Let's take a look at bleeding disorders but this is from a functional point of view.
Think about that for a second as you move forward with our differentials.
But functional, you don't necessarily have to have a decrease in platelet count, do you?
Functional, I want you think of the normal process of hemostasis that we've discussed.
When there's endothelial injury, you had expression of von Willebrand factor which is then bound to glycoprotein Ib.
If there's is a deficiency of glycoprotein Ib,
hereditary deficiency, this is then referred to as being Bernard-Soulier Syndrome
in which we can expect there to be lack of adhesion and there's an increase in bleeding time.
That's what your focus is going to be on when dealing with Bernard-Soulier.
What if the other glycoprotein, it was called IIb/IIIa, and it was responsible for what step?
So here also you would find an increase in bleeding time,
but the biggest difference between the two, would be the step in adhesion,
would be a lose in Bernard-Soulier.
The step in aggregation, would be lose in Glanzmann's Thrombasthenia.
Aspirin we talked about where you inhibit thromboxane therefore you don't have aggregation,
its a functional issue but it is an acquired type, isn't it?
Other NSAIDs of course, would be reversible including let's say ibuprofen.
Other issues in terms of drugs, remember the word or letters GREL,
and whenever you found the letters GREL in a drugs such as Clopidogrel, or Prasugrel, or Ticagrelor
then that was an issue or it was a target of your P2Y12 receptor antagonism for ADP
in which you are unable to then express glycoprotein IIb/IIIa.
So here, you prevent the step of aggregation on purpose.
Or Abciximab, that we talked about, it's going to particularly target glycoprotein IIb/IIIa,
and once again you will prevent platelet aggregation.
In other words, you are purposely creating function abnormalities with these drugs, aren't you?
Because you're trying to treat a patient who has platelet thrombi.