Brainscape's Knowledge GenomeTM

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


See full index

d. Regional exam 4(w13) > pain management 4/8/13 > Flashcards

pain management 4/8/13 Flashcards

0
Q
  1. what does pain control have to do with CRNAs?

2. what organizations have statements and standards for pain control?

A
  1. pain is a major concern with our patients: acute, chronic, cancer (especially in children) plus…(surgery causes pain)
  2. Joint commission (JCAHO) requires it; America pain society (APS) has standards; ASA (american society of anesthetists)has guidelines for pain management
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

objectives:

  1. verbalize relevant standards and regulatory guidelines in pain management.
  2. apply knowledge of the anatomy, physiology and psychology of pain to the safe care of patients with acute or chronic pain.
  3. list the effects of untreated pain
  4. perform competent assessment of pain
  5. describe the pharmacological and non pharmacological therapy of pain, with the advantages and disadvantages of various approaches
  6. for each pain syndrome discussed, describe any regional anesthesia block or injection which is indicated conserning anatomic, technical and pharmalogical considerations and adverse effects or contraindications.
A

-

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

according to the Joint Care Commission (in regards to pain control): hospitals must…

A
  1. recognize right of patient to assessment and management of pain
  2. assess existence, nature and intensity of pain in all patients
  3. record results of assessment for later re-assessment and follow up
  4. determine and assure new and existing staff competency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

TRANSDUCTION part 1

  1. what is transduction?
  2. what happens?
A
  1. noxious stimulus is translated into electrical activity
  2. peripheral terminals of primary AFFERENT SENSORY neurons are stimulated by heat, mechanical or chemical injury (noxious stimulus). This creates an action potential which is conducted to the DORSAL HORN of the spinal cord
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

opioid addiction vs. tolerance vs. dependence:

  1. what is addiction?
  2. what is tolerance?
  3. what is physical dependence?
A
  1. addiction: chronic, neuro-biologic disease with genetic, psychosocial and environmental factors. characterized by: impaired control over drug use, compulsive use, continued use despite harm, craving
  2. tolerance: state of adaptation in which receptors are less sensitive or down regulate- may be biochemical or physical, causing drugs to be less effective.
  3. physical dependence: adaptation classified by withdrawl symptoms from reduced dose, abrupt cessation or antagonist administration. the drug is needed to function.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what increases drug craving in drug addicted patients?

A

poor pain control

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

ASPMN position statement on patients with addiction disease includes:

A

have the right to be treated with dignity and respect; this includes maintaining the balance between effective pain management and protection of misuse of prescription medications. nurses advocate for patients with alcohol and drug recovery.

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

modulation:
1. what is modulation?
2. what inhibitory substances are used for modulation?
3. where do the inhibitory pathways from from and what do they run into?

A
  1. Once the brain has received a signal saying there is pain somewhere, it will try to modulate (minimize) the pain so that it still gets the point but not so strongly.
  2. It does this by using endogenous opiates such as enkephalins and also serotonin, norepinephrine and GABA.
  3. inhibitory pathways run from spinothalamic and medullary and intersect with primary afferent and or DH neurons to release inhibitors to inhibit pain transmission.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

TRANSMISSION: what is it?

A

transmission: Nerve impulses generated in the periphery are TRANSMITTED to the SPINAL CORD which then goes to the BRAIN (done in those 2 phases).

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

What are the steps in TRANSMISSION:
1. sensory nerve impulses travel via nerve axons of (primary ___ neurons) and travel to what part of the spinal cord?
2. in the spinal cord, sensory nerves then transfer the impulse to ___ by releasing what (substances and names)at the synapses?
3.neurons send nocioceptive impulses toward brain up ___?
name them and their destination:
–a.
–b.
–c.
–d.

A
  1. primary AFFERENT neurons to the DORSAL HORN of the spinal cord.
  2. primary afferet neurons transfer impulse to INTERNEURONS through the release of excitatory amino acids (glutamate, aspartate) and neuropeptides (substance P) at the synapses.
  3. ASCENDING TRACTS
    spinothalmic tract to thalamus;
    spinoreticular tract to reticular
    spinomesencephalic tract to mesencephalon
    spinohypothalamic to hypothalamus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

WHO pain relief ladder:
level 1:
level 2:
level 3:

A

level 1: non opioid
level1 top: pain persists or increases.
level 2: opioid for mild to moderate +/-non opiate; +/-adjunct
level 2 top: pain persists or increases.
level 3: opiate for moderate to severe +-/-non opiate; +/- adjunct
level 3 top: freedom from cancer pain

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

Transmission: trace the pain signal:
somatic pain:
visceral pain:

A
  1. somatic pain stimulus>A-delta (myelinated periph nv.)>dorsal horn>spinothalamic tract>limbic system and cortex
  2. visceral pain stimulus>C fibers (unmyelinated periph nv.)>dorsal horn>spinothalamic tract>limbic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  1. what is hyperalgesia?
  2. what is the cause of hypealgesia?
  3. what is the “phenomenon” that occurs from hyperalgesia? Where does it occur?
A
  1. decreased pain threshohd in inflamed area with hyperactive response to inappropriate levels of stimulus
  2. likely the result of chemical mediators (metabolites of arachadonic acid, prostaglandin and bradykinin)
  3. called “wind up” phenomenon in the dorsal horn (d/t prolongd stimulation) ; which is when the pain response snowballs and becomes harder to treat.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

perception:
1. what is pain perception?
2. what medications help to decrease the pain transmission?

A
  1. when the brain receives the electrical transduced and transmitted pain stimulus and interprets it (as pain)
  2. opioids, SSRI, SNRI, TCA, alpha-2 agonist
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Modulation:

  1. how do inhibitory substances work?
  2. what determines pain tolerances?
A
  1. bind to the receptors that will be receiving a painful stimulus and dont allow for it to receive that painful stimulus.
  2. modulation contributes to variances in pain response from person to person
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

modulation:

  1. how do opiates work in regards to modulation?
  2. how do gabapentin (neurontin) or pregabalin (lyrica) work?
  3. how does baclofen work?
A
  1. opiates/opioids inhibit nocioception in the DH by binding to opiate receptors and mimic-ing the effects of endogenous opiods
  2. gabapentin and pregabalin bind to opioid receptors in the brain and activate the descending pathways that further inhibit DH nocioception
  3. baclofen is a GABA agonist and binds to the receptors to mimic the inhibitory effects of GABA on nocioception transmission
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

modulation:

how do TCAs and MAO-Is inhibit pain?

A

by increasing the amount of NE and serotonin (5HT) at the synapses. NE and serotonin are pain blockers at the DH where the spinothalamic and medullary descending inhibitory fibers meet the DH neurons.

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

what is allodenia?

A

pain from non noxious stimulus (light touch, pressure of a blanket, etc.)

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

chronic post surgical pain (CPSP)

  1. what is it?
  2. what may be causes of it?
  3. what risk factors contribute to it?
A

1-phenomenon that is chronic pain caused from surgery that is at the surgical site
2-may be d/t nerve injury (surgery proximal to nerve pain), invasiveness of surgery, duration of surgery (>3 hours)
3-risk factors: anxiety, fear, gene polymorphisms, gender
-correlation between acute post op pain and chronic pain syndrome (CPSP)
-examples: thoracotomy

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

how to prevent CPSP

A

multimodal approach:
-regional, epidural, SAB, IV regional
adjuncts:
nsaids, clonidine, gaba drugs

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

opiod (induced) hyperalgesia

  1. what is the cause?
  2. how is pain increased?
  3. what is the treatment?
  4. when can this happen? what patients should you avoid this condition?
A
  1. mechanism not fully understood, not very common; in some patient high dose opiods cause upregulation in the receptors which causes receptor changes which end in releasing more pain transmitties.
  2. causes more pain due to a lower pain threshold
  3. nerves need to be reset. (have to come off opiods; will need alternative pain measures).
  4. during withdrawl, avoid in high risk patiets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

pre-emptive analgesia:

  1. what is the theory?
  2. what is an example with amputations?
A
  1. anagetsia given prior to stimulus which prevents establishment of altered central processing
  2. regional prevents prolonged signals from an amputated limb
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

pain response:

  1. what is it? what are the elements to pain perception?
  2. what factors influence it?
A
  1. subjective experience of perceiving pain: has 3 elements:
    - –sensory (location, duration, intensity)
    - –affective: (emotional, unpleasantness, motivational)
    - –cognitive: (awareness of implications, fear, anxiety)
  2. infulenced by: gentic, gender culture, chemical makeup and previous experience etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

acute pain:

  1. what is the definition?
  2. why do we have acute pain?
  3. what is it associated with?
  4. 2 types of acute pain; what are they?
A
  1. rapid, well defined onset with limited duration
  2. protective mechanism, provoked by tissue injury
  3. associated with anxiety, emotional resopnse and sympathetic hyperreactivity
  4. can be Monophasic (1 time cause…i.e. surgery, injury) or recurrent (headaches, menstrual cramps, inflamed bowel).
24
Q

managing acute pain:

  1. what meds are used?
  2. what methods of delivery?
  3. what is “bringing it all together” called?
A
  1. pharmacological: opioids, nsaids, adjuncts (SSRIs etc.)
  2. PCA vs. ATC (around the clock)
  3. multimodal
25
Q

Celebrex pre op; how is this possible?

A

less bleeding with cox2 (doesnt affect platelets) than with cox1

26
Q

factors associated with chronic pain

A 
20-60
women>men
genetics
race (african americans and hispanics)
previous injury
depression
27
Q

treating CPSP:

what approach is best? what does this entail?

A

mutimodal:

  • -regional anesthesla: epidural, SAB, IV regional, blocks
  • -adjuncts: nsaids, clonidine, precedex
  • -opioids
  • -gapapentin, pregabilin
28
Q

regional anesthesia and CPSP:

  1. why does CPSP deveolp?
  2. what does regional anesthesia do?
  3. what surgical patients does regional really help to reduce this in?
A
  1. there is a high correlation between severity of acute post op pain and CPSP
  2. reduces circulation of substance P and reduces neuronal input into dorsal horn; also reduces central sensitization
  3. shown to significantly reduce pain in thoracotomy, total hip and c-section
29
Q

multimodal philosophy: what is the action:

  1. opioids:
  2. gabapentin preop:
  3. pregabalin preop:
  4. celebrex preop:
  5. acetaminophin IV (affirmev) post op:
  6. Ketorolac post op:
  7. regional anesthesia:
  8. clonidine; dexmetatomidine:
  9. nitrous; ketamine:
A
  1. MU 1&2; delta; kappa
  2. enhances GABA, increased serotonin, decreases glutamate
  3. prevents Substance P and glutamate release
  4. selective Cox 2 antagonist
  5. central cyclooxygenase (COX) inhibitor (antagonist)
  6. NSAID- non selective COX antagonist
  7. prevent substance P release, prevents central sensitization
  8. alpha 2a receptor agonist
  9. NMDA antagonist
30
Q

TRANSDUCTION part 2

  1. what does the injury stimulate the release of?
  2. what “substance” is released after that?
A
  1. glutamate, prostaglandin, serotonin, bradykinins which activate pain fibers
  2. peripheral neurons release SUBSTANCE P which is a mediator along with othe mediators and activate Mast cells which releases vasodilaters and recruits other receptors.
31
Q

summary: what are the effects of TRANSDUCTION

A

Transduction in essence is a series of biochemical events associated with the reception of nociceptive stimulus in the generation of action potentials.
—-the arachadonic acid cascade (serotonin, bradykinin, substance P) has far reaching effects to aid the inflammatory response but also cause distant reactions (bronchoconstriction, vasodilation or vasoconstriction, increased vascular permeability, thrombosis, hyperalgesia).

32
Q

modulation:

how do sensory beta fibers arising from peripheral tissues affect modulation

A

rubbing the injury, TENS therapy, acupuncture help by over-riding pain sensations (gate theory) by utilizing the dorsal horn and or modulating spinothalmic neurons

33
Q

ketamine is good for

A

complex regional syndrome and depression

blocks NDMA receptors

34
Q

chronic pain:

  1. defn:
  2. could be an abarrency in the…?
  3. what are associated factors?
  4. what disorders might it be associated with?
A
  1. delayed and poorly defined onset of pain (which usually begins as acute pain); unpredictable and protracted duration; autonomous of independent trigger stimulus.
  2. could be an abarrency in the normal physiologic pathway;
  3. associated with depression, anxiety, sleep and mood issues
  4. may be associated with allodynia and hyperalgesia
39
Q
  1. how is windup prevented

2. what is induced by pre-, intra-, and post operative input

A
  1. preventing CNS sensitization throughout peri-opertive period as well as when incision is made by using preemptive analgesia
  2. central neuroplasticity
40
Q

pain response in the ANS (autonomic nervous system):

  1. what nervous system is stimulated in response to pain?
  2. what is the cascade of incidents at the site when pain is introduced?
  3. the “circle” leads to what?
A
  1. stimulates the sympathetic nervous system
  2. vasoconstriction>acidosis>tissue ischemia>chemical release>further chemical release (vicious circle)
  3. circle leads to Reflex Sypmathetic Dystrophy (RDS) aka CRPS or COMPLEX REGIONAL PAIN SYNDROME
41
Q

what is complex regional pain syndrome (CRPS):

  1. first discovered when? termed what?
  2. what is it?
  3. pathophysiology?
  4. what happens in early stages?
  5. what is the effect on the receptors?
  6. what happens to the pain pathways
  7. what receptor is activated
  8. what can trauma cause with CRPS?
A
  1. first described during civil war; termed causalgia
  2. involves extreme hyperalgesia or even allodynia
  3. underlying pathophysiology unknown: it involves peripheral and central nervous system
  4. in early stages nocioception is maintained by increased sympathetic activity
  5. prolonged afferent stimulation changes the receptor structure at all neuraxial levels
  6. leads to sensitization of pain pathways which initiates and maintains chronic neuropathy
  7. N-Methyl-D-Aspartate (NMDA) receptor activation is the primary mediator of sensitization in the dorsal horn and plays an important part in neuropathy.
  8. can be limited to one region but can spread to multiple sites through trauma.
42
Q

neurotransmitters in chronic pain:

  1. name the neurotransmitters involved in chronic pain transmission and modulation
  2. the bad : pain transmitters
  3. the good: pain modulators
A
  1. glutamate
    - –substance P
  2. enkephalins/endorphins
    - –serotonin
    - –norepinephrine
    - –GABA
44
Q

glutamate:

  1. what is it?
  2. what receptors does it stimulate and where does it act?
  3. what does it do?
A

glutamate

  1. is an afferent neuro transmitter;
  2. stimulates NDMA receptors in dorsal horn
  3. enhances pain transmission
45
Q

substance P:

  1. what is it?
  2. where does it work? what receptors does it stimulate?
  3. what pain fibers is it specific to?
A
  1. afferent neurotransmitter (NMT)
  2. stimulates neurokinin (NK) receptors in dorsal horn
  3. specific to type C nerve fibers
46
Q

Enkephalins/ Endorphins:

  1. what are they?
  2. where do they work?
  3. what do they do?
A
  1. descending neurotransmitter
  2. work on receptors in peri-aquaductal grey (PAG), para-giganto-cellularis nucleus
  3. inhibition of substance P release in the Dorsal Horn
47
Q

serotonin:

  1. what is it?
  2. what does it do? where?
A
  1. neurotransmitter

2. increases release of Enkephalins in the dorsal horn

48
Q

Norepinephrine:

  1. what is it?
  2. what does it do? where?
A
  1. neurotransmitter (sympathetic)

2. inhibitory NMT at Dorsal Horn via alpha 2a stimulation (pre-synaptic)

49
Q

GABA:

  1. what is it?
  2. what does it do? where?
  3. what ELSE does it do?
A
  1. inhibitory neurotransmitter
  2. stimulates GABA (inhibitory) receptors; in the Dorsal Horn
  3. reduces membrane potential
50
Q

the neurotransmitter is: GLUTAMATE:

  1. what drugs block it?
  2. why?
A
  1. ketamine: NDMA receptor blockers; glutamate stimulates NDMA receptors (which sensitize dorsal horn to pain)
  2. nitrous oxide: NDMA receptor blockers; glutamate stimulates NDMA (which sensitize dorsal horn to pain)
  3. dexmetomadine: inhibits pathways at dorsal horm where NDMA receptors are
  4. clonidine: inhibits pathways at dorsal horm where NDMA receptors are
51
Q

the neurotransmitter is: Substance P

1-4. what drugs block it and their action

A
  1. epidural- blocks sodium channels preventing impulse
  2. local anesthetic- blocks sodium channels preventing impulse
  3. dexmetatomidine: alpha-2a receptor agonist (blocks release of substance P)
  4. clonidine: alpha-2a receptor agonist (blocks release of substance P)
52
Q

the neurotransmitter is: Enkephalin/ Endorphin:

–what drugs augment it:

A

–opioids: increase release of enkephalins & endorphins

53
Q

the neurotransmitter is: Serotonin:
A. what does serotonin do at the synapse?
1-3. what drugs augment it?

A 
A. serotonin increases release of enkephalins in dorsal horn.
1. TCAs: elavil (amitriptyline)
2. SSRIs: celexa (citalopram)
3. SNRIs: effexor (venlafazine)
B. increase serotonin at synapse
54
Q

the neurotransmitter is: Norepinephrine:

  1. what does NE do to block pain?
  2. what drugs augment norepinephrine levels?
A
  1. inhibits transmission in dorsal horn

2. TCAs; SNRIs

55
Q

the neurotransmitter is: GABA

  1. what does GABA do to block pain
  2. what drugs augment GABA action?
A
  1. gaba is inhibitory of pain transmission at dorsal horn

2. pregabilin (Lyrica); gabepentin (neurontin)

56
Q

what can be added to local or regional to increase effectiveness (besides opiates and clonidine)?

A

Nsaids or affirmiv (acetaminophen)

57
Q
  1. what are blocks that are used for acute thoracic pain?

2. what are the risks?

A
  1. intercostal blocks (for rib fractures, thoracic surgery)

2. risk of ptx

58
Q
  1. what is pseudo-addiction?
  2. what does it result in (from staff)
  3. when does it resolve?
A
  1. an iatrogenic (hospital caused) condition from under treatment of real pain resulting in addicted person behaviors (anger, escalating demands for more pain med) they may hav tolerance or dependence
  2. staff assume patient is an addict and undertreat/ avoid
  3. condition is resolved when pain is effectively treated
59
Q

where are continuous regional blocks done?

A

brachial plexus, intercostals, intrapleural, femoral, sciatic

60
Q
  1. what is an intrapleural catheter block
  2. what uses?
  3. what is the risk (think vascular lungs)?
A
  1. catheter gives infusion or boluses of anesthetic into intrapleural space
  2. useful for post thoracic or abdominal surgery
  3. risk of toxicity from high absorption
61
Q

continuous epidural:

  1. what is given?
  2. when is it most useful?
  3. what methods of delivery?
A
  1. low dose opiates and low dose LA
  2. useful is started intra op to augment general anesthesia
  3. can be bolus, continuous or epidural pca (EPCA)
62
Q

anesthesia pearls:

  1. who should be consulted for post op pain control?
  2. what may be the best pain control route for surgery?
  3. what else should be used?
  4. which is better ATC or PRN?
  5. what method of pain control is good post op? what “rate” should be avoided? what should you do asap when pain is improved?
A
  1. involve pain management (if needed)
  2. regional or local may be optimal
  3. use adjuncts (clonidine, ssris etc.) when possible
  4. ATC better than PRN
  5. pca may be benificial (avoid basal rate if you can); convert to orals when possible
63
Q

fentanyl patch pre op?

A

may be best to remove and convert dose to iv intraop

d. Regional exam 4(w13) (2 decks)

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