module 5 lesson 5: pain management

Pain Assessment

• What is the undisputed standard for assessing existence and intensity of pain?

• What are the questions to ask?

→ how to quantify that 

→ ___: what makes it worse?

→ __: what have you done to make it better? 

→ __: how does it feel to you? Sharp? Stabbing? Throbbing? 

→ ___: how intense is it to you? How long have you had it for?

→ ___: where is it?

→ ___: has the pain moved to diff parts of body?

→ ___: how would you rate the pain?

→ timing: when d

→ treatment: what have you done?

→ understanding: believing the patient

• What happens if you think someone is pain seeking?

→ ___

Pain Assessment

• What is the undisputed standard for assessing existence and intensity of pain?

• What are the questions to ask?

→ how to quantify that 

→ provocative: what makes it worse?

→ palliative: what have you done to make it better? 

→ quality: how does it feel to you? Sharp? Stabbing? Throbbing? 

→ quantity: how intense is it to you? How long have you had it for?

→ region: where is it?

→ radiation: has the pain moved to diff parts of body?

→ severity: how would you rate the pain?

→ timing: when d

→ treatment: what have you done?

→ understanding: believing the patient

• What happens if you think someone is pain seeking?

→ treat their pain

Specific Patient Population Pain Assessments

Wong-Baker Faces

• face that reflects their pain

• for what age & which population? ___

CPOT: critical pain observation tool

-for someone who ____

FLACC

-Used for ___

Specific Patient Population Pain Assessments

Wong-Baker Faces

• face that reflects their pain

• ages 3+ & for someone who doesn’t understand english/ isn’t able to give you rating of their pain

CPOT: critical pain observation tool

-isn’t able to give their own assignment of their pain

-through your observations

FLACC-used for young children

-Used for very young children: aged 2 months to 7 years

Hierarchy of pain measures

• attempt at self report, consider condition, observe behavior, physiologic indicators, analgesic trial (give them something for their pain and see their reaction)

Acute/ transient	Chronic/ persistent non-cancer	Cancer	Chronic episodic	Idiopathic pain
____	___	___	___	___

Neuropathic pain: ___

Radicular pain: ____

Psychogenic pain: ___

Hierarchy of pain measures

• attempt at self report, consider condition, observe behavior, physiologic indicators, analgesic trial (give them something for their pain and see their reaction)

Acute/ transient	Chronic/ persistent non-cancer	Cancer	Chronic episodic	Idiopathic pain
-injury that doesn’t last very long (less than a couple days) -medical/ surgical condition -lasts hours to days	-long term -months to years	-acute/chronic pain -usually caused by tumor progression -related to pathologic process, invasive procedures, treatments, infection, and physical limitation	-intermittently over extended period of time -lasts hours, days, weeks -Ex. Sickle Cell, Migraine	-chronic in the absence of identifiable cause -perceived as excessive for the extent of condition -not sure why the pain is there

Neuropathic pain: nervous system: misfiring of the nerves

-abnormal processing of sensory input by PNS or CNS

-burning, shooting pain, pins & needles

-traumatic or nontraumatic

→ diabetes, compression, pinched nerve

-maladaptive neuroplasticity

-allodynia (pain when there shouldn’t be pain like when someone touches you and it hurts, “A for At All”)

-hyperalgesia (excessive reaction to something that should cause minimal pain)

Ex: phantom pain

-peripheral nerve pain

Radicular pain: comes at nerve root when the spinal cord root is compressed: tingling, nerves, (ex: in herniated disk)

Psychogenic pain: not attributable to specific injury but may be result of stress, depression, anxiety; 

Nociceptive Pathway

• Transduction: ___

• Transmission: ___

• Perception: ___

• Modulation: ___

→ what does GABA/ serotonin do? ___

→ what does substance P do? ___

→ Pain gate theory: pain and touch goes up to the brain, if we compress the injured part through squeezing the area, the signal can only let up so much so brain perceives less pain

Nociceptive Pathway

• Transduction: dialing phone number/ body receiving stimulus

• Transmission: sending like phone is ringing/ texting and sending the message/ message going up to the brain

• Perception: hears the message from the other end/ sympathetic/ parasympathetic nervous system activation

• Modulation: how’s the person reacting to what you say; is it positive (decreasing perception of pain) or negative (pass message incorrectly?)/ : GABA/ serotonin, which decrease sense of pain, substance P & others which increase sense of pain to send up to brain (opposite of opioid)

→ Pain gate theory: pain and touch goes up to the brain, if we compress the injured part through squeezing the area, the signal can only let up so much so brain perceives less pain

Classification of Pain

Somatic	Visceral
-___ -___ -ex: surgical, burn, RA, OA	-___ -___ -hollow viscus: ___

Classification of Pain

Somatic	Visceral
-bone pain, muscle, skin, connective tissue (more superficial, can point to where pain is) -aching, stabbing, throbbing, well localized -ex: surgical, burn, RA, OA S comes first in the alphabet, therefore its more superficial than V(isceral)	-visceral organs: GI tract, pancreas (more difficult for pt to identify where pain stems from) -organ capsule: aching, fairly well localized -hollow viscus: intermittent cramping (due to presence of smooth muscles)

Pain Management: Multi-Modal Approach

Intentionally + simultaneously combines medications & non-pharm interventions

Routes of Administration

-Oral: ___

-IV: __

-Rectal-alternative: ___

-Topical

-Transdermal: patches

-Neuroaxial-epidural: goes into epidural space, put numbing & pain

-Peripheral Nerve block: ____

Patient-Controlled Analgesia (PCA): can have with an IV and patient can press a button to administer themselves (with caps on how much they can PCA – patient controlled analgesia.

IV administration system where the patient initiates a small amount of opioid medication given IV by pressing a button when in pain. In some cases a continuous basal rate is prescribed, and the patient adds to it as necessary.

The system is set up with stringent dosing controls so that the patient cannot receive too much medication too quickly. There is a “lockout” period after each dose when the patient will not be able to access more medication.get & how frequently they get it)

Dose Timing

-Around-the-clock (ATC)

-As needed (PRN)

Pain Management: Multi-Modal Approach

Intentionally + simultaneously combines medications & non-pharm interventions

Routes of Administration

-Oral: easiest, well tolerated

-IV: fastest

-Rectal-alternative: if intubated/ sedated

-Topical

-Transdermal: patches

-Neuroaxial-epidural: goes into epidural space, put numbing & pain

-Peripheral Nerve block: will affect only one bundle of nerves, makes it numb/ pain free

Patient-Controlled Analgesia (PCA): can have with an IV and patient can press a button to administer themselves (with caps on how much they can PCA – patient controlled analgesia.

IV administration system where the patient initiates a small amount of opioid medication given IV by pressing a button when in pain. In some cases a continuous basal rate is prescribed, and the patient adds to it as necessary.

The system is set up with stringent dosing controls so that the patient cannot receive too much medication too quickly. There is a “lockout” period after each dose when the patient will not be able to access more medication.get & how frequently they get it)

Dose Timing

-Around-the-clock (ATC)

-As needed (PRN)

Opioid Analgesic- _____

Why	• ___
MOA	• ___
Adverse Effects	• ___

Opioid Antagonist- ___

Why	___
MOA	___
Adverse Effects	Tachycardia, dysrhythmias, BP changes
Expect effect	Half Life 30min-1hour
Route effect	___

Opioid Analgesic- Morphine

Why	• suppresses pain, decrease pain stimulus from moving up pathway • anesthesia
MOA	• Act on opioid receptor in CNS • Euphoria & sedation (monitor RR & O2 SATURATION)
Adverse Effects	• Respiratory depression: body less responsive to CO2 (which is responsible for breathing) ▪ Increased risk with people with respiratory disorders • Hypotension • N/V, constipation

Opioid Antagonist- Naloxone (aka Narcan)

Why	Reverse effects of opioids
MOA	Strongly bind to opioid receptors to block the receptor, but do not activate it, decrease in effects of opioid
Adverse Effects	Tachycardia, dysrhythmias, BP changes
Expect effect	Half Life 30min-1hour
Route effect	IM, IV, Intranasal

Important concepts

Physical dependence: __

Tapering Helps

___

Tolerance: ____

• ___

Substance Use Disorder (SUD): ____

• ___

• Compulsive use

Withdrawal

• Signs and symptoms: anxiety, nausea, vomiting diarrhea, insomnia, hot flashes

Important concepts

Physical dependence: withdrawal signs and symptoms

Tapering Helps

-dependance on the medications and some people get lots of the meds and when the med levels are given less, body needs more

-may result in the med used not as intended

Tolerance: decrease in effect over time

• Treated with increasing doses

Substance Use Disorder (SUD): chronic, relapsing neurologic disease

• impaired use and impaired control

• Compulsive use

Withdrawal

• Signs and symptoms: anxiety, nausea, vomiting diarrhea, insomnia, hot flashes

Non opioid analgesics

What’s important to know about COX?

COX-1: __	COX-2: ___
-___ -___ -___	-___ -___ -___ -___

its relation to prostaglandins: ___

Pharmacological Interventions: Non-opioid Analgesic

Nonsteroidal anti-inflammatory drugs (NSAIDs) & aspirin

Black Box Warning:

• ____

Non Opioid Analgesics

COX are receptors that allow cascade to occur

COX-1: any type of pain (think "Grip" on life)	COX-2: usually pain from tissue damage (think about someone who’s “too/ two” sick)
-decreases gastric mucosa -renal perfusion (long term use can be toxic to kidneys) -stimulate platelet aggregation	-inflammation -pain -fever -reduce platelets

Prostaglandins are key to inflammatory response:

-produced by COX 1&2

-increase thresholds & increase pain

With COX 1&2 blockage, body perceives pain as less due to blockage of prostaglandin production

Cox 1&2 inhibitors: ibuprofen, very strong

Pharmacological Interventions: Non-opioid Analgesic

Nonsteroidal anti-inflammatory drugs (NSAIDs) & aspirin

Black Box Warning:

• Cardiac Risk Factors: MI + Stroke (if chronic overuse: prostaglandins increase blood flow to an area. If body blocks perfusion to that area, it can cause the black box warning)

If chronically using NSAIDs and someone has cardiac issue, injury to that area is more likely bc NSAIDs decrease prostaglandins and causes bleeding

Take oral doses with food

Main Concern: BLEEDING

Long term use: NEPHROTOXIC (kidneys)

Pharmacological Interventions: Non-opioid Analgesic Centrally Acting

Acetaminophen (tylenol)

-exact MOA unknown

-___

-contraindicated with ___

-assess liver function hepatic damage: N/V, diarrhea, abdominal pain

-antidote: ___

Pharmacological Interventions: Non-opioid Analgesic Centrally Acting

Acetaminophen (tylenol)

-exact MOA unknown

-acts in CNS + no anti-inflammatory effects

-contraindicated with hepatic/ renal disease, alcoholism, hypersensitivity

-assess liver function hepatic damage: N/V, diarrhea, abdominal pain

-antidote: acetylcysteine (replenishes a liver antioxidant if overdose of acetaminophen)