part 8

Question 1

tumor specific monoclonal antibodies

Answer 1

ex. CD20 (used to treat b-cell lymphomas)
= rituximab
can cause direct apoptosis, complement activation or direct lysis

Question 2

radio-immunotherapies

Answer 2

add radioactive particles to immunoglobulines

Question 3

antibody-drug conjugate

Answer 3

add drug to antibodies

ex. brentuximab (anti CD30, causes apoptosis bc of cell arrest)

Question 4

bispecific T cell engager (BiTE)

Answer 4

zijn alleen antistoffen
ex. anti CD3 + anti CD19 antibodies stuck together
can bind 2 things

Question 5

CAR T cells

Answer 5

chimeric antigen receptor
uses viruses to change patient’s own T cells
ex CD19
side effect: cytokine release syndrome (hypotension, fever)

Question 6

tumor specific monoclonal antibodies: side effects

Answer 6

allergic reactions
tumor lysis syndrome (renal failure, release LDH)
anti-CD30: gives polyneuropathy

Question 7

trusseau syndrome

Answer 7

presence of thrombosis in relation to malignancy

Question 8

primary hemostasis

Answer 8

reduction in flow by vasoconstriction
AND
platelet plug

Question 9

secondary hemostasis

Answer 9

TF causes cascade to create fibrin

mediated by thrombin

Question 10

adhesion of platelets

Answer 10

done by: GP VI, Ia and Ib
GPVI and Ia are collagen receptors
GPIb binds vWF

Question 11

aggregation of platelets

Answer 11

GP IIb / IIIa, when activated bind to fibrinogen + vWF

Question 12

a-granules

Answer 12

release vWF and fibrinogen (precursor of fibrin)

Question 13

dense granules

Answer 13

release serotonin and ADP

Question 14

activation of platelets

Answer 14

through:
P2Y12 = ADP receptor
TXA2R = thromboxane A2 receptor
PAR1 = sensitive to thrombin

Question 15

thrombocytopenia

Answer 15

too few platelets
causes:
- reduced production (chemo, leukemia, aplastic anemia)
- increased consumption (ITP or DIC)
- loss/bleeding

Question 16

thromocytopathia

Answer 16

defective platelets
caused by:
- congenital platelet defects,
- acquired platelet defects, (kidney failure [uremia], liver cirrhosis)
- medication (platelet aggregation inhibitors)

Question 17

Bernard-Souiller syndrome

Answer 17

GPIb defective –> vWF can’t bind –> less aggregation

Question 18

Glanzmann thrombasthemia

Answer 18

GPIIb/IIIa defective –> less aggregation

Question 19

vWF: production

Answer 19

continuously: by epithelium stored in weibel-palade bodies

and regulatory: by megakaryotes / platelets, stored in a-granules

Question 20

vWF disease: type I

Answer 20

partial quantitive deficiency of vWF

Question 21

vWF disease: type II

Answer 21

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

Question 22

vWF disease: type III

Answer 22

virtually complete deficiency of vWF

also gives low factor VIII