Love Ozil and Messi hate bustards . clinical pharmacist. father .Editor @MyDoctors Facebook page. @FuckedUpFacts.husband .dreamer. African
Michigan, USA
Joined November 2011
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Urinalysis – The Liquid Kidney Biopsy indianjnephrol.org/urinalysi…
Suu🇦🇷🇺🇬 retweeted
#ECG From Scratch #61: Acute Pericarditis
Can you distinguish acute pericarditis from STEMI on the ECG?
In this episode, we cover:
🔲 Diffuse ST-segment elevation
🔲 PR-segment depression and reciprocal changes in aVR
🔲 Pericarditis vs. acute MI
🔲 Evolving ECG patterns and T-wave inversion
🔲 Diagnostic criteria and common pitfalls
⚠️ ECG findings must always be interpreted alongside the clinical presentation. Never dismiss possible ACS based on morphology alone.
Suu🇦🇷🇺🇬 retweeted
ALPRAZOLAM: Rule of 3
1. Hits fast within 30 mins. Used for sudden severe anxiety and extreme stress.
2. Highest addiction potential. Taking daily over 2 weeks leads to dependence.
3. NEVER mix with alcohol. Causes coma, sudden death.
CLONAZEPAM: Rule of 3
Suu🇦🇷🇺🇬 retweeted
Eplerenone vs. spironolactone in heart failure: long-term cardiorenal and mortality outcomes in a registry-based cohort
Compared with spironolactone, eplerenone was associated with lower all-cause mortality and lower risks of kidney function decline and mild hyperkalaemia.
academic.oup.com/ehjcvp/adva…
Suu🇦🇷🇺🇬 retweeted
🫀 CardioNugget™: AF + HFrEF — your AAD choices shrink FAST
Patient has AF + HFrEF (LVEF ≤40%) and needs long-term rhythm control?
✅ Amiodarone
✅ Dofetilide
🚫 Avoid flecainide/propafenone with significant structural heart disease or prior MI/scar.
🚫 Dronedarone is contraindicated in NYHA III/IV HF or recent decompensated HF.
Board shortcut:
❤️ Weak LV → think AMIO or DOFETILIDE
#CardioNugget #Cardiology #AFib #MedEd #CardioTwitter
Suu🇦🇷🇺🇬 retweeted
🔥 🩺 The US @CDCgov extends malaria Treatment with Artemether-Lumefantrine from 3 to 5 days!
Treatment of Uncomplicated Malaria | Malaria | CDC share.google/Fk8JoyHmGtnOULv…
Suu🇦🇷🇺🇬 retweeted
🔥 A multidisplinary team performs the first Radical nephro_ureterectomy, & radical cystoprostatectomy in Uganda!
🔥 We now have to manage that patient without a single kidney or bladder for the rest of his life.
@NakaseroHosp @PeaceBagasha #BadruSekitoleko @Internist_02
Suu🇦🇷🇺🇬 retweeted
A glimpse into the new curriculum: Modern Surgery from Day 1.
As the world moves towards minimally invasive surgery, our new generation of surgeons must be well equipped to meet the evolving demands of healthcare.
The future of Surgery starts now. 🚀
@mbiineron @Makerere
Suu🇦🇷🇺🇬 retweeted
AF + ACS: How should oral anticoagulation be managed?
When a patient with atrial fibrillation (AF) and an indication for long-term oral anticoagulation presents with acute coronary syndrome (ACS), treatment should balance two competing risks: stroke/systemic embolism and coronary ischemic events versus bleeding.
The contemporary default strategy is:
1. Short-term triple antithrombotic therapy
OAC + aspirin + a P2Y12 inhibitor, preferably clopidogrel, for the initial period after ACS/PCI. In the ESC strategy, triple therapy is generally limited to up to 1 week.
2. Dual antithrombotic therapy
Continue a DOAC + single antiplatelet agent, preferably clopidogrel, for up to 12 months.
3. Long-term therapy
After the combination-therapy period, OAC monotherapy is generally recommended when clinically appropriate.
DOACs are preferred over VKAs in eligible patients. Use the recommended stroke-prevention dose, unless the patient meets specific criteria for dose reduction.
The duration should always be individualized. In patients with high ischemic or stent-thrombosis risk and acceptable bleeding risk, triple therapy may be extended, generally up to 1 month. In patients with a high bleeding risk, antiplatelet therapy may be discontinued earlier.
Key principle: Keep triple therapy as short as possible, then continue OAC with a single antiplatelet agent before transitioning to OAC alone.
References
Collet JP, et al. 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. Eur Heart J. 2021;42:1289–1367. Section 5.2.3.
Rao SV, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. Circulation. 2025.
Suu🇦🇷🇺🇬 retweeted
Topical quinolone drops are the best-supported first-line choice for uncomplicated tubotympanic CSOM. Where they are inaccessible, boric acid or povidone-iodine are reasonable, evidence-consistent alternatives — not a compromise in outcome, just a lower evidence-certainty comparison.
Suu🇦🇷🇺🇬 retweeted
The reason Dr. Chris Baryomunsi, Dr. Jane Ruth Aceng and other senior doctors fighting medical interns yet Hon. Joel Ssenyoni a non medic is fighting for medical interns is simple.
I have spent most of my adult life around doctors but they're the worst people who front "EGO" in every discussion.
That's why you hear most doctors get furious when a patient questions them. The whole medical life, the ties, the books and titles shapes doctors to approach most situations with ego even sometimes at the expense of lives and it takes a lot of practice for a doctor to redeem his soul and see things with clarity.
Trust me, Dr. Chris Baryomunsi knows what he is doing is wrong, Dr. Jane Ruth Aceng did know she was wrong but to them this is a fight between intern doctors and their ego. These two doctors when they were interns did strike for the very issues interns are fighting for, so they know what they're doing but I can confidently tell you that they won't publicly say that they're wrong.
All senior doctors were paid during medical internship. I was paid, Dr. Chris Baryomunsi was paid, Dr. Omona was paid, Dr. Kiza Besigye was paid... Everyone you see Dr. And did internship in Uganda was paid for a reason and it is the same reason all countries do pay.
I don't blame the rest of Ugandans to fail to see this but fellow doctors well know all countries pay medical interns. All of them.
Kenya pays medical interns, and Dr. Chris Baryomunsi knows it.
Tanzania pays medical interns, and Dr. Chris Baryomunsi knows it.
Rwanda pays medical interns, and Dr. Chris Baryomunsi knows it.
Ghana pays medical interns/house officers, and Dr. Chris Baryomunsi knows it.
South Africa pays medical interns, and Dr. Chris Baryomunsi knows it.
Botswana pays medical interns, and Dr. Chris Baryomunsi knows it.
Namibia pays medical interns, and Dr. Chris Baryomunsi knows it.
Zambia pays medical interns, and Dr. Chris Baryomunsi knows it.
Zimbabwe pays medical interns/ junior doctors, and Dr. Chris Baryomunsi knows it.
The UK pays foundation doctors, and Dr. Chris Baryomunsi knows it.
Ireland pays intern doctors, and Dr. Chris Baryomunsi knows it.
Australia pays intern doctors, and Dr. Chris Baryomunsi knows it.
New Zealand pays first-year doctors/house officers, and Dr. Chris Baryomunsi knows it.
The United States pays resident physicians, and Dr. Chris Baryomunsi knows it.
Canada pays resident physicians, and Dr. Chris Baryomunsi knows it.
This list goes on....
I'm sure, the ego of doctors still will affect and blind the decision in this yet it's going to affect the whole medical training.
Suu🇦🇷🇺🇬 retweeted
Syncope with ST Elevation and T-wave inversion
drsmithsecgblog.com/syncope-…
@PMcardioApp
Suu🇦🇷🇺🇬 retweeted
I often explain this sign to my patients with allergic rhinitis. Many don't even know since they have had it for years and they dont know what allergic rhinitis is.
An allergic shiner is a dark discoloration below the eye that is associated with allergic rhinitis and is often seen in conjunction with bilateral Dennie–Morgan folds. These shiners are caused by venous congestion within the infraorbital groove, particularly from the nose. The characteristic infraorbital discoloration related to allergic shiners is due to a backup in the venous network supplying the mucous membranes of the paranasal and nasal cavities draining primarily via the branches of the sphenopalatine veins passing backward to the pterygoid plexus.[1] While a classic finding in pediatric patients with allergic rhinitis, these particular shiners will persist into adulthood if their allergies are not successfully addressed. The phenomenon was first documented in 1930, with the phrase being coined in 1954.[2][3]
Suu🇦🇷🇺🇬 retweeted
I'm breaking down this LFTs report like a pro clinician for my juniors today. A lot of you have been asking for a practical, real world way to read these. I promise you: if you read this thread to the end, you’ll never struggle with interpreting liver function tests again.
First of all remember this advice: never read LFTs randomly. Read in groups. Three groups. 🧵
Suu🇦🇷🇺🇬 retweeted
🩺 Excellent clinical pearl! The ABI is a quick, inexpensive, and highly useful bedside test for Peripheral Arterial Disease (PAD). Remember: ABI = ankle systolic pressure ÷ higher brachial systolic pressure. An ABI <0.90 suggests PAD, while <0.40 indicates severe limb ischemia requiring urgent vascular evaluation. Early diagnosis can save both limbs and lives. 💙🦵
This Post is from an account that no longer exists. Learn more
Suu🇦🇷🇺🇬 retweeted
Platelets >450,000 without an obvious cause:
Don’t just assume it’s reactive. Keep essential thrombocythemia in mind. Consider JAK2, CALR, and MPL mutation testing, especially if the elevation persists.
Hemoglobin >16 g/dL without a clear explanation:
Yes, smoking and dehydration can raise Hb, but don’t forget polycythemia vera. A JAK2 mutation can completely change the diagnosis.
Marked leukocytosis without an obvious infection:
A very high white cell count deserves a closer look. Review the peripheral smear and think about leukemia. If suspicious, involve hematology early.
Tear drop cells or nucleated RBCs on the peripheral smear:
These are never “normal.” Think of myelofibrosis or bone marrow infiltration until proven otherwise. Further work up, including a bone marrow biopsy, may be needed.
CBC tells you a story if you actually read it. Don’t just sign it.