• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/44

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

44 Cards in this Set

  • Front
  • Back

1. A bodily sensation with qualities like those reported duringtissue‐damaging stimulation


2. An experienced threat associated with this sensation


3. A feeling of unpleasantness or other negative emotion basedon this experienced threat

Pain - definition

What is the gender difference in pain expression?

• Pain perceptions and behavior are heavily influenced by ____ and bythe _______ (family support and expression of pain)


• Pain assessment may become particularly problematic when patientsand hospital workers have differing _____ background


• Pain is the ___ vital sign

culture and sociocultural context




cultural




5th

• The 5 racial categories are American Indian or Alaskan Native, Asian, black or African American, Native Hawaiian or Other Pacific Islander, and White.


• African American adults vs African American children experience in ED


• Black, Hispanic, and Asian women were less likely to receive epidural analgesia than white women.

Read it...

Which two types of afferents carry pain stimuli ?




Relative conduction velocity?




Predict Myelinated vs non-myelinated, and larger vs smaller?



Afferent pathway

Afferent pathway

nociceptors -> anterolateral fasciculus -> spinothalamic tract projects to 
-> reticular formation 
-> periaqueductal gray 
-> thalamus -> sensory cortex

nociceptors -> anterolateral fasciculus -> spinothalamic tract projects to


-> reticular formation


-> periaqueductal gray


-> thalamus -> sensory cortex

4 aspects of pain processing?

1. Transduction


2. Transmission


3. Modulation


4. Perception

noxious thermal, chemical, or mechanical stimuli are converted into an action potential

1. Transduction

action potential through 1st, 2nd and 3rd order neurons

2. Transmission

inhibition (by glycine and GABA) or augmentation (by norepinephrine, serotonin, and endorphins) of the afferent or efferent pain signals

3. Modulation

final common pathway: integration of painful input into the somatosensory and limbic cortices

4. Perception




• Endogenous Opioid receptor activation


• Neuronal circuit inhibition via interneurons


• Central inhibition via periaqueductal gray (PAG) andnucleus raphe magnus (nRM)


• Stress Induced Analgesia


These are mechs of?

Modulation

This mech of modulation


a) block neurotransmitter release byinhibiting Ca2+ influx into thepresynaptic terminal


b) open potassium channels, which hyperpolarizes neurons and inhibitsspike activity

Opioid receptors

morphine (mu), ketocyclazocine (kappa), vas deferens (delta), sigma receptors


These are types of what receptor family?

Opioid receptors

What is happening here? What mech of modulation?

What is happening here? What mech of modulation?



This mech of modulation occurs via stimulation produced analgesia (SPA). PAG or nRM -> inhibit spinal thalamic cells (i.e. spinal neurons that project monosynaptically to the thalamus) so that the noxious information from the nociceptors are modulated at the spinal cord level.


(descending tract: dorsolateral funiculus).


Central Inhibition



Central Inhibition

• Delayed pain in soldiers and athletes


• Flight or fight response


• influenced by variables such as age, sex, degree of sensitivityto opiates, and past stressful experiences.


• opioid and non‐opioid mechanisms (cannabanoid, endorphins)


Mech of modulation?

Stressed Induced Analgesia

• noxious stimulus


• tissue damage (eg, postoperative pain).


• somatic pain: injury to body tissues, localizable


• visceral pain. Mediated by stretch receptors. It is poorly localized, deep, dull, and cramping (eg, pain associated with appendicitis, cholecystitis, or pleurisy)


Type of pain?

Nociceptive pain

• abnormal neural activity secondary to disease, injury, or dysfunction ofthe nervous system. It commonly persists without ongoing disease (eg,diabetic neuropathy, trigeminal neuralgia, or thalamic pain syndrome)


Type of pain?

Neuropathic

Two types of Pathologic Pain

Central or Peripheral Sensitization

Central sensitization can cause?

Central sensitization can cause?

Hyperalgesia abnormally heightened sensitivity to pain.

Allodynia is pain, generally on the skin, caused by something that wouldn't normally cause pain

Hyperalgesia abnormally heightened sensitivity to pain.




Allodynia is pain, generally on the skin, caused by something that wouldn't normally cause pain

What type of pain is this?

What type of pain is this?

Pathologic; periperal sensitization

• Widespread musculoskeletal pain accompanied by fatigue,sleep, memory and mood issues


• Pathology in the all 4 pain pathways (transmission, transduction, modulation, and perception)


• NSAIDS (Non‐steroidal anti‐inflammatory drug)


• Acetaminophen


• Opiates


• Ketamine


Type of pain treatment?

Pharmacological

• Spinal


• Epidural


Type of pain treatment?

Regional Anesthesia

• Ketorolac


• Indomethacin


• Aspirin


• Naproxen (Aleve)


• Ibuprofen (Advil)


• Celecoxib


• Steroid


These are what kind of drugs for treating pain?

• NSAIDS (Non‐steroidal anti‐inflammatory drug)

Which drug blocks:
-synthesis of PLA ,inhibiting synthesis of AA?
-synthesis of COX-1 (and COX-2), inhibiting synthesis of PGs?

Which drug blocks:


-synthesis of PLA ,inhibiting synthesis of AA?


-synthesis of COX-1 (and COX-2), inhibiting synthesis of PGs?





Note the site of action!

Note the site of action!

• Ketorolac


• Indomethacin


• Aspirin


• Naproxen (Aleve)


NSAIDS + selectivity for inhibition of COX synthesis?

COX-1




KIAN

• Ibuprofen (Advil)


NSAIDS + selectivity for inhibition of COX synthesis?



Non-selective!

• Celecoxib


NSAIDS + selectivity for inhibition of COX synthesis?

COX-2


Celecoxib

Inc COX-1 selectivity -> increase effects here

Gastrointestinal effects

Inc COX-2 selectivity -> increase effects here

Cardiovascular effects



Cardiovascular risk associated with this NSAID



Mech of which drug?
Note the window!

Mech of which drug?


Note the window!

Acetaminophen/paracetamol

1. Block neurotransmitter releaseby inhibiting Ca2+ influx intothe presynaptic terminal


2. Open potassium channels,which hyperpolarizes neuronsand inhibits spike activity.




Does this look familiar? Mech of which class of synthetic drug?

Opiates




NB - these are the synthetic version of the endogenous opioids

Morphine
Hydromorphone
Oxymorphone
Fentanyl
Codeine
Hydrocodone
Methadone
Oxycodone
Belong to which class of drug?

Morphine


Hydromorphone


Oxymorphone


Fentanyl


Codeine


Hydrocodone


Methadone


Oxycodone


Belong to which class of drug?

Opiates

What class of drugs?

What class of drugs?

Opiates

Guess the drug!

Guess the drug!

Fentanyl!

• Cheap synthetic opioid


• More potent


• Fast acting


• Takes away the pain with intubation


• Unfortunately, it is a drug of abuse


The drug is?

Fentanyl!

• Risk factors:


• Alcohol Use


• Age: Youth


• Previous drug abuse (17X more)


• 4/5 users previously used painkillers


• Scare tactic advertisements prevent good pain management to those that need it




Addiction to these two similar drugs?

Heroin and Opiate addiction