Identify, discuss and define a disease and tell how it affects the body/specific organ

Published by Jeannie R. Ferrell

Nov 18, 2022


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I included all posted instructions for the paper that were submitted by professor.
Paper must cover following.
1. Identify, discuss and define a disease and tell how it affects the body/specific organ (or organ system). Be sure to
include information about who gets the disease (age, race, gender) and how many people in the United States
have it.
2. Review how the same organ or organ system functions in a healthy individual, then discuss how the disease
affects that system. For example, if you were discussing asthma, you would first briefly describe how the lungs function in
a healthy person. You would then contrast that with what happens in the lungs of an asthmatic patient (trigger events such
as histamine secretion, resulting constriction of bronchioles, etc.)
3. Discuss what (if anything) is known about the genetic component of the disease. Questions to consider include but
aren’t limited to: How much of the disease is a result of genetics? How much depends on environment? Are there multiple
ways of developing the disease? Who gets the disease? How is it inherited (autosomal dominant, X-linked recessive, etc.)?
How common is it? Are there genetic tests to detect the disease (assuming it has a genetic component)?
4. Discuss current therapies doctors and other health care professionals use. Include drugs or drug classes and
BRIEFLY discuss how the drug(s) work.
5. Discuss future treatments or therapies (gene therapies, new drugs, vaccines, innovative surgical procedures, etc.).
Follow these guidelines precisely when creating your paper
Notice the header that appears at the top of each page of this document on the research project. Use the
header/footer function in Word or WordPerfect to write your names, the date, and Bio 202 at the top of your paper. For the header only use a 9-point type of one of the following fonts: Arial, Times-Roman,
Helvetica, Palatino.
Can be a maximum of 1 inch on all sides. However, it’s likely you’ll need to make your margins smaller to fit all
your information on one page. You can make your margins as small as your printer will allow, but you may not
use smaller that 10-point type (again choose from Arial, Times-Roman, Helvetica or Palatino).
Title should appear two (single) spaces down from the header (from the top of the page, hit return twice and start
typing title). Use bold, 12-point font for the title only, and center the title.
Appears two, single spaces down from title. Use single-spaced 10- or 11-point font (Arial, Times-Roman,
Helvetica or Palatino) for the text of your summary. What size font you use may depend on how much
information you are trying to fit on one page. The paper should cover the questions listed under THE PROJECT
with one exception. You are NOT required to discuss how the healthy body operates nor very specifically how
the disease affects the body in the one-page summary. You will have ample time to cover this during the oral
You will turn in two copies of your group’s one-page summary. The first copy should look like the example I’ve
given you and will NOT contain citations. This is the one I will use to make copies to hand out in class. The
second copy is only for me and will contain the one-page summary along with a second sheet of paper containing
a list of citations used to compile the paper.
Follow APA style to format citations and title the second page
(citations) “References Used.” Do not put a reference in the list unless information from the reference specifically
appears in the one-page summary.
Good writers know that the first draft is simply that—a draft.
The next page contains a sample one-page summary on lupus erythematosus I made for you.
Tasneem Ashraf Bio 202
August 12, 2022
Systemic Lupus Erythematosus
Systemic lupus erythematosus (SLE), an autoimmune disorder, primarily strikes women of child-bearing age, though it
can also affect men and children. Lupus manifests when a patient’s immune system mistakenly begins to attack healthy
tissue in the body. This leads to inflammation and tissue damage.
Common SLE symptoms include extreme and/or chronic fatigue, osteoarthritis, kidney problems, skin rashes and sun
sensitivity. Chronic inflammation, which is a hallmark of the disease, can damage organs such as the heart, lungs and
central nervous system. Patients can experience long periods—sometimes even years—without symptoms, punctuated by
disease flare-ups. Generally, most patients lead normal, productive lives.
SLE is a chronic, non-fatal disease and is three times more common in African American women than in Caucasian
women. However, those of Asian, Native American and Hispanic descent also have a high rate of lupus. Nine out of 10
patients with SLE are women, a common statistic for many autoimmune diseases. SLE can run in families, but the risk
that offspring or siblings of an SLE patient will develop lupus is quite low.
There are three types of lupus: SLE, discoid lupus erythematosus (DLE) and drug-induced lupus. DLE mostly affects the
skin, producing a red rash across the cheeks and nose that resembles a wolf’s face. In fact, the disease derives its name
from the Latin word for wolf—lupus. Patients with DLE often later develop SLE. Drug-induced lupus can appear if a
patient takes prescription drugs known to produce lupus-like symptoms. The disease disappears when the patient
discontinues the medication.
Researchers aren’t sure what causes lupus, but believe a combination of genetic, environmental and perhaps hormonal
factors interact to produce the disease. Research suggests SLE is a polygenic disorder and that certain combination of
genes may make a person more susceptible to the disease. One line of research proposes that people with lupus carry a
defective gene(s) responsible for ridding the body of damaged or harmful cells (a process called apoptosis). If an
apoptotic gene is defective, harmful/damaged cells may stay in the body and injure other tissues. Other research suggests
that an autoimmune protein called interferon-alpha may induce the disease or that antibodies in lupus patients seem to
preferentially kill nerve cells by attaching to receptors located on neurons.
Though there is no one test for lupus, doctors can diagnose the disease based on the combined results of several tests. The
majority of these tests examine components of the patient’s immune system. For example, the antinuclear antibody
(ANA) test looks for autoantibodies that attack the nucleus of host cells. Other SLE autoantibody tests include anti-DNA,
anti-Sm (ribonuclear protein antibody), anti-RNP (cytoplasmic ribonuclear protein antibody) and anti-Ro (another nuclear
antibody). Physicians also commonly look for decreased complement levels (e.g. proteins C3, C4, CH50 and CH100) in the
blood, as complement levels typically drop during flare-ups.
There is no cure for SLE. Treatment for the disease varies depending on which symptoms are most prominent in the
individual. Generally, all patients benefit from bed rest and by reducing stress. Exposure to direct sunlight can cause
flare-ups or worsen symptoms, so a normal course of treatment includes avoiding the sun or wearing sunscreen.
Medications which treat the symptoms of lupus include anti-inflammatory drugs, antimalarials, corticosteroids and
immunosuppressives. Corticosteroids such as prednisone are the cornerstone of lupus treatment and work to quickly
reduce inflammation by suppressing the immune system. Anti-inflammatories such as ibuprofen directly decrease joint
inflammation, pain and fever. If lupus affects the kidneys or the central nervous system, immunosuppressives can also
restrain the patient’s overactive immune system. Antimalarials treat pain, fatigue, rashes and lung inflammation. Doctors
aren’t sure why antimalarial medications work to relieve lupus symptoms, but think the drugs may, like other
immunosuppresives, rein in parts of the immune system.
Current research is as varied as the treatment options for lupus. Geneticists continue their search for the genes which be
involved in lupus. Clinical researchers are developing a drug that would reduce or negate the effects of interferon-alpha.
Other scientists are focusing instead on how lupus affects the nervous system. Still others are concentrating on why lupus
is so prevalent in women and what role hormones may play in bringing on the disease. One hypothesis suggests that fetal
cells may remain in the mother’s bloodstream for years and thus may trigger an unwanted immune system response.


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