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OSCE

DR SUBHASISH DEB

Burdwan Medical College and Hospital

Department of General Medicine

09/12/2014DR SUBHASISH DEB

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CASE 1


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A 72 year old man presented with

generalized erythroderma with palmer and

planter hyperkeatosis and enlarged Lymph

nodes.

WBC= 24,000/ul (mico lit)

Peripheral smear shows the following

atypical cell.

Skin biposy showed epidermotropism of the

atypical cells


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(A)Typical erythroderma of Sézary syndrome, and

(B) solitary mycosis fungoides plaque,

(C) tumour nodule of large cell lymphoma (LCL). Histology reveals

(D) an upper band-like infiltrate with epidermotropism of atypical

lymphocytes and

(E) a typical Pautrier microabscess


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SEZARY SYNDROME

An aggressive form of CTCL (cutaneous T

cell Lymphoma)

Triad:

1. Erythroderma (diffuse)

2. Lymphadenopathy

3. Circulating atypical lymphocytes (Sezary

cells)


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DIAGNOSTIC CRITERIA

1 or more of the following should be present:

1. An absolute Sézary cell count of least 1000 cells/µL

2. Demonstration of an expanded CD4+ T-cell population CD4/CD8 > 10; loss of any or all of the T-cell antigens CD2, CD3, CD4, and CD5; or loss of both CD4 and CD5)

3. Identical T-cell clone in blood and skin. (by molecular assay like pcr)


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Mycosis fungoides and SS are the m/c

CTCLs

Lineage: Mature (peripheral) T cells

SS differentiated from MF by presence of

atypical lymphocytes in blood.


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CASE 2


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A 70 year old woman came with a c/o of

chest pain with radiation to left shoulder. She

has a medical h/o of hypercholesterolemia.

Her ECG showed the following.

Trop T – positive

CXR- NAD

Ur-30, Cr-1.0


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POSTERIOR WALL MI

PMI also called ‘dead angle infarction’

One of the m/c missed types of AMI

The term PMI is used for necrosis of the

dorsal infraatrial part of the left ventricle

located between the atrioventricular sulcus


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Occurs due to stenosis/ occlusion of RCX

Often accompanied by inferior and/or lateral

wall MI

Pts with ecg of isolated PMI often do not

receive the appropriate reperfusion t/t due to

lack of classical ST-segment elevation in

normal 12 lead ecg


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ECG FINDINGS

V1 and V2 are mirror images of V1 and V2 of

anterior wall MI

Vector cardiogram points ventrally due to

loss of the electrical forces normally aimed

dorsally, resulting in a prolonged R wave –

R/S >1 in V1 and V2

ST depression in precordial leads in acute

phase + tall upright T waves


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USE OF DORSAL LEADS

Mortality reduction is max when reperfusedwithin 6hrs if pain onset

POSTERIOR LEADS:

V7 – at the level of V6 at post Axillary line

V8 – left side of back at the tip of scapula

V9 – half way between V8 and the left paraspinal muscles

ST elevation >1mm in post leads is suggestive of PMI


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Sensitivity increases from 32% to 57% and

specificity 98% for RCX on the 15 lead ecg

instead of the normal 12 lead ecg


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CASE 3


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A 83 year old man with h/o heart disease

with repeated symptomatic episodes of CHF

presented with c/o cough and progessive

orthopnea and 3 weeks of PND. CXR

showed A

Pt was treated with iv furosemide, t. digoxin,

iv nitroglycerine and captopril. He improved

in 3 days and 6 days later, repeat CXR

showed B


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A B


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PHANTOM TUMOUR

The term phantom tumour is applied to a transudative interlobar pleural fluid collection in CHF which disappears spontaneously with compensation and may reappear on decompensation

USUALLY SEEN IN:

CHF

Renal Failure

Hypoalbuminemia

Due to transudation from pulmonary vasculature


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PATHOGENESIS

Involves the adhesion and obliteration of the

pleural space due to pleuritis that may be

transient, thereby preventing the free

accumulation of fluid.


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CASE 4


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A 56 year old woman with past h/o of HTN presented with flue like symptoms that were ongoing for last 3 days. While waiting in the observation room for 6 hrs, she developed chest pain. No family h/o of any cardiac problems.

ECG - showed the follwing

TROP t – positive

ECHO – hypokinetic walls with EF – 35%


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MYOCARDITIS

NON ISCHEMIC myocardial inflammation

resulting from a variety of infectious, immune

and toxic insults.

DCM and Chronic Heart Failure are the

mojor long term sequla of myocarditis.


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M/c/c in Europe and North America – VIRUS

m/c/c Worldwide – chagas disease

Less common non viral pathogens:

1. Borrelia Burgdorferi

2. Trypanosoma Cruzi

3. Hypersensitivity to drugs

4. Autoimmune reaction

(Streotococcal M protein and Coxsakie virus B epitopes are similar to cardiac myosin)


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As definitive diagnosis requires a heart

biopsy,which doctors are reluctant to do,

statistics on the incidence of myocarditis vary

widely.

Among HIV patients, myocarditis is the m/c

cardiac pathological finding at autopsy.


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SIGNS AND SYMPTOMS

1. Chest pain (stabbing)

2. CHF

3. Palpitation

4. Sudden death

5. Fever

6. Flue like symptoms


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DIAGNOSIS

ECG- diffuse t wave inversions, saddle

shaped ST-segment elevations (also in

pericarditis)

Gold standard – biopsy of myocardium

Generally done in a setting of angiography. A

small tissue sample of te endoand

myocardium is taken

Also useful are IgM against virus, ESR, CRP


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TREATMENT

Viral infections cannot be treated with direct

therapy – symptomatic

People who do not responf to convesional

therapy are candidayes for bridge thrapy with

Left ventricular assist device


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CASE 5


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A 20 years old man presented with this

rash and 1st degree heart block.

What is the diagnosis and what is the

treatment ?


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LYME DISEASE

Borrelia burgdorferi is transmitted to humans by the bite of infected hard ticks.

Early symptoms may include fever, headache, fatigue, depression, and a characteristic circular skin rash called erythema migrans(bull's eye rash) .

Left untreated, later symptoms may involve the joints, heart, and central nervous system.

Treatment: antibiotics-doxycycline, if have later complications- cefotaxime or ceftriaxone.


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