Educational game time!

[DwayneEMTP]

So it's been a while since we've done an education Round Robbin, so I thought I'd take my turn at starting one, with a little bit of a twist.

Each person answers the questions of the person before and then adds a new focus for the next question. The question will always be, more or less, "Define (X) and the anatomical/physiologic role that it plays, may play in EMS care."

I would like the answers in two parts. The first part being everything that you can pull out of your head. (Part A) And secondly what you can find to supplement that through research, but only a few minutes..you are going to be really pissed if you spend two hours researching something something only to find that you come back and the game has moved on by three questions.

Also, because I hate it when that happens, and most often I'm passed by by some shithead that gave a flippant answer just so he could ask his "no one will ever get THIS questions" we're going to try using place markers. If you read a question, and would like to answer it, Post, "I've got this one!" and then please answer within the next 30 mins or so...not sure how that will work, but lets try, ok?

And often these threads are dominated by those that are sitting at home doing nothing so that they can answer so quickly that no one else can participate. Please, participation is vital for people to learn...if you see your name more than twice or three times on a page, try and give someone else a chance to answer unless you see a lull in the thread.

Major points...

This is for learning. We should try to give topics that will help people be better practitioners, not to try and prove that we're smart enough to Google something that no one can answer, and worse, that no one cares about.

Please cit your sources! What got me thinking about this today is that I was mentally reviewing body system in my head and found that I maybe couldn't give a decent talk on ANY of them without some research. Though I have always been amazed by the information that comes to me when I need it in the ambulance. There is no shame in not knowing every body system down to the cellular level off the top of your head. The only shame is in forgetting that you should have that as a goal..And even more so claiming someone else's work as your own.

Give your BEST answer in A. It will allow people to say, "Ah, I see where you thought that, but maybe it will help if you think of it like this...." then show your research as well as anything you may have learned from it if you like.

Please stay in the spirit of the game. These are almost always ruined by someone that has to try and prove that they know the exact definition of Gynocockusrot, it's physiological paths, proper treatments, etc, "right off the top of their head" and it's just a coincidence that their answers match the first one Googled when you check.

Ok, so, your best answer, then your quickly researched answer, cited, then the topic for the next person that is likely at least partial knowable to them but also applicable to being in an ambulance. And if a question is obviously meant for our BLS brothers and sisters, please don't jump all over it with your medic degree without giving them a chance to answer.

And please remember that your answer is meant to teach those that read it...so speaking above everyone's head fails...Thanks for playing all!

Dwayne

Edited to add txt in bold.

First Topic....

As it's Cystic Fibrosis awareness month, lets start with that. Please be specific!

Define Cystic Fibrosis and the anatomical/physiologic role that it plays, may play in EMS care.

Edited May 2, 2011 by DwayneEMTP

[Bieber]

Define Cystic Fibrosis and the anatomical/physiologic role that it plays, may play in EMS care.

What I know:

Cystic fibrosis is an autosomal recessive disease that results from a mutation of a gene and is characterized by excessively salty skin, thickened pulmonary secretions, greasy stools and frequent pulmonary infections. The source of the increased and thickened secretions is due to a mutated protein in the ciliary epithelial cells. The same thickened mucous appears elsewhere in the body and can result in pancreatitis (and subsequently diabetes), GERD, splenic enlargement, appendicitis, and other symptoms of the disease include portal and pulmonary hypertension and right ventricular hypertrophy and frequent infections.

It's frequently screened for by testing the salinity of the skin and the long term prognosis is, frankly, poor. Lung transplants are often necessary, and most people with the disease die before reaching forty, if I'm recalling correctly.

What I learned:

Some further reading from my class notes and the internet reveals that the gene involved is the CFRT (cystic fibrosis transmembrane conductance regulator) gene, and that the specific mutation in about two-thirds of all patients is the deletion of F508, which comprises the codon for phenylalanine at position 508 and ultimately which is responsible for a halide anion channel that is involved in producing mucous and digestive secretions.

Without this protein (or without its proper functioning), those halides can't pass through the cell membrane (in the respiratory cells, the halides along with thiocyanite are trapped inside the cells, increasing the viscosity of the mucous produced and additionally with the entrapment of the thiocyanite, which is necessary for creating hypothiocyanite, an important antimicrobial in the respiratory system, this decreases the potency of the immune system, and on the skin they're trapped outside of the cells, causing the high salinity due to the combination of the chloride halide and sodium).

I also read that bowel obstruction and meconium ileus is common in children, poor growth, and cystic fibrosis can also present as a coagulative disorder due to vitamin K malabsorption. The most common respiratory infections in patients from 0-18 are due to staphylococcus aureus and haemophilus influenzae, after age eighteen pseudomonas aeruginosa becomes the dominant infectious agent in respiratory infections. Thickened mucous in the digestive tract is the underlying cause of the failure to growth (due to malabsorption), pancreatitis (blockage of the pancreatic ducts with these thickened digestive secretions), and bile duct blockage can result in cirrhosis.

What you should know:

EMS wise, the problem we're most likely to be presented with is dyspnea secondary to the thickened bronchial secretions. Probably the best treatments we in the prehospital realm can provide are going to be bronchodilators to open them up, IV fluids to help thin those secretions, and oxygen therapy. Corticosteroids may be beneficial too due to the inflammation caused by the mucous buildup.

I'll add some more about the long term treatment of cystic fibrosis tomorrow, unfortunately I can't finish this all tonight. In the meantime, I'd like to learn more about benign early repolarization.

[DwayneEMTP]

Outstanding!!

But you didn't leave the next question before you left!

[chbare]

Outstanding!!

But you didn't leave the next question before you left!

"I'd like to learn more about benign early repolarization."

Take care,

chbare.

[DarEMT]

"Delta F508" is the most common mutation of the defective gene. Cystic Fibrosis is often misdiagnosed as asthma, failure to thrive, and even Chrone's Disease. One in 20 of us is a symptomless carrier of the defective gene. It takes BOTH parents being carriers to produce a child with CF. When both parents are carriers, they have a 25% chance of EACH PREGNANCY of producing a carrier and a 50% chance of producing a child with CF. Thusfore, a female child with CF will find it difficult to conceive and the male with CF will almost certainly be sterile, because of the thick secretions of course. These thick secretions are present THROUGHOUT the body wherever mucus is found. Cystic Fibrosis affects caucasions predominantely, much like Sicle Cell affects african americans.

I disagree with the thought that 0-18 year olds staphylococcus aureus and haemophilus influenzae are the most common infections and, after age eighteen pseudomonas aeruginosa becomes the dominant infectious agent in respiratory infections. I see MRSA, as well as pseudomonas, in teenagers as well as adults and have seen it for years.....also, I believe Bieber is correct on the "median" age for life expectancy of someone with CF, however, please take into consideration that I believe that life expectancy isn't what's on paper....life expectancy is how you handle your body...treatments, medications, excercise, and a healthy mind will allow one to live just as long or longer than anyone else that is healthy otherwise.

Reference: Encyclopedia of "Mom of 2 CF girls"

***Please excuse any misspellings or non use of proper terminology, as it's late and I'm very tired***

[fiznat]

Bieber if that is really the information you had off the top of your head than hats off to you. That's some pretty thorough knowledge.

Stand by for a reply on BER.

[fiznat]

Benign Early Repolarization

What I know:

BER is one of the classic STEMI mimickers. The repolarization phase of the action potential, for some reason I don't know exactly, occurs slightly earlier resulting in an elevation of the ST segment of the ECG. I know that BER occurs more often in the young, especially thin African American males. Also, the usual presentation is precordial ST elevations in the absence of supporting cardiac signs or symptoms.

Research results:

There is no Wikipedia page on BER. LOL.

BER is a benign condition that exists in approximately 1% of the population. Interestingly, however, the percentage is much higher among patients presenting to the emergency department with chest pain. I've come across several estimates ranging from 25 to 50 percent. Of those patients, 80% will have precordial ST elevations of less than 2mm. Only 2% will have elevations above 5mm. Almost all of BER ST elevation occurs in the precordial leads V2-V5. Limb lead elevations are rare and usually much smaller (80% of the time less than 0.5 mm).

The etiology of BER has not been formally studied and to the best of my knowledge is not known.

BER is a STEMI mimicker and in the emergency medicine setting should be used as a diagnosis of exclusion. That means that patients should not be assumed to have BER until more dangerous conditions have been ruled out (AMI and pericarditis especially). In fact, though the condition has largely been considered benign (hence it's name!), recent studies (here and here) are suggesting that patients with BER actually have poor outcomes down the line.

Specific criteria for diagnosis of BER (from here):

1. ST segment elevation.

2. Upward concavity of the initial portion of the ST segment. (**like a smile not a frown**)

3. Notching or slurring of the terminal QRS complex.

4. Symmetric, concordant T waves of large amplitude.

5. Widespread or diffuse distribution of ST segment elevation on the ECG.

6. Relative temporal stability. (**ECG does not evolve, clinical condition remains stable**)

Also, here is an excellent 14 minute video on the subject that I found.

Sorry I couldn't find more information!

Next question: DKA is a fairly common condition that we run across. It produces a special kind of metabolic acidosis called an anion gap acidosis. Can someone tell us about DKA and how exactly it produces an anion gap acidosis (and what that is exactly!).

Edited May 4, 2011 by fiznat

[DwayneEMTP]

"Delta F508" is the most common mutation of the defective gene. Cystic Fibrosis is often misdiagnosed as asthma, failure to thrive, and even Chrone's Disease. One in 20 of us is a symptomless carrier of the defective gene. It takes BOTH parents being carriers to produce a child with CF. When both parents are carriers, they have a 25% chance of EACH PREGNANCY of producing a carrier and a 50% chance of producing a child with CF. Thusfore, a female child with CF will find it difficult to conceive and the male with CF will almost certainly be sterile, because of the thick secretions of course. These thick secretions are present THROUGHOUT the body wherever mucus is found. Cystic Fibrosis affects caucasions predominantely, much like Sicle Cell affects african americans.

I disagree with the thought that 0-18 year olds staphylococcus aureus and haemophilus influenzae are the most common infections and, after age eighteen pseudomonas aeruginosa becomes the dominant infectious agent in respiratory infections. I see MRSA, as well as pseudomonas, in teenagers as well as adults and have seen it for years.....also, I believe Bieber is correct on the "median" age for life expectancy of someone with CF, however, please take into consideration that I believe that life expectancy isn't what's on paper....life expectancy is how you handle your body...treatments, medications, excercise, and a healthy mind will allow one to live just as long or longer than anyone else that is healthy otherwise.

Reference: Encyclopedia of "Mom of 2 CF girls"

***Please excuse any misspellings or non use of proper terminology, as it's late and I'm very tired***

Awesome insight from a parent. Thanks for doing that!

Any experience with EMS in regards to your girls? Anything that you can share concerning attitudes, treatments, care of the CF patient that maybe we wouldn't normally think about but might allow us to provide better care for these patients?

Dwayne

Edited to correct some grammar..nothing substantial.

Edited May 4, 2011 by DwayneEMTP

[chbare]

"Delta F508" is the most common mutation of the defective gene. Cystic Fibrosis is often misdiagnosed as asthma, failure to thrive, and even Chrone's Disease. One in 20 of us is a symptomless carrier of the defective gene. It takes BOTH parents being carriers to produce a child with CF. When both parents are carriers, they have a 25% chance of EACH PREGNANCY of producing a carrier and a 50% chance of producing a child with CF. Thusfore, a female child with CF will find it difficult to conceive and the male with CF will almost certainly be sterile, because of the thick secretions of course. These thick secretions are present THROUGHOUT the body wherever mucus is found. Cystic Fibrosis affects caucasions predominantely, much like Sicle Cell affects african americans.

I disagree with the thought that 0-18 year olds staphylococcus aureus and haemophilus influenzae are the most common infections and, after age eighteen pseudomonas aeruginosa becomes the dominant infectious agent in respiratory infections. I see MRSA, as well as pseudomonas, in teenagers as well as adults and have seen it for years.....also, I believe Bieber is correct on the "median" age for life expectancy of someone with CF, however, please take into consideration that I believe that life expectancy isn't what's on paper....life expectancy is how you handle your body...treatments, medications, excercise, and a healthy mind will allow one to live just as long or longer than anyone else that is healthy otherwise.

Reference: Encyclopedia of "Mom of 2 CF girls"

***Please excuse any misspellings or non use of proper terminology, as it's late and I'm very tired***

Just to clarify, you agree or disagree?

Staphylococcus aureus, Haemophilus influenzae, and Pseudomonas aeruginosa are in fact the three most common bacteria that cause lung infections in CF patients. While I agree there are many others and some can be more common, the three mentioned are the most common when considering the CF population as a whole.

Take care,

chbare.

[Lone Star]

Next question: DKA is a fairly common condition that we run across. It produces a special kind of metabolic acidosis called an anion gap acidosis. Can someone tell us about DKA and how exactly it produces an anion gap acidosis (and what that is exactly!).

DKA

What I know about DKA:

Diabetic Ketoacidosis is a result of the body metabolizing fat stores instead of glucose for energy. This occurs because there isn't sufficient glucose stores, or the body isn't producing enough insulin. By metabolizing the fat (I believe this anerobic metabolism), it produces lactic acid.

Because the body isn't using the glucose stores (as in Type I diabetes), one of the signs is polyuria, leading to dehydration. Because of the dehydration, bicarbonate levels are low in the blood. This increases the acidity levels of the blood, and because of the volume drop (dehydration); sodium levels are elevated. This diffference between the cations (positive ions) and the low bicarbonate levels (one of the body's "buffer systems") produces the anion gap.

What I've learned:

While I don't fully understand lab values and osmolarity, I did learn that DKA treatments by using sodium bicarbonate is highly controversial as a treatment. I've also learned that it affects the immune system, and the DKA patient is highly susceptible to infections.

I found an article here that does a pretty good job of trying to explain it to dummies like me!

Can someone explain the actions of the heart during each segment of the EKG cycle?