(From the sidebar of QuittingKratom. Posting for those who are new, or may need a "refresher" or for those who are on the Reddit mobile app and have difficulty finding the sidebar information. If you encounter someone brand new here, feel free to link this to them. So many of us are "lost" when we're new and have no idea where to start. This wiki is a good place to start, along with the support from the wonderful members of this subreddit. If you're looking for more links to helpful information from the sidebar, scroll to the bottom of this post. I've added them there, after the Wiki information, for convenience.)
So you've decided you want to quit Kratom.

Withdrawal Symptoms

You may experience a number of withdrawal symptoms, both physical and psychological. Keep in mind that all humans are affected differently and experiences with symptoms will differ among us.

Physical Withdrawal Symptoms

The most common physical withdrawal symptoms experienced are outlined below.

Restless Leg Syndrome

Also known as RLS, this is the most common symptom of withdrawal. It can be described as an irresistible urge to move one's body to stop uncomfortable or odd sensations. It most commonly affects the legs, but can also affect the arms, torso, and head. Moving the affected body part modulates the sensations, providing temporary relief. On average, this symptom will be almost entirely gone by day 7.

Insomnia

As you would expect with RLS, insomnia is another commonly experienced withdrawal symptom. Lack of sleep usually occurs due to RLS, but it can continue even without RLS present.

Uncontrollable Body Temperature

This withdrawal symptom can be common, yet not as common as the two above. This symptom causes the body to experience drastic changes in temperature within a short period of time. This probably sounds much worse than it really is, but during the day it is fine. At night it involves being cold, putting the covers over you, then being really warm and throwing all the covers off.

Other symptoms

In addition to the above, you may experience a runny nose, teary eyes, sneezing, diarrhea, and an aching body. These are generally not a major problem. For diarrhea, loperamide can help (see below). For aches and pains, OTC pain relievers such as Advil can be useful.

Psychological Withdrawal Symptoms

Commonly referred to as PAWS (Post Acute Withdrawal Symptoms). Usually the psychological withdrawals tend to kick in after the physical withdrawals have passed. Described below are the most common psychological withdrawals that are experienced.

Lethargy

The lack of energy and enthusiasm is the most common psychological withdrawal experienced. This symptom can be minor for some, but it is quite commonly major. Although ironic, a good remedy for this lethargic feeling is exercise. It may be hard to get exercising initially due to the lethargy, but many people experience a huge improvement in their mood afterwards.

Cravings

Cravings are quite commonly experienced by addicts withdrawing from Kratom. Major cravings can cause addicts to relapse if the impulse is acted upon. Usually cravings don't last too long, and they seem to come in waves. Psychologically, cravings can play with your mind. You may find yourself thinking things like "I'll just take it this once, I've already made the decision to quit so I won't do it again".

Depression

Depression can play a big part in relapse when it comes to recovery from Kratom addiction. Although some users have existing mood disorders or depression, the PAWS during Kratom withdrawal hugely amplify these feelings/mindsets. Expect to experience some mild to moderate depressed feelings during PAWS and prepare your mind to acknowledge that these feelings are caused by the Kratom withdrawal. You WILL feel better. Once again exercise is a HUGE help to mitigate the depression experienced during withdrawal. It has been proven that regular exercise is as effective than the most common anti-depressants.

Taper vs. Cold Turkey

While one method may work for some, it may not work for another. We are all different and unique in many ways, including the way our body reacts to (lack of) substances.

Tapering

Tapering has been tried many times by different people. Some found tapering helpful, others did not. The main advantages of tapering are:

• Little to no physical withdrawals symptoms.
• Not as big of a shock on the body.
• Doesn't affect your day-to-day life as drastically as cold turkey (if you can't take time off work or don't have a weekend free).

Disadvantages of tapering off Kratom are:

• Requires a lot of self control and discipline.
• Easy to make an impulse decision to take more than your schedule planned.
• Although it may not impact your day-to-day life as drastically as cold turkey, the impact will be longer and more drawn out.

Note: Another effective method used is to taper with stem and vein kratom.

Cold Turkey

The cold turkey method seems to be the more preferable method as well as the most successful. The main advantages are:

• Getting it over and done with, no drawn out symptoms.
• Improvement is felt much sooner since the withdrawals are not drawn out.
• Day-to-day life is not affected for as long as it would be tapering.

Disadvantages of going cold turkey are:

• Physical withdrawal symptoms that are taxing on the body.
• The withdrawals are much worse over a short period of time compared to tapering.

Managing Your Withdrawals

There are a few tried and tested methods to dealing with various withdrawals symptoms. They are described below.

Exercise

The most effective way to make yourself feel better. It has been proven that regular exercise is as effective than the most common anti-depressants. The effects are very profound, and can remain present for hours. Exercise releases a flood of endorphins, directly stimulating your opioid receptors the same way Kratom does, reducing both physical and psychological withdrawal symptoms. Regular exercise will hasten the recovery process by bringing your body's endorphin system back online. It can be difficult to get started, but if you force yourself, you should find that it gets easier after only a few minutes as your heart starts pumping and the endorphins start flowing. Heavy weightlifting is one of the most efficient methods, in terms of benefits vs. time spent, but prolonged cardiovascular activity (jogging, bicycling, etc.) is also effective. Intense yoga is another option.

Orgasm

When you stop taking Kratom, your sex drive may return with a vengeance. Take advantage of it :). Orgasm, like exercise, causes a release of endorphins.

Meditation

It can be difficult when you are uncomfortable and your mind is racing, but a few minutes of meditation can significantly improve the way you feel. Close your eyes, and let your thoughts flow without trying to control or resist them. Take slow deep breaths, focusing on each inhale and exhale. Try not to think about anything else, but if a thought arises, let it be. Visualize each inhalation as bringing healing energy into your body, and each exhalation as removing negativity. Continue until you feel better, or longer, and repeat the process anytime you feel overwhelmed. Check out /meditation for great tips on meditation.

Supplements

Loperamide

Warning, kratom and loperamide.. We don't know if loperamide (in the recommended dosage for diarrhea (https://www.drugs.com/dosage/loperamide.html)) combined with kratom has health risks (in particular heart issues at higher doses), or people could start to abuse it. It had been reported that even the recommended loperamide doses can cause a rebound of withdrawal symptoms after you stop using it . Therfore we don't recommend to use loperamide. Other warnings: At recommended doses, the half-life of loperamide is approximately 10 hours. However, with higher doses, even as little as 16 mg, longer half-lives have been observed (upwards of 41 hours). News videos: "it's actually potentially even worse than using heroin...", "Kratom and Loperamide is a dangerous combination".

Supplements

There are a number of drugs and supplements that can improve mood, motivation, and sleep quality. Most of those listed are naturally derived, and many can be easily obtained at such locations as GNC, Vitamin Shoppe, pharmacies, and "natural" grocery stores, as well as online at sites like AllStarHealth, Bodybuilding.com, and Amazon.

• Black seed oil. some qk members reported that they used 3 x 2 teaspoons daily at the beginning.
• L-theanine: Found in green tea, this substance has a calming effect and improves cognition. Useful both during the day and to help with sleep.
• Ashwagandha: The "Indian ginseng," Ashwagandha is an adaptogen that improves overall well-being. Like L-theanine, can be used both day and night. "In anxiety and depression, ashwagandha has been demonstrated to be as effective as some tranquilizers and antidepressant drugs. Specifically, oral administration of ashwagandha for five days suggested anxiety-relieving effects similar to those achieved by the anti-anxiety drug lorazepam (Ativan®), and antidepressant effects similar to those of the prescription antidepressant drug imipramine (Tofranil®)": look here.
  
• Rhodiola rosea: Another adaptogen, this one has mild stimulating qualities (but without the jitters of caffeine). Best taken during the day. (Warning: Rhodiola has MAOI activity and could potentially interact with other meds/supplements. Be careful, do your research, and start with small amounts.)
  
• DLPA: A combination of the natural "L" form and the synthetic "D" form of the amino acid phenylalanine, DLPA has been shown to fight depression and reduce pain by boosting dopamine levels and preventing the breakdown of enkephalins (similar to endorphins).
  
• L-tyrosine: boosts dopamine.
  
• L-phenylalanine: Try L-tyrosine first. If the results are not satisfactory try L-phenylalanine.
  
• Valerian root: Sleep aid. Smells terrible but can be rather effective. Common in "sleepy" teas.
  
• 5-HTP: Precursor to serotonin. Improves mood and sleep. People who are taking antidepressant medications should not take 5-HTP, because in that case common side effects are : *Agitation or restlessness *Confusion *Rapid heart rate and high blood pressure *Dilated pupils *Loss of muscle coordination or twitching muscles *Heavy sweating *Diarrhea *Headache *Shivering *goosebumbs"
  
• Tryptophan: (propably superior to 5-HTP).
  
• SAM-e: Is a quick acting antidepressant.
  
• Chamomile and passion flower: These two herbs, widely available as teas, can help with anxiety and insomnia. At least one ex-Kratom addict has reported that, in does of 2-4 teabags, they can be very effective. WARNING: Passion flower is a MAO inhibitor, don't use it together with kratom.
  
• Melatonin: The body's sleep hormone, used for regulating the sleep/wake cycle. Tells the body that it's time to sleep. Taking too much (more than a milligram or two) can screw up the body's circadian rhythm and have the opposite of the intended effect. Good in combination with valerian root and 5-HTP. Some feel very groggy after taking melatonin.
  
• Kava: An herb that reduces anxiety, but can be hit-or-miss when it comes to sleep.
  
• Chocolate: Contains phenethylamine, which reduces anxiety and improves mood and cognition. Buy a generous amount of dark chocolate with a high cacao concentration, and eat as much of it as you want. The more, the better. Alternatively, phenethylamine is available as a supplement.
  
• Magnesium: Helps with sleep. Many people believe that Calcium needs to be taking with Magnesium for absorption, but this is not true. Calcium and Magnesium actually compete for the same transport system into the blood so it is better to take them at different times during the day. The only time this competition is eliminated is in the case where calcium and magnesium are bound to a single amino acid and are called calcium and magnesium amino acid chelates, as opposed to calcium carbonate/citrate or magnesium oxide/citrate. Minerals in the amino acid chelate form have double the absorption rate of calcium carbonate and magnesium oxide because they do not have to be altered in order to enter the bloodstream. Source.
  
• Cannabis: Given its legal status, not everybody is able or willing to obtain it, but cannabis can potentially aid with a wide spectrum of withdrawal symptoms. Indica-dominant strains are recommended for insomnia and anxiety, while Sativas are better suited for improving mood, motivation, and appetite. (However, it should be noted that Sativas can worsen anxiety in some cases.) Medical dispensaries, if you have access, are the best option due to the wide variety of strains available. If you have had problems with other drugs or drug substitution in the past, it is advised not to use Cannabis after quitting Kratom as it may lead to another substitution.
  

Warning: It's best to avoid using antihistamines (diphenhydramine, dimenhydrinate, hydroxyzine etc.) such as those found in Benadryl, Dramamine, NyQuil, Unisom, and Tylenol PM. While they can produce drowsiness under normal conditions, they are well known for exacerbating Restless Leg Syndrome, which will make your insomnia worse, not better.

Prescription drugs

In addition, there are various prescription drugs that can be of assistance. The ones listed below are prescription-only. These are not necessarily recommended; do your research before considering them. Be especially careful if you are taking any psychiatric prescriptions, such as SSRIs, MAOIs, or Wellbutrin. The following information is not a substitute for medical advice. Always consult your doctor. [We do not recommend to use this medications together with Kratom].

• Gabapentin: Gabapentin is an epilepsy and nerve pain drug, which is also prescribed for the restless leg syndrome. The drug acts as a sedative. It also helps with sleep and gives you energy. Don't abuse it, gabapentin causes a withdrawal syndrome if you use it for too long (use it maximal 5-6 days). Drug experts say the effects of using gabapentin for long periods of time or in very high quantities, particularly among sensitive populations like pregnant women, are not well-known. Attention:"treatment with gabapentin is associated with a substantial increase in the risk of opioid-related death".
• Clonidine: Due to its lack of abuse potential, doctors will generally not hesitate to prescribe it for a patient undergoing withdrawals. Clonidine can "stop" an opioid withdrawal relatively effectively, which is (simplified) due to the following mode of action: Adrenaline docks onto two receptors when released: α1 and α2. Clonidine docks onto α2-adrenergic receptors and “blocks” them. Also lowering blood pressure, works against the "adrenaline rush". Clonidine has an idiosyncrasy, i.e. the first dose of the active ingredient triggers an effect opposite to the actual effect !. Clonidine doses must be slowly increased, starting at a low dose. It should also be noted that clonidine must not be discontinued immediately; the dose has to be slowly reduced, because otherwise there can be a blood pressure crisis - with an already destabilized blood pressure (due to withdrawal), extreme caution is required here and we strongly recommend that treatment with clonidine is only carried out under medical supervision. Existing depression can be exacerbated or a new depression can be triggered by using clonidine. Existing depression can be exacerbated or a new depression can be triggered by using clonidine.
• Modafinil/adrafinil (Provigil, Nuvigil): [Warning: Do not use Modafinil together with Kratom (it may cause seizures)] A unique, non-euphoric stimulant, used to treat narcolepsy, shift-work disorders, and by Air Force pilots as a replacement for amphetamine. This drug, at levels of 100-200mg per day, can relieve the malaise and lack of motivation associated with withdrawal. Should not be taken within 12 hours of bedtime. While Modafinil is under Schedule IV in the US, Adrafinil, which metabolizes to Modafinil in the liver, is unscheduled and can be easily purchased.
• Selegiline (L-deprenyl): A MAO-B inhibitor used to treat Parkinson's, this drug increases levels of dopamine in the brain and has been shown to increase lifespan in rats. Unlike traditional MAOIs, selegiline does not require dietary restrictions, and is generally considered quite safe at levels of 5-10mg. Do not take near bedtime. Unscheduled in the US. .

Warning: Be mindful of the possibility of drug substitution. With addiction, drug substitution is a common problem when going through recovery. With all CNS depressant drugs (antidepressants, benzodiazepines, neuroleptics), it should be kept in mind that these drugs sedate in the long term and can trigger a so-called 'hangover', ie. they also lead to additional exhaustion during the day. In some cases, this can be perceived as a burden and can lead to losing sight of the desired goal or lowering the motivation to endure the withdrawal. Whether drug treatment makes the withdrawal easier or more difficult depends on personal factors and cannot be determined in general. Remember that your body can regenerate itself best and fastest if it is not exposed to other stresses.

Stem and Vein Kratom

Although total alkaloid levels are lower than in leaf, there is supposedly relatively more mitragynine present in S&V. The levels of mitraphylline, rhynchophylline (related to mitragynine) and corynantheidine are higher. In kratom communities on the internet it is sometimes reported that S&V can reduce tolerance to kratom, but this seems not to be the case. Anecdotal reports claim that S&V can be useful for mitigating withdrawal symptoms, and accelerating the brain's recovery from kratom addiction. There is a great guide on using stem and vein kratom to taper off here.

Relapse

Relapse is a normal part of recovery. It has happened to every single one of us. Try not to beat yourself up about it or feel like you are worthless and useless. That doesn't help a thing. It is just a small bump in your road to recovery. All you can do is get back up, dust yourself off and get back to quitting as soon as you are ready. You will know when you are ready.

More important information from the sidebar

• Quitting Kratom: What to Expect
  
• A list of possible Kratom withdrawal Symptoms
  
• Guide to Quitting Kratom Cold Turkey
  
• Tapering Guide
  
• Odds and ends of withdrawal symptoms
  
• PAWS (Post Acute Withdrawal Syndrome)
  
• So-called "Kratom Alternatives"
  
• Naltrexone: Important Information & Personal Experience
  
• Mega-Dosing Liposomal Vitamin C protocol for Withdrawal
  
• Wim Hof Method: An Awesome Set of Exercises
  
• Read Sub Rules and the "READ THIS FIRST if you're new..." Guide before posting
  
• How to add your Quit Date next to your username
  

The most popular post in this sub yesterday was about how fast everyone is zooming through the aisle and how slow and in the way store customers are. Almost 90% of the comments called out non-shoppers slow a hassle and “are they contemplating their life decision over this box of cereal?!”. Guys!!!! Have some humanity, of course we are doing a job and speed dictates how much we earn , BUT frankly it is not anyone’s problem to deal with. If anything if they run into shoppers who are being pushy and accidentally running into them, they would have a bad impression of us shoppers and some might report to the stores which will result in soft bans. It is not non-shoppers/store customers’ job to know who you are and accommodate. Treat others as how you want to be treated. Just because we are working it doesn’t mean we are better or should be prioritized over those who are making decisions to fill up their pantry for the week. PUT YOURSELF IN A CUSTOMER’S SHOES, if you’re shopping for yourself, would you want to be rushed in a COSTCO. Would you want to be bumped into on accident or not!!!!???
The post and its comments left me feeling disappointed in this community and how disgusting some of you feel about other people. BE BETTER!!!!

Oman has rugged coastlines and vast deserts, one of Arabia's hidden gems, where tradition and progress coexist. The nation that inspired the myths of Sinbad the Sailor is also abode to shifting sands and towering cliffs, colonial regiments, and the affluent sky-blue hydrosphere of the Indian Ocean. In addition to having a stunning array of natural and cultural highlights, this country also has colonial forts.
Get an opportunity to visit the stupendous strongholds at Nizwa, Jabrin, and Bahla; your process then, at that point, takes you on into the Bedouin deserts. Before traveling through the Qara Mountains to Salalah, you will camp here amid the shifting sands of Wahiba and the towering dunes of Rub al Khali. When you end this fantastic journey through Oman's second city's fertile palm and frankincense groves, you'll get a sense of Arabia's "perfume capital"'s distinctive charm and personality.
Omani culture is a fascinating mixture of various traditions. Despite the country's modernization, some traditional practices are still deeply ingrained in everyday life. Understanding Oman's way of life and lifestyle is fundamental, regardless of whether you well-conceived plan to visit and investigate the Viaggio In Oman momentarily.
Oman's people are also among the friendliest and most open to newcomers. Oman is one of those uncommon nations with something for everybody, from luxurious stays to those needing outside of what might be expected and from culture vultures to thrill seekers.
Reasons To Choose Oman, Your Next Destination!
There are wide-ranging benefits that you can capture while paying a visit to Oman; here are some of the essential reasons that can be captivated through Viaggi In Oman:-

• It is a location where the present and the past coexist harmoniously. Modern cities like Muscat, home to opulent hotels and shopping malls, are on one side. Then again, you have old towns like Nizwa with their memorable posts and customary souks. Oman is a fascinating destination that combines the old and the new in a way that will impress anyone who visits.
• The natural beauty of Oman is one of the most compelling reasons to travel there. The country has beautiful scenery, from rugged mountains to clean beaches. The Al Hajar Mountains' towering peaks can be explored by visitors, as can the Arabian Sea's crystal-clear waters. Oman also has several protected nature reserves, like the Wadi Shab Nature Reserve and the Ras al Jinz Turtle Reserve, where visitors can see the country's unique ecosystems and diverse wildlife.
• Additionally, Oman is a nation with a rich history and culture. It has a long history that goes back thousands of years, and the country has a lot of museums and historic sites where people can learn about it. The Bahla Fort, a UNESCO Heritage Site built in the 13th century, is among the most impressive. The post is one of the most outstanding saved instances of conventional Omani design and is an unquestionable requirement for anyone interested in the nation's experiences.
• Notwithstanding its set of experiences, Oman is additionally known for its warm cordiality. Visitors to Viaggio In Oman are frequently treated like family by the friendly and welcoming locals. Omanis are proud of their culture and happy to show it to tourists. This is apparent in the myriad festivals and occasions held nationwide, including the Muscat Festival and the Salalah Tourism Festival. These events are an excellent way to learn about Omani culture and get a firsthand look at the country's customs.
• One more motivation to visit Oman is its delectable cooking. Omani food is a mix of Bedouin, African, and Indian impacts, described by its intense flavors and utilization of new fixings. Local specialties like machboos, a spiced rice dish with fish or meat, and shuwa, a slow-roasted lamb dish, are available to visitors. Omani espresso is likewise a must-attempt, as it is customarily presented with dates and is an image of Omani cordiality.
• Oman is a secure and stable nation. It is regarded as one of the Middle East's safest nations due to its low crime rate. The government likewise has a stable political environment, which makes it an ideal objective for explorers searching for a serene and loosening-up escape.
• Omani cuisine has been influenced by the Middle East, its proximity to Asia, particularly India, and its location in the Middle East. Because of this, many of the dishes in this region of the Middle East combine various flavors and spices. The Omani public dish is shown, slow-cooked sheep or goat over sweet-smelling flavored rice, and it's a must-attempt if you are in the country.

In the past, this dish was only served on special occasions and was cooked in a ground-up oven; however, some Omani restaurants now do it. Mandrouba, also known as chicken rice and honey-soaked desserts, are two other Omani staples. Dates and Omani kahwa, which is Omani coffee with cardamom, are frequently given as tokens of hospitality.
Oman is a great destination to visit during Christmas or the October and February half-term holidays, when the climate is at its best, and the relatively short flight time makes traveling there with kids relatively stress-free. In addition, Viaggi In Oman is one of the safest and most stable countries in the Middle East, making it the ideal destination for families seeking something different. Scuba diving, camel rides, and other family-friendly activities are all available.
Conclusion
Visitors have a remarkable opportunity to interact with the Arab world without being influenced by excessive wealth. Bedouin significance remains at the heart of an Omani welcome, and Oman's low-rise towns maintain their traditional charm. Oman is the obvious choice for people who want to see modern Arabia but still feel ancient Arabia. It has stunning mountains, wind-blown deserts, and a pristine coastline. Whether staying in a hotel, dining out, or visiting a local home, visitors to the Viaggi In Oman can always expect a warm welcome. Omanis are proud of their country and everything it offers, so they're happy to welcome new people and show them respect with old-fashioned hospitality!

As I’ve live-posted about my vaginoplasty recovery, a lot of people have asked me about what hospital I’m at and how I chose this program. Now that I’m at home, I wanted to answer those questions publicly.
First off, I want to let you all know that I’m not the kind of person who does a bunch of research into my medical care. I often see people on this, and other trans-related subreddits, having super complex discussions about injectable hormones versus oral hormones or advances in surgical techniques and what’s happening in other countries for their medical advances. My mom is a nurse and I have had great medical care throughout my life, and so I just generally trust my medical professionals. I also want to acknowledge that there’s a HUGE level of privilege that allows me to do that. I’m white, middle class, have good health insurance, live near a major regional medical center, and have a great support system.
I live in Salt Lake City, Utah. It’s a bit like Austin, Texas, in that it’s a blue island in a red state. I could talk more about the general experience of transitioning here, but this post is focused on my surgical endeavors. It’s also home to the University of Utah Hospital, which is a teaching hospital with incredible amounts of funding and serves as a major regional medical center for the Mountain West (Idaho, Wyoming, Utah, Nevada). The UofU has offered vaginoplasties since 2018.
When I was considering the surgery, the UofU does online webinars where they talk about the different GC surgeries they offer. They have separate seminars for HRT, MTF bottom surgeries, FTM bottom surgeries, and maybe also top surgery webinars. I attended only the MTF bottom surgery webinar. They offer the webinars pretty regularly (maybe quarterly?). I didn’t personally think that the webinar was that helpful, because it mostly covered information that you could find out online, like the differences between procedures. The most helpful part in theory was hearing from previous patients who had gotten surgery there, but sometimes us queer folks can be a bit on the awkward and weird side and I felt like the particular person who spoke at my webinar was not helpful to hear from at all. She treated the webinar like it was a private appointment with her physician and was asking for dilation tips and the webinar manager kept having to be like “you should ask your physical therapist at your appointments” and it wasn’t easy to get any sense of what the recovery was like or what the aesthetics were or how sex was or anything.
Still, the convenience and in-network for my insurance made UofU a great option. I did have some reservations about the newness of the program and I had more questions and if I’m being totally honest here a lot of them were about aesthetics. I’m vain enough to want a pretty vagina.
The first step was a consult. I met with a PA for several hours and she answered all of my questions and gave much more in depth information about everything. It was exactly what I hoped that the webinar would be, but better because it was private.
After my consult, it became apparent that I’d have to delay the surgery. A good friend was getting married in Hawaii, since his now-wife is Hawaiian and all of her family is there. I couldn’t get the time off from work for that trip, plus surgery. I decided to delay my surgery a year so that I could be there for him.
During that year, two acquaintances had a vaginoplasty at the UofU, so I was able to get the inside scoop from them. They both reported very positively about the care they received, the appearance afterward, and their sexual experiences. One of them offered to let me see her real-live vagina, which I felt awkward about following up on so I said no, but I think I would have liked to see it and shouldn’t have let that hold me back from her generous offer.
After my year delay, I did the consult again with a different PA and once again got my questions answered and this time, the program had implementeda new part of the consult where they showed pictures of previous patients. They showed after photos from around the 3 month mark and a couple of photos from right immediately after. I thought that was the best part of the entire consult, and definitely the most reassuring. The vaginas all looked super natural, and I was fully confident in my decision to go forward at the UofU.
Meeting with the surgeons in advance wasn’t part of the consult process. I asked if I would meet them and they said surgeons aren’t usually met until day of, but that if it was important to me to meet them they could get that set up. It wasn’t important to me, so I didn’t bother. My questions had all already been answered.
Then the next two months were getting approval from my insurance. The biggest hurdle I had was getting all my letters lined up because I actually don’t regularly see a mental health provider. My mental health has been very good due to a career switch to a job I love and transitioning, so my mental health providers were a couple years old so it took some reaching out but they were happy to do my letters without seeing me for a new appointment. I did have to kind of call and email quite a few times on all providers to get those letters submitted. I just turned the letters over to the UofU and they handled my insurance approval.
I got the approval in January, and I signed up for the first available date with the surgeons that I wanted, which was the end of May. There are two teams of surgeons who do vaginoplasties at the UofU, and my friends both had Dr. Agarwal do theirs and she’s the head of the whole program, so I wanted her to do mine.
Between January and May, I just had two appointments. One was with PT to do some pelvic floor exercises to strengthen the area in advance and the other was another follow up with the PA where we reviewed surgery prep and I got a whole packet of info- what medications to discontinue and what I could eat the day before surgery etc.
Then I just showed up on the morning of surgery and you all know the rest.
I do want to note that while I publicly posted that I have BCBS insurance, starting in July of this year the UofU may be out of network for BCBS. Gap coverage may still exist.

One of our dogs seems to have a bad allergy to Farmer's Dog chicken recipe. They were ok for a few days, but then they started avoiding the food then eventually would eat it and yesterday they tried to scoot their butt raw and today they threw up their Farmer's Dog chicken from lunch after avoiding their dinner. I can see the food not digested in her throw up. We tried the chicken before and then switched to the beef formula because they didn't want to eat it. Then recently we tried chicken again so now I know its the chicken formula. She does fine with bland boiled chicken and rice and her chicken treats so theres something else than chicken thats in this formula thats upsetting her. I just want to see if anyone has had a similar experience with their dog. Will definitely stop giving her the Farmer's Dog chicken.

https://swisschems.is/product/arimidex-anastrozole-30mg-60-capsules/ code CHEMSEX10
FOR RESEARCH USE ONLY
---
Hello, fellow fitness enthusiasts of SwissChems! Today, I'd like to share a detailed guide on the usage of Anastrozole, a compound that has been gaining attention in the bodybuilding community.
What is Anastrozole?
Anastrozole, also known as Arimidex, is a non-steroidal aromatase inhibitor. It's primarily used in the medical field to treat postmenopausal women with hormone receptor-positive early breast cancer. However, in the bodybuilding world, it's often used to manage side effects related to estrogen levels that can occur when using certain anabolic steroids.
How Does Anastrozole Work?
Anastrozole works by inhibiting the enzyme aromatase, which is responsible for the conversion of testosterone to estrogen. By blocking this conversion, Anastrozole can help to control and reduce the levels of estrogen in the body.
Usage Guide for Bodybuilders

1. Dosage: The dosage of Anastrozole can vary depending on the individual's needs and the type of anabolic steroids being used. A common starting dose is 0.5mg every other day. However, some may need to adjust the dosage to 0.5mg every day or 1mg every other day, depending on their response and estrogen levels.
2. When to Take: Anastrozole can be taken at any time of the day, but it's often recommended to take it at the same time each day to maintain consistent blood levels.
3. Cycle Length: Anastrozole is typically used throughout the duration of a steroid cycle. It's important to start Anastrozole as soon as you start your steroid cycle to prevent estrogen-related side effects from occurring.
4. Post Cycle Therapy (PCT): After the end of the steroid cycle, Anastrozole should be discontinued. During PCT, other compounds like Selective Estrogen Receptor Modulators (SERMs) are typically used to help restore natural testosterone production.

Side Effects and Precautions
While Anastrozole can be beneficial in managing estrogen levels, it's important to be aware of potential side effects. These can include fatigue, joint pain, high blood pressure, and in some cases, a decrease in bone mineral density.
It's crucial to monitor your body's response to Anastrozole and adjust the dosage as needed. Overuse can lead to an excessive reduction in estrogen, which can lead to its own set of problems, such as impaired lipid profile and compromised immune function.
Conclusion
Anastrozole can be a useful tool for bodybuilders using anabolic steroids, helping to manage and prevent estrogen-related side effects. However, it's important to use it responsibly and under the guidance of a knowledgeable professional.
Remember, this post is for informational purposes only and does not constitute medical advice. Always consult with a healthcare provider before starting any new supplement regimen.
Stay strong, stay safe, and let's continue to support each other in our fitness journeys!
Disclaimer: Anastrozole is a prescription medication and should only be used under the supervision of a healthcare provider. The information provided in this post is for educational purposes only and is not intended to promote the use of this medication without a valid prescription.

I took a dab today for the first time in forever and was rippped. I decided to make myself some rice krispies cereal, and only realized what I had done when the microwave beeped to let me know the bag of minute rice i made was ready 🤦🏼‍♀️ i wasnt mad though, it was coconut jasmine rice and i still are it lmao

Smoking everyday is straight up KILLING my lungs, it's giving me permanent bronchitis. and that's no bueno, mang...so I've decided to make edibles to replace. The trouble is, those two times I tried to make butter, my results were very inconsistent. I made cocoa rice krispie treats, and even though I mixed the hell out of the treats when they were in the pot. One got me stoned and one just gave me a slight buzz. So I'm looking for methods that are foolproof. Don't wanna wast money on an ounce and have nothing to show for it.

Part 1: https://www.reddit.com/ReddXReads/comments/13lfqkw/vulturebeard_the_legbeard_that_ruined_roomies_fo
Hi everyone, bunny here. I’m having Ezekial post this for me because while I lurk on reddit, I’m on too many online communities and burn out quickly on all of them. I’m just here to tell this incredibly long tale. Pull up a chair, grab a snack, get comfy. This is a long ride.
The Cast List
Bunny (author): 33, female, a year or so out of a divorce that turned toxic and abusive and ultimately helped me realize I was gay. Recovering lifelong doormat slowly building a spine. Neuro spicy gym rat with major depressive disorder, general anxiety disorder, and most recently diagnosed with ADHD. Unfortunately very familiar with surviving trauma.
Z (poster): My partner. 31, nonbinary (they/them), also neuro spicy with depression, anxiety, OCD, BPD, autism, and also familiar with lifelong trauma.
One Liner Beard (OLB): 33, male, neuro spicy with ADHD and depression. He also suspects autism but isn’t pursuing a diagnosis. His nickname here comes from the fact that in messenger, he usually has one-word replies like “oof” or “mmm” as an acknowledgement he had seen the message but has nothing further to contribute.
VultureBeard (Vulture): 30, female, neuro spicy and disabled with multiple conditions. She has Ehlers-Danlos Syndrome, POTs (postural orthostatic tachycardia syndrome), autism, depression, anxiety, chronic migraines, but also possibly a list of things that may or may not be real – that will all be explained. The star of this unfortunate circus. Her name will be explained in this part.
Kid: 3. Female. OLB and Vulture’s child. Likely neuro spicy like we all are, but she’s also only 3 years old. Slightly speech delayed and not potty trained yet.
Minor mentions:
Shit ass ex-husband (SA): name is self-explanatory. 32, male. Divorce was amicable to keep the peace. I immediately went no contact with him after.
J2: Friend of OLBs.
You ready? Deep breath. Now let’s dive into this mess.
​
Chapter Two: VultureBeard, or the Walking Diagnosis
With the backstory of how we wound up with a neckbeard, a legbeard, and their kid out of the way, I’ll start on VultureBeard properly now.
J2 was the one who introduced her to OLB. He ran into her at a local convention, and they talked and spent the day together. He ended up sleeping over at her house, on her couch, since she lived a few minutes away from the convention center, and he introduced her to his D&D group that OLB was a DM for. He said that at first, he wanted to smash just based on looks (before she stopped caring for herself, before the pregnancy), until she opened her mouth.
Oh boy.
I met her on Halloween 2018 or 2019 (trauma made my memory absolute garbage, ain’t it fun?), when OLB wanted to run a one-shot Curse of Strahd campaign for our D&D group. J2’s group was called Party A, we were Party B. Both of our campaigns existed in the same universe that OLB created. It was a fun one shot. I liked her. We integrated her into our D&D campaign as a side character who joined our party.
With her autism, she talks a lot, and can have a conversation with anyone, but she does naturally miss a lot of social cues. She says it’s okay to be direct with her and say things like, “I can’t talk right now, I’m busy.” But in the wild, she just enjoys people. That in itself isn’t a bad thing.
When we met, she was a Mormon with long brown hair, glasses, and modest clothes with long ankle-length jean skirts. I don’t know if that was a lifelong practice or just the people she had associated with. She didn’t curse at all, and still substitutes “fudge” for my favorite and most often-used curse word. Over time, she dropped religion, but she only curses in text, and very rarely at that, like when she’s pushed to her mental limit. She still dresses in a lot of the modest clothes from before, but it’s mostly because she doesn’t go clothes shopping a lot. I have passed down some clothes I have shrunk out of to her.
Her fashion sense is a bit of Walmart-meets-Goodwill. The tired mom “this is clean, so I’ll wear it” kind of aesthetic. She’s big on thrifting, but so am I. Most of my wardrobe is thrifted or passed on from a few gym friends these days, so it’s not like I’m poking fun at secondhand clothes. It’s just that there’s a lack of style or effort on her part, like she just puts clothes on and sometimes remembers to brush her hair out. I think there’s a part of her that doesn’t recognize she’s plus sized after pregnancy because she once bought clothes that are size medium, and they didn’t fit. She fit my old 2X leggings. I traded her leggings once, my bigger size for her smaller size.
She and OLB don’t fold laundry or put it away, so she will have laundry stuffed in their hamper that they keep in our shoe closet next to the laundry room, or boxes on her desk, or on her desk chair. They kind of live out of that clothes pile. If she needs to dress in something nice, it likely is wrinkly because it was in an unfolded pile.
The first run-in with realizing that something was a little “off” with her was when she tried cooking for us. We had other friends over to play D&D and Magic with us, and she wanted to cook some kind of chicken and noodle dish. With her POTs (post orthostatic tachycardia syndrome), she’s usually sodium deficient so she adds way too much salt to whatever she’s eating. Not being used to cooking for others, she served us completely inedible chicken that was too salty.
One of my former friends was there for that debacle. What she also noticed was that Kid seemed to be behind some childhood markers. At 2, Kid was still using a bottle and didn’t seem to talk much. She was worried that Kid would keep falling behind. It was a red flag that got tucked away. At the time, I was still thinking of Vulture as a burned-out first-time neuro spicy mom. That’s a lot for a disabled woman to handle. As a disabled person myself, I tried to give her the benefit of the doubt. I gave her too much benefit of the doubt for way too long.
Vulture as a person focuses very much on herself. Because of the body aches and pains that come with both Ehlers-Danlos Syndrome and POTs, yes, I understand that her body regularly fights itself. But why is it that every time her body expressed pain, she had to do a loud, “AH, OW” or other pain noises as loud as she could? Or she will complain about whatever is giving her trouble. Some days she will be using her computer quietly, then when I come out of my bedroom, she starts to complain about her daily aches and pains. This happens pretty much every day, for different reasons. Her sneezes are likewise as loud, to where I can hear her across the house, through a closed door and over the show Z and I are watching.
Most awkward is Vulture’s bathroom habits. In Apartment #2, I guess Vulture got used to using the bathroom with the door cracked because they lived in a house without roommates, and she needed to keep an ear on Kid. Even now in a shared space, she keeps the door cracked, sometimes with the light off so I don’t think anyone is in the bathroom because it’s more migraine friendly.
Until I hear the grunting.
THE GRUNTING.
THE POOP GRUNTING.
I have heard it through my closed bedroom door, because her bathroom is right next to my bedroom. Usually, it’s when my bedroom is quieter, like when Z and I are off to sleep. But I hear her grunting as she’s using the bathroom, either because the door is open, or she is just that loud. I’m terrified to know which one it is.
Her hygiene is questionable at best. I know personally that Depression™ makes hygiene and self-care extremely difficult. I myself do the best I can, especially while being constantly sweaty at the gym and a Big Sad (depression) fighter. So, I get mental illness and hygiene. With Vulture and her long hair, she would leave it in a bun for days until it matted. She asked for my help with detangling it and it took me around two hours to safely work the mats and tangles out. When she cut it in a homemade attempt to do the popular wolf cut on Tik Tok, it was much more manageable. When it’s shorter, it has tight curls. She constantly has a natural body odor smell to her. I think with her sensitive skin, she has to wear a specific unscented deodorant, but I don’t think she applies it unless she’s leaving the house. The sink in her and OLB’s bathroom is used as mostly a storage space with things piled on top of it, so I don’t think it’s used for much. The bathtub needs a deep scrubbing, and she gives Kid a bath more than she herself showers.
Having heard the poop grunting, I’m afraid to look at their toilet.
In general, Vulture isn’t active, but to say that she’s sedentary is a vast understatement. The average sedentary person looks like an Olympic athlete next to her. She occupies two spots in the house: Her bed, or the couch in the living room. For most of the day. She will just have her laptop either on the table next to her or in her lap, and that’s where she spends most of the day, gaming.
With me being a gym rat, I am incredibly proud of how I went from a couch potato to a weightlifter. When I think about what would happen if I suddenly dropped to her levels of activity, I know my body would fall apart. I often wonder if her lying in bed or on the couch contributes to more of her body pains because her muscles are deteriorating from disuse. I mean what do I know, I’m not a doctor. That body pain cycles to her being even more inactive because she hurts. It’s a big cycle of negativity.
When the weather changes drastically, she will be hit with migraines or allergy attacks, to where she has to lay down all day as well. She takes OTC pain medicine frequently, as well as allergy meds. One of her desk cabinets is a well-stocked mini pharmacy of OTC medication and some prescription medication she has collected over time that expired over a year ago. When I’m hit with a rare migraine, I know she will have something in stock for it.
Her doctor says she needs to eat more frequently because she’s always shaky. She will hold up her hand to show me how much it’s shaking, and it always looks as though she’s making it shake from the wrist, instead of it being an actual hand movement. She always tells me, “Look at this,” and holds up her shaking hand, like she’s trying to show me how bad she’s doing, but it’s for different reasons every time. She didn’t eat, she’s too tired, she has a migraine, she has sinus pain – everything gives her shaky hands, which I joked about once.
If she has a new symptom, she goes to Doctor Google to look up what’s wrong with her, and then talk in our house chat on discord that she thinks she might have “so and so” wrong with her because the symptoms match. Or she will post screenshots of whatever her symptoms are. As far as I know in the time living with her, she’s never had close medical calls or anything that needed further treatment, except for a heart study where she wore a device to monitor her heart rate. Doctor Google gave her all sorts of things she could have, though.
Within the time I started writing this saga, I had this encounter with her in the house group chat on discord that she, OLB, and I are in, about how she thinks she’s allergic to mosquito bites because the bites swelled up and got inflamed:
Vulture: Just figured out something I’m most likely allergic to: mosquito’s saliva reaction is increased inflammation around the bite site and the condition is skeeter syndrome.
Me: You should get that confirmed by a doctor. It’s mosquito season.
(it sounds like she copy/pasted that bit about mosquito’s saliva from Google)
Mind you, my former in-laws thought I was allergic to mosquito bites because the same thing happened to me. My mosquito bites swelled up beyond what they should look like, and mosquitos have a good nose at finding me in particular compared to other people. I tried to empathize with her, even though it just seemed like she wanted to identify with a syndrome she found on the internet.
She said that she had the same symptoms her friend’s dad had for GERD because her acid reflux was acting up. The GERD saga is a fun one as well, which I’ll fully share later.
Funny enough, if I also have something similar to what her current issue is, she doesn’t play Oppression Olympics and say hers is worse. I’ve been dealing with vertigo on and off for the past month and I don’t have the ability to see a doctor for it at the moment. So, when she says that she’s dizzy or the room is spinning, I express empathy or at least a little “oh, same here,” because I have to carefully move my body in ways that don’t make the room spin. It might be her autism, it might be because she doesn’t care, but she never expresses empathy my way. She just moves on.
I’ve told her multiple times she needs to see a doctor to check for each new symptom she has, but somehow there’s an excuse. The latest I’ve heard is, “I will once my phone is turned back on. It hasn’t been paid in a while.” Valid yes, but then please get off Google. Because she’s on government assistance and doesn’t have a car and doesn’t know how to drive, she’s ferried to her appointments by a medical bus that stops at the house. They do need to be able to call her. Just please get off Google in the meantime! I’ve even told her that Doctor Google and WebMD will say everything is cancer or fatal and it’s not good for you, and she just kind of brushed it off.
One of my friends calls her the Professional Victim. Z is convinced she has Factitious Disorder (formerly called Munchausen’s). She loves to hide behind her illnesses as to why she can’t get out of bed or can’t do chores. If you were to listen to her every day, you’d think she was falling apart at the seams because it was always something. Migraine, body pain, allergies, sinus problems or sinus infections, stomach problems, dizziness, shakiness. Repeat. Forever.
She will ask me if her forehead feels hot, and when I can’t tell, she checks with a thermometer. She says, “My natural body temperature is low so 99 degrees is a fever to me.”
This is also where I gave her a lot of benefit of the doubt at the beginning, because EDS and POTs will affect the entire body in different ways. One of my friends, in her casual dark humor, will have conversations with me about how she’s just not going to be able to walk properly that day, because her ankle joint slid out of place, but she still finished her work shift. I talk to my friend regularly about her struggles with her body, but somehow it doesn’t have the same self-pity that Vulture’s does. Every disability presents differently between people. As rare as EDS and POTs is, it’s pretty common in online communities because it’s where people tend to flock to. In my time in varying disabled online communities, I’ve never seen someone who complains or fishes for attention as much as Vulture does.
If she’s having a relatively good day, she will either be gaming, or maybe she will get to one of the chores that OLB tries to get her to do during the day, like doing the dishes or cleaning Kid’s room. When OLB had prescription Adderall (before the shortage made him switch to a different ADHD med), she took one of his pills and was zooming around actually being productive. She has symptoms of ADHD but doesn’t have a formal diagnosis, so OLB thought it might help her. It seemed to.
If she has a bad day, which is most of her days, she stays rooted on the couch or moves between her couch and her bed, moving her laptop with her. She spends all day building in Minecraft, completing her Pokedex, or playing other games.
Sometimes when I come out of my room to cook, she says something along the lines of, “I planned on cleaning today,” followed by vague hand gestures of how she’s feeling. I never asked her about her daily plans, but she needed to tell me. Is it self-awareness or guilt?
If she’s doing a load of dishes, she will loudly proclaim that she’s dizzy and shaky and in pain and have to go sit down after 10 minutes of that. I don’t know if she actually has the body strength to stay upright for longer than ten minutes at a time, and I don’t know if that’s her actual chronic illnesses, or the fact that she doesn’t do anything at all.
I’ve given her the same advice I use myself for low spoon (low energy) days when I need to get things done. I’ve told her it’s okay to take ten-minute breaks and then get started again. Or an hour break, if her body is giving her trouble. I’ve told her it’s okay to clean the house while sitting on the ground or in a chair, if that’s easier on her body. In managing my broken mental health, I’ve taught myself all sorts of life hacks, or as I call them, “brain hacks,” to work around how gross depression makes me feel. And I’ve told her that if it’s a really bad day, the dishes aren’t going anywhere and can wait until tomorrow.
That’s meant to be compassionate, not taken in the “if you give an inch, they’ll take a mile” sort of way, but it must be interpreted as permission to not do The Thing. It just won’t get done if she feels she has permission to skip over it.
If she does anything, she will want metaphorical ass pats for her good work. OLB jokes that it’s a praise kink, but some days it really seems that way without anyone consenting to participate in her kink. She asks if I noticed she cleaned the kitchen or did some kind of cleaning and if I’m proud of her. I used to play along with the praise because I wanted to give her positive reinforcement, like maybe if I emphasized that it was a good thing, she’d be more encouraged to do it more. I’ve got jokes, apparently. Optimism was so strong early in the friendship.
If she cooks, usually it’s something frozen that she can heat up like pizza. Most of the time, she exists on boxed macaroni and cheese or sandwiches. Or what fast food OLB brings home. Most of her diet is processed, instant, or frozen. Or she eats odds and ends like what cereal and junk food is brought home from the food bank or when OLB goes shopping.
Since SA left the house, I took up cooking for myself and exploring what I like to cook, as SA was the main cook for the house. My gym regimen helped me meal prep and confront a lot of my bad eating habits, so I started prepping healthier foods. I am the stereotypical lifter that eats a lot of chicken, rice, and vegetables. Z also likes to cook, and it became a way for us to bond by cooking together or one of us watching the other cook and just vibe in each other’s company.
VultureBeard gets her name because, one, she is a legbeard. But two, every time I made something early on with her living with us, she always said something along the lines of, “Ooh, that smells so good! It’s making me hungry!”
Me, in my doormat stage, took the cue that she dangled and offered her some of my food. Back then, I always tried to cook enough for the whole house. It became a pattern. If I cooked something, she always popped up, hungry and unable to make actual food for herself or somehow her illnesses were acting up and preventing her from cooking for herself. If I said I was popping over to the store, sometimes she would ask if I could pick up a soda for her and occasionally, she would be able to pay me, always in loose change because her disability payments went right to the bills that she and OLB had. I always took the bait because yeah, doormats will doormat and vultures will vulture.
She does reciprocate in small ways, sharing some occasional treats with me or saying I can have some of her mac n cheese or Oreo cookies or French fries or whatever food she has some days. But for the most point, a lot of her behavior feels like fishing – fishing for attention, for food, for confirmations of her medical issues.
Her general attitude towards housework also contributes to her main other issue that makes me want to scream. She hoards. Empty salsa jars, Nesquik containers, pizza boxes, mac n cheese boxes. She holds onto things that Z and I see as garbage, because she has dozens of DIY projects in mind. She would be the person that followed 5 Minute Crafts for useful projects. To her credit, she did make a nifty sock organizer out of spare cardboard. But she has dozens of empty frozen pizza boxes and macaroni boxes piled up on her desk and ideas in her head, but no actual execution of them. I have pictures on my phone of her desk hoard, and while the desk itself is tall, the pile on the topmost part of the desk reaches the ceiling. That’s at least two feet of buildup.
It drives Z batty. With their OCD, Z can’t stand seeing the general mess in the house, but her desk makes them want to throw things. There was an empty Pizza Hut box that spent a week on the floor under the table in the living room before she finally picked it up and moved it to her desk. She scolded my cat for jumping on it.
Vulture: I want to save it for a project, I just don’t know what I want to use it for yet.
Me: Why not just throw it away? Isn’t it garbage?
She only gave a vague shrug, and the pizza box stayed on her desk for another few days until while cleaning the kitchen, Z got tired of looking at it and finally took it out to the outside garbage bin.
This is a constant pattern for her. She hoards things that she sees as something that could be useful in the future, but in the meantime it all stacks up and takes up space. She and OLB both are pack rats, which I think enables it further. OLB said that she also hoards food when she thinks there’s a food shortage in the house, but that also includes things that shouldn’t be eaten or are close to being spoiled. She freezes produce and even bread dough she made because she would start projects and then not have the energy to finish them or deal with them properly. I think if Z and I weren’t in the house, it would just be a rat’s nest of garbage.
That was why Z and I took on the majority of housework. We have a current setup to deep clean the common areas of the house monthly, and anything she doesn’t pick up that we read as trash will get thrown out. It’s barely making a change in the house, but it’s better for our mental health. It’s unfortunate that the house barely stays clean for two days after we clean it.
OLB usually has an excuse for not contributing towards the housework. His ADHD makes him forgetful, plus he hates dishes and purposefully avoids them until he knows he has to deal with it. He’s mostly just exhausted from work. With Vulture? Ten thousand excuses.
With OLB working an exhausting but consistent tech repair job, that leaves Vulture in charge of Kid during the day. If she exists entirely in her bed and the couch, how is she able to keep up with a toddler?
Oh, that’s going to be a huge tale on its own. Fuckle the buck up. We’ve got a long way to go. And yes, it will make you angry.

Hoping to hear from folks who have had any experiences like this. I am super stressed and borderline terrified at this point.
I have PsA, not RA, but I know both can be treated with anti TNF biologics. I recently transitioned from Humira to Simponi Aria (after several non-TNF blocker biologics). I have had increasingly severe symptoms, and after an extremely long wait I am finally seeing a neuro with musculoskeletal specialization. The appt is next week and I am honestly terrified. My concerns are that whatever is going on is not reversible, whether due to MS or other demyelination issues or something else.
There are so many things, all intermittent - as in daily but not 24/7. The most bothersome are: involuntary movement/tremors, dizziness and sensory issues (feeling freezing or burning hot, hands and feet in particular feeling cold , and hands and feet feeling heavy or like they are wet/being dipped in water, pins and needles especially in hands, arms and feet). The dizziness can be really intense at times, even while seated. Most upsetting for me, is involuntary movement. I feel like I am vibrating sometimes. I also have severe restless legs even just midday, while working.
Has anyone experienced these kinds of symptoms after or during TNF blockers? Were you able to get them to resolve after discontinuing the meds or with treatment of some kind? I am so scared. I hate not feeling in control of my body and I get so uncomfortable when I am visibly shaking, especially in professional settings.
Hoping someone can help put my mind at ease. Posted on the PsA board with minimal responses so far.

My hair type is thin, and I have had white hair since the age of 10, which I believe is due to using gel. Although I don't have any bald spots at the age of 28, I am unable to style my hair effectively. The rice-based conditioner I used to use for styling has been discontinued by the company. As a result, last month I purchased Set Wet gel again after all these years. However, I am now concerned about hair loss. If you have any suggestions or alternatives to hair gel, I would greatly appreciate it.

My [18m] father [48m] is a well respected man in my town, and most people know him and like, including all of my friends.
Now, let me get this clear, my father is Not abusive, but he's been through a lot and because of that he's had anger issues my whole life. He's also insanely stubborn and refuses to believe he can be wrong about anything. I don't think I've ever heard him apologize for lashing out. We've been walking on eggshells our whole life so we don't agitate him, because he's fucking terrifying. That being said, he has never laid a hand on any of us, [I have 2 sisters, we all still live at home, but I'm about to leave] but I can't say I personally haven't felt the mental impact.
Anyways, one year ago today, my father threw down a bowl because it was in his way. My mother, sisters, and I decided we weren't going to walk on eggshells anymore, and we weren't gonna clean up after him. He's a grown man, and at this point none of us are little kids anymore. So, that bowl has sat on the ground for an entire year.
This morning, when I walked in the kitchen, I got an idea. I consulted a friend of mine first, to make sure it was morally okay, and he thought it was hilarious so I did it. I got a mini party hat that I had in my room, a rice crispy treat, a candle, and some cake writing stuff we had from one of our birthdays.
I put the little hat on the bowl [it's upside down], wrote a 1 on the rice crispy treat, stuck a candle in it, lit it, and took a picture.
I sent it to a group chat of mine, with only 5 or 6 people in it [all my friends, no family] saying "Everyone say Happy Birthday to this Bowl!!!! It's a year old today because my father threw down in a fit of rage a year ago and still REFUSES to pick up and me and my sisters and my mom are sick and tired of cleaning up his rage messes so no one has picked it up 🥰"
I then went on to say how the bowl, named affectionately Bowlia, was practically a third sister to me, things like that, backhandedly insulting my father. My father doesn't know yet, but everytime I've brought up the monthly anniversaries, he gets pissed, and tells one of us to just pick it up.
It's his mess, so he should have to clean it. He told us a long time ago to keep any issues with him at home so it wouldn't affect his reputation in town, but this was only 5 or 6 of my friends.
So, am I the asshole knowing this will piss him off and possibly put a slight tarnish on his image in a few people?
Edit: I should add, the apple doesn't fall far from the tree, and I share a lot of the same anger issues and stubbornness, and we are similar in so many ways that I knew this would piss him off because I would be furious if it happened to me. So. Idk if that makes it worse.
Edit 2: I feel like I need to specify. He truly isn't abusive. He's a great man and a great father. When he isn't angry, he's a great and funny guy. I mean, he is a tad racist. And a bit homophobic. A pretty transphobic. Which is an issue because I'm trans. But he's a really good guy. He prides himself on not lying and he always supports us in everything we do. I haven't found anything yet he hasn't supported us in [I'm not coming out and never will to him] and he's really really good to us. In the past year, I've noticed significant improvement. He used to be angry a lot, but now he's angry much less often. Just, whenever he gets angry, he tends to get in a headspace and not come out of it for a while. He's nowhere near abusive, I just think he's a product of the environment.

My baby has always had rashes eversince she was born. Initially, our paediatrician diagnosed it as infantile rash. I was exclusively breastfeeding/ breast pumping, so for a really long time, the only thing my little one had was just breast milk.
Around the 5th or 6th month mark, her rashes just started to flare. The rashes were red, weepy, sometimes it bled. We went back to our paediatrician and she suggested it might be a milk protein allergy. I immediately decided against breastfeeding.
As soon as we switched her over to hypoallergenic formula, her face cleared up. Almost immediately. She was happy, bubbly, she could finally spend her time (when awake) playing and babbling, instead of rubbing her face like crazy.
Around 2.5 weeks ago, we decided to start trying to introduce her to solid food, i.e starter foods like rice cereal. Note that she's already 7th months at this point. As soon as we started, her rashes went insane again. I tried to be really careful & even picked PLAIN rice grain cereal. Meaning to say there are no other foods in the cereal besides white rice.
We went back to the paediatrician and he reccommended my babe to be on topical steroid but I am against it because I personally suffered from topical steroid withdrawal & it was a long and painful process.
I'm open to hearing your tip and tricks and what creams worked out for you.
Please reccommend some good baby safe eczema creams. We don't want to use steroid 😭

Welcome!
This is a series I am going to be working on where I endeavour to cover various topics in physiology intermixed with clinical pearls to impart some knowledge that doctors of most specialties and grades will hopefully find useful when looking after acutely unwell patients. Join me as we dredge through the depths of anaesthetic exam revision to answer important questions like "why do CT ask for a pink cannula", "why frusemide is okay to give in AKI", "why is hypoxic drive a bunch of horse manure" and many more. Pick up some of this material and you'll be well on your way to becoming a pernickety anaesthetist, whether you like it or not!
Questions, comments, feedback, and suggestions are both encouraged and welcome.

Previous installments:

• IV access, resuscitation, fluids, and the cardiovascular system
  
• The physiology of ageing and illness, and its impact on critical care decision making
  
• Respiratory failure, oxygen therapy, and gas exchange
  
• Reduced consciousness, intracranial events, and the central nervous system
  

Kidney function, acute kidney injury, and acid-base disorders

Next stop along our systems review are the mighty kidneys. I won't talk to you about Lupus nephritis or renal tubular acidosis, however I will try my best to cover some more typical things you might encounter like acute kidney injury (AKI) and drug dosing in renal impairment while trying to avoid embarrassing myself as a non-renal doctor.

What do the kidneys do?

An obvious question, they allow us to get rid of waste substances in urine. They are so much more than that however, they:

• Regulate electrolyte concentrations, water balance and plasma volume, plasma osmolality
• Regulate red blood cell production
• Regulate blood pressure via RAA system influencing vascular resistance
• Maintain acid-base homeostasis
• Control Vitamin D production
• Produce glucose from proteins and triglycerides (gluconeogenesis)

We will focus on only a few of these in this post, but the kidney's multiple roles and complex biochemical signalling deserves as mention as it can make diagnosing and understanding disease states difficult. It can also make us forget what other consequences there might be for patients in these disease states.

How do we measure kidney function?

In some respects knowing the heart or the brain aren't working is easy. Low blood pressure and infection? Septic shock. Low blood pressure + STEMI? Cardiogenic shock. Unconsciounsess or coma? Well whatever it is, it ain't working. So what about the kidneys, well we have creatinine, right? WRONG.
Although the kidney has many functions as we noted before, the easiest methods to quantify function look at the obvious: waste production. Its function is the sum of filtration through all the glomeruli in the kidneys, the glomerular filtration rate (GFR). When a substance is freely filtered through the kidneys and is neither secreted nor reabsorbed (which occur in the tubules rather than the glomeruli), the rate at which that substance is removed or cleared from the plasma can be used to measure GFR (in mL/min).
This substance is inulin and not creatinine. Because inulin isn't naturally present in our bodies, it has to be infused and then its concentration and the rate of decay measured. This is impractical clinically, so creatinine was selected as a practical alternative. The correlation between serum creatinine and measured GFR was researched and various formulas like MDRD and CKD-EPI were developed to estimate GFR (eGFR). This is why labs report eGFR as opposed to GFR. (There are also other methods to determine GFR like radionuclide scintigraphy...)

What's the problem?

The estimation of the GFR relies on assumptions that are not without problems. This review covers the topic at length, however the main points are:

• Creatinine is secreted, unlike inulin. As mentioned this occurs in the tubules, so changes in secretion will affect serum creatinine level despite a static filtration rate. As renal diseases progress, more and more creatinine is secreted, making serum concentrations less reflective of actual filtration.
  
• To truly reflect instrinsic renal function creatinine has to be in a steady state with stable generation and serum concentration. Creatinine is produced as a waste product of protein breakdown mainly from muscles. Therefore anything affecting catabolism, muscle activity, dietary protein intake, can alter this steady state. Frail sarcopenic patients will have artificially low creatinines and may not get as significant of a rise as a young muscular person in AKI.
  
• There has to be adequate delivery of creatinine to the glomeruli. The kidneys receive ~20% of the cardiac output, so the heart has to be pumping out effectively with healthy blood vessels, good volume and blood flow. A hypovolaemic patient with an MI may have a high creatinine despite working kidneys, they're just not being adequately perfused. Chronic diseases like hypertension, diabetes, heart failure, lead to upset of autoregulation of normal afferent (entering) arterioles, whereas ACE inhibitors and ARBs block AT-II from causing vasoconstriction of efferent (outgoing) arterioles, an imbalance can lead to renal impairment if perfusion isn't maintained, or improved blood flow and urine output if it is.
  
• The studies from which eGFR formulas are derived were conducted in mostly European and North American populations with elderly, black and CKD patients being significantly underrepresented. They only measured GFR a few times a year. With increasingly older, frailer, sicker patients, leading more sedentary industrialized diets and lifestyles, will the accuracy of these formulas hold up with time?
  
• eGFR correlates loosely with important indicators like proteinuria, fluid status, blood pressure, acidosis, anaemia, bone disease, iron deficiency, tubular function, etc. In the absence of those indicators, the elderly often have decreased GFR without increases in morbidity and mortality.
  

The takeaway is that creatinine and eGFR are tools developed from the assessment and monitoring of long term renal function. It is not designed for use in patients with acute fluctuations or those with zero kidney function (eg, anuric dialysis dependent).

What else we can monitor?

The example of the heart earlier was misleading. Blood pressure is influenced by many factors. Septic shock is actually a high cardiac output state with low systemic vascular resistance (SVR). Patients with heart failure can have normal blood pressures despite severe systolic dysfunction and poor exercise tolerance. Blood pressure is an easy surrogate marker because determining cardiac output and SVR is invasive and complex (of course we have focused echocardiography to help us these days).
A surrogate marker we can use for the kidneys is urine output (UO). After all the end product of glomerular filtration is the ultrafiltrate which will become the urine. If there is adequate urine output despite raised or increasing creatinine levels, we can be reasonably satisfied the kidneys are actually receiving enough blood flow to get rid of waste and perform its other functions.

Acute Kidney Injury

This leads us into one of the most commonly encountered entities in hospitalised patients: AKI. Let's look at the KDIGO criteria seen in the table below.

AKI Stage	Serum creatinine criteria	Urine output criteria
1	SeCr increase ≥26 umol/L <48hrs or SeCr increase ≥1.5 - 2x from baseline	<0.5mL/kg/hr for ≥6hrs
2	SeCr increase ≥2-3x from baseline	<0.5mL/kg/hr for ≥12hrs
3	SeCr increase ≥354 umol/L <48hrs or SeCr increase ≥3x from baseline or started on renal replacement therapy (any stage)	<0.3mL/kg/hr for ≥24hrs or anuria for ≥12hrs

^{Note: UO <0.5mL/kg/hr is the definition of oliguria.}
Definining by creatinine is a more practical screening test in most situations, allowing earlier diagnosis and intervention. UO can be monitored during the course of the day to identify patients who are borderline or not responding to treatment, may need re-evaluation of the cause, or escalation of care. This way a combination of the two can help offset the limitations of each method.
NICE guidance already exists on the diagnosis and management of AKI, most hospitals will have care bundles or even 'AKI nurses', so I'll run over a few important points.

• Pre-renal - This only means the cause lies outside the kidneys, and in at least in the early stages there is no histological change in the kidneys. In many cases like sepsis, diarrhoea, haemorrhage, there can be a relative or absolute fluid deficit and IV fluids are generally indicated. However excessive fluids can result in interstitial oedema in the kidneys, reducing the glomerular pressure gradient and so also reducing filtration. Similarly in poor cardiac output states where there is venous congestion there is a problem with the outflow of blood from the kidneys, so this is not a cause to reflexively withhold diuretics.
  
• Intrinsic - Here there are structural histological changes in the kidney, caused by many intrinsic renal diseases or nephrotoxic agents like aminoglycosides, vancomycin, NSAIDs, etc. If this is suspected, stopping the offending agent generally resolves AKI without needing a biopsy. Furosemide is not mentioned here as it is not inherently nephrotoxic. Acute tubular necrosis is often mentioned as a specific clinical entity, either due to nephrotoxic agents or sustained hypoperfusion from pre-renal causes. It is not a very helpful term since histological tubular damage has rarely been proven in studies, nor does it help with treatment.
  
• Post-renal - Obstruction may be incomplete, acute on chronic, with a normal ultrasound, no oligo/anuria, and may be associated with other pathologies like a kidney stone with pyelonephritis or sepsis. Catheters can get blocked too so don't forget a bladder scan if anuric, and obstruction can rarely be external such as by tumours or abdominal compartment syndrome.
  

When do I refer to renal or ICU?

Local protocols aside, advice should be sought when the patient does not appear to be responding to medical management and there may be a need for renal replacement therapy (RRT). This is often in the form of intermittent haemodialysis (iHD) on renal wards, and continuous venovenous haemodiafiltration (CVVHDF) in ICU. There are small differences in mechanism, efficacy, and indications of the many forms of RRT, the details of which aren't important for most non specialists. Generally accepted indications for RRT include:

• Symptomatic uraemia - Encephalopathy, neuropathy, pericarditis. Elevated urea on its own is not generally an indication.
  
• Hyperkalaemia - Persistent hyperkalaemia (>6.5) despite insulin/dextrose. Severe hyperkalaemia (>8 ) with arrhythmias, requiring pacing or isoprenaline. This can occur even without anuria and should be escalated as it obviously can be life threatening.
  
• Severe metabolic acidosis, pH <7.1 - This will depend upon the cause and patient's condition. Patients with DKA and pH <7 can almost always quickly be turned around with insulin and fluids. Severely septic patients may not be able to tolerate medical management long enough to improve without RRT.
  
• Toxins or overdose - Some medications and toxins may be removed by RRT (eg, lithium, vancomycin), with specific type of RRT better for some drugs than others. This is uncommon and decisions will depend on the input from renal, clinical state of the patient, and advice from toxbase or national poisons service. A drug may not be removed by RRT but if it leads to another entity such as acidosis it may still warrant RRT.
  
• Fluid overload or pulmonary oedema refractory to diuretics - If patient is anuric despite diuretics then it's more likely they'll end up requiring RRT. In contrast pulmonary oedema in decompensated heart failure with worsening renal function is not helped more by RRT than by adequate diuresis.
  

Absent from above include oligo/anuria or specific values of urea and creatinine. This doesn't exclude them as considerations, however the whole picture should be taken together to make decisions on an individualised basis. It might be that the patient improves despite a creatinine of 700, it might be they become acidotic and hyperkalaemic with a creatinine of 400. Even on the ICU we still don't know when the right time is to start RRT.
This is a reason why renal and ICU often advise the generic "monitor I/O" rather than taking over care. We do appreciate accurate monitoring is unrealistic on the wards, but we also don't have the ability to admit everyone when few will need a specific intervention like RRT. An adequate UO to aim for is above 0.5mL/kg/hr. As AKI resolves some patients enter a polyuric phase, this will resolve but watch that they don't become hypovolaemic in the process, it may require further fluids matching what is lost.

Renal vs ICU referral

This will depend on local arrangements and acuity. Refer to renal if:

• Single organ kidney failure - Normotensive haemodynamically stable patients, not septic or comorbid with poor cardiac function. The principal reason haemodialysis is intermittent because fluid is more rapidly removed therefore borderline hypotensive patients may not tolerate large volumes of blood and fluid being rapidly withdrawn from their intravascular space. I have seen patients arrest from starting dialysis!
  
• Unclear cause of AKI - ICU can offer RRT as a bridge, but the underlying cause has to be treated, if the cause is unclear or there is persistent renal dysfunction, this will require renal input. We refer for this from the ICU too.
  
• Diagnosis requiring specialist treatment - Immunosuppressive therapy for vasculitis.
  
• Renal transplant patients - Even with a clear cause and response to treatment, the precarious nature of immunosuppression, renal impairment and graft function mean these usually merit a call to transplant renal physicians.
  

Refer to ICU if:

• Multiorgan failure - Borderline blood pressure, high oxygen requirements, fluctuating consciousness level, coagulopathy, these patients are unlikely to tolerate iHD, but more importantly it suggests they are critically ill and may need rapid escalation of care (if appropriate) beyond what renal can provide (intubation, vasopressors, etc).
  
• No on-site dialysis service - In hours there may be arrangements to transfer to partnetertiary hospital particularly for complex patients. However hospitalised dialysis patients known to the renal team may require more urgent RRT than this allows. Some ICUs have the plumbing to offer dialysis (this will need a dialysis nurse however).
  
• Patient in extremis - ICU may be able to offer more timely input in patients needing urgent intervention especially if prior to surgery. A patient with bowel perforation and severe AKI will usually be septic and in multiorgan failure anyway, but a 70 year old with obstructive pathology may benefit from being close to theatre to offer RRT while awaiting a nephrostomy (or exchange). If it's reversible and there is somebody willing to operate, I would even dialyse a patient with a DNACPR we wouldn't otherwise admit.
  

Specific considerations

• AKI in heart failure
  
  • The heart-kidney interaction is complex and works both ways (see this review). Volume status and cardiac function needs to be carefully evaluated. Seeing CCF documented in the notes is meaningless. What does their most recent echo show? What did they present with? Stable HF with reasonable ventricular function and sepsis with no signs of overload can receive fluids. Acute cardiogenic pulmonary oedema with severe ventricular dysfunction probably has AKI rooted in the decompensation of heart failure (type 1 cardio-renal syndrome) and would benefit from diuresis.
  • Acute decompensated HF is usually a hypervolaemic state. Elevated right atrial pressures reduce the arteriovenous pressure gradient in the kidney leading to venous congestion, poor outflow. Inflow is also limited adding to the poor cardiac output so glomerular filtration is reduced, leading to a vicious cycle. Aggressive diuresis with furosemide reduces this congestion, improves glomerular pressure gradient and increasing filtration (as long as the patient does not become hypovolaemic). Furosemide's initial beneficial effects in venous congestion is preceded by its diuretic action and is thought to be due to it causing venodilation, reducing preload. The addition of acetazolamide may improve decongestion further.
  • Creatinine rising is not an indication to stop diuresis, it may in fact signify adequate decongestion with improved patient outcomes.
• AKI in liver disease
  
  • Like in heart failure this is a complicated topic (see this recent review). AKI is very common, occuring in up to 50% of hospitalised patients with cirrhosis. While we hear things like hepatorenal syndrome thrown around, common things being common we have to look at all the usual causes we've discussed first (so don't just throw terlipressin at everyone!)
  • Pre-renal causes are most common: Discontinue nephrotoxic drugs. Look for and cover for infections and spontaneous bacterial peritonitis. Hypovolaemia from diuretics or GI bleeds, resuscitate with crystalloids and blood as needed until euvolaemic (careful to avoid overload). Albumin has been found to improve survival in patients with SBP and can be considered if worsening renal function despite resuscitation (or following paracetensis for large volume >5L ascites). Hypervolaemia from congestion (cirrhotic cardiomyopathy leading to right heart failure can benefit from diuretics, abdominal compartment syndrome from tense ascites should be drained).
  • Intrinsic leaves us with tubulointerstitial causes and hepatorenal syndrome (HRS). Low fractional excretion of sodium and urine microscopy can help confirm HRS which offers a grim prognosis. Terlipressin may improve renal function at the cost of significant pulmonary oedema so regular volume assessment and avoidance of overload is paramount. RRT would only expected to be offered if waiting, or under consideration, for liver transplantation. If not, palliation will be the most likely alternative course.
• Drug dosing
  
  • I would avoid using the BNF in renal impairment. Many of its recommendations are different than common guidelines and frankly weird. Do talk to your pharmacist (also microbiologist where appropriate), they'll often refer to The Renal Drug Handbook which is a good resource and covers scenarios like RRT. Most drugs will be dosed based on creatinine clearance not eGFR so arm yourself with an app or calculator.
• Sodium bicarbonate
  
  • Bicarbonate infusions offer temporary extra buffering capacity, mopping up excess hydrogen ions resulting in a higher pH. This is beneficial in hyperkalaemia as a higher pH favours potassium moving intracellularly (for this reason saline is more harmful and Hartmann's more beneficial in hyperkalaemia). It also has accepted roles in tricyclic antidepressant overdose with adverse ECG findings (QRS, QT prolongation), urinary alkalinization (in salicylate poisonining, poor evidence in rhabdomyolysis), and normal anion gap metabolic acidosis (there is high cloride to replace loss of bicarbonate, see later).
  • Its use outside these indications is contentious. There is no evidence of benefit in DKA over conventional fluids even if normal saline's tendancy for acidosis may slow resolution of the acidaemia in DKA. It may be actively harmful in lactic acidosis and respiratory failure as the increased pH shifts the O2Hb dissociation curve to the left, causing reduced oxygen offloading. It also results in net CO₂ production (HCO₃⁻ + H⁺ → H₂CO₃ → H₂O + CO₂) which will have to be blown off with excess minute ventilation.
  • So why do ICU and renal advise it or use it themselves even with a lack of solid indications? Well, essentially it's a temporising measure. Severe acidaemia contributes to myocardial dysfunction, arrhythmias, and catecholamine resistance. In the critically ill it can be useful as a delay while you insert lines or in the hope it will avoid the need for RRT. The BICAR-ICU trial did find it delays the need for RRT and may even possibly reduce the need. I'm not entirely sold on the latter, but it can be reasonable to try if there are positive indicators like good UO.
  • How? Usually available in concentrated (8.4% with 1000mmol/L of each ion) or dilute (1.26% with 150mmol/L) forms. Due to the high tonicity of the former, 1.26% is generally preferrable especially if you can or want to give larger volumes. 8.4% should be reserved for fluid restricted states and should be given slowly via a central line except in an emergency. Slow infusions help combat significant CO₂ rises and hypernatraemia (especially with 8.4%). Dosing is 1 mmol/kg which is 1mL/kg of 8.4% or 6-7mL/kg of 1.26%. For real simplicity most patients can take a 50mL vial of 8.4% or 500mL bag of 1.26%.
• Iodinated contrast
  
  • The entity contrast induced nephropathy, better termed contrast associated acute kidney injury, is a contentious topic. There are many good reviews already on this topic.
  • The evidence is from old studies using high osmolality agents during PCI. Fluctuations in creatinine may not be indicative of actual renal function and may simply reflect the underlying illness requiring a scan rather than the contrast itself. Patients are not more likely to need long term RRT.
  • IV contrast with modern low osmolality agents isn't associated with AKI in patients who aren't and even those who are critically ill. There was no association in patients even with pre-existing AKI. Prophylaxis with intravenous saline nor sodium bicarbonate have been found to make a difference even in CKD patients with eGFR >30.
  • The tl;dr is unless you're in cath lab or IR suite bolusing large quantities of dye arterially it is probably irrelevant. The benefit of a quality contrast enhanced scan in diagnosing and treating the patient are likely to outweigh any miniscule risk. RCR guidelines mention appropriate consent and identification of patients at risk (eGFR <40) they do not exclude the use of contrast or require hydration, at any renal function. You are the doctor, it's up to you to discuss and determine need and benefit. (It's the radiographer's job to ask, don't @ them, but they shouldn't refuse either).

Acid-base disturbances

Now it would seem we are forced to consider the fundamental concept of what acid-base physiology even is. You might have heard about strong ion difference and become lost in confusion. You're not alone. Put simply, there are two competing theories that try to explain how pH changes occur in the body: the traditional model that uses the Henderson-Hasselbalch equation to mathematically explain pH with bicarbonate, and the Stewart model that uses the concept of strong ion difference to explain why changes in bicarbonate occur. The bottom line is that these are detailed explorations of physiology more useful for bed time reading than the bedside. For the interested details can be read elsewhere.
More practically, we can work through a blood gas in a systematic fashion to help decipher the type of acid-base disturbance. Start with pH → PO₂ (always check oxygenation) → PCO₂ (respiratory component) → HCO₃⁻ (metabolic component). I've reproduced this in a simple but limited table below for reference, but this is a more intuitive flowchart to work through.

pH	PCO₂	HCO₃⁻	Disturbance
<7.35	>6	↔	Acute respiratory acidosis
		↑	Chronic respiratory acidosis
	↔ /↓	<22	Metabolic acidosis
>7.45	<4.5	↔	Acute respiratory alkalosis
		↓	Chronic respiratory alkalosis
	↔ /↑	>26	Metabolic alkalosis

^{Numbers indicate primary abnormalities, arrows indicate compensatory changes. Respiratory compensation by altering ventilation occurs quickly, while renal compensation by altering bicarbonate excretion is a much slower process.}

Respiratory

With the topic being the kidney, I won't discuss respiratory acidosis here (see this earlier physiology bite). Acute respiratory alkalosis is due to hyperventilation blowing off CO₂. This can be due to obvious things like pain or anxiety, a compensation for hypoxaemia (eg, high altitude climbing), pregnancy (increased minute ventilation stimulated by progesterone), or salicylate poisoning (direct stimulation of respiratory centre).

Metabolic

Dipping back into some physiology, we can consider two concepts that can give us more information: base excess and anion gap. The purpose of these concepts is help narrow our differential diagnosis, rather than serve as pathophysiological explanations of illness.

• Base excess (BE) - This idea comes from Danish physicians during the polio epidemic where patients often experienced chronic CO₂ retention. For a standardised numerical way of gauging the degree of disturbance Siggaard-Andersen proposed BE to represent the quantity of acid in a lab that needed to be added to a solution of blood to normalise it to a pH to 7.40 and PCO₂ of 5.3. Not because the plan was to literally add acid, but this way you could easily quantify the degree of disturbance. Rather than use this concept Americans appear obsessed with the more complicated Winter's formula instead. Most blood gas analysers will calculate BE for us, often reported as standardised base excess (SBE), with a normal range of +/- 3. A negative base excess is sometimes described as a base deficit, they're the same thing.
  
  • SBE <-3 - There is a metabolic acidosis, alone or as compensation for a respiratory alkalosis.
  • SBE >3 - There is a metabolic alkalosis, alone or as compensation for a respiratory acidosis.
  • Mild -4 to -9, moderate -10 to -14, and severe <-15 (same but positive values for alkalosis)
  • It is especially helpful with mixed disorders or causes. A lactate of 4 doesn't explain a BE of -12 alone, are there other contributors to the acidosis? A bicarb of 30 doesn't explain a BE of +10, what else can be causing alkalosis?
• Anion gap (AG) - I have a more detailed reply here explaining anion gap. It is a theoretical number that exploits the body's need to maintain electroneutrality: we have a bunch of positively charged ions (cations) that are evenly matched with negatively charged ions (anions), and we measure some of these. When we have an excess of some anions that we don't measure like lactate this calculated number rises because one of the measured anions (bicarbonate) drops to compensate to maintain electroneutrality. Like BE, most blood gas analysers will calculate AG for you.
  

There are far too many causes and detailed physiology to discuss here exhaustively. If you want to read about the Cori cycle, Type A and B lactic acidosis, helpful mnemonics and more, head to this review or this section on Deranged Physiology.

Metabolic acidosis

Symptoms are non-specific, with the most obvious being hyperventilation for compensation. In severely acidotic states (pH <7) seek early ICU help. Awake patients will hyperventilate sometimes down to PCO₂ <2 which can dramatically increase work of breathing. Initiating invasive ventilation in this stage or patient fatigue can be very dangerous if hyperventilation isn't maintained, the acidosis can worsen and precipitate cardiac arrest. Hypotension from vasodilation and reduced cardiac contractility can occur, as well as arrhythmias, confusion, delirium, coma.

• High anion gap metabolic acidosis - The presence of unmeasured anions including: lactate, ketones (diabetes, starvation, alcoholic), salicylates, formate (metabolite of methanol), oxalate and glycolate (metabolites of ethylene glycol), other toxins.
  
• Normal anion gap metabolic acidosis - Losses of base (bicarbonate loss in GI tract via high ouput ileostomy or diarrhoea, renal loss via acetazolamide) or excess of acid (renal tubular acidosis, hyperchloraemia, adrenal insufficiency).
  
• Pitfalls: Albumin is an unmeasured anion, so low albumin can mask a high anion gap. Albumin corrected formulas have been developed. Similarly excessively high unmeasured cations like magnesium, calcium, and even lithium, can also lower the gap.
  

Treatment is aimed at eliminating the underlying cause with specific therapies as required like insulin in DKA, fomepizole for ethylene glycol poisoning, folinic acid in methanol poisoning, etc.

Metabolic alkalosis

Despite metabolic acidosis being the usual focus, metabolic alkalosis is actually the more common abnormality of the two in hospitalised patients and is frequently seen as a mixed disorder (like as a response to prolonged CO2 retention as seen in mechanically ventilated patients). In severe states it can lead to delirium, seizures, obtundation, arrhythmias.
The 'opposite' of acidosis, here we see a gain of alkali or loss of acid, with impaired bicarbonate excretion required to maintain this (via chloride or potassium depletion, impaired renal function, or volume depletion).

• Gain of alkali - Iatrogenic from bicarbonate infusions, citrate in transfused blood.
  
• Loss of acid - From the kidneys via diuretic therapy, or mineralocorticoid excess, hypokalaemia. From the GI tract by vomiting especially with pyloric stenosis or obstruction as there is gastric acid loss (with chloride) only, laxative abuse diarrhoea.
  

Treating the underlying cause is important as always. Where there is low chloride and hypovolaemia, this usually responds well to fluid replacement with saline and potassium as required. Acetazolamide can be given if there is hypervolaemia although in practice this is rarely required unless continued diuresis with other diuretics is required. Alkalosis results in low ionised calcium that can cause paraesthesias, but as calcium is buffered by albumin this rarely requires treatment and resolves with correction of the alkalosis.

Conclusion

This is another large topic where there was plenty to talk about. I had to cut down the scope significantly as it rapidly spun out of control, however I thought the nuances deserved a detailed writeup. Nothing is ever absolute so don't take any of this as incontrovertible evidence of the incompetence of a hated colleague (or their brilliance)! It will hopefully have given you some ideas to think about and research further when you see patients with AKI yourself.
Until next time!