CHOLELITHIASIS, NEPHROLITHIASIS SECONDARY HYPERTENSION, DM TYPE 2, HYDRONEPHROSIS

VELEZ COLLEGE – COLLEGE OF NURSING
A CASE STUDY OF PATIENT R.M DIAGNOSED WITH CHOLELITHIASIS, NEPHROLITHIASIS
SECONDARY HYPERTENSION, DM TYPE 2, HYDRONEPHROSIS
A Case Study Presented by:
Dave Jay S. Manriquez, RN.

CHAPTER ONE
INTRODUCTION
This is a case study on patient RM, 58 years old, male, Roman Catholic, Filipino, residing at Matabao Tubigon, Bohol and born on October 22, 1948 admitted for the 3rd time in Cebu
Velez General Hospital (CVGH) for complaints of right epigastric pain and vomiting. The patient was admitted under the service of Dr. Ceaar Quiza under the Department of Internal Medicine with
the case number of 88358.
The case was chosen by the researchers on June 28, 2007.
Nephrolithiasis (Alternative Names: Renal calculi; Kidney stones; Stones – kidney)
DEFINITION
The formation of crystal aggregates in the urinary tract results in kidney stones, the clinical condition referred to as nephrolithiasis. Kidney stones may produce no symptoms or may be associated
with one or several of the following: flank pain, gross or microscopic hematuria, obstruction of one or both kidneys, and urinary infections. The stones are usually formed by one of four substances:
(1) calcium, (2) uric acid, (3) magnesium ammonium phosphates (or struvite), or (4) cystine.1 Occasionally, calcium salts and uric acid will be present in the same stone.
CALCIUM STONE DISEASE
Calcium stone disease is the most common form of nephrolithiasis and represents about 70% of all stone-forming disease. It occurs most often in the third to fifth decade of life, more often in men
than women.
SIGNS AND SYMPTOMS
Patients often present with episodes of flank pain that radiates to the anterior abdomen or even to the genitalia. The pain is often severe and comes in waves. Often there is microscopic or gross
hematuria. Calcium oxalate crystals may be seen with urine microscopy, but this finding is not diagnostic since calcium oxalate crystals may be seen in the urine of non-stone-forming patients. In
some patients the renal stones are completely asymptomatic or may produce painless hematuria.
DIAGNOSIS
Stone analysis is the surest way to diagnose calcium oxalate or calcium phosphate stones. Calcium-containing stones are radiopaque on routine radiography but show up as bright objects on
computed helical tomography without contrast. Ultrasonography will detect all types of renal stones if the stone is larger than 3 to 5 mm and the ultrasound is technically satisfactory. Of the
conditions associated with calcium stones, only pyelotubular ectasia (medullary sponge kidney) is better demonstrated by intravenous urography.
URIC ACID STONE DISEASE
Uric acid stone disease is found in about 5% to 10% of stone formers. It is more common in patients with chronic diarrheal disorders and in those with hyperuricosuria. Most uric acid stone formers
do not have gout or hyperuricosuria. Uric acid stones may also be partially composed of calcium oxalate, and some patients have both uric acid and calcium oxalate stones.
SIGNS AND SYMPTOMS
Patients often present with episodes of flank pain that radiates to the anterior abdomen or even to the genitalia, as in calcium stone disease. The pain is often severe and comes in waves. Often there
is microscopic or gross hematuria.
DIAGNOSIS
Uric acid stone disease should be suspected in any patient with typical symptoms of renal colic in whom the plain radiographs do not show a calcified stone. Urate crystals may be present in the
urine, but occur in patients without stones as well. The urine pH will usually be less than 5.5. Stone analysis will provide sure diagnosis.

STRUVITE STONE DISEASE
Infection stones, also known as struvite or magnesium ammonium phosphate stones, occur in about 10% to 12% of patients, more often in women. They occur more often also in patients with spinal
cord injury, neurogenic bladder, vesicoureteral reflux, chronic indwelling Foley catheters, and recurrent urinary infections, and in those with chronic obstruction of the upper urinary tracts.
SIGNS AND SYMPTOMS
These stones may cause the typical symptoms of renal colic, but often they are discovered in the course of investigating a patient with recurrent urinary infections or in a patient with asymptomatic
bacteriuria. Since these stones can grow to significant size, they are often found in the renal pelvis and infundibula of the kidneys.
DIAGNOSIS
The diagnosis of struvite stones is suspected by finding large or branched stones in the kidneys of a patient with persistently infected urine. Stone analysis will confirm the diagnosis.
CYSTINE STONE DISEASE
PREVALENCE
Cystine stone disease occurs in less than 1% of all adult stone formers and in about 6% to 8% of children with nephrolithiasis.
SIGNS AND SYMPTOMS
The patient presents with symptoms of nephrolithiasis, often at a younger age than a person with calcium stone disease. The stones are radiopaque (ground-glass appearance) and amber. Family
history is often helpful (ie, siblings may have the disorder).
DIAGNOSIS
Normal urine contains less than 20-30 mg/d (<100mg/gm creatinine) of cystine. Urinary cystine excretion of greater than 250 mg/g creatinine in adults is clearly abnormal and is the usual amount
found in patients with cystinuria. The examination of a concentrated, acidic urine specimen will often reveal the presence of the cystine crystals, which are transparent and hexagonal. Cystine can be
detected qualitatively by adding sodium nitroprusside to the urine and observing a purple-red color. Stone analysis is diagnostic.
Foods and Drinks Containing Oxalate
People prone to forming calcium oxalate stones may be asked by their doctor to cut back on certain foods if their urine contains an excess of oxalate:
• beets
• chocolate
• coffee
• cola
• nuts
• rhubarb
• spinach
• strawberries
• tea
• wheat bran
People should not give up or avoid eating these foods without talking to their doctor first. In most cases, these foods can be eaten in limited amounts.
CAUSES, INCIDENCE AND RISK FACTORS:
Kidney stone formation may result when the urine becomes overly concentrated with certain substances. These substances in the urine may complex to form small crystals and subsequently stones.
Stones may not produce symptoms until they begin to move down the ureter, causing pain. The pain is severe and often starts in the flank region and moves down to the groin. Kidney stones are
common. About 5% of women and 10% of men will have at least one episode by age 70. Kidney stones affect about 2 out of every 1,000 people. Recurrence is common, and the risk of recurrence is

greater if two or more episodes of kidney stones occur. Kidney stones are common in premature infants. A personal or family history of stones is associated with increased risk of stone formation.
Other risk factors include renal tubular acidosis and resultant nephrocalcinosis.
SYMPTOMS:
• Flank pain or back pain on one or both sides progressive, severe, colicky (spasm-like) may radiate or move to lower in flank, pelvis, groin, genitals
• Nausea, vomiting
• Urinary frequency/urgency, increased (persistent urge to urinate)
• Blood in the urine
• Abdominal pain
• Painful urination
• Excessive urination at night
• Urinary hesitancy
• Testicle pain
• Groin pain
• Fever
• Chills
• Abnormal urine color
SIGNS AND TESTS
• Pain may be severe enough to require narcotics. There may be tenderness when the abdomen or back is touched. If stones are severe, persistent, or come back again and again, there may be
signs of kidney failure.
• Straining the urine may capture urinary tract stones when they are excreted.
• Analysis of the stone shows the type of stone.
• Urinalysis may show crystals and red blood cells in urine.
• Uric acid elevated
Stones or obstruction of the ureter may be seen on:
• Kidney ultrasound
• IVP (intravenous pyelogram )
• Abdominal x-rays
• Retrograde pyelogram
• Abdominal CT scan
• Abdominal/kidney MRI
MEDICAL THERAPY
The doctor may prescribe certain medications to prevent calcium and uric acid stones. These drugs control the amount of acid or alkali in the urine, key factors in crystal formation. The drug like:
1.) allopurinol - These drugs decrease the amount of calcium released by the kidneys into the urine by favoring calcium retention in bone. They work best when sodium intake is low.

2.) Thiola and Cuprimine – these help reduce the amount of cystine in the urine.
3.) acetohydroxamic acid (AHA) - AHA is used with long-term antibiotic drugs to prevent the infection that leads to stone growth
SURGICAL TREATMENT
Surgery should be reserved as an option for cases where other approaches have failed. Surgery may be needed to remove a kidney stone if it does not pass after a reasonable period of time
and causes constant pain is too large to pass on its own or is caught in a difficult place blocks the flow of urine causes ongoing urinary tract infection damages kidney tissue or causes constant
bleeding has grown larger.
1.) Extracorporeal shockwave lithotripsy (ESWL) is the most frequently used procedure for the treatment of kidney stones. In ESWL, shock waves that are created outside the body travel
through the skin and body tissues until they hit the denser stones. The stones break down into sand-like particles and are easily passed through the urinary tract in the urine.
Complications may occur with ESWL. Most patients have blood in their urine for a few days after treatment. Bruising and minor discomfort in the back or abdomen from the shock waves
are also common. To reduce the risk of complications, doctors usually tell patients to avoid taking aspirin and other drugs that affect blood clotting for several weeks before treatment.
2.) Percutaneous nephrostolithotomy allows fragmentation and removal of large calculi from the kidney and ureter and is often used for the many ESWL failures. A needle, and then a wire, over
which is passed a hollow sheath, are inserted directly in the kidney through the skin of the flank.
3.) Lithotripsy may be an alternative to surgery.
COMPLICATIONS
• Recurrence of stones
• Urinary tract infection
• Obstruction of the ureter, acute unilateral obstructive uropathy
• Kidney damage, scarring
• Decrease or loss of function of the affected kidney
PREVENTION
If there is a history of stones, fluids should be encouraged to produce adequate amounts of dilute urine (usually 6 to 8 glasses of water per day). Depending on the type of stone, medications or other
measures may be recommended to prevent recurrence.
HYPERTENSION (HPN)
 High blood pressure (140/90 mmHg or greater)
 Condition when the pressure inside of your large arteries is too high.
Three stages of HPN:
Sytolic (mmHg) Diastolic (mmHg)
Stage I 140-159 or 90-99
Stage II 160-179 or 100-109

Stage III >=180 or >=110
Types of HPN:
 ESSENTIAL - diagnosed when there is no identifiable cause for the occurrence of hypertension.
- condition that is most commonly seen.
 SECONDARY - an increase in the blood pressure as a result of another disease condition.
- Common disease entities that may cause HPN include renal artery stenosis, renal failure, phenochromocytoma, & adrenal
insufficiency.
Incidence Report:
 The latest local data (1998) shows a 21% prevalence among Filipinos.
 With a projected population of 78.4 million by year 2000, roughly 8.6 million Filipinos are hypertensive
 About 59% have target organ damage – heart attacks (myocardial infarction) in 3.4%, stroke in 11.5% and kidney damage in 53%
 Since hypertension causes minimal or no symptoms at all, only 13.6% of hypertensives are aware of their condition.
Causes
 Genes
 Lifestyle and environment- ex. smoking & alcohol intake
 Diet
 Certain medications
 Disorders of the kidneys or endocrine glands.
Signs and Symptoms
 High BP (pls. refer to the first page for values)
 Individuals with high BP rarely have symptoms
 Few complain of headache, nape pains or dizziness, which are usually mild and tolerable.
 Thus, hypertension is treated not only to relieve symptoms, but to prevent the development of target organ damage, which occur in those with chronic untreated, elevated blood pressure.
Complications
 Target organ damage is a general term used for the complications occurring as a result of uncontrolled hypertension. They include the brain, the eyes, the kidneys, and the heart.
 Stroke results when arteries in the brain burst (bleeding) or become blocked (thrombosis). Part of the brain dies and the patient becomes paralyzed

 Heart Attack occurs when coronary arteries in the heart are blocked. The heart muscle dies, and may stop beating. Patient dies as a consequence.
 Heart Failure results when the heart pumps too hard for too long, trying to keep blood flowing through the body. Eventually, the heart weakens. The patient now tires easily and is always
out-of-breath
 Kidney Failure happens when tiny vessels in the kidneys are blocked. The kidneys malfunction are unable to clean the body of wastes. Patient is slowly poisoned, becomes weak and
bloated. Unless “dialyzed”, the patient will die of poisoning from his own body wastes
 Blindness or Impaired Vision occurs when tiny blood vessels in the eye rupture or become blocked, damaging the surrounding eye tissues
BRAIN Prolonged hypertension predisposes and individual to the occurrence of strokes whether by occlusion (ischemic infarct) or by bleed (hemorrhagic infarct)
HEART Hypertension increases the work needed to be done by the heart to meet the demands of the body. This prolonged increase in the workload of the heart eventually results to enlargement of
the heart and predisposes to the occurrence of heart failure and heart attack.
KIDNEYS Prolonged hypertension can eventually result to kidney failure, which in the end-stage may necessitate dialysis treatment.
EYES Hypertension predisposes to development of hypertensive retinopathy with subsequent development of visual problems for the patient.
Risk factors
 Blood lipid levels, diabetes, obesity, family history, fibrinogen and other clotting factors, homocysteine and cardiac disorders.
Medical Management
 Diuretics, which initially increase urination to reduce salt and water retention and lower blood volume.
 Beta-blockers (BB’s), which slow the heart rate and lower the output of the heart.
 Angiotensin converting enzyme (ACE) inhibitors, which block production of a specialized hormone called angiotensin II. Angiotensin II causes the arteries to constrict and also stimulates
the release of another hormone that causes the kidneys to retain salt.
 Angiotensin II receptor blockers (ARBs or A II A’s), which relax blood vessels by blocking the action of angiotensin II.
 Calcium channel blockers (CCB’s) of which there are two types: Dihydropyridines (DHPs), and heart rate slowing calcium channel blockers. Both types relax blood vessels by slowing the
entry of calcium into cells. The DHPs increase the heart rate a little while the others slow it a little.
 Alpha-1 blockers work on the blood vessels to block the effect of constricting hormones such as norepinephrine. These are also commonly used to treat prostate problems.
 Alpha-2 agonists, which work in the brain to decrease the action of the nervous system to constrict blood vessels.
 Direct vasodilators, which relax the artery walls.
 Sympathetic nerve blockers, which prevent those nerves from constricting blood vessels.
http://www.pfizer.com.ph/ppg/disease_mgt/hbp.html
http://www.psh.org.ph/v2/index.php?page=lay-info
http://www.doh.gov.ph/faqs/hypertension
http://www.psh.org.ph/v2/index.php?page=how-low-is-low

Diabetes Mellitus Type 2
Mortality rate has increased by 92% over a ten year period from 1986 to 1995 and it is estimated that there are currently 3 million Filipinos who are diabetic. The World Health Organization
projected that by 2030, the number of cases of diabetes worldwide is estimated at 334 million. Based on the WHO study, the Philippines is projected to have an estimated number of 7.8 million
cases by 2030 and eventually may rank ninth in th elist of countries with the highest estimated cases worldwide. Given these figures, it is crucial to know and understand the facts about this disease.
Many patients with type 2 diabetes are asymptomatic, and their disease is undiagnosed for many years. Studies suggest that the typical patient with new-onset type 2 diabetes has had diabetes for at
least 4-7 years before it is diagnosed. Among patients with type 2 diabetes, 25% are believed to have retinopathy; 9%, neuropathy; and 8%, nephropathy at the time of diagnosis.
Prediabetes often precedes overt type 2 diabetes. Prediabetes is defined by a fasting blood glucose level of 100-125 mg/dL. Patients who have prediabetes have an increased risk for macrovascular
disease, as well as diabetes.
Risk Factors
• Age - Older than 45 years (though, as noted above, type 2 diabetes is occurring with increasing frequency in young individuals)
• Obesity - Weight >120% of desirable body weight (true for approximately 90% of patients with type 2 diabetes)
• Family history of type 2 diabetes in a first-degree relative (eg, parent or sibling)
• Hispanic, Native American, African American, Asian American, or Pacific Islander descent
• History of previous impaired glucose tolerance (IGT) or impaired fasting glucose (IFG)
• Hypertension (>140/90 mm Hg) or dyslipidemia (high-density lipoprotein [HDL] cholesterol level <40 mg/dL or triglyceride level >150 mg/dL)
• History of GDM or of delivering a baby with a birth weight of > 9 lbs
• Polycystic ovarian syndrome (which results in insulin resistance)
Signs and Symptoms
These may include frequent urination, unexplained weight loss, unusual or excessive thirst, extreme hunger, sudden changes in vision, tingling or numbness in hands or feet, presence of sores that
are slow to heal and feeling tired most of the time. According to the American Diabetes Association, either the Fasting Plasma Glucose (FPG or FBS) or an Oral Glucose Tolerance Test (OGTT)
can be used to diagnose the condition. The FPG or FBS is frequently used because it is less expensive and easier to perform.
Fasting blood sugar level between 100 to 125 mg/dl signals pre-diabetes. Pre-diabetes is a term which distinguishes individuals who are at a risk of developing diabetes which may be due to
impaired fasting glucose (IFG) or impaired glucose tolerance (IGT). If the fasting blood sugar is 126 mg/dl or higher, this may indicate that the person has diabetes.
Diagnostic Tests
1. Physical Examination
2. C-peptide blood test
3. Insulin level blood test
4. Urine Sugar Test

5. Urine Ketone Test
6. Oral Glucose Tolerance Test (OGTT)
7. Blood Glucose Tests:
a. Fasting Plasma Glucose (FPG)
b. Random Plasma Glucose
Complications
• Complications include hypoglycemia and hyperglycemia, increased risk of infections, microvascular complications (eg, retinopathy, nephropathy), neuropathic complications, and
macrovascular disease.
• Diabetes is the major cause of blindness in adults aged 20-74 years, as well as the leading cause of nontraumatic lower-extremity amputation and end-stage renal disease (ESRD).
Treatment Options
Individuals who suspect they have diabetes must visit their doctor for diagnosis. Healthy eating, maintaining an ideal body weight, regular physical activity and regular blood glucose testing are the
basic recommendations given. Many individuals with type 2 diabetes may require oral medicaiton, insulin or both to control their blood sugar levels depending on the case.
Persons with type 2 diabetes can still live long and healthy lives as long as proper treatment and management is given. They must consult an endocrinologist, a medical specialist who is an expert in
the management of diabetes and an opthalmologist for eye examinations. Based on several studies, regular physical activity or exercise can significantly reduce the risk of developing type 2
diabetes. Regular exercise of at least 3 times a week fro at least 30 minutes per session improves cardiovascular fitness, helps insulin to function well in maintaining blood sugar levels, controls
body weight and helps lower blood pressure and cholesterol levels. Individuals must first consult their physician before engaging in a regular exercise program. Other preventive measures include
having a healthy diet and attaining an ideal body weight.
ACUTE CHRONIC INFECTIONS
Severe glyperglycemia
Hyperosmolar Coma
Ketoacidosis
Lactic Acidosis
Hypogycemia
Microvascular (small blood vessels for the eyes,
kidneys, and nerves)
Macrovascular (large blood vessels for the brain,
heart, and limbs)
Neuropathy
Cataracts, glaucoma
Infections of the skin, eyes, ears, nose, throat,
lungs, gallbladder, kidneys, and genitor-urinary
tract
HYDRONEPHROSIS
Hydronephrosis is the distention of the pelvis and calices of the kidney with urine, as a result of obstruction of the ureter, with accompanying atrophy of the parenchyma of the organ. The
signs and symptoms of hydronephrosis depends upon whether the obstruction is acute or chronic. Unilateral hydronephrosis may even occur without symptoms.
Blood tests can show raised creatinine and electrolyte imbalance. Urinalysis may show an elevated pH due to the secondary destruction of nephrons within the affected kidney.

Symptoms that occur regardless of where the obstruction lies include loin or flank pain. An enlarged kidney may be palpable on examination. Where the obstruction occurs in the lower
urinary tract, suprapubic tenderness (with or without a history of bladder outflow obstruction) along with a palpable bladder are strongly suggestive of acute urinary retention, which left untreated is
highly likely to cause hydronephrosis. Upper urinary tract obstruction is characterised by pain in the flank, often radiating to either the abdomen or the groin. Where the obstruction is chronic, renal
failure may also be present. If the obstruction is complete, an enlarged kidney is often palpable on examination.
Etiology
The obstruction may be either partial or complete and can occur anywhere from the urethral meatus to the calyces of the renal pelvis.
The obstruction may arise from either inside or outside the urinary tract or may come from the wall of the urinary tract itself. Intrinsic obstructions (those that occur within the tract) include
blood clots, stones, sloughed papilla along with tumours of the kidney, ureter and bladder. Extrinsic obstructions (those that are caused by factors outside of the urinary tract) include pelvic or
abdominal tumours or masses, retroperitoneal fibrosis or neurological deficits. Strictures of the ureters (congenital or acquired), neuromuscular dysfunctions or schistosomiasis are other causes
which originate from the wall of the urinary tract.
Tests
Blood (U&E, creatinine) and urine (MSU, pH) tests should be taken. Ultrasounds, CTs and MRIs are also important tests. Ultrasound allows for visualisation of the ureters and kidneys and
can be used to assess the presence of hydronephrosis and/or hydroureter. An IVU is useful for assessing the position of the obstruction. Antegrade or retrograde pyelography will show similar
findings to an IVU but offer a therapeutic option as well. The choice of imaging depends on the clinical presentation (history, symptoms and examination findings). In the case of renal colic (one
sided loin pain usually accompanied by a trace of blood in the urine) the initial investigation is usually an intravenous urogram. This has the advantage of showing whether there is any obstruction
of flow of urine causing hydronephrosis as well as demonstrating the function of the other kidney. Many stones are not visible on plain xray or IVU but 99% of stones are visible on CT and
therefore CT is becoming a common choice of initial investigation.
Complications
Complications for untreated hydronephrosis may include:
1. pyelonephritis
2. kidney damage
3. kidney failure
Treatment
Treatment of hydronephrosis focuses upon the removal of the obstruction and drainage of the urine that has accumulated behind the obstruction. Therefore, the specific treatment depends
upon where the obstruction lies, and whether it is acute or chronic.
Acute obstruction of the upper urinary tract is usually treated by the insertion of a nephrostomy tube. Chronic upper urinary tract obstruction is treated by the insertion of a ureteric stent or
a pyeloplasty. Lower urinary tract obstruction (such as that caused by bladder outflow obstruction secondary to prostatic hypertrophy) is usually treated by insertion of a urinary catheter or a
suprapubic catheter.

RHEUMATOID ARTHRITIS
Rheumatoid arthritis is a systemic autoimmune disease that causes chronic inflammation of the joints. RA can also cause inflammation of the tissue around the joints, as
well as other organs in the body. Autoimmune diseases are illnesses that occur when body tissues are mistakenly attacked by its own immune system. The immune system is a
complex organization of cells and antibodies designed normally to “seek and destroy” invaders of the body, particularly infections. Patients with autoimmune diseases have
antibodies in their blood that target their own body tissues where they can be associated with inflammation.
The cause of rheumatoid arthritis is unknown. Even though infectious agents such as viruses, bacteria, and fungi have long been suspected, none have been proven as the
cause. Some scientist believed that the tendency to develop rheumatoid arthritis may be genetically inherited. Environmental factors also seem to play some role in causing
rheumatoid arthritis.
Rheumatoid Factor (an autoantibody directed against immunoglobulin G), antibodies against collagen, Epstein-Barr virus, encoded nuclear antigen, and certain other
antigens have been identified in clients with RA. The role of antibodies in RA is still unclear, but research has focused attention on pre-illness immunologic status in the
pathogenesis of RA. Anti-keratin antibody (AKA) and anti-perinuclear factor (APF) apper to be markers that predict the development of RA in RF-positive clients. RA may be
mild and relapsing, involving a few joints for a brief period, or markedly progressive, with the development of deformities and severe systemic disease.
The disease is three times more common in women as in men. It afflicts people of all races equally. The disease can begin at any age, but most often starts after age forty
and before sixty. In some families, multiple members can be affected, suggesting a genetic basis for the disorder.
Signs and symptoms include fatigue, lack of appetite, low grade fever, muscle and joint aches, stiffness, hoarseness of voice, pleuritis, and anemia. Also during flares,
joints frequently become red, swollen, painful, and tender. This occurs because the lining tissue of the joint becomes inflamed, resulting in the production of excessive joint fluid.
Optimal treatment for the disease involves a combination of medications, rest, joint strengthening exercises, patient (and family) education, joint protection to achieve the
primary goals of providing pain reduction, protecting articular surfaces to prevent bone and cartilage destruction, maintaining or restoring joint function, and controlling systemic
involvement. Treatment is most successful when there is close cooperation between the doctor, nurse, patient, and family member.
Two classes of medications are used in treating rheumatoid arthritis: fast-acting “first-line drugs” and slow-acting “second-line drugs” (also referred to as Disease-
Modifying Anti-rheumatoid drugs or DMARDs). The first-line drugs, such as aspirin and cortisone (corticosteroids), are used to reduce pain and inflammation. The slow-acting
second-line drugs, such as gold, methotrexate and hydroxychloroquine (plaquenil) promote disease remission and prevent progressive joint destruction, but they are not anti-
inflammatory agents
SURGICAL MANAGEMENT
Surgery may be used to reduce pain, improve function, and correct deformities.
 TENDON TRANSFER-can prevent progressive deformity. Nodules or benign bony tumors may be surgically removed and flexion contractures surgically
relieved.

 OSTEOTOMY- may improve the function of deformed joints or limbs. For example, a femoral head osteotomy may give symptomatic relief by changing the
position of the head of the femur when it is being subjected to the stress of impact against the acetabulum.
 SYNOVECTOMY- removal of synovia, as in the elbows, wrist, fingers, or knees. Help maintain joint function
 ARTHRODESIS- is a surgical procedure to produce bony fusion of a joint and is used for clients with bone loss after joint infection, tumors, musculoskeletal
trauma, and paralysis.
 JOINT REPLACEMENT- is the surgical replacement of natural diseased joint or joint components with artificial joints or joint components.
 SHOULDER ARTHROPLASTY- is the replacement of humeral head and glenoid articulating surface with a metal and polyethylene prosthesis.
 ELBOW ARTHROPLASTY- uses hinge joints made from metal and polyethylene. This metal and plastic joints allows for some medial to lateral and rotational
movements.
 HAND ARTHROPLASTY- surgery includes tendon transfers to improve pinch grasp and arthrodesis for strength and position of the thumb for opposition.
Cholelithiasis
Definition
Cholelithiasis is another name for gallstones. Gallstones are hard, solid lumps that form from bile in the gallbladder. Bile is a special liquid chemical made by the liver that helps the body
break down and digest fats. The gallbladder is a storage sack for bile. One may have just one or many gallstones that can be as small as a piece of sand or as large as golf balls.
There are different kinds of gallstones. The most common stone is made of cholesterol (a fat-like material). A pigment stone is made up from bilirubin, which is a part of old, dead blood
cells. Other kinds of stones may be a mixture of cholesterol and bilirubin.
Gallstones in the gallbladder or in the bile ducts can cause problems. Stones can block bile ducts (flexible tubes). Bile ducts go from the liver to the gallbladder or from the gallbladder to
the small intestine. Gallstones are more common in woman than in men between 20 and 50 years of age. But, as one gets older, anyone can get gallstones.
Symptoms
Symptoms usually manifest after a stone of sufficient size (larger than 8mm) blocks the cystic duct or the common bile duct. The cystic duct drains the gallbladder, and the common bile
duct is the main duct draining into the duodenum.
Collectively, these ducts form part of the biliary system. A stone blocking the opening from the gallbladder or cystic duct usually produces symptoms of biliary colic, which is right upper
quadrant abdominal pain that feels like cramping. If the stone does not pass into the duodenum and still continues to block the cystic duct, acute cholecystitis, an inflammation of the gallbladder,
results.
If the common bile duct is blocked for a substantial period of time, certain bacteria may find their way up behind the stone and grow in the stagnant bile, producing symptoms of cholangiti,
an inflammation to the bile ductss. This is a serious condition and usually requires hospitalization. Continued blockage of normal bile flow may produce jaundice.
Stones blocking the lower end of the common bile duct where it enters the duodenum may obstruct secretion from the pancreas, producing pancreatitis, an inflammation of the pancreas.
This condition can also be serious and may require hospitalization. In general, following symptoms must be observed closely:

• Abdominal pain in the right upper quadrant or in the middle of the upper abdomen, which may be:
o recurrent
o sharp, cramping, or dull
o radiate to the back or below the right shoulder blade
o made worse by fatty or greasy foods
o Occurs within minutes of a meal
• Jaundice
• Fever
Often there are no symptoms. Additional symptoms that may be associated with this disease include :
• Clay-colored stools
• Nausea and vomiting
• Heartburn
• Gas or excessive flatus
• Abdominal indigestion
• Abdominal fullness, gaseous
As for our patient, he currently manifested slight yellowish coloration of his skin or more commonly known as jaundice.
Causes
Cholelithiasis is usually incidentally discovered by routine x-ray study, surgery, or autopsy. Virtually all gallstones are formed within the gallbladder, an organ that normally functions to
store bile excreted from the liver.
Bile is a solution composed of water, bile salts, lecithin, cholesterol and some other small solutes. Changes in the relative concentration of these components may cause precipitation from solution
and formation of a nidus, or nest, around which gallstones are formed. The cystic duct drains bile from the gallbladder. The hepatic duct drains bile from the liver. The hepatic duct and cystic duct
join to form the common bile duct which carries bile to the small intestine. When gallstones block these ducts, they may lead to the following more serious conditions
These stones may be as small as a grain of sand, or they may become as large as an inch in diameter, depending on how much time has elapsed from their initial formation. Depending on
the main substance that initiated their formation (for instance, cholesterol), they may be yellow or otherwise pigmented in color.
Risk Factors
• Gender
- Women tend to get gallstones more frequently than men due to their higher estrogen levels.
• Oral Estrogen Use
- In addition, women who take oral contraceptives or postmenopausal hormone replacement therapy seem to have a higher risk of gallstones due to the estrogen these

therapies contain.
• Pregnancy
- Pregnancy also increases estrogen levels, thereby increasing risk of gallstones.
• Increasing Age
- As you get older, usually 40 and over, your risk of gallstones increases.
• Obesity and Diet
- Having mainly abdominal fat appears to raise your risk of getting gallstones. Being even moderately overweight increases cholesterol in your bile, which may easily form
gallstones. In addition, rapid weight loss or fluctuating weight can also increase your risk because low-calorie diets cause the gallbladder to contract less. People who have
had gastric-bypass surgery to lose weight quickly also have an increased risk for gallstones.
• Lack of Physical Activity
- Lack of exercise is associated with a higher risk of developing gallstones, perhaps because the gallbladder is contracting less.
• Family History of Gallstones
- Like many other conditions, gallstones tend to run in families.
• Native American Ethnicity
- Native Americans develop gallstones more frequently than any other ethnicity in the United States.
• Diseases of the Small Intestines
- Having a disease of the small or large intestine such as Crohn’s disease is associated with a higher risk of gallstones.
• Need for Long-term Intravenous Nutrition (Total Parenteral Nutrition)
- When it is necessary to provide nutrition through the veins, therefore bypassing the intestines, the gallbladder is less stimulated since there is no food going through the
intestines. This increases your risk of gallstones.
Diagnostic Tests:
o Blood Tests.
o ERCP is also called endoscopic retrograde cholangiopancreatography, a test done during an endoscopy to find stones, tumors, or other reasons for the problem. Dye is put into the
endoscopy tube. The dye then goes into your pancreas and bile ducts to help them show up better on x-rays. If one has stones, they can sometimes be removed during ERCP. People
who are allergic to shellfish (lobster, crab, or shrimp) may be allergic to this dye, thus assessment for allergies are important.
o HIDA scan is a nuclear medicine test. Radioactive material is given in IV fluids. Then x-rays are taken to help caregivers find blockages.
o Oral cholecystography is a test where one is given a shot or take pills with a special dye in them. X-rays are then taken over time. The test shows the gallbladder and any stones that
might be blocking the ducts. Some people are also allergic to this kind of dye. Assess for allergies to shellfish (lobster, crab, or shrimp).
o Ultrasound.
Our patient underwent ultrasound of his abdomen and revealed an 8.00mm stone within gallbladder with no evidence of cholecystitis.
Medical Management
o Changes in the diet such as eating foods that have less fat.
o Medicines for pain and nausea.
o ESWL is also called extracorporeal shockwave lithotripsy. Shock waves from a special machine are used to break up stones. The tiny pieces then pass through the bile ducts
without getting stuck.

Surgical Management
o Focused on removing the stones. The most common surgery is called a laparoscopic cholecystectomy.
- The surgical removal of the gallbladder, a muscular, pear-shaped organ that lies underneath the liver.
RATIONALE OF STUDY
In choosing this case study for the presentation, we first weighed the significance of the case. Though it was quite complex making this choice, but we had to make a stand firm.
Upon making our history and assessment of our patient, we learned that he is currently faced with 5 problems, which added more interest to the case. 1st
is Diabetes Mellitus, diagnosed 16
years ago. He has DM type 2, considered the most common form. It appears most often in middle-aged adults. It develops when the body doesn’t make enough insulin and doesn’t efficiently use the
insulin it makes (insulin resistance), thus is also known as non insulin-dependent diabetes mellitus.
2nd
is his Hypertension stage 2 diagnosed 6 years ago, a medical condition in which constricted arterial blood vessels increase the resistance to blood flow, causing an increase in blood
pressure against vessel walls. The heart then must work harder to pump blood through the narrowed arteries. This stage 2 hypertension is the type wherein blood pressure readings reach 160/100

mm Hg or higher. 3rd
is Cholelithiasis diagnosed last June 27, 2007, a condition wherein gallstones are formed within the gallbladder by accretion or concretion of normal or abnormal bile
components.
4th
is Nephrolitiasis diagnosed just recently on June 29, 2007. This is the formation of a stone within the urinary tract. Most of these stones are too large to pass through the narrow conduits
of the collecting system, thus obstruct the flow of urine and often cause severe pain. 5th
is his Rheumatoid Arthritis, diagnosed last 2000, which is an autoimmune disease that causes chronic
inflammation of the joints. This can also cause inflammation to the tissue around the joints, as well as other organs in the body.
With his present condition, this caught our attention and concern as good citizens of the society and as nursing students. In making this case study presentation of R.M., we seek to discover
more about these various conditions, how such conditions could complicate to other disease processes, and ways of preventive measures and management in dealing with his illnesses.
This study is guided by a theory. We opted to use Betty Neuman’s System Model, since it reflects the morals of our practice by focusing on the person as a complete system, and
provide a wholistic overview of the physiological, psychological, sociocultural, and developmental aspects of human beings. The use of nursing theories helps to serve as a framework for
the development of nursing knowledge
REVIEW OF RELATED LITERATURE
Diabetes mellitus is a group of metabolic diseases characterized by high blood sugar (glucose) levels, which result from defects in insulin secretion, or action, or both. Diabetes mellitus, commonly referred to
as diabetes (as it will be in this article) was first identified as a disease associated with “sweet urine," and excessive muscle loss in the ancient world. Elevated levels of blood glucose (hyperglycemia) lead to spillage of
glucose into the urine, hence the term sweet urine. Normally, blood glucose levels are tightly controlled by insulin, a hormone produced by the pancreas. Insulin lowers the blood glucose level. When the blood glucose
elevates (for example, after eating food), insulin is released from the pancreas to normalize the glucose level. In patients with diabetes, the absence or insufficient production of insulin causes hyperglycemia. Diabetes is a
chronic medical condition, meaning that although it can be controlled, it lasts a lifetime.
Proper nutrition is essential for anyone living with diabetes. Control of blood glucose levels is only one goal of a healthy eating plan for people with diabetes. A diet for those with diabetes should also help achieve and
maintain a normal body weight as well as prevent heart and vascular disease, which are frequent complications of diabetes.
There is no prescribed diet plan for those with diabetes. Rather, eating plans are tailored to fit an individual’s needs, schedules, and eating habits. A diabetes diet plan must also be balanced with the intake of insulin and
oral diabetes medications. In general, the principles of a healthy diabetes diet are the same for everyone. Consumption of a variety of foods including whole grains, fruits, non-fat dairy products, beans, and lean meats or
vegetarian substitutes, poultry and fish is recommended to achieve a healthy diet.
Many experts, including the American Diabetes Association, recommend that 50 to 60 percent of daily calories come from carbohydrates, 12 to 20 percent from protein, and no more than 30 percent from fat. People with
diabetes may also benefit from eating small meals throughout the day instead of eating one or two heavy meals. No foods are absolutely forbidden for people with diabetes, and attention to portion control and advance
meal planning can help people with diabetes enjoy the same meals as others in the family.
Some people with diabetes will benefit from using specific methods to help follow a diabetes meal plan. None of these diet plans is required for people with diabetes, but many people will find one them useful. Some of
these ways include:

Rating your plate is a meal planning system based upon portion size. Imaginary lines are used to divide a meal plate into two halves, and one half is further divided into fourths. One-fourth of the plate should contain
grains/starches, one-fourth should contain protein, and the remaining half should contain non-starchy vegetables.
Exchange lists help in the planning of balanced meals by grouping together foods that have similar carbohydrate, protein, fat, and calorie content. Meal planning exchange lists have been published by The American
Dietetic Association and the American Diabetes Association.
Carbohydrate counting is based upon the total carbohydrate intake (measured in grams) of foods.
Glycemic Index ranks carbohydrates according to the effects they have on blood sugar levels. [http://www.medicinenet.com/diabetes_mellitus/article.htm]
Nephrolithiasis: The process of forming a kidney stone, a stone in the kidney (or lower down in the urinary tract). Kidney stones are a common cause of blood in the urine and pain in the abdomen, flank, or
groin. Kidney stones occur in 1 in 20 people at some time in their life. The development of the stones is related to decreased urine volume or increased excretion of stone-forming components such as calcium, oxalate,
urate, cystine, xanthine, and phosphate. The stones form in the urine collecting area (the pelvis) of the kidney and may range in size from tiny to staghorn stones the size of the renal pelvis itself.
[ http://www.medterms.com/script/main/art.asp?articlekey=6806]
Calcium oxalate kidney stone formers are invariably advised to increase their fluid intake. In addition, magnesium therapy is often administered. Recently, a prospective study showed that a high dietary intake of calcium
reduces the risk of symptomatic kidney stones. The present study was performed to test whether simultaneous delivery of these factors--high fluid intake, magnesium ingestion and increased dietary calcium--could
reduce the risk of calcium oxalate kidney stone formation. A French mineral water, containing calcium and magnesium (202 and 36 ppm, respectively) was selected as the dietary vehicle. Twenty calcium oxalate stone-
forming patients of each sex as well as 20 healthy volunteers of each sex participated in the study. Each subject provided a 24-hour urine collection after ingestion of mineral water over a period of 3 days; after a suitable
rest period the protocol was repeated using local tap water (Ca: 13 ppm, Mg: 1 ppm). In addition, 24-hour urines were collected by each subject on their free diets. The entire cycle was repeated at least twice by each
subject. Several risk factors (excretion of oxalate; relative supersaturations of calcium oxalate, brushite and uric acid; calcium oxalate metastable limit; oxalate:magnesium ratio and oxalate:metastable limit ratio) were
favourably altered by the mineral water and tap water regimens but the former was more effective. In addition, the mineral water protocol produced favourable but unique changes in the excretion of citrate and
magnesium as well as in the relative supersaturation of brushite which were not achieved by the tap water regimen. To the contrary, tap water produced an unfavourable change in the magnesium excretion. The group
which benefitted most were male stone formers in whom 9 risk factors were favourably altered by the mineral water protocol. It is concluded that mineral water containing calcium and magnesium, such as that used in
this study, deserves to be considered as a possible therapeutic or prophylactic agent in calcium oxalate kidney stone disease. [http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd]
One in every 20 people develop a kidney stone at some point in their life. A kidney stone is a hard mineral and crystalline material formed within the kidney or
urinary tract. Kidney stones are a common cause of blood in the urine and pain in the abdomen, flank, or groin. Kidney stones are sometimes called renal calculi.
New research shows that lemonade is an effective -- and delicious -- way for kidney-stone-prone people to slow the development of new stones. "When treating
patients in our kidney stone center, we put everyone on lemonade therapy," says Steven Y. Nakada, chair and professor of urology at the University of Wisconsin,
Madison. If you've ever passed a kidney stone, you won't forget the sudden, intense pain in your flank. Some patients compare the pain with that of childbirth.
Kidney stones form when urine in the kidney becomes supersaturated with stone-forming salts -- and when the urine doesn't contain enough stone-preventing
substances. One of these substances is citrate. For people prone to stones, doctors usually prescribe potassium citrate. It can be taken as a pill or in liquid form. But
lemon juice is full of natural citrate. When made into low-sugar or sugar-free lemonade, Nakada and colleagues found, lemon juice increases the amount of citrate in
the urine to levels known to inhibit kidney stones. It doesn't work quite as well as potassium citrate. But for patients who'd rather avoid yet another medication,
lemonade is an attractive alternative. "The trend is going to be, if you can make a change in your diet and avoid medications, you are going to try to do that,"
Nakada said. "We see lemonade therapy as playing a role."
David Kang, a medical student and researcher at the Duke University Comprehensive Kidney Stone Center, found that this role can play for a long time. Kang and
colleagues followed 12 kidney-stone patients who had been on lemonade therapy for up to four years. Over the time they drank lemonade they had a lower burden
of kidney stones and appeared to form kidney stones at a slower rate than they did before starting lemonade therapy. Kang says a large-scale clinical trial will be

needed to confirm these findings. "None of the patients needed medical intervention over a mean treatment period of four years," Kang said. But lemonade alone
isn't the answer to kidney stones. It's only part of a stone-preventing diet. "First, you should reduce the amount of salt in the diet," Stoller says. "Get rid of the salt
shaker at the table. Use a potassium-based salt substitute. If you have a choice of two products, go to the one with less salt. Eat out less -- restaurant food is salty --
and never salt your food before tasting it." Second on Stoller's stone-prevention diet is eating smaller portions of meat and fish at each meal. "We are not saying to
eat less meat, just eat less at individual meals," he says. Third, increase fluid intake to where one is passing 1.5 to 2 liters of urine each day.
" In the quest for the causes of and potential treatments for rheumatoid arthritis, Japanese researchers have identified a protein that could be a target for
future therapy. Rheumatoid arthritis (RA) is a chronic and disabling autoimmune disease that first attacks the fluid that surrounds the joints, causing it to thicken and
grow abnormally, damaging the joints and surrounding cartilage rather than protecting them. More than 2 million Americans suffer from the illness, according to the
Arthritis Foundation. By identifying a protein that appears to be one of the culprits in the unhealthy buildup of this fluid, which is called synovial fluid, Dr. Yasushi
Miura and her colleagues at Kobe University School of Medicine hope that a new, targeted medication can be developed to treat the disease.
"The protein Decoy receptor 3 (DcR3) is one of the pathological factors of RA and can be a new therapeutic target for treatment," said Miura, an associate professor
in the division of orthopedic sciences at the medical school. DcR3 is a member of the large tumor necrosis factor receptor (TNFR) "super family," which has been
identified in the last decade as important in the regulation of cell growth and cell death, fundamental processes in biology, said Dr. Robert Hoffman, director of the
division of rheumatology and immunology at the University of Miami Miller School of Medicine in Florida. "We have known of the importance of cell growth and
cell death in studying cancer but more recently have found that it is also important in autoimmune diseases like RA and lupus," he said.
It was the similarity between the growth of malignant tumors and the abnormal growth of synovial tissue, called hyperplasia, that sparked Miura's research into
DcR3 and rheumatoid arthritis. DcR3 is known to be produced in tumor cells, including lung and colon cancers. What Miura and her colleagues found was that
DcR3 works with another member of the TNFR family to slow the normal cell death of synovial fluid cells, resulting in the hyperplasia that causes some of the
inflammation characteristic of rheumatoid arthritis. Hoffman said: "This is a novel application of the connection between this specific member of the TNFR super
family and RA, and studies like this are how we advance science. But it is currently a giant leap to suggest that this could be a therapy for RA."
For their study, Miura and her colleagues isolated and cultured synovial fluid from19 patients with rheumatoid arthritis, obtained during total knee replacement
surgery. For comparison, they also extracted synovial fluid in the same manner from 14 patients with osteoarthritis. The researchers then exposed the synovial fluid
to another TNFR protein called Fas, which induces cell death, called apoptosis. Finally, the fluid was incubated with a pro-inflammatory member of the TNFR
family, called TNFa. The TNFR family includes proteins that both induce and retard cell death, Miura explained. While DcR3 was present in the same amounts in
the fluids of both the rheumatoid arthritis and osteoarthritis patients, when the TNFa was introduced, DcR3 production increased in the fluid of the RA patients,
slowing down the Fas-induced cell death. The rate of cell death did not change in the fluid of the osteoarthritis patients, perhaps, Miura suggested, because the TNFa
levels were higher in the fluid of RA patients to begin with.
Miura said the results show that DcR3 acts in conjunction with TNFa to suppress the cell death necessary to keep synovial fluid healthy, and research aimed at
reducing the amount of DcR3 in the synovial fluid in rheumatoid arthritis patients could be productive. Dr. Stephen Lindsey, head of rheumatology at the Ochsner

Clinic Foundation., said, "We are always looking for better and more specific targets to control immune response, and this study is very intriguing." Lindsey said
there are drugs available that inhibit those proteins that suppress cell death, but because they are "global," rather than targeted to particular proteins, there are many
side affects, including infection. [http://ww2.arthritis.org/resources/news/womenmethotrexate.asp]
Gallstones are stones that form in the gall (bile). Bile is a watery liquid made by the cells of the liver that is important for digesting food in the intestine,
particularly fat. Liver cells secrete the bile they make into small canals within the liver. The bile flows through the canals and into larger collecting ducts within the
liver (the intrahepatic bile ducts). The bile then flows within the intrahepatic bile ducts out of the liver and into the extrahepatic bile ducts-first into the hepatic bile
ducts, then into the common hepatic duct, and finally into the common bile duct. From the common bile duct, there are two different directions that bile can flow.
The first direction is on down the common bile duct and into the intestine where the bile mixes with food and promotes digestion of food. The second direction is
into the cystic duct, and from there into the gallbladder (often misspelled as gall bladder). Once in the gallbladder, bile is concentrated by the removal (absorption)
of water. During a meal, the muscle that makes up the wall of the gallbladder contracts and squeezes the concentrated bile in the gallbladder back through the cystic
duct into the common duct and then into the intestine. (Concentrated bile is much more effective for digestion than the un-concentrated bile that goes from the liver
straight into the intestine.) The timing of gallbladder contraction-during a meal-allows the concentrated bile from the gallbladder to mix with food.
Yo-yo dieting may have another unhealthy and particularly painful side effect for men: gallstones. A new study shows men who repeatedly lose, then regain 20 or
more pounds through dieting are up to 76% more likely to develop gallstones later in life than men who maintain a constant weight. Gallstones occur when a solid
mass of cholesterol, bile, and calcium salts form in the gallbladder, often causing severe pain in the stomach area and requiring surgical treatment. Obesity and
rapid weight loss associated with dieting are known to increase the risk of developing gallstone disease, but researchers say the long-term effects of frequent weight
fluctuation on gallstone risk in men hasn't been clear.
In the study, published in the Archives of Internal Medicine, researchers analyzed data on nearly 25,000 men who participated in the Health Professionals Follow-up
Study. The men provided information on weight fluctuations from 1988 to 1992 and were followed from 1992 to 2002 for gallstones. The results showed gallstones
were more likely in men whose weight fluctuated more than 5 pounds than those who maintained a constant weight, and the risk of gallstones increased with the
degree of weight fluctuation.
Percentages take into account other factors, such as age, physical activity, alcohol intake, smoking, dietary factors, and use of certain medications. The risk of
gallstones also increased with the number of yo-yo dieting attempts. Men who lost and regained weight more than once had nearly double the risk of gallstones
when compared with men who maintained their weight. Researcher Chung-Jyi Tsai, MD, ScD of the University of Kentucky Medical Center, Lexington, and
colleagues say many factors associated with yo-yo dieting may work to raise the risk of gallstones, such as an increased concentration of cholesterol in the bile
associated with rapid weight loss.
High blood pressure or hypertension means high pressure (tension) in the arteries. Arteries are vessels that carry blood from the pumping heart to all the
tissues and organs of the body. High blood pressure does not mean excessive emotional tension, although emotional tension and stress can temporarily increase

blood pressure. Normal blood pressure is below 120/80; blood pressure between 120/80 and 139/89 is called "pre–hypertension", and a blood pressure of 140/90 or
above is considered high.
It seems that the association between body mass index (BMI) and high blood pressure or hypertension has decreased since 1989, researchers say. The finding
suggests that obesity may not have as much of an impact on heart-related disease as previously thought. "High blood pressure is a leading cause of the global burden
of disease," Dr. Pascal Bovet, of the University of Lausanne, Switzerland, and colleagues write in the medical journal Epidemiology. "The prevalence of
hypertension, and of several other conditions (including diabetes), is considered to be linked to the worldwide epidemic of obesity."
The researchers examined trends in blood pressure and BMI over a 15-year interval in the Seychelles. Their analysis was based on two independent surveys
conducted in 1989 and 2004 using representative samples of the population between the ages of 25 and 64 years. There was a slight decrease in average blood
pressure between 1989 and 2004 in both men and women. The prevalence of high blood pressure changed little during this time -- from 45 to 44 percent in men and
from 34 to 36 percent in women. The percentage of people who were overweight, defined as a BMI of 25 or more, increased from 39 percent to 60 percent between
1989 and 2004.
However, the association between BMI and BP decreased "substantially and consistently" between 1989 and 2004, irrespective of sex, Bovet's team writes. "If
confirmed, a decreasing association between BMI and blood pressure over time could imply that the impact of the overweight epidemic on cardiovascular disease
might be less important than predicted," the investigators conclude. "This decreased relationship could also help to explain the current favorable trends in
cardiovascular disease (declining incidence) observed in many countries despite the increasing prevalence of obesity," they point out.
[http://www.nlm.nih.gov/medlineplus/news/fullstory_51634.html]
Chocolate treat may be better than green or black tea at keeping high blood pressure in check. A new study suggests that dark chocolate and other cocoa-rich
products may be better at lowering blood pressure than tea. Researchers compared the blood pressure-lowering effects of cocoa and tea in previously published
studies and found eating cocoa-rich foods was associated with an average 4.7-point lower systolic blood pressure (the top number in a blood pressure reading) and
2.8-point lower diastolic blood pressure (the bottom number). But no such effect was found among any of the studies on black or green tea. Cocoa and tea are both
rich in a class of antioxidants known as polyphenols. But researchers say they contain different types of polyphenols, and those in cocoa may be more effective at
lowering blood pressure.
ANATOMY OF THE LIVER
- the largest organ in the body located under the diaphragm more on the right side of the body specifically at the upper right
quadrant of the body. The dark, reddish brown colored liver usually weighs 1.4 kg or about 3 lbs. It is enclosed by a fibrous
connective tissue known as capsule. It has four lobes and is suspended from the diaphragm and abdominal wall by a delicate
mesentery cord, the falciform ligament. It has many metabolic and regulatory roles; however, its digestive function is to produce
bile. Bile leaves the liver through the common hepatic duct and enters the duodenum through the bile duct. The functional unit
of liver is lobule and hepatocyte is the major cell.
Bile is a yellow-to-green, watery solution containing bile salts, bile pigments(chiefly bilirubin, a breakdown product of
hemoglobin), cholesterol, phospholipids, and a variety of electrolytes. Of these components, only the bile salts (derived from

cholesterol) and phospholipids aid the digestive process. Bile does not contain enzymes, but its bile salts emulsify fats by physically breaking large fat globules into smaller ones, thus providing more surface area for the
fat-digesting enzymes to work on.
From the liver, bile drips into the hepatic duct, which soon meets the cystic duct arriving from the gallbladder. Converging, they form one duct, the common bile duct, which meets the pancreatic duct, carrying enzymatic
fluid from the pancreas. Like a smaller river meeting a larger one, the pancreatic duct loses its own name at this confluence and becomes part of the common bile duct, which empties on demand into the duodenum.
When the sphincter of the bile duct is closed, bile from the liver is forced to back up into the cystic duct, and eventually into the gallbladder. There it is stored and concentrated until needed, when it flows back down the
cystic duct.
Lobes of liver:
- right and left lobes
* liver receives blood from 2 sources:
 Hepatic artery-will supply oxygen blood to the liver cells
 Hepatic portal vein- will bring deoxygenated
Functions of liver:
1. Detoxify poisonous and harmful chemicals like drugs and alcohol
2. maintaining blood glucose levels within normal range(70mg-110mg/dL or 80mg-120mg/dL)
 Glycogenesis- glucose converted to glycogen and stored in the liver.
 Glycogenolysis- stored glycogen converted to glucose
 Gluconeogenesis- glucose formation from no-carbohydrate substances such as fats and proteins. Also known as “formation of new sugar”
3. cholesterol metabolism and transport
 LDL’s- transports cholesterol and other lipids to body cells
-large amounts will be deposited on the arterial walls causing atherosclerosis
-tagged as bad lipoproteins
 HDL’s- good cholesterol because this is destined to be broken down and be eliminated from the body
Functions of bile:
- emulsifies fats
- absorption of fat-soluble vitamins(K,D, and A)
ANATOMY OF THE GALLBLADDER
- is a small, thin-walled green sac that snuggles in a shallow fossa in the inferior surface of the liver. When food digestion is not occurring,
bile backs up the cystic duct and enters the gallbladder to be stored. While being stored in the gallbladder, bile is concentrated by the
removal of water. Later, when fatty food enters the duodenum, a hormonal stimulus prompts the gallbladder to contract and spurt out
stored bile, making it available to the duodenum
Functions of gallbladder:
- Act as storage of to-be-used bile
Remember:

If bile is stored in the gallbladder for too long or too much water is removed, the cholesterol it contains may crystallize, forming gallstones. Since gallstones tend to be quiet sharp
blockage of the common hepatic duct or bile ducts prevents bile from entering the small intestine, and it begins to accumulate and eventually backs up into the liver exerting pressure into the liver cells. Then, bile salts
and bile pigments begin to enter the bloodstream. As it circulates through the body, the tissues become yellow, or jaundiced.
Jaundice caused by blockage of ducts more often results from actual liver problems such as hepatitis(liver inflammation) or cirrhosis, a chronic inflammatory condition in which the liver is severely damaged and
becomes hard and fibrous.
ANATOMY OF THE PANCREAS
It is an elongated, soft lobulated organ that stretches obliquely across the posterior abdominal wall in the epigastric region. It is situated behind the stomach and extends from the duodenum to the spleen. The
pancreas lies across the transpyloric plane. The pancreas is divided into a head, neck, body and tail.
The head of the pancreas is disc shaped and lies within the concavity of the deudenum. A part of the head extends to the left behind the superior mesenteric vessels. The neck is the constricted portion of the
pancreas and connects the head to the body. It lies in front of the beginning of the portal vein and the origin of the superior mesenteric artery from the aorta. The body runs upward and to the left across the midline. It is
somewhat triangular in cross section. The tail passes forward in the splenicorenal ligament in contact with the hilum of the spleen.
The pancreas is composed of two major type of cell, the acini and the islet of Langerhans. The acini secretes digestive juices into the deudenum and the islet of Langerhans secrete insulin and glucagons
directly into the blood.
The secretion of the exocrine portion of the pancreas is collected in the pancreatic duct, which joins the common bile duct and enters the deudenum at the ampulla of Vater. Surrounding the ampulla is the
sphincter of Oddi, which partially controls the rate at which secretions from the pancreas and gallbladder enter the deudenum.
The secretions of the exocrine pancreas are digestive enzyme high in protein content and an electrolyte-rich fluid. The secretions, which are very alkaline because of their high concentration of sodium
bicarbonate, are capable of neutralizing the high gastric juice that enters the duodenum. The enzyme secretions are amylase, trypsin and lipase. The enzyme amylase aids in the digestion of carbohydrate, the trypsin aids
the digestion of proteins and the lipase aids the digestion of fats. Other enzyme that promote the breakdown of more complex foodstuffs are also secreted. Hormones originating in the gastrointestinal tract stimulate the
secretion of these exocrine pancreatic juices. The hormone secretin is the major stimulus for increased bicarbonate secretion from the pancreas. The vagus nerve also influences exocrine pancreatic secretion.
The islet of Langerhans is the endocrine part of the pancreas. It is a collection of cells embedded in the pancreatic tissue. The islet of Langerhans contain three major type of cells, the alpha, beta and delta cells.
The alpha cells secrete glucagons, the beta cells secrete insulin and the delta cells secrete somatostatin.
Relations:
Anteriorly: from right to left, the transverse colon and the attatchment of the transverse mesocolon, the lesser sac, and the stomach.
Posteriorly: from right to left, the bile duct, the portal and spleenic veins, the inferior vena cava, the aorta, the origin of the superior mesenteric artery, the left psoas muscle, the left suprarenal gland, the left kidney, and
the hilum of the spleen.
Pancreatic Ducts:
The main duct of the pancreas begins in the tail and runs the length of the gland, receiving numerous tributaries on the way. It
opens in the second part of the deudenum at about its middle with the bile duct drains separately into the deudenum.
The accessory duct of the pancreas, drains the upper part of the head and then opens into the deudenum short distance above the
main duct. The accessory duct frequently communicates with the main duct.
Blood Supply:
Arteries: The spleenic and the superior and inferior pancreaticoduodenal arteries supply the panceas.
Veins: The corresponding vein drain into the portal systm.

Lymph drainage: Lymph nodes situated along the arteries supply the gland. The efferent vessels ultimately drain into the celiac and superior mesenteric lymph nodes.
Nerve Supply: Sympathetic and parasympathetic (vagal) nerve fibers supply the area.
Function of pancreas:
Exocrine- release of pancreatic enzymes
 Pancreatic lipases- responsible for final digestion of fats
 Pancreatic amylase- completes starch digestion
 Trypsin- splits proteins into shorter amino acids chains known as peptides
 Chymotrypsin, carboxypeptidase- carries about half of protein digestion
Endocrine- release of insulin and glucagons by the islets of langerhans
 Insulin- high blood glucose levels stimulates its release from the beta cells
 Glucagons- low blood glucose levels stimulates its release from the alpha cells
• without insulin, blood glucose levels rise to higher levels leading known as hyperglycemia. In such cases, glucose begins to spill into the urine because tubule cells of kidney cannot reabsorb it fast
enough. As glucose flushes into the body, water follows leading to dehydration. The clinical name for this condition is called diabetes mellitus. For cells cannot use glucose, fats and even protein are
broken down and used to meet body requirements. As a result, body weight begins to decline. Loss of body proteins leads to decreased ability to fight infections, so diabetic must be very careful in
hygiene and caring for even small cuts and bruises. When large amounts of fats(instead of sugars) are used for energy, blood becomes very acidic(acidosis)as ketones appear in the blood.
• Three cardinal signs are:
1. polyuria- increased urination
2. polydipsia- excessive thirst
3. polyphagia- hunger due to inability to use sugars and loss of fats and proteins
Pancreatic juice contains:
 Bicarbonates- responsible for its basicity (pH 8)
Hormones:
 Secretin- causes the liver to increase its output of bile
 Cholecystokinin(CCK)- causes gallbladder to contract and release stored bile into
the bile duct so that bile and pancreatic juice enter the
small intestine together
ANATOMY OF THE KIDNEYS
The kidneys balance the urinary excretion of substances against the accumulation within the body through ingestion and production.
They are a major controller of fluid and electrolyte balance. The kidneys also have several nonexcretory metabolic and endocrine functions,
including blood pressure regulation, erythropoietin production, insulin degradation, prostaglandin synthesis, calcium and phosphorus regulation
and vitamin D metabolism.
The kidneys are two reddish brown bean-shaped organs situated retroperitoneally on the posterior abdominal wall, one on each side of
the vertebral column. They lie between the 12th
thoracic and the 3rd lumbar vertebrae. The right kidney lies at a slightly lower level than the left
kidney (because of the bulk of the right lobe of the liver). The left kidney gives rise to a ureter that runs vertically downward the psoas muscle.

Both kidneys move downward in a vertical direction by as much as 1 inch with the contraction of the diaphragm. Adult kidneys average approximately 11cm in length, 5 to 7.5 cm in width, and 2.5 cm in thickness and
approximately weigh 113 to 170g.
Behind the parietal peritoneum is a mass of perirenal fat or the adipose capsule covers the fibrous capsule which forms the external covering of the kidney and is closely applied to its outer surface. The
condensation of connective tissue called Gerota’s fascia which lies outside the perirenal fat encloses the kidneys and suprarenal glands. It is contiuous laterally with the fascia transversalis. Lies external to the renal fascia
and often in large quantity is the pararenal fat which forms part of the retroperitoneal fat. The perirenal fat, renal facia and pararenal fat support the kidneys and hold them in position on the posterior abdominal wall. The
kidney is further protected externally by layers of muscle of the back, flank, and abdomen as well as by layers of fat, subcutaneous tissue, and skin.
The kidney has a curved shape with a convex distal edge and a concave medial boundary. The medial concave border of each kidney is a vertical slit that is enclosed by thick lips of renal substance which is
called the hilus. On The hilum extends into a large cavity called the renal sinus. The hilum transmits, the renal vein, two branches of the renal artery, the renal pelvis which is the upper extension of the ureter and the
third branch of the renal artery. Lymph vessels and sympathetic fibers also pass through the hilum.
Each kidney has a dark brown outer cortex and a light brown inner medulla. The cortex of the kidney lies just under the fibrous capsule and portions of it extend down into the medullary layer to form the
renal columns which is called the columns of Bertin. It is a cortical tissue that separates the renal pyramids. The medulla is divided into 8 to 18
cone-shaped masses of collecting ducts called the renal pyramids. Each renal pyramid has its base oriented toward the cortex. Their apices extend
toward the renal pelvis forming the renal papilla which projects medially.
The papillae have 10 to 25 openings each on the surface through which the urine empties into the renal pelvis. Eight or more groups of
papillae are present in each pyramid. Each pyramid empties into a minor calyx and several minor calices join to form a major calyx. The two to
three major calices channels the urine from the pyramids to the renal pelvis.
The renal pelvis is a cavity lined with transitional epithelium. The combined volume of the pelvis and calices is approximately 8 ml.
Volume in excess of this amount damage the renal parechymal tissue. The renal pelvis narrows as it reaches the hilus and becomes the proximal end
of the ureter.
Within the cortex lies the nephron, the functional unit of the kidney. Each kidney in the human is made up of about 1 million nephrons
each capable of forming urine. Each nephron consists of both vascular and tubular elements. The vascular element is the glomerulus through which
large amounts of fluid are filtered form the blood and the long tubular element in which the filtered fluid is converted into urine on its way to the
pelvis.
The glomerulus is composed of a network of branching and anastomosing glomelular capilliaries that have a high hydrostatic pressure
(about 60mmHg). The glomelular capilliaries are covered by epithelial cells. Filtration begins at the renal glomerulus. The glomelura tuft or the
glomerulus which is composed of a network of branching and anastomosing capiliaries and the beginning of the tubule system which is the
Bowman’s capsule. Filtrate from the glomerulus enters the Bowman’s capsule and then passes through a series of tubule segments which is the
proximal tubule that modify the filtrate as it passes through the renal cortex.
From the proximal tubule, fluid flows into the loop of henle that dips into the renal medulla. Each loop consist of a descending and an
ascending limb. The walls of the descending limb and the lower end of the ascending limb are very thin thus are called the thin segment of the loop
of Henle. After the ascending limb of the loop has returned part back to the cortex, its wall becomes thick like the other portions of the tubular
system.
At the end of the thick ascending limb is a short segment known as macula densa. Beyond the macula densa, fluid enters the distal tubule which lies also in the renal cortex. This is followed by the connecting
tubule and the cortical collecting tubule, which lead to the cortical collecting duct. The collecting ducts merge to form progressively larger ducts that eventually empty into the renal pelvis through the tips of renal
papillae.
A secondary capillary bed which is the peritubular capillaries carries the reabsorbed water and solutes back toward the vena cava.
Anterior organs of the right kidney are the suprarenal gland, the liver, the second part of the deudenum, and the right colic flexure. Posterior of it are the diaphragm, the twelfth rib, and the psoas and transverses
muscle. While in anterior to the left kidney is the suprarenal gland, the spleen, the stomach, the pancreas, the left colic flexure, and coils of jejunum. Posteriorly are the diaphragm, the eleventh and twelfth ribs and the
psoas.
ANATOMY OF CARDIOVASCULAR SYSTEM

Heart
Location & Size:
Approximately the size of a person’s fist, the hollow, cone-shaped heart weighs less than a pound. The heart
is located within the bony thorax and is flanked on each side by the lungs. Its more pointed apex is directed toward
the left hip and rests on the diaphragm, approximately at the level of the fifth intercostal space. Its broader posterosuperior aspect, or base, from which the great vessels of the body emerge, points toward the right
shoulder &
lies beneath the second rib.
Covering & Wall:
The heart is enclosed by a double sac of serous membrane, the pericardium. The thin visceral pericardium, or epicardium tightly hugs the external
surface of the heart and is actually part of the heart wall. It is continuous with the heart base with the loosely applied parietal pericardium, which is reinforced
on its superficial face by dense connective tissue. This fibrous layer helps protect the heart and anchors it to surrounding structures, such as the diaphragm and the
sternum.
The heart walls are composed of three layer. The outer epicardium (the visceral pericardium described above), the myocardium, and the innermost
endocardium. The myocardium consists of thick bundles of cardiac muscle twisted in ringlike arrangements. It is the layer that actually contracts. The
myocardium is reinforced internally by a dense, fibrous connective tissue network called the “skeleton of the heart.” The endocardium is a thin, glistening sheet
of endothelium that lines the heart chambers.
Chambers & Associated Great Vessels:
The heart has four hollow chambers of cavities—two atria and two ventricles. The superior atria are primarily receiving chambers. As a rule, they are
not important in the pumping activity of the heart. Blood flows into
the atria under low pressure from the veins of the body and then continues on to fill the ventricles. The inferior thick-walled ventricles are the discharging
chambers or actual pumps of the heart. When they contract, blood is propelled
out of the heart and into the circulation.
The septum that divides the heart longitudinally is referred to as the interventricular or interatrial septum, depending on which chamber it divides
and separates.
Although it is a single organ, the heart functions as a double pump. The right side works as the pulmonary circuit pump (pulmonary circulation) and
the left side is responsible for the systemic circulation.
Valves:
The heart is equipped with four valves, which allow blood to flow in only one direction through the heart chambers. The atrioventricular, or AV,
valves are located between the atrial and ventricular chambers on each side. The AV valves prevent backflow into the atria when the ventricles contract. The left
AV valve—the bicuspid or mitral valve consists of two cusps, or flaps, of endocardium. The right AV valve, the tricuspid valve, has three cusps. Tiny white
cords, the chordae tendianeae—literally “heart strings”, anchor the cusps to the walls of the ventricles. The second set of valves, the semilunar valves, guards
the bases of the two large arteries leaving the ventricular chambers. Thus, they are known as pulmonary and aortic semilunar valves. Each semilunar valve has three cusps.
Each set of valves operates at a different time. The AV valves are open during heart relaxation and closed when the ventricles are contracting. The semilunar valves are closed during hear relaxation and are
forced open when the ventricles contract.
Cardiac Circulation:
Although the heart chambers are bathed with blood almost continuously, the blood contained in the heart does not nourish the myocardium. The blood supply that oxygenates and nourishes the heart is provided
by the right and left coronary arteries. The coronary arteries branch from the base of the aorta and encircle the heart in the atrioventricular groove at the junction of the atria and ventricles. The coronary arteries and
their major branches (the anterior interventricular and circumflex arteries on the left, and the posterior interventricular and marginal arteries on the right) are compressed when the ventricles are contracting and fill
when the heart is relaxed. The myocardium is drained by the cardiac veins, which empty into a large vessel on the backside of the heart called the coronary sinus. The coronary sinus, in turn, empties into the right
atrium.
Conduction System of the Heart:

Two types of controlling systems act to regulate heart activity. One of these involves the nerves of the autonomic nervous system that act
like “brakes” and “accelerators” to decrease and increase the heart rate depending on which division is activated. The second system is the
intrinsic conduction system, or nodal system, that is built into the heart tissue.
The intrinsic conduction system is composed of special tissue found nowhere else in the body. This system cause heart muscle
depolarization in only one direction—from the atria to the ventricles. In addition, it enforces a contraction rate of approximately 75 beats per
minute on the heart; thus, the heart beats as a coordinated unit.
One of the most important parts of the intrinsic conduction system is a crescent-shaped node of tissue called the sinoatrial (SA) node,
located in the right atrium. Other components include the atrioventricular (AV) node at the junction the atria and ventricles, the atrioventricular
(AV) bundle (bundle of His), and the right and left bundle branches located in the interventricular septum, and finally the Purkinje fibers,
which spread within the muscle of the ventricle walls. Because the SA node has the highest rate of depolarization in the whole system, it starts
each heart beat and sets the pace for the whole heart. Consequently, it is often called the pacemaker.
SYSTEMIC CIRCULATION
Left Atrium
↓
Mitral valve
↓
Left Ventricle
↓
Aortic Semilunar Valve
↓
Aorta
↓
All parts of the body
Regulating Blood Pressure: The Renin-Angiotensin-Aldosterone System

STATEMENT OF THE PROBLEM
This case study aims to determine “How the patient acquired one illness to the development of another, and the process by which the body responds to the situation”.
This also specifically attempts to answer the following questions:
• What are Diabetes Mellitus, Hypertension, Cholelithiasis, Nephrolithiasis and Rheumatoid Arthritis?
• What system, organs or parts of the body are affected by the disease process?
• Where and how the illness was obtained, how it progressed and affected the body?
• What were the predisposing factors that lead the patient to acquire the diseases?
• Why dialysis is needed to be performed to the patient?
• What interventions are needed to manage such condition?
Were the interventions effective in helping the patient recover?

THEORETICAL BACKGROUND
The function of a theoretical framwework is to guide the research process. Nursing has passed the point where it operates within the framework of functionalism-
only relating one variable to another. The theory must be both understandable and applicable to the real world of nursing.
The Betty Neuman Health Care Systems Model
This health care systems model is called the “Total Person Approach to Patient Problems.” The conceptual framework encompassing this model vies people as
unique individuals with a composite of characteristics within a normal given range of response. Each person in a state of wellness or illness is a dynamic composite
of the interrelationship of physiological, psychological, sociocultural, and developmental variables. Although Neuman uses the term composite, the conceptual
framework encompasses the Gestalt theory, which holds that each of us is surrounded by a perceptual field that is in a dynamic equilibrium. A field theory approach
such as this maintains that all parts are intimately related and interdependent. The total organization of the field and its impact upon the functional behavior of the
individual is the primary focus. In this total person model, the organization of the field considers:
1. the effect of the stressors
2. The reaction of the organism to the stressors
3. The organism itself, while taking into consideration the simultaneous interaction of the physiological, psychological, sociocultural, and development
variables.

This total person framework, then, is an open system model with two major components, stress and the reaction to stress. In the Gestalt theory each stressor would
affect the individual’s reaction to any other stressor. The individual’s behavior then would be a function of the dynamic interaction between stressors and the
defenses against stressors supplied by the individual as well as the supporting environment.
Commonplaces
Commonplaces are topics commonly addressed by most theorists. These topics are usually vague, indicating locations rather than specific entities. The
commonplaces in a theory may be used to organize a theory or as structures with which to evaluate and understand a theory. Definitions of the commonplaces
utilized in the Neuman Systems Model are made by identifying the elements and relationships that have significance for Neuman.
Person
The conceptual framework encompassing this model views people as unique individuals who are a composite of characteristics within a normal given range of
response. Each person in a state of wellness or illness is a dynamic composite of the interrelationship of physiological, psychological, sociocultural, and
developmental variables. Person is an open system with interaction with the environment.
Nursing
Nursing is viewed as a unique profession in that it is concerned with all the variables affecting an individual’s response to stressors. The nurse has an obligation to
seek the highest potential level of stability for each individual.
Health
Wellness is considered the ability of an individual’s flexible line of defense against any stressor to maintain equilibrium. Any variances of wellness occur when
stressors are able to penetrate the flexible line of defense. Neuman views health on a continuum with levels of wellness and variances of wellness. If a person’s total
needs are met, he or she is in an optimal level of wellness. Hence, a reduced state of wellness is the result of needs not being met.
Person to Nurse
The nurse assesses and validates the individual’s response to stressors. Response to some stressors are known whereas others are manifested depending on the
meaning of the experience to the individual. The nurse has a knowledge of the relation of the environment and the person’s reaction to stress and reconstitution.
Person to Health
People retain harmony and balance with the environment by a process of interaction and adjustment. Persons are views as a total person composed of physiological,
psychological, sociocultural, and developmental variables. The interrelationship of these variables determines the degree of reaction and individual has to any

stressor. Each individual is seen as unique, but containing a blend of common attributes within a normal range of response. This normal range of response is known
as a normal line of defense- that which is necessary to maintain an individual’s equilibrium.
Nursing to Health
The nurse assists individuals, families, and groups to attain or maintain a maximum level of wellness by appropriate interventions. Nursing actions are interventions
at the primary, secondary, and tertiary prevention levels that will reduce stress factors, strengthen the line of defense, and maintain a reasonable degree of
adaptation.
Environment
The environment consists of internal and external factors. Internal is the flexible line of defense against stressors, such as the body’s immune response pattern or the
mobilization of white blood cells. External consists of an individual’s coping ability, lifestyle, developmental stage, and so forth, and is known as the normal line of
defense.
Stressors
Stressors may vary as to impact or reaction. There are three types of stressors:
1. Intrapersonal forces occurring within the individual.
2. Interpersonal forces occurring between one or more individuals.
3. Extrapersonal forces occurring outside the individual.
A stressor attempts to penetrate an individual’s normal line of defense to cause disequilibrium

CHAPTER TWO
Data Collection, Analysis and Interpretation
OPT Model
CLIENT IN CONTEXT PRESENT STATE INTERVENTIONS EVALUATION
R.M, 58 years old, male, Roman Catholic,
Filipino, residing at Matabao, Tubigon
Bohol, Birthdate October 22, 1948 , was
admitted for the 3rd time in Cebu Velez
General Hospital (CVGH) for complaints of
vomiting and right epigastric pain. Patient
was admitted under the services of Dr.Cesar
Quiza under the Department of Internal
Medicine with the case number of 88358.
History of Present Illness
1 month PTA, pt complained of
vomiting of previously ingested food with
an estimate of 1/8 cup per episode, every
after meal with 2-3 episodes per day for
duration of 1 week. He lost 10 kg in a month
and sought no consult nor self-medicated.
3 wks PTA, pt sought consult @
Ramiro Hospital in Bohol where he was
confined for a day and was ordered for UGI
endoscopies, UTZ, CBC,U.A,. The UTZ
ER Blotter
Accompanied by wife, patient arrived at CVGH-ER at
8:50am on June 27, 2007 per taxi, awake, conscious,
responsive, coherent, afebrile, with the following vital
signs: BP:120/80mmHg PR: 70 bpm RR: 30 cpm T:
36.0 C/axilla. At around 9:50 am, she was admitted to
the Medical-Surgical department under the services of
Dr. Cesar Quiza with case # 88358 and was transported
around 10:00 am to PPW 4th
floor per wheelchair.
DATE OF ASSESSMENT: June 28, 2007
Ht: 175cm
Wt: 85 kg
IBW: 68 kg
Physiologic Measurements
T°: 36.5°C/axilla
RR: 23 cpm
PR:84 bpm
BP: 110/80 mmHg
June 28, 2007
GENERAL APPEARANCE

was taken and revealed renal and gall
bladder stones and his UGI endoscopies
showed gastric erosions. No management
was done. He was discharged improved but
upon arriving home complained of left
flank, intermittent pain, which was
associated with urgency and frequency of
urination, but no pain and change in urine
color, was noted.
5 days PTA, pt sought consult with
an AP who advised for admission for further
treatment and monitoring. The night after
consult they went back to Bohol to settle
things at home before admission. Pt was
admitted @ CVGH 2 days after consult last
6/27/2007(Wednesday).
PAST HISTORY
Health History
1.) 16 yrs PTA diagnosed with DM
type 2 with poor compliance to
meds. CBG monitoring was not
practiced. His maintenance meds
include glipizide (Minidiab)
5mg/tab 1 tab OD and metformin
(Glucophage) 500mg/tab, 1 tab
BID. He had occasional complaints
of tingling sensation in the hands
but not in the feet and with
increased urgency and frequency of
urination especially at night,
voiding up to 4 times per night.
2.) 16 yrs PTA, he experienced one
episode of painless passing out of
urinary stone. He had reports of left
4pm >seen on bed, awake, conscious, responsive,
coherent, with IVF 1 PNSS 1 liter @ 10 gtts per minute
infusing well on left hand, with the following vital signs:
PR: 84 bpm RR: 23 cpm BP:110/80 mmHg T:
36.5°C/axilla
Skin and appendages: Presence of IV line on left arm,
Presence of jaundice on skin and soles of feet and palms
with good skin turgor, no edema, no lesions, long
fingernails and toenails with pale nail beds, with
presence of nail clubbing, with CRT >2 secs, no
cyanosis.
Head: normocephalic, (+) ROM, Hair is fine, wavy,
black, presence of dandruff but no lice infestations
Eyes : symmetrical, anicteric sclerae, smooth, moist and
pale palpebral conjunctivae and clear bulbar conjuctivae,
(-)discharges, equal distribution of eyebrows and
eyelashes, (+) Pupils Equally Round and Reactive to
Light and Accomodation, wears reading glasses with
unrecalled grade
Ears : symmetrical, no lesions, pinna is in line with the
outer canthus of the eye, no swelling, pinna is nontender,
no discharges noted on auditory meatus.
Nose: symmetrical, no masses, no discharges, nasal
septum at midline
Mouth and throat: lips are symmetrical but pale, no
ulcerations and no lesions, pinkish gums with no
ulcerations, tongue located at midline, uvula at midline,
with presence of tooth decays, no lesions, equal chest
expansion, presence of 2 molars,2 pre molars,2 canines
and 2 incisors on lower teeth
Lungs: Equal lung expansion, upon auscultation, clear
breath sounds, no rales and crackles heard upon
auscultation
Heart: distinct s1 and s2 heart sounds upon ausculation,
no murmurs heard, heart rate of 84 bpm with regular
rhythm.

flank, intermittent, non-radiating
pain. It was not relieved with
position changes. The symptoms
recurred 7 yrs PTA and no
consultation and meds were done
3.) 6yrs PTA was diagnosed with
Secondary HPN by Dr. Lara, their
family doctor with maintenance
meds of captopril (Capoten) 25mg
OD taken with good compliance. 5
days PTA med was shifted to
valsartan (Diovan) 80mg/tab 1 tab
OD. His wife monitors his BP
regularly with the usual readings of
110-140/80mmHg and with the
highest reading of 160/90mmHg.
4.) 7yrs PTA diagnosed with
Rheumatoid arthritis by Dr. Quiza
@ CVGH. His symptoms include
weakness and pain in both Calves
on legs upon eating internal organs.
He was given Celebrex 200mg 1
tab PRN as pain reliever.
Previous Hospitalizations:
Previous hospitalizations include
one in the 1960’s when R.M was still in his
20’S far inguinal Hernia @ CVGH by Dr.
Tambuyong. He went under Hernioraphy.
He suspected that the cause of his hernia
was because of not wearing a supporter
when playing basketball. He claimed to feel
pain and felt his testes becoming heavy
everytime he stands. He was given
unrecalled meds and was discharged 3 days
after with condition improved.
Abdomen: protuberant, no masses, no tenderness,
presence of bowel sounds at 8 gurgling sounds/minute
auscultated at right lower quadrant, (+) liver hook test,
(-)kidney punch, (-) Murphey’s sign
GUT-Reproductive: grossly male, no swelling, no
abnormal discharges, no lesions, no rashes.
Anus: no lesions, no hemorrhoids, no rashes.
Extremities: symmetrical, (+) ROM for all extremities,
no lesions, presence of bent little finger at right hand
Musculoskeletal: good muscle tone.
NEUROLOGIC ASSESSMENT
Mental Status/Cerebral Functioning
Awake, alert, conscious, responsive, coherent.
Motor/Cerebellar Functioning
Able to grasp student nurse’s wrist tightly. Extremities
symmetrically folded inward with good muscle tone.
Reflexes
(+) triceps reflex
(+) biceps reflex
(+) Achilles reflex
(+) patellar reflex
Sensory Functioning
Responsive to light touch (hanky) and pain (slight pinch) at
both upper and lower extremities and both sides of the face.
Cranial Nerve Testing
CN 1 (Olfactory) – distinguished the smell of lotion from
alcohol
CN 2 (Optic) – (+) PERRLA,(+) Blinking reflex
CN 3 (Oculomotor) – (+) PERRLA
CN 4 (Trochlear) – (+) PERRLA (+)Cardinal Gaze
CN 5 (Trigeminal) – (+) blink reflex, can open and close
mouth, can feel the touch of student nurse’s hand on face
CN 6 (Abducens) – (+) PERRLA (+)Cardinal Gaze
CN 7 (Facial) – able to close eyes, can smile, wrinkle forehead,
can clench jaw from side to side
CN 8 (Auditory) – (+) whisper test, can hear the tick of the

His second hospitalization was in
the 1980’s @ Ramiro hospital in Bohol for
pneumonia. His occasional complaints were
chest pains. He was given unrecalled meds
and was confined for five days. After
discharge, he transferred to CVGH by his
request for 2nd
opinion and further treatment
and monitoring. He was confined @ CVGH
for 3 days with condition improved.
His third hospitalization was in
1991 for MVA @ CVGH. Pt claimed to
have dislocated his right arm because he was
using it to hold his body up from falling
from the accident. Pt recalled being chased
by dogs from behind his motorcycle and
was forced into a post at the corner of the
road. His x-ray revealed no fractures. He
was given unrecalled meds and was on cast
for 3 mos. Where it was removed by Dr.
Mediano @ CVGH. He was confined for 3
days with condition improved.
His fourth hospitalization was last
Oct.23,2006 @ Ramiro hospital in Bohol for
complications from MVA 6 months PTA.
He recalled being chased again by dogs
from behind his motorcycle and he was
crashed to a nearby tree. Before
hospitalization R.M noticed swelling of his
feet. The next month, he went to Dr. Lim’s
clinic @ Ramiro hospital and was advised
for an x-ray of both femurs and it revealed
no fractures. He was advised to use crutches
from the swelling of his feet. He went back
to Dr. lim’s clinic 6 month’s PTA for
wrist watch at 1 foot away
CN 9 (Glossopharyngeal) – (+) gag reflex, able to swallow,
able, can taste sugar at the anterior part of the tongue
CN 10 (Vagus)- (+) gag reflex , able to swallow, can taste salty
food at the posterior part of the tongue
CN 11 (Accessory) – able to shrug shoulder against resistance
CN 12 (Hypoglossal) – mouth opens when nose is pinched,
tongue midline at protrusion
General Appearance:
4pm> Seen lying on bed, awake, conscious, responsive,
coherent, afebrile, with IVF of 1 PNSS 1 liter @ 10 gtts /
min, infusing well at left hand, with the following vital
signs:
Temperature: 36.3ºC/axilla
Pulse Rate: 85 bpm
Respiratory rate: 23 cpm
BP: 120/80mmHg
Significant findings:
Skin and appendages: Presence of IV catheter on left
arm, CRT of > 2 seconds, (+) jaundice on skin , in palms
of hand and soles of feet
Eyes: pale palpebral conjunctivae
Mouth and Throat: pale lips, presence of tooth decays,
Extremities:presence of bent little finger at right hand
General Appearance:
4pm> Seen sitting on bed, awake, conscious, responsive,
coherent afebrile, with IVF of 1PNSS 1 liter @ 10 gtts /
min, infusing well at left hand, with the following vital
signs:
Temperature: 36.5ºC/axilla
Pulse Rate: 85 bpm
Respiratory rate: 15 cpm
BP:120/80 mmHG

complaints of pain from his calves and was
advised for admission for his rheumatoid
arthritis. He was given celebrex 200mg BID
and was discharged 3 days after without
crutches and with condition improved.
Family History:
Herdofamilial diseases include cancer
(cervix, prostate) in the mother’s side and
DM, stroke and arthritis in the father’s side.
Genogram:
1. Health perception - Health
management Pattern
Pt is a hypertensive, diabetic,
non-asthmatic, occasional alcoholic
beverage drinker amounting to 4
Significant findings:
Skin and appendages: Presence of IV catheter on left
arm, CRT>2 seconds, presence of nail clubbing
Mouth and throat: presence of yellow teeth, presence of
tooth decays
Extremities: presence of bent little finger at right hand
LABORATORY FINDINGS
June 7, 2007
UREA BLOOD TESTING
Urea blood testing is done to determine
whether your kidneys are functioning
normally. It also determines whether your
kidney disease is getting worse. It monitors
treatment of your kidney disease. It determines
whether severe dehydration is present. It may
also help determine whether decreased kidney
function is the result of dehydration or kidney
disease.
Uric: 11.1 mg/dl ref range (2.3 – 8.2) ↑
Crea D: 6.2 mg/dl ref range (0.5 – 1.3) ↑
Urea: 50 mg/dl ref range (7 – 18) ↑
Implications:
Uric acid
♦ Clinical problems associated with
elevated serum uric acid levels arise
from the limited solubility of this
compound. Increase in uric acid in
serum rises above, it begins to
precipitate out of solution. May result
Maternal Paternal
Deceased female Deceased male
female male
patient
Legend:

CHOLELITHIASIS, NEPHROLITHIASIS SECONDARY HYPERTENSION, DM TYPE 2, HYDRONEPHROSIS

CHOLELITHIASIS, NEPHROLITHIASIS SECONDARY HYPERTENSION, DM TYPE 2, HYDRONEPHROSIS

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