Brainscape's Knowledge GenomeTM

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


See full index

ACVECC 2024 > Anesthesia/Analgesia > Flashcards

Anesthesia/Analgesia Flashcards

1
Q

What is the definition of suffering

A

“an experience of unpleasantness and aversion associated with perception of harm or threat of harm in an individual”

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

What is a primal alert signal

A

Linked to animals need to maintain homeostasis
Designed to alert animals to threats to these needs being met and drive aversive and adaptive behaviors

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

What are the four most common clinical signs associated with illness

A
  1. Fever 2. Lethargy 3. Anorexia, 4. Cachexia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What can sleep deprivation lead to

A

Systemic hypertension, higher mortality

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

What are 8 palliative measures in ICU for suffering

A

1) Provide adequate opportunity for uninterrupted sleep
-Low lighting overnight when feasible
2) Clustering treatments to minimize patient awakenings
3) Addressing thirst, hunger, and pain
4) Small amount of oral liquids to maintain membrane moisture -
5) Serial monitoring for pain
6) Vigilance for nausea
7) Nebulized furosemide may provide symptomatic relief from dyspnea as may opioid administration
8) Get patients outside for portion of the day to express normal behaviors

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

Definition of pain

A

an unpleasant sensory and emotional experience associated with actual or potential tissue damage.

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

10 consequences of uncontrolled pain

A
  1. increased blood pressure and heart rate
  2. peripheral vasoconstriction
  3. increased metabolic rate and oxygen consumption
  4. decreased immune function
  5. Immobility
  6. decreased pulmonary function and atelectasis
  7. increased incidence of pneumonia
  8. Inappetence
  9. Restlessness
  10. Insomnia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the four goal of treating pain

A
  1. relieve patient suffering
  2. promote healing
  3. decrease length of hospitalization
  4. minimize long-term changes to the animal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are physiological 4 parameters of pain

A

HR, RR, BP and pupil dilation

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

What is a measurable physiologic parameter and how does it relate to pain

A

Heart rate variability: variation in R-R interval obtained on ECG

Changes in parasympathetic and sympathetic nervous system tone have bigger impacts on high and low frequency components

Low HRV suggests dominance of once branch of ANS , typically the SNS if the evaluation made during noxious stimulation, stress, exercise

Correlated to chronic pain but not acute pain

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

What are endocrine markers of pain

A

epinephrine, NE, and cortisol

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

What are 10 altered behaviors of animals when in pain? Give an example of each

A
  1. Posture
    -Hunched back, base-wide stance position, prayer position (neck and head extended forward with front of body lowered to the ground), head and/or tail tucked under the body, tension and rigidity of the painful area, frequent position changes, reluctance to assume normal body positions (e.g., will not lie down, sit or stand when they normally would)
  2. Gait
    -Stiff, lameness, reluctance to move
  3. Abnormal movements
    -Shaking, trembling

4.Interaction
Reducing willingness to interact with people

  1. Demeanor
    Some animals become aggressive, some submissive

6.Attention to painful area
-Looking and staring, guarding, licking, chewing, and biting, self mutilation

  1. Palpation to painful area
    Turn or flinch, withdrawal, or escaping effort to biting and aggression when applying pressure
  2. Vocalization
    -Altered vocalizatio patterns
  3. Appetite
    -hyporexia/anorexia
  4. Grooming
    -Excessive grooming or chewing
    -In cats appropriate grooming decreased
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are two types of pain scales

A

Unidimensional and Multidimensional

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

What’s a unidimensional pain scale and what are its cons

A

Simple descriptive scale, numeric rating, scale, and visual analog scale

Poor interobserver agreement and sensitivity

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

Name 7 multidimensional scales and which ones are not validated?

A

1) 4AVetscale (validated for orthopedic pain)

2) Glasgow composite measure pian score (CMPS-C)
-validated for acute pain

3) Glasgow composite measure pain score short form
-validated for acute postop pain

4) university of melbourne pain scale
-acute pain

5) CSU pain scale
-not validated

6) UNESP-botucatu Multidimensional composite pain scale for cats
-validated

7) Glasgow composite measure pain score feline
-validated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is an action unit in pain

A

unique changes in facial expression produced by facial muscle activity
Involuntary and cannot be properly suppressed, amplified or stimulated

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

What are three AU’s in cats

A

Bases of pinane moving away, dorsal movement of the nose, mouth, and cheek area, and eyes narrowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

In a study of 351 dogs and cats hospitalized in the ICU, ___% were prescribed analgesics, and in __% of those cases, drug administration deviated from prescribed orders (__% decreased dose and ___% increased dose).

A

In a study of 351 dogs and cats hospitalized in the ICU, 39% were prescribed analgesics, and in 36% of those cases, drug administration deviated from prescribed orders (62% decreased dose and 38% increased dose).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

In above study What were reasons in above study for decreased dosing

A

sedation, hypothermia, hypotension, perceived absence of pain, and lack of access to controlled drugs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

In above study what were reasons for increased dosing

A

perceived pain, vocalizing, and anxiety.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What % PCV is necessary for adequate oxygen carrying capacity and oxygen delivery?

A

> 25%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

During anesthesia PCV can decrease by how much %?

A

3-5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What anesthetic protocols should be considered and administered for patient with renal insufficiency

A

Higher fluid rate may be required to maintain renal perfusion
Drugs excreted by kidney (ketamine in cats) may have delayed excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What anesthetic protocols should be considered and administered for patient with hepatic disease

A

Anesthetic protocols may be affected due to decreased glucose and albumin production, altered drug metabolism via cytochrome P-450 and decreased production of coagulation factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What anesthetic protocols should be considered and administered for patient with cardiac disease

A

Avoid fluid overload
Monitor BP carefully because hypotension may come from decompensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

MOA for anticholinergic?

A

competitively inhibits acetylcholine or other cholinergic stimulants at postganglionic parasympathetic neuroeffector sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Side effects of anticholinergics?

A

May make secretions more viscous

Increase anatomic dead space

Increase heart rate

Can increase myocardial work and oxygen consumption

Increase IOP, pupillary dilation

Glycopyrrolate does not cross blood–brain barrier or the placenta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Which U agonist has NMDA antagonist properties

A

Methadone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Pros and Cons of full u agonist

A

Complete reversal with naloxone

Analgesic- good for chronic and neuropathic pain

Minimal effect on CV performance

Give anticholinergic drug before starting CRI

Monitor for hyperthermia in cats

Cause respiratory depression

Cause bradycardia

Reduce reuptake of norepinephrine and serotonin, possible serotonin syndrome

morphine and meperidine cause histamine release => hypotension

GI effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Pros and cons of partial u agonist

A

Slow onset, effects difficult to reverse

Good for moderate pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Pros and cons of k agonist/u antagonist

A

Partial reversal of µ-agonist drugs

Minimal CV effects

Not good for severe pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

MOA of ketamine

A

binds N-methyl-D-aspartate (NMDA) receptors, reducing receptor activity and release of glutamate, an excitatory neurotransmitter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Pros and Cons of Ketamine

A

Cause salivation

Increase heart rate, CO via centrally mediated sympathetic response and endogenous catecholamine release, usually CV sparing

Increase ICP and intraoccular pressure

Analgesic

Renal elimination in cat

Cautious use in cats with HCM b/c increased cardiac contractility

Direct myocardial depressant effects in debilitated patients with decreased endogenous catecholamine response +. Hypotension and CV instability

Potential seizure as sole agent

doesn’t depress laryngeal protective reflexes and produces less ventilatory depression than opiods

Prevents response to nociceptive stimulie carried by p ain neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

MOA of benzodiazepines

A

antagonism of serotonin

increased release of and/or facilitation of gamma-aminobutyric acid (GABA) activity

diminished release or turnover of acetylcholine in the CNS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

MOA of phenothiazines

A

block postsynaptic dopamine receptors in the CNS and may inhibit the release of dopamine and increase its turnover rate

alpha 1 receptor blockade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Pros and cons of phenothiazine

A

Vasodilatory

Long duration of action

Not analgesic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

MOA of barbiturates

A

act directly on the CNS neurons in a manner similar to that of the inhibitory transmitter GABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Pros and Cons of barbiturates

A

Cause cardiovascular depression

Cause respiratory depression

Provide rapid induction

Decrease ICP and intraoccular pressure

Effects may be potentiated by concurrent acidosis or hypoproteinemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

MOA of propofol

A

Potentiates the effects of gamma-aminobutyric acid (GABA; an inhibitory neurotransmitter) by decreasing the rate of dissociation of GABA from its receptors.

This prolonged binding results in an influx of chloride, causing hyperpolarization of the postsynaptic cell membrane.

Propofol may also have activity at the glycine and N-methyl-D-aspartate (NMDA) receptors, but this is unclear.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Pros and Cons of Propofol

A

Rapidly acting with short duration of action

Causes respiratory depression

Causes peripheral vasodilation

Myocardial depressant

Can create arrhythmias

Not analgesic

Use with caution in patients with volume depletion or cardiovascular compromise; can cause significant depression

Increases ICP

Can cause Heinz body anemia in cats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

MOA of etomidate

A

Acts at the GABA receptor in the CNS to increase chloride conductance, causing hyper-polarization of postsynaptic neurons and resulting in hypnosis and CNS depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Pros and cons of etomidate

A

Maintains cardiovascular stability

Not used alone: otherwise retching and myoclonus

Suppresses adrenocortical function for 2–6 hr following single bolus dose

in cats repeated use => hemolysis due to propylene glycol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How are alpha 2 agonists metabolized

A

biotransformed by the liver, with inactive metabolites excreted in the urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Pros and cons of alpha 2 agonist

A

Causes cardiovascular depression

Can cause vomiting

Provides good sedation and analgesia

diuresis

peripheral vasoconcstriction

bradycardia

muscle relaxation

Can be combined with butorphanol or ketamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

MOA of alfaxalone

A

neuroactive steroid, binds to and activates the GABA cell surface receptor, inducing postsynaptic cell membrane hyperpolarization by activating chloride ion transport and enhancing the inhibitory action of GABA in the CNS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How is alfaxalone metabolized

A

undergoes phase I (cytochrome P450-dependent) and phase II (conjugation-dependent) metabolism in both species.27 Cats and dogs form the same 5 phase I metabolites. Phase II metabolites in cats are alfaxalone sulfate and alfaxalone glucuronide, with only alfaxalone glucuronide found in dogs. Alfaxalone metabolites are likely to be eliminated from dogs and cats by hepatic/fecal and renal routes, which is similar to other species studied.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

MOA of Lidocaine in analgesia

A

reducing ectopic activity of damaged afferent neurons, action at different molecular sites, such as Na+, Ca2+, and K+ channels and N-methyl-D-aspartate (NMDA) receptors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

MOA of inhalants

A

Acts on GAB receptors and voltage-gated channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Pros and cons of inhalants

A

Produces dose-dependent cardiovascular depression and peripheral vasodilation

Anesthesia depth can be adjusted rapidly

Potential for hypoxemia

Isoflurane and sevoflurane show rapid uptake and recovery

Nitrous oxide should be used with caution with closed gas spaces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Why is propoflo 28 not recommended in ill cats

A

Has benzyl alcohol as preservative which can be toxic when given in large doses

low capacity for glucuronic acid conjugation and therefore have limited ability to metabolize benzoic acid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What drug should be avoided in splenic tumor/fracture patients and why?

A

acepromazine, thiopental, and propofol can result in splenomegaly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What monitoring should you do during anesthesia?

A

Monitor ECG for changes in HR and rhythm
MAP > 60 mmHG to maintain renal perfusion
Perfusion parameters: CRT, MM, pulse quality
Depth
Oxygenation
Capnography
UOP
Temperature
Bloodwork (PCV/TP, BG in critical patietns)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What features do you look at in depth

A

eye position
pupil size
jaw tone
response to stimulus
heart rate
blood pressure
respiratory rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Pulse ox will read less than 100% when PaO2 falls under ____

A

140 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Steps to trouble shoot intraoperative hypotension

A

First step decrease inhalant
Next fluid bolus
Inotropic/vasopressor support
Add second agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is the goal of pain control?

A

state in which the pain is bearable but some of the protective aspects of pain, such as inhibiting use of a fractured leg, still remain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Where do opioids react (central, peripheral, transduction)?

A

centrally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

MOA of naloxone

A

bind to the same receptor as agonists but cause no effect and can competitively displace the agonist from the receptor and therefore reverse the agonist effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Which opioids reach a maximal effect at upper end of dose rang

A

butorphanol and buprenorphine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How is remifentanil metabolized

A

tisseu plasma esterases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Duration of action of fentanyl?

A

30 min an up to 2 hours when Im or SC

62
Q

Adverse effects of simbadol

A

hyperthermia, hypotension, bradycardia, or tachycardia

63
Q

Side effects of naloxone

A

acute pain, excitement, emergence delirium, aggression, and hyperalgesia

64
Q

What’s the benefit of using butorphanol as a reversal agent

A

that complete reversal of analgesia does not occur due to the κ-agonist effects of butorphanol. has sedative effects still

65
Q

Why is buprenorphine not as easily reversed

A

difficult to displace form receptor

66
Q

Draw arachidonic acid pathway

A
67
Q

How do nsaids decrease pain

A

NSAIDs decrease the pain input to the CNS, which may aggravate central hypersensitivity.
Inhibition of COX enzyme isoforms decreases inflammation

68
Q

Which COX pathway responsible for basal prostaglandin production and normal homeostatic processes

A

Cox 1

69
Q

Where are alpha 2 adrenergic agonists metabolized

A

biotransformed by the liver, with inactive metabolites excreted in the urine

70
Q

Cons of atipamazole

A

abrupt hypotension and/or aggression

71
Q

What can affect efficacy of fantanyl patch

A

Taken up by dermal blood flow
Hair, obesity and hypovolemic or hypothermic patients can alter

72
Q

What are adverse effects of bupivicaine

A

arrhythmias, reduced CO diaphragmatic paralsyis

73
Q

How does nocita work

A

multi-vesicular liposomes encapsulating bupivacaine
gradually released over several hours as the lipid bilayers break down

74
Q

Adverse effects epidural

A

vasodilation and subsequent hypotension

vomiting, urinary retention, pruritus, and delayed hair growth at the clipped epidural site

75
Q

Contraindications for epidural analgesia

A

include trauma over the pelvic region (with loss of appropriate landmarks), sepsis, coagulopathy, CNS disease, skin infection over the site of injection, hypovolemic shock, and severe obesity.

76
Q

Complications of epidural catheter

A

catheter dislodgement, discharge from the site, fecal contamination, line or filter breakage, and localized dermatitis.

77
Q

Why do you use lower dose if epidural goes into subarachinoid space

A

The lower dose is sufficient for an analgesic response because the roots of the spinal cord are more accessible within the subarachnoid space, where they are not protected by the dura

78
Q

Why is lidocaine beneficial to ischemia re-perfusion injury

A

inhibiting Na+/Ca2+ exchange and Ca2+ accumulation during ischemia, scavenging hydroxyl radicals, decreasing the release of superoxide from granulocytes, and decreasing polymorphonuclear leukocyte activation, migration into ischemic tissues, and subsequent endothelial dysfunction

79
Q

What % of human patients will experience ICUAW and can be u to 6 months

A

As much as 50% of muscle strength can be lost within 1 week of immobility

80
Q

What are benefits of rehabilitation therapy in critically ill patients

A
  • Decrease loss of muscle mass and strength
  • Maintain functional ability
  • Decrease pain and inflammation
  • Improve healing time
  • Reduce edema
  • Improve ventilation and circulation
  • Positive psychological benefits
  • Prevent injury
  • Decrease hospitalization time
  • Guide post hospitalization home care
81
Q

How does laser therapy work

A

photobiomodulation, involves the direct application of light energy (photons) to induce cellular responses in tissues

photons are absorbed by the cytochrome c complex in the mitochondria of target cells, which results in a biological cascade of events, including accelerated production of ATP, nitric oxide, and reactive oxygen species

reduces pain, inflamamtion, heals, improves muscle repair

82
Q

Where are contraindicated areas of treatment for laser therapy

A

neoplastic lesions, near a pregnant uterus, gonads, or cornea, near the presence of active bleeding, the endocrine glands, and active epiphyses.

83
Q

What’s Transcutaneous Electrical Nerve Stimulation

A

TENS is the application of high-frequency electrical current through electrodes placed on the skin.
TENS activates large cutaneous Aβ fibers, which is believed to stimulate inhibitory neurons in the spinal cord dorsal horn, interfering with transmission of C nerve fiber pain impulses to the brain (also known as the gate theory)

84
Q

What is pulsed electromagnetic field therapy

A

a device that transmits a nonthermal electromagnetic field when applied over an area of tissue to reduce pain and inflammation
increase intracellular Ca2+, which leads to increased calcium binding to calmodulin. It is believed that this reaction leads to a variety of downstream pathways, including the production of nitric oxide

85
Q

Contraindications to pulsed electromagnetic field therapy

A

not advisable to apply PEMF over tumor sites of hemangiosarcoma due to a potential increase in blood flow. Similarly, it should not be used with animals that have a pacemaker because of potential electrical interference.

86
Q

What is cryotherapy

A

application of cold to tissues, results in vasoconstriction, which decreases local blood flow, inflammatory response, and edema, thereby reducing pain

Pain relieving effects are achieved by slowing of nerve conduction velocity, increasing pain threshold and pain tolerance

87
Q

What is thermotherapy

A

Results in vasodilation, promotion of circulation of blood and lymphatics, edema reduction, release of muscular tension and spasm, pain reduction, and improved tissue elasticity

88
Q

How does Prom help

A

diffusion of nutrients from synovial fluid to cartilage, improves circulation and flexibility, and reduces the tension of periarticular muscles.
In patients with femoral fractures, PROM is required to prevent quadriceps

89
Q

What are three kinds of massage

A

1.Stroking 2. Effleurage 3. Petrissage

90
Q

What is stroking massage

A

slow gliding movement over the body using the palm of the hand in the direction of fur growth, cranial to caudal and proximal to distal

91
Q

What is effleurage massage

A

helps with fluid mobilization and lymphatic drainage; the palms of the whole hand are used for long strokes with light to moderate pressure distal to proximal and along the direction of muscle fibers towards the flow of lymphatic and drainage back to the heart.

92
Q

Where should

A
93
Q

massage not be performed

A

areas of active infection or acute inflammation, near a tumor, over open wounds, in cases of deep vein thrombosis or coagulopathies, in patients with unstable fractures, over painful areas, in patients in shock, and animals adversely reactive to touch

94
Q

What is neuromuscular electrical stimulation

A

low frequency, high pulse duration electrical stimulation to the muscles percutaneously through electrodes placed on the skin.
The current acts on motor nerves to achieve muscle contraction.

95
Q

When is neuromuscular electrical stimulation contra-indicated

A

pacemaker patients or seizure disorders

Application is not recommended over areas of neoplasia, infection, impaired sensation or skin damage, thrombosis or thrombophlebitis, directly over the heart, carotid sinus, or trunk during pregnancy

96
Q

Benefits of active movement

A

Active movement allows for natural joint motion and muscle contractions to maintain muscle strength and joint health

97
Q

What are rehab options for pulmonary therapy

A

Positioning-alternating recumbency

Postural drainage

Pervussion

98
Q

What is definition of pain

A

Unpleasant sensory and emotional experience associated with actual or potential tissue damage

99
Q

What is nociception

A

Neural process of encoding noxious stimuli. Conscious perception of pain

100
Q

What is physiologic pain

A

Noxious stimuli associated with the risk of injury

Proportional to stimulus intensity

Transient and characterized by a high stimulus threshold and narrow localization

Protective; Induces withdrawal reflexes and avoidance responses

101
Q

What is pathologic pain

A

Persistent noxious stimuli perpetuated by
inflammation or nerve damage

Implies that tissue damage has already occurred

Exaggerated pain response (Hyperalgesia) either at the site of injury or surrounding areas (Extraterritorial pain)

102
Q

What is adaptive pain

A

Transient normal response to tissue damage; confers tissue protection

Encompasses physiologic and pathologic pain

103
Q

What is maladaptive pain

A

Alteration of spinal cord and brain function from prolonged stimulus

Decrease of peripheral threshold of nociceptor

Altered neuronal gene expression and increased spinal neuron responsiveness

Secondary to inadequate management of adaptive pain

104
Q

What is allodynia

A

pain caused by a stimulus that doesn’t normally result in pain

105
Q

what is analgesia

A

absence of pain in response to stimulation that would normally be painful

106
Q

Causalgia

A

syndrome of sustained burning pain, allodynia, and hyperpathia after a traumatic nerve lesion, often combined with vasomotor and sudomotor dysfunction and later trophic changes

107
Q

What is distress

A

acute anxiety or pain

108
Q

Dysphoria

A

state of anxiety or restlessness, often accompanied by vocalization

109
Q

Hyperalgesia

A

Increased response to a stimulus that is normally painful

110
Q

What is paresthesia

A

abnromal sensation, whether spontaneous or evoked

111
Q

What is the Pathway of Nociception

A

Perception/Transduction
-Nociceptors

Transmission
-sensorry nerve fibers

Modulation
-spinal cord and brain

Conduction and central integration
-pain perception

112
Q

Draw pathway of nociception

A
113
Q

What are the nociceptors in perception and transduction

A

Nociceptors in cutaneous tissue, muscles and viscera

114
Q

What are the stimuli of nociceptors in perception and transduction

A

temperature, chemical ligands and mechanical shearing forces

115
Q

How do nociceptors stimulate pain

A

Activation of nonselective ion channels gated = Na+/Ca+ ion influx

Voltage-gated Na+ channel activated, leading to large Na+ influx and further depolarization

116
Q

What are chemical ligands that initiate nociception

A

Chemical ligands: pH, prostaglandins, leukotrienes, capsaicin, bradykinins, serotonin, anandamide, olvanil, resiniferatoxin

117
Q

What are the three transmission-sensory nerve fibers

A

Aβ fibers

A δ fibers

C fibers

118
Q

What do Aβ fibers do?

A

Conducts nonnoxious stimuli (Touch, vibration, pressure, rapid movement)

Large myelinated fibers activated by low-intensity stimuli

119
Q

What are A δ fibers

A

Responsible for sensation of physiologic pain, fast pain or ‘first pain’
-Sharp, localized, transient

Small receptive fields and high-threshold

Thermal and mechanical input

Small myelinated fibers, rapidly conducting

120
Q

What are C fibers

A

Responsible for slow pathologic pain (Poorly localized, dull/aching or burning sensation)

Polymodal (Activated by thermal, mechanical and chemical stimuli)

Most of the cutaneous nociceptic innervation
-Also found extensively in the muscles and viscera

Large receptive field, slow conduction (Non-myelinated)

121
Q

Where do sensory fibers synapse for modulcaton

A

dorsal horn of spinal cord

122
Q

What molecules inhibits transmission of nociceptive stimuli

A

GABA, glycine, endogenous opioid peptides (Encephalin and endorphins) inhibits transmission of nociceptive stimuli

123
Q

What are three principal pathways of modulation

A
  1. local interneurons (excitatory and inhibitory)
  2. neurons of segmental spinal reflexes
  3. Neurons that projects to supraspinal structures
    -wide dynamic range (WDR) neurons, nociceptive specific neurons
124
Q

What is the principal excitatory synaptic neurotransmitter (spinal cord and brain)? what are the receptors

A

glutamate and tachykinin

125
Q

What is glutamate’s receptor

A

NMDA, ampa, kainite

Intense stimulation required to overcome Mg2+-mediated receptor blockade- Pain remains after stimulus has disappeared

126
Q

Where is tachykinin released, and what does it mediate

A

c fibers, mediates pathologic pain

127
Q

What three area is Central Integration

A
  1. Brain stem (Medulla) and midbrain (Periaqueductal grey matter)
  2. Hypothalamus
  3. Cortex
128
Q

What three actions does brain stem and midbrain do in central integration

A

Cardiorespiratory center alert responses

Motor and emotional responses

Alertness mechanisms (Fight-or-flight response)

129
Q

What does hypothalamus do in central integration

A

Control of the autonomous nervous system response

Hormone release for stress control

130
Q

What does cortex in central integration

A

Pain perception (Quality, location, intensity and duration)

Generation of complex emotional response

131
Q

What causes peripheral sensitization

A
  1. Tissue inflammation
  2. Allodynia
  3. Hyperalesia
132
Q

How does tissue inflammation cause peripheral sensitization

A

Release of chemical ligands (H+, K+, ATP, proteases, COX-2, serotonin, histamine, chemokins and cytokines)

Lowers threshold of activation for A-δ and C-fiber

Recruits silent nociceptors

133
Q

How does central sensitization “wind up”occur

A

NMDA receptor dishinibition and glial cell activation

134
Q

How does nmda receptor dishinibition occur

A

Caused by repeated depolarization of the dorsal horn neurons

NMDA stimulation leads to intracellular Ca2+ mobilization → Increased glutamate responsiveness

↑ Dorsal horn neuron excitability
↓ Spinal cord neuron inhibition

135
Q

How does glial cell activation occur

A

Proinflammatory mediator production after nerve trauma

Role in reduction of opioid efficacy

136
Q

Three reasons to control pain

A
  1. sympathetic tone increase
  2. Counterregulatory hormone and RAAS activation
  3. Behavioral changes
137
Q

What does sympathetic tone increase do in pain

A

Proinflammatory mediator production after nerve trauma
Role in reduction of opioid efficacy

138
Q

What doe counter regulatory hormone and RAAS activation do in pain control

A

Cortisol, glucagon, ADH, growth hormone and IL-1 secretion, inhibition of insulin release

Catabolic state
-Hyperglycemia, proteolysis, lipolysis, sodium and water retention, decreased GFR, Immunosuppression, decreased wound healing

139
Q

Which analgesics medications inhibit perception?

A

Anesthetics

Opiods

alpha 2 agonists

benzodiazepines

Phenothiozines

140
Q

Which analgesics medications inhibit modulation?

A

Local anesthetics

opioids

alpha 2 agonists

tricyclic antidepressants

cholinesterase inhibitors

NMDA antagonsits

NSAIDS

Anticonvulsants

141
Q

Which analgesics medications inhibit transmission

A

Local anesthetics

alpha 2 agonists

142
Q

Which analgesics medications inhibit transduction

A

local anesthetics

opiods

NSAIDS

Corticosteroids

143
Q

When to use local blocks?

A

Enhance analgesia, lead to less use of systemic agents, decrease pain and wind up pain when used preemptively

144
Q

What are 6 types of loco-regional anesthesia

A
  1. Topical or surface
  2. Infiltrative
  3. Regional
  4. Neuraxial
  5. Intraarticular
  6. IV regional
145
Q

What is an epidural? vs spinal?

A

Administration of drugs into epidural (extra-dural) space.

Spinal = subarachnoid space

146
Q

What is the site of action for epidural

A

the nerve roots as they leave the spinal cord and travel out from the intervertebral foramina

147
Q

Describe how to perform an epidural

A
  1. Patient placed in sternal recumbence
  2. Clip an area a tthe lumbosacral junction.
  3. Aseptically prepare the skin
  4. After washing hands and while donning sterile gloves palpate the wings of the ilium with your thumb and middle finger. Using index finger palpate the spinous process of 7th lumbar vertebra
  5. Slide the index finger caudally down spinous process until LS space is palpable between L7 and S1
  6. Keeping index finger in place insert a 20-22 gauage, 1.5 to 2.0 inch spinal needle perpendicular to the skin on midline
  7. Advance needle to through ligamentum flavum usually a “pop” can be felt
  8. remove stylet and confirm placement with hanging drop “fill hub of needle with saline and fluid in needle should rop into epidural space”
  9. observe needle for blood
  10. slowly inject local anesthetic of choice , should be no resistance
  11. remove needle
148
Q

What are three layers for epidural

A

Skin -Fascia- ligamentum flavum

149
Q

What are contraindications for epidural

A
  1. Infection at the site (wounds/contamination)
  2. Coagulopathy
  3. Hypotension/hypovolemia
  4. Trauma in the region of injection
  5. CNS disease/increased ICP
150
Q
A

ACVECC 2024 (3 decks)

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