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**My Anesthesia ABA Advanced Study Cards > Central and Peripheral Nervous Systems > Flashcards

Central and Peripheral Nervous Systems Flashcards

1
Q

Which hypothalamic nucleus regulates circadian rhythm?

A

suprachiasmatic nucleus

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2
Q

Which hypothalamic nucleus regulates body temperature?

A

pre-optic anterior hypothalamus (also regulates thirst and non-REM sleep)

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3
Q

Where is vasopressin synthesized?

A

supraoptic and paraventricular hypothalamic nuclei, connected to the posterior pituitary

(SupraOptic & ParaVentricular hypothalamic nuclei= Va_SOP_ressin)

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4
Q

Which post-ganglionic sympathetic nerves use ACh as their neurotransmitter?

A

sweat glands and skeletal blood vessels

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5
Q

Which spinal levels provide sympathetics to the upper extremity?

A

T1-T4/5

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6
Q

Which anti-emetics should be avoided in patients with Parkinson’s disease?

A

metoclopramide, haloperidol, droperidol

(all are dopamine antagonists)

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7
Q

Why are patient’s with Parkinson’s disease poorly responsive to ephedrine?

A

catecholamine depletion

*direct-acting agents are preferable*

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8
Q

What makes a seizure “complex?”

A

impaired consciousness

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9
Q

How long should anti-epileptic drugs be continued in patients with severe TBI?

A

7 days

*anti-epileptics are very effective in preventing “early seizures” in the first 7 days, but ineffective in preventing “late seizures” after 7 days*

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10
Q

Which induction agent can cause extrapyramidal myoclonus prior to giving muscle relaxant?

A

etomidate

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11
Q

What is the most common cause of stroke during CEA?

A

embolism

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12
Q

Patients with which spinal cord lesions are at risk of autonomic hyperreflexia?

A

T6 and above

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13
Q

What are the common triggers for autonomic hyperreflexia?

A

distention of a hollow viscous

trauma

thermal stimulation

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14
Q

How do TCAs alter the effects of ephedrine?

A

can potentiate due to increased norepinephrine

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15
Q

How soon after the last alcoholic drink does delerium tremens become a concern?

A

2 days

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16
Q

At what point does hypoxia begin to affect cerebral blood flow?

A

Once PaO2 drops to 50, cerebral blood flow starts to rise exponentially

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17
Q

How does PaCO2 affect cerebral blood flow?

A

cerebral blood flow increases linearly with rising PaCO2 until the curve begins to flatten around 80 and completely flatten around 120

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18
Q

What techniques can cause a coupled decrease in both cerebral blood flow and CMRO2

A

hypothermia to 34 oC

barbiturates

propofol (greater reduction in CBF than in CMRO2)

19
Q

What are normal values for cerebral blood flow and CMRO2?

A

CBF: 50 mL / 100 g / min

CMRO2: 3.5 mL / 100 g / min

20
Q

What can lead to disruption of the blood-brain barrier?

A

extreme hypercapnea or hypoxia

sustained seizure

tumor

stroke

trauma

infection

21
Q

What is the normal volume of CSF and production rate of CSF in an adult?

A

normal volume: 150 mL

normal production: 500 mL / day

22
Q

How does dexamethasone decrease ICP?

A

limiting brain swelling

decreasing CSF production (in animal models)

23
Q

What is the transmural pressure of a cerebral aneurysm?

A

TMP = MAP - ICP (or - CVP, whichever is larger)

24
Q

How do opiates affect cerebral blood flow and CMRO2?

A

minimal effects on both

25
Q

What is the reverse steal effect (e.g., Robin Hood effect)?

A

brain vasculature to normal tissue vasocontricts in response to a stimulus (e.g., hypocarbia, propofol, barbiturates, benzodiazepines) while brain vasculature to damaged/ischemic areas can’t respond, thus redirecting blood flow to damaged/ischemic areas

26
Q

How does succinylcholine affect ICP?

A

transient, mild increase

*can be blunted with a defasciculating dose of non-depolarizing muscle relaxant*

27
Q

How much and how long does hypocarbia reduce cerebral blood flow?

A

2% reduction in CBF for every 1 mmHg reduction in PaCO2

effect lasts 6-24 h

28
Q

What are the most sensitive monitors for venous air embolism?

A

TEE > prechordial doppler > PA pressure changes > etN2

29
Q

Where should a CVL be placed to use for potential aspiration of a venous air embolism?

A

at the junction of the SVC and right atrium

30
Q

When should brain relaxation techniques be used in surgery for aneurysm clipping?

A

after the dura is open to avoid increasing aneurysm TMP by dropping ICP

*Before the dura is open: TMP = MAP - ICP

*After the dura is open TMP = MAP

31
Q

What are the two approaches to aneurysm clipping and how do they affect your BP management

A

Traditional: clips on either side of the aneurysm, better outcomes with induced hypotension or even circulatory arrest

Modern: temporary clip on feeding vessel(s), better outcomes with elevated MAPs to maintain collateral blood flow to the territory of the feeding vessel

32
Q

What are the ECG changes associated with SAH?

A

increased sympathetic outflow causing PVCs, prolonged QT, ventricular tachyarrhythmias, and ischemic changes from left heart strain

U waves from increasing ICP

33
Q

What is the Hunt and Hess scale for SAH?

A
34
Q

What is the incidence and timing of vasospasm after SAH?

A

15%

Risk peaks at 1 week, occurs rarely after 2 weeks

35
Q

What is the best monitor for cerebral vasospasm?

A

transcranial doppler and frequent neuro checks

36
Q

What is the approach to preventing cerebral vasospasm after SAH?

A

Triple H therapy: hypertension, hypervolemia, hemodilution

Nimodipine

Intra-arterial catheters for direct delivery of Ca2+ channel blockers in refractory cases

37
Q

What are the endocrinopathies of the pituitary gland?

A

anterior: GH, PRL, LH, FSH, ACTH, and TSH
posterior: oxytocin and vasopressin

38
Q

What happens to autoregulation and CO2 responsiveness in TBI?

A

autoregulation is lost

CO2 responsiveness is maintained

39
Q

At what ICP does herniation become an imminent risk?

A

30-40 mmHg

40
Q

What causes “neurogenic” pulmonary edema in the setting of TBI?

A

LV dysfunction from increased catecholamines

capillary leak syndrome of unclear etiology

41
Q

What are the causes of hyponatremia in the setting of TBI? How can they be distinguished?

A

SIADH: euvolemic, typically responsive to salt tabs and fluid restriction, can be treated with “vaptan” drugs (vasopressin receptor antagonists)

Cerebral salt wasting: hypovolemic, poorly responsive to fluid restriction and salt tabs

42
Q

How is spinal shock from a high cervical injury managed acutely?

A

fluid resuscitation (hypovolemia due to increased venous capacitance with unopposed vagal tone)

vasopressors with a ß1 component (counteract unopposed vagal tone)

43
Q

What kinds of injuries are associated with an unstable C-spine?

A

cervical burst fractures

ligamentous injury (esp. alar and tectorial)

dens fractures

44
Q

What is the Glasgow Coma Scale?

A

Eye response (out of 4)

Verbal response (out of 5)

Motor response (out of 6)

**My Anesthesia ABA Advanced Study Cards (35 decks)

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