Hypersensitivity Reactions

type II antibody mediated

antibodies attack cells directly, causign destruction

• timing: hours to days

• cells destroyed

• ex: hemolytic transfusion reaction, autoimmune hemolytic anemic, goodpasture sydrome, myasthenia gravis

type III immune complexes

antigen- antibody complexes deposit in tissues

• timing: days to weeks

• complexes clog

• ex: serum sickness, systemic lupus erythematosus, post- streptococcal glomerulonephritis

type IV t-cell mediated

t-cells cause inflammation without antibodies

• timing: 48- 72 hours (delayed)

• delayed dermatitis

• ex: contact dermatitis, tuberculin skin test (PPD), transplant rejection, graft vs host disease

hemolytic transfusion reaction

occurs when incompatible blood is transfused, causing rapid red blood cell destruction

• s/s: fever, back pain, hemoglobinuria, acute kidney injury

autoimmune hemolytic anemia

the immune system produces antibodies against one's own red blood cells

• s/s: chronic anemia, fatigue, jaundice, and splenomegaly

goodpasture syndrome

antibodies attack the basement membrane in lungs and kidneys

• s/s: pulmonary hemorrhage and rapidly progressive glomerulonephritis

myasthenia gravis

antibodies block acetylcholine receptors at neuromuscular junctions

• s/s: progressive muscle weakness and fatigue, especially affecting ftypeacial muscles

type II key clinical cues

• falling hemoglobin- monitor CBC results and assess for signs of decreased oxygen carrying capacity including tachycardia and dyspnea

• juandice- check bilirubin levels and assess for associated symptoms

• hemoglobinuria- dark tea colored urine, medical emergency immediate intervention

• acute kidney injury- monitor intake and output strictly and prepare for potential dialysis

type II priority nursing actions

• stop trigger

• maintain IV access

• monitor renal function

• support oxygenation

type II pharmacology

• corticosteroids- suppress immune response and reduce inflammation

  • prednisone, methylprednisone, dexamethasone

• immunosuppressants- decrease antibody production for chronic conditions

  • azathioprine, cyclophosphamide, rituximab

    • monitor for infection risk and bone marrow suppression

• IV fluids- provide renal protection by promoting hemoglobin clearance through kidneys

  • aggressive hydration with normal saline

serum sickness

develops 7- 21 days after exposure to foreign proteins (medications, antisera)

• s/s: fever, rash, and arthralgias

  • often caused by antibiotics, antivenom, or immunoglobulins

systemic lupus erythematosus

chronic autoimmune disease with widespread immune complex deposition affecting multiple organs

• s/s: butterfly rash, joint pain, and renal involvement are common

post streptococcal glomerulonephritis

follows streptococcal infection by 1-3 weeks

• immune complexes deposit in kidney glomeruli, causing hematuria, proteinuria, hypertension, and edema

type III key clinical cues

• fever

• joint pain- arthralgias result from synovial deposition of complexes causing inflammatory arthritis

• rash- vasculitic lesions or urticaria

• renal involvement:

  • kidney damage represents the highest priority concern

    • proteinuria, hematuria, rising creatinine, decreased urine ouput, periorbital or peripheral edema

type III priority nursing interventions

• monitor kidneys- strict intake and output measurement, daily weights, serum creatinine and BUN levels, watch for oliguria or fluid overload

• manage inflammation- admin anti-inflammatory meds

  • assess effectiveness by monitoring temperature, pain levels, and inflammatory markers

• prevent further injury- identify and eliminate triggering antigens

type III pharmacology

• corticosteroids- suppress inflammation and immune response

  • monitor blood glucose, blood pressure, signs of infection

  • prednisone, methylprednisone, dexamethasone

• NSAIDs- reduce pain and inflammation

  • give with food, monitor for GI bleeding, assess renal function

• immunosuppressants- control severe or chronic disease

  • strict infection precautions, monitor CBC for bone marrow suppression

  • azathioprine, cyclophosphamide, rituximab

type IV clinical cues

• delayed onset- rash or induration develosp 48- 72 hours after exposure, not immediately

• localized inflammation- reaction typically confined to area of contact or antigen exposure

• no antibodies involved- t-cell medicated responses means antihistamines provide minimal benefit

type IV nursing priority interventions

• remove exposure- eliminate trigger immediately

• protect skin- keep affected area clean, dry, avoid scratching, and apply cool compresses for comfort

• control symptoms- use topical or systemic corticosteroids to reduce inflammation, antihistamines alone are insufficient

type IV pharmacology

• topical corticosteroids- first line treatment for contact dermatitis

  • hydrocortisone, triamcinolone, betamethasone

• systemic corticosteroids- reserved for severe or widespread reactions

  • prednisone taper

• antihistamines- provide symptom relief for pruritus only, does not treat t cell response

  • diphenhydramine, cetirizine