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PHAC II > 1. Pain > Flashcards

1. Pain Flashcards

1
Q

What is the usual issue due to the subjective nature of pain? Undertreatment or overtreatment?

A

Undertreatment.

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2
Q

______ _____ last less than 6 month and stops once the healing process is done.

A

acute pain

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3
Q

_______ _____ involves complex processes and pathology, can alter anatomy and neural pathways, constant, lasts longer than 6 months and sometimes for life.

A

chronic pain

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4
Q

Briefly describe the pain theory.

A

when acute pain is severe AND unrelieved it can cause abnormally increased physiological responses.

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5
Q

Which systems are significantly affected by the pathophysiology of pain?

A

cardiovascular and respiratory systems

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6
Q

What are some harmful effects of pain?

A

-Adrenergic stimulation (SNS)
- increase HR
- increase CO
- increase heart oxygen use
- decrease in lung vital capacity
- decease in alveolar ventilation
- decrease in functional residual capacity
arterial hypoxemia
- suppressed immune function (increased risk of infections and sepsis)

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7
Q

What are some types of acute, unrelieved pain that can cause chronic pain?

A
  • multiple trauma
  • phantom limp pain after amputation
  • repeated back surgeries
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8
Q

What are some neuro-muscular disorders that can cause chronic pain?

A
  • fibromyalgia
  • rheumatoid arthritis
  • MS
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9
Q

What are 3 types of stimulation of pain pathways?

A
  • mechanical damage
  • extreme temperature
  • chemical irritation
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10
Q

Which neurons causes the first sharp pain?

A

A-delta, this is “protective pain”

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11
Q

Which neuron causes the second, dull pain?

A

neuron C, these cause learning and behavioral modification

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12
Q

What are the 4 distinct processes of the pain pathway?

A
  • transduction
  • transmission
  • modulation
  • perception
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13
Q

What is the local biochemical changes in nerve endings that generates a signal?

A

Transduction

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14
Q

What is the movement of a pain signal from the site of pain to the spinal cord and brain?

A

Transmission

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15
Q

What is the synthesis and analysis of the pain signal in the brain?

A

Perception

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16
Q

What is the process of the endogenous systems in place that can inhibit pain at any point along the pathway

A

Modulation

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17
Q

What are nociceptors?

A
  • free nerve endings that can differ between harmful and harmless stimuli
  • pain neurons
  • tissue damaged when exposed to mechanical, thermal or chemical stimuli
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18
Q

How does damaged tissue create the sensation of pain?

A
  • tissue damaged when exposed to mechanical, thermal or chemical stimuli
  • substances are released from the damaged tissue and creates the movement of the pain impulse to the spinal cord
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19
Q

What kind of substances are release from damaged tissue that cause pain?
How exactly do they cause this signal?

A
  • bradykinin
  • serotonin
  • substance P
  • histamine
  • prostaglandin
  • cause cell depolarization by sodium flux
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20
Q

What is the main role of histamine?

A

inflammation and exacerbation

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21
Q

What is the importance of prostaglandin?

A

they are the main target of NSAIDS

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22
Q

How do NSAIDS reduce pain?

A

they minimize the production of prostaglandins

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23
Q

How do corticosteroids reduce pain?

A

They inhibit prostaglandins as well as other inflammatory mediators

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24
Q

Where is pain processed?

A

the central structures of the brain

25
Q

Transmission requires _____________.

What inhibits this?

A
  • neurotransmitters

- opiods will inhibit their release

26
Q

How does the structure of A delta neurons contribute to its function?

A
  • they have large diameters –> therefore the signal will move FAST
  • causes the body to remove itself from the pain stimulus (“learning”)
27
Q

During the modulation phase, the pain sensation is reduced. What causes this?

A
  • Endorphins (endogenous opiods)
  • Descending fibers in the spinal tract and higher cortical centers will release these chemicals
  • they then bind to receptors in the pain pathway to block transmission and perception of pain
28
Q

How do antidepressants help reduce pain?

A
  • they decrease the reuptake of central NTs, such as serotonin and NE
  • these NTs can modulate perception
29
Q

What can activate the descending pain modulation system?

A 
STRESS
fear 
hunger/thirst
fatigue
prolonged motor activity
hypnosis
30
Q

What are the 3 categories of pain?

A
  1. nociceptic
  2. neuropathic
  3. visceral
31
Q

What is nociceptic pain caused by?

A

injury, trauma, infection

32
Q

What is neuropathic pain caused by?

A
  • damage or dysfunction of the peripheral or central NS

- abnormal processing of impulses also plays a part

33
Q

What is visceral pain caused by?

A

arises from an internal organ –> MI, appendicitis, small bowel obstrution, etc

34
Q

amputation/subsequent phantom limb, scar tissue from surgery, nerve entrapment or damaged nerves can all cause what type of pain?

A
  • neuropathic pain
35
Q

What are the 3 pharmacological effects of NSAIDS?

A
  1. analgesic
  2. anti-pyretic
  3. anti-inflammatory
  • these effect are all caused by the inhibition of prostaglandins
36
Q

How many types of cyclo-oxygenases (COX) are there?

Which one is responsible for pain, inflammation and fever?

A
  • 3 types

- COX-2 is involved with pain

37
Q

Describe the 3 phases of inflammation.

A
  1. Acute transient phase
    - local vasodilation, increased capillary permeability
  2. Delayed subacute phase
    - infiltration of leukocytes and phagocytes
  3. Chronic proliferative phase
    - tissure degeneration and fibrosis
38
Q

What would happen if a pt were injected with PGs?

What are some clinical uses of this?

A
  • would cause local inflammation, increased blood flow and severe pain
  • PGs can cause uterus cramping (used for abortions)
  • PG inhibitors can delay delivery
39
Q

Where are PGs released to induce a fever?

A

near the hypothalamus (the body temp regulator)

40
Q

NSAIDS can be better than ________ for inflammation-induced pain and even some post-op pain.

A

opiods (morphine, etc)

41
Q

Besides the role in pain/inflammation, what are 3 other effects the PGs have?

A
  1. critical with platelet aggregation and formation of clots (think about ASA)
  2. modulates stomach acid and mucus lining (think about how NSAIDS are bad for the stomach)
  3. important in uterine contraction (can cause painful cramps)
42
Q

What are the 2 mechanisms of action of ASA?

A
  1. ASA irreversibly acetylates COX enzymes (effect will last until new enzyme is made, not dependent on ASA elimination)
  2. a minor metabolite of ASA (gentisic acid) competitively inhibits COX enzymes (this effects will depend on elimination)
43
Q

What dosage of caffeine will increase the analgesic effect of non-opiod analgesics?

A

60-120 mg (found in a typical cup of coffee)

44
Q

What are the signs and sx of salicylate overdose?

What is the immediate danger?

A
  1. tinnitus
  2. increase in metabolic rate
    - initial hyperventilation
    - metabolic acidosis (overproduction of CO2)
    - severe hypoglycemia
  • immediate danger = hyperthermia, dehydration, hypoglycemia
45
Q

What is always and immediately used during salicylate overdose?

A

parenteral fluids and glucose

46
Q

What treatment is used for severe salicylate overdose?

A

hemodialysis

47
Q

What are 2 classes of NSAIDS?

A
  1. Salicylates
    - bismuth salicylates (pepto)
    - ASA
  2. Proprionic acid
    - ibuprofen (less GI effects)
    - naproxen (aleve, BID)
48
Q

This NSAID has:

  • high potency, but high risk of GI bleeds
  • Rx only
  • used for inflammatory pain (arthritis, post-op swelling, gout, sometimes endometriosis)
  • gel formulations that are used for muscular/joint pain
A

Diclofenac

49
Q

This NSAID is specifically used for gout and swelling. It is also less common for chronic conditions.

A

Indomethacin

50
Q

What type of COX inhibitor causes GI side effects most often?

A

non-selective COX inhibitors

51
Q

Describe the pathophysiology of GI issues caused by COX inhibitors.

A

COX-1 produces PGE2 and PGIs, these PGs suppress acid production, increase gastric blood flow and increase mucin secretion
- Therefore, if COX is inhibited, acid increases and mucus protection decreases

52
Q

What is misoprostol and what is its use?

A
  • is a PG analog (similar structure and function)

- used to supply the stomach with PG effect that is destroyed by non-selective COX inhibitors

53
Q

How do NSAIDS cause hypertension or angina?

A

By the increase in circulating blood volume

54
Q

How do NSAIDS cause bleeding disorders?

A

By inhibiting COX, the clotting process is compromised

55
Q

What is Reye’s syndrome and how do NSAIDs contribute?

A

fatal hepatic encephalopathy in children with viral infections (chicken pox, influenza)
- ASA can contribute to this syndrome

56
Q

What is the drug of choice in children? (Because of Reye’s syndrome)

A

Acetaminophen

57
Q

Explain the mechanism of action of acetaminophen overdose.

A
  • the highly reactive metabolite of acetaminophen has to broken down by glutathione (GSH).
  • if you have high doses of acetaminophen, the reactive metabolite with deplete GSH and the metabolite will no longer be broken down.
58
Q

What kind of damage is done to the liver after GSH is depleted?

A
  1. oxidative damage to liver cells (due to loss of anti-oxidant)
  2. direct damage to liver cells from the highly reactive intermediate
59
Q

What are the signs and sx of acetaminophen overdose?

A
  • severely elevated transaminase levels
  • hepatic encephalopathy
  • jaundice (tx is likely too late as this point)

PHAC II (9 decks)

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