Question What is atopy?

Function of IgE

Answer Genetic predisoposition to allergic reactions. (Involve IgE et Eosinophils -bind with antigen -trigger mast cell -release chemical mediators (histamine, leukotrienes, prostaglandins) -itchy/watery eyes -rahes -runny nose -edema -shunts blood away from core (makes periphery bright red) -SOB & CP -diarrhea 1) Histamine (H1 & H2) 2) Prostaglandins Causes constriction of bronchial smooth muscle Gastric secretion -Fever -Pain -Inflammation Leukotrienes

Effects of histamine

Primary mediators: H1: H2: What are prostaglandins responsible for?

Secondary mediator:

Cause smotth muscle contration & increased vascular permeability-> edema Type Type Type Type 1: 2: 3: 4: Anaphylactic/allergy Cytotoxic <---dont care about this one Immune Complex Delayed

4 types of hypersensitivity

Most severe form of hypersensitivity:

Type 1 - Anaphylactic -laryngeal/mucosal edema -hypotension -IgE antibodies -requires previous exposure -smooth muscle spasm -bronchospasm -inflammation -increased capillary permeability -How much u r exposed -Amount of chemical mediators released -Route of allergen entry (air, skin, ingesting) -extrinsic asthma -allergic rhinitis -systemic anaphylaxis -insect sting reactions Immune Complex (cluster of antibodies) The get stuck in the tissues et cause damage -lupus (SLE) -rheumatoid arthritis Immune complexes

Type 1 - Anaphylactic s/sx:

What does the severity of reaction depend on?

Examples of type 1 reactions:

Type 3 aka....

Examples of type 3 reactions:

Type 4 aka....

Delayed hypersensitivity -chemicals -latex -tape -tb test -contact dermatitis Prick/Scratch -least invasive -always preformed first -least risk for anaphylaxis 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)

Examples of type 4 reactions:

Skin test for allergies:

Blood sample test for allergies:

What can be used to decrease airway inflammation for management of anaphylaxis? Example et tx of atopic dermatitis Skin rash from internal medication administration: What's it look like? What needs to happen after a reaction like this? What can urticaria advance to?

Aminophylline or steroids Ex: Eczema Tx: antihistamines et corticosteroids Dermatitis Medicamentosa Intense, vivid color Needs to be listed as an allergy. Teach about future prevention 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 GI symptoms Pt teaching - elimination to exposure Immediate -rhinitis, conjunctivitis, asthma, anaphylaxis Delayed -most common type -vesicular akin lesions on back of hands, papules, pruritus ***Primary -caused by an inflammatory disorder (RHEUMATIC DISEASES); immune response

What do we need to be concerned about? What are the typical symptoms with food allergies? Nursing management for food allergies: Type 1 latex allergy:

Type 4 latex allergy:

Synovitis:

Secondary -caused by degenerative disease/injury/stuff like that Immune complexes AKA: scar tissue of a joint -development of granulation cells in the synovial fluid Bone destruction -overgrowth of bearing surface (spurs/osteophytes); huge noby joints -breakdown of joint surfaces Raynauds ESR: high with inflammation

What damages the tissue? What is pannus formation?

What does pannus formation lead to? What syndrome is VERY strongly linked to all rheumatic diseases?

Blood studies for rheumatic diseases:

ANA: specific to rheumatoid disease; elevated with autoimmune condition Rheumatoid factor: elevated with autoimmune condition

What will happen to a person with a rheumatic disease that does not remain active?

Their joints will fixate et they will lose ROM -Very important to have exercise program 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...) Major one is monitoring et managing potential complications - watch them closely: -not moving well=skin brkdwn, falls -autoimmune disorder=infection -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) Early: if dx'd here et sx controlled can remain here

Goals of management for rheumatic diseases:

Nursing intervention for rheumatic diseases:

Clinical manifestations of RA:

Stages of RA:

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 Gold standard drug for RA: Diet for RA: What worsens SLE? Systemic inflammation: RA vs. SLE Skin lesions c SLE: What's the primary cardiac symptom with SLE? Other systemic manifestations with SLE: Methotrexate High protein to control tissue wasting Low fat/low cal to keep wt under control to put less wt on their joints extended sun exposure or artificial UV light SLE has more systemic inflammation than RA -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 Pericarditis - auscultate for friction rub -renal failure -HTN -CNS diseases (subtle changes) Corticosteroids (solumedrol inpatient - prednisone outpatient) Main tx for SLE: ***take with food In the hands et feet Starts c Raynauds What makes the hard white nodules on the skin? What's the major concern in scleroderms? Calcinosis - calcium build up underneath the skin Hardening of esophagus, decreased esophageal mobility, HIGH risk of aspiration -Keep skin moist -ROM; will fixate -Pericarditis/pleural effusion -Avoid temp extremes (cannot sweat so cannot cool themselves) Do not smoke - causes massive vasoconstriction - encourage smoking cessation Relieve swelling et stop process before the spine fixates itself Help their respiratory status because they are hunched over What causes the problem with gout? Tx of gout: Management of fibromyalgia: Uric acid build up into urate crystals -***Allopurinol -low purine diet -Tricyclic antidepressants - help sleep, pain, et lifestyle is hindered -***Support/encouragement ***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 Why does increasing age have a higher rate of autoimmune diseases et cancer? Age-related gastric changes: 1)cannot recognize self from non-self 2)weakened surveillance system decreased gastric secretions & motility s/sx: fever, abd pain, bloating, nausea, gas, ***DIARRHEA If we have decreased nutritional intake we have an increased risk for infection. If we have an infection, we have an increased nutritional need Increased neutrophils= Increased lymphocytes= Increased eosinophils= bacterial infection viral infection allergic reactions Something you're just born with -genetic disorders -cellular defects -primarily in infants & young children CVID (Common Variable Immunodeficiency Disorder) Pernicious anemia

Where does scleroderma start?

Treating the sx of scleroderma:

Client education for scleroderma: Goal for ankylosing spondylitis:

What needs to be done for infectious arthritis?

Link between nutrition et infection:

What's a primary immunodeficiency?

Most common primary immunodeficiency: Clinical manifestation of CVID:

Dx of CVID: Very low levels of immunoglobulins or completely absent Tx of CVID: What are secondary immunodeficiencies most commonly secondary to? Teaching for secondary immunodeficiencies: What cell does the HIV virus bind to et proliferate in? IV immunoglobulin infusions AIDS Infection control, educate on handwashing, lifestyle changes, go to apts, etc... CD4 cells Shows up 3-12wks after expsoure HIV antibody test: EIA - test done FIRST; if positive then.... Western blot - confirms viral proteins If both tests are positive then the person is HIV positive Viral load test: 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. Indicates our overall level of immune suppression (how much is the virus killing of our CD4 count) 30 days to 3 months During this period, a person will test negative on HIV antibody test The balance between the amount of virus in the body and your immune reponse. Viral set point: The higher the viral set point the worse the prognosis. By the time the antibody test is positive, the virus is well established HAART - slows growth et reproduction of HIV Tx of HIV: ***Do viral load test & CD4 q 2-8wks after initiation of tx Pneumocystis Pneumonia (PCP) Respiratory complication of HIV/AIDS: Most common infection in AIDS clients Tx: Bactrim of Septra (TMP-SMZ) CD4 count less than 200 will get prophylactic tx GI complications of HIV/AIDS: -oral/esophageal candidiasis -chronic diarrhea -wasting syndrome -Kaposi's sarcoma (skin lesions, multiple organ involvement, disfigurement) -B-Cell lymphomas **most tx ineffective HIV Encephalopathy (AIDS dementia complex) s/sx: memory deficits, HA...progresses to psychosis, hallucinations, seizures, death Retinitis Leading cause of blindness c HIV: Prophylactic antibiotics (ganciclovir)

CD4/CD8 ratio: What's the "window period"?

Oncologic complications of HIV/AIDS:

Neurologic complications of HIV/AIDS:

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