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Pathological Processes > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

haemostasis

A

stopping of haemorrhage

involves vasoconstriction and platelet
plug formation as well

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2
Q

clotting

A

process whereby blood (a liquid in normal blood vessels)

becomes a solid mass when it makes contact with connective tissue.

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3
Q

three steps of haemostasis

A
  1. The severed artery contracts, not enough to stop the bleeding but enough to decrease the pressure downstream
  2. A primary haemostatic plug of activated platelets forms at the hole in the vessel sticking to the injured vessel and the connective
    tissue outside it. This is fragile but may control the bleeding. It forms in seconds to minutes.
  3. The secondary haemostatic plug forms as fibrin filaments stabilise the friable platelet plug into a blood clot. This forms in
    approximately 30 minutes.
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4
Q

what activates platelets

A

collagen
ADP
Thromboxane A2
Thrombin

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5
Q

what happens when platelets are activated

A
  1. Stick to the exposed subendothelium (basement membrane or
    collagen) specifically to von Willebrand factor which is
    concentrated on the subendothelial basement membrane.
  2. Aggregate with other platelets. This is how the platelet plug, and
    then the secondary haemostatic plug, grows. Fibrinogen binds to
    the platelets and sticks them together.
  3. Swell and change shape into sticky, spiny spheres.
  4. Secrete factors from platelet granules that help the platelet plug
    to grow and aid clotting, e.g., some fibrinogen, ADP,
    thromboxane A2.
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6
Q

how does aspirin work

A

aspirin irreversibly inactivates cyclooxygenase, one of the
enzymes responsible for the production of thromboxane A2. In this way
it decreases platelet aggregation.

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7
Q

intrinsic pathway

A

involves factors, all of
which are contained within the blood. It is triggered by a
negatively charged surface (e.g., the subendothelium or glass (it
was first described by scientists experimenting with blood in glass
test tubes) and no vessel needs to be broken open for it to occur.

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8
Q

extrinsic pathway

A

– so called because it needs a ‘tissue factor’
(thromboplastin, formerly called clotting factor III) which is
present outside of the blood. This pathway is triggered by
thromboplastin released from damaged cells adjacent to the area
of haemorrhage

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9
Q

factors that oppose clotting

A

dilution of clotting factors

natural anticoagulants- oppose the formation of fibrin- fibrinolysis

fibrin degradation products inhibit clotting

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10
Q

what is clot retraction

A

Platelets in the clot die. As they do so they cling to the fibrin and pull by
their actin-myosin filaments in a mechanism which is basically the same
as muscle contraction.

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11
Q

what are platelets

A

Disc shaped, anucleate cell fragments
• Megakaryocytes produce platelets in the
bone marrow

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12
Q

platelet adhesion

A 
• Initiating stimulus – damage to the vessel
wall
• Exposure of the underlying tissues
• vWF (critical role)
• Platelets adhere to collagen via
vWF/receptor
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13
Q

platelet activation/ secretion

A
  • ‘Release reaction’
  • Platelets contain granules
  • Alpha-granules
  • Dense granules
  • Platelets secrete these granules soon after adhesion
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14
Q

platelet aggregation

A
  • Cross linking of platelets to form a platelet plug.
  • Provides stability

platelet contraction

  • dependent on platelet cytoskeleton
  • creates an irreversibly fused mass of platelets
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15
Q

APTT anticoagulation tests

A
  • Intrinsic pathway
  • If prolonged suggests a deficiency in one of the factors
  • Factor VIII, IX, XI or XII deficiency
  • VIII (haemophilia A) and IX (haemophilia B)
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16
Q

PT

A

prothrombin time

extrinsic pathway
most commonly due to factor VII deficiency

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17
Q

TCT

A

thrombin clotting time

-measure of the final step of the pathway, the conversion of fibrinogen to fibrin via the action of thrombin

18
Q

how does tissue factor pathway inhibitor oppose clot formation

A

• Acts in the initiation phase of clotting
• Secreted mainly by endothelial cells
• Binds to tissue factor-factor VIIa complexes and inhibits the ability of these
complexes to generate factor Xa

19
Q

how does thrombin oppose clot formation

A

Binds to an endothelial cell receptor called thrombomodulin
• Eliminates thrombin’s clot producing effects and causes the bound thrombin
to bind Protein C and Protein S (plasma protein)
• Then inactivates Factors VIIIa and Va

20
Q

how does antithrombin III oppose clot formation

A

• Plasma protein that inactivates thrombin and several other clotting factors
• Activated by heparin on the surface of endothelial cells
• Prevents the spread of a clot by rapidly inactivating clotting factors that are
carried away from the immediate site of the clot by the flowing blood

21
Q

thrombocytopenia

A

Deficiency of platelets in the blood resulting in bleeding into the
tissues, bruising and slow blood clotting after injury

22
Q

fibrinolytic cascade

A

plasminogen activator causes plasminogen to be converted into into plasmin

fibrin breaks the clot and released d dimers

23
Q

how do clinical disorders of platelets present

A

purpura, petechiae, mucosal bleeding, epistaxis,

menorrhagia- heavy menstrual bleeding

24
Q

what causes decreased production of platelets

A
  • marrow aplasia or infiltration
  • megaoplastic anaemia
  • sepsis, systemic viral or bacterial infection
25
Q

what causes increased consumption of platelets

A

immune

  • Immune thrombocytopenic purpura
  • Thrombotic thrombocytopenic purpura
  • Post-transfusion purpura
  • Heparin-induced thrombocytopenia

non-immune

  • Disseminated intravascular coagulation (DIC)
  • Haemolytic uraemic syndrome
  • Hypersplenism
26
Q

immune thrombocytopenic purpura

A

• Isolated low platelet count with a normal bone marrow in the absence of
other causes of low platelets

27
Q

thrombotic thrombocytopenic purpura

A

• Blood disorder that results in blood clots forming in small vessel throughout
the body, resulting in consumption of platelets and red blood cells due to
their breakdown.

28
Q

haemolytic-uraemic syndrome

A

• Low RBCs, acute kidney injury and low platelets
• Bloody diarrhoea, fever, vomiting and weakness leading to kidney failure and low
platelets

29
Q

hypersplenism

A
  • Enlargement of the spleen
  • Reduction in the number of circulating blood cells
  • Compensatory proliferative response in the bone marrow
  • Potential for correction with splenectomy
30
Q

Von Willerbrand’s disease signs and symptoms

A
  • Spontaneous bleeding from mucous membranes (nosebleeds)
  • Excessive bleeding from wounds
  • Menorrhagia
  • Prolonged bleeding time in the presence of a normal platelet count
31
Q

whats the difference between the types of von willerbrand disease

A

• Type 1 and Type 3 associated with reduced quantity of circulating
vWF
• Type 2 – qualitative defects in vWF

32
Q

haemophilla A

A

FVIII deficiency
most common hereditary disorer associated with life threatening bleeding

easy bruising

prolonged APTT normal PT

33
Q

inhertance pattern of haemophilia A

A

x linked recessive

34
Q

haemophillia B

A

severe F9 deficiency

X linked recessive
prolonged APTT and normal PT

35
Q

treating Haemophillia

A

infusions with the factor absent

36
Q

disseminated intravascular coagulation

A

• Acute, subacute or chronic thrombohaemorrhagic disorder
characterised by excessive activation of coagulation which leads to
the formation of microthrombi in the microvasculature of the body.

37
Q

consequence of DIC

A

consumption of platelets, fibrin and

coagulation factors and secondarily activation of fibrinolysis

38
Q

signs and symptoms of DIC

A

tissue hypoxia and infarction

caused by the microthrombi

39
Q

causes of DIC

A
  • Sepsis
  • Surgery
  • Major Trauma
  • Cancer
  • Pregnancy Complications e.g. pre-eclampsia, amniotic fluid embolism, PPH)
  • Burns
  • Rhabdomyolysis
  • Snakebites (toxic reaction)
  • Frostbite
40
Q

congenital causes of vessel wall abnormalites

A

Hereditary Haemorrhagic Telangiectasia (HHT)

• Connective tissue disorders e.g. Ehlers Danlos syndrome

41
Q

acquired causes of vessel wall abnormalities

A
  • Senile purpura
  • Steroids
  • Infections e.g. measles, meningococcal infection
  • Scurvy – Vit C deficiency causes defective collagen production
42
Q

what is Virchow’s triad

A

endothelial damage
haemostasis
blood hypercoagulation

Pathological Processes (10 decks)

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