I want to help you guys - rachana

[ArchivalUser]

thanks ppl! appreciate these all...will u plz explain why manitol causes pulmonary edema? mechanism of action of indomethacine and hydrochlorthiazid and amiloride in DI nephrogenic? thanks

[ArchivalUser]

hi john2007, Iam having some presentation for my sat class so need to prepare today whole day, I will get back to you with the information u asked about by sat even,...

[ArchivalUser]

Hi Rachana,
Thanks a zillion! Very good work indeed. Helps all of us. Wish you nothing less than 99. Don't get any idea from my nick though! But may I just say, you have a lovely name(;-).

[ArchivalUser]

Too rapid infusion of large amounts of mannitol will cause a shift of intracellular water into the extracellular compartment resulting in cellular dehydration and overexpansion of the intravascular space with hyponatremia, congestive heart failure and pulmonary edema. Repeated doses should not be given to patients with persistent oliguria as this can produce a hyperosmolar state and precipitate congestive heart failure and pulmonary edema due to volume overload. Dosage must be carefully monitored and adjusted in accordance with the clinical situation to avoid the consequences of overdosage.

[ArchivalUser]

Hi, please can you explain in detail Horner Syndrome.

[ArchivalUser]

Horner's syndrome is a clinical syndrome caused by damage to the sympathetic nervous system. It is also known by the names Bernard-Horner syndrome or oculosympathetic palsy.

Signs
Signs found in all patients on affected side of face include ptosis (drooping upper eyelid from loss of sympathetic innervation to the Müller muscle, upside-down ptosis (slight elevation of the lower lid), and miosis (constricted pupil) and dilation lag. Enophthalmos (the impression that the eye is sunk in) and anhidrosis (decreased sweating) on the affected side of the face, loss of ciliospinal reflex and blood shot conjunctiva may occur depending on the site of lesion.
In children Horner's syndrome sometimes leads to a difference in eye color between the two eyes (heterochromia).This happens because a lack of sympathetic stimulation in childhood interferes with melanin pigmentation of the melanocytes in the superficial stroma of the iris.

Causes
Horner's syndrome is usually acquired but may also be congenital (inborn) or iatrogenic (caused by medical treatment). Although most causes are relatively benign, Horner's syndrome may reflect serious pathology in the neck or chest (such as a Pancoast tumor or thyrocervical venous dilatation) and hence requires workup.
¢Due to lesion of one side of the cervical sympathetic chain which affects on the same side of the lesion
¢Lateral medullary syndrome
¢Cluster headache - combination termed Horton's headache
¢Trauma - base of neck, usually blunt trauma, sometimes surgery.
¢Middle ear infection
¢Tumors - often bronchogenic carcinoma of the superior fissure (Pancoast tumor)
¢Aortic aneurysm, thoracic
¢Neurofibromatosis type 1
¢Goitre
¢Dissecting aortic aneurysm
¢Thyroid carcinoma
¢Multiple sclerosis
¢Carotid artery dissection
¢Klumpke paralysis
¢Cavernous sinus thrombosis
¢Sympathectomy
¢Syringomyelia
¢Nerve blocks, such as cervical plexus block, stellate ganglion or interscalene block

Pathophysiology
Horner's syndrome is due to a deficiency of sympathetic activity. The site of lesion to the sympathetic outflow is on the ipsilateral side of the symptoms. The following are examples of conditions that cause the clinical appearance of Horner's syndrome:
¢First-order neuron disorder: Central lesions that involve the hypothalamospinal pathway (e.g. transection of the cervical spinal cord).
¢Second-order neuron disorder: Preganglionic lesions (e.g. compression of the sympathetic chain by a lung tumor).
¢Third-order neuron disorder: Postganglionic lesions at the level of the internal carotid artery (e.g. a tumor in the cavernous sinus).

Diagnosis
Three tests are useful in confirming the presence and severity of Horner's syndrome:
1.Cocaine drop test - Cocaine blocks the reuptake of norepinephrine resulting in the dilation of a normal pupil. Due to the lack of norepinephrine in the synaptic cleft, the pupil will fail to dilate in Horner's syndrome.
2.Paredrine test:- This test helps to localize the cause of the miosis. If the 3rd order neuron (the last of 3 neurons in the pathway which ultimately discharges norepinephrine into the synaptic cleft) is intact, then the amphetamine causes neurotransmitter vesicle release, thus releasing norepinephrine into the synaptic cleft and resulting in robust mydriasis of the affected pupil. If the lesion itself is of the aforementioned 3rd order neuron, then the amphetamine will have no effect and the pupil remains constricted. There is no pharmacological test to differentiate between a 1st and 2nd order neuron lesion.
3.Dilation lag test

It is important to distinguish the ptosis caused by Horner's syndrome from the ptosis caused by a lesion to the oculomotor nerve. In the former, the ptosis occurs with a constricted pupil (due to a loss of sympathetics to the eye), whereas in the latter, the ptosis occurs with a dilated pupil (due to a loss of innervation to the sphincter pupillae). In an actual clinical setting, however, these two different ptoses are fairly easy to distinguish. In addition to the blown pupil in a CNIII (oculomotor nerve) lesion, this ptosis is much more severe, occasionally occluding the whole eye. The ptosis of Horner's syndrome can be quite mild or barely noticeable.
When anisocoria (unequal size of the pupils) occurs and the examiner is unsure whether the abnormal pupil is the constricted or dilated one, if a one-sided ptosis is present then the abnormally sized pupil can be presumed to be the one on the side of the ptosis.

Treatment depends on the location and cause of the lesion. In some cases surgical removal of a tumor is appropriate. If the tumor is malignant, radiation and chemotherapy may be recommended.

[ArchivalUser]

thanks rachana
wish you good luck

[ArchivalUser]

thanks rachana
wish you good luck

[ArchivalUser]

hey rachana!
hope u are had a great week...
if u can,, please summarize for us the different chromosomal abnormalities and the diseases,,,

Thanks...
c ya around...

sam

[ArchivalUser]

A chromosome abnormality reflects an abnormality of chromosome number or structure. Chromosome abnormalities usually occur when there is an error in cell division following meiosis or mitosis. There are many types of chromosome abnormalities. They can be organized into two basic groups, numerical and structural abnormalities.

Numerical abnormalities
When an individual is missing either a chromosome from a pair (monosomy) or has more than two chromosomes of a pair (trisomy). An example of a condition caused by numerical abnormalities is Down Syndrome, also known as Trisomy 21 (an individual with Down Syndrome has three copies of chromosome 21, rather than two). Turner Syndrome is an example of a monosomy where the individual is born with only one sex chromosome, an X.

The major numerical abnormalities that survive to term
Syndrome Abnormality Incidence per 10 000 births Lifespan (years)
Down Trisomy 21 15 40
Edward's Trisomy 18 3 <1
Patau's Trisomy 13 2 <1
Turner™s Monosomy X 2 (female births) 30-40
Klinefelter™s XXY 10 (male births) Normal
XXX XXX 10 (female births) Normal
XXY XYY 10 (male births) Normal

Structural abnormalities
Structural abnormalities can be unbalanced or balanced. The former are similar to numerical abnormalities in that genetic material is either gained or lost. The abnormalities range from the loss or duplication of whole chromosome arms to the deletion or duplication of tiny chromosome fragments barely visible under the microscope. However, even these tiny deviations (microdeletions and microduplications) can encompass several to many genes and have severe effects

Unbalanced structural abnormalities (p = short arm, q = long arm)
Syndrome Abnormality Incidence
Wolf-Hirschhorn Deletion, tip of 4p 1 in 50 000
Cri-du-chat Deletion, tip of 5p 1 in 50 000
WAGR Microdeletion, 11p
Prader-Willi/Angelman microdeletion, 15p
DiGeorge Microdeletion, 22q

Balanced structural abnormalities involve the rearrangement of genetic material but no overall gain or loss. Examples include inversions (where a segment is removed from a chromosome, turned on its axis and sealed back in place), translocations (where part of one chromosome becomes attached to another) and ring chromosomes (where the ends of the long and short arms fuse together to form a circle).
Balanced abnormalities can have an immediate effect if a gene is disrupted by the breakpoint, if two genes are fused together, or if the relocation of a gene causes it to be expressed at a higher or lower level than usual. However, the major consequence is to prevent normal chromosome pairing at meiosis, leading to the production of sperm and eggs with incomplete or partially duplicated chromosome sets.