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* NBME#5 block 1....................50Q
  maryam2009 - 03/24/11 00:56
  please choose and answer the Q in order,Thank you  
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* Re:NBME#5 block 1....................50Q
  drona99 - 03/24/11 01:51
  hi there ..thank you so much:)

1-AA ant cerebral aretry
back to homonculous again-

circle of willis pic

ACA supplies -
1-medial surface of frontal and parietal lobes
2-anterior 4/5 of corpus calllosum
3-anterior limb of internal capsule [thalamocortical fibres]

lesion of ASA-
1-contralateral spastic paresis and anaesthesia of lower limb
2-urinary incontinence
3-transcortical apraxia--cant move left arm in response to commond -this is becoz of lsion of corpus callosum--also called as disconnect syndrome-There is no motor weakness but becoz lesion of corpus callosum left wernikes cant communicate rt motor area.But person can rt arm becoz left werkines can communicate with lt motor so person can move rt hand.
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* Re:NBME#5 block 1....................50Q
  drona99 - 03/24/11 03:20
no symtoms at the time of fall --this is most differentiating point from epidural haematoma -
epidural presents with brief episode of unconscioness .

Sundural haematoma
more than half of all cases were seen in patients older than 60 years. The highest incidence of 7.35 cases per 100,000 persons occurs in adults aged 70-79 years.

Acute traumatic subdural hematoma often results from falls, violence, or motor vehicle accidents. The clinical presentation depends on the location of the lesion and the rate at which it develops. Often, patients are rendered comatose at the time of the injury. A subset of patients remain conscious; others deteriorate in a delayed fashion as the hematoma expands.
Chronic subdural hematomas are arbitrarily defined as those hematomas presenting 21 days or more after injury. Subacute subdural hematomas are defined arbitrarily as those that present between 4 and 21 days after injury

Epidural and subdural hematomas are alike in that they are masses of clotted blood (hematomas) caused by head trauma and deposited outside the brain but inside the skull. However, they differ in their locations relative to the dura mater. An epidural hematoma lies outside (on top of) the dura mater, while a subdural hematoma lies inside (beneath) the dura mater and outside the arachnoid mater. Thus, the locations of the two kinds of hematoma are encoded in their names -- "epi" is Greek for "upon" and "sub" is Latin for
"below." A third kind of hematoma caused by head injuries is traumatic intracerebral hemorrhage. These occur within the brain tissue itself and are no less serious than those outside the brain, but are not the subject of the current

Epidural and subdural hematomas are produced by ruptures of different blood vessels.

Epidural hematomas are usually caused by bleeding from an artery that nourishes the meninges known as the middle meningeal artery,

while subdural hematomas are usually due to bleeding from veins that drain
blood away from the surface of brain.

In epidural hematomas the blood is more limited in its spread because it has to push harder to move outward in the tight space between the inner surface of the skull and the outer surface of the dura mater. In contrast, the bleeding that produces subdural hematomas
is more free to spread in the looser space beneath the dura mater and typically runs from the front of the head to the rear.

One issue that applies to both kinds of hematomas is that they occupy space -- sometimes a lot of it --
within the braincase where there isn't a lot of extra space to go around. As they expand they compress the brain tissue next to them and additionally raise the pressure within the skull which can damage the rest of the brain.
Infants are also vulnerable to acute subdural hematomas. . In this case series, "shaken baby syndrome" was the most common cause.

for more differentiating points.
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* Re:NBME#5 block 1....................50Q
  drona99 - 03/24/11 04:56
cochlear nerve -

A- mamillary bodies?
B- cerebellar peduncles
C-VI cranial nerve
D-VII cranial nerve
E-cochlear nerve
F-and G cant figure out
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* Re:NBME#5 block 1....................50Q
  drona99 - 03/24/11 05:04
q is asking what increases in his Rbcs so its 2;3BPG - pt has hypoxia so to release more o2 from Hb Rbcs will secrete more 2;3BPG -
In hypoxia erythroetin also increases to cause polycythemia
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* Re:NBME#5 block 1....................50Q
  drona99 - 03/24/11 05:17

Alcohol withdrawal is characterized by neuropsychiatric excitability and autonomic disturbances similar to other sedative-hypnotic drugs.

delirium tremons-The main symptoms are confusion, diarrhea, disorientation and agitation and other signs of severe autonomic instability (fever, tachycardia, hypertension).

These symptoms may appear suddenly but can develop 23 days after cessation of drinking heavily with its highest peak/ intensity on the fourth or fifth day.
Also, these "symptoms are characteristically worse at night".
Other common symptoms include intense perceptual disturbance such as visions of insects, snakes or rats. These may be hallucinations, or illusions related to the environment, e.g., patterns on the wallpaper that the patient perceives as giant spiders attacking him or her. Unlike hallucinations associated with schizophrenia, delirium tremens hallucinations are primarily visual, but are also associated with tactile hallucinations such as sensations of something crawling on the subject a phenomenon known as formication


The exact pharmacology of ethanol is not fully understood; however, it is theorized that delirium tremens is caused by the effect of alcohol on the benzodiazepine-GABAA-chloride receptor complex for the inhibitory neurotransmitter GABA. Constant consumption of alcoholic beverages (and the consequent chronic sedation) causes a counterregulatory response in the brain in attempt to regain homeostasis.

This causes downregulation of these receptors, as well as an up-regulation in the production of excitatory neurotransmitters, primarily glutamate, and also such as norepinephrine, dopamine, epinephrine, and serotonin, all of which further the drinker's tolerance to alcohol. When alcohol is no longer consumed, these down-regulated GABAA receptor complexes are so insensitive to GABA that the typical amount of GABA produced has little effect; compounded with the fact that GABA normally inhibits action potential formation, there are not as many receptors for GABA to bind to meaning that sympathetic activation is unopposed. This is also known as an "adrenergic storm"; the effects of which can include (but are not limited to) tachycardia, hypertension, hyperthermia, hyperreflexia, diaphoresis, heart attack, cardiac arrhythmia, stroke, anxiety, panic attacks, paranoia, and agitation.

Delirium tremens due to alcohol withdrawal can be treated with benzodiazepines.
High doses may be necessary to prevent mortality.Pharmacotherapy is symptomatic and supportive. Typically the patient is kept sedated with benzodiazepines, such as diazepam

details --
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* Re:NBME#5 block 1....................50Q
  maryam2009 - 03/24/11 09:21
Compares a group with a given risk factor to a group wiyhout to assess whether the risk factor increased the likelihood of disease........COHORT STUDY
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* Re:NBME#5 block 1....................50Q
  maryam2009 - 03/24/11 09:40

Major neurotransmitters:

Amino acids: glutamate, aspartate, D-serine, γ-aminobutyric acid (GABA), glycine

Monoamines and other biogenic amines: dopamine (DA), norepinephrine (noradrenaline; NE, NA), epinephrine (adrenaline), histamine, serotonin (SE, 5-HT)

Others: acetylcholine (ACh), adenosine, anandamide, nitric oxide, etc.

Here are a few examples of important neurotransmitter actions:

Glutamate is used at the great majority of fast excitatory synapses in the brain and spinal cord. It is also used at most synapses that are "modifiable", i.e. capable of increasing or decreasing in strength. Modifiable synapses are thought to be the main memory-storage elements in the brain. Excessive glutamate release can lead to excitotoxicity causing cell death.

GABA is used at the great majority of fast inhibitory synapses in virtually every part of the brain. Many sedative/tranquilizing drugs act by enhancing the effects of GABA. Correspondingly glycine is the inhibitory transmitter in the spinal cord.

Acetylcholine is distinguished as the transmitter at the neuromuscular junction connecting motor nerves to muscles. The paralytic arrow-poison curare acts by blocking transmission at these synapses. Acetylcholine also operates in many regions of the brain, but using different types of receptors.

Dopamine has a number of important functions in the brain. It plays a critical role in the reward system, but dysfunction of the dopamine system is also implicated in Parkinson's disease and schizophrenia.

Serotonin is a monoamine neurotransmitter. Most is produced by and found in the intestine (approximately 90%), and the remainder in central nervous system neurons. It functions to regulate appetite, sleep, memory and learning, temperature, mood, behaviour, muscle contraction, and function of the cardiovascular system and endocrine system. It is speculated to have a role in depression, as some depressed patients are seen to have lower concentrations of metabolites of serotonin in their cerebrospinal fluid and brain tissue.

Substance P is an undecapeptide responsible for transmission of pain from certain sensory neurons to the central nervous system.
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* Re:NBME#5 block 1....................50Q
  maryam2009 - 03/24/11 09:54

motor or sensory symptoms ...parlysis ,blindness,mutism, often following an acute stressor.

Conversion disorder is a condition in which patients present with neurological symptoms such as numbness, blindness, paralysis, or fits without a physiological cause. It is thought that these problems arise in response to difficulties in the patient's life, and conversion is considered a psychiatric disorder.

One or more symptoms or deficits are present that affect voluntary motor or sensory function suggestive of a neurologic or other general medical condition.

Psychological factors are judged, in the clinician's belief, to be associated with the symptom or deficit because conflicts or other stressors precede the initiation or exacerbation of the symptom or deficit.
A diagnosis where the stressor precedes the onset of symptoms by up to 15 years is not unusual.
The symptom or deficit is not intentionally produced or feigned (as in factitious disorder or malingering).
The symptom or deficit, after appropriate investigation, cannot be explained fully by a general medical condition, the direct effects of a substance, or as a culturally sanctioned behavior or experience.
The symptom or deficit causes clinically significant distress or impairment in social, occupational, or other important areas of functioning or warrants medical evaluation.

The symptom or deficit is not limited to pain or sexual dysfunction, does not occur exclusively during the course of somatization disorder, and is not better accounted for by another mental disorder.
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* Re:NBME#5 block 1....................50Q
  drona99 - 03/24/11 12:07
  hey maryam q no 6-- ans is ee
we need to see wheather colonic polyps develop in to adenoca or not so for that we need ppl without polyps so ee..

***sarims all answer keys
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* Re:NBME#5 block 1....................50Q
  maryam2009 - 03/24/11 12:26
  Hi there,yes u r right I wanted to write E but I don't know how it is written A,my mistake,sorry
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