Autoimmune disorders

Autoimmune items ask whether you prevent an SLE flare, protect inflamed joints, keep a myasthenic airway open, and respect infection risk on immunosuppressants. Steroid hyperglycemia, taper, and adrenal rules are taught in depth in Oral antidiabetics and corticosteroids. This chapter owns lupus, RA versus OA framing, myasthenia crises, and immunosuppression safety.

SLE: flares and lupus nephritis

Systemic lupus erythematosus is a multisystem autoimmune disease in which autoantibodies and immune complexes injure skin, joints, serosa, kidneys, and other organs. Flares are not random mood swings — ultraviolet light, infection, surgery, and pregnancy commonly provoke activity. Teaching sunscreen (broad-spectrum, reapplied), sun-protective clothing, prompt treatment of infections, and medication adherence (hydroxychloroquine and immunosuppressants as ordered) is disease-modifying nursing. Malar rash and photosensitivity are visible cues; fatigue and arthritis are common. Fever in SLE can be disease or infection — never assume “just a flare” without assessment when the client is immunosuppressed.

Lupus nephritis changes the priority map. Immune complex deposition in glomeruli produces proteinuria, hematuria, rising blood pressure, edema, and climbing creatinine. Foamy urine and periorbital edema on stems should redirect you from lotion-for-the-rash thinking to renal monitoring, fluid and sodium guidance as ordered, and blood pressure control. Infection remains a top killer in treated lupus because therapy suppresses defenses — hand hygiene and fever reporting are not optional lifestyle tips.

RA joint protection versus OA

Rheumatoid arthritis is systemic autoimmune synovitis, typically symmetric small joints, with prolonged morning stiffness and constitutional symptoms. Joint protection means using larger joints for load (carry bags on forearms, not fingers), avoiding prolonged tight grips, pacing activity, splints as ordered, and balancing rest during flares with gentle ROM to prevent contractures. Hot packs may ease stiffness; ice can calm acute hot joints — match to the moment. Disease-modifying drugs slow destruction; infection and liver/lung monitoring follow specific agents.

Osteoarthritis is degenerative cartilage loss, often asymmetric weight-bearing joints, with pain that worsens with use and improves with rest, and brief stiffness. Teaching leans toward weight management, strengthening supporting muscles, assistive devices, and acetaminophen or topical NSAIDs as ordered — not the same immunosuppression package as RA. The exam distractor applies marathon exercise during an RA flare or assumes every “arthritis” client needs methotrexate. Keep the mechanism straight: immune-driven synovium versus mechanical wear.

• RA: symmetric, systemic, morning stiffness lasting longer.
• OA: activity pain, Heberden/Bouchard patterns as tested, local management.
• Never force a hot swollen RA joint through painful ROM contests.

Myasthenia: crisis versus cholinergic crisis

Myasthenia gravis is antibody-mediated attack on acetylcholine receptors at the neuromuscular junction — muscles fatigue with use, especially eyes, face, swallow, and respiration. Acetylcholinesterase inhibitors raise acetylcholine in the synapse and improve strength when dosed correctly. Myasthenic crisis is severe weakness from disease flare, infection, or underdosing: the airway and ventilation fail. Cholinergic crisis is overdose: muscarinic excess (salivation, lacrimation, urination, diarrhea, emesis, bradycardia, miosis) plus weakness from depolarization overload. Both can look like “can't breathe” — airway and ventilation come first.

Classic stems use edrophonium (Tensilon) testing: strength improves in myasthenic crisis and worsens or shows cholinergic signs in overdose — only where that test is still described. At the bedside without the test, history of missed doses versus extra pills, and presence of SLUDGE signs, guide you. Hold cholinesterase inhibitors in suspected cholinergic crisis; atropine may be ordered for muscarinic effects. Aspiration precautions, soft diet timing with peak drug effect, and infection prevention (infection triggers myasthenic crisis) are daily nursing. Never pile on more inhibitor because weakness continues without sorting which crisis you are in.

1. Airway equipment ready for any severe myasthenic weakness.
2. Give AChEI on time — late doses can precipitate crisis.
3. Treat infection early; it is a common crisis precipitant.

Immunosuppression and infection risk

Controlling autoimmune activity often means steroids, methotrexate, azathioprine, mycophenolate, or biologics that blunt immune surveillance. The tradeoff is infection — bacterial, viral, opportunistic — and slower wound healing. Teach clients to report fever, productive cough, dysuria, or wound changes immediately; avoid live vaccines when protocols forbid them; and practice food and exposure common sense during nadir-like risk periods. Hold or clarify immunosuppressants around active serious infection per provider — do not freelance stop/start. Detailed corticosteroid glucose and taper teaching belongs in Oral antidiabetics and corticosteroids; here, remember steroids plus other agents amplify infection risk in SLE, RA, and myasthenia care plans.

• Hand hygiene and vaccination status review at every teaching moment.
• TB and hepatitis screening appear before many biologics — nursing role is adherence to the checklist.
• Pregnancy plans matter for teratogenic DMARDs — send to provider counseling.

Priority map