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Pharmacology > Analgesic drugs > Flashcards

Analgesic drugs Flashcards

1
Q

Allodynia

A

a pain responce to an non-painful stimulus

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2
Q

Hyperalgesia

A

increased pain from a stimulus that normally provokes pain

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3
Q

Hypoalgesia

A

diminished pain in response to a normally painful stimulus

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4
Q

neuralgia

A

pain in the distribution of a nerve or nerves

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5
Q

neuritis

A

inflammation of a nerve or nerves

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6
Q

noxious stimulus

A

a stimulus that is damaging or threatens damage to normal tissues

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7
Q

nociception

A

the neural process of encoding noxious stimuli

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8
Q

nociceptor

A

a high threshold sensory receptor of the peripheral somatosensory system that is capable of transducting and encoding noxious stimuli

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9
Q

nociceptive pain

A

pain that arises from actual or threatened damage to a non-neural tissue and is due to the activation of nociceptors

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10
Q

neuropathic pain

A

pain causes by a lesion or damage or disease of the neurons or somatosensory nervous system

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11
Q

WHO therapeutic recommendations for mild pain 1-3/10

A

nonopioid analgesic NSAID ; regular scheduled dosing

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12
Q

WHO therapeutic recommendations for moderate pain 4-6/10

A

add an opioid to the nonopioid for moderate pain with regular scheduled dosing (weak opioid)

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13
Q

WHO therapeutic recommendations for severe pain 7+/10

A

switch to a high potency opioid; regular schedules dosing

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14
Q

what analgesics work at the transduction/ local level to modulate pain

A

LAs, Capsaicin, Anticovulsants, NSAIDs, ASA, acetaminophen and nitrate

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15
Q

what analgesics work at the transmission/ peripheral nerve level to modulate pain

A

LAs, opioids, and a2 - agonists

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16
Q

what analgesics work at the modulation level in the spinal cord to modulate pain

A

TCAs, SSRIs and SNRIs

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17
Q

what analgesics work at the brain/perception level to modulate the pain

A

Opioids, TCAs, SSRIs, SNRIs, and a2- agonists

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18
Q

what are the 2 types of analgesics

A

1) opioid
2) non-opioid

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19
Q

what are the 2 types of non-opioid analgestics

A

1) Non-Steroidal Anti Inflammatory Drugs (Cox, Ibuprofen, Naproxen etc.)
2) anti-inflammatory agents (NSAIDs or glucocorticoids)

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20
Q

what are the 3 endogenous opioid peptides

A

1) endorphins
2) enkephalins
3) dynorphins

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21
Q

what are endorphins derived from

A

POMC

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22
Q

what is the primary agonist of endorphins

A

mu and also has delta action

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23
Q

what are enkephalins derives from

A

proenkephalin

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24
Q

what are the primary agonist of enkephalins

A

mu and delta

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25
Q

what are dynorphins derived from

A

kappa agonist and have mu and delta action

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26
Q

what is a opioid

A

any natural occurring, semi-synthetic or synthetic compound that bind specifically to the opioid receptors and share the properties of one or more of the naturally occurring endogenous opioids

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27
Q

what is an opiate

A

any naturally occurring opioid derived from opium

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28
Q

what are strong agonists

A
  • morphine
  • fentanyl
  • hydromorpone
    -meperidine
  • oxymorphone
  • oxycodone
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29
Q

what do strong agonists have in common

A

they have a high affinity for certain receptors and are believed to interact primarily with mu opioid receptors in the CNS

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30
Q

Mild-to moderate agnoists

A
  • codeine
  • hydrocodone
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31
Q

mixed agonist-antagonist drugs

A

exhibit some of agonist and antagonist like activity at the same time because the drugs have the ability to act differently at specific classes or opioid receptors (for example they might bond to kappa but block mu)

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32
Q

what are some examples of mixed agonist-antagonist drugs

A
  • buprenorphine
  • nalbuphine
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33
Q

what are the opioid antagonists

A
  • naloxone and naltrexone
  • they block all opioid receptors expecually mu; and can be used to help treat overdoses and addition
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34
Q

nalxone

A

the primary agent in the US to treat opioid overdoses when administered in an emergence situation it can dramatically reduce the respiratory depression that is usually the cause of death

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35
Q

naltrexone

A

is commonly used in conjunction with behavioral therapy to maintain an opioid free state for addicts

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36
Q

what are the common primary therapeutic effects of all 3 opioid receptors (mu,kappa, and delta)

A

spinal and supraspinal analgesia

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37
Q

what are the other effects of Mu

A
  • sedation
  • respiratory depression
  • constipation
  • inhibits neurotransmitter release (acetylcholine and dopamine)
  • increases hormonal release
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38
Q

what are the other effects of kappa

A
  • sedation
  • constipation
  • psychotic effects
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39
Q

what are the other effects of delta

A
  • increases hormonal release (growth hormone)
  • inhibits neurotransmitter release (dopamine)
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40
Q

what type of receptors are opioid receptors (m,k and delta)

A

Gi/10 protein-coupled receptors

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41
Q

what are the 2 establishes direct Gi/10 protein coupled actions on neurons

A

1) close Ca2+ gated channels on presynaptic nerve terminals and thereby reduce transmitter release (glutamine and substance P)
2) they open K+ channels on post synaptic neurons and hyperpolarize them thus inhibiting postsynaptic neurons

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42
Q

what are the 3 sites of action of opioid analgesics on the afferent pathway

A

1) on inflamed or damaged peripheral nerves
2) at the SC (Dorsal root)
3) the amygdala

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43
Q

what are the action of agonists

A
  • analgesia
  • respiratory depression
  • spasm of smooth muscle of the GI and GU tracts, including the biliary tract
  • miosis (pinpoint pupils)
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44
Q

what is the CNS effect of opioids

A
  • analgesia
  • euphoria
  • sedation
  • respiratory depression
  • cough suppression
  • miosis
  • truncal rigidity
  • nausea and vomitiing
  • body temperature
  • sleep disturbances
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45
Q

what are the cardiovascular system effects of opioids

A
  • bradycardia (expect meperidine)
  • hypotension
  • increase in cerebral blood flow
  • increase in intracranial pressure
46
Q

what are the GI system effect of opioids

A

constipation

47
Q

what are the biliary tract effects of opioids

A

biliary colic (contraction of the biliary smooth muscles)

48
Q

what are the renal effects of opioids

A
  • decrease renal function
  • antidiuretic effect increases renal sodium absorption
  • urinary retention
49
Q

what are the endocrine effects of opioids

A
  • decrease testosterone with chronic use
  • decrease libio, energy and mood
  • dysmenorrhea and amenorrhea in women
50
Q

what are the pruritis effects of opioids

A

-produce flushing and warming of the skin accompanied sometimes by sweating, urticaria, and itching
- increase peripheral histamine release

51
Q

what are the clinical uses of opioid analgesics

A
  • analgesia
  • acute pulmonary edema
  • cough
  • diarrhea
  • anesthesia (pre-anesthetic medication regimen)
52
Q

what are some signs or opioid overdose

A
  • euphoria
  • unconsciousness
  • respiratory depression
  • miosis
  • pulmonary edema
  • seizures
  • hypothermia
  • death
53
Q

what is the opiate toxicity triad

A
  • CND depression Coma
  • respiration depression (cyanosis)
  • pupillary miosis
54
Q

what can a high degree of tolerance develop too

A

analgesic sedating and respiratory depressant

55
Q

what does optioid tolerance not develop to

A

miotic, convulsant and constipating action

56
Q

what is a moderate effect of opioid tolerance

A

bradycardia

57
Q

what are the 2 components of the dependance and withdrawal syndrome

A

1) physical dependance
2) symptoms of withdrawl

58
Q

what are some symptoms of opioid withdraw

A
  • rhinorrhea
  • lacrimation
  • yawning
  • chills
  • gooseflesh
  • hyperventilation
  • hyperthermia
  • mydriasis
  • muscular aches
  • vomiting
  • diarrhea
  • anxiety
  • hostility
59
Q

what are the 10 signs of overdose

A

1) respiratory depression
2) miosis
3) stupor
4) hepatic injury
5) myoglobinuric renal failure
6) rhabdomyolysis
7) absent or hypoactive bowel syndrome
8) compartment syndrome
9) hypothermia
10) possible signs of one or more fentanyl patches

60
Q

Pt controlled benefits (PCA)

A
  • may allow better pain control with fewer side effects
  • requires patient awareness, cognitive ability
  • increase patient satisfaction
61
Q

primary therapeutic effects of NSAIDS

A

analgesic, anti-inflammatory, antipyretic, anticoagulant, anticancer

62
Q

what are all the therapeutic effects of NSAIDs through

A

inhibition of prostaglandians (PG)

63
Q

What are prostaglandins

A
  • small lipid compounds produces in almost all cells
  • cells begin to synthesize PG in response to damage
64
Q

what are the functions of prostaglandins

A
  • PGs in the hypothalamus do thermoregulation
  • responsible for for coagulation
  • PGs can exaggerate pain
  • Promote inflammation
  • abnormal coagulation
65
Q

what do NSAIDs do

A
  • inhibit synthesis of prostaglandins
  • decrease prostaglandins by inhibiting cyclooxyrgenase enzyme
  • inhibits PG synthesis then all the important functions that the PG serve are affected by the ingestion of NSAIDs
66
Q

CYclooxygenase-1 (COX-1)

A

produces prostaglandins that mediate homeostatic functions constitutively expressed

67
Q

what are some homeostatic functions

A
  • protection of gastric mucosa
  • platelet activation
  • renal functions
  • macrophage differentiation
68
Q

cyclooxygenase-2 (COX-20

A
  • produces prostaglandins that mediate inflammation, pain and fever
  • induced mainly in sites of inflammation by cytokines
  • pathologic inflammation
69
Q

what are examples of pathologic inflammation

A

pain, fever and dysregulated proliferation

70
Q

List of common NSAIDS

A

aspirin, Ibuprofen, naproxen, indomethacin, meloxicam, diclofenac, celecoxIb

71
Q

what are some common side effects of NSAIDs

A
  • nausea and vomiting
  • Diarrhea
  • constipation
  • decreased appetite
  • rash
  • dizziness
  • headache
  • drowsiness
72
Q

what are the important side effects of NSAIDs

A
  • kidney failure
  • liver failure
  • ulcers
  • prolongs bleeding after injury or surgery
  • NSAIDs can cause fluid retention leading to edema
73
Q

What does COX-1 does to GI mucosa

A

produces PGE2: gastric protection (increased mucus secretion, increases bicardonate and increases mucosal blood flow)

74
Q

how does COX 1 and 2 impact the kidney

A

forms PGE2 and PGI2: afferent arteriolar vasodilation, increases sodium and water excretion

75
Q

how does COX 1 and 2 impact the cardiovascular system

A

PGI2 and TXA2: vasodilation and inhibit platelet aggregation; platelet aggregation and vasoconstriction

76
Q

what does COX1 inhibition impact the GI

A

peptic ulcers and GI bleeding

77
Q

how does COX inhibition impact the kidneys

A
  • Na and water retention
  • HTN
  • hemodynamic acute kidney injury
78
Q

how does COX 2 and COX1 inhibition

A

stroke and MI

79
Q

what is a COX-2 selective drug

A

Celecoxib (celebrex)

80
Q

what does Celecoxib do

A
  • inhibit the synthesis of PG that cause pain and inflammation
  • may decrease pain and inflammation with less toxicity
81
Q

what population is Celecoxib best for

A

for pts who need to be on long term NSAID use such as long term OA. that allow pt to remain active.

82
Q

where does Acetaminophen effect

A

PG in the nervous system

83
Q

what affects do acetaminophen not have

A

gastric irritation, anticoagulant effects, and no anti-inflammatory effects

84
Q

what are indications for acetaminophen

A

frequently 1st drug used to control the pain in the early stages of OA and other MSK pathologies that do not have an inflammatory component

85
Q

age groups and that use acetaminophen

A

children, adults, and pregnant women

86
Q

what is acetaminophen not indicated for

A

reyes syndrome

87
Q

what can acetaminophen toxicity lead to

A

liver toxicity

88
Q

steroidal anti-inflammatory drugs

A

powerful anti-inflammatory and immunosuppressive effects
- glucocortocoids

88
Q

non steroidal anti-inflammatory drugs

A

mild to moderate inflammation and needs to be taken continuously “take the whole prescription”

89
Q

what is glucocorticoids derived by

A

cholesterol

90
Q

what 3 adrenal steroids does the adrenal cortex produce

A

1) glucocorticoids
2) mineralocorticoids
3) other steroids

91
Q

what are examples for glucocorticoids

A

cortisol, and corticosterone

92
Q

what are example fo mineralocorticoids

A

aldosterone

93
Q

what do mineralocorticoids do

A

maintain fluid and electrolyte balance

94
Q

what are the physiological functions of glucocorticoids

A
  • control glucose metabolism
  • controls the body’s ability to deal with stress
  • decrease inflammation
  • suppresses the immune system
95
Q

what is the precursor for steroid synthesis

A

cholesteral

96
Q

what do glucocorticoids have effects on

A

anti-inflammatory and immunosuppressive effects

97
Q

what is the mechanism of action of glucocorticoids

A

drugs bind to glucocorticoid receptors in the cytoplasm, travels to the nucleus of the cells causing gene expression by binding to glucocorticoid response elements (GRE)

98
Q

what do GREs do

A

decrease expression of inflammatory proteins (cytokines) and increase expression of anti-inflammatory proteins.

99
Q

what are the 2 primary situations that glucocorticoids are used for

A

1) endocrine conditions
2) non endocrine conditions

100
Q

what do endocrine conditions do

A

systematically used to normalize adrenal cortical hypofunction

101
Q

what do non-endocrine conditions do

A

work on a variety of conditions for the purpose of anti inflammatory for immunosuppressive effects

102
Q

what are the most common nonendocrine conditions that PTs see

A

RA, myositis, tenosynovitis, collagen diseases, carpel tunnel syndrome

103
Q

what can the repeated injection of glucocorticoids do to tendons

A

cause them to breakdown, become week, and rupture. limited to 4 for fewer per year

104
Q

what is the suffix for anti inflammatory drugs

A

“sone”

105
Q

what are common glucocorticoid drugs

A
  • Betamethasone
  • mythyprednisolone
  • cortisone
  • prednisolone
  • dexamethasone
  • prednisone
  • hydrocortisone
  • triamcinolone
106
Q

Adverse effects of glucocorticoids

A
  • adrenocortical suppression
  • peptic ulcers
  • drug-induces cushing syndrome
  • adrenal crisis/ shock
  • breakdown of supporting tissues
  • decrease in the bodies ability to absorb Ca2+ leading to osteoporosis and delayed wound healing
107
Q

side effect of glucocorticoids

A
  • headache
  • irregular heart beat
  • sweating
  • dizziness
  • irritability
108
Q

drug induced cushing syndrome (hypercortisolism)

A
  • roundness and puffines in the face
  • fat deposition and obestity in the trunk
  • muscle wasting in extremities
  • HTN
  • osteoporosis
  • increased body hair
  • glucose intolerance
109
Q

adrenal crises/shock

A

causes vasodilation to the organs, vascular collapse, and sever HTN leading to S/S of pain in legs, low back and abdomin, vomiting and diarrhea, hyperkalemia and hyponatremia

Pharmacology (3 decks)

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