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Helper T Cells (CD4) release:

  • (Th1 helper T cells) →IL-2:
    • Maturation of cytotoxic T cells
    • Converts Natural Killer cell to Lymphokine Activated Killer (LAK)
  • (Th2 helper T cells) →IL-4:
    • Stimulates B cell to become plasma cell (antibody secreting)
    • Counteracts inflammatory cytokines and inhibits monocyte/macrophage function

IL-3:

  • Functions as hematopoietic growth factor
  • Targets mast cells and increases histamine release

IL-6: Most potent stimulus for production of hepatic acute phase response proteins.


IL-10: Interleukin that inhibits the macrophage form secreting cytokines


IgG, IgM:

  • Are opsonins, are able to fix complement (2 IgGs or 1 IgM is needed)

IgG:

  1. 1 in serum
  • The only antibody capable of crossing the placenta to give passive immunity to fetus.


IgM:

  • Secreted first, decreased levels after splenectomy

IgA: In secretions


IgD: Activate basophils and mast cells to produce antimicrobial factors


IgE:

  • Binds to allergens and triggers histamine release from mast cells and basophils
  • Is involved in allergy (type I hypersensitivity reactions)
  • Also protects against parasitic worms


Variable region of antibody: is responsible for antigen recognition


Complement cascade:

  • C3a, C5a are anaphylatoxins
  • C5-9 = membrane attack complex
  • Classic pathway initiated w/antibodies
  • Alternate pathway by bacteria
  • Classic and alternate paths converge on C3


MHC I: (HLA: A, B, C)

  • CD8 activation
  • On all nucleated cells
  • Single chain
  • Endogenous antigen


MHC II: (HLA: DP, DQ, DR)

  • CD4 activation
  • On B cells, dendrites, monocytes, macrophages, Langerhans, activated T cells and activated endothelial cells
  • 2 chains
  • Exogenous antigen


Natural Killer cells:

  • Neither T nor B cell
  • No antigen presentation needed
  • Recognize cells w/o self-MHC
  • Function: immunosurveillance against CA


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 24 hours before overt sepsis


Late sepsis:

  • Noted by decreased O2 extraction
  • So increase in SVO2 and decrease A-V O2 difference
  • SVO2 normal 66-77%
  • > 77% èsepsis or cyanide poisoning
  • < 66% èdecrease CO or decrease SA O2


4 intra-abdominal abscess locations:

  • Sub-diaphragmatic, sub-hepatic, inter-loop, and pelvic

C diff colitis: Tx is oral vancomycin or flagyl


ß-Strep and clostridial infections: can present w/in hours postop


Clostridial myonecrosis (C.Perfringens) drug of choice:

  • Penicillin G
  • Clindamycin if PCN allergy


Staph aureus:

  • Is coagulase negative
  • May produce clear 'slime' with chronic infection (vascular)


Aminoglycosides:

  • Bactericidal, irreversible binding to ribosome
  • Resistance due to decrease 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 ß-lactamase


Sulbactam and clavulanate: inhibit ß-lactamase


Amphotericin:

  • Binds sterols to alter fungal cell wall.
  • 80% get renal impairment also anemia, fever

Quinolones (Cipro):

  • Mechanism is DNA gyrase inhibition.
  • PO and IV routes equivalent
  • Prolonged QT interval (could contribute to Torsades)
  • Tendinitis, tendon rupture
  • May exacerbate muscle weakness in patients with myasthenia gravis

Pages in category "Immunology/Infection"

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