Pain, Inflammation, Gout Drug Therapy Flashcards

(34 cards)

1
Q

pain

A

5th vital sign
warning of disease/infection/injury
part of healing process

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2
Q

analgesics

A

drugs to relieve pain

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3
Q

nociceptors

A

nerve endings that respond to injury and pain

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4
Q

substances that trigger nociceptors

A

prostaglandins, histamine, bradykinin, serotonin, substance p

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5
Q

two elements of pain

A
local irritation (stimulation of peripheral nerves)
recognition of pain (CNS, anxiety and apprehension)
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6
Q

types of pain duration

A

acute and chronic

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7
Q

responses to pain

A

psychological-tired/irritable/insomina/anxiety/depression

physical- increased HR/decreased BP/weakened immune

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8
Q

opioid analgesics

A

derived from opium, act on opioid receptors scheduled, monitor for tolerance/dependance

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9
Q

nonopiod analgesics

A

NSAIDS, acetaminophen, silicates

treat mild pain

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10
Q

MOA of opioids

A

react on opiod receptors, mimic analgesic peptides, decrease CNS, inhibits substance P and glutamate and nociceptors

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11
Q

uses of opioids

A

moderate to severe pain, cough

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12
Q

pt teaching.SE of opioids

A

sedation, respiratory depression, changes in mood, decreased peristalsis causing constipation, may be unable to operate vehicle, miosis, muscle spams, orthostatic hypotension, oliguria, bradycardia, dry mouth, do not drink alcohol

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13
Q

MOA and use of narcotic “pure” agonists

A

block opiods from binding

used for addiction/overdose

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14
Q

MOA of narcotic “partial” agonists

A

produce respiratory depression/mild pain relief

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15
Q

uses for non-opioid analgesics

A

inflammation, arthralgia, HA, myalgia, fever, mild pain

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16
Q

arachidonic pathway

A

formation of arachidonic acid via enzyme conversion of phospholipids
COX form prostaglandins

17
Q

MOA of salicylates

A

blocks COX 1 and 2, inhibit synthesis of prostaglandins, suppress heat center, inhibit aggregation of platelets

18
Q

uses and pt teaching for salicylates

A

analgesic, antipyretic, anti-inflmmatory, anti-coagulation

reyes syndrome tinnitus

19
Q

MOA of NSAIDS

A

treat inflammation by inhibiting pathway of prostaglandin synthesis, inhibit COX

20
Q

pt teaching of NSAIDS

A

ulcers/GI upset, disrupts stomach lining

21
Q

MOA of COX 2 selective inhibitor

A

alleviate pain and inflammation without gastric mucosal disruption

22
Q

MOA of acetominophen (Tylenol®)

A

acts on regulation center, inhibits prostaglandin synthesis and formation in CNS, not anti-inflam

23
Q

pt teaching of acetaminophen (Tylenol®)

A

hepatotoxicity, no alcohol

24
Q

antidote for tylenol

A

acetylcysteine

25
combination drugs
narcotic + non narcotic
26
gout
inflammatory condition causing joint pain, accumlation of uric acid in joint fluid attacked by phagocytes avoid alcohol/beer/wine/cheese etc
27
subcategories of drugs used for gout
acute anti-gout hypouricemic agent uricosuric agent
28
MOA of acute anti-gout
alters ability of phagocytes to attack uric acid crystals
29
prophylactic therapy- long term anti gout
hypouricemic agent | uricosuric agent
30
MOA of hypouricemic agent
inhibits enzyme to produce uric acid
31
MOA of uricosuric agent
enhances renal excretion of uric acid, prevents reabsoprtion of uric acid
32
rheumatoid arthritis
autoimmune condition of joints | steroids, NSAIDS, analgesics, DMARDS
33
MOA of local anesthetics
decrease NA influx, interfere with nerve conduction
34
MOA of general anesthetics
increase GABA, inhibit glutamate | caution of malignant hyperthermia