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Intro to Clinical Medicine > Pain! > Flashcards

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”**

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2
Q

Acute/Temporary Pain Treatment
steps?
3

A
  1. 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**
  2. Use the least potent analgesic w/ the fewest side effects
  3. Properly titrate the dose & administer for an adequate amount of time
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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

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4
Q

Doasge for acetominophen?

max daily dose?

A

4000mg

4grams per day

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5
Q

Onset of acetominophen?

A

15 to 30 min

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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!

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7
Q

Mechanism of action for aspirin?

4

A
  1. Inhibits COX and platelet aggregation
  2. reduces pain by reducing inflammation
  3. Anti-pyretic
  4. Lower incidence of colon cancer and decreases DVT after CABG
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8
Q

Side effetcs of aspirin?

3

A

Gastric upset and ulcers
Hepatotoxicity and renal toxicity
Asthma and rashes

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9
Q

What is salicylism?

A

vomiting, tinnitus, decreased hearing and vertigo are reversible by reducing the dosage

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10
Q

What will toxic levels of aspirin cause?

4

A
  1. metabolic acidosis
  2. respiratory depression
  3. cardiotoxicity
  4. Overdoses are a medical emergency
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11
Q

Mechanism of action in NSAIDs?

A

Decreases prostaglasdins!! main mechanism of action

Non selective for COX1 and COX2

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12
Q

What do prostagladins cause?

A

inflammation

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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

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14
Q

What are the physiological effects of prostaglandin?

5

A
  1. Activation of the inflammatory response
  2. Elicitation of pain and fever
  3. Contraction and relaxation of smooth muscle** (can help with pain there)
  4. Inhibition of acid synthesis and increased secretion of the protective mucus in the stomach
  5. Increased blood flow to the kidneys
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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

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16
Q

GI Side Effects of NSAIDs?

4

A

N/V,
heartburn,
ulcers/bleeding,
diarrhea

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17
Q

Cant pregnant women take NSAIDS?

A

They shouldnt but can while lactating and postpartum

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18
Q

Renal side effects of NSAIDS

4

A
  1. Salt and water retention
  2. HTN**
  3. Can be particularly damaging if patient is taking other nephrotoxic drugs
  4. Interferes w/ platelet aggregation for 2-4 days
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19
Q

NSAIDs can cause photosensitivity

A

statement

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20
Q

What kind of patients do we see experiencing adverse renal events and acute kidney injury?
4

A
  1. Chronic kidney disease (decreased GFR)
  2. Volume depletion (diuresis, vomiting, diarrhea)
  3. CHF, nephrotic syndrome or cirrhosis
  4. Older age
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21
Q

Max dose for ibuprofen?

A

3200mg

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22
Q

Max dose for Naproxen (aleve)?

A

1000mg

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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

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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)
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25
Q

Opiod indications?

3

A

Acute postop pain
Severe pain for a limited duration
Chronic pain (by experienced provider)

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26
Q

MOA for opiods?

A

often inhibit Mu receptors in the CNS

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27
Q

What are Mu and Beta recetors for opiods associated with?

A

endorphins

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28
Q

What are delta receptors for opiosd associated with?

A

enkephalins

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29
Q

What are kappa receptors associated with?

A

dynorphins

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30
Q

Describe nociceptive pain?

A

cut your skin and it hurts where you cut it

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31
Q

Describe neuropathic pain?

A

neuropatnhy- nerves are causing symptoms of numbness adn tingling. source of pain is somewhere else

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32
Q

Side effects of opioids?

3

A

Constipation
Sedation
Addiction
are the big three

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33
Q

Everytime you prescribe an topioid what do you need to tell the patient?
4

A

Address ahead of time—constipation**
Warn of addiction
Sedation
Nausea and vomiting—may want to prescribe an anti-emetic

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34
Q

What causes the euphoria in opioids?

A

release of dopamine

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35
Q

Whats the difference between physical dependence and addiction?a

A

addiciton is the physcological dependance

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36
Q

If we push morphine too fast what can happen?

A

Hypotension (low BP)

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37
Q

Can you write for demerol pills?

A

NO, only IV and IM

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38
Q

How would the onset and duraiton of action differ in methadone than in other opioids?

A

Extended duration of action and slow onset of action

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39
Q

Side effects fo methadone?

3

A

Hypoglycemia
Hyponatremia
Death: prolonged QT interval—torsade de pointes

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40
Q

Methadone does not causes euphoria!

A

Statment

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41
Q

Oxycodone and acetominophen make what?

A

percocet

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42
Q

Oxycodone and aspirin make what?

A

percadan

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43
Q

Hydrocodone/acetaminophen makes what?

A

vicoden

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44
Q

Hydrocodone/ASA makes what?

A

Lortab

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45
Q

What is narcan used for?

A

opioid reversal medication

Only to get them breathing again not to reach full alertness

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46
Q

What kind of agonist is fentanyl?

What are its dosage forms?3

A

A very strong mu opioid agonist

Available in IV, transdermal patch and suckers

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47
Q

MOA of tramadol?

A

inhibits reuptake of epi and norepi

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48
Q

Side effects of tramadol?

3

A
  1. HA, dizziness
  2. Nausea, constipation (low risk for GI bleeding)
  3. Somnolence-stonrg desire to sleep
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49
Q

Purposes of a pain contract?

3

A
  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
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50
Q

What are Tricyclic Antidepressants (TCAs) used for regarding pain?

A

chronic pain states especially neuropathic pain

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51
Q

Issues with prescribing TCAs for pain?

A

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

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52
Q

Side effect categories for TCAs?

4

A

Anticholinergic -Neurologic

Cardiovascular -Gastrointestinal

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53
Q

Contraindicated for patients with?

4

A

severe cardiac diseas
conduction disturbances
get a pretreatment EKG
Avoid completely with patients with GI dysfunciton

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54
Q

What is the most common TCA given for neuropathic pain?

A

Amitriptyline (Elavil):

Strong anticholinergic effect

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55
Q

What are anticonvulsants used for in treating pain?

A

Used for the treatment of neuropathic pain and other mild/moderate chronic pain states

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56
Q

MOA for neurontin?

A

Binds to voltage gated ca channel sites

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57
Q

Why is neurontin usually used first line?

A

Well tolerated, effectivie and cheap

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58
Q

What do we not use Neurontin for?

A

trigeminal neuralgia

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59
Q

Side effects of neurontin?

4

A

Somnolence, Ataxia (thats why we start slow)
Nausea, diarrhea
Dizziness, fatigue
Mood swings

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60
Q

What is pregabalin used for (lyrics?)

A

peripheral neuropathy and fibromyalagia

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61
Q

Mode of action for Topiramate (Topamax)?

A

block voltage gated sodium channels

62
Q

What is the drug of choice for trigeminal neuralgia?

A

Carbamazepine (Tegretol)

63
Q

Why is Carbamazepine (Tegretol) dangerous?

A

Many drug interactions because it affects CYP enzymes

64
Q

What are the uses for Duloxatine (Cybalta)

MOA?

A

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
Q

What is an intrathecal injection?

3

A

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
Q

What is an epidural injection?

3

A

One time injection by anesthesiologist
Injects long acting anesthetic (Marcaine) and steroid
May be repeated if patient obtains relief

67
Q

What is Hyperalgesia

A

Increased response to a stimulus that normally is painful

68
Q

What is Hypoalgesia

A

Diminished response to a normally painful stimulus

69
Q

What is Analgesia

A

Absence of pain in response to stimulation that normally is painful- what we give for surgeries etc

70
Q

What is Hyperesthesia:

A

Excessive physical sensitivity

71
Q

What is Hypoesthesia

A

Diminished sensitivity to stimulation-numbness

72
Q

What is Dysesthesia

A

A unusual and frightening physical disorder- usually caused by nerves, burning or tingling sensation

73
Q

What is Paresthesia

A

An abnormal sensation, typically tingling or pricking

74
Q

What is Allodynia

A

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
Q

The A’s of pain treatment outcome?

4

A

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
Q

what are some invasive procedures we do to prevent pain?

4

A

Nerve blocks

Intra-spinal drug delivery

Short terms – intrathecal or epidural infusion

Long term – implants - pain pumps

77
Q

Central nerve blocks

A

Spinal

Epidural

78
Q

Peripheral nerve blocks

A

Femoral

Intercostal

79
Q

Autonomic Nerve blocks

A

Stellate ganglion

Lumbar Sympathectomy

80
Q

Facet block is for what pain?

81
Q

Cryolysis is for what pain?

A

nerve damage

82
Q

Radio frequency for what pain?

A

facet joint and nerve damage

83
Q

Neuropathic pain is caused by?

A

Pain caused by damage or disease affecting the somatosensory nervous system

84
Q

Common qualities?

3

A

Burning or coldness
“pins and needles”
Numbness and itching

85
Q

Neuropathic pain is divided into what kind of categories?

3

A

Peripheral neuropathic
Central neuropathic (brain/spinal cord)
Mixed

86
Q

What are the causes of neuropathic pain?

5

A 
Spinal cord injury
MS
Strokes
Diabetes
Herpes Zoster
87
Q

Neuropathic pain treatment?

4

A
  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
Q

Types of antidepressents?

A
  • Tricyclic antidepressants

- SNRI

89
Q

Types of anticonvulsants?

A

Pregabalin

  • Gabapentin
  • –Diabetic neuropathy
  • Carbamazepine
  • Oxcarbazepine
  • —-Trigeminal neuralgia
90
Q

Causes of Trigeminal neuralgia?

4

A
  1. Blood vessel pressing on the nerve
  2. MS
  3. Trauma/Surgery
  4. Cancer
    AFFECTS the 5th cranial nerve
91
Q

What kind of pain is associated with TN?

A

evere/stabbing
Constant aching/burning sensation
Pain rarely occur at night while sleeping- they aren’t sure why but it often happens

92
Q

An MRI should be done to make sure its TN and not what?

What risk factors are asscoiated with TN? 4

A

mass lesion or MS

Patients with sensory loss
Patients

93
Q

Medication for TN?

A

Carbamazepine 100-200mg qd to 600-1200 qd (first-line)

94
Q

Pathology of post herpetic neuralgia?

4

A
  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
Q

Where is the most common area for herpes zoster and where does it never cross?

A

never passes midline

most common area affected is T5-6 but it can go to any dermatome

96
Q

Medications to use for herpes zoter?

A

Analgesics (Capsaicin)
Anticonvulsants
TCAs

97
Q

Definition of chronic pain syndrome

3

A
  • 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
Q

What is chronic pain syndrome characterized by?

A

Prolonged or excessive pain

Mild or dramatic changes in skin color, temperature, and/or swelling

99
Q

Average age of CPS?

100
Q

Causes of CPS?

3

A

Fractures, sprains/strains, soft tissue injury
Limb immobilization
Surgical or medical procedures (needlestick)

101
Q

Type I CRPS is characterized how?

A

without a confirmed nerve injury

more common

102
Q

Type II CRPS is characterized how?

A

With a confirmed nerve injury

103
Q

Clinical presentations of CRPS?

5

A
  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
Q

Describe the 3 stages in CRPS?

A

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
Q

Medications/treatments to use along with physical therapy and psychotherapy for treatment of CRPS?
4 meds
1 procedure

A 
NSAIDS
Steroids
Anticonvulsants 
Opioids 
Nerve blocks
106
Q

What is the pathophysiology for tension headaches?

A

myofascial

107
Q

Medications for tension headaches?

3

A
  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
Q

What do migraine heachaches result frim?

A

dilation of blood vessels innervated by the trigeminal nerve caused by a release of neuropeptides from parasympathetic nerve fibers

109
Q

What are the four phases of headaches?

A
  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
Q

What are some triggers of migraine headaches?

A
  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
Q

Migraine Treatments?
First line?4
Second line?3

A

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
Q

Meds to use for nausea and vomiting?

A

Phenergan and zofran

113
Q

What meds could be used as preventative treatment for migraine headaches?
3

A

TCA’s
Beta Blockers
Calcium Channel Blockers

114
Q

Symptoms associated with cluster headaches?

5

A 
Watering of the eye
Nasal congestion
Swelling of the eye
Rhinorrhea 
Lacrimation
115
Q

Triggers for cluster headaches?

4

A

ETOH (alcohol)
Stress
Glare
Foods

116
Q

Clincial features of cluster headaches?

A
  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
Q

First line treatment for cluster headaches?

A

inhalation of 100% O2

Triptans

118
Q

What is the differential for TMJ?

5

A 
Infection
Temporal Arteritis
Dental problems
Trigeminal neuralgia
Parotid gland disorder
119
Q

Medications for TMJ?

5

A
  1. Muscle relaxants
  2. NSAIDs
  3. TCAs
  4. steriod joint injections
  5. Botox
120
Q

What is another name for acute pain?

2

A

eudynia

adaptive

121
Q

What is another name for chronic pain?

2

A

maldynia

maladaptive

122
Q

What is cutaneous pain?

A

Superficial structures such as skin and subcu

Papercut is an example of easily localized

123
Q

What is somatic pain?

A

deep body structures affected

sprained ankle- much swelling and vasculature involved

124
Q

What is viscceral/referred pain?

Where is it localized?

A

pain from an internal organ that is perceived to originate from a distant area of the skin.
to a dermatome

125
Q

Where is referred visceral pain in the heart localized?

Stomach?

Colon?

A

neck shoulder arm and jaw

above the umbilicus

below the umbilicus, pelvis

126
Q

What are the four physiological processes associated with pain?

A

Transduction
Transmission
Modulation
Perception

127
Q

What is transduction of pain?

A

Conversion of a noxious stimulusto electrical activity

128
Q

What is transmission of pain?

A

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
Q

What is the modulation of pain?

A

Refers to the alteration (augmentation or suppression) of sensory input

130
Q

What is the perception of pain?

A

Refers to the decoding of afferent input into the brain that gives rise to the individuals specific sensory experiene

131
Q

All pain receptors are?

A

free nerve endings

132
Q

What can pain receptors be stimulated by?

3

A

mechanical (stretch).
thermal.
chemical.

133
Q

What kind of chemical receptors enhance the sensitivity of pain endings but do not directly excite them.

A

prostaglandins and substance P

134
Q

What does the rate of tissue damage?

A

The cause of paiin

135
Q

What causes the most pain and may be the single agent most responsible for causing the tissue damage type of pain?

A

bradykinin

136
Q

First-order Neurons detect?

A

detect stimuli that threaten the integrity of innervated tissue

137
Q

Second order neurons do what?

A

located in the spinal cord and process nociceptive info

138
Q

Third order neurons do what?

A

project pain information to the brain

139
Q

In the neospinothalamic tract where does crossing over (decussation) occur?

A

When the 2nd neuron starts in the dorsal horn and crosses to the opposite side’s anterolateral tracts

140
Q

What kind of pain is in the neospinothalamic tract?

A

fast sharp pain

141
Q

What kind of pain is in the paleospinothalamic tract?

A

Slow pain types

142
Q

What is enkephalin believed to cause?

A

to cause both pre- and post-synaptic inhibition of type C and type Ad pain fibers where they synapse in the dorsal horns.

143
Q

Where are the enkephalins and dynorphin found?

A

found in the brain stem and spinal cord.

144
Q

the b-endorphin is found where?

A

in the hypothalamus and the pituitary.

145
Q

What is the fucntion of what opiate system in our brain?

A

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
Q

What comes with tissue damage and/or inflammation?

A

increase in permeability of capillaries and edema formation.

147
Q

Alergies we dont want are caused by?

A

histamine
bradykineins
leukotrienes

148
Q

What is causeing the inflammation, permeability of capillaries and edema formation in injury?

A

Algogenic substances

149
Q

Consequences of untreated acute pain?

3

A

increase metabolic rate and blood clotting,
impair immune function
induce negative emotions

150
Q

What is a procedural referral?

A

The patient has treatable pathology that I am not trained to treat.

151
Q

What is a cognitive referral?

A

There are diagnoses that I am considering that I am not trained to make.

Intro to Clinical Medicine (12 decks)

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