Basic - Neuro Flashcards

1
Q

When do you need to be careful administering Succinylcholine to patients who suffered burns?

A

Generally AFTER the first 24 hours - 2 years
- at that point, significant upregulation of nicotinic ACh receptors will occur

*same with pts with stroke and spinal cord injuries

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

Multiple sclerosis

  • ACh receptors (up/downregulated)
  • Depolarizing muscle relaxant
  • Nondepolarizing muscle relaxant
A

ACh receptors: Upregulated

Depolarizing muscle relaxant:
Careful, especially if flaccidity or spasticity

Nondepolarizing muscle relaxant:
May be more resistant or sensitive

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

Conditions that cause an upregulation of ACh receptors

A
  1. MS
  2. Burns
  3. Stroke
  4. Spinal cord injury
  5. GBS
  6. Prolonged immobility
  7. Muscular dystrophies
  8. Prolonged use of NMB

*can cause an exaggerated increase in K+ after giving Sux

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

Lambert eaton syndrome

  • disorder
  • Depolarizing muscle relaxant
  • Nondepolarizing muscle relaxant
A

prejunctional Ca2+ antibodies

Depolarizing muscle relaxant:
more sensitive

Nondepolarizing muscle relaxant:
more sensitive

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

Lambert eaton syndrome

  • disorder
  • Depolarizing muscle relaxant
  • Nondepolarizing muscle relaxant
A

ACh receptor:
- downregulation

Depolarizing muscle relaxant (sux):
more resistant

Nondepolarizing muscle relaxant (roc):
more sensitive

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

Myasthenia gravis

  • disorder
  • Depolarizing muscle relaxant
  • Nondepolarizing muscle relaxant
A

ACh receptor:
- downregulation

Depolarizing muscle relaxant (sux):
more resistant

Nondepolarizing muscle relaxant (roc):
more sensitive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
How do barbiturates affect :
ICP:
Cerebral blood flow: 
Cerebral autoregulation:
CMRO2:
A

ICP: Decrease
Cerebral blood flow: Decrease (dose dependent)
CMRO2: Decrease (dose dependent)
Cerebral autoregulation: Unaffected

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

Treatment for extrapyramidal symptoms or acute dystonic reactions?

A
  1. Anticholinergics
    - diphenhydramine (both anticholinergic and antihistamine)
  2. BDZ
  3. BB

*EPS: abnl movement when cholinergic-dopaminergic balance is off

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

________ on EEG is the goal target of reducing CMRO2 during an open cerebral aneurysm clipping

A

Burst suppression

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

What is the upregulation of postjunctional ACh receptors due to?

What risk does this pose?

A

Injury to nerves that cause decreased release of ACh or denervation or lack of ACh stimulus to the post-junctional receptor

hyperkalemia induced cardiac arrest

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

Cushing’s triad

A
  1. HTN
  2. Bradycardia
  3. Respiratory changes

= ominous sx of serious head injury -> urgent intubation

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

What is mannitol used for in neurosurgery?

A

osmotic diuretic -> quickly decrease ICP
- however, you NEED an intact BBB or else mannitol will raise brain osmolality, increase cerebral volume and risk herniation

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

Why is nitroglycerin not recommended in pts with head trauma if they are hypertensive?

A

Cerebral vasodilator -> may further raise ICP

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

What can cross the BBB

A

Small lipophilic molecules

  • oxygen
  • CO2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Treatment for elevated ICP intraop

A
hypertonic saline
diuretics
mannitol
- draw fluid back across the BBB in hopes of decreasing the edema
- however, you NEED an intact BBB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Effect of acute vs chronic use of phenytoin on nondepolarizing NMB

A

Acute:
- Potentiates blockade
(acute reduction in ACh release - less competitive inhibition)

Chronic:
- Increases resistance to blockade (ED95)
- Decreases duration of blockade
(increased postjunctional ACh receptor density - more receptors to block. and decreased sensitivity at the receptor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the ED95 in neuromuscular blocking drugs?

A

dose required to achieve desired effect in 95% of population

18
Q

Effect of phenytoin use on depolarizing NMB (succinylcholine)

A

Prolonged d/t upregulation in ACh receptors - higher risk of hyperK

Upregulation: denervation or lack of ACh stimulus to the post-junctional receptor

19
Q

Post op vision loss secondary to ANTERIOR ischemic neuropathy (AION) is most likely to occur after which type of surgery?

A

Cardiac surgery

*cardiac sx is done on the anterior = AION
posterior spine sx are done on the posterior = PION

20
Q

Post op vision loss secondary to POSTERIOR ischemic neuropathy (PION) is most likely to occur after which type of surgery?

A

posterior spine surgery

anterior ischemic optic neuropathy more common periop cause of vision blindness than posterior

21
Q

Decreasing a pts PaCO2 by 1mmHg will decrease CBF by ____

A

1mL/100g/min

22
Q

Pathway for eccrine sweat gland innervation (located all over the body except lips, and tip of penis and clit)

A

SYMPathetic preganglionic -> nicotinic receptor -> SYMPathetic postganglionic -> muscarinic receptor

23
Q

Pathway for apocrine sweat gland innervation (located in armpit and perianal areas)

A

PARAsympathetic preganglionic -> nicotinic receptor -> PARAsympathetic postganglionic -> muscarinic receptor

24
Q

_____ agents interfere with the sweating mechanism, which may lead to temp increases (esp child with fever)

A

Anticholinergic agents

- include in differential

25
Q

In pts with methemoglobinemia (toxic side effect of benzocaine admin), the only value that significantly changes on ABG is ____

A

PaO2
- partial pressure of arterial oxygen
-

26
Q

What is methemoglobinemia?

*occurs after exposure to substances that oxidize hgb faster than methemoglobin reductase can reduce it

A

Altered state of hgb where the FERROUS (Fe2+) form of heme is oxidized to the FERRIC form (Fe3+)
- cannot bind oxygen

27
Q

What can cause methemoglobinemia?

A
  • occurs after exposure to substances that oxidize hgb faster than methemoglobin reductase can reduce it
  • prilocaine
  • benzocaine
  • abx: dapsone, sulfonamides, trimetoprim
  • metoclopramide
  • nitrates / nitrites
28
Q

on ABG, which value is NOT directly measured, but calculated based on the assumption that ALL hgb is normal?

A

SaO2

- Can be falsely elevated in methemoglobinemia

29
Q

How many days of immobility leads pts to have increased risk of hyperkalemia with depolarizing muscle relaxants?

A

> 16 days

30
Q

The TOF of a nerve in a paralyzed extremity is ______

A

exaggerated

- production of extrajunctional ACh receptors in affected muscles -> increase response w/ stim

31
Q

CMRO2 and CBF decrease ___% for every 1C decrease in temperature

A

6%

32
Q

Increasing PaCO2 from 40-60 mmHg will cause an (increase/decrease) in CBF approximately __%

A

increase

60%

33
Q

CBF remains unchanged within the autoregulatory range of MAP ____ and PaO2 ____

A

MAP 50-150mmHg

PaO2 >50mmHg

34
Q

How do you calculate the diff in blood pressure in 2 different sites?

A

Height (cm) x 0.74

Subtract this value from the systolic and diastolic value at the heart

  • mneumonic:
  • pH = Pressure height
  • pH 15 20 = pressure 15 = height 20 cm
35
Q

Tetanus prevents neurotransmitter release (glycine and GABA) from ____ in the ____

A

inhibitory neurons
- inhibition of inhibitory neurons -> increased muscle contractions

Spinal cord

36
Q

Botulism prevents neurotransmitter release (ACh) from ____ at the ____

A

nerves

neuromuscular junction

37
Q

What illicit drug is a risk factor for tetanus contraction?

A

Heroin

38
Q

Neurogenic shock following acute high spinal cord injuries is associated with severe bradycardia and hypotension from _______

A

unopposed vagal or parasympathetic activity and loss of cardiac accelerator fibers (if injury is above T1-T4)

39
Q

Why would Pts with acute spinal cord injury become bradycardic during intubation?

A

Stimulation usually occurs above the level of spinal cord injury. Nerve transmission is unable ot descend and activate the thoracic sympathetic chain at T1-T4

40
Q

Why would Pts with acute spinal cord injury present with paradoxical shallow respirations?

A

implies level of injury is between C4-C7

- C3, C4, C5 keeps the diaphragm alive

41
Q

Autonomic hyperreflexia beings ___ weeks following acute spinal injury

A

2-3 weeks

42
Q

Etomidate and ketamine (Increases/decreases) amplitude of Somatosensory evoked potential stimulus (SSEP)

A

increases