Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/70

Click to flip

70 Cards in this Set

  • Front
  • Back
  • 3rd side (hint)
two types of of acquired hypofunction of immune system
iatrogenic and infectious
type IV is mediated by what two cells
type of hypersensitivity mediated by T-lymphocytes and Macrophages
Asthma, Hay Fever, and Insect Bites are examples of what kind of hypersensitivity
localized type I
Insect stings are an example of what kind of hypersensitivty
type I systemic
drug allergies, hives, and some food allergies are examples of what kind of hypersensitivity
type I
what are the two components of complement which are known as anaphylatoxins
C3a and C5a
what happens in the two phases of Type I (anaphylactic reactions)
Immediate: IgE on mast cell surface - degranulation of preformed mediators
Delayed: tissue infiltration by eosinophils, basophils, neutrophils, and some T cells; tissue injury, mucosal damage and remodeling
The initial response in type I reaction last how long and results in what kind at kind of tissue response
5 minutes to I hour -
vasodilation, vascular leakage, smooth muscle contraction, glandular secretion
The secondary response of type 1 hypersensitivty can last up to 2 hours or days and is characterized by what
tissue infiltrate by eosinophils, basohils, PMNs, and some T cells. tissue injury, mucosal damage and remodeling
biogenic amines (e.g histimine), chemotactic mediator, enzymes, and proteoglycans are all what kind of mediators
primary
leukotrienes, protaglandins, PAF, and cytokines are what kind of mediators
secondary
how do eosinophils ctntribute to Type I hypersensitivity damage
MBP feeds back and self amplifys the response. causes epithelial damage and mast cell degranulation.
Severe urticaria
caused by cold or hot. puffiness, facial edema, redening of skin. Not IgE mediated but does result from mast cell degranulation.
atopic keratoconjunctivitis is an example of what kind of reactoin
type one hypersensitivity. it results in puffy cornea
how might the smooth muscle change in someone with chronic asthma
sm muscle will replicate and hypertorophy. each time bronchoconstriction gets worse. also mucous glands get worse
which cells are key in the change in tissue seen in pts with chronic asthma
DCs -
In addition to changes in muscle and mucous glands in a patient with chronic asthma - what might happen to the epithelium
epithelial cell shedding
and BM pseudo-thickening
also see Edema

epithelial damage due to eosinophils
hemolysis is what type of reaction
type II
what is the difference between Acute and Delayed Hemolysis
Acute hemolysis requires pre-existant Ab and leads to rapid intravascular hemolysis. Delayed hemolysis involves a low/rising titer to Ab over 1-2 weeks and results in slow extravascular hemolysis
intravascular vs. extravascular
erythroblastosis fetalis is what kind of hypersensitivity reaction
Type II - RH incompatibility
in erythroblastosis fetalis youwould see RBC where in the liver
in Kupfer cells - broken down
what cells would you see alot of inthe liver which might be abnormal in a baby with erythroblastosis fetalis
tiny red cells - erythroblasts - may be in any organ - baby cant keep up with loosing reds
a disease which involves making Antibody against Type IV collagen (BM)
Goodpasture's disease (type II hypersensitivity)
what might you see in lung w/ goodspastures (rare)
hemmorrhage into lung
what type of hypersensitvity - rheumatic fever
type II
Cross reacting antibodies in strep infections has hyaluronidase which targets what and might lead to what
cartilage - lead to arthritis
Cross reacting antibodies in strep infections has Group A Carbohydrates which is an Ag similar to those found on heart valves which would cause
endocarditis

think fish mouth!
fish mouth deformity of the aortic valve might be seen in what kind of disease and what kind of hypersensitivity is this
rheumatic fever. type II
aschoff bodies are seen in what disease
seen in rheumatic heart disease due to inflammatory reaction. they are moncytes some have merged to form giant cells. looser organization than granulome (not a nodule)
Antibody has natural ligan activity on TSH receptor
Graves - leads to activaiton
Ab against AcH receptor - blocked
myasthenia gravis
key cell in type III reacation
PMNs (but MO also involved)
systemic type III reactions include what three diseases - mechanisms
serum sickness, SLE, drug interactions
arthus reaciton, vasculaitis, glomerulonephritis, arthritis is what kind of type III reaction
localized
why do PMNs lead to most of the tissue damage seen in type III reactions
enzymes that digest pretty much everything
post-streptococcal glomerulonephritis is what kind of reaciton
localized type III reaction
what kind of infiltrate are you likely to see in glomerulonephritis
PMNs
the lumpy bumpy pattern seen in a glomeruli would be an indication of what kind of reaction
type III
The inflammatory phase and necrotic phase of vasculitis is often due to what kind of reaction
type III -
small vessel vasculits caused by a type III reaction is often due to
drug
what two cells mediate the tuberculin reaction and the granulomatous reactions
CD4+ and macrophages
(delayed type)
what cells are primarily involved in reactions to tumors, viruses and allogenic cells
CD8+ (T cell mediated cytotoxicity
what two cells are involved in rejection of transplanted organ
Both CD4 and CD 8 (but B cells/Antibodies may be involved
what are the three microglial and monocyte cell products that are beneficial
TGFBeta
Growth and Trophic Factors
GM-CSF
What three cells are abolutely essential for Delayed Type hypersensitivity
T lymphocytes, APCs, Macrophages
what is injected with the tuberculin reaction
Purified Protein Derivitive (PPD) - last 2/3 dayrs
what are the two cells seen in the tuberculin reaction
T cells and macrophages
what causes the endothelium to become sticky for circulating leukocytes
T cells release cytokines which activate endothelial cells
what kind of graft rejection results in rapid thrombosis of vessels and involves preformed antibodies
hyperacute
what kind of graft rejection happens weeks to months afterward and may involve a cellular or humoral reaction
acute rejection
what kind of acute graft rejection involves lymphocyte and macrophage infiltrates
acute cellular
graft reaction inolves the possibility of vasculitis, thrombosis, endothelial proliferation
acute
what kind of rejection involves intimal fibrosis, obliteration of lumen, organ ischemia, interstial mononulcear cell infiltrate, organ atrophy, and chronic vasculitis
chronic rejection
what is the difference between the direct and indirect pathway in a graft rejection
direct inolves APCs w/in graft and Indirect involves recipients APCs with sample of graft
in what kind of rejection might you see graft arteriosclerosis and tubular atrophy
chronic
both the direct and indirect pathway in a graft reaction stimulate Th1 which secret IFN-gamma which activate what cells
macrophages
(IFN-gamma also increases vascular permeability and endothelial injury)
what histological change might you observe in the myocardial fibers if a pt has rheumatic fever
increased size of nuclei and hypertrophy of myocardium.
crescents are hallmarks of relatively severe glomerular injury and consist of
proliferating parietal epithelial cells as well as monocytes from the blood stream. With time they are organized into fibrous tissue which may or may not obliterate the glomerulus
cytokine produced by macrophages and DCS which are critical for induction of TH1
IL-12
Key mediator (cytokine) of DTH
IFN-gamma(powerful activator of MO)
autocrine and paracrine proliferation of T cells
IL-2
effects on endothelial cells. - all changes facilitate extravasation of lymphocytes and monocytes at site of DTH
TNF
activates eosinophils
IL-5
stimulates differentiation to the TH2 pathway
IL-4
two cytokines which down regulates immune system
IL10 and TGFbeta
two major components of granuloma in Type IV
epithoid cells surrounded by lympocytes
a common B cell deficiency which is mostly asymptomatic with some recurren tinfections and occurs 1/ 700 people
IgA Deficiency
cause of herediatry angioedma
C1 inhibitor deficiency - C proceeds unchecked - mast cells degranulated - vessel leaks etc...
what kind of immunity is effected in the follwoing diseases: hodgkins, tb, sarcoidosis, leprosy, measles
cellular immunity affected
chemotherapy and radiation are what kind of immunodeficiencies
iatrogenic (secondary)