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Hematology Exam 2 > 5. Hemostatis: Phys, Assessment, and Common Disorders > Flashcards

5. Hemostatis: Phys, Assessment, and Common Disorders Flashcards

1
Q
  1. 5 Hemostasis starts with platelets
    - Are platelets cells? Where do they come from?
    - Any organelles or granules?
A

Platelets are not really cells, but instead fragments. They split from huge cells in the bone marrow called megakaryocytes and then enter the circulation.

They do not have a nucleusor organelles, but contain many granules.

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2
Q

5.6 What are the layers of a typical artery?

A 
Tunica intima
Tunica media
Tunica externa (or adventitia)
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3
Q

5.7 What are two ways in which a vein’s anatomy is different than an artery?

A
  1. Thinner tunica media

2. Presence of venous valves within endothelium

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4
Q
  1. 8 Capillaries anatomy
    - What layers?
    - Thick or thin walls?
A

No tunica media or tunica externa

Tunica intima contains only endothelial cells and small amounts of collagen

Very “thin” walled

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5
Q

5.9 What are the three phases of hemostasis?

A
  1. Vasoconstrictive phase or vascular spasm
  2. Platelet plug formation
  3. Blood coagulation
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6
Q

5.9 What occurs in the first phase of hemostasis?

A

Vasoconstrictive phase or vascular spasm

- Smooth muscle in damaged blood vessels constrict (reduces blood flow to limit blood loss)

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7
Q

5.9 What are the triggers of the first phase of hemostasis?

A
  1. The direct injury itself

2. Sympathetic nervous system (reflexes of local pain receptors)

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8
Q
  1. 10 What occurs in the second phase of hemostasis?
    - Characterized by aggregation of what?
    - Attracted by what?
    - Effective mainly in what kind of injuries?
A

Characterized by aggregation of platelets

Platelets attracted to exposed collagen - stick, swell, and form spiked processes

Platelet plugs are effective in preventing blood loss due to small injuries

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9
Q

5.11 What two receptors do platelets have that allow them to adhere to the sites of injury?

A
  1. GP1a receptor - attaches to exposed collagen
  2. GP1b receptor - attaches to von Willebrand’s Factor (vWF) - a protein found in plasma, plaetlets, and the walls of blood vessels
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10
Q

5.11 GP1a receptors adhere to what structure present at damaged endothelium sites?

A

Exposed collagen

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11
Q

5.11 GP1b receptors adhere to what structure present at damaged endothelium sites?

A

von Willebrand’s Factor (vWF) - a protein found in plasma, platelets, and the walls of blood vessels

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12
Q

5.12 The successful adhesion of platelets to sites of damaged endothelium will trigger the secretion of what?

A

Adhesion triggers the secretion of multiple factors from granules of the platelets:

  1. ADP (adenosine diphosphate)
  2. Thromboxane A2 (TA2; TXA2; a prostaglandin)
  3. Serotonin (5-HT)
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13
Q

5.13 What do the secreted factors from platelets do?

A

ADP, TXA2 (thromboxane), and 5-HT (serotonin) will bind to specific receptors on other platelets
- This will stimulate those receptors to become more sticky and adhere to one another to form an aggregate

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14
Q

5.13 In addition to GP1a and GP1b, what other glycoprotein receptor plays an important role in platelet aggregation?

A

GPIIb/ GPIIIa

Fibrinogen and other macromolecules of platelets will bind to one another via GPIIb/GPIIIa

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15
Q
  1. 14 Third phase of hemostasis
    - When does it occur?
    - What factors are involved?
    - Where are these factors synthesized?
    - What is an example of these clotting factors?
A

Coagulation phase (blood clotting)

  • Occurs either to reinforce a platelet plug or to stop bleeding when a platelet plug fails
  • Involves numerous clotting factors (with roman numerals), which are mostly proteins synthesized by the liver
  • Fibrin is an example
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16
Q
  1. 15 Clotting factors
    - How many?
    - Most present in circulation in what form?
    - Usually activated by what?
A

20 different clotting factors

Most present in circulation as inactive proteins (zymogens) to prevent unwanted clotting

Usually activated by other clotting factors in order to take part in coagulation reaction

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17
Q
  1. 15 Clotting factors
    - What are the four vitamin K-dependent clotting factors? (Know this!)
    - Where do all four of these clotting factors originate?
A 
Factor II (Prothrombin)
Factor VII (Proconvertin)
Factor IX (Christmas factor)
Factor X (Stuart-Prower factor)

All made in the liver

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18
Q
  1. 15 Clotting factors

- Where is Clotting Factor III made?

A

“Tissue factor” or thromboplastin

Perivascular tissue (tissues that surround a blood vessel)

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19
Q

5.15 What is a clotting factor that originates from the diet?

A

Calcium

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20
Q

5.16 What are the three parts of the blood clotting cascade?

A
  1. Intrinsic
  2. Extrinsic
  3. Final common pathway
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21
Q

5.16 What initiates the intrinsic pathway and where?

A

Platelets - initiated within the blood

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22
Q

5.16 What initiates the extrinsic pathway and where?

A

Tissue thromboplastin - initiated outside the blood

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23
Q

5.16 Outline the extrinsic mechanism of the blood clotting cascade

A

Damaged perivascular tissues -> Thromboplastin (Factor III) —(Ca2+)—-> Factor VII —-(Factor V)—-> Factor X

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24
Q

5.16 Outline the intrinsic mechanism of the blood clotting cascade

A

Platelets —> Factor XII —-> Factor XI —-> Factor IX —(Ca2+, PF3) —> Factor VIII —–> Factor X

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25
Q

5.16 Outline the final common pathway

A

Factor X –(Factor III, Factor V, Ca2+, PF3)—> Prothrombin activator

Prothrombin (factor II) —(Prothrombin activator)—> Thrombin

Fibrinogen (Factor I) —(Thrombin)—> Fibrin —- (Factor XIII, Ca2+) —> Fibrin polymer

(This looks better on paper :( )

26
Q

5.17 What are “natural” anticoagulants?

A

Protease inhibitors that rapidly inactivate coagulation factors that escape the site of injury.

They maintain the homeostatic balance between coagulation and anti-coagulation.

27
Q

5.17 What are examples of “natural” anticoagulants?

A

Thrombomodulin
Antithrombin III (or just antithrombin)
Heparin cofactor II

28
Q
  1. 18 Thrombomodulin
    - Where is this present?
    - Combines with what protein?
    - What does it activate?
A

A natural anticoagulant glycoprotein that is present on endothelial cells.

Combines with thrombin to make a thrombomodulin-thrombin complex

Thrombomodulin-thrombin complex activates protein C

29
Q
  1. 18 Protein C
    - What is its cofactor?
    - Function?
A

Protein C’s cofactor is Protein S

They both degrade factors V and VIII

30
Q
  1. 19 Antithrombin III (antithrombin)
    - Produced where?
    - Function?
A

A natural anticoagulant glycoprotein produced by the liver.

Antithrombin binds to and inhibits factor X and thrombin (hence the name “anti-thrombin”)

31
Q
  1. 20 Heparin Cofactor II
    - Produced where?
    - Function?
A

A natural anticoagulant plasma protein produced by the liver.

Heparin cofactor II inhibits thrombin

(Not as important to humans as Thrombomodulin)

32
Q
  1. 21 What enzyme initiates the fibrinolytic system?

- What is it synthesized from?

A

Plasmin

Synthesized from an inactive plasma protein from the liver called Plasminogen.

33
Q
  1. 21 What enzyme converts plasminogen to plasmin?

- What releases this enzyme?

A

Tissue Plasminogen Activator (t-PA)

It is released into blood by the damaged endothelium of the blood vessels.

34
Q
  1. 21 Tissue Plasminogen Activator (t-PA)

- When is this enzyme released?

A

t-PA is released after several days (when the bleeding has stopped).

This is because plasminogen is trapped within the clot initially. As the plasminogen is activated, it breaks down the fibrin mesh.

35
Q

5.22 What are fibrinolysis inhibitors?

A

They prevent prolonged or unwanted degradation of fibrinogen.

36
Q

5.22 What are four examples of fibrinolysis inhibitors and where do each of them target the Fibrinolytic system?

A
  1. Plasminogen activator inhibitor 1 - targets tPA
  2. Plasminogen activator inhibitor 2 - targets tPA
  3. α2-antiplasmin - targets Plasmin
  4. α2-macroglobulin - targets Plasmin
37
Q

5.23 What are two clinical tests that are useful in assessing an individual’s clotting system?

A
  1. CBC - Platelet Count

2. Blood smear

38
Q
  1. 23 What is one result of a CBC - Platelet count that would signify an individual’s clotting system being at increased risk of bleeding?
    - Is this status a clinical concern?
A

Low platelet count - “Thrombocytopenia” - increased risk for bleeding

Not a clinical concern - occasionally, there may be bruising at the forearms, petechia (small purple spots around the body), nosebleeds, and/or bleeding gums

39
Q

5.23 What is the usefulness of a blood smear in assessing an individual’s clotting system?

A

Useful to confirm the automated platelet count and also allows the morphology of the platelets to be assessed
- Some inherited platelet disorders are associated with large platelets

40
Q
  1. 24 What is the basic premise of coagulation tests?

- How is citrate used in these tests?

A

Used to determine the function of the intrinsic and extrinsic components of the coagulation system.

Blood is collected in tubes containing sodium citrate.

The citrate binds calcium, inhibiting the normal coagulation cascade which requires calcium. Additional calcium needs to be added to form a clot.

41
Q

5.25 What are the four coagulation tests covered?

A
  1. Prothrombin Time (PT); Pro-time
  2. INR (International Normalized Ratio)
  3. Activated Partial Thromboplastin Time (APTT)
  4. Thrombin Clotting Time (TT)
42
Q
  1. 25 Prothrombin Time (PT); Pro-Time
    - Used to assess which pathway?
    - Procedure of the test?
A

Used to assess extrinsic pathway

Calcium is added to plasma to replace the Ca2+ removed by citrate and brain thromboplastin is added to substitute for tissue factor.

Clotting normally takes 12-15 seconds and the test time is compared with a standard normal control in a ratio.

43
Q

5.25 What is the point of the International Normalized Ratio (INR)?

A

Standardizes results between the different batches and manufacturers of tissue factor (as it is a biologically obtained factor).

Clinically, it monitors the effectiveness of drugs such as warfarin (Coumadin). Ideal INR for basic “blood-thinning” needs is 2.0 to 3.0 Patients with a high risk of clot formation need an INR of 2.5 to 3.5

44
Q
  1. 27 Activated Partial Thromboplastin Time (APTT)
    - Used to assess which pathway?
    - Procedure of the test?
A

Used to assess intrinsic pathway

Calcium is added to plasma to replace the Ca2+ removed by citrate and then kaolin and phospholipids are added to substitute for contact factor.

Clotting normally takes 25-36 seconds

45
Q
  1. 27 Activated Partial Thromboplastin Time (APTT)

- Clinically, this test is used to monitor what?

A

Clinically, APTT is most often used to monitor Heparin therapy. Therapeutic levels of UFH will typically prolong the aPTT to 2-2.5 times that of the normal value.

46
Q
  1. 28 Thrombin Clotting Time (TT)
    - Used to assess which pathway?
    - Procedure?
A

Used to assess the common pathway

Calcium is added to plasma to replace that removed by citrate and then thrombin is added to substitute for the products of the intrinsic and extrinsic pathways. This will assess the conversion of fibrinogen to fibrin.

47
Q
  1. 28 Thrombin Clotting Time (TT)

- Clinically, this test is used in what situations?

A

Clinically, TT is used when a Prothrombin Time (PT) and/or APTT is prolonged, particularly if abnormal fibrinogen level or function is considered

48
Q
  1. 28 Coagulation factor assays

- Used to determine what?

A

Used to determine actual deficiencies of specific clotting factors

49
Q

5.29 What are three examples of inherited clotting factor disorders?

A
  1. Hemophilia A (Factor VIII deficiency)
  2. Hemophilia B (Christmas disease)
  3. Von Willebrand’s Disease (vWD)
50
Q
  1. 29 Hemophilia A
    - What kind of genetic disorder?
    - What is the mutation?
    - How are APTT and PT results?
A

X-linked disorder (males normally)

Mutations in factor VIII gene - Factor VIII deficiency

Prolonged APTT (intrinsic); normal PT (extrinsic)

51
Q
  1. 30 Hemophilia B
    - What kind of genetic disorder?
    - What is the mutation?
    - How are APTT and PT results?
A

X-linked disorder (males normally)

Mutations in factor IX - Christmas disease

Prolonged APTT (intrinsic); normal PT (extrinsic)

52
Q
  1. 31 What is hemophilia?

- Increased risk of what?

A

Hemophilia leads to an increased risk of prolonged bleeding from common injuries or, in serious cases, bleeds may be spontaneous and without obvious cause - from abrasions or shallow abrasions

53
Q

5.31 What are four of the most serious sites of bleeding?

A
  1. Joint capsules (knees, elbows, hips)
  2. Skeletal muscles
  3. GI tract (food passing through GI)
  4. Brain
54
Q
  1. 32 Though not life threatening, which site is the most serious of hemophilia symptoms?
    - What is the mechanism of the permanent damage caused at this site?
A

Joint bleeds are the most serious symptoms of hemophilia.

Repeated bleeds in a joint capsule can cause permanent joint damage and disfigurement (chronic arthritis and disability).

Joint damage results from the repair, not the bleeding, as bone is damaged by enzymes.

55
Q

5.32 What is treatment for patients with low factor levels and who experience repeated and painful bleeds into their joints and skeletal muscles?

A

IV factor replacement

Apart from “routine” supplementation, extra factor replacement is also given around surgical procedure sand after trauma

56
Q

5.34 What is the most common inherited bleeding disorder?

A

Von Willebrand’s Disease (vWD) - affecting 125/million - leads to a mild bleeding disorder affecting males and females equally

57
Q
  1. 34 What are the two major roles of Von Willebrand Factor?

- Where is bleeding typically seen in Von Willebrand’s Disease?

A
  1. Mediating platelet adhesion
  2. Stabilizing factor VIII

Bleeding typically seen in skin and mucous membranes due to high capillary density - these tissues depend on the efficient formation of platelet plugs to stop bleeding

58
Q
  1. 34 Von willebrand Disease
    - APTT how?
    - Factor VIII clotting affected how?
    - PT affected how?
A

APTT prolonged

Factor VIII has reduced clotting activity

PT prolonged because of a failure in platelet-vessel wall interaction

59
Q

5.35 What are the causes of Thrombocytopenia?

A
  1. Impaired production of platelets
    - Drug induced
    - Bone marrow failure
  2. Increased destruction of platelets
    - Idiopathic thrombocytopenic purpura (ITP) - autoimmune response to platelets, which are removed prematurely by the reticuloendothelial system
60
Q
  1. 36 What are thrombophilias?

- What kind of “state” is the coagulation system swung towards?

A

Thrombophilias are conditions associated with excessive clotting

A defect or defiency in one of the natural anticoagulants will swing the balance of the coagulation system towards a hypercoagulable state and potential venous thromboembolism (VTE).

61
Q

5.36 What are four examples of inherited thrombophilias?

A

From most common to least common:

  1. Activated Protein C resistance
  2. Protein C deficiency
  3. Protein S deficiency
    - Both deficiencies inactivate Factor V and VIII
  4. Antithrombin III deficiency
62
Q

5.36 Explain the mechanism of Activated Protein C resistance

A

Not a protein C deficiency, but instead a poor response by Factor V to protein C

Major cause is a mutation in the Factor V gene (Factor V Leiden)

5% of caucasians have Factor V Leiden)

Hematology Exam 2 (4 decks)

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