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EasY Medical, Paris (2025)

22/09/2025

WARFARIN OVER DOSE TRATMENT
bleeding:
stop warfarin, vit K 5 mg IV, prothrombin complex concentration (if not available then FFP)
> 8 with minor bleeding:
stop warfarin, vit K 1-3 mg IV, if after 24 hours still INR is too high repeat the vit K dose IV and restart the warfarin when INR < 5
> 8 with no bleeding:
stop warfarin, vit K 1-5 mg orally, if after 24 hours INR is still high then repeat the vit K dose orally again, restart warfarin when INR < 5
5-8 with minor bleeding:
vit K 1-3 mg IV, restart warfarin when INR < 5
# INR between 5-8 with no bleeding: withhold one or two dose of warfarin and reduce subsequent maintenance dose.

06/09/2025

Wells Score for DVT
Mnemonic: SCARE THE Clot
S – Swelling of the leg (+1)
C – Cancer (+1)
A – Alternative diagnosis (−2)
R – Rest ≥3d (+1)
E – Edema (+1)
T – Tender calf (+1)
H – History of DVT (+1)
E – Enlarged veins (+1)
Clot – Can't move/Immobility (+1)

DVT likey

05/09/2025

New evidence supports immediate initiation of SGLT2 inhibitors and MRAs in all heart failure patients, regardless of LVEF, to reduce hospitalization and death.

Key Steps:
1️⃣ Suspect HF (symptoms + elevated NT-proBNP/BNP)
2️⃣ Start SGLT2i + MRA + diuretics (if congested)
3️⃣ Perform echocardiography & assess comorbidities
4️⃣ Tailor therapy based on LVEF and comorbidities

LVEF Categories:

· HFrEF (≤40%): ACE-I/ARB/ARNI, beta-blocker, SGLT2i, MRA
· HFmrEF (41–49%): SGLT2i, MRA ± ARNI/β-blocker*
· HFpEF (≥50%): SGLT2i, MRA

💡 Takeaway:
SGLT2i and MRAs are foundational across ALL HF types. Initiate early, even before echocardiography, to improve outcomes.

Source: PMID 40260636

04/09/2025

🩸 Erythropoietin Dosing – Anemia in CKD (Dialysis & Non-Dialysis)

✅ Starting Dose
IV or SC: 50–100 IU/kg, 3 times/week

🔄 Adjust Dose Based On Hemoglobin
📌 Check Hgb every 2–4 weeks
📈 If ↑ 1 g/dL in 2 weeks or Hgb >11 → Reduce dose by ≥25% or stop

🚫 Target Hgb: Stay ≤11 g/dL
Too high Hgb = ❗Risk of stroke, HTN, vascular events

02/09/2025

𝐖𝐡𝐞𝐧 𝐭𝐨 𝐇𝐨𝐥𝐝 𝐨𝐫 𝐒𝐭𝐨𝐩 𝐀𝐂𝐄 𝐈𝐧𝐡𝐢𝐛𝐢𝐭𝐨𝐫𝐬
𝐒𝐭𝐨𝐩 (𝐨𝐫 𝐡𝐨𝐥𝐝) 𝐀𝐂𝐄𝐢 𝐢𝐟:

• Hyperkalemia K⁺ ≥ 6.0 (or persistent >5.5 despite measures).
• AKI or eGFR falls >30% from baseline after starting.
• Symptomatic hypotension (dizziness, syncope).
• Pregnancy (contraindicated).
• Bilateral renal artery stenosis (or stenosis in a solitary kidney).
• Angioedema or severe cough due to ACEi.

𝐒𝐩𝐞𝐜𝐢𝐟𝐢𝐜 𝐂𝐥𝐢𝐧𝐢𝐜𝐚𝐥 𝐒𝐜𝐞𝐧𝐚𝐫𝐢𝐨𝐬

1. 𝐇𝐲𝐩𝐞𝐫𝐭𝐞𝐧𝐬𝐢𝐨𝐧
• Stop ACEi if patient develops uncontrolled hyperkalemia, AKI, or intolerable cough/angioedema. If BP remains uncontrolled, switch to another class (CCB, thiazide, ARB).

2. 𝐇𝐞𝐚𝐫𝐭 𝐅𝐚𝐢𝐥𝐮𝐫𝐞 (𝐇𝐅𝐫𝐄𝐅)
• ACEi are cornerstone therapy – only stop if contraindications develop.

• 𝐓𝐞𝐦𝐩𝐨𝐫𝐚𝐫𝐲 𝐡𝐨𝐥𝐝 𝐝𝐮𝐫𝐢𝐧𝐠:
• Severe hypotension (SBP 30% from baseline or eGFR risk.

3. 𝐂𝐡𝐫𝐨𝐧𝐢𝐜 𝐊𝐢𝐝𝐧𝐞𝐲 𝐃𝐢𝐬𝐞𝐚𝐬𝐞 (𝐂𝐊𝐃)
• ACEi/ARB are renal-protective (reduce proteinuria, slow progression).

•𝐂𝐨𝐧𝐭𝐢𝐧𝐮𝐞 𝐮𝐧𝐥𝐞𝐬𝐬:
• Creatinine rises >30% within 2–4 weeks of initiation.
• Persistent K⁺ >5.5 mmol/L despite correction.
• Advanced renal failure with symptomatic uremia.

𝐒𝐨𝐦𝐞𝐭𝐢𝐦𝐞𝐬 𝐧𝐞𝐩𝐡𝐫𝐨𝐥𝐨𝐠𝐢𝐬𝐭𝐬 “𝐭𝐨𝐥𝐞𝐫𝐚𝐭𝐞” 𝐦𝐢𝐥𝐝 𝐜𝐫𝐞𝐚𝐭𝐢𝐧𝐢𝐧𝐞 𝐫𝐢𝐬𝐞 (≤𝟑𝟎%) 𝐛𝐞𝐜𝐚𝐮𝐬𝐞 𝐢𝐭 𝐢𝐧𝐝𝐢𝐜𝐚𝐭𝐞𝐬 𝐞𝐟𝐟𝐞𝐫𝐞𝐧𝐭 𝐚𝐫𝐭𝐞𝐫𝐢𝐨𝐥𝐚𝐫 𝐝𝐢𝐥𝐚𝐭𝐢𝐨𝐧 (𝐩𝐚𝐫𝐭 𝐨𝐟 𝐛𝐞𝐧𝐞𝐟𝐢𝐭).

26/08/2025

;-
1-devlopment of heart failure in the last month of pregnancy or5 months after it
2- absence of any preexisting Heart disease
3- indeterminant cause
4-presence of echo findings( a together withb or c or all together)
a-LVEDD> 2.7CM/M
b-M mode fractional shortining

26/08/2025

Relative bradycardia occurs when the heart rate is lower than expected for a given fever. Normally, HR rises ~10 bpm per 1 °C increase in temperature. When this expected tachycardia is absent, it can point to specific causes, including non-infectious ones.

Non-infectious Causes & Mechanisms
1. Drug-induced
• Beta-blockers, non-dihydropyridine calcium channel blockers, digoxin
→ Direct suppression of sinus node, blunting HR rise.
• Other medications causing fever may also mask tachycardia if they affect cardiac conduction.

2. Electrolyte disturbances
• Hyperkalemia → Slows conduction through SA and AV nodes.
• Hypokalemia/hypocalcemia may rarely contribute indirectly via arrhythmias.

3. Endocrine disorders
• Hypothyroidism → Low basal metabolic rate; HR response to fever blunted.
• Adrenal insufficiency → Reduced catecholamine response.

4. Neurological / Autonomic causes
• Increased intracranial pressure (Cushing reflex) → Hypertension with bradycardia.
• Post-cardiac transplant → Denervated heart, absent sympathetic response to fever.

5. Other
• Severe hypothermia followed by fever → delayed HR response.
• Autonomic neuropathies (e.g., diabetic) → impaired HR modulation.

Key Clinical Point:
• In any patient with fever but lower-than-expected pulse, always review:
• Medications (beta-blockers, calcium channel blockers, digoxin)
• Electrolytes (especially potassium)
• Thyroid/adrenal status
• Neurological conditions or recent cardiac transplant

This helps distinguish non-infective relative bradycardia from classic infectious causes like typhoid or Legionella.

24/08/2025

β-Blockers in Hypertension with CKD

✅ Pathophysiology: Sympathetic overactivity in CKD drives hypertension, accelerates GFR decline, and increases CV morbidity & mortality.

✅ β-Blockers in CKD:

Cardioselective (Metoprolol, Atenolol) → slow renal disease progression, but less potent than RAAS blockade.

Vasodilating (Carvedilol, Nebivolol) → reduce renal vascular resistance, preserve GFR, slow albuminuria, and provide stronger cardiorenal protection.

Dialysis patients: β-blockers mitigate arrhythmias, reduce arterial stiffness & LVH.

✅ Lipid solubility matters:

Lipophilic (Metoprolol, Carvedilol, Propranolol): hepatic metabolism, CNS pe*******on, not dialyzable → better antiarrhythmic & cardioprotective effects.

Hydrophilic (Atenolol, Nadolol): renally cleared, risk of accumulation, dialyzable → less preferred in CKD.

Amphiphilic (Bisoprolol, Nebivolol): mixed clearance; nebivolol adds vasodilation.

✅ AASK Trial (African American Study of Kidney Disease and Hypertension):

Compared ramipril, metoprolol, amlodipine in CKD patients.

Metoprolol reduced ESRD and death more effectively than amlodipine.

Confirms β-blockers as valuable add-ons to RAAS blockade, especially with CVD.

👉 Takeaway:

RAAS blockade remains first-line in CKD hypertension.

Among β-blockers, Carvedilol (vasodilatory, cardiorenal protection) and Metoprolol (AASK outcome benefit, lipophilic) are the most preferred in CKD patients, including those on dialysis.

📚 Sources: PubMed | Springer | AASK Study

20/08/2025

Updated Treatment of Chronic Hepatitis C (2025)

Chronic hepatitis C (HCV) is now highly curable (>95% success rate) with direct-acting antivirals (DAAs). The choice of regimen depends on HCV genotype, liver disease severity, prior treatment, and comorbidities (e.g., CKD).

Recommended DAA Regimens

1. First-Line Therapies (Pan-Genotypic – Preferred)

- Glecaprevir/Pibrentasvir (GLE/PIB (Mavyret®)
- Indications: All genotypes (1-6), treatment-naïve or experienced, compensated cirrhosis or non-cirrhotic.
- Duration:
- No cirrhosis: 8 weeks
- Compensated cirrhosis: 12 weeks

- Sofosbuvir/Velpatasvir (SOF/VEL – Epclusa®)
- Indications: All genotypes (1-6), including decompensated cirrhosis (with ribavirin).
- Duration:
- No cirrhosis: 12 weeks
- Compensated cirrhosis: 12 weeks
- Decompensated cirrhosis (Child-Pugh B/C) : SOF/VEL + ribavirin × 12 weeks

- Sofosbuvir/Velpatasvir/Voxilaprevir (SOF/VEL/VOX – Vosevi®)
- Indications: Salvage therapy for prior DAA failure (all genotypes).
- Duration : 12 weeks (with/without cirrhosis).

2. Alternative Genotype-Specific Options
- Elbasvir/Grazoprevir (EBR/GZR – Zepatier®)
- Indications: GT1, GT4 (check for NS5A resistance-associated substitutions (RASs) in GT1a).
- Duration: 12-16 weeks (add ribavirin if RAS+).

---

Special Populations
- Decompensated Cirrhosis (Child-Pugh B/C):
- SOF/VEL + ribavirin × 12 weeks (avoid protease inhibitors like GLE/PIB or VOX).
- **Chronic Kidney Disease (CKD)**:
- GLE/PIB (safe in all CKD stages, including dialysis).
- Avoid SOF-based regimens if eGFR

17/08/2025

2025 AHA/ACC Hypertension Guidelines Summary

BP Categories
- Normal:

17/08/2025

Pregnancy & Diabetes – Key Points

1. Before Pregnancy (Preconception)
• Aim A1C < 6.5%.
• Stop medications unsafe in pregnancy: GLP-1 RAs, SGLT2i, ACEi/ARBs, statins.
• Take folic acid (400–800 µg daily).

2. During Pregnancy
• Preferred medication: Insulin.
• Safe oral: Metformin (sometimes glyburide).
• Avoid: GLP-1 RA, SGLT2i, thiazolidinediones.

• Blood sugar targets:
• Fasting:

17/08/2025

Clinical Monitoring of ACEi and ARB Therapy

ACE inhibitors (ACEi) and ARBs are highly effective but need careful monitoring.Here’s a practical monitoring approach (based on KDIGO, ESC, AHA guidelines):

Before starting ACEi/ARB

Baseline tests:
Serum creatinine & eGFR
Serum potassium
Blood pressure

After initiation or dose change
Check serum creatinine & potassium:
Within 1–2 weeks (earlier in high-risk: CKD, elderly, diuretics, heart failure).

Repeat in 4 weeks if stable.

Acceptable changes
Creatinine: Rise ≤30% from baseline or eGFR fall ≤25% → acceptable, continue and monitor.

Potassium:

K⁺ ≤5.5 mmol/L → usually continue
K⁺ >5.5 but 30%
Recurrent hyperkalemia
Bilateral renal artery stenosis

EasY Medical

22/09/2025

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