Week 11 Flashcards
what is type 1 hypersensitivity?
IgE mediated hypersensitivity - IgE bound to mast cells via Fc portion
what is type 2 hypersensitivity?
Ab mediated cytotoxic hypersensitivity
- cells are destroyed by bound Ab either by activation of complement or cytotoxic T cell (ADCC)
what is the biphasic response in effector phase of type 1 hypersensitivity?
initial: preformed mediator release (vasodilation, vascular leakage, SM spasm)
late phase: inflammatory cell influx (mucosal edema, music secretions, leukocyte infiltration, epithelial damage, bronchospasm)
where dose mast cell degradation and activation occur in type1?
GIT
nasal passage, eyes, airways
BV
what is type 3 hypersensitivity?
immune complex hypersensitivity
Ag:Ab complexes are deposited into sites of tissues which activates complement and attracts more neutrophils to the site of infection
what is type 4 hypersenstivity?
cell mediated hypersensitivity
Th1 cells secrete cytokines and activate macrophages which can accumulate at the site and CTLs
what are some immune complex related disease?
bacterial viral parasitic autoimmune serum sickness
how does a hapten work?
it can only trigger an immune response when coupled with an Ag
small molecules that contact skin and bind host proteins and converting that self Ag to highly immunogenic foreign peptides- bind to skin APC and activate T cells
upon subsequent exposure that same hapten triggers a memory T cell response
what are the 5Rs of radiotherapy?
radiosensitivity repair redistribution repopulation re-oxygenation
what causes acute effects to radiotherapy?
suppression of cell proliferation in tissues with high cell turnover (bone marrow, GI, airway mucosa)
what causes the late adverse effects of radiotherapy?
damage to non-proliferating tissues which cannot compensate for cell death
what is biphasic response of the effector phase in type 1 hypersensitivity
initial response is <15 min, release of preformed mediators = vasodilation, vascular leakage and smooth muscle spasm
late phase reaction is 4-24 hours, inflammatory influx = mucosal edema, mucosal secretions, leukocyte infiltration, epithelial damage, bronchospasm
where are mast cells found?
CT throughout the body, GIT, resp tract, heart
when are the connective tissue mast cells degranulated?
intravenous or subcutaneous mast cell degranulation
when are the mucosal mast cells degranulated?
inhalation or ingestion of allergen
symptoms of mast cell degranulation with intravenous allergen?
widespread histamine release which acts on BV to increase permeability = hives or anaphylactic shock
symptoms of mast cell degranulation with subcutaneous allergen?
local histamine release causes wheal and flare (red and swelling)
topical allergen penetrating can also be a cause of atopic asthma
symptoms of mast cell degranulation with inhaling an allergen?
allergic rhinitis - due to increased mucus production and nasal irritation
asthma due to contraction of bronchial smooth muscle and increased mucus secretion
symptoms of mast cell degranulation with ingestion of allergen?
contraction of intestinal SM induced vomitting
outflow fluid into the gut causes diarrhea
clinical signs of anaphylaxis?
pale gums cold limbs increased HR weak pulse urticaria (increased V perm) angioedema dyspnoea hypoxia hypotension contraction of intestinal SM = cramp and diarrhea swelling of lips, tongue, larynx = block respiration bronchoconstriction blocks expiration
examples of type 2 hypersensitivity?
incompatible blood transfusion
hemolytic disease newborn
hyperacute graft rejection
tx for anaphylactic reaction?
adrenalin which reforms the tight junctions of endothelial cell and relaxation of bronchial SM and heart
arthus reaction?
type 3 hypersensitivity
following penetration of Ag locally - ind gets vaccinated but already has pre-existing Ab to this Ag thus forms an immune complex initiating an inflammatory response
Arthus reactions (type III hypersensitivity reactions) are rarely reported after vaccination and can occur after tetanus toxoid–containing or diphtheria toxoid–containing vaccines. An Arthus reaction is a local vasculitis associated with deposition of immune complexes and activation of complement.
serum sickness?
eg, snake venom give the ind anti-venom serum however they already have Ab against anti-venom = form immune complex
bitten again = anti-anti venom Ab will bind anti venom serum and cause vasculitis
what are haptens?
small molecules that contact skin and bind host proteins thus converting self Ag into highly immunogenic foreign peptide which skin APCs can take up and sensitize naive hapten specific CD4 and CD8 T cells
upon subsequent exposure to the same hapten the hapten specific memory T cells in skin are activated = Th1 and CTLs
role of Th1 and CTLs in haptens?
Th1 secretes cytokines IFNy which activates macrophages to secrete IL1, IL6 and TNF
TH1 also activates keratinocytes which secrete IL1 and TNF
example of type 4 hypersensitivity?
mantoux skin test
IBD
RA
MS
what is injury prevention?
prevention from an accident from occurring which would have resulted in injury
reduction in the exchange of energy thus reducing the severity in injury
draw out haddon matrix for road trauma
see notes
what is the hierarchy of control? purpose?
system used to minimize and eliminate exposure to hazards
its unlikely people will change unless its made a rule or a law (eg, seat belts)
different components of hierarchy of control?
elimination- physically remove hazard
substitution- replace hazard
engineering controls- isolate people from hazard
administrative controls- change the way people work
personal protective equipment - protective the work with gloves etc
5 steps of project planning?
identify the problem analyze the problem design solutions plan your program evaluate (use SMART) - specific, measurable, achievable, relevant, timely
photon therapy?
better for deeper tumours travel in beam like visible light inverse square law entry and exit dose
electron therapy
for superficial tumours
entry dose only
small light particles that cannot penetrate all the way
what are the signs of early radiation toxicity?
alopecia
denudation of skin
erythema
inflammation
caused by suppression of cell proliferation in tissues with high cell turnover
radiation causes local damage of DNA in healthy cells and release of ROS
what are the signs of late radiation toxicity?
microvascular damage fibrosis telangectasia atrophy necrosis LOF hypo/hyperpigmentation glomerulonephritis
caused by damage to non-proliferating cells which are unable to compensate for cell death
which cancers are sensitive / resistant to radiotherapy?
sensitive: lymphoma, small cell, seminoma
resistant: pancreatic, renal, glioblastoma, melanoma
why do we fractionate radiotherapy treatment?
to allow hypoxic cells to become oxic (reoxygenation)
to allow greater chance of targeting sensitive stages of the cell cycle (redistribution)
to allow healthy cells to repair from radiotherapy as tumour cells don’t repair (repair)
how does radiotherapy work on a molecular and cellular level?
direct damage to DNA: radiation physically breaks sugar phosphate backbones of base pairs of DNA
indirect damage to DNA: due to production of toxic free radicals from interaction of radiation with water/ oxygen within cell
both result in single and double stranded breaks that if not repaired will accumulate and lead to reproductive death
double stranded breaks may persist without accurate repair resulting in mutations
external beam radiation therapy
delivered in photon beams
internal beam radiation
delivered from radiation sources placed inside or on the body
radioactive isotopes sealed in pellets implanted using delivery devices
can deliver higher doses to some cancers than some external beam while causing less damage to healthy cells
systemic radiation therapy
oral/ parenteral administration of radioactive substance bound to a monoclonal ab
used target delivery to specific tissues
3 principles to radiation safety?
time
distance
shielding
