Bandit Posted October 19, 2004 Share Posted October 19, 2004 alright rookies, time for the fast ball: By now you all should know that when you give amoxil to a patient with EBV they will pop with a rash. Now, to get uncle bandit off your ass for one entire week----what is the mechanism of action for that rash? Quote Link to comment Share on other sites More sharing options...
pahopeful Posted October 20, 2004 Author Share Posted October 20, 2004 Thanks for clearing up the TOF stuff, SirJL. After reading my answer, I realize that I must not be getting enough sleep! That's what I get for thinking that I know something for the test I have to take Thursday on that stuff! Bandit, I would like to take a stab at your pimp question. The rash that develops is a maculopapular rash. This rash can also occur with other penicillins, and without the concurrent EBV, but alas I am dodging the real question! Here's my humble guess: The rash is a hypersensitivity reaction that is due to the antigenic properties of a penicillin breakdown product, penicilloic acid. This antigenic metabolite reacts with proteins in the body, and acts as a hapten to cause the immune rxn (the rash). Sorry for the pathetic attempt, but that's all I've got for tonight. Am I on the right track?? Thanks for contributing a question...I appreciate the opportunity to learn from a veteran! Quote Link to comment Share on other sites More sharing options...
Bandit Posted October 20, 2004 Share Posted October 20, 2004 you are on the rigth track. think MHC and T cells. Quote Link to comment Share on other sites More sharing options...
pahopeful Posted October 20, 2004 Author Share Posted October 20, 2004 Ok, here's the follow-up on my previous guess... The antigen (penicilloic acid) is picked up by APCs (specifically B cells with Class II MHC). The APCs present the antigen to T-helper cells which in turn activate B cells to produce Ab (IgE specifically) to attack the antigen. The specified IgE binds to sites on mast cells and basophils which in turn release chemical mediators (examples include: histamine, cytokines, prostaglandins, etc). These chemical mediators when released in the skin cause the rash. This whole process is descriptive of a type IV hypersensitivy rxn. I have no idea if this is right Bandit, but there's my guess!! Have I continued on the right track or veered off course??! Quote Link to comment Share on other sites More sharing options...
merseur Posted October 20, 2004 Share Posted October 20, 2004 My guess is that the body produces an immune response particularly IgG and IgM and attacks amoxicillin. Quote Link to comment Share on other sites More sharing options...
Moderator EMEDPA Posted October 20, 2004 Moderator Share Posted October 20, 2004 TRY THIS ONE ON FOR SIZE: list presenting signs or symptoms for pulmonary embolism other than chest pain or dyspnea? Quote Link to comment Share on other sites More sharing options...
JenGintheED Posted October 21, 2004 Share Posted October 21, 2004 Finally, I can play!! How about sudden, unexplained tachycardia, JVD, hemoptysis? We were taught the classic S1Q3T3 but I think I read somewhere that that is actually rare to see that EKG pattern??? Quote Link to comment Share on other sites More sharing options...
JenGintheED Posted October 21, 2004 Share Posted October 21, 2004 And right-sided CHF symptoms when the blood can't get into the pulmonary circulatory circuit... dependent edema. Any more? :confused: Quote Link to comment Share on other sites More sharing options...
merseur Posted October 21, 2004 Share Posted October 21, 2004 dyspnea and hemoptysis Quote Link to comment Share on other sites More sharing options...
pahopeful Posted October 21, 2004 Author Share Posted October 21, 2004 acute pulmonary HTN possibly including: pink, frothy sputum severe dyspnea diaphoresis cyanosis Quote Link to comment Share on other sites More sharing options...
Bandit Posted October 21, 2004 Share Posted October 21, 2004 excellent job hopefull. what is the difference in anti pyritic properties between IBU and tylenol? Quote Link to comment Share on other sites More sharing options...
Bandit Posted October 21, 2004 Share Posted October 21, 2004 E, have you seen PEs ever present with fever? I have on many occasions only to hear docs tell me "nope!" Quote Link to comment Share on other sites More sharing options...
Moderator EMEDPA Posted October 21, 2004 Moderator Share Posted October 21, 2004 I have seen folks with pe have fever but not as the only sign/sx. no one mentioned unexplained syncope as a presentation for pe...that's the pimp question from hell"please give a ddx for syncope"...( shudder) anyway for more info on PE do a web search for the pioped study.( here is a summary http://www.emedicine.com/med/topic1958.htm lots of useful stuff like this.... * Patients with PE may present with atypical symptoms, where strong suspicion in a high-risk patient often leads to consideration of PE in the differential diagnosis. These symptoms include the following: o Seizures o Syncope o Abdominal pain o Fever o Productive cough o Wheezing o Decreasing level of consciousness o New onset of atrial fibrillation Quote Link to comment Share on other sites More sharing options...
pahopeful Posted October 23, 2004 Author Share Posted October 23, 2004 Ok Bandit, I'm ready to play again! Sorry that I've been slow on the response to the Tylenol/Ibuprofen question, but I had a major cardiovascular block test on Thursday and I have been studying for/recovering from that. :p About the acetaminophen/IBU question, from what I can tell, both drugs work similarly by inhibitin prostaglandins and therefore "resetting the thermostat" in the anterior hypothalamic heat regulatory center. However IBU and other NSAIDs act additionally in anti-pyresis by causing peripheral vasodilation which allows heat dissipation through the skin. That's all I got! Cardiology has fried my brain! Am I even close Bandit?? Quote Link to comment Share on other sites More sharing options...
isomerization Posted October 24, 2004 Share Posted October 24, 2004 Tylenol reduces fever by acting directly on the hypothalamus. It raises the pain threshold. No specific MOI is known by any sources I've inquired of. Ibuprofen reduces fever by acting on the souce of prostaglandins in inflammatory tissues(cox-2 or cyclooxygenase 2). I haven't even started chem classes yet so cut me some slack. I sooo wish I had a PDR. Quote Link to comment Share on other sites More sharing options...
Ames100 Posted October 24, 2004 Share Posted October 24, 2004 This is a great thread! Thanks to pahopeful for starting it! Here is something I learned today during my ER rotation: Besides corneal abrasion, what ocular condition(s) can be detected by examination of the eye with fluorescein stain? Quote Link to comment Share on other sites More sharing options...
JenGintheED Posted October 24, 2004 Share Posted October 24, 2004 herpes simplex keratitis Quote Link to comment Share on other sites More sharing options...
pahopeful Posted October 24, 2004 Author Share Posted October 24, 2004 Thanks for appreciating the thread Ames...I'm really enjoying answering the questions and reading answers from others too! As for the uses of fluorescein stain, I would guess that the next obvious use is to ascertain prescence of a foreign body. How'd I do?? I'm sure that there are other uses, but that's all I can think of for tonight. Thanks so much for contributing a pimp question...got anymore?? Quote Link to comment Share on other sites More sharing options...
Ames100 Posted October 24, 2004 Share Posted October 24, 2004 Yes, you are both correct! The most serious thing to not miss is herpes simplex keratitis (which shows up as a dendritic lesion under fluorescein stain - sort of like a little fern leaf), but you can also pick up foreign bodies, corneal ulcers, and conjunctival abrasions. The symptoms of herpes keratitis can present like conjunctivitis, so if you have any suspicion for herpes, you must stain the eye to make the diagnosis. Let's see.... other questions.... How about this: Your patient presents with low back pain. What question must you be sure to ask in order to rule out a rare but serious condition? (I learned this yesterday in the ER too!) Quote Link to comment Share on other sites More sharing options...
isomerization Posted October 24, 2004 Share Posted October 24, 2004 By Ames100 Your patient presents with low back pain. What question must you be sure to ask in order to rule out a rare but serious condition? (I learned this yesterday in the ER too!) Could be renal,pancreatic, perforated ulcer, malignancy/infection in the spinal colum, AAA, appendicitis or just musculoskeletal. They are all serious but not what I would call "rare". The AAA is the most life-threatening but not something one would need a hx to diagnose so I'll go with spinal infection as vertrebral diskitis with abcess. I would look for neurologic deficit. All the speculation aside, I don't know of one question that would sufficiently rule out any of these but it's fun. Quote Link to comment Share on other sites More sharing options...
isomerization Posted October 25, 2004 Share Posted October 25, 2004 Ames100, Bandit, Did I answer correctly or is it cheating to look in a book? I was hoping for some discussion about what was right and wrong to get a deeper understanding from people that have the actual experience. All I can go by is the books in front of me. Quote Link to comment Share on other sites More sharing options...
Ames100 Posted October 26, 2004 Share Posted October 26, 2004 Could be renal,pancreatic, perforated ulcer, malignancy/infection in the spinal colum, AAA, appendicitis or just musculoskeletal. They are all serious but not what I would call "rare". The AAA is the most life-threatening but not something one would need a hx to diagnose so I'll go with spinal infection as vertrebral diskitis with abcess. I would look for neurologic deficit. All the speculation aside, I don't know of one question that would sufficiently rule out any of these but it's fun. Sorry, Isomerization, I was waiting to make sure there weren't any other answers out there before I wrote back... Your answers were all very good, and some of them came to my mind too (when my preceptor asked me this question) - but he was looking for cauda equina syndrome, which can be ruled out by asking the patient if they have bowel or bladder function. Cauda equina is a severe neurologic disorder that most commonly results from a disc herniation in the lumbar region. Symptoms include severe low back pain, urinary or bowel incontinence, motor weakness or sensory loss in both legs, and saddle anesthesia (unable to feel anything in the body areas that would sit on a saddle). So any patient that presents with low back pain should be asked if they are able to urinate and defacate, and also if they have any numbness or weakness in their legs or saddle area. Thanks for answering my question!! Anybody else have one? Quote Link to comment Share on other sites More sharing options...
doboy Posted October 26, 2004 Share Posted October 26, 2004 Patient comes into your office, CC- continous headache, suboccipital region, general weakness. PE : downward nystagnus, upper extremity weakness, disturbed gait. Hx: pt. denies trauma, no hydrocephelus @ birth. Labs Ordered LP- glucose/protien levels normal, no bacteria in CSF. Low CSF pressure in spinal compartment (hint). other labs normal. MRI findings: tonsilar herniation of cerebellum below foramen magnum to level of C1. Can you name the Dx and Tx? Good Luck Quote Link to comment Share on other sites More sharing options...
Ames100 Posted October 26, 2004 Share Posted October 26, 2004 Hmmmm.... This is a tough one. I am going to guess Arnold-Chiari I type malformation? But I'm not sure if you would have increased or decreased CSF pressure on LP.. :confused: Quote Link to comment Share on other sites More sharing options...
isomerization Posted October 26, 2004 Share Posted October 26, 2004 Ames100, Thanks for the response. If anyone is interested: http://www.emedicine.com/emerg/topic85.htm Quote Link to comment Share on other sites More sharing options...
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