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213 Cards in this Set
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4 clinical symptoms in Parkinsons and patient population
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akinesia
tremor rigidity gait disturbances affect 1% of population of 65 |
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Cause of Parkinson's
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The Nigrostriatal Projection
dies in Parkinson’s |
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Role of acH dopamine and gaba in Parkinson's
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Dopamine inhibits gaba release
ACh stimulates gaba release without dopamine Gaba cannot be shut off |
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Selegiline mechanism
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inhibits MAO-B which and MPTP cannot be broken down to MPP+,
MPP+ damages substantia nigra |
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precursor for dopamine
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L-Dopa
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where is most L-DOPA metabolized
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the periphery
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side effects of L-DOPA
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nausea, cardiac arrhythmias
orthostatic hypotension psychotic symptoms, dyskinesias on-off pheenomenon |
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What is the on-off pheenomenon
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PD symptoms are controlled (may have dyskinesias)
off - symptoms are not controlled (may have dystonia) due to fluctuating level of drug |
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How is on-off pheenomenon reduced
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inhibit COMT and MAO-B
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3 contraindications for L-Dopa
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psychosis
melanoma (dopa is precursor for melanin) narrow angle glaucoma (a agonist) |
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extracerebral metabolism of L-DOPA is enhanced by
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B6
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How do non-selective MAO inhibitors interact with L-DOPA
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prevent dopamine metabolism which could lead to hypertensive crisis
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When is L-DOPA most effective
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first 3-4yrs then get side effects
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What two symptoms of parkinson's is L-DOPA best at treating
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bradykinesia and akinesia
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This drug inhibits L-AAD (which metabolizes L-DOPA) in the periphery
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carbidopa
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Mechanism of tolcapone
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inhibits COMT in periphery and brain so L-DOPA can enter the brain.
entacopone only inhibits in periphery |
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What isnt helped by LAAD and COMT inhibitors
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CNS effects may be worsened due to increased DA
includes dyskinesias psychotomimesis |
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How is on-off pheenomenon reduced
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inhibit MAO-B and COMT
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Side effects of carbidopa and tolcapone
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Tolcapone - diarrhea, liver tox >entacapone
worsen side effects of L-DOPA may need to reduce L-DOPA dose with tolcapone |
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Drug that inhibits metabolism of Central DA by inhibiting MAO-B
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Selegiline
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Why are smokers at less risk for getting parkinsons
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Nicotine is neuroprotective and releases DA
smoking may inhibit MAO-B |
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Two side effects of selegiline
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L-DOPA side effects worsened
hypertensive crisis if patient is also on non-selective MAO inhibitor |
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Two drugs that stimulate D2 receptors centrally
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bromocriptine
ropinirole |
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use of D2 agonists
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ldopa dose reduction
alleviates on-off use in patients desensitized to ldopa |
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Side effects of D2 agonists, how can one of these side effects be relieved
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nausea
hypotension (give dopamine antagonist that does not cross bbb) |
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Central side effects of D2 agonist
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dyskinesia, psychosis
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advantages of ropinirole over bromocriptine
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titrated easily
fewer gi problems good for young patients |
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Contraindications for D2 agonists 5
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psychosis
recent MI peripherial vascular disease peptic ulcers |
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This drug enhances dopamine release by inhibiting its uptake
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Amantidine
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uses for release enhancers
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initial therapy
reduce bradykinesia, tremors, rigidity early on may be short lived |
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Amantidine side effects
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mild
restlessness, depression, irritability, insomnia, agitation, excitement, confusions, hallucinations overdose can produce acute toxic psychosis |
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mechanism of benztropine
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muscarinic antagonist
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anticholinergics are most useful for what symptoms in parkinsons
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mild parkinsons tremor and rigidity over bradykinesia
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side effects of anti aCH centrally
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drowsy
confusion inattention restlessness |
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side effects of anti aCH peripherilly
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dry mouth
blurred vission mydriasis urinary retention nausea vommiting |
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contraindications for anti aCH 3
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prostatic hypertrophy
obstructive GI disease narrow angle glaucoma |
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mechanism of all antipsychotics
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block D2 receptors, increase cAMP
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Amphetamines effect on DA
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increases release through facilitated transport
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How long does it take for d2 blockers to work and why
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4-6 weeks since neuron will rapidly fire initially but then dies off
"depolarization inactivation" |
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D1, D5 function
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activate CAMP
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D3 location
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limbic
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D4 receptors have a high affinity for this drug
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clozapine
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reason for parkinsons effects with a D2 blockers
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your blocking dopamine in nigrostraiatal projection
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this drug is a phenothiazine, used for acute tx of psychosis, potentiates anesthesia (puts people to sleep)
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chlorpromazine
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advantage of haldol over chlorpromazine
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less sedation
less alpha block |
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2 ways atypical antipsychotics differ from typical
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lower EPS side effects
increased ratio 5HT2:D2 blockade |
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first atypical, no eps, selective for causing DPI only in mesolimbic pathyway
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Clozapine
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which generation of antipsychotics is used to treat negative and positive symptoms of schizo
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atypicals
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major side effects of Clozapine
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Agranulocytosis, diabetes
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dose-dependent atypical, no risk of agranulocytosis
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Resperidone
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atypical antipsychotic associated with diabetes, and serious weight gain
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Olanzapine
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This drug is a partial agonist at D2 receptors, blocks 5HT2 and partial agonist at 5HT1a
no risk of diabetes |
Aripiprazole
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advantage of partial D2 agonist
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decrease dopamine in accumbens
increase in cortex |
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APS side effects 1-5 days
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acute dystonia (muscle spasms)
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APS side effect 5-30 days
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parkinsoniasm
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aps side effect 5-60 days
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akathisia (restlessness)
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Late occuring APS side effect
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tardive dyskinesia
often irreversible |
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tardive dyskinesia mechanism
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dopamine receptor supersensitivity
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Neuroleptic Malignant syndrome
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Fever, Encephalopthy, Vitals unstable, elevated enzymes, rigidity of muscles
D2 block in hypothalmus |
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Why don't you add an anti ach with Tardive dyskinesia
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due to D2 upregulation, this will make the symptoms worse
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specifically, which drugs are used to treat Parkinson's
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Bromocriptine, Amantadine, Levodopa, Selegiline, Antimuscarinics (BALSA)
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opiod pruritis caused by..
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histamine release
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opiod GI effect
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antidiarrheal/constipation
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opiod mood effect
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euphoria
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opiod bladder effect
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urinary retention
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opiod labor effect
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prolonged labor
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opiod pupil effect
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miosis
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three families of opiods are
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POMC - beta endorphin
Enkephalins Dynorphins |
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where do pro-enkephalins and pro-dynorphins act
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the brain
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prime opiod receptor for most drugs
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Mu - analgesia, respiratory depression, euphoria, dependence
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two non-opiod receptors and their effects
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sigma - agitation, hallucinations, dysphoria
DM- antitussive |
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opiods effects on cAMP, Ca, K+ channels
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inhibit camp, inhibit ca channels, activate k+ channels
decreases firing of neuron and inhibits neurotransmitter release |
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opiods effect on pulmonary edema
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reduces preload, afterload, anxiety to help acute PE
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opiod site of action
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SAme DAve
afferent pain nerves dorsal horn thalmus, limbic system, cortex |
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opiod action on ascending pathways
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inhibits
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opiod action on descending pathways
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excites
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opiods are ineffective against what types of pain
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fast, and neuropathic
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antitussive effects are mediated by which receptor
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DM receptor which is not stereoselective, so d and l steroisomers will bind DM.
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opiod effect on gastric empyting
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delayed, this is a source of drug-drug interaction
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Does tolerance develop to peripheral opiods that are anti-diarrheal
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NO
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cause of death from opiod overdose
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respiratory depression
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triad of opiod overdose
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respiratory depression
coma pinpoint pupils |
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opiod effect on temp.
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hyperthermia
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opiod effect on thoracic compliance
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decreases
truncal rigidity |
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opiod effect on bilary tract
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contraction/spasm > bilary colic
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hormones increased by opiods
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GH, ADH, prolactin (inhibits sexy time)
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hormones decreases by opiods
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(FSH, LH, CRF, ACTH)
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opiod effect on intracranial pressure
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increases
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opiod effect on immune function
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inhibits
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opiod cautions and contraindications
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head injuries
pregnancy asthma/copd impaired renal/liver function addisions/hypothyroidism (lower dose) substance abuse history |
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common opioid drug interactions
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MAOIs
sedative-hypnotics;anti-psychotics -respiratory depression |
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why do oral doses of opioids have to be higher then IV
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1st pass metabolism
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morphine 6 glucorinide
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full agonist at mu receptor
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morphine 3 glucuronide
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not opioid mediated, seizures at high does
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how is merperidine metabolized in the liver
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demethylated to normerperidine which is toxic in the CNS
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How is codeine metabolized in the liver
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demthylated to morphine
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what effects do not exhibit opioid tolerance
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constipation and miosis
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opiod effect on tolerance
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Tolerance does NOT affect safety: the therapeutic index remains unchanged, as the analgesic effects and respiratory effect tolerances go up in parallel.
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define Equi-Analgesia
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the ability of all full agonists to achieve the same analgesic affect (i.e. same level of pain reduction)
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4 high efficacy opioid agonists
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morphine, fentanyl are first line
merperidine and heroin are second line |
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use of fentanyl
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short acting for anesthesia
transdermal for maintenance buccal for breakthrough pain |
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How is heroin different from morphine
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o Pro-Drug Deacetylation Turns into Morphine
o Crosses the BBB within seconds (=ADDICTIVE) |
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There are greater in meperidine than morphine
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vomiting
dizziness antimuscarinic activity toxicity |
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These are less in merperidine than morphine
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potency
duration cough suppression smooth muscle effects |
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normeperidine adverse effects
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2. Inhibits MAO
a. ↑ NE Release from displacement – i.e. Tyramine Hypertensive Crisis |
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Three low efficacy opioid analgesics
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codeine, oxycodone, propoxyphene
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Use of codeine
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codeine produces an antitussive (anti-cough) effect at much lower concentrations than required for an analgesic effect
o Causes significant histamine-release |
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Highest efficacy of the low medium oral opioids
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Oxy, pill is crushed in drug users causing a higher effective dose
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Propoxyphene toxicities
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) CNS Toxicity (like meperidine) 2)Cardiotoxicity
o Norprophoxyphene – TOXIC METABOLITE |
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This drug has mixed opioid receptors effects
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pentazocine
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Benefits of a mixed agonist
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lower dependence
toxicity uncommon however there is a ceiling on analgesia and it can cause withdrawel in pts on full agonists |
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dextromethorphan and loperamide are what class
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non-analgesic opioids
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dextra use
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cough syrup
DM receptors |
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loperamide use
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antidiarrheal
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Opiod antagonist
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Naloxone
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ADME of Naloxone
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rapid acting, short duration
if you give this drug to someone who has passed out due to opioid overdose, that person may literally “jump up off the gurney” once the drug has taken effect (because it will stop the toxic affects that have rendered the person comotose) |
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What are the two systems that metabolize alcohol.
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ADH (liver and gut)
Microsomal Ethanol Oxidizing System |
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What enzymes metabolizes etOH below .1%
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ADH
MEOS is above .1% |
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What is the basis for a breathalyzer test
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etOH can be excreted through the lungs
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what substances may cause a disulfaram like reaction?
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oral hypogylcemics
metronidazole some cephalosporins |
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What drugs when taken with acute alcohol can cause CNS depression
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antihistamines
TCA narcotics anticonvulsives benzodiazepines |
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chronic alcohol use with what drug increases risk for hepatotoxicity
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acetaminophen
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etoh concentration (weight/vol)
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1g/100ml
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vd for alcohol
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.7L/Kg
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how long does it take for ADH to metabolize 1 drink
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1-1.5hrs
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mechanism for metabolic tolerance of etOH
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induction of MEOS system
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possible mechanism for FAS
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aberrant neuronal and glial migration during development
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drug of choice for etOH withdrawal symptoms
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clonidine
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reason for use of Naltrexone in alcoholics
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naltrexone is a mu opiod receptor antagonist.
Opioid receptors are upregulated by alcohol. Naltrexone reduces relapses by short circuting the reward pathway |
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possible mechanism of acamprosate
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decrease gaba
increase nmda its an antiepileptic medication similar to Topiramate |
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drug used to treat methanol and ethylene glycol metabolism
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Fomepizole
blocks ADH |
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toxic metabolites of methanol
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formaldehyde - acidosis, retinal damage
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toxic metabolite of ethylene glycol
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oxalic acid - acidosis, nephrotoxicity
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beta blocker used to reduce etOH withdrawal
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propanolol
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benzo used to treat etOH withdrawal
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diazapem
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Ondansetron mechanism and use
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5HT blocker
Ondansetron lowers the cravings for alcohol, especially in early-onset alcoholics. In one cognitive-behavioral therapy study, ondansetron patients with early-onset alcoholism had fewer drinks per day and reported more days without drinking at all, as compared to the other groups in the study |
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Function of ergosterol
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it is used in fungal cell membranes as a membrane stabilizer.
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mechanism of Azole drugs
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• Azoles decrease the synthesis of ergosterol by inhibiting fungal cytochrome P450 enzymes, which converts Lanosterol (a precursor) to Ergosterol. Blocking a certain P450 enzyme reduces the amount of ergosterol
fungicidal |
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azole spectrum
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They are broad spectrum, with coverage that includes candida, Cryptococcus, blastomycosis, histoplasmosis, dermatophytes
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Unique to fluconazole
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o Best penetration of all the azoles in the cerebral spinal fluid
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When two situations is fluconazole the drug of choice?
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cryptococcal meningitis
o A drug of choice for prophylaxis in high risk neutropenic patients (e.g. bone marrow transplant) and HIV/AIDS patients with recurrent oral or esophageal candidiasis, but resistant strains becoming more common |
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Fluconazole adverse affects
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Rash, Steven Johnson
inhibits CYP2C9 - increases serum phenytoin, warfarin |
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This is the drug of choice for dimorphic fungi (histoplasma, blastomyces, and sporothrix), it is also inhibited by h2 antagonists and proton pump inhibitors
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Itraconazole
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Itraconazole adverse effects
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bioavailability reduced with rifampins
congestive HD in pts w/ LVD inhibits CYP3A4 - contraindicated w/statins must take with low pH |
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which drug causes visual disturbances in the first 30min of dosing?
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Voriconazole
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what is voriconazole the drug of choice for?
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invasive aspergillosis (its voracious voriconazole)
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This azole is used topically, inhibits cyp450, may cause nausea, pruitis and hepatitis
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Ketoconazole
• First azole, not used IV any more due to high level of inhibition of human CYP450 enzymes |
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This drug inhibits B(1-3) glucan synthesis leading to a defective cell wall
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Capsofungin
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This antifungal is Used in invasive aspergillosis in patients not responsive to amphotericin B or voriconazole. Also used in candidemia
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Capsofungin
administered IV monitor for liver toxicity |
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Two polyenes
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Nystatin, Amphotercin B
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mechanism of polyenes
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o Amphipathic (i.e. having polar and non-polar regions) polyene that binds to ergosterol in the cell membrane.
The lipid portion binds to the ergosterol and the aqueous portion of the molecules forms an ion channel pore (a hydrophilic region in the membrane that allows ions to flow through) |
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Cause of polyenes adverse effects
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• Most adverse effects likely due to unwanted binding to cholesterol in cells of the host
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Amphotercin B route of admin
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IV
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Amphotercin half life
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15 days
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Amphotercin spectrum?
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very broad
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What must you warn patients about who are taking Amphotercin B
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immediate infusion reactions, fever, chills, muscle spasms, heading , vomiting, hypotension
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Long term damage of Amphotercin
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renal
At first this is reversible (decreased perfusion) Then after ~2 g total administered, you are at risk for irreversible damage (tubular injury) It’s not how much you give per day, it’s how much you give total cumulatively that’s important |
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Advantages of • Amphotericin B Lipid Formulations
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less renal toxicity
less infusion rxns |
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disadvantages of • Amphotericin B Lipid Formulations
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hepatoxicity
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Main uses of Amphotericin B
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systemic fungal infection
pregnancy |
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Uses of nystatin
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used topically and orally for GI infections. Not absorbed by GI
Nasty Nystatin is very toxic o Localized candidal infections, including oropharyngeal thrush and vaginal candida |
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This drug blocks the enzyme that normally converts squalene to a product that eventually gets converted to lanosterol, which gets converted to ergosterol.
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Terbinafine
squalane builds up and its toxic to the fungus |
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Terbinafine use
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• Keratophilic like griseofulvin, but also has direct fungicidal properties
fungal nail infections (onychomycosis) safe drug |
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Griseofulvin mechanism
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o Griseofulvin is a mitotic inhibitor because it interferes with microtubule assembly. Without that, you don’t have mitosis.
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How long is Griseofulvin used for
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• Griseofulvin becomes deposited in newly growing keratin of skin and nails, and prevents fungal infection of the new growth
o Griseofulvin is also keratophilic • Treatment must persist 2-6 weeks or more until old infected tissue is no longer present |
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Adverse effects of Griseofulvin
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• Adverse: a potential adverse that is rarely seen is allergic syndrome similar to serum sickness; hepatitis; GI disturbances
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Mechanism of Flucystosine
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Flucytosine is taken up into the cell and converted to toxic anti-metabolites that block DNA/RNA synthesis.
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What is flucytosine used in combo with
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• With amphotericin B to treat systemic Cryptococcus neoformans
• With itraconazole for chromoblastomycosis |
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flucytosine toxicity
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bone marrow depression
nasuea vommiting diarrhea |
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Antihelminth infections are generally effective against what stage of worm.
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these drugs are generally affective against the larvae form of the worm, also known as microfilariae stage in roundworms
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benzimidizoles kill what stage of the parasite
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benzimidizoles are known to be effective at killing the eggs and larvae, with some evidence for killing adult worms.
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benzimidizole mechanism
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They work by inhibiting microtubule (MT) polymerization in the organism by inhibiting assembly of beta tubulin at the same binding site as colchicine
Remember, they affect the polymerization process, not the depolymerization of MT |
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other benzimidizole actions
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• Inhibition of glucose uptake
• Inhibition of mitochondrial fumarate reductase • Uncoupling of oxidative phosphorylation So benizimidizoles affect energy production and MT synthesis. |
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2 mechanisms of resistance for benzimidizoles
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There are 2 mechanisms of resistance to benzimidizoles. Some roundworms change their B tub isotype usage, to a resistant isotype. The second mechanism is thru selection and mutation. You start selecting for mutations that select for resistant strains. For example, a point mutation in β-tubulin: phenylalanine to tyrosine at position 200 reduces drug binding to the mutant tubulin.
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What type of infections in mebenziole used for?
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Mebendizole is used for infections restricted to GI lumen because it is poorly absorbed.
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What benzimidizole is used for systemic infections
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Albendizole has a variable and erratic absorption, but it is used for systemic infections. Its absorption can be improved with fatty foods or with bile salts. It needs to undergo first pass metabolism to form the active metabolite, which is albendazole sulfoxide
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Benzo’s contraindications
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pregnant women, young children
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Benzo’s adverse effects
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GI disturbances, headache, dizziness, tiredness, Alopecia
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Mebendazole toxicity, if it gets absorbed
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Rash
agranulocytosis occipatal seizures liver enzyme abnormalities |
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Albendazole toxicity
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• GI symptoms, dizziness, headache
• Transient liver enzyme abnormalitiesaminotransferase elevations • Rash, pruritis • Rare bone marrow depression |
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CYP inhibitor effect on albendazole
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increases its levels
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What is given with Ivermectin to control inflammation following death of microfilarie
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corticosteroids
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ivermectin is effective against what form of parasite
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larva form. that is why you give it with albendazole in LF if there are adults
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Ivermectin
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Ivermectin inhibits feeding behavior by inducing tonic paralysis of muscles in the parasite. This results in inhibition of feeding behavior. Ivermectin also targets an invertebrate specific glutamate-sensitive Cl channel that is only present in invertebrates (not to be confused with the glutamate sensitive NMDA channels from the alcohol lecture!) and binding leads to opening of the channel, hyperpolarization and muscle
Paralysis. Ivermectin also binds to GABA-gated Cl- channel, that may be a cause for worm death. There is selectivity that is going on because ivermectin can also bind to human GABA-gated channels but at 100 x the concentration that binds nematode channels. |
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Ivermectin resistance
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Resistance: the worm can start expressing an ATP-dependent P-glycoprotein transporter that mediates drug efflux out from the parasite. Alternatively, specific mutations in channel may cause the drug to become ineffective.
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Ivermectin toxicity
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mild, toxicity due to Mazzoti reaction
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Ivermectin is contraindicated in
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Ivermectin is contraindicated in patients with impaired blood brain barriers, and in loa loa infected it is patients, this drug should not be used because it can lead to marked disability and encephalopathy.
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Praziquantal is the drug of choice for?
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schistosomiasis
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Praziquantal is effect against what life stage of the parasite?
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. It is effective for adult worms and immature
stages (i.e. microfilariae) |
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Praziquantal mechanism
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Increased influx of calcium across the tegument (outer covering of the worm) leads to the disruption of the tegument and antigen exposure that further will lead to a host immune response. The increased influx of calcium will also lead to muscular contraction followed by spastic paralysis. Note that in this case it is spastic paralysis, in CONTRAST to the tonic paralysis caused by ivermectin.
Resistance is not a problem with praziquantel, but know that there are two reported “resistant” populations in Northern Senegal and in Egypt, and the resistance is probably due to a mutation in voltage-gated Ca2+ channel β subunit. |
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Praziquantal contraindications
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Ocular cysticercosis- the parasite killing leads to a host response in the eye leading to irreversible damage. Ocular cysticercosis is caused by larval form of the pork tapeworm in the eye and killing the parasite in the eye may lead to irreversible damage due the to inflammatory response.
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Diethylcarbamazine effective against what stage of parasite
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adult
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Diethylcarbamazine is contraindicated in?
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river blindness
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River blindness treatmeant
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ivermectin with corticosteroids
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Diethylcarbamazine possible mechanism
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It produces paralysis in the worms, alters worm surface membrane resulting in
enhanced killing by the host immune system and stimulates platelet aggregation around membrane-damaged parasites and also may alter arachidonic acid metabolism in host immune cells to promote immune response. Finally there is worm organelle damage and apoptosis. |
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acidic or basic urine prolongs effects of DEC
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Alkalinized urine- elevate plasma levels and prolong half-life leading to increased therapeutic effects
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Diethylcarbamazine major toxicities
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Mazzoti
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Pyrantel pamoate kills what stage of parasite
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Pyrantel pamoate kills both the adult form and larva form in the intestines, not when its mirgrating
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Pyrantel pamoate mechanism
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Pyrantel works as a depolarizing neuromuscular blocker and stimulates nicotinic receptors, leading to a depolarizing block of worm nicotinic receptors at the neuromuscular junction. Pyrantel also causes release of acetylcholine and
inhibits cholinesterase, which leads to spastic paralysis in the worm, and the worm is expelled from GI tract. |