This is a post about oPortfolio - a project that Meducation and Podmedics are collaborating on. We have a Kickstarter project and would love your support!
Students? Junior Doctors? Senior Doctors?
Over the last two days we've been asked by lots of people who oPortfolio is for. Some people want it for students, others to replace junior doctor systems, and some for revalidation purposes. The simple answer is that it's for everyone going through their medical careers from student to consultant and on to retirement.
There are two challenges to building a system that's relevant for such a wide variety of people. The first is to make something that has all the features that are needed for all the people. We are strong believers in self-directed learning and want that to be at the core of oPortfolio. We want people to be able to build their own personal portfolios, keeping a log of everything they want to - their own personal space for reflection and learning. oPortfolio should be something that you find useful at all stages, and that's crucial to our vision.
The second challenge is working with existing ePortfolio systems, and to have functionality that deaneries and Colleges need to adopt our platform if they want to. Making a system that is incompatible with existing systems, or that involves doctors still having to use other horrible software defies the whole point of what we're doing. If a user's oPortfolio has to be manually copied & pasted into another system, everyone loses out. This, therefore, also has to be a large consideration as we move forwards.
At all times, we will have to balance these two challenges up against each other.
oPortfolio is for everyone. It certainly won't have all the features that everyone needs from day one, but our aim is to build a solid base everyone can use, and then expand it from there. With regards to who we give our initial focus to, it will be the people who support us on Kickstarter. They are showing genuine support for what we're doing, and therefore deserve to be prioritised. That only seems fair.
Please support us today. Thank you.
It was a Saturday, about tea-time in the quaint village of Athelstaneford, East Lothian. Mrs Alexandria Agutter sat in her cottage, enjoying the delights of the late-summer evening with a glass of gin and tonic. She listlessly sipped from the rather generous pick-me up, no doubt chewing over the happenings of the day. Blast! The taste was much too bitter to her liking. She stood up. And promptly crumpled to the floor in a dizzied heap. It had not been five minutes when a fiery pain gripped her parched throat and in her frenzied turn she watched the bleary room become draped in a gossamery silk.
How Dame Agatha would approve. But this is no crime novel, on that fateful day, 24th August 1994, poor Mrs Agutter immortalised herself in the history books of forensic medicine; she was the victim of a revered toxin and a vintage one it was too. She had unwittingly imbibed a G&T laced with a classic poison of antiquity.
A clue from the 21st century: do you recall the first Hunger Games film adaption? Those inviting purple-black berries or as Suzanne Collins coined them ‘Nightlock’; a portmanteau of hemlock and Deadly Nightshade. True to the laters’ real life appearance those onscreen fictional fruits played a recurring cameo role.
Deadly Nightshade is a perennial shrub of the family Solanaceae and a relative of the humble potato (a member of the Solanus genus). It is a resident of our native woodland and may be found as far afield as Europe, Africa and Western Asia. The 18th century taxonomist, Carl Linnaeus gave the plant an intriguing name in his great Species Plantarum. The genus Atropa is aptly named after one of the three Greek Fates, Atropos. She is portrayed shearing the thread of a mortal’s life so determining the time and manner of its inevitable end. The Italian species name belladona (beautiful woman) refers to the striking mydriatic effect of the plant on the eye. The name pays homage to Pietro Andre Mattioli, a 16th century physician from Sienna, who was allegedly the first to describe the plant’s use among the Venetian glitterati - ladies of fashion favoured the seductive, doe-eyed look. Belladona is poisonous in its entirety. It was from the plant’s roots in 1831, the German apothecary Heinrich F. G. Mein isolated a white, odourless, crystalline powder: it was (surprise, surprise) atropine.
Atropine is a chiral molecule. From its natural plant source it exists as a single stereoisomer L-atropine, which also happens to display a chiral potency 50-100 times that of its D-enantiomer. As with many other anaesthetic agents it is administered as a racemic mixture. How strange that atropine now sits among the anaesthetist’s armamentarium, its action as a competitive antimuscarinic to counter vagal stimulation belies its dark history. It was a favourite of Roman housewives seeking retribution against their less than faithful husbands and a staple of the witch’s potion cupboard. Little wonder how belladona became known as the Devil’s plant. Curiouser still it’s also the antidote for other poisons, most notably the organophosphates or nerve gases.
On account of its non-selective antagonism, atropine produces a constellation of effects: the inhibition of salivary, lacrimal and sweat glands occurs at low doses; dry mouth and skin are early markers. Pyrexia is a central effect exacerbated by the inability to sweat. Flushing of the face due to skin vessel vasodilatation. Low parasympathetic tone causes a moderate sinus tachycardia. Vision is blurred as the eye becomes dilated, unresponsive to light and accommodation is impaired. Mental disorientation, agitation and ataxia give the impression of drunkedness or a delirium tremens like syndrome. Visual hallucinations, often of butterflies or silk blowing in the wind, are a late feature.
It was then that Mr Agutter, seemingly untroubled by the sight of his wife’s problematic situation, proceeded to leave a message with the local practitioner. How fortunate they were to have the vigilant locum check the answering machine and come round to the Agutter’s lodge accompanied by an ambulance crew. The attending paramedic had the presence of mind to pour the remainder of Mrs Agutter’s beverage into a nearby jam jar, while Mr Agutter handed over what he suspected to be the offending ingredient: the bottle of Indian tonic water. As it soon transpired there were seven other casualties in the surrounding countryside of East Lothian – all involving an encounter with tonic water.
In fact by some ironic twist of fate, two of the victims were the wife and son of Dr Geoffry Sharwood-Smith, a consultant aneasthetist. Obviously very familiar with the typical toxidrome of anticholinergic agents, he was quick to suspect atropine poisoning. Although for a man of his position with daily access to a sweetshop of drugs, it was not something to draw attention to.
Through no small amount of cunning had the poisoner(s) devised the plan. It was elegant; atropine is very bitter. So much so that it can be detected at concentrations of 100 parts per million (0.001%). Those foolish enough to try the berries of belladonna during walks in the woods are often saved by the berry’s sour taste. They are soon spat out. But the quinine in the tonic water was a worthy disguise. The lethal dose for an adult is approximately 90-130mg, however atropine sensitivity is highy variable. In its salt form, atropine sulfate, it is many times more soluble: >100g can be dissolved in 100ml of water. So 1ml may contain roughly tenfold the lethal dose.
There ensued a nationwide scare; 50 000 bottles of Safeway branded Indian tonic water were sacrificed. Only six bottles had been contaminated. They had all been purchased, tops unsealed, from the local Safeway in Hunter’s Tryst. Superficially this looked like the handiwork of a psychopath with a certain distaste for the supermarket brand, and amidst the media furore, it did have some verisimilitude: one of the local papers received a letter from 25 year old, Wayne Smith admitting himself as the sole perpetrator.
The forensic scientist, Dr Howard Oakley analysed the contents of the bottles. They all contained a non-lethal dose, 11-74mg/litre of atropine except for the Agutter’s, it contained 103mg/litre. The jam jar holding Mrs Agutter’s drink bore even more sinister results, the atropine concentration was 292mg/L. It would appear Mrs Agutter had in some way outstayed her welcome. But she lived. A miscalculation on the part of the person who had added an extra seasoning of atropine to her drink. According to the numbers she would have had to swallow a can’s worth (330ml) to reach the lethal dose. Thankfully she had taken no more than 50mg.
The spotlight suddenly fell on Dr Paul Agutter. He was a lecturer of biochemistry at the nearby University of Napier, which housed a research syndicate specialising in toxicology. CCTV footage had revealed his presence at the Safeway in Hunter’s Tryst and there was eye witness evidence of him having placed bottles onto the shelves. Atropine was also detected by the forensic investigators on a cassete case in his car. Within a matter of two weeks he would be arrested for the attempted murder of his wife. Despite the calculated scheme to delay emergency services and to pass the blame onto a non-existent mass poisoner, he had not accomplished the perfect murder. Was there a motive? Allegedly his best laid plans were for the sake of a mistress, a mature student from Napier. He served seven years of a twelve year sentence. Astonishingly, upon his release from Glenochil prison in 2002, he contacted his then former wife proclaiming his innocence and desire to rejoin her in their Scottish home. A proposition she was not very keen on. Dr Agutter was employed by Manchester University as a lecturer of philosophy and medical ethics. He is currently an associate editor of the online journal Theoretical Biology and Medical Modelling.
We will never know the true modus operandi as Dr Agutter never confessed to the crime. Perhaps all this story can afford is weak recompense for the brave followers of the Dry January Campaign. Oddly these sort of incidents never appear in their motivational testimonials.
Emsley J. Molecules of Murder. 2008, Cambridge, RSC Publishing, p.46-67.
Lee MR. Solanaceae IV: Atropa belladona, deadly nightshade. J R Coll Physicians Edinb. March 2007; 37: 77-84.
Illustrator Edward Wong
This blog post is a reproduction of an article published in the The Medical Student Newspaper January issue, 2014
This is an excerpt from "Fluids and Electrolytes Made Incredibly Easy! 1st UK Edition" by William N. Scott. For more information, or to purchase your copy, visit: http://tiny.cc/Fande. Save 15% (and get free P&P) on this, and a whole host of other LWW titles at lww.co.uk when you use the code MEDUCATION when you check out!
The chemical reactions that sustain life depend on a delicate balance – or homeostasis – between acids and bases in the body. Even a slight imbalance can profoundly affect metabolism and essential body functions. Several conditions, such as infection or trauma, and certain medications can affect acid-base balance. However, to understand this balance, you need to understand some basic chemistry.
Understanding acids and bases requires an understanding of pH, a calculation based on the concentration of hydrogen ions in a solution. It may also be defi ned as the amount of acid or base within a solution.
Acids consist of molecules that can give up, or donate, hydrogen ions to other molecules. Carbonic acid is an acid that occurs naturally in the body. Bases consist of molecules that can accept hydrogen ions; bicarbonate is one example of a base.
A solution that contains more base than acid has fewer hydrogen ions, so it has a higher pH. A solution with a pH above 7 is a base, or alkaline.
A solution that contains more acid than base has more hydrogen ions, so it has a lower pH. A solution with a pH below 7 is an acid, or acidotic.
Getting your PhD in pH
A patient’s acid-base balance can be assessed if the pH of their blood is known. Because arterial blood is usually used to measure pH, this discussion focuses on arterial samples.
Arterial blood is normally slightly alkaline, ranging from 7.35 to 7.45. A pH level within that range represents a balance between the concentration of hydrogen ions and bicarbonate ions. The pH of blood is generally maintained in a ratio of 20 parts bicarbonate to 1 part carbonic acid. A pH below 6.8 or above 7.8 is usually fatal.
Under certain conditions, the pH of arterial blood may deviate significantly from its normal narrow range. If the blood’s hydrogen ion concentration increases or bicarbonate level decreases, pH may decrease. In either case, a decrease in pH below 7.35 signals acidosis.
If the blood’s bicarbonate level increases or hydrogen ion concentration decreases, pH may rise. In either case, an increase in pH above 7.45 signals alkalosis.
Regulating acids and bases
A person’s well-being depends on their ability to maintain a normal pH. A deviation in pH can compromise essential body processes, including electrolyte balance, activity of critical enzymes, muscle contraction and basic cellular function. The body normally maintains pH within a narrow range by carefully balancing acidic and alkaline elements. When one aspect of that balancing act breaks down, the body can’t maintain a healthy pH as easily, and problems arise.
Amended from Wikipedia and other sources
Stage means spread
Grade means histology
Prostate cancer staging – spread of the cancer
There are two schemes commonly used to stage prostate cancer. TMN and Whitmore Jewett
Stage I disease is cancer that is found incidentally in a small part of the sample when prostate tissue was removed for other reasons, such as benign prostatic hypertrophy, and the cells closely resemble normal cells and the gland feels normal to the examining finger
Stage II more of the prostate is involved and a lump can be felt within the gland.
Stage III, the tumour has spread through the prostatic capsule and the lump can be felt on the surface of the gland.
In Stage IV disease, the tumour has invaded nearby structures, or has spread to lymph nodes or other organs.
Grading - Gleason Grading System is based on cellular content and tissue architecture from biopsies, which provides an estimate of the destructive potential and ultimate prognosis of the disease.
TX: cannot evaluate the primary tumor
T0: no evidence of tumor
T1: tumor present, but not detectable clinically or with imaging
• T1a: tumor was incidentally found in less than 5% of prostate tissue resected (for other reasons)
• T1b: tumor was incidentally found in greater than 5% of prostate tissue resected
• T1c: tumor was found in a needle biopsy performed due to an elevated serum PSA
T2: the tumor can be felt (palpated) on examination, but has not spread outside the prostate
• T2a: the tumor is in half or less than half of one of the prostate gland's two lobes
• T2b: the tumor is in more than half of one lobe, but not both
• T2c: the tumor is in both lobes but within the prostatic capsule
• T3: the tumor has spread through the prostatic capsule (if it is only part-way through, it is still T2)
• T3a: the tumor has spread through the capsule on one or both sides
• T3b: the tumor has invaded one or both seminal vesicles
• T4: the tumor has invaded other nearby structures
It should be stressed that the designation "T2c" implies a tumor which is palpable in both lobes of the prostate. Tumors which are found to be bilateral on biopsy only but which are not palpable bilaterally should not be staged as T2c.
Evaluation of the regional lymph nodes ('N')
NX: cannot evaluate the regional lymph nodes
• N0: there has been no spread to the regional lymph nodes
• N1: there has been spread to the regional lymph nodes
Evaluation of distant metastasis ('M')
• MX: cannot evaluate distant metastasis
• M0: there is no distant metastasis
• M1: there is distant metastasis
• M1a: the cancer has spread to lymph nodes beyond the regional ones
• M1b: the cancer has spread to bone
• M1c: the cancer has spread to other sites (regardless of bone involvement)
Evaluation of the histologic grade ('G')
Usually, the grade of the cancer (how different the tissue is from normal tissue) is evaluated separately from the stage; however, for prostate cancer, grade information is used in conjunction with TNM status to group cases into four overall stages.
• GX: cannot assess grade
• G1: the tumor closely resembles normal tissue (Gleason 2–4)
• G2: the tumor somewhat resembles normal tissue (Gleason 5–6)
• G3–4: the tumor resembles normal tissue barely or not at all (Gleason 7–10)
Of note, this system of describing tumors as "well-", "moderately-", and "poorly-" differentiated based on Gleason score of 2-4, 5-6, and 7-10, respectively, persists in SEER and other databases but is generally outdated. In recent years pathologists rarely assign a tumor a grade less than 3, particularly in biopsy tissue. A more contemporary consideration of Gleason grade is:
• Gleason 3+3: tumor is low grade (favorable prognosis)
• Gleason 3+4 / 3+5: tumor is mostly low grade with some high grade
• Gleason 4+3 / 5+3: tumor is mostly high grade with some low grade
• Gleason 4+4 / 4+5 / 5+4 / 5+5: tumor is all high grade
Note that under current guidelines, if any Pattern 5 is present it is included in final score, regardless of the percentage of the tissue having this pattern, as the presence of any pattern 5 is considered to be a poor prognostic marker.
The tumor, lymph node, metastasis, and grade status can be combined into four stages of worsening severity.
Stage Tumor Nodes Metastasis Grade
Stage I T1a N0 M0 G1
Stage II T1a N0 M0 G2–4
T1b N0 M0 Any G
T1c N0 M0 Any G
T1 N0 M0 Any G
T2 N0 M0 Any G
Stage III T3 N0 M0 Any G
Stage IV T4 N0 M0 Any G
Any T N1 M0 Any G
Any T Any N M1 Any G
T (Primary tumour)
• TX Primary tumour cannot be assessed
• T0 No evidence of primary tumour
• Ta Non-invasive papillary carcinoma
• Tis Carcinoma in situ (‘flat tumour’)
• T1 Tumour invades subepithelial connective tissue
• T2a Tumour invades superficial muscle (inner half)
• T2b Tumour invades deep muscle (outer half)
• T3 Tumour invades perivesical tissue:
• T3a Microscopically
• T3b Macroscopically (extravesical mass)
• T4a Tumour invades prostate, uterus or vagina
• T4b Tumour invades pelvic wall or abdominal wall
N (Lymph nodes)
• NX Regional lymph nodes cannot be assessed
• N0 No regional lymph node metastasis
• N1 Metastasis in a single lymph node 2 cm or less in greatest dimension
• N2 Metastasis in a single lymph node more than 2 cm but not more than 5 cm in greatest dimension,or multiple lymph nodes, none more than 5 cm in greatest dimension
• N3 Metastasis in a lymph node more than 5 cm in greatest dimension
M (Distant metastasis)
• MX Distant metastasis cannot be assessed
• M0 No distant metastasis
• M1 Distant metastasis.
Urothelial papilloma – non cancerous (benign) tumour
•Papillary urothelial neoplasm of low malignant potential (PUNLMP) – very slow growing and unlikely to spread
•Low grade papillary urothelial carcinoma – slow growing and unlikely to spread
•High grade papillary urothelial carcinoma – more quickly growing and more likely to spread