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Pathophysiology > Nervous system Part 1 > Flashcards

Nervous system Part 1 Flashcards

1
Q

What is Multiple sclerosis?

A
  • autoimmune disease of the CNS
    • immune system attacks the myelin or oligodendrocytes
  • Local area will develop inflammation causing demyelination
    • stiff, like scar tissue
    • nerves no longer conduct signals efficiently leading to muscular, sensory, and autonomic defects
  • highly variable depending on person
    • can have asymptomatic life or deteriorate rapidly
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2
Q

What is the cause of Multiple sclerosis?

A
  • no specific cause identified
  • there is a genetic susceptibility
  • it is a delayed hypersensitivity T-cell response to antigens and injuring the myelin
    • lymphocytes and macrophages mediate the destruction of the myelin
  • possible dysfunction in ion channels
  • Environment plays a role
    • higher incidence in norther countries
      • if pt moves from place of higher incidence to place of lower incidence before 15, they will assume the risk of the new home
      • same for opposite
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3
Q

What is the incidence of MS worldwide?

When is it diagnosed?

what increases incidence of relapse?

A
  • 1 million worldwide
    • 1:1,000 in the US
  • usually diagnosed btw 18-40 years (later diagnosis usually indicates slower disease progression
  • women 2x more likely than men
  • pregnancy is protective against relaps
  • increased incidence of relapse with stress
    • post birth of baby
    • viral illness/infection
    • surgery
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4
Q

What are the signs and symptoms of Multiple sclerosis?

A
  • paralysis (this can cause extra junctional receptors!!)
  • sensory disturbances- may cause pain
  • autonomic disturbances- req. more support in OR
  • lack of coordination
  • visual impairment
  • seizures
  • cognitive and emotional disturbances (usually mild)
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5
Q

What is the overall life expectancy of a patient with MS?

How long do exacerbations last?

A
  • 80% of normal
  • Severity is variable pt to pt
    • some will live long lives with few exacerbations, some will die within months of diagnosis
  • Incidence of remission and exacerbation intervals are difficult to predict
  • exacerbations are where symptoms are worse for a few days, then stabalize for 2-3 weeks, then start to improve
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6
Q

What do increases in temperature do for pts with MS?

A

increases in temperature will increase symptoms through further neuronal conduction impairment

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7
Q

How is MS diagnosed?

A
  • Clinical signs and symptoms
    • often visual disturbances first
  • Oligoclonal abnormalities in immunoglobulins (released in response to myelin breakdown)
    • increased gamma globulin in the CSF
  • Prolonged latency of evoked potentials
  • Cranial MRI sensitive marker for demyelinative plaques
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8
Q

What is an evoked potential?

A
  • tests the integrity of the motor and sensory pathways
  • motor: put an electrode on the skull and look for the motor response
  • Sensory: some kind of peripheral or central stimulation and try to sense and action potential in the brain
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9
Q

Multiple Sclerosis treatment

A
  • No cure
  • NSAIDS
  • Corticosteroids
    • for exacerbations, not for long term
  • Interferon B- good for person with lots of relapses
  • Glatiramer Acetate- mix of polypeptides that mimics myelin (like a decoy) and attracts whatever is killing the myelin
  • Mitoxantrone- decreases lymphocyte regeneration
    • very cardiotoxic, only given for severe MS
  • Azathioprine- immunosupressant
  • Methotrexate
  • immune modulators: natalizumab and fingolimod
    *
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10
Q

Guillian-Barre Syndrome pathophysiology

A
  • Theory: Antigens create an immune response against nerve fibers and or block presynaptic voltage-gated Ca channels and postsynaptic nAChr channels, causing NM weakness
  • Sudden onset of ascending, symmetrical acute generalized paralysis and areflexia
  • segmental demyelination of PNS by macrophages and lymphocytes and channelopathies
    • motor, sensory, and autonomic affects
    • starts with legs and ascends up
  • Autoimmune
  • These ppl have a Na channel blocking factor found in CSF
  • Follows some kind of infection or immunization
    *
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11
Q

What is the incidence of Guillian-Barre Syndrome?

mortality?

What is usually the cause of death?

A
  • Incidence = 1: 50,000
  • 3-8% mortality
  • Most die from: ANS dysfunction, respiratory failure, sepsis, PE, cardiac arrest
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12
Q

What is the difference between segmental demyelination and axonal degeneration?

A
  • Segmental demyelination- injury to the myelin
    • recovery within a couple of weeks
  • Axonal degeneration- the actual axon is ruined/ “dies”
    • recovery can be incomplete and takes months
    • some pts have chronic pain
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13
Q

What are the signs and symptoms of Guillian-Barre syndrome?

A
  • Autonomic nervous system dysfunction
  • bilateral facial paralysis
    • red flag b/c nerves that control face are close to nerves that control airway
  • difficulty swallowing- pharyngeal muscle weakness
  • impaired ventilation- intercostal muscle paralysis
  • flaccid/decreased deep tendon reflexes
  • extremity paresthesias
  • pain- HA, backache, muscle tenterness
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14
Q

What are the signs and symptoms of autonomic nervous system dysfunction you might see in a pt with guillian-barre ssyndrome?

A
  • labile BP - hypertensive to hypotensive
  • diaphoresis
  • peripheral vasoconstriction
  • tachycardia at rest
  • ECG- conduction abnormal
    • risk for MI
    • severe orthostatic hypotension (just lifting head to pillow)
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15
Q

How is Guillian Barre syndrom diagnosed?

A
  • clinical signs and symptoms
  • high normal protein counts in CSF
    • the Na channel blocking proteins
  • develops after respiratory or GI infection in 50% of patients
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16
Q

How is Guillian-Barre treated?

A
  • supportive care
    • mechanical ventilation when VC < 15 ml/kg or poor ABG
    • cuffed ETT to prevent aspiration
    • treat hyper or hypotension
    • maybe plasmapheresis
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17
Q

What is the pathophysiology of parkinson’s disease?

A
  • Degenerative CNS disease
  • degeneration in dopaminergic pathways between substantia nigra and basal ganglia (to the caudate nucleus and putamen)
    • dopamine provides inhibitory , ACh is unopposed, causing tremors (extrapyramidal movements)
  • cause unknown, deffinitely a genetic predisposition
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18
Q

What usually causes the death of pts with Parkinsons?

A
  • Without dopamine, the cholinergic neurons are left unopposed and extrapyramidal motor symptoms develop
  • progressive disease over 10-15 years
  • death usually from fall or infection
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19
Q

What are the signs and symptoms of Parkinson’s disease?

A
  • Classic triad:
    • skeletal muscle tremor (pill rolling)
    • rigidity (neck)
    • akinesia- difficulty starting movement
    • bradykinesia- slow movement
  • loss of facial expression and decreased blinking
  • 1st signs:
    • rigidity in proximal neck muscles
    • loss of arm swings when walking
    • loss of head turn with body turn
  • General:
    • seborrhea (exzema of scalp)
    • oily skin
    • pupillary changes
    • diaphragmatic spasms
    • oculogyric crisis (eyes stuck in one position)
    • dementia
    • depression
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20
Q

How is parkinson’s diagnosed?

A
  • physical symptoms
  • will try on l-DOPA and if there is improvement, they it will be diagnosed as parkinson’s
  • easy to spot during the stair or even hall walk in basic physical
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21
Q

How is parkinson’s treated?

A
  • Goal to increase the concentration of dopamine in basal ganglia or the receptor response to dopamine
  • Levodopa- DA precursor can get to the brain
    • SE psychosis
  • decarboxylase inhibitor- travels with the Levodopa so that it doesnt get metabolized. L-DOPA crosses the BBB, decarboxylase inhibitor does not
  • Amantadine- increases dopamine release
  • Type B MAOs- increase dopamine release (B’s are more specific to dopamine)
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22
Q

What is the surgery that is used to treat Parkinson’s when it becomes end-stage?

A
  • Deep brain stimulation
    • head is placed in frame and taken to MRI
    • burr hole into brain
    • place electrode into specific nuclei
    • generator pack implanted below clavicle or in abdomen
  • Very effective! but reserved for end of stage because it is so risky of hemorrhagic stroke
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23
Q

What is the experimental treatment for parkinsons disease?

A
  • Gene therapy/stem cell transplant of dopaminergic/adrenal medullary fetal tissue
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24
Q

What are the side effects to dopamine treatments?

A
  • motor (dyskinesias)
  • psychiatric (mania, agitation, hallucinations, paranoia)
  • CV- increased contractility and heart rate, orthostatic hypotension
  • Gastointestinal- N/V- stimulation of chemoreceptor trigger zone by DA
25
Q

What is the pathophysiology that causes a disc herniation?

A
  • the compressible nucleus pulposus protrudes through the fibrocartilaginous annulus fibrosis which surrounds it and compresses the nerve root
26
Q

What are the statistics regarding disc herniation?

A
  • low back pain is 2nd most common reason for MD visits in US
  • 70% of adults will experience LBP
  • LBP most common cause of disability in pts <45 yrs
  • most common cause is disc herniation
  • 1% pts with LBP have metastatic cancer of vertebral bodies
  • CT to confirm
27
Q

Where is the pain for a C5-6 protrusion?

A
  • pain starts in neck and radiates to shoulder and down the lateral arm to the thumb
  • biceps muscle and reflex are weak
28
Q

Where is the pain for a C6-7 protrusion?

A
  • pain in the scapula, triceps region, and middle and index fingers
29
Q

How is cervicle disc herniation treated?

A

rest

pain control

epidural corticosteroids

surgical decompression

**immobility worsens symptoms

30
Q

What are the symptoms of disc herniation in L4-5 region?

A

low back pain radiating down lateral/posterior thighs and calves (sciatica)

31
Q

What are the sumptoms of disc herniation in the L5-S1 region?

A
  • low back pain radiating down lateral/posterior thigs and calves (sciatica)
  • sensory loss and weakness
32
Q

How is thoracic disc herniation treated?

A
  • epidural corticosteroids
  • surgical laminectomy or microdiskectomy
33
Q

How is spinal cord injury diagnosed?

A
  • Hx of high impact accident, fall or penetrating injury
  • pain or tenderness over vertebra
  • flaccid areflexia
  • loss of rectal sphincter tone
  • paradoxical respiration
  • bradycardia (w/hypovolemia)
34
Q

What are pts with MS and rheumatoid arthritis also at risk for?

A

spinal cord injury

35
Q

How is a spinal cord injury measures as complete vs incomplete?

A
  • look at 28 dermatomes and 10 muscle groups
    • A= no sensory or motor function below lesion
    • B= sesnory but not motor function preserved below lesion
    • C&D= motor function preserved below injury (D group’s muscles get a higher score)
    • E= normal sensory and motor funtion
36
Q

What is spinal shock?

A
  • transient period of absolute flaccidity/atony- peripheral blood vessel dilation and reflex loss below the lesion
    • lasts days to weeks
  • similar to “symathectomy”
37
Q

What is neurogenic shock?

A
  • decreased BP and HR secondary to vasomotor paralysis and loss of SNS innervation of the heart
    • baroreceptors controlled by SNS and PNS, with a high injury the SNS cannot respond to low BP
  • depression of descending sympathetic pathways in spinal cord common with high thoracic injury
  • lasts 3-5 dyas
38
Q

What are the symptoms of spinal cord injury “shock”?

A
  • flaccid paralysis
  • total absence of sensation
  • loss of temp regulation
  • loss of spinal cord reflexes
  • decreased BP and HR (if>T6)
  • PVC’s and ST-T wave ECG changes
  • **Greatest threats to life are alveolar hypoventilation, unprotected airway, PNA, PE
39
Q

What happens to reflexes after a couple weeks after injury?

A
  • spinal cord reflexes come back, responding overly agressively to normal stimuli (like a full bladder)
  • with a lesion, the brain cannot mediate (or inhibit) reflexes
  • thermoregulatory, CV, GI, GU–no input from brain
40
Q

Why would you need to be careful in giving ACE inhibitors to a patient with a spinal cord injury?

A
  • Because the Renin-angiotensis-aldosterone system compensates for the inability of the SNS to maintain BP
  • There will be a lot of renin in the system, so if you give an ACE inhibitor, BP may plummet
41
Q

how high can an injury be to maintain prenic innervation of the diaphragm?

A

C5 or below

*C5 or 6 will have innervation of diaphragm intact but will not have innervation of accessory inspiratory muscles (will do better in supine position, LMA prob non enough)

42
Q

What causes pulmonary edema in pts right after a spinal cord injury?

A
  • Catecholamine surge after injury causes rapid increase in pulmonary vascular volume combined with excessive fluid administration in resuscitation phase
43
Q

In what position do quadriplegic patients breath best?

A

Supine

44
Q

Why does a pt with a high spinal transection brady with almost any noxious stimuly?

A
  • With a high spinal transection, the patient would have unopposed vagal stimuli
  • this may cause bradycardia and cardiac arrest
    • especially during hypoxemia
45
Q

How can we prevent agains secondary injury in a patient with a spinal cord injury?

A
  • must maintain a robust BP and prevent hypoxia
  • immobilization of spine
  • intubation if high C-spine involved
    • inline stabilization with standard DVL
    • be careful with cricoid pressure
46
Q

What are some problems associated with chronic spinal cord injury?

A
  • impaired ventilation
  • chronic infection
  • prone to renal stones (nephrolitiasis) b/c they are unable to completely empty bladder
  • anemia
  • impaired thermoregulation
  • DVT
  • depression and chronic pain
    • baclofen for muscle spacsticity (do not interrupt baclofen; can seize)
  • Autonomic dysreflexia
47
Q

How does autonomic dysreflexia work?

A
  • Pts at risk for dysreflexia upon resolution of spinal shock and return of SNS reflexes
  • Basic problem: the CNS and upper spinal cord are isolated from the spinal cord below the lesion
  • afferent impulse sent when there is stimulation below the lesion
    • this impulse has no inhibitory “check and balance”
    • profound vasoconstriction below the lesion occurs
  • the carotid sinus senses the increased BP and causes a reflexive drop in SNS outflow above the lesion, leaving PNS “unchecked” above the lesion, causing bradycardia
48
Q

Where is the cut-off for spinal injury location that will cause AD?

A

spinal injury at or above T6 will cause AD

49
Q

Why does somebody who has no sensation because of a spinal cord injury need anesthesia for a surgery?

Which is better spinal or epidural?

A

they will still have an autonomic response to a surgery, so anesthesia is used to prevent AD

Spinal is better because it is more reliable that it is in the right spot (because you draw back for CSF)

Dont really know if it is placed right with epidural b/c the person is difficult to assess

50
Q

How will pts with spinal injuries respond to administration of catecholamines?

A

Exaggerated BP response, super sensitive

Quadriplegic pts BP may increase 5-10 times with exogenenous angiotensin and catecholamines

51
Q

What is a seizure?

A

rhythmic, repetative depolarization of neurons

*clinical manifestations depend on location of neurons

52
Q

What things can cause seizure?

A
  1. D/C of sedative-hypnotic drugs or ETOH
  2. drug use (opioids, amphetamines, cocaine)
  3. uremia
  4. traumatic injury
  5. neoplasms
  6. infection
  7. congenital malformation
  8. birth injury
  9. electrolyte imbalance (glucose!)
  10. blood in a ventricle
  11. hypoxia
  12. vascular disease
  13. CVA
  14. Fever (peds)
  15. unknown causes
53
Q

What classifies a seizure disorder as epilepsy?

A
  • epilepsy- recurrent seizures resulting from congenital or acquired factors
  • partial (focal/local)
    • simple partial (no loss of consciousness)
    • complex partial (consciousness affected)
    • partial that becomes generalized
  • generalized
    • Absance
    • myoclonic (brief jerk of a muscle or muscle group)
    • clonic-tonic
    • Atonic (sudden loss of muscle tone)
54
Q

How are seizure disorders treated?

A
  • Pharmacologic therapy that tries to decrease neuronal excitability or increase neuronal inhibition
  • start with one drug and increase dose/add others as needed
55
Q

which seizure medications induce CYP450?

A
  • Carbamazepine
  • phenobarbital
  • phenytoin
56
Q

Which seizure medications dont induce CYP450?

A
  • Gabapentin
  • Topiramate
  • Valproate- increases surgical bleeding
57
Q

What surgical treatment is used for patients with seizures?

A
  • Resection of pathologic foci
    • usually a temporal lobectomy
    • high risk for permanent hemiparesis
58
Q

What is considered status epilepticus?

What kind of treatment is required?

A
  • Continuous sz activity or > 2 seizures in a row with no return to consciousness in between
  • This is life threatening
    • requires pharmacologic termination of sz
    • ABC support
  • rule out hypoglycemia
  • expect metabolic acidosis and hyperthermia after

Pathophysiology (26 decks)

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