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216 Cards in this Set
- Front
- Back
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what is the Neuromuscular blockers' MOA?
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competitive blockade of ACH at the pre (decreasing amount of ACH produced) and post (competes with receptor sites)synaptic neuromuscular junctions.
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what are the 2 general types of NMB drugs?
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non-depolarizing- antagonistic
depolarizing- excess depolarizing agent blocks transmission (succinyl choline) |
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all NMB drugs bear a structural resemblance to what?
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ACH - not lipid soluble, does not cross CNS, has to be given by injection
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what is succinylcholine metabolized by?
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plasma cholinesterase. It is the only depolarizng agent. Works fast and wears off fast.
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what is the fastest NMB?
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succinylcholine
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what are the 2 phases of MOA for succinylcholine?
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1- reacts with nicotinic channels, opening them, and causing depolarization
2- desensitized to the effects of acetylcholine |
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describe the MOA for the non-depolarizing drugs
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bind to the same receptors but do not cause depolarization
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with the non-depolarizing drugs, the duration of action is in direct correlation with what?
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Route of elimination
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all of the steroidal muscle relaxants are metabolized by what?
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3-hydroxy, 17-hydroxy, and 3,17-dihydroxy products mainly in the liver.
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which of the hydroxy products produces a metabolite that is still as potent as the parent drug?
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3-hydroxy
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pancuranium?
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long DOA
first one cardiovascular effects adjust dose in hepatic and renal failure |
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vecuronium?
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DOA depends on age and dose
minimal cardiovascular effect less histamine release not eliminated by the kidney |
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rocuronium?
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similar to vecuronium by has a very fast onset. 30 min DOA
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Atracurium?
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intermediate DOA
no cumulative affect 20% histamine release possilbe cis-atracuriam is its isomer metabolized by hofman producing laudanosine. |
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what are the bad things involved with laudanosine?
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crosses BBB and can cause seizures
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what is the difference between cisatracuriam and atracuriam?
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cis is a stereoisomer of it, it has less histamine and less laudanosine effect than it's parent drug. It also is metabolized the same way as the parent, by Hofmann elimination.
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which NMB is long lasting and does not have cardiovascular effects?
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doxacurium
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which NMB is the shortest DOA of all the non-depolarizing and also induces histamine release?
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mivacurium
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how is the NMB drug monitioring done?
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diaphragm strength
transdermal stimulation head lift peripheral nerve stimulation |
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does doing the peripheral nerve stimulation hasten the patient recovery?
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no
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which drugs have no cardiovascular effect?
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cisatracurium
vecuronium doxacurium |
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which drugs cause hypotension?
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atracurium
mevicurium metocurine tubocurarine |
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what can you do to leesen the effect of the hypotension causing drugs?
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pre-medicate with an antihistamine
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which drug causing tachycarida and an increase in CO?
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pancuronium
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what drug can cause bradycardia in infants and tachycardia in adults?
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succinylcholine
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what are the other side effects that can be seen with depolarizing agents?
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release of potassium into the blood (hyperkalemia). and intraocular pressure. Increased intragastric pressure.
muscle pain due to unsyncronized contraction of muscle fibers that haven't been paralyzed yet. |
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how do the NMB react with anesthetics?
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it deepens their effects, especially with isoflurane.
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with antibiotics?
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aminoglycosides, clindamycin, and tetracyclines
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what happens if you mix a nondepolarizing NMB with a depolarizing NMB?
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they tend to cancel eachother out and a larger dose will be needed.
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what affect do local anesthetics and antiarrythmics have on NMBs?
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smaller doses enhance the block from both the depolarizing and the nondepolarizing NMBs
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what affect do corticosteroids have on NMBs?
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tend to decrease their effectiveness and cause prolonged muscle weakness and myopathy.
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what drugs tend to increase the NMB
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tacrine, oral contraceptives, metoclopramide
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what about with Myasthenia gravis?
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increases the effects of teh disease
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what about with increased age?
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increased age increased the DOA
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what do you need to do if their liver is bad?
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decrease the dose
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what about with paitients with severe burns?
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require higher doses because they tend to be resistent to the non-depolarizing agents
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what can reverse their effects?
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cholinesterase inhibitors- neostigmine, physostigmine, and edrophonium (aCH-E only)
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which NMB do they not have an effect on?
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mivacurium
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what is the difference between spasm and spasticity?
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spasm- sudden, violent, involuntary, accompanied with pain
spasticity- increased tone , heightened deep tendon reflexes, hypertonicity, and involuntary jerks, often associatred with muslce weakness. |
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what rugs are used to control spasticity?
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dantroline, diazepam, tinazadine, baclofen
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WHAT OTHER EFFECT DO ALL OF THE MUSCLE RELAXANTS HAVE?
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sedating, enhanced by alcohol, are not superior to the analgesics or anti-inflammatories
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what is the MOA for the muscle relaxants?
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unknown
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what is baclofen?
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GABA-mimetic agent (GABA-B). Inhibits the release of substance P. Used in spinal spasticity and MS. 10-20 oral, or .5-2 intrathecally
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side effects?
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drowsy, fatigue, nausea, vertigo, muscle weakness, depression, headache, may control seizure control in epilepsy patients. Careful with MS and elderly, cause they are more sensetive to it. Best to gradually increase the dose
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Botultoim toxin?
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blocks pre-synaptic release of ACh.
used to treat strabismus and blepharospasm. |
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Carisoprotol?
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releives spasm better than placebo, but sucks otherwise. Good at conroling acute musculoskelatal condtions.
|
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sideeffects?
|
drowsy, decreased heart rate, flushing, CNS depressant, trembling, headache, hiccups, angiodema
|
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Chlorzoxasone?
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superior to diazepam, good for short term relief, not good for long term relief.
|
|
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side effects?
|
hepatocellular toxicity
same as cariprotol. Take with food or milk. |
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clonidine?
|
A-agonist
rarely used alone HoTN |
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Cyclobenzaaprine?
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drowsiness, dizziness, lightheadedness, xerostomia
long half life. helpful with patients with trauma or acute muscluar skelatal pain. |
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Dantroline?
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used to treat spasticity
small effect on cardiac and smooth muscle can cause dose-dependant muscle weakness. Used to treat malignant hyperthermia |
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Diazepam?
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GABA-A receptors
very sedating at doses needed to alter muscle tension can cause drowsiness, fatigue, and ataxia |
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Metaxalone?
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sedative properties. Helps patient sleep. Careful with seizure patients
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Methocarbomol?
|
adjunctive medicationused in the treatment of tetanus
sedative same sideeffecrts |
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orphenadrine?
|
structurally related to diphenhydamine
no direct skeletal muscle relaxant activity can intereact with propoxyphene- causing confusion, anxiety, and tremor. |
|
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Tizanidine?
|
antispastic. A-agonist
NOT SEDATING better tolerated than baclofen and diazepam dry mouth, hallucinations interacts with Cipro, and fluvoxitine. Care ful with oral contraceptives, causes levels to go down. |
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what does an increase in gout correlate with?
|
age, serum creatinine, blood urea nitrogen, male, BP, body weight, and alcohol intake
|
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what drugs are capable of causing gout?
|
diuretics
Salicyates cytotoxic drugs Ethanol L-Dopa Pyrazinamide Ethambutol Nicotinic Acid Vit B-12 Cyclosporine |
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what drug is used to prevent the recurrent episodes of gout and meditarranean fever, and can have a mild beneficial effect on sarcoid arthrtitis?
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Colchicine
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MOA of colchicine?
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binds to intracellular protein tubulin, preventing polymerization into microtubules. Inhibits leukocytes migration, phagocitation, and formation of leukotrienen B4.
|
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side effects of Colchicine?
|
diarrhea, nausea, abdominal pain.
GI toxicity elderly can become dehydrated and lose electrolytes. hair loss bone marrow depression peripheral neuritis myopathy fatal ascending CNS depression do NOT take with Alcohol |
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|
Dose?
|
give early.
.5-1 mg initially .5-.6 grams every 2 hours until episode subsides, side effects occur, or pt. has taken 12 tablets. (no more than 8 mg in 24 hours) prophylaxis= .5 mg 1-3 times/day PO= initial 2mg, 1 mg 6-12 hours later. total dose is 4 mg |
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who should not get colchicine?
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neutropenia
difficult to inject veins renal problems liver problems |
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what is the success rates with using colchicine?
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<12 hours after attack = 75-95%
>24 hours much less START IT EARLY |
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how do NSAIDs treat gout?
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inhibit prostaglandin synthesis and urate crystal phagosytosis.
don't use aspirin Oxaprozin lowers serum uric acid. Don't use it during an attack. |
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what NSAID is most often used to treat gout?
|
Indomethacin
50-75mg initially, then 50mg every 6 hours for 1-2 days, then 25-50mg every 8 hours for 1-3 days |
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why don't you want to give indomethacin to elderly patients?
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becuase of the prostaglandin inhibiton in renal function
|
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what are the uricosuric agents?
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probenacid and sulfenpyrazone
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what do they do, and when are they usually used?
|
they decrease the body pool of urate. Usually used when tophi are determined, when thet patiet has several gouty attacks, or the patient has a high level of plasma uric acid.
2-3 weeks after the gouty attack. don't use in high secreters. maintain a high urine flow. |
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what is the MOA of the uricosuric drugs?
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they decrease the amount of uric acid that is reabsorbed in the tubules in the kidneys so that more of it is excreted.
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ADRs?
|
GI irritation (sulf)
rash (pro) nephrotic syndrome (pro) aplastic anemia (both) |
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doses?
|
pro-500mg, then to 1g after a week. Increase dose by 500mg every 6 months until 2-3 grams/day.
sulf- not often used |
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fenofibrate?
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lipid lowering agent, also limits reabsortion of uric acid in distal tubules.
|
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losartan?
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raises urine pH so the risk of stones is less. also acts as a uricosuric
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Allpurinol?
|
lifetime therapy
works for under-excreters and over producers reduces UA synthesisby inihibiting xanthine oxidase also used for the treatment of cancer to prevent the high uric acid levels that follow chemotherapy. |
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|
when is it used?
|
chronic gout,
not for acute use 24-hour uric acid test when the uricosurics don't work used for renal stones or impariments |
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ADRs?
|
N/V, diarrhea, skin rash, maculopapular lesions, exfoliative dermatitis
acute atttacks neuritis bone marrow suppression hepatic toxicity aplastic anemia interstitial nephritis |
|
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dose?
|
100 mg, can increase it
|
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Febuxostat
|
xanthine oxidase inhibitor indicatred for chronic managment
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ADRs?
|
upper respitory infections
diarrhea can block clearance of xanthine-based drugs like azathioprine or theophyline, but does not interact with naproxen, colchicine, or indomethacin |
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Rasburicase MOA?
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oxidizes urate to allantonin, it also breaks down pre-existing UA as well, where allopurinol does not. Also is used for tuomr lysis syndrome
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what are the non-pharmacoligical treatments for RA?
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rest
excersize diet/weight control physical/occupational therapy |
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what do we need to consider when deciding what to give to patients concerning NSAIDs?
|
Cost
DOA patient tolerability acceptance NSAIDs do not modify disease progression or joint destruction they are used for the analgesic effect, and eventually the anti-inflammatory effect. |
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why are corticosteroid used to treat RA?
|
used to treat the inflammation until the DMARDs start working, or if the DMARDs don't work, or with acute flares. Want to use them sapringly to avoid ADRs (prednisone 10 mg/day, can cause bone loss)
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what is the problem with using them chronically for anti-inflammatory uses?
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stop working after a year
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what 2 cytokines are overproduced with RA?
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TNF-alpha
IL-1 |
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what role does IL-1 take?
|
destruction of the bone.
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what role does TNF-alpha take?
|
growth of rheumatoid synovial tissue
WBC production of proteases production of other inflammation causing cytokines (IL-1, IL-12, IL-8) |
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what is the best way to stop the progression of RA?
|
non-biological DMARD + MTX + TNF inhibitor
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what are the advantage of using DMARD's?
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reduce S&S
reduce functional disability retard radiographic progression |
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Methotrexate?
|
drug of choice for moderate to severe disease.
decreases TNF and increases IL-10 60-70% show goodd response |
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ADR's?
|
GI, cirrhosis, myelosuppression, alopecia, stomatitis,
check CBC every 4 months and liver every year folate can help with ADR's |
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sulfasalazine?
|
anti-inflammatory and immunosuppressive and antimicrobial
suppresses TNF, IL-1, neutrophil migration and chemotaxis, and enhances the release of adenosine. |
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ADR's?
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25% stop taking it due to ADR's
GI rash hepatitis blood dyscrasia |
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Leflunomide?
|
prevents CD4 proliferation, alters conc. of IL-2 and growth factors, and inhibits leukocyte adhesion, can work for a long time. It is very expensive compared to methotrexate
is changed to an active metabolite quickly. 1/2 life = 2 weeks |
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what are the ADRs?
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alopecia, rash, diarrhea.
Do not use in women of child bearing years that are not using contraception |
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what is Hydroxychloroquine
|
MOA: suppresses lysosomal enzymes, inhibits B and T cells and IL-release.
Used for mild early therapy. can take up to 4 months to see results. |
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ADRS?
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rash
bone marrow suppression irreversible retinopathy (mostly with chloroquine) GI issues |
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Azathioprine?
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inferior to methotrexate
usually only tried on patients that don't respond to other treatments. |
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ADRs?
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N/V/D
bone marrow suppression hepatic inflammation lymphoproliferative cancer |
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what other antibiotics are used in treating RA?
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minocycline (most common)
doxycycline azithromycin rifampin metronidazole usually only used early in the disease. used in patients during the refractory period. |
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inflixamab is a chimeric molecule, what does it indicate?
|
part mouse, part human for the IgG molecule. It binds to TNF-A. It is very expensive.
used for RA chrone's disease psoriatic arthritis and plaques ankylosing spondylitis |
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ADRs?
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N/V/D
headache abdominal pain respiratory problems can develop antinuclear antibodies to dounvle stranded DNA. Don't use with anakinra give any vaccinastiond before giving this drug |
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Etanercept?
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anti-TNF
14-90 days to start working can be combined with methotrexate |
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ADR's?
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same as inflixamab, but can cause more infections. Causes injection site reactions
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Adalimumab?
|
TNF antagaonist
fully human recombinant monoclonal antibody 3 month onset inhibits progression of RA and decreases the damage. subQ injection can be used alone or with methotrexate don't use with anakinra |
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what are the 3 previously mentioned drugs mostly used for?
|
moderate to severe RA.
inhibits the progression of physical damage best when used with methotrexate |
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MOA of Anakinra?
|
blocks IL-1
don't use with TNF blockers can be used with other DMARDs injection site reactions don't use if patient is on an antibiotic OK to use with pregnancy |
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Abatacept?
|
soluble cytotoxic T-lymphocyte associated antigen for Ig.
Can be used with the non-biological DMARDs decreases cytokine release and B cell activation and autoantibody production. |
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Rituximab?
|
Anti CD20 Chimeric Mab
depletes B cells with CD20 on thier surface associated with hypersensitivity reaction (steroids reduces rxn) can give with methotrexate |
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what is sodium hyaluronate?
|
a lubricant that is injected into the joint.
do not use in sites that have inflammation or infection. don't use if patient is allergic to eggs or feathers |
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what is glucosamine sulfate?
|
a building block necassary for building new cartilage.
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ADR's?
|
drowsiness
Headache high blood glucose in diabetics insomnia |
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why do seizures occur?
|
hereditary
mental retardation elderly- CV disease, tumor, trauma, metabolic disorders, CNS abnormal potassium deficiency in ATPase idiopathic neurotransmitters |
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what is the difference between partial and generalized seizures?
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partial (60%) originate on one side of the brain, while generalized originate from both.
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describe what is commonly seen in a simple partial seizure?
|
still conscious
unilateral clonic jerking sensory abnormalities flushing or piloerecrtion deja vu |
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what are complex partial seizures?
|
same but also causes unconsciousness.
Aura may precede a partial seizure that grows into a generalized seizure. |
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what is an absence seizure?
|
common in children
generalized abrubt episodes of loss of awareness like a staring spell. can have coordinated involuntary movement or clonic movement |
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what is a primary generalized tonic-clonic seizure
|
aura (can feel it coming on)
immediate pre-tonic clonic phase loss of consciuosness flexion and extention of extremities (tonic) followed by jerking (clonic) and afterwards is drousy and confused. |
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how do antiepileptics control seizures?
|
elevates the threshold of neurons to chemical snd electrical stimuli
.limit propagation of the seizure discharge from the origin. these are done by depression of the synaptic transmission or reduction of nerve conduction. |
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what are the 3 different MOAs of the antiepileptics?
|
1- Na channel inactivation (prolongs it, reducing it from firing at high frequencies, phenytoin)
2- Ca slow channel current reduction (reduces current in generalized absence seizures, thosuximide) 3. potentiate GABAergic inhibition (makes more GABA available and enhances CL influx, benzodiazepines) |
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what types of seizures is phenytoin the drug of choice for?
|
partial simple and complex, generalized tonic clonic and status epilipticus. (it is not the drug of choice for absence and myoclonic)
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what type of seizure is carbamazepine the drug of choice for?
|
myoclonic.
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what type of seizure is ethosuximide the drug of choice for?
|
absence
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what type of seizure uses phenytoin and aslo diazepam together as the first drug of choice?
|
status epilipticus
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other than just the Na channel inactivation, what elee is effected by phenytoin?
|
Ca channel inhibition during depolarization
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why does phenytoin not want to be used with absence seizures?
|
it can make them worse.
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ADRs of phenytoin?
|
CNS depression (cerebellum or vestibular)
N/V gingival hyperplasia megaloblastic anemia behavior changes inhibition of ADH teratogen |
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since phenytoin is metabolized by CYP-450, which drugs can stimulate it to go quicker and which ones will inhibit it?
|
inducer- carbamazepine, phenobarbital, alcohol
inhibitor- phenobarbital, diazepam, fluconazole, estrogen, isoniazid. |
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what is fosphenytoin?
|
prodrug for phenytoin. faster rate of administration. Works better but can only be used for 5 days.
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how does carbamazepine work?
|
Na channel blocker in brain. It is also used for trigeminal neuralgia and manic depression
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adrs?
|
stupor and coma
respitory problems N/V apalstic anemia liver toxicity highly lipid soluble autoinduction (shortens half life after a few weeks). |
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what are the inducers and inhibitors for carbamazepine?
|
inducers- phenobarbital, phenytoin, valproic acid
inhibitors- cimetidine, diltiazem, erythromycin, isoniazid, propoxyphene |
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|
Risk factors for developing thrombi are what?
|
age
obesity oral contraceptives immobilization cancer trauma or major surgery COPD MI ulcerative colitis |
|
|
describe a clot formation
|
vasc injury- collagen released- platelet adhesion- platelet release reaction- activation of the 2b-3a integrin receptor- platelet aggregation
|
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what does the intrinsic coagulation system start with?
|
factor 12
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what does the extrensic coagulation system start with?
|
factor 7
|
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what are the body's inherent anticoagulation system?
|
protein C
protein S antithrombin 3 |
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what is factor 1 in the complement system?
|
fibrinogen
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what is factor 2 and what affects it?
|
prothrombin- heparin and warfarin
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what is factor 7 and what affects it?
|
proconvertin - warfarin
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what is factor 9 and what affects it?
|
christmas factor, CPT - warfarin
|
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what is factor 10 and what affects it?
|
stuart prower factor- heparin and warfarin
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heparin MOA?
|
stimulates antithrombin 3
inactivates thrombin and factors 9-12. |
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what is heparin used for?
|
pulmonary embolsim
deep vein thrombosis stroke |
|
|
ADR'S?
|
bleeding
osteoporosis thrombocytopenia alopecia paradoxical thromboembolism heparin induced thrombocytopenia |
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contraindications?
|
heavy bleeding
hemophilia thrombocytopenia active hepatic or renal disease |
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how is it given and how is it monitored?
|
IV, SQ
monitored by APTT and platelet count |
|
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antidote to heparin?
|
protamine sulfate
|
|
|
LMWH MOA?
enoxaparin, dalteparin |
activate antithrombin 3
more specific for factor 10 |
|
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uses?
|
DVT- prophylaxix and treatment
unstable angima and non Q wave MI |
|
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adrs?
|
bleeding
thrombocytopenia rash |
|
|
contraindications?
|
active bleeding
thrombocytopenia |
|
|
administering and monitoring?
|
SQ
anti factor 10 |
|
|
antidote?
|
protamine sulfate
|
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|
which is UH or LMWH more specific to factor 10 and has a hgher % of bioavailabilitiy?
|
LMWH
|
|
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what is the warfarin MOA?
|
interferes with hepatic synthesis of vitamin K depedant factors 2 7 9 10
impairs function of protein C and S |
|
|
what is warfarin used for?
|
atrial fibrillation
heart valves PE DVT stroke hypercoagulable states |
|
|
describe the availability of warfarin
|
100% bioavailable
99% bound to albumin CYP 450 metabolized to inactive long half life 36-42 hours S-warfarin stronger than R. |
|
|
what order are the vit K factors inactivated?
|
7,9,10, 2
|
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ADRs
|
bleeding
skin necrosis alopecia |
|
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contraindications
|
pregnancy
active bleeding |
|
|
how is warfarin administered and monitored, and what is the antidote?
|
PO, IV
PT/INR Vitamin K |
|
|
what drugs will enhance the effect of warfarin?
|
amiodarone
sulfamethoxazole ketoconazole itraconazole |
|
|
what drugs decrease the effect of warfarin?
|
rifampin
barbituates carbamazepine phenytoin |
|
|
what other things don't necassarily enhace warfarin itself, but indirectly can increase the systemic effect of warfarin?
|
NSAIDS
COX2 inhibitors ASA fever diarrhea hyperthyroidism CHF cirrhosis |
|
|
what are the thrombin inhibitors?
|
bivaliruden
refludin hirudin argatroban- only acts at binding site the rest directly inhibit thrombin. |
|
|
ADR's?
|
bleeding
fever abnormal LFTs |
|
|
CI?
|
hypersensitivity
|
|
|
administration?
monitoring? antidote? |
IV
aPTT, ACT none |
|
|
what is the factor 10a inhibitor?
|
fondaparinux
|
|
|
uses?
|
prophylaxis of DVT and treatment of DVT and PE
|
|
|
ADR's?
|
bleeding
fever anemia |
|
|
CI's?
|
hypersensitivity
bleeding severe renal impirment BW less than 50 Kg. |
|
|
administration?
monitoring? antidote? |
SQ
antifactor 10a none |
|
|
MOA for Danaparoid?
|
prevents fibrin formation in the coagulation pathway
|
|
|
use?
|
prevent DVT
|
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|
ADR's?
|
bleeding
fever |
|
|
CI's?
|
hypersensitivity
active bleeding |
|
|
admin?
monitoring? antidote? |
SQ
anti factor 10a none |
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what are thrombolytics?
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break up a already formed clot.
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alteplase?
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preferentially activates plasminogen that is bound to the fibrin.
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streptokinase?
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combines with proactivator plasminogen
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urokinase?
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directly changes plasminogen to active plasmin.
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when evualating someone for hyperlipidemia, what is considered a high risk patient?
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someone with congestive heart disease and a ldl level over 100.
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what is a considered a moderately high risk?
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2+ risk factors and cholesterol above 130
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what is considered a moderate level?
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2 risk factors and a cholesterol above 160
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what is considered a low risk?
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0-1 risk factor and cholesterol above 190.
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what are the risk factors associated with hyperlipidemia?
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waist size - men=40, women=35
triglycerides count >150 HDL count men<40, women<50 HTN fasting glucose >110 smoking homocysteine conc. >8 males older than 45 females older than 55, or younger with menopause. Familial history of father before age 55, or mother before age 65. |
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what is considered a negative risk factor?
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a HDL higher than 60.
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what is the therapy of choice for high cholesterol?
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statin
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what is the MOA for statins?
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reduce hepatic cholesterol synthesis, which increases the uptake of non-HDL particles from the systemic circulation.
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what are the common side effecs for statins?
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myalgia- complain of elbows and knees hurting.
GI intolerance complain of flu symptoms |
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how much of a change do you get by increasing the dose with statins?
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not much, you get the biggest change with the smallest dose.
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how does statins affect the triglyceride levels?
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the higher your triglycerides, the bigger the effect of the statins.
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what is the second drug of choice for hyperlipidemia?
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BAR's- bile acid resins
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what are the BAR's MOA?
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they decrease the LDLs by decreasing the bile reabsorption.
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what are the major adverse effects for BARs?
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flatulence
bloating |
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what are the contraindications for using BARs?
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triglycerides >400 - it will actually increase the levels.
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what is the MOA for nicotinic acid (niacin)?
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decreases the hepatic production of VLDL and apo B.
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what are the side effects for Niacin?
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flushing- aspirin beforehand will help combat the flushing.
can also increase the risk of hepatotoxicity. |
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what are the MOA for the fibrates?
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increase the VLDL clearance and synthesis
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side effects?
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GI
rash myalgia gallstones |
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what are the benefits of the fibrates?
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reduce major coronary events
reduce progression of coronary lesion does not decrease the chance of mortality. |
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what is the MOA of ezetimibe.
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stops cholesterol absorption in the GI
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how is it usually used?
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an add on to a statin.
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what is an important contraindication for ezetimibe?
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cyclosporine
causes severe liver enzyme elevation category C for pregnancy |
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what things can be used as add-ons with statins?
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ezetimibe
bile acid sequestarents PPAR Fish Oil Niacin |
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what are the pros of adding these things to a statin?
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better control
increased HDL decreased TG decrease LDL increase LDL particle size |
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what are the cons of adding on to a statin?
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increased cost
increased myositis risk increased hepatic risk increased potential for other drug interaction lack of outcome data. |
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what are some other effects of adding fish oil to a statin other than lowering your cholesterol level?
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reduction in malignant ventricular arrythmias
increased heart rate antithrombc efects anti-inflammatory effects slight lowering of blood pressure |
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what is the difference between drug abuse and drug misuse?
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abuse- use in a manner inconsistent with social norms in the attempt to alter mood or feeling state.
misuse- inappropriate use of a drug intended for therapeutic reasons. |
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what is the difference between addiction and physical dependance?
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abuse- psychological
dependance- physical change when drug is taken away. |
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what is the difference between tolerance and withdrawal?
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tolerance- bigger dose with same effect
withdrawal- happens with a person that is physically dependant. |
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what is cross tolerance and dependance?
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ability of one drug to suppress the manifestations of physical withdrawal produced by another drug and to maintain the physically dependant state.
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