This book I found on GoogleBooks looks like it might be interesting. It looks like it's designed to take you from nursing practice down to A&P, rather than the other way 'round. It might be more useful for any remaining diploma nurses out there, or those going into an RN-to-BSN program, although it couldn't hurt for anyone else to look at it. I think I'll probably try to get it, but my guess is that I'll get more out of it after practicing for a while (assuming I graduate...).
It's available from Amazon as a regular book, or a kindle book. And the author has put out other books as well, like the Biological Basis of Cancer Nursing.
Nurses fired for photos, new viruses, depressed doctors
Friday via BoingBoing:
Research shows that we are likely to find more viruses.
Doctors are depressed and more likely to kill themselves, but are nurses? I couldn't find anything with a quick Google search.
Two nurses in Wisconsin were fired after taking photos of a patient's X-ray. The article raises the spectre of HIPAA, although you would really have to know more of the details before making that call. For example, did the photos show the patient's name? Anyhow, they were acting in bad taste. I think the hospital was probably justified in firing them, although if it was out of "HIPAA fear," that would be a bad thing.
Research shows that we are likely to find more viruses.
Doctors are depressed and more likely to kill themselves, but are nurses? I couldn't find anything with a quick Google search.
Two nurses in Wisconsin were fired after taking photos of a patient's X-ray. The article raises the spectre of HIPAA, although you would really have to know more of the details before making that call. For example, did the photos show the patient's name? Anyhow, they were acting in bad taste. I think the hospital was probably justified in firing them, although if it was out of "HIPAA fear," that would be a bad thing.
ketosis vs. ketoacidosis, part 2
Okay, I think I figured out yesterday's question about the etiology of ketoacidosis vs. ketosis. To recap, all the metabolic processes that lead to ketone production in ketoacidosis are present in ketosis, yet dietary carbohydrate starvation doesn't lead to an acidotic condition. This left me wondering what, exactly, causes ketoacidosis.
I feel pretty good about my conclusions yesterday. I narrowed down the cause to relative acidosis caused by volume depletion associated with the hyperglycemia that is not present in starvation, or an imbalance in the production-to-utilization ratio in ketosis. (If the body could burn and/or excrete ketones as fast as it produced them, there would be no acidosis.) And in fact, one of these was the reason.
First, as to the hyperglycemia-dehydration hypothesis, I discovered a condition called "euglycemic diabetic ketoacidosis," which pretty much rules that one out. Interestingly, while a western medical journal referred to this as a rare condition, a Pakistani medical journal says it accounts for 30% of patients presenting with DKA. I wonder what would account for that?
I finally found the answer in section 8.2 of Kerry Brandis' Acid-Base Physiology, an outstanding (and open access!) publication I had run across before but forgotten about. It's quite simple. Insulin is an antagonist to free fatty-acid release by cells. Without insulin, higher rates of free fatty-acids are available to act as increased substrate for ketone production. The odd imbalanced ratio of acetoacetate-to-ß-hydroxybutyrate is caused by an imbalance in NAD+to-NADH ratio caused by lactic acidosis.
I don't think I ever could have figured this out on my own because the answer depends on knowing rates. I would have had to figure out all the math behind the physiology first. So, I don't feel too bad.
Of course, that's not the whole story. FFA production is also increased by stress hormones, which explains why DKA is often precipitated by an infection.
Also, it appears that there may be some contribution of the feeding state on the rate of ketone uptake by mitochondria. I wonder about this one though. Essentially, it's suggested that in starvation ketone uptake is accelerated by glucagon, but as we know glucagon and other catabolic hormones rise in DKA. Again, it's a question of degree, I guess. Maybe glucagon is much higher in starvation.
Two articles that should have led me to the answer are the eMedicine articles on DKA and AKA. Actually, I did look at them yesterday. Not sure why they didn't register.
Finally, I almost went down a wrong path today looking at Dr. Johan Koeslag's article on oxalaoacetate. He suggests that glycogen is a necessity in order for cells to upregulate mitochondrial metabolism. Consider, then, a cell metabolism model focused on both fuel and rate regulation. The body might interpret the lack of normal fuel as a state of exertion rather than pathology and try to upregulate mitochondria, but, unable to do this in a state of glycogen depletion, then try to increase metabolic outputs by increasing substrates. I'm not totally convinced that there isn't something here. You will find some connection between DM1, DKA, and enlarged liver from over-storage of glycogen, for instance, if you start Googling.
Anyhow, I'm done with this for now. I think my Nur464 instructor should be encouraged for getting me to back and focus on the insulin issue and not squelching my interest in physiology, as was done in previous courses. Of course, I'm probably going to fail Nur464 since this won't be on the tests, but really that's all about the Community Health course, not this little side distraction...
I feel pretty good about my conclusions yesterday. I narrowed down the cause to relative acidosis caused by volume depletion associated with the hyperglycemia that is not present in starvation, or an imbalance in the production-to-utilization ratio in ketosis. (If the body could burn and/or excrete ketones as fast as it produced them, there would be no acidosis.) And in fact, one of these was the reason.
First, as to the hyperglycemia-dehydration hypothesis, I discovered a condition called "euglycemic diabetic ketoacidosis," which pretty much rules that one out. Interestingly, while a western medical journal referred to this as a rare condition, a Pakistani medical journal says it accounts for 30% of patients presenting with DKA. I wonder what would account for that?
I finally found the answer in section 8.2 of Kerry Brandis' Acid-Base Physiology, an outstanding (and open access!) publication I had run across before but forgotten about. It's quite simple. Insulin is an antagonist to free fatty-acid release by cells. Without insulin, higher rates of free fatty-acids are available to act as increased substrate for ketone production. The odd imbalanced ratio of acetoacetate-to-ß-hydroxybutyrate is caused by an imbalance in NAD+to-NADH ratio caused by lactic acidosis.
I don't think I ever could have figured this out on my own because the answer depends on knowing rates. I would have had to figure out all the math behind the physiology first. So, I don't feel too bad.
Of course, that's not the whole story. FFA production is also increased by stress hormones, which explains why DKA is often precipitated by an infection.
Also, it appears that there may be some contribution of the feeding state on the rate of ketone uptake by mitochondria. I wonder about this one though. Essentially, it's suggested that in starvation ketone uptake is accelerated by glucagon, but as we know glucagon and other catabolic hormones rise in DKA. Again, it's a question of degree, I guess. Maybe glucagon is much higher in starvation.
Two articles that should have led me to the answer are the eMedicine articles on DKA and AKA. Actually, I did look at them yesterday. Not sure why they didn't register.
Finally, I almost went down a wrong path today looking at Dr. Johan Koeslag's article on oxalaoacetate. He suggests that glycogen is a necessity in order for cells to upregulate mitochondrial metabolism. Consider, then, a cell metabolism model focused on both fuel and rate regulation. The body might interpret the lack of normal fuel as a state of exertion rather than pathology and try to upregulate mitochondria, but, unable to do this in a state of glycogen depletion, then try to increase metabolic outputs by increasing substrates. I'm not totally convinced that there isn't something here. You will find some connection between DM1, DKA, and enlarged liver from over-storage of glycogen, for instance, if you start Googling.
Anyhow, I'm done with this for now. I think my Nur464 instructor should be encouraged for getting me to back and focus on the insulin issue and not squelching my interest in physiology, as was done in previous courses. Of course, I'm probably going to fail Nur464 since this won't be on the tests, but really that's all about the Community Health course, not this little side distraction...
ketosis vs. ketoacidosis
We got let of class early today, right before the instructor was going to explain the physiology of DKA. Reviewing the book and online sources, I can't figure out what makes the difference between dietary ketosis and DKA. I understand the clinical findings, but why does the DKA patient fall into an extreme acidotic state? To see what I'm talking about, check out the clinical profiles.
I dismiss the role of lactic acidosis since, as I understand it, lactic acidosis occurs as an effect rather than cause of DKA.
This leaves two possibilities: (1) relative increased ratio of production to utilization of ketones in DKA (either absolute ratio or ratio of rate); or (2) the pH change is wholly attributable to the dehydration caused by glucosuria in DKA.
I could make a story for either of these, but it's also possible there's some other contributing factor like kidney damage that I'm missing.
Anyone have any insights? Please reply.
| ketosis | ketoacidosis | |
| insulin | ↓ | ↓ |
| ketogenesis | ↑ | ↑ |
| ketonemia | ↑ | ↑ |
| ketonuria | ↑ | ↑ |
| pH | - | ↓ |
| Anion gap | - | ↑ |
| Lactic acidosis | - | ↑ |
| glucose | ↓ | ↑ |
| gluconeogenesis | ↑ | ↑ |
| glucosuria | - | ↑ |
I dismiss the role of lactic acidosis since, as I understand it, lactic acidosis occurs as an effect rather than cause of DKA.
This leaves two possibilities: (1) relative increased ratio of production to utilization of ketones in DKA (either absolute ratio or ratio of rate); or (2) the pH change is wholly attributable to the dehydration caused by glucosuria in DKA.
I could make a story for either of these, but it's also possible there's some other contributing factor like kidney damage that I'm missing.
Anyone have any insights? Please reply.
Carnival today, ashes tomorrow
Press play before reading on...
Tomorrow is Ash Wednesday, the start of Lent. Today is Mardi Gras, and I guess Carnival has been going on in Rio de Janeiro, Brazil, since the beginning of the month...
Everyone dresses up in costume. Of course, someone had to dress up like a sexy nurse (boring), but there were also all manner of interesting costumes and floats, as displayed in this great Telegraph photo set.
Brazil's president was present at the festivities as well:
The two samba dancers chosen to dance at the head of the parade this year were older women, which is making some older women happy, although honestly, if you take a look at the photos from that Telegraph photo set above, you'll have to agree that their "older women" don't like the older women you see in your local Wal-Mart.
And of course, there are always job openings for nurses at Carnival. Actually, I am surprised at how much experience and certification they want. I guess you sort of have to rely on yourself, although you would think they have telemedicine by now...
Tomorrow is Ash Wednesday, the start of Lent. Today is Mardi Gras, and I guess Carnival has been going on in Rio de Janeiro, Brazil, since the beginning of the month...
Everyone dresses up in costume. Of course, someone had to dress up like a sexy nurse (boring), but there were also all manner of interesting costumes and floats, as displayed in this great Telegraph photo set.
Brazil's president was present at the festivities as well:
President Luiz Inacio Lula da Silva spent eight hours watching the parades staying till 5 a.m. At one point, he tossed condoms down from his box seat onto those parading, taking an active part in a government anti-AIDS campaign to distribute 65 million prophylactics this month.65 million condoms!!
The two samba dancers chosen to dance at the head of the parade this year were older women, which is making some older women happy, although honestly, if you take a look at the photos from that Telegraph photo set above, you'll have to agree that their "older women" don't like the older women you see in your local Wal-Mart.
And of course, there are always job openings for nurses at Carnival. Actually, I am surprised at how much experience and certification they want. I guess you sort of have to rely on yourself, although you would think they have telemedicine by now...
The Ship's Nurses are responsible to care for the nursing needs (routine and emergency needs) of the guests and crew. Registered Nurses with valid registration in the United States, Canada, New Zealand, Australia, South Africa, Ireland, or European Union country with a minimum of three recent years of emergency or critical care nursing experience with competency in emergency/critical care nursing care are eligible to apply. Current BLS certification is required. Current ACLS certification (Advanced Cardiac Life Support) or its equivalent, is highly recommended. Some willingness to learn simple laboratory/x-ray procedures. Must be proficient with IV cannulation and venipuncture.
Xigris : how does it work, really?
Xigris, or "recombinant human activated Protein C," is an anticoagulant used to treat septic shock. How does Xigris work?
What does Protein C do?
Protein C is a key component of the body’s natural negative feedback loop for the coagulation cascade. The final steps in coagulation are the conversion of Prothrombin to Thrombin by Factor X and Factor V. Factor X is activated by Factor VIII.
Thrombin produces Fibrin, which is the building block of blood clots, but it also activates Protein C (PC) by converting it to activated Protein C (aPC). Activated Protein C (aPC) is an enzyme that breaks down Factor V and Factor VIII. By breaking down these factors, Factor X is inhibited and Factors X and V are inhibited from producing Thrombin. Hence the negative feedback loop: as Factors V and VIII increase the production of Thrombin, Thrombin increases the production of aPC, which then decreases the production of Factors V and VIII.
Figure: Coagulation cascade.
How does this apply to septic shock?
In inflammation, blood vessels are exposed to chemicals of inflammation like Interleukins (IL) and Tumor Necrosis Factor (TNF). Inflammation makes the blood vessels "leaky," which exposes the outside of the blood vessels to blood. (Normally, only the inside of the blood vessel is exposed to blood.)
When the cells on the outside of blood vessels are exposed to blood, they release a chemical called Tissue Factor. Also, the cells on the inside of blood vessels release Tissue Factor if they are damaged by inflammation. Tissue Factor starts the coagulation cascade.
Normally, the coagulation cascade started by Tissue Factor is kept in check by the Protein C negative feedback loop.
However, in sepsis, the inflammation response occurs systemically in the body. Because it is occurring everywhere at the same time, Protein C begins to get used up. When there is no Protein C left, the coagulation cascade's negative feedback loop stops. Without the negative feedback loop, coagulation occurs systemically in the body, since the inflammation is systemic.
Systemic coagulation causes micro-blood clots in the body's small blood vessels. These micro-clots can stop blood flow to some tissues, which causes systemic tissue damage and helps lead to multiple organ failure.
By giving activated Protein C (aPC), we can artificially maintain the coagulation cascade's negative feedback loop, which helps prevent tissue damage from systemic micro-clots.
Why don't we use warfarin to treat septic shock?
Since warfarin (Coumadin) is a relatively cheap anti-coagulant, it would seem logical to use it instead of activated Protein C. However, because of warfarin's specific pharmacodynamics, it actually decreases the body's Protein C before its anti-coagulant effect starts. In patients with A-Fib or other relatively harmless conditions, a temporary decrease in Protein C has no ill effects. However, it could be dangerous in patients with septic shock.
Why don't we use heparin to treat septic shock?
Since heparin is a relatively cheap anti-coagulant, it would seem logical to use it, too, instead of activated Protein C. However, think back to the coagulation cascade for a moment. Remember that there is an "extrinsic pathway" and an "intrinsic pathway" that lead to coagulation. What do these terms extrinsic and intrinsic mean?
Essentially, the intrinsic pathway is coagulation that is started due to conditions intrinsic to the body. Think of an MI. The blood clotting that leads to an MI is started by the body's response to the conditions of its blood vessels.
On the other hand, the extrinsic pathway is coagulation that is started due to conditions outside, foreign, or extrinsic to the body. Think of a cut. The blood clotting that is produced by a cut occurs when trauma damages blood vessels.
"Heparin" is actually a collection of different molecules that work on different parts of the coagulation cascade. Some heparin molecules work on the common pathway, but the others work on the intrinsic pathway, although coagulation that occurs due to septic shock is through the extrinsic pathway.
(In fact, research on whether heparin could help in sepsis is unclear. Because many patients are already receiving heparin for DVT prophylaxis, it is hard to create a robust trial of heparin for sepsis treatment. It does appear that it is safe to give Xigris and heparin together.)
Does activated Protein C do anything else?
Besides its role in the coagulation cascade's negative feedback loop, activated Protein C also inhibits some Interleukins, which helps to decrease the systemic inflammation occurring during shock. Both the body's natural aPC and Xigris have this property. And they both also inhibit the body's PAI-1, a chemical that helps to stop blood clots from breaking up. (That's an inhibitor of an inhibitor--i.e., aPC essentially increases the body's natural tPA.)
Does Xigris treat anything else besides septic shock?
Choi et al. (2007) tried to determine whether Xigris would be effective in a single-organ treatment. Citing research showing Xigris was especially effective in the treatment of sepsis occurring from pneumonia, they tried to determine whether Xigris would have a protective effect for the lung in treating ventilator-associated pneumonia. Taking samples from several human patients, they inoculated rats with P. aeruginosa and then treated them with either aPC, tPA, or heparin and had a control group treated with saline.
Interestingly, the results indicated that while Xigris had an anti-coagulant effect, it did not have the anti-inflammatory effect described above, as measured by neutrophil density in the lung tissue. As the authors indicate, this rat model of pneumonia cannot determine effects in people either for pneumonia or for sepsis. However, citing evidence that anti-inflammatories and anti-coagulants failed to improve mortality in sepsis, the authors imply the mechanisms by which Xigris actually works (as I have described above) may not actually explain its efficacy in improving outcomes.
How is Xigris made?
Mammalian cells are genetically modified to produce Protein C. They are then grown in lab cultures. The cells excrete the Protein C (PC) into the cultures, where the culture medium converts it to activated Protein C (aPC). The activated Protein C is then purified from the culture medium. Therefore the name "recombinant [i.e., genetic recombination] human activated Protein C," or rhAPC.
What does Protein C do?
Protein C is a key component of the body’s natural negative feedback loop for the coagulation cascade. The final steps in coagulation are the conversion of Prothrombin to Thrombin by Factor X and Factor V. Factor X is activated by Factor VIII.
Thrombin produces Fibrin, which is the building block of blood clots, but it also activates Protein C (PC) by converting it to activated Protein C (aPC). Activated Protein C (aPC) is an enzyme that breaks down Factor V and Factor VIII. By breaking down these factors, Factor X is inhibited and Factors X and V are inhibited from producing Thrombin. Hence the negative feedback loop: as Factors V and VIII increase the production of Thrombin, Thrombin increases the production of aPC, which then decreases the production of Factors V and VIII.
Figure: Coagulation cascade.
How does this apply to septic shock?
In inflammation, blood vessels are exposed to chemicals of inflammation like Interleukins (IL) and Tumor Necrosis Factor (TNF). Inflammation makes the blood vessels "leaky," which exposes the outside of the blood vessels to blood. (Normally, only the inside of the blood vessel is exposed to blood.)
When the cells on the outside of blood vessels are exposed to blood, they release a chemical called Tissue Factor. Also, the cells on the inside of blood vessels release Tissue Factor if they are damaged by inflammation. Tissue Factor starts the coagulation cascade.
Normally, the coagulation cascade started by Tissue Factor is kept in check by the Protein C negative feedback loop.
However, in sepsis, the inflammation response occurs systemically in the body. Because it is occurring everywhere at the same time, Protein C begins to get used up. When there is no Protein C left, the coagulation cascade's negative feedback loop stops. Without the negative feedback loop, coagulation occurs systemically in the body, since the inflammation is systemic.
Systemic coagulation causes micro-blood clots in the body's small blood vessels. These micro-clots can stop blood flow to some tissues, which causes systemic tissue damage and helps lead to multiple organ failure.
By giving activated Protein C (aPC), we can artificially maintain the coagulation cascade's negative feedback loop, which helps prevent tissue damage from systemic micro-clots.
Why don't we use warfarin to treat septic shock?
Since warfarin (Coumadin) is a relatively cheap anti-coagulant, it would seem logical to use it instead of activated Protein C. However, because of warfarin's specific pharmacodynamics, it actually decreases the body's Protein C before its anti-coagulant effect starts. In patients with A-Fib or other relatively harmless conditions, a temporary decrease in Protein C has no ill effects. However, it could be dangerous in patients with septic shock.
Why don't we use heparin to treat septic shock?
Since heparin is a relatively cheap anti-coagulant, it would seem logical to use it, too, instead of activated Protein C. However, think back to the coagulation cascade for a moment. Remember that there is an "extrinsic pathway" and an "intrinsic pathway" that lead to coagulation. What do these terms extrinsic and intrinsic mean?
Essentially, the intrinsic pathway is coagulation that is started due to conditions intrinsic to the body. Think of an MI. The blood clotting that leads to an MI is started by the body's response to the conditions of its blood vessels.
On the other hand, the extrinsic pathway is coagulation that is started due to conditions outside, foreign, or extrinsic to the body. Think of a cut. The blood clotting that is produced by a cut occurs when trauma damages blood vessels.
"Heparin" is actually a collection of different molecules that work on different parts of the coagulation cascade. Some heparin molecules work on the common pathway, but the others work on the intrinsic pathway, although coagulation that occurs due to septic shock is through the extrinsic pathway.
(In fact, research on whether heparin could help in sepsis is unclear. Because many patients are already receiving heparin for DVT prophylaxis, it is hard to create a robust trial of heparin for sepsis treatment. It does appear that it is safe to give Xigris and heparin together.)
Does activated Protein C do anything else?
Besides its role in the coagulation cascade's negative feedback loop, activated Protein C also inhibits some Interleukins, which helps to decrease the systemic inflammation occurring during shock. Both the body's natural aPC and Xigris have this property. And they both also inhibit the body's PAI-1, a chemical that helps to stop blood clots from breaking up. (That's an inhibitor of an inhibitor--i.e., aPC essentially increases the body's natural tPA.)
Does Xigris treat anything else besides septic shock?
Choi et al. (2007) tried to determine whether Xigris would be effective in a single-organ treatment. Citing research showing Xigris was especially effective in the treatment of sepsis occurring from pneumonia, they tried to determine whether Xigris would have a protective effect for the lung in treating ventilator-associated pneumonia. Taking samples from several human patients, they inoculated rats with P. aeruginosa and then treated them with either aPC, tPA, or heparin and had a control group treated with saline.Interestingly, the results indicated that while Xigris had an anti-coagulant effect, it did not have the anti-inflammatory effect described above, as measured by neutrophil density in the lung tissue. As the authors indicate, this rat model of pneumonia cannot determine effects in people either for pneumonia or for sepsis. However, citing evidence that anti-inflammatories and anti-coagulants failed to improve mortality in sepsis, the authors imply the mechanisms by which Xigris actually works (as I have described above) may not actually explain its efficacy in improving outcomes.
How is Xigris made?
Mammalian cells are genetically modified to produce Protein C. They are then grown in lab cultures. The cells excrete the Protein C (PC) into the cultures, where the culture medium converts it to activated Protein C (aPC). The activated Protein C is then purified from the culture medium. Therefore the name "recombinant [i.e., genetic recombination] human activated Protein C," or rhAPC.
- MDConsult article on Xigris. Retrieved February 23, 2009, from http://www.mdconsult.com/das/pharm/body/122118849-7
- Medscape article on pathogenesis of septic shock. Retrieved February 23, 2009, from www.medscape.com/viewarticle/412839
- Coagulation. (2009). Wikipedia. Retrieved February 24, 2009, from en.wikipedia.org/wiki/Coagulation
- Protein C. (2008). Wikipedia. Retrieved February 24, 2009, from en.wikipedia.org/wiki/Protein_C
- Goda Choi, Jorrit-Jan H. Hofstra, Joris J. T. H. Roelofs, Sandrine Florquin, Paul Bresser, Marcel Levi, Tom van der Poll, Marcus J. Schultz (2007). Recombinant human activated protein C inhibits local and systemic activation of coagulation without influencing inflammation during Pseudomonas aeruginosa pneumonia in rats Critical Care Medicine, 35 (5), 1362-1368 DOI: 10.1097/01.CCM.0000261888.32654.6D
- M. Levi, M. Levy, M. D. Williams, I. Douglas, A. Artigas, M. Antonelli, D. Wyncoll, J. Janes, F. V. Booth, D. Wang, D. P. Sundin, W. L. Macias (2007). Prophylactic Heparin in Patients with Severe Sepsis Treated with Drotrecogin Alfa (Activated) American Journal of Respiratory and Critical Care Medicine, 176 (5), 483-490 DOI: 10.1164/rccm.200612-1803OC
- Fabián Jaimes, Gisela De La Rosa, Clara Arango, Fernando Fortich, Carlos Morales, Daniel Aguirre, Pablo Patiño (2006). A randomized clinical trial of unfractioned heparin for treatment of sepsis (the HETRASE study): design and rationale [NCT00100308] Trials, 7 (1) DOI: 10.1186/1745-6215-7-19
- Marcel Levi, Tom van der Poll (2004). Coagulation in sepsis: all bugs bite equally Critical Care, 8 (2) DOI: 10.1186/cc2816
- Warfarin necrosis. (2009). Wikipedia. Retrieved February 24, 2009, from http://en.wikipedia.org/wiki/Warfarin_necrosis
Nurses becoming prostitutes
I was doing some research for an op-ed I have to write on recruitment/retainment, when I came across this for-real article about nurses becoming prostitutes in Australia:
In the spirit of stones and glass houses, I should point out that if becoming a gigolo (gigoloing? gigolation?) was a realistic option for me, I would certainly be tempted to make this move by the bullshit of nursing school (viz., this op-ed assignment...).
EXHAUSTED and demoralised nurses would rather work as prostitutes than in Queensland's crumbling hospitals, The Courier-Mail reports.
A former registered nurse of 10 years' experience has told how she and at least four of her colleagues have found new jobs working in brothels.
"We could no longer work in such an understaffed and stressful environment," said the mother of two, who wanted to be known only as Jenna.
"I was overworked, poorly paid and a mistake could have led to charges if I caused a death," she said.
"I came to the conclusion the nursing shortage wasn't my problem but it was my responsibility to protect myself from burning out or making a fatal mistake."
...
The QNU survey also found 45 per cent of nurses had experienced workplace violence, which is more prevalent in the public and aged-care sectors than in the private sector. Jenna said violence was more of a concern in hospitals than in the sex industry.
"The security (at the brothel) is wonderful. We have buzzers in our room, there are bracelets we can request if you have a client you're a bit suspicious of."
Jenna said she had gone to great lengths to hide her new occupation from her family. "I wear my nurse's uniform to work, I carry my hospital ID. But when I get to work I change. There's a couple of others who do the same," she said.
Health Minister Stephen Robertson said it was disappointing some nurses were seeking alternative careers.
In the spirit of stones and glass houses, I should point out that if becoming a gigolo (gigoloing? gigolation?) was a realistic option for me, I would certainly be tempted to make this move by the bullshit of nursing school (viz., this op-ed assignment...).
Your Nishank Bhalla guide
When I opened up my university's homepage today, I discovered that a student named Nishank Bhalla had been given an award for his genetic research. Nishank is a really nice guy who I met in my virology class last semester. A "full course load" here is 12 credits. Nishank was taking 32 credits, and he was auditing the virology class in addition. He said maybe he wanted to work in the third world for a while after graduation. I think he should go straight to medical school so he can get out well before he's in his 30's, but that's just my opinion. (He could always do Doctors without Borders or something later...) I'm happy for him. Here's your guide to Nishank Bhalla online:
In 2007, Nishank won an award at the Sigma Xi Annual Student Research Conference. He was working on genetic material from the teeth of ancient Mayans. Here's a photo from the 2007 conference. I think he is the mustachio'd fellow in the back row...
At some point,
Nishank Bhalla
got on Facebook.
Then in 2008, Nishank again won an award at the Sigma Xi 2008 Annual Student Research Conference. He was again working on sequencing DNA from the Mayans.
I have my own piece to add, as well. Nishank was sitting in on my Bio416 Virology class last semester and running intellectual rings around the rest of us. At the beginning of the semester, he was already ready to be a TA/instructor. Here is my Flickr photo of Nishank explaining Picornavirus replication to us:
Congrats, Nishank!
In 2007, Nishank won an award at the Sigma Xi Annual Student Research Conference. He was working on genetic material from the teeth of ancient Mayans. Here's a photo from the 2007 conference. I think he is the mustachio'd fellow in the back row...
At some point,
Nishank Bhalla
got on Facebook.
Then in 2008, Nishank again won an award at the Sigma Xi 2008 Annual Student Research Conference. He was again working on sequencing DNA from the Mayans.
I have my own piece to add, as well. Nishank was sitting in on my Bio416 Virology class last semester and running intellectual rings around the rest of us. At the beginning of the semester, he was already ready to be a TA/instructor. Here is my Flickr photo of Nishank explaining Picornavirus replication to us:
Congrats, Nishank!
At the intersection of nursing and chimpanzees
Who would think that the recent story about Travis the chimpanzee, who had to be shot after attacking a woman, could have any even marginal connection with nursing?
The attack was really quite gruesome. I won't repeat, but the AP report has parts of the 911 call transcript if you want. So, what's the connection? Xanax. At least that's one theory:
The attack was really quite gruesome. I won't repeat, but the AP report has parts of the 911 call transcript if you want. So, what's the connection? Xanax. At least that's one theory:
Police said that Travis was agitated earlier Monday and that Herold had given him the anti-anxiety drug Xanax in some tea. Police said the drug had not been prescribed for the 14-year-old chimp.
In humans, Xanax can cause memory loss, lack of coordination, reduced sex drive and other side effects. It can also lead to aggression in people who were unstable to begin with, said Dr. Emil Coccaro, chief of psychiatry at the University of Chicago Medical Center.
"Xanax could have made him worse," if human studies are any indication, Coccaro said.
Stephen Rene Tello, executive director of Primarily Primates, a sanctuary for chimps in Texas, said it is difficult to say what effect Xanax would have on a chimp, but he noted that chimps and humans have similar physiology.
Investigators said they were also told that Travis had Lyme disease, a tick-borne illness with flu-like symptoms that can lead to arthritis and meningitis in humans.
"Maybe from the medications he was out of sorts," Stamford police Capt. Richard Conklin said.
A lousy camel
I'm not a huge fan of music written after, say, the development of the electric guitar, but I do have periodic enjoyment of music from my parents' heyday, for whatever reason. Anyhow, I just discovered Steppenwolf about 5 days ago, and I like it. Playing around with seeqpod, I started listening to Magic Carpet Ride and heard the line "I looked around, a lousy camel's all I found". I thought it was odd to write a song about a camel, but hey...
Last night I held Aladdin's lamp
And so I wished that I could stay
Before the thing could answer me
Well, someone came and took the lamp away
I looked around, a lousy candle's all I found
Last night I held Aladdin's lamp
And so I wished that I could stay
Before the thing could answer me
Well, someone came and took the lamp away
I looked around, a lousy candle's all I found
MRI embroidery
It's been busy for me lately, so I present just a simple image today. Becky Stern embroidered an image from her MRI...
via boingboing
via boingboing
Cory Doctorow: How to not be cxlxmx
I'm sitting here with a ton of work that needs to be done this weekend before I go to work, and guess what I'm doing? Surfing the web of course, and coming across an article by Cory Doctorow of BoingBoing about how to not be distracted by the Interwebs. Ha!
Namaste, diploma nursing
For nursing education, the wheel has come... [folding hands in namaste and bowing] ...full circle:
Via SmartBrief, comes an article in the MohaveDailyNews reporting on the increasing popularity of internships, residencies, and mentoring programs to maintain nurse retention.
These government/nursing association programs seem to suggest either that (1) nursing schools are an inherently poor forum for training in a profession like nursing, or (2) nursing schools are simply doing a crappy job. My guess is that the stress should be more on #2. There is not enough recognition of reality in nursing school: viz., daily care planning is simply not done in hospitals anymore, and work loads are maybe 5x as much as clinical loads. Care plans need to either be jettisoned altogether or be a more abstract and managerial tool used/created by the CNS. Oh, and then there's all that reflective learning BS that needs to go, too. Honestly, if you were a patient talking to a nursing instructor, would you tell her you wanted the patients to be more reflective or know med administration more thoroughly?
Via SmartBrief, comes an article in the MohaveDailyNews reporting on the increasing popularity of internships, residencies, and mentoring programs to maintain nurse retention.
...Many novice nurses like O'Bryan are thrown into hospitals with little direct supervision, quickly forced to juggle multiple patients and make critical decisions for the first time in their careers. About 1 in 5 newly licensed nurses quits within a year, according to one national study.It's funny, I was just thinking the other day about the fact that it's been about three years since I started down this path, and that in three years, if I had simply been given a stack of textbooks and had 2-3 days per week on the job training without clinical write-ups, I would probably have learned a hell of a lot more. Imagine that: 3 days per week for 3 years, plus almost unlimited time to read about physiology, pharmacology, psychology, and other relevance! That would kick ass!
That turnover rate is a major contributor to the nation's growing shortage of nurses. But there are expanding efforts to give new nursing grads better support. Many hospitals are trying to create safety nets with residency training programs.
‘‘It really was, 'Throw them out there and let them learn,''' said University of Portland nursing professor Diane Vines. The university now helps run a yearlong program for new nurses.
...Medical school grads get on-the-job training during formal residencies ranging from three to seven years. Many newly licensed nurses do not have a similar protected period as they build their skills and get used to a demanding environment.
Some hospitals have set up their own programs to help new nurses make the transition. Often, they assign novices to more experienced nurses, whom they shadow for a few weeks or months while they learn the ropes. That's what O'Bryan's hospital did, but for her, it wasn't enough.
So more hospitals are investing in longer, more thorough residencies. These can cost roughly $5,000 per resident. But the cost of recruiting and training a replacement for a nurse who washed out is about $50,000, personnel experts estimate.
...The American Association of Colleges of Nursing and the University HealthSystem Consortium teamed up in 2002 to create a residency primarily for hospitals affiliated with universities. Fifty-two sites now participate in that yearlong program and the average turnover rate for new nurses was about 6 percent in 2007.
...The federal government has jumped on the bandwagon. Since 2003, it has awarded $17 million in grants for 75 hospitals to start first-year training programs.
The National Council of State Boards of Nursing is considering a standardized transition program. It cited a study showing a link between residencies and fewer medical errors, but also pointed to the inconsistency among current efforts.
These government/nursing association programs seem to suggest either that (1) nursing schools are an inherently poor forum for training in a profession like nursing, or (2) nursing schools are simply doing a crappy job. My guess is that the stress should be more on #2. There is not enough recognition of reality in nursing school: viz., daily care planning is simply not done in hospitals anymore, and work loads are maybe 5x as much as clinical loads. Care plans need to either be jettisoned altogether or be a more abstract and managerial tool used/created by the CNS. Oh, and then there's all that reflective learning BS that needs to go, too. Honestly, if you were a patient talking to a nursing instructor, would you tell her you wanted the patients to be more reflective or know med administration more thoroughly?
Comin' to America: Marburg Hemorrhagic Fever
I like this understated headline from the RockyMountainNews: "Rare Marburg hemorrhagic fever shows up in Denver". Well, golly gee! Of all the fevers you don't want to just show up on your doorstep, Marburg hemorrhagic is one of the rarest. In fact, this is the first reported case in the United States. The CDC's Dr. Pierre Rollin (seen here and here doing field work in Africa... and by the way, you don't expect the first search hit for an infectious disease doctor to be IMDB...) says the patient recovered fully. Apparently, the case was unconfirmed until just days ago (my guess is that since the incubation period isn't longer than two weeks, the CDC was waiting to make sure the infection was contained before making an announcement).Maramagambo Python Cave
The AP article says the unidentified patient had been visiting #CDC photo removed# the "python cave" of Maramagambo Forest in Uganda and had come in contact with fruits bats. If you have any interest in hemorrhagic fevers, you will recognize that fruit bats are also the reservoir for Ebola, Marburg's cousin in the Filoviridae family, and the cave connection has been a feature of pop virology since at least The Hot Zone, which featured Kitum Cave. So why is it called the python cave, anyway?
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18-Oct-2009
EDITED PER BLOGGER DMCA POLICY:
I received a DMCA takedown notice from Blogger. Blogger set this post to "Draft" status so that it was no longer published on the web. Blogger's takedown notice didn't say what the offending material in this post was (!!), and, of this date, the notice has not been posted on ChillingEffects.org as Google's DMCA policy says it will be.
However, based on the comments section below, I'm guessing the complainant is a certain Flickr user who posted photos of a cave in Maramagambo Forest, so I'm removing his photo of the cave. That's a shame as it was a nicely illustrative photo. Complainants like this are sort of a pain. While within the letter of the law, the question of the ethics of reproducing a freely found photo is quite different. I was not obscuring authorship, I linked back to the photo's source, I don't get any financial gain of any sort from this blog, and the photo was originally published on the web for everyone to see for free.
The act of publishing in and of itself implies the intention for intellectual works to be disseminated to the public. (That's not just my idea but a component of American copyright law--it's why there is a public domain for things to eventually end up in.) So, to publish your work for free and then restrict its dissemination is sort of, um... well, how would you put it?
As an aside:
Some commenters on this post were upset by the offhand way I say it was "stupid" to visit the cave (see below). I didn't mean so much to call the photographer, per se, stupid (as I don't know the circumstances of the photo and the photographer--for example, perhaps the photographer had never even heard of these sorts of viruses before visiting Uganda) as to call the whole business of visiting these caves a general stupidity. Commenters said, essentially, "hey, we're not stupid 'cause the photos were taken before the government said the fruit bats were a possible reservoir for the virus." I would like to point out, however, as The Hot Zone was published in the early 1990s and identified caves like this as a likely source of the virus, I find it impossible to believe there wasn't long-standing scientific speculation about these caves. This doesn't make specific tourists stupid, but it does make a case for the general stupidity of these cave visits.
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... stupid people! Actually, it's hard to imagine, but the [now removed] photos... were potentially taken within a few feet of a virus that could kill thousands or millions of people throughout America or Europe. In fact, the international community recognized this, and Uganda closed down tourism to the python cave after another tourist from The Netherlands brought Marburg back to Europe and died last summer.
Lutheran Medical Center
The patient was cared for at Lutheran Medical Center in Wheat Ridge, CO, # photo removed # a 400-bed hospital employing about 500 Registered Nurses and 5 Nurse Practitioners. As part of a protocol for an unknown infection, they followed standard contact precautions, including gowns and gloves. I was just thinking that at my hospital "standard precautions" really just means gloves and actually gloves only when making certain types of patient contact. Maybe this patient's symptoms were such that they took more precautions with him. The CDC has posted guidelines for US health care workers dealing with viral hemorrhagic fevers and linked to it from their Marburg page.
A 2003 study in Emerging Infectious Diseases could identify only two risk factors for contracting Marburg. One was working as a miner and the other was receiving an injection. So, as long as a nurse doesn't have a needle-stick incident, contraction probably isn't too big a worry. In fact, of the all health care workers who were enrolled in the study, none had antibodies for Marburg: "Types of patient contact included administering injections (38%); cleaning up blood, vomitus, urine, or feces (28%); washing bed clothes (7%); washing corpses (6%); and receiving a needlestick injury (2%)."
VSV-G vaccines and tetherin
But what if you were a nurse who had a needle-stick incident? Well, right now you'd be screwed, I think. But maybe in the near future, there will be a prophylactic. Feldmann et al. (2007), working with the related Ebola virus, were able to protect monkeys from lethal doses of virus by using a post-exposure dose of vaccine created by integrating an Ebola glycoprotein into a vesicular stomatitis virus: "treatment is particularly suited for use in accidentally exposed individuals and in the control of secondary transmission during naturally occurring outbreaks or deliberate releases." And although Feldmann et al. were working with Ebola, Daddario-DiCaprio et al. (2006) produced a similar experiment using the Marburg glycoprotein. This 2006 study looked at the efficacy of this antigenic delivery method as a preventive vaccine, but since the 2007 study uses the same essential methodology in a post-exposure context, it seems highly likely that a post-exposure treatment for Marburg could be created as well.
An emerging treatment option that has just been published in February and March issues of Journal of Virology involves the use of tetherin (formerly CD317), a cellular component that keeps new virions from detaching from infected cells. (See some great photos of budding Ebola virus at PLoS Pathogens.) Two teams (Sakuma et al & Jouvenet et al) found that tetherin has specific action on a spectrum of viruses including Marburg. However, Vincent Racaniello over at virology blog recently blogged a PNAS article showing that Ebola glycoprotein inhibits tetherin activity on the cell surface.
The announcement of this whole Marburg episode occurs just shortly after a Filipino man contracted Ebola from pigs...
- Bausch DG, Borchert M, Grein T, Roth C, Swanepoel R, Libande ML, et al. (2003). Risk Factors for Marburg Hemorrhagic Fever, Democratic Republic of the Congo Emerging Infectious Diseases, 9 (12)
- K. M. Daddario-DiCaprio (2006). Cross-Protection against Marburg Virus Strains by Using a Live, Attenuated Recombinant Vaccine Journal of Virology, 80 (19), 9659-9666 DOI: 10.1128/JVI.00959-06
- Heinz Feldmann, Steven M. Jones, Kathleen M. Daddario-DiCaprio, Joan B. Geisbert, Ute Ströher, Allen Grolla, Mike Bray, Elizabeth A. Fritz, Lisa Fernando, Friederike Feldmann, Lisa E. Hensley, Thomas W. Geisbert (2007). Effective Post-Exposure Treatment of Ebola Infection PLoS Pathogens, 3 (1) DOI: 10.1371/journal.ppat.0030002
- N. Jouvenet, S. J. D. Neil, M. Zhadina, T. Zang, Z. Kratovac, Y. Lee, M. McNatt, T. Hatziioannou, P. D. Bieniasz (2008). Broad-Spectrum Inhibition of Retroviral and Filoviral Particle Release by Tetherin Journal of Virology, 83 (4), 1837-1844 DOI: 10.1128/JVI.02211-08
- T. Sakuma, T. Noda, S. Urata, Y. Kawaoka, J. Yasuda (2008). Inhibition of Lassa and Marburg Virus Production by Tetherin Journal of Virology, 83 (5), 2382-2385 DOI: 10.1128/JVI.01607-08
Journals in public health
If you are a resourceful and interested nursing student, you will not have any problem finding articles in public health. However, if you are not, here is a hint for you: try open access.
First of all, be aware of the Online Journal of Rural Nursing and Health Care. I think it is one of the first (and maybe the first) open access nursing journal.
Second, BioMed Central now hosts a large amount of public health and systems-oriented journals. For example:
First of all, be aware of the Online Journal of Rural Nursing and Health Care. I think it is one of the first (and maybe the first) open access nursing journal.
Second, BioMed Central now hosts a large amount of public health and systems-oriented journals. For example:
- Australia and New Zealand Health Policy
- AIDS Research and Therapy
- BMC Ecology
- BMC Health Services Research
- BMC International Health and Human Rights
- BMC Nursing
- BMC Public Health
- Conflict and Health
- Cost Effectiveness and Resource Allocation
- Environmental Health
- Epidemiologic Perspectives & Innovations
- Globalization and Health
- Health and Quality of Life Outcomes
- Health Research Policy and Systems
- Human Resources for Health
Most self-serving comment from an instructor
In one of our courses, there is confusion over the syllabus. What, exactly, are the assignments and when are they due? We had a post-conference tonight with a clinical instructor who said that she's done this course for seven years and that there are always complaints about the syllabus. We had to understand, she said, that the syllabus was a learning exercise in critical thinking--we're supposed to read it and "figure out" what we're supposed to be doing.
What??!!
I've been matriculated at several institutions, including a highly regarded one, and I've been taking undergraduate courses for nigh on a decade now. Never, never, have I heard such a dishonest, cowardly, self-serving comment, and never have I had a professor who has suggested that the syllabus is a critical learning tool. This program is incredible! And I mean incredible as in, I can't believe she just said that...
What??!!
I've been matriculated at several institutions, including a highly regarded one, and I've been taking undergraduate courses for nigh on a decade now. Never, never, have I heard such a dishonest, cowardly, self-serving comment, and never have I had a professor who has suggested that the syllabus is a critical learning tool. This program is incredible! And I mean incredible as in, I can't believe she just said that...
Taza chocolate
I've gotten tired of things like Lindt, which I find to be over-hyped. There's a lot of disappointing chocolate out there. And you usually end up eating more than you want/need when the quality is low. At least, I do.
I had some Green & Black's a while back and thought it was pretty good, so I went to the local food co-op only to discover that they weren't carrying it anymore. Not green enough? Too pricey? Who knows. Anyhow, the proprietress suggested I try Chocolove, and the co-op also had a "stone ground" chocolate in nice packaging (as seen above). So, I picked up 33% and 55% Chocolove bars, and the 70% stone ground bar, which is made by a company called Taza.
The Chocolove milk chocolate was disappointing (hard dry texture, with excessive caramel-like flavor and weak strength in general), but in their defense, I noticed too late that it was marked "Best if sold before January 2009." The Chocolove dark chocolate was fairly okay (sell by May 2010).
I was really looking forward to the stone ground Taza chocolate. I imagined it would have a raw, earthy flavor. It did not. I was actually shocked at my first bite. Disappointed. I felt like I had been taken. Not at all the foresty, root-dirt flavor I imagined it to be, the stone ground chocolate was almost sour. If I had been told it was something besides chocolate, I would have believed it.
But not one to trust in my own instincts after being raised on Hershey's and Lindt--although here I have to digress to say that I was an early recognizer of the fraud that is Toblerone, though other peers in my hometown thought it was great when newly imported some years ago--I decided to wait a couple days and try it again.
Again, bleh, but not quite so bleh. This time, after two pieces each of Chocoloves and 2 of Taza, I had had 6 pieces of chocolate and was unsatisfied, so I went online to find out more about chocolate production and discovered that, while I always thought chocolate came from a bean/plant similar to coffee, it actually comes from the seeds of big pods that look like this:
I tried two pieces of Taza again tonight after dinner. Okay, I can see how this might be enjoyable, I thought, but I'm still not getting it. However, after a little reading on the subject, I discovered that Taza's flavor comes from its relative lack of processing. It is lightly roasted and not treated to blend the cocoa butter as much. Actually, the whole thing makes sense to me. When I was a Boy Scout, we went on an overnight wilderness survival trip where we tried to scavenge acorns for dinner. Oh my goodness, they are horrible!! If you don't roast acorns, they have an overpoweringly sharp bitter/sour quality. We tried to boil it out, but no go. The cocoa seeds must be similar--if you roast them long, it removes more of the sharp qualities. A lighter roast leaves more of the seed's inherent flavor in the chocolate.
Anyhow, after more consideration, I came to the conclusion that Taza is neither better or worse than other fine chocolates. It is something a little different. And I've been pleased to see that other more knowledgeable reviewers essentially agree with my assessment of the taste:
David Lebovitz: "decidedly on the fruity side rather than 'roasty', like so many other chocolates."
Casey Meshbesher: "the flavor really is a barrage of fruity juices, champagnes, and vinegar."
(Well, I don't know about champagne, but fruit and vinegar sound right.)
In addition to Taza's chocolate bars, they also offer inside views of their chocolate-making process on their website and sell roasted or unroasted cocoa. I think it would be fun to be able to have a spread of unroasted cocoa, different roasts of cocoa, and the pure chocolate made from them, all from different growers, to be able to taste the differences that the processing imparts. Maybe when I win the lottery.
This is not the end of CxLxMx
Amazingly, I passed the aforementioned pharmacology test! Now there just the HESI next week!
Is this the end of CxLxMx?
In about a 1/2 hour, I have to take a pharmacology test that's being given in my "Issues in Nursing" class. Since I haven't had clinicals since last spring and was counting on using extra free time from cutting back on work to review pharm all this semester, I'm not ready yet. The test requires a 90% (or, presumably, you don't pass the class/graduate). That won't happen today. When will it happen? If it doesn't, what will happen? Will I be out of the program?
I'm a little annoyed as I think this is a self-serving move on the part of the nursing department here. After all, I have passed the previous Med-Surg, Psych, Maternity, etc. classes. That indicates I have the ability to master the material. And it's the responsibility of the national NCLEX boards, and not individual nursing schools, to ensure competent practice at an individual level. It seems to me that the purpose could only be to wash people out of the program, which should theoretically raise the school's scores in NCLEX pass rates. That's what they do at the local community college, which has comprehensive exit exams and high NCLEX pass rates. I don't think it's ethical anyhow. If you're going to boot someone, you don't wait til the semester before graduation to do it.
I'm a little annoyed as I think this is a self-serving move on the part of the nursing department here. After all, I have passed the previous Med-Surg, Psych, Maternity, etc. classes. That indicates I have the ability to master the material. And it's the responsibility of the national NCLEX boards, and not individual nursing schools, to ensure competent practice at an individual level. It seems to me that the purpose could only be to wash people out of the program, which should theoretically raise the school's scores in NCLEX pass rates. That's what they do at the local community college, which has comprehensive exit exams and high NCLEX pass rates. I don't think it's ethical anyhow. If you're going to boot someone, you don't wait til the semester before graduation to do it.
Superbowl XLIII commercials
This afternoon is supposed to be Superbowl XLIII. I've never watched the Superbowl. In fact, I don't think I've ever watched a football game from start to finish. Once, when I young many years ago, before the death of one of my father's friends, there was some sort of bowl game that we had a party for. I remember being extremely excited over chips, dips, soda, burgers, dogs, ice cream, etc., and then disappointed over not be allowed to spend the entire game eating (which is what I thought the point was).
Anyhow, the following commercial was supposedly pulled from the line-up this year.
Anyhow, the following commercial was supposedly pulled from the line-up this year.
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