Immunopathology of infections.

Question 1

Lectin Pathway

Answer 1

Mannose Binding protein binds to non reduced mannose, fucose, and glucosamine working to activate complement through the C3 converatse.

Question 2

alteernate complement activated by

Answer 2

bacterial cell surfaces, componnents, endotoxins, microbial polysaccharides and aggregated IgA

Question 3

Stages of infection

Answer 3

aborted infection, prodromal, inapparent infection, sub clinical infection, clinical infection,

Question 4

Clinical infections can be calssified as

Answer 4

fulminating, acute, subacute, chronic, inapparent

Question 5

exotoxins can be produced by

Answer 5

gram positive or grame negative bacteria

Question 6

exotoxins include

Answer 6

cytolitic enzymes and receptor binding proteins.

Question 7

Superantigens

Answer 7

group of toxins that activate T cells without(bind to MHC II and t-cell receptor) requiring antigen

Question 8

Superantigens cause the release of

Answer 8

IL-1 and IL2 (large amounts of interleukin

Question 9

Superantigens include

Answer 9

S. Aureus, Staph enterotoxins and erythrogenic toxin A or C of S. pyogenes.

Question 10

Immune deficiency may result from

Answer 10

genetic deficiencies, starvation, drug induced, chemotherapy, cancer, disease. being born, being pregnant.

Question 11

Pateints with elevated levels of CRP have increased risk for

Answer 11

diabetes, hypertension or CV disease

Question 12

CRP receptor is on

Answer 12

macrophage

Question 13

how to lower your CRP

Answer 13

exercise, lose weight, stop smoking, flax seed, aspirin, niacin, statins, clean teeth.

Question 14

excessive immune and inflammatory responses are triggered by

Answer 14

the infection and can cause disease

Question 15

acute phase response to cell wall componinents

Answer 15

is a protective antibacterial repsonse when limited and controlled

Question 16

Tissue damage induced by neutrophils, macrophage and complement at site of infection and granuloma formation induced by

Answer 16

CD4 T cells and macrohages . for TB - leads to tissue destruction.

Question 17

M protein of S. pyogenes mimics

Answer 17

heart cell tissues, so that anti M protein antibodies cross react with heart muscle to cause damage (rhematic fever, immune complexes deposited in the golmeruli of the kidney poststreptococal golmerulonephritis. )

Question 18

three bacteria that are imporant causes of diseas symptoms in patients

Answer 18

chlamydia, treponema, borrelia

Question 19

Type 1 hypersensitivity

Answer 19

IgE antibody which binds to the Fc receptor on the mast cells and becomes a cells urface receptor for antigens. can cause anaphylactic reactions

Question 20

type II hypersensitivity

Answer 20

mediated by antibody and complement activation. - good pastures, Rh factor, and autoimune endocrinopathies. ADCC- antibody dependent cellular cytotoxicity.

Question 21

Type III hypersensitivity

Answer 21

immune compelxes are trapped in the kidney and elsewhere and can activate teh complement - serum sickness, nephritis, associated with chronic hep B infection, and arthus reaction.

Question 22

Type IV delayed hypersensitivity

Answer 22

mediated by CD4 TH1 cells, chemically modified self proteins are processed and presensted to CD4 T cells which release cytokines (IFN)- tuberculin response (purifed protein derivative test) and reaction to metals such as nickel. APC TCR, T cell receptor.

Question 23

antigen excess can occur early and form

Answer 23

soluble antigen antibody complexes

Question 24

Nephrotic syndrome immunofluorescense

Answer 24

granular pattern, corresponds