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D - first q - ? multiple sclerosis
GBS should not effect sensory system right? so i will not go for LP
Second Q - A - Unknown time of onset - no tpa, some centers are doing intra-areterial tpa until 6hrs after stroke, i donno if this is up on step3 yet.
Third Q - ASA, ASA/Dipyridamole are good in all cases. In pts who cannot tolerate ASA or in pts with PAD, Clopidogrel is the choice. BP control certainly reduces stroke - best agents are ramipril and HCTZ. I think its statin thats not useful in secondary prevention. Some studies have actually showed increased hemorrhagic stroke with statin
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Q3 Ans may be warfarin - because the Q says "atheroembolic" not cardioembolic. please post answer . thank you guest
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c
a
e
hey pindi thanks buddy .....
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any 1 please explain why Q1 suspects multiple sclerosis? why in MS we do ANA?
many thanks.
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---- CORRECT ANSWERS ARE-----
B
C
E
will try to post the explainations ...as well....not too long from now!
welcome..strongdoc and goody!
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* EXPLAINATION FOR Q # 1 *
ans is B.
This patient has a history and examination consistent with a myelopathy.
The rapidity of onset and the lack of other antecedent symptoms (e.g., pain) make a noncompressive etiology most likely.
An MRI is the initial test of choice and will easily identify a structural lesion such as a
neoplasm or subluxation. Noncompressive myelopathies result from five basic causes: spinal
cord infarction; systemic disorders such as vasculitis, systemic lupus erythematosus (SLE), and sarcoidosis; infections (particularly viral); demyelinating disease such as multiple sclerosis; and idiopathic.
Therefore, serologies for antinuclear antibodies, viral serologies such as HIV and
HTLV-I, and lumbar puncture are all indicated. Because the clinical scenario is consistent with a myelopathy, an electromyogram is not indicated
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* EXPLAINATION FOR Q # 2 *
answer is C...
Cerebrovascular diseases account for up to 200,000 deaths a year in the United States and are major cause of morbidity. Acute ischemic stroke results from an acute occlusion of an
intracranial vessel from in situ thrombosis or an embolic source.
The magnitude of the flow
reduction is a function of the collateral blood flow, and this depends largely on the vascular
anatomy of the individual patient.
Brain tissue dies within minutes of a fall in cerebral blood
flow. Therefore, reestablishment of flow and prevention of widening of the territory of
infarction are two of the major goals of stroke therapy.
A pivotal National Institute of
Neurological Disorders and Stroke (NINDS) study showed that patients who received
intravenous recombinant tissue plasminogen activator (rTPA) within 3 h of the onset of
symptoms had a significant clinical benefit. This was the case despite a 6.4% risk of
intracerebral hemorrhage.
Other, more recent trials have looked at intraarterial delivery of rTPA
by a catheter-based approach within a 6-h time frame for middle cerebral artery (MCA) territory infarctions, and there appears to be a significant benefit.
Although this has not been approved by the U.S. Food and Drug Administration, based on early clinical trials, it is rapidly becomingthe standard of care for patients with MCA strokes that fall out of the 3-h window for intravenous rTPA. Numerous studies have shown the benefit of aspirin administered within 48 h of stroke onset.
Aspirin offers a modest benefit in regard to further stroke recurrence. Some literature supports a benefit of clopidogrel in ischemic stroke patients as a means of secondary prevention.
Although frequently used, heparin remains unproven as a beneficial agent in the
treatment of acute stroke. Because this patient has no contraindication to thrombolytic therapy but falls outside the 3-h window for intravenous rTPA, catheter-delivered rTPA is the next best option if the support facilities exist and should be recommended for this patient.
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