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آرشیو پست ها
🔴 Coronary Artery Diseases (CAD/ischemic Heart Disease IHD)
▪︎It's The Most Common Cause Of Chronic Stable Angina & Acute Coronary Syndrome (Myocardial infarction & Unstable Angina)
▪︎Most Common Cause Of Death Worldwide
▪︎Mostly Results From Lipid Deposition inside The Coronary Arteries (Atherosclerosis) That Leads To Arterial Narrowing & Myocardial Ischaemia (Angina) Or Infarction (MI)
🔷Risk Factors For CAD
1. Atherosclerosis
2. Diabetes & Hypertension
3. Smoking & Obesity
4. Old Age & Male
5. Family Hx Of Heart Disease
🔰Chronic Stable Angina (Angina Pectoris) ▪︎Chronic Fixed Narrowing Of Coronary Arteries Due To Atherosclerosis Leads To Transient Myocardial Ischaemia During Supply-Demand Mismatch (On Exertion) ▪︎Predictable Onset Of Symptoms ▪︎Other Causes Of Stable Angina ➡️ Hyprtrophic Obstructive Cardiomyopathy/Aortitis/Aortic Stenosis/Prinzmetal Angina/Syndrome X 🔷Clinical Features Of Chronic Stable Angina 📍1. Diffuse Retrosternal Constricting Chest Pain ▪︎After Exertion/Heavy Meal/Cold Weather/Intense Emotions/Lying Flat/Vivid Dream ▪︎Radiating To Neck/Jaw/Arms/Shoulders ▪︎Subside With Rest & GTN Within 5 Min 📍2. Normal ECG & Cardiac Biomarkers 🔹Dx Of Chronic Stable Angina 📍1. ECG Stress Test (Treadmill) ➡️ ST Depression ≥1mm 📍2. High Suspicious But Normal Stress ECG ➡️ Then Do : ▪︎Myocardial Perfusion Scan ▪︎Stress Echocardiography ▪︎CT Coronary Angiography 🔹Mx Of Chronic Stable Angina 🔸A. During Acute Attack ▪︎Give Nitroglycerin (GTN Sublingual/Buccal Fast Acting Repeated After 5Min If No Response) 🔸B. Prevention Of Attacks (Maintenance) 📍1. Sublingual GTN + BB (Metoprolol 50-200mg Daily/Bisoprolol 5-15mg Daily/Carvedilol) 📍2. If No Response : ▪︎Add CCB (Amlodipine/Nifedipine/Verapamil/Diltiazem) ▪︎Or Long Acting Nitrate (IsoSorbide DiNitrate/MonoNitrate) ▪︎Or Nicorandil (K Channel Blocker Has No Risk Of Tolerance) ▪︎Or Ivabradine (If Channel Blocker) ▪︎Or Ranolazine ▪︎Or Do Revascularisation (PCI/CABG) 📍3. Prevent Complications (MI) ▪︎Low Dose Aspirin (75 Mg) Or Clopidogrel (75 Mg Alternative To Aspirin) ▪︎ACE Inhibitors Or ARBS ▪︎High intensity Statins (Atorvastatin 20-80mg)
🔰Prnizmental Angina (Variant) ▪︎Vasospasm Of Coronary Arteries Leading To Heart Muscle Ischaemia & Chest Pain 🔹Mx Of Prnizmental Angina ➡️ CCB/Long Acting Nitrates
🛑Methotrexate is contraindicated in several groups of patients. These include:
✅Patients who are pregnant (or may become pregnant) ✅Patients with liver disease ✅Patients who consume more than one alcoholic drink daily ✅Patients with moderate to severe impairment of kidney function (estimated glomerular filtration rate [eGFR] less than 30 mL/min/1.73 m2
🛑Cardiovascular effects of hyperthyroidism⬆️Heart rate ⬆️Pulmonary artery pressure ⬆️Cardiac output ⬆️Ejection fraction ⬆️Diastolic relaxation ⬆️Systolic blood pressure ⬆️Myocardial oxygen consumption ⬇️Systemic vascular resistance ⬇️Diastolic blood pressure
🏆 2026 Nobel Prize in Physiology or Medicine
The Nobel Prize was awarded to Karl Deisseroth, Peter Hegemann, and Georg Nagel for discoveries that led to optogenetics.
🧠 What is Optogenetics?
Optogenetics is a technique that uses light to control specific neurons.
The researchers discovered and developed light-gated ion channels, such as channelrhodopsins. When light activates these channels, ions flow across the neuronal membrane, changing its membrane potential and allowing researchers to activate or inhibit specific neurons with high precision.
💡 Light → Ion channel → Membrane potential change → Neuronal activity
🔬 Why does it matter?
Optogenetics has revolutionized neuroscience by allowing scientists to study the causal role of specific neural circuits in:
• Learning & memory
• Movement
• Sensory processing
• Emotion & behavior
It also has potential therapeutic applications, including vision restoration and neurological disorders.
«٧ أكتوبر | ذكرى طوفان الأقصى. فلسطين حاضرة في الوجدان؛ نحيّي صمود أهلها وارتباطهم بأرضهم، ونتطلع إلى الحرية والكرامة والسلام. من زيتون فلسطين تبدأ الحكاية… وتبقى جذورها شاهدة.»
🔥Cases and its management of
📍Hypertension.
📍Angina.
📍Heart failure.
Easy Files.
د. أشرف خلوف
psychiatric_book
تقريبا هذا افضل كتاب معتمد في ال Psychiatry
عدد الصفحات 130 صفحة باللغة الإنجليزية
ما عُمَرُه كان الدكتور الذي يُصعّب المادة على الطلبة معيارًا للدكتور المثالي.
بل على العكس، الدكتور المثالي هو الذي يجعل الطالب يحب المادة، ويفهمها بطريقة بسيطة وواضحة، ويزرع فيه الفهم الحقيقي بدلًا من الحفظ المؤقت.
فالهدف من أي مادة دراسية ليس أن تكون عقبة أمام الطالب، وإنما أن تمنحه علمًا ينتفع به، ويخرج منها فاهمًا ومستفيدًا.
هذه هي ثمرة التدريس الحقيقي، وهذا هو الدكتور الذي يستحق أن يُوصف بالمثالي ..🤍✨.
Topics of the day
#Heart_Failure@Clinicalinternalmedicine
#Hypertension@Clinicalinternalmedicine
🔷Complications Of HT📍1. Acute Coronary Syndrome (MI) & Stroke 📍2. Chronic Kidney (Hypertensive NephroPathy) & Eye Disease (Hypertensive Retinopathy) 📍3. Aortic Dissection Or Aneurysm 📍4. Heart Failure
🔷Mx Of HT🔸A. Target Blood Pressure 1. Age >80 اكبر ➡️ Clinic BP <150/90 2. Age <80 اصغر ➡️ Clinic BP <140/90 3. Diabetic ➡️ Clinic BP <130/80 🔸B. Life Style Changes 1. Weight Reduction 2. Stops Smoking & Alcohol 3. Salt & Saturated Fat Restriction 4. Eats Fruits/Vegetables/Fish Oil 5. Regular Exercise 🔸C. Drugs Tx
🪀Indications For Drugs :📍1. Stage One HT (≥135/85) + Organs Damage Or Cardiovascular Risk >20% 📍2. Stage Two Hypertension (≥150/95)
🪀Drugs Regime :▪︎Ist Line (Standard) Drugs ➡️ ACEI/ARBS/CCB/Thiazide ▪︎Stage One HT ➡️ Start Single Drug ▪︎Stage Two HT ➡️ Start Two Drugs ▪︎ACEI With ARBS Never Combined Together 📍1. Age <55 ➡️ Start With ACEI Or ARBS 📍2. Age >55 Or Black ➡️ Start With CCB 📍3. No Good Control : ▪︎ACEI Or ARBS + CCB ▪︎Still No Good Control ➡️ ACEI Or ARBS + CCB + Thiazide (Triple Therapy) ▪︎Still No Good Control (Resistant HT) ➡️ Triple Therapy + Increase Dose Of Diuretics Or Add Further Diuretics Or Alpha Or Beta Blockers
🪀Drugs Names :📍1. Thiazide Diuretics (BendroFlumethazide 2.5mg Daily/CycloPenthiazide 0.5mg Daily) ▪︎Better for Old Ages ▪︎Needs Months For Full Effect 📍2. Loop Diuretics (Furosemide 40mg Daily/Bumetanide 1mg Daily) ➡️ Useful During Renal Impairment Or Refractive Edema Or To Mixed With ACEI 📍3. ACE Inhibitors (Enalapril 20mg/RamiPril 5-10mg/Lisinopril 10-40mg) ➡️ 1st Line For Patients With Kidney Disease 📍4. ARBS (Irbesartan 150-300mg/Valsartan 40-160mg) ➡️ Better Tolerance Than ACEI (No Cough) 📍5. CCB : ▪︎Amlodipine (5-10mg)/Nifedipine (30-90mg) ➡️ Better For Older Ages ▪︎Rate Limiting CCB (Verapamil 240mg & Diltiazem 200-300mg ➡️ For HT + Angina 📍6. BB (Metoprolol 100-200mg/Atenolol 50-100mg/Bisoprolol 5-10mg/Labetolol 200mg-2.4g/Carvedilol 6.25-25mg 2x Daily) ➡️ For HT + CAD (Angina/Post MI) 📍7. Alpha Blockers (Prazosin/indoramin/Doxazosin) ➡️ For HT + BBH (Benign Prostatic Hyperplasia) 📍8. Spironolactone (K Sparing Diuretic) ➡️ For Refractive HT 📍9. Aspirin ➡️ For Hypertensive Patients + Age >50 Or Have Organs Damage Or Cardiovascular Risk 15% Or Diabetes 📍10. Statins ➡️ For Hypertensive Patients + Cardiovascular Risk 10%
🔸D. Causes Of No Improvement (Resistant HT)📍1. No Compliance To Tx ما يتلزم 📍2. New Drug Resistance العلاج نفسة بدة يقل مفعولة بسبب تشبع الجسم 📍3. Undiagnosed Causes 🔸E. Accelerated (Malignant HT/Hypertensive Crisis) ▪︎Very High BP (180/120 mmHg) ▪︎With End Organ Damage (Retinopathy Grade 3-4/Renal Failure/LV Failure/Hypertensive Encephalopathy/Death) 🪀Clinical Features Of Malignant HT 📍1. Severe Headache & Visual Disturbances With Altered Mental State 📍2. Intracranial Hemorrhage & Papilloedema 📍3. Oliguria & Renal Failure 📍4. Pulmonary Edema 📍5. Aortic Dissection 📍6 Seizures 📍7. Myocardial infarction (MI) & Heart Failure 🪀Mx Of Malignant HT : ▪︎Controlled Slow BP Reduction To 150/90 Over 24-48h Using : 📍1. IV/IM Labetalol (2mg/Min | Maximum 200mg) 📍2. IV GTN (0.6-1.2mg/hr) 📍3. IM Hydralazine (5-10mg Every 30Min) 📍4. IV Sodium NitroPrusside (0.3-1μg/kg/Min) 🔸F. Hypertensive Urgency ▪︎High Elevation in BP (>160/100 mmHg) But No Evidence Of Organ Damage ▪︎Mx By Oral AntiHypertensive ➡️ Captopril/Clonidine/Labetalol/Nifedipine/Diazoxide https://t.me/Clinicalinternalmedicine
🔴Hypertension▪︎is Chronic Elevation in Arterial Blood Pressure To Level At Which Increase in Cardiovascular Morbidity & Mortality
🔷Causes Of HT🔸A. Essential HT (Most Common 95%) ▪︎No Specific Cause Identified ▪︎High Occurrence in 1st Degree Relatives & Identical Twins
🪀Risk Factors For Essential HT :📍1. Old Ages (>60 Years) & Male 📍2. African American/Japanese 📍3. High Salt & Heavy Alcohol intake 📍4. Obesity & Lack Of Exercise 📍5. Family Hx Of HT
🔸B. Secondary HT (5%)▪︎Specific Cause Present
🪀Causes Of Secondary HT :📍1. Renal (Most Common Secondary Causes Of HT) : ▪︎Renal Artery Stenosis ▪︎PKD (Polycystic Kidney Disease) ▪︎Glomerulonephritis ▪︎Diabetic Nephropathy ▪︎Parenchymal Renal Disease ▪︎Chronic Renal Failure 📍2. Endocrine : ▪︎Pheochromocytoma ▪︎Cushing's Syndrome ▪︎Primary HyperAldosteronism (Conn' Syndrome) ▪︎Congenital Adrenal Hyperplasia ▪︎Thyrotoxicosis/Hyperparathyroidism/Hypothyroidism ▪︎Acromegaly ▪︎Liddle' Syndrome ▪︎11β-Hydroxysteroid Dehydrogenase Deficiency 📍3. Aortic Coarctation 📍4. Obesity/Pregnancy/Obstructive Sleep Apnea (OSA) 📍5. Drugs (Steroids/NSAIDS/Oral Contraceptives/TCA/Decongestants/Cocaine/Alcohol)
🔷Clinical Features Of HT📍1. HT Mostly Asymptomatic (Silent Killer) 📍2. Findings Indicate The Cause : ▪︎RadioFemoral Delay ➡️ Corcacation Of Aorta ▪︎Kidneys Enlargement ➡️ PKD ▪︎Abdominal Bruits ➡️ Renal A Stenosis ▪︎Moon face ➡️ Cushing Syndrome 📍3. Findings Indicate The Risk Factors : ▪︎Central Obesity ▪︎Hyperlipidemia 📍4. Findings indicate The Complications : ▪︎LV Hypertrophy & Failure ▪︎Atrial Fibrillation (AF) ▪︎Aortic Aneurysm ▪︎Stroke ▪︎Peripheral Arterial Disease ▪︎Hypertensive Retinopathy (Cotton Wool Exudates)
🔷Dx Of HT🪀Ways Of BP Measurement 📍1. At The Clinic ➡️ Accurate BP Measurement By The Doctor 📍2. Out Side The Clinic (Ambulatory ABPM/Home HBPM) : ▪︎Used For Patients With Liable BP/Refractive HT/Symptomatic Hypotension/White Coat HT ▪︎Ambulatory Measurement (ABPM) ➡️ Automated Device Used To Measure The Patient's Blood Pressure For 24h During Normal Patient's Activity (It's 12/7 mmHg Lower Than Clinic Measurements But Provide Better Profile) ▪︎Home BP Measurement By The Patient (HBPM Not Well Reliable)
🪀Dx Of HT Confirmed When :▪︎BP >140/>90 (Or >130/>80 in Another Staging) in At Least Two-Three Different Times During Complete Mental & Physical Rest
🪀Staging OF HT :🔸A. From Davidson المصدر من 📍1. Within Normal : ▪︎Normal <130/85 ▪︎Optimal <120/80 ▪︎High Normal 130-139/85-89 📍2. Hypertension : ▪︎Grade One HT 140-159/90-99 ▪︎Grade Two HT 160-179/100-109 ▪︎Grade Three HT ≥180/>110 📍3. Isolated Systolic HT : ▪︎Grade One 140-159 ▪︎Grade Two ≥160
🔸B. Other Staging (American Heart Association)📍1. Normal <120/<80 📍2. Elevated 120-129/<80 📍3. Hypertension : ▪︎Stage One HT 130-139/80-89 ▪︎Stage Two HT ≥140/≥90
🔷Dx Of HF📍1. Chest Xray : ▪︎Upper Lobe Pulmonary Vein Distension ▪︎Increase Lung Vascularity ▪︎Interstitial Edema (Kerley B Lines) ▪︎Alveolar Edema (Hazy Opacification) ▪︎Pleural Effusion ▪︎Cardiac Dilatation 📍2. Echo (Confirm Dx) : ▪︎Reduced EF <40% (Most Common) ➡️ Systolic Dysfunction (Congestive HF) ▪︎Preserved EF >50% ➡️ Diastolic Dysfunction ▪︎BorderLine EF 41-49% ➡️ Mixed Systolic & Diastolic Dysfunction ▪︎Normal EF 55-70% 📍3. BNP & NT-ProBNP Enzymes (Used For Dx & Follow Up) ➡️ Elevated (Due To Atrial Dilatation)
🔷Complications Of HF📍1. Renal Failure (Due To Poor Renal Perfusion Or Drugs [Diuretics/ACEI/ARBS]) 📍2. Liver Failure (Due To Poor Perfusion & Congestion) 📍3. Electrolytes Disturbances : ▪︎Hypo Or Hyperkalemia ▪︎Hyponatremia 📍4. Thromboembolism (DVT & Pulmonary Embolism) 📍5. Arrhythmia 📍6. Sudden Death (50% Risk & Mostly Due To Ventricular Arrhythmia)
🔷Mx Of HF🔶A. Acute Heart Failure & Pulmonary Edema 📍1. IV Morphine (Decrease Distress) 📍2. Sit The Patient Up (Decrease Preload) 📍3. High Flow Oxygen & CPAP (5-10mmHg To Decrease Hypoxia) 📍4. Nitrates (IV 10-200μg/min Or Buccal 2-5mg To Decrease Preload & AfterLoad) 📍5. Loop Diuretic (IV Furosemide 50-100mg To Decrease Volume Overload) 📍6. +Ve inotropic Agents (IV Dobutamine 2.5-10μg/Kg/Min To Increase Cardiac Output) 🔶B. Chronic HF 📍1. Life Style Changes : ▪︎Salt Restriction (<3g/Day) ▪︎Avoids Smoking & Alcohol ▪︎Regular Moderate Exercise ▪︎Influenza & Pneumococcal Vaccine 📍2. Drugs : ▪︎Standard Combination ➡️ ACEI/ARBS/ARNI + BB (Beta Blockers) ▪︎Drugs Increase Myocardial Contraction (Decrease AfterLoad) ➡️ Better For Systolic Dysfunction ▪︎Drugs Decrease PreLoad ➡️ Better For Diastolic Dysfunction 🪀I. Diuretics ➡️ Decrease Systemic & Pulmonary Congestion ▪︎Loop Diuretics (Oral Furosemide [Lasix] 1st Line) ▪︎Aldosterone Blockers (Spironolactone & Eplerenone) ➡️ For Post STEMI HF (HF With Severe LV Systolic Dysfunction) ▪︎For Resistant Edema Use : •IV Furosemide (5-10mg/h) •Loop + Thiazide Diuretics (BendroFlumethiazide 5mg Daily) 🪀II. ACE Inhibitors (Captopril/Enalapril/Lisinopril) ▪︎DecreaseNeuroHumoral Activity (Decrease Peripheral VasoConstriction & Salt & Water Retention) & Improve Morbidity & Mortality ▪︎Usually Not Tolerated Due To Chronic Cough 🪀III. ARBS (Losartan/Valsartan) ➡️ Better Tolerance Than ACE Inhibitors 🪀IV. BB (Bisoprolol/Carvedilol/Metoprolol) ▪︎Decrease Sympathetic Activity & Risk Of Arrhythmia & Sudden Death (More Effective Than ACE Inhibitors in Mortality Reduction) ▪︎Started At Low Dose Then Increase Gradually To Prevent Acute On Chronic HF (Bisoprolol Given At 1.25mg Then Increase Gradually Over 12w Till 10mg Daily Reached) 🪀V. Sacubitril (Neprilysin Inhibitors) + ARBS (ARNI) ➡️ For Resistant HF 🪀VI. Ivabradine ➡️ Alternative To BB Or Elevated Heart Rate Despite BB Use Or No Improvement On Triplet Therapy (ACEI/BB/Aldosterone Blockers) 🪀VII. Hydralazine + Nitrate ➡️ If No Improvement No Other Drugs (Useful For Afro-Caribbean Patients) 🪀VIII. Digoxin ➡️ For Rate Control In [HF + AF] Or Resistance HF 🪀IX. Amidarone ➡️ Last Choice For Arrhythmia in HF 📍3. Non-Pharmacological Tx : 🪀I. Implantable Cardiac Defibrillator (For HF + Ventricular Arrhythmia) 🪀II. Resynchronisation Devices (For Severe IntraVentricular Delay Or Complete Heart Block) 🪀III. Coronary ReVascularization (PCI Or CABG) 🪀IV. Cardiac Transplantation 🪀V. Ventricular Assist Devices (VAD Increase Cardiac Output While Waiting For Cardiac Transplantation)
▪︎Drugs Reduce Mortality ➡️ BB/ACEI/Hydralazine + Nitrates/Neprilysin Inhibitors/Spironolactone/Ivabradine/Resynchronisation Devices ▪︎ACEI/ARBS/Spironolactone ➡️ Risk Of Hyperkalaemiahttps://t.me/Clinicalinternalmedicine
🔴Heart Failure (HF)▪︎inability Of The Heart To Produce Cardiac Output Sufficient To Meet The Body Demands ▪︎More in Elderly (1% At 50-59 Years & 10% At 80-89 Years)
🔷Risk Factors For HF📍1. Coronary (Stenosis) & Ischaemic (MI) HD 📍2. Valvular HD 📍3. Hypertension (HT) & Diabetes (DM) 📍4. Cardiomyopathy
🔷Most Causes Of Death in HF Due To📍1. Pump Failure (No Blood Ejection) 📍2. Ventricular Arrhythmia
🔷Severity Of HF📍1. Mild To Moderate ➡️ Symptoms Occur Only When Metabolic Demands Increase 📍2. Severe ➡️ Symptoms Present At Rest
🔷Causes Of HF🔶A. Ventricular Dysfunction (Most Common Cause) 📍1. Systolic Dysfunction (Reduced Ejection Fraction <40%) ▪︎Impaired LV Contraction Due To Myocardial Disease (IHD/MI/Myocarditis) Results in Low Cardiac Output 📍2. Diastolic Dysfunction (Preserved Ejection Fraction >50%) ▪︎Impaired LV Relaxation During Diastole Due To LV Hypertrophy/Cardiac Tamponade/Restrictive & Constrictive Pericarditis 📍3. Both Systolic & Diastolic Dysfunction ➡️ in Patients With CAD (Coronary Artery Disease) 🔶B. High Output Failure ▪︎Increase in Body Demands Can't Be Meet By The Usual Normal Cardiac Output (CO) ▪︎Seen in Large AV Shunt (in Dialysis)/Thiamine Deficiency (Wet Beri Beri)/Severe Anemia/Thyrotoxicosis/Pregnancy (All These Conditions Require More CO) 🔶C. Valvular Diseases Causing HF 📍1. Impaired Ventricular Filling (M & T Stenosis) 📍2. Ventricular OutFlow Obstruction (A & P Stenosis/Hypertrophic Cardiomyopathy/HT/Pulmonary HT) 📍3. Ventricular Volume Overload (M & A Regurgitation/VSD/ASD) 🔶D. Arrhythmia Causing HF ➡️ AF/Tachycardia/Complete Heart Block 🔶E. Acute HF Due To 📍1. DeCompensation Of Chronic HF ➡️ Precipitated By Sudden Diuretics Cessation/Respiratory Infection 📍2. New Onset Acute HF ➡️ Due To Acute Coronary Syndrome (MI)/Acute MR & AR/Malignant HT 🔶F. RHF (Right Side HF) Due To ▪︎LHF (Most Common) ▪︎Lung Disease (Pulmonary HT/Pulmonary Embolism PE) ▪︎Valve Diseases (TR/PR/PS/ASD)
🔷Clinical Features Of HF🔶A. Acute HF 📍1. No Compensatory Mechanisms ➡️ Acute Pulmonary Edema Develops 📍2. Present As Sudden Onset Of : ▪︎Dyspnea & ARDS (Adult Respiratory Distress Syndrome) ▪︎Orthopnea (Dyspnea On Lying Down) ▪︎Rapid Pulse & High BP (Blood Pressure) ▪︎Elevated JVP/Gallop Rhythm (S3) ▪︎Agitation/Pale/Cold Peripheries ▪︎Bilateral Basal Lung Crepitations/Expiratory Wheeze (Cardiac Asthma) ▪︎New Systolic Murmur (MR/VSD) ▪︎If Blood Pressure (BP) is Normal Or Low ➡️ indicates Cardiogenic Shock Developed (Bad Sign) 🔶B. Chronic HF 📍1. Compensatory Mechanisms Present ➡️ Symptoms Only At Exacerbations (No Pulmonary Edema) 📍2. Chronic Symptoms Of Low Cardiac Output : ▪︎Fatigue/Weakness ▪︎Low BP/Cold Peripheries ▪︎Poor Effort Tolerance ▪︎Oliguria/Uremia ▪︎Weight Loss 📍3. Chronic LHF (Pulmonary Congestion) ➡️ Pulmonary Edema/Pleural Effusion/Cardiomegaly 📍4. Chronic RHF (Peripheral Body Congestion) ➡️ Elevated JVP/Peripheral Pitting Edema/Ascites/Liver Congestion/Mild Jaundice https://t.me/Clinicalinternalmedicine
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