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Patho > Pain > Flashcards

Pain Flashcards

1
Q

Allodynia

A

Abnormal perception of pain from a stimulus that shouldn’t be painful

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2
Q

Dysesthesia

A

Not pain. Just an uncomfortable sensation.

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3
Q

Anesthesia

A

Reduced perception of ALL sensation, mainly touch

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4
Q

Pallanesthesia

A

Loss of perception of vibration

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5
Q

Causalgia

A

Burning pain in the distribution of one or more peripheral nerves

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6
Q

Protopathic sensation

A

noxious

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7
Q

Epicritic sensation

A

Non-noxious sensation

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8
Q

Cancer pain involves both

A

acute and chronic pain

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9
Q

These types of pain use both pain pathways

A

Thermal and mechanical

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10
Q

This pain uses mostly slow fibers

A

Chemical pain. Mediated by the following NTs

Bradykinin
Substance P
Proteolytic enzymes
All of this increase the permeability of ions

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11
Q

Nociception involves these four processes

A

Transduction
Transmission
Modulation
Perception

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12
Q

Modulation

A

Neurons originating in the brainstem descend to the level of the spinal cord, releasing substances to modulate the nociceptive impulses

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13
Q

First order neurons

A

Send axons via the dorsal root ganglia, and then synapse with interneurons, sympathetic neurons, motor neurons (ventral horn), or second order neurons.

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14
Q

Neurons traveling along the STT may end up in the

A

Thalamus
RF
Nucleus raphe magnus
Periaqueductal gray

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15
Q

Where is the STT?

A

Anterolaterally in the white matter of the spinal cord

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16
Q

Third order neurons

A

Send fibers from the thalamus to:
Somatosensory areas I and II in the parietal cortex
Superior wall of the sylvian fissure

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17
Q

Tracks alternative to the STT

A

1) Spinoreticular (will cause insomnia)
2) Spinomesencephalic (activates the antinociceptive, descending pathways. It mediates the pain!)
3) Spinohypothalamic and spinotelencephalic (activate the hypothalamus to evoke emotional behavior)

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18
Q

Fast pain pathway (neospinothalamic tract)

A

1st order- via A-delta to lamina I (lamina marginalis) on the dorsal horn of spinal cord

2nd order- Decussate through the anterior white commisure, and and pass up through the white anterolateral columns (STT)
Some of these will end on the reticular formation (nag you enough not to fall asleep), but most will end on the ventrobasal complex (VBC) of the thalamus

3rd order then communicate with somatosensory cortex

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19
Q

Slow pain pathway (paleospinothalamic tract)

A

1at order- via C fibers to laminae II and III (substantia gelatinosa)

2nd order- either connect II or III to V within the dorsal horn

3rd order- now connect with the fast pain pathway, by decussating via the anterior white commissure, and traveling up the STT

Where do the 3rd order neurons terminate?
10% in thalamus
Rest go to pons, midbrain, and the tectum of the midbrain mesencephalon periaqueductal grey

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20
Q

When is fast pain easily localized?

A

If the a-delta fibers are stimulated long with tactile receptors

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21
Q

3 major components of the brain analgesia system

A

1) Periaqueductal grey (in the midbrain)
2) Nucleus raphe magnus (in the medulla)
3) Nociceptive inhibitory neurons in the dorsal horn of the spinal cord (work to inhibit those neurons carrying pain signals)

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22
Q

Periaqueductal grey

A

Area surrounding the cerebral aqueduct in the midbrain
Epicenter of analgesia**
Plays a role in the descending modulation of pain and in defensive behavior

23
Q

Nucleus raphe magnus

A

This is the PAIN MEDIATOR
Sends fibers to the dorsal horn of the spinal cord to directly inhibit pain
Also sends fibers to the cortex to tell you how much the injury should really hurt
This system is stimulated from axons in the spinal cord and cerebellum

24
Q

Chemical mediators of pain

A

1) Substance P (Elicits the SLOW pathway. It’s released slowly and builds over a few minutes. Results in slow chronic pain. This is a big one for us in anesthesia)
2) Glutamate (FAST pathway. Acts instantly and lasts for only a few miliseconds)
3) CGRP (Calcitonin Gene-Related Peptide. Newer one found in chronic pain, especially migraines)

25
Q

What receptor does ketamine work on?

A

NMDA. It is an NMDA antagonist, which is why it may be useful in chronic pain.

26
Q

Cell physiology for acute pain

A

1) Pain signals arrive to the dorsal horn via a-delta and C fibers
2) These fibers release Substance P and Excitatory Amino Acids (EAAs)
3) Substance P- activates neurokinin-1 (NK-1) receptors
EAA activate AMPA
4) Pain neurons are now depolarized and carry their signals to the brain

27
Q

Cell physiology for chronic pain

A

1) Constant barrage of pain signals depolarizes the neuron in a way that results in the removal of Mg from NMDA receptors.
2) Calcium floods in, activating nitric oxide synthase (cNOS)
3) cNOS converts L-arginine to nitric oxide (NO), which rapidly diffuses out of the cell because it is a gas
4) NO then works pre-synaptically to cause an exaggerated release of substance P and EAAs, and post-synaptically to cause a release of substance P and ACh

28
Q

Neuroendocrine response to pain

A

Increase in catabolic hormonesDecrease in anabolism, insulin, and testosterone
Stress response
ACTH release
Hyperglycemia

29
Q

Cardiac response to pain

A

Increase in HR, SVR, BP, and CO
MI, CHF, dysrhythmia
Increased O2 demand and decreased supply
Secondary atelectasis
Coronary vasoconstriction due to high catecholamines
Increased plasma viscosity and platelet aggregation

30
Q

Release of ______ may induce coronary vasospasm

A

Serotonin

31
Q

Pulmonary response to pain

A

Increase in O2 consumption and CO2 production
Increase in minute ventilation- rapid shallow breaths
Decrease in TV, VC, and FRC
Decrease in FRC is huge *****. As FRC decreases, resting lung volume approaches the closing volume, resulting in atelectasis, V/Q mismatch, and hypoxemia.

32
Q

Visceral pain is often referred to ________

A

somatic sites

33
Q

GI/GU response to pain

A

Think about what happens to the gut with SNS activation

1) Increased sphincter tone (urinary retention)
2) Decrease in gastric motility (ileus)
3) Increase in gastric juices (stress ulcers)

34
Q

Muscular and emotional responses to pain

A

Muscle- Periosteal and somatic irritation initiate motor reflex leading to muscle spasm
Emotional- anxiety and anger if lack of pain control

35
Q

What is the best course of action for post-op pain control?

A

Pre-emptive analgesia! Load them up from with pain meds.

36
Q

Benefits of regional anesthesia

A

Less morbidity
Less CV failure
Fewer infections (d/t increase in blood flow from the sympathectomy)
Lower cortisol levels (surgeries above the level of L1 tend to have a large neuroendocrine response to surgery)
Overall lower post-op complication rate

37
Q

When do you want to incorporate regional anesthesia?

A

Whenever possible! It’s good for both intra and post-op care

38
Q

COX inhibitors

A

Work by inhibiting prostaglandin synthesis
COX1- widespread in the body
COX2- mostly deals with inflammation

39
Q

Benefits of PCAs

A

Cost-effective
Patients consume less drug (although males use more than females)
Higher patient satisfaction
Shorter hospital stays

40
Q

Nearly all overdoses from PCAs have been due to _____

A

Errors in programming the PCA

41
Q

Define chronic pain

A

Pain that persists for one month longer than expected

42
Q

Most common examples of chronic pain

A

1) Low-back pain
2) HA
3) Facial pain, cancer pain, and arthritic pain
4) Pain can also be psychogenic in nature

43
Q

Causes of chronic pain

A

1) Chronic somatic or visceral pathology
2) Psychological mechanisms
3) Peripheral mechanisms (associated with chronic inflammation)
4) Peripheral-central mechanism (Lesions of peripheral nerves, dorsal roots, or dorsal ganglia. Happens in causalgias, reflex sympathetic dystrophy, and phantom pain)
5) Central mechanism (lesions to thalamus and spinal cord)
6) Reflex role (Excessive muscle tension. SNS hyperactivity also can create local ischemia)
7) Circle mechanism (intense nerve stimulation causes closed loop with interneurons)
8) Chronic nerve compression (fixed surgically)
9) Psychophysiologic (severe stress causes chronic tension HAs and spasms in shoulder, back, and chest)
10) Learned mechanisms- hypochondriacs convince themselves so much that they’re in pain that they actually get pain

44
Q

Why are minor injuries more painful for those with chronic pain?

A

Because their serotonin and endorphins are depleted

45
Q

Patients with chronic pain can develop these changes to their personality

A

Neuroticism, anxiety, anger, hopelessness. These tend to go away when the pain is relieved.

46
Q

Are cancer patients more or less likely to become addicted to narcotics?

A

Less

47
Q

Causes of cancer pain

A

1) Bone involvement

2) Compression of peripheral nerves

48
Q

Importance of pain relief in cancer patients

A

Patients with pain have more emotional disturbances and die sooner than those whose pain is controlled

49
Q

Why are most people so hesitant to give narcotics?

A

Lack of knowledge of pharmacology of analgesics
Fear of addiction
Fear of resp repression

50
Q

3 step recommendation for cancer pain

A

1) ASA, tylenol, NSAIDS
2) Codein and oxycodone
3) IV morphine and dilaudid

51
Q

This medication can cause opioid induced hyperalgesia

A

Fentanyl. Long-term use can increase the person’s sensitivity to pain

52
Q

Parts of the brain activated during acute stress

A

1) RAS or thalamus (increases alertness)
2) Amygdala (linked to your behavior under stress- crying, anger, etc)
3) Arcuate nucleus (releases NPY)
4) Locus coeruleus (releases norepi)
5) Paraventricular nucleus (PVN)- releases CRH

53
Q

How is chronic stress maladaptive?

A

Because it involves a dampening of negative feedback of the stress response
Humans are prepared to deal with acute stress, but are not designed for chronic stress

Patho (14 decks)

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