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Good job, my friend!

 

The fibrinogen and immunoglobins released in inflammatory states cause RBCs to form stacks called Rouleaux bodies. They look like stacks of coins that have been pushed to the side. It is different from agglutination, in which the RBCs form clumps.

 

Here's a picture of what they look like.

 

Like you said, Monika, sed rate is the rate at which RBCs settle in anti-coagulated blood; Rouleaux bodies are heavier and therefore settle quicker than individual RBCs.

 

{At least that is my understanding; any comments/criticisms?}

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it is a point of connection between 4 bones of the cranium... sphenoid fonatella,.... greater wing of sphenoid b., squamosal temporal b., frontal b., and parietal b.... I think the middle meningeal a. rests on it, at the point of connection. Useful land mark in neuro-surg... ect. doc me my 1/2 points for spelling :P. I can't remember any more... agghh!! been up since crack of dawn on weds. I hope this helps.... good luck :D

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Good job, Do, for not having any sleep! Hope those exams went well!

 

Yup - the pterion is an H-shaped spot on the side of the skull where the greater wing of the sphenoid joins with the frontal, parietal & temporal bones.

 

And it is the location of the shenoid fontanel.

 

And it overlies the middle meningeal artery & vein.

 

But what makes this spot more prone to injury than other spots on the calvarium?

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  • 2 weeks later...
Good job, Do, for not having any sleep! Hope those exams went well!

 

Yup - the pterion is an H-shaped spot on the side of the skull where the greater wing of the sphenoid joins with the frontal, parietal & temporal bones.

 

And it is the location of the shenoid fontanel.

 

And it overlies the middle meningeal artery & vein.

 

But what makes this spot more prone to injury than other spots on the calvarium?

 

The pterion is the thinnest point in the skull - and the most common site of injury in traumatic epidural hematomas ;)

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Epidural was what we learned in class, but I looked it up to be sure (the memory only holds so much, ya know :D )...

 

"The thinnest part of the lateral wall of the skull is ... the pterion. Clinically, this is an important area because it overlies the anterior division of the middle meningeal artery & vein" Snell, Clinical Anatomy

 

"90% of epidural hematomas are caused by head trauma with a skull fracture that crosses a portion of the middle meningeal artery or vein. The middle meningeal artery is torn in 60% of cases." Wayne State University Neuroradiology Teaching File

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  • 3 weeks later...

If I'm remembering right, the 2 most common causes of hypercalcemia are:

1. primary hyperparathyroidism

2. cancer metastasis to bone (most likely from prostate cancer)

 

I am stumped on the 2 most commonly seen in the ER though!

 

Thanks for getting the thread restarted, Angel!

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Guest bluiz1997

With which genetic disorder are you likely to see blue/purple sclera? I saw a patient with this disorder my first year in practice and may never see another one. It is a rare condition.

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Guest bluiz1997

OK this is a fun one.....

 

Explain why when anticoagulating a patient you should concominantly start them on Heparin and oral anticoagulant (Warfarin) prior to maintaining on Warfarin.

 

Explain full physiology in regards to the clotting mechanism.

 

What complication is likely to occur at a higher incidence if you start a patient directly on Warfarin without first initiating Heparin?

 

How long should the patient be on Heparin in conjunction with the Warfarin?

 

How does Warfarin work?

What is the antidote for Warfarin?

What is the antidote for Heparin?

 

 

If a patient was directly started on Warfarin without first loading with Heparin...which conditions would increase the incidence of complications?

 


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All right...I had to finish studying for an incredibly difficult GI exam before I could tackle this one, but I'm ready to take a stab at it!

 

HERE GOES!!....

Explain why when anticoagulating a patient you should concominantly start them on Heparin and oral anticoagulant (Warfarin) prior to maintaining on Warfarin.

Heparin has a faster onset (peak levels in 2-4 hrs) whereas warfarin is slower in onset (peak levels at 72-96 hrs). Therefore you want to start the Heparin for quick anti-coag and then use warfarin as an oral maintenance therapy

 

Explain full physiology in regards to the clotting mechanism.

Heparin: heparin in combination with antithrombin III can inhibit thrombosis by inactivating activated Factor X and inhibiting the conversion of prothrombin to thrombin. Once active thrombosis has developed, larger amounts of heparin can inhibit further coagulation by inactivating thrombin and preventing the conversion of fibrinogen to fibrin. Heparin also prevents the formation of a stable fibrin clot by inhibiting the activation of the fibrin stabilizing factor.

 

Warfarin: inhibitsthe synthesis of vitamin K dependent clotting factors, which include Factors II, VII, IX and X, and the anticoagulant proteins C and S

 

What complication is likely to occur at a higher incidence if you start a patient directly on Warfarin without first initiating Heparin?

it may enhance the release of atheromatous plaque emboli (systemic cholesterol embolization causing, among other things..."purple toes syndrome")

 

How long should the patient be on Heparin in conjunction with the Warfarin?

My sources say "several days"...maybe 3 ??

 

How does Warfarin work?

see above info about clotting cascade

 

What is the antidote for Warfarin?

Vitamin K

 

What is the antidote for Heparin?

fresh frozen plasma

 

If a patient was directly started on Warfarin without first loading with Heparin...which conditions would increase the incidence of complications?

you got me here...someone with more energy will have to figure this one out! :p

 

 

Thanks bluiz for contributing to the thread...be kind in how many ways I got my answers wrong! :D

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Guest pac4hire

Pahopeful....you were great except the reversal for heparin...any new ideas? FFP can be used in the all to controversial DIC however what one drug can be used to reverse heparin?

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Guest pac4hire

1. What are the defining structures in distinguishing between a direct hernia and an indirect hernia?

 

2. (A)In any adult,what concominent dz(s) must be ruled out if a new direct/indirect hernia is found? (B) How do this/these cause hernia's?

 

3. What is the (1)least invasive and cheapest diagnostic test to help dx a hernia in a pt with a good clinical history but a questionable exam?

 

 

These are easy, don't overthink them. These are Rotation day 1 pimp questions...

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Guest bluiz1997

You did an excellent job answering that question!!! I was asked this question on the spot as a student. Your preceptors will be very impressed if you can explain this with physiological mechanism because it is difficult.

 

Some Key points

 

*Antidote of Heparin is Protamine Sulfate; FFP can also be administered

 

*Heparin loading dose is given because the full Coumadin effect can take

up to 48-72 hours. Hence Heparin is usually continued for at least 2-3 days.

Factor 2 is the slow guy with half life of 42-72 hours.

 

*Coumadin acts by blocking the biosynthesis of the Vitamin K dependant clotting factors 2,7,9&10 and Protein C&S (Very Good; this is likely to be incorporated into a board question)

 

* Important to remember Proteins C&S are generally the problem causers. Protein C has a short half life of 8 hours. Depleting the Protein C too quickly can cause a hypercoagulable state. Never** start a high loading dose of Coumadin as this will increase the likelihood of hypercoagulability due to quick depletion of Protein C increasing the likelihood of Coumadin Induced Necrosis. Usually Coumadin is started at 5-7.5mg and never higher than 15mg in inital dosing. Always start Heparin first until adequate INR is achieved.

 

*Coumadin Induced Necrosis is rare but more likely to occur with those whom have Protein C, Protein S, or Antithrombin III deficiency. Specifically at an even higher rate if the clinician does not start Heparin first!!!!

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Very good! You are correct!!! :p That (and that it goes away within a couple of weeks) is pretty much all that we were told about this condition.

 

 

I just learned that one this past Wednesday!

 

Harlequin phenomenon occurs when one half of a neonate's body turns red and the other half is pale, with a striking line of demarcation down the center. It is thought to be benign... {that's all I remember off the top of my head}

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  • 5 weeks later...

There is Klinefelter's with the extra chromosome XXY. There are a host of Y-linked recessive disorders such as Cystic Fibrosis, but I do believe the way this is worded, I am not getting the gist of just what is being sought here.

It has been said, at times it is not the answer that is so important, but the ability to ask the correct questions. LOL!

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