Inflammatory, Autoimmune & Immune Disorders — Core Concepts

This is about chronic inflammation, autoimmunity, and immune system behavior (plus a few neuro + GI conditions driven by inflammation). The key is recognizing:

• “Is this autoimmune, degenerative, or acute inflammation?”

• “Is my biggest risk infection, respiratory failure, or organ damage?”

• “What’s the nurse’s priority right now?”

  
  

🛡️ Safety Anchors (Inflammatory & Immune)

• 🔥 Inflammation ≠ always infection. Red, warm, swollen joint → think inflammation first, not automatically antibiotics.

• 🧬 Autoimmune disease = high infection risk, especially on steroids or immunosuppressants – teach to report slight changes in health.

• 🫁 Neuro-immune conditions (GBS, MS, encephalitis) → always ask: “Can they protect their airway and breathe?”

• 🌞 SLE & photosensitivity → strict sun protection (hats, sunscreen, avoid midday sun).

• 💉 Antineoplastics & high-dose steroids are big causes of immunosuppression.

• 🧠 ↑ICP signs (projectile vomiting, blurred vision, bradycardia + hypertension) are emergencies.

• 💪 Rheumatic diseases: nursing goals focus on pain control + activity tolerance, not “cure.”

Clinical Judgment Chain (Immune):Identify immune/inflammatory pattern → decide autoimmune vs degenerative vs acute → protect airway, brain, vital organs → prevent infection & immobility complications → long-term education & self-management.

🦴 Autoimmune & Rheumatic Disorders

Disorder	Pathophysiology / Type	Incubation & Transmission	Key Clinical Features	Diagnostics	Isolation / Infection Control	Priority Nursing Care / Exam Pearls
Rheumatoid Arthritis (RA)	Chronic autoimmune synovial inflammation → pannus → joint destruction & deformity	Chronic autoimmune; no incubation or transmission; often gradual onset.	Symmetric small-joint pain & swelling (hands, wrists), early morning stiffness, fatigue, possible nodules later.	Rheumatoid factor, anti-CCP, ESR/CRP, X-ray (joint space narrowing).	None; not contagious.	Main goals: pain control & activity tolerance. Early RA sign = early morning stiffness. RA development sequence: synovitis → pannus → ankylosis. Nursing dx often activity intolerance r/t fatigue & pain.
Osteoarthritis (OA)	Degenerative joint disease; cartilage wear in weight-bearing joints	Chronic wear-and-tear; noninfectious; non-autoimmune.	Pain worsens with use, better with rest; crepitus; affects weight-bearing joints (knees, hips, spine, hands). Minimal systemic symptoms.	X-ray: joint space narrowing, osteophytes.	None.	Focus on weight reduction, assistive devices, heat, analgesics, low-impact exercise. In exam: arthritis affecting hands, knees, hips, spine = likely OA.
Gout	Uric acid crystal deposition in joints causing acute inflammation	Chronic metabolic; no incubation; triggered by hyperuricemia, high purine diet, alcohol, renal issues.	Sudden severe pain, redness, warmth and swelling in great toe (podagra) most common; can involve other joints.	Serum uric acid, synovial fluid analysis (needle-shaped crystals).	None.	Acute attack: pain control (NSAIDs if allowed), joint rest. Long-term: low-purine diet, avoid alcohol, maintain hydration, allopurinol as ordered. Exam clue: swollen, hot, painful great toe = gout.
Systemic Lupus Erythematosus (SLE)	Multisystem autoimmune disease; immune complexes deposit in tissues (skin, joints, kidneys, etc.)	Chronic autoimmune; no incubation; flares triggered by sun, stress, infection, some meds.	Butterfly rash over cheeks & nose, photosensitivity, malaise, arthralgia, possible mouth ulcers, renal involvement (proteinuria).	ANA, anti-dsDNA, anti-Smith antibodies, complement levels, UA for protein.	None, but infection precautions if immunosuppressed.	Teach: avoid sun (wear large-brimmed hats, sunscreen), avoid tanning beds, rest during flares. Watch for renal involvement & infection (esp. on steroids like prednisone).
Polymyositis	Chronic inflammatory myopathy with immune attack on skeletal muscle → weakness	Chronic autoimmune; not infectious. Often gradual onset.	Proximal muscle weakness (difficulty climbing stairs, rising from chair, lifting arms), fatigue.	CK elevated, muscle biopsy, EMG.	None.	Key nursing dx: impaired physical mobility. Safety: fall prevention, assistive devices, energy conservation, PT. Monitor swallowing/resp muscles in advanced disease.
Psoriatic Arthritis	Inflammatory arthritis associated with psoriasis; joint & skin involvement	Chronic autoimmune/inflammatory; no incubation.	Joint pain/swelling, morning stiffness + psoriatic skin plaques (silvery scales), nail pitting/onycholysis.	Clinical + imaging; RF often negative.	None.	Injections of corticosteroids may be used for periodic flares. Long-term oral steroid use not recommended due to risk of psoriatic skin flare when stopping, plus osteoporosis and systemic side effects. Emphasize adherence to DMARDs/biologics as prescribed.
“Rheumatic Disease” (general goal)	Group of chronic inflammatory or autoimmune musculoskeletal diseases	N/A	Chronic pain, inflammation, fatigue, reduced mobility.	Depends on specific disorder.	None.	Major goal: maintain activity tolerance & pain control, and reduce risk of infection & deformity. Encourage joint protection, planned rest, gentle ROM, non-pharmacologic pain relief (heat/cold, relaxation).

🧬 Immune System & Immunodeficiency Basics

Disorder / Concept	Pathophysiology / Type	Incubation & Transmission	Key Clinical Features	Diagnostics	Isolation / Infection Control	Priority Nursing Care / Exam Pearls
Primary Immune Deficiency	Inherited defect of immune system (B cells, T cells, complement, or phagocytes)	Present from birth; not contagious; no incubation.	Recurrent, unusual, or severe infections; poor response to standard treatment; failure to thrive in children.	Immune panel (immunoglobulins, lymphocyte subsets), genetic tests.	Standard; avoid exposure to sick people.	Needs ongoing infection-control precautions and monitoring. Exam wording: inherited deficit → likely primary immune deficiency. Teach family to seek care early for fevers or new symptoms.
Drug-Induced Immunosuppression	Immune suppression from antineoplastics, high-dose steroids, some immunosuppressants	Onset depends on drug course; not transmissible.	↑ risk of infections, poor wound healing, atypical fever response.	CBC (neutropenia), immune function tests.	Protective isolation sometimes, strict hand hygiene.	Exam: antineoplastic drugs most likely cause immunosuppression. Teach: avoid crowds, sick contacts, fresh flowers/uncooked foods (per protocol); report minor health changes (cough, low-grade fever, SOB).
Stages of Immune Response	1) Recognition of antigen; 2) Proliferation of lymphocytes; 3) Response (antibody production or cell-mediated response); 4) Effector (destruction of antigen).	N/A	In infection (like pneumonia): early fever & symptoms → recognition/proliferation; later antibodies & T cells act → response/effector; patient begins to feel better and becomes afebrile.	Mostly theoretical; supported by serology (antibodies).	N/A	Exam style: patient with pneumonia who is now afebrile and feels better is in the later response/effector stages where antigen is being cleared.
Active Immunity	Body produces its own antibodies after antigen exposure (disease or vaccination)	Develops over days–weeks after exposure; long-lasting (years to lifetime).	None specific; confers protection against repeat infection.	Serology (antibody titers).	N/A	Disease and vaccination are examples of active immunity. Immunization = active artificial immunity (exam point).
Passive Immunity (Breastfeeding & Ig)	Ready-made antibodies transferred; no antibody production by recipient’s immune system	Immediate but short-term protection (weeks–months).	N/A clinically, but provides protection in infants or post-exposure.	N/A	N/A	Colostrum/breast milk provides passive immunity to diseases mother is immune to. Also rabies immune globulin = artificial passive immunity.

🧫 Immune Cells & Functions (What the Questions Were Really Asking)

Disorder / Concept	Pathophysiology / Type	Incubation & Transmission	Key Clinical Features	Diagnostics	Isolation / Infection Control	Priority Nursing Care / Exam Pearls
Neutrophils	Innate immune phagocytes; first responders to acute inflammation	N/A	Not a “disease,” but neutrophils are the first cells at inflammation sites.	CBC with differential (neutrophilia, bands).	N/A	Remember: Neutrophils are the first cells to arrive at the site of inflammation. Key for acute bacterial infections.
Monocytes / Macrophages	Monocytes in blood → migrate to tissues → become macrophages (phagocytes & antigen-presenting cells)	N/A	N/A	CBC; tissue histology.	N/A	Function: capture antigens via phagocytosis and present them to lymphocytes. That’s how they link innate and adaptive immunity.
Cytotoxic T Cells (CD8)	Adaptive, cell-mediated immunity; directly kills infected or abnormal cells	N/A	N/A	Flow cytometry, immune profiling.	N/A	Direct destruction of foreign microorganisms or cancer cells is done by cytotoxic T cells. Exam: “attacking and killing cancer cells” → cytotoxic T cell.
Plasma Cells (B-Cell Derived)	Activated B cells that secrete antibodies	N/A	N/A	Bone marrow studies, immunoglobulin assays.	N/A	Plasma cells produce and secrete antibodies; these circulate in humoral immunity. Not RBCs or bacteria.
Basophils	Innate immune cells; release histamine & other mediators	N/A	N/A	CBC differential.	N/A	Among innate cells listed, basophils do NOT phagocytose (unlike neutrophils, macrophages, eosinophils).
Humoral Immunity	Adaptive immunity that uses antibodies in plasma against extracellular antigens	N/A	N/A	Measurement of antibodies (IgG, IgM, etc.).	N/A	Humoral immunity results in circulation of antibodies, not antigens or NK cells.

🧠 Neuro-Inflammatory & Neuro-Immune Disorders

Disorder	Pathophysiology / Type	Incubation & Transmission	Key Clinical Features	Diagnostics	Isolation / Infection Control	Priority Nursing Care / Exam Pearls
Guillain–Barré Syndrome (GBS)	Acute autoimmune demyelination of peripheral nerves, often post-infection	Usually occurs 1–3 weeks after viral or GI illness; not contagious between people.	Ascending weakness starting in legs, areflexia; can progress to paralysis; may involve respiratory muscles and cranial nerves (facial weakness, drooling).	Nerve conduction studies, LP (↑protein, normal cells).	Standard.	Priority: respiratory function. Continuous eval of breathing; drooling = bulbar weakness → immediate concern (risk aspiration). Monitor vital capacity; be ready for intubation. Pain and paresthesia common but not top priority versus airway.
Multiple Sclerosis (MS)	Chronic immune-mediated demyelination in CNS (brain, spinal cord)	Chronic; no incubation; often relapsing-remitting course.	Visual changes (diplopia, scotomas), muscle weakness, spasticity, fatigue, ataxia, dysarthria, dysphagia.	MRI (white matter plaques), CSF oligoclonal bands.	Standard.	Pathophys sequence (simplified): T cells cross blood-brain barrier → immune attack causes inflammation & myelin destruction → plaques form on demyelinated axons → nerve conduction disrupted → neurologic symptoms. Exam: immediate intervention needed when MS pt has congested cough + dysphagia (aspiration risk).
Encephalitis	Inflammation of brain parenchyma, often viral or post-infectious	Acute; depends on virus; not usually directly transmitted person-to-person outside vector route.	Fever, headache, altered mental status, seizures, neuro deficits.	CT/MRI, LP, EEG, viral studies.	Standard; droplet if concurrent meningitis suspected.	Nursing dx for encephalitis: altered cerebral perfusion or risk for ↑ICP. Management: VS & neuro checks, seizure precautions, control fever (tepid sponge), orientation for confusion; restraints only if absolutely necessary and safe.
Myelomeningocele (Newborn)	Neural tube defect with sac containing meninges & spinal cord through vertebral defect	Present at birth; not infectious.	Visible sac on back (usually lumbosacral), possible motor/sensory deficits below lesion, risk for infection and CSF leakage.	Prenatal US; postnatal physical exam, imaging.	Standard; protect sac from contamination.	Priority problem: risk for infection. Position prone, keep sac covered with moist sterile saline dressings, strict sterile technique. Do NOT use petrolatum or leave open to air.
Increased Intracranial Pressure (ICP) / Subdural Hematoma with Mannitol	Volume increase (blood, brain, CSF) in fixed skull → ↑ICP	Acute after head injury, hemorrhage, edema.	Headache, vomiting (often projectile), blurred vision, decreased LOC, Cushing’s triad: ↑BP, ↓HR, ↓RR, sometimes high temp.	CT/MRI, ICP monitoring.	Standard.	Mannitol (osmotic diuretic) effect: best shown by increased urine output and improved neuro status. Vital sign trend for rising ICP in exam: increasing temp, decreasing pulse, decreasing respirations, increasing blood pressure.
Subarachnoid Hemorrhage (SAH)	Bleeding into subarachnoid space (often from aneurysm) → sudden ↑ICP	Acute; not infectious.	“Worst headache of my life,” nuchal rigidity, vomiting, photophobia, possible LOC changes.	CT scan, LP if CT negative and ICP not elevated.	Standard.	Lumbar puncture is contraindicated when ICP is elevated, because it can precipitate herniation. SAH pt with signs of ↑ICP → no LP.
Meningeal Irritation (Signs)	Inflammation/irritation of meninges (infection, hemorrhage)	N/A	Nuchal rigidity (inability to flex neck forward), Kernig’s sign (pain/resistance on knee extension with hip flexed), Brudzinski’s sign (involuntary hip/knee flexion when neck flexed).	Clinical exam.	Depends on cause (e.g., droplet for meningitis).	Opisthotonos (body arched, head and heels backward) can also be seen in severe meningeal irritation / tetanus. Recognize these as classic meningitis signs in Select-all-that-apply questions.

💩 GI & Hepatic Inflammatory Disorders

Disorder	Pathophysiology / Type	Incubation & Transmission	Key Clinical Features	Diagnostics	Isolation / Infection Control	Priority Nursing Care / Exam Pearls
Ulcerative Colitis (UC)	Inflammatory disease limited to colon & rectum; continuous lesions; thought to be related to altered immunity	Chronic; not infectious.	Watery stools with blood and mucus, urgency, abdominal cramping (often LLQ), weight loss, anemia.	Colonoscopy with biopsy (distinguishes from Crohn’s & IBS), stool studies.	Standard.	During exacerbation: monitor stool frequency & blood loss, fluid & electrolytes, low-residue diet, rest. Etiology in exam: altered immunity.
Crohn’s Disease / IBS Differentiation	Crohn’s: transmural inflammation anywhere in GI; IBS: functional disorder with no structural lesions	Chronic; not contagious.	Crohn’s: abdominal pain, diarrhea, weight loss, possible steatorrhea, fistulas. IBS: pain relieved by defecation, no blood, normal colonoscopy.	Colonoscopy with biopsy is the test that differentiates Crohn’s/UC from IBS.	Standard.	Exam: if they ask which test differentiates IBS from Crohn’s/UC → colonoscopy with biopsy.
Appendicitis	Obstruction of appendix lumen → inflammation, infection, risk of perforation	Acute; not contagious.	Periumbilical pain shifting to RLQ (McBurney’s point), anorexia, nausea, mild fever. Sudden relief of pain may indicate rupture.	Clinical exam, WBC, ultrasound/CT.	Standard.	Priority nursing dx: Risk for infection related to possible rupture of appendix. Immediate intervention when pt says, “The pain seems to be gone now” (possible perforation). Pre-op: NPO; post-op: monitor infection, pain, ambulate early.
Liver Cirrhosis with Asterixis	Chronic liver damage → scarring & portal hypertension; hepatic encephalopathy causes asterixis	Chronic; not infectious by itself.	Jaundice, ascites, spider angiomas, bruising, mental changes; asterixis = flapping tremor of hands when wrists extended.	LFTs, ultrasound, ammonia levels.	Standard; contact if also infectious (e.g., Hep B/C).	To assess for asterixis: ask pt to extend arms and dorsiflex wrists; look for flapping. Manage with lactulose for encephalopathy, low-protein diet per order, safety for confusion.

🩸 Endocrine / Metabolic: Type 1 Diabetes Mellitus (T1DM)

Disorder	Pathophysiology / Type	Incubation & Transmission	Key Clinical Features	Diagnostics	Isolation / Infection Control	Priority Nursing Care / Exam Pearls
Type 1 Diabetes Mellitus	Autoimmune destruction of pancreatic β-cells → absolute insulin deficiency	Autoimmune; not infectious. Often onset in childhood/young adults.	“3 P’s”: polyuria, polydipsia, polyphagia, weight loss, fatigue. Child with frequent thirst and urination → ask “How is your appetite?” to support suspicion.	Fasting blood glucose, random BG, HbA1c.	Standard.	Teaching: test blood sugar regularly (e.g., ≥4×/day), stay hydrated, recognize infection early. Foot care: never walk barefoot even at home (exam wrong answer is “As long as I’m in my house, I can walk barefoot.”).

🧠 Quick Checks (Division 2)

Try answering mentally:

1. Which arthritis is autoimmune and symmetric, and which is degenerative and weight-bearing?

2. SLE patient teaching: what is the most important sun-related instruction?

3. In GBS, which finding is most urgent: tingling feet, BP 106/50, absent reflexes, or continuous drooling?

4. A patient with cirrhosis is being checked for asterixis. What should you ask them to do?

5. Ulcerative colitis stool description in a flare?

6. Appendicitis patient says, “The pain seems to be gone now” → what are you concerned about?

7. First cells at the site of inflammation?

8. Which drug class is most likely causing immunosuppression in a cancer patient?

✅ Answers (peek):

1. RA = autoimmune, symmetric small joints; OA = degenerative, weight-bearing joints.

2. Wear large-brimmed hats / strict sun avoidance (and sunscreen).

3. Continuous drooling → bulbar weakness → airway risk.

4. Extend the arms and dorsiflex the wrists; watch for flapping.

5. Watery stools with blood and mucus.

6. Possible ruptured appendix → high risk for peritonitis.

7. Neutrophils.

8. Antineoplastic (chemotherapy) drugs.