Hello! I'm 3wpo and having pain still, internally, that I just can't stand. Now, I've had my dr refill oxy once but I'm reluctant to ask again.
I take warfarin (blood thinners) so NSAIDS (ibuprofen, advil, etc) are off the table. (Naproxin is as well.) Tylenol is great for minor headaches but basically a sugar pill against the pain I'm having.
So! My question is... does anyone either in my situation or otherwise, know of alternatives to help? I mean, I could live with it but I don't... want to.
Edit - I had a laprascopic total keeping my ovaries.

My father was released from the hospital two weeks ago after battling covid pneumonia (vaccinated and boosted but had not received most recent vaccination yet.) I have moved back in with my parents to take care of him during the overnight hours. We are gradually increasing physical activity, but mobility is still fairly limited. He spends most of the day/night in his lift chair (2L 02 delivered via cannula whenever he sleeps as he has apnea that he has refused to treat) so I can only imagine that this isn't really helping things. I would imagine he has tremendous anxiety about his mortality as well.
My question is: is there anything I can do to help eliminate what I can only imagine to be a terrifying experience? Right now it seems like the only thing that helps is that mom makes him a nice cup of tea and rubs his hand/head until he's asleep, but she's 86 and I would like for her to be able to get a good night's rest as well. Would massage help? Is it even worth considering an SSRI or would that be too much of a risk at his age?
Current meds are warfarin, and blood pressure (not sure exactly which but I could check if that's helpful) and Tylenol (325 mg) as necessary for any pain. I believe he is on flomax as well... Home health care comes by at least once a week to check his numbers and we check O2 at least once an hour.
Thank you for your time, it is greatly appreciated!

Mystery itching making my dad miserable, autoimmune connection?
My dad (71M, 250 lbs, 6’1 white) has been experiencing life-ruining itching since Oct. 2019. He takes a beta blocker, blood thinners, warfarin, a multivitamin, tylenol, melatonin and zzzquil for sleep. He does not drink, smoke, or do drugs.
He had three heart valves replaced in his thirties after heart problems developed from a childhood bout with rheumatic fever.
He was about 10-11 when he had rheumatic fever and remembers his joints and body aching so much his mom had to carry him to the hospital.
Between that rheumatic fever and his heart valve surgery in his 30s, his health gradually declined, blood pooling in his feet and legs, sweating and vomiting.
He doesn’t give me a ton of details, but basically he only went to the ER when he was in extremely dire straits and they figured out something was wrong with his heart and he got the surgery done soon after.
His health was never good, when he got sick he got incredibly sick.
Before the itching began, he couldn’t walk long distances because he would get extremely winded and he got a handicapped placard for that reason.
When the itching began in Oct. 2019, it was immediately full body with a rash all over. It seemed like he had a fever and was freezing cold when it was still warm outside (we live in a desert). We thought at first that it was shingles, or an extreme allergic reaction to a dog we had just gotten the month before.
Doctors were perplexed, some said eczema or called them just ulcers or cysts. But it looks nothing like typical diabetes ulcers, venous ulcers or anything of the sort.
We ruled all that out but the itching remained and has intensified over the years. Doctors prescribed a round of oral steroids, prednisone in the beginning and during particularly bad flare ups, and he uses topical steroids and over the counter pain medicine to cope.
His skin, mainly his ankles and legs, is covered in raised pustules or nodules all over that have hard white lumps in them that can be popped out, leaving behind an open wound or crater that scars. The surrounding skin has become scaly and almost looks dead from how much he scratches.
He can get obsessive in popping the pustules, which probably isn’t good, but there’s no stopping him.
He said it is the most intense itch he’s ever felt, worse than any pain. It wakes him out of a deep sleep, he often doesn’t get more than a few hours of sleep a night and constantly keeps himself distracted online and with video games to stop himself from itching.
After hours of research he finally found pictures online that looked like what he had: prurigo nodularis which a dermatologist later agreed with. While researching it, he became frustrated that it basically said its a mystery and there’s no known cause.
That caused him to give up on going to doctors and give up on asking for medicine since then. He recently went back to the dermatologist after a long bout away because he’s having an extremely bad flare up, and he’s on steroids right now and feeling so much better.
He was able to sleep without being woken up from itching for the first time in years he said he felt “euphoric” and told my mom in the morning “you haven’t seen your husband this happy in years.
When we are having a discussion about it, I wondered aloud if he should go to a rheumatologist, and that’s when he told me about his childhood rheumatic fever.
I felt like there was some connection there, between the rheumatic fever and this autoimmune itching, but he’s skeptical.
My question is: can this prurigo nodularis be related to or caused by a childhood rheumatic fever? If so, what treatments could help this, biologics, or Dupixent? Will that medicine be approved by medicare?
If not, is it possible for him to be on a low dose of steroids indefinitely, because it seems to give him so much relief? (edited post for formatting issues)

Hi been having headaches and not sleeping. I take warfarin, been three months now and I been basically raw dogging pain not taking medicine at all. This headache have been unbearable I can’t even sleep , is it safe to take a Tylenol PM?

Current regimen. The sequence was the hardest thing to determine.
Morning:
- Levothyroxine 75 mcg 1 tablet
- Amiodarone 200 mg 1 tablet(replaced Amlodopine)
- Spironolactone 25 mg 1 tablet
- Warfarin 2.5mg 1 tablet (replaced Eliquis) (Mon-Thu: 2.5mg, Fri: 5mg)
- Farxiga 10mg 1 tablet (replaced Xigduo)
- Metformin 1000 mg 1 tablet (replaced Xigduo)
- Entresto 97/103 mg (replaced Edarbi) 1 tablet TWICE DAILY
- Vascepa - 2 capsules TWICE DAILY
- Carvedilol 12.5 mg 1 tablet TWICE DAILY (replaced Metoprolol)
- Ozempic - .5 mg - WEEKLY
​
Evening:
- Atorvastatin 80 mg 1 tablet
- Aspirin 81 mg 1 tablet
- 97/103 mg Entresto
- 12.5 mg Carvedilol
- Vascepa
​
As needed:
- [ ] Tylenol
​
​
SEQUENCE:
- 7:00 AM Levothyroxine (no food)
Wait 30 minutes
- 25 mg Carvedilol (with food)
Wait 2 hours
- Amiodarone, Spironolactone, Warfarin, Farxiga, 97/103 mg Entresto.
Wait 1-2 hours
- Metformin, Vascepa (with food)
- 7:00 PM: Atorvastatin, Aspirin, Vascepa, 25 mg Carvedilol (with food)
Wait 2 hours
- 9:00 PM: 97/103 mg Entresto
​

Hello 👋
TLDR: Is it normal to have more extreme pain after starting Xarelto, and during/after elevating? If so, why? Is worsening leg pain a symptom of worsening clot? When does one go back to the ER (if no PE symptoms)? Does one have to wait it out after diagnosis with extreme pain or can the clot cause more damage in the leg and there is something they can do to dissolve it?
My DVT caused only swelling and not much pain. The night of being diagnosed, in the ER, they gave me 15mg of Xarelto. I woke up at 3 am in extreme pain, after elevating comfortably all night. To my shock the calf swelling subsided from a balloon leg to stick figure leg. I was so happy. But the pain was 10x worse than I ever felt. Searing fire from the calf through the toes. Lasted about 3-4 hours.
It got better during the day. But the swelling returned by afternoon. I took a second dose of Xarelto, and elevated my leg about 1 hr later, and the pain became excruciating immediately. I had to finally take half tramadol (my first ever) after tylenol was not helping. It just slightly dulled the pain.
Is this worsening pain a possible side effect of Xarelto or is this the signal the medicine is working? I haven't had extreme pain at all at ER. I am willing to take other classical medicine like warfarin if it has fewer side effects.
Background:
I am new here. 43 yo female with no other risks, but I had minor ankle surgery. Symptoms started 2 days post-op with tingling and numbness in my foot, dead toes, and bizarre swelling. No pain in the calf. I was wearing a splint and did not see the foot until I removed it due to discomfort. As I also had a nerve block I had absolutely no way to tell what is happening. Because my surgeon was away I had to go to urgent clinic. The urgent clinic sent me home with antibiotics thinking it was cellulitis.
When the swelling started moving up to my calf, the urgent clinic doctor sent me for Ultrasound. I only started experiencing cramping calf pain the morning of the ultrasound where they diagnosed DVT of calf. Popliteal, tibial, and peroneal veins. (8th day after surgery.)
By that afternoon I was in the ER. After 5 hrs, they took blood and sent me home on Xarelto 15 mg twice a day and recommended I reach out to a vascular surgeon.
My main worry currently is the worsening pain but also the fact that I cannot feel half my foot and looks like my nerves were compromised, either in surgery or due to the blood constriction.
To be clear because of the ankle surgery I am unable to walk to help the flow, and can only use crutches and wheelchair. I sweta a lot due to the extra effort but my painful leg is still immobile. I am supposed to receive a walking boot on 8/28 but doubt it, because cannot put any weight on my foot at all now.
It is miserable situation and I question how life will be with this level of pain.

Hello! I was diagnosed with CVST in June 2023 and this summer I've spent so much time reading helpful posts on ClotSurvivors that I wanted to share my experience too in case it helps anyone. Sorry in advance for the post length and happy to answer any questions that folks have!
In late June this year I got a sudden sharp pain in my head on a Sunday after coming back from a semi-long, hot walk. I had donated blood on the Friday before so figured it was related to dehydration, took some ibuprofen and continued on with my day. On Monday I tried to work (I work from home and am pretty much in Zoom calls all day) but just couldn't focus because of the pain so took the day off. Tuesday was pretty much the same--I was lying in a dark room attempting to call into meetings but something definitely felt off. I called a nurse hotline and asked about the headache and they suggested I go to the ER so I did.
When I got to the ER my headache wasn't too bad but I had blurry vision. I am so, so grateful that the ER doctor ordered a CT scan (I think it was because I mentioned I rarely get headaches and I'd never had one this bad) and the results showed a density on the right transverse and sigmoid venous sinus thrombosis. The ER doctor ordered a follow up MRI that confirmed the clot and I was admitted to the hospital (very slowly, there were no rooms so spent the night in the ER). I ended up staying in the hospital for 3 days on heparin drip under observation. I had a chest CT and and ultrasound of my legs to look for other clots and they actually found a small PE that I had ZERO symptoms for. The neurologist assigned to my case asked me to choose between warfarin or a direct anti-coagulant, and the way he described warfarin did NOT make it sound attractive so i chose the DOAC. He prescribed Xarelto and I transitioned from heparin to that the day before I was discharged.
The only cause identified so far for my clots was my birth control (I had been on Portia for many years) so I stopped taking that right away. This had the fun side effect of causing my period to come early while I was still in the hospital. The way surprise blood just gushed out of me was concerning and I thought it might be a sign of internal bleeding from medication, but just a fun preview of periods to come :)
After I was discharged I took two weeks off of work and tried to take it easy. My appetite was pretty good, energy levels okay. Prior to this event I was super active, running, walking, doing lots of yoga, so it was really hard for me to sit still and rest. I had a lot of head pressure after the hospital and also some weird issues with my eustachian tube (I constantly needed to equalize pressure by blowing my nose--this symptom still comes and goes and I was told to just use a nasal spray) that kept me from getting out and about too much. After about a week at home I started taking small walks and car rides. I went back to work slowly after about two weeks but every now and then I need to take a day or half day off because of headache/fatigue. I've taken Tylenol just a few times since I've been discharged and have staying hydrated (thanks to all the people on this subreddit who recommend good hydration!!).
It's now August and I'm almost at my 3 month clot anniversary. This morning I decided to go to the ER for a nagging new headache I've had for the past two weeks on my left temple/eye, sometimes radiating to my cheek. The headache does not respond to Tylenol and gets worse throughout the day. I've also had bad neck pain on the left (which my GP sent me to physical therapy for). The ER doctors today ordered a CT scan and found no new issues (woo!) and saw evidence of my original clot slowly dissolving (also woo!). I was discharged after a few hours and here I am! Happy but wishing I had more information about what was causing this new annoying headache.
Over the past few weeks I've been getting back into my old routine: some short runs, yoga classes, longer walks. My job also causes me a good amount of stress on any given day, so I'm thinking I might just be taking things too quickly and I need to slow things back down. Last week I was also on my period. I've had 3 periods since being discharged and they are definitely heavier and more liquidy than before, but thankfully they end after ~3 days of heavy bleeding. So perhaps that played into my new headache too.
I have a follow up with my neurologist later this week and more bloodwork to rule out additional possible causes for the clots in September. My neurologist suggested that if things continue to look good I can end the Xarelto (currently on 20mg 1x day) but I'm of the mind set of wanting to stay on some level of blood thinner just to help with my anxiety...
Anywho, this is already a long post but I wanted to say thank you again to this subreddit and the wonderful posters! Your experiences and positive responses to posters have really helped feel like I'm not alone these past few months <3
​
​

Thuốc Glivec (https://bacsi247.org/blog/thuoc-glivec-cong-dung-cach-dung-va-nhung-luu-y-truoc-khi-su-dung) 100mg là thuốc điều trị bệnh ung thư máu. Tại bài viết này, bacsi247.org cung cấp các thông tin chuyên sâu về thuốc. Một sản phẩm nổi bật trong danh mục thuốc bệnh lý về ung thư được đội ngũ bác sĩ và dược sĩ của chúng tôi tin dùng.

Thông tin thuốc Glivec 100mg

• Tên Thuốc: Glivec 100mg
• Số Đăng Ký: VN-13289-11
• Hoạt Chất: Imatinib mesilate 100mg
• Dạng Bào Chế: Viên nén bao phim
• Quy cách đóng gói: Hộp 6 vỉ x 10 viên
• Hạn sử dụng: 24 tháng
• Công ty Sản Xuất: Novartis Pharma Stein AG (Schaffhauserstrasse CH-4332 Stein Switzerland)
• Công ty Đăng ký: Novartis Pharma Services AG (Lichtstrasse 35 – 4056 Basel Switzerland)

Thuốc Glivec 100mg là gì?

Glivec 100mg là thuốc chống ung thư có sự khác biệt về mặt cấu trúc và dược lý học so với các thuốc chống ung thư khác. Thuốc được chỉ định nhằm điều trị ung thư máu.

Công dụng của Glivec 100mg

Thuốc Glivec 100mg có tác dụng dùng để điều trị cho:
Bệnh nhân người lớn và trẻ em có nhiễm sắc thể Philadelphia (bcr-abl) dương tính (Ph +) bệnh bạch cầu mạn tính dòng tủy (CML) mới được chẩn đoán mà ghép tủy xương không được coi là phương pháp điều trị đầu tiên.
Bệnh nhân người lớn và trẻ em bị Ph + CML trong giai đoạn mãn tính sau khi thất bại điều trị interferon-alpha, hoặc trong giai đoạn tăng tốc hoặc khủng hoảng bùng phát.
Bệnh nhân người lớn và bệnh nhi mắc bệnh bạch cầu nguyên bào lympho cấp tính nhiễm sắc thể Philadelphia (Ph + ALL) mới được chẩn đoán tích hợp với hóa trị.
Bệnh nhân người lớn có Ph + ALL tái phát hoặc khó chữa như đơn trị liệu.
Bệnh nhân người lớn bị bệnh tăng sinh tủy / bệnh tăng sinh tủy (MDS / MPD) liên quan đến sự sắp xếp lại gen của thụ thể yếu tố tăng trưởng có nguồn gốc từ tiểu cầu (PDGFR).
Bệnh nhân người lớn bị hội chứng tăng bạch cầu ái toan (HES) và / hoặc bệnh bạch cầu tăng bạch cầu ái toan mãn tính (CEL) với sự sắp xếp lại FIP1L1-PDGFRα.
Ảnh hưởng của Glivec 100mg đến kết quả của việc cấy ghép tủy xương vẫn chưa được xác định:
Điều trị bệnh nhân người lớn với các khối u mô đệm đường tiêu hóa ác tính không thể cắt bỏ và / hoặc di căn (GIST) có Kit (CD 117).
Điều trị bổ trợ cho bệnh nhân người lớn có nguy cơ tái phát đáng kể sau khi cắt bỏ GIST dương tính với Kit (CD117). Những bệnh nhân có nguy cơ tái phát thấp hoặc rất thấp không nên điều trị bổ trợ.
Điều trị cho bệnh nhân người lớn mắc bệnh u xơ tử cung không cắt bỏ được (DFSP) và bệnh nhân người lớn mắc bệnh DFSP tái phát và / hoặc di căn không đủ điều kiện phẫu thuật.
Ở bệnh nhân người lớn và trẻ em, hiệu quả của Glivec 100mg dựa trên tỷ lệ đáp ứng huyết học và di truyền tế bào tổng thể và tỷ lệ sống sót không tiến triển trong CML, tỷ lệ đáp ứng huyết học và di truyền tế bào trong Ph + ALL, MDS / MPD, tỷ lệ đáp ứng huyết học trong HES / CEL và về tỷ lệ đáp ứng khách quan ở bệnh nhân người lớn với GIST và DFSP không thể cắt bỏ và / hoặc di căn và về tỷ lệ sống không tái phát ở GIST bổ trợ.

Cách hoạt động của thuốc Glivec 100mg

Imatinib là một loại thuốc chống ung thư. Một loại enzyme protein, bcr-abl tyrosine kinase, chịu trách nhiệm cho sự phát triển tăng sinh bất thường của tế bào ung thư. Thuốc này ức chế sự tăng sinh và gây ra apoptosis (tế bào chết theo kế hoạch) ở các tế bào dương tính bcr-abl (tế bào ung thư). Đây là cách nó hoạt động để ngăn chặn hoặc làm chậm sự lây lan của ung thư.

Liều dùng thuốc Glivec 100mg bao nhiêu?

Liều dùng trẻ em > 2 tuổi

• Có thể uống 1 lần hoặc chia 2 lần/ngày.
• Bệnh bạch cầu mạn tính dòng tủy Ph+ (giai đoạn mạn, thể tái phát hoặc dai dẳng) 260 mg/m2/ngày.
• Bệnh bạch cầu mạn tính dòng tủy Ph+ (giai đoạn mạn, thể mới chẩn đoán) 340 mg/m2/ngày, tối đa 600 mg/ngày.

Liều dùng người lớn

• Liều thông thường 400 – 800 mg/ngày. Uống 1 lần/ngày nếu liều 400 – 600 mg/ngày, chia làm 2 lần với liều 800mg/ngày.
• Bệnh bạch cầu mạn tính dòng tủy Ph+ giai đoạn mạn 400mg/ngày, có thể tăng liều lên đến 600 mg/ngày nếu đáp ứng với điều trị kém sau 3 tháng điều trị; giai đoạn cấp hoặc quá nhiều tế bào non trong máu 600 mg/ngày và có thể tăng liều lên đến 800 mg/ngày nếu đáp ứng điều trị kém.
• Bệnh bạch cầu cấp dòng lympho Ph+ tái phát hoặc điều trị thất bại với trị liệu khác: 600 mg/ngày.
• U tổ chức liên kết dạ dày – ruột: Điều trị hỗ trợ sau phẫu thuật cắt bỏ khối u: 400mg/ngày; trường hợp bệnh nhân không thể phẫu thuật hoặc di căn ác tính: 400mg/ngày, có thể tăng liều lên đến 800 mg/ngày
• Bệnh lý tăng tế bào mast xâm lấn toàn thân: Liều ban đầu 100mg/ngày, có thể tăng liều lên đến 400 mg/ngày.
• Trường hợp imatinib sử dụng như thuốc bước 2 điều trị bệnh bạch cầu dòng tủy mạn tính: 400 – 600 mg imatinib/ngày.

Hiệu chỉnh liều trong một số trường hợp

Tránh sử dụng imatinib phối hợp với các thuốc cảm ứng CYP3A4 mạnh (dexamethason, carbamazepin, phenobarbital, phenytoin, rifampicin), nếu cần thiết phải phối hợp thì phải tăng liều imatinib lên ít nhất 50% và theo dõi cẩn thận.
Trường hợp bệnh nhân có suy thận, Cục Quản lý thực phẩm và dược phẩm Hoa Kỳ (FDA) khuyến cáo như sau:

• Suy thận nhẹ (Clcr 40 – 59 ml/phút) liều tối đa 600 mg/ngày.
• Suy thận vừa (Clcr 20 – 39 ml/phút) liều tối đa 400 mg/ngày.
• Suy thận nặng (Clcr < 20 ml/phút) cần thận trọng, liều có thể dung nạp: 100 mg/ngày.

Trường hợp bệnh nhân có suy gan:

• Suy gan nhẹ và vừa: Không cần điều chỉnh liều.
• Suy gan nặng: Giảm liều 25%.
• Bệnh nhân có tổn thương gan nhiễm độc trong quá trình điều trị: Ngừng điều trị (nếu bilirubin > 3 lần giới hạn trên hoặc transaminase > 5 lần giới hạn trên), khi bilirubin < 1,5 lần giới hạn trên và transaminase < 2,5 lần giới hạn trên thì có thể dùng lại imatinib với liều như sau:
• Trẻ em > 2 tuổi: Liều hiện tại 260 mg/m2/ngày, giảm xuống 200 mg/m2/ngày; liều hiện tại 340 mg/m2/ngày, giảm xuống 260 mg/m2/ngày.
• Người lớn: Liều hiện tại 400mg/ngày, giảm xuống 300mg/ngày; liều hiện tại 600mg/ngày, giảm xuống 400mg/ngày; liều hiện tại 800mg/ngày, giảm xuống 600 mg/ngày.

Quên liều thuốc Glivec 100mg

Liều đã quên nên được thực hiện càng sớm càng tốt. Bạn nên bỏ qua liều đã quên nếu đã đến thời gian cho liều dự kiến ​​tiếp theo. Không sử dụng thêm thuốc để bù cho liều đã quên.

Quá liều lượng của Glivec 100mg

• Tìm kiếm sự chăm sóc y tế ngay lập tức hoặc liên hệ với bác sĩ nếu nghi ngờ quá liều thuốc Glivec 100mg.
• Đem theo đơn thuốc Glivec 100mg và hộp thuốc cho bác sĩ xem.

Cách dùng thuốc Glivec 100mg

Dùng thuốc Glivec 100mg chính xác theo quy định của bác sĩ. Thực hiện theo tất cả các hướng dẫn trên nhãn thuốc của bạn và đọc tất cả các hướng dẫn thuốc hoặc tờ hướng dẫn. Bác sĩ của bạn đôi khi có thể thay đổi liều của bạn. Sử dụng thuốc chính xác theo chỉ dẫn.

Tác dụng phụ Glivec 100mg

Hầu hết các tác dụng phụ không cần chăm sóc y tế và biến mất khi cơ thể bạn thích nghi với thuốc. Tham khảo ý kiến ​​bác sĩ nếu họ vẫn tiếp tục hoặc nếu bạn lo lắng về họ
Tác dụng phụ thường gặp của Glivec 100mg

• Phù (sưng)
• Buồn nôn
• Nôn mửa
• Chuột rút cơ bắp
• Đau cơ xương (xương, cơ hoặc khớp)
• Bệnh tiêu chảy
• Phát ban
• Mệt mỏi
• Đau bụng

Thận trọng khi dùng thuốc Glivec 100mg

Bạn không nên sử dụng imatinib nếu bạn bị dị ứng với nó.
Hãy cho bác sĩ biết nếu bạn đã từng:

• Bệnh gan (đặc biệt là viêm gan B);
• Bệnh thận;
• Tuyến giáp kém hoạt động , phẫu thuật tuyến giáp gần đây hoặc sắp tới;
• Bệnh tim, huyết áp cao , suy tim sung huyết ;
• Một loét dạ dày hoặc chảy máu;
• Bệnh tiểu đường;
• Hóa trị liệu .

Bạn có thể cần phải thử thai âm tính trước khi bắt đầu điều trị này.
Không sử dụng imatinib nếu bạn đang mang thai. Nó có thể gây hại cho thai nhi hoặc gây dị tật bẩm sinh. Sử dụng biện pháp tránh thai hiệu quả để tránh mang thai trong khi bạn đang sử dụng imatinib và ít nhất 14 ngày sau liều cuối cùng của bạn.
Không cho con bú trong khi bạn đang sử dụng thuốc này và ít nhất 1 tháng sau liều cuối cùng của bạn.

Tương tác thuốc Glivec 100mg

Hãy cho bác sĩ biết nếu bạn đang dùng bất kỳ loại thuốc nào khác, bao gồm cả những loại thuốc bạn mua không cần đơn từ hiệu thuốc, siêu thị hoặc cửa hàng thực phẩm chăm sóc sức khỏe.
Một số loại thuốc và Glivec 100mg có thể gây nhiễu lẫn nhau. Chúng bao gồm nhiều loại thuốc được thải trừ khỏi cơ thể qua gan:

• St. John’s wort, một loại thảo dược có trong nhiều sản phẩm mà bạn có thể mua mà không cần đơn
• Paracetamol, một loại thuốc được tìm thấy trong nhiều loại thuốc giảm đau và thuốc chữa cảm lạnh thông thường (ví dụ như Panadol, Panadeine, Codral, Tylenol) được biết là có liên quan đến nhiễm độc gan.
• Một bệnh nhân đang dùng paracetamol thường xuyên để hạ sốt đã tử vong do suy gan cấp. Mặc dù hiện nay chưa rõ nguyên nhân nhưng cần đặc biệt thận trọng khi sử dụng paracetamol và Glivec 100mg.
• Thuốc kháng sinh như rifampicin, ketoconazole, erythromycin, clarithromycin, itraconazole
• Thuốc kháng vi-rút dùng để điều trị HIV / AIDS
• Dexamethasone, một loại thuốc steroid
• Thuốc điều trị cholesterol cao, chẳng hạn như simvastatin
• Thuốc dùng để điều trị chứng động kinh, chẳng hạn như phenytoin, carbamazepine, phenobarbitone
• Warfarin, một loại thuốc dùng để ngăn ngừa cục máu đông
• Một số loại thuốc dùng để điều trị rối loạn tâm thần và trầm cảm
• Một số loại thuốc dùng để điều trị huyết áp cao và các vấn đề về tim
• Cyclosporin

Bạn có thể cần dùng các lượng thuốc này khác nhau hoặc bạn có thể cần dùng các loại thuốc khác nhau.

Has anyone done this? I had a PE a few months ago after getting covid (despite being vaccinated), and they put me on Eliquis for 6 months. The clot cleared quickly and my blood levels are normal, but I'm worried that MDMA would increase the bleeding risk. Thanks in advance for any insights!
EDIT - Reporting back in case anyone else finds themselves in this position:
I ended up taking MDMA, LSD, and Vyvanse (not prescribed) on different days of the festival (as well as a fair bit of Tylenol). It's now a couple weeks later and I haven't noticed any unusual side effects or interactions with the Eliquis. Before taking any of these drugs I also checked with a couple pharmacists, as well as three of my friends (doctophysician's assistant/nurse practitioner). None could think of any reason they would interact. I also asked my doctors (hemo/pulmo/primary), but they didn't know anything.
For added context, I've also been on Remicade for years to treat ulcerative colitis, which was threatening to flare up a bit during the fest.
I still don't recommend doing this or anything (especially at a festival because of injury risk due to lowered coordination), but I figured I should at least share my experience for science or whatever. Other than the two commenters in this thread who combined MDMA with Warfarin, I haven't seen a single other anecdote in my extensive googling about mixing MDMA with blood thinners. There was one other post on reddit from someone who mixed Eliquis with LSD and shrooms without issue, but that's all I've seen. I would love to see more illegal drugs documented in medical literature (and also legalized, but that's a different discussion).

Hello kava lovers!
I took quite a bit of time today to dig into this. It's been a long running issue that when you type in "Kava" in google you get some dubious results on the first page. I'm taking it upon myself to list those here, and refute them where they have issues.
Search Results for "Kava" on google in incognito window.
Result 1: Webmd

1. Overview

• Point 1: “Kava is a beverage or extract that is made from Piper methysticum, a plant native to the western Pacific islands. The name "kava" comes from the Polynesian word "awa," which means bitter. In the South Pacific, kava is a popular social drink. It is consumed as a beverage in ceremonies to promote relaxation.”

1. No issues with point one.

• Point 2: “There have been some safety concerns about kava. Cases of liver damage and even some deaths have been traced to kava use. Because of these reports, kava was withdrawn from the market in Europe and Canada in the early 2000s. However, most countries have allowed kava to return to the market since that time. Kava has never been taken off the market in the U.S.”

1. And my issues start here. “Cases of liver damage and even some deaths have been traced to kava use” is a hotly contested conclusion, and rather inflammatory when such paltry evidence exists to support it. The paragraph then goes on to state “However, most countries have allowed kava to return to the market since that time.” My issue here is; why are we not seeing these cases of liver failures and injury in countries where it’s freely available today, if it’s as liver toxic as it was said to be?

• Point 3: “Kava is most commonly used for anxiety. Some people take kava for stress, restlessness, sleeping problems (insomnia), and many other conditions. But there is no good scientific evidence to support these uses.”

1. “But there is no good scientific evidence to support these uses.” Hilariously they give quite good scientific evidence to support these uses directly in their references. Kava and kava extracts have been proven in double blind placebo controlled studies to reduce anxiety scores, and increase sleep duration/quality.
2. How does it work?

• Point 1: “Kava affects the brain and other parts of the central nervous system. The kavalactones in kava are believed to be responsible for its effects.”

1. No issues with this. This has been demonstrated repeatedly in research.
2. Possibly Effective for

• Point 1: “Anxiety. Most research shows that taking kava extracts that contain 70% kavalactones can lower anxiety and might work as well as some prescription anti-anxiety medications. Most studies have used a specific kava extract (WS 1490, Dr. Willmar Schwabe Pharmaceuticals). It seems that kava supplements containing at least 200 mg kavalactones daily should be taken for at least 5 weeks for symptoms to improve.”

1. Strangely, they just got finished saying there is no good scientific information on which to support these theories. Extra note: WS-1490 is an extract that has been embroiled in controversy. The extract is contested on the grounds that it was changed several times throughout the research periods from an ethanolic extract to an acetonic extract with no indication. You can see this by noting how the kavalactone percentage changes arbitrarily from 30% to 70%.
2. Possibly Ineffective for

• Point 1: “A type of persistent anxiety marked by exaggerated worry and tension (generalized anxiety disorder or GAD). Several early studies show that taking kava doesn't improve symptoms in people with GAD.”

1. They conveniently don’t mark their sources in the article, but this one comes from Dr. Sarris in Australia in 2020. This research concluded that kava was more suitable for the reduction in stress and tension related to ‘situational’ anxiety, than it was for direct treatment of G.A.D.
2. Insufficient Evidence for

• Point 1 “Withdrawal from drugs called benzodiazepines. Early research suggests that slowly increasing the dose of kava extract over the course of one week while decreasing the dose of benzodiazepines over the course of two weeks can prevent withdrawal symptoms and reduce anxiety in people who have been taking benzodiazepines for a long period of time.”

1. It can reduce anxiety, but the actual physical withdrawal is not treated by any action of the kavalactones themselves. It’s likely that the steady tapering of the BZP drug was what allowed these participants to cease their use with less acute withdrawal. Kava definitely helps, but it has different actions at the GABA-A receptor that are not similar to that of benzodiazepine drugs. Benzos target the BZP allosteric site on the GABA-A receptor where they exert their effect. Kava and flumazenil (a very potent anti-benzo or BZP antagonist) were administered at the same time in studies, and the effect of kava was not blocked.

• Point 2 “Cancer. There is some early evidence that taking kava might help to prevent cancer.”

1. I would say this “insufficient evidence” is actually an order of magnitude more studied and documented than the “liver damage” at the very beginning of this article. I’ve added additional citations below this papers citations, and I stopped citing at 12 research studies that show anti-cancer effects.

• Point 3 “Insomnia. Research on the effectiveness of kava in people with sleeping problems is inconsistent. Some research shows that taking kava extract daily for 4 weeks reduces sleeping problems in people with anxiety disorders. But other research suggests that taking kava three times daily for 4 weeks does not reduce insomnia in people with anxiety.”

1. The World Health organization monograph (2002) describes insomnia as a state supported by clinical data. This is generally accepted, however there were participants in studies on kava that dropped out due to insomnia complaints. While kava is overall a good fit for sleep issues, it likely won’t present that way to 100% of the people who drink it. We actually do see people complain about not being able to get to sleep after a strong kava. I say this to agree with the above paragraph where it states the research is inconsistent. It helps me with sleep, but that doesn’t mean it will be the same for everyone.

• Point 4 “Symptoms of menopause. Early research shows that taking kava daily for 3 months might reduce depression, anxiety, and hot flashes.”

1. While maybe insufficient, there is good evidence to support this. Two individual studies found improvement in mood, reduction in depression, and reduction in anxiety in perimenopausal individuals.

• Point 5 “Stress. Early research suggests that taking a single dose of kava by mouth might reduce symptoms associated with mentally stressful tasks.”

1. This is an odd one to say has insufficient evidence. A number of researchers including Münte, Sarris, Cropley, and Aporosa have found kava reduces symptoms associated with mentally stressful tasks.

• Point 6 “Seizure disorder (epilepsy).”

1. This is in line with reality. We only see glimpses into kava’s ability to modulate glutamate. Kavain was shown to inhibit veratridine-activated sodium channels. It’s possible that kava may help reduce seizures, but as said, there is insufficient evidence to say it precisely.

• Point 7 “Muscle pain.”

1. This I don’t agree with, and it’s a strange one to be saying there’s insufficient evidence for. Kava has marked antinociceptive (pain relieving) and muscle-relaxing properties. A good number of independent research studies have confirmed this.

• Point 8 “Other conditions”

1. I’m not really sure what to say here. I suppose it’s quite accurate to say that there is insufficient evidence for kava causing superhero-like powers to emerge.
2. Side Effects

• Paragraph 1 “When taken by mouth: Kava is POSSIBLY SAFE when taken for up to 6 months. Using kava can make you unable to drive or operate machinery safely. Do not take kava before you plan on driving. "Driving-under-the-influence" citations have been issued to people driving erratically after drinking large amounts of kava tea.”

1. This is good, and goes pretty far based on the double blind placebo controlled studies. The one issue I have is the 6 month limit. There really isn’t any indication that taking kava beyond this time frame causes issues, it’s just when they cut the time limit of the study. Empirical evidence suggests kava, when consumed as a beverage, is safe indefinitely as shown by the South Pacific people who drink kava on a daily basis and have for generations. In regards to driving, I fully agree. If you’re consuming anything that makes you question your abilities with driving, call an ubelyft.The risk is simply not worth it.

• Paragraph 2 “People may have heard that use of kava can cause liver damage. The use of kava for as little as 1-3 months has resulted in the need for liver transplants and even death in some people. Early symptoms of liver damage include yellowed eyes and skin (jaundice), fatigue, and dark urine. But these cases appear to be relatively rare. Most people who have used kava have not experienced liver toxicity. Also, some experts believe that the liver toxicity seen in these cases cannot be directly linked to kava. Other factors may have contributed to these toxic effects. To be on the safe side, people who choose to use kava can get liver function tests.”

1. That’s pretty honest, however the phrase “The use of kava for as little as 1-3 months has resulted in the need for liver transplants and even death in some people” really understates “some people”. The number of individuals allegedly harmed by kava is limited to less than 10. There has been no intrinsic (unable to be separated) toxicity seen in kava or any kava extracts, however idiosyncratic reactions of the immunologic type have occurred. This is extremely rare. I can’t say that enough. We’re talking on the scale of winning the lottery, being hit by lightning, and finding Jimmy Hoffa all at the same instant. If we turn our attention to things such as green tea extracts or acetaminophen we see intrinsic, predictable toxicity to the liver. This does not exist with kava.
2. Special Precautions and Warnings

• Point 1 “Pregnancy and breast-feeding: Don't use kava if you are pregnant or breast-feeding. Kava is POSSIBLY UNSAFE when taken by mouth. There is a concern that it might affect the uterus. Also, some of the dangerous chemicals in kava can pass into breast milk and might hurt a breast-fed infant.”

1. They’re speaking about kavalactones, and they’re not “dangerous chemicals” however we don't fully understand the function of GABAergic substances on the developing brain. Kavalactones are known as lipophilic, meaning they tend to combine or dissolve in fats. This means they could likely also pass on through breastfeeding. There is no data confirming this suspicion, however with no experience available, kava is not recommended for use by pregnant or breast-feeding women. It’s much better to err on the side of caution. In regards to kava affecting the uterus, I’m afraid there is absolutely nothing confirming this. It’s an old myth from Fiji that kava stimulates the uterus, this doesn’t happen, and shouldn’t be listed as a precaution. Histopathology was performed on rats at 2.0g/kg of kavalactones and found no-effect level on the uterus. (2012. “Toxicology and Carcinogenesis Studies of Kava Kava Extract (CAS No. 9000-38-8) in F344/N Rats and B6C3F1 Mice (gavage Studies).” National Toxicology Program 571 (1): 1–186. https://ntp.niehs.nih.gov/publications/reports/t500s/tr571/index.html)

• Point 2 “Liver disease: Kava might cause liver problems, even in healthy people. People who have a history of liver problems should avoid kava.”

1. Well this sounds familiar. This will be the 3rd time this website has decided it was pertinent to warn us of liver damage. What they’ll throw at you sometimes is the instance of GGT elevation in metabolism tests seen in kava users in the late 80s and early 90s in Australia's Northern Territory. This is NOT indicative of liver damage. It indicates liver adaptation and is seen in kava drinkers that consume about a pound of dried kava per week. AST and ALT increases are not seen. I would even go as far to say here that kava is not even detrimental to those with liver problems. Kava is not intrinsically toxic to the liver in any way.

• Point 3 “Parkinson disease: Kava might make Parkinson disease worse. Do not take kava if you have this condition.”

1. This one is interesting. You have research on one side saying kava has no or very little activity at dopamine, then you have other research indicating that some kavalactones drop dopamine levels considerably. The one kavalactone in question here is Yangonin. Yangonin has shown in research to lower dopamine to below detectable levels. I personally believe that this is happening evidenced by the extrapyramidal movements seen in kava drinkers that went way overboard. They end up looking like they have parkinsons. If you are on medication such as levodopa that is specifically meant to increase free dopamine levels in the brain, kava can counteract this effect and cause the resurgence of parkinson's symptoms. So yes, I agree with this statement. If you have parkinsons it’s best to skip the kava.

• Point 4 “Surgery: Kava affects the central nervous system. It might increase the effects of anesthesia and other medications used during and after surgery. Stop using kava at least 2 weeks before a scheduled surgery.”

1. This is not talked about very much but should be taken into close consideration when approaching a surgery. Kava has many properties that haven’t been studied all that intensively. Kava has shown to have some mild antithrombotic actions. This means it may be able to prevent, to a degree, blood clotting. Give yourself at least a week if not two before any surgery to let your system flush out. Kava has also been shown to increase the sedation of anesthetic drugs. You’ll want to observe this just to be on the safe side.
2. Major Interactions

• Point 1 Alprazolam “Kava can cause drowsiness. Alprazolam (Xanax) can also cause drowsiness. Taking kava along with alprazolam (Xanax) may cause too much drowsiness. Avoid taking kava and alprazolam (Xanax) together.”

1. Agreed

• Point 2 “Kava might cause sleepiness and drowsiness. Medications that cause sleepiness are called sedatives. Taking kava along with sedative medications might cause too much sleepiness.Some sedative medications include clonazepam (Klonopin), lorazepam (Ativan), phenobarbital (Donnatal), zolpidem (Ambien), and others.

1. Agreed as well. Sedation seems to be the pharmacodynamic interaction here.
2. Moderate Interactions

• Point 1 “Levodopa interacts with KAVA - Levodopa affects the brain by increasing a brain chemical called dopamine. Kava might decrease dopamine in the brain. Taking kava along with levodopa might decrease the effectiveness of levodopa.”

1. I believe this to be correct. Levodopa is a medication meant to increase the levels of dopamine in the brain. Yangonin can decrease dopamine levels in the brain and counteract this medication.

• Point 2 “Medications changed by the liver (Cytochrome P450 1A2 (CYP1A2) substrates) interact with KAVA - Some medications are changed and broken down by the liver.- Kava might decrease how quickly the liver breaks down some medications. Taking kava along with some medications that are changed by the liver might increase the effects and side effects of some medications. Before taking kava talk to your healthcare provider if you take any medications that are changed by the liver. Some of these medications that are changed by the liver include clozapine (Clozaril), cyclobenzaprine (Flexeril), fluvoxamine (Luvox), haloperidol (Haldol), imipramine (Tofranil), mexiletine (Mexitil), olanzapine (Zyprexa), pentazocine (Talwin), propranolol (Inderal), tacrine (Cognex), theophylline, zileuton (Zyflo), zolmitriptan (Zomig), and others.

1. This is also correct. CYP1A2 is the pathway of metabolization for caffeine. Kava causes inhibitory actions at this pathway and as such causes caffeine to appear in serum levels for much longer than without kava in the system. The individual effect of this combination may differ from person to person. CYP1A2 activity has a range of 40% between individuals. As such it’s quite difficult to make predictions of which drugs will do what when this pathway is inhibited.

• Point 3 “Medications changed by the liver (Cytochrome P450 2C19 (CYP2C19) substrates) interact with KAVA - Some medications are changed and broken down by the liver Kava might decrease how quickly the liver breaks down some medications. Taking kava along with some medications that are broken down by the liver can increase the effects and side effects of your medication. Before taking kava talk to your healthcare provider if you take any medications that are changed by the liver. Some of these medications changed by the liver include amitriptyline (Elavil), clomipramine (Anafranil), cyclophosphamide (Cytoxan), diazepam (Valium), lansoprazole (Prevacid), omeprazole (Prilosec), lansoprazole (Protonix), phenytoin (Dilantin), phenobarbital (Luminal), progesterone, and others.

1. Correct as well; however, issues at this cytochrome with drugs that use this pathway are not heavily researched in regards to kava. They generally encompass the sedative effects and their increase when in combination with the drugs above. Caution should still be taken when combining these drugs with kava as it will likely make them stay in your system for considerably longer periods of time. DMY seems to be the most potent inhibitory kavalactone in this regard.

• Point 4 “Medications changed by the liver (Cytochrome P450 2C9 (CYP2C9) substrates) interacts with KAVA - Some medications are changed and broken down by the liver. Kava might decrease how quickly the liver breaks down some medications. Taking kava along with some medications that are broken down by the liver can increase the effects and side effects of some medications. Before taking kava talk to your healthcare provider if you take any medications that are changed by the liver. Some medications that are changed by the liver include amitriptyline (Elavil), diazepam (Valium), zileuton (Zyflo), celecoxib (Celebrex), diclofenac (Voltaren), fluvastatin (Lescol), glipizide (Glucotrol), ibuprofen (Advil, Motrin), irbesartan (Avapro), losartan (Cozaar), phenytoin (Dilantin), piroxicam (Feldene), tamoxifen (Nolvadex), tolbutamide (Tolinase), torsemide (Demadex), warfarin (Coumadin), and others.

1. This inhibition was seen strongest with methysticin, the number 6 on chemotypes. The effect seen with methysticin was low, with only 1% of the strength of their positive control (Sulfaphenazole). I truly believe this would not have a strong impact on drugs that also use this pathway being kava/kavalactones have such a low affinity for it.

• Point 5 “Medications changed by the liver (Cytochrome P450 2D6 (CYP2D6) substrates) interact with KAVA - Some medications are changed and broken down by the liver. Kava might decrease how quickly the liver breaks down some medications. Taking kava along with some medications that are change by the liver can increase the effects and side effects of your medication. Before taking kava talk to your healthcare provider if you take any medications that are changed by the liver. Some medications that are changed by the liver include amitriptyline (Elavil), clozapine (Clozaril), codeine, desipramine (Norpramin), donepezil (Aricept), fentanyl (Duragesic), flecainide (Tambocor), fluoxetine (Prozac), meperidine (Demerol), methadone (Dolophine), metoprolol (Lopressor, Toprol XL), olanzapine (Zyprexa), ondansetron (Zofran), tramadol (Ultram), trazodone (Desyrel), and others.

1. This is incorrect. Kava has no inhibition property at this cytochrome even at absurdly high concentrations, and as such this is wrong.

• Point 6 “Medications changed by the liver (Cytochrome P450 2E1 (CYP2E1) substrates) interact with KAVA - Some medications are changed and broken down by the liver. Kava might decrease how quickly the liver breaks down some medications. Taking kava along with some medications that are change by the liver can increase the effects and side effects of your medication. Before taking kava talk to your healthcare provider if you take any medications that are changed by the liver.Some medications that are changed by the liver include acetaminophen, chlorzoxazone (Parafon Forte), ethanol, theophylline, and drugs used for anesthesia during surgery such as enflurane (Ethrane), halothane (Fluothane), isoflurane (Forane), and methoxyflurane (Penthrane).

1. Again methysticin is the only kavalactone shown to interact with this cytochrome and it does it quite weakly. I wouldn’t suspect any immediate issues with drugs that use this pathway combined with kava.

• Point 7 “Medications changed by the liver (Cytochrome P450 3A4 (CYP3A4) substrates) interact with KAVA - Some medications are changed and broken down by the liver. Kava might decrease how quickly the liver breaks down some medications. Taking kava along with some medications that are broken down by the liver can increase the effects and side effects of some medications. Before taking kava, talk to your healthcare provider if you are taking any medications that are changed by the liver. Some medications changed by the liver include lovastatin (Mevacor), ketoconazole (Nizoral), itraconazole (Sporanox), fexofenadine (Allegra), triazolam (Halcion), and many others.

1. This effect, if present, will be very light. Kava has shown very slight inhibitory properties at CYP3A4 with methysticin being the most potent inhibitor. Methysticin has shown to be about 1% the inhibitory properties of their positive control, Ketoconazole. I would not expect major interactions with pharmaceuticals along this pathway with kava.

• Point 8 “Medications moved by pumps in cells (P-Glycoprotein Substrates) interacts with KAVA - Some medications are moved by pumps in cells. Kava might make these pumps less active and increase how much of some medications get absorbed by the body. This might increase the amount of some medications in the body, which could lead to more side effects. But there is not enough information to know if this is a big concern. Some medications that are moved by these pumps include etoposide, paclitaxel, vinblastine, vincristine, vindesine, ketoconazole, itraconazole, amprenavir, indinavir, nelfinavir, saquinavir, cimetidine, ranitidine, diltiazem, verapamil, corticosteroids, erythromycin, cisapride (Propulsid), fexofenadine (Allegra), cyclosporine, loperamide (Imodium), quinidine, and others.”

1. A single dose of 800mg kavain gave a serum concentration level of 40ng/ml or .1um. This plasma level is unlikely to cause any significant inhibition of P-gp in vivo. Also, 800mg of kavain is quite unlikely to be consumed at once in a typical kava consuming session. The likelihood of inhibition here is very low. Results obtained in vitro vs in vivo were contradictory.

• Point 9 “Medications that can harm the liver (Hepatotoxic drugs) interact with KAVA - Kava might harm the liver. Taking kava along with medication that might also harm the liver can increase the risk of liver damage. Do not take kava if you are taking a medication that can harm the liver. Some medications that can harm the liver include acetaminophen (Tylenol and others), amiodarone (Cordarone), carbamazepine (Tegretol), isoniazid (INH), methotrexate (Rheumatrex), methyldopa (Aldomet), fluconazole (Diflucan), itraconazole (Sporanox), erythromycin (Erythrocin, Ilosone, others), phenytoin (Dilantin), lovastatin (Mevacor), pravastatin (Pravachol), simvastatin (Zocor), and many others.”

1. It should be obvious to limit the intake of liver toxic compounds, however some of them are rather ubiquitous. Acetaminophen, also known as APAP, Panadol, Paracetamol, and Tylenol is a potent hepatotoxic drug due to its metabolites. Kava likely does not interact with these drugs other than APAP. There is research leaning to indicate that the combination of APAP and kava should be avoided on the issue of glutathione degradation. IF kava does indeed reduce glutathione levels, mixing it with APAP would increase its toxicity.
2. Dosing
3. Paragraph 1 “By Mouth: For anxiety: 50-100 mg of a specific kava extract (WS 1490, Dr. Willmar Schwabe Pharmaceuticals), taken three times daily for up to 25 weeks, has been used. Also, 400 mg of another specific kava extract (LI 150, Lichtwer Pharma) taken daily for 8 weeks has been used. Five kava tablets each containing 50 mg of kavalactones have been taken in three divided doses daily for one week. One to two kava extract tablets has been taken twice daily for 6 weeks. Calcium supplements plus 100-200 mg of kava taken daily for 3 months have also been used.”
4. This really doesn’t tell us anything to go by for our own personal dosing. In truth, there is no recommended dosage for powdered kava. These dosage recommendations come from several studies as well as the German Commission E. I take it that these numbers indicate the minimum amount of kavalactones it requires to see any effect without seeing intoxication. Seeing that many of us aim for intoxication these numbers are simply meaningless.

Citations Removed for length. See kavaforums post for full citations.
Kavaforums Discussion Thread: https://kavaforums.com/forum/threads/webmds-article-on-kava.19070/

Saw that someone was requesting some useful trials to know for IM and thought I'd post this little summary I made a while back. Didn't post it because I didn't think it was fully ready and I was hoping to make a video on it but it seems like now would be a good timing. Hopefully it's useful to some people - obviously WikiJournalClub is super clutch when it comes to this. Would be cool to see what other articles people thought were useful / important and maybe even different specialties could post important trials in their fields also which would be interesting!
These are some studies I think you probably should just know before you start intern year. ​ Highly recommend using WikiJournalClub.com to look up landmark trials and studies. ​ My Tier List (based on how often I needed to know certain trials): S Tier = AFFIRM, RACE II, ARDSNet, PROSEVA A Tier = ACCORD, NICE-SUGAR, ALLHAT, SPRINT, FAIR-HF, REDUCE B Tier = SELECT-D, EMPA-REG, LEADER C Tier = the rest of the articles below ​

Diabetes

Okay, you definitely need to know these trials. Maybe not so much the UKPDS and ADVANCE ones but definitely the principle that good glucose control decreases microvascular but not macrovascular complications. But ACCORD, EMPA-REG + CANVAS, LEADER + REWIND, and the ADA 2021 guidelines are huge! ​ ACCORD = targeting a goal A1c <6% increases mortality compared to goal A1c <8% EMPA-REG = SGLT2 inhibitors decrease CV events in diabetic patients (recommended for heart failure) LEADER = GLP-1 agonists decrease CV events in diabetic patients (recommended for CAD) UKPDS 33 and ADVANCE = intensive BG control in diabetes reduces microvascular complications (retinopathy, nephropathy, neuropathy) but NOT macrovascular complications (ischemic heart disease, peripheral vascular disease, cerebrovascular disease) ADA 2021 Guidelines = recommends goal A1c <7% in most adults, <8% in patients with history of severe hypoglycemia, limited life expectancy, multiple comorbidities, etc. NICE-SUGAR = goal BGs for inpatients (studied in ICU patients) is 140-180. Intensive control led to more deaths. RABBIT-2 = basal bolus insulin regimens are more effective than sliding scale insulin regimens ​

Hypertension

People talk about these trials a lot. You should definitely know the basics of them. Basically ACCORD-BP said one thing and SPRINT said another, so now we target a goal BP <130/80 which is kind of in between both lol. I just threw the PATHWAY one in there because it says why our first-line agent is spironolactone for resistant HTN but it's not as high-yield. ​ ALLHAT = established CCBs, ACEIs, and thiazides (chlorthalidone) as the first line antihypertensives ACCOMPLISH = ACEI + CCB reduces mortality better than ACEI + thiazide. Criticism is that they used HCTZ rather than chlorthalidone. PATHWAY-2 = why we add spironolactone for resistant HTN (defined as patients on ACEI/ARB + CCB + diuretic) ACCORD-BP = intensive SBP control <120 compared to <140 did not reduce adverse outcomes in pts WITH diabetes SPRINT = intensive SBP control <120 compared to <140 improved CV outcomes in pts WITHOUT diabetes 2017 ACC/AHA Guidelines = recommends treating to goal BP <130/80 based on the prior studies in ALL patients ​

Atrial Fibrillation

You freaking better know AFFIRM and RACE II like the back of your freaking hand!!! There's some other ones that are sort of whatever. BRIDGE tells us that when you hold warfarin prior to surgery, you don't need to give heparin in the interim to patients if their CHADSVASc scores are <2-3 . ARISTOTLE, RE-LY, ROCKET AF, ENGAGE AF-TIMI 48 basically all tell us that DOACs are as good if not better than warfarin. But damn, AFFIRM and RACE II are always going to guide your practice and EAST-AFNET might be a new game changer. ​ AFFIRM = rate control is equivalent to rhythm control in nonvalvular AF, but rhythm trends towards increased mortality RACE II = why our target heart rate for afib is <110 bpm rather than <80 bpm EAST-AFNET 4 = new study showing rhythm control actually might be better than rate control now . . . ! ​

Heart Failure

You really don't need to know the specifics . . . just know that the establishing of "guideline-directed medical therapy" is backed by a ton of research.
CONSENSUS, V-HeFT II, SOLVD = ACEIs are a first line medication for reducing mortality in HFrEF MERIT-HF, COPERNICUS, CIBIS-II = beta-blockers are a first line medication for reducing mortality in HFrEF RALES, EMPHASIS-HF, EPHESUS = aldosterone antagonists are indicated for HFrEF <35% **[A-HeFT](https://www.wikijournalclub.org/wiki/A-HeFT)** = isosorbide dinitrate + hydralazine improves survival in black patients with HFrEF. Per AHA 2013 guidelines, all black patients should be on nitrates/hydralazine for HFrEF if already on optimal medical therapy, and ALL patients should be considered for this if they can't tolerate ACEI/ARB therapy. Kind of a controversial study because race and genetic variations don't always correlate strongly. **PARADIGM-HF, PARAGON-HF** = ARNIs (sacubitril-valsartan) was better than ACEI in reducing mortality in HFrEF but not HFpEF. Per 2016 ACC heart failure guidelines, if patients are tolerating ACE-I or ARB, replacement with ARNI is recommended. **MADIT-II, SCD-HeFT** = the studies that showed ICD reduced all cause mortality in EF <30% (we do in EF <35%) **DANISH** = ICDs don't show a significant mortality benefit in NON-ischemic cardiomyopathy <35% but did reduce sudden cardiac death, decision to place ICD should be made on case-by-case basis **RAFT** = Cardiac resynchronization therapy (CRT-P or CRT-D) is indicated if LBBB, QRS >150, and EF <35% DAPA-HF = in patients with HFrEF with or WITHOUT T2DM, SGLT2 inhibitors decreased mortality! Important study to know because it's changing our current practice! FAIR-HF = in patients with HFrEF and iron deficiency, IV iron improves NYHA class, 6-minute walk distance, and QOL DOSE = why we use 2-2.5x home dose when patient comes with acute decompensated heart failure, also continuous vs intermittent loop diuretics is equivalent Val-HeFT, CHARM-Added = ARBs can be added to ACEI if aldosterone antagonist is not indicated or poorly tolerated (note this strategy does not have any benefit in diabetic nephropathy per the VA-NEPHRON D trial) CHARM-Preserved = ARBs in HFpEF may reduce hospitalizations but have no effect on mortality ​

Acute Respiratory Distress Syndrome

ARDSNet, PROSEVA, and ACURASYS are the ones to know here. ​ ARDSNet = low tidal volume ventilation (6 mL/kg) was superior to high tidal volume ventilation (12 mL/kg) Daily ICU Sedation Holidays and Awakening and Breathing Controlled Trial (ABC or "wake up and breathe" trial) = daily sedation holidays reduce days on ventilators, days in ICU, and days in hospital PROSEVA = in patients with severe ARDS (P:F <150), prone positioning reduces mortality. Proned patients may have been healthier however and there was a higher rate of unscheduled extubation, ET tube obstruction, and pressure ulcers (which are higher in proned patients) were not reported ACURASYS = paralysis for 48 hours in patients with early severe ARDS improved 90 day survival ROSE = paralysis did NOT show improved mortality . . . so we're not doing it as much as before FLORALI = high-flow nasal cannula was better than non-invasive ventilation (CPAP, BiPAP) in patients with acute hypoxemic respiratory failure ​

Acute Coronary Syndrome

​ This is a bit of a weak spot for me. I have to admit I don't know which ones are the highest yield at this current time. I'll keep updating. Work in progress! ​ COLCOT = interesting newer study showing colchicine may reduce the risk of CV events after MI! No guidelines yet but practice may change in the near future. PLATO = ticagrelor (Brilinta) is better than clopidogrel (Plavix) in ACS VA Cooperative Study = the landmark trial in 1983 which showed aspirin reduces mortality from acute MI or UA AVOID = supplemental oxygen for patients having a STEMI but who are not hypoxic may increase MI size and risk for recurrent MI . . . later trial DETO2X-AMI also supported these results ​

Sepsis / Shock

​ Dang, I didn't know about all these trials before but they all seem pretty high-yield. There are some pretty legit and interesting studies in this group! ​ Annane Trial, CORTICUS, HYPRESS, ADRENAL, APPROCHS = Annane in 2002 showed short-term mortality benefit with IV hydrocortisone and fludrocortisone in septic shock in patients with evidence of adrenal insufficiency. CORTICUS and HYPRESS showed faster reversal of shock but possible increased infection rates. 2018 ADRENAL again showed no difference in death at 90 days between hydrocortisone and placebo but there was faster time to reversal of shock, shorter time to discharge from ICU, time to extubation, and decreased number of blood transfusions. 2018 APPROCHS confirmed Annane Trial's findings of reduced mortality. Notably, the patients in Annane Trial and APPROCHS were more critically ill than in CORTICUS, HYPRESS, and ADRENAL which may account for some of these findings. Conclusion: there may be a benefit to steroids in shock, but even if so it is modest at best. Still worth trying though Hydrocortisone, Vitamin C, and Thiamine in Severe Sepsis and Septic Shock = 2017 study showing 32% decrease in mortality (P < 0.001) with Vitamin C administration, thought to be due to synergistically reducing inflammation along with hydrocortisone. But this was a very low-quality study and with only 97 patients VITAMINS = 2020 study showing that IV vitamin C, thiamine, and hydrocortisone did not lead to faster resolution of septic shock compared to hydrocortisone alone Rivers Trial, ARISE, ProCESS, ProMISe = early goal-directed therapy was introduced by Rivers Trial in 2001, suggesting all patients should get an arterial line and central line with continuous ScvO2 monitoring. The 2014 ARISE, 2014 ProCESS, and 2015 ProMISe trials showed that EGDT is not superior to usual care so now we don't do all these lines for no reason. BAM MIC DROP. HEAT = tylenol doesn't improve mortality in patients with probable infection and fevers, but shortens ICU length of stay in survivors and delays death in non-survivors SEPSISPAM = goal MAP 80-85 didn't reduce all-cause mortality compared to MAP 65-70, was associated with less renal dysfunction but higher rates of afib ​Sepsis-3 = updated guidelines in 2016. Sepsis was first described in 1992 with Sepsis-1, and introduced the SIRS criteria and sepsis steps (sepsis, severe sepsis, septic shock, multi-organ dysfunction syndrome). Sepsis-3 removed SIRS and replaced it with SOFA and q-SOFA. The term severe sepsis was also removed as it was considered redundant. SOAP II = norepinephrine is the first-line antiarrhythmic, dopamine is similar but has higher risk of arrhythmias VASST = addition of low-dose vasopressin did not reduce mortality when compared to norepinephrine alone. Main use is as a catecholamine-sparing agent. Also the power of the study was a little limited IDEAL-ICU = no difference between early-initiation vs delayed-initiation RRT strategies in patients with septic shock and AKI without urgent need for dialysis ATHOS-3 = angiotensin II is a really good vasopressor in patients with severe vasodilatory shock on multiple pressors CRISTAL = colloids did not give mortality benefit over crystalloids in ICU patients with hypovolemic shock . . . HOWEVER there was a mortality benefit at 90 days which should be further explored. This was a follow-up to the 2004 SAFE study which showed no benefit of albumin over normal saline BICAR-ICU = giving bicarbonate for severe metabolic acidosis didn't improve mortality except in patients with AKI PRORATA = HIGH-YIELD!! Procalcitonin-guided antibiotic strategy resulted in fewer days of antibiotics without an >10% increase in mortality. Don't use procalcitonin to guide when to START antibiotics. But you can use it and trend it to guide when to STOP antibiotics! Criticism is that the trial used a >10% increase in mortality threshold rather than >5%. SEDCOM = no difference between dexmedtomidine and midazolam in achieving sedation, but dexmedetomidine resulted in less time in ventilator, delirium, tachycardia, and hypertension at the cost of bradycardia SMART = among medical and surgical ICU patients, LR or plasma-lyte reduce rate of death or RRT compared to NS Yang-Tobin Study = the study that came up with the rapid shallow breathing index, in 1991! Maybe before you were born! ​

Hyperlipidemia

​ There are a lot of studies that showed why statins are so good for reducing cardiovascular mortality in patients with HLD. Here's the main landmark study. There's plenty more to look into if you want to see why we do high-intensity statins, and why we are now starting to add ezetimibe and PCSK9 inhibitors! ​ 4S = Scandinavian Simvastatin Survival Study, LANDMARK study showing statins reduce all-cause mortality in patients with hyperlipidemia and prior MI or angina ​

Alcoholic Hepatitis

Idk I've just heard of the STOPAH trial a few times so it's probably a good one to know. ​ STOPAH = newest study which showed neither prednisolone or pentoxifylline showed mortality benefit in alcoholic hepatitis, though there was a trend towards improved mortality with prednisolone (P = 0.06) ​Pentoxifylline in Severe Alcoholic Hepatitis = 2000 study suggesting pentoxifylline may improve survival Prednisolone in Severe Alcoholic Hepatitis = 1992 study suggesting prednisolone improves survival ​

Cirrhosis

There's a couple situations where giving albumin to cirrhotics is indicated - SBP or large volume paracentesis.
Albumin for SBP = IV albumin reduces renal impairment in cirrhotic patients with SBP, leading to AASLD 2012 guideline stating we should give 1.5 g albumin per kg body weight within 6 hours of presentation and 1g/kg on day 3 ​

Anemia

Just transfuse everyone to goal Hgb > 7. Unless they have CAD. Then you can do Hgb > 8. Now you know the names of the trials that figured this out.
TRICC = in ICU patients transfusion to goal Hgb > 7 had better survival compared to goal Hgb > 10 Transfusion Strategies for Acute Upper GI Bleeding = goal Hgb > 7 had reduced mortality compared to goal Hgb > 10 TRISS = in patients with septic shock, transfusion to goal Hgb > 7 had similar mortality compared to goal Hgb > 9. This article led to rewriting of Surviving Sepsis Guidelines which previously had suggested transfusing to goal Hgb > 10! ​

COPD

Yeah, know this one.
REDUCE = 5 days of steroids for COPD exacerbation is non-inferior to a 14-day course ​ Well, I guess you could know some other ones too because they are the reason we do LAMA -> LABA -> ICS, why we say oxygen gives mortality benefit, etc. but I don't have time to write them right now ​

VTE in Cancer

​ If a patient with cancer gets a VTE, you can send them home on LMWH or rivaroxaban. Less bleeding with LMWH, decreased recurrent VTE with rivaroxaban. ​ SELECT-D = rivaroxaban can be used to decrease risk of recurrent VTE in cancer patients but at the expense of increased rates of bleeding (particularly in patients with GI malignancies . . . so send them home with LMWH if GI malignancy but if they are low risk for bleeding you can consider rivaroxaban). Was actually better than LMWH at decreasing rates of VTE though! CLOT = 2003 trial which showed LMWH was as effective as warfarin for VTE prevention in cancer patients ​

Appendicitis

Not sure why I put this one here because it's more surgery . . . but it's an interesting one to know! ​ APPAC = medical management with antibiotics may be better than surgical management in patients with uncomplicated appendicitis

I injured my big toe right foot at 9:30 pm mst.i accidentally kicked a hard surface. It was dark, It hurt and bled a lot. F 65, 5’5”, 150 lbs, non smoker, non drinker, mitral valve replaced 8 yrs ago. Ejection fraction now 60%. On warfarin for a fib, and metroprol (sp), on trazadone to sleep 100 mg at night.7.5 warfarin, once a week and 5 the other six., Ativan .5 bid pen, torsemide,aldactone, cymbalta, bentyl, oxycodone 5 mg with Tylenol. Bid prn, stage 4 renal failure, congestive heart failure, mild copd ibs, migraine, spinal stenosis. Tbi in dec 2000. My iNR was 2.1, create was 2.2, bun 50, hct 36, hb12.2, calcium 1.16 I went to urgent care 12 hrs l8tr. Wrapped it loosely to contain bleeding. As of now the tip is still oozing fluid. They did not drill a hole. They squirted some soapy water and attached steri strips to keep nail down. It bleeds onto my sandle, eww. odd pain along arch that runs under the toe. Main question is is my toenail doomed? I have a pic, not allowed to post pic. shrug thanking you in advance. I hope I met your standards this time.

I saw a meme about Pradaxa, Eliquis, and Xarelto essentially ending warfarins career and it got me thinking, what drugs would you put in the pharmacy hall of fame? The loose criteria being what drug lived the longest being one of the only drugs in its class and when it went generic, sort of kept its its exclusivity ability to still be brand only/patient requested brand only? Coumadin certainly has a case, I’d say viagra would be the “Tom Brady”, Tylenol, Adderall. The brand recognition that transcends the normal brand gone generic cycle.

For an entire year, I've been trying to find and keep a job as a Pharmacy Assistant. In each of the places where I worked, I did my tasks far slower than everyone else. I never lasted very long in any of these pharmacies. I was so slow because I was terrified of making a mistake. That's all it takes. Just one misspelled number can lead to someone taking double the dose of a dangerous drug like warfarin or Tylenol 3.
​
I don't understand how everyone else is so unfazed by this. Compared to me, the other assistants work so fast. They never seem worried about making a mistake. Damn it, I don't know what to do. I performed very poorly at all the places I've worked. I tried so hard to push back my fear. I pushed myself so hard, I meditated, I ate healthy, I excersized, I talked to my employment counsellor about my issues. Nothing worked. Now all I'm left with is a handful of negative references for interviews to shake their heads at, and a family who thinks I'm just a lazy freeloader.
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There is no way I can go back to being a Pharmacy Assistant. I can't deal with the panic I feel whenever I get stuck putting together a medication blister pack. I doubt anyone would be willing to hire me with my abysmal work history.
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Damn it, I'm either just completely devoid of determination and willpower, or I'm scared of doing things wrong and having to deal with the consequences for an inhumane length of time.
​
Does anyone have any suggestions? Are there any healthcare jobs that don't involve checking things to prevent harm? Will my poor job history prevent me from getting any job above mopping floors at mcdonald's? How can I prove to my family that I'm not just a loser?

26 F here. Had my first blood clot in my left leg roughly one week ago. My mother and my grandmother both had issues with hormonal birth control, so I'm assumimg that's what got me. I also vape (very low nic, but still) which I'm sure didn't help much. Currently trying to abstain from any and all nicotine as much as possible so I can wean myself off. The withdrawals on top of the pain have not been fun.
The pain is the absolute worst, though. This is my 5th day since visiting the ER and I've never felt anything this bad in my life. I was not prescribed nor given any form of painkiller; only Warfarin to stop the clotting. The first 2 days, I resorted to using a medical grade cannabis pen to dull the pain, but being kind of broke atm it was just a temporary "fix" and I used it up super quickly. I can't exactly afford to keep that up when a shitty disposable pen is $55 at the local dispensary. Not to mention any potential interactions with Warfarin.
Is there anything else I can take to help the pain? I've tried Tylenol, which is apparently "safe," but the results weren't great. I asked my family doctor this very question but haven't received a response yet.
Also, is it "normal" to have severe complications when standing/walking for a bit? I've found I can generally handle the pain until I have to go to the bathroom or something...But the second I stand up, even with crutches, the pain is just unbearable. I haven't been able to get into the bathtub without assistance. Getting up the courage to hop to the toilet on one leg is a whole ordeal.
Just please, for the love of all this is good, tell me this gets better...Because after only a week, I'm starting to lose it.

How long does Modafinil last? I found this in an article about Modafinil half life but just want to verify the legitimacy of the claim. I have a lot of experience with Modafinil and I've personally found that some brands last longer than others, but I'm not sure if it's placebo or what.
​

How Long does Modafinil Last?

Measuring how long modafinil lasts means looking at a few different metrics.
We need to know how long it takes for modafinil to start producing effects when it reaches its peak, and how long it takes for enough of the compound to be eliminated from the bloodstream so that it no longer produces any of its effects.
​
Step 1. Modafinil Absorption
Roughly 40–65% of the modafinil you take is absorbed into the bloodstream [1].
This can vary depending on the health of your gastrointestinal tract.
It’s very common for people to have chronic inflammatory states in the gastrointestinal tract, which can reduce the amount of modafinil that’s absorbed into the bloodstream.
People suffering from even mild inflammation, but especially from more severe inflammatory states like Celiac disease, IBD, or IBS may have a significantly lower absorption rate through the intestinal tract.
In most people, modafinil is absorbed relatively quickly over the course of 45 minutes. If taken with food, or you have a slow digestive function, this can take as long as 2 hours.
​
2. The Onset of Effects
Once the drug is absorbed through the digestive tract, 45-60 minutes later, it quickly reaches peak concentrations.
Around the 4–6 hour mark, you will feel the strongest effects of the modafinil. This usually lasts another two hours.
​
3. The Half-Life of Modafinil
The half-life of modafinil is about 12 to 15 hours.
A lot of websites discuss half-life, but don’t actually tell you what this means or why it’s important.
Drug half-life is a measurement of the time it takes for exactly half the drug to be eliminated from the bloodstream.
This means the compound was either destroyed in the bloodstream or eliminated from the body through the kidneys or digestive tract, or both.
Half-life doesn’t work like you probably think it does.
If the half-life says 10 hours, it doesn’t mean the drug is completely gone in 20 hours. Instead, the dose is cut in half every 10 hours.
For example: If you take 500 mg of a drug and the half-life is 10 hours, it means that there will be 250 mg left at the 10-hour mark—makes sense right?— 10 hours later, there will be 125 mg left, 10 more hours and there will be 62.5 mg left…
You get the picture.
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Modafinil Has a Long Half-Life
Modafinil has a very long half-life compared to other drugs, such as Tylenol with a half-life of 2–3 hours, and caffeine with a half-life of 5–6 hours.
Some drugs, like Warfarin (a blood thinning medication), has a much longer half-life, which can range from 20–60 hours.
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The Importance of Half-Life
We use information about the half-life of drugs to determine the dose of a medication, and how often it should be taken.
Tylenol, for example, needs to be taken every 3 or 4 hours for best results, while modafinil should only be taken once per day because its effects last much longer.
​
Adding Up Modafinil’s Half-Life to Figure Out How Long it Lasts:
A normal dose of Modafinil is about 200 mg.
We only absorb about 40–65% of the modafinil into our bloodstream.
This means that we have about 80–130 mg in our bloodstream once it’s all absorbed.
Let’s go in the middle of this range and say that we absorb about 100 mg modafinil from the average 200 mg dose.
Since we know the half-life of modafinil is about 14 hours, this means that at the 14-hour mark we’ll have about 50 mg left in our system. We would still be feeling the effects at this dose, but they would be much weaker.
After 28 hours, we would then have 25 mg modafinil in our system, which we would likely no longer be feeling the effects of.
After 42 hours, we would still have about 12 mg of modafinil coursing around our bloodstream.
This would continue until there was nothing left. After 56 hours, 6 mg, 70 hours, 3 mg, 84 hours, 1.5 mg, 98 hours, less than 1 mg.
The takeaway from this is that with a 200 mg dose, based on the 14-hour half-life and 40-65% absorption rate of modafinil, the drug will produce effects for about 16-22 hours.
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Piecing It All Together

1. Onset: 45 minutes to 2 hours
2. Time Until Peak Effects: 1–2 hours
3. Peak Effects: 2–4 Hours
4. Tapering Off Effects: 12–16 hours.
5. Total Duration Of Effects: 16–22 hours.

How Long Does Modafinil Stay in Your System?

Although the effects of modafinil usually disappear after about 16–22 hours, it can remain in the body for up to 4 days.
As mentioned, the body will still have about 1.5mg in the bloodstream 84 hours after taking it.
That’s 3 days later!

Hi everyone. This summer I developed multiple clots in my brain leading to Cerebral Venus Sinus Thrombosis (CVST). From what I understand, this is a rarer form of thrombosis, ~5 in 1 million people affected per year (why didn't I get those odds with the lottery?!) and there isn't much information online about it so I wanted to share my story. The large detail is partly because I have tried to not think about what happened to me. No one probably cares much about the details, but writing it is therapeutic for me.
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tl;dr

• I had multiple blood clots in my brain in June causing CVST
  • From what it sounded like to me, basically, every vein in my brain had a clot.
• I spent a total of 2 weeks in the hospital, 2 separate visits.
  • The catalyst for the second stay was double vision & a subdural hematoma.
• I'm on warfarin for recovery and should be able to go off blood thinners when the clots are gone.
• I experienced double vision that went away about 2.25 months after the stroke.
• Reason for clots - Still TBD (likely birth control)
  • I have no genetic factors for clotting.
  • I was on hormonal birth control which is believed to be the reason, however, I'll be going to a hematologist later for further testing.
• My last MRI (3 months post CVST) showed significant improvement. I only have a trace amount of one clot left.
• I have more follow-ups in December. Hopefully, I will be at a full recovery.

​
My takeaway from all of this: Enjoy life and be present in each moment! I used to work so much and would focus on that over everything else. Work will never be as important as family and friends. From now on, I will work to live, not live to work. I'd rather use that time connecting with loved ones.
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The Incident
For about 1.5-2 weeks in June I started having headaches every day. They went away with tylenol so I didn't think much of it until I had a splitting headache that caused me to take a day off work. Even then I still didn't think much of that headache. I figured I was just starting to get migraines even though I had never been diagnosed with migraines before. The next day everything escalated. In the morning, I was nauseated. By the afternoon, I was vomiting and couldn't even keep water down. Should I have gone to the doctor? Probably and my husband was urging me to go, but I'm stubborn and at this point, I thought I just had food poisoning. By the evening, something was obviously not right. I was confused about where the rooms were in the house. At this point, my husband made the executive decision that we were going to the ER. They ran a ton of tests on me and found the blood clots in my CT scan. I was rushed to a hospital in Seattle (we live in a suburb) as that's where all the neurologists work. My poor husband was not able to be with me through any of this. I'm not sure if it was specific to Covid restrictions or normal procedure. For me, I was pretty much out of it through this whole time. I don't remember anything other than the Covid test and them telling me I had clots in my brain. However, on my husband's side, he was anxiously waiting for a call to find out what was wrong with me and had absolutely no idea about what was going on until they rushed me to Seattle.
Hospital Stays
ICU Round 1- After being rushed to the hospital, I was in the ICU for a few days. I don't remember much of this either. I really thought the whole thing was a dream and not reality. I remember my husband being there, my parents on Facetime saying hi, and our friend who is a nurse at the hospital stopping by to check on me. I was in here for about 3 days before I was moved to a regular room.
Regular Room - My stay in a regular room started off with a bang. Apparently, I have tiny veins and getting an IV was a nightmare. However, after that was done, I was more awake and able to actually talk with my husband. I started to eat, mainly graham crackers & bananas. Overall, it was fairly pleasant, at least as pleasant as it can be when you're in the hospital. The hospital beds get uncomfortable after a while and my headaches would flair up before I could get tylenol again, but I was alive and getting better! Luckily, my husband works for a gracious company and he was able to take time off to be with me in the hospital each day. After about 1 week in the hospital, I went home with a blood thinner prescription. I was super happy to be going home!
ER & ICU Round 2 - After a couple of days of being home, I started experiencing double vision. I called the stroke clinic and had to go back to the ER. I spent a whole day in the ER, got a couple of CT scans and they found a subdural hematoma. I was back in the ICU and getting IVs this time around was even worse. I had a couple of CT scans to check on the hematoma. Luckily, I was able to only spend one night and one day in the ICU before I was moved to a regular room.
Regular Room - Once I moved to the regular room, I felt a lot more comfortable. I got an eye patch, so that helped with my double vision. This time around, I physically felt better, which was good. I spent time listening to podcasts and audiobooks. Awaiting the dreaded blood draws every few hours. The food at this hospital was pretty good so I enjoyed meals as I had an appetite again. This time around, I was planned to go on warfarin. For those that don't know, warfarin takes a while to build up in your system in order to hit a therapeutic range. Basically, this stay was waiting to hit that range. I spent a total of another week in the hospital before I got to go home again. When I went home this time, I was actually feeling better physically and really looked forward to sleeping in my own bed.
​
Recovery
Physical (Independence) - I needed assistance walking around the house for a few weeks after the hospital. About 2-3 weeks after I got home, I was able to move around by myself.
Physical (Fatigue) - The first week at home, I slept almost the whole time. After that, I started to stay awake longer during the day, but would still take naps. I think it took about 1 month to feel like I less fatigued.
Physical (Headaches) - I took tylenol round the clock when I first got home. After about a month, I found that I only needed it when I woke up in the morning and when it was close to bedtime. After about 1.5 months, I didn't rely on tylenol anymore and only need to take it on occasion.
Double Vision - This was the most frustrating aspect of my recovery! I only had double vision when both eyes were open so I used eye patches to mitigate this issue. I would switch the eye patch between my left and right eye every 30 min-1 hour. Additionally, I tried to only wear the eye patch as needed. After ~2 months, my vision started to recover. I now have no double vision issues. I went to a neuro-ophthalmologist a month ago to confirm. I had some swelling of the optic nerve, but that was due to clots. I'm on medicine to improve that and should hopefully hear good news at my follow up appointment.
Mental - I don't have any issues with memory or thought process thankfully. However, the emotional aspect can be hard. I still don't think I've really dealt with the fact that I almost died. It's a scary thing to think about and not something I want to dwell on. I do have some stressors around headaches now. I'm also worried about going off blood thinners and the what-ifs. I haven't sought therapy through this as I have felt good overall. However, I will start to look into that if I start to feel more stressed or anxious.
Overall, my recovery experience has been a positive one so far. I feel very lucky and thankful to have improved so quickly. I'm not in the clear just yet, but getting closer every day!

Surgical intern here. I feel like I call my pharmacists an ungodly amount of times a day, and wanted to know if maybe I was missing some basic knowledge (or basic ways to get to that knowledge). My hospital has Micromedex for free, so I'll always try to give it a cursory glance or Google quickly before I call about a drug. (E.g. I no longer call about the usual dose for X indication unless it's not on Micromedex.)
My main clinical questions:

• how to convert from IV to PO and vice versa (Google can help with metoprolol and that's about it...)
• which drugs are oral suspension vs. oral liquid and how the dose changes when I order different formulations (e.g. recently learned oral liquid Tylenol is like 950 mg while tablet is 1000 mg)
• if a drug that we don't have on formulary is similar to any that we do have (I can tell if they're in the same family but other than that I'm SOL...)
• pediatric dosing (at what point/weight are they adult-sized and how do I find the max dose for something? e.g. ceftriaxone and Flagyl weight based have max caps of 2g and 1.5g)
• warfarin dosing please send help
• vancomycin dosing and troughs please send help pleaseeeee

My non-clinical questions:

• how do I find out if something's covered by my patient's insurance? I've always been told to prescribe and send to our hospital pharmacy, but occasionally I hear back and get told something isn't covered and then I literally do not know what to do with that info besides panic-call pharmacy for help
• how do I figure out the proper way of writing a prescription amount? e.g. if someone's taking some 5 mg/5mL formulation but I need to give that to them QID for 1 months, do I write a "1 unit" or is "100 mL" reasonable? How big can those bottles get? I usually get calls from pharmacy to correct my order but I'd like to do it properly on the first try - I just don't know how.
• is there any other resource besides Micromedex? That's what I've seen my clinical pharmacists use at least

My hospital doesn't have a lot of the standard doses (or they'll have weird doses that we don't use), so a lot of times I have to dig and figure it out the proper dose. A great big thank you to pharmacists that catch my errors and fix them! I just want to be better and make less work for everyone else lol. Thanks!
EDIT: Wow, all the responses have been so wholesome and helpful!! It's exactly what I was looking for, and my phone is now several apps fuller. Thanks for taking the time to answer a dumb intern's questions!!

Hey all,
Currently laying on my couch in fairly bad pain. Long story short, I had an infected cyst on my tailbone drained a few hours ago and boy does it hurt.
I was prescribed tramadol to help with the pain, but due to an apparent mixup or miscommunication or something with CVS pharmacy in Target, I left without my med because it's on "national backorder." I had already been waiting around for about a half hour to get it and the lidocaine from the procedure was wearing off, and my doctor was unavailable when I called the clinic to ask for a different medication. Not wanting to limp around anymore, I left a message and drove home.
I took a dose of Tylenol about an hour and a half ago, (1000mg) but it's barely reduced the pain at all; which I figured would be the case since it's been bothering me since last week and tylenol has been less and less effective, and why the doctor prescribed tramadol. I figured once the doctor called me back, I'd have them send the rx to a closer pharmacy (CVS is a half hour round trip) and pick it up there.
Sooo now, I got a text from CVS saying my rx has been filled and is ready to pick up. Confusing, cause they told me they didn't have any. But ok. I haven't heard back from my doctor yet. In looking up the possible issues with combining Tramadol and Warfarin, I saw that it can cause respiratory depression--basically difficulty breathing. I've already been experiencing that a little more than usual on the last week and it's causing me a lot anxiety... which of course makes it more difficult to breathe.
So now I'm not even sure I want to get the Tramadol if it'll cause breathing issues. I trust my doctor wouldn't prescribe anything that I couldn't have safely when taken appropriately, but I don't want to add more anxiety and discomfort to what I already have. But at the same time, tylenol isn't doing much to help and I'm supposed to take a soak in the bath later to help the wound drain completely and heal, and I can't imagine being able to sit without intense pain. I don't wanna take more tylenol just because I'm not sure what my INR is at currently and I don't want to make that drop or spike.
In summary.... has anyone taken Tramadol while on Warfarin, and if so, how were the side effects?
If you made it this far, thanks for reading my rant, I'm frustrated and in pain and cranky. Lol

I've seen plenty of articles and talks about how Vascepa is simply just another Lipitor drug that helps reduce triglyceride levels. I'm not an expert in finance with Biotechs but reading their clinical trials shows that Vascepa isn't related to Lipitor because Lipitor is a statin therapy that has already been standardized in the medical industry. Vascepa is recommended to be used with statin therapy and not replace it because Vascepa itself isn't a statin (HMG CoA reductase inhibitor for biochem people) but is in the same drug class as blood thinners (Platelet Aggregation Inhibitors) like Tylenol (Section 8.2 in https://pubchem.ncbi.nlm.nih.gov/compound/Icosapent-ethyl#section=Pharmacology-and-Biochemistry). That's why the biggest side effect is internal bleeding (10-12%) because AMRN said "The incidence of bleeding was greater in patients receiving concomitant antithrombotic medications, such as aspirin, clopidogrel or warfarin". This is a huge disclaimer that most likely skewed their results because the patients are essentially doubling up on their blood thinners which will increase internal bleeding anyways regardless of the specific drug at hand.
With this information I truely believe AMRN was shorted this week (possibly in the future as well) but mid to long term I believe AMRNs valuation is worth immensely more than the $7.5b it currently has after increasing their revenue for the quarter and year.
Take this as Chemistry DD because big money will manipulate the stock the best they can to profit off retail investors.

I (27F) am on Warfarin for life (blood clotting disorder), so I can’t take NSAIDs. I’ve torn my rotator cuff (ouch!), and Tylenol (acetaminophen) isn’t helping. I even gave up and took some Advil (Ibuprofen), despite it being contraindicated with blood thinners, and thats not helping. Anyone know of a pain killer that’s good for pain like this, that’s ok to take with blood thinners?