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93 Cards in this Set
- Front
- Back
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what is the overall MOA for NSAIDs
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inhibition of prostaglandin synthesis by inhibition of cyclooxygenase(COX)
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what is the pathologic process that causes fever?
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pyrogens increase the production of IL-1 in phaocytic cells IL-1 acts on the anterior hypothalamus to increase the production of prostaglandins. Prostaglandins increase the set-point temperature, setting in motion the heat-generating mechanism that increase body temperature and produce fever.
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what is the pathology behind peripheral pain sensation?
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b. Peripheral sensory pain receptors are free nerve endings in the skin, muscle, and viscera (nociceptors). Substance P is a neurotransmitter for nociceptors. Sensations of pain are processes by the anterolateral system.
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what is the pathology behind inflammation
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d. Acute and chronic inflammation involve products of arachadonic acid metabolism, namely prostaglandins and leukotrienes.
i. Prostacyclin (PGI2): vasodilation, inhibits platelet aggregation ii. Thromboxane A2: causes vasoconstriction, promotes platelet aggregation iii. Prostaglandin D2 and E2: vasodilation, increased vascular permeability iv. 5-HETE and LTB4: chemotaxis of inflammatory cells v. Leukotriene C4, D4, and E4: vasoconstriction, bronchospasm, increased vascular permeability |
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Describe the mechanism of action of analgesic-antipyretic and non-steroidal anti-inflammatory drugs (NSAIDs).
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a. These drugs inhibit the synthesis of prostaglandins by inhibiting the enzyme cyclooxygenase (aka prostaglandin synthetase).
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what are the three isozymes of the cyclooxgenase?
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cox-1-houskeeping isozyme its product plays a role in normal body functions and homiostatis
cox-2 is the inducible isozyme and its products promote inflammations cox-3 isnt important |
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what iszymes do NSAIDs analgesic and antipyretics work on
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Cox -1
and Cox-2 |
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what do prostaglandins cause
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alterations of vascular permeability, bronchial constriction, increased secretions
this manifests as bronchospasm, congestion, and mucus plugging |
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what are the two types of NSAIDS
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NONspecific NSAIDs-(aspirin) inhibit both cox 1 and cox-2
specific NSAIDs- inhibit only cox 2 |
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what does lipooxygenase do?
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creates leukotrienes which facilitate inflamation
some NSAIDS affect these as well as the COX |
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what are the therapeutic uses of NSAIDs
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analgesics(mainly pain from inflammation) - lower maximal effect than opoids, no addiction, free of CNS effects
antipyretic- lowers temp only during fever, by lowering prostaglandins which mediate as pyrogens and by blocking IL-1 antiinflammatory-by inhibition of PG other(dysmenorrhea, patent ductus arteriosus, colon cancer prevention |
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what are some side effects of NSAIDS
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GI ulcerations and intolerance
blockade of platelet aggreegation(inhibition of synthesis)from cox 1 inhibition of uterine motility (inhibtion of induction of labor) inhibition of prostaglandin mediated renal effects hypersensitivity reactions: asthmatic attacks, urticaria and angioedema |
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aspirin causes what irriversable effect
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inhibtion of thomboxane and loss of platelt aggregations
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if patient has hypersensitity to aspirin what could happen
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cross sensitivity to other NSAIDs
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what can be given to aleaveate GI issue caused by NSAIDs
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misoprostol(cytotec) synthetic PGE1 analog
can cause diarrhea |
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what side effects do COX 2 inhibitors not have that nonselective COX inhibitor do
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GI ulcerations and tolerance
inhibtion of platelet function |
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what is effect of aspirin
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analgesic antipyretic and antiinflammartory agent
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what is MOA of aspriin
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inhibits COX1 and COX2 through irreversible acytylation
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what is duration of Aspirin
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effects on platlets persist for 8-10days
15-30min half life |
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what are some adverse effects specific to aspirin?
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tinnitus or deafness
hepatotoxicity |
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what are sign of aspirin intoxication
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distubance of acid base balance
respiratory alkalosis(initial) metabolic acidosis(eventual) salicyclism: headache, dizziness, ringin in the ears, mental confusion, drowsiness, and sweating |
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what is a contraindication for aspirin?
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GI ulcers
asthma gout young children(reyes syndrome) |
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what are some other uses for aspirin
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juvenile rheumatoid arthritis
preventative for MI decreased incidence of colon cancer |
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what are some characteristics of diflunisal(dolobid)
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more effective and longer duration than aspirin (8-12h)
less auditory side effects than aspirin |
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what is the use of mesalamine
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local effects on treatment of inflammatory bowel disease
effective in ulcerative colitis:asacol not an NSAID |
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what is acetaminophen used for
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very good analgesic and antipyretic, but weak antiinflammatory
COX2 inhibitor so lacks many side effects of aspirin can use in GI patients |
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what are some adverse effects of acetaminophen
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fatal hepatic necrosis
increased risk in alcoholics |
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what can be used as antidote to acetaminophen overdose?
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nacetylcysteine(mucomyst)
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waht is the duration of acetaminophen
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1-4hour half life
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what is the MOA of acetaminophen overdose that leads to fatal liver necrosis
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P450 breaks acetaminophen down into a toxic intermediate N-aceyl-beta-benzoquinone imine
in normal doses that intermediate is conjugated with glutathione to become mercapturic acid which is nontoxic and excreted if there is to much of the toxic intermediate then it can bind to macromolecules in nucleophilic cells and cause cell death |
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what is a drug interaction of inomethacin(indocin)
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probenecid inhibits renal excretion of inodocin
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what are some adverse effects of inodocin
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GI: nausea, vomiting, anorexia, abdominal pain
CNS: severe frontal headache(15%) |
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what are two other uses of indomethacin
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treat acute gouty arthritis
managment of patent ductus arteriosus |
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what is sulindac a prodrug for?
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sulindae sulfide
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what are some uses for sulindae
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less ulcerogenic NSAID than aspirin
suppress polyp formation in colon cancer |
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what is a rare complication of sulindae
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renal stones
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what is the duration of sulindae
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half life of sulindae is 7hrs
half life of active sulindae is 18hrs taken twice a day |
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what are the adverse effects of tolmetin
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GI: epigastric pain, nasuea, vomiting
CNS; less common than inomethacin |
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what is another use of tolmetin
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juvenile rheumatoid arthritis
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what is MOA of diclofenac
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blocks COX and lipoxygenase so blocks both PG and leukotrienes
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what is the duratino of diclofenac
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2h half life
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what is the adverse effects of diclofenac
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less likly to cause peptic ulcer than aspirin
hepatotox not recommended for kids or mothers nursin or preg |
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what is ketorolac give as
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injection
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what is ketorolac used for
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short term management of moderatel severe acute pain
can reach opoid level pain managment with no addiction or CNS effects |
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what is ibuprofen used for
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mild antiinflammatory and analgesic
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what is durartion of ibuprofen
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2hr half life
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what dosage level is needed for anti inflammatory effects
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1200-2400mg/d
OTC only come in 200mg form so for treatement of inflammation you need prescription for higher dose tablets |
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what is duration of Naproxen
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14hr half life so fairly long
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what is the potency of naproxen
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20x that of aspririn
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what is the adverse affects of naproxen
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less GI irritation than aspirin
renal tox |
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what is MOA of ketoprofen
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inhibits both COX and lipooxygenase
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what is duration of ketoprofen
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short 2hr half life
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what are adverse effects of ketoprofen
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CNS and GI
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what is a benifit of oxaprozin
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very long half life 40-60hr
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what is duration of prioxicam
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long half life 50hr
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what is meloxicam MOA
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preferential COX 2
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what is the duration of meloxicam
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half life of 20hrs
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What is unique about nabumaetone
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ketone prodrug
preferential COX 2 inhibitor low incidence of side effects long duration(24h 1/2life) |
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what is the MOA of celecoxib(celebrex)
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the first truely COX-2 selective NSAID
only one available so it does not affect platelet aggregation or prothrombin time and does not cause ulcers |
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what is the risk of taking celebrex
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cardiovascular risk
bc of this VIOXX a similar drug was withdrawn |
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what is the black box warning for celebrex
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risk in cardiovascular patients
for long term or high dose use low dose effects uknown |
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what are the three disease modifying antirheumatic drugs?
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Abatacept
rituximab TNF-alpha blocking agents: etanercept, adalimumab, infliximab |
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what is the use of disease modifying antirheumatic drugs
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reserved fro pts who are refractory to therapeutic regimens of NSAIDs
(RA, juvenile RA) |
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what is MOA of ketoprofen
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inhibits both COX and lipooxygenase
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what is duration of ketoprofen
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short 2hr half life
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what is the MOA of abatacept(orencia)
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selective costimulation modulator, inhibits T cell activation
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what is mode of administration of disease modifying antirheumatic drugs
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IV infustion
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what are adverse effects of ketoprofen
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CNS and GI
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what is the MOA of rituximab
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monoclonal antibody binds to antigen CD20 B lymphocyts
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what is a benifit of oxaprozin
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very long half life 40-60hr
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what is the adverse reaction associated with rituximab
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fatal infusino reaction)death within 24hrs
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what is duration of prioxicam
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long half life 50hr
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what is meloxicam MOA
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preferential COX 2
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what is MOA of etanercept
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binds to TNF and blocks interaction with TNF receptors
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what is MOA of adalimumab
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binds specifically TNFalpha and blocks p55 and p75 cell survace TNF receptors
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what is the duration of meloxicam
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half life of 20hrs
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what is the duration of the TNF alpha blockng drugs
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often its quite high which allows for once or twice weakly injections
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What is unique about nabumaetone
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ketone prodrug
preferential COX 2 inhibitor low incidence of side effects long duration(24h 1/2life) |
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what is the MOA of celecoxib(celebrex)
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the first truely COX-2 selective NSAID
only one available so it does not affect platelet aggregation or prothrombin time and does not cause ulcers |
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what is the risk of taking celebrex
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cardiovascular risk
bc of this VIOXX a similar drug was withdrawn |
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what is the black box warning for celebrex
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risk in cardiovascular patients
for long term or high dose use low dose effects uknown |
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what are the three disease modifying antirheumatic drugs?
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Abatacept
rituximab TNF-alpha blocking agents: etanercept, adalimumab, infliximab |
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what is the use of disease modifying antirheumatic drugs
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reserved fro pts who are refractory to therapeutic regimens of NSAIDs
(RA, juvenile RA) |
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what is the MOA of abatacept(orencia)
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selective costimulation modulator, inhibits T cell activation
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what is mode of administration of disease modifying antirheumatic drugs
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IV infustion
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what is the MOA of rituximab
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monoclonal antibody binds to antigen CD20 B lymphocyts
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what is the adverse reaction associated with rituximab
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fatal infusino reaction)death within 24hrs
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what is MOA of etanercept
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binds to TNF and blocks interaction with TNF receptors
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what is MOA of adalimumab
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binds specifically TNFalpha and blocks p55 and p75 cell survace TNF receptors
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what is the duration of the TNF alpha blockng drugs
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often its quite high which allows for once or twice weakly injections
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what can occur when on adalimumab(humira)
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infections
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what is the MOA of infliximab
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neutralize the activity of TNFalpha inhibits binding of TNFalpha with its receptors
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what is a risk of taking infliximab
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increased risk of infection
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