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Pathophysiology 201 > Final - brain and nerves > Flashcards

Final - brain and nerves Flashcards

(54 cards)

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1
Q

upper motor neuron damage (upper brain lesion)

A

Weakness and loss of voluntary motion

Spinal reflexes remain intact but cannot be modulated by the brain
- Increased muscle tone
- Hyperreflexia
- Spasticity

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2
Q

lower motor neuron damage (lower brain lesion)

A

Neurons directly innervating muscles are affected.
- Irritated neurons:
Spontaneous muscle contractions: fasciculations
- Death of neurons:
Spinal reflexes are lost
- Flaccid paralysis
Denervation atrophy of muscles

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3
Q

muscular dystrophy s/s

A

Initial weakness is in legs/pelvic girdle -> walk with a waddle, difficulty climbing steps
gower maneuver
Weakness spreads to other muscles
- Respiratory
- Cardiac -> cardiac myopathy
(DMD (2-3)earlier than BMD (adolescence))

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4
Q

myasthenia gravis pathophysiology

A

Autoimmune disease
- Gradual destruction of acetylcholine receptors
- Associated with thymus tumor or hyperplasia

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5
Q

myasthenia gravis s/s

A

gradual development of weakness proximally to distal
- Facial and ocular muscles, Arms and legs
- impaired vision, speech, facial drooping

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6
Q

myasthenia gravis treatment

A

Anticholinesterase drugs
Immunosuppressive drugs
Thymectomy
Plasmapheresis

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7
Q

multiple sclerosis pathophysiology

A

Progressive demyelination of neurons in brain + spinal cord
Demyelinated or sclerotic patches develop through white matter of the CNS
- degenerative disease but periods of remission

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8
Q

multiple sclerosis etiology

A
  • age 20-40
  • usually women
  • unknown cause (probs auto immune disorder)
  • multifactoral: genetic, immunologic and environmental components
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9
Q

multiple sclerosis s/s

A
  • depends on areas of demylination
    Blurred vision
    Weakness in legs
    Double vision
    Numbness, burning tingling in certain areas sensory fibers damaged
    Ulcers related to immobility
    Bladder dysfunction
    Abnormal gait
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10
Q

multiple sclerosis treatment

A

Treat acute attacks or initial demyelination
Modify the course of the disease
Treat symptoms
- Glucocorticoids control acute attacks
Block immune system
Beta interferon: decreases number of exacerbations due to effect on immune system
Glatiramer: blocks demyelination
Ocrevus
Physical therapy

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11
Q

Mononeuropathies

A

damage to one nerve (carpal tunnel syndrome) can resolve with immobilization

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12
Q

Polyneuropathies

A

damage to many nerves, slim chance of recovery

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13
Q

parkinson pathophysiology

A

Progressive degenerative changes in the basal nucleus - decreased production of dopamine (an inhibitory neurotransmitter)

Imbalance between excitatory and inhibitory signals in the basal nucleus  excessive stimulation

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14
Q

parkinson s/s

A

Fatigue
Muscle weakness and aching
Loss of spontaneous facial expressions
Tremors in hands at rest
Postural instability
If patients also has degeneration of cortical neurons  dementia
Bradykinesia (slow movement)

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15
Q

parkinson treatment

A

Dopamine replacement therapy
L-DOPA
Drugs that blocks the breakdown of L-DOPA

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16
Q

ALS patho

A

Damages both upper and lower motor neurons
Survival 2-5 years from onset
UMN damage - weakness, lack of motor control
Loss of control over spinal reflexes - stiffness, spasticity
LMN damage
Irritation - fasciculations
Decreased neuron firing - weakness, denervation atrophy, hyporeflexia

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17
Q

s/s als

A

Muscle cramping
Weakness
Muscular atrophy
Impaired chewing
Impaired swallowing
Impaired speech

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18
Q

als treatment

A

riluzole but only extends life 2-3 months w/o relieving symptoms

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19
Q

Vasogenic edema

A

ECF
- Impaired function of blood-brain barrier
- Transfer of water and proteins from vascular to interstitial space

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20
Q

Cytotoxic edema

A

Increase in intracellular fluid
Can result from hypoosmotic state

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21
Q

Noncommunicating or Obstructive hydrocephalus

A

normal flow of CSF is blocked

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22
Q

Communicating hydrocephalus

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A

malabsorption of CSF

23
Q

primary brain injuries

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A

immediate
Focal lesions: contusions, hemorrhage
Diffuse injuries: concussion, diffuse axonal injury

24
Q

Secondary injuries

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A

Brain swelling
Infection
Ischemia

25
epidural hematoma
Between the skull and the dura mater - rapid bleeding
26
Subdural Hematoma
Between the dura mater and the arachnoid mater - slower bleeding
27
intracerebral hematoma
Within the brain tissue itself
28
concussion
transient neurological impairment caused by mechanical force to the brain and can lead to loss of consciousness - usually recovery occurs within 24 hours
29
concussion s/s
headache, irritability, insomnia, poor concentration, amnesia
30
Contusions
bruising on the surface of the brain - Direct force, depressed skull fracture or closed acceleration-deceleration injury s/s depends on size and amount of cerebral edema (neurological deficits) Want to prevent secondary injury
31
Transient ischemic attack (TIA)
TIA: temporary local reduction in blood flow in the brain - focal ischemia Partial occlusion of an artery due to atherosclerosis Small embolus Vasospasm - 15% chance of having a stroke within 3 months of a TIA
32
TIA s/s
Varies depending on location of the ischemia Effects are transient (weakness, aphasia, visual, confusion)
33
Cerebrovascular accident (CVA) or Stroke
Infarct in the brain - tissue necrosis Total occlusion of cerebral blood vessels - Emboli or thrombi - Ruptured vessel
34
Etiology of CVA
Diabetes, hypertension, elevated cholesterol, hyperlipidemia, atherosclerosis, history of TIA’s, embolli
35
S/S Stroke
sudden onset Weakness in face/arms Usually affecting one side numbness Vision loss in one eye Aphasia, slurred speech Sudden ataxia Damage depends on collateral circulation
36
Treatment Stroke
Preserving brain tissue, secondary stroke prevention and minimizing long term disability Clot busters (tPA) but only if you have ruled out hemorrhagic stroke Surgery
37
Tonic–clonic seizure
muscle contraction, loss of consciousness
38
Absence seizure
non-convulsive, disturbances in consciousness - No physical signs of seizure
39
Myoclonic seizure
brief involuntary, jerking type of muscles movement - face, trunk, extremities
40
Tonic seizure
voluntary muscles of the legs and arms contract - body stiffens, legs and arms extended
41
Clonic seizure
bilateral, symmetric, rhythmic muscle contractions
42
Atonic seizure
loss of muscle tone
43
alzheimers
amyloid plaques/neuritic plaques, brain atrophy and neurofibrillary tangles in the cytoplasm, decreased Ach - begins with memory issues - Loss of short term memory and sometimes confusion about events in long term memory - Personality changes
44
Vascular dementia
caused by cerebrovascular disease - small brain infarctions, ischemia (memory loss as brain tissue dies)
45
Frontotemporal dementia
atrophy of frontal and temporal lobes of the brain - presents with disruptive behavior - Behavioral and language changes - Disruptive behavior, impulsive actions or apathy
46
initial stage of dementia
short-term memory loss (2-4 years)
47
Moderate stage of dementia
global cognitive impairment (2-10 years) - Language, spatial relationships, problem solving, depression, confusion, disorientation, lack of insight, inability to carry on daily activities
48
Severe stage of dementia
loss of ability to respond to environment; require total care, bedridden (1-3+ years)
49
Focal ischemia
(cerebral artery occlusion) - stroke (only specific area of the brain loses blood flow)
50
global ischemia (cerebral disorder)
loss of perfusion to the entire brain resulting in loss of function - can’t meet the metabolic demands of the whole brain - Secondary to severe shock - Cardiac arrest
51
most common brain tumor
Astrocytoma
52
most aggressive brain tumor
Glioblastoma multiform
53
Focal (unprovoked) Seizures Without Impairment of Consciousness or Awareness
Limited to one hemisphere May be preceded by a aura Clinical s/s depends on the area of the brain affected
54
Focal (unprovoked) Seizures With Impairment of Consciousness or Awareness
Abnormal discharge moves from one hemisphere to other Accompanied by repetitive activity including lip smacking, patting or rubbing clothing Confusion during postictal period Hallucinations

Pathophysiology 201 (23 decks)

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