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
2
Q
Acute Pain
A
- Immediate response to an illness or injury that resolves once causative factor is relieved.
3
Q
Chronic Pain
A
- Persists for extended periods of time and does not resolve when cause is treated
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.
5
Q
Pain Receptors
A
- Activated by 3 pathways
- Mechanical (pressure)
- Thermal
- Chemical (Bradykinin, Serotonin, Histamine)
6
Q
Prostglandins
A
- Prostaglandins and substance P enhance sensitivity to pain receptors to activation, but do not activate them.
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.
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.
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
10
Q
Visceral
A
- Stimulation deep in tissue/organs
- More diffuse pain
- Deep, boring pain
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
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.
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
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.
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
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
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.
18
Q
COX-1
A
- Found in platelets, GI Mucosal cells, renal tubule cells.
- Responsible for house keeping chores.
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.
