Noorul Seckam Group 9

Disease of Central Nervous System

Slide 167 Suppurative mengitis

1) Histological and gross view signs

Focal and segmental

Neutrophilic exudate is seen covering the meninges , with prominent dilated

vessels. There is edema and focal inflammation (extending down via the Virchow-
Robin space) in the cortex to the right. This acute meningitis is typical for bacterial
infection.

This edema can lead to herniation and death. Resolution of infection may be
followed by adhesive arachnoiditis with obliteration of subarachnoid space
leading to obstructive hydrocephalus.
Microscopically, a gram stain reveals gram negative diplococci within a
neutrophil, typical for Neisseria meningitidis.

2)Complications
hearing loss, which may be partial or total – people who have had meningitis ,
recurrent seizures (epilepsy)
problems with memory and concentration , co-ordination, movement and
balance problems , learning difficulties and behavioural problems , vision loss,
which may be partial or total
, loss of limbs – amputation is sometimes necessary to stop the infection
spreading through the body and remove damaged tissue ,
bone and joint problems, such as arthritis, kidney problems.

3) Pathogenesis.
The organisms that cause bacterial meningitis colonize the nasopharynx and, from
there, they get into the blood stream. They enter the subarachnoid space by
passing through endothelial cells (transcytosis), getting across the porous choroid
plexus capillaries, or being carried by granulocytes. The CSF is an ideal medium for
the spread of bacteria because it provides enough nutrients for their
multiplication and has few phagocytic cells, and low levels of antibodies and
complement.
Bacterial products can damage the brain and blood vessels directly. Bacterial
toxins cause neuronal apoptosis, and cell wall lipopolysaccharide (endotoxin),
released from bacteria, activates clotting causing disseminated intravascular
coagulation (DIC). 

Slide 39 Gouty tophy

1) Histological and gross view signs

Focal and segmental

On gross pathologic examination, tophaceous gout deposits appear as yellow-

white chalky material. Urate within aspirated or scraped material is seen as
strongly negative, birefringent, ,needle-shaped crystals under polarized light
Histologically, gouty tophi appear as amorphous amphophilic material similar to
amyloid deposits ). The crystals within these tissue deposits are difficult to
visualize with routine fixation, tissue processing, and staining because they are
dissolved by aqueous solutions during formalin processing.

2)Complications
Tophi. Tophi are clumps of urate crystals that harden under your skin. ...

•Joint damage and deformity. When you have chronic gout, you have swelling in
your joints regularly. ...

•Kidney disease and kidney failure

•Psychological and emotional problems.

•Severe degenerative arthritis

•Secondary infections
•Urate or uric acid nephropathy

•Increased susceptibility to infection

•Urate nephropathy

•Renal stones

•Nerve or spinal cord impingement

•Fractures in joints with tophaceous gout

3) Pathogenesis
Gout can be considered a disorder of metabolism that allows uric acid or urate to
accumulate in blood and tissues. When tissues become supersaturated, the urate
salts precipitate, forming crystals. In addition, the crystals also are less soluble
under acid conditions and at low temperatures, such as occur in cool, peripheral
joints (eg, the metatarsophalangeal joint of the big toe).
Various factors including genetics , obesity ,medications can lead to
hyperurecemia
||
Reduced solubility of urate
||
Acute inflammation in joints.