Agon Turkaj

🫀💊Anti-arrhythmic drugs are an absolute struggle to learn Let’s simplify it a little based on mechanism of action You are going to remember the phrase “Some Block Potassium Channels” Some do… but how is that going to help you remember? Class 1 Drugs - “Some” = Sodium Blockers Class 2 Drugs - “Block” = Beta Blockers Class 3 Drugs - “Potassium” = Potassium Blockers Class 4 Drugs - “Channels” = Calcium Channel Blockers

Suggested algorithm for diuretic resistance. mdpi.com/2077-0383/14/9…

As the physician, what's the solution to this

🚨🦠 𝗦𝗲𝗽𝘀𝗶𝘀 𝟮𝟬𝟮𝟲 ⬇️⬇️⬇️⬇️ ⚠️ 𝘿𝙚𝙛𝙞𝙣𝙞𝙘𝙞𝙤́𝙣 🧬 Infección + respuesta desregulada → 𝙛𝙖𝙡𝙡𝙖 𝙤𝙧𝙜𝙖́𝙣𝙞𝙘𝙖 ⏱️ 𝙂𝙤𝙡𝙙𝙚𝙣 𝙃𝙤𝙪𝙧 🧪 Lactato 🩸 Hemocultivos 💊 ATB amplio 𝘼𝙎𝘼𝙋 💧 Fluidos si hipotensión / lactato ≥4 💧 𝙍𝙚𝙨𝙪𝙘𝙞𝙩𝙖𝙘𝙞𝙤́𝙣 💉 30 mL/kg cristaloides👀👀 ❌ No usar PVC aislada ✅ Usar dinámicos (PLR, VS) ⚠️ Evitar sobrecarga 💊 𝙑𝙖𝙨𝙤𝙥𝙧𝙚𝙨𝙤𝙧𝙚𝙨 🥇 Noradrenalina 🎯 PAM ≥65 mmHg ➕ Vasopresina/adrenalina si refractario 🧪 𝙇𝙖𝙘𝙩𝙖𝙩𝙤 🔁 Reevaluar cada 2–4 h 📉 ↓ lactato = mejor pronóstico 🔥 𝘾𝙡𝙖𝙫𝙚 𝙩𝙚𝙧𝙖𝙥𝙚́𝙪𝙩𝙞𝙘𝙖 🦠 Control de foco = 𝙘𝙧𝙞́𝙩𝙞𝙘𝙤 💊 Desescalar antibióticos 💉 Esteroides solo shock refractario 🫁 𝙍𝙚𝙨𝙥𝙞𝙧𝙖𝙩𝙤𝙧𝙞𝙤 🎯 SpO₂ 90–96% 🌬️ Vt ~6 mL/kg + Pplat ≤30 🔄 Prono en ARDS ‼️Si te sirve: ❤️ Me gusta | 🔁 Repost | ➕ Follow para más #MedED en #ClubCrit 😄🧠🫶 👇🏼👇🏼👇🏼👇🏼 📚📖#ClubCrit #Sepsis #Shock #CritCare #UCI #ICU #CriticalCare #Diagnóstico #icu #intensivecare #diagnosis #management #POCUS #VExUS #MedicinaBasadaEnEvidencia #Terapia #MedEd #Medicina #FOAMed #FOAMcc #CuidadoCrítico #MedX #EducaciónMédica #MedIntensiva #MedXCommunity #MedicinaCrítica #MedED #CritCare #ICUManagement #MustRead #LecturaRecomendada

This image is highly valuable, highlighting key diseases and their most characteristic features.

Pediatric Dose Calculation 💊👦👶🏻

The complex multi-organ network involved in obesity-induced insulin resistance (IR) and its progression toward type 2 diabetes. It highlights how metabolic stress in one tissue creates a feedback loop that affects the entire body. nature.com/articles/s4139…

Medications used for the prevention and treatment of migraine headaches, categorized by drug type, dosage, indications, contraindications, and key considerations. instagram.com/p/DW4UAKTjDxb/…

The key differences between Hemolytic Uremic Syndrome (HUS) and Thrombotic Thrombocytopenic Purpura (TTP), which are both types of thrombotic microangiopathies (TMA) characterized by hemolytic anemia and low platelet counts. facebook.com/share/p/1GwXQV…

Stop guessing transfusions—match the problem to the right blood product. Follow NICE Blood Transfusion Guideline (2026).

The solar, lunar, and serpentine motifs embedded in Albanian folk art and ritual practice represent a continuous symbolic tradition traceable to the Illyrian period. From mountain-top sun ceremonies and east-facing burial rites, to the domestic veneration of the house serpent as a totemic guardian, these motifs are structural elements of a pre-Christian cosmology. They survived occupation, conversion, and centuries of cultural pressure precisely because they were encoded into everyday objects: cradles, door frames, grave crosses, and the skin itself.

This chart is a helpful clinical summary for interpreting coagulation panels, which are essential for diagnosing bleeding disorders and monitoring anticoagulant therapy. anesthguide.com/topic/coagulat…

🧵 Antiemetic Cheat Sheet: Stop giving Ondansetron for all vomiting 📌 Quick Reference •Pregnancy ➡️ Doxylamine + Pyridoxine •Motion sickness ➡️ Scopolamine •Chemotherapy ➡️ Ondansetron •Gastroparesis ➡️ Metoclopramide •Vestibular causes ➡️ Promethazine 🔴 Mechanism-based approach 1️⃣ Pregnancy vomiting Drug: Doxylamine + Vit B6 Mechanism: Antihistamine + central modulation 2️⃣ Motion sickness Drug: Scopolamine Mechanism: Anticholinergic (vestibular suppression) 3️⃣ Chemo-induced vomiting Drug: Ondansetron Mechanism: 5-HT3 receptor blockade 4️⃣ Gastroparesis Drug: Metoclopramide Mechanism: D2 blockade → prokinetic 5️⃣ Vertigo-related vomiting Drug: Promethazine Mechanism: H1 blockade

Recordamos la regla 3-6-9 para los diámetros intestinales, más allá del cual existe riesgo de perforación 🚨 -Intestino delgado: < 3 cm -Intestino grueso: < 6 cm -Ciego: < 9 cm

A high-level clinical roadmap designed to help healthcare professionals diagnose and manage common electrolyte imbalances. It breaks down complex physiological processes into logical flowcharts based on lab values and clinical signs. @DharSaty

@DrMedica_13 Can’t pee, can’t see and can’t climb the tree. Reactive Arthritis (Reiter’s Syndrome)

A patient presents within 3 hours of stroke onset. Drug? A) Aspirin B) Alteplase (tPA) C) Heparin D) Warfarin

@ZahoorAhmed1450 Lidocaine is bets choice here and have given it many times but guidance now is makindo.co.uk/topics/20.php

🩸 Hemostasis vs Thrombosis: Pathology Summary 🧠DOAC Targets ->Api-Xa-ban / Rivaro-Xa-ban: The name literally tells you the target. Contains "Xa" = Targets Factor Xa. ->Da-bi-gatran: Contains "bi" = Think "2" (Factor II is Thrombin). Dabigatran is a Direct Thrombin Inhibitor. 🧠PT has 2 (less) letters; VII the only factor. It’s short and fast-Extrinsic PTT has 3(many)letters: So many factors are involved-Intrinsic 📌Big Picture: Clotting = Balance ⚖️ Hemostasis = Normal clotting to stop bleeding ✅ Thrombosis = Pathologic clots in vessels ❌ 🩸The body maintains a tight equilibrium between forces: ->Pro-clotting: Intact vessels, platelets 🧱, and the coagulation cascade ⚡. ->Anti-clotting: Natural anticoagulants (Protein C, S, Antithrombin) 🛡️ and fibrinolysis (clot breakdown) ✂️. 🩸The Clotting Process in 3 Steps Step 1: Primary Hemostasis (Platelet Plug 🧱) ->Injury exposes collagen. von Willebrand Factor (vWF) binds it. Platelets adhere, activate, and aggregate to form a temporary plug 🧱. Needs: Adequate functional platelets, vWF. Receptors: GpIb, GpIIb/IIIa. Step 2: Secondary Hemostasis (Coagulation Cascade ⚡) Goal: Generate thrombin ➡️ forms a stable fibrin clot. Key Pathways (Labs): Intrinsic Pathway (PTT): Factors XII ➡️ XI ➡️ IX ➡️ VIII 🔵. Extrinsic Pathway (PT): Tissue Factor (TF) + Factor VII 🔴. Common Pathway: Connects both to activate Thrombin ➡️ forms Fibrin 🟩. 📌Key Concepts: Reactions happen on platelet membranes to increase speed 🚀. Thrombin acts as a feedback amplifier 🔊. Vitamin K is essential to activate Factors II, VII, IX, X 🥬, enabling membrane binding. Step 3: Fibrinolysis (Clot Breakdown ✂️) Plasminogen ➡️ Plasmin, which breaks down the fibrin clot. Too much fibrinolysis = delayed bleeding. 📌Clinical Connections: Bleeding disorders occur from low platelets (petechiae), low vWF (mucosal bleeding), or factor deficiencies (deep bleeding). Thrombosis occurs from low anticoagulants or increased tissue factor. Lab Testing Summary 🧪 🩸PT (Prothrombin Time): Measures the Extrinsic Pathway (Factor VII) 🔴. INR-guided. 🩸PTT (Partial Thromboplastin Time): Measures the Intrinsic Pathway (Factors XII, XI, IX, VIII) 🔵. Heparin-guided. Prolonged PT/PTT: Decision Guide 🟩 PT Normal, PTT Normal: Bleeding still occurring? Think: vWD, Platelet problem, or Factor XIII deficiency (missed by standard labs) 🤔. 🟥 Prolonged PT ONLY: Common causes: Warfarin, early Vitamin K deficiency, liver disease. Targets Factor VII (extrinsic) 🔴, which has the shortest half-life and drops first. 🟦 Prolonged PTT ONLY: Common causes: Heparin, Hemophilia A/B, vWD, Lupus Anticoagulant (prolongs PTT in lab, causes CLOTTING clinically) ⚠️. 🟪 BOTH Prolonged: Indicates a common pathway issue or systemic disorder. Common causes: Liver disease, DIC, advanced Vitamin K deficiency, or deficiencies in X, V, II, fibrinogen. 🩸Diagnostic Approach: Unexplained prolongation? Start with a Mixing Study 🧬. ✅ Corrects (Normalizes): Factor Deficiency (fixes the missing piece). ❌ Fails (Remains prolonged): Inhibitor Present (something is blocking clotting). 🧠Deep Dive into Key Concepts & Diagnoses 📌Natural Anticoagulant Systems 🛡️ Keep clotting in check to prevent thrombosis: 🩸Antithrombin: Inhibits thrombin and Xa; potentiated by heparin. 🩸Protein C/S: Thrombin-activated; inhibits Factors Va, VIIIa. (Needs S as a cofactor). Clinical: Factor V Leiden mutation prevents APC from cleaving Va ➡️ gain of function ➡️ thrombosis ⚠️. Protein C/S deficiency causes venous thrombosis ⚠️. 🩸Fibrinolytic System ✂️ Plasmin breaks down the clot. Deficiencies in inhibitors lead to excessive breakdown and bleeding. 🩸Thrombin Time (TT) Measures fibrinogen ➡️ fibrin conversion. Prolonged by low fibrinogen, heparin, and direct thrombin inhibitors. 📌The "Don't Miss" Diagnoses 🚨 ⚡️Dysfibrinogenemia Normal fibrinogen antigen but low functional fibrinogen ➡️ bleeding OR thrombosis. Autosomal Dominant. Tests functional < antigen. Prolonged TT. Treat with fibrinogen concentrate or cryoprecipitate. ⚡️Factor XIII Deficiency or Acquired Inhibitor Normal PT and PTT! The standard tests MISS it entirely. Causes severe, delayed bleeding and poor wound healing. Test Result: Normal labs, but severe bleeding ➡️ get a CLOT SOLUBILITY test. The unstable clot dissolves in 5M urea or acid. Acquired inhibitors: New-onset bleeding in older patients ➡️ requires immunosuppression. High mortality from treatment infection, not bleeding. 📌Key One-Liners 🧠 Factor VII drops first on Warfarin. Normal labs ≠ normal hemostasis. History > labs for bleeding approach. When PT+PTT are both prolonged, trust history and consider systemic issues or the common pathway. Mixing study always first. Acquired inhibitors ➡️ older patients with new bleeding. 🎯 Master Summary Hemostasis is a balance between platelets 🧱, coagulation ⚡, endothelium, and fibrinolysis ✂️. PT=VII (extrinsic) 🔴. PTT=VIII, IX (intrinsic) 🔵. Missing study separates deficiency vs inhibitor 🧬. Factor XIII deficiency is a normal-lab bleeder missed without solubility test 🚨. #MedTwitter, #MedEd, #Hematology, #Thrombosis, #Thrombophilia, #Hemostasis, #VTE, #Anticoagulation, #Coagulation, #FOAMed @ASH, @Bloodjournal, @NEJM, @HemOncToday @VTEHemostasis, @MedEdHacks, @HematologyNews1 @oncodaily @Hema_News @J_Hematology @realbowtiedoc @IMG_Oncologists @ASH_hematology @ASCOPost

Diuretics 😍