Neuro Quiz 1 Flashcards Preview

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Flashcards in Neuro Quiz 1 Deck (36):
1

CVA

non-traumatic brain injury-disruption of blood flow in the brain

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CVA Types

ischemic & hemorrhagic

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Ischemic types

thrombotic (clot in artery), embolic (dislodged clot that moves to brain), TIA

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Hemorrhagic types

HTN-Intracerebral (burst blood vessel), Aneurysm (weak spot in artery forms balloon and pops), Subarachnoid (blood vessel bursts near surface of brain)

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CVA location-presentation: anterior

○ Anterior: contralateral motor and sensory deficit, sucking or rooting reflex, rigidity and gait problems, loss of proprioception, fine touch

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CVA location-presentation: posterior cereberal

Dominant side—aphasia, motor/sensory deficits, hemianopsia
■ Non-dominant side—motor/sensory deficit, neglect, hemianopsia

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CVA location-presentation: Vertebral

CN deficits, diplopia (double vision), dizziness, N/V, dysarthria (slurred, slow speech), dysphagia/coma

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CVA location-presentation: Left hemisphere

Left hemisphere: aphasia (language disorder, not understand), right side deficits, math/scientific reasoning impaired

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CVA location-presentation: Right hemisphere

spatial/perceptual deficits, left side deficits, art/creativity impaired

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CVA diagnosis

○ BEFAST: Balance, Eyes, Face, Arms, Speech, Time
○ Non-contrast CT scan
○ Complications: DVT, pneumonia, seizures, impaired skin integrity, motor deficits, safety, vision deficits, sensory/perceptual complications, dysphagia, alterations in elimination

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Guillain-Barre Syndrome

involves degeneration of the myelin sheath of PNS

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Guillain-Barre Syndrome Patho

usually bacterial/viral infection triggers antibodies to attack peptides within peripheral myelin sheath

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Guillain-Barre Syndrome clinical manifestations

ascending paresthesia, paresis, paralysis, absent DTR, resp failure

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Guillain-Barre Syndrome Diagnosis

lumbar puncture (↑ protein), electromyography/EMG (nerve conduction)

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Guillain-Barre Syndrome Treatment

Plasmapheresis, IV Ig

16

Multiple Sclerosis

demyelination and scarring of neurons in CNS

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Multiple Sclerosis affected Population

400,000 annually; 20-50 years (women>men); caucasians; cold climates

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Multiple Sclerosis Patho

destruction of myelin sheath surrounding neurons in CNS (maybe triggered by virus)

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Multiple Sclerosis Clinical manifestation

vision problems (“Di”plopia OOOOOOOO DOUBLE VISION), paresthesia (tingling sensation), ataxia (loss of bodily movement), spasticity (certain muscles contract)

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Multiple Sclerosis Diagnosis

history, MRI brain/spinal cord

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Multiple Sclerosis Treatment

corticosteroids, immunosuppressive agents (Interferon-B)

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Myasthenia Gravis affected population

○ 60,000 people; 20-30 in women; after 50 in men

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Myasthenia Gravis patho

autoantibodies block skeletal muscle receptor sites, prevents acetylcholine from attaching to them--muscle contraction does not occur

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Myasthenia Gravis clinical manifestation

Ptosis (eye lid drooping), diplopia, dysphagia (difficulty swallowing), dysarthria (slow speech), myasthenic snarl, resp failure

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Myasthenia Gravis diagnosis

Serum acetylcholine receptor antibodies, Tensilon test, EMG

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Myasthenia Gravis treatment

Thymectomy (removal of Thymus), anticholinesterase drugs, corticosteroids, immunosuppressants, plasmapheresis, IV Ig

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-Cholinergic Poisoning antidote

Atropine)

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SLUDGE

S salivation
L lacrimation
U urinary incontinence
D diarrhea
G GI cramps
E emesis

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Amyotrophic Lateral Sclerosis (ALS or Lou Gehrig’s Disease

rare progressive neuromuscular degeneration

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Amyotrophic Lateral Sclerosis (ALS or Lou Gehrig’s Disease affected population

5,000 annually; 40-60 years, men>women; fatal within 3-5 years

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ALS clinical manifestation

muscle twitching/atrophy (including resp muscles), positive Babinski reflex
■ Amyotrophy- Process of muscle atrophy
■ Lateral- Loss of nerves on each side of the spinal cord
■ Sclerosis- Hardened scar tissue when nerve cells die

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Parkinson’s Disease

chronic progressive neuro degeneration

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Parkinson’s Disease affected population

1 million annually; 65 years and older at risk

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Parkinson’s Disease patho

degeneration of substantia nigra leads to decrease in production of Dopamine, ACh is inhibited resulting in muscle tremors/rigidity, accumulation of abnormal proteins in neurons

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Parkinson’s Disease clinical manifestations

rest tremor, rigidity (“Cogwheel”), bradykinesia (slow movement), decreased arm swing, infrequent blinking, drooling, mumbled speech

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Parkinson’s Disease treatment

Levodopa/carbidopa, deep brain stimulation