clinic presents

10

ATOMIC BLONDE (2017)

DIR: David Leitch

As I stated in my Instagram post, Atomic Blonde is the film that redefined sexiness for me in 2017. As someone who feels uncomfortable watching a majority of sex scenes, I finally was not. There is something comforting in this pairing of girls, and finally we have a bisexual film hero who, although overly sexualized, is badass, confident, and will take a man down. This is so important to me because it is so rarely seen, and when it is, it’s usually referenced or joked about. Her bisexuality passes naturally through the diegesis. I never had any particular feelings about Charlize Theron before this movie, but now I wonder why I slept on her so long. She was stunning for the part. Yet another admirable bit about this movie is her fashion and shoes: mostly black and white to contrast the lighting, and naturally sexual. 

Although not an 80s movie, this film harkens back to the time for me with the soundtrack. Made up of Bowie & Queen, George Michael, New Order, and Depeche Mode, as well as a few of the popular German songs of the 80s, it feels vibrant and pulsing with energy. The setting and lighting bring us back to the 1980s feel, and the stunning color combinations of neon lighting give flavor to the darkness of Cold War Berlin, and give intense energy to the nightlife of a torn city. It heightens the sexual tension of the love scenes, and this is in clear contrast to the cold, clinical light of the present day and action sequences. 

A killer soundtrack. A stunning, fashionable bisexual heroine. Colorful neon lighting. Bomb action sequences. Comfortable sex scenes. An 80s throwback. As one of the pull quotes I read stated: “This is the movie we need right now.” How correct it is. 

Scientists discover shared genetic origin for MND and schizophrenia

Researchers from Trinity College Dublin have shown for the first time that Motor Neurone Disease (MND) – also known as Amyotrophic Lateral Sclerosis (ALS) – and schizophrenia have a shared genetic origin, indicating that the causes of these diverse conditions are biologically linked. The work has just been published in the prestigious journal Nature Communications

By analysing the genetic profiles of almost 13,000 MND cases and over 30,000 schizophrenia cases, the researchers have confirmed that many of the genes that are associated with these two very different conditions are the same.

In fact, the research has shown an overlap of 14% in genetic susceptibility to the adult onset neuro-degeneration condition ALS/MND and the developmental neuropsychiatric disorder schizophrenia.

While overlaps between schizophrenia and other neuropsychiatric conditions including bipolar affective disorder and autism have been shown in the past, this is the first time that an overlap in genetic susceptibility between MND and psychiatric conditions has been shown.

Dr Russell McLaughlin, Ussher Assistant Professor in Genome Analysis at Trinity College Dublin, and lead author of the paper said: “This study demonstrates the power of genetics in understanding the causes of diseases.“

"While neurological and psychiatric conditions may have very different characteristics and clinical presentations, our work has shown that the biological pathways that lead to these diverse conditions have much in common.”

Professor Hardiman said: “Our work over the years has shown us that MND is a much more complex disease than we originally thought. Our recent observations of links with psychiatric conditions in some families have made us think differently about how we should study MND. When combined with our clinical work and our studies using MRI and EEG, it becomes clear that MND is not just a disorder of individual nerve cells, but a disorder of the way these nerve cells talk to one another as part of a larger network.”

She continued: “So instead of thinking of MND as a degeneration of one cell at a time, and looking for a ‘magic bullet’ treatment that works, we should think about MND in the same way that we think about schizophrenia, which is a problem of disruptions in connectivity between different regions of the brain, and we should look for drugs that help to stabilise the failing brain networks.”  

“The other significant issue that this research brings up is that the divide between psychiatry and neurology is a false one. We need to recognise that brain disease has many different manifestations, and the best way to develop new treatments is to understand the biology of what is happening. This will have major implications for how we classify diseases going forward, and in turn how we train our future doctors in both psychiatry and neurology. That in itself will have knock-on consequences for how society understands, approaches and treats people with psychiatric and neurological conditions.“

The new research was prompted by earlier epidemiological studies by researchers at Trinity, led by Professor Hardiman. These studies showed that people with MND were more likely than expected to have other family members with schizophrenia, and to have had another family member who had committed suicide.

This was first noted as family histories were ascertained from people with MND in the National ALS Clinic and was subsequently investigated as part of case control studies in Ireland in which over 192 families with MND and 200 controls participated. Details of over 12,000 relatives were analysed and the rates of various neurological and psychiatric conditions calculated in family member of those with MND and controls. This work was subsequently published in the prestigious American journal the Annals of Neurology in 2013.

This led the Trinity group to team up with European collaborators in MND including the University of Utrecht, Kings College London and members of the Project MinE and Psychiatric Genome Consortia to see if these epidemiological observations could be due to a genetic overlap between MND and schizophrenia.

The Trinity group, along with their partners in the University of Utrecht, will continue to study the links between MND and psychiatric conditions using modern genetics, epidemiology and neuroimaging, and in this way will develop new and more effective treatments that are based on stabilizing disrupted brain networks.

anonymous asked:

Psychiatry is not abusive and self diagnosing is dangerous. You're not a doctor and you don't know the details about all the disabilities and illnesses that are out there. Researching things on your own is fine and all, but not everything on the internet is true. Many people are often delusional and claim they have a certain disability or illness when in reality they do not, and they're merely attention seekers.

Oh gosh… here we go. First, I should probably point out that you shouldn’t assume things about other people on the Internet. You’re right, I’m not a doctor: I’m a psychologist and I most certainly have a solid understanding of the myriad diagnosable mental disorders recognized by the American Psychiatric Association. Oops.

I also have over ten years experience as a peer advocate for people who have mental health problems and/or are suffering violence at the hands of the psychiatric institution.

With that out of the way, my dear Dunning Kruger acolyte, let’s talk about all the interesting ways in which you’re painfully wrong:

First, you don’t understand what a psychiatric diagnosis even is. Diagnostic criteria for psychiatric conditions are not diseases because they do not describe an underlying disease process. They are syndromes. What that means is that your precious psychiatric diagnoses are nothing more than descriptions of various symptoms that the psychiatric profession has concluded are often seen in combination. Moreover these diagnostic criteria are:

  • Not culturally neutral. Psychiatric diagnostic criteria were developed through the observation of patients in European (incl. North American) cultures. There is extensive research by cultural anthropologists researching mental disability in non-European cultures that shows not only that psychiatric diagnoses did not seem to fit the studied population but that the importation of European psychiatry fundamentally changed the clinical presentation of the local patients.
  • Not without controversy, even within the psychiatric profession. I can think of several psychiatric diagnoses enumerated in the DSM-V that psychiatrists can’t stop bickering about regarding their validity, and that’s not including the infighting having to do with the fundamental nature of various disorders.
  • Constantly changing. Every few years a new edition of the Diagnostic and Statistical Manual of Mental Disorders comes out and diagnoses are added, dropped, and often radically changed. Two of the diagnoses that I carry, bipolar I disorder and autism spectrum disorder, changed radically in the transition from the DSM-IV-TR to the DSM-V. The latter wasn’t even a ‘real diagnosis’ until a few months ago.
  • Imprecise and subjective. Mental health professionals treating the same patient will regularly give different diagnoses from each other. Incidentally, in science we call this failing a test/retest check for reliability which is an indication that something is horseshit.
  • Helpfully bound and presented in a single volume, in plain English, for anyone with a library card or a bit of spare change to browse. Seriously. The fact that you don’t think that people who self diagnose mental disorders don’t even bother to consult a copy of the DSM-V is downright insulting. Do you really think that people who are struggling with getting help for a serious, potentially life-threatening condition restrict their research to Yahoo Answers? Grow up and give me a break. 

How is a psychiatric diagnosis made? It starts with a patient who is complaining about a symptom, or a group of symptoms that are causing them distress. You then ask them what they think is wrong with them and they give you symptoms. Having a fairly good idea of what’s wrong with your patient you now ask follow-up questions in order to differentially diagnose similar conditions. If you are very, very lucky you might even be able to directly observe a symptom or two. Then, you make your diagnosis and move on to discussing treatment options.

You wanna know what’s really useful? When a patient already has a good idea what’s wrong with them and is informed enough to know what information to volunteer. Now all you need to do is confirm the diagnosis. Having an informed patient is critical to providing quality health care of any kind.

But let’s talk about what happens when self diagnosis gets vilified by mental health professionals, as you so dearly seem to want. An anecdote from my personal life:

Before I was formally diagnosed with bipolar disorder I had serious problems with depression. My general practitioner referred me to a psychiatrist and I told her that I thought I was bipolar based on some hypomanic episodes that I felt that I had in the past. The psychiatrist brushed me off and did not ask the questions necessary to investigate my concern. She prescribed a high dose of antidepressants and sent me on my way.

If you don’t know, antidepressants cause Very Bad Things™ to happen to people who are bipolar. This is the reason why ‘bipolar II’ is a distinct diagnosis from major depression. I knew this but I also knew that if it did cause a mania it would confirm my diagnosis, so I took the drugs.

Not only did the resulting mania land me in the hospital but the drugs did permanent and severe damage. I no longer have a manageable bipolar II condition, I have a poorly controlled bipolar I condition.

So why do people self-diagnose? Because something is causing them to suffer and they either do not have access to the medical resources necessary for a formal diagnosis or they have tried to get a diagnosis but for some reason have been unable to get one.

Self-diagnosis is empowering. Self-diagnosis allows people to access the care they need from mental health professionals because they will be able to present their complaint in a way that is understandable to their healthcare provider. Self-diagnosis also allows people to research ways to cope with their symptoms without involving medical professionals.

Can a self-diagnosis be wrong? Yes. Are mental health professionals alert to errors in self-diagnosis? Yes. But here’s the thing: A mental health self-diagnosis is almost never far from the eventual, formal diagnosis.

All this being said: You’re just angry that certain people, who aren’t you, are able to advocate for themselves without going through a gauntlet of potentially abusive gatekeepers. In other words, you’re fucking scum and please get off my blog.

Basic Drug Calculations: How to Survive Clinical Rotations #4

When I matriculated into clinical rotations, the thing that I probably was most terrified of was messing up a drug dosage or calculation. So much math, and when you are stressed? It can be easy to mess up! So let’s go through a basic drug calculation together! 

-First things first: Unless it’s a very specific drug that states otherwise, in general, ALL OF YOUR WEIGHTS WILL NEED TO BE IN KGS (kilograms), NOT POUNDS!!!!!  How do you do this? Take your weight in pounds and divide by 2.2!! So a 14 pound dog is 6.36kgs!!!!

Okay, so you have a 14 pound dog (6.36 kg) named PooPoo that you want to give Miraclemycin to that is in a bottle. It states in your pharmacy book (Drugs R Us) that you should give 3.0 mg/kg of MIraclemycin. That means you need 3.0 mg (MILLIGRAMS) PER KILOGRAM of body weight. We just that PooPoo is 6.36 kgs, so simply multiply THE WEIGHT (IN KGS) BY THE MGS PER KILOGRAM. That is 3.0 mg/kg X 6.36 kg to get 19.08 mgs!  Whoohoo, we know how much to give!!! 

…But it’s in a bottle that is liquid and it says that the bottle has 15 mg/ml… Never fear! This means there is 15 MG (milligrams) of medication per 1 ML (Milliliter) of liquid. So if we want 19.08 milligrams, we take the amount of milligrams we want divided by how many MG/ML. So 19.08 mg divided 15 mg/ml= 1.2 mls! That means we would draw up 1.2 mls in our syringe! 

(Below is the calculation again in a little more streamlined fashion):

14 pounds / 2.2 = 6.36 kgs

6.36 kgs X 3.0 mg/kg = 19.08 mgs

19.08 mgs/ 15 mg/ml = 1.2 mls of Miraclemycin!  

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Other useful links: Surviving clinical rotations #1 (how to be prepared for clinical rotations), #2 (Presenting a case: Signalment), #3 (How to take a history), what is a clinical rotation

anonymous asked:

Can you explain the different type of paralysis. I have a character who is magical and has the paralysis where it's an on and off thing with their legs. I was wondering if it was possible for them to be able to drive or operate Machinery like a motorcycle or a car. What would be the limits to what they can do because I want them to pose as human as possible.

Hey there nonny. A lot of what I’m going to say is going to go out the window, because you specifically mentioned magic and you specifically mention temporary paralysis (”on again / off again”). 

And this may be uncomfortable advice to get, but I’m going to ask you to read this answer all the way through, read it again, think about it, and read it a third time. 

First, talking about your character “posing as human as possible” gives me some really uncomfortable feelings about the way you may be planning to represent disability. This may be a function of the character limits in the ask box, or English may not be your first language, but the words you used implied that your character is disabled and thus not human. BAD. (Your character may be an elf or piskie or merwolf, I don’t know, but if your character is human, take a good hard look at how you’re looking at them.) 

Next: Yes, paralyzed people can drive, as long as they have some function in their arms. In fact, I worked for a quadriplegic man as his home health aide (search for Tom if you want the whole story). He could brush his teeth and comb his hair if you velcroed the implement to his hand, but he operated a car safely and effectively. Hand levers operated the brake and gas, and a control knob for the steering wheel, worked for him just fine. 

I don’t know about motorcycles, but I would assume that if he’s wheelchair-dependent, getting into and out of a motorcycle would be problematic. 

Now, on to the “on again off again” paralysis. This does exist, but not following trauma. Periodic paralysis is caused by a group of genetic disorders which change the way the body’s muscles process ions. (Muscle movement are triggered by nerves, which rely on ion changes to send electrical signals; changes in the ion channels changes or prevents electrical signals from processing). Most of them are triggered by something: heat, cold, high-carb meals. Some will have problems with high potassium (with glucose being the treatment), others will have problems with high sugar (with potassium being the treatment). 

This group of diseases is always genetic and always inherited. 

I’ll be honest: this isn’t my area of expertise. For a better understanding of the way these diseases work, I suggest you do some homework on the clinical presentation of periodic paralyses. (There’s a very good resource here; may require a free account.) 

Take care, good luck, and make sure that you take the lives of paralyzed people into account. 

xoxo, Aunt Scripty

(Samantha Keel)

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Tips on How to Take a History (How to Survive Clinical Rotations #3)

Nothing is more daunting to a newbie clinical vet student that to be thrown into a random room with a client and to accurately assess what is wrong with their pet in 15 minutes or less. Here are some quick tips to make your history taking experience hopefully a little less scary!

-> First of all, what in the world is a history??  Taking a history, in a nutshell, is listening to the presenting complaints and asking the right questions to further assess and lead you to (hopefully) the correct diagnosis. Everyone has been to the doctor and has been a part of a history!  For example, where does it hurt? How long has this been going on? What medications are you currently taking?

-> A good history can be just as vital as your physical and diagnostics. Do not underestimate how important a history can be! You can literally find the diagnosis in the history, if you know what to ask. It may be tempting to skip “the boring” questions (”what medications does Poofy get”, “what does Puddle eat”), but it might just give you a hint into what is going on! 

-> Ask open ended questions! This is SUPER important! For instance, a close ended question would be something that can be answered with a yes or no response, like “So YoYo is vomiting?”  Instead, use a question that requires a more thorough answer, such as “Oh no so I hear YoYo isn’t feeling well. Can you tell me what has been going on with YoYo?”

-> Don’t be afraid to reword your question. For instance, let’s say you ask “Did your pet get into any toxins?” “No.” **Reworded** “Did your pets receive or eat any animal or human medication?” (Or “what medications does your dog get” if you are being proper and using an open ended question!) “Oh yeah he wasn’t feeling well so I gave him 5 ibuprofen…”  

-> Keeping a list of questions to ask in specific situations can be helpful. For example, in a pupper that has been having diarrhea, I learned to ask questions like “What does Tubbers eat normally? Has he had a diet change or human food recently?” “What toys or other objects does Flufferbutt like to chew?” “Has Ubersnoodle been dewormed recently? Do you remember when and with what medication?” 

-> Their answers might change. The most frustrating thing that happens to me is that I will ask something, get response X, and then my attending vet will come in, ask the same question, and get another answer! That’s okay! Sometimes it take repetitive questions for a client to remember something. Have heart, it happens to everyone!

-> Don’t beat yourself up if you forget to ask something. I promise you, even though I have been doing this for almost a year, I always forget to ask something. And that’s okay! It takes time, practice, and experience with other cases to know what to ask and how to ask it. Just like everyone else in clinical rotations, it will come in time. 


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Other useful links: Surviving clinical rotations #1 (how to be prepared for clinical rotations), #2 (Presenting a case: Signalment)what is a clinical rotation

Before the videotapes were found, the extent of Karla Homolka’s involvement in the rapes and murders perpetrated by her husband Paul Bernardo was unknown, but once they were viewed, it showed her role was that of a willing participant.

All of the following quotes are from Invisible Darkness by Stephen Williams.

Tammy Homolka

While hesitant at first, Karla eventually agreed to let Paul rape her younger sister Tammy, a plan that came to a fatal conclusion on December 24, 1990. After plying her with alcoholic drinks laced with the Halcion she stole from her work, Tammy passed out. Karla stripped and then used a Halothane-soaked cloth to cover Tammy’s nose and mouth while Paul retrieved his video camera. Karla told Paul to put on a condom several times before giving up and saying, “Fucking do it. Just do it.” She sucked on her sister’s breasts as Paul told her to do. Then, as she was kneeling between Tammy’s legs, “Paul pushed her head down and Karla started to perform cunnilingus on her sister.” She became distraught because Tammy had her period. Paul urged Karla to finger her sister and then demanded she taste it, which she did. When Paul asked if it tasted good, “Karla looked into the camera, daubed her lips on the cuff of her white turtleneck and said, ‘fucking disgusting.’“ She later tried to claim that remark was towards the act itself. Tammy died by choking to death on her vomit.

Jane Doe

Jane Doe refers to the unidentified girl Karla knew from a former job at an animal clinic. As a wedding present, Karla invited her over to 57 Bayview Drive, spiked her drinks with Halcion, which caused her to pass out and had her waiting for Paul in their bedroom. He was worried Karla was using the same drugs that caused Tammy’s death, but she insisted everything would be fine. The following are excerpts of Karla’s role in the rape:

“Next, Karla started performing cunnilingus on Jane. She licked Jane and then raised her head, licked her lips, wagged her tongue back and forth and smiled wantonly for the camera. Then, she did the extreme close-up thing, just the way she had the previous Christmas. Only this time Karla pretended to plant a big, fat kiss on the camera lens.
Then she sucked Jane’s breasts, fir the right, then the left. When she sat up, Paul caught her smiling face.”

“Karla had kept her sleeveless lifeguard tank top on, but she was naked from the waist down. She climbed over Jane’s face, held up the tank top and rubbed her clitoris on Jane’s nose and mouth.
‘Okay, okay,’ Paul said. ‘Take her hand and put it in your cunt.’
Kneeling beside Jane, with her legs apart, Kala took Jane’s lifeless hand and rubbed it against her labia. She rotate her hips lasciviously and then got that incredible look in her eyes - that look of incomparable lust and evil that Paul loved so much.
‘Put the fingers inside you,’ he said, and Karla did just as she was told.”

Leslie Mahaffy

After Paul had kidnapped Leslie Mahaffy in the early morning hours of June 15, 1991, he woke up Karla and told her to stay in the bedroom because he had brought someone home. She then fell back asleep. When she woke up for the day and went downstairs, she suddenly became furious  Paul had used their fancy champagne glasses on Leslie. Later that day, Paul led her upstairs to the bedroom where Karla was and asked Leslie whether she’d like to have to sex with two people. She began to whimper, so Karla told Paul to “tell her the other person’s a woman.”
“Paul told her she was going to get a big kiss. He turned on the camera and watched as Karla moved in front of Leslie and bent over to give her a kiss, pushing on the younger girl’s lips twice, making it squishy and moist. Leslie did not move, but Karla knew full well that sharing this kind of kiss with another woman would excite Paul.”

“She spread the comforter and one of their electric blankets in front of the hope chest, along with her new king-size pillows. Leslie was lying with her legs spread, with Karla kneeling and kissing her vagina. Paul tried for a close-up of Karla’s face. Raising her head, she smiled and wagged her tongue with that devilish glint in her eye.”

“Karla was splayed on her back, eyes closed like a happy sunbather, while Leslie lay on her stomach with her blindfolded head between Karla’s legs.
‘Is she making you feel okay?’ Paul asked Karla, and he saw her smile.
Whatever Paul got, Karla wanted too. She moved to a kneeling position, arching her buttocks while Paul told Leslie to ‘caress and make her feel good.’
‘Put your tongue right in her asshole, push it right in.’ he said. Lesle touched Karla’s thigh, and did as she was told.
The whole scene lasted a little more than twenty-five minutes.”

In the final sequence, Karla videotaped Paul anally raping Leslie and ignored her cries in pain for help.

Kristen French

On April 16, 1992, Kristen French was kidnapped while walking home from school. This time, Karla assisted in the abduction by asking the teenager for directions as Paul forced her into the front seat of his car at knife-point. Karla made sure she didn’t move on the drive back to their house by yanking on her hair. Once inside the master bedroom, Karla directed behind the camera, telling Kristen to smile as Paul raped her and assured her she was doing a good job. The next day, Karla dressed up in the closest thing to a schoolgirl outfit she could find to match Kristen and Paul videotaped them doing “girl stuff,” such as putting on makeup and perfume. After that, “Karla knelt between Kristen’s legs and began exploring her vagina with her tongue.” Then, “While Karla lay back on the bed with both hands behind her head, Paul told Kristen to put her fingers inside, and he moved in for a close-up.
Are my nails hurting you?’ she inquired with some concern, but Karla told her it felt ‘real good.’
‘I like little girls,’ said Karla.”

“Karla brought Kristen’s hand to her breast and told her that she was a ‘good, little sex slave.’“

Karla was operating the camera once again as Kristen was performing fellatio on Paul. “Okay,’ Karla said, cuing Kristen to say a line about how she hated her boyfriend and Paul was her boyfriend and he should ‘fuck all the girls at Holy Cross,’ if it would make him happy. The bedsprings were squeaking faster and faster, when Karla interjected with the breathless information that she ‘got some good mouth shots.’
Suddenly, from the basement, there was a loud whine. The dog was feeling deprived. The sound distracted Paul but Karla urged Kristen on, calling her a ‘good cock sucker.’
‘I want to see a mouth full of cum, Kristen,’ Karla said, over the whirring motor of the camera and the baleful sound of the dog.”

In the next sequence, “the title track from Ice-T’s Power boomed over Karla, who smiled as she put the neck of an empty wine bottle all the way up Kristen’s vagina.
Using both of her hands, Karla forced the glass bottle in and out of Kristen French more than forty times.”

So get this

Today, Planned Parenthood was in my clinic to do a presentation on birth control options so that we can be informed and can offer family planning and education to our patients. I was pretty excited, since, you know, we’re in FLORIDA and PP doesn’t get Sec. 10 funding or any state assistance here.. so I honestly didn’t even know there WERE any PP clinics around until this training was scheduled.

So these two young reps walk in.. both looking like your average Starbucks™ blond chicks, one with a turtleneck and 90s glasses on and the other in a knit sweater with a septum piercing…


And they’re going through a super informative session on birth control (which is VERY descriptive and makes lots of my coworkers super uncomfortable and I LOVE it) but then they talk about some side effects and are talking about how some cultural beliefs keep women from using hormonal contraception bc it can prevent them from having a cycle….

And then she uses the example of “Hispanic” women who believe that if you don’t bleed, the blood will filter elsewhere into your body like “into your brain”

What the actual fuck? My nursing supervisor (a badass Puerto Rican woman) just gives me this LOOK like “WHAT KIND OF RACIST BULLSHIT IS THIS?”

Like seriously.. these gringas walk into an addiction clinic with a staff of 22 people where 9 of them are poc and 4 of those 9 are Latinas… Chica you picked the wrong group to try and make out as hysterical and superstitious…

I was dumbfounded.. I couldn’t believe what I was hearing.

South African nine-year-old becomes third HIV infected child to go into remission

A South African nine-year-old is the world’s third child born with HIV to go into remission, scientists have said.

The child has had a healthy immune system for more than eight years after receiving a short course of treatment in early life, according to a new study.

Researchers believe aggressive treatment soon after infection could enable long-term remission of the disease – which, if it lasts, would be a form of cure for the deadly virus.

HIV-positive individuals must take daily antiretroviral drugs (ART) for their whole lives to control the infection’s progression.

But experts were surprised by the results of the clinical trial, presented at a conference in Paris, which appears to have left the child with no need for medication.

The study was sponsored by the US National Institute of Allergy and Infectious Diseases, which previously found that early treatment helped babies survive.

Researchers did not identify the minor but said they started on HIV drugs when they were two months old and stopped 40 weeks later.

Tests when the child was nine and a half years old found signs of the virus in a small number of immune system cells, but none capable of reproducing.

The child does not have a gene mutation that gives natural resistance to HIV infection, the researchers said, so remission seems likely due to the early treatment.

Experts have stressed the case is extremely rare, and does not suggest a simple path to a future cure for Aids, which killed an estimated 1.1 million people worldwide in 2015.

Linda-Gail Bekker, president of the International Aids Society, said the study raises the “interesting notion that maybe treatment isn’t for life” but was “clearly a rare phenomenon”.

“It’s a case that raises more questions than it necessarily answers,” she told Reuters.

So far, similar results have been seen in two other children, one in the US and another in France.

A French woman who was born with HIV and is now around 20 has had her infection under control despite no HIV medication since she was around six years old.

And the infection was suppressed in a baby born with the virus in Mississippi in 2010 for 27 months after stopping treatment before it reappeared in her blood. She was able to control the virus again after treatment resumed.

Around 18 million people – half of all those living with HIV around the world – take ART, which can cause unpleasant side effects.

These drugs could in future be replaced with six yearly injections that slowly and continuously release HIV medication into the blood, scientists also revealed in separate research.

At least a dozen adults have had remissions lasting for years after stopping HIV medication.

A study under way now is testing whether treating HIV-infected newborns within two days of birth can control the virus later after treatment stops.

It started in 2014 in South America, Haiti, Africa and the United States, and some of the earliest participants might be able to experiment with stopping treatment later this year.

Access to drugs and fewer people being infected with HIV have led to a steep fall in the number of deaths related to the virus, according to the World Health Organisation. In 2015, 45 per cent fewer people died of the virus compared to in 2005.

Dr Michael Brady, medical director of the Terrence Higgins Trust, said the case report was “really interesting” and called for further research into the phenomenon.

“Early HIV therapy, in both children and adults, has been shown to reduce some of the damage to the immune system that HIV causes in the first few weeks and months of infection,” he said.

“If we can understand this mechanism better it will hopefully lead to novel treatment strategies and, maybe one day, a cure.

“Further research is needed, but this case adds to the hope that, one day, we may be able to prevent the need for life-long therapy with a short course of early HIV treatment in infancy.

“For now, however, early diagnosis and life-long treatment for HIV remain our best options for fighting the epidemic.”

So, fun story. For every major operation/milestone, I bring my vet clinic treats. When I had my Mexican street dog spayed, I brought them chips and salsa, and a large piñata filled to the brim with candy.

Later that evening, I was sent a video of the entire staff beating the piñata and laughing maniacally.

Moral of the story: Give your vet clinic fun presents. They will appreciate it, and you will be forever loved by the staff.

There are plenty of mnemonics out there to help medics organise the way information about a condition is presented, e.g. Dressed In a Surgeon’s Gown A Physician Might Make Progress. I follow a similar structure when writing notes on conditions, but don’t keep to any mnemonic.

Here’s my structure:

[CONDITION NAME] - one liner definition

  • Aetiology - including relevant pathophysiology (I know they are different…) & risk factors.
  • Epidemiology - only significant demographic details (sex, age, ethnicity, geography)
  • Screening programs / Prevention (e.g. vaccines) - if relevant
  • Clinical presentation - including symptoms/signs and history details (e.g. rate of onset)
    • Diagnostic criteria & other scoring systems
  • Investigations - can be split into:
    • Basic work-up
    • Diagnostic tests
    • Monitoring disease activity
  • Treatment - can be split into:
    • Acute & long-term
    • Conservative (e.g. advice/lifestyle tips), Medical (i.e. drugs), Surgical
  • Prognosis - usually one line (good/bad) & any significant details (e.g. short lifespan)
  • Complications - disease-related & therapy-related

I try to only write things down that are clinically relevant - i.e. what info would help me recognise and manage this condition correctly in the real world? I keep the science pretty basic when comes to aetiology/pathophysiology - enough to offer a robust explanation to a patient and if asked on a ward round. I’m pretty fluid about the level of detail depending on the condition.

Another advantage of digital notes is the ability to add photos/illustrations, especially helpful for x-ray signs or funny rashes. My notes are tailored to me and aim to be concise & comprehensive, which means:

  • Lots of personal abbreviations
  • Very little text - love bullet points, hate reading
  • Only images/words which clarify things I don’t think I will know when I need to revise 

When condensing a complicated disease down into punchy bullet points, keep asking yourself, ‘will I be able to re-piece together how this management plan flows in the real word from these few words?’ I have fallen into a trap of over simplifying.

It’s important to find a system that works for you and stick with it consistently. You’ll thank yourself for it when you’ve made exam revision that little bit more doable.

My Uworld notes- 6
  • serum sickness is a type 3 HSR characterized by deposition of circulation complement fixing immune complexes and resulting vasculitis. Associated findings include fever, urticaria, arthralgias, glomerulonephritis, lymphadenopathy and a low serum c3 level 5-10 days after intravascular exposure to antigen. type 3 HSR typically activate complement at local site where immune complexes containing IgG and or IgM complement fixing antibodies have been deposited. This often results in hypocomplementemia including decreased C3 level

  • liver dz-a/w AFP

  • carcinoembryonic antigen (CEA) a/w colorectal cancer

  • CA125 -ovarian cancer. Both CEA and ca125 are fr monitoring purposes

  • PSA prostate specific antigen is most useful in establishing extent of prostate cancer and evaluating response to prostate cancer tx.

  • Iced water think cold – cold think cold agglutinins – cold agglutinin associated with infection with mycoplasma pneumonia

  • another cold agglutinin is EBV

  • free air in peritoneal cavity= bowel perforation

  • pancreatic calcification= chronic pancreatitis

  • heavily calcified vessels = atherosclerosis and vascular dz

  • distended bladder= urinary retention

  • air in billiary tract a/w gallstone ileus

  • fluoxetine a/w anorgasmia and decreased libido and increase latency to orgasm. They can however be used to tx premature ejaculation

  • phenelzine= MAO-I used in tx of depression monoamine oxidase is a mitochondrial enzyme that deaminates primary and secondary aromatic amines

  • tricyclic antidepressants can cause orthostatic hypotension example imipramine

  • trazadone- priapism

  • paroxysmal breathlessness and wheezing in young patient unrelated to ingestion of aspirin, pulmonary infection inhaled irritant stress and or exercise should raise a strong suspicion for extrinsic allergic asthma. The granule containing cells in sputum are most likely eosinophils and the crystalloid bodies are most likely Charcot Leyden crystals (contain eosinophil membrane protein)

  • chronic eosinophilic bronchitis in asthmatics involves bronchial wall infiltration by numerous activated eosinophils largely in response to IL5 released by TH2 cells

  • digestion and absorption of nutrients primarily occurs in small intestine. SI cells produce enzymes responsible for nutrient absorption. Proteins in ingested food exist primarily as polypeptides and require hydrolysis to dipeptides tripeptides and amino acid for absorption. Hydrolysis of these polypeptides is accomplished by proteolytic enzymes such as pepsin and trypsin

  • these enzymes are secreted inactive proenzymes trypsinogen and pepsinogen from stomach and pancreas

  • trypsin activates other proteolytics enzymes including chymotrypsin carboxypeptidase and elastase. Activation of trypsinogen to trypsin is achieved by enteropeptidase (or enterokinase)an enzyme produced in duodenum

  • enteropeptidase deficiency results in defective conversion of trypsinogen to active trypsin

  • lipase secreted from exocrine pancreas is the most important enzyme of digestion of triglycerides. Chronc pancreatitis is a painful condition that causes lipase deficiency. This leads to poor fat absorption and steatorrhea

  • secretin is a peptide hormone secreted by S cells of duodenum un response to low duodenal pH. Secretins timulates secretion of bicarbonate from the pancreas and gall bladder and reduces acid secretion in the stomach by reducing production of gastrin. Neutralizing the acidic pH of food entering the duodenum from the stomachis necessary for proper function of pancreatic enzymes (amylase, lipase)

  • trisomy 18 (47XX: Edwards syndrome

    • face: micrognathia, microstomia, eye defects (microphthalmis, cataracts) low set ears and malformed ears prominent occiput

    • CNS: microcephaly, neural tube defects (meningocele, anencephaly), holoprosencephaly, arnold chiri malformation, severe MR delayed psychomotor development

    • musculoskeletal: clenched hands with overlapping fingers (index finger overrides the middle fingerand fifth finger overrides the fourth finger) rocker bottom feet short sternum and hypertonia

    • cardiac: VSD, PDA

    • distinguishing features: clenched hands and or overlapping finger

    • GI: Meckel diverticulum, malrotation

    • ultrasound: intrauterine growth restriction and polyhydramnios especially ina fetus with abnormal hand arrangement

  • unlike patients with Edward’s syndrome neonates with Patau syndrome (trisomy 13) have cleft lip and palate, polydactyly and omphalocele. Patau syndrome is not a/w low set ears and overlapping fingers but do present with rocker bottom feet also

  • 47XXX karyotype is clinically silent however, some affected women have slightly decreased IQ scores. Female newborns with this karyotype are phenotypically normal with no obvious dysmorphism

  • 47XXY Kleinfelter’s syndrome: may be a/w mild mental retardation or normal intelligence. The typical patient is tall mall adult with gynecomastia small testes and infertility. Male newborns with this karyotype are phenotypically normal with no obvious dysmorphism. The clinical findings do not become apparent until adulthood.

  • Sudden onset of abdominal or flank pain hematuria and left sided varicocele together suggests renal vein thrombosis a well known complication of nephrotic syndrome. Nephrotic syndrome is a hypercoagulable state d/t increased loss of anticoagulant factors especially anti thrombinIII (responsible for the thrombotic and thromboembolic complications of nephrotic syndrome)

  • venous drainage from left testes travels throught the left testicular vein into the left renal vein and from there the IVC. In contrast to the right testicular vein which empties directly into the IVC. This difference in venous drinage gives diagnostic significance to left sided varicocele in that it often indicates an occlusion of the left renal vein by a malignant tumour or thrombus

  • malaise low grade fever followed by a facial rash. Feels better now but still has the rash- red flushed cheeks with – clinical presentation of erythema infectiosum aka fifth dz. As the facial rash fades an erythematous rash in reticular lace like pattern often appears on trunk and extremities. The rash of erythema infectiosum is thought to result at lest partly from local immune complex deposition once serum levels of virus specific IgM and IgG have attained high enough levels.

  • Erythema infectiosum= non enveloped DNA virus called parvo B19. The blood group P antigen globoside is a parvovirus B19 is highly tropic for erythrocyte precursors particularly erythrocytes and erythroid progenitor cells

  • Parvo B19 replicates predominantly in the bone marrow

  • anthracyclines daunorubicin doxorubicin epirubicin and idarubicin are chemotherapeutic agents a/w severe cardiotoxicity because of their unique ability to generate free radicals.. Dilated cardiomyopathy is dose dependent and may present months after discontinuation of the drug . Swelling of sarcoplasmic reticulum is the morphologic sign of early stage doxorubicin associated cardiomyopathy. Followed by loss of cardiomyocytes and its symptoms are those of biventricular CHF including dyspnea on exertion orthopnea and peripheral edema

  • dexrazoxane prevents Doxorubicin associated cardiomyopathy because dex is a iron chelating agent that decreases formation of free radicals by anthracyclines.

  • Restrictive cardiomyopathy a/w hemochromatosis amyloidosis sarcoidosis and radiation theraapy : remember -osis

  • hypertrophic cardiomyopathy caused by mutation of beta myosin heavy chain

  • focal cardiomyopathyscarring commonly results in MI

  • pericardial fibrosis usually follows cardiac surgery radiation therapy or viral infections of the pericardium

  • PCP aka angel dust aka phencyclidine commonly associated with violent behaviour

  • LSD can also cause aggressive behaviour but it is more typically characterized by affective liability thought disruption )delusion) and visual hallucination whereas PCP produces more psychomotor agitation including clonic jerking of extremities

  • angel dust can be put on marijuana and smoked LD is ingested orally

  • secobarbital is a street barbiturate a CNS depressant which leads to drowsy drunken state of consciousness without the violent behaviour

  • heroin (opioid) produces CNS psychomotor depression and respiratory depression miosis and bradycardia are common

  • dry tap with no splenomegaly or lymphadenopathy – think aplastic anemia which causes pancytopenia

  • aplastic anemia= hypo cellular bone marrow with fat cells and fibrotic stroma

  • hyper cellular marrow with increased blasts found in myeloproliferative d/o and certain leukemias

  • most common side effect of streptokinase= hemorrhage . Streptokinase is a thrombolytic agent that acts by converting plasminogen to plasmin which subsequently degrades fibrin. It is a foreign protein derived from streptococci and induce HSR.

  • Dissection of ascending aorta manifests as tearing chest pain that radiates to the inter-scapular area commonly occurs in hypertension marfans and ehlers danlos

  • hyperactive jaw jerk reflex when lightly tapped= chvostek’s sign- Hypocalcemic – facial m contraction elicited by tapping facial nerve just anterior to ear. The most common cause of outpatient hypocalcemia is primary hypoparathyroidism which is often d/t prior loss of parathyroid tissue during thyroidectomy

  • scotoma is visual defect that occurs d/t pathologic processes that involve parts of retina or optic nerve resulting in discrete area of altered vision surrounded by zones of normal vision. Lesions of macula cause central scotomas.. examples would include MS, diabetic retinopathy and retinitis pigmentosa

  • verapamil is a calcium channel blocker that slows SA and AV node phase 0 depolarization (in nodal cells, the phase of depolarization is mediated by calcium influx)

  • phase 0 depolarization of cardiac conduction system occurs during diastole thus verapamil slows diastolic depolarization

Let’s get rid of the term ‘borderline personality disorder’

The psychological diagnosis of Borderline Personality Disorder (or BDP) continues to be one of the more heavily debated of the psychological disorders.  The straight-up truth, however, is that it’s a full on pejorative label with stigma that all too often causes clinicians to view borderline clients in a negative and resentful fashion.  The significant majority of people identified as borderline are women and the diagnostic criteria reflects a largely male-oriented ideas of healthy psychological functioning.

It can be true that psychotherapy with borderline clients can often be extremely difficult and arduous and it is not uncommon for therapists to feel exhausted and manipulated by their borderline clients.  Although I feel that the specific ways in which BPD is conceptualized and understood often contributes to this negative outlook.

Psychological theorists, such as Judith Herman, Basil Van der Kolk  and many others, argue that BDP is often better understood as a ‘complex’ form of posttraumatic stress disorder (PTSD). Complex PTSD is a more pervasive and ingrained form of chronic difficulties with stress and anxiety that stem from significant experiences of trauma.  Many of the symptoms entailed in complex PTSD can look very similar to the clinical presentation of BDP.

The idea of seeing BPD as a complex form of PTSD is supported by multiple research findings that have found that a significantly high percentage of people diagnosed with BPD have histories of being victims of substantial traumas (Courtois, 2009; Van der Kolk et al., 2006; Driessen et al., 2000; Zanarini et al., 1997; Ogata et al., 1990).

A study reported by Zanarini et al. (1997), for example, looked a large sample of individuals diagnosed with BPD and found that a significant majority of these people had experiences with sexual abuse at some point during their childhoods. Based on these results, and the results of additional studies, Zanirini and her colleagues concluded that severe experiences of trauma appear to be a substantial etiological factor in most cases of BPD.

Judith Herman (1997) notes that identifying someone as being the victim of a trauma tends to elicit a more sympathetic reaction from psychotherapists and other mental healthcare providers. That is to say, a therapist who sees her client as having trauma-related difficulties is less likely to feel annoyed and resentful toward the client as opposed one who is identified as borderline. Complex PTSD is simply a more compassionate diagnosis… one that fosters a greater degree of understanding and empathy (factors that are often essential if a treatment is going to be effective).

Research reported by Courtois et al. (2009) and Van der Kolk et al. (2006) found that treatments that are based on a primary diagnosis of Complex PTSD are substantially more effective and successful compared to those based upon a primary diagnosis of BPD.  Considering that these two diagnostic labels essentially refer to the same condition, it would appear that the therapist’s perspective, compassion, and understanding concerning the root cause of psychological difficulties might often be a key factor in determining a treatment’s ability to succeed and bring about positive results.

Of course there are plenty of people in the professional community who argue against this whole idea, who reject the notion of re-conceptualizing BDP as a complex form of PTSD.  And many would site the neurological evidence gathered that suggests BPD is a largely organic condition caused by subtle neurological abnormalities that lead to greater sensitivity and vulnerability to negative affect.  This idea is largely supported by functional MRI scans that demonstrate significant alterations in the brain scans of subjects identified with BPD versus neurotypical controls.

These opponents argue that the high rates of histories of trauma among those identified with BPD is merely a co-morbid correlation.  Some have even gone so far as to suggest that the increased prevalence of histories of childhood sexual abuse in BPD may itself be a result of these neurological factors. The argument here is that the reduced abilities for impulse control and social inhibition acts as a factor that increase the likelihood that a specific child will be a victim of sexual abuse (Siever, 1997; Siever et al., 1998).  

Yes, you read that right…  These guys actually came up with a neurological version of blaming the victim.  It’s deplorable and the kind of arcane thinking that makes us headshrinkers look like assholes.   

What I feel these arguments fail to take into account, however, is the fact that the brain is a much more plastic and dynamic organ than many give it credit for.  Neurological structures are just as likely to be shaped and affected by our experiences as the other way around.  More current research has shown similar structural abnormalities among combat veterans diagnosed with PTSD.  This shows that traumatic experiences can impact on the functioning and even the structural anatomy of the brain. 

And the heightened sensitivity in limbic regions of those identified with PTSD are not all that different compared to similar findings among patients identified with BPD.

Now of course the real problem with re-conceptualizing BPD as complex PTSD is that there are many people diagnosed with BPD who do not have histories of significant abuse and trauma (Zlotnick et al., 2003). When considering this factor, however, it is important to keep in mind that what constitutes a psychological trauma can be an extremely relative and subjective matter.  Physical and sexual abuse is clearly traumatic and it can be easy to understand how such experiences might impact on psychological functioning. Other instances of trauma, however, can be much more subtle and covert, yet nonetheless be just as psychologically damaging.

In my own research (Goldblatt et al., 2003), my colleagues and I found that children who were neglected and who were separated from primary attachment figures were indistinguishable from children who had experienced severe physical and/or sexual abuse on a number of empirical rating scales. 

These results, coupled with the results of similar studies (Bradley, 2000; Salzman et al., 1997; Van der Kolk, 1994) indicate that neglect and attachment difficulties can be just as traumatic and psychologically damaging as childhood experiences of sexual and/or physical abuse.

What this indicates is that people diagnosed with BPD who do not have histories of severe childhood trauma may still be understood as possibly experiencing a complex form of PTSD.

With the publication of the new Diagnostic and Statistical Manual of Mental Disorders (the DSM-5), Complex PTSD has been recognized as an official diagnostic label.  Unfortunately, the research has found that the inclusion of this disorder has not correlated with a reduction of cases where patients are identified as BPD.  There are a number of factors that may be contributing to this finding… not the least of which being that, as a new diagnosis, clinicians might shy away from utilizing Complex PTDS for worries that insurance providers will reject reimbursement claims.  

Hopefully things will change soon and we will see less and less cases of BPD.  We’ll see…




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  • American Psychological Association (2000). The Diagnostic and Statistical Manuel of Psychological Disorders, Volume IV, Text Revised (TR). Washington, DC: American Psychological Association Press. 
  • Bradley, S.J. (2000). Affect Regulation and the Development of Psychopathology. New York: The Guilford Press. 
  • Driessen, M., Herrmann, J., Stahl, K., Zwaan, M. et al., (2000). Magnetic Resonance Imaging Volumes of the Hippocampus and the Amygdala in Women with Borderline Personality Disorder and Early Traumatization. Archives of General Psychiatry, Vol. 57(12), pp. 113-123. 
  • Courtois, C.A. Ford, J.D. (2009). Treating Complex Posttraumatic Stress Disorder: An Evidence-Based Guide. New York: The Guilford Press. 
  • Goldblatt, N.G.F., Mercer, B.L., & Wood, P. (2003). Assessing Object Relations in Foster Children. Berkeley, CA: The Wright Institute. 
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  • Herman, J. (1997). Trauma and Recovery: The aftermath of Violence – From Domestic Abuse to Political Terror. New York: Basic Books Press.

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Kalat, J.W. (2008). Biological Psychology, Tenth Edition. Pacific Grove, CA: Brooks-Cole 
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  • Zlotnick, C., Johnson, D.M., Yen, S., Battle, C.L., Sanislow, C.A., Skodol, A.E., Grilo, C.M., McGlashan, T.H., Gunderson, J.G., Bender, D.S., Zanarini, M.C., & Shea, T.M. (2003). Clinical Features and Impairment in Women with Borderline Personality Disorder (BDP) with Posttraumatic Stress Disorder (PTSD), BDP Without PTSD, and Other Personality Disorders with PTSD. The Journal of Nervous and Mental Disease, Vol. 191(11), pp. 706-713.
Dear Rookie,

I hope for you that you find an incredible partner. Find a mentor, a veteran on there last leg, “retired on duty”, and spark thier creativity to teach again. So much more credit should be given to experience. Find a veteran and pic thier brain. Challenge them in a respectful way. Watch them. Learn from them. Understand this field is fluid and constantly changing but some things never change. Understand that patient presentation is largely first hand experience. Those text book presentations are few and far between. You will rarely have the exact answers….and that’s ok. Base your treatment decisions on clinical presentation and a solid foundation in physiological understanding and you will be just fine. Signed, A Paramedic Friend