Immune, rhum, allergic disorders

Leukopoiesis -- Formation of leukocytes from hematopoietic stem cells in bone marrow
First line of defense -- Skin and mucous membrane barriers
Second line of defense -- Innate immune response with leukocytes, NK cells, inflammation, and fever
Third line of defense -- Adaptive immunity with memory and specific pathogen defense
Innate immunity -- Rapid response without memory
Adaptive immunity -- Slower response with immunologic memory
Natural killer cells (NK cells) -- Innate lymphocytes that destroy abnormal cells without prior exposure
NK cell receptors -- Non-antigen-specific surface receptors that detect foreign cells
NK cell cytokines -- Released to enhance immune signaling
B cells -- Adaptive lymphocytes that mature in bone marrow and produce antibodies
Activated B cell -- Becomes a plasma cell that secretes antibodies
T cells -- Mature in thymus, include cytotoxic, helper, regulatory, and memory subtypes
Helper T cell (CD4) -- Activates other immune cells via cytokines
Cytotoxic T cell (CD8) -- Kills infected or cancerous cells
Memory T cell -- Provides rapid secondary immune response
Neutrophils -- Short-lived WBCs that fight bacteria via phagocytosis and degranulation
Absolute neutrophil count (ANC) -- Measures circulating neutrophils to assess infection risk
Moderate neutropenia -- ANC 500–1000
Severe neutropenia -- ANC <500
Eosinophils -- Fight parasites; increase in allergies and autoimmune disorders (“worms, wheezes, weird diseases”)
Basophils -- Release histamine, heparin, and leukotrienes in allergic responses
Mast cells -- Tissue-resident cells releasing histamine, cytokines, and heparin to recruit leukocytes
Monocytes -- Circulating cells that become macrophages in tissues
Macrophage subtypes -- M1 (microbicidal) and M2 (tissue repair/tumor)
Dendritic cells -- Antigen-presenting cells using receptor-mediated endocytosis
Complement system -- 30+ liver-produced proteins aiding innate and adaptive immunity
Complement activation -- Leads to opsonization, inflammation, or cell lysis

Humoral immunity (B cell) -- Recognize, react, and remember pathogens via antibody production
Primary immune response -- First exposure → IgM then IgG
Secondary immune response -- Memory B cells rapidly produce IgG
Antibody neutralization -- Antibodies render toxins or viruses harmless
Complement fixation -- IgM/IgG activate complement to lyse pathogens
Agglutination -- Antibodies bind insoluble pathogens, clumping them
Precipitation -- Antibodies bind soluble antigens forming complexes for removal
Natural active immunity -- Infection-induced antibody formation
Artificial active immunity -- Vaccine-induced antibody formation
Natural passive immunity -- Antibodies transferred from mother to infant
Artificial passive immunity -- Injection of antibodies (e.g., IVIG)

Cellular immunity (T cell) -- T cells directly destroy infected or foreign cells
Helper T cell cytokines -- Interleukins stimulate macrophages, neutrophils, and lymphocytes
Cytotoxic T cell actions -- Release perforin, interferons, and TNF to kill target cells
Memory T cells -- Long-lived, respond rapidly on re-exposure

IgA -- Found in mucosa; prevents adhesion and provides newborn passive immunity
IgD -- B-cell receptor involved in activation
IgE -- Mediates allergic and parasitic responses
IgG -- Main circulating antibody; secondary response; crosses placenta
IVIG therapy -- Passive antibody infusion for infection or autoimmune suppression
IgM -- First antibody made; indicates acute/new infection

Type I hypersensitivity -- IgE-mediated, immediate reaction (allergy, asthma, anaphylaxis)
Type II hypersensitivity -- IgG/IgM attack host cells (cytotoxic autoimmune)
Type III hypersensitivity -- Immune complex deposition (SLE, PSGN, serum sickness)
Type IV hypersensitivity -- Delayed T-cell-mediated (poison ivy, TB test, Hashimoto’s)

Anaphylaxis mechanism -- IgE-dependent reaction from mast cells and basophils
Anaphylaxis onset -- Within 30 minutes of exposure
Anaphylaxis symptoms -- Urticaria, hypotension, bronchospasm, GI upset
Anaphylaxis labs -- Elevated tryptase and histamine
Anaphylaxis treatment -- Epinephrine 0.5 mg IM q5 min × 3, airway, fluids, steroids, antihistamines

Angioedema causes -- Allergic vs bradykinin-mediated (ACE inhibitors)
Bradykinin-mediated angioedema -- Poor response to epi; treat with TXA or bradykinin blockers

Urticaria -- Vascular skin reaction from allergy or infection; treat with antihistamines

Drug-induced cytopenia -- Type II; IgG + complement; caused by penicillin, sulfa, etc.
Drug-induced interstitial nephritis -- Type IV; AKI with eosinophilia; biopsy diagnostic
Maculopapular rash -- Benign T-cell drug reaction
DRESS -- Fever, rash, eosinophilia, organ involvement; needs steroids
AGEP -- Pustules, neutrophilia; stop offending drug
SJS/TEN -- Mucosal sloughing, epidermal necrosis; supportive (burn unit)
AERD -- COX-1 inhibition → ↑leukotrienes → asthma/nasal polyps
Red man syndrome -- Non-IgE mast cell activation from vancomycin infusion

Osteoarthritis (OA) -- Degenerative, non-inflammatory arthritis; pain ↑ with activity
OA imaging -- Joint-space narrowing and osteophytes
OA labs -- Normal ESR
OA treatment -- NSAIDs, acetaminophen, steroid injections, arthroplasty

Gout -- Monosodium urate crystal arthritis (negative birefringence)
Gout treatment -- NSAIDs, colchicine (≤36 h), steroids if refractory
Chronic gout prevention -- Allopurinol or febuxostat; avoid thiazides/alcohol

CPPD (pseudogout) -- Calcium pyrophosphate deposition; chondrocalcinosis on XR
CPPD treatment -- NSAIDs; colchicine prophylaxis

Seronegative spondyloarthropathies -- HLA-B27+, RF-negative; AS, PsA, ReA, IBD-related

Ankylosing spondylitis -- Young men, chronic back pain, uveitis, “bamboo spine” on XR
Ankylosing spondylitis treatment -- NSAIDs → TNF inhibitors

Psoriatic arthritis -- Asymmetric DIP arthritis with nail pitting; “pencil-in-cup” XR
Psoriatic arthritis treatment -- NSAIDs → methotrexate → TNF inhibitors

Reactive arthritis (Reiter’s) -- Arthritis + urethritis + conjunctivitis post-GI/STI
Reactive arthritis treatment -- NSAIDs; prolonged antibiotics if chlamydia-associated

Septic arthritis -- Monoarthritis, fever, >50 k WBCs in synovial fluid
Septic arthritis organisms -- S. aureus, E. coli, Pseudomonas
Septic arthritis treatment -- Hospitalize, IV antibiotics

Gonococcal arthritis -- Migratory polyarthritis, tenosynovitis, pustular rash
Gonococcal arthritis treatment -- Ceftriaxone + azithromycin

Osteomyelitis -- Bone infection (S. aureus common); ↑ESR/CRP; MRI sensitive
Osteomyelitis treatment -- Long antibiotics ± surgical debridement

Sarcoidosis definition -- Multisystem inflammatory disease with non-caseating granulomas
Sarcoidosis organs -- Lungs, lymph, skin, eyes, heart
Sarcoidosis CXR -- Bilateral hilar adenopathy
Sarcoidosis labs -- ↑ACE, hypercalcemia
Sarcoidosis diagnosis -- Biopsy
Sarcoidosis treatment -- Prednisone → methotrexate/azathioprine if chronic
Lupus pernio -- Chronic facial sarcoidosis lesion
Löfgren’s syndrome -- Erythema nodosum + hilar adenopathy + uveitis
Sarcoid liver findings -- ↑Alk phos, ↑transaminases
Sarcoid hematologic -- Lymphopenia, anemia
Sarcoid cardiac -- Arrhythmia or heart failure risk

Sjögren’s syndrome -- Autoimmune exocrinopathy causing dry eyes and dry mouth
Sjögren’s associations -- RA, SLE, scleroderma, thyroid, PBC
Sjögren’s genetics -- HLA-DQA1*0501, IRF5, STAT4
Sjögren’s complication -- Lymphoma
Sjögren’s diagnosis -- Minor salivary gland biopsy

Polyarteritis nodosa (PAN) -- Necrotizing vasculitis of small/medium arteries
PAN distribution -- Segmental lesions at bifurcations; spares lungs
PAN renal findings -- Hypertension, microaneurysms
PAN labs -- ↑WBC (neutrophils), ↑ESR
PAN serology -- ANCA-negative; screen for Hep B/C
PAN diagnosis -- Biopsy or angiography showing aneurysms
PAN prognosis untreated -- 10–20% 5-year survival