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csv-export (3) Flashcards

1
Q

What is Levodopa administered with?

A

carbidopa (it is unable to cross the BBB and inhibits the enzyme that converts L?dopa to DA, so L?dopa crosses the BBB)

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2
Q

What are indications for carbidopa?levodopa?

A

parkinsons disease (GOLD STANDARD)
parkinsonian symptoms in other diseases (lewy body dementia)
restless leg syndrome

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3
Q

which symptoms of parkinsons does carbidopa?levodopa effective in treating?

A

bradykinesia, tremor, and rigidity, NOT postural instability

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4
Q

side effects of L?dopa

A

dose dependent:
nausea/vomiting?? esp with carbidopa
orthostatitc hypotension
psychosis

or dskinesia (can be choreic or dystonic)

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5
Q

metabolism of dopamin

A

L dopa converted to dopamin intracellulary, then DA is metabolized into homovanillic acid via the enzyme monoamine oxidase

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6
Q

older dopamine agonist

newer dopamin agonist

A

bromcriptine
pramipexole and ropinirole are newer

mnuemonic: bros are old news. the new thing to do is to rope people into going to the prom

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7
Q

what is bromocriptine used for?

A

suppress secretion of prolactin from anterior pituitary, used in treatement of prolactoma and endrocrine disorder
** risk of cardiac valve fibrosis

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8
Q

what is pramipexole and ropinirole used for?

A

restless leg syndrome and parkinsons
can be started in early course of PD before Ldopa is necessry, but can be used later to to reudce Ldopa induced dyskinesias and motor fluctuations

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9
Q

side effects of dopamine agonist

A

N/V, orthostatic hypotension, visual hallucinations
bromocriptine: heart valve fibrosis
pramipexole/ropinirole: sleep attacks

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10
Q

drug interaction for ropinirole

A

uses CYP1A2 in metabolism, cannot be used with ciprofloxacin (elderly patients with PDs and UTIs)

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11
Q

MAOb inhibitors

A

selegiline and rasgiline

way to remember: people had to LINE up behind dictator MAO

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12
Q

risk for MAO inhibitors

A

because it breaks down tyrosine too, you have the risk of hypertensive crisis when taken with tyramine containing food
but selegine and rasgiline are MAOb specfic so they are safer

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13
Q

use of MAObs

side effects

A

benefit in early parkinsons disease
selegine and rasagiline are associated with nausea and heachache
selegiline can cause confusion and insomnia

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14
Q

which drugs should you not take with MAOis

A

SSRIs or tricylclic antidepressants due to risk of serotonin syndrome

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15
Q

amantadine

A

NMDA glutamate antagonist, increases DA release and blocks DA reuptake

remember: glutamate is excitatory?? a man does not get excited too often
(not great)

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16
Q

indicaitons for amantadine

A

early tremor predominant parkinsons disease or late in parkinsons to treat dyskinesia and motor fluctuations

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17
Q

side effects of amantadine

A

ankle edema, confusion, insomnia

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18
Q

COMT inhibitors

A

tolcapone, entacapone

this is a stretch?? al capone has to use computers to do all his bad guy stuff
(and he needs his hit men just like COMT inhibitors need L dopa to work)

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19
Q

what are COMT inhibitors used with?

A

its inefective wihtout carbidopa/L?dopa

used to treat pt with L dopa motor fluctuations who are experiencing end of dose wearing off” periods

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20
Q

anticholinergics

A

trihexyphenidyl and benztropine
used bc dopamine depletion produces state of cholinergic sensitivity, so anticholinergic agents improve parkinsonian symptoms

most often used for treatment of drug?induced parkinsonism

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21
Q

side effects of anticholinergics

A

dont give to elderly?? memory impairment, confusion, hallucinations
also anti?muscarinic effects: dry mouth, orthostatic hypotension, blurred vision, constipation, nausea, urinary retention

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22
Q

depolarizing neuromuscular blockers

non?depolarizing neuromuscular blockers

A

depo: succinylcholine (agonist)

non?depo: cisatracurium, pancuronium, rocuronium, vecuronium (competitive antagonist)

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23
Q

indications of NMJ blockers?

A

paralytic agents: facilitates tracheal intubaiton, prevents movements during surgery

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24
Q

side effects of succinylcholine

A

stimulates nicotinic receptors at PNS, SymNS, muscarinic receptors at SA node:
CV effects: arrhythmias, bradycardia, tachycardia, hypotension

not metabolized by acetylcholinesterase: prolonged muscle contraction, skeletal muscle depo cause hyperkalemia and myalgias (also trigger for malignant hyperthermia)

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25
Q

non depolarizing agents side effects

cistacurium, pancuronium, rocuronium, vecuronium

A

histamine release (cistracurium)
tachycardia
hypo/hypertension
vecuronium has minimal CV side effects and histamine release, so its popular in children

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26
Q

drug interactions for NMJ blockers

A

dont use with antibiotics, anticonvulsants, antiarrhythmias, cholinesterase inhibitors, Mg, Li, inhalation anesthesias

conditions: burn, muscular dystrophy, myasthenia graivs, nerve injury

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27
Q

cholinesterase inhibitors

A

pyridostigmine and neostigmine

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28
Q

indications for pyridostigmine

A

increase muscle strength in myasthenia gravis, help to combat orthostatic hypotension

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29
Q

indications for neostigmine

A

to reverse effects of non?depo muscle relaxants at end of surgery

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30
Q

side effects of pyridostigmine and neostigmine

A 
muscarinic:
GI: diarrhea, N/V, abd cramp
increase bronchial and oral secretions
miosis
diaphoresis

nictoinic: muscle cramps, fasciculations, muscle weakness if dose too high

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31
Q

DONT use neostigmine and pyridostigmine with…

A

they prevent breakdown of Ach, so they potentiate drugs with cholinergic properties

centrally acting acetylcholinesterase inhibitors
eye drops to treat glaucoma (act via Psymp)
NMJ blocking agents

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32
Q

indications for NSAIDS

A

antipyretic, analgesic, anti?inflammatory (except acetaminophen)

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33
Q

what is indomethacin used for?

A

to close patent ductus arteriosus

its one of the most potent inhibitors of COX and has adverse effects

34
Q

what do NSAIDs do biochemically?

A

inhibitors of cyclooxygenase (COX)?? enzyme that catalyses synthesis of prostaglandin from arachidonic acid
so it decreases production of prostaglandins (which play a role in pain, inflammation, fever)

35
Q

how do prostaglandins work?

A

sensitize sensory nerve endings to nocioceptive stimuli
promote tissue inflammation
induce increase in setting of body’s thermostat
but they also play important role in cytoprotection of GI tract, homeostasis, and renal homeostasis

36
Q

what is special about aspirin?

A

it irreversibly inhibits COX

37
Q

3 forms of COX:

A

Cox 1: contitutive enzyme found in constant levels in tissues?? important role in GI tract, homeostasis, renal homeostasis

COX 2: inducible enzyme?? can be upregulated during inflammation by cytokines

COX3: inhibited by acetaminophen and other analegeis/anytipyretic drugs

38
Q

where do NSAIDS work?

A

nonselective inhibitors of COX 1 and COX 2 except celecoxib?? selectively inhibits COX?2 and acetaminophen selectively inhibits COX 3

39
Q

side effects of NSAIDS:

A 
GI irritation, pepticu ulcers, incresed bleeding and bruising
hepatic toxicity (ESPECIALLY acetaminophen)
renal toxicity (EXCEPT acetaminophen)
dont use during second half of pregnancy EXCEPT acetaminophen
40
Q

drug interactions with which 4 drugs?

A

oral anticoagulants? inc risk of bleeding
lithium?? inc risk of lithium toxicity
antihypertensive agents? antagonism of antihypertensive effects
corticosteroids? inc risk of GI complications

41
Q

acetaminophen: how is it different in action and use?

A

can be used concurrently with NSAIDS (which should not be taken together)
?lacks significant antiplatelet and anti?inflammatory activity

42
Q

Reye syndrome

A

virus?infected children who are treated with aspirin

43
Q

unique features of aspirin

A

?irreversibly acetylates platelet COX?? has anti?platelet effects for 14 days
? excessive doses stimulate respiratory center in medulla, cause hyperventialion, respiratory alkalosis with an anion?gap metabolic acidosis

44
Q

treatment of salicylate poisoning

A

?induce vomiting to remove unabsorbed durg
?IV admin of sodium bicarb to counteract metabolic acidosis and enhance rate of exretion of salicylate
?admin fluids, electrolytes, supportive care

45
Q

why is acetaminophne hepatotoxic?

A

bc a small amount is converted by cytochrome p450 into a potentially hepatotoxic quinone intermediate (is ok if therapeutic dose taken)

46
Q

what is acetaminophen overdose treatment?

A

acetylcysteine

47
Q

ketolorolac

A

first NSAID available for parenteral use (IV or IM)? dental surgery

48
Q

celecoxib

A

selective COX2 can cause antiinflammaotry without GI tox, bu tit was withdrawn from the market due to increased risk of CV events

49
Q

derived from poppy; frequently abused IV for its strong euphoric effect

A

heroin

50
Q

administered by various routes for control of severe pain

A

morphine

51
Q

approximatley 100x more potent than morphine, frequently used in anesthetic practice bc it has short time to peak analgesic effect, rapid termination of effect after small bolus doses and relative CV stability
administered IV

A

fentanyl

52
Q

administered orally
?used for relief of chronic pain, treatment of opioid abstinence syndromes, treatment of heroin addiction
?racemic mix: one stereoisomer acts as NMDA receptor antagonist, one is mu agonist

A

methadone

53
Q

rapid synthetic opioid is no longer used for pain control bc metabolite toxicity resulting in seizures
** does not constrict the sphincter of oddi?? drug of choice for gall bladder pain

A

meperidine

54
Q

codeine

what is it used for?

A

analgesic, antitussive, antidiarrheal

less potent than morphine

55
Q

hydrocodone

A

most frequently used opiate in teh US; usually combined with weaker analgesic such as acetaminophen, ibuprofen, aspirin

56
Q

oxycodone

A

stucturally similar to codeine and hydrocodone, usually used for moderate to severe pain

57
Q

tramadol

A

synthetic codeine analog, well absorbed orally

2 adverse reactions: seizures and serotonin syndrome

58
Q

partial agonist

how does it work?

A

buprenorphine
high affinity but low efficacy at the mu receptor
also acts as a kappa antagoinst, making it useful in opioid deterrance, detox, maintenance

59
Q

mixed agonist?antagonist

A

nalbuphine

competitive mu receptor antagonist but exerts analgesic effects by acting as kappa receptor agonist

60
Q

indications for nalbuphine

A

for opioid induced pruritis

61
Q

opioid antagonists

A

naloxone, naltrexone

62
Q

indications for naloxone

A

treatment for opioid intoxication/overdose?? half life is an hour?? may need to be redosed

63
Q

naltrexone

A

longer half life?? 24 hours after moderate oral doses, used for treatment of alcoholism

64
Q

which drugs are used for an acute attack?

A

triptans, dihyroergotamine, analgesics (aspirin, NSAIDs, opioids), anteemetics (promethazine)

65
Q

which drugs are used for migraine prophylaxis?

A 
beta blockers (propanolol)
tricyclic antidepressants (amitriptyline)
anticonvulsants (valproate and topiramate)
66
Q

sumatriptan

A

selective agonist for serotonin 5?HT1B and 5?HT1D receptors in cranial arteries?? cause vasoconstriction and reduces neurogenic inflammation associated with activation of trigeminovascular system neuronal transmission

67
Q

side effects of sumatriptan

A

self limited: transient dizziness, tingling, chest discomfort
serious: temporary elevation of BP (vasoconstriction)
myocardial ischemia (vasoconstriction)
stroke (vasoconsriction)
?? avoided with CAD pts

68
Q

drug interactions iwth sumatriptan

A

dont co?administer sumatriptan with ergotamines or MAO inhibitors

69
Q

ergotamine derivatives

mechanism of action

A

dihydroergotamines
dual: alpha adrenergic blocker that simulates vascular smooth msucle to vaso constrict and an agonist of serotonin receptors

70
Q

use for dihydroergotamine

A

treatment for acute migraine in patients who fail triptans (nasal spray as outpatient, IV or IM in hospital)

71
Q

side effects of dihyrdoergotamine

A

self limited: rhinitis, taste disorders, nausea (need coadmin with anti?emetics)
and signifacant vasoconstriction?? myocardial and cerebrovascular ischemia

72
Q

drug interactions for dihydroergotamine

A

SO MANY== dangerous! used with great caution

73
Q

side effects of opioids:

A

nausea and vomiting?? can give mixed agonist/antagonist (nalbuphine)

constipation
pruritis?? antihistamines

74
Q

when should high dose chronic acetaminophen be avoided?

A

liver disease

75
Q

when should chronic systemic NSAIDS be avoided?

A

PUD and chronic kidney diease

also NSAIDS are are assoc with increased risk of myocardial infarction

76
Q

what are the mainstay of therapy for neuropathic pain?

A

tricyclic antidepressants, anticonvulsants, topical local anesthetics

77
Q

side effects of local anesthetics

A

hypersensitivity reaction: more common with esteres secondary to one of their metabolic products (para?aminobenzoic acid, PABA)
perioral numbness
seizures

78
Q

amides

A

lidocaine
buprivicaine
ropivacaine

79
Q

esters

A

benzocaine
procaine
tetracaine
cocaine

80
Q

what determines how rapidly the drug’s onset of action is?

A
  1. the more closely the pKa approximates the physiologic pH of tissues (7.35?7.45), faster the onset of action
  2. drugs potency (lipid solubility)
  3. tissue pH?? if pH is decreased, the drug is shifted to its ionized form and the onset of action is delayed (why local anesthetics are slower acting in inflammation due to acidic environment)
81
Q

which drugs will have longer duration of action?

A

those that are lipid soluble and heavily protein bound

82
Q

how do you treat neuropathic pain?

A

tricylclic antidepressants, anticonvulsants, topical local anesthetics

Neurodisorders (3 decks)

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