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Pharmacology > Pain Management Part I > Flashcards

Pain Management Part I Flashcards

1
Q

Describe general anesthetics

A
  • used for major surgeries
  • induces a reversible state of unconsciousness
  • provides amnesia
  • often used in conjunction
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2
Q

Describe the ideal anesthetic

A
  • Rapid onset
  • Loss of consciousness & sensation
  • Amnesia
  • Skeletal muscle relaxation
  • Inhibition of sensory & autonomic reflexes
  • Easy dose adjustment
  • Minimum toxic side effects
  • Recovery rapid & uneventful
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3
Q

What are the stages of anesthesia

A
  • Stage I Analgesia: still conscious, somewhat aware, loss of sensation
  • Stage II Excitement: unconscious, amnesiac, appears agitated & restless
  • Stage III Surgical Anesthesia: ideal level for surgery, regular & deep respirations
  • Stage IV Medullary Paralysis: should be avoided, cessation of spontaneous respirations, cardiovascular collapse
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4
Q

Routes of administration for anesthetics

A
  • Inhalation: gases/volatile liquids; longer onset to stage III; easier to adjust dose & maintain anesthesia
  • Intravenous (IV): several categories of CNS depressants; rapid onset to stage III; risk of over medication
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5
Q

Describe inhalation anesthetics

A
  • Gases: Nitrous oxide, used for short procedures
  • Volatile liquids: several chemically similar agents available; Desflurane or Sevoflurane are preferred due to rapid onset, faster recovery, & better anesthesia control
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6
Q

Describe intravenous (IV) anesthetics

A
  • Barbiturates: induction of anesthesia, fast onset, relatively safe
  • Benzodiazepines: induction & maintain of anesthesia
  • Opiod analgesics: induction & maintain of anesthesia
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7
Q

Describe Ketamine

A
  • dissociative anesthesia
  • pt appears detached from surroundings
  • awake but sedated & unable to recall events
  • useful for short procedures
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8
Q

Adverse effects and advantages of Ketamine

A
  • Adverse effects: hallucinations, strange dreams, & other psychotic reactions
  • Advantages: less respiratory adverse effects & less cardiac dysfunction
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9
Q

Describe Propofol (IV anesthesia)

A
  • Short acting hypnotic
  • Rapid onset
  • Induction & maintenance
  • Rapid recovery
  • Continuous infusion: sedation of mechanically ventilated patients
  • Rare adverse effect: Propofol related infusion syndrome (PRIS)
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10
Q

Describe Etomidate (IV anesthesia)

A
  • Hypnotic like drug
  • Rapid onset
  • Short duration
  • Quick recovery
  • Minimal cardiopulmonary side effects
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11
Q

Describe Dexmedetomidine (IV anesthesia)

A
  • Alpha 2 agonist
  • No respiratory depression
  • Adjunct during surgery
  • Short term sedation for mechanically ventilated patients
  • Hypotension
  • Bradycardia
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12
Q

Describe anesthesia pharmacokinetics

A
  • widely and uniformly distributed
  • high degree of lipid solubility
  • stored in adipose tissue: slow washout, longer based on duration of anesthesia or patient weight
  • Elimination: excretion from the lungs, biotransformation in the liver
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13
Q

Describe the mechanism of action for anesthesia

A
  • Inhibit neuronal activity in the CNS: sedation, hypnosis, amnesia
  • Inhibit neuronal function in spinal cord: immobility, inhibiting motor response to painful stimuli
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14
Q

Describe neuromuscular blockers

A
  • Adjunct to general anesthesia
  • Skeletal muscle paralysis
  • Does not provide anesthesia, sedation, analgesia, or amnesia (DO NOT USE ALONE)
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15
Q

Neuromuscular blockers mechanism of action

A
  • block transmission of nerve impulses (depolarizing or non-depolarizing)
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16
Q

Adverse effects of neuromuscular blockers

A
  • Tachycardia
  • Increased histamine release
  • Hyperkalemia
  • Residual muscle pain & weakness
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17
Q

Physical therapy considerations with neuromuscular blockers varying washout period

A
  • Increased confusion
  • Disorientation
  • Lethargy
  • Delirium
  • Muscle weakness
  • Bronchial secretions
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18
Q

Describe local anesthetics (LA)

A
  • Loss of sensation in a specific area
  • Used prior to minor surgical procedures
  • Rapid recovery with minimal side effects
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19
Q

Non- surgical use of local anesthesia (LA)

A
  • Short term pain relief: musculoskeletal & joint pain
  • Chronic pain: cancer, complex regional pain syndrome
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20
Q

How can a PT deliver local anesthesia (LA)

A
  • phonophoresis
  • iontophoresis
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21
Q

What factors go into the selection of local anesthetics (LA)

A
  • Operative site
  • Nature of procedure
  • Type of regional anesthesia
  • Anesthetic duration
  • Patient characteristics
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22
Q

Describe the pharmokinetics of local anesthetics (LA)

A
  • Drug to remain at administration site: trigeminal nerve for dental procedure; spinal cord (epidural, spinal)
  • Commonly used with vasoconstrictor: epinephrine prevents “washout” from site; prevent from reaching the bloodstream (decreases systemic side effects)
  • Eliminated by hydrolysis
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23
Q

Clinical uses of local anesthetics (LA)

A
  • Topical
  • Transdermal
  • Infiltration
  • Peripheral nerve block
  • Central nerve blockade
  • Sympathetic blockade
  • Intravenous (IV) regional anesthesia
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24
Q

Describe topical local anesthetics (LA)

A
  • Applied directly to produce analgesia: skin, mucous membranes, cornea
  • Used for minor surface irritation or injury: burns, abrasions, inflammation
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25
Q

Describe transdermal local anesthetics (LA)

A
  • Applied to skin surface
  • Enhanced with electrical current (iontophoresis) and/or ultrasound (phonophoresis)
  • Used in dermatologic & minor surgical procedures
  • Transdermal patch: musculoskeletal pain, neuropathic pain
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26
Q

Describe infiltration anesthesia (LA)

A
  • Injection directly into selected tissue
  • Diffuse sensory nerve endings
  • Used for performing surgical repair
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27
Q

Describe peripheral nerve block local anesthetics (LA)

A
  • Injected close to nerve trunk
  • Interrupt transmission along the nerve
  • Used in dental procedures
  • Minor nerve black: single peripheral nerve
  • Major nerve block: several nerves or nerve plexus
28
Q

Describe central nerve blockade (LA)

A
  • Injected in spaces surrounding the spinal cord
  • Epidural nerve blockade: injected into the space b/w the bony vertebral column & the dura mater
  • Caudal block: injected into lumbar epidural space via sacral hiatus
  • Spinal nerve blockade: injected into subarachnoid space
29
Q

Describe sympathetic blockade (LA)

A
  • Selective interruption of sympathetic efferent discharge
  • Used for complex regional pain syndrome (CRPS)
  • Injected into area surrounding the sympathetic chain ganglion innervating the limb: usually involves a series of 5 injections; goal is decreased sympathetic outflow not analgesia
30
Q

Describe intravenous regional anesthesia (LA)

A
  • Injected into peripheral vein in selected extremity
  • Local vessels carry anesthetic to the nerves in that extremity
  • Requires use of a tourniquet to localize the medication
  • Used for short surgical procedures or to treat CRPS
31
Q

What is the mechanism of action (MOA) of local anesthetics (LA)

A
  • Inhibit opening of sodium channels on nerve membranes
  • Blocks action potential along neuronal axons
  • Only 2-3 nodes of Ranvier in a myelinated neuron need to be affected to block the action potential
32
Q

Describe differential nerve block

A
  • Local anesthetics block specific nerve fiber groups depending on their size & myelination
  • Smallest fibers first then progressively larger fibers
  • Different diameter fibers transmit different information: Smallest (type C) transmit pain & Largest (Type A-alpha) transmit impulses to skeletal muscle
33
Q

Systemic effects of local anesthetics (LA)

A
  • Temperature
  • Local Anesthetic Systemic Toxicity (LAST): early symptoms include ringing in the ears, agitation, restlessness, decreased sensation in the tongue, around the mouth, & areas of the skin
34
Q

CNS and cardiac effects of local anesthetic systemic toxicity (LAST)

A
  • CNS: somnolence, confusion, agitation, excitation, seizures, impaired respiratory function
  • Cardiac: decreased cardiac excitation, HR, & force contraction
35
Q

PT considerations with local anesthetics (LA)

A
  • PTs may be involved in administration of LAs to treat musculoskeletal pain: iontophoresis and phonophoresis
  • Working with patients post anesthesia: decreased sensation below the blockade, risk of damage during exercise due to analgesia, impaired motor function
  • Working with CRPS patients: schedule PT right after administration of LA
36
Q

What is chronic pain linked to

A
  • Restrictions in mobility
  • Dependence on opioids
  • Anxiety and depression
  • Poor perceived health or quality of life
37
Q

Describe the pain ladder

A
  • Step 1: non-opioids +/- adjuvants
  • Step 2: opioids from mild to moderate pain +/- non-opioids +/- adjuvants
  • Step 3: opioids from moderate to severe pain +/- non-opioids +/- adjuvants
  • Step 4: invasive and minimally invasive treatments
38
Q

What are the pharmacologic properties of NSAIDs (non-steroidal anti-inflammatory drugs)

A
  • Anti-inflammatory: reduces inflammation
  • Analgesic: relieves pain
  • Antipyretic: reduces fever
  • Anticoagulant: inhibits platelet aggregation
39
Q

NSAIDs history

A
  • Aspirin (ASA) considered the original NSAID
  • Newer NSAIDs compared to ASA: efficacy and safety
  • Acetaminophen (APAP) lacks anti-inflammatory & anticoagulant effects (not true NSAID, though blocks COX in CNS)
40
Q

Describe eicosanoids

A
  • Eicosa: 20-carbon
  • Enoic: containing double bonds
  • Prostanoid: specific eiconsanoids (Prostaglandins, thromboxanes, & prostacyclins)
  • Prostaglandins: group of lipid like compounds that regulate cell function (produced in every cell except RBC; thromboxanes & leukotrienes derived from same precursor)
41
Q

Effects of excessive prostaglandins

A
  • Inflammation
  • Pain
  • Fever
  • Dysmenorrhea
  • Thrombus formation
  • Other pathologies
42
Q

Describe COX-1 (cyclooxygenase)

A
  • synthesizes beneficial prostaglandins
  • maintains cellular hemostasis
  • most NSAIDs are nonselective
  • inhibition may cause stomach & kidney issues
43
Q

Describe COX-2 (cyclooxygenase)

A
  • produces prostaglandins in response to injury
  • selective NSAIDs inhibit only COX-2: less GI adverse effects; risk of HTN, heart failure, & infarction
  • Celecoxib
44
Q

Adverse effects of NSAIDs

A
  • GI damage
  • Cardiovascular problems
  • Kidney damage
  • Hepatotoxicity
  • Hypersensitivity
  • Reye syndrome
45
Q

PT considerations related to NSAIDs

A
  • NSAID use is common
  • Effective for mild to moderate pain & inflammation w/o cognitive side effects
  • Use with caution in people with GI problems, liver damage, kidney damage, heart failure, & diabetes
  • May increase bleeding
46
Q

Describe Acetaminophen (Paracetamol)

A
  • Analgesic and antipyretic effects
  • Lacks anti-inflammatory or anticoagulant effects
  • Not associated with GI irritation
  • MOA: inhibition of cyclooxygenase in the CNS
47
Q

Adverse effects of acetaminophen

A
  • Liver toxicity in high doses causing hepatic necrosis and potentiated by pre-existing liver damage & alcohol abuse
48
Q

PT considerations for acetaminophen

A
  • Use is common, often combined with other medications
  • Effective for mild to moderate pain
  • Use with caution in people with liver disease
  • Understand the difference between NSAIDs and acetaminophen
49
Q

Epidemiology of rheumatoid arthritis (RA) and osteoarthritis (OA)

A
  • RA: affects 0.5-1% of population; 3x more likely in women
  • OA: ~50% of people aged 65; most common joint disease in the U.S.
50
Q

Describe RA

A
  • Characterized by synovitis & destruction of articular tissue
  • Chronic, systemic disorder
  • Pain, stiffness, inflammation
  • Periods of exacerbation & remission
  • Progressive joint damage and bone erosion
51
Q

Goals for treatment of RA

A
  • Decrease joint inflammation
  • Arrest progression of the disease
52
Q

Medications that can be used for RA

A
  • NSAIDs: decrease joint inflammation & pain; short term use
  • Glucocorticoids: decrease joint inflammation & pain; bridge to DMARD or acute flare
  • Disease-Modifying Antirheumatic Drugs (DMARDs): diverse group of medications; slows RA progression, modifications of immune response
53
Q

Describe glucocorticoids

A
  • decreased joint inflammation & pain
  • decrease joint erosion & damage (high dose)
54
Q

Significant adverse effects of glucocorticoids

A
  • Increased bone loss
  • Muscle wasting, weakness
  • HTN
  • Aggravation of DM, glaucoma, cataracts
  • Increased risk of infection
55
Q

Describe DMARDs

A
  • Loosely define cluster of agents
  • Slow or halt the progression of RA
  • Early use to control synovitis & erosive changes
  • Used with NSAIDs and glucocorticoids
  • Highly effective
  • Significant adverse effects
56
Q

Traditional (nonbiological) DMARDs

A
  • Antimalarials (Hydroxychloroquine): use in combination with newer DMARDs or pts who cannot tolerate newer agents
  • Immunosuppressant (Azathioprine): use to treat severe cases not responding to other agents
  • Gold therapy: no longer available
  • Leflunomide (Arava): decreases pain, inflammation, & joint effusion; slows formation of bone erosions; works early ~1 mo
  • Methotrexate: antimetabolite used in cancer tx, decreases synovitis & bone erosion, less narrowing of joint space, used alone or in combination, rapid onset ~2-3 wks
57
Q

Adverse effects of antimalarials (Hydroxychloroquine), immunosuppressant (Azathioprine), Leflunomide (Areva), and Methotrexate

A
  • Antimalarials: high doses = irreversible retinal damage; headache; GI distress
  • Immunosuppressant: fever/chills, sore throat, fatigue, nausea/vomiting, loss of appetite
  • Leflunomide: GI distress, allergic reactions (skin rashes), hair loss, pneumonitis
  • Methotrexate: GI distress (loss of appetite, nausea), long term = pulmonary problems, hematological disorders, liver dysfunction, hair loss
58
Q

Describe tumor necrosis factor (TNF) inhibitors

A
  • Inhibit TNF- α: cytokine released from cells involved in inflammatory response
  • Slow progression of inflammatory joint disease
  • Improve symptoms & QOL
  • Must be administered parenterally
59
Q

Adverse effects of TNF inhibitors

A
  • infections
  • malignancy
  • liver disease
  • heart failure
  • lupus-like disease
  • demyelinating disorders
60
Q

Other biologicals

A
  • Abatacept: targets T cell activation; used second line
  • Anakinra: blocks interleukin-1 on joint tissue; moderately effective
  • Rituximab: depletes B lymphocytes; beneficial in select patients
  • Tocilizumab: blocks the interleukin-6 receptor; alternative for select patients
61
Q

Describe osteoarthritis (OA)

A
  • intrinsic defect in remodeling of joint cartilage & bone
  • progressive degeneration of articular cartilage
  • degenerative bony changes: thickening of subchondral bone, creation of subchondral bone cysts, & formation of osteophytes
  • occurs inn large wbing joints & spine
62
Q

Goals of treatment for OA

A
  • manage pain
  • maintain an active lifestyle
63
Q

Medications for treatment of OA

A
  • NSAIDs: decrease joint inflammation & pain
  • Acetaminophen: decrease joint pain
  • Disease Modifying Osteoarthritic Drugs (DMORDs): viscosupplementation, Glucosamine, & Chondroitin sulfate
64
Q

Describe viscosupplementation

A
  • Uses hyaluronan to restore lubricating properties of synovial fluid: reduces pain & improves function
  • Tx consists of weekly injections
  • Responders may benefit for 6-12mo
  • Temporarily attenuates progression
  • May delay need for invasive Tx
65
Q

Describe Glucosamine & Chondroitin Sulfate

A
  • Key ingredients for production of glycosaminoglycans, proteoglycans, & hyaluronic acid
  • Proposed benefit of decreased pain & improved function
  • Inconsistent results in clinical trials
  • Available OTC (over the counter) as dietary supplement
  • Well tolerated
66
Q

Physical therapy considerations for RA and OA

A
  • Treatments for RA and OA play a role in optimizing rehabilitation
  • Be aware of medication regimens: adverse effects should be considered when designing therapy programs
  • MOADs may have a positive effect on ability to participate in rehabilitatio

Pharmacology (12 decks)

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