Few minutes with Dr.Das

Few minutes with Dr.Das Dr.Apurba Das
M.B.B.S( CU) FCPS part 2( Medicine)
MRCP (Paces)

09/11/2025

Painless ulcer + Painless LN :
Syphilis
Painless ulcer + Painful LN :
LGV
Painless beefy red ulcer,bleeds easily + No LN :
Granuloma inguinale

20/10/2025

🧭 Hemolytic anemia made Easy🧭
_____________________________________

🔹 Main Classification of Hemolysis
••••••••••••••••••••••••••••••••••••••••••••••••

🔷Extravascular Hemolysis → RBC destruction in spleen → splenomegaly present

🔷Intravascular Hemolysis → RBC destruction in circulation → no splenomegaly

A. EXTRAVASCULAR HEMOLYSIS
~~~~~~~~~~~~~~~~~~~~~~~

1. RBC Membrane Defects (Inherited)
----------------------------------------------------------------

Hereditary spherocytosis
Hereditary elliptocytosis
Hereditary stomatocytosis
Hereditary pyropoikilocytosis
Hereditary xerocytosis

2. Hemoglobinopathies (Inherited)
-----------------------------------------------------------

🔷Quantitative (↓ production)

Beta-thalassemia (major, intermedia, minor)
Alpha-thalassemias

🔷Qualitative (abnormal Hb structure)

Sickle cell anemia (Hb S)
Sickle Hb C disease
Sickle β-thalassemia
Hb C disease
Hb D disease
Hb E disease

3. Autoimmune
-----------------------------

Warm autoimmune hemolytic anemia (AIHA)

🌄 Clues to Common Causes
~~~~~~~~~~~~~~~~~~~~

🔸 Thalassemia (Major/Intermedia)
----------------------------------------------------------------

🧬Autosomal recessive
Clues: Mongoloid facies, prominent maxilla, repeated transfusions, iron overload signs

🔸 Sickle Cell Disease
------------------------------------------

🧬Autosomal recessive
Splenomegaly early → autosplenectomy later
Crises: abdominal/bone pain, osteomyelitis, avascular necrosis, stroke, acute chest syndrome

🔸 Hereditary Spherocytosis
------------------------------------------------

🧬Autosomal dominant

Strong Family history, jaundice post-infection, gallstones

🔸 Warm AIHA
--------------------------------

✓Search underlying cause ⤵️
⭕SLE (young females)
⭕CLL (≥50 yrs, high lymphocytes)
⭕NHL (any age, B-symptoms)

⭕Drugs: Penicillin, cephalosporins

B. INTRAVASCULAR HEMOLYSIS
~~~~~~~~~~~~~~~~~~~~~

1. Inherited 🧬
----------------

⭕G6PD deficiency
⭕Pyruvate kinase deficiency (mixed intra/extravascular)

2. Immune
----------------

⭕Cold AIHA
⭕Alloimmune (incompatible transfusion)
⭕Drug-induced (Penicillin, Cephalosporins, Methyldopa)

3. Mechanical
--------------------------------

⭕Microangiopathic (TTP, HUS, DIC, HELLP, malignant HTN, scleroderma)
⭕Prosthetic valves
⭕March hemoglobinuria (after walking)

4. Paroxysmal intravascular Hemolysis
----------------------------------------------------------------

⭕Paroxysmal nocturnal hemoglobinuria (PNH)
⭕Paroxysmal cold hemoglobinuria

5. Infections
------------------------

⭕Protozoa: Malaria, Babesiosis
⭕Bacteria: Clostridium infection

6. Toxic
----------------
Snake venom

7. Systemic
-----------------------
Wilson’s disease

💥 Clues to Common Intravascular Causes
~~~~~~~~~~~~~~~~~~~~~~~~~~~~

🔸 G6PD Deficiency
--------------------------------

🧬X-linked recessive

Hemolysis triggered by:
✓Fava beans
✓Drugs: sulfa, antimalarial, ciprofloxacin, dapsone
✓Infections

🔸 Cold AIHA
--------------------------------

Secondary to:
✓Infections: Mycoplasma pneumoniae, EBV/IMN
✓Lymphoproliferative disorders

🔸 Paroxysmal Cold Hemoglobinuria
----------------------------------------------------------------
Hemolysis after cold exposure

🔸 Incompatible Blood Transfusion
------------------------------------------------------------

Immediate (fatal) or delayed

C/P :Dyspnea, AKI, severe hemolysis after transfusion

🔸 PNH
----------------

Hemolysis ± thrombosis ± aplastic anemia (BM failure)

🔸 Mechanical Valve Hemolysis
--------------------------------------------------------

You must exclude other causes

🔸 MAHA (TTP/HUS/DIC)

✍️TTP: ≥3/5 → MAHA, ↓plts, renal impairment, fever, confusion/stroke + schistocytes

✍️HUS: Triad → MAHA + ↓plts + renal failure + schistocytes

✍️DIC: Sepsis/cancer/liver disease → bleeding + ↑PT/PTT/INR, ↓plts, ↓fibrinogen

🔸 Wilson’s Disease
--------------------------------

🧬 AR inheritance

C/P Acute/chronic liver disease + neuro signs (tremor, chorea, ataxia, dementia) + hemolysis ± AKI + Kayser–Fleischer rings

🩺 Focused History
~~~~~~~~~~~~~~

🔸 Present History

Ask about the following ⤵️

✓Onset, duration, course, first vs recurrent attack

✓Urine color, left flank pain

✓Precipitating factors ⤵️
Drugs/fava beans → G6PD
Infection → G6PD, Sickle cell, Cold AIHA
Night hemolysis → PNH
Post-transfusion → Alloimmune hemolysis

🔸 Associated Features
------------------------------------------------

🕵️Sickle cell: recurrent pain, osteomyelitis, stroke, ulcers, chest crises

🕵️TTP: fever, confusion, bleeding, purpura

🕵️HUS: bleeding + renal signs + diarrhea

🕵️Lymphoma/CLL: weight loss, lymphadenopathy

🕵️SLE: rash, photosensitivity, arthritis, oral ulcers, nephritis, seizures

🕵️Wilson: tremors, abnormal movements.

🔸 Past History
~~~~~~~~~~~~

Recurrent hemolytic episodes → Sickle cell anemia & G6PD deficuency

Thrombosis history → PNH, APS, SLE

Frequent transfusions → Thalassemia

Cholecystectomy → Hereditary Spherocytosis or Sickle Cell Anemia

Drugs: sulfa/antimalarial (G6PD), antibiotics/NSAIDs (drug-induced)

Family history: HS, sickle cell anemia , G6PD deficiency

Gynecologic: amenorrhea (iron overload), abortions (APS/SLE)

🔍 Focused Examination
~~~~~~~~~~~~~~~~~

🔸 General
----------------

✓Pallor + jaundice (universal)

✓Mongoloid facies, frontal bossing → Thalassemia

🔸 Extremities
----------------------------

✓Leg ulcers → Sickle cell anemia (SCA)

✓Hemiplegia (stroke) → SCA/PNH/APS

✓DVT → PNH, APS

✓LL edema → Thalassemia (heart failure )

🔸 Skin/Lymph Nodes
-----------------------------------------

✓Lymphadenopathy → Lymphoma/CLL

✓Butterfly/discoid rash → SLE

🔸 Abdomen
-------------------------

Splenomegaly → Extravascular hemolysis

No splenomegaly → Intravascular causes

🧪 Diagnostic Workup
~~~~~~~~~~~~~~~

🅰️ Basic Investigations

✓CBC: ↓Hb, normocytic/normochromic; high MCV if reticulocytosis

✓Low MCV → Thalassemia

✓Lymphocytosis → CLL ( absolute lymphocytic count > 5000 with lymphocytic leukocytosis

✓Bicytopenia → TTP/HUS/DIC, Evans syndrome, SLE, PNH

🔷Blood film ⤵️

✓Schistocytes → TTP/HUS/DIC
✓Spherocytes → HS, warm AIHA
✓Sickled cells → SCA
✓Heinz bodies → G6PD

🔷LFTs: ↑indirect bilirubin

🔷RFTs: ↑creatinine in intravascular hemolysis (ABO mismatch, Wilson, TTP/HUS, DIC, SLE)

🔷Urinalysis looking for ⤵️

✓Hemoglobin/hemosiderin → Intravascular Hemolysis
✓Urobilinogen → Extravascular Hemolysis

🔷ESR: high in SLE, lymphoma, CLL

🅱️ Specific Investigations
~~~~~~~~~~~~~~~~~

⭕Reticulocyte % ≥ 2.5 % → proves hemolysis

⭕LDH: high in all types

⭕Haptoglobin: low in intravascular Hemolysis

🔷Ultrasound: spleen evaluation

🔷Hb electrophoresis: for thalassemia/sickle anemias

🔷HS tests: Osmotic fragility / EMA binding (flow cytometry)

🔷AIHA: Direct Coombs test

⭕SLE workup: ANA, anti-dsDNA, C3/C4

⭕CLL: Blood film (smudge cells), flow cytometry (CD5,19,23)

🔷Lymphoma: LN biopsy, imaging, immunophenotyping

🔷Cold AIHA: Coombs test

🔷G6PD deficiency:

⭕During attack → Heinz bodies

⭕Between attacks → G6PD assay

🔷PNH: CD55, CD59, FLAER test

🔷MAHA/DIC: PT↑, PTT↑, INR↑, ↓plts, ↓fibrinogen, ↑FDPs

🔷Wilson’s: ↓ceruloplasmin, ↑24h urinary copper ± liver biopsy

🔷Mechanical valve: Echocardiography

✅ If cause unclear:
→ Blood film + Coombs test + CD55/59
+ G6PD assay + DIC screen + Wilson screen

AIDP (Acute Inflammatory Demyelinating Polyradiculoneuropathy) — the classic and most common variant of Guillain–Barré S...
14/10/2025

AIDP (Acute Inflammatory Demyelinating Polyradiculoneuropathy) — the classic and most common variant of Guillain–Barré Syndrome (GBS) — can present in several clinical and pathologic variants, depending on which fibers (motor, sensory, cranial, or autonomic) are predominantly involved.

Below are the main variants and subtypes of AIDP/GBS:

---

🔹 1. Classic AIDP

The most common form in Europe and North America.

Immune-mediated demyelination of peripheral nerves and roots.

Features:

Symmetric ascending weakness (legs → arms → cranial muscles).

Areflexia or hyporeflexia.

Mild sensory symptoms (paresthesia, numbness).

May have autonomic dysfunction.

Pathology: Segmental demyelination with inflammatory infiltrates (lymphocytes, macrophages).

---

🔹 2. AMAN (Acute Motor Axonal Neuropathy)

Pure motor form (no sensory loss).

Common in Asia and Latin America.

Often follows Campylobacter jejuni infection.

Pathogenesis: Antibodies against gangliosides (e.g., GM1, GD1a) target axolemma at nodes of Ranvier.

Features:

Rapid, symmetric motor weakness.

Reflexes absent or reduced.

Sensory exam normal.

Recovery may be slower than in AIDP.

NCS: Axonal loss without demyelination.

---

🔹 3. AMSAN (Acute Motor and Sensory Axonal Neuropathy)

Severe variant involving both motor and sensory axons.

Features:

Profound motor paralysis.

Severe sensory loss.

Slow or incomplete recovery.

NCS: Axonal degeneration of both motor and sensory fibers.

---

🔹 4. Miller Fisher Syndrome (MFS)

A cranial variant of GBS.

Triad:

Ophthalmoplegia (eye movement paralysis).

Ataxia.

Areflexia.

Often mild or without limb weakness.

Antibody marker: Anti-GQ1b IgG.

NCS: Often normal in limbs; absent H-reflex.

---

🔹 5. Pharyngeal–Cervical–Brachial Variant

Weakness confined to oropharyngeal, neck, and upper limb muscles.

Reflexes absent in arms but preserved in legs.

May have facial diplegia.

Antibodies: Often anti-GT1a or anti-GQ1b positive.

---

🔹 6. Bickerstaff Brainstem Encephalitis

Overlaps with Miller Fisher syndrome but includes altered consciousness or hyperreflexia (CNS involvement).

Antibody: Anti-GQ1b positive.

---

🔹 7. Pure Sensory GBS

Rare form.

Acute sensory ataxia with areflexia but no weakness.

NCS: Sensory demyelination; motor studies normal.

---

🔹 8. Pandysautonomic GBS

Extremely rare.

Severe autonomic dysfunction dominates (hypotension, arrhythmia, pupillary changes).

Weakness mild or absent.

---

🔹 9. Paraparetic Variant

Weakness limited to lower limbs.

May mimic transverse myelitis or spinal cord disease.

Reflexes absent in legs but normal in arms.

---

Summary Mnemonic – “AIDP Spectrum”

👉 AIDP – AMAN – AMSAN – MFS – PCB – BBE – Sensory – Autonomic – Paraparetic

14/10/2025

Auto antibodies collection

**1. ANA (Antinuclear Antibody)**
- Associated disease: Systemic Lupus Erythematosus (SLE)
- Screening test, high sensitivity but low specificity

***

**2. Anti-dsDNA**
- Associated disease: SLE, especially lupus nephritis
- Specific and correlates with disease activity

***

**3. Anti-Smith (Sm)**
- Associated disease: SLE
- Highly specific, but not sensitive. Most specific for SLE, low sensitivity

***

**4. Anti-Ro/SSA & Anti-La/SSB**
- Associated disease: Sjogren's Syndrome, neonatal lupus
- Also seen in congenital heart block in neonates

***

**5. Anti-centromere**
- Associated disease: Limited cutaneous systemic sclerosis (CREST)
- Linked to pulmonary hypertension

***

**6. Anti-Scl-70 (Anti-topoisomerase I)**
- Associated disease: Diffuse cutaneous systemic sclerosis
- Associated with interstitial lung disease and poor prognosis

***

**7. Anti-RNA polymerase III**
- Associated disease: Diffuse systemic sclerosis
- Risk of scleroderma renal crisis

***

**8. Anti-Mi-2**
- Associated disease: Dermatomyositis (classic form)
- Suggests classic skin findings, good prognosis

***

**9. Anti-Jo-1**
- Associated disease: Polymyositis, antisynthetase syndrome
- Mechanics hands, interstitial lung disease, antisynthetase syndrome

***

**10. ANCA (c-ANCA/PR3, p-ANCA/MPO)**
- Associated diseases: GPA (c-ANCA), MPA/EGPA (p-ANCA)
- Helps subtype vasculitis, guides therapy

***

**11. Rheumatoid Factor (RF)**
- Associated disease: Rheumatoid arthritis
- Non-specific; can be positive in infections and aging

***

**12. Anti-CCP (ACPA)**
- Associated disease: Rheumatoid arthritis
- Highly specific, correlates with erosive RA, prognostic value

***

**13. HLA-B27**
- Associated disease: Seronegative spondyloarthropathies (e.g., ankylosing spondylitis)
- Not an antibody, marker of genetic predisposition

***

**14. Antiphospholipid Antibodies (aCL, anti-β2GP1, lupus anticoagulant)**
- Associated disease: Antiphospholipid Syndrome, primary or secondary to SLE
- Associated with venous/arterial thrombosis, recurrent miscarriages, thrombocytopenia. Can prolong aPTT but is prothrombotic

***

**15. Anti-histone**
- Associated disease: Drug-Induced Lupus
- Seen in 95% of DIL cases. Associated with drugs like hydralazine, procainamide, isoniazid, methyldopa. Usually no renal or CNS involvement

***

**16. Anti-GBM (antiglomerular basement membrane)**
- Associated disease: Goodpasture Syndrome, Anti-GBM disease
- Causes rapidly progressive glomerulonephritis and pulmonary hemorrhage. Linear IgG deposits on renal biopsy. Often confused with vasculitis

***

**17. Anti-neuronal antibodies (Anti-NMDA, Anti-ribosomal P)**
- Associated disease: Neuropsychiatric SLE (NPSLE)
- Anti-ribosomal P: psychosis; anti-NMDA: cognitive dysfunction. Diagnosis is clinical with MRI, CSF studies

***

**18. Anti-U1 RNP**
- Associated disease: Mixed Connective Tissue Disease (MCTD)
- Overlap syndrome with features of SLE, systemic sclerosis, polymyositis. High titers are characteristic. Presents with Raynaud’s, arthritis, muscle weakness

***

**19. Anti-GQ1b**
- Associated disease: Miller Fisher Syndrome (variant of Guillain-Barré)
- Triad of ophthalmoplegia, ataxia, areflexia. Often post-infectious. Antibodies present in most cases

***

**20. Anti-AChR (acetylcholine receptor), Anti-MuSK**
- Associated disease: Myasthenia Gravis
- Fluctuating muscle weakness, ptosis, diplopia. Anti-AChR is most common; Anti-MuSK in AChR-negative cases. Thymoma association

***

**21. Anti-VGCC (PQ-type voltage-gated calcium channels)**
- Associated disease: Lambert-Eaton Myasthenic Syndrome (LEMS)
- Proximal muscle weakness, autonomic symptoms, improves with activity. Associated with small cell lung cancer. Antibodies impair presynaptic Ca²⁺ release

***

**22. Anti-Aquaporin-4 (AQP4-IgG, NMO-IgG)**
- Associated disease: Neuromyelitis Optica (Devic disease)
- Optic neuritis, transverse myelitis. Highly specific. Distinguished from MS by long spinal cord lesions and lack of brain MRI lesions

3You are a General Medical Senior House Officer (SHO) in a District General Hospital. You are asked to see a 20-year-o...
01/07/2024

3
You are a General Medical Senior House Officer (SHO) in a District General Hospital.
You are asked to see a 20-year-old man in the Emergency Department (ED) who is breathless. He gives a history of recent air travel to South America within the last 10 days. He denies any past medical history, but says that he has a chronic smokers’ cough. The patient is not taking any regular medications.
On examination, he is a thin man with tachypnoea at rest. His baseline observations include a blood pressure (BP) of 120/80 mmHg, and a pulse of 100 beats per minute (bpm). His oxygen saturation is 89% on room air and his temperature is 38.5oC. He is noted to have bi-basal crepitations and ill-defined heart sounds on auscultation. Routine
bloods reveal an elevated white blood cell count (WCC) and c-reactive proTIEN...

*WHAT ARE YOU THINKING WITH THIS ECG

What is the next step of management??

Interesting but true u will do a chest xray and strat antibiotics!!!!

And thats the twist😌

2Widow maker sign!!!!😵‍💫Isn’t it interesting?? 🤔A 69 year old man presents with central crushingChest pain.He also fee...
30/06/2024

2
Widow maker sign!!!!😵‍💫

Isn’t it interesting?? 🤔

A 69 year old man presents with central crushing
Chest pain.He also feels nauseous. He states that the pain came on rest.Past medical history HTN and poorly controlled T2DM

Look at the ecg...🔎

There is➡️ biphasic T waves ( up than down or down than up) in V2 to V4...

Are u thinking it is nonspecific !!!🥲

Don’t make the women widow!!!!!🌑

This is 'syndrome☢️type 2

Significance💥
✅Pathognomic of critical stenosis of proximal left anterior descending artery(LAD)
✅high risk of ACS within days/ weeks if unteated

1A 38 years old male smoker diabetic pt comes to you with chest pain for last 4 hours*Look at the ECGThere is1.ST elev...
29/06/2024

1

A 38 years old male smoker diabetic pt comes to you with chest pain for last 4 hours

*Look at the ECG
There is
1.ST elevation in lead 3 but not any other inferior leads
2.ST depression in v5 and v6
3.slight ST elevation in lead v1 Higher than ST

🤔What are u thinking?? Is it a NSTMI!!!treat him as NSTMI!!🤨

Wait a sec▶️......!!! No, no no dude🚫, this is pattern 2020. About 6.3% NSTMI follows this pattern...

So What is the significance??

* Though only lead 3 ST elevation, there could be a huge inferior infract ( inferior MI)
* patient may have multi vessel Disease!!!

So, Don't miss the twist☺️
Ecg From liftl.com

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