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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
Limit to Levodopa Therapy
Loss of effectiveness: fluctuations (dyskinesia/akinesia), end of dose failure, on-off phenomena
26
COMT Inhibitor
Entacapone
27
Entacapone MOA
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
28
Entacapone adverse effects
related to increased levodopa exposure
29
Advanced PD uses what
Combinations of levodopa/carbidopa, DA agonists, amantadine, MAO-B inhibitor
30
Drug-Induced Parkinsonism caused by
Antipsychotic therapy: antagonists at D2 receptors (haloperidol) Shown as tremor, rigidity, bradykinesia
31
Treatment of drug-induced parkinsonism
Reduce dose or switch antipsychotic Anticholinergics Amantadine NEVER L-DOPA
32
Treatment of myasthenia gravis
immunosuppressants: azathioprine, cyclosporine, IVIg plasmapheresis quaternary anticholinesterases
33
Azathioprine MOA
Converted to mercaptopurine: interferes with purine nucleic acid metabolism, interferes with lymphoid cell proliferation that follows Ag stimulation
34
Problem with Azathioprine and its also used with what other treatment
clinical benefits may not be observed for several months | often used along with thymectomy/steroids
35
Azathioprine SE
``` bone marrow suppression GI signs (diarrhea, vom) at high dose ```
36
Cyclosporine MOA and why better than azathioprine
inhibits production of helper t cells | works quicker than azathioprine
37
Cyclosporine SE
nephrotoxicity and HTN (dont use in patient with preexisting renal disease or HTN)
38
IVIg speed of action
much faster than azathioprine or cyclosporine
39
IVIg SE
During infusion: headache, muscle ache, chills | Post-infusion: fatigue, fever, nausea (1 day), migraines and allergic reactions
40
what is plasmapheresis
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
Plasmapheresis SE
dizziness, nausea, numbness, tingling, lightheadedness but should pass quickly infection if central line is used
42
Plasmapheesis vs immunosuppression
plasma is faster in onset of action
43
Plasmapheresis is used for
myasthenic crisis pt scheduled for thymectomy/post operatively covering increased weakness of steroid tx
44
anticholinesterases what kind of drugs
``` 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
Drug used in Tensilon Test
Short acting anticholinesterase edrophonium
46
How tensilon test works
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
Spasmolytics
CNS: baclofen, diazepam, tizanidine, riluzole, gabapentine PNS: dantrolene
48
What is spasticity and what are the causes of spasticity
Velocity-dependent increase in tonic stretch reflexes cause hyperactive reflex, spasms, weakness and loss of dexterity; spinal injury, stroke, ALS, MS, cerebral palsy
49
Baclofen MOA
``` 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
SE of Baclofen
drowsiness, lassitude, ataxia, muscular weakness, constipation, urinary retention
51
Diazepam MOA
Centrally acting spasmolytic MS, spinal lesions, NOT ALS increases GABAergic neurotransmission leading to enhanced presynaptic inhibition
52
Tizanidine MOA
Centrally acting spasmolytic Mechanism not understood reinforces inhibitory effects in spinal cord, reduces pain conduction Used for spasms, MS
53
SE of Tizanidine
Result from alpha-2 agonist adrenergic effects (hypotension, drowsiness)
54
Riluzole MOA
Centrally acting spasmolytics Tx of ALS (extends survival and tiem to tracheostomy) Mechanism not clear
55
SE of Riluzole
GI hemorrhage Sepsis Convulsion Neoplasm
56
CI of Riluzole
Lactation
57
Gabapentin MOA
Centrally acting spasmolytic Antiseizure drug, MS patients Peripheral neuropathies for pain reduction
58
Danrolene MOA
Peripheral spasmolytic | Skeletal muscle relaxant, interferes with release of Ca ions from SR
59
Uses of Dantrolene
Used: cerebral spasticity, not ALS, malignant hyperthermia, external sphincter hypertonicity
60
SE of Dantrolene
Muscle weakness | Dose related hepatocellular injury
61
Types of Headaches to Tx pharmacologically
Tension headaches Migraine headaches Cluster headaches
62
Acute treatment for tension headache
NSAIDs alone (aspirin, acetaminophen, ibuprofen) NSAIDs + caffeine NSAIDs + a barbiturate NSAIDs + butalbital + caffeine (overuse of NSAIDs provokes headache)
63
NSAID MOA
Inhibit PG synthesis Analgesis (mild to moderate pain) Anti-inflammatory Cause gastric irritation and GI bleeding, cardiac events
64
Butalbital MOA
Barbiturate (sedative-hypnotic family) Facilitate GABA neurotransmission Sedation/anxiolytic
65
Butalbital CI
Alcohol Significant dependence potential if doses higher than prescribed are taken Rebound headaches from withdrawal
66
Caffeine MOA
Competitive antagonist at adenosine receptor | used + NSAID
67
SE of Caffeine
Palpitations and anxiety | Termination of caffeine in patient who are dependent causes headaches
68
Prophylactic Tx for Tension Headache
Older antidepressants: amitriptyline, doxepin, imipramine (not SSRIs) --> takes 2 to 6 weeks
69
Amitriptyline and doxepin MOA and SE
anticholinergic SE: dry mouth, urinary retention, tachycardia, CNS intoxication, sedation and drowsiness Amitriptyline is deadly in overdose, alters cardiac electrical properties
70
Tx of Migraine
Anti-inflammatory 5-HT1b/d agonists Ergotamines Dopamine antagonists
71
5-HT1b/d or Triptans
``` Agonists Rizatriptan Zolmitriptan Sumatriptan Naratriptan Frovatriptan ```
72
Migraine tx problems
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
5HT1 Mechanism
Triptans: act a presynaptic trigeminal nerve endings to inhibit release of vasodilating peptides (substance P and CGRP) Vasoconstrictor
74
Triptans SE
``` 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
Ergot Alkaloids MOA
Ergotamine Dihydroergotamine 5HT1b/d stimulation Only if used early in attack
76
Ergot Alkaloid SE
Nausea Alpha agonist effects: constrict blood vessel Stim other tryptamine receptors - hallucinations, bizarre behavior, gangrene, abortion
77
D2 Antags to treat migraine
Chlorpromazine Prochlorperazine Metoclopramide Use for moderate migraines with nausea and severe migraines IM
78
SE of DA Antag
Rare but disabling Parkinsonism Dystonias Neuroleptic Malignant Syndrome
79
Types of dystonias
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
Prophylaxis of Migraine
``` Beta blockers: propranolol and timolol Verapamil Valproate Topiramax Methysergide Older antidepressants: amitriptyline ```
81
Methysergide interactions
interacts with numerous 5HT receptors (antags and partial agonists)
82
Prophylaxis of migraine work at these receptors best
5HT2a and 5HT2c
83
Methysergide SE
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
Predominant tx of cluster headache
Prophylaxis: prednisone, lithium (good for chronic form), methysergide, ergotamine, valproate, verapamil
85
Bout of cluster headaches tx with
oxygen | triptans
86
Lithium toxicity
``` 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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