infection

Question 1

antibiotic classes

Answer 1

cell wall synthesis: Beta- lactams (cephalosporins, penicillins), glycosides

cell membrane function: polymixins

protein synthesis: tetracyclins, aminoglycosides, macrolides

nucleic acid synthesis: quinolones, rifampicin, trimethoprim

Question 2

endogenous pathway of antigen presentation

Answer 2

expressed by all cells

Virus enters cytosol
detected by proteasome and broken down into viral peptides
Transported into ER by TAP proteins
associate with HLA-A,B,C ; leaves cytoplasm to present to a CD8+ T cell

Question 3

exogenous pathway of antigen presentation

Answer 3

expressed only by antigen presenting cells

Bacteria enters cell by phagocytosis/micropinocytosis
Bacteria broken down in endosomes
endosome fuses with large vesicle containing MHC class 2 complex
presented to CD4+ T cells

Question 4

Hep B serology

Answer 4

First= surface antigen (HBsAg) within 6 weeks, followed by e-antigen (HBeAg) shows high infectivity, core antibody (IgM) is first antibody produced, followed by e-antibody (anti-HBe/HBeAb) representing disappearance of e-antigen and infectivity, surface antibody represents clearance of virus (HBsAb), core antibody (IgG) persists for life

Question 5

actions of cytokines

Answer 5

IL-1: acts on hypothalamus to increase body temperature

IL-6: acts on bone marrow to mobilise neutrophils, acts locally to vasodilate, increase vascular permeability and attract neutrophils

TNF-alpha: acts on liver to stimulate production of opsonins

Question 6

complement proteins

Answer 6

7+8=15

C3b+C4b: opsonisation

C5a+C3a: recruitment of phagocytes

C5-C9: killing of pathogens (membrane attack complex/MAC)

Question 7

primary immunodeficiencies + age of onset

Answer 7

onset < 6 months: suggests T cells or phagocyte deficiency

6 months < onset < 5 yrs: indicates B cell, antibody or phagocyte defect

onset > 5 yrs: indicates B cell, antibody, complement defect or secondary immunodeficiency

Question 8

extrinsic pathway of immune activation

Answer 8

CD4 binds to B cell receptors, activating it
antigen processing + presentation occurs
B7 costimulators are increased
TCR engagement occurs (antigen specific)
B7 binds to CD28 on helper cells causing it to present MHC class 2 molecules
CD40 activation and cytokine release allows antibody switching