Term
| what is the cause of a surface infection, what are two examples |
|
Definition
failure to spread to deeper tissues, cant evade innate defenses to colonize deper
ex: vacoule in bladder, extrintestinal E.coli |
|
|
Term
| explain how a microbe could make a vacoule in the bladder and cause symptoms |
|
Definition
vacoule has biofilm colony in it
it releases cytotoxin and endotoxins that cause inflammation
dissemination causes pyeloneophritis and sepsis |
|
|
Term
| explain how extraintestinal E.coli infects and causes symptoms |
|
Definition
1. uropathogenic E.coli (UPEC) attaches to uroepithelium via type 1 pilli and signals apoptosis
2. attaches to a3B1 integrins via type 1 pilli and internalizes itself forming intracellular bacterial communities (IBC)
3. releases hemylysin A toxin to inhibit Akt protein and cause apoptosis and expholiation
4. expholiation allows it to invade new layer of cells inside qiescent intracellular reserivors (QIR) |
|
|
Term
| how does a systemic infection occur |
|
Definition
1. entry into the body (bite, drugs, etc)
2. capillary
3. CT matrix
4. histocyte
5. lymphatic capillary
5. raplication, interference with macrophages, enterance into T/B cells
6. dissemination of CNS, bones, organs, skin |
|
|
Term
| explain how salmonella typhi (typhoid fever) invades and causes symptoms |
|
Definition
1. fecal oral introduction
2. adherence to mucosa and invasion
3. encounters APC in submucosa
4. T3SS2 allows it to live in phagocytes which help them colonize
5. inside salmonella containing vacoule they inject proteins into cytoplasm
6. enters pyer's patches by invading M cells
7. go to mesentrial nodes or redoculendothelial system
8. blood
9. secondary infection in marrow, liver, spleen, and gallblader
10. reinfect via bile release from gall bladder |
|
|
Term
| what are the symptoms of typhoid fever |
|
Definition
| diarrhea, fever, abdominal pain, myocardtis, necrosis of peyers patches, peritonitis, sepsis, rose spots on skin |
|
|
Term
| what are the virulance factors of typhoid fever |
|
Definition
encoded salmonella pathogenicity islands that affect cytoskeleton signaling
peptidyglycan, outer and inner membrane, lipopolysaccharides
fibrae, pilli, flagella
plasmids with anti-microbal resistance genes
inhibit apoptosis of host cell |
|
|
Term
| why does typhoid fever sometimes have persistant infections |
|
Definition
produces IL-10 and NO which reduce immune response
limits CD4 and CD8 proliferation
IL-22 promotes INF-y secretion by Th2 to maintain infection
TNF-a maintains infection
re-infection via bile |
|
|
Term
| what is different when a microbe is spreading via nerves |
|
Definition
rate of spread depends on axonal flow
host defenses are weak
can get to brain (especially via olfactory)
can invade brain, ependymal, and meningeal cells |
|
|
Term
| what are examples of diseases that infect via nerves, how do they get in, which one is associated with olfactory |
|
Definition
cross BBB: WNV, EEE
cross BBB on carrier: HIV, CMV
go through olfactory nerveL naegleria fowleri
also: rabies, URI, influenza, herpes simplex, varicella zoster, neonatal meningitis E. cili |
|
|
Term
| how does neonatal meningitis E.coli cross the BBB (3 ways) |
|
Definition
attach type 1 pilli to CD48 and increase Ca to rerange actin
OmpA attaches to ECGP96 causing actin rerangement
CNF1 and 67RL attach causing RAC1 production and myosin rerangement |
|
|
Term
| how is neonatal meningitis E.coli aquired and how does it infect and cause symptoms, what protects it |
|
Definition
aquired at birth > invades macrophages > crosses BBB > neutrophilia > inflammation
protected via K1 capsule and outer membrane protein A (OmpA) |
|
|
Term
| what factors influence infection |
|
Definition
| primary and secondary immune deficiencies |
|
|
Term
| what is a primary immune deficiency |
|
Definition
| genetic deficiency of immune cells, receptors, ILs, etc |
|
|
Term
| what is a secondary immune deficiency |
|
Definition
| nutrition, disease, medication, stress, MHC genes, blood groups, antibiotic resistance, toxins, antigen alteration, similarity of antigen to host, interference with antigen processing or barriers, mutations, penetration into cells, adhesion |
|
|
Term
| how are mast cells activated (or inactivated) |
|
Definition
| recognize PRR and PAMP via TLR (without physical contact) |
|
|
Term
| what issues can mast cells cause when they over do it |
|
Definition
granuloma development
epithelial apoptosis
increased degranulation
cause systemic effects
attract many immune cells (neutrophils)
make pro-inflammatory cytokines |
|
|
Term
| what cytokines do mast cells make, what do they do |
|
Definition
TNFa: neutrophil migration, upregulate E-selectin and VCAM-1 on vessels to attract lymphocytes, lymphocyte proliferation
IL-6: bacterial clearance
cathelicidins, IL-4, MC protease-6 |
|
|
Term
| what cytokines cause the most inflammation |
|
Definition
|
|
Term
| what cytokines amplify inflammation |
|
Definition
| IL-6, IL-8, NO, prostaglandins, PAF |
|
|
Term
| what cytokine is induced by TNFa and IL-1, what does it do |
|
Definition
| IL-8, mediates neutrophil chemo-attratant responses |
|
|
Term
| what cytokine increases BBB permeability |
|
Definition
|
|
Term
| how can something avoid death by phagocyte |
|
Definition
killing or inhibiting it first
running away
enzymes like leukocidins, hemolysis and C5a peptidase stop intracellular death
encapsulation
make salic acid or factor H to stop C3b
inhibit MAC attack lysis
inhibit phagolysosome formation |
|
|
Term
| what innate defenses does a microbe need to dodge (5) |
|
Definition
phagocytes
interfere with cillia action
interfere with complement (mimic regulator, inhibit or destory, block, disguise)
make Fe binding molecules
block interferons |
|
|
Term
| what are the 5 ways a microbe can dodge adaptive immune system |
|
Definition
silent invasion (dont form toxin)
live inside host cells
hit and run infection
modulate host immune system
antigenic variation
immunosupression
interfere with immune expression |
|
|
Term
| if a microbe wants to do a hit and run infection to avoid adaptive systems, what does it need to do (4) |
|
Definition
mimic host antigens
hide MHC
hide in areas without lymphocytes
create biofilm |
|
|
Term
| how can a microve hide its MHC |
|
Definition
put it in vacolue inside the cell
stop it from getting to surface
stop NK and CD8 damage (ok it didnt hide it, but eh)
f-ed up MHC that causes NK cells to die when they attach |
|
|
Term
| explain areas or methods microbes can use or go to to stay away from lymphotyctes |
|
Definition
skin keratin layer is safe
nervos system, joints, testis, placenta
could make its own spot: cyst
hide DNA in host DNA (retrovirus) |
|
|
Term
| what microbes make a cyst to stay hidden |
|
Definition
| echinooccus spp., trichinella spiralis, toxoplasma gondii |
|
|
Term
| how can microbes modulate the host immune system to stay safe (7) |
|
Definition
produce a small or poor immune response to limit antigens
infect embryo and be learned as self (anergy)
produce a huge immune rsponse and create tolerance (anergy) (saturates TCR and BCR)
make 'host campflauge'
exploit gaps in host immune system
upset Th1/Th2 balance
induce downregulation signals to immune response (T17, IL-10) |
|
|
Term
| how can a microbe camoflauge themselves as host |
|
Definition
fibrin in capsule
hyaluronic capsule
fibronectin on surface
salic acid on capsule |
|
|
Term
| what are examples of microbes that undergo antigenic variation |
|
Definition
borreila recurrents (relapsing fever)
trypanosoma brucei (african sleeping sickness)
influenze (via hemoagglutin adherence factor) |
|
|
Term
| how can microbes cause immune supression |
|
Definition
induce cytokines, release immunosupressive molecules or inducers
, kill T cells, divert T cells, interfere with signals, interfere with MHC |
|
|
Term
| how can microbes interfere with local immune expression |
|
Definition
inhibit phagocytosis of antibody coated bacteria via protein A on cell wall
anti IgA enzymes
fake Fc receptors to IgG or IgA |
|
|
Term
| what are the adherence factors for bordetella pertussis and their functions |
|
Definition
| filamentous hemagglutin, pertactin attract regulatory T cells to help supress immune system |
|
|
Term
|
Definition
infects B cells by attaching to C3d receptor (CD21)
prevents apoptosis, cause B cells to make antibodies (IgM)
can become latent |
|
|
Term
|
Definition
fever, sore throat, petechiae on hard papalte, splenomeagyl, anorexia, lethargy
can cause in immunosupressed: hepatitis, splenic rupture, janudice, hairy tounge |
|
|
Term
| what cancers can EBV make, list major identifiers of these cancers |
|
Definition
nasopharyngeal carcinoma: no oncogenes, high IgA to EBV before carcinogens, co-carcinogens
burkitt's lymphoma: oncogene c-myc, B cells wont rest, especially in young boys
hidkins lymphoma (immunosupressed associated lymphoma): T cells keeping EBV in check are reduced, often in people with HIV |
|
|
Term
| what serotypes cause cervical cancer, where do they infect |
|
Definition
| serotypes 6, 11, 16, 18 infect keratinocytes or basal layer of skin and mucosa |
|
|
Term
| what does cervical cancer mess up in cells |
|
Definition
| oncogene E6 which codes for p53 |
|
|
Term
| what are co-carcinogens for cervical cancer |
|
Definition
| cigarettes, herpes simplex, UV light (some of the same serotypes make skin cancer like 16 and 18) |
|
|
Term
| kaposki's sarcoma: cause, location, common patients, treatment |
|
Definition
cause: herpes (HV8) sexually transmitted
location: tumor of endothelial cells
more common in AIDs and HIV patients
treatment: can only treat in lytic stage, latent is antiviral |
|
|
Term
| give an example of a bacteria that causes chancer, what are the other complications / symptoms |
|
Definition
helicobacter pylori
causes stomach / duodnal cancer and MALT lymphoma
chronic inflammation and peptic ulcers |
|
|
Term
| give and example of a liver cancer |
|
Definition
hepatic carcinoma (HBV via DNA and HCV via RNA)
persistant infection especially in young |
|
|
Term
| once the virus has infected what are its next options (5) |
|
Definition
budding from the cell to spread
lysis of the cell to spread
persistance in the host
latency
transformation into a tumor cell |
|
|
Term
| explain what is going on in the body when a virus is latent |
|
Definition
may be a symptomless carrier or..
small release of virons or toxins that have cumelative effects that become an issue (HIV, HBV) |
|
|
Term
| what are the 4 ways of transmission or infection of a tumor cell / oncogene |
|
Definition
direct: virus expresses oncogene and transform cell
indirect: virus causes disturbance that activates an oncogene
vertical transmission: mother to offspring (placenta, milk, genetically)
horizontal transmission: saliva, urine, sex, personal contact |
|
|
Term
| in a person without cancer, what did and are the proto-oncogenes doing |
|
Definition
they were active during embryogenesis and turned on after development
they coded for cell surface receptors or intracellular proteins that act as signal acceptors or carriers for growth, differentiation, and stopping cell death |
|
|
Term
| what can increase expression or activity of an oncogene (turn proto-oncogene into oncogene) |
|
Definition
| mutation, virus insertion next to one |
|
|
Term
| what happens to the cell when an oncogene is turned on |
|
Definition
| hyperactive gene products, increased transcription, loss of growth control, increased division, decreased differentiation, reduced apoptosis, loss of contact inhibition |
|
|
Term
| what are examples of viruses that cause activation / insertion of oncogenes |
|
Definition
|
|
Term
| what are two names for HTLV1, what causes it |
|
Definition
human T lymphotrophic virus-1 infection / adult t cell lukemia
tax causes synthesis of IL-2 and IL-2 receptor, causes milagnant transformation immortalizing CD4 cells, promoting division and growth, and stopping apoptosis |
|
|
Term
| what is the treatment to HTLV1 |
|
Definition
|
|
Term
| what are two names for HTLV2, what disease is it associated with |
|
Definition
human T lymphotrophic virus-1 infection / hairy T cell lukemia
non milagnant, associated with neuro and chronic inflammation conditions |
|
|
Term
| what are the RNA segments of retroviruses, what are their functions |
|
Definition
GAG: p12 for matrix and structure, p24 for capsid
POL: reverse transcriptase
ENC: envelope proteins gp120, gp41, gp160 to bind to host
NEF: multifunctional, virulence
TAT, REF, TAX |
|
|
Term
| what is the most opportunistic infection in HIV patients |
|
Definition
|
|
Term
| what is different in AIDS from HIV |
|
Definition
| less infective, latent until stimulated, smaller viral load, slow (lentivirus) |
|
|
Term
|
Definition
1. enters mucosa
2. contacts APC (macrophages not so much)
3. binds with gp120 to CD4 receptors
4. conformational changes
5. binds with gp120 and other co-receptors and brings host cell closer
6. binds with gp41 to fuse to host
7. enters, uncoats, and replicates |
|
|
Term
| what are the co-receptors HIV attaches to, what makes them different from eachother |
|
Definition
CCR co-receptors
CCR5B is resistant to HIB
CCR4a is more suspectible to HIV and came from hematopoetic stem cell via growth factor 1 |
|
|
Term
| what are the acute retroviral symptoms of HIV when to they start |
|
Definition
after 2-4 weeks incubation
fever, malaise, lymphadenopathy
maybe: lymphopenia, atypical T cells, meningitis, mucosal ulcers
positive viral load, neutralizing antibodies |
|
|
Term
| what is the latent symptoms of HIV, why are they different |
|
Definition
they are different because there has been enough time for CD8 to create antibodies to fight, it wont last forever but it is helping
acute symptom resolution, opportunist infections, dermatology issues, virus replication, aids, dementia, kaopski's sarcoma, impaired memory, mental slowing, loss of flexibility, clumsiness, tremor, wealness, apathy, withdrawl, iritability, depression |
|
|
Term
| how does HIV progress to AIDs |
|
Definition
viral invasion of CNS
encephalopathy due to nodules of inflammatory cells
AIDS opportunistic infection |
|
|
Term
|
Definition
early with p24 antigen via ELISA
HIV RNA
antibody to HIV
CD4 count
monitor opportunistic infections and symptoms
GAG or INT gene count
flow cytometer: labels CD3, CD4, CD8
laser detection to T cells and dye labeled antibodies |
|
|
Term
| what is a normal CD4 count |
|
Definition
|
|
Term
|
Definition
1. with ELISA for anti-HIB antibody to recombinant antigen p25, gp41, gp120, gp36. if positive...
2. western blot: HIV on nitrocellulose paper. add patient sample. conjugate antihuman IgG. add substrate. color bands show HIV |
|
|
Term
| how is HIV confirmed positive, why do we need so much proof |
|
Definition
TWO antigens show positive p24, pg1, gp120, gp160
because ELISA can show false positive after influenza vaccine, hepititis, autoimmune disease, transfusions |
|
|
Term
| when and why might HIV diagnosis be missed |
|
Definition
p24 not made anymore and antibodies not made yet
late stage disease when antibody numbers are falling |
|
|
Term
| what are the treatments for HIV |
|
Definition
reverse transcriptase inhibitor, protease inhibitor, fusion inhibitor, integrase inhibitor
HAART: highly active anti-retroviral therapy |
|
|
Term
| when there is overproduction of cytokines, what things are overproduced |
|
Definition
| endotoxins, superantigens, cytokine storm, TNF, complements, |
|
|
Term
| where do endotoxins come from, give general and examples |
|
Definition
gram negative bacteria like nisseria meningitides, enterobacteriaceae, shigella, bordello pertussis.
LPS is an endotoxin |
|
|
Term
| what are the parts of LPS, what makes it an endotoxin |
|
Definition
conserved lipid portion: lipid A most toxic part
polysaccharide core
variable O serologic region
it binds CD14 and TLR4 on macrophages and dendritic cells |
|
|
Term
|
Definition
endotoxins cause cytokine release (especially TNF)
vascular collapse
cardiovascular failure |
|
|
Term
| what is the most likley cause of fever |
|
Definition
| IL-1 and TNF made by macrophages in response to LPS act on hypothalamus |
|
|
Term
| how do superantigens work |
|
Definition
connect a chain MHC II and variable region TCR beta
cause release of IL-1, IL-2, INFy, TNFa and B
cause capillary leaking, rash, desqumation, fever |
|
|
Term
| what are the cytokines involved in a cytokine storm, put them into categories by effect |
|
Definition
primary contributers: TNFa and IL-6
inflammatory mediators: cytokines, ROS
pro-inflammatory: TNFa, IL-1, IL-6
anti-inflammatory: IL-10, IL-1 agonist |
|
|
Term
| what cytokines does TNF need to have full effects |
|
Definition
|
|
Term
| what is the difference between hypersensitivity and autoimmune |
|
Definition
hypersensitiviey is caused by over reaction of immune system in response to harmless antigen
autoimmune is hypersensitivie response to self tissue |
|
|
Term
| what is the fell and coombs classification based on, what is it for type 1 hypersensitivity |
|
Definition
based on immunomechanism and time
antibody mediated |
|
|
Term
| what defines type 1 hypersensitivity, how does it begin |
|
Definition
1. allergin contacts mucosa and gets on APC
2. it is presented to Th0 which differentiates into Th2
3. Th2 makes IL-4 and induces B cell to class switch to IgE
4. IgE attaches to IceRI receptor on mast cell
5. antigen binds to IgE Fc receptor on mast cells and causes degranulation |
|
|
Term
|
Definition
| indication of an allergic response |
|
|
Term
| what are the major granules of mast cells, what do they do |
|
Definition
histamine: contract smooth muscle, vasodilate, mucous secretion, increased GI motility
serotnin and proteases: smooth muscle contraction, increased respiratory rate
TNFa: activates endothelial cells
leukotrienes: like histamine but slower
prostaglandin: dilate and permeability of vessels, attract neutrophils
RANTES (CCL5) |
|
|
Term
| how is RANTES made, what does it do |
|
Definition
TNFa and IL-1 from mast cell degranulation cause RANTES production
recruits leukocytes to inflammatory sites |
|
|
Term
| how is a mast cell activated by an antigen |
|
Definition
| repetitive epitopes cross link IgE |
|
|
Term
| what are examples of systemic and localized allergins |
|
Definition
localized: food, pollen, dust, dander
systemic: bee toxin, drugs, food |
|
|
Term
| what are the symptoms of an immediate hypersensitivity 1 reaction |
|
Definition
acute urticaril: wheal and flare
IgE mase cell degranulation > local sweling
primary mediators released: histamine, seritonin, proteases |
|
|
Term
| what are the symptoms of a later hypersensitivity 1 reaction |
|
Definition
wide spread swelling at the injection site
secondary mediator release: IL-1, 2, 3, 4, 6, 9, 13, TNFa, GM-CSF, RANTES
leukotrienes and prostaglandins |
|
|
Term
| what causes systemic anaphylaxis |
|
Definition
mast cells contract smooth muscle and swell CT
death is caused by aspiration and airway constriction due to epiglottis swelling
circulatory collapse, edema, increased permeability |
|
|
Term
| what are the causes and symptoms of allergic rhinitis (hay fever). what type of reaction is this |
|
Definition
type 1 hypersensitivity
symptoms: sneezing, mucous, tears, itchy eyes, inflammation
causes: pollen, dander, dust mite feces |
|
|
Term
| what are the symptoms (early and late) and causes of allergic asthma, what is the type of reaction |
|
Definition
type 1 hypersensitivity
early somptoms: acute bronchoconstriction
late: mast cell, esoinophil and neutrophil release mediators
symptoms: epithelial damage, mucus, bronchial muscle contract, shortness of breath
causes: irritants, allergins cold air, exercise |
|
|
Term
| what are the treatments of type 1 hypersensitivity |
|
Definition
albuterol (smooth muscle relaxor)
avoidance of allergen
desensitizaion
cromolyn sodium
mediator antagonism |
|
|
Term
| how does desensitization work |
|
Definition
increase dose of allergen causes IgG blocking antibodies to compete for allergen
Activates Th1 and inhibits Th2 IgE production by inhibiting IL-4 |
|
|
Term
| how does cromolyn sodium work |
|
Definition
| maintains resting state by reducing triggering of mast cells by stopping Ca influx |
|
|
Term
| what drugs are used in mediator antagonism |
|
Definition
antihistamines: block H1 and H2 receptors
B2 agonist: bronchodilate
leukotriene agonist: prevent smooth muscle contraction
throphylline: phosphodiesterase inhibitor
epinepherine: binds B receptors on mast cells
cortizone: reduces histamine by blocking production |
|
|
Term
| how can hypersensitivity type 1 be detected |
|
Definition
intradermal testing: scratch and injection
RAST: radioallergosorbent test: dilute patient serum and add allergin, add anti-IgE, measure binding |
|
|
Term
| what is Atopy, what is it associated with |
|
Definition
genetic disposition to an allergy
associated with HLA types |
|
|
Term
| what does HLA DR3 indicate |
|
Definition
| graves, addisons, sjogrens |
|
|
Term
| what does HLA DR2 indicate |
|
Definition
|
|
Term
| what does HLA DR8 indicate |
|
Definition
|
|
Term
| what does HLA DR4 indicate |
|
Definition
|
|
Term
| what does HLA B-27 indicate |
|
Definition
| ankylosing spondylitis, reiter's syndrom |
|
|
Term
| what is beta lactam, why is it unique |
|
Definition
| it is the reactive ring in penicillin that can cause ALL the types of hypersensitivity reaction. it is essential for antibiotic activity |
|
|
Term
| what is needed to cause differentiation into Th2 |
|
Definition
IL-4, CD40, CD145
and IL-4, IL-5 and TL-10 to block Th1 |
|
|
Term
| what is central tolerance |
|
Definition
| T cells go through negative selection in thymus and B cells in marrow. if they react too strong their eliminated |
|
|
Term
| how can central tolerance get messed up |
|
Definition
inheritance of two genetic polymorphisms (HLA)
self peptides not all or presented properlly to the T cells
large amounts of low reactive protein presented to immune cells in infection |
|
|
Term
| how are immunologically privlidged sites considered to be a T cell tolerance |
|
Definition
| because they are not presented cells from these sites in central tolerance, it hides self antigens from auto-reactive T cells |
|
|
Term
| how can the tolerance, immunologically provlidged areas, be broken |
|
Definition
exposire of T cells to these molecules (trauma)
molecular mimicry: immune response makes antibodies that cross react with host tissues |
|
|
Term
| what causes PANDA, what are other similar forms of this disease |
|
Definition
pediatric autoimmune neurophycjiatric disorder
caused by strep pyogenes when it gets into the brain tissue
(also can get into muscle (syndenham's chorea) and myosin (rheumatic fever)) |
|
|
Term
| what is peripherial tolerance of autoimmune |
|
Definition
autoreactive T cells enter tissue and body mechanisms prevent them
anergy: T or B cells block signals
regulatory T cells inhibit |
|
|
Term
| what are the symptoms of autoimmune disease |
|
Definition
| rash, FUO, muscle weakness, ataxia, arthritis, hair loss |
|
|
Term
| what is the gell and coombs classification of type 2 hypersensitivity |
|
Definition
|
|
Term
| what defines type 2 hypersensitivity |
|
Definition
| molecules bind to human cells and the immune system does not recognize them so B cells make IgG, complements, and phagocytes to come destory them |
|
|
Term
| what diseases / issues are included in type 2 hypersensitivity |
|
Definition
blood type incompatability
transplant rejection (MHC incompatability)
drug reactions
myasthenia gravis
graves disease |
|
|
Term
| what are the Rh loci, what is its inheritence, what makes someone positive |
|
Definition
loci: C, D, E
Rh is recessive, need DD or Dh to be positive. Dd is negative |
|
|
Term
| what happens when Rh postiive and negative are mixed |
|
Definition
the first time nothing except making anti-D IgG antibodies.
the second time the antibodies do their thing and break RBC into fragments (autoimmune hemolysis) |
|
|
Term
| what is the difference between Rh and ABO antibodies |
|
Definition
| anti-A and anti-B (isohemagglutin-antibodies) dont need previous exposure to be made. they are there at birth and are IgM activating |
|
|
Term
| what are other blood groups other than ABO and Rh |
|
Definition
| I, kelly, duffy, kidd, lewis, lutheran |
|
|
Term
| why do we care about I antigens |
|
Definition
because sometimes they can act as autoantigens for anti-a and andi-B antibodies
normally behaves as a self antigen |
|
|
Term
| what is worse, Rh or ABO incompatability and why |
|
Definition
| ABO because the reaction is more rapid and uses IgM which is more efficient |
|
|
Term
| hemolytic disease of the newborn: explain, treatment, preventitive |
|
Definition
mom is Rh-. first baby is +. mom builds anti-D antibodies. second baby is + antibodies kill baby spleen and liver
treatment: UV light, exchange transfusion for fetus
preventing: anti-D antibody injections (rhogam) |
|
|
Term
| explain allograft (hyperacute) rejection |
|
Definition
| recipient has formed anti-HLA or Rh antibodies from previous transfusion or pregnacy or anti-A or anti-B react to graft destorying it via IgG and IgM and NK cells |
|
|
Term
|
Definition
| drug (hapten) attaches to membrane proteins and illicts an immune response causing loss of tolerance to self tissue |
|
|
Term
| what causes myasthenia gravis |
|
Definition
| autoantibodies bind to ACh recptors on NMJ and complements cause damage |
|
|
Term
| what are the early and late symptoms of myasthenia gravis and treatment |
|
Definition
early: drooping eyelids, double vision
late: weak facial expression, trouble breathing
treatment: inhibiting acetocholinesterase |
|
|
Term
| what causes effects of graves disease, what are some symptoms |
|
Definition
autoantibody binds to TSH receptor and mimics hormone effects
neonatal hypothyroidism, protruding eyes |
|
|
Term
| what is the gell and coombs classification of type 3 hypersensitivity |
|
Definition
|
|
Term
| what defines type 3 hypersensitivity |
|
Definition
| immune complexes are not cleared properlly by the complement system and cause hypersensitivity |
|
|
Term
| how are immune complexes normally cleared |
|
Definition
complement system: many Fc close together activate complement pathway and complements break up lattice of immune complex (especialy C3)
RBC: move immune complex to phagocytes in liver and spleen. complement receptor 1 (CR1) activates C3 to help |
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Term
| why are complexes not cleared correctly |
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Definition
clearence mechanisms saturated
lack of complement
predispositional to immune comlex disease
complexes deposit in skin, heart, kidney, and joints
complexes lodge in tissue or vessels by binding IgG and proteins |
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Term
| how do not cleared complexes cause symptoms |
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Definition
activate innate immune system which causes chemotaxis and mast cell degranulation
neutrophils and macrophages form enzymes, ROS, NOS, TNF, IL-1 which causes tissue damage
platelets are activated causing thrombi and ischemia |
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Term
| what diseases are associated with type 3 hypersensitivity |
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Definition
| serum sickness, systemic lupus erythematosus, farmer;s lung, post strep disease, RA, pigeon breeders diseae, cheese washer;s disease, subacute sclerosing panencephalitis (via measles), glomerulonephritis |
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Term
| what causes serum sickness |
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Definition
injection of foreign serum makes immune complexes
monoclonial antibody treatement, horse serum antitoxin |
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Term
| what is the gell and coombs classification for type 4 hypersensitivity |
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Definition
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Term
| explain the process in a type 4 hypersensitivity |
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Definition
1. sensitizing agent causes reaction
2. macrophages signal inflammation
3. dendeitic cells take antigen to node
4. Th1 cells and macrophages stimulate cytokines
5. necrosis, fibrosis, granuloma |
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Term
| what sensitizing agents cause type 4 hypersensitivity |
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Definition
microbes (mycobaceria, systemic fungi, tissue protozoa)
chemicals or metals
topical meds
foreign tissue |
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Term
| what cytokines are released in type 4 hypersensitivity |
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Definition
macrophages releasE: TNF, ROS, NO
TNF does most damage
INFy, IL-2, 2, 3, GM-CSF, MCAF, MIF |
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Term
|
Definition
| Th1 cells, multinucleated cells, epitheloid cells, intracellular bacteria, activated macrophages |
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Term
| what are examples of microbes that cause granuloma |
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Definition
| TB, M. leprae, fungal (histoplasmosis) |
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Term
| what are the symptoms of RA |
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Definition
synovial membranes and tendon sheaths are swollen due to chronic inflammatory cells, T cells, and macrophages
TNF does most of the damage. attracts neutrophils, induces them to digest matrix, induces osteoclasts to destory bone |
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Term
| what is the evidence of type 3 and 4 hypersensitivity in RA |
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Definition
| IgM, IgG, cells involved, long term damage |
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Term
| what is the treatment for RA |
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Definition
anti-inflammatory: steroidal and non
monoclonial antibodies: anti-TNF-RA, INF-B-MS |
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Term
| explain the process in contact dermititis |
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Definition
1. antigen binds
2. makes a hapten / carrier complex
3. APC take it to lymph node
4. T cells make DHT memory cells
5. re-exposure
6. hapten complex is presented to Th1 DHT
7. INFy and monocyte chemotactic factor made
8. CD8 causes tissue damage |
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Term
| what are three diseases that change surface recognition from self to non-self and on what tissue |
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Definition
MS: on myelin
type 1 diabetes mellitus: beta cells
celiac disease: grain-protein gluten |
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