Immune Disorders Flashcards
Types of Immune Responses:
Altered Immune Responses:
Type I: IgE-mediated Anaphylactic reactions
-anaphylaxis, angioedema, atopic reactions (allergic rhinitis, eczema, asthma), urticaria
Type II: Cytolytic/toxic reactions
-hemolytic blood transfusion reaction
Type III: Immune Complex reactions
-autoimmune diseases (SLE)
Delayed Hypersensitivity Reactions:
Type IV: Cell-mediated response (contact dermatitis)
Immunocompetence
the body is able to identify, inactivate and destroy foreign substances
appropriate way to respond
Altered Immune Response:
Incompetent/under-responsive: severe infection, immunodeficiency disease, malignancy may occur
Overresponsive:
hypersensitivity, allergies, autoimmune diseases
Type I: Overview
occurs in pts who are highly susceptible to certain allergens
first exposure: IgE antibodies form and attach to mast cells and basophils
second and subsequent exposure: allergens attach to IgE causing cells to release chemicals-histamine, ECF-A, leukotrienes, serotonin, kinin, bradykinin which target organs/tissues and cause sx
Type I: Sx
Smooth muscle contraction increased vascular permeability Vasodilation Hypotension Pruritis increased mucus production
Type 1: Anaphylactic Reactions
Anaphylaxis:
usually occurs w/in minutes
life threatening d/t bronchial constriction and vascular collapse
if d/t injection or insect bite initially will see itching, edema, erythema at site
Shock (vascular collapse): rapid weak pulse decrease BP dilated pupils dyspnea possible cyanosis
Bronchial and angioedema
Type 1: Tx
ABC's O2 Epinephrine (0.5ml every 5-10min) Antihistamine IV steroid
*these vasoconstrict and increase BP
Type 1: Angioedema
swelling in deeper layers of skin (eyelids, lips, tongue, larynx, hands, feet, GI tract, genitalia)
progression
skin may appear normal or have reddish hue
if lesions may be itchy
several hours to days
Type 1: Atopic Reaction
occurs in 20% of population
form of allergy which is hypersensitive and occurs in part of the body that is not in contact with the allergen
inherited tendency to be sensitive to environmental allergies includes: allergic rhinitis, asthma, atopic dermatitis/eczema, urticaria
Type 1: Asthma
bronchial action d/t ECF -A (slow reacting substance of anaphylaxis) & histamine
bronchial smooth muscle contraction
excessive mucus
edema of bronchial mucosa
Type 1: Atopic Dermatitis
Eczema: chronic inherited skin disorder caused by environmental allergens an "itch that rashes" skin reaction is more generalized or can be patchy-redness, swelling, cracking, weeping of clear fluid, scaling and crusting
Tx: hydrocortison, moisturizer, hydration
Type 1: Urticaria
acute skin reaction to systemic allergen occurring in atopic person
sx: transient wheals varying in size and shape with flaring caused by histamine
rapid development post-exposure
lasting minutes to hours
itching
tx: antihistamines, epinephrine if sever and no response to antihistamine
Type II: Cytotoxic and Cytolytic Reactions Overview
Reaction d/t activated complement system which mediates the reaction - involves IgG and IgM
causes cell destruction-erythrocytes, leukocytes, platelets
seen in:
- ABO and Rh incompatibility blood transfusion reactions
- autoimmune and drug related hemolytic anemias, leukopenia, thrombocytopenia
Type II: Acute Hemolytic Transfusion Reaction Overview
90% d/t mislabeled blood product or wrong pt
develop in first 15 min of starting blood product transfusion
agglutination of RBC obstructs capillaries which blocks clotting factors and can allow bleeding
RBC destruction releases Hgb which is filtered by kidney
Kidney tubules blocked can lead to Acute Renal Injury (ARI)
Type II: Acute Hemolytic Transfusion Reaction Sx
fever, chills low back pain flushing tachycardia tachypnea hypotension vascular collapse dark urine watch for shock *can lead to cardiac arrest, ARI, death
Type II: Acute Hemolytic Transfusion Reaction Nursing Interventions
Stop transfusion and keep vein open (kvo) with NS
remain w/ pt, VS and focused assessment
notify HCP
frequent monitoring for Sx of complications, monitor I&O
collect necessary blood and urine samples
blood and tubing returned to lab for sampling/testing
Febrile Reaction (Other type of blood product transfusion reaction):
caused by leukocyte incompatibility
commonly caused by multiple blood transfusions
Sx: sudden fever, chills, HA, flushing, muscle pain
Interventions: Stop transfusion, kvo, notify MD, antipyretics
Prevention: additional filter on tubing, use of leukocyte-poor blood products
Allergic Reaction (other type of blood product transfusion reaction - type I immune response)
sensitive to plasma proteins
increases in pts with allergies
may be mild or anaphylactic
sx: hives, itching, flushing, wheezing, cyanosis, shock, cardiac arrest
Interventions: stop transfusions, kvo, notify MD
- antihistamine
- restart if sx transient and mild
- do not restart if fever or resp sx
- epinephrine
Prevention: admin antihistamine prior to transfusion if known hx allergies per order
Circulatory Overload (other type of blood product transfusion reaction)
infusion rate too fast and/or pt with decreased cardiac or renal function
elderly at increased risk
Sx: dyspnea, cough, lungs-crackles, tachycardia, increased BP, distended neck veins
Interventions:
- decrease infusion rate
- raise HOB with feet dependent
- notify MD
- O2
- diuretics
Prevention: adjust rate per pt size and tolerance
Septicemia Reaction (other type of blood product transfusion reaction)
transfusion of contaminated blood products
Sx: rapid onset of chills, high fever, V, D, decrease BP, shock
Interventions:
- stop transfusion, kvo, notify MD, VS
- blood cultures, return blood and tubing to lab for testing
- O2, IVF, antibiotics, vasopressors, volume expanders
Prevention: infuse within 4 hours
*general rule: blood products should never infuse longer than 4 hours (2-4 hours is good range)
Type III: Immune Complex Reactions Overview
Complexes form (antigens and immunoglobulins) are deposited in tissues and capillaries, become fixed and release chemotactic factors leading to inflammation and destruction of involved tissue
Local or systemic, immediate or delayed
common sites: kidneys, skin, joints, blood vessels, lungs, heart
Autoimmune: ex) RA, SLE, Myesthenia Gravis, Type 1 DM
Autoimmunity
immune system no longer differentiates self from non-self
cause is unknown: age, gender, hormones play part
principle factors include:
- inheritance of susceptibility gene
- initiation of autoreactivity by triggers (usually viral infection)
Type III: SLE Overview
chronic progressive multi-system inflammatory disease, extremely variable, difficult to predict progression
periods of exacerbations and remissions
more common in women of child bearing age
African Americans, Asians, Native Americans
Cause is unknown, probably has genetic component
Type III: SLE Precipitating Factors/ Triggers
menarche or pregnancy (esp the immediate postpartum period) due to hormonal fluctuations
sun exposure (can be from tanning beds due to UV light)
Meds
Stress (can cause flair up)
Type III: SLE Sx (Early Symptoms, Skin, Musculoskeletal, Cardiopulmonary, PV, Renal, Nervous)
onset or exacerbation after menarche
Prodrome (early symptoms): excessive fatigue, fever, weight loss, arthralgia (joint pain)
*classic Sx when they all occur together
Skin: dry, scaly rash on sun exposed areas
- butterfly rash on cheeks and nose (50% SLE pts have this)
- ulcers of mouth and nose
- alopecia w or w/o lesions (hair regrows except where lesions were)
Musculoskeletal: polyarthralgia w/ AM stiffness, arthritis (90%) non erosive but may have deformities
Cardiopulmonary: tachypnea, cough-restrictive lung disease)
- arrhythmias d/t fibrosis of SA and AV node
- HTN, CAD accelerates and need aggressive therapy
- Pericarditis, endocarditis
Peripheral Vascular: Raynauds phenomenon - arterial vasospasm in response to cold/stress
Kidneys: Lupus nephritis (40% w/in 5 years of dx
- starts with mild proteinuria and progresses rapidly to glomerulonephritis
- goal of tx: to slow progression and preserve function by managing disease
Nervous system: seizures, peripheral neuropathy
-organic brain syndrome: disordered thought process, memory prob, depression, psychosis, probable recovery but with some residual impairment
Type III: SLE Hematologic Sx
anemia, antibody formation against blood cells, bleeding and clotting problems
- leukopenia-infection: increases susceptibility, pneumonina
- common cause of death, fever needs to be taken super seriously, no live vaccines
thrombocytopenia: bleeding OR
hypercoagulability: excessive clotting and requires treatment with coumadin
Type III: SLE Diagnostic Tests
ANA (antinuclear titer antibody) titer: positive 97% of time
Antismith antibodies (Anti-Sm): positive 30-40% of time and are considered diagnostic
ESR and CRP: used to monitor disease activity and response to treatment
Complement system: C3 and C4 are diagnostic for SLE - become depleted due to exaggerated inflammatory response
-CBC, BUN and creatinine, UA
Type III: SLE Interventions
manage active phase of disease (exacerbations) while preventing long-term tissue damage
- better prognosis associated with early dx
- monitor for complications of disease (infection, bleeding/clotting, heart and lung, renal, neuro, and perform necessary interventions to address these problems)
Type III: SLE Medications
corticosteroid: acute phase for inflammation and immunosuppression
NSAIDS: pain and inflammation
Plaquenil (antimalarial): decrease inflammatory response in joints, fever and fatigue (takes 2-3 months to take effect, not for acute, used for chronic)
Immunosuppressive Drug: methotrexate, imuran - chronic tx of inflammation and disease progression
MVI, Folic Acid, and Fe supplement
Type III: SLE Tx
Plasmapheresis: done through IV access
- removal of plasma containing antibodies, complexes, and inflammatory mediators (complements) that are causing tissue destruction
- used in exacerbation phase when pt is not responding to corticosteroid tx
- plasma volume is replaced with NS or LV
Acute phase: documentation of therapy, fever pattern, joint inflammation, fatigue
- monitor respiratory and cardiac function (daily weight, I&Os d/t corticosteroid use, watch for sx of FVE)
- monitor kidney function and watch for signs of renal failure
- watch for s/sx of bleeding or clotting
- neuro status, peripheral neuropathy
Type III: SLE Education
Educate on disease process, therapy, risk for infertility
Avoid/ eliminate exposure to precipitating factors - fatigue, sun exposure, stress, infection
Type III: SLE Psychological Considerations
vague onset - undiagnosed
hereditary considerations - genetic counseling
self-esteem issues as well as fatigue and pain interfering with quality of life
family/friend education re disease process
young adults have difficulty with decreased sun exposure and physical limitations
Type IV: Delayed Hypersensitivity Overview
Sensitized T-lymphs attack antigens or release cytokines which attract macrophages, releasing enzymes causing tissue destruction
takes 24-48 hours for reaction to occur after exposure
ex) contact dermatitis, microbial hypersensitivities (TB), transplant rejections, some drug sensitivities
Type IV: Contact Dermatitis
skin is first introduced to substance and epidermal proteins become antigenic. Memory cells form 7-14 days later)
subsequent exposure: person develops eczematous rash in 48 hours
-metals (nickle, mercury), catechols (poison ivy, oak, sumac), cosmetics, rubber compounds (latex)
acute sx: skin edematous, red, papules, vesicles, itchy, burning, stinging
latex allergies can be type I or type IV
Type IV: Latex delayed hypersensitivity
caused by chemicals in manufacturing process of gloves
6-48 hours post-exposure
Sx: dryness, itching, fissures, redness, swelling, crusting (24-48 hours)
chronic exposure: leads to lichenification (thickening of skin), scaling, and hyperpigmentation
