Hi all! Ive just received my track for GPST1 in Royal preston
Just wanted to know if anyone has done these at RPH and how they found them? Slightly worried for paeds + obgyn as i have zero experience in these :/
I enjoyed ED in my previous DGH for FY2 but scared it will be a big step up
Any advice will be appreciated :))
Hello GPUK,
looking for some honest perspectives from GPs working in Scotland, particularly Edinburgh, as well as anyone who has worked in both Scotland and England.
I’m currently an ST3 in England and have a salaried GP role lined up in London after CCT. I’ve built a really good relationship with the partners there and there seems to be a genuine potential route into partnership longer term. On the other hand, my wife has a strong chance of being offered a funded PhD in Edinburgh in a fairly competitive subspecialty area (surgical), so a move there is on the table. She has been offered a prestigious PHD in London but currently not funded.
I’m conscious this is essentially a relationship compromise decision, and I’m trying to weigh up potentially stepping away from a very good opportunity in London with a clear, if uncertain, pathway for something more unknown in Scotland. There is also the consideration of leaving friends and family. We also have Young children. Just trying to get broader perspectives from those who’ve been there or are currently working in Scotland or Edinburgh.
A few things I’m trying to understand:
I appreciate this will vary massively depending on urban vs rural and individual practices, but I would really value hearing people’s actual experience! THANKS
How are we feeling then? One week to go!
The panic is setting in and I can't seem to quell it. For those who have taken it, how did it feel one week to results?
GP registrars and trainers,
Please sign the BMA petition to hold optum to account. It is important that we all come together to send a clear message!
I’m starting GP training this August and I wanted to ask whether any of you guys have had a fleet vehicle during it or got an approval for one at the start of training. If so, when should I apply, so as to cover the 36 month period and sort out the approvals etc.
Doing a bit of locum to keep myself above 40 NHS sessions and the most convenient work is SystmOne. I avoided it since CCT but now I'm confronting this demon.
Got my head around simple consultations, prescribing acutes, pathology requests... But any tips to help would be gratefully received.
hi all,
I am looking for a remote job and saw this advert. is being expected to do 30 triages an hour every hour all day totally insane or people are doing these numbers now? even just the sick notes take me 3 minutes including sending the attachment and having a quick look back at the notes
interested to hear peoples thoughts
link to ad for reference
I recently had a patient who “demanded” a vaginal examination. They presented with some light spotting and I saw that they were overdue a smear test and so I advised that they go get their smear test ASAP as the vaginal examination would not alter management (as they would need the smear test regardless). However, the patient was adamant that they needed a vaginal examination there and then and pressured me into doing it in the end against my judgement.
I have been reflecting on this and was wondering what others would have done in this scenario? I am a male GP and have also reflected on if I had been a female GP and the genders were reversed, and a male patient had “demanded” an intimate examination, would that have made the situation more inappropriate? And if so why should that be the case?
As part of my role as a registrar, I partake in a weekly ward round review at a care home. Context - it’s a private contract between the practice and the care home, one of the GP partners also does a ward round during the week. I was late on one occasion and they asked my practice where I was. I have flexible working and later morning starts as per my OH adjustments. I was doing admin work in the morning and having laptop issues. As well as this, I’ve had significant life circumstances. Despite all of this, my CS has decided to investigate why I was late on this particular day with the care home (I get along with the staff here). They’ve gone as far as to review CCTV footage as to when I arrived to the car park. There’s a disparity of about 1-2 hours as when I disclosed I was there (I acknowledged this could be an error on my part due to stress). All jobs were completed in a timely fashion. Now I’m being reprimanded for it and a note on my portfolio, simply because I was late: I feel this is over the top, especially having CCTV reviewed as a doctor.
Please advise.
I’m ST3, was supposed to CCT in August and start radiology training right after. Unfortunately, I failed my recent SCA sitting and the next possible one is not until September. I’m in a dilemma at present as I really wanted to start radiology training and can’t go through the process of applying again in the next cycle. At the same time, I don’t want to lose all the grind I poured into GP. Can anyone with experience on this guide me on what my options are?
Much appreciated
How to do revision on work days after job when exam is in July? Any tips? Thanks
I’m a solo developer in Doncaster building a secure platform for clinics to issue verified, uneditable test results that patients can share safely. When someone shares a result, the recipient can be very sure it:
- came from the clinic
- hasn’t been tampered with
- is linked to the correct person
I don’t think anything on the market does this as reliably as I want to.
I’m trying to talk to UK clinics about a small, low-risk pilot, but so far emails and cold calls aren’t getting much traction.
My question is: for an industry as sensitive and regulated as medical/healthcare, what’s the best way to get clinics or small healthcare businesses to partner on an idea like this?
Should I keep trying emails and calls, or is there a better approach
Who is the right person to contact (owner, practice manager, clinical director, IT/compliance)?
What kind of message or offer works best in a regulated industry where people are cautious about new tools?
If you’ve worked with clinics, GPs, or other healthcare providers, or have experience partnering in a regulated sector, I’d really appreciate your advice.
Hi there. I am a pregnant ST2 who will be going on maternity leave 3 months into ST3. I need to set PDPs for ST3, should I set long term PDPs to be completed over the course of ST3, or should I set short term goals to be completed over the 3 months before I go on mat leave?
These deep dives provide a physiological anchor for those who want to understand the 'why' behind the guidelines. Protocol-driven medicine is boring and easy to forget.
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Thirty percent of UK adults aged 16 and over are obese, as of 2024.
For decades, the clinical response was diet, exercise, and surgical referral for a small minority, with medical therapy (orlistat and the like) occupying an uncomfortable middle ground of modest efficacy and poor tolerability.
That has changed. GLP-1 agonists and dual GLP-1/GIP agonists now produce headline-grabbing weight loss. Less spoken about is lean mass loss, accelerating bone turnover, and near-universal weight regain on discontinuation.
A 48-year-old woman with a BMI of 36 and prediabetes is considering starting "Mounjaro." She has tried multiple weight loss programmes without sustained success. What are the realistic expectations and risks?
A 54-year-old man on tirzepatide for 14 months has lost 24% of his body weight. He is asking whether to continue, as he's read on Facebook about the drug causing muscle loss. How should this be approached?
A 62-year-old woman discontinues semaglutide after 18 months because of supply issues. Within 9 months she has regained two-thirds of the weight she lost. What predicts this?
A 39-year-old patient on tirzepatide is scheduled for elective laparoscopic cholecystectomy in 10 days. Should the GLP-1 be held, and for how long?
These four scenarios capture the everyday GP challenges with this drug class. We're usually not the ones prescribing these medications, and yet every third patient seems to be taking them.
The goal of this deep dive is to explain the mechanistic rationale behind the current generation of obesity pharmacotherapy: why incretin mimetics work where calorie restriction fails, what dual GIP/GLP-1 agonism adds beyond GLP-1 alone, where the real-world efficacy differs, and what specifically to counsel for in primary care.
Body weight is controlled by a neuroendocrine network linking peripheral fat stores, the gastrointestinal tract, and the central nervous system.
## Hypothalamic Integration
The hypothalamic arcuate nucleus is the primary sensory gateway for peripheral energy signals. It contains two opposing populations of neurons with their own neurohormonal mediators: a pro-satiety group that suppresses appetite and increases sympathetic energy expenditure, and a pro-hunger group that does the opposite. The balance of activity between these groups determines whether the brain tells the body to eat or stop eating.
## The Adipose Hormone: Leptin
Leptin is secreted by fat cells in direct proportion to fat mass. It crosses the blood-brain barrier, activates the pro-satiety neurons, and suppresses the pro-hunger neurons. In the healthy state, rising fat mass raises leptin, which reduces appetite and increases energy expenditure. Falling fat mass (as in fasting or caloric restriction) reduces leptin sharply, activating the starvation response. In effect, leptin secretion is a negative feedback loop that regulates fat stores and satiety.
## The Gut: GLP-1, GIP, Ghrelin, and PYY
The gastrointestinal tract provides both the primary hunger signal and the primary satiety signal.
Ghrelin, secreted by the empty stomach during fasting, activates the pro-hunger neurons. It is the only major orexigenic gut hormone and rises predictably before meals and during caloric restriction.
After meals, the small intestine releases satiety hormones: GLP-1, GIP, and PYY. These reach the brain by two routes - both directly across the blood-brain barrier (at sites where it is permeable), and indirectly via the vagus nerve.
GLP-1 is the central hormone. It augments insulin secretion in a glucose-dependent way (which is why GLP-1 drugs do not cause hypoglycaemia in non-diabetic patients), slows gastric emptying, and suppresses appetite centrally. GIP synergises with GLP-1 in the brain and directs lipids into peripheral fat depots rather than the liver and skeletal muscle, which is why dual agonists improve cardiometabolic markers beyond what weight loss alone would predict.
ELI5: The brain has two switches in the appetite control centre. One switch ("eat") is turned on by the hunger hormone ghrelin from the empty stomach. The other ("stop eating") is turned on by leptin from fat tissue and by gut hormones released after meals — the most important being GLP-1. GLP-1 drugs work by mimicking that natural "stop eating" signal, but at much higher and longer-lasting doses than the body produces on its own.
Obesity is more complicated than just excess calorie intake. Rather, it's better to think of it as the failure of the homeostatic system that controls energy balance.
Adipose inflammation and insulin resistance. Adipose tissue first accommodates weight gain by recruiting new fat cells. Once that capacity is exceeded, existing cells enlarge until they outgrow their blood supply. Hypoxic fat cells trigger local inflammation, recruit inflammatory macrophages, and release cytokines (notably TNF-α and IL-6) that interfere with insulin signalling. This is the bridge between central obesity and type 2 diabetes: the inflammation is what drives systemic insulin resistance, not the fat itself.
Central leptin resistance. Despite very high circulating leptin, the brain stops responding to it. The receptor signalling pathway becomes desensitised through chronic over-stimulation. The clinical consequence is that the brain becomes "blind" to fat stores. Because the leptin signal is not received, the brain perceives the body as energy-depleted even when fat mass is high, and continues to demand food. This is why simply reducing calorie intake fails in the long term: the brain is not receiving the signal that there is enough fat already.
Ectopic lipid deposition. When fat cells cannot expand further, lipids are deposited where they should not be; namely, the liver (MASLD), skeletal muscle, and pancreas. This drives the clinical features of metabolic syndrome: dyslipidaemia, insulin resistance, hypertension, and dysglycaemia.
The starvation defence. Once weight has been lost, the body initiates an evolutionarily conserved response against starvation. Leptin falls disproportionately faster than fat mass; ghrelin rises and remains elevated; resting energy expenditure drops; muscle becomes mechanically more efficient at producing the same work. These changes persist for at least 12 months after weight loss and may be permanent. This is why "just stop eating" fails as a long-term strategy: the body fights weight loss with the same intensity it would fight starvation.
ELI5: As fat cells fill up beyond capacity, they trigger inflammation that disrupts the brain's ability to read the leptin signal from fat, and drives insulin resistance. The brain thinks there isn't enough fat even when there's plenty, so it keeps demanding food. When weight loss is attempted, the body also fights back with a slower metabolism and greater hunger.
## Reward Circuitry
Obesity is also driven by non-homeostatic, reward-based eating. Two distinct reward systems govern this:
Dopaminergic "wanting". This is the urge to seek food when you see, smell, or think about it.
Opioidergic "liking". This is the pleasure of consumption itself.
In chronic obesity, both systems become blunted by repeated exposure to highly palatable food. The "wanting" signal is downregulated, so larger caloric hits are required to feel satisfied. The "liking" signal is downregulated, so more food is needed for the same pleasure.
As leptin resistance develops in obesity, leptin's normal inhibitory effect on the reward circuit is also lost, removing the brake on reward-driven eating.
ELI5: The brain has two separate systems that drive eating beyond hunger. One creates the urge to seek food (dopamine, "wanting"), which is what makes you go downstairs to the kitchen at 10pm. The other creates the pleasure of eating (opioids, "liking"), which is what makes the first bite feel so good. Both become numb in obesity, so you need more food to feel the same.
GLP-1 agonists (semaglutide, liraglutide, dulaglutide) are structurally modified peptides that resist degradation by the enzymes that rapidly inactivate native GLP-1. Modifications extending half-life from minutes to approximately one week enable weekly subcutaneous dosing.
Pharmacological actions occur at multiple distinct sites:
Brain (appetite centre): Sustained activation of the pro-satiety neuronal population produces durable suppression of appetite that persists across days, not just at meal times. This is the dominant mechanism for weight loss.
Brain (reward centre): GLP-1 receptors are expressed in the reward centre. GLP-1 drugs reduce reward-system activation in response to food cues, which is why patients describe food noise (the persistent intrusive thoughts about food) simply going away. The same mechanism likely explains why patients also report reduced cravings for alcohol, nicotine, and gambling on semaglutide and tirzepatide.
Brainstem (nausea centre): The same receptors that produce satiety also mediate the principal adverse effect of nausea. Tolerance develops over weeks, which is why GI symptoms typically improve with continued therapy.
Pancreas: Glucose-dependent augmentation of insulin secretion (the incretin effect). Because the effect requires elevated blood glucose to manifest, GLP-1 drugs do not cause hypoglycaemia in non-diabetic patients, and only rarely in patients with type 2 diabetes not on drugs that promote insulin secretion (e.g. sulfonylureas).
Stomach: Slowed gastric emptying contributes to satiety but undergoes rapid tolerance within weeks, whereas the central appetite effect does not. So most of the durable weight loss is driven by the brain, not the stomach.
ELI5: GLP-1 drugs copy a hormone the gut releases after eating, but engineered to last a whole week instead of minutes. For obesity, most weight loss comes from the brain effect, not the slowed stomach emptying--that part wears off after a few weeks. They suppress appetite and reduce reward from eating.
Tirzepatide is a single peptide that activates both GLP-1 and GIP receptors with high affinity. The pharmacology is more complex than a simple "two for one":
At the GLP-1 receptor, tirzepatide is an "imbalanced" agonist. Without going into too much biochemistry, this design reduces receptor downregulation over time, helping the drug remain effective for longer.
At the GIP receptor, tirzepatide is a high-affinity full agonist. GIP receptor activation in the brain enhances the appetite-suppressing effect of GLP-1 whilst, paradoxically, potentially mitigating the high-dose nausea typically associated with GLP-1 monoagonism.
GIP receptor activation increases blood flow to fat depots and enhances their lipid-buffering capacity, directing lipids into peripheral fat rather than the liver or skeletal muscle. This may explain why tirzepatide produces greater improvement in cardiometabolic markers than semaglutide for any given amount of weight loss.
The net result is greater weight loss with similar tolerability; head-to-head trials show tirzepatide produces about 6 percentage points greater weight loss than semaglutide.
ELI5: Tirzepatide hits two targets instead of one. The second target boosts appetite suppression, reduces nausea, and helps direct fat into the right places rather than the liver or muscles. The result is about 6% more weight loss than semaglutide in head-to-head trials.
NB: this section only covers non-diabetic adverse effects. Diabetes-specific issues (including retinopathy worsening) are outside the scope of this deep dive.
## Gastrointestinal Effects
GI effects are the predominant class of adverse effects. The mechanism is dual: central, via aversive signalling in the brainstem nausea centre; peripheral, via vagal feedback from the delayed gastric emptying. Eighty-six percent of patients in trials report some GI adverse event versus 31% on placebo. Severe nausea and vomiting are most common.
GI symptoms are predominant in the dose-titration phase. They typically attenuate over weeks as central tolerance develops.
## Biliary Disease
Cholelithiasis and cholecystitis occur at approximately 30% increased rate. This is due to a combination of reduced gallbladder motility, because the gut hormone CCK which normally stimulates gallbladder contraction is suppressed, and bile cholesterol supersaturation during rapid weight loss.
This could also lead to increased risk of gallstone-associated pancreatitis. While large-scale meta-analyses have failed to demonstrate a causal increase in pancreatitis, the MHRA has issued an alert in 2026 warning of "the potential risk of severe acute pancreatitis with these products, including rare reports of necrotising and fatal pancreatitis". Pre-existing pancreatitis history is a relative contraindication.
## Perioperative Aspiration Risk
GLP-1 agonists increase pyloric sphincter tone and reduce gastric contractility, significantly delaying gastric emptying. Standard fasting protocols prior to anaesthesia (6 hours solids, 2 hours clear fluids) are often insufficient. While most patients develop tolerance to gastric effects within weeks, "slow-adapting" patients experience clinically significant gastroparesis indefinitely.
Current guidance from the Association of Anaesthetists (UK) and the ASA recommends withholding weekly GLP-1 agonists for at least one week before elective surgery, and daily agonists for at least 24 hours.
## Medullary Thyroid Carcinoma
This is a regulatory contraindication based on rodent data. Thyroid C-cells in rats and mice express GLP-1 receptors at high levels, and chronic stimulation produces C-cell hyperplasia and MTC. Healthy human C-cells have negligible GLP-1 receptor expression. The theoretical risk in humans with pre-existing C-cell pathology (e.g. multiple endocrine neoplasia type 2) is the reason for current contraindications, though these drugs have been used for years for diabetes, and no evidence of increased risks of MTC has been found.
ELI5: The most common side effects are nausea and vomiting, which improve over time. Gallbladder problems are slightly more common because the gallbladder doesn't empty as well. Pancreatitis is a theoretical risk. The most important practical issue is surgery: the stomach empties slowly even when you've fasted, so the drug needs to be held for a week before anaesthesia. Thyroid cancer risk was a concern from animal studies, but human cells respond differently and no evidence has emerged in a decade of widespread use.
## Real-World Efficacy
The trial data for these drugs suggests they work in motivated, supervised, well-resourced groups of patients. Real-world effectiveness is significantly lower at 70-80% of trial efficacy. Real-world tolerability is notably worse, with patients persisting for a median of 11 months before abandoning treatment, primarily due to GI intolerance, supply chain disruptions, and cost.
## Loss of Lean Body Mass
DEXA studies indicate that 25-40% of weight lost on incretin therapy is lean body mass i.e. muscle, bone, and water.
The mechanism is not fully understood but is thought to be a combination of:
This is concerning because:
- Lean mass loss reduces resting metabolic rate, which compounds the weight regain problem.
- In elderly patients, accelerated loss of muscle mass can permanently impair functional independence.
Trial protocols mandate 150 minutes of weekly exercise plus optimum amounts of dietary protein to prevent the loss of lean body mass. But trial participants are highly motivated, health-literate, and adherent to lifestyle co-interventions. This is why real-world lean mass loss is likely worse than trial DEXA substudies suggest.
## The Rebound Effect
Discontinuation of GLP-1 agonists produces rapid weight regain. RCT evidence shows that after drug cessation, the majority of lost weight is regained within 12 months, at a rate substantially faster than weight regain following lifestyle-based weight loss alone.
Ghrelin rebounds, leptin remains suppressed (because fat mass has fallen), yet leptin resistance persists. The pharmacological appetite suppression is removed, yet the underlying biology that drove the original obesity is unchanged. Worse is that patients seem to predominantly regain fat and do not easily recover lost lean mass, leaving them with worse body composition than baseline.
The implication is that incretin therapy is not a cure for obesity, but a chronic suppression of an underlying biological drive. This must be discussed before initiation. A patient who cannot commit to indefinite therapy should not be started on it; they will lose weight, stop the drug, regain the weight, and end up with a worse metabolic state than baseline.
## Hedonic Blunting
A subset of patients report broader anhedonia (reduced enjoyment of activities) during GLP-1 therapy. This is thought to be due to suppression of the reward pathways.
ELI5: The headline trial figures (15% on semaglutide, 21% on tirzepatide) are achieved by motivated patients who don't drop out and who exercise and eat enough protein. About one-third of the weight lost is muscle, not fat, which is why the drugs only really work safely if patients also do resistance training. Real-world patients lose less than that because they stop the drug, can't tolerate the maximum dose, or can't access it. When the drug stops, the weight comes back fast. The drug suppresses obesity; it does not cure it. Some patients find that they experience reduced pleasure in doing anything, and not just eating.
As GPs, we rarely start these drugs ourselves, but many of our patients have heard about them, and some of them will ask. Here are a few key points to counsel on:
Salaried GPs, what is the best thing and the worst thing you have found about transitioning from ST3 to a Salaried role? Are there any tips you can share with us lot inching towards CCT in August? TIA!
I recently CCT‘d and started a new salaried job on 1st April this year. Other salaried GPs at the practice have received the DDRB recommended pay rise backdated to April. Do you think I should be receiving the payrise too or have I missed the boat by starting my contract too late?
Hi all,
My GPST1 starting in Aug has its ST1 year solely in GP practices, whole of ST2 in hospital and then ST3 back in GP land.
Is this normal? I thought ST1 was in hospital setting?
Top tips for starting on GP? What is expected of you as a ST1 in the GP setting?
Thanks.
Got GP offer in North Staffordshire VTS. Any ideas on how is the training quality/ loving like in those areas?
Looking for a salaried GP for the first time and thinking where to advertise? Indeed? NHS jobs?