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Sarah's Apex > Neuro complete > Flashcards

Neuro complete Flashcards

1
Q

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

A

Astrocytes- most abundant of the glial cells, regulation of metabolic environment, repair neuron after neuronal injury

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

oligodendrocytes- Form the myelin 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 and 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

Mnemonic Oh OH OH to touch and feel a girls v. ahhh heavenly
1. Olfactory - sensory- smell
2. Optic - Sensory - vison
3. Oculomotor - Motor - Eye movement, pupil constriction
4. Trochlear - Motor - eye movement
5. Trigeminal - Both
* V1- ophthalmic- somatic sensation of face
* V2- maxillary - somatic sensation to anterior 2/3 of tongue
*V3- Mandibular- muscles of mastication
6. Abducens- Motor- Eye movement
7. Facial ( temporal, zygomatic, Buccal, Mandibular, cervical) - both- facial movement except mastication, eyelid closing
8. Vestibulocochlear (acoustic) - sensory- hearing and balance
9. Glossopharyngeal - both- Somatic Sensation and taste to posterior 1/3 of tongue, anterior of epiglottis
10. Vagus- Both- Swallowing
11. Accessory - Motor - Shoulder shrug
12. Hypoglossal - motor- tongue movement

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4
Q

which cranial nerve resides in the central nervous system? what is the implication of this?

A

With the exception of the optic nerve (CN2) all of the cranial nerves are part of the peripheral nervous system. This means that the optic n is the only cranial nerve that is surrounded by the dura.

because the optic nerve is part of the CNS, it is bathed by CSF. If you inject a local anesthetic into the optic nerve during regional anesthesia of the eye, you will have a big problem.

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5
Q

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

A

Tic douloureux (trigeminal neuralgia CN 5) causes excruciating neuropathic pain in the face

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6
Q

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

A

Bell’s palsy results from injury to the facial nerve (CN7). This causes ipsilateral facial paralysis.

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7
Q

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

A

The CSF cushions the brain, provides buoyancy, and delivers optimal conditions for neurologic function. It is located in the:
* Ventricles ( left lateral, right lateral, third, and fourth)
* Cisterns around the brain
* Subarachnoid space in the brain and spinal cord

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8
Q

What regions of the brain are NOT protected by the blood-brain-barrier?

A

The blood-brain barrier separates the CSF from the plasma. It has tight junctions that restrict passage of large molecules and ions

The BBB is not present at the chemoreceptor trigger zone. posterior pituitary gland, pineal gland, choroid plexus, and parts of the hypothalamus

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9
Q

What is the normal amount of volume and specific gravity of CSF?

A

CSF volume= 150mL
Specific gravity = 1.002-1.009

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10
Q

What is the production, circulation, and absorption of CSF?

A

CSF production: ependymal cells of the choroid plexus at a rate of 30mL/hr
Circulation: Remember- Love My 3 Silly 4 Lorn Magpies
Lateral ventricles- foramen of monroe- Third ventricle (site of production (choroid plexus)- Aqueduct of Sylvius, Fourth Ventricle site of production (choroid plexus)- Foramen of Luschka and Magendie- subarachnoid space (brain and spinal cord)
Reabsorption: venous circulation via the arachnoid villi in the superior sagittal sinus

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11
Q

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

A

CBF= CPP/Cerebral vascular resistance
Global = 45-55 mL/100g tissue/min or 15% of cardiac output
Cortical= 75-80 mL/100g tissue/min
Subcortical: 20mL/100g tissue/min

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12
Q

What are the 5 determinants of cerebral blood flow?

A
  1. Cerebral metabolic rate of oxygen (CRMO2)
  2. CPP
  3. Venous pressure
  4. PaCO2
  5. PaO2
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13
Q

What is the normal value for CRMO2? What factors cause it to increase? To decrease?

A

CRMO2 describes how much O2 the brain consumes per minute. The reference value is 3-8mL/O2/100g brain tissue/min
* Decreased by hypothermia (7% per 1 degree decrease), halogenated anesthetics, propofol, etomidate, and barbiturates
* increased by hyperthermia, seizures, ketamine, and nitrous oxide

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14
Q

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

A

CPP= MAP-ICP (or CVP), whichever is higher
The cerebrovasculature autoregulates its resistance (vessel diameter) to provide a constant cerebral perfusion pressure of 50-150mmHg
* this ensures a relatively stable blood flow and confers protection against swings in blood pressure.
* Autoregulation is influenced by products of local metabolism, myogenic mechanisms, and autonomic innervation

To ensure a CPP of 50mmHg, MAP must b 55-65 if ICP is in the normal range of 10-15mmHg.If ICP is increased, CPP will require a higher MAP.

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15
Q

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

A

0- 50mmHg Low= Max dilation: vessels are maximally dilated, CBF becomes pressure dependent, risk of cerebral hypoperfusion

50-150 mmHg Autoregulation: CBF is constant over a range of pressure

> 150mmHg Max constriction: CBF becomes pressure dependent, risk of cerebral edema and hemorrhage

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16
Q

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

A

A high venous pressure decreases cerebral venous drainage and increases cerebral volume. This creates a backpressure of the brain that reduces the arterial/venous pressure gradient (MAP-CVP), which means CPP decreases…
Conditions that impair venous drainage:
* jugular compression secondary to improper head positioning
* increased intrathoracic pressure secondary to coughing or PEEP
* Vena cava thrombosis
*Vena cava syndrome (blood flow is slowed ex pregnancy)

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17
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/100 g brain tissue/min

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18
Q

at what PaCO2 does maximal cerebral vasodilation occur? how bout maximal cerebral vasoconstriction?

A

for every 1 mmHg increase (or decrease) in PaCO2, CBF will increase (or decrease) by 1-2mL/100g brain tissue/min
* maximal vasodilation occurs at a paCO2 of 80-100 mmHg
* Maximal vasoconstriction occurs at a PaCO2 of 25mmHG

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19
Q

What is the relationship between CMRO2 and CBF?

A

As a general rule:
* things that increase the amount of O2 the brain uses (CRMO2) tend to cause cerebral vasodilation (increased CBF). Examples include hyperthermia or ketamine.
* things that decrease the amount of O2 the brain uses (CRMO2) tend to cause cerebral vasoconstriction (decreased CBF). Examples include hypothermia, propofol, and thiopental.

Halogenated anesthetics are an exception- they decouple the relationship between CRMO2 and CBF. Said another way, they reduce CMRO2, but they cause cerebral vasodilation. This explains why a patient with intracranial HTN is better served with TIVA.

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20
Q

How do acidosis and alkalosis affect CBF?

A

Respiratory acidosis increases CBF
Respiratory alkalosis decreases CBF
Metabolic acidosis or alkalosis do not directly affect cerebral blood flow. This is because H+ does not pass through the blood-brain barrier. A compensatory change in minute ventilation can, however, affect CBF.

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21
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 cerebral blood flow

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22
Q

What is the normal intracranial pressure? what values are considered abnormal?

A

Intracranial pressure is the supratentorial CSF pressure.

Normal ICP is 5-15 mmHg
cerebral HTN occurs if ICP >20

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23
Q

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

A

ICP measurement is indicated with a glasgow coma scale score < or equal to 7
An intraventricular catheter is the gold standard for ICP measurement. ICP can also be measured with a subdural bolt or a catheter placed over the convexity of the cerebral cortex.

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24
Q

List the signs and symptoms of intracranial HTN

A

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

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25
Q

Discuss the Monroe-Kellie Hypothesis

A

the brain lives in a rigid, bony box. within this box, there are three components: brain, blood and csf

the Monroe-Kellie hypothesis describes the pressure-volume Equilibrium between the brain, blood, and CSF within the confines of the cranium. It says that an increase in one of the components must be countered with a decrease in one or both of the others. If not, then the pressure inside the cranium will rise.

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26
Q

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

A

Cushing’s triad indicates intracranial HTN. It includes:
HTN, bradycardia, and irregular respirations
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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27
Q

Name 4 areas where brain herniation can occur

A

Brain herniation can occur at any of these 4 locations:
* 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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28
Q

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

A

CO2 dilates the cerebral vessels -> decrease cerebral vascular resistance -> increase CBF -> Increase ICP

Hyperventilation (PaCO2 30-35 mmHg) constricts the cerebral vessels -> Increase cerebral vascular resistance -> decrease cerebral blood flow -> decreased ICP

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

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29
Q

How do nitroglycerine and nitroprusside affect ICP?

A

These agents are cerebral vasodilators. By increasing CBF (volume of blood in the brain), they increase ICP

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30
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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31
Q

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

A

Osmotic diuretics (mannitol 0.25-1 g/kg) increases serum osmolarity and “pulls” water across the blood-brain barrier towards the bloodstream

  • if the 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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32
Q

Describe the anterior and posterior circulation of the brain. Where do these pathways converge?

A

The cerebral circulation can be divided into 2 separate circulations: anterior and posterior. They converge at the Circle of Willis.

Anterior Circulation:
* The internal carotid arteries supply the anterior circulation. They enter the skull through the foramen lacerum.
* Aorta-> carotid a-> internal carotid artery-> circle of willis-> cerebral hemispheres

Posterior circulation:
* the vertebral arteries supply the posterior circulation. They enter the skull through the foramen magnum.
* Aorta-> subclavian a-> vertebral a-> Basilar-> posterior fossa structures and cervical spinal cord

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33
Q

Describe the anatomy of the circle of Willis

A

The anterior and posterior circulations converge at the circle of willis. The 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 the other side should theoretically be able to perfuse the affected areas of the brain

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34
Q

Which population of stroke patients should receive a thombolytic agent?

A

The type of CVA must be determined prior to treatment because a thrombolytic should NOT be given to a patient with hemorrhagic stroke. Since the etiology of CVA cannot be determined by clinical criteria alone, the patient should receive an emergent non-contrast CT

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35
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.

Think about this when administering IV fluids that contain dextrose.

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36
Q

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

A

An increased transmural pressure predisposes the aneurysm to rupture. As the vessel bursts, blood flows into the subarachnoid space.

Tansmural pressure = MAP-ICP

We like to think of MAP as the pressure pushing outwards against the aneurysmal sac and ICP as the counter pressure that pushes against it. In essence, ICP creates a tamponade effect. Using this model, it’s easy to see that the risk of rupture is increased by HTN and/or an acute reduction in ICP (opening of the dura)

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37
Q

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

A

the most common in a patient with SAH is an intense headache that is often described as the “worst one in my life”

Consciousness is lost about 50% of the time, an other s/sx include focal neurologic deficits, N/V, photophobia, and fever. Meningismus (signs of meningitis) occurs as blood spreads throughout and irritates the subarrachnoid space. Furthermore, blood can block CSF flow, causing obstructive hydrocephalus and increasing ICP

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38
Q

What is the most significant source of Morbidity and mortality in the patient with SAH?

A

Cerebral vasospasm is a delayed contraction of the cerebral arteries. It can lead to cerebral infarction and is the most significant source of morbidity and mortality in the patient with SAH.

Free Hemoglobin that is in contact with the outer surface of the cerebral arteries increases the risk of vasospasm. Indeed, there is a positive correlation between the amount of blood observed on CT and the incidence of vasospasm

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39
Q

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

A

It occurs in about 25% of patients following SAH, and it’s most likely 4- 9 days following SAH

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40
Q

What is the tx for cerebral vasospasm?

A

Triple H therapy (hypervolemia, HTN, and hemodilution to HCT 27-32%) is the standard of care for vasospasm following SAH. Liberal hydration supports blood pressure and CPP. It also creates a state of hemodilution, which reduces blood viscosity and cerebrovascular resistance. Together these improve cerebral blood flow.

Nimodipine is the only calcium channel blocker shown to reduce morbidity and mortality associated with vasospasm. Interestingly, it does not actually relieve the spasm. But instead, it increases collateral blood flow.

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41
Q

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

A

Patients who undergo endovascular coiling require heparinization during the procedure.
If the aneurysm ruptures during the procedure, you should give protamine (1mg of protamine per 100 U of heparin given). MAP should be lowered into the low/normal range.
While it wasn’t cited in our references, adenosine can be given to temporarily arrest the heart, so the interventional radiologist can control the bleeding.

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42
Q

Calculate the Glasgow coma scale.

A

The GCS provides an objective of neurologic status. A GCS< 8 is consistent with traumatic brain injury.

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43
Q

how do you treat a patient 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 is not the best option for acute warfarin reversal

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44
Q

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

A

Clopidogrel, aspirin, or both can be reversed with platelet transfusion. There is also evidence of reversal with recombinant factor VIIa

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45
Q

What are 2 common ways of reducing ICP that should specifically be avoided in the patient with traumatic brain injury?

A

there are 2 things you should specifically avoid in the patient with TBI:
* Hyperventilation can worsen cerebral ischemia in patients with TBI. Hyperventilation is only indicated as temporary measure to acutely reduce ICP.
* Steroids worsen neurologic outcome

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46
Q

Is nitrous oxide safe in the patient with a traumatic brain injury?

A

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

Nitrous oxide can rapidly expand a pneumothorax or cause pneumocephalus. Do not use it in the patient with TBI.

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47
Q

Compare and contrast the 5 types of seizures

A

Grand mal- tonic clonic, resp arrest-> hypoxia, increased O2 consumption d/t increased brain activity and muscle contraction
* acute tx- propofol, diazepam, and thiopental
* surgical tx- vagal nerve stimulator or resection of foci

Focal cortical-Localized to a particular cortical region, can be motor or sensory, usually no loss of consciousness

Absence ( petit mal)- temporary loss of awareness (but remains awake), more common in children

Akinetic- temporary loss of consciousness and postural tone, can result in fall -> head injury, more common in children

Status Epilepticus- Seizure activity that lasts >30 min or 2 grand mal seizures without regaining consciousness in-between
Resp arrest-> hypoxia d/t O2 consumption increase
Acute tx- phenobarbital, thiopental, phenytoin, benzos, propofol, and even GA

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48
Q

What is the relationship between etomidate and seizures?

A

Etomidate commonly causes myoclonus (muscle jerk). This is not associated with increased EEG activity in patients that do not have epilepsy.

In patients with seizure disorders, etomidate (or methohexital or alfentanil) increases EEG activity and can be used to help determine the location of seizure foci during cortical mapping

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49
Q

Describe the pathophysiology of alzheimer’s disease.

A

Key findings include the development of diffuse beta amyloid-rich plaques and neurofibrillary tangles in the brain.
Consequences of plaque formation include:
* dysfunctional synaptic transmission. This is most noticeable in nicotinic Ach neurons.
* Apoptosis (programmed cell death)

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50
Q

What class of drugs is used to treat alzheimers disease? How do they interact with succinylcholine?

A

Tx for alzheimers dx is palliative and aims to restore the concentration of Ach. This is accomplished with cholinesterase inhibitors, such as tacrine, donepezil, rivastigmine, and galantamine.
Cholinesterase inhibitors increase the duration of action of succinylcholine, although the clinical significance of this is debatable.

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51
Q

Describe the pathophysiology of Parkinson’s dx.

A

the dopaminergic neurons in the basal ganglia are destroyed.
Decreased dopamine + normal acetylcholine= relative acetylcholine increase -> suppression of corticospinal motor system + overactivity of extrapyramidal motor system

classic triad is akinesia, rigidity and skeletal muscle tremor

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52
Q

What drugs increase the risk of extrapyramidal s/sx in the patient with Parkinson’s dx?

A

Drugs that antagonize dopamine should be avoided.
-metoclopramide
-Butyrophenones (haloperidol & droperidol)
-Phenothiazines (promethazine)

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53
Q

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

A

Corneal abrasion is the most common eye complication
Ischemic optic neuropathy is the most common cause of vision loss

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54
Q

Describe the pathophysiology of ischemic optic neuropathy

A

Venous congestion in the optic canal reduces perfusion pressure. Increased intraabdominal and/or intrathoracic pressure can also increase intraocular pressure
OPP = MAP- Intraocular pressure
the central retinal and posterior ciliary arteries are the highest risk because they are “watershed” areas- they lack anastomoses with other arteries. A rise in intraocular pressure can compress these vessels, which reduces oxygen delivery to the retina.

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55
Q

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

A

ION is most common after spinal surgery in the 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 sex, obesity, diabetes, HTN, smoking, old age atherosclerosis

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56
Q

Discuss the blood flow to the spinal cord

A

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

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57
Q

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

A

The artery of Adamkiewicz is the most important radicular artery.
Along with the anterior spinal artery, the artery of Adamkiewicz supplies the anterior cord in the thoracolumbar region. It most commonly originates between T11-T12

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58
Q

envision the anatomy of the spinal cord and spinal nerve cross-section

A

The spinal cord lines the peripheral nerves to the brain.
* sensory neurons enter from the periphery via the dorsal nerve root
* motor and autonomic neurons exit the ventral nerve root
Central canal: CSF pathway
White matter: axons and supporting cells
Grey matter: cell bodies
Ventral root: motor and autonomic
Dorsal nerve root: sensory

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59
Q

Describe the organization of the three neuron pathway common to the spinal tracts.

A

Each Pathway Consist of three neurons
* the first order neuron travels from the periphery to the spinal cord or brainstem
* the second order neuron travels from the spinal cord or brainstem to a subcortical structure
*the third order neuron links the subcortical structure to the cerebral cortex

60
Q

Compare and contrast the structure and function of the dorsal column with the spinothalamic tract

A

Dorsal column- medial lemniscal system:
* Transmits mechanoreceptive sensations: fine touch, proprioception, vibrations, and pleasure.
* Capable of two point discrimination- a high degree of localizing the stimulus.
* Consists of large, myelinated, rapidly conducting fibers
* Transmits sensory information faster than the anterolateral system
* think of this area as a more evolved system

Anterolateral system - spinothalamic tract:
* Transmits: pain, temperature, crude touch, tickle, itch, and sexual sensation
* two point discrimination is not present.
* consists of smaller, myelinated, slower conducting fibers
* think of this as a more primitive system

61
Q

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

A

The corticospinal tract is the most important motor pathway. THis is often referred to as the pyramidal tract. All of the other motor pathways outside of the corticospinal (pyramidal) tract are known collectively as the extrapyramidal tract.
The Babinksi test is a method to test the integrity of the corticospinal tract. A firm stimulus is applied to the underside of the foot yields the following responses:
Normal- downward motion of all the toes
upper motor neuron injury: upward extension of the big toe with fanning of the other toes
Lower motor neuron injury: no response

62
Q

How can you differentiate neurogenic shock from hypovolemic shock?

A

Neurogenic shock-> bradycardia, hypotension, hypothermia with pink, warm extremities (cutaneous vasodilation)

Hypovolemic shock-> tachycardia, hypotension, and cool, clammy extremities

63
Q

Discuss the use of succinylcholine in the patient with spinal cord injury

A

Succs should be avoided 24hrs after injury and should not be used for at least 6 months thereafter (some books say 1 year after)

64
Q

When does a patient with spinal cord 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. there is a return of spinal sympathetic reflexes below the level of injury, however, without inhibitory influences that would normally come from above the level of injury, the sympathetic reflexes below the level of injury exist in an overactive state. This places the pt at risk for autonomic hyperreflexia (mass reflex)

While up to 85% of pts with injury above T6 will develop AH, it is very unlikely to occur in patients with an injury below T10. The higher the level of injury, the more intense the response

65
Q

list 6 situations that can precipitate AH

A

Stimulation of the hollow organs -bladder, bowel, uterus
Bladder catheterization
surgery- especial cystoscopy or colonoscopy
bowel movement
cutaneous stimulation
childbirth

66
Q

Discuss the presentation and pathophysiology of autonomic hyperreflexia

A

the classic presentation is htn and bradycardia

Stimulation below the level of SCI triggers a sympathetic reflex arc that creates a profound degree of vasoconstriction below the level of injury. This activates the baroreceptor reflex in the carotid sinus, which slows heart rate. the body attempts to reduce afterload and vasodilation above the level of injury.

Other S/sx include:
*Reflex vasodilation above the level of spinal cord injury -> nasal stuffiness
*HTN-> Headache and blurred vision
*Malignant hypertension-> stroke, seizure, left ventricular failure, dysrhythmias, pulm edema, and/or myocardial infarction

67
Q

Detail the anesthetic management of the patient with AH.

A

even though the pt does not have sensation below the level of SCI, stimulation of the affected areas can elicit autonomic hyperreflexia- prevention is paramount!
* General or spinal anesthesia are the best options
* An epidural may be used for a laboring mother, however when compared to a spinal anesthetic, an epidural does not inhibit the sacral nerve roots to the same degree
* HTN is best treated with removal of the stimulus, deepening the anesthetic, and a rapid acting vasodilator, such as sodium nitropruside
* Bradycardia can be treated with atropine or glyco
* Administration of a positive chronotrope with vasoconstrictive properties will worse HTN
* adding lidocaine jelly to the cystoscope or foley catheter does not prevent AH
* Succinylcholine should be avoided for at least 6 months following SCI
* AH may present in the postoperative period as the effects of anesthesia wear off; close postoperative monitoring is warranted

68
Q

Discuss the pathophysiology of amyotrophic lateral sclerosis.

A

Amyotrophic lateral sclerosis (ALS) causes progressive degeneration of motor neurons in the corticospinal tract. Astrocytic gliosis replaces the affected motor neurons. Both the upper as well as the lower motor neurons are affected

the etiology is unknown.

69
Q

Detail the anesthetic management of ALS.

A
  • There is no evidence that supports a clear benefit of any particular anesthetic technique.
  • Succ’s can cause lethal hyperkalemia. Lower motor neuron dysfunction is associated with the proliferation of postjuctional nicotinic receptors.
  • There is increased sensitivity to nondeploarizing neuromuscular blockers
  • Bulbar muscle dysfunction increases the risk of pulmonary aspiration.
  • chest weakness reduces vital capacity and maximal minute ventilation
  • consider postoperative mechanical ventilation
70
Q

Describe the pathophysiology of myasthenia gravis

A

Myasthenia gravis is an autoimmune disease. IgG antibodies destroy post-junctional, nicotinic, acetylcholine receptors at the neuromuscular junction. Although Ach is present in sufficient quantity, there aren’t enough receptors to translate the extracellular signal into an intracellular response. This manifests as skeletal muscle weakness.
A key feature of myasthenia gravis is skeletal muscle weakness that becomes worse later in the day or that develops with exercise. Periods of rest allow for recovery of skeletal muscle function.

71
Q

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

A

The thymus gland plays a key role in MG, and thymectomy brings symptom relief to many pts.
* thymectomy reduces circulating Anti-ACHR IgG in most pts
* Surgical approach may be via median sternotomy or by the transcervical approach

72
Q

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

A

in 1/3 of women, pregnancy intensifies the symptoms of myasthenia gravis.
Anti-AchR IgG antibodies cross the placenta and cause weakness in 15-20% of neonates. this can persist up to 2-4 weeks, which is consistent with the half-life of the Anti-AchR IgG antibodies in the neonate’s circulation. These neonates may require airway management.

73
Q

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

A

Pyridostigmine (an anticholinesterase) is the first- line treatment for myasthenia gravis. An overdose can cause a cholinergic crisis, which can include skeletal muscle weakness. Since myasthenic crisis also presents with skeletal muscle weakness, it can be difficult to distinguish from a cholinergic crisis.

The diagnosis is made by administering 1-2 mg edrophonium, otherwise known as the “Tensilon test”
* If muscle weakness is made worse, then the patient has a cholinergic crisis (treatment = anticholinergics)
* if there is an improvement in muscle strength, then the patient had an exacerbation of myasthenic symptoms (treatment = anticholinesterase, immunosuppression, plasmapheresis)

74
Q

How do pts with myasthenia gravis respond to neuromuscular blockers?

A

Because there is a reduction in the number of nicotinic receptors (type-m) at the neuromuscular junction, patients with myasthenia gravis have an increased sensitivity to non-depolarizing NMBs and a resistance to succinylcholine.
Remember that volatile anesthetics cause skeletal muscle relaxation by acting in the ventral horn of the spinal cord. In many cases, this eliminates the need for neuromuscular blockers.

75
Q

Why are patients with myasthenia gravis prone to aspiration?

A

Bulbar muscle weakness (mouth and throat) manifest as difficulty handling oral secretions. This increases the risk of pulmonary aspiration.

76
Q

Describe the pathophysiology of Eaton-Lambert syndrome.

A

Eaton-Lambert syndrome is caused by IgG-mediated destruction of the presynaptic voltage-gated calcium channel at the presynaptic nerve terminal

When the action potential depolarizes the nerve terminal, Ca +2 entry into the presynaptic neuron is limited, thereby reducing the amount of Ach that is released into the synaptic cleft.

The postsynaptic nicotinic receptor is present in normal quantity and functions normally.

76
Q

Describe the pathophysiology of Eaton-Lambert syndrome.

A

Eaton-Lambert syndrome is caused by IgG-mediated destruction of the presynaptic voltage-gated calcium channel at the presynaptic nerve terminal

When the action potential depolarizes the nerve terminal, Ca +2 entry into the presynaptic neuron is limited, thereby reducing the amount of Ach that is released into the synaptic cleft.

The postsynaptic nicotinic receptor is present in normal quantity and functions normally

77
Q

Compare and contrast myasthenia gravis to Eaton- lambert syndrome in terms of pathophysiology,
Common co-morbidities, and response to neuromuscular blockers/reversals.

A

Eaton lambert / Myasthenia gravis
region aff. Ca channel / Nm receptor (post-syn)
defect: Decreased Ach / decreased response to Ach
NMJ aff: presynaptic neuron /post sy at motor endplate
Common co-mor: Small cell carcinoma / Thymoma
succs : sensitive / resistant
NDMBs: sensitive / sensitive
AchE inhibitors: Poor / Adequate

78
Q

Describe the pathophysiology of Guillain-Barre syndrome

A

Guillain-Barre Syndrome (acute idiopathic polyneuritis) is characterized by an immunologic assault on myelin in the peripheral nerves. The action potential can’t be conducted, so the motor endplate never receives the incoming signal

it usually persist for approx. 2 weeks and ends with full recovery in approx 4 weeks

79
Q

Discuss the presentation of guillain-barre syndrome.

A

A flue- like illness usually precedes paralysis by 1-3 weeks.

S/sx include:
*Flaccid paralysis begins in the distal extremities and ascends bilaterally towards the proximal extremities, trunk, and face.
* intercostal muscle weakness impairs ventilation
* facial and pharyngeal weakness causes difficulty swallowing
*sensory deficits include: paresthesias, numbness, and/or pain.
* Autonomic dysfunction is common: tachycardia or bradycardia, htn or hotn, diaphoresis or anhidrosis, and orthostatic hotn.

80
Q

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

A

Familial periodic paralysis are two distinct disease processes that are characterized by acute episodes of skeletal muscle weakness that is accompanied by either hypo- or hyperkalemia

*hypokalemic periodic paralysis- is diagnosed if skeletal muscle weakness follows a glucose-insulin infusion. the patient becomes weak after the serum K + is reduced. Associated with calcium channelopathy.
*Hyperkalemia periodic paralysis- is diagnosed if skeletal muscle weakness follows oral potassium administration. The patient becomes weak after the serum K+ is increased. Sodium Channelopathy.

81
Q

What drugs should be avoided in the patient with each type of familiar periodic paralysis? How about temperature?

A

Acetazolamide is the tx both forms of this disease. It creates a non-anion acidosis, which protects against hypokalemia. It also facilitates renal potassium excretion, which guards against hyperkalemia.

  • Avoid hypothermia for both hypo- and hyperkalemic periodic paralysis!
         Hypokalemic                                 Hyperkalemic
  Don't: glucose containing solutions          Succ's           
 K+ wasting diuretic / K+ containing solutions (LR)
     Beta 2 agonists                                     
             Succs

Safe: NDMBs / glucose containing solutions
Acetazolamide / K wasting diuretics
/ Beta 2 agonists
/ NDMBs
/ Acetazolamide

82
Q

Detail the functions of the following receptors in skeletal muscle: nicotinic dihydropyridine, ryanodine, and SERCA2. Which is dysfunctional in the patient with Malignant hyperthermia?

A

when the T-tubule is depolarized (Ach binds to nicotinic receptor at the NMJ), extracellular Ca2+ enters the myocyte via the dihydropyridine receptor at the T-tubule.

This activates the defective ryanodine receptor (RYR1), which instructs the sarcoplasmic reticulum to release way too much calcium into the cell. You can think of RYR1 receptor as a Ca2+ faucet that can’t be turned off. Not only is there more Ca2+ to engage with the contractile elements, but the cell attempts to return the excess Ca+2 to the SR via the SERCA2 pump. Both processes consume a substantial amount of ATP, increase oxygen consumption, an increase CO2 production.

When the skeletal myocyte consumes all of its ATP, there is no ATP available to maintain the integrity of cell membranes. As a consequences, they break down and intracellular components (myoglobin and K+) are released into the systemic circulation.

83
Q

list 8 consequences of too much Ca 2+ inside the skeletal myocyte

A
  • sustained muscle contraction
  • Accelerated metabolic rate and rapid depletion of ATP
  • increased oxygen 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
84
Q

Identify 3 conditions that are definitively linked to MH.

A

MH is definitively lined to only three other co-existing diseases:
1. King-Denborough syndrome
2. Central core disease
3. Multiminicore disease

some texts say Evan myopathy as the third disease, not nagelhout

85
Q

list 6 conditions that are NOT definitively linked to MH

A
  1. Duchenne muscular dystrophy
  2. Becker muscular dystrophy
  3. neuroleptic malignant syndrome
  4. Myotonia congenita
  5. Myotonic dystrophy
  6. Osteogenesis Imperfecta

Duchenne muscular dystrophy is associated with an MH-like condition characterized by rhabdomylosis. It is possible that halogenated agents and succs can initiate this MH-like syndrome in the patient with DM, so it is prudent to avoid these agents. Dantrolene does not treat this condition

86
Q

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

A

The most sensitive indicator is an EtCO2 that rises out of proportion to minute ventilation. MH can occur as late as 6 hours after exposure to a triggering agent

Early: tachycardia, tachypnea, masseter spasm, warm soda lime, irregular heart rhythm

Intermediate: cyanosis, irregular heart rhythm, patient warm to touch

Late: muscle rigidity, cola-colored urine, coagulopathy, irregular heart rhythm, overt hyperthermia

87
Q

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

A

Trismus and masseter muscle rigidity are two entities that exist on a continuum.

  • trismus describes a tight jaw that can still be opened
  • masseter muscle rigidity describes a jaw that cannot be opened

Trismus is a normal response to succinylcholine, so it’s ok to proceed with surgery if trismus occurs in isolation. Even so, it’s probably wise to convert to a non-triggering agent

Masseter muscle rigidity complicates airway management. Spasm is due to increased Ca+ in the myoplasm. Since this site of action is distal to the neuromuscular junction, a neuromuscular blocker will not relax the jaw. If the patient experiences masseter muscle rigidity, assume MH until proven otherwise.

88
Q

What is the definitive test for susceptibility to malignant hyperthermia?

A

Anyone who has experienced MH or masseter spasm should be referred for a halothane contracture test for diagnosis. Although this is the definitive test for diagnosis, it only has an 80% specificity, so there is a risk of a false negative result.

89
Q

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

A

Dantrolene is classified as a muscle relaxant. It has two mechanisms of action:
* it halts Ca2+ release from the RyR1 receptor
* It prevents Ca2+ entry into the myocyte, which reduces the stimulus for calcium-induced calcium release

the most common side effects are muscle weakness and venous irritation

90
Q

How is dantrolene formulated? How is it prepared?

A

Each vial contains 20mg of dantrolene + 3g of mannitol. The vials must be reconstituted with preservative-free water.
NaCl introduces additional solute, which prolongs the time required for dantrolene to dissolve into the diluent. Coming from someone who has experience with this, mixing dantrolene is a chore. Enlist help early. Warming the diluent will make the process much faster

91
Q

How do you treat MH?

A
  • Discontinue the triggering agent
  • Call for help
  • Administer 100% oxygen at >10L/min
  • Administer dantrolene (or ryanodex) 2.5mg/kg IV and repeat q5-10 min.
  • Correct lactic acidosis w/ sodium bicarbonate
  • Treat hyperkalemia (CaCl 5-10 mg/kg IV and insulin 0.15units/kg + D50 1mL/kg)
  • protect against dysthymias (class 1 agents: lidocaine 2mg/kg or procainamide 15mg/kg)
  • Maintain urine output (IV hydration, mannitol 0.25g/kg, furosemide 1mg/kg)
  • Cool the patient until the temperature drops below 38 decrees C (cold IVF, cold fluid lavage, ice packs)
  • Monitoring coagulation (DIC is a late complication and signals impending demise)
  • calcium channel blockers should not be given with dantrolene because dangerous hyperkalemia will result
92
Q

Describe the pathophysiology of Duchenne Muscular Dystrophy.

A

(Psuedohypertorphic muscular dystrophy) Dystrophin is a critical structural component of the cytoskeleton of skeletal and cardiac muscle cells. It helps anchor actin and myosin to the cell membrane. The absence of dystrophin destabilizes the sarcolemma during muscle contraction and increases membrane permeability. The affected skeletal muscle appears hypertrophic due to fatty infiltration.

The absence of dystrophin allows extrajunctional receptors to populate the sarcolemma. This predisposes these patients to hyperkalemia following succinylcholine administration. Indeed, succinylcholine sports a black box warning in details the risk of cardiac arrest and sudden death secondary to hyperkalemia in children and undiagnosed skeletal muscle myopathy. Classic teaching suggests that DM increases the risk of malignant hyperthermia, however, a more recent meta-analysis refutes this claim.

93
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

94
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, and congestive heart failure.
* signs of cardiomyopathy include resting tachycardia, jugular venous distension, S3/S4 gallop, and displacement of the point of maximal impulse.
* the gold standard of cardiac evaluation is an echocardiogram

EKG changes:
Impaired cardiac conduction -> sinus tachycardia and short PR interval
* Scarring of the posterobasal aspect (black/bottom) to the left ventricle as increased R wave amplitude in lead 1, and deep Q in the limb leads

95
Q

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

A

the cobb angle describes the magnitude of the spinal curvature
Cobb angle (degrees)
40-50 : indication for surgery
60: decreased pulmonary reserve
70: pulmonary symptoms present
100: gas exchange significantly impaired. Higher risk postoperative pulmonary complications

96
Q

Contrast the early and late complications of scoliosis.

A

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

Early: Restrictive ventilatory defect- FEV1 and FRC are decreased, FEV1/FVC ratio is normal
* decreased lung volumes and capacities: VC, TLC, FRC, RV
(Decreased chest wall compliance)

Late: V/Q mismatching, hypoxemia, hypercarbia (sign of impending respiratory failure), Pulmonary HTN, Reduced response to hypercapnia, Cor Pulmonale, Cardiorespiratory failure

97
Q

List 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)
98
Q

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

A

Antlantoaxial subluxation is the most common airway complication of RA.

this is due to weakening of the transverse axial ligament, which allows the odontoid to directly compress the spinal cord at the level of the foramen magnum. The patient is at risk for quadriparesis or paralysis

As an aside, patients with Down Syndrome are also at risk for AO subluxation

99
Q

Discuss the pathophysiology of rheumatoid arthritis

A

Rheumatoid arthritis is an autoimmune disease that targets the synovial joints. There is 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 a central role in the pathogenesis of RA.

The hallmark of RA is morning stiffness that generally improves with activity. The joints are painful, swollen, and warm. Other symptoms include weakness, fatigue, and anorexia. Lymph node enlargement in the cervical, axillary, and epitrochlear regions may be noted as well. This condition is 2-3 times more common in women.

100
Q

Using as systems approach, list the complications of rheumatoid arthritis.

A

eyes: sjogrens syndrome- risk of corneal abrasion
Airway: TMJ synvoitis- limited mouth opening, cyrcoarytenoid arthritis- narrow glottic opening, AO instability- risk of spinal cord and vertebral a. compression
Nervous system: peripheral neuropathy due to nerve entrapment
Endocrine: adrenal insufficiency and infections due to chronic steroid therapy
Renal: renal insufficiency due to - vasculitis and NSAIDS
Pulmonary: Pleural effusion, restrictive ventilatory pattern - diffuse interstitial fibrosis, costochondral involvement limits chest wall expansion
Cardiac: pericardial effusion or tamponade, restrictive pericarditis, aortic regurgitation, valvular fibrosis, coronary artery arteritis, dilation of aortic root
GI: NSAIDs, Steroids
Hematologic: anemia, platelet dysfunction secondary to NSAIDs

101
Q

Describe the pathophysiology of systemic lupus erythematosus.

A

Systemic lupus erythematosus is an autoimmune disease characterized by the proliferation of antinuclear antibodies. SLE affects nearly every organ system, and most of the consequences are the direct result of antibody-induced vasculitis and tissue destruction

102
Q

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

A

SLE is a disease that targets young women (approx 1:1000). The most common problems of SLE are polyarthritis and dermatitis. Arthritis can affect any joint, but it generally does not involve the spine.
Only 33-50% of theses pts develop the malar “butterfly” rash.
Airway: crycoarytenoiditis-> hoarseness, stridor, and airway obstruction
Nervous system: stroke, psychosis/dementia, peripheral neuropathy
Renal: nephritis with proteinuria
Pulmonary: Restrictive ventilatory defect, pulmonary HTN, Interstitial lung dx impaired diffusing capacity, pleural effusion, recurrent pulm emboli
Cardiac: pericarditis (tamponade is uncommon), raynaud’s phenomenon, HTN, conduction defects, endocarditis
Hematologic: Antiphospholipid antibodies, hypercoagulability, anemia, thrombocytopenia, leukopenia

103
Q

What drugs can exacerbate SLE?

A

Exacerbation of SLE can occur as a result of stress or drug exposure. Drug induced lupus generally persists for several weeks to months and presents with mild symptoms of arthralgia, anemia, leukopenia, and fever. Here are the most common offenders: PISSED CHIMP
P: Pregnancy
I: infection
S: surgery
S: stress
E: enalapril
D: D-Penicillamine
C: Captopril
H: Hydralazine
I; Isoniazid
M: Methyldopa
P: Procainamide

104
Q

What is the relationship between SLE and antiphospholipid syndrome?

A

Patients with SLE are prone to developing antiphospholipid antibodies. Although aPTT is prolonged, these patients are prone to a state of hypercoagulability and thrombosis. They are at risk for stroke, DVT, and pulmonary embolism.
Pregnant patients with SLE are at higher risk.

105
Q

Discuss the pathophysiology of myotonic dystrophy

A

Myotonic dystrophy is characterized by a prolonged contracture after a voluntary contraction. This is the result of dysfunctional calcium sequestration by the sarcoplasmic reticulum. Contractions can be so severe that they interfere with ventilation and intubation.

106
Q

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

A
  • Succinylcholine
  • Reversal of NMB with anticholinesterases (theoretical)
  • hypothermia (shivering -> sustained contractions)
107
Q

Discuss the pathophysiology of Marfan Syndrome.

A

Marfan syndrome is an autosomal dominant trait (not acquired). It is a connective tissue disorder that’s associated with an elevated risk of aortic dissection, mitral valve prolapse, mitral regurgitation, and aortic insufficiency.
Dissection of the ascending aorta can extend into the pericardium, an this increases the risk of cardiac tamponade. Remember Beck’s Triad? (JVD, HoTN, and muffled heart tones)
As an aside, spontaneous pneumothorax is a very common complication in the patient with Marfan syndrome

108
Q

Discuss the pathophysiology of Ehlers-Danlos syndrome

A

Ehlers-Danlos syndrome is an inherited disorder of procollagen and collagen. There are several types, but only type IV is associated with blood vessel rupture (think AAA).

Arguably the most important thing to remember about Ehlers-Danlos syndrome is that there is an increased bleeding tendency. This is the result of a lack of blood vessel integrity and not coagulopathy. Since hematoma is a common complication, we tend to avoid regional anesthesia and IM injections. Invasive line placement or trauma during airway management poses a threat as well.

Pneumothorax is also a common complication, so be careful with the peak inspiratory pressure

109
Q

what type of CNS cell is most prone to brain tumors?

A

Glial cell

110
Q

What are the 3 anatomic structures of the brainstem?

A

Midbrain
Pons
Medulla oblongata

111
Q

what cranial nerve is part of the CNS?

A

CN 2- Optic nerve

112
Q

Tic douloureux affects which cranial nerve?

A

Trigeminal nerve CN5

113
Q

where in the brain is the blood-brain barrier NOT present?

A

Chemoreceptor trigger zone
hypothalamus
pineal gland
posterior pituitary gland
choroid plexus

114
Q

Maximal cerebral constriction and vasodilation occur at a PaCO2 of?

A

PaCO2 of 25mmhg and 80-100 mmHg

115
Q

What are the 5 determinants of cerebral blood flow?

A

Cerebral metabolic rate of oxygen
cerebral perfusion pressure
PaCO2
PaO2
Venous pressure

116
Q

The brain autoregulates cerebral blood flow between a cerebral perfusion pressure of:

A

50-150mmHg

117
Q

Most common site of transtentorial herniation and what nerve can be injured?

A

The temporal uncus and oculomotor nerve (CN3) causing fixed pupil dilation

118
Q

7 signs/sx of increased ICP

A

Headache
N/V
Papilledema-optic disc edema
neuro deficit
pupil dilation and non-reactivity to light
altered LOC
seizure

119
Q

What is the diagnostic criteria for intracranial HTN

A

ICP>20mmHg

120
Q

Nitroprusside effects on vasculature

A

Reduces Systemic BP, and dilates cerebral vasculature and increases CBF and ICP

121
Q

D5 LR effects on the brain with high ICP

A

in the setting of cerebral ischemia, excess glucose in the brain is converted to lactic acid, thereby worsening outcomes

122
Q

Donepezil, tacrine, rivastigmine, and galantamine are what kind of medications and what are they used for?

A

cholinesterase inhibitors meds, used for alzheimers

123
Q

Arterial bleeding occurs most commonly between what two layers?

A

Arachnoid and pia mater

124
Q

Central nervous system: nuclei
peripheral nervous system: ?

A

Ganglia

Nuclei are clusters of neuronal cell bodies that exist in the CNS. Ganglia are clusters of cell bodies that exist in the peripheral nervous system

125
Q

which spinal tract is monitored by somatosensory evoked potentials?

A

Dorsal column- sensory pathway of spinal cord
common nerves used: median, and posterior tibial

paraplegia can still occur, since it is not monitoring motor.

126
Q

Loss of somatosensory evoked potentials during spinal fusion is MOST likely due to interruption of the:

A

Posterior spinal artery.

Posterior spinal arteries (2):
* Supply the sensory pathways (1/3 of cord)
* SSEPs monitor this region

Anterior spinal artery
* Supplies the motor pathways (anterior 2/3 of cord)
* MEPs monitor this region

127
Q

Prolonged aortic cross clamp time is MOST likely to result in loss of:

A

Movement and bowel control

others: loss of temperature and pain sensation
bladder dysfunction

proprioception and touch remain intact

128
Q

which region of the spinal cord is MOST commonly injured in a traumatic accident?

A

cervical, 55% of the time

Know the 6 P’s of suspected spinal cord injury:
* Paralysis
* Pain
* paresthesia
* Priapism (prolonged erection without sexual contact)
* Ptosis (may indicate C-spine injury)
* Position (holding head upright, raising arms over head, or prayer position/arms folded across chest may indicate c-spine injury)

most common cause of death from SCI are respiratory failure and aspiration of gastric contents

129
Q

Anesthetic considerations of osteogenesis imperfecta

A

it is an autosomal dominant disease of the connective tissue. It effects the bone, sclera, and the inner ear.
* dysfunctional collagen production leads to brittle bones, so careful positioning is a must. Fractures can even occur during NIBP inflation or following fasciculations caused by Succ’s!
* a difficult airway is the result of reduced cervical ROM and extremely high risk of fractures to the c-spine and mandible
* Kyphoscoliosis and pectus excavatum (sunken chest) reduce chest wall compliance and vital capacity (not hyperinflated lungs). In turn, this sets the stage for V/Q mismatching, thereby increasing the incidence of arterial hypoxemia.
* Serum thyroxine is increased in >50% of the patients with osteogenesis imperfecta. This increases oxygen consumption, which may lead to hyperthermia. The risk of MH is NOT increased.
* Interestingly, this pt can present with blue sclerae which are easily fractured.

130
Q

according to the FDA black box warning, succ’s administration to children may cause:

A

rhabdomyolysis

(not MH)

131
Q

What are the MOST important anesthetic considerations for scleroderma?

A

Epistaxis, Pulm HTN, renal insufficiency

Scleroderma causes excessive fibrosis in the skin and organs. Microvascular involvement affects many organs in the body.

  • Airway: Skin fibrosis -> limits mouth opening and mandibular mobility
  • Lungs: pulmonary fibrosis and pulmonary HTN
  • Heart: Dysrhythmias and CHF
  • Blood vessels: Decreased compliance -> HTN
  • Kidneys: Renal failure and renal artery stenosis-> HTN
  • Peripheral and cranial nerves-> nerve entrapment by tight connective tissue -> neuropathy
  • Eyes -> dryness predisposes to corneal abrasion

some pts with scleroderma develop CREST syndrome menmonic (Calcinosis, Raynaud’s phenomenon, Esophageal hypomotility, Sclerodactyly, Telangiectasia (spider veins))

132
Q

Which statements are true regarding acute idiopathic polyneuritis?

A

Epstein- Barr is a common etiology
There is an exaggerated response to ephedrine
Succ’s should be avoided

(guillian barre syndrome)
Most common culprits are Campylobacter jejuni bacteria, epstein-barr virus, and cytomegalovirus. Other causes are vaccinations, surgery, and lymphomatous disease.

flaccid paralysis begins distal and ascends bilaterally

avoid succ;s due to hyperkalemia risk from proliferation of extrajunctional Ach receptors

There is an exaggerated response to indirect acting sympathomimetics (ephedrine) due to upregulation of postjunctional adrenergic receptors

Steroids are not useful

133
Q

which diseases are associated with vasculitis?

A

SLE and RA

134
Q

Paget’s disease

A

associated with excess osteoblastic (bone synthesis) and osteoclastic (bone reabsorption) activity that causes abnormally thick, but weak, bone deposits. IT’s caused by excessive parathyroid hormone or calcitonin deficiency. No vascular involvement.

135
Q

Glycogen storage diseases

A

inherited conditions with defective enzymes responsible for glycogen synthesis and metabolism. > 12 kinds. The major clinical features of GSD are metabolic acidosis, hypoglycemia, and cardiac and hepatic dysfunction (due to accumulated glycogen disrupting normal tissue)

Type V McArdle glycogen build up in skeletal muscle leads to exercise intolerance, muscle cramping, and episodic myoglobinuria. Severe lactic acidosis can occur in stressful situations . There is typically no hepatic involvement in Type V GSD

Type I Von Gierke is caused by a defect in glucose-6-phosphatase, the enzyme that catalyzes the breakdown of G-6-phosphate to glucose. Type Ia is the most severe with features including short stature, hepatomegaly, developmental delay, failure to thrive, osteoporosis, and inflammatory bowel disease, among others

*** increases risk of MH

136
Q

In a pt with scoliosis, what is the threshold value for predicted forced vital capacity that indicates the need for postoperative ventilation?

A

40% is strongly suggested that planning for postoperative ventilation is warranted. Preop FVC less than 30 to 35% is associated with prolonged postoperative ventilation.

137
Q

Which components of the central nervous system degenerate in amyotrophic lateral scerlosis?

A

Alpha motor neurons in anterior horn in spinal cord and Descending upper motor neurons or corticospinal tract

Both upper and lower motor neurons degenerate in ALS. Spasticity and hyperreflexia are cardinal signs of upper motor neuron involvement

Degeneration of neurons in the pars compacta leads to parkinsons disease

138
Q

Choreiform movement is due to an excess of which neurotransmitter in the basal ganglia?

A

dopamine

Huntington’s disease is an autosomal dominant inherited dx. resulting in degeneration of the basal ganglia, neuronal death, and altered GABA, dopamine, and glutamate signaling in the cortex.
(Excessive cystosine-adenine-guanine)
presenting sign is considered chorea (rapid, jerky, involuntary movement), it may be preceded by behavior changes (depression, aggression, mood swings, and dementia). Bulbar dysfunction is common, increasing the risk of respiratory complications and aspiration.

139
Q

Multiple sclerosis

A

autoimmune dx of the central nervous system which results in inflammation, demyelination, and axonal injury. Demyelination and denervation result in limb weakness and the proliferation of extrajunctional acetylcholine receptors (referred to as fetal or immature)

The extrajunctional ACh receptors, when depolarized, have a 2 to 10 times longer open channel time during which potassium exits the cells according to its concentration gradients (inside»»>outside). With use of Succ’s abnormal amts of K is released and may precipitate hyperkalemic cardiac arrest.

140
Q

A patient with poorly controlled epilepsy is under general anesthesia with muscle paralysis. What signs may indicate seizure activity?

A

Abrupt onset of tachycardia and BP
increasing ET CO2

141
Q

Signs and symptoms of serotonin syndrome

A

Hyperthermia
Brisk reflexes
clonus

Life threatening drug induced syndrome following the administration of serotonergic drugs, stimulating the 5HT-1A and 5HT-2A receptors. THe syndrome generates autonomic hyperactivity (HTN, tachycardia, tachypnea, hyperthermia, and diaphoresis), neuromuscular hyperactivity (tremors, clonus, and muscle rigidity), and changes in neurologic function (agitation, anxiety, disorientation, and excitement)

142
Q

Lithium

A

Associated with decreased tubular response to ADH
Impaired parathyroid hormone secretion

Lithium decreases the tubular response to ADH and can cause increases or decreases in sodium levels. Lithium also impairs PTH release, which can lead to hypocalcemia. For these reasons, a full electrolyte panel should be evaluated in these pts. Due to its narrow therapeutic index, lithium level is also recommended (normal 0.8 to 1.2 mEq/L)

Thiazide diuretics increase lithium reabsorption, thus increasing the risk of toxicity. Loop diuretics are preferred as they do not promote these effects. NSAIDs and ACEI’s can also increase the risk of toxicity

Lithium is associated with decreased anesthetic requirement and prolongs neuromuscular blockade. Lithium is monovalent alkali cation- just like sodium and potassium. It appears to mimic sodium at several cellular membrane pumps, including the nephron (where Na reabsorption occurs) and in excitable cells (where it can replace Na).

143
Q

what are the effects of a intracranial tumor on cerebral autoregulation?

A

Autoregulatory responses are abolished
blood flow becomes pressure-dependent

144
Q

Charcot-Marie- Tooth

A

hereditary motor- sensory neuropathy caused by mutation of the genes responsible for myelin production. It is characterized by slow and progressive muscle weakness, atrophy, and loss of sensation in the lower extremities

145
Q

Depression is thought to be caused by:

A

Norepinephrine and serotonin

decreased available NE and 5 HT neurotransmitters have been associated with clinical depression. Tx is largely based on increasing the availability of these neurotransmitters by inhibiting reuptake processes SSRIs, SNRIs, NDRIs

Sarah's Apex (14 decks)

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