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Pathophysiology I > Neuro Pathophysiology > Flashcards

Neuro Pathophysiology Flashcards

1
Q

What are the three divisions of the afferent division in the peripheral nervous system?

A

somatic sensory
visceral sensory
special sensory (olfaction and vision)

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2
Q

What are the 2 divisions of the efferent division in the peripheral nervous system?

A 
somatic motor
autonomic motor (sympathetic, parasympathetic, enteric)
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3
Q

What is an example of an ANS reflex that Dr. Walker loves to talk about?

A

baroreceptor reflex, baroreceptors sense increase in pressure/stretch and send signal (afferent) to NTS which sends the signal to the VMC to be integrated and then transmitted down CNX to SA node and decreases HR

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4
Q

Describe the somatic reflex.

A

Sensory stretch receptors start AP that is send toward spinal cord, signal is transmitted through interneuron or directly to motor nerve which comes out of ventral portion of spinal cord and innervates the muscle to cause contraction

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5
Q

What are the primary functions of the CNS?

A
  • integrates many incoming signals and coordinates appropriate outgoing neural signals
  • carries out higher mental function - including memory and learning
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6
Q

What is the primary function of the PNS?

A
  • connects CNS with peripheral structures
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7
Q

The spinal cord is an extension of the _______.

A

medulla oblongata

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8
Q

When do spinal nerves become apart of the PNS?

A

As soon as they exit the spinal cord, even though they still have their cell bodies in the spinal cord, if they exit they are considered part of the PNS

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9
Q

Where do the nerves for the cauda equina originate?

A

conus medullaris

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10
Q

What is the cauda equina?

A

Bundle of spinal nerves that resemble a horse’s tail, includes 2nd-5th lumbar nerve pairs, 1st-5th sacral nerve pairs, and coccygeal nerve

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11
Q

What regions/organs does the cauda equina innervate?

A

Pelvic organs, lower limbs, PSNS innervation to bladder and internal and external anal sphincters

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12
Q

What are the 3 demyelinating disorders?

A

multiple sclerosis (MS)
amyotrophic lateral sclerosis (ALS)
guillan barre syndrome (GBS)

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13
Q

What is the pathophysiology behind MS?

A

chronic degenerative disease of the CNS caused by misdirection of the immune system & T cells attacking CNS myelin protein; results in decreased number of dendrites and axons in the CNS; transmission along axon is slow

sclerosis refers to multiple scars (or scleroses) on the myelin sheaths

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14
Q

Does MS occur more in males or females?

A

females

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15
Q

What are some of the clinical features of MS?

A

fatigue, parathesias, unsteady gait, muscle weakness and atrophy, respiratory insufficiency, ANS dysfunction

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16
Q

What are some of the manifestations of brain demyelination in MS?

A
  • seizures, spasticity
  • emotional lability
  • visual loss
  • dysarthria, dysphagia
  • cognitive dysfunction
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17
Q

What are some of the manifestations of spinal cord lesions with MS?

A

paresthesias, limb weakness, bowel and bladder symptoms

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18
Q

What are some of the manifestations of brain stem lesions with MS?

A

autonomic dysfunction

abnormal ventilatory drive

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19
Q

What causes relapses in MS?

A

Autoimmune assault on myelin which causes focal inflammatory demyelination

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20
Q

What causes remissions in MS?

A

inflammation subsides and conduction restored; Na+ channels restored and myelin repaired; can last weeks, months, or longer

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21
Q

What causes permanent dysfunction in MS?

A

axons are destroyed and no longer able to conduct signal

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22
Q

What are some of the anesthetic implications for MS?

A
  • stress associated with anesthesia may worsen symptoms
  • spinal anesthesia was avoided but now OK
  • epidural and other regional techniques have been used w/o adverse effects
  • Altered cardiovascular responses possible
  • Avoid succ. due to hyperkalemia
  • Prevent hyperthermia - slows conduction
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23
Q

Do patients with MS have upregulated, downregulated, or normal amount of NAchR at the NMJ?

A

upregulated

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24
Q

How does hyperthermia affect nerve conduction with MS?

A

slows conduction, 0.5 C temp increase may block nerve conduction in demyelinated fibers

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25
Q

Do patients with MS have increased, decreased, or normal amounts of Ach?

A

Decreased

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26
Q

What is the pathophysiology behind ALS or Lou Gehrig’s disease?

A

Progressive, degenerative motor disease involving both upper and lower motor neurons, bulbar involvement

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27
Q

What types of muscle are affected by ALS?

A

any striated muscle of the body

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28
Q

Does ALS occur more in males or females, and at what age?

A

males > females, usually begins after 4th decade and peak occurrence is at 50

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29
Q

What cranial nerves are not involved with ALS?

A

CN III, IV, and VI–motor control of eye movement spared

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30
Q

What can cause the initial pathophysiology of ALS?

A
  • heavy metal exposure
  • glutamate excitotoxicity
  • oxidant stress
  • hereditary component (mutation in SOD1 which is a powerful antioxidant)
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31
Q

What does the term “amyotrophic” mean?

A

lower motor neuron symptoms due to destruction of the ventral (anterior) horn neurons (destruction of neurons that exit the spinal cord)

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32
Q

What does the term “lateral sclerosis” mean?

A

scarring of lateral cortic-spinal tracts with upper motor neuron symptoms (destruction of neurons that transverse from brain down to spinal cord before point of exit)

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33
Q

What are some of the lower motor symptoms in ALS?

A

Flaccid paresis:

  • muscle weakness, atrophy, hypotonia –> paralysis (plegia)
  • lower motor neuron damage more likely to result in permanent paralysis
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34
Q

What are some of the upper motor neuron symptoms in ALS?

A

spastic paresis:
- stiff and tight muscles causing weakness of movement patterns
- upper motor neuron damage more likely to be repaired
(no modulation of reflex arc)

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35
Q

What are general clinical manifestations of ALS?

A
  • muscle atrophy, fasciculations
  • difficulty swallowing
  • dysarthria (articulation)
  • dysphonia (volume)
  • sensory, autonomic, and cognitive functions preserved
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36
Q

Are the NAchR upregulated, downregulated, or normal with ALS?

A

upregulated

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37
Q

What should you consider with ND-NMBA and ALS?

A

use sparingly because can cause a prolonged response (Less Ach in NMJ to compete with them)

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38
Q

Can you give succ. to someone with ALS?

A

no, increased NAchR density causes widespread depolarization and hyperkalemia

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39
Q

What are some anesthetic implications for someone with ALS?

A
  • cognition and sensation intact
  • respiratory care (progressive muscle weakness, aspiration risk, difficult mechanical ventilation weaning)
  • subclinical autonomic dysfunction could lead to exaggerated decreases in cardiovascular function in response to anesthesia
  • awake extubation
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40
Q

What is the definition of Guillain-Barre Syndrome (GBS)?

A
  • “acute inflammatory demyelinating polyneuropathy”
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41
Q

What is the pathophysiology of GBS?

A

inflammatory/immune disorder of the peripheral nerves immune cells/Ab attack the Schwann cells resulting in destruction of the myelin sheath; demyelination slows transmission of nerve signals, weakens them over long distances (myelin sheaths of many axons are attacked which leads to a wide array of symptoms)

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42
Q

Is GBS inherited or contagious?

A

No

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43
Q

What is the peak disability time and recovery time for someone with GBS?

A

peak disability 10-14 days and recovery time takes weeks to months

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44
Q

What is the prognosis of someone with GBS and do they have residual effects?

A

prognosis good if axons are spared or regenerate, most patients recover with minimal or no residual deficits

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45
Q

Why is there a 1-5% mortality with those with GBS?

A

mortality secondary to autonomic dysfunction or PE

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46
Q

What are some of the clinical features of GBS?

A
  • muscle weakness (more often in legs than arms) that is progressive
  • areflexia
  • cranial nerve and autonomic involvement
  • glove and stocking distribution of parasthesias - “pins and needles”
  • elevated CSF protein
  • sensory action potentials are low-amplitude or absent (d/t demyelination)
  • respiratory muscle failure requiring ventilation
  • pulmonary aspiration
  • ANS - sinus tachycardia, bradyarrhythmia resulting from trivial vagal stimulation, postural hypotension, excessive sweating, ileus
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47
Q

What manifestations of GBS require supportive treatment?

A
  • dysrhythmias and autonomic instability (tachycardia-give lowest dose possible of beta blockers, severe bradycardia-may need pacing)
  • thromboembolic complications as a result of stasis due to decreased muscle tone (prophylactic anticoagulation)
  • ileus (prokinetics)
  • bulbar weakess (related to bulbar nerves found in medulla and can affect CNVII-XII, can lead to speech deficit) - enteral feeding, aspiration
  • respiratory paralysis (postop ventilation)
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48
Q

What are some anesthetic implications for someone with GBS?

A
  • succ. contraindicated - causes hyperkalemia

- ND-NMBA should be used sparingly because they cause a prolonged response due to less Ach available to compete with

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49
Q

What are the 2 disorders of the NMJ?

A 
myasthenia gravis (MG)
Lambert-Eaton Myasthenic Syndrome (LEMS)
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50
Q

What is the pathophysiology behind MG?

A

is a chronic autoimmune neuromuscular disease with varying degrees of muscle weakness, caused by Abs blocking nAchR at the muscle endplate and increases their turnover; Abs also flatten post-synaptic folds and damage post-synaptic membrane

decreased endplate potentials cause decreased change of AP

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51
Q

What are the clinical features of MG?

A
  • muscle weakness (increases with exercise - fatigability)
  • eye, facial, bulbar, and limb muscle weakness
  • respiratory muscle weakness rare but possible post-op complication
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52
Q

What are some of the anesthetic implications for MG?

A
  • depends on the severity of the disease
  • preop planning and periop care important
  • assessment of respiratory and bulbar function
  • avoid sedative premedication if evidence of respiratory compromise
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53
Q

What should you do if a patient with MG is taking acetylcholinesterase inhibitors and is scheduled for surgery?

A
  • withheld on the day of surgery; MG patients generally have a decreased requirement for these drugs int he post-op period
  • Ach inhibitors may prolong action of suxamethonium and increase need for nondepolarizing neuromuscular blocking agents
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54
Q

What should you consider with induction and maintenance of anesthesia with someone with MG?

A
  • show increased senstivity to neuromuscular blockade
  • relatively resistant to suxamethonium (high doses lead to dual block - indistinguishable from a nondepolarizing -type block)
  • extremely sensitive to nondepolarizing neuromuscular blockers (faster onset and a more prolonged action in MG)
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55
Q

What should you consider with post-op management of someone with MG?

A
  • short period of post-op mechanical ventilation may be needed
  • careful monitoring of respiratory function
  • acetylcholinesterase inhibitor therapy restarted in postop period, dose increased as the patient starts to mobilize
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56
Q

What is the pathophysiology of LEMS?

A

autoimmune disease of the NMJ that involves pathogenic antibodies downregulating presynaptic calcium channels which causes decreased Ach release and muscle weakness

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57
Q

What is LEMS commonly associated with?

A

60% of LEMS associated with small cell lung cancer, autoantibody produced against tumor expressed in voltage-gated calcium channels

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58
Q

What are some anesthetic implications of LEMS?

A
  • paralytics should be titrated to a minimum
  • paralytic reversal is often ineffective
  • prepare for post-op ventilation
  • 3,4-diaminopyridine (VG-K+ channel inhibitor) can be used post-op
  • autonomic disturbances may be present
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59
Q

What are some considerations with LEMS and paralytics?

A
  • increased senstivity to succ (in contrast to MG)

- increased effectiveness of NDNMB

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60
Q

What is a difference between MG and LEMS and their pathophysiologies?

A

MG affects post-synaptic membrane and LEMS affects pre-synaptic membrane

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61
Q

What is the pathophysiology of muscular dystrophy?

A

defect of muscle fiber from absence of dystrophin protein in muscle which leads to progressive weakness

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62
Q

Is muscular dystrophy genetic?

A

Yes, located on x-chromosome (more common in males) and is recessive trait

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63
Q

What are some anesthetic implications for muscular dystrophy?

A
  • succ causes hyperkalemia and malignant hyperthermia

- hypersensitive to NDNMR

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64
Q

What protein do patients with muscular dystrophy lack?

A

dystrophin protein

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65
Q

What is the pathophysiology of scoliosis?

A

lateral rotational curvature of the spine; muscles, ligaments and soft tissue become shortened on the concave side of the curvature (may be neurologic in origin); over time deformities of vertebral column and ribs occur; the greater the compressive forces the greater the deformity

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66
Q

What is the pathophysiology behind structural scoliosis?

A

rotation of the spine itself

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67
Q

What is the pathophysiology behind non-structural scoliosis?

A

rotation due to reasons other than spine (pain, posture, leg discrepancy)

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68
Q

What are some clinical manifestations of scoliosis?

A
  • spine curvature, rounded shoulders, prominence of one hip, rib prominence
  • non-structural scoliosis can be rectified with traction or supine position
  • structural scoliosis compromises alveolar ventilation
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69
Q

What are some anesthetic implications of scoliosis?

A
  • not associated with sensory or motor deficit
  • respiratory dysfunction occurs - reduce alveolar ventilation - may reduce effectiveness of mechanical ventilation
  • associated with increased risk of mitral valve prolapse, increased pulmonary resistance and pulmonary hypertension
  • spine curvature may impact location of spinal anesthesia needle
  • kyphosis is a posterior rotation of spine and kyphoscoliosis is both a posterior and lateral curvature of spine
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70
Q

What is the pathophysiology behind ankylosing spondylitis?

A

chronic inflammatory joint disease cause by inflammation at various regions within a joint (primarily vertebral joints); leads to joint remodeling; stiffening and/or fusion of spine and sacroiliac joints results; genetic predisposition; autoimmune disease attacks antigens on cartilage

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71
Q

What are some of the clinical manifestations of ankylosing spondylitis?

A
  • low back pain and stiffness is an early sign (mid 20’s)
  • restricted motion of the spine occurs
  • reflex muscle spasms may occur
  • chest movement can become restricted
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72
Q

What is an anesthetic implication for someone with ankylosing spondylitis?

A

positioning of patient and ability to ventilate independently in post-op

73
Q

What is the pathophysiology of spina bifida?

A

congenital disorder characterized by defect in closure of the neural tube; vertebral laminae remain unfused (most often at the lumbosacral level); no serious neurological dysfunction except those associated with the lumbosacral region

neural tube is surgically closed in the neonatal period

74
Q

What are some of the clinical manifestations associated with spina bifida?

A
  • associated with nerves of the lumbosacral region
  • lower limb muscle weakness leads to gait changes and abnormal positioning of the feet
  • sphincter disturbance at bowel and bladder
75
Q

What are some anesthetic implications for someone with spina bifida?

A
  • if patients are in a prone position then watch for injury to eyes, brachial plexus, or abdomen
  • prone position may impair ventilation
  • special consideration for the positioning of the patient due to deformity - may make intubation more difficult
76
Q

What is the pathophysiology behind cauda equina syndrome?

A

caused by compression of nerve roots below L1 caused by spine fracture or disk herniation

77
Q

What are some clinical manifestations of cauda equina syndrome?

A
  • lower extremity motor deficits
  • variable sensorimotor dysfunction
  • variable reflex dysfunction
  • variable bowel, bladder and sexual dysfunction
78
Q

What are some anesthetic implications for cauda equina syndrome?

A
  • can be caused by spinal anesthesia and pooling of hyperbaric local anesthetics
  • to reduce risk of anesthesia-induced cauda equina syndrome avoid 5% lidocaine
79
Q

Where does the spinal cord extend from?

A

base of skull to L1-L2

80
Q

Where are the cell bodies for the spinal nerves in the lower vertebrae below the spinal cord?

A

conus medularis

81
Q

How many segments is the spinal cord divided into?

A

31 segments each with a pair of ventral (motor) and dorsal (sensory) spinal nerve roots

82
Q

What is in the gray matter of the spinal cord?

A

Nerve cell bodies

83
Q

What is in the white matter of the spinal cord?

A

ascending and descending nerve tracts

84
Q

Which gender is more prone for spinal cord injuries?

A

males age 16-30

85
Q

What is the most common cause of spinal cord injuries?

A

MVA (55%)
sports (18%)
penetrating injuries (15%)

86
Q

What do half of the kids with SCI also have?

A

TBI

87
Q

Where do most spinal cord injuries occur?

A

C1-C2
C4-C7
T1-T2
- most mobile portions of the vertebral column
- cord occupies much of the vertebral canal in cervical and lumbar regions (more easily injured)

88
Q

What is a primary spinal cord injury?

A

spinal cord stretching, tearing, compression of tissue, penetrating injury

89
Q

What is a secondary spinal cord injury?

A

cytokine and amino acid release from injured cells which leads to inflammation, free radical formation, cellular edema, and cellular apoptosis

90
Q

What can compound spinal cord injury?

A
  • systemic hypotension and hypoxia
  • local cord edema (injury may spread 2 SC levels above or below)
  • destruction of axons nerve cell bodies and the supporting glia
91
Q

Not only does SCI cause neurologic dysfunction, but it also causes what?

A

important disturbances in the body’s other systems (so many other peripheral systems are controlled by nerves that project through the spinal cord Ex: bladder function, defecation, and sexual function)

92
Q

What can spinal cord injury lead to?

A

spinal cord shock

93
Q

What is spinal cord shock?

A
  • temporary loss or depression or all (or almost all) spinal reflex activity below the level of the injury (spinal cord reflex arcs immediately above the level of injury may also be severely depressed)
  • involves spinal cord reflex arcs of autonomic and somatic nervous systems
94
Q

What is the onset/resolution of spinal cord shock?

A
  • onset occurs in hours

- resolution happens in weeks to months (depending in definition of resolution)

95
Q

What is the definition of resolution in someone that had spinal cord shock?

A

return of somatic (i.e. muscle spindle) and autonomic (i.e. sympathetic reflex arcs)

96
Q

Above what level would spinal cord shock require ventilatory support?

A

C4-C5

97
Q

What are some of the signs and symptoms of spinal cord shock?

A
  • ## all s/s result from interruption in both somatic and visceral sensation that results in absent somatic (flaccid paralysis) and autonomic (hypotension) reflexes
98
Q

What is the role of oligodendrocytes?

A

form myelin around CNS axons

99
Q

What is the role of astrocytes?

A

help regulate composition of interstitial fluid in CNS and provide glucose to and remove ammonia from neurons

100
Q

What is the role of microglia cells?

A

specialized macrophages that perform immune functions in the CNS

101
Q

What is a nucleus?

A

collection of nerve cells in the brain or spinal cord

102
Q

What is a ganglion?

A

cluster of nerve cell bodies with similar functions found outside the brain and spinal cord

103
Q

What is a nerve?

A

bundle of nerve fibers in the peripheral nervous system held together with connective tissue, most contain sensory and motor fibers

104
Q

What is a nerve tract?

A

bundle of nerve fibers in the CNS with a common origin and destination; generally classified as ascending or descending

105
Q

What are afferent neurons?

A

convey information from tissues and organs into the CNS, peripheral ends of sensory receptors, have a single process (axon) that divides after leaving the cell body, one branch ends at a receptor and the other at a bouton

106
Q

What are efferent neurons?

A

convey information from the CNS out to the effector cells (muscles, glands, or other nerve cells), cell bodies and dendrites of efferent neurons are within the CNS and the axons extend out to the periphery

107
Q

Where do interneurons lie?

A

entirely in CNS

108
Q

What is the role of an interneuron?

A

connects afferent and efferent neurons within the CNS

109
Q

How many interneurons and efferent neurons are there for each afferent neuron entering the CNS?

A

200,000 interneurons
10 efferent neurons
(number of interneurons interposed between specific afferent and efferent neurons varies according to teh complexity of the activity they control)

110
Q

How close do neurons have to be to capillary to receive diffusion of nutrients?

A

50 micrometers

111
Q

What is the range of BPs the brain is able to regulate CBF?

A

60 mmHg - 160 mmHg

112
Q

What is a protective mechanism the brain and heart have utilized if they undergo anaerobic metabolism?

A

able to use lactic acid as a fuel, not only is it important that they are able to use the lactic acid, but it also takes acid out of the internal milieau and helps protect brain

113
Q

What are the 5 processes that are activated by cellular ischemia?

A
  1. lactic acid accumulation and cellular swelling
  2. decreased function of Na+/K+ pump
  3. neuroexcitotoxicity
  4. enzymatic activation
  5. inflammation
114
Q

What anesthetic agents can precipitate a seizure (decrease seizure threshold)?

A
  • enflurane
  • laudanosine (metabolite of atracurium and cisatracurium)
  • methohexital
  • ketamine
  • normeperidine
115
Q

What are some risk factors for seizures?

A
  • hyperthermia
  • alkalosis
  • hypoglycemia/hyperglycemia (altered metabolism and increased glutamate and dec. gaba)
  • hypoxia (increase glutamate and dec. gaba)
  • hyponatremia (cellular swelling)
  • sleep disorders
  • genetic
  • tumor, trauma, infection or fever
  • SAH, stroke damage
  • drugs or alcohol overdose or withdrawal
  • fatigue or stress
  • excessive sensory stimuli
116
Q

What is a prodroma?

A

early manifestations: malaise, HA hours to days prior before onset of seizure

117
Q

What is an aura?

A

peculiar sensation preceding onset of generalized seizure

118
Q

What is postictal state?

A

time period immediately following seizure activity (disorientation, confusion, fatigue, HA)

119
Q

What is a seizure?

A

sudden explosive disorderly discharge of cerebral neurons

120
Q

How much does cerebral oxygen demand increase during a seizure?

A

60%

121
Q

How much does cerebral ATP demand increase during a seizure?

A

250%

122
Q

What is an epileptogenic focus?

A

group of neurons with sudden changes in normal membrane potential, change in neuronal membrane potential means membranes and more permeable and increased chance of neuronal depolarization

123
Q

How does sensory stimulation alter seizure activity?

A

interferes with ability to recruit brain structures that transmit paroxysmal activity to other regions
1. high intensity auditory stimuli
2. somatosensory stimulation - sustained touch, rubbing, movement of the limgs
3. olfactory stimuli - prevention
(puts neurons in refractory stage)

124
Q

What are things that increase the seizure threshold?

A
  • benzos
  • volatiles
  • propofol
  • barbituates
  • acidosis
125
Q

Why is cerebral blood flow important?

A

removes waste and brings O2, maintains physical environment

126
Q

How much of the CO does the brain get?

A

15%

127
Q

Why is CBF highly regulated?

A

little reserve of nutrients and O2, constant blood flow required

128
Q

What is the average CBF?

A

50 mL/100 g/min

129
Q

What is the formula for CBF?

A

CBF = CPP/R

130
Q

How will CBF of 20-25 affect EEG?

A

slowing of EEG

131
Q

How will CBF of 15-20 affect EEG?

A

flat EEG

132
Q

How will CBF

A

irreversible brain damage

133
Q

How can you calculate CPP?

A

MAP - ICP

134
Q

What is normal ICP?

A
135
Q

At what ICP is CPP compromised?

A

> 30

136
Q

What is CPP primarily dependent on?

A

MAP

137
Q

What is a normal CPP?

A

80-100 mmHg

138
Q

CBF is ____ proportional to CPP.

A

directly

139
Q

Which artery carries majority of the blood to the brain?

A

middle cerebral artery (80%)

140
Q

What are the 2 mechanisms for autoregulation?

A

myogenic and metabolic

141
Q

What is the myogenic mechanism?

A

if CPP or MAP decreases, then vasculature will vasodilate and if CPP or MAP increases, then cerebral vasculature will vasoconstrict to help ensure that the CBF remains constant/appropriate for whatever the metabolic activity of the brain is

142
Q

What is different for children and their cerebral autoregulation

A

have lower MAP so they are more susceptible to reduced CBF in the event of reduced MAP

143
Q

How does chronic HTN affect cerebral autoregulation?

A

shifts cerebral autoregulation curve to the right

144
Q

What is the metabolic autoregulation mechanism?

A

when metabolic demand exceeds CBF get release of metabolites that cause vasodilation, can also work in reverse and cause vasoconstriction

145
Q

What systems innervate the cerebral vasculature?

A

SNS
PSNS (different than systemic)
non-cholinergic/non-adrenergic fibers

146
Q

CO2 is ____ proportional to CBF.

A

directly

147
Q

How much does CBF change per 1 mmHG change in paCO2

A

1-2 mL/100 g/min above 40 mmHg

148
Q

How does hypothermia influence CBF and CMRO2?

A

decreases both

149
Q

How does hyperthermia affect CBF and CMRO2?

A

increases both

150
Q

How much does CBF change per 1 degree change in body temperature?

A

5-7%

151
Q

How does viscosity affect CBF?

A

increased viscosity decreases CBF

152
Q

What is the optimal Hct for CBF?

A

0.30

153
Q

How do anesthetics affect CBF and CMRO2?

A

increase CBF and decrease CMRO2

154
Q

What is the average CMRO2?

A

3-3.8 mL O2/100 g/min or about 50 mL/min

155
Q

Cerebral metabolism is how much of the body’s total O2 consumption?

A

20%

156
Q

What is the brain’s average glucose consumption?

A

5 mg/100 g/min or 75 mg/min

157
Q

How much of the glucose utilized by the brain is metabolized aerobically?

A

90%

158
Q

What do neurons use as their primary energy source?

A

glucose

159
Q

What can pass easily through the BBB?

A

lipids, H2O, CO2, O2, anesthetic agents

160
Q

What cannot easily pass through the BBB?

A

ions and large molecules, proteins, H+, HCO3-, mannitol

161
Q

What requires a transport protein to cross the BBB?

A

glucose

162
Q

Marked abnormalities in serum sodium and glucose should be corrected slowly or quickly?

A

slowly, can cause rapid brain fluid shifts

163
Q

What can disrupt the BBB?

A 
infection
cerebral ischemia
hypertension
severe hypercapnea
hypoxia
tumor
trauma
stroke
seizure activity
164
Q

What are ependymal cells?

A

glial cells with loose intercellular junctions that line the ventricles and form a permeable barrier between the brain ISF and CSF

165
Q

What is different about the ependymal cells in the choroid plexus?

A

tight intercellular junction

166
Q

What is the function of the choroid plexus?

A

form CSF, don’t let much fluid move from ISF to CSF with good pumping action that pump ions into ventricles and water follows

167
Q

How much CSF is produced per day?

A

21 mL/hr or 500 mL/day

168
Q

CSF composition is iso, hypo, or hypertonic with blood plasma?

A

isotonic

169
Q

What electrolytes are higher in the CSF compared to blood?

A

Na+, Cl-, Mg++

170
Q

What electrolytes/substances are lower in the CSF compared to blood?

A

glucose, K+, Ca++, HCO3-

171
Q

How does the CSF flow through the brain?

A

lateral ventricles to the 3rd ventricle and then the 4th ventricle and then circulates around brain and spinal cord

172
Q

Where does CSF empty?

A

arachnoid villi

173
Q

Where does CSF go once it goes into the arachnoid villi?

A

empties into sagittal sinus which drains into the jugular vein and then back into the heart

174
Q

The brain has high or low intracranial compliance?

A

high compliance, the high amount of volume in the cranium does not significantly change the pressure

175
Q

The brain has high or low intracranial elastance?

A

low elastance, no change in pressure for an increased volume

176
Q

The doral column medial lemniscal tract carries what?

A

discriminating touch

177
Q

Does the DCML tract dessicate high or low?

A

crosses high

178
Q

The spinothalamic tract carries what?

A

pain and temperature

179
Q

Does the spinothalamic tract dessicate high or low?

A

low

Pathophysiology I (2 decks)

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