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

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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.
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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
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4
Q

Signs and Symptoms

A
  • LOCALIZED RESPONSE:
  • localized edema
  • andioedema
  • Pruritus “itching”
  • Rhinitis “stuffy, runny nose”
  • Rash
  • Redness
  • Fever “usually low”
  • Urticaria “hives”
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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
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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
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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
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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
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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.
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10
Q

Nursing Interventions

for anaphylactic reaction

A
  1. Stop the blood transfusion
  2. Call an RRT
  3. Place an oxygen mask on the patient at 10L/min.
  4. Administer 0.9% NS at 1L/hr.
  5. Give the patient Epinephrine 1:1000 dilution SQ.
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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!!!!!
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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.
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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.
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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
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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)
  • 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.
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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
    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
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