Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
47 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
Types of Drugs Used in Treatment of Pain
|
1. Analgesics
2. Anti-Inflammatories |
|
|
|
Types of Analgesic Drugs
|
1. Opiods
2. Non opiods |
|
|
|
Types of Anti-Inflammatory Drugs
|
1. NSAIDS
2. Glucocorticoids |
|
|
|
Function of Analgesics
|
Decrease and manage pain
They are NOT Anesthetics |
|
|
|
Types of Analgesic Drugs
|
1. Opiod (Narcotic describes sx so use opiod as term)
2. Non opiod |
|
|
|
Purpose of opiods?
Usage of opiods |
Alter the perception of pain
Used in moderate/severe pain |
|
|
|
Morphine
|
Grandfather of opiods, all others compared relative to this prototype
|
|
|
|
Mechanism of opiod action:
Primary system. Binding sites |
Acts primarily on CNS tissue
Dorsal gray matter of the spinal cord Medial thalamus and hypothalamus in the brain |
|
|
|
Opiod receptor sites
|
Specific receptors on:
pre synaptic nerve terminals post synaptic neurons |
|
|
|
Effect of opiod binding
|
DOUBLE EFFECT:
Pre synaptically decreases release of neurotransmitter Post synaptically decreases excitability of neuron |
|
|
|
How opiods developed
|
Disccovery of opiod receptors led to search for endogenous opioid like substances
|
|
|
|
Adverse effects of opiods
|
Sedation
Mood changes Confusion Respiratory depression Orthostatic hypotension Nausea and vomiting (transient) Constipation (ongoing) Tolerance and Dependence |
|
|
|
Most potentially harmful adverse effects opiods
|
Respiratory depression: decreaed sensitivity of control mechanism @ brainstem **even at therapeutic doses**
Orthostatic hypotension: dx w/ drop of 10mm hg diastolic, 20 mm hg diastolic bp |
|
|
|
Tolerance and Physical Dependence def:
|
Tolerance: increased dose to achieve same effect
Dependence: onset of withdrawal if drug suddenly stopped |
|
|
|
Old school vs new school on T & D:
Implications |
OS: > 3wks usage T & D occur
NS: English study: match dose to need no T & D Involve patient more in dosing |
|
|
|
PCA features
|
"Pt. controlled anesthesia"
Self Administered Programmed to prevent OD "Demand Dose" Lock out period Much better at maintaining dosage in "therapeutic window" vs large fluctuations in traditional administration |
|
|
|
PCA study observations
|
Better pain control w/ decreased side effects (less sedation, tolerance, dependence)
Increased pt. satisfaction (locus of control) Requires awareness and cognitive ability |
|
|
|
Non opiod Analgesics
|
NSAIDS
Acetaminophen |
|
|
|
NSAID effects
|
Analgesic
Antiinflammatory Antipyretic Anticoagulant Anticancer? (esp colorectal polyps) Aspirin the grandfather of NSAID's |
Aspirin the grandfather of NSAID's
|
|
|
Specific OTC NSAID's
|
Aspirin
Ibuprofen Anaproxen Ketoprofen |
|
|
|
Specific Rx NSAID's
|
Etodolac
Fenoprofen Kelorolac Meclofenamate Piroxicam |
|
|
|
OTC vs Rx NSAIDS
|
Therapeutic difference: no
Safety difference: no (above if used in same relative doses) Cost differences: YES |
|
|
|
Mechanism of action of NSAIDS
|
Inhibit the synthesis of prostaglandins in all cells EXCEPT mature RBC's
|
|
|
|
Prostaglandins Biosynthesis
|
Membrane Phospholipid x Phospholipase>>Arachadonic Acid x Cyclooxygenase>>PGG2>>(all PG's and Thyroxane)
|
|
|
|
Leukotrine Biosynthesis
|
Membrane Phospholipid x Phospholipase>>Arachadonic Acid x Lipoxygenase>>(all leukotrines)
|
|
|
|
NSAID mechanism on PG's
|
Inhibits production of PG"s by preventing cycloogenase enzyme (COX) from converting arachodonic acid to PGG2
|
|
|
|
Cyclooxygenase subtypes
|
COX 1
-Normal constituent in certain cells -synthesizes PG's to potect cells and maintain fuction (stomach, kidney, platelets etc) COX2 -Induced when cell is injured -synthesize PG's that mediate pain/inflammation and other pathologies |
|
|
|
NSAID specificity
|
TRADITIONAL NSAID's are non-specific: inhibit both COX1and COX2
|
|
|
|
COX2 selective drugs action
|
-Inhibit synthesis of PG's in pain/inflammation
-spare beneficial PG's in stomach, kidney, platelets -May decrease pain/inflammation w/ less toxicity (decreased gastritis) |
|
|
|
First Developed COX@ selective drug and effects
|
Celexicob (Celebrex)
-Very effective but d/t pt. variability not effective for all -cardiovascular side effects |
|
|
|
2nd & 3rd generation COX2 selectives
|
Vioxx (Rofecoxib)
Bextra (Valbecoxib) Both recalled d/t severe side effects (MI/Stroke) |
|
|
|
Acetaminophen: Name and properties
|
Tylenol
Analgesic & Antipyretic No gastric irritation Effects CNS PG production, little on peripheral No Anti Inflammatory or Anticoagulant effects |
Inform patients: NSAID and Acetaminophen are not the same
|
|
|
Acetaminophen and Liver Toxicity
|
15 g can cause damage in a healthy liver
Much less can cause damage w/ liver toxicity Very serious drug Mechanism of Acetaminophen biotransformation in Liver |
Acetaminophen>>N acetyl-p-bensoquinonimine x GSH(amino acid)>>mercapturic acid (excreted in kidneys or urine)
W Increased dose or decreased GSH, N acetyl-p-benzoquinonimine builds up and is VERY toxic to liver enzymes |
|
|
Acetaminophen & Opiod combos
|
Lortab, Lorcet (Hydrocodone & Acet)
Ultracet (Tramadol & Acet) Darvocet: (Propoxyphene & Acet) Percocet (Oxycodone & Acet) Often undercut the opiod and results in decreased pain control |
|
|
|
Non opiod concerns
|
Gastric irritation (esp nsaids)
Hepatic, renal toxicity (esp if pathologies) **Impaired bone and cartilage healing** Overdose: ASA intoxication: decrease hearing, tinnitus, confusion, ha, CN VIII reacting as a barometer to toxicity |
** From animal studies
--possibly d/t effect on pg's **do not use them if you don't have to in bone and cartilage |
|
|
Glucocorticoids General Info
|
Steroids
Powerful Antiinflammatory effects and Immunosuppressive effects Many uses and indications Can resolve inflammation, but dz process continues (treat sx's only) |
|
|
|
Major families of Steroids
|
Antiinflammatory: Corticosterone
Mideral: Aldosterone (retain salt and water) Sex Hormones: Androtenedione |
Structurally similar and all made from cholesterol
|
|
|
Common Glucocorticod drugs
|
Betamethasone
Cortisone Prednisone Prednisolone Hydrocortisone Paramethasone Dexamethasone |
|
|
|
Glucocorticoid effects
|
Acto on inflammatory cells
macrophages, leukocytes |
|
|
|
Glucocorticoid mechanism of action
|
Bind to receptor in cytoplasm
Receptor travels to nucleus Decreaed expression of inflammatory proteins: cytokines, enzymes ets increased expression of antiinflammatory protiens (to a lesser extent) |
|
|
|
Action common to ALL steroids
|
Got to genomic components of cell and effect mrna and protein synthesis
|
|
|
|
Glucocorticoid Administration Methods
|
Oral/Systemic:
Regular maintenance dose Dose packs (taper dose after dumping large dose) Injections( 3-4 intraarticular/yr can be very effective) Other |
Inhalation
Topical Nasal Opthalmic Otic |
|
|
Glucocorticoid Adverse Effects
|
Primary: Catabolic effect on
Bone Muscle Ligament Tendon Skin (All Collagenous tissues) |
|
|
|
How Glucocorticoids have catabolic effect
|
Takes collagen from tissues to generate glucose in liver (nl function of endogenous glucocorticoids)
W/ intro of external drug, this accelerates process and breaks tissue down |
|
|
|
Role of Rehab w/ catabolic effect of Glucocorticoids
|
Right combination of resistive/wb/aquatic exercise can offset catabolic effect
|
|
|
|
Glucocorticoid side effects continued
|
Salt and water retention (bloated face)
increased infection increased gastric ulcers glucose intolerance glaucoma Adrenal suppression |
|
|
|
Adrenal Cortical shock
|
Sudden stop of glucocorticoid can produce:
profound drop in bp systemic vascular collapse organ damage** |
Can occur affter 3-4 wks of continuous use.
Be aware when pt says they want to stop taking gc's |
