Sign in to view Sepideh’s full profile
Welcome back
By clicking Continue to join or sign in, you agree to LinkedIn’s User Agreement, Privacy Policy, and Cookie Policy.
New to LinkedIn? Join now
or
New to LinkedIn? Join now
By clicking Continue to join or sign in, you agree to LinkedIn’s User Agreement, Privacy Policy, and Cookie Policy.
Sign in to view Sepideh’s full profile
Welcome back
By clicking Continue to join or sign in, you agree to LinkedIn’s User Agreement, Privacy Policy, and Cookie Policy.
New to LinkedIn? Join now
or
New to LinkedIn? Join now
By clicking Continue to join or sign in, you agree to LinkedIn’s User Agreement, Privacy Policy, and Cookie Policy.
Los Angeles, California, United States
Sign in to view Sepideh’s full profile
Welcome back
By clicking Continue to join or sign in, you agree to LinkedIn’s User Agreement, Privacy Policy, and Cookie Policy.
New to LinkedIn? Join now
or
New to LinkedIn? Join now
By clicking Continue to join or sign in, you agree to LinkedIn’s User Agreement, Privacy Policy, and Cookie Policy.
2K followers
500+ connections
Sign in to view Sepideh’s full profile
Welcome back
By clicking Continue to join or sign in, you agree to LinkedIn’s User Agreement, Privacy Policy, and Cookie Policy.
New to LinkedIn? Join now
or
New to LinkedIn? Join now
By clicking Continue to join or sign in, you agree to LinkedIn’s User Agreement, Privacy Policy, and Cookie Policy.
View mutual connections with Sepideh
Welcome back
By clicking Continue to join or sign in, you agree to LinkedIn’s User Agreement, Privacy Policy, and Cookie Policy.
New to LinkedIn? Join now
or
New to LinkedIn? Join now
By clicking Continue to join or sign in, you agree to LinkedIn’s User Agreement, Privacy Policy, and Cookie Policy.
View mutual connections with Sepideh
Welcome back
By clicking Continue to join or sign in, you agree to LinkedIn’s User Agreement, Privacy Policy, and Cookie Policy.
New to LinkedIn? Join now
or
New to LinkedIn? Join now
By clicking Continue to join or sign in, you agree to LinkedIn’s User Agreement, Privacy Policy, and Cookie Policy.
Sign in to view Sepideh’s full profile
Welcome back
By clicking Continue to join or sign in, you agree to LinkedIn’s User Agreement, Privacy Policy, and Cookie Policy.
New to LinkedIn? Join now
or
New to LinkedIn? Join now
By clicking Continue to join or sign in, you agree to LinkedIn’s User Agreement, Privacy Policy, and Cookie Policy.
About
Saber Plastic Surgery
16260 Ventura Blvd, Suite…
Welcome back
By clicking Continue to join or sign in, you agree to LinkedIn’s User Agreement, Privacy Policy, and Cookie Policy.
New to LinkedIn? Join now
Activity
Sign in to view Sepideh’s full profile
Welcome back
By clicking Continue to join or sign in, you agree to LinkedIn’s User Agreement, Privacy Policy, and Cookie Policy.
New to LinkedIn? Join now
or
New to LinkedIn? Join now
By clicking Continue to join or sign in, you agree to LinkedIn’s User Agreement, Privacy Policy, and Cookie Policy.
-
I am so proud of our team RetractOrtho and Evolve Medtech Partners, for helping get a second patent issued today by USPTO. This is the second patent…
I am so proud of our team RetractOrtho and Evolve Medtech Partners, for helping get a second patent issued today by USPTO. This is the second patent…
Liked by Sepideh Saber
Experience & Education
-
Saber Plastic Surgery
******* *******
-
******* ***** **********
******* *******
-
********* ******
*******, **************, *** **** *******
-
******** ********** ****** ** ********
*.*. undefined
-
-
********** ** ******** **********
******* *** ************** ******* undefined
-
View Sepideh’s full experience
See their title, tenure and more.
Welcome back
By clicking Continue to join or sign in, you agree to LinkedIn’s User Agreement, Privacy Policy, and Cookie Policy.
New to LinkedIn? Join now
or
By clicking Continue to join or sign in, you agree to LinkedIn’s User Agreement, Privacy Policy, and Cookie Policy.
Licenses & Certifications
Languages
-
English
-
-
German
-
-
Persian
-
View Sepideh’s full profile
-
See who you know in common
-
Get introduced
-
Contact Sepideh directly
Other similar profiles
-
Roshan P. Morbia, MD, FACS
Roshan P. Morbia, MD, FACS
Owner | Founder | Plastic Surgeon, Virginia Plastic Surgery
Suffolk, VA -
M. Whitten Wise MD
M. Whitten Wise MD
Reconstructive Plastic Surgeon at Center for Restorative Breast Surgery
New Orleans, LA
Explore more posts
-
Dr. S.0 MIKAYE
Status Epilepticus (SE) Definition • A neurological emergency where seizures are: • Continuous for >5 minutes, OR • Recurrent without recovery of consciousness in between. (Old definition used >30 min, but >5 min is now accepted because prolonged seizures rarely stop spontaneously and cause brain damage.) Types 1. Convulsive SE (most common, tonic–clonic). 2. Non-convulsive SE (prolonged absence or focal seizures with impaired awareness). Causes (Precipitating Factors) • Poor adherence / withdrawal of antiepileptic drugs. • Stroke, brain tumor, trauma, CNS infection. • Hypoglycemia, electrolyte imbalance (Na⁺, Ca²⁺). • Alcohol withdrawal, drug overdose. • Idiopathic (in known epileptic patients). Clinical Features • Generalized convulsive SE: • Prolonged tonic–clonic movements. • Unconsciousness. • Tongue biting, frothing, incontinence. • Cyanosis, tachycardia, hypertension. • Non-convulsive SE: • Altered behavior, confusion, staring spells, subtle twitching. Complications if untreated: • Hypoxia, lactic acidosis. • Rhabdomyolysis, hyperthermia. • Arrhythmias, hypotension. • Neuronal injury → permanent brain damage, death. Management (Emergency Protocol) 1. ABCs (Airway, Breathing, Circulation): • Ensure airway, give oxygen. • Secure IV access. • Monitor vitals, blood glucose, electrolytes. 2. First-line (within 5 min): • IV benzodiazepines: Lorazepam 0.1 mg/kg IV (max 4 mg) OR • Diazepam 10 mg IV (can repeat once) OR • Midazolam IM if no IV access. 3. Second-line (if seizure persists >10–20 min): • IV antiepileptics: Phenytoin, Valproate, or Levetiracetam. • Alternative: Phenobarbital. 4. Refractory SE (if persists >30–60 min): • Continuous IV anesthetic infusion (midazolam, propofol, thiopental). • ICU admission, mechanical ventilation. 5. Treat underlying cause: • Correct hypoglycemia (give IV dextrose if needed). • Manage infection, stroke, trauma, electrolyte imbalance. Key Points to Remember • SE = seizure >5 min or repeated without recovery. • Always secure ABC first before drugs. • Benzodiazepines first-line, then longer-acting antiepileptics. • Can cause permanent brain damage if not controlled quickly.
98
4 Comments -
Dr. S.0 MIKAYE
Tramadol Class • Centrally acting analgesic. • Weak opioid agonist (μ-opioid receptors). • Also inhibits serotonin & norepinephrine reuptake → dual mechanism. Mechanism of Action 1. μ-opioid receptor agonism → weak opioid effect for pain relief. 2. Serotonin + norepinephrine reuptake inhibition → enhances descending pain inhibitory pathways. Uses • Moderate to moderately severe pain (postoperative, musculoskeletal, neuropathic). • Alternative in patients not tolerating NSAIDs or when stronger opioids not needed. • Sometimes used in chronic pain and neuropathic pain (with caution). Adverse Effects • Common: Nausea, vomiting, dizziness, constipation, sedation. • Serious: • Seizures (lowers seizure threshold). • Serotonin syndrome (esp. if combined with SSRIs, SNRIs, MAOIs). • Respiratory depression (less than morphine, but possible at high doses/with other depressants). • Dependence & withdrawal (lower risk than morphine, but still present). Contraindications • Epilepsy or history of seizures (risk ↑). • Concomitant use with MAO inhibitors, SSRIs, SNRIs → risk of serotonin syndrome. • Severe respiratory depression. • Head trauma (can increase intracranial pressure). Dose (adults) • 50–100 mg orally every 4–6 hours as needed. • Max: 400 mg/day (300 mg/day in elderly >75 years). • Extended-release forms available. Key Points for Exams • Acts on both opioid + monoaminergic systems. • Less potent than morphine. • Seizures & serotonin syndrome = major red flags. • Safer than NSAIDs in patients with gastric ulcers or renal impairment. • Can still cause dependence, so not risk-free. ✅ Memory Aid “Tra-MAD-ol” → May make patients MAD (seizures, serotonin syndrome, dependence).
76
1 Comment -
Dr. S.0 MIKAYE
🔹 Atropine Class: Anticholinergic (muscarinic receptor antagonist) Mechanism of action: • Blocks parasympathetic (vagal) effects by inhibiting acetylcholine at muscarinic receptors. • Leads to ↑ heart rate, ↓ secretions, relaxation of smooth muscles. Uses: • Bradycardia (emergency management of severe low heart rate) • Pre-anesthetic (reduce salivary/respiratory secretions) • Organophosphate poisoning (antidote) • Eye exams (mydriasis – pupil dilation) Side effects: (anticholinergic effects) • Dry mouth, blurred vision, constipation • Urinary retention • Tachycardia • Confusion (especially in elderly) Typical dose (bradycardia): • 0.5 mg IV every 3–5 minutes, up to 3 mg max 🔹 Adrenaline (Epinephrine) Class: Sympathomimetic (acts on α and β adrenergic receptors) Mechanism of action: • α1 stimulation: vasoconstriction → ↑ BP, ↓ mucosal swelling • β1 stimulation: ↑ heart rate, ↑ contractility • β2 stimulation: bronchodilation, ↓ allergic mediator release Uses: • Anaphylaxis (life-saving drug of choice) • Cardiac arrest (as part of ACLS protocol) • Severe asthma attack (when not responding to standard treatment) • Added to local anesthetics (to prolong action, reduce bleeding) Side effects: • Palpitations, tachycardia • Hypertension • Tremors, anxiety • Arrhythmias in high doses Typical doses: • Anaphylaxis: 0.3–0.5 mg IM (1:1000 solution), repeat every 5–15 min as needed • Cardiac arrest: 1 mg IV (1:10,000 solution) every 3–5 minutes during CPR ✨ Quick difference: • Atropine → blocks parasympathetic tone (used for bradycardia, secretions, poisoning). • Adrenaline → stimulates sympathetic system (used for anaphylaxis, cardiac arrest, severe asthma).
87
4 Comments -
Dr. S.0 MIKAYE
Structured overview of ways to correct hyperkalemia (high serum potassium >5.5 mmol/L): 🔹 1. Stabilize the Heart (Immediate – if ECG changes present) • IV Calcium gluconate (or calcium chloride) • Onset: 1–3 minutes, lasts 30–60 minutes • Does not lower K⁺, but stabilizes cardiac membranes and prevents arrhythmias 🔹 2. Shift Potassium into Cells (Temporary measures) • Insulin + glucose (e.g., 10 units regular insulin IV + 25–50 g glucose IV) • Onset: 15–30 minutes • β2-agonists (Salbutamol/albuterol nebulization or IV) • Onset: 30 minutes • Caution: may cause tachycardia • Sodium bicarbonate IV (especially if metabolic acidosis present) • Less effective, mainly in acidotic patients 🔹 3. Remove Potassium from the Body (Definitive measures) • Loop diuretics (e.g., furosemide) – if patient has adequate kidney function • Potassium binders • Sodium polystyrene sulfonate (Kayexalate) • Patiromer / Sodium zirconium cyclosilicate (newer, safer) • Dialysis (Hemodialysis or Peritoneal dialysis) • Most effective and rapid in severe/refractory hyperkalemia or renal failure 🔹 4. Supportive / Preventive Measures • Stop exogenous potassium (IV fluids, diet, drugs like spironolactone, ACE inhibitors) • Treat underlying cause (renal failure, rhabdomyolysis, hemolysis, acidosis) ✅ Summary (Stepwise Approach): 1. Stabilize heart → IV calcium 2. Shift K⁺ into cells → insulin + glucose, β-agonist, bicarbonate 3. Remove K⁺ → diuretics, binders, dialysis 4. Prevent recurrence → address underlying cause
185
-
Dr. S.0 MIKAYE
Jaundice 1. Definition • Jaundice = Yellowish discoloration of skin, sclera, and mucous membranes caused by elevated bilirubin in the blood (hyperbilirubinemia). • Clinically visible when serum bilirubin > 2–3 mg/dL. 2. Bilirubin Metabolism (Quick recap) 1. RBC breakdown → heme → unconjugated bilirubin (water-insoluble). 2. Transported to liver bound to albumin. 3. Liver: conjugation with glucuronic acid → conjugated bilirubin (water-soluble). 4. Excreted in bile → intestines → converted to urobilinogen & stercobilin (gives stool brown color). 5. Some reabsorbed, some excreted in urine. 3. Types of Jaundice A. Pre-hepatic (Hemolytic) • Due to increased bilirubin production (mostly unconjugated). • Causes: Hemolytic anemia, malaria, sickle cell disease, thalassemia, transfusion reaction. • Features: • Mild jaundice, no bilirubin in urine (since unconjugated not water-soluble). • Dark stools (↑ stercobilin). B. Hepatic (Hepatocellular) • Due to liver cell dysfunction → impaired conjugation & excretion. • Causes: Viral hepatitis, alcoholic hepatitis, cirrhosis, drugs, liver cancer. • Features: • Mixed ↑ conjugated & unconjugated bilirubin. • Dark urine (conjugated bilirubin present). • Pale stools possible. • Other liver failure signs (ascites, coagulopathy, encephalopathy). C. Post-hepatic (Obstructive/Cholestatic) • Due to bile duct obstruction → impaired bilirubin excretion. • Causes: Gallstones, pancreatic cancer, cholangiocarcinoma, biliary atresia, strictures. • Features: • Conjugated hyperbilirubinemia. • Dark urine (bilirubinuria). • Pale/clay-colored stools (no stercobilin). • Itching (pruritus) due to bile salt deposition. 4. Clinical Features • Yellow sclera (earliest sign). • Yellow skin & mucous membranes. • Associated symptoms depend on cause: • Fever, malaise (hepatitis). • Abdominal pain (gallstones, malignancy). • Weight loss (cancer). • Pruritus (cholestasis). 5. Investigations • Liver function tests (LFTs): • ↑ Unconjugated → hemolysis, hepatic dysfunction. • ↑ Conjugated → obstruction. • Urine test: Bilirubin, urobilinogen. • CBC, reticulocyte count → hemolysis. • Viral hepatitis serology. • Ultrasound abdomen → obstruction, gallstones, liver pathology. • CT/MRCP/ERCP if needed. 6. Management 👉 Depends on cause: • Hemolytic: Treat underlying hemolysis, blood transfusion if severe. • Hepatic: Antivirals (hepatitis), stop hepatotoxic drugs, supportive care. • Obstructive: Surgery or endoscopic removal of gallstones, stenting for tumors. • General: Hydration, nutrition, avoid hepatotoxins (alcohol, drugs). 7. Complications • Chronic liver disease → cirrhosis, portal hypertension. • Vitamin deficiencies (fat-soluble A, D, E, K). • Coagulopathy (due to ↓ vitamin K absorption). • Hepatic encephalopathy.
56
1 Comment -
Dr. S.0 MIKAYE
Diabetes Insipidus (DI) and Syndrome of Inappropriate Antidiuretic Hormone (SIADH): 🧪 1. Diabetes Insipidus (DI) Definition: A disorder caused by lack of antidiuretic hormone (ADH) or resistance to its effect, leading to excessive loss of dilute urine and dehydration. 🔹 Types: • Central DI – deficiency of ADH (posterior pituitary problem) • Nephrogenic DI – kidneys do not respond to ADH 🔹 Causes: • Central: head injury, brain tumors, pituitary surgery • Nephrogenic: kidney disease, lithium use, genetic 🔹 Symptoms: • Excessive urination (polyuria) • Excessive thirst (polydipsia) • Dehydration • Dilute urine with low specific gravity 🔹 Lab findings: • High serum sodium (hypernatremia) • Low urine osmolality • High serum osmolality 🔹 Treatment: • Central: Desmopressin (DDAVP) • Nephrogenic: thiazide diuretics, low-salt diet, treat cause 💧 2. Syndrome of Inappropriate ADH (SIADH) Definition: Excessive release or action of ADH, causing water retention, dilution of blood sodium, and concentrated urine. 🔹 Causes: • Brain injury, stroke, infection (e.g., meningitis) • Lung cancer (especially small-cell carcinoma) • Certain drugs (SSRIs, carbamazepine, vincristine) 🔹 Symptoms: • Nausea, vomiting • Headache • Confusion or seizures (due to low sodium) • Reduced urine output 🔹 Lab findings: • Low serum sodium (hyponatremia) • High urine osmolality • Low serum osmolality 🔹 Treatment: • Fluid restriction • Hypertonic saline (for severe cases) • Demeclocycline or vasopressin receptor antagonists in chronic cases 📌 Key Differences: Feature DI SIADH ADH Low or ineffective Excessive Sodium High Low Urine output High (polyuria) Low Urine osmolality Low (dilute) High (concentrated) Treatment Desmopressin or supportive Fluid restriction, correct sodium
109
6 Comments -
Dr. S.0 MIKAYE
Congestive Heart Failure (CHF) CHF is a chronic, progressive condition where the heart is unable to pump blood effectively to meet the body’s needs, leading to congestion (fluid buildup) in the lungs and/or other parts of the body. It can result from structural or functional heart disorders that impair ventricular filling or ejection of blood. Causes • Coronary artery disease (most common) • Hypertension (long-term high blood pressure) • Valvular heart disease (e.g., aortic or mitral valve defects) • Cardiomyopathy (dilated, hypertrophic, or restrictive) • Arrhythmias • Post-myocardial infarction damage Types 1. Left-sided heart failure • Systolic failure: Reduced ejection fraction (HFrEF) due to poor contraction. • Diastolic failure: Preserved ejection fraction (HFpEF) due to stiff ventricle with poor filling. 2. Right-sided heart failure • Often secondary to left-sided failure or lung diseases (cor pulmonale). 3. Biventricular failure • Both sides affected. Pathophysiology • Reduced cardiac output → activation of compensatory mechanisms (RAAS, sympathetic nervous system) → fluid retention and increased afterload → worsening heart function. • Backward failure → congestion in lungs (left-sided) or systemic veins (right-sided). • Forward failure → inadequate tissue perfusion. Symptoms Left-sided failure • Dyspnea on exertion • Orthopnea (breathlessness when lying flat) • Paroxysmal nocturnal dyspnea • Fatigue, exercise intolerance Right-sided failure • Peripheral edema • Ascites • Hepatomegaly • Jugular venous distension Signs • Tachycardia, hypotension (late stages) • Crackles in lungs • S3 gallop • Pitting edema • Cool extremities Complications • Pulmonary edema • Arrhythmias • Renal impairment • Cardiogenic shock • Death Diagnosis • History & physical exam • Chest X-ray: Cardiomegaly, pulmonary congestion • Echocardiography: Ejection fraction, wall motion abnormalities • BNP or NT-proBNP: Elevated in heart failure • ECG: Arrhythmias, ischemic changes Management Non-pharmacologic • Low-sodium diet • Fluid restriction (in some cases) • Weight monitoring • Physical activity as tolerated Pharmacologic • ACE inhibitors / ARBs / ARNI (sacubitril–valsartan) • Beta-blockers (e.g., carvedilol, metoprolol succinate) • Diuretics (for symptom relief of congestion) • Mineralocorticoid receptor antagonists (spironolactone) • SGLT2 inhibitors (dapagliflozin, empagliflozin) • Ivabradine (selected patients) Advanced • Implantable cardioverter-defibrillator (ICD) • Cardiac resynchronization therapy • LV assist devices • Heart transplant Prognosis • Progressive but manageable with early intervention • Prognosis depends on cause, severity, comorbidities, and adherence to treatment
61
1 Comment -
Dr. S.0 MIKAYE
Cardioselective Beta Blockers 1. Definition • β1-selective blockers that predominantly block β1 receptors in the heart (↓ HR, ↓ contractility, ↓ cardiac output) with less effect on β2 receptors in bronchi and peripheral vessels. • Called cardioselective because they are safer in patients with asthma, COPD, and peripheral vascular disease, though selectivity is dose-dependent (lost at higher doses). 2. Examples • Atenolol • Metoprolol (tartrate, succinate) • Bisoprolol • Esmolol (short-acting, IV) • Nebivolol (also causes NO-mediated vasodilation) • Acebutolol (has partial agonist activity) 3. Mechanism of Action • Block β1 receptors in the heart → • ↓ Heart rate (negative chronotropy) • ↓ Contractility (negative inotropy) • ↓ Conduction through AV node (negative dromotropy) • ↓ Renin release from kidneys (helps in hypertension). 4. Indications • Hypertension (especially with comorbid heart disease). • Angina pectoris (reduce myocardial O₂ demand). • Myocardial infarction (reduce mortality). • Heart failure (bisoprolol, metoprolol succinate, carvedilol—though carvedilol is nonselective). • Arrhythmias (SVT, AF rate control, PVCs). • Thyrotoxicosis (control symptoms). • Migraine prophylaxis (metoprolol). 5. Side Effects • Bradycardia, AV block. • Hypotension. • Fatigue, dizziness. • Worsening of acute heart failure (if started abruptly or in decompensated state). • Can still cause bronchospasm at high doses. • Mask symptoms of hypoglycemia (caution in diabetics). 6. Contraindications • Severe bradycardia, heart block. • Acute decompensated heart failure. • Severe asthma or COPD (relative, especially at high doses). • Peripheral arterial disease (relative). ✅ Summary: Cardioselective β-blockers (β1 blockers) like atenolol, metoprolol, bisoprolol, and esmolol mainly act on the heart with fewer bronchial and vascular side effects. They are widely used in hypertension, angina, arrhythmias, MI, and heart failure but must be used cautiously in patients with bradycardia, severe asthma, or heart block.
61
1 Comment -
Dr. S.0 MIKAYE
Pulmonary Oedema • Definition: Accumulation of fluid within the lung interstitium and alveoli. • Causes: • Cardiogenic (commonest): Left-sided heart failure, hypertension, valvular heart disease, myocardial infarction. • Non-cardiogenic: ARDS, sepsis, high altitude, toxins, renal failure. • Pathophysiology: Increased hydrostatic pressure (cardiogenic) or increased capillary permeability (non-cardiogenic) → fluid leaks into alveoli → impaired gas exchange. • Symptoms: • Severe shortness of breath, especially when lying flat (orthopnea). • Pink frothy sputum (classic). • Cough, wheeze, rapid breathing. • Signs: • Fine inspiratory crackles (rales) at lung bases. • Tachypnea, hypoxia, cyanosis. • Signs of left heart failure (raised JVP, gallop rhythm). • Investigations: • Chest X-ray: “Bat-wing” or perihilar opacities, Kerley B lines. • Echocardiography for cardiac cause. • Treatment: • Oxygen. • Diuretics (e.g. furosemide). • Vasodilators (nitrates). • Treat underlying cause (heart failure, sepsis, etc.). Pleural Effusion • Definition: Accumulation of fluid in the pleural space (between lung and chest wall). • Causes: • Transudative: Heart failure, nephrotic syndrome, cirrhosis. • Exudative: Pneumonia, TB, malignancy, pulmonary embolism. • Pathophysiology: Imbalance between pleural fluid formation and absorption (↑ hydrostatic pressure, ↓ oncotic pressure, or ↑ capillary permeability). • Symptoms: • Progressive shortness of breath. • Pleuritic chest pain. • Dry cough. • Signs: • Reduced breath sounds. • Stony dull percussion note. • Reduced chest expansion on affected side. • Decreased tactile fremitus. • Investigations: • Chest X-ray: Blunting of costophrenic angle, meniscus sign. • Ultrasound: Detects small effusions, guides aspiration. • Pleural fluid analysis (protein, LDH, cytology, cultures) → Light’s criteria to differentiate transudate vs exudate. • Treatment: • Therapeutic aspiration / chest drain if large or symptomatic. • Treat underlying cause (e.g. antibiotics for pneumonia, diuretics for heart failure, anti-TB drugs, chemo for malignancy). ✅ Key Difference: • Pulmonary oedema → fluid inside alveoli/lung tissue → mainly cardiac-related → crackles. • Pleural effusion → fluid outside lung (pleural space) → compresses lung → stony dullness and reduced breath sounds.
90
7 Comments -
Dr. S.0 MIKAYE
💊 Metformin 1. Class • Oral antihyperglycemic agent (biguanide). • First-line drug for Type 2 Diabetes Mellitus (T2DM). 2. Mechanism of Action • ↓ Hepatic glucose production (inhibits gluconeogenesis). • ↑ Insulin sensitivity in peripheral tissues (especially muscles). • ↓ Intestinal absorption of glucose. • Does not stimulate insulin secretion (so low risk of hypoglycemia). 3. Indications • Type 2 Diabetes Mellitus (first-line). • Sometimes in PCOS (Polycystic Ovary Syndrome) for improving insulin resistance and ovulation. • May be used in metabolic syndrome, pre-diabetes, and obesity (off-label). 4. Dosage (Adults) • Usual starting dose: 500 mg once or twice daily with meals. • Titrated gradually to reduce GI side effects. • Maintenance dose: 1500–2000 mg/day (max ~2550 mg/day depending on formulation). 5. Side Effects • Common: GI upset (nausea, vomiting, diarrhea, abdominal discomfort, metallic taste). • Serious (rare): Lactic acidosis (especially in renal/hepatic impairment, alcoholism, or hypoxia). • Long-term: ↓ Vitamin B12 absorption → risk of deficiency. 6. Contraindications • Severe renal impairment (eGFR < 30 mL/min/1.73 m²). • Acute/chronic metabolic acidosis (e.g., DKA). • Severe liver disease, alcoholism, or conditions predisposing to hypoxia (e.g., heart failure, respiratory failure). 7. Advantages • Weight neutral or slight weight loss. • Low risk of hypoglycemia. • Cardiovascular protection (shown in studies like UKPDS). ✅ Summary: Metformin is the first-line oral drug for T2DM, effective, safe, and affordable. Its main drawbacks are GI side effects and rare lactic acidosis.
62
1 Comment -
Dr. S.0 MIKAYE
🔹 Definition Ischemic Heart Disease is a condition where there is reduced blood supply (ischemia) to the heart muscle due to narrowing or blockage of the coronary arteries, usually from atherosclerosis (fatty plaque buildup). 🔹 Causes / Risk Factors 1. Non-modifiable: • Age (older age) • Male gender (higher risk, though risk increases in women after menopause) • Family history of premature heart disease 2. Modifiable: • Hypertension • Diabetes mellitus • Smoking • High cholesterol (↑ LDL, ↓ HDL) • Obesity • Sedentary lifestyle • Excessive alcohol intake • Stress 🔹 Types of Ischemic Heart Disease 1. Stable Angina – chest pain with exertion, relieved by rest or nitroglycerin. 2. Unstable Angina – chest pain at rest, unpredictable, medical emergency. 3. Myocardial Infarction (Heart Attack) – prolonged ischemia causing permanent heart muscle damage. 4. Silent Ischemia – no symptoms, but reduced blood supply seen on tests. 5. Sudden Cardiac Death – usually from severe arrhythmia due to ischemia. 🔹 Symptoms • Chest pain or pressure (angina) radiating to left arm, jaw, back. • Shortness of breath. • Fatigue, sweating, nausea. • Palpitations. • In silent cases (esp. diabetics, elderly) – minimal or no symptoms. 🔹 Complications • Heart failure • Arrhythmias (e.g., ventricular fibrillation) • Myocardial infarction • Sudden cardiac death 🔹 Diagnosis • ECG (resting & stress test) • Echocardiography • Cardiac enzymes (Troponins, CK-MB) in MI • Coronary angiography (gold standard) • CT coronary angiogram 🔹 Management 1. Lifestyle modification • Stop smoking • Healthy diet (low saturated fats, high fiber, fruits, vegetables) • Exercise (as tolerated) • Weight reduction • Stress management 2. Medications (main pillars) • Antiplatelets (Aspirin, Clopidogrel) • Beta-blockers (Metoprolol, Atenolol) • Nitrates (Nitroglycerin) • Statins (Atorvastatin, Rosuvastatin) • ACE inhibitors / ARBs (for BP, heart protection) 3. Interventional / Surgical • Percutaneous Coronary Intervention (PCI) – angioplasty + stent • Coronary Artery Bypass Grafting (CABG) – open-heart surgery ✅ Summary: Ischemic Heart Disease is the leading cause of death worldwide. Prevention through lifestyle modification and risk factor control is as important as treatment.
157
3 Comments -
Dr. S.0 MIKAYE
Gout vs. Pseudogout Gout • Definition: A type of arthritis caused by deposition of monosodium urate crystals in joints due to hyperuricemia. • Common Sites: Big toe (1st metatarsophalangeal joint), ankle, knee. • Causes/Risk Factors: • High uric acid (diet rich in red meat, alcohol, seafood). • Kidney disease (decreased uric acid excretion). • Obesity, hypertension, diuretics, chemotherapy. • Symptoms: • Sudden, severe joint pain (often at night). • Redness, swelling, warmth of joint. • Recurrent attacks if untreated. • Diagnosis: • Synovial fluid analysis: needle-shaped, negatively birefringent crystals under polarized light. • Elevated serum uric acid (may be normal during an acute attack). • Treatment: • Acute attack: NSAIDs (indomethacin), colchicine, corticosteroids. • Long-term: Allopurinol or febuxostat (uric acid lowering), lifestyle modification. Pseudogout (Calcium Pyrophosphate Deposition Disease – CPPD) • Definition: Arthritis caused by deposition of calcium pyrophosphate dihydrate (CPPD) crystals in the joints. • Common Sites: Knee, wrist, shoulder, ankle. • Causes/Risk Factors: • Aging (most common in elderly). • Joint trauma, osteoarthritis. • Metabolic disorders (hemochromatosis, hyperparathyroidism, hypomagnesemia). • Symptoms: • Sudden joint pain, swelling, redness (resembles gout). • Chronic joint stiffness and pain in some cases. • Diagnosis: • Synovial fluid: rhomboid-shaped, positively birefringent crystals. • X-ray: Chondrocalcinosis (calcification of cartilage). • Treatment: • NSAIDs, colchicine (less effective than in gout). • Corticosteroid injections for severe flares. • No specific crystal-lowering therapy
40
-
Dr. S.0 MIKAYE
Deep Venous Thrombosis (DVT) is the formation of a blood clot (thrombus) in the deep veins, usually of the legs (calf, femoral, popliteal, iliac), but sometimes in the upper limbs. It’s dangerous because it can lead to pulmonary embolism (PE). 🔹 Risk Factors (Virchow’s Triad) 1. Venous stasis • Prolonged immobility (bed rest, long flights, casts) • Heart failure • Obesity 2. Endothelial injury • Trauma, surgery • Central venous catheters • IV drug use 3. Hypercoagulability • Pregnancy, postpartum, OCPs, HRT • Malignancy • Thrombophilias (Factor V Leiden, Protein C/S deficiency) • Dehydration 🔹 Clinical Features • Swelling (usually unilateral leg) • Pain, tenderness (often calf) • Warmth & redness • Dilated superficial veins • Homan’s sign (calf pain on dorsiflexion) – not reliable, rarely used now ⚠️ Many DVTs are asymptomatic until complication develops. 🔹 Complications • Pulmonary embolism (PE) → sudden dyspnea, chest pain, hemoptysis • Post-thrombotic syndrome → chronic leg swelling, pain, ulcers • Recurrent DVT 🔹 Diagnosis • Clinical prediction: Wells’ score • D-dimer test (sensitive, not specific; good to rule out) • Duplex Doppler ultrasound (first-line) • Venography (gold standard, rarely used) • CT/MR venography (when ultrasound is inconclusive) 🔹 Management 1. General Measures • Bed rest with limb elevation (acute phase) • Compression stockings (to prevent post-thrombotic syndrome) 2. Anticoagulation (cornerstone of treatment) • Initial: Low molecular weight heparin (LMWH), unfractionated heparin, or fondaparinux • Long-term: Oral anticoagulants (warfarin, DOACs like rivaroxaban, apixaban) • Duration: • First episode, provoked → 3 months • Unprovoked or recurrent → ≥6 months or lifelong 3. Thrombolysis / Thrombectomy • Selected cases: massive iliofemoral DVT with threatened limb 4. Inferior Vena Cava (IVC) filter • If anticoagulation contraindicated or recurrent PE despite therapy 🔹 Prevention • Early mobilization after surgery • Prophylactic LMWH in high-risk patients • Compression stockings during travel/immobility • Adequate hydration ✅ Key Point: DVT is dangerous not just because of local symptoms but mainly because of the risk of pulmonary embolism, which can be fatal. Early recognition, anticoagulation, and prevention are critical.
80
-
Dr. S.0 MIKAYE
🔹 What are Benzodiazepines? • A class of psychoactive drugs that enhance the effect of the neurotransmitter GABA (gamma-aminobutyric acid) at the GABA-A receptor. • They produce sedative, anxiolytic, muscle relaxant, and anticonvulsant effects. 🔹 Common Examples • Diazepam (Valium) • Lorazepam (Ativan) • Alprazolam (Xanax) • Clonazepam (Klonopin) • Midazolam (short-acting, used in anesthesia) 🔹 Clinical Uses • Anxiety disorders (short-term relief) • Insomnia (short-term use) • Seizures & epilepsy (e.g., status epilepticus) • Alcohol withdrawal (to prevent seizures, agitation) • Pre-anesthetic / procedural sedation • Muscle spasms 🔹 Side Effects • Sedation, drowsiness, dizziness • Impaired memory and concentration • Dependence and tolerance with long-term use • Withdrawal symptoms if stopped abruptly • Respiratory depression (especially when combined with alcohol or opioids) 🔹 Contraindications & Precautions • History of substance abuse • Severe respiratory disease (e.g., COPD, sleep apnea) • Elderly patients (risk of falls, confusion) • Pregnancy (risk of congenital malformations, floppy infant syndrome) 🔹 Key Point Benzodiazepines are effective but risky if misused. They’re best for short-term management of acute conditions, not long-term daily use, due to dependence and withdrawal risks.
92
-
Dr. S.0 MIKAYE
Opioids Definition • Opioids are a class of drugs (natural, semi-synthetic, or synthetic) that act on opioid receptors in the central and peripheral nervous system to produce pain relief, sedation, and euphoria. • They include both opiates (natural from opium, e.g., morphine, codeine) and synthetic analogues (e.g., fentanyl, methadone). 1. Mechanism of Action • Bind to opioid receptors (µ, κ, δ): • Mu (µ) receptor → analgesia, euphoria, respiratory depression, physical dependence. • Kappa (κ) receptor → analgesia, sedation, dysphoria. • Delta (δ) receptor → analgesia, mood regulation. • Result: ↓ neurotransmitter release, ↓ pain transmission. 2. Common Examples • Natural: Morphine, Codeine. • Semi-synthetic: Heroin, Oxycodone, Hydromorphone. • Synthetic: Fentanyl, Methadone, Tramadol, Pethidine (Meperidine), Buprenorphine. 3. Clinical Uses • Analgesia (moderate to severe pain: trauma, post-op, cancer pain). • Cough suppression (codeine, dextromethorphan). • Diarrhea treatment (loperamide, diphenoxylate). • Anesthesia adjunct (fentanyl, remifentanil). • Opioid dependence treatment (methadone, buprenorphine). 4. Side Effects • CNS: Sedation, dizziness, confusion, euphoria. • Respiratory: Respiratory depression (major cause of death in overdose). • GI: Constipation, nausea, vomiting. • Other: Miosis (pinpoint pupils), itching, urinary retention, hypotension. 5. Tolerance, Dependence & Withdrawal • Tolerance: Need higher doses with repeated use. • Dependence: Physiological adaptation; abrupt stop → withdrawal. • Withdrawal symptoms: Anxiety, sweating, runny nose, muscle aches, yawning, diarrhea, piloerection (“cold turkey”). 6. Overdose • Signs: Respiratory depression, coma, pinpoint pupils, hypotension, bradycardia. • Treatment: Naloxone (opioid receptor antagonist, rapid reversal). 7. Contraindications / Caution • Respiratory disease (COPD, asthma, sleep apnea). • Head injury (↑ CO₂ retention → ↑ ICP). • History of substance abuse. • Pregnancy (risk of neonatal respiratory depression & withdrawal). ✅ Summary: Opioids are powerful analgesics that work on opioid receptors to reduce pain and produce sedation. While essential in pain management, they carry major risks: respiratory depression, tolerance, dependence, and withdrawal. Naloxone is the antidote for overdose.
69
1 Comment -
Dr. S.0 MIKAYE
Dura-based tumors are tumors that arise from, or are attached to, the dura mater (the tough outer covering of the brain and spinal cord). They can be primary (originating from the dura itself) or secondary (metastatic or locally invading from nearby structures). Common Dura-Based Tumors 1. Meningioma • Most common dura-based tumor. • Usually benign, slow-growing. • Arises from arachnoid cap cells attached to the dura. • Can cause mass effect and seizures. • Imaging: extra-axial, well-circumscribed lesion, often with a “dural tail” sign on MRI with contrast. 2. Hemangiopericytoma / Solitary Fibrous Tumor • Rare, aggressive tumors that can mimic meningiomas. • Tend to recur and metastasize. 3. Metastases to the dura • From breast, prostate, lung, kidney, or melanoma. • Often multifocal. • May present with subdural spread (“carcinomatous meningitis”). 4. Lymphoma (Primary dural lymphoma) • Rare. • Can mimic meningioma radiologically. 5. Other rare types • Sarcomas • Plasmacytoma (solitary form of multiple myeloma) • Dural chondrosarcoma or osteosarcoma (rare) Key Radiological Features (especially on MRI/CT) • Extra-axial location (outside the brain parenchyma). • Broad dural base of attachment. • Dural tail sign (seen in meningioma, but not pathognomonic). • Mass effect on adjacent brain parenchyma.
35
-
Dr. S.0 MIKAYE
Gamma-Glutamyl Transferase (GGT) Overview • Definition: GGT is an enzyme found mainly in the liver, but also in the kidneys, pancreas, and bile ducts. • Function: It helps in the transfer of gamma-glutamyl groups between molecules, playing a role in amino acid transport and glutathione metabolism. • Clinical importance: GGT is a sensitive marker of bile duct function and alcohol-related liver injury. Normal Reference Range (Values may vary slightly depending on the lab) • Men: 8–61 U/L • Women: 5–36 U/L Clinical Uses 1. Detection of liver and bile duct disease • Elevates in cholestasis, biliary obstruction, hepatitis, cirrhosis. 2. Alcohol abuse marker • Highly sensitive to chronic alcohol intake (even before symptoms appear). 3. Differentiate source of alkaline phosphatase (ALP) elevation • If ALP ↑ + GGT ↑ → liver or bile duct origin. • If ALP ↑ + GGT normal → bone origin. 4. Monitor recovery in alcoholic liver disease (falls after abstinence). Causes of Elevated GGT • Liver disease: • Hepatitis (viral, alcoholic, toxic) • Cirrhosis • Biliary obstruction (gallstones, tumors) • Alcohol consumption (even moderate intake can increase GGT) • Medications: • Phenytoin • Phenobarbital • NSAIDs • Some antibiotics • Pancreatic disease • Congestive heart failure (secondary liver congestion) Key Points for Interpretation • Sensitive but not specific → GGT rises in many liver conditions, so it must be interpreted alongside other liver function tests (LFTs). • Best use: • Confirm liver/biliary origin of ALP elevation. • Detect alcohol-induced liver damage.
42
2 Comments -
Dr. S.0 MIKAYE
Statins – Cholesterol-lowering drugs that inhibit cholesterol synthesis in the liver. Mechanism of Action • Inhibit HMG-CoA reductase (the rate-limiting enzyme in the cholesterol synthesis pathway) • This lowers LDL cholesterol production • Increases LDL receptor expression on liver cells → more LDL removed from the blood Examples • Atorvastatin • Simvastatin • Rosuvastatin • Pravastatin • Lovastatin Uses 1. Hyperlipidemia – especially high LDL 2. Prevention of cardiovascular disease • Secondary prevention (post–heart attack or stroke) • Primary prevention in high-risk patients 3. Familial hypercholesterolemia Benefits • Lower LDL cholesterol (20–60%) • Mildly increase HDL cholesterol • Reduce triglycerides • Reduce risk of heart attack, stroke, and death from cardiovascular causes Side Effects • Common: headache, nausea, constipation, mild muscle aches • Serious but rare: • Myopathy → can progress to rhabdomyolysis (muscle breakdown → kidney injury) • Liver enzyme elevation (monitor liver function) • New-onset diabetes (small risk) Contraindications • Active liver disease • Pregnancy & breastfeeding • Caution in heavy alcohol users Monitoring • Baseline liver function tests (LFTs) before starting • Creatine kinase (CK) if muscle symptoms occur • Lipid profile after 4–12 weeks, then every 3–12 months Key Counseling Points • Take preferably at night (for short-acting statins like simvastatin) since cholesterol synthesis is higher overnight • Avoid grapefruit juice (especially with simvastatin, atorvastatin) — can increase statin levels and risk of toxicity • Report any unexplained muscle pain, weakness, or dark urine immediately
56
4 Comments -
Dr. S.0 MIKAYE
Phenytoin • Class: Antiepileptic drug (AED). • Mechanism of action: • Blocks voltage-gated sodium channels in neurons → stabilizes neuronal membranes → prevents repetitive firing. Pharmacokinetics • Oral and IV forms. • Nonlinear kinetics (small dose changes → large changes in serum level). • Highly protein bound. • Metabolized in the liver (CYP450 inducer → interacts with many drugs). • Narrow therapeutic range (10–20 µg/mL). Uses • Generalized tonic-clonic seizures. • Focal (partial) seizures. • Status epilepticus (IV, but usually lorazepam/diazepam first, then phenytoin for maintenance). • Cardiac arrhythmias (rare use, class IB antiarrhythmic). Adverse Effects Dose-related (toxic): • Nystagmus. • Ataxia. • Diplopia, dizziness. • Confusion, sedation. Chronic use: • Gingival hyperplasia (classic exam question). • Hirsutism. • Coarsening of facial features. • Megaloblastic anemia (↓ folate). • Osteopenia/osteoporosis (↑ vitamin D metabolism). • Peripheral neuropathy. Serious reactions: • Stevens–Johnson syndrome, toxic epidermal necrolysis. • Hepatotoxicity. • Blood dyscrasias (agranulocytosis, aplastic anemia). • Teratogenicity: Fetal hydantoin syndrome (cleft lip/palate, congenital heart defects, growth deficiency, developmental delay). Monitoring • Serum phenytoin levels (due to narrow therapeutic index). • CBC, liver function tests, vitamin D status (long-term). Contraindications • Pregnancy (teratogenic, but sometimes used if benefits outweigh risks). • Caution with hepatic impairment. 👉 Key point to remember: Phenytoin = Na⁺ channel blocker, effective in seizures, but causes gingival hyperplasia, hirsutism, teratogenicity, and narrow therapeutic i
28
2 Comments
Explore top content on LinkedIn
Find curated posts and insights for relevant topics all in one place.
View top content