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Pearls on acute upper GI bleeding from #UEGWeek - take home messages courtesy of @iangralnek💡🩸
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One of the gamechanging advances in gastroenterology is tissue transglutaminase (TTG) antibody testing for coeliac disease. But what exactly is it?
TTG is a naturally occurring enzyme. In coeliac disease, B-cells produce antibodies against this enzyme (anti-TTG antibodies).
The test is so accurate that patients with a high anti-TTG titre (>10x above the upper limit of normal) is sufficient to diagnose coeliac disease.
🤖 Made with AI
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Homi Bhabha, Robert Oppenheimer, Paul Dirac, Lise Meitner, and other scientists photographed together, dated unknown.
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Here's a curious thing that happens when you try mixing liquids that won't chemically blend, like water and oil 🧪 On Earth, oil floats on top of water because of the difference in density. In space, there's no weight from gravity, so that natural separation never happens. The two liquids stay mixed together as a floating suspension of droplets, until rotation steps in: spin the container, and inertia pushes the denser water outward while the oil gathers toward the center 🌀🌌
Microgravity turns everyday physics upside down ✨🚀
Credit:ISS
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A 60-year-old patient presents with a chronic, relapsing eruption of flaccid superficial pustules forming annular and circinate configurations over the trunk, proximal extremities, and intertriginous areas. The pustules arise on erythematous plaques and contain sterile-appearing purulent material.
Histopathology shows a subcorneal pustule packed predominantly with neutrophils, with minimal acantholysis.
What is the most likely diagnosis?
A) Sneddon-Wilkinson disease (Subcorneal pustular dermatosis)
B) Pemphigus foliaceus
C) Generalized pustular psoriasis
D) IgA pemphigus
Dr. Harinder Sandhu
Drop your answer in the comments!
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A long-term cigarette smoker suddenly develops acute shortness of breath. A chest X-ray is shown below.
What is the most likely diagnosis, and what is the immediate management?
A) Pulmonary embolism
B) Spontaneous pneumothorax
C) Pleural effusion
D) Pneumonia
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A 50-year-old patient presents with chronic, bilateral violaceous-to-brown papules and plaques around the ankles and dorsal feet, associated with edema, venous stasis changes, pruritus, and occasional tenderness.
Dermoscopy reveals prominent superficial vessels, hemorrhagic dots, and a violaceous background.
Dr. Harinder Sandhu
What is the most likely diagnosis?
A) Kaposi sarcoma
B) Acroangiodermatitis of Mali
C) Hypertrophic lichen planus
D) Stasis dermatitis
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A 55-year-old patient presents with recurrent, widespread, tense inflammatory bullae, erosions, crusted plaques, and post-inflammatory dyspigmentation, predominantly affecting the hands, forearms, and extensor surfaces.
Histopathology reveals a neutrophil-rich subepidermal blister. Direct immunofluorescence demonstrates linear IgG and C3 deposits along the basement membrane zone, with dermal-side binding on salt-split skin testing.
What is the most likely diagnosis?
A. Bullous pemphigoid
B. Epidermolysis bullosa acquisita
C. Linear IgA bullous dermatosis
D. Dermatitis herpetiformis
E. Anti-p200 pemphigoid
Dr. Harinder Sandhu.
What is the key diagnostic finding?
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What is the most likely diagnosis based on these annular erythematous plaques with raised, scaly borders and central clearing?
A. Tinea corporis
B. Granuloma annulare
C. Nummular eczema
D. Psoriasis
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Dx: Nonuremic calciphylaxis associated w/ futibatinib (Lytgobi®️), likely precipitated by acute hypercalcemia/hyperphosphatemia.
The severe pain, stellate black necrotic plaques w/ surrounding livedoid violaceous erythema, & B/L lower-extremity distribution are classic for calciphylaxis. Although she had normal renal function and PTH, she developed acute hypercalcemia (11.1 mg/dL) & hyperphosphatemia (7.4 mg/dL) after calcium supplementation for tumor lysis syndrome. X-ray demonstrated vascular calcifications, & Bx subsequently confirmed small-vessel calcification w/ lobular fat necrosis, establishing nonuremic calciphylaxis. The close temporal relationship to futibatinib, an FGFR inhibitor known to cause hyperphosphatemia & associated w/ calciphylaxis, further supports a drug-associated process.
Tx: Futibatinib was held, w/ sodium thiosulfate & sevelamer initially used for calcium-phosphate control. Despite progression & inability to continue these agents because of hypocalcemia/hypophosphatemia, a 72-hour IV epoprostenol infusion (2 ➡️ 8 ng/kg/min) produced rapid cessation of ulcer progression & regression of livedoid changes. Epoprostenol may therefore have a role as rescue therapy for refractory FGFR inhibitor–associated calciphylaxis through improved tissue perfusion.
A woman in her 60s w/ stage IIIC intrahepatic cholangiocarcinoma was referred for suspected vasculitis after developing severe pain & progressive purpuric plaques 2 wks after starting Lytgobi®️ (futibatinib).
O/E: Black necrotic stellate plaques w/ surrounding livedoid violaceous erythema on the B/L lower legs. Recent Ca/Phos peaks were 11.1/7.4 mg/dL after calcium supplementation for TLS; Cr, BUN, & PTH were normal.
What’s the diagnosis❓
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Dx: Refractory disseminated granuloma annulare (GA), w/ marked response to systemic (Rhapsido®️) remibrutinib.
The patient had an 8-year hx of Bx-proven disseminated GA, characterized by recurrent, intensely pruritic erythematous annular plaques involving the trunk & B/L extremities. Repeat Bx again showed dermal granulomatous inflammation w/ mucin deposition, elastophagocytosis, & dermal elastolysis, confirming GA. His disease was highly refractory, w/ inadequate or transient responses to topical/IL corticosteroids, prednisone, hydroxychloroquine, phototherapy, multiple systemic agents, biologics, & targeted therapies. Mycophenolate mofetil produced the best prior response (~90% improvement) but was discontinued because of concerns regarding long-term immunosuppression.
Tx: (Rhapsido®️) Remibrutinib 25 mg PO BID was initiated after failure of deucravacitinib, resulting in 75% improvement at 4 weeks & 95% improvement by 4 months, w/ sustained control & no reported adverse effects. Remibrutinib is a selective, irreversible Bruton tyrosine kinase (BTK) inhibitor that may suppress BTK-dependent macrophage & innate immune signaling implicated in granulomatous inflammation. This case suggests BTK inhibition as a potential targeted therapy for refractory disseminated GA.
A man in his 60s w/ a PMHx notable for BCC & HSV presented w/ an 8-year hx of a recurrent, progressively symptomatic eruption. He now reported a severe flare of intensely pruritic, erythematous annular plaques involving the B/L extremities & trunk. Similar episodes had occurred intermittently over the preceding years, w/ the most recent flare approximately 1 year earlier.
What’s your diagnosis❓
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A 7-year-old child presents with several well-demarcated, asymptomatic, uniformly brown macules on the cheek and upper extremity. Dermoscopy shows homogeneous pigmentation with a regular, delicate pigment network and no atypical structures. The lesions are stable, with no preceding inflammation or trauma.
What is the most likely diagnosis?
A. Café-au-lait macules
B. Lentigo simplex
C. Post-inflammatory hyperpigmentation
D. Melanocytic nevus
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A 52-year-old patient presents with multiple progressively enlarging, smooth, firm, pink-to-violaceous nodules densely clustered over the scalp and periauricular region, producing a characteristic “turban-like” appearance.
Histopathology demonstrates well-circumscribed nests of basaloid cells arranged in a “jigsaw puzzle” pattern, surrounded by thick hyaline basement-membrane material.
What is the most likely diagnosis?
A. Trichoepithelioma
B. Cylindroma
C. Spiradenoma
D. Basal cell carcinoma
Can you guess the diagnosis?
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🔥 🔥 🔥
You can never say never.
Some things in health can be incidental findings.
Yesterday I aw a 6yr old boy with complaint of lower abdominal pain,fever and vomiting. No history of trauma to the abdomen, my assessment ruled out gastritis and Gastroenteritis.
Due to the right iliac fossa tenderness, I had high suspicion of appendicitis, so I requested for an abdominopelvic scan, which showed a highly inflamed appendix with possible rupture.
But what got my attention was something I noticed about his skull, he had a pulsating skull.
I want my medical chiefs and our amazing doctors, health practitioners to look at this video and tell me what they think.
Video was made with consent from the parent, patient details weren't disclosed.
This wasn't there primary concern but I had to bring it to their notice and counselled them.
Medics what do you think.
Happy sunday my people.
Much ❤️ from here.




































