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Principles of Med Neuroscience > L.2.2 > Flashcards

L.2.2 Flashcards

1
Q

what are primary sensory nerve fibres

A

nerve fibres that transmit different sensory modalities (ex: chemical, mechanical or thermal)

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2
Q

What are the features of large sensory nerve fibres

A
  • conduct signals more quickly
  • faster signal transmission
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3
Q

Why do large primary sensory nerve fibres conduct signals faster

A
  • greater diameter (less resistance)
  • more myelination
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4
Q

What are examples of large primary sensory nerve fibres

A

proprioception and touch fibres

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5
Q

What are features of small sensory nerve fibres

A
  • conducts signals more slowly
  • slower signal transmission
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6
Q

Why do small sensory nerve fibre conduct signals slower

A
  • they have a smaller diameter (more resistance)
  • little to myelination
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7
Q

What is the function of tactile receptors close to the surface of the skin

A
  • important for detecting light touch and texture
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8
Q

Name 2 tactile receptors that are close to the surface of the skin

A
  • Merkel’s disk
  • Meissner’s corpuscle
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9
Q

What is the function of deeper tactile receptors

A

specialised for sensing deeper pressure and skin stretching

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10
Q

What are the differences in receptive field size between tactile receptors

A
  • close to surface: small receptive fields
  • deep: large receptive fields
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11
Q

What does the size of the receptor field mean

A
  • small receptor field = smaller area of skin = allows more precision
  • larger receptor field = larger skin area = no precision and allows gross movement
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12
Q

What are rapid adapting receptors

A
  • respond strongly at the start of stimulus and continue even if the stimulus is gone
  • good for detecting changes in stimuli
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13
Q

What are the slowly adapting receptors

A
  • continue to fire as long as the stimulus is present
  • good for detecting continuous pressure or stretch
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14
Q

How does mechanical transduction work

A
  1. touch is transduced by mechanically sensitive ion channels
  2. channels open to the deformation of the cell membrane by skin/receptors
  3. this leads to action potential
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15
Q

What are the 2 ways in which sensory information is coded by primary sensory neurons

A
  • rate coding
  • temporal coding
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16
Q

What is rate coding

A
  • frequency of action potentials
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17
Q

How does rate coding code sensory information

A
  • stronger stimulus = higher frequency of APs = higher rate of coding
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18
Q

What is temporal coding in sensory information processing?

A
  • Temporal coding refers to the timing of action potentials
  • helps to know when a stimulus occurs
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19
Q

How does the CNS interpret sensory information?

A

based on the rate (frequency) and timing (temporal coding) of action potentials

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20
Q

What is spatial resolution

A

the ability to distinguish between two close touches.

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21
Q

How is spatial distribution measured

A

using the 2-point discrimination test.

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22
Q

What is the significance of the 2-point discrimination test?

A
  • can be used to assess nerve damage
  • if nerve damage = can’t separate even at large distances
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23
Q

Why is the density of tactile receptors greater on the hand and face

A

it allows for better spatial resolution

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24
Q

How does the spatial distribution of tactile receptors vary across the body?

A

Some areas of the body have more tactile receptors than others, which affects sensitivity and spatial resolution

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25
Q

What is the difference between sensation and perception?

A
  • Sensation: Direct result of activating sensory receptors
  • Perception: brain’s interpretation of sensations, influenced by past experiences and emotions
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26
Q

Why can the same touch feel different depending on context?

A

Perceptions are influenced by past experiences and emotions

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27
Q

What are the two types of sensory information carried in ascending tracts?

A
  • proprioceptive
  • exteroceptive
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28
Q

What does proprioceptive information mean

A

information originating from inside the body (muscle, joints)

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29
Q

What does exteroceptive information mean

A

information originating from outside the body (pain, touch)

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30
Q

What are the 3 main neurons in the anatomy of the ascending sensory tracts?

A
  • first-order neurons
  • second-order neurons
  • third-order neurons
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31
Q

What do first-order neurons do

A

they carry information by entering the spinal cord via the dorsal root ganglion

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32
Q

What do second-order neurons do

A

they carry information by ascending from the spinal cord to the brainstem

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33
Q

What do third order neurons do

A

they carry information from brainstem to the cortex

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34
Q

What does the dorsal column-medial lemniscus pathway transmit?

A
  • fine touch
  • vibration
  • proprioception
  • from the PNS to the brain
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35
Q

What is the mnemonic for the DCML Pathway

A
  • Feeling Very Patient
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36
Q

What types of receptors are involved in proprioception?

A

muscle spindles, Golgi tendon organs, joints

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37
Q

Outline the DCML Pathway

A
  • first-order neurons enter spinal cord via the fasciculus cuneatus & gracilis
  • they ascend via dorsal column
  • synapse & decussate w/ second-order neurons in medulla at the nucleus cuneatus and gracilis
  • third order neurons project to somatosensory cortex
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38
Q

What is the function of the Fasciculus cuneatus & fasciculus gracilis

A
  • Fasciculus cuneatus = carries upper limb sensation to nucleus cuneatus
  • Fasciculus gracilis = carries lower limb sensation to nucleus gracilis
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39
Q

Where do first-order neurons synapse in the dorsal column pathway?

A

First-order neurons synapse on second-order neurons in the medulla at the nucleus cuneatus and nucleus gracilis

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40
Q

What is the function of second-order neurons, and where are they located? DCML Pathway

A
  • Location: Medulla
  • Receive input from first-order neurons, decussate (cross over), and form the medial lemniscus
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41
Q

What is the location and function of third-order neurons? DCML Pathway

A
  • Location: Thalamus
  • Project sensory input to the somatosensory cortex for interpretation
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42
Q

What is the location and function of first-order neurons in the dorsal column pathway?

A
  • Location: Spinal cord (Fasciculus cuneatus & fasciculus gracilis)
  • Receive sensory input from peripheral receptors and ascend through dorsal columns
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43
Q

What happens when the dorsal column (DCML) in the spinal cord is damaged?

A

Loss of tactile discrimination and proprioception on the same side as the damage

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44
Q

Why does damage to the dorsal column cause loss of sensation on the same side?

A
  • sensory signals do not cross over until the medulla
  • damage in the spinal cord interrupts signals from the same side before they decussate.
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45
Q

What is clinical test that can be used to determine if someone has had DCML damage

A

Romberg’s sign

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46
Q

What is the Rombergs sign test

A
  • Tests for sensory ataxia
  • present when a patient is able to stand with feet together and eyes open, but sways or falls with eyes closed
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47
Q

What is the spinothalamic tract responsible for

A

carrying non-discriminative touch, pain and thermal sensory information from the body the brain

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48
Q

Where do first-order neurons of the spinothalamic tract enter?

A

First-order neurons enter the spinal cord and form the tract of Lissauer.

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49
Q

where do first-order neurons synapse the spinothalamic tract

A

dorsal horn of the spinal cord

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50
Q

After crossing the spinal cord, where do second-order neurons travel? (spinothalamic tract)

A

They ascend in the anterolateral column of the spinal cord to the thalamus.

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51
Q

How are the fibres in the spinothalamic tract organized?

A

Lower limb fibres: Located laterally anterolateral column
Upper limb fibres: located anterior anterolateral column

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52
Q

What is the function of third-order neurons in the spinothalamic tract?

A

Project sensory information from the thalamus to the somatosensory cortex

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53
Q

What is the effect of a lesion of the spinal cord in the spinothalamic tract?

A

Loss of pain, temperature, and crude touch on the opposite side of the body.

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54
Q

Why does a lesion on one side of the spinal cord affect sensations on the opposite side? (spinothalamic tract)

A

they decussate in the spinal cord

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55
Q

What happens with outer tract injury (e.g., cord compression from a herniated disk)? (spinothalamic tract)

A

Loss of lower limb pain first, as lower limb fibers are located laterally.

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56
Q

What happens with inner tract injury (e.g., grey matter tumor)?

A

Loss of upper limb pain first, as upper limb fibers are located medially.

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57
Q

What kind of sensory information does the spinocerebellar tract carry

A

unconscious proprioceptive information from peripheral receptors (muscle spindles, Golgi tendon organs and joint capsules) to the cerebellum.

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58
Q

What are the effects if a lesion occurs at the spinocerebellar tract

A
  • uncoordinated muscle activity on the same side
  • the tract doesn’t cross over, damage affects the same side of the body
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59
Q

What are the 2 tracts that make up the spinocerebellar tract

A
  • posterior (or dorsal) spinocerebellar tract
  • anterior (or ventral) spinocerebellar tract
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60
Q

What is the function of the anterior (or ventral) spinocerebellar tract

A

involved in carrying proprioception from the lower limb

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61
Q

What is the function of the posterior (or dorsal) spinocerebellar tract

A

carries unconscious proprioceptive information from the lower limb and trunk

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62
Q

Outline the pathway of the spinocerebellar tract

A

1)First-order neurons enter the spinal cord and synapse in the dorsal horn
2)Second-order neurons ascend the lateral column to cerebellum via fast axons

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63
Q

What is pain?

A

An unpleasant sensory experience associated with tissue damage, involving both physical sensations and emotional reactions (e.g., fear and anxiety).

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64
Q

Why might two people experience the same injury differently?

A

Pain involves emotional reactions, which vary based on individual factors like past experiences and personal thresholds.

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65
Q

Why do we feel pain?

A
  • Protective mechanism: Alerts the body to danger
  • Prevent further damage: Encourages healing
  • Learning: Emotional memory of pain helps avoid harmful situations.
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66
Q

What are the common sensations of pain?

A

sharp, itch & ache

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67
Q

Where do pain signals start in the body?

A

In nociceptors, located in the skin and muscles

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68
Q

What is the role of nociceptors in pain?

A

They detect harmful stimuli and send signals to the spinal cord via nerves.

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69
Q

How does the spinal cord contribute to pain processing?

A

It relays pain signals to the brain for further processing

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70
Q

Which brain regions process pain sensations and emotional responses?

A
  • Somatosensory cortex: Processes the physical sensation of pain.
  • Limbic system: Handles emotional responses to pain.
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71
Q

What are the two main components of pain mechanisms?

A
  • Peripheral Component: Nociceptors detect harmful stimuli and send signals to the spinal cord.
  • Central Component: The spinal cord relays signals to the brain, which processes the sensation and emotional reaction.
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72
Q

What is nociceptive pain?

A

Pain Caused by activation of nociceptors due to actual or potential tissue damage

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73
Q

What are examples of injuries that cause nociceptive pain?

A

Injuries to tissues such as skin, muscles, and joints

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74
Q

What is neuropathic pain?

A

Pain caused by injury or dysfunction of the nervous system, leading to abnormal pain signals

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75
Q

What are nociceptors?

A

Primary sensory neurons that detect pain

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76
Q

Where are nociceptors located?

A
  • skin
  • muscles
  • meninges
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77
Q

How do nociceptors transmit pain signals?

A

Nociceptors send pain signals to the dorsal horn in the spinal cord, which then transmits them to the brain.

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78
Q

What are the two primary sensory nerve fibres for transmitting pain?

A
  • A-delta fibres
  • C fibres
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79
Q

What do A-delta fibres transmit

A

Transmit sharp and acute pain quickly (e.g., touching a hot surface).

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80
Q

What do C fibres transmit

A

Transmit dull and aching pain slowly.

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81
Q

Why are pain signals transmitted slowly via small-diameter nerve fibres?

A

To keep pain in the brain’s awareness longer, encouraging proper rest and avoiding further injury

82
Q

What are free nerve endings?

A

Unspecialised nerve endings of nociceptors make them versatile in detecting a range of painful stimuli

83
Q

What types of stimuli can nociceptors detect?

A

thermal, mechanical and chemical

84
Q

what kind of special structure do nociceptors have

A

they have free nerve endings in the periphery

85
Q

What are features of first-pain response

A
  • well-localised
  • fast transmission
  • conducted by alpha-delta fibres
86
Q

What are features of secondary pain responses

A
  • poorly localised
  • slow transmission
  • conducted by C-fibres
87
Q

What are polymodal nociceptors?

A

Nociceptors that respond to multiple types of stimuli, such as thermal and chemical.

88
Q

What type of nociceptors are mostly polymodal?

A

C fibres

89
Q

How does the brain differentiate between pain stimuli (e.g., heat or mechanical force)?

A

The central nervous system decodes signals from peripheral nerves to determine the pain source.

90
Q

What is pressure transduction in nociceptors?

A

Mechanically sensitive ion channels at the nerve receptor ends respond to pressure, causing membrane deformation

91
Q

What happens during pressure transduction?

A
  1. Membrane deformation causes ion channels to open
  2. Calcium and sodium ions enter the cell, causing depolarization.
  3. Action potential generated
92
Q

What channels are responsible for temperature transduction?

A

Transient receptor potential (TRP) channels transduce different temperatures

93
Q

Which specific TRP channel responds to heat and capsaicin?

A

The Vanilloid (TRPV1) channel responds to heat and capsaicin (found in chillies)

94
Q

How does inflammation affect nociceptors?

A

Inflammatory chemicals released during tissue injury excite nociceptors, enhancing pain sensitivity.

95
Q

What are examples of chemicals that sensitize nociceptors during inflammation?

A
  • ATP
  • H+
  • serotonin
96
Q

What happens to nociceptors during tissue injury or inflammation?

A

Chemicals are released that activate nociceptors, triggering pain signals.

97
Q

Which chemical binds to purinergic receptors to activate nociceptors?

A

ATP binds to purinergic receptors

98
Q

Which chemical binds to 5-HT3 receptors to activate nociceptors?

A

serotonin

99
Q

How do protons (H+) activate nociceptors?

A

Protons bind to acid-sensing channels and increase during tissue acidosis (ex: lactic acid build up during exercise)

100
Q

What is neurogenic inflammation?

A

Activation of one branch of a nociceptor spreads inflammation to other areas

101
Q

What chemicals are released during neurogenic inflammation?

A

Substance P and calcitonin gene-related peptide (CGRP).

102
Q

What are the effects of Substance P and CGRP?

A
  • Vasodilation: Blood vessels dilate, increasing blood flow.
  • Mast Cell Activation: Mast cells release histamine, increasing inflammation.
103
Q

What is hyperalgesia?

A

A condition where noxious stimuli produce an exaggerated pain response

104
Q

What is allodynia?

A

A condition where non-noxious stimuli cause a painful response.

105
Q

What is an example of hyperalgesia

A

A small pinch on inflamed skin feels extremely painful

106
Q

What is an example of allodynia

A

Brushing against sunburned skin feels painful

107
Q

Why does inflammation cause hypersensitivity?

A

Hypersensitivity protects injured tissues by preventing interference, promoting healing

108
Q

What are the two main mechanisms of pain hypersensitivity?

A
  • Peripheral sensitisation
  • Central sensitisation
109
Q

What is peripheral sensitisation

A

Increased responsiveness of nociceptor ends due to tissue injury/inflammation.

110
Q

What is central sensitisation

A

Enhanced response within the spinothalamic tract, common in neuropathic pain.

111
Q

How does bradykinin contribute to peripheral sensitisation?

A
  • Reduces the threshold of heat-activated TRPV1 channels
  • Causes heat-sensitive nociceptors to fire more easily, increasing sensitivity to warmth
112
Q

How does nerve growth factor (NGF) affect nociceptors?

A

It reduces the threshold of TRPV1 channels, making heat-sensitive nociceptors fire more easily.

113
Q

How do prostaglandins contribute to pain hypersensitivity?

A
  • Reduce the threshold of sodium and TRPV1 channels.
  • Nociceptors fire more easily, leading to hypersensitivity
114
Q

What is the mechanism of action of bradykinin in nociceptor sensitisation?

A
  1. Bradykinin binds to its metabotropic G protein-coupled receptor on the nociceptor
  2. Protein kinases are activated within the neuron
  3. Phosphorylation occurs on the TRPV1 channel, making it more sensitive
115
Q

What is the result of bradykinin’s action on the TRPV1 channel?

A

The TRPV1 channel becomes more sensitive, firing at lower temperatures

116
Q

What is the role of first-order neurons in the spinothalamic tract?

A

First-order neurons (nociceptors) detect pain at the site of injury (skin, muscles, organs) and send signals to the spinal cord via the dorsal horn

117
Q

What happens to first-order neurons once they enter the spinal cord? (spinothalamic tract – pain)

A
  • Their fibres travel through the tract of Lissauer.
  • They synapse in the substantia gelatinosa (lamina I and II).
  • Glutamate and substance P are released to excite second-order neurons.
118
Q

Where are second-order neurons located, and what is their function? (spinothalamic tract)

A

Second-order neurons are in the dorsal horn of the spinal cord:
- Cross to the opposite side of the spinal cord.
- Ascend to the thalamus through the anterolateral column.

119
Q

What is the role of third-order neurons in the spinothalamic tract?

A
  • Sensory component: Project to the primary somatosensory cortex to encode location and modality of pain.
  • Emotional component: Project to the insula and cingulate cortex (limbic system, prefrontal cortex) to encode emotional responses to pain.
120
Q

Why does referred pain happen?

A

Visceral nociceptors and skin nociceptors converge on the same second-order neurons in the spinal cord, leading the brain to misinterpret the source of pain

121
Q

What is referred pain?

A

Referred pain occurs when the brain misinterprets visceral pain (from organs) as coming from the skin or muscles

122
Q

What is an example of referred pain?

A

In angina (heart pain), the pain is perceived in the left arm or upper chest because the brain receives signals from both the heart and these skin areas through the same spinal neurons

123
Q

What is stress-induced analgesia?

A

the body’s ability to temporarily reduce pain during stressful or dangerous situations, allowing for survival or focus on a demanding task

124
Q

How does the body achieve stress-induced analgesia?

A
  • The brain activates a descending modulatory system to reduce pain signals travelling from the body to the brain.
  • Higher cortical regions initiate these pathways to suppress pain
125
Q

What role does the periaqueductal grey matter (PAG) play in pain regulation?

A

The PAG initiates pain suppression by activating descending modulatory pathways

126
Q

What is the function of the rostral ventromedial medulla (RVM)?

A

The RVM sends inhibitory or excitatory signals down the spinal cord to modulate pain in the spinothalamic tract

127
Q

Outline the pathway of pain modulation

A
  1. Cortical regions trigger the pathway and send signals to the PAG.
  2. PAG sends signals to the RVM.
  3. RVM sends modulatory signals to the dorsal horn where pain is inhibited or amplified
128
Q

What is the order of regions in the descending pain modulation pathway?

A

Cortical regions → PAG → RVM → Dorsal horn

129
Q

How does the inhibition of pain occur in the dorsal horn?

A
  1. The PAG activates serotonergic neurons in the RVM.
  2. These neurons excite inhibitory interneurons in the dorsal horn.
  3. Inhibitory interneurons release neurotransmitters that reduce spinothalamic tract activity, blocking pain signals.
130
Q

What is the result of pain inhibition in the dorsal horn?

A

Pain signals from nociceptors are blocked, resulting in fewer pain signals traveling to the brain.

131
Q

What are the opioid peptides used by the body to inhibit pain?

A

Endorphins and enkephalins.

132
Q

How do opioids inhibit pain?

A
  • Opioids bind to inhibitory metabotropic receptors.
  • This reduces the activity of neurons and blocks pain signals
133
Q

What is the role of opioids in the PAG and RVM?

A
  • Opioids inhibit inhibitory interneurons that normally suppress the pain pathway.
  • Result: The pain inhibition pathway remains active.
134
Q

How do opioids act in the dorsal horn to inhibit pain?

A

Opioids act directly on second-order neurons, preventing them from transmitting pain signals to the brain

135
Q

What is the overall effect of the endogenous opioid system?

A

The endogenous opioid system reduces or blocks the transmission of pain signals along the pain pathway

136
Q

What are opioids

A

Opioids are drugs used for pain relief.

137
Q

how do opioids work?

A

they work by binding to specific opioid receptors in the brain, which reduces pain perception and creates a sense of calm.

138
Q

What is Naloxone

A

an opioid antagonist that binds to opioid receptors without activating them displacing opioids.

139
Q

why is Naloxone useful?

A

It reverses opioid effects and can treat opioid overdose by displacing opioids from receptors

140
Q

what are examples of opioids for severe pain and mild pain?

A

Morphine (for severe pain) and codeine (for mild pain).

141
Q

What are semi-synthetic opioids

A

chemically modified versions of naturally occurring opioids

142
Q

What are examples of semi-synthetic opioids

A

heroin

143
Q

What are synthetic opioids and what are some examples?

A
  • completely man-made
  • Fentanyl
144
Q

When are synthetic opioids used for

A

severe pain

145
Q

What are the risks associated with opioid use?

A
  • Dependency: Physical and psychological reliance.
  • Tolerance: Need for higher doses over time to achieve the same effect.
  • Overdose: Potentially fatal respiratory depression
146
Q

What does PCA stand for, and how is it administered?

A
  • Patient-Controlled Analgesia
  • it allows patients to self-administer pain relief using an IV pump
147
Q

How does an infusion differ from PCA?

A

An infusion delivers medication continuously through an IV line, while PCA allows self-administration on demand.

148
Q

What is intramuscular administration?

A

It involves injecting medication directly into a muscle.

149
Q

How are oral medications administered, and what is a key characteristic of this method?

A
  • by mouth;
  • it is convenient but slower due to the digestive process
150
Q

Where are medications delivered in epidural/spinal administration, and what is it commonly used for?

A
  • injected into the epidural space or spinal fluid
  • commonly for regional pain relief during childbirth or surgery
151
Q

Where in the brain are opioid receptors that play a role in pain transmission located?

A

In the pons and midbrain

152
Q

What is the function of the periaqueductal grey matter, and where is it located?

A
  • in the midbrain
  • crucial for pain suppression and is a key site for opioid action
153
Q

What is the role of the nucleus raphe magnus in pain modulation?

A

It inhibits pain signals as they ascend to the brain

154
Q

Why can opioids cause constipation?

A

Opioid receptors in the gastrointestinal tract affect digestive processes, often leading to constipation

155
Q

How do peripheral opioid receptors influence pain and inflammation?

A

They act locally in peripheral tissues to modulate pain and inflammation.

156
Q

What is the primary function of MU receptors?

A

They are the primary opioid receptors (e.g., morphine) responsible for powerful pain relief (analgesia) but also cause side effects like nausea and itching.

157
Q

What role do delta receptors play in pain and mood?

A

involved in pain modulation and emotional responses, influencing mood and the emotional aspects of pain

158
Q

What is the key benefit and limitation of kappa receptors?

A

provide pain relief with fewer side effects, like respiratory depression, but can cause dysphoria instead of euphoria, limiting addiction potential

159
Q

To which type of receptor does morphine bind, and what is the effect?

A

Morphine binds to MU receptors in the brain and spinal cord to reduce the perception of pain

160
Q

What are the common side effects of morphine?

A

Respiratory depression, nausea, vomiting, constipation

161
Q

Why can morphine cause respiratory depression?

A

It slows down breathing, which can be dangerous at high doses.

162
Q

How does morphine affect the gastrointestinal tract?

A

It slows down movement, leading to constipation.

163
Q

Against which specific opioid side effect is naloxone most effective?

A

Respiratory depression

164
Q

What does the acronym ABC stand for when managing a patient?

A

Airway, Breathing, and Circulation.

165
Q

Why is checking the airway a critical first step?

A

To ensure it is clear, as an obstructed airway prevents oxygen from reaching the lungs.

166
Q

What does assessing breathing ensure?

A

That the lungs are ventilating properly and oxygen is reaching the blood.

167
Q

Why is checking circulation important in patient care?

A

To ensure that blood is carrying oxygen properly to tissues

168
Q

What can happen when a patient regains consciousness rapidly after naloxone administration?

A

They may wake up quickly and agitated as they regain consciousness

169
Q

Why is close monitoring required after naloxone administration?

A

Its short duration means opioid effects can return once naloxone wears off, causing the patient to collapse suddenly.

170
Q

What is ketamine primarily used for?

A

It is a fast-acting anesthetic and analgesic used for pain relief and sedation

171
Q

How does ketamine reduce pain?

A

It blocks NMDA receptors in the brain, reducing pain signals, and interacts with kappa and delta receptors for additional pain relief

172
Q

What makes ketamine a suitable anesthetic for patients with low blood pressure?

A

Its sympathomimetic effect increases heart rate and blood pressure.

173
Q

What is emergence phenomena in patients recovering from ketamine?

A

Vivid dreams or hallucinations experienced as the patient wakes up.

174
Q

What are the three main properties of NSAIDs?

A

Analgesic (pain relief), antipyretic (fever reduction), and anti-inflammatory.

175
Q

How do NSAIDs work to reduce pain and inflammation?

A

By inhibiting the Cyclooxygenase (COX-1 and COX-2) enzymes.

176
Q

What are common side effects of NSAIDs on the gastrointestinal system?

A

Gastric irritation

177
Q

How can NSAIDs affect the respiratory system in some patients?

A

They can cause bronchospasm, leading to breathing difficulties.

178
Q

How does aspirin, a type of NSAID, affect blood clotting?

A

It inhibits platelet function, reducing the ability of blood to clot.

179
Q

What enzymes does aspirin inhibit to reduce pain, fever, and inflammation?

A

Cyclooxygenase (COX) enzymes

180
Q

How can high doses of aspirin affect cellular energy production?

A

It disrupts oxidative phosphorylation

181
Q

What is “air hunger,” and how is it related to aspirin?

A

Difficulty breathing caused by excessive aspirin intake.

182
Q

What are paracetamol’s primary uses?

A

Pain and fever relief.

183
Q

What is the main risk of paracetamol overdose?

A

liver damage

184
Q

How do anxiolytics help with pain management?

A

They reduce anxiety, which can indirectly lower pain perception

185
Q

What is the role of local anesthetics in pain management?

A

They block pain at the nerve level for specific procedures

186
Q

Which types of medications, like gabapentin, are used for chronic pain?

A

Antidepressants and antiepileptics.

187
Q

How does ether stimulate the cardiovascular system?

A

stimulates the sympathetic nervous system, helping maintain cardiovascular stability, especially in cases of severe blood loss

188
Q

Why is ether’s high blood/gas partition coefficient a challenge in anesthesia?

A

It causes slow uptake into the blood, making it difficult to achieve and maintain an appropriate anesthetic depth.

189
Q

What is the primary purpose of anti-emetic drugs?

A

To prevent nausea and vomiting, especially as a side effect of anesthesia.

190
Q

Name three additional anti-emetics used based on patient needs.

A

Steroids, prochlorperazine, and cannabinoids

191
Q

Name three common benzodiazepines

A

Midazolam, Diazepam, Lorazepam.

192
Q

What are the routes of administration for benzodiazepines?

A

Oral, Intravenous, Intramuscular.

193
Q

What are the risks of over-sedation with benzodiazepines?

A

Impaired awareness and responsiveness, loss of airway reflexes, and respiratory depression, especially when combined with other sedatives

194
Q

What is the reversal agent for benzodiazepine overdose?

A

Flumazenil, which blocks benzodiazepine effects

195
Q

What is the primary difference between amides and esters in local anesthetics?

A

Amides have a longer duration of action and are broken down more slowly, while esters have a shorter duration and are metabolized quickly

196
Q

Give three examples of amide local anesthetics.

A

Lignocaine (lidocaine), prilocaine, bupivacaine

197
Q

What is the primary target of local anesthetics in nerve cells?

A

Sodium channels.

198
Q

Describe the first step in the mechanism of action for local anesthetics.

A

The un-ionized drug crosses the cell membrane into the inside of the nerve cell.

199
Q

What happens to the drug once it is inside the nerve cell?

A

It becomes ionized, enabling it to block sodium channels.

200
Q

What is the ultimate effect of local anesthetics blocking sodium channels?

A

Inhibition of action potentials, preventing pain signals from traveling to the brain.

201
Q

Why is there a toxicity risk with local anesthetics?

A

Blood vessels and nerves are closely associated, increasing the chance of accidental vascular injection.

Principles of Med Neuroscience (12 decks)

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