طب عام (سنة سادسة)⛧

هذه قناة أشرح بيها مادة الاطفال الفكرة هي نسوي ذاكرة صورية ، لأن أشوف هاي الطريقة من أكثر الطرق الي تساعد على التذكر . كل هاي الصور ما جاية من مكان واحد ، وإنما دا أجمع المعلومات من المحاضرات النوتات ملاحظات الدكاترة الأسئلة الوزارية وكل شغلة مريت عليها أثناء الدراسة واسفل كل صوره دازيلكم شرح وتوضيح والاسئله المهمه وافكار عن كل موضوع ... وبشكل مجاني 🔽🔽 https://t.me/RM_01pediatric

قد زين الأشعار اسم المصطفى وبــه علا بين الورى الإبـــداعُ..

يتسابقون بمدحهم لشفيعهم في شعرهم يشدو به الإجماعُ..

هيَّا معي حيّوا الفضيل تحيةً حتى تسرّ من اللقـــاء بقـــاعُ..

درب التوسط لا غلوٌ أو جفا إذ يقتدي في فعله الأتبــــاعُ..

فصلاتنا وسلامنا صوب الهدى في طيبة العظمى هناك مُذاعُ..ﷺ

﴿‏اللَّهُمَّ صَلِّ وَسَلِّمْ وَبَارِكْ عَلَى سَيِّدُنَا مُحَمَّدٍ وعلى آله ﷺ ﴾.. *🌹💓صلوا على الحبيب💓🌹* ✍🏻💚🕊️🌴

🔴Gastroenteritis (GE) & Dehydration

▪︎Clinical Syndrome Of Diarrhea & Vomiting Due To Infectious & Inflammatory Process Affect The GIT

🔹Types Of Diarrhea

📍1. Acute ➡️ Acute Onset Of Excessive Loose Stool (>10ml/Kg/Day in Infants & >200g/24h in Older Children) For <14 Days 📍2. Chronic (Persistent) ➡️ Acute Episode Of Diarrhea Persist >14 Days 📍3. Secretary ➡️ Direct Stimulation Of Intestinal Mucosa To Secrets Fluids & Electrolytes Into The Bowel Lumen (Mostly Due To Cholera Toxins) ▪︎Stool Volume >200ml/Day ▪︎Na Content >70mEq/L ▪︎Ph >5 📍4. Osmotic ➡️ Malabsorption Of Ingested Substances Causing Water Pulling From intestinal Walls Into The Lumen (Mostly Due To Lactose Intolerance/Laxatives) ▪︎Stool Volume <200ml/Day ▪︎Na Content <70mEq/L ▪︎Ph <5 ▪︎Diarrhea Resolve By Stops Feeding ▪︎+Ve Reducing Substances 👇 هذي مواد لها القدرة على امتصاص الماء من جدران الخلايا (وجودها بالستول معناه ان الدياريا اوزموتك)

🔹Causes Of GE

📍1. Viral ➡️ Mostly Occur in Winter/Mild & Self Limited in 3-7 Days/Watery/With Low Grade Fever ▪︎RotaVirus ➡️ Most Common Cause Of Diarrhea In Children ▪︎NoroVirus ➡️ Most Common Cause Of Gastroenteritis Outbreaks (Highly Contagious) & Occurs At Any Age 📍2. Bacterial ➡️ More in Summer/With Cramping Abdominal Pain & High Grade Fever/Severe in Nature ▪︎Bloody (Dysentery Due To Colon & Rectum Involvement) : •Salmonella/Shigella •Enterohaemorrhagic & Invasive E.coli •C.Difficile (After Antibiotics) •Yersinia ▪︎Watery (Secretary) : •Cholera •EnteroPathogenic & Toxigenic (Traveller's Diarrhea) E.coli •Food Poisoning (Staph/Bacillus/C.Perfringens) ▪︎Start Watery Then Becomes Bloody ➡️ Campylobacter Jejuni (Most Common Cause Of Bacterial Gastroenteritis) 📍3. Protozoal ▪︎Giardia ➡️ Offensive Watery Diarrhea/Abdominal Pain & Distension & Bloating/Malabsorption (Resemble Celiac)/Secondary Lactose Intolerance & Weight Loss ▪︎Entamoeba Histolytica (Amoebiasis) ➡️ Bloody Offensive Diarrhea With Mucous & Tenesmus & RLQ Abdominal Pain (Mimic Appendicitis) & Flask Shape Ulcers

🔹Complications

1. Dehydration ➡️ Main Cause Of Death 2. Hypovolaemic & Septic Shock 3. Acute Renal Failure (Due To Renal Hypoperfusion) 4. Metabolic Acidosis (Due To Bicarbonate Loss in Stool Or Acute Renal Failure) 5. Electrolytes Disturbances ▪︎Low K ➡️ Paralytic Ileus/Hypotonia/Apathy/Arrhythmia ▪︎Low Ca ➡️ Tetany & Convulsions ▪︎Low Or High Na & Hypoglycemia ➡️ Convulsions 6. Bleeding (DIC & Sepsis)/Persistent Diarehea 7. Hemolytic Uremic Syndrome (By Enterohemorrhagic E.Coli)

🔹DDX

1. Coeliac Disease/Cow's Milk Allergy 2. Acute Appendicitis/Pyloric Stenosis/Hirschsprung's/Intussusception/Necrotizing Enterocolitis 3. DKA/Hemolytic Uremic Syndrome 4. Hepatitis A/UTI/Respiratory Infection/Otitis Media/Meningitis/Septicaemia

🔹Mx ➡️ Supportive

📍1. Correct Dehydration 📍2. AB If Indicated ➡️ Bloody Diarehea/Cholera/Protozoa/Severe Malnutrition/Toxic Febrile Child/Age <3m/Associated Pneumonia ▪︎Ciprofloxacin ➡️ Salmonella/Shigella/Yersinia ▪︎Vancomycin/Metronidazole/Fidaxomicin ➡️ C.Difficile ▪︎Tetracycline/Doxycycline/Ciprofloxacin ➡️ Cholera ▪︎Metronidazole ➡️ Protozoa 📍3. Continue Feeding 📍4. Zinc Supplements (10-20mg For 10-14 Days) ..... Most Common Viral GE ➡️ RotaVirus Most Common Bacterial GE ➡️ Campylobacter Jejuni Malabsorption ➡️ Giardia Flask Shape Ulcer/Resemble Appendicitis ➡️ Entamoebia Histolytica Topic of the day is #Gastroenteritis @Clinicalpediatricround

🔴Cerebral Palsy (CP)

▪︎It's A Group Of Permanent Neurological Dysfunctions Arise From Structural Abnormalities in The Developing Brain Of The Baby Before Or After Birth

▪︎It's The Most Common Cause Of Motor Impairment in Children ▪︎Usually Dx At Age Of 18m After Delayed in The Motor Development ▪︎Characterized By :

📍1. Permanent Non-Progressive Dysfunction (But Changing)

يعني يبقى على حاله لا يسوء اكثر ولا يتحسن بس شوية تصير اختلافات بمرور الوقت

📍2. Usually Affects Motor Functions (Movement & Posture Impairment Due To Dysfunction in Motor Centres Like Cerebral Cortex/Cerebellum/Basal Ganglia)

📍3. Associated With Mental Retardation/Behavioural & Emotional Disturbances/Vision & Hearing Impairment/Epilepsy

🔷Causes & Risk Factors Of CP 🔸A. During Pregnancy (Pre-Natal 80%) :

📍1. Congenital Causes (Congenital Brain Malformations/Congenital Infections TORCH/Genetic Syndromes) 📍2. Maternal Risk Factors (Low Socioeconomic State/Seizures/Eclampsia/Diabetes & Hypertension/Drugs/Bleeding/Infection/Polyhydramnios/Abnormal Fetal Presentation/Multiple Births)

🔸B. During Birth (Natal Or Peri-Natal 10%) :

📍1. Low Birth Weight & Prematurity 📍2. Hypoxia Ischemic Encephalopathy (HIE Most Important) 📍3. Birth Trauma

🔸C. After Birth (Post-Natal 10%) :

📍1. Meningitis & Head Trauma (Most Common Cause Of Acquired CP) 📍2. Other Causes : ▪︎Encephalitis ▪︎Hypoglycemia ▪︎Hyperbilirubinemia (Kernicterus) ▪︎Hydrocephalus ▪︎Inborn Errors Of Metabolism (PKU) ▪︎IntraVentricular Haemorrhage in VLBW Infants

🔷Types Of CP 🔸A. According To Site Of Body Involvement

📍1. HemiParesis (HemiPlegia) ➡️ Motor Impairment Of One Side Of The Body (Unilateral Impairment Of Arm & Leg On The Same Side) 📍2. DiPlegia ➡️ Motor Impairment Of The Lower Limbs (If Only Lower Limbs Affected It's Called ParaPlegia But If Lower Limbs + Some Limitations in Upper Limbs It's Called DiPlegia) 📍3. QuadriPlegia ➡️ Motor Impairment Of All Limbs (Whole Body) 📍4. MonoPlegia ➡️ Motor Impairment Of Only One Limb

🔸B. According To Type Of Motor Disorder

📍1. Spastic CP : ▪︎Most Common Form Of CP (70-80%) ▪︎Results From Injury To Upper Motor Neurons Of The Pyramidal Tract ▪︎Usually Bilateral ▪︎Characterized By : I. Increase Muscle Tone (Spasticity) II. Pathological Reflexes (+Ve Babinski & HyperReflexia/Persistent Primitive Reflexes) III. Abnormal Movement IV. Pseuedo-Bulbar Palsy (Poor Sucking & Swallowing/Squint/Speech Abnormalities) V. Types : ▪︎Spastic DiPlegia (35%) ▪︎Spastic HemiPlegia (25%) ▪︎Spastic QuadriPlegia (20%) ▪︎Spastic ParaPlegia & MonoPlegia 📍2. DysKinetic CP (10-15%) ➡️ Results in Abnormal Movement & Involuntary Uncontrolled Recurrent Movements 📍3. Ataxic CP (<5%) ➡️ Results in Abnormal Posture & Movement & Loss Muscle Coordination Due To Cerebellar Injury 📍4. Dystonic CP ➡️ Results in Stiff Movements & Hypotonia & Reduced Activity (Floppy Infant) 📍5. ChoreAthetotic CP ➡️ Results in Combination Of Ataxia (Loss Balance & Coordination) & Rigidity (HyperTonia) & DysKinesia (Involuntary Movements) 📍6. Mixed CP (10-15%) ➡️ More Than One Pattern Of Motor Abnormality Present (More Complications)

🔷Clinical Features & Complications Of CP

📍1. Feeding Difficulty 📍2. Developmental Delay 📍3. Abnormal Movements & Postures 📍4. Seizure Episodes 📍5. Behavioural & Sensory Abnormalities 📍6. Mental Retardation Or Learning Difficulties

🔷Mx Of CP

📍1. Exclude Reversible Causes Of The Neurological Dysfunction (CT/MRI/Metabolic & TORCH Screen/Genetic Tests) 📍2. Evaluation Of Associated Abnormalities (Hearing & Visual Impairment/Seizures) 📍3. Physical & Occupational Therapy 📍4. Symptomatic Tx : ▪︎Sedatives ▪︎Muscle Relaxants ▪︎Surgical Correction Of The Deformities https://t.me/Clinicalpediatricround

🔴GIT Bleeding

🔰Upper GIT Bleeding

▪︎Bleeding Source Above The Ligament Of Treitz Of The Duodenum ▪︎Most Common GIT Emergency

🔹Causes

📍A. From Esophagus

1. Reflux Esophagitis (Recurrent GERD Due To Hiatus Hernia) 2. Mallory Weiss Tear in Esophagus (Due To Recurrent Retching & Forceful Vomiting) 3. Esophageal Varices (Due To Portal HT) 4. Esophageal Cancer

📍B. From The Stomach

1. Gastric Ulcers 2. Gastric Erosion & Gastritis (Due To NSAIDS/Aspirin/Alcohol/H.pylori) 3. Portal Hypertensive Gastropathy 4. Vascular Malformations (Gastric Varices/Dieulafoy Lesion/Antral Ectasia) 5. Gastric Cancer

📍C. From Doudenum

1. Duodenal Ulcer 2. Duodenitis 3. AngioDysplasia 4. Aorto-Duodenal Fistula (After Aortic Surgery)

🔰Lower GIT Bleeding

▪︎Bleeding Source Below The Ligament Of Treitz Of The Duodenum

🔹Causes 📍A. Severe Acute

1. Diverticulae (Most Common) ➡️ Arterial Erosion Inside The Mouth Of The Diverticulum/Always Stops Spontaneously 2. Angiodysplasia (Vascular Malformation) ➡️ More in Elderly/Stops Spontaneously But Recur 3. Bowel Ischaemia 4. Meckle's Diverticulum ➡️ More in Children & Adolescents/Dx By Laparotomy Or ⁹⁹Tc 5. IBD

📍B. SubAcute & Chronic

1. Haemorrhoids ➡️ Bright Red Rectal Bleeding During Or After Defecation (No Pain) 2. Anal Fissure ➡️ Fresh Rectal Bleeding & Anal Pain During Defecation (Pain) 3. Colonic Cancer 4. Large Polyps 5. Angiodysplasia 6. Solitary Rectal Ulcer 7. Radiation Enteritis 8. IBD

🔹Presentation Of GIT Bleeding 🔰Upper

1. Hematemesis ➡️ Vomiting Of Red Fresh Blood With Clots (Severe) Or Dark Coffee Ground (Less Severe) Blood 2. Melena ➡️ Black Tarry Stool With Offensive Odour (Digested By Stomach Acids) 🔰Lower ➡️ Hematochezia (Passage Of Red Fresh Blood Through The Rectum)

🔹Ix & Mx Of GIT Bleeding

📍1. Two Large IV Lines ➡️ Then Give Crystalloids Fluids (If Low BP) Or Blood Transfusion (If Active Bleeding & Low BP) 📍2. Oxygen ➡️ If Patient in Shock 📍3. Draw Blood For IX & Cross Match ▪︎Low MCV (Iron Deficiency Anemia)➡️ Chronic Or SubAcute Bleeding ▪︎Normal HB/Normocytic Anemia ➡️ Acute Bleeding ▪︎Thrombocytopenia ➡️ Chronic Liver Disease ▪︎PT ➡️ Check Liver Disease & Anticoagulants Drugs ▪︎Elevated Urea + Normal Creatinine (Increase BUN-Creatinine Ratio) ➡️ Severe Upper Git Bleeding 📍4. Suspected Causes ▪︎Peptic Ulcer ➡️ Give High Dose IV PPI (Omeprazole) ▪︎Esophageal Varices ➡️ Give Octreotide/Telipressin + Antibiotics/Endoscopic Banding & Sclerotherapy Injection/Balloon Tamponade/TIPSS 📍5. Unknown Cause ➡️ Do Upper Or Lower Endoscopy For Dx & Tx 📍6. Open Surgery Or Angiographic Embolization ➡️ If Endoscopy Fails To Detect & Stop The Source/Rebleeding Occur/Hemodynamically Unstable Patient فضلاً وليس أمرا يرجى الاشتراك في القناة ومشاركة مع الآخرين للاستفادة https://t.me/Clinicalsurgeryround

جنا نضحك انو راتب العقود 300 الف يعني 200 دولار هسا مابيهن 170 دولار

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🤍🤍🤍 📌 Reye Syndrome▫️

▫️ Definition :

is a rare but serious pediatric condition characterized by: 🔖Acute noninflammatory encephalopathy 🔖Hepatic dysfunction with microvesicular fatty change 🖊It classically occurs in children following a viral infection (especially influenza or varicella) who receive aspirin (salicylates).💊

⚙ Pathophysiology :

The core problem is mitochondrial dysfunction in hepatocytes. 🔖Aspirin + viral illness → → Impaired mitochondrial β-oxidation of fatty acids → Accumulation of microvesicular fat in liver cells → Decreased ATP production 💭Consequences: 🔖↑ Ammonia (hyperammonemia) 🔖Cerebral edema 🔖Hypoglycemia (due to impaired gluconeogenesis) 🔖Elevated AST/ALT

❓ Clinical Features :

Usually affects children 4–12 years old. 💭Typical scenario: Child recovering from viral infection → given aspirin → develops: ✔️Persistent vomiting ✔️Lethargy ✔️Confusion ✔️Seizures ✔️Rapid progression to coma 🌟Labs show: ↑ AST/ALT ↑ Ammonia Hypoglycemia Normal bilirubin (often)

💡 Diagnosis :

🤍Clinical suspicion + history of salicylate exposure. 🤍Liver biopsy (if performed) shows: Microvesicular fatty change No inflammation

🚀 Management :

🎉Supportive ICU care 🎉Control intracranial pressure 🎉Correct hypoglycemia 🎉Avoid aspirin in children✖️ #𝑺𝒚𝒏𝒅𝒓𝒐𝒎𝒆 🤍🤍🤍

‼️🔰D. Rickets الكساح‼️

▪︎Weakening & Softening Of The Child Bones After Defective Mineralization Due To Ca & Phosphate Deficiency (Impaired Mineralization Of Growing Bones) ▪︎Affects Growing Bones Of Children Mostly At 6m-2Years (Before Epiphyseal Closure)

🔹Pathophysiology

▪︎Vitamin D Roles ➡️ Absorption Of Ca & Phosphate From Git & Kidney Then Deposit Them in The Bone Matrix ▪︎Low Vitamin D ➡️ Low Ca & Phosphate ➡️ Rickets ▪︎PTH Roles ➡️ When Serum Ca Level Low ➡️ Increase PTH ➡️ Increase Bone OsteoClastic Activity ➡️ Increase Ca Release From Bone To Blood ➡️ Raise Serum Ca Level Again (But Can't Raise Phosphate Level) ▪︎Breast Milk ➡️ Low in Vitamin D ▪︎Formula Milk ➡️ Sufficient in Vitamin D ▪︎Transplacental Vitamin D ➡️ Enough Only For 1st 2m Of Infant's Life

🔹Causes Of Rickets

🔶A. Nutritional (Infantile Or Primary Rickets) ▪︎Most Common Cause ▪︎Mostly Affect Infants Due To : 📍1. Maternal Vitamin D Deficiency 📍2. Infants Diet Low in Vitamin D Or Ca Or Phosphate Due To ▪︎Exclusive Breast Feeding After 6m Age ▪︎Prolonged Parenteral Nutrition ▪︎Weaning Diet Not Rich in Vitamin D/Ca/Phosphate 📍3. Poor Infants Cutaneous Synthesis Of Vitamin D Due To ▪︎Dark Skin Pigmentation ▪︎Full Body Clothing ▪︎Winter & Spring/indoor Living 🔶B. Secondary Rickets Due To : 📍1. Malabsorption ▪︎Celiac Disease ▪︎Pancreatic Insufficiency (Cystic Fibrosis) ▪︎Cholestatic & Chronic Liver Disease ▪︎Diet High in Phytic Acid 📍2. Increase Vitamin D Metabolism ➡️ By Enzyme Induction (Anticonvulsants Phenobarbital) 📍3. Defective Production Of Vitamin D ▪︎Type I Vitamin D Dependent Rickets ▪︎Familial HypoPhosphoataemic Rickets ▪︎Chronic Renal Disease ▪︎Fanconi's Syndrome 📍4. Organs Resistant (Type II Vitamin D Dependent Rickets)

🔹Clinical Features Of Rickets

📍1. Proximal Muscle Weakness & Delayed in Teeth Eruption & Crawling & Walking (Waddling Gait) 📍2. Irritability/Insomnia/Anorexia/Forehead Sweating 📍3. Head ➡️ ▪︎CranioTabes (1st Sign) (Thinning Of Inner Bones Of Skull) Detected By Pressing Over Occipital Or Parietal Bones ▪︎Large Box Shape Head With Frontal & Parietal Bossing & Large Depressed Anterior Fontanelles (Asymmetric Skull Shape) ▪︎CranioSynoStosis (Early Closure Of Skull Sutures) 📍4. Chest & Abdomen ➡️ ▪︎Rachitic Rosaries (No Ribs Ossification At Costochondral Junction) ▪︎Harrison Sulcus (Transverse Groove Near The Diaphragm) ▪︎Abdominal Protrusion & Umbilical Hernia 📍5. Extremities ➡️ ▪︎Broadening At Wrist & Ankle (Expansion Of Metaphysis) ▪︎Marfan Sign (Transverse Groove Felt Over Medial Malleolus Due To Two Unfused Parts Of Malleolus) ▪︎Deformity (Varus/Valgus/Kyphosis/Scoliosis/Lordosis)

🔹Dx Of Rickets

1. Low Serum Vitamin D & Ca & Phosphate 2. High PTH & ALP 3. Wrist Xray ➡️ ▪︎Broadening & Widening The Distal End Of Metaphysis ▪︎Cupping (Concavity) The Distal End Of Metaphysis ▪︎Loss Sharp Line Of Metaphysis (Fraying) ▪︎Wide Joint Space ▪︎Green Stick Fractures At Shaft

🔹Complications

1. Hypocalcemia Causing Tetany & Seizures & Laryngeal Spasms ➡️ Give Immediate IV 1-2ml/Kg 10% Ca Gluconate Over 5-10 Min Followed By Maintenance Oral Ca Over 2-6w 2. Skeletal Deformities & Bone Fractures ➡️ Avoid Walking & Crawling To Prevent Deformity 3. Short Stature & Failure To Thrive 4. Gastroenteritis & Chest infections Due To Hypotonia & Stasis (Decrease Intestinal Motility & Weak Cough Reflex)

🔹Mx Of Rickets

1. Oral 2000-5000 IU/Day Vitamin D For 4-6w 2. Or Single IM 300k-600k IU For 2-4 Doses Over 1 Day (Shock Or Stoss Therapy) ➡️ Used If No Compliance 3. Then Daily Vitamin D Maintenance ▪︎400 IU/Day (Age <1 Year) ▪︎600 IU/Day (Age >1 Year)

🔹Improvement Criteria

1. Zone Of Calcification Seen On Xray 2. ALP Back To Normal 3. Improved Muscle Tone #Rickets https://t.me/Clinicalpediatricround

معقولة فلوس ال250 مال طلاب السادسة يلي تخرجو ليهسا مامرجعينهن؟! شني ينرادلهن موازنة؟

▪️وزارة الصحة تعلن وصول علاج العامل الثامن لعلاج نزف الدم الوراثي

🔷DDX Of Fibroids

1. Adenomyosis 2. Uterine Sarcoma 3. Ovarian Mass 4. Pelvic Kidney 5. Colonic Cancer 6. Inflammatory Bowel Mass 7. Diverticulae

🔷Mx Of Fibroids

🔸A. Conservative ▪︎For Asymptomatic Fibroids That Detected Incidentally 🔸B. Medical

🔺Disadvantages Of Medical Tx :

1. Ineffective in Cases Of Sub-Mucoal Fibroids Or Enlarged Uterus Palpable Abdominally (>12w Gestation Uterine Size) 2. Regrowing Of The Fibroids After Drugs Discontinuation

🔺Drugs Used in Medical Tx : 📍1. GnRh Agonist

▪︎Decrease GnRh Hormone Release From The Pituitary (-Ve FeedBack) That Decrease Estrogen Production From The Ovaries Within 2-3w ▪︎Given Every 1-3m As Injections Or Nasal Spray ▪︎40% Reduction in Fibroid Volume ▪︎Risk Of Post-Menopausal Symptoms (Osteoporosis/Hot Flushes & Vaginal Dryness) ▪︎Can Used Before Surgery To Decrease Fibroid Size & Vascularity

📍2. UliPristal Acetate (SPRM)

▪︎Acts As Selective Progesterone Receptor Modulater (Blocker) ▪︎Reducing Fibroid Volume & Bleeding Without Causing Estrogen Deficiency (No Post-Menopausal Symptoms) ▪︎Available Orally

📍3. For Fibroids With Bleeding

▪︎LevoNorgestrel Intra-Uterine Device (LNG-IUS Mirena) ▪︎Tranexamic Acid ▪︎NSAIDS (Mefenamic Acid) ▪︎Progesterone Only Pills ▪︎Combined Oral Contraceptives 🔸C. Surgical 🔺Indications For Surgery : 1. Failed Medical Tx 2. Continuous Heavy Menstrual Bleeding 3. Pressure Symptoms 4. Recurrent Miscarriage Or Unexplained Infertility 5. Suspicious Of Malignancy (Rapidly Growing Or Suspicious Features On US) 6. Torsion Or Degeneration

🔺Types Of Surgery :

📍1. MyoMectomy (Fibroid Removal Using Hysteroscopy Or Laparotomy) ▪︎Preserve Fertility ▪︎Less Complications ▪︎Risk Of Fibroid Recurrence ▪︎Hysteroscopic MyoMectomy Used Only For Submucoal Fibroids Protruding into Uterine Cavity ▪︎Open MyoMectomy For Intra-Mural & Sub-Serosal Fibroids 📍2. Hysterectomy ▪︎For Patient Completed Her Family ▪︎Complete Cure 📍3. Uterine Artery Embolization ▪︎50% Reduction in Fibroid Volume ▪︎Complications ➡️ Postoperative Pain (Fibroid Ischaemia)/Ovarian Failure/Infection/Fibroid Expulsion 📍4. Endometrial Ablation ▪︎Significant Reduction in Fibroid Size & Bleeding ▪︎High Risk Of Infertility (Amenorrhea) 📍5. High-Intensity Focused US Ablation

🔸D. Mx Of Acute Degeneration

📍1. Fluids & Analgesic 📍2. Antibiotics 📍3. Bed Rest

🔴Uterine Fibroids (Leiomyoma) تليفات الرحم

▪︎Estrogen Dependent Benign Tumours Of The Uterine Smooth Muscles That Arise From Neoplastic Transformation Of A Single Smooth Muscle Cells Of The MyoMetrium ▪︎Most Common Benign Tumors Of The Female Genital Tract (Affect 40% Of Women) ▪︎Usually Multiple ▪︎More in Middle Age & Old Woman (70% in 6th Decade Of Life) ▪︎Fibroids Have More Estrogen & Progesterone Receptors Than Other Smooth Muscle MyoMetrial Cells ▪︎High Rate Of Recurrence

🔷Risk Factors For Fibroids

1. NulliParous ما عدها حمل لحد هسة 2. Obesity 3. Family Hx Of Fibroids 4. African Origin

🔷Classification (Sites) Of Fibroids

📍1. Sub-Mucoal ➡️ More Risk Of Bleeding & Subfertility 📍2. Intra-Mural 📍3. Sub-Serosal 📍4. Cervical

🔷Clinical Features & Complications Of Fibroids

📍1. Most Fibroids Are Small & Asymptomatic (60% Incidental Finding) 📍2. Abnormal Uterine Bleeding (Heavy Menstrual & Intermenstrual Bleeding) 📍3. SubFertility Or Recurrent Miscarriage (Reproductive Failure) ➡️ Due To Mechanical Occlusion Or Distortion Of Fallopian Tubes Or Endometrial Cavity 📍4. Pressure Effects On Adjacent Organs ▪︎Urinary Frequency/Nocturia/Urine Retention/Hydronephrosis (Ureter Obstruction) ▪︎Abdominal Discomfort Or Distention (Bloating) Or Constipation ▪︎Pelvic Pressure & Heaviness ▪︎Lower Limb Varicosity 📍5. Severe Acute Pain Due To Acute Degeneration Or Torsion ▪︎Red Degeneration ➡️ Haemorrhage & Necrosis Within The Fibroids During The Mid-2nd Trimester Of Pregnancy That Results in Acute Pain & Tenderness Over The Uterus With Low Grade Fever & Vomiting ▪︎Hyaline Degeneration ➡️ Asymptomatic Softening & Liquefaction Of The Fibroids ▪︎Cystic Degeneration ➡️ Asymptomatic Central Necrosis Leaving Cavity Inside The Fibroids ▪︎Sarcomatous Degeneration ➡️ Malignant Transformation Of The Fibroids (Low Risk But More Suspicious in Post-Menopausal Women With Rapidly increasing Size Fibroids) 📍6. Abnormal Lie Or Mal-Position Or Mal-Presentation Of The Fetus During Pregnancy ➡️ Due To Fibroids in The Cervix Or Lower Uterine Segment 📍7. Postpartum Haemorrhage & Delayed Uterine Involution & Uterine Infections 📍8. Chronic Anemia 📍9. Fibroids Enlargement During Pregnancy (1st Trimester) 📍10. Fibroids Calcification After Degeneration 📍11. DysPareunia (Painful Sex) ➡️ Due To Posterior Fibroids Near The Vaginal Cul-De Sac

🔷Dx Of Fibroids

🔸A. Clinical Features (Hx) 🔸B. Examination 📍1. Visible Palpable Abdominal Mass Arise From The Pelvis 📍2. Firm Irregularly Palpable Enlarged & Non-Tender Uterus 📍3. General Signs Of Anemia (Pallor) 🔸C. Ix 📍1. US (1st Gold Standard) ➡️ Well-Defined Rounded Or Lobulated Myometrial Lesion ▪︎TVUS (Trans-Vaginal) ➡️ For Sub-Mucoal & Small Intra-Mural Fibroids ▪︎TAUS (Trans-Abdominal) ➡️ For Large Intra-Mural & Sub-Serosal Fibroids & Exclude Hydronephrosis ▪︎Doppler US ➡️ CircumFerential Vascularization 📍2. MRI (Most Accurate) ➡️ For Suspected Malignancy & Before Uterine Artery Embolization 📍3. Hysteroscopy ➡️ For Dx & Removal Of Sub-Mucoal Fibroids 📍4. Saline Infusion SonoHystroGraphy (SIS) ➡️ Detecting Submucoal Fibroids & Endometrial Polyps

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🔻 Alport Syndrome..

📌 Definition : 🙂

هي مرض وراثي تصيب الكُلى ✨ بشكل أساسي، وتؤثر كذلك على الأذن 👂 والعين 👁. المرض ناتج عن خلل في Type IV collagen وهو مكوّن أساسي في Glomerular Basement Membrane (GBM). يعني ببساطة :

Defect in collagen ▫️ weakening of the glomerular basement membrane (GBM) ▫️ leakage of blood and protein into the urine ▫️ progressive deterioration of kidney function.

📌 Pathophysiology : 😒

📌Mutation in genes: 💜COL4A5 (الأكثر شيوعًا – X-linked). 💜COL4A3. 💜COL4A4. ⬅ هذا الخلل يؤدي إلى: 💜Thinning ثم       Thickening and Splitting في GBM. 💜Progressive          glomerulosclerosis Eventually      ➜ Chronic Kidney Disease.

📌 Symptoms : 😠

💜 Renal : • Persistent hematuria " أول عرض" • Proteinuria. • Hypertension. • Progressive renal failure. • ESRD "غالبًا في سن الشباب" 💜Ear : • Sensorineural hearing loss. 💜Eye : • Anterior lenticonus. "علامة مميزة جدًا" •Retinal flecks. •Visual disturbance.

📌 Diagnosis : 🤓

💜 Investigations : • Urine analysis ➜   Hematuria ± Proteinuria. • Renal function tests ➜ ↑ Creatinine. • Audiometry ➜ Hearing loss. • Eye examination. 💜 Genetic testing :       "Definitive diagnosis" ⬅ يكشف الطفرة في COL4 genes. 💜 Renal biopsy : • Electron microscopy ➜   “Basket weave appearance” of    GBM.

📌 Treatment : 🤷‍♂️

لا يوجد علاج نهائي شافي للطفرة، لكن نبطئ التدهور! 💜 ACE inhibitors / ARBs تقلل proteinuria وتحمي الكلى. 💜 Control hypertension. 💜 Dialysis عند الوصول إلى ESRD. 💜Kidney transplantation أفضل خيار طويل المدى.

📌 Prognosis : 🙂

•in X-linked males ➜ غالبًا ESRD قبل عمر 30–40 سنة. • الإناث غالبًا أعراض أخف. • كلما بدأ البروتين في البول مبكرًا, كان التدهور أسرع.

📌 Important Clinical Points : ☕️

• Persistent hematuria  + تاريخ عائلي لفشل كلوي = فكر في Alport!! • Hematuria + Hearing loss = Red    flag. •  Anterior lenticonus علامة شبه Pathognomonic. -------------------------------------------------------

📎 MEN 1 Syndrome || Multiple Endocrine Neoplasia Type 1 ➡️Previously called Wermer's Syndrome🔥.

📎Definition:

➡️A rare inherited (Autosomal Dominant) disorder caused by proliferate lesions ( Hyperplasia , Adenoma, carcinoma) of multiple endocrine glands.

✅Cause:

➡️Mutation in the MEN1 tumor suppressor gene on chromosome 11q13, which encodes the protein menin.

💡Mnemonic:

❤️MEN1 ➡️ “3 Ps” ✔️Parathyroid ✔️Pancreas ✔️Pituitary

1️⃣ Parathyroid Glands:

✅ Most common manifestation (>90%) ⏺️ Usually due to: • Hyperplasia • Adenoma ⤵️ Causes Primary Hyperparathyroidism ⚠️Results: • ↑ PTH • ↑ Calcium (Hypercalcemia) ✅ Symptoms: • Kidney stones • Bone pain • Fatigue • Depression & psychiatric symptoms

2️⃣ Pancreatic / Enteropancreatic Tumors

📳 Functional neuroendocrine tumors ( leading Cause of death in MEN1) 💡Common types: ✅Gastrinoma ➡️Secretes Gastrin 💭Causes: ⏺️Zollinger–Ellison Syndrome • Recurrent peptic ulcers • Severe gastric acid secretion • Diarrhea ✅ Insulinoma ➡️Secretes Insulin 💭Causes: • Hypoglycemia • Sweating • Tremors • Confusion ✅ VIPoma ➡️Secretes VIP (vasoactive intestinal peptide) 💭Causes: • Watery diarrhea • Hypokalemia • Achlorhydria ❓Known as: WDHA Syndrome

3️⃣ Pituitary Tumors

Occur in about 40% of patients 💡Most common: Prolactin _Secreting Macroadenoma ➡️Secretes Prolactin 💭Causes: • Amenorrhea • Galactorrhea • Infertility

✔️Diagnosis:

❗️Genetic testing for MEN1 mutation ❗️Hormonal studies: • Calcium • PTH • Gastrin • Prolactin ❗️Imaging: • MRI • CT scan

❤️ Treatment:

⚠️ Surgery is the main treatment ( Parathyroidectomy ) ✅ Medications may control hormone excess: • PPIs for gastrinoma • Dopamine agonists for prolactinoma ------------------------------------------------------ https://t.me/Clinicalsurgeryround

🖊 Marfan Syndrome ❔

📌 Definition ▫️:

Marfan syndrome is an inherited (runs in families) medical problem that affects the strength of connective tissues in the body. Since connective tissue is found throughout the body, 🔸Marfan syndrome can affect many areas, such as the bones, joints, eyes, heart, blood vessels, nervous system, skin, and lungs.

📍 Causes 💡 :

1⃣-mutation in the FBN1 gene on chromosome 15, which disrupts the production of fibrillin-1, a protein essential for building connective tissue. 2⃣-Marfan syndrome is inherited in an autosomal dominant manner. This means if a parent has Marfan syndrome, each child has a 50% chance of having it too.

🔹 Signs 🔍 :

✔️Arms, legs, fingers, and toes that are longer in relation to the rest of the body. ✔️Chest wall (sternum) that caves in or sticks out. ✔️Curvature of the spine. ✔️Flat feet. ✔️Headaches.

⚠️ Diagnosis 👥:

♦️Clinical Examination:⬇  Doctors look for specific physical features, including long limbs, crowded teeth, flat feet, and joint hypermobility. ♦️Imaging Tests: 🔸Echocardiogram: Measures the aorta's diameter to check for enlargement. ♦️CT or MRI Scan: Provides detailed images of the chest and spine.

📌 Treatment:🤩

Although there is no cure❕, the most common treatment is surgery for Marfan syndrome. The aortic root is the part of the aorta that connects to the heart, and it can be weakened or bulge. Surgery may involve replacing the aortic root with a synthetic graft. 🔹 🌟

تم رفع ادمن جديد بالقناة من اخوتنا في اليمن ادعوا الله له بالتسديد والتوفيق اخونا دكتور عبود مفتاح

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