3545 Exam 4 (Svetlana's Set)

What is a hypersensitivity reaction?

An exaggerated immune response to an antigen that causes tissue injury instead of protection.

What does normal immunity do?

Defends against pathogens, neutralizes invaders, clears cellular debris, and promotes tissue healing and repair.

What is the mechanism of Type I hypersensitivity?

IgE-mediated; allergen binds IgE on mast cells, triggering rapid release of histamine and bradykinin.

What are examples of Type I hypersensitivity?

Anaphylaxis, angioedema, allergic rhinitis, urticaria.

What is the mechanism of Type II hypersensitivity?

Cytotoxic; autoantibodies bind to self cells carrying an attached foreign protein, forming an immune complex.

What are examples of Type II hypersensitivity?

Heparin-induced thrombocytopenia (HIT), hemolytic transfusion reactions, immune thrombocytopenic purpura (ITP).

What is the mechanism of Type III hypersensitivity?

Immune complex mediated; excess circulating antigens bind antibodies, forming complexes that deposit in small vessels.

What is an example of Type III hypersensitivity?

Systemic lupus erythematosus (SLE).

What is the mechanism of Type IV hypersensitivity?

Delayed, T-lymphocyte (T-cell) mediated; no antibody involvement.

What are examples of Type IV hypersensitivity?

TB skin test reaction, poison ivy contact dermatitis.

What do histamine and bradykinin cause in Type I reactions?

Vasodilation, capillary leak, increased mucus production, and bronchoconstriction.

What role do mast cells play in allergies?

Allergen binds to antibodies on mast cells, triggering mediator release that causes sneezing, runny nose, itchy eyes, and hives.

What are mild symptoms of Type I hypersensitivity?

Itchy eyes, sneezing, hives.

What are moderate symptoms of Type I hypersensitivity?

Urticaria, wheezing.

What are severe symptoms of Type I hypersensitivity?

Anaphylaxis with airway closure and circulatory collapse; angioedema.

What is a critical cue for Type I severity?

Symptoms escalate within minutes of exposure.

What are common triggers of anaphylaxis?

Medications, foods, latex, insect stings, and IV contrast media.

What are early manifestations of anaphylaxis?

Anxiety, a feeling of impending doom, pruritus, and hives.

What are respiratory manifestations of anaphylaxis?

Wheezing, stridor, dyspnea, throat tightness.

What are circulatory manifestations of anaphylaxis?

Hypotension and tachycardia.

What are GI manifestations of anaphylaxis?

Abdominal cramping and vomiting.

What is the first priority action in anaphylaxis?

Activate the Rapid Response Team and give IM epinephrine immediately.

Are there contraindications to IM epinephrine in anaphylaxis?

No, there are no absolute contraindications.

Why is epinephrine used in anaphylaxis?

It reverses vasodilation (raises BP) and reverses bronchoconstriction (opens the airway).

How often should epinephrine be redosed in anaphylaxis?

Repeat every 5 to 15 minutes, up to 3 doses.

What is included in the anaphylaxis acute management bundle?

IM epinephrine, maintain airway, high-flow O2, rapid normal saline bolus, recumbent position, stop causative agent, and give adjunct drugs.

What are adjunct medications in anaphylaxis?

Albuterol, H1 antihistamines, H2 antihistamines, glucocorticoids, and glucagon.

What is the recommended positioning in anaphylaxis?

Recumbent with legs and feet elevated, if tolerated.

What should be monitored after anaphylaxis?

Continuous cardiac monitoring and pulse oximetry; watch for wheezing, stridor, and hypotension.

What is the timing for rebound (biphasic) reactions?

A second reaction can occur 4 to 6 hours after the initial episode resolves.

What should be taught about using an epinephrine auto-injector?

Carry two devices, inject into the mid-outer thigh, hold for 3 seconds, then massage for 10 seconds.

What is angioedema?

Deep tissue swelling of the face, lips, tongue, and neck caused by a Type I mechanism.

What are priority cues in angioedema?

Stridor, dysphagia, and a reported lump in the throat.

What are common medication triggers of angioedema?

ACE inhibitors and NSAIDs.

What is a key teaching point about ACE inhibitor angioedema?

It can occur years after the medication was started.

What are interventions for angioedema?

Apply oxygen, prepare for intubation or tracheostomy, give epinephrine and corticosteroids.

What is the pathophysiology of Heparin-Induced Thrombocytopenia (HIT)?

Heparin binds platelet factor 4 (PF4), forming IgG antibodies that cause platelet activation and destruction.

What is the difference between HIT Type I and Type II?

Type I is non-immune and transient; Type II is immune-mediated and causes significant thrombocytopenia.

What is the hallmark sign of HIT?

Thrombocytopenia — platelet count below 150,000 or a drop greater than 50 percent from baseline.

Why is HIT considered paradoxical?

Despite low platelets, the patient clots due to platelet activation.

What are key cues for HIT?

Sudden pain, redness, or swelling in one limb; skin discoloration at the injection site.

What is the first priority nursing action in HIT?

Immediately stop all heparin sources.

What are alternative anticoagulants in HIT?

Argatroban, bivalirudin, or fondaparinux.

Why should warfarin not be started immediately in HIT?

Warfarin must wait until platelets are above 150,000 to avoid worsening clotting risk.

What should be documented in HIT?

Document heparin allergy clearly in the EHR and check for hidden sources.

How far back can heparin exposure matter in HIT?

Up to 100 days prior.

What is the pathophysiology of Immune Thrombocytopenic Purpura (ITP)?

A Type II reaction where autoantibodies target and destroy the patient's own platelets.

What are hallmark manifestations of ITP?

Petechiae, easy bruising, mucosal bleeding, and severe thrombocytopenia.

What is the key difference between ITP and HIT?

ITP causes bleeding from platelet destruction; HIT causes clotting despite low platelets.

What platelet count raises bleeding risk?

Below 50,000 raises bleeding risk with trauma.

What are priority nursing interventions in ITP?

Bleeding precautions, monitoring for bleeding, and neurologic checks.

What should ITP patients be taught about bleeding precautions?

Use a soft toothbrush, avoid contact sports, and apply pressure to puncture sites.

When should an ITP patient seek urgent care?

Headache, vision changes, confusion, uncontrolled bleeding, blood in urine or stool, or vomiting blood.

What medications are used in ITP?

Corticosteroids, IV immunoglobulin (IVIG), immunosuppressants, thrombopoietin receptor agonists, and platelet transfusion for severe active bleeding.

What is systemic lupus erythematosus (SLE)?

An autoimmune disorder where inflammatory and immune attacks occur against multiple self-tissues and organs.

What happens to complement in lupus?

Complement is overactivated by trapped immune complexes, leading to inflammation; low C3/C4 levels indicate active disease.

Why does SLE affect blood vessels heavily?

Vessels are major deposition sites for immune complexes, causing vasculitis and reduced organ perfusion.

What are common triggers for SLE?

UV light, medications, stress, pregnancy, infection, and genetics.

What are the musculoskeletal features of SLE?

Arthralgias, joint pain, myositis, and osteonecrosis.

What are the integumentary features of SLE?

Malar rash, photosensitivity, alopecia, oral ulcers, and skin lesions.

What are the renal features of SLE?

Proteinuria, hematuria, and glomerulonephritis.

What are the cardiovascular features of SLE?

Pericarditis, Raynaud phenomenon, atherosclerosis, myocarditis, and hypertension.

What are the neurologic features of SLE?

Peripheral neuropathy, confusion, seizures, and altered level of consciousness.

What are the hematologic features of SLE?

Anemia, leukopenia, and thrombocytopenia.

What are the most common causes of death in SLE?

Chronic kidney disease from glomerulonephritis and cardiovascular disease from atherosclerosis and myocarditis.

What key labs are used to diagnose SLE?

ANA, ESR, CRP, CBC with differential, complement levels C3 and C4, BUN and creatinine, and urinalysis.

What are signs of an SLE flare?

Fever, increased joint pain, and new or worsening rash.

What does new hematuria or hypertension in SLE indicate?

Lupus nephritis, which can progress to acute kidney injury.

What does dyspnea or chest pain in SLE indicate?

Pericarditis or pleural effusion.

Why are SLE patients at high infection risk?

Immunosuppressive therapy suppresses the immune response.

What are priority nursing problems in SLE?

Persistent pain, fatigue, and risk for organ failure.

How is pain managed in SLE?

NSAIDs for mild pain, corticosteroids for flares, and warm baths for stiffness.

How is fatigue managed in SLE?

Prioritize tasks, encourage rest, promote low-impact activity, and address stressors.

What is the role of hydroxychloroquine in SLE?

It reduces flares and organ damage; requires regular eye exams due to toxicity risk.

What dietary interventions are recommended for SLE?

High-vitamin and high-iron diet; high-protein only if no renal disease.

What vaccinations should SLE patients receive?

Get immunized but avoid all live vaccines due to immunosuppression.

What are the skin care interventions for SLE?

Monitor skin integrity, provide oral care, use mild soap, and avoid sunlight.

What are the complications to monitor in SLE?

BUN and creatinine levels, proteinuria, pleuritis, nephritis, and infection.

What is the action of epinephrine?

Causes vasoconstriction and bronchodilation; first-line for anaphylaxis.

What is the action of antihistamines?

Block histamine receptors; relieve itching and hives.

What is the action of corticosteroids?

Suppress inflammation and immune response; used in anaphylaxis and SLE flares.

What is the action of immunosuppressants?

Reduce autoimmune attack on self-tissue; used in SLE and IBD maintenance.

What is the depth of involvement in Crohn's disease?

Transmural, involving all layers of the bowel wall.

What is a characteristic lesion pattern in Crohn's disease?

Skip lesions with a cobblestone appearance.

What is the pain location for Crohn's disease?

Right lower quadrant.

What is the stool pattern in Crohn's disease?

5 to 6 loose stools per day, typically without gross blood.

What are the structural complications of Crohn's disease?

Strictures and deep ulcerations that lead to fistulas and abscesses.

What types of fistulas can occur in Crohn's disease?

Enterovesical, enteroenteric, enterocutaneous, and enterovaginal.

Why does Crohn's disease cause malabsorption?

Transmural inflammation of the small bowel, especially the ileum, impairs nutrient absorption.

What are the physical assessment findings in Crohn's disease?

Low-grade fever, weight loss, fatigue, RLQ abdominal tenderness, and poor nutrition and hydration status.

What are the lab findings in Crohn's disease?

Decreased hematocrit and hemoglobin, increased WBC, increased CRP and ESR, low folic acid and B12, electrolyte abnormalities, and hypoalbuminemia.

What diagnostic tests are used for Crohn's disease?

MRE, upper and lower endoscopy.

What are the priority collaborative problems in Crohn's disease?

Impaired nutrition, acute or persistent pain, and potential for infection.

What nutritional support may be required in Crohn's disease?

May require TPN and 3000+ calories per day to heal.

What is the surgical management for Crohn's disease?

Fistula repair or bowel resection; surgery is not curative.

What is the recommended diet during a flare of Crohn's disease?

Low-residue, high-protein diet.

Where does ulcerative colitis (UC) begin?

In the rectum and spreads upward through the colon.

What is the depth of involvement in ulcerative colitis?

Mucosa and submucosa only.

What is the lesion pattern in ulcerative colitis?

Continuous, not patchy.

What is the pain location for ulcerative colitis?

Left lower quadrant.