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APEXANESTHESIA COPY COPY > UNIT 7 Neuro > Flashcards

UNIT 7 Neuro Flashcards

1
Q

Name 4 types of glial cells and describe the function of each

A

astrocytes

  • most abundant
  • regulation of metabolic environment
  • repair neuron after neuronal injury

ependymal cells

  • concentrated in roof of 3rd/4th ventricles & SC
  • form the choroid plexus, which produces CSF

oligodendrocytes

  • form the myeline sheath in the CNS
  • schwann cells form the myelin sheath in the PNS

microglia
- act as macrophages and phagocytize neuronal debris

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2
Q

list the name and function of the 4 lobes of the cerebral cortex

A

frontal: contains the motor cortex
parietal: contains somatic sensory cortex
occipital: contains vision cortex
temporal: contains auditory cortex & speech centers
- Wernicke’s area: understanding speech
- Broca’s area: motor control of speech

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3
Q

Name the 12 cranial nerves

A 
I olfactory
II optic
III oculomotor
IV trochlear
V trigeminal
VI abducens
VII facial
VIII vestibulochochlear
IX glossopharyngeal
X vagus
XI spinal accessory
XII hypoglossal
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4
Q

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

A

CN III:

  • up (in, out, and straight)
  • in
  • down (out and straight)

CN IV
- in and down

CN VI
- out

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5
Q

What bedside tests are used to assess the CN?

A 
I smell
II vision
III eye movement, pupil constriction
IV eye movement
V facial sensation (+ ant 2/3 tongue sensation)
VI eye movement
VII facial movement except chewing 
VIII hearing, balance
IX posterior 1/3 tongue sensation
X swallowing
XI shoulder shrug
XII tongue movement
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6
Q

Which CN resides in the CNS? What is the implication of this?

A

CN II is the only CN that is part of the CNS (the rest are part of the PNS). This means that CN II is the only CN that is surrounded by dura.

It is bathed in CSF. If you inject LA into the optic nerve during RA of the eye, you will have a big problem.

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7
Q

What is tic douloureux? What CN contributes to this problem?

A

trigeminal neuralgia
CN V

causes excruciating neuropathic pain in the face

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8
Q

What is Bell’s palsy? What CN contributes to this problem?

A

CN VII

causes ipsilateral facial paralysis

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9
Q

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

A

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

It is located in the:

  • ventricles (lateral, 3rd, and 4th)
  • cisterns around the brain
  • subarachnoid space in brain & SC
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10
Q

What regions of the brain are NOT protected by the BBB?

A

BBB separates the CSF from the plasma. It has tight junctions that restrict pass of large molecules & ions.

The BBB isn’t present at the chemoreceptor trigger zone, posterior pituitary gland, pineal gland, choroid plexus, and parts of the hypothalamus

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11
Q

What is the normal volume and specific gravity of CSF?

A

volume 150mL

spec grav 1.002-1.009

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12
Q

Describe the production, circulation, and absorption of CSF.

A

CSF production: ependymal cells of the choroid plexus (of lateral ventricles), rate of 30mL/hr

circulation: lateral ventricles –> foramen of Monro–> 3rd vent –> aqueduct of Sylvius –> 4th vent –> paired foramen of Luschka/midline foramen of Magendie –> subarachnoid space –> superior sagittal sinus
absorption: arachnoid villi within the superior sagittal sinus (to the venous circulation)

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13
Q

What is the formula for CBF? what are the normal values for global, cortical, and subcortical flow?

A 
CBF = CPP/CVR 
(CVR = cerebral vascular resistance)

global 45-55mL/100g (or 15% of CO)
cortical 75-80mL/100g
subcortical 20mL/100g

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14
Q

What are the 5 determinants of CBF?

A 
CMRO2
CPP
venous pressure
PaCO2
PaO2
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15
Q

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

A

CMRO2 describes how much O2 the brain consumes per minute.

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

decreased by hypothermia (7%/1C), IA, propofol, etomidate, barbs

increased by hyperthermia, ketamine, N2O

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16
Q

What is the formula for CPP? What is normal?

A

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

autoregulation via vessel diameter changes to provide a constant CPP of 50-150mmHg

  • i.e. MAP needs to be higher
  • autoreg 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

CPP <50

  • vessels are maximally dilated
  • CBF becomes pressure dependent
  • risk of cerebral hypoperfusion

CPP >150

  • vessels are maximally constricted
  • CBF becomes pressure dependent
  • risk of cerebral edema & hemorrhage
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18
Q

list 4 conditions that reduce CPP as a function of increased venous pressure.

A

a high venous pressure decreased cerebral venous drainage & increases cerebral volume –> backpressure is created to the brain that reduces the arterial/venous pressure gradient (MAP-CVP)

conditions that impair drainage:

  • jugular compression d/t head position
  • increased intrathoracic pressure d/t cough, PEEP
  • vena cava thrombosis
  • vena cava syndrome
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19
Q

What is the relationship b/n PaCO2 and CBF? What physiologic mechanism is responsible for this?

A

linear

  • pH of the CSF around the arterioles controls the cerebral vascular resistance
  • at a PaCO2 of 40mmHg, CBF is 50mL/100g tissue/min
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20
Q

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

A

for every 1mmHg change in PaCO2, CBF will change by 1-2mL/100g tissue/min

max vasodilation occurs at PaCO2 of 80-100mmhg
max vasoconstriction occurs at PaCO2 of 25mmHg

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21
Q

What is the relationship b/n CMRO2 and CBF?

A

as a general rule

  • things that increase the amount of O2 the brain uses (CMRO2) tend to cause cerebral vasodilation (increased CBF) –> hyperthermia, ketamine
  • things that decrease CMRO2 tend to cause cerebral vasoconstriction (decreased CBF) –> hypothermia, propofol, TPL

halogenated anesthetics are an exception; they decouple the relationship: reduce CMRO2, but also cause cerebral vasodilation
- this is why TIVA is a better choice w/ intracranial hypertension

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22
Q

How do acidosis & alkalosis affect CBF?

A

resp acidosis = increased CBF
resp alkalosis = decreased CBF

met acidosis/alkalosis don’t directly affect CBF. This is because H+ doesn’t pass through the BBB. A compensatory change in MV can, however, affect CBF.

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23
Q

How does PaO2 affect CBF?

A

PaO2 <50-60mmHg causes cerebral vasodilation & increases CBF

When PaO2 is >60mmHg, it doesn’t affect CBF.

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24
Q

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

A

ICP is the supratentorial CSF pressure
normal = 5-15mmHg
cerebral HTN > 20mmHg

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25
Q

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

A

when GCS <7

intraventricular catheter is the gold standard

other ways:

  • subdural bolt
  • catheter placed over the convexity of the cerebral cortex
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26
Q

List the s/s of intracranial HTN

A 
HA
N/V
papilledema (swelling of the optic nerve)
focal neurologic deficit
decreased LOC
seizures
coma
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27
Q

discuss the monroe-kellie hypothesis

A

brain lives in a rigid, bony box containing brain, blood, and CSF

  • if one component increases in volume, another component must decrease in order to maintain constant pressure
  • remember intracranial compliance curve
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28
Q

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

A

indicates intracranial HTN

  • HTN
  • bradycardia
  • irregular respirations

increased ICP –> decreased CPP w/ compensatory HTN
–> baroreceptor reflex activation
compression of medulla –> irregular respirations

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29
Q

name 4 areas where brain herniation can occur.

A
  1. of the cingulate gyrus under the falx
  2. transtenotorial
  3. cerebellar tonsils via the foramen magnum
  4. via 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 vessels –> decreased CVR –> increased CBF –> increased ICP

hyperventilation –> decreased ICP in this manner

lowering PaCO2 <30 increases the risk of cerebral ischemia d/t vasoconstriction & L shift of the oxyHgb dissociation curve

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31
Q

How do NTG & SNP affect ICP?

A

cerebral vasodilators –> increases CBF –> 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 & ICP

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33
Q

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

A

0.25-1g/kg increases serum osm & “pulls” water across the BBB towards the bloodstream for excretion

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

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34
Q

describe anterior & posterior circulation of the brain. Where do these pathways converge?

A

converge at the circle of willis

anterior
ICA enter skull via foramen lacerum
aorta –> carotid –> ICA –> circle of willis –> cerebral hemispheres

posterior
vertebral a enter skull via foramen magnum
aorta –> SC –> vertebral –> basilar –> posterior fossa structures & cervical SC

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35
Q

describe the anatomy of the circle of willis.

A

primary function of the circle of willis is to provide redundancy of blood flow in the brain. If one side of the circle becomes occluded, the other side should theoretically be able to perfuse the affected areas of the brain

basilar
PCA
pcomm
MCA
ACA
acomm
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36
Q

Which population of stroke patients should receive a thrombolytic agent?

A

CVA d/t thrombosis
diagnosis must be made by emergent head CT prior to administration

if tx can begin <3hrs after onset of symptoms, the pt should receive tPA
- aspirin is acceptable if tPA cannot be administered

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37
Q

What is the relationship b/n hyperglycemia & cerebral hypoxia?

A

During cerebral hypoxia, glucose is converted to lactic acid. Cerebral acidosis destroys brain tissue & is associated w/ worse outcomes

monitor serum glucose, treat hyperglycemia, be careful administering dextrose containing IVF

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38
Q

in the context of cerebral aneurysm, how is transmural pressure calculated?

A

an increased transmural pressure predisposes the aneurysm to rupture.

transmural pressure = MAP - ICP

MAP = pressure pushing outward against the aneurysmal sac
ICP = counterpressure that pushes against it.
–> creates a tamponade effect

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

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39
Q

What is the most common clinical finding in a patient w/ SAH? What are the other s/s?

A

WHOL (worst HA of life)

others

  • LOC (50%)
  • neurologic deficits
  • N/V
  • photophobia
  • fever
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40
Q

What is the most significant source of M&M in the patient w/ SAH?

A

cerebral vasospasm (delayed contraction of the cerebral arteries); can lead to cerebral infarction

free Hgb that is in contact w/ the outer surface of the cerebral arteries increases the risk –> +correlation b/n amount of blood observed on CT & vasospasm incidence

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41
Q

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

A

25% of patients

most likely 4-9days after SAH

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42
Q

What is the treatment for cerebral vasospasm?

A

triple H therapy (hypervolemia, HTN, permissive hemodilution to Hct 27-32%)

nimodipine (CCB) reduces M&M associated w/ vasospasm –> doesn’t actual reduce the spasm, but increases the collateral blood flow

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43
Q

during endovascular coil placement for a cerebral aneurysm, the aneurysm ruptures. What is the best treatment at this time?

A

protamine 1mg/100U heparin
low/normal MAP
+/- adenosine to temporarily arrest the heart

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44
Q

be able to calculate the Glascow coma scale

A

eyes (1-4)
motor (1-6)
verbal (1-5)

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45
Q

How do you treat the patient w/ an ICH who is on warfarin?

A

FFP, prothrombin complex concentrate, and/or recombinant factor VIIa to reverse the warfarin

vitamin K isn’t the best option for acute warfarin reversal

46
Q

How do you treat the patient w/ an ICH who is on clopidogrel?

A 
platelet transfusion (aspirin can be reversed this way too)
there is also evidence of reversal w/ recombinant factor VIIa
47
Q

What are two common ways of reducing ICP that should specifically be avoided in the patient w/ a TBI?

A

hyperventilation (can worsen cerebral ischemia + it’s only indicated as a temp measure)

steroids (worsen neurologic outcome)

48
Q

Is N2O safe in the pt w/ TBI?

A

No

other injuries, such as pneumothorax, may only become evident after anesthetic induction & PPV

49
Q

compare and contrast the 5 types of seizures.

A

grand mal

  • generalized tonic/clonic activity
  • respiratory arrest –> hypoxia
  • tx: propofol, diazepam, TPL
  • surgical: vagal nerve stim or rsxn of foci

focal cortical

  • localized to a particular cortical region
  • can be motor or sensory
  • usually no LOC

absence (petit mal)

  • temporary loss of awareness
  • more common in children

akinetic

  • temp LOC & postural tone (can result in fall & TBI)
  • more common in children

status epilepticus

  • seizure activity >30min or 2 grand mal w/out regaining consciousness in between
  • resp arrest –> hypoxia
  • tx: phenobarb, phenytoin, benzos, propofol, and even GA
50
Q

What is the relationship b/n etomidate and seizures

A

etomidate commonly causes myoclonus. This is not associated w/ increased EEG activity in those that do not have epilepsy.

In those w/ sz disorders, etomidate (or methohexital or alfentanil) increases EEG activity and can be used to help determine location of seizure foci during cortical mapping

51
Q

Describe the patho of Alzheimer’s disease

A

diffuse beta amyloid rich plaques and neurofibrillary tangles in the brain

consequences:
- dysfunctional synaptic transmission (most notable at nACh neurons)
- apoptosis (programmed cell death)

52
Q

What class of drugs is used to treat Alzheimer’s disease?How do they interact w/ succinylcholine?

A

tx is palliative & aims to restore the [ACh]; cholinesterase inhibitors (tacrine, donepezil, rivastigmine, galantamine)

cholinesterase inhibitors increase the DOA of succ, although the clinical significance is debatable

53
Q

Describe the patho of Parkinson’s disease.

A

dopaminergic neurons in the basal ganglia are destroyed —> imbalance of DA & ACh (relative ACh increase)

this leads to suppression of corticospinal motor system + overactivity of extrapyramidal motor system

54
Q

What drugs increase the risk of extrapyramidal s/s in the pt w/ Parkinson’s disease?

A

reglan
butyrophenones (haldol, droperidol)
phenothiazines (promethazine)

55
Q

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

A

corneal abrasion

ischemic optic neuropathy = most common cause of vision loss

56
Q

Describe the patho of ischemic optic neuropathy.

A

ischemia of the optic nerve. Most likely explanation is that venous congestion in the optic canal reduces perfusion pressure

ocular PP = MAP - intraocular pressure

central retinal & posterior ciliary arteries are at highest risk b/c they are “watershed” areas – they lack anastomoses w/ other arteries

57
Q

What surgical procedure presents the most significant risk of ION? What are other procedure & patient risk factors?

A

spinal surgery in the prone position = most significant risk

other factors:

  • prone
  • use of Wilson frame
  • long duration of anesthesia
  • large EBL
  • low colloid:crystalloid resus
  • hypotension
  • male
  • obesity
  • DM
  • HTN
  • smoking
  • old age
  • atherosclerosis
58
Q

discuss the blood flow to the SC

A

SC is perfused by:
1 anterior spinal artery (anterior 2/3 of SC)
2 posterior spinal arteries (posterior 1/3 of SC)
6-8 radicular arteries

59
Q

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

A

artery of Adamkiewicz

along w/ the anterior spinal artery, the artery of adamkiewicz supplies the anterior cord in the thoracolumbar region. Most commonly originates b/n T11-T12

60
Q

Envision the anatomy of the SC & spinal nerve in cross section.

A

sensory neurons from the periphery via the dorsal nerve root

motor & autonomic neurons exit via the ventral nerve root

61
Q

describe the organization of the 3 neuron pathway common to the spinal tracts.

A

each pathway consists of three neurons:

  1. first order: peripheral nerve to SC or brainstem
  2. second order: SC or brainstem to subcortical structure
  3. third order: subcortical structure to the cerebral cortex.
62
Q

compare the structure & function of the dorsal column with the spinothalamic tract.

A

dorsal column (medial lemniscal system)

  • transmits mechanoreceptor sensations (fine touch, proprioception, vibration, pressure)
  • capable of 2 point discrimination (high degree of localization)
  • large, myelinated, rapidly conducting fibers
  • faster transmission than anterolateral system
  • a “more evolved” system

anterolateral system (spinothalamic tract)

  • transmits pain, temp, crude touch, tickle, itch, sexual sensation
  • no 2 point discrimination
  • smaller, myelinated, slower conducting fibers
  • more “primitive” system
63
Q

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

A

most important motor pathway (often referred to as the pyramidal tract, all others are collectively the extrapyramidal tract)

Babinski test (firm stimulus to underside of foot) yields:

  • normal: downward motion of all the toes
  • upper motor neuron injury: upward extension of big toe + fanning of the others
  • lower motor neuron injury: no response
64
Q

contrast the presentation of upper vs. lower motor neuron injury

A

upper motor neurons begin in the cerebral cortex & end in the ventral horn of the SC, while the lower motor neurons begin in the ventral horn & end at the NMJ

upper motor neuron injury presents w/ hyperreflexia & spastic paralysis

lower motor neuron injury presents w/ impaired reflexes & flaccid paralysis

65
Q

discuss the patho of neurogenic shock.

A

impairment of cardioaccelerator fibers (T1-T4) –> unopposed cardiac vagal tone –> bradycardia & decreased inotropy

decreased SNS tone –> vasodilation –> venous pooling –> decreased CO & BP

impairment of sympathetic pathways from hypothalamus to blood vessels –> inability to vasoconstrict or shiver –> hypothermia

66
Q

how can you differentiate neurogenic shock from hypovolemic shock?

A

neurogenic: bradycardia, hypotension, hypothermia w/ pink, warm extremities d/t cutaneous vasodilation
hypovolemia: tachycardia, hypotension, cool, clammy extremities.

67
Q

Discuss the use of succinylcholine in the patient w/ SC injury.

A

avoid if >24hrs post injury

do not use for at least 6months thereafter, some books say 1yr

68
Q

When does a pt w/ SC injury become at risk for autonomic hyperreflexia? What factor (other than time) contributes to this risk?

A

After the neurogenic shock phase ends (1-3 weeks), the body begins to mend itself in a pathologic and disorganized way, putting the pt at risk for autonomic hyperreflexia.

up to 85% of patients w/ injury >T6 will develop, very unlikely to occur in those w/ injury

69
Q

List 6 situations that can precipitate autonomic hyperreflexia

A 
sitmulation of the hollow organs (bladder, bowel, or uterus)
bladder catheterization
surgery (esp cysto, CLN)
bowel movement
cutaneous stimulation
childbirth
70
Q

Discuss the presentation & pathophysiology of autonomic hyperreflexia.

A

classic presentation = HTN & bradycardia.

stimulation below the level of SCI triggers sympathetic reflex arc that creates a profound degree of vasoconstriction below the level of injury –> baroreceptor activation in carotid bodies (bradycardia) –> body attempts to reduce afterload w/ vasodilation above the level of the injury.

other s/s:

  • reflex vasodilation above level of SC injury –> nasal stuffiness
  • HTN –> HA/blurred vision
  • malignant HTN –> CVA, sz, LV failure, dysrhythmias, pulmonary edema, and/or MI
71
Q

detail the anesthetic management of the patient w/ autonomic hyperreflexia.

A

prevent stimulation to the area below level of injury to prevent AH!

  • GA or spinal = best
  • epidural not as good for laboring mother b/c doesn’t inhibit sacral nerve roots as much
  • tx HTN w/ removal of stim, deepen IA, + rapid vasodilator (SNP)
  • tx bradycardia w/ atropine/glyco
  • avoid meds that increase HR & vasoconstrict
  • avoid sux x6months
  • monitor for AH closely in the immediate post-op period, when anesthesia is wearing off.
72
Q

Discuss the patho of amyotrophic lateral sclerosis.

A

causes progressive degeneration of motor neurons in the corticospinal tract. Astrocytic gliosis replaces the affected motor neurons. Both the upper & the lower motor neurons are affected.

Etiology is unknown

73
Q

Detail the anesthetic management of ALS

A
  • no clear evidence that supports one technique over another
  • avoid sux (hyperK+)
  • increased sensitivity to NDMR
  • bulbar m dysfunction increases risk of aspiration
  • chest weakness decreases VC & MMV
  • consider post-op mechanical ventilation
74
Q

describe the patho of myasthenia gravis

A

autoimmune disease
IgG Ab destroy post-junctional nAChR at the NMJ. (ACh is present in sufficient quantity, the receptors just aren’t there)
–> skeletal m weakness.

Key feature is skeletal m weakness that becomes worse later in the day or that develops w/ exercise & can recover some w/ rest.

75
Q

What surgical procedure can reduce symptoms in the patient w/ myasthenia gravis?

A

the thymus gland plays a key role in MG, and thymectomy brings symptom relief to many patients

  • it reduces circulating anti-AChR IgG in most patients
  • surgical approach may be via median sternotomy or by the transcervical approach
76
Q

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

A

in 1/3 of women, pregnancy intensifies the symptoms of MG.

Anti-AChR IgG Ab cross the placenta and cause weakness in 15-20% of neonates. This can persist x2-4 weeks, which is consistent w/ the half-life of these antibioties in the neonates circulation
- they may require airway management.

77
Q

How can you tell the difference b/n cholinergic crisis and myasthenic crisis?

A

Pryidostigmine (anticholinesterase) is the first line tx for MG. An OD can cause cholinergic crisis, which can include skeletal m weakness (makes differentiation difficult)

diagnosis is made by administering 1-2mg IV edrophonium (“Tensilon test”)

  • if weakness is made worse, then the pt has cholinergic crisis (tx = anticholinergic)
  • if weakness improves, then it was an MG exacerbation (tx = anticholinesterase, immunosuppression, plasmapheresis)
78
Q

How do patients with myasthenia gravis respond to NMB?

A

bc there is a reduction in the number of m-nAChR at the NMJ, those w/ MG have an increased sensitivity to NDMR and a resistance to succinylchline.

IA cause skeletal m relaxation by acting in the ventral horn of the SC - in many cases this eliminates the need for NMB.

79
Q

WHy are patients w/ myasthenia gravis prone to aspiration?

A

bulbar m weakness (mouth and throat) manifests as difficulty handling oral secretions –> increased risk of aspiration

80
Q

describe the patho of Eaton Lambert syndrome

A

IgG mediated destruction of the presynaptic v-gated Ca++ channel at the presynaptic nerve terminal.

When the AP depolarizes the nerve terminal, Ca++ entry into the presynaptic neuron is limited, thereby reducing the amount of ACh that is released into the synaptic cleft.

Postsynaptic nAChR is normal

81
Q

compare and contrast myasthenic gravis to eaton-lambert syndrome in terms of patho, common comorbidities, and response to NMB

A

eaton-lambert

  • v-gated Ca++ channels
  • decreased ACh release
  • presynaptic neuron of NMJ
  • comorb: small cell lung CA
  • sensitive to NMB (both)
  • AChE inhibitors doesn’t improve symptoms

MG

  • Nm receptor (post)
  • decreased ACh response
  • postsynaptic motor endplate
  • comorb: thymoma
  • resistant to sux, sensitive to NDMR
  • AChE inhibitors improve symptoms
82
Q

describe the patho of Guillain-Barre syndrome.

A

characterized by an immunologic assault on the myelin in the peripheral nerves. The AP can’t be conducted –> the motor endplate never receives the incoming signal

usually persists for approx 2 weeks and ends w/ full recovery in approx 4 weeks.

83
Q

discuss the presentation of guillian-barre

A

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

s/s:

  • flaccid paralysis begins in the distal extremities and ascends bilat toward proximal extremities, trunk, face
  • intercostal m weakness impairs ventilation
  • facial, pharyngeal weakness causes dysphagia
  • sensory deficits: paresthesias, numbness, +/- pain
  • autonomic dysfunction is common: HR, BP, sweating abnormalities, orthostatic hypotension
84
Q

What is familial periodic paralysis and how can the 2 variants of this disease be distinguished from each other?

A

two distinct disease processes that are characterized by acute episodes of skeletal m weakness that is accompanied by hypo or hyperkalemia

hypokalemia: diagnosed if skeletal m weakness follows a glucose-insulin infusion
hyperkalemia: diagnosed if skeletal m weakness follows oral K+ administration

85
Q

What drugs should be avoided in the patient w/ each type of familial period paralysis? How about temperature?

A

hypokalemic: avoid:
- glucose containing slns
- K+ wasting diuretics
- B2 agonists

hyperkalemia avoid:

  • succinylcholine
  • K+ containing slns (LR)

acetazolamide is the tx for both forms bc it creates a nonanion gap acidosis, which protects against hypokalemia. It also facilitates renal K+ excretion which guards against hyperkalemia

avoid hypothermia for both types.

86
Q

detail the functions of the following receptors in skeletal m:

  • nicotinic
  • dihydropyridine
  • ryanodine
  • SERCA2

which is dysfunctional in the patient w/ MH?

A

when T-tubule is depolarized, extracellular Ca++ enters the myocyte via the dihydropyridine receptor at the T-tubule

this activates the ryanodine receptor (RYR1), which instructs the SR to release massive Ca++ into the cell. In the case of MH, it releases WAY TOO MUCH
(consumes ATP, O2, produces CO2)

cell attempts to return some Ca++ into the SR via the SERCA2 pump (in MH, this pump becomes overworked)
(consumes ATP, O2, produces CO2)

when the skeletal m consumes all of its ATP, cell membrane integrity is no longer maintained & intracellular components (myoglobin & K+) are released into the systemic circulation I

87
Q

list 8 consequences of too much Ca++ inside of the skeletal myocyte

A
  • sustained muscular contraction
  • accelerated metabolic rate & rapid ATP depletion
  • increased O2 consumption
  • increased CO2 & heat production
  • mixed respiratory and lactic acidosis
  • sarcolemma breaks down
  • K+ & myoglobin leak into the systemic circulation
  • rigidity from sustained contraction
88
Q

identify 3 conditions that are definitively linked to MH

A
  1. King-Denborough syndrome
  2. central core disease
  3. multiminicore disease

some texts list that Evans myopathy is also definitively linked to MH (not according to the MHAUS website)

89
Q

list 6 conditions that are NOT definitively linked to MH

A
  • Duchenne muscular dystrophy
  • Becker muscular dystrophy
  • neuroleptic malignant syndrome
  • myotonia congenita or dystrophy
  • osteogenesis imperfecta
90
Q

what is the most sensitive indicator of MH? What is the time course of the other s/s?

A

MH can occur as late as 6hrs after exposure to a triggering agent.

most sensitive: EtCO2 rises out of proportion to MV

early:
- tachycardia
- tachypnea
- masseter spasm
- warm soda lime
- irregular heart rhythm

intermediate:
- cyanosis
- pt warm to touch
- irregular heart rhythm

late:
- muscle rigidity
- cola-colored urine
- coagulopathy
- irregular heart rhythm

91
Q

what is the difference b/n trismus and MH? How should you proceed if the patients presents with either condition?

A

trismus & masseter m rigidity exist on a continuum

  • trismus: jaw can still be opened
  • masseter m rigidity: cannot open jaw

trismus is a normal response to succinylcholine - ok to proceed w/ surgery if occurring in isolation, but may want to avoid other triggering agents.
if the pt has masseter m rigidity, assume MH until proven otherwise
- as an aside, NMB will not help this since it’s occurring distal to the NMJ

92
Q

What is the definitive test for susceptibility to MH?

A

halothane contracture test

- it only has an 80% specificity, so there is a risk of false-negative result

93
Q

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

A

classified as a muscle relaxant.
two mechanisms of action:
- halts Ca++ release from the RyR1 receptor
- prevents Ca++ entry into the myocyte which reduces the stimulus for calcium induced calcium release.

the most common side effects are muscle weakness & venous irritation

94
Q

How is dantrolene formulated? How is it prepared?

A

each vial contains 20mg dantrolene + 3g mannitol & must be reconstituted w/ preservative free H2O

NaCl introduces additional solute which prolongs the time required for dantrolene to dissolve into the dilutent

enlist help early!!

95
Q

How do you treat MH?

A 
d/c triggering agent
100% FiO2 >10L/min
dantrolene 2.5mg/kg IV 
- repeat Q5-10mins
hyperventilate
correct lactic acidosis w/ bicarb
treat hyperK+
- CaCl 5-10mg IV 
- insulin 0.15U/kg + D50 1mL/kg
protect against dysrhythmias
- class I agents (lido, procain)
- avoid CCB w/ dantro to avoid hyperK+
maintain UOP
- IV hydration
- 0.25mg/kg mannitol
- 1mg/kg lasix
cool the pt until temp <38C
- cold IVF
- cold fluid lavage
- ice packs
monitor coags, avoid DIC
96
Q

describe the patho of Duchenne muscular dystrophy

A

dystrophin is a critical structural component of the cytoskeleton of skeletal and cardiac m cells. It helps anchor actin & myosin to the cell membrane. Absence of it destabilizes the sarcolemma during muscular contraction & increases membrane permeability

extrajunctional receptors populate –> avoid succinylcholine

classic teaching suggests that DM increases the risk of MH, but more recent meta analysis refutes this claim.

97
Q

How does Duchenne muscular dystrophy affect pulmonary function?

A

kyphoscholiosis (restrictive lung disease) –> decreased pulmonary reserve –> increased secretions & risk of PNA

respiratory muscle weakness also occurs

98
Q

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

A

cardiac considerations:

  • degeneration of cardiac m –> decreased contractility, pap m dysfunction, mitral regurg, cardiomyopathy, CHF
  • signs of cardiomyopathy = resting tachycardia, JVD, S3/S4 galllop
  • gold standard = echo

EKG changes

  • ST + short PR
  • scarring of posterobasal aspect of LV manifests as increased R wave amplitude in lead 1 & deep Q waves in the limb leads
99
Q

What is the Cobb angle and what is its significance?

A

describes the magnitude of the spinal curvature

40-50degrees = indication for surgery
60 = decreased pulmonary reserve
70 = pulmonary symptoms present
100 = gas exchange significantly impaired, higher risk of post-op pulmonary complications
100
Q

contrast the early & late complications of scoliosis

A

alters thoracic geometry, which compresses the lungs & creates a restrictive ventilatory defect. One side of the thorax becomes smaller than the other

early:
- restrictive ventilatory defect (same lung volume, capacity decreases as any)
- decreased chest wall compliance

late:
- VQ mismatching
- hypoxemia
- hypercarbia (sign of impending failure)
- pHTN
- reduced response to hypercapnia
- cor pulmonale
- cardiorespiratory failure

101
Q

List 3 ways that rheumatoid arthritis affects the airway.

A
  1. TMJ: limited mouth opening
  2. cricoarytenoid joints: decreased diameter of glottic opening
  3. cervical spine: A-O subluxation w/ flexion + limited extension
102
Q

What is the most common airway complication of rheumatoid arthritis? What’s it’s clinical significance?

A

AO subluxation is the most common airway complication of RA

This is d/t the weakening of the transverse axial ligament, which allows the odontoid to directly compress the SC at the level of the foramen magnum.

  • puts the pt at risk for quadriparesis or paralysis
  • side note: pts w/ Down syndrome are also at risk for AO subluxation
103
Q

Discuss the pathophysiology of RA.

A

autoimmune disease that targets the synovial joints. There is also widespread systemic involvement d/t infiltration of immune complexes in teh small & medium arteries –> vasculitis.

cytokines (TNF & interleukin-1) play a central role in the pathogenesis.

Hallmark of RA: morning stiffness that improves w/ activity
joints are painful, swollen, and warm

other symptoms:

  • weakness
  • fatigue
  • anorexia
  • lymph node enlargement
104
Q

using a systems approach, list the complications of RA.

A

airway:
- TMJ synovitis
- cricoarytenoid arthritis
- AO instability

pulmonary

  • pleural effusion
  • restrictive pattern d/t diffuse interstitial fibrosis + costochondral involvement that limits chest wall expansion

cardiac

  • pericardial effusion/tamponade
  • restrictive pericarditis
  • aortic regurgitation
  • valvular fibrosis
  • coronary artery arteritis

hematologic

  • anemia
  • platelet dysfunction d/t NSAIDs

renal
- renal insufficiency d/t vasculitis, NSAIds

endocrine
- adrenal insufficiency & infections d/t steroids

GI
- gastric ulcerations d/t NSAIDs, steroids

Eyes
- Sjogren’s syndrome - risk of corneal abrasion

PNS
- peripheral neuropathy d/t nerve entrapment

105
Q

describe the patho of systemic lupus erythematosus.

A

SLE is an autoimmune disease characterized by the proliferation of antinuclear Ab.
SLE affects nearly every organ system & most consequences are the direct result of Ab-induced vasculitis and tissue destruction

106
Q

Using a systems based approach, list the complications of systemic lupus erythematosus

A

targets young women
most common problems are polyarthritis (generally not the spine) & dermatitis

only 33-50% develop the “butterfly rash”

airway:
- cricoarytenoiditis: hoarseness, stridor, a/w obstruction
- RLN palsy

pulmonary

  • restrictive
  • pHTN
  • interstitial lung dz w/ impaired diffusing capacity
  • pleural effusion
  • recurrent PE

CV

  • pericarditis
  • Raynaud’s
  • HTN
  • conduction defects
  • endocarditis

hematologic

  • antiphospholipid Abs
  • hypercoagulability
  • anemia
  • thrombocytopenia
  • leukopenia

renal: nephritis w/ proteinuria

CNS: stroke

107
Q

what drugs can exacerbate SLE?

A

occurs d/t stress or drug exposure
drug induced usually persists for several weeks-months & presents w/ mild symptoms

most common offenders (PISSED CHIMP)
Pregancy
Infection
Surgery
Stress
Enalapril
D-penicillamine
Captopril
Hydralazine
Isoniazid
Methyldopa
Procainamide
108
Q

what is the relationship b/n SLE & antiphospholipid syndrome?

A

those w/ SLE are prone to developing antiphospholipid antibodies. Although aPTT is prolonged, these pts are prone to a state of hypercoagulability & thrombosis

  • risk for stroke, DVT, PT
  • pregnant pts are at higher risk
109
Q

Discuss the patho of myotonic dystrophy.

A

characterized by prolonged contracture after a voluntary contraction. This is the result of dysfunctional Ca++ sequestration by the SR. Contractions can be so severe that they interfere w/ ventilation & intubation

110
Q

What 3 things can increase the risk of contractures in the patient w/ myotonic dystrophy?

A
  1. succinylcholine
  2. reversal of NMB w/ anticholinesterases (theoretical)
  3. hypothermia (shivering –> sustained contractions)
111
Q

Discuss the patho of Marfan syndrome.

A

autosomal dominant trait
connective tissue disorder that’s associated w/ an elevated risk of aortic dissection, MV prolapse, mitral regurg, aortic regurg.

dissection of the ascending aorta can extend into the pericardium, and this increases the risk of cardiac tamponade. Becks’ triad: JVG, hypotension, muffled heart tones.

as an aside, spontaneous pneumo is a common complication in these patients.

112
Q

Discuss the patho of Ehlers-Danlos syndrome

A

inherited disorder of procollagen and collagen. There are several types, but only type IV is associated w/ vascular rupture (i.e. AAA)

increased bleeding tendency d/t lack of blood vessel integrity+ coagulopathy.

  • avoid RA
  • avoid IM injections
  • be careful during airway management & line placement.

PTX is also a common complication; avoid high PIP

APEXANESTHESIA COPY COPY (12 decks)

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