Basic neurophysiology Flashcards
Glutamate agonizes which 3 receptors? Is glutamate excitatory or inhibitory? How are action potentials generated?
In the CNS, glutamate is a major excitatory neurotransmitter and there are three main receptor targets: AMPA, Kainate, and NMDA receptors.
Glutamate receptor agonism results in the flow of cations across a channel. With this flow of sodium (and in some cases calcium) into the cell, and potassium out of the cell, the resting membrane potential of the cell changes and thus generates an action potential.
Is GABA excitatory, or inhibitory? How does it work-GABA A vs GABA B?
GABA is a major inhibitory neurotransmitter in the CNS, which in the case of the GABA-A receptor, opens chloride channels, hyperpolarizing them and making the generation of action potentials more difficult.
The GABA-B receptor also responds to GABA but works through a second messenger and does not involve chloride channels.
NMDA-excitatory or inhibitory? What does it let in? What does it let out? What excites it? What blocks it?
NMDA receptors are excitatory and allow Na+ and Ca++ in and K+ out. Glutamate excites this receptor and leads to membrane depolarization. There are multiple substances that can antagonize this receptor, therefore making depolarization (and in the spinal cord pain transduction) less likely (inhibited). The two substances you need to know are ketamine (which binds at the PCP binding site) and Mg++. Remember this is not a complete description, please crack open your favorite text and read more.
The agonism of the opioid receptor results in:
A. Changing the resting potential to be less negative
B. Changing the resting potential to be more negative
C. Changing the threshold potential to be less negative
D. Changing the threshold potential to be more negative
B: Changing the resting potential to be more negative
To answer this tricky question you need to first know that the opioid receptor activation results in neuronal hyperpolarization (making it more difficult to generate an action potential)
Opioid agonism probably changes only the resting potential and not the threshold potential (in other words, generation of an action potential still requires a certain positive inflection of mV, its just starting from a more negative point)
In the setting of starvation, which of the following substances will the brain increase the utilization of most to provide a source of energy:
Ketones
Normally glucose provides the overwhelming majority of ATP for energy utilized by the brain, but in starvation (after 3 days) glucose utilization by the brain decreases by about 25% and ketone utilization increases by 1300%!
Among all the cellular processes of the brain (maintenance, transportation, metabolism, synaptic transmission),________ is the largest consumer of energy
electrical activity (transporting ions across the cell membranes to maintain a resting potential and fire action potentials)
What is coupling? Which drugs de-couple? How much CO does the brain need to receive?
when less energy is being used by the brain, less oxygen is delivered.
the degree of cerebral blood flow is coupled to the cerebral metabolic rate)
Other drugs decouple this relationship, such as fluorinated volatile anesthetics. In this case, despite less energy being consumed, more oxygen is delivered (increased blood flow). Under normal circumstances, the brain needs to receive about 15-20% of cardiac output to cover the metabolic needs
Look at #5 graph in this basic neurophys section
Ok
Is BIS reliable for global ischemia due to hypotension?
Also because general anesthesia shares many features with brain ischaemia, processed EEG (BIS monitor, etc) is not a reliable monitor for this issue.
Which volatile anesthetic is NOT a cerebral vasodilator?
N2O
Highest CBF and intracranial pressure with the volatile (main 3)
Of the anesthetics you’ll be expected to know, CBF is highest with isoflurane, followed by desflurane, followed by sevoflurane (at a given MAC). Because of the increased CBF, intracranial pressure tends to increase with volatile anesthetics (highest with desflurane, then isoflurane, then sevoflurane)
Brain is a fixed space-explain what can increase that pressure? What’s normal ICP? And above what number do neurological symptoms start to show?
The cranial vault is a fixed space and any increase in brain mass (usually from swelling or malignancy), CSF production or decreased CSF absorption, or increased blood volume from increased CBF will increase ICP. Normal ICP is less than 10 mm Hg and above 20 cm Hg, the pressure volume relationship is such that small increases in increased volume will lead to exponentially large increases in pressure.
Sustained very high ICP (well above 20 mm Hg, more like 40 mm Hg+) can result in brain herniation and death. This is discussed in more detail in the clinical neurophys section. What is important to tell from the graph is that the change from normal to danger zone (20 mm Hg) to life threatening (40+ mm Hg) can all occur with a very small volume change (because the pressure-volume relationship increases exponentially). Now you know why you’re doing a hemicrani at 2 am on a patient with an MCA stroke prior to malignant swelling.
When auto regulation is interrupted such as a pathological state like trauma or stroke, blood volume increases in relation to blood pressure.
T/F
True
Propofol, etomidate, and many barbituates including thiopental decrease CBF and increase what?
these agents (especially the first three) cause an increase in cerebral vascular resistance.
In general, what do opioids do to CBF? What are the two exceptions?
In general, opioids will slightly decrease CBF. Primarily Sufenta and fentanyl
Which substances can NOT cross the BBB?
Electrolytes, mannitol, glucose, dextrose, amino acids, proteins, and hydrophilic compounds cannot cross.
Which of the following decrease the production of cerebral spinal fluid:
A. Mannitol
B. Furosemide
C. Fentanyl
D. Ketamine
What other drug does this?
Furosemide
This is trivial, admittedly, but it is a board classic! That is why this is the second time this is discussed in the M5 for such a small piece of minutiae. There are two drugs you should know that decrease CSF production and those are acetazolamide and furosemide (acetazolamide is more commonly used for this purpose).
Opioids and barbiturates and how they relate to CSF
Fentanyl and other opioids probably have little to no effect on CSF production, although they do increase CSF absorption, and the same is for benzodiazepines, barbituates, and etomidate (more important minutiae)
Lidocaine and CBF and CMR
Most IV anesthetics such as propofol, etomidate, barbituates, and to a lesser extent benzodiazepines, will decrease CMR and CBF. Lidocaine acts just like these IV anesthetics in that both CBF and CMR are decreased.
As compared to the serum, which of the following has proportionately the lowest levels in the CSF:
A. Protein
B. Sodium
C. Bicarbonate
D. Glucose
Osmolality of CSF and serum are the same? pH of serum vs CSF?
Normal CSF has about the same concentration of sodium as the serum, moderately lower concentrations of other cations, increased chloride, slightly decreased bicarbonate and glucose, but far lower levels of protein (7,000 mg/dL in serum and 28 mg/dL in CSF). The osmolality of CSF and serum are the same. The pH of normal serum is 7.4 and normal CSF is 7.3.
Class a nerves: Alpha delta A-alpha A-beta A-gamma
Class A nerves are large and myelinated and have further subdivisions.
A-delta nerves are myelinated, have a low threshold for activation, and conduct signal fast-they deal with nociception. A-alpha fibers are used for motor and proprioception. A-beta and A-gamma are used for cutaneous touch, pressure and muscle spindles.
Class C nerves are used in:
A. Nociception B. Preganglionic autonomic system C. Post-ganglionic autonomic system D. A & B E. A & C
E.
Class C fibers are non-myelinated or lightly myelinated nerves with slow conduction velocities. Slow-pain and post-ganglionic conduction are mediated through these nerves
Pain signal:
The first order neuron has a cell body in the dorsal root ganglion and sends fibers to the periphery (where nociceptors can be activated), and sends the signal through the dorsal root ganglion (in most cases but not all) and synapses on the second order neuron in the dorsal horn of the spinal cord (as well as a variety of other places including sympathetic nerves in the dorsal root). The second order neuron’s cell body is also in the dorsal horn of the spinal cord and sends the transmission to the contralateral hemisphere of the spinal cord (in many cases but not all) and sends signal up the spinothalamic tract (in some cases but not all) and synapses in a variety of places, with the three most important being: reticular formation, periaqueductal gray, and thalamus.
Which of the following increases in response to pain:
A. Cortisol B. Antidiuretic hormone (ADH) C. Cellular and humoral immune function D. A&B E. All of the above
D: A&B
Cortisol, angiotensin II, ADH, catecholamines, cytokines, adrenocorticotropic hormone, growth hormone, & glucagon increase in response to pain. Cellular and humoral immune function decreases. Pain is associated with a stress response independent of surgery.
