Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHYSIOLOGY II > WEEK IV (Platelets) > Flashcards

WEEK IV (Platelets) Flashcards

1
Q

How many platelets are present in each millilitre of blood?

A

250 million platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are Platelets/Thrombocytes?

A

Small cell fragments shed from the outer edges of extraordinarily large bone-marrow bound cells called MEGAKARYOCYTES

[Platelets are DETACHED VESICLES containing pieces of megakaryocyte cytoplasm wrapped in plasma membrane]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are Megakaryocytes derived from?

A

Undifferentiated stem cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How long do Platelets remain functional for?

A

10 days until they are removed from circulation by TISSUE MACROPHAGES & replaced by new platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the hormone that increases the level of platelets in the blood?

A

THROMBOPOIETIN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Cells from which organ especially remove platelets from circulation?

A

Spleen & Liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the properties of Thrombopoietin?

A
  • Produced by the liver
  • Increases the number of megakaryocytes in bone marrow
  • Stimulates each megakaryocyte to produce more platelets as needed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the properties of platelets?

A
  • Lack nuclei
  • Contain organelles and cytosolic enzyme systems for GENERATING ENERGY and SYNTHESISING SECRETORY PRODUCTS
  • Store cytosolic enzymes in cytoplasmic granules
  • Contain high concentrations of ACTIN and MYOSIN (enable them to contract)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is Hemostasis?

A

The stopping of bleeding from a broken blood vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why is bleeding from a severed artery more dangerous than from a severed vein?

A

Arterial blood pressure is higher than venous blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is needed for bleeding to take place?

A
  • A break present in the vessel wall
  • The pressure inside must be greater than the pressure outside to force blood out the defect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the three major steps of hemostasis?

A

1) Vascular spasm
2) Formation of a platelet plug
3) Blood coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is Vascular Spasm

A

When a cut or torn blood vessel immediately constricts which slows blood flow through the defect and thus minimises blood loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What happens to the endothelial surfaces of the blood vessel during Vascular spasm?

A

The opposing endothelial surfaces of the vessel are pressed together and become sticky and adhere to each other which seals off the damaged vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the properties of Vasoconstriction?

A
  • First line of defence against bleeding
  • Occurs in response to endothelial damage
  • Key mediator are ENDOTHELINS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the properties of Endothelins?

A
  • Proteins
  • Potent vasoconstrictors (regulate blood pressure by constricting blood vessels)
  • Released by ENDOTHELIAL CELLS near site of damage
  • ENDOTHELIN receptor blockers used in PULMONARY HYPERTENSION
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What happens when the endothelial lining is disrupted because of vessel injury?

A

von Willebrand factor (vWF) adheres to the exposed collagen which is found in the underlying endothelial lining -> vWF has BINDING SITES to which fast-moving platelets attach using their cell-surface receptors specific for this Plasma protein -> vWF serves as a BRIDGE between platelets & injured vessel wall -> Adhesion prevents platelets from being swept forward in the circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What activates the sound platelets at the Platelet plug?

A

Collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the properties of activated platelets?

A
  • Spiky processes helping to adhere to COLLAGEN & other PLATELETS
  • Release chemicals from their storage granules
  • Release ADENOSINE DIPHOSPHATE (ADP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the difference between normal platelets and activated platelets?

A
  • Normal platelets = disc-shaped & smooth surface
  • Activated platelets = Reorganise their actin cytoskeletal elements to develop spiky processes (helps to adhere to collagen & other platelets)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the importance of ADP?

A

Causes the surfaces of nearby circulating platelets to become STICKY so they adhere to the first layer of AGGREGATED PLATELETS & are activated -> Newly aggregated platelets release more ADP -> More platelets pile on forming a platelet plug using POSITIVE FEEDBACK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the aggregating process reinforced by?

A

The ADP-stimulated formation of an eicosanoid paracrine called THROMBOXANE A2 from a component of the platelet plasma membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the properties of Thromboxane A2?

A
  • Directly promotes & indirectly enhances platelet aggregation
  • Triggers the release of even more ADP from platelet granules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the three events leading to the formation of a Platelet plug?

A

1) Adhesion
2) Activation
3) Aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Why does the platelet plug not continue to expand over the surface of the adjacent normal vessel lining?

A

ADP discharged by activated platelets stimulates release of PROSTACYCLIN and NITRIC OXIDE from the adjacent normal endothelium -> Both chemicals inhibit PLATELET AGGREGATION -> Platelet plug is limited and does not spread to the nearby undamaged vascular tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the other roles of the aggregated platelet plug apart from sealing the vessel?

A
  • ACTIN-MYOSIN COMPLEX within aggregated platelets contracts to COMPACT & STRENGTHEN a fairly loose plug
  • Releases VASOCONSTRICTORS to reinforce initial VASCULAR SPASM
  • Releases chemicals that enhance blood coagulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are other platelet functions besides thwarting blood loss?

A
  • Releasing growth factors to help damaged tissue rebuild
  • Inducing inflammation
  • Serving as detectors of disease-causing microorganisms
  • Promoting NET release by neutrophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Summarise the steps of Primary Hemostasis (Platelet plug formation)

A

1) ENDOTHELIN is released from damaged cell and circulating platelets adhere to and are activated by EXPOSED COLLAGEN at the site of vessel injury since vWF binds to exposed collagen
2) Activated platelets release ADP and thromboxane A2
3) ADP and Thromboxane A2 work together to activate other platelets passing by. ADP helps platelets adhere to endothelium.
4) Newly activated platelets aggregate onto the growing platelet plug and release even more platelet-attracting chemicals
5) Normal endothelium releases PROSTACYCLIN and NITRIC OXIDE which inhibit platelet aggregation so platelet plug is confined to the site of injury

29
Q

What is Blood coagulation/Clotting?

A

The transformation of blood from a liquid into a solid gel

30
Q

What are the benefits of blood coagulation/clotting?

A
  • Formation of a clot on top of the platelet plug reinforces the seal over a break in a vessel
  • As blood in the vicinity of the vessel defect SOLIDIFIES, it can no longer flow
31
Q

What is the difference between Fibrinogen and Fibrin?

A

Fibrinogen = a large, soluble plasma protein produced by the liver and normally always present in plasma

Fibrin = an insoluble, threadlike molecule

32
Q

Describe the conversion of Fibrinogen into Fibrin and its importance

A
  • Catalysed by THROMBIN
  • Fibrin molecules adhere to the damaged vessel surface forming a loose, netlike meshwork that traps blood cells, including aggregating platelets
33
Q

What accounts for stretchiness of blood clots?

A

The highly elastic property of Fibrin

34
Q

Describe the fibrin web

A

Original fibrin web is weak since fibrin strands are LOOSELY INTERLACED but CHEMICAL LINKAGES rapidly form between adjacent strands to strengthen and stabilise the clot meshwork

35
Q

What is the cross-linkage of the Fibrin web catalysed by?

A

A clotting factor called Factor XIII (fibrin-stabilising factor)

36
Q

What are the roles of Thrombin?

A
  • Converts Fibrinogen into Fibrin
  • Activates Factor XIII to stabilise the resultant fibrin mesh
  • Acts in a positive-feedback fashion to facilitate its own formation
  • Enhances platelet aggregation
37
Q

Why does Thrombin exist in the blood as Prothrombin?

A

Thrombin exists in the plasma in the form of an inactive precursor called PROTHROMBIN which is converted into thrombin by the CLOTTING CASCADE when blood clotting is desirable -> This is because thrombin must normally be absent from the plasma except during vessel damage otherwise blood would always be COAGULATED

38
Q

What are the properties of Coagulation factors?

A
  • Proteins synthesised in LIVER
  • Soluble in plasma
  • Activate when triggered by ENDOTHELIAL DAMAGE
  • Form an insoluble protein called FIBRIN
  • Fibrin mesh prevents blood loss
  • Circulate as INACTIVE ENZYMES (ZYMOGENS)
  • Activated forms are Ia, Va & Xa
  • Many activate to become SERINE PROTEASES
39
Q

What are the properties of the Coagulation Cascade?

A
  • SEQUENTIAL ACTIVATION of clotting factor zymogens
  • Constant low level of activation in serum
  • AMPLIFICATION occurs with endothelial damage
  • Leads to FIBRIN GENERATION
40
Q

The activation of which clotting factor is the centre of cascade?

A

The activation of X to Xa

[this is because Activation X to Xa makes fibrin]

41
Q

Describe how the activation of X to Xa makes a platelet plug

A

1) Activation of X to Xa
2) Xa converts PROTHROMBIN (II) to THROMBIN (IIa)
3) THROMBIN (IIa) converts FIBRINOGEN (I) to FIBRIN (Ia)
4) Fibrin forms plug to stop bleeding

42
Q

What are the properties of the Tissue Factor Thromboplastin?

A
  • Glycoprotein
  • Constitutively expressed in SUB-ENDOTHELIAL cells
  • NOT expressed by ENDOTHELIAL CELLS
  • No significant contact with circulating blood
  • Exposed by ENDOTHELIAL DAMAGE
  • Major activator of COAGULATION SYSTEM
43
Q

What is the Primary event of the Coagulation cascade?

A

Exposure of tissue factor

44
Q

What happens after the exposure of the tissue factor?

A
  • Tissue factor interacts with factor VII forming VIIa
  • VII activates Xa
45
Q

What are the properties of Thrombin?

A
  • Thrombin (IIa) makes more thrombin -> activates a positive feedback cascade
  • XIa, VIIIa, Va, Thrombin (IIa) & IXa (using VIIIa as a cofactor) all activate Xa
46
Q

What are the properties of Factor VIII?

A
  • Produced in endothelial cells (NOT LIVER)
  • Circulates bound to VON WILLEBRAND FACTOR
  • Released from vWF in response to VASCULAR INJURY (vascular injury -> increased thrombin -> becomes VIIIa)
47
Q

What is the importance of the von Willebrand Factor?

A
  • vWF is critical for PLATELET AGGREGATION
  • vWF produced by ENDOTHELIAL CELLS & MEGAKARYOCYTES
  • Binding to vWF increases VIII plasma half life
48
Q

What are the properties of Multicomponent complexes?

A
  • Two complexes for conversion of X to Xa
  • Three components bound together
    (Active clotting factor as enzyme, Co-factor & Substrate (factor X))
  • Require Phospholipids and Calcium
    (Phospholipid occur on surfaces of cells & Calcium is a co-factor)
49
Q

What are the three complexes that bind together to form a multicomponent complex?

A
  • Active clotting factor functioning as enzyme
  • Co-factor
  • Substrate (always factor X)
50
Q

What are the properties of Extrinsic Xase?

A
  • PHOSPHOLIPID: Tissue Factor-bearing cells
  • ENZYME: Factor VIIa
  • CO-FACTOR: Tissue Factor
  • SUBSTRATE: Factor X
51
Q

What are the properties of Intrinsic Case?

A
  • PHOSPHOLIPID: Platelets
  • ENZYME: Factor IXa
  • CO-FACTOR: Factor VIII (VIIIa)
  • SUBSTRATE: Factor X
52
Q

What are the properties of Calcium?

A
  • Factor IV
  • Required for clot formation
  • Activated platelets release calcium
  • EDTA binds calcium in blood samples
  • Prevents clotting
53
Q

What are the properties of Factor XIII?

A
  • Crosslinks fibrin
  • Stabilises fibrin plug
  • Absence of XIII leads to INADEQUATE CLOT FORMATION
  • Requires CALCIUM as co-factor
  • Activated by thrombin (IIa) formation
54
Q

What are the properties of Factor XII (Hageman factor)?

A
  • Activates factor XI to XIa
  • Important for testing of COAGULATION SYSTEM
  • Activated by CONTACT with NEGATIVE CHARGES
  • Factor XII is turned into XIIa via contact with SILICA
  • Basis for PARTIAL THROMBOPLASTIN TIME (PTT)
55
Q

What causes Hemophilia A, B & C?

A
  • HEMOPHILIA A = deficiency of factor VIII
  • HEMOPHILIA B = deficiency of factor IX
  • HEMOPHILIA C = deficiency of factor XI
56
Q

How many plasma clotting factors participate in the final conversion of fibrinogen into a stabilised fibrin mesh?

A

12

57
Q

What are the properties of Factor X?

A
  • Converts Prothrombin & Thrombin
  • Normally present in blood in inactive form
  • Must be activated by another activated factor
58
Q

What are the pathways involved in the Clotting cascade?

A

Intrinsic & Extrinsic Pathways

59
Q

What are the properties of the Intrinsic Pathway?

A
  • Precipitates clotting with damaged vessels and clotting of blood samples in test tubes
  • 7 steps
  • Set off when Factor XII (HAGEMAN FACTOR) is activated by coming into contact with EXPOSED COLLAGEN in an INJURED VESSEL or a FOREIGN SURFACE
  • Aggregated platelets secret PF3 which enhances platelet aggregation
60
Q

What are the properties of the Extrinsic Pathway?

A
  • 4 steps
  • Requires contact with tissue factors EXTERNAL to the blood
  • Initiates clotting of blood that has escaped into tissues
  • Traumatised tissue release TISSUE THROMBOPLASTIN which directly activates factor X which bypasses all the steps of the intrinsic pathway
61
Q

How long does it take a clot to form?

A

3-6 minutes

62
Q

How do the intrinsic and extrinsic pathways operate?

A

Simultaneously

63
Q

What happens during Clot Retraction?

A
  • Platelets trapped within the clot contract and shrink the fibrin mesh, pulling the edges of the damaged vessel closer together
  • SERUM is squeezed from the clot (plasma minus fibrinogen & other clotting precursors)
64
Q

How do platelets promote vessel repair?

A

Aggregated platelets secrete a chemical that promotes the invasion of FIBROBLASTS from the surrounding connective tissue into the wounded area of the vessel -> Fibroblasts form a scar at the vessel defect

65
Q

Which enzyme dissolves the clot?

A

Plasmin

66
Q

What would happen if clots weren’t removed after performing their hemostatic function?

A

Accumulation would obstruct vessels especially the small vessels that regularly endure rib ruptures

67
Q

What are the properties of Plasmin?

A
  • Plasma protein produced by Liver
  • Present in blood in inactive precursor form (PLASMINOGEN)
  • Activated in a fast cascade of reactions involving many factors
  • Becomes trapped in the clot and later dissolves by slowly breaking down the FIBRIN MESHWORK
68
Q

What is Plasmin activated by which removes unwanted blood clots?

A

Tissue Plasminogen Activator (TPA)

PHYSIOLOGY II (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions