Exam 4 Immunological Abnormalities Flashcards
(33 cards)
1
Q
Hypersensitivity
A
Types of hypersensitivity reactions
Type I: Anaphylactic #1 concern in a Hospital
Type II: Cytotoxic
Type III: Immune complex
Type IV: Delayed
2
Q
Type I: Anaphylactic
A
- Most common and severe type of hypersensitivity reaction.
- May be localized or systemic - 2 types
- Results from the over-production of an antigen-specific IgE after exposure to an offending allergen
- Common allergens: drugs, chemicals, food, insect venom, seasonal: (grass, pollen, ragweed), mold, mildew, dust, animals, etc.
- Requires previous exposure to the specific antigen. (patient must be exposed twice to develop a response) 1st exposure=no reaction; 2nd exposure=reaction!
- Reaction begins immediately after exposure to the antigen.
3
Q
Common Allergens causing Anaphylactic shock
A
- In a hospital setting, we worry about: Latex, Antibiotics, and Contrast Dye
- The faster the reaction after contact with the allergent, the more severe the reaction
- Drugs:
- Penicillins, Sulfonamides, Insulins, Asa, Tetracycline, Cephalosporins, Chemo agents, NSAID’s
- Foods:
- Eggs, milk, peanuts, shellfish, chocolate, strawberries
- Treatment Measures:
- Blood products, Iodine-contrast media (contrast dye is made from this), latex based products
- Insect Venoms:
- Wasps. Hornets, yellow jackets, bumblebees, ants,
- Animal Sera:
- Tetanus antitoxin, Rabies antitoxin, snake venom antitoxin
4
Q
Signs and Symptoms
A
- LOCALIZED RESPONSE:
- localized edema
- andioedema
- Pruritus “itching”
- Rhinitis “stuffy, runny nose”
- Rash
- Redness
- Fever “usually low”
- Urticaria “hives”
5
Q
Treatment for Local Response
A
- Antihistamines:
- FIRST RESPONSE Benadryl (Diphenhydramine) Side effect: drowsiness
- Claritin, Zyrtec, Allegra (may also contain “D”- decongestant) “seasonal allergies”
- May need Prednisone burst for sustained effect “for localized response”
- May need Albuterol MDI if wheezing is present.
- SE: Tremor, Tachycardia
6
Q
Type 1 :Anaphylaxis
A
-
SYSTEMIC RESPONSE: WORSE TYPE OF REACTION- MAY BE FATAL IF NOT TREATED QUICKLY!!!
- Window of time: 2-3 minutes
- Massive vasodilation: causes sudden drop in BP
- This is the histamine response of Cytokines, bradykinin which causes the Vasodilation
- Increased capillary permeability
- Smooth muscle contraction: gastrointestinal and uterine spasm
- Laryngeal stridor and edema: bronchospasm
- Less than 3 mintues to intubae *throat will close* tube must go in
- Angioedema
- Tounge, lips swell = difficulty talking
7
Q
Clinical Manifestations
of an anaphylactic reaction:
A
- ASSESS 1ST FOR ABC
- If BP goes down, infuse with fluids, 18 bore if possible. Need a minimum of 90/50 to perfuse organs
- Cardiovascular
- Hypotension
- Arrhythmias
- Tachycardia
- Cardiac arrest
-
Respiratory
- Hoarseness
- Coughing
- Sensation of narrowing airway
- Wheezing
- Stridor
- Dyspnea, tachypnea
- Respiratory arrest
- Neurologic
- Headache
- Dizziness
- Paresthesia
- Feeling of Impending Doom
- Gastrointestinal
- Cramping
- Abdominal pain
- Nausea/Vomiting
- Diarrhea
- Integument
- Pruitus
- Angioedema
- Erythema
- Urticaria
8
Q
Medical Management
Anaphylactic Reaction
A
- CPR: ABC’s are assessed immediately.
- Oxygen by face mask or CPAP may be needed. Monitor airway for stridor- ET intubation may be required.
- Epinephrine 1 : 1,000 dilution injection subcutaneously in upper arm or thigh. May follow with IV infusion of Epinephrine.
- Antihistamines: (Benadryl) Diphenhydramine 25-50 mg IV push.
- Corticosteroids: Solucortef (fast) or Solumedrol- 150 mg IV push
- H2 receptor blocker intravenously
- this protects from stress ulcers forming
- Drugs: Pepcids
9
Q
Nursing Management
Anaphylactic Reaction
A
- Monitor V.S. and respiratory status: call RRT as needed.
- Monitor for signs of increasing laryngeal edema- stridorous breath sounds, wheezing- Prepare to intubate if present. Administer Oxygen in high concentrations as ordered.
- CPR: continuous assessment of ABC’s.
- Administer Epinephrine 1:1,000 dilution
- Establish IV access for Epinephrine infusion
- Prepare to administer emergency medications (Benadryl, Solumedrol) and IV fluids to keep blood pressure up.
- Document interventions and patient’s response to treatment.
- Epinephrine causes vasoconstriction
- Assess peripheral pulses
- Job as bedside nurse for RTT: Brief team on vitals, chart everything.
10
Q
Nursing Interventions
for anaphylactic reaction
A
- Stop the blood transfusion
- Call an RRT
- Place an oxygen mask on the patient at 10L/min.
- Administer 0.9% NS at 1L/hr.
- Give the patient Epinephrine 1:1000 dilution SQ.
11
Q
Nursing Management
for anaphylactic reaction
A
- Prevention: careful assessment of patient
- Patient Education: Patient MUST ALWAYS CARRY AN EPI PEN!!!!!!!
- Self administration of Epinephrine (Epi-pen)
- Avoidance of precipitating factor
- Allergy testing by allergist
- Pharmacologic therapy- antihistamines
- Allergen Immunotherapy
- Food Allergy bracelet while in hospital
- Latex Allergy bracelet while in hospital
- PATIENT NEEDS MEDIC-ALERT BAND!!!!!
12
Q
Type II: Cytotoxic
(Antibody Mediated Disorders)
A
- The immune system mistakenly identifies a normal constituent of the body as foreign and activates the complement cascade.
- Examples include mismatched blood reaction, hemolytic anemias, some severe drug reactions
- Involves the binding of either IgG or IgM antibody to the cell bound antigen. The result of this antigen-antibody binding is activation of the complement cascade and destruction of the cell to which the antigen is bound.
13
Q
Type III Hypersensitivity:
Immune Complex Mediated Disorders
A
- Vascular response: there is an increase in vascular permeability and tissue injury causing pathologic inflammatory response.
- Kidneys and joints are particularly susceptible to this type of injury.
- Examples: Vascular damage that occurs in the autoimmune diseases:
- Systemic Lupus Erythematosus
- Rheumatoid Arthritis
- Raynaud’s phenomenon.
14
Q
Type IV
(Cell Mediated Disorders)
A
- Hypersensitivity is mediated by cells, not antibodies
-
Response is usually delayed for 24-72 hours after exposure to antigen
- *difficult to diagnose
- Cells involved in response are T8 lymphocytes (cytotoxic killer cells) and lymphokines producing cells
- Other inflammatory cells are involved: monocytes, neutrophils, eosinophils, basophils
- Examples: reaction to TB test, contact dermatitis
15
Q
Medical Management for Type II, III, and IV reactions include immunosuppressive therapies.
A
- Immunosuppressant drugs can be classified into four categories: Patients should never stop taking abruptly!!!!
- If stopped abrutply, body will not be producing cordisol → body goes into Addisonian Crisis
- 1st Response is injection of Hydrocrotisone
- Addisonian Crisis S&S:
- Pain in your lower back, abdomen or legs.
- Severe vomiting and diarrhea, leading to dehydration.
- Low blood pressure.
- Loss of consciousness.
- High potassium (hyperkalemia) and low sodium (hyponatremia)
- Addisonian Crisis S&S:
-
Anti rejection meds for transplants
- Azathioprine (Imuran)
- Cyclosporine (Neoral, Sandimmune, SangCya)
- Monoclonal antibodies, which include: basiliximab (Simulect), daclizumab (Zenapax), and muromonab (Orthoclone OKT3)
- Corticosteroids such as Prednisone (Deltasone, Orasone)
- Most potent immune suppressing drug
- SE: Tremors, anxious, insomnia, edema, can lead to Steroid Phsychosis
- Most patients are prescribed drugs from more than one category. Patients must be on these medications for life.
16
Q
Addisonian Crisis
A
- LIFE THREATENING
- If a patient abrubtly stops taking immunosuppressive therapy, body will not be producing cordisol = body goes into Addisonian Crisis
- 1st Response is injection of Hydrocrotisone
Addisonian Crisis S&S:
- Pain in your lower back, abdomen or legs.
- Severe vomiting and diarrhea, leading to dehydration.
- Low blood pressure.
- Loss of consciousness.
- High potassium (hyperkalemia) and low sodium (hyponatremia)
17
Q
Rheumatoid Arthritis
vs.
Osteo Arthritis
A
Osteo Arthritis
- Heberden’s Nodes → 2 nodes
- unilateral
- localized
- attacks joints only
Rheumatoid Arthritis
- 1 nodule
- bilateral symmerical
- systemic
- Peripheral joints, muscles, tendons, ligaments and blood vessels
18
Q
Autoimmune and Rheumatic Diseases
A
- Also called arthritis, rheumatic diseases include more than 100 different disorders
- They primarily affect the joints, but also muscles, bone, ligament, tendons, and cartilage
- Classification:
- Monoarticular or polyarticular
- Inflammatory or non-inflammatory
19
Q
Autoimmune Disorders:
Rheumatoid Arthritis
A
- Systemic inflammatory Autoimmune disease
- disease that results from the body’s production of an antibody (Rheumatoid factor) that reacts with IgG as if it were an antigen
- Rheumatoid Factor is produced by lymphocytes
- RF + IgG = immune complex
- (IgG) Immunoglobulin G → an anitbody
20
Q
Rheumatoid Arthritis
A
21
Q
Rheumatoid Arthritis
A
Septic Joints Possible
- Inflammatory fluids → treat w/NSAID + heat
- Fluid w/bacteria → septic joint; treat w/antibiotics (10 days-6 weeks)
- Occurs more commonly in women ages 35-50
- Attacks peripheral joints, muscles, tendons, ligaments, and blood vessels
- Inflammation of the synovial membranes is followed by formation of pannus, an inflammatory exudate, and destruction of cartilage, bone, and ligaments.
- Pannus is replaced by fibrotic tissue and calcification, which causes subluxation of the joint
22
Q
Assessment and Diagnostic Findings with Rheumatoid Arthritis
A
- Clinical presentation: rheumatoid nodules and joint inflammation bilaterally. Lymph node enlargement, tenderness, swelling, and temperature changes (warmth) in joints. Symptoms are typically bilateral.
- Health history: include onset of symptoms, family history, past health history, and contributing factors
- Functional assessment: ADL’s
- Arthrocentesis: removal of fluid from swollen joint and testing of that fluid → for infection
- Radiologic Tests: X-rays, bone scans, CT scans, and MRIs
- Tissue biopsy → rare
-
Serum studies:
- CBC → checks for infection
- Chem 25 → checks for liver function, electrolytes
- Complement → checks for immunity
- Anti- Nuclear Antibodies
- Erythrocyte Sedimentation Rate, C-Reactive Protein → non-specific
- Rheumatoid Factor → disease activity in the body
23
Q
Laboratory Findings
A
- Laboratory findings:
- Serum rheumatoid factor is present in 80 % → factor we can test in blood
- Elevated erythrocyte sedimentation rate (ESR) indicates inflammation
- C-reactive protein is positive (CRP) indicates inflammation
- RBC’s decreased
- C4 complement is decreased
- Serum Antinuclear antibody (ANA) is positive
- Synovial fluid may display a straw colored fluid with fibrin flecks and the WBC count may be elevated.
- X-rays may reveal bone demineralization and soft tissue swelling during early phases. Later may reveal narrowing of joint spaces, destruction of articular cartilage, erosion, and deformity.
24
Q
RA Clinical Manifestations/Assessments
A
- Joint pain, redness and warmth with swollen effusions
- Lack of joint mobility and function bilaterally
- Joint instability, contractures
- Deformities of the hands and feet
- Fatigue, malaise, anorexia
- Elevated body temperature
- Subcutaneous nodules on joints
- Limited ROM, paresthesias of hands/feet
- Morning stiffness and crepitus
- Pericarditis, Leukopenia
- Splenomegaly, Enlarged lymph nodes
25
Systemic clinical manifestations of RA
* Fever: low grade \<101.5 F
* Weight loss → anorexia; no appetite
* Fatigue
* Anemia
* Lymph node enlargement
* Peripheral Neuropathy
* Raynaud’s phenomenon- cold and stress induced vasospasm of the hands and feet giving them a cyanotic (bluish) appearance.
* To check for Pericartitis
1. Tell patient to hold breath
2. Put Stethescope on sub-xiphoid process
3. Listen for crinkle sounds like the sound of hair rubbing together
4.
26
Characteristic Degenerative Changes
Typical deformities
A. Ulnar drift
B. Boutonniere deformity
C. Hallux Valgus
D. Swan-neck deformity
27
Medical management
of Rheumatoid Arthritis
**RA affects blood vessels → 4x higher chances of developing coronary artery disease**
* NSAID’s (Ibuprofen) and rest
* NSAID's can cause kidney hypo perfussion → can cause acute kidney failure
* Frequent follow-up care → every 3 months
* Physical and occupational therapy to maintain joint function and muscle strength.
* check for functional status: ADL → jar opening, buttoning clothes
* Exercsie → Swimming, yoga
* \* **Remember the maximum dose of Ibuprofen is 2400 mg/day. May cause renal toxicity**
* Meds: Low-dose corticosteroids, hydroxychloroquine (antimalarial), initially for mild disease.
* Short Term
* Long term cause bone weakness/loss
* For moderate disease, Methotrexate is prescribed. Imuran is also given.
* Methotrexate treats breast cancer → in pill form suppresses immune response
* For severe disease, biologic therapy is prescribed. Enbrel, Remicade, Kineret, and Humira slow disease progression.
* Treat pain and prevent progression of the disease → not currative
28
Goals & Medical Management
for Rheumatoid Arthritis
MAJOR GOALS
■Suppress inflammation and autoimmune response
■Control pain
■Maintain or improve joint mobility
■Maintain or improve functional status
■Increase patient’s knowledge of disease
■Promote self-management with therapy
MEDICAL MANAGEMENT
■NSAID’s, anti-Rheumatic’s, corticosteroids, immunosuppressives
■NSAID’s, splints, thermal heat, relaxation
■Exercise programs and muscle strengthening
■Adaptive devices
■Provide and reinforce patient teaching
■Emphasize therapeutic regimen and lifestyle
29
Connective Tissue Diseases
* A group of chronic disorders characterized by diffuse inflammation and degeneration in the connective tissue
* Cause is unknown but thought to have an immunologic basis
* Characterized clinically with exacerbations and remissions
* Includes Rheumatoid Arthritis (RA), Systemic Lupus Erythematosus (SLE), Scleroderma, Polymyositis, and Polymyalgia Rheumatica
* Look out for: kidney, lungs, neurological status, skin and musculo skeletal
30
Systemic Lupus Erythmatosus
* Chronic inflammatory disease that affects all organ systems: renal, pulmonary, neurological, integumentary, and musculoskeletal.
* Look for BUN & Creatine, lung status, and neuro status
* Predominantly occurs in women ages 20-40.
* May be due to B lymphocyte hyperactivity with ↑ antibody production that abnormally targets self.
* Two types: Discoid – superficial lesions and Systemic – recurrent remissions and exacerbations with widespread organ involvement,
* Genetic, hormonal, immunologic, and environmental factors may play a role.
* May be drug induced:
* Methyldopa → can treat parkinsons disease
* Isoniazid → can treat TB
* Penicillins → BP
* Hydralazine
* Procainamide → cardiac drug
31
SLE- Clinical Manifestations
* Musculoskeletal: 90% joint involvement, similar to RA but no RF and no joint destruction
* Integumentary: rashes, “butterfly” rash on nose, cheeks; alopecia, sun sensitivity, mucous membrane lesions
* Cardiovascular: pericarditis, ischemic heart disease
* Pulmonary: pleural effusion, pneumonitis, PE
* Renal: glomerulonephritis, nephrotic syndrome
* Neurological: 30-75%; vasculitis leads to CVA, seizures, depression, psychiatric complications
* Hematopoietic: hemolytic anemia, leukopenia, lymphopenia, thrombocytopenia, lymphadenopathy with lesions on head, scalp, neck
32
Medical Management
of Systemic Lupus Erythmatosus
* Corticosteroids are the single most important medication used for treatment.
* Prednisone: Used in low oral doses for remissions and in high doses (IV if needed) for exacerbations. Must NEVER be stopped abruptly!! Always a tapered reduction of dose.
* Anti-malarial medications, alkylating agents and purine analogs are used for serious forms that do not respond to conservative therapies.
* SE: Chipmunk cheeks, hirsutism, balding, large trunk
33
Nursing Management
* Decreasing fatigue
* Promoting restorative sleep
* Providing protection for impaired skin integrity
* Sun and ultraviolet light exposure can increase disease activity or cause exacerbation-
* Facilitating self-care
* Improving body-image and coping
* Monitoring and managing potential complications- cardiac and renal involvement
