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APEX Study Guide > Unit 7: Neuro > Flashcards

Unit 7: Neuro Flashcards

1
Q

What are the 4 types of glial cells? What are their functions?

A

Astrocytes: most abundant type – regulation of metabolic environment, repair neuron after neuronal injury

Ependymal Cells: concentrated in the roof of the 3rd and 4th ventricles spinal canal – from the choroid plexus, which produces CSF

Oligodendrocytes: from the myelin sheath in the CSF

Microglia: act as macrophages and phagocytize neuronal debris

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2
Q

What are the four lobes of the cerebral cortex and their functions?

A

Frontal Lobe - contains the motor cortex

Parietal Lobe - contains somatic sensory cortex

Occipital Lobe - contains vision cortex

Temporal Lobe - contains auditory cortex and speech centers

  • Wernicke’s area = understanding speech
  • Broca’s area = motor control of speech
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3
Q

What are the 12 cranial nerves?

On Occasion Our Trusty Truck Acts Funny Very Good Vehicle Any How

A

CN I - Olfactory
CN II - Optic
CN III - Oculomotor
CN IV - Trochlear
CN V - Trigeminal (V1 Ophthalmic; V2 maxillary; V3 mandibular)
CN VI - Abducens
CN VII - Facial (temporal, zygomatic, buccal, mandibular, cervical)
CN VIII - Vestbulocochlear
CN IX - Glossopharyngeal
CN X - Vagus
CN XI - Accessory
CN XII - Hypoglossal

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4
Q

What cranial nerves provide motor control of the eyes? How does each nerve contribute to the eye’s movement?

A

CN III (Oculomotor) – inferior oblique (extorsion-elevation); superior rectus (supraduction); medial rectus (adduction); inferior rectus (infraduction)

CN IV (Trochlear) – superior oblique (intorsion-depression)

CN VI (Abducens) – lateral recuts (abduction)

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5
Q

What bedside tests are used to assess each cranial nerve?

A

CN I (Olfactory): Smell
CN II (Optic): Vision
CN III (Oculomotor): Eye movement; Pupil constriction
CN IV (Trochlear): Eye movement
CN V (Trigeminal): Somatic sensation to face and anterior 2/3 of tongue, muscles of mastication
CN VI (Abducens): Eye movement
CN VII (Facial): Facial movement except mastication, eyelid closing, taste to anterior 2/3 of tongue
CN VIII (Vestibulocochlear): Hearing and balance
CN IX (Glossopharyngeal): Somatic sensation and taste to posterior 1/3 of tongue
CN X (Vagus): Swallowing
CN XI (Accessory): Shoulder shrug
CN XII (Hypoglossal): Tongue movement

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6
Q

Which cranial nerve resides in the central nervous system? What is the implication of this?

A

CN II (Optic) is the only cranial nerve that is part of the CNS

It is the only cranial nerve surrounded by the dura
*if you inject a local anesthetic into the optic nerve during regional anesthesia of the eye it will go directly into the CSF

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7
Q

What is tic douloureux? What cranial nerve contributes to this problem?

A

Tic Douloureux = Trigeminal Neuralgia (CN V)

-causes excruciating neuropathic pain in the face

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8
Q

What is Bell’s Palsy? What cranial nerve contributes to this problem?

A

Results from injury to the facial nerve (CN VII)

Causes ipsilateral facial paralysis

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9
Q

What is the function of CSF and where is it located?

A

It cushions the brain, provides buoyancy, and delivers optimal conditions for neurologic function

Located in:
-ventricles (left lateral, right lateral, third, and fourth)
-cisterns around the brain
-subarachnoid space in the brain and spinal cord

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10
Q

What regions of the brain are NOT protected by the BBB? (5)

A

-Chemoreceptor trigger zone
-Posterior pituitary gland
-Pineal gland
-Choroid plexus
-Parts of the hypothalamus

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11
Q

What is the normal volume and specific gravity of CSF?

A

CSF Volume = 150 mL

Specific Gravity = 1.002 - 1.009

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12
Q

Describe the production, circulation, and absorption of CSF

A

Production: ependymal cells of the choroid plexus at a rate of 30 mL/hr

Circulation: Left/Right lateral ventricles –> Foramen of monro –> Third ventricle –> Aqueduct of sylvius –> Fourth ventricle –> Foramen of luschka –> Foramen of magendie

Absorption: venous circulation via the arachnoid villi in the superior sagittal sinus

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13
Q

What is the formula for cerebral blood flow? What are the normal values for global, cortical, and subcortical flow?

A

Cerebral Blood Flow = Cerebral Perfusion Pressure / Cerebral Vascular Resistance

-Global: 45-55 mL/100g tissue/min or 15% of CO
-Cortical: 75-80 mL/100g tissue/min
-Subcortical: 20 mL/100g tissue/min

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14
Q

What are the 5 determinants of cerebral blood flow?

A
  1. Cerebral metabolic rate for oxygen (CMRO2)
  2. Cerebral perfusion pressure
  3. Venous pressure
  4. PaCO2
  5. PaO2
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15
Q

What is the normal value for CMRO2? What factors cause it to increase? To decrease?

A

Normal = 3.0 - 3.8 mL/O2/100g brain tissue/min

Decreased by: hypothermia (7% per 1*c), halogenated anesthetics, propofol, etomidate, and barbiturates

Increased by: hyperthermia, seizures, ketamine, and nitrous oxide

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16
Q

What is the formula for cerebral perfusion pressure? What is normal?

A

CPP = MAP - ICP (or CVP, whichever is higher)

Cerebral vasculature autoregulates its resistance to provide a constant cerebral perfusion pressure of 50-150 mmHg

  • this ensures a relatively stable blood flow and confers protection against swings in BP
  • autoregulation is influenced by products of local metabolism, myogenic mechanisms, and autonomic innervation
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17
Q

What are the consequences of a CPP that exceeds the limits of autoregulation (too high and too low)?

A

Max Dilation (CPP <50): vessels are maximally dilated – CBF becomes pressure dependent – risk of cerebral hypoperfusion

Autoregulation (CPP 50-150): CBF is constant over a range of pressure

Max Constriction (CPP >150): vessels are maximally constricted – CBF becomes pressure dependent – risk of cerebral edema and hemorrhage

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18
Q

What are four conditions that reduce CPP (cerebral perfusion pressure) as a function of increased venous pressure?

A

Conditions that impair venous drainage:

  • jugular compression secondary to improper head position
  • increased intrathoracic pressure secondary to coughing or PEEP
  • vena cava thrombosis
  • vena cava syndrome

**high venous pressure decreases cerebral venous drainage and increases cerebral volume – creates a backpressure to the brain that reduces the arterial/venous pressure gradient (MAP-CVP)

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19
Q

What is the relationship between PaCO2 and CBF? What physiologic mechanism is responsible for this?

A

There is a linear relationship between PaCO2 and CBF

-the pH of the CSF around the arterioles controls cerebral vascular resistance
-at a PaCO2 of 40 mmHg CBF is 50 mL/100g brain tissue/min

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20
Q

At what PaCO2 does maximal cerebral vasodilation occur? How about max cerebral vasoconstriction?

A

For every 1 mmHg increase (or decrease) in PaCO2, CBF will increase (or decrease) by 1-2 mL/100g brain tissue/min

Max Vasodilation occurs at PaCO2 of 80-100 mmHg
Max Vasoconstriction occurs at PaCO2 of 25 mmHg

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21
Q

What is the relationship between CMRO2 and CBF?

A

Things that increase the amount of O2 the brain uses (CMRO2) tend to cause cerebral vasodilation (increased CBF) – ex) hyperthermia or ketamine

Things that decrease the amount of O2 the brain uses (CMRO2) tend to cause cerebral vasoconstriction (decreased CBF) – ex) hypothermia, propofol, and thiopental

*halogenated anesthetic are an exception – they decouple the relationship between CMRO2 and CBF (they reduce CMRO2 but cause cerebral vasodilation)

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22
Q

How do acidosis and alkalosis affect CBF?

A

Respiratory Acidosis increases CBF
Respiratory Alkalosis decreases CBF

Metabolic acidosis and alkalosis do not directly affect CBF

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23
Q

How does PaO2 affect CBF?

A

a PaO2 below 50-60 mmHg causes cerebral vasodilation and increases CBF

when PaO2 is above 60 mmHg it does not affect CBF

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24
Q

What is the normal ICP? What values are considered abnormal?

A

Normal ICP = 5-15 mmHg

Cerebral HTN occurs if ICP >20 mmHg

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25
Q

When is ICP measurement indicated? What is the gold standard for measurement?

A

Indicated with a GCS <7

-an intraventricular catheter is the gold standard for ICP measurement
-can also be measured with a subdural bolt or a catheter placed over the convexity of the cerebral cortex

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26
Q

What are the signs and symptoms of intracranial HTN?

A

-Headache
-N/V
-Papilledema (swelling of optic nerve)
-Focal neurologic deficit
-Decreased LOC
-Seizure
-Coma

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27
Q

What is the Monroe-Kellie hypothesis?

A

Brain lives in a rigid, bony box – within the box there are 3 components: brain, blood, and CSF

Monroe-Kellie hypothesis describes the pressure-volume equilibrium between the brain, blood, and CSF within the confines of the cranium
– an increase in one of the components must be countered with a decrease in one or both of the others – if not the pressure inside the cranium will rise

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28
Q

What is Cushing’s triad? What is the clinical relevance of this reflex?

A

Hypertension
Bradycardia
Irregular Respirations

Indicates intracranial hypertension

*increased ICP reduces CPP – to preserve cerebral perfusion, blood pressure increases - HTN activates the baroreceptor reflex leading to bradycardia - compression of the medulla causes irregular respirations

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29
Q

Where are the four areas where brain herniation can occur?

A

-Herniation of the cingulate gyrus under the falx
-Herniation of contents over the tentorium cerebelli (transtentorial herniation)
-Herniation of the cerebellar tonsils through the foramen magnum
-Herniation of contents through a site of surgery or trauma

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30
Q

How does hyperventilation affect CBF? What is the ideal PaCO2 to achieve this effect?

A

CO2 dilates the cerebral vessels –> decreasing cerebral vascular resistance –> increased CBF –> increased ICP

Hyperventilation (30-35) constricts cerebral vessels –> increased cerebral vascular resistance –> decreased CBF –> decreased ICP

*lowering PaCO2 <30 increases risk of cerebral ischemia due to vasoconstriction and shifting the oxyhemoglobin dissociation curve to the left (reduces oxygen offloading)

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31
Q

How do nitroglycerine and nitroprusside affect ICP?

A

Cerebral Vasodilators

-increases CBF, thus increase ICP

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32
Q

How does head position affect ICP?

A

Head elevation >30 degrees facilitates venous drainage away from the brain

Neck flexion or extension can compress the jugular veins, reduce venous outflow, increase CBV, and increase ICP

Head down positions increase CBV and ICP

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33
Q

How does mannitol reduce ICP? What problems can arise when mannitol is used in this way?

A

Mannitol = Osmotic Diuretic
-increases serum osmolarity and ‘pulls’ water across the BBB towards the bloodstream

-if BBB is disrupted, mannitol enters the brain and promotes cerebral edema
-mannitol transiently increases blood volume, which can increase ICP and stress the failing heart

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34
Q

Describe the anterior circulation of the brain

A

Internal carotid arteries supply the anterior circulation (enter the skull through the foramen lacerum

Aorta –> Carotid a. –> Internal Carotid a. –> Circle of Willis –> Cerebral Hemispheres

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35
Q

Describe the posterior circulation of the brain

A

Vertebral arteries supply the posterior circulation (enter the skull through the foramen magnum

Aorta –> Subclavian a. –> Vertebral a. –> Basilar a. –> Posterior fossa structures and Cervical Spinal Cord

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36
Q

Where do the anterior and posterior circulation pathways converge in the brain?

A

Circle of WIllis

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37
Q

What is the function of the circle of Willis?

A

Primary function = provide redundancy of blood flow in the brain

-if once side of the circle becomes occluded – the other side should theoretically be able to perfuse the affected areas of the brain

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38
Q

How do you determine which stroke patient can receive a thrombolytic agent?

A

Emergent Non-Contrast CT

Thrombolytic should NOT be given to hemorrhagic strokes

-if treatment can begin <4.5 hrs after onset of symptoms, the pt with an ischemic CVA should recieve an IV thrombolytic (ex tPA)
-ASA is an acceptable alternative if tPA can’t be administered

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39
Q

What is the relationship between hyperglycemia and cerebral hypoxia?

A

During cerebral hypoxia, glucose is converted to lactic acid – cerebral acidosis destroys brain tissue and is associated with worse outcomes

-monitor serum glucose and treat hyperglycemia with insulin

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40
Q

How is transmural pressure calculated in the context of cerebral aneurysm?

A

Increased transmural pressure predisposes the aneurysm to rupture

-MAP = pressure pushing outwards against the aneurysmal sac
-ICP = the counter pressure that pushes against it

*risk of rupture is increased by HTN and/or acute reduction in ICP

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41
Q

What is the most common clinical finding in a pt with subarachnoid hemorrhage? What are other signs/symptoms?

A

Most Common = intense headache (“worst one in my life”)

-Loss of consciousness (50% of the time)
-Focal neurologic deficits
-N/V
-Photophobia
-Fever
-Signs of meningismus (occurs as blood spreads throughout and irritates the Subarachnoid space)

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42
Q

What is the most significant source of morbidity and mortality in the patient with subarachnoid hemorrhage?

A

Cerebral Vasospasm

-delayed contraction of the cerebral arteries – can lead to cerebral infarction
-free Hgb that is in contact with the outer surface of the cerebral arteries increases the risk of vasospasm

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43
Q

What is the incidence of cerebral vasospasm? When it is most likely to occur?

A

Occurs in ~25% of pts following SAH

Most likely 4-9 days following SAH

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44
Q

What is the treatment for cerebral vasospasm?

A

Triple H Therapy – Hypervolemia, HTN, Hemodilution to hct 27-32%

-liberal hydration supports BP and CPP (also creates state of hemodilution – reduces blood viscosity and cerebrovascular resistance)

Nimodipine – increases collateral blood flow

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45
Q

What is the best treatment if a cerebral aneurysm ruptures during coiling?

A

Give protamine (1mg per 100U heparin administered)

Lower MAP into low/normal range

*isn’t cited but, adenosine can be given to temporarily arrest the heart, to IR can control the bleeding

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46
Q

What are the motor response scores in the Glasgow Coma Scale?

A

1 = No motor response
2 = Abnormal extension to pain
3 = Abnormal flexion to pain
4 = Withdrawal response to pain
5 = Localizing response to pain
6 = Obeys commands

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47
Q

What are the verbal response scores in the Glasgow Coma Scale?

A

1 = No verbal response
2 = Incomprehensible sounds
3 = Inappropriate words
4 = Confused
5 = Oriented

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48
Q

What are the eye opening scores in the Glasgow Coma Scale?

A

1 = No eye opening
2 = Eye opening to pain/pressure
3 = Eye opening to sound
4 = Eyes open spontaneously

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49
Q

What Glasgow Coma Scale score is consistent with TBI?

A

Less than 8

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50
Q

How do you treat the pt with an intracerebral bleed who is on warfarin?

A

Warfarin can be reversed with FFP, prothrombin complex concentrate, and/or recombinant factor VIIa

*vitamin K = not the best option

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51
Q

How do you treat the pt with an intracerebral bleed who is on clopidogrel?

A

Clopidogrel and ASA can be reversed with platelet transfusion

*no evidence of reversal with recombinant factor VIIa

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52
Q

What are 2 common ways of reducing ICP that should be specifically avoided in the pt with a TBI?

A

-Hyperventilation (can worsen cerebral ischemia)

-Steroids (worsen neurologic outcome)

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53
Q

Is N2O safe in the pt with a TBI?

A

No

-other injuries, such as pneumothorax, may only become evident after anesthetic induction and positive pressure ventilation

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54
Q

What are the five types of seizures?

A

-Grand Mal
-Focal Cortical
-Absence (Petit Mal)
-Akinetic
-Status Epilepticus

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55
Q

Describe a Grand Mal seizure

A

Generalized tonic-clonic activity
-tonic phase = whole body rigidity
-clonic phase = repetitive jerking motions

Respiratory Arrest –> Hypoxia
-oxygen consumption d/t increased brain activity and muscle contraction

Acute treatment = propofol, diazepam, and thiopental
Surgical treatment = vagal nerve stimulator or resection of foci

56
Q

Describe a Focal Cortical seizure

A

Localized to a particular cortical region

-can be motor or sensory
-usually no loss of consciousness

57
Q

Describe an Absence (Petit Mal) seizure

A

Temporary loss of awareness (but remains awake)

-more common in children

58
Q

Describe an Akinetic seizure

A

Temporary loss of consciousness and postural tone

-can result in fall –> head injury
-more common in children

59
Q

Describe Status Epilepticus. How is it treated?

A

Seizure activity lasting more than 30 minutes or 2 grand mal seizures without regaining consciousness in between

Respiratory arrest –> Hypoxia
-increased O2 consumption

Acute Treatment: phenobarbital, thiopental, phenytoin, benzos, propofol, and even GA

60
Q

What is the relationship between etomidate and seizures?

A

Etomidate commonly causes myoclonus – not associated with increased EEG activity in patients that don’t have epilepsy

Patients with seizure disorders – Etomidate increases EEG activity and can be used to help determine the location of seizure foci during cortical mapping

61
Q

What is the pathophysiology of Alzheimer’s Disease?

A

Development of diffuse beta amyloid-rich plaques and neurofibrillary tangles in the brain

Consequences of plaque formation:
-dysfunctional synaptic transmission – most noticeable in nicotinic ACh neurons
-apoptosis

62
Q

What class of drugs is used to treat Alzheimer’s disease? How do they interact with SUX?

A

Cholinesterase Inhibitors (Tacrine, Donepezil, Rivastigmine, and Galantamine)

Cholinesterase inhibitors increase the duration of action of SUX (clinical significance is debatable)

63
Q

What is the pathophysiology of Parkinson’s disease?

A

Dopaminergic neurons in the basal ganglia are destroyed

-decreased dopamine + normal ACh = relative ACh increase –> suppression of corticospinal motor system and overactivity of extrapyramidal motor system

64
Q

What drugs increase the risk of extrapyramidal signs/symptoms in the pt with Parkinson’s?

A

Drugs that antagonize dopamine – Should be avoided

-Metoclopramide
-Butyrophenones (haloperidol & droperidol)
-Phenothiazines (promethazine)

65
Q

What is the most common eye complication in the periop period? what is the most common cause of vision loss?

A

Most common eye complication = Corneal Abrasion

Most common cause of vision loss = Ischemic Optic Neuropathy

66
Q

What is the pathophysiology of ischemic optic neuropathy?

A

Consequence of ischemia of the optic nerve

-most likely explanation is that venous congestion in the optic canal reduces prefusion pressure
-increased intraabdominal and/or intrathoracic pressure can also increase intraocular pressure

*central retinal and posterior ciliary arteries = at highest risk

67
Q

What surgical procedure presents the most significant risk of ischemic optic neuropathy? What are other procedure (6) and patient (7) risk factors?

A

Most common after spinal surgery in prone position

Procedure Risk Factors:

  • prone
  • use of wilson frame
  • long duration of anesthesia
  • large blood loss
  • low ratio of colloid to crystalloid resuscitation
  • hypotension

Patient Risk Factors:

  • male
  • obesity
  • diabetes
  • hypertension
  • smoking
  • old age
  • atherosclerosis
68
Q

How is the spinal cord perfused?

A

One anterior spinal artery –> anterior 2/3 of spinal cord

Two posterior spinal arteries –> posterior 1/3 of spinal cord

6-8 Radicular arteries

69
Q

What is the most important radicular artery? Which spinal segment does it typically enter the spinal cord?

A

Artery of Adamkiewicz

Commonly originates between T11-T12

*supplies the anterior cord in the thoracolumbar region

70
Q

What is the 3 neuron pathway common to the spinal tracts?

A

First Order Neuron: travels from periphery to spinal cord or brainstem

Second Order Neuron: travels from spinal cord or brainstem to a subcortical structure

Third Order Neuron: links the subcortical structure to the cerebral cortex

71
Q

What is the structure and function on the dorsal column?

A

Doral Column - Medial Lemniscal System

Structure: large, myelinated, rapidly conducting fibers

Function:
-transmits mechanoreceptive sensations (fine touch, proprioception, vibration, and pressure)
-capable of two point discrimination (high degree of localizing the stimulus)
-transmits sensory information faster than the anterolateral system

72
Q

What is the structure and function of the spinothalamic tract?

A

Anterolateral System - Spinothalamic Tract

Structure: smaller, myelinated, slower conducting fibers

Function:
-transmits pain, temp, crude touch, tickle, itch, and sexual sensation
-two point discrimination is not present

73
Q

What bedside exam can assess the integrity of the corticospinal tract? How do you interpret it?

A

Corticospinal Tract (Pyramidal Tract) = most important motor pathway

Bed Side Exam = Babinski test

-normal: downward motion of all toes
-upper motor neuron injury: upward extension of the big toe with fanning of other toes
-lower motor neuron injury: no response

74
Q

What is the difference in presentation between an upper and lower motor neuron injury?

A

Upper motor neurons – begin in cerebral cortex, end in ventral horn of spinal cord
-presents with hyperreflexia and spastic paralysis

Lower motor neurons – begin in ventral horn, end at neuromuscular junction
-presents with impaired reflexes and flaccid paralysis

75
Q

What is the pathophysiology of neurogenic shock?

A

-Impairment of cardioaccelerator fibers (T1-T4) –> Unopposed cardiac vagal tone –> Bradycardia and reduced inotropy
-Decreased SNS tone –> Vasodilation –> Venous pooling –> Decreased CO and BP
-Impairment of sympathetic pathways from hypothalamus to blood vessels –> Inability to vasoconstrict or shiver –> Hypothermia

*hypothermia is the result of the inability of the cutaneous vasculature to vasoconstrict, causing redistribution of blood flow towards the periphery and allowing more heat to escape from the body

76
Q

How can you differentiate neurogenic shock from hypovolemic shock based on symptoms?

A

Neurogenic Shock = bradycardia, hypotension, hypothermia w/ pink, warm extremities

Hypovolemic Shock = tachycardia, hypotension, and cool, clammy extremities

77
Q

Is SUX ok to use in a patient with spinal cord injury?

A

SUX should be avoided 24 hours after injury and should not be used for at least 6 months after injury

78
Q

When is autonomic hyperreflexia? What factors contributes to this risk of development?

A

After neurogenic shock phase ends (1-3 weeks) – body begins to mend in a pathologic and disorganized way

Return of spinal sympathetic reflexes below level of injury without inhibitory influences that normally come from above the injury creates sympathetic reflexes below the level injury to exist in an overactive state
-this puts patient at risk for autonomic hyperreflexia (mass reflex)

Up to 85% of patients w/ injury above T6 develop AH
*very unlikely to occur w/ injury below T10
*higher the injury the more intense the response

79
Q

What are the 6 situations that can precipitate autonomic hyperreflexia?

A
  • Stimulation of the hollow organs (bladder, bowel, uterus)
  • Bladder catheterization
  • Surgery (especially cystoscopy or colonoscopy)
  • Bowel movement
  • Cutaneous stimulation
  • Childbirth
80
Q

What is the classic presentation of autonomic hyperreflexia?

A

Hypertension and Bradycardia

Other signs/symptoms:
-reflex vasodilation above level of injury –> nasal stuffiness
-hypertension –> headache and blurred vision
-malignant HTN –> stroke, seizure, LV failure, dysrhythmias, pulm edema, and/or MI

81
Q

What is the pathophysiology of autonomic hyperreflexia?

A

-Stimulation below level of injury triggers a sympathetic reflex arc that creates a profound degree of vasoconstriction below level of injury
-Activates the baroreceptor reflex in carotid sinus – slows HR
-Body’s attempt to reduce afterload w/ vasodilation above the level of injury

82
Q

What is the anesthetic management of a patient with autonomic hyperreflexia?

A

PREVENTION is paramount

-general or spinal are the best options
-epidural may be used for a laboring mom (epidural doesn’t inhibit sacral nerve roots to the same degree as a spinal)
-HTN is best treated w/ removal of the stimulus, deepening the anesthetic, and a rapid acting vasodilator (ie. sodium nitroprusside)
-bradycardia can be treated w/ atropine or glyco
-administration of a positive chronotrope w/ vasoconstrictive properties will worsen HTN
-adding lidocaine jelly to cysto or foley does not prevent AH
-SUX should be avoided for at least 6 months following injury
-may present in postop period – close postop monitoring

83
Q

What is the pathophysiology of amyotrophic lateral sclerosis (ALS)?

A

Causes progressive degeneration of motor neurons in the corticospinal tract

Astrocytic gliosis replaces the affected motor neurons

Both upper and lower motor neurons are affected

*unknown etiology

84
Q

What are the anesthetic considerations of ALS?

A

-No evidence that supports any particular anesthetic technique
-SUX can cause lethal hyperkalemia (lower motor neuron dysfunction is associated w/ proliferation of postjunctional nicotinic receptors)
-Increased sensitivity to NDMRs
-Bulbar muscle dysfunction increases risk of pulmonary aspiration
-Chest weakness reduces vital capacity and maximal minute ventilaiton
-Consider postop ventilation

85
Q

What is the pathophysiology of myasthenia gravis?

A

Autoimmune disease

-IgG antibodies destroy post-junctional, nicotinic, ACh receptors at the neuromuscular junction
-although ACh is present in sufficient quantity, there isn’t enough receptors to translate the response – manifests as skeletal muscle weakness

*Key feature = muscle weakness that becomes worse later in the day or develops with exercise

86
Q

What surgical procedure can reduce symptoms in the pt with myasthenia gravis?

A

Thymectomy (thymus gland plays key role in myasthenia gravis)

-thymectomy reduces circulating Anti-AchR IgG in most patients
-surgical approach may be via median sternotomy or by the transcervical approach

87
Q

How does myasthenia gravis affect the pregnant mother and the fetus?

A

In 1/3 women – pregnancy intensifies the symptoms

-Anti-AchR IgG antibodies cross the placenta and cause weakness in 15-20% of neonates
-can persist up to 2-4 weeks (neonate may require airway management)

88
Q

How can you tell the difference between cholinergic crisis and myasthenic crisis?

A

Diagnosis is made by administering 1-2 mg IV Edrophonium – “Tensilon Test”

-Cholinergic Crisis = muscle weakness worsens (treat w/ anticholinergic)
-Myasthenic Crisis = improvement in muscle strength (treat with anticholinesterase, immunosuppression, plasmapheresis)

89
Q

How do patients with myasthenia gravis respond to neuromuscular blockers?

A

Increased sensitivity to NDMRs

Resistance to SUX

*due to reduction in number of nicotinic receptors at NMJ

90
Q

Why are patients with myasthenia gravis prone to aspiration?

A

Bulbar muscle weakness (mouth and throat) manifests as difficulty handling oral secretions

*increases risk of pulmonary aspiration

91
Q

What is the pathophysiology of Eaton-Lambert syndrome?

A

Caused by IgG-mediated destruction of the presynaptic voltage-gated calcium channel at the presynaptic nerve terminal

-when action potential depolarizes the nerve terminal, Calcium entry into the presynaptic neuron is limited – reduces the amount of ACh that is released into the synaptic cleft
-postsynaptic nicotinic receptor is present in normal quantity and functions normally

*common co-morbidity = small-cell lung carcinoma (oat-cell carcinoma)
*sensitive to SUX and NDMRs

92
Q

What is the pathophysiology of Guillain-Barre syndrome (acute idiopathic polyneuritis)?

A

Immunologic assault on myelin in the peripheral nerves

-action potential can’t be conducted – motor endplate never receives the incoming signal
-usually persists for ~2 weeks and ends with full recovery in ~4 weeks

93
Q

How does Guillain-Barre syndrome present?

A

A flu-like illness usually precedes paralysis by 1-3 weeks

-flaccid paralysis begins in the distal extremities and ascends bilaterally towards the proximal extremities, trunk, and face
-intercostal muscle weakness impairs ventilaiton
-facial and pharyngeal weakness causes difficulty swallowing
-sensory deficits include paresthesias, numbness, and/or pain
-autonomic dysfunction is common (tachycardia or bradycardia, hyper or hypotension, diaphoresis or anhidrosis, and orthostatic hypotension)

94
Q

What is familial periodic paralysis? How can the two variants be distingushed from each other?

A

Familial Periodic Paralysis = acute episodes of skeletal muscle weakness that is accompanied by either hypo or hyperkalemia

  • Hypokalemic periodic paralysis: diagnosed if skeletal muscle weakness follows a glucose-insulin infusion (pt becomes weak after serum K is reduced)
  • Hyperkalemic periodic paralysis: diagnosed if skeletal muscle weakness follows oral potassium administration (pt becomes weak after serum K increases)

*Acetazolamide = treatment for both forms
-creates non-anion gap acidosis (protects against hypokalemia)
-facilitates renal potassium excretion (guards against hyperkalemia)
*AVOID hypothermia

95
Q

What drugs should be avoided and which are safe in the patient with hypokalemic periodic paralysis?

A

Do Not Administer:
-glucose containing solutions
-potassium wasting diuretics
-beta-2 agonists
-SUX

Safe to Administer:
-NDMRs
-Acetazolamide

96
Q

What drugs should be avoided and which are safe in the patient with hyperkalemic periodic paralysis?

A

Do Not Administer:

  • SUX
  • Potassium containing solutions (LR)

Safe to Administer:

  • glucose containing solutions
  • potassium wasting diuretics
  • beta-2 agonists
  • NDMRs
  • Acetazolamide
97
Q

What is the pathophysiology of malignant hyperthermia?

A

T-tubule is depolarized (ACh binds to nicotinic receptor at neuromuscular junction) –> extracellular calcium enters the myocyte via the dihydropyridine receptor at the t-tubule –> activates the DEFECTIVE RYANODINE RECEPTOR (RYR1)

Defective RYR1 receptor instructs the sarcoplasmic reticulum to release way too much calcium into the cell –> causes more calcium to engage with the contractile elements and the cell attempts to return the excess calcium to the SR via the SERCA2 pump
-both processes consume a substantial amount of ATP, increase O2 consumption, and increase CO2 production

When skeletal myocyte consumes all of its ATP – no ATP to maintain integrity of the cell membranes –> breakdown and intracellular components (myoglobin and K+) are released into systemic circulation

98
Q

What are the 8 consequences of too much calcium inside a skeletal myocyte?

A

-Sustained muscle contraction
-Accelerated metabolic rate and rapid depletion of ATP
-Increased O2 consumption
-Increased CO2 and heat production
-Mixed respiratory and lactic acidosis
-Sarcolemma breaks down
-Potassium and myoglobin leak into the systemic circulation
-Rigidity from sustained contraction

99
Q

What three conditions are definitively linked to malignant hyperthermia?

A

-King-Denborough Syndrome
-Central Core Disease
-Multiminicore Disease

100
Q

What six conditions are not definitively linked to malignant hyperthermia?

A

-Duchenne muscular dystrophy
-Becker muscular dystrophy
-Neuroleptic malignant syndrome
-Myotonia congenita
-Myotonic dystrophy
-Osteogenesis imperfecta

101
Q

What is the most sensitive indicator of malignant hyperthermia? What are the early, intermediate, and late symptoms?

A

Most Sensitive Indicator = EtCO2 that rises out of proportion to minute ventilation

Early Symptoms:

  • Tachycardia, Tachypnea, Masseter spasm, Warm soda lime, Irregular heart rhythm

Intermediate Symptoms:

  • Cyanosis, Irregular heart rhythm, Patient warm to touch

Late Symptoms:

  • Muscle rigidity, Cola-colored urine, Coagulopathy, Irregular heart rhythm, overt hyperthermia
102
Q

What is the difference between trismus and malignant hyperthermia? How should you proceed if the pt presents with either condition?

A

Trismus = tight jaw that can still be opened

Masseter Muscle Rigidity = jaw that cannot be opened (MH)

-Trismus is normal response to SUX – ok to proceed with surgery
-Masseter muscle rigidity complicates airway management (spasm due to increased calcium in myoplasm)

103
Q

What is the definitive test for susceptibility to malignant hyperthermia?

A

Halothane Contracture Test

-anyone who has experienced MH or masseter spasm should be referred
-only has 80% specificity (risk of false negative result)

104
Q

How does dantrolene treat MH? What are its most common side effects?

A

Dantrolene = Muscle relaxant

-halts calcium release from the RyR1 receptor
-prevents calcium entry into the myocyte (reduces stimulus for calcium induced calcium release)

Most common side effects are muscle weakness and venous irritation

105
Q

How is dantrolene formulated and prepared?

A

One Vial = 20mg dantrolene + 3g mannitol

Must reconstitute with preservative free water

106
Q

How do you treat MH?

A

-Discontinue triggering agent
-Call for help
-Administer 100% oxygen at >10 L/min
-Administer dantrolene (or Ryanodex) 2.5 mg/kg IV and repeat q5-10 min
-Hyperventilate
-Correct lactic acidosis w/ sodium bicarb
-Treat hyperkalemia (CaCl 5-10 mg/kg IV and insulin 0.15 u/kg + D50 1 mL/kg)
-Protect against dysrhythmias (class 1 agents: lidocaine 2mg/kg or procainamide 15 mg/kg)
-Maintain urine output (IV hydration, mannitol 0.25 g/kg, furosemide 1mg/kg)
-Cool the patient until temp drops below 38*C (cold IV fluid lavage, ice packs)
-Monitoring coagulation (DIC = late complication and signals impending demise)

107
Q

What is the pathophysiology of Duchenne muscular dystrophy?

A

The absence of dystrophin – destabilizes the sarcolemma during muscle contraction and increases membrane permeability

-dystrophin is a critical structural component of the cytoskeleton of skeletal and cardiac muscle cells – helps anchor actin and myosin to the cell membrane
-absence of dystrophin allows extrajunctional receptors to populate the sarcolemma – predisposes pt to hyperkalemia following SUX administration

108
Q

How does Duchenne muscular dystrophy affect pulmonary function?

A

Kyphoscoliosis (restrictive lung disease) –> Decreased pulmonary reserve –> Increased secretions and risk of pneumonia

Respiratory muscle weakness

109
Q

How does Duchenne muscular dystrophy affect cardiac function? What EKG findings might you expect?

A

Cardiac Considerations:
-degeneration of cardiac muscle –> reduced contractility, papillary muscle dysfunction, mitral regurgitation, cardiomyopathy, CHF
-signs of cardiomyopathy include resting tachycardia, JVD, S3/S4 gallop, displacement of the point of maximal impulse
-Gold standard of cardiac evaluation = Echo

EKG Changes:
-impaired cardiac conduction –> sinus tach and short PR interval
-scarring of the posterobasal aspect (back/bottom) of LV manifests as increased R wave amplitude in lead 1 and deep Q wave in limb leads

110
Q

What is the Cobb angle, and what is its significance?

A

Cobb Angle = Magnitude of spinal curvature

40-50 Degrees: Indication for surgery
60 Degrees: Decreased pulmonary reserve
70 Degrees: Pulmonary symptoms present
100 Degrees: Gas exchange significantly impaired – Higher risk postop pulm complications

111
Q

What are the early respiratory complications of scoliosis?

A

Restrictive Ventilatory Defect:
-decreased FEV1 and FRC
-normal FEV1/FVC ratio

Decreased Lung Volumes and Capacities:
-VC
-TLC
-FRC
-RV

Decreased Chest Wall Compliance

112
Q

What are the late respiratory complications of scoliosis?

A

-V/Q mismatching
-Hypoxemia
-Hypercarbia (sign of impending resp failure)
-Pulmonary HTN
-Reduced response to hypercapnia
-Cor pulmonale
-Cardiorespiratory failure

113
Q

What are the three ways rheumatoid arthritis affects the airway?

A

Temporomandibular Joint – limited mouth opening

Cricoarytenoid Joints – decreased diameter of glottic opening

Cervical Spine – atlanto-occipital subluxation with flexion / limited extension

114
Q

What is the most common airway complication of rheumatoid arthritis? What is its clinical significance?

A

Atlantoaxial Subluxation

-due to weakening of the transverse axial ligament – allows odontoid to directly compress the spinal cord at the level of the foramen magnum

*Patient is at risk for quadriparesis or paralysis

115
Q

What is the pathophysiology of rheumatoid arthritis?

A

Autoimmune disease that targets synovial joints

-also widespread systemic involvement due to infiltration of immune complexes into the small and medium arteries leading to vasculitis
-cytokines (TNF and interleukin-1) play central role

*Hallmark of RA = morning stiffness that generally improves with activity
-joints are painful, swollen, and warm
-weakness, fatigue, and anorexia =other symptoms

-2-3x more common in women

116
Q

What are the eye complications of rheumatoid arthritis?

A

Sjogren’s syndrome (risk of corneal abrasion)

117
Q

What are the nervous system complications of rheumatoid arthritis?

A

Peripheral neuropathy due to nerve entrapment

118
Q

What are the endocrine complications of rheumatoid arthritis?

A

Adrenal insufficiency and infections due to chronic steroid therapy

119
Q

What are the renal complications of rheumatoid arthritis?

A

Renal insufficiency due to:

-vasculitis
-NSAIDs

120
Q

What are the pulmonary complications of rheumatoid arthritis?

A

Pleural effusion

Restrictive ventilatory pattern:
-diffuse interstitial fibrosis
-costochondral involvement limits chest wall expansion

121
Q

What are the cardiac complications of rheumatoid arthritis?

A

-Pericardial effusion or tamponade
-Restrictive pericarditis
-Aortic regurgitation
-Valvular fibrosis
-Coronary artery arteritis

122
Q

What are the GI complications of rheumatoid arthritis?

A

NSAIDs

Steroids

123
Q

What are the hematologic complications of rheumatoid arthritis?

A

Anemia

Platelet dysfunction secondary to NSAIDs

124
Q

What is the pathophysiology of systemic lupus erythematosus?

A

Autoimmune disease characterized by the proliferation of antinuclear antibodies

-affects nearly every organ system
-most of the consequences are the direct result of antibody-induced vasculitis and tissue destruction

125
Q

What are the most common problems of systemic lupus erythematosus?

A

Polyarthritis

Dermatitis

*targets young women

126
Q

What are the airway complications of systemic lupus erythematosus?

A

Cricoarytenoiditis:

  • hoarseness
  • stridor
  • airway obstruction
127
Q

What are the nervous system complications of systemic lupus erythematosus?

A

Stroke

Psychosis/dementia

Peripheral neuropathy

128
Q

What are the Renal complications of systemic lupus erythematosus?

A

nephritis with proteinuria

129
Q

What are the pulmonary complications of systemic lupus erythematosus?

A

-Restrictive ventilatory defect
-Pulmonary HTN
-Interstital lung disease w/ impaired diffusing capacity
-Pleural effusion
-Recurrent pulmonary emboli

130
Q

What are the cardiac complications of systemic lupus erythematosus?

A

-Pericarditis (tamponade is uncommon)
-Raynaud’s phenomenon
-HTN
-Conduction defects
-Endocarditis

131
Q

What are the hematologic complications of systemic lupus erythematosus?

A

-Antiphospholipid antibodies
-Hypercoagulability
-Anemia
-Thrombocytopenia
-Leukopenia

132
Q

What drugs can exacerbate systemic lupus erythematosus?

(PISSED CHIMP)

A

P - pregnancy
I - infection
S - surgery
S - stress
E - enalapril
D - d-penicillamine

C - captopril
H - hydralazine
I - isoniazid
M - methyldopa
P - procainamide

133
Q

What is the relationship between systemic lupus erythematosus and antiphospholipid syndrome?

A

Patients with SLE are prone to developing antiphospholipid antibodies

-although aPTT is prolonged – pt is prone to a state of hypercoagulability and thrombosis
-at risk for stroke, DVT, and PE

134
Q

What is the pathophysiology of myotonic dystrophy?

A

Characterized by a prolonged contracture after voluntary contraction

-result of dysfunctional calcium sequestration by the sarcoplasmic reticulum
-contractions can be so severe that they interfere with ventilation and intubation

135
Q

What three things can increase the risk of contractures in the patient with myotonic dystrophy?

A

SUX

Reversal of NMB w/ anticholinesterase (theoretical)

Hypothermia (shivering –> sustained contractions)

136
Q

What is the pathophysiology of Marfan syndrome?

A

Autosomal dominant trait

Connective tissue disorder associated with:
-elevated risk of aortic dissection
-mitral regurgitation
-aortic insufficiency

*dissection of ascending aorta can extend into the pericardium (increases risk of cardiac tamponade)
*Spontneous pneumothorax is very common

137
Q

What is the pathophysiology of Ehlers-Danlos syndrome? Which type is associated with blood vessel rupture?

A

Inherited disorder of procollagen and collagen

-only type IV is associated with blood vessel rupture (ie AAA)
-increased bleeding tendency (result of a lack of blood vessel integrity and not coagulopathy)

*typically avoid regional anesthesia and IM injections
*pneumothorax is also common complications

APEX Study Guide (13 decks)

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