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Med School Year 2 Flash Cards > Pharmocology > Flashcards

Pharmocology Flashcards

1
Q

Mechanism of Action (MOA) of Selegiline

A

MAO-B selective inhibitor (MAO-B is the primary isoenzyme responsible for degradation of DA in the striatum).

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2
Q

Benefit of Selegiline selectivity

A

They inhibit DA metabolism in the striatum without greatly affecting degradation of catecholamines in other brain regions.
So decreased risk of hypertensive crisis due to accumulation of peripheral NE

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3
Q

what is responsible for insomnia side effectof selegiline

A

methamphetamine and amphetamine

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4
Q

Best use of selegiline

A

adjunctive agent to improve response to levodopa

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5
Q

selegiline interactions

A

TCAs, serotonin, SSRIs with an effect of serotonin syndrome (sympathetic activity with hyperthermia)

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6
Q

MOA of Rasagiline

A

MAO-B selective inhibitor; more neuroprotective than selegiline and maybe less behavioral side effects

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7
Q

Bromocriptine MOA

A

Ergot-derived dopamine agonists

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8
Q

SE (side effects) of Bromocriptine

A

Vasospasm. psychotomimetic and dyskinetic effects, profound nausea, vomiting

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9
Q

Pramipexole MOA

A

Affects D3 receptors as DA agonists, neuroprotective agent, both early and advanced PD

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10
Q

Ropinirole MOA

A

Selective D2 agonists; effective in early or advanced PD alone or combo

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11
Q

Anticholinergics

A

Biperiden
Trihexyphenidyl
Benztropine

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12
Q

Anticholinergics MOA

A

Centrally acting competitive inhibitor or muscarinic cholingeric receptors
Improve tremor and rigidity but not bradykinesia

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13
Q

SE of antimuscarinics

A

Dry mouth, urinary retention, constipation, will make demntia worse

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14
Q

CI (contraindications) of antimuscarinics

A

prostatic hyperplasia, obstructive GI disease, glaucoma

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15
Q

MOA of Amantadine

A

Facilitate DA function (poorly understood)

short lived benefits

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16
Q

SE of Amantadine

A

insomnia, restlessness, depression, GI disturbances, toxic psychosis in overdose

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17
Q

CI of Amantadine

A

seizure disorders, CHF

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18
Q

why use L-DOPA instead of DA

A

DA doesn’t penetrate the CNS but L-DOPA is the precursor that can be converted after transport by dopa decarboxylase

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19
Q

why is L-DOPA not use initially as much

A

Limited period of effectiveness of this drug

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20
Q

after substantial degeneration of DA neurons what drug could still be effective

A

direct dopamine receptor agonists becasue dont depend on functional capacity of DA neurons

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21
Q

difference between DA agonists and L-DOPA

A

DA agonists - reduce endogenous DA release and reduce need for exogenous levodopa
DA agonists should RETARD the disease progression whereas levodopa therapy would accelerate the progression (DA metabolism contributes to progression of the PD neurodegenerative process)

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22
Q

Carbidopa MOA

A

Does not cross blood brain barrier; it inhibits peripheral DA formation allowing levodopa dose to be lowered while increasing its availability to the CNS (allows levodopa dose to be lowered while increasing its availability to the CNS)

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23
Q

SE of Levodopa

A

GI: nausea and vomiting (tolerance after 4-6 weeks)
Cardio: arrhythmia due to increased catecholamines
Dyskinesia: chora, ballismus, athetosis, tics, tremor
Behavior: mood, hallucination, sleep disturbance

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24
Q

Drugs you can’t use to treat SE of levodopa

A

Phenothiazine: as antiemetics (DA receptor blocker)
Haloperidol: for dyskinesia (DA receptor blocker)
Conventional antipsychotics because anti-dopaminergic
MAOA Inhibitors

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25
Q

Limit to Levodopa Therapy

A

Loss of effectiveness: fluctuations (dyskinesia/akinesia), end of dose failure, on-off phenomena

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26
Q

COMT Inhibitor

A

Entacapone

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27
Q

Entacapone MOA

A

inhibition of dopa decarboxylase in the periphery causes activation of COMT pathway in the periphery increasing 3-O-MD (competes with levodopa absorption into brain) so the capones may smooth response to levodopa and may permit lowering of levodopa drugs
only periphery

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28
Q

Entacapone adverse effects

A

related to increased levodopa exposure

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29
Q

Advanced PD uses what

A

Combinations of levodopa/carbidopa, DA agonists, amantadine, MAO-B inhibitor

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30
Q

Drug-Induced Parkinsonism caused by

A

Antipsychotic therapy: antagonists at D2 receptors (haloperidol)
Shown as tremor, rigidity, bradykinesia

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31
Q

Treatment of drug-induced parkinsonism

A

Reduce dose or switch antipsychotic
Anticholinergics
Amantadine
NEVER L-DOPA

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32
Q

Treatment of myasthenia gravis

A

immunosuppressants: azathioprine, cyclosporine, IVIg
plasmapheresis
quaternary anticholinesterases

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33
Q

Azathioprine MOA

A

Converted to mercaptopurine: interferes with purine nucleic acid metabolism, interferes with lymphoid cell proliferation that follows Ag stimulation

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34
Q

Problem with Azathioprine and its also used with what other treatment

A

clinical benefits may not be observed for several months

often used along with thymectomy/steroids

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35
Q

Azathioprine SE

A 
bone marrow suppression
GI signs (diarrhea, vom) at high dose
36
Q

Cyclosporine MOA and why better than azathioprine

A

inhibits production of helper t cells

works quicker than azathioprine

37
Q

Cyclosporine SE

A

nephrotoxicity and HTN (dont use in patient with preexisting renal disease or HTN)

38
Q

IVIg speed of action

A

much faster than azathioprine or cyclosporine

39
Q

IVIg SE

A

During infusion: headache, muscle ache, chills

Post-infusion: fatigue, fever, nausea (1 day), migraines and allergic reactions

40
Q

what is plasmapheresis

A

procedure that filters the blood’s plasma component (centrifuged, plasma removed, cells returned to patient and diluted with fresh plasma or a substitute)
removes abnormal Ab in specific cases

41
Q

Plasmapheresis SE

A

dizziness, nausea, numbness, tingling, lightheadedness but should pass quickly
infection if central line is used

42
Q

Plasmapheesis vs immunosuppression

A

plasma is faster in onset of action

43
Q

Plasmapheresis is used for

A

myasthenic crisis
pt scheduled for thymectomy/post operatively
covering increased weakness of steroid tx

44
Q

anticholinesterases what kind of drugs

A 
Quaternary drugs (dont penetrate CNS)
Must use antimuscarinic to block excess ACh in the PNS while leaving the enhancement of nicotinic effects at skeletal muscle ACh receptors intact
45
Q

Drug used in Tensilon Test

A

Short acting anticholinesterase edrophonium

46
Q

How tensilon test works

A

Add edrophonium to see if patient gets better or worse; if better then underdosed and if worse then overdosed
Nicotinic receptors are ion channels and can’t reset until agonist dissociates so if too much anticholinesterase present then ACh is the agonists that continuous depolarization of membrane
Muscle weakness in over and under dose

47
Q

Spasmolytics

A

CNS: baclofen, diazepam, tizanidine, riluzole, gabapentine
PNS: dantrolene

48
Q

What is spasticity and what are the causes of spasticity

A

Velocity-dependent increase in tonic stretch reflexes cause hyperactive reflex, spasms, weakness and loss of dexterity; spinal injury, stroke, ALS, MS, cerebral palsy

49
Q

Baclofen MOA

A 
Centrally acting spasmoclytic
GABA analogue (GABA-B receptor agonists) so inhibits release of excitatory amino acids and substance P

More effective in spinal and MS and ALS

50
Q

SE of Baclofen

A

drowsiness, lassitude, ataxia, muscular weakness, constipation, urinary retention

51
Q

Diazepam MOA

A

Centrally acting spasmolytic
MS, spinal lesions, NOT ALS
increases GABAergic neurotransmission leading to enhanced presynaptic inhibition

52
Q

Tizanidine MOA

A

Centrally acting spasmolytic
Mechanism not understood
reinforces inhibitory effects in spinal cord, reduces pain conduction
Used for spasms, MS

53
Q

SE of Tizanidine

A

Result from alpha-2 agonist adrenergic effects (hypotension, drowsiness)

54
Q

Riluzole MOA

A

Centrally acting spasmolytics
Tx of ALS (extends survival and tiem to tracheostomy)
Mechanism not clear

55
Q

SE of Riluzole

A

GI hemorrhage
Sepsis
Convulsion
Neoplasm

56
Q

CI of Riluzole

A

Lactation

57
Q

Gabapentin MOA

A

Centrally acting spasmolytic
Antiseizure drug, MS patients
Peripheral neuropathies for pain reduction

58
Q

Danrolene MOA

A

Peripheral spasmolytic

Skeletal muscle relaxant, interferes with release of Ca ions from SR

59
Q

Uses of Dantrolene

A

Used: cerebral spasticity, not ALS, malignant hyperthermia, external sphincter hypertonicity

60
Q

SE of Dantrolene

A

Muscle weakness

Dose related hepatocellular injury

61
Q

Types of Headaches to Tx pharmacologically

A

Tension headaches
Migraine headaches
Cluster headaches

62
Q

Acute treatment for tension headache

A

NSAIDs alone (aspirin, acetaminophen, ibuprofen)
NSAIDs + caffeine
NSAIDs + a barbiturate
NSAIDs + butalbital + caffeine

(overuse of NSAIDs provokes headache)

63
Q

NSAID MOA

A

Inhibit PG synthesis
Analgesis (mild to moderate pain)
Anti-inflammatory
Cause gastric irritation and GI bleeding, cardiac events

64
Q

Butalbital MOA

A

Barbiturate (sedative-hypnotic family)
Facilitate GABA neurotransmission
Sedation/anxiolytic

65
Q

Butalbital CI

A

Alcohol
Significant dependence potential if doses higher than prescribed are taken
Rebound headaches from withdrawal

66
Q

Caffeine MOA

A

Competitive antagonist at adenosine receptor

used + NSAID

67
Q

SE of Caffeine

A

Palpitations and anxiety

Termination of caffeine in patient who are dependent causes headaches

68
Q

Prophylactic Tx for Tension Headache

A

Older antidepressants: amitriptyline, doxepin, imipramine (not SSRIs) –> takes 2 to 6 weeks

69
Q

Amitriptyline and doxepin MOA and SE

A

anticholinergic
SE: dry mouth, urinary retention, tachycardia, CNS intoxication, sedation and drowsiness
Amitriptyline is deadly in overdose, alters cardiac electrical properties

70
Q

Tx of Migraine

A

Anti-inflammatory
5-HT1b/d agonists
Ergotamines
Dopamine antagonists

71
Q

5-HT1b/d or Triptans

A 
Agonists
Rizatriptan
Zolmitriptan
Sumatriptan
Naratriptan
Frovatriptan
72
Q

Migraine tx problems

A

Short t1/2 life that headache may re-emerge
Slowest onset agent is least efficacious
Route of admin impacts speed of onset (mild - oral; moderate - oral, intranasal, parenteral; severe - parenteral)

73
Q

5HT1 Mechanism

A

Triptans: act a presynaptic trigeminal nerve endings to inhibit release of vasodilating peptides (substance P and CGRP)
Vasoconstrictor

74
Q

Triptans SE

A 
Altered sensation (tingling, warmth, dizziness, muscle weakness)
Pain at injection site 
Chest discomfort (vasoconstriction) - don't use if have CAD, prinzmetal angina, uncontrolled HTN
75
Q

Ergot Alkaloids MOA

A

Ergotamine
Dihydroergotamine

5HT1b/d stimulation
Only if used early in attack

76
Q

Ergot Alkaloid SE

A

Nausea
Alpha agonist effects: constrict blood vessel
Stim other tryptamine receptors - hallucinations, bizarre behavior, gangrene, abortion

77
Q

D2 Antags to treat migraine

A

Chlorpromazine
Prochlorperazine
Metoclopramide
Use for moderate migraines with nausea and severe migraines IM

78
Q

SE of DA Antag

A

Rare but disabling
Parkinsonism
Dystonias
Neuroleptic Malignant Syndrome

79
Q

Types of dystonias

A

Torticollis: muscle contraction leading to twisting of the neck w/ unnatural head position
Facial distortion
Tongue protrusion
Dysarthria: imperfect articulation of speech
Opisthotonus: whole body spasm
Scoliosis: bending of the spine
Oculogyric crisis: rapid eye movement
Akathisia: inability to sit, pacing, restlessness

80
Q

Prophylaxis of Migraine

A 
Beta blockers: propranolol and timolol
Verapamil
Valproate
Topiramax
Methysergide
Older antidepressants: amitriptyline
81
Q

Methysergide interactions

A

interacts with numerous 5HT receptors (antags and partial agonists)

82
Q

Prophylaxis of migraine work at these receptors best

A

5HT2a and 5HT2c

83
Q

Methysergide SE

A

GI burning, diarrhea, nausea, vom
Can’t be given with triptans because HTN and vasospasm risk
Long term tx: inflammatory fibrosis (retroperitoneal fibrosis, pleuropulmonary fibrosis, coronary fibrosis) thats reversible

84
Q

Predominant tx of cluster headache

A

Prophylaxis: prednisone, lithium (good for chronic form), methysergide, ergotamine, valproate, verapamil

85
Q

Bout of cluster headaches tx with

A

oxygen

triptans

86
Q

Lithium toxicity

A 
low therapeutic index
polydipsia/polyuria
tremor
gastric distress
edema
weight gain
hypothyroidism
cardiac conduction problems
mild cognitive impairment

Med School Year 2 Flash Cards (18 decks)

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