia.d. constipation. pressure. nausea. vomiting. skeletal and smooth muscle. hemorrhage. resuscitation cart may contain both calcium gluconate and calcium chloride • Monitor calcium levels frequently • Report abnormalities • Review methods of preventing constipatient and endorse his to patient as his medication may cause constipation • Encourage to have adequate vitamin D intake • Avoid milk products Venticular fibrillation.DRUG STUDY DRUG ORDER (Generic name.

fragility. osteoprosis. adrenal • Monitor vital signs • Monitor intake and output • Stress importance of proper hygiene such as handwashing • Maintain a clean environment to prevent infection Classification: corticosteroid Dosage: 100 mg Route: IVTT Frequency: q6h sufficiency. euphoria. anorexia. increased susceptibility to infection.DRUG STUDY DRUG ORDER (Generic name. decreased wound healing. Depression. cushingoid appearance. petechiae. hirsutism. classification. Lactation. dosage. route. adrenal suppresion. headache NURSING CARE PLAN . acne. hypertension. Tartrazine hypersensitivity or intolerance. ecchymoses. brand name. frequency) Generic Name: Hydrocortisone MECHANISM OF ACTION CONTRAINDICATIONS INDICATIONS ADVERSE EFFECTS OF THE DRUG NURSING RESPONSIBILITIES/ PRECAUTIONS Supress inflammation and the normal immune response Autoimmune disorder – Systemic Lupus Erythematosus Active untreated infection. muscle wasting.

Report relief from pain with a scale of 3/10 b. client will be able to: a. The client was able to verbalize and understand other ways of being relieved from pain. o Relaxation exercises Techniques are used to bring about a state of physical and mental awareness and tranquility. temperature.ASSESSMENT DATA (Subjective & Objective Cues) Subjective: “sakit akong koto-koto. Pain scale: 3/10 . The goal of these techniques is to reduce tension. Some people deny the experience of pain when it is present.” As verbalized by the client Objective: Facial grimace Muscle guarding restlessness Pain Scale: 7/10 NURSING DIAGNOSIS (Problem and Etiology) Acute Pain related to biological injuring agents secondary to disease condition of systemic lupus erythematosus GOALS AND OBJECTIVES Following 8-hours of nursing intervention. color and moisture of skin. Demonstrate use of relaxation skills and diversional activities NURSING INTERVENTIONS AND RATIONALE *Assess pain characteristics for baseline data * Observe or monitor signs and symptoms associated with pain. sleep. and ability to focus. Attention to associated signs may help the nurse in evaluating pain. heart rate. EVALUATION Goals were met. 1. such as BP. subsequently reducing pain. restlessness. * Provide rest periods to facilitate comfort. She was able to demonstrate proper breathing techniques to facilitate relaxation. Nonpharmacological methods include the following: o Distraction techniques Heighten one’s concentration upon nonpainful stimuli to decrease one’s awareness and experience of pain. Verbalize nonpharmacologic methods that provide relief c. and relaxation. Some methods are breathing modifications and nerve stimulation. * Eliminate additional stressors or sources of discomfort whenever possible.

dry. * Clean. and moisturize skin. twice daily or as indicated by incontinence or sweating. * Encourage ambulation if patient is able. especially over bony prominences. restricting time in one position to 2 hours or less and customizing the schedule to patient’s routine and caregiver’s needs.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 DIAGNOSIS (Problem and Etiology) Impaired skin integrity related to immunological deficit secondary to lupus nphritis NURSING CARE PLAN GOALS AND NURSING INTERVENTIONS AND OBJECTIVES RATIONALE After 8-hours of nursing interventions. client will be able to: • Participate in prevention measures and treatment program • Verbalize understanding on the process and overt symptoms of the disease EVALUATION o Encourage implementation and posting of a turning schedule. The patient demonstrated understanding on her course of treatment . • Encourage adequate nutrition and hydration: • Instruct on proper wound care and application of pressure right after puncture or withdrawal of blood sample Goals were met.

The client was able to verbalized understanding on her condition and how she can help to alleviate it. intake and output. client will be able to: • Verbalize understanding of condition • Specify causative factors NURSING INTERVENTIONS AND RATIONALE Documented urine color and characteristic. Reported any changes for Observed voiding pattern fro Urine characteristics help notifying diagnosis Discuss with patient the nature of her condition EVALUATION Goals were met. .NURSING CARE PLAN 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 GOALS AND OBJECTIVES After 8-hours of nursing interventions. and pt daily weight.

The client was able to verbalize and understand other ways of being relieved from pain. She was able to demonstrate proper breathing techniques to facilitate relaxation.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 DIAGNOSIS (Problem and Etiology) Impaired skin integrity related to immunological deficit secondary to lupus nephritis NURSING CARE PLAN GOALS AND NURSING INTERVENTIONS AND OBJECTIVES RATIONALE After 8-hours of nursing interventions. client will be able to: • Participate in prevention measures and treatment program • Verbalize understanding on the process and overt symptoms of the disease EVALUATION Goals were met. Pain scale: 3/10 .

VII. T (Treatment) H (Hygiene) Short walks are encouraged but not to the extent of fatigue . A full diet is required with provision and adherence to a healthy diet/ eating of nutritious foodd S (Spirituality) . Discharge Planning .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. . for only short periods. Go to church every Sunday .Strengthen spirituality by allowing the significant others to spend time in prayer. dosage. and so on up to 1520 minutes at a time.Provide a well organized plan for administering and taking in of medication.Follow strict compliance to the medications as prescribed by the attending physician following the right medication. Daily bathing is necessary O (Outpatient) . Self-care must be done to promote proper hygiene and well- being. M (Medications) E (Exercise) - Expose the self to the sun because sunlight provide natural source of vitamin D. a little more the next day. beginning with 3-5 minutes the first day. time and route.Seek medical attention if any unusualities happens.

we learn from it. It would make us realize how we should do better next time. 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. I felt very fortunate of the things that I have. I learned a lot and I’m very happy about the things that happened during the rotation. More than contented even. Mistakes does not have to end as is. Furthermore. The experience enabled me to realize the realities of life. I felt as if I was able to really help other people. I am very contented with everything. the patent and the watchers.Learning Experience This rotation was awesome.

10th ed. David’s drug Guide for Nurses. et al. 2002. Joyce E. A. Doenges. J. Nursing Care Plans: Guidelines for Individualizing Patient Care.XII. F. Philippines.A.col1 . Smeltzer. 2004. Medical-Surgical Nursing: Clinical Management for Continuity of Care. 2003.com/p/articles/mi_m0ICF/is_2_27/ai_n18610685/pg_12/? tag=content.A. Inc. Springhouse. Bangkok. Textbook of Medical Surgical Nursing. Black. Lippincot Williams & Wilkins. Marilynn E. et al.H. 10th ed.H and Vallerand. Merriam Webster Bookstore. 6th ed. F. http://findarticles. 5th ed. 1997. Philadelphia. Pennsylvania. Davis company. et al. Thailand. Davis Company. Bibliography Deglin. Suzanne E.

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