Dr. Rakib's Med Academy

21/09/2025

😴 Dizziness Made Easy 😴
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🔷Dizziness = one of the most common challenging complaints in clinical practice.

🔷It is not a diagnosis, but a symptom with multiple possible underlying causes.

🔷First and most important step: clarify what the patient actually means by “dizzy.”

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✅ Three Main Categories of Dizziness
⚡|⚡|⚡|⚡|⚡|⚡|⚡|⚡|⚡|⚡|⚡|

ℹ️ Vertigo (Spinning / Rotation sensation)
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ℹ️ℹ️ Presyncope (Impending faint / blackout sensation)
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ℹ️ℹ️ℹ️Non-Specific Dizziness (lightheadedness, malaise, fatigue)

🚩اولا 🚩

ℹ️ Vertigo (Spinning / Rotation sensation)
________________________________________

👉 Definition: False sense of movement (self or surroundings spinning).

👉 Origin: Disorder of balance system → either central (cerebellum) or peripheral (inner ear / vestibular system).

💁Peripheral vertigo vs Central vertigo 💁
``````````````````````````````````````````````````````````

🟪Peripheral Vertigo – Key Features:
~~~~~~~~~~~~~~~~~~~~~~~~~

⚡Sudden, severe, episodic attacks (seconds–minutes).

⚡Nystagmus: horizontal or rotatory.

⚡Often associated with auditory symptoms (hearing loss ± tinnitus).

⚡NO neurological findings (no cerebellar signs).

🚩Peripheral Causes:
•••••••••••••••••••••••••••••

1️⃣BPPV (Benign Paroxysmal Positional Vertigo):
________________________________________

✔️Brief, position-induced vertigo (turning head, lying down, sitting up suddenly).

✔️Due to dislodged otoconia.

✔️Diagnosis: Dix–Hallpike test (+ve).

2️⃣Vestibular Neuritis:
_______________________

✔️Post-viral inflammation of vestibular branch of CN VIII.

✔️Severe vertigo for days, sudden onset.

✔️No hearing loss.

✔️+ve Head thrust test.

✔️Symptoms: imbalance, oscillopsia, nausea, vomiting.

3️⃣Labyrinthitis:
_________________

✔️Inflammation of both vestibular + cochlear branches.

✔️Vertigo + Hearing loss + Tinnitus.

🚩Types:
`````````````

✔️Viral (post-URTI).

✔️Serous (chronic otitis media).

✔️Suppurative (bacterial, toxic patient, severe).

✔️Toxic (drug-induced e.g. aminoglycosides).

✔️Chronic (fistula-related).

4️⃣Ramsay Hunt Syndrome
_________________________
→ unilateral facial palsy + vesicular rash + hearing loss + vertigo.

5️⃣Ménière’s Disease:
________________________

✔️Classic triad:

1. Episodic vertigo.

2. Sensorineural hearing loss.

3. Tinnitus.

✔️Attacks in clusters, with long symptom-free intervals.

💻Central Vertigo – Key Features:
~~~~~~~~~~~~~~~~~~~~~

⚡Gradual, continuous, or long-lasting (days–weeks).

⚡Nystagmus: vertical / downbeat.

⚡Not affected much by head position.

⚡Associated with neurological features (ataxia, dysarthria, diplopia, sensory changes).

⚡NO auditory symptoms.

🔷Central Causes:
____________________

1️⃣Cerebellar hemorrhage: sudden, severe vertigo + headache, vomiting, ataxia (hypertensive elderly).

2️⃣Cerebellar infarction: sudden vertigo + cerebellar signs (ataxia, nystagmus) in stroke-risk patients (HTN, DM, AF).

3️⃣Vertebrobasilar insufficiency: recurrent vertigo + brainstem/cerebellar signs.
⤵️⤵️⤵️
“5 Ds”: Dizziness, Diplopia, Dysarthria, Dysphagia, Drop attacks.

4️⃣Vestibular Migraine:⤵️⤵️

⚡≥5 episodes (5 min – 72 hrs) with vestibular symptoms.
⚡History of migraine.
⚡Migraine features (headache, photophobia, aura, nausea).

5️⃣Basilar Migraine:
migraine with brainstem aura (dysarthria, diplopia, tinnitus, vertigo, ataxia, bilateral paresthesia, ↓ consciousness).

6️⃣Multiple Sclerosis: demyelination → cerebellar involvement (ataxia, dysmetria, dysdiadochokinesia), plus optic neuritis / pyramidal signs.

7️⃣ Cerebellar tumours ; vertigo plus other features of cerebellar syndrome plus headache with signs of ↑ ICT

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🚩ثانيا 🚩

ℹ️ℹ️ Presyncope (Impending faint / blackout sensation)

👉 Definition: Feeling about to lose consciousness, sometimes with real syncope.

🔷Main Causes:
~~~~~~~~~~~~

🚩Orthostatic Hypotension:⤵️
______________________________

✓Definition: ↓ SBP ≥20 mmHg or ↓ DBP ≥10 mmHg on standing.

✓Causes:
__________

1️⃣Diabetic autonomic neuropathy.

2️⃣Autonomic dysfunction (amyloidosis, Shy–Drager syndrome, elderly).

3️⃣Addison’s disease (chronic: pigmentation, weight loss / acute: steroid withdrawal, stress).

4️⃣Acute hypovolemia: dehydration, diarrhea, hemorrhage, DKA.

🚩Reflex Syncope:
____________________

1️⃣Vasovagal: fear, prolonged standing → pallor, sweating, collapse, hypotension.

2️⃣Carotid sinus hypersensitivity: triggered by neck pressure (shaving, collar, massage).

🚩Cardiac Syncope: 🚨 dangerous
____________________________________

1️⃣Obstructive: Aortic stenosis, HOCM.

2️⃣Bradyarrhythmias: 2nd/3rd degree block (Adams–Stokes attacks → pallor → syncope → flushing).

3️⃣Tachyarrhythmias: SVT, AF, VT; may be associated with chest pain in MI.

4️⃣Sudden death syndromes: Brugada, Long QT.

Mimics: المتشابهات خلى بالك ‼️
~~~~~~~

⭕Hypoglycemia: dizziness, sweating, tremor, palpitations → neuroglycopenia (confusion, coma) if untreated.

⭕Psychogenic: anxiety, panic attacks (dyspnea, suffocation, globus, palpitations).

===========================

🚩ثالثا 🚩

ℹ️ℹ️ℹ️Non-Specific Dizziness (lightheadedness, malaise, fatigue)

🔷Common Causes:
_____________________

1️⃣Anemia: pallor, exertional SOB, fatigue.

2️⃣Infection: fever, myalgia, systemic symptoms.

3️⃣Depression: low mood, guilt, anhedonia.

4️⃣Tension headache: often with anxiety/depression.

5️⃣Hypertension: sometimes with high BP (>160/100), headache ± dizziness.

7️⃣Drug-induced:

⚡Antidepressants, Antipsychotics.

⚡Anticonvulsants, Sedatives.

⚡Antihypertensives.

⚡Chemotherapeutics.

🔑 Clinical Approach (Step-by-step)
___________________________________

1️⃣ Clarify type of dizziness (Vertigo vs Presyncope vs Non-specific).

🗣️Ask: “Do you feel the world spinning? About to faint? Or just vague lightheadedness?”

2️⃣ History:

Onset, duration, triggers, associated symptoms (hearing loss, tinnitus, neurological, chest pain, palpitations).

3️⃣ Examination:

signs (BP lying/standing, HR).

exam (cerebellar signs).

exam (nystagmus, hearing).

exam (murmurs, irregular pulse).

4️⃣Investigations guided by suspicion:

, Echo (cardiac).

-Hallpike, Head thrust (ENT).

brain (neurological).

tests: CBC (anemia), glucose, electrolytes, cortisol (a m) if suspected Addison's disease

20/09/2025

🟪 Approach to Myopathy made Easy 💻
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🎯approach to myopathy

✍️Note : Photos for approaches in comments

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Myopathy and Muscle Weakness
==↘️=====↘️====↙️======↙️==

🌄To reach the diagnosis of myopathy , you have to take all such considerations into your mind 🧠

ℹ️Regarding Patterns of Muscle Involvement
~~~~~||||~~~~~|||~~~~~|||~~~~|||~~~~~~

👨‍⚕️The distribution of weakness is an important diagnostic clue:

🔷Proximal Weakness( weakness affecting proximal muscles of the limbs)
••••••••••••••••••••••••••••••••••••••••••••••••••••••••

⭕Causes ⤵️

⚡Muscular dystrophies such as⤵️
dystrophy
dystrophy
-girdle dystrophy
dystrophy
myopathy

⚡Congenital myopathies such as
core disease
disease
myopathy
rod myopathy

⚡Metabolic myopathies such as
storage disorders
storage disorders
myopathies

⚡Inflammatory myopathies such as , dermatomyositis, -mediated necrotizing myopathy, and syndrome

⚡Endocrine ( e g $, disorders etc)

⚡Toxic myopathies ( toxins & drug induced )

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🔷Distal Weakness( weakness affecting mainly the distal muscles of the limbs)
••••••••••••••••••••••••••••••••••••••••••••••••••••••••

⭕Causes ⤵️

⚡Distal muscular dystrophies and myofibrillar myopathies

⚡Congenital myopathies (late-onset centronuclear myopathy, nemaline rod myopathy)

⚡Metabolic disorders such as glycogen storage disease and lipid storage disease
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🔷Proximal Arm with Distal Leg Weakness
••••••••••••••••••••••••••••••••••••••••••••••••••••••••••

⭕Causes ⤵️

⚡Facioscapulohumeral dystrophy

⚡Scapuloperoneal myopathy

⚡Myofibrillar myopathies

⚡Emery-Dreifuss muscular dystrophy

⚡Bethlem myopathy
--------------------

🔷Distal Arm with Proximal Leg Weakness
••••••••••••••••••••••••••••••••••••••••••••••••••••••••••

⭕Causes ⤵️

⚡Inclusion body myositis (involving finger flexors and quadriceps)

⚡Myotonic dystrophy (in some cases)

🔷Axial Weakness
••••••••••••••••••••••••••

⭕Causes ⤵️

⚡Inflammatory myopathy

⚡Hereditary inclusion body myopathy

⚡Myotonic dystrophy type 2

⚡Neck extensor myopathy leading to “dropped head syndrome”
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🔷Eye Muscle Weakness (Ptosis or Ophthalmoplegia)
••••••••••••••••••••••••••••••••••••••••••••••••

⭕Causes ⤵️

⚡Myotonic dystrophy

⚡Congenital myopathies

⚡Mitochondrial myopathies

⚡Neuromuscular junction disorders such as myasthenia gravis and Lambert-Eaton myasthenic syndrome

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🔷Episodic Weakness or Myoglobinuria
••••••••••••••••••••••••••••••••••••••••••••••••••••••••

⭕Causes ⤵️

⚡Related to exercise:
••••••••••••••••••••••••••••••
storage disorders such as McArdle disease
disorders such as carnitine palmitoyltransferase deficiency,
myopathies such as cytochrome b deficiency

⚡Not related to exercise:
•••••••••••••••••••••••••••••••••••
hyperthermia and
rhabdomyolysis,
paralysis syndromes
and
-induced causes such as statins

⚡Delayed or unrelated to exercise: causes such as viral myositis, and endocrine or electrolyte-related causes

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🔷Muscle Stiffness and Delayed Relaxation
•••••••••••••••••••••••••••••••••••••••••••••••••••••••••••

⭕Causes ⤵️

⚡Myotonic dystrophy types 1 and 2

⚡Paramyotonia congenita

⚡Hyperkalemic periodic paralysis with myotonia

⚡Potassium-aggravated myotonia

⚡Neuromyotonia such as Isaac’s syndrome

»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»

ℹ️ℹ️Approach to Intermittent Weakness
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Step 1️⃣: Look for Myoglobinuria
-----------------------------------------------------

🔷If present → suspect metabolic myopathies such as
storage disorders
metabolism disorders
disorders

⚡Use the forearm exercise test:

lactic acid rise → glycolytic pathway defect , it would be storage disorders ( disease)

lactic acid rise → fatty acid metabolism disorder such as carnitine deficiency

Step 2️⃣: If Myoglobinuria is Absent
--------------------------------------------------------

🔷If there is Normal strength between attacks with proximal greater than distal weakness during episodes , order ECG ‼️⤵️⤵️⤵️

⚡Abnormal electrocardiogram → consider syndromes with dysmorphic features such as Andersen-Tawil syndrome ( prominent U waves and risk of bidirectional ventricular tachycardia

⚡Normal electrocardiogram → check for myotonia

🚩If no myotonia → periodic paralysis (hypokalemic or hyperkalemic)

🚩If myotonia is present → confirm by genetic testing

🔷If there is Variable weakness including extraocular muscles, ptosis, bulbar, and limb muscles
⤵️⤵️⤵️⤵️⤵️

⚡Order Acetylcholine receptor antibody or muscle-specific kinase antibody positive → acquired myasthenia gravis (screen for thymoma)

🚩If antibody negative → perform repetitive nerve stimulation or single-fiber electromyography

🚩If abnormal → consider the diagnosis of Lambert-Eaton myasthenic syndrome (screen for small cell lung cancer, check voltage-gated calcium channel antibody)

🚩If normal → consider seronegative myasthenia gravis, congenital myasthenia, or functional weakness

»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»

ℹ️ℹ️ℹ️ Approach to Persistent Weakness
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Step 1️⃣: Identify the Pattern of Weakness
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🔷 If there is Proximal greater than distal weakness →possibilities ⤵️⤵️
myopathies (polymyositis, dermatomyositis
# immune-mediated necrotizing myopathy), dystrophies
myopathies
myopathies

myopathies

🔷If there is Ptosis and extraocular muscle weakness →possibilities ⤵️⤵️
muscular dystrophy, myopathy
myopathy

🔷If there is Facial weakness and scapular winging → muscular dystrophy

🔷 If there is Facial weakness with distal myotonia → dystrophy

🔷 If there is Proximal and distal weakness (hand grip and quadriceps) → body myositis

🔷If there is Distal weakness only → myopathies

🔷 If there is Dropped head or axial weakness → possibilities ⤵️⤵️
gravis

lateral sclerosis,
myopathy

Step 2️⃣: Confirm with Diagnostic Testing
-------------------------------------------------------------------
🔷يتم طلبهم فى أغلب الحالات 🔷

🔷Electromyography → confirms myopathy and helps exclude motor neuron disease such as amyotrophic lateral sclerosis

🔷Repetitive nerve stimulation → may reveal neuromuscular junction disorder such as myasthenia gravis, Lambert-Eaton syndrome, or botulism

🔷Serum creatine kinase elevation → supports diagnosis of myopathy

🔷DNA testing → useful for hereditary myopathies

🔷Muscle biopsy → often required for final diagnosis and to distinguish between disorders

✅ Summary
•••••••••••••••••
🟪Patterns of weakness (proximal, distal, axial, ocular, episodic, stiffness) are central to narrowing the differential diagnosis.

🟪Intermittent weakness → think about neuromuscular junction disorders, periodic paralysis syndromes, and metabolic myopathies.

🟪Persistent weakness → use distribution of weakness plus investigations such as electromyography, creatine kinase, genetic testing, and muscle biopsy for diagnosis.

19/09/2025

✍️Nutshell Notes about Adrenal Insufficiency ( Addison disease = Primary Adrenal insufficiency Vs Secondary Adrenal insufficiency)
=========================================
🎯Adrenal insufficiency in any exam may present as any of the following scenarios :

(* The critical presentation is Adissonian Crisis in which the patient will have hemodynamic instability with marked hypovolemia and electrolytes disturbance).
1- Neurological : Syncope ( Should be differentiated from Seizure), Recurrent Falls, Gait abnormality or imbalance.
2- Fatigue
3- Recurrent Hypoglycemia ( in patient with Background of long term use of steroids that stopped abruptly)
4- GIT symptoms ( Abdominal pain with Normal Abdominal examination , alternating bowel habits , recurrent loose motions or Constipation )
5- Anemia related symptoms
6- Symptoms due to electrolyte disturbance ( Hyponatremia/Hyperkalemia)

💉The Most common Presentation is secondary Adrenal Insufficiency and The most common cause is related to Exogenous Steroid Administration which will affect HPA if suddenly withdrawal.
💉Steroid dose 5 mg per day for 3 weeks or more usually affect HPA axis and therefore gradual withdrawal is needed to avoid adrenal suppression.
=======================================
💉The most common causes of Primary Adrenal insufficiency include :

1- Infections : CMV, Tuberculous , Histoplasmosis , Meningococcemia , sepsis ( especially in immunosuppressed patient and those presents with disseminated cutaneous fungal infection).
2- Vascular : Hemorrhage , Thrombosis due to APLS , Myeloproliferative , HIT , DIC
3- Infiltrative : Hemochromatosis , Sarcoidosis , Histiocytosis , Amyloidosis
4- Metastatic tumors
5- Drug induced ( Ketoconzole , Myterapone , Etomidate , Over warfariniztion )
6- Adrenalectomy
7-Autoimmune Adrenalitis ( Alpha 21-hydroxylase Antibody).

💉The most common causes of secondary Adrenal insufficiency related to Pituitary Thalamic diseases ( Trauma , radiation, Infarction , Adenoma . infilterations , infection ..)

==========================================

✍️Adrenal insufficiency Patient may present with reversible Ataxia ( reversible Cerebellar Ataxia) related to marked Hyponatremia or due to other causes like Celiac ataxia or vitamins deficiency.

✍️One of important differentials between Primary and secondary Adrenal insufficiency is that in case of Primary Adrenal insufficiency (Addison disease) there is cutaneous Hyperpigmentation , Why? ---> Because there is loss of Negative feedback with overproduction of Pro-Opiomelanocortin ( POCM) a precursor molecule that is cleaved into ACTH and alpha-Melanocyte stimulating Hormone both of them stimulating Melanocytes to produce more melanin resulting in Hyperpigmentation.

=========================================
✍️Laboratory investigations suggestive of Adrenal insufficiency :

Normal Anion Gap Metabolic Acidosis ( VBG/ABG)
Hypoglycemia ( Low BG Measurement)
Hyponatremia / Hyperkalemia
Eosinophilia
Lymphocytosis
Anemia

✍️Once suspected , Measure Morning Cortisol level and ACTH level ( Cortisol level < 100nmol/ml) or level is less than 3 microgram/dl is suggestive of the diagnosis. ACTH level is expected to be elevated in presence of Low Cortisol level in case of primary Adrenal Insufficiency. ( * Cutoff morning cortisol level > 13-18microgram/dl is sufficient to rule out Adrenal insufficiency and levels between 3-13 microgram/dl requires further investigation like short synacthen test to rule out the diagnosis).

✍️The confirmatory test is short synacthen Test ( 250 Microgram Cosyntropin) given IV or IM and cortisol level should be measured 30, 60, 90 minutes after.. Failure to raise serum cortisol level > 550nmol/ml after 30 minutes or failure to raise cortisol level > 200 nmol/L from baseline confirms inappropriate response ( Adrenal insufficiency) which can be either primary or secondary. The next step is to measure ACTH level which will be elevated in case of Primary Adrenal insufficiency.

✍️To Do short synacthen Test --> The patient should not Take estrogen, Spironolactone Tablet for last 6 weeks and should stop steroid dose 1 day before the test.

✍️If suspecting Addison disease ---> request for 21-Hydroxylase Antibody .

✍️Other important tests will be needed according to the scenario include --> Viral screening , TB screening , Adrenal or pituitary imaging , ECG due to electrolytes disturbance , other autoimmune markers in case of Polyglandular syndrome.

=========================================
🎯The Broad Map for Treatment of Adrenal insufficiency include :
☑️Treat the underlying cause, Correct The Volume status with IV crystalloids , Correct electrolytes disturbance.

☑️ Steroid replacement ( the dose should follow the Circadian Rhythm with 2/3 dose in the morning and 1/3 dose at Midday the usual dose 20-30 mg daily Hydrocortisone )--> avoid giving dose at Night as it it may induce insomnia or psychosis.

☑️The recommended equivalent prednisolone dose is range from 2-4 mg OD which has the benefit of being long acting and taken once daily at morning compared to Hydrocortisone ( 3 mg prednisolone equivalent to 20 mg Hydrocortisone taken 10 mg morning , 5 mg at noon and 5 mg afternoon).

☑️to make sure about the appropriate dose of prednisolone for steroid replacement in adrenal insufficiency , measure cortisol level 8 h after the dose , if the cortisol level between 15-25mcg/dL then replacement is adequate.

☑️ Importantly should know there is no superiority of using Hydrocortisone over prednisolone for steroid replacement in adrenal insufficiency regarding clinical response , bone profile and quality of life.

☑️In case of Treating Adrenal Crisis : The treatment include IV crystalloids , IV hydrocortisone dose 100 mg Loading then 50 mg IV/6h or 200 mg Continuous infusion over 24 h for 48hours till patient is able to take oral .

☑️There is no need to provide mineralocorticoid ( Fludrocortisone) during management of Adrenal crisis with Hydrocortisone.

☑️IV Dexamethasone is not recommended in the management of Adrenal crisis as it lacks mineralocorticoid effect.

☑️In case of persistent symptoms despite appropriate Cortisol replacement in adrenal insufficiency : Add fludrocortisone 100-150 mic/day.
=======================================
☑️Steroid dose should be Doubled ( steroid Sick Day Rules ) during criticall illness or planned major surgery and also during pregnancy especially in Third trimester.
☑️ If the patient is having Long haul travel ( > 12 hours ) should take extra dose 1mg of regular prednisolone daily dose till arrival then next day take his regular doses.

☑️The patient should be counseled about red flags of adrenal insufficiency and should have Steroid Emergency Card ( Card contains : Name , dose steroid you are on , and indication , the dose during emergency situation , First contact Number if patient is unwell and Q code that can be scanned to contact with relevant health care provider ) or Medical Alert Bracelet.

☑️The patient should be counseled that this replacement dose is unlikely to cause systemic side effects as it is replacement of already deficient body Hormone and given in a lower dose.

15/07/2025

🩺20 Atrial Fibrillation Facts Every Physician Needs to Know in 2025.
💖https://www.pointofcaremedicine.com/blog-post/20-atrial-fibrillation-facts-every-physician-needs-to-know-in-2025.

Summary
Atrial fibrillation is the most common sustained cardiac arrhythmia, affecting approximately 10.55 million adults in the US with a lifetime risk of up to 1 in 3 people.
Atrial fibrillation is classified into four stages reflecting disease progression: stage 1 (at risk), stage 2 (pre-AF), stage 3 (clinical AF), and stage 4 (permanent AF).
Oral anticoagulation is indicated for AF patients with an estimated thromboembolic risk of ≥2% per year (CHA₂DS₂-VASc ≥2 for men, ≥3 for women), as anticoagulation reduces stroke risk by 60-80% compared to placebo.
Catheter ablation is first-line therapy for symptomatic paroxysmal AF and is superior to antiarrhythmic drugs for maintaining sinus rhythm and improving quality of life.
Patients with AF and heart failure with reduced ejection fraction (HFrEF) benefit significantly from rhythm control with catheter ablation, showing improvements in mortality, hospitalization rates, and ventricular function.
Early rhythm control (within 12 months of AF diagnosis) is associated with better outcomes, including reduced cardiovascular mortality, stroke, and hospitalizations compared to rate control.
Rate control in AF targets a resting heart rate of

This guide compiles essential facts to help physicians optimize their approach to AF, from diagnosis and risk stratification to treatment selection and addressing health disparities.

15/07/2025

15/07/2025

Some Important test in Hepatology..

31/05/2025

🌼💮 causes of OPTIC DISC SWELLING 💮🌼
এটা সহজে মনে থাকতে চায় না। but যদি একটু মেকানিজম চিন্তা করে পড়ি, তাহলেই পানির মত সোজা হয়ে যাবে।
☘️ optic disc কী?
↔️ Optic nerve head. সোজাকথায়, optic nerve এর একমাত্র visual portion, যেটা fundoscopy করলে দেখা যায়। central retinal artery & vein এখানেই যথাক্রমে entry & exit করে। তারমানে, optic nerve head যখন elevated/enlarged হয়, তখন optic disc টা swollen দেখায়। উল্লেখ্য, যখন optic Nerve এর উপর প্রেসারের কারনে ২চোখের optic disc swelling হয়, সেটাকে papilloedema বলা হয়।
তাহলে, মোটাদাগে, optic disc swelling এর কারন ৪ ধরনের:
1. optic nerve এর উপর প্রেসার (raised ICP)
2. Venous obstruction(local causes)
3. Arterial causes (systemic causes)
4. Optic nerve (itself) damage (various causes)
[ to remember: pressure, vein, artery, nerve]

◑ optic nerve এর উপর বাহ্যিক প্রেসার (raised ICP-Papilloedema) ➡️
> solid: mass; tumor, abscess
>liquid : obstructive hydrocephalus
>? : idiopathic intracranial HTN

◑ venous obstruction: ➡️
>central retinal vein occlusion
>cavernous sinus thrombosis

◑arterial causes : ➡️
>HTN
>vasculitis
>hypercapnia
(Hypercapnia → cerebral vasodilation → ↑ cerebral blood flow → ↑ ICP → pressure on optic nerve)

◑optic nerve damage :➡️
> demyelination: multiple sclerosis
>ischemia of nerve itself: AION(Anterior Ischaemic Optic Neuropathy)
>toxic: methanol
>infiltrative: sarcoidosis, lymohoma, glioma, TB
>hereditary: leber's hereditary optic neuropathy
>infective: syphilis, lyme's disease

31/05/2025

💁Topics: Pulse + Common abnormalities of the apex beat🏃

🔹 Q1. A 65-year-old man with a history of aortic stenosis is found to have a slow-rising, low-amplitude carotid pulse. What is the most likely term used to describe this pulse?
A. Pulsus paradoxus
B. Pulsus alternans
C. Anacrotic pulse
D. Bisferiens pulse
E. Collapsing pulse
✅ Answer: C. Anacrotic pulse
Explanation:
Anacrotic (slow-rising) pulse is characteristic of aortic stenosis.
Features: low amplitude, delayed upstroke.
It reflects the prolonged ejection phase due to obstructed LV outflow.
Best felt in the carotid artery.

🔹 Q2. A patient with severe aortic regurgitation is found to have a rapidly rising and collapsing radial pulse. What is the classical name for this pulse?
A. Pulsus bisferiens
B. Collapsing pulse
C. Dicrotic pulse
D. Pulsus alternans
E. Anacrotic pulse
✅ Answer: B. Collapsing pulse
Explanation:
Collapsing (water hammer) pulse is typical of aortic regurgitation.
It results from:
High stroke volume
Rapid diastolic runoff back into LV
Best appreciated with the arm elevated above the head.

🔹 Q3. A 40-year-old woman with constrictive pericarditis is found to have an elevated JVP with a prominent y descent. What is the most likely underlying cause?
A. Tricuspid stenosis
B. Cardiac tamponade
C. Right heart failure
D. Constrictive pericarditis
E. Pulmonary embolism
✅ Answer: D. Constrictive pericarditis
Explanation:
In constrictive pericarditis, the y descent is prominent due to rapid early diastolic filling being abruptly halted.
Other JVP features: elevated JVP, Kussmaul's sign (inspiratory rise).
Tamponade, by contrast, shows absent y descent.

🔹 Q4. A 32-year-old man with hypertrophic cardiomyopathy is found to have a bifid carotid pulse with two palpable peaks in systole. What is the correct term for this pulse?
A. Anacrotic pulse
B. Bisferiens pulse
C. Pulsus alternans
D. Collapsing pulse
E. Pulsus paradoxus
✅ Answer: B. Bisferiens pulse
Explanation:
Bisferiens pulse: two systolic peaks felt during a single cardiac cycle.
Seen in:
Hypertrophic cardiomyopathy (HOCM)
Combined aortic stenosis + regurgitation
Mechanism: dynamic obstruction of LVOT.

🔹 Q5. You are examining a patient’s neck veins. You see a biphasic waveform that is not palpable and changes with posture and respiration. What is the most likely structure you are observing?
A. Carotid artery
B. External jugular vein
C. Internal jugular vein
D. Subclavian vein
E. Vertebral artery
✅ Answer: C. Internal jugular vein
Explanation:
Internal jugular pulse:
Not palpable
Biphasic waveform (a and v waves)
Varies with respiration and posture
Carotid is palpable, monophasic, and not affected by respiration.

🔹 Q6. A 68-year-old man with mitral regurgitation has a displaced and hyperdynamic apex beat. Which of the following best explains this apex beat abnormality?
A. Pressure overload of LV
B. Volume overload of LV
C. Right ventricular hypertrophy
D. Pericardial effusion
E. Constrictive pericarditis
✅ Answer: B. Volume overload of LV
Explanation:
Hyperdynamic and displaced apex beat suggests LV volume overload.
Seen in:
Mitral regurgitation
Aortic regurgitation
Apex is diffuse and forceful.

🔹 Q7. A patient with cardiac tamponade presents with hypotension, elevated JVP, and a large decrease in systolic BP during inspiration. What is the term for this finding?
A. Pulsus alternans
B. Pulsus paradoxus
C. Dicrotic pulse
D. Anacrotic pulse
E. Collapsing pulse
✅ Answer: B. Pulsus paradoxus
Explanation:
Pulsus paradoxus: exaggerated fall in systolic BP (>10 mmHg) during inspiration.
Seen in:
Cardiac tamponade
Severe asthma
Tension pneumothorax
Caused by impaired LV filling due to interventricular dependence.

🔹 Q8. A 70-year-old patient with atrial fibrillation is found to have an irregularly irregular pulse with absent 'a' waves in the jugular venous pulse. What is the reason for this JVP finding?
A. AV dissociation
B. Absence of atrial contraction
C. Tricuspid stenosis
D. Right atrial tumor
E. Complete heart block
✅ Answer: B. Absence of atrial contraction
Explanation:
In atrial fibrillation, there is no coordinated atrial contraction → no 'a' wave in JVP.
Pulse is irregularly irregular, and varying intensity.

🔹 Q9. On cardiac examination, a patient is found to have a tapping, non-displaced apex beat and a loud first heart sound. What is the likely diagnosis?
A. Aortic stenosis
B. Mitral regurgitation
C. Mitral stenosis
D. Aortic regurgitation
E. Cardiomyopathy
✅ Answer: C. Mitral stenosis
Explanation:
Tapping apex beat: palpable S1.
Indicates mobile mitral valve leaflets closing loudly.
Common in mitral stenosis, often rheumatic in origin.
Apex is not displaced.

🔹 Q10. A 60-year-old man is found to have a sustained, heaving apex beat located in the 6th intercostal space, lateral to the midclavicular line. What is the most likely cause of this apex beat abnormality?
A. Left ventricular hypertrophy from hypertension
B. Atrial septal defect
C. Right ventricular hypertrophy
D. Mitral stenosis
E. Pericardial effusion
✅ Answer: A. Left ventricular hypertrophy from hypertension
Explanation:
Heaving (sustained) apex beat suggests pressure overload of LV.
Seen in:
Aortic stenosis
Chronic hypertension
It is localized, forceful, and sustained.
Displacement reflects long-standing disease.