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Hemorrhagic Fever
II
Submitted By:
Wincy S. Banayad
Submitted To:
Mrs. Raquel Makarambon
Introduction:
Dengue Hemorrhagic fever is a wide spread disease in our country. This is brought
about by a mosquito called Aedes Aegypti, which dwells in any clean stagnant water.
This case study, aims to provide knowledge to the possible treatment or any medical
management that can be done in a patient who is infected by this vector borne illness
Objectives:
Name:
Age and Gender:
Birthday:
Address:
Religion:
Jennievive P. Ocfemia
13 yrs. Old, female
12 28 1997
Madjaas St. Payatas, Quezon City
Roman Catholic
Clinical History:
Physical Examinations:
Laboratory Exam:
Pathophysiology of Dengue:
Dengue virus is primarily transmitted by Aedes mosquitoes, particularly A. aegypti.
These mosquitoes usually live between the latitudes of 35 degrees North and
35 degrees South below an elevation of 1,000 metres (3,300 ft). They bite primarily
during the day. Other mosquito speciesA. albopictus, A polynesiensis and several A.
scutellarismay also transmit the disease. Humans are the primary host of the virus,
but it may also circulate in nonhuman primates.An infection may be acquired via a
single bite.A mosquito that takes a blood meal from a person infected with dengue
fever becomes itself infected with the virus in the cells lining its gut. About 810 days
later, the virus spreads to other tissues including the mosquito's salivary glands and is
subsequently released into its saliva. The virus seems to have no detrimental effect on
the mosquito, which remains infected for life. Aedes aegypti prefers to lay its eggs in
artificial water containers and tends to live in close proximity to humans, and has a
preference for feeding off them rather than other vertebrates.
Dengue may also be transmitted via infected blood products and through organ
donation.In countries such as Singapore, where dengue is endemic, the risk is
estimated to be between 1.6 and 6 per 10,000 transfusions.Vertical transmission (from
mother to child) during pregnancy or at birth has been observed.Other person-toperson modes of transmission have been reported, but are very unusual.
When a mosquito carrying DENV bites a person, the virus enters the skin together
with the mosquito's saliva. It binds to and enters white blood cells, and reproduces
inside the cells while they move throughout the body. The white blood cells respond
by producing a number of signalling proteins (such as interferon) that are responsble
for many of the symptoms, such as the fever, the flu-like symptoms and the severe
pains. In severe infection, the virus production inside the body is much increased, and
many more organs (such as the liver and the bone marrow) can be affected, and fluid
from the bloodstream leaks through the wall of small blood vessels into body cavities.
As a result, less blood circulates in the blood vessels, and the blood pressure becomes
so low that it cannot supply sufficient blood to vital organs. Furthermore, dysfunction
of the bone marrow leads to reduced numbers of platelets, which are necessary for
effective blood clotting; this increases the risk of bleeding, the other major
complication of dengue.
After entering the skin, DENV binds to Langerhans cells (a population of dendritic
cells in the skin that identifies pathogens).The virus enters the cells through binding
between viral proteins and membrane proteins on the Langerhans cell, specifically the
C-type lectins called DC-SIGN, mannose receptor and CLEC5A.DC-SIGN, a nonspecific receptor for foreign material on dendritic cells, seems to be the main one. The
dendritic cell moves to the nearest lymph node. Meanwhile, the virus genome is
replicated in membrane-bound vesicles on the cell's endoplasmic reticulum, where the
cell's protein synthesis apparatus produces new viral proteins, and the viral RNA is
copied. Immature virus particles are transported to the Golgi apparatus, the part of the
cell where the some of the proteins receive necessarily sugar chains (glycoproteins).
The now mature new viruses bud on the surface of the infected cell and are released
by exocytosis. They are then able enter other white blood cells (such as monocytes
and macrophages).
The initial reaction of infected cells is to produce the interferon, a cytokine that raises
a number of defenses against viral infection through the innate immune system by
augmenting the production of a large group of proteins (mediated by the JAK-STAT
pathway). Some serotypes of DENV appear to have mechanisms to slow down this
process. Interferon also activates the adaptive immune system, which leads to the
generation of antibodies against the virus as well as T cells that directly attack any cell
infected with the virus.Various antibodies are generated; some bind closely to the viral
proteins and target them for phagocytosis (ingestion by specialized cells) and
destruction, but some bind the virus less well and appear instead to deliver the virus
into a part of the phagocytes where it is not destroyed but is able to replicate further.
Dengue virus
Dengue (DF) and dengue hemorrhagic fever (DHF) are caused by one of four closely
related, but antigenically distinct, virus serotypes (DEN-1, DEN-2, DEN-3,
and DEN-4), of the genus Flavivirus.
Immunity
Infection with one of these serotypes provides immunity to only that serotype for life,
so persons living in a dengueendemic area can have more than one dengue infection
during their lifetime. If an individual develops immunity to one subtype and then tries
to launch an immune response to another subtype then they will develop DHF/DSS.
Work has been done on a tetravalent vaccine that will attempt to give the individual
immunity to all four of the subtypes at the same time.
Mechanism of complications
It is useful to understand why certain individual develop DHF/DSS. The Dengue
virus has been shown to have 4 subtypes. These 4 subtypes are different strains of
dengue virus that have 60-80% homology between each other. The major difference
for humans lies in subtle differences in the surface proteins of the different dengue
subtypes. After a person is infected with dengue, he or she develops an immune
response to that dengue subtype. The immune response produces specific antibodies
to that subtype's surface proteins that prevent the virus from binding to macrophage
cells (the target cell that dengue viruses infect) and gaining entry. However, if another
subtype of dengue virus infects the individual, the virus will activate the
immune system to attack it as if it was the first subtype. The immune system is tricked
because the 4 subtypes have very similar surface antigens. The antibodies bind to the
surface proteins but do not inactivate the virus. The immune response attracts
numerous macrophages, which the virus proceeds to infect because it has not been
inactivated. This situation is referred to as Antibody-Dependent Enhancement (ADE)
of a viral infection. This makes the viral infection much more acute. The body
releases cytokines that cause the endothelial tissue to become permeable
which results in hemorrhage and plasma loss from the blood vessels. Increased
vascular permeability leads to plasma loss from the vascular compartment. This
results in haemoconcentration, low pulse pressure. When the plasma loss becomes
critical, shock ensues. Both quantitative and qualitative platelet defects can develop.
Therefore bleeding time can be prolonged even when platelet counts are above
100,000 per cubic millimeter. In the liver there is focal necrosis of hepatocytes,
swelling, appearance of Councilman bodies and hyaline necrosis of
Kupffer cells.
Anatomy and Physiology:
Diet
No specific diet is necessary for patients with dengue fever, but the EDCF diet
is most preferably.
Patients may become dehydrated from fever, lack of oral intake, or vomiting.
Patients who are able to tolerate oral fluids should be encouraged to drink oral
rehydration solution, fruit juice, or water to prevent dehydration.
Return of appetite after dengue hemorrhagic fever or dengue shock syndrome
is a sign of recovery.
Activity
Bedrest is recommended for patients with symptomatic dengue fever, dengue
hemorrhagic fever, or dengue shock syndrome.
Assessment
Diagnosis
S = nome
Imabalance
Nutrition:
lessthan the
body
requirements
r/t
prevaling
condition:
DHF II
Objectives:
Dry Skin
Planning
Intervention
Rationale
After series of
nursing
increase fluid
intake
This will
prevent
intervention,
patient
will be able to
consume
dehydration
and
further
complications
food serve
Evaluation
Provided
Health
teachings
about the
food
importance
and constant
hydartion
On bed most of
the time
ang importansya ng
pagkain"