Patho: Nervous system

Helpfulness: 0
Set Details Share
created 5 years ago by hcarrera
show moreless
Page to share:
Embed this setcancel
code changes based on your size selection

Identify the high risk groups for head injury

Young people 15-24 years

infants 6 months-2 years

young school aged kids and the elderly


most common causes of head injury.

Falls (35%)
Transportation-related events (17%)
Struck by moving objects or moving against stationary objects (16.5%)
Assaults (10%)
Others (sports-related injuries, blasts; 21%)


Distinguish between coup and contrecoup

Occurs as a continuous motion
Head strikes fixed object (coup) and rebounds (contrecoup)

front and back


primary head injury

-Caused by impact
-Involves neuronal and glial injury and the vascular response
-Focal (direct impact)
-Diffuse (acceleration/deceler-ation rotational)


Secondary head injury

-Cerebral edema, brain swelling, hemorrhage, infection and high ICP
-Occurs from reduced circulation and brain shift


Tertiary head injury

Caused by apnea, low BP and other lung and cardiac problems


Focal brain injury

-Blunt trauma
.Epidural hematoma
.Subdural hematoma
-Intracerebral hemorrhage, subarachnoid hemorrhage
-Compound fracture
-Penetrating trauma


Diffuse brain injury

-Concussions (mild to severe)
-Diffuse axonal injury (mild to severe; injury over a widespread area)


Explain what a CVA is

Most common clinical manifestation
A sudden, nonconvulsive focal neurological deficit
4th leading cause of death in the US


identify and define the 3 main types of CVA

Arterial occlussions caused by thrombi—(blood clots)
Fragments breaking from a thrombus outside the brain
Intracranial bleeding



(Thrombotic CVA)

Transient ischemic attacks

May be due to intermittent blockage by thrombotic particles or spasm
-All neurological deficits clear in 24 hours leaving no residual deficit
-35% completed strokes preceded by TIAs


Stroke in evolution

(Thrombotic CVA)

-Step-by-step process over minutes to hours
-Intermittent progression over hours to days characteristic of thrombotic stroke or slow hemorrhage


Completed stroke

(Thrombotic CVA)

CVAs that reach maximum destructiveness in producing neurological deficits


Cerebral infarction

-Results when area of brain loses blood supply due to vascular occlusion
-May be ischemic or hemorrhagic


Cerebral hemorrhage

-Primary cause is hypertension
-Walls of small arteries and arterioles thicken
-Microaneurysms may form and bleed
-Bleeding may displace/compress adjacent brain and cause ischemia and edema


Inter-cranial aneurism

-Result from vascular wall defects, which allow thinning and ballooning of vessel wall
-Potential for bleeding and rupture occurs


AV malformations

Arteriovenous malformations

-Vascular malformation
-Tangled masses of dilated vessels that may be congenital


Subarachnoid Hemorrhage

-Blood from injured/defective vasculature enters subarachnoid space
-Blood clogs:
.Arachnoid granulations (so CSF not reabsorbed)
.Foramina within ventricular system (so CSF circulation impaired)


Identify the early manifestations of cerebral hemorrhage.

-Headache, altered mental status, motor weakness, numbness and tingling
-Vasospasm is a complication causing brain ischemia and infarction


Parkinsons disease

-disease of basal ganglia
-Primary forms involve degeneration of dopamine-secreting nigrostriatal pathway, which causes dopamine depletion and excess cholinergic activity
-Tremor and rigidity caused by excessive cholinergic activity
Secondary (drug-induced) forms


Parkinson's disease cont'

-Mainstay of treatment involves L-dopa, dopamine precusor
-Complete invalidism may occur in 15-20 years
-New research suggests occupational exposure to organic groundwater contaminant (trichloroethylene) and dry cleaning chemical (perchloroethylene) increases risk


Huntington disease

Rare hereditary disease involving the basal ganglia and cerebral cortex
Autosomal dominant trait with high penetrance
Defect on short arm of chromosome 4
Depletion of g-aminobutryic acid (GABA; inhibitory neurotransmittor)-secreting neurons causes involuntary, fragmented movements


Alzheimers disease

Cause unknown; theories proposed
Loss of neurotransmitter stimulation by choline acetyltransferase
Genetic defects involving amyloid precusor protein
Alteration of apolipoprotein E, which binds beta amyloid
Pathologic activation of N-methyl-D-asparate (NMDA) receptors with excess calcium influx
Prions and autoimmune reactions


Forms of Alzheimers

-Early onset familial gene defects
Amyloid precursor protein on chromosome 21
Presenilin on chromosome 14 (PSEN1)
Presenilin on chromosome 1 (PSEN2)
-Late-onset familial
Defect in apolipoprotein E on chromosome 19
APOE2, APOE3 and APOE4 occur most frequently
APOE4 allele is marker of increased susceptibility…but NOT a determinant



(multiple sclerosis)

Degenerative disease in which CNS demyelinization may result from immunogenic-viral causes
Viruses/antigens may attack myelin and cause hypersensitivity reaction
Steroids can shorten duration of acute exacerbations
Immunosuppressant therapy may slow progression



(Amyotrophic lateral sclerosis)

Rare degenerative disorder involving lower and upper motor neurons
Flaccid paresis progressing to paralysis characterizes this syndrome
Genetic factors now thought to be involved and may involve SOD
Glutamate toxicity may cause neuron degeneration
New research suggests NFL players may be at higher risk of death from neurodegenerative diseases like ALS or Alzheimer’s (associated with CTE)


Myasthenia Gravis

Neuromuscular disorder of voluntary muscle characterized by weakness and fatigability

Postsynaptic acetylcholine receptors on muscle cell not recognized as self
Elicits antigenic response
Antibody binding blocks acetylcholine binding
Receptors destroyed and impulse transmission diminished across neuromuscular junctions


Myasthenia crisis

Severe muscle weakness causes:
Quadriparesis or quadriplegia
Respiratory insufficiency with reduced tidal volume and vital capacity
Extreme difficulty swallowing, in danger of respiratory arrest


Cholinergic crisis

Arises from anti-cholinesterase drug toxicity
Caused by too much acetylcholine at neuromuscular junctions

LIKE MYASTHENIA CRISIS BUT ASSOCIATED WITH:Increased intestinal motility, diarrhea, intestinal cramps, bradycardia, pupillary constriction, increased salivation and sweating