Exam 1 · Week 3 · Standalone study page
M3 · Allergic, Inflammatory & Immunologic Disorders
This page keeps all of the original course information, while reducing the decision to one module: hypersensitivity, inflammation and emergency response.
▸M3Allergic, Inflammatory & Immunologic DisordersWeek 3
💡 The one idea
Hypersensitivity is the immune system attacking the wrong thing. Four types, and the exam wants you to tell them apart by timing and mechanism.
| Type | Mechanism | Timing | Example |
|---|---|---|---|
| I — Immediate | IgE + mast cells → histamine | Seconds to minutes | Anaphylaxis, hay fever, asthma |
| II — Cytotoxic | IgG/IgM attack a cell surface | Hours | Transfusion reaction, ITP |
| III — Immune complex | Antigen–antibody clumps deposit | Hours to days | SLE, RA, serum sickness |
| IV — Delayed | T cells, no antibody | 48–72 hours | TB skin test, poison ivy, latex |
⭐ How to remember the four
“ACID” — Allergic (I), Cytotoxic (II), Immune complex (III), Delayed (IV).
Type IV is the odd one: no antibodies, and it takes days. That is why you read a TB test at 48–72 hours, not immediately.
🚨 Anaphylaxis — the order is the answer
Epinephrine is first, not Benadryl. Antihistamines and steroids never rescue an airway.
Adult dose 0.3–0.5 mg IM of 1:1000, repeat every 5–15 minutes as needed.
🧠 Lupus, in five facts
- Butterfly rash across the cheeks and nose, worse with sun
- Photosensitivity — teach sunscreen and cover up, always
- Follows a flare and remission pattern; fatigue and joint pain between
- Lupus nephritis is the complication that determines survival — watch proteinuria
- Labs: ANA screens (sensitive), anti-dsDNA and anti-Smith confirm (specific)
⭐ High-yield — what the exam actually asks
Show 5 moreHide these 5
- Hypersensitivity types — I: IgE/immediate (anaphylaxis, urticaria, food, latex). II: cytotoxic (transfusion reactions). III: immune complex (lupus, serum sickness). IV: delayed T-cell
24–72 hr(poison ivy, TB skin test, transplant rejection). - Urticaria can be the opening act of anaphylaxis. Assess lips, tongue and airway before calling it minor.
- Latex allergy cross-reacts with banana, avocado, kiwi, chestnut. Latex-free for the whole stay, not just procedures.
- RA hits joints symmetrically with morning stiffness
>1 hour. Lupus can hit any organ — kidneys most often, but heart, lung and brain involvement is the scary kind. - Both get NSAIDs, steroids, methotrexate. Methotrexate → pancytopenia. Steroids → immunosuppression. Never stop either abruptly.
Show 5 moreHide these 5
- Lupus teaching is built around sun/UV protection. Exercise between flares is encouraged and does not trigger one.
- Workup labs: CBC, ANA, ESR, CRP.
- Gout: allopurinol is the long-term drug (monitor kidneys, push
2+ Lfluid/day); colchicine treats the acute attack and causes diarrhea. Avoid organ meats, seafood, alcohol. Also caused by chemo, aspirin and diuretics — not just diet. - Raynaud's: cold triggers a white → blue → red vasospasm. Gloves in cold environments, including the freezer aisle.
- Fibromyalgia is not inflammatory — ESR, CRP and ANA are normal. Low-impact exercise, sleep hygiene, duloxetine/pregabalin/milnacipran. Not opioids.
🎧 From the LSC exam-prep recording
What the faculty actually said in the review session for this week — their numbers, their worked calculations, their priority rulings. On an exam, this beats the textbook.
Show 5 moreHide these 5
- Never start allopurinol during an acute gout flare — it can worsen it. Flare treatment is naproxen or colchicine, with corticosteroids if neither can be used. Infliximab is not a gout drug (a -mab, for autoimmune disease); apixaban is an anticoagulant.
- Their conceptual hook: most flaring conditions — gout, asthma, COPD, migraine — split into PRN rescue drugs and daily preventive drugs. Allopurinol is the daily preventive and is taken flare or no flare; you simply do not start it mid-attack.
- Colchicine hits the GI tract hard — expect horrendous diarrhea and cramping. NSAID no-go list: peptic ulcer disease, chronic renal failure or a rising creatinine, hypertension, heart failure.
- Apixaban is an anticoagulant like warfarin but needs no INR monitoring. Bleeding precautions still apply.
- Acute inflammatory condition, their SATA: give corticosteroids on schedule, monitor for GI bleeding on NSAIDs and steroids alike, give antipyretics for fever, and check renal function before high-dose NSAIDs. Do not delay anti-inflammatories until the diagnostics come back.
Show 6 moreHide these 6
- The type I cue set they scored as relevant: onset 10 minutes after the infusion started, itching, dizziness, diarrhea, BP 86/52, HR 118, RR 24. Temp 37.3 °C and SpO₂ 96% were scored not indicative. About 90% of anaphylaxis has urticaria or rash.
- Their five anaphylaxis systems, in order: skin (hives), respiratory (wheeze, SOB), cardiovascular (hypotension, tachycardia), GI (vomiting, diarrhea — the forgotten one), upper airway (lip and tongue swelling).
- After epinephrine, monitor for cardiac dysrhythmias. Not respiratory depression, sedation or hypotension — those are the opposite of what a sympathomimetic does. Sinus tachycardia after a dose is expected, not an emergency.
- Hypersensitivity with their examples: I allergy/anaphylaxis + allergic rhinitis, minutes · II antibody attacks a cell — hemolytic transfusion reaction · III antibody binds a molecule — serum sickness, lupus attacking DNA · IV delayed, days later — PPD read at 72 hours, poison ivy, nickel dermatitis.
- Reported penicillin allergy: first clarify what actually happened. Rash, itching or swelling → notify the provider before giving. Do not document an allergy on a vague report — a false penicillin allergy also takes away the cephalosporins.
- Their rule of thumb: always ask "what happens when you take it?" Most reported allergies are adverse effects. Itching and nausea on morphine is an adverse effect, and the provider may still give it with premedication.
Show 7 moreHide these 7
- Salicylate toxicity: tinnitus is the red flag. The action is hold and notify, not treat the symptom. Acute overdose looks GI; chronic looks neuro (fatigue, confusion). Hyperventilation is the acid-base tell. Usually reversible if caught early.
- RA is never diagnosed on one test — rheumatoid factor plus ESR, CRP and a CBC, to tell it apart from other joint disease. Morning stiffness lasting hours points at RA and away from osteoarthritis; so do symmetry and chronic progression.
- SLE priority triad: rising BUN/creatinine, BP 160/98 with dark frothy urine (lupus nephritis), and SOB with pleuritic chest pain (lupus pneumonitis). The butterfly rash is expected, not a priority — famous, but it needs no intervention.
- Their timing hook: NSAID relief within about 60 minutes; DMARDs take weeks to months. That is why the two are prescribed together — nobody waits months in pain for the DMARD to land.
- Hydroxychloroquine: any visual change = possible irreversible retinal toxicity → stop the drug. Nausea and headache are ordinary side effects. Routine eye exams are required.
- Their drug matrix: methotrexate → RA · duloxetine and pregabalin → fibromyalgia · hydroxychloroquine and azathioprine → SLE · physical therapy → all three. Resting a painful joint is the intuitive answer and the wrong one.
- Fibromyalgia: the therapeutic answer validates — "your pain is real and valid" — and names why tests come back normal. It is muscle pain from central pain processing, not joint inflammation; expect fibro fog and sleep disturbance.
Show 3 moreHide these 3
- "Requires immediate discontinuation" is asking for an adverse effect, not a side effect. A side effect is mild and can often be premedicated; an adverse effect changes the prescription.
- Matrix and select-all items deduct for wrong picks — start from what you actually know and stop there.
- Calc: diphenhydramine 25 mg from 12.5 mg/5 mL → 25 ÷ 12.5 × 5 =
10 mL→2 teaspoons. Any of formula, ratio or dimensional analysis gets you there — do not round until the last step.
⚠️ Exam traps
- Allopurinol is prevention; colchicine is the acute attack. Reversing them is the classic miss.
- Fibromyalgia's normal labs versus RA and lupus's abnormal ones is the fastest way to tell them apart.
⚠️ What it turns into — the complication for each one
The disorder cards below run definition, causes, signs, diagnostics, management and nursing. This is the part they do not have, and it is where the exam lives: so what happens if this is missed or left? The allergic ones kill fast through the airway; the autoimmune ones damage slowly through organs — and their treatment, immunosuppression, brings its own risk.
| Disorder | What it turns into |
|---|---|
| Anaphylaxis | Laryngeal edema closing the airway and cardiovascular collapse. A biphasic reaction can return 1–72 hours after the first settles, which is why she is observed and not sent home early |
| Latex allergy | Anaphylaxis on re-exposure, and loss of a career for a health worker. Cross-reacts with banana, avocado, kiwi and chestnut — ask about those foods |
| Allergic rhinitis | Sinusitis, otitis media with effusion, worsening asthma, and broken sleep that shows up as poor concentration and irritability |
| Systemic lupus erythematosus | Lupus nephritis progressing to renal failure — the leading cause of death. Pericarditis, myocarditis, pleuritis, stroke, seizures. Infection from immunosuppression, and pregnancy loss |
| Rheumatoid arthritis | Joint deformity and lost function, atlantoaxial subluxation threatening the cord, vasculitis, Sjögren syndrome, pericarditis. Infection from DMARDs and biologics; osteoporosis from long-term steroids |
| Immunodeficiency | Recurrent and opportunistic infection, sepsis, poor response to vaccines, and raised malignancy risk |
🤕 Allergic, inflammatory and immunologic disorders, section by section
Hypersensitivity first, then autoimmunity, then too little immune function. Same six sections every time.
AnaphylaxisEpinephrine firstOpenClose
Definition and Overview
A severe, rapid, whole-body type I hypersensitivity reaction. Mast cells and basophils dump histamine and other mediators all at once, so vessels dilate and leak, airways constrict and the airway swells. It kills by airway obstruction or by circulatory collapse, sometimes within minutes, and it requires previous sensitisation — the first exposure primes, the next one reacts.
Causes and Risk Factors
Foods (peanuts, tree nuts, shellfish, eggs, milk), drugs (penicillins and other antibiotics, NSAIDs, contrast media, anaesthetic agents), insect stings, and latex. Higher risk with a history of atopy, asthma — especially poorly controlled asthma — and any previous reaction, however mild. The severity of a past reaction does not predict the severity of the next one.
Clinical Manifestations
Onset within seconds to minutes, and the faster the onset the worse the reaction. Skin: urticaria, flushing, itching, angio-edema of the lips, tongue and face. Airway: hoarseness, stridor, throat tightness, wheeze, cough, dyspnea. Circulation: tachycardia, hypotension, dizziness, collapse. Gut: cramping, vomiting, diarrhea. And a sense of impending doom, which clients describe consistently and which should be taken entirely seriously. Skin signs can be absent — their absence does not rule out anaphylaxis.
Assessment and Diagnostic Findings
It is a clinical diagnosis and it is made at the bedside. Assess airway, breathing and circulation continuously; listen for stridor and wheeze; watch the tongue and lips; monitor blood pressure, heart rate and oxygen saturation. Serum tryptase drawn within a few hours supports the diagnosis afterwards but must never delay treatment. Referral for allergy testing once recovered.
Medical Management
Intramuscular epinephrine 1:1000 into the outer mid-thigh, immediately, repeated every 5 to 15 minutes if needed. Nothing else substitutes for it. Then remove the trigger, high-flow oxygen, lie flat with legs raised unless breathing is easier sitting up, large-volume IV crystalloid for hypotension, nebulised bronchodilators for wheeze, and H1 and H2 antihistamines and corticosteroids as adjuncts — adjuncts, not treatment. Prepare for intubation or surgical airway.
Nursing Management and Client Education
Give the epinephrine first — do not stop to give diphenhydramine, and do not wait for the blood pressure to fall. Stay with the client; call for help rather than leaving. Keep intubation equipment and a second dose to hand. Observe for a biphasic reaction for up to 12 hours, because a second wave can arrive after everything has settled. Then teach: carry two auto-injectors at all times, how and where to inject through clothing into the thigh, to check the expiry date, to go to the emergency department after every use even if it worked, and to wear medical identification. Teach label reading and cross-reactivity, teach the family and the school or workplace to use the injector, and make sure the allergy is documented in every record and on the wristband.
Latex AllergyOpenClose
🖼️ InfographicsAllergy & Cough
Definition and Overview
Hypersensitivity to natural rubber latex proteins. It comes in two forms that are often confused: an irritant or type IV delayed contact dermatitis, appearing hours to days later as dry cracked itchy skin where the glove sat, and a type I immediate IgE-mediated reaction, appearing within minutes as urticaria, rhinitis, wheeze or full anaphylaxis. Only the type I reaction is life-threatening.
Causes and Risk Factors
Repeated exposure is the risk — health care workers, and above all children with spina bifida or urogenital anomalies who have had many surgeries and catheterisations. Also rubber-industry workers, people with multiple past operations, and anyone with atopy. Cross-reactivity with foods is the classic exam point: banana, avocado, kiwi, chestnut, tomato and potato share proteins with latex.
Clinical Manifestations
Contact dermatitis: redness, dryness, cracking and itching in the pattern of the glove, developing over 24 to 48 hours. Immediate reaction: hives at the contact site within minutes, then rhinitis, conjunctivitis, wheeze, angio-edema and anaphylaxis. Symptoms that appear during a procedure or after a rectal or vaginal examination with latex gloves should raise it at once.
Assessment and Diagnostic Findings
The history is the assessment, and it must be asked before every procedure: reactions to gloves, balloons, condoms, dental dams or elastic; itching or swelling of the mouth with banana, avocado, kiwi or chestnut; and how many operations the person has had. Skin-prick or serum-specific IgE testing confirms it. Document it as an allergy everywhere and band the client.
Medical Management
Avoidance is the treatment. A latex-safe environment: non-latex gloves, equipment and supplies, and for a known type I allergy the client is scheduled as the first case of the day, before latex particles have been stirred into the air. Antihistamines and topical steroids for dermatitis; epinephrine and full anaphylaxis management for a type I reaction.
Nursing Management and Client Education
Ask about latex allergy before every procedure and act on the answer. Prepare a latex-free cart — and check the small things, because the catch is that latex hides in tourniquets, blood pressure cuffs, IV tubing ports, tape, elastic bandages, stoppers on medication vials and the reservoir bag. Teach the client to carry an auto-injector if the reaction has been type I, to wear medical identification, to tell every dentist and clinician, and to avoid the cross-reactive foods if they cause symptoms. For contact dermatitis, teach glove alternatives, thorough hand drying and moisturiser — and that powdered latex gloves make everything worse for everyone in the room.
Allergic RhinitisOpenClose
Definition and Overview
An IgE-mediated inflammation of the nasal mucosa on exposure to an inhaled allergen — hay fever. Seasonal disease follows pollens; perennial disease follows dust mites, moulds, cockroaches and animal dander. It is not dangerous, but it is genuinely disabling: it wrecks sleep, concentration and school or work performance, and it is closely tied to asthma and sinusitis.
Causes and Risk Factors
Family or personal history of atopy — eczema, asthma, food allergy. Exposure to pollens, house dust mites, moulds, pets and cockroaches. Made worse by tobacco smoke, air pollution and strong odours, which irritate without being true allergens.
Clinical Manifestations
Sneezing in runs, clear watery rhinorrhoea, nasal congestion, and itching of the nose, palate, eyes and ears. Pale, boggy, bluish nasal turbinates on examination. Postnasal drip and a chronic throat clearing. In children, allergic shiners — dark under-eye circles — and the allergic salute, a transverse crease across the nose from pushing it upward. The discharge is clear; purulent discharge with facial pain and fever suggests sinusitis instead.
Assessment and Diagnostic Findings
History with attention to timing, setting and what makes it better or worse — that is usually enough. Nasal examination. Skin-prick testing or serum-specific IgE identifies the allergen when avoidance or immunotherapy is planned; antihistamines must be stopped several days before skin testing or the test will be falsely negative. Assess for coexisting asthma, sinusitis and otitis media with effusion.
Medical Management
Allergen avoidance first. Then intranasal corticosteroids, which are the most effective single treatment, second-generation oral antihistamines (loratadine, cetirizine, fexofenadine), intranasal antihistamines, leukotriene receptor antagonists, and saline irrigation. Decongestants for short-term use only. Allergen immunotherapy for disease that avoidance and drugs do not control.
Nursing Management and Client Education
Teach that intranasal steroids take days to weeks to work and must be used daily, not as needed — clients abandon them at day three otherwise. Teach the spray technique: aim away from the septum, toward the outer wall of the nostril, to prevent nosebleeds. Topical decongestant sprays must not be used beyond three days — rebound congestion makes the problem permanent. Warn that first-generation antihistamines such as diphenhydramine cause sedation and anticholinergic effects, and are a falls and confusion risk in older adults. Practical avoidance: allergen-proof mattress and pillow covers, wash bedding in hot water weekly, keep humidity below 50%, remove carpets where possible, keep pets out of the bedroom, keep windows shut and shower after being outdoors in pollen season. For immunotherapy, teach that injections are given where resuscitation is available and that the client waits 30 minutes afterwards.
Systemic Lupus ErythematosusOpenClose
🖼️ InfographicsLupus
Definition and Overview
A chronic autoimmune disease in which autoantibodies and immune complexes attack connective tissue anywhere in the body — skin, joints, kidneys, blood, heart, lungs and brain. It runs in flares and remissions and looks different in every person, which is exactly why it is hard to diagnose. Kidney involvement, lupus nephritis, is what most often determines the outcome.
Causes and Risk Factors
Overwhelmingly women of childbearing age, and more common and more severe in Black, Hispanic, Asian and Native American women. Genetic susceptibility with triggers: ultraviolet light, infection, stress, pregnancy and the postpartum period, and certain drugs — hydralazine, procainamide and isoniazid can produce a drug-induced lupus that resolves when the drug is stopped.
Clinical Manifestations
Fatigue, fever, weight loss and symmetrical joint pain are the everyday burden. The recognisable sign is the butterfly (malar) rash across the cheeks and bridge of the nose, sparing the nasolabial folds, along with a discoid rash, photosensitivity, painless oral or nasal ulcers, alopecia and Raynaud phenomenon. Then organ involvement: proteinuria and hypertension from nephritis, pleuritis and pericarditis, anemia, leukopenia and thrombocytopenia, and neuropsychiatric disease from headache to seizures and psychosis.
Assessment and Diagnostic Findings
ANA is positive in almost everyone with lupus, so it screens but does not diagnose. The specific ones are anti-double-stranded DNA and anti-Smith, and anti-dsDNA titres and complement C3 and C4 track disease activity — the antibody rises and the complement falls in a flare. Add CBC, ESR and CRP, creatinine, urinalysis for protein, red cells and casts at every visit, antiphospholipid antibodies for clotting risk, and renal biopsy to classify nephritis.
Medical Management
Hydroxychloroquine for essentially everyone, because it reduces flares and improves survival. Corticosteroids for flares, at the lowest dose for the shortest time. Immunosuppressants — methotrexate, azathioprine, mycophenolate, cyclophosphamide — and biologics such as belimumab for significant organ disease. NSAIDs for joint and serosal pain. Aggressive control of blood pressure and lipids, and an ACE inhibitor or ARB for proteinuria.
Nursing Management and Client Education
Sun protection is treatment, not advice: broad-spectrum SPF 30 or higher every day, hats, long sleeves, avoid the middle of the day, and be aware that fluorescent light can provoke a flare. Teach the client to recognize their own early flare pattern and to report new swelling, frothy urine, chest pain, fever or a change in thinking. Hydroxychloroquine needs an annual eye examination for retinal toxicity, and it takes months to work — say so, or it gets stopped. On steroids, teach infection risk, glucose, bone protection with calcium and vitamin D, and never stopping corticosteroids abruptly. Because infection is a leading cause of death, teach hand hygiene, keeping vaccinations up to date (no live vaccines while immunosuppressed), and reporting fever early. Balance rest with activity, plan pregnancy for a period of remission and discuss it in advance, and acknowledge the invisible illness — the fatigue and the being disbelieved are real, and depression is common.
Rheumatoid ArthritisOpenClose
🖼️ InfographicsRheumatoid Arthritis
Definition and Overview
A chronic systemic autoimmune inflammation of the synovium. The inflamed synovium forms a pannus that erodes cartilage and bone, permanently deforming the joint. It is symmetrical, affects the small joints first, and is systemic — that is what separates it from osteoarthritis, which is asymmetrical, mechanical, and confined to the joint.
Causes and Risk Factors
Two to three times more common in women, usually beginning between 30 and 60. Genetic susceptibility (HLA-DR4), smoking, which is the strongest modifiable risk, obesity, family history, and possibly periodontal disease and the gut microbiome.
Clinical Manifestations
Morning stiffness lasting more than an hour — the single most useful discriminator, because osteoarthritis stiffness eases within minutes. Symmetrical swelling, warmth and pain in the small joints of the hands and feet: the metacarpophalangeal, proximal interphalangeal and metatarsophalangeal joints, with the distal interphalangeal joints spared. Later, the classic deformities — ulnar deviation, swan-neck and boutonniere fingers. Systemic features: fatigue, low-grade fever, weight loss, anemia, rheumatoid nodules, dry eyes and mouth, pleuritis, pericarditis and vasculitis.
Assessment and Diagnostic Findings
Rheumatoid factor and anti-CCP antibodies, of which anti-CCP is the more specific and predicts erosive disease. ESR and CRP to measure activity. CBC for anemia of chronic disease. X-rays showing joint space narrowing and erosions; ultrasound or MRI detects synovitis earlier. Assess function directly — grip strength, ability to dress, open jars, manage a toothbrush — because that is what the client actually cares about.
Medical Management
Start a disease-modifying drug early — within weeks of diagnosis — because the window to prevent erosion is short. Methotrexate is the anchor drug, given weekly with folic acid. Then biologics (TNF inhibitors, abatacept, rituximab, tocilizumab) and JAK inhibitors when methotrexate is not enough. Corticosteroids as a bridge or for flares. NSAIDs for symptoms only — they do not slow the disease. Physiotherapy, occupational therapy, and joint replacement for damaged joints.
Nursing Management and Client Education
Balance rest and activity: rest the joint during a flare, but keep moving it through range of motion, because immobility causes contracture. Heat for stiffness, cold for an acutely inflamed joint. Splints at night. Occupational therapy for assistive devices and joint protection — use large joints instead of small ones, slide rather than lift, use both hands, and take frequent breaks. Teach the drugs carefully: methotrexate is taken weekly, not daily — a daily dose has killed people — and it needs folic acid, regular liver function tests and CBC, no alcohol, and reliable contraception, because it causes birth defects. On biologics, teach infection risk, screening for tuberculosis before starting, no live vaccines, and reporting any fever. Plan the day around morning stiffness — a hot shower on waking, appointments in the afternoon. Address the fatigue and the depression openly, and connect the client with a support group.
ImmunodeficiencyOpenClose
🖼️ InfographicsAllergic, Inflammatory & Immunologic
Definition and Overview
A failure of part of the immune system, so infections are more frequent, more severe, longer, and caused by organisms that should not trouble anyone. Primary immunodeficiency is inherited and usually appears in childhood — a defect in antibodies, T cells, phagocytes or complement. Secondary immunodeficiency is acquired and is far more common in adult practice.
Causes and Risk Factors
Secondary causes are what you will meet: HIV, chemotherapy and radiotherapy, corticosteroids and other immunosuppressants, biologics, transplantation, splenectomy, diabetes, chronic kidney or liver disease, malnutrition, and extremes of age. Primary causes are suggested by a family history and by infections beginning in infancy.
Clinical Manifestations
The pattern matters more than any single infection: recurrent sinus, ear or chest infections, infections that need intravenous antibiotics or do not clear, two or more serious infections such as pneumonia or sepsis, persistent thrush after infancy, deep abscesses, poor growth in a child, and opportunistic organisms like Pneumocystis, Aspergillus or disseminated fungal disease. A client who is neutropenic may not mount a fever or produce pus — the usual signs of infection can simply be absent, so a single low-grade temperature is an emergency.
Assessment and Diagnostic Findings
CBC with differential and the absolute neutrophil count — below 500/mm³ is severe neutropenia and high risk. Quantitative immunoglobulins, specific antibody responses to vaccines, lymphocyte subsets including CD4 count, complement levels, HIV testing, and genetic testing for suspected primary disease. Culture everything before antibiotics, and inspect the usual quiet sites — mouth, perineum, IV lines, skin folds — at every shift.
Medical Management
Treat the cause where you can and support what is missing. Immunoglobulin replacement, intravenous or subcutaneous, for antibody deficiency. Prophylactic antimicrobials. Growth factors such as filgrastim to shorten chemotherapy-induced neutropenia. Antiretroviral therapy for HIV. Haematopoietic stem cell transplantation for severe primary immunodeficiency. Prompt, aggressive, broad-spectrum treatment of every febrile episode.
Nursing Management and Client Education
Hand hygiene is the whole game — yours, the client's, and every visitor's. Protective measures for the severely neutropenic: private room, no one with an infection in the room, no fresh flowers, plants or standing water, and no raw or undercooked food. Avoid rectal temperatures, suppositories and enemas — breaking that mucosa lets gut organisms straight into the blood. Meticulous mouth care with a soft brush, daily skin and perineal inspection, and minimal invasive devices. Teach the client to take their temperature and to call for a single reading of 100.4°F (38°C) rather than waiting. Teach food safety, avoiding crowds during nadir periods, no gardening or cleaning litter trays without gloves, no live vaccines while immunosuppressed, and that household contacts should be vaccinated. For immunoglobulin infusions, watch for headache, chills and fever, and slow the rate. Name the isolation for what it is — lonely — and plan around it.
🧠 Mind maps 2
One per disorder, built from the structure of your ATI chapter.
🎯 Who gets it
- Lupus risk rises with genetic predisposition and female sex aged
15-44. - Lupus is more common in African American, Asian, Hispanic, or Indigenous clients.
- Lupus flares can be triggered by trauma, infection, UV light, or stress.
- Gout risk rises with BMI over
30, heredity, and trauma.
👀 What you see
- Lupus: fatigue, joint pain/swelling, hair loss, dry eyes, headaches.
- Lupus: fever signals a flare; watch for pericarditis and anemia.
- Lupus: classic butterfly rash across the nose and cheeks.
- Lupus: discoid form causes coin-shaped lesions on sun-exposed skin.
🧪 What confirms it
- ANA titers are positive in
90%of clients who have lupus. - Lupus depletes complement proteins C3 and C4, so both drop.
- ESR is elevated in lupus from systemic inflammation.
- Lupus kidney involvement raises BUN and creatinine, with protein and RBCs in urine.
🩺 What you do
- Lupus: monitor vital signs, especially blood pressure, and systemic symptoms.
- Lupus: watch for hypertension and edema signaling kidney involvement.
- Lupus: diminished breath sounds may indicate pleural effusion.
- Lupus: tachycardia with sharp inspiratory pain suggests pericarditis.
💊 Drugs
- NSAIDs treat lupus inflammation; avoid in clients with ulcers.
- Prednisone immunosuppresses in lupus; watch for fluid retention and bruising.
- Colchicine treats acute gout pain; use cautiously with kidney impairment.
- Gout NSAIDs (indomethacin, naproxen, ibuprofen) are avoided with kidney disease or ulcers.
💬 What you teach
- Lupus: taper steroids gradually; never stop corticosteroids abruptly.
- Lupus: wear sunscreen, hats, and long sleeves to avoid UV flares.
- Hydroxychloroquine needs frequent eye exams to monitor for visual changes.
Read left to right: who gets it → what you see → what confirms it → what you do → what goes wrong. Cover a column and rebuild it out loud.
🎯 Who gets it
- RA risk is higher in females aged
30 to 60years. - Genetic predisposition and prior bacterial or viral infection raise RA risk.
- Stress, smoking, and environmental factors also increase RA risk.
- Older age is an added risk factor for RA.
👀 What you see
- Morning stiffness and pain after rest or long sitting are typical.
- Joint swelling, warmth, and erythema are common RA findings.
- Joint deformity is a late manifestation of RA.
- RA commonly affects fingers, hands, wrists, knees, and feet.
🧪 What confirms it
- Anti-CCP antibodies are more sensitive for RA than RF antibody.
- RF antibody normal range is under
20 U/mL; not RA-specific. - ESR rises with inflammation, infection, or tissue necrosis.
- CRP normal range is under
1.0 mg/dL; tracks treatment response.
🩺 What you do
- Encourage physical activity and safe mobility aids to protect joints.
- Recommend assistive devices like grab bars and raised toilet seats.
- Initiate fall precautions; refer to physical and occupational therapy.
- Monitor for medication effectiveness: less pain, more mobility.
💊 Drugs
- RA treatment typically starts with NSAID therapy first.
- NSAIDs relieve pain, fever, and inflammation in RA.
- NSAIDs can cause significant GI distress in some clients.
💬 What you teach
- After arthrocentesis: take acetaminophen for pain; avoid strenuous exercise a few days.
- X-rays track joint damage progression; keep still during the scan.
- Take NSAIDs with food, milk, or antacids to protect the stomach.
Read left to right: who gets it → what you see → what confirms it → what you do → what goes wrong. Cover a column and rebuild it out loud.
🎥 Lecture recordings 3
Tap a card to open that recording in Google Drive. The same list lives in the lecture library.
All NUR 258 recordings →🖼️ Infographics 6
Tap a card to open the matching graphics in your infographic library.
📄 Simple Nursing handouts for this module — 3 of them, straight from your Drive.
📋 Active Learning Templates 2
One per disorder. Every row is filled from that section of the ATI chapter — print it, cover the right, rebuild it.
📋 Lupus Erythematosus, Gout, and Fibromyalgia6 parts
Filled from ATI chapter 87, row by row from that chapter’s own sections — 12 of 12 rows have content.
🧭 What it isAlterations in Health (Diagnosis) · Health Promotion & Disease Prevention
Alterations in Health (Diagnosis)
- This chapter covers three distinct conditions: lupus erythematosus, an autoimmune disease causing chronic inflammation across organs; gout, a hyperuricemia disorder that deposits uric acid crystals in joints; and fibromyalgia, a chronic widespread pain and fatigue syndrome.
Health Promotion & Disease Prevention
From this module — built from the notes above on this page, not a section of the ATI chapter.
- Lupus: strict sun protection — ultraviolet light triggers both rash and systemic flares. Sunscreen, hats, long sleeves.
- Gout: limit purines — organ meats, shellfish, sardines, beer — and keep well hydrated.
- Fibromyalgia: graded aerobic exercise, sleep hygiene and stress management are the core treatment, not the extras.
- Infection prevention and vaccination in anyone on immunosuppression.
- Recognize and treat depression, which is common in all three and worsens every symptom.
👀 How it shows upAssessment — Risk Factors · Assessment — Expected Findings
Assessment — Risk Factors
- Lupus risk rises with genetic predisposition and female sex aged
15-44. - Lupus is more common in African American, Asian, Hispanic, or Indigenous clients.
- Lupus flares can be triggered by trauma, infection, UV light, or stress.
- Gout risk rises with BMI over
30, heredity, and trauma. - Gout risk also rises with alcohol use, diuretics, and chemo agents.
- Gout risk increases with chronic kidney disease as well.
- Fibromyalgia risk rises in females over age
40with sleep deprivation. - Fibromyalgia risk rises with trauma, infection, or autoimmune disease history.
Assessment — Expected Findings
- Lupus: fatigue, joint pain/swelling, hair loss, dry eyes, headaches.
- Lupus: fever signals a flare; watch for pericarditis and anemia.
- Lupus: classic butterfly rash across the nose and cheeks.
- Lupus: discoid form causes coin-shaped lesions on sun-exposed skin.
- Lupus: Raynaud's phenomenon causes color changes in fingers with cold or stress.
- Gout: acute attacks last
1 to 2 weeks. - Gout: severe pain, redness, swelling, and warmth in the great toe joint.
- Gout: chronic disease can form tophi, urate deposits under the skin.
🧪 How it is confirmedLaboratory Tests · Diagnostic Procedures
Laboratory Tests
- ANA titers are positive in
90%of clients who have lupus. - Lupus depletes complement proteins C3 and C4, so both drop.
- ESR is elevated in lupus from systemic inflammation.
- Lupus kidney involvement raises BUN and creatinine, with protein and RBCs in urine.
- CBC in lupus often shows pancytopenia, a drop in all cell lines.
Diagnostic Procedures
- Skin biopsy confirms discoid lupus by finding lupus cells and inflammation.
- Synovial fluid aspiration checks for uric acid crystals to confirm gout.
🩺 What you doNursing Care · Medications · Therapeutic Procedures
Nursing Care
- Lupus: monitor vital signs, especially blood pressure, and systemic symptoms.
- Lupus: watch for hypertension and edema signaling kidney involvement.
- Lupus: diminished breath sounds may indicate pleural effusion.
- Lupus: tachycardia with sharp inspiratory pain suggests pericarditis.
- Lupus: check hands/feet color changes from Raynaud's vasospasm.
- Lupus: monitor mental status changes for neurologic involvement.
- Lupus: track BUN, creatinine, and urine output for renal status.
- Lupus: offer small frequent meals and limit salt with steroid therapy.
- Lupus and fibromyalgia: provide emotional support to client and family.
Medications
- NSAIDs treat lupus inflammation; avoid in clients with ulcers.
- Prednisone immunosuppresses in lupus; watch for fluid retention and bruising.
- Colchicine treats acute gout pain; use cautiously with kidney impairment.
- Gout NSAIDs (indomethacin, naproxen, ibuprofen) are avoided with kidney disease or ulcers.
- Gout prednisone requires gradual tapering, never abrupt discontinuation.
- Allopurinol/febuxostat lowers uric acid production for chronic gout maintenance.
- Probenecid promotes uric acid excretion; monitor uric acid levels.
- Pegloticase IV, given every other week, converts uric acid for excretion.
Therapeutic Procedures
From this module — built from the notes above on this page, not a section of the ATI chapter.
- Lupus: hydroxychloroquine as the backbone, with steroids and immunosuppressants for flares. Baseline and annual eye examination — retinal toxicity.
- Gout, acute: NSAIDs, colchicine or corticosteroids. Do not start or stop allopurinol during an acute attack — it makes it worse.
- Gout, long term: allopurinol or febuxostat with generous fluids; joint rest and elevation during an attack.
- Fibromyalgia: duloxetine, milnacipran or pregabalin, alongside exercise and cognitive behavioral therapy.
- Energy conservation, joint protection and pacing across all three.
💬 Around the patientClient Education · Interprofessional Care
Client Education
- Lupus: taper steroids gradually; never stop corticosteroids abruptly.
- Lupus: wear sunscreen, hats, and long sleeves to avoid UV flares.
- Hydroxychloroquine needs frequent eye exams to monitor for visual changes.
- Lupus: report peripheral or periorbital swelling and any infection signs.
- Lupus: avoid crowds and sick contacts to prevent flares.
- Lupus nephritis/pericarditis: report chest pain and take meds as prescribed.
- Gout: follow a low-purine diet, avoiding organ meats and shellfish.
Interprofessional Care
- Ophthalmologists monitor for visual deficits from hydroxychloroquine therapy.
- Refer lupus clients to support groups as appropriate.
- Physical therapy can help reduce pain from fibromyalgia symptoms.
- Refer fibromyalgia clients to national foundations and local support groups.
⚠️ What goes wrongComplications
Complications
From this module — built from the notes above on this page, not a section of the ATI chapter.
- Lupus nephritis — the complication that determines prognosis. Monitor urine protein and creatinine.
- Lupus: pericarditis, pleuritis, neuropsychiatric involvement, and accelerated atherosclerosis.
- Gout: tophi, joint destruction, and uric acid kidney stones.
- Fibromyalgia: disability, sleep disorder, depression, and the harm of repeated unnecessary investigation.
- Infection and osteoporosis from long-term corticosteroids.
📋 Rheumatoid Arthritis6 parts
Filled from ATI chapter 88, row by row from that chapter’s own sections — 12 of 12 rows have content.
🧭 What it isAlterations in Health (Diagnosis) · Health Promotion & Disease Prevention
Alterations in Health (Diagnosis)
- This chapter explains rheumatoid arthritis, an autoimmune disease where white blood cells inflame joint synovium bilaterally, causing pain, deformity, and systemic effects on the lungs, heart, and eyes, alternating between flares and remission.
Health Promotion & Disease Prevention
- Keep using affected joints and stay active to preserve range of motion.
- Aim for
150 minof moderate activity weekly, or30 mindaily,5 daysa week.
👀 How it shows upAssessment — Risk Factors · Assessment — Expected Findings
Assessment — Risk Factors
- RA risk is higher in females aged
30 to 60years. - Genetic predisposition and prior bacterial or viral infection raise RA risk.
- Stress, smoking, and environmental factors also increase RA risk.
- Older age is an added risk factor for RA.
Assessment — Expected Findings
- Morning stiffness and pain after rest or long sitting are typical.
- Joint swelling, warmth, and erythema are common RA findings.
- Joint deformity is a late manifestation of RA.
- RA commonly affects fingers, hands, wrists, knees, and feet.
- Finger deformities include ulnar deviation, swan neck, and boutonniere changes.
- Subcutaneous nodules can form over joints or pressure points.
- Low-grade fever, fatigue, and muscle weakness are common.
- Xerostomia, anorexia, and weight loss can also occur.
🧪 How it is confirmedLaboratory Tests · Diagnostic Procedures
Laboratory Tests
- Anti-CCP antibodies are more sensitive for RA than RF antibody.
- RF antibody normal range is under
20 U/mL; not RA-specific. - ESR rises with inflammation, infection, or tissue necrosis.
- CRP normal range is under
1.0 mg/dL; tracks treatment response. - ANA titer is often positive in RA but not RA-specific.
Diagnostic Procedures
- Arthrocentesis aspirates synovial fluid; RA shows raised WBCs and protein.
🩺 What you doNursing Care · Medications · Therapeutic Procedures
Nursing Care
- Encourage physical activity and safe mobility aids to protect joints.
- Recommend assistive devices like grab bars and raised toilet seats.
- Initiate fall precautions; refer to physical and occupational therapy.
- Monitor for medication effectiveness: less pain, more mobility.
- After arthrocentesis, check the joint site for bleeding, pain, fever, or swelling.
- NSAID use: watch for fluid retention, hypertension, and renal dysfunction.
- Corticosteroid use: monitor for Cushingoid changes, weight gain, and high BP.
- DMARDs: monitor for allergic reaction, low WBCs, and rising liver enzymes.
- Sjögren's syndrome: give eye drops, artificial saliva, and vaginal lubricants.
Medications
- RA treatment typically starts with NSAID therapy first.
- NSAIDs relieve pain, fever, and inflammation in RA.
- NSAIDs can cause significant GI distress in some clients.
Therapeutic Procedures
- Plasmapheresis removes circulating antibodies to reduce severe RA flares.
- Total joint arthroplasty replaces joints unresponsive to medication therapy.
- Synovectomy is surgical removal of the affected synovial membrane.
💬 Around the patientClient Education · Interprofessional Care
Client Education
- After arthrocentesis: take acetaminophen for pain; avoid strenuous exercise a few days.
- X-rays track joint damage progression; keep still during the scan.
- Take NSAIDs with food, milk, or antacids to protect the stomach.
- Watch for GI bleeding: coffee-ground emesis or dark, tarry stools.
- Corticosteroids aren't for long-term RA use due to osteoporosis and hyperglycemia risk.
- Corticosteroids can also cause immunosuppression and cataracts with prolonged use.
- Report vision changes, high blood sugar, poor healing, or weight gain on steroids.
Interprofessional Care
- Refer clients to RA support groups for peer support.
- Occupational therapy provides adaptive devices to aid ADLs and prevent deformity.
⚠️ What goes wrongComplications
Complications
From this module — built from the notes above on this page, not a section of the ATI chapter.
- Joint deformity — ulnar deviation, swan-neck and boutonnière changes, and loss of function.
- Cervical spine instability at C1–C2 — matters enormously before intubation or any neck manipulation.
- Extra-articular disease: rheumatoid nodules, pleural effusion, interstitial lung disease, pericarditis, scleritis.
- Sjögren syndrome — dry eyes and mouth — commonly accompanies it.
- Anemia of chronic disease, osteoporosis, and accelerated cardiovascular disease, which is the leading cause of death.
- Immunosuppression from DMARDs and biologics — screen for TB before starting a TNF inhibitor.
📝 Notes & key concepts
The lines from this module that carry a number, a dose or an absolute rule — the ones that decide questions. Everything else is on the cards above.
- Hypersensitivity types — I: IgE/immediate (anaphylaxis, urticaria, food, latex). II: cytotoxic (transfusion reactions). III: immune complex (lupus, serum sickness). IV: delayed T-cell
24–72 hr(poison ivy, TB skin test, transplant rejection). - RA hits joints symmetrically with morning stiffness
>1 hour. Lupus can hit any organ — kidneys most often, but heart, lung and brain involvement is the scary kind. - Both get NSAIDs, steroids, methotrexate. Methotrexate → pancytopenia. Steroids → immunosuppression. Never stop either abruptly.
- Gout: allopurinol is the long-term drug (monitor kidneys, push
2+ Lfluid/day); colchicine treats the acute attack and causes diarrhea. Avoid organ meats, seafood, alcohol. Also caused by chemo, aspirin and diuretics — not just diet. - Never start allopurinol during an acute gout flare — it can worsen it. Flare treatment is naproxen or colchicine plus corticosteroids. Infliximab is not a gout drug. Colchicine hits the GI tract hard; NSAIDs are off-limits in renal impairment.
- The type I cue set they scored as relevant: onset 10 minutes after the infusion started, itching, dizziness, diarrhea, BP 86/52, HR 118, RR 24. Temp 37.3 and SpO2 96% were scored as not indicative. About 90% of anaphylaxis has urticaria or rash.
- Hypersensitivity with their examples: I allergy/anaphylaxis + allergic rhinitis · II hemolytic and transfusion · III serum sickness · IV delayed — PPD read at 72 hours, poison ivy, nickel dermatitis.
- Reported penicillin allergy: first clarify what actually happened. Rash, itching or swelling → notify the provider before giving.
- SLE priority triad: rising BUN/creatinine, BP 160/98 with dark frothy urine (lupus nephritis), and SOB with pleuritic chest pain (lupus pneumonitis). The butterfly rash is expected, not a priority.
- Their timing hook: NSAID relief within about 60 minutes; DMARDs take weeks.
- Hydroxychloroquine: any visual change = possible irreversible retinal toxicity → stop the drug. Routine eye exams required.
- Calc: diphenhydramine 25 mg from 12.5 mg/5 mL = 10 mL = 2 teaspoons.
🎯 Module quiz
Questions for this module. They also feed the Mega Quiz.
Nothing here yet — drop it in when you have it