Lecture - Blood (Haemostasis #2 Coag Tests)

Question 1

So that Y shaped diagram for the blood coagulation is kinda made for the tests. The tests that I want you to explain are APTT, PT, and TCT.

1. What do you need to do to the blood first in order to carry out these tests on it?
2. APTT:
   - explain which pathway you use this for and what factors are involved
   - what are the two stages about?
   - what is the end point?
   - what test is this useful for?
3. PT:
   - explain which pathway this is used for and what factors
   - is it physiological?
   - how do you use APTT with this to find out what the problem is (e.g. if one if prolonged and other isn’t etc)
4. TCT:
   - what do you add to the plasma to cause fibrinogen to clot quickly?
   - what are you screening for?

Answer 1

1. Proteins shouldn’t be activated, Ca cheated with citrate, platelets removed in APTT, blood needs to be fresh for all tests

Question 2

In the table for the four tests, what factors are clinically important that they detect and what deficiencies detected aren’t clinically important:

• APTT
• PT
• TCT
• Fibrinogen assay

Answer 2

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Question 3

Coagulation factor assays:

1. What are they usually performed as?
2. Activity is measured as a percentage of what? What does this mean?
3. How is fibrinogen assayed?
4. Do you just wanna recite to a wall how the coagulation factor assays work?

Answer 3

2. Percentage of biological clotting activity so like, normal would be 100% and you see how the patient performs
3. Basically, put in activaor and phospholipid with pateint plasma and plasma deficinet in the factor you want to measure

Wanna see hwo well pateint’s plasma will coreect that deficincy

Measure time it takes to clot and assess that against a standard curve

Question 4

Okay, this is like a summary really but what are the 4 causes of bleeding?

Answer 4

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Question 5

How do you assess bleeding disorders:

1. History
   - what do yo look at (4)
2. Tests
   - what 2 sets of tests and then if appropriate, what else?

Answer 5

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Question 6

Moving onto the first of the 2 bleeding disorders we’re gonna talk about: Disseminated Intravascular Coagulation (DIC)

1. What is it?
   - coagulopathy arises from what?
   - is it bad in the mild form?
   - inside what?
2. What are two possible causes?
3. Potential results for mild DIC, moderate+severe DIC?
4. Pathogenesis:
   - what can be released into blood that causes it?
   - or what else triggers it? Any cause of…..
   - some form of _____ ____ can also cause it
5. Once it starts, what does it result in? (4)
6. Fibrinolysis is ALWAYS activated in DIC - by what factor that is secreted by endothelium?
   - So fibrin is cleared from most small blood vessels but that means high levels of what?
   - Inadequate activation of fibrinolysis results in what?
7. What two things can you say about the clinical features?
8. Lab findings:
   - what happens to the fibrinogen conc? So what happens to TCT?
   - what happens to platelet count?
   - high/rising levels of what?
   - those three are the top things but what happens to the coagulation factors? So what happens to APTT and PT?
   - Protein C and Antithrombin - what happens to them?
   - what can you see in the blood film?
9. Diseases causing DIC #1
   - what one kind of organism/infection can cause DIC?
   - what does the endotoxin from it activate?
   - what does this cause to be expressed by monocytes and where?
   - does this occur in all cases of gram -ve septicaemia?
   - especially in what is very high levels of endotoxins released?
   - What are some control mechanisms? But these may be overcome by prothrombin factors and result in what becoming clinically important?
   - what three things are used up?
10. Treatment of DIC:
    - what should you treat if possible so the DIC will stop? Like, with what?
    - Secondary bleeding that is caused by DIC - what to do? So if have thrombocytopenia, low fibrinogen, what do you give? If severe cases aren’t controlled by cyroprecipitate?
    - Extremely severe case that you can’t fix with replacement, what do you do?
11. Other disorders causing DIC #2
    - any severe or widespread tissue injury can cause it so what does this include?
    - what about brain- what can cause DIC that’s related to brain?

Answer 6

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Question 7

So this is the second cause of bleeding - Vit K deficiency

1. So we know that you need Vit K to permit addition of COO group to factors 2, 7, 9 and 10, Protein C and S. This means, lack of Vit K would result in what?
2. Vit K deficiency occurs in 3 groups of clinical conditions - what are the three?
3. From question 2, this is the first group of Vit K deficiency: adults and Vit K deficiency
   - Is Vit K fat soluble?
   - What can be the cause of deficiency - 3 of them
   - Liver stores of Vit K when you can’t absorb it (I think) will usually last how many weeks? SO what happens to the PT and APTT? What should you beware of though?
4. Second group of Vit K deficiency: Vit K and liver disease
   - Where are most coag factors synthesised?
   - In severe liver disease, what happens? What falls more than others? What can improve coagulation status before liver biopsy or surgery?
5. Third and last group of Vit K: Vit K and Neonate
   - In neonate, there is limited Vit K transport across the placement so what are the levels of Vit K-dependent factors at birth like?
   - So what is always given after birth?
   - What about premature infants?

Answer 7

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Question 8

Warfarin!

1. What does it affect?
2. Who are the benefits (2)?
3. What are the potential problems? (3)
4. What’s the standardising of the PT about? What’s the radio called?
5. What are some common causes for warfarin treatment to go out of control? (4)

Answer 8

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