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Pathophysiology > 11.1 Pain and Fever > Flashcards

11.1 Pain and Fever Flashcards

1
Q

Pain

A
  • Localized or generalized unpleasant body sensation that cause mild to severe physical discomfort and emotional distress
  • Only the patient can accurately state when pain is present and how it is experienced.
  • Most common symptom for patients seeking healthcare
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2
Q

Acute Pain

A
  • Immediate response to an illness or injury that resolves once causative factor is relieved.
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3
Q

Chronic Pain

A
  • Persists for extended periods of time and does not resolve when cause is treated
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4
Q

Neurophysiologic Basics of Pain

A
  • Net result of activity in two opposing neural pathways

- Pain impulses are carried from site of origin to the brain and generate pain sensation through pain receptors.

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5
Q

Pain Receptors

A
  • Activated by 3 pathways
  • Mechanical (pressure)
  • Thermal
  • Chemical (Bradykinin, Serotonin, Histamine)
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6
Q

Prostglandins

A
  • Prostaglandins and substance P enhance sensitivity to pain receptors to activation, but do not activate them.
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7
Q

Second Pathway of Pain

A
  • Originates in the brain and suppresses pain conduction along the first pathway which diminishes pain.
  • Suppresses using endogenous opioids (enkephalins and beta-endorphins).
  • Released from brain and spinal chord.
  • Opioid medication activates these endogenous pain suppressing systems.
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8
Q

Nociceptive Pain

A
  • Caused by activation of A-delta and C nociceptors in response to injury, disease, and inflammation.
  • Actual or potential tissue damage
  • Responds well to analgesics such as NSAIDS and opioids.
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9
Q

Somatic Pain

A
  • Ongoing activation of nociceptors in bone, muscle, and soft tissue.
  • Well localized.
  • Gnawing, throbbing, burning, or cramping
  • Intermittent/constant
  • Deep/superficial
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10
Q

Visceral

A
  • Stimulation deep in tissue/organs
  • More diffuse pain
  • Deep, boring pain
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11
Q

Neuropathic Pain

A
  • Abnormal processing of stimuli in peripheral or CNS.
  • Injury to receptors, afferent fibers, or CNS
  • Shooting, burning, stabbing, jabbing, tearing, numb, dead, cold, and radiating pattern.
  • Caused by trauma, infection, toxin, metabolic disturbance, inflammation and etc
  • Responds poorly to opioids and analgesics
  • Responds to
    Antidepressants - Imipramine
    Anticonvulsants - Carbamazepine, Gabapentin
    Local Anesthetics - Lidocaine
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12
Q

Endogenous Analgesics

A
  • Opioid peptides react with opioid receptors to inhibit transmission of pain signals
  • These include enkephalins, beta-endorphins, dynorphins.
  • They are found in Peripheral and Central NS tissue.
  • Believed to moderate our response to pain
  • They serve as neurotransmitters, neuromodulators, and neurohormones.
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13
Q

ABC’s of Pain Management

A

A - Ask and Assess pain Regularly and Systematically
B - Believe family/client report of pain
C - Choose appropriate pain control options
D - Deliver interventions timely/logically/coordinated
E - Empower and Enable patients to control the treatment to the greatest extent possible

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14
Q

Pain Assessment

A
  • Location, Intensity, Relation to Time, Activities, Other Signs and Symptoms.
  • Assess patient before and after providing analgesics.
  • Pain is measured on a 1-10 scale.
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15
Q

Fever

A
  • Caused by chemical called pyrogens
  • Helps immune system fight infectious agents such as bacteria and viruses which are sensitive to temperature changes
  • Hypothalamus regulates bodies temperature
  • Pyrogens react with hypothalamus to raise body temperature
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16
Q

Prostaglandins

A
  • Chemical mediator found in most body tissue

- Assist in many body functions, inflammatory response, pain, fever, and formed with cell injury occurs

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17
Q

COX

A
  • Cyclooxygenase is responsible for synthesis of prostaglandins (PGE2), prostacyclin (PGl2) and thromboxane A2 (TXA2).
  • Found in all tissues that exert local effects.
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18
Q

COX-1

A
  • Found in platelets, GI Mucosal cells, renal tubule cells.

- Responsible for house keeping chores.

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19
Q

COX-2

A
  • Found in fibroblasts, chondrocytes, endothelial cells, macrophages, mesangial cells.
  • Produces effects at site of tissue injury, mediating inflammation, sensitizing pain receptors.
20
Q

PGE2 & PGl2

A
  • Promote inflammation and sensitize pain receptors to stimuli at site of injury.
  • In the stomach they protect gastric mucosa
  • In the kidneys they maintain renal blood flow
  • In the brain PGE2 mediate pain, fever, pain perception
  • TXA2 stimulates stimulates platelet aggregation
21
Q

COX Inhibitors and Acetaminophen

A
  • Analgesic, Anti-Inflammation, Antipyretic
    Cox 1 inhibition can cause gastric erosion, ulceration, bleeding tendencies and renal impairment
    Cox 2 inhibition can decrease inflammation, decrease pain, decrease fever, but cause renal impairment
22
Q

Cox Inhibitors

A
  • First Generation NSAID’s (Non Selective)

- Second Generation NSAID’s (Specific COX-2 Inhibitor)

23
Q

NSAID’s Mechanism of Action

A
  • Inhibit prostaglandin synthesis in CNS and PNS
  • Inhibit COX1 and COX2 enzymes required to create prostaglandins
  • Relieve pain by blocking pain impulse transmission
  • Decrease fever by resetting hypothalamus thermostat to lower temperature
  • Antiplatelet
24
Q

Indications for NSAID’s

A
  • Treat/prevent mild to moderate pain and inflammation (arthritis, bursitis)
  • Relieve pain (headache, minor trauma, minor surgery)
  • Not recommended for Visceral Pain
  • Reduce Fever
  • Suppress platelet aggregation (ischemic stroke, TIA, acute MI)
25
Q

Contraindications NSAID’s

A
  • Increased risk of GI Adverse effects such as bleeding and ulcerations
  • Impaired renal function, alcohol use, peptic ulcer disease
  • Avoided in children with viral infections due to connectivity with Reye’s syndrome.
  • Pregnancy may cause GI blood loss, anemia, post partum hemorrhage.
  • Risk to fetus
26
Q

Second Generation NSAID (COX2 Inhibitor)

A
  • Developed to minimize adverse effects of NSAID’s
  • Suppress pain and inflammation with less risk to gastric ulcerations
  • Can still cause severe ulcerations, renal impairment, increase risk of MI and stroke.
  • Celecoxib
27
Q

Second Generation NSAID’s

A
  • Reserved for patients at high risk of GI bleed
  • Oral, metabolized in liver and excreted in kidneys
  • Risk of MI, stroke, CV events.
  • May increase effect of warfarin and decrease effect of ACE inhibitors, furosemide.
28
Q

Acetaminophen

A
  • Mild to moderate pain/fever
  • NOT AN NSAID
  • Inhibits COX1 and COX2 within CNS
  • Does not inhibit in PNS which is why it does not have anti-inflammatory properties or adverse GI, platelet and kidney effects.
  • Metabolized in liver but small amounts remain in body as toxic metabolite.
  • Can cause liver damage or fatal liver necrosis
29
Q

Acetaminophen toxicity

A
  • 4g a day is maximum dose
  • 2g for people who use excessive alcohol
  • Overdose causes hepatotoxicity
  • Jaundice, vomiting, CNS stimulation, excitement, delirium, coma, death
30
Q

Acetaminophen toxicity treatment

A
  • Administer charcoal if overdose present
  • N-acetylcysteine is the antidote
  • Antidote does not reverse damage already done
31
Q

Opioid Analgesic

A
  • Used for moderate to severe acute or chronic pain
  • Morphine, codeine, fentanyl, oxycodone, hydrocodone, methadone
  • 70% of overdose involve opioids.
32
Q

Opioid/Opiate/Narcotic

A

Opioid - Natural/Synthetic drug similar to morphine
Opiate - Drugs with opium
Narcotic - Not a useful term

33
Q

Characteristics of Opioid Analgesic

A
  • Relieve moderate to severe pain by inhibiting pain signal transmission.
  • Metabolized in liver and excreted in urine.
34
Q

Mechanism of Action Opioid

A
  • Bind to opioid receptors in brain, spinal cord and peripheral tissue. Activates endogenous analgesic system.
35
Q

Pharmacological Effect Opioid

A
  • Analgesia, CNS depression, decreased mental/physical activity, respiratory depression, pupillary constriction
  • Nausea, vomiting, slow motility, constipation, bowel spasms
36
Q

Black Box Warning Opioids

A
  • All opioids have black box warnings due to potential for abuse and risk of fatal overdose due to respiratory depression
37
Q

Indications for Opidoids

A
  • Prevent/relieve severe/chronic pain
  • Promote sedation, decrease anxiety, decrease amount of anesthesia needed for pre/post op surgery
  • Treatment of abdominal cramping and diarrhea.
38
Q

Contraindications Opioids

A
  • Existing respiratory depression
  • Chronic lung disease
  • liver/kidney disease
  • Prostatic hypertrophy
  • Objective is to use least potent medication that is effective
39
Q

Pharmacotherapeutics Morphine

A
  • Moderate to severe pain
  • Dyspnea associated with left heart failure
  • Acute MI
  • Post-op sedation
40
Q

Pharmacokinetics Morphine

A
  • Not very lipid soluble so only part passes BBB

- Oral has high first-pass metabolism so doses are higher orally than parentally

41
Q

Adverse Effects Morphine

A
  • Respiratory depression, hypoventilation, apnea, respiratory arrest, circulatory depression, cardiac arrest
42
Q

Contraindications Morphine

A
  • Patient with pre-existing respiratory depression
  • Bronchial asthma
  • Airway obstruction
  • Heart failure
43
Q

Precautions

A
  • Receiving other CNS depressants including alcohol.
44
Q

Opioids and Elderly

A
  • Use great caution as they are sensitive to respiratory depression, confusion, sedation.
  • Use nonpharmacological therapies whenever possible
  • Use drugs with shorter half-lives because less likely to accumulate
  • Start small dose and increase gradually
45
Q

Opioids in Children

A
  • May need to be given in other ways not IM

- Not all are appropriate for children

46
Q

Opioid Antagonist

A
  • Naloxone and Naltrexone

- Nalmefene (Longer acting reversal agent)

47
Q

Narcan

A
  • Rapidly reverses affect of opioids.
  • Used for patients with respiratory depression
  • IV, IM, Intranasal
  • Onset 2-5 min after IV injection, short half life so may need to be given repeatedly
  • Monitor closely with airway support, oxygen and suction.

Pathophysiology (18 decks)

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