Regjistruar: 16/01/2005
Vendbanimi: Raccon City
Mesazhe: 3634

Citim:

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Po citoj ato që tha Aljohin
ej pse nuk mund te postoj nje foto?

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akoma nuk osh rregullo ajo puna e fotove

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Modifikuar nga NS-6 datė 27/01/2006 ora 00:00

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Regjistruar: 07/07/2003
Vendbanimi: Padova
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At the follow-up examination two and a half
months later, the patient said that the swelling in her
feet had improved, but that the pain in her left foot
was radiating into the leg. She again had a small
blister over the second finger on the right hand and
said that the right hand occasionally turned “purple
and red.” She was taking oxycodone–acetaminophen
and calcium and iron supplements but was
not taking the gabapentin regularly because it sedated
her.
On examination, sensation of a pinprick and of
temperature was decreased distally in all the extremities,
particularly in the right hand and left foot,
and there was anesthesia with respect to all types of
sensation in the right median-nerve distribution.
Vibratory sensation was reduced in the left foot.
Strength was normal throughout all the muscle
groups on detailed examination. The deep-tendon
reflexes were ++ and symmetric, and the plantar responses
were flexor. Cerebellar function remained
normal.
The urine was normal. Tests for antinuclear antibodies,
anti–Jo-1 antibodies, anti–Scl-70 antibodies,
and anti–hepatitis B core antibodies were negative.
The results of additional laboratory tests are
shown in Table 1.
An electromyographic study was performed on
the right arm and both legs. There was evidence of a
sensorimotor axonal neuropathy; sensory responses
were absent. The disorder was asymmetric, with
a low-amplitude motor response in the tibial nerve
on the left side and normal-amplitude responses on
the right side. Needle-electromyographic examination
showed only slight changes in reinnervation in
the tibialis anterior and extensor digitorum brevis
on the left side and the abductor pollicis brevis on
the right side.
A diagnostic procedure was performed.


mbaroi prezantimi i rastit...tani mendohet t'i keni te gjitha informacionet qe u nevojiten....

__________________
"I believe there are more instances of the abridgement of the freedom of the people by gradual and silent encroachments of those in power than by violent and sudden usurpations." James Madison

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analiza e porteinave te sieros tregon qe nuk kemi te bejme me nje mielome multiple per faktin se nuk kemi nje rritje monoklonale te te paktes njeres prej imunoglobulinave sic ndodh zakonisht ne rastin e mielomes...dhe ajo rritje e IgG duket se nuk te con asgjekundi sepse nuk eshte ndonje rritje teper e madhe qe te mund te merrej per baze si shenje infeksioni a tjeter gje...pak qe me huton eshte ajo rritja e atyre transaminazeve...nuk eshte qe jane rritur shume por prap jane gati 3x normalen....

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Kurre mos debato me nje idiot!Njerezit mund te mos e bejne dallimin! (Ligj i Marfit)
Think Different!Think Again! (National Geographic Channel)

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differential diagnosis

Dr. David A. Chad:
This 49-year-old woman presented
with a painful peripheral neuropathy. We must
first define the attributes of the neuropathy and
then develop a differential diagnosis.

characterizing a peripheral neuropathy:

We begin by reviewing the defining characteristics
of the neuropathy.
1-3
The most important of these
are the time course, the type of neuron or fiber involved,
the clinical and anatomical pattern of
deficits, the type of nerve-fiber abnormality, the type
of neuropathy (inherited or acquired), and the availability
of clues to the possible presence of an associated
systemic disease (Table 2).
The record indicates that the neuropathy in this
patient is chronic. Her right hand had been numb
for several years, and the burning paresthesias in her
hands and feet had been present for four months.
Small sensory fibers were predominantly affected,
and the neuropathy was painful, with trophic changes
in the skin of the right hand. There was a loss of
large-fiber vibratory sensation, particularly in the
territory of the median nerve in the right hand and
in both feet. The presence of intact reflexes indicates
that the large-diameter, heavily myelinated 1A afferent
neurons were spared. Some motor-fiber involvement
was evident both on physical examination and
on electromyography.
The clinical and anatomical pattern of the patient’s
deficits is complex. There is bilateral but
asymmetric involvement of the upper and lower extremities
(with the distal extremities much more
affected than the proximal extremities). In addition,
the electromyogram points to at least two superimposed
mononeuropathies: a painful mononeuropathy
of the right median nerve, with the site of involvement
probably above the transverse carpal
ligament, because of some loss of sensation in the
palm, and with features resembling those of causalgia,
and both sensory and motor neuropathy of
the left tibial nerve. Finally, there appears to have
been involvement of the maxillary division of the
left trigeminal nerve. This pattern suggests the presence
of an evolving mononeuritis multiplex that is
passing through the stage of overlapping mononeuropathies
on its way to a mostly distal, symmetric
polyneuropathy.
The nerve-fiber abnormality appears to be a mix
of axon loss and demyelination. Axonal involvement
of the motor fibers is indicated by the slight
changes in motor-unit potential in the territories of
the right median and left peroneal nerves and by
the reduced amplitude of the left tibial motor re-
sponse. There are also features of demyelination,
since the motor velocities are reduced more than
can be explained by loss of amplitude alone. Pronounced
sensory involvement, with relative sparing
of the motor responses, may be caused by loss
of the neurons of the dorsal-root ganglia,their axons,
or both, but in this instance it is more likely a
result of damage to the nerve fibers rather than to
the cell bodies.
The neuropathy in this patient is more likely to
be acquired than inherited. The absence of a family
history, the age at onset, and both its duration and
the fact that it is asymmetric, with prominent paresthesias,
are features typical of acquired peripheral
neuropathy.
There are clues that a systemic disorder may be
present. The episodes of color changes in the right
hand suggest Raynaud’s phenomenon, and the mild
polyclonal hypergammaglobulinemia suggests immune
activation. The mild abnormalities in the levels
of aspartate aminotransferase and alanine aminotransferase
suggest that there is inflammation
of the liver. These features raise the possibility of
an underlying connective-tissue disorder. The fact
that the patient had emigrated from India and the
subtle, hypopigmented skin lesion raise the possibility
of infection by
Mycobacterium leprae.

__________________
"I believe there are more instances of the abridgement of the freedom of the people by gradual and silent encroachments of those in power than by violent and sudden usurpations." James Madison

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Ky file ėshtė shkarkuar 44 herė.

tabela 2

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"I believe there are more instances of the abridgement of the freedom of the people by gradual and silent encroachments of those in power than by violent and sudden usurpations." James Madison

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Regjistruar: 16/01/2005
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hmmmmm....me te vertete shume gjera te vyera keto!sme kishte shkuar ne mendje qe nje rritje aq e paket e IgG mund te sherbente si parameter!...iher me shkoi ne mend qe mund te ishte infeksion meqe kishte edhe transaminazit ishin rritur por hoqa dore duke pare qe bilirubina ishte ne rregull dhe se po te ishte hepatit do kishte nje forme me te zgjeruar...duhet me e pase parasysh per here tjeter...
tani nese ke mundesi,si ti edhe une te bejme nje pergjithsim per konceptet dhe semundjet qe jane permend ketu...ska nevoje me detaje fare...vetem sa jane permend ketu,dhe pastaj kalojme tek nje rast tjeter...me pati rene ne dore nje,te shof a e gjej dot me!

__________________
Kurre mos debato me nje idiot!Njerezit mund te mos e bejne dallimin! (Ligj i Marfit)
Think Different!Think Again! (National Geographic Channel)

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rasti nuk ka mbaruar akoma

the process of differential diagnosis

Table 3 lists the diagnoses that would match the
characteristics I have described: a chronic, acquired,
painful, overlapping mononeuritis multiplex that
predominantly affects sensory fibers, with a combination
of axon loss and demyelination and with
some features suggesting a connective-tissue disease
and others that raise the possibility of leprosy.
Table 3 also lists the reasons for including or ruling
out each possible diagnosis.
A predominantly sensory neuropathy presenting
in midlife raises the possibility of a paraneoplastic
manifestation.
Because small dorsal-root
ganglia may be targeted initially, the disorder may
begin with painful asymmetric paresthesias, commonly
in the hand or arm, but, unlike the disorder
seen in this case, evolves to affect large sensory fibers,
with pronounced sensory ataxia and attenuation
or loss of tendon reflexes. The predominance
of small-fiber involvement in the current case suggests
sensory perineuritis
and other forms of
small-fiber sensory neuropathy in which the reflexes
remain intact.
Their relatively benign nature, or
relapsing–remitting character, however, suggests
that they are unlikely candidates for the diagnosis
in this case.
A predominantly small-fiber neuropathy in primary
systemic amyloidosis is classically manifested
as a distal, symmetric polyneuropathy with prominent
autonomic signs and major-organ involvement.
It is a consideration here for several reasons:
it is characterized by sensory symptoms that spread
very rapidly to the hands, with carpal tunnel syndrome
as the presenting feature in 25 percent of
patients
; cranial neuropathy, including trigeminal
involvement, may occur; and perhaps most important,
tendon reflexes are preserved until the condition
is in its advanced stages — a point emphasized
by David Dawson at one of these conferences in
1979.
He pointed out that preservation of tendon
reflexes narrows the range of diagnostic possibilities
to just a few conditions: amyloidosis, leprosy,
and slowly advancing sensory diabetic neuropathy.
There are no clinical or laboratory findings in this
case, however, that would support a diagnosis of
amyloid neuropathy.


narrowing the differential diagnosis

The process of differential diagnosis leads to a consideration
of vasculitic neuropathy in the context of
systemic vasculitis or connective-tissue disease and
leprous neuropathy. Although cryoglobulinemic
neuropathy is associated with Raynaud’s syndrome
and although it may produce painful asymmetric
neuropathy and be associated with liver dysfunction
due to hepatitis C infection,
the absence in
this case of skin lesions suggesting leukocytoclas-
tic vasculitis and the absence of serum protein abnormalities
make this diagnosis unlikely. Vasculitic
neuropathy occurs in Sjögren’s syndrome, a chronic
autoimmune disorder of the exocrine glands. Patients
with Sjögren’s syndrome may have Raynaud’s
phenomenon and hypergammaglobulinemia, and
the peripheral nerves may be affected.
18
One of the
major manifestations of the neuropathy of Sjögren’s
syndrome is a sensory ganglionopathy that is manifested
predominantly as a sensory ataxia, although
there may also be vasculitic involvement of individual
nerve trunks. Sjögren’s syndrome is one of the few

__________________
"I believe there are more instances of the abridgement of the freedom of the people by gradual and silent encroachments of those in power than by violent and sudden usurpations." James Madison

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Ky file ėshtė shkarkuar 37 herė.

Po shkruaj nga pak qe mos merziteni t'i lexoni te gjitha pernjehere

__________________
"I believe there are more instances of the abridgement of the freedom of the people by gradual and silent encroachments of those in power than by violent and sudden usurpations." James Madison

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Regjistruar: 16/01/2005
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Mesazhe: 3634

me fal
kujtova se kishte mbaruar atje ...

__________________
Kurre mos debato me nje idiot!Njerezit mund te mos e bejne dallimin! (Ligj i Marfit)
Think Different!Think Again! (National Geographic Channel)

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Si thoni a ti japm fund rastit sonte? Eshte goxha i gjate po edhe i bukur


connective-tissue disorders that affects the trigeminal
ganglion.
Peripheral neuropathy may predate or
overshadow symptomatic glandular involvement,
and testing for anti-SSA and anti-SSB autoantibodies
is helpful but not definitive. In the current case,
I initially favored a diagnosis of vasculitic neuropathy,
possibly in the context of Sjögren’s syndrome.
The patient was known, however, to have come
from a region where leprosy is endemic, and she
presented with a predominantly small-fiber neuropathy
and intact reflexes. These factors, along with
the presence of a subtle, hypopigmented skin lesion,
raise the possibility of leprous neuropathy.
Several features of the case are not typical of this diagnosis,
including the severe pain and causalgia,
large-fiber sensory involvement, and absence of demonstrable
enlargement of peripheral nerves.
However, there was a greater reduction of pinprick
sensation over the dorsal surfaces of the hands
than over the palmar aspects — regions equidistant
from the trunk and served by the same upper-limb
nerves. Indeed, the pattern in this case, as outlined
by Sabin in his classic description of sensory loss in
leprosy,
. . . attracts attention because it does not
follow the distribution of the named subcutaneous
sensory nerves, of the mixed nerve
trunks, of the sensory roots, or of the distal
symmetrical sensory loss with fading upper
borders commonly associated with the various
hereditary, toxic and metabolic neuropathies.
Comparison of this pattern of sensory
loss with thermographic pictures of the arm
suggests that local temperature differences
might provide an explanation for this unique
configuration of sensory loss.
Figure 1 shows Sabin’s examples of temperaturelinked
sensory loss in lepromatous neuropathy. In
addition, the allodynia and sensory loss on the face
involve the malar region, an area that is cooler than
other regions of the body. Thus, the involvement
that I originally considered a manifestation of a trigeminal
neuropathy could be viewed as temperature-
linked cutaneous sensory loss. The intact deeptendon
reflexes and preserved H reflexes in the face
of pronounced sensory loss in the feet for smalland
large-fiber modalities (pain and light touch,
respectively) in the absence of sensory-nerve action
potentials point to very distal (intracutaneous) sensory-nerve
involvement, which is typical of lepromatous
neuropathy.
There is also evidence of
lesions involving more proximal portions of the
peripheral nerves — specifically, the right median
nerve and the left tibial nerve. Such mononeuropathies
may also be seen in leprous neuropathy.
The causative organism of leprosy is
M. leprae,
an
acid-fast, obligate, intracellular gram-positive bacillus
that reproduces maximally at 27°C to 30°C.
Consequently, infection is most prominent in cooler
regions of the body (34°C to 35°C).
The organism
infects the skin and cutaneous nerves, its
principal target being the Schwann-cell basal lamina.
Five major clinical subtypes of leprosy, which reflect
the immunologic status of the host, have been
defined.
Tuberculoid leprosy occurs in persons
with relatively intact cell-mediated immunity to the
organism, limiting the spread of the disease. Typically,
there are a small number of skin lesions in
cool regions, with adjacent nerve-trunk involvement.
Histopathological examination of the skin
and nerves shows granulomas but no or few bacilli.
Lepromatous leprosy occurs in persons with no immune
response to
M. leprae.
Large numbers of bacilli
are found in the skin, nerves, and nasal mucosa.
Borderline leprosy is intermediate in its manifestations
between those two subtypes and is subdivided
into forms that more closely resemble tuberculoid
leprosy (so-called borderline tuberculoid leprosy)
and forms that are closer to lepromatous leprosy
(so-called borderline lepromatous leprosy).
In tuberculoid leprosy, sensory loss is pronounced
in the skin lesions as a result of damage to
the dermal nerves. There may be damage to nerve
trunks in the vicinity of the skin lesions, and on occasion
painful mononeuropathies develop in swollen
or enlarged nerves.
In lepromatous leprosy, a
progressive symmetric polyneuropathy favoring
cool regions is the chief manifestation.
There is
also damage to peripheral-nerve trunks, resulting in
superimposed mononeuropathies that may evolve
into mononeuritis multiplex. The incidence of neuropathic
complications is probably highest in patients
with borderline leprosy.
These patients
have an unstable immune response to the organism,
so that the clinical manifestations vary along the tuberculoid-
to-lepromatous spectrum. Impaired immunity
results in extensive spread of the organism,
whereas retained immunity generates a destructive
inflammatory granulomatous response.
Leprous neuropathy explains several key clinical
manifestations in this case. The painful dysesthesias
affecting the hands, with sensory loss more
pronounced on the dorsal than on the palmar surfaces,
can be explained by temperature-dependent
invasion of dermal nerves by
M. leprae
. The exquisitely
painful right median neuropathy in the forearm
is related to involvement of the proximal mediannerve
trunk. The retention of the deep-tendon reflexes
probably indicates that the deep-seated 1A
afferent nerves were spared. The absence of sensory
responses stems from very distal axon loss in intracutaneous
nerves. Finally, motor-nerve conduction
velocities that have decreased out of proportion to
amplitude loss reflect demyelination due to the destruction
of Schwann cells.
I believe that the likeliest diagnosis in this case
is leprous neuropathy and that the diagnostic procedure
was a sural-nerve biopsy. Because the clinical
features are most consistent with the presence

__________________
"I believe there are more instances of the abridgement of the freedom of the people by gradual and silent encroachments of those in power than by violent and sudden usurpations." James Madison

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