Apex Unit 7 Neuro Flashcards
Match each glial cell with its physiologic function. Astrocytes Microglia Oligodendrocytes Ependymal cells
Increase neuronal conduction velocity
Phagocytosis
CSF production
Metabolic support to neurons
Astrocytes + Metabolic support to neurons
Ependymal cells + CSF production
Microglia + Phagocytosis
Oligodendrocytes + Increase neuronal conduction velocity
There are four types of glial cells in the central nervous system.
Astrocytes provide metabolic support to the neurons
Ependymal cells are involved in CSF production
Microglia act as macrophages and phagocytize neuronal debris
Oligodendrocytes form the myelin sheath and increase conduction velocity
*Note that Schwann cells form the myelin sheath in peripheral nerves.
Match each brain lobe with its function.
Frontal + Motor cortex
Occipital + Vision
Parietal + Sensation
Temporal + Audition
The cerebral cortex is divided into four lobes.
Frontal + Motor cortex Occipital + Vision Parietal + Sensation Temporal + Audition Try and find ways to relate this to other areas. In this case, you may think about evoked potentials or perhaps the spinothalamic tract. Always look for ways to build connections between topics.
Which cranial nerve is MOST likely to be compressed by a pituitary tumor?
Facial
Oculomotor
Olfactory
Optic
Optic
The optic nerve runs in very close proximity to the pituitary gland. A pituitary tumor can compress the optic nerve, resulting in visual changes.
Regarding cerebrospinal fluid dynamics, match the corresponding items.
Site of CSF production + Choroid plexus
Site of CSF reabsorption + Arachnoid villi
Pathway between lateral and third ventricle + Foramen of Monro
Pathway between third and fourth ventricle + Aqueduct of Sylvius
Know the pathway of CSF from its site of production to its site of absorption.
A fixed and dilated pupil suggests herniation of the:
choroid plexus.
cerebellar tonsils.
temporal uncus.
cingulate gyrus.
Temporal uncus
The Monro-Kellie doctrine states that the brain, blood, and CSF are relegated to the confines of the cranium. If there is an increase in any one of these constituents, there must be a reduction in one or both of the others. If not, the pressure inside the cranium will rise.
The risk of elevated ICP is cerebral herniation, and the most common site of transtentorial herniation is at the temporal uncus. As ICP rises, the temporal uncus is forced from the supratentorial space into the infratentorial space. This increases pressure on the midbrain.
Since the oculomotor nerve (CN III) originates from the midbrain and crosses near the tentorium, herniation of this region puts pressure on and causes ischemia to CN III. Clinically this manifests as a fixed and dilated pupil.
Anesthetic management for the patient with an ICP of 25 mmHg undergoing craniotomy for tumor resection includes: (Select 3.)
PaCO2 30 mmHg. dexamethasone. nitroprusside. phenylephrine. D5LR. PEEP 10 mmHg.
Dexamethasone
Phenylephrine
PaCO2 30 mmHg
This patient has an elevated ICP and is at risk for cerebral ischemia. Anesthetic management is tailored to reduce ICP while preserving CPP.
Hyperventilation (PaCO2 30-35 mmHg) constricts the cerebral vessels, decreases cerebral blood volume, and reduces ICP. Dexamethasone reduces swelling around the tumor (it does not shrink the actual tumor). Phenylephrine is used to support CPP.
That patient has an elevated ICP (25 mmHg), so we don’t want to do anything that might increase it further. Although nitroprusside reduces systemic blood pressure, it dilates the cerebral vasculature and increases CBF and ICP. D5LR contains glucose and in the setting of cerebral ischemia, excess glucose in the brain is converted to lactic acid, thereby worsening outcome. PEEP increases intrathoracic pressure and reduces venous outflow away from the brain.
The following vascular structures exist as pairs EXCEPT the: vertebral artery. basilar artery. middle cerebral artery. posterior communicating artery.
Basilar artery
There is only one basilar artery. It is the main blood supply to the brain’s posterior circulation.
The basilar artery gives rise to the paired posterior communicating arteries.
The subclavian arteries give rise to the paired vertebral arteries.
The internal carotid arteries give rise the paired middle cerebral arteries.
Within how many hours can IV recombinant tissue plasminogen activator be given after a patient exhibits symptoms of an acute ischemic stroke?
(Enter your answer in hours)
Three hours
tPA must be given within three hours of the onset of symptoms.
Prevention and treatment of cerebral vasospasm following subarachnoid hemorrhage includes: (Select 3.)
controlled hypotension. hematocrit 30%. daily transcranial Doppler exams. nifedipine. mannitol. nimodipine.
Nimodipine
Hematocrit 30%
Daily transcranial Doppler exams
Vasospasm is the leading cause of morbidity and mortality after subarachnoid hemorrhage.
Prevention consists of nimodipine and triple H therapy (hemodilution, hypervolemia, and hypertension). Additionally, the patient should receive frequent neurologic evaluation as well as daily transcranial Doppler examinations.
Since nimodipine is the only calcium channel blocker that reduces morbidity and mortality associated with vasospasm, nifedipine isn’t indicated. Controlled hypotension and mannitol go against triple H therapy.
Management for the patient with traumatic brain injury on clopidogrel includes: (Select 2.)
fresh frozen plasma.
methylprednisolone.
platelet transfusion
hypertonic sodium chloride.
Platelet transfusion
Hypertonic sodium chloride
This question is twofold. First, you need to know how to treat the head injury, and second you need to know how to reverse the anticoagulant so the patient can proceed to surgery.
Although steroids have been used for decades in the patient with TBI, their use is no longer recommended as they’re associated with a poorer neurologic outcome.
Hypertonic saline supports hemodynamics and creates an osmotic effect that reduces brain water.
Clopidogrel is reversed with platelet transfusion. FFP can be used to reverse warfarin, although there may be better alternatives.
Which agent should be avoided in the patient with epilepsy? Sufentanil Dexmedetomidine Propofol Ketamine
Ketamine
Of the answer choices provided, ketamine is the most likely to produce a seizure in the patient with epilepsy.
Opioids can cause myoclonic activity as well as chest wall rigidity. These effects may be confused with seizure activity.
There are a few case reports that implicate propofol as a cause of seizures and opisthotonos (rigid posture with an arched back). In spite of this, propofol is a first line anticonvulsant.
Dexmedetomidine appears to be safe in the patient with epilepsy.
Which drug is excreted unchanged by the kidneys? Gabapentin Carbamazepine Valproic acid Phenytoin
Gabapentin
Gabapentin is unique among the anticonvulsants, because it is excreted unchanged by the kidneys.
Valproic acid, carbamazepine, and phenytoin are metabolized by the liver.
Carbamazepine, and phenytoin induce hepatic enzymes.
Valproic acid inhibits hepatic enzymes.
The duration of action of which drug will be prolonged in the patient treated with donepezil for Alzheimer’s disease?
Succinylcholine
Vecuronium
Rocuronium
Cisatracurium
Succinylcholine
Cholinesterase inhibitors are the mainstay of medical therapy for Alzheimer’s disease. Inhibition of pseudocholinesterase in the plasma increases the duration of action for succinylcholine and mivacurium.
Which factors contribute to the pathophysiology of Parkinson’s disease? (Select 2.)
Increased glutamate in the substantia nigra
Increased GABA in the thalamus
Decreased dopamine in the basal ganglia
Decreased acetylcholine in basal ganglia.
Decreased dopamine in the basal ganglia
Increased GABA in the thalamus
In a nutshell, the pathophysiology of Parkinson’s disease can be characterized by an imbalance between dopamine and acetylcholine in the basal ganglia. Destruction of dopaminergic neurons favors a state of cholinergic over activity. In turn, this increases GABA activity in the thalamus leading to thalamic suppression. The final result is an inhibition of the cortical motor system and an overactivity of the extrapyramidal system.
Ischemic optic neuropathy MOST commonly occurs after:
spinal surgery.
corneal abrasion.
radical neck dissection.
cardiopulmonary bypass.
Spinal surgery
Ischemic optic neuropathy is the most common cause of perioperative vision loss. It occurs most often after surgery on the spine
The artery of Adamkiewicz: (Select 2.)
usually arises between T4 and T8
more commonly arises from the left side.
occlusion can cause flaccid paralysis.
provides collateral circulation to the posterior spinal cord.
More commonly arises from the left side
Occlusion can cause flaccid paralysis
The artery of Adamkiewicz arises from the aorta. In 75% of the population, it originates between T8-T12. It supplies the anterior spinal artery, which serves the anterior (not posterior) two-thirds of the spinal cord.
Occlusion of the artery of Adamkiewicz during aortic cross clamping can cause anterior spinal artery syndrome. This results in:
Flaccid paralysis of the lower extremities
Bowel and bladder dysfunction
Loss of temperature and pain sensation (spinothalamic tract is impaired)
Preserved touch and proprioception (dorsal column function is preserved)
All of the following statements about the dorsal column are true EXCEPT:
the second order neuron decussates in the medulla.
it transmits nociceptive input to the thalamus.
it transmits sensory information faster than the anterolateral system.
the first order neuron enters the spinal cord via the dorsal root ganglia.
It transmits nociceptive input to the thalamus
The anterolateral system (not the dorsal column), transmits nociceptive input to the thalamus.
All the other answer choices are stated correctly.
Which pathway transmits afferent nociceptive input to the brain? Corticospinal tract Lissauer tract Anterolateral system Medial lemniscal system
Anterolateral system
The anterolateral system (spinothalamic tract) transmits afferent nociceptive input to the brain.
What about the other tracts?
The medial lemniscal system (dorsal column) transmits fine touch, proprioception, vibration, and pressure.
The Lissauer tract is an intermediary pathway that relays sensory input in the spinal cord.
The corticospinal tract transmits motor impulses.
Injury to the corticospinal tract above the level of decussation in the medulla will result in: (Select 2.)
flaccid paralysis.
contralateral paralysis.
ipsilateral paralysis.
spastic paralysis.
Contralateral paralysis
Spastic paralysis
The corticospinal tract carries motor signals from the cerebral cortex to the muscles of the body. Where the injury occurs determines the location and type of paralysis the patient will experience.
Injury above decussation = spastic paralysis on contralateral side
Injury below decussation = flaccid paralysis on ipsilateral side
Which findings are MOST likely to occur during the acute phase of spinal cord transection at C7?
Tachycardia and hypotension
Hypothermia and tachycardia
Autonomic hyperreflexia and hypothermia
Bradycardia and hypothermia
Bradycardia and hypothermia
The patient with an acute C7 transection will endure neurogenic shock. This is characterized by bradycardia, hypotension, and hypothermia with pink and warm extremities.
By contrast, hypovolemic shock presents with tachycardia, hypotension, and cool, clammy extremities.
A patient with a two year old C7 spinal cord transection presents for cystoscopy under general anesthesia. Insertion of the cystoscope causes the heart rate to decrease from 75 to 30 bpm. Which of the following statements are MOST likely to be true? (Select 3.)
Ephedrine is a better option than atropine.
There is vasodilation above C7.
Nitroprusside is a better option than hydralazine.
This patient is at risk for intracerebral hemorrhage.
The Bezold-Jarisch reflex caused the heart rate to decrease.
An epidural would have prevented this response.
There is vasodilation above C7
Nitroprusside is a better option than hydralazine
This patient is at risk for intracerebral hemorrhage
The patient experiencing autonomic hyperreflexia will vasodilate above the level of injury and vasoconstrict below the level of injury (risk of severe hypertension).
Consequences of HTN:
HTN produces bradycardia via the baroreceptor reflex. Anticholinergics are the treatment of choice, as sympathomimetic agents can increase BP further.
Hypertension must be treated promptly, as it can cause stroke, LV failure, and pulmonary edema. Nitroprusside will take effect much sooner than hydralazine (onset = 10 – 20 min).
When compared to epidural anesthesia, general or spinal anesthesia will more reliably prevent AH.
Consequences of amyotrophic lateral sclerosis include all of the following EXCEPT:
hyperkalemia with succinylcholine.
risk of pulmonary aspiration
increases sensitivity to nondepolarizing neuromuscular blockers.
cardiomyopathy.
Cardiomyopathy
Amyotrophic lateral sclerosis (ALS) causes progressive degeneration of motor neurons in the corticospinal tract (upper and lower motor neurons).
Bulbar muscle weakness increases the risk of aspiration.
Extrajunctional receptors at the NMJ can cause life-threatening hyperkalemia.
ALS does not affect cardiac muscle (cardiomyopathy is not a risk).
Friedreich’s ataxia is a motor neuron disease that affects skeletal and cardiac muscle. These patients commonly have an associated cardiomyopathy and congestive heart failure.
Select the statement that BEST describes myasthenia gravis.
Neonates of affected mothers are at risk for muscle weakness.
Edrophonium impairs muscle strength during symptom exacerbation.
Pregnancy reduces the severity of symptoms.
Acetylcholine production is decreased.
Neonates of affected mothers are at risk for muscle weakness
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.
Myasthenia and Pregnancy:
Pregnancy exacerbates the symptoms of myasthenia gravis.
Anti-AchR IgG antibodies cross the placenta. This can cause weakness in the neonate for 2 - 4 weeks after delivery.
The patient with myasthenia gravis will be: (Select 2.)
sensitive to vecuronium.
resistant to succinylcholine.
resistant to rocuronium.
sensitive to succinylcholine.
Sensitive to vecuronium
Resistant to succinylcholine
In the last question, we established that there are too few receptors at the motor endplate.
Since neurotransmission is already impaired, it takes less nondepolarizer to causes paralysis.
For the same reason, it takes more succinylcholine to depolarize the motor endplate.
Identify the characteristics common to Eaton-Lambert syndrome. (Select 3.)
Increased sensitivity to succinylcholine Small cell lung carcinoma Diagnosed with Tensilon test Destruction of the nicotinic receptor Bulbar muscle weakness Destruction of voltage-gated calcium channels
Destruction of voltage-gated calcium channels
Increased sensitivity to succinylcholine
Small cell lung carcinoma
Eaton-Lambert syndrome is easily confused with myasthenia
gravis, so we think it’s best to learn about them side by side
Eaton-Lambert syndrome is associated with destruction of presynaptic voltage-gated calcium channels, increased sensitivity to succinylcholine, and close association with small cell lung carcinoma.
Myasthenia gravis is associated with destruction of the nicotinic receptor, bulbar muscle weakness, and diagnosis with Tensilon test.
Which disease begins with an influenza-like illness that is followed by ascending paralysis?
Myotonic dystrophy
Guillain-Barre syndrome
Charcot-Marie-Tooth
Familial periodic paralysis
Guillain-Barre syndrome
Guillain-Barre syndrome is characterized by ascending paralysis that is preceded by an influenza-like illness.
Familial periodic paralysis is a group of diseases characterized by intermittent attacks of skeletal muscle weakness that are associated with hypo- or hyperkalemia.
Myotonic dystrophy is a group of diseases where the hallmark is prolonged muscle contracture (myotonia) after a voluntary skeletal muscle movement.
Charcot-Marie-Tooth disease is an inherited peripheral neuropathy that presents as skeletal muscle weakness and wasting. It is usually confined to the lower third of the legs, but it can also affect the quadriceps, hands, and forearms.
Which agents are safe to administer to the patient with hypokalemic periodic paralysis? (Select 2.)
Terbutaline
D5LR
Rocuronium
Acetazolamide
Rocuronium
Acetazolamide
Familial periodic paralysis is characterized by acute episodes of skeletal muscle weakness accompanied by changes in the serum potassium concentration. There are two variants of this disease: hypokalemic and hyperkalemic.
Acetazolamide is the treatment for both variants of this condition.
Patients are more sensitive to the effects of nondepolarizing neuromuscular blockers, so a short-acting agent is preferred.
The wrong answer choices will make more sense after you review the pathophysiology.
Malignant hyperthermia is primarily associated with the genetic mutation of the: actin myofilament. dihydropyridine receptor. SERCA2 pump. ryanodine receptor.
Ryanodine receptor
MH is an inherited disease of skeletal muscle that is characterized by disordered calcium homeostasis.
Exposure to halogenated anesthetics and/or succinylcholine activates the defective ryanodine receptor (RYR1), which stimulates the sarcoplasmic reticulum to release way too much calcium into the cell.
The earliest signs of malignant hyperthermia include: (Select 3.)
disseminated intravascular coagulation. hyperthermia. tachycardia. masseter spasm. cola colored urine. increased EtCO2.
Tachycardia
Increased EtCO2
Masseter spasm
Knowing the signs and symptoms of MH isn’t enough. You’ll need to know the time course of the events.
Early signs are the result of the hypermetabolic state of skeletal muscle: tachycardia, increased EtCO2, masseter spasm.
Later signs include hyperthermia, cola colored urine (rhabdomyolysis), and DIC.
