PATHOPHYSIOLOGY OF MENINGITIS

INFECTION/INFLAMMATION OF THE

MENINGES COVERING THE BRAIN AND SPINAL CORD.

Infective organisms enter the CNS

Organisms quickly disseminate into the meninges and ventricles

Dissemination result in:

 Meningeal congestion, cerebral edema, increases ICP, pus formation. 

 Ø INFANT: hydrocephalus happens, if exudates block ventricles. 

Skull is capable of expanding.

Ø ADULT: blockage of the ventricles would to increases ICP.

PATHOPHYSIOLOGY OF HUNTINGTON'S DISEASE

hereditary disease that causes degeneration of cerebral cortex and basal ganglia.

Involves disturbance in neurotransmitter substance primarily 

> Gamma Aminobyutric Acid (GABA)

> Dopamine 

GABA neurons in basal ganglia, frontal cortex and cerebellum are destroyed

 GABA neurotransmitter production 

Excess of dopamine causes abnormal nerotransmisson along

the affected pathway

Chorea and mental deterioration

Enlargement of the ventricles in HD patients due to atrophy of 

the head of the caudate from neuronal loss.

PATHOPHYSIOLOGY OF BELL'S PALSY

Disorder CN VII unilateral facial paresis/paralysis

Compression of the facial nerve 

due to demyelination.

Inflammation or ischemia (inadequate blood supply)

The facial nerve is responsible for contraction

of the muscle of the face in expression, lacrimation

and the senses of taste and hearing.

PATHOPHYSIOLOGY OF ALZHEIMER'S DISEASE

 progressive degeneration and atrophy of brain. 

The brain of patients with alzheimer’s has 3 distinguishing features

Neurofibrillatory tangles (fibrous protein)

Amyloid plaques (composed of degenerating axons and dendrites)

Granulovacuolar degeneration(fibrous protein)

Normal brain weighs 1,380 g

>autopsy of alzheimers brain
>reveals brain atrophy
>weighs 1,000 g or less (fibrous protein)

PATHOPHYSIOLOGY OF INCREASED INTRACRANIAL PRESSURE

 increase in any three intracranial components.






EDEMA

INCREASED INTRACRANIAL PRESSURE

BLOOD VESSEL COMPRESSION

DECREASED PERFUSION

DECREASED OXYGEN

BRAIN CELL DEATH

PATHOPHYSIOLOGY OF GUILLAINE BARRE SYNDROME

An acute, rapidly progressive and fatal form of polyneuritis. 

WHITE BLOOD CELLS (WBC) ATTACK PERIPHERAL NERVES

DESTRUCTION OF MYELIN SHEATH (DEMYELINATION)

WIDENING OF THE NODES OF RANVIER

DELAY OR IMPAIRMENT OF IMPULSES TRANSMISSION

WEAKNESS / PARALYSIS / LOSS OF SENSATION

PATHOPHYSIOLOGY OF MULTIPLE SCLEROS

A progressive demyelination of the white mater of the brain and spinal cord.

INFECTION / AUTOIMMUNE RESPONSE

ATTACKS WHITE MATER OF BRAIN

DESTRUCTION OF MYELIN SHEATH

SCARRING (GLIOSIS, HARD YELLOW PLAQUES)

DISRUPTION OF NERVE CONDUCTION

NEUROLOGIC DYSFUNCTION

PATHOPHYSIOLOGY OF AMYOTROPIC LATERAL SCLEROSIS

The defining feature of ALS is the death of both upper and lower motor neurons 

in the motor cortex of the brain, the brain stem, and the spinal cord.

MOTOR NEURONS IN MO AND SPINAL CORD DIE

MUSCLES THEY SERVE ATROPHY

WEAKNESS / PARALYSIS OF THE MUSCLES

SIGNS ANG SYMPTOMS VARY ACCORDING TO

 WHAT NEURON IS AFFECTED AND WHAT MUSCLES THEY SERVE

PATHOPHYSIOLOGY OF SEIZURE

a sudden malfunction in the brain that causes someone to collapse, convulse, or have another temporary disturbance of normal brain function, often with a loss or change in consciousness.

GROUP OF NEURONS LOSE AFFERENT STIMULATION

BECOME EPILEPTOGENIC FOCUS

THESE NEURONS ARE HYPERSENSITIVE AND EASILY ACTIVATED

FIRE ABNORMALLY

SEIZURE

PATHOPHYSIOLOGY OF MYASTHENIA GRAVIS

A progressive disorder affecting neuromuscular transmission of impulses in voluntary muscles.

BLOOD CELL AND THYMUS PRODUCE ANTIBODIES

ANTIBODIES: BLOCK AND DESTROY/ 
WEAKEN NEURO RECEPTORS IN NEUROMUSCULAR JUNCTION (ACH RECEPTORS)

FAILURE IN TRANSMISSION OF ACH NEUROTRANSMITTER TO MUSCLES

MUSCULAR WEAKNESS OR PARALYSIS