Chronic Kidney Disease Secondary To Type 2 Diabetes Mellitus
Chronic Kidney Disease Secondary To Type 2 Diabetes Mellitus
Angeles City
College of Nursing
AY 2008-2009
Presented by:
Group No. 4
N-402
Presented to:
Mr. Christian G. Garcia RN
INTRODUCTION
renal function over a period of months or years. It is diagnosed by screening people that are at
risk of the disease such as those with hypertension, Diabetes Mellitus and one who has a
history of renal disease in their family. The loss of protein and red blood cells through the
urine may indicate an early stage of the disease. The progression of it is characterized and
identified with increased creatinine levels from blood test which indicates falling of the
glomerular filtration rate as a result of the kidneys’ decreased ability to excrete waste
products. Some diagnostics to fully investigate the disease and its progression includes blood
CKD is classified according to its severity in five stages. Stage 1 being the mildest
and causing no signs and symptoms while stage 5 which is a severe illness and with poor life
expectancy, it is also known as the established chronic kidney disease and synonymous to
End-Stage Renal Disease (ESRD), Chronic Kidney Failure (CKF), or Chronic Renal Failure
(CRF). There are no specific treatments that can hamper the progression of the disease. If
there is an underlying cause, such as in vasculitis, this may be treated directly and slow the
damage. Dialysis and kidney transplant are forms of renal replacement therapy that are
According to data collected from 120 countries with dialysis programs, at the end of
2005 about 1,900,000 people were receiving renal replacement therapy (RRT). Among these
individuals, 1,297,000 (68%) received hemodialysis and 158,000 (8%) received peritoneal
dialysis; although an additional 445,000 (23%) were living with a kidney transplant. Precise
(http://clinicalevidence.bmj.com/ceweb/)
Worldwide, the highest incidence and prevalence rates are reported from the USA,
Taiwan, and Japan. In America, 34% of cases of ESRD each year are caused by diabetes,
In the Philippines, as of 2005, there is 2.6% of the total population of ages 20 years
and above that suffers from stage 3-5 of the disease. 2.2% comes from stage 3, 0.2% from
stage 4 and the other 0.2% from the stage 5 or the end stage.
End Stage Renal Disease (its progressed state) is already the 7th leading cause of
death among Filipinos. The population of ESRD patients requiring dialysis therapy in Asia is
expanding at a faster rate than in the rest of the world. In Philippines, the dialysis population
is growing at a rate of 10% or more annually. It is said that a Filipino is having the disease
hourly or 120 Filipinos per million populations per year. This shows that about 10, 000
Filipinos need to replace their kidney function. Unfortunately though only 73% or about 7,
267 patients received treatment. An estimate of about a quarter of the whole population
Sugar mommy, a patient at Angeles Medical Center in the female ward bed 1, was
diagnosed with Chronic Kidney Disease (CKD) secondary to Diabetes Mellitus type 2. Her
current condition (as to what made her rush to the hospital), which is CKD, may be brought
deficiency of insulin, resulting to glucose intolerance. This lack of insulin results to failure to
transfer glucose from the plasma to the cells. Insulin is a hormone that is needed to convert
sugar, starches and other food into energy needed for daily life. The body responds by the
is in the fasting state. Generally there are two types of Diabetes Mellitus namely type 1
(Insulin-dependent diabetes mellitus, IDDM) and type 2 (non-insulin-dependent diabetes
mellitus, NIDDM). It is the accumulation of the glucose absorbed from the meal in the blood
factors. First is the impaired insulin release resulting to failure of normal handling of the
glucose absorbed from the food. Second is the defect in tissue response to insulin which is
caused by the defective insulin receptors on the target cells. And third is inflammation.
Genetics, obesity and lack of exercise are believed to be the cause of the disease.
Per record, there are more than 24 million people in the United States and 190 million
people worldwide with diabetes (95% Type 2). Diabetes continues to grow at epidemic levels
as it affects more children and kills more people each year than AIDS and breast cancer
combined. “Diabetes is the fifth-deadliest disease in the United States, and it has no cure. But
let us bring the picture to the Philippines; it has 95% comprising the Type 2 diabetes (adult
onset). If we are going to plot diabetes, Type 2 form is much higher in percentage compared
to Type 1 diabetes, mostly obese individuals are affected and in the Philippines it is the Type
General Objective:
The main goal of the group is to be able to present the case study of our chosen client
that would provide a comprehensive discussion of the pathological mechanism of the disease
Specific Objectives:
interpret the pertinent data gathered from the patient and her significant others;
discuss the anatomy and physiology of the organ involved in the patient’s
disease;
NURSING HISTORY
1. Personal History
A. Demographic Data
Sugar mommy, a 50 year old female married to Sugar Daddy living in Angeles City.
Sugar mommy was born on February12, 1960. She was blessed with 4 children, one of them
is married, the two are working in Manila and the other one stays at home to take care of her.
She was admitted last June 19, 2010 at Angeles Medical Center.
Sugar mommy never got a chance to work since she got married at an early age. Her
husband already stopped working, in the construction, site to take care of her. Currently, her
2 children in Manila are providing for them. Medical bills as well as expenditures at home
are being shouldered by these two daughters. According to sugar mommy, she also has a
monthly allowance of 2,000 pesos. With this money, she buys a bottle of soft drinks every
day and she eats a lot of rice too though she knows that these should not be part of her diet.
Sugar mommy finished high school at Holy Angel University. She failed to attend
college due to financial constriction. She also got married at a young age.
Sugar mommy is a Roman Catholic. She used to be a regular church goer but the
worsening of her condition January of 2009 led to her non-attendance of mass every Sunday.
She watch televised mass instead.
Mrs. Sugar Mommy goes to “mananawas” for minor illnesses such as cough and
colds and tend to self medicate. Only when the illness is severe that she and her family go to
the hospital to seek medical treatment.
Sugar mommy’s father died of diabetes. While on her mother’s side, they are known
to have hypertension and a lot died of stroke.
Father Mother
Sugar
Mommy
- Diabetes Mellitus type 2
- Hypertension
Sibling - Stroke
- Goiter
- Dead
Sibling
History of past illness
Sugar mommy had already chicken pox, measles, mumps and rubella. When she was
17 years old, she had goiter and undergone thyroidectomy. She was hospitalized 12 years ago
and was diagnosed with type 2 diabetes. After a year, she was hospitalized again due to a
recurring goiter. Last January, 2009 she became very ill and her diabetes affected her kidney.
She was comatose at the Intensive Care Unit of Angeles Medical Center and had undergone
11 sessions of hemodialysis. Being unable to pay the bills right away, she stayed in the
Mrs. Sugar Mommy came to the hospital with a chief complaint of right upper
quadrant pain and body weakness night of June 19, 2010. A few days prior to admission,
Sugar Mommy experienced nausea and vomiting, loss of appetite, body weakness, frequent
urination with dark yellow urine. Two days before admission she began experiencing pain
in the right upper quadrant. She also had edema on both feet.
III.
PHYSICAL ASSESSMENT
NIDDM
General Description
Sugarmommy is 50 years old, about five feet and 1 inch tall, petit and frail-looking. She
has a typical Filipina feature. She was sitting on bed when we first visited her, wearing a
light green blouse and chequered shorts and looking generally neat and presentable despite
her medical condition. She was accommodating, actively engages in conversation despite
experiencing abdominal pain that afternoon. Her husband was present during the interview
and from time to time, joins the conversation to confirm some of the information being
Vital Signs
T=37.8 ◦ C
P=81bpm
R=20 bpm
HEAD
Scalp is slightly paler than body complexion and is free of redness and inflammation
(-) infestations
Face
Facial features are symmetrical ( eyebrows, nasolabial folds, and sides of the mouth)
Eyes
Ears
(-) tinnitus
Nose
External nose is not tender, no lesions, masses, and nodules noted upon palpation
Mouth
an Tongue is pink in color, moist, and with presence of whitish coating and papillae,
NECK
Horizontal, linear scars on the center and the right side of the neck from previous
thyroidectomy
UPPER EXTREMITIES
CHEST
URINARY SYSTEM
Infrequent urination
LOWER EXTREMITIES
Skin is light brown in thigh area, scaly on the lower legs with both feet almost
mahogany in color
Presence of scars, dark brown in color, round shaped about 2 cm in size on the left
anterior thigh
Presence of sore just below the right big toe with signs of delayed healing.
General Description
During the next nurse-patient interaction, Sugarmommy was wearing a blue “duster”
and looking generally neat and presentable despite her medical condition. She was
accommodating as the other day and actively engages in conversation despite experiencing a
mild headache that afternoon. Her husband was present during the interview and from time
to time, joins the conversation to confirm some of the information being shared by his wife.
Vital Signs
T=36.7◦ C
P=79bpm
R=20 bpm
HEAD
Scalp is slightly paler than body complexion and is free of redness and inflammation
(-) infestations
Skull
Face
Eyes
Ears
(-) tinnitus
Nose
Mouth
Tongue is pink in color, moist, and with presence of whitish coating and papillae,
NECK
Horizontal, linear scars on the center and the right side of the neck from previous
thyroidectomy
UPPER EXTREMITIES
CHEST
ABDOMEN
URINARY SYSTEM
Infrequent urination
No difficulty upon urination
LOWER EXTREMITIES
Skin is light brown in thigh area, scaly on the lower legs with both feet almost
mahogany in color
Presence of edema on both feet, 2 to 4 mm deep, with the right foot looking fuller and
more swollen.
Presence of scars, dark brown in color, round shaped about 2 cm in size on the left
anterior thigh
Presence of sore just below the right big toe with signs of delayed healing.
General Description
During the nurse-patient interaction, Sugarmommy was wearing a white shirt and
with blue shorts with her hair unneatly tied up. She was accommodating as the previous days
and actively engages in conversation. Her husband was present during the interview and from
time to time, joins the conversation to confirm some of the information being shared by his
wife.
Vital Signs
T=36.1◦ C
P=84bpm
R=18 bpm
BP= 130/80 mmHg
HEAD
Scalp is slightly paler than body complexion and is free of redness and inflammation
(-) infestations
Skull
Face
Facial features are symmetrical ( eyebrows, nasolabial folds, and sides of the mouth)
Eyes
Ears
(-) tinnitus
Nose
External nose is not tender, no lesions, masses, and nodules noted upon palpation
Mouth
Tongue is pink in color, moist, and with presence of whitish coating and papillae,
NECK
Horizontal, linear scars on the center and the right side of the neck from previous
thyroidectomy
UPPER EXTREMITIES
ABDOMEN
URINARY SYSTEM
Infrequent urination
LOWER EXTREMITIES
Skin is light brown in thigh area, scaly on the lower legs with both feet almost
mahogany in color
Presence of edema on both feet, 2 to 4 mm deep, with the right foot looking fuller and
more swollen.
Presence of scars, dark brown in color, round shaped about 2 cm in size on the left
anterior thigh
Presence of sore just below the right big toe with signs of delayed healing.
DIAGNOSTIC/LA NORMAL
DATE ORDERED
BORATORY
INDICATIONS/PURPOS VALUES ANALYSIS AND
DATE RESULTS RESULTS
PROCEDURES E (UNITS INTERPRETATION
WERE
USED IN
RELEASED
HOSPITAL)
Hemoglobin To determine the oxygen June 19, 2010 9.0 11.6-15.5 It is below normal.
carrying capacity of the
blood. It evaluates the June 21,2010 8.8 It indicates that the level of
hemoglobin content of oxygen in the blood of the
erythrocytes. patient and factor that gives
blood red color is low. It is an
indication of possible pallor and
even anemia of the patient.
Also, it may lead to decrease
oxygen transfer and delivery to
cells.
Hematocrit To determine the percentage June 21, 2010 25.9 36.0-37.0 It is below normal.
of total blood volume
composed of RBC. 26.3 Decreased Hematocrit
percentage indicates that the
solid part or formed elements of
the blood like the hemoglobin
are in less concentration than the
liquid part which is the plasma.
RBC To determine the number of June 19, 2010 2.75 4.20-5.40 It is below normal.
RBC per cubic millimeter of
blood. It indicates anemia.
WBC Determine presence of June 19, 2010 22.91 4.8-10.8 It is above normal.
infection and inflammation
This indicates that infection is
present.
Neutrophils To check if there is acute June 19, 2010 90.8 40-74 It is above normal.
bacterial infection
It indicates that there is acute
inflammation.
Lymphocytes To determine the number of June 19, 2010 2.5 19-48 It is below normal.
antibodies responsible for
allergic reactions. There are insufficient antibodies
that can affect the immunity.
Monocytes They circulate in the June 19, 2010 5.7 3-9 Normal
peripheral blood prior to
emigration into the tissues. No infection present.
Platelets They are vital to June 19, 2010 290 150-400 Normal
coagulation of the blood to
prevent bleeding. Immunologic functions with
regard to platelets is still
functional leading to resistance
to bleeding.
Before:
Explain test procedure. Explain that slight discomfort maybe felt when skin is punctured.
Avoid stress if possible because altered physiologic status influence and changes normal hemoglobin values.
During:
Provides privacy.
Collect a venous sample according to the protocol of the laboratory
After:
Apply manual pressure and dressings to the puncture site on removal of the needle.
Bruising at the puncture site is not uncommon signs of inflammation are unusual and should be reported if the inflamed
BLOOD CHEMISTRY
DIAGNOSTIC/LA NORMAL
DATE ORDERED
BORATORY INDICATIONS VALUES ANALYSIS AND
DATE RESULTS RESULTS
PROCEDURES (UNITS USED INTERPRETATION
PURPOSE WERE
IN
RELEASED
HOSPITAL)
Creatinine It is used to diagnose June 19, 2010 7.02 mg/dl 0.5-1.69 mg/dl It is above normal.
impaired kidney function
It indicates kidney damage.
BUN To measure of the amount June 20, 2010 58.79 mg/dl 7.21mg/dl It is above normal.
of nitrogen in the blood in
the form of urea, and a It indicates a moderate-to-
measurement of renal severe degree of renal failure.
function.
Before:
Explain the test procedure and blood drawing procedure. Obtain history of s/sx of the hypoglycemia.
Ensure that the patient fasts, except for water, for 8 to 12 hours before blood is drawn.
During:
Provide privacy.
After:
Ph The pH is a June 19, 2010 7.38 7.35-7.45 Within the normal range.
measurement of the
acidity or alkalinity Normal because of the
of the blood. compensatory mechanism of the
body making it able to have a
In order for normal normal metabolism.
metabolism to take
place, the
PCO2 The by-product of June 19, 2010 23.5 35-45 Lower than the normal range.
the cells that when
combined to water Metabolic acidosis brought by
in the body the failure of the kidneys, the
produces carbonic body compensates as it lowers
acid, thus, lowering the CO2 levels by altering the
the Ph of the blood. respiration. Low levels may
indicate respiratory alkalosis.
PO2 The partial pressure June 19, 2010 68.7 80-100 Lower than the normal range.
of oxygen that is Inadequate supply of oxygen
dissolved in arterial present in the blood, indicates
blood. hypoxemia
HCO3 Through the help of June 19, 2010 12.4 22-26 Lower than the normal range.
the kidneys,
bicarbonate when With the kidney failure, there is
retained will deficit base in the blood or
increase the Ph and excess acid other than CO2.
when excreted will Low levels indicate Metabolic
then lower the Ph acidosis.
of the blood.
B.E. The base excess June 19, 2010 -11.3 meq/L 1-2 meq/L Lower than the normal range.
indicates the
amount of excess or Negative values indicates deficit
insufficient level of of base in the blood brought by
bicarbonate in the the kidney failure.
system.
O2 Saturation Indicates how June 19, 2010 93.2% 97% Lower than the normal range.
saturated the
circulating blood in Less percentage of oxygen the
the arteries with blood carries as it circulates in
oxygen. the body.
CAPILLARY BLOOD GLUCOSE
URINALYSIS
URINALYSIS To monitor the June 19, 2010 2.5 mg/dl Ketones: negative
kidney function of (quantitative 0.5–3.0
persons with mg/dL). It is normal.
diabetes mellitus. In
diabetics, the
excretion of greater It indicates that there is no any
than 200 μg/mL presence of acidosis.
albumin is
predictive of
impending kidney
disease.
Before:
Withhold diuretics for 3 days before the test. Check with clinician.
Determine the patient’s usual liquid intake and request that intake not to be increase beyond this daily amount during
testing.
During:
Provide privacy.
After:
Patient can resume normal fluid and dietary intake and medication unless specifically ordered otherwise.
ENDOCRINE SYSTEM
In general, the endocrine system is in charge of body processes that happen slowly,
such as cell growth. Faster processes like breathing and body movement are monitored by the
nervous system. But even though the nervous system and endocrine system are separate
systems, they often work together to help the body function properly.
The Pancreas
produce a clear fluid (pancreatic juice) that flows into the duodenum through a common duct
along with bile from the liver. Pancreatic juice contains three digestive enzymes: tryptase,
amylase, and lipase along with intestinal enzymes, complete the digestion of proteins,
carbohydrates, and fats, respectively. Scattered among the enzyme-producing cells of the
pancreas are small groups of endocrine cells, called the islets of Langerhans that secrete two
The pancreatic islets contain several types of cells: alpha-2 cells, which produce the
hormone glucagon; beta cells, which manufacture the hormone insulin; and alpha-1 cells,
which produce the regulatory agent somatostatin. These hormones are secreted directly into
the bloodstream, and together, they regulate the level of glucose in the blood. Insulin lowers
the blood sugar level and increases the amount of glycogen (stored carbohydrate) in the liver;
glucagon has the opposite action. Failure of the insulin-secreting cells to function properly
results in diabetes.
Function
Exocrine functions of pancreas are carried out by the Acinar, within the tubular and
acinar units of the gland. These cells secrete digestive enzyme that catalyze the digestion of
Endocrine functions of pancreas are carried out by the islet of langerhans. The islet,
containing Alpha, beta, and delta cells are scattered throughout the pancreatic tissue. The islet
cells are arranged in cords and are separated by a rich blood supply of capillaries. Insulin and
glycogen are two hormones secreted by the islets, play a vital role in the control of
carbohydrate metabolism.
Insulin synthesized by the beta cells, also helps control fat and protein metabolism.
Insulin is a powerful hypoglycemic agent it lowers blood sugar levels by promoting passage
of glucose in the cell. Insulin helps stimulate the active transport of glucose into muscle and
adipose tissue cells and protein synthesis within the tissues and inhibits the breakdown of
protein into amino acids. It also regulate the rate at which carbohydrate are used by cells for
energy.
gastrin are synthesized by the duct cells. Gastrin is used in the metabolism of foods and
somatostatin decreased the secretion of insulin, glycogen, growth hormone, gastrin and
secretion. And the secretion of pancreatic polypeptides is carried out by the F-cells. Any
alterations in the exocrine and endocrine functions of the pancreas would mean alterations in
the insulin and blood glucose level that may bring several abnormalities.
Actions of Insulin
hyperglycemia-generating hormones and to maintain low blood glucose levels. Because there
are numerous hyperglycemic hormones, untreated disorders associated with insulin generally
peptide is removed in the cisternae of the endoplasmic reticulum and it is packaged into
secretory vesicles in the Golgi, folded to its native structure, and locked in this conformation
by the formation of 2 disulfide bonds. Specific protease activity cleaves the center third of the
molecule, which dissociates as C peptide, leaving the amino terminal B peptide disulfide
metabolism. The increase in metabolism leads to an elevation in the ATP/ADP ratio. This in
of the cell leading to Ca2+ influx and insulin secretion. In fact, the role of K+ channels in
insulin secretion presents a viable therapeutic target for treating hyperglycemia due to insulin
insufficiency.
Glucose Metabolism
Uncontrolled IDDM leads to increased hepatic glucose output. First, liver glycogen
stores are mobilized then hepatitis gluconeogenesis used to produce glucose. Insulin
deficiency also impairs non-hepatic tissue utilization of glucose. In particular in adipose
tissue and skeletal muscle, insulin stimulates glucose uptake. This is accomplished by insulin-
mediated movement of glucose transporter proteins to the plasma membrane of these tissues.
Reduced glucose uptake by peripheral tissues in turn leads to a reduced rate of glucose
blood. Other enzymes involved in anabolic metabolism of glucose are affected by insulin
production and reduced peripheral tissues metabolism leads to elevated plasma glucose
levels. When the capacity of the kidneys to absorb glucose is surpassed, glucosuria ensues.
Glucose is an osmotic diuretic and an increase in renal loss of glucose is accompanied by loss
of water and electrolytes, termed polyuria. The result of the loss of water (and overall
volume) leads to the activation of the thirst mechanism (polydipsia). The negative caloric
balance which results from the glucosuria and tissue catabolism leads to an increase in
URINARY SYSTEM
hollow bulb known as Bowman's capsule. Bowman's capsule leads into a long, convoluted
tubule consisting of four sections: the proximal tubule, loop of Henle, distal tubule, and
collecting duct. The collecting ducts empty into the central cavity of the kidney, the renal
pelvis, which connects to the ureter. Each human kidney has about a million nephrons.
Glomerulus refers to two unrelated structures in the body, both named for their globular
form.
For the olfactory bulb structure of converging axons from the olfactory epithelium
Capillaries are the smallest of a body's blood vessels, measuring 5-10 μm. They
connect arteries. Blood is filtered by the glomerulus, and the resultant "prourine" passes
through the tubular system where water, electrolytes and nutrients are reabsorbed. The
dissociates free ions when dissolved (or molten), to produce an electrically conductive
medium. Because they generally consist of ions in solution, electrolytes are also known as
ionic solutes.
Potassium is a chemical element in the periodic table that has the symbol K (L.
kalium) and atomic number 19. The name potassium comes from potash the source it was
first isolated from. This is a soft, silvery-white metallic alkali metal that occurs naturally
bound to other elements in seawater and many minerals. It oxidizes rapidly in air, is very
Urine Formation
The primary functions of the nephrons include removing waste substances from the
blood and regulating water and electrolyte concentrations within the body fluids. The end
product of these functions is urine, which is excreted to the outside of the body, containing
wastes, excess water, and excess electrolytes. Urine formation involves glomerular filtration,
Glomerular Filtration
much like the filtration that occurs at the arteriole ends of other capillaries throughout the
body.
The glomerular capillaries, however, are many times more permeable than the capillaries in
other tissues due to the presence of numerous tiny openings (fenestrae) in their walls.
Filtration Pressure
As in case of other capillaries, the main force responsible for moving substances
through the glomerular capillary wall is the pressure of the blood inside (glomerular
hydrostatic pressure). This movement is also influenced by the osmotic pressure of the
plasma in the glomerulus and by the hydrostatic pressure inside the glomerular capsule. An
increase in either of these pressures will oppose movement out of the capillary and, thus,
reduce filtration. The net pressure acting to force substances out of the glomerulus is called
capsule, and it has about the same composition as the filtrate that becomes tissue fluid
elsewhere in the body. That is, glomerular filtrate is largely water and contains essentially the
same substances as the blood plasma, except for the larger protein molecules, which the
filtrate lacks.
Filtration Rate
Consequently, the factors that affect the glomerular hydrostatic pressure, glomerular plasma
osmotic pressure, or hydrostatic pressure in the glomerular capsule will also affect the rate of
filtration.
blood backs
up into the glomerulus, the glomerulus, the glomerular hydrostatic pressure increases, and
the filtration rate rises. Converse effects are produced by vasodilation of these vessels. In
the capillaries, the blood pressure, acting to force water and dissolved substances outward, is
opposed by the effect of the plasma osmotic pressure that attracts water inward. As
filtration occurs through the capillary wall, the proteins remaining in the plasma cause the
osmotic pressure within the glomerular capillary to rise. When this pressure reaches a
certain high level, filtration ceases. Conversely, conditions that tend to decrease plasma
the filtration rate. The hydrostatic pressure in the glomerular capsule sometimes changes as
gland pressing on the urethra. If this occurs, fluids tend to back up into the renal tubules and
cause the hydrostatic pressure in the glomerular capsules to rise. Since any increase in
capsular pressure opposes glomerular filtration, the rate of filtration may decrease
significantly.
In an average adult, the glomerular filtration rate for the nephrons of both kidneys is about
125 milliliters per minute, or 180,000 milliliters (180 liters) in 24 hours. Since this 24-hour
volume is nearly 45 gallons, it is obvious that not all of it is excreted as urine. Instead, most
of the fluid that passes through the renal tubules is re absorbed and reenters the plasma.
which was described previously, and two negative feedback mechanisms. These mechanisms
are triggered whenever the filtration rate is decreasing. For example, as the rate decreases,
the concentration of chloride ions reaching the macula densa in the distal convoluted
tubule also decreases. In response, the macula densa signals the smooth muscles in the wall
of the afferent arteriole to relax, and the vessel becomes dilated. This action allows more
blood to flow into the glomerulus, increasing the glomerular pressure, and as a consequence,
the filtration rate rises toward its previous level. At the same time that the macula densa
signals the afferent arteriole to dilate, it stimulates the juxtaglomerular cells to release renin.
Angiotensin II is a vasoconstrictor, and it stimulates the smooth muscle cells in the wall for
the efferent arteriole to contract, constricting the vessel. As a result of this action, blood
tends to back up into the glomerulus, and as the glomerular hydrostatic pressure increases, the
filtration rate also increases. These two mechanisms operate together to ensure a constant
blood flow through the glomerulus and a relatively stable glomerular filtration rate, in spite of
Tubular Reabsorption
If the composition of the glomerular filtrate entering the renal tubule is compared with
that of the urine leaving the tubule, it is clear that changes occur as the fluid passes through
the tubule. For example, glucose is present in the filtrate, but absent in the urine. Also, urea
and uric acid are considerably more concentrated in the urine than they are in the glomerular
filtrate. Such changes in fluid composition are largely the result of tubular reabsorption, a
process by which substances are transported out of the glomerular filtrate, through the
epithelium of the renal tubule, and into the blood of the peritubular capillary.
Since the efferent arteriole is narrower than the peritubular capillary, the blood flowing from
the former into the latter is under relatively slow pressure. Also, the wall of this capillary is
more permeable than that of other capillaries. Both of these factors enhance the rate of fluid
active transport.
Water also is reabsorbed rapidly though the epithelium of the proximal tubule by osmosis;
however, portions of the distal tubule and collecting duct are almost impermeable to
water. This characteristic of the distal tubule and collecting duct is important in the regulation
These carriers transport passenger molecules through the membrane, release them, and return
to the other side to transport more passenger molecules. Such a mechanism has a limited
transport capacity; that is, it can only transport a certain number of molecules in a given
amount of time, because the number of carriers is limited. Usually all of the glucose in the
glomerular filtrate is reabsorbed, because there are enough carrier molecules to transport it.
Sometimes, however, the plasma glucose concentration increases, and if it reaches a critical
level, called the renal plasma threshold, there will be more glucose molecules in the filtrate
than the active transport mechanism can handle. As a result, some glucose will remain in the
Amino acids also enter the glomerular filtrate and are reabsorbed in the proximal
mechanism is though to reabsorb a different group of amino acids, whose members have
molecular similarities. As a result of their actions, only a trace of amino acids usually remains
in the urine. Although the glomerular filtrate is nearly free of protein, some albumin may be
present. These proteins have relatively small molecules, and they are reabsorbed by
pinocytosis through the brush border of the epithelial cells lining the proximal convoluted
tubule. Once they are inside an epithelial cell, the proteins are converted to amino acids and
moved into the blood of the peritubular capillary. Other substances reabsorbed by the
epithelium of the proximal convoluted tubule include creatine, lactic acid, citric acid, uric
acid, ascorbic acid (vitamin C), phosphate ions, sulfate ions, calcium ions, potassium ions,
and sodium ions. As a group, these substances are reabsorbed by active transport mechanisms
with limited transport capacities. Such a substance usually does not appear in the urine until it
Substances that remain in the renal tubule tend to become more and more
concentrated as water is reabsorbed from the filtrate. Most water reabsorption occurs
passively by osmosis in the proximal convoluted tubule and is closely associated with the
water moves through cell membranes from regions of lesser solute concentration (hypotonic)
from the renal tubule into the peritubular capillary. Because of the movement of solutes and
water into the peritubular capillary, the volume of fluid within the renal tubule is greatly
reduced.
Tubular Secretion
This is a process by which certain substances are transported from the plasma of the
peritubular capillary into the fluid of the renal tubule. As a result, the amount of
particular substance excreted into the urine may be greater than the amount filtered from the
body fluids.
Although most of the potassium ions in the glomerular filtrate are actively reabsorbed in the
proximal convoluted tubule, some may be secreted passively in the distal segment and
collecting duct. During this process, the active reabsorption of sodium ions out of the fluid
produces a negative electrical charge within the tube. Because the positively charged
potassium ions (K+) and hydrogen ions (H+) are attracted to regions that are negatively
charged, these ions move through the tubular epithelium and enter the tubular fluid.
2. Pathophysiology Precipitating factors
Stress
PATEINT-CENTERED (SCHEMATIC DIAGRAM) Sedentary lifestyle
Predisposing factors Unhealthy eating habits
Age ( 50 years old) Hypertension
Race (Asian) Alcoholism
Hereditary ( father side) smoking
Death
Anemia (RBC2.75)
Fatigue
b. Synthesis of the Disease
blood glucose (hyperglycemia) resulting from defects in insulin production and secretion,
decreased cellular response to insulin or both. Hyperglycemia may lead to acute metabolic
Type 2 diabetes accounts to about 90% to 95% of diabetic. It results from a decreased
Type 2 is first treated with diet and exercise, then oral hypoglycemic agents as needed. And
type 2 most frequently occurs in patients older than 30 years of age and in obese patients.
a. Age (50 years old) – Type 2 DM usually occurs at the age 45 years old and above
(Braunwald,ed.., 2001). Type 2 DM occurs most commonly in people older than 30 years
b. Race (Asian) – Type 2 DM is more prevalent among colored races although Type 1 DM is
c. Hereditary - A genetic predisposition, lowered beta-cell mass either through genetic and/or
b. Diet – Foods rich in carbohydrates can easily promote the increasing level of glucose along
the bloodstream.
c. Sedentary lifestyle - a sedentary lifestyle is damaging to health and bears responsibility for
the growing obesity problems." Inactivity and being overweight go hand in hand towards a
diagnosis of type 2.
d. Unhealthy eating habits – 90% of people who have been diagnosed with type 2 diabetes
are overweight. Unhealthy eating contributes largely to obesity. Too much fat, not enough
fiber and too many simple carbohydrates all contribute to a diagnosis of diabetes.
e. Excessive drinking of alcohol - Alcohol is processed in the body very similarly to the way
fat is processed, and alcohol provides almost as many calories. Therefore, drinking alcohol in
f. Smoking (15 sticks a day) - Smoking raises your blood glucose (sugar) and reduces your
body's ability to use insulin, making it more difficult to control your diabetes.
g. Hypertension – Blood flows slowly due to its difficulty passing through the narrow blood
vessels.
1. Hyperglycemia
This is due to the excessive blood volume secondary to increase volume of water in the
Due to dehydration brought by frequent urination, in return, thirst center of the brain will be
triggered making the patient to urge for thirst and also ude to the activation of the thirst center
as a result of dehydration.
4. Hypertension
Due to increase blood flow secondary to increased blood viscosity, in return due a decrease
5. Fatigue (malaise)
6. Nephropathy
Occurs when there is too much inflammation and glucose in the bloodstream, clogging the
Chronic kidney disease (CKD), also known as chronic renal disease, is a progressive loss
pressure or diabetes and those with a blood relative with chronic kidney disease. Chronic
excrete waste products. Creatinine levels may be normal in the early stages of CKD, and the
condition is discovered if urinalysis (testing of a urine sample) shows that the kidney is
allowing the loss of protein or red blood cells into the urine. To fully investigate the
underlying cause of kidney damage, various forms of medical imaging, blood tests and often
renal biopsy (removing a small sample of kidney tissue) are employed to find out if there is a
reversible cause for the kidney malfunction. Recent professional guidelines classify the
severity of chronic kidney disease in five stages, with stage 1 being the mildest and usually
causing few symptoms and stage 5 being a severe illness with poor life expectancy if
synonymous with the now outdated terms end-stage renal disease (ESRD), chronic kidney
Stage 1
Slightly diminished function; Kidney damage with normal or relatively high GFR (>90
mL/min/1.73 m2). Kidney damage is defined as pathologic abnormalities or markers of
damage, including abnormalities in blood or urine test or imaging studies.[1]
Stage 2
Mild reduction in GFR (60-89 mL/min/1.73 m2) with kidney damage. Kidney damage is
defined as pathologic abnormalities or markers of damage, including abnormalities in blood
or urine test or imaging studies.[1]
Stage 3
Moderate reduction in GFR (30-59 mL/min/1.73 m2).[1] British guidelines distinguish
between stage 3A (GFR 45-59) and stage 3B (GFR 30-44) for purposes of screening and
referral.[4]
Stage 4
Severe reduction in GFR (15-29 mL/min/1.73 m2)[1] Preparation for renal replacement
therapy
Stage 5
Established kidney failure (GFR <15 mL/min/1.73 m2, or permanent renal replacement
therapy (RRT
b.2. Signs and Symptoms with rationale
1. blood pressure is increased due to fluid overload and production of vasoactive hormones,
increasing one's risk of developing hypertensionand/or suffering from congestive heart
failure
2. 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").
3. Erythropoietin synthesis is decreased (potentially leading to anemia, which
causes fatigue)
4. Fluid volume overload - symptoms may range from mild edema to life-
threatening pulmonary edema
5. 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)
6. Higher levels of creatinine, BUN indicate a falling glomerular filtration rate and as a
result a decreased capability of the kidneys to excrete waste products.
VI.
A. Medical Management
Plain NSS Normal Saline Solution To increase both Date Ordered: June 19, Patient’s blood volume increases
1000ml x 40 is an isotonic crystalloid blood volume and 2010 and cells are rehydrated.
ugtts/min that contains 0.9 % to rehydrate the
(KVO) sodium chloride (salt) in cells. Date Started: June 19, 2010
sterile water.
NURSING RESPONSIBILITIES:
Prior:
B. Drugs
Generic and General
Indication D/O, D/S, D/C Client’s Response
Brand name Description
BEFORE:
Explain the procedure to the patient the importance of the drug, its uses, and effects.
Prepare the right medication at the right time and with the right dosage.
should be used with caution in patients with renal impairment or in those at risk of fluid retention
DURING:
AFTER:
Pantoprazole ANTI-ULCER/ To treat gastrophageal reflux D/O: June 19, 2010 Patient’s risk for stomach ulcers
Sodium Gastric Acid disease. D/S: June 19, 2010 due to medications was prevented.
Pantoloc Proton Pump To treat or reduce the risk of D/C: June 21, 2010
Inhibitor stomach ulcers due to
medications.
BEFORE:
Prepare the right medication at the right time and with the right dosage.
Do not chew or crush the tablets, and take them with a glass of water in the morning before, during, or after breakfast.
DURING:
AFTER:
BEFORE:
Explain the procedure to the patient the importance of the drug, its uses, and effects.
Prepare the right medication at the right time and with the right dosage.
Shake the oral liquid well before each use to mix the medicine evenly
DURING:
AFTER:
Monitor for upset stomach, vomiting and belching
Paracetamol/ ANTI- Commonly used for relief of fever, D/O: June 19, 2010 Patient’s headache and minor
Acetaminophe PYRETIC headaches, and other minor pains D/S: June 19, 2010 pains are relieved.
n ANALGESIC and aches. D/C: June 23, 2010
Tylenol
BEFORE:
Explain the procedure to the patient the importance of the drug, its uses, and effects.
Prepare the right medication at the right time and with the right dosage.
AFTER:
Kremizin Oral absortive Can delay the progression of D/O: June 22, 2010 The progression of chronic kidney
chronic renal failure in undialyzed D/S: June 22, 2010 disease of the patient was can be
patients with uremic syndrome delayed.
BEFORE:
Explain the procedure to the patient the importance of the drug, its uses, and effects.
Determine hypersensitivity to the drug.
Prepare the right medication at the right time and with the right dosage.
DURING:
AFTER:
Serum creatinine and blood pressure levels were measured every month for 6 months
Ferrous Anti-anemic/ To preven iron defeincy and to D/O: June 22, 2010 Patient was provided with iron
Sulfate nutritional provide iron supplementation. D/S: June 22, 2010 supplements.
supplement
Fergon
BEFORE:
Explain the procedure to the patient the importance of the drug, its uses, and effects.
Prepare the right medication at the right time and with the right dosage.
DURING:
Dilute and administer with straw because it can cause staining of teeth
Milk, eggs, or caffeine beverages when taken with the iron preparation may inhibit absorption.
Give on an empty stomach if possible because oral preparations are best absorbed then. Minimize gastric distress if needed by giving
AFTER:
Monitor patient for iron overdose which may include abdominal pain, diarrhea, nausea and sharp abdominal cramping
Dolacet ANALGESIC To treat moderate to severe back D/O: June 23, 2010 The patient reported decreased
Dolacet pain and pain from arthralgia, D/S: June 23, 2010 pain.
cancer, dental procedures,
headache and myalgia
BEFORE:
Prepare the right medication at the right time and with the right dosage.
DURING:
AFTER:
Monitor signs of overdose such as blurred vision, cold, clammy skin, confusion and dizziness
Epoetin Alfa ANTI- Anti – anemic D/O: June 21, 2010 Well tolerated and no
Renogen ANEMIC *To treat infection like D/S: June 21, 2010 further aggravation of
septicemia and skin D/C: June 21, 2010 infection resulted. No
infection due to necrosis adverse effects noted. Side
effects include experience
of soft stools.
BEFORE:
Explain the procedure to the patient the importance of the drug, its uses, and effects.
Prepare the right medication at the right time and with the right dosage.
DURING:
AFTER:
Generic and
General Description Indication D/O, D/S, D/C Client’s Response
Brand name
Cefuroxime 2ND GENERATION Treatment of infections D/O: June 22, 2010 Well tolerated and no
Zinnat CEPHALOSPORIN specifically in the upper further aggravation in
ANTIBIOTIC respiratory tract. D/S: June 22, 2010 infection resulted. Side
effects experienced include
nausea and presence of soft
stools during defecation.
No adverse effects noted.
BEFORE:
Explain the procedure to the patient the importance of the drug, its uses, and effects.
Determine hypersensitivity to the drug.
Prepare the right medication at the right time and with the right dosage.
DURING:
AFTER:
Generic and
General Description Indication D/O, D/S, D/C Client’s Response
Brand name
Cephalexin 1ST To treat infection like D/O: June 21, 2010 Well tolerated and no
HCL GENERATION septicemia and skin further aggravation of
Kefox CEPHALOSPORIN infection due to necrosis D/S: June 21, 2010 infection resulted. No
ANTIBIOTIC D/C: June 21, 2010 adverse effects noted. Side
effect includes experience
of soft stools.
BEFORE:
Explain the procedure to the patient the importance of the drug, its uses, and effects.
Prepare the right medication at the right time and with the right dosage.
DURING:
AFTER:
Monitor for hypersensitivity and adverse reaction
Generic and
General Description Indication D/O, D/S, D/C Client’s Response
Brand name
Calcium ANTACID / To alleviate heart burn D/O: June 22, 2010 Well tolerated and
Carbonate ANTIHYPER- due to hyperacidity and to D/S: June 22, 2010 hyperacidity decreased.
Calsan, Tums PHOSPHATEMIC treat hyperphosphatemia D/C: June 22, 2010 Side effects experienced
due to renal disorder include nausea and
sensation of warmth in the
skin. No adverse effects
noted.
BEFORE:
Explain the procedure to the patient the importance of the drug, its uses, and effects.
DURING:
Urge patient to chew them thoroughly before swallowing and to drink a glass of water afterwards
AFTER:
C. DIET
Low salt, Low fat diet The low fat and salt diet Indicated for bed patient Date Ordered: June 19, >The client complied
is design to limit the whose condition
total amount of fat, salt required modified diet in 2010 with the prescribed diet.
and cholesterol in the order to prevent further
diet to reduce serum aggravation, like not
lipid levels and avoid increase fat levels in the Date Started: June 19, >Well tolerated and no
excessive sodium blood and to prevent 2010 complaints.
retention further damage to
kidneys
BEFORE:
DURING:
Enumerate the foods that the patient may or may not take.
AFTER:
> Investigate
changes in > Changes in
mentation/ mentation can
sensorium. be due to
abnormally high
or low glucose,
electrolyte
abnormalities,
and decreased
cerebral
perfusion.
VIII.
DISCHARGE PLAN
Topic: Diet