Questions in class Flashcards

(43 cards)

1
Q

Which factor does not lead to platelet activation?

  • Thrombin
  • Serotonin
  • VEGF
A

VEGF

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2
Q

How do platelets sense damage of the blood vessels?

  • By chemotaxis
  • By collagen mobilized on vWF
  • By extravasation of … into the tissue
  • By Erythropoietin release
A

By collagen mobilized on vWF

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3
Q

How does acetylsalicylic acid lead to haemodilution?

  • Via vasodilation
  • Via inhibition of the coagulation cascade
  • By the inhibition of the cyclooxygenase
  • By the reduction of the erythrocyte count
A

By the inhibition of the cyclooxygenase

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4
Q

GPIV is recognised by…

A

Collagen (receptor?)

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5
Q

Coagulation is needed for..

  • Vessel occlusion
  • Protection against atherosclerosis
  • Wound healing
  • Acid base balance
A

Wound healing

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6
Q

Which cells produce prostacyclin that causes vasodilatation and inhibits platelet activation?

  • Platelets
  • Endothelial cells
  • Smooth muscle cells
  • Leukocytes
A

Endothelial cells

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7
Q

Which of the following statements is correct?

  • Inhibition of platelet binding to leukocytes is sufficient to prevent thrombosis
  • Inhibition of secondary-feedback platelet activation is sufficient to prevent thrombosis
  • In order to block thrombosis platelet interaction with the subendothelial matrix needs to be blocked
  • Inhibition of RNA synthesis in platelets prevents thrombosis
A

Inhibition of secondary-feedback platelet activation is sufficient to prevent thrombosis

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8
Q

The megakaryocyte is found in..

  • Bone marrow
  • Lymph nodes
  • Liver
  • Kidney
A

Bone marrow

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9
Q

What is the function of PAF (platelet activating factor) released after platelet activation?

  • It reduces the thrombotic risk
  • It recognizes damaged blood vessels
  • It enhances fibrin cross-linking
  • It leads to recruitment of further paletes
  • Chemotaxis
A

It leads to recruitment of further paletes

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10
Q

Which of the following statements is correct?

  • Fibrogen activates GPIIb/IIIa
  • Fibrinogen binds to activated GPIIb/IIIa
  • Fibrogen inactivates GPIIb/IIIa
  • GPIIb/IIIa binds inactivated fibrogen
A

Fibrinogen binds to activated GPIIb/IIIa

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11
Q

Thromoxan A2…

  • Enhances platelet aggregation
  • Inhibits blood coagulation
  • Activates neutrophil granulocytes
  • Leads to vasodilation
A

Enhances platelet aggregation

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12
Q

What phospholipid derived factors are not cyclooxygenase dependant?

  • Leukotriene
  • Thromboxane
  • Prostaglandine
  • Prostacyclin
A

Leukotriene

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13
Q

How do paletes interfere with secondary haemostasis? Via release of..

  • Fibrogen and collagen
  • Thrombin and prothrombin
  • Calcium, FV, FVIII
  • FVIIa and FIXa
A

Calcium, FV, FVIII

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14
Q

Which sort of enzyme is ADAMTS13?

  • Catalase
  • Coagulase
  • Protease
  • Decarboxylase
A

Protease

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15
Q

Which process is a result of platelet activation?

  • Uptake of thromboxan
  • Calcium integration into the palette membrane
  • Conformational change of surface GPIIb/IIIa
  • Conformational change of intraplatelet GPIIb/IIIa
A

Conformational change of surface GPIIb/IIIa

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16
Q

How does the factor IIa get activated?

  • By the coagulation factors TF/VIIIa
  • By the coagulation factors TF/VIIIa
  • By fibrin
  • By activated protein C
A

By the coagulation factors TF/VIIIa

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17
Q

Which statement about protein C (PC) is not true?

  • PC is a natural occurring anticoagulant which circulates in plasma
  • PC is synthesised in the liver
  • PC is activated by phosphorylation
  • PC is a serin protease
A

PC is activated by phosphorylation

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18
Q

How does vWF syndrome affect platelet function?

  • GPIIa/IIIa conformational change is inhibited
  • Platelets adhesion is affected
  • Platelet crosslinking is affected
  • Platelet membrane flip is not possible
A

Platelets adhesion is affected

19
Q

Which of the following answers is true for Antithrombin?

  • Heparin decreases the inhibitory effect of AT on coagulation
  • AT forms an inhibitory complex with FXa
  • AT inhibits the activating factors V, VIIa, VIIIa and Xa
  • AT is a cofactor of Protein S, required for enhancing the inhibitory interaction
A

AT forms an inhibitory complex with FXa

20
Q

How is Protein C activated?

  • By interaction with factor V and VIII
  • By thrombin/ thrombomodulin by cleavage
  • By thrombin/ thrombomodulin by addition of an amino group
  • By separation of Protein S
A

By thrombin/ thrombomodulin by cleavage

21
Q

Which of the following statements about thrombin is not correct?

  • It’s factor II and a serin protease
  • It’s part of the coagulation, catalyses generation from fibrin to fibrinogen
  • It’s synthesized by the liver as an inactive proenzyme
  • Plays a role in anticoagulatory task
A

It’s factor II and a serin protease

22
Q

A lack of defect of FIX results in:

  • Haemophilia A
  • Haemophilia B
  • Glanzmann syndrome
  • Bernard Soulier syndrome
A

Haemophilia B

23
Q

Haemophilia A is caused by the lack of factor VIII,…

  • Which is, under normal conditions, able to activate itself
  • Which is, under normal conditions, activated by thrombin and inhibited by protein C
  • Which is, under normal conditions, part of the extrinsic tenase complex, activating factor X
  • Who’s loss can either be acquired or inherited
A
  • Which is, under normal conditions, activated by thrombin and inhibited by protein C
  • Who’s loss can either be acquired or inherited
24
Q

Which of the following statements is correct?

  • Binding of thrombin to thrombomodulin activates TAFI, which is responsible for the activation of fibrinolysis
  • Thrombin is able to promote the activation of coagulation factors V, XI and VIII as well as its own release (positive feedback loop)
  • Thrombin is a serine protease with a structural similarity to tryptophan
  • One of the properties of anticoagulatory thrombin is to activate protein C after binding to vWF
A

Thrombin is able to promote the activation of coagulation factors V, XI and VIII as well as its own release (positive feedback loop)

25
The Prothrombinase complex… - Consists of factors Xa and Va - Directly activates Fibrinogen to Fibrin - Leads to the generation of active thrombin by linking two prothrombins - Gets inactivated by activity of aPC
- Consists of factors Xa and Va | - Gets inactivated by activity of aPC
26
Leukocyte rolling on endothelial cells is initiated by - P-selectin - ICAM-1 - VCAM - E-Selectin
P-selectin
27
Which of the following statements is NOT correct? - VEGF binds to FIk1 (VEGF-R2) - VEGF binds to FIt1 (VEGF-R1) - Angiopoetin-1/-2 binds to Flt1 (VEGF-R1) - Angiopoetin-1/-2 binds to Flk1 (VEGF-R2)
Angiopoetin-1/-2 binds to Flt1 (VEGF-R1)
28
What is the consequence of VEGF binding to VEGF-R2? - Recruitment of pericytes - Differentiation of endothelial cells - Stabilisation of blood vessels - Reconstruction of the basal membrane
Differentiation of endothelial cells
29
How can angiogenesis be induced during tumor development? - Matrix metalloproteases degrade the basal membrane, which leads to sprouting of endothelial cells - Oxygen shortage of the tumor leads to induction of HIF-1, which induces VEGF expression - Vessel injury during tumor growth leads to new vessel formation - Tumor express VEGF-R2 which induces the differentiation of endothelial cells
Oxygen shortage of the tumor leads to induction of HIF-1, which induces VEGF expression
30
Which is the function of the lymphatic system? - Transportation of liquids into tissue - Transportation of dendritic cells - Transportation of antibodies - Transportation of coagulation factors
Transportation of liquids into tissue
31
At what developmental stage does vasculogenesis occur? - Late embryogenesis - Early embryogenesis - Only in adults - During embryogenesis and in adults
Early embryogenesis
32
What is the correct sequence? (Angiogenesis)
Angiogenic stimulus → degradation of the basal matrix → initial endothelial migration → endothelial cell-proliferation → formation of capillaries → maturation and recruitment
33
Angiopoetin-1 binds to… - VEGF-R1 - VEGF-R2 - Tie2 - Tie1
Tie2
34
Which factor is no angiogenic stimulus? - Hypoxia - Inflammation - Degradation of the basal membrane - Tissue injury
Degradation of the basal membrane
35
Which statement about vasculogenesis is correct? - During intraembryonal development angioblasts are formed in the ectoderm, which differentiate to endothelial cells - During intraembryonal development angioblasts are formed in the endoderm, which differentiate to endothelial cells - Vasculogenesis is regulated by VEGF and erythropoietin - During embryonic development in the yolk sac vessel and blood development are coupled
During embryonic development in the yolk sac vessel and blood development are coupled
36
Which statement about veins and arteries is correct? - Veines can be exposed to higher blood pressure compared to arteries - Arteries have valves toprevent reflux of blood - Venoles collect blood of the capillaries, which is then further transported in veins - Veins are the blood storage pool, which ⅓ of the blood being in the veins
Venoles collect blood of the capillaries, which is then further transported in veins
37
Which factor induces vasculogenesis? - Angiopoetin-1 - Tie2 - VEGF - bFGF
VEGF
38
Which vessels have valves? - Arteries - Veins - Capillaries - Veins and lymphatic vessels
Veins and lymphatic vessels
39
Which molecule induces vasoconstriction? - NO - Angiotensin II - Bradykinin - cGMP
Angiotensin II
40
Stabilisation of newly formed vessels is very important. Which protein is important for the recruitment of pericytes? - Platelet-derived Growth Factor - Serpin - Angiopoetin 1 - VEGF-2
Angiopoetin 1
41
Which vessel has the thickest vessel wall? - Veins - Arterioles - Lymphatic vessels - Arteries
Arteries
42
VEGF binds to … consequence of this interaction in the yolk sac during embryonic development? - Endothelial cell differentiation - Hematopoietic stem cell development - Stabilisation of newly formed vessels - Vessel formation
Vessel formation
43
What starts secondary haemostasis? - Platelet activation - Erythrocyte activation - Activation of plasma factors - Proliferation of endothelial cells
Activation of plasma factors