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BCIT Module 3 > Module 3 > Flashcards

Module 3 Flashcards

1
Q

What are the anatomical/structural divisions of the nervous system?

A

CNS and PNS

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2
Q

What makes up the CNS?

A

Brain

Spinal cord

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3
Q

What makes up the PNS?

A

Cranial nerves
Spinal nerves
Autonomic nervous system

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4
Q

What are the divisions of the autonomic nervous system?

A

sympathetic

Parasympathetic

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5
Q

What are the functional divisions of the nervous system?

A 
Spinal cord level (controls automatic motor responses)
Brain stem/subcortical level (controls BP, resps, equilibrium, primitive emotions)
Cortical level (responsible for cognition, the storage and retrieval of info, thinking, memory, abstract thought)
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6
Q

What are the 3 major areas of the brain?

A

Cerebrum
Brain stem
Cerebellum

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7
Q

What does the cerebrum contain?

A

Hemispheres
Diencephalon
Basal ganglia

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8
Q

What does the diencephalon contain?

A

Thalamus

Hypothalamus

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9
Q

What does the brain stem contain?

A

Midbrain
Pons
medulla
RAS

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10
Q

What are the functions of the cerebellum?

A

Coordination of muscle groups
control of fine movement
Control of balance
Maintenance or feedback loops to correct movement

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11
Q

What are the lobes of the cerebrum?

A 
Frontal
Parietal
Occipital
Temporal
Limbic (rhinencephalon)
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12
Q

What are the functions of the frontal lobe?

A

High level cognitive functions
Motor control of speech (Broca’s area)
Voluntary motor function

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13
Q

What are the functions of the parietal lobe?

A

Contralateral sensation
Contralateral visual fields
Receptive speech, language comprehension, calculation, L/R discrimination

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14
Q

What are the functions of the occipital lobe?

A

visual perception
Visual reflexes
Smooth eye movements

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15
Q

What are the functions of the temporal lobe?

A

Auditory reception (Wernicke’s) new memory, smell, upper lateral vision
Interpretation of sensation
Detailed past memories

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16
Q

What are the functions of the limbic lobe?

A

Self preservation

Recall of events related to emotion

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17
Q

Where does the crossing of motor fibres occur?

A

Medulla

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18
Q

What is the RAS?

A

Reticular Activating System
Brain stem portion: responsible for sleep/wakefulness
Thalamic portion: responsible for cognition and attention

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19
Q

What is the tentoria and what is it’s significance?

A

A fold of the dura mater that covers the cerebellum and supports the occipital lobes of the cerebrum.

Brain can herniate through this bone resulting on pressure to CN III and unequal pupils.

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20
Q

What are the mechanisms of protection for the CNS?

A

Cranial/spinal nerves
Meninges
CSF
Blood-brain barrier

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21
Q

Where is CSF contained?

A

Between the pia mater and the arachnoid mater in the subarachnoid space

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22
Q

What are the layers of meninges?

A 
*brain* 
Pia mater
Arachnoid mater
Dura mater
*skull*
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23
Q

Where is CSF produced?

A

Secreted by the choroid plexus (mainly) and the capillaries in the pia mater

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24
Q

Where is CSF reabsorbed?

A

Through the arachnoid villi

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25
Q

What is foramen of Monro and what is it’s significance?

A

Hole between the lateral ventricle and the 3rd ventricle where CSF flows through.

It is where the EVD transducer is levelled to.

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26
Q

What does CSF contain?

A

Lymphocytes
Glucose
Protein

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27
Q

What is the blood-brain barrier permeable to?

A 
Water
Oxygen
Carbon dioxide
Glucose
Lipid soluble compounds
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28
Q

What are the 2 main sets of vessels that supply blood to the brain?

A

Left/right common carotid (anterior circulation)

left/right vertebral arteries (posterior circulation)

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29
Q

What are afferent nerves of the PNS?

A

Sensing nerves (body -> cord) denoted by “spino”

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30
Q

What are efferent nerves of the PNS?

A

Motor nerves (cord -> body) denoted by “spinal”

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31
Q

what are the components of a neurological assessment?

A 
The patient’s story
Pt’s level of consciousness
Cranial nerves
Motor strength
Vital signs
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32
Q

What tests should you do to assess cranial nerve function (and associated nerves)?

A
  • pupillary response (optic II, occularmotor III)
  • corneal reflex (trigeminal V, facial VII)
  • gag/cough reflex (glossopharangeal IX, vagus X)
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33
Q

What is Cushing’s triad?

A

Bradycardia, hyperventilation, hypertension with widened pulse pressure. Indicated worsening ICP

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34
Q

What is the equation for cerebral oxygen supply?

A

PaO2 + cerebral blood flow

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35
Q

What controls cerebral blood flow?

A

Cerebral perfusion pressure / cerebral vascular resistance

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36
Q

What are the components of CPP?

A

MAP - ICP

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37
Q

What is normal CPP?

A

60-100 mmHg

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38
Q

What factors influence cerebral vascular resistance?

A
  • The diameter of the blood vessels

- ICP

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39
Q

What factors influence the diameter of cerebral blood vessels?

A

Autoregulation

Cerebral metabolic demand

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40
Q

Under what circumstances does autoregulation fail?

A

When CPP < 60
When ICP > 30
When MAP 60-150
TBI

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41
Q

What is the biophysical theory of autoregulation?

A

Autoregulation is controlled by stretch receptors in blood vessels

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42
Q

What is the chemical theory of autoregulation?

A

CO2 and H+ cause cerebral vasodilation

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43
Q

What are the major factors that influence cerebral metabolic rate?

A

Stress (physical and emotional)
Temperature
Activity level

44
Q

What are the contents of the cranial vault?

A

brain 80%
CSF 10%
Blood 10%

45
Q

What is the Monroe-Kellie hypothesis?

A

ICP = cerebral blood volume + brain tissue volume + CSF volume

If one of the components increases in volume, one or both of the other components must decrease in volume for ICP to remain unchanged.

46
Q

What are factors that increase brain volume?

A

Tumours
Hematoma
Cerebral edema (abscess, CVA, trauma, hypoxic injury)

47
Q

What are factors that increase cranial blood volume?

A

Vasodilation (increased PaCO2, drugs)

Jugular vein compression (tight collar, ET ties, head torsion)

48
Q

What are factors that increase CSF volume?

A 
Impaired drainage (tumour, spina bifida)
Impaired reabsorbtion (subarachnoid hemorrhage, infection)
Overproduction (rare)
49
Q

What is the primary injury in TBI?

A

Injury that occurs at the moment of impact as a result of mechanical forces to the head

50
Q

What is a secondary injury in TBI?

A

Biochemical and cellular response to the initial trauma that can exacerbate the primary injury and cause additional damage and impairment in brain recovery.

51
Q

What are the top 2 culprits of secondary injury in TBI?

A

Hypoxia

Hypotension

52
Q

What is the difference between and open and closed skull fracture?

A

In an open fracture the dura mater is exposed, in a closed one it is not.

53
Q

What are the types of cerebral hematomas?

A

Epidural
Subdural
Intracerebral

54
Q

What is a concussion?

A

Brain injury accompanied by a brief LOC, diagnosed primarily based on history.

55
Q

What is an epidural hematoma?
Arterial or venous?
Presentation?
Symptoms?

A

Blood that creates a space-occupying lesion between the skull and the dura mater.

Occurs as a result of trauma to the skull and meninges.
2/3 are associated with arterial bleeding.
Usually presents as a brief LOC, lucidity then rapid deterioration due to arterial bleeding.
Symptoms: localized headache, sleepy, dilated/fixed pupil.

56
Q

What is a subdural hematoma?
Arterial or venous?
Common MOI?
Classifications?

A

Accumulation of blood between dura and arachnoid membrane.

Usually venous
Commonly seen in acceleration-deceleration, rotational forces.
Classified as acute, subacute (4 days-3 weeks) or chronic (> 22 days after injury)

57
Q

What is an intracerebral hematoma?
Common MOI?
Presentation?
Treatment?

A

When bleeding occurs deep within cerebral tissue.

MOI: depressed skull fractures, penetrating injuries,sudden acceleration-deceleration injuries.
Presents as sudden deterioration of patient 6-10 days after trauma
May or may not be treated surgically.

58
Q

What are the type of missile injuries and what are they?

A
  • depressed (indentation in skull)
  • penetrating (enters but does not leave skull)
  • perforating (enters and leaves skull)
59
Q

What is DAI?

A

Diffuse axonal injury.

Prolonged post-traumatic coma that is not caused by mass lesion. Occurs as a result of damage to the axons or disruption of axonal transmission of the neural impulses. May not by visible on CT/MRI

60
Q

What is a mild brain injury?

A

GCS 13-15

LOC < 15 mins

61
Q

What is a moderate brain injury?

A

GCS 9-12

LOC 15 mins-6 hrs

62
Q

What is a severe brain injury?

A

GCS <8 after resus or who deteriorate to 8 within 48 hrs

LOC > 6 hrs

63
Q

What is the minimum MAP required to peruse the brain?

A

60

64
Q

What is normal ICP?

A

0-15 mmHg

65
Q

What should your normal PaCO2 target be in TBI?

A

35-40 (never less than 20, can cause cerebral ischemia).

66
Q

What are the mechanisms of injury in spinal cord injury?

A

Hyperflexion (deceleration I.e. head-on collision)
Hyper extension (rear end MVC)
Rotation
Axial loading (fall from height onto feet)
Penetrating injuries

67
Q

What is the target MAP in spinal cord injury?

A

MAP 85-90 for 5-7 days

68
Q

What is the primary difference between spinal shock and neurogenic shock?

A

Spinal shock originates in the spinal cord (will only affect organs below the injury). Usually results in tachycardia (to compensate for reduced preload).

Neurogenic shock affects how the brain communicates with the heart and vasculature (more global). Usually results in bradycardia.

69
Q

What is autonomic dysreflexia?

A

Caused by massive sympathetic response to a noxious stimuli.

Results in hypertension, bradycardia, flushing, diaphoresis, headache.

Can also cause seizures and cerebral hemorrhage.
Frontline treatment is to remove the stimulus.

70
Q

What is the most accurate way of monitoring ICP?

A

Intraventricular catheter

71
Q

What is intracranial hypertension?

A

Elevated ICP. ICP > 20 mmHg

72
Q

Where is the tip of an IVC located?

A

In the 3rd ventricle

73
Q

Describe an intracranial pressure wave.

A

P1 - percussion wave, pulsation of the choroid plexus, should be tallest wave.
P2 - tidal wave, represents compliance, pathologically raised when ICP is elevated.
P3- dicrotic wave

74
Q

What are the nursing responsibilities of an EVD?

A
  • make sure it is levelled (between corner of eye and external auditory meatus)
  • confirm if you want it in the open or closed position
  • confirm the drain settings
  • confirm that it is secure to the pole
  • confirm that there is fluid fluctuation levels with the patient’s pulse to confirm that drain is patent
  • confirm that there is an accurate ICP waveform on the monitor
75
Q

What is the highest PEEP setting you should have on someone with concerning ICP?

A

20.

76
Q

What is a concern with giving vasodilators to someone with a TBI?

A

A lot of peripheral vasodilators also cause cerebral vasodilation (increased intracranial blood volume). Treatment with metoprolol or labetalol can blunt this effect.

77
Q

When can you not use hyperosmolar therapy in TBI?

A

When the blood-brain barrier is not intact.

78
Q

What are first line therapies for blunting noxious stimuli?

A

Benzodiazepines and narcotics

79
Q

What is a jugular bulb catheter?

A

Catheter inserted into the jugular vein and threaded upward into cerebral venous circulation to monitor cerebral oxygenation.

80
Q

What is SjVO2?
What are the normal values?
What is its limitation?

A

Jugular venous oxygen saturation (SaO2 of jugular bulb catheter).

Normal is 60-80%

It only tests for overall extraction, not localized ischemia.

81
Q

What is CerO2?

What are the normal values?

What are its limitations?

A

Cerebral oxygen extraction ratio.

SjVO2 - SaO2.

25-30% is normal. >40% indicates an imbalance between supply/demand.

Does not detect cerebellum or brain stem CerO2.

82
Q

What treatment options do you have if CerO2 is > 40%?

A
  • increase FiO2
  • Increase Hgb
  • increase PaCO2
  • treat fever
  • treat pain
  • reduce stimulation
83
Q

What should you monitor when giving mannitol?

A

Osmolarity (should be >320)
Na+
K+

84
Q

What is PbtO2?

What are normal/abnormal values?

A

Brain tissue oxygenation, monitors regional tissue oxygenation

Normal is 23-35 mmHg
<20 represents compromised brain oxygen

85
Q

what are the complications of TBI?

A
  • prolonged immobility (ulcer formation, DVT)
  • pneumonia
  • GI problems (stress ulcers, vomiting, gastroparesis, gastritis, diarrhea, malnutrition)
  • seizures
  • fluid/electrolyte disorders (diabetes insipidus, SIADH, cerebral salt wasting syndrome)
86
Q

What is diabetes insipidus?

What is the most common injury associated?

What is the treatment?

A

Lack of ADH (compounded by pt’s inability to drink fluids), results in copious amounts of dilute urine.

Most common in basal skull fractures.

Thx: hypotonic IV fluids, synthetic ADH (vasopressin)

87
Q

What is SIADH?

What are the symptoms?

What are the treatments?

A

Syndrome of inappropriate antidiuretic hormone secretion. Excessive ADH causes H2O retention (poor urine output) causing dilution of sodium (relative hyponatremia).

Symptoms: nausea, vomiting, lethargy, decreased urine output, no peripheral edema.

Tx: fluid restriction (500-1000 mL/day), SLOW Na+ replacement (8 mEq/L rise per 24 hrs), vasopressin receptor antagonists, hypertonic saline, intermittent Lasix

88
Q

What is the most common site for ischemic stroke presentation?

A

Middle cerebral artery

89
Q

What are the types of hemorrhagic stroke?

A

Subarachnoid

Intracerebral

90
Q

What are the secondary causes of death from stroke?

A
  • edema (#1)
  • Seizures
  • secondary hemorrhage (hemorrhagic conversion)
91
Q

What are the most important clinical manifestations of stroke?

A
  • weakness
  • trouble speaking
  • vision problems
  • headache
  • dizziness
92
Q

What is the time frame for rtPA?

A

Within 3 hours but can be given up to 4.5 with additional criteria.

93
Q

What are blood pressure goals in stroke?

A

Initial HTN should not be managed (it is compensatory) unless it is > 220/120 (target 180/105)

When giving tPA BP is controlled to < 180/105 (higher risk of bleeding)

94
Q

What is the dose of tPA?

A

0.9 mg/kg to a max of 90 mg.

10% of total dose given as bolus.
Remaining 90% given as infusion over 1 hr.

95
Q

Why not give D5W to a stroke patient?

A

It can leak into cerebral tissue and cause edema (glucose can pass through and it is hypotonic). It also may impair the movement of cerebral glucose.

96
Q

What is the most common cause of SAH?

A

The rupture of a cerebral aneurysm.

97
Q

What are the symptoms of subarachnoid hemorrhage?

A 
Abrupt onset of pain
Brief LOC
Nausea
Vomiting
Focal neurological deficits
Stiff neck
Photophobia
98
Q

What are the treatments for cerebral aneurysms?

A
  • clipping
  • removal
  • embolization (silicone beads, coil)
  • stenting
99
Q

What is the most important cause of intracerebral hemorrhage?

A

Hypertension

100
Q

What is SAH grading?

A

1 - asymptomatic or minimal headache
2- moderate- severe headache, maybe CN palsy
3 - drowsiness, confusion, mild focal deficit
4 - stupor, moderate-severe hemiparesis
5 - deep coma, decerebrate rigidity

101
Q

What are the complications of a surgically treated aneurysm?

A
  • seizures (irritation from blood)
  • hydrocephalus (blood blocks reabsorption from the arachnoid villi)
  • vasospasm(most common)
102
Q

How do you treat vasospasm in the post-surgical aneurysm patient?

A
  • hemodynamic augmentation (Triple H therapy)
  • nimodipine 60 mg q 4 hrs
  • cerebral angioplasty (when pharmacologic management has failed)
103
Q

What is Triple H therapy and what is it used for?

A

Used to augment hemodynamics in the setting of vasospasm (decreases blood visocity and increases volume and flow pressure through the vasospastic area).

  • hypervolemic expansion (CVP 8-10) with crystalloid or colloid
  • hemodilution (HCT 32-35%)
  • hypertension (30% increase in MAP via a vasopressor, target 200-180 systolic with a clipped aneurysm).
104
Q

How much CSF is produced?

A

20 ml/h or 500 ml/day

105
Q

What is the dose of mannitol?

A

0.25-1g/kg q 6 hrs

BCIT Module 3 (1 decks)

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