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AUTOLOGOUS...tissue is moved from one location to other in same individual.
SYNGENEIC..transplant b/w genetically identical individuals(monozygotic twins)
ALLOGENEIC..translants b/w genetically diffrent members of same species.
XENOGENEIC..transplant b/w members of diffrent species.


-hyperacute rejection..within minutes to hours...due to preformed anti-donar antibodies and complement
-accelerated...takes days...because of reactivation of sensitized Tcells.
-acute..takes days to weeks...due to primary activation of T cells.
-chronic....months to years..causes r unclear: antibodies,immune complexes,slow cellular reaction,recurrence of disease.
-graft versus host..weeks to months...grafted bone marroe T cells attack the host.


in cns i think localisation of a lesion according to the presenting complaint wud be hy. its really a waste of neurons if u try memorising ALl the syndroems and try to fit a given clinical picture ..hence we'll figure out hte approach to such a question.

firstly the broad categorisation..

is it a brain stem lesion?

is it below the BS ( SC) ?

is it above the BS( cortex eg)


look for two regions..

above the neck?

if deicit is on the same side above and below, think ABOBE THE BRAINSTEM--corex/capsule

( this is a contralateral lesion)

below the neck?


if long tract signs are contralateral tofacial deficits, think brainstem.

the CN deficits are ipsi tot he lesion.

the lomng tract deficits are contra to it.


if there are long trasct findings, and the face isnt involved..analyse the long tract deficits. pain and temp will be opp to the rest ( in general)..these point to a sc hemisection


remember when u review these points do not confuse DEFICITS with reference to the face and lower body..

with deficits compared to the lesion.

an internal capsule infarct wil produce motor/sensory deeficits contralateral to the lesion itsllef ..but the same side of the face and body will be involved.


once i got familiar withthis basic pattern, i tried learning the different syndromes...

im assuming this is HY..if any experienced examinee thinks otherwise do post smiling face


thax a lot ..really appreaciate that..



rubella is caused by RNA toga virus.
posterior cervical and post auricular lymhadenopathies are charecterstic of rubella.
palms and soles are also not involved

Edited by sheena2005 on Sep 04, 2006 - 5:56 PM


gram positive bugd forming spores.

bacillus anthracis
clostridium perferinges
clostridium tetani

they have dipicolinic acid in their core.have no metabolic activity.


gram stain limitations

treponema--too thin to be visualized----dark field microscopy and flourescent antibody staining.

Rickettesia--intracellular parasite

Mycobacteria-- high lipid content cell wall requires acid fast stain

Mycoplasma-- no cell wall

legionella pneumophilia--intracellular-- silver stain

chlaymydia--intracellilar parasite.


rheumatoid nodules are dur to focal vasculitis.


tay sach's-hexosaminidase A


great smiling face



ALPHA...secondary to gene deletion.4 genese can be deleted

1 deleted....silent carrier

2 deleted..trait

3 deleted HBH disease

4 deleted ...hydropes fetalis,bart hb

CLINICAL PICTURE..variable clinical severity, non alpha chain aggregates less toxic, mild hemolysis and anemia tend to be milder; brts in neonate leads to anoxia and intrauterine death.


defects in mRNAprocessing.

homozygous..beta thalacemia major

heterozygous..beta thalacemia monir.

CLINICAL PICTURE..mediterranean countries,africa,south asia.

relative excess of alpha chains..hb aggregates and become insoluble

intra and extra medullary hemolysis , extramedullary hemopoises ,secondary hemochromatosis.



-alpha thalacemia: normal HbA2 and HbF

-beta thalacemia minor(trait):elevated HbA2,HbF


I DUN KNO THATS H/Y OR NOT..but i was readin it so put it here just to rewise in last..


dry cough with use of ACE inhibitors is due to increasd production of bradykinins, substance p,thromboxanes and prostaglandins.


when an individual focuses on nearby objects after looking at distant objects,3 events occurs..

1.ACCOMODATION..parasympathetic fibers contract the ciliary muscle, which relaxes suspensory ligaments,allowing lense to increase its convexity..increase in refractive index of the lens..thereby focusing a near object on retina

2. CONVERGENCE..both medial rectus muscles contract,adductin both eyes.

3. PUPILLARY CONSTRICTION...parasympathetic fibers contractthe pupillar sphincter muscle....miosis.

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