Analgesic drugs Flashcards
(110 cards)
1
Q
Allodynia
A
a pain responce to an non-painful stimulus
2
Q
Hyperalgesia
A
increased pain from a stimulus that normally provokes pain
3
Q
Hypoalgesia
A
diminished pain in response to a normally painful stimulus
4
Q
neuralgia
A
pain in the distribution of a nerve or nerves
5
Q
neuritis
A
inflammation of a nerve or nerves
6
Q
noxious stimulus
A
a stimulus that is damaging or threatens damage to normal tissues
7
Q
nociception
A
the neural process of encoding noxious stimuli
8
Q
nociceptor
A
a high threshold sensory receptor of the peripheral somatosensory system that is capable of transducting and encoding noxious stimuli
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
10
Q
neuropathic pain
A
pain causes by a lesion or damage or disease of the neurons or somatosensory nervous system
11
Q
WHO therapeutic recommendations for mild pain 1-3/10
A
nonopioid analgesic NSAID ; regular scheduled dosing
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)
13
Q
WHO therapeutic recommendations for severe pain 7+/10
A
switch to a high potency opioid; regular schedules dosing
14
Q
what analgesics work at the transduction/ local level to modulate pain
A
LAs, Capsaicin, Anticovulsants, NSAIDs, ASA, acetaminophen and nitrate
15
Q
what analgesics work at the transmission/ peripheral nerve level to modulate pain
A
LAs, opioids, and a2 - agonists
16
Q
what analgesics work at the modulation level in the spinal cord to modulate pain
A
TCAs, SSRIs and SNRIs
17
Q
what analgesics work at the brain/perception level to modulate the pain
A
Opioids, TCAs, SSRIs, SNRIs, and a2- agonists
18
Q
what are the 2 types of analgesics
A
1) opioid
2) non-opioid
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)
20
Q
what are the 3 endogenous opioid peptides
A
1) endorphins
2) enkephalins
3) dynorphins
21
Q
what are endorphins derived from
A
POMC
22
Q
what is the primary agonist of endorphins
A
mu and also has delta action
23
Q
what are enkephalins derives from
A
proenkephalin
24
Q
what are the primary agonist of enkephalins
A
mu and delta
25
what are dynorphins derived from
kappa agonist and have mu and delta action
26
what is a opioid
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
27
what is an opiate
any naturally occurring opioid derived from opium
28
what are strong agonists
- morphine
- fentanyl
- hydromorpone
-meperidine
- oxymorphone
- oxycodone
29
what do strong agonists have in common
they have a high affinity for certain receptors and are believed to interact primarily with mu opioid receptors in the CNS
30
Mild-to moderate agnoists
- codeine
- hydrocodone
31
mixed agonist-antagonist drugs
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)
32
what are some examples of mixed agonist-antagonist drugs
- buprenorphine
- nalbuphine
- pentazocine
33
what are the opioid antagonists
- naloxone and naltrexone
- they block all opioid receptors expecually mu; and can be used to help treat overdoses and addition
34
nalxone
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
35
naltrexone
is commonly used in conjunction with behavioral therapy to maintain an opioid free state for addicts
36
what are the common primary therapeutic effects of all 3 opioid receptors (mu,kappa, and delta)
spinal and supraspinal analgesia
37
what are the other effects of Mu
- sedation
- respiratory depression
- constipation
- inhibits neurotransmitter release (acetylcholine and dopamine)
- increases hormonal release
38
what are the other effects of kappa
- sedation
- constipation
- psychotic effects
39
what are the other effects of delta
- increases hormonal release (growth hormone)
- inhibits neurotransmitter release (dopamine)
40
what type of receptors are opioid receptors (m,k and delta)
Gi/10 protein-coupled receptors
41
what are the 2 establishes direct Gi/10 protein coupled actions on neurons
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
42
what are the 3 sites of action of opioid analgesics on the afferent pathway
1) on inflamed or damaged peripheral nerves
2) at the SC (Dorsal root)
3) the amygdala
43
what are the action of agonists
- analgesia
- respiratory depression
- spasm of smooth muscle of the GI and GU tracts, including the biliary tract
- miosis (pinpoint pupils)
44
what is the CNS effect of opioids
- analgesia
- euphoria
- sedation
- respiratory depression
- cough suppression
- miosis
- truncal rigidity
- nausea and vomitiing
- body temperature
- sleep disturbances
45
what are the cardiovascular system effects of opioids
- bradycardia (expect meperidine)
- hypotension
- increase in cerebral blood flow
- increase in intracranial pressure
46
what are the GI system effect of opioids
constipation
47
what are the biliary tract effects of opioids
biliary colic (contraction of the biliary smooth muscles)
48
what are the renal effects of opioids
- decrease renal function
- antidiuretic effect increases renal sodium absorption
- urinary retention
49
what are the endocrine effects of opioids
- decrease testosterone with chronic use
- decrease libio, energy and mood
- dysmenorrhea and amenorrhea in women
50
what are the pruritis effects of opioids
-produce flushing and warming of the skin accompanied sometimes by sweating, urticaria, and itching
- increase peripheral histamine release
51
what are the clinical uses of opioid analgesics
- analgesia
- acute pulmonary edema
- cough
- diarrhea
- anesthesia (pre-anesthetic medication regimen)
52
what are some signs or opioid overdose
- euphoria
- unconsciousness
- respiratory depression
- miosis
- pulmonary edema
- seizures
- hypothermia
- death
53
what is the opiate toxicity triad
- CND depression Coma
- respiration depression (cyanosis)
- pupillary miosis
54
what can a high degree of tolerance develop too
analgesic sedating and respiratory depressant
55
what does optioid tolerance not develop to
miotic, convulsant and constipating action
56
what is a moderate effect of opioid tolerance
bradycardia
57
what are the 2 components of the dependance and withdrawal syndrome
1) physical dependance
2) symptoms of withdrawl
58
what are some symptoms of opioid withdraw
- rhinorrhea
- lacrimation
- yawning
- chills
- gooseflesh
- hyperventilation
- hyperthermia
- mydriasis
- muscular aches
- vomiting
- diarrhea
- anxiety
- hostility
59
what are the 10 signs of overdose
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
Pt controlled benefits (PCA)
- may allow better pain control with fewer side effects
- requires patient awareness, cognitive ability
- increase patient satisfaction
61
primary therapeutic effects of NSAIDS
analgesic, anti-inflammatory, antipyretic, anticoagulant, anticancer
62
what are all the therapeutic effects of NSAIDs through
inhibition of prostaglandians (PG)
63
What are prostaglandins
- small lipid compounds produces in almost all cells
- cells begin to synthesize PG in response to damage
64
what are the functions of prostaglandins
- PGs in the hypothalamus do thermoregulation
- responsible for for coagulation
- PGs can exaggerate pain
- Promote inflammation
- abnormal coagulation
65
what do NSAIDs do
- 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
CYclooxygenase-1 (COX-1)
produces prostaglandins that mediate homeostatic functions constitutively expressed
67
what are some homeostatic functions
- protection of gastric mucosa
- platelet activation
- renal functions
- macrophage differentiation
68
cyclooxygenase-2 (COX-20
- produces prostaglandins that mediate inflammation, pain and fever
- induced mainly in sites of inflammation by cytokines
- pathologic inflammation
69
what are examples of pathologic inflammation
pain, fever and dysregulated proliferation
70
List of common NSAIDS
aspirin, Ibuprofen, naproxen, indomethacin, meloxicam, diclofenac, celecoxIb
71
what are some common side effects of NSAIDs
- nausea and vomiting
- Diarrhea
- constipation
- decreased appetite
- rash
- dizziness
- headache
- drowsiness
72
what are the important side effects of NSAIDs
- kidney failure
- liver failure
- ulcers
- prolongs bleeding after injury or surgery
- NSAIDs can cause fluid retention leading to edema
73
What does COX-1 does to GI mucosa
produces PGE2: gastric protection (increased mucus secretion, increases bicardonate and increases mucosal blood flow)
74
how does COX 1 and 2 impact the kidney
forms PGE2 and PGI2: afferent arteriolar vasodilation, increases sodium and water excretion
75
how does COX 1 and 2 impact the cardiovascular system
PGI2 and TXA2: vasodilation and inhibit platelet aggregation; platelet aggregation and vasoconstriction
76
what does COX1 inhibition impact the GI
peptic ulcers and GI bleeding
77
how does COX inhibition impact the kidneys
- Na and water retention
- HTN
- hemodynamic acute kidney injury
78
how does COX 2 and COX1 inhibition
stroke and MI
79
what is a COX-2 selective drug
Celecoxib (celebrex)
80
what does Celecoxib do
- inhibit the synthesis of PG that cause pain and inflammation
- may decrease pain and inflammation with less toxicity
81
what population is Celecoxib best for
for pts who need to be on long term NSAID use such as long term OA. that allow pt to remain active.
82
where does Acetaminophen effect
PG in the nervous system
83
what affects do acetaminophen not have
gastric irritation, anticoagulant effects, and no anti-inflammatory effects
84
what are indications for acetaminophen
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
age groups and that use acetaminophen
children, adults, and pregnant women
86
what is acetaminophen not indicated for
reyes syndrome
87
what can acetaminophen toxicity lead to
liver toxicity
88
steroidal anti-inflammatory drugs
powerful anti-inflammatory and immunosuppressive effects
- glucocortocoids
88
non steroidal anti-inflammatory drugs
mild to moderate inflammation and needs to be taken continuously "take the whole prescription"
89
what is glucocorticoids derived by
cholesterol
90
what 3 adrenal steroids does the adrenal cortex produce
1) glucocorticoids
2) mineralocorticoids
3) other steroids
91
what are examples for glucocorticoids
cortisol, and corticosterone
92
what are example fo mineralocorticoids
aldosterone
93
what do mineralocorticoids do
maintain fluid and electrolyte balance
94
what are the physiological functions of glucocorticoids
- control glucose metabolism
- controls the body's ability to deal with stress
- decrease inflammation
- suppresses the immune system
95
what is the precursor for steroid synthesis
cholesteral
96
what do glucocorticoids have effects on
anti-inflammatory and immunosuppressive effects
97
what is the mechanism of action of glucocorticoids
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
what do GREs do
decrease expression of inflammatory proteins (cytokines) and increase expression of anti-inflammatory proteins.
99
what are the 2 primary situations that glucocorticoids are used for
1) endocrine conditions
2) non endocrine conditions
100
what do endocrine conditions do
systematically used to normalize adrenal cortical hypofunction
101
what do non-endocrine conditions do
work on a variety of conditions for the purpose of anti inflammatory for immunosuppressive effects
102
what are the most common nonendocrine conditions that PTs see
RA, myositis, tenosynovitis, collagen diseases, carpel tunnel syndrome
103
what can the repeated injection of glucocorticoids do to tendons
cause them to breakdown, become week, and rupture. limited to 4 for fewer per year
104
what is the suffix for anti inflammatory drugs
"sone"
105
what are common glucocorticoid drugs
- Betamethasone
- mythyprednisolone
- cortisone
- prednisolone
- dexamethasone
- prednisone
- hydrocortisone
- triamcinolone
106
Adverse effects of glucocorticoids
- 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
side effect of glucocorticoids
- headache
- irregular heart beat
- sweating
- dizziness
- irritability
108
drug induced cushing syndrome (hypercortisolism)
- 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
adrenal crises/shock
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
