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Blood 2 Flashcards

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1
Q

Function of platelets

A

To seal breaks in blood vessels

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2
Q

Other name for platelets

A

Thrombocytes

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3
Q

What are platelets derived from?

A

Cell fragments shed from megakaryocytes

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4
Q

Structure of platelets

A

Lack nuclei

Have organelles and cytosolic enzymes for generating energy and synthesizing secretory products

High concentrations of actin and myosin

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5
Q

Lifespan of platelets

A

Remain functional for an average of 10 days

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6
Q

How are platelets removed from circulation?

A

by tissue macrophages

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7
Q

Do platelets leave blood like WBCs?

A

No

About 1⁄3 are stored in blood-filled spaces in spleen

Released when needed by sympathetically induced splenic contraction

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8
Q

How is platelet production regulated?

A

Self-regulating process

Regulation factors (Thrombopoietin (TPO), Interleukin-3 (IL-3), IL-6, IL-11)

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9
Q

How is TPO produced and what is its effect?

A

Hormone produced by liver

increases number of megakaryocytes and therefore increases platelet production

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10
Q

How do intact endothelial cells prevent platelets from aggregating

A

Release prostacyclin and nitric oxide

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11
Q

Steps for formation of hemostatic plug

A

1) Vessel injury exposes underlying collagen fibers
2) Platelets adhere. A large plasma protein called the von Willebrand factor stabilizes the platelets by forming bridge with collagen fibres
3) Platelets swell, form spiked processes and become sticky.
4) Prostaglandin synthesis in platelets occurs, and thromboxane A2 (TXA2) is produced. Serotonin is also released. These messengers enhance vasoconstriction and platelet aggregation
5) ADP release causes platelets to well and aggregate

Primary hemostatic plug is formed

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12
Q

Stability of primary hemostatic plug

A

Unstable

Temporary control of bleeding

Becomes stabilized by fibrin network

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13
Q

Function of hemostasis

A

Prevents blood loss from a broken blood vessel

essential to life

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14
Q

Three major steps of hemostasis

A

Vascular spasm (constriction of vessel)

Formation of platelet plug

Blood coagulation (clotting)

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15
Q

Reason for vascular spasm in hemostasis

A

Reduces blood flow through damaged vessel

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16
Q

General outcome of blood clotting

A

Transformation of blood from liquid into a solid gel

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17
Q

What is the purpose of clot formation?

A

Reinforce platelet plug

Converts blood in the vicinity to non flowing gel

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18
Q

When are clotting factors present in blood plasma?

A

Clotting factors are always present in blood plasma in inactive precursor form

Vessel damage that exposes collagen initiates cascade of reactions that involve successive activation of clotting factors

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19
Q

Fibrinogen

A

Precursor of fibrin

Insoluble protein - creates protein meshwork of clot

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20
Q

Thrombin

A

Converts fibrinogen to fibrin at site of injury

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21
Q

Factor XIII

A

Fibrin stabilizing factor

xlink fibrin molecules

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22
Q

Factor X

A

Last component of clotting cascade that activates thrombin from prothrombin

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23
Q

Platelet factor 3

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A

Stimulator of clotting cascade secreted by platelets

24
Q

What is the clotting cascade?

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A

series of steps

involves 12 plasma clotting factors

Leads to conversion of fibrinogen into a fibrin mesh

25
How is the clotting cascade triggered?
Intrinsic pathway Extrinsic pathway See figure
26
Number of steps in intrinsic pathway of clotting cascade
Seven separate steps
27
When does intrinsic pathway start?
When factor XII (Hageman factor) is activated by coming into contact with exposed collagen in injured vessel or foreign substance such as test tube
28
What are all the clotting factors in the intrinsic pathways
Either cofactors or enzymes All enzymes except factor XIII are serine protease
29
Scale of amplification in intrinsic pathway
1 mol of activated factor XI -> IX -> X -> prothrombin -> 2x108 mol of fibrin
30
Number of steps in extrinsic pathway
Four
31
When does extrinsic pathway start?
Requires contact with tissue factors external to the blood Tissue thromboplastin released from traumatized tissue directly activates factor X
32
Why is the clotting cascade so extensive?
Ensure coagulation occur only when needed Otherwise, serious consequences e.g. atherosclerosis -> thrombus -> emboli -> heart attack or stroke Amplification at each step (reduces loss of blood)
33
Why is ASA (aspirin) used to prevent heart attack/ stroke?
ASA blocks platelet aggregation -> prevents clot formation
34
Clot dissolution
Tissue heals (new tissue formed) -> plasminogen converted to plasmin by action of factor XII (Hageman factor) -> plasmin slowly dissolves clot Fibrin also produced by healthy vessels -> dissolved by tissue plasminogen activator (tPA)
35
Anticoagulant drugs
Heparin Hirudin (lepirudin) Warfarin
36
Fibrinolytic drugs
Streptokinase Urokinase Anistreplase Tissue plasminogen activator (t-PA)
37
Antiplatelet drugs
Aspirin Ticlopidine
38
Thrombus
Abnormal intravascular clot attached to a vessel wall
39
Emboli
Freely floating clots
40
Factors that cause thromboembolism
Roughened vessel surfaces associated with atherosclerosis Imbalances in the clotting-anticlotting systems Slow-moving blood Occasionally triggered by release of tissue thromboplastin into blood from large amounts of traumatized tissue
41
Septicemic shock
Widespread clotting that is caused by toxins released by infectious bacteria
42
Hemophilia (cause and treatment)
Excessive bleeding caused by deficiency of one of the factors in the clotting cascade (80% defect in making Factor VIII) Treatment by infusion of factor VIII and IX
43
Thrombocytopenia purpura
Condition in which individual develops many small purple blotches Arise from small ruptures in capillaries and vessels Lack platelets to seal sites (reduced or no formation of platelet plugs) Blood leaks -> excessive bleeding at these sites
44
Vitamin K deficiency
Vitamin K is required for prothrombin synthesis in liver
45
How does thrombocytopenia purpura arise?
Rare autoimmune disorder break down of platelets in the blood by autoantibodies (detected in 60-70% patients) low platelet count thought to be triggered viral infection, after which young children develop large bruises and petechiae (small purple dots under the skin). Exact mechanism unclear
46
Von Willebrand disease
Genetic mutation in chromosome 12 3 types categorized depending on vWF levels Lab findings: increased bleeding time, normal PT, activated partial thromboplastin time decreases, decrease in Factor VIII, decrease in vWF
47
Symptoms of deep vein thrombosis
swelling, pain, or unusual redness or warmth in one of the legs
48
How to prevent deep vein thrombosis
annual checkups take medication as prescribed avoid being sedentary (lifestyle & flight) stretching weight quit smoking watch for symptoms
49
Diagnosis of deep vein thrombosis
d-Dimer test ultrasound scan of the legs blood samples to check for clotting problems (such as inherited biochemical conditions) venogram
50
Treatment of deep vein thrombosis
LMW Heparin (iv or sc), warfarin Prevent larger clot, pulmonary embolism, new clot formation, post-thrombotic syndrome (PTS)
51
Who does hemophilia A affect?
Males X-linked disorder
52
What happens in hemophilia A?
Reduced synthesis of factor VIII <1% - frequent spontaneous bleeding 1-5% severe bleeding following injury >5% bleeding after injury or surgery
53
What occurs in disseminated intravascular coagulation?
Widespread generation of fibrin within blood vessels
54
What can severe disseminated intravascular coagulation cause?
Organ dysfunction
55
Myeloproliferative neoplasms
Incluces many diseases Abnormal megakaryocytic proliferation Common mutation: Janus Kinase 2 (JAK2), V617F RCT ongoing: TPO receptor agonists, JAK2 inhibitors

Physiology (19 decks)

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