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Haemostasis Flashcards

1
Q

What is haemostasis?

A

The stopping of blood flow

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2
Q

List the 3 mechanisms that the immediate arrest of a haemorrhage depends on

A
  1. Vasoconstriction
  2. Adhesion
  3. Aggregation
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3
Q

What is the quantitative platelet disorder that causes primary haemostasis?

A

Thrombocytopenia

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4
Q

What is the qualitative cause of platelet disorders that cause primary haemostasis?

A

Functional defect that is either inherited or acquired

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5
Q

What are some acquired causes of primary haemostasis?

A

Drugs
Alcohol
Uremia
Myeloproloferative disorders

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6
Q

What is a normal platelet count?

A

150-350 x10^9/L

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7
Q

What is thrombocytopenia?

A

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

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8
Q

How is thrombocytopenia diagnosed?

A

By carrying out a full blood count, followed by a blood film, and a platelet sample

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9
Q

List 3 of the possible causes of thrombocytopenia

A
  1. Exposure to drugs
  2. Viral infections i.e HIV
  3. Autoimmune diseases that result in a low blood count
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10
Q

What is ITP?

A

Immune thrombocytopenic purpura

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11
Q

How does ITP present clincally?

A

Has an incidence rate of 2.5/100, 000, 4.5/100, 000 in those over 60
Petechnial rash or bleeding

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12
Q

Explain thrombotic microangiopathies

A

A group of disorders involving small blood clots (thrombi) in the microcirculation, leading to hemolytic anemia, thrombocytopenia, and organ damage

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13
Q

List the conditions included in thrombotic mircoangiopathies

A

Thrombotic Thrombocytopenic Purpur (TTP)
Hemolytic Uremic syndrome (HUS)
Haemolytic anaemia with elevated liver enzymes and low platelet count (HELLP)

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14
Q

How is TTP treated?

A

Thrombotic thrombocytopenic purpur is treated by plasma exchange

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15
Q

How is HUS treated?

A

Hemolytic Uremic syndrome is treated with withdrawal of drugs due to condition usually being due to heperin (blood thinner)

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16
Q

How is HELLP treated?

A

Haemolytic aneamia wiht elevated liver enzymes and low platelet count is treated through the delivery of fetus and placenta, and is usually self-resolved after this

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17
Q

How is HIT treated?

A

Heparin-Induced Thrombocytopenia is treated by stoppping heparin and the administration of anti thrombotic agents to a patient

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18
Q

What is Bernard Soulier GP 1b-IX-V?

A

A rare inherited bleeding disorder caused by a defect in platelets, the cells involved in blood clotting.
The condition primarily affects the ability of platelets to adhere to blood vessel walls, leading to prolonged bleeding or difficulty in forming blood clots.

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19
Q

What is Glanzmann thrombasthenia?

A

A rare bleeding disorder caused by a defect in platelet function due to a deficiency in glycoprotein IIb/IIIa, which is needed for platelet aggregation.
Platelets fail to bind to fibrinogen

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20
Q

Which 2 thrombotic mircoangiopathies is a platelet tranfusion harmful for and why?

A

TTP and HIT
In both conditions, the underlying problem involves abnormal platelet activation and clot formation, which could be worsened by giving additional platelets.

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21
Q

Summarise primary haemostasis

A

-Results in the formation of the platelet plug
- Doesn’t involve the coagulation pathways
- Includes disorders of platelet numbers, size and functionality

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22
Q

Define secondary haemostasis

A

The process that stabilises a blood clot by forming a fibrin mesh, reinforcing the initial platelet plug.
Ensures the clot is stable and effective in stopping bleeding, allowing tissue healing

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23
Q

List the key steps in secondary haemostasis

A
  1. Coagulation Cascade: Activation of coagulation factors through intrinsic, extrinsic, and common pathways.
  2. Thrombin Generation: Factor X is activated to Xa, converting prothrombin to thrombin.
  3. Fibrin Formation: Thrombin converts fibrinogen to fibrin, forming a mesh.
  4. Clot Stabilization: Factor XIII cross-links fibrin, strengthening the clot.
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24
Q

Summarise the extrinsic pathway

A

The main pathway for initiation of coagulation
Exposure to TF binds to factor VII, which activates factor X
The promthrombinase complex (FX, FV, Ca and plt phospholipid activates prothrombin to thrombin) which then activates the intrinsic FXI- leading to the intrinsic pathway

25
Summarise the intrinsic pathway
Amplifies the coagulation cascade The tenase complex amplifies activation of FX, generating large amounts of thrombin Thrombin cleaves fibrinogen to form soluble fibrin monomers which poloymerise to form solubles fibrin polymers Thrombin activates FXIII which cross links with Ca and stabilises the fibrin polymer forming an insoluble fibrin
26
What makes up the tenase complex?
Factor IXa, FVII, Ca and a phospholipid
27
Explain the process of positive feedback, in terms of blood clotting
Thrombin activates FXI on the platelet surface which activates FIX to enhance FXa generation High levels of thrombin can cleave PAR4- plt shape change (stabilisation of the platelet plug) High levels of thrombin generated at propagation phase bind to fibrin and are protected from inhibition by antithrombin
28
Summarise the process of localisation
-Thrombin is released form the platelet plug is rapidly inactivated by antithrombin -FXa is quickly inhibited by TFPI -Thrombin binds to thrombomodulin, which changes it's activity to no longer cleave fibrinogen -Process is further controlled by protein C inhibitor, allowing thrombomodulin to activate protein C
29
What does activated protein C do?
Along with protein S, they inactivate FVa and FVIIIa This limits thrombin generation to the injury site and prevents clotting on healthy endothelium
30
What do deficiencies in protein C and S result in?
Prevention of cleavage and inactivation of FV Allows for the spread of thrombin into the vascualte and is associated with venous thrombisis
31
What is fibrinolysis?
The breakdown of a blood clot when an injury has healed
32
What is the central enzyme to fibrinolysis?
Plasminogen
33
Give the 2 fibrinolysis defects
Hyperfibrinolysis- clotting too quick, disposes to bleeding and throbosis. Plasmin inhibitor and plasminogen inhibitor 1 prevents this Hyperfibrinolysis- deficiencies of t-PA or u-PA, plasminogen, contact factors. Associated with thromboembolic disease
34
Explain the 4 steps of cell based coagulation
1. Initiation- occurs on the surface of a tissue factor presenting cell 2. Amplification- platelets are activated and release cytokines. Coagulation factors are attracted to the platelet surface 3. Propagation- thrombin is produced in large amounts on activated platelet surface 4. Fibrin formation- stable clot formed 5. Termination- natural anticoagulants
35
What does a factor 8 deficiency result in?
Haemophillia A- X-linked disease effects 1 in 10,000 people Results in spontaneous/ prolonged bleeding and easy bruising
36
How is Haemophillia A treated?
Factor VIII Replacement Therapy: Infusions of Factor VIII to treat or prevent bleeding episodes. Prophylactic: Regular infusions to prevent bleeding, especially in severe cases.
37
What is Haemophillia B caused by?
A Factor IX deficiency
38
What doews a combined FV and FVIII deficiency result in?
a rare autosomal recessive bleeding disorder found around the Mediterranean sea
39
What does a Factor X disorder result in?
An inherited- autosomal recessive disease More common than others as it is an acquired disorder presents as easy bruising, bleeding gums, nosebleeds and prolonged injury after trauma
40
Which factor deficiency results in Haemophilia C?
Factor XI There are 3 mutations that cause this: 1. Type II- stop codon in exon 5 2. Type III- Phe283 is replaced with Leu 3. Type II/III- heterozygotes
41
How is a FXI deficiency treated?
FFP or FXI concentrate (half life 52hrs)
42
Explain the results of a Factor XII deficiency
A rare autosomal recessive bleeding disorder, where blood clots are unstable Homozygotes present with life long bleeding from the umbilical cord
43
What is APTT?
Activated Partial Thromboplastin Time
44
What effect does liver disease have on coagulation factors?
Decrease of extrinsic factors synthesised in the liver, meaning the prothrombin time increases APTT and fibrinogen synthesis also affected
45
What are the effects of Vitamin K deficiency?
Factors 2, 7, 9 and 10 (all depednet of VitK) are affected, whic hcauses an increase in the prothrombin time
46
List the advantages of automation
Reduces human error CTS reduces health and safety risks Large volume of work can be carried out Reduction in assay time
47
What is Prothrombin time (PT)?
A measure of the efficiency of the EXTRINSIC clotting system (FVII, FV, FX, prothrombin and fibrinogen)
48
What is APTT sensitive to?
Heparin Factors: VIII, IX, XI, XII Lupus anticoagulant Liver disease Vit K
49
What is Clauss fibrinogen?
Based on the addition of an excess of thrombin to platelet poor plasma Fibrinogen concentration becomes the rate-limiting factor and the clotting time is a function of the fibrinogen concentration. Not affected by heparin Can be affected by degradation products
50
List 3 further tests that can be done after abnormal coagulation results have been found
Thrombin time (TT) Reptilase time (RT) Factor assays
51
How do factor assays work?
Patients plasma is mixed with factor deficient plasma and the appropriate test repeated The time taken to clot can be read from the graph to determine patient factor level
52
What levels of Factor VIII would a patient with severe Haemophillia present with?
Between 50-150%
53
What is anticoagulant therapy?
When agents are given to inhibit platelet function
54
What does Warfarin do?
Inhibits the vitamin K-dependent posttranslational modification of coagulation factors
55
What is INR?
International Normalised Ratio Monitored using the PT test and calculated according to: INR=PR^ISI
56
What does Heparin do?
Complexes with Anti-Thrombin III to inhibit thrombin and increase the clotting time ATIII complexed to heparin is 1000- fold moore efficient at binding thrombin due to a conformational change indiced by heparin revealing a crucial ariginline residue
57
List 3 direct oral anticoagulants
Thrombin inhibitor Xa inhibitors Rivaroxban (7-11 hrs)
58

AP0509 (4 decks)

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