cosmetic neurology

This is an interesting paper by Dr. Chaterjee, a very well respected neurologist. I find this subject matter endlessly fascinating, ultimately I do not think there is a difference between therapy and enhancement but in their use. I put my perspective/comments in green!

University of Pennsylvania

ScholarlyCommons

Neuroethics Publications Center for Cognitive Neuroscience

8-1-2004

Cosmetic Neurology: For Physicians the Future is Now

Anjan Chatterjee

University of Pennsylvania, anjan@mail.med.upenn.edu

Published in Virtual Mentor: Ethics Journal of the American Medical Association Volume 6, Number 8.

Publisher URL: http://www.ama-assn.org/ama/pub/category/12799.html

Basic neuroscience and neuropharmacology are beginning to yield therapies for cognitive disorders. While we can eagerly anticipate treatments for dementing illnesses, stroke, traumatic brain injury, and developmental abnormalities, these very treatments raise uncomfortable questions. If we can improve cognitive systems in disease, can we also do so in health? Should we practice cosmetic neurology?

I do not agree with the set up because it frames anything outside of treating an acute decrease in health, i.e. -disease, as "cosmetic". The word cosmetic is taken from the greek kosmetikos, meaning to adorn, that usage connotes a preoccupation with the exterior. I believe improving our cognitive systems is the same as "improving" our blood pressures, nutrition, or life spans.

The possibility of “better brains” has captured the imagination of the press, policy pundits, and ethicists [1-10]. With few exceptions, physicians have not contributed to these discussions, despite their central role in this unfolding drama [11,12]. Cosmetic neurology includes the use of botulinum toxin to brush away wrinkles.

I'll agree, using botox for wrinkles seems less "necessary" than using it for migraines or dystonias.

However, it also alters how we function and feel, rather than just how we look. Many interventions to improve cognitive and emotional systems are available now, and others are on the horizon. The risks and benefits of newer medications remain to be worked out. However, we can assume that some version of these medications will be relatively efficacious and safe. The accompanying article on neuroethics by Martha Farah reviews the anticipated pharmacopeia of cosmetic neurology and the deep ethical concerns raised for individuals and society (also see [12]). The focus here is on the role of the physician in managing the use of cosmetic neurologicinterventions.

Framing the Issue: the Purpose of Medicine

Ethical discussions of cosmetic neurology often frame the issue as one of therapy versus enhancement [6,13]. Therapy treats disease and enhancement improves normal abilities. Most people consider therapy desirable. By contrast, many pause at enhancement. Francis Fukayama, for example, opines, “the original purpose of medicine is to heal the sick, not turn healthy people into gods” [14].

So I'll take issue with Fukayama's quote, which in my opinion is hyperbole. I believe the underlying assumption that guides an ethical pursuit of enhancement is that mankind is mortal and can never be "gods" moreover that is not the purpose of improving "normal" function. The purpose for improving normal function is create opportunity for the growth, development, and evolution of our existence. Also, "normal" is a statistical measure of central tendency, it is descriptive- think how the "normal" human lifespan has improved over the last millennia, no one argues against pursuing this similar "enhancement". Again "healthy" people are defined by their state of health, derived from heilen, meaning "whole", but that definition does not indicate what the whole is.

He suggests that public policy should restrict research for enhancement.

...and as a consequence risk falling behind those that do.

For 2 reasons, the distinction between therapy and enhancement is less useful than one might hope. First, notions of disease often lack clear boundaries. For example, if individuals of short stature can be “treated” with growth hormone [15], does it matter whether they are short because of a growth hormone deficiency or because of other reasons [13]?

I agree, in most cases no- it would not matter.

Second, promoting research for therapy and restricting it for enhancement ignores the simple fact that research in one often applies to the other. The therapy versus enhancement distinction also obscures what for physicians may be the critical question:

What is the purpose of medicine? The strength of allopathic medicine has been its scrutiny of disease mechanisms. Understanding the biology of malfunction provides insight into how to fix that malfunction. Despite its undoubted successes, this approach has limits. Most notably, the quality of patients' lives does not always correspond well to biomarkers and symptoms of disease. The symptoms of Parkinson's disease that are most responsive to dopamine agonists are not those that bother patients most [16]. Measures of disease activity may not be the best indicator of the impact of multiple sclerosis on patients [17]. Recognizing the limits of clinical and pathological indices, assessing patients' quality of life is now a routine practice in therapeutic trials. Such assessments seem eminently reasonable. After all, the point of treating a disease is to improve patients' quality of life. However, if a purpose of medicine is to improve quality of life

for people who happen to be sick, then why not apply medical knowledge to improve the quality of life of those who happen to be healthy?

Inevitability

Cosmetic neurology raises several serious ethical concerns. These interventions challenge fundamental notions of character and individuality; it is likely that they will be used coercively, and cosmetic neurology will not lessen the burden of distributive justice in a country in which the quality of health care is polarized by economic class. It is improbable, however, that cosmetic neurology will be restrained significantly by journalistic consternation, religious admonition, and government regulation. More likely, such restraints will be overwhelmed by free markets and military innovations.

Excellent paragraph, issues of coercion and distributive justice must be addressed but are not grounds for restricting the investigation into the field. I think what has come from

the field of reproductive endocrinology can inform how we implement advances in this field.

The market.

Pharmaceutical companies stand to make substantial profits and will probably support social pressures that encourage wide use of cosmetic neurology. According to Carl Elliott, in 2001 GlaxoSmithKline spent $91 million dollars in direct advertising to consumers for its medication Paxil [8], more than Nike spends on its top shoes. Advertisements for better brains would undoubtedly prey on an insecure public. Gingko Biloba, despite underwhelming effects on cognition [18], is a billion dollar industry. Pharmaceutical companies are not oblivious to the marketing possibilities of new “interventions” that could apply to the entire population [19, 20]. Sadly, the academy is unlikely to restrain Industry.

But I don't think this is the academy's role.

Scientific leaders who discover new therapeutic possibilities are quick to stake biotech claims [20]. Joint ventures between universities and pharmaceutical companies are increasingly common.

The military. Imagine a soldier who is stronger, faster, more enduring, learns more quickly, needs less sleep, and is not hampered by disturbing combat memories. The military's deep interests in cognitive enhancements date back to “go-pills” (amphetamines) for World War II soldiers [20], and continue to the present [20, 21]. For example, military investigators found that modafinil [a wakefulness-promoting agent] has its greatest effects in helicopter simulation performances at the combined nadir of sleep deprivation and circadian troughs [22]. Relevant findings from military research are likely to trickle down to civilians. Over-fed Hummer vehicles maneuver through the cobbled streets of Philadelphia. Perhaps Hummer brains are around the corner.

Seems a bit glib, lots of great technologies had their roots in the military, the internet -for one. Hummers were originally popularized by a movie actor and civilian, Arnold Schwarzenegger, and this was long before the masses used these vehicles as a proxy for their manhood.

The Role of Physicians

Americans believe that the pursuit of happiness is an inalienable right. This pursuit assumes we know what constitutes happiness [23]. Fame and fortune have been standard proxies for happiness in American culture. Better brains may very well join the list, either as a means to fame and fortune or as a direct source of happiness [24]. Scientific, economic, marketing, and regulatory forces are likely to shape the role physicians will play. The details are difficult to predict, but what is certain is that physicians will engage in cosmetic neurology.

Again, I take issue with calling this practice "cosmetic neurology", these issues are much deeper than that!

This practice will be complicated by the fact that physicians will not be able to rely on the conventions of traditional practice. Neurologists may have special understanding of the potential risks and benefits of quality of life interventions that work through the nervous system, but they have no special insight into the underpinnings of happiness. One plausible scenario is that physicians will become quality-of-life consultants.

But I would posit that the physician as quality of life consultant is already the case in many specialties. In past eras physicians once even had moral authority to say what is right and wrong. For these reasons I do not believe that we will be able to rely on conventions of practice.

Physicians might offer a menu of options, with the likely outcomes and the incumbent risks stated in generalities. The role would be to provide information while abrogating final responsibility for decisions to patients.

This reminds me of a lecture during 2nd year of medical school discussing the new paradigm in American healthcare writ large. The demise of paternalistic medicine gave rise to the autonomous patient and the "provider" (read technician, not physician) role being as stated above. The meat of Dr. Chatterjee's statement I believe is the physician abrogation of final responsibility. This is akin to "buck passing" and its a phenomenon in the new era of medicine that I believe is creating major identity problems for physicians. When I was and when I will again be the patient, I want a physician who takes final responsibility for my health, it is the physician opinion that I want. So when a patient asks, "do you think i should take this pill to make me smarter?", in addition to informing risks/benefits I would take a stance, "I think you should/should not... because...xyz, and that is my medical opinion."

Abrogation of such responsibility is promoted by current practice norms. Financial incentives in medicine are now driven by paper trails and diagnostic studies, rather than by personal engagement with patients.

Sad but true and hopefully unsustainable in the long run.

A comfortable stance would be to let people decide for themselves. After all, isn't autonomy what patients want? It turns out that the degree of autonomy patients want is not so clear, especially when they are sick (as reviewed in [25]). Furthermore, the bewildering array of choices available to American consumers in almost every domain of life is a source of considerable anxiety [26 ]. A practice of medicine that encourages patients to be consumers is in danger of compounding these anxieties. I am not advocating that physicians become disengaged purveyors of quality-of-life elixirs. I am suggesting that this role is a distinct possibility given current trajectories of medical practice. In a litigious society, many physicians would gladly shed the irksome traditional mantle of beneficence.

Where do you stand?

Since 1997, the FDA has permitted direct marketing to consumers. Physicians can anticipate facing questions from “patients” and advocacy groups in which distilling principle from prejudice is not easy. To make these issues concrete, I invite readers to consider the following questions.

1. Would you take a medication with minimal side-effects half an hour before Italian lessons if it allowed you to learn the language more quickly?

Market cap $25billion.

2. Would you give your children a medication with minimal side-effects half an hour before piano lessons if it allowed them to learn better?

Not until long term data came out about safety and adverse events with respect to their growth and development. e.g. - stimulants used as treatment for ADHD were found to make kids physically smaller (height and weight) at 10/20 yr follow up. Second, the child can decide for themselves when they are no longer a minor. It could be argued that having a beer or beta blocker before recital may make them perform better, but no one is credibly supporting that idea in a child either.

3. Would you pay more for flights whose pilots were taking a medication that made them react better in emergencies?

I would be happy to if it was shown to reduce the risk of death.

4. Would you want residents to take medications after call nights that would make them less likely to make mistakes in caring for patients because of sleep-deprivation?

Planning on at least trying this, but I believe (anecdotally) that one will eventually need to pay the sleep debt. I think that would be a great investigation, whether or not these medications reduce errors resulting from sleep deprivation. But I think another question in this debate is whether we should treat sleep deprivation, or prevent it!

5. Would you take a medicine that selectively dampened disturbing memories?

Great question!! Maybe...

This article has put forward legitimate concerns regarding the ethical practice of medicine where it relates to improving the healthy. For me, there have yet to be any convincing arguments against

the use and development of enhancing agents save for adverse events. Maybe one question worth asking is, given that these agents are not good or bad except for how they are used, would it be

right to use them knowing that most use could be "bad"?

This is such an exciting topic,

References

1. Groopman J. Eyes wide open. The New Yorker. December 3, 2001. 52-57.

2. Marcus S. Neuroethics: Mapping the Field. New York: Dana Press; 2002.

3. Rose S. Smart drugs: do they work, will they be legal? Nature Reviews Neuroscience. 2002;3:975-979.

4. The ethics of brain science: open your mind. The Economist. May 25, 2002; 77-79.

5. Farah MJ. Emerging ethical issues in neuroscience. Nature Neuroscience. 2002;5:1123-1129.

6. Wolpe P. Treatment, enhancement, and the ethics of neurotherapeutics. Brain and Cognition. 2002;50:387-305.

7. Plotz D. The ethics of enhancement. Slate. March 12, 2003. Accessed July 27, 2004.

8. Elliot C. American bioscience meets the American dream. The American Prospect. 2003;14:38-42.

9. President's Council on Bioethics. Beyond Therapy: Biotechnology and the Pursuit of Happiness. Washington, DC; President's Council on Bioethics. 2003. Accessed July 27, 2004.

10. Baily R. The battle for your brain. Reasononline. February 2003. Accessed July 26, 2004.

11. Whitehouse P, Juengst E, Mehlman M, Murray T. Enhancing cognition in the intellectually intact. Hastings Center Report. 1997;27 (May-June):14-22.

12. Chatterjee A. Cosmetic neurology: the controversy over enhancing movement, mentation and mood. Neurology. 2004 (in press).

13. Daniels N. Normal functioning and the treatment-enhancement distinction. Cambridge Quart Healthcare Ethics. 2000;9:309-322.

14. Fukayama F. Our Posthuman Future. New York: Farrar, Straus & Giroux, 2002.

15. Cuttler L, Silvers J, Singh J, et al. Short stature and growth hormone therapy: a national study of physician recommendation patterns. JAMA. 1996;276: 531-537.

16. Harris Interactive. Inc. The impact of Parkinson's disease on quality of life. Online Survey. 2003.

17. Nortvedt M, Riise T. The use of quality of life measures in multiple sclerosis research. Multiple Sclerosis.

2003;9:63-72.

18. Solomon P, Adams F, Silver A, Zimmer J, DeVeaux R. Ginkgo for memory enhancement: a randomized controlled trial. JAMA. 2002;288:835-840.

19. Langreth R. Viagra for the brain. Forbes. February 4, 2002: 46-52.

20. Hall S. The quest for a smart pill. Scientific American. 2003;289:54-65.

21. George M. Stimulating the brain. Scientific American. 2003;289:67-77.

22. Caldwell JJ, Caldwell J, Smythe NR, Hall K. A double-blind, placebo-controlled investigation of the efficacy of modafinil for sustaining the alertness and performance of aviators: a helicopter simulator study. Psychopharmacology. 2000;150:272-282.

23. Elliot C. Better than Well: American Medicine Meets the American Dream. New York: WW Norton & Company; 2003.

24. Kass L. The pursuit of biohappiness. Washington Post. October 16, 2003: A25.

25. Schneider C. The Practice of Autonomy: Patients, Doctors and Medical Decisions. New York: Oxford Press; 1998.

26. Schwartz B. The Paradox of Choice: Why Less Is More. New York: Ecco, 2004.

Anjan Chatterjee, MD, is associate professor in the Department of Neurology and a faculty member of the Center for Cognitive Neuroscience at the University of Pennsylvania, Philadelphia, Pa.

medicine rotation reflection...

i couldn't figure out why i was so tired at the end of every day. then the answer was given to me one evening when my sig. other said to me when i was staring blankly off into the distance, "dude you are out to lunch right now, you look emotionally exhausted" thats exactly it- people in milstein are going through so much it just takes its toll after a while.

-als patient who has to use eye movements to communicate every last thing, "itch her, thirsty, cramping, done..."

-guy who had traumatic brain injury, and is brain dead but kept alive

-guy with pulmonary issue who yells "i wanna die, i wanna die i wanna die" over and over and over (especially when we round) -he died

-woman who took previous guy's room w/CHF who can't recline past 45degrees or suffocates, "do you know what its like to want to die?", "please let me die" -she dies too

-undocumented woman w/no known family from mexico who is unresponsive and sits in mckeen for 100+ days and counting..."

-guy out of prison after 10 year stint w/drug problem and a-fib who doesn't take meds and elopes in the middle of one night despite not being able to walk >200ft without hacking

-woman w/MS with one functioning (but paretic) distal upper limb.

-woman stuck in nursing home with (choose at least one) pneumonia/sepsis/altered mental status/dementia/infected wound/vomit x10

-women w/cirrhosis and renal failure refusing dialysis for reason, "god will save me if its not my time, you doctor's don't care about anythings except money"

-women w/ severe mental retardation who is medically ok but all care is done by aging mother...

-woman (age 65, young!) w/cancer x2 and renal failure who is deaf and shivering literally falling apart

-alcoholic guy (with wife kids and other girlfriend) who drinks himself into acute pancreatitis and is demanding and entitled

the patients on our particular service average 80+ years old and are chronically sick. many of there health problems exist because of poor social situations.

i get the sense that the physician-patient relationship in inpatient medicine differs greatly compared to the outpatient setting. i put myself "in the patient's bed", like this one woman was visited by so many people one day (~20) its hard to keep track of who is doing what. consider the fact that the attendings dont spend as much time with the patients (like a few minutes in the morning x10 patients per service= less than an hour a day at best), the resident's have to rotate and cross cover so the patient never knows who's who and where's what, plus there is the cast consulting physicians, nurses, pt, ot, respiratory, speech and swallow, social worker. its a real production. this rotation has shown me that inpatient medicine is a lot like general contracting, and much of the day's work consists in lining things up for a client's project (in this case the patient's health). my conception as physician as a moral authority who sits at the bedside and chats w/patients about their children or swaps recipes and smiles and is generally happy emotionally available etc etc has been greatly challenged- a lot of "physicians" are specialty technicians, and the patient can see many "doctors" in one day. its probably because milstein is an incredibly busy place, i can't wait to try out another hospital and see how the physician/patient relationship differs.

renal clinical notes

renal notes

immune complex GN

post strep/infectious

SLE (full house)

MPGN (HCV)

IgA nephropathy

anti-GBM (very fast onset)

affects renal, lung or both (goodpastures)

pauci immune

vasculitis

sore throat + GN same day = IgA (no time lag)

sore throat + GN later = post strep

microscopic polyangiitis - lungs are whited out

wegener's - lung nodules

systemic disease (nodules, purpura, ulcers, sinusitis)

Pulmonary and Renal

lung vasculitis - lupus, henoch schonlein purpura, wegeners, microscopic polyangiitis

pneumonia/sepsis major cause of ATN

ANCA is to RPGN as antiDNA is to lupus

tx of vasculitis - cytoxan + steroids + plasmapharesis

IgA nephropathy -renal

HSP - systemic

IgA nephropathy treatment - ACEi

if > 1gm protein in urine 50% loss of renal function in ten years

Lupus - endocaopillary proliferation

Serum complement is low with

MPGN

Lupus

Post infectious

Complement is normal with

IgA neph

anti-GBM

ANCA-RPGN/Wegeners

Anemia + decrease plts? could be thrombotic microangiopathy

when doing a kidney biopsy a drop in Hgb of 1.0g/dL is no problem

radiology lecture

dont need chest ct for pneumonia should be able to use cxr, persistent pneumonia is indication for chest ct

indications

known interstitial lung disease

f/u to therapy

lung ca staging

immunocompromised

for pulmonary embolism test is CTA

aneurysm ask for contrast and noncontrast, noncontrast first to see acute blood

ascending aorta is surgical management, descending is medical management

anterior mediasinal mass differ

Teratoma

Terrible lymphoma

Thymoma

Thyroid tumors

Thoracic aorta

air bronchograms are airways traversing through consolidated lung - alveoli are filled

clinical notes

80% of all GI bleeds UGIB - dx includes PUD, varices, AVM, GAVE, gastritis

fecal antigen test for H. pylori ~100% sensitive

pepto bismo makes stool look melanic

mycobacterial infections increased in north carolina because greater numbers of them in the soil

anti dsDNA antibodies used to monitor lupus

doing an LP? send for VZV, EBV, HSV, AFB, bacterial, india ink, toxo, jc and lyme

"cant correlate response to tx of crypto meningitis by using titers, use clinical symptoms, you can follow serum titers"

tx amphotericin and fluconazole

ICP>25cm should be drained

HCV Ab takes ~12wks to seroconvert but when do are 98% sensitive

acute HAV big rise in ALT ~2months,

dont be fooled- hep B surface antibody can go away (become undetected) patient still has immunity

HBV mainly sexually transmitted disease

tx - IFNalpha2b nucleotide/side inhibitors,

pros - 1 year treatment, increased clearance

cons - subq injection, depression/psych side fx

15-40% will clear acute HCV infxn

normally transmitted parenterally (blood to blood)

test is elisa if + then look for RNA,

HCV elisa false negative w/early test and immunosuppressed

normal ALT does not rule out HCV

HCV tx PEG-IFNalpha

random fact - dysgeusia - an alteration in taste

c. diff colitis can occur 6months after abx

mammography guidelines - 40-50 nada (would need to expose 3000 women to ten years of radiation to pick one cancer)

50-60 every two years, 60+ yearly

mammography not a great screen for young denser breast tissue anyway

Mollaret's meningitis - recurrent HSV-2 mediated

"gastric ulcer bleeding is arterial- not venous"

"an ulcer in the antrum is almost never cancerous"

ulcer healing while on PPI ~90%, while on ranitidine/famotidine -85%

when you get ulcers in the antrum the problem is pyloric stenosis

risk of PUD - bleeding and perforation

Obstruction? differential - malignancy, crohn's, pancreatitis, gastric polyp, tb, gastric bezoars (foreign body)

IgG4 deficiency predisposes to atelectasis

heard on the wards-

"patient complains of losing hearing? check the ear for cockroaches"

senna/docusate - softens bowel movements

dulcolax/miralax/enema -heavy duty

"don't give epi/terbutaline for asthma exacerbation to patient w/htn and h/o cad or other risk factors, iatrogenic MI well described"

pulmonary

contraindications to permissive hypercapnia

1. pregnancy

2. increased ICP

heliox - 70/30 blend of helium and o2 allows for more laminar flow, have to reset ventilator settings

inhaled anesthetics are great bronchodilators

ascites photo borrowed from internet

This patient presented with alcoholic cirrhosis and a MELD score of 19. His management involves normalizing several aspects of his physiology. I would like to take the time to review the pathophysiology of cirrhosis as it applies to this case. The word cirrhosis derives from the greek kirrhos meaning tawny or brown/orange. This is because cirrhotic livers have a burnt brownish orange appearance. Physiologically, cirrhosis is an irreversible fibrosis of the liver whereby the cellular architecture is destroyed and unable to be regenerated. As a result dysfunctional nodular tissue forms in place of viable parenchyma, and this ensuing disordered tissue greatly increases intrahepatic vascular resistance. This resistance creates a pressure gradient between the portal vein and hepatic, the so-called hepatic vein portal gradient (HVPG). Because passage through portal circulation is greatly impeded over time, the HVPG increases. When the gradient reaches ~12mmHg, a diagnosis of portal hypertension can be made, although clinical symptoms are not usually apparent until this gradient is greater than 20mmHg¹. The portal hypertension is necessary for the accumulation of fluid in the peritoneal cavity, ascites. Specifically, ascites comes as a direct result of this increased HVPG. A sustained HVPG over time develops porto-systemic collaterals through angiogenic mechanisms. These new shunts in addition to the known shunts (gastric vein, rectal vein, umbilical veins) greatly decrease systemic vascular resistance and increase cardiac output. Also the increased pressure in the portal system in concert with increased levels of bacterial endotoxin from decreased portal flow has been found to induce high levels of NO release from the endothelium. This NO release is the prime mechanism for the great splanchnic vasodilation found in cirrhotic patients with ascites. Thus the portal system becomes greatly dilated and “stopped up” while the systemic circulatory systemic becomes one of high flow and low resistance. This high flow system also reduces mean arterial pressure thus decreasing the carotid and renal baroreceptor “stretch” and activating the neurohumoral responses of the renin angiotensin-aldosterone activating system (RAAS), sympathetic activation and ADH. Chronic activation of these factors leads to sodium retention and an inability to excrete salt that can greatly derange volume status. Decreased urine sodium excretion (sometimes as little as 10meq/day) is commonly found in cirrhotics². Chronically unopposed ADH action resulting from underperfusion of the carotid baroreceptors doubly impedes the body’s ability to regulate volume because the kidneys no longer can excrete free water (inhibited by ADH). Overtime a refractory dilutional hyponatremia results from this response. In fact with cirrhosis, the patient is volume and salt overloaded despite having a low intravascular volume and hyponatremia. Unfortunately, these mechanisms of maintaining volume ultimately fail because as the synthetic capability of the liver declines so too does the synthesis of a prime mediator of the intravascular volume, albumin. The decreasing oncotic effects of these proteins and increased splanchnic capillary dilation give are greatly hindered and this excess volume is transmitted to the interstitial spaces and potential spaces of the peritoneum. Finally because the intravascular volume cannot be maintained, this cycle continues unbroken.

Ascites in liver cirrhosis is but one of many medical problems that this patient faces. There is a risk of the peritoneal fluid becoming septic, so called spontaneous bacterial peritonitis (SBP). This is associated with great mortality and requires chronic antibiotic prophylaxis. Particularly relevant to this patient is the risk of catastrophic bleeding from portosystemic varices that evolve as a result of increased portal pressures and high flow portosystemic shunting. It is presumed that this likely contributed in significant ways to creating his evolving anemia, and although he was not found to have active bleeding on EGD, his guaiac was positive, leading one to believe that he suffers from intermittent gastrointestinal bleeding. Hepatic encephalopathy is another complication of chronic cirrhosis resulting from the portosystemic shunting of toxic gut contents (ammonia and other nitrogen based molecules, bacterial derived toxins) to the cerebral vasculature that can greatly alter mental status and possibly result in cerebral edema and herniation³. In fact the patient is being treated with the standard lactulose; a non-absorbable substrate that acidifies the GI lumen which has been found to be bactericidal to urease producing species⁴. As well he is being treated with rifaximin, a rifamycin antibiotic that inhibits bacterial RNA synthesis that has been found to have similar efficacy and faster onset⁴. Other manifestations of liver cirrhosis not covered here are hepatorenal and hepatopulmonary syndromes, hepatocellular carcinoma, and portal vein thromboses.

References:

1. Bosch J., Garcia-Tsoa G. “Management of Varices and Variceal Hemorrhage in Cirrhosis” N Engl J Med 2010 362:823-832.

2. Such J., Runyon B. “Pathogenesis of ascites in patients with cirrhosis” www.uptodate.com

3. Fauci, Braunwald, Kasper, Hauser, Longo, Jameson, Loscalzo. Harrison’s Principles of Internal Medicine 17^th Edition. McGraw Hill 2008.

4. Zeneroli et al. “Management of Hepatic Encephalopathy: Role of Rifaximin.” Chemotherapy 2005 51:90-95.

5. Mansfield P. 2010. “Clinical features, diagnosis, and staging of gastric cancer” www.uptodate.com

6. Goldberg E., Chopra S., “Overview of the complications, prognosis, and management of cirrhosis” www.uptodate.com

furosemide to spironolactone ratio

- 2/5

triad of acute interstitial nephritis

-fever

-eos

-rash

etiology- drugs, infection

angioedema and rash (urticaria)

IgE mediated

direct mast cell mediated (nsaids, contrast)

vasculitis

Pulmonary infiltrates

farmer's lung

parasitic (strongyloides, aspergillosis) - eos!

loeffler's endocarditis - eos

autoimmune churg strauss

HCV + rash = type II cryoglobulinemia (30-40%) can get palpable purpura and cidp (chronic inflammatory demyelinating polyneuropathy), type I membranoproliferative

what is the classic paraneoplastic syndrome w/dermatologic manifestations?

dermatomyositis (lung cancer)

asymptomatic eosinophilia? could be strongyloides DONT give steroids - causes devastating sepsis

give ivermectin

DRESS- drug rash w/eosinophilia and systemic symptoms

eosinophilic leukemia? very rare entity but when happens ^^^^^^eos

eosinophilia mnemonic

Neoplasm (ovarian)

Asthma

ASA/adrenal

Connective tissue disorder

Parasitic

chronic urticaria think thyroiditis

^^^B12 seen in polycythemia vera

hypereosinophilic syndrome marker - anti-PDGRFalpha/beta

aspirin allergy - nasal polyps

what estimates risk of stroke in non rheum a-fib?

CHADS2

chf

htn >140/90

age >75

dm

stroke (prior)

nares swab for influenza - 66% specific 100% sensitive

causes of A-fib mnemonic

Pulmonary (pe/copd)

Iatrogenic

Rheumatic

Atherosclerotic

Thyroid (hyper)

Endocarditis

Sick sinus

cardinal rule for history if you suspect environmental exposure - anyone else w/same sickness?

cholesterol emboli can mimic vasculitis.

wegener's patients may have a neuropathy

two cases in which you would expect a thrombocytosis?

1. anemia

2. thrombocytosis as an acute phase reactant

bacterial causes of hemoptysis

klebsiella, tb, pneumococcus, staph aureus

UGIB is 80% of all GI bleed

dx pud, avm, varices, gastritis, gave

surgeons ask for the hematocrit, physicians ask for the hemoglobin - hemoglobin is better because it is measured

shingles vaccine is a live vaccine, its more effective when you give it younger, effective even if you've already had an outbreak of shingles

heart rate best way to test for orthostasis, not bp

fecal antigen test for h. pylori ~100% sensitive

anti dsDNA levels used to monitor severity of lupus

which antibiotics cross the BBB?

azithromycin at high doses

vancomycin

zosyn does not cross bbb

tubes and lines radiology

icu tubes and lines

endotracheal tube should be ~T4-T5 on portable chest xray for good position

flexion/extension can move the ETT as much as 2cm

complications of ET tubes

dislodgment

vocal cord injury

mainstem bronchus

put in esophagus

laceration

tracheostenosis/malacia

tracheostomy tube put in level of 3rd tracheal cartilage, not effected by motion of head

complications

emphysema, pneumomediastinum, pneumothorax

get xray after putting them in

central venous catheter

usually from IJ, tip should be in SVC, not atrium b/c can cause arrhythmias

malposition

air embolism

pneumothorax/hemothorax

cardiac perf

sepsis

venous perf

picc

small caliber

can left for long duration

preferred to end in svc

do NOT ever attempt power injecting into these lines

malposition

ectopic infusion into mediastinum or pleural space

catheter breaking/embolism

puncture blood vessel

clot

air embolization

chest tube

should always run medial to inner margins of ribs

chest tube

posteoinferior for effusion

anterosuperior for pneumothorax

complications

bleeding/laceration, rapid expansion leads to flash pulmonary edema

bp fistula

ng tubes

at least 10 cm should be in stomach

risk malposition, perf the esophagus, over time indwelling tubes reflux

intra-aortic balloon pump

inflate during diastole - increase return to coronary arteries,

pulmonary artery catherter aka swan ganz

dx cariac and non cardiac pulmonary edema

should be in pulmonary artery WITHIN THE MEDIASTINAL SHADOW

can cause pulmonary infarction (balloon inflated for long time)

embolization (tip breaks off)

perf the artery

more clinical tips in internal medicine

metastatic thyroid looks like miliary on cxr

miliary cxr?

pcp

tb

histoplasmosis

varicella

sarcoid increased cd4/cd8 ratio

increased AST/ALT + ^MCV + ^GGT = alcohol

BNP is falsely low in obese and falsely high in kidney failure

^K+? tx kayexolate, calcium gluconate

rifaximin - to treat hepatic encephalopathy

lasix/aldactone ratio is 2/5

spontaneous bacterial peritonitis ppx = ceftriaxone 1mg iv daily

triad of acute interstitial nephritis = fever, eosinophilia, rash

etiology mostly likely drugs or infection

angioedema + urticaria etiology is...

IgE mediated

direct mast cell activation (contrast nsaids ...)

vasculitis

Pulmonary infiltrates + eosinophilia

farmer's lung

parasitic (strongyloides, aspergillus, loeffler's)

autoimmune (churg strauss..)

cxr 101

chest x-ray 101

methodology - look at

bones, soft tissues, heart/mediastinum, lungs, airways, upper abdomen

pa view preferred because doesn't magnify the heart

spine sign - decreasing intensity of spin as you go caudal on the lateral view xray

silhouette sign - loss of margins bc two structures of similar densities sitting next to each other

atelectasis - incomplate expansion of portion of lung

sail sign - silhouetteing of left diaphragm for left lower lobe atelactasis, mass

s sign of golden - right upper lobe collapse, (anterior collapse), reverse s sign on pa, right side - obstructive mass causing collapse

pneumonias -

PCP pneumonia seldom if ever cause pleural effusion

with PCP you get sharp costophrenic angles and possible cystic structures (PCP)

septic emboli - rh valves peripheral thrombophlebitis etc.. predominant peripheral lung disease, ct more sensitive than cxr, see nodles, feeding vessel sign, cavitation, wedge lesions

tb can look like anything!

ghon complex, cavitary, miliary, they appear everywhere- (spread by blood)

left hilum normally higher than right hilum, if reversed indicates potential atelectasis

intersitial edema - kerley b lines (transverse near lower lung fields, septal lines)

alveolar edema - begin to lose vessels

medicine day one odds and ends

volvulus - section of bowel twists on itself creating and obstruction and proximal dilation

ogilvie's syndrome - an acute pseudo obstruction of colon in absence of any mechanical cause normally 2/2 neuro, post-op, parkinson's

infxs megacolon picture is more tenderness/sick/fever

Sinemet can give decrease peristalsis

Amitiza (lubiprostone) ^NaCl secretion in lumen of GI used for constipation/hard stool

Miralax = polyethylene glycol, an osmotic agent for constipation/hard stool

Colace - coats stool to help movement

Pericolace - docusate +senna

decubitus ulcer tx - wound vac/pack it w/gauze, keep off it!

calling a consult?

1. identify yourself

2. patient name and mrn

3. one-liner, relevant labs/imaging

4. whats the question??

start medicine rotation tomorrow

in church today i was reading 1 timothy a few interesting points

"do not muzzle an ox that is treading grain" in reference to letting those that are doing god's work be able to preach teach talk etc..

don't speak harshly

speak to older men and women as if they were your fathers or mothers

speak to younger men and women as is they were brothers and sisters

sins can be conspicuous and precede a man into judgment, other mens' sins follow them into judgment

and the sermon had a message i agreed with, the central thesis was "do not prepare your defense in advance" in my opinion referring to the mental emotional state of having a clean conscience such that your positions on matters of the past and present are at your fingertips, unified with your own personal integrity, there is no clever planning or posturing or trying to create a defense. if you have to defend your position, just draw from what you know thinking "on your feet"*, which is the truth, hopefully that you are in harmony. that spoke to me.

*if there are details that you need to remember that are subtle i think its ok to go over those in advance

internal medicine rotation starts tomorrow!

Urological emergencies notes...

urology

causes of enterocutaneous fistula

FRIEND

Foreign body

Radiation

Infection/Inflammation

Epithelialization

Neoplasm

Distal obstruction

7 Urologic Emergencies (means take action now!)

1. Torsion - testicle twists- acute severe pain. 4-6 hour window before tissue death

diagnosis is US, tx can try and detorse (open book) turn each testicle laterally, will still need to operate orchiopexy

2. Priapism - either low flow or high flow. Low flow is emergency, drain it w/needle, tx w/phenylephrine,

low flow associated w/leukemias, multiple myeloma, sickle cell, can also try PDE5 inhibitors

high flow let go

3. Paraphimoses - 4-6 hour window before tissue death in glans, squeeze on glans and it goes back in (most times), still no? dorsal foreskin gets cut

4. Ureteral obstruction w/fever - no flow past stone soon to be urosepsis, patient w/diabetes even worse

5. Acute urinary retention - etiiology clot or bph, fix w/catheter

6. Ureteral damage - most often iatrogenic from not pushing the catheter all the way in, when balloon expands trauma to prostate PUSH THE CATHETER ALL THE WAY IN

7. Fornier's gangrene - infxn of perineum increased in diabetics, immunosuppression, chronic etoh, normal polymicrobial, requires empiric Abx and debridement bad news

bad news

ob/gyn clinical reflection

This rotation was my first experience with childbirth. It took just a few short weeks to gain some valuable insight into a really very truly dangerous right of passage. What a great privilege to be side by side with these mothers and witness for me this heretofore completely unknown event known as childbirth. First I should say that I was really surprised the first time I saw a mother's water break- water for me has always had a connotation of purity and cleansing and life (from baptism and all its religious symbolism to the water's obvious symbolism of life etc). The mother's water breaking and spilling all over the table and floor is a clarion call to the unstoppable force of life, the water breaks the baby is coming, the baby is pure and has not been in this world, it is clean, the baby waits for no one, not even tocolytics. It was really amazing. And then mix the water with blood. So much blood! For me blood has its own symbolism as well, blood is life and passion, in this context blood is the mother's life and it is literally spilling out onto the table with the newborn. The mother gives part of her life to the newborn and to the birth. These two fluids water and blood, have such gravity in the context of childbirth. It was apparent after seeing just one childbirth why for ages these two vital substances have held such great esteem throughout all of human culture. You can't name a culture that won't respect the sanctity of water and blood. What's more, during the OB portion of our rotation I really developed a sense for the cost of life, both in our more modern times and in the past. Even today it became clear that childbirth is an extremely dangerous event, even with packed red blood cells, and FFP and a team of skilled physicians standing by, how unpredictable and completely at the mercy of God, the universe, or who knows what else it is to be the mother bringing life into this world. I caught the spirit of the mystery of life, if only as a spectator. Can you imagine how dangerous it must have been to labor and deliver before such modern luxuries?? When faced with these mortal risks, to say nothing of the intense pain, the true cost of life becomes apparent to those women who choose to undertake its passing forward. The moment of delivery in its pain and suffering stands in stark contrast to the moment of pleasure and romance during conception, how diametrically opposed these two marvelous events are, both lived by the mother! I learned just how easy it is for mom to bleed uncontrollably, to give her life for another, half a liter of blood minute right out of the womb, life could be over in as short as 12 minutes. The gravity and sobriety of a delivery leaves its mark on the mother, especially the younger nulliparous. But despite these high costs, I saw that a mom can get what she paid for in the intense joy and mother's love toward the newborn, it seems that feeling is worth the risk, worth putting your up your life and limb to fortune. Now after this rotation, I can fully appreciate the cause for celebration when fortune smiles and a mother gives birth to a healthy baby with minimal complications. It really is a miracle.

ob/gyn abortion notes

6.3 million pregnancies a year US

50% of pregnancies unintended

1/2 of unintended from women who don't use contraceptive

low SES account for more unintended pregnancies

unintended pregnancies how they end up

40% abortion

40% birth

10% fetal loss

induced abortion

20-24 yrs 33% of abortion

25-29 yrs 23% of abortion

30-34 yrs 15% of abortion

86% of abortions unmarried

>60% of abortions are less than 9 weeks

80% done under 12 weeks

7/100,000 births are fatal for mom

safer to have abortion early than to carry pregnancy 2/100,000 if early abortion

medical abortion 5-9 weeks

surgical 5-14 weeks

medical

advantages

performed w/o delay

no anesthesia

psychological easier

misoprostol, mifepristone, methotrexate rarely used (used for ectopics)

complications of medical abortion

bleeding 9-16 days

failure

infection (rare)

surgical procedure

manual <10>10 weeks

2nd trimester - laminaria (cervical dilators, wrapped in sea weed), need anesthesia

complications of surgical

infection, incomplete, perf, bleeding, clots, asherman,

2nd tri medical induction

option for patient desiring to hold or view fetus, give misoprostol or pitocin every 4-6 hours

30% chance of retained placenta - would need d&c

ob/gyn clinical notes

2nd half of 2nd trimester is when estrogen upregs oxytocin receptors
hemabate

giving a uterotonic must ask two questions?
asthmatic or hypertensive?
postpartum hemorrhage? what do you do?
vaginal exam
1. where bleeding?
uterus, cervix (laceration), vagina
2. stop the bleeding

risk of cervical laceration - leep (changes nature of tissue), big baby, compound presentation (finger on head), sulcal tear vagina, tears can go all the way back.
drusian's incicsions cut cervix 12, 4, 8 oclock, don't cut 3&9 oclock where uterine arteries

risk factors for atony - multiple gestations, polyhydramnios, big baby, tocolytic (mag), prolonged labor, fibroids
blynch sutures - suspenders for the uterus to stop it from bleeding

then
uterine artery ligation
then
hysertectomy

hyaline casts in lungs - pathognomonic for amniotic fluid embolism

eclampsia - seizure and htn (don't need proteinuria)

code right after birth? think amniotic fluid embolism

boggy uterus - massage, not working give uterine tonics- stick w/one agent max it out
1mg cytotec (misoprostol),
methergine or hemabate, or pit wide open

flagyl - metronidazole - anearobes

subcutaneous emphesyma - used for laparoscope (rice krispies sign)

hpv vaccine - tetravalent insures against warts and cancers

endometritis = uterine tenderness postpartum + fever, physical diagnosis

gentamicin - covers aerobes, clinda- covers ug aneareaboes
ampicillin -