Lab Rats In Lab Coats
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Always give slow IV (never IM or SC) → risk of tissue necrosis.
Continuous cardiac monitoring during infusion (arrhythmia risk).
• If fits continue → repeat dose or start infusion.
• Treat underlying cause (vitamin D deficiency, hypoparathyroidism, hypomagnesemia, renal disease).
Hypokalemia and Hypocalcemia
1. Hypokalemia causes metabolic alkalosis
• Low K⁺ shifts H⁺ ions into cells → blood becomes more alkaline.
• This is called a contraction alkalosis.
2. Alkalosis increases calcium binding to albumin
• In alkalosis, albumin has more negative charges → it binds more calcium.
• This lowers the amount of free ionized Ca²⁺ (the biologically active form).
3. Ionized calcium falls, total calcium may remain normal
• So, even if lab “total calcium” looks okay, the patient develops symptomatic hypocalcemia (tetany, seizures, paresthesias).
Causes of Hypocalcemia

1. Neonatal & Pediatric Causes
Prematurity (immature parathyroid response)
Vitamin D deficiency / rickets
Hypoparathyroidism (congenital or post-surgical)
Hypomagnesemia (impairs PTH release/action)
High phosphate load (e.g., cow’s milk in infants, tumor lysis, renal failure)

2. Systemic / Adult Causes
Hypoparathyroidism (autoimmune, surgical, genetic)
Vitamin D deficiency or resistance (CKD, malabsorption, anticonvulsant therapy)
Chronic kidney disease (↓ 1α-hydroxylase activity → ↓ calcitriol)
Pancreatitis (fat saponification traps calcium)
Massive blood transfusion (citrate binds calcium)

3. Electrolyte-related Causes
Hypomagnesemia (↓ PTH secretion, ↓ bone response)
Alkalosis (↑ Ca²⁺ binding to albumin → ↓ ionized calcium)
The classical triad of congenital toxoplasmosis is:
1. Chorioretinitis
2. Hydrocephalus
3. Intracranial calcifications (classically diffuse, especially basal ganglia)

Presence of this triad strongly suggests congenital toxoplasmosis, although not all infants present with all three.
Transplacental (Congenital) Varicella Infection

Limb Hypoplasia
• Underdeveloped or shortened extremities.
• Caused by viral damage to fetal blood vessels and nerves.
2. Cutaneous Scars
• Linear, cicatricial scars on the skin, often along dermatomes.
• Appear like burn or surgical scars, present at birth.
• Pathognomonic for transplacental varicella infection.
Prenatal infection,
Classical clinical features:
1. Skin → cicatricial skin scars (burn-like, linear or zig-zag).
2. Limbs → limb hypoplasia or underdeveloped extremities.
3. Central Nervous System → microcephaly, seizures, cortical atrophy, developmental delay.
4. Eyes → cataracts, chorioretinitis, microphthalmia, nystagmus.
5. Growth → intrauterine growth restriction (IUGR), low birth weight.
Reactivation of Congenital Varicella (Shingles in children)
• If a fetus is infected with varicella-zoster virus (VZV) in utero, the virus remains latent in the sensory ganglia.
• Later in childhood, the virus can reactivate as herpes zoster (shingles), even in very young children.
• Unlike adults, shingles in these children may occur without a history of chickenpox (since their “primary infection” was congenital).
• Reactivation usually causes:
Dermatomal vesicular rash (localized to a single dermatome).
Neuropathic pain (less severe in children than adults).
• May be associated with eye complications if the trigeminal ganglion is involved.
For Congenital Varicella Syndrome, the Central Nervous System (CNS) features mainly include:
Microcephaly (small head size due to poor brain development).
Seizures (from cortical scarring/atrophy).
Cortical atrophy (loss of brain tissue).
Developmental delay / intellectual disability.
Congenital Rubella Syndrome (CRS)
Classical Triad (Gregg’s Triad)
1. Sensorineural deafness (most common, ~60–70%)
2. Eye defects (cataracts, retinopathy, microphthalmia)
3. Congenital heart disease (especially PDA and pulmonary artery stenosis)
Salt & Pepper Retinopathy
• Seen in congenital rubella.
• Pigmentary changes in the retina → mottled “salt and pepper” appearance.
• May cause reduced vision but sometimes asymptomatic.

2. Radiolucency of the Long Bones

• Radiographs show areas of decreased density in the metaphysis and epiphysis.
• Represents congenital rubella arthropathy (non-infectious bone disease).
• Can mimic osteomyelitis but usually symmetrical.
• Often involves knees, femur, tibia.
Blueberry muffin rash
CMV

Microcephaly
• Head circumference below normal.
• Due to impaired brain growth from CMV infection in utero.

2. Periventricular Calcifications (– ultrasound & CT)
• Calcium deposits around the ventricles.
• Very characteristic for CMV (contrast with diffuse/basal ganglia calcifications in toxoplasmosis).
Forwarded from Dabi🏴‍☠️
Arrhythmia tree
Forwarded from Ameer lectures (Ameer Ahmed 313)
مرحبا طلاب…………
1-انفتح التسجيل ع كورس الكسور ان شاء الله،

2-سعر الاشتراك 15 الف دينار للطالب الواحد واذا اكثر يصير ع 10 لكل طالب.، الكورس يفيد خامس وسادس

3-الكورس يشمل جميع محاضرات الكسور
trauma,diseases

4-المحاضرات المشروحه هي خاصه بطب الانبار، واكو محاضره مجانيه اذا احد يحب يشوف الشرح هذه رابط الكورس
(https://medmasters.app/item/course/1206)

5-طريقة الاشتراك عن طريق ماستر كارد تحويل (6425473680)وارسال صوره لعملية التحويل حتى يتم الاضافه

6-المحاضرات مرفوعه ع برنامج medmaster
2-IOS—https://apps.apple.com/us/app/medmasters/id6447317197)

7-كل مشترك بعد الدفع يوصله كوود يستخدم لجهاز واحد فقط مجرد ادخال الكود يتفعل الكورس
داخل التطبيق تختارون حساب اسمه Ameer lectures
بس تدخلون الكوود الي اني ادزه يتفعل الكورس ان شاء الله
1-وهذه معرفي @amory129
Forwarded from 0/0 (Haidar A. Fahad)
أمير من العشرة الأوائل عالكلية وكلش خوش يشرح (باعتباره الـ roommate ف جنة مستغليه أبشع استغلال)
Forwarded from 0/0 (Haidar A. Fahad)
0/0
أمير من العشرة الأوائل عالكلية وكلش خوش يشرح (باعتباره الـ roommate ف جنة مستغليه أبشع استغلال)
بتخرجي جان لازم اشكر الله وأهلي (وأمير)
Different types of aphasia