part 8 Flashcards
(22 cards)
tumor specific monoclonal antibodies
ex. CD20 (used to treat b-cell lymphomas)
= rituximab
can cause direct apoptosis, complement activation or direct lysis
radio-immunotherapies
add radioactive particles to immunoglobulines
antibody-drug conjugate
add drug to antibodies
ex. brentuximab (anti CD30, causes apoptosis bc of cell arrest)
bispecific T cell engager (BiTE)
zijn alleen antistoffen
ex. anti CD3 + anti CD19 antibodies stuck together
can bind 2 things
CAR T cells
chimeric antigen receptor
uses viruses to change patient’s own T cells
ex CD19
side effect: cytokine release syndrome (hypotension, fever)
tumor specific monoclonal antibodies: side effects
allergic reactions
tumor lysis syndrome (renal failure, release LDH)
anti-CD30: gives polyneuropathy
trusseau syndrome
presence of thrombosis in relation to malignancy
primary hemostasis
reduction in flow by vasoconstriction
AND
platelet plug
secondary hemostasis
TF causes cascade to create fibrin
mediated by thrombin
adhesion of platelets
done by: GP VI, Ia and Ib
GPVI and Ia are collagen receptors
GPIb binds vWF
aggregation of platelets
GP IIb / IIIa, when activated bind to fibrinogen + vWF
a-granules
release vWF and fibrinogen (precursor of fibrin)
dense granules
release serotonin and ADP
activation of platelets
through:
P2Y12 = ADP receptor
TXA2R = thromboxane A2 receptor
PAR1 = sensitive to thrombin
thrombocytopenia
too few platelets causes: - reduced production (chemo, leukemia, aplastic anemia) - increased consumption (ITP or DIC) - loss/bleeding
thromocytopathia
defective platelets
caused by:
- congenital platelet defects,
- acquired platelet defects, (kidney failure [uremia], liver cirrhosis)
- medication (platelet aggregation inhibitors)
Bernard-Souiller syndrome
GPIb defective –> vWF can’t bind –> less aggregation
Glanzmann thrombasthemia
GPIIb/IIIa defective –> less aggregation
vWF: production
continuously: by epithelium stored in weibel-palade bodies
and regulatory: by megakaryotes / platelets, stored in a-granules
vWF disease: type I
partial quantitive deficiency of vWF
vWF disease: type II
subtype A: decreased platelet binding + deficiency of HMV vWF multimers
subtype B: increased affinity for GPIb, gets removed from circulation so deficient
subtype M: decreased platelet binding, no loss of HMV vWF multimers
subtype N: decreased affinity for F VIII
vWF disease: type III
virtually complete deficiency of vWF
also gives low factor VIII
