Essex County College

Department of Nursing
Nursing Assessment & Plan of Care

Student Name_Don Prem Legaspi____________ Grade__________

Date__10/7/2010_________

Data Base

Name (Pt. Initials)______B.K.____ Room #____718B_______ Date of

Admission___8/11/10_______

Age__77___ Date of Birth___12/13/1933______ Place of Birth______USA___________

Sex__M___ Marital Status___married______ Religion__Islam______

Occupation___retired_______

Admitting Diagnosis (es)

1. non healing wound below the left thigh
2. left knee stump
3. gangrene of the right foot

Current Surgical Interventions

1. left above knee amputation

Surgical History:
Left below knee amputation

Medical History: left below knee amputation, End Stage renal disease on hemodialysis, diabetes
mellitus type 2, hypertension, coronary artery disease

Allergies (Food/Drugs): NKA

 Medical Diagnosis Evaluation

Diagnosis: End stage renal disease

Pathophysiology:
Approximately 1 million nephrons are present in each kidney, each contributing to the total
GFR. Regardless of the etiology of renal injury, with progressive destruction of nephrons, the
kidney has an innate ability to maintain GFR by hyperfiltration and compensatory
hypertrophy of the remaining healthy nephrons. This nephron adaptability allows for
continued normal clearance of plasma solutes so that substances such as urea and creatinine
start to show significant increases in plasma levels only after total GFR has decreased to
50%, when the renal reserve has been exhausted. The plasma creatinine value will
approximately double with a 50% reduction in GFR. A rise in plasma creatinine from a
baseline value of 0.6 mg/dL to 1.2 mg/dL in a patient, although still within the reference
range, actually represents a loss of 50% of functioning nephron mass.

The residual nephron hyperfiltration and hypertrophy, although beneficial for the reasons
noted, has been hypothesized to represent a major cause of progressive renal dysfunction.
This is believed to occur because of increased glomerular capillary pressure, which damages
the capillaries and leads initially to focal and segmental glomerulosclerosis and eventually to
global glomerulosclerosis. This hypothesis has been based on studies of five-sixths
nephrectomized rats, which develop lesions that are identical to those observed in humans
with chronic kidney disease.

Factors other than the underlying disease process and glomerular hypertension that may
cause progressive renal injury include the following:

- Systemic hypertension
- Acute insults from nephrotoxins or decreased perfusion
- Proteinuria
- Increased renal ammoniagenesis with interstitial injury
- Hyperlipidemia
- Hyperphosphatemia with calcium phosphate deposition
- Decreased levels of nitrous oxide
- Smoking

Etiology:
The most common causes of ESRD are diabetic nephropathy, hypertension, and
glomerulonephritis. Together, these cause approximately 75% of all adult cases. Certain
geographic areas have a high incidence of HIV nephropathy.
Historically, kidney disease has been classified according to the part of the renal anatomy that is
involved, as:
- Vascular, includes large vessel disease such as bilateral renal artery stenosis and small
vessel disease such as ischemic nephropathy, hemolytic-uremic syndrome and vasculitis
- Glomerular, comprising a diverse group and subclassified into:
 - Primary Glomerular disease such as focal segmental glomerulosclerosis and IgA
nephritis
- Secondary Glomerular disease such as diabetic nephropathy and lupus nephritis
- Tubulointerstitial including polycystic kidney disease, drug and toxin-induced chronic
tubulointerstitial nephritis and reflux nephropathy
- Obstructive such as with bilateral kidney stones and diseases of the prostate
- On rare cases, pin worms infecting the kidney can also cause idiopathic nephropathy

Clinical Signs:
ESRD is initially without specific symptoms and can only be detected as an increase in
serum creatinine or protein in the urine. As the kidney function decreases:
- blood pressure is increased due to fluid overload and production of vasoactive
hormones, increasing one's risk of developing hypertension and/or suffering from
congestive heart failure
- Urea accumulates, leading to azotemia and ultimately uremia (symptoms ranging
from lethargy to pericarditis and encephalopathy). Urea is excreted by sweating and
crystallizes on skin ("uremic frost").
- Potassium accumulates in the blood (known as hyperkalemia with a range of
symptoms including malaise and potentially fatal cardiac arrhythmias)
- Erythropoietin synthesis is decreased (potentially leading to anemia, which causes
fatigue)
- Fluid volume overload - symptoms may range from mild edema to life-threatening
pulmonary edema
- Hyperphosphatemia - due to reduced phosphate excretion, associated with
hypocalcemia (due to vitamin D3 deficiency). The major sign of hypocalcemia is
tetany.
- Later this progresses to tertiary hyperparathyroidism, with hypercalcaemia, renal
osteodystrophy and vascular calcification that further impairs cardiac function.
- Metabolic acidosis, due to accumulation of sulfates, phosphates, uric acid etc. This
may cause altered enzyme activity by excess acid acting on enzymes and also
increased excitability of cardiac and neuronal membranes by the promotion of
hyperkalemia due to excess acid (acidemia)
People with chronic kidney disease suffer from accelerated atherosclerosis and are more
likely to develop cardiovascular disease than the general population. Patients afflicted
with chronic kidney disease and cardiovascular disease tend to have significantly worse
prognoses than those suffering only from the latter.

Nursing Care:

Intervention:
Record accurate intake and output
Weigh daily at same time of day, on same
Rationale:
Accurate i&o is necessary for determining
renal function and fluid replacement needs
and reducing risk of fluid overload
Daily body weight is best monitor of fluid
 scale, with same equipment and clothing
Assess skin, face, dependent areas for edema
Plan oral fluid replacement with patient,
within multiple restrictions
Administer/ restrict fluids as indicated
Administer medication as indicated
(diuretics)
Administer medication as indicated
(antihypertensives)
status
Edema occurs primarily in dependent tissues
of the body (hands, feet, lumbosacral area).
Patient can gain up to 10 lbs of fluid before
pitting edema is detected
Helps avoid periods without fluids,
minimizes boredom of limited choices, and
reduces sense of deprivation and thirst.
Fluid management is usually calculated to
replace output from all sources plus
estimated insensible losses
Given early in oliguric phase of renal failure
in an effort to convert to non-oliguric phase,
flush the tubular lumen of debris, reduce
hyperkalemia, and promote adequate urine
volume.
May be given to treat hypertension by
counteracting effects of decreased renal
blood flow and/or circulating volume
overload.

Medical Diagnosis Evaluation

Diagnosis: diabetes mellitus type 2

Pathophysiology:
Insulin resistance means that body cells do not respond appropriately when insulin is present.
Unlike type 1 diabetes mellitus, insulin resistance is generally "post-receptor", meaning it is a
problem with the cells that respond to insulin rather than a problem with the production of
insulin.
This is a more complex problem than type 1, but is sometimes easier to treat, especially in the
early years when insulin is often still being produced internally. Severe complications can result
from improperly managed type 2 diabetes, including renal failure, erectile dysfunction,
blindness, slow healing wounds (including surgical incisions), and arterial disease, including
coronary artery disease. The onset of type 2 diabetes has been most common in middle age and
later life, although it is being more frequently seen in adolescents and young adults due to an
increase in child obesity and inactivity. A type of diabetes called MODY is increasingly seen in
adolescents, but this is classified as a diabetes due to a specific cause and not as type 2 diabetes.
Diabetes mellitus with a known etiology, such as secondary to other diseases, known gene
defects, trauma or surgery, or the effects of drugs, is more appropriately called secondary
diabetes mellitus or diabetes due to a specific cause. Examples include diabetes mellitus such as
MODY or those caused by hemochromatosis, pancreatic insufficiencies, or certain types of
medications (e.g., long-term steroid use).

Etiology:
Type 2 diabetes is due primarily to lifestyle factors and genetics. It was also found that oligomers
of islet amyloid polypeptide (IAPP), a protein that forms amyloid deposits in the pancreas during
type 2 diabetes, triggered the NLRP3 inflammasome and generated mature IL-1β. One therapy
for type 2 diabetes, glyburide, suppressed IAPP-mediated IL-1β production in vitro.
Lifestyle
A number of lifestyle factors are known to be important to the development of type 2 diabetes. In
one study, those who had high levels of physical activity, a healthy diet, did not smoke, and
consumed alcohol in moderation had an 82% lower rate of diabetes. When a normal weight was
included the rate was 89% lower. In this study a healthy diet was defined as one high in fiber,
with a high polyunsaturated to saturated fat ratio, and a lower mean glycemic index. Obesity has
been found to contribute to approximately 55% type 2 diabetes, and decreasing consumption of
saturated fats and trans fatty acids while replacing them with unsaturated fats may decrease the
risk. The increased rate of childhood obesity in between the 1960s and 2000s is believed to have
led to the increase in type 2 diabetes in children and adolescents.
Environmental toxins may contribute to recent increases in the rate of type 2 diabetes. A positive
correlation has been found between the concentration in the urine of bisphenol A, a constituent
of some plastics, and the incidence of type 2 diabetes.
Medical conditions
There are many factors which can potentially give rise to or exacerbate type 2 diabetes. These
include obesity, hypertension, elevated cholesterol (combined hyperlipidemia), and with the
condition often termed metabolic syndrome (it is also known as Syndrome X, Reavan's
syndrome, or CHAOS). Other causes include acromegaly, Cushing's syndrome, thyrotoxicosis,
pheochromocytoma, chronic pancreatitis, cancer and drugs. Additional factors found to increase
the risk of type 2 diabetes include aging, high-fat diets and a less active lifestyle.
Subclinical Cushing's syndrome (cortisol excess) may be associated with type 2 diabetes. The
percentage of subclinical Cushing's syndrome in the diabetic population is about 9%. Diabetic
patients with a pituitary microadenoma can improve insulin sensitivity by removal of these
microadenomas.
Hypogonadism is often associated with cortisol excess, and testosterone deficiency is also
associated with type 2 diabetes, even if the exact mechanism by which testosterone improve
insulin sensitivity is still not known.
Genetics
There is also a strong inheritable genetic connection in type 2 diabetes: having relatives
(especially first degree) with type 2 increases risks of developing type 2 diabetes very
substantially. In addition, there is also a mutation to the Islet Amyloid Polypeptide gene that
results in an earlier onset, more severe, form of diabetes.
About 55 percent of type 2 diabetes patients are obese at diagnosis —chronic obesity leads to
increased insulin resistance that can develop into type 2 diabetes, most likely because adipose
tissue (especially that in the abdomen around internal organs) is a (recently identified) source of
several chemical signals to other tissues (hormones and cytokines).
Other research shows that type 2 diabetes causes obesity as an effect of the changes in
metabolism and other deranged cell behavior attendant on insulin resistance.
However, environmental factors (almost certainly diet and weight) play a large part in the
development of type 2 diabetes in addition to any genetic component. This can be seen from the
adoption of the type 2 diabetes epidemiological pattern in those who have moved to a different
environment as compared to the same genetic pool who have not. Immigrants to Western
developed countries, for instance, as compared to lower incidence countries of origins.
There is a stronger inheritance pattern for type 2 diabetes. Those with first-degree relatives with
type 2 diabetes have a much higher risk of developing type 2 diabetes, increasing with the
number of those relatives. Concordance among monozygotic twins is close to 100%, and about
25% of those with the disease have a family history of diabetes. Genes significantly associated
with developing type 2 diabetes, include TCF7L2, PPARG, FTO, KCNJ11, NOTCH2, WFS1,
CDKAL1, IGF2BP2, SLC30A8, JAZF1, and HHEX.[24] KCNJ11 (potassium inwardly
rectifying channel, subfamily J, member 11), encodes the islet ATP-sensitive potassium channel
Kir6.2, and TCF7L2 (transcription factor 7–like 2) regulates proglucagon gene expression and
thus the production of glucagon-like peptide-1. Moreover, obesity (which is an independent risk
factor for type 2 diabetes) is strongly inherited.
Monogenic forms, e.g., MODY, constitute 1–5 % of all cases.
Various hereditary conditions may feature diabetes, for example myotonic dystrophy and
Friedreich's ataxia. Wolfram's syndrome is an autosomal recessive neurodegenerative disorder
that first becomes evident in childhood. It consists of diabetes insipidus, diabetes mellitus, optic
atrophy, and deafness, hence the acronym DIDMOAD.
Gene expression promoted by a diet of fat and glucose as well as high levels of inflammation
related cytokines found in the obese results in cells that "produce fewer and smaller
mitochondria than is normal," and are thus prone to insulin resistance.
Medications
Some drugs, used for any of several conditions, can interfere with the insulin regulation system,
possibly producing drug induced hyperglycemia. Some examples follow, giving the biochemical
mechanism in each case:
Atypical Antipsychotics - Alter receptor binding characteristics, leading to increased insulin
resistance.
Beta-blockers - Inhibit insulin secretion.
Calcium Channel Blockers - Inhibits secretion of insulin by interfering with cytosolic calcium
release.
Corticosteroids - Cause peripheral insulin resistance and gluconeogensis.
Fluoroquinolones - Inhibits insulin secretion by blocking ATP sensitive potassium channels.
Niacin - causes increased insulin resistance due to increased free fatty acid mobilization.
Phenothiazines - Inhibit insulin secretion.
Protease Inhibitors - Inhibit the conversion of proinsulin to insulin.
Somatropin - May decrease sensitivity to insulin, especially in those susceptible.
Thiazide Diuretics - Inhibit insulin secretion due to hypokalemia. They also cause increased
insulin resistance due to increased free fatty acid mobilization.

Clinical Signs:
The classical symptoms of diabetes are polyuria (frequent urination), polydipsia (increased
thirst), polyphagia (increased hunger), fatigue and weight loss.
Nursing Care:
Intervention:
Observe for signs of infection and
inflammation
Promote good handwashing by nurse and
patient
Maintain aseptic technique for IV insertion
procedure, administration of meds, and
providing maintenance and site care.
Rotate IV sites as indicated.
Provide catheter or perineal care. Teach
the female patient to clean from front to
back after elimination.
Provide conscientious skin care, gently
massage bony areas. Keep the skin dry,
linens dry and wrinkle free.
Place in semi-fowler position
Encourage adequate dietary and fluid
intake of 3000 ml per day.
Obtain specimen for culture and
sensitivities as indicated.
Medical Diagnosis Evaluation
Rationale:
Patient may be admitted with infection,
which could have precipitated the
ketoacidotic state, or may develop a
nosocomial infection.
Reduces the risk of cross-contamination
High glucose in the blood creates an
excellent medium for bacterial growth.
Minimizes the risk for infection.
Peripheral circulation may be impaired,
placing patient at increased risk for skin
irritation or breakdown and infection.
Facilitates lung expansion and reduces
risk of aspiration.
Decrease susceptibility to infection.
Identifies organisms so that most
appropriate drug therapy can be instituted.
Diagnosis: Hypertension

Pathophysiology:

Most of the mechanisms associated with secondary hypertension are generally fully
understood. However, those associated with essential (primary) hypertension are far less
understood. What is known is that cardiac output is raised early in the disease course, with
total peripheral resistance (TPR) normal; over time cardiac output drops to normal levels but
TPR is increased. Three theories have been proposed to explain this:
- Inability of the kidneys to excrete sodium, resulting in natriuretic factors such as
Atrial Natriuretic Factor being secreted to promote salt excretion with the side effect
of raising total peripheral resistance.
- An overactive Renin-angiotensin system leads to vasoconstriction and retention of
sodium and water. The increase in blood volume leads to hypertension.
- An overactive sympathetic nervous system, leading to increased stress responses.

It is also known that hypertension is highly heritable and polygenic (caused by more than one
gene) and a few candidate genes have been postulated in the etiology of this condition.
Recently, work related to the association between essential hypertension and sustained
endothelial damage has gained popularity among hypertension scientists. It remains unclear
however whether endothelial changes precede the development of hypertension or whether
such changes are mainly due to long standing elevated blood pressures.

Etiology:

Essential hypertension

Essential hypertension is the most prevalent hypertension type, affecting 90–95% of

hypertensive patients.Although no direct cause has identified itself, there are many factors such
as sedentary lifestyle, stress, visceral obesity, potassium deficiency (hypokalemia), obesity (more
than 85% of cases occur in those with a body mass index greater than 25), salt (sodium)
sensitivity, alcohol intake, and vitamin D deficiency that increase the risk of developing
hypertension. Risk also increases with aging, some inherited genetic mutations, and having a
family history of hypertension. An elevation of renin, a hormone secreted by the kidney, is
another risk factor, as is sympathetic nervous system overactivity. Insulin resistance which is a
component of syndrome X, or the metabolic syndrome is also thought to contribute to
hypertension. Recent studies have implicated low birth weight as a risk factor for adult essential
hypertension.

Secondary hypertension

Secondary hypertension by definition results from an identifiable cause. This type is important to
recognize since it's treated differently than essential hypertension, by treating the underlying
cause of the elevated blood pressure. Hypertension results in the compromise or imbalance of the
pathophysiological mechanisms, such as the hormone-regulating endocrine system, that regulate
blood plasma volume and heart function. Many conditions cause hypertension, some are
common and well recognized secondary causes such as Cushing's syndrome, which is a
condition where the adrenal glands overproduce the hormone cortisol. In addition, hypertension
is caused by other conditions that cause hormone changes such as hyperthyroidism,
hypothyroidism (citation needed), and certain tumors of the adrenal medulla (e.g.,
pheochromocytoma). Other common causes of secondary hypertension include kidney disease,
obesity/metabolic disorder, pre-eclampsia during pregnancy, the congenital defect known as
coarctation of the aorta, and certain prescription and illegal drugs.

Clinical Signs:
High blood pressure usually causes no symptoms and high blood pressure often is labeled "the
silent killer." People who have high blood pressure typically don't know it until their blood
pressure is measured. Sometimes people with markedly elevated blood pressure may develop:

- headache,

- dizziness,

- blurred vision,

- nausea and vomiting, and

- chest pain and shortness of breath.

People often do not seek medical care until they have symptoms arising from the organ damage
caused by chronic (ongoing, long-term) high blood pressure. The following types of organ
damage are commonly seen in chronic high blood pressure:

- Heart attack

- Heart failure

- Stroke or transient ischemic attack (TIA)

- Kidney failure

- Eye damage with progressive vision loss

- Peripheral arterial disease causing leg pain with walking (claudication)

- Outpouchings of the aorta, called aneurysms

About 1% of people with high blood pressure do not seek medical care until the high blood
pressure is very severe, a condition known as malignant hypertension.
 - In malignant hypertension, the diastolic blood pressure (the lower number) often
exceeds 140 mm Hg.

- Malignant hypertension may be associated with headache, lightheadedness, nausea,

vomiting, and stroke like symptoms

- Malignant hypertension requires emergency intervention and lowering of blood

pressure to prevent brain hemorrhage or stroke.

It is of utmost importance to realize that high blood pressure can be unrecognized for years,
causing no symptoms but causing progressive damage to the heart, other organs, and blood
vessels.

Nursing Care:
Intervention:
Define and state the limits of desired BP.
Explain hypertension and its effect on the
heart, blood vessels, kidney, and brain
Assist the patient in identifying modifiable
risk factors like diet high in sodium,
saturated fats and cholesterol.
Reinforce the importance of adhering to
treatment regimen and keeping follow up
appointments.
Suggest frequent position changes, leg
exercises when lying down.
Help patient identify sources of sodium
intake.
Encourage patient to decrease or
eliminate caffeine like in tea, coffee, cola
and chocolate.
Stress importance of accomplishing daily
rest periods.
Provide information regarding community
resources, and support patients in making
lifestyle changes.
Rationale:
Provides basis for understanding
elevations of BP, and clarifies
misconceptions and also understanding
that high BP can exist without symptom or
even when feeling well.
These risk factors have been shown to
contribute to hypertension.
Lack of cooperation is common reason for
failure of antihypertensive therapy.
Decreases peripheral venous pooling that
may be potentiated by vasodilators and
prolonged sitting or standing.
Two years on moderate low salt diet may
be sufficient to control mild hypertension.
Caffeine is a cardiac stimulant and may
adversely affect cardiac function.
Alternating rest and activity increases
tolerance to activity progression.
Community resources like health centers
programs and check ups are helpful in
controlling hypertension.