immunology

Immunology & Infection

IL 4 stimulates B cell to become plasma cell (antibody secreting)
IgG, IgM are opsonins, are able to fix complement (2 IgG's or IgM needed)
IgM made first. Decreased levels after splenectomy
IgA in secretions
IgD a helper, largely unknown
IgG #1 in serum, Crosses placenta
IgE allergic reactions, type I hypersensitivity reactions, histamine release (mast cell, basophil), parasites

Variable region of antibody is responsible for antigen recognition
Complement cascade: C3a, C5a are anaphylatoxins; C5-9 = Membrane Attack Complex.
- classic pathway initiated with antibodies; alternate pathway by bacteria
- classic and alternate paths converge at C3
MCH I: CD8 activation; on all necleated cells; single chain
MCH II: CD4 activation; on B cells, dendrites, monocytes; 2 chains

Natural Killer cells: neither T nor B. No antigen presentation is needed. Recognize cells w/o self MHC. Natural killer is responsible for immunosurveillance against CA.
IL 2 converts Natural Killer cell to Lymphokine Activated Killer
Intradermal skin test - best test to evaluate cell-mediated immunity
Basophils - source of histamine in blood
Mast Cells - source of histamine in tissue
Endotoxin is lipopolysaccharide A from gram negative bacteria
Hyperglycemia comes 24hrs before overt sepsis
Late sepsis noted by decreased O2 extraction so increased SvO2 and decreased A-V O2 difference. SvO2 normal 66-77%; >77% = sepsis or cyanide poisoning; <66% due to decreased cardiac output or decreased SaO2
4 intraabdominal abscess locations: sub-diaphragmatic, sub-hepatic, inter-loop, and pelvic

C. Diff colitis: Rx is ORAL vancomycin or flagyl
B-Strep and Clostridial infections can present within hours post-op
Staph Aureus is coagulase +; may produce clear 'slime' with chronic infection (vascular)
Aminoglycosides: bactericidal, irreversible binding to ribosome; resistence due to decreased active transport
Clindamycin, tetracycline, erythromycin: bacteriostatic, reversible binding to ribosome
Vancomycin: binds plasma membrane; resistance is due to altered cell wall
MRSA resistance due to change in bacteria binding protein, not due to a B-lactamase
Sulbactam and clavulanate inhibit B-lactamase
Amphotericin: binds sterols to alter fungal cell wall. 80% get renal impairment; see anemia, fever
Quinolones (cipro): mechanism is DNA Gyrase inhibition. PO and IV routes equivalent