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Week 6
Immune Disorders
Infection
Human Immunodeficiency Virus
Genetics
Altered Immune Responses and Transplantation
Nursing Care of Clients with Lymph Disorders
Bacterial, Viral, and Fungal Infections: Prevention,
Assessment and Interventions.
Infectious Diseases are leading cause of death worldwide.
Previously controlled infections are re-emerging like malaria,
tuberculosis, and pertussis.
Newer infections have emerged over the last several decades
including Lyme disease, Human Immunodeficiency virus
(HIV), and Coronavirus (SARS)
Infectious Diseases in the US
 The resistance of microorganisms produced a level of
concern similar to infections in the pre-antibiotic era.
Example: VRE, MRSA.
 Bioterrorism is the latest threat involving
microorganism like smallpox, tularemia, plague and
anthrax.
 Virulence – the ability of the pathogen (disease
producing microorganism) to invade and injure the
host (person).
Risk Factors for Infections
Environmental
 Excessive alcohol consumption →→ malnutrition
 Smoking
 Malnutrition
Medication therapy (immunosuppressive agents)
 Glucocorticosteroid
 Cancer Chemotherapy
Chronic Diseases
 DM
 Adrenal Insufficiency
 Renal Failure
 Hepatic Failure
 Chronic Lung Disease
Causes of Infections
 Bacteria
 Micrograph of a bacteria colony forming. The bacterial colony is well
developed, and is showing the initial development of a biofilm. Some
of the round Cocci type bacteria are suspended in an adhesive matrix.
Virus
AIDS Virus
Virus are pathogenic organisms that use the host’s genetic
machinery to reproduce ( HIV, Hepatitis, Herpes Simplex)
Fungus
 Fungus in the head
Skin Fungus
Molds and yeast (Candida Albicans, Aspergillus)
Prions – Protein particles
Prions
 Prion is an infectious agent that is composed primarily
of protein. To date, all such agents have been
discovered to propagate by transmitting a misfolded
protein state; as with viruses the protein itself does not
self-replicate, rather it induces existing polypeptides in
the host organism to take on the rogue form.
 The misfolded form of the prion protein has been
implicated in a number of diseases in a variety of
mammals, including bovine spongiform
encephalopathy (BSE, also known as "mad cow
disease") in cattle and Creutzfeldt–Jakob disease (CJD)
in humans. All known prion diseases affect the
structure of the brain or other neural tissue.
Parasites – Protozoa/Helminths
Protozoa – Malaria, Toxoplasmosis
Helminths – Worms , flukes
Chain of Infection
↑ →→→→→→→Causative Agents→→→↓
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Cycle of Infection
Reservoir
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Portal of exit
Susceptible Host
from the host
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Port of entry to the host ←←←Mode of transmission
Diagnostic Procedures and Nursing Interventions
 White Blood Cell Count with Differential
- provide information about type of infection and the
body’s response to it.
-Normal is 5,000 to 10, 000 mm3.
-Count less than 4, 300/mm3 is called leukopenia. It
may indicate compromised inflammatory response or
viral infection.
- A count greater than 10, 000/mm3 indicates an
inflammatory response to a pathogen or a disease
process.
Differential on the laboratory report
Note: The percentage of one type of cell increases, the
percent of other types decreases.
Neutrophils – are among the first cells to respond to a
bacterial infection.
* a 70% increase in neutrophils indicates bacterial
infection.
This increase is often referred to as a “ shift to the
left.”
* A decrease in neutrophils is known as neutropenia.
An overwhelming infection can deplete the bone marrow of
neutrophils and produce neutropenia. Many antineoplastic drugs used
to treat cancer produce bone marrow depression and can significantly
lower the neutrophil count. Types of drugs that can produce
neutropenia include some antibiotics, the psychotropic drug lithium,
phenothiazines, and tricyclic antidepressants.
Lymphocytes – are the second most commonly occuring WBC’s .
Primarily respond to viral infections but also maybe elevated in case of
mononucleosis, TB, and some tumors.
Eosinophils – are elevated with allergic reactions and parasitic
infections.
Culture and Sensitivity
 Use standard precaution in collecting and handling
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specimens.
Properly labeled and deliver promptly.
Results are usually available preliminary bet. 24-48
hours and final results in 72 hours.
If the C and S result reveals the at the cultured
organism is not sensitive to prescribed antimicrobial
agents, it is the nurse’s responsibility to report the
result to the PCP before administering the subsequent
doses of ineffective antimicrobial.
An ATB that is sensitive to the organsism should be
prescribed.
Erythrocyte Sedimentation Rate
ESR – The rate at which RBCs settle out of plasma.
Normal adult value is between 15 to 20 mm/hr.
An increase indicates an active inflammatory
process or infection.
Immunoglobulin Electrophoresis
- Determines the presence of quantity of specific
immunoglobulin (IgG, IgA, IgM).
- Used to detect hypersensitivity disorders, autoimmune
disorders, chronic viral infections, immunodeficiency,
multiple myeloma, and intrauterine infections.
Antibody Screening Tests
 Detect the presence of antibodies against specific
causative agents.
 Positive antibody test indicates exposed client and
developed antibodies to a specific antigen but does not
indicate information whether client or not the client is
currently infected (e.g. HIV antibodies).
 Auto-antibody Screening Test – detects the presence of
antibodies against a persons own DNA (self cell).
Associated with autoimmune conditions such as
systemic lupus erythematosus, rheumatic arthritis.
Antigen test
 Detects the presence of a specific pathogen (e.g. HIV)
 Used to identify certain infections or disorders.
Gallium Scan
 A nuclear scan that uses a radioactive substance to
identify hot spots of WBCs within the client’s body.
 Radioactive Gallium citrate is injected IV and
accumulates in areas where inflammation is present.
 Other tests include CT scan, MRI, Biopsies to
determine the presence of infection, abscesses, and
lesions.
Sign and symptoms of Infections ( depends on type and
organ/tissue involve.
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Fever, chills
Fatigue, malaise
Enlarge lymph nodes
Rash, skin lesions, purulent wound drainage,
erythema
Change level of consciousness, dysphagia, nuchal
rigidity, photophobia, headache
Sore throat, hyperemia, enlarge tonsils
Nausea, vomiting, anorexia, abdominaal cramping
diarrhea.
Dyspnea, cough, purulent sputum, crackles.
Dysuria, urinary frequency, hematuria, pyuria.
NANDA Nursing Diagnosis for infection
 Fatigue
 Hyperthermia
 Pain (mild to moderate)
Nursing Interventions
 Administer antipyretics for fever and discomfort as prescribed.
 Administer antimicrobial therapy as prescribed.
 Encourage increased fluid intake or maintain IV replacement to
prevent dehydration.
 Implement infection control measures – standards, airborne, droplet,
and contact.
 Provide diversional activities if needed.
 Teach the client regarding:
- any infection control measures needed at home.
- Self administration of medication therapy.
- Complications that need to be reported immediately.
Complications
 Multi Drug resistant infections
 Sepsis
Meeting needs of Older Adult in Infections
Order adults are at increased risk for infection due to:
-Slowed response to ATB therapy
- Slowed immune response
- Loss of SC tissue, thinning of skin.
- Decreased vascularity and slowed wound healing
- Decreased cough and gag reflex
- Increased chronic illnesses
- Decreased gastric acid production
- Decreased mobility
- Bowel/bladder incontinence
- Dementia
- Greater incidence of invasive devices ( urinary catheter, TF,
tracheostomies, IV lines.
HIV/AIDS
HIV/AIDS
 Human Immunodeficiency virus is a retrovirus that is
transmitted through blood and body fluids.
 HIV Targets are CD4 lymphocytes also known as TCells or T-Lymphocytes.
 T-cells work in concert with B- Lymphocytes, both are
part of specific acquired (adaptive) immunity.
 HIV integrates its RNA into host cell DNA through
reverse transcriptase, reshaping the host’s immune
system.
Human Immunodeficiency Virus Infection
 Human Immunodeficiency Virus (HIV)
is a retrovirus that infects cell expressing CD4 on
their cell membranes primarily TH cells.
The HIV copies its RNA into the host cell’s DNA and
then remains quiescent until the host cell is activated
to mount an immunologic response.
Activation of the host TH CD4 cells also initiates
replication and production of the HIV RNA which is
released into the circulation. This newly made HIV
then infects other TH CD4 cells
HIV
 Transmission
- intimate sexual contact, unprotected sex (vaginal,
anal, oral)
- Multiple sex partners
- Occupational exposure (healthcare workers)
- contaminated needles ( needle sharing).
- contaminated blood products (unscreen blood
products)
- from mother to fetus (delivery), perinatal exposure
- mother to breast –feeding infant
HIV is found in different body parts and fluids:
 Transmitted though blood and body fluids (semen,
vaginal secretions)
 Found in breast milk, amniotic fluid, urine, feces,
saliva, tears, CSF, lymph nodes, cervical cells, corneal
tissue, and brain tissue but epidemiological studies
indicated that these are unlikely sources of infection.
HIV -Stages
Primary HIV-1 infection
 Initial Stage– 4-8 weeks – High level of virus are in the blood.
 Symptoms are generalized similar to flue.
 Marked by rapid rise in HIV viral load, decreased CD4+ cells and
decreased CD8 cells
CD8+ T-cells or killer T cell) belongs to a sub-group of T lymphocytes
(a type of white blood cell) that are capable of inducing the death of
infected somatic or tumor cells; they kill cells that are infected with
viruses (or other pathogens), or are otherwise damaged or
dysfunctional
 Resolution of clinical manifestations conincides with
decline in Viral HIV copies.
 Lymphadenopathy persist throughout the disease process.
Latent Stage – Chronic
 Inactive in infected, resting, T-CD4 host cells.
When the resting CD4 host is activated for an
immune response, the virus begins to replicate.
Levels of virus are high in the lymph nodes where
TH CD4 reside but low in the blood.
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Maybe prolonged and clinically silent (asymptomatic)
Client may be asymptomatic for 10 years or more.
Anti-HIV antibodies are produced (HIV positive)
Over time, the virus begins active replication using the
host’s genetic machinery.
- CD4 cells are destroyed, Viral load increases, and
dramatic loss of immunity.
Body Response
 T-cells and B- cells attepmts to destroy the Th CD4 cells
harvoring virus. However, the Tc cells and B cells are
cripled without adequate TH CD4 support.
 This latent stage can last 2 to 12 years, during which time
the patient is asymptomatic.
 During this time the number of CD4 cells declines.
Third Stage - AIDS
 The client begins to experience opportunistic infections.
Level of TH CD4 cells are usually below 500 cells/mm3 and
declining while levels of virus in the blood are increasing.
 Characterized by life threatening OIs.
 End Stage of HIV infection.
 This stage can last 3-5 years without treatment.
 Once the CD4 cells levels drops below 200 cells/mm3, the
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patient is considered to have acquired
immunodeficiency syndrome
(AIDS). Virus level in the blood is high, This stage ends in
death, usually within 1 year.
 ALL persons with AIDS have HIV, but not all persons with
HIV have AIDS.
Diagnostic Tests
Antibody Essay (+ within 3 weeks to 3 months
following infection)
ELISA
 ELISA less expensive screening of HIV antibody.
 Positive result on an enzyme linked immunosorbent
assay (ELISA) and confirmed with a positive result on a
WESTERN BLOT TEST
 Western blot should be done to confirm the results
because false positive do occur with ELISA.
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CD4+ Cell Count
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T cell count (CD4 Test) – decreased 750 cells/mm3
Measures the extent of immune damage from HIV.
Predicts disease process.
Clients with values below 200 cells/mm3 have an 85%
likelihood of progressing to AIDS within 3 years.
The CD4 Test
The main cell HIV attacks is called a T-helper cell
or CD4 cell. The T-helper cell plays an important
part in the immune system. It helps to coordinate
all the other cells to fight illnesses. Any damage to
T-helper cells can have a serious effect on the
immune system.
The CD4 Test
 The CD4 test measures the number of CD4 or
T-helper cells in the blood.
 The more CD4 cells in the client’s blood per
cubic millimeter, the stronger the client
immune system.
 The stronger the immune system, the better
the body can fight illnesses.
 A low CD4 count does not mean that client will
certainly become ill, but it makes it more
likely.
The CD4 Test
 The T-helper cell has a protein CD4 on its
surface.
 HIV needs the CD4 in order to enter the cells it
targets to infect.
 If HIV is able to enter the T-helper cell, it can
take over the cell and then use it to duplicate
itself.
 When HIV produces more copies of itself, the
amount of CD4 cells decreases.
 As a result, there are fewer cells available to
help the immune system to fight illnesses.
CD4 Test
 It is recommended that all patients with a CD4
count consistently below 200 should start
antiretroviral therapy.
 However, data suggest that it is better to take
action before the count has fallen so low.
 The general recommendation is for treatment
to begin when the CD4 count is between 200
and 350.
Other Blood tests/Tests
 CBC with Differential – abnormal – denotes anemia,
thrombocytopenia, and leukopenia.
 Platelet count decreased – prone to bleeding.
 Biochemical profile – e.g. liver studies – altered for
client receiving drug therapy.
 Brain or Lung MRI or CT scan - abnormal
Plasma HIV-1 RNA - The Viral Load Test
 Viral load refers to the amount of HIV in client’s
blood. The result of a viral load test indicates how
much virus there is in the blood and which can harm
the immune system.
 Increased ( > 1,5000 copies) – non detectable to
highly elevated (>100, 000 copies/ml)
Viral load increases coincides with active viral
replication.
Major complications
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Opportunistic Infections
fungal (candida albicans /thrust); red bleeding gums and oral
mucuous membranes.
Bacterial Infections – Mycobacterium
avium/tuberculosis.
Protozoan Infections - PCP, cryptosporidium,
toxoplasmosis
Viral Infections – cytomegalovirus (lung inflammation, colitis,
blindness); Herpes Simplex virus – painful vascular lesions, seizures,
blindness, deafness.
Wasting Syndrome – secondary to OP, malnutrition.
Secondary cancers (Kaposi sarcoma – purplish or brown lesions
Non-Hodkin’s B –Cell lymphomas (weight loss, fever, night sweats)
Dementia
Pt. With AIDS are high risk for Opportunistic Infections
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Fungal ( thrust)- Oral candidiasis
Parasitic Viral Infection – Herpes Simplex
Cytomegalovirus retinitis
Pneumocystis carinii Pneumonia
Cryptosporidium enteritis
Cryptococcus neoformans meningitis
Toxoplasmosis.
Pt. With AIDS are high risk for cancers (40%) of
patient with HIV
 Kaposi’s sarcoma
 Non-Hodgkin’s Lymphoma
 Anal cancer
 Cervical cancer
CNS effect
 Encephalophaty
 Cognitive impairment
 Dementia
Sign and Symptoms
 Initial stage – general flu-like symptoms
 Second and latent stage – may not experience any
symptoms
 Third stage – Pt may present for medical care complaining
of frequent persistent symptoms
 Fever, night sweats, swollen lymph nodes, or other
symptoms specific to the site of infection such as
headache, skin lesions that do not heal, sore throat,
dyspnea,
 Burning with urination, or diarrhea.
 Extreme fatigue and weight Loss
 Any of these symptoms coupled with Hx unprotected Sex
with person possibly infected with HIV, Hx of IV drug
abuse using shared needles, or a history of a blood
transfusion before 1989 warrants consideration of
diagnosis of HIV
Medical Treatment
 There is no cure for HIV. The medical treatment of
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HIV infection is symptomatic and aimed at reducing
the viral load, preventing and treating infections and
treating malignancies.
Early stages – outpatient treatment
Maintain balance diet
Exercise regularly
Maintain good dental hygiene
Stop smoking and using illicit drugs
Minimize stress
And practice safe sexual habits.
NANDA NURSING DIAGNOSIS
 Risk for infection
 Imbalanced Nutrition: less than body requirements
 Fatigue/activity Intolerabce
 Fluid Volume Deficit
 Ineffective Coping
 Ineffective therapeutic regimen management.
Nursing Interventions
 Provide Client teaching
- Transmissions, infection control measures, safe sex practices.
- Need for well balanced diet, self administration of prescribed
medications and potential s/e.
- s/s that need to be reported immediately (infection).
- The need for frequent follow-up monitoring CD4 and viral count.
- Identify factors that may interfere with nutrition and correct if possible
- Encourage activity alternated with rest periods
- Administer supplemental Oxygen as needed
- Provide analgesia as needed.
- Provide skin care as needed/
- Emphasize the importance of carefully complying with anti-retroviral
dosing schedules.
- Encourage use of constructive coping mechanisms.
- Assist the client with identifying primary support systems.
- Refer the client to local AIDS support groups as appropriate.
Opportunistic Infections Management
 Implement and maintain anti-retroviral drug therapy as
prescribed. (HARRT- highly active antiretroviral therapy)
Protease Inhibitor – Indinavir, Saquinavir
Nucleoside reverse transcriptase inhibitors – didasone, zidovudine.
Nonnucleoside reverse transcriptase inhivitors – nevirapine,
delavirdine
Antineoplastic-interferon alpha 2a,
interferon alpha 2 b
Antibiotics – Isoniazid, azithromycin, ripamfin
Antifungals – amphotecirin B, Fluconazole
Antidiarrheals – diphenoxylate HCL, atropine
Antidepressant – Paroxetine, sertraline
Analgesics – Opioids, NSAIDS
Appetitte stimulants ( Megace)
Antivirals – ganciclovir.
Nursing Interventions
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Monitor for skin breakdown
Maintain fluid intake
Maintain nutrition
Teach client to report s/s of infection immediately to PCP.
Wasting syndrome – Maintain nutrition orally or by TPN if
indicated. Provide between meal supplemental snack.
Serve at least six small frequent feedings with high value
protein.
 Fluid/Electrolyte Imbalance – Monitor fluid/electrolyte
status. Report abnormal lab. Data promptly, Maintain IV
fluid replacement.
 Seizures (HIV encephalopathy)
maintain client safety. Implement seizure precautions.
HIV Structure
 These pictures show the structure of the Human Immunodeficiency Virus (HIV). The
outer shell of the virus is known as the viral envelope. Embedded in the viral envelope is a
complex protein known as env, which consists of an outer protruding cap glycoprotein (gp)
120, and a stem gp41.
Within the viral envelope is an HIV protein called p17 (matrix), and within this is the viral
core or capsid, which is made of another viral protein p24 (core antigen).
The major elements contained within the viral core are two single strands of HIV RNA, a
protein p7 (nucleocapsid), and three enzyme proteins, p51 (reverse transcriptase), p11
(protease) and p32 (integrase).
Nucleoside Analogs - NRTIs
 AIDS drugs known as nucleoside analogues. The first group of
antiretroviral drugs are the Nucleoside Reverse Transcriptase
Inhibitors (NRTIs). They were the first type of drug available to
treat HIV and AIDS in 1987 and are better known as nucleoside
analogues or nukes. HIV needs an enzyme called reverse
transcriptase in order to be able to infect healthy cells and
reproduce itself in a person's body. As the name says, NRTIs
inhibit reverse transcriptase. The drugs slow down the
production of the reverse transcriptase enzyme and make
HIV unable to infect cells and duplicate itself.
Protease Inhibitors - PIs
 Protease inhibitors (PI). They were first approved in 1995.
 Protease inhibitors, as the name says, inhibit protease. Almost every living cell
contains protease.
 Protease is a digestive enzyme that breaks down protein and is one of
the many enzymes that HIV uses to reproduce itself. The protease in HIV
attacks the long healthy chains of enzymes and proteins in the cells and
cuts them into smaller pieces.
 These infected smaller pieces of proteins and enzymes continue to infect
new cells.
 The protease inhibitors take effect before the protease in HIV has the
chance to break down the protein and enzymes. This way the protease
inhibitors slow down the duplication of the virus and thus prevent the
infection of new cells. The NRTIs and NNRTIs only have an effect on newly
infected cells.
 Protease inhibitors are able to slow the process of immature noninfectious virus becoming mature and infectious. Protease inhibitors
also work in cells that have been infected for a long time, by slowing
down the reproduction of the virus.
Antiretroviral treatment
Antiretroviral treatment for HIV infection consists of
drugs, which work against HIV infection itself by
slowing down the reproduction of HIV in the body.
The drugs are often referred as antiretrovirals, antiHIV drugs or HIV antiviral drugs
AZT - Antiviral Medication
This is a picture of AZT, the first approved antiretroviral drug for treatment
of HIV and AIDS. In March 1987, the U.S Food and Drug Administration
(FDA) approved AZT to be used as a treatment for AIDS.
CANCERS
Cancer – Neoplastic Disease Process
 Abnormal cell growth and differentiation
 Exact cause – unknown
 Cancer cells invade surrounding tissues and spread to
other areas.
 Trigger factors may include viruses, physical and
chemical agents, hormones, genetic and diet.
Carcinomas – epithelial tissues
Adenocarcinomas – glandular glands
Sarcomas – mesenchymal tissues
Leukemias – malignancies of blood forming cells
Lymphomas – lymph tissues
Multiple myeloma – plasma cells and affects the bone.
Risk Factors
 Age
 Genetic Predispositions
 Exposures t chemicals, viruses, tobacco, and alcohol
 Diet high in fat and red meat, low in fiber
 Sun, ultraviolet light, or radiation exposure, (radon)
 Sexual lifestyle, Multiple sexual partners, STD,
HIV/AIDS
 Other risk factors are poverty, obesity, and chronic
GERD
Diagnostic Procedure
 Tissue biopsy – definitive diagnosis of abnormal
cancer cells.
 CBC and Differential – screening for leukemias
 Chest X-Ray, CT scan, MRI, PET scan – visualized
tumors, metastasis or progression of cancer.
 Tumor Marker Essay – CEA,CA 124, Alphafetoprotein)
– screening for cancers of the colon, pancrease,
prostate, liver, uterus, and ovaries. Elevated values
suggestive of cancer.
Therapeutic procedures
 Radiation – ionizing radiation of tissue by the path of the radiation
beam resulting to death of cells. S/E include skin changes, hair loss,
and debilitating fatigue.
 Internal Radiation Therapy- Client should be place on a private room and bath
- Appropriate signage should be place on the door
warning of the radiation source.
- healthcare personnel should wear a dosimeter film badge that
records the amount of radiation exposure.
- visitors should be limited to 30 min visits and maintain distance of 6
feet.
- Visitors and health care personnel who are pregnant or under the age
of 16 should not come in contact with the client.
- A lead container should be kept in the client’s room if the delivery
method could allow spontaneous loss of radioactive material.
- Precautions listed above should be carried out at home if the client is
discharge during therapy.
External Radiation
 Wash skin over irradiated area gently with mild soap
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and water and dry thoroughly using patting motions.
Do not remove radiation “tattoos” that are used to
guide therapy.
Do not apply powders, ointments, lotions or perfumes
to irradiated skin.
Wear soft clothing over irradiated skin and avoid tight
or constricting clothes.
Do not expose irradiated skin to sun or heat source.
Surgical Excision
 Diagnostic , curative, or palloative. Risk of seeding.
 Chemotherapy
certified provider administers systemic or local
cytotoxic medications to destroy rapid dividing cells.
Often combination of anticancer medications are used
and significant adverse effect is
IMMUNOSUPPRESSION ( bone marrow supression).
measures must be employed to reduce the risk
especially at the medications “nadir”.
Nausea and vomiting, alopecia, and mucositis are
common side effects. Take measures to prevent
extravasation of vesicants.
Sign and Sypmtoms
 CAUTION
C – change in bowel or bladder habits
A – a sore that does not heal
U – unusual bleeding or discharge
T- thickening of a lump in the breast or elsewhere
I – Indigestion or difficulty swallowing
O- obvious change in warts or moles
N- nagging cough or hoaseness
Weight loss
Fatigue and weakness
Pain
Nausea and anorexia.
NANDA Nursing Diagnosis
 Anticipatory grieving
 Risk for infection
 Fear/anxiety
 Imbalanced Nutrition: Less than body requirements
 Ineffective Tissue perfusion
Nursing Interventions
 Encourage screenings (pap smears , mammogram,
colonospcopy, stool for OB)
 Implement pain control measures as prescribed.
 Encourage /maintain fluid intake – premdedicate prior to
eating antinausea (odansetron- Zofran)
administer appetite stimulant (megace)m add protein
powder to feedings.
Reduced risk for Neutropenia
 Protect client from possible source of infection.
 Use hand hygiene
 Avoid crowds while undergoing chemotherapy
Administer colony-stimulating factors Neupogen – stimulate
WBC production.
Nursing Interventions
 Reduce risk of anemia administer recombitant
erythropoeitin alpha as prescribed.
 Reduce risk of Thrombocytopenia – avoid NSAIDs and
IM injections if platelet count is decrease.
 Maintain IV fluids
 Implement post-radiation care if applicable
Interventions are based on site of radiation.
Antidiarrheals for GI Tract, Mouthcare for head and neck,
administer Octrotide ( Sandostine) as prescribed.
 Encourage female client to wear hat or wig if undergoing
radiation or chemotherapy that produces alopecia.
Children – offer a baseball
 LISTEN TO CLIENT’s CONCERN
 Avoid false reassurance
 Allow time to disscuss feelings regarding loss and grieve.
Complications and Nursing Implications
 Oncologic Emergencies
Syndrome of Inappropriate Antidiuretic Hormone
( SIADH). Monitor hyponatremia and serum osmolality.
Administer Lasix IV, IV NS and/or Hypertonic saline as
prescribed for severe hyponatremia.
Spinal Cord Compression – related to metastasis. Assess
the client’s neurological status, including motor, and
sensory deficits. Administer corticosteroid as prescribed.
Support the client during radiation therapy.
Hypercalcemia
Superior vena cava Syndrome – Position in high Fowler’s
position.
Dissiminated intravascular Coagulation – Observe the
client for bleeding and apply pressure as needed.
Autoimmune Disorders
 Normally, the immune system recognizes that the
tissues in the body are not "foreign" and does not
attack them. If a transplant is performed, however, the
immune system usually recognizes that the organs that
are transplanted are different and attacks them, a
process called rejection.
 Drugs that reduce the activity of the immune system
(immunosuppressants) are typically given to persons
who have received transplants, unless the donor is an
identical twin.
 Cancer cells are sometimes different enough from
normal cells that the immune system attacks them,
but the immune response alone is usually not enough
to keep a cancer from spreading.
What are autoimmune disorders?
 Autoimmune disorders are diseases caused by the
body producing an immune response against its
own tissues. The cause of autoimmune diseases is
unknown, but it appears that there is an inherited
predisposition to develop autoimmune disease in
many cases.
 In a few types of autoimmune disease (such as
rheumatic fever), a bacteria or virus triggers an
immune response, and the antibodies or T-cells
attack normal cells because they have some part of
their structure that resembles a part of the
structure of the infecting germ.
Localized Autoimmune Diseases
 Rheumatoid arthritis (joints; less commonly lung,
 Lupus [Systemic Lupus Erythematosus] (skin,
joints, kidneys, heart, brain, red blood cells, other)
 Scleroderma (skin, intestine, less commonly lung)
 Sjogren's syndrome (salivary glands, tear glands,
joints)
 Wegener's granulomatosis (sinuses, lungs,
kidneys)
 Primary biliary sclerosis, Sclerosing cholangitis,
Autoimmune hepatitis (liver)
 Polymyalgia Rheumatica (large muscle groups)
 Temporal Arteritis / Giant Cell Arteritis (arteries of
the head and neck) skin)
Systemic Autoimmune Diseases
 Type 1 Diabetes Mellitus (pancreas islets)
 Hashimoto's thyroiditis, Graves' disease (thyroid)
 Celiac disease, Crohn's disease, Ulcerative colitis
(GI tract)
 Multiple sclerosis, Guillain-Barre syndrome
(central nervous system)
 Goodpasture's syndrome (lungs, kidneys)
 Addison's disease (adrenal)
 Raynaud’s phenomenon (fingers, toes, nose, ears)
Rheumatoid Arthritis
 Is a chronic, systemic, progressive inflammatory disease of the synovial
tissue.
 A bilateral systemic inflammatory disease process involving multiple
joints.
 Classified as an autoimmune disease process which antibodies are
formed against synovial tissues include synovial membrane, articular
cartilage, joint capsule, tendon and ligaments surrounding the joints,
involvement of the disease is one of exacerbations and remissions.
 The natural course of the disease is one of exacerbations and remisions.
 Inflammation and tissue damage can cause severe deformities that
greatly restrict function.
Risk Factors
 Female gender
 Age 20 to 50 years
 Genetic Predisposition
 Epstein Barr Virus  The Epstein-Barr Virus (EBV), also called Human
herpesvirus 4 (HHV-4), is a virus of the herpes family
(which includes Herpes simplex virus and
Cytomegalovirus ), and is one of the most common
viruses in humans. Most people become infected with
EBV, which is often asymptomatic but commonly causes
infectious mononucleosis.
Diagnostic Procedures
Diagnostic Procedures and Nursing Interventions
Rheumatoid Factor ( RF) antibody
 Diagnostic for Rheumatoid Arthritis + 1:40 to 1:60 (
normal < 1:20 Antinuclears Antibody ( ANA) titer (
antibody produced against one’s own DNA) high titer
correlate with severe disease.
 A ( +) ANA titer is associated with RA ( normal is
negative ANA titer at 1:20 dilution).
 Erythrocyte Sedimentation Rate (ESR) : ELEVATED
 20 – 40 mm/hr = mild inflammation
 40 – 70 mm/hr = moderate inflammation
 70- 150 mm/hr = severe inflammation
Arthrocentesis
 Synovial fluid aspiration by needle
 With RA, increased white blood cells ( WBC) and RF are present.
 S/S (clinical findings depend on the area affected by the disease process)
- Pain at rest and with movement
- Morning stiffness
- joint deformity
- Anorexia/weight loss
- Fever ( generally low grade)
- Fatigue
- Muscle weakness/atrophy
What to assess or monitor?
 Pain ( character, intensity, effectiveness of relief measure)
 Functional ability
 Indications of infections
NANDA NURSING Diagnosis
 Fatigue
 Impaired physical mobility
 Chronic pain
 Disturbed body image
 Risk for injury
Nursing Interventions
1.
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2.
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3.
4.
5.
6.
Apply heat or cold to areas affected as indicated based on
client response.
Morning stiffness (hot shower)
Pain ( heated paraffin)
Edema ( cold therapy)
Assist with and encourage physical activity to maintain
joint mobility ( w/in capabilities of the client)
Maximize functional activity, minimize pain, conserve
energy ( pacing activities and rest periods)
Provide a safe environment - facilitte use of assistive
device.
Utilize progressive muscle relaxation.
Monitor the client for s/s of fatigue.
Refer the client to support groups as appropriate
Nursing Interventions
7. Administer medications as prescribed.

Analgesics

Anti-inflammatories – NSAIDS
e.g. Plaquinel (hydroxychloroquine), Azulfidine
(sulfasalazine)
 Steroid e.g. Prednisolone ( Prednisone) – monitor for
fluid retention , HTN and renal dysfunction.
 Immunosuppressants - slow the progression of
disease e.g. Methotrexate ( rheumatrex),
cyclophosphamide( Cytoxan), Leflunomide ( e.g
Arava). Monitor for toxic effects ( bone marrow
suppressions, increased liver enzymes).
Nursing Interventions
 Administer Biological response Modifiers – inhibit the
action of tumor necrosis factor ( TNF)
- E.g etanercept ( Enbrel), infliximab ( Remicade),
adalimumab (Humira) and Anakinra ( kineret)
- Do not administer if client have serious infection.
- Monitor for injection/infusion reactions
- Monitor CBC and the client for signs of infections.
 Monitor for medication effectiveness ( reduced pain,
increased mobility)
 Teach the client regarding s/s that needs to be
reported immediately ( fever, infection).
Complications and Nursing Implications
 Sjoren’s syndrome ( dry eyes, dry mouth, dry vagina)
 Joint deformity ( tendon rupture, secondary
osteoporosis).
 Vasculitis ( ischemic organs)
 Cervical sublaxation ( risk of quadriplegia and
respiratory compromise).
GENETICS
Genetics
 Genetics has profound impact on health and disease.
 More than 4000 diseases are though to be related to
mutated genes.
 Common disorders like heart diseases and most
cancers arise from a complex interplay among multiple
genes and between genes and factors in the
environment.
 The study of principles of genetics is very important to
nursing. The ability to know basic genetic principles
will enable nurses to become prepared to assist the
patient and their family in dealing with genetic issues.
Basic Principles of Genetics
 Genes are transmitted from parents to their offspring.
 Genes are basic units of heredity – approximately
20,000 to 25,000 genes in each person’s genetic makeup or genome.
 Any change in gene structure leads to a mutation that
may alter the type and amount of protein produces.
 Each gene has a specific location on a chromosome
termed a locus.
 Alelle is one of two or more alternative forms of a gene
that occupy corresponding loci on homologous
chromosomes.
Basic Principles of Genetics
 Chromosomes are contained in the nucleus of the cell
and occurs in pairs. There are 23 pairs of chromosomes
and are said to be homologous and are termed
autosomes.
 Autosomes are the same is males and females.
 The sex-chromosomes make-up the 23rd pair of
chromosomes. A female has two X chromosomes. A
male has one X and one Y chromosomes. One
chromosome of each pair is inherited from the mother
and the father.
 The sperm cell of the father carries either a X or Y
chromosomes.
Basic Principles of Genetics - DNA
 DNA – Genes are made up of a nucleic acid called
deoxyribonucleic acid that stores genetic information
and encodes the instruction for synthesizing specific
proteins needed to maintain life.
 DNA also dictates the rate at which protein will be
made.
 DNA is made up of 4 nitrogeneous bases known as
adenine, thymine, guanine, and cytosine.
Basic Principles of Genetics- RNA
 Ribonucleic acid is very similar to DNA . Lack thymine and
instead contains uracil. RNA is single stranded and
contains ribose instead of deoxyribose sugar.
 RNA transfers the genetic information obtained from DNA
to the proper location for protein synthesis and plays a
critical role during synthesis of protein.
 Protein synthesis – transcription and translation.
 Human Genome Project – initiated in 1990 and completed
in 2003 is international effort to map all 20,000 to 25,000
human genes and determine the complete sequence of
more than 3 billion DNA bases.
Basic Principles of Genetics - Alleles
 When two gene pairs are different alleles, the allele that is
fully expressed is the dominant allele. The other allele that
lacks the ability to express itself in the presence of a
dominant allele is the recessive allele.
 Physical traits expressed by a person are termed the
phenotype, and the actual genetic makeup of a person is
termed as genotype.
 Cell Division
Mitosis – results in formation of genetically identical
daughter cells.
Meiosis – occurs in sexual reproductive cells.
 Nondisjunction – results to disorders such Down
Syndrome and Turner Syndrome. These disorders are
characterized by physical and/or mental defects.
Disorders Resulting from Nondisjunction
 Nondisjunction – failure of the two chromosomes to
separate during meiosis causing an abnormal number of
chromosomes. The oocyte or the sperm may have two
copies of the same chromosomes or missing one.
 Down Syndrome - trisomy 21, or trisomy G, is a
chromosomal disorder caused by the presence of all or part
of an extra 21st chromosome.
 Often Down syndrome is associated with some impairment
of cognitive ability and physical growth , and a particular
set of facial characteristics. Down syndrome in a fetus can
be identified with amniocentesis during pregnancy, or in a
baby at birth.
 Individuals with Down syndrome tend to have a lower than
average cognitive ability, often ranging from mild to
moderate developmental disabilities.
Turner Syndrome
 Turner syndrome or Ullrich-Turner syndrome (also
known as "Gonadal dysgenesis" encompasses several
conditions, of which monosomy X (absence of an entire sex
chromosome) is most common. It is a chromosomal
abnormality in which all or part of one of the sex
chromosomes is absent (unaffected humans have 46
chromosomes, of which two are sex chromosomes).
 Typical females have two X chromosomes, but in Turner
syndrome, one of those sex chromosomes is missing or has
other abnormalities.
 In some cases, the chromosome is missing in some cells but
not others, a condition referred to as mosaicism or 'Turner
mosaicism'.
Inheritance Pattern
 Genetics disorders can be categorized into autosomal
dominant, autosomal recessive, or sex-linked (xlinked) recessisve disorders
 If the mutant gene is located on an autosome, the
genetic disorder is called autosomal.
 If the mutant gene is located on the x-chromosome,
the genetic disorder is called x-linked.
Autosomal Dominant Disorders
 Caused by mutation of a single gene pair (heterozygous) on
a chromosome. Dominant allele prevails over a normal
allele. Shows variable expression.
 Variable expression means that the symptoms expressed by
the individual with the mutual gene vary from person to
person even if they have the same mutated gene.
 Although autosomal dominant disorders have a high
probability of occurring in families, sometimes these
disorders caused a new mutation or skip a generation. This
is called incomplete penetrance.
Autosomal Dominant Disorders
(The Pediatric Orthopaedic Society of North America 2010
(www.posna.org)
 Autosomal dominant disorders are relatively commonly seen in orthopedic
practice.
 Affected individuals are heterozygous, with one normal and one mutated gene.
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Since the mutated gene determines phenotypic expression, the disorder is
characterized as dominant.
Homozygosity is generally fatal. Variable expressivity is characteristic of
autosomal dominant disorders.
Transmission is characterized by one half of offspring of affected individuals
being affected, regardless of sex.
Examples of autosomal dominant disorders are achondroplasia,
pseudoachondroplasia, the multiple epiphyseal dysplasias, chondrodysplasias,
osteogenesis imperfecta, Marfan syndrome, polydactyly, hereditary motor
sensory neuropathies I and II (Charcot-Marie-Tooth disease), myotonic
dystrophy, and neurofibromatosis.
A common feature of autosomal dominant disorders is that they are structural
disorders. While they may impair function and have some reduction in life
expectancy, survival to at least reproductive age is the rule.
Autosomal Dominant Disorders
Autosomal Dominant Disorders
 In the case of autosomal dominant genes, a single
abnormal gene on one of the autosomal chromosomes
(one of the first 22 "non-sex" chromosomes) from
either parent can cause the disease. One of the parents
will have the disease (since it is dominant) in this
mode of inheritance and that person is called the
CARRIER. Only one parent must be a carrier in order
for the child to inherit the disease.
Common Diseases on each category
 Autosomal Dominant:
- Huntington’s Disease
- Familial Hypercholesterolemia
- Neurofibromatosis
- Breast and Ovarian Cancer elated to BRCA genes
- Marfan Syndrome
- hereditary nonpolyposis colorectal cancer
 Autosomal Recessive:
- Cystic Fibrosis
- Tay-Sach’s Disease
- Phenylketonuria
- Sickle –Cell Disease
- Thallasemia
 Sex-linked Recessive
- Hemophilia
- Duchenne Muscular Dystrophy
- Wiscott-Aldrich Syndrome
Gene Therapy
Autosomal Recessive Disorders
 Are caused by mutation of two gene pairs
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(homozygous) on a chromosomes.
A persons who inherits one copy of the recessive allele
does not develop the disease because the normal allele
predominates. However such person is a carrier.
The risk of two heterozygotes, or carriers, having an
affected child is 25%, 1 in 4, for each child that they
have. On the contrary, there is a 3 in 4 chance that
each child will not be affected.
Males and females are at equal risk for being affected.
Two affected individuals usually produce children all
of whom are affected as well.
Autosomal Recessive Disorders
X-linked Recessive Disorders
 They are caused by mutation of the X-chromosomes.
 Usually men are affected by this disorder because
women who carry the mutated gene on one Xchromosome have another X chromosome to
compensate for the mutation.
 However, women who carry the mutated gene can
transmit the mutated gene to their offspring.
X-linked Diseases
 X-linked diseases usually occur in males. Males have only one X
chromosome. A single recessive gene on that X chromosome will cause
the disease.
 The Y chromosome is the other half of the XY gene pair in the male.
However, the Y chromosome doesn't contain most of the genes of the X
chromosome. It therefore doesn't protect the male. This is seen in
diseases such as hemophilia and Duchenne muscular dystrophy .
 TYPICAL SCENARIOS
For a given birth, if the mother is a carrier (only one abnormal X
chromosome) and the father is normal:
 25% chance of a normal boy
 25% chance of a boy with disease
 25% chance of a normal girl
 25% chance of a carrier girl without disease
If the father has the disease and the mother is normal:
 100% chance of a normal boy
 100% chance of a carrier girl without disease
X-linked Diseases
 X-LINKED RECESSIVE DISORDERS IN FEMALES
 Females can get an X-linked recessive disorder, but this is very rare. An
abnormal gene on the X chromosome from each parent would be required,
since a female has two X chromosomes. This could occur in the two scenarios
below.
For a given birth, if the mother is a carrier and the father has the disease:
 25% chance of a healthy boy
 25% chance of a boy with the disease
 25% chance of a carrier girl
 25% chance of a girl with the disease
If the mother has the disease and the father has the disease:
 100% chance of the child having the disease, whether boy or girl.
 The odds of either of these two scenarios are so low that X-linked recessive
diseases are sometimes referred to as “male only” diseases. However, this is not
technically correct.
 Female carriers can have a normal X chromosome that is abnormally
inactivated. This is called "skewed X-inactivation." These females may have
symptoms similar to those of males.
Multifactorial Inhireted Conditions
 These are caused by a combination of genetic and
environmental factors.
 These disorders run in the families but do not show
the same inherited characteristics as the single-gene
mutation conditions.
 Mutifactorial conditions are poorly understood but
include Diabetes Millitus, Obesity, Hypertension,
Cancer, and Coronary Artery Diseases
Gene Therapy
 Is an experimental technique that is used to replace or
repair defective or missing genes with normal genes.
 It is currently only being tested for the treatment of
diseases that have no other cures
 Started with gene therapy trials in children with severe
combined immunodeficiency disease caused by adenosine
deaminase deficiency. T Lymphocytes from these children
were obtained, and the missing gene was inserted into
these T Cellsto produce the missing enzymes, and these
children were capable of developing a functioning immune
system.
Nursing Management
 The role of the nurse in Genetics is to be able to assist
client and family in making critical decision related to
genetic issues such as genetic testing.
 Collaborate with the team or physician to involve a
genetic counselor.
 Give client and families accurate information
pertaining to genetics, genetic diseases and
probabilities of genetic disorders. (See Punnet squares
figure 14.4 Lewis pp. 218.
Stem Cells
 Use of stem cells may allow for regeneration of lost tissue
and restoration of function in diseases such as Parkinson’s
Disease, Alzheimer’s Disease, Heart Disease, Diabetes
Millitus and Spinal Cord Injuries.
 Stem cells in the body that have ability to differentiate into
other cells. Stem cells can be divided into two types:
embryonic and adult.
 Embryonic stem cells have the ability become anyone of the
hundred of types of cells in the human body.
 Adult stem cells – are undifferentiated cells that are found
in small numbers in most adult tissues.
 Found in children and can be extracted from umbilical
cords. Their role in the body are to maintain and repair
tissues in which they are found. Multipotent cells.
Normal Immune Response
 Immunity is a state of responsiveness to foreign substances
such as microorganisms and tumor proteins.
Immune Response serves three functions:
 Defense – The body protects against invasion by
microorganisms and prevents the development of infection
by attacking foreign antigens and pathogens.
 Homeostasis – Damaged cellular substances are digested
and removed. Through this mechanism, the body’s
different cell types remain uniform and unchanged.
 Surveillance – mutations continually arise in the body but
are normally recognized as foreign cells and destroyed.
Types of Immunity
 Innate ( Natural)
 Acquired
 Innate immunity exist in a person without prior
contact with an antigen. Involves nonspecific response
and neutrophils and monocytes are primary WBC
involved. Ex. Species specificity of infectious agents
 Acquired Immunity – is the development of immunity,
either actively or passively.
Types of Immunity
 Active Acquired Immunity – results from the invasion
of the body by foreign substances such as
microorganisms and subsequent development of
antibodies and sensitized lymphocytes. With each
reinvasion of the microorganisms, the body responds
more rapidly and vigorously to fight off the invader.
May results naturally from a disease or artificially
through inoculation of a less virulent antigen (e.g.
immunizations). Immunity develop on this is long
lasting.
Active Acquired Immunity
e.g. Natural contact with antigen through clinical
infection (from chickenpox (varicella), measles
(rubeola), and mumps).
e.g. Artificial – immunization with antigen
(immunization with live attenuated virus or killed
vaccines). E.g. MMR, DTaP, HAV, HBV.
Passive Acquired Immunity
 Implies that the host receives antigen rather than
synthesizing them.
 This may take place naturally through the transfer of
immunoglobulins across the placental membrane
from the mother to fetus.
 Artificial passive acquired immunity occurs through
injection with gamma globulin ( serum antibodies).
 Immunity provides immediate benefits but passive
immunity is short lives because the host did not
synthesize the antibodies and consequently does not
retain memory cells for the antigen.
Antigens
 Substance that elicit an immune response.
 Most are composed of protein.
 Some are large polysaccharides, lipoproteins, and
nucleic acids.
 All of the body organs have antigens on their surface
that are unique to each person and enable the body to
recognize itself.
 The immune system becomes “ tolerant” to the body’s
own molecules and therefore nonresponsive to “self”
antigens.
Lymphoid Organs
 The lymphoid system is composed of central and
peripheral lymphoid organs.
 Central lymphoid organs are the thymus glands and
bone marrow.
 Peripheral lymphoid organs are the tonsils, gut,
genital, bronchial, and skin associated lymphoid
tissues, lymph nodes, and spleen.
Lymphocytes
 They are produced in the bone marrow and eventually
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migrate to the peripheral organs.
Thymus is important in the differentiation and
maturation of T-Lymphocytes therefore essential for a
cell- mediated immune response.
Thymus is large during childhood and shrink with age.
Tonsils are typical lymphoid tissue.
Skin associated lymphoid tissue – Lymphocytes and
Langerhans cells. When Langerhans cells are depleted,
the skin can neither initiate an immune response nor
support a skin localized delayed hypersensitivity
response.
Lymphocytes
 Antigens introduced to the body.
 Antigens interact with B and T Lymphocytes and
macrophages in the lymph nodes.
 Lymph nodes – filter foreign material brought to the
site and circulation of lymphocytes.
 Spleen – is important as the primary site for filtering
foreign substances from the blood. Consist of white pulp
containing B and T lymphocytes and red pulp containing
RBC.
 Macrophages line the pulp and sinuses of the spleen.
 The spleen therefore is the major site of immune response
for blood-borne antigens.
Cells Involved in Immune Response
Mononuclear Phagocyte –
 Monocytes in the blood and macrophages.
 Mononuclear phagocytes have critical role. Involve in
capturing, processing, and presenting the antigen to
the lymphocytes.
 Stimulates humoral or cell-mediated immune
response.
 Macrophage –bound antigen (highly immunogenic) is
presented to circulating T or B Lymphocytes and thus
triggers an immune response.
Lymphocytes
 B Lymphocytes – produced from bone marrow.
Differentiate into plasma cells when activated. Plasma
cells produced antibodies (immunoglubolins).
 T Lymphocytes – cells that migrate from bone marrow
to thymus to differentiate into T – Lymphocytes.
Thymosin – helps in maturation and differentiation of
T-Lymphocytes.
 T-Lymphocytes are primarily responsible for immunity
to intracellular viruses, tumor cells, and fungi.
 T-Lymphocytes are categorized into T cytotoxic and T
helper cells.
T-Cytotoxic Cells
 Also known as CD8 cells are involve in attacking
antigens on the cells membrane of foreign pathogens
and releasing cytolytic substances that destroy the
pathogen.
 Have antigen specificity and are sensitized by exposure
to antigen.
 They can also remain as a memory T-Cell. Sensitized
T-cells that are not attacking.
 Provides more rapid and intense cell-mediated
immune response on the 2nd exposure.
T-Helper Cell
 Also known as CD4 cells involved in the regulation of
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cell-mediated immunity and the humoral antibody
response.
Differentiates into subsets and produce distinct
cytokines TH2 and TH1 cells.
TH1 cells – stimulates phagocyte mediated immunity.
TH2 cells – stimulates phagocytes independent,
eosinophil-mediated immunity which is effective
against parasites.
Also involve in allergic response.
Natural Killer Cells
 NK Cells are also involved in cell-mediated immunity.
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These cell are not T or B cells but are large lymphocytes
with numerous granules in the cytoplasm.
NK Cells do not require prior sensitization for their
generation. Involve in killing of virus infected cells, tumor
cells, and transplanted grafts.
Has significant role in immune surveillance for malignant
changes.
Dendritic Cells- important in cell mediated immune
response. Called Langerhans cells in the skin. Found in
lining of the nose, lungs, stomach, and intestine.
Dendrites capture antigens at site and then transport the
antigen until it encounters a T Cell with specificity for the
antigen.
Cytokines
 Soluble factors secreted by WBC and other cells in the
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-
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body that acts as messengers between the cell types.
See page 222 of Lewis for Types and Functions of
specific Cytokins .
Types
Interleukin (Ils) Interferons
Tumor Necrosis Factor (TNF)
Colony stimulating Factors ( CSFs)
Erythropoietin
Cytokines
 Have a beneficial role in hematopoiesis and immune
function. They can also have detrimental effects such
as those seen in chronic inflammation, autoimmune
diseases and sepsis.
 There are currently at least 100 different cytokines.
They acts as immunomodulatory factors, colonystimulating factors acts as growth regulating fasctors
for hematopoeietic cells, and interferons are antiviral
and immunomodulartory.
Comparison of Humoral and Cell-Mediated
Immunity
 Humoral Immunity - consist of antibody-mediated immunity.
Production of antibody is an essential component in a humoral
immune response.
 Cell –Mediated Immunity – Immune response are initiated
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through specific antigen recognition by T cells. The cell types
involve include T lymphocytes, macrophages, and NK cells. Cell
– mediated immunity is of primary importance in
1. immunity against pathogens that survive inside of cells,
including viruses and some bacteria
2. fungal infections
3. rejection of transplanted tissues
4. contact hypersensitivity reactions
5. tumor immunity
Altered Immune Response
 1.
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Hypersensitivity reactions – occurs when the body
fails to recognize self-protein. ( see Lewis pg. 225 table
14-9.
Type 1 – IgE – mediated reactions – pollens, food,
drugs , dust. Involve antibody - IgE
Type II – Cytotoxic Reactions – cells surface of
RBC’s basement membrane IgG, IgM frequently.
Type III – Immune Complex Reactions –
Extracellular fungal, viral, bacterial. IgG, IgM
Type IV _ Delayed Hypersensitivity Reactions –
intracellular or extracellular. NO antibody involve.
Emergency Management for Anaphylactic Shock
 Etiology – injection of, ingestion of, or topical exposure to substance that
produces profound allergic response.
 Initial
- Ensure patent airway
- remove insect stinger if present.
- Epinephrine 1:1000, 0.2 – 0.5 ml SC for mild symptoms; repeat at 10-15 minutes
intervals.
- Epinephrine 1:10,000, 0.5 ml IV at 5 to 10 minte intervals for severe reactions.
- administer high flow oxygen via non-rebreather mask.
- Place recumbent and elevate legs.
- Keep warm.
- administer Diphenhydramine ( Benadryl) IM or IV
Administer histamine H2 blocker such as Cimetidine ( Tagamet)
Maintain blood pressure with fluids, volume expanders, vasopressors, e.g.
dopamine ( Intropin), norepinephrine bitartrate (Levophed).
Ongoing Monitoring
Monitor V/S , respiratory effort, O2 sat, LOC, and Cardiac rhythm.
Anticipate intubation with severe Respiratory distress.
Anticipate cricothyrotomy or tracheostomy with severe laryngeal edema.
Graft versus Host Disease
 Graft vs. Host Disease occurs when an immunoincompetent
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
(immunodeficient) pt. is tranfused or transplanted with
immunocompetent cells.
In transplantation the biggest concern is host’s rejection of the
graft.
The GVH response may have its onset 7 to 30 days after
transplantation.
It involves donor T-cells attacking and destroying vulnerable
host cells.
No adequate treatment of GVH disease once it is established.
Corticosteroid are often used. They enhance susceptibility to
infection. The use of immunosuppressive agents has been most
effective as a preventive rather than a treatment measure.
Radiation of blood products before they are administered is
another measure to prevent T cell replication.
Organ Transplantation
 Organs that can be transplanted:
- Cornea
- Heart valves
- Lungs
- Kidneys
- Small intestine
- Pancreas/Islets cell
- Tendons/Cartilages
- Bone/Bone marrow
- Skin
Donor Sources
 Cadaver
 Living Donors
 How to be come a donor. The individual has to notify
the state of his/her decision when receiving a new
driver’s license. Will receive an organ donor card. An
organ donor should also notify his/her family because
the family members are ultimately the people who give
the medical community the approval to enroll a
deseased individual as an organ donor.
Requirement: Donor and Recipient Matching
 Factors to consider for matching:
 ABO Blood and human leukocyte antigen ( HLA)
typing, medial urgency, time on the waiting list, and
geographic locations
 Histocompatibility studies – to identify the HLA for
both donors and potential recipients.(PCR test is done
to type for the antigens at all five loci (A,B,C,D, and
DR)
Transplant Rejection
 Hyperacute rejection – occurs minutes to hours after
transplantation. No treatment. Organ is removed.
 Acute rejection – most commonly occurs days to month
after transplantation. This type of rejection is mediated by
the recipients T-cytotoxic lymphocytes which attack the
foreign organ. Immunosuppressive Therapy helps. Long
term used of immunosuppressants place clients in high
risk for infections for a longer period of time.
 Chronic rejection – is a process that occurs over months or
years and is irreversible. No definitive therapy for this type
of rejection. Treatment is mainly supportive.
 7Please read pg. 239 Lewis for Drug Therapy used for
Immunosuppressive Therapy.