Neuro Patho

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Neuro Patho
2013-03-26 15:35:31

Patho exam 2 spring 2013
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  1. Name two neurotransmitters and where they exist.
    • Acetylcholine (one of the most important!)
    • -preganglionnic for both ANS divisions
    • -postgangiononic for PNS
    • -at neuromuscular junctions
    •  (Ach converts Epi to Norepi)

    • Norepi/Epi
    • -neurotransmitters for SNS
  2. Humans secrete ___ml of CSF daily.
  3. NORMAL CSF pressure is ___ mmH20
  4. CSF is made in the ___ ___ and circulate through the 3rd, 4th ventricles and ______ space.
    Lateral ventricles; subarachnoid space
  5. Brain cells can function without oxygen for ____.
    10 seconds
  6. In cardiac arrest, death of brain cells occur in _____minutes.
    4-6 minutes
  7. ____ is major fuel of nervous system however it has NO PLACE to STORE it.
  8. Are YOUNG men or women more likely to stroke?
  9. Are OLD me or women more likely to stroke?
  10. Overall, are men or women more likely to stroke?
  11. Who is more likely to stroke African Americans or Caucasians?
    African Americans
  12. Whats the difference between a Transient Ischemic Attack (TIA) and a Ischemic attack (Stroke)?
    TIA: <24 hrs symptoms resolve, NO INFARCT on scans

    Stroke: >24 hrs process that leads to DESTRUCTION of neural tissue and consequent brain damage
  13. Name four causes of Ischemic stroke (which is the most common kind of stroke BTW!)
    • 1. Large artery thrombosis (atherosclerotic disease)
    • 2. Small penetrating artery thrombosis (lacunar-white matter)
    • 3. Cardiogenic embolitic (Afib, PFO, valve dx)
    • 4. Cryptogenic (no apparent cause, although further investigation usually finds one!)
  14. ISCHEMIA vs ISCHEMIC, what's the difference?
    Ischemia: decreased blood supply

    Ischemic: death of tissue
  15. What is the goal of treatment for a stroke?
    Save the Penumbra!!
  16. Right side stroke will show what s/s?
    • Spatial-perceptual deficits
    • Tendency for distraction
    • Impulsive behavior
    • Poor judgement
    • Deficits in L visual fields
    • (jump out of bed/crazy, don't know limits, no special or limb awareness)
  17. Left side stroke will show what s/s?
    • Language problems (expressive aphasia, receptive aphasia, global aphasia)
    • Intellectual impairment
    • Slow/cautious behavior
    • Deficits in R visual fields
    • (Unable to communicate, disturbed thought process)
  18. Pathophysiology of an ISCHEMIC stroke?
    • Blood vessels narrow/occlude
    • Creates a change in cerebral blood flow
    • Severity of stroke depends on the loss of flow (lg artery=lg damage, & vice versa)
    • Minimal blood at center of the infarct
    • Margins of infarct blood vessels dilate
    • Increased edema surrounding ischemia (pneumbra)
  19. The goal of treatment for an ischemic stroke is to save the pneumbra. How do we do this?
    • Give TPA & ASA
    • Increase perfusion:
    •  -increasing BP
    •  -give fluids
    •  -give O2 (2-3L for O2Sats <92)
    •  -Temp (99.6+), bed rest
  20. Why place a patient on a heart monitor for an ischemic stroke?
    Monitor VS and rhythm (arrhythmia like Afib will decrease cerebral perfusion!)
  21. A patient was treated with Thrombolysis for an ischemic stroke. Where do you want to keep their blood pressure? When do you start anticoagulants?
    • SBP ≥ 180mmHg or DBP ≥ 105mmHg
    • No Heparin, ASA, warfarin, clopidogrel or dipyridamole for 24hrs
    • (CT or MRI after tPA therapy
    • Monitor for bleeding)
  22. A patient had an ischemic stroke but could not be treated w/thrombolytic therapy (too late!). Where do you want to keep their blood pressure and when should you start anticoagulants?
    • SBP > 220 or DBP >120
    • Antithrombotics started WITHIN 24 hrs
    • Repeat CT or MRI for 24-48hrs after stroke or  PRN
  23. Define TBI
    • A blow or jolt to the head!
    • Or a penetrating head injury that disrupts the function of the brain
  24. TRUE or FALSE
    TBI's can range from mild (brief change in mental status or consciousness) to severe (extended period of unconsciousness or amnesia after the injury).
    TRUE. Can result in short or long term problems with independent function. There is a BROAD spectrum of disabilities/symptoms
  25. TBI are diagnosed by the Glascow Coma Scale. What are the categories and what is the range for mild, moderate, severe?
    GCS categories: eye opening, verbal response, & best motor response.

    • Severity: 
    •    Mild (13-15)
    •    Mod (9-12)
    •    Severe (3-8)
  26. How do you confirm a diagnosis for a TBI?
    with imaging. (CT/MRI)
  27. There are two types of TBI. Name them.
    Primary or Direct: damage caused by impact (Diffuse axonal injury, focal lesions of laceration, contusion, hemorrhage)

    Secondary: from subsequent brain injury like brain swelling, infection, & cerebral hypoxia
  28. Diffuse Axonal Injury is a Primary type of TBI. How does it happen?
    Results from acceleration/deceleration (ex: shaken baby)
  29. Explain a mild DAI (diffuse axonal injury)
    • Coma 6-24 hrs
    • follows commands by 24 hr
    • outcome of DEATH is UNCOMMON
    • Neuro deficits are common
  30. Explain a moderate DAI (diffuse axonal injury)
    • Coma > 24 hrs w/out prominent brainstem signs
    • Outcome INCOMPLETE RECOVERY of those who survive
  31. Explain a severe DAI (diffuse axonal injury)
    • Coma prolonged with brainstem signs
    • (Decortication/Decerebration)
  32. What are the FOUR types of focal lesions of lacerations (Primary kind of TBI)?
    • contusions or hemorrhages
    • epidural (extradural) hematoma
    • subdural hematoma
    • intracerebral hematoma
  33. Which has a worse prognosis, an epidural or subdural hematoma?
    EPIDURAL IS WORSE (instant)

    Subdural: hours, days, or weeks. Can lead to chronic progressive dementia.
  34. Who is at risk for getting a subdural hematoma?
    Elderly, alchoholics, basically anyone who falls easily!

    ↑ age = ↓ brain size = more jiggle room
  35. What causes hydrocephalus?
    • Damage to flow or absorption of CSF. 
    • Direct pressure causes degeneration of surrounding white matter. 
    • Results in neuro changes (declining memory & cognitive ability)
    • May cause coma in ↑ ICP is acute.
  36. What are some s/s of hydrocephalus?
    • Enlarged ventricles = pressure
    • ↑ICP
    • Decreased memory/cognition
    • Sleepy/coma
    • HA, N/V
    • seizures
    • (infants, eye bulging & head swellling)
    • midline deviations can occur
  37. Congenital hydrocephalus is considered non-communicating. What does this mean?
    • There is an obstruction so the CSF in the ventricular system does not properly communicate w/the subarachnoid space.
    • This could be from structural lesions (malformation or myelomeningcele)
  38. Acquired hydrocephalus is considered communicating. Explain more about this.
    • There are too few or poor functioning arachnoid villa so they are unable to absorb the CSF. 
    • This is seen in adults w/subarachnoid hemorrhage, meningitis, head injury, or neoplasia.
  39. What is normal pressure hydrocephalus and who usually gets it?
    Accumulation of CSF causes ventricles of the brain to enlarge but may not cause ↑ ICP like other types of hydrocephalus. 

    • Occurs in adults 60yr+.
    • 10% of pt w/symptoms of dementia have it!
  40. How do you diagnose normal pressure hydrocephalus?
    • Have patient walk 20 ft and measure time (do this 3x and take best of 3)
    • Md then does LP and removes some CSF
    • 3 hrs later, repeat the walk test
    • (if ↑ speed or ability, likely to have NP hydrocephalus)
  41. What does adequate Cerebral blood flow depend on?
    • Cerebral blood volume
    • Cerebral blood flow
    • Cerebral Perfusion pressure
  42. How do you calculate cerebral perfusion pressure?
    MAP - ICP = CPP
  43. What cerebral perfusion pressure do you need for cell nourishment?
  44. What cerebral perfusion pressure do you need after injury?
  45. How is cerebral perfusion pressure regulated?
    • By constriction or dilation of vessels.
    • CO2 is potent vasodilator so we purposefully hyperventilate or keep pt alkalotic (so you get vasoconstriction) to increase brain perfusion.

    (also can give O2)
  46. What is a normal intracranial pressure?
  47. What happens to cerebral flow if ICP increases?
    Flow decreases. If ICP>CPP then get hypoxia & hypercapnia which causes brain damage!!!
  48. Besides an increase in CSF, what else can cause increased ICP?
    • edema
    • hemorrhagee
    • neoplasia
  49. What are the cardinal signs of increased ICP?
    • HA
    • vomiting without nausea
    • ocular palsies
    • altered LOC
    • back pain
    • papilledema
    • Cushing's triad
  50. What is papilledema?
    • Optic disk swelling caused by increased ICP
    • The hydrostatic pressure pushes fluid out and that fluid is reabsorbed by papilla nerve of eye.
    • Get enlarged blind spot which can cause permanent vision loss
  51. What will you see if ICP gets so high that displacement of brain tissue occurs?
    Dilated pupils & inward facing eye
  52. What is CUSHING's triad? (seen when ↑ICP)
    ↑ BP, ↓ RR, ↓ HR (think opposite of shock)

    • Wide pulse pressure
    • Abnormal breathing
  53. What is the Monroe Kellie Hypothesis?
    • The pressure/volume relationship between ICP, volume of CSF, blood & brain tissue, & cerebral perfusion pressure.
    • States that the cranial compartment is incompressible.
    • Fixed volume inside cranium (any ↑ of one constituent must be compensated by a ↓ of another)
  54. According to the Monroe Kellie Hypothesis, an increase in edema will cause a _____ in CSF & blood flow.
  55. What is a coma?
    • A type of altered consciousness state
    • In an irreversible coma (aka cerebral death) there will be hemeostatic mechanisms left intact but they are unarousable.
    • No sleep wake cycles, eyes remain closed
  56. Altered arousal = ____
    Altered content of thought = _____
    • coma
    • awareness
  57. Describe a Persistant Vegitative State ("minimally conscious state)
    • Sleep/wake cycle
    • BP, resp, & digestion are normal
    • eyes may open but no tracking or sustained function
    • inconsistent evidence of perception & communication
  58. Describe Vegetative state
    • Absence of awareness of self and environment
    • Inability to interact with others
    • Absence of sustained or reproducible voluntary behavioral responses
    • Lack of language comprehension
    • Hypothalamic & brain stem function maintains life
    • Bowel/bladder incontinence
    • Variable preserved cranial nerve/spinal cord reflexes
    • Condition has continued for at least 1 month (can recover if less than 1 Month!)
  59. Brain death is described as the ABSENCE of what 4 things?
    • absence of all responses to light, noise, motion, and pain
    • absence of all reflexes (blink, cough) unless of spinal cord origin
    • absence of spontaneous resp. off vent (w/PCO2 60mmHg)
    • Absence of cranial nerve reflexes (fixed pupils)
    • EEG isoelectric!
  60. What is a seizure?
    • Single event of an abnormal discharge in the brain.
    • Results in an abrupt and temporary altered state of cerebral function
  61. What is epilepsy?
    • Chronic disorder of abnormal, recurrent, excessive and self-terminating discharge from neurons
    • *Alterations in membrane potentials that predispose certain hyperactive hypersensitive neurons (lowers threshold for firing)*
  62. Describe status epilepticus
    Continuous seizure lasting at least 5 minutes or 2+ discrete seizures w/incomplete recovery of consciousness.
  63. Partial seizures involve ONE part of the brain (focal).

    Name the three partial types of seizures
    • Simple: consciousness not impaired
    • Complex: consciousness impaired
    • Evolving: into secondary generalized
  64. Generalized seizures will fire from both hemispheres. 
    Name the six types of generalized seizures.
    • Absence: common in kids; interrupts consciousness but not postural control
    • Myoclonic: sporadic jerks
    • Clonic: repetitive rhythmic that are bilateral and symmetric
    • Tonic: stiffening musculature
    • Tonic-clonic: most common!
    • Atonic: abrupt loss of postural control
  65. You must get an _____ to diagnose and classify a seizure!!!
  66. Explain the pathophysiology of a seizure
    • You need excitable neurons.
    • Then get an increase in excitatory glutaminergic activity for recurrent connection to spread discharge.
    • Reduction in activity of the normal inhibitory (GABA) projection
    • *Imbalance between excitation & inhibition of CNS*
  67. What drugs do we give to treat seizures?
    • Keppra (1st choice)
    • Dilantin
    • Ativan (status)
  68. Spina Bifida is a type of ___ ___ ___ and can be caused by a deficiency of ___ ___ during pregnancy.
    • neural tube defect
    • folic acid
  69. What type of spina bifida has an unfused vertebral arch?
    Occulta-will see tuft of hair on back
  70. What types of spina bifida has a cyst like sac on back?
    Meningocele-cord placement OK, ↑ CSF in pocket)

    Meningomyelocele-displaced spinal cord (lots of deficits)
  71. What type of spina bifida has an open spinal cord?
  72. A demyelination of white matter in the  brain and spinal cord (mainly around ventricles) results in sclerotic plaques. What is this?
    Multiple Sclerosis
  73. There are a few postulated pathophysiologies mechnisms of MS. What are they?
    • Autoimmune response to latent virus in genetically susceptible individual
    • Sensitized T cells attack myelin protein
    • Susceptibility genes thought to be on HLA locus
  74. In MS, there is chronic inflammation, demyelination, and scarring of myelin. These lesions have an affinity for ___ ____.
    OPTIC Nerves (common first symptom is double vision)
  75. What is the age of onset for MS?
    20-40 years
  76. TRUE or FALSE
    MS is more prevalent in colder northern latitudes and those of northern european ancestry.
  77. There are double the amount of women compared to men that have ____ ____.
    Multiple Sclerosis
  78. What is the most common type of Multiple Sclerosis?
    Relapsing-Remitting MS (80%) have this.
  79. What are some S/S of MS? (PS they are highly variable)
    • Ataxia (lack of voluntary muscle control)
    • Optic neuritis
    • Spasticity
    • Paresthesias
    • Fatigue
    • Bladder & sexual dysfunction
    • Dizziness & Vertigo
    • Pain
    • Cognitive impairment (memory, attention, & problem solving)
  80. Describe the pathophysiology of Amyotrophic Lateral Sclerosis (ALS).
    • Progressive motor neuron disease that involved both upper and lower motor neurons.
    • Degenerative changes. 
    • UMN:spasticity reduced muscle strengths
    • LMN: flaccidity, paralysis, & muscle atrophy
    • Weakness start in arms or legs and begins to effect speech, progression continues....
  81. TRUE or FALSE
    Intellect, sensory, vision, hearing, & bowel/bladder functions are spared until the end of ALS.
  82. In ALS ____ are more affected than ___.
    Men are more affected than women (The opposite is true for MS)
  83. What is the common age group for ALS?
  84. What is parkinson's disease?
    Degeneration of basal ganglial cells with ↓ secretion of dopamine.
  85. What are the characteristics of parkinson's disease?
    • Tremor (pin rolling), tremor w/intentional movement
    • Rigidity
    • Bradykinesia (slowness of movement)
  86. Treatment for Parkinson's

    Given as carbodopa bc if administered on it's own, breaks down completely in periphery (doesn't cross BBB)
  87. According to WHO _____ is a syndrome due to disease of the brain.
  88. TRUE or FALSE
    Dementia is usually chronic and progressive
  89. Dementia is a disturbance of multiple cortical functions including...
    calculation, learning capacity, language, & judgement
  90. Does dementia fluctuate during the day?
    NO, delirium does
  91. Dementia of Alzheimer Type (DAT) involves cortical (frontal and temporal lobes). The enzymes can make ___
    • TANGLES.
    • Senile plaques & neurofibrillatory tangles = degenerated nerve endings and axons as well as abnormal amyloid deposition.
  92. What is the pathophysiology of Alzheimer's dementia?
    • Loss of apolipoprotein E (apoE)
    • Mutation in the ApoE gene (homozygous 15 fold increased risk & heterzygous have 3 fold increased risk)
  93. What is the difference between primary and secondary spinal cord injuries?
    • Primary: occurs at time of impact
    • Secondary: after primary d/t complex systemic & biochemical processes on cellular function
  94. True or False
    In spinal cord injuries, the degree of injury depends on the force
  95. Describe the pathophysiology of spinal cord injury.
    • Changes in blood flow (ischemia)
    • edema spreads above/below injury (leads to further changes in blood flow & ischemia)
    • Hemorrhage (ischemia)
    • Electrolyte imbalances (change in Ca level which impairs mitochondrial function)
    • Cascade of inflammatory response
  96. What is spinal shock?
    • complete loss of all segments below injury/lesion
    • Reflexes may return in 2-3weeks
  97. What happens immediately following a spinal cord injury (1st part of sequelae)
    microscopic hemorrhages, edema in the white matter-decreased perfusion
  98. What happens within 4 hours of spinal cord injury (2nd part of the sequelae)
    disruption of myelin, axonal degeneration, & ischemic endothelial injury
  99. What happens during the last stage of the spinal cord injury sequelae?
    • Necrosis progresses
    • 40% in 4 hrs
    • 70% in 24 hrs
  100. If you have an spinal cord injury at C4, will you be able to eat?
    Possibly. You have head/neck sensation. You can elevate your shoulders and diaphragm
  101. At C7-C8 SCI, may you use a manual wheelchair?
    Yes, you have finger control so you can.
  102. Could you ambulate a short distance if you have a SCI at T11-L5?
    YES, ambulate short distances with with assistance