Neuro

Question 1

A 70-year-old man with diabetes mellitus presents with pain sensation in his limb that was amputated for gangrene 4 weeks prior to consult. The diagnosis of neuropathic pain, more specifically phantom limb pain is made. Which of the following is a feature of neuropathic pain?
A. Associated with tissue damage
B. Caused by direct stimulation of pain receptors
C. Characterized by dull, aching pain
D. Responds favorably to antidepressants and anticonvulsants

Answer 1

The correct answer is that it responds favorably to antidepressants and anticonvulsants. Unlike other types of pain, neuropathic pain does not respond well to the administration of nonsteroidal anti-inflammatory drugs (NSAIDs).
Neuropathic pain is a chronic type of pain that is caused by damage to the sensory system within the central or peripheral nervous system. It is not usually caused by tissue damage but from damage to the nervous system. The damage can be secondary to trauma, disease, surgery, or even chemotherapy.
Common examples of central neuropathic pain include post spinal cord injury pain, post-stroke pain, Wallenberg syndrome, and multiple sclerosis. On the other hand, common disorders that are associated with peripheral neuropathic pain include neuroma, diabetes, phantom limb pain, trigeminal neuralgia, cervical radiculopathy, lumbosacral plexopathy, postherpetic neuralgia, and brachial plexus avulsion.
The pain in neuropathy is not caused by direct stimulation of pain receptors, and it may occur in a continuous or intermittent fashion in an area with sensory loss. It may be characterized as burning, lancinating, aching pain, and in some cases allodynia, or abnormal sensitivity to innocuous stimuli such as running water or cold air. It can also be accompanied by dysesthesias and hyperalgesia.

Question 2

You’re examining a 46-year-old female complaining of a two-week history of dyspnea, palpitations and generalized fatigue. Her past medical history is remarkable for alcoholism, and hypertension, well controlled with lisinopril. Visually the patient appears dyspneic, orthopneic, edematous with warm and well-perfused extremities. Her vital signs are a blood pressure of 162/65 mmHg, a heart rate of 87 bpm, SpO2 98% on ambient air. The physical exam is remarkable for bounding quick upstroke pulse, followed by a rapid collapse; subungual capillary pulsations, and a systolic bruit over the carotids. The exam is also remarkable for a hyperdynamic precordium and a scratchy mid-systolic murmur over the third left intercostal space. A transthoracic echocardiography is remarkable for a dilated LV cavity (LV end-diastolic dimension of 72mm), and an EF of 61%. An ECG is ordered and reveals nonspecific ST-T segment changes. What is the most likely diagnosis for this patient’s symptoms?
A. High Output Heart Failure due to Wet beriberi
B. Cor Pulmonale due to COPD
C. Heart failure with preserved ejection fraction due to uncontrolled hypertension
D. Alcoholic Cardiomyopathy

Answer 2

This case describes a patient with signs and symptoms of heart failure. Her ejection fraction is preserved, there is good capillary refill, Corrigan pulse, wide pulse pressure, Quincke’s pulse and a Means-Lerman scratch; all signs of high-output heart failure. Her ejection fraction is also preserved meaning option B is unlikely. Option C would be associated with classic congestive heart failure signs and is unlikely as the patient’s hypertension is well controlled. Option D, alcoholic cardiomyopathy, maybe an exacerbating factor however does not fully explain the patient’s symptoms as the dilation of the LV here would be expected to result in a reduced LV ejection fraction. Option A, is the most likely diagnosis in this patient. Beriberi is caused by the deficiency of Vitamin B1 and is seen among alcoholics. The wet form of beriberi presents with tachycardia, dyspnea and peripheral edema associated with cardiomyopathy (usually dilated) and high-output HF; consistent with his patient’s presentation. Minor electrocardiographic changes (e.g. nonspecific ST-T wave changes) such as in this patient are also common. As such, Option A is the correct answer.

Question 3

A 37-year-old woman is scheduled for a fertility procedure. She has had numerous operative procedures and anesthetic techniques since an MVA 3 years ago and is constantly bothered by postoperative nausea and vomiting (PONV). You are unable to give her a guarantee about eliminating her PONV, but you do everything you can during the case to prevent it, in particular, by avoiding all narcotics. A good anatomic reason for this is because the chemoreceptor trigger zone (CRTZ), located on the floor of the fourth cerebral ventricle, is not protected by what structure?
A. Pia Mater
B. Dura Mater
C. Choroid Plexus
D. Blood-Brain Barrier

Answer 3

D is the correct answer because the CRTZ is outside of the blood brain barrier, therefore sensitive to medications, such as narcotics, which can cause nausea.
A is not correct because all areas of the brain have the closely applied, vascular, pia mater.
B is not correct because the fourth cerebral ventricle, being inside the brain, is covered by dura.
C is not correct because the choroid plexus is a means of absorbing CSF and is not in this area.

Question 4

Shortly after a craniotomy, a 22-year-old man has a blood pressure of 120/80, heart rate of 90, and he is producing 5 ml/kg of urine per hour. His serum sodium level is 149 and urine sodium is 8 mEq/L. Which is the most appropriate treatment of his hypernatremia?
A. Fludrocortisone
B. Methylene blue
C. Desmopressin
D. Furosemide
E. Hydrochlorothiazide

Answer 4

This question describes a patient who has central diabetes insipidus (DI). DI creates disturbances in serum and urine sodium levels because the body does not have enough of the hormone vasopressin, also known as antidiuretic hormone (ADH). It can result because of damage to the hypothalamus or pituitary gland. With DI, plasma sodium levels are markedly elevated because patients cannot concentrate their urine. Because the main issue in central DI is a deficient secretion of ADH, control of polyuria can be achieved by hormone replacement.
Desmopressin (DDAVP) is the substitute of ADH that has potent antidiuretic but no vasopressor activity. The constellation of symptoms is often included on the differential with syndrome of inappropriate anti-diuretic hormone secretion (SIADH) and cerebral salt wasting (CSW). With SIADH, patients are normovolemic with elevated urinary sodium and low plasma sodium. With CSW, patients are hypovolemic with a similarly elevated urinary sodium and low plasma sodium. Patients with CSW have a reduced effective arterial blood volume.

Question 5

A 55-year-old man presents to the clinic with complaints of hemoptysis, dyspnea, and chronic cough. Upon examination, he is seen to be wheezing and has clubbing on his fingers. CT scan shows bronchial dilation. The patient has no comorbidities. What is the most likely diagnosis?
A. Status asthmaticus
B. Bronchiectasis
C. Bronchitis
D. COPD

Answer 5

Status asthmaticus is a life-threatening condition in which a patient of asthma suffers from a bout of bronchospasm that is not relieved in spite of treatment. This is a medical emergency that requires prompt treatment. The diagnosis of status asthmaticus requires a history of unresponsive asthma. Bronchiectasis causes irreversible airway dilation which presents with hemoptysis, breathlessness and chest pain. Clubbing of fingers is a characteristic sign that differentiates it from COPD. The diagnosis is made via CT scan, without contrast, which will show bronchial dilation or thickening of bronchial walls.
Pulmonary function changes vary considerably and hence are not diagnostic for bronchiectasis. COPD is characterized by dyspnea upon exertion or rest, chronic cough, and chronic sputum production. It is often seen in chronic smokers or those with chronic occupational exposure to dust and chemicals.
Lung function tests can help in its diagnosis. COPD is characterized by a decreased FEV1: FVC ratio and increased FRC and TLC. Bronchitis also presents with cough for several weeks, along with dyspnea, wheezing and chest pain and sputum production. Chest X-ray and CT will be normal in bronchitis.

Question 6

Where is the largest redicular artery located?

Answer 6

The great redicular artery is the largest of all redicular spinal artery, also called artery of adamkiewicz.

Located between T9-T12 in 75% but it might also seem below which explains why infrarenal aneurysm associated with 0.25% of paraplegia

Question 7

How long hyperventilation to decrease CBF is effective

Answer 7

CBF continues to vasoconstrict until PaCO2 reaches 30, below it the effect is stabilized and beyond 24-48 hours, any change in PCO2 will not effect CBF

Question 8

CSF composition compared to plasma

Answer 8

A little acidic than plasma (pH 7.33), more CO2 (50), lower protein (0.2) resulting in lower buffering system

The BBB only allows lips soluble to cross, and this helps to maintain the composition of CSF

Question 9

Medication that you never give as inotropy for HFrEF patients?

Answer 9

CCBs

Because of their negative inotropy

Question 10

Carotid sinus reflex

Answer 10

Carried by vagus.

Stimulated by high BP or pressure -> suppresses SNS and activates PSNS

Question 11

Why Etomidate is avoided in neuro anesthesia

Answer 11

Because of its myoclonus and of course adrenal suppression. It also precipitate epileptic EEG activity

Question 12

When to avoid succyincholine in MS patient? What about avoiding atropine or glycopyrolate?

Answer 12

If they have muscle contractured that leads to paralysis or paresis.

Patients on chronic muscarinic agonists first example bethanechol for urinary retention, care must be taken when given glyco or atropine as this can lead to further urinary retention.

Question 13

N2O effect on ICP

Answer 13

When it’s used with IV anesthetics, it has minimal effect on CMR or CBF and ICP

But if used with volatiles it will increase CBF and ICP

Question 14

Which volatile that has epliptogenic side effect

Answer 14

Enuflurane

Question 15

Volatiles effect on CBF and ICP

Answer 15

All increase CBF with decrease CMR but dose dependent

Sevo & Des: increases CBF at MAC 2 and above
Enflurane: lesser than halothane
Isoflurane: lesser vasodilator than halothane at MAC 1-1.5, but it has greater reduction in CMR which why preferred over halothane for ptn with high ICP.
Halothane: most potent vasodilation of CBF at MAC < 1

Question 16

Monitoring interval after single neuroaxial injection with fentanyl vs morphine?

Answer 16

Fentanyl -> continues monitoring for 20 min then hourly for 2 hours

Morphine or dilaudid is 24 hours continues monitoring

Question 17

CBF changes with increase PaCO2 vs Temp

Answer 17

For every 1 mmHg PaCO2 -> 1mL/100g/min (the overall % of CBF increase in response to PaCO2 change is 2%)

For every change in Temp -> 6mL/100g/min change in CBF

Question 18

At what CBF, ischemia results? Isoelectric on EEG? And permanent neuronal death?

Answer 18

At 20 mL/100g/100 -> risk for ischemia

At 15 mL/100g/min -> cortical EEG is isoelectric

Below 15 mL/100g/min -> permanent neuronal damage. (Although evidence of such won’t be seen on EEG until flow is 6 mL/100g/min or below).

Question 19

Explain how hypoCa causes tetany

Answer 19

A low Ca prevents Na channels to be fully closed between each action potential leading to constant Na leak which contributes into constant depolarization or repetitive firing of cell membranes causing tetany. Strider is vocal cord in tetany mode.

Question 20

N2O effect on CBF and CMR and ICP?

Answer 20

Nitrous has cerebral vasodilation and cause sympathoadrenal stimulation

Increases CBF, CMR and ICP

Question 21

The sequence of normal pain transmission is as follows:

Answer 21

(1) pain is sensed by A-delta and C-fibers projected from dorsal root innervating peripheral tissue and viscera;
(2) these primary nociceptors synapse with neurons in the dorsal horn of the gray matter of the spinal cord;
(3) projections from dorsal horn ganglia ascend the spinal cord via the spinothalamic tract to synapse, through the brainstem, to neurons in the thalamus; and
(4) neurons in the thalamus send terminal projections to the somatosensory cortex.

This model represents a general framework, acknowledging that between nociceptors in the periphery and terminal projections to the brain can be multiple excitatory and inhibitory interneurons, as well as spinal reflex arcs.

Question 22

A 20-year-old man is planned to undergo orthopedic surgery for a leg fracture he sustained during a motor vehicle accident. After induction of anesthesia with desflurane, his respiratory minute ventilation decreases notably. This patient is likely to experience which of the following other effect of this drug?
A. Decrease responsiveness of area postrema
B. Increased cerebral metabolic rate
C. Increased intracranial pressure
D. Decreased seizure threshold

Answer 22

The correct option is increased intracranial pressure (ICP). The patient in the question stem has been given a fluorinated inhalational anesthetic. A rise in ICP results after giving a patient inhaled anesthetic, such as desflurane. Fluorinated anesthetics result in a rise in cerebral blood flow, by a somewhat unknown mechanism, this causes raised ICP. This is a result of Monro-Kellie theorem. Decrease responsiveness of area postrema is incorrect as that is a result of antiemetic drugs like ondansetron. Desflurane stimulates the area postrema. Increased cerebral metabolic rate is incorrect as inhaled anesthetics cause the opposite. Decreased seizure threshold is incorrect as desflurane suppresses seizure activity, which results in an increased seizure threshold.

Question 23

A 55-year-old man in intensive care on the second postoperative day after emergent coronary artery bypass grafting has flaccid paralysis. There is a lack of bilateral patellar reflex with impaired touch and thermal sensation from bilateral knees and below and intact proprioceptive and vibration sensation. Cranial nerves and upper limbs are neurologically intact. Bilateral peripheral pulses are symmetrical and palpable. Lower extremity Doppler sonography showed normal arterial and venous blood flow. CT angiogram of lower limbs revealed atherosclerotic plaques but no emboli. MRI of the thoracic spine showed no abnormality. The patient has a history of smoking 2 packs per day for thirty years and medical history of hypertension, type 2 diabetes mellitus, and chronic obstructive pulmonary disease. Which of the following is a possible clinical diagnosis?
A. Anterior spinal artery syndrome
B. Posterior spinal artery syndrome
C. Brown Sequard syndrome
D. Spinal shock

Answer 23

The patient's clinical presentation in the intensive care, two days post-operatively is suggestive of ischemia in the territory supplied by the anterior spinal artery (A). The anterior spinal artery which supplies the anterior two-thirds of the spinal cord, receives supplies from the artery of Adamkiewicz. The internal mammary artery used for bypass grafting in coronary artery bypass is a collateral supplier of the artery of Adamkiewicz and has been implicated as a cause for anterior spinal ischemia.
A patient with posterior spinal artery syndrome (B) will present with loss of proprioception, vibration sensation, two-point discrimination, and light touch but will have preservation of motor function abnormalities below the level of the lesion and feel pain.
Clinical features of Brown Sequard syndrome (C) are paralysis and loss of proprioception on the ipsilateral side with loss of pain and temperature sensation on the contralateral side. The patient in the question stem did not have these clinical features.
Spinal shock (D) is characterized clinically by loss of both cutaneous and deep tendon reflexes below the level of the lesion along with autonomic dysfunction leading to hypotension and bradycardia.

Question 24

A 45-year-old female is scheduled to undergo resection of her cerebellopontine angle tumor via a suboccipital approach. Her lab results are: Hemoglobin: 10.5gm/dL Leukocyte count: 15,000/cmm 2 Sedimentation rate: 60 mm/h Platelets: 250,000/cmm 2 Blood urea nitrogen (BUN): 15mg/dL Serum creatinine: 1.1mg/dL Serum sodium: 140 mEq/L Serum potassium: 3 mEq/L Serum chlorides: 110m Eq/L Which one of the following agents can be safely used to reduce intracranial pressure intra-operatively?
A. Mannitol
B. Hypotonic saline
C. Normal saline
D. Hypertonic saline 3%

Answer 24

Hyperosmolar therapy with mannitol or hypertonic saline solution is the main strategy for the management of intracranial hypertension (IH) and cerebral edema. One of the most common problems associated with the use of hypertonic saline (HTS), either in the form of repeated doses or in continuous infusion, is hyperchloremic, hypokalemic acidosis. Other problems include ARF, arrhythmias, hemolysis, acute lung edema and pontine myelinolysis. Mannitol is associated with hypokalemic, hypochloremic acidosis and acute renal injury with high doses. This patient’s baseline serum electrolyte values are indicative of borderline hyperchloremia with hypokalemia. So, in this patient, mannitol (A) is preferable instead of HTS (D).

Question 25

You're evaluating a 19-year-old male patient following a motor vehicle accident in the ER. He states he has a headache, chest pains and is otherwise feeling well. His vitals are, blood pressure 138/82 mmHg, heart rate 92 beats per minute and respiratory rate 14 breaths per minute. The exam is unremarkable except for marks, abrasions on the chest consistent with seatbelt use. While you're talking with the patient, the patient loses consciousness and the monitor shows vitals at blood pressure 158/101 mmHg, heart rate 52 beats per minute and irregular respiration. Which of the following explains this patient's symptoms?
A. Pericardial effusion
B. Increased ICP
C. Pneumothorax
D. Splenic rupture

Answer 25

This case describes a patient with traumatic injuries with sudden onset of hypertension, bradycardia and irregular respiration. Option B, increased intracranial pressure is the most likely cause due to the Cushing reflex. Increased cerebral pressure results in hypoperfusion of the brain, which causes hypertension. Hypertension then leads to bradycardia secondary to the baroreceptor reflex. And finally, irregular respiration is secondary to impaired brainstem function.

Question 26

Neurotoxicity caused by Nitric oxide (NO) is due to which of the following?

A. Cerebral vasodilation
B. Increase in MABP
C. Increase in CBF
D. The formation of lethal free radicals

Answer 26

Nitric oxide (NO) plays several roles in the central nervous system as a messenger molecule. However, when generated in excess, NO can be neurotoxic. It has been postulated that neurotoxic actions of NO are mediated by peroxynitrite (ONOO-), the reaction product from NO and superoxide anion (D). In pathologic conditions, peroxynitrite and oxygen free radicals can be generated in excess of a cell antioxidant capacity resulting in severe damage to cellular constituents including proteins, DNA and lipids. The inherent biochemical and physiological characteristics of the brain, including high lipid concentrations and energy requirements, make it particularly susceptible to free radical and oxidant mediated insult.
NO causes cerebral vasodilation (A), increase in MABP (B) and increase in CBF (C). All of these actions are not associated with neurotoxicity.

Question 27

You use succinylcholine to assist intubation during an operation for a 48-year-old woman undergoing pituitary surgery. An increase in intracranial pressure following the use of succinylcholine during general anesthesia is due to which of the following?

A. Histamine release
B. Direct relaxation of cerebral vascular smooth muscle
C. Effect of cholinergic blockade on cerebral blood vessels
D. Indirect stimulation of the reticular activating system

Answer 27

Succinylcholine is depolarizing muscle relaxant is widely used in anesthesia. Its onset of action is within 30 seconds of administration and its effect lasts for three to five minutes. It binds to nicotinic receptors at the neuromuscular junction and opens ligand gated channels leading to depolarization and inhibition of neuromuscular transmission. It causes an increase in intracranial pressure by indirectly stimulating the reticular activating system. (D) Complete neuromuscular blockade with vecuronium has been shown to prevent succinylcholine induced increase in intracranial pressure.
It does not influence smooth muscular vascular endothelium (B) (C) nor does it release histamine (A).

Question 28

N2O effect on CBF and CMRO2

Answer 28

While most inhaled anesthetics decrease cerebral metabolism, nitrous has been shown to increase it. All inhaled agents increase cerebral blood flow primarily through vasodilation