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Anatomy and Physiology
Fisher
Case Study A
Sarah, a forty-nine year old Anglo woman, visits her physician complaining of weight
loss, sweating, listlessness and flu-like symptoms (fever, headache, scratchy throat,
generalized body ache). After checking her history the physician notes that Sarah is
married, has four children and no previous history of chronic illness. Her weight has
decreased 15 pounds over the past three months and she presents with a temperature
of 101o F, a slightly elevated pulse (85 beats per minute), normal blood pressure
(112/78 mm Hg) and slightly labored breathing. Sarah has a negative family history of
cardiovascular and respiratory disease. All of her family members are living and are free
of cardiovascular or respiratory diseases. Sarah does not smoke and is current on all
immunizations. She does report that she developed these symptoms a few days after
visiting a friend whose son was home with a cold. After a chest X-ray and physical
examination of Sarah’s ear, nose and throat, the physician confirms the diagnosis and
prescribes bed rest, aspirin and a nasal decongestant. The physician also cautions
Sarah from returning to her normal activities until she has been afebrile for a minimum
of 24 hours.
Sarah’s condition continues to worsen such that a week later she returns to her
physician’s office. She has pain on the left side of her chest, is coughing more
frequently and her sputum has a yellow color. Her respiratory rate is 32 breaths per
minute and her breathing is labored. Her blood pressure is unchanged and does not
demonstrate postural changes. Breath sounds indicate inspiratory rates and a chest Xray indicates a dense infiltrate within the lungs. Physical examination
reveals lymphadenopathy. The physician suspects pneumonia and orders laboratory
tests on Sarah’s blood and sputum. The results of the sputum tests indicate the
presence of gram positive diplococci and polymorphonucleocytes that are too
numerous to count. What concerns the physician, however, are the results of Sarah’s
blood test. Her blood tests indicate leukopenia, anemia, and thrombocytopenia. In
addition, the differential leukocyte count indicates that the concentration of helper T
cells has decreased. The physician now suspects that Sarah has been infected with the
human immunodeficiency virus (HIV) and that she has developed pneumonia as a
result of the immune suppression.
In reviewing her history, the physician notes that Sarah has been married for the past
30 years and does not admit to any extramarital affairs. She has not received any blood
transfusions or blood products and does not use intravenous drugs. She is a selfemployed certified public accountant and has not visited any countries with high
incidences of HIV infection. Upon further discussion, Sarah does mention to the
physician that she and her husband were separated a few years ago for approximately
6 months as a result of his extramarital affair. The physician asks Sarah if he can run
another test to determine whether or not she has contacted HIV and asks Sarah to talk
to her husband about being tested for HIV as well. The physician also begins treating
Sarah for the pneumonia that has developed and asks her to return the next day for the
results of the HIV test.
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The next day Sarah and her husband return to the physician’s office and the physician
confirms that the enzyme-linked immunoadsorbent assay confirms that Sarah is HIV
positive. The physician does mention that a second more sensitive test will be
conducted to confirm this finding, however, he is doubtful that the result will indicate a
false positive in the first test. Her husband admits to having numerous extramarital
affairs with both women and men and consents to a blood test to determine his HIV
status, which subsequently is positive. The physician then discusses the replicative
cycle of HIV, the concept of a retrovirus, and treatment options with both Sarah and
her husband. Sarah immediately starts on a regimen of protease inhibitors and
nucleoside analogs (azidothymidine, AZT, and ddI). In addition, the physician discusses
with Sarah and her husband the necessity of practicing "safe sex" even though both are
HIV positive and the importance of not exposing themselves to opportunistic diseases.
In addition, he mentions that some of the drugs they will be taking to minimize viral
replication may cause nausea. He cautions them to take all medications as scheduled
and to return to his office at the first sign of any disorder. He also reiterates that this
disease can not be transferred by casual contact, but can be transferred through an
exchange of body fluids (blood, semen and vaginal secretions).
1. Define each of the bold terms in the description.
Term
Definition
Afebrile
not feverish
Anemia
an abnormally low number of erythrocytes,
concentration of hemoglobin, hematocrit, or any
combination of these measures
the inability of the immune system to mount a
normal response to an antigen or antigens
Immunodeficiency
Leukopenia
abnormally low numbers of leukocytes, usually less
than 5000 per cubic mm
Lymphadenopathy
swollen lymph nodes, often indicating diseased
lymph nodes
Polymorphonucleocytes
a white blood cell with a multilobed nucleus; a
granulocyte
Protease inhibitors
enzymes that inhibit the actions of proteolytic
enzymes (proteases)
Retrovirus
a virus that contains ribonucleic acid as its genetic
material and utilizes reverse transcriptase to
synthesize a complementary DNA molecule that
becomes integrated into a chromosome of the host
cell
Thrombocytopenia
abnormally low numbers of thrombocytes, usually
less than 130,000 per cubic mm
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2. Why was HIV not initially considered as a possible cause for the symptoms
Sarah presented with?
Infection with HIV was not initially considered since Sarah did not present with any of the
risk factors. She has been in a monogamous relationship for at least 30 years and has
not received any blood transfusions or blood products. She does not use intravenous
drugs and her travel has not taken her to areas where she would be at risk for HIV
infection.
3. Why did Sarah’s symptoms worsen and develop into pneumonia?
The initial symptoms worsened due to the inability of her immune system as a result of
her positive HIV status, to mount an adequate response to the bacteria which were
present in her respiratory tract. Since her immune system was unable to respond, the
bacteria were able to become established in the airway. The polymorphonucleocytes
increase in concentration in the sputum to respond to the bacteria. These cells, while
part of the immune response, are not specifically affected by HIV and would continue to
mount a response to a pathogenic organism. These cells were not sufficient to prevent
the development of pneumonia.
4. Identify the specific types of leukocytes and the function of each cell.
The different types of leukocytes and the functions attributed to each are shown in the following
table.
Leukocyte
Function(s)
Basophil
Release of heparin and histamine
Eosinophil
Destruction of antibody-coated pathogens
Neutrophil
Phagocytosis of antibody-coated pathogens
Monocyte
Develop into macrophage
Macrophage
Phagocytosis of pathogens and activation of T cells
B lymphocyte
Antibody production and differentiation into memory cells
T lymphocyte
Destruction of virus-infected cells
Natural killer cell
Attack and lyse virus-infected cells or cancer cells
5. Why does HIV specifically affect one type of leukocyte?
A single type of lymphocyte, the CD4+ T lymphocyte or helper T cell, is the only
subpopulation of leukocyte infected by HIV. This occurs because the HIV binds specifically
to a receptor on the surface of the helper T cells. The virus has a specific glycoprotein
known as gp120 which binds to the CD4 molecules on the surface of the helper T cells. This
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binding allows for the HIV to then fuse with the plasma membrane of the helper T cell and
infect the cell.
6. Why can protease inhibitors and nucleoside analogs be used in minimizing the
replication of the HIV virus?
Protease inhibitors can be used because the genome of HIV encodes for a protease which is
required for the formation of viral proteins from larger proteins produced by translation in the cell.
Inhibiting this protease by the use of protease inhibitors would block the formation of viral proteins
and subsequently viral production. The use of nucleoside analogs will block the production of viral
RNA. These nucleoside analogs are added to the growing RNA strand and since they lack a free
2’ hydroxyl group, the synthesis of the RNA molecule ceases. If the cell is unable to synthesize
the RNA for the assembly of the virus, then viral replication is minimized. Using these drugs in
combination with each other has proven more effective than using each drug alone.
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