Exam 4 Immunological Abnormalities Flashcards
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
Q
Systemic clinical manifestations of RA
A
- 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
- Tell patient to hold breath
- Put Stethescope on sub-xiphoid process
- Listen for crinkle sounds like the sound of hair rubbing together
4.
26
Q
Characteristic Degenerative Changes
A
Typical deformities
A. Ulnar drift
B. Boutonniere deformity
C. Hallux Valgus
D. Swan-neck deformity
27
Q
Medical management
of Rheumatoid Arthritis
A
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
Q
Goals & Medical Management
for Rheumatoid Arthritis
A
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
Q
Connective Tissue Diseases
A
- 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
Q
Systemic Lupus Erythmatosus
A
- 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
Q
SLE- Clinical Manifestations
A
- 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
Q
Medical Management
of Systemic Lupus Erythmatosus
A
- 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
Q
Nursing Management
A
- 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
