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Pathology 2 > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

hemostasis

A

stopping blood loss in response to vascular injury

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2
Q

What is the stages of hemostasis (be straightforward)

A

vascular constriction –> formation of platelet plug –> formation of blood clot –> fibrous organization

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3
Q

When does the formation of the platelet plug occur

A

primary homeostasis

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4
Q

Describe the formation of the platelet plug

A

platelet aggregation –> vWF connects platelets to endothelium –> exposed collagen allows more aggregation –> fibrinogen connects the platelets together = platelet plug

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5
Q

What occurs during secondary homeostasis

A

formation of the blood clot

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6
Q

describe the formation of the blood clot

A

coagulation cascade = fibrinogen –> fibrin

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7
Q

what occurs during fibrous organization

A

involves fibrinolysis in which the clot is broken up by proteins in the plasma

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8
Q

Petechiae

A

small (1 to 2 mm), round, red or brown lesions resulting from hemorrhage into the skin and are present primarily in areas with high venous pressure, such as the lower extremities

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9
Q

Purpura

A

Extravasation of red blood from cutaneous vessels into skin or mucous ; membranes results in reddish-purple lesions ; NO blanching

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10
Q

Vasculitis

Commonly seen in?

A

inflammation of and damage to blood vessels; most commonly has an infectious or immune-mediated cause.

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11
Q

Hematoma

A

Hemorrhage within a closed space

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12
Q

Ecchymosis

A

bruise; the most common form of hemorrhage in the skin; blanch with pressure

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13
Q

Thrombosis

A

hemostasis in the wrong place; end result is vessel occlusion and tissue ischemia

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14
Q

Embolism/thromboembolism

A

a substance that forms within or enters the vascular system at one site and is carried through the blood stream to another area of the body, where it lodges in a blood vessel and produces its effects (usually infarcts)

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15
Q

Infarction

A

irreversible ischemic or hypoxic damage to cells/tissues resulting in necrosis of the cells/tissue

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16
Q

Physical characteristics of platelets

A

1) form from hematopoietic tissue
2) not a cell; lack a nucleus
3) metabolically active
4) 2-3µM Diameter, 6-8fL
5) Life span= 7-10 days

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17
Q

Chemical Characteristics + Role in clotting

A

Plugs up injury sites by binding to collagen to stop bleeding: releases adhesive glycoprotein and ADP to increase aggregation and size of plug
platelets, damaged blood vessels and plasma promote cascade of 13 plasma proteins to give rise to fibrin to trap RBC, leukocytes and platelets to make blood clot (thrombus)

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18
Q

Describe the general mechanisms of blood coagulation

A

1) conversion of prothrombin to thrombin
2) conversion of fibrinogen to fibrin
3) development of a blood clot = fibrin threads mix in
4) clot retraction
5) lysis of blood clots= plasminogen –> plasmin (fibrinolysin). Fibrinolysin lyses fibrin and helps remove the clot.

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19
Q

what leads to activation of prothrombin to thrombin?

A

Factor Xa

20
Q

What are the common pathways used in the intitation of clotting?

A

Extrinsic, Intrinsic and Common

21
Q

Explain the Extrinsic Pathway

A

Extrinsic Pathway (tested by prothrombin time (PT): Injury to a tissue -> release of tissue factor -> activates factor VII ­– activates factor X

22
Q

Explain the Intrinsic Pathway

A

Intrinsic Pathway (tested by partial thromboplastin time (PTT): Factor XII -> activated factors XI then IX and then VIII (VIIIa) combine to activate factor X

23
Q

Explain the Common Pathway

A 
Common Pathway (both extrinsic and intrinsic)= regulated by antithrombin III (which inactivates excess thrombin) 
Factor X ­-> II (prothrombin) -> Thrombin -> I (Fibrinogen) -> Fibrin (which makes a clot and removes excess thrombin regulating the cycle so the clot doesn’t get to big)
24
Q

role of Vitamin K in the formation of blood clotting factors

A

Vitamin K activates clotting factors II (prothombin), VII, IX, X, C, S. –> Warfarin is an anticoagulant (prevents blood clots)

25
Q

hemophilia

A
  • blood does not clot normally
  • an X-linked recessive disorder of factor VIII deficiency or inactivity.
  • bruise easily and hemorrhage at points of trauma, most notably in the joints (referred to as hemarthrosis).

Physiology: VIII is deficient and we know factor VIII is part of the intrinsic pathway, PTT is therefore prolonged. The PT and bleeding time, however, will be normal because the extrinsic pathway is still intact and the platelets are still functional.

26
Q

deep vein thrombosis

A

-occlusion of the venous system (LE)
Causes: blood stasis (most common), hypercoagulability and endothelial damage.
-95% of all PE’s (pulmonary emboli) derive from deep leg vein thrombosis
-increased with pregnancy, cardiac failure, prolonged bed rest, ortho surgery.
-Thombosis accompanied by inflammation is called thrombophlebitis.

27
Q

thrombocytopenia

A
  • decreased number of platelets NOt an abnormality in function
  • AIDS, SLE and viral infections, heparin use.
28
Q

pulmonary embolism

A

blood clot that has traveled to the lungs.

-are derived from DVT’s.

29
Q

disseminated intravascular coagulation

A
  • primarily involves thrombus formation due to activation of the coagulation cascade.
  • occurs secondary to another disease.
  • if all the clotting factors are used up, excessive bleeding could occur
30
Q

Bleeding time test

A

A small cut is place don the patient’s forearm, with a BP cuff kept on the arm at 40mm Hg to resist venous flow. Normal bleeding time may be 2-7 minutes. If the bleeding time is prolonged, this usually suggests a defect in platelet function.

31
Q

Platelet count (Normal Range)

A

Normal range: 150,000-400,000

32
Q

Partial thromboplastin time (PTT)

A

intrinsic and common pathways ; prolonged PTT= defect in INTRINSIC

33
Q

prothrombin time (PT)

A

defect in EXTRINSIC: extrinsic and common pathways: prothrombin –> thrombin –> fibrinogen –> fibrin

34
Q

D-dimer

A

the degradation product of crosslinked fibrin. It reflects the ongoing activation of the hemostatic system

helps rule out DVT, evaluate thrombus formation, monitor tx

elevated: pregnancy, postop, trauma, inflammation, liver dz, heart dz

35
Q

platelet function test

A

assessed using platelet aggregometry

36
Q

The normal prothrombin time is about

A

12 sec

37
Q

The reference range of the PTT is

A

60-70 sec

38
Q

What was devised to standardize measurements of prothrombin time?

A

international normalized ratio (INR)

39
Q

INR

A

a ratio that relates a person’s prothrombin time compared to a normal control sample

40
Q

normal range INR for a health person is

A

0.9-1.3

41
Q

What does a low INR mean? High INR?

A

high INR (4 or 5) –> high PT (longer time=Extrinsic defect) a high risk of bleeding

low INR (e.g., 0.5) –> that there is a chance of having a clot

42
Q

Describe the antithrombotic mechanisms which prevent excessive thrombosis

A

1) Fibrin
2) anti-thrombin III
3) heparin
4) plasminogen

43
Q

How does fibrin help prevent excessive thrombosis?

A

Fibrin in the clot absorbs excess thrombin

44
Q

How does anti-thrombin III help prevent excessive thrombosis?

A

Anti-thrombin III (present in the clot area) inactivates excess thrombin

45
Q

How does heparin help prevent excessive thrombosis?

A

Heparin (a powerful anticoagulant made by mast cells and basophils) enhances the activity of anti-thrombin III (which inactivates excess thrombin)

46
Q

How does plasminogen help prevent excessive thrombosis?

A

Plasminogen –>plasmin. Plasmin lyses fibrin and helps remove the clot. The process of plasminogen activation occurs at least a day after the clot has formed to allow time for the initiation of wound healing. It is activated by tissue plasminogen activator, which is released by the damaged tissue.

47
Q

conditions that predispose a patient to developing pathologic thromboses

A

Thrombophilia can be acquired or hereditary. Causes:

  • antiphospholipid antibodies (your immune system mistakenly produces antibodies against certain normal proteins in your blood)
  • thrombocytosis (high platelet counts) & myeloproliferation (excess cells are produced)
  • medications (such as oral contraceptives)
  • malignancy, orthopedic surgery, trauma or infection (microangiopathic)
  • Hereditary predispositions include anticoagulant deficiencies (Protein C, S and Antithrombin II), Factor V Leiden, Prothrombin mutation, fibrinolytic defects (rare).

Pathology 2 (6 decks)

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