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77 Cards in this Set
- Front
- Back
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What is atopy?
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Genetic predisoposition to allergic reactions. (Involve IgE et Eosinophils
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Function of IgE
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-bind with antigen
-trigger mast cell -release chemical mediators (histamine, leukotrienes, prostaglandins) |
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Effects of histamine
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-itchy/watery eyes
-rahes -runny nose -edema -shunts blood away from core (makes periphery bright red) -SOB & CP -diarrhea |
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Primary mediators:
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1) Histamine (H1 & H2)
2) Prostaglandins |
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H1:
H2: |
Causes constriction of bronchial smooth muscle
Gastric secretion |
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What are prostaglandins responsible for?
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-Fever
-Pain -Inflammation |
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Secondary mediator:
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Leukotrienes
Cause smotth muscle contration & increased vascular permeability-> edema |
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4 types of hypersensitivity
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Type 1: Anaphylactic/allergy
Type 2: Cytotoxic <---dont care about this one Type 3: Immune Complex Type 4: Delayed |
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Most severe form of hypersensitivity:
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Type 1 - Anaphylactic
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Type 1 - Anaphylactic s/sx:
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-laryngeal/mucosal edema
-hypotension -IgE antibodies -requires previous exposure -smooth muscle spasm -bronchospasm -inflammation -increased capillary permeability |
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What does the severity of reaction depend on?
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-How much u r exposed
-Amount of chemical mediators released -Route of allergen entry (air, skin, ingesting) |
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Examples of type 1 reactions:
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-extrinsic asthma
-allergic rhinitis -systemic anaphylaxis -insect sting reactions |
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Type 3 aka....
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Immune Complex (cluster of antibodies)
The get stuck in the tissues et cause damage |
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Examples of type 3 reactions:
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-lupus (SLE)
-rheumatoid arthritis Immune complexes |
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Type 4 aka....
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Delayed hypersensitivity
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Examples of type 4 reactions:
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-chemicals
-latex -tape -tb test -contact dermatitis |
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Skin test for allergies:
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Prick/Scratch
-least invasive -always preformed first -least risk for anaphylaxis |
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Blood sample test for allergies:
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RAST
-SAFEST way to test for allergies -Very expensive -Take a blood sample and then expose the blood to the allergen (look for clumping and IgE antibodies) |
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What can be used to decrease airway inflammation for management of anaphylaxis?
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Aminophylline or steroids
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Example et tx of atopic dermatitis
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Ex: Eczema
Tx: antihistamines et corticosteroids |
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Skin rash from internal medication administration:
What's it look like? What needs to happen after a reaction like this? |
Dermatitis Medicamentosa
Intense, vivid color Needs to be listed as an allergy. Teach about future prevention |
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What can urticaria advance to?
What do we need to be concerned about? |
Angioneurotic edema
-involves deeper layers of the skin, eyelids, lips, hands, feet, tongue Airway. Need to be watched carefully for 3-4 days in an intensive care setting and may need a trach |
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What are the typical symptoms with food allergies?
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GI symptoms
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Nursing management for food allergies:
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Pt teaching - elimination to exposure
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Type 1 latex allergy:
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Immediate
-rhinitis, conjunctivitis, asthma, anaphylaxis |
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Type 4 latex allergy:
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Delayed
-most common type -vesicular akin lesions on back of hands, papules, pruritus |
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Synovitis:
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***Primary
-caused by an inflammatory disorder (RHEUMATIC DISEASES); immune response Secondary -caused by degenerative disease/injury/stuff like that |
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What damages the tissue?
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Immune complexes
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What is pannus formation?
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AKA: scar tissue of a joint
-development of granulation cells in the synovial fluid |
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What does pannus formation lead to?
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Bone destruction
-overgrowth of bearing surface (spurs/osteophytes); huge noby joints -breakdown of joint surfaces |
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What syndrome is VERY strongly linked to all rheumatic diseases?
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Raynauds
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Blood studies for rheumatic diseases:
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ESR: high with inflammation
ANA: specific to rheumatoid disease; elevated with autoimmune condition Rheumatoid factor: elevated with autoimmune condition |
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What will happen to a person with a rheumatic disease that does not remain active?
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Their joints will fixate et they will lose ROM
-Very important to have exercise program |
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Goals of management for rheumatic diseases:
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Suppress inflammation
-NSAIDS, ASA Suppress autoimmune response -DMARDS (Plaquenil, Humira, Embrel) Control pain -meds, hot/cold therapy Maintain/improve joint mobility -exercise plain Increase knowledge -teach et reinforce Promote self management -evaluate home situation (stairs, handrails, etc...) |
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Nursing intervention for rheumatic diseases:
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Major one is monitoring et managing potential complications - watch them closely:
-not moving well=skin brkdwn, falls -autoimmune disorder=infection |
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Clinical manifestations of RA:
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-joint pain
-swelling -***warmth & erythema -loss of function -spongy or boggy joint tissue -***begins with small joints (hands, wrist, feet; then progresses to knees & hips) -***acute onset -bilateral & symmetric stiffness -extra-articular symptoms (wt loss, anemia, hair loss, thin skin, reynauds) -milky synovial fluid (normally clear) |
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Stages of RA:
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Early: if dx'd here et sx controlled can remain here
Moderate: erosive - PT/OT; meds to stop disease et decrease pain Persistant: erosive - corticosteroids to decrease inflammation; consider reconstructive surgery Advanced: unremitting - give pain meds, anti-inflammatories, antidepressants |
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Gold standard drug for RA:
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Methotrexate
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Diet for RA:
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High protein to control tissue wasting
Low fat/low cal to keep wt under control to put less wt on their joints |
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What worsens SLE?
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extended sun exposure or artificial UV light
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Systemic inflammation: RA vs. SLE
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SLE has more systemic inflammation than RA
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Skin lesions c SLE:
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-annular polycyclic; raised acne-like rash, kind of lumpy
-discoid lupus lesions; round with itty bitty spots inside (looks like ringworm) -butterfly rash; very characteristic of lupus |
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What's the primary cardiac symptom with SLE?
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Pericarditis - auscultate for friction rub
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Other systemic manifestations with SLE:
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-renal failure
-HTN -CNS diseases (subtle changes) |
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Main tx for SLE:
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Corticosteroids (solumedrol inpatient - prednisone outpatient)
***take with food |
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Where does scleroderma start?
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In the hands et feet
Starts c Raynauds |
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What makes the hard white nodules on the skin?
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Calcinosis - calcium build up underneath the skin
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What's the major concern in scleroderms?
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Hardening of esophagus, decreased esophageal mobility, HIGH risk of aspiration
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Treating the sx of scleroderma:
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-Keep skin moist
-ROM; will fixate -Pericarditis/pleural effusion -Avoid temp extremes (cannot sweat so cannot cool themselves) |
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Client education for scleroderma:
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Do not smoke - causes massive vasoconstriction - encourage smoking cessation
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Goal for ankylosing spondylitis:
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Relieve swelling et stop process before the spine fixates itself
Help their respiratory status because they are hunched over |
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What causes the problem with gout?
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Uric acid build up into urate crystals
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Tx of gout:
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-***Allopurinol
-low purine diet |
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Management of fibromyalgia:
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-Tricyclic antidepressants - help sleep, pain, et lifestyle is hindered
-***Support/encouragement |
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What needs to be done for infectious arthritis?
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***Considered a medical emergency - need to find out C&S because it causes RAPID jt degeneration then sepsis
***Need to immobilize jt to prevent further friction et damage |
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Why does increasing age have a higher rate of autoimmune diseases et cancer?
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1)cannot recognize self from non-self
2)weakened surveillance system |
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Age-related gastric changes:
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decreased gastric secretions & motility
s/sx: fever, abd pain, bloating, nausea, gas, ***DIARRHEA |
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Link between nutrition et infection:
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If we have decreased nutritional intake we have an increased risk for infection.
If we have an infection, we have an increased nutritional need |
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Increased neutrophils=
Increased lymphocytes= Increased eosinophils= |
bacterial infection
viral infection allergic reactions |
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What's a primary immunodeficiency?
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Something you're just born with
-genetic disorders -cellular defects -primarily in infants & young children |
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Most common primary immunodeficiency:
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CVID (Common Variable Immunodeficiency Disorder)
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Clinical manifestation of CVID:
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Pernicious anemia
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Dx of CVID:
Tx of CVID: |
Very low levels of immunoglobulins or completely absent
IV immunoglobulin infusions |
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What are secondary immunodeficiencies most commonly secondary to?
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AIDS
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Teaching for secondary immunodeficiencies:
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Infection control, educate on handwashing, lifestyle changes, go to apts, etc...
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What cell does the HIV virus bind to et proliferate in?
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CD4 cells
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HIV antibody test:
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Shows up 3-12wks after expsoure
EIA - test done FIRST; if positive then.... Western blot - confirms viral proteins If both tests are positive then the person is HIV positive |
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Viral load test:
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Measures the progression of the disease (shows plasma level of the virus). The higher the viral load the worse the prognosis. The lower the viral load the longer its going to take them to reach AIDS.
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CD4/CD8 ratio:
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Indicates our overall level of immune suppression (how much is the virus killing of our CD4 count)
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What's the "window period"?
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30 days to 3 months
During this period, a person will test negative on HIV antibody test |
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Viral set point:
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The balance between the amount of virus in the body and your immune reponse.
The higher the viral set point the worse the prognosis. By the time the antibody test is positive, the virus is well established |
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Tx of HIV:
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HAART - slows growth et reproduction of HIV
***Do viral load test & CD4 q 2-8wks after initiation of tx |
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Respiratory complication of HIV/AIDS:
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Pneumocystis Pneumonia (PCP)
Most common infection in AIDS clients Tx: Bactrim of Septra (TMP-SMZ) CD4 count less than 200 will get prophylactic tx |
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GI complications of HIV/AIDS:
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-oral/esophageal candidiasis
-chronic diarrhea -wasting syndrome |
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Oncologic complications of HIV/AIDS:
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-Kaposi's sarcoma (skin lesions, multiple organ involvement, disfigurement)
-B-Cell lymphomas **most tx ineffective |
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Neurologic complications of HIV/AIDS:
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HIV Encephalopathy (AIDS dementia complex)
s/sx: memory deficits, HA...progresses to psychosis, hallucinations, seizures, death |
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Leading cause of blindness c HIV:
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Retinitis
Prophylactic antibiotics (ganciclovir) |
