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Pharmacology > Mod 3 > Flashcards

Mod 3 Flashcards

1
Q

What is pain?

A

Pain, a basic protective mechanism, is a symptom of an underlying physiologic or psychologic problem.

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2
Q

If pain is subjective how does the nurse know what it is?

A

Pain is whatever sensation the patient perceives it to be; perceptions vary individually

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3
Q

what do you need to take in to consideration when it comes to pain?

A

Emotional states and ethnic, cultural, and religious factors all contribute to the patient’s pain perception.

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4
Q

what is acute pain?

A

sudden onset usually subsides with tx, ex: MI, kidney stones

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5
Q

What is chronic pain?

A

persistent or recurring pain that continues for more than 6 months
Ex: cancer or rheumatoid arthritis

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6
Q

what is visceral pain?

A

originates in smooth muscle or organ systems. Difficult to localize because is dull aching and may be referred.
Ex: gallbladder pain

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7
Q

what is somatic pain?

A

arises from skeletal muscle, fascia, ligaments, vessels or joints. Localized, constant, aching, throbbing. Somatic pain may present as nociceptive pain or neuropathic pain.
Somatic pain responds best to NSAID’s, visceral pain usually responds well to opioids.

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8
Q

Somatic pain may present in what two ways?

A

nociceptive pain or neuropathic pain

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9
Q

what is nociceptive pain?

A

where tissue damage results in peripheral nerve stimulation, usually an inflammatory component.

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10
Q

what is neuropathic pain?

A

— is caused by peripheral nerve injury and not stimulation. Called paresthesia, it is a burning, shooting and/or tingling sensation.
Ex: cancer invasion, diabetes

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11
Q

What kind of medication does neuropathic pain respond to?

A

Responds less well to opioids, requires adding adjunct med such as an anticonvulsant like Gabapentin (Neurontin) or tricyclic antidepressant like Amitriptyline (Elavil) to the client’s drug regimen.

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12
Q

how do we make pain more objective?

A

by using a pain scale like the FLACC or PAIN AD

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13
Q

Inflammation is what kind of process?

A

an immune-mediated process

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14
Q

Some of the chemical mediators of the pain are what?

A

prostaglandins, bradykinin, and histamine, which also mediate the inflammatory response

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15
Q

what increase body temperature by causing production of prostaglandin E1 in the hypothalamus?

A

Pyrogens

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16
Q

what are the Nonnarcotic Analgesic, Antipyretic, and NSAID’s?

A
  • Salicylates
  • Para-aminophenol derivatives
  • NSAID’s
  • DMAR’s – Disease Modifying AntiRheumatic Drug
  • Urinary tract analgesic
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17
Q

what are the Salicylates mechanism of action?

A

produces analgesia by inhibiting prostaglandin synthesis; reduces fever through hypothalamic stimulation leading to vasodilation and increased diaphoresis; and reduces inflammation by inhibiting prostaglandin synthesis. Also inhibits platelet aggregation

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18
Q

what are examples of Salicylates?

A
  • aspirin (A.S.A, Bayer)
  • Trilisate
  • diflunisal (Dolobid)
  • Salicylate (Disalcid)
  • Ecotrin
  • Ascriptin
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19
Q

aspirin (A.S.A, Bayer)

A

-Most widely used, relieves headache, neuritis, neuralgia, myalgia, rheumatoid arthritis and dysmenorrhea.
-contraindicated in children, under the age of 12, with varicella or influenza, may lead to Reye’s syndrome.
-used to prevent TIA & MI
(stroke)

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20
Q

Trilisate

A

used to treat osteo and rheumatoid arthritis

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21
Q

diflunisal (Dolobid)

A

requires a prescription

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22
Q

Ecotrin

A

enteric coated so that is doesn’t cause gi irritation

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23
Q

Ascriptin

A

ASA and Maalox so that is doesn’t cause gi irritation

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24
Q

what are the adverse effects of Salicylates?

A
  • -most common is GI, (N/V, GI distress)
  • -Tinnitus, hearing problems
  • Salicylism (toxicity) - N/V, diarrhea, thirst, diaphoresis, confusion, hyperventilation, dizziness and tinnitus
  • in asthmatics with nasal polyps, bronchospasm and asthma
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25
Q

when are Salicylates Contraindicated?

A
  • GI bleeding, gastric ulcer

- pregnancy, viral illness in children under 12

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26
Q

when should precautions be used with Salicylates?

A

hepatic or renal impairment, bleeding disorders

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27
Q

what are the drug interactions with Salicylates?

A
  • Potentiate effects of other drugs
    a. alcohol-leading to GI bleeding
    b. anticoagulants
    c. corticosteroids increased ulcerogenic effect
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28
Q

What are Para-aminophenol derivatives

mechanism of action?

A

analgesic and antipyretic, does not act on inflammation or platelet function. Inhibits prostaglandin synthesis

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29
Q

what is an example of a Para-aminophenol derivatives?

A

Acetaminophen (Datril, Tylenol)

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30
Q

Acetaminophen (Datril, Tylenol)

A
  • drug of choice for osteoarthritis
  • drug of choice for fever and viral symptoms in children
  • used in codeine compounds
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31
Q

what are the Adverse effects of Para-aminophenol derivatives such as Acetaminophen (Datril, Tylenol)?

A
  • rarely causes GI distress. Chronic use of high doses can cause kidney damage and hepatoxicity (monitor ALT, AST, bilirubin, albumin
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32
Q

what is the Antidote for Acetaminophen (Datril, Tylenol) toxicity?

A

acetylcysteine (Mucomyst) (also used as respiratory drug, smells like rotten eggs)

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33
Q

what are NSAID’s mechanism of action?

A
  • Relieve pain and alter pain perception by acting in the peripheral nervous system to inhibit the formation or reactivity of prostaglandins. They inhibit the Cox enzyme (the first enzyme in the prostaglandin pathway)
  • Reduce inflammatory response triggered by trauma, microorganisms, drugs, or other foreign substances
  • Control fever, probably by inhibiting prostaglandin release
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34
Q

what are examples of NSAID’s?

A
  • diclofenac (Zipsor)
  • fenoprofen (Nalfon)
  • flurbiprofen (Ansaid)
  • ibuprofen (Motrin)
  • indomethacin (Indocin)
  • kitoprofen (Orudis)
  • ketorolac (Toradol)
  • meloxicam (Mobic)
  • naproxen (Naprosyn)
  • piroxicam (Feldene)
  • sulindac (Clinoril)
  • tolmetin sodium (Tolectin)
  • etodolac (Lodine)
  • nabumetone (Relafen)
  • ocelecoxib (Celebrex)
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35
Q

diclofenac (Zipsor)

A

on the HESI and it is the same thing as Motrin

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36
Q

ibuprofen (Motrin)

A

TX fever and mild to severe pain

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37
Q

indomethacin (Indocin)

A

TX gout

38
Q

ketorolac (Toradol)

A

po, IM, or IV; only injected NSAID for short term pain management
Used for breakthrough pain with epidural or PCA pain management

39
Q

celecoxib (Celebrex)

A

COX-2 Inhibitor (second generation NSAID)( hard on the stomach)

40
Q

nabumetone (Relafen)

A

first NSAID to remain inactive until leaves the stomach

41
Q

what are the Adverse effects of NSAID’s?

A

In general better tolerated then salicylates or steroids

  • GI disturbances - N/V, dyspepsia, diarrhea, GI ulceration, hemorrhage
  • CNS - vertigo, insomnia, confusion, tinnitus, depression, blurred vision, decreased acuity
  • Renal - cystitis, hematuria ( toxic to the kidneys – nephrotoxic)
42
Q

what are the contraindications of NSAIDS?

A
  • GI bleeding, gastric ulcer
  • asthma, nasal polyps
  • renal compromise
43
Q

when administrating NSAID what should the nurse do?

A
  • Give salicylates with at least 8 oz. of liquid
  • Administer NSAID’s with food or milk to decrease GI irritation
  • Determine level of pain & effectiveness of analgesics
44
Q

what should the nurse monitor for when giving NSAID?

A
  • observe for signs of salicylate toxicity –Monitor for signs of bleeding, including monitoring of H & H
  • Withhold acetaminophen & notify MD if pt develops rash, fever, angioedema
  • For NSAID’s, monitor for fluid retention
45
Q

what should the nurse teach the patient taking NSAIDS

A
  • -Teach patient to be aware of any alterations in hearing (salicylates)
  • Caution female client of childbearing age that NSAID’s may interfere with blood clotting and prolong duration of pregnancy and labor.
  • -Teach client to take NSAID with a full glass of water and to remain in an upright position for 30 minutes.
  • -Advise client to take NSAID with meals to decrease the risk of gastrointestinal side effects.
46
Q

DMAR’s – Disease Modifying AntiRheumatic Drug

A

Biologic Response Modifiers
Mechanism of action: immunomodulators, slow the joint destruction of RA. Block the TNF ( tumor necrosis factor )which has inflammatory effects.

47
Q

what are some examples of DMARs?

A
  • leflunomide (Avara) po
  • etanercept (Enbrel) SQ 2 times a week
  • adalimumab (Humira)
  • infliximab (Remicade)
48
Q

infliximab (Remicade)

A

prototype

49
Q

what are the adverse effects of DMARs?

A

increased risk for infection, headache, injection site pain

50
Q

what is a Urinary tract analgesic?

A

phenazopyridine (Pyridium)

51
Q

phenazopyridine (Pyridium)

A
  • produces a local analgesic effect on urinary tract in 24-48 hours; relieves the dysuria & urgency of UTI
  • Colors urine orange-red, permanently stains
  • Short term treatment - 2 days only.
  • Administer with food to avoid GI distress
  • OTC – Azo-standard
52
Q

what is the Narcotic Agonist Mechanism of action?

A

-inhibiting the transmission of pain impulses in sensory
pathways to the spinal cord
-reducing cortical responses to painful stimuli in the brain stem, thalamus and limbic system
-altering behavioral responses to pain

53
Q

why may the use of Narcotic Agonist lead to repeated drug use even in the absence of pain, possibly resulting in dependence?

A

because it has a less tense and more tranquil, maybe even euphoric effect

54
Q

what schedule are Narcotic Agonist?

A

schedule II drugs (because opium derivatives and synthetic narcotics)

55
Q

Other narcotics compared to how much Morphine?

A

10 mg IM

56
Q

what are Narcotic Agonist used to TX?

A

Used to relieve severe pain in acute, chronic, & terminal illnesses and to reduce preanesthesia anxiety; possess antidiarrheal & antitussive effects. Morphine reduces dyspnea of pulmonary edema & Lt ventricular failure by reducing anxiety and producing peripheral vasodilation, thus decreasing cardiac workload. Used with caution in OB, because crosses the placenta & can cause neonatal respiratory compromise

57
Q

how can Narcotic Agonist be administered?

A

Available by many routes : oral, IV, IM, sq, epidural, sublingual, intrathecal: ( places drug directly into the CSF avoiding absorption barrier between blood and brain)Transdermal, rectal and implanted pumps.

58
Q

Morphine Sulfate (Duramorph)

A

MS does not exhibit a ceiling effect, level of analgesia increases as the dose is increased

59
Q

Morphine sustained

A

release (MS Contin) released slowly as med travels through GI tract. Patient remains pain free 6-12 hours( long term and terminal/ ma use morphine sulfate for break through pain)+

60
Q

Codeine

A

combined with aspirin or acetaminophen for additive analgesic effect; also antitussive; ceiling effect.

61
Q

fentanyl (Sublimaze)

A

only parenteral; used for epidural analgesia or Duragesic (patch) (it is used for 3-72 hr/ remember to look for the patch)

62
Q

hydromorphone (Dilaudid)

A

more potent then morphine X6

63
Q

methadone (Dolophine)

A

synthetic narcotic; used for detoxification treatment for narcotic addiction - although drug produces tolerance, physical & psychological dependence

64
Q

what are adverse effects of Narcotic Agonist?

A

–Respiratory depression,
-vasodilation –> flushing,
–orthostatic hypotension,
–N/V,
-biliary colic,
–constipation,
reduced peristalsis,
–BPH –> urinary retention,
may prolong labor,
–miosis,
–contraindicated in head injury - masks changes in LOC, euphoria, sedation, tolerance, dependence. (remember we don’t relieve pain with these during head injury because we cant assess LOC, once diagnosed you can TX pain)

65
Q

what drugs interact with Narcotic Agonist?

A

Alcohol, barbiturates, Tagamet, MAO inhibitors

66
Q

what do Mixed Narcotic Agonist do?

A

Risk of drug dependence is lower; no antitussive effects; produce fewer GI effects; less likely to cause respiratory depression, but increases systemic arterial pressure and overall cardiac workload. (remember you don’t want to give to the patient with chest pain)

67
Q

what are examples of mixed narcotic agonist?

A
  • butorphanol (Stadol)
  • dezocine (Dalgan)
  • pentazocine (Talwin)
  • pentazocine & acetaminophen (Talacen) –Nalbuphine (Nubain)
68
Q

Nalbuphine (Nubain)

A

Not cardiac friendly

69
Q

dezocine (Dalgan)

A

can increase cardiac index, stroke volume, and pulmonary vascular resistance

70
Q

Tramadol (Ultram)

A

-mod or severe pain
- meals not needed (GI friendly)
side affects: dizziness, constipation, seizures, tolerance, dependence

71
Q

what are adverse reactions to mixed narcotic agonist?

A

Usually affect CNS & GI tract; N/V, sedation, B/p changes
(increased B/P)

72
Q

when administering mixed narcotic agonist what should the nurse be aware of?

A
  • Monitor respiratory status during and after administration
  • -Count resp rate prior to administration. Withhold the drug & contact HCP if rate is 10 /min or less
  • -Side rails up and bed in low position
73
Q

Do you administer a mixed narcotic agonist to a narcotic dependent patient?

A

No, may precipitate withdrawal symptoms

74
Q

how do you Dispose of Duragesic patch?

A

by folding in half, flush down toilet or put in sharps container

75
Q

Should you discontinue narcotics abruptly in the narcotic-dependent client?

A

NO

76
Q

what daily monitoring and measurements should be done for a patient receiving narcotic?

A
  • Determine level of pain and effectiveness of analgesics
  • -Monitor vital signs, will decrease B/P
  • -Measure respiratory rate, pattern, and depth, O2 sats
  • Watch for signs of dependence
  • -Encourage clients to achieve optimal pain control by taking medication before pain becomes severe
  • -Teach client nonpharmacologic pain relief measures to augment analgesic use
  • -When in pain geriatric patients may become restless, agitated and confused, don’t know how to report pain or request pain med.
77
Q

what do you need to teach the patient when it come to narcotics?

A
  • Caution client that alertness may be impaired
  • Tell client to avoid concomitant use of alcohol and other CNS depressants
  • Tell client not to give drug to friends or family members.
  • Warn client about possibility of dependence
78
Q

what is the Narcotic Antagonists

Mechanism of action?

A

they work by competitive inhibition at the opiate receptor sites, displacing narcotic molecules and preventing them from exerting their effects

79
Q

What is an example of a Narcotic Antagonists?

A

naloxone (Narcan)

80
Q

naloxone (Narcan)

A

drug of choice for reversal of respiratory depression caused by narcotic overdose. IV, IM, SQ (IV route preferred in emergency) Small dose q 2-3 minutes as needed, if pt does not respond after 10 mg re-evaluate the diagnosis of narcotic overdose.( remember don’t push to rapidly because narcotic will no longer relieve the pain)
Also reverses the analgesic effects of narcotic drug. Monitor carefully, the effects of the narcotic overdose may last longer than the effects of the antagonist and repeated doses may be indicated.

81
Q

naltrevone (Trexan)

A

used as adjunct to psychotherapy or counseling for detoxified addicts. Will cause withdrawal symptoms if given when also receiving narcotics.

82
Q

what are the adverse effects of Naloxone?

A

N/V, increased B/P, tachycardia

83
Q

What is the General Anesthetic Agent mechanism of action?

A

General anesthetic agents depress CNS to produce loss of consciousness, unresponsiveness to pain stimuli, and muscle relaxation

84
Q

how are General Anesthetic Agent administered?

A
  • inhalation
  • injection
  • combination
85
Q

what are 3 parts to anesthesia administration?

A
  • induction - initiation usually by IV agent. Purpose is to produce a rapid, pleasant, and stress less transition from consciousness to sleep.
  • maintenance - administration of primary anesthetic, begins during induction; can be continued until surgery is complete
  • emergence - follows withdrawal of anesthetic agents. Drugs administered to reverse effects
86
Q

what is Stage I - anesthesia?

A

begins with onset of anesthesia and ends with loss of consciousness; smell and pain sensations are gone; may have hallucinations and dreams

87
Q

what is Stage II - excitement?

A

begins with loss of consciousness; reflexes more prominent, resp irregular. Complications occur most commonly in this stage

88
Q

what is Stage III - surgical anesthesia?

A

procedure can be performed safely

89
Q

what is Stage IV - medullary paralysis?

A

toxic stage, resp cease, circulatory collapse, anesthetic overdose

90
Q

Inhalation anesthetics

A
  • -are absorbed at varying rates, distributed most rapidly to organs with high blood flow, (brain, liver, kidneys and heart), metabolized, and excreted mainly by the lungs, but also the liver
  • -all cross the blood - brain barrier
  • -absorption is affected by alveolar ventilation - the provision of air or gas to the alveoli - and perfusion - the amount of blood passing through the alveoli
  • Used for surgery because they offer more precise and rapid control of depth of anesthesia than injection anesthetics
  • Most commonly used are Ethrane & Forane, usually with nitrous oxide
91
Q

what are adverse affects of Inhalation anesthetics?

A
  • -hypotension,
  • -prolonged respiratory depression, –prolonged recovery,
  • cardiopulmonary depression,
  • confusion,
  • -sedation,
  • nausea/vomiting,
    • ataxia,
    • hypothermia (causes shivering, increases BMR, apply O2 and monitor O2 sats )
92
Q

What are the SX of withdrawal syndrome?

A 
Irritability 
Diaphoresis 
Restlessness 
Muscle twitching 
Increased pulse and BP

Pharmacology (9 decks)

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