Pain! Flashcards
1
Q
Factor’s influencing pain
3
A
Patient’s fear of what is causing the pain- when they find out it is lessened
Psychological stressors and past pain experiences
Pain “threshold”**
2
Q
Acute/Temporary Pain Treatment
steps?
3
A
- Identify source of pain:
- Remove the cause if possible
- There is a lag period before pain subsides
- Treat pain EARLY before it has increased to a level where it is more difficult to control** - Use the least potent analgesic w/ the fewest side effects
- Properly titrate the dose & administer for an adequate amount of time
3
Q
Mechanism of action for acetaminophen?
3
A
Weak COX-1 & COX-2 inhibitor in peripheral tissues
Decreases pain but has NO anti-inflammatory effect
Anti-pyretic
4
Q
Doasge for acetominophen?
max daily dose?
A
4000mg
4grams per day
5
Q
Onset of acetominophen?
A
15 to 30 min
6
Q
Side effects of acetominophen?
3
A
Large doses can cause liver toxicity & be lethal
Large doses can cause dizziness and disorientation
Renal damage can occur even w/ normal dosages!
7
Q
Mechanism of action for aspirin?
4
A
- Inhibits COX and platelet aggregation
- reduces pain by reducing inflammation
- Anti-pyretic
- Lower incidence of colon cancer and decreases DVT after CABG
8
Q
Side effetcs of aspirin?
3
A
Gastric upset and ulcers
Hepatotoxicity and renal toxicity
Asthma and rashes
9
Q
What is salicylism?
A
vomiting, tinnitus, decreased hearing and vertigo are reversible by reducing the dosage
10
Q
What will toxic levels of aspirin cause?
4
A
- metabolic acidosis
- respiratory depression
- cardiotoxicity
- Overdoses are a medical emergency
11
Q
Mechanism of action in NSAIDs?
A
Decreases prostaglasdins!! main mechanism of action
Non selective for COX1 and COX2
12
Q
What do prostagladins cause?
A
inflammation
13
Q
So acetominophen is a weak COX inhibitor. What does this indicate about inflammation?
A
Since it is a weak inhibitor it does not decrease prostaglandin activity and thus does not decrease inflammation
14
Q
What are the physiological effects of prostaglandin?
5
A
- Activation of the inflammatory response
- Elicitation of pain and fever
- Contraction and relaxation of smooth muscle** (can help with pain there)
- Inhibition of acid synthesis and increased secretion of the protective mucus in the stomach
- Increased blood flow to the kidneys
15
Q
Why is prostaglandin good for the GI tract?
A
can help with pain there because it controls contraction and relaxation of smooth muscle
inhibits acid synthesis and increases protective mucous for the stomach
16
Q
GI Side Effects of NSAIDs?
4
A
N/V,
heartburn,
ulcers/bleeding,
diarrhea
17
Q
Cant pregnant women take NSAIDS?
A
They shouldnt but can while lactating and postpartum
18
Q
Renal side effects of NSAIDS
4
A
- Salt and water retention
- HTN**
- Can be particularly damaging if patient is taking other nephrotoxic drugs
- Interferes w/ platelet aggregation for 2-4 days
19
Q
NSAIDs can cause photosensitivity
A
statement
20
Q
What kind of patients do we see experiencing adverse renal events and acute kidney injury?
4
A
- Chronic kidney disease (decreased GFR)
- Volume depletion (diuresis, vomiting, diarrhea)
- CHF, nephrotic syndrome or cirrhosis
- Older age
21
Q
Max dose for ibuprofen?
A
3200mg
22
Q
Max dose for Naproxen (aleve)?
A
1000mg
23
Q
What are COX-2 inhibitors good for?
3
A
They are just as effective as other NSAIDs
Less GI toxic
Good for treating artritis
24
Q
Considerations/risk for gastroduodenal toxicity in NSAIDS?
A
Age >65 Use of anticoagulant therapy Previous GI bleed Acute PUD Concomitant use of glucocorticoids (if on steriods give them something else besides both can cause ulcers)
25
Opiod indications?
| 3
Acute postop pain
Severe pain for a limited duration
Chronic pain (by experienced provider)
26
MOA for opiods?
often inhibit Mu receptors in the CNS
27
What are Mu and Beta recetors for opiods associated with?
endorphins
28
What are delta receptors for opiosd associated with?
enkephalins
29
What are kappa receptors associated with?
dynorphins
30
Describe nociceptive pain?
cut your skin and it hurts where you cut it
31
Describe neuropathic pain?
neuropatnhy- nerves are causing symptoms of numbness adn tingling. source of pain is somewhere else
32
Side effects of opioids?
| 3
Constipation
Sedation
Addiction
are the big three
33
Everytime you prescribe an topioid what do you need to tell the patient?
4
Address ahead of time—constipation**
Warn of addiction
Sedation
Nausea and vomiting—may want to prescribe an anti-emetic
34
What causes the euphoria in opioids?
release of dopamine
35
Whats the difference between physical dependence and addiction?a
addiciton is the physcological dependance
36
If we push morphine too fast what can happen?
Hypotension (low BP)
37
Can you write for demerol pills?
NO, only IV and IM
38
How would the onset and duraiton of action differ in methadone than in other opioids?
Extended duration of action and slow onset of action
39
Side effects fo methadone?
| 3
Hypoglycemia
Hyponatremia
Death: prolonged QT interval—torsade de pointes
40
Methadone does not causes euphoria!
Statment
41
Oxycodone and acetominophen make what?
percocet
42
Oxycodone and aspirin make what?
percadan
43
Hydrocodone/acetaminophen makes what?
vicoden
44
Hydrocodone/ASA makes what?
Lortab
45
What is narcan used for?
opioid reversal medication
| Only to get them breathing again not to reach full alertness
46
What kind of agonist is fentanyl?
What are its dosage forms?3
A very strong mu opioid agonist
Available in IV, transdermal patch and suckers
47
MOA of tramadol?
inhibits reuptake of epi and norepi
48
Side effects of tramadol?
| 3
1. HA, dizziness
2. Nausea, constipation (low risk for GI bleeding)
3. Somnolence-stonrg desire to sleep
49
Purposes of a pain contract?
| 3
1. To provide informed consent regarding risks and benefits of opioid treatment
2. To foster adherence to the treatment program and limit the potential for abuse
3. To improve the efficacy of the pain treatment program
50
What are Tricyclic Antidepressants (TCAs) used for regarding pain?
chronic pain states especially neuropathic pain
51
Issues with prescribing TCAs for pain?
We prescrib eit at a much lower dose than for depression and titrate up from there. This leads to the drug taking much longer to work and we mind not see any effects for 4-6 weeks or not at all
52
Side effect categories for TCAs?
| 4
Anticholinergic -Neurologic
| Cardiovascular -Gastrointestinal
53
Contraindicated for patients with?
| 4
severe cardiac diseas
conduction disturbances
get a pretreatment EKG
Avoid completely with patients with GI dysfunciton
54
What is the most common TCA given for neuropathic pain?
Amitriptyline (Elavil):
| Strong anticholinergic effect
55
What are anticonvulsants used for in treating pain?
Used for the treatment of neuropathic pain and other mild/moderate chronic pain states
56
MOA for neurontin?
Binds to voltage gated ca channel sites
57
Why is neurontin usually used first line?
Well tolerated, effectivie and cheap
58
What do we not use Neurontin for?
trigeminal neuralgia
59
Side effects of neurontin?
| 4
Somnolence, Ataxia (thats why we start slow)
Nausea, diarrhea
Dizziness, fatigue
Mood swings
60
What is pregabalin used for (lyrics?)
peripheral neuropathy and fibromyalagia
61
Mode of action for Topiramate (Topamax)?
block voltage gated sodium channels
62
What is the drug of choice for trigeminal neuralgia?
Carbamazepine (Tegretol)
63
Why is Carbamazepine (Tegretol) dangerous?
Many drug interactions because it affects CYP enzymes
64
What are the uses for Duloxatine (Cybalta)
MOA?
Duloxatine (Cybalta)
1. Antidepressant
2. Indicated for treating diabetic peripheral neuropathy
3. Found to work in other chronic pain conditions such as fibromyalgia, and chronic LBP
Blocks serotonin and norepi reuptake
65
What is an intrathecal injection?
| 3
An injection into the space around the spinal cord
Used for patient’s with chronic LBP
Usually there is a reservoir of an opioid analgesic that is pumped in
66
What is an epidural injection?
| 3
One time injection by anesthesiologist
Injects long acting anesthetic (Marcaine) and steroid
May be repeated if patient obtains relief
67
What is Hyperalgesia
Increased response to a stimulus that normally is painful
68
What is Hypoalgesia
Diminished response to a normally painful stimulus
69
What is Analgesia
Absence of pain in response to stimulation that normally is painful- what we give for surgeries etc
70
What is Hyperesthesia:
Excessive physical sensitivity
71
What is Hypoesthesia
Diminished sensitivity to stimulation-numbness
72
What is Dysesthesia
A unusual and frightening physical disorder- usually caused by nerves, burning or tingling sensation
73
What is Paresthesia
An abnormal sensation, typically tingling or pricking
74
What is Allodynia
Pain resulting from a stimulus that does not normally elicit pain. so out of normal. brushing a feather or throwing a cotton ball at someone causes severe pain
75
The A's of pain treatment outcome?
| 4
Analgesia- reduce pain
Activities of Daily Living- so they can do them
Adverse effects- try to reduce SE
Aberrant behaviors- not deviating from the course that youre trying to achieve
76
what are some invasive procedures we do to prevent pain?
| 4
Nerve blocks
Intra-spinal drug delivery
Short terms – intrathecal or epidural infusion
Long term – implants - pain pumps
77
Central nerve blocks
Spinal
| Epidural
78
Peripheral nerve blocks
Femoral
| Intercostal
79
Autonomic Nerve blocks
Stellate ganglion
| Lumbar Sympathectomy
80
Facet block is for what pain?
back pain
81
Cryolysis is for what pain?
nerve damage
82
Radio frequency for what pain?
facet joint and nerve damage
83
Neuropathic pain is caused by?
Pain caused by damage or disease affecting the somatosensory nervous system
84
Common qualities?
| 3
Burning or coldness
“pins and needles”
Numbness and itching
85
Neuropathic pain is divided into what kind of categories?
| 3
Peripheral neuropathic
Central neuropathic (brain/spinal cord)
Mixed
86
What are the causes of neuropathic pain?
| 5
```
Spinal cord injury
MS
Strokes
Diabetes
Herpes Zoster
```
87
Neuropathic pain treatment?
| 4
1. Antidepressants (first-line)
- Tricyclic antidepressants
- SNRI
2. Anticonvulsants (first-line)
- Pregabalin
- Gabapentin
- --Diabetic neuropathy
- Carbamazepine
- Oxcarbazepine
- ----Trigeminal neuralgia
3. Topical lidocaine
- ----Post-herpetic neuralgia
4. Opioids
- Not recommended as first-line treatment
88
Types of antidepressents?
- Tricyclic antidepressants
| - SNRI
89
Types of anticonvulsants?
Pregabalin
- Gabapentin
- --Diabetic neuropathy
- Carbamazepine
- Oxcarbazepine
- ----Trigeminal neuralgia
90
Causes of Trigeminal neuralgia?
| 4
1. Blood vessel pressing on the nerve
2. MS
3. Trauma/Surgery
4. Cancer
AFFECTS the 5th cranial nerve
91
What kind of pain is associated with TN?
evere/stabbing
Constant aching/burning sensation
Pain rarely occur at night while sleeping- they aren’t sure why but it often happens
92
An MRI should be done to make sure its TN and not what?
What risk factors are asscoiated with TN? 4
mass lesion or MS
Patients with sensory loss
Patients
93
Medication for TN?
Carbamazepine 100-200mg qd to 600-1200 qd (first-line)
94
Pathology of post herpetic neuralgia?
| 4
1. Virus lies dormant until opportune moment
2. Gains entry into the sensory dorsal root ganglia
3. Travels down sensory nerve and is the cause for dermatomal distribution
4. Virus damages sensory nerves, sensory dorsal root ganglia, and dorsal horns of spinal cord
95
Where is the most common area for herpes zoster and where does it never cross?
never passes midline
| most common area affected is T5-6 but it can go to any dermatome
96
Medications to use for herpes zoter?
Analgesics (Capsaicin)
Anticonvulsants
TCAs
97
Definition of chronic pain syndrome
| 3
- Chronic pain condition affecting one of the limbs
- Most cases are preceded by direct physical trauma, often of relatively minor nature, to the soft tissue, bone or nerve.
- Often follows surgical repair
98
What is chronic pain syndrome characterized by?
Prolonged or excessive pain
| Mild or dramatic changes in skin color, temperature, and/or swelling
99
Average age of CPS?
40 years
100
Causes of CPS?
| 3
Fractures, sprains/strains, soft tissue injury
Limb immobilization
Surgical or medical procedures (needlestick)
101
Type I CRPS is characterized how?
without a confirmed nerve injury
| more common
102
Type II CRPS is characterized how?
With a confirmed nerve injury
103
Clinical presentations of CRPS?
| 5
1. Prolonged and constant pain
2. Constant or intermittent changes in temperature, skin color, and swelling
3. May change color
- Blotchy
- Blue
- Purple or red
4. Abnormal jerking or tremors
5. Skin is shiny and thin
104
Describe the 3 stages in CRPS?
Stage 1: After even with or without apparent cause, pt. develops pain in limb – burning, throbbing, sensitive to touch or cold with localized edema
Stage 2: Progression of edema, thickening of skin, muscle wasting, brawny skin.
Stage 3: Limitation of movement, contracture of digits, waxy trophic skin changes, brittle ridged nails.
105
Medications/treatments to use along with physical therapy and psychotherapy for treatment of CRPS?
4 meds
1 procedure
```
NSAIDS
Steroids
Anticonvulsants
Opioids
Nerve blocks
```
106
What is the pathophysiology for tension headaches?
myofascial
107
Medications for tension headaches?
| 3
1. Aspirin 325mg 1-2 po every 4-6 hrs prn headache
Acetaminophen (Tylenol)325mg 1-2 po every 4-6 hrs prn
NSAIDS
Ibuprofen 200mg, 400mg, 800mg 1 po tid prn
2. 2nd line
Above meds with caffeine
3. Adjunct therapy
butalbital
108
What do migraine heachaches result frim?
dilation of blood vessels innervated by the trigeminal nerve caused by a release of neuropeptides from parasympathetic nerve fibers
109
What are the four phases of headaches?
1. Premonitory (non headache symptoms up to 2 days pre migraine)
- crankiness, food cravings, depression
2. Aura (visual and or speech focal symptoms)
3. Headache
4. Postdromal- exhausted, euphoria
110
What are some triggers of migraine headaches?
1. Skipping meals or eating too little
2. Having too little or too much caffeine
3. Sleeping too much or too little
4. Emotional stress
111
Migraine Treatments?
First line?4
Second line?3
ASA (anti-inflammatory drug)
Acetaminophen
NSAIDS
Indomethacin - used for gouts
Zolmitriptan (Zomig) 1.25-2.5mg every 2 hrs (max 10mg/24 hrs)
Rizatriptan (Maxalt) 5-10mgq2hrs max 30mg/24hrs
Sumatriptan (Imitrex) 4-6mg SC. May repeat in 1 hr. Max
112
Meds to use for nausea and vomiting?
Phenergan and zofran
113
What meds could be used as preventative treatment for migraine headaches?
3
TCA's
Beta Blockers
Calcium Channel Blockers
114
Symptoms associated with cluster headaches?
| 5
```
Watering of the eye
Nasal congestion
Swelling of the eye
Rhinorrhea
Lacrimation
```
115
Triggers for cluster headaches?
| 4
ETOH (alcohol)
Stress
Glare
Foods
116
Clincial features of cluster headaches?
1. Unilateral pain, begins around eye or temple
2. Begins quickly, maximum intensity in minutes
3. Deep and excruciating “ice pick” pain
4. Ipsilateral lacrimation and redness of the eye
5. rhinorrhea
6. Ipsilateral nasal congestion
117
First line treatment for cluster headaches?
inhalation of 100% O2
| Triptans
118
What is the differential for TMJ?
| 5
```
Infection
Temporal Arteritis
Dental problems
Trigeminal neuralgia
Parotid gland disorder
```
119
Medications for TMJ?
| 5
1. Muscle relaxants
2. NSAIDs
3. TCAs
4. steriod joint injections
5. Botox
120
What is another name for acute pain?
| 2
eudynia
| adaptive
121
What is another name for chronic pain?
| 2
maldynia
| maladaptive
122
What is cutaneous pain?
Superficial structures such as skin and subcu
| Papercut is an example of easily localized
123
What is somatic pain?
deep body structures affected
| sprained ankle- much swelling and vasculature involved
124
What is viscceral/referred pain?
Where is it localized?
pain from an internal organ that is perceived to originate from a distant area of the skin.
to a dermatome
125
Where is referred visceral pain in the heart localized?
Stomach?
Colon?
neck shoulder arm and jaw
above the umbilicus
below the umbilicus, pelvis
126
What are the four physiological processes associated with pain?
Transduction
Transmission
Modulation
Perception
127
What is transduction of pain?
Conversion of a noxious stimulusto electrical activity
128
What is transmission of pain?
refers to the passage of action potentials from the peripheral terminal along axons to the central terminal of nociceptors in the central nervous system.
129
What is the modulation of pain?
Refers to the alteration (augmentation or suppression) of sensory input
130
What is the perception of pain?
Refers to the decoding of afferent input into the brain that gives rise to the individuals specific sensory experiene
131
All pain receptors are?
free nerve endings
132
What can pain receptors be stimulated by?
| 3
mechanical (stretch).
thermal.
chemical.
133
What kind of chemical receptors enhance the sensitivity of pain endings but do not directly excite them.
prostaglandins and substance P
134
What does the rate of tissue damage?
The cause of paiin
135
What causes the most pain and may be the single agent most responsible for causing the tissue damage type of pain?
bradykinin
136
First-order Neurons detect?
detect stimuli that threaten the integrity of innervated tissue
137
Second order neurons do what?
located in the spinal cord and process nociceptive info
138
Third order neurons do what?
project pain information to the brain
139
In the neospinothalamic tract where does crossing over (decussation) occur?
When the 2nd neuron starts in the dorsal horn and crosses to the opposite side's anterolateral tracts
140
What kind of pain is in the neospinothalamic tract?
fast sharp pain
141
What kind of pain is in the paleospinothalamic tract?
Slow pain types
142
What is enkephalin believed to cause?
to cause both pre- and post-synaptic inhibition of type C and type Ad pain fibers where they synapse in the dorsal horns.
143
Where are the enkephalins and dynorphin found?
found in the brain stem and spinal cord.
144
the b-endorphin is found where?
in the hypothalamus and the pituitary.
145
What is the fucntion of what opiate system in our brain?
Pain suppression during times of stress.
An important part of an organism’s response to an emergency is a reduction in the responsiveness to pain.
effective in defense, predation, dominance and adaptation to environmental challenges.
146
What comes with tissue damage and/or inflammation?
increase in permeability of capillaries and edema formation.
147
Alergies we dont want are caused by?
histamine
bradykineins
leukotrienes
148
What is causeing the inflammation, permeability of capillaries and edema formation in injury?
Algogenic substances
149
Consequences of untreated acute pain?
| 3
increase metabolic rate and blood clotting,
impair immune function
induce negative emotions
150
What is a procedural referral?
The patient has treatable pathology that I am not trained to treat.
151
What is a cognitive referral?
There are diagnoses that I am considering that I am not trained to make.
