platelet and vessel wall interaction

Question 1

clot formation in vivo:
exposure of sub endothelial — –> accumlation of activated — at the site of injury — > — deposition and – formation

Answer 1

proteins
platelets
fibrin
clot

Question 2

-Circulate as quiescent cells, survey vascular integrity – described as the ‘unmanned drones of the vasculature’1 is known as —
-Undergo explosive activation upon — damage
- — discs derived from –
-Very – - 2-4μm
- — life-span ~ 10 days
- Normal platelet count: 150 400 x 109/litre

Answer 2

platelet
vessel wall
anucleated discs
megakarocyte
very small
long

Question 3

fragmentation of cytoplasm each MK produces —-

Answer 3

4000 platelets

Question 4

ultrastructural feature of the platelet:
1- —- :
Gp VI
Gp Ib-IX-V complex
Gp IIb-IIIa complex
2- — granules :
- —
- —–
- —-
3- — granules as:
- —
- —
- —-
- —
4- also has — , — membrane , — cannalucaltion system and —

Answer 4

surface receptors
dense
Ca+2
ADP/ATP
serotonin
alpha
VWF
firbongen
factor v
PF4
glycogen , phopsholipid membrane , open, mitochondria

Question 5

platelts find the site of vascular damage by —

Answer 5

platelet adhesion

Question 6

1-Von Willebrand factor (VWF):
- — — circulating – protein
-Contains – sites for platelets and sub-endothelial tissue
-Must be ‘ — ’ for these binding sites to be exposed
2- GPIb-V-IX complex receptor :
- is a — receptor composed of – subunits which are:
- coupled to underlying —

Answer 6

globular multi metric
plasma
binding sites
tethered
platelet
4 subunits which are:
GPIbα
GPIbβ
GPIX
GPV
cytoskeleton

Question 7

VWF-GPIbα complex:
-Interaction between a – plasma protein (Von Willebrand Factor; VWF)…
- and a — receptor (glycoprotein Ib; GPIbα)
- Crucial for — in – shear conditions
- how VWF adheres to platelet:
1-Becomes — to the site of – injury
2- — , exposing — sites for GPIbα
3-Platelets become – to site of injury

Answer 7

circulating plasma protein
platelet surface
platelt adhesion
high
tethered
vascular
unravels
biding site
bound

Question 8

—- happens when VWF binding platelet GPIbα is compromised
- — common bleeding disorder (1 in 1000):
-Genetic defects in VWF which result in:
1. – VWF levels
2. inability to bind —
3. prevent binding to – or –

Answer 8

von willebrand disease VWD
most common
low
collagen/plaetelt
sub- endothelial tissues or platelets

Question 9

bernard soulier syndrom:
- – genetic defect in – that prevent normal– interaction
- Prevents normal – formation, – tendency

Answer 9

rare
GPIbα
VWF
normal thrombus
bleeding

Question 10

-platelet activation:
1-Change in platelet –
2-Activation of — - GpIIb/IIIa
3- — secretion
4- — of plasma membrane
- what’s the purpose does platelet activation serve:
-Conversion from ‘ — ’ state to – ‘ — ’ state:
1-Adopt – changes to help – formation
2-Secretion of – that facilitate – formation
3-Activate — to make them ‘— ’ for other – and– factors

Answer 10

shape
cell surface interns
granule
“Flip/Flop”
quiescent
active haemostat state
structural changes
clot formation
secretion of factors for clot formation
cell surface molecules
stickily
platelet and coagualtion factors

Question 11

1- platelet shape change:
-Within – of – - change in shape
becomes — or —
-Reorder of – and — polymers of cytoskeleton

Answer 11

seconds of adhesion
spherical or pseudopodia
actin and tubular

Question 12

-release of platelet granules:
1- Dense Granules
Rich in – messengers that promote further platelet — and –
2- Alpha Granules
Rich in – proteins, contributes to further—
- open canalicular system OCS: – surface with periodic invaginations
entrances into OCS
Extensive system of – membrane –
– serves as – system for granule –

Answer 12

chemicals
activation and aggregation
clotting proteins
clot formation
flat
internal
tunnels
conduit system
release

Question 13

inhibitors of platelet activation:
-Used to prevent — (rich in aggregated platelets)
-Most common example is —
-Inhibits – pathways that lead to platelet –

Answer 13

arterial thrombosis
aspirin
signalling
activation

Question 14

making the platelet sticky:
1- “ flip-flop” of phospholipids:
- — charged phospholipids previous on inner leaflet of platelet membrane become —
-Necessary for — dependent coagulation factor binding
2- GPIIb/IIIa activation:
-Platelet activation causes platelet membrane activation of —-
-An important platelet receptor for – and –
- Acts to cause platelet –
- GPIIb/IIIa deficiency:
— fails to accumulate at the site of vessel injury when GPIIb/IIIa is absent
-Patients deficient in this receptor have —

Answer 14

-ve
externalised
vitamine k
glycoprotein complex IIB/IIIA
VWF and firbongen
platelet aggregation
platelet plug
Glansmann’s thrombasthenia

Question 15

GPIIb/IIIa inhibitors - Abciximab:
- — directed against GPIIb/IIIa
-Inhibits —
-Preventing the formation of – during procedures to open – arteries

Answer 15

monoclonal antibody
platelet aggregation
blood clot
open blocked arteries

Question 16

diagnostic tests for thrombosis:
- — is a specific degradation fragment of cross-linked fibrin
-It is produced – as part of the — process by –
-It has a – half-life in plasma
-Measurement of plasma D-dimer levels is useful to aid in the – of —

Answer 16

d-dimer
naturally
wound healing
plasmin degradation of thrombus
long
diagnosis
pulmonary thromboembolism (PTE)

Question 17

application of d dimer:
- — levels of D-dimer indicates the occurrence of recent thrombotic event
-A — D-dimer concentration excludes thromboembolic events such as deep vein thrombosis and pulmonary embolism with a high probability
-A — D-Dimer test is not definitive evidence for the presence of thrombosis - definitive diagnosis must be accompanied by MRI scanning, angiography, CAT scan etc

Answer 17

elevated
normal
positive