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OSCE
DR SUBHASISH DEB
Burdwan Medical College and Hospital
Department of General Medicine
CASE 1
A 42 year old woman was admitted to hospital with
a one month history of progressive forgetfulness,
irritability and confusion. There was no history of
tremor or confabulation. There was no history of
fever, headache, neck-ache or neck stiffness.
Further inquiry revealed she had developed rash
around her neck and in the distal parts of all four
limbs a month prior to the onset of the altered
mental status. The guardians also reported that the
patient had had diarrhea which was watery and had
lasted a week prior to admission. There was no
history of vomiting. She was on Cat 1 for the past 4
months.
Diagnosis?
PELLAGRA (ISONIAZID INDUCED)
 Pellagra is due to B3 (niacin) deficiency
 Isoniazid induced pellagra is caused by deficiency
of B3 DUE TO a deficiency of B6 (thiamine)
 The picture : Casal’s necklace
B6
CAUSES
1. Deficiency of niacin (maize eating population)
2. Deficiency of tryptophan
 Decreased intake (meat, fish)
 Lucine (inhibits QRPT enzyme)
 B6 deficiency (needed by kynunreninase
enzyme)
3. Carcinoid syndrome (conversion to serotonin)
4. Factors causing decreased absorption – Crohn’s
disease, Gasteroenterostomy, chronic alcoholism,
Hartnup’s disease
FEATURES:
 4 D’s
 Dermatitis
 Diarrhoea
 Dementia
 Death
 Others-
Glossitis, loss of appetite, generalized weakness ,
vomiting, abdominal pain.
DUE TO B6 DEFICIENCY:
 Microcytic Hypochromic anemia (B6 reqired by
delta ALA – 1st enzyme of heme sys)
 Seizures :
glutamate
glutamate decarboxylase B6
GABA
Hyperactivity of neurons due to excess of glutamate
 Homocysteinuria :
Cystathianone B synthase requires B6 (PLP) to convert
homocysteine to cystathione – increased CVA chances
TREATMENT
 Always give Pyridoxine with isoniazid
 B3 deficincy treated by:
oral nicotinamide (niacin) 100-200mg TDS x 5days
 Adverse effects of niacin: FLUSHING
 Due to tachyphylaxsis
 Premedication with ASPIRIN
 Niacin combined with
LAROPIPRANT a
prostaglandin D2 receptor 1
antagonist
CASE 2
A 58 year old woman came with a chief
complaint of syncope. She also had low
grade fever 38C.
Her 12 lead ecg showed..
BRUGADA SYNDROME
 First described in 1992 by Pedro and Josepg
Brugada
 Associated with sudden cardiac death
 Individuals are usually healthy with structurally
normal hearts
 Generally considered a hereditary disease
 More common cause of sudden cardiac death than
previously recognized
HOW COMMON IS IT??
 Responsible for up to 20% of sudden deaths in pts
without any structural heart abnormality
 Responsible for 4-5% of all sudden deaths
 Incidence varies in different populations
 Most common in young males
 First onset of symptoms (syncope. Sudden death) ~
40 yrs
BRUGADA SYNDROME
 Mortality ~10% per year if not treated with internal
cardioverter-defibrillator (ICD)
 Antidsyrhythmics have no effects on prognosis
 Syndrome characterized by:
 ECG abnls. in lead v1-v3
 Polymorphic or monomorphic VT
 Structurally normal heart
 Familial occurrence in ~ half of the pts
BRUGADA SYNDROME
ECG findings in v1-v3:
 RBBB or IRBBB
 ST segment elevation --- 2 types
 “Coved-type” – most common
 “Saddle-type”
 Findings can vary depending on may factors including
fever/ambient temp
Definitive diagnosis: EPS (electrophysiology study
in EP labs)
Saddle
type
Cove
type
TYPES:
1. Type 1 :
 Coved ST segment
 J point elevation with ST segment elevation >=0.2mV
 Negative T wave
2. Type 2:
 Saddle back configuration of ST
 High take off of ST >0.2mV
 Ending in positive or biphasic t wave without touching base
line
3. Type 3:
 ST elevation <0.1 with either of the morphologies
UNCOMPLICATED RBBB
ST depression
CASE 3
 Papules extending to form a yellow–red plaque
covered with telangiectatic vessels on the
patient's forearm. CBG 330. ???
NECROBIOSIS LIPOIDICA
DIABETICORUM
 Necrobiosis lipoidica was first described by
Oppenheim in 1929 as a chronic granulomatous
dermatitis of unknown cause.
 female:male ratio of 3:1
 Mostly associated with Type 1 DM
FEATURE:
 initially presents with well-circumscribed
erythematous papules, which develop into large,
irregularly delineated plaques with a waxy, yellow
center
 the epidermis becomes thin and transparent,
allowing underlying vasculature to become visible
 The involved peripheral tissue is slightly raised and
has a reddish-blue color
Pathophysiology
 Exact cause not known
 an inflammatory disorder characterised by collagen
degeneration, combined with a granulomatous response
Diagnosis
 Skin biopsy
 demonstrating superficial and deep perivascular and
interstitial mixed inflammatory cell infiltrate
 necrotising vasculitis with adjacent necrobiosis and
necrosis of adnexal structures
 Presence of lipid in necrobiotic areas may be
demonstrated by Sudan stains
No clearly defined cure.
CASE 4
 A 18yr old boy came with deafness to the ENT opd. The
new female resident finds it to be SNHL and refers him
to MOPD. The physician asked for an MRI and saw this
plate (Fig 1)
 The physician referred the pt to SOPD for a biopsy. After
having completed the up hill task of getting an aesthetic
fitness, finally the pathologist in his exam found
VEROCAY bodies in the specimen and told to correlate
clinically!
 The surgeon meanwhile didn’t understand much as
usual and send the pt back to MOPD.
 The physician gave a diagnosis of__________ and send
the pt back to the surgeon for surgical treatment.
NEUROFIBROMATOSIS 2
 A/k MISME syndrome- Multiple Inherited
Schwannomas, meningiomas and ependymomas
 Less common than NF-1
 Due to mutation of merlin (a/k schwannomin) in ch
22q12 , AD
 Symptoms generally occur at late teen to 20yrs
CLINICAL FEATURES:
 Hallmark of NF2 is hearing loss due to vestibular
schwannoma
 Others:
 Headache
 Balance problems and peripheral vertigo
 Facial weakness- compression of VII nerve
 Deafness and tinnitus
 Other brain and spinal tumours
DIAGNOSIS:
 Confirmed diagnosis:
 bilateral vestibular schwannomas (may also be known
as acoustic neuroma)
 Probable diagnosis:
 family history of NF2 AND
 unilateral vestibular schwannomas or any 2 of the
following tumor types: meningioma, glioma,
schwannoma, juvenile posterior subcapsular lenticular
opacity, juvenile cortical cataract
TREATMENT
 Surgery is the primary treatment for most peripheral
nerve tumors associated with NF2.
 Systemic medical treatment:
 Bevacizumab (still in trial)
 Management of hearing loss:
 Cochlear implant, ABI- auditory brain stem implant
 For meningioma;
 Sunitinib (in trial)
 For vestibular schwannoma:
 Lapatinib (in trial)
THANK YOU

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OSCE

  • 1. OSCE DR SUBHASISH DEB Burdwan Medical College and Hospital Department of General Medicine
  • 3. A 42 year old woman was admitted to hospital with a one month history of progressive forgetfulness, irritability and confusion. There was no history of tremor or confabulation. There was no history of fever, headache, neck-ache or neck stiffness. Further inquiry revealed she had developed rash around her neck and in the distal parts of all four limbs a month prior to the onset of the altered mental status. The guardians also reported that the patient had had diarrhea which was watery and had lasted a week prior to admission. There was no history of vomiting. She was on Cat 1 for the past 4 months.
  • 5. PELLAGRA (ISONIAZID INDUCED)  Pellagra is due to B3 (niacin) deficiency  Isoniazid induced pellagra is caused by deficiency of B3 DUE TO a deficiency of B6 (thiamine)  The picture : Casal’s necklace
  • 6. B6
  • 7. CAUSES 1. Deficiency of niacin (maize eating population) 2. Deficiency of tryptophan  Decreased intake (meat, fish)  Lucine (inhibits QRPT enzyme)  B6 deficiency (needed by kynunreninase enzyme) 3. Carcinoid syndrome (conversion to serotonin) 4. Factors causing decreased absorption – Crohn’s disease, Gasteroenterostomy, chronic alcoholism, Hartnup’s disease
  • 8. FEATURES:  4 D’s  Dermatitis  Diarrhoea  Dementia  Death  Others- Glossitis, loss of appetite, generalized weakness , vomiting, abdominal pain.
  • 9. DUE TO B6 DEFICIENCY:  Microcytic Hypochromic anemia (B6 reqired by delta ALA – 1st enzyme of heme sys)  Seizures : glutamate glutamate decarboxylase B6 GABA Hyperactivity of neurons due to excess of glutamate  Homocysteinuria : Cystathianone B synthase requires B6 (PLP) to convert homocysteine to cystathione – increased CVA chances
  • 10. TREATMENT  Always give Pyridoxine with isoniazid  B3 deficincy treated by: oral nicotinamide (niacin) 100-200mg TDS x 5days  Adverse effects of niacin: FLUSHING  Due to tachyphylaxsis  Premedication with ASPIRIN  Niacin combined with LAROPIPRANT a prostaglandin D2 receptor 1 antagonist
  • 12. A 58 year old woman came with a chief complaint of syncope. She also had low grade fever 38C. Her 12 lead ecg showed..
  • 13.
  • 14. BRUGADA SYNDROME  First described in 1992 by Pedro and Josepg Brugada  Associated with sudden cardiac death  Individuals are usually healthy with structurally normal hearts  Generally considered a hereditary disease  More common cause of sudden cardiac death than previously recognized
  • 15. HOW COMMON IS IT??  Responsible for up to 20% of sudden deaths in pts without any structural heart abnormality  Responsible for 4-5% of all sudden deaths  Incidence varies in different populations  Most common in young males  First onset of symptoms (syncope. Sudden death) ~ 40 yrs
  • 16. BRUGADA SYNDROME  Mortality ~10% per year if not treated with internal cardioverter-defibrillator (ICD)  Antidsyrhythmics have no effects on prognosis  Syndrome characterized by:  ECG abnls. in lead v1-v3  Polymorphic or monomorphic VT  Structurally normal heart  Familial occurrence in ~ half of the pts
  • 17. BRUGADA SYNDROME ECG findings in v1-v3:  RBBB or IRBBB  ST segment elevation --- 2 types  “Coved-type” – most common  “Saddle-type”  Findings can vary depending on may factors including fever/ambient temp Definitive diagnosis: EPS (electrophysiology study in EP labs)
  • 19. TYPES: 1. Type 1 :  Coved ST segment  J point elevation with ST segment elevation >=0.2mV  Negative T wave 2. Type 2:  Saddle back configuration of ST  High take off of ST >0.2mV  Ending in positive or biphasic t wave without touching base line 3. Type 3:  ST elevation <0.1 with either of the morphologies
  • 20.
  • 21.
  • 22.
  • 24.
  • 25.
  • 27.  Papules extending to form a yellow–red plaque covered with telangiectatic vessels on the patient's forearm. CBG 330. ???
  • 28. NECROBIOSIS LIPOIDICA DIABETICORUM  Necrobiosis lipoidica was first described by Oppenheim in 1929 as a chronic granulomatous dermatitis of unknown cause.  female:male ratio of 3:1  Mostly associated with Type 1 DM
  • 29. FEATURE:  initially presents with well-circumscribed erythematous papules, which develop into large, irregularly delineated plaques with a waxy, yellow center  the epidermis becomes thin and transparent, allowing underlying vasculature to become visible  The involved peripheral tissue is slightly raised and has a reddish-blue color
  • 30.
  • 31.
  • 32. Pathophysiology  Exact cause not known  an inflammatory disorder characterised by collagen degeneration, combined with a granulomatous response Diagnosis  Skin biopsy  demonstrating superficial and deep perivascular and interstitial mixed inflammatory cell infiltrate  necrotising vasculitis with adjacent necrobiosis and necrosis of adnexal structures  Presence of lipid in necrobiotic areas may be demonstrated by Sudan stains No clearly defined cure.
  • 34.  A 18yr old boy came with deafness to the ENT opd. The new female resident finds it to be SNHL and refers him to MOPD. The physician asked for an MRI and saw this plate (Fig 1)  The physician referred the pt to SOPD for a biopsy. After having completed the up hill task of getting an aesthetic fitness, finally the pathologist in his exam found VEROCAY bodies in the specimen and told to correlate clinically!  The surgeon meanwhile didn’t understand much as usual and send the pt back to MOPD.  The physician gave a diagnosis of__________ and send the pt back to the surgeon for surgical treatment.
  • 35.
  • 36. NEUROFIBROMATOSIS 2  A/k MISME syndrome- Multiple Inherited Schwannomas, meningiomas and ependymomas  Less common than NF-1  Due to mutation of merlin (a/k schwannomin) in ch 22q12 , AD  Symptoms generally occur at late teen to 20yrs
  • 37. CLINICAL FEATURES:  Hallmark of NF2 is hearing loss due to vestibular schwannoma  Others:  Headache  Balance problems and peripheral vertigo  Facial weakness- compression of VII nerve  Deafness and tinnitus  Other brain and spinal tumours
  • 38. DIAGNOSIS:  Confirmed diagnosis:  bilateral vestibular schwannomas (may also be known as acoustic neuroma)  Probable diagnosis:  family history of NF2 AND  unilateral vestibular schwannomas or any 2 of the following tumor types: meningioma, glioma, schwannoma, juvenile posterior subcapsular lenticular opacity, juvenile cortical cataract
  • 39. TREATMENT  Surgery is the primary treatment for most peripheral nerve tumors associated with NF2.  Systemic medical treatment:  Bevacizumab (still in trial)  Management of hearing loss:  Cochlear implant, ABI- auditory brain stem implant  For meningioma;  Sunitinib (in trial)  For vestibular schwannoma:  Lapatinib (in trial)

Editor's Notes

  1. On autopsy, normal hearts. No athereosclerosis no hocm. Its purely a electro phenomenon What was described in ealy 1990’s has become a hot topic in electrocardiology. There have been several consensus conferences and now the brugada syndrome is not just a Zebra diagnosis as though of before
  2. In other words 1 out of every 20 to 25 cardiac arrests in the genearl population are due to brugada syndrome
  3. Only treatment is ICD More often polymorphic v tachs. And if you are lucky, it will terminate on its own, person wakes up from his collapse and wakes up saying that he had a syncopal episode. If they are not lucky, it degenerates from v tach to v fib and sudden death So syncope and sudden death may be a part of the same disease in a spectrum
  4. Most specefic and sensitive is the cove type It is a sodium channelopathy, so if yu have sodium channel blockers like cocaine, tca, anticholinergics, it will increse the chnces of syncopal episodes. Infact electrophysiologist use a sodium channel blocker to test from this condition which induces v tach and confirms the diagnosis, then they place the ICD
  5. Coved type, irrespective of sympotms must be investigated
  6. Hammer the head as pattern recognition is important Unusual St elevation in v1 and v2
  7. The elecrophysiologist gave a diag of brugada at 1st look and the non electrophysiologist cariologist gave a diag of acute MI