Immune Slide cquired immunity by benbenzhou

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Immune Slide cquired immunity

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									Slide 1 This section discusses care of clients with selected alterations of the
immune system.

Slide 2 Self versus Non self. This is what immunity is all about. It is the
ability of the cells of the body to be able to recognize cells or things that are
not part or the normal body. How does the immune system know what is
self? Each of us has specific cell surface characteristics which don’t
perfectly match anyone else. An exception is identical twins. This is called
our Human Leukocytic Antigens or HLA’s. Auto-immune problems occur
when the body doesn’t recognize self & attacks it. Organ transplants are
rejected because the donated organ has a different HLA than the host. The
host’s immune system doesn’t recognize the HLA & attacks & destroys the
transplant. Functions of the immune system are: (1) defense against
bacteria, viruses, fungi and parasites. (2) homeostasis by removing and
destroying damaged cells, and (3) surveillance by identifying continuous
malignant cells and destroying them.

Slide 3 Immunity is classified as innate or acquired. Innate immunity
(natural immunity) is present at birth and exists in a person without prior
contact with an antigen.

Slide 4 Acquired immunity is classified as (1) active or natural which
occurs following exposure to a disease such as measles, chickenpox or
mumps; (2) active or artificial which occurs as the result of an injection of
an antigen such as immunizations. These types take time to develop but last
a long time.

Slide 5 Acquired passive immunity can occur naturally as the result of
antibodies being passed from mother to fetus or may be acquired artificially
through injection of gamma-globulin (GG) to produce short term protection
from disease. These types are short lived because no memory cells are
present.

Slide 6 Please review anatomy and physiology of the immune system from
your text and notes from Fundamentals. Video tapes 137 and 134 found in
the Nursing Lab also offer a good review.

Slide 7 There are two types of immune responses. They are humoral or
plasma mediated and cell-mediated. In humoral immunity, an invading
antigen causes the B cells to divide and differentiate into plasma cells which
secrete antigen-specific immunoglobulins ( Ig)

Slide 8 There are five types of Ig. IgA, IgG and IgM respond to viral and
bacterial invasion. IgD may assist in B cell binding with the antigen. IgE is
present during inflammatory responses and causes allergic reactions..

Slide 9 During the humoral response, complement which consists of
approximately 25 enzymes, works with antibodies to puncture the bacterial
cell walls to destroy them.

Slide 10 In cell-mediated immunity,the antigen such as bacteria, virus,
fungus or cancer, lives within the body cell and is present on the cell surface.
Macrophages identify the antigen and T cells defend against it. This is a
delayed response such as might occur in graft rejection, hypersensitivy
reactions, tumor immunity and immunity against bacteria, virus and fungus.

Slide 11 Immunocompetence exists when the immune system is able to
identify and destroy foreign substances. When the immune system in not
competent to recognize or destroy foreign substances, infeciton,
immunodeficiency diseases and cancer occur. When the immune system is
overactive, hypersensitivies such as allergies and autoimmune diseases
occur.

Slide 12 There are four types of hypersensitivities, Type 1 is known as an
anaphylactic reaction. On the first exposure to the allergen, IgE antibodies
are produced and bind to mast cells and basophils. On next exposure, the
allergen attaches to the IgE bound to mast cells or basophils, and causes
release of chemical mediators from the cells. These chemicals cause
vasodialation, hypotension, increased secretion of mucus, and itching.. A
cutanous response, a wheal-and-flare reaction occurs. An example is a
mosquito bite. Examples of the cause for local anaphylaxis is food, pollen,
medication, and dust.

Slide 13 Anaphylaxis occurs when the chemical mediators are released
systemically. Anaphylaxis may be caused by food, particularly, shellfish,
nuts, eggs and strawberries, drugs like PCN and Sulfa, insect bites (bees and
wasps) antitoxins like Rabies or tetanus, and iodine-contrast media for IVPs
and MRIs. Anaphylaxis can occur rapidly and is a medical emergency.
Symptoms of anaphylactic shock include rapid, weak pulse, hypotension,
dyspnea, bronchial edema, crackles, wheezing, laryngeal edema,
angioedema, increased mucous, strider and death, if not treated immediately.

Slide 14 Treatment for shock must be initiated STAT. Respiratory and
cardiovascular systems must be assessed and monitored. Epinephrine
1:1000, 0.2 to 0.5 ml should be given either SQ or IV if severe to cause
vasoconstriction and bronchodilation. Benadryl IM or IV and Histamine H2
blockers such as Tagamet are given to decrease angioedema and urticaria

Slide 15 Oxygen is given to maintain O2 sat at above 90%. The head of the
bed should be raised to 45 degrees to assist with respiration. Blood pressure
should be maintained with fluids and vasopressors such as dopamine and
norepinephrine. Aminophylline is given IV at 6 mg/kg for severe
bronchospasns. Albuterol nebs may be given every 2 – 4 hours.

Slide 16 Vital signs, O2 sat, level of conscientious, cardiac and respiratory
status should continue to be monitored and the RN should anticipate CPR,
intubation and tracheotomy if necessary.

Slide 17 Other examples of anaphylactic reactions are called Atopic
reactions. These include allergic rhinitis, commonly known as hay fever,
bronchial asthma, atopic dermatitis, urticaria, and angioedema. Individuals
who experience these disorders have inherited an increased tendency to be
sensitive to the environmental allergens. Hay fever is the most common.
Symptoms are runny nose and eyes, sneezing, mucosal swelling and puritus
around the eyes, nose, throat and mouth. Symptoms of asthma are listed on
this slide.

Slide 18 Atopic dermatitis involves generalized skin lesions which are
vesicular and edematous. Urticaria or hives develops rapidly after exposure
to an allergen and lasts for minutes to hours. Hives represents a wheal-flare
response to the allergen. Angioedema is a localized skin reaction similar to
hives but involving deeper layers of skin and submucosa. Swelling is
usually seen in the eyelids, lips, tongue, larynx, hands, feet, GI tract and
genitalia. This can be a medical emergency if respiration is compromised.

Slide 19 Type II hypersensivity reactions are cytotoxic and cytolytic and
destroy cells by binding IgM and IgE to cell surfaces which activates
complement and phagocytosis. Examples of Type II reactions are blood
transfusion reactions because of blood incompatibility, and drug- related
hemolytic anemias. Goodpasture sysdrome is a rare disease in which the
lungs and kidneys are damaged due to endogenous antibodies interacting
with tissue antigens. Pulmonary hemorrhage and glomerulonephritis result.

 Slide 20 IgG and IgM form immune complexes in the body that get
deposited in vessel walls and extravascular tissues. Complement is activated
and chemical mediators of inflammation like histamine are released.
Neutrophils respond to the inflammation that is created by the immune
complexes, increasing tissue damage. Streptococcal infections are also
causes of Type III reactions.

Serum sickness caused by foreign serums like horse serum for anti tetanus.
Pencillins and sulfonamides can cause serum sickness. Serum sickness
produces fever, arthritis, uticaria, enlarged spleen and lymph nodes, 7 to 14
days after exposure .It is treated with adrenal cortical hormones-
glucocorticords and mineral corticoids- these medications decrease the
inflammatory process.

Slide 21 A Type IV reaction is a cell-mediated response, causing tissue
damage. The response takes 24 to 48 hours to occur. It is characterized by
an interaction between antigens and antigen-responsive T lymphocytes.
Examples are contact dermatitis, poison ivy, PPD and transplant rejection.

Slide 22 After the cause of the allergic response has been identified, the
client should avoid the allergen. This may simply involve avoiding certain
foods, but may require making life changes such as moving to a different
climate, changing occupations or giving up a pet. If a drug is the cause, he
should avoid it and wear a Medic Alert bracelet, identifying the allergy.
Drug therapy includes antihistimines for allergic rhinitis and urticaria. They
work by blocking the histamine receptor sites.
Sympathomimetic/decongestant drugs include Epinephrine (Adrenalin) is
the treatment of choice for anaphylactic reactions. Minor decongestants
include NeoSynephrine and Sudafed to treat allergic rhinitis. Corticosteroid
nose sprays are effective for allergic rhinitis and oral corticosteroids are
given for more severe allergic reactions. Antipruritics include topicals -
calamine lotion, coal tar solutions, menthol and camphor. Mast cell-
stabilizing drugs are used to asthma and allergic rhinitis. Examples are
Cromolyn (Nasalcrom) and nedocromil (Tilade). They block release of
histamines, leukotrienes and other chemicals from the mast cell after
antigen- IgE interaction.
Slide 23 The elderly have a decline in the immune system such as decreased
size and activity of the thymus, decreased production of T and B cells,
delayed hypersensitivity responses, decreased cell-mediated immunity,
greater susceptibility to infection and higher incidence of tumors.
The older adult should be encouraged a to eat well-balanced diet, drink
adequate fluids, and to get flu & pneumonia shots. They should practice
good handwashing. They should be taught to report fever or other signs of
infection, and changes in mental status, behavior or levels of activity

Slide 24 The symptoms listed above may indicated an problem with
immunity.

Slide 25 These sypmtoms are indicative of chronic allergies

Slide 26 Diagnostic tests used to confirm immunodeficiency problems
include a CBC with WBC differential including an absolute lymphocyte and
eosinophil count. Cellular immunodeficiency is diagnosed if the
lymphocyte count is below 1200/microliters. The eosinophil count is
elevated with type I hypersensitivity reactions involving IgE
RAST test measures the quantity of antigen-specific Ig E in the blood. It is
less sensitive and more expensive than skin testing and has no risk of
anaphalaxis. Skin tests involve pricking the skin with suspected allergens or
injecting interdermally. A local wheal-and-flare response indicates an
allergy to the allergen. A very sensitive person is at risk for having an
anaphylactic reaction.

Slide 27 HLA is done to determine if it matches the HLA of the donor prior
to transplant. Histocompatibility is essential prior to matching donors and
recipients of blood, bone marrow and organ transplants. The human
leukocyte antigen system is a series of inherited genes that occur on the sixth
chromosome in humans. If the HLA matches on 5 – 6 antigens, there is less
likelihood of rejection of the tissue. Crossmatching mixes blood from the
donor and potential recepient to determine any cytotoxic (anti-HLA)
antibodies to the donor blood. A negative crossmatch indicates no cytotoxic
antibodies are present and transplant should have a positive outcome.

Slide 28 In GVHD, the graft rejects the host. The new donor cells
recognize the host as foreign and within 7 to 30 days, the donor T cells
attack and destroy vulnerable host cells. GVHD targets the skin, GI tract
and liver. Symptoms include a painful, itching rash that begins on the soles
and palms and covers the chest, back and legs, causing desquamation. Liver
involvement includes mild jaundice and elevated liver enzymes. GI
symptoms include diarrhea, abdominal pain, bleeding and malabsorption.
The biggest problem is infection – bacterial, viral and fungal. GVHD is
most often seen following bone marrow transplant.

Slide 29 Calcineurin inhibitors inhibit production of T cytoxic lymphocytes.
Amtimetabolites suppress proliferation of T and B cells. Corticosteroids
suppress inflammatory response and inhibit cytokine production and T cell
activation. Typically, these three categories are used together. Please
review side effects in your Pharmacology and Nursing textbooks. Infections
are treated with antibiotics, antivirals or antifungals.

Slide 30 Risk for infection is the biggest problem with GVHD. Careful
handwashing for both client and the healthcare team is essential. Reverse
isolation, adequate hydration and nutrition, and good oral hygiene are a must
and careful monitoring for signs of infection and complications are required.

Slide 31 If the client has received an organ transplant, he should be
continually assessed for graft rejection. Signs of rejection include erythemia
and swelling over the site, and elevated temperature along with increased
WBC’s. This client should be assessed for GVHD and is treated with
immunosuppressive therapy and should be monitored for infection.

Slide 32 Autoimmune diseases are grouped according to organ-specific and
systemic diseases. Several systemic diseases will be covered in this course.
Organ-specific diseases will be covered in Advanced Adult Nursing and
Pediatric Nursing

Slide 33 This section discusses selected systemic autoimmune disorders of
the connective tissue.

Slide 34 Osteoarthritis, also known as degenerative joint disease, involves a
progressive deterioration and loss of cartilage in the joints. The cartilage
becomes soft and yellow resulting in a narrowing of the space between
joints. Bone spurs develop and there is uneven stress on the joints and
decreased motion.
Slide 35 A single cause for OA has not been identified, but it is related to
advancing age. Approximately 60% of clients over the age of 65 years have
symptoms of the disease. After the age of 50, it is twice as great in females,
which suggests decreased estrogen as a cause. Obesity is related to OA of
the knee. Strenuous exercise and sports injuries have been linked to OA.
Signs and symptoms include first, joint pain which gets worse with joint use.
As OA progresses, joints become more painful, and enlarged. Heberden’s
and Bouchards’ nodes may be found on the fingers. If the spine is involved,
the client may have difficulty sitting and rising from a chair. Knee
involvements results in altered gait. Joint pain is increased with falling
barometric pressure before rain. It is true that the client can predict rain “in
his bones”.

Slide 36 OA is diagnosed by history and physical. There are no lab tests,
although the Sed rate may be elevated if synovitis is present. Bone scan, CT
and MRI may show early joint changes and x-rays will show joint space
narrowing

Slide 37 The client with mild to moderate pain can use Tylenol and
Capsaicin cream for relief. The cream should not be used with a heating
pad. Other clients benefit from the NSAIDs or ASA. If the client
experiences muscle spasms, muscle relaxants such as Flexeril may be
necessary. Review your Pharmacology notes for more information on these
drugs.

Slide 38 The OA client needs to balance rest with activity. During acute
pain, the joint should be rested and placed in a functional position, using
pillows, splints, or braces. The joints should not be immobilized more than
one week to prevent joint stiffness. Heat or cold applications may be
helpful. Glucosamine and chrondroitin sulfate may help with synthesis of
new cartilage.

Slide 39 Weight loss is very beneficial for OA of the knee in the obese
client. A healthy diet should be followed for all OA clients. Surgery may be
indicated for some clients.

Slide 40 This slide lists some of the surgical treatment options.

Slide 41 Hyperuricemia is caused by increased uric acid production,
underexcretion of uric acid by the kidneys of increase of foods containing
purines (sardines, herring, muscles, liver, goose, sweetbreads). Stress,
alcohol, thiazide diuretics, immunosuppressive drugs, and prolonged fasting
can induce gout. Gouty arthritis usually affects no more than four joints, the
most common being the great toe. The onset is rapid and it usually subsides
in 2 to 10 days. Attacks can reoccur if not treated. Chronic gout involves
multiple joints and tophi develop, causing deformity

Slide 42 Diagnosis can usually be made on clinical symptoms alone. Serum
and urine uric acid levels will be elevated as will as WBC’s. Synovial fluid
aspiration is usually not necessary. Treatment includes life style changes
such as watching diet, losing weight if necessary and decreasing or avoiding
alcohol. The client should be monitored for kidney stones. Rest of the joint,
heat and cold applications may be helpful


Slide 43 Medications useful for treating gout are (1)Zyloprim which is
useful during the acute stage and as a maintanence drug to prevent further
attacks, (2) Colchicine used with NSAIDs and (3) Benemide which can’t be
used for clients who have reduced creatinine clearance. ASA must be
avoided because it inactivates Banemid. Cozaar may be useful in promoting
urate diuresis . Cozaar and Zyloprim may be given together

Slide 44 . RA is a chronic, systemic disease characterized by inflammation
of connective tissue in the synovial joints. The cause is unknown but it is
known to affect women between the age of 40 and 60, 2-3 times more often
than men. Smoking has also been linked to RA.

Slide 45 The autoimmune and genetic theories explains that a genetically
susceptible individual develops an abnormal IgG in response to a antigen,
and then develops autoantibodies known as rheumatoid factor (RF) against
the abnormal IgG. These combine to form immune complexes and are
deposited in the joints, causing inflammation and joint changes followed
later by cartilage and destruction by a pannus.

Slide 46 The pannus usually effects fingers, knees, and is worse in toes,
ankles, and feet.

Slide 47 This slide shows a pannus.
Slide 48 This slide list signs and symptoms of RA. Morning stiffness
usually occurs for one hour in the morning.
Please refer to your text for pictures of deformities on p 1726. Also note
complications of RA on p 1727

Slide 49 This slide lists several associated problems of RA. Caplan’s
syndrome causes fibrosis in the lungs and is seen a lot with coal miners.
Felty’s causes splenomegaly.

Slide 50 Diagnostic tests used to determine RA include (1) the ANA which
indicates the presence of an autoimmune disease and is positive in some
cases of RA, (2) the RF which is positive in about 80% of cases,

Slide 51 (3) and the sed rate and C-reactive protein tests which detect acute
and chronic inflammation. Elevated WBCs are present in synovial fluid
analysis. Bone scans, MRI and CT show early joint changes and can
confirm RA. As RA progresses, narrowing between joints and deformity
can be seen on x-ray.

Slide 52 DMARDs should be started early in the disease to prevent
disability. Plaquenil is indicated for mild cases. It is important that the
client have an eye exam every 6 months to monitor for irreversible retinal
degeneration.

Slide 53 NSAIDs , especially the Cox 2 inhibitors are frequently
prescribed. Aspirin relieves pain, but does not stop disease.
Gold Salts- decrease disease activity. Given PO or IM, but IM is more
effective.
Cytotoxic medications may slow down the disease.
Methotrexate is the drug of choice in moderate to severe cases. It has a
rapid antiinflammatory effect & relives symptoms in days to weeks.
Analgesics are used for pain control. Review these drugs in your
Pharmacology text.

Slide 54 Clients can benefit from hot and cold compresses and mild exercise
after the acute phase. Complementary therapies may be helpful. Clients
should be taught to eat a balanced diet, take NSAIDs with food, and to get
frequent mild exercise. Assistive devices may useful to protect the joints.

Slide 55 Systemic Lupus Erthmatosus is a chronic, multisystem disease that
occurs mostly in women in their 30sand 40s. The cause is unknown but it is
considered to be an autoimmune

Slide 56 Auto antibodies are produced by b cell hyperactivity, complement
is activated and immune complexes are deposited in body organs. SLE may
be drug induced by drugs such as procainamide and hydralazine. Symptoms
disappear when the Rx is discontinued.

Slide 57 Signs and symptoms depend on the organs involved. Vascular
lesions usually develop in sun-exposed areas with the classic butterfly rash
across the nose occurring in alopecia over lesions is common. Arthritis
occurs in more than 90% of cases. Arrhythmias can be fatal. Renal damage
can result in glomerulonephritis. Seizures and Organic Brain Syndrome
result from deposits of immune

Slide 58 No specific tests are diagnostic for SLE. ANA is present along
with other antibodies. Tests that are most specific are anti-double stranded
DNA and anti-Smith which are rarely found in other diseases. RF may be
positive because of the relation of RA to SLE ESR may be used to monitor
disease activity. Steroids are the drug of choice.

Slide 59 The client should be taught to monitor the skin for infection, to
avoid sun and to keep skin clean and dry. Because many clients are
immunosuppessed, they need to monitor for systemic infection and may
need reverse isolation. Depending on which organs are involved, symptoms
such as decreased urine output , neurological changes, and chest pain should
be assessed.

Slide 60 Systemic sclerosis is a chronic disease of the connective tissue in
which there is excessive formation of fibrous connective tissue and fibrosis
of the skin. The cause is an abnormal production of collagen. Clients
present with joint pain, tight shiny skin, no wrinkles, renal symptoms,
dysphasia, and GERD.

Slide 61 This slide lists CREST manifestations of Systemic Sclerosis.
Raynaud’s which is described as paroxysmal vasospasm in digits which
limits arterial blood flow when exposed to cold. Client experiences
blanching, followed by cyanosis and then erythema during rewarming phase.
May procede onset of SS by months or decades.) Skin changes are seen in
fingers & hands & the trunk. The face becomes expressionless. Joints in the
jaw and hands lose ROM. Internal organ involvement includes fibrosis of
the esophagus, causing GERD & difficulty swallowing . Lung involvement
causes pulmonary abnormalities. Congestive Heart Failure occurs from
fibrosis. Renal disease is progressive and is the major cause of death due to
renal failure. Drugs are used to treat the symptoms, but there is no cure.
There is no diagnostic test; the Sed rate may be elevated.

Slide 62 Nursing care is aimed at maintaining ROM and preventing
complications such as aspiration. The respiratory, cardiac and renal systems
need to be monitored closely for complications.

Slide 63 This section discusses HIV and Persons with AIDS.

Slide 64 Please review the etiology of HIV and AIDS from your
Fundamentals course.

Slide 65 The incidence of AIDS is increasing worldwide, especially in the
under 25 y/o population.

Slide 66 The Elisa test is used to diagnose HIV antibodies which can be
detected after 12 weeks. The Western blot test is used to confirm the
diagnosis. There are other tests on the market now, including ones that can
be done at home.

Slide 67 Normal CD 4 count is above 1000. When the count is 500 or
below, symptoms of HIV are seen. When the count is below200,
opportunistic infections begin and the client is sero converting to AIDS. The
amount of CD4 cell presence reflects the severity of the infection, as does
the viral load, referring to the amount of HIV in the bloodstream. The
higher the viral load, the more advanced the disease. As the virus continues
to kill cells bearing CD4 receptors, the CD4 cell count drops, signaling
progressive immunosuppression. Ultimately, after the development of an
AIDS defining illness, AIDS is diagnosed. Criteria for Diagnosis is CD4 +T
cell count below 200cells/microliter, or development of an opportunistic
infection or indicator condition such as TB, pneumonias, and invasive
cervical cancer. End-stage AIDS is defined as CD4 counts below 50.

Slide 68 There is no cure for AIDS, but medications are increasingly able to
control the disease and clients are living longer, healthier lives. New drugs
are being developed every day. The drugs of choice at present are the
antivirals in the reverse transcriptase inhibitors and the protease inhibitors
groups. The next 5 slides offer a brief review. Also, please review your
notes from your Medication Administration course.

Slides 69 – 73 Review

Slide 74 and 75 Because opportunistic diseases are frequently seen in the
AIDS client, medications are given to prevent or treat these diseases. Slides
75 and 76 are examples of prophylactic drugs which are used.

Slide 77 Two newer medications are Pentafuside, a fusion inhibitor which
prevents HIV’s binding to healthy T-cells, and Proleukin which boosts the
immune system.

Slide 78 Typically, a combination of several medications (HAART) is used.
Also, efforts to boost the immune system, such as a bone marrow transplant
and use of interleukins is used in some cases. Although drug therapy is the
major treatment, emphasis should also be placed on promoting health in the
immunosuppressed client. Diet, careful handwashing, avoiding infection and
taking medications properly are necessary components of treatment.

Slide 79 Education of the client with HIV is highly important in preventing
the spread of AIDS. Clients and their families need correct information to
prevent isolation of the client. The client and family also need to know the
signs and symptoms of opportunistic diseases, so that immediate treatment is
provided.

Slide 80 There are numerous nursing diagnoses that apply to the AIDS
client. Nutrition is a common problem due to nausea from medication and
the presence of thrush. Soft foods and high calorie, high protein foods
should be offered. Diarrhea is a common problem. Good skin care is
necessary to prevent further infections. The client will be fearful and may
lack support because of discrimination from others. He may have low self
esteem related to his diagnosis. This is a physically and emotionally
draining disease that always ends in death. The client may react with anger
or denial and may be noncompliant. He must be encouraged to make any
necessary lifestyle changes to modify the disease process. Individual and
group therapy is usually helpful.
Slide 81 Opportunistic infections may be caused by fungus, bacteria or
virus. The more common ones are pneymocystis carinii pneumonia,
cryptococcal meningitis, cytomegalovirus retinitis, mycobacterium avium
complex, Kaposi’s sarcoma, and AIDS – dementia complex

Slide 82 PCP is sometimes the first indication that the client has AIDS. In
HIV positive clients, it can be prevented by use of maintenance antibiotics.
Nursing intervention includes monitoring the respiratory status, fever
symptoms, administering oxygen, IV fluids and antifungals and nutrition.

Slide 83 This disease is caused by a fungus and is treated with antifungal
drugs. It is important that the client remain on maintenance drugs after the
acute stage is over because 50-75% will have a recurrence within a year
without them.

Slide 84 CMV can also effect the respiratory, GI and CNS. Ocular disease
does not appear until there is severe immunosuppression. Clients with AIDS
should have frequent eye exams so that CMV is detected and early treatment
with antivirals can begin.The goal is to prevent loss of vision, but even with
treatment, blindness may occur.

Slide 85 MAC frequently causes GI symptoms, especially chronic diarrhea
in HIV clients. Positive cultures can be isolated from the lymph nodes, bone
marrow or blood. Symptoms of MAC include diarrhea, abdominal pain,
fever, weight loss, malaise, anemia, neutropenia, malabsorption syndrome
and obstructive jaundice. Treatment is with the same antiinfectives that are
used for TB, which is also frequently seen in the immunosuppressed client.

Slide 86 KS is the most common neoplasm seen in AIDS clients. It occurs
in 21% of clients. It is thought to be caused by Human herpes virus. Small
lesions which are not painful are typically found on the skin and mouth.
Lesions may also be found in the lungs & GI tract and can cause bleeding &
respiratory distress. Diagnosis is made with biopsy. Successful treatment
with ARTs can resolve the disease. Other malignancies are treated with
chemotherapy as indicated.

Slide 87 ADC occurs in the terminal stages of AIDS and is caused by HIV
infection of the brain or other systemic opportunistic problems. If the cause
is reversible, such as dehydration, appropriate treatment is started. If not,
the client and family is supported to a comfortable death.

								
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