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A.

Introduction

Diabetes is a metabolic disorder characterized by a relative or absolute


lack of the hormone insulin or insulin resistance, or both, which is impaired
use of carbohydrates and altered metabolism of fats and protein. The word
diabetes, from the Greek meaning “a siphon”, suggests urine formation, the
word mellitus, from the Greek meaning “honey”, suggests sweetness. Type 2
diabetes was formerly known by a variety of partially misleading names,
including “adult-onset diabetes,” obesity-related diabetes”, or non-insulin-
dependent diabetes” (NIDDM). It is characterized by “insulin resistance” as
body cells do not respond appropriately when insulin is present. This is more
complex problem than type 1, but it is sometimes easier to treat, since insulin
is still in many, especially in the initial years. Type 2 may go unnoticed for
years in a patient before diagnosis, since the symptoms are typically milder
and can be sporadic. The 3 cardinal signs of Type 2 DM are polyphagia
(excessive hunger), polydipsia (excessive thirst), and polyuria (excessive
urination). Other signs and symptoms of this disease are weight loss or gain,
blurred vision, headaches lethargy, impotence, vaginal discharge, increased
vaginal infection, increased wound healing time, orthostatic hypertension,
decreased pedal pulses, paresthesics, and decreased sensations
(extremities). If these signs and symptoms were not given proper or enough
attention, it may lead to the following complications” diabetic neurophatics
(low of sensation in extremities), Charcot’s syndrome, Retinopathy, kidney
failure, Atherosclerosis of the heart and large vessels and amputation.
In 2004, according to the World Health Organization, more than 150
million people worldwide suffer from diabetes. Its incidence is increasing
rapidly, and it is estimated that by the year 2025 this number will double.
Diabetes mellitus occurs throughout the world, but it is common (especially
Type 2) in the more developed countries. In 2002 there were about 18.2
million diabetics in the United States alone. Diabetes is in the top 10, and
perhaps the top 5, of the most significant disease in the developed world, and
is gaining insignificance. For at least 20 years, diabetes rates in North
America have been increasing substantially. The Centers for Disease Control
has termed the change an epidemic. The National Diabetes Information
Clearing house estimates that diabetes costs $132 billion in the United States
alone every year.
Diabetes has become a multibillion dollar industry in Europe
specifically; Type 2 Diabetes contributes to an annual economic cost of 129
billion among developed countries. Due to this, the traditional urine testing
as the only method for gauging blood glucose levels of patients, a variety of
devices designed to monitor glucose while easing the burden of frequent
blood tests. There is a growing demand for portable glucose meters that are
compact user friendly in monitoring blood glucose levels efficiently accurate.
Through technological improvements, Point of Case Testing (POC) is the
largest profit making segment in the market. POC testing provides simple and
quick results. With this, POC testing is expected to play a key role in the fight
against Diabetes and will dominate the market over clinical diagnostics
Glycosylated hemoglobin (HbAlc) is another test that is expected to rise
slightly and is being processed and prices for cheaper than hospital-based
laboratories since it is already adopted by health Care Teams even outpatient
clinics and small hospital based laboratories. Manufacturers will identify
customers unmet needs and develop competent technologies that focus on
dedicated systems to improve efficiency and profitability. New technologies
and challenges may occur; it will remain for more patient friendly screening
and treatments. The future care for Diabetes will non-invasive and make
glucose regulation for more accurate and easier to manage.
Current Trends CDC Criteria for Anemia in Children and Childbearing-Aged
Women
Hemoglobin (Hb) and hematocrit (Hct) measurements are the
laboratory tests used most commonly in clinical and public health settings for
screening for anemia. Because most anemia in children and women of
childbearing age is related to iron deficiency (1), the main purpose of anemia
screening is to detect those persons at increased risk for iron deficiency.
Proper anemia screening requires not only sound laboratory methods and
procedures but also appropriate Hb and Hct cutoff values to define anemia.
The "normal" ranges of Hb and Hct change throughout childhood and during
pregnancy, and are higher for men than women (1,2). Thus, criteria for
anemia should be specific for age, sex, and stage of pregnancy. Current major
reference criteria for anemia, however, are not based on representative
samples and fail to take into account the normal hematologic changes
occurring during pregnancy. To address these limitations, CDC has formulated
new reference criteria for use in clinical practice for public health and
nutrition programs and the CDC Pediatric and Pregnancy Nutrition
Surveillance Systems. The new criteria may also be useful for defining
anemia in clinical research and nutrition surveys.
The anemia reference values for children, nonpregnant women, and
men are derived from the most current nationally representative sample--the
Second National Health and Nutrition Examination Survey, 1976-1980
(NHANES II). Because representative data are not yet available for pregnant
women, anemia reference values are based on the most current clinical
studies available. Adjustment values of Hb and Hct cutoffs are provided for
persons who reside at higher altitudes and for those who smoke cigarettes.
Anemia Cutoffs for Children, Nonpregnant Women, and Men
Because hematologic values normally change as children grow older, it is
necessary to use age-specific criteria for diagnosing anemia in children (1).
The best hematologic reference data for the United States are available from
the NHANES II. The Hb and Hct cutoffs recommended represent the age-
specific fifth percentile values for "healthy" persons from NHANES II (Table 1)
(3, 4). The healthy sample was defined by excluding persons who were likely
to have iron deficiency based on multiple iron biochemical measures. The
anemia cutoff values based on these NHANES II studies for younger children
are in close agreement with the cutoff values recommended by the American
Academy of Pediatrics, which were based on a sample of healthy white
middle-class children (5). Even though no data are available from NHANES II
to determine anemia cutoffs for infants less than 1 year of age, cutoff values
for children 1-2 years can be extrapolated back to 6 months of age. In
general, anemia screening to detect iron deficiency is not indicated for
infants less than 6 months of age because younger infants usually have
adequate iron nutritional status (6). Anemia Cutoffs during Pregnancy
During a normal pregnancy, a woman's hematologic values change
substantially (2). For women with adequate iron nutrition, Hb and Hct values
start to decline during the early part of first trimester, reach their nadir near
the end of second trimester, then gradually rise during the third trimester
(2,7-10). Because of the change of Hb and Hct during pregnancy, anemia
must be characterized according to the specific stage of pregnancy. The
normal range of Hb and Hct during pregnancy is based on data aggregated
from four European studies of healthy iron-supplemented pregnant women
(7-10). These studies provide similar findings at each specific month of
pregnancy. The month-specific fifth percentile values for Hb of the pooled
data have been adopted for use in the CDC Pregnancy Nutrition Surveillance
System (Table 2). In addition, trimester-specific cutoffs also have been
developed for use in the clinical setting (Table 2). These trimester-specific
cutoffs are based on the mid-trimester values; cutoffs for the first trimester,
the time at which most women are initially seen for prenatal care, are based
on a late-trimester value. Adjustment of Hb and Hct Cutoffs for Altitude and
Smoking

Persons residing at higher altitudes ( greater than 1000 meters (3300


feet)) have higher Hb and Hct levels than those residing at sea level. This
variation is due to the lower oxygen partial pressure at higher altitudes, a
reduction in oxygen saturation of blood (11), and a compensatory increase in
red cell production to ensure adequate oxygen supply to the tissues. Thus,
higher altitude causes a generalized upward shift of the Hb and Hct
distributions. This shift may be associated with the underdiagnosis of anemia
for residents of higher altitudes when sea-level cutoffs are applied (CDC,
unpublished data). Therefore, the proper diagnosis of anemia for those
residing at higher altitudes requires an upward adjustment of Hb and Hct
cutoffs. The values for altitude-specific adjustment of Hb and Hct are derived
from data collected by the CDC Pediatric Nutrition Surveillance System on
children residing at various altitudes in the mountain states (Table 3). Altitude
affects Hb and Hct levels throughout pregnancy in a similar way (J.N.
Chatfield, unpublished data).
The influence of cigarette smoking is similar to that of altitude, in that
smoking increases Hb and Hct levels substantially. The higher Hb and Hct of
smokers is a consequence of an increased carboxyhemoglobin from inhaling
carbon monoxide during smoking. Because carboxyhemoglobin has no
oxygen carrying capacity, its presence causes a generalized upward shift of
the Hb and Hct distribution curves (CDC, unpublished data). Therefore, a
smoking-specific adjustment to the anemia cutoff is necessary for the proper
diagnosis of anemia in smokers. The smoking-specific Hb and Hct
adjustments are derived from the NHANES II data (Table 4). The altitude and
smoking adjustments are additive. For example, a woman living at 6000 feet
and smoking two or more packs of cigarettes per day would have her cutoff
for anemia adjusted upward by a total of 1.4 grams of Hb or 4% Hct.
Reported by: Div of Nutrition, Center for Chronic Disease Prevention and
Health Promotion; Div of Environmental Health Laboratory Sciences, Center
for Environmental Health and Injury Control; Div of Health Examination
Statistics, National Center for Health Statistics; Div of Host Factors, Center for
Infectious Diseases, CDC.

Hypertension is a common clinical problem faced by both primary care


clinicians and specialists. While the exact prevalence of resistant
hypertension is unknown, clinical trials suggest that it is not rare, involving
perhaps 20% to 30% of study participants. As older age and obesity are 2 of
the strongest risk factors for uncontrolled hypertension, the incidence of
resistant hypertension will likely increase as the population becomes more
elderly and heavier. The prognosis of resistant hypertension is unknown, but
cardiovascular risk is undoubtedly increased as patients often have a history
of long-standing, severe hypertension complicated by multiple other
cardiovascular risk factors such as obesity, sleep apnea, diabetes, and chronic
kidney disease. The diagnosis of resistant hypertension requires use of good
blood pressure technique to confirm persistently elevated blood pressure
levels. Pseudoresistance, including lack of blood pressure control secondary
to poor medication adherence or white coat hypertension, must be excluded.
Resistant hypertension is almost always multifactorial in etiology. Successful
treatment requires identification and reversal of lifestyle factors contributing
to treatment resistance; diagnosis and appropriate treatment of secondary
causes of hypertension; and use of effective multidrug regimens. As a
subgroup, patients with resistant hypertension have not been widely studied.
Observational assessments have allowed for identification of demographic
and lifestyle characteristics associated with resistant hypertension, and the
role of secondary causes of hypertension in promoting treatment resistance is
well documented; however, identification of broader mechanisms of
treatment resistance is lacking. In particular, attempts to elucidate potential
genetic causes of resistant hypertension have been limited.
Recommendations for the pharmacological treatment of resistant
hypertension remain largely empiric due to the lack of systematic
assessments of 3 or 4 drug combinations. Studies of resistant hypertension
are limited by the high cardiovascular risk of patients within this subgroup,
which generally precludes safe withdrawal of medications; the presence of
multiple disease processes (eg, sleep apnea, diabetes, chronic kidney
disease, atherosclerotic disease) and their associated medical therapies,
which confound interpretation of study results; and the difficulty in enrolling
large numbers of study participants. Expanding our understanding of the
causes of resistant hypertension and thereby potentially allowing for more
effective prevention and/or treatment will be essential to improve the long-
term clinical management of this disorder.

Furuncles are very common. They are caused by staphylococcus


bacteria, which are normally found on the skin surface. Damage to the hair
follicle allows these bacteria to enter deeper into the tissues of the follicle
and the subcutaneous tissue. Furuncles may occur in the hair follicles
anywhere on the body, but they are most common on the face, neck, armpit,
buttocks, and thighs.
Furuncles are generally caused by Staphylococcus aureus, but they may be
caused by other bacteria or fungi. They may begin as a tender, red,
subcutaneous nodule but ultimately become fluctuant (feel like a water-filled
balloon). A furuncle may drain spontaneously, producing pus. More often the
patient or someone else opens the furuncle.
Furuncles can be single or multiple. Some people have recurrent bouts with
abscesses and little success at preventing them. Furuncles can be very
painful if they occur in areas like the ear canal or nose. A health care provider
should treat furuncles of the nose. Furuncles that develop close together may
expand and join, causing a condition called carbunculosis.
Electrolytes are salts that conduct electricity and are found in the body
fluid, tissue, and blood. Examples are chloride, calcium, magnesium, sodium,
and potassium. Sodium (Na+) is concentrated in the extracellular fluid (ECF)
and potassium (K+) is concentrated in the intracellular fluid (ICF). Proper
balance is essential for muscle coordination, heart function, fluid absorption
and excretion, nerve function, and concentration.

The kidneys regulate fluid absorption and excretion and maintain a


narrow range of electrolyte fluctuation. Normally, sodium and potassium are
filtered and excreted in the urine and feces according to the body's needs.
Too much or too little sodium or potassium, caused by poor diet, dehydration,
medication, and disease, results in an imbalance. Too much sodium is called
hypernatremia; too little is called hyponatremia. Too much potassium is called
hyperkalemia; too little is called hypokalemia.

B. Reasons for choosing such case for Presentation

One of the formidable parts in doing a case study is choosing what


case is to present. We had this unanimous decision of choosing our patients
case, first and foremost because with our initial contact we already
established harmonious relationship with the patient and his significant
others. We had established the “trust” we yearn from them and that makes it
easy for us to ask certain questions we need for our case and interact with
them properly. Another thing is because we find them kind and humorous
that is why our previous interaction with them is smooth and conventional.
Most importantly, our patient’s case is very critical because he has five
diagnoses. With that thought alone, we want to further enhance our
knowledge about the disease such as to ensure appropriate evaluation of the
etiology, reassess and address the course of the illness takes in its
progression. Also, to have an experience in handling and providing
humanitarian health services to a patient who has it and provide any
intervention or treatment indicated based on the specific etiology and the
course it follows in that specific patient. With that scenario, it is not only the
knowledge that was enhanced but also our skills as health care practitioners.

II. NURSING ASSESSMENT


A. Personal History
1. Demographic Data

Mr. Mickey (not his real name) is a 52 years old married male, Filipino
who was born on February 16, 1954 in Angeles City. He is the eldest among
the eight siblings of Disney family (not their real family name) and has 5
unmarried sisters. He, together with Mrs. Minnie (not her wife’s real name)
and their eight children, currently resides near main road in Robinson’s mall,
Angeles City, Pampanga. He is religiously affiliated as a Roman Catholic. He is
presently working as a Barangay Tanod. He was admitted at Ospital Ning
Angeles (ONA) on April 27, 2008 because of hypertension and Diabetes
Mellitus type 2.

2. Socio-economic and cultural factors


Mr. Mickey was able to finish a full course of elementary until second
year college but had not gone to school to continue his studies due to
financial constraints.
Mr. Mickey was a construction worker before and now he is presently
working as a barangay tanod. He doesn’t earn much, he just earn 2000 per
month that’s why he cannot able to support his family. They spend about 300
pesos a day through the financial support of his children.
Mr. Mickey, does not like having exercises, he has a sedentary lifestyle.
He gets easily stressed because of their financial status plus his job as a
barangay tanod. He usually comes home at 2 am in the morning. He does not
engage in any vices such as drinking alcoholic beverages nor smoking
cigarettes. As for the foods he eats before he acquired hypertension and
diabetes mellitus type 2, Mr. Mickey preferred fatty and salty foods and also
those glucose rich or sweets.
Mr. Mickey and his family also believe in consulting the “herbolaryos
or manghihilot” for any problems or illness that would occur. They also use
herbal medicines as alternative in treating illnesses like guava decoction.
The family of Mr. Mickey lived in one of those small concrete houses, situated
near main road of Robinson’s Mall in Angeles. They have a one storey house
but cemented. It has only three bedrooms though they are ten in the family
living in that house. Some of them are sleeping in the sala at night. Their
sala serves both as a receiving and recreational area for the family; a kitchen
at the back portion of the house, and a comfort room. Their residence is
fortunately, nearby the community market. So everyday, his wife buys fresh
foodstuffs like meat, fish, and vegetables to cook. There are also clinics and
health center but not close to the proximity. There are also no factories near
their house.

B. Family Health Illness History

Grandfather Grandmother Grandfather Grandmother


(deceased): (deceased): (deceased): (deceased):
Hypertension Kidney Failure Heart Attack Tuberculosis

Mommy Mouse Papa Mouse


(Mother-deceased): (Father-deceased):
Stroke and DM Lung Cancer

Mr. Sister 1 Brother Sister Sister Sister Sister 5 Sister


Mickey:
eldest

- Normal

- With diabetes

- With hypertension

- With Diabetes type 2, Hypertension 2


C. History of Past illnesses
Mrs. Minnie mentioned that it was actually her husbands first time to
be confined in a hospital. According to Mrs. Minnie, her husband had Measles
when he was in grade five. Mr. Mickey had Arthritis; he used “katingko” as a
pain remedy. He took Mefenamic acid and Biogesic for his arthritis and
Headache. He also had cough and colds and he used to drink lots of water as
self medication. He also suffered from hypertension and was diagnosed when
he was still single, it was just starting then (mild hypertension). He didn’t take
any medications nor consult any health care provider. Five years ago, Mr.
Mickey noticed that he has an insatiable appetite for food, excessive thirst,
and at the same time he urinates frequently. He easily gets fatigue and feels
weak or lethargic that’s why he used to sleep most of the time.

D. History of Present Illness

Two years ago, Mr. Mickey went to the clinic and consulted the Doctor.
He complained of pain and loss of hearing in his left ear. The Doctor
prescribed him antibiotic (eardrops) and advised him to wear hearing aid.
One year after, two ears became affected. In January 2008 when he went to
health center, his blood pressure was increased, it was 140/90. Last April 23,
morning, when he sought medical help in the OPD of ONA. During that time,
he has no appetite in eating and his furuncle was still small. The Doctor
prescribed him to take Amoxicillin, Appebon with Iron and Cetrizine
Dihydrochloride. On the night of April 27, 2008, he was admitted to the
hospital for the first time with admitting diagnosis of intractable vomiting,
Electrolyte imbalance, Anemia, furuncle, Diabetes Mellitus type 2,
Hypertension 2.

The following doctor’s orders were given: (lifted from the Mr. Mickey’s
chart):
Initial V/S were, T-36.0 PR-84 RR-21 BP-170/100
 Pls admit to medical ward
 Secure consent from admin and management
 NPO temporarily except meds
 IVF PNSS 1L x 30 gtts/min
 Dxtic: CBC-done RBC-done
 U/A-done
 Na, K-done
 Creatinine-Requested
 BUN
 FBS
 Lipid profile
 CXR-PA
 12 lead ECG
 Tx: Ceftriaxone 1g/IV q 12
 Metformin 500mg 1 tab BID
 Plasil tab TID PRN for Vomiting
 FeSO4 tab BID
 Monitor VS q4
 Refer accordingly
 Amlodipine (Lopicard) 5g I tab OD

E. Physical Examination

Physical Assessment/Doctor’s Notes: April 27, 2008 (admission-lifted


from the chart)
Diagnosis: Intractable Vomiting, Electrolyte Imbalance,
Anemia, Furuncle, DM type 2, Hypertension 2

• Vomiting, three times


• Body weakness

• BP= 170/100 mmHg

• Pulse Rate= 84 beats per minute

• Respiratory Rate= 21 cycles per minute


• Temperature= 36.6 ˚C
*** for Lipid profile, triglycerides, BUA, CXR posterior-anterior view, ECG

Physical Assessment: April 28, 2008

Vital Signs:
T- 37°C RR- 17 cpm
PR- 74 bpm BP- 150/90 mmHg

1. General Appearance
a. Body built is ectomorphic
b. Presence of halitosis for the breath odor
c. Attitude is cooperative
d. Affect or mood is appropriate for the situation

2. Skin
a. There is good skin turgor
b. Skin is dry, pale on the palms and soles of the feet, with scars on lower
extremities
c. Absence of facial and periorbital edema
d. (+) 3-cm-diameter furuncle on left upper arm, draining purulent
secretion

3. Head
a. Skull is round in shape and has normal contour, with no palpated
depressions
b. Hair is thick, with fine strands; scalp is excessively oily with no masses
palpated
c. Facial features are symmetrical with no noted abnormalities

4. Eyes
a. Pupils are equally round and reactive to light and accommodation
b. Palpebral conjunctiva are pale
c. Eyebrows are symmetrically aligned, hair is thick, evenly distributed;
skin is intact
d. Eyelashes are equally distributed and curled slightly outward
e. No discharges present
f. Absence of periorbital edema
g. Cornea is transparent, smooth and shiny
h. Details of the iris are visible, color brown
i. Sclera appears white

5. Ears
a. Ears are symmetrical and aligned with the outer canthus of the eye,
with no lesions noted.
b. Color is same as facial skin
c. Ears have no foul smelling discharges, with impacted cerumen on the
middle ear
d. Pinna recoils after being folded

6. Nose
a. Nose has no discharge, no lesions, not occluded & with patent airway
b. Color is same as facial skin

7. Throat and Mouth


a. Throat & mouth have no sores and swellings/inflammation
b. Lips are dry and pinkish
c. There is slight difficulty in swallowing
d. Grade of (+) 1 for tonsils-normal; pale, smooth, with no inflammation
e. Tongue is positioned at the center, furry, white, moist, rough, with
fissures
f. Gums are pale and with firm texture

8. Neck
a. Color is slightly darker than facial skin
b. Absence of enlarged thyroid area
c. Absence of jugular vein distention
d. Movement is coordinated and smooth

9. Chest
a. Breasts are not enlarged, with no lesions
b. No masses assessed upon palpation

10. Cardiovascular
a. Absence of chest pain and murmurs
b. Normal heart rhythm, PR = 74 bpm

11. Respiratory
a. Chest is symmetric; anteroposterior to transverse diameter ratio is 1:2
b. Chest expansions are symmetrical
c. Absence of rales on both lung fields
12. Gastrointestinal
a. Presence of bowel sounds 5/min, presence of flatus
b. Absence of bowel movement
c. Absence of organomegaly

13. Extremities
a. Upper- symmetrical, absence of edema; capillary refill >2 seconds; (+)
3-cm-diameter furuncle on left upper arm, draining purulent secretion
b. Lower- symmetrical, absence of edema

14. Urogenital
a. Urine output: approximately 30cc per hour, amber yellow in color,
cloudy
b. Genitals- no foul smelling discharges

Neurological Assessment
Cranial Nerve Normal Findings Actual Findings
1. Olfactory Client must be able to Client was able to
Type: Sensory identify the scent of identify the scent of
Fxn: Sense of smell perfume when allowed to perfume when allowed
smell it. to smell it.
2. Optic Client must see the pen or Client was able to see
Type: Sensory penlight clearly from a the pen or penlight
Fxn: Sense of vision and certain distance; must be from a certain distance,
visual fields able to read newspaper but was not able to
print. read newspaper print.
Client needs to wear
eyeglasses for better
vision.
3. Oculomotor Eyes must follow the The client was able to
Type: Motor direction of the movement follow the movement of
Fxn: Pupil constriction and of the penlight; the penlight through
raising of eyelid In lightly dimmed her eyes.
environment, the pupils of
the eyes will dilate but
upon the introduction of
light, pupils will constrict.
4. Trochlear The eye must follow the The client was able to
Type: Motor movement of a pen in follow the pen with her
Fxn: Downward inward different directions with eyes without moving
eye movement coordination. her head.
5. Trigeminal The client must elicit The client elicited
Type: Sensory and Motor blinking reflex upon blinking reflex upon
Fxn: Jaw movements, touching the cornea with touching the cornea.
chewing and mastication the use of cotton.
(Corneal Sensitivity Test)
6. Abducens Client must follow the The client was able to
Type: Motor index finger of the follow the index finger
Fxn: Lateral movements examiner and its of the examiner and its
of the eyes movements. movements.
7. Facial Client must be able to The client was able to
Type: Motor and Sensory raise eyebrows, show raise eyebrows, show
Fxn: Movement of teeth, frown, smile, pout teeth frown, smile, pout
muscles of the face and and puff out cheeks. Also, and puff out cheeks.
sense of taste on the the client must also be Also, the client was not
anterior two-thirds of the able to distinguish sweet, able to distinguish
tongue sour, and salty foods. sweet, sour, and salty
foods. Test not
performed due to
anorexia and vomiting.
8. Acoustic Client must be able to The client was not able
(Vestibulocochlear) hear a snap of the finger. to hear the snap of the
Type: Sensory finger.
Fxn: Sense of hearing
9. Glossopharyngeal The patient must be able The client was not able
Type: Motor and Sensory to swallow foods that were to taste the food. Test
Fxn: Pharyngeal chewed and taste bitter not performed due to
movements and foods. Also, the gag reflex anorexia and vomiting.
swallowing should be stimulated.
Sense of taste on the
posterior one-third of the
tongue
10. Vagus The patient must be able The client was able to
Type: Motor to speak clearly. speak clearly.
Fxn: Swallowing and
speaking
11. Accessory The patient must able to The client was able to
Type: Motor elevate her shoulders elevate her shoulders
Fxn: Movement of against resistance. against resistance.
shoulder muscles (Sternocleidomastoid and
Trapezius muscles function
test)
12. Hypoglossal The patient must able to The patient was able to
Type: Motor move her tongue side to move her tongue side
Fxn: Movement of tongue side and protrude her to side and protrude
and strength of the tongue. her tongue.
tongue
Diagnostic and Laboratory Procedures

DIAGNOSTIC DATE ORDERED INDICATIONS OR RESULTS NORMAL ANALYSIS AND


OR AND DATE PURPOSES VALUES INTERPRETATIO
LABORATORY RESULTS IN N
PROCEDURES

CLINICAL
CHEMISTRY
FBS/RBS Date Ordered: A test that is 137 (70-105mg/dl) A fasting blood
04-27-08 routinely done in all sugar level of
clients with possible 126 mg/dL or
Date Results In: cardiovascular higher is
04-27-08 disorders to determine consistent with
blood glucose levels. either type 1 or
type 2 diabetes.
Patient’s FBS is
exceeds the
normal limits
indicating the
patient has
diabetes.
113.4 135 – 150 mEq/L
• SODIUM The sodium
- To monitor the electrolyte level
electrolytes and check is below normal
for imbalances any range. It
imbalance in the fluid indicates that the
and electrolytes. patient has
Sodium plays a major hyponatremia.
role in homeostasis in
a variety of ways
including the renal
retention and excretion
of water.
3.8 3.5 – 5.2 mEq/L
• POTASSIUM The potassium
- While, Potassium electrolyte level
is checked in order to is within normal
assess a known and range.
suspected disorder
associated with renal
disease, glucose
metabolism, trauma or
burns.

URINALYSIS Date Ordered: It indicates that


04-27-08 Color: Yellow there is impaired
kidney function
Transparency due to decrease
Date Results In: : organ perfusion.
04-27-08 SL cloudy
3.5-4.5 Ph is slightly
Ph: 5.0 basic which could
indicate
This is a measure of metabolic
acidity for your urine. alkalosis.
This measures how 1.010-1.030 Water would
dilute your urine is. Specific have a SG of
Gravity: 1.000 . Most
1.010 urine is around
1.010, but it can
vary greatly
depending on
when you drank
fluids last, or if
you are
dehydrated. This
means that the
Microscopic value in the
Findings result is within
normal range.

Normally
Pus negative.
cells/HPF: Leukocytes are
3-6 the white blood
cells (or pus
cells). This looks
for white blood
cells by reacting
with an enzyme
in the white cells.
White blood cells
in the urine
suggests a
urinary tract
infection.
Normally there is
RBC/HPF: no blood in the
5-8 urine. Blood can
indicate an
infection, kidney
stones, trauma,
or bleeding from
a bladder or
kidney tumor.
The technician
may indicate
whether it is
hemolyzed
(dissolved blood)
or non-
hemolyzed
(intact red blood
cells). Rarely,
muscle injury can
cause myoglobin
to appear in the
urine which also
causes the
3.2-5.0 g/dl reagent pad to
falsely indicate
blood.
Albumin:
Positive (3+) Albumin is
slightly below
normal. Lower
levels indicate
Sugar: infection, kidney
(Negative) disease, and
inadequate iron
HEMATOLOGY: intake.

HEMOGLOBIN Date Ordered: ▪ HGB M: 140-180g/l


04-27-08 - to monitor Hgb F: 120-160g/l
value in the RBC
Date Results In: - to suggest the
04-27-08 presence of body fluid 95
deficit due to elevated
Hgb level The level of
hemoglobin is
below normal
WBC To detect infection or 5-10 x 109/L which indicates
inflammation. This anemia and
blood test evaluates decrease tissue
the number of 14.5 perfusion.
condition and
differentiates causes of The WBC count
alteration in the total exceeds the
WBC count including normal range
inflammation, infection which indicates
and tissue necrosis. presence of
infection.

HEMATOCRIT to aid diagnosis of M: 0.40-0.52L/L


abnormal states of F:0. 37-0.47L/L
hydration,
polycythemia and 0.29
anemia.
- It measures the The level of
concentration of RBC hematocrit is
within the blood below normal
volume and is which also
expressed as a indicates anemia
percentage. and decrease
tissue perfusion.
18 - 48 %
LMPHOCYTES
To detect presence of
infection within the 0.5
body.
The number of
lymphocyte is
slightly elevated
which indicates
Bacteria: presence of
Epithelial cells: Some infection.
CLINICAL Date Ordered: Some (74-110mg/dl)
CHEMISTRY 04/27/08
FBS/RBS A test that is routinely
done in all clients with 88
Date Results In: possible cardiovascular
04-28-08 disorders to determine A fasting blood
blood glucose levels. sugar level of
126 mg/dL or
higher is
consistent with
CHOLESTEROL M: 123 – 270 either type 1 or
F: 150 to 250 type 2 diabetes.
Used to estimate Patient’s FBS is
risk of developing a 160.7 within normal
disease — specifically range
heart disease. Because
high blood cholesterol The cholesterol
has been associated level is within the
with hardening of the normal range.
arteries, heart disease
and a raised risk of
death from heart
attacks, cholesterol
testing is considered a
routine part of
preventive health care.

CLINICAL Date Ordered: (74-110mg/dl)


CHEMISTRY 04-28-08
FBS A test that is routinely
Date Results In: done in all clients with 117.5
04-29-08 possible cardiovascular
disorders to determine
blood glucose levels. Patient’s FBS is
exceeds the
This calculation is a normal limits
good measurement of indicating the
kidney and liver patient has
BUN function. (7-18 mg/dl) diabetes.

93

The BUN value is


significantly
higher than the
M: 123 – 270 normal range. It
CHOLESTEROL F: 150 to 250 may indicate
Used to estimate risk possible kidney
of developing a 192.5 or liver failure.
disease — specifically
heart disease. Because
high blood cholesterol The cholesterol
has been associated level is within the
with hardening of the normal range.
arteries, heart disease
and a raised risk of
death from heart
attacks, cholesterol
testing is considered a
routine part of
preventive health care.

LIPID PROFILE: Date Ordered:


04-28-08

HDL C Date Results In: -It has the lowest 33.2 M=30-75 The HDL is within
04-29-08 concentration of normal limit
cholesterol and which indicates a
transport endogenous healthy
cholesterol to body metabolic
cells. system.

LDL C 145.22 M=66-178


- The cholesterol- The LDL is within
containing lipid fraction normal limit
most likely associated which indicates
with atherogenesis there is no
(CHD). One of the narrowing of
enzymes most blood vessels.
commonly used to
detect myocardial
infarction.

TRIGLYCERIDES - A test to determine


the cholesterol level 70.4 36-165
circulating in the The triglycerides
bloodstream. level is within the
normal range.
SGPT/ALT 17.0 0-30 U/L
- used to determine if
there is any condition The SGPT level is
necrosis of within normal
hepatocytes, limit.
myocardial cells,
erythrocytes, or
skeletal muscle cells. 19.9 0-40 U/L

SGOT/AST
- used o determine any The SGOT level is
condition involving within normal
necrosis of limit.
hepatocytes,
myocardial cells, or
skeletal muscle cells.

NURSING RESPONSIBILITIES
.
BLOOD TESTING
Before the Procedure:
a. Explain the procedure to the client in order to gain cooperation.
b. Inform the client that she may feel pain during needle insertion.
c. Prepare the materials necessary for the test.
d. Practice aseptic technique by cleaning the area of blood extraction with alcohol in an outward circular
motion.

During the Procedure:


a. Provide comfort to the client.
b. Encourage the patient to relax and refrain from unnecessary movements.

After the Procedure:


a. Apply pressure on the site of puncture to prevent bleeding.
b. Handle the blood sample carefully to prevent hemolysis.

URINALYSIS
Before the Procedure:
a. Explain the procedure to the client in order to gain her
b. Inform the client that there is no need for NPO.
c. Educate the patient on the proper way of collecting urine (clean catch midstream specimen).
d. Prepare the container for the urine.

During the Procedure:


a. Provide privacy.
b. Assist the patient if unable to get her urine sample on her own.
c. Instruct the patient to prevent contamination of the urine and not to add water to the urine specimen , to
prevent alteration of reslts.

After the Procedure:


a. Refrigerate the specimen.
b. Continue taking the medications that were stopped prior to the procedure.
III . ANATOMY AND PHYSIOLOGY

The Cardiovascular System

The heart and circulatory system make up the cardiovascular system.


The heart works as a pump that pushes blood to the organs, tissues, and cells
of the body. Blood delivers oxygen and nutrients to every cell and removes
the carbon dioxide and waste products made by those cells. Blood is carried
from the heart to the rest of the body through a complex network of arteries,
arterioles, and capillaries. Blood is returned to the heart through venules and
veins.
The one-way circulatory system carries blood to all parts of the body.
This process of blood flow within the body is called circulation. Arteries carry
oxygen-rich blood away from the heart, and veins carry oxygen-poor blood
back to the heart. In pulmonary circulation, though, the roles are switched. It
is the pulmonary artery that brings oxygen-poor blood into the lungs and the
pulmonary vein that brings oxygen-rich blood back to the heart.
Twenty major arteries make a path through the tissues, where they
branch into smaller vessels called arterioles. Arterioles further branch into
capillaries, the true deliverers of oxygen and nutrients to the cells. Most
capillaries are thinner than a hair. In fact, many are so tiny, only one blood
cell can move through them at a time. Once the capillaries deliver oxygen
and nutrients and pick up carbon dioxide and other waste, they move the
blood back through wider vessels called venules. Venules eventually join to
form veins, which deliver the blood back to the heart to pick up oxygen.
Vasoconstriction or the spasm of smooth muscles around the blood
vessels causes and decrease in blood flow but an increase in pressure. In
vasodilation, the lumen of the blood vessel increase in diameter thereby
allowing increase in blood flow. There is no tension on the walls of the vessels
therefore, there is lower pressure.
Various external factors also cause changes in blood pressure and
pulse rate. An elevation or decline may be detrimental to health. Changes
may also be caused or aggravated by other disease conditions existing in
other parts of the body.
The blood is part of the circulatory system. Whole blood contains three
types of blood cells, including: red blood cells, white blood cells and platelets.
These three types of blood cells are mostly manufactured in the bone
marrow of the vertebrae, ribs, pelvis, skull, and sternum. These cells travel
through the circulatory system suspended in a yellowish fluid called plasma.
Plasma is 90% water and contains nutrients, proteins, hormones, and waste
products. Whole blood is a mixture of blood cells and plasma.
Red blood cells (also called erythrocytes) are shaped like slightly
indented, flattened disks. Red blood cells contain an iron-rich protein called
hemoglobin. Blood gets its bright red color when hemoglobin in red blood
cells picks up oxygen in the lungs. As the blood travels through the body, the
hemoglobin releases oxygen to the tissues. The body contains more red blood
cells than any other type of cell, and each red blood cell has a life span of
about 4 months. Each day, the body produces new red blood cells to replace
those that die or are lost from the body.
White blood cells (also called leukocytes) are a key part of the body's
system for defending itself against infection. They can move in and out of the
bloodstream to reach affected tissues. The blood contains far fewer white
blood cells than red cells, although the body can increase production of white
blood cells to fight infection. There are several types of white blood cells, and
their life spans vary from a few days to months. New cells are constantly
being formed in the bone marrow.
Several different parts of blood are involved in fighting infection. White
blood cells called granulocytes and lymphocytes travel along the walls of
blood vessels. They fight bacteria and viruses and may also attempt to
destroy cells that have become infected or have changed into cancer cells.
Certain types of white blood cells produce antibodies, special proteins
that recognize foreign materials and help the body destroy or neutralize
them. When a person has an infection, his or her white cell count often is
higher than when he or she is well because more white blood cells are being
produced or are entering the bloodstream to battle the infection. After the
body has been challenged by some infections, lymphocytes remember how to
make the specific antibodies that will quickly attack the same germ if it
enters the body again.
Platelets (also called thrombocytes) are tiny oval-shaped cells made in
the bone marrow. They help in the clotting process. When a blood vessel
breaks, platelets gather in the area and help seal off the leak. Platelets
survive only about 9 days in the bloodstream and are constantly being
replaced by new cells.
Blood also contains important proteins called clotting factors, which
are critical to the clotting process. Although platelets alone can plug small
blood vessel leaks and temporarily stop or slow bleeding, the action of
clotting factors is needed to produce a strong, stable clot.
Platelets and clotting factors work together to form solid lumps to seal
leaks, wounds, cuts, and scratches and to prevent bleeding inside and on the
surfaces of our bodies. The process of clotting is like a puzzle with
interlocking parts. When the last part is in place, the clot is formed.
When large blood vessels are cut the body may not be able to repair
itself through clotting alone. In these cases, dressings or stitches are used to
help control bleeding.
In addition to the cells and clotting factors, blood contains other
important substances, such as nutrients from the food that has been
processed by the digestive system. Blood also carries hormones released by
the endocrine glands and carries them to the body parts that need them.
Blood is essential for good health because the body depends on a
steady supply of fuel and oxygen to reach its billions of cells. Even the heart
couldn't survive without blood flowing through the vessels that bring
nourishment to its muscular walls. Blood also carries carbon dioxide and
other waste materials to the lungs, kidneys, and digestive system, from
where they are removed from the body.

The Urinary System

The components of the urinary system are: two kidneys, two ureters, urinary
bladder and urethra. The kidneys process blood and form urine by filtering
blood plasma (glomerular filtration) and returning most of the water and
solutes to the bloodstream (tubular reabsorption). The remaining water and
solutes constitute the urine (secretion) which passes through ureters, are
stored in the urinary bladder, then excreted from the body through the
urethra.

The main functions of the kidneys are to regulate blood volume and
composition, help regulate blood pressure, synthesize glucose, release
erythropoietin, participate in vitamin D synthesis and excrete wastes in the
urine.

The nephron is functional unit of the kidney. The parts of the nephron are:
renal corpuscle- where blood plasma is filtered and renal tubule- into which
filtered fluid passes. The renal corpusclelies within the renal cortex and
consists of two components: glomerulus and the glomerular (Bowman's)
capsule- a double-walled epithelial cup that surrounds the glomerulus. The
parts of a renal tubule are: proximal convoluted tubule- lies within the renal
cortex, loop of Henle (nephron loop)- extends into the renal medulla, distal
convoluted tubule- lies within the renal cortex, distal convoluted tubules of
several nephrons empty into a single collecting duct.

Malfunctioning of one of the small portions that make up the nephron will
cause impairment in the functioning of the kidneys. Glomerular filtration rate
may decrease, and as a result, large molecules are drained out and secreted
in the urine. Examples of which are RBC and protein molecules. Likewise,
accumulation of sodium causes formation of crystals, which, when dislodged,
may either block passageways of urine, or be excreted and seen as crystals
in the urine.

The Endocrine System


The endocrine system is made up of glands that produce and secrete
hormones. These hormones regulate the body’s growth, metabolism (the
physical and chemical processes of the body), and sexual development and
function. The hormones are released into the bloodstream and may affect
one or several organs throughout the body.

The role of the endocrine system is to maintain the body in balance


through the release of hormones which transfer information and instructions
from one set of cells to another. Many different hormones move through the
bloodstream, but each type of hormone is designed to affect only certain
cells.

Hormones are chemical messengers created by the body. They transfer


information from one set of cells to another to coordinate the functions of
different parts of the body. Hormones can act on some specific cells because
they themselves do not actually cause an effect. It is only through binding
with a receptor (part of the cell specifically designed to recognize the
hormone) like a key into a lock - that causes a chain reaction to occur,
changing the activity of the cells. If a cell does not have a receptor for a
hormone then there will be no effect. Also, there can be different receptors
for the same hormone, and so the same hormone can have different effects
on different cells.

The major glands of the endocrine system are the pituitary, thyroid,
parathyroids, adrenals, pineal body, thymus, and the reproductive organs
(ovaries and testes). The pancreas is also a part of this system; it has a role
in hormone production as well as in digestion. A gland is a group of cells that
produces and secretes chemicals. A gland selects and removes materials
from the blood, processes them, and secretes the finished chemical product
for use somewhere in the body. The endocrine gland cells release a hormone
into the blood stream for distribution throughout the entire body. These
hormones act as chemical messengers and can alter the activity of many
organs at once.

The hypothalamus controls all the processes undergone by the anterior


and posterior pituitary glands. It initiates the production of hormones by the
APG. The APG is controlled by releasing hormones which are chemical signals
produced by the nerve cells of the hypothalamus, causing either stimulation
or inhibition of hormone production. Secretion of hormones by the PPG is
controlled by nervous system stimulation of nerve cells in the hypothalamus.
Parathyroid glands secrete parathyroid hormone which is essential for the
regulation of blood calcium levels. Adrenal glands produce epinephrine and
norepinephrine which are fight-or-flight hormones that prepare the body for
vigorous physical activity. Testes and ovaries produce hormones that are
responsible for secondary sex characteristics, spermatogenesis, and
oogenesis. The thymus gland secretes thymosin which aids in the synthesis
of WBC for fighting infection. This gland decreases in size in some older
adults. The pineal body releases melatonin that is thought to decrease the
secretion of LSH & FSH by decreasing the release of hypothalamic-releasing
hormones. The thyroid gland, located on either side of the trachea, is
controlled by the thyroid stimulating hormone releases by the anterior
pituitary gland, which was initially stimulated by the TSH releasing hormone
from the hypothalamus.

The pancreas is also part of the body's hormone-secreting system,


even though it is also associated with the digestive system because it
produces and secretes digestive enzymes. The pancreas produces two
important hormones, insulin and glucagon. They work together to maintain a
steady level of glucose, or sugar, in the blood and to keep the body supplied
with fuel to produce and maintain stores of energy. The pancreas completes
the job of breaking down protein, carbohydrates, and fats using digestive
juices of pancreas combined with juices from the intestines, secretes
hormones that affect the level of sugar in the blood, and produces chemicals
that neutralize stomach acids that pass from the stomach into the small
intestine by using substances in pancreatic juice. It contains Islets of
Langerhans, which are tiny groups of specialized cells that are scattered
throughout the organ.

In humans, the pancreas is a 15-25 cm (6-10 inch) elongated organ in


the abdomen adjacent to the small intestine and lies toward the back. It has
three regions: a head (abuts a part of the duodenum), body (at the level of L2
of the spine) and tail (extends toward the spleen).

The pancreatic duct (also called the duct of Wirsung) runs the length of
the pancreas and empties into the second part of the duodenum at the
ampulla of Vater. The common bile duct usually joins the pancreatic duct at or
near this point. Many people also have a small accessory duct, the duct of
Santorini, which extends from the main duct more upstream (towards the tail)
to the duodenum, joining it more proximal than the ampulla of Vater.

The pancreas is supplied arterially by the Pancreaticoduodenal arteries


and the splenic artery: the splenic artery supplies the neck, body, and tail of
the pancreas; the superior mesenteric artery provides the inferior
pancreaticoduodenal artery; and the gastroduodenal artery provides the
superior pancreaticoduodenal artery.

Venous drainage is via the pancreaticoduodenal veins which end up in


the portal vein. The splenic vein passes posterior to the pancreas but is said
to not drain the pancreas itself. The portal vein is formed by the union of the
superior mesenteric vein and splenic vein posterior to the neck of the
pancreas. In some people (some books say 40% of people), the inferior
mesenteric vein also joins with the splenic vein behind the pancreas (in
others it simply joins with the superior mesenteric vein instead).

The pancreas is a compound gland in the sense that it is composed of


both exocrine and endocrine tissues. The exocrine function of the pancreas
involves the synthesis and secretion of pancreatic juices. The endocrine
function resides in the million or so cellular islands (the islets of Langerhans)
embedded between the exocrine units of the pancreas. Beta cells of the
islands secrete insulin, which helps control carbohydrate metabolism. Alpha
cells of the islets secrete glucagon that counters the action of insulin.
There are four main types of cells in the islets of Langerhans. They are
relatively difficult to distinguish using standard staining techniques, but they
can be classified by their secretion:

Name of % of islet
Endocrine product Representative function
cells cells
beta cells Insulin and Amylin 50-80% lower blood sugar
alpha cells Glucagon 15-20% raise blood sugar
delta cells Somatostatin 3-10% inhibit endocrine pancreas
PP cells Pancreatic polypeptide 1% inhibit exocrine pancreas

The islets are a compact collection of endocrine cells arranged in


clusters and cords and are crisscrossed by a dense network of capillaries. The
capillaries of the islets are lined by layers of endocrine cells in direct contact
with vessels, and most endocrine cells are in direct contact with blood
vessels, by either cytoplasmic processes or by direct apposition.

There are two main types of exocrine pancreatic cells, responsible for
two main classes of secretions:

Name of cells Exocrine secretion Primary signal


Centroacinar cells bicarbonate ions Secretin
digestive enzymes
Basophilic cells (pancreatic amylase, Pancreatic lipase, CCK
trypsinogen, chymotrypsinogen, etc.)

THE INTEGUMENTARY SYSTEM


Integumentary System
The skin is the largest organ in the body: 12-15% of body weight, with a
surface area of 1-2 meters. Skin is continuous with, but structurally distinct
from mucous membranes that line the mouth, anus, urethra, and vagina. Two
distinct layers occur in the skin: the dermis and epidermis. The basic cell type
of the epidermis is the keratinocyte, which contain keratin, a fibrous protein.
Basal cells are the innermost layer of the epidermis. Melanocytes produce the
pigment melanin, and are also in the inner layer of the epidermis. The dermis
is a connective tissue layer under the epidermis, and contains nerve endings,
sensory receptors, capillaries, and elastic fibers.
The integumentary system has multiple roles in homeostasis, including
protection, temperature regulation, sensory reception, biochemical synthesis,
and absorption. All body systems work in an interconnected manner to
maintain the internal conditions essential to the function of the body.
Follicles and Glands
Hair follicles are lined with cells that synthesize the proteins that form hair. A
sebaceous gland (that secretes the oily coating of the hair shaft), capillary
bed, nerve ending, and small muscle are associated with each hair follicle. If
the sebaceous glands becomes plugged and infected, it becomes a skin
blemish (or pimple). The sweat glands open to the surface through the skin
pores. Eccrine glands are a type of sweat gland linked to the sympathetic
nervous system; they occur all over the body. Apocrine glands are the other
type of sweat gland, and are larger and occur in the armpits and groin areas;
these produce a solution that bacteria act upon to produce "body odor".
The Digestive System
The human digestive system, as shown in Figure 2, is a coiled, muscular tube
(6-9 meters long when fully extended) stretching from the mouth to the anus.
Several specialized compartments occur along this length: mouth, pharynx,
esophagus, stomach, small intestine, large intestine, and anus. Accessory
digestive organs are connected to the main system by a series of ducts:
salivary glands, parts of the pancreas, and the liver and gall bladder (bilary
system).
III. THE PATIENT AND HIS ILLNESS
A. Pathophysiology
a. Schematic Diagram

PATHOPHYSIOLOGY: HYPERTENSION (book-


centered)
Non-modifiable Factors Modifiable Factors
- Age – 35 years and older - Alcohol use - Excess dietary sodium
- Gender – men and post-menopausal women - Lack of exercise - Stress
- Race – black and brown race
- Family history of hypertension
- Obesity - Diabetes
- Kidney disease - Hormonal disorders
- Porphyria - Toxemia of pregnancy
- Oral Contraceptives - Steroids
- Decongestants - Diet pills
- Antidepressants - History of high BP during
pregnancy
- Nonsteroidal anti-inflammatory drugs

Cell membrane alteration Hyperinsu- Renin- SNS over- ↓ Filtering Renal Na


linemia Angiotensi activity surface retention
n Excess

Venous ↑Fluid
Constriction Volume
Structural Functional
hypertrophy Constriction
Decreased organ perfusion

Impaired Impaired Impaired ↑Contractilit ↑Preload


ocular cerebral renal y
↑Peripheral functioning functioning functioning
Resistance

Retinal Altered level of ↑↑BUN, Left ↑BP = ↑Cardiac


↑Blood pressure changes, consciousness, ccreatinine ventricular Output
papilledema dizziness,
PATHOPHYSIOLOGY: DIABETESheadache hypertroph
MELLITUS TYPE II (book-centered )
y
Non-modifiable Factors Modifiable Factors
- Age - Older than 40 years - History of previous impaired glucose tolerance (IGT) or impaired fasting glucose (IFG)
- Family history of type 2 diabetes - Obesity - Weight >20% of desirable body weight (true for approximately 90% of
- Hispanic, Native American, African American, patients with type 2 diabetes)
Asian American, or Pacific Islander descent, - Hypertension (>140/90 mm Hg) or dyslipidemia (high-density lipoprotein [HDL]
Asian 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)
- Viruses: certain viruses may destroy beta cells
- Faulty Immune System: multiple factors may cause the immune system to destroy beta
cells, such as infection
- Physical Trauma: injury or trauma may destroy the ability of the pancreas to produce
insulin
- Drugs: drugs used for other conditions could cause the development of diabetes
- Stress: hormones at times of stress may block the effectiveness of insulin
- Pregnancy: hormones produced during pregnancy can block the effectiveness of insulin

HYPERGLYCEMIA

↑Blood Blood Sugar Level exceeds Glucose uptake


Osmolarity renal threshold by the cells
Normal = 180mg/dl

Fluid shifting from Cellular starvation ↓Energy


intracellular to extracellular Level
Excretion of excess glucose
in the urine
Hunger due to the Body
Intracellular dehydration stimulation of Satiety Center
/ volume depletion malaise
Glucosuria of Hypothalamus

Thirst sensation due to the


Glucose attracts water Polyphagia
stimulation of Thirst Center
of hypothalamus
↑Urine Output: Polyuria

Polydipsia

Sluggish blood flow Delayed biochemical


mediation

Decreased organ perfusion


Slow-healing cuts or
sores

Dry, Nephropat Neuropath Confusio Blurred


itchy vision,
skin retinopath
Numbness y
and
tingling
sensation

PATHOPHYSIOLOGY: ELECTROLYTE IMBALANCE - HYPONATREMIA (book-centered)


modifiable Factors:
Non-modifiable Factors - Diet – low Na intake
- Age - Old age - Climate – acclimatization to warm weather
- Sex - female - Intensive physical activities
- Conditions that impair the body's water excretion
including chronic conditions that cause organ failure

↓Renal perfusion/ ineffective blood supply to the


kidneys

Renal tissue hypoxia

Impairment in renal functioning

↓ tubular reabsorption

↑ Sodium excretion Excretion of albumin

Albuminuria fluid shifting from intravascular to intracellular


space causing an urge to expel excess water

↓ serum Na ↓ BP Nausea, Fluid


levels: vomiting, accumulati
abdominal on in the
cramping, alveoli
hyperactive
Greater proportion of bowel
water in the blood sounds

compared to sodium
Fluid shifting from interstitial
↓impulse to intracellular
Intravascular fluid
Alteration in brain Crackles Tachypnea
transmission
esp. in thetobrain which is volume
Weakness functioning Dry skin
thesensitive
muscles to serum Na
Lethargy
PATHOPHYSIOLOGY: IRON DEFICIENCY ANEMIA (book-centered)
Non-modifiable Factors: Modifiable Factor:
- Sex - females - Diet low in iron
- - Pregnant women - Children with poor nutrition, including low-income children,
- Age - Young Children - Infants and toddlers 6- Children with lead in their blood, Infants fed cow's milk before 1
24 months of age; Premature and low-birth- year of age, Breastfed infants older than 4 months who are not
weight babies receiving iron-rich solid foods or iron supplements
- Adults With Intestinal Bleeding - It also includes people who use
medicines that can cause intestinal bleeding (for example,
aspirin).
- People who are on kidney dialysis, vegetarians, with low
socioeconomic status and older adults who have poor diets.

↓ Iron absorption
at the intestines

↓ Iron available to
the tissues (red
blood cells)

Depletion of iron stores


at the bone marrow to
compensate for
decreased availability
Impaired
hemoglobin and red
blood cell synthesis

Decrease
circulating red
blood cell along
with its hemoglobin Enlarged
Spleen

Decrease in
hemoglobin

Decrease Decrease decreased


oxygen supply Pallor Decreased oxygenation and perfusion to
to the oxyen circulating blood any affected
integument supply to the that provides heat part causing
body delay in
Increased need biochemical
Swelling or for the heart to mediation
soreness of Fatigue Cold hands
pump more
the tongue and feet,
blood to meet
and cracks brittle nails
oxygen demand
Frequen
t
Infectio
Shortness of
breath,
tachypnea
PATHOPHYSIOLOGY: FURUNCLE (patient-centered)
Modifiable Factors
 Poor hygiene
 Insect bite
 Excessive perspiration
 Increased pressure
 Increased friction

Development
of wound

↑Biochemical
mediation through ↑
blood flow

Enlargement of wound,
turning red, firm and swollen

Development of a single,
small, firm, swollen,
red/pink, tender nodule
(furuncle) draining
purulent secretions

PATHOPHYSIOLOGY (patient-centered)
Non-modifiable Factors Modifiable Factors
- Age – 54 y/o - Excess dietary sodium
- Gender – male - Lack of exercise
- Race – brown race - Stress
- Family history of - Diabetes
hypertension

Cell membrane alteration Ineffective Renin- SNS over- Renal Na


utilization Angiotensi activity retention
of insulin n Excess

Venous ↑Fluid
Functional Constriction Constriction Volume

↑Peripheral Resistance
↑Contractility ↑Preload

↑BP: 170/100 mmHg: April 27, 2008;


150/90mmHg: April 28, 2008, 140/100
mmHg: April 29, 2008 ↑↑Cardiac Output

Modifiable Factors
↓Perfusion to the pancreas - Diabetes mellitus;
Non-modifiable Factors
- Age – 54 years old - active electrolyte loss from
vomiting; current low Na intake
Impairment in the
functioning of the pancreas
↓Renal perfusion/ ineffective blood supply to the
Impaired insulin secretion kidneys

Hyperglycemia
Non-modifiable Factors Modifiable Factors
- Age - Older than 40 - History of previous impaired Renal
years fasting glucose tissue
- Family history of DM - Hypertension (>140/90 mm Hg); hypoxia
dyslipidemia (HDL level <40
mg/dl)
- Stress: hormones at times of

Impairment BUN: 93
in mg/dl –
↑Blood Blood Sugar Level Glucose uptake ↓Energy renal April
Osmolarity exceeds renal by the cells Level functioning 29,
threshold : 137 2008
mg/dl: April 27,
2008, 117.5mg/dl:
Fluid shifting April 28, 2008 Cellular Body malaise,
from starvation Fatigue: April 27-30,
intracellular to 2008
extracellular
Excretion of excess Hunger due to the ↓ tubular
glucose in the urine stimulation of Satiety reabsorption
Center of Hypothalamus
Intracellular
dehydration /
Excretion of
volume
albumin
depletion Glucose attracts water Polyphagia

↑ Sodium Albuminuria
↑Urine Output: excretion : +3 : U/A-
polyuria April
Thirst Sluggish blood Anorexia: ↓ serum Na
sensation April 23-30, levels: 113.4 27, 2008
due to the Modifiable Factor: 2008 mEq/l: April
stimulatio ↓ Iron intake & low 27, 2008
n of Thirst Depletion of iron stores
socio-economic status
Center of at the bone marrow to
↓ Iron available to
hypotha- compensate
↓ Iron for
absorption
the tissues (red
lamus decreased
atblood availability
the intestines
cells)
↓organ Delayed
perfusio biochemical ↓ sodium
n mediation intake

Greater proportion of
Dry ↓ Iron absorption water in the blood
skin: Modifiable at the intestines compared to sodium:
April Factor:
Hemodilution: Hct –
Polydipsi 28- -Insect bite
0.29: April 27, 2008
a 30,
200
↓ Iron available to
8
the tissues (red
Development
blood cells) Fluid shifting from ↓cerebral
of wound
Intravascular to perfusion/

↓ interstitial intracellular esp. in ineffective
interstitial the brain which is blood supply
Depletion of iron stores fluid
fluid sensitive to serum to the brain
↑Biochemic at the bone marrow to volume Na changes
al mediation volume
compensate for
through ↑ decreased availability
blood flow
Dry skin:
April 28-30,
Alteration in brain
2008
functioning
Enlargement of wound, Impaired
turning red, firm and swollen hemoglobin and red
blood cell synthesis

↓impulse Lethargy:
transmission to April 29,
Development of a single,
Decrease the muscles 2008
red, swollen firm furuncle
(approx. 3cm diameter, circulating red
located at the left upper blood cell along
arm) draining purulent with its hemoglobin
secretions: Weakness: April
April 27-30, 2008 27-30, 2008
Decrease in
hemoglobin: 95
Increased need
g/l: April 27, 2008
for the heart to
Decreased pump more of
Shortness
Pallor: Fatigue -
oxyen blood
breath,to meet
April 28- April 27-30,
supply to the oxygen
tachypneademand
b. Synthesis of the Disease

b.1 Hypertension
b.1.1 Definition

Hypertension is defined as systolic pressure greater than 140 mmHg


and a diastolic pressure greater thank 90 mmHg based on the average of two
or more accurate blood pressure measurements taken during two or more
contacts with a health care provider. Blood pressure of less than 120/80
mmHg diastolic as normal, 120 to 129/80 to 89 mmHg as pre-hypertension,
and 140/90 mmHg or higher as hypertension. (Bare, B. et. al. , 2008)

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. An elevation of the
systolic and/or diastolic blood pressure increases the risk of developing heart
(cardiac) disease, kidney (renal) disease, hardening of the arteries
(atherosclerosis or arteriosclerosis), eye damage, and stroke (brain damage).
These complications of hypertension are often referred to as end–organ
damage because damage to these organs is the end result of chronic (long
duration) high blood pressure. For that reason, the diagnosis of high blood
pressure is important so efforts can be made to normalize blood pressure and
prevent complications.

b.1.2 Non-modifiable and Modifiable Risk Factors


***factors specific to the patient are highlighted
Non-modifiable Risk Factors:
 Age – 35 years and older
 Gender – men and post-menopausal women
 Race – black and brown race
 Family history of hypertension

Modifiable Risk Factors:


 Alcohol use  History of high blood pressure
 Excess dietary sodium during pregnancy

 Lack of exercise  Toxemia of pregnancy

 Stress  Oral Contraceptives (Birth Control

 Obesity Pills)
 Steroids
 Diabetes
 Nonsteroidal anti-inflammatory
 Kidney disease
drugs
 Hormonal disorders
 Decongestants
 Porphyria
 Diet pills
 Antidepressants

b.1.3 Signs and Symptoms, Complications with Rationale


***factors specific to the patient are highlighted

 high blood pressure – due to vasoconstriction and increase in circulating


fluid (↑BP: 170/100 mmHg: April 27, 2008; 150/90mmHg: April 28, 2008,
140/100 mmHg: April 29, 2008)
 retinal changes and papilledemea (swelling of the optic disk) –due to
increased pressure exerted by the walls of the vessels supplying the eye
and increased intraocular pressure related to cranial nerve II affectation
 increased blood urea nitrogen (93mg/dl: April 29, 2008) and serum
creatinine levels – due to poor oragn (kidney) perfusion which alters renal
processes and causes destruction and release of substances (i.e.
creatinine)
 left ventricular hypertrophy – may occur in response to increased
workload placed on the ventricle as it tries to contract against higher
systemic pressure
 cerebrovascular involvement which may be manifested by dizziness,
headache and impaired level of consciousness – related to ineffective
blood supply to the brain which causes impairment in the functioning of
brain structures
 impairment in organ function – occurs to the organs being supplied by the
narrowed vessels; takes place due to decreased perfusion brought about
by narrowed arteries

b.2 Diabetes Mellitus


b.2.1 Definition

Diabetes mellitus type 2 (diabetes mellitus type II, non insulin-


dependent diabetes (NIDDM), obesity related diabetes, or adult-onset
diabetes) is a metabolic disorder that is primarily characterized by insulin
resistance, relative insulin deficiency, and hyperglycemia. It is often managed
by engaging in exercise and modifying one's diet. It is rapidly increasing in
the developed world, and there is some evidence that this pattern will be
followed in much of the rest of the world in coming years. It is a non-ketosis
prone hyperglycemia and glucose intolerance due to defects in insulin
secretion and peripheral insulin action. DM type 2 comprises 80% of diabetic
cases.

Type 2 diabetes often goes undetected for long periods of time, since
symptoms are usually not pronounced. Insulin is produced, but it is not
enough, or it does not work properly to transport glucose through the
receptor cells. Type 2 diabetics can often be controlled with a carefully
planned diet, an exercise program, oral medication, or insulin, used as
necessary.Uncontrolled Type 2 diabetes results in hyperglycemia. Since
symptoms have an insidious onset, the patient may not recognize that there
is any difficulty. Left uncontrolled for a long period of time, Type 2 diabetics
develop more serious symptoms such as severe hyperglycemia, dehydration,
confusion, and shock. This is called “hyperglycemic hyperosmolar non-ketotic
coma.” These symptoms are most common in the elderly population and
people suffering from illness or infection.

The following are the criteria for the diagnosis of DM Type 2:


o Symptoms of diabetes (polyuria, polydipsia, weight loss) plus casual
(random) plasma glucose ≥ 200 mg/dL (11.1 mmol/L)
o Fasting plasma glucose ≥ 126 mg/dL (7.0 mmol/L) on 2 occasions
o 2 hour plasma glucose ≥ 200 mg/dL (11.1 mmol/L) during OGTT with
75 g glucose load
o LFTs, amylase, lipase - abd pain

b.2.2 Non-modifiable and Modifiable Risk Factors


***factors specific to the patient are highlighted

Non-modifiable Factors:
 Age - Older than 40 years
 Family history of type 2 diabetes
 Hispanic, Native American, African American, Asian American, or Pacific
Islander descent, Asian

Modifiable Factors:
 History of previous impaired glucose tolerance (IGT) or impaired fasting
glucose (IFG) – FBS:137 mg/dl: April 27, 2008; 117.5mg/dl: April 28, 2008
 Obesity - Weight >20% of desirable body weight (true for approximately
90% of patients with type 2 diabetes)
 Hypertension (>140/90 mm Hg)(↑BP: 170/100 mmHg: April 27, 2008;
150/90mmHg: April 28, 2008, 140/100 mmHg: April 29, 2008), 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)
 Viruses: certain viruses may destroy beta cells
 Faulty Immune System: multiple factors may cause the immune system to
destroy beta cells, such as infection
 Physical Trauma: injury or trauma may destroy the ability of the pancreas
to produce insulin
 Drugs: drugs used for other conditions could cause the development of
diabetes
 Stress: hormones at times of stress may block the effectiveness of insulin
 Pregnancy: hormones produced during pregnancy can block the
effectiveness of insulin

b.2.3 Signs and Symptoms, Complications with Rationale

 Polyuria – due to excretion of excess glucose that causes more water


attraction in the urine
 Polydipsia – due to the stimulation of the thirst center of the
hypothalamus brought about by intracellular dehydration
 Polyphagia – due to the stimulation of the satiety center of the
hypothalamus which brought about by cellular starvation from inadequate
glucose uptake
 Weight loss – due to cellular starvation from inadequate glucose uptake
 Weakness – due to cellular starvation which causes decreased energy
levels (April 27-30, 2008)
 Fatigue – due to cellular starvation which causes decreased energy levels
(April 27-30,2008)
 Blurred vision, retinopathy – related to poor organ perfusion brough about
by sluggish blood flow
 Slow-healing cuts or sores – related to poor peripheral perfusion due to
sluggish blood flow
 Dry, itchy skin – related to poor organ perfusion due to sluggish blood
flow(April 28-30, 2008-manifested by dry skin)
 Frequent infections – related to poor perfusion due to sluggish blood flow
thereby decreasing number and speed of readily available WBC; delay in
biochemical mediation
 Hyperglycemia – related to inadequate insulin production FBS:137 mg/dl:
April 27, 2008; 117.5mg/dl: April 28, 2008
 Dehydration – due to increased blood osmolarity leading to fluid shifting
from intracellular to extracellular compartment(April 28-30, 2008-
manifested by dry skin)
 Confusion – related to inadequate cerebral perfusion due to sluggish blood
flow
 Numbness and tingling sensation – related to poor peripheral perfusion
due to sluggish blood flow
 Nephropathy, neuropathy – common to older patients – related to poor
organ perfusion due to sluggish blood flow, causing impairment in organ
function

b.3 Electrolyte Imbalance: Hyponatremia


b.3.1 Definition

Hyponatremia refers to a serum level that is below normal (<135


mEq/l). (Bare, B. et. al. , 2008) When the blood sodium is too low, the cells
malfunction — causing swelling. In chronic hyponatremia, sodium levels drop
gradually over several days or weeks — and symptoms are typically
moderate. In acute hyponatremia, sodium levels drop rapidly — resulting in
potentially dangerous effects, such as rapid brain swelling, which can result in
coma and death.

Hyponatremia (hypervolemic) occurs when the sodium in the blood is


diluted by excess water. Hyponatremia (euvolemic, hypervolemic) may result
from medical conditions that impair excretion of water from your body, or by
a significant increase in water consumption(hypovolemic), such as by
athletes competing in marathons and other high-endurance events.
b.3.2 Non-modifiable and Modifiable Risk Factors
***factors specific to the patient are highlighted

Non-modifiable Factors:

 Age. Low blood sodium is more common in older adults. This is due to
age-related changes and increased prevalence of chronic disease that
may impair the body's normal sodium balance.
 Sex. Hyponatremia is more common in women than in men.

Non-modifiable Factors:

 Diet. Patient may be at an increased risk of hyponatremia if following a


low-sodium diet, especially if combined with diuretic intake.
 Intensive physical activities. People who take part in marathons,
ultramarathons, triathlons and other long-distance, high-intensity
activities are at an increased risk of hyponatremia.
 Climate. Not being acclimated to hot weather can increase the amount of
sodium you lose through sweating during exercise.
 Conditions that impair the body's water excretion. Medical conditions that
may increase your risk of hyponatremia include kidney disease, syndrome
of inappropriate anti-diuretic hormone (SIADH) and heart failure, and other
chronic diseases that cause organ failure.

b.3.3 Signs and Symptoms, Complications with Rationale

 Serum sodium level that is below normal (<135 mEq/l): 113.4 meQ/l:April
27
 Neurologic manifestations such as headache, lethargy (April 29, 2008),
confusion, apprehension – due to fluid shifting from intravascular to
intracellular space in an attempt to raise the proportion of Na with water
 Decreased BP, orthostatic hypotension – due to decreased vascular
volume secondary to water and sodium loss
 Tachycardia – compensatory response which is a direct result of triggering
sympathetic catecholamine
 Sympathetic responses of the heart – due to stimulation of
chemoreceptors on the aortic and carotid bodies
 Crackles in the lungs – due to fluid shifting to the pulmonary alveoli
secondary to increased pressure of circulating fluids in the pulmonary
capillaries
 Greater blood volume (water component>serum Na) – Hct of 0.29: April
27
 Tachypnea (April 27, 2008), dyspnea, othopnea, shortness of breath – fluid
accumulation in the alveoli alters oxygen-carbon dioxide exchange
transport
 Nausea, vomiting, abdominal cramping, hyperactive bowel sounds – due
to fluid shifting from intravascular to intracellular space causing an urge to
expel excess water
 Dry skin (April 28-30, 2008), tongue and mucous membranes – due to
decrease in interstitial fluid caused by sodium deficit in the blood

b.4 Anemia (Iron Deficiency)


b.4.1 Definition

Iron-deficiency anemia typically results when the intake of dietary iron


is inadequate for hemoglobin synthesis. (Bare, B. et. al. , 2008) It is the most
common type of anemia. A lack of iron in the body can come from bleeding,
not eating enough foods that contain iron, or not absorbing enough iron from
food that is eaten. (Retieved at
http://www.nhlbi.nih.gov/health/dci/Diseases/anemia/anemia_whatis.html
accessed on May 1, 2008, 8:22 pm)

The term anemiais used for a group of conditions in which the number
of red blood cells in the blood is lower than normal, or the red blood cells do
not have enough hemoglobin. Hemoglobin—an iron-rich protein that gives the
red color to blood—carries the oxygen from the lungs to the rest of the body.
In people with anemia, the blood does not carry enough oxygen to the rest of
the body. Red blood cells also remove carbon dioxide, a waste product, from
cells and carry it to the lungs to be exhaled.

There are many types of anemia. The three major causes of anemia
are blood loss, decreased production of red blood cells, or increased
destruction of red blood cells. White blood cells and platelets are the two
other kinds of blood cells. White blood cells help fight infection. Platelets help
blood to clot. In some kinds of anemia, there are low amounts of all three
types of blood cells. The most common symptom of all types of anemia is
feeling tired because the body is not receiving enough oxygen.

In iron-deficiency anemia, the body does not have enough iron to form
hemoglobin, which means there is not enough hemoglobin to carry oxygen to
the whole body. The body gets its iron from food. The main foods that contain
iron are meat and shellfish as well as iron-fortified foods. A steady supply of
iron is needed to form hemoglobin and healthy red blood cells.
The four main causes of IDA include: Blood loss, either from disease or
injury, Not getting enough iron in the diet, Not being able to absorb the iron
in the diet. Iron-deficiency anemia also can develop when the body needs
higher levels of iron, such as during pregnancy

b.4.2 Non-modifiable and Modifiable Risk Factors


***factors specific to the patient are highlighted

Non-modifiable Factors:

 Sex - Women - Women who lose a lot of blood during their monthly
periods are at higher risk of developing iron-deficiency anemia. About 1 in
5 women of childbearing age has iron-deficiency anemia. - Pregnant
women need twice as much iron in their diet than women who are not
pregnant. If a pregnant woman doesn't get enough iron for herself and the
growing baby, she can develop iron-deficiency anemia. About half of all
pregnant women have this type of anemia.
 Age - Young Children - Infants and toddlers 6-24 months of age need a lot
of iron to grow and develop. Premature and low-birth-weight babies are at
even greater risk for iron-deficiency anemia because they don't have as
much iron stored in their bodies.

Modifiable Factors:

 Diet low in iron – decreased intake of Iron-rich foods


 Blood loss – causes decrease in blood volume
 Other children at risk for anemia are: Children with poor nutrition,
including low-income children, Children with lead in their blood, Infants fed
cow's milk before 1 year of age, Breastfed infants older than 4 months
who are not receiving iron-rich solid foods or iron supplements
 Adults With Intestinal Bleeding - Adults who bleed in their intestinal tract
are at risk for iron-deficiency anemia. This includes people who have
bleeding ulcers or colon cancer. It also includes people who use medicines
that can cause intestinal bleeding (for example, aspirin).
 Other Adults - Other adults who are at risk for iron-deficiency anemia
include those who are on kidney dialysis, vegetarians, with low
socioeconomic status and older adults who have poor diets.

b.4.3 Signs and Symptoms, Complications with Rationale

 Fatigue (April 27-30, 2008) is caused by having too few red blood cells to
carry oxygen to the body. This lack of oxygen in the body can cause
people to feel weak or dizzy, have a headache, or even pass out when
changing position (for example, standing up).
 Shortness of breath, tachypnea (April 27, 2008) and chest pain - Since the
heart must work harder to move the reduced amount of oxygen, signs and
symptoms may include shortness of breath and chest pain. This can lead
to a fast or irregular heartbeat or a heart murmur.
 Pallor (April 28-30, 2008) - In anemia, the red blood cells don't have
enough hemoglobin. Common signs of lack of hemoglobin include pale
skin, tongue, gums, and nail beds.
 Cold hands and feet as well as brittle nails – due to decrease oxygenation
and circulating blood that provides heat to the body
 Swelling or soreness of the tongue and cracks in the sides of the mouth –
due to decrease oxygen supply to the integument causing easy bruising
 An enlarged spleen – due to increased number of dead RBC
 Frequent infections – due to compromised immune system and decreased
perfusion to any affected part causing delay in biochemical mediation
 Some of the signs and symptoms of iron-deficiency anemia are related to
its causes, such as blood loss. Blood loss is most often seen with very
heavy or long lasting menstrual bleeding or vaginal bleeding in women
after menopause. Other signs of internal bleeding are bright red blood in
the stool or black, tarry-looking stools.
 Decreased hemoglobin on lab exams – 95g/l: April 27, 2008

b.5 Furuncle
b.5.1 Definition

A furuncle or boil is an acute inflammation arising deep in one or more


hair follicles and spreading in the surrounding dermis. It is a deep form of
follliculitis. Furunculosis refers to multiple or recurrent lesions. Furuncles may
occur anywhere in the body but are more prevalent in areas subjected to
irritation, pressure, friction and excessive perspiration, such as the buttocks,
back of the neck and the axilla. (Bare, B. et. al., 2008)

A furuncle may start as a small, red, raised, painful pimple. Frequently


the infection progresses and involves the skin and subcutaneous fatty tissue,
causing tenderness, pain and surrounding cellulites. The area of redness and
induration represents and effort of the body to keep the infection localized.
The bacteria, usually staphylococci, produce necrosis of invaded tissue. The
characteristic pointing of a boil follows in a few days. When this occurs, the
character becomes yellow or black, and the boil is said to have “come to a
head.”

b.5.2 Non-modifiable and Modifiable Risk Factors


***factors specific to the patient are highlighted

Non-modifiable Factors – no particular non-modifiable factors


Modifiable Factors
 Poor hygiene
 Insect bite
 Excessive perspiration
 Increased pressure
 Increased friction

b.4.3 Signs and Symptoms, Complications with Rationale

 The lesions themselves are the primary symptoms:


- Small firm tender red nodule in skin (early)
- Fluctuant nodule (later)
- Located with hair follicles
- Tender, mildly to moderately painful
- May be single or multiple
- Usually pea-sized, but may be as large as a golf ball
- Swollen
- Pink or red
- May grow rapidly
- May develop white or yellow centers (pustules)
- May weep, ooze, crust
- May join together or spread to other skin areas and progress into a
carbuncle
- Decreasing pain as the area drains
The above-mentioned are characteristics of a furuncle. The furuncle is the
symptom itself. Its characteristics are changes in the site of indurations due
to biochemical mediation. Whenever there is an injury or any break in the
skin integrity, the body attempts to localize the infection by increasing blood
flow to the affected part in order to supply necessary chemicals that will aid
in controlling infection. Localized infection is generally characterized by the
following:
- Increasing pain as pus and dead tissue fills the area – due to release of
prostaglandins
- Skin redness or inflammation around the lesion
- Swollen, tender – due to increased blood flow and accumulation of
dead bacteria and WBC that engulf them
- Pink or red – due to increased blood flow
V. The Patient and His Care
A. Medical Management
a. IVFs, NGT feeding, BT, Nebulization, TPN, Oxygen therapy, etc...
Medical Date General Description Indication(s) or purposes Client’s
management ordered Reponse to the
or / Date treatment
treatment performed:
D5LRS D.O.: Lactated Ringer’s Injection, USP is This medication is an The patient was
04-27-08 a sterile, nonpyrogenic solution intravenous (IV) solution used to supplied with
04-28-08 containing isotonic concentrations supply water and electrolytes adequate fluid.
04-29-08 of electrolytes in water for (e.g., calcium, potassium, No adverse
injection. It is administered by sodium, chloride), either with or responses were
D.P.: intravenous infusion for without calories (dextrose), to noted.
04-27-08 parenteral replacement of the body. It is also used as a
04-28-08 extracellular losses of fluid and mixing solution (diluent) for
04-29-08 electrolytes other IV medications.
D5NM D.O. Hypertonic solutions draw fluid It is a sterile, nonpyrogenic The patient was
04-30-08 solution for fluid and electrolyte supplied with
out of the intracellular and
replenishment and caloric adequate fluid.
D.P. interstitial compartments into the supply. No adverse
04-30-08 responses were
vascular compartment, expanding
noted.
vascular volume.

Nursing Responsibilities:
Prior to:
1. Prepare the equipment
2. Verify doctor’s order
3. Use strict aseptic technique
4. Explain the procedure to the S0 and give formation about the purpose of IVF to be inserted
5. Identify the client
6. Assess vital signs for baseline data
7. Assess skin turgor, allergy to tape
8. Check the status or veins to determine appropriate venipuncture site
During:
9. Use the smallest gauge needle possible.
10.Check for patency of the tubing
11.Spike the solution container
12.Cleanse the fluid to be given, make sure it is the same with the prescribed fluid.
13.Partially fill the drip chamber gently with solution.
14.Select a suitable vein for venipuncture
15.Dilate the vein
16.Put on clean gloves and clean the venipuncture site.
After:
17.Label the IVF (name, date started, number)
18.Ensure appropriate infusion flow.
19.Adjust the rate of fluids appropriate to the needs f the patient as ordered. If there is any question with the flow
rate ordered, check with the physician who gave the order.
20.Monitor IV flow and patient’s response
21.Monitor patient for evidence of IV infiltrations
22.Check for presence of air in the tubing, if air is present, remove immediately
23.Check for the patency of the line always.
24.Regulate and monitor the IV rate of fluid.
25.Document relevant data.

b. Drugs
Name of Drugs: Date Route Indication(s) or Client’s Nursing Responsibilities
ordered, Dosage Purpose(s) Response
performed and to the
, Frequency Treatment
Generic Name: D.O. 1g/IV q 12 Treatment of: No adverse 1.Assess for infection (vital signs;
ceftriaxone 04-27-08 Skin and skin reaction appearance of wound, sputum,
structure with urine, and stool; WBC) at
Brand Name: D.P. infections, bone Ceftriaxone beginning of and throughout
Rocephin 04-27-08 and joint was noted. therapy.
04-28-08 infections,
04-29-08 urinary and 2.IV: Monitor injection site
04-30-08 gynecologic frequently for phlebitis (pain,
infections redness, swelling)
including
gonorrhea, resp. 3.Advise patient to report signs of
tract infections, superinfection (furry overgrowth
intra-abdominal on the tongue, loose or foul
inmfections, smelling stools) and allergy.
septicemia,
meningitis.
Generic Name: D.O. 500mg 1 Management of The 1. Observe for signs and
Metformin 04-27-08 tab BID type 2 diabetes patient’s symptoms of hypoglycemic
mellitus; may be blood reactions (abdominal pain,
Brand Name: D.P. used with diet, glucose sweating, hunger,
Fortamet 04-28-08 insulin, or decreased weakness,dizziness,
04-29-08 sulfonylurea oral from 137 to h/a,tremor,tachycardia,anxi
04-30-08 hypoglycemics. 88 on April ety) when combined with
28, 2008 oral sulfonylureas.
AEB lab 2. PO: Administer metformin
results with meals to minimize GI
(FBS/RBS). effects.
3. Explain to explain that
metformin helps control
hyperglycemia but does
not cure diabetes.
Treatment is usually long
term.

Generic Name: D.O. 1 tab TID Disturbances of No adverse 1. Assess pt. for nausea,
Metoclopramide 04-27-08 for GI motility. reaction vomiting, abdominal
Vomiting Nausea & with Plasil distention, and bowel
Brand Name: D.P. vomiting of was noted. sounds before and after
Plasil 04-28-08 central & administration.
04-29-08 peripheral origin 2. PO: Administer doses
04-30-08 associated w/ 30min. before meals and at
surgery, bedtime.
metabolic 3. Advise pt. to avoid
diseases, concurrent use of alcohol
infectious & and other CNS depressants
drug-induced while taking this
diseases. medication.
Facilitate small
bowel intubation
& radiological
procedures of
GIT
Generic Name: D.O. 1 tab BID Simple Fe The patient 1. Assess nutritional status
FeSO4 04-27-08 deficiency & Fe- responded and dietary history to
deficiency well with determine possible cause
Brand Name: D.P. anemia. Patient the of anemia and need for
Feosol 04-28-08 intolerant to medication patient teaching.
04-29-08 conventional Fe and no 2. Discontinue oral iron
04-30-08 & those prone to adverse preparations prior to
GI upsets reaction parenteral administration.
was noted. 3. Advise patient that stools
may become dark green or
black and that this change
is harmless.
Generic Name: D.O. 5g 1 tab Hypertension, The 1. Monitor BP and pulse
Amlodipine 04-27-08 OD angina, patient’s before therapy, during dose
myocardial blood titration, and periodically
Brand Name: D.P. ischemia. pressure during therapy.
Norvasc 04-28-08 Reduce the risk decreased 2. PO: May be administered
04-29-08 of coronary from without regard to meals.
04-30-08 revascularizatio 170/100 to 3. Advise pt. to take
n. 150/100 on medication as directed,
April 28, even if feeling well.
2008.
Generic Name: D.O. 300 Treatment of No adverse 1. Assess for infection (vital
Clindamycin 04-28-08 mg/tab q serious reaction signs; appearance of
12 anaerobic with wound, sputum, urine, and
Brand Name: D.P. infections esp Clindamyci stool; WBC) at beginning of
Clindal 04-28-08 those caused by n was and during therapy.
04-29-08 Bacteroides noted. 2. PO: administer with a full
04-30-08 fragilis. glass of water. May be
Alternative to given with meals. Do not
penicillin in refrigerate.
some severe 3. Instruct pt. to notify HCP
Staph & Strep immediately if diarrhea,
infections, abdominal cramping, fever,
including Staph or bloody stools occur and
osteomyelitis. not to treat with
antidiarrheals without
consulting HCP.
Generic Name: D.O. 1 cap OD Underwt due to The 1. May be taken with or
Pizotifen 04-29-08 lack of appetite patient’s without food (May be taken
associated w/ appetite w/ meals to reduce GI
Brand Name: D.P. vit B deficiency was discomfort.).
Mosegor Vita 04-30-08 secondary to enhanced 2. Timed-release tablets and
cap impaired dietary as capsules should be
intake or verbalized swallowed whole, without
absorption; by himself. crushing, breaking or
nervous chewing.
disorders in 3. Emphasize the importance
puberty of follow-up examinations
(anorexia to evaluate progress.
nervosa) old
age when
prevention of
deficiency of B-
group vit is
indicated.
Nursing Responsibilities:
Prior:
1. Check the written medication order for completeness. It should include the drug name, dosage, frequency,
and duration of the therapy.
2. Check if IV in.
3. Check to see if there are any special circumstances surrounding administration of the dose to the patient.
4. Be certain that you know the expected action, safe dosage range, special instructions for administration and
adverse effects associated with drug orders.
5. Prepare the necessary equipment.
6. Wash your hands.
7. Check the label on the medications three times before administering any drug.
8. Prepare the dosage as ordered.
9. Explain the procedure to the patient. The action of the drug and its side effects.
During:
10.Identify the patient.
11.Identify if the patient expresses any doubt about the medication; always recheck the order, drug label and
dosage on the medication card.
12.For oral meds do special regulation and precaution to avoid or prevent aspiration.
After:
13.Following administration, be certain that the patient is comfortable, then immediately record the procedure.
14.Maintain patient’s safety
15.Monitor patient for side effects
16.Instruct the patient to report signs of superinfection and allergy.
17.Inspect IV insertion sites for sign of phlebitis.
18. Document and assess the patient's reaction to the given drug
c. Diet
Date General Indications Specific Client’s
Type of Diet ordered, Description or Purposes foods taken response
date and
performed reaction to
the diet

D.O. The low fat Indicated for Low salt and The client
complied
04-27-08 and salt diet bed patients low fat
with the
is designed whose foods. prescribed
diet.
D.P. to limit the condition
Low Fat, Low 04-27-08 total requires
Salt Diet 04-28-08 amount of modified
04-29-08 fat, salt and diet in order
04-30-08 cholesterol to prevent
in the diet further
to reduce aggravation
serum lipid of condition.
levels and
avoid
excessive
sodium
retention

Nursing Responsibilities:
Prior to:
1. Check the doctor’s order for the type of diet prescribed
2. Explain the importance of the diet given.
3. Explain the importance of compliance to the diet given.
4. Inform dietary department on the patient’s diet
During:
5. Give appropriate foods to the patient.
6. Enumerate the foods that the patient may or may not take.
7. Emphasize strict compliance to diet
8. Reiterate diet frequently
After:
9. Document the patient’s tolerance to the diet given.
April 28, 2008
7am – 7pm shift

S>Ø

O>received supine on bed; asleep; with an ongoing IVF #1 0.9 NaCl 1L @ 550
ml level, regulated @ 30gtts/min, infusing well on right hand; appears weak;
with 3cm-diameter open wound on left upper arm, with erythematous,
inflamed surroundings, draining purulent secretions; with dry, scaly skin on
left upper arm; with difficulty hearing; (+) pallor; with cold, clammy skin;
capillary refill in 3 seconds; with VS taken and recorded as follows: T=37°C,
PR=74bpm, RR=17cpm, BP=150/90mmHg.

A>Decreased cardiac output related to decreased afterload as evidenced by


blood pressure elevation, cold, clammy skin, prolonged capillary refill >2
seconds, and pallor.

P>After 4 hours of nursing interventions, patient will display hemodynamic


stability as evidenced by decrease in blood pressure from 150/90 to
130/80mmHg.

I>Established rapport
>Assessed patient’s condition
>VS taken and recorded
>Assessed character of wound and wound drainage
>Reviewed laboratory data for any deviations from the normal range
>Assessed for capillary refill through blanch test
>Assisted in position changes
>Maintained aseptic technique during wound care
>Advised to inform health care provider should vomiting occur
>Instructed to dangle feet first before standing and walking
>Emphasized the importance of hand washing technique before and after
would cleaning
>Instructed SO on the proper and aseptic method of doing wound cleaning
>Encouraged rest periods
>Encouraged to avoid sweet, fatty and salty foods
>Seen on rounds by Dr. Delmas @ 7am with orders made and carried out
- FBS, lipid profile SGPT, SGOT, BUN, Creatinine – requested
- daily wound cleaning – done
- IVF to FF D5LRS 1 liter x 30gtts
- start Clindamycin 300mg/tab q 12 hrs – prescribed
- refer
>Monitored and regulated IVF as ordered
>Due meds given as prescribed
>Needs attended
>Refer accordingly
>Endorsed

E>Goal met; patient will displayed hemodynamic stability as evidenced by


decrease in blood pressure from 150/90 to 130/80mmHg.

_______________________________________________Kathleen Kaye D. Tobias, AUF-


SN

April 29, 2008

S>Ø

O>received lying on bed; awake, unconscious and incoherent; with an


ongoing IVF #53 D5LRS 1L @ 350 ml level, regulated @ 30gtts/min, infusing
well on right hand; appears weak, pale and lethargic; with dry skin; inflamed
3-cm-diameter furuncle with purulent secretion @ left upper arm noted; with
pale conjunctiva; vomitus noted, thick in consistency, approximately 50 cc
within the shift; with VS taken and recorded as follows: T=37.1°C,
PR=80bpm, RR=19cpm, BP=140/100mmHg.

A> Impaired Skin Integrity related to presence of inflamed 3-cm-diameter


eruption (wound) on left upper arm.
P> After 4 hours of nursing interventions, the patient will understand and
cooperate to the health teachings and interventions given.

I> Established Rapport


> Assessed condition
> Monitored and Recorded Vital Signs
> Assessed presence of cyanosis
> Assessed Skin Turgor
> Instructed on proper and aseptic wound care
> Instructed to increase fluid intake
> Instructed to eat foods rich in protein and vitamin C once DAT
>Emphasized the importance of hand washing especially before and after
wound care
>Reinforced low salt, low fat diet
>Practiced aseptic technique in wound cleaning
>Due meds given
>Regulated IVF as ordered
>Needs attended
>Refer accordingly
>Endorsed

E> Goal met. Patient cooperated in nursing interventions given and


verbalized understanding of the health teachings.

___________________________________________Kathleen Kaye D. Tobias, AUF-SN

April 30, 2008


7am – 7pm shift

S>Ø
O>received sitting on bed; awake, conscious and coherent; with an ongoing
IVF #5 D5LRS 1L @ 900 ml level, regulated @ 30gtts/min, infusing well on
right hand; appears weak; (+) pallor; with purulent secretion draining from
inflamed 3-cm-diameter furuncle @ left upper arm; with dry, scaly skin; with
vomiting 2x, vomitus is thick in consistency, yellowish color, approximately
100cc within the shift; with difficulty hearing; with pale conjunctiva; capillary
refill within 2 seconds; with VS taken and recorded as follows: T=36.2°C,
PR=73bpm, RR=20cpm, BP=110/70mmHg.

A>Risk for deficient fluid volume related to loss of fluid through normal route
(vomiting).

P>After 4 hours of nursing interventions, patient will not manifest evidences


of fluid volume deficit such as poor skin turgor, dry mucous membranes,
increased PR and temperature, and decreased BP.

I>Established rapport
>Assessed patient’s condition
>Monitored and recorded vital signs
>Determined ability to chew, swallow, taste
>Assessed skin turgor and capillary refill
>assessed body built, activity, rest level
>Reviewed laboratory results
>Auscultated bowel sounds
>Practiced aseptic technique in wound cleaning
>Promoted relaxing environment to enhance intake
>Encouraged small frequent feedings
>Reinforced low salt, low fat diet
>Instructed SO on the proper way of doing wound care
>Emphasized the importance of hand washing before and after wound care
>Seen on rounds by Dr. Bondoc @ 9:00 am with orders made and carried out
- continue meds
- D5NM 1L x 8hrs
- change dressing OD – done
- refer
>Due meds given as prescribed
>Regulated IVF as ordered
>Needs attended
>Refer according ly
>Endorsed

E>Goal met; patient did not manifest evidences of fluid volume deficit such
as poor skin turgor, dry mucous membranes, increased PR and temperature,
and decreased BP.

_______________Charmaigne Hazelyn Cruz, AUF-SN/Kathleen Kaye Tobias, AUF-


SN

VI. CLIENT’S DAILY PROGRESS CHART


1. Client’s Daily Progress Chart
April 27
(Admission) April 28 April 29 April 30
Nursing Diagnosis

>
*
Decreased
cardiac output
related to
decreased
afterload as
evidenced by
blood pressure
elevation,
cold, clammy
skin,
prolonged
capillary refill
>2 seconds,
and pallor.
*

> Impaired
Skin Integrity.

*
> Risk for
deficient fluid
volume
related to loss
of fluid
through
normal route
(vomiting).

April 27 April 28 April 29


April 30
7am 7pm 7am 7pm 7am 7pm 7am 7pm
Vital Signs to to 7 to to 7 to to 7 to to 7
7pm am 7pm am 7pm am 7pm am
Temperature (degrees 36.6 37 36.6 37.1 37.2 36.2
Celsius)
Pulse Rate (beats per
84 74 82 80 78 73
minute)
Respiratory Rate (cycles
21 17 21 19 22 20
per minute)
170- 150- 140- 140- 110- 110-
Blood Pressure (mmHg) 100 90 90 100 60 70
Diagnostic/ Laboratory procedures

27 28 29
30
FBS/RBS
(70-100mg/dl) 137 88 117.5

Na
(135-150 mg/dl) 113.4

K
(3.5-5.2 mg/dl) 3.8

Urinalysis *

Hgb
(140-180 gm/L) 95

WBC
(5-10 x 10 ^9/L) 14.5

Hct.
(0.40-0.54 L/L) .29

Seg. 0.90 .90

Lymph.= 0.10
.10

BUN= 93
(7-18 mg/dl) 93

Cholesterol= 192.5
(150-250 mg/dl) 160.7 192.5

Creatinine= 18
(0.4-1.4) 18.0

HDL C=33.2
(30-75) 33.2

LDL C= 145.22
(66-178) 145.22

Triglycerides= 70.4 (36-


165) 70.4

SGPT/ALT= 17
(up to lu/ml) 17.0

SGOT/AST= 19.9
(up to 40 lu/ml) 19.9
Medical Management

IVF’S 27 28 29 30

D5LRS * * *

D5NM *

April 27 April 28 April 29 April 30


MEDICATIO 7am- 7pm- 7am- 7pm- 7am- 7pm- 7am- 7pm-
NS 7pm 7am 7pm 7am 7pm 7am 7pm 7am
Ceftriaxone
* * * * * *
1g/IV q 12
Metformin
500mg 1 tab * * * * *
BID
Plasil tab TID
* * * *
for Vomiting
FeSO4 tab
* * * * *
BID
Amlodipine
* * *
5g 1 tab OD
Clindamycin
300 mg/tab * * * * *
q 12
Mosegor Vita
*
cap

Diet am pm am pm am pm am pm

Low fat, low


* * * * * *
salt

Conclusion:

The Groups’ Goal in this study is to at least help the patient deal with
the situation in order to prevent further complications and gain cooperation
with the nurses and to somewhat help in stabilizing and improve the patient’s
health and well-being because the patient is still responsible in achieving his
health goal. Many Interventions were done according to the level of
knowledge and understanding of the student nurses about the diseases he is
afflicting right now in order to meet the said Goal. Through constant
monitoring of his Vital Signs, laboratory results and checking the patient’s
Daily Progress chart, the Group was able to identify if their Goals were
achieved. During the first day of handling the patient, his vital signs were
monitored and blood pressure appeared to be elevated and at the same time
he feels weak. Vital signs were normal during the second day except for the
blood pressure same with the third day. On the last day that the group
handled the patient, Vital Signs were normal and the patient was still
appeared weak, pale and lethargic. Medications were given on time at the
desired dose. Other records such as laboratory results show that there are
still complications particularly the Random Blood Sugar, however, some
laboratory findings show within normal range. The Goal was not totally met
because there are still abnormalities presented during the first until the last
day that the group handled him though he is cooperative when it comes to
medical regimen.

VIII. BIBLIOGRAPHY

Bare, B. et. al. (2008). Brunner and Suddarth’s Textbook of Medical-Surgical


Nursing. Philadelphia:Lippincott-Williams & Wilkins

Deglin, J. and Velerand, A. (2007). Davis’s Drug Guide for Nurses.


Pensylvania: E.A. Davis Company.

Doenges, Marilynn E. Nursing Care Plans: Guidelines for Planning Patient Care

Seely, R., Stephens, T., Tate, P. (2005). Essentials of Human Anatomy &
Physiology. New York: McGrw-Hill.

Wolff L: Fundamentals of Nursing, 7th edition, JB Lippincott Co.


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ANGELES UNIVERSITY FOUNDATION
Angeles City
College of Nursing

CASE STUDY:
HYPERTENSION II
DIABETES MELLITUS TYPE II
ELECTROLYTE IMBALANCE
(HYPONATREMIA)
IRON DEFICIENCY ANEMIA
FURUNCLE