Dr. Sayada Sultana Nipa

04/02/2026

6 BRAIN TUMORS IN ADULTS :

1️⃣ Glioblastoma Multiforme (GBM)
🔬 Most common PRIMARY brain tumor. THE DEADLY ONE
Imaging shows ring-enhancing mass crossing corpus callosum. the “butterfly glioma.”
⚠️ Histology: pseudopalisading necrosis + microvascular proliferation.
GFAP positive.
🔍 Dx: MRI shows butterfly lesion crossing midline with central necrosis.
🏥 Tx: Surgery + temozolomide + radiation.

2️⃣ Meningioma
🔬 Most common BENIGN tumor. ATTACHED TO DURA
⚠️ Extra-axial mass with “dural tail” sign.
Histology: whorled spindle cells + psammoma bodies.
🔍 Dx: MRI shows homogeneously enhancing dural-based mass.
🏥 Tx: Surgical resection is curative. Observe if small and asymptomatic.

3️⃣ Schwannoma (Acoustic Neuroma)
🔬 CN VIII tumor. CEREBELLOPONTINE ANGLE
Bilateral = NF2 (chromosome 22).
⚠️ Histology: Antoni A (dense, Verocay bodies) and Antoni B (loose, myxoid).
S-100 positive.
🔍 Dx: MRI shows CP angle mass extending into internal auditory canal.
🏥 Tx: Observation vs surgery vs gamma knife depending on size/symptoms.

4️⃣ Pituitary Adenoma
🔬 Sella turcica.
They’ll give you hormonal symptoms (prolactinoma = galactorrhea/amenorrhea. GH = acromegaly. ACTH = Cushing)
OR bitemporal hemianopia from optic chiasm compression.
🔍 Dx: MRI of sella + hormone panel + visual fields.
🏥 Tx: Prolactinoma = dopamine agonists first (NOT surgery).
Others = transsphenoidal surgery.

5️⃣ Oligodendroglioma
🔬 Calcified frontal tumor. BETTER PROGNOSIS
Slow-growing, often long seizure history before diagnosis.
⚠️ Histology: “fried egg” cells (clear cytoplasm, central nuclei) + “chicken wire” capillaries.
🔍 Dx: CT shows calcified frontal mass. Test for 1p/19q codeletion.
🏥 Tx: Surgery + PCV chemo or temozolomide.

6️⃣ Metastatic Brain Tumors
🔬 Most common OVERALL brain tumor. MULTIPLE LESIONS
⚠️ Multiple lesions at gray-white junction = metastases.
🔍 Dx: MRI shows multiple ring-enhancing lesions. Find the primary.
🏥 Tx: Surgery or radiosurgery if few lesions.
Whole brain radiation if multiple.
Dexamethasone for edema.

30/01/2026

SIADH (Syndrome of Inappropriate Antidiuretic Hormone)

Key Diagnostic Criteria

Hypotonic hyponatremia
→ Low serum sodium 40 mEq/L

Clinical euvolemia
(No edema, no dehydration)

Normal renal, adrenal, and thyroid function
No recent diuretic use

29/01/2026

DLCO (Diffusing Capacity of Lung for CO) measures how well gas moves from alveoli → pulmonary capillary blood.

DLCO~~ {Surface Area * Pulmonary blood flow} / {Membrane thickness}

27/01/2026

27/01/2026

Young thin patient + rapid weight loss / low BMI + post-prandial epigastric pain + early satiety / vomiting = Think: Superior Mesenteric Artery (SMA) Syndrome

26/01/2026

👩‍⚕️👩‍⚕️Hospital-acquired and ventilator-associated pneumonia :

Whilst the majority of patients with pneumonia develop outside of hospital ('community-acquired) it is common for patients to develop significant chest infections whilst admitted. These require special consideration as the causative organisms (and hence recommend antibiotic regimes) are often different.

Definitions
hospital-acquired pneumonia (HAP): pneumonia that occurs ≥ 48 hours after admission
ventilator-associated pneumonia (VAP): pneumonia that develops ≥48 hours after endotracheal intubation

👾👾Common causative organisms
*Staphylococcus aureus (methicillin-sensitive, MSSA)
*methicillin-resistant Staphylococcus aureus (MRSA)
*Pseudomonas aeruginosa - particularly in ventilated patients, most common cause in patients ventilated > 5 days
*gram-negative bacilli (e.g. Escherichia coli, Klebsiella pneumoniae, Enterobacter spp, Acinetobacter spp) - particularly in late-onset HAP (after 4 days)
polymicrobial infections
multidrug-resistant (MDR) pathogens

🔴Features
clinical findings also seen with community-acquired pneumonia
cough
sputum
dyspnoea
fever
consolidation/infiltrates on chest x-ray
raised white cell count and CRP
increased respiratory rate, decreased oxygenation saturations may be seen on observations charts
ventilated patients may have
decreased tidal volume
increased inspiratory pressures
decreased oxygenation
diagnosis is complicated by the fact that many hospitalised patients will have confounding features due to reason for underlying admission, e.g. dyspnoea or raised CRP

Investigations
chest x-ray
bloods
CRP
WBC
microbiology
peripheral blood cultures
lower respiratory tract sample e.g. sputum sample or bronchoalveolar lavage sample
should be done prior to the initiation of antibiotics

✅Management
antibiotic choices should of course be guided by microbiology results and local protocols
BNF guidance for non-severe signs or symptoms and not at higher risk of resistance
oral co-amoxiclav
BNF guidance for severe signs or symptoms or at higher risk of resistance
IV piperacillin with tazobactam OR IV third-generation cephalosporin ceftazidime OR IV meropenem
if MRSA is suspected then add IV vancomycin

26/01/2026

Snowstorm appearance in CXR:
🔴 Metastatic Cancer: (esp Medullary thyroid cancer or choriocarcinoma)
⚪️Calcified varicella infection
🟣Fat Embolism Syndrome.
⚫️Pulmonary Alveolar Microlithiasis
🔴Miliary Tuberculosis
⚫️sarcoidosis

25/01/2026

🤔Young patient + Cough + Dyspnea + Fatigue + Bilateral hilar lymphadenopathy + Hypercalcemia + Skin lesions / Eye symptoms
👩‍⚕️👩‍⚕️👩‍⚕️Think: Sarcoidosis

🔍🔍Key Diagnostic Features
• Non-caseating granulomas on biopsy
• Bilateral hilar lymphadenopathy on CXR / CT
• T ACE levels (supportive, not diagnostic)
• Hypercalcemia / hypercalciuria
→ due to 1 1-a hydroxylase activity in macrophages
• Restrictive lung disease on PFTs
• Always exclude TB, fungal infections, and lymphoma before labeling sarcoidosis
• PTH is low or suppressed despite hypercalcemia
• Tuberculin skin test often negative (anergy)

24/01/2026

Restless Leg Syndrome 🔻🔻
IRLSSG diagnostic criteria

Should include :
• Urge to move legs
• Worse at rest
• Relieved by movement
• Worse in evening/night
• Not explained by another condition

first step is to correct IDA
Treat if ferritin

24/01/2026

Young female + postpartum / OCP + severe headache + seizures = Think: CVST (Cerebral Venous Sinus Thrombosis)

Extra supportive Features (if present):
Papilledema / vomiting (↑ ICP)
Blurred vision / diplopia (VI nerve palsy)
Focal deficits (weakness, aphasia)
Hemorrhagic venous infarct on imaging

Best test: MRI brain + MRV (or CT venogram)
Treatment: Anticoagulation (heparin) even if hemorrhagic infarct

24/01/2026

5 Types OF Nephrotic Syndrome👇👇👇
1️⃣ Minimal Change Disease

🔬 T-cell mediated
💡 T-cell dysfunction causes loss of negative charge on the GBM. Albumin leaks because it’s no longer repelled.

Classic presentation:
They’ll give you a child with periorbital edema after a viral URI.
No blood in the urine.

⚠️ LM is NORMAL. That’s why it’s “minimal change.”
EM shows podocyte effacement.
Highly responsive to steroids.
In adults, think Hodgkin.

2️⃣ Focal Segmental Glomerulosclerosis (FSGS)

🔬 Podocyte injury
💡 Direct podocyte damage causes scarring.
Focal = some glomeruli
Segmental = part of each glomerulus

Classic presentation:
They’ll give you HIV, he**in use, or sickle cell with nephrotic syndrome.

⚠️ Most common nephrotic syndrome in HIV
Over 50% progress to ESRD. Worst prognosis.
NOT as responsive to steroids.
LM shows segmental sclerosis.

3️⃣ Membranous Nephropathy

🔬 Immune complex deposition
💡 Anti–phospholipase A2 receptor antibodies deposit on the epithelial side of the GBM, causing thickening.

Classic presentation:
Nephrotic syndrome plus hepatitis B, sulfa drugs, gold salts, or underlying cancer.

⚠️ Most common nephrotic syndrome in Caucasian adults
LM shows thickened pink capillary walls.
EM shows “spike and dome” subepithelial deposits.

4️⃣ Diabetic Nephropathy

🔬 Non-enzymatic glycosylation
💡 Hyperglycemia glycosylates the GBM.
First hyperfiltration → then thickening → then proteinuria → then failure.

Classic presentation:
Long-standing diabetic with progressive proteinuria.

⚠️ #1 cause of ESRD worldwide
Start ACE/ARB even if BP is normal. Nephroprotection is independent of BP control.
LM shows Kimmelstiel–Wilson nodules. Pink hyaline circles.

5️⃣ Renal Amyloidosis

🔬 Light chain deposition
💡 Myeloma overproduces light chains. They misfold into β-pleated sheets and deposit in the kidney.

Classic presentation:
Multiple myeloma plus nephrotic syndrome plus Bence-Jones proteinuria.

⚠️ “Multiple myeloma = most common cause of renal amyloidosis”
Congo red stain shows apple-green birefringence under polarised light.

24/01/2026

Approach to Livedo Reticularis

Livedo reticularis is a sign, not a diagnosis.
It reflects disturbed vascular flow due to:
• Vasospasm
• Vascular inflammation (vasculitis)
• Vascular occlusion (thrombotic / embolic)

Key Principle

Persistent livedo reticularis is pathological and requires evaluation.

Pattern Recognition
• Livedo + DVT + pregnancy loss
Think: Antiphospholipid syndrome (APS)

• Livedo + neuropathy + abdominal pain
Think: Polyarteritis nodosa (PAN)

• Livedo + ischemic stroke in a young woman
Think: Sneddon syndrome

• Livedo + blue toe syndrome + AKI after angiography
Think: Cholesterol embolization

• Livedo + arthralgia + purpura
Think: Cryoglobulinemic vasculitis

Persistent livedo reticularis = vascular pathology until proven otherwise. Always investigate
Diagnosis depends on recognizing the associated clinical pattern rather than the skin finding alone.