Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ABA Advanced Exam > Central and Peripheral Nervous Systems > Flashcards

Central and Peripheral Nervous Systems Flashcards

1
Q

Which hypothalamic nucleus regulates circadian rhythm?

A

suprachiasmatic nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which hypothalamic nucleus regulates body temperature?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where is vasopressin synthesized?

A

supraoptic and paraventricular hypothalamic nuclei, connected to the posterior pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

sweat glands and skeletal blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Which spinal levels provide sympathetics to the upper extremity?

A

T1-T4/5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

metoclopramide, haloperidol, droperidol

(all are dopamine antagonists)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

catecholamine depletion

*direct-acting agents are preferable*

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What makes a seizure “complex?”

A

impaired consciousness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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*

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

etomidate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the most common cause of stroke during CEA?

A

embolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

T6 and above

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the common triggers for autonomic hyperreflexia?

A

distention of a hollow viscous

trauma

thermal stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do TCAs alter the effects of ephedrine?

A

can potentiate due to increased norepinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

2 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

ABA Advanced Exam (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions