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Thalassemia
Thalassemiaalso called Mediterranean anemiais an inherited blood disorder
characterized by less hemoglobin and fewer red blood cells in your body than normal.
Defects in the genes that make hemoglobin cause thalassemia. Hemoglobin is the
substance in red blood cells that allows the cells to carry oxygen from your lungs tothe other parts of your body. Because of low hemoglobin and a low amount of red
blood cells, thalassemia results in anemia.
If you have a mild form of thalassemia, you may not require any treatment. But, ifyou
have a more severe form, you may need blood transfusions on a regular basis.Although in some
cases severe thalassemia can be life-threatening, milder forms ofthalassemia usually can be
effectively treated.
Although thalassemia causes anemia, don't confuse thalassemia with iron deficiency
anemia. People with thalassemia often have more iron in their bodies than they need.For this reason, if you have thalassemia, don't take iron supplements unless your
doctor recommends it.
Symptoms
Signs and symptoms of thalassemia include:
Fatigue
Weakness
Shortness of breath
Yellow discoloration of the skin (jaundice)
Bone deformities in the face
Slow growth
Protruding abdomen
The signs and symptoms you experience depend on your type and severity of
thalassemia. Some babies show signs and symptoms of thalassemia at birth, whileothers may not develop signs or symptoms until they're about 6 to 12 months old.
Some people who have only one hemoglobin gene affected don't experience any
thalassemia symptoms.
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Causes;
Blood consists of liquid, called plasma, and three types of cells that float within the
plasma:
White blood cells. These blood cells fight infection.
Platelets. These blood cells help your blood clot after a cut.
Red blood cells (erythrocytes). These blood cells carry oxygen from your
lungs, through you
r bloodstream, to your brain and your body's other organs
and tissues. Your body needs a supply of oxygenated blood to function.
Oxygenated blood helps give your body its energy and your skin a healthy
glow.
Red blood cells contain hemoglobina red, iron-rich protein that gives blood its red
color. Hemoglobin enables red blood cells to carry oxygen from your lungs to allparts of your body and to carry carbon dioxide from other parts of your body to your
lungs so that it can be exhaled. Most blood cells, including red blood cells, are
produced regularly in your bone marrowa red, spongy material found within the
cavities of many of your large bones.
Thalassemia disrupts the normal production of hemoglobin and leads to a low level of
hemoglobin and a high rate of red blood cell destruction, causing anemia. When
you're anemic, your blood doesn't have enough red blood cells to carry oxygen to your
tissuesleaving you fatigued.
Thalassemia is caused by defects in the genes that make hemoglobin. The only way to
get thalassemia is to inherit one or more defective hemoglobin genes from your
parents.
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There are two types of thalassemia: alpha and beta, named for the two protein chains
that make up normal hemoglobin. The type of thalassemia you have depends on the
type of defective gene you inherit.
Alpha-thalassemia
Four genes are involved in making the alpha hemoglobin chain. You get two from
each of your parents. If one or more of the alpha hemoglobin genes are defective, you
develop alpha-thalassemia.
The more defective genes you have, the more severe your alpha-thalassemia:
One gene. If only one of your alpha hemoglobin genes is defective, you'll
have no signs or symptoms of thalassemia. But, you're a carrier of the disease
and can pass it on to your children.
Two genes. If you have two defective alpha hemoglobin genes, thalassemia
signs and symptoms are mild. This condition is called alpha-thalassemia
minor.
Three genes. If three of your alpha hemoglobin genes are defective, your
signs and symptoms will be moderate to severe. This condition is also called
hemoglobin H disease.
Four genes. When all four alpha hemoglobin genes are defective, the
condition is called alpha-thalassemia major or hydrops fetalis. It usually
causes a fetus to die before delivery or shortly after birth.
Beta-thalassemia
Two genes are involved in making the beta hemoglobin chain. You get one from each
of your parents. If one or both of the beta hemoglobin genes are defective, you
develop beta-thalassemia.
One gene. If one of your beta hemoglobin genes is defective, you have mild
signs and symptoms. This condition is called beta-thalassemia minor.
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Two genes. If both of your beta hemoglobin genes are defective, your signs
and symptoms will be moderate to severe. This condition is called beta-
thalassemia major or Cooley's anemia. Babies born with two defective beta
hemoglobin genes usually are healthy at birth, but develop signs and
symptoms within the first year of life.
Risk factors
Factors that increase your risk of thalassemia include:
Family history. Thalassemia is an inherited disorder, passed from parents to
children through defective hemoglobin genes.
Ancestry. Thalassemia occurs most often in people of Italian, Greek, Middle
Eastern, southern Asian and African ancestry. Alpha-thalassemia affects
mainly people of Southeast Asian, Chinese and Filipino descent.
When to seek medical advice
Make an appointment with your child's health care provider for an evaluation if he or
she has any of the following signs or symptoms of thalassemia:
Fatigue
Weakness
Shortness of breath
Yellow discoloration of the skin (jaundice)
Bone deformities in the face
Slow growth
Protruding abdomen
Dark urine
Tests and diagnosis
Most children who have moderate to severe cases of thalassemia show signs and
symptoms within their first two years of life. If your doctor suspects your child has
thalassemia, he or she may confirm a diagnosis using blood tests. If your child has
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thalassemia, blood tests may reveal a low level of red blood cells. The red blood cells
may be smaller than normal, pale (a sign of low hemoglobin), varied in size and
shape, and have uneven hemoglobin distributiongiving the cells a bull's-eye
appearance under the microscope.
Blood tests may also be used to measure the amount of iron in your child's blood andto evaluatehis or her hemoglobin. In some cases, a blood test may be used for DNAanalysis to diagnose
thalassemia or to determine if a person is carrying defective
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Dengue hemorrhagic fever
Dengue, the most common arboviral illness transmitted worldwide, is caused by infection
with 1 of the 4 serotypes of dengue virus, family Flaviviridae, genus Flavivirus (single-stranded
no segmented RNA viruses). Dengue is transmitted by mosquitoes of the genusAedes, which are
widely distributed in subtropical and tropical areas of the world, and is classified as a major
global health threat by the World Health Organization (WHO)
Dengue is a mosquito-borne infection that in recent decades
has become a major international public health concern. Dengue is found in tropical and sub-
tropical regions around the world, predominantly in urban and semi-urban areas. Dengue
hemorrhagic fever (DHF), a potentially lethal complication, was first recognized in the 1950s
during dengue epidemics in the Philippines and Thailand. Today DHF affects most Asian
countries and has become a leading cause of hospitalization and death among children in the
region. There are four distinct, but closely related, viruses that cause dengue. Recovery from
infection by one provides lifelong immunity against that virus but confers only partial and
transient protection against subsequent infection by the other three viruses. There is good
evidence that sequential infection increases the risk of developing DHF.
Global burden of dengue
The incidence of dengue has grown dramatically around the world in recent decades.
Some 2.5 billion peopletwo fifths of the world's populationare now at risk from dengue.
WHO currently estimates there may be 50 million dengue infections worldwide every year. In2007 alone, there were more than 890 000 reported cases of dengue in the Americas, of which 26
000 cases were DHF. The disease is now endemic in more than 100 countries in Africa, the
Americas, the Eastern Mediterranean, South-east Asia and the Western Pacific. South-east Asia
and the. Western Pacific is the most seriously affected. Before 1970 only nine countries had
experienced DHF epidemics, a number that had increased more than four-fold by 1995.Not only
is the number of cases increasing as the disease is spreading to new areas,
butexplosive outbreaks are occurring. In 2007, Venezuela reported over 80 000 cases, including
more than 6 000 cases of DHF. Some other statistics:
During epidemics of dengue, infection rates among those who have not been previouslyexposed to the virus are often 40% to 50%, but can reach 80% to 90%.An estimated 500 000
people with DHF require hospitalization each year, a very large proportion of whom are children.
About 2.5% of those affected die. Without proper treatment, DHF fatality rates can exceed 20%.
Wider access to medical care from health providers with knowledge about DHF - physicians and
nurses who recognize its symptoms and know how to treat its effects - can reduce death rates to
less than 1%.
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The spread of dengue is attributed to expanding geographic distribution of the
four dengue viruses and their mosquito vectors, the most important of which is the
predominantly urban species. A rapid rise in urban mosquito populations is bringing ever greater
numbers of people into contact with this vector, especially in areas that are favorable for
mosquito breeding, e.g. where household water storage is common and where solid waste
disposal services are inadequate. Dengue viruses are transmitted to humans through the bites of
infective female mosquitoes. Mosquitoes generally acquire the virus while feeding on the blood
of an infected person. After virus incubation for eight to 10 days, an infected mosquito is
capable, during probing and blood feeding, of transmitting the virus for the rest of its life.
Infected female mosquitoes may also transmit the virus to their offspring by trans ovarial (via the
eggs) transmission, but the role of this in sustaining transmission of the virus to humans has not
yet been defined .Infected humans are the main carriers and multipliers of the virus, serving as a
source of the virus for uninfected mosquitoes. The virus circulates in the blood of infected
humans for two to seven days, at approximately the same time that they have a fever mosquitoes
may acquire the virus when they feed on an individual during this period. Some studies haveshown that monkeys in some parts of the world play a similar role in transmission.
Dengue fever is a severe, flu-like illness that affects infants, young children and adults,
but seldom causes death. The clinical features of dengue fever vary according to the age of the
patient. Infants and young children may have a fever with rash. Older children and adults
may have either a mild fever or the classical incapacitating disease with abrupt onset and high
fever, severe headache, pain behind the eyes, muscle and joint pains, and rash.
Dengue hemorrhagic fever (DHF) is a potentially deadly complication that is characterized
by high fever, often with enlargement of the liver, and in severe cases circulatory failure. The
illness often begins with a sudden rise in temperature accompanied by facial flush and other flu-like symptoms. The fever usually continues for two to seven days and can be as high as 41C,
possibly with convulsions and other complications in moderate DHF cases, all signs and
symptoms abate after the fever subsides. In severe cases, the patient's condition may suddenly
deteriorate after a few days of fever; the temperature drops, followed by signs
of circulatory failure, and the patient may rapidly go into a critical state of shock and die within
12 to 24 hours, or quickly recover following appropriate medical treatment (see below).
There is no specific treatment for dengue fever.
For DHF, medical care by physicians and nurses experienced with the effects and progression of
the complicating hemorrhagic fever can frequently save livesdecreasing mortality ratesfrom more than 20% to less than 1%. With four closely related viruses that can cause the disease,
the vaccine must immunize against all four types to be effective.
There is limited understanding of how the disease typically behaves and how the virus interacts
with the immune system. There is a lack of laboratory animal models available to test immune
responses to potential vaccines. Despite these challenges, two vaccine candidates
have advanced to evaluation in human subjects in countries with endemic disease, and several
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potential vaccines are in earlier stages of development. WHO provides technical advice and
guidance to countries and private partners to support vaccine research and evaluation.
At present, the only method of controlling or preventing dengue virus transmission is to
combat the vector mosquitos .In Asia and the Americas, breeds primarily in man-
made containers like earthenware jars, metal drums and concrete cisterns used for domesticwater storage, as well as discarded plastic food containers, used automobile tires and other items
that collect rainwater. In Africa the mosquito also breeds extensively in natural habitats such as
tree holes, and leaves that gather to form "cups" and catch water
.In recent years,, a secondary dengue vector in Asia, has becomeestablished in the United
States, several Latin American and Caribbean countries, parts of Europe and Africa. The rapid
geographic spread of this species is largely attributed to the international trade in used tires, a
breeding habitat. Vector control is implemented using environmental management and chemical
methods. Proper solid waste disposal and improved water storage practices, including covering
containers to prevent access by egg-laying female mosquitoes are among methods that areencouraged through community-based programs. The application of appropriate insecticides to
larval habitats, particularly those that are useful in households, e.g. water storage vessels,
prevents mosquito breeding for several weeks but must be re-applied periodically. Small,
mosquito-eating fish and copepods (tiny crustaceans) have also been used with some success.
During outbreaks, emergency vector control measures can also include broad application of
insecticides as space sprays using portable or truck-mounted machines or even aircraft. However,
the mosquito-killing effect is transient, variable in its effectiveness because the aerosol droplets
may not penetrate indoors to microhabitats where adult mosquitoes are sequestered, and the
procedure is costly and operationally difficult. Regular
monitoringof the vectors' susceptibility to widely used insecticides is necessary to ensure theappr
opriate choice of chemicals. Active monitoring and surveillance of the natural mosquito
population should accompany control efforts to determine program effectiveness.
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PHYSICAL ASSESSMENT
Date assessed: September 6 2011
General assessment: conscious and coherent
Initial vital signs: T=36.2C, RR=23, BP=90/60, PR=70
Area Assessed Technique Normal Findings Actual Findings Evaluation
Skin
Color Inspection Light brown,tanned skin (vary
according to race)
Light brown skin Normal
Soles and palms Inspection Lighter colored
palms, soles
Lighter colored
palms, soles
Normal
Moisture Inspection/
Palpation
Skin normally dry Skin normally dry Normal
Temperature Palpation Normally warm Normally warm Normal
Texture Palpation Smooth and soft Smooth and soft NormalTurgor Palpation Skin snaps back
immediately
Skin snaps back
immediately
Normal
Skin
appendagesa. Nails Inspection Transparent,
smooth and convex
Transparent,
smooth and convex
Normal
Nail beds Inspection Pinkish Pale Due to
decreased
blood flow
Nail base Inspection Firm Firm Normal
Capillary refill Inspection/
Palpation
White color of nailbed under pressureshould return to
pink within 2-3
seconds
Returns within 2-3seconds
Normal
b. Hair
Distribution Inspection Evenly distributed Evenly distributed Normal
Color Inspection Black Black Normal
Texture Inspection/
Palpation
Smooth Smooth Normal
Eyes
Eyes Inspection Parallel to eachother
Parallel to eachother
Normal
Visual Acuity Inspection
(penlight)
PERRLA- Pupils
equally round reactto light and
accommodation
PERRLA- Pupils
equally round reactto light and
accommodation
Normal
Eyebrows Inspection Symmetrical in
size, extension, hair
Symmetrical in
size, extension, hair
Normal
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texture and
movement
texture and
movement
Eyelashes Inspection Distributed evenly
and curved outward
Distributed evenly
and curved outward
Normal
Eyelids Inspection Same color as the
skin
Blinks involuntarily
and bilaterally up to
20 times per minute
Do not cover the
pupil and the
sclera, lids
normally closesymmetrically
Same color as the
skin
Blinks involuntarily
and bilaterally up to
18 times per minute
Do not cover the
pupil and the sclera,
lids normally close
symmetrically
Normal
Normal
Normal
Conjunctiva Inspection Transparent withlight pink color
Transparent withlight pink color
Normal
Sclera Inspection Color is white Color is white Normal
Cornea Inspection Transparent, shiny Transparent, shiny Normal
Pupils Inspection Black, constrictbriskly
Black, constrictbriskly
Normal
Iris Inspection Clearly visible Clearly visible Normal
Ears
Ear canalopening
Inspection Free of lesions,discharge of
inflammation
Canal walls pink
Free of lesions,discharge of
inflammation
Canal walls pink
Normal
Normal
Hearing Acuity Inspection Client normallyhears words when
whispered
Client normallyhears words when
whispered
Normal
NoseShape, size and
skin color
Inspection Smooth, symmetric
with same color asthe face
Smooth, symmetric
with same color asthe face
Normal
Nares Inspection Oval, symmetric
and withoutdischarge
Oval, symmetric
and withoutdischarge
Normal
Mouth and
PharynxLips Inspection Pink, moist
symmetric
Light pink, dry,
symmetric
Lack of fluid
intake
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Buccal mucosa Inspection Glistening pink soft
moist
Glistening pink soft
moist
Normal
Gums Inspection Slightly pink color,
moist and tightly fit
against each tooth
Slightly pink color,
moist and tightly fit
against each tooth
Normal
Tongue Inspection Moist, slightlyrough on dorsalsurface medium or
dull red
Moist, slightlyrough on dorsalsurface medium or
dull red
Normal
Teeth Inspection Firmly set, shiny Firmly set, shiny
With tooth decay
Normal
Hard and soft
palate
Inspection Hard palate- dome-
shaped
Soft Palate- lightpink
Hard palate- dome-
shaped
Soft Palate- lightpink
Normal
Neck
Symmetry ofneck muscles,
alignment of
trachea
InspectionNeck is slightlyhyper extended,
without masses or
asymmetry
Neck is slightlyhyper extended,
without masses or
asymmetry
Normal
Neck ROM Inspection Neck moves freely,without discomfort
Neck moves freely,without discomfort
Normal
Thyroid gland Palpation Rises freely withswallowing
Rises freely withswallowing
Normal
Thorax andLungs
Auscultation Clear breath sounds Clear breath sounds Normal
Abdomen
Bowel sounds
Inspection
Auscultation
Skin same color
with the rest of thebody
Clicks or gurgling
sounds occur
irregularly andrange from 5-35 per
minute
Skin same color
with the rest of thebody
Clicks or gurgling
sounds occur
irregularly andrange from 20 per
minute
Normal
Normal
Extremities
Symmetry
Skin color
Hair distribution
Inspection
Inspection
Inspection
Symmetrical
Same with the color
of other parts of thebody
Evenly distributed
Symmetrical
Same with the color
of other parts of thebody
Evenly distributed
Normal
Normal
Normal
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Skin
Temperature
Presence of
lesionROM
Palpation
Inspection
Inspection
Warm to touch
No lesions
Moves freelywithout discomfort
Warm to touch
No lesions
Able to move butwith assistance
Normal
Normal
Due to bodyweakness
Neurology
system
Level ofconsciousness
Inspection Fully conscious,respond to
questions quickly,
perceptive of
events
Fully conscious,respond to
questions quickly
perceptive of events
Normal
Behavior andappearance
Inspection Makes eye contactwith examiner,
hyperactive
expresses feelingswith response to the
situation
Makes eye contactwith examiner,
hyperactive
expresses feelingswith response to the
situation
Normal
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ANATOMY AND PHYSIOLOGY OF THE BLOOD
BLOOD
Blood is considered the essence of life because the uncontrolled loss of it can result to
death. Blood is a type of connective tissue, consisting of cells and cell fragments surrounded by aliquid matrix which circulates through the heart and blood vessels. The cells and cell fragments
are formed elements and the liquid is plasma. Blood makes about 8% of total weight of the body.
Functions of Blood:
>transports gases, nutrients, waste products, and hormones
>involve in regulation of homeostasis and the maintenance of PH, body temperature, fluidbalance, and electrolyte levels
>protects against diseases and blood loss
PLASMA
Plasma is a pale yellow fluid that accounts for over half of the total blood volume. It
consists of 92% water and 8% suspended or dissolved substances such as proteins, ions,nutrients, gases, waste products, and regulatory substances.
Plasma volume remains relatively constant. Normally, water intake through the GITclosely matches water loss through the kidneys, lungs, GIT and skin. The suspended and
dissolved substances come from the liver, kidneys, intestines, endocrine glands, and immune
tissues as spleen.
FORMED ELEMENTS
Cell Type Description Function
Erythrocytes (RBC) Biconcave disk, no nucleus, 7-8 micrometers in diameter
Transport oxygen and carbondioxide
Leukocytes (WBC):
Neutrophil
Basophil
Spherical cell, nucleus with
two or more lobes connectedby thin filaments, cytoplasmic
granules stain a light pink or
reddish purple, 12-15
micrometers in diameter
Spherical cell, nucleus, with
two indistinct lobes,cytoplasmic granules stain
blue-purple, 10-12
micrometers in diameter
Phagocytizes microorganism
Releases histamine, which
promotes inflammation, andheparin which prevents clot
formation
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Eosinophil
Lymphocyte
Monocyte
Spherical cell, nucleus often
bilobed, cytoplasmic granules
satin orange-red or bright red,
10-12 micrometers in diameter
Spherical cell with roundnucleus, cytoplasm forms athin ring around the nucleus,
6-8 micrometers in diameter
Spherical or irregular cell,nucleus round or kidney or
horse-shoe shaped, contain
more cytoplasm thanlymphocyte, 10-15micrometers in diameter
Releases chemical that reduce
inflammation, attacks certain
worm parasites
Produces antibodies and otherchemicals responsible fordestroying microorganisms,
responsible for allergic
reactions, graft rejection,tumor control, and regulation
of the immune system
Phagocytic cell in the bloodleaves the circulatory system
and becomes a macrophage
which phagocytises bacteria,dead cells, cell fragments, anddebris within tissues
Platelet Cell fragments surrounded by
a cell membrane and
containing granules, 2-5
micrometers in diameter
Forms platelet plugs, release
chemicals necessary for blood
clotting
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PREVENTING BLOOD LOSS
When a blood vessel is damaged, blood can leak into other tissues and interfere with the
normal tissue function or blood can be lost from the body. Small amounts of blood from the body
can be tolerated but new blood must be produced to replace the loss blood. If large amounts of
blood are lost, death can occur.
BLOOD CLOTTING
Platelet plugs alone are not sufficient to close large tears or cults in blood vessels. When
a blood vessel is severely damaged, blood clotting or coagulation results in the formation of a
clot. A clot is a network of threadlike protein fibers called fibrin, which traps blood cells,platelets and fluids.
The formation of a blood clot depends on a number of proteins found within plasma
called clotting factors. Normally the clotting factors are inactive and do not cause clotting.
Following injury however, the clotting factors are activated to produce a clot. This is a complexprocess involving chemical reactions, but it can be summarized in 3 main stages; the chemical
reactions can be stated in two ways: just as with platelets, the contact of inactive clotting factorswith exposed connective tissue can result in their activation. Chemicals released from injured
tissues can also cause activation of clotting factors. After the initial clotting factors are activated,
they in turn activate other clotting factors. A series of reactions results in which each clottingfactor activates the next clotting factor in the series until the clotting factor prothrombin activator
is formed. Prothrombin activator acts on an inactive clotting factor called prothrombin.
Prothrombin is converted to its active form called thrombin. Thrombin converts the inactive
clotting factor fibrinogen into its active form, fibrin. The fibrin threads form a network whichtraps blood cells and platelets and forms the clots.
CONTROL OF CLOT FORMATION
Without control, clotting would spread from the point of its initiation throughout the
entire circulatory system. To prevent unwanted clotting, the blood contains several
anticoagulants which prevent clotting factors from forming clots. Normally there are enoughanticoagulants in the blood to prevent clot formation. At the injury site, however, the stimulation
for activating clotting factors is very strong. So many clotting factors are activated that the
anticoagulants no longer can prevent a clot from forming.
CLOT RETRACTION AND DISSOLUTION
After a clot has formed, it begins to condense into a denser compact structure by aprocess known as clot retraction. Serum, which is plasma without its clotting factors, is squeezed
out of the clot during clot retraction. Consolidation of the clot pulls the edges of the damaged
vessels together, helping the stop of the flow of blood, reducing the probability of infection andenhancing healing. The damaged vessel is repaired by the movement of fibroblasts into damaged
area and the formation of the new connective tissue. In addition, epithelial cells around the
wound divide and fill in the torn area.
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The clot is dissolved by a process called fibrinolysis. An inactive plasma protein calledplasminogen is converted to its active form, which is called plasmin. Thrombin and other clotting
factors activated during clot formation, or tissue plasminogen activator released from
surrounding tissues, stimulate the conversion of plasminogen to plasmin. Over a period of a few
days the plasmin slowly breaks down the fibrin.
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LABORATORY EXAMINATIONS
Hematology Report
Date: September 6 2011
PARAMETER NORMAL
FINDINGS
ACTUAL FINDINGS ANALYSIS
White Blood Cells 5-10 x 10^g/L 3.9 x 10^g/L Decreased due to
inadequate
inflammatory
defenses to suppress
infection and humoral
immunity takes place
Hemoglobin 120-160g/L 152g/L N0RMAL
Hematocrit 39-54 % 31 % Decreased due to poor
oxygen supply
Segmenters 0.60-0.70 0.73 Increased; indicate
high glucose level in
the blood
Lymphocytes 28-40 42.2
Platelet Count 150-450 x 10^g/L 22x10^g/L Deceased due to
hemolysis
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Hematology Report
Date: September 4 2011
PARAMETER NORMAL
FINDINGS
ACTUAL FINDINGS ANALYSIS
White Blood Cells 5-10 x 10^g/L 2.9 x 10^g/L Decreased due to
inadequate
inflammatory
defenses to suppress
infection and humoral
immunity takes place
Hemoglobin 120-160g/L 152g/L
Hematocrit 39-54 % 29 % Decreased due to poor
oxygen supply
Segmenters 0.60-0.70 0.65 Normal
Lymphocytes 28-40 28.6 NORMAL
Platelet Count 150-450 x 10^g/L 45X10^g/L Hemolysis
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Urinalysis Report
Date: September 4 2011
PARAMETER NORMAL
FINDINGS
ACTUAL FINDINGS ANALYSIS
Color Yellow Amber Yellow normal
Transparency Clear clear normal
Reaction 4.5-8 6.5 normal
Specific Gravity 1.005-1.030 1.005 normal
Sugar Negative Negative normal
Protein Negative Negative normal
Squamous Epithelial
Cells
Few Occasional normal
HEMATOLOGY REPORT
Date: September 5 2011
PARAMETER NORMALFINDINGS
ACTUAL FINDINGS ANALYSIS
White Blood Cells 5-10 x 10^g/L 2.7 x 10^g/L Decreased due toinadequate
inflammatory
defenses to suppressinfection and humoral
immunity takes place
Hemoglobin 120-160g/L 162g/L Decreased due to poor
oxygen supply
Hematocrit 39-54 % 29 % Decreased due to pooroxygen supply
Segmenters 0.60-0.70 0.68 normal
Lymphocytes 28-40 44 Increased due to the
bodys increasedimmune system
Platelet Count 150-450 x 10^g/L 29x 10^g/L hemolysis
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Date: September 5 2011
PARAMETER NORMAL
FINDINGS
ACTUAL FINDINGS ANALYSIS
White Blood Cells 5-10 x 10^g/L 4.8 x 10^g/L Decreased due to
inadequate
inflammatorydefenses to suppress
infection and humoral
immunity takes place
Hemoglobin M: 13.0-18.0 g/dL 10.3 g/dL Decreased due to poor
oxygen supply
Hematocrit 39-54 % 31 % Decreased due to pooroxygen supply
Segmenters 0.60-0.70 0.57 Decreased; indicatelow glucose level in
the blood
Lymphocytes 0.20-0.30 0.43 Increased due to thebodys increased
immune system
Platelet Count 150-450 x 10^g/L 95 x 10^g/dL hemolysis
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OBJECTIVES
General objectives:
To be knowledgeable about the nature of Dengue Fever Syndrome,
management and treatment to be able to render effective nursing care to
the client.
Specific Objectives:
To be familiar with the etiology of the disease
To know the pathophysiology of the disease
To be aware of the signs and symptoms
To know its complications
To be knowledgeable on how to prevent the diseaseTo know the treatment and how to apply it
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PATIENTS PROFILE
Name: VF
Age: 15 years old
Gender: Female
Address: Mallig Isabela
Date of Birth: January 3 1996
Nationality: Filipino
Religion: Roman Catholic
Civil Status: Single
Date of Admission: Sept. 4 2011
Time of admission: 3:00 pm
Physician: Dr. Rema Parallag
Place of Admission: CVMC
Admitting Diagnosis: Dengue hemorrhagic fever 3
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Discharge Planning
Patient's Name:
> VF 15 year-old male patient, who was diagnosed with Dengue
Hemorrhagic Fever.
Diet:
> Encourage nutritious foods like vegetables, meat and fruits.
Medications:
> Give acetaminophen in case the temperatures increases.
> Treatment:
> Increased oral fluid intake.
Health Teaching:
> D- discusses the possible source of infection of the disease.
> E- educate the family/patient on how to eliminate those vectors.
> N- Never stocked water in a container without cover.
> G- Gallon, container and tires must have proper way of disposal.
> U- Use insecticides at home to kill or reduce mosquito.
> E- Encourage the family of the patient to clean the surroundings to destroy the
breeding area.
>Give aerosol to replace fluid in the body.
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PATHOPHYSIOLOGY
Non- predisposing Factor: Predisposing Factor
- Age15y/o immunocompromised
environment
Bite of aedes aegypti mosquito carrying a virus
Virus goes into the circulation
Infects cells & generate cellular response
Initiates destruction of the platelet
Potential for haemorrhage
Stimulates intense inflammatory response
Release of exogenous pyrogens the body releases anti-
Inflammatory
mediators
WBC (Neutrophils & Macrophages) (Histatin, Kinins)
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Release of endogenous pyrogens vascular response
Reset of hypothalamic thermostat Redness & Heat
Fever Headache, Vomiting
Epistaxis, Abdominal
pain
Muscle contract Blood vessels Circulatory CollapseShock
To produce construct to
Additional heat prevent loss of body heat DEATH
SHIVERING CHILLS
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NURSING CARE PLAN
Assessment NursingDiagnosis
Planning NursingIntervention
Rationale Evaluation
Subjective:Mainit po ang katawan koasverbalized by the patient.
v/S takenBP 110/70mmHgTemp. 38.4CRR 26bpmPR 90bpm
- Flushing of skin- Skin warm to touch
Elevated bodytemperaturerelated toincreasepyrogenscirculating inthe body
Within 8 hoursof effectivenursinginterventionpatient bodytemperaturewill bedecrease from38.4- 37.5C
IndependentNursingAction:-Monitoredvital sign
- Monitoredintake andoutput
- Performed
TSB
-Increasedoral fluidintake
- Providedsafe & quiteenvironment
-Informed thepatient aboutpropermanagementof fever
Dependentnursingintervention:- Administeredmedicationsas order byphysicianssuch asParacetamolor any antipyretic drugs.
- Serves atbaseline data.-To know thefluid balanceof the body
- To reducebodytemperature
through theprocess ofconduction- To preventdehydrationand supportcirculatingvolume.- To provideconduciveplace to rest.Inform thepatient about
propermanagementof fever- To be ablefor the patientto know thepropermanagement.
-To elevatethe patientsbodytemperature.
After 8 hours ofrendering effectivnursing interventthe goal wascompletely met aevidenced bypatients bodytemperaturedecreases from38.4-37.5C.Patients skin not
warm to touch.Normal complexiof the skin.
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Assessment Nursing Diagnosis Planning NursingIntervention
Rationale Evaluatio
bjective:asakit ang tiyanas verbalized bypatient.
uarding ofmachacial grimaceain scale of 8/10
Acute pain relatedto clinicalmanifestations ofdenguehemorrhagic fever
Within 8 hours ofeffective nursingintervention patientwill be able to feelless pain on hisabdomen.
.
IndependentNursing Action:-Performed acomprehensiveassessment of pain
- Providednonpharmacologicmanagement likechange of position
& applying warmcompress
- Encourageddivers ionalactivities- rest period
-encouraged pt. todo deep breathingexercises
- To improvequality, frequency &location of pain.
-To alleviate pain.
-To divert hisattentions to thepain- To prevent fatigue
After 8 hours rendering effenursing intervthe goal waspartially met aevidenced byguarding ofstomach andpatients verbapartial relieve
pain.
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Assessment NursingDiagnosis
Planning NursingIntervention
Rationale Evaluation
Subjective:Nangangati akoas verbalized bythe patient
- Redness of theskin- Skin rashes
Risk for impairedskin integrityrelated toitchiness
Within 2hours ofnursingintervention,
patient willdemonstratebehavior inpreventing skinimpairment.
.
IndependentNursing Action:-Monitored vitalsigns
- Provided skinhygiene throughsponge bathing &changing regularly
- Kept bedlinensdry, use non-irritating materials,& keep bedwrinkled free
- Palpated skinlesions for size,shape,consistency,texture & hydration
- Encouragedrepositionschedule for client
-Providedinformation to theclient about the
importance ofregularobservation &effective skin care
- Serves asbaseline data to
determine anydiscrepancies-To maintain skinintegrity at optimallevel.
-To avoid lesions,scratching of skin& harboring ofmicroorganism.
- To assess extentof involvement ofskin impairment.
-To preventfriction that maycause irritation ofthe skin
- To promotewellness bygaining
knowledge ontreatment/ therapy
After 8 hours ofrendering effectivenursing interventiothe goal was
completely met asevidenced bypatientsdemonstration ofbehavior inpreventing skinimpairment.-patient verbalizescomfortability,decrease feeling oitchiness andgradualdisappearance of
rashes.-patients skincolor(pigmentatiobecomes normal(absence ofredness)
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DRUG ACTION INDICATION CONTRAINDICATION ADVERSE
REACTION
NURSING
RESPONSIBILTIES
PATIENT
TEACHING
Dobutamine
Hydrochloride
Stimulateshearts beta1receptors to
increase
myocardial
contractility and
stroke volume.At therapeutic
dosages, drug
increases
cardiac output
by decreasing
peripheral
vascular
resistance,
reducing
ventricular
filling pressure,
and facilitating
AV node
conduction
Increase cardiacoutput in short-tern
treatment of cardiac
decompensation
cause by depressed
contractility, such
as during refractoryheart failure;
adjunctive therapy
in cardiac surgery
Contraindicatedin patients
hypersensitive to
drug or its
components and
in those w/
idiopathichypertrophic
subaortic stenosis
CNS:headache
CV:hypertension,
increasedheart rate
Before startingtherapy, give a
plasma volume
to correct
hypovolemia an
a cardiac
glycoside Continuously
monitor ECG,
blood pressure,
pulmonary
artery wedge
pressure,
cardiac output
and urine
output
Tell patiento report
adverse
reactions
promptly,
especially
laboredbreathing a
drug-induc
headache
Instructpati8ent to
report
discomfort
I.V. inserti
site
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