Altered Immunity Study Guide
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If you are immunoincompetent what sort of problems will you have?
system is incompetent or under responsive
- severe infections
- immunodeficiency disease
If you have immunohyperresponse issue, what sort of problems will you have?
- auto-immune diseases
WBC's involved in innate immunity
Active Acquired Immunity
results from invasion of the body by a foreign object and development of antibodies.
With each invasion the body responds quicker
Passive Acquired Immunity
results from person receiving antibodies to an antigen by an injection or from the mom across the placenta.
Type I Hypersensitivity
Anaphylaxis....mediated by IgE
this is any sort of an allergic response
But it can be a severe and quick response to a specific allergen....bronchial constriction
Atopic Type I Hypersensitivities
Sensitive to environmental allergens
- Allergic Rhinitis/hay fever
- Atopic Dermatitis
Type II Hypersensitivities
Involve IgG and IgM
Cytotoxic and Cytolytic Reaction
Describe Cytotoxic and Cytolytic Type II Hypersensitivity
Involves erythrocytes, platelets and leukocytes
- Seen when patient receives ABO incompatible blood from a donor causing agglutination (clumping)
- Rh Imcompatability too
Type III Hypersensitivity
Involve IgG and IgM
Associated with Auto-Immune Disorders
tissue damage secondary to antigen-antibody complex
Where do you typically see Type III Hypersensitivity Reactions occur? (Immune-Complex Reaction)
- Blood Vessels
Examples of Type III diseases
- Acute Glomerulonephritis
Type IV Hypersensitivity Reaction
Delayed Hypersensitivity Reaction
Reaction that occurs 24-48 hrs after contact
When T lymphocytes attack antigens or release cytokines that attract macrophages and release enzymes that cause tissue destruction
Examples of Type IV Delayed Hypersensitivity Reactions
- Contact Dermititis:
- Poison Ivy, Poison Oak
- Microbial Hypersensitivity:
- Transplant Rejection
Antigen responsible for Type I Anaphylaxis Hypersensitivity
Exogenous pollen, food, drugs, dust
Antigen responsible for Type II Cytotoxic Rxn
Cell surface of RBC, basement membrane
Antigen Responsible for Type III Immune-complex Hypersensitivity
Extracellular, fungal, viral, bacterial
Local Anaphylactic Response
cause a localized cutaneous response, a pale wheal containing endematous fluid surrounded with a erythemous flare (mosquito bite)
Systemic Anaphylactic Response
- mediators are released systemically causing:
- weak, rapid pulse
- dilated pupils
- bronchial edema
**occurs within minutes and can be life threatening
swollen eyelids, lips, tongue larynx, hand, feet.
Starts at the face and spreads
Assessment for Type I Allergic Hypersensitivities
- Patient health history-family history
- Past and present allergies-Id them and get info about clinical manifestations
- Physical exam of skin manifestations
Diagnostic studies for Type I Allergic Hypersensitivities
- CBC with differential (Increase of eosinophils)
- Serology (ag and ab in blood)
- Sputum, nasal and bronchial secretions (eosinophils)
- Skin test
What test is good to detect food and drug allergies?
Collaborative Care for Type I Allergy Hypersensitivity
- Reduce exposure to allergens
- Treat symptoms
- Desensitize thru immunotherapy if needed
If a person has anaphylaxis...what do I do?
- Maintain patent airway: oxygen or intubation
- Prevention of spread of allergen by a tourniquet (bee sting or bite)
- Administer epinephrine, solumedrol and Benadryl
Epinephrine does what for anaphylaxis
- causes vasoconstriction for increase of BP
- and dilates bronchioles to keep airway open
What does Solumedrol do for anaphylaxis?
decreases inflammation causing vasodilation for bronchioles to open
Cardiovascular response to anaphylaxis
- cardiac arrest
Respiratory response to anaphylaxis
- respiratory arrest
Skin response to anaphylaxis
What do you teach a person who has had anaphylaxis reaction?
Avoid allergens that cause systemic anaphylaxis
Antibodies involved with Type II Cytotoxic and Cytolytic reactions....specific
IgM-primary response to ABO blood antigen
IgG-secondary immune response
causing complement lysis and macrophages in the tissues
What does Type II Hypersensitivity lead to?
- Bleeding-low platelets
- Agranulocytosis....increased infections
cant differentiate self from non self proteins which leads to development of autoantibodies and auto-sensitized T cells causing tissue damage based on the self-antigen involved.
the removal of plastma containing components causing the disease. The plasma is replaced with normal saline or albumin. Circulating antibodies and antigen-antibody complexes known to cause autoimmune disorders are removed as well as inflammatory mediators
Systemic Type III Auto-Immune Hypersensitivity
- Systemic Lupus
- Scleroderma (hardening of skin)
Organ Specific Type III Auto Immune Hypersensitivity
Blood, CNS, Muscle, Heart, Endocrine, GI, Kidney, Liver, Eye
Who mostly gets Lupus? When?
Women during childbearing years....also cause flare ups
Interventions for Acute Lupus Exacerbations
- Document severity of symptoms and response to therapy
- Monitor Fever
- Joint inflammation, ROM limitations, pain, fatigue?
- Any signs of hematological problems? (anemia/bleeding)
If a persons on corticosteroids what do I need to watch closely?
I&O...fluid retention and possible renal failure
Protein and creatinine clearance
Health promotion and teaching for a person with Lupus
- Disease process...what do they know? Fill in rest
- Drugs...side effects/schedule
- Avoid stress
- Pain and stress management
- Avoid sick
- Avoid skin drying agents, sun
- Marital and Pregnancy counseling
Mediators of injury for Type IV delayed Hypersensitivity reactions
cytokines and T cytotoxic cells
- NO ANTIBODIES!!
- Involves phagocytes, Cytotoxic T cells....cytokines are NOT always present
With Type IV hypersensitivity what gets rid of the antigens?
- T lymphocytes induce apoptosis
- Macrophages and Natural Killer cells destroy the pathogen
Type I Latex allergic rxn
it's an immediate response to the rubber.
- red skin
- anaphylactic shock
Type IV Latex allergic rxn
caused by the chemical used in manufacturing the latex gloves....a delayed reaction that occurs within 6-48 hrs.
- cracking of skin
- crusty by 24-48 hrs.
Goal of immunosuppressive therapy
to suppress the immune response to prevent rejection of transplanted organ while maintaining sufficient immunity to prevent overwhelming infection and minimize side effects
Example of 3 immunosuppressive drugs
- Cell Cept
Primary immunodeficiency disorders
immune cells are improperly developed or absent
Secondary Immunodeficiency disorders
deficiency is caused by an illness or treatment
- Drug induced is most common (immunosuppressive drugs)
- but also caused by....
- stress response
- surgical removal of lymph nodes, thymus or spleen
- HIV (viral transmission)
Describe gerontological considerations related to the immune response
- decreased # of T lymphocytes
- increased risk for tumors cuz less NK cells
- increased risk for flus and pneumonia cuz shrinking thymus and decrease in t cell prod.
- decline in effective immune response
Dermatologic Manifestations of SLE
- butterfly rash over the cheeks and bridge of nose
- ulcerations of mouth
Musculoskeletal problems from SLE
- arthritis that causes deformities in hands
Cardiopulmonary problems from SLE
- cardiac dysrhythmias as the disease advances
- restrictive lung disease
Renal problems seen with SLE
*Preserve renal function is goal!!*
Nervous System problems seen with SLE
- generalized or focal seizures
Hematologic problems seen with SLE
- mild leukopenia
Infections seen with SLE
infections, pneumonia are common cuz of immunosuppressive effects and many anti inflammatory meds.
Treat fevers aggressively cuz can cause death
If a person with SLE needs a vaccination make sure it is
not with a live virus
Tests to confirm SLE
- anti-double stranded DNA
- anti-Smith antibodies
Maintenance drugs for SLE
- NSAIDS for pain
- Steroid sparing drugs for RA
- Antimalarials to block autoantibodies
Exacerbation drugs for SLE
- Immunosuppressive drugs
How is HIV transmitted
- vaginal secretions
- breast milk
Variables in transmission of HIV
- duration and frequency of contact
- volume of fluid
- virulence and concentration of organism
- host immune status
Patho of HIV
- Has to be inside a living cell
- virus goes from RNA to DNA with the help of reverse transciptase
- strand copies itself and becomes a double stranded viral DNA
- it enters the cells nucleus and its genome and it is now a permanent part of the cells genetic structure.....replicates again, and again, and again
initial infection of HIV is a large amount of virus in the blood
Why is the viral load in the initial stage of HIV low?
Cuz the B cells are able to make HIV specific antibodies to reduce the viral load and the T cells are still able to mount a cellular immune response.
CD4 T cells normal life span? when HIV positive?
What causes the immune dysfunction in HIV positive people
caused by damage/destruction of T helper cells and T lymphocytes
What are the #s of CD4 T cells to maintain a healthy immune response?
200-499 you will start to have immune problems
under 200 sever problems
Acute Phase of HIV
- CD4 T >500
- person will have flu like symptoms
- GI problems
- sore throat
Early Chronic Phase of HIV
- CD4 T 200-499
- patient unaware they have HIV
- can last 10-12 yrs
- very vague flu like symptoms
- virus is replicating
Intermediate Chronic Phase of HIV
- CD4 T 200-499
- Immunity is decreasing
- Most common sign: THRUSH
- PERSISTENT Fever
- DRENCHING night sweats
- CHRONIC diarrhea
- RECURRENT headaches
- SEVER fatigue
Late Chronic Phase of HIV
- IT IS NOW AIDS!!
- CD4 T <200
- Manifestations of life threatening opportunistic cancers, infections, wasting syndrome, dementia
- Invasive cervical
- Karposis carcinoma
- #1 FUNGAL-thrush, oral hair leukoplakia, pneumocystitis jiroveci PNA
- Viral- Herpes, shingles, Hep A & B
- Protazoal-Toxoplasmosis of brain
What's wasting syndrome?
loss of 10% or more of ideal body wt
Abnormal labs in Late chronic stage of HIV....which is now AIDS
- low WBC
- low neutrophils
- low platelets
- low erythrocytes
- abnormal LFT
In order to dx a person with AIDS you must have... a CD4 T cell count of <200 plus one of these....
- opportunistic cancer
- opportunistic infection
- wasting syndrome
May have more than 1, but need at least 1.
Enzyme Immunoassay (EIA)
- detects serum antibodies that bind to HIV antigens.
- if positive, test is repeated at 3 or 6 weeks, or 3 months
If it is positive again, do a Western Blot of Immunofluorescence Assay
If a person gets a false negative test for HIV with EIA....what do I do?
check for risky behaviors and counsel to retest-early testing may have occurred
Western Blot and Immunofluorescence Assay
How do they work?
WB-ID's antibodies in the serum after mixing with purified HIV antigens
IFA-identifies the HIV in infected cells
If either is + then HIV +
Goal of drug therapy for HIV
- decrease RNA levels
- maintain/raise CD4T count >200
- delay the development of HIV related symptoms and manifestations of opportunistic diseases
Entry inhibitor drugs
work by inhibiting the finding of HIV
Reverse Transcriptase Inhibitors
interfere with the ability of HIV to make a DNA copy
prevents HIV from entering the viral genetic material into the host cell
prevents the protease enzyme from cutting HIV proteins in to appropriate lengths for replication
Entry Inhibitor drug
- skin irritation at injection site
Nucleoside Reverse Transcriptase Inhibitor (2)
- AZT-N/V, anemia, leukopenia, myopathy
- Viramune-Steven Johnson, rash, hepatitis
- Viread-N/V, vaginal irritation, renal impairment
Major problem with ART therapy
- Resistance develops rapidly when taken alone or in inadequate doses
- Its combo therapy and can have drug-drug interactions
- Non compliance of dose and length of time
- Keep up with f/u appt and labs
What med will you give somebody with Pneumocystitis jiroveci pneumonia and Toxoplasmosis and Mycobacterium avium complex?
What med will you give a person with Varicella Zoster Virus?
What med will you give a person with TB?
What med will you give a person with pneumococcal pneumonia, influenza virus, Hep A and B?
What are your assessments for a person with HIV/Aids?
- Risky behaviors
- previous STD's
- Foreign travel
- frequen infections
Planning goal for HIV/Aids pt.
- Adherence to drug regimens
- promotion of healthy life style
- protect others from HIV
- develop/maintain healthy and supportive relationships
- maintain role fxn
- come to terms with disease, disability, death
- cope with symptoms of disease and drug therapy
Safe drug use
don't use injectable drugs, do not share injection equipment with others, use sterile equipment through community need and syringe exchange programs
Rick reducing-clean equipment before use with bleach
Safe Perinatal activity
if are HIV + use birth control and don't get prego
Risk Reducing-treat with AZT before prego, during and after
S/S HIV patients need to report immediately
- change in LOC
- headache with N/V
- vision changes
- persistent SOB related to activity and isn't relieved by a short rest period
- N/V with abdominal pain
- Vomiting blood
- Yellow skin
- pain in flank and unable to urinate for 6 hrs
- blood in urine
- new onset of weakness
- chest pain
- new rash or oral lesion accompanied by fever
- ideas to hurt self
What are the side effects of long term ART
- metabolic disorders...
- bone disease
- insulin resistance
- cardiovascular disease
Type II Cytotoxic and Cytolytic Rxn
disorder that involves lungs and kidneys resulting in hemorrhage and glomerulonephritis
Local anaphylactic response
The anaphylaxis cardinal principle is
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