Flashcards in Exam 4: NSAIDs/Non-Opioids yo-Part 1 to Aspirin Deck (100):
Patients who ________ having pain or who have fear and anxiety will perceive more pain.
_______: “an unpleasant sensory or emotional experience associated with actual or potential tissue damage, or described in terms of such damage”
_______ = absence of pain in response to a stimulus that is normally painful
________ = absence of all sensory modalities
2 Types of pain: _______ = non- steroidal anti-inflammatory analgesics (NSAIDS) are most effective.....AND...._________ = opiates (narcotics) are most effective
Dull, aching, inflammatory......AND......Sharp, piercing, lancinations
Hey, I don't think I saw this enough...Narcotics are NOT __________.
Degrees of Pain & what to use: _____ = Salicylates, NSAIDS most effective...._______ = Salicylates, NSAIDS most effective....________ = opiates are best
Locus of Action...haha that sounds cool: Non-opioid Analgesics- Act primarily at ________ nerve endings...._______ effect mediated centrally... Mechanism: inhibit _________ synthesis
Locus of Action...haha that sounds cool: Opioid Analgesics-Act primarily within ______.....Mechanism: _______ CNS which reduces response to pain (pain reaction)
Locus of Action...haha that sounds cool: ________ (local pain control) = analgesia, anti-inflammatory effects THEREFORE ________, _______ are used; few side effects....All non-opioid analgesics work on the ________
nervous system (as well as CNS)
Periphery...salicyclates and NSAIDs....PNS
Locus of Action...haha that sounds cool: ________ = analgesia, anti- inflammatory effects, ANTIPYRETIC effect.....NSAIDS; acetaminophen (Tylenol).....opiates = more side effects
The WAR- NSAIDs VS Opioids- _______ = true analgesics; stop the pain from where it is occurring
The WAR- NSAIDs VS Opioids- ________ = diminish your awareness of pain, so act as analgesics (don’t feel pain)
The WAR- NSAIDs VS Opioids- NSAIDS inhibit _________ synthesis; they accomplish this by inhibiting the __________ enzyme.
The WAR- NSAIDs VS Opioids- NSAIDs inhibit ________ PG as well as PG associated with _________.
What is another name for salicyclics?
How many drugs approved by the US are in the NSAIDs family? Whats one example?
acetaminophen (Tylenol) = classified as a “__________” analgesic (not NSAID), as it works on COX-___ in the CNS, and is NOT ________.
What is the grandfather molecule of prostaglandin synthesis?
What are the four steps to forming prostaglandins? Where do NSAIDs/Salicyclics intervene?
Arachidonic Acid-->Cyclooxygenase (Salicyclics/NSAIDs inhibit here)-->Endoperoxidases--->Prostaglandins
Non-selective NSAIDs are COX-__ & ____ inhibitors.
COX-1 & 2
COX-1 leads to ________ prostaglandins which promote _________. ERGO- blocking COX-1 will lead to side effects in the _____, ______, and ______ aggregation.
cytoProtective....homeostasis....stomach, kidneys, platelet
What are the three end products of COX-1?
1.Prostacyclin-stomach endothelium 2.Prostaglandin E2-kidneys 3.Thromboxane A2-platelets
COX-2 leads to the prostaglandins that are correlated with ________...which is our goal!
Salicyclates and NSAIDs block which COX(s)?
COX-1 AND COX-2 non selectively
COX-___ Regulates the amount of stomach acid produced
Blocking COX-___ with aspirin or NSAIDS decreases production of protective _______ in the gastric lining = explains side effect of GU ulceration and bleeding
COX-___ is the inducible form which is produced when you experience trauma and need inflammatory response for healing
Drugs that block COX 2 are primarily used for ______.
COX-___ have no effect on the stomach = leave cytoprotective prostaglandins intact.
What is THE ONLY COX-2 selective inhibitor on the market?
COX-__: Recently discovered (2002), Works in the central nervous system, Suppresses prostaglandin synthesis, No anti-inflammatory effects, this is how acetaminophen (Tylenol) works (pain control but no anti-inflammatory effects)
COX-3: Works in the ______.
COX-3: Suppresses _______ synthesis
COX-3: NO _______ effects
COX-3: This is how __________ (Tylenol) works (pain control but no anti-inflammatory effects)
Non-selective NSAIDs = block both COX-__ and COX-__...MOST NSAIDs in use today (eg. ibuprofen)
COX-1 and COX-2
Selective NSAIDS = block COX-__ only....Only one available on U.S. market: _______ (_______) used primarily for arthritis pain.
Remember that acetaminophen (Tylenol) blocks COX-__ but it is NOT categorized as an _____.
What is the abbreviation of Aspirin? What is its pharmalogic class? Comes from extracts of _______.
What is the most useful salicyclate for analgesia?
What is the chemical structure of Aspirin?
Most of aspirin’s effects are due to inhibition of __________.
Prostaglandins are synthesized _______ by inflammatory stimuli.
locally...shop local broooo
Prostaglandins sensitize pain ________ to substances such as bradykinin, therefore reduction in _________ = reduction in pain.
Aspirin is MORE effective if given ______ painful stimuli are experienced
Aspirin is more effective against _______ pain (caused by inflammation) versus ______ pain (direct irritation of nerve endings)
Kinetics of ASA-Rapidly and completely absorbed from stomach and small intestine, producing peak effect on empty stomach in ___ minutes
Kinetics of ASA- Widely distributed; poorly bound to _______
Kinetics of ASA- Hydrolyzed to ________ in GI tract and via _______ effect in liver
Kinetics of ASA- Conjugated with ______ and ________ acid by liver
Kinetics of ASA- Half-life is ______-dependent, small doses = half life of __-__ hours...Higher dose = 15-30 hours
DOSE...small=2-3 hours...higher =15-30 hours
Kinetics of ASA- It follows ______ order kinetics.
Kinetics of ASA- May lead to ________ situation if take too much
Kinetics of ASA- _______ increased by alkalinization with sodium bicarbonate which increases the proportion of the aspirin that is in the ______ form that is therefore excreted
Effects of Aspirin-Analgesic:Relieves _____ to _____ pain, not potent enough for intense pain, use an opioid.
mild to moderate
Effects of Aspirin-Considered an antipyretic because it inhibits ________ synthesis in the _________....it also induces peripheral ________ and sweating.
Effects of Aspirin-Anti-inflammatory: Prostaglandins are potent vasodilating agents that also increase capillary permeability.....Inhibition causes decreased erythema and _______ of inflamed area
Effects of Aspirin-Anti-inflammatory: Important because almost all dental pain is __________ in nature....High dose aspirin is used to relieve pain and inflammation of ______ too!
Effects of Aspirin- the Analgesic dose = dosing used for pain control is NOT ENOUGH for ________ effects!
HOW many mg of aspirin is needed for anti-inflammatory effect? What are the 2 side effects of this high of a dose?
3500 mg....stomach ulceration and bleeding
Effects of Aspirin-Large/high doses (greater than ___ g per day) – produces _______ effect = excretion of uric acid in urine...At one time, aspirin was used to treat ____ but, Aspirin is no longer used for this purpose
What analgesic should a person with gout stay away from?
Aspirin...patient takes probenecid (Benemid) to excrete uric acid (stops absorption of uric acid back into bloodstream)...aspirin can ANTAGONIZE these effects
Effects of Aspirin:Anti-platelet effect = _________ effect that lasts for the life of the platelet (___-___ days)...Reduces platelet adhesiveness/aggregation by interfering with _________ (____) release = prolongs bleeding time
irreversible....7-10 days...adenosine diphosphate (ADP)
Effects of Aspirin: Aspirin inhibits cyclooxygenase which inhibits the formation of __________, which facilitates clotting, so by reducing this, aspirin reduces the risk for _______ and ______! AT about ____ mg/day
thromboxane A2...blood clots and stroke!...81 mg
￼Adverse effects of aspirin ________: dyspepsia, nausea, vomiting, gastric bleeding...WHY?
Gastointestinal..inhibits the COX-1 Cytoprotective enzymes!!
￼Adverse effects of aspirin-Stimulates chemoreceptor ______ zone in the CNS (nausea and vomiting)
￼Adverse effects of aspirin--Exacerbates ________ ulcers, gastritis, hiatal hernia, reflux disease
￼Adverse effects of aspirin- What is it called when aspirin inhibits the production of PROTHROMBIN?
Inhibits production of prothrombin = hypo-prothrombin-emia!!
￼Adverse effects of aspirin-the GI bleeding caused by aspirin is often ______!
What is the name of this syndrome??? aspirin contraindicated in children/adolescents with viral infections
Reye's Syndrome can manifest with fluid in _____ (encephalitis) and ________ = often fatal
What do we use instead of aspirin if a child is sick? (most of the time its viral origin!)
What is a classic warning sign of Salicyism (toxicity of aspirin)?
Aspirin toxicity- At high doses = _________ = produces _________; then compensatory renal loss of _______, Na and K = leads to respiratory AND _______ acidosis!!!
Death from aspirin poisoning is usually ______ and ______ imbalance
acidosis and electrolyte
Aspirin toxicity-Usually occurs in overdose ranges from __-___ grams in adults
Allergies to aspirin are pretty rare...Less than __% incidence
These are signs of a ________: rash, wheezing, urticaria (hives), angioneurotic edema, anaphylaxis
TRUE aspirin allergy
Allergy to aspirin CAN mean a person has __________ to other NSAIDs!
________ are more likely to have hypersensitivity reaction to aspirin (incidence ranges from 5- 15%)...STEEEEEVVVEEEE....THEREFORE ________ is a CONTRAINDICATION for aspirin use.
What is the ASPIRIN hypersensitivity TRIAD??
1. Aspirin Hypersensativity 2.ASTHMA 3.Nasal Polyps
Mechanism of aspirin allergy...Shift in COX cascade to inhibit
￼bronchodilating ______.....Shifts to favor unopposed lipoxygenase pathway and formation of ________ (bronchoconstrictors)
Allergic reactions look like _______ attacks = bronchial effects...in fact, in asthmatics, aspirin sensitivity develops over about ____ exposures
Cray cray patients- When aspirin is applied directly to oral mucosa, ester in water splits to ______ acid and salicylic acid and makes an "______"
Oral ulcerations = chewing aspirin-containing ____.
gum...whaaaa they make that?!
Summary...time to use your memory tricks! What are the 4 contraindications to aspirin?
1.Allergy (bronchal rxn) 2.Chronic Gastritis 3.Gout 4.Anticoagulants
Aspirin displaces ______ from plasma proteins and therefore increases risk for a hemmorage.
When is Aspirin contraindicated in pregnancy? What is the FDA category? BUT _______ aspirin has not been shown to be teratogenic.
The 3rd trimester!....C/D woah!..low dose
Aspirin and Prego-Can ______ labor (decreases prostaglandins responsible for uterine contractions)......Increases risk for _______ complications in mother....Risk of premature closing of the ________ in fetus, resulting in pulmonary vasculature abnormalities and pulmonary hypertension in newborn.
prolong (AINT NOBODY GOT TIME FOR THAT!)....BLEEDING....ductus arteriosus
Aspirin DOSING-___ mg for cardio-protective...____ mg for full strength dose (during a M.I.)
81 mg...325 mg
Aspirin Dosing- ____-____ mg every ___-___ hours UP TO ____ g per DAY!!!
325 - 650 mg...4-6 hours...up to 4 grams per day
Aspirin dosing: Children: ___-___ mg/kg/dose every 4-6 hours, up to a total of __ grams per day
10-15...4 g per day
Discontinue Aspirin? ______ aspirin therapy (81 mg daily) = NO need to discontinue
1 single dose of aspirin exerts an effect for a minimum of __ days
Discontinue Aspirin? For highly invasive surgeries, must weigh risk to patient versus bleeding risks...Eg: patients with cardiac stents are on aspirin and antiplatelet drug (Plavix) = discontinue _______ but not _______ before surgery
If patient is taking aspirin because of cardiac history, then __________ before advising the patient to discontinue the drug = benefit must outweigh risks to the patient
consult the patient’s physician!!!!
Potential for “________” risks (MI, stroke) if suddenly discontinue the use of aspirin!!
What makes a person on aspirin clot why wouldn't they just bleed out??? _____ AND endothelial cells continue to make ___________.