Immunopath

Question 1

type 1 autoimmune rxns

Answer 1

anaphalctic- mediated by mast cells releasing vasoactive/spasmogenic substances

IgE binds to mast cells. next time IgE recognizes Ag, it crosslinks IgE receptors it releases vasoactive substances

Question 2

type 1 autoimmune rxn types

Answer 2

localized (asthma, hay fever) or systemic (stings, hives)

Question 3

2 types of substances in mast cells

Answer 3

preformed- granules- histamine

actively formed

Question 4

2 stages of type 1 rxns

Answer 4

immediate- mast cells release preformed mediators. vasodilation, vasoleakage, muscle contraction

delayed- releases synthesized mediators. infiltration via basophils, neutrophils and T cells; tissue injury and remodeling

Question 5

eosinophil contribution to type 1 rxns

Answer 5

releases major basic protein, leads to mast cell degranulation and epithelial damage

releases leukotriene 4, platelet activating factor

Question 6

severe urticaria

Answer 6

induced by heat or cold- no need for IgE

localized

Question 7

atopic keratoconjunctivitis

Answer 7

type 1 rxn

localized inflammation of eyes

Question 8

asthma

Answer 8

type 1 rxn abnormal repair response to epithelial injury

over time, causes epithelial shedding, gland hyperplasia, matrix remodeling, muscle hyperplasia, inflammatory infiltrate, and basement membrane thickening

Question 9

anaphylaxis

Answer 9

systemic type 1 rxn

resipratory and heart rate dramatically increase, BP drastically decreases

Question 10

type 2 rxns

Answer 10

mediated by Abs

damage defined by where Ab binds

Question 11

hemolytic transfusion rxns

Answer 11

acute- high levels of preexisting Abs bind and lyse transfused blood. cells destroyed via complement

delayed- low levels of Abs, over 1-2 weeks cause slow hemolysis. cells destroyed via phagocytes

Question 12

erythroblastosis fetalis

Answer 12

child born anemic, edema, liver hypertrophy

caused by Rh- mom attacking Rh+ child blood cells

Question 13

goodpasture’s disease

Answer 13

Abs bind basement membrane of glomeruli

visualized w/ stain for IgG

causes renal failure and pulmonary hemorrhages

Question 14

rheumatic fever

Answer 14

Abs that develop in response to strep throat cross react w/ other host tissue

causes arthritis, endocarditis, chorea, and myocarditis

immune complexes deposit and cause vasculitis

Question 15

graves disease

Answer 15

cause autoimmune stimulation of TSH receptors- causes massive thyroid hormone relase

Question 16

myasthenia gravis

Answer 16

autoimmune blockade of AcH receptors in muscle motor plates

Question 17

type 3 rxns

Answer 17

immune system produces Abs, repeated exposure to Ags, Ag-Ab complexes form and are deposited in the tissues. complement cascade causes attraction and activation of PMNs and macrophages. end result is damage and inflammation

Question 18

post streptococcal glomerulonephritis

Answer 18

type 3 rxn

Abs form to streptococci Ag form. Ag-Ab complexes form and deposit in glomerulus causing damage

Question 19

vascullitis

Answer 19

Ab-Ag complexes deposit in blood vessel walls outside epithelium

often seen in Hep B

Question 20

serum sickness

Answer 20

injection of horse serum caused Ag-Ab complexes to buildup and deposit in many places in the body causing massive complement activation

Question 21

type 4 rxns

Answer 21

driven by lymphocytes and macrophages

delayed type- CD4 driven

viral- CD8 driven

transplant rejection- both

Question 22

granuloma formation

Answer 22

result of type 4 rxn where Ag cannot be cleared