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Case-based MCQ

Case-based MCQ

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Enhance Your Medical Expertise with Case Based MCQ โ€“ Your Go-To Telegram Channel for Challenging, Real-World MCQs and Continuous Learning. Admin: @Mohamm_ADs

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๐Ÿ“ˆ Analytical overview of Telegram channel Case-based MCQ

Channel Case-based MCQ (@casebasedmcq) in the English language segment is an active participant. Currently, the community unites 19 283 subscribers, ranking 1 204 in the Medicine category and 22 979 in the India region.

๐Ÿ“Š Audience metrics and dynamics

Since its creation on ะฝะตะฒั–ะดะพะผะพ, the project has demonstrated rapid growth, gathering an audience of 19 283 subscribers.

According to the latest data from 12 June, 2026, the channel demonstrates stable activity. Although there has been a change in the number of participants by -202 over the last 30 days and by -5 over the last 24 hours, overall reach remains high.

  • Verification status: Not verified
  • Engagement rate (ER): The average audience engagement rate is 2.15%. Within the first 24 hours after publication, content typically collects 1.06% reactions from the total number of subscribers.
  • Post reach: On average, each post receives 414 views. Within the first day, a publication typically gains 205 views.
  • Reactions and interaction: The audience actively supports content: the average number of reactions per post is 1.
  • Thematic interests: Content is focused on key topics such as boardvital, bmj, journal, usmle, drug.

๐Ÿ“ Description and content policy

The author describes the resource as a platform for expressing subjective opinions:
โ€œEnhance Your Medical Expertise with Case Based MCQ โ€“ Your Go-To Telegram Channel for Challenging, Real-World MCQs and Continuous Learning. Admin: @Mohamm_ADsโ€

Thanks to the high frequency of updates (latest data received on 13 June, 2026), the channel maintains relevance and a high level of publication reach. Analytics show that the audience actively interacts with content, making it an important point of influence in the Medicine category.

19 283
Subscribers
-524 hours
-527 days
-20230 days
Posts Archive
Correct Answer Is A This clinical finding is known as external auditory exostosis (EAE) or โ€˜Surferโ€™s earโ€™ and is a common condition among both professional and recreational surfers. The exact cause of the condition is unknown, but it is thought that exposure to cold water and wind may stimulate osteoblasts in the temporal bone to produce bony growths that project into the ear canal. Surferโ€™s ear is a benign but irreversible condition and is often asymptomatic in the early stages. Patients are recommended to avoid cold and windy conditions, and the use of ear plugs and a protective hood may also be helpful as a preventative measure. Ear plugs, however, will not resolve exostoses that are already present. Surgical treatment is reserved for patients with severe and symptomatic external auditory exostosis. Referral is indicated for large lesions, progressive hearing loss, and recurrent ear infections

A 25 year old male patient who attends with right-sided ear discomfort. He tells you that he has had discomfort for a few months and has a feeling like his ear is โ€˜blockedโ€™. He is a keen early morning surfer and thinks that the blocked feeling might just be some trapped water in his ears. He has not noticed any ear discharge. He has no fevers and feels systemically well. However, the aching sensation is getting progressively worse in his right ear and he is keen to know if there is any problem. You perform an otoscopic examination of his ears and note the following finding on both left and right sides: What is the most appropriate advice to provide to him today about his ear complaint? A. Advise him that he has an increased risk of developing otitis externa and conductive hearing loss B. Advise him that he will require oral flucloxacillin 500mg 6 hourly for five days C. Advise him that the condition is aggravated by sand in the auditory canals D. Advise him that wearing ear plugs while surfing will assist with resolution of the condition. E. Advise him that he will require an urgent review with an Ear Nose Throat (ENT) surgeon due to the malignant potential of this condition

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Correct Answer Is A Of the options, labyrinthitis, Meniereโ€™s disease and lateral medullary syndrome can cause acute onset vertigo, tinnitus and hearing loss. Ataxia can be a presentation in patients with cerebellar or vestibular disease. Of these three and given the inconclusive neurological examination, labyrinthitis is the most likely diagnosis. Another hint that pointed towards labyrinthitis is that the vertigo provoked with changes in head position as stated in the context. Acute labyrinthitis presents with acute vertigo often followed by nausea and vomiting, tinnitus andย  hearing loss. A history of preceding viral upper respiratory tract infection is present in up to 50% of patients. Change in head position provokes vertigo. Each episode of vertigo lasts from few seconds to minutes. Meniereโ€™s disease also presents with episodes of acute onset vertigo, tinnitus and hearing loss. However, patients with Meniereโ€™s disease often complain of ear fullness because the pathophysiology is excess endolymph in the labyrinth. Patients are usually middle-aged women with a positive family history for the condition. Finally, Meniereโ€™s disease is much less common compared to labyrinthitis. Given these, Meniereโ€™s disease in this patient is a less likely diagnosis compared to labyrinthitis. Vestibular neuronitis is the inflammation of the vestibular nerve often by a viral infection. Patients usually have a preceding viral upper respiratory infection or herpes zoster. Vertigo and imbalance are the prominent features of vestibular neuronitis and there is no hearing loss or tinnitus. Loss of balance is more prominent in vestibular neuronitis compared to other causes of vertigo and patient commonly present with vertigo and falls. Symptoms in vestibular neuronitis are aggravated by change in the position of the head. Neurological examination in patients with vestibular neuronitis is otherwise normal. Acoustic neuromas are intracranial tumors that arise from the Schwann cell sheath of either the vestibular or cochlear nerve. As acoustic neuromas increase in size, they eventually occupy a large portion of the cerebellopontine angle. Although 5-15% of patients with acoustic neuroma present with acute onset of unilateral hearing loss, deafness has an insidious onset in this condition, making it a less likely diagnosis. Gradual hearing loss is overwhelmingly the most common presenting symptom of patients with acoustic neuroma . Imbalance and vertigo is not a prominent feature because as the tumor growth disrupts the vestibular nerve function slowly, there is enough time for compensation. Other features that may be present in patients with acoustic neuroma are headache and facial sensory impairment. Lateral medullary syndrome, also known as Wallenberg syndrome or posterior inferior cerebellar artery (PICA) syndrome has other clinical features in addition to vertigo, hearing loss,and tinnitus. Such features include cross-body sensory impairment (sensory impairment of the face on the affected side and that of the body on the other side), Hornerโ€™ssyndrome, and signs and symptoms indicative of the involvement of cranial nerves or their nucleus. Such signs and symptoms may include dysphagia(due to involvement of nucleus ambiguus that supplies the vagus and glossopharyngeal nerves),dysarthria, dysphonia, disrupted temperature and pain sensation, palatal clonus and heart rate and blood pressure dysregulation (due to involvement of the vagus nerve)

A 54-year-old woman presents to the emergency department with complaints of sudden onset vertigo, nausea, vomiting and hearing loss in her left  ear. Vertigo provoked with changes in head position. On examination, her vitals are within the normal  range. Hearing is decreased on the left side on whisper test. Rinne and Weber tests establish sensori neural deafness of the left ear. She has also nystagmus with the rapid eye to the left side. The rest of the examination is inconclusive.Which one of the following could be the most likely diagnosis? A. Labyrinthitis B. Vestibular neuronitis C. Acoustic neuroma D. Meniere's disease E. Lateral medullary syndrome

Correct Answer Is E The inner ear contains the endolymphatic fluid-filled semicircular canals (which convey movement and position of the head) and the cochlea (which is the sensory organ of hearing).  Conditions that cause disruption of endolymph flow can present with vertigo (semicircular canals) and/or sensorineural hearing loss (cochlea). Perilymphatic fistulas are a rare, but debilitating, complication of head injury or barotrauma.  They cause leakage of endolymph from the semicircular canals and cochlea into surrounding tissues, resulting in characteristic clinical features: Progressive sensorineural hearing loss caused by damage to cochlear hair cells from loss of endolymph. Episodic vertigo with nystagmus triggered by pressure changes in the inner ear (eg, Valsalva maneuver, elevation changes [eg, riding in elevator]) due to acutely increased endolymph leakage.  This can be demonstrated clinically by performing a loud clap (ie, pressure change due to sound conduction through the ossicles) near the patientโ€™s ear and observing for nystagmus (Tullio phenomenon). Patients are advised to limit activities that increase inner ear pressure; they also require ENT referral for further management. Benign paroxysmal positional vertigo is caused by debris (otoliths) that temporarily alters endolymph flow through the semicircular canals.  Therefore, patients typically have sudden, brief (<1-min) episodes of vertigo triggered by head movement. Eustachian tube dysfunction can result in fluid in the middle ear space (not the inner ear vestibular system) and can cause ear popping, cracking, and hearing loss in response to changes in pressure.  However, it also causes a sense of ear fullness or pain, not episodic vertigo with nystagmus. Mรฉniรจre disease is caused by increased endolymphatic fluid volume or pressure in the vestibular system.  It also causes episodic vertigo with hearing loss, but episodes are accompanied by aural fullness or tinnitus, last 20 minutes to 24 hours, and often lack specific, identifiable triggers. Orthostatic hypotension causes lightheadedness, presyncope, or syncope when the patient assumes a standing position due to cerebral hypoperfusion.  It does not involve the vestibular system and therefore does not cause true vertigo or nystagmus. A perilymphatic fistula can occur after head trauma and result in episodic vertigo triggered by sudden pressure changes (eg, Valsalva maneuvers) or loud noises (Tullio phenomenon).

A 34-year-old man comes to the office due to intermittent dizziness over the past 3 months.ย  The patient has had episodes of a sudden spinning sensation, accompanied by nausea, that resolve spontaneously after approximately a minute.ย  Symptoms occur when he is lifting heavy weights, riding on an elevator, or after sneezing.ย  He has had no headache or ear pain but has trouble hearing out of the right ear.ย  The patient had a concussion after a bicycle collision 4 months ago but has no other medical conditions and has had no recent upper respiratory illness.ย  Vital signs are within normal limits.ย  Physical examination shows normal ears, including tympanic membranes.ย  There is no extremity weakness or sensory loss.ย  No nystagmus is present at rest but performing a Valsalva maneuver provokes nystagmus and the other reported symptoms.ย  Which of the following is the most likely diagnosis? A. Benign paroxysmal positional vertigo B. Eustachian tube dysfunction C. Mรฉniรจre disease D. Orthostatic hypotension E. Perilymphatic fistula

Correct Answer Is B There is an increased risk of floppy iris syndrome with the use of selective-alpha blockers (especially tamsulosin) and interrupting treatment does not reduce this risk. The ophthalmologist may need to use a different operative technique and therefore it is important that the ophthalmologist is aware of past and / or current selective-alpha blocker use prior to surgery. While prazosin is a cheaper option, it has more side effects and requires multiple doses each day. Therefore, it is not recommended in international BPH guidelines. Tamsulosin is likely to reduce blood pressure and is not likely to worsen his hypertension. The 5-alpha reductase inhibitors (rather than the alpha-adrenoreceptor antagonists) can take several months to reach maximal effect in terms of symptoms. While sildenafil may improve voiding symptoms, it is not traditionally prescribed as a first-line option for BPH

A 67 year old male presents to see you for review after being started on tamsulosin two months ago by a colleague for symptomatic management of benign prostatic hyperplasia. He wishes to discuss the new medication with you today and is keen to know more about alternative options as his friends with similar problems are taking different medications to him. He has a past history of hypertension and is having cataract surgery in two weeks. Which piece of advice below is most appropriate for him? A. You advise him that prazosin may be a cheaper option compared with tamsulosin with less adverse effects B. You advise him that the tamsulosin may affect his cataract surgery and the ophthalmologist will need to be notified prior to surgery C. You advise him the tamsulosin is likely to worsen his hypertension and should be ceased D. You advise him that the tamsulosin can take several months to provide maximal improvement in symptoms and he should continue taking it for now E. You advise him that sildanafeil is a more effective first-line treatment for benign prostatic hyperplasia compared with tamsulosin

Repost from EDL Backup Channel
"Dear followers, Our previous medical book sharing channel, โ€œEDLMEDICOSโ€, was unfortunately blocked due to DMCA rules. Our goal is to continue providing a free and accessible platform for the exchange of educational materials in the field of medicine. We believe that knowledge should be shared freely, and we are committed to creating a community of learners and educators. We thank you for your continued support and look forward to your engagement in this new chapter." ๐Ÿ“Subscribe: https://t.me/EDLMedicos_info EDLMEDICOS administration team, Jul 27 2025

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Repost from Medical Mnemonics
STOP WAR IN GAZA โ—

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Repost from Medical Mnemonics
๐Ÿงฉ Medical Mnemonics Short metacarpals Differentials โ€œThe fingerTIPS are shortโ€ ๐Ÿ– โ–ซTurnerโ€™s syndrome โ–ซInjury ๐Ÿ“Iatrogenic ๐Ÿ“
๐Ÿงฉ Medical Mnemonics Short metacarpals Differentials โ€œThe fingerTIPS are shortโ€ ๐Ÿ– โ–ซTurnerโ€™s syndrome โ–ซInjury ๐Ÿ“Iatrogenic ๐Ÿ“Infection ๐Ÿ“Idiopathic โ–ซPseudohypoparathyroidism ๐Ÿ“Pseudopseudohypoparathyroidism โ–ซSickle cell disease (post- dactylitis) #radiology   ใ€ฐใ€ฐใ€ฐใ€ฐใ€ฐใ€ฐใ€ฐใ€ฐใ€ฐใ€ฐใ€ฐ ยฉMedical Mnemonics

Repost from EDL Backup Channel
โš ๏ธ ๐Ÿ”” ๐’๐€๐•๐„ ๐“๐‡๐ˆ๐’ ๐‹๐ˆ๐’๐“ ๐…๐Ž๐‘ ๐€ ๐‘๐€๐ˆ๐๐˜ ๐ƒ๐€๐˜ !   โฌ‡๏ธ 1. ๐Ÿงฉ ๐— ๐—˜๐——๐—œ๐—–๐—”๐—Ÿ ๐— ๐—ก๐—˜๐— ๐—ข๐—ก๐—œ๐—–๐—ฆ (๐—Ÿ๐—˜๐—”๐—ฅ๐—ก ๐—˜๐—”๐—ฆ๐—œ๐—Ÿ๐—ฌ) 2. ๐—–๐—”๐—ฆ๐—˜ - ๐—•๐—”๐—ฆ๐—˜๐—— ๐— ๐—–๐—ค๐—ฆ โ” 3. ๐Ÿ‡จ๐Ÿ‡ฆ ๐— ๐—–๐—–๐—ค๐—˜ ๐—ฃ๐—ฅ๐—˜๐—ฃ๐—”๐—ฅ๐—”๐—ง๐—œ๐—ข๐—ก 4. ๐Ÿฉบ ๐—˜๐——๐—Ÿ ๐— ๐—˜๐——๐—œ๐—–๐—ข๐—ฆ (๐— ๐—˜๐——๐—œ๐—–๐—”๐—Ÿ ๐—•๐—ข๐—ข๐—ž๐—ฆ ๐—”๐—ก๐—— ๐—Ÿ๐—œ๐—ก๐—ž๐—ฆ) 5. ๐Ÿ“š ๐—˜๐——๐—Ÿ ๐—ฃ๐—›๐—”๐—ฅ๐—  6. ๐Ÿ›๐Ÿ“ท ๐—ข๐—ก๐—Ÿ๐—œ๐—ก๐—˜ ๐— ๐—˜๐——๐—œ๐—–๐—”๐—Ÿ ๐—ฆ๐—–๐—›๐—ข๐—ข๐—Ÿ 7. ๐—ฅ๐—˜๐—ฆ๐—œ๐——๐—˜๐—ก๐—–๐—ฌ ๐—œ๐—ก ๐—š๐—˜๐—ฅ๐— ๐—”๐—ก๐—ฌ ๐Ÿ‡ฉ๐Ÿ‡ช 8. ๐—ฃ๐—ฅ๐—”๐—–๐—ง๐—œ๐—–๐—˜ ๐—œ๐—ก ๐—”๐—จ๐—ฆ๐—ง๐—ฅ๐—”๐—Ÿ๐—œ๐—” ๐Ÿ‡ฆ๐Ÿ‡บ 9. ๐— ๐—•๐—•๐—ฆ & ๐—ฅ๐—˜๐—ฆ๐—œ๐——๐—˜๐—ก๐—–๐—ฌ ๐—œ๐—ก ๐—œ๐—ง๐—”๐—Ÿ๐—ฌ ๐Ÿ‡ฎ๐Ÿ‡น 10. ๐—ฅ๐—˜๐—ฆ๐—œ๐——๐—˜๐—ก๐—–๐—ฌ ๐—œ๐—ก ๐—จ๐—ž ๐Ÿ‡ฌ๐Ÿ‡ง 11. ๐—ฅ๐—˜๐—ฆ๐—œ๐——๐—˜๐—ก๐—–๐—ฌ ๐—œ๐—ก ๐—จ๐—ฆ ๐Ÿ‡บ๐Ÿ‡ธ 12. ๐—ฅ๐—˜๐—ฆ๐—œ๐——๐—˜๐—ก๐—–๐—ฌ ๐—œ๐—ก ๐—–๐—”๐—ก๐—”๐——๐—” ๐Ÿ‡จ๐Ÿ‡ฆ 13. ๐—™๐—ฅ๐—˜๐—ก๐—–๐—› ๐— ๐—˜๐——๐—œ๐—–๐—”๐—Ÿ ๐—•๐—ข๐—ข๐—ž๐—ฆ ๐Ÿ‡ซ๐Ÿ‡ท 14. ๐—š๐—˜๐—ฅ๐— ๐—”๐—ก ๐— ๐—˜๐——๐—œ๐—–๐—”๐—Ÿ ๐—•๐—ข๐—ข๐—ž๐—ฆ ๐Ÿ‡ฉ๐Ÿ‡ช 15. ๐— ๐—˜๐——๐—œ๐—–๐—”๐—Ÿ ๐—ฅ๐—˜๐—ฆ๐—˜๐—”๐—ฅ๐—–๐—› ๐ŸŽ“๐Ÿซฅ 16. ๐Ÿ“ธ ๐——๐—˜๐—ฅ๐— ๐—”๐—ง๐—ข๐—Ÿ๐—ข๐—š๐—ฌ ๐—”๐—ง๐—Ÿ๐—”๐—ฆ 17. ๐—ข๐—˜๐—ง ๐—ฃ๐—ฅ๐—˜๐—ฃ๐—”๐—ฅ๐—”๐—ง๐—œ๐—ข๐—ก โœ… 18. ๐— ๐—˜๐——๐—œ๐—–๐—”๐—Ÿ ๐—”๐— ๐—”๐—ญ๐—ข๐—ก  ๐ŸŒ 19.  ๐—–๐—”๐—ฅ๐——๐—œ๐—ข๐—Ÿ๐—ข๐—š๐—ฌ ๐—–๐—”๐—ฆ๐—˜๐—ฆ ๐Ÿซ€ 20. ๐Ÿ’  ๐—จ๐—ช๐—ข๐—ฅ๐—Ÿ๐—— ๐—˜๐——๐—จ๐—–๐—”๐—ง๐—œ๐—ข๐—ก๐—”๐—Ÿ ๐—ข๐—•๐—๐—˜๐—–๐—ง๐—œ๐—ฉ๐—˜๐—ฆ 21. ๐— ๐—˜๐——๐—œ๐—–๐—–๐—ข๐—จ๐—ก๐—ง - ๐— ๐—˜๐——๐—œ๐—–๐—”๐—Ÿ ๐—”๐—–๐—–๐—ข๐—จ๐—ก๐—ง ๐Ÿ”„ 22. ๐Ÿ› ๐— ๐—˜๐——๐—œ๐—–๐—”๐—Ÿ ๐—ฆ๐—–๐—œ๐—˜๐—ก๐—–๐—˜๐—ฆ ๐—”๐—ฃ๐—ฃ๐—Ÿ๐—ฌ

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