Heparin vs. Aspirin

[Pox in a box]

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I'm having some trouble dealing with a concept in pharmacology. Heparin is for anticoagulation and aspirin, due to its inhibition of cyclooxygenase, prevents platelet aggregation. I can see how administering both to a patient could cause major problems in bleeding time (very increased PT) but I don't understand why you can't just put a patient on aspirin instead of putting them on heparin/warfarin. Aspirin is cheap and OTC. Heparin/warfarin are very painstaking to administer and patient compliance may not be as good. Aspirin has some good effects (like antipyretic, analgesic, anti-inflammatory) but I guess the adverse effects (GI bleeding, tinnitus, hypersensitivity, etc.) are too overwhelming for most patients long term. Am I thinking wrong here?

 

[Samoa]

There are head-to-head trials addressing this very issue. In fact, there was one in NEJM a few years ago that you might want to read. go to www.nejm.org and do a search.

 

[phdmed07]

I would assume that the main reason to put a patient on anticoags like heparin/warfarin deals with what these drugs treat. The anticoags are used for Deep Vein thrombosis and pulmonary emboli, the problem is blood clots and these drugs are antagonizing clotting Fs and decreasing the chance of developing these conditions. Aspirin is affecting platelet aggregation which isnt the problem that the anticoags are treating.
Just my 2 cents.
ECU Med 07

 

[me454555]

B/c heparin and aspirin work on different parts of clotting

Aspirin - inhibits platelet aggregation so increased bleeding time but normal PT and PTT

Heperin - inhibits clotting factors so normal bleeding time but increased PT and PTT

 

[p53]

Heperin - inhibits clotting factors so normal bleeding time but increased PT and PTT

Really? You better type up this theory and send it to Kumar for his next draft of Big Robbin's.

ONLY AN UNEDUCATED person would think that heparin inhibits clotting factors. DON'T POST MISINFORMATION AGAIN. Students preparing for the USMLE deserve ACCURATE information.

HEPARIN activates antithrombrin III. Antithrombrin III is responsible for inactivating the serine proteases in the clotting pathway. HEPARIN HAS NO PHYSICAL EFFECT ON CLOTTING FACTORS!

 

[north2southOMFS]

Yep, what he said above me.

it is coumadin that will increase PT. (But not PTT)

 

[Wrigleyville]

1) Calm down.

2) Warfarin increases both PT and PTT. PT is a more accurate measure of the drug's action (fewer non-vitamin K dependent factors in the pathway), which is why it is used to monitor the drug.

 

[me454555]

Hey P53, relax buddy, don't blow a gasket its really not that big a deal. I think everyone here knew what I meant by "inhibits the clotting factors" and I was just trying to simplify a concept. I appologize for the oversight.

Don't call people "uneducated" on this board b/c we are all soon to be doctors. Have a little bit of professional courtisy and correct a mistake in a constructive, respectful manor and try not to demean your fellow colleagues.

 

[omarsaleh66]

I would assume that the main reason to put a patient on anticoags like heparin/warfarin deals with what these drugs treat. The anticoags are used for Deep Vein thrombosis and pulmonary emboli, the problem is blood clots and these drugs are antagonizing clotting Fs and decreasing the chance of developing these conditions. Aspirin is affecting platelet aggregation which isnt the problem that the anticoags are treating.
Just my 2 cents.
ECU Med 07

yeah i agree, i just want to add to this. A good way to look at it is 2 different clots. In arterial clots think aspirin for prophylaxis, and in new coronary stents think clopidgrel cuz what u want here is platelet inhibition.

In venous clots think heparin, warfarin to prevent DVTs.

later

 

[HiddenTruth]

Really? You better type up this theory and send it to Kumar for his next draft of Big Robbin's.

ONLY AN UNEDUCATED person would think that heparin inhibits clotting factors. DON'T POST MISINFORMATION AGAIN. Students preparing for the USMLE deserve ACCURATE information.

HEPARIN activates antithrombrin III. Antithrombrin III is responsible for inactivating the serine proteases in the clotting pathway. HEPARIN HAS NO PHYSICAL EFFECT ON CLOTTING FACTORS!

1. Why are you YELLING? There isn't a code BLUE here.
2. I can help set up some counseling sessions for you. All you have to do is ask.
3. If I remember correctly, you were the one who was raving "MISINFORMATION" about murmurs and criticizing people in the other thread. I don't think anyone else got too personal. If you think so highly of yourself, why are you on these forums, other than the personality disorder that others have "diagnosed" you with. So, to cut a long story short, and to prevent myself from acting like yourself, apply your post above (which I have nice quoted for you) to yourself before you criticize others.
4. I think there is a general concensus of your behavior and persistent negative attitute on this board. Maybe that should ring some bells. Good luck!

To the OP: what everyone has said is pretty much correct. They both have different mechanism of actions first off. Heaprin activ AT III which INCREASES the inactivation of factor 11a and 10a primarily by ATIII. Infact, the major difference between enoxaparin (LMWH) and heparin is that the low molecular wt heparin is too short (only 15 polysacchs i think) to fully wrap around ATIII and increase its activity. So, larger coag factors such as IIa are not affected by LMWH because ATIII still has some normal inactivation activity due to short LMWH. Therefore factor IIa is not affected by LMWH. But, anyways, so heaprin increases PTT, while aspirin inhibits platelet aggregation, which only prolongs BT. Remember, platelet aggregation will occur before the clotting cascade is initiated. And, like omar mentioned, their uses are for different clinical conditions. I think that is the most we'll have to know for step 1 in respect to this question. Good luck!

 

[NIQ]

1. Why are you YELLING? There isn't a code BLUE here.
2. I can help set up some counseling sessions for you. All you have to do is ask.
3. If I remember correctly, you were the one who was raving "MISINFORMATION" about murmurs and criticizing people in the other thread. I don't think anyone else got too personal. If you think so highly of yourself, why are you on these forums, other than the personality disorder that others have "diagnosed" you with. So, to cut a long story short, and to prevent myself from acting like yourself, apply your post above (which I have nice quoted for you) to yourself before you criticize others.
4. I think there is a general concensus of your behavior and persistent negative attitute on this board. Maybe that should ring some bells. Good luck!

To the OP: what everyone has said is pretty much correct. They both have different mechanism of actions first off. Heaprin activ AT III which INCREASES the inactivation of factor 11a and 10a primarily by ATIII. Infact, the major difference between enoxaparin (LMWH) and heparin is that the low molecular wt heparin is too short (only 15 polysacchs i think) to fully wrap around ATIII and increase its activity. So, larger coag factors such as IIa are not affected by LMWH because ATIII still has some normal inactivation activity due to short LMWH. Therefore factor IIa is not affected by LMWH. But, anyways, so heaprin increases PTT, while aspirin inhibits platelet aggregation, which only prolongs BT. Remember, platelet aggregation will occur before the clotting cascade is initiated. And, like omar mentioned, their uses are for different clinical conditions. I think that is the most we'll have to know for step 1 in respect to this question. Good luck!

Great answer, thanks for clarifying differences in LMWH and heparin