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HMS301 Blood & Neoplasia > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

Define Hemostasis

A

the process of blood clot formation at the site of vessel injury.

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2
Q

Hemostasis is a complex process & depends on interactions between the?

A
  • vessel wall
  • platelets
  • coagulation & fibrinolytic mechanisms
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3
Q

Antithrombic factors

A
  • thrombomodulin
  • heparin sulphate
  • prostacyclin
  • nitric oxide
  • plasminogen activator
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4
Q

Platelets
1) Exposure
2) Platelet adhesion

A

intimal injury & exposure of subendothelial elements leads to platelet adherence via platelet membrane receptor glycoprotein Ib (GpIb), to collagen & vWF in the subendothelial matrix.

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5
Q

Platelets

A
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6
Q

4 stages of Hemostasis

A

1) constriction of the blood vessel
2) formation of a temporary platelet plug
3) activation of the coagulation cascade
4) formation of fibrin plug or final clot

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7
Q

Vaso-constriction

A
  • injury to vessels leads to immediate vasoconstriction = reducing blood flow to the injured area & endothelial damage results in loss of antithrombotic properties = leading to extracellular matrix/collagen exposure to the blood components.
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8
Q

Platelet Adhesion

A
  • ECM releases cytokines & inflammatory markers that lead to adhesion of the platelets & their aggregation at that site = which leads to the formation of a platelet plug & sealing of the defect.
  • The platelet adhesion is a complex process mediated by interactions between various receptors and proteins including tyrosine kinase receptors, glycoprotein receptors, other G-protein receptors as well as the von Willebrand Factor (vWF) (functions via binding to the Gp 1b-9 within the platelets).
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9
Q

Platelet Activation

A

The platelets that have adhered undergo very specific changes:
= they release their cytoplasmic granules that include ADP, thromboxane A2, serotonin, & multiple other activation factors.
= they also undergo a transformation of their shape into a pseudopodal shape which in-turn leads to release reactions of various chemokines. P2Y1 receptors help in the conformational changes in platelets.

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10
Q

Platelet Aggregation

A
  • various platelets are activated, adhered to each other & the damaged endothelial surface leading to the formation of a primary platelet plug.
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11
Q

Coagulation

A
  • involves a series of enzymatic reactions leading to the conversion of soluble plasma fibrinogen to fibrin clot.
  • initiated by tissue damage
  • local generation of fibrin enmeshes & reinforces the platelet plug.
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12
Q

Extrinsic Pathway

A
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13
Q

Intrinsic Pathway

A
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14
Q

Fibrin Clot Formation

A
  • conversion of fibrinogen to fibrin monomers which polymerizes & forms fibrin polymer mesh and result in a cross-linked fibrin clot.
  • this reaction is catalyzed by activated factor XIII (factor XIIIa) that stimulates the lysine and the glutamic acid side chains causing cross-linking of the fibrin molecules and formation of a stabilized clot.
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15
Q

Clot Resolution (Tertiary Hemostasis)

A
  • activated platelets contract their internal actin and myosin fibrils in their cytoskeleton, which leads to shrinkage of the clot volume.
  • plasminogen then activates to plasmin, which promotes lysis of the fibrin clot; this restores the flow of blood in the damaged/obstructed blood vessels.
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16
Q

Physiological limitation of coagulation

A
  • could lead to dangerous occlusion of blood vessels if it’s not limited to the site of injury by protective mechanisms.
  • activity is increased by Heparin.
  • antithrombin binds to & forms complexes with coagulation factors thereby inactivating them.
  • activated protein C inactivates factors V & VIII = enhanced by the cofactor protein S.
  • venous thromboembolism = inherited deficiencies of natural anticoagulant proteins places patient at increased risk of venous thromboembolism.
17
Q

Deficiency of
- platelet membrane receptor glycoprotein 1b (Gp1b)
or
- vWF
leads to congenital bleeding disorders…

A
  • Bernard–Soulier disease
  • von Willebrand’s disease
18
Q

Aneurysms

A
  • occurs when a weak blood vessel begins to swell or blow up like a balloon.
  • most dangerous cases = aneurysm can burst, causing blood to spill on the surface of the brain.
  • ruptured brain aneurysm = most common & most deadly vascular brain abnormality, with a 50% fatality rate.
19
Q

Arteriovenous Malformation (AVM)

A
  • believed to a congenital condition.
  • happens when tangle of blood vessels either irritates another part of the brain, causing a stroke, or ruptures and causes bleeding within the brain.
  • AVM patient can continue to re-bleed over time & develop serious neurological problems.
20
Q

Difference between Arteriovenous Malformation (AVM) & Cavernous Malformation

A
  • AVM holds blood flowing at high pressure.
  • AVM described as a tangle but CVM described as small balls of blood vessels.
21
Q

Cavernous Malformation

A
  • small ball of blood vessels that carries low BP blood.
  • least lethal
  • can lead to seizures, brain bleeds & serious neurological deficits.
22
Q

Symptoms of vascular abnormalities

A
  • most patients are asymptomatic until a rupture occurs.
  • minor symptoms = difficulty seeing, enlarged pupils.
  • Aneurysm = moment of rupture = worst headache of a lifetime.
23
Q

Risk factors for vascular abnormalities

A
  • Family history
  • High BP = puts extra strain on blood vessel walls.
  • Medical history
  • Sex = women
  • Smoking
24
Q

Treatment options for vascular abnormalities

A
  • Craniotomy (removing a section of the skull) = to stop the bleeding before damage is done.
  • Endovascular surgery = allows the surgeon can make an incision in a patient’s leg andsnake a very narrow catheter up through the blood vessels to the brain = when the catheter reaches the brain, the surgeon can then fill the aneurysm with ametallic thread called coils, which prevent blood from getting into the aneurysm & protect the patient from another rupture.
25
Q

Define Thrombocytopenia

A
  • defined as = platelet count below the lower limit of the reference range.
26
Q

Thrombocytopenia severity can be further subdivided by platelet count:

A
  • Mild = 100,000 to 149,000/microL
  • Moderate = 50,000 to 99,000/microL
  • Severe = <50,000/microL
27
Q

True or False

Correlation between platelet count & bleeding risk is relatively weak

A

True

28
Q

Give an example to explain how the correlation between platelet count & bleeding risk is relatively weak

A
  • surgical bleeding is generally not a concern with platelet counts >50,000 micro/L = some procedures may be safely performed at lower platelet counts e.g. cataract surgery, bone marrow aspiration.
29
Q

Explain this comment:
Bleeding risk in Immune thrombocytopenia may be slightly lower compared with other conditions for the same platelet count.

A

We are less concerned about bleeding in an individual with Immune thrombocytopenia and a platelet count of 30,000 micro/L than we are about bleeding in an individual with aplastic anemia and a platelet count of 30,000 micro/L.

30
Q

Heparin-induced thrombocytopenia (HIT)

A
  • an uncommon complication of heparin exposure in which antibodies to a platelet factor 4 epitope induced by heparin can cause thrombocytopenia & platelet activation, leading to life-threatening venous &/or arterial thrombosis.
  • should be considered in a patient recently exposed to heparin who develops thrombocytopenia, thrombosis, anaphylaxis, or skin reactions.
  • treatment involves immediate discontinuation of heparin & administration of a non-heparin anticoagulant.
31
Q

Vaccine-induced immune thrombotic thrombocytopenia (VITT)

A
  • rare syndrome that occurs after vaccination with a coronavirus disease 2019 adenoviral vector vaccine.
  • resemble spontaneous Heparin-induced thrombocytopenia.
32
Q

Paroxysmal nocturnal hemoglobinuria (PNH)

A
  • rare condition caused by loss of glycosylphosphatidylinositol from cell membranes.
  • thrombosis often involves unusual locations such as intraabdominal or cerebral veins.

HMS301 Blood & Neoplasia (8 decks)

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