Chapter 5 Flashcards
Means by which body is made urgently aware of the presence of tissue damage
Sensation of pain
Protective reflex for self preservation
Pain
The physical component of pain
Perception
The psychological component of pain
Reaction
Where does pain go?
Cortex (brain)
Unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage
IASP definition of pain
pain where the injury is
Nociceptive
Feeling pain in normal structures
Nociceptive
Is the site of pain always the source of pain?
NO
Classification of analgesic agents
Nonopiods, nonnarcotics
Opioids, narcotics
Salicylates, aspirin, nonaspirinxsalicylates
Nonopioids or nonnarcotics
Nonopioid analgesics act primarily at peripheral nerve endings, although their antipyretic effect is mediated centrally. Opioids act primarily in the central nervous system
Site of action
Nonopioid analgesics inhibit prostaglandin synthesis. Opioids affect the response to pain by depressing the CNS
Mechanism of action
Acetylsalicylic acid (aspirin) is broken down into
Acetic acid (HA) + salicylic acid (SA)
Acetylsalicylic acids mechanism of action
Inhibit prostaglandin synthesis, enzyme cycle-oxygenase (COX 1 and ll)
Sensitize pain receptors, lower pain threshold to painful stimuli, cause inflammation and fever, affect vascular tone and permeability
Prostaglandins
Where is acetylsalicylic acid absorbed?
Stomach and small intestine
With the addition of a buffer the half life of unhydrilyzed aspirin is
About 15 minutes
The half life of hydrolyzed aspirin is what?
Dose dependent
Half life of small doses of acetylsalicylic acid
2-3 hours
Half life of high doses of acetylsalicylic acid
15-30 hours
What has zero order kinetics
Acetylsalicylic acid
A constant amount rather than a constant percentage of the drug is metabolized per hour
Zero order kinetics
Addition of a buffer in aspirin facilitates what
Dispersing, dissolving, and absorption of the aspirin
Aspirin is poorly bound to what?
Plasma proteins
Pharmacologic effects of acetylsalicylic acid
Analgesic effect Antipyretic effect Anti inflammatory effect Uricosuric effect Antiplatelet effect
What is aspirins analgesic effect
Mild to moderate pain such as arthritis, headache, and toothache
The ability of aspirin to reduce fever (antipyretic) results from
Inhibition of prostaglandin syntheses in the hypothalamus
Aspirins antiinflammatory effect is derived from what
It’s ability to inhibit prostaglandin synthesis (COX l and ll). While prostaglandins are potent vasodilation agents, inhibition if prostaglandins causes decreased erythema and swelling of the inflamed area
Large doses of aspirin have a uricosuric effect which means
It can increase the elimination of uric acid
Aspirin irreversibly binds to
Platelets
Inhibits aggregation
Prostacyclin
Stimulates aggregation
Thromboxane A2
Acetylsalicylic acid adverse reactions
GI effects Bleeding Reye’s syndrome Hepatic and renal effects Pregnancy and nursing considerations Hypersensitivity (allergy)
What is aspirins most frequent side effect?
GI Tract (dyspepsia, nausea, vomiting, gastric bleeding)
At usual therapeutic doses, aspirin irreversibly interferes with clotting mechanism by
Reducing platelet adhesiveness. Bleeding time is prolonged and each platelet is affected until new platelets are formed in 4-7 days
What is Reye’s syndrome associated with
Hepatotoxicity
Acetylsalicylic acid toxicity
Salicylism, tinnitus, headache, nausea, vomiting, dizziness, dimness of vision, hyperventilation , respiratory alkalosis, death
Tinnitus
Ringing in ear
When blood levels of salicylates reached a certain level, a toxic reaction occurs
Salicylism
Cause of death from aspirin poisoning is usually what?
Acidosis and electrolyte imbalance
Prevention of toxicity
Education of parents
Lethal dose of acetylsalicylic acid for children and adults
Child: 4 gm
Adult: 10-30 gm
Warfarin interaction with acetylsalicylic acid
Bleeding and hemorrhage
Acetylsalicylic acid interaction with probenecid
Precipitates gout attack
Acetylsalicylic acid interaction with methotrexate
Causes increased serum concentration and MTX toxicity
Acetylsalicylic acid interaction with sulfonylureas
Hypoglycemia
Aspirin interaction with antihypertensives
Reduce the effects of hypertensive agents
Uses of aspirin
Analgesia for mild to moderate pain, antiinflammatory, low dose aspirin therapy
Chemical classification of nonsteroidal antiinflammatory drugs
Propionic acids Acetic acids Fenamates Pyrazolones Oxicams
What are NSAID’s similar to
Aspirin- inhibition of prostaglandin synthesis by inhibiting COX
What enzymes do NSAID’s inhibit
COX l and ll
NSAID mechanism of action results in
Reduction in formation of prostaglandin precursors and thromboxanes from arachidonic acid
Most NSAID’s peak in
1-2 hours
Where are NSAID’s metabolized
Liver
Where are NSAID’s excreted
Kidneys
NSAID’s are useful for treating what
Dysmenorrhea and gout
Gastrointestinal effects of NSAID’s
Irritation, pain, bleeding, interfere with normal stomach protective mechanisms
Central nervous system effects of NSAID’s
Sedation Dizziness Confusion Mental depression Headache Vertigo Convulsions
NSAID adverse reactions
Blood clotting and myocardial infarction or stroke Muscle weakness Ringing ears Hepatitis Hematologic problems Blurred vision Celecoxib
Renal effects of NSAID’s
Hypertension Renal failure Cystitis Increased urinary tract infection Decrease in renal blood flow Decrease in glomerular filtration rate
Oral effects of NSAID’s
Ulcerative stomatitis
Gingival ulceration
Dry mouth
Hypersensitivity reactions of NSAID’s
Hives or itching Angioneurotic edema Chills and fever Steven Johnson’s syndrome Exfoliative dermatitis Epidermal necrolysis
Pregnancy and nursing considerations of NSAID’s
Prolong gestation
Delay parturition
Produce dystocia
What drugs are FDA pregnancy category B
Fenoprofen
Ibuprofen
Naproxen
What drugs are FDA pregnancy category c
Diflunisal
Tolmetin
Medenamic acid
NSAID drug reactions
Lithium Digoxin Antihypertensives Probenecid Cyclosporin and MTX
Lithium
May increase lithium toxicity
May increase effect of digoxin
Digoxin
May decrease effects
Antihypertensives
May increase serum levels of NSAID’s
Probenecid
Increased toxicity
Cyclosporin and MTX
NSAID medical therapeutic uses
Osteoarthritis Rheumatoid arthritis Gouty arthritis Fever Dysmenorrhea Pain Bursitis and tendinitis
NSAID dental therapeutic uses
Pain
Equivalent in analgesia efficacy to opioid analgesics in many clinical situations
How long is the half life of ibuprofen (Advil, Motrin)
2 hours
Onset of action for ibuprofen (Advil, Motrin)
1/2 hour
Duration of ibuprofen
4-6 hours
NSAID examples
Naproxen (naprosyn)
Naproxen sodium (anaprox)
Naproxen sodium otc (aleve)
Longer half life than ibuprofen!
Other NSAID’s
Cyclo-oxygenase ll specific agent ( fewer adverse reactions)
Celecoxib (Celebrex)
(Less irritating to stomach)
Member of the p-aminophenols
Acetaminophen (Tylenol)
Where is acetaminophen absorbed from
GI Tract
Peak plasma level of Tylenol
1-3 hours
Half life of Tylenol
1-4 hours
Tylenol is
Hepatotoxic possibly nephrotixic
Tylenol does not..
Have antiinflammatory effects
Produce gastric bleeding
Affect platelet adhesiveness
Affect uric acid excretion
Toxic dose of Tylenol
12 gm or more
Adverse reactions of Tylenol
Hepatic necrosis
Nephrotoxicity
Who should avoid Tylenol
Patients with hepatic disease or who ingest 3 or more alcoholic beverages a day (me on the weekends) 🍺
Treatment of toxicity of Tylenol
Gastric lavage
Activated charcoal
Sulfhydryl groups- oral N-acetylcysteine
Associated with long term consumption of acetaminophen
Nephrotoxicity
Acetaminophen + aspirin or NSAID’s
Risk of analgesic nephropathy, renal papillary necrosis, end stage renal disease, and cancer of the kidney or bladder
Skin reactions to Tylenol
Steven Johnson’s syndrome
Toxic epidermal necrolysis
Acute generalized exanthematous pustulosis
Drug interactions of Tylenol
Hepatotoxicity can be potentiated by agents that induce hepatic microsomal enzymes
Chronic, large doses of alcohol
Uses of Tylenol
Analgesic
Antipyretic
Patients with aspirin hypersensitivity
Patients with aspirin induced gastric irritation
Regular adult dose of Tylenol
325 mg 2 tabs every4-6 hours
Extra strength adult dose of Tylenol
650 mg 2 tabs every 6 hours
Infant suspension of Tylenol
Per prescribing practitioner
JR strength Tylenol for what ages
6-11 years
Drugs used to treat gout
Colchicine
Allopurinol (zyloprim)
Probenecid (benemid)